Category: Alcoholism

There has been an abundance of research on the associations between drinking behavior and marital status, but many questions remain regarding the timing of when an individual gets married and divorced and if there is any relation to alcohol use.

A new study released in the April 2011 issue of Alcoholism: Clinical & Experimental Research, which is currently available at Early View, explores that subject in detail and found that alcohol dependence was a strong predictor of both delays in marriage and early separation.

According to Mary Waldron, an assistant professor at the Indiana University School of Education and lead author, few studies have examined the impact of alcohol involvement on timing in marital transitions across development.

"Previous research documented associations between adolescent substance use and early marriage or cohabitation, but much of this work did not follow participants past their 20s," she said.

The researchers recruited over 5,000 Australian twins in the early 1980s, assessing physical, psychological and physical manifestations of alcohol use, including age at onset of alcohol dependence. The researchers also established age of first marriage and age of separation from the marriage in twins who were between the ages of 28 and 92 at last assessment.

Although early drinking is one of the best predictors of later alcohol dependence, the results showed that there was a strong association between alcohol dependence and delayed marriage, as well as early separation. It was also found that genetic influences contributed to these associations for both men and women. According to Waldron, while heritable risks appear to be important, additional research is needed to better understand the role of genes and their interplay with environmental influences.

While follow-up studies with more diverse samples are also needed, the results of this study underscore the fact that problem drinking affects more people than simply the alcoholic.

"Young adults who drink alcohol may want to consider the longer-term consequences for marriage," said Waldron. "If drinking continues or increases to levels of problem use, likelihood of marriage, or of having a lasting marriage, may decrease."

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Journal Reference:

1. Mary Waldron, Andrew C. Heath, Michael T. Lynskey, Kathleen K. Bucholz, Pamela A. F. Madden, Nicholas G. Martin. Alcoholic Marriage: Later Start, Sooner End. Alcoholism: Clinical and Experimental Research, 2011; DOI: 10.1111/j.1530-0277.2010.01381.x

Drinking is a popular pastime for most adolescents, but when copious amounts of alcohol are consumed (known as binging) on a regular basis, it could be indicative of a deeper problem. Therefore, researchers in the Netherlands set out to answer two questions: Why do some adolescents engage in binging so frequently, and is there a possible genetic component?

The answers will be published in the April 2011 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.

Carmen S. van der Zwaluw, senior author of the study and PhD candidate at Radboud University in the Netherlands, said that this study is the first to examine the possible association between different genes, coping drinking, and risky alcohol use in adolescents.

"Other studies have shown that alcohol use, and especially risky alcohol use, is partly heritable," said van der Zwaluw. "These studies did not show, however, which specific genes are involved in the genetic predisposition for risky alcohol use. Thus, one of the things that alcohol researchers are now trying to clarify is which genes make up the genetic vulnerability for alcohol (mis)use."

The researchers examined 282 Dutch adolescents that had consumed alcohol at least once during their lives, collected DNA samples and administered questionnaires to determine their reasons for drinking and the intensity of alcohol-related problems that they had experienced.

For the DNA analysis, variations in two different genes were examined: the dopamine D2 receptor gene (DRD2) that is involved in the reward pathway, and the serotonin transporter gene (SLC6A4), which plays a role in emotional states. The results showed that the risk allele of the DRD2 variation, and not in the SLC6A4 gene, implicates a genetic vulnerability for both binge drinking and alcohol-related problems that may only appear if they drink to suppress or eliminate negative emotions.

"I am thrilled about the gene-environment interaction that was found in this study indicating that the relation between coping motives and alcohol consumption was stronger among the DRD2 risk allele carriers," said Helle Larsen, a PhD candidate at the Behavioural Science Institute, Radboud University. "This relation should definitely be investigated more thoroughly in future research."

Van der Zwaluw agrees that since the research is the first of its kind, it must be replicated to show that it was correct and not just an anomaly.

"[The next step] would be examining whether other genetic variants increase the risk for drinking problems, and if this risk can be decreased by learning other coping styles to handle the problems."

