TEEN BRAIN AND ALCOHOL

Brain Damage Risks report by the American Medical Association
http://ok.gov/odmhsas/documents/Adolescent%20Brain%20and%20Alcohol.pdf

De Bellis, Michael D.; Narasimhan, Anandhi; Thatcher, Dawn L.; Keshavan, Matcheri S.; Soloff, Paul; Clark, Duncan B.;"Prefrontal Cortex, thalamus, and cerebellar volumes in adolescents and young adults with adolescent-onset alcohol use disorders and comorbid mental disorders", ALCOHOLISM: CLINICAL AND EXPERIMENTAL RESEARCH (2005), 29(9):1590-1600. "In adults, prefrontal, thalamic, and cerebellar brain injury is associated with excessive ethanol intake. As these brain structures are actively maturing during adolescence, we hypothesized that subjects with adolescent-onset alcohol use disorders, compared with control subjects, would have smaller brain volumes in these areas. Thus, we compared prefrontal-thalamic-cerebellar measures of adolescents and young adults with adolescent-onset alcohol use disorders (AUD, defined as DSM-IV alcohol dependence or abuse) with those of sociodemographically similar control subjects.

"Magnetic resonance imaging was used to measure prefrontal cortex, thalamic, and cerebellar volumes in 14 subjects (eight males, six females) with an AUD (mean age, 17.0 +/- 2.1 years) and 28 control subjects (16 males, 12 females; 16.9 +/- 2.3 years). All AUD subjects were recruited from substance abuse treatment programs and had comorbid mental disorders.

"Subjects with alcohol use disorders had smaller prefrontal cortex and prefrontal cortex white matter volumes compared with control subjects.

"These findings suggest that a smaller prefrontal cortex is associated with early-on set drinking in individuals with comorbid mental disorders. Further studies are warranted to examine if a smaller prefrontal cortex represents a vulnerability to, or a consequence of, early-on set drinking."

"The prefrontal cortex is a key region for complex thinking, planning, inhibition, and emotional regulation, said Tapert. It could be that, with less while matter in the prefrontal cortex, information does not transfer in this area as quickly and efficiently as is needed for the sorts of complex decision making young people need to do.

NIAAA Consortium Furthers Knowledge of Alcohol's Effects on Brain Development in Adolescents http://www.ehd.org/health_alcohol_8.php

"Alcohol and the Adolescent Brain--Human Studies" by Susan Tapert, Lisa Caldwell and Christina Burke. https://pubs.niaaa.nih.gov/publications/arh284/205-212.htm

Teen Brain Affected by Alcohol
Monti, Peter M.; Miranda, Robert, Jr.; Nixon, Kimberley; Sher, Kenneth J.; Swartzwelder, H. Scott; Tapert, Susan, White, Aaron, Crews, Fulton T.; "Adolescence: booze, brains and behavior", ALCOHOLISM: CLINICAL & EXPERIMENTAL RESEARCH (2005); 29 (2): 207-220. The adolescent brain is designed to learn; yet the same plasticity that facilitates neuromaturation also renders it particularly vulnerable to the damaging effects of alcohol. Some of the findings presented were:
-The neurochemical, cellular, synaptic, and structural organization of the adolescent brain makes it more vulnerable than the adult brain to disruption from activities such as binge drinking. Adolescent rats that were exposed to binge drinking appear to have permanent damage in their adult brains.
-Research has identified subtle but important brain changes occurring among adolescents with Alcohol Use Disorder (AUD), resulting in a decreased ability in problem solving, verbal and non-verbal retrieval, visuospatial skills, and working memory.
-The association between antisocial behavior during adolescence and alcoholism may be explained by abnormalities in the frontal limbic system, which appears to cause "blunted emotional reactivity".
-Alcohol-induced memory impairments, such as "blackouts", are particularly common among young drinkers and may be at least in part due to disrupted neural plasticity in the hippocampus, which is centrally involved in the formation of autobiographical memories.
- The symposium concluded that many serious adult mental disorders have their onset during childhood, and are risk factors for heavy alcohol involvement, especially attention deficit disorder, schizophrenia spectrum disorders, and bipolar spectrum disorders. The nature and extent of alcohol's effects on the neurodevelopmental and clinical aspects of these disorders should be a priority.

