Although heavy drinking can cause a great deal of health damage ranging from cirrhosis of the liver to pancreatitis, horror stories of alcoholic brain damage are largely a myth. Although wet brain is real, it can be prevented by proper nutrition and is not directly caused by alcohol itself.Alcohol, Brain Cells, and Brain Shrinkage
It has long been an established fact that actively drinking, alcohol dependent subjects have smaller brain volumes than normal control subjects who do not drink alcohol. Early researchers assumed that this was because alcohol killed the brain cells of alcohol dependent subjects, but current research proves that this hypothesis is largely untrue. Unless there has been brain damage as a result of liver failure or thiamine deficiency, the majority of brain cells of heavy drinkers are intact even though the brain has shrunk. We have also discovered that a long period of abstinence or moderate drinking tends to restore the volume of heavy drinker’s brains back to normal.
The human brain consists of white cells and gray cells. The gray cells are responsible for thinking and feeling and decisions–they correspond to the Central Processing Unit (CPU) of your computer. The white cells are like the cables of your computer which connect the keyboard and the monitor to the CPU. In 1993 Jensen and Pakkenberg did brain cell counts which compared the number of cells in the brains of heavy drinkers with those of nondrinkers. What they found was that the number of gray cells was the same in both the heavy drinkers and the nondrinkers. However, there were fewer white brain cells in the brains of the drinkers which implies that alcohol kills white brain cells.
In 2009 George Fein discovered that there was one part of the brain in the parietal lobe–which is associated with spatial processing–where alcohol kills gray cells. Fein claims that this explains why even after alcohol dependent subjects regain use of all their other cognitive functions they still seem to have difficulties with spatial processing.
Studies by Pfefferbaum (1995, 1998) show that with long periods of abstinence or moderate drinking the brains of alcoholic dependent subjects return to nearly the same size as their nondrinking counterparts.
It is not conclusive whether shrinkage is more pronounced in males, in females, or the same in both (Hommer, 2003).
To summarize: The brains of long term, heavy drinkers shrink, but they return to almost full normal size after a long period of abstinence or moderate drinking. Long-term, heavy drinking kills some white brain cells and some of the gray cells responsible for spatial processing; however, it does not kill any other gray cells. In particular, the gray cells which are responsible for our thinking, decision making, and other cognitive processes remain intact even in long-term, heavy drinkers. Unless there is brain damage which is due to thiamine deficiency or liver failure nearly all brain functions of alcohol dependent drinkers can be returned to normal with a long period of abstinence or moderate drinking. Cognitive functioning tends to return to normal when brain size returns to normal.
There is some evidence that both the amount of brain shrinkage and the amount of cognitive deficit are dependent on the quantity of alcohol consumed and the number of years of heavy drinking; it is not established whether this relationship is linear or not.
Amnesia and Dementia Due To Thiamine Deficiency – Wernicke-Korsakoff Syndrome Aka Wet Brain
The condition known as wet brain or Wernicke-Korsakoff Syndrome is a form of brain damage which is characterized by severe amnesia, confabulation, and sometimes dementia (Emsley, et al. 1996). It is not caused by direct effects of alcohol on the brain. It is caused by a severe deficiency of Thiamine (vitamin B1) and is often precipitated by a sudden influx of glucose. A number of things have been shown to lead to a severe enough thiamine deficiency to trigger wetbrain. These include a diet consisting solely of polished rice, prolonged bouts of morning sickness, bulimia and severe alcohol dependence.
Wetbrain has a sudden onset–it is not something which happens gradually over time. The first stage of wetbrain is called Wernicke’s encephalopathy. When there is a sudden influx of glucose in a brain which is deprived of thiamine the brain cells begin to die. This is because the chemical reactions which supply these brain cells with energy for life use thiamine to turn glucose into energy in a chemical process called the Krebs cycle. When there is an influx of glucose and no thiamine to help metabolize it, these brain cells burn out like a car engine running on high octane gasoline at high speed with no oil. The brain cells which die first are the ones which require the most thiamine to function. These brain cells are located around the middle of the brain and are the brain cells which are associated with memory and muscular movement. The brain cells of the cerebellum, which controls balance, are also affected.
The symptoms of Wernicke’s encephalopathy are confusion, lack of coordination, and involuntary eye movements. If Wernicke’s encephalopathy is immediately treated with thiamine it can be stopped and largely reversed. However, if Wernicke’s encephalopathy is not immediately treated, it quickly turns into Korsakoff’s psychosis, which is permanent and largely resistant to treatment. Symptoms of Korsakoff’s syndrome include loss of past memories, inability to learn new things, confabulation (remembering things which never happened), lack of coordination and unsteady gait, and in severe cases dementia. In some cases physicians who should have known better have precipitated Wernicke-Korsakoff syndrome in patients by putting them on a glucose drip instead of a thiamine drip.
Alcohol tends to block absorption of thiamine by the human body, so all people who drink alcohol should be careful to eat well and should also take vitamin B1 pills to make sure that they are getting enough thiamine. Severely heavy drinkers who consume around a fifth or a quart of vodka per day are often too nauseous too nauseous to eat well and may tend to vomit up what they do eat. Moreover, if these people are living on the streets, they may be unwilling to spend money on food which could be used to buy alcohol. These people are in the greatest danger of developing Wernicke-Korsakoff syndrome.
Breedlove (2007) tells us that all cases of wetbrain due to alcohol ingestion could be prevented by regulations requiring that thiamine be added to alcoholic beverages. It is unfortunate that our puritanical US society prefers to send people to abstinence-based programs which fail rather than to eliminate much human suffering by implementing the simple harm reduction policy of adding thiamine to alcoholic beverages.
HAMS recommends that all drinkers be sure to eat nutritious meals and take vitamins–especially thiamine–to help ward off wetbrain. It is also good to try and have some abstinence days or otherwise reduce alcohol intake to help prevent this.
Wetbrain is sometimes complicated by hepatic encephalopathy.
Hepatic encephalopathy is damage to the brain which is a result of liver failure, which may be caused by cirrhosis, hepatitis, etc. One job of the liver is to screen out toxins so that they can be disposed of as waste rather than circulate in the blood and damage delicate tissues like the brain. When the liver fails it is believed that toxins like ammonia and manganese cross the blood-brain barrier and cause damage to the brain–i. e. hepatic encephalopathy.
Symptoms of hepatic encephalopathy include lethargy, apathy, disorientation, inappropriate behavior, and slurred speech. In severe cases there may be coma.
If alcohol causes liver failure then hepatic encephalopathy can be one result.