[citation needed] Impairment of the liver will also allow more alcohol to reach the brain and hasten the individual's blackout.
[5] It is a common misconception that blackouts generally occur only in alcoholics; research suggests that individuals who engage in binge drinking, such as many college students, are often at risk as well.
[6] In one study, a sample of individuals was gathered and divided into groups based on whether they had a fragmentary blackout within the last year or not.
In their beverage challenge, participants were given one drink per ten minutes until the target of 0.08% blood alcohol level was achieved.
Together, these findings suggest that the differential effects of alcohol on free and cued recalls may be a result of substance altering neural activity in conceptual rather than sensory networks.
As such, a person experiencing an en bloc blackout may not appear to be doing so, as they can carry on conversations or even manage to accomplish difficult feats.
However, not all subjects experience blackouts which implies that genetic factors play a role in determining central nervous system (CNS) vulnerability to the effects of alcohol.
[12] In another study hospital file data showed, that of 67 participants who consumed excess alcohol, 39 had reported a blackout.
The presence of blackouts was associated to some degree with some indications of severity such as withdrawal and loss of control, but not with duration of problem drinking, physical complications or abnormal liver function.
The hypothesis that blackouts either reflect a general vulnerability to the cerebral consequences of alcohol use disorder or are associated with other forms of more enduring cognitive impairment did not receive any support.
Current findings show that subjective responses to alcohol have direct effects on both the final BAC achieved and on the experiences of blackouts and hangover that are not explained by level of intoxication.
[15] Memory disruptions by alcohol leading to blackout have been linked to inhibition of long-term potentiation, particularly in the hippocampus, by affecting gamma-Aminobutyric acid (GABA) and N-methyl-D-aspartate neurotransmission.
Activation during correct inhibitory-responses relative to go-responses in the left and middle frontal gyri at baseline predicted future blackout experience, after controlling for follow-up externalizing behaviors and lifetime alcohol consumption.
Benzodiazepines (such as flunitrazepam, midazolam, and temazepam), barbiturates (such as phenobarbital), and other drugs which also act as GABAA agonists, are known to cause blackouts as a result of high dose use.
[18] Alternatively, two studies have indicated that there appears to be a genetic predisposition towards blacking out, suggesting that some individuals are more susceptible to alcohol-related amnesia.
As expected in a complex condition like alcohol dependence, the disagreement in the association between AD and 5-HTTLPR likely reflects the impossibility for a single genetic determinant to explain the whole of the risk.
Blackouts were reported during activities such as spending money (27%), sexual conduct (24%), fighting (16%), vandalism (16%), unprotected intercourse (6%), and driving a car (3%).