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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
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