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

Source: Daily Telegraph,  London  reported Nov. 9.2004

Record numbers of teenagers are requiring drug treatment as a result of smoking skunk, the highly potent cannabis strain that is 25 times stronger than resin sold a decade ago.

More than 22,000 people were treated in 2007  for cannabis addiction – and almost half of those affected were under 18. With doctors and drugs experts are warning that skunk can be as damaging as cocaine and heroin, leading to mental health problems and psychosis for thousands  – an IoS editorial states that there is growing proof that skunk causes mental illness and psychosis.

The decision comes as statistics from the NHS National Treatment Agency show that the number of young people in treatment almost doubled from about 5,000 in 2005 to 9,600 in 2006, and that 13,000 adults also needed treatment.

The skunk smoked by the majority of young Britons bears no relation to traditional cannabis resin – with a 25-fold increase in the amount of the main psychoactive ingredient, tetrahydrocannabidinol (THC), typically found in the early 1990s. New research being published in this week’s Lancet (2008)  will show how cannabis is more dangerous than LSD and ecstasy. Experts analysed 20 substances for addictiveness, social harm and physical damage. The results will increase the pressure on the Government to have a full debate on drugs, and a new independent UK drug policy commission being launched next month will call for a rethink on the issue.

The findings last night reignited the debate about cannabis use, with a growing number of specialists saying that the drug bears no relation to the substance most law-makers would recognise. Professor Colin Blakemore, chief of the Medical Research Council, who backed the original Independent  campaign for cannabis to be decriminalised, has also changed his mind.

He said: “The link between cannabis and psychosis is quite clear now; it wasn’t 10 years ago.”

Many medical specialists agree that the debate has changed. Robin Murray, professor of psychiatry at London’s Institute of Psychiatry, estimates that at least 25,000 of the 250,000 schizophrenics in the UK could have avoided the illness if they had not used cannabis. “The number of people taking cannabis may not be rising, but what people are taking is much more powerful, so there is a question of whether a few years on we may see more people getting ill as a consequence of that.”

“Society has seriously underestimated how dangerous cannabis really is,” said Professor Neil McKeganey, from Glasgow University’s Centre for Drug Misuse Research. “We could well see over the next 10 years increasing numbers of young people in serious difficulties.”

Politicians have also hardened their stance. David Cameron, the Conservative leader, has changed his mind over the classification of cannabis, after backing successful calls to downgrade the drug from B to C in 2002. He abandoned that position last year, before the IoS revealed that he had smoked cannabis as a teenager, and now wants the drug’s original classification to be restored.

Source  IoS  Dec. 2008

Physicians who encounter myocardial infarction in teenagers should consider the possibility that the teens may have ingested K2, a form of synthetic cannabinoid, researchers said.

“Although chest pain is a common presenting complaint of teenagers seen in emergency departments, chest pain from cardiac causes remains exceedingly rare,” Colin Kane, MD, a pediatric cardiologist at the UT Southwestern Medical Center in Dallas, and colleagues wrote in the December issue ofPediatrics. “Use of illicit drugs causing chest pain and myocardial ischemia, however, must remain part of the differential diagnosis.”

The researchers reported on three cases of myocardial infarction in teenagers following ingestion of K2. Designer drugs containing synthetic cannabinoids have become more popular among teens, but little is known about their health implications.

K2 is a collection of herbs and spices that have been treated with a synthetic cannabinoid. The effects are said to be stronger than naturally occurring cannabis.

“These types of drugs give a marijuana-like effect but do not show up on drug screens,” Kane explained to MedPage Today. Therefore, careful questioning may be needed to elicit information about K2 exposure, the authors suggested.
All three cases involved 16-year-old males with no previous health problems. Each complained of chest pains of at least three days’ duration and presented between August and November of 2010.

Initial electrocardiograms revealed ST-segment elevation and high troponin levels. There was no personal or family history of early cardiac problems. Urine drugs screens noted the presence of THC in two patients. No other drugs, including cocaine and amphetamines, were found.

“When the first patient came we initially thought it was a virus that was affecting his heart,” said Kane. “The day after he was hospitalized, the chest pain, ECG, and laboratory test all changed dramatically. We went back to the patient and were more persistent about anything else he might have done. It just isn’t normal for a 16-year-old to have a heart attack.”
Shortly thereafter, two new cases presented with similar findings. After establishing that these males also had smoked K2, Kane and colleagues became concerned because their patients were not having just chest pains, but actual heart attacks.

“I have since then seen a number of kids in my practice who have smoked K2 and complained of chest pains,” said Kane. “I haven’t seen any other frank heart attacks.”

This led them to wonder if there was something different about the K2 that was in circulation at that time. Another option is that teenagers were showing up in the emergency room, but the heart attacks were not found because it is so atypical in the age group.

“It is disconcerting and frightening that K2 is relatively easy to obtain and could have such serious health consequences,” said Kane. “Emergency and primary care doctors need to ask patients specifically about the use of K2 and synthetic marijuana. If the clinical findings fit, physicians should take the extra step and look for heart damage, even in previously healthy teenagers.”

Source:   www.pediatrics.aappublications.org at University of Florida on November 14, 2011

ABSTRACT: The aim of the present study was to determine the risk of lung cancer associated with cannabis smoking.

A case–control study of lung cancer in adults less than55 yrs of age was conducted in eight district health boards in New Zealand. Cases were identified from the New Zealand Cancer Registry and hospital databases. Controls were randomly selected from the electoral roll, with frequency matching to cases in 5-yr age groups and district health boards. Interviewer-administered questionnaires were used to assess possible risk factors, including cannabis use. The relative
risk of lung cancer associated with cannabis smoking was estimated by logistic regression.

In total, 79 cases of lung cancer and 324 controls were included in the study. The risk of lung cancer increased 8% (95% confidence interval (CI) 2–15) for each joint-yr of cannabis smoking, after adjustment for confounding variables including cigarette smoking, and 7% (95% CI 5–9) for each pack-yr of cigarette smoking, after adjustment for confounding variables including cannabis smoking. The highest tertile of cannabis use was associated with an increased risk of lung cancer (relative risk 5.7 (95% CI 1.5–21.6)), after adjustment for confounding variables including cigarette smoking.

In conclusion, the results of the present study indicate that long-term cannabis use increases the risk of lung cancer in young adults.

Source Eur Respir J 2008; 31: 280–286 2008

Feinstein says the marijuana users performed significantly worse than the non-users on tests measuring attention, speed of thinking, visual perception, and cognition related to planning and organizing.  Scores on one test measuring speed of processing information were about a third lower among marijuana users compared to non-users.  Thirty-two percent of non-users and 64% of users met the definition of globally cognitively impaired, meaning that they had measurable impairments in two or more aspects of intellectual functioning.
 
Neurologist Lily Jung Hensen, MD, of Seattle’s Swedish Neurosciences Institute, tells WebMD that the findings make a strong argument that the cognitive risks associated with marijuana use outweigh potential benefits for MS patients.
 
Source: http://www.cbs47.tv/webmd/ms/story/Medical-Marijuana-May-Impair-Thinking-of-MS/FmQ00ndFKkKhQ199RrPTDQ.cspx  Oct.2011

A single cannabis joint has the same effect on the lungs as smoking up to five cigarettes in one go, indicates research published ahead of print in the journal Thorax.

The researchers base their findings on 339 adults up to the age of 70, selected from an ongoing study of respiratory health, and categorised into four different groups.

These comprised those who smoked only cannabis, equivalent to at least one joint a day for five years; those who smoked tobacco only, equivalent to a pack of cigarettes a day for at least a year; those who smoked both; and those who did not smoke either cannabis or tobacco.

All the participants had high definition x-ray scans (computed tomography) taken of their lungs and they took special breathing tests designed to assess how well their lungs worked.

They were also questioned about their smoking habits.
Seventy five people smoked only cannabis, and 91 smoked both. Eighty one people did not smoke either, and 92 smoked only tobacco.

Combined smokers tended to use less tobacco, the findings showed.
Cannabis smokers complained of wheeze, cough, chest tightness and phlegm. But emphysema, the progressive and crippling lung disease, was only seen in those who smoked tobacco, either alone or in combination.
But cannabis still damaged the lungs and stopped them from working properly.

It diminished the numbers of small fine airways, which are important for transporting oxygen and waste products to and from the blood vessels effectively.
And it damaged the large airways of the lung, blocking airflow, and forcing the lungs to work harder.
The extent of this damage was directly related to the number of joints smoked, with higher consumption linked to greater incapacity.

The effect on the lungs of each joint was equivalent to smoking between 2.5 and five cigarettes in one go.
The authors explain that the impact of cannabis is strongly associated with the way in which it is smoked. It is usually smoked without a filter, and at a higher temperature. Smokers tend to inhale more deeply and to hold their breath for longer.

Source:  Retrieved August 8, 2009, from http://www.sciencedaily.com

Important insights into the continued spread of hepatitis C among injecting drug users are provided by two studies published in the online edition of the Journal of Infectious Diseases. An international team of investigators showed that infectious quantities of hepatitis C could survive on inanimate surfaces for up to seven days. However, the virus can be rendered inactive by commercially available disinfectants, or heating to a temperature of 65-70° for approximately 90 seconds.

In a separate study, French investigators detected the virus on 80% of alcohol swabs obtained from injecting drug users. They suggest that the swabs may be shared by users, risking the transmission of hepatitis C.

Holly Hagan of the New York University College of Nursing in an accompanying editorial stated: “The studies contribute new knowledge to our understanding of the mechanisms by which HCV [hepatitis C virus] may be transmitted among PWID [people who inject drugs] via injection-related materials.”

There are an estimated 130 million hepatitis C infections worldwide. Hepatitis C is a blood-borne infection and a major mode of transmission is injecting drug use. Needle and syringe exchange programmes have been introduced in many countries to control the epidemic. The have been highly effective at preventing new HIV infections, but hepatitis C transmissions still continue. This is possibly because viral load tends to be high in individuals with chronic hepatitis C infection, and even small quantities of contaminated blood are potentially infectious.

A team of investigators led by Juliane Doerrbecker wished to establish a clearer understanding of the survival of the virus, and the effectiveness of disinfectants and heat at rendering the virus non-infectious. Steel discs were contaminated with infectious quantities of hepatitis C which were then allowed to dry. Reassuringly, commercially available disinfectants were also shown to have “a high virucidal efficacy against HCV.”

Tests also showed that infectious quantities of hepatitis C of approximately 30 TCID50/ml could still be detected on inanimate surfaces up to seven days after contamination. However, the investigators emphasised that “all tested biocides were able to inactivate HCV infectivity to undetectable levels.”

The investigators then examined the effect of heat on the virus. Spoons and/or cookers are used to heat diluted heroin into solutions. The liquid is then drawn into a syringe, potentially contaminating the spoon if hepatitis C-infected blood is present in the syringe. The investigators therefore contaminated spoons with the virus, which were then heated to various temperatures using tea candles.

Infectivity started to decrease at temperatures of approximately 50°. Levels of the virus fell below the limit of detection when temperatures reached 67-70°. It generally took between 80 to 95 seconds for heating to produce small bubbles in the spoon.

“Reusing HCV contaminated cookers could lead to infection even if using sterile syringes,” comment the investigators. Holly Hagan emphasised that injecting drug users rarely heat spoons for more than 15 seconds.

In separate research, Dr Vincent Thibault and his colleagues collected drug-using paraphernalia from individuals known to be infected with hepatitis C. The used paraphernalia included syringes, filters and water cups, swabs for cleaning of skin before injecting and pads employed to stop bleeding after withdrawal of needles. A total of 160 pieces of equipment were collected.

The virus was detected on 44% of the pooled materials. A further 620 items used by individuals of unknown infection status were also obtained. Approximately 83% of the pools obtained from swabs had detectable hepatitis C. Moreover, viral load was highest (above 3 log10 iu/ml) within these swab pools. Hepatitis C was also commonly detected in syringes, but viral load tended to be at low levels (12 to 890 iu/ml). The investigators therefore believe that there is “a higher chance for PWID to be contaminated though sharing of a tainted spoon rather than a tainted syringe.”

They note that blood was often visible on swabs. The researchers therefore suggest that transmission of the virus could occur if swabs were being used inappropriately. “The chaotic and rushed atmosphere of the injection setting, where swab sharing and mixing could take place, is…an important factor that should be considered.”

Holly Hagan believes the two studies have important implications for hepatitis C prevention programmes. “Cleaning cookers or perhaps impregnating injection equipment with safe biocides may help reduce the incidence of new infections. Promoting safe swab use to emphasize avoidance of reuse seems a prudent measure.”

Reference
Doerrbecker J et al. Inactivation and survival of hepatitis C virus on inanimate surfaces. J Infect Dis, online edition, doi: 101093/infdis/jir535 (click here for the abstract).

Thibault V et al. Hepatitis C transmission in injecting drug users: could swabs be the main culprit? J Infect Dis, online edition, doi: 101093/infdis/jir650 (click here for the abstract).

Source: www.aidsmap.com 4th Nov.2011

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

A significant increase (more than 10-fold) in the number of newly diagnosed HIV-1 infections among injecting drug users (IDUs) was observed in Greece during the first seven months of 2011. Molecular epidemiology results revealed that a large proportion (96%) of HIV-1 sequences from IDUs sampled in 2011 fall within phylogenetic clusters suggesting high levels of transmission networking. Cases originated from diverse places outside Greece supporting the potential role of immigrant IDUs in the initiation of this outbreak.

Source: Eurosurveillance, Volume 16, Issue 36, 08 September 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

It was the party drug of the 90s. But alarmingly Ecstasy’s popularity seems to be rising again. A worrying trend is re-emerging for the illegal substance after U.S. hospital admissions involving Ecstasy leapt 74.8 per cent in just four years, according to a national study.
Most of the Ecstasy-related hospital visits involved patients aged 18 to 29, but notably 17.9 per cent involved children as young as 12
The Substance Abuse and Mental Health Services Administration (SAMHSA) study indicated the number of hospital emergency visits involving Ecstasy increased from 10,220 in 2004 to 17,865 visits in 2008.
Slightly more than half (52.8 per cent) of the emergency visits were male, the study found. More than a third of the Ecstasy-related visits were made in the South (34.0 per cent) while nearly a third were in the West (31.4 per cent).
Nearly a fifth were made in the Midwest (18.5 per cent), and nearly a sixth were made in the Northeast (16.1 per cent).
But in another alarming trend the study also found that 77.8 per cent of these visits – almost 8 in 10 cases – also involved the use of at least one of more other substances alongside Ecstasy.
The most common drugs used in combination with Ecstasy are marijuana, alcohol and cocaine.
In cases where patients were 21 or older 39.7 per cent had taken Ecstasy with three or more other drugs.
‘The resurgence of Ecstasy use is cause for alarm that demands immediate attention and action,’ said SAMHSA Administrator Pamela S Hyde, J D.

The drug induces feelings of euphoria but can produce psychedelic and stimulant side effects such as anxiety attacks, hypertension and even hypothermia.
The variety and severity of these can increase when the drug is used in combination with other substances.
Dr Peter Delany, director of the Centre for Behavioural Health Statistics and Qualities at SAMHSA, said the agency ‘needed to start digging’ to find the cause of the spike in admissions. ‘Kids are getting it (Ecstasy) at raves and parties, which may indicate a return to social gatherings,’ he said. ‘It is also probably a very cheap drug,’ he added.
‘The largest group of people (doing Ecstasy) are 18 to 29. These are people who have a lot more freedom and a lot more money,’ he said. He also cited the need for prevention education to continue well into adulthood to address this age group.
The more pressing issue, Dr Delany said was the people who were admitted to hospital with more than one substance in their system. ‘Ignorance is part of it,’ he said. ‘There is a lot of risk taking in that age group. ‘This (Ecstasy) is not a safe drug. The first time out of the door can have some serious side effects. When you are mixing it with multiple drugs you don’t know what the reaction will be. Everyone is different,’ he said.
Dr Delany also cited so-called ‘pharm’ or ‘trail mixing’ parties, when young people put a collection of drugs into a bowl and it becomes a very dangerous lucky dip.
But these bowls don’t just contain illegal drugs, they also contain prescription drugs raided from parents’ medical cabinets. Another report by SAMHSA found there has also been a dramatic rise in emergency visits associated with the misuse of prescription drugs.
From 2004 to 2008 these rose from 144,644 visits to 305,885 visits a year and occurred among men and women, as well as among those younger than age 21 and those 21 and older.
The three prescription opioid pain relievers most frequently involved were Oxycodone products (rose 152 percent), Hydrocodone products (rose 123 per cent) and Methadone products (rose 73 per cent).
‘These alarming findings provide one more example of how the misuse of prescription pain relievers is impacting lives and our health care system,’ said SAMHSA administrator Pamela S Hyde. ‘This public health threat requires an all-out effort to raise awareness of the public about proper use, storage, and disposal of these powerful drugs.’

Source: www.dailymail.co.uk 25th March 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

Chronic cannabis abuse raises nerve growth factor serum concentrations in drug-naive schizophrenic patients
Maria C. Jockers-Schertibi, Uta Matthies. Heidi Danker-Hopfe, Undine E. Lang Richard
Ivlahlberg and Rainer heliweg
Department of Psychiatry and Psychotherapy, Char ftc-University Medicine Berlin Campus Benjamin F,thjkiin. Berth,. German
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 NOF 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 senim 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 (Fig. I).
NGF-plasma le ‘els 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 a!., 1999 By contrast, in our much larger sample of patients, we found no significant differences with respect to senim 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 antipsvchotics for various time spans. It is known that haloperidol can remain in the cerebral tissue for as long as year after application (Konihuber et at, 1999) thereby possibly modulating and influencing NGF values by its antidopaminergic properties. For this reason, a drug-free period of l days might be too short to rule out the pharmacologEca effects of footer antipsychotic medication on the NOF concentration. Haloperidol reduces the basal tTGF plasma levels in eight formerly neuroleptic’ free schizophrenic patients (ALoe et at. 1997). One explanation could he cosecretion of ‘1GF with prolactin. with both being contro by activation of the dopamirie D: receptor subtype Missale er a!.. L 996) that, in turn, can be blocked by the antidopaminer dnig haloperidol. Moreover brain-derived neurotrophic factor (BDNF). another NGF-re]ated neurotrophin. was 1-cc shown to be decreased in he serum of chronic schizophrenic patients who were already treated with neuroleptics Tovooka ci at. 2002). However. we demonstrated highly signLticant elevations ot he NOF serum levels in schizophrenic patients who had consumed significant amounts of cannabis in the past i 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 { neurochenhical) studies to supporr this. Schizophrenia. a disease of alleged neurodevelopmental origin. o begins in M. C. JOCKERS-SCHERCJBL ETAL.: SCHIZOPHRENIA! CANNABIS AND NERVE GROWTH FACTOR 443 1 I
adolescence at age 6—24 years and is thought to coincide with increased vulnerability to cannabinoids. sometimes avert triggered by them (Andreasson era!.. 1987: Linszen eta!.. 994). In analogy to the situation in neurodegenerative disease (for reviews, see Heliweg et a!, 1998; Siegel and Chauhan, 2000). the high levels of NOF 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 NGE levels is due to disease development (enhanced by cannabis) as a stale marker or whether NOF 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 NOF concentrations as a risk-trait variable. 1 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 NOF measurements in the serum. The same was true when serum NGF concentrations were measured in otherwise healthy controls acutely intoxicated with cannabis ( 5; Anders and He unpublished data), These findings indicate that the rise in NOF 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 consum ing patients (Table I) further substantiates this hypothesis.
Greatly raised NGF serum concentrations have been demon strated hi chronic diseases such as alcohol dependence (Aloe a at.. 1996) or Behcet’s disease (lockers-Scherlibi C a 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 NOF concen [ in schizophrenic patients with a long-terni consumption of additional substances with neuroroxic effects is consistent with the hypothesis of an NOF 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 ?TGF concentrations reported for man to date. Accordingly, cumulative doses of ecstacy have been demonstrated to be neurotoxic and exert delayed and/or chronLc cerebral alterations (Ricaurte and \lcCann. 992). showing altered glucose metabolism in Positrone emission tomography studies in the hippocampus and amygdala of seven chronic ecstacy users (Obrocki er a!,. 1999). Previous magnetic resonance imaging studies with chronic drug abusers of various drugs including cocaine, amphetamines and psvchedelics. also showed minor structural brain changes (Aasley et at.. 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 re basis, This explains the lack of a control group vith polvsubstance 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 mse arch.
The origin of the NOF 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 preclinical Alzheimer’s disease (Schaub er a!.. 2002). On the other hand, it could retlect a peripheral immun ological reaction in terms of a cytokine released from peripheral immune cells (for reviews, see Levi-Montalcini el c 1996; Hel er a!.. 1998). Schizophrenia has been connected to autoimmune disease (Ganguli er aI.. 1994; Jones and Cannon. 1998) and to inflammatory disease (Lin eLa!.. 199B). both possibly resulting in central or peripheral immune responses. An argument could be made about the principal evidence for a role of the neurotrophins NOF 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 NOF as not only having a role as a peripheral cytokine. but also as a factor relevant to schizophrenia (for a review, see Aloe et ci., 2000).
In summary, we suggest that the raised NOF 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 cerebra! 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 concen ations in our confirmatory study design, we also demonstrated an earlier ons of disease in schizophrenic patients consuming cannabis chronically, thereby underlining a precipitating effect of the drug on disease onset. Those two findings am suggestive of a correlation but further studies are required to confirm this hypo thesis. 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 NOR production.
Acknowledgement
We would like to thank Dr Hans Scherubl manuscript and giving valuable advice.
Address for correspondence
darth C Jockers-Scherubi Department of Psychiatry and Psychotherapy C h an re-University
‘ledicine Berlin Eschenn 3 :4050 Berlin Germany
Email: mar i .joc ke rs @ med i zi ii. fu—be ri in. de
References
for looking over the
Aasley .1 Storsaeter 0, tqilsen C, Smevik 0, Rinck P (1993) Minor structural brain changes in young drug abusers. Acta Neurol Scand 87:210-214

