Lecithin:
Prevention for booze-induced liver disease?
By Dr. Anthony G. Payne
If you drink or know someone who does, you may want to print off or email him or her this article.
Alcohol-induced disease is fairly commonplace among persons who abuse alcohol. Fibrosis and cirrhosis by-and-large head the list. In both cases, abnormal
changes take place in liver tissue that compromise this vital organ's ability to function optimally. For many people who drink, a doctor's finding of liver
pathology (disease) is sufficient to effect a change in drinking patterns, i.e., either curtailed ingestion or abstinence (On a temporary or permanent basis)
. For others, however, a diagnosis of cirrhosis or other alcohol-induced disease does not put "the fear of G-d in 'em" with sufficient force to overpower
the craving to elbow bend. For them especially, what I am about to share may be a lifesaver. Literally!
In at least two separate animal studies carried out during the past fifteen years, a wheat-derived phospholipid rich oil called lecithin protected animals
who were given and/or consumed booze at high levels were protected from developing many of the pathologic abnormalities common when alcohol is abused.
Furthermore, when animals bend their elbows or paws sans lecithin, their livers developed telltale pathologic changes. Here are the details of this very
compelling body of research:
In a study involving rats, 28 male littermates were pair-fed liquid diets containing 36% of energy either as ethanol (alcohol) or as additional
carbohydrates for 21 days. Half of these rodents were given polyenylphosphatidylcholine (A component of lecithin) at 3 grams per liter of their food
substrate (Liquid meals). The other group was given safflower oil (3 grams/liter) and choline (A chemical part of lecithin) as a bitatrate salt. The
polyenylphosphatidylcholine (PPC) did not influence diet intake or alcohol consumption, but the booze-induced liver enlargement and accumulation of
specific fats (lipids - triglycerides and cholesterol esters) and proteins were about half those in rats not given PPC. In rats that consumed PPC,
post-eating rise in serum lipids was lower than was true of their littermates who had no PPC. The researchers, who worked at the Alcohol Research and
Treatment Center, Bronx Veteran Affairs Medical Center (New York City), concluded that "These beneficial effects of PPC at the initial stages of alcoholic
liver injury may prevent or delay the progression to more advanced forms of alcoholic liver disease" (1).
In a separate 10 year-long study involving baboons, also carried out at the Bronx Veteran Affairs Center (Section of Liver Disease and Nutrition), the
suggested benefits of lecithin ingestion were even more encouraging. In the study, twelve baboons (eight females, four males) were fed a liquid diet
supplemented with polyunsaturated lecithin (50% of total energy) or isocaloric carbohydrate. This group was compared with another group of eighteen baboons
who were fed an equivalent diet (with or without alcohol), but without of lecithin. (2) Both groups developed increases in specific lipids (associated with
alcohol use), but there were significant differences in the degree of liver injury (fibrosis) seen. For one thing, septal fibrosis (with cirrhosis in two
animals) and transformation of their fat cells (lipocytes) into transitional cells developed in seven of the nine baboons fed the regular diet with alcohol,
septal fibrosis did not develop in any of the animals fed lecithin. In fact, they did not progress beyond the stage of perivenular (area around veins)
fibrosis and had significantly lesser activation of fat cells to transitional cells. (3) The clincher came when the scientists took three of the
lecithin-consuming animals off same, but maintained their customary diet and alcohol mix. They very rapidly progressed to cirrhosis, accompanied by an
increased transformation of their fat cells to transitional cells! The fact these researchers found that choline exerted no protective effect in animals
ingesting large quantities of alcohol led them to conclude that the polyunsaturated phospholipids might be responsible for the protective effect. This is
underscored by the rodent study cited above, in which choline did not protect the animals from alcohol-induced liver damage, whereas PPC (Lecithin component)
did. (4)
Baboon livers are remarkably similar to human livers (This is one reason an attempt was made many years back to transplant baboon livers into humans whose
livers had failed). Given this, it seems logical that lecithin should provide human drinkers at least some of the benefits seen in the baboons. Accordingly,
for those who drink -- especially heavily -- lecithin may be an invaluable form of health insurance. Of course, curtailing or quitting is ideal, but we
obviously do not live in an ideal world. And until we have a cure for alcohol habituation and addiction, prevention will at least help offset some of the
injury heavy boozers do to themselves. And if only a small fraction of alcohol users take lecithin religiously and reap clear clinical benefits, the savings
in terms of payouts for medical care could prove very substantial!
Lecithin is sold over-the-counter in the USA as a health food supplement and is generally quite economical.
References
Navder KP, Baraona E, Lieber CS. 'Polyenylphosphatidylcholine attenuates alcohol-induced fatty liver and hyperlipidemia in rats'. J. Nutrition,
Sep;127 (9): 1800-6.
2. Liber CS, DeCarli LM, Mak KM, Kim CI, Leo MA. 'Attenuation of alcohol-induced hepatic fibrosis by polyunsaturated lecithin'. Hepatology 1990 Dec;12
(6):1390-8 3. IBID 4. IBID
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