Abstract

OBJECTIVE:

Moderate to heavy levels of prenatal alcohol exposure have been associated with alterations in child behavior, but limited data are available on adverse effects after low levels of exposure. The objective of this study was to evaluate the dose-response effect of prenatal alcohol exposure for adverse child behavior outcomes at 6 to 7 years of age.

METHODS:

Beginning in 1986, women attending the urban university-based maternity clinic were routinely screened at their first prenatal visit for alcohol and drug use by trained research assistants from the Fetal Alcohol Research Center. All women reporting alcohol consumption at conception of at least 0.5 oz absolute alcohol/day and a 5% random sample of lower level drinkers and abstainers were invited to participate to be able to identify the associations between alcohol intake and child development. Maternal alcohol, cigarette, and illicit drug use were prospectively assessed during pregnancy and postnatally. The independent variable in this study, prenatal alcohol exposure, was computed as the average absolute alcohol intake (oz) per day across pregnancy. At each prenatal visit, mothers were interviewed about alcohol use during the previous 2 weeks. Quantities and types of alcohol consumed were converted to fluid ounces of absolute alcohol and averaged across visits to generate a summary measure of alcohol exposure throughout pregnancy. Alcohol was initially used as a dichotomous variable comparing children with no prenatal alcohol exposure to children with any exposure. To evaluate the effects of different levels of exposure, the average absolute alcohol intake was relatively arbitrarily categorized into no, low (>0 but <0.3 fl oz of absolute alcohol/day), and moderate/heavy (>/=0.3 fl oz of absolute alcohol/day) for the purpose of this study. Six years later, 665 families were contacted. Ninety-four percent agreed to testing. Exclusions included children who missed multiple test appointments, had major congenital malformations (other than fetal alcohol syndrome), possessed an IQ >2 standard deviations from the sample mean, or had incomplete data. The Achenbach Child Behavior Checklist (CBCL) was used to assess child behavior. The CBCL is a parent questionnaire applicable to children ages 4 to 16 years. It is widely used in the clinical assessment of children’s behavior problems and has been extensively used in research. Eight syndrome scales are further grouped into Externalizing or undercontrolled (Aggressive and Delinquent) behavior and Internalizing or overcontrolled (Anxious/Depressed, Somatic Complaints, and Withdrawn) behaviors. Three syndromes (Social, Thought, and Attention Problems) fit neither group. Higher scores are associated with more problem behaviors. Research assistants who were trained and blinded to exposure status independently interviewed the child and caretaker. Data were collected on a broad range of control variables known to influence childhood behavior and/or to be associated with prenatal alcohol exposure. These included perinatal factors of maternal age, education, cigarette, cocaine, and other substances of abuse and the gestational age of the baby. Postnatal factors studied included maternal psychopathology, continuing alcohol and drug use, family structure, socioeconomic status, children’s whole blood lead level, and exposure to violence. Data were collected only from black women as there was inadequate representation of other racial groups.

STATISTICAL ANALYSES:

Statistical analyses were performed using the SPSS statistical package. Frequency distribution, cross-tabulation, odds ratio, and chi(2) tests were used for analyzing categorical data. Continuous data were analyzed using t tests, analyses of variance (ANOVAs) with posthoc tests, and regression analysis.

RESULTS:

Testing was available for 501 parent-children dyads. Almost one fourth of the women denied alcohol use during pregnancy. Low levels of alcohol use were reported in 63.8% and moderate/heavy use in 13% of pregnancies. Increasing prenatal alcohol exposure was associated with lower birth weight and gestational age, higher lead levels, higher maternal age, and lower education level, prenatal exposure to cocaine and smoking, custody changes, lower socioeconomic status, and paternal drinking and drug use at the time of pregnancy. Children with any prenatal alcohol exposure were more likely to have higher CBCL scores on Externalizing (Aggressive and Delinquent) and Internalizing (Anxious/Depressed and Withdrawn) syndrome scales and the Total Problem Score. The odds ratio of scoring in the clinical range for Delinquent behavior was 3.2 (1.3-7.6) in children with any prenatal exposure to alcohol compared with nonexposed controls. The threshold dose was evaluated with the 3 prenatal alcohol exposure groups. One-way ANOVA revealed a significant between group difference for Externalizing (Aggressive and Delinquent) and the Total Problem Score

Source: Pediatrics. 2001 Aug;108(2):E34.PMID: 11483844 [PubMed – indexed for MEDLINE]

Abstract

BACKGROUND:

The development of the fetal endocannabinoid receptor system may be vulnerable to maternal cannabis use during pregnancy and may produce long-term consequences in children. In this study, we aimed to determine the relationship between gestational cannabis use and childhood attention problems and aggressive behavior.