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Journal Reference:

1. Carmen S. van der Zwaluw, Emmanuel Kuntsche, Rutger C. M. E. Engels. Risky Alcohol Use in Adolescence: The Role of Genetics (DRD2, SLC6A4) and Coping Motives. Alcoholism: Clinical and Experimental Research, 2011; DOI: 10.1111/j.1530-0277.2010.01393.x

 A Letter to the Editor entitled "What should we advise about alcohol consumption?" was recently published by Maurizio Ponz de Leon in the journal Internal and Emergency Medicine. Dr. de Leon argues that the message of health benefits of moderate drinking "seems to me hazardous and extremely dangerous to diffuse in the general population."

His reasons included (1) many people may be unable to distinguish between low-moderate and high consumption of wine, beer or spirits, and alcohol metabolism may differ remarkably from one subject to another; (2) alcohol remains a frequent cause of car crash, and governments (in almost all western countries) try to convince or force people to abstain from drinking before driving; and (3) to consider alcohol as a medication whose consumption may contribute to improved health is another source of concern.

Dr. de Leon asks: "Are we truly at the point of prescribing alcohol consumption in order to reduce the risk of stroke and coronary damage?" He concluded "more studies are needed before we can give sensible recommendations on alcohol consumption to the general population."

The de Leon editorial has prompted considerable response from other scientists, including further Letters to the Editor of the journal by Di Castelnuovo, Costanzo, Donati, Iacoviello, and de Gaetano, and by Estruch and Lamuela-Raventos.

In addition, the original editorial has stimulated considerable debate among members of the International Scientific Forum on Alcohol Research. Among key arguments presented by the Forum members, all experts in scientific research on alcohol, are that messages to the public should not be "paternalistic" (we will tell you what is best for you since you are not smart enough to understand the facts), and that guidelines must always be based on sound, balanced scientific data rather than on uninformed opinion. Forum members emphasized that there are certain people who should not drink at all (including former abusers of drugs or alcohol, people with certain medical conditions, children and adolescents, and people with religious or moral proscriptions against alcohol), and there can never be a general recommendation for everybody to consume alcohol.

On the other hand, physicians should not withhold from their patients and the public scientifically sound and balanced data on alcohol and health. And the data are extremely strong supporting a role for moderate alcohol intake, for appropriate adults, for the reduction in risk of coronary artery disease and other diseases of ageing.

Several Forum members pointed out that it was unfortunate that the journal had chosen to publish the original letter that castigates alcohol from an author with good scientific credentials, but little to no apparent research expertise in the subject of alcohol and health. Many Forum members disagreed with the statement of de Leon that "Many people may be unable to distinguish between low-moderate and high consumption of wine, beer or spirits."

A leading scientist dealing with this subject for decades, Dr. Arthur Klatsky, has written: "Most people know very well what the difference is between light to moderate drinking and binge or excessive drinking. While some patients may rationalize their heavy drinking because of its purported health effects, I have yet to find someone who had developed alcohol abuse because of messages about the health effects of moderate drinking." Medical practitioners, in his view, "have a 'solemn duty' to tell the truth about alcohol consumption, as they understand it, to all of their patients."

While pointing out that certain individuals will not benefit from the consumption of alcohol, several Forum members believed that it would be unethical for physicians to withhold from middle-aged or elderly subjects at risk of cardiovascular disease information on the potential benefits of light-to-moderate drinking

Contributions to this critique by the International Scientific Forum on Alcohol Research were provided by the following members:

• Francesco Orlandi, MD, Dept. of Gastroenterology, Università degli Studi di Ancona. Italy
• Fulvio Ursini, MD, Dept. of Biological Chemistry, University of Padova, Padova, Italy
• R. Curtis Ellison, MD, Section of Preventive Medicine & Epidemiology, Boston University School of Medicine, Boston, MA, USA
• Arne Svilaas, MD, PhD, general practice and lipidology, Oslo University Hospital, Oslo, Norway
• Harvey Finkel, MD, Hematology/Oncology, Boston University Medical Center, Boston, MA, USA
• Andrew L. Waterhouse, PhD, Marvin Sands Professor, Department of Viticulture and Enology, University of California, Davis
• Erik Skovenborg, MD, Scandinavian Medical Alcohol Board, Practitioner, Aarhus, Denmark
• Maritha J. Kotze, PhD, Human Genetics, Dept of Pathology, and David Van Velden, MD, Dept. of Pathology, University of Stellenbosch, South Africa
• Ulrich Keil, MD, PhD, Institute of Epidemiology and Social Medicine, University of Münster, Münster, Germany
• Tedd Goldfinger, DO, FACC, Desert Cardiology of Tucson Heart Center, Dept. of Cardiology, University of Arizona School of Medicine, Tucson, Arizona, USA

