- Alcohol-induced blackouts are more common than many think, occurring in 55 percent of college drinkers.
- Blackouts are influenced by one's genetic vulnerability as much as by the amount one drinks.
- Blackouts are due to dysfunction in the part of the brain responsible for memory formation—the hippocampus.
- Blackouts predict increased drinking in later years and a greater likelihood of developing alcohol dependence.
I once asked a group of alcoholics in rehab how many had experienced a blackout in the first years of their drinking. Nearly all raised their hand. Then I asked those with their hands in the air how many of them had an alcoholic parent. All but two kept their hand up, and one who had lowered his hand said he was adopted and did not know about his parents.
Alcohol-induced blackouts have a genetic foundation. Twin studies show that if one twin is prone to blackouts, the other is much more likely to also be prone if they are identical, rather than fraternal. Identical twins share 100 percent of their DNA, while fraternal twins only share 50 percent.
In the words of an important review of alcohol-induced blackouts, “… individual differences, not just alcohol consumption, increase the likelihood of experiencing an alcohol-induced blackout.”(1) You do not have to be alcohol-dependent to experience blackouts, and not all people addicted to alcohol experience them. Binging, pre-partying, and alcohol games, especially on an empty stomach, all produce a rapid rise in blood alcohol levels that make blackouts more likely.
And the higher blood alcohol levels reach, the more likely a person will black out. But I have known people who blacked out with only one or two drinks. The more genetically susceptible an individual is, the less alcohol is required to black out.
What Happens During a Blackout
People often confuse blacking out with passing out. The two are fundamentally different.
People pass out when they have had so much to drink that it is like going under anesthesia. Consciousness lapses and people become comatose, unable to be aroused. Blackouts, on the other hand, have no objective signs of their presence and no alteration in the level of consciousness. During a blackout, people can carry on conversations and complete complex tasks. I once interviewed a surgeon who had successfully removed a patient’s appendix while in a blackout.
Alcohol-induced blackouts are defined as amnesia, or memory loss, for all or part of a drinking episode. This memory loss can be sputtering, called fragmentary, or continuous, called en bloc.
The experience can be compared to snapping photos only to discover later that there was no film in the camera. There is no way to recover the pictures you thought you were taking. The difference with a blackout is that, not only are there no pictures in the camera, but your mind has absolutely no memory of having taken the pictures.
During a blackout, the mind is not functioning properly because the brain is not functioning properly. The fundamental mental dysfunction is that short-term memory is no longer being uploaded into longer-term memory. Short-term memory is sometimes called scratchpad memory—it records events for only about three minutes before they fade.
It is not difficult to navigate through an evening with full awareness of your life before the blackout began and of only what happened in the last three minutes since the blackout began. The gap in memory between the beginning of amnesia and the last three minutes continues to grow as long as the blackout lasts. There is a lot of information during the last three minutes, enough to keep people oriented and appearing quite normal, even to themselves.
From my discussions with people who have experienced blackouts, the amnesia has nearly instantaneous onset and ending. One man told me of having gone to a magic show after dinner and suddenly, as though teleported through space and time, finding himself on stage with the magician being asked to pick a card from a deck he was handed. It was as though a light inside his mind had just been switched on.
The only objective evidence of a blackout is to give someone three unrelated words, have them repeat the words, and then wait five minutes before asking them what the three words were. This is sufficient time for all short-term memory to be lost without transfer to long-term memory. Someone in a blackout will have no memory of having been given three words to remember and may think you are playing a trick on them. The movie Memento illustrated this condition on a permanent basis due to brain injury. The most common cause of permanent blackouts is thiamine deficiency due to poor diet in chronic alcoholics, called Korsakoff’s Syndrome.
The brain area where short-term memory is formed is the hippocampus. The speed with which short-term memory is formed depends on the amount of theta rhythm (7-13 Hertz) organizing the hippocampus. Theta rhythm comes from areas in the midline of the lower parts of the brain. In Korsakoff’s, these source areas of theta are destroyed, which leaves the hippocampus disorganized enough that the link between short- and long-term memory is severed.
Temporary blackouts are probably due to temporary disruption of theta rhythm input to the hippocampus. Such experiences are relatively common. Approximately 50 percent of college students who drink have experienced a blackout.
A lot of ridiculous things do happen during blackouts, and you may laugh at them, deny them, or just say you got “really f**ked up last night,” but blackouts are no joke. They predict increased drinking in later years, especially in men. They are clear evidence of having genetic vulnerability to alcohol. The earlier and more frequently blackouts occur in your drinking career, the greater your risk of eventually developing alcohol dependence. And that is not a good thing.
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1. R Wetherill and K Fromme, Alcohol-induced blackouts: A review of recent clinical research with practical implications and recommendations for future studies, Alcoholism, May 2016, Vol 40(5): 922-935