Following the Scottish example, England has piloted drug courts using specially trained magistrates to closely supervise treatment-based community sentences. This initial report found no major glitches but low throughput and uncertain cost-benefits.

Summary The Dedicated Drug Court framework for England and Wales provides for specialist courts which exclusively handle cases relating to drug misusing offenders from conviction through sentence to completion (or breach) of a community order with a Drug Rehabilitation Requirement (DRR). Two magistrates’ courts (Leeds Magistrates’ Court and West London Magistrates’ Court) have been piloting drug courts implemented in line with the Ministry of Justice’s framework.

The critical factors for implementation success are an understanding of local context and scale of need, the enthusiasm of the local judiciary and partner agencies, good partnership working, availability of resources to deliver the drug court and its associated treatment services, the depth of understanding by all staff of offender motivation and, in particular, recognition of the points at which an offender is most likely to make progress in reducing or stopping drug use. Continuity of judiciary is key to successful implementation of a drug court. It provides the focus for communication between the court and the offender and across magistrate panels. Continuity of judiciary was a strong planned feature of both courts. Based on analysis undertaken with data from the Leeds pilot, there is strong evidence that continuity of magistrates has a statistically significant impact on several key drug court outcomes. Greater continuity of magistrates experienced by offenders is associated with their being less likely to miss a court hearing, more likely to complete their sentence, and less likely to be reconvicted.

Break-even analysis showed that (compared to normal adjudication) an extra 8% of offenders seen by the courts would need to stop taking drugs for five years or more following completion of the sentence to provide a net economic benefit to the wider society, and 14% in order to provide a net economic benefit to the criminal justice system. A robust quantification of impact was not possible because of the difficulties in collecting sufficient data on a comparison group of offenders not processed through drug courts.

Findings Commissioned by the UK Ministry of Justice, the report describes the implementation rather than the outcomes of England’s pilot drug courts. In line with international understandings, the courts were intended to specialise in drug-related offenders, presided over by sentencers specially trained for this task who order treatment-based sentences and closely supervise the offender’s progress, aided by regular tests for illegal drug use. The aim is maximise the rehabilitative impact of the sentence by increasing compliance and engagement with treatment through criminal justice pressure (ultimately the prospect of receiving a more typical punishment-based sentence if the drug court’s order fails) and rewards (of which one of the most powerful seems to be the unfamiliar experience of being congratulated by a judge or magistrate).

The report identified no critical fault lines in the implementation of the courts. However, these were particularly promising sites: the Leeds court built on a pre-existing system and in London, court staff were enthusiastic about the proposal and had already been working towards creating a drug court. Nevertheless, offender throughput was lower than expected. Over the 17 months of the evaluation, the London court sentenced just 60 new offenders while in Leeds the total was 276. Low throughput raised costs per offender. Compared to a standard 12-month drug rehabilitation requirement order implemented through normal adjudication, supervising the order through the drug courts cost £4633 extra per offender.

With no comparison group of normally adjudicated offenders, the evaluation was unable to say whether this was money well spent. They were, however, able to calculate the drug use reductions the courts would have to ‘buy’ in order to meet their extra costs – as noted in the abstract, the answer was 8% of offenders ceasing drug use for at least five years compared to the numbers doing so on a normally adjudicated drug rehabilitation requirement order. This calculation though excludes the base costs of normal adjudication and of a normally supervised drug rehabilitation requirement order. This seems to mean that the 8% would also have to be over and above the proportion of offenders who remain abstinent after normal judicial processing. The report gives no indication of how much success would be needed to match the total costs incurred by the criminal justice system in implementing all the elements of a drug court-supervised drug rehabilitation requirement order.

The report’s emphasis on offenders seeing the same magistrate(s) for their sentencing and throughout subsequent progress reviews is backed by evidence from Leeds that continuity is substantially associated with better compliance and drug use and crime outcomes. Steps were taken to reduce the risk that continuity was caused by high compliance and good progress rather than vice versa. However, without actually allocating offenders at random to see or not see the same magistrates, it is impossible to eliminate this possibility. Assuming the effect was real, it is of concern that organising continuity was a challenge, and especially so for ‘breach’ hearings dealing with unacceptable failures to comply with the order, which national regulations required to occur within a set period. Unfortunately, these crucial junctures are just when continuity is most needed, requiring an understanding of whether the offender will do better on a revised order, or the order has failed and should be revoked, often resulting in imprisonment.

A final caution over any such report is that some leading criminologists accuse the UK government of manipulating and distorting criminological research for political gain, to the point where the professor of criminology at the Open University has called for a boycott of government-commissioned work. The featured report was commissioned by the UK Ministry of Justice, a ministry carved out in part from the Home Office, one of the main targets of these accusations.

Scotland preceded England in formally piloting drug courts in Glasgow from 2001 and in Fife the following year. As in England, implementation was not entirely smooth but better than might have been expected. There was a high but it was thought acceptable failure rate, probably aided by Scotland’s more flexible application of drug treatment and testing orders, predecessors to the drug rehabilitation requirements used later by the English courts. However, crime impacts were questionable. Within one year 50% of drug court offenders had been reconvicted and within two years 71%, and the average frequency of reconvictions only slightly dipped in the two years after the order was imposed compared to the two years before. There was no clear crime-reduction benefit from supervising the orders through the drug courts (at an average cost of nearly £18,500 per order) as opposed to normal adjudication. But, as in England, the costs imposed on society by persistent, high-rate offending and drug-related mortality and morbidity, are such that even modest improvements might be cost-beneficial overall.

International experience and research relating to drug courts suggests it is important for courts to emphasise rewards as well as punishments, see offenders frequently enough to apply these swiftly in response to progress, deploy a range of rewards and sanctions short of revocation which are consistently applied, have a strong and sure ultimate sanction when the programme fails, make these consequences absolutely clear to offenders, have rapid access to a range of treatment options, maintain continuity in the judge dealing with the case, and to attend to the range of the individual’s needs. Willingness to continue despite some initial offending makes the structure imposed by stringent requirements and monitoring a positive feature rather than one which leads most offenders to fail. Consistent judicial supervision, the fact that this forces addicts (back) in to treatment, and drug testing which provides a shared measure of how treatment is progressing, probably all play their parts.

Source: www.findings.org.uk March 2009

   Adopted children are twice as likely to abuse drugs if their biological parents did too, suggesting that genetics do indeed play a role in the development of substance abuse problems.However, trouble or substance abuse in the adoptive family is also a risk factor, according to a study of more than 18,000 adopted children inSweden.

This suggests that both environment and biological family history can influence a child’s likelihood of future drug use.”For someone at low genetic risk, being in a bad environment conveys only a modestly increased risk of drug abuse,” says lead study author Dr. Kenneth S. Kendler, professor of psychiatry and human genetics at Virginia Commonwealth University in Richmond. “But if you are at high genetic risk, this can put your risk for drug abuse much higher.”

 The findings should be reassuring to adoptive parents, and to people who are thinking about adopting, because they show the importance of a positive environment, experts say.  “A child who is adopted, just like a child who is biological, does carry a certain genetic risk, but this shows that the environment they’re being raised in and how their genetic risk interacts with that is probably much more important for the potential development of any disease, including substance abuse and dependence,” says Dr. Lukshmi Puttanniah, director of child and adolescent psychiatry at Lenox Hill Hospital in New York, who was not involved with the study.

 The study, published this week in the Archives of General Psychiatry, included 18,115 children born inSwedenbetween 1950 and 1993 and later adopted. Overall, 4.5% of adopted individuals had drug-abuse problems as identified by Swedish medical, legal and pharmacy records, versus 2.9% of people in the general population.

But 8.6% of those who had at least one biological parent who abused drugs had their own abuse problems versus 4.2% of adoptees whose biological parents did not have a history of drug abuse.

 Adopted children had roughly double the risk of drug abuse if their biological full- or half-sibling had similar issues. But the risk was about the same if their adoptive siblings — those who had no biological connection to them — had abused drugs.

In general, trouble in the adoptive family, such as parental divorce, death, criminal activity, and alcohol problems was linked to a higher risk of drug abuse in the adopted child. There are a number of things adoptive parents — and biological parents for that matter — can do to minimize the risk of their children experimenting with drugs and alcohol, say experts.

“If parents are responsible, are monitoring their children’s behavior, paying attention to them, spending time with them, that’s going to have a positive effect and protect them from going down the path of alcohol and drug abuse,” says Maria M. Wong, Ph.D., associate professor of psychology at Idaho State University in Pocatello.

 ”Knowing the medical history of children who will be adopted is always a good idea, however . . . genes are not destiny,” adds Dr. Wilson Compton, director of the division of epidemiology, services, and prevention research at the National Institute on Drug Abuse, which helped fund the study. “This study shows that in a healthy, safe, and secure environment with little exposure to drug abuse and other problems in the adoptive relatives, even children with multiple drug abusing biological relatives do much better than those whose adoptive families don’t provide such advantages.”

But the current study omitted some factors, some of which might be important to current and future adoptive parents.For instance, the researchers didn’t know when the adopted child joined his or her new family.

“Children who are adopted at age 5 are in a different risk category from newborns,” says Dr. Lisa Albers, director of the Adoption Program at Children’s Hospital Boston.

 And the study probably underestimates the number of drug users given that drug abuse was identified only if a person had had a brushwith the law, had been hospitalized or had a certain prescription history. That sets a “relatively high bar,” Albers says.  In any event, rates of drug abuse in theU.S.tend to be higher than inSwedenor other Scandinavian countries, says Kendler.  Also, researchers didn’t take into account changes in adoption in the last 50 years.

 For instance, many more children placed for adoption today have birth parents with a history of substance abuse compared with 50 years ago, says Albers.

On the other hand, the medical community has moved forward “light years” in its understanding and ability to handle other risk factors for substance abuse, such as ADHD, impulse control challenges, mental health concerns like anxiety or significant trauma, which may have occurred prior to the child coming into the family — all of which are risk factors for substance abuse, says Albers.

“If we have parents with a history of drug abuse, we can probably do better . . .. if we address the early signs that put the child at risk for drug abuse,” says Albers.

“Joining an adoptive family that is supportive even if you’re genetically at high risk is a very positive thing,” she adds.

Source:   www.health.com  5th March 2012

  Context Marijuana smoke contains many of the same constituents as tobacco smoke, but whether it has similar adverse effects on pulmonary function is unclear.

 Objective To analyze associations between marijuana (both current and lifetime exposure)and pulmonary function.

Design, Setting, and Participants The Coronary Artery Risk Development in Young Adults (CARDIA) study, a longitudinal study collecting repeated measurements of pulmonary function and smoking over 20 years (March 26, 1985-August 19, 2006) in a cohort of 5115 men and women in 4 US cities. Mixed linear modelling was used to account for individual age-based trajectories of pulmonary function and other covariates including tobacco use, which was analyzed in parallel as a positive control. Lifetime exposure to marijuana joints was expressed in joint-years, with 1 joint-year of exposure equivalent to smoking 365 joints or filled pipe bowls.

Main Outcome Measures Forced expiratory volume in the first second of expiration (FEV1) and forced vital capacity (FVC).

Results Marijuana exposure was nearly as common as tobacco exposure but was mostly light (median, 2-3 episodes per month). Tobacco exposure, both current and lifetime, was linearly associated with lower FEV1 and FVC. In contrast, the association between marijuana exposure and pulmonary function was nonlinear (P_.001): at low levels of exposure, FEV1 increased by 13 mL/joint-year (95% CI, 6.4 to 20; P_.001) and FVC by 20 mL/joint-year (95% CI, 12 to 27; P_.001), but at higher levels of exposure, these associations levelled or even reversed. The slope for FEV1 was −2.2 mL/joint-year (95% CI, −4.6 to 0.3; P=.08) at more than 10 joint-years and −3.2 mL per marijuana smoking episode/mo (95% CI, −5.8 to −0.6; P=.02) at more than 20 episodes/mo. With very heavy marijuana use, the net association with FEV1 was not significantly different from baseline, and the net association with FVC remained significantly greater than baseline

(eg, at 20 joint-years, 76 mL [95% CI, 34 to 117]; P_.001).

Conclusion Occasional and low cumulative marijuana use was not associated with adverse effects on pulmonary function.

JAMA. 2012;307(2):173-181 www.jama.com

RESPONSE TO ASSOCIATION BETWEEN MARIJUANA EXPOSURE AND PULMONARY FUNCTION OVER 20 YEARS STUDY

 1. Research validity

The study appears well designed and there is no reason to think it was not done according to description.  But they only look at limited lung function parameters FeV1 and FVC. No microscopic analysis of tissue was done and certainly other areas of potential damage were not addressed. 

The investigators also admit that there were limitations in the study.  A significant problem is that cannabis use is often difficult to quantify precisely due to smokers sharing joints, different inhalation techniques and different ways of smoking cannabis including joints, pipes and bongs.  By comparison, the average amount of tobacco in a commercial cigarette of standard length is 1 gram.  Therefore, the comparison between nicotine smokers and marijuana smokers is moot because the amount of smoke exposure in the two groups was vastly different and a comparable marijuana cohort was not recruited.

Clearly there was a reduction in lung function between 7-10 joint-years, but significant reductions at more than 20 joints per month.

The increased function was found with under 10 joint-years – that could be 1 joint per day for 10 years or 2 joints per week for 30 years. Numerous other studies have demonstrated damage- I am including some that are attached.

What is telling is that they did not have heavy users but still found evidence to suggest that heavy use causes lung damage.  There is no accounting for changing patterns of use over the life time and lung recovery potential, which is great.

A key sentence is occasional and low cumulative marijuana use is not associated with adverse effects on pulmonary function.  Occasional and low tobacco use is also not associated with adverse consequences. They did not have enough heavy marijuana users to draw conclusions of detrimental effects on pulmonary function. If nicotine smokers are using about 8-9 cigarettes/day and marijuana users 2-3 episodes in past 30 days, this is not really a valid comparison.

The authors note that “some investigators have proposed that the deep inspiratory manoeuvers practiced by marijuana smokers could stretch the lungs resulting in larger lung volumes.”  It is true that cannabis smokers inhale more deeply, hold their breath for longer, and perform Valsalva manoeuvre at maximal breath hold which could result in a stretching of the lungs.  However, it is important to note that cannabis is usually smoked without a filter and to a shorter butt length, and the smoke is a higher temperature than tobacco, thus exposing the cannabis smoker to greater levels of carboxyhaemoglobin and tar inhaled when compared with a tobacco cigarette of the same size. (Tashkin)

Another speculative possibility they note is “strengthening of chest wall musculature or another ‘training’ effect that allows marijuana users to inspire more fully (closer to total lung capacity) on spirometry testing.” The functional effects of this association on lung health or respiratory function in daily life are unclear.  “Hypothetically speaking, a positive effect from marijuana in the short term (the stretch/training effect) and a negative effect in the long term (damage from smoke exposure) should result in a nonlinear association as observed. According to this explanation, the predominant effect for FEV1 at very high exposure (more than 40 joint-years) reflects cumulative damage

Their findings suggest an accelerated decline in pulmonary function with heavy use and a resulting need for caution and moderation when marijuana use is considered.  Additionally, marijuana potency has increased dramatically in recent years and this study was initiated 20 years ago. The authors conclude that they did find an association with calendar time, but this assumption is questionable because the people were recruited a long time ago and their smoking habits (dose/unit) may or may not remain stable.

  2. What this study lacked

This study did not compare light cigarette smokers (2-3 cigarettes in past 30 days) with light marijuana smokers (2-3 episodes in past 30 days) (or heavy with heavy). They provide no comforting conclusions. Lung capacity (how much air you can force your lungs to exhale) was the only measure presented. Deep inhalation may have increased the ability of lungs to store more air and enable exhalation. But studies have shown that marijuana smoking is associated with large airway inflammation, symptoms of bronchitis, increased airway resistance and lung hyperinflation. They should have availed themselves of more lung tests than simply “blowing out air.”

There are many other studies that have demonstrated health concerns about smoking marijuana.  (Below are summaries of some studies.  A fuller report of these and other studies are available upon request.)

S Aldington, et al.  2007. Effects of cannabis on pulmonary structure, function and symptoms. Thorax Online First.

 METHODS: 339 adults from the Greater Wellington region.  Their respiratory status was assessed using high-resolution CT (HRCT) scanning, pulmonary function tests and a respiratory and smoking questionnaire.  Associations between respiratory status and cannabis use were examined by analysis of covariance and logistic regression.

 RESULTS: A dose-response relationship was found between cannabis smoking and reduced force expiratory volume in 1 s to forced vital capacity ratio and specific airways conductance, and increased total lung capacity.  Cannabis smoking was associated with decreased lung density on HRCT scans.

 CONCLUSIONS:  Smoking cannabis was associated with a dose-related impairment of large airways function resulting in airflow obstruction and hyperinflation.  In contrast, cannabis smoking was seldom associated with macroscopic emphysema.  The most important finding was that one joint of cannabis was similar to 2.5-5 tobacco cigarettes in terms of causing airflow obstruction.  This dose equivalence is consistent with the reported 3-5 fold greater levels of carboxyhaemoglobin and tar inhaled when smoking a cannabis joint compared with a tobacco cigarette of the same size.  The findings suggest that the predominant effects of cannabis on pulmonary structure, function and symptoms are in causing the symptoms of wheezing, cough, chest tightness and sputum production, large airways obstruction and hyperinflation, but not emphysema.

 S Aldington, et al.  2008.  Cannabis use and risk of lung cancer: a case-control study.  European Respiratory Journal.

 METHODS:  A case-control study of lung cancer in adults greater than ≤0 years of age was conducted in eight district health boards inNew Zealand.  In total, 79 cases of lung cancer and 324 controls were included in the study.  The aim of the study was to determine the risk of lung cancer associated with cannabis smoking.

 RESULTS: The risk of lung cancer increased 8% for each joint-year of cannabis smoking, after adjustment for confounding variables included cigarette smoking, and 7% for each pack-year of cigarette smoking, after adjustment for confounding variables including cannabis smoking.  The highest percentile of cannabis use was associated with an increased risk of lung cancer, after adjustment for confounding variables including cigarette smoking.

 CONCLUSION:  The result indicated that long-term cannabis use increases the risk of lung cancer in young adults.  The results also provided a quantification of the effect of cannabis smoking: the increased risk for each joint-year of cannabis smoking was similar to that for each pack-year of cigarettes.  In other words, the risk of lung cancer increased by 8% for each joint-year of cannabis exposure after adjustment for confounding variables, including tobacco smoking.

 D Moir, et al.  2008.  A Comparison of Mainstream and Sidestream Marijuana and Tobacco Cigarette Smoke Produced under Two Machine Smoking Conditions. American Chemical Society.

 METHODS:  In this study a systematic comparison of the smoke composition of both mainstream and side stream smoke from marijuana and tobacco cigarettes prepared in the same way and consumed under two sets of smoking conditions was undertaken.  The study examined the suite of chemicals routinely analyzed in tobacco smoke.

 RESULTS:  As expected, the results showed qualitative similarities with some quantitative differences.  Ammonia was found in mainstream marijuana smoke at levels up to 20-fold greater than that found in tobacco.  Hydrogen cyanide, and some aromatic amines were found in marijuana smoke at concentrations 3-5 times those found in tobacco smoke.  Mainstream marijuana smoke contained selected poly7chclic aromatic hydrocarbons (PAHs) at concentrations lower than those found in mainstream tobacco smoke, while the reverse was the case for side stream smoke, with PAHs present at higher concentrations in marijuana.

 CONCLUSION:  The presence, in both mainstream and side stream smoke of marijuana cigarettes, of known carcinogens and other chemicals implicated in respiratory diseases was confirmed.

 BMoore.  2004.  Respiratory Effects of Marijuana and Tobacco Use in aU.S.Sample.  JGIM.

 METHODS:  This study examined respiratory effects of marijuana and tobacco use in a nationally representative sample while controlling for age, gender, and current asthma.  The Design was analysis of the nationally representative third National Health and Nutrition Examination Survey (NHANES III) and the Setting wasU.S.households.  Participants were a total of 6,728 adults age 20-59 who completed the drug, tobacco, and health sections of the NHANES III questionnaire in 1988 and 1994.  Current marijuana use was defined as self-reported 100+ lifetime use and at least 1 day of use in the past month. 

 RESULTS: Self-reported respiratory symptoms included chronic bronchitis, frequent phlegm, shortness of breath, frequent wheezing, chest sounds without a cold, and pneumonia.  A medical exam also provided an overall chest finding and measure of reduced pulmonary functioning.  Marijuana use was associated with respiratory symptoms of chronic bronchitis, coughing on most days, phlegm production, wheezing, and chest sounds without a cold.

 CONCLUSION:  The impact of marijuana smoking on respiratory health has some significant similarities to that of tobacco smoking.

 SW Hii, et al. 2007.  Bullous lung disease due to marijuana.  Asian Pacific Society of Respirology.

 METHODS:  A report on a series of 10 patients (mean age 41 ± 9 years, eight male, two female), who presented over a period of 12 months with new respiratory symptoms and who admitted to regular chronic marijuana smoking (≥ 1 year continuously).  Symptoms on presentation were dyspnoea, pneumothorax, and chest infection.

 RESULTS:  High-resolution CT revealed symmetrical, variably sized, emphysematous bullae in the upper and mid zones.  However, the CXR was normal in four patients and lung function was normal in five.

 CONCLUSION:  Marijuana smoking leads to asymmetrical bullous disease, often in the setting of normal CXR and lung function.  In subjects who smoke marijuana, these pathological changes occur at a younger age (approximately 20 years earlier) than in tobacco smokers.

  Another example: Ann Epidemiol. 2010 Apr;20(4):289-97. Associations between duration of illicit drug use and health conditions: results from the 2005-2007 national surveys on drug use and health. Han B, Gfroerer JC, Colliver JD.

 METHODS: Data from respondents aged 35 to 49 (N = 29,195) from the 2005-2007 National Surveys on Drug Use and Health (NSDUH) were analyzed.

RESULTS: The prevalence rates of a broad range of health conditions by duration of use of specific illicit drug among persons 35 to 49 years of age in the United States were estimated and compared: Positive associations between duration of marijuana use and anxiety, depression, sexually transmitted disease (STD), bronchitis, and lung cancer were found. 

  3.  Impact on the debate over medical marijuana

 The use of marijuana daily for “chronic medical conditions” or for psychoactive purposes is not captured by this study and therefore cannot inform the public about the ongoing “medical marijuana” effects and effects of heavy marijuana use.

 Marijuana is being used by many individuals on a daily (and several times a day) as a so-called medicine for prolonged and indefinite periods of time.   The authors’ own conclusions were that they did not have enough people who were heavy users (e.g. daily) to draw any conclusions and the trend towards accelerated decline in lung capacity was seen in heavy users (but not statistically because not enough users). Sadly, because it is a longitudinal study they did not start with current trends of high dose marijuana and increased number of heavy users, especially those using for purported medical purposes.

 Until such time that specific substances have proven effects there is no place for marijuana in modern medicine.  Medications have side effects that have to be managed and risks weighed against benefit; but, for most of evidence-based medical practitioners, there is no place for a smoked medicine without proven efficacy.

  4. Additional thoughts

 This will fuel the debate among those already committed to marijuana but it will not advance public health.

It is important to not forget the numerous other serious consequences of marijuana use: cognitive, learning, psychosis, addiction, criminal behaviour, impaired drivers on the highway and in workplaces, etc. – none of which were considered in this study.

 Source:  Document written byCalvinaFay, Bertha Madras, Andrea Barthwell, and Eric Voth  International Task Force on Global Drug Policy   January 2012

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Hospitalizations for alcohol and drug overdoses – alone or in combination – increased dramatically among 18- to 24-year-olds between 1999 and 2008, according to a study by researchers at the National Institute on Alcohol Abuse and Alcoholism (NIAAA), part of the National Institutes of Health.

Led by Aaron M. White, Ph.D. and Ralph W. Hingson, Sc.D., of NIAAA’s division of epidemiology and prevention research, the study examined hospitalization data from the Nationwide Inpatient Sample, a project of the U.S. Agency for Healthcare Research and Quality designed to approximate a 20 percent sample of U.S. community hospitals. The findings appear in the September issue of the Journal of Studies on Alcohol and Drugs.

Drs. White, Hingson, and their colleagues report that, over the 10-year study period, hospitalizations among 18-24-year-olds increased by 25 percent for alcohol overdoses; 56 percent for drug overdoses; and 76 percent for combined alcohol and drug overdoses.

“In 2008, 1 out of 3 hospitalizations for overdoses in young adults involved excessive consumption of alcohol,” noted Dr. White. “Alcohol overdoses alone caused 29,000 hospitalizations, combined alcohol and other drug overdoses caused 29,000, and drug overdoses alone caused another 114,000. The cost of these hospitalizations now exceeds $1.2 billion per year just for 18-24-year-olds.”

According to the authors, this is a growing problem for those outside of the 18-24 age range, as well.

“Among the entire population 18 and older, 1.6 million people were hospitalized for overdoses in 2008, at a cost of $15.5 billion, and half of these hospitalizations involved alcohol overdoses,” added Dr. Hingson.
The current study also showed an increase of 122 percent in the rate of poisonings from prescription opioid pain medications and related narcotics among 18-24 year olds. An alcohol overdose was present in 1 of 5 poisonings on these medications.

“The combination of alcohol with narcotic pain medications is particularly dangerous, because they both suppress activity in brain areas that regulate breathing and other vital functions,” Dr. White said.

The researchers noted that the steep rise in combined alcohol and drug overdoses highlights the significant risk and growing threat to public health of combining alcohol with other substances, including prescription medications. They call for stronger efforts to educate medical practitioners and the general public about the dangers of excessive alcohol consumption alone or in combination with other drugs.

“An increase in screening for alcohol misuse would help clinicians identify patients at particularly high risk for excessive drinking and for alcohol and medication interactions,” said NIAAA Acting Director Kenneth Warren, Ph.D. “Clinicians should use brief intervention techniques to help young adults evaluate their relationship with alcohol and other drugs and make wise choices regarding future use

Source www.cadca.org Sept. 2011

Guernsey’s Health and Social Services Department has issued a warning about the danger of a toxic chemical found locally in cocaine.
The department said levamisole had been detected in recent samples of the drug.
It said that some people who ingested the chemical developed agranulocytosis, a potentially fatal condition that harms the immune system.
Dr Roland Archer, the States analyst, said: “This is the first time that it has been detected in Guernsey.”
He said: “Once levamisole has been added to cocaine, it is nearly impossible to remove it and it even survives processing of cocaine into ‘crack’.”
New equipment costing £80,000 has enabled the department to examine drugs at a molecular level.
A gas chromatograph mass spectrometer, recently purchased by the department, helped find the substance.
Dr Archer said: “It gives us a lot more confidence when presenting the data on controlled drugs.”

Source: www.bbc.co.uk 26th August 2011

AstraZeneca is adding a new heart warning to the labels of Seroquel, a antipsychotic drug, at the request of the Food and Drug Administration. The revised label, posted on the Federal Food and Drug Administration website, says Seroquel and extended-release Seroquel XR “should be avoided” in combination with at least 12 other medicines (including methadone) linked to a heart arrhythmia that can cause sudden cardiac arrest.

Source: http://www.nytimes.com/2011/07/19/health/19drug.html?_r=1 July 2011

A new study from the Department of Energy’s Brookhaven Natural Laboratory released this week suggests that people addicted to certain types of drugs might actually have lower density in crucial parts of their brain.
This and previous studies have shown that cocaine-addicted individuals, relative to non-addicted individuals, have lower gray matter density in frontal parts of the brain – which is important for paying attention and organizing one’s own behavior – and in the hippocampus, a brain region important for learning and memory.
But it doesn’t stop at cocaine. The study revealed that persistent alcohol or cigarette consumption may have a similar effect.
The longer cocaine, alcohol, and cigarettes were abused, the lower gray matter was found in the hippocampus and frontal regions of the brain.

This result means that curtailing drug use may be protective against such brain changes.
The study did not test the effects of other substances. It did, however, clarify that genetic makeup may predispose certain individuals to lose brain matter over

Source: www.huffingtonpost.com 2011/03/13

This week, The National Center on Addiction and Substance Abuse at Columbia University released the National Survey of American Attitudes on Substance Abuse XVI: Teens and Parents. This year’s survey reveals that teens who regularly use social networking sites are at increased risk of smoking, drinking and using drugs. The survey finds that compared to teens who in a typical day do not spend any time on a social networking site, those who do are five times likelier to use tobacco, three times likelier to use alcohol, and twice as likely to use marijuana.

The CASA Columbia survey also reveals that 40 percent of all teens surveyed have seen pictures on Facebook, Myspace or other social networking sites of kids getting drunk, passed out, or using drugs and kids who have seen such pictures at also at increased substance abuse risk.

This year’s survey explored teen TV viewing habits in relation to teen substance abuse and found that compared to teens that do not watch suggestive teen programming, those who do are likelier to smoke, drink and use drugs.

According to Joseph A. Califano, Jr., CASA Columbia’s Founder and Chairman and Former U.S. Secretary for Health, Education, and Welfare: “The relationship of social networking site images of kids drunk, passed out, or using drugs and of suggestive teen programming to increased teen risk of substance abuse offers grotesque confirmation of the adage that a picture is worth a thousand words. The time has come for those who operate and profit from social networking sites like Facebook to deploy their technological expertise to curb such images and to deny use of their sites to children and teens who post pictures of themselves and their friends drunk, passed out or using drugs. Continuing to provide the electronic vehicle for transmitting such images constitutes electronic child abuse.”
Source: www.CADCA.org Aug. 2011

BRIAN DONNELLY

THE controversial heroin substitute methadone was implicated in more deaths than the drug itself in two areas of Scotland last year.
The figures for the Lothians show methadone was implicated in 33 deaths, while the comparable figure for heroin was 26. In Grampian, another historical centre of drug abuse, the substitute was a factor in 19 deaths, set against 14 for heroin.
The Scottish Drugs Forum (SDF), the national non- government drugs policy and information agency, said the prevalence of the substitute was “concerning”, while Tory health spokesman Murdo Fraser MSP said the figures showed there was a clear breakdown in the support system.

Source: www.Herald Scotland.com 17th Aug. 2011

Smoking is an important risk factor in brain shrinkage and a decline in brain function in later years, a new study suggests. The study found smoking, along with high blood pressure, diabetes and excess weight, all contributed to potentially dangerous changes in the brain that could lead to a decline in mental functioning as soon as 10 years later. The study appears in the journal Neurology.
HealthDay reports the study included 1,352 people without dementia whose average age was 54. Each person was weighed, measured, given blood pressure, cholesterol and diabetes tests and underwent brain MRI scans over 10 years. The researchers found smokers lost brain volume overall and in the hippocampus—the part of the brain which converts short-term memory into long-term memory—at a faster rate than nonsmokers. They were also more likely to have a rapid increase in small areas of damage to the brain’s blood vessels.
Study author Charles DeCarli, M.D., of the University of California at Davis Alzheimer’s Disease Center, said in a journal news release, “Our findings provide evidence that identifying these risk factors early in people of middle age could be useful in screening people for at-risk dementia and encouraging people to make changes to their lifestyle before it’s too late.”

Source: ThePartnership @drugfree.org. Aug.2011

Men who use marijuana may increase their risk for developing testicular cancer. A
recent study of several hundred Washington State men with testicular cancer showed an association between current marijuana use and the more aggressive of the two types of the disease. Moreover, the association was strongest among men with a long history of regular marijuana use.

To firmly link marijuana use and the cancer, however, scientists will need to replicate the findings among large groups of men across many geographical regions and identify the underlying biological mechanisms, says NIDA-funded researcher Dr. S. K. Dey of the Cincinnati Children’s Hospital Medical Center, who collaborated on the study with Drs. Janet Daling and Stephen M. Schwartz and colleagues at the Fred Hutchinson Cancer Research Center and the University of Washington.

During the past 50 years, the number of new cases of testicular cancer reported annually in the United States has nearly doubled. So has the percentage of the general population who report having smoked marijuana at least once. Dr. Dey suspected that the two trends might be related, although exposure to various environmental factors may also be involved. Along with the simultaneous rise in rates, there are biological reasons to hypothesize a connection between the drug and the cancer. Research has shown that marijuana smoking reduces sperm production and male fertility, and other work has linked diminished fertility to increased risk of testicular cancer. Cannabinoid receptors— the cell-membrane proteins that bind to a component of marijuana as well as to the naturally occurring compounds known as endocannabinoids—occur on the cell
membranes of sperm, the testes (see photograph), the uterus, and embryos, as well as on brain neurons. Marijuana smoking causes widespread effects in the endocrine and reproductive systems and might alter the growth of somatic and germ cells in the testes, resulting in testicular cancer.

The research team interviewed 369 men who were diagnosed with testicular cancer between 1999 and 2006 and 979 men who never had the disease. They recruited all of the study participants from three counties in Washington State and controlled statistically for smoking, drinking, and other testicular cancer risk factors. Approximately 70 percent of each group reported smoking marijuana at least once. The researchers found that the odds of having testicular cancer were 70 percent higher among men who reported current marijuana use compared with nonusers. In addition, the researchers observed 80 percent higher odds of testicular cancer among men who started to use marijuana before age 18 compared with nonusers. They also found that the odds for testicular cancer among men who used marijuana at least weekly were twice that of nonusers.

Of the two categories of testicular cancer, nonseminomas and seminomas, the former was strongly associated with a history of marijuana smoking, but the latter had little or no association, Dr. Dey says. Nonseminomas occur in younger men, grow more rapidly, and have lower survival rates. While a man diagnosed with seminomas is 98 percent as likely as someone without the disease to still be alive 10 years later, the figure for someone diagnosed with a nonseminoma ranges from 46 percent to 92 percent, depending on the tumor subtype.
The association between marijuana smoking and nonseminomas, but not seminomas, is difficult to explain, says Dr. Dey. The rates for both types of cancer have been rising, and subnormal fertility and certain environmental exposures during puberty—such as chemicals that affect estrogen and androgen production—are risk factors for both.
“My colleagues and I hope our study sparks similar epidemiological investigations of the relationship between testicular cancer and marijuana abuse around the world,” says Dr. Dey. “These results may also spur animal research, which is essential for interpreting our findings.” Animal research, he says, will be required to determine whether marijuana’s psychoactive ingredient, delta-9 tetrahydrocannabinol (THC), or its other components increase the risk of testicular cancer. Studies with animals may also search for molecular pathways connecting marijuana and testicular cancer. Such studies would probably focus
on marijuana’s activation of the neurotransmitter system that underlies its psychoactive, endocrine, and reproductive effects.
“If these interesting findings are replicated in a large, nationally representative group of participants, then future research should delve into the molecular mechanism underlying the association,” says Dr. Vishnudutt Purohit of NIDA’s Division of Basic Neuroscience and Behavioral Research. He notes that the study by Drs. Dey, Daling, and Schwartz is part of NIDA-supported research to determine how drugs of abuse affect the cardiovascular, pulmonary, reproductive, and immune systems of the body.
(For more information on these cancers, see http://seer.cancer.gov/publications/survival/surv_testis.pdf.)

SOURCE
Daling, J.R., et al. Association of marijuana use and the incidence of testicular germ cell tumors. Cancer 115(6):1215–1223, 2009.
December 2010 NIDA Notes/ Volume 23, Number 3

Celebrities and millionaires with no history of addiction research or helping addicts to reclaim destroyed lives campaigned globally in June to make drugs even more available – citing reasons based on theory not fact. David Raynes tells the truth

COMPARE STATISTICS: HARMS OF LEGAL vs ILLEGAL DRUGS

• “More deaths are caused each year by tobacco use than by all deaths from HIV, illegal drug use, alcohol use, motor vehicle injuries, suicides, and murders combined,” states the US Centre for Disease Control (www.cdc.gov/tobacco/data_ statistics/fact_sheets/health_effects/tobacco_related_
mortality). UK figures are below.

• 880 deaths/year involve heroin or morphine
(latest figures from the Office of National Statistics at http://www.statistics.gov.uk/pdfdir/poi0311.pdf)

• 8,664 deaths/year involve alcohol (http://www.statistics.gov.uk/cci/nugget.asp?id=1091

• 81,400 deaths of people in England alone aged 35+ were attributable to tobacco (http://www.ic.nhs.uk/pubs/smoking10)

• An estimated 462,900 hospital admissions in England alone of people aged 35+ were attributable to smoking (ibid).

Source: Addiction Today July/August 2011

People who abused methamphetamine or other amphetamine-like stimulants were more likely to develop Parkinson’s disease than those who did not, in a new study from the Centre for Addiction and Mental Health (CAMH).
The researchers examined almost 300,000 hospital records from California covering 16 years. Patients admitted to hospital for methamphetamine or amphetamine-use disorders had a 76 per cent higher risk of developing Parkinson’s disease compared to those with no diagnosis. Globally, methamphetamine and similar stimulants are the second most commonly used class of illicit drugs.
“This study provides evidence of this association for the first time, even though it has been suspected for 30 years,” said lead researcher Dr. Russell Callaghan, a scientist with CAMH. Parkinson’s disease is caused by a deficiency in the brain’s ability to produce a chemical called dopamine. Because animal studies have shown that methamphetamine damages dopamine-producing areas in the brain, scientists have worried that the same might happen in humans.
It has been a challenge to establish this link, because Parkinson’s disease develops in middle and old age, and it is necessary to track a large number of people with methamphetamine addiction over a long time span. The CAMH team took an innovative approach by examining hospital records from California – a state in which methamphetamine use is prevalent – from 1990 up to 2005. In total, 40,472 people, at least 30 years of age, had been hospitalized due to a methamphetamine- or amphetamine-use disorder during this period.
These patients were compared to two groups: 207,831 people admitted for appendicitis with no diagnosis of any type of addiction, and 35,335 diagnosed with cocaine use disorders. A diagnosis of Parkinson’s disease was identified from hospital records or death certificates. Only the methamphetamine group had an increased risk of developing Parkinson’s disease.
While the appendicitis group served as a comparison to the general population, the cocaine group was selected for two reasons. Because cocaine is another type of stimulant that affects dopamine, this group could be used to determine whether the risk was specific to methamphetamine stimulants. Cocaine users also served as a control group to account for the health effects or lifestyle factors associated with dependence on an illicit drug.
“It is important for the public to know that our findings do not apply to patients who take amphetamines for medical purposes, such as attention deficit hyperactivity disorder (ADHD), since these patients use much lower doses of amphetamines than those taken by patients in our study,” said Dr. Stephen Kish, a CAMH scientist and co-author.
To put the study findings into numbers, if 10,000 people with methamphetamine dependence were followed over 10 years, 21 would develop Parkinson’s, compared with 12 people out of 10,000 from the general population. “It is also possible that our findings may underestimate the risk because in California, methamphetamine users may have had less access to health-care insurance and consequently to medical care,” said Dr. Callaghan.
The current project is significant because it is one of the few studies examining the long-term association between methamphetamine use and the development of a major brain disorder. “Given that methamphetamine and other amphetamine stimulants are the second most widely used illicit drugs in the world, the current study will help us anticipate the full long-term medical consequences of such problematic drug use,” said Dr. Callaghan.
Media Contact: Michael Torres, Media Relations, CAMH; 416-595-6015

Source: www.camh.net 26th July 2011

Electronic cigarettes, or “e-cigarettes,” are crude drug delivery systems for refined nicotine that pose unknown risks, two experts write in this week’s New England Journal of Medicine. Researchers from the American Legacy Foundation’s Steven A. Schroeder National Institute for Tobacco Research and Policy Studies write that e-cigarettes have more in common with asthma inhalers than with cigarettes, according to Science Daily.
E-cigarettes are designed to deliver nicotine in the form of a vapor, which is inhaled by the user. They usually have a rechargeable, battery-operated heating element, a replaceable cartridge with nicotine or other chemicals and a device called an atomizer that converts the contents of the cartridge into a vapor when heated. E-cigarettes often are made to look like regular cigarettes.
The Food and Drug Administration (FDA) announced in April that it would regulate e-cigarettes as tobacco products, not as drug-delivery devices.
Last year, the FDA lost a court case after it tried to treat e-cigarettes as drug-delivery devices, which must satisfy stricter requirements than tobacco products, including clinical trials to prove they are safe and effective. FDA tests found that the liquid in some e-cigarettes contained toxins besides nicotine, as well as cancer-causing substances found in tobacco. Some public health experts say the level of the cancer-causing agents is similar to those found in nicotine replacement therapy, which contains nicotine extracted from tobacco.
The authors list several safety concerns about e-cigarettes. They note that the devices do not reliably deliver nicotine, and have not been sufficiently studied in the same way the FDA requires other smoking-cessation drugs and devices to be evaluated. Therefore, smokers who try to use e-cigarettes to help them quit smoking are likely to find them ineffective because of their variable nicotine content and unreliable delivery, they say.
They also note that smokers may use e-cigarettes in places where traditional tobacco smoking is not allowed, thus encouraging them to keep smoking instead of quitting. E-cigarettes also may become a smoking “starter” product for young people. E-cigarette cartridges can be bought over the Internet with flavors such as chocolate and grape, they write.

Source: DrugFreee.org 21st July 2011

Researchers from the Medical Research Council (MRC) have uncovered for the first time how excess alcohol can cause irreparable damage to our DNA. In a new study published in the journal Nature today, MRC scientists also discovered a two-tier defence system in our cells that limits the threat of permanent genetic damage.
Scientists at the MRC’s Laboratory of Molecular Biology (LMB) have discovered that an overload of a toxic chemical called acetaldehyde, a by-product from the breakdown of alcohol in our body, can cause damage to DNA. They showed that our cells have two natural ways of protecting us against acetaldehyde. Firstly, this toxin can be removed by specialised enzymes. If this step fails, acetaldehyde builds up and damages DNA, but a second mechanism kicks in to repair the damaged DNA, using another set of enzymes known as the Fanconi proteins.
In pregnant mice which were genetically altered not to have these two defences, the equivalent of a single binge drinking session of alcohol caused catastrophic damage to the fetus. Not only did alcohol damage the fetus, but in the adult modified mice, this alcohol consumption damaged blood stem cells, obliterating the production of blood.
Dr KJ Patel, lead author of the paper from the MRC Laboratory of Molecular Biology, said:
“The findings show how critically reliant we are on both these control systems to prevent alcohol from causing irreversible mutations to DNA, both in the fetus and in our own cells.
“The effects of alcohol in the modified pregnant mice resembled fetal alcohol syndrome, where excessive drinking by pregnant women causes permanent damage to the unborn child, leading to birth defects and learning difficulties. Our work suggests that binge drinking could generate enough acetaldehyde to overwhelm the body’s two natural defence mechanisms.
“This new knowledge transforms our view of precisely how excess alcohol causes damage – ultimately changing our DNA. Quite apart from this, our conclusions suggest potentially simple approaches to treat Fanconi anaemia – currently a terminal incurable illness in humans.”
The study highlights how two groups who have inherited failures of the natural control mechanisms are particularly at risk of severe DNA damage from alcohol. Individuals with a rare disease called Fanconi anaemia, which affects around 20,000 people worldwide, do not have the enzymes which repair DNA and are likely to be very sensitive to acetaldehyde. This could explain why such people are highly susceptible to both blood disorders and cancer. More commonly, around 500 million people from South East Asia with a condition called the ‘Asian alcohol flushing mutation’ have a greatly reduced capacity to break down acetaldehyde. This research suggests these individuals may be susceptible to lifelong DNA damage and could explain why alcohol consumption greatly increases their risk of gullet cancer.
Dr Hugh Pelham, director of the MRC Laboratory of Molecular Biology, said:
“We know that there’s a complex interplay between genetics, our body’s natural resilience to disease and our environment. By determining the molecular reason behind the toxic effects of alcohol to our DNA, our researchers have shown how vulnerable we can be to DNA damage from excess alcohol and even more so in the womb. Despite the existence of protective mechanisms, long-term genetic damage must be added to the risks of excessive alcohol consumption.”
The research was also funded by the Children’s Leukaemia Trust UK and the Fanconi Anaemia Research Fund USA.

Source: www.mrc.ac.uk 6th July 2011

Exposure to second hand smoke has a direct, measurable impact on the brain—and the effect is similar to what happens in the brain of the person doing the smoking. In fact, exposure to this secondhand smoke evokes cravings among smokers, according to a study funded by the National Institute on Drug Abuse (NIDA), part of the National Institutes of Health.

The study, published in Archives of General Psychiatry, used positron emission tomography to demonstrate that one hour of secondhand smoke in an enclosed space results in enough nicotine reaching the brain to bind receptors that are normally targeted by direct exposure to tobacco smoke. This happens in the brain of both smokers and non-smokers.

Previous research has shown that exposure to secondhand smoke increases the likelihood that children will become teenage smokers and makes it more difficult for adult smokers to quit. Such associations suggest that secondhand smoke acts on the brain to promote smoking behavior.

“This study gives concrete evidence to support policies that ban smoking in public places, particularly enclosed spaces and around children,” said Arthur Brody, M.D., of the University of California at Los Angeles Department of Psychiatry and Biobehavioral Sciences and corresponding author for the article

Source: www.cadca.org 5th May 2011

Scientists at Anglia Ruskin University have revealed for the first time the serious long-term health risks associated with Benzylpiperazine (BZP), dubbed the “new ecstasy”.
BZP was a popular legal high before it was reclassified as a controlled substance in December 2009. According to Dean Ames, the Forensic Science Service’s drugs intelligence adviser, the designer drug has replaced MDMA as the main ingredient in ecstasy tablets.
Dean Ames said:
“It’s a rare drug now, MDMA. There are hundreds of thousands of tablets in circulation in the UK that look like ecstasy tablets, but which actually contain piperazines (a class of compounds that includes BZP).

The tablets are still being sold as ecstasy and because they have an effect, young people may think they are taking ecstasy.”
Anglia Ruskin’s research, led by Professor Mike Cole and Dr Beverley Vaughan, is the first of its kind to examine the health implications of taking piperazines and will help to educate medical staff as to the most serious symptoms associated with their ingestion, namely liver and kidney damage.
“The market for and abuse of clandestinely synthesised designer drugs has increased significantly over the last decade and this has been accompanied by an increase in the number of reports of death and serious illnesses related to the ingestion of these substances,” said Professor Cole, whose preliminary findings were presented at the American Academy of Forensic Sciences’ annual conference.

“Before our research there had been no systematic study of the toxicity of these drugs and this is needed if we are to treat drug users effectively and inform people of the potential hazards associated with taking them.”
The data produced by Professor Cole and Dr Vaughan provides clear evidence of the cellular cytotoxicity of BZP and its synthetic by-products at levels likely to occur following their ingestion. It also indicates that in general the liver, the site of detoxification for the body, is most sensitive to the actions of these drugs.
“Cells derived from the liver and kidney were exposed to BZP – its starting materials and its impurities – at concentrations which reflected a dose for a user of these drugs. The cells were examined to determine whether significant changes had occurred, including apoptosis (cell suicide) and necrosis (cell murder),” explained Professor Cole.

“It was found that BZP itself is toxic to the kidney whilst the starting material, piperazine hexahydrate, showed toxicity in only the liver. In general the study showed that water soluble drugs, impurities and mixtures were toxic to liver cells, whilst compounds and mixtures which are fat soluble are toxic to the kidney.

“Mixtures of drugs and impurities, synthesised to reflect street samples, produced a variety of toxic effects depending upon the composition of the mixture – but all were significantly toxic. The work is important because it begins to provide an explanation of why people who have taken these drugs exhibit the symptoms that they do in A&E rooms.

“It also shows that different batches of drugs will have different effects because of the different proportions of drug and impurity in the material, and that users are exposed to toxic mixtures of drugs for which both the short and longer-term effects will not be known and cannot easily be predicted.”

Addictions expert Sarah Graham, who is a spokesperson for the Government drugs helpline FRANK, said: “BZP is not safe – it is an entirely synthetic party drug which mimics the effects of ecstasy and speed. It is a stimulant which can raise your blood pressure and may lead to a fit or heart attack. You never know what you are getting because the chemical make up continually changes and mixing the drug with alcohol can increase the risks.”

Source: www.anglia.ac.uk May 2011

May 2, 2011

CANCER COUNCIL AUSTRALIA has revised dramatically upwards its estimate of alcohol’s contribution to new cancer cases and issued its strongest warning yet that people worried by the link should avoid drinking altogether.
New evidence implicating alcohol in the development of bowel and breast cancer meant drinking probably caused about 5.6 per cent of cancers in Australia, or nearly 6500 of the 115,000 cases expected this year, a review by the council found. This was nearly double the 3.1 per cent figure it nominated in its last assessment, in 2008.
The council’s chief executive, Ian Olver, said the updated calculations revealed breast and bowel cancer accounted for nearly two-thirds of all alcohol-related cancers, overtaking those of the mouth, throat and oesophagus.
”The public really needs to know about it because it’s a modifiable risk factor,” said Professor Olver, calling for awareness campaigns to alert people to the link. ”You might not be able to help your genes but you can make lifestyle choices.”
Professor Olver said public advice should not conflict with the National Health & Medical Research Council’s 2009 recommendation people should drink no more than two standard alcohol units daily, already half the previous safe threshold for men.
But people should also be told there was no evidence of a safe alcohol dose below which cancer-causing effects did not occur – either from direct DNA damage, increased oestrogen levels or excessive weight gain. ”If you want to reduce your cancer risk as far as possible [abstinence] would be the option you have,” he said.
Public advice was especially important, Professor Olver said, because studies that suggested alcohol could protect against heart disease were increasingly being challenged by new findings that people gave up drinking when they became ill or old – meaning any potential benefits of moderate alcohol use for cardiovascular health had probably been oversold.

Source: : http://www.theage.com.au/lifestyle/wellbeing/quit-drinking-to-cut-cancer-risk-20110501-1e38g.html#ixzz1LTPjlgEi May 2011

Dutch researchers find that the hippocampus of long-term ecstasy users is 10.5% smaller than peers who don’t use drugs.
Dutch researchers found that long-term ecstasy users had an increased risk of hippocampal damage, which can contribute to the eventual onset of Alzheimer’s.
Long-term Ecstasy users risk brain damage, memory loss and an increased chance of developing Alzheimer’s disease, new research suggests.
Dutch researchers used MRI scans to study the brains of 10 men in their mid-20s who had taken an average of 281 ecstasy tablets over the previous six and a half years, and seven peers who had taken other drugs.
They found that the hippocampus – the part of the brain controlling memory – was 10.5% smaller among the ecstasy users, and their overall grey matter 4.6% less.
“These data provide preliminary evidence that Ecstasy users may be prone to incurring hippocampal damage”, and may help explain the memory loss witnessed among such people in previous studies, the co-authors wrote in the Journal of Neurology, Neurosurgery and Psychiatry.
“Hippocampal atrophy is a hallmark for disease of progressive cognitive impairment in older patients, such as Alzheimer’s disease”, they added.
Professor David Nutt, the government’s former lead adviser on drugs misuse, said, however, that the “interesting pilot study … is underpowered to provide definitive evidence of an effect of ecstasy”. Evidence suggests that many drugs, including alcohol, can damage someone’s memory, Nutt added.

Source: guardian.co.uk, Wednesday 6 April 2011

“Many studies have linked marijuana use with early onset of psychosis. The question is, does smoking marijuana cause earlier psychosis? A new review of 83 studies involving more than 22,000 participants seeks an answer.

The meta-analysis found that people who smoked marijuana developed psychotic disorders an average 2.7 years earlier than people who did not use cannabis
Context  A number of studies have found that the use of cannabis and other psychoactive substances is associated with an earlier onset of psychotic illness.
Objective  To establish the extent to which use of cannabis, alcohol, and other psychoactive substances affects the age at onset of psychosis by meta-analysis.
Data Sources  Peer-reviewed publications in English reporting age at onset of psychotic illness in substance-using and non–substance-using groups were located using searches of CINAHL, EMBASE, MEDLINE, PsycINFO, and ISI Web of Science.
Study Selection  Studies in English comparing the age at onset of psychosis in cohorts of patients who use substances with age at onset of psychosis in non–substance-using patients. The searches yielded 443 articles, from which 83 studies met the inclusion criteria.
Data Extraction  Information on study design, study population, and effect size were extracted independently by 2 of us.
Data Synthesis  Meta-analysis found that the age at onset of psychosis for cannabis users was 2.70 years younger (standardized mean difference = –0.414) than for nonusers; for those with broadly defined substance use, the age at onset of psychosis was 2.00 years younger (standardized mean difference = –0.315) than for nonusers. Alcohol use was not associated with a significantly earlier age at onset of psychosis. Differences in the proportion of cannabis users in the substance-using group made a significant contribution to the heterogeneity in the effect sizes between studies, confirming an association between cannabis use and earlier mean age at onset of psychotic illness.
Conclusions  The results of meta-analysis provide evidence for a relationship between cannabis use and earlier onset of psychotic illness, and they support the hypothesis that cannabis use plays a causal role in the development of psychosis in some patients. The results suggest the need for renewed warnings about the potentially harmful effects of cannabis.
Matthew Large, BSc(Med), MBBS, FRANZCP; Swapnil Sharma, MBBS, FRANZCP; Michael T. Compton, MD, MPH; Tim Slade, PhD; Olav Nielssen, MBBS, MCrim, FRANZCP
Source: Arch Gen Psychiatry. Published online February 7, 2011. doi:10.1001/archgenpsychiatry.2011.5

 A growing body of research is showing that when it comes to treatments for alcohol use disorders, women’s needs are different from men’s. Scientists who recently presented studies at the Research Society on Alcoholism are exploring gender differences in alcohol treatment and moving beyond a one-size-fits-all strategy.

“Women have different barriers to treatment than men,” says Elizabeth Epstein, PhD, Research Professor in the Clinical Division of theCenterofAlcohol StudiesatRutgersUniversityinNew Brunswick,NJ. “They are less likely to seek alcohol treatment in a dedicated alcohol facility, and more likely to seek treatment with a general practitioner or psychiatrist for depression or fatigue.” However, many of these doctors don’t routinely screen for an alcohol or drug use problem, she explains.