METHODS:

Using a large general population birth cohort, we examined the associations between parental prenatal cannabis and tobacco use and childhood behavior problems at 18 months measured using the Child Behavior Checklist in N=4077 children. Substance use was measured in early pregnancy.

RESULTS:

Linear regression analyses demonstrated that gestational exposure to cannabis is associated with behavioral problems in early childhood but only in girls and only in the area of increased aggressive behavior (B=2.02; 95% CI: 0.30-3.73; p=0.02) and attention problems (B=1.04; 95% CI: 0.46-1.62; p<0.001). Furthermore, this study showed that long-term (but not short term) tobacco exposure was associated with behavioral problems in girls (B=1.16; 95% CI: 0.20-2.12; p=0.02). There was no association between cannabis use of the father and child behavior problems. CONCLUSIONS: Our results suggest that intrauterine exposure to cannabis is associated with an increased risk for aggressive behavior and attention problems as early as 18 months of age in girls, but not boys. Further research is needed to explore the association between prenatal cannabis exposure and child behavior at later ages. Our data support educating future mothers about the risk to their babies should they smoke cannabis during pregnancy. Source: http://www.ncbi.nlm.nih.gov/pubmed/21470799 4th April 2011

Reports that school prevention programs aimed at curbing alcohol misuse in children are somewhat helpful, enough so to deserve consideration for widespread use, according to a large, international systematic review.

The most significant program effects were reductions in episodes of drunkenness and binge drinking, reviewers found.

“School-based prevention programs that take a social skills-oriented approach or that focus on classroom behavior management can work to reduce alcohol problems in young people,” David Foxcroft, lead review author said. “However, there is good evidence that these sorts of approaches are not always effective.”

The reasons for inconsistent results with these programs are unclear, said Foxcroft, from Great Britain’s Oxford Brookes University.

Foxcroft and co-author Alexander Tsertsvadze, at the University of Ottawa Evidence-Based Practice Center, in Canada, analyzed 53 randomized controlled trials done in a wide range of countries with youth ages 5 to 18 when studies began.

Forty-one studies took place in North America, six in Europe and six in Australia. One was conducted in India and one in Swaziland. Two studies transpired in multiple locations.

Most studies assessed generic prevention programs that targeted several risky behaviors, such as drinking, smoking and drug abuse, while the rest focused on alcohol-specific programs.

The researchers compared drinking among the youngsters who took part in various school-based programs to the drinking done by students who were not. The youngsters in the comparison groups might have participated in other alcohol-prevention programs, such as family-based ones, or they might have just experienced the ordinary school curriculum.

The authors concluded that their evidence supported the use of certain generic prevention programs over alcohol-specific ones. They cited the Life Skills Training Program, the Unplugged Program and the Good Behavior Game as particularly effective interventions.

The review appears in the May 2011 issue of The Cochrane Library, a publication of The Cochrane Collaboration, an international organization that evaluates medical research. Systematic reviews draw evidence-based conclusions about medical practice after considering both the content and quality of existing medical trials on a topic.

“These findings are important,” David Jernigan, Ph.D., director of the Center on Alcohol Marketing and Youth at the Johns Hopkins Bloomberg School of Public Health, said. “Efforts to reduce young people’s drinking through school-based programs are legion. A $300 million federal program supporting school-based prevention ended last year, partly based on research findings that these programs do not work. This review does not find that. Instead it indicates that there is something in certain school-based programs that in fact can work.”

Jernigan emphasizes that “school-based programs are so often expected to do the whole job of prevention, and this is an unfair expectation.” He describes school-based programs functioning as “lonely voices” in an environment saturated with marketing messages promoting youthful drinking. The amount of drinking in a youngster’s home and community and the price of alcohol are other major influences that need addressing, he said. Until then, “we can’t expect large effects from school-based programs alone.”

Health Behavior News Service is part of the Center for Advancing Health.

Source: www.cadca.org 12th May 2011

This study sets out to broaden the evidence base by running a trial, based in UK general practice, where only brief support was available for participants while they compared nicotine nasal spray to placebo. It was based in 27 general practices and there was a total of 761 heavy smokers (at least 15 cigs/day for at least 3 years) who received brief support and 12 weeks of treatment with either nicotine nasal spray or placebo. The primary outcome was biochemically-verified complete abstinence from smoking throughout weeks 3-12.

