Preventing adolescent alcohol use

Preventing Alcohol Use with a Voluntary After School Program for Middle School Students: Results from a Cluster Randomized Controlled Trial of Project CHOICE
Prev Sci. 2012 Aug; 13(4): 415–425.
Elizabeth J. D’Amico, et al.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3353018

journalistic version:
http://www.npr.org/sections/health-shots/2015/11/12/455654938/to-prevent-addiction-in-adults-help-teens-learn-how-to-cope

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5 or less alcohol drinks per week is healthy

The Addicted Brain.
Coursera, 2014. Emory University.
by Michael Kuhar, Ph.D.
https://www.coursera.org/course/addictedbrain

The amount that we can drink safely has been explored.
A weekly intake of no more than five drinks for men and two drinks for women is associated with lowest mortality. This suggests than a low level use of alcohol may be, in fact, healthy.

The NIAAA (National Institute for Alcohol Abuse and Alcoholism) recommends:
No more than 14 drinks per week for men
No more than 7 drinks per week for women.

Daily use of over 15 drinks per day for men and 10 for women will likely lead to dependence.

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drinks for summer
http://www.npr.org/templates/story/story.php?storyId=127217858

Predictors of adolescent alcohol misuse

Neuropsychosocial profiles of current and future adolescent alcohol misusers
Robert Whelan, et al.
Nature (02 July 2014)
http://www.nature.com/nature/journal/vaop/ncurrent/full/nature13402.html

A comprehensive account of the causes of alcohol misuse must accommodate individual differences in biology, psychology and environment, and must disentangle cause and effect.
Animal models can demonstrate the effects of neurotoxic substances; however, they provide limited insight into the psycho-social and higher cognitive factors involved in the initiation of substance use and progression to misuse.

One can search for pre-existing risk factors by testing for endophenotypic biomarkers in non-using relatives; however, these relatives may have personality or neural resilience factors that protect them from developing dependence.
A longitudinal study has potential to identify predictors of adolescent substance misuse, particularly if it can incorporate a wide range of potential causal factors, both proximal and distal, and their influence on numerous social, psychological and biological mechanisms.

Here we apply machine learning to a wide range of data from a large sample of adolescents (n = 692) to generate models of current and future adolescent alcohol misuse that incorporate brain structure and function, individual personality and cognitive differences, environmental factors (including gestational cigarette and alcohol exposure), life experiences, and candidate genes.

These models were accurate and generalized to novel data, and point to life experiences, neurobiological differences and personality as important antecedents of binge drinking.
By identifying the vulnerability factors underlying individual differences in alcohol misuse, these models shed light on the aetiology of alcohol misuse and suggest targets for prevention.

Pharmacotherapy for Alcohol Use Disorders

Pharmacotherapy for Adults With Alcohol Use Disorders in Outpatient Settings
A Systematic Review and Meta-analysis
JAMA. May 14, 2014;311(18):1889-1900.
http://jama.jamanetwork.com/article.aspx?articleid=1869208
Daniel E. Jonas, MD, MPH, et al.

Importance: Alcohol use disorders cause substantial morbidity and early mortality yet remain greatly undertreated. Medications are considerably underused.

Results:
Most assessed acamprosate, naltrexone, or both.
The NNT to prevent return to any drinking for acamprosate was 12
Among medications used off-label, moderate evidence supports an association with improvement in some consumption outcomes for nalmefene and topiramate.

Conclusions and Relevance: Both acamprosate and oral naltrexone were associated with reduction in return to drinking.
When directly compared with one another, no significant differences were found between acamprosate and naltrexone for controlling alcohol consumption.
Factors such as dosing frequency, potential adverse events, and availability of treatments may guide medication choice.

journalistic version:
http://www.npr.org/blogs/health/2014/05/13/312152578/meds-can-help-problem-drinkers-but-many-doctors-dont-know-that

Beer Flavor Provokes Striatal Dopamine Release

(c) Subjects rated the desire for beer, and the number of beers wanted.

Beer Flavor Provokes Striatal Dopamine Release in Male Drinkers: Mediation by Family History of Alcoholism
Neuropsychopharmacology (15 April 2013)
Brandon G Oberlin, et al.
http://www.nature.com/npp/journal/v38/n9/full/npp201391a.html

Striatal dopamine (DA) is increased by virtually all drugs of abuse, including alcohol.
However, drug-associated cues are also known to provoke striatal DA transmission– a phenomenon linked to the motivated behaviors associated with addiction.

To our knowledge, no one has tested if alcohol’s classically conditioned flavor cues, in the absence of a significant pharmacologic effect, are capable of eliciting striatal DA release in humans.
Employing positron emission tomography (PET), we hypothesized that beer’s flavor alone can reduce the binding potential (BP) of [11C]raclopride (RAC; a reflection of striatal DA release) in the ventral striatum, relative to an appetitive flavor control.
Forty-nine men, ranging from social to heavy drinking, mean age 25, with a varied family history of alcoholism underwent two [11C]RAC PET scans: one while tasting beer, and one while tasting Gatorade.
Relative to the control flavor of Gatorade, beer flavor significantly increased self-reported desire to drink, and reduced [11C]RAC BP, indicating that the alcohol-associated flavor cues induced DA release.
BP reductions were strongest in subjects with first-degree alcoholic relatives.

These results demonstrate that alcohol-conditioned flavor cues can provoke ventral striatal DA release, absent significant pharmacologic effects, and that the response is strongest in subjects with a greater genetic risk for alcoholism.
Striatal DA responses to salient alcohol cues may thus be an inherited risk factor for alcoholism.