Monti, Peter M.; Miranda, Robert, Jr.; Nixon, Kimberley; Sher, Kenneth J.; Swartzwelder, H. Scott, Tapert, Susan, White, Aaron, Crews, Fulton T.; "Adolescence: booze, brains and behavior", ALCOHOLISM : CLINICAL AND EXPERIMENTAL RESEARCH (2005), 29 (2): 207-220. This article represents the proceedings of a symposium at the 2004 Research Society on Alcoholism meeting in Vancouver, British Columbia, Canada. The presentations were (1) Introduction, (2) Adolescent Binge Drinking Causes Life-Long Changes in Brain, (3) Functional Neuro-imaging Studies in Human Adolescent Drinkers, (4) Abnormal Emotional Reactivity as a Risk Factor for Alcoholism, (5) Alcohol-Induced Memory Impairments Including Blackouts, and the Changing Adolescent Brain and (6) Discussion.

Teen Brain Affected by Depression, Alcoholism : Girls With Family History of Alcoholism Have Altered Brain Waves. ACER News Release.

Many patients diagnosed with depression have abnormalities in brain electrical activity. Research has found that teen-age girls with a personal history of depression, not current depression, have enhanced alpha (slow wave) brain electrical activity.

Teen-age girls with a family history of alcoholism have enhanced beta (fast wave) activity.

The effects of a family history of alcoholism occurred in the left frontal brain; the effects of a personal history of depression occurred in the right frontal brain.

Numerous studies have documented abnormalities in brain electrical activity in patients diagnosed with depression. A study in the November issue of Alcoholism: Clinical & Experimental Research examines teen-age girls with a history of depression, rather than active depression, to see if they exhibit a subtle abnormality in brain function. The study also investigates if the presence of depression or alcoholism among family members exaggerates the abnormality in brain function.

"Researchers and clinicians have often raised the question of whether clinical depression is a state or a trait," said Lance O. Bauer, professor of psychiatry at the University of Connecticut School of Medicine and lead author of the study. "That is, do patients with clinical depression possess normal brain function that only becomes abnormal when they are in a state of active depression? Or, alternatively, do these patients possess a subtle brain abnormality which is always present, in other words, a trait?"

Researchers examined 151 adolescent females, 15 to 20 years of age, divided into six categories: depressed or non depressed, those with a positive or negative family history of alcoholism, and those with a positive or negative family history of depression. Of the total, 58 met Diagnostic and Statistical Manual of Mental Disorders - Third Edition, Revised DSM-IIIR) criteria for a personal lifetime diagnosis for depression (only 4 of these met the criteria for a current episode of depression). Researchers recorded electroencephalographic (EEG) activity from 31 electrode sites while the subjects sat relaxed inside a shielded, soundproofed chamber with their eyes open.

Results showed that a personal history of depression and a family history of alcoholism had opposite effects on the EEG power spectrum. Teen-age girls with a history of depression, not active depression, showed an enhanced amount of eight to 12 cycles per second brain electrical activity. This is referred to as alpha or slow-wave activity. "In other words," said Bauer, "a subtle abnormality in brain electrical activity is consistently present in these girls, even after the period of acute depression has passed."

A family history of alcoholism was associated with a qualitatively different abnormality in brain function: an enhancement of 19-30 cycles per second. This is referred to as beta or fast-wave activity. A family history of depression did not seem to have an effect on EEG activity, a finding that Adolf Pfefferbaum, director of the Neuropsychiatry Program at SRI International, calls both "interesting" and "intriguing."

"This pattern of association and dissociation suggests potential and different biological markers for liability for alcoholism or depression," he explained. "This possibility for a predictor of alcoholism is strengthened when taken together with another recent publication by Bauer in which he found increased beta power in alcoholics, more so in the men than women."

Another finding of the study was that the effects of a family history of alcoholism occurred in a different region of the brain (left frontal) than the effects of a personal history of depression (right frontal).

"These results suggest that the brain is a very complex organ," said Bauer. "Individuals who possess multiple personal and family risk factors might therefore possess a brain in which multiple areas are affected."

Bauer said the study adds to scientists' growing knowledge base in several areas. "For example," he said, "we found subtle abnormalities in brain function in young girls who have not yet experienced repeated episodes of depression and who have not yet been chronically exposed to antidepressant medication. We also found that a family history of alcoholism is associated with a subtle abnormality in brain function which is different from the abnormality associated with depression."

Although the results of the study have no immediate implications for current treatment, Bauer said that, if replicated, their findings suggest that "treatment for depression might be improved by a thorough assessment of personal history as well as family history.

The presence of both depression and a family history of alcoholism," he said, "might call for a different, or more intensive, treatment strategy than would apply to a depressed patient without a family history of alcoholism."

The co-author of the Alcoholism: Clinical & Experimental Research paper was Victor M. Hesselbrock of the Department of Psychiatry at the University of Connecticut School of Medicine. The study was funded by the National Institute on Alcohol Abuse and Alcoholism and the National Institute on Drug Abuse.