“We know that 85 percent of people who have alcohol problems in their lifetime don’t seek treatment for it, so we are focusing most of our treatment research resources on the 15 percent who do,” according to Dr. Epstein. “We need to look beyond that, to who is struggling without treatment.” More training in alcohol use disorders is needed for emergency department physicians, obstetrician/gynecologists and family practitioners, she states. “We need to develop interventions that allow doctors to screen for alcohol use problems, since we know that women are not likely to come in and say they drink too much.”

Alcohol tends to affect women more than men for several reasons. Dr. Epstein explains, “A woman who weighs the same as a man and consumes the same amount of alcohol over the same length of time is likely to have a higher blood alcohol level. Women have less body water than men, leading to a higher blood alcohol concentration, and they also have less lean muscle mass and fewer enzymes in the stomach that break down alcohol. That means more ethanol is going into the bloodstream and directly to organs like the heart, brain and liver, and doing damage.”

She notes that women develop a host of alcohol-related health problems more quickly than men, even though they tend to start drinking later. “Older womens’ bodies are not processing anything as well as younger women, including alcohol,” she says. “And we are seeing younger women’s drinking patterns catching up with men’s, which is not a good thing. That means that as this generation progresses, we’ll see more and more older women with alcohol problems.”

Success With Individual Therapy

Dr. Epstein is leading the Rutgers Women’s Treatment Project at theCenter ofAlcohol Studies. This five-year clinical research study, funded by the National Institute of Alcohol Abuse and Alcoholism, is testing the effectiveness of therapies for women with drinking problems.

She and her colleague, Dr. Barbara McCrady, looked at marital therapy combined with alcohol therapy for women, testing it against individual alcohol therapy for women. “The women in both groups did very well, reducing their drinking days from an average of about 70 percent before the study, to 20-30 percent while in and after treatment,” states Dr. Epstein. The coupled treatment conferred a slight advantage in terms of maintaining the gains in the year following treatment. That study required women to be in a committed relationship or marriage to a male to be eligible. Many women didn’t want to sign up, because their spouse had to be involved.

Both doctors then offered a choice of either individual therapy or couples therapy in a two-armed clinical research study to treat alcohol use disorders. For that study, women had to be in a committed relationship, but did not need to bring their partner in if they chose individual therapy. Most women in that study chose individual therapy. Women who chose individual therapy were randomly assigned to regular cognitive behavioral therapy (CBT) or female-specific CBT. In CBT, emphasis is placed on the importance of breaking the drinking habit and learning coping skills.

The female-specific treatment also emphasized womens’ rights to care for themselves, and helped them feel more self-confident and less sensitive to what other people thought about them. The treatment provided assertiveness training and helped women address how to deal with a partner who drinks heavily, and with anxiety and depression. Women learned about anger management and how to make connections with sober people who treat them well and don’t abuse them.

While women in both groups showed improvement in their drinking, Dr. Epstein and her colleagues found that women who chose individual therapy were more likely to stick with therapy than those who chose couples therapy.

Currently Dr. Epstein is investigating the effectiveness of female-specific-CBT treatment delivered in women-only groups. She explains, “We want to be able to develop treatments for a broad range of women, which could be integrated into community-based therapy.”

Trauma and Substance Abuse Linked

Many women with substance abuse disorders also suffer from post-traumatic stress syndrome (PTSD), resulting from interpersonal violence, says Denise Hien, PhD, ABPP, who presented data at the meeting about promising treatments for women who suffer from PTSD and substance use disorders. “They drink in response to trauma,” says Dr. Hien, Professor at the City University of New York, and Adjunct Senior Research Scientist at Columbia University College of Physicians and Surgeons inNew York.

Dr. Hien compared a type of CBT called “Seeking Safety” for substance abuse and PTSD with a relapse prevention treatment. “Seeking Safety” is a short-term treatment for both trauma and substance abuse in women. Both disorders are treated at the same time by the same clinician. Secondary analyses indicate that trauma therapy may be most effective for women who are also receiving some type of self-help, such as being part of a 12-step group. “If a person is not affiliated with a self-help group, she may actually get worse from trauma therapy alone,” Dr. Hien says.

Last year, she published a study in the American Journal of Psychiatry that found if you treat the PTSD symptoms first, in women who suffer from both substance abuse and PTSD, it led to a reduction in substance abuse. The study found little evidence that treating substance abuse first improved PTSD symptoms. Currently, patients who suffer from both disorders often are not treated for PTSD until they receive addiction treatment and stop using drugs and alcohol. This sequence is based on the assumption that addressing trauma could worsen a person’s substance abuse.

Dr. Hien is also conducting a clinical trial that is examining whether adding the antidepressant sertraline HCI (Zoloft) to trauma therapy benefits women with PTSD and alcohol misuse or alcohol use disorders.

Source: The Partnership@DrugFree.org  July 2011

There has been much debate about whether cannabis might cause or exacerbate psychotic illnesses or whether characteristics of persons who tend to develop these conditions make them more likely to use the drug.

Authors of a new meta-analysis that found that earlier use of cannabis may trigger earlier onset of psychotic disorders say that their study supports a causative role.

Source: JAMA, March 2, 2011 – Vol. 305, No. 9

Abstract

Objective To examine the association between smoking and risk of invasive breast cancer using quantitative measures of lifetime passive and active smoking exposure among postmenopausal women.

Design Prospective cohort study. Setting 40 clinical centres in the United States. Participants 79?990 women aged 50–79 enrolled in the Women’s Health Initiative Observational Study during 1993–8. Main outcome measures Self reported active and passive smoking, pathologically confirmed invasive breast cancer.

Results In total, 3520 incident cases of invasive breast cancer were identified during an average of 10.3 years of follow-up. Compared with women who had never smoked, breast cancer risk was elevated by 9% among former smokers (hazard ratio 1.09 (95% CI 1.02 to 1.17)) and by 16% among current smokers (hazard ratio 1.16 (1.00 to 1.34)). Significantly higher breast cancer risk was observed in active smokers with high intensity and duration of smoking, as well as with initiation of smoking in the teenage years. The highest breast cancer risk was found among women who had smoked for =50 years or more (hazard ratio 1.35 (1.03 to1.77) compared with all lifetime non-smokers, hazard ratio 1.45 (1.06 to 1.98) compared with lifetime non-smokers with no exposure to passive smoking). An increased risk of breast cancer persisted for up to 20 years after smoking cessation. Among women who had never smoked, after adjustment for potential confounders, those with the most extensive exposure to passive smoking (=10 years’ exposure in childhood, =20 years’ exposure as an adult at home, and =10 years’ exposure as an adult at work) had a 32% excess risk of breast cancer compared with those who had never been exposed to passive smoking (hazard ratio 1.32 (1.04 to 1.67)). However, there was no significant association in the other groups with lower exposure and no clear dose response to cumulative passive smoking exposure.

Conclusions Active smoking was associated with an increase in breast cancer risk among postmenopausal women. There was also a suggestion of an association between passive smoking and increased risk of breast cancer.

Source: BMJ 2011; 342:d1016

Although growing literature suggests that long-term marijuana use is associated with a wide range of adverse health consequences, many people believe it is relatively harmless and should be legalized, the researchers noted. “However, this study shows long-term, heavy cannabis use causes significant brain injury, memory loss, difficulties learning new information, and psychotic symptoms, such as delusions of persecution [paranoia], delusions of mind-reading, and bizarre social behaviors in even non-vulnerable users,” said lead researcher Murat Yucel, from the ORYGEN Research Centre and the Neuropsychiatry Centre at the University of Melbourne.
This new evidence plays an important role in further understanding the effects of marijuana and its impact on brain functioning, Yucel said. “The study is the first to show that long-term cannabis use can adversely affect all users, not just those in the high-risk categories such as the young, or those susceptible to mental illness, as previously thought,” he said.
The report was published in the June issue of the Archives of General Psychiatry.
In the study, Yucel’s team did high-resolution MRIs on 15 men who smoked more than five joints a day for more than 10 years. They compared those with scans of 16 men who did not In addition, all the men took verbal memory tests and were examined for symptoms of psychiatric disorders. “The more marijuana used, the more these individuals were likely to show reduced brain volumes in the hippocampus and amygdala, as well as being more likely to develop symptoms of psychotic disorders and to have significant memory impairment,” Yucel said.
In fact, the hippocampus of marijuana users was 12 percent smaller, and the amygdala was 7.1 percent smaller than among nonusers. In addition, men who used marijuana also had symptoms of psychiatric disorders, Yucel’s group found. The hippocampus is associated with the regulation of emotion and memory, while the amygdala controls fear and aggression.
“There is ongoing controversy concerning the long-term effects of cannabis on the brain,” Yucel said. “These findings challenge the widespread perception of cannabis as having limited or no harmful effects on brain and behavior. Although modest use may not lead to significant neurotoxic effects, these results suggest that heavy daily use might indeed be toxic

SOURCE: Murat Yucel, Ph.D., ORYGEN Research Centre, Melbourne Neuropsychiatry Centre, University of Melbourne, Australia; Adam Bisaga, M.D., assistant professor, psychiatry, Columbia University, and addiction psychiatrist, New York State Psychiatric Institute, New York City; June 2008, Archives of General Psychiatry

Summary

Background

Whether cannabis can cause psychotic or affective symptoms that persist beyond transient intoxication is unclear. We systematically reviewed the evidence pertaining to cannabis use and occurrence of psychotic or affective mental health outcomes.

Methods

We searched Medline, Embase, CINAHL, PsycINFO, ISI Web of Knowledge, ISI Proceedings, ZETOC, BIOSIS, LILACS, and MEDCARIB from their inception to September, 2006, searched reference lists of studies selected for inclusion, and contacted experts. Studies were included if longitudinal and population based. 35 studies from 4804 references were included. Data extraction and quality assessment were done independently and in duplicate.

Findings

There was an increased risk of any psychotic outcome in individuals who had ever used cannabis (pooled adjusted odds ratio=1•41, 95% CI 1•20—1•65). Findings were consistent with a dose-response effect, with greater risk in people who used cannabis most frequently (2•09, 1•54—2•84). Results of analyses restricted to studies of more clinically relevant psychotic disorders were similar. Depression, suicidal thoughts, and anxiety outcomes were examined separately. Findings for these outcomes were less consistent, and fewer attempts were made to address non-causal explanations, than for psychosis. A substantial confounding effect was present for both psychotic and affective outcomes.

Interpretation

The evidence is consistent with the view that cannabis increases risk of psychotic outcomes independently of confounding and transient intoxication effects, although evidence for affective outcomes is less strong. The uncertainty about whether cannabis causes psychosis is unlikely to be resolved by further longitudinal studies such as those reviewed here. However, we conclude that there is now sufficient evidence to warn young people that using cannabis could increase their risk of developing a psychotic illness later in life.

Source: The Lancet, Volume 370, Issue 9584, Pages 319 – 328, 28 July 2007

Abstract:

Context A number of studies have found that the use of cannabis and other psychoactive substances is associated with an earlier onset of psychotic illness.
Objective To establish the extent to which use of cannabis, alcohol, and other psychoactive substances affects the age at onset of psychosis by meta-analysis.
Data Sources Peer-reviewed publications in English reporting age at onset of psychotic illness in substance-using and non–substance-using groups were located using searches of CINAHL, EMBASE, MEDLINE, PsycINFO, and ISI Web of Science.
Study Selection Studies in English comparing the age at onset of psychosis in cohorts of patients who use substances with age at onset of psychosis in non–substance-using patients. The searches yielded 443 articles, from which 83 studies met the inclusion criteria.
Data Extraction Information on study design, study population, and effect size were extracted independently by 2 of us.
Data Synthesis Meta-analysis found that the age at onset of psychosis for cannabis users was 2.70 years younger (standardized mean difference = –0.414) than for nonusers; for those with broadly defined substance use, the age at onset of psychosis was 2.00 years younger (standardized mean difference = –0.315) than for nonusers. Alcohol use was not associated with a significantly earlier age at onset of psychosis. Differences in the proportion of cannabis users in the substance-using group made a significant contribution to the heterogeneity in the effect sizes between studies, confirming an association between cannabis use and earlier mean age at onset of psychotic illness.
Conclusions The results of meta-analysis provide evidence for a relationship between cannabis use and earlier onset of psychotic illness, and they support the hypothesis that cannabis use plays a causal role in the development of psychosis in some patients. The results suggest the need for renewed warnings about the potentially harmful effects of cannabis.
(Full text available here) – http://archpsyc.ama assn.org/cgi/content/full/archgenpsychiatry.2011.5

Source: . Archives of General Psychiatry, 7th February 2011

Individual health risks
The assessment of individual health risks includes consideration of mephedrone’s acute and chronic toxicity, its dependence potential, and similarities and differences to other reference stimulants.

Systematic data are not routinely collected in Europe on acute toxicity related to mephedrone or closely comparable recreational drugs. Therefore, information on these effects of mephedrone is limited to user reports and clinical data on individuals presenting with acute problems. The reported short-term effects of mephedrone use have much in common with those of other stimulants. Some self-reports from users favourably compare mephedrone’s effects, saying the high can be both better and longer lasting than cocaine.

The main routes of administration for mephedrone are reported as snorting (nasal
insufflation) and swallowing (oral ingestion), sometimes after dissolving with water. As mephedrone is primarily available in powder form, injecting use is reported but appears to be rare.

Adverse effects reported by users include sweating, headaches, tachycardia, palpitations, nausea, chest pain, bruxism (teeth grinding), agitation/aggression and paranoia. In addition, nasal insufflation of mephedrone is reported to be associated with significant nasal irritation and pain which has led to some users switching to oral use of mephedrone. Users report increased sexual arousal but there is insufficient information to detect whether this is associated with highrisk sexual behaviour.
Some detailed information on the patterns of acute mephedrone toxicity is available from clinical case series from poisons information services and specialist hospitals in the United Kingdom and Sweden, including one series of analytically confirmed acute mephedrone toxicity from the United Kingdom. In this data, patients typically present with sympathomimetic features (dilated pupils, agitation, tachycardia, hypertension); severe clinical features such as chest pain, significant hypertension, arrhythmias and seizures have been reported in a small number of cases to date. Similar to other stimulant drugs, it is likely that the risk of toxicity is related to the dose of mephedrone used; however there is insufficient information available from toxicity
reports to determine a ‘dose threshold’ and/or whether particular routes of use are more likely to be associated with toxicity. It is possible that certain rare, but clinically significant, severe effects are associated with mephedrone use. However, as experience of the toxicological profile of the drug is currently limited to a few hundred cases it is difficult to be sure.

Data from individuals presenting with acute mephedrone toxicity suggest that the majority of individuals have used at least one other substance together with mephedrone. However there are analytically confirmed cases of lone mephedrone toxicity. This is similar to individuals presenting with acute toxicity related to other stimulant drugs. There are two reported fatalities in which mephedrone appears to be the sole cause of death (one in Sweden and one in the United Kingdom). In addition to these cases, there are at least another 37 deaths in the United Kingdom and Ireland in which mephedrone has been detected in post-mortem blood and/or urine toxicology screening. In some of these cases it is likely that other drugs and/or other medical conditions or trauma may have contributed to or been responsible for death. The inquests into the deaths are pending for the majority of these cases
therefore it is not possible at this time to determine the contribution of mephedrone.

Strong craving for the substance is reported by some users’ self-reports, sometimes rated higher than that experienced with other stimulant drugs. This is cited as a main reason for using more mephedrone than intended, and for using for longer periods than planned. Withdrawal symptoms do not appear to be significant for most users with the primary symptoms of nasal congestion and fatigue most probably related to route of use and lack of sleep secondary to staying up late. However the other reported findings, in heavier users, would be consistent with a stimulant withdrawal syndrome. There is some evidence that the drug has a high abuse liability with over 30 % of the UK telephone survey sample reporting three or more DSM criteria
of dependence and being classified as dependent. Tolerance, loss of control, a strong urge to use and using despite problems predominate. In addition, there are reports from the United Kingdom of mephedrone dependence being reported to drug treatment services that suggest psychological rather than physical dependency similar to other stimulant drugs.
No studies have been published investigating the potential for chronic mephedrone toxicity associated with mephedrone use, including reproductive toxicity, genotoxicity and carcinogenic potential. Reports suggest mephedrone may be used as an alternative to illicit stimulants. The reasons given for using mephedrone include: value for money, product purity and consistency as well as the poor availability or low quality of other stimulants (cocaine, ecstasy/MDMA). Some users
noted a preference for mephedrone over other stimulant drugs with data from the UK clubbers rating mephedrone above ecstasy and cocaine for strength and pleasurable high. Mephedrone users in the UK telephone survey reported on the considerable impact mephedrone had on their consumption of cocaine and ecstasy, with approximately two thirds of the sample reporting that they now took less MDMA, and a third reporting that they now consumed less cocaine. Just under half of the group reported they would choose mephedrone over cocaine and only a quarter said that they would take mephedrone over ecstasy
.
The physical effects reported by mephedrone users are typical of other stimulants and may be particularly similar to MDMA. However, mephedrone’s relatively short duration of action, leading to repeat dosing, is more analogous to cocaine.
In summary, from the data sources available, it appears that the effect profile and clinical presentations of mephedrone intoxications share some features seen with MDMA and some features seen with cocaine. Additionally, there are very limited reports of fatalities directly related to mephedrone. Some users have reported negative effects and in some cases these have required medical attention. Similar to other stimulant drugs, the extent to which users experience problems requires further investigation. Data also suggest that mephedrone has a potential to cause dependency. However, more in-depth studies would be required to explore in
detail the dependence potential of this drug.

Source: excerpt from DEA report 2010

A promising new cognitive therapy, or brain training, approach to drug addiction was published in the recent issue of Biological Psychiatry.
Drug addiction is considered a brain disease, according to the National Institute on Drug Abuse, because the abuse of drugs leads to changes in the structure and function of the brain. Drug prevention, education, and awareness programs seem to be quite effective for some individuals because they realize the long term repercussions of abusing substances. For those that are vulnerable to addictions, these measures often fall short. One theory for this may be the “delayed discounting” sometimes present in those who are vulnerable to addictions.
Addicts tend to exhibit a trait called “delay discounting”, or the tendency to devalue rewards and punishments that occur in the future. Addicts may at the same time have a predisposition towards “reward myopia” which is the tendency towards the immediate gratification that drugs can provide with addictions.
Dr. Warren Bickel, from the Center for Addiction Research in Little Rock, Arkansas, and his colleagues borrowed a rehabilitation approach used successfully with patients suffering from stroke, or traumatic brain injury.
The therapy approach utilized working memory training. Subjects addicted to stimulants were given brain exercises that focused on strengthening the areas of the brain associated with storing and managing information reasoning to guide behavior. Dr. Bickel’s team had stimulant abusers repeatedly perform a working memory task and found that by strengthening the brain circuitry, they also reduced the addicts devaluation of longer term rewards.
Dr. John Krystal, Editor of Biological Psychiatry comments on the article:
“The legal punishments and medical damages associated with the consumption of drugs of abuse may be meaningless to the addict in the moment when they have to choose whether or not to take their drug. Their mind is filled with the imagination of the pleasure to follow. We now see evidence that this myopic view of immediate pleasures and delayed punishments is not a fixed feature of addiction. Perhaps cognitive training is one tool that clinicians may employ to end the hijacking of imagination by drugs of abuse.”
“Dr. Bickel says, “Although this research will need to be replicated and extended, we hope that it will provide a new target for treatment and a new method to intervene on the problem of addiction.”
Source Published in Biological Psychiatry reported in e-max health.com 27th Jan 2011

1. 12/17 states (including DC) with “medical” marijuana” have 20% + traffic fatalities involving drugs
70.6% of states with MMJ laws have driver fatalities testing positive for drugs of 20% or greater

2. 13/17 states with “medical” marijuana” has 19% + traffic fatalities involving drugs (Arizona)
76% of states with MMJ have driver fatalities testing positive for drugs of 19% or higher

3. 3/17 states with “medical” marijuana” laws that have low rates of driver fatalities also have low rates of testing for drugs (Oregon, Rhode Island, Maine: not tested 79%, 41%, 100% ).

4. 1/17 states with “medical” marijuana”, New Mexico, tests all, but has anomalous 1% positive tests (an outlier, along with Mississippi, North Carolina).
Drug testing of drivers in fatal accidents should be 100%!

STATES WITHOUT “MEDICAL MARIJUANA” LAWS HAVE LOWER PREVALENCE OF DRIVER FATALITIES INVOLVING DRUGS: 27%

1. 24/33 states with no “medical” marijuana” laws have fewer than 20% of driver fatalities involving drugs
73% of states with no “medical marijuana” laws have fewer than 20% driver fatalities testing positive for drug.

2. 9/33 states with no “medical” marijuana” approval have 20% or more driver fatalities involving drugs.
27% of states with no “medical marijuana” laws have 20% or more of driver fatalities involving drugs

3. Ct, state with highest number of fatalities also has highest rate of testing, 99%
Prevalence of driver fatalities involving drugs is three times higher, on average, in states with approved “medical marijuana” laws.

Source: Bertha Madras PhD Harvard Medical School Dec. 2010

Admiral Regina M. Benjamin, released a new report that shows that tobacco smoke, even occasional smoking or secondhand smoke, damages the human body and leads to disease and death.

The 700-page report, “A Report of the Surgeon General: How Tobacco Smoke Causes Disease-The Biology and Behavioral Basis for Smoking,” finds that cellular damage and tissue inflammation from tobacco smoke are immediate, and that repeated exposure weakens the body’s ability to heal the damage.

Even brief exposure to secondhand smoke can cause cardiovascular disease and could trigger acute cardiac events, such as heart attack. The report describes how chemicals from tobacco smoke quickly damage blood vessels and make blood more likely to clot. The evidence in this report shows how smoking causes cardiovascular disease and increases risks for heart attack, stroke, and aortic aneurysm.

The report also explains why it is so difficult to quit smoking. According to the research, cigarettes are designed for addiction. The design and contents of current tobacco products make them more attractive and addictive than ever before. Today’s cigarettes deliver nicotine more quickly and efficiently than cigarettes of many years ago.

You can read the full report at www.surgeongeneral.gov. Last week, CADCA hosted a webinar on tobacco cessation and smoking prevention. A recording of this session, as well as the PowerPoint presentations used during the session, can be accessed online.

Source: www.cadca.org Dec. 2010

[Correspondence]
Tashkin, Donald P.; Roth, Michael D.; Dubinett, Steven M.
UCLA School of Medicine; Los Angeles, CA 90095-1690

———————————————-

To the Editor: You point to largely experiential evidence of the medicinal
benefits of marijuana and the apparent absence of serious short-term toxicity.
However, a note of caution is warranted. Although it is true that smoking
marijuana carries no immediate risk of death, there may be serious adverse
effects in the very patients for whom medicinal marijuana is most commonly
considered (i.e., those whose immune defenses are already compromised by AIDS or
cancer plus chemotherapy). For example, in patients with AIDS, marijuana use has
been associated with the development of both fungal and bacterial pneumonias.
[1,2] Moreover, among HIV-positive persons, marijuana use has been shown to be a
risk factor for rapid progression from HIV infection to AIDS and the acquisition
of opportunistic infections or Kaposi’s sarcoma, or both. [3]

Cellular studies and studies in animals lend support to these potential health
consequences of marijuana. For example, delta-9-tetrahydrocannabinol has been
shown to have immunosuppressive effects on macrophages, natural killer cells,
and T cells, as well as on the response of mice to opportunistic infection. [4]
In our own studies, [5] (and unpublished data) we recovered alveolar macrophages
from the lungs of habitual marijuana smokers and found a significant reduction
in their ability to kill fungi, bacteria, and tumor cells, as well as a
deficiency in their ability to produce protective inflammatory cytokines, such
as tumor necrosis factor (alpha).

Donald P. Tashkin, M.D.

Michael D. Roth, M.D.

Steven M. Dubinett, M.D.

UCLA School of Medicine; Los Angeles, CA 90095-1690

REFERENCES

1. Denning DW, Follansbee SE, Scolaro M, Norris S, Edelstein H, Stevens DA.
Pulmonary aspergillosis in the acquired immunodeficiency syndrome. N Engl J Med
1991;324:654-62. Bibliographic Links

2. Caiaffa WT, Vlahov D, Graham NM, et al. Drug smoking, Pneumocystis carinii
pneumonia, and immunosuppression increase risk of bacterial pneumonia in human
immunodeficiency virus-seropositive injection drug users. Am J Respir Crit Care
Med 1994;150:1493-8. Bibliographic Links

3. Tindall B, Cooper DA, Donovan B, et al. The Sydney AIDS Project: development
of acquired immunodeficiency syndrome in a group of HIV seropositive homosexual
men. Aust N Z J Med 1988;18:8-15. Bibliographic Links

4. Newton CA, Klein TW, Friedman H. Secondary immunity to Legionella pneumophilia
and Th1 activity are suppressed by delta-9-tetrahydrocannabinol. Inject Infect
Immun 1994;62:4015-20.

5. Sherman MP, Campbell LA, Gong H Jr, Roth MD, Tashkin DP. Antimicrobial and
respiratory burst characteristics of pulmonary alveolar macrophages recovered
from smokers of marijuana alone, smokers of tobacco alone, smokers of marijuana
and tobacco, and nonsmokers. Am Rev Respir Dis 1991;144:1351-6. Bibliographic
Links Accession Number: 00006024-199704170-00025

Even mild alcohol intoxication can seriously impair drinkers’ visual acuity, according to a study from the University of Washington.
Researchers found that test subjects who consumed just enough alcohol to reach half the legal alcohol intoxication level in the U.S. performed poorly on tests of their ability to notice an unexpected visual object when they were performing another simple task. Researchers said this was the first study to demonstrate that alcohol can cause such “inattentional blindness.”
“We rely on our ability to perceive a multitude of information when we drive (speed limit, road signs, other cars, etc.),” said study lead author Seema Clifasefi. “If even a mild dose of alcohol compromises our ability to take in some of this information, in other words, limits our attention span, then it seems likely that our driving ability may also be compromised.”
The study was published in the July 2006 issue of the journal Applied Cognitive Psychology.
Reference:
Clifasefi, S. L., Takarangi, M. K. T., Bergman, J. S. (2006) Blind drunk: the effects of alcohol on inattentional blindness. Applied Cognitive Psychology, 20(5): 697-704.

Source:Reported in Medical News Today July 7, 2006

Yes, despite what potheads claim. Doctors in Greece compared the mental abilities of 20 people who had smoked dope four times a week for 15 years with 20 who had used it for less than seven years, and 24 never-smokers. They were given 15 words to learn, and asked to repeat them later. The average score for the long-term smokers was 7; for the shorter-term smokers, 9; for the never-users, 12. It is the latest in many studies showing repeated ‘soft’ drug abuse damages the brain. This isn’t surprising because marijuana’s active ingredient, tetrahydro cannabinol (THC), is highly fat-soluble. As our brain is the organ with the highest concentration of fat, THC makes a beeline for it and stays there for

Source: The Guardian Saturday September 30, 2006

27 October 2006

People addicted to cocaine have an impaired ability to perceive rewards and exercise control due to disruptions in the brain’s reward and control circuits, according to a series of brain-mapping studies and neuropsychological tests conducted at the U.S. Department of Energy’s Brookhaven National Laboratory.
“Our findings provide the first evidence that the brain’s threshold for responding to monetary rewards is modified in drug-addicted people, and is directly linked to changes in the responsiveness of the prefrontal cortex, a part of the brain essential for monitoring and controlling behavior,” said Rita Goldstein, a psychologist at Brookhaven Lab. “These results also attest to the benefit of using sophisticated brain-imaging tools combined with sensitive behavioral, cognitive, and emotional probes to optimize the study of drug addiction, a psychopathology that these tools have helped to identify as a disorder of the brain.”
Goldstein will present details of these studies at a press conference on neuroscience and addiction at the Society for Neuroscience (SfN) annual meeting in Atlanta, Georgia, on Sunday, October 15, 2006, 2 to 3 p.m., and at a SfN symposium on Wednesday, October 18, 8:30 a.m.
Goldstein’s experiments were designed to test a theoretical model, called the Impaired Response Inhibition and Salience Attribution (I-RISA) model, which postulates that drug-addicted individuals disproportionately attribute salience, or value, to their drug of choice at the expense of other potentially but no-longer-rewarding stimuli – with a concomitant decrease in the ability to inhibit maladaptive drug use. In the experiments, the scientists subjected cocaine-addicted and non-drug-addicted individuals to a range of tests of behavior, cognition/thought, and emotion, while simultaneously monitoring their brain activity using functional magnetic resonance imaging (fMRI) and/or recordings of event-related potentials (ERP).
In one study, subjects were given a monetary reward for their performance on an attention task. Subjects were given one of three amounts (no money, one cent, or 45 cents) for each correct response, up to a total reward of $50 for their performance. The researchers also asked the subjects how much they valued different amounts of monetary reward, ranging from $10 to $1000.
More than half of the cocaine abusers rated $10 as equally valuable as $1000, “demonstrating a reduced subjective sensitivity to relative monetary reward,” Goldstein said.
“Such a ‘flattened’ sensitivity to gradients in reward may play a role in the inability of drug-addicted individuals to use internal cues and feedback from the environment to inhibit inappropriate behavior, and may also predispose these individuals to disadvantageous decisions – for example, trading a car for a couple of cocaine hits. Without a relative context, drug use and its intense effects – craving, anticipation, and high – could become all the more overpowering,” she said.
The behavioral data collected during fMRI further suggested that, in the cocaine abusers, there was a “disconnect” between subjective measures of motivation (how much they said they were engaged in the task) and the objective measures of motivation (how fast and accurately they performed on the task).
“These behavioral data implicate a disruption in the ability to perceive inner motivational drives in cocaine addiction,” Goldstein said.
The fMRI results also revealed that non-addicted subjects responded to the different monetary amounts in a graded fashion: the higher the potential reward, the greater the response in the prefrontal cortex. In cocaine-addicted subjects, however, this region did not demonstrate a graded pattern of response to the monetary reward offered. Furthermore, within the cocaine-addicted group, the higher the sensitivity to money in the prefrontal cortex, the higher was the motivation and the self-reported ability to control behavior.
The ERP results showed a similarly graded brain response to monetary reward in healthy control subjects, but not in cocaine-addicted individuals.
“The dysfunctional interplay between reward processing and control of behavior observed in these studies could help to explain the chronically relapsing nature of drug addiction,” Goldstein said. “Our results also suggest the need for new clinical interventions aimed at helping drug abusers manage these symptoms as part of an effective treatment strategy.”

Source: Medical Research News 18th Oct.2006

27 October 2006

Researchers have found altered neural synchronization in people who smoke cannabis, providing evidence to support the link between the use of this drug and schizophrenia.

Altered neural synchronization has previously been demonstrated in patients with schizophrenia. This led Patrick Skosnik (Indiana University, Bloomington, USA) and team to suggest that such alterations may represent a neurophysiological link between schizophrenia symptoms and the neurobehavioral effects of cannabis.

The researchers assessed neural synchronization using electroencephalograms (EEG) to measure auditory steady-state potentials, eg, auditory click trains at specific frequencies – 20, 30, and 40 Hz – in 17 cannabis users and 16 drug naïve individuals.

The cannabis users showed decreased EEG power and signal-to-noise ratio at the stimulation frequency of 20 Hz compared with non-drug users.

Skosnik and colleagues note that there was no significant difference between the two groups with regard to noise power, indicating that the altered neural synchronization in cannabis users was due to decreased signal strength of oscillating circuits and not the increased noise stemming from neural background activity.

The cannabis users also demonstrated increased schizotypal personality characteristics, as assessed on the Schizotypal Personality Questionnaire, compared with controls. However, there was no significant difference between the two groups in scores on the Wechsler Adult Intelligence Scale. This demonstrates that any alterations in neural synchrony were not associated with generalized cognitive or sensory deficits, the researchers note.

Further analysis revealed that scores on the Schizotypal Personality Questionnaire positively correlated with total years of cannabis use. In addition, schizotypy scores negatively correlated with 20 Hz power, indicating that cannabis-using individuals scoring higher in schizotypy had larger deficits in neural synchronization.

“These data provide evidence for neural synchronization and early-stage sensory processing deficits in cannabis use,” the team writes in the American Journal of Psychiatry.

“Given that there is tight coupling of the endocannabinoid and dopamine systems, it appears possible that genetic anomalies leading to altered dopamine activity may interact with early cannabis exposure to produce overt psychosis.”

Source: Am J Psychiatry 2006; 163: 1798–1805
©2006 Current Medicine Group Ltd

The Inextricable Link

Research substantiates the link between violence and alcohol/drug use among adolescents. This link exists not only
for the perpetrators of violence, but also for those who are victims of violence. Eliminating the State Grants portion of the Safe and Drug Free Schools and Communities (SDFSC) program will undoubtedly lead to increases in violence,alcohol and drug use among school-aged youth.

Student Alcohol Use and Violence

• Alcohol use is an independent risk factor for delinquent and violent behaviors among young people.
• Adolescents who abuse alcohol are three times more likely to commit violent offenses than those who do not drink to excess.
• Youth aged 12-17 who reported violent behaviors in the past year also reported higher rates of past year alcohol use compared with youths who did not report violent behavior.

65.9% of those youth reporting heavy alcohol use, 56.8% of those reporting binge drinking, and 43.7% of those reporting past 30-day use of alcohol had also engaged in one or more of the following delinquent behaviors: participating in a serious fight at school or at work; participating in a group-against-group fight; attacking someone with the intent to seriously hurt them; stealing or attempting to steal something worth $50 or more; selling illegal drugs; and/or carrying a hand gun within the last year.

• Alcohol use among adolescents co–occurs with a range of other risky behaviors including violence, tobacco use, sexual activity, drinking and driving and suicide.

Student Alcohol Use and Victimization

• Those who drink, including adolescents, may experience an increased risk of violence because of reduced physical coordination, poor decision-making in threatening situations and isolation while out late at night.
• Alcohol increases vulnerability to victimization above levels of vulnerability brought about other factors.

Student Drug Use and Violence

• Youths who had engaged in fighting or other delinquent behaviors were more likely than other youths to have
used illicit drugs.
• Of those students who reported carrying a gun to school during the 2005-2006 school year, 63.9% report also
using marijuana, 39.9% report using cocaine, and 36.8% report using crystal meth in the past year.
• Of those students who reported hurting others with a weapon at school, 68.4% had used marijuana, 48.3%
had used cocaine, and 44.1% had used crystal meth in the past year.
• Of those students who reported being hurt by a weapon at school, 60.3% reported using marijuana, 41.1% reported
using cocaine and 38.3% reported using crystal meth in the past year.
• Past month illicit drug use was reported by 17.3% of youths who had gotten into serious fights at school or
work in the past year compared with 7.6% of those who had not.
• The incidences of youth physically attacking others, stealing, and destroying property increased in proportion
to the number of days marijuana was smoked in the past year.
• Marijuana users were twice as likely as non-users to report they disobeyed school rules.
• Of those students who reported threatening someone with a gun, knife or club or threatening to hit, slap or kick
someone during the 2005-2006 school year, 27% also reported using marijuana, 7.8% reported using cocaine and 6.2% reported using crystal meth in the past year.
• During the 2005-2006 school year, of those students who reported any trouble with the police, 39.6% also reported
using marijuana, 12.2% reported using cocaine, and 9% reported using crystal meth in the past year.

Community Anti-Drug Coalitions of America > 625 Slaters Lane, Suite 300 > Alexandria, VA 22314 > T 800.542.2322 > cadca.org
CSSourmunity Anti-Drug Coalitions of America > 625 Slaters Lane, Suite 300 > Alexandria, VA 22314 > T 800.542.2322 > cadca.org

Footnotes

1 Komro, K.A., Williams, C.L., Foster, J.L., et al. (1999).
The relationship between adolescent alcohol use and delinquent
and violent behaviors. Journal of Child Adolescent
Substance Abuse, 9(2):13-28.
2 Fergusson, D.M., Lynskey, M.T., Horwood, L.J. (1996).
Alcohol misuse and juvenile offending in adolescence. Addiction,
91(4): 495-510.
3 Office of Applied Studies, Substance Abuse and Mental
Health Services Administration. (2005). The NSDUH report:
Alcohol use and delinquent behaviors among youths. Available:

http://www.oas.samhsa.gov/2k5/alcDelinquent/

alcDelinquent.pdf
4 Ibid.
5 Windle, M. Alcohol Use Among Adolescents. Thousand
Oaks, CA: Sage, 1999.
6 Shepherd, J.P.(1998). Emergency room research on links
between alcohol and violent injury. Addiction, 93(8): 1261–
1262.
7 Shepherd, J.P.; Sutherland, I.; Newcombe, R.G. (2006)
Relations between alcohol, violence and victimization in
adolescence. Journal of Adolescence, 29(4): 539-553.
8 Office of Applied Studies, Substance Abuse and Mental
Health Services Administration. National Survey on Drug
Use and Health: National Findings. (2005). Youth Prevention-
Related Measures: Fighting and Delinquent Behavior.
64. Available: http://oas.samhsa.gov/
nsduh/2k5nsduh/2k5results.pdf.
9 Pride Surveys. (2006). Questionnaire report for grades 6-
12: 2006 national summary. 184. Available: http://
www.pridesurveys.com/customercenter/us05ns.pdf.
10 Pride Surveys. (2006). Questionnaire report for grades 6-
12: 2006 national summary. 197. Available: http://
www.pridesurveys.com/customercenter/us05ns.pdf.
11 Pride Surveys. (2006). Questionnaire report for grades 6-
12: 2006 national summary. 199. Available: http://
www.pridesurveys.com/customercenter/us05ns.pdf.
12 Office of Applied Studies, Substance Abuse and Mental
Health Services Administration. National Survey on Drug
Use and Health: National Findings. (2005). Youth Prevention-
Related Measures: Fighting and Delinquent Behavior.
64. Available: http://oas.samhsa.gov/
nsduh/2k5nsduh/2k5results.pdf.
13 Office of National Drug Control Policy. (2006). Marijuana
Myths and Facts: The Truth Behind 10 Popular Misperceptions.
10. Available: http://www.whitehousedrugpolicy.gov/
publications/marijuana_myths_facts/
marijuana_myths_facts.pdf
14 Ibid.
15 Pride Surveys. (2006). Questionnaire report for grades 6-
12: 2006 national summary. 194. Available: http://
www.pridesurveys.com/customercenter/us05ns.pdf.
16 Pride Surveys. (2006). Questionnaire report for grades 6-
12: 2006 national summary. 195. Available: http://www.pridesurveys.com/customercenter/us05ns.pdf.ourceThe Inextricable S
Source: Cadca online Nov. 2006

Steroid users appear more likely to commit crimes involving weapons and fraud, scientists in Sweden report.
Steroids are linked to manic episodes, depression, suicide, psychotic episodes and increased aggression and hostility, occasionally triggering violent behavior, including murder.
Researchers at Uppsala University in Sweden studied the relationship between crime and steroid use in 1,440 Swedish residents tested for the drugs between 1995 and 2001 from clinics, including substance abuse facilities, as well as police and customs stations.
Of those involved in the study, 241 tested positive, with an average age of about 20.
The research team found those who tested positive for steroid use were roughly twice as likely to have been convicted of a weapons offense and one-and-a-half times as likely to have been convicted of fraud.
When the researchers excluded people from substance abuse facilities from their analysis the connection with armed crime remained, but the link between steroid use and fraud disappeared.
While steroids are linked with outbursts of uncontrolled violence known as “‘roid rage,” they did not appear to be connected with sexual offenses, violent crimes such as murder, assault and robbery, or crimes against property such as theft.
This investigation instead reveals that steroid use may be linked with premeditated crimes—those involving preparation and advance planning.
One explanation the researchers suggest for the findings is that criminals involved in serious crimes such as armed robbery or the collection of crime-related debts might benefit from the muscularity, heavy build and increase in aggression that comes with steroid use.
The scientists report their findings in the November issue of the Archives of General Psychiatry.

Source: Fox News Live Science Monday , November 06, 2006

Does Ketamine Cause Bladder Damage?

Special K and Cystitis.

In early 2008, researchers sat up and took notice of a report published in BJU International, a urology journal. “The destruction of the lower urinary tract by ketamine abuse: a new syndrome?”
The report details the discovery by physicians in Hong Kong of 59 ketamine abusers who had been admitted to urology units in local hospitals from 2000 to 2007. Interstitial cystitis, also known as painful bladder syndrome, can vary from mild to severe, and its cause is often not known. Symptoms include painful, frequent, or urgent urination. The researchers found that 71 % of the patients “showed various degrees of epithelial inflammation similar to that seen in chronic interstitial cystitis. All of 12 available bladder biopsies had histological features resembling those of interstitial cystitis.”

The authors conclude that “secondary renal damage can occur in severe cases, which might be irreversible, rendering patients dependent on dialysis.”
What is believed to be the first official report of the problem appeared in 2007 in Urology, documenting the case of nine Canadian ketamine users with bladder complications. The authors, affiliated with the University of Toronto, conclude: “As illicit ketamine becomes more easily available, ulcerative cystitis and potential long-term bladder sequelae related to its use may be a more prevalent problem confronting urologists.”

This year, similar reports from Bristol in the UK were published in Clinical Radiology. Researchers with the National Health Service and the Bristol Royal Infirmary discovered “a series of 23 patients, all with a history of ketamine abuse, who presented with severe lower urinary tract symptoms.” Various imaging techniques revealed smaller bladder volume, bladder wall thickening, inflammation, urethral strictures, and other bladder pathologies. The patients all reported symptoms similar to those reported by the earlier Hong Kong ketamine users.

The report concludes that “many users are well aware, but are often not forthcoming with this information.” They also maintain that “the key to the effective management of ketamine-induced bladder pathology is early diagnosis.”

Frequent recreational use of ketamine appears ill advised until more research can confirm the true scope of the problem.

Source: http://addiction-dirkh.blogspot.com Oct. 2010

Health and social services are facing a new challenge, as many illicit drug users get older and face chronic health problems and a reduced quality of life. That is one of the key findings of research published in the September issue of the Journal of Advanced Nursing.
UK researchers interviewed eleven people aged 49 to 61 in contact with voluntary sector drug treatment services.
“This exploratory study, together with our wider research, suggest that older people who continue to use problematic or illegal drugs are emerging as an important, but relatively under-researched, international population” says lead author Brenda Roe, Professor of Health Research at Edge Hill University, UK.
“They are a vulnerable group, as their continued drug use, addiction and life experiences result in impaired health, chronic conditions, particular health needs and poorer quality of life. Despite this, services for older drug addicts are not widely available or accessed in the UK.”
Figures from the USA suggest that the number of people over 50 seeking help for drug or alcohol problems will have risen from 1.7 million in 2000 to 4.4 million by 2020. And the European Monitoring Centre for Drugs and Drug Addiction estimates that the number of people aged 65 and over requiring treatment in Europe will double over the same period.
The nine men and two women who took part in the study had an average age of 57. All were currently single and their homes ranged from a caravan, hostel or care home to social housing. Key findings from the study – by the Evidence-based Practice Research Centre at Edge Hill University and the Centre for Public Health at Liverpool John Moores University – included:
• Most started taking drugs as adolescents or young adults, often citing recreational use, experimenting or being part of the hippy era. Child abuse and the death of a parent were also mentioned.
Some started taking drugs late in life due to stressful life events like divorce or death. Meeting a drug using partner was another trigger. One man started taking drugs later in life to shock his drug taking partner into stopping and ended up developing a drug habit himself.
• First drug use varied from magic mushrooms, LSD, amphetamines and cannabis to heroin and methadone. Alcohol and smoking often featured alongside drug use.
• Some increased their drug use over time, while others had periods when they tried to reduce or even abstain from drugs. All but two of the participants were taking methadone, either as maintenance or as part of a reduction strategy in order to give up drugs.
• A number of the participants said they were trying to use drugs responsibly and it was felt that their age and the influence of drug treatment services were factors in this. They also appeared more aware of the need to maintain their personal safety, based on previous experiences.
• Most recognised that their drug use was having detrimental and cumulative effects on their health, as they had developed a range of chronic and life-threatening conditions that required hospitalisation and ongoing treatment.
• Physical health conditions included: circulatory problems such as deep vein thrombosis, injection site ulcers, stroke, respiratory problems, pneumonia, diabetes, hepatitis and liver cirrhosis. Malnutrition, weight loss and obesity also featured, as did accidental injuries due to falls and drug overdoses.
• Common mental health problems included memory loss, paranoia and changed mood states, with anxiety or anger also featuring.
• All wished they hadn’t started taking drugs and would advise young people not to. A few were keen to give up, but others felt it was too hard. One man described his drug use as “disgusting and squalid” while another said that the older he got the worse his drug use got and that it was a “crazy” situation.
• All were single or divorced and drug use was a common factor in relationship breakdowns. Most lived alone, with three relying on carers who were also drug users. Pets were often important for some, providing companionship as well as a sense of responsibility and structure to their day.
• Drug use was often associated with chaotic lifestyles and relationships and some reported periods of imprisonment.
• Participants were positive about the support they received from voluntary drug services, but had mixed experiences of primary and hospital care. Some felt stigmatised by healthcare professionals, while others received compassion and acknowledgement of their drug use.
“Our population is ageing and the people who started using drugs in the sixties are now reaching retirement age” says Professor Roe.
“It is clear that further research is needed to enable health and social care professionals to develop appropriate services for this increasingly vulnerable group. We also feel that older drug users could play a key role in educating younger people about the dangers of drug use.”

Source: ww.news-medical.net/news 9th Sept 2010

Both drinking and withdrawal from chronic drinking can raise circulating glucocorticoid levels, known as cortisol in humans and corticosterone in rodents. Prolonged and high concentrations of glucocorticoids can have damaging effects on neuronal function and cognition. Evidence shows that glucocorticoids are associated with neurotoxicity during abstinence after withdrawal from alcohol dependence (AD), and that glucocorticoid receptor antagonism may represent a pharmacological option for recovery.

A review of this evidence will be published in the December 2010 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.
“Prolonged and elevated levels of glucocorticoid hormones can damage or destroy neurons, and lead to an increased vulnerability to other situations that can damage neurons, such as raised excitatory amino acid activity,” explained A.K. Rose, a lecturer in psychology at the University of Liverpool and corresponding author for the review. “This can underlie loss of memory functions.”
“High levels of brain cortisol associated with stress have long been linked to deficits in neuronal function, which can be seen in aging,” added John Littleton, a professor in the department of pharmaceutical sciences at the University of Kentucky.
Among the review’s key points:
Brain glucocorticoid concentrations increase and glucocorticoid receptor occupancy decreases during prolonged abstinence after withdrawal from alcohol.
“Our evidence shows that brain concentrations of corticosterone remain raised for long periods after alcohol withdrawal, even after the blood concentrations return to normal levels,” said H.J. Little, a professor in addiction science at King’s College London and who conducted this research. “Furthermore, the corticosterone concentrations remained increased in rodent brains for up to two months, approximately five human years, following cessation of prolonged alcohol drinking.”
“One of the most important questions for research and treatment is why alcoholics can relapse after many months of abstinence,” observed Littleton. “Partly this can be attributed to the effects of conditioning in which ‘cues’ provoke craving for alcohol, as well as a ‘protracted withdrawal syndrome’ which includes anxiety, sleep disturbances, and general feelings of being unwell. Prolonged high levels of brain cortisol after withdrawal from alcohol may explain the strength of these cues, and many of the symptoms of protracted withdrawal.”
Increased glucocorticoid levels in the brain after alcohol treatment are associated with cognitive deficits seen during abstinence, affecting both treatment efficacy and quality of life.
“Cessation of drinking is clearly linked to cognitive deficits,” said Little. “For example, visuospatial learning can be worse in abstinent alcoholics than in those still intoxicated, and memory and learning deficits have been found in rats after alcohol withdrawal, but not during alcohol intake. Furthermore, greater neuronal degeneration has been reported after cessation of chronic alcohol intake than during its consumption, and multiple withdrawal episodes cause greater neuronal damage than a single withdrawal episode.”
“This point is important because cognitive deficits in alcoholics during attempted abstinence can interfere with treatment options such as ‘cognitive behavior therapy’ and also drug treatment,” said Littleton. “Drugs targeting the effects of cortisol in the brain might therefore both reduce the chances of relapse and reduce the cognitive deficits that interfere with treatment.”
Glucocorticoids are involved in the neuropathological consequences of AD.
“Animal and cell-culture research show very convincingly that cortisol/corticosterone can increase neurotoxicity associated with periods of alcohol withdrawal,” said Littleton. “Since the highest cortisol levels were found in the prefrontal cortex and hippocampus, this may explain why these areas are damaged in alcoholics. This makes the brain cortisol glucocortcoid receptors a potential target for prevention of alcohol-induced brain damage.”
“If cognitive impairments could be reduced, patients would be more likely to engage in, and thus benefit from, psychosocial treatments,” added Rose. “Better cognitive function coupled with better treatment engagement is likely to produce better treatment outcomes and quality of life. A person with greater cognitive function is likely to be more able to find work and re-build relationships.
“In summary,” said Littleton,” stress, the hypothalamo-pituitary adrenal axis, and cortisol are very important determinants of the natural history of alcoholism — affecting an individual’s drinking behavior, the effects on cognition and memory, and the likelihood of relapsing into alcoholism during abstinence. We can also see that hypotheses applicable to animals can now be applied to inform new human research.”
Add’l Contact: H.J. Little, Ph.D. hilary.little@sgul.ac.uk 44.207.848.0436 (England) King’s College London

Source: Alcoholism: Clinical & Experimental Research, 7 SEP 2010 DOI: 10.1111/j.1530-0277.2010.01298.x

Recent research has clarified a number of important questions concerning adverse effects of cannabis on health. A causal role of acute cannabis intoxication in motor vehicle and other accidents has now been shown by the presence of measurable levels of Delta(9)-tetrahydrocannabinol (THC) in the blood of injured drivers in the absence of alcohol or other drugs, by surveys of driving under the influence of cannabis, and by significantly higher accident culpability risk of drivers using cannabis. Chronic inflammatory and precancerous changes in the airways have been demonstrated in cannabis smokers, and the most recent case-control study shows an increased risk of airways cancer that is proportional to the amount of cannabis use. Several different studies indicate that the epidemiological link between cannabis use and schizophrenia probably represents a causal role of cannabis in precipitating the onset or relapse of schizophrenia. A weaker but significant link between cannabis and depression has been found in various cohort studies, but the nature of the link is not yet clear. A large body of evidence now demonstrates that cannabis dependence, both behavioral and physical, does occur in about 7-10% of regular users, and that early onset of use, and especially of weekly or daily use, is a strong predictor of future dependence. Cognitive impairments of various types are readily demonstrable during acute cannabis intoxication, but there is no suitable evidence yet available to permit a decision as to whether long-lasting or permanent functional losses can result from chronic heavy use in adults. However, a small but growing body of evidence indicates subtle but apparently permanent effects on memory, information processing, and executive functions, in the offspring of women who used cannabis during pregnancy. In total, the evidence indicates that regular heavy use of cannabis carries significant risks for the individual user and for the health care system.

Source: Prog Neuropsychopharmacol Biol Psychiatry. 2004 Aug;28(5):849-63.

Neurobiology of cannabis–recent data enlightening driving disturbances

Abstract

During the last decades a new landscape of cannabis has been designed on account of: the increase in its use the greater youth of its users; the increase in the content of its main active constituent tetrahydrocannabinol (THC) and a lot of new epidemiological and neurobiological data. THC displays an exceptional lipophilicity, allowing its cerebral storage, leading to long lasting effects, by far more lasting than its presence in blood, and beyond the period throughout the intoxicated people feel a disablement. This is linked to its slow release from brain areas in which large proportion of spare receptors exists (reserve receptors). THC disturbs cognition and various skills required in driving. It may be responsible for psychiatric troubles: anxiety, depression, suicide attempt, psychotic attack, triggering of schizophrenia. It potentiates the alcohol effects and incites to alcohol drinking. It displays close relationships with dependence to heroin. This new landscape of cannabis urges to make a radical alteration in the public communication about this drug of abuse as it has yet collected so many troubles, accidents or tragedies.

Source: Ann Pharm Fr. 2006 May;64(3):148-59.

Dose related risk of motor vehicle crashes after cannabis use.

Abstract

The role of Delta(9)-tetrahydrocannabinol (THC) in driver impairment and motor vehicle crashes has traditionally been established in experimental and epidemiological studies.
Experimental studies have repeatedly shown that THC impairs cognition, psychomotor function and actual driving performance in a dose related manner. The degree of performance impairment observed in experimental studies after doses up to 300 microg/kg THC were equivalent to the impairing effect of an alcohol dose producing a blood alcohol concentration (BAC) >/=0.05 g/dl, the legal limit for driving under the influence in most European countries. Higher doses of THC, i.e. >300 microg/kg THC have not been systematically studied but can be predicted to produce even larger impairment.
Detrimental effects of THC were more prominent in certain driving tasks than others. Highly automated behaviors, such as road tracking control, were more affected by THC as compared to more complex driving tasks requiring conscious control.
Epidemiological findings on the role of THC in vehicle crashes have sometimes contrasted findings from experimental research. Case-control studies generally confirmed experimental data, but culpability surveys showed little evidence that crashed drivers who only used cannabis are more likely to cause accidents than drug free drivers.
However, most culpability surveys have established cannabis use among crashed drivers by determining the presence of an inactive metabolite of THC in blood or urine that can be detected for days after smoking and can only be taken as evidence for past use of cannabis. Surveys that established recent use of cannabis by directly measuring THC in blood showed that THC positives, particularly at higher doses, are about three to seven times more likely to be responsible for their crash as compared to drivers that had not used drugs or alcohol.
Together these epidemiological data suggests that recent use of cannabis may increase crash risk, whereas past use of cannabis does not. Experimental and epidemiological research provided similar findings concerning the combined use of THC and alcohol in traffic. Combined use of THC and alcohol produced severe impairment of cognitive, psychomotor, and actual driving performance in experimental studies and sharply increased the crash risk in epidemiological analyses.

