Pathophysiology
Binge drinking has the propensity to result in brain damage faster as well as more severely than chronic drinking (alcoholism), due to the neurotoxic effects of the repeated rebound withdrawal effects. During the repeated alcohol free stages associated with binge drinking, a larger amount of glutamate is released than occurs during withdrawal from chronic alcohol abuse; additionally this extreme release of glutamate happens on a repeated basis in binge drinkers leading to excitotoxicity. The tolerance that occurs during chronic ('non-stop') drinking delays alcohol-related brain damage compared to binge drinking which induced immediate and repeated insults to the brain.
Impairments in impulse control in binge drinkers, which is more prominent in female binge drinkers, is due to dysfunction of the frontal lobe. The findings in humans have been largely concordant with animal studies. Such animal studies find that heavy and regular binge drinking causes neurodegeneration in corticolimbic brain regions areas which are involved in learning and spatial memory, such as the olfactory bulb, piriform cortex, perirhinal cortex, entorhinal cortex, and the hippocampal dentate gyrus. A study in rats found that a heavy 2 day drinking binge caused extensive neurodegeneration in the entorhinal cortex with resultant learning deficits. While brain damage from binge drinking is known to occur as a result of binge drinking patterns, it is unclear how long drinking sessions last and how regular binge drinking is done to cause brain damage in humans. One study found that humans who drank at least 100 drinks (male) or 80 drinks (female) per month (concentrated to 21 occasions or less per month) throughout a 3 year period had impaired decision making skills compared to non-binge drinkers. Repeated acute withdrawal from alcohol which occurs in heavy binge drinkers has been shown in several studies to be associated with cognitive deficits as a result of neural kindling; neural kindling due to repeated withdrawals is believed to be the mechanism of cognitive damage in both binge drinkers and alcoholics. Neuronal kindling also leads to each subsequent acute withdrawal episode being more severe than previous withdrawal episodes.
Blackouts, a form of amnesia which occurs in binge drinkers may be due to suppressed hippocampus function with rebound NMDA (glutamate) activity combined with excessive glucocorticoid release induced by the stress of repeated intoxication followed by acute withdrawal/abstinence is the proposed mechanism of neural kindling leading to neurotoxicity of structures involved in learning and memory within the brain of binge drinkers. Frontal lobe processing may become impaired as a result of binge drinking with resultant neurocognitive deficits and impaired working memory.
Alcohol suppresses brain function during intoxication; but upon withdrawal rebound effects occur in the glutamate/NMDA system and with excess glutamate activity glucocorticoid release; due to the repeated intoxication, followed by acute withdrawal a neurotoxic effect develops which damages the central nervous system, leading to persisting impairments in verbal and nonverbal cognitive abilities as well as impairment of spatial orientation. Due to developmental processes occurring during adolescence including myelinization and restructuring of the synapses, adolescents are thought to be more vulnerable to the neurotoxic effects of alcohol.
Age and genetic factors influence the risk of developing alcohol-related neurotoxicity. Adolescence, especially early adolescence (i.e. before age 15), is a critical and delicate developmental stage for specialised neuronal and synaptic systems mature. This critical developmental stage is where lifelong adult traits e.g., talents, reasoning and complex skills mature; however alcohol and in particular binge drinking may disrupt and interfere with this developmental process. Adolescence is also a period of development characterised by a high level of novel seeking, thrill seeking and risk taking behaviour and thus alcohol and other drug experimentation and abuse is common. An adolescent rat study found that a relatively short exposure to high levels of alcohol resulted in long-lasting changes to functional brain activity with corresponding abnormalities in EEG brain waves which persisted into adulthood, including persisting disturbances in sleep EEG with a reduction in slow wave sleep. These EEG findings are similar to premature aging. According to one review of the literature, if the developmental stage of adolescence is similar to the developmental stage of the fetus with regard to sensitivity to the neurotoxic effects of alcohol, and if long-lasting or permanent damage to the brain occurs similar to what animal studies suggest, then this represents a major public health issue due to the high levels of alcohol use by adolescents. Indeed, alcohol can affect the remodeling and functional changes in synaptic plasticity and neuronal connectivity in different brain regions that occurs during adolescence (see this related article).
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