The results showed that nicotine nasal spray more than doubled the number who successfully stopped smoking (15.4% vs 6.7%) from weeks 3-12 giving an odds ratio of 2.6 (95% CI 1.5-4.4). Although many reported minor irritant adverse effects it was noted to be particularly effective amongst those who were highly dependent on nicotine.

SMMGP comment: Tobacco harm reduction strategies is a neglected area although we know
that replacing smoking with a smokeless delivery system for the primary drug, nicotine, can reduce risks by about 99%, about the same as abstinence. Because smoking is so popular, the total health benefits from tobacco harm reduction dwarf those from any other area of HR.
There is an increasing array of nicotine replacement therapy options and this study shows one effective way of delivery. One interesting facet was the tiny number (0.2%) that went on to achieve abstinence if they were still smoking at one week. This infers that it may be worth prescribing a single week of nicotine nasal spray and reassessing abstinence. It?s a relatively small, inexpensive punt and it can double the chance of abstinence for that individual – even without the more comprehensive smoking cessation services which some prescribing is based around.

Source: Stapleton JA, Sutherland G. Addiction 2011;106:824-832

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

A single 15-minute exposure to nicotine caused a long-term increase in the excitability of neurons involved in reward, according to a study published in The Journal of Neuroscience. The results suggest that nicotine and cocaine hijack similar mechanisms of memory on first contact to create long-lasting changes in a person’s brain.
“Of course, for smoking it’s a very long-term behavioral change, but everything starts from the first exposure,” said Danyan Mao, PhD, postdoctoral researcher at the University of Chicago Medical Center. “That’s what we’re trying to tackle here: when a person first is exposed to a cigarette, what happens in the brain that might lead to a second cigarette?”
Learning and memory are thought to be encoded in the brain via synaptic plasticity, the long-term strengthening and weakening of connections between neurons. When two neurons are repeatedly activated together, a stronger bond forms between them, increasing the ability of one to excite the other.
Previous research in the laboratory of Daniel McGehee, PhD, neuroscientist and associate professor in the Department of Anesthesia & Critical Care at the Medical Center, discovered that nicotine could promote plasticity in a region of the brain called the ventral tegmental area (VTA). Neurons that originate in the VTA release the neurotransmitter dopamine, known to play a central role in the effects of addictive drugs and natural rewards such as food and sex.
“We know that a single exposure to physiologically relevant concentrations of nicotine can lead to changes in the synaptic drive in the circuitry that lasts for several days,” said McGehee, senior author of this study. “That idea is very important in how addiction forms in humans and animals.”
In the new experiments, Mao monitored the electrical activity of VTA dopamine neurons in slices of brain dissected from adult rats. Each slice was bathed for 15 minutes in a concentration of nicotine similar to the amount that would reach the brain after smoking a single cigarette. After 3-5 hours, Mao conducted electrophysiology experiments to detect the presence of synaptic plasticity and determine which neurotransmitter receptors were involved in its development.
Mao discovered that nicotine-induced synaptic plasticity in the VTA is dependent upon one of the drug’s usual targets, a receptor for the neurotransmitter acetylcholine located on the dopamine neurons. But another element found necessary for nicotine’s synaptic effects was a surprise: the D5 dopamine receptor, a component previously implicated in the action of cocaine. Blocking either of these receptors during nicotine exposure eliminated the drug’s ability to cause persistent changes in excitability.
“We found that nicotine and cocaine employ similar mechanisms to induce synaptic plasticity in dopamine neurons in VTA,” Mao said.
While the subjective effects of nicotine and cocaine are very different in humans, the overlapping effects of the two drugs on the reward system of the brain may explain why both are highly addictive substances, the researchers said.
“We know without question that there are big differences in the way these drugs affect people,” McGehee said. “But the idea that nicotine is working on the same circuitry as cocaine does point to why so many people have a hard time quitting tobacco, and why so many who experiment with the drug end up becoming addicted.”
The overlap between nicotine and cocaine effects at the D5 receptor may also offer a novel strategy for preventing or treating addiction. However, currently-known blockers of the receptor also block another dopamine receptor, D1, that is important for normal, healthy motivation and movement.
“This dopamine receptor is attractive as a potential target,” McGehee said. “The real challenge is to tweak the addictive effect of drugs like nicotine or other psychostimulants without totally crushing the person’s desire to pursue healthy behavior.”
Future research will also focus on whether repeated exposure to nicotine, as would occur in a regular smoker, changes the drug’s effects on synaptic plasticity in the VTA. In the meantime, the current study builds evidence that addictive drugs appropriate the neurobiological tools of learning and memory to create long-term changes in brain reward pathways.
“It’s all fitting with the overriding idea that changes in synaptic strength are part of the way these drugs motivate behavior in a persistent way,” McGehee said.
The study, “Nicotine Potentiation of Excitatory Inputs to Ventral Tegmental Dopamine Neurons,” will be published May 4, 2011 by The Journal of Neuroscience. In addition to Mao and McGehee, Keith Gallagher of the University of Chicago is a co-author.
The research was supported by grants from the Women’s Council of the Brain Research Foundation and the National Institutes of Health.

