HAMS: Harm Reduction for Alcohol

What Is Wet Brain?

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Introduction

Wet brain is a form of brain damage. Wet brain is also called Wernicke-Korsakoff syndrome, Korsakoff's psychosis, Wernicke's encephalopathy, and beri beri. The symptoms of wet brain may sometimes improve with therapy but it is often permanent and irreversible.

Wet brain is caused by a deficiency of thiamine which is also known as vitamin B1. Chronic, heavy alcohol consumption can lead to a thiamine deficiency which can then lead to wet brain. This is because alcohol interferes with the absorption of thiamine. Wet brain can also occur in people who have never consumed alcohol. A diet of nothing but polished rice can cause wet brain because of the lack of thiamine in the diet. Wet brain can also be brought on by periods of vomiting which last for several days such as might result from severe morning sickness or bulimia.

Wet brain is not caused by alcohol killing brain cells. A study by Jensen and Pakkenberg suggests that chronic heavy drinking does not result in the loss of gray matter--the thinking part of the brain--although it can result in the loss of white matter. The exact nature of the impact of chronic heavy drinking on cognitive abilities in well nourished individuals remains something of a matter of dispute. For more information on this topic please visit our page Myths and Facts about Alcohol and Brain Damage.

Wet brain is not a case of gradual brain damage occurring over time--wet brain has a sudden onset and is often brought on by an sudden large dose of glucose in an individual suffering from a severe thiamine deficiency. It is generally agreed that wet brain occurs in two stages. The first stage of wet brain is Wernicke's encephalopathy which results from a severe thiamine deficiency and which may be precipitated by a sudden influx of glucose. If Wernicke's encephalopathy is immediately treated with thiamine injections it can be completely reversed and the patient can return to normal. If the Wernicke's encephalopathy goes untreated then it will progress to the second stage of wet brain which is known as Korsakoff's psychosis. Korsakoff's psychosis is not reversible although it can be improved somewhat through treatment.

Prevention of wet brain:

Anyone who drinks alcohol should always try to eat well and be careful to take their vitamins. Very heavy drinkers may always feel too nauseous to eat very much--they or their loved ones should at least try to make sure they get adequate vitamin supplements, particularly thiamine (B1). When malnourished heavy drinkers show up for medical treatment doctors should be sure to give them vitamin shots or an IV with thiamine. Heavy drinkers need to be careful to get much more thiamine in their diet than non-drinkers because heavy drinking prevents much of the thiamine from being absorbed.

Symptoms of wet brain:

Glucose and wet brain:

A sudden influx of glucose in a malnourished drinker can precipitate the onset of wet brain. It is potentially dangerous for malnourished heavy drinkers to eat large amounts sweets and no vitamins or other food--this can bring on wet brain. Some medical professionals who should know better have also caused wet brain in patients by putting them on a glucose drip.

Treatment for wet brain:

Abstinence from alcohol, thiamine, and time can help lead to some improvements of Korsakoff's psychosis. Total recovery is extremely unlikely.

REFERENCES:

MedlinePlus Medical Encyclopedia - Wernicke-Korsakoff syndrome

http://www.nlm.nih.gov/medlineplus/ency/article/000771.htm

(accessed August 5, 2009)

Heye N, Terstegge K, Sirtl C, McMonagle U, Schreiber K, Meyer-Gessner M. (1994). Wernicke's encephalopathy--causes to consider. Intensive Care Med. 20(4), 282-6.

PubMed Abstract: http://www.ncbi.nlm.nih.gov/pubmed/8046122

Jensen GB, Pakkenberg B. (1993). Do alcoholics drink their neurons away? Lancet. 342(8881), 1201-4.

PubMed Abstract: http://www.ncbi.nlm.nih.gov/pubmed/7901529

Meier S, Daeppen JB. (2005). [Prevalence, prophylaxis and treatment of Wernicke encephalopathy. Thiamine, how much and how do we give it?] [French]. Rev Med Suisse. 1(26), 1740-4.

PubMed Abstract: http://www.ncbi.nlm.nih.gov/pubmed/16117048

Watson AJ, Walker JF, Tomkin GH, Finn MM, Keogh JA. (1981). Acute Wernickes encephalopathy precipitated by glucose loading. Ir J Med Sci. 150(10), 301-3

PubMed Abstract: http://www.ncbi.nlm.nih.gov/pubmed/7319764

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