For the detailed critique of this paper by the International Scientific Forum on Alcohol Research: http://www.bu.edu/alcohol-forum/critique-029-differing-opinions-on-the-message-to-the-public-regarding-alcohol-consumption16-january-2011/

The 40 alcohol and health specialists who are members of the Forum are happy to respond to questions from Health Editors regarding emerging research on alcohol and health and will offer an independent opinion in context with other research on the subject.

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Journal References:

1. Maurizio Ponz de Leon. What should we advise about alcohol consumption. Internal and Emergency Medicine, 2010; DOI: 10.1007/s11739-010-0487-1
2. Augusto Castelnuovo, Simona Costanzo, Maria Benedetta Donati, Licia Iacoviello, Giovanni Gaetano. What should we advise about alcohol consumption: reply letter by A. Di Castelnuovo. Internal and Emergency Medicine, 2011; DOI: 10.1007/s11739-010-0502-6
3. Ramon Estruch, Rosa Ma Lamuela-Raventós. What should we advise about alcohol consumption: reply letter by R. Estruch. Internal and Emergency Medicine, 2011; DOI: 10.1007/s11739-010-0503-5

Marketing efforts that encourage mixing caffeinated "energy" drinks with alcohol often try to sway young people to believe that caffeine will offset the sedating effects of alcohol and increase alertness and stamina.

But a new study led by researchers from the Boston University School of Public Health and the Center for Alcohol and Addiction Studies at Brown University has found that the addition of caffeine to alcohol — mixing an energy drink with vodka, for example — has no effect on enhancing performance on a driving test or improving sustained attention or reaction times.

"There appears to be little or no protective benefit from the addition of caffeine to alcohol, with respect to the safe execution of activities that require sustained attention with rapid, accurate decisions," says the study, published in the February edition of the journal Addiction.

"The results of this study suggest that public education, via media and warning labels, should be considered regarding the safety of CABs [caffeinated alcoholic beverages], and that regulators should scrutinize energy drink and CAB advertising as it relates to promoting safety-related expectancies."

The study, headed by Jonathan Howland, professor of community health sciences at BUSPH, comes amid increased government scrutiny of energy drinks, particularly when mixed with alcohol. Denmark has banned the sale of energy drinks, and the governments of Canada and Sweden have issued warnings about mixing energy drinks with alcohol.

In 2009, the US Food and Drug Administration issued a statement expressing concern about a lack of safety data on CABs, after survey results showed that the consumption of such beverages correlated with risky behavior among college students.

Howland and his co-authors note that while energy drink companies do not explicitly advertise that their products should be mixed with alcohol, "non-traditional youth-oriented marketing strategies" include claims that such drinks will "enhance attention, endurance, performance, weight loss, and fun, while reducing performance decrements from fatigue from alcohol."

In the new study, the research team randomized 129 participants, ages 21 to 30, into four groups: one group that consumed caffeinated beer; a second that consumed non-caffeinated beer; a third that consumed caffeinated non-alcoholic beer; and a fourth that consumed non-caffeinated, non-alcoholic beer. Those receiving alcohol attained an average blood alcohol level of .12 grams percent — somewhat higher than 0.8 grams percent, the legal per se level for driving under the influence.

Thirty minutes after drinking, the participants were tested on a driving simulator and on a sustained attention/reaction time test.

The results indicate that caffeine does not mitigate the impairment effects of alcohol. On the driving test, the effect of alcohol on performance was significant — but the addition of caffeine did not make a noticeable difference. On the test for sustained attention and reaction times, the addition of caffeine made only a slight difference that the study deemed "borderline significant."

Howland summed up the study results: "It is important that drinkers understand that adding caffeine to alcohol does not enhance safety."