Source:
Journal of Psychopharmacology 17(4) (2 439—445
V2003 British Aisociatlon For Psychopharmacology (ISSN Oz I
SAGE PublicaUons. London. Thousand Oaks. CA and Naw Delhi
0269—08111200312117:4: 439—445; O38O3

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

The story that broke one afternoon in mid-March was startling, even to editors who have been around for a while.
A 19-year-old man had died and 10 others were sickened in a mass overdose after experimenting with a synthetic drug during a party in Blaine.
We have written before about the problems of designer synthetic drugs, which are molecularly different from illegal drugs and sometimes can be acquired legally in shops or over the Internet. But this was the first time we had seen such deadly ramifications. After covering the case in Blaine, which resulted in one man being charged with third-degree murder, we set out to discover just how big a problem these drugs are posing in society. Our preliminary research revealed that this was a growing problem nationally, with devastating consequences across the country.
In the months since, we have researched or acquired dozens of these synthetic drugs, to discover how easy they are to buy and whether consumers are given any warnings at all when they buy the drugs.
We have talked to users, victims and witnesses across the country about some of the unintended consequences of ingesting synthetic drugs. And we have enlisted a number of experts, researchers and businesses in the greater Twin Cities community to help us identify what exactly is in the most common compounds so we can pinpoint the true risk to consumers. For example, Internet Exposure, a web development and marketing firm, is conducting research for us on how people are using the Internet to research and buy drugs, while MedTox Laboratories in St. Paul is testing chemicals for us.
The results of our investigation will unfold in stories that we will publish over the next few months, with the first appearing online today. It is a tragic story of a party that went wrong in a small town in Oklahoma, with eerie similarities to the party in Blaine earlier this year. We went to Oklahoma to illustrate that if synthetic drugs are a problem in such a small, tight-knit community like Konawa, they can create trouble anywhere in Middle America.
Police officer Kat Green, who arrives at the party in Oklahoma to find her own son nearly incapacitated, repeatedly wonders why her son would put something in his body without knowing exactly what it was.
Why indeed, would anyone?
The answer to that question seems to be that these partygoers are taking synthetic drugs because they think it will be fun, the drugs are often touted as legal, and the drugs are easily acquired, making them seem less dangerous than illegal drugs like marijuana, cocaine or hallucinogens. (Some people also take synthetic drugs because they may not show up on drug tests. )
Pamela Louwagie, who has been one of the primary reporters on this investigation, said that some of the partygoers in both Blaine and Oklahoma had researched the drugs they thought they were acquiring, while others “simply seemed to trust that their friends had done enough research to be safe.
“It was striking that, in each case, they didn’t get what was ordered,” Louwagie said. “That showcases the true danger in these things. Many of these substances, while they have been around … for a while, are truly untested. And if you buy them, you don’t know what they have been mixed with and, in some cases, whether you’re even getting the right thing.”
What’s also striking is the trust buyers put in the notion that it is safe to acquire a synthetic drug over the Internet, from an unproven source.
We hope that when we have finished our investigation, we will have helped parents, teenagers and other adults truly understand the risk that synthetic drugs pose — as well as the dangers of buying substances from some unknown source somewhere around the globe who just happens to advertise on the Internet.
I’ll be sharing this story with my own daughters; I urge others to share it with friends and family as well.

Source: Nancy Barnes, Editor, www. StarTribune.com 24th July 2011

A new study suggests that abuse of prescription opioids may be a first step on the path toward misuse of heroin and other injected drugs.
Science Daily reports that the researchers found four out of five injection drug users misused an opioid drug before they injected heroin. They also found that almost one out of four young injection drug users first injected a prescription opioid, and most later switched to injecting heroin.
The study, published in the International Journal of Drug Policy, found that risk factors for misusing opioid drugs include family history of drug misuse, and a past history of receiving prescriptions for opioids.
“Participants were commonly raised in households where misuse of prescription drugs, illegal drugs, or alcohol, was normalized,” lead researcher Dr. Stephen Lankenau, from Drexel University in Philadelphia, said in a news release. “Access to prescription medications – either from a participant’s own source, a family member, or a friend – was a key feature of initiation into prescription drug misuse.”
The study included 50 injection drug users between the ages of 16 to 25. They had all misused a prescription drug at least three times in the past three months. Nearly three-fourths of participants had been prescribed an opioid, often for dental procedures or sports injuries. Most had family members who misused one or more substances. The authors called on parents to carefully monitor and safeguard prescription drugs, especially opioids, in their home

Source: International Journal of Drug Policy June 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

Prolonged prenatal exposure to nicotine decreases the number of newborn cells in the hippocampus, a brain area important in learning and memory, according to preliminary research presented at Neuroscience 2010, the annual meeting of the Society for Neuroscience, held in San Diego. The study offers a neurobiological explanation for why the children of women who smoke during pregnancy are at an increased risk of developing learning disabilities.

“Previous research has shown that nicotine, cocaine, and other addictive drugs decrease the number of newborn cells in adults. Our research suggests that these effects may be even more dramatic in newborn animals,” said Robin Lester, PhD, of the University of Alabama at Birmingham, who directed the study. “These findings provide further warnings to expectant mothers that they should seek help in refraining from smoking during pregnancy,” Lester said.
To mimic the conditions of moderate to heavy smoking in a pregnant mother, Lester and his colleagues treated pregnant rats with nicotine through an implanted mini-pump, which acts similarly to a nicotine patch. The researchers then counted the number of newborn cells in the offsprings’ dentate gyrus, a section of the hippocampus known to contain neuronal stem cells. They also monitored synaptic plasticity — the reorganization of neural pathways considered essential to learning.
“We found a reduced number of dividing stem cells and altered plasticity in the newborn animals exposed to nicotine,” Lester said. These findings may lead to new approaches to treating learning disabilities and other behavior deficits associated with prenatal nicotine exposure.

Source: Society for Neuroscience (2010, November 15). Prenatal exposure to nicotine affects stem cells in hippocampus. ScienceDaily. Retrieved May 8, 2011, from http://www.sciencedaily.com¬ /releases/2010/11/101115155215.htm

Prescription narcotics were involved in more drug overdose deaths in 2007 than heroin and cocaine combined, according to a new article. And in some states, the number of deaths from prescription painkiller overdose is higher than suicide or car crashes.
Approximately 27,500 people died from unintentional prescription narcotics overdoses in 2007, driven to a large extent by prescription narcotics overdoses, said researchers from the Centers for Disease Control and Prevention (CDC), Duke University and the University of North Carolina at Chapel Hill. Narcotics pain medications were also involved in about 36 percent of all poisoning suicides in the U.S. in 2007.
many deaths from both Operation Iraqi Freedom and Operation Enduring Freedom in Afghanistan, from the beginning of both wars through Feb. 20, 2011, said study researcher Dr. Richard H. Weisler, an adjunct professor of psychiatry at UNC Chapel Hill and Duke University.
Alternatively, the drug overdose deaths would be equivalent to losing an airplane carrying 150 passengers and crew every day for six months, researchers said.
The study findings come on the tail of another article published this month in the Journal of the American Medical Association, which showed that the risk of fatal overdose increases with the dose of drugs taken (though taking the medications as needed or as prescribed was not associated with overdose risk).
In 2009, the CDC’s National Youth Risk Behavior Survey revealed that 1 in 5 high school students in the United States have abused prescription drugs, including the narcotics painkillers OxyContin, Percocet and Vicodin. Narcotics, also called opioids, are synthetic versions of opium that are used to treat moderate and severe pain.
And in June last year, the CDC reported that visits to hospital emergency departments involving nonmedical use of prescription narcotic pain relievers has more than doubled, rising 111 percent, between 2004 and 2008.
Researchers said one of the key reasons for the increase in prescription drug overdose deaths is increased nonmedical use of narcotics without a prescription because of the feeling it produces. They also said that medical providers, psychiatrists and primary care physicians may fail to anticipate the extent of overlap between chronic pain, mental illness and substance abuse among their patients.
For example, 15 percent to 30 percent of people with unipolar, bipolar, anxiety, psychotic, non-psychotic and attention deficit/hyperactivity disorders will also have substance abuse problems, said study researcher Dr. Ashwin A. Patkar, associate professor of psychiatry and behavioral sciences at Duke University.
“Similarly, people with substance abuse are more likely to have another mental illness and a significant number of patients with chronic pain will have mental illness or substance abuse problems,” Patkar said in a statement.
Moreover, narcotics, benzodiazepines, antidepressants and sleep aids are commonly prescribed even though they are harmful and addictive when abused, researchers said. It’s the combinations of these drugs that are frequently found in the toxicology reports of people dying of overdoses.
Researchers suggest that before prescribing narcotics, doctors should try non-narcotic medications as well as — when possible — physical therapy, psychotherapy, exercise and other nonmedicinal methods.
The study was published last week in the Journal of Clinical Psychiatry.
Pass it on: Overdosing on narcotic painkillers accounts for more deaths than from heroin and cocaine combined.

Source:www.myhealthnewsdaily.com 27th April 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

Ronald I. Herning, PhD, Warren E. Better, MS, Kimberly Tate, BS and Jean L. Cadet, MD

From the Molecular Neuropsychiatry Branch, National Institute on Drug Abuse, National Institutes of Health,Baltimore,MD.

Address correspondence and reprint requests to Dr. Ronald I. Herning, Molecular Neuropsychiatry Branch, National Institute on Drug Abuse, PO Box 5180, Baltimore, MD21224; e-mail: rherning@intra.nida.nih.gov

Objective: To determine possible effects of prolonged marijuanause on the cerebrovascular system during a month of monitoredabstinence and to assess how the intensity of current use mighthave influenced cerebrovascular perfusion in these marijuanausers.

Method: The authors recorded blood flow velocity in the anteriorand middle cerebral arteries using transcranial Doppler sonographyin three groups of marijuana users who differed in the intensityof recent use (light: n = 11; moderate: n = 23; and heavy: n= 20) and in control subjects (n = 18) to assess the natureand duration of any potential abnormalities. Blood flow velocitywas recorded within 3 days of admission and 28 to 30 days ofmonitored abstinence on an inpatient research unit in orderto evaluate subacute effects of the drug and any abstinence-generatedchanges.

Results: Pulsatility index, a measure of cerebrovascular resistance,and systolic velocity were significantly increased in the marijuanausers vs control subjects. These increases persisted in theheavy marijuana users after a month of monitored abstinence.

Conclusions: Chronic marijuana use is associated with increasedcerebrovascular resistance through changes mediated, in part,in blood vessels or in the brain parenchyma. These findingsmight provide a partial explanation for the cognitive deficitsobserved in a similar group of marijuana users.

Source:  NEUROLOGY 2005;64:488-493

The number of under-16s arriving drunk at accident and emergency inAberdeenhas soared by a shocking 60 per cent.

And health chiefs have warned that more and more vital hospital beds are now being filled up with booze-binge schoolchildren.

Alarming statistics reveal the number of people treated for alcohol-related emergencies by NHS Lothian has soared by 68 per cent.

There were 4,751 cases in 2008/09, up from 2,823 in 2006/07. And inAberdeen, the number has risen from 1,712 people five years ago to 2,220 in 2008/09.

The figure for the same period in Aberdeenshire increased from 900 to 1,051.

The numbers were only topped by Greater Glasgow andClyde, with 13,592 alcohol-related discharges in 2008/09.

Worried politicians last night called for urgent action to tackleScotland’s underage drinking shame.

MSP Murdo Fraser, the Tory shadow health secretary, said: “These are frightening figures that show just how deep the problem is. We have to target problem drinks and problem drinkers, give better education on the dangers of alcohol abuse, and crack down on those who sell to children.”

A Labour spokesman called the new statistics “highly alarming”.

He added: “The SNP Government has to bring forward measures that actually work. They need to crack down on the rogue shops that openly sell booze to kids.”

And north-east MSP Maureen Watt said: “The scale of the increase inAberdeenis deeply alarming.

“It is the second largest increase acrossScotlandand more than three times the national average.”

The Nats MSP added: “Aberdeen Royal Infirmary is not the only hospital in which, on any night of the week, beds and trolleys are blocked by people sleeping off the effects of drink.

“Do taxpayers think that is a good use of their money and health professionals’ time? I do not think so.”

Dr Pauline Strachan, director of acute services at NHS Grampian, told a Holyrood committee: “If we look at accident and emergency attendance it was traditionally 20 to 30-year-olds.

“Now we see children as young as 10, 11 or 12 being presented in a drunken state.

“There had been a 60 per cent increase in children under 16 being admitted drunk at accident and emergency.

“Also about 20 or 25 years ago, it tended to be 50 or 60-year-olds who had chronic liver disease.

“Now it’s not unusual for people in their 20s.”

Ambulance chiefs inAberdeenrecently revealed they dealt with more than 6,000 calls during popular drinking times last year.

NHS Grampian said: “Alcohol misuse places an unnecessary burden on emergency services.”

Source:scottish-sun@the-sun.co.uk   15^th June 2010

A new assessment tool may allow doctors to evaluate the impact of methamphetamine on babies exposed in the womb. The tool may help identify which babies will go on to develop problems due to exposure to the drug, according to a new study.

Medical News Today reports that doctors at the Warren Alpert Medical School of Brown University andWomen & InfantsHospital inProvidence,RI, looked at the effects of prenatal exposure to methamphetamine in 185 newborns and compared them with 195 newborns who were not exposed to meth, but were exposed to alcohol, tobacco or marijuana before birth.

They reported at the Pediatric Academic Societies meeting inDenver that an assessment tool called the NICU Network Neurobehavioral Scale (NNNS) was used to evaluate the babies during the first four days of life and again when they were one month old.  The tool evaluates the babies’ muscle tone, reflexes, behavior, motor development and stress.

The researchers said that the tests could help identify which babies are doing well and which are the ones who could benefit from intervention and prevention services.

Source: www.drugfree.org/join-together  3^rd May 2011

The blood pressure drug propranolol may help treat cocaine addiction, a new animal study suggests. The study investigated the behavior of rats repeatedly given injections of cocaine in a particular cage. The rats learned to associate the positive feelings of cocaine with the cage, much as humans associate the high of cocaine with the environment in which they use the drug, Time reports.

The researchers found that rats given propranolol before they were allowed to enter the cocaine cage, no longer showed a preference for it over any other cage. Rats who were given shots of saline instead of the blood pressure drug continued to seek out the cocaine cage for at least two weeks.

In humans, propranolol might dull the pleasant associations of cocaine, the article says. The cravings that accompany those feelings might also dissipate, and that in turn could reduce the risk of a relapse. The article notes that propranolol has been studied as a treatment for post-traumatic stress disorder, with mixed results.

The new study appears in the journal Neuropsychopharmacology

Source:www.drugfree.org.  July 2011

Background

Alcohol is responsible for a significant portion of the global burden of disease. There is widespread concern reported in the media and other sources about drinking trends among young people, particularly heavy episodic or “binge” drinking. Prominent among policy responses, in theUKand elsewhere, have been attempts to manage antisocial behaviour related to intoxication in public spaces. Much less attention has been given to the longer term effects of excessive drinking in adolescence on later adult health and well-being. Some studies suggest that individuals “mature out” of late adolescent drinking behaviour, whilst others identify enduring effects on drinking and broader health and social outcomes in adulthood.

If adolescent drinking does not cause later difficulties in adulthood then intervention approaches aimed at addressing the acute consequences of alcohol, such as unintentional injuries and anti-social behaviour, may be the most appropriate solution. If causal relationships do exist, however, this approach will not address the cumulative harms produced by alcohol, unless such intervention successfully modifies the long-term relationship with alcohol, which seems unlikely. To address this issue a systematic review of cohort studies was conducted, as this approach provides the strongest observational study design to evaluate evidence for causal inference.

Methods

A systematic review was undertaken of the available literature using relevant online databases and standard systematic review literature search techniques. The search parameters included database articles from 1964 to 2008. This approach was supplemented through the use of hand searching of key journals, citation searching and contact with the primary authors of relevant studies. A data collection protocol was developed and the entire process was undertaken independently on two occasions by different researchers. All subsequent study tasks were also duplicated. Only peer-reviewed published data were used and further unpublished information was not sought from authors.

Studies of drinking behaviour were included if they collected data on at least two points in time, were at least 3 years apart, and from the same cohort. Cohorts formed from general population sources, including college students and military conscripts, were included. Studies based on selected or special populations such as children of alcoholics, mental health patients, and offenders were excluded.

We evaluated the strength of causal inference possible in these studies by assessing whether all possible contributing factors (confounders) had been taken into account. We also gave greater weight to studies that had follow-up rates of 80% or greater, and which had sample sizes of 1,000 participants or more.

Results

Fifty-four studies were eligible for inclusion in this review. Approximately half of all reports (n = 26) were from US studies, ten were fromSweden, eight fromBritain, four fromNew Zealand, three fromAustralia, two fromFinland, and one from theNetherlands. More than half (n = 30) originated from school-based cohorts. Birth cohorts were more likely to be the subject of multiple studies (n = 11/14). Nineteen (35%) studies, based on eight different cohorts, were assessed as having stronger capacity for causal inference), and we focussed primarily on these studies.

The main results were as follows –

• The majority of the studies provided evidence for a link between adolescent drinking and drinking behaviour in later adulthood.
• All studies assessing alcohol problems or dependence in adulthood found statistically significant associations with late adolescent drinking.
• Mortality was examined in only one cohort; the Swedish Conscript Study. It found that late adolescent heavy drinkers were twice as likely to have died compared to moderate drinkers by the mid-thirties. The majority of these deaths were due to car crashes and suicides. The risk of death due to alcohol specific causes (e.g. alcohol intoxication, liver cirrhosis) was also higher for this group.
• One study found no effect of adolescent drinking on court convictions or property offences by age 21, however one other study found that adolescent alcohol problems were predictive of official recorded criminal convictions by the mid-thirties.
• There was no effect of adolescent drinking on any of the mental health outcomes included in the studies, apart from the study noted above which did find that heavier adolescent drinkers had a higher risk of suicide in adulthood.
• One of the studies identified a small but significant effect of adolescent alcohol use on later tobacco use, however a similar relationship was not observed in other studies once confounding factors present in late adolescence were controlled.
• The majority of studies found that there was no association between adolescent drinking and drug use or dependence, after controlling for confounding.
• One study found a link between adolescent drinking at age 16 and educational attainment at age 42, however this effect was only evident in men.

Discussion

This systematic review investigated whether late adolescent alcohol consumption is a time-limited activity without significant longer term consequences or whether it impacts upon adult health and well being. It is clear that the evidence base on long-term consequences is not as extensive nor as compelling as it could be. There is a large evidence base attesting to the ongoing impacts of late adolescent drinking on adult drinking behaviours, though most studies cannot strongly support causal inferences because of their designs. There is robust evidence from one US National school cohort that apparent effects on later alcohol consumption persist beyond the age of 30, which is longer than had previously been understood. Possible effects on subsequent alcohol problems including dependence are somewhat more complex than effects upon subsequent alcohol consumption per se. Evidence from multiple well-designed cohort studies indicates that other factors indicative of heightened psychosocial risk more broadly are also implicated. It is nonetheless striking that effects on alcohol problems assessed at ages in the mid 30s appear to have been produced by elevated consumption in late adolescence. Findings from a rigorousNew Zealandbirth cohort study on nonalcohol outcomes, however, demonstrate that many apparent effects of late adolescent drinking are actually due to other factors. Certainty about the long-term consequences of late adolescent drinking is thus not easily achieved.

