One can imagine a debate between an alcohol user and a non-drinker. “A few drinks could reduce my chances of getting Alzheimer’s!” the first exclaims. “But drinking can CAUSE dementia!” the second insists. Which one is right? What does the evidence say?
Actually, both statements have merit.
Alcohol as Preventive
Researchers at London’s Imperial College combined data from a number of studies in a meta-analysis. With several cautions, they concluded “there is some evidence to suggest that limited alcohol intake in earlier adult life may be protective against incident dementia later.” (Peters, R, et al. Age and Ageing 2008)
Alcohol Dementia
On the other hand, consuming alcohol also increases risk of one type of dementia—alcohol dementia (or alcoholic dementia). And the dementia can occur years after stopping alcohol use.
A quick grounding in terminology: “Dementia” is an umbrella word, covering all the diseases that produce progressive loss of brain function, and including especially memory loss. The most common cause of dementia in the US is Alzheimer's Disease. About 2% of dementias are alcoholic dementia in some studies, more in other studies.
Binge drinking seems especially dangerous. Finnish investigators found that people who drank more than five bottles of beer or one bottle of wine once a month were over three times as likely to get dementia. Passing out from drinking at least twice produced a ten times greater risk of dementia. (Jarvenpaa, T. Epidemiology July 2006)
How Alcohol Causes Dementia--Indirect Effects
Thiamin, or a lack of it, often is the culprit here. Thiamin, a “B” vitamin (B1), is essential for nerve cell health. (Heart cells are also especially dependent on thiamin.) Why are many alcoholics thiamin deficient?
Poor nutrition. This is the traditional explanation. It is presumed alcoholics consume alcohol in place of yeast, whole grains, liver, and vegetables, the usual sources of dietary thiamin. This explanation is often thrust on the homeless street alcoholic. But many alcoholics have normal diets.
Poor thiamin absorption or utilization. Thiamin is mostly absorbed from the gut via a carrier protein, must be carried by special proteins to cells, and then requires special proteins for incorporation into cells. Many genetic defects can impede these processes, so relative thiamin deficiency may occur with a normal diet. Alcohol use may expose weaknesses in several ways. For example, alcohol can directly disrupt thiamin absorption. Also, alcohol can contribute to magnesium deficiency, and magnesium is essential for binding thiamin within cells.
How Alcohol Causes Dementia--Direct Effects
Alcohol is a nerve toxin. It appears to cause damage by excitotoxicity. Alcohol can damage NMDA receptors, leading to uncontrolled glutamate production. Glutamate, in turn, leads to calcium flooding into nerve cells, damaging and ultimately killing them. In this theory, damaged NMDA receptors continue to produce excitotoxicity, even after alcohol use is stopped, leading to accumulating brain damage—dementia years after alcohol use has stopped, and progressing in spite of abstinence.
Alzheimer's also produces excitotoxicity. The co-occurrence of Alzheimer's and Alcohol dementia is not uncommon.
The Picture of Alcohol Dementia
Alzheimer's dementia starts with short term memory loss. Alcohol dementia may not have much memory loss at first. Instead, it often becomes evident by frontal lobe signs:
- poor planning
- personality change
- poor judgments
- difficulty handling complex situations
Alcohol may also destroy brain cells in the cerebellum, the coil of nerves in back and below the main brain. The cerebellum controls muscle movement; damage may affect walking and fine muscle control. Falling down is a risk from cerebellum damage.
Ultimately, Alcohol Dementia may progress to be indistinguishable from Alzheimer's. However, the course is less predictable. Sometimes it is much slower in progression.
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