Consumption of energy drinks mixed with alcohol has mushroomed since 2001, with some surveys showing that one in four college students report mixing the two. Some studies have found that caffeine reverses alcohol-related performance impairment on tests of reaction time, attention and psychomotor speed, but not on error rates. Other studies have found that caffeine does not significantly impact alcohol-induced impairment of motor coordination.

Howland said the new study was one of the first to provide "a controlled evaluation of the acute effects of caffeine on driving impairment" after drinking to intoxication levels. The institutional review boards of Boston Medical Center, Brown University and the University of Michigan approved the study.

In addition to Howland, researchers on the study include: Damaris J. Rohsenow of the Center for Alcohol and Addiction Studies at Brown University; J. Todd Arnedt of the Sleep and Chronophysiology Laboratory of the University of Michigan Medical School; Daniel J. Gottleib of the Boston University School of Medicine; and Caleb A. Bliss, Sarah K. Hunt, Tamara Vehige Calise, Timothy Heeren, Michael Winter and Caroline Littlefield, all of BUSPH.

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Journal Reference:

1. Jonathan Howland, Damaris J. Rohsenow, J. Todd Arnedt, Caleb A. Bliss, Sarah K. Hunt, Tamara Vehige Calise, Timothy Heeren, Michael Winter, Caroline Littlefield, Daniel J. Gottlieb. The acute effects of caffeinated versus non-caffeinated alcoholic beverage on driving performance and attention/reaction time. Addiction, 2011; 106 (2): 335 DOI: 10.1111/j.1360-0443.2010.03219.x

Previous research regarding the association between alcohol consumption and dementia or cognitive impairment in later life suggests that mild to moderate alcohol consumption might be protective of dementia. However, most of the research has been conducted on subjects already rather elderly at the start of the follow-up.

A new study published in the December issue of the Journal of Alzheimer's Disease addresses this problem with a follow-up of more than two decades.

The study, conducted at the University of Turku, University of Helsinki and National Institute for Health and Welfare in Finland based on subjects from the Finnish Twin Cohort, shows that midlife alcohol consumption is related to the risk of dementia assessed some 20 years later. The study indicates that both abstainers and subjects consuming large amounts of alcohol have a greater risk for cognitive impairment than light drinkers.

"Our finding is significant as the changes typical of Alzheimer's disease — the most common dementia syndrome — are thought to start appearing two to three decades before clinical manifestation and therefore identification of early risk factors is imperative," states Jyri Virta, researcher at University of Turku, Finland.

In addition to total alcohol consumption, the authors were able to assess the effects of different drinking patterns. The study suggests that drinking large amounts of alcohol (defined as a bottle of wine or the equivalent) at a single occasion at least monthly is an independent risk factor for cognitive impairment. Such binge drinking doubles the risk of cognitive impairment even when total alcohol consumption was statistically controlled for.

Similarly, passing out because of heavy drinking on one occasion was also found to increase the development of subsequent cognitive impairment. Thus, it is not only the amount of alcohol, but also the pattern by which alcohol is consumed that affects the risk of cognitive impairment. The published study is among the first to report these effects.

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Journal Reference:

1. Jyri J. Virta, Tarja Järvenpää, Kauko Heikkilä, Markus Perola, Markku Koskenvuo, Ismo Räihä, Juha O. Rinne and Jaakko Kaprio. Midlife Alcohol Consumption and Later Risk of Cognitive Impairment: A Twin Follow-up Study. Journal of Alzheimer's Disease, 2010; 22 (3): 939-948 DOI: 10.3233/JAD-2010-100870

 Addiction researchers at Washington University School of Medicine in St. Louis have found that a risk for alcoholism also may put individuals at risk for obesity.

The researchers noted that the association between a family history of alcoholism and obesity risk has become more pronounced in recent years. Both men and women with such a family history were more likely to be obese in 2002 than members of that same high-risk group had been in 1992.

"In addiction research, we often look at what we call cross-heritability, which addresses the question of whether the predisposition to one condition also might contribute to other conditions," says first author Richard A. Grucza, PhD. "For example, alcoholism and drug abuse are cross-heritable. This new study demonstrates a cross-heritability between alcoholism and obesity, but it also says — and this is very important — that some of the risks must be a function of the environment. The environment is what changed between the 1990s and the 2000s. It wasn't people's genes."