Notwithstanding the limitations of the evidence base and of this review, and attenuations over time in the strength of the direct effects, late adolescent alcohol consumption appears a probable cause of increased drinking well into adulthood, through to ages at which adult social roles have been achieved. Heavier drinking seems most likely, however, to be only one component in a complex causal process. The contribution of adolescent drinking has probably been overestimated in previous studies through not taking accouint of other possible explanations. There are also uncertainties induced by self-reported data. The importance of these findings is highlighted in the context of work showing strong stability of drinking patterns through the fourth and fifth decades of life. A wide range of health and other harms, such as liver cirrhosis, are caused by alcohol at middle and older ages. Late adolescent drinking, by virtue of its probable effect on long-term adult alcohol consumption is likely to contribute to the burden of alcohol-related disease. Continuities from adolescence to adulthood in drinking patterns have been observed across a range of measures including frequency of consumption and heavy drinking.

In this study it seems that alcohol consumption confers additional risk of alcohol problems both on those who are already more vulnerable in various ways to poorer health and psychosocial outcomes, and strikingly also among those who are not otherwise vulnerable. Possible effects on adult alcohol problems and dependence including hospitalisation identified here result from heavier drinking in adolescence without necessarily involving problems at younger ages. If these effects are confirmed, there are two important implications: (1) Reducing late adolescent alcohol consumption in the general population may be expected to make a long-term contribution to reducing the incidence of adult alcohol problems; (2) In more vulnerable populations, late adolescent drinking may be one cause among many of later difficulties, and its effects may be more severe and long-lasting than for other groups. Having relatively secure psychosocial resources may somewhat buffer these risks, and their consequent potential for adverse effects, but it does not remove them. These statements should be read with some caution given studies of mediators and moderators of these effects are lacking, limiting our understanding of their nature. Nevertheless, this systematic review affords more secure inference of the likely existence of these effects than has been possible previously. It is possible that relationships with alcohol forged during late adolescence may have cumulative lifetime drinking related consequences that are also simply not well captured by the existing literature.

In addition to making both alcohol and heavy drinking less available, less acceptable, and more expensive, these findings indicate a need for policy makers to encourage young people to be more cognisant of the long-term risks to adult health and well-being, and to act on this awareness in their decision making about whether and how much to drink. This encouragement requires much more than the provision of accurate information about risks if it is to have any real prospect of influencing actual behaviour. Alcohol harm reduction has largely been concerned with reducing various risks inherent in drinking situations and their immediate aftermaths. This study demonstrates the need to develop a longer term perspective on harm reduction.

Source:Alcohol Insights No.80

Abstract

A review of the existing literature on the occurrence of challenging behavior among children with prenatal drug exposure was conducted. While a large number of studies were identified that evaluated various outcomes of prenatal drug exposure, only 37 were found that directly evaluated challenging behaviors. Of the 37 studies, 23 focused on prenatal cocaine exposure, and 14 focused on prenatal alcohol exposure; most studies relied on broadband measures such as the CBCL for the assessment of challenging behavior. Among the 37 studies, a clear role for the postnatal environment on developing challenging behaviors was evident; however, prenatal alcohol exposure showed a much clearer independent effect upon challenging behaviors than was noted in the prenatal cocaine studies. Additionally, only 3 of the 37 studies addressed interventions for challenging behaviors, each of which showed an improvement in child behavior or parent-child interactions. As researchers have continued to show the importance of the postnatal environment, it is likely that interventions addressing specific environmental risk factors will be helpful to reduce or prevent challenging behaviors among this population.

Source:  http://www.ncbi.nlm.nih.gov/pubmed/18037268  Dec. 2008

 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

The NDPA have encouraged many individual users to get into treatment for their addiction. In some cases they have had to ‘fight’ for funding to get into residential rehab – with a further fight to stay for secondary treatment, i.e. 24 weeks instead of 12. The best chance for long term drug dependent users is a minimum of 6 months residential rehab. We can guarantee that no users in a residential rehab would ever be rewarded with drugs.

Heroin and cocaine addicts on the government’s treatment programme are being given drugs as a reward for clean urine samples, the BBC has learned. The National Treatment Agency (NTA), which runs the £500m-a-year scheme, admits the practice is “unethical”. Its own survey of almost 200 clinics in England found users were being offered extra methadone, a heroin substitute, or anti-depressants for good behaviour. Health Minister Dawn Primarolo has asked for a report into the survey. She said the survey had raised “very serious issues”. She said, “It is unacceptable, unethical, it should not happen that prescription drugs and doses are used, or suggested that they should be used, as either incentives or withheld as sanctions as part of a treatment programme.”

Best principles

A third of clinics in the survey said users who produced a drug-free urine sample may be offered increased doses of heroin substitute as a reward – known as “contingency management”. A quarter admits that clients can choose the type of substitute drugs they want. The survey also found clinicians offering anti-depressants, cash vouchers or access to detox as a reward. The NTA said offering drugs for anything other than clinical need was wrong and it wanted certain practices “squeezed out of the system”.

The agency’s chief executive Paul Hayes told the BBC, “One of the things that’s important before we start rewarding people through things like contingency management is to make sure that we’re doing it according to the best principles for drug treatment.”

“There are a range of practices associated with drug misuse in this country that are not what we would want them to be.”  He said the NTA was set up to not only expand the provision of drug treatment, but also to improve its quality.

Very different

He added, “It is entirely appropriate to prescribe other drugs alongside prescription drugs that are to deal with withdrawal. Not as a reward, which is why we wouldn’t advocate it.”

“What we would say is the dose people get ought to be determined by the individual’s needs, not by whether or not they’re co-operating with the regime. That’s why the contingency management programme that we’re thinking of introducing, based on American research, is going to be very different to the ad hoc rewards that operate in not very well managed services in this country at the moment.”

Martin Barnes, chief executive of drug information charity DrugScope, said it was “appalling” to offer drugs as a reward. “It is a complete distortion of the principles of ‘contingency management’,” he said. “The practice is unethical, contrary to official guidance and creates potentially serious risks for the drug user.”

Matthew Taylor, of the Royal Society of Arts, a think tank looking at how best to get addicts off drugs, said an overhaul of current policies was needed.

General problem

“I think the reality is that our drug strategy just isn’t working,” he told BBC One’s Breakfast.

“Only a very small proportion of those people who are put through drug detoxification successfully complete the programme, and even when people do successfully complete the programme they revert to drug use very quickly.”

“So we need a different approach, and the fact that some people feel that they need to incentivise drug users with other drugs in order to keep them off illegal drugs is, I think, part of that general problem.”

Dr Michael Ross, former clinical director of Bradford’s drug dependency service, said drug addicts needed to be self-motivated to achieve results. “The idea of bribing the patient to achieve a result which wasn’t actually something they felt important is quite abhorrent.” he said.

The drugs treatment project is the centrepiece of government strategy. Only about 6% of users on the programme leave free of drugs each year. However, there is evidence that giving addicts access to services can reduce crime and improve health even if they continue to take drugs.

Source: Daily Dose. Oct. 18^th, 2007

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

Opioid use just before conception or in early pregnancy has been associated with an increased risk for birth defects, including hypoplastic left heart syndrome, one of the most critical heart defects.
According to an ongoing, population-based study conducted by the Centers for Disease Control and Prevention (CDC), women receiving opioid analgesic treatment in early pregnancy had a 2- to 3-fold increased risk of delivering infants with conoventricular septal defects, atrioventricular septal defects, hypoplastic left heart syndrome, spina bifida, or gastroschisis.
“It’s important to acknowledge that although there is an increased risk for some types of major birth defects from an exposure to opioid analgesics, that absolute risk for any individual woman is relatively modest,” principal investigator Cheryl S. Broussard, PhD, from the CDC’s National Center on Birth Defects and Developmental Disabilities, said in a news release.
“However, with very serious and life-threatening birth defects like hypoplastic left heart syndrome, the prevention of even a small number of cases is very important,” she said.

Source: The study was published online February 24 in the American Journal of Obstetrics and Gynecology.

• Those who started smoking the drug at college were 90 per cent more likely to have psychotic symptoms in their mid-20s
• Some users suffered psychotic symptoms including hallucinations, delusions and disordered thoughts
Young people who use cannabis are doubling their risk of developing psychotic symptoms, experts warn. And mental health problems persist among those who continue using it compared with those who stop, according to research by an international team of scientists.
Their study adds to mounting evidence that smoking cannabis can trigger psychotic illnesses such as schizophrenia in vulnerable youngsters. It appears to demolish counter-arguments that cannabis does not cause symptoms of mental illness, or that some turn to the drug as a form of self-medication to deal with them.
The research also shows a link with psychosis at a very early stage of use among young people who previously never experienced such symptoms. They include paranoid ideas, hallucinations, hearing voices or bizarre behaviour.
The study, by a team from Germany, the Netherlands and the Institute of Psychiatry in London, focused on more than 1,900 volunteers aged 14 to 24 living in Germany. It followed up with the group after three years and eight years.
Those who had not previously used cannabis but began to during the study had double the risk of developing psychotic symptoms, it found. If they carried on using it, they were at an increased risk of psychotic experiences compared with those who did not. There was also no evidence that suffering psychotic symptoms was likely to result in people turning to cannabis for relief.
Reporting on their findings in the British Medical Journal, the team concluded: ‘Cannabis use precedes the onset of psychotic symptoms in individuals with no history of them.’
Cannabis may also increase the risk of lasting harm to mental health by making such symptoms persist with continued use. Last month, Australian researchers found that cannabis use accelerates the onset of full-blown mental illness almost three years earlier in people at risk.
Sir Robin Murray, professor of psychiatric research at the Institute of Psychiatry, said of the latest study: ‘It is one of ten prospective studies all pointing in this same direction. In short, it adds a further brick to the wall of evidence showing that use of traditional cannabis is a contributory cause of psychoses like schizophrenia.
‘It adds new information by showing that it is those who show psychotic symptoms within a few years of initiating cannabis use who are especially likely to develop persistent psychotic symptoms if they persist in their use of cannabis.’
Previous research has shown that a quarter of the population has a genetic predisposition which makes them ten times more likely to develop psychosis and other schizophrenia-like symptoms after smoking cannabis. Experts warn that anyone with pre-existing mental health problems or family history is at increased risk of mental illness if they use cannabis.
In a BMJ commentary, Professor Wayne Hall, from the University of Queensland, and Professor Louisa Degenhardt, from the Burnet Institute in Melbourne, say the link is biologically plausible and more information should be given to young people about the risks. ‘The case is strengthened by evidence that regular cannabis use in adolescence predicts poorer educational outcomes, increased risk of using other illicit drugs, increased risk of depression and poorer social relationships in early adulthood’, they added.

Source: http://www.dailymail.co.uk/health/article 2nd March 2011

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

Just under 9% of HIV-positive individuals in the UK are co-infected with hepatitis C virus, investigators report in the Journal of Viral Hepatitis.
“In comparison with other large cohort studies, the overall HCV [hepatitis C virus] prevalence of 8.9% in the UK…is low,” comment the investigators. They believe that this is because of the low prevalence of HIV among injecting drug users in the UK. However, approximately 20% of HIV-positive patients in the UK have never been tested for hepatitis C, despite guidance that all patients should be screened annually.
Encouragingly, there was no evidence that co-infection resulted in a poorer response to antiretroviral therapy. Liver disease caused by hepatitis C is now a major cause of illness and death in HIV-positive patients. However, detailed information on the prevalence of hepatitis C among HIV-positive individuals in the UK is lacking. There is also little information on hepatitis C testing and the impact of co-infection on responses to HIV therapy
Therefore investigators from the UK Collaborative HIV Cohort (UK CHIC) undertook an observational study involving 31,765 patients provided with care at ten specialist HIV clinics between 1996 and 2007. Prevalence of co-infection (determined by a positive hepatitis C antibody result), trends in testing, and responses to HIV therapy were monitored. Overall, 64% of patients had been tested for hepatitis C at least once. The proportion of patients screened for the virus increased from 9% in 1996 to 80% in 2007.
“There has been a clear instruction that all HIV-positive patients should be screened since at least 2004,” write the investigators. Nevertheless, “20% of patients under follow-up in 2007 had not apparently ever been tested. The latest BHIVA [British HIV Association] guidelines recommend screening all HIV-positive patients at diagnosis, with annual repeat testing in those who are negative.”
Testing rates differed according to HIV risk group, and was highest for gay men (74%), followed by heterosexual men and women (63%). Although injecting drug use is a well-established risk factor for hepatitis C, only 50% of individuals with a history of injecting drug use had been tested for the virus.
However, the investigators think that the true prevalence of testing in this group is likely to be higher. They comment: “these patients may be more likely to have been tested previously.” The researchers also suggest that the higher rates of mortality and loss to follow-up among injecting drug users could also mean this group were less likely to be screened for hepatitis C.
Overall prevalence of hepatitis C was 9%, and prevalence was 8% among those who were receiving care in 2007. By contrast, prevalence in the general UK population is estimated to be 0.44%. The investigators suggest that the significantly higher prevalence of the infection among patients in the UK CHIC reflects “the shared transmission routes of HCV and HIV.”
Prevalence of hepatitis C differed between HIV risk groups. It was highest in injecting drugs users (84%), followed by gay men (7%), and heterosexual men and women. However, the investigators suggest that some hepatitis C infections in gay men may actually be due to injecting drug use, who suggest that this behaviour may be “underreported by some MSM [men who have sex with men], sufficient to place them at risk of HCV infection…underreporting of IDU as a risk for HCV transmission in MSM may also affect other cohorts.”
Most co-infected patients were men (80%), white (82%), and their median age was 37. The strongest independent risk factor for co-infection with hepatitis C was HIV transmission group. Injecting drug users were significantly more likely to be co-infected than all other risk groups (p < 0.0001).
The impact of co-infection on responses to antiretroviral therapy was analysed in the 9669 patients who started HIV treatment after 2000. A total of 4% of these patients were co-infected. Overall, 91% of patients achieved an undetectable viral load. Co-infected patients were just as likely as individuals who were only infected with HIV to achieve this outcome. There was no association between co-infection and subsequent rebound in viral load. In addition, CD4 cell count increases were comparable between co-infected and HIV-mono-infected patients.
“We found no association between HCV co-infection and either the initial virological response, the rate of viral rebound or the CD4 count response,” emphasise the investigators. They note that results from the Swiss HIV cohort study showed that co-infection did not have an impact on virological responses to therapy.
“The overall cumulative prevalence of HCV of 8.9% in UK CHIC is lower than other cohorts among whom the proportion of IDU is higher,” conclude the researchers. However, they emphasise that this rate of co-infection still “represents a substantial burden of disease.”

Source:www.aidsmap.com Feb 14th 2011

Young people who misuse drugs and alcohol are at a greater risk for continuing this behavior into their middle-aged years, according to research by Yasmina Molero Samuelson at Sweden’s Center for Psychiatric Research (CPF), Karolinska Institutet. They are also more likely to suffer from physical, financial and mental health problems and experience more accidents, suicide attempts and premature death.
“What we can see is that adolescent antisocial behavior, manifested through substance misuse and delinquency, significantly increases the risk of various types of psychosocial problems in adulthood, even into middle age,” said Samuelson.
Samuelson analyzed two large groups of adolescents who had been in treatment for drug use at a clinic in Stockholm, Sweden during the end of the 1960s and the beginning of the 1980s. The analysis ended in 2002, and the participants were compared to two matched samples from the average population.
The results revealed that teens treated for substance abuse continued to suffer from psychosocial problems well after treatment, even up to age 50, to a far greater extent than those in the matched samples. They also had a higher risk of experiencing several coexisting problems in adulthood.
Interestingly, females with substance abuse issues and delinquency showed an equal risk of developing psychosocial problems as adults as their male counterparts. A significant number of girls who were treated at the clinic committed crimes in both adolescence and adulthood. Overall, the crimes committed by both males and females included non-violent crimes, violent crimes, and substance-related crimes.
“This emphasizes the importance of early and effective interventions in order to prevent a negative development that risks being maintained for most of a person’s life,” said Samuelson.
The variety of problems still experienced well into adulthood suggests that treatment interventions during teen years should not only focus on the specific substance abuse or delinquency, but should also evaluate and treat problems in other areas of life as well.
“The results also clearly show the importance of not overlooking young girls in these types of contexts, since they too demonstrate severe antisocial behavior, and are equally at risk of developing problems throughout their lives as their male counterparts,” said Samuelson.

Source: www.psychcentral.com 11 Feb.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

Academics at Northumbria University have demonstrated a link between teenage binge drinking and damage to prospective memory.

Prospective memory is an important aspect of day-to-day memory function and is defined as the cognitive ability to remember to carry out an activity at some future point in time. Examples include remembering to attend an appointment at the dentist or to carry out a task such as remembering to pay a bill on time.

In the first study to examine the effects of binge drinking on prospective memory in teenagers, researchers tested the ability of fifty students from universities in North East England to remember a series of tasks. The students were shown a 10-minute video clip of a shopping district in Scarborough and were asked to remember to carry out a series of instructions when they saw specified locations.
Twenty-one of the students were categorized as binge drinkers. For women, this meant that they drank the equivalent of six standard glasses of wine or, for men, six pints of beer, two or more times a week. The remaining 29 participants were categorised as non-binge drinkers.

The study found that the binge drinkers recalled significantly fewer location-action/items combinations than their non-binging peers. These findings were observed after screening out teenagers who used other substances (such as ecstasy, cannabis and tobacco), those who had used alcohol within the last 48 hours, and after observing no between-group differences on age, anxiety and depression.

Dr Tom Heffernan led the study. He comments: “The mechanisms that may underlie such everyday cognitive impairments associated with binge drinking are not yet fully understood. It is possible that excessive drinking may interfere with the neuro-cognitive development of the teenage brain.

“It is important to realise that there no ‘safe’ levels of drinking set for teenagers and that the amount of bingeing revealed in the present study represents a high volume of alcohol intake across the two to three bingeing sessions which were the norm in the group. The high levels of drinking amongst teenagers is particularly worrying given the mounting evidence that the teenage brain is still maturing and undergoing significant development in terms of its structure and function.
“Given that teenagers are inexperienced drinkers who have both a low tolerance for alcohol and immature neuro-physiological systems, they should therefore be drinking much less than the ‘safe’ levels recommended for adults.”

Intriguingly, one other finding of the study is that binge drinkers do not perceive themselves to have a poor memory, suggesting teenagers do not appreciate the damage that is being done.

Source: T. Heffernan, R. Clark, J. Bartholomew, J. Ling, S. Stephens. Does binge drinking in teenagers affect their everyday prospective memory? Drug and Alcohol Dependence, 2010; 109 (1-3): 73 DOI: 10.1016/j.drugalcdep.2009.12.013 Northumbria University (2010, July 29).

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

BY MARK HENDERSON, SCIENCE CORRESPONDENT

ONE in four people carries genes that increases vulnerability to psychotic illnesses if he or she smokes cannabis as a teenager, scientists have found.
A common genetic profile that makes cannabis five times more likely to trigger schizophrenia and similar disorders has been identified, increasing pressure on the Government to reverse the drug’s reclassification from Class B to Class C.