Source¨ Drug Alcohol Depend. 2004 Feb 7;73(2):109-19

Schizophr Bull. 2010 Mar 11. [Epub ahead of print]
The Impact of Substance Use on Brain Structure in People at High Risk of Developing Schizophrenia.
Welch KA, McIntosh AM, Job DE, Whalley HC, Moorhead TW, Hall J, Owens DG, Lawrie SM, Johnstone EC.
1Division of Psychiatry, School of Molecular and Clinical Medicine, University of Edinburgh, Royal Edinburgh Hospital, Edinburgh EH10 5HF, UK.
Abstract
Ventricular enlargement and reduced prefrontal volume are consistent findings in schizophrenia. Both are present in first episode subjects and may be detectable before the onset of clinical disorder. Substance misuse is more common in people with schizophrenia and is associated with similar brain abnormalities. We employ a prospective cohort study with nested case control comparison design to investigate the association between substance misuse, brain abnormality, and subsequent schizophrenia. Substance misuse history, imaging data, and clinical information were collected on 147 subjects at high risk of schizophrenia and 36 controls. Regions exhibiting a significant relationship between level of use of alcohol, cannabis or tobacco, and structure volume were identified. Multivariate regression then elucidated the relationship between level of substance use and structure volumes while accounting for correlations between these variables and correcting for potential confounders. Finally, we established whether substance misuse was associated with later risk of schizophrenia. Increased ventricular volume was associated with alcohol and cannabis use in a dose-dependent manner. Alcohol consumption was associated with reduced frontal lobe volume. Multiple regression analyses found both alcohol and cannabis were significant predictors of these abnormalities when simultaneously entered into the statistical model. Alcohol and cannabis misuse were associated with an increased subsequent risk of schizophrenia. We provide prospective evidence that use of cannabis or alcohol by people at high genetic risk of schizophrenia is associated with brain abnormalities and later risk of psychosis. A family history of schizophrenia may render the brain particularly sensitive to the risk-modifying effects of these substances.

Vlahov, D. et al. Increased Use of Cigarettes, Alcohol, and Marijuana among Manhattan, New York, Residents after the September 11th Terrorist Attacks. American Journal of Epidemiology. 155(11):988-996, June 1, 2002.
Found that New Yorkers who increased their use of marijuana, tobacco or alcohol in after September 11 had increased chances of developing Post Traumatic Symptoms. Marijuana increased both PTS symptoms and depression more than the other substances.

In a large drug use survey of men born between 1944-1954, found that marijuana users who use the drug to cope with problems are more depressed than those who do not use to cope with problems.
Musty, R. Kaback, L. Relationships between motivation and depression in chronic marijuana users. Life Sciences. Volume 56, Issues 23-24, 5 May 1995, Pages 2151-2158.
Compared heavy and moderate marijuana users on several motivation and depression scales. Found that heavy users’ lack of motivation is correlated with their level of depression.
Bovasso, G. Cannabis Abuse as a Risk Factor for Depressive Symptoms.
Am J Psychiatry 158:2033-2037, December 2001.
People with a diagnosis of cannabis abuse at baseline were four times more likely than those with no cannabis abuse diagnosis to have depressive symptoms at the follow-up assessment, after adjusting for age, gender, antisocial symptoms, and other baseline covariates. In particular, these participants were more likely to have experienced suicidal ideation and anhedonia during the follow-up period.

Source: GREEN B. RITTER C. Marijuana use and depression. Journal of health and social behavior. 2000, vol. 41, no1, pp. 40-49 (1 p.3/4)

Smoking cannabis is more harmful than cigarettes and more likely to
trigger cancer, according to a report.

Just three cannabis ‘joints’ a day can cause the same amount of damage to the lungs as an entire packet of 20 cigarettes.

The British Lung Foundation says that when cannabis and tobacco are
smoked together, the harmful effects are significantly worse.

Its research suggests young cannabis smokers may also be at greater risk of throat and gullet cancers.

The foundation found that tar from cannabis joints contains 50 per cent more cancer-causing toxins than cigarettes made from tobacco alone.

Eight million Britons are thought to smoke cannabis, which some experts believe is a ‘gateway’ to harder drugs such as heroin and cocaine.

Earlier this year, researchers found that 79 per cent of children
thought cannabis was safe while only 2 per cent recognised there are
health risks from smoking the drug.

Dame Helena Shovelton, chief executive of the British Lung Foundation, said the harmful effects of cannabis had been swept under the carpet.

‘People are under the illusion it is safe to smoke cannabis. Our report
shows it is very dangerous to lung health, at least as dangerous as tobacco.

‘It seems society is in the same position as when research first showed the harm caused by tobacco. It took 15 years for the Government to take notice but we don’t want to repeat the mistakes of the past.’

Dame Helena said cannabis available today is 15 times stronger than the drug smoked in the 1960s. ‘This means studies carried out at that time will probably have underestimated the effects of cannabis smoking,’ she explained.

‘Puff and inhalation volume with cannabis is up to four times higher
than with tobacco – in other words you inhale deeper and hold your
breath with the smoke for longer before exhaling.

‘This results in more poisonous carbon monoxide and tar entering into
the lungs,’ Dame Helena said.

The foundation’s report – A Smoking Gun? – analyses research from around the world.

It found cannabis smokers have a higher level of chronic and acute
respiratory-conditions such as coughingwheezing and bronchitis. ‘When cannabis is smoked together with tobacco then the effects are additive’, it says.

Some studies suggest cannabis smoking may trigger chronic obstructive pulmonary disease which kills 32,000 people in Britain every year, the foundation’s report adds.

‘Research linking cannabis smoking to the development of respiratory
cancer exists although there have also been conflicting findings.

‘Not only does the tar in a cannabis cigarette contain many of the same carcinogens as tobacco smoke, but the concentrations of these are up to 50 per cent higher in the smoke of a cannabis cigarette,’ it says.

Benzyprene, found in the tar of cannabis joints, can change the make-up of one of the genes which suppresses tumours and could therefore make cancer more likely for people who smoke joints.

There are also more than 75 case studies of young cannabis smokers with cancers of the throat and gullet – diseases usually rare in people under 60.

Source: Daily Mail
Monday 11 Nov 2002

A new compound similar to the active component of marijuana (cannabis) might provide effective pain relief without the mental and physical side effects of cannabis, according to a study in the July issue of Anesthesia & Analgesia, official journal of the International Anesthesia Research Society (IARS).

The synthetic cannabinoid (cannabis-related) compound, called MDA19, seems to avoid side effects by acting mainly on one specific subtype of the cannabinoid receptor. “MDA19 has the potential for alleviating neuropathic pain without producing adverse effects in the central nervous system,” according to the study by Dr Mohamed Naguib of The University of Texas M.D. Anderson Cancer Center.

MDA19 Works on a Single Cannabinoid Receptor
The researchers performed a series of experiments to analyze the pharmacology and effects of the synthetic cannabinoid MDA19. There are two subtypes of the cannabinoid chemical receptor: CB1, found mainly in the brain; and CB2, found mainly in the peripheral immune system.

Dr. Naguib’s group has been doing research to see if the cannabinoid receptors—particularly CB2—can be a useful target for new drugs to treat neuropathic pain. Neuropathic pain is a difficult-to-treat type of pain caused by nerve damage, common in patients with trauma, diabetes, and other conditions.

MDA19 was designed to have a much stronger effect on the CB2 receptor than on the CB1 receptor. In humans, MDA19 showed four times greater activity on the CB2 receptor than on the CB1 receptor. In rats, the difference was even greater. The experiments also showed that MDA19 had “protean” effects, so-called after the shape-shifting Greek sea god Proteus—under different conditions, it could either block or activate the cannabinoid receptors.

In rats, treatment with MDA19 effectively reduced specific types of neuropathic pain, with greater effects at higher doses. At the same time, it did not seem to cause any of the behavioral effects associated with marijuana.

Potential to Develop Effective Pain Drugs that Avoid Side Effects
The “functional selectivity” of MDA19—the fact that it acts mainly on the CB2 receptor and has a range of effects under differing conditions—could have important implications for drug development. “[W]ith functionally selective drugs, it would be possible to separate the desired from the undesired effects of a single molecule through a single receptor,” Dr. Naguib and colleagues write.
This means that MDA19 could be a promising step toward developing medications that have the pain-reducing effect of cannabinoids while avoiding the mental and physical side effects of marijuana itself. However, more research will be needed before MDA19 or other agents that act on the CB2 receptor are ready for testing in humans.

“These elegant studies by Professor Naguib demonstrate remarkable analgesic properties for this synthetic cannabinoid,” comments Dr. Steven L. Shafer of Columbia University, Editor-in-Chief of Anesthesia &Analgesia. “The studies suggest a novel mechanism for this protean agonist. Although preliminary, these studies suggest that synthetic cannabinoids may be significant step forward for patients suffering from neuropathic pain.”

SOURCE : www.news-medical.net 2nd July 2010

A typical drug user’s transition to addiction could result from a persistent impairment of synaptic plasticity in a key structure of the brain, suggests a new French study.
The research, by the teams of Pier Vincenzo Piazza and Olivier Manzoni, at the Neurocentre Magendie in Bordeaux, appears in the journal Science.

This study is the first demonstration that a correlation exists between synaptic plasticity and the transition to addiction. The results from the teams at Neurocentre Magendie call into question the hitherto held idea that addiction results from pathological cerebral modifications, which develop gradually with drug usage.

Their results show that addiction may, instead, come from a form of anaplasticity, i.e. from incapacity of addicted individuals to counteract the pathological modifications caused by the drug to all users.

The voluntary consumption of drugs is a behaviour found in many species of animals. However, it had long been considered that addiction, defined as compulsive and pathological drug consumption, is behaviour specific to the human species and its social structure.

In 2004, the team of Pier Vincenzo Piazza showed that the behaviours which define addiction in humans, also appear in some rats which will self administer cocaine. Addiction exhibits astonishing similarities in men and rodents, in particular the fact that only a small number of consumers (humans or rodents) develop a drug addiction. The study of drug dependent behaviour in this mammal model thus opened the way to the study of the biology of addiction.

Today, thanks to a fruitful collaboration, the teams of Pier Vincenzo Piazza and Olivier Manzoni are reporting discovery of the first known biological mechanisms for the transition from regular but controlled drug taking to a genuine addiction to cocaine, characterised by a loss of control over drug consumption.

Chronic exposure to drugs causes many modifications to the physiology of the brain. And researchers wanted to find out which of these modifications is responsible for the development of an addiction.
The addiction model developed in Bordeaux provides a unique tool to answer this question. Thus it allows comparing animals who took identical quantities of drugs, but of which only few become addicted.

By comparing addict and non-addict animals at various time points during their history of drug taking, the teams of Pier Vincenzo Piazza and Olivier Manzoni have demonstrated that the animals which developed an addiction to cocaine exhibit a permanent loss of the capacity to produce a form of plasticity known as long-term depression (or LTD).

LTD refers to the ability of the synapses (the region of communication between neurons) to reduce their activity under the effect of certain stimulations. It plays a major role in the ability to develop new memory traces and, consequently, to demonstrate flexible behaviour.

After short-term usage of cocaine, LTD is not modified. However, after a longer use, a significant LTD deficit appears in all users. Without this form of plasticity, which allows new learning to occur, behaviour with regard to the drug becomes more and more rigid, opening the door to development of a compulsive consumption.

The brain of the majority of users is able to produce the biological adaptations which allow to counteract the effects of the drug and to recover a normal LTD.
By contrast, the anaplasticity (or lack of plasticity) exhibited by the addicts leaves them without defences and hence the LTD deficit provoked by the drug becomes chronic.

This permanent absence of synaptic plasticity would explain why drug seeking behaviour becomes resistant to environmental constraints (difficulty in procuring the substance, adverse consequences of taking the drug on health, social life, etc.) and consequently more and more compulsive. Gradually, control of the taking of the drug is lost and addiction appears.

For Pier-Vincenzo Piazza and his collaborators, these discoveries also have important implications for developing new treatment of addiction.

“We are probably not going to find new therapies by trying to understand the modifications caused by a drug in the brains of drug addicts,” explain the researchers, “since their brain is anaplastic.” For the authors, “The results of this work show that it is in the brain of the non-addicted users that we will probably find the key to a true addiction therapy.

Indeed,” the authors estimate, “understanding the biological mechanisms which enable adaptation to the drug and which help the user to maintain a controlled consumption could provide us with the tools to combat the anaplastic state that leads to addiction”. (ANI)

Source: www.sify.com/news 2010-06-29

Researchers have found that a specific and remarkably small fragment of RNA appears to protect rats against cocaine addiction – and may also protect humans.
The discovery could lead to better ways of predicting drug abuse risk and treating addictions

In the study, researchers at The Scripps Research Institute in Jupiter, Florida found that cocaine consumption increased levels of a specific microRNA sequence in the brains of rats, named microRNA-212.

As its levels increased, the rats exhibited a growing dislike for cocaine, ultimately controlling how much they consumed.
On the other hand, as levels of microRNA-212 decreased, the rats consumed more cocaine and became the rat equivalent of compulsive users.

The study’s findings suggest that microRNA-212 plays a pivotal role in regulating cocaine intake in rats and perhaps in vulnerability to addiction.
Interestingly, the same microRNA-212 identified in this study, is also expressed in the human’s dorsal striatum, a brain region that has been linked to drug abuse and habit formation.

“This study enhances our understanding of how brain mechanisms, at their most fundamental levels, may contribute to cocaine addiction vulnerability or resistance to it,” Nature quoted National Institute on Drug Abuse (NIDA) Director Dr. Nora D. Volkow, as saying.

“This research provides a wonderful example of how basic science discoveries are critical to the development of new medical treatments and targeted prevention,” he added.

Rats with a history of extended cocaine access can demonstrate behavior similar to that observed in humans who are dependent on the drug.
Current data show that about 15 percent of people who use cocaine become addicted to it.
The findings suggest that microRNAs may be important factors
contributing to this vulnerability.

“The results of this study offer promise for the development of a totally new class of anti-addiction medications. Because we are beginning to map out how this specific microRNA works, we may be able to develop new compounds to manipulate the levels of microRNA-212 therapeutically with exquisite specificity, opening the possibility of new treatments for drug addiction,” said Paul J. Kenny, senior author on the study.
The study is published in the journal Nature. (ANI)

Source:www.sify.com/news 9th July 2010-07-10

Marijuana used for medical purposes has the same long term effect on the user as marijuana used for recreation. Marijuana use can cause impairment of short-term memory, attention, motor skills, reaction time, and the organization and integration of complex information.

Marijuana use alters perceptions and creates time distortion and can cause drowsiness and lethargy. Heavy marijuana use can cause apathy, decreased motivation, and impair cognitive performance and can cause mental health problems.

Employees who use marijuana off-duty are still effected by it. Impaired cognition that can cause lapses in judgement can remain for a long period. Memory defects can last as long as six weeks. See: Abbie Crites-Leoni, Medicinal Use of Marijuana: Is the Debate a Smoke Screen for Movement Toward Legalization? 19 J. Legal Med. 273, 280 (1998) (citing Schwartz, et al., Short- Term Memory Impairment in Cannabis-Dependent Adolescents, 143 Am. J. Dis. Child. 1214 (1989)

Employers may be liable for the actions of employee who use marijuana especially those employees in safety sensitive positions. The more chronic the use of “medical” marijuana the higher the risk.

VIOLATIONS OF FEDERAL LAW

Will employers have to accommodate marijuana use that violates federal law? Marijuana, remains illegal under federal law because of its “high potential for abuse,” its lack of any “currently accepted medical use in treatment in the United States,” and its “lack of accepted safety for use … under medical supervision.”Gonzales v. Raich, 545 U.S. 1 (2005); United States v. Oakland Cannabis Buyers’ Cooperative, 532 U.S. 483 (2001)

IF THIS BILL PASSES “MEDICAL” MARIJUANA WILL RESULT IN MORE MARIJUANA USE AMONG EMPLOYEES

As consumers we all pay for lost productivity and job-related accidents in the final costs of the produced goods and higher insurance premiums due to workplace accidents. Drug using employees are not as safe. They are 3.6 times more likely to be involved in a work-related accident than their non-using employee, and 5 times more likely to file workers’ compensation claims. As many as 50% of all workers’ compensation claims may involve substance abuse.[FN1]

The U.S. Postal Service did a study that showed that substance abusers have 55% more accidents, experience 85% more on-the-job injuries, and have a 78% higher rate of absenteeism when compared to non-substance abusing employees.[FN2] A report by the National Safety Council claimed that 80% of those injured in serious drug-related work accidents are not the drug using employees, but innocent employees and others.[FN3]

Drug using employees commit workplace crimes. There is a very significant statistical correlation between drug use and criminal conduct.[FN4]

Substance abuse also causes:
Domestic and financial difficulties for employees;
Poor judgment in employment decision making;
Potential embarrassment to the employer as a result of off-duty conduct, which may be publicized, including criminal charges, diversion of supervisory and managerial time;
Damage to company property; and
Time devoted to discipline and grievance matters.[FN5]

While the studies vary somewhat, it is clear that there is substantial substance abuse in the workplace and it has a powerful negative impact on our economy and productivity. The increased use of “medical” marijuana will magnify all these problems.

References

[FN1] Current, The Truth About Drug Testing: Answers to the Questions Everyone Is Asking, p. 3 (1st Ed., Fort Lauderdale, FL, 1998).

[FN2] “Pre-employment Drug Testing: Association with EAP, Disciplinary, and Medical Claims Information” U.S. Postal Service, Personnel Research and Development Branch, Office of Selection and Evaluation, July 1992.

[FN3] Wisotsky, The Ideology of Drug Testing [Ideology of Drug Testing], 11 Nova L Rev 763, 768 (1987).

[FN4] See Stewart, Proof Positive of Drug Link to Crime, Wall St J, May 28, 1987, at 26, col 3.

[FN5]Alcohol & Drugs in the Workplace: Costs, Control and Controversies, A BNA Special Report [Costs, Control and Controversies], 7 (Bureau of National Affairs, Washington, D.C. 1986)

Source: David Evans sent to DFAF May 2010

A new study from the David Geffen School of Medicine at UCLA suggests that increasing cigarette taxes could be an effective way to reduce smoking among individuals with alcohol, drug or mental disorders.

The study, published online in the American Journal of Public Health, found that a 10 percent increase in cigarette pricing resulted in an 18.2 percent decline in smoking among people in these groups.

The findings demonstrate that increasing cigarette taxes could be a way to curb smoking, which is still the leading preventable cause of death in the United States, according to the study’s lead author, Dr. Michael Ong, an assistant professor of medicine in the division of general internal medicine and health services research at the Geffen School of Medicine.
“Whatever we can do to reduce smoking is critical to the health of the U.S.,” said Ong, who is also a researcher at UCLA’s Jonsson Cancer Center. “Cigarette taxes are used as a key policy instrument to get people to quit smoking, so understanding whether people will really quit is important.

Individuals with alcohol, drug or mental disorders comprise 40 percent of remaining smokers, and there is little literature on how to help these people quit smoking.”

Prior research on the effect of cigarette pricing on smoking, which had been conducted using information from 1991, suggested that individuals with mental illness were less likely than other individuals to quit due to price increases. Unlike that research, however, the current study expanded the research to include people with alcohol and drug disorders.

The researchers based their work on data from 7,530 individuals from the 2000-01 Healthcare for Communities Household Survey. Of those, 2,106 people, or 23 percent, had alcohol, drug or mental disorders during the previous year. Of that group, 43.8 percent were smokers — a much higher proportion than among rest of the population.

Though the researchers found that people with alcohol dependence did not cut down on cigarettes when prices rose, people with binge-drinking problems, substance-use disorders and mental disorders were significantly more likely to quit smoking if prices rose, as would occur with a cigarette tax increase.

While the study does suggest that increasing cigarette prices through taxation could reduce smoking among individuals with alcohol, drug or mental disorders, the authors note that further study is needed to determine if recent cigarette price increases have reduced smoking among individuals with such disorders, and whether the identified association is causal.

Source: http://www.sciencedaily.com/releases June 3, 2010

California data on drivers involved in passenger vehicle fatal crashes using Marijuana were analyzed to determine the impact on traffic safety and to provide information on the possible impact of an initiative, the Tax and Regulate Cannabis Initiative or “TC2010” which is on the California ballot in November 2010 to reform and partially legalize Marijuana.

A total of 1240 persons were killed in the last five years in fatal motor vehicle crashes involving Marijuana. 230 were killed in 2008. Use has increase steadily in the last ten years and is now at 5.5% in fatal passenger vehicle crashes. The use in single vehicle fatal crashes where most drivers are tested shows an involvement rate of 8.3%.

The largest increases occurred in the 5 years following the establishment of the Medical Marijuana Program in January 2004. For the five years following legalization there were 1240 fatalities in fatal crashes, compared to the 631 fatalities for the five years prior, for an increase of almost 100%.

In 2008 there were 8 counties where more than 16% of the drivers in fatal crashes tested positive for Marijuana. Five of the 8 counties had rates over 20% Based on this experience, a use rate of 16% to 20% is very likely. A rate increase to only 16%, would result in 670
fatalities, and at 20% we would have about 840 fatalities annually. The 20% level would be more than triple the present level of 230 fatalities in 2008. At these levels, Marijuana would rival alcohol at 17.9%, as the top cause of traffic fatalities.

If “TC2010” passes, tax income on Marijuana is estimated at $1.4 billion annually compared to an estimated $4 billion or more economic loss from Marijuana related fatal crashes.
Over 80% of the Marijuana drivers are male, with a median age of 25. In addition, about half (48%) of the drivers using Marijuana also were legally intoxicated. About 75% of the drivers that used Marijuana did not use any other drug. About 1.2 fatalities were reported for each Marijuana involved driver.

Authors: Alfred Crancer and Alan Crancer

Source: -Received June 2010 from Drug Free America Foundation

“This report summarises the key findings from a report exploring public attitudes towards illegal drugs and drug misuse in Scotland, based on data from the 2009 Scottish Social Attitudes survey. It focuses in particular on attitudes towards opiate misuse, and on views of potential policy responses to this. However, it also places such attitudes in the context of wider views and experiences of illegal drugs.”

Main Findings
■ Support for legalising cannabis – which increased in Scotland (as in the rest of the UK) in the late 1990s – has fallen considerably in more recent years, from 37% in 2001 to 24% in 2009. Attitudes towards prosecution for possession of cannabis for personal use also hardened between 2001 and 2009.

■ Most people said taking cocaine occasionally is wrong – 76% rated it as 4 or 5 on a scale where 5 meant ‘very seriously wrong’.

■ 45% of people agreed that ‘Most people who end up addicted to heroin have only themselves to blame’, while just 27% disagreed.

■ Around half (53%) disagreed that ‘most heroin users come from difficult backgrounds’ (29% agreed).

■ Among those in paid employment, around half (47%) said they would be ‘very’ or ‘fairly comfortable’ working alongside someone they knew had used heroin in the past, while around 1 in 5 would be uncomfortable.

■ Just a quarter (26%) said they would be comfortable with someone who was receiving help to stop using heroin moving near to them, while half (49%) would be uncomfortable.

■ There was no public consensus on what should be the top government priority for tackling heroin use in Scotland – 32% chose ‘tougher penalties for those who take heroin’, 32% ‘more help for people who want to stop using heroin’ and 28% ‘more education about drugs’.

■ Just 16% agreed that people who possess heroin for personal use should not be prosecuted (compared with 34% for cannabis).

■ Public support for providing clean needles to injecting drug users fell from 62% in 2001 to 50% in 2009.

■ Opinion on educating young people about safer drug use was split – 44% agreed that young people should be given information about how to use drugs more safely, but 40% disagreed.

■ Four out of five (80%) agreed that ‘the only real way of helping drug addicts is to get them to stop using drugs altogether’. However, 29% agreed that ‘most heroin users can never stop using drugs completely’, while 27% said they neither agreed nor disagreed or did not know.

■ 63% disagreed that ‘Someone who has been a heroin addict can never make a good parent, even if their drug problems are in the past’.

■ Around two thirds (64%) said that young children of heroin users should be placed into temporary foster care until the parents stop taking heroin. A further 1 in 5 believed the child should stay at home while the family receives help from social workers and just 8% said the child should be permanently adopted by another family.

The full report is also accessible online.

Source: http://uwsnealb.wordpress.com/2010/05/28/scottish-social-attitudes-survey-2009-public-attitudes-to-drugs-and-drug-use-in-scotland/ May 25 2010

Levels of the serotonin transporter are low in the brains of users of ecstasy, according to a US National Institute of Drug Abuse-funded study by Toronto’s Centre for Addiction and Mental Health (CAMH) and The Hospital for Sick Children (SickKids) published today in the journal Brain.

Ecstasy (MDMA) is a stimulant drug widely used recreationally that is also being tested in clinical trials for the treatment of post-traumatic stress disorder.
Led by Dr. Stephen Kish at CAMH, this study provides confirmation of a previous finding from Johns Hopkins University that levels of the serotonin transporter (SERT) are low in cerebral cortex of chronic ecstasy users. The subjects were “typical” ecstasy users who used about two tablets of the drug twice a month.

SERT is a protein responsible for regulating levels of serotonin, a neurotransmitter important for mood and impulse control. Ecstasy interacts with SERT to cause the release of serotonin, an action that probably explains some of the behavioral effects of the drug such as increased sociability.

Scientists have long suspected that ecstasy might harm brain cells that use serotonin, but 12 years of brain scan studies have produced contradictory results, even within the same laboratory.
The CAMH study used a large subject size (49 drug users, 50 control subjects), confirmed by hair analysis that ecstasy users actually used the drug, and used an imaging probe that could measure SERT throughout the brain.
“We were surprised to discover that SERT was decreased only in the cerebral cortex and not throughout the brain, perhaps because serotonin nerves to the cortex are longer and more susceptible to changes. This finding is almost identical to newer data from Johns Hopkins and is the first time that one laboratory has actually been able to replicate results of another independent laboratory in a SERT study of ecstasy users.” said Dr. Kish.

Drug hair analysis indicated that many ecstasy users, probably unknowingly, also used methamphetamine, which might itself damage serotonin cells; however, low SERT was found both in ecstasy users who used and who did not use methamphetamine. Dr. Jason Lerch at SickKids showed that those ecstasy users who also used methamphetamine had a slightly thinner cerebral cortex.

Does low SERT equal “structural brain damage”? “Not necessarily” said co-author Dr. Isabelle Boileau of CAMH. “There is no way to prove whether low SERT is explained by physical loss of the entire serotonin nerve cell, or by a loss of SERT protein within an intact nerve cell.”
Dr. Kish suggests that low SERT might explain why many ecstasy users need to keep increasing the dose to experience the same effects, since SERT is necessary for the action of ecstasy. “Most of the ecstasy users of our study complained that the first dose is always the best, but then the effects begin to decline and higher doses are needed. The need for higher doses, possibly caused by low SERT, could well increase the risk of harm caused by this stimulant drug,” said Dr. Kish.

Media Contact: Michael Torres, Media Relations, CAMH ; 416 595 6015 or email media@camh.net

Source: www.camh.net 18th May 2010

Steroids are linked to manic episodes, depression, suicide, psychotic episodes and increased aggression and hostility, occasionally triggering violent behavior, including murder.

Researchers at Uppsala University in Sweden studied the relationship between crime and steroid use in 1,440 Swedish residents tested for the drugs between 1995 and 2001 from clinics, including substance abuse facilities, as well as police and customs stations.

Of those involved in the study, 241 tested positive, with an average age of about 20.
The research team found those who tested positive for steroid use were roughly twice as likely to have been convicted of a weapons offense and one-and-a-half times as likely to have been convicted of fraud.

When the researchers excluded people from substance abuse facilities from their analysis the connection with armed crime remained, but the link between steroid use and fraud disappeared.
While steroids are linked with outbursts of uncontrolled violence known as “‘roid rage,” they did not appear to be connected with sexual offenses, violent crimes such as murder, assault and robbery, or crimes against property such as theft.

This investigation instead reveals that steroid use may be linked with premeditated crimes—those involving preparation and advance planning.
One explanation the researchers suggest for the findings is that criminals involved in serious crimes such as armed robbery or the collection of crime-related debts might benefit from the muscularity, heavy build and increase in aggression that comes with steroid use.

The scientists report their findings in the November issue of the Archives of General Psychiatry.

Source: Fox News Live Science Monday , November 06, 2006

The brain’s nucleus accumbens (NAC) is a core region of the mesocorticolimbic dopaminergic system and is interconnected with the ventral tegmental area (VTA) and the prefrontal cortex. The mesocorticolimbic system is thought to be central to the reinforcing effects of many drugs and plays an important role in addiction. A new study has found that alcohol abuse elevated the expression of a distinct set of genes in the NAC and VTA, while nicotine blunted this effect in the VTA.

Results will be published in the July 2010 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.

“In spite of their differences in pharmacology, alcohol and tobacco consumption are often intimately linked,” said Traute Flatscher-Bader, a postdoctoral research fellow at The University of Queensland and corresponding author for the study. “Nonetheless, the molecular mechanisms that underlie alcohol and nicotine abuse, and particularly their co-abuse, are still incompletely understood.”

“One thing that researchers have encountered is that it is often difficult to find ‘pure’ alcoholics, that is, alcoholics that only abuse alcohol and nothing else,” agreed Simon Worrall, director of postgraduate coursework programs in molecular biology at The University of Queensland. “Many alcoholics are poly-drug abusers, with the most common other drug being nicotine. Thus, many studies which have studied the effects of alcohol on the brain and other organs have been compromised because they have not taken account of the effects of nicotine addiction which is often superimposed on the effects of alcohol addiction.”

In the first part of the current study, Flatscher-Bader and her colleagues used DNA microarray technique to study the expression of many thousands of genes in the brains of non-smoking and smoking alcoholics and non-drinking smokers.

“We examined the impact of alcoholism and smoking on gene expression in the NAC in 20 chronic alcohol abusers and controls with and without recent smoking history,” said Flatscher-Bader. “The results revealed that in this brain region, the abuse of alcohol and nicotine had distinct effects on the expression of genes. In addition, altered expression of a number of genes was associated with both alcohol and nicotine abuse. Within the latter group was a set of genes which play a crucial role in a molecular pathway regulating cell structure.”

The researchers then went on to investigate in more detail the altered expression of six selected genes within the pathway regulating cell structure in two brain regions, using 30 cases comprised again of smoking and non-smoking controls and alcohol abusers. For this part of the study they used the method called “real time polymerase chain reaction.”

“This expanded investigation revealed that one of the genes, called RHOA, was elevated by alcohol abuse and its highest expression was evident in the smoking alcoholics in both brain regions,” said Flatscher-Bader. “The RHOA gene had previously been implicated in the initiation of tobacco smoking. In the NAC, the expression of a further four of the six selected genes was increased by alcohol abuse. Interestingly, the highest expression for each of the genes in the NAC was in the smoking alcoholics. In the other brain region called the VTA, alcohol abuse had a similar effect and elevated the expression of all six selected genes. In contrast to the NAC, however, concurrent smoking dampened the induction of five of these alcohol-sensitive genes in the VTA.”

“Many studies have analyzed the changes in gene expression in this brain system to try to untangle the molecular pathology of alcohol addiction,” said Worrall, “but this is amongst the first to take into account the effect of co-administration of nicotine with alcohol.

Flatscher-Bader stressed that there are several cell types in the brain and there are several steps between gene expression and impact on cell structure and function. “It has to be emphasized that our study is important as a first step in identifying molecular pathways underlying the effects of alcohol abuse and smoking and their co-joint abuse on the human NAC and VTA, “she said. “It now needs to be tested if our findings are, indeed, associated with changes to neuronal structure and function.”

“A better understanding of the molecular basis of withdrawal may help in the development of new treatments to ameliorate the symptoms,” added Dr Worrall. “Not many previous studies took into account the potential effects of nicotine addiction that may be superimposed on top of those from alcohol, so these results may help clinicians better use present therapy/drugs to treat patients abusing both alcohol and/or nicotine and may also lead to the development of new drugs.”

Source: www.medicalnewstoday.com 5.5.2010

Recent research has clarified a number of important questions concerning adverse effects of cannabis on health.

A causal role of acute cannabis intoxication in motor vehicle and other accidents has now been shown by the presence of measurable levels of Δ9-tetrahydrocannabinol (THC) in the blood of injured drivers in the absence of alcohol or other drugs, by surveys of driving under the influence of cannabis, and by significantly higher accident culpability risk of drivers using cannabis.

Chronic inflammatory and precancerous changes in the airways have been demonstrated in cannabis smokers, and the most recent case-control study shows an increased risk of airways cancer that is proportional to the amount of cannabis use.

Several different studies indicate that the epidemiological link between cannabis use and schizophrenia probably represents a causal role of cannabis in precipitating the onset or relapse of schizophrenia.

A weaker but significant link between cannabis and depression has been found in various cohort studies, but the nature of the link is not yet clear. A large body of evidence now demonstrates that cannabis dependence, both behavioral and physical, does occur in about 7–10% of regular users, and that early onset of use, and especially of weekly or daily use, is a strong predictor of future dependence.

Cognitive impairments of various types are readily demonstrable during acute cannabis intoxication, but there is no suitable evidence yet available to permit a decision as to whether long-lasting or permanent functional losses can result from chronic heavy use in adults. However, a small but growing body of evidence indicates subtle but apparently permanent effects on memory, information processing, and executive functions, in the offspring of women who used cannabis during pregnancy. In total, the evidence indicates that regular heavy use of cannabis carries significant risks for the individual user and for the health care system.

Source: Progress in Neuro-Psychopharmacology and Biological Psychiatry, Volume 28, Issue 5, August 2004, Pages 849-863

An 18-year-old male presents complaining of crampy abdominal pain, nausea, and intractable vomiting for the past year. The symptoms are episodic, lasting several weeks and remitting for weeks to months.

The patient states that his abdominal pain is 10 out of 10 in severity, and that he has been vomiting up to 20 times each day. He has been evaluated at multiple hospitals, and he has had numerous upper endoscopies, colonoscopies, swallowing studies, and CT and MRI imaging studies, all of which were unrevealing.

He underwent a cholecystectomy, but had no improvement in his symptoms after the surgery. His pain and nausea are unresponsive to antacids and antiemetics.

The patient’s only relief is with hot water bathing: he spends hours each day in the shower with the temperature set as hot as he can bear. The patient’s history is otherwise unremarkable, except that he admits to daily marijuana use beginning at the age of 14.

This patient’s story is typical of cannabinoid hyperemesis, a clinical syndrome characterized by intractable vomiting and abdominal pain associated with the unusual learned behavior of compulsive hot water bathing, occurring in the setting of long-term heavy marijuana use.
Treatment consists of medication for immediate symptomatic relief and marijuana cessation for long-term relief. Symptoms usually remit within weeks of becoming abstinent.

If this disorder is so easily diagnosed and treated, why were the patient’s past doctors confused to the point of performing what might have been an unnecessary surgery? Cannabinoid hyperemesis is a new diagnosis, first described in 2004, and currently sixteen papers on the subject have been published.

Therefore, it is likely that the patient’s prior doctors had never considered this disorder. Second, the pathogenesis of cannabinoid hyperemesis is poorly understood.
How can marijuana, which is used in cancer clinics as an anti-emetic, cause intractable vomiting? And why would symptoms abate in response to high temperature?

The connection between marijuana, vomiting, and heat is non-intuitive, and a medical team unfamiliar with this syndrome would be hard-pressed to reach the diagnosis.
The largest study of cannabinoid hyperemesis to date was the landmark report by Allen et al in 2004 in an area of Southern Australia where marijuana use is largely decriminalized.

The report tracked 10 patients who presented with cyclic vomiting after 3 to 27 years of cannabis abuse and no other history of drug abuse. All but one displayed compulsive hot water bathing; the remaining patient had only experienced his symptoms for 6 months, and the authors theorize that he had not yet learned to associate hot water with symptom palliation.

The 9 compulsive bathers reported that this bizarre behavior occupied hours of their days and said that their symptoms were ameliorated within minutes of bathing and returned when the water cooled. All 10 patients were counseled to cease cannabis use, and 7 did so. Within weeks of cessation, the symptoms resolved for these 7 patients; the remaining 3 patients did not cease cannabis use and continued to have cyclic vomiting and abdominal pain.

After several years of abstinence, 3 patients resumed cannabis use and were hospitalized again with cyclic vomiting and abdominal pain. Once again, 2 of these patients successfully stopped using cannabis, and their symptoms resolved. The remaining patient continued to use cannabis and continued to experience symptoms at the time of publication.
Following the first case report, further cases have been described on three continents.

All patients presented with the classic triad of symptoms described by Allen et al: cyclic vomiting and abdominal pain, an extensive history of cannabis abuse, and palliation with hot water bathing. The fact that this unique triad is preserved in diverse patient populations suggests that there is a pathogenic mechanism that underlies this syndrome.

Several authors have speculated about the pathophysiology of cannabinoid hyperemesis, and though the specifics remain unclear, there is consensus over some of the basic principals: It appears that the high lipophilicity of delta-9-tetrahydrocannabinol (Δ9-THC, the active compound in marijuana) causes cumulative increases in concentration with chronic use, which may lead to toxicity in susceptible patients.

The abdominal pain and vomiting are explained by the effect of cannabinoids on CB-1 receptors in the intestinal nerve plexus, causing relaxation of the lower esophageal sphincter and inhibition of gastrointestinal motility. This finding is supported by gastric emptying studies performed on one of the patients presented by Allen et al, which revealed severely delayed emptying. While cannabis appears to have anti-emetic effects that are centrally mediated, it is possible that these effects predominate at low doses whereas the gastrointestinal effects predominate at the high concentrations that occur with long-term use.

The proposed explanation for compulsive hot water bathing is based on the fact that cannabis disrupts autonomic and thermoregulatory functions of the hippocampal-hypothalamic-pituitary system. There is a high concentration of CB1 receptors within the limbic system, and the hypothalamus in particular is known to be responsible for integrating central and peripheral thermosensory input. Furthermore, Δ9-

THC induces hypothermia in mice in a dose-dependent manner. While this evidence links cannabis to the hypothalamus and to thermoregulation, it does not provide a causal relationship. Two mechanisms proposed by Chang et al are that (1) cannabinoid-induced hypothermia causes the desire for hot water bathing, or (2) hot water bathing is the direct result of CB1 activation in the hypothalamus.

The true mechanism underlying hot water bathing remains enigmatic, and further studies are needed to elucidate the relationship between this bizarre learned behavior and the other features of cannabinoid hyperemesis.

A timely diagnosis of cannabinoid hyperemesis is essential not only to effect proper treatment but also to prevent iatrogenic morbidity and mortality from unnecessary diagnostic procedures and surgical interventions. There are, however, several obstacles to effective diagnosis:

First, the legal status of marijuana makes eliciting an accurate drug history challenging. Second, the bizarre hot water bathing is likely often attributed to psychological conditions such as obsessive-compulsive behavior. Third, the knowledge of the anti-emetic effects of cannabis likely disguises cases of cannabinoid hyperemesis, leading to the erroneous belief that cannabis is treating cyclic vomiting rather than causing it.

Finally, the fact that this syndrome is so recently described and relatively unknown outside an esoteric subset of the GI literature means that most clinicians are unaware of its existence. The following diagnostic criteria adapted from Sontineni et al can be used to facilitate a diagnosis of cannabinoid hyperemesis syndrome:

ESSENTIAL FEATURES
History of chronic cannabis use
Nausea and cyclic vomiting over months
Relief with cessation of cannabis use
SUPPORTING FEATURES
Compulsive hot water bathing with transient relief of symptoms
Colicky abdominal pain
Exclusion of other etiologies (especially gall-bladder and pancreas)
In the case of the 18-year-old patient presented above, asking the open-ended question, “What makes you feel better?” followed by more focused questions regarding the temperature of the water and the history of marijuana use were sufficient to suggest the diagnosis of cannabinoid hyperemesis.
We propose that these questions be used as a screening tool for all patients presenting with cyclic vomiting. Based on our experience and a review of the literature, we believe that these questions may be both sensitive and specific for detecting this unusual syndrome.
The patient presented in this case was counseled on his likely diagnosis.

Though he was initially skeptical, giving him printouts of case reports on cannabinoid hyperemesis syndrome and discussing the etiology of the disease were sufficient to convince him of the diagnosis. He was treated symptomatically in the hospital. Two weeks after discharge, he remains abstinent from marijuana and reports that his symptoms are improving.
Sarah A. Buckley and Nicholas M. Mark both are 4th year medical students at NYU School of Medicine
Faculty reviewed by Robert Hoffman, MD, Director NYU Poison Control Center, Associate Professor Departments of Medicine and Emergency Medicine, NYU Langone Medical Center

Source http://www.clinicalcorrelations.org/?p=2877 July 15th 2010

A LEADING medic at the Edinburgh Royal Infirmary today warned of the growing toll of Scots’ drinking habits as new figures showed liver disease deaths at the hospital have doubled in seven years.
The hospital, which is a referral centre for acute cases from across the whole of Scotland, had 67 fatalities from cirrhosis of the liver in 2005. A further 17 people died from the disease at the Western General Hospital in 2005 which, along with 2003, is the highest level for eight years.
Professor Peter Hayes today said there had been an “exponential rise” in cases among middle-aged men, in particular, in recent years which was showing no signs of slowing.
“The main problem is alcohol,” he said. “On the Continent, the problem seemed to peak in the 1970s and 1980s and cases have been falling since. They’re doing something very right, we’re doing something very wrong. I suspect it’s down to culture and the amount we consume.”
Prof Hayes, of the department of hepatology at the ERI, said more than half the cases were due to long-term alcohol abuse, typically people who have drunk a bottle of spirits a day for 20 years.
However, obese people and drug users who contracted hepatitis C by sharing needles in the 1970s and 1980s also account for a large proportion.
Prof Hayes warned that these health problems – although not as high as in some areas such as Paisley, near Glasgow – are growing in Edinburgh and Lothian.
“Deaths from liver disease in the UK, and Scotland in particular – and among middle-aged men in particular – are rising exponentially. Figures published in 2006 showed deaths in Scotland just massively increased, almost rising in a straight line.
“This is a national problem but one we are also seeing in Edinburgh and the Lothians.
“The problem is worse in Paisley, for example, but I’m sure it’s going up in Edinburgh, probably at the same rate just starting at a lower level.”
Some people are showing the signs of long-term alcohol abuse after just a few years of drinking, and there are also more female patients, but the most common sufferers continue to be men in their 50s and 60s.
Prof Hayes said: “We do see people in their 20s, they always catch your eye because they are so young, but the majority are older, and we still get more men than women.
“Alcohol is undoubtedly the most important reason for the rise. Hepatitis C is increasing – it takes a long time to cause sclerosis – but we are seeing a lot of people now who may have experimented with drugs, even just for a short time, 20 or 30 years ago.
“The third factor is obesity and diabetes. People are getting obese younger but living longer because of efforts to stop them dying from heart disease. This is putting pressure on their liver.”
Across Scotland 976 people died from liver disease in 2005, along with the same figure in 2003, the highest in eight years.
The figures, obtained by SNP MSP Christine Grahame, also showed that in 2005, 41,250 people were discharged from Scottish hospitals with an explicit diagnosis of an alcohol-related condition, 5441 in the Lothians.
She said the best way of turning the corner was by targeting the next generation of drinkers.
“We have to go back into schools with a determined education message,” she said.
“We think we’re immortal when we are young. When we do find young people with extreme difficulty with drinking we have to find residential places for them straight away.”

Source: Scotsman.com 27th Jan 2007

Research Summary
New research finds that smoking three or four marijuana cigarettes a week for six years could harm lung function and destroy antioxidants that protect cells against heart disease and cancer, Reuters reported Dec. 5.
“Smoking cannabis on a regular basis actually depletes your lung of protective antioxidant substances and this may have chronic long-term implications for young individuals,” said Dr Sarah Nuttall of the University of Birmingham in England.
The study involved a group of 20 people ages 19 to 30 who were either nonsmokers, cigarette smokers, and/or marijuana users. Researchers took blood samples, conducted lung function measurements, and tested for antioxidant markers.
“We found that smokers, compared to nonsmokers, had impaired lung function,” Nuttall said.
Nuttall said that when compared to nonsmokers, marijuana smokers had substantially lower levels of a protective antioxidant and nitric oxide, which is linked to lung function.
“These findings are important in young individuals in which the use of cannabis is increasing and may have serious long-term implications for what is currently regarded as a relatively harmless recreational habit,” she said.
The study’s findings were presented at a meeting of the held recently in London, England.

Source: British Thoracic Society Dec.2003

Research Summary

Background

Despite the high prevalence of cannabis use in schizophrenia, few studies have examined the potential relationship between cannabis exposure and brain structural abnormalities in schizophrenia.
Aims To investigate prefrontal grey and white matter regions in patients experiencing a first episode of schizophrenia with an additional diagnosis of cannabis use or dependence (n=20) compared with similar patients with no cannabis use (n=31) and healthy volunteers (n=56).
Method Volumes of the superior frontal gyrus, anterior cingulate gyrus and orbital frontal lobe were outlined manually from contiguous magnetic resonance images and automatically segmented into grey and white matter.
Results Patients who used cannabis had less anterior cingulate grey matter compared with both patients who did not use cannabis and healthy volunteers.
Conclusions A defect in the anterior cingulate is associated with a history of cannabis use among patients experiencing a first episode of schizophrenia and could have a role in poor decision-making and in choosing more risky outcomes.
Philip R. Szeszko, PhD, Delbert G. Robinson, MD and Serge Sevy, MD et al
Correspondence: Dr Philip R. Szeszko, Zucker Hillside Hospital, Psychiatry Research, 75–59 263rd Street, Glen Oaks, NY11004, USA. Tel: +1 718 470 8489; fax: +1 718 343 1659; email: szeszko@lij.edu

Source: The British Journal of Psychiatry (2007) 190: 230-236. doi: 10.1192/bjp.bp.106.024521
© 2007 The Royal College of Psychiatrists

James M. Howard,
Independent Biologist

It is my hypothesis that schizophrenia results from reduced fetal brain growth and development due to low maternal DHEA. This is exposed later in life by hormones that interfere with DHEA availability, that is, cortisol and testosterone, along with the natural decline of DHEA that begins around age twenty. Therefore, schizophrenia often occurs following a stressful event (cortisol) in the late teens or early twenties (testosterone and loss of DHEA) or later in life as DHEA reaches very low levels. Schizophrenia is characterized by low DHEA. Individuals with normal DHEA along with reduced fetal DHEA may not develop schizophrenia.
I suggest that the psychoactive chemicals of cannabis exert their effects by binding to androgen receptors. It has been found that THC and CBN inhibit binding of dihydrotestosterone to the androgen receptor (Endocrinology 1980; 107: 848-50). This binding to receptors in the advanced forebrain would reduce executive function and increase lower brain function by redistributing DHEA. That is, blocking access to upper brain receptors would increase lower brain function and increase lower brain functions such as appetite, etc.
DHEA binds to the androgen receptor. Cannabis use would reduce DHEA binding to the androgen receptor. It is this blocking of DHEA at its upper level receptors and subsequent redistribution of availability for lower brain activity that I think produces the effects of cannabis.
It is known that DHEA directly affects the anterior cingulate cortex (Psychopharmacology (Berl) 2006; 188: 541-51). Interference of DHEA binding in the anterior cingulate cortex of individuals with reduced growth and development in this area may reduce both function and maintenance of this area with the result being the symptoms of schizophrenia.

The brains of alcoholics can show measurable improvement in volume, chemical activity, and functionality after as little as seven weeks of abstinence, a new study published in the journal Brain today reveals.

Researchers from Germany, the UK, Switzerland and Italy collaborated on a study of ten men and five women alcoholics who had achieved an average of 38 days abstinence at the time of the study. Alcoholics who used psychoactive medications or who smoked more than 10 cigarettes a day after they stopped drinking were excluded from the data. Researchers used functional magnetic resonance imaging (fMRI) and proton MR spectroscopy, laboratory tests for levels of brain chemicals that measure nerve integrity and repair, and performance tests for attention and concentration.

Brain volume increased an average of two percent, researchers found, and there were major increases in the substances that measured nerve health and regrowth. There were also improvements in performance. However, in one subject, who had the longest history of alcoholism in the study (more than 25 years), the evidence of brain recovery was not visible within the relatively short time span of the study.

The leader of the research, Dr Andreas Bartsch from the University of Wuerzburg, Germany, said:
“The core message from this study is that, for alcoholics, abstinence pays off and enables the brain to regain some substance and to perform better. However, our research also provides evidence that the longer you drink excessively, the more you risk losing this capacity for regeneration. Therefore, alcoholics must not put off the time when they decide to seek help and stop drinking; the sooner they do it, the better.”

Source. Journal ‘Brain’ SUNDAY, DECEMBER 17, 2006

Research in Archives of Dermatology observed the effect by looking at the upper part of the inner arm in smokers and non-smokers.

Previous studies have focused on the face, where skin can also be damaged by exposure to the sun.

But the University of Michigan, Ann Arbour, team say this study shows smoking alone makes the skin age, which may help persuade some to quit.

The researchers photographed 82 people’s upper inner right arms.

Participants were aged 22 to 91. Such a wide age range was used in order to record the natural state of old and young skin.
There is strong evidence suggesting cigarette smoke has a negative effect on the appearance of skin
Indy Rihal, British Skin Foundation

Half of those studied had a history of smoking and had smoked, on average, for 24 years.

The number of packs of cigarettes they smoked ranged from a quarter of a packet to four packs per day.

The team created a nine-point scale to measure damage to skin which is not exposed to the light.

In those aged over 65, there was almost a two-point difference between smokers and non-smokers.

In the over-45s, the difference was around a point.

Writing in Archives of Dermatology, the researchers led by Dr Yolanda Helfrich, said: “We found that the number of packs of cigarettes smoked per day, total years of smoking and pack-years of smoking [an average of packs per day over the number of years of smoking] were correlated with the degree of skin aging.

“After controlling for age and other variables, we found that only packs of cigarettes smoked per day was a major predictor of the degree of photo-protected skin ageing.”

Evidence ‘mounting up’

Dr Helfrich said: “Previous studies have shown that smokers have a greater degree of skin ageing, but those have looked at facial skin.

“There are some sceptics who said the sun was having some of the effect.

“We have demonstrated that there was a significant degree of damage just from smoking.”

She added: “The evidence is certainly mounting up that smoking is not good for you. This just adds to all of that.”

She said more research was needed to show exactly how smoking damaged the skin.

Indy Rihal, of the British Skin Foundation, said: “In addition to UV light from the sun and sun beds, cigarette smoke is a main environmental factor that causes changes in the skin often associated with ‘looking old’ such as coarse wrinkling and a sallow, leathery texture.

“There is strong evidence suggesting cigarette smoke has a negative effect on the appearance of skin.

“Smoking enhances an enzyme in the skin, matrix metalloproteinase-1, resulting in increased collagen breakdown and diminished collagen production. The overall effect causes wrinkling and inelasticity.

“In addition the constriction of tiny blood vessels in the skin caused by smoking reduces the oxygen supply to the skin negatively affecting skin health and appearance in general.”

Amanda Sandford, of Action on Smoking and Health (ASH) said: “This study provides further evidence of the detrimental effects that smoking can have on the skin.

“No amount of anti-ageing cream will remove the wrinkles caused by cigarettes so the best way for smokers to avoid the wrinkled prune look is to stop smoking.”

Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/1/hi/health/6466041.stm

Published: 2007/03/21 00:03:21 GMT

© BBC MMVII

Summary

27 Mar 2007

Death, injury and illness caused by substance use are among the top ten contributors to global disease burden measured in disability-adjusted life-years – what was once seen by many in developing countries as the disease of industrialised nations is now a worldwide trend. Alcohol alone contributed to 27% of all deaths involving 15-”29-year-olds in economically developed countries in 2002, and illicit drugs a further 4%.

John Toumbourou (Deakin University, Australia), Tim Stockwell (University of Victoria, Canada), and colleagues review approaches and strategies to prevent substance abuse in young people and state that rates of tobacco use, harmful alcohol use, and illicit drug use can be substantially reduced through the concerted application of a combination of regulatory, early-intervention, and harm-reduction approaches.

However, the authors note that the current state of knowledge about the extent of adolescent substance use, and what works in reducing problems, is restricted to knowledge from a few high-income countries. Furthermore, investigations to test the efficacy of interventions are scarce, and many interventions have yet to be evaluated in real-world settings.

In an accompanying Comment, Isidore Obot looks at substance-use interventions in developing countries and notes: “Although developing countries have something to learn from the experiences of industrialised countries, success in preventing substance use and reducing related harms will come not in the application of one strategy or group of strategies, but by addressing the issue within the context of developmental planning. These are countries faced with the reality of poverty; where drug policy is often limited to law enforcement, prevention is sporadic. . .resources are limited, and drugs and alcohol problems compete with what policymakers might regard as more immediate problems of survival”.

Source: Article URL: http://www.medicalnewstoday.com 27 March 2007

Cannabis smoking may cause 5 per cent of lung cancer cases in people up to middle age, according to a New Zealand study which challenges international thinking on the drug.  Around 15 per cent of New Zealand adults under 46 use cannabis, drug-use surveys have found.
 
Researcher Dr Sarah Aldington, of the Medical Research Institute in Wellington, presented the new case-control study to the Thoracic Society conference in Auckland yesterday.
 
Cannabis users may have thought they were safe from lung cancer after a Californian study of more than 1600 people last year found no link between the disease and smoking the drug.  Dr Aldington said the evidence on cannabis and the risk of lung cancer was limited and conflicting. Her study found the risk rose more than five-fold among the third of users smoking the most cannabis.
 
“In conclusion there is a relationship between cannabis smoking and lung cancer in this study,” she said. “Approximately 5 per cent of lung cancer cases in those aged 55 and under may be attributable to cannabis…”   This equates to about 15 new cases a year – in 2002, 306 people aged 18-55 were diagnosed with lung cancer in New Zealand.  The study questioned about 60 people with lung cancer from eight health districts between Waikato and Canterbury and more than 200 “controls” – people randomly selected from electoral rolls in the same areas.
 
They were asked about risk factors, including cannabis and tobacco use.   The researchers calculated that the risk of developing lung cancer increased by about 8 per cent a year for people whose cumulative exposure equated to smoking one joint a day. This was about the same as the increase for someone with a one-pack-a-day tobacco habit.   The younger someone started smoking cannabis, the higher their risk of lung cancer.
 
“Long-term cannabis use increases the risk of lung cancer in young adults, particularly in those who start smoking cannabis at a young age,” the researchers conclude.
 