Obesity in the United States has doubled in recent decades from 15 percent of the population in the late 1970s to 33 percent in 2004. Obese people — those with a body mass index (BMI) of 30 or more — have an elevated risk for high blood pressure, diabetes, heart disease, stroke and certain cancers.

Reporting in the Archives of General Psychiatry, Grucza and his team say individuals with a family history of alcoholism, particularly women, have an elevated obesity risk. In addition, that risk seems to be growing. He speculates that may result from changes in the food we eat and the availability of more foods that interact with the same brain areas as addictive drugs.

"Much of what we eat nowadays contains more calories than the food we ate in the 1970s and 1980s, but it also contains the sorts of calories — particularly a combination of sugar, salt and fat — that appeal to what are commonly called the reward centers in the brain," says Grucza, an assistant professor of psychiatry. "Alcohol and drugs affect those same parts of the brain, and our thinking was that because the same brain structures are being stimulated, overconsumption of those foods might be greater in people with a predisposition to addiction."

Grucza hypothesized that as Americans consumed more high-calorie, hyper-palatable foods, those with a genetic risk for addiction would face an elevated risk from because of the effects of those foods on the reward centers in the brain. His team analyzed data from two large alcoholism surveys from the last two decades.

The National Longitudinal Alcohol Epidemiologic Survey was conducted in 1991 and 1992. The National Epidemiologic Survey on Alcohol and Related Conditions was conducted in 2001 and 2002. Almost 80,000 people took part in the two surveys.

"We looked particularly at family history of alcoholism as a marker of risk," Grucza explains. "And we found that in 2001 and 2002, women with that history were 49 percent more likely to be obese than those without a family history of alcoholism. We also noticed a relationship in men, but it was not as striking in men as in women."

Grucza says a possible explanation for obesity in those with a family history of alcoholism is that some individuals may substitute one addiction for another. After seeing a close relative deal with alcohol problems, a person may shy away from drinking, but high-calorie, hyper-palatable foods also can stimulate the reward centers in their brains and give them effects similar to what they might experience from alcohol.

"Ironically, people with alcoholism tend not to be obese," Grucza says. "They tend to be malnourished, or at least under-nourished because many replace their food intake with alcohol. One might think that the excess calories associated with alcohol consumption could, in theory, contribute to obesity, but that's not what we saw in these individuals."

Grucza says other variables, from smoking, to alcohol intake, to demographic factors like age and education levels don't seem to explain the association between alcoholism risk and obesity.

"It really does appear to be a change in the environment," he says. "I would speculate, although I can't really prove this, that a change in the food environment brought this association about. There is a whole slew of literature out there suggesting these hyper-palatable foods appeal to people with addictive tendencies, and I would guess that's what we're seeing in our study."

The results, he says, suggest there should be more cross-talk between alcohol and addiction researchers and those who study obesity. He says there may be some people for whom treating one of those disorders also might aid the other.

This work was supported by grants from the National Institute on Alcohol Abuse and Alcoholism and the National Institute on Drug Abuse of the National Institutes of Health.

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Journal Reference:

1. R. A. Grucza, R. F. Krueger, S. B. Racette, K. E. Norberg, P. R. Hipp, L. J. Bierut. The Emerging Link Between Alcoholism Risk and Obesity in the United States. Archives of General Psychiatry, 2010; 67 (12): 1301 DOI: 10.1001/archgenpsychiatry.2010.155

 A multinational research team led by scientists at the National Institutes of Health has found that a genetic variant of a brain receptor molecule may contribute to violently impulsive behavior when people who carry it are under the influence of alcohol. A report of the findings, which include human genetic analyses and gene knockout studies in animals, appears in the Dec. 23 issue of Nature.

"Impulsivity, or action without foresight, is a factor in many pathological behaviors including suicide, aggression, and addiction," explains senior author David Goldman, M.D., chief of the Laboratory of Neurogenetics at the NIH's National Institute on Alcohol Abuse and Alcoholism (NIAAA). "But it is also a trait that can be of value if a quick decision must be made or in situations where risk-taking is favored."

In collaboration with researchers in Finland and France, Dr. Goldman and colleagues studied a sample of violent criminal offenders in Finland. The hallmark of the violent crimes committed by individuals in the study sample was that they were spontaneous and purposeless.