The increased risk applies to people who inherit variants of a gene named COMT who also smoked cannabis as teenagers. About a quarter of the population have this genetic make-up, and up to 15 per cent of the group are likely to develop psychotic conditions if exposed to the drug early in life.
Neither the drug nor the gene raises the risk of psychosis by itself.
The study, led by Avshalom Caspi and Terrie Moffitt, of the Institute of Psychiatry at King’s College London, offers the best explanation yet for the way that cannabis has a devastating psychiatric impact on some users but leaves most unharmed. Scientists had suspected that genetic factors were responsible for this divide, but a gene had not been pinpointed.
The findings, to be published in Biological Psychiatry, also reinforce a growing consensus that nature and nurture are not mutually exclusive forces but combine to affect behaviour and health. The King’s team has previously identified genes that raise the risk of depression or aggression, but only in conjunction with environmental influences.
Mental health campaigners said that the results vindicated their concerns about the decision last year to downgrade cannabis to a Class C drug, which means that possession is no longer an arrestable offence.
Marjorie Wallace, chief executive of the mental health charity Sane, said that it was becoming clear that cannabis placed millions of users at risk of lasting mental illness. About fifteen million Britons have tried cannabis, and between two million and five million are regular users, according to the Home Office British Crime Survey. The research suggests that a quarter could be at risk.
The evidence will be considered by a review of the drug’s classification announced last month by the Home Secretary. It may be possible to develop a test for genetic susceptibility to cannabis. “If we were able genetically to identify the vulnerable individuals in advance, we would be able to save thousands of minds, if not lives,” Ms Wallace said.
Dr Caspi, however, rejected the idea of screening based on the COMT gene. “Such a test would be wrong more often than it is right. Cannabis has many other adverse effects, especially on developing teenagers, on respiratory health and possibly on cognitive function. Effects may be pronounced among a genetically vulnerable group but that doesn’t mean we should encourage others not genetically vulnerable to use cannabis.”
The King’s team tracked 803 men and women born in Dunedin, New Zealand, in 1972 and 1973, who were enrolled at birth in a research project. Each was interviewed at 13, 15 and 18 about cannabis use, tested to determine which type of COMT genes they had inherited, and followed up at 26 for signs of mental illness.
COMT was chosen as it is known to play a part in the production of dopamine, a brain-signalling chemical that is abnormal in schizophrenia. It comes in two variants, known as valine or methionine, and every person has two copies, one from each parent.
Among people with two methionine variants, the rate of psychotic illness was 3 per cent, the background rate for the general population, regardless of whether they had used cannabis as teenagers.
Among those with two valine variants the rate was 3 per cent for non-users but 15 per cent for those who had smoked cannabis in their teens.
Dr Caspi said research had shown that the valine gene variant and cannabis affect the brain’s dopamine system in similar fashion, suggesting that they deliver a “double dose” that can be damaging. The work needs to be replicated by others to confirm the findings, Dr Caspi said. It also is possible that the gene involved is not COMT but a neighbour.
THE DRUG OF CHOICE FOR MILLIONS
• Cannabis was reclassified from a Class B to a Class C drug in January 2004. Possession remains illegal, but is not an arrestable offence. The Home Secretary has asked for a review by November
• The Home Office estimates that fifteen million people have tried cannabis, two million to five million are regular users and reclassification has saved 199,000 hours’ police work
• Liberalisation campaigners argue that millions smoke the drug with fewer ill-effects than others suffer from alcohol or tobacco
• A recent study at Maastricht University found that cannabis doubles the risk of schizophrenia, hallucinations and paranoia among a genetically susceptible group

Source: www.timesonline.co.uk 14 April 2005

Half of all U.S. children live in a house where a parent or other adult uses tobacco, drinks heavily or uses illegal drugs, according to a report released on Tuesday.
These adults are three times more likely to abuse their children and four times more likely to neglect them than parents who do not abuse alcohol or drugs or use tobacco, said the report from Columbia University’s National Center on Addiction and Substance Abuse.
“Children of alcohol and drug abusers are at increased risk of accidents, injuries and academic failure. Such children are more likely to suffer conduct disorders, depression or anxiety, conditions that increase the risk children will smoke, drink and use drugs,” the center said in a statement.
The report is an analysis of the center’s own research as well as dozens of reports from groups ranging from Alcoholics Anonymous, U.S. government surveys on families and health behavior and the Children’s Defense Fund, a nonprofit social welfare organization. It found that 35.6 million U.S. children, about half of all children in the country, live in a home where a parent or other adult uses tobacco, drinks heavily or uses illicit drugs.
More than 37 percent of U.S. children live with an adult who uses tobacco, nearly 24 percent live with a binge or heavy drinker and 12.7 percent live in a household where a parent or other adult uses illicit drugs, the report found.
Several studies show that children exposed to household cigarette smoke have a higher risk of sudden infant death syndrome, asthma and ear infections. They are more likely to have their tonsils or adenoids surgically removed and recent studies show they have a bigger risk of cancer and heart disease.
“If substance abusing parents are not concerned about what drugs, alcohol and tobacco are doing to themselves, they should be concerned about the ill effects they have on their children,” center Chairman Joseph Califano said.
“Children of substance abusing parents are much likelier to become substance abusers themselves,” he added.
“A child who gets through age 21 without smoking, using illegal drugs or abusing alcohol is virtually certain never to do so.”

Source: WASHINGTON (Reuters) Mar 29, 2005

[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

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

New research shows that a synthetic analogue of the active component [THC] of marijuana may reduce the inflammation and prevent the mental decline associated with Alzheimer’s disease.

“This research is not only a major step in our understanding [of] how the brain reacts to Alzheimer’s disease, but may also help open a route to novel anti-Alzheimer’s drugs,” says Raphael Mechoulam, professor emeritus of medicinal chemistry at Hebrew University in Jerusalem and discoverer of marijuana’s active component.

To show the preventive effects of cannabinoids on Alzheimer’s disease, researchers at the Cajal Institute and Complutense University in Madrid, led by Maria de Ceballos, conducted studies using human brain tissue, as well as experiments with rats.

Source:The Journal of Neuroscience February 23, 2005

The active ingredient in marijuana may stall decline from Alzheimer’s disease, research suggests. Scientists showed a synthetic version of the compound may reduce inflammation associated with Alzheimer’s and thus help to prevent mental decline. They hope the cannabinoid may be used to developed new drug therapies. The research, by Madrid’s Complutense University and the Cajal Institute, is published in the Journal of Neuroscience.

Source:http://www.biopsychology.com/index. Feb 2005

A cannabis-based drug could help people with Alzheimer’s disease by giving them the “munchies”, researchers say.

Patients with the condition often experience weight loss because they stop recognising when they are hungry. The study does not suggest they should be given cannabis to smoke – instead, they tested a synthetic version of a cannabis extract. It was found the cannabinoid led to weight and reduced agitation, another symptom of the disease. The researchers from the Meridian Institute for Aging in New Jersey looked at a drug called dronabinol which is an artificial version of delta-9 THC, the active ingredient in cannabis.

Dronabinol may reduce agitation and improve appetite in patients with Alzheimer’s disease

Dr Joshua Shua-Haim, Meridian Institute for Aging

Source: BBC report 21 Aug.2003

June 28, 2004
Vol. 13, Issue 26

Nine behaviours and attitudes differentiate students who used marijuana before age 15 from those who had not, according to an analysis of data from the 2002 Maryland Adolescent Survey (MAS). Overall, one-fifth of Maryland 12th grade students reported using marijuana before age 15. A scale of 9 warning signs of early marijuana use among 12thgraders was developed from an analysis of the MAS data (see below). The scale also detected early use among 8th and 10th graders. The more warning signs a student had, the more likely he or she was to have used marijuana early . For example, approximately three-fourths of 12th graders with 6 or more warning signs were early marijuana users, compared to 3% of 12th graders with no warning signs. Students with more warning signs also reported using a greater number of other illegal drugs*and experiencing a greater number of serious problems **resulting from drug and alcohol use report, “Warning Signs for Early Marijuana Users Among Maryland’s Public School Students,” discusses the implications of these findings for intervening with youth and implementing prevention programs. Complimentary copies of the report can be ordered by contacting CESAR at cesar@cesar.umd.eduor 301-405-9770.

Behaviors•
Cigarette use before age 15
•Alcohol use before age 15
•20 or more unexcused absences
•Drug arrest
•Alcohol arrest
Attitudes/Opinions
•Smoking marijuana is safe
•Smoking cigarettes is safe
•My parents think it’s okay to smoke marijuana
•My parents think it’s okay to smoke

SOURCE: Maryland Drug Early Warning System (DEWS), CESAR, “Warning Signs for Early Marijuana Users Among Maryland’s Public School Students,” DEWS Investigates, June 2004. For more information, contact Dr. Eric Wish at ewish@cesar.umd.edu.

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

Long-term alcoholics are running the risk of permanent brain damage, according a study published today.
Research has shown that while the brain can regenerate following damage caused by drink, it struggles more after longer periods.
Scanning technology and computer software was used to analyse how the form, function and size of brains in 15 patients changed over a period of six to seven weeks after they gave up alcohol. The researchers, from the UK, Switzerland and Italy, found that brain size increased by an average of almost 2 per cent 38 days after the start of the study.
Levels of chemicals that indicate how intact the brain’s nerve cells and sheaths are also rose significantly, by around 10 per cent to 20 per cent.
Only one patient appeared to continue to lose brain volume and he was the one who had been drinking the longest, for 25 years, the study found.
Dr Andreas Bartsch, from the University of Wuerzburg in Germany, who led the research, said: “The core message from this study is that, for alcoholics, abstention 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 the capacity for regeneration.” The results of such brain scans could be used to help keep alcoholics motivated on staying sober, Dr Bartsch added.
Furthermore, the findings, published in the online edition of the journal Brain, did not simply reflect rehydration.
“Instead, the adult human brain, and particularly its white matter [where nerve fibres are], seems to possess genuine capabilities for regrowth,” Dr Bartsch said.

Scotsman Source: www.aa-uk.org.uk Dec/ 18 2006

How serious is the child and teenage alcohol problem in your area?
More than 20 children and teenagers are being treated in hospital every day for alcohol-related illnesses, including mental disorders, poisoning and liver disease, according to newly released official data.
The figures, labelled “staggering” by one of Britain’s most senior doctors, show that in the year 2005-6, during which Labour introduced 24-hour drinking, the number of under-18s seeking treatment for alcohol-related health problems leapt by 13% to 8,894, an average of 24 a day.
The research, released in parliament by Caroline Flint, the health minister, shows that the number treated has gone up by 33% since Labour came to power in 1997.
Professor Ian Gilmore, president of the Royal College of Physicians, said: “This is a staggering rise and it is only the tip of the iceberg.
“Drinks sold by supermarkets and off-licences are cheaper than ever, and those shops have been at the front of the queue for 24-hour licences, so it has never been more available.
“The younger they drink, the more likely they are to have alcohol-related problems later in life. It is now commonplace to see men and women in their twenties with end-stage alcoholic liver damage.”
The disease figures released by Flint do not include those people treated for injuries sustained in incidents such as drunken fights or drink-driving.
Separately, the government has released figures for patients treated for alcohol-related conditions in accident and emergency wards, showing that alcohol-related medical emergencies and hospital treatments have doubled since 1997.
In some parts of the country the rise is even steeper. The worst areas include the region formerly covered by Cheshire and Merseyside Strategic Health Authority, where 742 young people were treated last year, a rise of more than 25% in just a year. In Northumberland, Tyne and Wear, the number went up by a quarter.
By contrast, some southern health authorities experienced an improvement. In Bedfordshire and Hertfordshire, for example, there were only 119 cases, a fall of 30%.
In addition to the figures for children and teenagers, the Department of Health data also show that the number of people aged 18 and over treated for alcohol-related illness has gone up from 124,925 to 253,603 since 1997, a rise of more than 100%.
The data, released in a written answer, appear to contradict the government’s claims that the liberalisation of pub opening and supermarket off-sales time would lead to more responsible drinking. They bear out research published earlier this year by the British Association for Emergency Medicine, which found an increase in alcohol-related injuries treated in hospital among all age groups since the change to the drinking laws.
Ahead of its launch of 24-hour opening in November 2005, the government assured voters that there would be tougher controls on underage drinking.
It announced on-the-spot fines for children buying alcohol and tougher penalties for staff serving them.
Tessa Jowell, the culture secretary, said at the time: “The result will be more freedom for responsible adults and tougher treatment for the yobbish minority.”
Labour’s approach to teenage drinking has not always lived up to the responsible image that it likes to project.
In the run-up to the 2001 general election, the party sent text messages to first-time voters telling them, “Don’t give a XXXX for last orders? Vote Labour”. This was an allusion to advertisements for Castlemaine XXXX, the Australian beer.
Dr Gray Smith-Laing, a consultant at the Medway Maritime hospital in Gillingham, Kent, who treats patients with liver disease, said last week: “What we’re seeing is the numbers going up, the age coming down.
“The idea that (24-hour opening) just smooths out the drinking and people drink the same amount over a longer period of time is complete rubbish.”
The Department of Health says that levels of binge drinking have peaked and new facilities such as walk-in centres could explain the growth in treatment for drink-related injuries.
The department said yesterday: “The increased attendances at A&E departments, as seen in recently published figures, began some years ago. Evidence suggests that increased rate of growth of attendances predates the change in licensing laws by several years. In fact, this year growth has actually slowed.”

SOURCE: POSTED BY ALCOHOLICS ANONYMOUS UK AT 7:50 AM MON 25.12.06

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

The number of young people needing treatment for mental or other serious problems caused by smoking cannabis has rocketed by a third, experts revealed last night.
The NHS National Treatment Agency for Substance Misuse revealed cannabis use had taken a heavy toll on 4,400 youngsters last year – or more than ten every day.
They were referred for treatment by psychiatric services or families worried the person’s life was falling apart. In many cases, the user was aged just 18 or 19., the NTA said.
The figures come amid significant falls in the number of 18-24 year old’s needing treatment for abusing other illegal drugs – including cocaine and heroin. Experts say it reflects drug users increasingly opting for cannabis rather than other banned substances.
Four years ago, the number of youngsters with serious cannabis problems was only 3,300. Last year, it was around 3,700. Cannabis users accounted for 29 per cent of all new treatment cases aged under 25 in 2009-10, up from 18 per cent four years previously.
Young people are also turning to so-called legal highs as they seek alternatives to poor-quality cocaine on the streets. NTA chief executive Paul Hayes said: ‘As young adults turn their backs on heroin, crack and cocaine, more of the 18 to 24 age group are seeking treatment for problems with cannabis.
‘There are also indications that some who shun cocaine are taking risks with designer drugs like methedrone, dubbed a legal high until it was banned.
‘Treatment services need to be on the alert, able to respond to changing patterns of drug use and drug dependency. ‘In relation to legal highs, we don’t know what the treatment demand will be. They haven’t been around long enough, we don’t know what their potential to cause addiction is. We know they can cause health harms.’
It follows concern about the increasing availability of the super-strength skunk variety of cannabis – which now accounts for between 70 and 80 per cent of police seizures.
Doctors warn that people who smoke skunk are 18 times more likely to develop psychosis than those who use milder forms of the drug. The researchers, from the Institute of Psychiatry in London, compared data on the health and habits of almost 200 cannabis users.
More than half were being treated for psychosis, in which hallucinations and delusions leave people unable to distinguish between reality and their imagination.
Analysis showed skunk was the drug of choice of those being treated for psychosis, while hash was more likely to be smoked by those without mental health problems.
Cannabis has been linked to a string of vicious killings by young people, including the murder and mutilation of teenager Jodi Jones by her boyfriend Luke Mitchell and the stabbing of fashion designer Lucy Braham by Oxford University student William Jaggs.
In 2004, the then Home Secretary David Blunkett approved the reclassification of cannabis from Class B to Class C. The decision was reversed four years later, on the orders of Prime Minister Gordon Brown, on the grounds it was sending out the wrong message to children that cannabis was harmless.
The government has also stated a determination to crack down on the so-called legal highs. Mephedrone – also known as Meow, Bubbles and M-Cat – was banned and made a class B drug in April.
The Home Office has also announced plans for year-long bans that could be put in place quickly to take new drugs off the market while a comprehensive review of their potential harm is carried out. Roger Howard, chief executive of the UK Drug Policy Commission, said: ‘With the changing nature of drug use, we do need to pay more focus on these new emerging drugs. ‘I think that’s something that people in the field are very aware of. ‘How quickly can the system adjust?’

Source: www.dailymail.co.uk 8th October 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

Exposure to alcohol in the womb can have devastating physical and mental effects – and children in care often suffer disproportionately
Six out of 10 children in care are there because they were abused or neglected, and parental drinking is often a significant factor. But professionals are becoming increasingly aware that some of these children may be victims of alcohol misuse twice over. An estimated 7,000 children are born with foetal alcohol syndrome (FAS) in the UK each year and experts believe that a disproportionate number of them end up in care.
FAS is caused by drinking during pregnancy and falls under the umbrella of foetal alcohol spectrum disorders (FASD), which are characterised by lifelong brain damage and physical defects. The consequences include learning disabilities, hyperactivity, autistic traits and problems with social skills, language and memory.
Life chances
Gareth Crossman, executive director of external affairs at The Adolescent and Children’s Trust (Tact), a charity provider of adoption and fostering services, says: “Young people in care have some of the worst life-chances of children, generally. They are more likely to be homeless, have mental health problems and come into contact with the criminal justice system. These issues are compounded [by FASD] because they cannot interact with the world in the same way as the rest of us.”
FASD have so far failed to register on the government’s radar, suggesting a pressing need for more integrated working between health and social care. Dr Mary Mather, medical adviser to Tact’s foetally affected children’s service, says: “Here we are doing nothing, and we suspect we have a bigger problem than other countries because we have one of the highest rates of teenage pregnancy and binge drinking in Europe.”
Research suggests that lack of diagnosis and support leads to chronic “secondary disabilities” including clinical depression with a high risk of suicide. In theory FAS is easier to diagnose than other disorders on the spectrum because of its characteristic facial features – such as small eyes, a smooth philtrum above the lip and a thin upper lip – but it depends on digital facial photography and computer analysis which is not widely available.
“You need a documented history of involvement with alcohol before birth and obstetric and neonatal records and that’s difficult with children in care,” says Mather. “When a baby is being placed for adoption it is virtually impossible to be sure of the diagnosis.”
Frequent placement breakdowns are likely to be the result. Most referrals to the FASD clinic run by Surrey and Borders Partnership NHS Foundation Trust – the only NHS diagnostic clinic – have been for adopted or fostered children, says consultant psychiatrist Dr Raja Mukherjee. “[The carers] have parented normally before but found they were struggling with this child and have sought help. The thing that causes the biggest problem lifelong is not how you look, but how you behave.”
Addressing behaviour involves using consistent routines, simple language, repetition of instructions and rules, a structured environment and constant supervision – talking therapies do not work. And what needs to be remembered, says Mather, is that “these are not children who won’t, but children who can’t”.
The Adolescent and Children’s Trust: tinyurl.com/32hhm9w
Surrey and Borders NHS partnership NHS Trust: tinyurl.com/3x5gn5z

Source: www.guardian.co.uk September 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)

The number of people admitted into hospital because of GHB poisoning has quadrupled in the period 2004-2009. In total, 1200 persons were admitted in the ER’s of hospitals who had swallowed the party drug (23 persons per week). This was reported by the Consumer and Safety Foundation last Sunday.
Almost sixty percent of the treatments took place in the weekend. It mainly concerns males (69 percent). Something more than half of the victims was in the age of 20 to 29 years, one in five in the age of 30 to 39 (22 percent) and fourteen percent between 15 and 19.

Many of the patients not only used GHB, but also alcohol (34%) or other drugs like XTC (10%), cocaine (7%) or speed (1%). Almost all victims at the ER’s suffer from GHB poisoning, 40 percent need to be admitted into hospital, half of which even at the IC department.

Going ‘out’ because of GHB is regarded as something normal. The Consumer and Safety Foundation wants there to be more education and information on GHB. According to the foundation the party drug now has a too positive image: “It’s cheap, simply to get, people break loose and become jolly and do not suffer a hangover. That image has to change for reality. GHB is addictive and can even be life threatening. And the long term damage to health is not yet known.”

(Source: http://www.veiligheid.nl/csi/veilighe id.nsf/wwwVwContent/M_7CC86ED715F24DE9C125778500330C70) Aug 2010

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

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

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

Combining a randomised trial with a ‘real-world’ test, studies of the Dutch Drinking Less programme have gone further than any others to establish the beneficial impacts of web-based alcohol self-help interventions.

The study was a ‘real-world’ test of a promising Dutch internet-based self-help intervention for problem drinking.
A previous randomised trial employing the methodological safeguards possible in tightly controlled research (particularly the recruitment of a comparison group not given access to the intervention) had established that the intervention reduced drinking. At issue in the featured study was whether similar drinking reductions would be seen when the intervention was made freely available to the general public. If they were, then the assumption could be made that these too were caused by having access to the intervention.

Drinking Less is an on-line, interactive programme with no personal therapist input. Aimed at risky drinkers among the general adult population, the intervention is based on principles derived from motivational interviewing, cognitive-behavioural therapies and self-control training. Its home page offers links to alcohol-related information, treatment services, a discussion forum, and the

Drinking Less self-help programme, the core of the intervention. Over a recommended six weeks (though this is entirely up to the user) the programme guides visitors in preparing to change their drinking, setting goals , implementing change, and finally sustaining it, preferably by drinking within recommended limits.

The earlier trial had found that six months later, at least 17% of adult problem drinkers randomly allocated to this intervention had reduced their drinking to within Dutch guidelines, compared to just 5% allocated to an on-line alcohol education brochure. Before the study, both groups had averaged about 55 UK units a week.

At follow-up, the Drinking Less group had cut consumption to about 36 UK units a week, but the brochure group had barely changed.

The featured study monitored what happened when over 10 months spanning 2007 and 2008 the web site was advertised to the Dutch public. During this time round 27,500 people visited the site, of whom 1625 signed up for the self-help programme, accessing it on average 23 times.

Typically they were well educated, employed, middle-aged men. On average they drank about 50 UK units a week, and nearly all who completed the on-line AUDIT screening questionnaire scored in a range indicative of alcohol abuse or dependence.
During the first seven of the 10 months, 378 of site visitors who signed up to the Drinking Less programme also agreed to participate in research to assess its impact. On average they drank roughly the same amount (95% exceeded Dutch guidelines) as all 1625 who signed up and were also similar in age, sex, employment, and motivation to change.