Dr Aldington said cannabis was the most commonly used recreational drug in the world, used by 161 million people, and its use was increasing in many countries. She said cannabis contained 50 per cent more cancer-causing chemicals than tobacco.  The study has found what the University of California researchers had expected to find but didn’t.   A researcher from that study, Dr Donald Tashkin, said in the Washington Post his group had thought cannabis smokers’ deeper inhalation and tendency to hold smoke in their lungs for longer than tobacco users would contribute to an increased cancer risk.
 
He said earlier work had shown cannabis contained cancer-causing chemicals as potentially harmful as those in tobacco. But cannabis also contained the chemical THC, which might kill ageing cells and keep them from becoming cancerous.
 
Middlemore Hospital clinical director of medicine Associate Professor Jeff Garrett, a leader of the Thoracic Society, said the Aldington study was “a good pilot study. It’s early work, it’s interesting, but there needs to be more work done.”

Source:  New Zealand Herald
Tuesday March 27, 2007

________________________________________
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The number of people admitted to hospital in England with alcoholic liver disease has more than doubled in just 13 years, figures show.
Between 1989 and 2003 admissions for the disease increased by 116% in men and 108% in women.
The figures, from London’s St George’s Hospital and the Office for National Statistics, were presented at a British Society of Gastroenterology meeting.
They underline just how much of a drain alcohol abuse is on NHS resources.

The figures show that there was a rise in admissions in people of all ages – including young adults.
In the year 2002/03, the admission rate for alcoholic liver disease was 42.4 per 100,000 men, and 27.6 per 100,000 women.
Many health campaigners have voiced concern that changes to licensing laws, allowing more pubs and clubs to stay open for longer, could lead to increases in alcohol-related illness and public disorder in the UK.
Lead researcher Dr Mark Fullard said that with hospitals already struggling to cope with demand, the rising number of cases of alcoholic liver damage was a potentially huge problem.
“The research findings highlight an important problem in public education and health planning and how we are going to manage alcohol related problems in this country.
“If it doubles again, it is going to have tremendous implications for the future burden of care in hospitals.”

The actual number of women admitted with alcoholic liver problems is about half that of men – but the rate of increase in cases is similar.
The diseases included in the study range from mild alcoholic hepatitis – mild inflammation of the liver – through to very severe cirrhosis and liver cancer.
Dr Fullard said: “If you are young and have alcoholic liver disease and carry on drinking, then you will get severe alcoholic liver disease.”
Dr Elwyn Elias, of the British Society of Gastroenterology, said: “It is very important that we are flagging this up at a time when the consumption of alcohol in this country is continuing to increase.
“I think we are unmasking an iceberg effect where we are storing up enormous problems for the NHS in the future.”

Source: BBC News Reported in Daily Dose 15th March 2005

By Jane Kirby, PA Health Correspondent
Published: 25 June 2007

The dance drug ecstasy significantly affects both long and short-term memory, according to analysis published today.

Researchers found verbal, not visual, memory was most affected by the drug, which sells in British clubs for as little as a few pounds per tablet.

Studies have previously noted ecstasy affects memory but the new research examined 26 studies involving 600 users.

Experts from the University of Hertfordshire found the number of tablets taken over a lifetime had little effect on the results.

The average number of tablets taken by people in the study was 327, with a range of 16 to 902.

Professor Keith Laws and Joy Kokkalis, from the University’s School of Psychology, led the study, which will be published in the journal Human
Psychopharmacology: Clinical and Experimental.

They found ecstasy had a medium to large effect on impairing short and long-term memory.

In more than three-quarters of ecstasy users, long and short-term verbal memory was below the average of those who had not used the drug.

Dr Laws said: “To summarise, this meta-analysis confirms that ecstasy users show significantly impaired short-term and long-term memory when compared with non-ecstasy users.

“The ecstasy users also displayed significantly worse verbal than visual memory.

“Indeed, their visual memory was relatively normal and seems to be affected more by concurrent cannabis use.”

Ecstasy is a class A drug used by an estimated 500,000 people in the UK.

Studies have shown long-term or heavy ecstasy use can damage neurons in the brain and cause depression, anxiety and difficulty sleeping.

One study published last year by researchers in Amsterdam found even short-term light use could damage blood flow to the brain.

Source:http://news.independent.co.uk/health/article2705536.eceJune 2007

The report, published online in the International Journal of Cancer, found that people who drink 15 grams of alcohol a day – equivalent to about two units – have about a 10 per cent increased risk of bowel cancer.
Those who drank more than 30 grams of alcohol – equivalent to three to four units which is less than a couple of pints of strong lager – increased their bowel cancer risk by around 25 per cent.

Source: Internatinal Journal of Cancer July 2007

Smoking marijuana in early pregnancy can cause infertility. A study at Vanderbilt University found that marijuana influences a signal that helps embryos pass safely from the ovary to the lining of the uterus.
Investigators found that when mice were given tetrahydrocannabinol, the major active component of marijuana, the embryos failed. They speculated that the chemical caused a fatty acid deficiency triggering a breakdown in the signaling system and making the embryo miss the crucial window for implantation in the uterus.
“We have shown before if you tinker with the normal timing of implantation in the uterus, it can create adverse ripple effects throughout the course of pregnancy leading to compromised pregnancy outcome,” said Dr. Sudhansu Dey of Vanderbilt University. Now the scientists are learning what happens on the molecular level that influences implantion.
“The take-home message would be, if you have fertility problems and you are smoking either marijuana or tobacco cigarettes, stop,” said Herbert Schuel, professor emeritus of anatomy and cell biology in the School of Medicine at the University of New York at Buffalo. “The same kinds of effects are produced by nicotine and tobacco smokers.”

Source NewsMax.com Sept.2006

Alcohol related hospital admissions double in last ten years according to latest official figures
The latest compendium of figures issued today (26 June) by the independent provider of official health and social care statistics, the Information Centre (The IC) show how hospital admissions specifically related to alcohol consumption have more than doubled in the last ten years.
In 2005/06, there were 187,640 NHS hospital admissions among adults aged 16 and over with either a primary or secondary diagnosis specifically related to alcohol. This has increased from 89,280 in 1995/96.
In its alcohol statistics bulletin, the most comprehensive and up to date compendium of facts and figures about alcohol consumption in England, The IC also found that:
• Among children under 16 there were 5,280 NHS Hospital admissions in 2005/06 with either a primary or secondary diagnosis specifically related to alcohol. This represents an overall increase of just over a third from 3,870 in 1995/96.
• In 2005, 6,570 people died from causes directly linked to alcohol consumption, of these just under two thirds (4,160) died from alcoholic liver disease. Two thirds (67 per cent) of those dying from alcoholic liver disease were men.
• In England in 2005, 73 per cent of men and 58 per cent of women reported drinking an alcoholic drink on at least one day in the week prior to interview. Thirteen per cent of men and 8 per cent of women reported drinking on every day in the previous week.
• Thirty-four per cent of men and 20 per cent of women had drunk more than the recommended number of units on at least one day in the week prior to interview. Eighteen per cent of men and 8 per cent of women had drunk more than twice the recommended daily intake.
• Older people were more likely to drink regularly – 28 per cent of men and 18 per cent of women aged 45-64 drank on five or more days in the week prior to interview compared to 10 per cent of men and 5 per cent of women aged 16-24. Younger people were more likely to drink heavily, with 42 per cent of men and 36 per cent of women aged 16-24 drinking above the daily recommendations compared to 16 per cent of men and 4 per cent of women aged 65 and over.
• Among men, 24 per cent reported drinking on average more than 21 units in a week. For women, 13 per cent reported drinking more than 14 units in an average week.
The bulletin also looked at awareness of the Government’s alcohol warnings and found that whilst 69 per cent of people reported that they had heard of the government guidelines on alcohol consumption, of these people, more than a third said that they did not know what the recommendations were. Thirty two per cent of adults however had seen units of alcohol displayed on labels of alcoholic drinks, compared to 23 per cent in 2000.
In England in 2005, 45 per cent of pregnant women did not drink at all during pregnancy, while 39 per cent reported drinking on average less than 1 unit a week and only 8 per cent drank 1 to 2 units Alcohol is more affordable than ever according to the figures.
In 2006, alcohol was 65 per cent more affordable than it was in 1980. Household expenditure on alcohol has increased steadily since 1980 as has total household expenditure; however expenditure on alcohol as a proportion of total household expenditure has decreased steadily over the same period standing at 5.2 per cent in 2006 compared to 7.5 per cent in 1980. In 2004, the Government estimated that alcohol misuse costs the health service between £1.4 and £1.7 billion per year.
Commenting on the figures, Professor Denise Lievesley, Chief Executive of The Information Centre, says:
“These figures show some worrying trends about the effects on society of consuming excessive amounts of alcohol. The doubling of alcohol related hospital admissions and increases in serious illness and death caused by alcohol gives cause for concern. We hope Government and other policy makers will use these figures to inform the development and implementation of policies to help reduce the harm that excessive alcohol consumption can cause.”

Source:: pubs/alcoholeng07 June 2007

Abstract

The goal of the present study was to examine the rate of cannabis use among participants in the Cognitive Assessment and Risk Evaluation (CARE) Program, a longitudinal program for individuals who are “at risk” for developing a psychotic disorder. Cannabis abuse was assessed in 48 individuals identified as at risk for psychosis based on subsyndromal psychotic symptoms and/or family history. At 1 year follow-up, 6 of the 48 (12.5%) at risk subjects had made the transition to psychosis. Of the 32 subjects who had no use or minimal cannabis use, one subject (3.1%) converted to psychosis. Of the 16 subjects who met criteria for cannabis abuse/dependence, five (31.3%) converted to psychosis. The results show a significant association between cannabis abuse and conversion to psychosis in this sample. Nicotine use was also found to be significantly associated with later conversion. The significant associations between cannabis and nicotine abuse and conversion to psychosis in individuals at risk for schizophrenia suggest that early identification and intervention programs should screen for and provide education about the deleterious effects of these substances.
Winston De La Haye, M.D., M.P.H. Lecturer and Consultant Psychiatrist Dept. of Community Health & Psychiatry, University of the West Indies, Mona, JAMAICA

Source: Source: Psychiatry Research 2007; 151: 151-154

A British “legal drugs” manufacturer based in Belgium has told Sky News the UK is about to be flooded with a deadly new drug called naphyrone.
Dave Llewellyn, who admits supplying large quantities of mephedrone to customers in the UK, said the new chemical is so dangerous he was refusing to sell it on his website – although it would not be against the law.
“This stuff is absolutely evil – it’s going to cause all sorts of psychological problems,” he told Sky News. “It will cause long-term brain damage from the very first hit and eventually it’s going to end up with bodies.”
Naphyrone is already being marketed as a mephedrone replacement, but according to Mr Llewellyn it is far more toxic than many illegal drugs like cocaine and ecstasy.
The substance is sold online under the name NRG-1 and costs as little as 25 pence a hit.  We know a little about its chemistry. We know it’s a variant of other substances both legal and illegal that can cause psychological and physical harm.   Dr Ken Checinski, from charity Addaction
The fact it is so cheap means, according to Mr Llewellyn, that it is likely to become hugely popular with youngsters.  “I think it really could be Europe’s crystal meth. I can see an epidemic where people are getting into it without realising what they’re getting into and then having to go back for more.”
For the moment naphyrone is not widely available in the UK, but its presence is a concern for many established scientists.  Medical director of the charity Addaction Dr Ken Checinski has warned those considering taking the designer drug to think again.
“We know a little about its chemistry. We know it’s a variant of other substances both legal and illegal that can cause psychological and physical harm,” he said.   The Government is currently trying to outlaw mephedrone – but naphyrone is likely to escape the ban for the moment.
Dave Llewellyn says naphyrone ‘could be Europe’s crystal meth’  Mephedrone has been linked to the deaths of a number of people across Europe.  Mr Llewellyn says the UK’s lucrative legal drugs market, which is worth hundreds of millions of pounds every year, is being targeted by dealers based in the Far East.
“The Chinese have been getting this ready for the last six months to take over the moment mephedrone is banned.
“It has been ready but why have two things banned at the same time – they want to keep their factories churning over these chemicals.”
Naphyrone will present legislators with another headache.   It is also likely to reignite the debate about how best to deal with the wave of new legal synthetic drugs which continue to hit the market, despite the ban of previous substances.
Source:  http://news.sky.com  1st April 2010

Have you ever forgotten to post an important letter or let an appointment slip your mind? A new study from UK researchers suggests that for those who regularly use ecstasy or other recreational drugs, this kind of memory lapse is more common. Their research, which uncovered potential links between memory deficits and cocaine for the first time, appears in the Journal of Psychopharmacology, published by SAGE.

Florentia Hadjiefthyvoulou, John Fisk, and Nikola Bridges from the University of Central Lancashire and Catharine Montgomery from Liverpool John Moores University wanted to delve deeper into the link between deficits in prospective memory (remembering to remember, or remembering to perform an intended action) and drug use.

The new research into prospective memory expands on previous studies, which have shown that ecstasy or polydrug users are impaired in performing a number of cognitive tasks, including verbal and spatial exercises. A team led by Fisk also published evidence in 2005 that those using ecstasy perform worse in deductive reasoning, too. Prospective memory tasks can be either time or event based, which means that the external trigger to remember could be in response to an event, or because it is time to do something. The distinction is important because these memory tasks use somewhat different brain processes.

The researchers recruited 42 ecstasy/polydrug users (14 males, 28 females) and 31 non-users (5 males, 26 females) for the study – all were students. The students were quizzed about their drug habits (including tobacco, cannabis and alcohol), and given questionnaires to assess their everyday memory, cognitive failures and prospective and retrospective memory. They were then given a number of lab-based memory tests, including some that required students to remember something several weeks later. The results showed that recreational drugs such as ecstasy, or the regular use of several drugs, affect users’ memory functions, even when tests are controlled for cannabis, tobacco or alcohol use. According to Fisk, memory deficits were evident in both lab-based and self-reported measurements of subjects’ prospective memory.

The results also suggested that ecstasy/polydrug users “possess some self awareness of their memory lapses.”
The authors say that although ecstasy/polydrug users as a whole are aware of their memory problems they may be uncertain as to which illicit drug is behind the defects they perceive. “The present results suggest that these deficits are likely to be real rather than imagined and are evident in both time- and event-based prospective memory contexts,” Fisk says.

Source: www.cadca.org l8 March 2010

Summary

While there is a wealth of research into the health impact of tobacco smoking, there is relatively little on the effects of cannabis smoking.
Research investigating whether the inhalation of cannabis smoke causes damage to the lungs and airways focuses on whether this effect is independent of the effects of tobacco smoke or not.
In general, the studies indicate that there is an increased negative health impact on those who smoke cannabis compared to those who do not smoke at all. When cannabis is smoked together with tobacco then the effects are additive.
However, what is not clear is whether it is the addition of the cannabis or the tobacco which is more harmful or whether this is the result of the combined effects of equally harmful substances.
Some key findings emerge from the research:
• The cannabis smoked today is much more potent that that smoked in the 1960s. The average cannabis cigarette smoked in the 1960s contained
about 10mg of tetrahydrocanabinol (THC), the ingredient which accounts for the psychoactive properties of cannabis, compared to 150mg of THC today. This means that longitudinal studies carried out in the 1960s and 1970s may not be
indicative of the effects of cannabis cigarettes
smoked today.
• Studies comparing the clinical effects of habitual cannabis smokers versus nonsmokers demonstrate a significantly higher prevalence of chronic and acute respiratory symptoms such as chronic cough and sputum production, wheeze and acute bronchitis episodes.
• 3-4 Cannabis cigarettes a day are associated with the same evidence of acute and chronic bronchitis and the same degree of damage to the
bronchial mucosa as 20 or more tobacco cigarettes a day.
• Cannabis tends to be smoked in a way which increases the puff volume by two-thirds and depth of inhalation by one-third. There is an
average fourfold longer breath-holding time with cannabis than with tobacco. This means that there is a greater respiratory burden of carbon
monoxide and smoke particulates such as tar than when smoking a similar quantity of tobacco.
• Cannabis smoking is likely to weaken the immune system. Infections of the lung are due to a combination of smoking-related damage to the
cells lining the bronchial passage (the fine hair-like projection on these cells filter out inhaled microorganisms)and impairment of the principal immune cells in the small air sacs caused by cannabis.
• The evidence concerning a possible link between cannabis smoking and Chronic Obstructive Pulmonary Disease (COPD) has not
yet been conclusively established. A number of studies indicate a causal relationship between the two whereas others contradict these findings.
• Research linking cannabis smoking to the development of respiratory cancer exists although there have also been conflicting findings. Not
only does the tar in a cannabis cigarette contain many of the same known carcinogens as tobacco smoke but the concentrations of these are up to 50% higher in the smoke of a cannabis cigarette. It also deposits four times as much tar on the respiratory tract as an unfiltered cigarette of the same weight. Smokers of cannabis and tobacco have shown a greater increase in cellular abnormalities indicating a cumulative effect of smoking both.
• The THC in cannabis has been shown to have a short term bronchodilator effect. This has lead to suggestions that THC may have therapeutic benefits in asthma. However, the noxious gases, chronic airway irritation or malignancy after long term use associated with smoking would seem likely to negate these benefits.

Recommendations
From a clinical perspective the main effects of smoking cannabis on the lungs are increased risk of pulmonary infections and respiratory cancers. Benzpyrene, a known constituent of the tar of cannabis cigarettes has been shown to promote alterations in one of the most common tumour suppressor genes, p53, hence facilitating the development of respiratory cancer. Gene p53 is
thought to play a role in 75% of all lung cancers. The British Lung Foundation recommends a public health education campaign aimed at young people to ensure that they are fully aware of the increased risk of pulmonary infections and respiratory cancers associated with cannabis smoking. The increased potency of the cannabis smoked today compared to the cannabis smoked twentythirty years ago suggests that earlier studies may underestimate the effects of cannabis smoking. In addition the lack of conclusive evidence concerning
the link between cannabis smoking and Chronic Obstructive Pulmonary Disease (COPD) underlines the need for further research.
The British Lung Foundation recommends that further research is undertaken to take into account the increased potency of today’s cannabis and to establish what link (if any) there is between COPD and cannabissmoking.

Source: British Lung Foundation Report ‘A Smoking Gun’ 2007

November 9, 2006

Men diagnosed with cancer are less likely to survive the disease if they were smokers or heavy drinkers. Smoking and drinking are well-known risk factors for cancer, but researchers have begun looking into how these addictions affect survivability, as well. Researcher Young Ho Yun and colleagues at the National Cancer Center in Goyang, South Korea tracked 14,578 cancer patients for about nine years and compared mortality data to patients’ history of smoking and alcohol use.
The researchers found that former smokers were more likely to die from any kind of cancer than nonsmoking cancer patients, possibly because smoking causes tumors to grow more aggressively. Smokers also may be less likely to get cancer screening tests, the authors noted, so their disease is often further advanced when treatment begins.
Among patients with head, neck, or liver cancer, heavy drinkers were more likely to die than nondrinkers, with risk increasing with consumption levels.
“Our findings suggest that groups at high risk of cancer need to be educated continually to improve their health behaviors — not only to prevent cancer, but also to improve prognosis,” the study authors noted.

Source: Journal of Clinical Oncology Nov. 1, 2006.

Reference:
Park, S.M., Lim, M.K., Shin, S.A., Yun, Y.H. (2006) Impact of Prediagnosis Smoking, Alcohol, Obesity, and Insulin Resistance on Survival in Male Cancer Patients: National Health Insurance Corporation Study. Journal of Clinical Oncology, 24(31): 5017-5024.

In a study published today in the journal Addiction, researchers in the United States have discovered that accidental overdose deaths involving cocaine rise when the average weekly ambient temperature passes 24 degrees Celsius (75 degrees Fahrenheit).  Using mortality data from New York City’s Office of the Chief Medical Examiner for 1990 through 2006, and temperature data from the National Oceanic and Atmospheric Association, researchers found that accidental overdose deaths that were wholly or partly attributable to cocaine use rose significantly as the weekly ambient temperature passed 24 degrees Celsius.  The number of cocaine-related overdose deaths continued to rise as temperatures continued to climb. 
Cocaine-related overdose deaths increase as the ambient temperature rises because cocaine increases the core body temperature, impairs the cardiovascular system’s ability to cool the body, and decreases the sense of heat-related discomfort that ordinarily motivates people to avoid becoming overheated.  Cocaine users who become overheated (hyperthermic) can overdose on lower amounts of cocaine because their bodies are under more stress. 
The study’s findings correct previous research that associated an increase in cocaine-related mortality with much higher temperatures (31.1 degrees Celsius, or 87.9 degrees Fahrenheit).  Because cocaine-related overdose fatalities begin to rise at lower ambient temperatures than was previously thought, it is now apparent that cocaine users are at risk for longer periods of each year.  Between 1990 and 2006, the average weekly temperature in New York City rose above 24 degrees Celsius for about seven weeks per year.
The study showed no difference in the number of drug overdoses in New York City among those weeks where the average temperature was between -10 and 24 degrees Celsius. Above 24 degrees Celsius, however, there were 0.25 more drug overdoses per 1,000,000 residents per week for every two degrees increase in weekly average temperature.  Given that over 8.2 million people live in New York City, the study’s findings predict that at least two more people per week will die of a drug overdose in the city for each two degree rise in temperature above 24 degrees Celsius, compared to weeks with average temperatures of 24 degrees and below.
The authors of this study point out the need for public health interventions in warm weather, such as delivering health-related warnings to high-risk groups.  Prevention efforts could also include making air conditioning available in locations where cocaine use is common such as urban areas with a known high prevalence of cocaine use, and within those urban areas, particular neighbourhoods with elevated numbers of cocaine-related deaths or arrests.  As lead author Dr. Amy Bohnert explains, “Cocaine users are at a high risk for a number of negative health outcomes and need public health attention, particularly when the weather is warm.”

Source: Bohnert A., Prescott M., Vlahov D., Tardiff K., and Galea S. Ambient temperature and risk of death from accidental drug overdose in New York City, 1990-2006. Addiction 2010; 105: doi:10.1111/j.1360-0443.2009.02887.x

Smoking marijuana as a teenager could raise the risk of developing schizophrenia and psychotic symptoms as a young adult, according to a new study that compared the prevalence of mental illness among marijuana users and non-users.

Bloomberg News reported March 2 that researcher John McGrath of the University of Queensland, Australia, and colleagues studied 3,801 young-adult sibling pairs and concluded that those who used marijuana the longest (six or more years) were twice as likely to develop schizophrenia or delusional disorders. They also were four times more likely than non-users to score highly on a test gauging psychotic-like experiences.

Higher scores on the test also were seen among those who used marijuana for less than three years.

Source: www.jointogether.org  March 2010

Alcohol-related death rates by sex, United Kingdom, 1991-2008

The number of alcohol-related deaths in the United Kingdom has consistently increased since the early 1990s, rising from the lowest figure of 4,023 (6.7 per 100,000) in 1992 to the highest of 9,031 (13.6 per 100,000) in 2008. Although figures in recent years suggested that the trend was levelling out, alcohol-related deaths in males increased further in 2008. Female rates have remained stable.

There are more alcohol-related deaths in men than in women. The rate of male deaths has more than doubled over the period from 9.1 per 100,000 in 1991 to 18.7 per 100,000 in 2008. There have been steadier increases in female rates, rising from 5.0 per 100,000 in 1991 to 8.7 in 2008, less than half the rate for males. In 2008, males accounted for approximately two-thirds of the total number of alcohol-related deaths. There were 5,999 deaths in men and 3,032 in women.

Source: Office of National Statistics 29th January 2010

Theresa H M Moore, Stanley Zammit, Anne Lingford-Hughes, Thomas R E Barnes, Peter B Jones, Margaret Burke, Glyn Lewis
Summary
Background – Whether cannabis can cause psychotic or affective symptoms that persist beyond transient intoxication is unclear. We systematically reviewed the evidence pertaining to cannabis use and occurrence of psychotic or affective mental health outcomes.
Methods – We searched Medline, Embase, CINAHL, PsycINFO, ISI Web of Knowledge, ISI Proceedings, ZETOC, BIOSIS, LILACS, and MEDCARIB from their inception to September, 2006, searched reference lists of studies selected for inclusion, and contacted experts. Studies were included if longitudinal and population based. 35 studies from 4804 references were included. Data extraction and quality assessment were done independently and in duplicate.
Findings – There was an increased risk of any psychotic outcome in individuals who had ever used cannabis (pooled adjusted odds ratio=1•41, 95% CI 1•20–1•65). Findings were consistent with a dose-response eff ect, with greater risk in people who used cannabis most frequently (2•09, 1•54–2•84). Results of analyses restricted to studies of more clinically relevant psychotic disorders were similar. Depression, suicidal thoughts, and anxiety outcomes were examined separately.
Findings for these outcomes were less consistent, and fewer attempts were made to address non-causal explanations, than for psychosis. A substantial confounding eff ect was present for both psychotic and aff ective outcomes.
Interpretation The evidence is consistent with the view that cannabis increases risk of psychotic outcomes independently of confounding and transient intoxication eff ects, although evidence for aff ective outcomes is less strong. The uncertainty about whether cannabis causes psychosis is unlikely to be resolved by further longitudinal studies such as those reviewed here. However, we conclude that there is now suffi cient evidence to warn young people that using cannabis could increase their risk of developing a psychotic illness later in life.

Source: The Lancet Vol.370 pp 319-328 July 2007

The results of this study suggest that many drug abusers may experience similar changes in the patterns of global gene expression in their brains, irrespective of their drug of choice. Whether longtime drug abusers favor cocaine, marijuana, or PCP, their autopsied brains showed a number of common gene changes consistent with diminished brain plasticity— i.e., the ability to learn from new experiences and adapt to new situations. Therefore, brain functions may be similarly impaired as the result of chronically abusing different drugs.

Background: Chronic drug abuse can change the structure and function of several brain regions. Recent advances in genomic technologies allow us to monitor the expression level of thousands of genes simultaneously in specific parts of the brain, including the anterior prefrontal cortex (aPFC), a region that plays an important role in decision making. A dysfunctional aPFC appears to be a characteristic feature of the brains of drug abusers. Researchers wanted to know if different drugs of abuse can compromise the normal patterns of gene expression that converge in common pathways, resulting in similar changes in the brains of drug abusers.

Study Design: NIDA scientists compiled clinical case histories and toxicology reports to establish the primary drug of abuse of 42 deceased drug abusers. The drugs examined included cocaine, marijuana, and PCP. The researchers then measured the level of expression of more than 9000 individual genes in small brain tissue samples obtained from the aPFC.

What They Found: Although many effects were specific to each drug, the scientists also found that nearly 80 percent of the drug abuse cases displayed similar alterations in genetic output compared to the controls. For example, genes involved in calcium signaling were turned down, while genes involved in lipid- and cholesterol-related pathways were turned up.

Comments from the Authors: The aPFC is characterized by a particularly dense and complex network of neural connections. Our results show that cocaine, marijuana, and PCP can alter the function of this critical brain area in similar ways, which could threaten the drug abuser’s ability to make sound decisions.

What’s Next: Many of the gene families identified here point to common downstream pathways that should be studied further in order to understand their specific contributions to the long-term effects of abused drugs on the human brain.

Source: The study, led by Dr. Elin Lehrmann of the Cellular Neurobiology Research Branch in NIDA’s Intramural Research Program in Baltimore, was published in the open access journal PLoS ONE on December 27, 2006 (PLoS ONE 1:e114).

Cannabis use has been found to co-exist with a range of mental health symptoms and disorders (a concurrence referred to hereafter as co-morbidity). Large-scale epidemiological surveys have found higher rates of psychotic, affective, anxiety, and behavioural disorders among individuals with substance use disorders than in the general population (Degenhardt, Hall & Lynskey, 2001; Farrell et al., 2001; Merikangas et al., 1998). The majority of individuals seen at publically-funded mental health services have psychosis (including schizophrenia), bipolar disorder, or severe personality disorder, especially borderline personality disorder. Though there has been a dearth of studies on the latter, there have been several attempts to develop treatments for cannabis use for the former conditions (Edwards et al., 2006; Barrowclough et al., 2001; Baker et al, 2006; Kavanagh et al., 2002). Recent Australian studies have found cannabis use in individuals with psychosis to be significantly greater than have comparable international studies (Wade et al., 2006; Wade et al., 2007; Hinton, Edwards & Elkins, 2008) in a similar population of patients with recent-onset psychosis.
Source: www.npic.au 2009 Management of Cannabis and Related Disorders

Using a highly sensitive new test, scientists in Europe are reporting “convincing evidence” that marijuana smoke damages the genetic material DNA in ways that could increase the risk of cancer.

Researchers note that toxic substances in tobacco smoke can damage DNA and increase the risk of lung and other cancers. However, there has been uncertainty over whether marijuana smoke has the same effect. Scientists are especially concerned about the toxicity of acetaldehyde, present in both tobacco and marijuana. However, it has been difficult to measure DNA damage from acetaldehyde with conventional tests.
The research was carried out by Rajinder Singh, Jatinderpal Sandhu, Balvinder Kaur, Tina Juren, William P. Steward, Dan Segerback and Peter B. Farmer from the Cancer Biomarkers and Prevention Group, Department of Cancer Studies and Molecular Medicine and Karolinska Institute, Sweden.
Raj Singh said: “Parts of the plant Cannabis sativa, also known as marijuana, ganja, and various street names, are commonly smoked as a recreational drug, although its use for such purposes is illegal in many countries.
The scientists describe development and use of a modified mass spectrometry method that showed clear indications that marijuana smoke damages DNA.
“There have been many studies on the toxicity of tobacco smoke. It is known that tobacco smoke contains 4000 chemicals of which 60 are classed as carcinogens. Cannabis in contrast has not been so well studied. It is less combustible than tobacco and is often mixed with tobacco in use. Cannabis smoke contains 400 compounds including 60 cannabinoids. However, because of its lower combustibility it contains 50% more carcinogenic polycyclic aromatic hydrocarbons including naphthalene, benzanthracene, and benzopyrene, than tobacco smoke.”
The authors added: “It is well known that toxic substances in tobacco smoke can damage DNA and increase the risk of lung and other cancers. Scientists were unsure though whether cannabis smoke would have the same effect. Our research has focused on the toxicity of acetaldehyde, which is present in both tobacco and cannabis.”
The researchers add that the ability of cannabis smoke to damage DNA has significant human health implications especially as users tend to inhale more deeply than cigarette smokers, which increases respiratory burden. “The smoking of 3-4 cannabis cigarettes a day is associated with the same degree of damage to bronchial mucus membranes as 20 or more tobacco cigarettes a day,” the team adds.
“In conclusion, these results provide evidence for the DNA damaging potential of cannabis [marijuana] smoke, implying that the consumption of cannabis cigarettes may be detrimental to human health with the possibility to initiate cancer development,” the article states. “The data obtained from this study suggesting the DNA damaging potential of cannabis smoke highlight the need for stringent regulation of the consumption of cannabis cigarettes, thus limiting the development of adverse health effects such as cancer.”

Source Chemical Research in Toxicology, 2009; 22 (6): 1181 DOI: 10.1021/tx900106y

Here’s another reason to “keep off the grass.” Researchers in Canada report that marijuana smoke contains significantly higher levels of several toxic compounds — including ammonia and hydrogen cyanide — than tobacco smoke and may therefore pose similar health risks.

David Moir and colleagues note that researchers have conducted extensive studies on the chemical composition of tobacco smoke, which contains a host of toxic substances, including about 50 that can cause cancer. However, there has been relatively little research on the chemical composition of marijuana smoke.
In this new study, researchers compared marijuana smoke to tobacco smoke, using smoking machines to simulate the smoking habits of users. The scientists found that ammonia levels were 20 times higher in the marijuana smoke than in the tobacco smoke, while hydrogen cyanide, nitric oxide and certain aromatic amines occurred at levels 3-5 times higher in the marijuana smoke, they say. The finding is “important information for public health and communication of the risk related to exposure to such materials,” say the researchers.
The study, “A Comparison of Mainstream and Sidestream Marijuana and Tobacco Cigarette Smoke Produced under Two Machine Smoking Conditions,” is scheduled for the Dec. 17 issue of ACS’ Chemical Research in Toxicology.

Source: ScienceDaily. Retrieved December 29, 2009, from http://www.sciencedaily.com /releases/2007/12/071217110328.htm

In a finding that challenges the increasingly popular belief that smoking marijuana is less harmful to health than smoking tobacco, researchers in Canada are reporting that smoking marijuana, like smoking tobacco, has toxic effects on cells.

Rebecca Maertens and colleagues note that people often view marijuana as a “natural” product and less harmful than tobacco. As public attitudes toward marijuana change and legal restrictions ease in some countries, use of marijuana is increasing.
Scientists know that marijuana smoke has adverse effects on the lungs. However, there is little knowledge about marijuana’s potential to cause lung cancer due to the difficulty in identifying and studying people who have smoked only marijuana.
The new study begins to address that question by comparing marijuana smoke vs. tobacco smoke in terms of toxicity to cells and to DNA. Scientists exposed cultured animal cells and bacteria to condensed smoke samples from both marijuana and tobacco. There were distinct differences in the degree and type of toxicity elicited by marijuana and cigarette smoke.
Marijuana smoke caused significantly more damage to cells and DNA than tobacco smoke, the researchers note. However, tobacco smoke caused chromosome damage while marijuana did not.

Source: The Genotoxicity of Mainstream and Sidestream Marijuana and Tobacco Smoke Condensates. Chemical Research in Toxicology, Online July 17, 2009 DOI: 10.1021/tx9000286

People with multiple sclerosis (MS) who smoke marijuana are more likely to have emotional and memory problems, according to new research.

“This is the first study to show that smoking marijuana can have a harmful effect on the cognitive skills of people with MS,” said study author Anthony Feinstein, MPhil, PhD, of the University of Toronto. “This is important information because a significant minority of people with MS smoke marijuana as a treatment for the disease, even though there are no scientific studies demonstrating that it is an effective treatment for emotional difficulties.”
Feinstein noted that MS itself can cause cognitive problems. “In addition, cognitive problems can greatly affect the quality of life for both patients and their caregivers,” he said.
For the study, researchers interviewed 140 Canadian people with MS. Of those, 10 people had smoked marijuana within the last month and were defined as current marijuana users. The marijuana users were then each matched by age, sex, the length of time they had MS, and other factors to four people with MS who did not smoke marijuana.
The researchers then evaluated the participants for emotional problems such as depression, anxiety and other psychiatric disorders. They also tested the participants’ thinking skills, speed at processing information, and memory.
The study found marijuana smokers performed 50 percent slower on tests of information processing speed compared to MS patients who did not smoke marijuana. There was also a significant association between smoking marijuana and emotional problems such as depression and anxiety.
People with MS have higher rates of depression and suicide compared to the general population. “Since marijuana can induce psychosis and anxiety in healthy people, we felt it was especially important to look at its effects on people with MS,” Feinstein said.

Source: the online edition of Neurology, February 13, 2008

Testicular germ cell tumors (TGCTs) are the most common type of cancer in American men between the ages of 15 and 34. For the last 50 years, the incidence of TGCTs has increased yearly in the United States and many other Western countries. A corresponding increase in marijuana abuse during this time period has been suggested as a potential causative factor. Chronic marijuana use is known to affect the body’s hormone and reproductive systems, disruption of which can potentially lead to cancer development. To test this hypothesis, researchers funded by NIDA interviewed 371 men aged 18 to 44 in Seattle and Puget Sound, Washington who had been treated for an invasive TGCT between 1999 and 2006, and 979 men from the same area who had not had testicular cancer. The researchers asked all participants about their lifetime marijuana and hashish use, as well as cigarette, alcohol, and other recreational drug use. They also collected data on other suspected risk factors for TGCT, including cryptorchidism (an undescended testicle) and a family history of TGCT. The researchers found that current marijuana use was associated with a 70 percent increased risk of nonseminoma TGCTs, but was not associated with risk of seminoma. (Seminoma and nonseminoma are the two subtypes of TGCT.) For nonseminoma tumors, the risk increased more for frequent (at least weekly) marijuana use and for use beginning in adolescence. This increased risk was independent of any other measured risk factor. The authors conclude that additional studies are needed to confirm these results, and to understand the biological processes that may link marijuana use to an increase in risk for nonseminoma TGCTs.

Daling JR, Doody DR, Sun X, Trabert BL, Weiss NS, Chen C, Biggs ML, Starr JR, Dey SK, Schwartz SM. Association of marijuana use and the incidence of testicular germ cell tumors. Cancer. 2009 Mar 15;115(6):1215-23.

Source: NIDA Addiction Research News December 11, 2009

http://www.drugabuse.gov/newsroom/09/NS-12.html

A new study funded by NIDA has used brain-imaging technology to show that during a decision game, chronic marijuana users show less activity in an error-processing part of their brains than peers who do not use marijuana. These results provide preliminary evidence in the debate on whether substance abusers willfully ignore their problem or whether cognitive deficits prevent them from fully understanding their addiction and its potential consequences. Functional magnetic resonance imaging (fMRI) of 16 heavy marijuana users and 16 non-drug-using peers provided real-time pictures of brain activity during the decision game. The marijuana abusers in the study did not make more mistakes during the game than participants who did not use the drug, but they were significantly less likely to recognize that they had made the mistakes. Non-marijuana-using participants were aware of 91 percent of their mistakes during the game, and marijuana abusers were aware of only 77 percent of their mistakes. fMRI revealed that when they made errors that they did not consciously recognize, the marijuana abusers showed less activity than the other participants in an area of the brain called the anterior cingulate cortex (ACC). The authors caution that marijuana withdrawal may have played some role in the lack of error awareness, as higher scores in several categories on a marijuana craving questionnaire were associated with poorer error awareness. However, if drug abusers cannot monitor their behavior accurately, this deficit in awareness may contribute to their continued use of a drug despite the consequences or to their continued associations with situations that make them liable to relapse.

Hester R, Nestor L, Garavan H. Impaired Error Awareness and Anterior Cingulate Cortex Hypoactivity in Chronic Cannabis Users. Neuropsychopharmacology. 2009 Jun 24. [Epub ahead of print]

Source: NIDA Addiction Research News December 11, 2009

http://www.drugabuse.gov/newsroom/09/NS-12.html

Scientists have been studying cannabinoids, substances that are chemically related to the ingredients found in marijuana, for more than two decades, hoping to learn more about how the drug produces its effects–both therapeutic and harmful. Marijuana has been reported effective in the treatment of multiple sclerosis, glaucoma, nausea caused by chemotherapy and wasting caused by AIDS. However, like all drugs, it also causes numerous unwanted side effects, including hypothermia, sedation, memory impairment, motor impairment and anxiety. Research on cannabinoids could someday yield new, more effective drugs or drug combinations.

At Temple University’s School of Pharmacy and Center for Substance Abuse Research (CSAR), one of only a few centers in the nation focused on the basic science of substance abuse, several researchers are investigating how cannabinoids produce pharmacological effects in rats.
One such study, “L-NAME, a nitric oxide synthase inhibitor, and WIN 55212-2, a cannabinoid agonist, interact to evoke synergistic hypothermia,” published in the February issue of the Journal of Pharmacology and Experimental Therapeutics, reveals how cannabinoids produce one of the drug’s most robust actions, hypothermia, or decreased body temperature.
According to lead author Scott Rawls, Ph.D., assistant professor of pharmacodynamics at Temple’s School of Pharmacy, “To operate at maximum efficiency, the body needs to maintain a stable, normal temperature. When the body’s temperature is altered, as in hypothermia, normal body functions, such as blood pressure and circulation, are impaired.”
Marijuana operates via two receptors in the body. One receptor, called CB1, is located in the brain and produces the drug’s psychoactive effects, including euphoria and dizziness. The other receptor, CB2, is found throughout the body and impacts the immune system. Substances in marijuana bind to one of these receptors and set off a chemical process that leads to an effect, such as hypothermia. Scientists have focused on this chemical process at the molecular level to pinpoint the exact molecules involved.
Knowing that the molecule nitric oxide (NO) plays an important role in the regulation of body temperature, the Temple researchers set out to determine what role it might play in cannabinoid-induced hypothermia. By combining a cannabinoid with a substance that blocked NO synthesis, they found that cannabinoid-induced hypothermia increased more than two-fold.
“This demonstrates the possibility that NO plays a part in regulating the impact of cannabinoids on body temperature and other cannabinoid-mediated actions,” said Rawls. “These findings could be helpful in determining the mechanisms that underlie some of the pharmacological actions of marijuana,” he added.
Rawls’ research team is currently investigating the impact of cannabinoids on other physiological systems, such as analgesia and movement, and the brain neurotransmitters that mediate those systems.

Source: . ScienceDaily. Retrieved July 18, 2008, from http://www.sciencedaily.com¬ /releases/2004/03/040309071927.htm

Patients with chronic hepatitis C (HCV) infection should not use marijuana (cannabis) daily, according to a study published in Clinical Gastroenterology and Hepatology, the official journal of the American Gastroenterological Association (AGA) Institute. Researchers found that HCV patients who used cannabis daily were at significantly higher risk of moderate to severe liver fibrosis, or tissue scarring. Additionally, patients with moderate to heavy alcohol use combined with regular cannabis use experienced an even greater risk of liver fibrosis. The recommendation to avoid cannabis is especially important in patients who are coinfected with HCV/HIV since the progression of fibrosis is already greater in these patients.

“Hepatitis C is a major public health concern and the number of patients developing complications of chronic disease is on the rise,” according to Norah Terrault, MD, MPH, from the University of California, San Francisco and lead investigator of the study. “It is essential that we identify risk factors that can be modified to prevent and/or lessen the progression of HCV to fibrosis, cirrhosis and even liver cancer. These complications of chronic HCV infection will significantly contribute to the overall burden of liver disease in the U.S. and will continue to increase in the next decade.”

This is the first study that evaluates the relationship between alcohol and cannabis use in patients with HCV and those coinfected with HCV/HIV. It is of great importance to disease management that physicians understand the factors influencing HCV disease severity, especially those that are potentially modifiable. The use and abuse of both alcohol and marijuana together is not an uncommon behavior. Also, individuals who are moderate and heavy users of alcohol may use cannabis as a substitute to reduce their alcohol intake, especially after receiving a diagnosis like HCV, which affects their liver. Researchers found a significant association between daily versus non-daily cannabis use and moderate to severe fibrosis when reviewing this factor alone. Other factors contributing to increased fibrosis included age at enrollment, lifetime duration of alcohol use, lifetime duration of moderate to heavy alcohol use and necroinflammatory score (stage of fibrosis). In reviewing combined factors, there was a strong (nearly 7-fold higher risk) and independent relationship between daily cannabis use and moderate to severe fibrosis. Gender, race, body mass index, HCV viral load and genotype, HIV coinfection, source of HCV infection, and biopsy length were not significantly associated with moderate to severe fibrosis.

Of the 328 patients screened for the study, 204 patients were included in the analysis. The baseline characteristics of those included in the study were similar to those excluded with the exception of daily cannabis use (13.7 percent of those studied used cannabis daily versus 6.45 percent of those not included). Patients who used cannabis daily had a significantly lower body mass index than non-daily users (25.2 versus 26.4), were more likely to be using medically prescribed cannabis (57.1 percent versus 8.79 percent), and more likely to have HIV coinfection (39.3 percent versus 18.2 percent).

The prevalence of cannabis use amongst adults in the U.S. is estimated to be almost 4 percent. Regular use has increased in certain population subgroups, including those aged 18 to 29.

Hepatitis is an inflammation of the liver. Hepatitis C is the most common form of hepatitis and infects nearly 4 million people in the U.S., with an estimated 150,000 new cases diagnosed each year. While it can be spread through blood transfusions and contaminated needles, for a substantial number of patients, the cause is unknown. This form of viral hepatitis may lead to cirrhosis, or scarring, of the liver. Coinfection of hepatitis C in patients who are HIV positive is common; about one quarter of patients infected with HIV are infected with hepatitis C. The majority of these patients, 50 to 90 percent, were infected through injection drug use. Hepatitis C ranks with alcohol abuse as the most common cause of chronic liver disease and leads to about 1,000 liver transplants yearly in the U.S.

Source: http://www.medicalnewstoday.com/articles/95434.php 29.01.08

HONG KONG (Reuters) – Smoking a joint is equivalent to 20 cigarettes in terms of lung cancer risk, scientists in New Zealand have found, as they warned of an “epidemic” of lung cancers linked to cannabis.
Studies in the past have demonstrated that cannabis can cause cancer, but few have established a strong link between cannabis use and the actual incidence of lung cancer.
In an article published in the European Respiratory Journal, the scientists said cannabis could be expected to harm the airways more than tobacco as its smoke contained twice the level of carcinogens, such as polyaromatic hydrocarbons, compared with tobacco cigarettes.
The method of smoking also increases the risk, since joints are typically smoked without a proper filter and almost to the very tip, which increases the amount of smoke inhaled. The cannabis smoker inhales more deeply and for longer, facilitating the deposition of carcinogens in the airways.
“Cannabis smokers end up with five times more carbon monoxide in their bloodstream (than tobacco smokers),” team leader Richard Beasley, at the Medical Research Institute of New Zealand, said in a telephone interview.
“There are higher concentrations of carcinogens in cannabis smoke … what is intriguing to us is there is so little work done on cannabis when there is so much done on tobacco.”
The researchers interviewed 79 lung cancer patients and sought to identify the main risk factors for the disease, such as smoking, family history and occupation. The patients were questioned about alcohol and cannabis consumption.
In this high-exposure group, lung cancer risk rose by 5.7 times for patients who smoked more than a joint a day for 10 years, or two joints a day for 5 years, after adjusting for other variables, including cigarette smoking.
“While our study covers a relatively small group, it shows clearly that long-term cannabis smoking increases lung cancer risk,” wrote Beaseley.

“Cannabis use could already be responsible for one in 20 lung cancers diagnosed in New Zealand,” he added.
“In the near future we may see an ‘epidemic’ of lung cancers connected with this new carcinogen. And the future risk probably applies to many other countries, where increasing use of cannabis among young adults and adolescents is becoming a major public health problem.”
(Reporting by Tan Ee Lyn; Editing by Alex Richardson)

Source: http://www.reuters.com/article/healthNews/ Jan. 29 2008

The study’s demonstration of a
strong association between cannabis
use and periodontitis experience by
age 32 years indicates that long-term
smoking of cannabis is detrimental to
the periodontal tissues and that public
health measures to reduce the prevalence
of cannabis smoking may have
periodontal benefits for the population.

To our knowledge, no previous
studies have examined this relationship,
so there are no data with which
to compare the findings. Determining
whether the association exists in other
populations should be a priority for
periodontal epidemiological research.

The nature of the biological mechanism
for the observed association is
currently unclear. The periodontal
effects of tobacco smoke are thought
to occur via the systemic effects of
nicotine and other toxic constituents
on immune function and the inflammatory
response within the periodontal
tissues. Cannabis contains more
than 400 compounds, including more
than 60 cannabinoids; the noncannabinoid
constituents are similar to
tobacco (except for nicotine), and
those have been reported to carry systemic
health risks and have histopathological
effects that are similar to
those of tobacco smoke.

Although definitively establishing the
periodontal effects of exposure to cannabis
smoke we should await confirmation
in other populations and settings,
health promoters and dental and medical
practitioners should take steps to
raise awareness of the strong probability
that regular cannabis users may be
doing damage to the tissues that support
their teeth.

Source: Jama Feb.6 2008 Vol.299 No.5

Murat Yu¨ cel, PhD, MAPS; Nadia Solowij, PhD; Colleen Respondek, BSc; Sarah Whittle, PhD; Alex Fornito, PhD;
Christos Pantelis, MD, MRCPsych, FRANZCP; Dan I. Lubman, MB ChB, PhD, FRANZCPContext:

Cannabis is the most widely used illicit drug in the developed world. Despite this, there is a paucity of research examining its long-term effect on the human
brain.

Objective: To determine whether long-term heavy cannabis use is associated with gross anatomical abnormalities in 2 cannabinoid receptor–rich regions of the brain, the hippocampus and the amygdala.

Design: Cross-sectional design using high-resolution (3-T) structural magnetic resonance imaging.
Setting: Participants were recruited from the general community and underwent imaging at a hospital research facility.
Participants: Fifteen carefully selected long-term (_10 years) and heavy (_5 joints daily) cannabis-using men (mean age, 39.8 years; mean duration of regular use, 19.7
years) with no history of polydrug abuse or neurologic/mental disorder and 16 matched nonusing control subjects (mean age, 36.4 years).
Main Outcome Measures: Volumetric measures of the hippocampus and the amygdala combined with measures of cannabis use. Subthreshold psychotic symptoms and verbal learning ability were also measured.
Results: Cannabis users had bilaterally reduced hippocampal and amygdala volumes (P=.001), with a relatively (and significantly [P=.02]) greater magnitude of reduction in the former (12.0% vs 7.1%). Left hemisphere hippocampal volume was inversely associated with
cumulative exposure to cannabis during the previous 10 years (P=.01) and subthreshold positive psychotic symptoms (P_.001). Positive symptom scores were also associated with cumulative exposure to cannabis (P=.048).
Although cannabis users performed significantly worse than controls on verbal learning (P_.001), this did not correlate with regional brain volumes in either group.
Conclusions: These results provide new evidence of exposure-related structural abnormalities in the hippocampus and amygdala in long-term heavy cannabis users and corroborate similar findings in the animal literature. These findings indicate that heavy daily cannabis use across protracted periods exerts harmful effects on brain tissue and mental health.
Arch Gen Psychiatry. 2008;65(6):694-701
THERE IS CONFLICTING evidence regarding the long-term effects of regular cannabis use. Although growing literature suggests that long-term cannabis use is associated
with a wide range of adverse health consequences,1-4 many people in the community,
as well as cannabis users themselves, believe that cannabis is relatively harmless and should be legally available.

