Does Underage Drinking Cause Brain Damage?

Dr. Howard Moss, US NIAAA Assistant Director of Clinical Research, presented , "Does Underage Drinking Cause Brain Damage - Convergent Evidence from Imaging Research" to a packed audience at the 12th Annual International Society of Addiction Medicine Conference, University of Bicocca, Milan, Italy, 2010.
He noted first that there was a distinct phase of development distinguishing Adult from Adolescent and that this was in agreement with other mammalian research.
This phase was typified by 1. Engagement in disproportionate amount of risk taking behaviour 2. Increased Appetitive Drive 3. Emotional Volatility 4. Greater autonomic and neuroendrocrine reactivity to stress. 5. Greater cognitive disruption during stress (eg. impulsive responding) 6. Decreased sensitivity to behavioral effects of psychosomatic substances (Note, paradoxically, Decreased not increased) 7. Decreased sleep drive and phase delay
Adolescent brain development was studied and reviewed by Tapert and Schwienburg. There was first increased growth, especially in the preadolescent period followed by pruning which resulted in synaptic refinement. Synaptic pruning: there are many connections between neurons and those not used get pruned away and this results in improvement in attention. By end of adolescence half of the synapses have been pruned. Grey matter is replaced by white matter. 1% of the brain's gray matter is pruned per year during teen years. Glutaminergic neurons are replaced.
Adolescence is the highest risk period for initiation of regular drug use in the US. Cigarettes, for instance have their peak initiation by age 16.
Drug use prevalences in 8th grade show 17 % use alcohol, 8% use illicit drugs, 8% use cigarettes. By 12th grade 45% use alcohol, 21% use illicit drugs and 22% use cigarettes.
Adolescent drinking is less frequent than adults but adolescent drinking is associated with high dose, they drink to get drunk. Adults drink more frequently at a lower dose.
Morphometry studies of the brains of adolescents comparing heavy drinkers with controls show that heavy drinkers have smaller hippocampus. The hippocampus is associated with memory and learning. Morphometry studies also show that heavy drinkers have smaller prefrontal cortexes. The prefrontal cortex is what makes homo sapiens different from other species in planning, goal direction etc. Mylenization studies, using Defusioin Tensor Imaging ( D.L. Thatcher, S. Pajtec, D.B. Clark, 2010) show that the brains of adolescents in the substance abuse samples show decreased myelinization and brains which don't function in a synchronous way. The Fractional Anisotrophy studies show the region of impairment most in the Superior Longitudinal Fasciularis. Heavy drinking adolescents have deficits in large white matter areas.
P Magnetic Resonance Spectroscopy studies brain metabolism showing the energy use of the brain by following phospholipid turnover. The studies of adolescents with alcohol, conduct disorder and Substance Abuse Disorders show that their synapses are not be pruned which explains well the attentional problems and executive function failure seen behaviorally.
Functional MRI studies show regional changes in Oxygen use and can identify areas involved in a task. The Spatial Memory Task changes rapidly in pre adolescents. Heavy drinking adolescents actually did better on this test but the MRI studies showed that they had to use many more areas of their brain to accomplish the task.(Tapert et al, 2004). However after 4-5 years of heavy drinking Spatial Memory Tasks evidence decreased performance, and less activation in superior or inferior parietal areas. Heavy drinkers showed less memory retrieval and poor spatial memory while heavy marijuania users showed decreased learning of tasks, decreased sequencing and increased error. Heavy drinkers showed decreased hippocampus and decreased prefrontal development and decreased white matter integrity. f MRI studies showed decreased performance.

Dr. Moss in conclusion said that the evidence collectively points to negative brain changes as a consequence of alcohol and drug abuse. These negative brain changes constitute brain damage. The question he said that the studies didn't show was whether this was delayed development which could potentially 'catch up' or more permanent deficits. The other question the research did not answer as yet was whether these changes were precursors to later dependence. However he said the epidemiological evidence to date shows very clearly that the heavier the drinking in early adolescence the greater the likelihood of later dependence. What was further not shown was how these changes impacted on other psychopathology. The conclusion remained though that these changes associated with alcohol and drug abuse looked like brain damage.
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