Despite some statistically significant differences, they were also broadly similar to participants in the earlier randomised trial. Over 8 in 10 had never received professional help for their drinking. A few weeks later a survey suggested that after signing up, nearly 9 in 10 went on to use the programme, though generally only a few times.
Of the 378 in the baseline sample, 153 responded to an on-line follow-up survey six months later. Before signing up to the programme, just 4% had confined their drinking within Dutch guidelines; six month later, 39% did so. They had also nearly halved their average consumption from 50 UK units to 27. On the ‘fail-safe’ assumption that the intervention had no impact on people who were not followed up, still the drinking reductions were statistically significant; from 5%, the proportion drinking within guidelines rose to 19%, and consumption fell from 51 UK units to 42.

Next the analysts compared these results with those from the six-month follow-up in the randomised trial. Based only on respondents to the follow-up surveys, and adjusting for differences between the samples, in the ‘real-world’ test over twice as many (unadjusted figures 36% v. 19%) people moved to drinking within Dutch guidelines. When the assumption was made that in both trials the intervention had no impact on people not followed up, the figures still favoured the ‘real-world’ test (15% v. 10%), but the difference was no longer statistically significant.

The researchers concluded that the featured study had shown that the benefits established by the randomised controlled trial would be sustained when the intervention was made routinely and generally available to the public. The expected throughput of 3000 Drinking Less programme users a year would amount to nearly 3% of the country’s problem drinkers who would otherwise not have received professional help. Probably because they require the drinker to take the initiative and visit the site, such interventions reach people who, compared to the totality of problem drinkers, are more likely to be women, employed, highly educated, and motivated to change their drinking. Given its low cost per user, this type of intervention seems to have a worthwhile place in a public health approach to reducing alcohol-related problems.

Though only a minority of site visitors may sign up for web-based alcohol programmes, nevertheless the numbers engaged can be very large, and the risk-reductions seem of the order typical in studies of brief advice to drinkers identified in health care settings. In these settings screening programmes typically identify people who are not actually seeking help for drinking problems – ‘pushing’ them towards intervention and change – while web sites ‘pull’ in people already curious or concerned about their drinking. As such these two gateways can play complementary roles in improving public health and offering change opportunities to people who would not present to alcohol treatment services. However, in Britain and elsewhere, both tactics reach only small fractions of the population who drinking excessively, leaving the bulk of the public health work to be done by interventions which drinkers generally cannot avoid and do not have seek out, such as price increases and availability restrictions.

With its combination of a randomised trial and a ‘real-world’ test, the featured research programme has gone further than any other in establishing the beneficial impacts of web-based alcohol interventions. However, largely because many site users do not complete research surveys, it remains impossible to be sure that the results seen in such studies will be replicated across the entire usership of the sites. Details below.

Strengths and limitations of the featured study
The featured study’s combination of a randomised trial with all its methodological safeguards, and a ‘real-world’ trial approximating normal conditions, affords what seems to be the best indication to date of the contribution web-based self-help interventions could make to reducing heavy drinking and associated health risks. However, its twin pillars are weakened by the fact that many people either did not join the studies or did not supply follow-up data; those who did may not have been typical of all the people who might access such sites.

In the randomised trial, 40% of the baseline sample did not complete the six-month follow-up survey, and in the featured study, nearly 60%. Though on the measures taken by the study the respondents generally seemed typical of the baseline sample, clearly something was sufficiently different to cause them to respond while the others did not. In both studies this problem was catered for by assuming that non-responders were also non-changers. Though this almost certainly underestimated the impact of the intervention, still in both there remained significant and worthwhile improvements.

What could not be catered for in either study was the degree to which people who join such studies differ from the much greater number who would use the web sites, but decline participation in research. This problem was especially apparent in the featured study, in which it seems that around 6% of site visitors signed up for the self-help programme. Of these, perhaps a third or slightly more of the people who signed up for the programme during the relevant period also agreed to participate in the research. In some important ways (including amount drunk and motivation to change) they seemed similar to the bulk of programme sign-ups, though the researchers suspect they were more likely to have engaged with the programme.

Opening more doors to change for more people
A review of computer-based alcohol services for the general public has rehearsed the advantages: immediate, convenient access for people (the majority in developed nations) connected to the internet; consequently able to capitalise on what may be fleeting resolve; anonymous services sidestep the embarrassment or stigma which might deter help-seeking; such services are available to people unwilling or less able to talk about their problems to a stranger; generally they are free and entail no travel costs or lost income due to time off work; very low operating cost per user if widely accessed; easily updated.

In consumption terms, the drinking problems of web site users are comparable to those of drinkers who seek treatment, yet few have received professional help, perhaps partly because their higher socioeconomic status and greater resources have enabled them to restrict the consequential damage. People who actually engage with web-based assessments of their drinking problems have more severe problems than those who just visit and leave. Including the randomised trial which paved the way for the featured study, the review found eight studies which evaluated the effectiveness of computer-based interventions for the general public.

In all but one the users significantly improved on at least one of the alcohol-related measures recorded by the studies.
A particular role for alcohol self-help sites may be to offer an easy, quick and accessible way to for drinkers to actualise their desire to tackle their problems, especially when that desire is allied with the resources to implement and sustain improvements without face-to-face or comprehensive assistance. After conducting the Project MATCH trial, some of the world’s leading alcohol treatment researchers argued that “access to treatment may be as important as the type of treatment available”. The implication is that in cultures which accept ‘treatment’ as a route to resolving unhealthy and/or undesirable drinking, having convincing-looking and accessible ‘treatment doors’ to go through may be more important than what lies behind those doors, as long as this fulfils the expectations of the client or patient. This is likely to be especially the case for people who retain a stake in conventional society in the form of marriages, jobs, families, and a reputation to lose. These populations – the kind the featured study suggests are attracted to self-help alcohol therapy web sites – have more of the ‘recovery capital’ resources needed to themselves do most of the work in curbing their drinking.

The British Down Your Drink site
The best known British alcohol self-help web site is the Down Your Drink site run by a team based at University College London, an initiative originally funded by the Alcohol Education and Research Council and now by the Medical Research Council’s National Prevention Research Initiative. In 2007 this was revised to offer set programmes from a one-hour brief intervention to several weeks, but also to generally give the user greater control over the use they made of the site. The approach remained based on principles and techniques derived from motivational interviewing and cognitive-behavioural therapies.

The previous version had been structured as six consecutive modules to be accessed weekly. An analysis of data provided by the first 10,000 people who registered at the site after piloting ended in September 2003 revealed that most were in their 30s and 40s, half were women, nearly two-thirds were married or living with a partner, just 4% were unemployed, and most reported occupations from higher socioeconomic strata.

As an earlier study commented, site users were predominantly middle class, middle aged, white and European. Six in 10 either did not start the programme, or completed just the first week. About 17% completed the six weeks. Of these, 57% returned an outcome questionnaire. Compared to their pre-programme status, on average they were now at substantially lower risk, and functioning better and living much improved lives.
The sample had been recruited over about 27 months, a registration rate of about 4500 a year. By way of comparison, in England during 2008/09, around 100,000 adults were treated for their alcohol problems at conventional services. User profile and site usage had been similar during the earlier pilot phase. Results from surveys sent to pilot programme completers indicated that three quarters had never previously sought help for their drinking.

Source: Published in Findings 19 May 2010 Alcoholism: Clinical and Experimental Research: 2009, 33(8), p. 1401–1408

How serious is the child and teenage alcohol problem in your area?

More than 20 children and teenagers are being treated in hospital every day for alcohol-related illnesses, including mental disorders, poisoning and liver disease, according to newly released official data.

The figures, labelled “staggering” by one of Britain’s most senior doctors, show that in the year 2005-6, during which Labour introduced 24-hour drinking, the number of under-18s seeking treatment for alcohol-related health problems leapt by 13% to 8,894, an average of 24 a day.

The research, released in parliament by Caroline Flint, the health minister, shows that the number treated has gone up by 33% since Labour came to power in 1997.

Professor Ian Gilmore, president of the Royal College of Physicians, said: “This is a staggering rise and it is only the tip of the iceberg.
“Drinks sold by supermarkets and off-licences are cheaper than ever, and those shops have been at the front of the queue for 24-hour licences, so it has never been more available.

“The younger they drink, the more likely they are to have alcohol-related problems later in life. It is now commonplace to see men and women in their twenties with end-stage alcoholic liver damage.”
The disease figures released by Flint do not include those people treated for injuries sustained in incidents such as drunken fights or drink-driving.

Separately, the government has released figures for patients treated for alcohol-related conditions in accident and emergency wards, showing that alcohol-related medical emergencies and hospital treatments have doubled since 1997.

In some parts of the country the rise is even steeper. The worst areas include the region formerly covered by Cheshire and Merseyside Strategic Health Authority, where 742 young people were treated last year, a rise of more than 25% in just a year. In Northumberland, Tyne and Wear, the number went up by a quarter.
By contrast, some southern health authorities experienced an improvement. In Bedfordshire and Hertfordshire, for example, there were only 119 cases, a fall of 30%.

In addition to the figures for children and teenagers, the Department of Health data also show that the number of people aged 18 and over treated for alcohol-related illness has gone up from 124,925 to 253,603 since 1997, a rise of more than 100%.
The data, released in a written answer, appear to contradict the government’s claims that the liberalisation of pub opening and supermarket off-sales time would lead to more responsible drinking.

They bear out research published earlier this year by the British Association for Emergency Medicine, which found an increase in alcohol-related injuries treated in hospital among all age groups since the change to the drinking laws.

Ahead of its launch of 24-hour opening in November 2005, the government assured voters that there would be tougher controls on underage drinking.
It announced on-the-spot fines for children buying alcohol and tougher penalties for staff serving them.
Tessa Jowell, the culture secretary, said at the time: “The result will be more freedom for responsible adults and tougher treatment for the yobbish minority.”

Labour’s approach to teenage drinking has not always lived up to the responsible image that it likes to project.
In the run-up to the 2001 general election, the party sent text messages to first-time voters telling them, “Don’t give a XXXX for last orders? Vote Labour”. This was an allusion to advertisements for Castlemaine XXXX, the Australian beer.

Dr Gray Smith-Laing, a consultant at the Medway Maritime hospital in Gillingham, Kent, who treats patients with liver disease, said last week: “What we’re seeing is the numbers going up, the age coming down.

“The idea that (24-hour opening) just smooths out the drinking and people drink the same amount over a longer period of time is complete rubbish.”
The Department of Health says that levels of binge drinking have peaked and new facilities such as walk-in centres could explain the growth in treatment for drink-related injuries.

The department said yesterday: “The increased attendances at A&E departments, as seen in recently published figures, began some years ago. Evidence suggests that increased rate of growth of attendances predates the change in licensing laws by several years. In fact, this year growth has actually slowed.”

SOURCE: POSTED BY ALCOHOLICS ANONYMOUS UK AT 7:50 AM MON 25.12.06

It is well-known that maternal smoking during pregnancy can have long-term effects on the physical health of the child, including increased risk for respiratory disease, ear infections and asthma. New research shows that prenatal smoking also can lead to psychiatric problems and increase the need for psychotropic medications in childhood and young adulthood.

Finnish researchers found that adolescents who had been exposed to prenatal smoking were at increased risk for use of all psychiatric drugs especially those uses to treat depression, attention-deficit/hyperactivity disorder (ADHD) and addiction compared to non-exposed youths. The study was presented Tuesday, May 4 at the Pediatric Academic Societies (PAS) annual meeting in Vancouver, British Columbia, Canada.

“Recent studies show that maternal smoking during pregnancy may interfere with brain development of the growing fetus,” said Mikael Ekblad, lead author of the study and a pediatric researcher at Turku University Hospital in Finland. “By avoiding smoking during pregnancy, all the later psychiatric problems caused by smoking exposure could be prevented.”

Ekblad and his colleagues collected information from the Finnish Medical Birth Register on maternal smoking, gestational age, birthweight and 5-minute Apgar scores for all children born in Finland from 1987 through 1989. They also analyzed records on mothers’ psychiatric inpatient care from 1969-1989 and children’s use of psychiatric drugs.

Results showed that 12.3 percent of the young adults had used psychiatric drugs, and of these, 19.2 percent had been exposed to prenatal smoking.

The rate of psychotropic medication use was highest in young adults whose mothers smoked more than 10 cigarettes a day while pregnant (16.9 percent), followed by youths whose mothers smoked fewer than 10 cigarettes a day (14.7 percent) and unexposed youths (11.7 percent).

The risk for medication use was similar in males and females, and remained after adjusting for risk factors at birth, such as Apgar scores and birthweight, and the mother’s previous inpatient care for mental disorders.

Smoking exposure increased the risk for use of all psychotropic drugs, especially stimulants used to treat ADHD (unexposed: 0.2 percent; less than 10 cigarettes/day: 0.4 percent; and more than 10 cigarettes/day: 0.6 percent) and drugs for addiction. An increased risk for use of drugs to treat depression also was seen (unexposed: 6 percent; less than 10 cigarettes/day: 8.6 percent; and more than 10 cigarettes/day: 10.3 percent).

“Smoking during pregnancy is still quite common even though the knowledge of its harmful effects has risen in recent years,” Ekblad concluded. “Recent studies have shown that smoking during pregnancy has negative long-term effects on the health of the child. Therefore, women should avoid smoking during their pregnancy.”

Source: MediLexicon International Ltd 6th May 2010
American Academy of Pediatrics

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

Combining a randomised trial with a ‘real-world’ test, studies of the Dutch Drinking Less programme have gone further than any others to establish the beneficial impacts of web-based alcohol self-help interventions.

Abstract

The study was a ‘real-world’ test of a promising Dutch internet-based self-help intervention for problem drinking. A previous randomised trial employing the methodological safeguards possible in tightly controlled research (particularly the recruitment of a comparison group not given access to the intervention) had established that the intervention reduced drinking. At issue in the featured study was whether similar drinking reductions would be seen when the intervention was made freely available to the general public. If they were, then the assumption could be made that these too were caused by having access to the intervention.

Drinking Less is an on-line, interactive programme with no personal therapist input. Aimed at risky drinkers among the general adult population, the intervention is based on principles derived from motivational interviewing, cognitive-behavioural therapies and self-control training. Its home page offers links to alcohol-related information, treatment services, a discussion forum, and the Drinking Less self-help programme, the core of the intervention. Over a recommended six weeks (though this is entirely up to the user) the programme guides visitors in preparing to change their drinking, setting goals , implementing change, and finally sustaining it, preferably by drinking within recommended limits.
The earlier trial had found that six months later, at least 17% of adult problem drinkers randomly allocated to this intervention had reduced their drinking to within Dutch guidelines, compared to just 5% allocated to an on-line alcohol education brochure. Before the study, both groups had averaged about 55 UK units a week. At follow-up, the Drinking Less group had cut consumption to about 36 UK units a week, but the brochure group had barely changed.
The featured study monitored what happened when over 10 months spanning 2007 and 2008 the web site was advertised to the Dutch public. During this time round 27,500 people visited the site, of whom 1625 signed up for the self-help programme, accessing it on average 23 times. Typically they were well educated, employed, middle-aged men. On average they drank about 50 UK units a week, and nearly all who completed the on-line AUDIT screening questionnaire scored in a range indicative of alcohol abuse or dependence.
During the first seven of the 10 months, 378 of site visitors who signed up to the Drinking Less programme also agreed to participate in research to assess its impact. On average they drank roughly the same amount (95% exceeded Dutch guidelines) as all 1625 who signed up and were also similar in age, sex, employment, and motivation to change. Despite some statistically significant differences, they were also broadly similar to participants in the earlier randomised trial. Over 8 in 10 had never received professional help for their drinking. A few weeks later a survey suggested that after signing up, nearly 9 in 10 went on to use the programme, though generally only a few times.
Of the 378 in the baseline sample, 153 responded to an on-line follow-up survey six months later. Before signing up to the programme, just 4% had confined their drinking within Dutch guidelines; six month later, 39% did so. They had also nearly halved their average consumption from 50 UK units to 27. On the ‘fail-safe’ assumption that the intervention had no impact on people who were not followed up, still the drinking reductions were statistically significant; from 5%, the proportion drinking within guidelines rose to 19%, and consumption fell from 51 UK units to 42.
Next the analysts compared these results with those from the six-month follow-up in the randomised trial. Based only on respondents to the follow-up surveys, and adjusting for differences between the samples, in the ‘real-world’ test over twice as many (unadjusted figures 36% v. 19%) people moved to drinking within Dutch guidelines. When the assumption was made that in both trials the intervention had no impact on people not followed up, the figures still favoured the ‘real-world’ test (15% v. 10%), but the difference was no longer statistically significant.
The researchers concluded that the featured study had shown that the benefits established by the randomised controlled trial would be sustained when the intervention was made routinely and generally available to the public. The expected throughput of 3000 Drinking Less programme users a year would amount to nearly 3% of the country’s problem drinkers who would otherwise not have received professional help. Probably because they require the drinker to take the initiative and visit the site, such interventions reach people who, compared to the totality of problem drinkers, are more likely to be women, employed, highly educated, and motivated to change their drinking. Given its low cost per user, this type of intervention seems to have a worthwhile place in a public health approach to reducing alcohol-related problems.
Though only a minority of site visitors may sign up for web-based alcohol programmes, nevertheless the numbers engaged can be very large, and the risk-reductions seem of the order typical in studies of brief advice to drinkers identified in health care settings. In these settings screening programmes typically identify people who are not actually seeking help for drinking problems – ‘pushing’ them towards intervention and change – while web sites ‘pull’ in people already curious or concerned about their drinking. As such these two gateways can play complementary roles in improving public health and offering change opportunities to people who would not present to alcohol treatment services. However, in Britain and elsewhere, both tactics reach only small fractions of the population who drinking excessively, leaving the bulk of the public health work to be done by interventions which drinkers generally cannot avoid and do not have seek out, such as price increases and availability restrictions.
With its combination of a randomised trial and a ‘real-world’ test, the featured research programme has gone further than any other in establishing the beneficial impacts of web-based alcohol interventions. However, largely because many site users do not complete research surveys, it remains impossible to be sure that the results seen in such studies will be replicated across the entire usership of the sites. Details below.

Strengths and limitations of the featured study

The featured study’s combination of a randomised trial with all its methodological safeguards, and a ‘real-world’ trial approximating normal conditions, affords what seems to be the best indication to date of the contribution web-based self-help interventions could make to reducing heavy drinking and associated health risks. However, its twin pillars are weakened by the fact that many people either did not join the studies or did not supply follow-up data; those who did may not have been typical of all the people who might access such sites. In the randomised trial, 40% of the baseline sample did not complete the six-month follow-up survey, and in the featured study, nearly 60%. Though on the measures taken by the study the respondents generally seemed typical of the baseline sample, clearly something was sufficiently different to cause them to respond while the others did not. In both studies this problem was catered for by assuming that non-responders were also non-changers. Though this almost certainly underestimated the impact of the intervention, still in both there remained significant and worthwhile improvements.
What could not be catered for in either study was the degree to which people who join such studies differ from the much greater number who would use the web sites, but decline participation in research. This problem was especially apparent in the featured study, in which it seems that around 6% of site visitors signed up for the self-help programme. Of these, perhaps a third or slightly more of the people who signed up for the programme during the relevant period also agreed to participate in the research. In some important ways (including amount drunk and motivation to change) they seemed similar to the bulk of programme sign-ups, though the researchers suspect they were more likely to have engaged with the programme.

Opening more doors to change for more people

A review of computer-based alcohol services for the general public has rehearsed the advantages: immediate, convenient access for people (the majority in developed nations) connected to the internet; consequently able to capitalise on what may be fleeting resolve; anonymous services sidestep the embarrassment or stigma which might deter help-seeking; such services are available to people unwilling or less able to talk about their problems to a stranger; generally they are free and entail no travel costs or lost income due to time off work; very low operating cost per user if widely accessed; easily updated. In consumption terms, the drinking problems of web site users are comparable to those of drinkers who seek treatment, yet few have received professional help, perhaps partly because their higher socioeconomic status and greater resources have enabled them to restrict the consequential damage. People who actually engage with web-based assessments of their drinking problems have more severe problems than those who just visit and leave. Including the randomised trial which paved the way for the featured study, the review found eight studies which evaluated the effectiveness of computer-based interventions for the general public. In all but one the users significantly improved on at least one of the alcohol-related measures recorded by the studies.
A particular role for alcohol self-help sites may be to offer an easy, quick and accessible way to for drinkers to actualise their desire to tackle their problems, especially when that desire is allied with the resources to implement and sustain improvements without face-to-face or comprehensive assistance. After conducting the Project MATCH trial, some of the world’s leading alcohol treatment researchers argued that “access to treatment may be as important as the type of treatment available”. The implication is that in cultures which accept ‘treatment’ as a route to resolving unhealthy and/or undesirable drinking, having convincing-looking and accessible ‘treatment doors’ to go through may be more important than what lies behind those doors, as long as this fulfils the expectations of the client or patient. This is likely to be especially the case for people who retain a stake in conventional society in the form of marriages, jobs, families, and a reputation to lose. These populations – the kind the featured study suggests are attracted to self-help alcohol therapy web sites – have more of the ‘recovery capital’ resources needed to themselves do most of the work in curbing their drinking.