Source: University of Chicago Medical Center (2011, May 4). Nicotine and cocaine leave similar mark on brain after first contact. ScienceDaily. Retrieved May 8, 2011, from http://www.sciencedaily.com¬ /releases/2011/05/110503171745.htm

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

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

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

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

Source: www.cadca.org 5th May 2011

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

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

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

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

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

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

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

Source: www.anglia.ac.uk May 2011

May 2, 2011

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

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

It requires 70 gallons of diesel fuel to produce one indoor Cannabis plant, or 140 gallons with smaller, less-efficient gasoline generators. In California, the top-producing state, indoor cultivation is responsible for about 3% of all electricity use or 8% of household use, somewhat higher than estimates previously made
for British Columbia.17 This corresponds to the electricity use of 1 million average
California homes, greenhouse-gas emissions equal to those from 1 million average cars, and energy expenditures of $3 billion per year. Due to higher electricity prices and cleaner fuels used to make electricity, California incurs 70% of national energy costs but contributes only 20% of national CO2 emissions from indoor Cannabis cultivation.

From the perspective of individual consumers, a single Cannabis cigarette represents 2 pounds of CO2 emissions, an amount equal to running a 100-watt light bulb for 17 hours assuming average U.S. electricity emissions (or 30 hours on California’s cleaner grid).

The emissions associated with one kilogram of processed Cannabis are equivalent to those of driving across country 5 times in a 44-mpg car. One single production module doubles the electricity use of an average U.S. home and triples that of an average California home. The added electricity use is equivalent to running about 30 refrigerators.

Producing one kilogram of processed Cannabis results in 3,000 kilograms of CO2 emissions. The energy embodied in the production of inputs such as fertilizer, water, equipment, and building materials is not estimated here and should be considered in future assessments.

Source: http://evan-mills.com/energy-associates/Indoor.html April 2011

Many mothers and fathers think that allowing their children to have a supervised drink is a good way of exposing them to alcohol safely and taking away its illicit thrill. But new research suggests it sends mixed signals that result in them being more likely to abuse alcohol as they enter their core teenage years.
A joint American-Australian study of more than 1,900 12 and 13-year-olds found that those whose parents took such a “harm minimisation” approach were more likely to have experienced “alcohol-related consequences” – such as not being able to stop drinking, getting into fights, or having blackouts – two years later than those whose parents had a “zero-tolerance” strategy.
A year into the study, almost twice as many Australian teenagers (67 per cent) had drunk alcohol in the presence of an adult than their American counterparts (35 per cent), reflecting general attitudes in Australia and the US when it comes to supervised underage drinking.
The following year, just over a third (36 per cent) of the Australians had experienced alcohol-related consequences compared to only a fifth (21 per cent) of the Americans.
While cultural differences alone could feasibly account for the disparity, the results also found that teens who had been allowed to drink while supervised were more likely to have had such experiences regardless of which country they were from.
The results of the study, conducted by the Centre for Adolescent Health in Melbourne, Australia, and the Social Development Research Group in Seattle, USA, are published today in the Journal of Studies on Alcohol and Drugs.
British attitudes to teenage drinking are more similar to those in Australia than America, a matter reflected in law. While in the UK and Australia one can buy an alcoholic drink in a pub or off-licence from the age of 18, in the US the minimum age is 21. However, two years ago Sir Liam Donaldson, then England’s chief medical officer, said children under 15 should never be given alcohol, even though it is legal for parents to give a child over five alcohol in the home.
A separate Dutch study of 500 12-to-15-year-olds, also published in the JSAD today, found that it was the amount of alcohol available at home, and not how much parents drank, that determined teenage drinking habits – suggesting parents should keep their drinks cabinets locked.
Dr Barbara McMorris, of Minnesota University, who led the first study, said: “Both studies show that parents matter. “Despite the fact that peers and friends become important influences as adolescents get older, parents still have a big impact.” She added: “Kids need parents to be parents and not drinking buddies. Adults need to be clear about what messages they are sending. Kids need black and white messages early on. “Such messages will help reinforce limits as teens get older and opportunities to drink increase.”

