Fatty liver disease, or hepatic steatosis, is an excessive accumulation
of fat within the liver cells. Since multiple disorders can cause fatty liver, in most cases the only cure is to address the
underlying disorder.
In the absence of alcohol or other known cause, the patient may be diagnosed
with non-alcoholic fatty liver disease. This is a relatively new disorder, and associated risk factors include female gender,
obesity, hyperlipidemia and diabetes. Some authorities estimate its prevalence at 5% of the general population and over 25%
in patients with obesity and type II diabetes. In most cases the course of the disease is benign, with some patients progressing
to cirrhosis and complications. Case Western researchers theorize that the generation of fatty liver involves two steps: 1)
insulin resistance, which causes the liver to synthesize fat in greater amounts. 2) oxidation of the fats, which inflame the
liver.
The theory of the cause of fatty liver explains the current attempts at
a solution. Weight loss, presumably from a low fat diet, lowers total body weight and total body fat, decreasing the burden
on the liver. Decreasing body fat decreases insulin resistance. Exercise also lowers the resistance of body cells to insulin
and so limits the creation of fat by the liver. Anti-oxidants such as vitamin E, N-acetylcysteine, betaine, and others counteract
the oxidation of the lipids present.
The most positive studies on fatty liver have been done with ursodeoxycholic
acid (UDCA), which improved fatty liver significantly in rats and has been used successfully in humans for a variety of liver
disorders. What is ursodeoxycholic acid (UDCA)? A secondary bile acid, normally found in trace amounts and a closely related
to a primary bile acid. Bile acids are absorbed by passive diffusion along the entire gut and actively transported by the
distal ileum. They are rapidly absorbed by liver cells and resecreted. In the course of a normal digestion, the bile acid
pool (2-4g) circulates 5 to 10 times a day. Bile acid reabsorption suppresses creation, but maximum creation is about 5 g
a day which may not be sufficient to offset intestinal malabsorption. Adding UDCA into the diet helps the liver process fats
more efficiently and may bring oxidized fats from the liver back into the gut to be excreted.
Other studies have shown that a deficiency of choline, necessary for many
body functions, actually caused fatty liver in rats. Choline is actually an essential nutrient if the body is not getting
enough methionine and folate.
Supplementation with conjugated linoleic acid, while not weight reducing
in humans, resulted in a 4% decrease in proportion of body fat over twelve weeks.
Given other research, it is possible to make some general dietary suggestions:
Avoid sugar. Rats fed high sugar diets of up to 50% pure sugar developed
fatty livers in proportion to the amount of sugar they were fed.
Use mono-unsaturated, cold pressed oils like olive oil. Unsaturated oils
oxidize more rapidly. Use all oil sparingly, except oil necessary to get essential fatty acids.
Add soy to your diet. Soy isoflavones affect fat in the blood positively.
Avoid alcohol, preservatives and pesticides. Tax your liver's abilities
to detoxify as little as possible.
Since a deficiency in the amino acid arginine may cause fatty liver, be
careful to get sufficient protein.
Consider a multivitamin high in choline and anti-oxidants unless your diet
can be very high in vegetables and fruits.
Consider eating primarily low glycemic index (slow burning) carbohydrates
to slow insulin resistance.
Strongly consider supplementing with bile acids, particularly UDCA.
Strongly consider exercise or movement to decrease insulin resistance in
the cells.