The British Down Your Drink site

The best known British alcohol self-help web site is the Down Your Drink site run by a team based at University College London, an initiative originally funded by the Alcohol Education and Research Council and now by the Medical Research Council’s National Prevention Research Initiative. In 2007 this was revised to offer set programmes from a one-hour brief intervention to several weeks, but also to generally give the user greater control over the use they made of the site. The approach remained based on principles and techniques derived from motivational interviewing and cognitive-behavioural therapies.
The previous version had been structured as six consecutive modules to be accessed weekly. An analysis of data provided by the first 10,000 people who registered at the site after piloting ended in September 2003 revealed that most were in their 30s and 40s, half were women, nearly two-thirds were married or living with a partner, just 4% were unemployed, and most reported occupations from higher socioeconomic strata. As an earlier study commented, site users were predominantly middle class, middle aged, white and European. Six in 10 either did not start the programme, or completed just the first week. About 17% completed the six weeks. Of these, 57% returned an outcome questionnaire. Compared to their pre-programme status, on average they were now at substantially lower risk, and functioning better and living much improved lives. The sample had been recruited over about 27 months, a registration rate of about 4500 a year. By way of comparison, in England during 2008/09, around 100,000 adults were treated for their alcohol problems at conventional services. User profile and site usage had been similar during the earlier pilot phase. Results from surveys sent to pilot programme completers indicated that three quarters had never previously sought help for their drinking.

Source: Published in Findings 19 May 2010 Alcoholism: Clinical and Experimental Research: 2009, 33(8), p. 1401–1408

Combining a randomised trial with a ‘real-world’ test, studies of the Dutch Drinking Less programme have gone further than any others to establish the beneficial impacts of web-based alcohol self-help interventions.
Abstract The study was a ‘real-world’ test of a promising Dutch internet-based self-help intervention for problem drinking. A previous randomised trial employing the methodological safeguards possible in tightly controlled research (particularly the recruitment of a comparison group not given access to the intervention) had established that the intervention reduced drinking. At issue in the featured study was whether similar drinking reductions would be seen when the intervention was made freely available to the general public. If they were, then the assumption could be made that these too were caused by having access to the intervention.

Drinking Less is an on-line, interactive programme with no personal therapist input. Aimed at risky drinkers among the general adult population, the intervention is based on principles derived from motivational interviewing, cognitive-behavioural therapies and self-control training. Its home page offers links to alcohol-related information, treatment services, a discussion forum, and the Drinking Less self-help programme, the core of the intervention. Over a recommended six weeks (though this is entirely up to the user) the programme guides visitors in preparing to change their drinking, setting goals , implementing change, and finally sustaining it, preferably by drinking within recommended limits.
The earlier trial had found that six months later, at least 17% of adult problem drinkers randomly allocated to this intervention had reduced their drinking to within Dutch guidelines, compared to just 5% allocated to an on-line alcohol education brochure. Before the study, both groups had averaged about 55 UK units a week. At follow-up, the Drinking Less group had cut consumption to about 36 UK units a week, but the brochure group had barely changed.
The featured study monitored what happened when over 10 months spanning 2007 and 2008 the web site was advertised to the Dutch public. During this time round 27,500 people visited the site, of whom 1625 signed up for the self-help programme, accessing it on average 23 times. Typically they were well educated, employed, middle-aged men. On average they drank about 50 UK units a week, and nearly all who completed the on-line AUDIT screening questionnaire scored in a range indicative of alcohol abuse or dependence.
During the first seven of the 10 months, 378 of site visitors who signed up to the Drinking Less programme also agreed to participate in research to assess its impact. On average they drank roughly the same amount (95% exceeded Dutch guidelines) as all 1625 who signed up and were also similar in age, sex, employment, and motivation to change. Despite some statistically significant differences, they were also broadly similar to participants in the earlier randomised trial. Over 8 in 10 had never received professional help for their drinking. A few weeks later a survey suggested that after signing up, nearly 9 in 10 went on to use the programme, though generally only a few times.
Of the 378 in the baseline sample, 153 responded to an on-line follow-up survey six months later. Before signing up to the programme, just 4% had confined their drinking within Dutch guidelines; six month later, 39% did so. They had also nearly halved their average consumption from 50 UK units to 27. On the ‘fail-safe’ assumption that the intervention had no impact on people who were not followed up, still the drinking reductions were statistically significant; from 5%, the proportion drinking within guidelines rose to 19%, and consumption fell from 51 UK units to 42.
Next the analysts compared these results with those from the six-month follow-up in the randomised trial. Based only on respondents to the follow-up surveys, and adjusting for differences between the samples, in the ‘real-world’ test over twice as many (unadjusted figures 36% v. 19%) people moved to drinking within Dutch guidelines. When the assumption was made that in both trials the intervention had no impact on people not followed up, the figures still favoured the ‘real-world’ test (15% v. 10%), but the difference was no longer statistically significant.
The researchers concluded that the featured study had shown that the benefits established by the randomised controlled trial would be sustained when the intervention was made routinely and generally available to the public. The expected throughput of 3000 Drinking Less programme users a year would amount to nearly 3% of the country’s problem drinkers who would otherwise not have received professional help. Probably because they require the drinker to take the initiative and visit the site, such interventions reach people who, compared to the totality of problem drinkers, are more likely to be women, employed, highly educated, and motivated to change their drinking. Given its low cost per user, this type of intervention seems to have a worthwhile place in a public health approach to reducing alcohol-related problems.
Though only a minority of site visitors may sign up for web-based alcohol programmes, nevertheless the numbers engaged can be very large, and the risk-reductions seem of the order typical in studies of brief advice to drinkers identified in health care settings. In these settings screening programmes typically identify people who are not actually seeking help for drinking problems – ‘pushing’ them towards intervention and change – while web sites ‘pull’ in people already curious or concerned about their drinking. As such these two gateways can play complementary roles in improving public health and offering change opportunities to people who would not present to alcohol treatment services. However, in Britain and elsewhere, both tactics reach only small fractions of the population who drinking excessively, leaving the bulk of the public health work to be done by interventions which drinkers generally cannot avoid and do not have seek out, such as price increases and availability restrictions.
With its combination of a randomised trial and a ‘real-world’ test, the featured research programme has gone further than any other in establishing the beneficial impacts of web-based alcohol interventions. However, largely because many site users do not complete research surveys, it remains impossible to be sure that the results seen in such studies will be replicated across the entire usership of the sites. Details below.
Strengths and limitations of the featured study
The featured study’s combination of a randomised trial with all its methodological safeguards, and a ‘real-world’ trial approximating normal conditions, affords what seems to be the best indication to date of the contribution web-based self-help interventions could make to reducing heavy drinking and associated health risks. However, its twin pillars are weakened by the fact that many people either did not join the studies or did not supply follow-up data; those who did may not have been typical of all the people who might access such sites. In the randomised trial, 40% of the baseline sample did not complete the six-month follow-up survey, and in the featured study, nearly 60%. Though on the measures taken by the study the respondents generally seemed typical of the baseline sample, clearly something was sufficiently different to cause them to respond while the others did not. In both studies this problem was catered for by assuming that non-responders were also non-changers. Though this almost certainly underestimated the impact of the intervention, still in both there remained significant and worthwhile improvements.
What could not be catered for in either study was the degree to which people who join such studies differ from the much greater number who would use the web sites, but decline participation in research. This problem was especially apparent in the featured study, in which it seems that around 6% of site visitors signed up for the self-help programme. Of these, perhaps a third or slightly more of the people who signed up for the programme during the relevant period also agreed to participate in the research. In some important ways (including amount drunk and motivation to change) they seemed similar to the bulk of programme sign-ups, though the researchers suspect they were more likely to have engaged with the programme.
Opening more doors to change for more people
A review of computer-based alcohol services for the general public has rehearsed the advantages: immediate, convenient access for people (the majority in developed nations) connected to the internet; consequently able to capitalise on what may be fleeting resolve; anonymous services sidestep the embarrassment or stigma which might deter help-seeking; such services are available to people unwilling or less able to talk about their problems to a stranger; generally they are free and entail no travel costs or lost income due to time off work; very low operating cost per user if widely accessed; easily updated. In consumption terms, the drinking problems of web site users are comparable to those of drinkers who seek treatment, yet few have received professional help, perhaps partly because their higher socioeconomic status and greater resources have enabled them to restrict the consequential damage. People who actually engage with web-based assessments of their drinking problems have more severe problems than those who just visit and leave. Including the randomised trial which paved the way for the featured study, the review found eight studies which evaluated the effectiveness of computer-based interventions for the general public. In all but one the users significantly improved on at least one of the alcohol-related measures recorded by the studies.
A particular role for alcohol self-help sites may be to offer an easy, quick and accessible way to for drinkers to actualise their desire to tackle their problems, especially when that desire is allied with the resources to implement and sustain improvements without face-to-face or comprehensive assistance. After conducting the Project MATCH trial, some of the world’s leading alcohol treatment researchers argued that “access to treatment may be as important as the type of treatment available”. The implication is that in cultures which accept ‘treatment’ as a route to resolving unhealthy and/or undesirable drinking, having convincing-looking and accessible ‘treatment doors’ to go through may be more important than what lies behind those doors, as long as this fulfils the expectations of the client or patient. This is likely to be especially the case for people who retain a stake in conventional society in the form of marriages, jobs, families, and a reputation to lose. These populations – the kind the featured study suggests are attracted to self-help alcohol therapy web sites – have more of the ‘recovery capital’ resources needed to themselves do most of the work in curbing their drinking.
The British Down Your Drink site
The best known British alcohol self-help web site is the Down Your Drink site run by a team based at University College London, an initiative originally funded by the Alcohol Education and Research Council and now by the Medical Research Council’s National Prevention Research Initiative. In 2007 this was revised to offer set programmes from a one-hour brief intervention to several weeks, but also to generally give the user greater control over the use they made of the site. The approach remained based on principles and techniques derived from motivational interviewing and cognitive-behavioural therapies.
The previous version had been structured as six consecutive modules to be accessed weekly. An analysis of data provided by the first 10,000 people who registered at the site after piloting ended in September 2003 revealed that most were in their 30s and 40s, half were women, nearly two-thirds were married or living with a partner, just 4% were unemployed, and most reported occupations from higher socioeconomic strata. As an earlier study commented, site users were predominantly middle class, middle aged, white and European. Six in 10 either did not start the programme, or completed just the first week. About 17% completed the six weeks. Of these, 57% returned an outcome questionnaire. Compared to their pre-programme status, on average they were now at substantially lower risk, and functioning better and living much improved lives. The sample had been recruited over about 27 months, a registration rate of about 4500 a year. By way of comparison, in England during 2008/09, around 100,000 adults were treated for their alcohol problems at conventional services. User profile and site usage had been similar during the earlier pilot phase. Results from surveys sent to pilot programme completers indicated that three quarters had never previously sought help for their drinking.
Source: Published in Findings 19 May 2010 Alcoholism: Clinical and Experimental Research: 2009, 33(8), p. 1401–1408

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 2010-30-

Researchers have discovered that ¬consuming a very high amount of alcohol in a short time can cause irreversible damage. In the long run youngsters risk becoming absent-minded and forgetful.
Previous research found that high levels of alcohol act as a poison and prevent the brain working properly. Now scientists say that excess alcohol can actually destroy grey matter called the hippocampus, which stores and recalls events and forms mental images, known as spatial reasoning.
A US team gave alcohol for one hour a day to teenage macaque monkeys, who drank until they were drunk. Their brains produced fewer cells and suffered more neural degeneration than a control group. Last year, a survey of 35 countries found the UK had the third highest number of 15 and 16-year-olds with an alcohol problem. Girls were worse than boys.
Don Shenker, chief executive of Alcohol Concern, said the Government needed “to force the drinks industry to ensure consumers are aware of the dangers”.

Source: Daily Express 1st June 2010

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 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 52 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
Source: The Lancet. Sept. 11 2004

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

Source: Daily Telegraph, London reported Nov. 9.2004

Scientists at Melbourne’s Howard Florey Institute have discovered a system in the brain that stops an alcoholic’s craving for alcohol, as well as prevent relapse once they have recovered from alcohol addiction.
________________________________________
The ‘Orexin’ system is a group of cells in a part of the brain called the hypothalamus. These cells produce Orexin, which was originally implicated in the regulation of feeding, but it soon became apparent that Orexin was also involved in the ‘high’ felt after drinking alcohol or taking illicit drugs.

In studies conducted with rats, Dr Andrew Lawrence and his Florey colleagues used a drug that blocked Orexin’s euphoric effects in the brain and the results were remarkable.
“In one experiment, rats that had alcohol freely available to them stopped drinking it after receiving the Orexin blocker.” Dr Lawrence said. “In another experiment, rats that had gone through a detox program and were then given the Orexin blocking drug, did not relapse into alcohol addiction when they were reintroduced to an environment in which they had been conditioned to associate with alcohol use.

“Orexin reinforces the euphoria felt when drinking alcohol, so if a drug can be developed to block the Orexin system in humans, we should be able to stop an alcoholic’s craving for alcohol, as well as preventing relapse once the alcoholic has recovered,” he said.
Dr Lawrence said that this research could also lead to treatments for eating disorders, such chronic over-eating, which leads to obesity. “Our research shows that alcohol addiction and eating disorders set off common triggers in the brain, so further investigations may uncover drug targets in the Orexin system to treat both conditions,” Dr Lawrence said.

The Florey scientists are now conducting multiple experiments to discover the precise circumstances that activate the Orexin system. “To explore this discovery further we are now investigating how different experimental paradigms and environmental situations impact on the Orexin system, which will hopefully pinpoint therapeutic drug targets,” Dr Lawrence said.
“Before a therapeutic Orexin-blocking drug can be developed, we need to ensure that it will be safe to use in the long-term and that issues surrounding a person’s compliance in taking the drug are considered,” he said.

According to the World Health Organisation, alcohol is one of the most widely used and abused substances in the world and causes as much, if not more death and disability as measles, malaria, tobacco, or illegal drugs.
Dr Lawrence and his colleagues were the first in the world to demonstrate the Orexin system’s involvement in alcohol addiction and their research paper was recently published in the prestigious British Journal of Pharmacology. Dr Lawrence’s paper was downloaded 658 times by researchers from around the world in the first three months of its publication, making it the most downloaded research paper in that issue and supporting the research’s importance.
The Howard Florey Institute is Australia’s leading brain research centre. Its scientists undertake clinical and applied research that can be developed into treatments to combat brain disorders, and new medical practices. Their discoveries will improve the lives of those directly, and indirectly, affected by brain and mind disorders in Australia, and around the world. The Florey’s research areas cover a variety of brain and mind disorders including Parkinson’s disease, stroke, motor neuron disease, addiction, epilepsy, multiple sclerosis, autism and dementia.

Source: ScienceDaily. Retrieved March 28, 2010 Howard Florey Institute (2006, December 13).
.
________________________________________

A recent study by investigators at the Vanderbilt Kennedy Center for Research on Human Development may help explain the long-term behavioral and neurological problems associated with prenatal exposure to cocaine. In a recent issue of the Journal of Neuroscience, Gregg Stanwood, Ph.D., and Pat Levitt, Ph.D., report that prenatal cocaine exposure in rabbits causes a long lasting displacement of dopamine receptors in certain brain cells, which alters their ability to function normally.
Though this effect has not yet been assessed in cocaine-exposed children, the findings give researchers a place to start looking.
“The hysteria surrounding the ‘crack baby’ was sort of overblown,” said Stanwood, research assistant professor of Pharmacology and lead author on the study.
Incredibly high levels of cocaine — usually coupled with the abuse of other drugs — can lead to premature labor, preterm birth and low birth weight, Stanwood said.
“But in women who have abused relatively low recreational doses of cocaine, it is actually very hard to distinguish those children at birth from children born to anyone else,” he said. “However, as those children age, they do develop deficits in their cognitive and emotional development.”
These children often exhibit attention and arousal problems, similar to children with attention deficit hyperactivity disorder (ADHD). However, the standard treatments for ADHD — Ritalin and other stimulants — are not always effective in these children.
Studying the effects of prenatal cocaine exposure on the developing brain is difficult in human populations because cocaine abusers often abuse other drugs. Animal models can help determine how prenatal cocaine exposure might influence brain development to cause these subtle cognitive impairments.
“We thought that it was important to set up an animal model that recapitulates a key feature of human abuse — that being intravenous exposure to low doses of cocaine,” Stanwood said.
A few years ago, Stanwood and Levitt, professor of Pharmacology and director of the Vanderbilt Kennedy Center, established such a model in rabbits. They found that exposure to low levels of intravenous cocaine during a very short window of time during gestation — equivalent to the late first trimester and early second trimester in humans — caused specific alterations in brain circuits that use the neurotransmitter dopamine. Additionally, these cocaine-exposed offspring showed attention problems as well as insensitivity to stimulants like amphetamine, suggesting that cocaine exposure had altered the development of the dopamine pathways in the brain.
“In collaboration with Dr. Eitan Friedman of the City University of New York, we had previously shown a decrease in signaling of a particular receptor protein, the dopamine D1 receptor,” Stanwood said. “We know that this receptor is involved in regulating the formation of cortical circuitry. It’s also involved in the behavioral effects of amphetamines and cocaine.”
“The current study was an attempt to look at the mechanism of this decrease in D1 receptor signaling,” he said.
Stanwood examined the levels of D1 receptor in brain cells taken from “teenage” rabbits that were exposed to cocaine during that short, sensitive prenatal period.
He found that cocaine exposure did not alter the total amount of D1 receptor produced in the brain. However, there was a dramatic alteration in the location of the protein within the cell.
“It’s not where it should be,” he said. D1 receptors are normally found at the cell surface, but neurons from the cocaine-exposed animals showed the receptor was predominantly sequestered inside the cells.
“The fascinating thing is that this effect appears permanent,” said Stanwood. This implies that cocaine exposure during a brief, sensitive period of neural development can lead to long-lasting effects at the cellular level.
This change also altered the growth of neuronal processes, suggesting that the altered D1 receptor trafficking may underlie the changes in neuronal architecture and behavior that Stanwood and others have previously observed.
What remains to be determined, he cautioned, is whether D1 receptor localization is affected in humans exposed to cocaine prenatally.
If found in humans, “it gives us a new way to think about helping those children as they continue to mature.” Because cocaine exposure seems to alter the distribution of the D1 receptor, Stanwood suggests that researchers might find a way to “steer” the receptor into the correct cellular location. That could provide new avenues for treating the attention problems in cocaine-exposed children, as well as in children with stimulant-resistant ADHD.
“Neither we nor anyone else has yet identified whether this mechanism occurs in the human population,” Stanwood said, “so that is a critical next step.”
Note: This story has been adapted from a news release issued by Vanderbilt University Medical Center.

Source ScienceDaily.com 13th January 2007

The Journal of Pediatrics has published a new study which brings to light another troubling consequence of smoking marijuana, particularly during pregnancy.
“Barros and her team looked at 561 infants born to adolescent mothers. Twenty-six of them had been exposed to marijuana, as revealed by tests on the mother’s hair and the infant’s stool. Just one of the mothers had reported smoking pot while pregnant.
Trained examiners, who did not know a child’s marijuana exposure status, tested the neurobehavioral responses of all infants. On average, marijuana-exposed infants scored differently on measures of arousal, regulation and excitability compared to the non-exposed infants…
..Infants exposed to marijuana in the womb show subtle behavioral changes in their first days of life, researchers from Brazil report.
These newborns were more irritable than non-exposed infants, less responsive, and more difficult to calm, Dr. Marina Carvalho de Moraes Barros and colleagues from the Federal University of Sao Paulo and colleagues report. They also cried more, startled more easily, and were more jittery. Such changes, Barros and her team say, have the potential to interfere with mother-child bonding.
Here’s the key point: “It is necessary to counter the misconception that marijuana is a ‘benign drug’ and to educate women regarding the risks and possible consequences related to its use during pregnancy,” Barros and colleagues conclude.”

