That the liver is the organ of the body most sensitive to the
noxious effects of prolonged excessive drinking is a received
truth. The liver is the canary of the body in relation to alcohol.
To find, therefore, that alcohol in certain circumstances may
be good for ones liver is in no small measure a surprise.
Transient and isolated over-indulgence may irritate the liver,
but, with its enormous regenerative capacity,it quickly heals.
Repetitive major insults over the years, however, are likely to
lead to lasting damage, in sequential order of gravity: inflammation
(alcoholic hepatitis), fatty liver (hepatic steatosis), and, finally,
cirrhosis. In each case, structural abnormalities are accompanied
by disorder of the vital almost unimaginable complex of liver
functions. While the degree of damage is in general proportional
to the quantity of alcohol imbibed, there are wide individual
differences in susceptibility.
Alcoholic cirrhosis is a common cause of disability and death
among heavy drinkers. It accounts for much of the steeply increasing
death rate of the right side of the J-shaped curve. (The curve
illustrates that light to moderate drinkers live longer and healthier
than abstainers, and do very much better than those who drink
to excess.) Those with cirrhosis of the liver of any cause are
also at higher risk of development of hepatoma (liver cancer),
nearly always fatal.
In addition to causing liver damage by excess, alcohol, at least
when abused, inhibits liver regeneration (healing) from any damage,
by viral hepatitis, toxin, medication overdose (acetaminophen),
hemochromatosis (hereditary iron overload), or alcohol itself.
Let us turn to the surprising study of Manna Zhang, et al., published
in the November, 2000, issue of the journal Gastroenterology.
Working in the laboratory of Gerald Minuk at the University of
Manitoba Liver Diseases Unit in Winnipeg, Canada. They fed laboratory
rats light, moderate, or heavy portions of alcohol, or tap water,
for 30 days before removal of a substantial proportion of the
rats livers. The regeneration of the liver was then measured by
sophisticated techniques. The rats engaging in heavy consumption
of alcohol clearly showed impairment of regeneration. The moderate
consumers were negligibly impacted, perhaps a trace tilt toward
impairment. The light-drinking rats, however, exhibited enhanced
regeneration, that is, they did considerably better than those
who drank only water.
The mechanisms of improved liver regeneration among the light-drinking
rats are not known. Two proposed are favorable effects upon cell
membranes and inhibition of inhibitors of regeneration. It must
be borne in mind that this is just one experiment, and that it
is in rats, not humans, so, before assigning these results as
still another illustration of the increasingly universal J-shaped
curve, conventional prudence would dictate abstinence for those
of us with active liver disease.
Can the body generate alcohol?
I once saw a film about a non-drinking man who got into trouble
with the law because of alcoholic intoxication. He got out of
trouble when it was demonstrated that the alcohol had been manufactured
in his gastro-intestinal tract. An amusing fantasy, I thought.
Now, in the same issue of Gastroenterology, Cope, Risby, and Diehl,
at John Hopkins University, Baltimore, propose that the fatty
livers occurring in obese individuals may be caused by alcohol
generated within the intestine.
This time its mice, obese versus lean mice, that were studied.
The mice were abstinent of alcohol, yet ethyl alcohol, our favourite
kind, was detectable in the exhaled breaths of the mice. Obese
mice had more than thrice the alcohol of lean mice. The peak concentration
occurred in the morning. Breath alcohol of the obese mice increased
with age; not so in lean mice. The antibiotic, neomycin, administered
orally, reduced alcohol levels by 50 percent.
It is thought that micro-organisms normally living in the intestine
produce the alcohol, which flows via the blood stream to the liver,
its next station. Obesity is thought to slow intestinal motility,
thereby enabling bacterial over growth, with resultant increased
production of alcohol and other noxious factors. The occurrence
of abnormal (fatty) livers in obese mice is quite similar to that
seen in obese humans. It sometimes leads to even more serious
liver damage. Are safe limits of alcohol consumption lower for
obese people? We dont know yet.
Certainly further studies are needed, but one may wonder about
corrective measures, such as weight reduction, prudent use of
antibiotics, and enlistment of beneficial competing microorganisms,
*Dr. Finkel, clinical professor of medicine at Boston University
Medical Center, founding chairman of the Committee on Health of
the Society of Wine Educators, and award-winning wine writer,
writes and lec-tures internationally on the influences of wine
upon health. He is a member of AIMs editorial board.