Source: www.telegraph.co.uk/health 28th April 2011

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

Background

Methamphetamine (METH), an abused illicit drug, disrupts many cellular processes, including energy metabolism, spermatogenesis, and maintenance of oxidative status. However, many components of the molecular underpinnings of METH toxicity have yet to be established. Network analyses of integrated proteomic, transcriptomic and metabolomic data are particularly well suited for identifying cellular responses to toxins, such as METH, which might otherwise be obscured by the numerous and dynamic changes that are induced.

Methodology/Results

We used network analyses of proteomic and transcriptomic data to evaluate pathways in Drosophila melanogaster that are affected by acute METH toxicity. METH exposure caused changes in the expression of genes involved with energy metabolism, suggesting a Warburg-like effect (aerobic glycolysis), which is normally associated with cancerous cells. Therefore, we tested the hypothesis that carbohydrate metabolism plays an important role in METH toxicity. In agreement with our hypothesis, we observed that increased dietary sugars partially alleviated the toxic effects of METH. Our systems analysis also showed that METH impacted genes and proteins known to be associated with muscular homeostasis/contraction, maintenance of oxidative status, oxidative phosphorylation, spermatogenesis, iron and calcium homeostasis. Our results also provide numerous candidate genes for the METH-induced dysfunction of spermatogenesis, which have not been previously characterized at the molecular level.

Conclusion

Our results support our overall hypothesis that METH causes a toxic syndrome that is characterized by the altered carbohydrate metabolism, dysregulation of calcium and iron homeostasis, increased oxidative stress, and disruption of mitochondrial functions.

Source: . PLoS ONE 6(4): e18215. doi:10.1371/journal.pone.0018215. (2011)
Sun L, Li H-M, Seufferheld MJ, Walters KR Jr, Margam VM, et al. Sun L, Li H-M, Seufferheld MJ, Walters KR Jr, Margam VM, et al.

A public-smoking ban in Australia has led more parents to smoke at home, raising health risks for kids, researchers say.
The research from the Australian National University’s Research School of Social Sciences concluded that “bans in recreational public places can perversely increase tobacco exposure of nonsmokers … Children seem to be particularly affected. The level of cotinine (a nicotine by product measurable in saliva) in children considerably increases as a result of bans in public places.”
Public smoking bans tend to “displace smokers to private places where they contaminate nonsmokers,” said authors Jerome Adda, Ph.D., and Francesca Cornaglia, Ph.D., visiting scholars from University College London.

Source: Medical Post April 4 2006

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

The research demonstrates for the first time that cannabinoid receptors called CB2, which can be activated by cannabis use, are present in human sensory nerves in the peripheral nervous system, but are not present in a normal human brain.
Drugs which activate the CB2 receptors are able to block pain by stopping pain signals being transmitted in human sensory nerves, according to the study, led by researchers from Imperial College London.
Previous studies have mainly focused on the other receptor activated by cannabis use, known as CB1, which was believed to be the primary receptor involved in pain relief. However, as CB1 receptors are found in the brain, taking drugs which activate these receptors can lead to side-effects, such as drowsiness, dependence and psychosis, and also recreational abuse.
The new research indicates that drugs targeting CB2 receptors offer a new way of treating pain in clinical conditions where there are currently few effective or safe treatments, such as chronic pain caused by osteoarthritis and pain from nerve damage. It could also provide an alternative treatment for acute pain, such as that experienced following surgical operations.

The new study showed that CB2 receptors work to block pain with a mechanism similar to the one which opiate receptors use when activated by the powerful painkilling drug morphine. They hope that drugs which target CB2 might provide an alternative to morphine, which can have serious side effects such as dependency, nausea and vomiting.

Praveen Anand, Professor of Clinical Neurology and Principal Investigator of the study from the Division of Neurosciences and Mental Health at Imperial College London, said: ”Although cannabis is probably best known as an illegal recreational drug, people have used it for medicinal purposes for centuries. Queen Victoria used it in tea to help with her period pains, and people with a variety of conditions say that it helps alleviate their symptoms.

“Our new study is very promising because it suggests that we could alleviate pain by targeting the cannabinoid receptor CB2 without causing the kinds of side-effects we associate with people using cannabis itself.”
The researchers reached their conclusions after studying human sensory nerve cells in culture with CB2 receptor compounds provided by GlaxoSmithKline, and also injured nerves from patients with chronic pain.
The researchers are now planning to conduct clinical trials of drugs which target CB2 in patients with chronic pain at Imperial College Healthcare NHS Trust, which has integrated with Imperial College London to form the UK’s first Academic Health Science Centre.