Source: Journal of Pediatrics Vol.149 Issue 6 Dec. 2006

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

Fact sheet September 2006

Overall Mortality
• Tobacco use is the leading preventable cause of death in the United States.1 Cigarette smoking causes an estimated 438,000 deaths, or about 1 of every 5 deaths, each year.2,3 This estimate includes approximately 38,000 deaths from secondhand smoke exposure.2

• Cigarette smoking kills an estimated 259,500 men and 178,000 women in the United States each year.2

• More deaths are caused each year by tobacco use than by all deaths from human immunodeficiency virus (HIV), illegal drug use, alcohol use, motor vehicle injuries, suicides, and murders combined.2,4

• On average, adults who smoke cigarettes die 14 years earlier than nonsmokers.5

• Based on current cigarette smoking patterns, an estimated 25 million Americans who are alive today will die prematurely from smoking-related illnesses, including 5 million people younger than 18.6
Mortality from Specific Diseases
• Lung cancer (124,000), heart disease (108,000), and the chronic lung diseases of emphysema, bronchitis, and chronic airways obstruction (90,000) are responsible for the largest number of smoking-related deaths.2

• The risk of dying from lung cancer is more than 22 times higher among men who smoke cigarettes and about 12 times higher among women who smoke cigarettes compared with never smokers.7

• Since 1950, lung cancer deaths among women have increased by more than 600%.1 Since 1987, lung cancer has been the leading cause of cancer-related deaths in women.1

• Cigarette smoking results in a two- to three-fold increased risk of dying from coronary heart disease.7

• Cigarette smoking is associated with a ten-fold increased risk of dying from chronic obstructive lung disease.6 About 90% of all deaths from chronic obstructive lung diseases are attributable to cigarette smoking.1,7

• Pipe smoking and cigar smoking increase the risk of dying from cancers of the lung, esophagus, larynx, and oral cavity.8 Smokeless tobacco use increases the risk for developing oral cancer.8,9
References
1. U.S. Department of Health and Human Services. Women and Smoking: A Report of the Surgeon General. Atlanta, GA: U.S. Department of Health and Human Services, CDC, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health; 2001. Available at: http://http://www.cdc.gov/tobacco/sgr/sgr_forwomen/index.htm. Accessed December 2006.

2. CDC. Annual Smoking–Attributable Mortality, Years of Potential Life Lost, and Productivity Losses — United States, 1997–2001. MMWR 2005: 54(25) 625-628. Available at http://0-www.cdc.gov.mill1.sjlibrary.org:80/mmwr/preview/mmwrhtml/mm5425a1.htm. Accessed: September 2006.

3. CDC. Health United States, 2005 With Chartbook on Trends in the Health of Americans. ( PDF–119KB) Hyattsville, MD: U.S. Department of Health and Human Services, CDC, National Center for Health Statistics; 2006. Accessed September 2006.

4. McGinnis J, Foege WH. Actual causes of death in United States. Journal of American Medical Association 1993;270:2207–2212.

5. CDC. Annual smoking-attributable mortality, years of potential life lost, and economic costs—United States, 1995–1999. MMWR 2002; 51(14):300–303. Accessed September 2006.

6. CDC. Perspectives in disease prevention and health promotion, smoking-attributable mortality and years of potential life lost—United States, 1984. MMWR 1997;46:444–451. Available at: http://0-www.cdc.gov.mill1.sjlibrary.org:80/mmwr/preview/mmwrhtml/00047690.htm. Accessed February 2004.

7. Novotny TE, Giovino GA. Tobacco use. In: Brownson RC, Remington PL, Davis JR (eds). Chronic Disease Epidemiology and Control. Washington, DC: American Public Health Association; 1998;117–148.

8. U.S. Department of Health and Human Services. Reducing the Health Consequences of Smoking—25 Years of Progress: A Report of the Surgeon General. Atlanta, GA: U.S. Department of Health and Human Services, CDC; 1989. DHHS Pub. No. (CDC) 89–8411. Available at: http://profiles.nlm.nih.gov/NN/B/B/X/S/. Accessed September 2006.

9. U.S. Department of Health and Human Services. The Health Consequences of Using Smokeless Tobacco: A Report of the Advisory Committee to the Surgeon General, 1986. Bethesda, MD: U.S. Department of Health and Human Services, Public Health Service. NIH Pub. No. 86–2874. Accessed September 2006.
Note: More recent information may be available at the CDC’S Office on Smoking and Health Web site: http://0-www.cdc.gov.mill1.sjlibrary.org:80/tobacco.

Source: Centers for Disease Control and Prevention
National Center for Chronic Disease Prevention and Health Promotion
Office on Smoking and Health. tobaccoinfo@cdc.gov Sept.2006

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
A study by the British Lung Foundation determined that smoking marijuana is more harmful to the lungs than smoking cigarettes, the BBC reported Nov. 11.
According to the study, smoking three marijuana cigarettes a day can cause the same damage as 20 cigarettes. And those who smoke both marijuana and cigarettes are further increasing their risk of lung damage.
Dr. Mark Britton, chairman of the foundation, said that tar from cannabis cigarettes contains 50 percent more carcinogens than tobacco. Since marijuana smokers tend to inhale up to four times more deeply than tobacco users, more poisonous carbon monoxide and tar enter the lungs, he added.
“These statistics will come as a surprise to many people, especially those who choose to smoke cannabis rather than tobacco in the belief it is safer for them,” said Britton. “It is vital that people are fully aware of the dangers so they can make an educated decision and know the damage they may be causing.”
As a result of the study’s findings, the group is urging the British government to implement a public-health education campaign on the health risks of marijuana smoking.

Source: Link from Join Together February 2007

Maoris have the world’s highest lung-cancer rate, and heavy marijuana use could be a culprit, the New Zealand Herald reported Oct. 10.
About one in five New Zealanders are regular users of marijuana. Researcher Richard Beasley of the Medical Research Institute in Wellington, New Zealand, is working on a study that compares cancer rates between marijuana smokers, tobacco smokers, and nonusers. He recently released a research review concluding that marijuana smoking is more cancerous than tobacco smoking.
Beasley performed the research review for a Wellington coroner who has called for a tougher approach than harm reduction to marijuana use in New Zealand.

Source: New Zealand Herald Oct.l7 2005

Strategies teenagers use to minimise alcohol-related harm
• Aims: To examine strategies of harm minimization employed by teenage drinkers.
• Findings: The teenagers participating in the present study were more concerned about social than health risks. The informants monitored their own level of intoxication, but in order to reduce alcohol consumption they depended upon support from their peers. The informants preferred drinking in the company of well-known and trusted peers, and during drinking episodes they supervised and intervened in each others’ drinking to the extent that they deemed it necessary and possible. In regulating the social context of drinking they relied on their personal experiences more than on formalized knowledge about alcohol and harm, which they had learned from prevention campaigns and educational programmes.
• Conclusions: The study found that teenagers may help each other to minimize alcohol-related harm, and teenage peer groups should thus be considered a resource for health promotion.
Morten Hulvej Jørgensen, Tine Curtis, Pia Haudrup Christensen, Morten Grønbæk (2007) Harm minimization among teenage drinkers: findings from an ethnographic study on teenage alcohol use in a rural Danish community

Source: Addiction 102 (4), 554–559

Viewing videotape of themselves while experiencing delirium tremens could reduce the relapse rate in alcohol-dependent patients
• The aim of this prospective randomized controlled study was to determine whether viewing videotape of themselves while experiencing delirium tremens (DT) reduces the relapse rate in alcohol-dependent patients.
• Findings: The patients with videotape experience had a significantly lower relapse rate after the first month (0% versus 20%), 2 months (13.33% versus 46.67%) and 3 months (26.67% versus 53.33%). Patients with videotape experience had less severe relapses and consumed fewer units of alcohol than controls.
• Conclusions: Videotape exposure in delirium tremens is an original therapeutic method which seems to be effective in reducing relapse risk in patients with alcohol dependence.
Adriana Mihai, Cristian Damsa, Michael Allen, Bertrand Baleydier, Coralie Lazignac, Andreas Heinz (2007) Viewing videotape of themselves while experiencing delirium tremens could reduce the relapse rate in alcohol-dependent patients

Source: Addiction 102 (2), 226–231.

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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By Maggie Fox

WASHINGTON (Reuters) – The marijuana being sold across the United States is stronger than ever, which could explain a growing number of medical emergencies that involve the drug, government drug experts on Wednesday.

Analysis of seized samples of marijuana and hashish showed that more of the cannabis on the market is of the strongest grade, the White House and National Institute for Drug Abuse said.

They cited data from the University of Mississippi’s Marijuana Potency Project showing the average levels of THC, the active ingredient in marijuana, in the products rose from 7 percent in 2003 to 8.5 percent in 2006.

The level had risen steadily from 3.5 percent in 1988.

National Institute on Drug Abuse Director Dr. Nora Volkow fears the problem is not being taken seriously because many adults remember the marijuana of their youth as harmless.

“It’s really not the same type of marijuana,” Volkow said in a telephone interview. “This could explain why there has been an increase in the number of medical emergencies involving marijuana.”

According to the Substance Abuse and Mental Health Administration, marijuana was involved in 242,200 visits to hospital emergency rooms in 2005. This means that the patient mentioned using marijuana and does not mean the drug directly caused the accident or condition being treated, SAMHSA says.

The number is up from 215,000 visits in 2004.

The pharmacy department at Mississippi has compiled data on 59,369 samples of cannabis, 1,225 hashish samples, and 443 hash oil samples confiscated since 1975. “The highest concentration of (THC) found in a cannabis (marijuana) sample is 33.12 percent from Oregon State Police,” the report reads.
Hashish and hash oil concentrations are far higher, as they consist of processed plant product.

“Researchers and treatment experts have argued for some time that today’s more powerful marijuana has more harmful effects on users. This report underscores that we are no longer talking about the drug of the 1960s and 1970s — this is Pot 2.0,” John Walters, director of National Drug Control Policy, said in a statement.

Volkow said demand has driven growers to cultivate the stronger stuff. “It is the market,” she said. “Like in the market you favor the best tomatoes. When people buy marijuana, they don’t want a weak cigarette.”

Volkow’s institute has been studying the effects of cannabis, whose active ingredients are very similar to important brain chemicals called endogenous cannabinoids. “It clearly is addictive,” she said.

If children and adolescents use marijuana, it could affect their still-developing brains, she said.

The report said more than 60 percent of teens receiving treatment for drug abuse or dependence report marijuana as their primary drug of abuse.

“Although the overall number of young people using marijuana has declined in recent years, there is still reason for great concern, particularly since roughly 60 percent of first-time marijuana users are under 18 years old,” Volkow said.

According to the National Survey on Drug Use and Health 4.1 million Americans, or 1.7 percent of the population, report they use marijuana.

Source: Reuters Health. 26th April 2007

Abstract:
The use of Cannabis sativa preparations, such as hashish and marijuana, is wide-spread among young people, including pregnant women. Despite this concern, the consequences of cannabis exposure on the brain during periods of active brain development, such as the prenatal phase and adolescence, is not well known. Several epidemiological studies support the cannabis gateway hypothesis, where early cannabis use is suggested to increase the risk of initiating use of other illicit drugs, e.g., amphetamine or heroin. However, the nature of such direct links are unclear. Therefore, the aim of this thesis was to test experimentally the cannabis gateway hypothesis, i.e., to determine whether cannabis exposure during periods of active brain development alters reward-related behavior and neurobiology for psychostimulant and opioid drugs by the use of animal models.
In the first study, we examined the effects of early adolescent exposure (postnatal day; PND; 28-32, one injection per day) with the synthetic cannabinoid CB1 receptor agonist WIN55,212-2 and the main psychoactive substance in C. sativa, Δ9-tetrahydrocannabinol (THC) on amphetamine-induced motor behavior and dopamine release in the nucleus accumbens during adolescence. No alterations were evident in the cannabinoid exposed rats, results which did not support the cannabis gateway hypothesis in relation to subsequent psychostimulant abuse.
Next, we investigated the effects of adolescent exposure on subsequent opioid reward-related behavior and the neurobiology of opioid and cannabinoid systems during adulthood. We studied THC exposure across the full adolescent period (PND 28-49), and administered the drug once every third day in order to better mimic the pattern of intermittent use seen in teenagers. The results revealed discrete opioid-related alterations within brain regions highly implicated in reward and hedonic processing (e.g., increased proenkephalin gene expression in the nucleus accumbens and increased mu opioid receptors in the ventral tegmental area). This was coupled to increased heroin intake in a self-administration paradigm and increased morphine conditioned place preference, indicating altered sensitivity to the reinforcing properties of opioids.
Furthermore, in evaluating the adolescent ontogeny of the opioid and cannabinoid systems within limbic-related brain areas, we found that active endocannabinoid- and opioid- related neurodevelopment takes place to a very high extent during this period. Most pronounced were the alterations in endocannabinoid levels in cognitive brain areas, even though alterations were also apparent in reward-related regions.
Finally, we investigated the effects of prenatal cannabis exposure (gestational day 5- PND 2) on subsequent opioid reward-related behavior and neurobiology of the opioid and cannabinoid systems in adulthood. Similar to adolescent cannabis exposure, prenatal exposure induced discrete opioid-related alterations within brain regions highly implicated in reward and hedonic processing. Moreover, elevated heroin-seeking observed during extinction and after food deprivation was evident in the THC exposed rats, suggesting an increased motivation for drug use under conditions of stress.
Taken together, this thesis presents neurobiological support for the cannabis gateway hypothesis in terms of adult opiate, but not amphetamine, abuse, with underlying long-term disturbances of discrete opioid-related systems within limbic brain regions.
ISBN: 978-91-7357-064-0

Source: Karolinska Institute online 9th Feb.2007

Abstract: Spano MS, Ellgren M, Wang X, Hurd YL.

Karolinska Institute, Department of Clinical Neuroscience, Psychiatry Section, S-17176 Stockholm, Sweden.

BACKGROUND: Prenatal cannabis exposure is a growing concern with little known about the long-term consequences on behavior and neural systems relevant for reward and emotional processing.
METHODS: We used an animal model to study the effects of prenatal exposure to Delta(9)-tetrahydrocannabinol (THC) on heroin self-administration behavior and opioid neural systems in adult males (postnatal day 62). Rats were exposed to THC (.15 mg/kg) or vehicle from gestational day 5 to postnatal day 2. RESULTS: Both pretreatment groups showed similar heroin intake, but THC-exposed rats exhibited shorter latency to the first active lever press, responded more for low heroin doses, and had higher heroin-seeking during mild stress and drug extinction. THC exposure reduced preproenkephalin (PENK) mRNA expression in the nucleus accumbens during early development, but was elevated in adulthood; no adult striatal changes on preprodynorphin mRNA or PENK in caudate-putamen. PENK mRNA was also increased in the central and medial amygdala in adult THC-exposed animals. THC animals had reduced heroin-induced locomotor activity and nucleus accumbens mu opioid receptor coupling.
CONCLUSIONS: This study demonstrates enduring effects of prenatal THC exposure into adulthood that is evident on heroin-seeking behavior during extinction and allostatic changes in mesocorticolimbic PENK systems relevant to drug motivation/reward and stress response.

Source: : Biol Psychiatry. 2007 Feb 15;61(4):554-63. Epub 2006 Jul 28.

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

Scientists have shown how cannabis may trigger psychotic illnesses such as schizophrenia.
A King’s College London team gave healthy volunteers the active ingredient tetrahydrocannabinol (THC).
They then recorded reduced activity in an area of the brain which keeps inappropriate thoughts at bay. THC levels are thought to have doubled in street cannabis in recent years – at the expense of other ingredients which may have a beneficial effect.

A separate study has shown that one of these ingredients – cannabidiol (CBD) – has the potential to dampen down psychotic symptoms, and could form the basis of new treatments. The research will be discussed at a conference on the impact of cannabis use to be held at the Institute of Psychiatry at King’s College this week.
Dependency
Although figures are not kept, it is estimated that as many as 500,000 people in the UK may be dependent on cannabis. Increasing numbers of people are seeking help for cannabis problems at specialist clinics. In 2005, only heroin users accounted for a greater proportion of patients. Experts are concerned that street cannabis is becoming increasingly potent. It is thought that average THC content has risen from 6% to 12% in recent years.
The Institute of Psychiatry study gave THC, CBD or placebo capsules to adult male volunteers who had not abused cannabis. They then carried out brain scans, and a battery of tests, and found that those who took THC showed reduced activity in an area of the brain called the inferior frontal cortex, which keeps inappropriate thoughts and behaviour, such as swearing and paranoia in check.
The effects were short-lived, but some people appeared more vulnerable than others.
In a second study, a team from Yale University administered THC intravenously. Even at relatively low doses, they found 50% of healthy volunteers began to show symptoms of psychosis. Volunteers who already had a history of psychotic symptoms appeared to be particularly vulnerable.
Side effects
A third study, by the University of Cologne, compared the effect of CBD and a commonly used anti-psychotic medicine, Amisulpride, on 42 patients with a history of schizophrenia.
After four weeks both groups showed a reduction in psychotic symptoms, but the CBD group were less prone to side effects, such as muscle stiffness and weight gain.

The researchers warned that THC and CBD compete with each other biochemically, so a rise in THC levels would blunt any positive impact of CBD. Professor Robin Murray, a consultant psychiatrist at the Institute of Psychiatry, said the research provided the strongest evidence that cannabis had a significant impact on the brain.
He said proving a long-term effect was extremely difficult, as it was not ethical or feasible to stimulate long-term psychosis in volunteers.
However, he said: “If something has an active effect in inducing the symptoms of psychosis after one dose, then it would not be at all surprising if repeated use induced the chronic condition.”
Professor Murray also warned that the high potency cannabis now widely available was likely to pose a much bigger risk to health than the significantly weaker formulations of previous years. “It is similar to comparing the effect of drinking a glass of wine at the weekend with drinking a bottle of vodka every day.”
Marjorie Wallace, of the mental health charity Sane, called the research a “significant contribution” to the understanding of the dangers of cannabis.
“Sane has been saying for years that there is a link between psychosis and the drug, particularly in its more potent forms.
“We strongly urge the government to heed the growing evidence and take urgent action to warn young people that some of them are risking lifelong mental illness – that they are playing Russian roulette with their minds.”

Source: BBC NEWS: 2007/04/30

A steady rise in long-term heavy drinking has led to a doubling of alcohol-related deaths among men over the past decade, according to official figures.
The study of “preventable mortality” found that the rate of alcohol-related deaths had risen sharply among women too, with two thirds more dying of diseases such as cirrhosis over the period.
The rise in alcohol-related deaths is in stark contrast to sharp falls in the rest of the top five “preventable causes of mortality”.
Lung cancer and other pulmonary diseases are both down by a third, while suicide is down by 14 per cent. The data were released in the Office for National Statistics’ quarterly survey of the nation’s health.
Alcohol Concern said that the biggest increase in alcohol-related deaths was among those aged 35 to 54, a generation of people who started drinking heavily in their youth and carried on into middle age.

Source: From The Times Online May 25, 2007

According to experimental scientists a common antipsychotic drug used in emergency rooms to treat methamphetamine overdose can damage nerve cells in an area of the brain known to regulate movement.
Investigators from the Boston University School of Medicine used a rat model to determine that only the combination of the medication, haloperidol, and methamphetamine causes the destructive effects, not either one alone.
Senior author Bryan Yamamoto, PhD, and his team suspect the damage results from the exaggerated stimulation of cells by the amino acid glutamate, which proves toxic to cells producing the neurotransmitter gamma-aminobutyric acid (GABA).
Their results are published in the May 30 issue of The Journal of Neuroscience.
“This work in laboratory animals raises immediate concerns that a standard treatment for methamphetamine overdose in humans might worsen drug abuse-related brain injuries,” says William Carlezon, PhD, at Harvard’s McLean Hospital, who was not affiliated with the study.
“A crucial next step is to determine how atypical antipsychotic medications would affect methamphetamine toxicity in the same model.”
The rats in the experiment were injected with either methamphetamine or a saline solution over a period of eight hours. When the rats were given haloperidol before and nearly halfway through the eight-hour period, Yamamoto and his colleagues noted more than a fivefold rise in base levels of glutamate in the substantia nigra, a part of the brain known to play a role in movement disorders such as Huntington’s disease.
After examining the long-term effects of the combination, they found that glutamate concentrations in the substantia nigra were twice as high in methamphetamine-treated rats as in saline-treated ones two days after injections.
Yamamoto and his colleagues were able to link this rise in glutamate to the death of GABA-containing cells in one part of the substantia nigra. This may predispose some people who have been treated for a methamphetamine overdose to seizures and the development of movement disorders, they say, although the study did not measure movement specifically.
In addition to future studies of other antipsychotic medications, says Yamamoto, “we hope to examine if the loss of cells results in abnormal involuntary movements resembling Tourette’s syndrome and Huntington’s disease.”

Source: Society for Neuroscience May 30th 2007

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

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.

Cannabinoids may suppress tumor invasion in highly invasive cancers, according to a study published online December 25 in the Journal of the National Cancer Institute.
Cannabinoids, the active components in marijuana, are used to reduce the side effects of cancer treatment, such as pain, weight loss, and vomiting, but there is increasing evidence that they may also inhibit tumor cell growth. However, the cellular mechanisms behind this are unknown.
Robert Ramer, Ph.D., and Burkhard Hinz, Ph.D., of the University of Rostock in Germany investigated whether and by what mechanism cannabinoids inhibit tumor cell invasion.
Cannabinoids did suppress tumor cell invasion and stimulated the expression of TIMP-1, an inhibitor of a group of enzymes that are involved in tumor cell invasion.
“To our knowledge, this is the first report of TIMP-1-dependent anti-invasive effects of cannabinoids. This signaling pathway may play an important role in the antimetastatic action of cannabinoids, whose potential therapeutic benefit in the treatment of highly invasive cancers should be addressed in clinical trials,” the authors write.