Crego, A.; Holguin, S. R., Parada, M.; Mota, N., Corral, M.; Cadaverira, E.; "Binge drinking affects attentional visual working memory processing in young university students", ALCOHOLISM: CLINICAL AND EXPERIMENTAL RESEARCH (2009), 33 (11): 1870-9. Binge drinking (BD) typically involves heavy drinking over a short time, followed by a period of abstinence, and is common among young people, especially university students. Animal studies have demonstrated that this type of alcohol consumption causes brain damage, especially int nonmature brain. The aim of this study was to determine how BD affects brain functioning in male and female university students, during the performance of a visual working memory task. The researchers used event-related electrophysiological brain response (ERP) technique to measure the students' brain response to a visual working memory task. The study found: students who were binge drinkers displayed anomalies during execution of the task, even when they correctly executed the task; binge drinkers required greater attentional processing during the task to finish it correctly; the binge drinking students had difficulties differentiating between relevant and irrelevant stimuli; and binge drinking students displayed less efficiency in distributing attentional and working memory resources between the different information presented during the task. The authors concluded that healthy adolescents and young people who binge drink--even only once or twice a week, and who do not display chronic alcohol consumption or alcohol dependence, "may suffer alterations at the electrophysiological level in attentional and working memory processing. This study is another in the long list of research that shows that binge-type drinking is harmful and can have long-term consequences.


"Drinking in America: myths, realities, and prevention policy," U. S. Department of Justice, Office of Juvenile Justice Programs, Office of Juvenile Justice and Delinquency Prevention, Updated for 1999 National Household Survey Data.

Most Americans either abstain from alcohol or drink very infrequently--less than once a week. Our public policies and social norms, however, do not reflect this fact and make alcohol readily accessible at low prices. Alcohol sales are dominated by a relatively small minority of the population who drink heavily. Policies and norms that promote alcohol availability support and encourage these problematic drinking behaviors. Most Americans consume very little alcohol, so it is not surprising that large majorities of the population support stricter alcohol policies designed to reduce drinking problems, especially among young people. These policy reforms have been shown to be effective in reducing alcohol consumption problems.

Foster, Susan El; Vaughan, Roger D.; Foster, William H.; Califano, Joseph A.; "Estimate of the commercial value of underage drinking and adult abusive and dependent drinking to the alcohol industry", ARCHIVES OF PEDIATRICS AND ADOLESCENT MEDICINE (May, 2006). Underage drinkers and adult pathological drinkers (those that meed the clinical DSM-IV criteria for alcohol abuse or addiction) consume between 37.5 percent and 48.8 percent of the value of all alcohol in the United States. $22.5 billion in consumer spending on alcohol came from underage drinking and $25.8 billion came from adult pathological drinking. Other findings include: Alcohol abuse and addiction cost the nation an estimated $220 billion in 2006 - more than cancer ($196 billion and obesity ($133 billion). Each day more than 13,000 children and teens take tier first drink. The 25.9 percent of underage drinkers who are alcoholics and alcohol abusers consume 47.3 percent of alcohol drunk by underage drinkers. The 9.6 percent of adult pathological drinkers consume 25 percent of alcohol drunk by adult drinkers. Children and teens that begin drinking before age 15 are four time likelier to become alcohol dependent that those who do no drink before age 21.
http://archpedi.ama-assn.org/cgi/content/full/160/5/473

Hingson RW ; Heeren T ; Winter MR; "Age at drinking onset and alcohol dependence: age at onset, duration, and severity", ARCHIVES OF PEDIATRIC ADOLESCENT MEDICINE (2006), 160(7): 739-46. "Results: Relative to respondents who began drinking at 21 years or older, those who began drinking before age 14 years were more likely to experience alcohol dependence ever and within 10 years of first drinking (adjusted hazard ratios and 95% confidence intervals [CIs], 1.78 [1.51-2.11] and 1.69 [1.38-2.07], respectively). They also more often experienced past-year dependence and multiple dependence episodes (adjusted odds ratios, 1.93 [95% CI, 1.40-2.64] and 3.09 [95% CI, 2.19-4.35], respectively). Among alcohol-dependent persons, the odds were 2.62 (95% CI, 1.79-3.84) for having at least 1 episode exceeding 1 year and 2.89 (95% CI, 1.97-4.23) for meeting 6 or 7 dependence diagnostic criteria. There is a need to screen and counsel adolescents about alcohol use and to implement policies and programs that delay alcohol consumption."

updated 12/26/16