Massachusetts Beverage Business


Article By: Harvey Finkel, MD

Like the canary in an old coal mine, the liver is the sensitive sentinel, the first organ to sustain permanent damage from abusive drinking. A large portion of the excessive mortality depicted by the right upward sweep of the J-shaped curve is due to alcoholic liver disease – chiefly cirrhosis. Liver damage by alcohol abuse can take other forms, ranging from mild reversible fat deposition and inflammation all the way to liver cancer (hepatoma).

Fatty liver is one of these common way stations, often reversible with reduction or cessation of drinking. Like the rest of the spectrum of liver disorders, fatty liver is not exclusively tied to alcohol. It may afflict non-drinkers who are, for example, obese, diabetic or exposed to certain toxins, but, in our perceptions, this and some other forms of liver disease are, especially in the western world, inexorably associated with drinking too much for too long. Globally, hepatitis viruses and iron overload bear much of the blame. Almost all of us would say that drinking to excess causes liver damage; that drinking moderately is liver-neutral – no harm, no benefit.

The results of medical research, however, once more counterintuitively surprise, most recently in three published scientific papers, one from Japan, one from Sweden, one from California. Hiramine, et al., reporting in the journal of gastroenterology, find that while the risk of fatty liver is associated with obesity, the risk is significantly decreased, by as much as 56 percent, in drinkers compared to abstainers. The benefit was especially related to frequency of drinking, not so much to quantity. This study tends to add to the increasingly accepted notion of the J-shaped curve and that more or less regularly spaced drinking of moderate quantity is most beneficial to health.

Kechagias, et al., as described in the annals of medicine, had Swedish men and women drink, respectively, two glasses or one of red wine daily for three months, then compared them to a matched group of abstainers. Here, too, the risk of fatty liver is increased by obesity and by insulin resistance (a precursor of diabetes), but there is zero evidence of liver damage in the drinking group, who, however, experienced a 16 percent drop in “bad” cholesterol and were probably less grumpy.
Dunn, et al., in the journal of hepatology, report from California on the very common nonalcoholic fatty liver disease (NAFLD), which often produces no or few symptoms. They found that among those with NAFLD, people who drank moderately (up to two drinks per day, and no binges) had half the risk of abstainers of their liver disorder worsening.

A search of the scientific literature turns up other support for moderate alcohol’s liver innocence, even benefit, on which I have commented previously. Several studies in the US and in Japan between 2OO7 and 2O1O also indicated protection of the liver in humans by moderate drinking. Zhang, et al., in 2OOO, demonstrated in rats that light alcohol consumption enhanced liver regeneration, and Szabo, in 2OO7, that mice enjoying moderate drinking had less rather than more inflammation in their livers compared to their unfortunate teetotaling counterparts.

The mechanisms involved are not clear. The anti-inflammatory effects of alcohol (and of wine’s polyphenols) deserve more study. Alcohol-associated benefits to blood lipids (e.g., raising “good cholesterol”) and insulin sensitivity should also be considered. Obesity of any cause seems part of the equation, perhaps rendering the liver vulnerable to alcoholic and other insults. The California group foresees the time when, after risks are more clearly delineated, selected individuals with NAFLD will be advised modest alcohol consumption to sooth both their hearts and livers.

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