Source: Anand et al. Cannabinoid receptor CB2 localisation and agonist-mediated inhibition of capsaicin responses in human sensory neurons. Pain, 2008; 138 (3): 667 DOI: 10.1016/j.pain.2008.06.007

Cannabis contains a chemical called THC, which binds to, and activates, proteins in the brain known as ‘CB1 cannabinoid receptors’. Activating these receptors can relieve pain and prevent epileptic seizures; but it also causes the mood-altering effect experienced by people who use cannabis as a recreational drug.

Now, Professor Maurice Elphick and Dr Michaela Egertová from Queen Mary’s School of Biological and Chemical Sciences may have found a way of separating out the effects of cannabis – a discovery which could lead to the development of new medicines to treat conditions such as epilepsy, obesity and chronic pain. The research is described in the December issue of the journal Molecular Pharmacology.

Working in collaboration with scientists based in the USA*, they have identified a protein that binds to the CB1 receptors in the brain. But unlike THC, this ‘Cannabinoid Receptor Interacting Protein’ or CRIP1a, suppresses the activity of CB1 receptors.

Professor Elphick explains: “Because CRIP1a inhibits the activity of the brain’s cannabinoid receptors, it may be possible to develop drugs that block this interaction, and in turn enhance CB1 activity. This may give patients the pain relief associated with CB1 activity, without the ‘high’ that cannabis users experience.”

Leslie Iversen FRS, Professor of Pharmacology at the University of Oxford and author of The Science of Marijuana, commented on the new findings: “This interesting discovery provides a completely new insight into the regulation of the cannabinoid system in the brain – and could offer a new approach to the discovery of cannabis-based medicines in the future.”

“CB1 Cannabinoid Receptor Activity Is Modulated by the Cannabinoid Receptor Interacting Protein CRIP1a” is published online in the December issue of Molecular Pharmacology.
The Elphick laboratory in the School of Biological & Chemical Sciences at Queen Mary is supported by grants from UK research councils (BBSRC, MRC) and the Wellcome Trust.

Source:
The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Queen Mary, University of London. 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

Background

Many studies have suggested that adolescence is a period of particular vulnerability to neurocognitive effects associated with substance misuse. However, few large studies have measured differences in cognitive performance between chronic cannabis users who started in early adolescence(before age 15) with those who started later.

 Aims

To examine the executive functioning of individuals who started chronic cannabis use before age 15 compared with those who started chronic cannabis use after 15 and controls.

Method

We evaluated the performance of 104 chronic cannabis users (49 early-onset users and 55 late-onset users) and 44 controls who undertook neuropsychological tasks, with a focus on executive functioning. Comparisons involving neuropsychological measures were performed using generalised linear model analysis of variance (ANOVA).

 Results

The early-onset group showed significantly poorer performance compared with the controls and the late-onset group on tasks assessing sustained attention, impulse control and executive functioning.

Conclusions

Early-onset chronic cannabis users exhibited poorer cognitive performance than controls and late-onset users in executive

functioning. Chronic cannabis use, when started before age 15, may have more deleterious effects on neurocognitive functioning.

Source:  The British Journal of Psychiatry (2011) 198, 442–447. doi: 10.1192/bjp.bp.110.077479

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

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

A new study suggests that the brain damage suffered by children whose mothers used metamphetamine during pregnancy may be even worse than the effects that alcohol has on a fetus.

Researchers at the University of California, Los Angeles, found that some of the brain regions of meth-exposed children were even smaller than in alcohol-exposed children. One such region is the caudate nucleus, which plays a role in learning, memory, motor control, and motivation.

“Our findings stress the importance of drug abuse treatment for pregnant women,” said research team leader Elizabeth Sowell.

According to Sowell and her colleagues, being able to identify which brain structures are affected in meth-exposed children may help predict the specific types of leaning and behavioral problems that will afflict these children.

 Source:  The Journal of Neuroscience. March 17 2011

Brain abnormalities could be help explain why certain people could have a pre-disposition to cocaine dependency, according to research published today.

In a report in The Herald newspaper today, researchers at theUniversity of Cambridge have identified the abnormalities in the frontal lobe of cocaine users’ brains which are linked to their compulsive cocaine-using behaviour. Scientists think these abnormalities could help explain why some people are more prone to drug dependency.