With nearly 15 million Americans using cannabis in a given month, 3.4 million using cannabis daily for 12 months or more, and 2.1 million commencing use every year,5 there is a clear need to conduct robust investigations that elucidate the long-term sequelae of long-term cannabis
use.
The strongest evidence against the notion that cannabis is harmless comes from the animal literature6-9 in which longterm cannabinoid administration has been shown to induce neurotoxic changes in the hippocampus, including decreases in neuronal volume, neuronal and synaptic density, and dendritic length of CA3 pyramidal neurons. Although such work suggests
that exposure to cannabinoids may be neurotoxic in animals, much less is known about the neurobiologic consequences of long-term cannabis exposure in humans.
Only a handful of brain imaging studies have been conducted in human cannabis users, with inconsistent findings reported.
Early cannabis research using pneumoencephalography10 reported cerebral atrophy in a small sample (N=10) of cannabis users, but further studies using computed tomography11-13 did not detect any abnormalities, despite the potential confounds of polydrug use, comorbid neurologic/
psychiatric diagnoses, and a lack of appropriate comparison groups.
Author Affiliations: ORYGEN
Research Centre (Drs Yu¨ cel,Whittle, and Lubman) and Melbourne Neuropsychiatry Centre, Department of Psychiatry, The University of Melbourne and Melbourne Health (Drs Yu¨ cel, Whittle, Fornito, and Pantelis), Melbourne, Australia; School of Psychology and Illawarra
Institute for Mental Health, University of Wollongong, Wollongong, Australia (Dr Solowij and
Ms Respondek); and Schizophrenia Research Institute, Sydney, Australia (Dr Solowij).
(REPRINTED) ARCH GEN PSYCHIATRY/VOL 65 (NO. 6), JUNE 2008 WWW.ARCHGENPSYCHIATRY.COM

©2008 American Medical Association. All rights reserved.
Downloaded from www.archgenpsychiatry.com , on June 3, 2008 recent structural magnetic resonance imaging (MRI) studies have also reported contradictory findings, ranging from
no global or regional changes in brain tissue volume or composition14-16 to gray and white matter density changes, either globally17 or in focal regions, most notably in the
hippocampal and parahippocampal areas.18,19 However, these previous studies used imaging techniques with relatively coarse spatial and anatomical resolution and typically focused on samples with multiple substance use or comorbid psychiatric disorders and on only moderate levels of cannabis use (ie, _2 joints per day). Indeed, despite strong evidence of neurotoxicity in the animal literature, 6-9 to our knowledge, no neuroimaging study has examined the neurobiologic sequelae of long-term heavy cannabis use while controlling for the important confounds of polydrug abuse and co-occurring psychiatric disorders.
In this study, we used high-resolution 3-T MRI to assess volumetric changes in 2 cannabinoid-rich regions of the brain (the hippocampus and the amygdala) known to be susceptible to the neurotoxic effects of cannabis exposure in a sample of long-term heavy users carefully
screened for polysubstance abuse and mental disorders.
Given the growing literature regarding an association between cannabis use and the development of psychosis20 and cognitive impairment,16,21 we also assessed for subthreshold
psychotic symptoms and verbal learning ability in this otherwise psychologically healthy sample.
METHODS
PARTICIPANTS
Male cannabis users with long histories of regular and heavycannabis use (n=15) and nonusing healthy male volunteers (n=16) matched on age, estimated premorbid intelligence (National
Adult Reading Test),22 years of education, and state and trait anxiety (Spielberger State-Trait Anxiety Inventory)23 were recruited from the general community via a variety of advertisements
(Table). Cannabis users had lower Global Assessment of Functioning scale scores and greater depressive symptoms (as measured using the Hamilton Depression Rating Scale)24 than the comparison group; however, there were no current or lifetime histories of diagnosable medical, neurologic, or psychiatric conditions as assessed using the Structured Clinical Interview
for DSM-IV Axis I Disorders, Patient Edition.25 All the control subjects also underwent a Structured Clinical Interview for DSM-IV Axis I Disorders, Non-Patient Edition.25 Subthreshold
psychotic symptoms were probed using the Scale for the Assessment of Positive Symptoms26 and the Scale for the Assessment of Negative Symptoms.27 Regarding alcohol use, the
groups did not differ in levels of current consumption, lifetime use, or history of abuse or dependence; and no participant drank more than 24 standard alcoholic drinks per week.
Significantly more cannabis users were also tobacco smokers (_2=22.9, P_.001) (Table). For all users, cannabis was the primary drug of abuse, with only limited experimental use of other
illicit drugs (generally _10 lifetime episodes).
PROCEDURE
Participants were assessed on 2 occasions, usually 1 week apart. In the first test session, participants completed demographic, clinical, and substance use history assessments. In the second test session, they completed the Rey Auditory Verbal Learning
Test (RAVLT) and underwent structural MRI.
Participants were asked to abstain from using substances for at least 12 hours before each test session, and cannabis users reported abstaining from cannabis for a mean of 21.3 hours before
the first test session (median, 14 hours; range, 10-72 hours) and a mean of 19.8 hours before the second test session (median, 17 hours; range, 12-48 hours). Urine samples were obtained
from users on 4 occasions and from controls on 2 occasions to corroborate self-reported abstinence. Specifically, for cannabis users, samples were obtained on the evening before
each test session and on the day of testing. For controls, samples
were collected only on the day of testing. Examination of these
samples demonstrated that all but 1 cannabis user had cannabinoid
metabolites (11-nor-_9-tetrahydrocannabinol-9-
carboxylic acid creatinine normalized) detected in urine samples
from the first test session, and levels were generally high
(evening: median, 467 ng/mg [range, 0-2320 ng/mg]; day of
testing: median, 447 ng/mg [range, 0-11 293 ng/mg]). From the
second test session, 2 users returned a 0 reading; otherwise,
cannabinoid metabolite levels were again high (evening: median,
456 ng/mg [range, 0-3511 ng/mg]; day of testing: median,
389 ng/mg [range, 0-4470 ng/mg]). The levels of urinary
cannabinoid metabolites generally corroborate the selfreported
patterns of heavy cannabis use in the sample. All but
2 control subjects returned a 0 reading for cannabinoid metabolites
across both test sessions. The 2 controls with positive
urine samples reported only minimal and very occasional
exposure to cannabis. The median level of cannabinoid metabolites
in controls at the first test session was 0 ng/mg (range,
0-184 ng/mg) and at the second test session was 0 ng/mg (range,
0-180 ng/mg).
STRUCTURAL MRI
The MRI data were obtained using a 3-T scanner (Intera; Phillips
Medical Systems NA, Bothell, Washington) at the Symbion
Clinical Research Imaging Centre, Prince of Wales Medical
Research Institute, Sydney. A 3-dimensional volumetric
spoiled gradient–recalled echo sequence generated 180 contiguous
coronal slices. The imaging parameters were as follows:
echo time, 2.9 milliseconds; repetition time, 6.4 milliseconds;
flip angle, 8°; matrix size, 256_256; and 1-mm3 voxels.
Hippocampal, amygdala, whole brain, and intracranial volumes
were measured using established reliable protocols28-31
and were delineated by a trained rater (S.W.) masked to group
information. Specifically, the hippocampal boundaries were as
follows: posterior, the slice with the greatest length of continuous
fornix; medial, the open end of the hippocampal fissure
posteriorly, the uncal fissure in the hippocampal body, and the
medial aspect of the ambient gyrus anteriorly; lateral, the temporal
horn of the lateral ventricle; inferior, the white matter inferior
to the hippocampus; superior, the superior border of the
hippocampus; and anterior, the alveus was used to differentiate
the hippocampal head from the amygdala. The anterior border
was the most difficult to identify consistently and was aided
by moving between slices before and after the index slice. The
amygdala boundaries were as follows: posterior, the appearance
of amygdala gray matter above the temporal horn; superolateral,
the thin strip of white matter that separates the amygdala
from the claustrum and the tail of the caudate; medial, the
angular bundle, which separates the amygdala from the entorhinal
cortex; superomedial, the semilunar gyrus; inferior, the
hippocampus; inferolateral, the temporal lobe white matter and
the extension of the temporal horn; and anterior, the slice anterior
to the appearance of the optic chiasm. Whole brain volumes
were estimated using the Brain Extraction Tool method32
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to separate brain from nonbrain tissue. After brain/nonbrain
segmentation, each voxel was classified into gray matter, white
matter, or cerebrospinal fluid using FAST Model statistical software.
33 Only gray and white matter were used in the estimate
of whole brain volumes. The intracranial cavity was delineated
from a sagittal reformat of the original 3-dimensional data
set. The major anatomical boundary was the dura mater below
the inner table, which was generally visible as a white line.
Where the dura mater was not visible, the cerebral contour was
outlined. Other landmarks included the undersurfaces of the
frontal lobes, the dorsum sellae, the clivus, and the posterior
arch of the craniovertebral junction.
Interrater and intrarater reliabilities were assessed by means
of the intraclass correlation coefficient (ICC) (absolute agreement)
using 15 brain images from a separate MRI database established
specifically for this purpose and that has previously
been delineated by another expert rater. For the hippocampus,
interrater ICC reliabilities were 0.92 (right) and 0.91 (left)
and intrarater ICC reliabilities were 0.98 (right) and 0.95 (left).
For the amygdala, interrater ICC reliabilities were 0.85 (right)
and 0.88 (left) and intrarater ICC reliabilities were 0.93 (right)
and 0.97 (left). Once reliability was established, the rater (S.W.)
delineated the regions of interest for the images acquired from
the present study.
STATISTICAL ANALYSES
Whole brain volume, age, educational level, and estimated IQ
were not significantly different between the 2 groups and were,
therefore, not used as covariates (Table). Regional gray matter
volumes for the hippocampus and amygdala were corrected for
the effect of the intracranial cavity using a previously described
formula34 and were analyzed using analyses of variance,
with hemisphere (left or right) and region (hippocampus
and amygdala) as within-subject factors and group as the
between-subject factor. Main effects and interactions were evalu-
Table. Demographic, Clinical, Drug Use, and MRI Volumetric Measures
Measure
Long-term Cannabis Users
(n=15)
Nonusing Control Subjects
(n=16) P Valuea
Age, mean (SD), y 39.8 (8.9) 36.4 (9.8) .31
IQ, mean (SD) 109.2 (6.3) 113.9 (8.1) .09
RAVLT score, mean (SD)
Sum of 5 learning trials 43.8 (8.8) 57.4 (10.1) _.001
20-min delay 8.9 (4.1) 12.3 (3.7) .009b
Educational level, mean (SD), y 13.4 (3.2) 14.8 (3.7) .28
GAF scale score, mean (SD) 72.0 (11.2) 80.8 (9.4) .02
HAM-D score, mean (SD) 5.87 (3.2) 2.56 (1.9) _.001b
STAI, mean (SD)
State anxiety 34.3 (9.8) 32.9 (9.4) .67
Trait anxiety 39.3 (9.7) 39.0 (8.2) .92
SAPS score, mean (SD) 8.1 (7.9) 0.6 (1.2) _.001b
SANS score, mean (SD) 11.7 (8.5) 1.4 (1.4) _.001b
Cannabis use
Duration of regular use, mean (SD) [range], yc 19.7 (7.3) [10-32] NA NA
Age started regular use, mean (SD) [range], yc 20.1 (6.9) [12-34] NA NA
Current use, mean (SD), d/mod 28 (4.6) NA NA
Current use, mean (SD), cones/mod,e 636 (565) NA NA
Cumulative exposure, past 10 y, mean (SD)f 77 816 (66 542) NA NA
Cumulative exposure, lifetime, mean (SD)f 186 184 (210 022) 12.7 (12.2) _.001
Estimated episodes of use, median (range) 62 000 (4600-288 000) 11 (0-30) _.001
Alcohol use, mean (SD), standard drinks/wk 9.6 (6.1) 6.8 (5.0) .19
Tobacco use, mean (SD), cigarettes/d 16.5 (8.9) 7.5 (9.2) .20
Brain volumes, mean (SD), mm3
Intracranial cavity 1 546 237 (94 018) 1 607 590 (136 386) .14
Whole brain 1 310 780 (90 778) 1 374 123 (105 673) .09
Hippocampus .002g
Left hemisphere 2849 (270) 3240 (423)
Right hemisphere 2949 (244) 3348 (400)
Amygdala .01g
Left hemisphere 1766 (98) 1878 (190)
Right hemisphere 1601 (143) 1744 (158)
Abbreviations: GAF, Global Assessment of Functioning; HAM-D, Hamilton Depression Rating Scale; MRI, magnetic resonance imaging; NA, not applicable;
RAVLT, Rey Auditory Verbal Learning Test; SAPS, Scale for the Assessment of Positive Symptoms; SANS, Scale for the Assessment of Negative Symptoms;
STAI, State-Trait Anxiety Inventory.
aTwo-tailed t test unless otherwise indicated.
bMann-Whitney test.
cRegular use was defined as at least twice a month.
dCannabis users had used at this level for most of their drug-using history.
eA cone is the small funnel into which cannabis is packed to consume through a water pipe in a single inhalation. Without the loss of sidestream smoke, the
quantity of tetrahydrocannabinol delivered by this method is estimated as equating 3 cones to 1 cigarette-sized joint. Thus, the cannabis users in this study
smoked the equivalent of 212 joints per month, or approximately 7 joints per day.
fExpressed as cones for users and as episodes for controls. Estimates of lifetime exposure beyond 10 years in these very long-term users became skewed and
unreliable; hence, the 10-year estimate was used in correlational analyses.
gRegion_group analysis of variance.
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ated using Greenhouse-Geisser–corrected degrees of freedom,
with _=.05. Effect sizes, expressed as Cohen d, are also reported
for pairwise contrasts. Only effects involving group (cannabis
users vs nonusers) and associations with cannabis use
parameters are reported because this was the primary focus of
the present study. Group comparisons of performance on the
RAVLT and measures of subthreshold psychotic symptoms
(using the Scale for the Assessment of Positive Symptoms and
the Scale for the Assessment of Negative Symptoms) were conducted
using independent-samples t tests or Mann-Whitney tests
for nonnormally distributed data. Pearson product moment correlational
analyses were conducted to examine the behavioral
(ie, symptom and cognitive) relevance of any identified group
differences in regional brain volumes and the association
between these brain changes and parameters of cannabis use.
These analyses were necessarily exploratory given the limited
sample size.
RESULTS
GROUP CONTRASTS
In the analysis of regional gray matter volumes, there
was a significant main effect of group (F1,29=12.98,
P=.001) and a region_group interaction (F1,29=6.25,
P=.02). This result and the post hoc pairwise analyses
demonstrated reduced hippocampal volumes in cannabis
users (F1,29=11.14, P=.002 corrected; a reduction of
12.1% in the left and 11.9% in the right hippocampus
relative to controls), with a very large effect size (Cohen
d: left hippocampus, 1.17; and right hippocampus,
1.27) (Figure 1). Cannabis users also had smaller
amygdala volumes (F1,29=7.31, P=.01 corrected; a
reduction of 6.0% in the left amygdala and 8.2% in the
right amygdala relative to controls), with large effect
sizes (Cohen d: left amygdala, 0.80; and right amygdala,
0.99). The region _ group interaction reflects that the
overall reduction in hippocampal volume was relatively
(and significantly) greater than the reduction in amygdala
volume (12.0% in the hippocampus vs 7.1% in the
amygdala). In the analysis of subthreshold psychotic
symptoms, cannabis users reported significantly higher
positive symptoms (Scale for the Assessment of Positive
Symptoms; z=−3.57, P_.001) and negative symptoms
(Scale for the Assessment of Negative Symptoms;
z=−3.66, P_.001) than nonusing controls. Regarding
verbal learning, cannabis users displayed significantly
poorer performance than controls on the RAVLT measures
(sum of words recalled across the 5 learning trials:
z=−3.97, P_.001; and free recall after a 20-minute
delay: z=−2.61, P=.009).
CORRELATIONAL ANALYSES
There was a significant inverse association between left
hippocampal volume and cumulative cannabis exposure
during the previous 10 years (r=−0.62, P=.01; accounting
for 38% of the variance in left hippocampal volume)
(Figure 2A). When 1 participant with relatively
higher cumulative cannabis exposure and small hippocampal
volume was excluded, 22% of the variance was
still accounted for despite falling short of significance in
the reduced sample (r=−0.47, P=.09). There was also an
association between left hippocampal volume and positive
symptoms (r=−0.77, P_.001) (Figure 2B) and between
positive symptoms and cumulative cannabis exposure
(r=0.52, P=.048) (Figure 2C). The associations
between left hippocampal volume and cumulative cannabis
exposure and between left hippocampal volume and
positive symptoms remained after controlling for the effects
of global functioning (Global Assessment of Functioning
scale) and depressive symptoms (Hamilton Depression
Rating Scale). No other associations were found
between other brain volumetric measures, cannabis use,
and psychotic symptoms, and they did not vary as a function
of alcohol or tobacco use. Measures of RAVLT performance
did not correlate with hippocampal or amygdala
volumes in either controls or cannabis users.
COMMENT
To our knowledge, this is the first human study of longterm
heavy cannabis users to demonstrate marked
exposure-related hippocampal volume reductions.
These findings corroborate previous animal research,6-9
suggesting that long-term heavy cannabis use is associated
with significant and localized hippocampal volume
reductions that relate to increasing cumulative cannabis
exposure. In addition, the present findings are consis-
tent with the view that cannabis use increases the risk
of psychotic symptoms and informs the debate concerning
the potential long-term hazardous effects of cannabis
in this regard. The bilateral reduction in amygdala
volume is a novel but not unexpected finding given the
dense concentration of cannabinoid receptors in this
region.35
Although these findings are consistent with those of
a previous study,18 it is difficult to directly compare these
results with those of other human studies given that past
work used MRI with lower magnetic field strength and
spatial resolution and did not conduct region-of-interest–
based analyses (eg, performed whole-brain voxel-based
analyses18). Tzilos et al14 conducted the only other study,
to our knowledge, that investigated cannabis users with
a relatively long history of use (specifically, an average
duration of use of 22.6 years, or 18.9 years of daily use)
and their study is, therefore, most comparable with the
present study. Although they found no effects of longterm
cannabis use on hippocampal volume, the authors
acquired their images at a lower field strength and with
a coarser spatial resolution (1.5 T with 3-mm-thick slices
vs 3 T with 1-mm-thick slices in the present study), an
important consideration given the size of the brain structures
investigated. Moreover, their region of interest was
less specific to the hippocampus relative to the present
measure because they also included the parahippocampal
gyrus. Furthermore, there was a relatively large age
discrepancy between their users and controls (38.1 vs 29.5
years), and the minimum duration of exposure to cannabis
was considerably lower in their sample (as little as
1 year of cannabis exposure), but, overall, their sample
reported an average of 20 100 lifetime episodes of use.
In contrast, the minimum duration of exposure to cannabis
in the present sample was 10 years, with an average
of 62 000 episodes of use. Thus, despite a similar mean
duration of use, the present sample used more than 3 times
as much cannabis, which may explain the finding of a
dose-response relationship between hippocampal volume
and cumulative cannabis use. Further highresolution
MRI work is necessary to characterize precisely
the dosage of cannabis required for significant brain
changes to occur.
The pattern of use in the present sample is consistent
with heavy cannabis use patterns that have previously
been reported in other Australian studies. For example,
Copeland and colleagues36 reported median daily intake
of 8 cones (the small funnel into which cannabis is packed
to consume through a water pipe in a single inhalation)
in an Australian sample of cannabis users seeking treatment
for cannabis dependence, ranging up to 125 cones
per day in the heaviest user, with 11% reporting cannabis
smoking throughout the day. The heaviest user herein
reported smoking 80 cones per day (approximately 25
joints smoked throughout the day). This pattern of cannabis
use is not dissimilar to the heaviest cannabis users
from other studies of non–treatment-seeking samples of
Australian cannabis users.37,38
Despite the large magnitude of effects observed, it remains
unclear whether these volumetric reductions
reflect neuronal or glial loss, a change in cell size, or a
reduction in synaptic density (eg, dendritic arborization),
all of which have been reported in rodent studies.
6-9 For example, Scallet and colleagues9 found striking
tetrahydrocannabinol-induced residual decreases in
the mean volume of hippocampal neurons and their nuclei
and a 44% reduction in the number of synapses up
to 7 months after the last exposure to tetrahydrocannabinol.
Moreover, Landfield and colleagues7 administered
tetrahydrocannabinol 5 times a week for 8 months
(approximately 30% of the rat lifespan, and comparable
in frequency and duration to the present sample) and
found significant tetrahydrocannabinol-induced decreases
in neuronal density in the hippocampus. Such
findings may help explain the mechanisms underlying
gross hippocampal and amygdala volume loss seen in this
sample of long-term heavy cannabis users.
Left Hippocampal Volume, mm3
In the present study, hippocampal volume in the cannabis-
using group was inversely correlated with cumulative
exposure to the drug in the left, but not right, hemisphere.
Previous functional imaging studies16,39 have found
reduced left hippocampal activation during cognitive performance
in cannabis users, and there is evidence to suggest
that hippocampal abnormalities in psychiatric disorders
such as schizophrenia are more prominent in the
left hemisphere.40 These findings converge to suggest that
the left hippocampus may be particularly vulnerable to
the effects of cannabis exposure and may be more closely
related to the emergence of psychotic symptoms. In this
context, it is interesting that we found a significant inverse
correlation between left hippocampal volume and
positive symptoms. Cannabis use was also positively correlated
with positive symptoms, suggesting that there are
complex associations among exposure to cannabis, hippocampal
volume reductions, and psychotic symptoms.
Given these relationships, it is possible that the exposurerelated
hippocampal reduction may reflect heavy cannabis
use in response to preexisting or developing psychotic
symptoms. However, there is limited empirical
support for long-term self-medication of subthreshold psychotic
symptoms with cannabis and stronger support for
the induction of psychotic symptoms subsequent to cannabis
exposure.20 As such, it seems more likely that prolonged
heavy use of cannabis induced subthreshold psychotic
symptoms and that both of these factors are
associated with hippocampal volume loss. These symptoms
were subthreshold because these cannabis-using participants
were carefully screened for current and past history
of mental disorders. Furthermore, the fact that the
mean age of the present cannabis-using sample was nearly
40 years suggests that these symptoms are unlikely to reflect
a prodrome. One speculation is that the present participants
were less genetically vulnerable to developing
a psychotic disorder subsequent to cannabis use,41,42 allowing
them to smoke heavily for many years. Future longitudinal
work assessing the emergence of hippocampal
reductions and psychotic symptoms with continued exposure
to cannabis, and how these are related to polymorphic
variations in susceptibility genes for psychotic
disorders, will prove useful in better characterizing these
relationships.
Given that cannabis users had significantly greater depressive
symptom scores than controls and that there is
an association between depression and hippocampal volume
reduction,43 it could also be argued that depressive
symptoms may be another mediating factor in the relationship
between cannabis use and hippocampal volume
reduction. However, there are a variety of important
considerations that make this unlikely. First, there
was no significant association between hippocampal volumes
and depressive symptom scores. Second, the relationship
between left hippocampal volume and quantity
of cannabis used was maintained after statistically
controlling for depressive symptoms. Finally, the overwhelming
evidence suggests that hippocampal reductions
in major depressive disorder tend to occur in the
more persistent forms of the disorder (eg, multiple episodes,
repeated relapses, or long illness duration).43,44 This
was not the case in the present sample of cannabis users,
who scored less than 6.0 on the Hamilton Depression
Rating Scale, had never been diagnosed as having
major depression, and did not seek treatment for any depressive
disorder.
Cannabis users showed poorer performance on measures
of verbal learning, consistent with previous findings.
Although some functional imaging studies have
found reduced left hippocampal blood flow and activation
during verbal (and visual) learning tasks in cannabis
users, we found no correlation between RAVLT
performance measures and hippocampal volume in either
controls or cannabis users. It is likely that anatomical volume
is a less sensitive measure than brain activation for
identifying correlations with behavioral performance. This
is a particularly pertinent consideration given that the
performance measures on the RAVLT are likely to reflect
the operation of numerous cognitive processes not
necessarily related to hippocampal function. Future work
using experimental tasks designed to more specifically
probe memory functions mediated by the hippocampus
may be useful in this regard.
The bilateral reduction in amygdala volume is a novel
but not unexpected finding given the dense concentration
of cannabinoid receptors in this region.35 There were
no cognitive, psychotic, or depressive symptom associations
with reduced volume in the amygdala. However,
this region has been significantly implicated in cannabinoid-
associated emotional and reward-related learning
and memory processes.47,48 Given that these aspects of
learning have not been examined in human cannabis users,
they would seem to serve as a potentially informative
avenue forward to help elucidate the functional relevance
of such volumetric reduction in the amygdala.
The relationship between long-term cannabis use and
brain abnormalities is complex. Although a limitation of
this study may be the residual effects of cannabis in light
of the fact that the cannabis users in this study were required
to be cannabis free for only 12 to 24 hours before
MRI, such issues are likely to be more pertinent for studies
examining more dynamic aspects of brain functioning
(eg, activations and cognition).49 The present structural
findings are unlikely to relate to the recent effects
of cannabis use because we are unaware of any evidence
that suggests that the hippocampus and amygdala can
change in volume by 6% to 12% in short periods. However,
although we maintain that the present results reflect
brain changes associated with long-term heavy cannabis
use rather than the consequences of recent exposure,
further longitudinal work is required to assess whether
such changes are reversible across more protracted periods
of abstinence.
Another limitation of this study is the relatively small
sample size, although the sample was exceptionally unique
in that participants were very long-term and heavy cannabis
users (mean of 5-7 joints per day for _10 years)
without polydrug use or co-occurring neurologic or diagnosable
mental disorders. As such, we conducted the
first, to our knowledge, “pure” examination of the effects
of heavy and protracted exposure to cannabis in humans.
The large effect sizes of the main findings suggest
that these results are robust and reproducible. These findings
are further strengthened by the observed dose-
response relationships between hippocampal volume reductions
and cumulative cannabis use.
There is ongoing controversy concerning the longterm
effects of cannabis on the brain. These findings
challenge the widespread perception of cannabis as having
limited or no neuroanatomical sequelae. Although
modest use may not lead to significant neurotoxic effects,
these results suggest that heavy daily use might indeed
be toxic to human brain tissue. Further prospective,
longitudinal research is required to determine the
degree and mechanisms of long-term cannabis-related
harm and the time course of neuronal recovery after abstinence.
Correspondence: MuratYu¨ cel, PhD,MAPS,ORYGENResearch
Centre, 35 Poplar Rd (Locked Bag 10), Melbourne,

Source: Arch.Gen.Psychiatry. Vol.65 June 2008

New report finds carrying of knives a key factor
DRINK PROBLEM: research suggests killings and suicides are linked to alcohol and drugs
Alcohol and drug abuse is pushing Scots to kill or take their own lives almost twice as often as people in other parts of Britain, a report revealed today.
Researchers found there were 500 killings in Scotland over five years and 5,000 suicides over six years. Both these figures are almost double those in England and Wales.The culprits were normally young men attacking other young men, they said, and the carrying of knives was a key factor.Scientists also found the North-South divide was highest among teenagers . The findings were revealed in a Scottish Government-commissioned report, Lessons for Mental Health Care in Scotland, carried out at the University of Manchester.
Scientists looked at all suicides and homicides in the population north of the border, as well as those committed by people who had sought help from mental health services. Homicide rates in Scotland were 2.12 per 100,000 people compared to 1.23 per 100,000 in England and Wales. And suicide rates in Scotland were 18.7 per 100,000 of the population, compared to 10.2 per 100,000 in England and Wales. Rates for suicide and killing among the mentally ill were also found to be higher in Scotland.
A total of 12% of killers and 28% of those who took their own lives had mental health problems.
Research director Professor Louis Appleby said the number of killings and suicides linked to alcohol and drug misuse was “striking”. He said: “Alcohol and drug misuse runs through these findings and it appears to be a major contributor to risk in mental health care and broader society. The findings suggest alcohol and drugs lie behind Scotland’s high rates of suicide and homicide.”
Referring to the high homicide figure, Prof Appleby said: “National homicide rates are high because of particularly high rates in certain areas of the country, namely Glasgow and Clyde and Argyll.” In Scotland, as across Britain, homicide is a crime committed primarily by young men against young men, the report said. Alcohol and drugs had often been taken and the weapon was usually a knife or another sharp object.
Prof Appleby said politicians should focus on drugs and alcohol and the carrying of knives, rather than mental health, when seeking to tackle the problem. He said: “Drugs and knives are a dangerous mix, so policy response to these deaths should focus on alcohol and drug abuse in young people and on the carrying of knives by young men. The rise in homicide rates in recent years is the result of an increase in killings by young people, mainly men under 25 years, but most are not mentally ill. A public health approach to homicide would target alcohol and drug use before mental health illness.”
Of 1,373 suicides among the mentally ill studied, there was a history of alcohol misuse in 57% of cases and drug abuse in 38%. Of 58 killings looked at among the mentally ill, more than 70% were committed by people with alcohol problems and around 77% had drug problems.
The report also made a string of recommendations. These included improving mental health services for young people, removal of ligature points from hospital wards and tightening up security on wards.
Source:The Press & Journal : 16/06/2008

Drug addiction accelerates aging in addicts.

Addictive drugs have been shown to impair stem cell regeneration and potentate programmed cell death leading to accelerated aging.

Drug addicts are known to suffer many pathologies including cancer and elevated mortality.

Surveys of addicts aged between 19 and 45 years in Australia disclosed higher levels of infections, dental and mental pathologies and hair graying consistent with aging were present in addicts.

Degenerative changes related to aging like skin thinning, wrinkling, dementias, muscle wasting, cardiovascular disease, psychiatric disturbances were common in addicted populations.

Source: Clinical Correlates of Accelerated Aging in Addiction, Reece S & Lavin M 2009)

To assess the effect of alcohol use on prostate cancer risk, researchers analyzed data from 10,920 men participating in the Prostate Cancer Prevention Trial. Participants age 55 years or older and without prostate cancer were randomized to receive either finasteride or placebo and followed for 7 years. Baseline questionnaire data on quantity, frequency, and type of alcohol consumed were used to calculate average grams of ethanol per day. At baseline, 79% of subjects reported no drinking, 12% reported consumption of 0.1–14.9 g alcohol per day, 6% reported consumption of 15–49.9 g per day, and 2.4% reported consumption of ≥50 g per day.

• Prostate cancer was diagnosed in 2129 men (19.5%) during follow-up. Of these, 67% had low-grade cancer (Gleason score, 2–6), 26.5% had high-grade cancer (Gleason score, 7–10), and 6.5% had cancer of unknown grade.
• Compared with no alcohol use, heavy use (≥50 g per day) was associated with a significantly increased risk of total, low-grade, and high-grade prostate cancer in the finasteride group (relative risk [RR]=1.89, 2.01, and 2.15, respectively) and with a nonsignificant increased risk of high-grade cancer in the placebo group (RR=1.67). Lower levels of alcohol use were not associated with increased prostate cancer risk.
• Heavy beer and wine use were associated with increased prostate cancer risk, but liquor was not.
Comments:
This interesting study suggests that heavy alcohol use may increase prostate cancer risk and may also prevent a beneficial effect of finasteride on that risk. It should be noted that the threshold for increased risk in this study (50 g per day) is equal to about 4 standard drinks per day and, therefore, well above published hazardous drinking thresholds for men. Still, these results may be useful to clinicians when counseling their patients about lower-risk alcohol use and/or prostate cancer prevention. Kevin L. Kraemer, MD, MSc

Source:Gong Z, Kristal AR, Schenk JM, et al. Alcohol consumption, finasteride, and prostate cancer risk. Cancer. 2009;115(16):3661–3669.

In this new study, researchers compared marijuana smoke to tobacco smoke, using smoking machines to simulate the smoking habits of users. The scientists found that ammonia levels were 20 times higher in the marijuana smoke than in the tobacco smoke, while hydrogen cyanide, nitric oxide and certain aromatic amines occurred at levels 3-5 times higher in the marijuana smoke, they say. The finding is “important information for public health and communication of the risk related to exposure to such materials,” say the researchers.

Source: American Chemical Society (2007, December 18). Marijuana Smoke Contains Higher Levels Of Certain Toxins Than Tobacco Smoke

Conflicting evidence exists regarding the long-term effects of cannabis use, according to background information in the article. “Although growing literature suggests that long-term cannabis use is associated with a wide range of adverse health consequences, many people in the community, as well as cannabis users themselves, believe that cannabis is relatively harmless and should be legally available,” the authors write. “With nearly 15 million Americans using cannabis in a given month, 3.4 million using cannabis daily for 12 months or more and 2.1 million commencing use every year, there is a clear need to conduct robust investigations that elucidate the long-term sequelae of long-term cannabis use.”

Murat Yücel, Ph.D., M.A.P.S., of ORYGEN Research Centre and the Melbourne Neuropsychiatry Centre at the University of Melbourne, Australia, and colleagues from the University of Wollongong performed high-resolution structural magnetic resonance imaging on 15 men (average age 39.8 years) who smoked more than five joints daily for more than 10 years. Their results were then compared with images from 16 individuals (average age 36.4) who were not cannabis users. All participants also took a verbal memory test and were assessed for subthreshold (below the standard of disease diagnosis) symptoms of psychotic disorders, which include schizophrenia and mania.

The hippocampus, thought to regulate emotion and memory, and the amygdala, involved with fear and aggression, tended to be smaller in cannabis users than in controls (volume was reduced by an average of 12 percent in the hippocampus and 7.1 percent in the amygdala). Cannabis use also was associated with sub-threshold symptoms of psychotic disorders. “Although cannabis users performed significantly worse than controls on verbal learning, this did not correlate with regional brain volumes in either group,” the authors write.

“There is ongoing controversy concerning the long-term effects of cannabis on the brain,” the authors write. “These findings challenge the widespread perception of cannabis as having limited or no neuroanatomical sequelae. Although modest use may not lead to significant neurotoxic effects, these results suggest that heavy daily use might indeed be toxic to human brain tissue. Further prospective, longitudinal research is required to determine the degree and mechanisms of long-term cannabis-related harm and the time course of neuronal recovery after abstinence.”

Source: Arch Gen Psychiatry, 2008;65(6):694-701

Because of widespread concern that the present economic crisis, particularly its effect on unemployment, will adversely affect population health, the research team investigated how economic changes have affected mortality rates over the past three decades in European Union countries. The research team, which is comprised of researchers from the University of California, San Francisco; University of Oxford, and London School of Hygiene and Tropical Medicine, used data from the World Health Organization and the International Labor Organization. They analyzed more than 50 causes of death in 26 EU countries between 1970 and 2007 and compared the results to unemployment data. They also examined the different levels of government social spending during the same period, taking into account other factors that might affect rising death rates, such as population aging and the different ways that countries monitor employment rates and causes of death.

The stress of recessions, particularly of unemployment, seemed to markedly increase rates of death from intentional violence, with women particularly affected by homicide and men by suicide, according to study results.

“Suicides are just the tip of the iceberg” said lead author David Stuckler, PhD, of the University of Oxford and London School of Hygiene and Tropical Medicine. “Rising suicide rates are a sign of many failed suicide attempts and high levels of mental distress among workers and families.”

Employers need to be aware that workers often turn to alcohol during times of stress and need to be aware of the signs of alcohol abuse. For help on launching a workplace substance abuse prevention program, visit the Department of Labor’s Working Partners Web site.

Source: www.cadca.org Sept.l9 2009

Heavy alcohol use is associated with an increased

risk of chronic pancreatitis, which may put patients

at risk for pancreatic cancer. In this study, an increased risk

was seen among subjects who reported either no alcohol

consumption (a group that probably contained former

drinkers) or consuming 3 or more drinks per day of liquor.

I agree with the conclusions of the authors that, although

moderate alcohol use was not a risk factor for pancreatic

cancer in this study, heavy alcohol use, particularly of liquor,

may play a role in its etiology. R. Curtis Ellison, MD

Source: Alcohol use and risk of pancreatic cancer: the NIH-AARP

Diet and Health Study. Am J Epidemiol. 2009;169(9):1043–1051.

Regular moderate alcohol consumption may be a protective

factor for cardiovascular disease. However, the effect

of alcohol consumption immediately prior to cardiovascular

events has not been studied extensively. Researchers conducted

a “case-crossover” study in 250 first-time nonfatal

acute myocardial infarction (AMI) cases to assess the influence

of alcohol consumption in the 12 hours preceding

AMI. Each case served as its own control; i.e., the control

information for each subject was based on his or her own

past behavior. The 12 hours preceding AMI was considered

the hazard period, while the corresponding time period a

week before AMI was the control period.

Drinking any alcohol in the hazard period increased

the risk for AMI threefold (odds ratio [OR], 3.1); even

moderate drinking (U24 g of ethanol for women and

U36 g for men) more than doubled it (OR, 2.3).

 Of the 187 subjects who drank any alcohol, 15 men

and 2 women reported heavy episodic drinking (4+

drinks per occasion for women and 5+ drinks for

men). The association between heavy episodic drinking

and AMI was not significant (OR, 3.0).

 These results were not influenced by known risk factors

for AMI (age, gender, smoking status, family history

of AMI, hypertension, hyperlipidemia, diabetes,

prior unstable angina pectoris, physical exertion

shortly before the event, psychological stress, or cocaine

use) in adjusted analyses.

 Compared with an age- and sex-matched general

population sample, subjects with AMI had more frequent

heavy episodic drinking (less than monthly, 21%

versus 11%; monthly or more, 7% versus 3%) and were

more likely to drink irregularly, i.e., less than weekly

(29% versus 16%).

Comments: Drinking any alcohol increased the risk for AMI in

the next 12 hours in this study. Researchers were not able

to demonstrate a significant association between heavy episodic

drinking and AMI due to the small number of exposed

subjects; however, the sample had higher rates of heavy and

irregular drinking compared with the general population,

giving some support to the hypotheses that heavy drinking

increases AMI risk, and that pattern of drinking is important

when assessing the risk for cardiovascular events. The relationship

between alcohol use and cardiovascular events is

likely not as simple as is commonly thought.

Source: Gerlich MG, Krämer A, Gmel G, et al. Patterns

Gerlich MG, Krämer A, Gmel G, et al. Patterns

of alcohol consumption and acute myocardial infarction: a

case-crossover analysis. Eur Addict Res. 2009;15(3):143–149

2. Injecting into the groin and the injection of crack cocaine, which are associated with higher levels of
infection and risky injecting, have become more common.

3. Injecting site infections are common, with around one third of injecting drug users reporting having had an
abscess, sore or open wound at an injecting site in the last year.

4. Transmission of HIV and HCV infection through injecting drug use remains higher than in the late 1990s, with a fifth of recent initiates having hepatitis C and around one in 100 having HIV. Overall almost half of injecting drug users are now infected with hepatitis C and about one in 90 with HIV.

5. There has been a marked increase in the number of injecting drug users receiving the hepatitis B vaccine,
with two-thirds now reporting vaccination.

6. Services to reduce injecting related harms and support for those who want to stop injecting should continue to be developed in line with published guidance.

Key Findings
Behaviours: Levels of reported needle and syringe (direct) sharing have declined in recent years, following an increase in the late 1990s. In 2007, around a quarter of injecting drug users (IDUs) reported direct sharing in the previous month; this level remains higher than in the mid-1990s when about a sixth reported this. The sharing of other injecting equipment remains even more common. There are also indications that
two other factors associated with a greater risk of infection have become more common, with almost one in three IDUs now reporting injecting into the groin (femoral vein) and athird reporting the injection of crack-cocaine.

Hepatitis C: Overall, almost half of IDUs in the UK have been infected with hepatitis C. However, there are marked variations in hepatitis C prevalence within the UK, with low prevalences found in some areas. The overall prevalence of hepatitis C infection among IDUs has probably increased in recent years. Current levels of hepatitis C transmission remain higher than in the late 1990s with a fifth of IDUs becoming
infected within three years of starting to inject.

HIV: The incidence of HIV among IDUs is higher than in the late 1990s with around one in 100 now becoming infected within three years of starting to inject. The overall prevalence of HIV infection among IDUs however remains low compared to many other countries. In England & Wales, the overall HIV
prevalence among IDUs is currently around one in 90. Within England and Wales prevalence has increased amongst IDUs outside London: where it has risen from around one in 400 in 2002 to about one in 150 in 2007. However, the prevalence is higher in London, with around one in 20 HIVinfected. In Scotland, the prevalence of HIV among IDUs was around one in 350 in 2007, which is the lowest level reported
since this was first measured in 1989.

Voluntary confidential diagnostic testing: Uptake of testing for hepatitis C among IDUs in contact with drug services, after increasing markedly, now appears to be levelling off with around three-quarters having ever had a test. It is estimated that around half of IDUs with hepatitis C in contact with these services remain unaware of their infection, and that this proportion has not changed in recent years. There are also likely to be many current and former IDUs not in contact with services that will be unaware they have hepatitis C. Whilst most IDUs in contact with services report having had a test for HIV at some point, only two thirds
of those with HIV are aware of their infection.

Vaccination: The proportion of IDUs reporting uptake of hepatitis B vaccination has increased in recent years, with around two-thirds now reporting accepting at least one vaccine dose. However, the transmission of hepatitis B continues among IDUs.

Bacterial infections: Injecting site infections, which may cost the NHS as much as £47 million per annum, remain common with around one-third of IDUs reporting having had an abscess, sore or open wound at an injecting site in the last year. There are continuing problems ranging from localised injection site infection through to invasive disease associated with meticillin resistant Staphylococcus aureus and severe
group A streptococcal infection. The ongoing occurrence of wound botulism and tetanus cases also remains a concern.

Dope smokers have a 40 per cent increased risk of developing schizophrenia, and taking it regularly drives the risk up two-fold, Australian research shows.
A new study by psychiatrists has reviewed the latest evidence of links between cannabis use and mental illness, concluding the association is “stronger and clearer than ever”.
A pot smoker is 40 per cent more likely to suffer a psychotic episode than a non-smoker, according to the review of major published international research.
And for people who smoke daily over long periods their risk is 200 per cent higher.
“On the world stage, Australians excel in smoking cannabis, so there are very many people who fit into this category,” said lead researcher Dr Martin Cohen, a psychiatrist at the Hunter New England Mental Health Service.
“In fact we’re number one in the world.
“We know now more than ever that this bodes badly for our mental health.”
The review, published in the latest Australian and New Zealand Journal of Psychiatry, calculates that about 14 per cent of all cases of psychosis would never have occurred had the patient not picked up a joint.
A third of all Australians have smoked at least once in their life, with about 300,000 using daily. And while all had increased their risk to some degree, there was growing evidence that genetics predisposed some people even more.
Scientists have found a gene called COMT that, when faulty, is unable to break down the brain chemical dopamine.
An overload of dopamine triggers psychosis and, as cannabis produces an excess of the chemical, people with this “fault” are vulnerable.
Between 10 and 25 per cent of the population are believed to have the faulty gene, but as yet there is no way to test for it.
The risk is also higher for people who start smoking young and those who use heavily.
A 1998 national drug survey of 14 to 19 year olds showed 20 per cent had smoked in the last week, and 20 per cent of these took their first puff before they turned 12.
“These teenagers are the ones we really need to worry about because their use is changing a developing brain,” Dr Cohen said.
Professor Jan Copeland, director of the National Cannabis Prevention and Information Centre, said the levels of cannabis use had declined significantly since the 1998 survey, especially among school-aged Australians.
“But while we’re deterring many from ever trying, established regular users are still finding it very difficult to give up, putting them at risk of not just psychosis but depression as well,” she said.
Source:  The West.com.au  21st May 2008

Ian Sample, science correspondent
The Guardian
Tuesday June 3 2008

Smoking cannabis for long periods of time may shrink parts of the brain that govern memory, emotion and aggression, according to researchers in Australia. Scientists used magnetic resonance imaging to scan the brains of people who admitted to smoking more than five joints a day for at least 10 years and compared them with brain images taken from non-drug users.

Those who smoked cannabis regularly had on average a 12% smaller hippocampus, the part of the brain which is thought to be involved with emotion and memory, and a 7% smaller amygdala, which plays a role in regulating fear and aggression.

For the study, researchers imaged the brains of 15 cannabis smokers and 16 individuals who did not use the drug. The scientists, led by Murat Yücel at the University of Melbourne and colleagues at the University of Wollongong, said scans on larger numbers of people were needed to confirm the extent of the effect.

“Although modest use may not lead to significant neurotoxic effects, these results suggest that heavy daily use might indeed be toxic to human brain tissue,” the scientists report in the journal Archives of General Psychiatry.

Cannabis users also fared worse in tests of verbal memory and were more likely to have low-level symptoms of psychotic disorders such as schizophrenia and mania.

Last month, a team at New York University scanned the brains of a group of 17- to 30-year-olds who had smoked cannabis two to three times a week for at least a year. In that study, the brains of drug users looked no different from those who had never taken cannabis.

In 2004, Cyril D’Souza, a professor of psychiatry at Yale University, reported that THC, the active ingredient in cannabis, caused fleeting schizophrenia-like symptoms in users, ranging from suspiciousness and delusions to poor memory and attention span.

Source: http://www.guardian.co.uk/science/2008/jun/03/drugs.drugsandalcohol

Wednesday, September 10, 2008NEW YORK (Reuters Health) – Researchers from Spain have found a strong and independent link between cannabis use and the onset of psychosis at a younger age. The association, they say, cannot be explained by chance, and is not related to gender or the use of other drugs. It is, however, related to the amount of cannabis used.

“The clinical importance of this finding is potentially high,” Dr. Ana Gonzalez-Pinto from Santiago Apostol Hospital in Vitoria, and colleagues write in the Journal of Clinical Psychiatry, given that cannabis use is extremely prevalent among young people.”

The researchers also report that “estimates of the attributable risk suggest that the use of cannabis accounts for about 10 percent of cases of psychosis.”

The findings are based on 131 patients ages 15 to 65 years who needed inpatient care for a first psychotic episode during a 2-year period. The subjects were evaluated using the Structured Clinical Interview for DSM-IV Axis I Disorders, and clinical and demographic data were also collected.

The results showed a significant gradual reduction in the age at which psychosis began that correlated with an increased dependence on cannabis. Compared with nonusers, age at onset was reduced by 7, 8.5, and 12 years among users, abusers and dependents, respectively, the researchers report.

In further analysis, the effect of cannabis on age at onset “was not explained by the use of other drugs or by gender,” they also note. The finding was similar in the youngest patients, suggesting that this effect was not due to chance.

These results “point to cannabis as a dangerous drug in young people at risk of developing psychosis,” Gonzalez-Pinto and colleagues conclude.

SOURCE: Journal of Clinical Psychiatry, August 2008.

New research suggests that it takes less exposure to tobacco to increase the risk of colorectal cancer among women than men.
Researchers Joseph C. Anderson, M.D., of the University of Connecticut and Zvi A. Alpern, M.D. of Stony Brook University conducted a large cross-sectional study, analyzing data on patients who underwent colonoscopies. Utilizing a measurement called “pack years” — determined by multiplying the number of cigarettes smoked per day by the number of years smoked — researchers compared the amount of tobacco exposure in men and women to increased colorectal cancer risk.
The analysis, controlling for age, body mass index and family history, showed that women who smoked up to 30 pack-years had an 82 percent greater risk for significant colorectal neoplasia than nonsmoking women, while men who smoked up to 30 pack-years showed 21 percent greater risk than nonsmoking men. Female smokers faced double the risk or more of colorectal cancer if they smoked less than 30 pack years, while men achieved the same level of risk only when they smoked more than 30 pack years.
The study was presented at the American College of Gastroenterology’s annual scientific meeting.
 
Source: Reported in Join Together Oct. 7 2008

The latest Drug Abuse Warning Network (DAWN) report—drawn from a sample of hospital emergency departments across the Nation—indicates that more than 1.7 million visits to emergency departments (ED) were associated with some form of substance misuse or abuse. The 2006 DAWN report, developed by the Substance Abuse and Mental Health Services Administration (SAMHSA), provides the latest estimates on how substance use affects this critical part of the Nation´s healthcare system.

Of the of 113 million ED visits in the United States, DAWN estimates that 1,742,887 were associated with drug misuse or abuse, with illicit drugs responsible for 31 percent of the cases and prescription drugs for 28 percent of the cases.

Among the report’s more notable findings:

• Cocaine was involved in 548,608 emergency department visits.
• Marijuana was involved in 290,563 emergency department visits. The rates were highest among those aged 18-24.
• Heroin was involved in 189,780 emergency department visits.
• There were 126,704 emergency department visits by patients under age 21 where alcohol was the only substance involved in the visit.
• Stimulants, including amphetamines and methamphetamines, were involved in 107,575 emergency department visits.

Prescription and over-the-counter drugs were responsible for 741,425 of the ED visits and the majority of these visits (54 percent) involved multiple drugs.

While most of the data was similar to previous years, there was a notable increase in the number of ED visits related to prescription drugs, with a 44 percent increase from 2004 to 2006.

Source:  CADCA Coalitions OnLine  11th Dec. 2008

Two recently published research papers have used functional MRI (fMRI) to show how the two main constituents of cannabis Tetrahydrocannabinol (THC) and Cannabidiol (CBD) act on the brain to modulate cognitive function and psychiatric  symptoms.
Cannabis is the world’s most widely used illicit drug and has a wide range of psychological and symptomatic effects.  In the short term cannabis can induce psychotic symptoms and anxiety, while regular use is associated with cognitive impairments and an increased risk of schizophrenia.  
Talking about the latest research published by the Institute of Psychiatry at King’s College London, into the effects of cannabis, Professor Philip McGuire one of the authors said: “The Institute has been at the forefront of research into the adverse psychiatric effects of cannabis use.  These new findings further develop scientific understanding in this area by indicating how the two main psychoactive constituents of cannabis act on the brain to alter cognitive function and induce psychiatric symptoms.
The studies were initiated by Philip McGuire and Zerrin Atakan from the Institute of Psychiatry at King’s, Jose Crippa from Ribeirão Preto, Brazil and Rocio Martin-Santos in Barcelona, Spain.   They and a team of researchers at the Institute used functional magnetic resonance imaging and behavioural measures to assess the impact on brain function in healthy male volunteers.  Each subject was scanned on three occasions at monthly intervals, with each scan preceded by the administration of either THC, CBD or a placebo.
In the first paper published in Biological Psychiatry in December 2008, ‘Neural Basis of Δ-9-Tetrahydrocannabinol and Cannabidiol: Effects During Response Inhibition’ the researchers considered the effects of THC and CBD on brain function during a Go/No Go task which requires subjects to over-ride a regular button pressing response.  They found that THC reduced activation in the part of the prefrontal cortex that is normally critical for this ‘response inhibition’ process.  Please refer to the journal for a full copy of the paper. (Biological Psychiatry 64 (11), pp. 966-973) doi:10.1016/j.biopsych.2008.05.011)
In the second paper published in the Archives of General Psychiatry (12 January 2009) ‘Distinct Effects of _9-Tetrahydrocannabinol and Cannabidiol on Neural Activation During Emotional Processing’  the researchers investigated the neurophysiological basis of the effects of cannabis on anxiety, using faces that had fearful expressions.  Normally viewing fearful faces provokes anxiety, activates the amygdala, and increases skin conductance (a measure of autonomic arounsal).  Administration of CBD reduced the response of the amygdale to fearful faces, and this effect was correlated with its effect on skin conductance.  Please refer to the Archives of General Psychiatry, January 2009 issues for full copies of this paper.  (Arch Gen Psychiatry, 2009;66 (1): 95-105.)
Professor Philip McGuire concludes, “These studies show that THC and CBD have distinct effects on brain function in humans, and these may underlie their correspondingly different effects on cognition and psychiatric symptoms.  Determining how the constituents of cannabis act on the brain is fundamental to understanding the role of cannabis use in the aetiology of psychiatric disorders.”
Source:  Institute of Psychiatry  20th Jan 2009 

WASHINGTON (Reuters) – About a fifth of people with tuberculosis in the United States report abusing drugs or alcohol, and the figure is even higher when only U.S.-born patients are included, government researchers said on Monday.
The substance abusers were more contagious than others with the disease and remained contagious longer, the U.S. Centers for Disease Control and Prevention researchers wrote in the journal Archives of Internal Medicine.
About a third of people worldwide are infected with the bacterium that causes TB. Only a small percentage of people ever develop the disease. But the effect of substance abuse on the body may raise the chances that the latent infection turns into active disease, and substance abusers may be less likely to be screened for TB, the researchers said.
The researchers tracked 153,268 people with TB in the United States from 1997 to 2006, accounting for nearly everyone age 15 and older with the disease during that span.  Overall, 19 percent of them reported that they abused drugs and/or alcohol, according to the study. Among the 76,816 U.S.-born people with TB, 29 percent reported substance abuse.
The United States has very low rates of TB compared to many other parts of the world, and about half of the people with TB were born elsewhere.
“The most commonly reported risk factor for TB was substance abuse,” CDC epidemiologist Eric Pevzner, one of the researchers, said in a telephone interview. It was greater than are other leading risk factors such as HIV infection or homelessness, the researchers said.
TB is an infectious bacterial disease typically attacking the lungs. It can be spread by breathing in droplets from a cough or sneeze of an infected person.
Pevzner said the findings had important public health implications as the United States attempts to lower its TB rates even further, Pevzner said.  “We can’t treat the TB in isolation,” Pevzner said. “We have to bring in people who are experts in substance abuse and also treat the life circumstances that people are facing so that we can help cure this disease and help end a chain of transmission.”
Substance abusers are less likely to complete TB treatment, the researchers said. They also may have TB diagnosed later and have less access to routine medical care.

Source:  Reuters  16th January 2009

Drug addicts find it harder than non-addicts to derive pleasure from everyday life, new Australian research shows.
The study took in 33 heroin addicts on opiate replacement, whose brain activity was measured as they looked at pictures of drug and non-drug related scenes.
Associate Professor Dan Lubman said the addicts showed elevated responses to drug-related images compared with a control group of non-drug users, but the key finding was their disinterest in otherwise pleasurable non-drug scenes.  “Looking at pictures of heroin, needles, people injecting heroin, and social drug use … the heroin group found the drug pictures much more pleasant and rewarding, it lit up the brain activity,” said Dr Lubman, of Melbourne University’s Orygen Youth Health Research Centre.  “Whereas they were under-responsive and found the emotionally pleasant pictures much less pleasant.”
Dr Lubman said the alternative images included attractive people engaged in fun activities, delicious food, and “things that people normally rank as being quite pleasurable … there were also a few puppy dogs in there”.
The same drug addicts were assessed again six months later to see who had kicked their habit, with surprising results as the critical factor was not those who enjoyed drug-related pictures the most.  “It was actually the under-responsiveness to emotional positive pleasurable stimulus that predicted who was using the most heroin,” Dr Lubman said.
He said the findings held implications for drug treatment programs and the public, who often grappled with an addict’s inability to stop using.  Dr Lubman said the results suggested drug users had a reduced ability to enjoy everyday pleasures, and their brains remained excited by the prospect of continued drug use.
It also showed why threats of punishment, which Dr Lubman calls the “big stick” approach, may not work in discouraging addicts. “They haven’t got anything else in their lives to turn to,” he said.
“Our research shows the focus should be not only just the drugs but getting them (addicts) to be passionate about something else in some way, because that’s the best predictor about whether they will stop using.”
Dr Lubman said he expected similar results to be associated with all drugs of addiction, including alcohol, and further research was needed to explain a possible “chicken and egg” problem.  Which came first, addiction leading to less pleasure in life or drug taking to overcome a pre-existing lack of enjoyment?
“There is evidence to suggest that people who are vulnerable to addictions already have an underlying emotional problem,” Dr Lubman said.
The research findings were published in the journal Archives of General Psychiatry.

Source:  www.theage.com.au  Feb. 3rd 2009

People with mental illness alone are no more likely than anyone else to commit acts of violence, a new study by UNC researchers concludes. But mental illness combined with substance abuse or dependence elevates the risk for future violence.
“Our study shows that a link between mental illness and violence does exist, but it’s not as strong as most people think,” said Eric B. Elbogen, Ph.D., lead author of the study and assistant professor in the forensic psychiatry program at the University of North Carolina at Chapel Hill School of Medicine.
“We found that several other factors – such as a history of past violence or substance abuse or a recent divorce or loss of one’s job – are much more predictive of future violence than mental illness alone,” Elbogen said. “Only when a person has both mental illness and substance abuse at the same time does that person’s risk of future violence outweigh anyone else’s.”
UNC co-author Sally C. Johnson, M.D. added, “These findings challenge the perception some people have, and which you often see reflected in media coverage, that mental illness alone makes someone more dangerous. Our study shows that this perception is just not correct.”  Elbogen and Johnson’s study is published in the February 2009 issue of Archives of General Psychiatry. To arrive at their findings, they conducted statistical analyses of data collected previously as part of the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) conducted by the National Institute of Alcohol Abuse and Alcoholism.
A total of 34,653 people completed interviews during the two separate waves of NESARC. Wave 1 took place from 2001-2002 while wave 2 was from 2004-2005. Wave 1 data on severe mental illness – including schizophrenia, bipolar disorder and major depression – were analyzed to predict wave 2 data on violent behavior.
The results show “that if a person has severe mental illness without substance abuse and history of violence, he or she has the same chances of being violent during the next 3 years as any other person in the general population,” Elbogen and Johnson wrote. 
When mental illness is combined with substance abuse, the risk for future violence reaches the level of statistical significance. However, even mental illness combined with substance abuse ranks only ninth on the study’s list of the top 10 predictors of future violence. The higher ranking predictors, listed in order of their predictive value, are age (younger people are more likely to commit acts of violence), history of violence, sex (males are more prone to violence), history of juvenile detention, divorce or separation in the past year, history of physical abuse, parental criminal history and unemployment for the past year. Victimization in the past year was the tenth predictor.
“The data shows it is simplistic as well as inaccurate to say the cause of violence among mentally ill individuals is the mental illness itself … the current study finds that mental illness is clearly relevant to violence risk but that its causal roles are complex, indirect, and embedded in a web of other (and arguably more) important individual and situational cofactors to consider,” the study concludes.
Source:   ScienceDaily (Feb. 3, 2009)

The United Kingdom has one of the highest rates of illicit drug use in the developed world.In 2007, it was estimated that more than eleven million adults aged between 16 and 59 in England and Wales had taken illegal drugs in their lifetime, including over three million who had taken an illicit drug in the past year. Many drug users have taken cannabis only a few times in their lives and no other drugs. For a minority, drug use becomes regular and prolonged, and is associated with a high degree of harm to themselves and others.

