The Pathology of Alcoholism

This presentation is restricted to a discussion of the visible effects of alcohol on hu­man tissues as seen at post-mortem examina­tions.

By C. S. SMALL, M. D., Assistant Professor of Pathology, C. M. E., Loma Linda

This presentation is restricted to a discussion of the visible effects of alcohol on hu­man tissues as seen at post-mortem examina­tions. A summary of evidence is given, with a few specific references. This writer, not a physiologist or psychologist, but a pathologist, feels incompetent to discuss adequately the func­tional results of alcohol, but from some experi­ence in autopsy work, can speak about its visible naked-eye and microscopic effects.

 

Two types of death from alcohol must be distinguished. First, so-called acute alcoholism, the results of an excessive dose taken within a few hours or days ; and second, chronic alco­holism, signifying the slower cumulative effects of persistently repeated sub-lethal indulgences.

The effects of alcohol are dependent largely on the amount consumed, regardless of mixture with, or dilution by, other substances, but it must be recognized that the more dilute the beverage, the less marked the effect, within certain limits. We must also realize that alco­hol, like work, heat, or cold, is better tolerated by some people than by others.

I remember as a child having seen drawings of the extremely bloodshot or congested brain of the drunkard, bearing the obvious implication that everyone addicted to alcohol died from the effects of some such circulatory derangement of the brain. However, in the course of several hundred of my post-mortem examinations, I have seen no certain invariable or even conspic­uously frequent pathology which would set a given brain apart from others as coming from an alcoholic devotee. True, there are certain progressive deteriorations of mentality due to alcohol, but these are not accompanied by diag­nostic naked-eye or microscopic evidences. The most common visible damage to the brain from alcoholic indulgence is that caused by accidental injury to the incoordinate victim of its influ­ence.

There is, however, a quite characteristic find­ing in those who die during extreme alcoholic excess, and that is the "wet" brain, known as cerebral edema. Occasionally caused by other factors, it is nevertheless very frequently found after death from acute alcoholism. It does not accompany chronic indulgence unless this is terminated by an acute episode.

It is sometimes said that the heart and blood vessels are affected by alcohol, but there is little evidence to support such an idea. High blood pressure, or hypertension, and alcohol have no definite relationship. Likewise, arteriosclerosis or hardening of the arteries, contrary to com­mon belief, is not occasioned by alcohol.

Damage to the lungs is very meager, and no criteria exist for distinguishing the lungs of chronic alcoholics from those of abstainers. However, as with the brain, if the victim suc­cumbs from a single debauch, there is pulmo­nary edema or "wet" lungs, a condition brought about by several other and much more frequent causes.

Drinkers have frequently been warned of the relationship between ulcer of the stomach and alcohol. While it is quite true that a single excess may cause shallow destruction of patches of the gastric lining, it is also true that these usually heal uneventfully, and seldom result in the more chronic and dangerous ulcer, which has causes distinctly apart, in many cases, from excesses in drink or in food. Therefore we may not say that alcohol bears any definite re­lationship to typical chronic ulcer of the stomach or duodenum. A much debated question is whether alcohol can cause a slow shriveling of the stomach lining (atrophic gastritis), accom­panied by burning pain and faulty gastric digestion. A certain fraction of sufferers from this disease can justifiably blame alcohol, but few drinkers contract the disease, and some abstainers have it. Nevertheless it is agreed that alcohol does cause a significant number of such cases. The vast majority of chronic drinkers show no visible effect on the stomach or intestine.

A furious battle raged for many years over the so-called "gin-drinker's liver" or alcoholic cirrhosis of the liver, and the debate is not yet closed. It is to be noted that this fatal but pro­longed malady afflicts many total abstainers, and that many alcoholics escape. In fact, about forty per cent of all such cases have not tasted intoxicants, and only eight per cent of chronic steady drinkers die of cirrhosis of the liver. But looking at the figures in a little different way, we see that death from cirrhosis is much more common among alcoholics than among those not so addicted.

In a series of about 20,000 post-mortems at a large Western hospital, a very striking fact was noted. Before alcohol was outlawed by the Volstead Act, eighteen out of every one thou­sand autopsies revealed the disease cirrhosis. During the years when alcoholic consumption was really diminished, this figure declined to six out of every thousand, and upon the resumption of the widespread use of alcohol in the early '30's, it promptly returned to eighteen and is now above that!

Beer (alcohol 2-8%) has no definite visible effect upon the liver. Wine (alcohol 8-20%) in large quantities certainly has. So-called hard liquor (alcohol up to 6o%) is the worst and most consistent offender.

The clinching proof of this alcohol-cirrhosis relationship was elicited experimentally only four years ago. It was found in certain animals who were fed enough fats to cause so-called fatty degeneration of the liver, that the addi­tion to their feedings of amounts of alcohol comparable to those taken by human drinkers of "hard liquor" caused the shrinkage of the liver known as cirrhosis, but only in animals deprived of sufficient food, and particularly vitamin B. They also found that, in an animal with a fatty liver, deficiency of vitamin B would produce the disease without the intervention of alcohol at all ! So cirrhosis in non-alcoholic people can be logically explained. These results also ex­plain cirrhosis in the alcoholic, for he frequently lives on almost nothing but alcohol for days at a time, thus depriving himself of necessary foods, including vitamins, and setting the stage for cirrhosis.

The time was when nephritis or Bright's disease was blamed on alcohol, but no scientific evidence is forthcoming to support the claim. The kidney may be functionally damaged to a slight degree, but not visibly so.

Alcohol and some diseases, such as pneu­monia, syphilis, gonorrhea, have a definite rela­tionship, but only because the inebriate fails to protect himself against them.

This summary of the effects of alcohol on human organs is not very impressive as tem­perance promotion material, but a knowledge of some things alcohol does not do is as valu­able as information on the more obvious things that it does do.

In conclusion, alcohol does cause edema of the brain, edema of the lungs, atrophic gastritis, and cirrhosis of the liver. It is not the sole cause of any of them, and certain conditions must be met before it will cause any one of them. Alcohol does not cause hardening of the arteries, high blood pressure, heart disease, or kidney disease. It does not cause chronic ulcers of the stomach or duodenum. The propa­ganda against alcohol is best directed at its effects on the mind and character, which are consistent, and appallingly dangerous.

BIBLIOGRAPHY

Henderson, Yandell, "A New Deal in Liquor," Doubleday, Doran & Co.

Carroll, Robert S., "What Price Alcohol," Mac­millan.

Emerson, Haven, "Alcohol and Man," Macmillan. Strecker and Chambers, "Alcohol—One Man's Meat," Macmillan.

Bogen, Emil, "What About Alcohol?" Angelus Press.

Wright, A. W,, "General Pathology and Some Spe­cial Complications of Alcoholism," Archives of Path­ology, 32:670, 10-41

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By C. S. SMALL, M. D., Assistant Professor of Pathology, C. M. E., Loma Linda

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