The researchers, led by Dr Karen Ersche of the University’s Behavioural and Clinical Neuroscience Institute,  scanned the brains of 120 people, half of whom had a dependence on cocaine.   They found that the cocaine users had widespread loss of grey matter which was directly related to the duration of their cocaine use and that this reduction in volume was associated with greater compulsivity to take cocaine.

The scientists also found that parts of the brain reward system where cocaine exerts its actions were significantly enlarged in cocaine users. This was not linked to the duration of the user’s habit.

The researchers believe this may suggest that alterations in the brain’s reward system predate cocaine use, possibly making these individuals more vulnerable to the effects of the drug.

The Advisory Council on the Misuse of Drugs is currently carrying out a review of the harms associated with cocaine.

Source:  www.heraldscotland.com  11^th June 2011

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

Teenagers – especially girls – who binge drink could be damaging the part of their brain which controls memory and spatial awareness, say Californian researchers.

Young women’s brains are particularly vulnerable to harm from alcohol because they develop earlier than men’s.  Tests on 95 adolescents aged 16 to 19 were carried out by researchers at severalUSuniversities.

The study is published in Alcoholism: Clinical & Experimental Research.

Researchers recruited 27 binge-drinking males and 13 females and gave them neurophsychological tests and “spatial working memory” tests to complete.

Binge-drinking young women were defined as those drinking more than three pints of beer or more than four glasses of wine at one sitting. Binge-drinking men drank four pints of beer or a bottle of wine.   The same tests were then carried out on 31 males and 24 females who did not have episodes of drinking heavily and the results compared.

Using MRI scans, the study team found that female teenage heavy drinkers had less brain activation in several brain regions than female non-drinking teens when doing the same spatial task.  They suggested that this could cause problems when driving, playing sports involving complex moves, using a map or remembering how to get somewhere.

Susan Tapert, professor of psychiatry at theUniversityofCaliforniaand lead study author, said these differences in brain activity negatively affected other functions, like concentration and “working memory”.

The study describes “working memory” as using and working with information that is in your mind, like adding up numbers. It is also critical to logical thinking and reasoning.  But the young men studied were not affected to the same extent, Dr Tapert said.   “Male binge drinkers showed some, but less, abnormality as compared to male non-drinkers. This suggests that female teens may be particularly vulnerable to the negative effects of heavy alcohol use.”

Fluctuations

Previous research has shown that among adult alcoholics, women are more vulnerable to the damaging effects of alcohol on the brain than men.

Edith Sullivan, a professor in psychiatry and behavioural sciences atStanfordUniversity, said that the brains of adolescent boys and girls appear to be affected differently by alcohol.  “Females’ brains develop one to two years earlier than males, so alcohol use during a different developmental stage – despite the same age – could account for the gender differences.

“Hormonal levels and alcohol-induced fluctuations in hormones could also account for the gender differences. Finally, the same amount of alcohol could more negatively affect females since females tend to have slower rates of metabolism, higher body fat ratios, and lower body weight.”

Don Shenker, from Alcohol Concern, said the research demonstrates why reducing binge drinking among young people must be an urgent priority. “Ministers should go much further to clamp down on off-licence promotions which are driving under-age drinking and reviewing the extent of alcohol marketing which young people are exposed to and which makes drinking appear attractive.

“We have to also look at intervening as early as possible so that when teenagers go to A&E as a result of drinking or in trouble with the police or at school, they are provided with the right advice and support to reduce their risky drinking and make healthier choices.”

A Department of Health spokeswoman said “We are already taking action to tackle problem drinking, including plans to stop supermarkets selling below cost alcohol and working to introduce a tougher licensing regime.   “Our recent white paper set out our plan to ring-fence public health spending and give power to local communities to improve the health of local people and this includes improving alcohol treatment services through a greater focus on outcomes and payment by results.   We will also be publishing a new alcohol strategy later this year to follow on from the public health white paper.”

Source: www.bbc.co.uk  16^th July 2011

Abstract

OBJECTIVE:

Prenatal cocaine exposure has been associated with alterations in neonatal behavior and more recently a dose-response relationship has been identified. However, few data are available to address the long-term behavioral effects of prenatal exposures in humans. The specific aim of this report is to evaluate the school-age behavior of children prenatally exposed to cocaine.