"We conducted this study in Finland because of its unique population history and medical genetics," says Dr. Goldman. "Modern Finns are descended from a relatively small number of original settlers, which has reduced the genetic complexity of diseases in that country. Studying the genetics of violent criminal offenders within Finland increased our chances of finding genes that influence impulsive behavior."

The researchers sequenced DNA of the impulsive subjects and compared those sequences with DNA from an equal number of non-impulsive Finnish control subjects. They found that a single DNA change that blocks a gene known as HTR2B was predictive of highly impulsive behavior. HTR2B encodes one type of serotonin receptor in the brain. Serotonin is a neurotransmitter known to influence many behaviors, including impulsivity.

"Interestingly, we found that the genetic variant alone was insufficient to cause people to act in such ways," notes Dr. Goldman. "Carriers of the HTR2B variant who had committed impulsive crimes were male, and all had become violent only while drunk from alcohol, which itself leads to behavioral disinhibition."

"Discovery of a genetic variant which predicts impulsive behavior under certain conditions in one human population may have much wider implications," says NIAAA Acting Director Kenneth R. Warren, Ph.D. "The interaction with alcohol intoxication is interesting, as is the apparent involvement of a neurotransmitter pathway that has been regarded as important in addictions and other behavior."

The researchers then conducted studies in mice and found that when the equivalent HTR2B gene is knocked out or turned off, mice also become more impulsive. Studies of any alcohol interaction in the knockout mice are ongoing.

Taken together, the findings could lead to a better understanding of some aspects of impulsivity and ultimately may lead to strategies for diagnosing and treating some clinically important manifestations of impulsive behavior. The researchers caution, however, that impulsivity is a complex trait with multiple genetic and environmental causes.

"Although relatively common in Finland, the genetic variant we identified in this study is unlikely to explain a large fraction of the overall variance in impulsive behaviors, as there are likely to be many pathways to impulsivity in its various manifestations," says Dr. Goldman.

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Journal Reference:

1. Laura Bevilacqua, Stéphane Doly, Jaakko Kaprio, Qiaoping Yuan, Roope Tikkanen, Tiina Paunio, Zhifeng Zhou, Juho Wedenoja, Luc Maroteaux, Silvina Diaz, Arnaud Belmer, Colin A. Hodgkinson, Liliana Dell’Osso, Jaana Suvisaari, Emil Coccaro, Richard J. Rose, Leena Peltonen, Matti Virkkunen, David Goldman. A population-specific HTR2B stop codon predisposes to severe impulsivity. Nature, 2010; 468 (7327): 1061 DOI: 10.1038/nature09629

 A little-used medication can help treat alcoholism, an updated review of studies confirms. At any given time, about 5 percent of the population suffers from an addiction to alcohol, often with devastating consequences to work, family, friends and health. Twelve-step programs have been the mainstay for helping alcoholics to quit drinking, but a significant number of people who try these programs do not find them helpful or suffer relapses.

The Cochrane review finds that the medication naltrexone — brand names are Depade and ReVia — when combined with counseling or interventions like Alcoholics Anonymous, can help cut the risk of heavy drinking in patients who are dependent on alcohol.

Naltrexone works by blocking the pleasurable feelings, or "high," a person gets from drinking alcohol, thereby reducing motivation to drink. Naltrexone can be taken daily as a pill and is available as a long-acting injection.

The review was published by 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.

"Hundreds of drugs have been tried for relapse prevention [in alcoholism] and basically all others have failed," said Michael Soyka, M.D., senior author of the review. "From a clinical point of view, there are few pharmacologic options for the treatment of alcohol dependence, so it is important to study those options that look promising." Soyka and lead review author Suanne Roesner are associated with the psychiatric hospital at the University of Munich.

Alcohol dependence is different from alcohol abuse or misuse. The symptoms of alcohol dependence include craving for alcohol, an inability to control drinking, the presence of withdrawal symptoms if one tries to quit and tolerance — the need to increase alcohol amounts to feel the same effect. People who only abuse alcohol and are not dependent on it have no trouble controlling their drinking, once they decide to do so.

