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Introduction:
The “Drunk” Phase:
Drunk Physiology:
Drunk Neurochemistry:
The “Blackout” Phase:
Blackouts are a reaction to the consumption of alcohol which impacts memory. It’s the inability to recall any memories that may have been formed during the period of intoxication. During this period a person can often remember what they are doing and saying for a two minute period and thus carry on conversations (Blacking Out vs. Passing Out, 2018).
Type's of Blackouts:
There are two kinds of blackouts; the first is referred to as an en bloc or a complete blackout which nothing is remembered from the previous night. The second is a partial or fragmentary blackout where cueing can assist in memory recall. During extreme intoxications levels, one’s episodic memory can dysfunction, that is their ability to encode memories with spatial and social context (Lee, Roh & Kim, 2009). While there are multiple memory systems within the brain, recent publications show that alcohol may alter the hippocampus and related structures on a cellular level. Typically, blackouts occur when there is a rapid increase in blood alcohol consumption. Despite this, not all individuals experience blackouts suggesting genetic factors influence the CNS vulnerability to alcohol (Lee, Roh & Kim, 2009). As a result, some individuals are more likely to develop alcoholism, some may have altered perceptions of their experiences when intoxicated while some experience positive aspects and others negative (Lee, Roh & Kim, 2009).
Blackout Physiology:
A recent study done in Washington University School of Medicine, scientists have identified certain brain cells involved in blackouts (Dryden, 2011). While the previous understanding of the effects of alcohol on the brain suggested that it lead to cell death, new research shows that alcohol actually interferes with receptors in the brain. These interferences manufacture steroids that inhibit long-term potentiation (LPT), a process that strengthens the connections between neurons and is crucial to memory & learning (Dryden, 2011). The specific mechanism involves receptors NMDA that transmit glutamate. Glutamate is a neurotransmitter that carries signals between neurons. Interestingly, NMDA receptors must maintain a fine balance where too much activity and too little can be toxic. When alcohol exposure reaches these receptors some are inhibited while others later become activated, which causes neurons to release steroids that inhibit LTP and thus memory formation. These brain cells are found in the hippocampus, and their dysfunction interferes with your brains synaptic plasticity (Dryden, 2011).
Blackout Neurochemistry:
The “Hungover” Phase:
Hungover Physiology:
Hungover Neurochemistry:
Treatments:
References:
Blacking Out Vs. Passing Out - Alcohol and Drug Education Program - Boston College. (2018). Bc.edu. Retrieved 25 March 2018, from https://www.bc.edu/offices/healthpro/alcohol-and-drug-education-program/info-resources/blackout.html
Dryden, J. (2011). The biology behind alcohol-induced blackouts | The Source | Washington University in St. Louis. The Source. Retrieved 25 March 2018, from https://source.wustl.edu/2011/07/the-biology-behind-alcoholinduced-blackouts/
Lee, H., Roh, S., & Kim, D. (2009). Alcohol-Induced Blackout. International Journal Of Environmental Research And Public Health, 6(11), 2783-2792. http://dx.doi.org/10.3390/ijerph6112783