METHODS:

All black non-human immunodeficiency virus-positive participants in a larger pregnancy outcomes study who delivered singleton live born infants between September 1, 1989 and August 31, 1991 were eligible for study participation. Staff members of the larger study extensively screened study participants during pregnancy for cocaine, alcohol, cigarettes, and other illicit drugs. Prenatal drug exposure was defined by maternal history elicited by structured interviews with maternal and infant drug testing as clinically indicated. Cocaine exposure was considered positive if either history or laboratory results were positive. Six years later, 665 families were contacted; 94% agreed to participate. The child, primary caretaker (parent), and, when available, the biologic mothers were tested in our research facilities. Permission was elicited to obtain blinded teacher assessments of child behavior with the Achenbach Teacher’s Report Form (TRF). Drug use since the child’s birth was assessed by trained researchers using a structured interview.

RESULTS:

Complete laboratory and teacher data were available for 499 parent-child dyads, with a final sample size for all analyses of 471 (201 cocaine-exposed) after the elimination of mentally retarded subjects. A comparison of relative Externalizing (Aggressive, Delinquent) to Internalizing (Anxious/Depressed, Withdrawn, Somatic Complaints) behaviors of the offspring was computed for the TRF by taking the difference between the 2 subscales to create an Externalizing-Internalizing Difference (T. M. Achenbach, personal communication, 1998). Univariate comparisons revealed that boys were significantly more likely to score in the clinically significant range on total TRF, Externalizing-Internalizing, and Aggressive Behaviors than were girls. Children prenatally exposed to cocaine had higher Externalizing-Internalizing Differences compared with controls but did not have significantly higher scores on any of the other TRF variables. Additionally, boys prenatally exposed to cocaine were twice as likely as controls to have clinically significant scores for externalizing (25% vs 13%) and delinquent behavior (22% vs 11%). Gender, prenatal exposures (cocaine and alcohol), and postnatal risk factors (custody changes, current drug use in the home, child’s report of violence exposure) were all related to problem behaviors. Even after controlling for gender, other prenatal substance exposures, and home environment variables, cocaine-exposed children had higher Externalizing-Internalizing Difference scores. Prenatal exposure to alcohol was associated with higher total score, increased attention problems, and more delinquent behaviors. Prenatal exposure to cigarettes was not significantly related to the total TRF score or any of the TRF subscales. Postnatal factors associated with problem behaviors included both changes in custody status and current drug use in the home. Change in custody status of the cocaine-exposed children, but not of the controls, was related to higher total scores on the TRF and more externalizing and aggressive behaviors. Current drug use in the home was associated with higher scores on the externalizing and aggressive subscales.

CONCLUSIONS:

Results of this study suggest gender-specific behavioral effects related to prenatal cocaine exposure. Prenatal alcohol exposure also had a significant impact on the TRF. Postnatal exposures, including current drug use in the home and the child’s report of violence exposure, had an independent effect on teacher-assessed child behavioral problems.

Source:  Pediatrics. 2000 Oct;106(4):782-91.

A highly-toxic class-A drug is being sold inScotland, according to senior police officers. ParaMethoxyMethylAmphetamine (PMMA) has been found in tablets which look like ecstasy.

The substance has also been found in drugs being sold as “legal highs” inScotland.

The Association of Chief Police Officers Scotland said it had recovered quantities of PMMA after a series of raids. It has been produced in pink tablets with a Rolex crown logo, and in white tablets with a four-leaf clover logo.

PMMA has also been recovered in powder form and police said it may also be present in other products and tablets.

Det Inspector Tommy Crombie, of the Scottish Crime and Drug Enforcement Agency, said: “PMMA is a stimulant similar to ecstasy but it is not as potent. Users… may be tempted to take more tablets to achieve the desired effect, increasing the risk of a potentially fatal overdose.”

“I would strongly advise drug users to avoid such products and follow harm reduction advice where necessary.”

From BBC News Scotland July 2011

Gil Kerlikowske, Director of National Drug Control Policy released the Administration’s 2011 National Drug Control Strategy in July .This Strategy coordinates an unprecedented government-wide public health and safety approach to reduce drug use and its consequences in the United States.  The Administration’s new Strategy continues to expand upon a balanced approach to drug control that emphasizes community-based drug prevention, integration of drug treatment into the mainstream health care system, innovations in the criminal justice system to break the cycle of drug use and crime, and international partnerships to disrupt transnational drug trafficking organizations.  The final paragraph of the report says:

“Overall drug use in theUnited Stateshas dropped substantially over the past thirty years. In response to comprehensive efforts to address drug use at the local, state, Federal, and international levels, the rate of Americans using illicit drugs today is roughly half the rate it was in the late 70s. More recently, there has been a 46 percent drop in current cocaine use among young adults (age 18 to 25 years) over the past five years, and a 68 percent drop in the rate of people testing positive for cocaine in the workplace since 2006.”

Source:  DFAF  July 2011