Soyka and colleagues examined the results of 50 previously published high-quality studies on naltrexone and alcohol dependence. Overall, the studies enrolled nearly 7,800 patients diagnosed with alcohol dependence. Of these, about 4,200 patients took naltrexone or a similar drug called nalmefene. The rest of the patients took a placebo or had some other type of treatment. Treatment with naltrexone ranged from four weeks to a year, with most patients receiving about 12 weeks of treatment. Most patients also received counseling.

Researchers found that patients who received naltrexone were 17 percent less likely to return to heavy drinking than were patients who received a placebo treatment. "That would mean that naltrexone can be expected to prevent heavy drinking in one out of eight patients who would otherwise have returned to a heavy drinking pattern," Soyka said.

Naltrexone also increased the number of people who were able to stay abstinent by 4 percent.

While at first glance that might not seem like a miracle cure for alcoholism, Soyka said that the effectiveness of naltrexone is on par with medications used for other psychiatric conditions.

"Naltrexone is moderately effective in reducing alcohol intake. It's about as effective as antidepressants in depressive disorders," he said. "From a safety point of view, there are few safety concerns. Nausea is the most frequent side effect."

Carlton Erickson, Ph.D., director of the Addiction Science Research and Education Center at the University of Texas in Austin, says naltrexone can help a person with alcohol dependence move toward the goal of abstinence.

"Anytime you reduce the severity of drinking, the individual is more open to treatment for abstinence," he said. "It's almost like putting them through a series of steps if you can get them to cut down; once they start to cut down they are more likely to become abstinent with continued treatment and continued exposure to 12-step programs." Erickson is not associated with the review or any of its authors.

Despite its possible benefits in treating alcohol dependency, naltrexone is not widely used in the United States or elsewhere, Erickson said. Some addiction specialists fear that the widespread use of naltrexone or other medications will result in patients not receiving the counseling or psychological interventions they need.

There is also a lingering attitude that the treatment of alcohol dependency must rely solely on psychological or spiritual methods.

"People in 12-step programs typically don't believe in medications for the treatment of alcoholism," Erickson said. "Therefore they are unlikely to accept anyone into their 12-step meetings who is on a medication like naltrexone. Secondly, they would not want to accept it for themselves, unless a physician talked them into it as part of their treatment plan."

In addition, most large alcohol treatment centers, with the exception of Hazelden, do not advocate for the use of medications in the management of addiction, he said.

However, Erickson said that naltrexone is FDA-approved only as an adjunct to abstinence-based therapies, like Alcoholics Anonymous. "Naltrexone is not something you give to someone who says 'I want to stop drinking, give me a pill.' Naltrexone is only a helper to that process. The medication itself is not a magic bullet."

The review discloses that two authors received speaker/consultancy/advisory board honoraria from pharmaceutical companies.

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Journal Reference:

1. Roesner S, et al. Opioid antagonists for alcohol dependence. Cochrane Database of Systematic Reviews, 2010, Issue 12

Not a happy holiday thought, but an important one: The number of babies who die of SIDS, or sudden infant death syndrome, surges by 33 percent on New Year's Day. The suspected reason? Alcohol consumption by caretakers the night before.

Led by sociologist David Phillips of the University of California, San Diego, the study documenting the dramatic rise in SIDS deaths on New Year's is published in the journal Addiction. The spike, write Phillips and his coauthors, is beyond the normal winter increase in SIDS.

The study examined 129,090 SIDS cases from 1973 to 2006 using three multiyear nationwide datasets: computerized death certificates, the linked birth and infant death dataset, and the Fatality Analysis Reporting System. The authors say it is the first, large-scale U.S. study to explore possible connections between alcohol and SIDS.

Though SIDS has decreased significantly since the 1994 implementation of the "Back to Sleep" campaign, which urges caregivers to put infants on their backs to sleep, among other "safe-sleep" recommendations, SIDS continues to be the leading cause of death for children aged 1 month to 1 year. Also known as "crib death" and "cot death" because it strikes seemingly healthy babies in their sleep, SIDS is usually ruled the cause of death only when other causes are ruled out.

Phillips and his coauthors found three types of evidence linking SIDS to alcohol. In addition to rising, just like alcohol consumption, more on New Year's than at any other day of the year, SIDS and alcohol consumption also increase every weekend. And the SIDS death rate is abnormally high for children of alcohol-consuming mothers: Babies of mothers who drink are more than twice as likely to die of SIDS.