Drug misuse is defined by the World Health Organisation as the use of a substance for a purpose not consistent with legal or medical guidelines, for example the non-medical use of prescription medications or the recreational use of illegal drugs. Drug misuse is not necessarily problematic, though it can never be considered risk-free.

 More people take cannabis than any other drug, but problematic drug use, particularly dependence, is most frequently associated with opiates. For example, the National Treatment Agency for Substance Misuse report that heroin is the main drug misused by 66%of their clients aged 18 or over, with a further 8%naming other opiates as their main drug of misuse. The annual
social and economic cost of Class A drug use has been estimated at £15.4 billion a year; 99%of this is accounted for by problem drug users.

A number of adverse health outcomes have been associated with drug misuse. Injecting drug users are vulnerable to thrombosis, abscesses, blood-borne diseases (particularly hepatitis B and C and HIV), and respiratory problems. Frequent cannabis use has also been associated with respiratory problems.
There is significant co-morbidity between drug misuse and poor mental health. Problematic use of one drug often co-occurs with misuse of or dependence on other drugs and alcohol.

Drug misuse and drug dependence are more prevalent in adults with various psychiatric problems, from common mental disorders to personality disorders and severe psychotic illness. For example, cannabis use has been linked to the development of acute and long term psychotic symptoms, though the causal pathways for the latter remain unclear. In prisoners in England and Wales, severe dependence on cannabis or stimulants, such as amphetamines or cocaine, was associated with an increased risk of psychosis. Significant proportions of those being treated as inpatients or in the community for severe mental illness have substance misuse problems, and this has treatment implications that are not
always satisfactorily addressed. ( Psychiatric comorbidity, including with drug
dependence, is considered in Chapter 12 of this report.)

The number of admissions to NHS hospitals with a primary or secondary diagnosis of drug related mental health or behavioural disorder has risen from 19,018 episodes in 1996/97 to 38,170 in 2006/07.15 In the same period, the number of admissions with a primary diagnosis of poisoning by drugs rose from 7057 to 10,047. Between 1993 and 1999, deaths in England attributable to drug misuse rose from 786 to 1538.16 Since then the level has remained constant; in 2006, 1469 deaths were attributable to drug misuse.

 In 2007/08, 202,666 individuals were in contact with structured drug treatment services in England. Though the health impacts of drug dependence are significant, the harm to society of drug related crime is also great. It has been estimated that between a third and a quarter of acquisitive crime – including burglary, theft, fraud and the sale of sex – is drug-related. Surveys of offenders have shown high rates of recent heroin and cocaine use, and made explicit the link between criminal behaviour and the need to get money to buy drugs. Other types of crime are less strongly linked to drug use, although drug dealing may be linked to high levels of community violence.

The risk factors for drug use are similar to those for criminal behaviour, including social and economic deprivation and family breakdown. In young people, truancy, exclusion from school, serious or frequent offending and homelessness are linked to an increased risk of frequent drug use and the use of Class A drugs.  The harm caused by problem drug use also extends to the families of drug users and to the communities in which they live. The children of people with problematic drug use have been described as being at risk from conception to adulthood, from multiple and cumulative harms to their mental and physical health, and to their social, emotional and educational development. Already-deprived communities are most at risk of drug-related harm, through the direct effect on users, as well as increased rates of crime and antisocial behaviour.

Increasing concern about the harm caused by drug misuse and dependence during the 1990s led to the publication of the first ten-year drugs strategy in 1998, updated in 2002.  Its overall aim was to ‘reduce the harm caused by illegal drugs’, with objectives relating to four themes: preventing young people from becoming drug users, treatment of problem drug users, reducing the supply of drugs, and reducing drug-related crime.

The first drug strategy could claim some successes, including a reduction in the prevalence of lifetime drug use, a doubling between 1998 and 2008 of the numbers of drug users receiving treatment, and a reduction in recorded acquisitive crime. In 2008 the second ten year drug strategy was published. This strategy focused on:

• Protecting communities through tackling drug supply, drug-related crime     and anti-social behaviour;
• Preventing harm to children, young people and families affected by drug misuse;
• Delivering new approaches to drug treatment and social re-integration; and
• Public information campaigns, communications and community engagement.

The major source of data on the prevalence of drug use by adults aged 16 and over in England is the annual British Crime Survey (BCS). The 2006/07 BCS estimated that 35.5% of adults in England and Wales aged between 16 and 59 had taken illegal drugs at some time, including 13.8%of adults who had taken one or more Class A drugs.

10.0%of adults had taken drugs in the past year. Cannabis was the most commonly used drug; 8.2% of adults had taken cannabis in the past year. 3.4%of adults had taken a Class A drug in the past year.

Men were more likely than women to have taken drugs. Drug use in the past year was most common in 16 to 19 year olds (23.3%) and 20 to 24 year olds (24.8%), but declined sharply with age thereafter. Around half of adults in their twenties had taken drugs at some time in their lives. This was increasingly less likely in older adults; among 55 to 59 year olds, the oldest age group for whom data were available, 18.1%had taken drugs at least once.

It is acknowledged that using a household survey of this kind to measure drug use may underestimate several key groups whose patterns and levels of drug use may be atypical. These include students in halls of residence, the homeless, and those in institutions, including hospitals and prisons. Additionally, drug dependent people living in private households may be relatively less likely to participate in surveys, given that they may lead chaotic lives which make them less available, able or willing to answer survey questions. Comparisons of the BCS with the numbers of drug users in treatment confirm that surveys significantly underestimate the number of dependent drug users.

Source:  Adult Psychiatic Morbidity in England. Report for NHS Information Centre Feb. 2009 National Centre for Social Research morbidity in England.

This case-control study investigated cannabis use as a possible cause for the increase in testicular tumours in recent decades. Testicular tumours typically affect men in their 20s, 30s and 40s. There are two main types of testicular cancer: seminomas and nonseminomas. They are both types of germ (seed) cell tumours. The peak age for developing these types of tumour is between 20 and 35 years for nonseminomas and between 30 and 45 years for seminomas. The aim of this study was to compare previous cannabis use in men who had developed testicular cancer with a group of matched controls who had not.
The ATLAS study recruited men between 18 and 44 years living in three counties of Washington State who had been diagnosed with invasive testicular cancer between January 1999 and January 2006. Of the possible 550 cancer cases, the researchers interviewed and enrolled 369 men in their study.
Men who did not have testicular cancer were identified for the control group by a technique called random digit dialling. This involves calling random phone numbers and establishing if there is somebody matching certain criteria living at that address. In this case, the controls were male, matched to the cases by age and had to have been living in the same area during the diagnosis period. The researchers interviewed 979 of 1,875 eligible controls.
All cases and controls were interviewed using a questionnaire asking about demographics, cigarette smoking, alcohol use, recreational drug use, family history and other known risk factors for testicular cancer. The cases were asked to give their exposure to these risks for the time before they were diagnosed with cancer. The controls were then asked about their behaviour from that same date. Each man who reported marijuana use was asked to recall the times in his life when he used marijuana or hashish (or both), the age at which he first and last used it, and the frequency (times per day, week, month or year).
The researchers carried out statistical analyses for all testicular cancers combined, and then separately for type of cancer: seminomas, nonseminomas and each particular subtype of nonseminomas. They looked at risk of cancer according to marijuana use, while adjusting for (taking into account) confounders such as smoking and alcohol use.
What were the results of the study?
Compared with controls, cases were more likely to be from a lower socioeconomic background and to have less than college education. There were also no men of African-American origin in the cases. Cases were also more likely to have a first-degree relative with testicular cancer and to have a history of cryptorchidism (undescended testis/testes).
A slightly higher proportion of men with testicular cancer had ever smoked marijuana (72.6%) compared to the controls (68.0%). However, from this, the calculated risk of testicular cancer with ever having used marijuana was only borderline significant (OR, 1.3; 95% CI, 1.0-1.8). A higher proportion of cases reported being current marijuana users (26% versus 20%), and to have started using marijuana below the age of 18 years (21% versus 15%). How many years the men had used marijuana did not significantly affect the risk of testicular cancer.
Men with testicular cancer more commonly used marijuana once or more times per week (15% versus 10% of the control group). Using marijuana once or more times per week doubled the risk of testicular cancer (OR, 2.0; 95% CI, 1.3-3.2) compared with never using it. Using marijuana less than once a week was not associated with a significantly increased risk.
When the researchers carried out subgroup analyses by type of testicular cancer they found that the increased risk of seminoma from current marijuana use was non-significant, but the increased risk for nonseminoma was significant (OR, 2.3; 95% CI, 1.3-4.0).
What interpretations did the researchers draw from these results?
The researchers conclude that they found a link between marijuana use and the occurrence of nonseminomas. They say that additional studies are needed to test further the theory of a link between marijuana use and testicular cancer, and to explore the possible biological reasons for this.

Source:  medical journal Cancer Feb 2009

Down in your cups? … researchers find a link between alcohol dependency and depression.
Excessive alcohol drinking may increase the risk of depression, a long-term study conducted over 25 years in New Zealand has found.
The study, published in the Archives of General Psychiatry, involved a group of 1,055 children who were monitored and interviewed at various times over 25 years.
“At all ages, there were clear and statistically significant trends for alcohol abuse or dependency to be associated with increased risk of major depression,” wrote the researchers, led by David Fergusson at the University of Otago’s department of psychological medicine.
The study found 19.4 percent of the participants between 17 and 18 were either abusing or dependent on alcohol, and 18.2 percent were diagnosed with depression.
“Individuals who fulfilled the criteria for alcohol abuse or dependency were 1.9 times more likely to also fulfill the criteria for major depression,” the researchers wrote.
The link between the two was significant even after factoring in other possible causes, such as use of cannabis and other illegal drugs, affiliation with “deviant peers,” unemployment and a partner who committed crimes.
“It has been proposed that this link may arise from genetic processes in which the use of alcohol acts to trigger genetic markers that increase the risk of major depression,” the researchers said.
“Further research suggests that alcohol’s depressant characteristics may lead to periods of depressed effect among those with alcohol abuse or dependency.”

Source:  theAge.com.au  3rd March 2009

Cannabis is a common drug of abuse that is associated with various long-term and short-term adverse effects. The nature of its association with vomiting after chronic abuse is obscure and is underrecognised by clinicians. In some patients this vomiting can take on a pattern similar to cyclic vomiting syndrome with a peculiar compulsive hot bathing pattern, which relieves intense feelings of nausea and accompanying symptoms. In this case report, we describe a twenty-two year-old-male with a history of chronic cannabis abuse presenting with recurrent vomiting, intense nausea and abdominal pain. In addition, the patient reported that the hot baths improved his symptoms during these episodes. Abstinence from cannabis led to resolution of the vomiting symptoms and abdominal pain. We conclude that in the setting of chronic cannabis abuse, patients presenting with chronic severe nausea and vomiting that can sometimes be accompanied by abdominal pain and compulsive hot bathing behaviour, in the absence of other obvious causes, a diagnosis of cannabinoid hyperemesis syndrome should be considered.

Source:  Cannabinoid hyperemesis syndrome: Clinical diagnosis of an underrecognised manifestation of chronic cannabis abuse. Sontineni SP et al
World J Gastroenterol 2009 March;15(10):1264-1266

The daily consumption of cannabis predisposes to the appearance of psychosis and schizophrenia, and those episodes of psychosis which are fruit of this substance present certain specific characteristics, both before their appearance and in the clinical presentation of the psychosis.

This is one of the conclusions of the doctoral thesis “Neurodevelopment and environmental stress in initial psychosis: transversal analysis of the ESPIGAS study”, carried out by researcher Miguel Ruiz Veguilla, of the Institute of Neurosciences of the University of Granada (Spain) and supervised by professors Manuel Gurpegui Fernández de Legaria and Jorge Cervilla Ballesteros. Ruiz Veguilla is also the person in charge fo the Unit of Development Neuropsychiatry of Jaén (Spain).
This work has studied the risk factors associated with schizophrenia, identifying and characterizing in depth those psychosis associated with a continual consumption of cannabis. They carried out a study with 92 subjects, 50 of which had developed a psychosis without presenting signs of an “abnormal neurodevelopment”, this is, they had been doing well academically, they had a group of friends (no social isolation) and they presented a good motor coordination. In addition, these subjects did not show a family history of episodes of psychosis in first or second degree.

Identifying a new type of psychosis
The research work carried out by Miguel Ruiz Veguilla has identified a connection between cannabis consumption and psychosis in subjects with a good premorbid performance, and without signs of minor neurological alterations, which in his opinion might point out “a psychopathological way associated with psychosis in subjects with less predisposition”.
Thus, 66% of the patients with psychosis who participated in the study and had a normal neurodevelopment admitted to have consumed cannabis daily or almost every day, whereas 43% of the participants with markers of an abnormal neurodevelopment (those already indicated: bad previous social and academic behaviour, a family history and a “clumsier” attitude when they carry out tasks of motor coordination and complex motor acts) were drug users too.
In the light of the results of his doctoral thesis, the researcher of the University of Granada says that, after having identified a type of psychosis where the environmental factor plays a more relevant role, we should now answer the question of which is the prognosis, in the long term, of those subjects with a good previous behaviour, whose psychosis is associated with a high consumption of cannabis.
The results of this research work have been published in the journals Schizophrenia Research and European Psychiatry.

Source: University of Granada (2009, March 26). Daily Consumption Of Cannabis Predisposes To Appearance Of Psychosis And Schizophrenia,

Conflicting evidence exists regarding the long-term effects of cannabis use, according to background information in the article. “Although growing literature suggests that long-term cannabis use is associated with a wide range of adverse health consequences, many people in the community, as well as cannabis users themselves, believe that cannabis is relatively harmless and should be legally available,” the authors write.  “With nearly 15 million Americans using cannabis in a given month, 3.4 million using cannabis daily for 12 months or more and 2.1 million commencing use every year, there is a clear need to conduct robust investigations that elucidate the long-term sequelae of long-term cannabis use.”
Murat Yücel, Ph.D., M.A.P.S., of ORYGEN Research Centre and the Melbourne Neuropsychiatry Centre at the University of Melbourne, Australia, and colleagues from the University of Wollongong performed high-resolution structural magnetic resonance imaging on 15 men (average age 39.8 years) who smoked more than five joints daily for more than 10 years. Their results were then compared with images from 16 individuals (average age 36.4) who were not cannabis users. All participants also took a verbal memory test and were assessed for subthreshold (below the standard of disease diagnosis) symptoms of psychotic disorders, which include schizophrenia and mania.
The hippocampus, thought to regulate emotion and memory, and the amygdala, involved with fear and aggression, tended to be smaller in cannabis users than in controls (volume was reduced by an average of 12 percent in the hippocampus and 7.1 percent in the amygdala). Cannabis use also was associated with sub-threshold symptoms of psychotic disorders. “Although cannabis users performed significantly worse than controls on verbal learning, this did not correlate with regional brain volumes in either group,” the authors write.
“There is ongoing controversy concerning the long-term effects of cannabis on the brain,” the authors write. “These findings challenge the widespread perception of cannabis as having limited or no neuroanatomical sequelae. Although modest use may not lead to significant neurotoxic effects, these results suggest that heavy daily use might indeed be toxic to human brain tissue. Further prospective, longitudinal research is required to determine the degree and mechanisms of long-term cannabis-related harm and the time course of neuronal recovery after abstinence.”

Source:  JAMA and Archives Journals (2008, June 3). Long-term Cannabis Users May Have Structural Brain Abnormalities

The number of alcohol and drug abusers being treated by mental hospitals has leapt by almost a third in five years.   Doctors have also charted a rising number of patients being sectioned because of psychiatric problems – many in private hospitals at NHS expense.
Critics last night blamed the binge drink and drug culture for creating more mental health disorders, while cuts in NHS beds are increasing dependency on the private sector.  Critics blame binge drink and drug culture for creating more mental health disorders
A report by three psychiatrists in the British Medical Journal says there is concern about an era of ‘re-institutionalisation’ within mental hospitals.
The number of hospital beds dropped from 150,000 in the 1950s to less than 55,000 in 1995 in favour of community care but demand appears to be rising, they say.   The number of sectioned patients – taken into hospital under compulsory orders – has increased by 20 per cent over the last decade.
The psychiatrists found a 29 per cent rise in admissions by alcohol and drug abusers since 2003.  They say the numbers have changed the environment on psychiatric wards with reports of patients with depression feeling intimidated and even attacked by those with drink and drug problems.
Tories claimed the increase was not being helped by Labour ‘mixed messages’ on the dangers of drugs and its rolling out of 24-hour drinking.

Source:  www.MailOnline  Oct.2008

Men who smoke marijuana frequently have significantly less seminal fluid, a lower total sperm count and their sperm behave abnormally, all of which may affect fertility adversely, a new study in reproductive physiology at the University at Buffalo has shown.
This study is the first to assess marijuana’s effects on specific swimming behavior of sperm from marijuana smokers and to compare the results with sperm from men with confirmed fertility. Marijuana contains the cannabinoid drug THC (tetrahydrocannabinol), which is its primary psychoactive chemical, as well as other cannabinoids.   Results of the study were presented today (Oct. 13, 2003) at the annual meeting of the American Society of Reproductive Medicine in San Antonio.
“The bottom line is, the active ingredients in marijuana are doing something to sperm, and the numbers are in the direction toward infertility,” said Lani J. Burkman, Ph.D., lead author on the study. Burkman is assistant professor of gynecology/obstetrics and urology and head of the Section on Andrology in the UB School of Medicine and Biomedical Sciences. UB’s andrology laboratory also carries out sophisticated diagnosis for infertile couples.
“We don’t know exactly what is happening to change sperm functioning,” said Burkman, “but we think it is one of two things: THC may be causing improper timing of sperm function by direct stimulation, or it may be bypassing natural inhibition mechanisms. Whatever the cause, the sperm are swimming too fast too early.” This aberrant pattern has been connected to infertility in other studies, she noted.
Burkman collaborated on earlier, published UB research that was the first to show that human sperm contains cannabinoid receptors, and that the naturally occurring cannabinoid, anandamide, which activates cannabinoid receptors in the brain and other organs, also activates receptors in sperm. This evidence indicated an important role in reproduction for natural cannabinoids.
Further research in the andrology laboratory showed that human sperm exposed to high levels of THC displayed abnormal changes in the sperm enzyme cap, called the acrosome. When researchers tested synthetic anandamide equivalents on human sperm, the normal vigorous swimming patterns were changed and the sperm showed reduced ability to attach to the egg before fertilization. Only about 10 laboratories in the U.S. perform this array of sperm function tests.
In the current study, Burkman received seminal fluid from 22 confirmed marijuana smokers and subjected the samples to a variety of tests. The volunteers reported smoking marijuana approximately 14 times a week, and for an average of 5.1 years.  Control numbers were obtained from 59 fertile men who had produced a pregnancy. All men abstained from sexual activity for two days before the lab analysis.
The samples from both groups were tested for volume, sperm-count-per-unit of seminal fluid, total sperm count, percent of sperm that was moving, velocity and sperm shape. Sperm also were assessed for an important function called hyperactivation (HA), a closely regulated and very vigorous type of swimming that is required as the sperm approaches the egg. The researchers evaluated HA and velocity while the sperm was in seminal fluid and again after washing and incubation, when the dead sperm were eliminated.
Results showed that both the volume of seminal fluid and the total number of sperm from marijuana smokers were significantly less than for fertile control men. Significant differences also appeared when HA and velocity, both before and after washing, were assessed, the study found.
“The sperm from marijuana smokers were moving too fast too early,” said Burkman. “The timing was all wrong. These sperm will experience burnout before they reach the egg and would not be capable of fertilization.”
Burkman noted that many men who smoke marijuana have fathered children. “The men who are most affected likely have naturally occurring borderline fertility potential, and THC from marijuana may push them over the edge into infertility,” she said.
As to the question of whether fertility potential returns when smokers stop using marijuana: Burkman said the issue hasn’t been studied well enough to provide a definitive answer.
“THC remains stored in fat for a long period, so the process may be quite slow. We can’t say that everything will go back to normal. Most men who have borderline fertility are unaware of that fact. It’s difficult to know who is at risk. I definitely would advise anyone trying to conceive not to smoke marijuana, and that would include women as well as men.”

Source: University At Buffalo : 14th October 2003

Classify this item in the “not good news” file. Hepatitis C—it’s not just for syringe users anymore. Contrary to previous theory, dirty needles or direct blood exposure may not be necessary. While bodily fluids have always been suspect, researchers at the University of Rochester Medical Center and other institutions have discovered evidence of the hepatitis C virus (HCV) in nasal secretions left in straws used to sniff drugs.

It is no secret that the regular practice of snorting or sniffing drugs can lead to inflammation and bleeding in the tender mucous membranes in the nose. This complicates the risk of using “shared drug-sniffing implements,” as the study refers to them.

According to a report of the work in NIDA Addiction Research News, the method of disease transmission is unknown in an estimated 20 percent of Hepatitis C infections. NIDA said the researchers “asked participants to snort air through a straw in a way that would mimic their normal drug-sniffing behavior to determine whether sniffing implements became contaminated. The straws were then tested for blood and HCV.”

In the study of 38 intranasal drug users, all of whom had active Hepatitis C infections, “researchers found trace amounts of blood in 74 percent of mucus samples and on 8 percent of the straws used for sniffing. In addition, they detected HCV in 13 percent of mucus samples and on 5 percent of the straws.” The Hepatitis C virus is capable of surviving on surfaces for as long as 16 hours. The scientists conclude that the results, while preliminary, “lend important virological and clinical support to the intranasal HCV transmission hypothesis.”

In fact, the authors of the study suggest that the findings are quite likely conservative, given that the Hepatitis C virus is more likely to “occur in the nasal secretions with greater frequency during episodes of active drug sniffing, which may exacerbate the discharge of nasal fluids and blood.”

Source: Clinical Infectious Diseases. October 1, 2008

People who smoked marijuana had changes in the blood flow in their brains even after a month of not smoking, according to a study published in the February 8 issue of Neurology, the scientific journal of the American Academy of Neurology.

The findings could explain in part the problems with thinking or remembering found in other studies of marijuana users, according to study authors Ronald Herning, PhD, and Jean Lud Cadet, MD, of the National Institute on Drug Abuse in Baltimore, Md.

The study involved 54 marijuana users and 18 control subjects. The marijuana users volunteered to take part in a month-long inpatient program. The blood flow velocity in brain arteries was tested with transcranial Doppler sonography in all participants at the beginning of the study and again at the end of the month for the marijuana users.

The blood flow velocity was significantly higher in the marijuana users than in the control subjects, both at the beginning of the study and after a month of abstinence from marijuana use. The marijuana users also had higher values on the pulsatility index (PI), which measures the amount of resistance to blood flow. This is thought to be due to narrowing of the blood vessels that occurs when the circulation system’s ability to regulate itself is impaired.
“The marijuana users had PI values that were somewhat higher than those of people with chronic high blood pressure and diabetes,” Herning said. “However, their values were lower than those of people with dementia. This suggests that marijuana use leads to abnormalities in the small blood vessels in the brain, because similar PI values have been seen in other diseases that affect the small blood vessels.”

The PI values for light and moderate marijuana users improved over the month of abstinence. There was no improvement for heavy marijuana users. The light users smoked two to 15 joints per week. The moderate users smoked 17 to 70 joints per week, and the heavy users smoked 78 to 350 joints per week.

Source:. American Academy Of Neurology (2005, February 13). Marijuana Use Affects Blood Flow In Brain Even After Abstinence. ScienceDaily. Retrieved May 12, 2009

When depression and substance abuse occur together, as
is common, either condition can hamper effective treatment
of the other. Behavioral interventions that address
both conditions have not been rigorously tested. Although
delivering such interventions by computer holds promise
for extending their reach, their effectiveness in treating
these co-occurring disorders remains unknown. In a randomized
trial, researchers measured the effectiveness of an
intervention combining principles of motivational interviewing
(MI) and cognitive behavioral therapy (CBT) in the
treatment of depression and co-morbid alcohol and/or cannabis
use. After a single baseline brief-intervention session,
97 persons with co-occurring depression and heavy alcohol
and/or cannabis use were randomized to receive either no
further treatment (n=30) or nine 1-hour sessions of MI/
CBT treatment delivered either by a therapist (n=35) or by
computer (n=32). Sixty-seven patients completed the
study. Depression and alcohol/cannabis use were assessed
at 3, 6, and 12 months following treatment completion.
• Although the initial treatment session demonstrated
modest efficacy for depression as well as alcohol and/
or cannabis use, outcomes across all 3 conditions were
further improved among MI/CBT recipients.
• The proportion of participants with improved depressive symptoms (Beck Depression Inventory score,
<17) and with diminished alcohol and/or cannabis use
(<50% as many hazardous use days per month) at 12
months did not differ significantly among recipients of
therapist- or computer-delivered interventions.
Comments: These data provide clear evidence that combining
interventions to target depression as well as alcohol
and/or cannabis use can improve outcomes in both conditions,
and that delivering such interventions by computer
may be effective and reduce costs associated with therapist
time. The results might have been less favorable had intent-to-
treat analyses assumed that participants lost to follow-up
had resumed drug use. In addition, the intensity of the
intervention (10 hour-long sessions) raises questions about
feasibility in typical practice settings. As computer-delivered
interventions gain acceptance, further studies to define
cost- effectiveness and completion rates outside of research
settings are warranted.

Source: . Addiction. 2009; 104(3):378–388. . Computer-
based psychological treatment for comorbid depression
and problematic alcohol and/or cannabis use: a randomized
controlled trial of clinical efficacy.

A UK study based on a cohort of more than 1 million
women related baseline alcohol intake to the relative risk
(RR) of incident invasive cancer at 21 sites. A quarter of
the cohort reported drinking no alcohol; 98% of those who
drank consumed fewer than 21 drinks per week and had an
average consumption of 10 g of alcohol per day (1 standard
drink as defined in this study). Only current drinkers were
included in dose-response analyses; both lifetime abstainers
and ex-drinkers were excluded. During an average of 7.2
years of follow-up, 68,775 invasive cancers occurred. Results
included the following:
• Increased alcohol consumption was associated with
increased risk of cancers of the oral cavity and pharynx
(increase in RR per 10 g daily increase in alcohol intake,
29%), esophagus (22%), larynx (44%), rectum
(10%), liver (24%), breast (12%), and total cancer (6%).
• For cancers of the upper aerodigestive tract, alcoholassociated
risk was confined to current smokers, with
little or no effect among never or past smokers.
• Increased alcohol consumption was associated with a
decreased risk of thyroid cancer, non-Hodgkin lymphoma,
and renal cell carcinoma.
• Trends were similar in women who drank wine exclusively
compared with consumers of other types of alcohol.
• For every additional drink regularly consumed per day,
the increase in incidence up to age 75 years per 1000

women in developed countries was estimated to be
about 11 for breast cancer; 1 for cancers of the oral
cavity and pharynx; 1 for cancer of the rectum; and 0.7
each for cancers of the esophagus, larynx, and liver.
Comments: The results of this study support what has been
known for many decades: there is an association between
alcohol intake, especially heavy intake, and upper aerodigestive
cancers. Further, even moderate drinking may increase
the risk of other cancers, including breast cancer.
There are, however, a number of analytic problems with
this paper: the authors were unable to compare results of
current drinkers with lifetime abstainers and ex-drinkers
separately; no data were provided on pattern of drinking
(regular or binge); and only linear analysis was used, making
it difficult to judge if the association between alcohol
and these cancers was U-shaped, J-shaped, or showed a
threshold effect. While it is important to emphasize that
alcohol can be associated with cancer, it will be especially
important for additional studies based on this large cohort
to report the net effects of drinking on other diseases and
on total mortality.

Source: Allen NE, Beral V, Casabonne D, et al. Moderate
alcohol intake and cancer incidence in women. J Natl Cancer
Inst. 2009;101(5):296–305.

Research Summary
Drivers ages 21 to 34 comprise a disproportionate share of fatal motor vehicle crashes in which at least one of the drivers was legally intoxicated (had a BAC of .08 or greater), according to data from the National Highway Traffic Safety Administration (NHTSA).
Although drivers ages 21 to 34 were involved in 31% of all fatal crashes in 2006, they were involved in 43% of all fatal crashes in which at least one driver was intoxicated.
On the other hand, drivers ages 45 or older were involved in 36% of all fatal crashes, but just 23% of drunk-driving fatal crashes.
These findings suggest that prevention efforts may be most effective if they focus on educating young adult drivers about the dangers of driving while intoxicated.
Source: , from The Center on Substance Abuse Research (CESAR) at the University of Maryland. October 1, 2007

Research Summary
Researchers at Heidelberg University in Germany have found that it takes only six minutes for a change in brain cells to occur after drinking the equivalent of about three glasses of beer or two glasses of wine, Science Daily reported June 15.
Researchers gave 15 healthy subjects (eight male and seven female) enough alcohol to produce a blood alcohol level of 0.05 to 0.06 percent — sufficient to impair driving but not severe intoxication.
Using magnetic resonance spectroscopy (MRS), the researchers found that the concentration of creatine, a substance that protects brain cells, decreased as the amount of alcohol increased. Chloine, a component of cell membranes, was also reduced. Lead author Armin Biller of Heidelberg’s Department of Neuroradiology said that the reduction in chloine probably indicated that alcohol triggered changes in the composition of cell membranes.
The researchers also found that the day after the subjects had consumed alcohol, their brain metabolism had reverted to what it had been prior to the experiment. However, Armin warned that, “The brain’s ability to recover from the effect of alcohol decreases or is eliminated as the consumption of alcohol increases. The acute effects demonstrated in our study could possibly form the basis for the permanent brain damage that is known to occur in alcoholics. This should be clarified in future studies.”
The study found no differences between male and female subjects, suggesting that the brains of female and male subjects reacted to alcohol consumption the same way.
Source: Journal of Cerebral Blood Flow & Metabolism. June 22, 2009

30 June 2009 – Injecting drug use is responsible for an increasing proportion of HIV infections in many parts of the world. It is estimated in the World Drug Report 2009 that between 11 and 21 million people worldwide inject drugs, and of those, between 0.8 and 6.6 million are infected with HIV.
Brazil, China, the Russian Federation and the United States of America are estimated to have the largest populations of injecting drug users (IDUs), and together account for 45 per cent of the estimated total worldwide population of IDUs. In addition, injecting drug use appears to be an emerging phenomenon in many countries where it had not been reported previously. By 2008, injecting drug use had been reported in 148 countries and territories together accounting for 95 per cent of the world’s population.
HIV infection among people who inject drugs has been reported in 120 countries, and the prevalence of HIV among IDUs varies dramatically. Regions with the largest numbers and highest concentrations of HIV-positive IDUs include Eastern Europe, East and South-East Asia and Latin America. In those regions, the prevalence of HIV is higher than 40 per cent among many national and subnational injecting drug user populations.
Except for sub-Saharan Africa, IDUs account for a sizeable proportion of the total number of people living with HIV. In Eastern Europe and Central Asia, more than half of those living with HIV are IDUs.
The dynamics of the spread of HIV infection are notable. A decade ago, HIV had not been detected among IDUs in Estonia. By contrast, a more recent estimate now suggests that the prevalence of HIV infection in that country has, in one sample, increased to 72 per cent of IDUs. Yet in Australia and New Zealand, levels of HIV infection have remained very low (1.09 and 0.73 per cent, respectively), despite the fact that the prevalence of injecting drug use is higher there than in some other countries.
This difference has been attributed to the geographic isolation of those two countries, as well as to their swift introduction of needle and syringe programmes and the expansion of opiate substitution treatment programmes after HIV infection was first documented in 1984.
The increase in the spread of HIV among IDUs calls for investment in comprehensive public health interventions.
UNODC is helping countries to review and develop laws, policies and standards of care that enable them to put in place effective services for IDUs. It also encourages greater proactive involvement of law enforcement agencies in HIV prevention and care and promotes collaboration among the health and criminal justice sectors and community-based and civil society organizations.
In addition, UNODC helps countries to expand evidence-informed drug dependence treatment services, particularly opioid maintenance therapy for IDUs, and to raise awareness among drug dependence treatment services regarding the need to address HIV prevention and care issues and to develop interventions to prevent the transition from non-injecting drug use to injecting drug use.
UNODC promotes services such as voluntary and confidential HIV counselling and testing, the treatment of sexually transmitted infections, the provision of antiretroviral therapy and interventions for specific sub-groups, including prisoners, sex workers who inject drugs and IDUs who may exchange sex for drugs or money.
Source eNews@UNODC July 2009

All other things being equal, adolescents and young adults who smoked marijuana more
than 50 times at the first contact were six times more likely to become heavy cocaine
users than those who did not smoke marijuana. This finding supports the suggestion that
preventing adolescents and young adults from using substantial amounts of marijuana
may lead to a considerable decrease in the number of future heavy cocaine users.

Source: Office of National Drug Control Policy Washington, DC February 2004

Studies of these three “gateway drugs”—alcohol, tobacco, and marijuana—show that adolescents who use one or more of these are at greater risk to go on to use cocaine or heroin.

Regular or heavy use of cannabis was associated with increased risk of using other illicit drugs”
Addiction 2006, 101: 556-569

25-year longitudinal study affirms link between marijuana use and other illicit drug use”
Congress of the United States, 14 March 2006

Risk of using cocaine has been estimated to be more than 104 times greater for those who have used marijuana than for those who have never tried it.
Source: www.cocineabuse.net

A new federal report concludes the younger children are when they first use marijuana, the more likely they are to use cocaine and heroin and become dependent on drugs as adults.
The report, “Initiation of Marijuana Use: Trends, Patterns and Implications,” found that 62% of adults age 26 or older who initiated marijuana before they were 15 years old reported that they had used cocaine in their lifetime. More than 9% reported they had used heroin and 53.9% reported nonmedical use of psychotherapeutics.
Source www.highbeam.com Sept 2002
Long-term studies of high school students and their patterns of drug use show that very few young people use r drugs without first trying marijuana. The risk of using cocaine has been estimated to be more than 104
“It appears that the biochemical changes induced by marijuana in the brain results in a drug-seeking, drug taking behavior, which in many instances will lead the user to experiment with other pleasurable substances. The risk of progressing from marijuana to cocaine or heroin is now well documented.
“Marijuana users are sixty-six times more likely to use cocaine subsequently than subjects who have never consumed marijuana. This 1990 survey of PRIDE documents further the fact that marijuana is a “gateway” drug to more destructive dependency-producing drugs such as heroin or cocaine. Such a most significant risk of escalating from marijuana to cocaine was reported by Kandel and colleagues in 1975 (Science 190 (1975): 912). Clayton and Voss (U.S. Journal of Drug and Alcohol Dependence, Jan. 1982) confirmed Kandel’s observation and reported that the risk for a marijuana user to progress to cocaine consumption is ten times greater than the risk of a heavy tobacco smoker to develop cancer of the lung. Dr. Herbert Kleber (Journal of Clinical Psychiatry, 1988, 48:3) reports that 75% of frequent users of marijuana have used cocaine at least once. It is a fact that the major epidemic of cocaine consumption besetting the country since the mid-eighties was preceded by the marijuana epidemic of the seventies.”
Gabriel Nahas in the preface to 1990′s 5th edition of Keep Off the Grass :

heavy cannabis use by adolescents predicts an increased risk of harder drug use (MacCoun,1997).
Source The FAS Drug Policy Analysis Bulletin Issue Number Seven June 1999

Thousands of middle-aged professionals who experimented with drugs during their student days will be warned in a major government health campaign this autumn that they may be infected with hepatitis C.

It is thought that up to 400,000 British people may be carrying the potentially fatal virus without knowing it, because there is such a long delay between infection and symptoms appearing.

Ministers have decided to go ahead with a national public awareness campaign in September, warning that anyone who has ever injected drugs, particularly sharing a needle, used straws to sniff cocaine or had a blood transfusion before 1991, is at risk and should consider having a blood test. However, they are worried about causing mass panic and want to adopt a ‘softly-softly’ approach by focusing on the treatment available for the disease, rather than its potential consequences.

The co-ordinators are hoping to find a celebrity who has been infected with the virus to spearhead the campaign, but so far those approached have declined publicity, such is the embarrassment associated with the condition. The general public view about hepatitis C is that only hardened drug addicts are at risk, but increasingly doctors are seeing patients who have been infected after just one or two injections.

The virus is passed on through blood-to-blood contact, and those at risk also include people who had a blood transfusion before blood screening was brought in 13 years ago. Sexual transmission, tattooing and piercing are the other possible methods of transmission.

At present only 2,000 people a year are treated for hepatitis C on the NHS, but estimates of the numbers infected in the UK vary from around 0.4 per cent of the population, some 240,000, to 1 per cent, some 600,000.

It is potentially fatal, but effective new antiviral drugs can cure between 50 to 80 per cent of sufferers who have a chronic form of the disease. Of those who carry hepatitis C, about 80 per cent go on to develop a chronic infection in the liver, and about one-fifth of these will develop serious liver disease.

However, many people do not know they are carriers until they have serious symptoms such as severe liver pain. Many of those at risk will be people who experimented with drugs in their youth. Charles Gore, chief executive of the Hepatitis C Trust, said: ‘How do you reach the man on the street, who might have had a blood transfusion 20 years ago, or who might have injected drugs in his youth. and warn him that he could be wandering around with this virus?’

People can have the disease for 20 years or more before they develop symptoms, which means those who experimented at college might not realise the risks.

‘Typically, it might be someone who didn’t know how to inject drugs into the vein and who borrowed a syringe from someone who was more experienced. The virus can then be passed directly into the bloodstream.’

Gore added: ‘Between 1975 and 1985, in particular, there was a huge experimentation with drugs. It was before the Aids crisis, no one was aware of the dangers of blood-borne viruses, and many more were injecting than was commonly supposed.’

Gore, who backs the government’s efforts, says that Britain is far behind other European countries in identifying patients. ‘It is hard to get people to admit that they might be at risk. It involves them owning up to their past.’

The chair of the Department of Health’s advisory group on hepatitis, Professor Howard Thomas, re-iterated the warning that patients don’t have to be drug addicts to be at risk. ‘Many of those infected will be people in influential positions who dabbled with drugs years ago while at college,’ he told the Health Service Journal last week. While admitting there is more to be done in making GPs aware of the disease, he said that they have now taken the first steps in setting up a national system of clinical centres for hepatology, or liver disease.

The first signs of the disease are not easy to spot. They commonly include fatigue and aching joints, which are fairly usual for people in their middle age. Patients also experience differing degrees of pain. Some have a mild form of the virus and are in acute pain, others have serious liver damage before they realise anything is wrong.

Ministers, highly aware of how the HIV campaign in the Eighties scared a generation of people, want to take a more ‘softly-softly’ approach. They started last week by sending out an action plan to all GPs and health professionals.

A spokeswoman for the Department of Health would say little about the campaign, other than to state that an outside consultancy firm had been brought in to work on strategy. ‘We will have a public awareness campaign, but in order not to get people panicked, you have to do it in stages, so the first stage is to make the professionals aware of the potential problems.’

  For more information, call the Hepatitis C Trust’s helpline on 0870 200 1200.

A new survey reveals that one in five mothers smoke while pregnant. The habit causes low birth-weight babies with dramatically increased chances of mental impairment, disability and sudden death as infants. Baby health charity Tommy’s conducted the poll.

Smoking is also linked to ectopic pregnancy.

New research from Sweden has shown that smokers puff clouds of poison in to the air which can seriously affect the breathing around them. The discovery has prompted ASH to urge the government to ban indoor smoking in workplaces. Swedish scientists found that endotoxins, which are made by bacteria and occur naturally in the air, are produced by tobacco smoke in high concentrations. Tobacco is known to contain over 4,000 chemicals, including 50 substances known to cause cancer. Low concentrations of endotoxins are not harmful and may even play a role in protecting people against allergies. However, in high concentrations, endotoxins can cause serious inflammatory reactions in the respiratory tract, leading to bronchitis and asthma. The researchers also concluded that tobacco endotoxins appeared to be the most aggressive among the various types that exist. ASH spokeswoman Amanda Sandford noted that the research could lead to a greater understanding of how tobacco smoke can trigger respiratory diseases such as asthma: “There are lots of sources of pollution we don’t have much control over, but we can control tobacco smoke in enclosed areas,” she said. She added that the study reinforced the need for a ban on smoking ban on indoor places.

Source: Morning Star, Times, 23 August, 2004

Dr. Richard Garey of Tulane University  theorized that the very strong pot people smoke today is causing common reactions nowdays that were rarely seen back in the 60s and 70s when pot was only about one tenth as powerful as it is now. He spoke of how THC stimulates the pleasure centers located in the midbrain. But also located in the midbrain are the violence and unpleasant emotion centers. The stronger pot evidentally causes neural firing (or misfiring) that lights up not only the pleasure centers but nearby violence centers. The MJ user damages feeder cells by thickening the myelin sheaths of those neurons (because THC is fat soluble and myelin sheaths are fatty) and causing fatty blockages in the synaptic gaps. That causes reduced ability to receive any natural highs, makes one emotionally flat and explains in part the amotivational syndrome. One could theorize that huge amounts of THC would be needed to stimulate any pleasure in the advanced user and adjoining areas would get lit up so to speak. Violence could actually trigger a strong response in the pleasure center by stimulating intense neural activity in the midbrain…activity no longer provided by natural highs thanks to damage by marijuana.

It has been known for more than two decades that many illicit drugs inflict damage on the immune system leaving the body open to a host of opportunistic infections, not the least of which is the HIV virus. Other drugs accelerate the progression of HIV to full blown AIDS. A study published in the American Journal of Public Health 87:585-590, noted that the risk of AIDS mortality in marijuana users versus non-users was approximately doubled, though the authors insisted this phenomenon was related more to male homosexuality behaviour than to smoking marijuana, a drug known to undermine the immune system.

A new study presents the highest risk for dependence on alcohol is about age 20-21 years but that for marijuana it is about 17 years. The peak for cocaine dependence was seen to occur at about age 24-26 years and was estimated to be between 18.4-24.5%. Additionally, the authors noted that 5-6% of cocaine users become dependent in the first year of use and 15- 16% had become dependent within 10 years of first use, For those who use marijuana at least once, the probably of becoming dependent was 9% by age 30 though most cases of dependence occurred when users were 15-25 years old. For those who used alcohol at least once, the “estimated cumulative probability of alcohol dependence by age 55 was about 20%… Most cases met that criteria, however, between the ages of 15 and 35 years.”

For recovering alcoholics and ex-smokers, as well as former users of illicit drugs, the mundane trappings of their addictions—ice cubes, ashtrays, straws, needles—exert a strong, long-lasting power to trigger relapse. A new University of Michigan study, published in the current (October 2001) issue of the Journal of Neuroscience, provides experimental evidence supporting a neurological explanation for why cues as innocent as the sound of ice cubes tinkling in a glass can cause “recovered” addicts to experience dangerous drug cravings. “Drug use is known to sensitize’ certain neural systems within the brain, causing changes that are relatively permanent,” says U-M psychologist Kent C. Berridge, co-author of the study with U-M psychologist Cindy L. Wyvell. “This study shows that the brain is vulnerable to cues that trigger irrational ‘wanting,’ even after a long period of remaining drug-free, once sensitized by prior drug use or exposure.” The research was supported by the National Science Foundation and by the National Institute on Drug Abuse.
For the study, Wyvell and Berridge designed an experiment with rats that eliminated several alternative explanations, such as withdrawal symptoms, learned habits or drug pleasure, for the increase in compulsive drug-seeking that is commonly triggered in human addicts by encounters with drug cues.

First, in order to avoid withdrawal symptoms, they trained the rats to press a lever to get a reward of sugar pellets, not an addictive drug. They also taught the rats to associate a 30-second tone with getting sugar pellets, without needing to press the lever. Then they sensitized one group of rats by administering a series of amphetamine injections, while injecting controls with a saline solution. Next, the researchers waited 10 to 14 days to make sure both groups were drug-free, then resumed the experiment. While the rats pressed the lever in hope of getting the sugar reward, they were presented intermittently with the sound cue, to assess the cue’s ability to trigger excessive pursuit of reward.

In the sensitized rats, the cue triggered excessive wanting,” says Berridge. “Whenever a sugar cue (a sound) occurred, rats pressed in a frenzy on a lever that had previously earned them a sugar reward.” In fact, the researchers found that sensitized rats pressed the lever 200 percent more than rats in the control group, an increase equivalent to the behaviour produced in other rats by injecting amphetamine directly into their brains. This showed that sensitization of the brain and direct drug activation of the brain’s dopamine reward-craving system amplified equally the ability of reward cues to trigger excessive ‘wanting.” “Much more remains to be done before we understand how this process works in humans, with drug rewards such as cocaine and heroin, and to a lesser extent, alcohol or nicotine,” says Berridge. ‘But this study is an important step, because it provides the first pure demonstration that neural sensitization causes a specific process— irrational cue-triggered ‘wanting’ for reward—that is a plausible psychological mechanism for relapse. These results from animals based on a natural sugar reward this may be a useful step toward understanding brain mechanisms of cue-triggered relapse in human drug addiction”

When confronted with evidence of how their behaviour is harming their bodies, some people will adopt healthier attitudes and lifestyles, according to a review of existing research. Modifiable behaviours, such as smoking, obesity, alcohol and lack of exercise are responsible for nearly half of the leading causes of American deaths, according to the review, published in the April issue of the American Journal of Preventive Medicine. “Increasing awareness that one has some personal risk of harm, or has already caused physical harm through unhealthy habits, may increase motivation for health behaviour change. Studies that assess the use of biological indicators of health status, referred to as biomarkers, to motivate people to take better care of themselves have produced mixed results, but when analyzed together a pattern emerges, McClure says.

In her analysis of eight randomized studies, those studies that did not show a significant effect on motivation or behaviour change used a single health indicator, tested on one occasion. In contrast, studies that showed positive results used a single indicator assessed at multiple visits or multiple indicators assessed at a single visit. For example, in one study, patients informed of their carbon monoxide levels (resulting from smoking) and genetic susceptibility for lung cancer were twice as likely to attempt to quit smoking compared with similar subjects who were not provided feedback on their personal disease risk. The health indicators reviewed include cholesterol level, carbon monoxide level, lung cancer susceptibility genes, depressed breathing function and other pulmonary symptoms and physical fitness. The studies explored the effects of health indicators on tobacco use, dietary change and physical activity. The number of participants in each study varied from 90 to more than 2,000. “The prevalence of behaviour-related disease in our society makes it critical
that we continue to improve our ability to promote more healthful behaviour. To be effective, this work should be based on empirically validated techniques, says Mcclure. Although the results of this work suggest that health indicators that convey quantitative information about harm exposure, disease risk or impaired physical functioning may increase motivation to engage in more healthful behaviors, appropriate treatment may be necessary for lasting behaviour change. However, conclusions are limited by the dearth of randomized studies on this subject. This field of research has also so far not explored the potential psychological damage that could result from telling people they have done harm to themselves, she says.

 Memory tests and brain scans performed on 22 subjects who had recently used Ecstasy revealed they suffered memory deficiencies and changes in certain brain cells. The scans showed the damage was most pronounced on cortical neurons linked to memory function. In Ecstasy users, those brain cells had a decreased density of receptors for the neurotransmitter serotonin, which transports messages between cells and is known to affect mood. Previous research has suggested that Ecstasy causes a flood of serotonin in the brain, followed by a drop-off when the drug wears off. Brain scans performed on 16 former Ecstasy users who had abstained from the drug for at least a year did not show lasting damage to the serotonin receptors in cortical neurons. But former users did not perform as well on memory tests as 13 control subjects who had never used the drug. While the neurons of former users seemed to recover, the consequences on memory from the earlier Ecstasy use may be irreversible, said study author Liesbeth Reneman of the Academic Medical Center in Amsterdam. The longer that Ecstasy was used and the higher the dosages, the worse the memory impairment, the study found.

“We identified that MDMA [Ecstasy] use is associated not only with short-term consequences [on memory] but with long-term consequences as well,” Reneman wrote in the October issue of the medical journal Archives of General Psychiatry. Study participants, who ranged in age from 18 to 45, agreed not to use psychoactive drugs for three  weeks before the testing. The study noted that Ecstasy users were more likely to smoke marijuana than the control group, which might have influenced the memory test results. Previous research has shown Ecstasy, sometimes known as MDMA or by its chemical name 3,4-methylenedioxymetharrphetamine, can cause dramatic changes in heart rate and blood pressure. It can also lead to dehydration and has been shown to cause lasting changes in the brain’s chemical systems that control mood and memory. Animal studies have shown damage to brain cells connected to memory function.

Ecstasy Use During Pregnancy Can Cause Memory Damage

New research indicates that use of the drug ecstasy during pregnancy can cause long-term learning and memory problems in children, the Associated Press reported April 30.  A research team led by Charles V. Vorhees of  Children’s Hospital Research Foundation and the University of Cincinnati College of Medicine in Cincinnati, Ohio, found that rats given ecstasy on days 11-20 of their life suffered from impaired learning and memory in maze tests. During the first 11 to 20 days, a rat’s still developing brain is used to approximate exposing a woman to the drug in her third trimester of pregnancy. The researchers found that the damage suffered early in life continued when the rats
reached adulthood. “These findings suggest that ecstasy may pose a previously unrecognized risk to the developing brain,”said Vorhees.

I entirely support the conclusion of Dr. William Bennett, co-chair of DWI, concerning the acute and chronic irreversible damaging effects of ‘Ecstasy’ (3-4 methylenedoxyrnethamphetamine ) its methylated derivatives. These effects have been reported for the past 15 years in dozens of articles published in the biomedical specialized literature (Pharmacology, Toxicology, Pathology) MDMA is a neurotoxic substance associated with acute and chronic brain damage and cardiovascular toxicity,- along with impairment of reproductive function and fetal development (see Ellenhorn, Medical Toxicology, Elsevier 1995).

MDMA is a ring substituted amphetamine derivative chemically related to both hallucinogens and stimulants.

Marked tolerance occurs with an increase to 10 times the initial dose. After one ingestion, the main complications reported are hallucinations, paranoia, insomnia, tachycardia, muscle rigidity (trismus) which resolves within 48 hours. Regular users present weight loss, exhaustion, jaundice, paranoia, damage to hepatic function and spontaneous intracranial hemorrhage. Signs can develop several hours after ecstasy ingestion. These complications occur unpredictably and require immediate action with a treatment similar to that used by anesthetist to treat severe hyperthermia (dantrolene) No pharmaceutical company has ever made MDMA nor has the FDA given its approval. In 1985 the DEA classified MDMA as a Schedule I compound with a high potential of abuse and without any current medical use.
Effects of MDMA on brain and behaviour are mediated by its effect on serotoninergic nerve terminals and impairment of turnover of this neuromediator. Intrauterine growth abnormalities, complications of pregnancy and delivery including maternal death, and neurophysiologic and neurobehavioral abnormalities in neonates have been described with antenatal methamphetamine drug exposure. Intrauterine death has followed an intravenous injection of amphetamine.
Methamphetamine studies in pregnancy describe an increased incidence of intrauterine growth retardation, prematurity and perinatal complications. Body weight, length, and head circumference changes in the infant are described. At birth, withdrawal symptoms may include abnormal sleep patterns, tremors, hypertonicity, a high—pitched cry, poor feeding patterns, sneezing, and frantic sucking. During the first year, the infant may exhibit lethargy, poor feeding, poor alertness, and severe lassitude.

More evidence has emerged that long-term users of the drug Ecstasy may have permanent changes in the way their brains work. In particular, using the drug may be killing cells which produce a vital mood chemical called seratonin. But it is not yet confirmed whether the loss of these cells has an adverse effect on brain health. The latest clues come from an autopsy of a 26-year-old Canadian – a long-term heavy user of Ecstasy – who died of an overdose of a different drug. When his brain was tested, it was found to have between 5O°/o and 80% less serotonin than the brain of other patients.
While the researchers, from the Centre for Addiction and Mental Health in Toronto, concede it is difficult to draw conclusions from a single case, they say the finding is significant.
Dr Stephen Kish said: “ This is the first study to show that this drug can deplete the level of serotonin in humans.” Seratonin is a neurotransmitter chemical, released by nerve cells in the brain, which controls mood, pain perception, sleep, appetite and emotion. A massive release of seratonin stimulated by Ecstasy is widely thought to be the principal mechanism of the drug.

Ecstasy hangover

Additionally, the “Ecstasy hangover” – feelings of excessive tiredness and irritability, alongside an inability to think clearly – is thought to be caused by an over-depletion of the chemical as the drug ceases to have an effect. The man whose brain was the subject of the study started using Ecstasy once a month at the age of 17. In the last few years of his life, he used it four or five nights a week at nightclubs, usually including a three-day weekend “binge” during which he took six to eight tablets. It is still uncertain whether a low level of serotonin in those who take Ecstasy is due to the action of the drug, or whether naturally occurring deficits in the chemical make you more likely to take it. Studies on animals given the drug suggest the former is more likely. Dr Philip Robson, a senior research fellow in psychiatry at Oxford University, said: ‘We simply don’t know what the long term effects of losing these nerve cells is.”

Addiction specialists have determined that people who use cocaine get sick more often because the drug hampers production of a body protein that triggers  immune responses.

For the study, researchers at McLean Hospital and  Harvard Medical School injected cocaine in the arm of  participants who said they used the drug in the previous month. Another group was injected with a placebo. In the other arm, a catheter was placed in all participants. Generally, the presence of a foreign device, such as a catheter, increases the level of interleukin-6, a protein that tells the immune system to fend off the invader. In the group receiving the placebo injection, the protein performed normally.. But among participants receiving cocaine, the interleukin-6 level increased only one-third as much as the placebo group after four hours.
Dr. John Halpern, a training doctor in a drug-detoxification unit, said the results help to explain why ‘a every single person coming in had a cold.” The study is published in the March 2003 issue of the Journal of Clinical Endocrinology and Metabolism.

RAC Foundation research suggests that drug—driving is now a bigger problem than drink-driving among 17—24 years olds. Edmund King of the RAC Foundation said: “We hear that more people smoke cannabis as a recreational drug. The danger now is that mixing that with alcohol could produce a deadly cocktail that motorists may not be aware of. Cannabis may make people feel more laid back but combined with alcohol gives them the impetus to drive. They may think they are not over the limit  and in fact could be under the drink-drive limit,  but still be more dangerous.”