Source: Journal of the National Cancer Institute (2007, December 27). Cannabinoids May Inhibit Cancer Cell Invasion. ScienceDaily. Retrieved July 18, 2008, from http://www.sciencedaily.com¬ /releases/2007/12/071226004546.htm

Alcohol-related deaths in England and Wales are twice as high among people born in Scotland or Ireland compared with the rest of the population, a study has shown
Alcohol-related deaths in England and Wales are twice as high among people born in Scotland or Ireland compared with the rest of the population, a study has shown.
Research, conducted by the University of Edinburgh and the Office for National Statistics, also found that men born in India – but living in England and Wales – had similar rates of alcohol-related death as Scottish- and Irish-born people.
The findings showed too that people born in parts of Asia or Africa were at greater risk of dying from liver cancer, but generally had lower rates of alcohol-related deaths. The higher rate of death from liver cancer could be attributable to the fact that viral hepatitis is more common in ethnic minority communities.
The team used information on deaths for England and Wales from 1999 to 2003 and figures from the 2001 census to quantify the link between a person’s country of birth and the likelihood of dying from an alcohol-related condition.
The difference in alcohol-related deaths rates could be explained by cultural differences in rates of alcohol consumption. For example, adults who are Scottish or Irish have been shown on average to drink more than the recommended limit of alcohol.
The study, published in the Journal of Public Health, follows recent reports that alcohol-related hospital admissions in the over 65s are rising.
Dr Neeraj Bhala, who led the study, said: “Deaths from alcohol-related conditions, liver disease and liver cancer are increasing in the UK, but little is known about the role of ethnicity or country of birth. Some ethnic groups appear to be setting an example for the population as a whole with very low rates of liver disease, almost certainly as a result of low alcohol consumption.”
“These findings show significant differences in death rates by country of birth for both alcohol-related deaths and liver cancer. We now need to focus on developing new policy, research and practical action to help address these differences.”
Alcohol is thought to cause as much death and disability worldwide as tobacco use or high blood pressure. In England alone, alcohol misuse is estimated to costs more than £20 billion a year.

Source: EurekaAlert. 19th March 2009

Key findings from Professor Martin Plant, Alcohol Health and Research Unit,Faculty of Health and Sciences, University of the West of England and AlcoholConcern, the national agency on alcohol misuse.

Professor Plant and his team were commissioned by Alcohol Concern in April 2009 to investigate what the future may hold for the nation’s drinking habits and associated harms. Professor Plant’s forecasting allows us to answer how our drinking patterns are likely to affect the state of the nation’s health in 2035.

For the first time in the UK, the relationship between alcohol consumption and mortality has been calculated. The research indicates a definitive link: the higher our society’s alcohol consumption, the more deaths occur as a result. Based on this, it is possible to forecast how health harms from alcohol may increase in the next 10 years if we continue to drink at the rate of the last 15 years.

Source: www.Alcoholconcern.org.uk Oct 2009

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

My first appointment was with Dr Diana Fishbein, a Senior Fellow in behavioral neuroscience at the Research Triangle Institute (RTI) which is an international not-for-profit research organisation .

Diana is the Director of the Transdisciplinary Behavioural Science Program at RTI. In this role she focuses on bringing interdisciplinary teams of researchers together to try to answer some of the big questions that need to be asked in the behavioural sciences. Her overarching goal is to focus on the nexus between research and practice and to facilitate the “Translation of Research into Evidence Based Practice”. In fact RTI International organisational by line is Turning Knowledge into Practice.    

Diana’s personal research career has been in the area of criminology and drug abuse taking a prevention science approach.  She is particularly interested in why some young people respond well to a prevention approach while others don’t, and ultimately in determining “who responds to what treatment at what time point and why”?

To explore these questions she uses interdisciplinary methods and a developmental approach and sees the plasticity of neurobiological systems as one of the keys to finding the answer. Dr. Fishbein  pointed out that neuroplasticity enables neurobiological systems to be shaped by inputs from the environment and so can be altered for better or worse depending on the nature of these inputs. This is highly relevant to a prevention or early intervention approach and can guide the development of interventions. Research in this area is now beginning to focus on the mechanisms through which developmental risk factors impact on the developing systems and also on the type of interventions which have the most impact, how they are affecting neuroplastic change and when they are having the most effect.  

For instance there is evidence that the neurobiological functions underlying drug misuse and aggression are quite complex and include executive functioning, coping skills and affect regulation. The part of the brain associated with these functions (prefrontal-limbic brain networks) is not consolidated until early adulthood. Therefore is we can understand the type, effect and developmental timing of environmental impact on this brain function we may be able to plan intervention programs that alter negative impact and increase positive impact.  We may also need to tailor interventions to particular risk factors in the young person’s environment. Diana is confident this translational approach promises to eventually offer some direction for the design of effective interventions to prevent drug misuse and associated aggression.

This cutting-edge evidence-based research with the capacity to not only make a difference but to provide us with the scientific evidence to show how change has come about.  The message that again seems to be coming through to me is that one size is not likely to fit all. The other message is one that Professor Alan Hayes a member of the external advisory group for this project has written about in his chapter entitled Why early in life is not enough! (Hayes, 2007. In France, A & Homel, R (Eds) Pathways and crime prevention: Theory policies and practice  Willian (pps 202-225)

Dr Fishbein and I also talked about the need for parent and community involvement in interventions.  She also indicated to me that she and her organisation are very interested in innovative collaborative international research. Perhaps this is something to think about for the future.

Source: http://shapingbrains.wordpress.com  3^rd March 2010

BABIES born to mothers who take methadone during pregnancy have developed a range of visual problems, according to a report by medical experts in Glasgow.

The study discovered that the mothers of all 20 infants referred to a specialist clinic for vision defects had taken opiates during pregnancy.  The problems included blurred vision, nystagmus (rapid and involuntary eye movement from side to side), squints, short-sightedness and cerebral visual impairment – signs that the brain was not processing the signals from the eyes correctly.  The results of the study are likely to add to the controversy surrounding the prescription of the heroin substitute methadone to drug users.The latest official statistics show that 572 babies were born to drug misusers in 2006-7, including 370 births to users of opiates such as methadone and heroin. The study, published in the Scottish Medical Journal, was carried out by doctors at the Royal Hospital for Sick Children at Yorkhill and Princess Royal Maternity. It is the first major investigation into how the use of opiates during pregnancy affects the development of vision in babies.

Researchers said there were “growing concerns” about the scale of the vision problems being picked up by eye examinations and about how long they would persist.

Neonatal consultant Helen Mactier said: “We were seeing a disproportionate number of babies who had visual difficulties whose mothers had a history of drug abuse.”
Ruth Hamilton, a consultant clinical scientist and an expert in vision who is involved in the research project, said: “This is about the long-term outcomes for these children. It may be that these babies will go on to develop problems later in life, and it is very important that we discover if there is something we can do.”

In the study, 19 babies had blurred vision, 14 nystagmus, six had squints, six were short-sighted and five had cerebral visual impairment.

A preliminary summary of the research has been presented to the Scottish Paediatric Society. It suggests routine eye examinations for children who were exposed to methadone in the womb, saying: “Children with a history of in-utero opiate exposure may benefit from a vision screening programme.”

Mactier said: “We deliver 150 babies a year to drug-using women and around 45 per cent of them are treated for withdrawal. These babies stay in hospital for a longer period, they are often sick and small. Their mothers are often heavy smokers, they may be from very socially deprived backgrounds, they have a high risk of depression.

“There is an increasing amount of evidence that babies born to drug-addicted mothers have a whole range of health problems.”  She said that, because of the often chaotic lifestyle of drug users, it was hard to single out methadone or any other factor as the principal cause of eye problems.

“Between two-thirds and four-fifths of women on prescribed methadone are also using illicit opiates, valium or similar drugs.” A secondary study will try to pinpoint which factors were most likely to cause of eye problems in the babies of drug-abusing mothers.

There are now 22,000 addicts in Scotland on a methadone programme. A study by Glasgow University’s Centre for Drug Misuse Research found that people on methadone programmes still take heroin. There are concerns the programme replaces one addictive drug with another, and that people are “parked” on methadone for years. There have also been cases of addicts’ children gaining access to methadone.

Earlier this month, the £50 million policy was criticised when an addict’s free supply was cut after almost 20 years.  A Scottish Government spokesman said official policy was to recommend methadone treatment for pregnant drug users on the grounds that prescribed drugs carried a lower risk than continuing to use illegal drugs.  He said: “Pregnant women who misuse drugs receive extra support and care suited to their personal needs.”

Source: ScotlandonSunday  28^th Feb 2010

Professor Fabrizio Schifano at the University’s School of Pharmacy, is lead author of the paper which will be published online in Neuropsychobiology.

Professor Schifano and his colleagues at St George’s, University of London’s International Centre for Drug Policy, which runs the National Programme on Substance Abuse Deaths (np-SAD), reviewed stimulant-related deaths from the np-SAD database and from the British Crime Survey 2001-2007 results and found that identified 832 amphetamine and methylamphetamine-related deaths and 605 ecstasy-related deaths. What was of more concern to Professor Fabrizio and the researchers was the fact that the fatalities from ecstasy during that period were typically identified in victims who were young and healthy.

The report, which covered an 11-year, UK-wide analysis of mortality from these drugs, noted that deaths seemed to have dropped in 2000 to peak once again over the following years and then after a drop again in 2003, it increased again over the following years.
Commenting on the findings, Professor Schifano said: “These data seem to support the hypothesis that young individuals seem to suffer extreme consequences after excessive intake of ecstasy. This is an issue of public health concern which deserves further studies.”

Source: ScienceDaily (Feb. 1, 2010

Teens who smoke marijuana are at a greater risk of developing schizophrenia and psychotic symptoms in the future, a new study has found.
After observing more than 3800 youngsters, researchers learnt that people who used the drug for six or more years were twice as likely to suffer from delusional disorders than those who never used it. Researchers from Queensland Brain Institute, at the University of Queensland, quizzed 3801 young adults who were born in Brisbane between 1981 and 1984.
Among the 1272 participants who had never used marijuana, 26 (2 per cent) were diagnosed with psychosis, while the 322 people who had used marijuana for six or more years, 12 (3.7 per cent) were diagnosed with the illness. The average age of the participants was about 20. According to the authors, the study was the first to look at sibling pairs to discount genetic or environmental influence.
“This is the most convincing evidence yet that the earlier you use cannabis, the more likely you are to have symptoms of a psychotic illness,” the Sydney Morning Herald quoted Dr McGrath, a professor at the institute, as saying in a statement.
McGrath added: “The message for teenagers is: if they choose to use cannabis they have to understand there’s a risk involved.” The study noted: “Apart from the implications for policy makers and health planners, we hope our findings will encourage further clinical and animal-model research to unravel the mechanisms linking cannabis use and psychosis.”
The research has been published online by the Archives of General Psychiatry.

Source: Health Wise Feb 28 2009

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

Beshay M, Kaiser H, Niedhart D, Reymond MA, Schmid RA.
Division of General Thoracic Surgery, University Hospital Berne, Switzerland.

Background: We observed a remarkable increase in the number of young patients who presented with lung emphysema and secondary spontaneous pneumothorax (SSP) at our institution for over a period of 30 months; most of them have a common history of marijuana abuse. Study design: Retrospective case series. Methods: Seventeen young patients presented with spontaneous pneumothorax with bullous lung emphysema were systematically evaluated over a period of 30 months. All were regular marijuana smokers. Clinical history, chest X-ray, CT-scan, lung function test, and laboratory and histological examinations were assessed. We compared the findings of this group (group I) with the findings of non-marijuana smoking patients (group II) in the same period. The findings of this series were also compared with the findings of 75 patients presented with pneumothorax in a previous period from January 2000 till March 2002 (group III). Results: In group I, there were 17 patients: the median age of the patients was 27 years (range 19-43 years), 16 males and 1 female. All were living in Switzerland. All but one smoked marijuana daily for a mean of 8.8 years and tobacco for 11.8 years. CT-scan showed multiple bullae at the apex or significant bullous emphysema with predominance in the upper lobes only in two patients. Only two patients had reduced forced first second expiratory volume (FEV1) and one reduced vital capacity (VC) below the predicted 50%. This correlated with the subjectively asymptomatic condition of the patients. All but two patients were treated by video-assisted thoracoscopic surgery (VATS) for prevention of relapsing pneumothorax. Histology showed severe lung emphysema, inflammation, and heavily pigmented macrophages. In group II, there were 85 patients: there were 78 males, the median age was 24 years (range 17-40 years), 74 patients smoked tobacco for 13.4 years but no marijuana. CT-scan in 72 patients showed only small bullae at the apex but no significant emphysema; other clinical, laboratory, and histopathological findings showed no significant difference in group I. In group III, there were 75 patients: there were 71 males and 4 females. Mean age was 25 years (range 16-46 years). Six smoked marijuana daily for a mean of 3.2 years, and 62 smoked tobacco for 14 years. CT-scan done in 59 patients showed few small bullae at the apex but no significant lung emphysema. The presence of lung emphysema on CT-scan in group I was significantly different than in groups II and III (p=0.14). No significant difference was found among all groups in the form of clinical, laboratory, and histopathological findings. Conclusions: In case of emphysema in young individuals, marijuana abuse has to be considered in the differential diagnosis. The period of marijuana smoking seems to play an important role in the development of lung emphysema. This obviously quite frequent condition in young and so far asymptomatic patients will have medical, financial, and ethical impact, as some of these patients may be severely handicapped or even become lung transplant candidates in the future.

Source: Pubmed. Eur J Cardiothorac Surg. 2007 Oct 9;

Research Summary
There is compelling evidence that second hand smoke can trigger heart attacks, according to a new report from the Institute of Medicine (IOM), and people with heart conditions are urged to avoid exposure to tobacco smoke, the Associated Press reported Oct. 15.
The report, requested by the U.S. Centers for Disease Control and Prevention (CDC), said there is no safe level of exposure to second hand smoke, and that people with cardiovascular disease could risk heart attack with less than an hour’s exposure to environmental tobacco smoke, which restricts blood vessels and increases clotting.
“If you have heart disease, you really need to stay away from second hand smoke. It’s an immediate threat to your life,” said researcher Neal Benowitz of the University of California at San Francisco.
Benowitz added that everyone, in fact, should avoid second hand smoke, since many people who have heart disease are not aware of the problem if they have never had a heart attack. “Even if you think you’re perfectly healthy, second hand smoke could be a potential threat to you,” he said.
“The evidence is clear,” said CDC head Thomas Frieden. “Smoke-free laws don’t hurt business … but they prevent heart attacks in non-smokers.”
Researchers found “clear and consistent” evidence that smoking bans cut the rate of heart attacks, according to statistician Stephen Feinberg of Carnegie Mellon University, a member of the IOM committee that compiled the report.
Source: Associated Press Oct.15th 2009

Research Summary
A recent University of California at Riverside study found that second hand smoke from tobacco can lead to nonalcoholic fatty liver disease (NAFLD), which can cause fat to accumulate in the liver of people even if they drink moderately or don’t drink alcohol at all.
Researchers studied mice exposed to second hand smoke for a year and found that fat accumulated in their liver cells, a sign of NAFLD.
The researchers focused their attention on two main fat metabolism regulators that are also found in human cells: the protein that stimulates synthesis of fatty acids in the liver and AMPK (adenosine monophosphate kinase), which regulates that protein. They found that AMPK activity is inhibited when exposed to second hand smoke, leading the other protein to synthesize more fatty acids. The result is NAFLD, according to the report.
“Our study provides compelling experimental evidence in support of tobacco smoke exposure playing a major role in NAFLD development,” said Manuela Martins-Green, who led the study.
Source: Journal of Hepatology September 2009.

The heart attack rate fell 10 percent in England and 14 percent in Scotland after the U.K. countries imposed bans on public smoking, the Similar results are expected from a study in Wales.
“We always knew a public smoking ban would bring rapid health benefits, but we have been amazed by just how big and how rapid they are,” said John Britton, director of the U.K. Center for Tobacco Control Studies at Nottingham University. The research is expected to boost calls for further curbs on secondhand smoke, such as banning smoking in cars with children.
“Exposure to cigarette smoke induces rapid changes in blood chemistry, making it much more prone to clotting,” explained Ellen Mason, a senior cardiac nurse at the British Heart Foundation. “In someone who has narrowed or damaged coronary arteries, smoke exposure can tip the balance and cause a heart attack.”
The findings echo those in other nations where public smoking has been banned, such as France, Ireland and Italy.

Source: Sunday Times reported Sept. 13th.2009

Research Summary
A genetic study has found that children who were exposed to secondhand smoke are more likely to develop lung cancer as adults, according to researchers from the National Cancer Institute and the Mayo Clinic.
Childhood exposure to secondhand smoke raised lung-cancer risk even among study subjects who never smoked themselves. Researchers drew their conclusions in part from analysis of a gene called MBL2, known to increase susceptibility to respiratory diseases.
Source: Cancer Epidemiology, Biomarkers and Prevention. December 2009

Animal studies show that daily marijuana use could permanently alter serotonin and norepinephrine levels in the brain, raising the risk of depression and anxiety, according to researcher Gabriella Gobbi of McGill University.
The Canadian Press reported Dec. 17 that Gobbi studied the brain chemistry of 18 adolescent lab rats exposed daily to marijuana and found that they had decreased levels of mood-controlling serotonin and higher levels of the stress hormone norepinephrine.
Gobbi said that the effects were magnified because the adolescent brain is still developing. “These permanent changes in the brain are also linked to certain mental illnesses, like schizophrenia,” she said. “And we showed that even if we stopped the cannabis use at the end of adolescence, the changes were still detectable in adulthood.”
A future study will concentrate on adolescent marijuana use among humans.
Source: Neurobiology of Disease. 5th Dec.2009

Comments on above article:

Posted by JBrennan on 08 Jan 10 07:25 PM EST
I smoked marijuana daily at 17 years old and have felt different ever since stopping that, I ended up having more difficulty relaxing, sleeping, and finding energy than I did before daily marijuana use. Today I take amino acids that increase the amount of serotonin and norepinephrine, and it makes me feel normal again. It’s true that my one case doesn’t necessarily prove or disprove anything about marijuana, but I find it funny that there are people who immediately dismiss evidence of marijuana’s harmful affects while immediately claiming that marijuana is harmless, as if the brain is so easy to figure out that they already know everything there is to know about marijuana’s affects on the brain.
Posted by Paula D. Gordon on 09 Jan 10 04:30 AM EST
For additional information and perspectives on the harmfulness of marijuana, see http://gordondrugabuseprevention.com and http://spiritualharmofmarijuana.com It is interesting to note that there are references to work on both website that speak about the long term effects of marijuana use.

Posted by jgogek on 08 Jan 10 03:24 PM EST
The conclusions of this research would not surprise me at all. I find it disturbing when I read the comments in JoinTogether from advocates of recreational and medical marijuana immediately trying to denigrate any new finding on neurologic and other impacts of marijuana. Caring people should be concerned about the possible health impacts of commonly used substances — if not for themselves then at least for other people. Personal beliefs about marijuana use should be trumped by public health concerns. The science on marijuana impact continues to unfold and it should guide public policy. Personal wishes about individual marijuana use should not affect public policy.

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

Progression to daily marijuana use in adolescence may hasten the onset of symptoms leading up to psychosis, an Emory University study finds. The study was published in the November issue of the American Journal of Psychiatry.

The researchers analyzed data from 109 hospitalized patients who were experiencing their first psychotic episode. The results showed that patients who had a history of using marijuana, or cannabis, and increased to daily pot smoking experienced both psychotic and pre-psychotic symptoms at earlier ages.
“We were surprised that it wasn’t just whether or not they used cannabis in adolescence that predicted the age of onset, rather it was how quickly they progressed to becoming a daily cannabis user that was the stronger predictor,” said Michael Compton, lead author and assistant professor of psychiatry in the Emory School of Medicine.
The study also found a gender difference: The female subjects who progressed to daily pot smoking had a greater increased risk for the onset of psychosis than the males.
Marijuana is the most abused illicit substance among people with schizophrenia, the most extreme form of psychosis, and previous research has shown that smoking pot is likely a risk factor for the disease.
The Emory study also focused on what is known as the prodromal period, when a person has symptoms such as unusual sensory experiences, which are often precursors to frank hallucinations and delusions. Prodromal symptoms can occur months, or years, before a diagnosis of psychosis. About 30 to 40 percent of prodomal teenagers will eventually develop schizophrenia or another psychotic disorder.
“The prodromal period is especially important because it’s considered to be a critical time for preventive intervention,” says Elaine Walker, a co-investigator of the study and professor of psychology and neuroscience at Emory.
The study also involved researchers from Emory’s Rollins School of Public Health and Georgia State University. It was funded by the National Institute of Mental Health.

Source: American Journal of