The study also found a rise in SIDS just after April 20 (or 4/20), a counterculture celebration of cannabis, and after July 4, which is also known as an inebriated time, though the rise on neither of these dates is as dramatic as on New Year's.

To see if parental sleeping-in might be at fault — rather than intoxication itself — the authors also checked to see what happens during the autumn shift to daylight savings, when many sleep later because an hour has been added to the day. There was no rise in SIDS, Phillips said.

The authors acknowledge important limitations to the current study. The large datasets contain very little information per case, Phillips said, so "we could not specify the detailed mechanisms and cannot determine whether alcohol is an independent risk factor for SIDS, a risk factor only in conjunction with other factors or a proxy for risks associated with occasions when consumption increases."

The study doesn't, and can't, point definitively to alcohol consumption as a cause of SIDS, but the connections are concerning, Phillips said. He worries that parents may not be as good at parenting — following the "Back to Sleep" recommendations, for example — when they've been drinking.

"We know that when people are under the influence of alcohol their judgments are impaired and they are not as good at performing tasks. This would include caretaking," Phillips said.

Phillips urges further studies that might shed additional light on the relationship between alcohol and SIDS. Nonetheless, he said, it is not unreasonable even now to suggest that SIDS investigations inquire about the recent alcohol consumption of the infant's caretakers and that pediatricians advise new parents that alcohol impairs their abilities and may endanger their children.

"The 'Back to Sleep' campaign was largely successful," the authors write. "A similar campaign might now be implemented: There should be increased efforts to inform caretakers that alcohol impairs parental capacity and might be a risk factor for SIDS."

Phillips' coauthors are Kimberly M. Brewer and Paul Wadensweiler of UC San Diego.

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Journal Reference:

1. David P. Phillips, Kimberly M. Brewer, Paul Wadensweiler. Alcohol as a risk factor for sudden infant death syndrome (SIDS). Addiction, 2010; DOI: 10.1111/j.1360-0443.2010.03199.x

The effects of alcohol abuse, as well as recovery from it, have been intensely studied. However, incarcerated women have remained an extremely understudied population despite steadily increasing in recent decades. One of the main ways to help individuals (as well as prisoners) with their recovery is through a 12-step program like Alcoholics Anonymous (AA).

A new study released in the March 2011 issue of Alcoholism: Clinical & Experimental Research, which is currently available at Early View, explores that subject in detail and found that AA attendance of at least once per week greatly increased the chance of a positive outcome.

According to Yael Chatav Schonbrun, a researcher in Butler Hospital at Brown University, this research is only the first step to help a population at risk of mental health disorders, risky sexual behavior and physical health problems.

"Despite the recent growth in this population, and despite the public health problems encountered, incarcerated women remain understudied. It is clear that AA is a widely available and familiar resource for underserved populations, and so it was logical to examine predictors of AA attendance, and how useful it would be for incarcerated women," he said.

The researchers recruited 223 hazardously-drinking women (averaged around 12 drinks per drinking day) from the women's facility at the Rhode Island Department of Corrections Adult Correctional Institute and ran two sessions — one during incarceration and one after release — along with a one-, three- and six-month follow-up to determine alcohol and treatment use. During the sessions, a timeline method was used to assess the alcohol use of the participants in the previous 90 days, as well as determining the severity of their involvement with alcohol, exposure to other drugs and participation in AA.

The data showed that if the women attended AA once a week or more, there was a significant decrease in the levels of alcohol-related consequences, and an overall decrease in the total days spent drinking.

This research is the first of its kind to evaluate AA attendance and alcohol-related outcomes among incarcerated hazardously-drinking women returning to the community. According to Schonbrun, "given that AA is so widely available, and is a familiar resource among incarcerated women, finding a method to increase utilization of AA might have great utility for improving alcohol and alcohol-related outcomes for incarcerated women."

However, future research is still required to answer questions regarding the duration and frequency of AA attendance needed for positive results, as well as evaluating if incarcerated men behave in a similar way.

"We hope that this study will call further attention to the needs of incarcerated women," said Schonbrun, "and that this research will help to arouse increased interest in addressing the needs of this underserved population."