Objective: To determine whether cannabis use in adolescence predisposes to higher rates of depression and anxiety in young adulthood.

Design: Seven wave cohort study over six years.

Setting: 44 schools in the Australian state of Victoria
.
Participants: A state wide secondary school sample of 1601 students aged 14-15 followed for seven years.

Main outcome measure: Interview measure of depression and anxiety (revised clinical interview schedule) at wave 7.

Results: Some 60% of participants had used cannabis by the age of 20; 7% were daily users at that point. Daily use in young women was associated with an over fivefold increase in the odds of reporting a state of depression and anxiety after adjustment for intercurrent use of other substances (odds ratio 5.6, 95% confidence interval 2.6 to 12). Weekly or more frequent cannabis use in teenagers predicted an approximately twofold increase in risk for later depression and anxiety (1.9, 1.1 to 3.3) after adjustment for potential baseline confounders. In contrast, depression and anxiety in teenagers predicted neither later weekly nor daily cannabis use.
Conclusions: Frequent cannabis use in teenage girls predicts later depression and anxiety, with daily users carrying the highest risk. Given recent increasing levels of cannabis use, measures to reduce frequent and heavy recreational use seem warranted.

The BMA has called on the UK government to develop a campaign to highlight that taking drugs—whether prescribed, over the counter, or illegal—can impair driving capacity in a similar way to alcohol.
The BMA has recommended that the government should coordinate scientific research to establish effective drug testing devices and should educate the public on the association between taking some drugs and impaired driving ability.
To help publicise the problem, the BMA has developed a website www.bma.org.uk that reviews trends in road traffic fatalities and injuries, as well as research on drugs and driving performance. The website highlights research from the Transport Research Laboratory showing that the number of people involved in fatal collisions who tested positive for illegal drugs increased sixfold between the periods 1985-87 and 1996-99

While researching information about ecstasy on the Scientific American website, this article from its December 2000 issue was noted.  The use of the word “Firmly” is the journal’s choice, giving an indication of how strongly they feel the link of marijuana use to infertility really is.  Perhaps this explains the escalating business in infertility clinics in the past 20 years – the results of baby boomers indulging in cannabis in the 1960s and 70s.”

Scientists from the University of Buffalo have smoked out what may cause some cases of infertility: marijuana. Today at the annual meeting of the American Society for Cell Biology, Herbert Schuel and his colleagues describe a cellular signaling system that responds to THC–the active substance in marijuana–and that may regulate sperm functions necessary for normal egg fertilization. The signalling system may be activated by anandamide, a cannabinoid-like molecule which this study shows for the first time is found in human seminal plasma, mid-cycle oviductal fluid and follicular fluid.

“These findings suggest that defects in the cannabinoid receptor-signalling system could account for certain types of infertility,” Schuel says. “A better understanding of these mechanisms might lead to the development of novel drugs useful in reproductive medicine. For heavy marijuana users, the study results raise the possibility they are jeopardizing fertility by overloading this system.” To be sure, the process by which sperm prepare to fertilize an egg in the female reproductive tract is still mysterious. They must first become “capacitated” before they can begin swimming vigorously towards an egg and secrete the enzymes necessary to penetrate the egg’s protective coat, a process called the acrosome reaction. But Schuel’s work shows that both AM-356–a synthetic version of natural anandamide–and THC affect this sequence of events in three distinct ways: first, although low amounts of AM-356 stimulate sperm to swim more vigorously, too much of it has the exact opposite effect. Both AM-356 and TCH inhibit structural changes over the acrosome. And AM-356 significantly impairs sperm from binding to an egg’s protective coat.

“The increased load of cannabinoids in people who abuse marijuana could flood natural endocannabinoid-signal systems in reproductive organs and adversely impact fertility,” Schuel adds. “This possibility may explain observations made over the past 30 to 40 years that marijuana smoke drastically reduces sperm production in males.” –Kristin Leutwyler

Men who smoke marijuana frequently have significantly less seminal fluid, a lower total sperm count and their sperm behave abnormally, all of which may affect fertility adversely, a new study in reproductive physiology at the University at Buffalo has shown.
This study is the first to assess marijuana’s effects on specific swimming behavior of sperm from marijuana smokers and to compare the results with sperm from men with confirmed fertility. Marijuana contains the cannabinoid drug THC (tetrahydrocannabinol), which is its primary psychoactive chemical, as well as other cannabinoids.

Results of the study were presented today (Oct. 13, 2003) at the annual meeting of the American Society of Reproductive Medicine in San Antonio. “The bottom line is, the active ingredients in marijuana are doing something to sperm, and the numbers are in the direction toward infertility,” said Lani J. Burkman, Ph.D., lead author on the study.
Burkman is assistant professor of gynecology/obstetrics and urology and head of the Section on Andrology in the UB School of Medicine and Biomedical Sciences.
UB’s andrology laboratory also carries out sophisticated diagnosis for infertile couples. “We don’t know exactly what is happening to change sperm functioning,” said Burkman, “but we think it is one of two things: THC may be causing improper timing of sperm function by direct stimulation, or it may be bypassing natural inhibition mechanisms. Whatever the cause, the sperm are swimming too fast too early.” This aberrant pattern has been connected to infertility in other studies, she noted.
Burkman collaborated on earlier, published UB research that was the first to show that human sperm contains cannabinoid receptors, and that the naturally occurring cannabinoid, anandamide, which activates cannabinoid receptors in the brain and other organs, also activates receptors in sperm. This evidence indicated an important role in reproduction for natural cannabinoids. Further research in the andrology laboratory showed that human sperm exposed to high levels of THC displayed abnormal changes in the sperm enzyme cap, called the acrosome. When researchers tested synthetic anandamide equivalents on human sperm, the normal vigorous swimming patterns were changed and the sperm showed reduced ability to attach to the egg before fertilization. Only about 10 laboratories in the U.S. perform this array of sperm function tests. In the current study, Burkman received seminal fluid from 22 confirmed marijuana smokers and subjected the samples to a variety of tests. The volunteers reported smoking marijuana approximately 14 times a week, and for an average of 5.1 years. Control numbers were obtained from 59 fertile men who had produced a pregnancy. All men abstained from sexual activity for two days before the lab analysis. The samples from both groups were tested for volume, sperm-count-per-unit of seminal fluid, total sperm count, percent of sperm that was moving, velocity and sperm shape. Sperm also were assessed for an important function called hyperactivation (HA), a closely regulated and very vigorous type of swimming that is required as the sperm approaches the egg.

The researchers evaluated HA and velocity while the sperm was in seminal fluid and again after washing and incubation, when the dead sperm were eliminated. Results showed that both the volume of seminal fluid and the total number of sperm from marijuana smokers were significantly less than for fertile control men. Significant differences also appeared when HA and velocity, both before and after washing, were assessed, the study found.

“The sperm from marijuana smokers were moving too fast too early,” said Burkman. “The timing was all wrong. These sperm will experience burnout before they reach the egg and would not be capable of fertilization.”

Burkman noted that many men who smoke marijuana have fathered children. “The men who are most affected likely have naturally occurring borderline fertility potential, and THC from marijuana may push them over the edge into infertility,” she said. As to the question of whether fertility potential returns when smokers stop using marijuana: Burkman said the issue hasn’t been studied well enough to provide a definitive answer.

“THC remains stored in fat for a long period, so the process may be quite slow. We can’t say that everything will go back to normal. Most men who have borderline fertility are unaware of that fact. It’s difficult to know who is at risk. I definitely would advise anyone trying to conceive not to smoke marijuana, and that would include women as well as men.”
Additional scientists on the study included Herbert Schuel, Ph.D., UB professor of pathology and anatomical sciences, and the staff of the andrology laboratory.

Cardiovascular complications of recreational drugs are an important cause of morbidity and mortality.
The consumption of recreational drugs has reached epidemic proportions. Forty five million European Union citizens have used cannabis at some time, with proportionately higher use among younger people. The consumption of harder drugs such as cocaine and heroin is rising, with an estimated 1.5 million problem users in the European Union. Drug use is commonly associated with complications, including an increased risk of premature death. In particular,recreational drugs have profound effects on cardiovascular function. Some studies suggest that adverse cardiac events are relatively uncommon, though recent data from the United States indicate that one in four myocardial infarcts in people aged 18-45 years can be linked to cocaine use,suggesting that variation in definitions may contribute to under-reporting. Many physicians will encounter patients with cardiovascular problems related to recreational drug misuse. In addition to the problems posed by self administration, massive overdoses may occur in individuals who attempt to smuggle illegal drugs by ingesting packets which rupture in the gastrointestinal tract; and inadvertent ingestion of recreational drugs by children has been reported. Successful management can be difficult, since many patients will be unwilling or unable to provide an accurate history. An awareness of the pathophysiological effects of these compounds is therefore an important aid to diagnosis.
Cocaine, ecstasy, and amphetamine share similar adverse effects on the cardiovascular system,related predominantly to activation of the sympathetic nervous system. Cocaine acts by inhibiting norepinephrine reuptake in peripheral sympathetic nerve terminals as well as stimulating central sympathetic outflow. Circulating catecholamine concentrations can be raised as much as fivefold.Amphetamine and its derivative ecstasy produce indirect sympathetic activation by releasing norepinephrine, dopamine, and serotonin from central and peripheral autonomic nervous system terminals, and serious cardiovascular complications have been well documented. Sympathetic activation can lead to varying degrees of tachycardia, vasoconstriction, and unpredictable blood pressure effects, depending on the dose taken and the occurrence of coexisting cardiovascular disease. Hypotension as a result of a relative catecholamine depletion state, paradoxical suppression of the central nervous system (amphetamine), or acute myocardial depression (due to ischaemia or a direct toxic effect of the drug) can occur. Myocardial ischaemia and infarction may be related to the raised catecholamine concentration causing an increase in oxygen demand, coronary artery spasm, platelet aggregation, and thrombus formation. Repetitive episodes of coronary artery spasm and paroxysms of hypertension may result in endothelial damage,coronary artery dissection, and acceleration of atherosclerosis. Paroxysmal increases in blood pressure can lead to aortic dissection or valvular damage, which increases the risk of endocarditis.Cocaine and amphetamine have been associated with non-cardiogenic pulmonary oedema and a dilated cardiomyopathy. The adverse cardiovascular changes and sympathetic stimulation associated with these agents predispose to myocardial electrical instability and a wide range of tachyarrhythmias. The class 1 antiarrhythmic properties of cocaine can impair cardiac conduction,precipitating conduction defects and bradyarrhythmias, including sinus arrest and atrioventricular block.

The mechanisms of action of the hallucinogens lysergic acid (LSD) and psilocybin (magic mushrooms) are complex, with various effects on serotonergic, dopaminergic, and adrenergic receptors. These drugs have mild adrenergic effects, producing manifestations of sympathetic arousal such as dilated pupils, sinus tachycardia, hypertension, and hyper-reflexia. Cardiovascular complications are rarely serious, although the potential for arrhythmias and myocardial infarction exist.

Morphine and its semisynthetic analogue heroin are the most commonly misused narcotic analgesics,accounting for almost half of drug related deaths.   They act centrally to increase parasympathetic and reduce sympathetic activity, resulting in bradycardia and hypotension. Various bradyarrhythmias and tachyarrhythmias have been reported. Bacterial endocarditis, affecting mainly right sided cardiac structures, is a well known complication of intravenous narcotic misuse. Non cardiogenic pulmonary oedema (which may not develop until 24 hours after admission) can occur in heroin overdose.

Volatile substance misuse is a common problem in adolescents, with most deaths occurring in boys. In the United Kingdom butane gas lighter refills-which are cheap and easily available-are the most commonly misused substances. Cardiac arrhythmias are the main cause of sudden cardiac death. Tachyarrhythmias may be induced by sympathetic activation or myocardial sensitisation to circulating catecholamines.  Some volatile substances can reduce sinoatrial node automaticity and suppress cardiac conduction. Myocardial ischaemia and infarction as well as a poorly characterised cardiomyopathy have been reported.

Cannabis is the most widely consumed recreational drug. Low or moderate doses increase sympathetic and reduce parasympathetic activity, producing a tachycardia and an increase in cardiac output. Higher doses inhibit sympathetic and increase parasympathetic activity, resulting in bradycardia and hypotension. The haemodynamic effects of consumption of low or moderate doses increase myocardial oxygen consumption, reducing the threshold for induction of angina in patients with pre-existing coronary artery disease. These adverse haemodynamic changes may also trigger plaque rupture in vulnerable individuals. The risk of plaque rupture is short lived, and induction of myocardial infarction is rare.

All these drugs have important effects on cardiovascular function that significantly contribute to adverse events. Most adverse cardiac events occur in young adults and are potentially reversible. The key to diagnosis is a high index of suspicion, particularly when unexplained or unusual cardiovascular problems occur in association with central nervous system dysfunction, together with awareness of the pathophysiological effects of the drugs. There are no adequate randomised controlled trials to guide therapy, which is based principally on an understanding of the cardiovascular actions of the drugs, along with experience gained from observational studies.

Exposure to marijuana or THC (its active ingredient) produces damage to the embryo and retarded feotal growth in fish, rodents, rabbits, the rhesus monkey and humans. The most serious adverse consequences occur in the earliest stage of reproductive function on germ cells of mice and men. Decreased sperm production and abnormal forms of sperm were observed on volunteer studies in a University Hospital in 1975 – 1977. In the 70′s and 80′s, experimental studies on several animal species reported dose-related cellular damage on the testis.

The National Institute of Drug Abuse (NIDA) sponsored most of these studies that were performed by seasoned investigators and published in peer reviewed journals. NIDA, in its mandated Annual Report to Congress of 1979 and 1980 on the health hazards of marijuana, did not issue a formal warning on the subject similar to that of Surgeon General Koop of the Public Health Service who reported in a special declaration of September 1982: “That marijuana decreased sperm count and activity while interfering with ovulation and prenatal development.”During the 1990′s NIDA stopped sponsoring any additional studies on this subject, though it funded dozens of clinical controlled studies of addicts who smoked NIDA-dispensed marijuana cigarettes (and cocaine).

The protocol of these later studies did not include investigations of germ cell, sperm, or ova and did not explicitly warn the subjects on the potential risk to their reproductive function. These risks were again detailed in an international conference on ‘Marijuana and Medicine” held in 1998 at New York University Medical Center. In this conference, reports of the 70′s were validated and confirmed by current studies in molecular biology. As summarized by Professor H. Schuel who reported at the conference the presence of THC receptor sites on sperm cells:
“THC is known to affect all phases of reproduction function studies thus far in humans and laboratory animals by:
* inhibiting secretion of hormones by the pituitary gland
* affecting secretion of steroids by sexual glands
* inhibiting ovulation
* inhibiting sperm production and increasing the incidence of sperm with abnormal cells
* inhibiting the motility of ejaculated sperm
* affecting early embryonic development
* affecting implantation of the embryo into the uterine mucosa
* reducing the number of pregnancies carried to term.”

In brief, marijuana smoking puts at risk future generations before they are conceived.

A new study concludes that people who misuse alcohol and other drugs are responsible for about 25 percent of all violent crimes. Seena Fazel of the University of Oxford in England and Martin Grann of the Karolinska Institute in Stockholm, Sweden, compared Sweden’s national crime register for the years 1988-2000 with hospital discharges of individuals diagnosed with alcohol and other drug misuse and psychoses. The researchers found that 16 percent of violent crimes, including murder, robbery, assault, and rape, were committed by individuals who had been discharged from the hospital after treatment for alcohol misuse, while 10 percent were linked to those who misused drugs such as amphetamines and opiates.

“It is likely you will find the same sort of figures in Western Europe and North America,” said Fazel. “There needs to be more integration between the criminal-justice system and mental-health services because of this close association between crime and people who leave hospital with drug and alcohol problems.” The researchers concluded that, “Using resources to treat people with these problems could be cost-effective in terms of crime reduction.” In particular, Fazel said that treatment should be considered if a person has been convicted of a violent crime. “Probation officers and mental health professionals should continue to work more closely,” he said.

Physicians nationwide are beginning to see the health impact of the increasing popularity of methamphetamine (meth), especially in rural areas, Obstetrician-gynecologist Mary Holley, M.D., who founded Mothers against Methamphetamine, said about 10 percent of her patients are addicted to the stimulant. “We’re seeing devastation,” she said. “Infant mortality is high. The kids who are born won’t feed. They’re underweight. They’re sick. They are going to have ADHD almost guaranteed, and they grow up in a home with an addicted mother who doesn’t care about them.

In the 1950s and 1960s, meth was only available by prescription and was mainly prescribed for weight loss. In the 1980s, illegal meth labs began popping up in California and moving to other states. According to the Substance Abuse and Mental Health Services Administration (SAMHSA), more than 12 million Americans reported having used methamphetamine in 2002. “It has a lot of appeal,” said Barry Lester, Ph.D., professor of psychiatry at Brown Medical School in Providence, R.I. “You can make it in your home and bypass the illegal drug trade. It’s cheap. Everything you need to make it you can get between your hardware store and your pharmacy and the recipes are on the Web.”

Public-health experts are greatly concerned over the growing number of people who use meth, in particular pregnant women. Infants born to meth-using mothers generally have a higher risk for low birth weight and developmental and behavioral problems. “Methamphetamine has really replaced cocaine as the drug of choice for pregnant women,” said Lester. “But the evidence would say that it’s at least as bad, if not worse.” Anti-drug advocates are urging primary-care physicians to better screen their pregnant patients for addiction and, when necessary, refer them to treatment.

“Pregnancy is a powerful motivator, and a prime moment that you find people receptive to treatment,” said Randy Stevens, M.D., an addictionologist at Hamilton Center in Terre Haute, Ind., and a clinical assistant professor of family medicine at Indiana University School of Medicine. “If you’re able to get away from it during your pregnancy, that can carry over to a time when you’re not pregnant.” But doctors are concerned that resources are few and hard to access for patients who agree to treatment. “They need extensive counseling, and I can’t do it,” said Holley. “We’ve got several rehab centers, but they want $1,000 upfront. The total cost will be $20,000. The majority of rehab that goes on here is in the county jail.”

NEW YORK, Apr 20 (Reuters Health) — People who have smoked marijuana daily for many years display more aggression when they are going through withdrawal than do infrequent and former users, according to study results reported by researchers at Harvard University in Boston, Massachusetts.The study is “further evidence that a withdrawal syndrome is associated with abstinence from long-term marijuana use,” according to a statement issued by the National Institute on Drug Abuse (NIDA), which funded the study.

“People addicted to marijuana may continue to use the drug at least partly to prevent the onset of withdrawal symptoms,” said NIDA Director Dr. Alan I. Leshner in a statement. ”Identifying the exact nature of this syndrome is crucial to developing treatment strategies for those attempting to stop their marijuana use.” NIDA reports that marijuana is the most widely used illicit drug in the United States.  According to the 1997 National Household Survey on Drug Abuse, more than 11 million Americans used marijuana in the past month.

The Harvard researchers studied the behavior of 17 long-term heavy users of marijuana and 20 people who were infrequent or former smokers. The subjects were placed in a chamber facing a computer monitor and a response panel that had two buttons, labeled A and B. They were told that they would compete against another subject in a separate chamber, although they were actually responding solely to the computer. If the person pressed the A button 100 times, he or she gained 1 point, while pressing the B button 10 times subtracted points from the opponent. The subjects participated in five sessions, scheduled during marijuana use in the case of current users, and after days 1, 3, 7 and 28 of abstinence.

Current marijuana users became significantly more aggressive 3 and 7 days after withdrawal, compared with those who were infrequent or former marijuana users, according to the NIDA. The lead investigator, Dr. Elena Kouri of Harvard Medical School in Boston, Massachusetts, told Reuters Health that the computer test has been used in number of studies to measure aggressive responses to other substances. She emphasized that the new results do not suggest that heavy marijuana users would be aggressive outside the laboratory setting. The study findings are published in the April issue of the journal Psychopharmacology.

Withdrawal from marijuana, as with other addictive drugs, produces symptoms such as irritability, nervousness, depression, restlessness, sleep difficulty, and decreased appetite, all of which are alleviated when use recommences. A paper published in the journal Psychopharmacology (2003) examined the use of the drug nefazodone to treat anxiety associated with marijuana withdrawal and found that though it eased some symptoms of withdrawal the patients remained significantly agitated and uncomfortable. The authors noted that Nefazodone can caused blurred vision, dizziness, and light headedness, but stressed that more research was needed to determine if higher doses of the drug would be more effective in relieving withdrawal symptoms. They concluded by stating: “Given the mounting evidence of marijuana withdrawal symptoms, the vast numbers of daily users, and the difficulty treatment-seekers have in maintaining abstinence, it is clear that more behavioral and pharmacological treatment options for marijuana-dependent individuals are needed.”


This paper illuminates the addictiveness of marijuana, the difficulty of treatment and, unfortunately, the growing number of marijuana users [many of whom are now attaining the drug under the guise of medicinal use]. Delta-9 THC (Dronabinol) is the major psychoactive ingredient in cannabis and is so highly addictive that it is outlawed in Europe, even as a prescription drug. Because of the high THC content of cannabis today (often ten+ times more potent than it was 20 years ago) addiction is likely to occur much more rapidly today than it has in the past and perhaps is associated with the plethora of adverse consequences leading to emergency medical and psychiatric episodes.

Reference: Haney et al, Nefazodone decreases anxiety during marijuana withdrawal in humans, Psychopharmacology (2003) 165:157-165

A British team researching psychotic symptoms, such as paranoia and hallucination, has found that there is a relatively strong link between cannabis consumption and psychosis in a recent report.According to the study conducted at King’s College Hospital in London, more than one in 20 people in Britain have experienced psychotic symptoms such as paranoid thoughts or hallucinations.

The study of 8,580 people found that 5.5 percent had experienced one or more of the five psychotic symptoms measured, including feeling their thoughts were being interfered with or suffering strange experiences. Psychotic symptoms were linked to drug and alcohol dependence, recent stressful life events and lower intellectual ability. In terms of drug dependence, the relationship between cannabis and psychotic symptoms was the strongest.

Louise Johns from the Institute of Psychiatry said: “We looked at factors associated with these symptoms and it was cannabis dependence that was most linked to psychosis.”What we don’t know is the direction – whether cannabis dependence leads to psychosis or psychotic symptoms lead to cannabis use,” she said.

Although psychosis is generally thought of as an “all-or-nothing” phenomenon,the researchers said there was increasing evidence that it exists in the population as a continuum rather than as a categorical diagnosis.This meant that most people who reported one or more psychotic symptoms were not clinically mentally ill, they said.

Chronic cannabis use can lead to regular bouts of non-stop vomiting and an obsession with hot showers, Australian researchers have found. General practitioner, Dr Hugh Allen of Mount Barker Hospital in South Australia, and team report this rare new syndrome in the November issue of the journal Gut.

Allen said he encountered the first case, dubbed patient Y in the paper, in the late 1990s. The patient came to him after a severe bout of vomiting.

“He would vomit continuously for two or three days,” Allen told ABC Science Online. “It was so bad he had to go to hospital and be put on a drip.”

Two or three months later it happened again, and then the vomiting episodes became more frequent, occurring every month. The patient was a heavy user of marijuana at the time, said Allen, having started smoking at the age of 19 with the vomit attacks starting when he was 22.

“In all honesty, he was smoking 20 to 40 cones a day,” Allen said.

When the patient was in hospital he started to act strangely, said Allen. The patient would sit in a hot shower, which he said relieved his nausea and vomiting.

“It became an obsession with him. He would have 10 to 15 showers a day.”

After 15 months of cyclical vomiting, Allen said the patient concluded that his cannabis use was to blame. So he stopped using it and didn’t vomit severely for nine months. But Allen said the patient started using the drug again, and two months later was vomiting.

Behind the vomit Allen and team set out to test the theory that chronic cannabis use could be behind otherwise unexplained cases of vomiting. They identified 19 chronic cannabis users from the state of South Australia, which has fairly liberal laws regarding the possession of small quantities of marijuana for personal use.Five patients refused to follow through with the study because they did not believe cannabis was behind the vomiting, said Allen. Another five patients were excluded as there were other potential explanations for their vomiting, including schizophrenia and other drug use.

But the remaining nine cases, plus one from Sydney, demonstrated a link between chronic cannabis use and vomiting. “They all had exactly the same syndrome,” said Allen.

“Out of the 10 cases, seven abstained and all got better. Three took up smoking again and got sick again,” he said. “Of these three, two gave up again and got better and one continued smoking and remained ill.”

Allen said the illness, called cannabinoid hyperemesis, was “reasonably rare”, affecting perhaps 1% of chronic users.”But some people are very sensitive to cannabis.”

Body temperature Allen said experiments in mice had shown that cannabis lowers body temperature and lowered body temperature can affect how the gut works, and can lead to vomiting.In people with vomiting sickness, cannabis could be interacting with the hypothalamus, which controls the body’s temperature and gut motility, he said. And this interaction could explain why such people find relief in hot showers.

“It could be that by having a shower, people are heating themselves up and restoring their normal gut motility,” said Allen.

He said further research was needed to test this.

  Source: Anna Salleh. ABC Science Online  14^th October 2004

A study of women attending a medium-sized university in New York finds that college women were nine times more likely to experience sexual aggression on occasions when they drank five or more drinks, Health Day News reported April 14.

The study showed that college women who drank moderately were three times more likely to be sexually victimized than if they hadn’t had a drink at all. In addition, college women who drank heavily were seven times more likely to experience non-sexual aggression, while moderate drinkers were three times more likely to be accosted compared to days when they didn’t drink.

“We’re not saying that drinking per se is the only reason this is occurring,” said R. Lorraine Collins, a senior research scientist at the University of Buffalo’s Research Institute on Addictions. “We’re just saying the risk increases with alcohol intake, and with heavier drinking the risk is even greater.”

This is the first study to analyze college women’s daily drinking behavior and both sexual and nonsexual victimization over a period of weeks. Based on the findings, researchers recommended that college women reduce their alcohol consumption so that they would be more aware and more capable of resisting sexual and nonsexual victimization.

“We need to be able to understand our environment to defend against the perpetrators,” said Karen Johnson, executive vice president of the National Organization for Women. “That means that if you’re going out drinking that you go out with friends who are not drinking.”
Source: Journal Alcoholism: Clinical and Experimental Research April 2004

Two new studies show that individuals with alcohol or other drug addictions often have accompanying medical or psychiatric conditions, such as bone fractures, muscle injuries, pain disorders, depression, anxiety, and psychoses, according to the National Institute on Drug Abuse (NIDA).

For the first study, Jennifer Mertens and a research team at Kaiser Permanente and researchers at the University of California at San Francisco analyzed 12-month data from 747 people who entered the Kaiser Permanente addiction-treatment program.

The data was compared with a control group of 3,690 patients who were members of the HMO, but not diagnosed with an addiction.

The researchers found that those undergoing addiction treatment were significantly more likely to have injuries, depression, and anxiety disorders. Furthermore, addicted individuals were more likely to require treatment for lower back pain, headache, and arthritis.

The second study, conducted by researchers at Northwestern University Feinberg School of Medicine and Children’s Memorial Hospital in Chicago, used data from the Northwestern Juvenile Project. The researchers also interviewed 1,829 youth ages 10 to 18 who were in the Cook County Juvenile Temporary Detention Center.

The study found that more than 10% of the boys and almost 14% of the girls had an addiction and a major mental disorder, such as psychosis, manic episode, or major depressive episode.

“The findings from these studies highlight the need for medical screening and treatment of comorbid conditions,” said NIDA Director Dr. Nora D. Volkow. “These studies provide more evidence that substance abuse does not occur in a vacuum, but rather often exists together with a number of conditions that have serious health consequences and may influence the success of substance-abuse interventions provided alone. Physicians and other healthcare providers need to keep in mind that a diagnosis of substance abuse should be an important warning signal to look for co-existing medical or psychiatric conditions.”
Source Archives of Internal Medicine Nov. 20032 and Archives of General Psychiatry Nov. 2003

Cannabis use in Australia is at an all-time high and is putting heavy users at risk of experiencing schizophrenia, a conference in Melbourne has heard.

The National Cannabis and Mental Illness Conference in Melbourne today heard Australian rates of use were higher than the US, UK and much of Europe and that one in 10 regular users would become dependent on the drug.

Professor David Castle from the Mental Health Research Institute and the University of Melbourne said there was no doubt cannabis use could worsen mental illnesses like schizophrenia.

But he said it was more difficult to say how many people would never have become ill if they had not used cannabis.

Professor Castle said there were cumulative causes for schizophrenia and cannabis could act as “the straw that broke the camel’s back”.

“The debate is how many people, if they never had that straw, would not have their back broken,” he said.

Professor Wayne Hall of Queensland University’s Institute for Molecular Bioscience said large-scale surveys showed 60% of young adults had used cannabis.

Professor Hall said studies also showed around 10% of people who were regular users of cannabis would become dependent daily users who found it hard to control their drug use.

Richard McLean, 31, had a cannabis dependency that he believes contributed to the schizophrenia he experienced for five years.

Mr McLean said he stopped using cannabis when he became psychotic, but the symptoms continued.

“My feeling is I did have a predisposition and my stresses and my use of marijuana led to my psychosis,” he said.

Mr McLean said his mental illness caused pain and confusion for his family, friends and himself.

“It’s just a tragic situation that I had to go through years of losing friends, I had to go through years of losing job opportunities, being depressed and navigating my way through the mental health system,” he said.

Mr McLean said he had not entirely overcome his mental illness, but he now knew the signs and had surrounded himself with people who could help.

He has now written a book, “Recovered Not Cured”, about his experiences.

Mr McLean said despite his experiences he was not anti-drugs, but urged young people to learn about the risks of the drugs they took and to “take care of each other”.

The conference continues tomorrow at The Royal Melbourne Hospital.
Source: AAP NEWSFEED BYLINE: By Alex Wilson
DATELINE: MELBOURNE, Aug 16 2004

SASKATOON – A study of homeless youth in Saskatoon has come up with some disturbing findings.

Nearly 10% of the young people who took part in the research tested positive for hepatitis C. That’s more than double the rate of any other Canadian city where the disease has been studied. The research was conducted by Saskatoon community health nurse Jocelyn Andrews. It was the first study to focus on street kids rather than all drug users in the community.

Andrews also discovered that a drug routinely prescribed for children with an attention deficit disorder was abused by many of the 186 homeless kids who were studied. “What we saw in this subset of this street youth population is injection drug use is a risk for hep C, but what we found in Saskatoon is that use of Ritalin by injection was strongly associated with the hepatitis C virus.”

Andrews says the jury is still out on the role a needle-exchange program could play in reducing infection in youth. Most users of needle exchanges are in their 20s or older – and just having a clean needle is not the answer. “The needle-exchange service offers just the needle,” Andrews says. “With hep C we know it’s readily transmitted through not only the syringe that people are using to inject, but also the other paraphernalia that goes on with that practise: the water, the filter, the spoon.”

Andrews says there’s a positive spinoff from this study. Those who tested positive for hepatitis C have now been told where they can get medical help.
Source:CBC Saskatchewan – Saskatchewan,Canada
Apr 23 2004 http://sask.cbc.ca/regional/servlet/View?filename=hepcyouth04232004

Teenagers and young adults who frequently smoke cannabis are much more likely to develop mental problems, new research has revealed today.

The study of 2,500 people aged 14 to 24 found the more often they used the drug the greater their chance of suffering hallucinations, delusions or mental confusion.

Those who had a pre-existing vulnerability to psychosis, a loss of contact with external reality, had an even greater risk but the research showed they were not significantly more likely to want to smoke the drug.

Anti-drug campaigners said the study, published on bmj.com, confirmed the potentially serious risks to health linked to cannabis use. The results are likely to add further pressure on the Government following its move in January which downgraded cannabis from a class B to class C drug.

As a result of the change those now caught carrying the drug will, in most cases, be given a caution rather than arrested. Past research into other drugs, including cocaine, has also suggested links to mental illness.

Professor Jim van Os, from the Department of Psychiatry and Neuropsychology at Maastricht University, assessed drug use among 2,437 young people and also assessed their predisposition for psychotic symptoms over a four-year period.

The researchers found that being predisposed to psychosis did not significantly predict cannabis use during the four years.

This went against past suggestions that people may start using cannabis because they are predisposed to psychosis rather than the cannabis causing the psychosis to appear.
Source: Evening Standard 1 December 2004

THE MOST nostalgic of the 1968 emotionally scarred generation still believe that there is no association between cannabis and psychosis. Some will even suggest that cannabis smoking is preferable to drinking alcohol.

This week a leading police officer advanced the theory on radio that crushing cannabis smoking in a district was detrimental to both the individual’s health and to the law and order within the community. He said that in his experience the amount of cocaine taken in any one area is inversely proportional to the amount of cannabis used. Come down hard on the cannabis users and the result could be that there would be a cocaine problem.

Doctors who have been dealing with the ill effects of cannabis smoking were therefore relieved to read in the BMJ about a recent study of cannabis use, and its ability to precipitate psychotic symptoms in young people, especially if they had already shown symptoms which suggested a predisposition to psychiatric problems. Most medical practices have had patients who were young, bright and amusingly bizarre who appeared to have a good future awaiting them, only to have it dashed once they started to smoke marijuana.

There was a relationship between the amount of cannabis smoked and the likelihood that the user would develop psychotic symptoms. The more someone smoked the greater the likelihood of psychotic symptoms. These symptoms are not always so serious as to be described as a psychotic breakdown, but even lesser symptoms can affect the ability of a young person to do their job properly or to make good social relationships.

The research published in the BMJ was carried out by psychiatrists in Maastricht in the Netherlands. They took great trouble to adjust the findings for any confounding factors, such as concurrent use of alcohol, cigarettes, or other drugs, which might have given a bias to results.

The survey not only clearly demonstrated that exposure to cannabis during adolescence and young adulthood increased the risk of psychotic symptoms later in life but also confirmed other elements of the anecdotal evidence related by GPs. It showed, for instance, that as has always been suspected the association between smoking cannabis and the development of psychosis is much stronger if the smoker already has the type of personality that is associated with a predisposition to psychotic disease. This predisposition was assessed after a psychological study of the patient’s personality.

Many doctors, who haven’t the skill and experience to do this, have noticed that a family history of a predisposition to psychotic diseases also increases the risk for cannabis smokers.

It has been my habit to tell young people in families where this tendency is obvious that smoking cannabis may be, and in fact is, undesirable for most students but it can be disastrous for those who carry these genes.

The results of the Dutch study confirms anecdotal evidence and three earlier studies that cannabis may precipitate a serious psychotic breakdown and can lead to the emergence of less severe symptoms. These changes in personality can undermine someone ’s domestic life and career and lead to a lifetime of troubles.

Studies published five years ago also showed that the more cannabis smoked the more likely a patient would be to develop cancer. Regular light marijuana smoking more than doubled the likelihood of developing cancer of the head and neck (this includes the tongue and mouth). Daily users of cannabis who smoke more than one spliff a day increase the chances of developing one of these tumours by five times. If they both smoked cigarettes regularly and took cannabis the chances increased 36 times.

Marijuana appears as a stronger carcinogen than cigarettes, according to Professor Li Mao, from the M D Anderson Cancer Centre in Houston, Texas.

Although cannabis may not be as detrimental to the heart and cardiovascular system as cocaine, researchers at Harvard found that the heart attack rate is five times higher for someone in the first hour after smoking a joint than it is at other times.
Source The Times. January 2005

NEW YORK (Reuters Health) – A part of the brain involved in both drug craving and judgment appears to be smaller in cocaine addicts than in healthy people, researchers have found. Analyzing brain scans from 27 people addicted to cocaine and 27 healthy adults of the same age, the researchers found that in the drug abusers, a brain structure called the amygdala was smaller than normal.

Exactly what the finding means is not yet clear, but several pieces of evidence suggest that reduced volume in the amygdala may predispose a person to cocaine addiction, the study’s senior author told Reuters Health.

The amygdala is a collection of nuclei in the brain involved in the processing of emotion. Brain-imaging studies have tied drug craving to activity in the amygdala, and recent research has also suggested that the brain structure aids in sizing up the potential negative outcomes of an action.

It’s such judgment that people with drug addiction typically lack, Dr. Hans C. Breiter of Massachusetts General Hospital in Boston noted in an interview with Reuters Health.

His team’s study, published in the November 18th issue of the journal Neuron, cannot answer the question of whether smaller amygdala volume is a contributor to or consequence of cocaine addiction, Breiter said.

However, he pointed to evidence that supports a causal role. For example, amygdala volume did not correspond with the level of a person’s drug abuse; cocaine users in the study had abused the drug for anywhere from one to 27 years, yet had similar reductions in amygdala size.

In addition, Breiter explained, during normal development, the right-hemisphere amygdala becomes larger than the left. However, in these cocaine addicts, he said, “there was a loss of this asymmetry.”

It seems unlikely, the researcher noted, that drug abuse would have affected only one side of the brain in these individuals. Instead, he said, such a loss of asymmetry in the amygdala would seem to have genetic underpinnings.

But if a reduction in amygdala volume is involved in cocaine addiction, the implications would be great regardless of whether it’s a cause or effect, according to Breiter.

If even short-term cocaine abuse can cause such “dramatic” degenerative change in the brain, he said, that would highlight a prime danger of the drug.

On the other hand, if smaller amygdala volume raises a person’s vulnerability to cocaine addiction, then it offers a potential way to reveal that risk. According to Breiter, it might become possible for people with a family history of any forms of addiction to get a brain scan of the amygdala to see if they have this structural predisposition.

The fact that the amygdala appears to be involved in judging the potential pitfalls of an action may help explain how an abnormality in its structure could make a person susceptible to cocaine addiction, according to Breiter.

However, there is also the amygdala’s role in drug craving. An interesting finding, Breiter noted, was that “the smaller the amygdala was, the more they craved for cocaine.”

Whether the findings are unique to cocaine is not yet clear. The study is part of a larger project by Breiter and his colleagues that is using advanced brain imaging to find potentially inherited “markers” in the brain – such as differences in structure or nerve activity – that are associated with addiction and mood disorders such as depression.

British doctors have connected marijuana use with rising rates of depression, psychosis and schizophrenia.

The Royal College of General Practitioners said that acceptance of the drug and greater availability of stronger forms of it were leading to rising rates of depression, psychosis and schizophrenia, The Telegraph of London reported Sunday.

“Health warnings are falling on deaf ears, drowned out by the cries of powerful liberal pro-legalization groups,” said Dr. Clare Gerada of the college’s drugs misuse unit.

“There is clear evidence that high levels of use, especially among teenagers who are physically and mentally still developing, carries with it the increased risk of psychosis and respiratory conditions such as asthma,” she said.

More worrying, Gerada said, was the increase in super-strong versions of the drug, known as skunk. “The truth is, genetically modified forms of the drug are the norm,” she said.

The British Medical Journal in its January 2005 issue revealed that smoking cannabis once or twice a week almost doubled the risk of developing psychotic symptoms later in life.

Robin Murray, a professor of psychiatry at King’s College London, has said that since the 1980s doctors have begun to see a link between psychotic symptoms and cannabis.

The American Psychiatric Association lists harmful mental effects caused by marijuana, including psychotic disorder, hallucinations, anxiety disorder, impaired judgement, sensation of slowed time, social withdrawal, perceptual disturbances, impaired motor coordination, memory deficit, depersonalization, delusions, paranoia – and others. (Diagnostic and Statistical Manual of Mental Disorders (DSM) IV, APA. Washington DC 1994)

Marijuana may cause depression, flashbacks, aggressive feelings and has been associated with loss of motivation.

A history of unemployment or of violent behaviour was associated with more frequent cannabis use.

Marijuana use causes antisocial personality traits and symptoms.

Marijuana use linked to homicide. It is clear that abnormal behaviour induced by the use of psychoactive drugs plays a significant role in violent crimes which are completely unrelated to either drug profits or trafficking. Many of the murderers interviewed for this study stated they felt that marijuana use was a factor in their crime.

New research suggests that people who smoke and drink heavily are more at risk for oral cancer, the Researchers from King’s College in London, England, found an increase in oral cancer among men and women in their 20s and 30s who smoke and binge drink.

The researchers said that when tobacco smoke combines with alcohol, it produces dangerous levels of cancer-causing chemicals that attack the lining of the mouth.

“Our data show that smoking, drinking and poor diet are major risk factors, and that the younger people start smoking and drinking, the higher the risk,” said Newell Johnson, a professor of oral pathology at King’s College

EXCESSIVE use of cannabis might lead to brittle bone disease, new research has shown.Scottish scientists found that the drug can cause increased bone loss, which in turn leads to osteoporosis. The findings add to a growing body of evidence on the dangers of cannabis and prompted campaigners to renew their calls for the government to rethink its drugs law.

Researchers at Aberdeen University made the discovery while carrying out a study, which was funded by the Arthritis Research Campaign, into chemicals produced naturally in the body called endogenous cannabinoids. The good news is that through understanding for the first time that cannabinoids regulate bone density, scientists have paved the way for new drugs to treat bone disorders.

But the study, published in the journal Nature Medicine, also sounded a warning for the 3.5 million cannabis users in the UK. Professor Stuart Ralston, who led the study, said: “I wouldn’t want to strike fear into everyone who uses the drug, but our tests lead us to the conclusion that it might cause bone loss.”

Cannabinoids act in the same way as chemicals in cannabis by attaching themselves to receptors in the body, stimulating appetite or bone metabolism. Prof Ralston said: “These experiments were not carried out on human patients, but the prediction is that if someone is continually exposed to cannabis, then it would stimulate the cells that would cause a loss of bone. The drugs which stimulate these receptors – and mimic the effects of cannabis – were detrimental to bone and caused increased bone loss, which could, in turn lead to osteoporosis.”

Prof Ralston, now based at Edinburgh University, said the discovery opened the door to drugs used to treat obesity being used to prevent and treat osteoporosis. He said the drugs that block cannabinoid receptors to suppress appetite could also be used to stop bone loss.

He explained: “We were looking at the role of these cannabinoid receptors – the molecules that, like cannabis, would bind on to the bone.

“We started using drugs that would block these receptors and we found that they completely prevented bone loss. It was a very, very impressive effect.”

More than 250,000 people in Britain suffer osteoporosis-related fractures each year, but Prof Ralston said that the most widely used drug treatments for osteoporosis, cancer-related bone diseases, rheumatoid arthritis and other bone diseases were inconvenient to take and can be associated with various undesirable side-effects.

He added: “There is a real need to identify new drugs that can inhibit bone loss, and it looks like blockers of cannabinoid receptors may fit the bill as a new class of drugs for the treatment of bone disease.”

Prof Ralston is now leading further research into the effects of cannabis on bone disease.

Source: The Scotsman Monday 23rd May 2005

New Zealand and U.S. researchers found that non-smokers who lived with a smoker were 15% more likely to have died during a three-year study period than those who never smoked and lived with non-smokers, the Times of London reported April 5.

The study, conducted by researchers at the Department of Public Health at Wellington School of Medicine and Health Sciences and the Harvard School of Public Health, compared census data from 1981 and 1996, which included information about smoking behavior, with mortality statistics over the following three years.

“The results from this study add to the weight of evidence of harm caused by passive smoking and support steps to reduce exposure to other people’s smoke — in the home and in other settings,” the researchers said.

The study’s findings are published in the online version of the British Medical Journal.

A Canadian-led international study finds that the causes of a heart attack are the same for people throughout the world, with cigarette smoking one of the main risk factors, the “There hasn’t been a study like this ever in the world,” said lead investigator Dr. Salim Yusuf, head of the Population Health Research Institute at McMaster University in Hamilton. “The risk factors that we’ve been able to measure account for 90 percent or more of heart disease. The impact of these risk factors in developing heart disease is global. It’s there in every ethnic group, in men, in women, in every region of the world, in young and old. It means we should be able to prevent the majority of premature heart attacks in the world.”

The research concluded that cigarette smoking and a poor ratio of bad to good cholesterol contribute to two-thirds of all heart attacks worldwide.

The five-year study involved 30,000 people in 5A2 countries. About half of the participants had suffered a heart attack. They were compared to an equal number of people with no heart disease, matched for age, sex, and city of residence.

“So now we’ll say: What causes the risk factor, not what causes the disease. And from a public-health point of view, there should be no more wallowing about that we need more information. We’ve got it,” said Dr. Sonia Anand, a specialist in vascular medicine and a member of the McMaster research team.

The latest figures show that 15 million people died from heart attacks worldwide in 1998. “The important issue is that the risk factors outlined in this study, the vast majority of them are modifiable,” said Toronto cardiologist Anthony Graham, a spokesman for the Heart and Stroke Foundation of Canada. “And what it suggests is that tobacco control is going to be as important in the developing world as it is in the western world.”

The study’s findings are published in issue of the British medical journal 

Heavy cannabis use could be a cause of Maori having the world’s highest lung cancer rate, groundbreaking research suggests.

Many Maori from children to kaumatua use cannabis in “epidemic proportions”, says a study by Richard Beasley of the Medical Research Institute in Wellington.

But cannabis might not be as safe as the proponents of its legalisation say. A paper by professor Beasley on the health effects of cannabis was among the research that prompted Wellington coroner Garry Evans to urge ast week that government policy on illicit drugs be changed from “harm minimisation” to campaigning against drug use.

The paper reviews the literature on cannabis and suggests it is more cancer-causing than tobacco, and, like tobacco, causes bronchitis.
Smoking three cannabis cigarettes a day is equal to smoking more than 20 tobacco cigarettes, it says.

Professor Beasley said last night that his institute was close to finishing what he believed was the world’s first study on links between cannabis and lung cancer.

The study reviews all lung cancer cases from Hamilton to Canterbury with a focus on whether the sufferer used cannabis. A tandem study is looking at 300 New Zealanders in four groups of 75 to find the effects of cannabis smoking on human lungs. One group is cannabis smokers only, another smokes cannabis and tobacco, the third tobacco only and the fourth group is non-smokers.

In his paper for the coroner, Professor Beasley said information was urgently needed on the potential role of marijuana in New Zealand’s high lung cancer rate, particularly among Maori, who had the world’s highest rate and were heavy cannabis users.

Research showed cannabis use had reached epidemic proportions and was generally accepted and tolerated among Maori. “Users range from children through to kaumatua.”
Cannabis use was rising. The proportion of the population to have tried it rose from 43 per cent in 1990 to 52 per cent by 1998 and the proportion of regular users from 18 per cent to 21 per cent.

Studies showed regular smokers of three to four cannabis joints a day had chronic bronchitis and other symptoms similar to those of smokers of 20 or more tobacco cigarettes a day.

Professor Beasley said the institute’s two studies should be finished within a month or two but it could take till well into next year before their publication in a medical or scientific journal.

Meanwhile, the evidence supported the coroner’s plea for a close look at how health authorities responded to illicit drug use. The institute also hoped to conduct research into so-called party pills, which were
restricted in the United States but legally sold in New Zealand to over-18s despite little knowledge of their effects.

Source: Study by Richard Beasley of the Medical Research Institute in Wellington. October 2005

A study funded in part by the National Institute of Drug Abuse (NIDA) that was published in the Archives of Internal Medicine looked at nearly 750 people that entered an HMO addiction treatment program. The data gathered regarding other social and medical conditions was compared to over 3,600 other patients who were also members of the HMO but who were not identified as having an addiction.

The study found that those receiving treatment for substance abuse were more likely to have the by products of lower back pain, headaches, arthritis and of course depression and anxiety, which are common with most drug users.

Though this study has only recently been done, it has been known for decades that somatic illnesses can result from the ingestion of toxins such as drugs, both legal and illicit.

Many people throughout society have some type of nutritional deficiencies. Since drug use depletes the body of essential vitamins and minerals their overall health condition naturally worsens, in addition to the more prevalent physical, mental and social problems caused by drug addiction. What wasn’t reported in this study is that in most cases when drug use ceases and overall health is restored the other symptoms often diminish substantially.

Rats given doses of the active ingredient in marijuana early in life were more sensitive to other drugs later in life, according to Swedish researchers.

Researchers led by Yasmin Hurd of the Karolinska Institute exposed young rats to THC, the main psychoactive ingredient in marijuana, then studied their response to heroin use. The THC-exposed rats tended to be more responsive to lower doses of heroin and self-administer more of the drug than the non-exposed rats.

The study could have implications for teenage humans who use marijuana, perhaps making them more susceptible to other drug use later on, researchers said. “The developing brain is definitely more sensitive,” Hurd said, noting that the human brain continues to develop up to age 25. “Many people think that all cannabis does is to give you a calm, relaxed feeling and no long-term effects.”

Commenting on the study, professor Robin Murray of the Institute of Psychiatry in London said, “Clearly it needs to be replicated, but there is already evidence that, in animals, cannabis and amphetamine show cross-tolerance. So that rodents given THC, the active ingredient of cannabis, show greater effects when given amphetamine. This suggests that it may be easier to come to grief when you try heavy drugs if you have already sensitized your brain receptors with cannabis. We need more basic and clinical research into the long-term effects.”

Source: Daily Telegraph. June 2005

Although the public debate about the legalization of marijuana has continued for as long as 25 years, few controlled studies have been conducted to assess its potential medical benefits. The present study examined the antiemetic effect of smoked marijuana cigarettes (8.4 and 16.9 mg Δ9-tetrahydrocannabinol [THC]) compared to a highly potent antiemetic drug, Ondansetron (8 mg) in 13 healthy volunteers. Nausea and emesis were induced by syrup of Ipecac. Marijuana significantly reduced ratings of “queasiness” and slightly reduced the incidence of vomiting compared to placebo. Ondansetron completely eliminated the emetic effects of Ipecac. These findings support and extend previous results, indicating that smoked marijuana reduces feelings of nausea and also reduces emesis in this model. However, its effects are very modest relative to Ondansetron, and the psychoactive effects of marijuana are likely to limit its clinical usefulness in the general population.

Delta9-Tetrahydrocannabinol (THC) is frequently found in the blood of drivers suspected of driving under the influence of cannabis or involved in traffic crashes. The present study used a double-blind crossover design to compare the effects of medium (16.5 mg THC) and high doses (45.7 mg THC) of hemp milk decoctions or of a medium dose of Dronabinol (20 mg synthetic THC, Marinol(R)) on several skills required for safe driving. Forensic interpretation of cannabinoids blood concentrations were attempted using the models proposed by Daldrup (cannabis influencing factor or CIF) and Huestis and coworkers. First, the time concentration-profiles of THC, 11-hydroxy-Delta9-tetrahydrocannabinol (11-OH-THC) (active metabolite of THC), and 11-nor-9-carboxy-Delta9-tetrahydrocannabinol (THCCOOH) in whole blood were determined by gas chromatography-mass spectrometry-negative ion chemical ionization. Compared to smoking studies, relatively low concentrations were measured in blood. The highest mean THC concentration (8.4 ng/mL) was achieved 1 hour after ingestion of the strongest decoction. Mean maximum 11-OH-THC level (12.3 ng/mL) slightly exceeded that of THC. THCCOOH reached its highest mean concentration (66.2 ng/mL) 2.5-5.5 hours after intake. Individual blood levels showed considerable intersubject variability. The willingness to drive was influenced by the importance of the requested task. Under significant cannabinoids influence, the participants refused to drive when they were asked whether they would agree to accomplish several unimportant tasks, (e.g., driving a friend to a party). Most of the participants reported a significant feeling of intoxication and did not appreciate the effects, notably those felt after drinking the strongest decoction. Road sign and tracking testing revealed obvious and statistically significant differences between placebo and treatments. A marked impairment was detected after ingestion of the strongest decoction. A CIF value, which relies on the molar ratio of main active to inactive cannabinoids, greater than 10 was found to correlate with a strong feeling of intoxication. It also matched with a significant decrease in the willingness to drive, and it matched also with a significant impairment in tracking performances. The mathematic model II proposed by Huestis et al. (1992) provided at best a rough estimate of the time of oral administration with 27% of actual values being out of range of the 95% confidence interval. The sum of THC and 11-OH-THC blood concentrations provided a better estimate of impairment than THC alone. This controlled clinical study points out the negative influence on fitness to drive after medium or high dose oral THC or Dronabinol.

Background

Increasing attention has been given by researchers to cannabis use in individuals with psychosis. As psychoses are relatively low-prevalence disorders, research has been mostly been restricted to small-scale studies of treatment samples. The reported prevalence estimates obtained from these studies vary widely. Aims

 To provide prevalence estimates based on larger samples and to examine sources of variability in prevalence estimates across studies. Method Data from 53 studies of treatment samples and 5 epidemiological studies were analysed.

Results 

Based on treatment sample data, prevalence estimates were calculated for current use (23.0%), current misuse (11.3%), 12-month use (29.2%), 12-month misuse (18.8%), lifetime use (42.1%) and lifetime misuse (22.5%). Epidemiological studies consistently reported higher cannabis use and misuse prevalence in people with psychosis. Conclusions

The factor most consistently associated with increased odds of cannabis prevalence was specificity of diagnosis. Factors such as consumption patterns and study design merit further consideration.

Long-term cannabis abuse may increase the risk of schizophrenia. Nerve growth factor (NGF) is a pleiotropic neurotrophic protein that is implicated in development, protection and regeneration of NFG sensitive neurones. We tested the hypothesis that damage to neuronal cells in schizophrenia is precipitated by the consumption of cannabis and other neurotoxic substances, resulting in raised NGF serum concentrations and a younger age for disease onset. The NGF serum levels of 109 consecutive drug-naive schizophrenic patients were measured and compared with those of healthy controls. The results were correlated with the long-term intake of cannabis and other illegal drugs. Mean (± SD) NGF serum levels of 61 control persons (33.1 ± 31.0 pg and 76 schizophrenics who did not consume illegal drugs (26.3 ± 19.5 pg/mi) did not differ significantly, Schizophrenic patients with regular cannabis intake (> 0.5 g on average per day for at least 2 years) had significantly raised NGF serum levels of 412.9 ± 288.4 pg/mI Cu 21) compared to controls and schizophrenic patients not consuming cannabis (p c 0001). In schizophrenic patients who abused not only cannabis, but also additional substances, NGF concentrations were as high as 2336.2 ± 1711.4 pg C = 12). On average, heavy cannabis consumers suffered their first episode of schizophrenia 3.5 years (n = 21) earlier than schizophrenic patients who abstained from cannabis. These results indicate that cannabis is a possible risk factor for the development of schizophrenia. This might be reflected in the raised NGF-serum concentrations when both schizophrenia and long-term cannabis abuse prevail.

Discussion

These results demonstrate that serum NGF concentrations in untreated schizophrenic patients differed greatly depending on their long-term intake of drugs of abuse. Whereas he drug-naive schizophrenic patients who had not consumed illegal substances n the past showed no significant difference in serum NGF concentrations, those abusing cannabis for longer than 2 years showed significantly elevated N compared to healthy controls. This has been shown unequivocally not only by a descriptional data analysis, but also by a confirmatory study design (Table 2). Schizophrenic patients with long-term abuse of multiple substances showed an even greater increase in their serum NGF concentrations up to 90-fold above non-abusing schizophrenic patients .

NGF-plasma levels in 26 male schizophrenic patients who had been kept free of neuroleptics for 14 days were reported to be significantly lower than those observed in controls (Bersani er al., 1999).  By contrast, in our much larger sample of patients, we found no significant differences with respect to serum NGF concentrations between schizophrenic patients and controls. However, our patients were comp!etely drug-naive whereas the patients of the formerly cited study previously had been treated with antipsychotics for various time spans. It is known that haloperidol can remain in the cerebral tissue for as long as year after application (Konihuber et al, 1999) thereby possibly modulating and influencing NGF values by its antidopaminergic properties. For this reason, a drug-free period of l day might be too short to rule out the pharmacological effects of footer antipsychotic medication on the NGF concentration. Haloperidol reduces the basal TGF plasma levels in eight formerly neuroleptic free schizophrenic patients (Aloe et al. 1997). One explanation could be cosecretion of NGF with prolactin. with both being controlled by activation of the dopamirie D receptor subtype (Missale et al. 1996) that, in turn, can be blocked by the antidopamine drug Haloperidol. Moreover brain-derived neurotrophic factor (BDNF). another NGF-related neurotrophin. was shown to be decreased in the serum of chronic schizophrenic patients who were already treated with neuroleptics (Tovooka ci at. 2002). However. we demonstrated highly signficant elevations of the NGF serum levels in schizophrenic patients who had consumed significant amounts of cannabis in the past,  more than 0.5 per day over at least 2 years). There’s strong circumstantial evidence for neuronal damage by toxic drugs, but only a few neurochemical studies to support this.    Schizophrenia. a disease of alleged neurodevelopmental origin begins in  adolescence at age 16—24 years and is thought to coincide with increased vulnerability to cannabinoids. sometimes even triggered by them (Andreasson et al. 1987: Linszen et al. 1994). In an analogy to the situation in neurodegenerative disease (for reviews, see Heliweg et al, 1998; Siegel and Chauhan, 2000). the high levels of NGF observed in our study might reflect the assumed adverse effects induced by cannabis consumption in schizophrenia development.

At present, the causes and mechanisms of the observed rise in NGF serum concentrations in schizophrenia following long-term cannabis abuse remain speculative. Similarly, from the present data, it is not possible to establish whether the rise in NGF levels is due to disease development (enhanced by cannabis) as a state marker or whether NGF was even already high before disease onset. Theoretically, patients at risk for an unfavourable outcome of schizophrenia due to repeated cannabis consumption could be assumed to be a different patient population altogether and show premorbid rises in NGF concentrations as a risk-trait variable. a small sample (n = I of subjects without schizophrenia, but regular cannabis consumption of at least 0.5 g per day for longer than 2 years. We found no such elevation of NGF measurements in the serum. The same was true when serum NGF concentrations were measured in otherwise healthy controls acutely intoxicated with cannabis ( 5; Anders et al,  unpublished data), These findings indicate that the rise in NGF concentrations is not an effect of chronic cannabis consumption per se but rather reflects the combined damaging effects of cerebral vulnerability in schizophrenia and the chronic toxicity of long-term cannabis abuse. The earlier onset of schizophrenia in the cannabis consuming patients further substantiates this hypothesis.

Greatly raised NGF serum concentrations have been demonstrated in chronic diseases such as alcohol dependence (Aloe a at.. 1996) or Behcet’s disease (Lockers-Scherlibi C, 1996). They are not specific for a certain diagnosis. but rather are a marker for chronicity of disease, and possibly for poor prognosis as seen in Behcet’s disease. Our finding of even greater serum NGF concentration in schizophrenic patients with a long-term consumption of additional substances with neuroroxic effects, is consistent with the hypothesis of an NGF correlation with the cumulative dose and toxicity of drugs. The rise was up to 90-fold of the mean NGF serum concentrations of schizophrenic patients without drug consumption, which corresponds to the highest endogenous NGF concentrations reported for man to date. Accordingly, cumulative doses of ecstasy have been demonstrated to be neurotoxic and exert delayed and/or chronic cerebral alterations (Ricaurte and McCann. 1992). showing altered glucose metabolism in positron emission tomography studies in the hippocampus and amygdala of seven chronic ecstasy users (Obrocki et al. 1999). Previous magnetic resonance imaging studies with chronic drug abusers of various drugs including cocaine, amphetamines and psychedelics. also showed minor structural brain changes (Ansley et al. 1993). However, the investigators did note that the study probands had also been consuming alcohol, Therefore, the structural central nervous system changes did not clearly reflect those effects exclusively attributable to illegal drugs, but possibly also those due at least in part to alcohol. To avoid such confounding factors in our study, we excluded those patients who consumed alcohol on a regular basis, This explains the lack of a control group with polysubstance abuse but no schizophrenia because we were unable to find probands that were otherwise reasonably healthy and consumed no alcohol. Certainly, this remains a field for future research.

The origin of the NGF measured in serum is speculative: on the one hand, serum NGF could well stem from a central source and reflect the contral neurotrophin state, especially in pathological conditions such as pre-clinical Alzheimer’s disease (Schaub et al. 2002). On the other hand, it could reflect a peripheral immun ological reaction in terms of a cytokine released from peripheral immune cells (for reviews, see Levi-Montalcini et al. 1996;). Schizophrenia has been connected to autoimmune disease (Ganguli et al. 1994; Jones and Cannon. 1998) and to inflammatory disease (Lin et al. 1998). both possibly resulting in central or peripheral immune responses. An argument could be made about the principal evidence for a role of the neurotrophins NGF or BDNF in conjunction with schizophrenia. In the meantime, there are a number of experiments indicating a connection between BDNF and schizophrenia (Toyooka et at 2002) and some indicating NGF as not only having a role as a peripheral cytokine. but also as a factor relevant to schizophrenia (for a review, see Aloe et al.  2000).

In summary, we suggest that the raised NGF serum concentrations found in schizophrenics with long-term cannabis abuse, and more so in schizophrenics with long-term abuse of additional drugs, reflect the amount of cerebral damage by the combined effects of a primary cerebral vulnerability resulting from schizophrenia and the supposed additional drug-neurotoxicity. Apart from the biochemical evidence of an additive effect of schizophrenia and cannabis consumption on NGF serum concentrations in our confirmatory study design, we also demonstrated an earlier onset of disease in schizophrenic patients consuming cannabis chronically, thereby underlining a precipitating effect of the drug on disease onset. Those two findings are suggestive of a correlation but further studies are required to confirm this hypothesis. Thus, cannabis use may be a risk factor in schizophrenia development, but a predisposition to schizophrenia and cannabis use combined (but neither one independently) appears to be linked to increased NGR production.

High incidence of aneurysms found in users, study finds
Cocaine users seem to have an unusually high incidence of coronary artery aneurysms, weakened areas of heart blood vessels that raise the risk of heart attacks, new research finds.

The study included 191 men and women in their 40s who had angiography, an X-ray of blood vessels, because of known or suspected heart disease. Aneurysms were found in 34 of the 112 persons who reported using cocaine and only six of 91 nonusers.

The study, by physicians at the Minneapolis Heart Institute Foundation, appears in the May 10 issue of Circulation.

That higher incidence of aneurysms may help explain why cocaine users have been found to have a high risk of heart attacks, said Dr. Timothy D. Henry, director of research at the foundation.

Henry suggested two possible explanations for the increased incidence of aneurysms.

“Cocaine use causes periodic hypertension, periods when the blood pressure goes up sharply,” he said. “Having such episodes of high blood pressure over the course of time can lead to formation of aneurysms.”

Cocaine is also known to damage the endothelium, the delicate lining of blood vessels, which could contribute to the weakening of the arteries, Henry said.

Whatever the explanation, the report is “another reason to tell people how dangerous cocaine is,” he said.

The study cited estimates by the federal Substance Abuse and Mental Health Services Administration that 27.7 million Americans – 12% of those 12 and over – had used cocaine at least once in 2001, and that 1.7 million had used it in the previous month.

Most studies of cocaine and heart damage have concentrated on immediate problems, Henry noted. The new study raises the possibility that even short-term use can cause damage decades later, he said. One man in the study who was found to have an aneurysm said he had used cocaine heavily for a two-year period 15 years earlier, Henry said, so the drug “can cause long-term damage that you have to live with the rest of your life.”

Dr. Murray Mittleman, director of the Cardiovascular Epidemiology Research Unit at Beth Israel Deaconess Medical Center in Boston, said the new study “provides clues to the mechanisms of heart attacks occurring in people who are cocaine users.”

“It is an important step forward in understanding the biology of what happens in cocaine use,” Mittleman said.

But follow-up studies are needed because of the way the study was carried out, he said.

“They didn’t start out looking at people who used cocaine,” Mittleman said. “They looked at people who had angiography for some clinical reason. It is possible that this is a special group of cocaine users.”

Nevertheless, the report “gives some insight into why we observe a higher rate of cardiac problems in cocaine users,” he said.

SOURCES: Timothy D. Henry, M.D., director, research, Minneapolis Heart Institute Foundation; Murray Mittleman, M.D., director, Cardiovascular Epidemiology Research Unit, Beth Israel Deaconess Medical Center, Boston; May 10, 2005, Circulation

The practice of dipping marijuana cigarettes in embalming fluid has been around for years. But some experts say the potent combination is becoming more of a problem in New Jersey, where it figured in a recent shootout that left one user dead, one wounded and one other person injured. Known on the street by numerous nicknames including “illy,” “leek,” “crazy Eddie,” “wet,” “amp” and “purple rain,” the formaldehyde-laced marijuana, sometimes with PCP added as well, has been around for at least 20 and possibly 30 years, said Doug Collier, a spokesman for the U.S. Drug Enforcement Administration in Newark.

Tests Driving Drug-Affected Motorists Off The Road 

Victoria’s world-first random roadside saliva tests have highlighted an alarming rate of drug use among drivers, the Minister for Police & Emergency Services, Tim Holding, said today.

Mr Holding said independent laboratory analysis had shown drug driving was more than three times as prevalent as drink driving, with one in every 73 drivers testing positive for cannabis or methamphetamine-based drugs. This compares to an average of one in every 250 drivers who are breathalysed testing positive for alcohol.

“Drug driving tests have been an outstanding success in reliably identifying drivers whose capacity to drive is dangerously compromised,” Mr Holding said. “There can be no mistake that driving under the influence of illicit drugs is just as dangerous as driving while affected by alcohol and is a major contributor to death and trauma on Victoria’s roads.

“The first four months of the saliva drug testing program have identified a worrying level of substance use among drivers that will not be tolerated.” Mr Holding said a three-step process ensured the integrity of the tests. Drivers are initially asked to provide a saliva sample by placing a small absorbent pad on their tongue for a few seconds.

Drivers who return a positive test are then asked to accompany police into a drug bus, similar to a booze bus, for two further saliva samples – one to be kept by the driver and the other for further on-the-spot analysis. If this indicates a positive result, the sample is sent to a laboratory for verification. Motorists who return positive laboratory results for cannabis or methamphetamines are fined $307 and lose three demerit points, or are prosecuted in court. If the offence progresses to court, the maximum penalty for a first offence is $614 and three months’ licence cancellation. Subsequent convictions can result in fines of up to $1227 and up to six months’ licence cancellation.

Mr Holding said in the four months to 17 March 2005, a total of 4619 drivers were tested, with 63 drivers testing positive for drugs. He said 21 drivers tested positive for cannabis and methamphetamine-based drugs. Five drivers tested positive for only cannabis, with 37 testing positive to only methamphetamine-based drugs.

Of the 3488 car drivers tested, 47 returned a positive result. Sixteen out of 1131 truck drivers tested positive for drugs. Eight preliminary tests were not confirmed by the drug bus.

Mr Holding said test handling procedures had been reviewed after three drivers’ final tests ultimately came up negative in the very early stages of the program. “Independent laboratory tests since have conclusively verified the accuracy of saliva drug testing,” Mr Holding said.

The nature of ecstasy-group related deficits in associative learning
Catherine Montgomery, John E. Fisk and Russell Newcombe

Rationale/objectives Research has revealed associative learning deficits among users of ecstasy; the present study explored the component processes underlying these deficits.

Methods: 35 ecstasy users and 62 non-ecstasy users completed a computer-based, verbal paired-associates learning task. Participants attempted to learn eight sequentially presented word pairs. After all eight had been presented, the first member of each pair was displayed and participants attempted to recall the second. Eight trials were administered. Correct responses on each trial, forgetting at various levels of learning, perseveration errors and the rate at which the associations were learned (trials to completion) were all recorded.

Results: MANOVA revealed that ecstasy users performed worse overall and subsequent ANOVAs showed that users performed significantly worse on virtually all measures. Regression analysis revealed that over half of the ecstasy-group related variance in trials to completion was attributable to group differences in initial learning and forgetting. In relation to forgetting, it appears that cannabis use may be an important determinant. In relation to rate of learning (trials to completion) and initial learning, both ecstasy and cannabis may be implicated.

Conclusions: There appears to be abundant evidence of associative learning deficits among ecstasy users. However, it appears that a range of illicit drugs including cannabis and ecstasy may contribute to these deficits

 DUBLIN (Reuters) – Clubbers using ecstasy to keep them dancing through the night may damage their immune systems, while those suffering from depression induced by the drug could be more difficult to treat, a neuroscientist said on Wednesday.Developed as an appetite suppressant but now used at raves and nightclubs to reduce inhibitions, ecstasy has been linked to psychiatric illnesses but Dr. Thomas Connor of Trinity College Dublin believes it may also put physical health at risk.

“Ecstasy has potent immunosuppressant qualities which have the ability to increase an individual’s susceptibility to disease,” Connor told journalists at the British Association for the Advancement of Science annual festival in Dublin.

The environment in which ecstasy, also known as MDMA, is taken further increases the risk of contracting infectious diseases, he said.

“People ingest these drugs in crowded nightclubs full of young people with lots of bugs (germs) going around.”

Connor said evidence so far suggested somebody taking two tablets during a night out would experience a weakening in the body’s natural defences lasting up to 48 hours. Scientists have yet to study the long-term impact on the immune system but the potential was there for damage in hard-core users, he added.

Connor pointed to anecdotal evidence suggesting a higher risk of illness such as web sites used by clubbers advising that they eat plenty of fruit and vegetables in order to boost their immune systems before taking the drug.

There had been instances of unusual illnesses in young users such as shingles of the eye and cases of meningitis, which causes inflammation of the membrane covering the brain and spinal cord, shortly after ingesting the drug, he said.

In the face of evidence that MDMA can lead to depression, anxiety and psychosis, Connor said there were growing signs the physical damage done by the drug reduced the effectiveness of anti-depressants such as Prozac.

“In ecstasy users the proteins that Prozac works on are greatly diminished in number,” he said, cautioning however that results so far were based on studies on animals rather than clinical trials.

Epidemic of liver disease hits women drinkers. By Steve Bloomfield and Sophie Goodchild

Carly Gooding knows she drinks too much. Doctors say young females like her are now showing signs of cirrhosis

Teenage girls are suffering the kind of serious liver damage normally found in women 20 years older because of the growing binge-drinking crisis, one of Britain’s leading liver experts has revealed.

In an exclusive interview with The Independent on Sunday, Professor Ian Gilmore, liver specialist at the Royal Liverpool University Hospital, warned of a health “time bomb” among young women caused by soaring levels of alcohol consumption. Doctors are treating increasing numbers of women in their late teens and early twenties with alcohol-induced liver problems, he said.

And the nation’s binge-drinking crisis has become so bad that cases of cirrhosis – once the preserve of serious, middle-aged alcoholics – are now “commonplace” among women in their late twenties, he added.

A recent study of pupils aged 11 to 15 showed that for the first time girls were as likely as boys to have drunk alcohol, and were drinking very similar amounts.

Health campaigners are increasingly concerned about the amount of alcohol that young women are consuming. A spokeswoman for Alcohol Concern, the national agency on alcohol misuse, said: “We have seen a big increase in the amount of alcohol that women drink over recent years. We are now seeing the knock-on effects of that as women are starting to experience serious health problems at a much younger age.”

Professor Gilmore, the spokesman on alcohol for the Royal College of Physicians, said five years of concentrated binge drinking could lead to the development of cirrhosis. The Chief Medical Officer, Professor Sir Liam Donaldson, said cirrhosis rates among women aged between 35 and 44 have risen sevenfold since the 1970s.

The British Liver Trust echoed Professor Gilmore’s warning. A spokeswoman for the trust said: “Up until very recently we were seeing people in their forties and fifties developing liver disease. Now it is people in their twenties and thirties. We were not getting 30-year-olds with cirrhosis 10 years ago. It is a growing, and very worrying, trend.”

Typical of young women who drink copiously and regularly is Carly Gooding, 25, a sales assistant from Kent, who notches up 58 units a week – 44 more than the maximum 14 recommended by health professionals.

“Every night when I get home I will open a bottle of wine, but on a weekend I like to let my hair down,” she said. “I have tried to cut down.  This New Year I am going to. My skin is disgusting.”

The availability and price of alcohol are to blame for Britain’s cirrhosis rates, which are higher than anywhere else in Europe, said Professor Gilmore. “Alcohol has never been cheaper in real terms and it has never been more available,” he said.

Changes in licensing laws, due to come into force on 24 November, will only lead to an increase in Britain’s growing cirrhosis crisis, warned Martin Plant, professor of addiction studies at the University of the West of England. “The situation is bad, and it is getting worse. The prospect of extended liquor licensing hours is most unwelcome,” he said.

At a conference in Bristol this week, Professor Plant will present evidence that extending licensing hours in different countries has had a damaging effect on public health. “Even if they are extended by as little as an hour, it drastically increases health problems,” he said.

In Western Australia, bars that chose to open for one extra hour experienced a doubling of alcohol-related violence. In Iceland, the effect was so alarming the new law was rescinded.

The Government was “opening up a can of worms” by extending opening hours in pubs, clubs and off-licences, warned a spokesman for the British Liver Trust. “Young people now drink as much as possible in as short a time as possible,” she said.

The new licensing laws will allow bars, clubs, off-licences and supermarkets to apply for a licence to serve alcohol for 24 hours a day.

Doctors and health officials have warned that increased opening hours could lead to increased levels of drinking, and the Association of Chief Police Officers has called on the Government to delay implementation of the reforms.

Ministers argue that staggered closing times will lead to a decrease in alcohol-fuelled town-centre violence. They also claim that longer opening hours will lead to people taking more time over their drink rather than trying to fit in more rounds.

Doctors are concerned about the lack of research into alcohol-related disease. Professor Gilmore said it is “very hard” to get funding and called on the Government to invest in new studies.

Teenage girls are suffering the kind of serious liver damage normally found in women 20 years older because of the growing binge-drinking crisis, one of Britain’s leading liver experts has revealed.

In an exclusive interview with The Independent on Sunday, Professor Ian Gilmore, liver specialist at the Royal Liverpool University Hospital, warned of a health “time bomb” among young women caused by soaring levels of alcohol consumption. Doctors are treating increasing numbers of women in their late teens and early twenties with alcohol-induced liver problems, he said.

And the nation’s binge-drinking crisis has become so bad that cases of cirrhosis – once the preserve of serious, middle-aged alcoholics – are now “commonplace” among women in their late twenties, he added.

A recent study of pupils aged 11 to 15 showed that for the first time girls were as likely as boys to have drunk alcohol, and were drinking very similar amounts.

Health campaigners are increasingly concerned about the amount of alcohol that young women are consuming. A spokeswoman for Alcohol Concern, the national agency on alcohol misuse, said: “We have seen a big increase in the amount of alcohol that women drink over recent years. We are now seeing the knock-on effects of that as women are starting to experience serious health problems at a much younger age.”

Professor Gilmore, the spokesman on alcohol for the Royal College of Physicians, said five years of concentrated binge drinking could lead to the development of cirrhosis. The Chief Medical Officer, Professor Sir Liam Donaldson, said cirrhosis rates among women aged between 35 and 44 have risen sevenfold since the 1970s.

The British Liver Trust echoed Professor Gilmore’s warning. A spokeswoman for the trust said: “Up until very recently we were seeing people in their forties and fifties developing liver disease. Now it is people in their twenties and thirties. We were not getting 30-year-olds with cirrhosis 10 years ago. It is a growing, and very worrying, trend.”

What is the leading known cause of mental and physical birth defects, surpassing both spina bifida and Downs syndrome? Which drug produces more severe abnormalities in a developing foetus than heroin, cocaine, or marijuana?

The answer to both questions is the same: alcohol. Alcohol (wine, beer, or liquor) is the most common preventable cause of birth defects in the United States.

When a woman drinks alcohol during pregnancy, she risks giving birth to a child who will pay the price – in mental and physical deficiencies – for the rest of his life. Yet many pregnant women do drink alcohol, and it is estimated that one in every 750 infants is born with full-blown Foetal Alcohol Syndrome (FAS) each year in the United States. Another 50,000 children are born with Foetal Alcohol Effects (FAE) each year. Read this article to learn more about FAS and FAE, including characteristics and risk factors.

Signs and Symptoms of FAS

FAS is identified as a pattern of physical, developmental, and functional abnormalities in a child resulting from a woman’s drinking alcohol during pregnancy. Characteristics of children with FAS include:

Low birth weight Small head circumference. Failure to thrive. Developmental delay. Organ dysfunction. Facial abnormalities, including smaller eye openings, flattened cheekbones, and indistinct philtrum (an underdeveloped groove between the nose and the upper lip). Epilepsy. Poor coordination/fine motor skills. Poor socialization skills, such as difficulty building and maintaining friendships and relating to groups Lack of imagination or curiosity Learning difficulties, including poor memory, inability to understand concepts such as time and money, poor language comprehension, poor problem – solving skills Behavioral problems, including hyperactivity, inability to concentrate, social withdrawal, stubbornness, impulsiveness, and anxiety

Children with FAE display the same symptoms, but to a lesser degree, and are less likely to have mental retardation.

The Hidden Handicap

It was not until 1973 that alcohol was officially recognized as a teratogen, a substance that can cause damage to a foetus. Today, FAS and FAE are still largely misunderstood by the general public.

Children with FAE are often at a disadvantage because they are frequently undiagnosed, says Georgiana Wilton, coordinator of the National Family Empowerment Network: Supporting Families Affected by FAS and FAE. This also applies to children with Alcohol-Related Neurodevelopmental Disorder (ARND), a recently recognized category of prenatal damage that refers to those children who exhibit only the behavioral and emotional problems of FAS/FAE, without any signs of developmental delay or physical growth deficiencies.

“These kids fall through the cracks and suffer for it,” Wilton says. “Their behavior can look like belligerence or obstinacy, when in fact the kids are acting out of their own limited understanding of what is expected of them.” Wilton explains that although children with FAE or ARND may score well on intelligence tests, their behavioral deficits often interfere with their ability to succeed. Extensive education and training of health care professionals, parents, and teachers are essential to caring for these children.

Diagnosis and Long-Term Effects

“Early diagnosis is essential,” affirms Ronnie Jacobs of the Bergen County, New Jersey Council on Alcohol and Drug Abuse. “We must remember that it’s not that these kids are a problem, but that they have a problem. We need to change our mindset, because the children are not going to change. FAS, FAE, and ARND are lifelong conditions. There is no cure.”

Psychologist Ann Streissguth, a pioneer in the field of FAS, has conducted numerous studies mapping the long-term effects of FAS/FAE. Her research shows that the problems associated with FAS actually intensify as children move into adulthood. A majority of the adults in her studies had mental health problems, experienced trouble with the law, and were unable to live independently.

Professionals who work on a daily basis with the families of FAS/FAE victims see important changes beginning to take place. “Recent research has led to an awareness of the importance of providing early intervention to children diagnosed with FAS,” says Wilton. “Development and stimulation programs begun between birth and age 5 have made enormous differences.”

How Much Alcohol Is Too Much?

It is clear that abusing alcohol during pregnancy is dangerous, but what about the occasional drink? How much alcohol constitutes too much during pregnancy? No evidence exists that can determine exactly how much alcohol ingestion will produce birth defects. Individual women process alcohol differently. Other factors vary the results, too, such as the age of the mother, the timing and regularity of the alcohol ingestion, and whether the mother has eaten any food while drinking.

Many doctors believe that an occasional glass of wine during pregnancy presents no risk to the foetus. But as Linda Nicholson, a genetic counsellor, points out, “We don’t know how much alcohol is safe so we just say, ‘Don’t drink at all.’” Although full-blown FAS is the result of chronic alcohol use during pregnancy, FAE and ARND may occur with only occasional or binge drinking.

Because alcohol easily passes the placental barrier and the foetus is less equipped to eliminate alcohol than its mother, the foetus tends to receive a high concentration of alcohol, which lingers for longer periods than it would in the mother’s system.
Source: KidsHealth.org July 2005

Executive figures show 156 people died from drug abuse, while 134 died on the roads. The figures, for 2003, were uncovered by SNP justice spokesman Kenny MacAskill in a response to questions he tabled to the Executive.

Glasgow MSP Nicola Sturgeon, the SNP’s Holyrood leader, said it was a “staggering revelation”. She added: “This only underlines the fact that Glasgow’s drug epidemic has grown out of all proportion. “Even with the large reduction in the number of deaths from drug misuse over the past year there are still 16% more deaths from drugs than there are on our roads.

“We must act now to free Glasgow from the oppression of drugs in our communities.” 

Atrial defibrillation, a heart-rhythm problem, is far more common in men who consume 45 alcoholic drinks or more per week than among those who have less than one drink weekly, Reuters reported Sept. 13.

Researchers from Beth Israel Deaconess Medical Center in Boston said that the study showed than men who drink heavily were 45% more likely to suffer heart arrhythmia than light drinkers. In atrial fibrillation, the upper chambers of the heart beat erratically, leading to possible blood clots and stroke.

“I think the clinical assumption has always been that if there is a higher risk of atrial fibrillation among alcohol drinkers, it is among people who drink a lot. Our results confirm this belief,” said lead study author Dr. Kenneth J. Mukamal.

Researchers looked at coronary-health data on 16,415 men and women for the study. They said that heart problems are probably just as common among female drinkers, but the data did not include enough female heavy drinkers to support that conclusion.

About 5% of all atrial defibrillation cases among men are caused by alcohol, the authors estimated.

Heavy drinking quickly leads to memory loss and learning problems, according to animal studies conducted by researchers at Saint Louis University.

Medical Study News reported June 15 that rats fed a diet that included 20% alcohol for eight weeks, then kept off of alcohol, showed signs of brain damage. The damage persisted even after the mice abstained from alcohol for 12 weeks. Researchers said that the study showed that even short periods of excessive drinking could cause lasting memory and learning problems.

The mice were given the ethanol equivalent of a person drinking six to eight beers a day or a bottle of wine daily for six years.

Blood Flow to Brain Altered Weeks After Smoking Pot

The effects of marijuana in the brain may linger long after the last joint goes out.

A new study shows that blood flow to the brain in people who smoked marijuana remained altered up to a month after they last smoked pot.

Researchers say the findings may help explain the problems with memory and thinking found in previous studies of chronic marijuana users.

Marijuana’s Effects on the Brain

In the study, which appears in the Feb. 8 issue of Neurology, researchers studied the blood flow in brain arteries of 54 marijuana users and 18 nonusers.

The marijuana users volunteered to participate in an inpatient program and abstained from marijuana use for a month.

Blood flow in the brain was analyzed at the beginning of the study and at the end of the month for the marijuana users.

Researchers found blood flow was significantly higher in marijuana users than in nonusers, both at the beginning and at the end of the study.

However, the marijuana users also had higher scores on the pulsatility index (PI), which is a measure of resistance to blood flow.

Researchers say the level of resistance to blood flow among light and moderate marijuana users improved over the course of the abstinence month. But there was no improvement among heavy marijuana users.

This resistance is thought to be caused by the narrowing of blood vessels that happens when the body’s own ability to regulate the circulatory system becomes impaired.

“The marijuana users had PI values that were somewhat higher than those of people with chronic high blood pressure and diabetes,” says researcher Ronald Herning, PhD, of the National Institute on Drug Abuse in Baltimore, Md., in a news release. “However, their values were lower than those of people with dementia. This suggests that marijuana use leads to abnormalities in the small blood vessels in the brain, because similar PI values have been seen in other diseases that affect the small blood vessels.”

Light marijuana users smoked two to 15 joints per week, moderate users smoked 17 to 70 joints per week, and heavy users smoked 78 to 350 joints per week.

Teratological investigations have demonstrated that agents that are relatively harmless to the mother may have significant negative consequences to the foetus.
Among these agents, prenatal alcohol, nicotine or cannabis exposure have been related to adverse offspring outcomes. Although there is a relatively extensive body of literature that has focused upon birth and behavioral outcomes in newborns and infants after prenatal exposure to maternal smoking, drinking and, to a lesser extent, cannabis use, information on neurobehavioral and cognitive teratogenic findings beyond these early ages is still quite limited. Furthermore, most studies have focused on prenatal exposure to heavy levels of smoking, drinking or cannabis use. Few recent studies have paid attention to low or moderate levels of exposure to these substances. This review endeavors to provide an overview of such studies, and includes animal findings and potential mechanisms that may explain the mostly subtle effects found on neurobehavioral and cognitive outcomes. It is concluded that prenatal exposure to either maternal smoking, alcohol or cannabis use is related to some common neurobehavioral and cognitive outcomes, including symptoms of ADHD (inattention, impulsivity), increased externalizing behavior, decreased general cognitive functioning, and deficits in learning and memory tasks.

OCALA – Methamphetamine abuse continues to spread, despite new laws and public education campaigns aimed at stamping it out. Now, medical researchers are warning that meth is not only addictive, it literally causes brain damage – all the more so when mixed with an HIV infection.

Both methamphetamine abuse and HIV infection distort different parts of the brain, diminishing thought processes such as memory, problem-solving and attention span, researchers at the HIV Neurobehavioral Research Center of the University of California-San Diego report in this month’s American Journal of Psychiatry.

Dr. Jay Rubin, a neurologist in Ocala, said the findings agree with what doctors already know about drugs and other stresses on the brain.

“Things like cocaine abuse can cause strokes,” Rubin said. “There may be some certain areas of the brain that are probably more susceptible to damage. It’s known, for instance, that suffocation or near-suffocation causes damage in the parts of the brain like the hippocampus.”

Ocala Police Maj. Guy K. Howie, who commands Marion County’s multi-agency drug enforcement team, said the findings likewise bear out with his own observations of the growing numbers of local meth abusers.

“It doesn’t surprise me at all,” he said. “When you talk to somebody that’s on meth, you know. You watch the way they talk, the way they twitch. And I’ve known some to be up for two to three days at a time. All of the toxic chemicals used to make it has got to do something to both the body and the brain.”

The researchers in San Diego analyzed brain scans of 103 adults divided into four groups: meth abusers, HIV-positive, HIV-positive meth abusers and a control group with neither problem. They also tested each group on their attention span and memory, the speed at which they mentally process information, their ability to learn, verbal skills, motor skills and other brain functions.

Methamphetamine abuse, they found, is related to swelling of the parietal cortex, which helps people understand and pay attention to their surroundings, as well as the basal ganglia, which is linked to motor skills and motivation.

HIV, on the other hand, appears to shrink three parts of the brain: the cerebral cortex, which plays a role in higher thinking, reasoning and memory; the hippocampus, involved in learning and memory; and the basal ganglia.

Both meth abuse and HIV appear to damage the brain separately, and cause the most damage when paired together.

“In HIV-infected people, the . . . impairments are associated with decreased employment and vocational abilities, difficulties with medication management, impaired driving performance and problems with general activities of daily living, such as managing money,” Terry Jernigan, leader of the research team, explained in a released statement.

While the impact of meth is less understood, “abusers of the drug have impaired decision-making abilities,” he said. “These could potentially affect treatment and relapse prevention efforts, as well as things like money management and driving performance.”

The findings are especially significant given the risky sexual behavior and contaminated needles that tend to link meth abuse with HIV infection, according to Nora D. Volkow, director of the National Institute on Drug Abuse (NIDA).

They are also significant given the rate at which meth use is gaining. A recent survey by the National Association of Counties revealed that the white crystalline drug poses a bigger problem for law enforcement agencies across 45 states than cocaine, heroine or marijuana.

In Marion County, Howie said, police have identified 21 meth labs compared to three at this time in 2004. They have also confiscated 1,584 grams of the drug, compared to 475 grams at this time last year. The 12 cases of meth possession in 2005 – not including the labs – represents an increase as well.

“It’s starting to get popular among teenagers, but it’s more popular with the 20- to 30-year-old crowd,” Howie said. “There are a lot of people in their 40s using it, too.”

Relatively cheap, highly addictive and too-often mistaken as harmless, meth cuts across most economic classes but has been more popular with whites than blacks, Howie said. Abusers of the white, crystalline drug usually develop pock marks on the skin, and scabs that result from scratching.

Lately, meth trafficking has been up locally while production has dropped slightly – but only slightly, Howie said. “That’s because we put several of the people cooking it in jail.”

Beating the epidemic is going to require continued, aggressive education about the drug’s effects and addictiveness, he said – otherwise, “This is going to just take over like crack did in the 1980s.”

More than a third of America’s 46 million adult smokers try to stop each year, but fewer than 10 % succeed. Some relapse because they cannot tolerate the discomfort and craving associated with nicotine withdrawal. In recent animal studies, NIDA-supported scientists identified sites on some brain cells that appear to be key promoters of the negative psychological symptoms of nicotine withdrawal. The sites, called glutamate receptors, are part of the communication network that uses the neurotransmitter glutamate as a chemical messenger.

Neurobiologists have previously shown that glutamate helps produce the good feelings smoking causes. When nicotine attaches to receptors on cells in the brain’s ventral tegmental area (VTA), the cells release glutamate, which in turn triggers other VTA cells to release dopamine, a neurotransmitter that produces pleasure. Dr. Athina Markou of The Scripps Research Institute (TSRI) in La Jolla, California, and colleagues reasoned that just as glutamate surges caused by nicotine give rise to smoking pleasure, glutamate depletion related to nicotine abstinence might underlie the displeasure of withdrawal. The researchers speculated that when nicotine is withdrawn after chronic use, the feedback system that restores glutamate to normal levels following surges could overshoot its mark, resulting in a glutamate dearth—and symptoms of depression and irritability.

Blocking an Inhibitory Glutamate System Reduces Discomfort of Nicotine Withdrawal in Rats           Rats that had been exposed to nicotine for 7 days showed discomfort 12 hours after withdrawal from nicotine. Rats that were injected, at 18 hours into withdrawal, with a compound that blocked mGluII receptors showed no increase in withdrawal-associated discomfort. (Discomfort measurement technique is described in “Asking a Rat, ‘How Do You Feel?’”). Untreated rats experienced increasing discomfort through 24 hours of withdrawal.

To test this idea, Dr. Markou and Dr. Paul Kenny at TSRI, along with Dr. Fabrizio Gasparini of Novartis Institutes for Biomedical Research in Basel, Switzerland, focused on a specific group of glutamate receptors called group II metabotropic glutamate (mGluII) receptors. These inhibitory receptors are key components of the glutamate feedback system: They detect high glutamate levels and signal glutamate-producing cells to reduce their activity to bring the levels back down. Inactivating the mGluII receptors interrupts this process, leaving glutamate levels high. The researchers hypothesized that if they inactivated rats’ mGluII receptors while subjecting the animals to nicotine withdrawal, the plunge in glutamate levels may be avoided, and the animals’ withdrawal symptoms attenuated.

The scientists implanted tiny pumps under the skin on the backs of adult male rats. The pumps dispensed a nicotine solution that maintained high nicotine levels equivalent to those produced in a human who smokes 30 cigarettes per day. After the rats had been exposed to nicotine for 7 days, the investigators removed the pumps, depriving the animals of nicotine and thus leading to nicotine withdrawal. Then, after 18 hours of withdrawal, half the rats were injected with a chemical that blocks the action of mGluII receptors, in effect switching off the inhibitory feedback signals to the glutamate-producing cells. Over the next 72 hours the scientists evaluated the rats at regular intervals using a technique, called intracranial self-stimulation (see “Asking a Rat, ‘How Do You Feel?’”), that measures withdrawal-like depression in laboratory animals. As the scientists had predicted, the rats with active mGluII receptors exhibited significant discomfort; the withdrawal discomfort rapidly dissipated in those in which mGluII receptors were turned off.

To help confirm the association between mGluII receptors and withdrawal-like symptoms, Dr. Markou’s team treated nicotine-dependent rats with a compound that stimulates the same receptors. In these animals, activation of the inhibitory glutamate loop triggered discomfort comparable with that in nicotine withdrawal. “Other research has shown how nicotine changes regulation of excitatory glutamate signalling,” Dr. Markou says. “Our study helps explain how nicotine also commandeers inhibitory glutamate circuits. The altered function of the mGluII receptors appears to mediate, at least partly, the depression like aspects of nicotine withdrawal.” The effect, she explains, is a carrot-and-stick influence strong enough to thwart the most sincere attempts to quit smoking. “Nicotine provides a positive effect through the excitatory circuits, making smoking a rewarding and reinforcing experience. Now we see that nicotine has a similarly powerful aversive effect through the inhibitory circuits, making withdrawal an unpleasant experience.”

The role of mGluII receptors in withdrawal suggests that these receptors might also offer a target for therapeutic intervention, Dr. Markou adds. “Easing the depression like aspects of withdrawal would significantly decrease discomfort and make it easier for people to maintain abstinence and resist the temptation to relapse to smoking.”

Recreational cannabis use has been associated with psychotic reactions, but this is the first such report in closely monitored subjects participating in a clinical trial, note Dr. Bernard Favrat and colleagues at Institut Universitaire de Medicine Legale in Lausanne.

Favrat’s group was conducting a study to examine the effects of ingestion of  THC (delta-9-tetrahydrocannabinol) on psychomotor function and driving performance in eight occasional cannabis users.

The first case of psychosis was in a 22-year-old man given 20 milligrams of dronabinol, a synthetic THC. Ninety minutes after dronabinol administration he experienced severe anxiety and symptoms of psychosis, and was unable to perform the two psychometric tests.

Levels of THC and its active metabolite 11-OH-THC in the blood at the time of the strong adverse effects were 1.8 and 5.2 nanograms per millilitre, respectively.

The second case was also a 22-year-old man who developed severe anxiety one hour after taking 16.5 milligrams of a THC compound, when his THC blood level was 6.2 nanograms per milligram and 11-OH-THC was 3.9 nanograms per milligram. For several hours he was unable to perform psychometric tests

The authors note that smoking a 3.5-% marijuana cigarette leads to blood concentrations of THC in the range of 50 to 100 nanograms per millilitre. They believe that oral administration produces higher levels of 11-OH-THC, with slower elimination.

Alternatively, they suggest that “consuming oral cannabis may produce more potent, yet unknown psychotomimetic metabolites of THC.”

“Doctors and users should be aware of the increasing availability of oral cannabis in ‘special’ drinks or food as well as in medications under development,” which can result in “significant psychotic reactions,” Favrat’s group cautions.

Spray Shows Benefits for Rheumatoid Arthritis in Small British Study

Nov. 8, 2005 – A spray containing two chemicals extracted from marijuana improved pain and sleep in rheumatoid arthritis (RA) patients, British researchers report.

The study, which appears in Rheumatology, was small, brief, and likely the first of its kind, note the researchers. They write that the “encouraging” results warrant larger, longer studies. The spray, called Sativex, is made by GW Pharmaceuticals, the British drug company that funded the study. It is sprayed into the mouth and the medication is absorbed under the tongue or the inside part of the cheek.One of the researchers is GW Pharmaceuticals’ medical director. Two others disclose having received honoraria from GW Pharmaceuticals.

Spray Study

The study included 58 RA patients. They had no history of psychiatric disorders, substance misuse, epilepsy, or severe heart, kidney, or liver problems.

First, patients rated their pain at rest, during movement, and first thing in the morning. They also rated their quality of sleep.

Next, the patients were given one of two sprays to use every evening for about a month. Sativex was one of those sprays. The other was an empty spray (placebo).

Sativex was given to 31 patients. The other 27 patients got the placebo. No one knew which patients had gotten Sativex.

Sativex contains THC (delta-9-tetrahydrocannabinol) and CBD (cannabidiol). Those are key therapeutic compounds in cannabis that have been shown by other studies to produce effects on pain and inflammationhave been shown by other studies to produce effects on pain and inflammation, write the researchers.

They included rheumatologist David R. Blake of the Royal National Hospital for Rheumatic Diseases in Bath, England.

Study’s Results

Compared with the placebo group, patients taking Sativex had notable improvements in pain (including pain during movement and pain at rest), sleep quality, and RA disease activity, the researchers report.

Morning pain didn’t change much but was “surprisingly low” to begin with, write Blake and colleagues.

The sprays were only used in the evening to minimize any intoxication. The most common side effects with Sativex were dizziness (eight patients, or 26% of the Sativex group), dry mouth (four patients, or 13%), and lightheadedness (three patients, or 10% of those taking Sativex).

PATIENTS suffering the effects of cannabis abuse are being treated by Tasmanian public hospitals every day, says a leading health authority.

People with short-term drug-induced psychosis and longer-term mental illness, compounded by pot smoking, are seeking medical help at an increasing rate. Mental Health Services clinical statewide director Peter Norrie said the Royal Hobart Hospital was seeing many cannabis cases.

First-time pot smokers were turning up at the Royal with full-blown psychosis — delusional, confused and anxious. Other more regular pot smokers with long-term mental illness were fronting for treatment for episodes likely to have been triggered or related to using cannabis.

“These days it’s close to every day,” said Dr Norrie, who is a senior clinical consultant psychiatrist at the Royal. He said he was talking about “drug-induced psychosis or long-term mental illness associated with pot smoking”. Dr Norrie said it was “very common” for first-time users to present with “floridly psychotic” behaviour.

He said psychiatrists were increasingly concerned with the link between substance abuse and mental illness. Cannabis use had been linked with depression, anxiety and schizophrenia. International studies show modern strains of marijuana are from three to 10 times stronger than those used by previous generations.

“Clinically psychiatrists have suspected a link for many years and the latest research seems to confirm this,” Dr Norrie said.

“The chicken-and-egg debate has raged for years – whether pot causes psychosis or people with a tendency to psychotic illness are predisposed to smoke pot.”

Dr Norrie said the first signs of schizophrenia were often a lack of engagement with society. But those symptoms could also be what is commonly known as “typically teenage” or a sign of the onset of depression.

Disengaged teenagers could then turn to cannabis.

If psychosis did occur it was hard to tell whether smoking pot was a cause or a symptom. Dr Norrie said some pot smokers appeared to be able to continue the habit without serious mental illness but others were prone to individual cases of psychosis or longer-term mental disease.

“There’s a certain group of people who smoke pot who are unlikely to develop mental illness but there’s certainly a significant number of the population who suffer from mental illness and pot smoking adds to the risk,” Dr Norrie said.

Drug-induced psychosis usually consists of paranoia, confusion and anxiety.

Sufferers present with memory problems and delusions. They can believe they have special powers, hear and see things that are not there and are unable to distinguish what is real.

Rate of mental illness combined with drug abuse up by more than 60% in five years Source : Moneyplans.net Archives

The rate of mentally illness combined with drug abuse has climbed more than 60% in five years across England and Wales, finds research in the Journal of Epidemiology and Community Health.

And those affected are becoming younger: the average age has fallen from an average of 38 to 34, the findings show.

The researchers assessed information submitted by family doctors to the General Practice Research Database on the extent of combined mental illness and drug abuse seen at surgeries in England and Wales. The information covered adults between the ages of 16 and 84.

Drug abuse excluded alcohol and tobacco, but included prescription and illegal drugs.

The data were taken from 230 general practices – equivalent to just over 3% of the population of England and Wales – for the five years between 1993 and 1998.

The authors used patient years of exposure as a unit of measurement to reflect how long patients were treated, rather than how many were registered.

Between 1993 and 1998, the rate of combined mental illness and substance abuse rose from 50 per 100,000 patient years of exposure (PYE) to 80/100,000 PYE, equivalent to an increase of 62%.

Men were more likely to be affected than women. Rates climbed 79% among men during the study period compared with 44% for women.

Applying these figures to the population suggests that the number of people with mental illness and drug abuse problems rose from 23,624 in 1993 to 37,361 in 1998. Numbers in the age band 25 to 34 more than doubled in five years.

The problem was greatest in certain types of mental illness. The rate of psychosis and drug abuse soared by 147% in five years, while that of paranoia and drug abuse rose by 144%. Rates of schizophrenia combined with drug abuse rose 128%.

Based on their findings, the authors suggest that the average family doctor practice sees seven patients who are both mentally ill and misusing drugs, and that this will double to 14 by 2006. The problem seems to be greater and rising more rapidly among those with serious mental illness, they say.

“Clinicians have observed a connection between these two disorders for years, so we are excited to have found what could be a molecular underpinning for that association,” said Alison Goate, a psychiatric geneticist who led the study.

According to Goate, a variation or alteration of the CHRM2 gene appears to influence why some people are susceptible to alcoholism, others to depression, some to both diseases, and others to neither. The CHRM2 gene is involved in attention, learning, memory, and cognition.

The study’s findings resulted from a DNA analysis of 2,310 people from 262 families in which at least three members were alcoholics. Some individuals in the families were also depressed alcoholics.

Goate said additional research is needed to determine any underlying biology for the two disorders. “What you want is to see someone obtain the same results in an independent study,” she said.

Wang, J. et al. (2004) Evidence of common and specific genetic effects: association of the muscarinic acetylcholine receptor M2 (CHRM2) gene with alcohol dependence and major depressive syndrome. Human Molecular Genetics, 13(17): 1903-1911.

Objective: Although a number of studies have examined the respiratory impact of marijuana smoking, such studies have generally used convenience samples of marijuana and tobacco users. The current study examined respiratory effects of marijuana and tobacco use in a nationally representative sample while controlling for age, gender, and current asthma.

Design: Analysis of the nationally representative third National Health and Nutrition Examination Survey (NHANES III).

Setting: U.S. households.

Participants: A total of 6,728 adults age 20 to 59 who completed the drug, tobacco, and health sections of the NHANES III questionnaire in 1988 and 1994. Current marijuana use was defined as self-reported 100+ lifetime use and at least 1 day of use in the past month.

Measurements and Main Results: Self-reported respiratory symptoms included chronic bronchitis, frequent phlegm, shortness of breath, frequent wheezing, chest sounds without a cold, and pneumonia. A medical exam also provided an overall chest finding and a measure of reduced pulmonary functioning. Marijuana use was associated with respiratory symptoms of chronic bronchitis (P=.02), coughing on most days (P=.001), phlegm production (P=.0005), wheezing (P<.0001), and chest sounds without a cold (P=.02).

Conclusion: The impact of marijuana smoking on respiratory health has some significant similarities to that of tobacco smoking. Efforts to prevent and reduce marijuana use, such as advising patients to quit and providing referrals for support and assistance, may have substantial public health benefits associated with decreased respiratory health problems.
Brent A. Moore, PhD, Erik M. Augustson, PhD, MPH2, Richard P. Moser, PhD, Alan J. Budney, PhD, Department of Psychiatry, Yale University School of Medicine, New Haven, CT, USA; Tobacco Control Research Branch, Division of Cancer Control and Population Sciences, and Behavioral Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, Rockville, MD, USA; Departments of Psychology and Psychiatry, University of Vermont, Burlington, VT, USA

Women trying to get pregnant may be less likely to succeed if they are exposed to secondhand smoke, according to a new study.

The Associated Press reported May 25 that a study of 225 women seeking fertility treatment found that smokers and nonsmokers who lived with a smoker were half as likely to get pregnant as nonsmokers who did not live with a smoker.

The study group included 39 smokers, who smoked an average of 11 cigarettes per day, as well as 40 smokers who lived with other smokers and 146 women who did not smoke and lived with nonsmokers.

“We found that embryo quality and fertilization rates were similar in the three groups, but there was a significant difference in the pregnancy rates per embryo transfer, with the nonsmokers achieving around 48 %, the smokers around 19% and the side-stream smokers 20%,” said lead author Michael Neal, who led a team of researchers from Canada’s McMaster University and Hamilton Health Sciences.

It was unknown, however, whether secondhand smoke hurt the chances of getting pregnant among women who don’t require interventions like in-vitro fertilization. Women with fertility problems may be particularly sensitive to secondhand smoke, researchers said.

The rate of breast cancer among young female smokers is double the rate among nonsmokers, and nonsmokers who are exposed to tobacco smoke also are at elevated risk, according to Canadian researchers.

The Toronto Globe and Mail reported June 3 that premenopausal women who smoke are far more likely to get breast cancer, and that women exposed to tobacco smoke as children or adults had virtually the same risk as smokers — even if they themselves had never smoked.

“Essentially, we see a doubling of risk,” said researcher Kenneth Johnson of the Public Health Agency of Canada. About 20 % of breast-cancer cases occur in premenopausal women. Scientists speculate that the toxins in cigarette smoke affect estrogen levels, which could explain why both smokers and those exposed to secondhand smoke share a similar risk of getting breast cancer.

The study, a meta-analysis of previously published articles, was published in the.

Reuters reported Jan. 31 that the study by the research group CBS for the Dutch government concluded that lung-cancer cases among women have risen over the past few decades in step with an increase in female smoking. Further, Dutch women with lung cancer died, on average, at age 70, while their healthy peers had a life expectancy of 81.

Men had a life expectancy of 76, but lung-cancer victims lived an average of 73 years.

“Women who died from lung cancer were younger than men who died from the same cause. This means the harmful effects of smoking are more serious for women than for men,” the study concluded.

AMSTERDAM – Cigarette smoking is more harmful to women than to men, cutting more than a decade off female smokers’ life expectancy but much less for their male peers, Dutch government research suggested today.

Statistics agency CBS said a comparison of the numbers of Dutch who died of lung cancer in 2003 and smoking trends showed the habit cut a Dutch woman’s life expectancy by 11 years, versus three for a man.

“Women who died from lung cancer were younger than men who died from the same cause. This means the harmful effects of smoking are more serious for women than for men,” it said, but did not suggest a reason for the difference.

Cigarette smoking is believed to be one of the main causes of lung cancer as well as other cancers and lung diseases.

The CBS said a rise in lung cancer among Dutch women since the 1970s correlated with an increase in smoking by women.

On average, female lung cancer sufferers died at age 70 versus an average life expectancy for Dutch women of 81.

Male lung cancer sufferers lived to an age of 73 on average, compared with an average expectancy of 76 years for Dutch men.

The CBS said life expectancy for men in the Netherlands has increased by about five years since the 1970s as they have smoked less.

“The fall in cases of lung cancer among men can be attributed to their smoking habits,” it said. Source: Reuters News Service Jan. 31, 2005, 9:28AM

A recent national study of over 43,000 U.S. adults by scientists at the National Institute on Alcohol Abuse and Alcoholism (NIAAA) and the National Institute of Drug Abuse (NIDA) found that substance abusers are more likely than the general public to have antisocial disorders, including conduct disorder, antisocial personality disorder, and adult antisocial behavior. Experts said the findings stress the need for coalitions to include criminal justice professionals in their substance abuse prevention efforts.

“The strong and significant association between substance abuse or addiction and conditions such as antisocial personality disorder, conduct disorder, and adult antisocial behavior, suggests that prevention and treatment strategies need to apply an integrated approach,” said NIDA Director Dr. Nora Volkow. “By also treating antisocial syndromes, particularly those that develop in adolescence or persist over time, we may be able to substantially reduce substance abuse and addiction.”

Antisocial personality disorder, conduct disorder, and adult antisocial behavior are typified by behaviors that can lead to interaction with the criminal justice system, including physical aggression, reckless disregard for one’s own safety and the safety of others, indifference regarding pain inflicted on others, destructive behavior, and stealing.

Jane Callahan, Director of CADCA’s National Coalition Institute, said the new data underscores the need for collaboration between all sectors of the community. “Due to the link between substance abuse and antisocial syndromes and the behaviors associated with these disorders, it’s important that coalitions address treatment in the local correction system as part of a comprehensive criminal justice response,” Callahan said. “Coalitions should make sure criminal justice professionals are at the table, especially when planning treatment initiatives.”

NIDA and NIAAA scientists conducted their research utilizing data from the 2001-2002 National Epidemiologic Survey on Alcohol and Related Conditions.

A federal research team has discovered more clues behind the long-suspected role of the carcinogen acetaldehyde in the link between alcohol consumption and some forms of cancer.

Researchers at the National Institute on Alcohol Abuse and Alcoholism (NIAAA) and the National Institute of Standards and Technology report that natural compounds called polyamines react with acetaldehyde – which is formed as the body metabolizes alcohol – to generate reactions that damage DNA. This can lead to the formation of cancer.

“This work provides an important framework for understanding the underlying chemical pathway that could explain the association between drinking and certain types of cancer,” said NIAAA director Ting-Kai Li, M.D. Alcohol consumption has been associated with increased risk of upper gastrointestinal cancer and other cancers.

Polyamines, which are essential for cell growth, generally protect DNA from damage. But researchers found that when these compounds react with acetaldehyde, they facilitate its conversion to crotonaldehyde, which has been shown to cause cancer in animals.

“We were able to demonstrate that these reactions can take place with acetaldehyde concentrations that have been measured in human saliva during alcohol consumption,” said lead NIAAA researcher P.J. Brooks, Ph.D.