Phosphatidyl choline is the clinical term used for lecithin.
Lecithin is a phosphoplipid composed of glycerol, two fatty acids and a phosphatidic acid. The primary phosphatides in lecithin are phosphatydlethanolamine (PE) and phosphatydlcholine (PC). The latter is of particular interest to researchers studying treatments to slow or reverse the senile dementia known as Alzheimer's disease.
Lecithin is the dietary precursor of choline. Choline is a precursor of acetylcholine, a neurotransmitter required for normal brain function. Both lecithin and choline have been studied for their capacity to lower serum cholesterol and to slow or reverse the effects of Alzheimer's disease.
Naturally occurring choline is ingested primarily in the form of phosphatidylcholine from lecithin. It is estimated at least 300 milligrams per day of choline is consumed as lecithin and free choline. The average person takes in about 400 to 900 milligrams in the diet daily. Persons eating liver or eggs, however, ingest more than three times that amount in their diet.
Lecithin sold in health food stores and by over-the-counter pharmacies is extracted from egg or soybean. Since lecithin nutritional supplements usually contain only about 20% to 30% phosphatidylcholine (PC), they may not the best sources of PC. PC concentrates are available and sold primarily to licensed health practitioners for therapeutic use.
Those dietary sources rich in choline by comparison to lecithin are listed below:
Lecithin 2200 Lentils 223 Egg yolk 1490 Split peas 201 Liver 550 Rice bran 170 Whole egg 162 Roasted peanuts 162 Wheat germ 406 Oatmeal 156 Soybeans 340 Peanut butter 145 Rice germ 300 Bran 143 Barley 139 Blackeye peas 257 Ham 122 Garbanzo beans 245 Brown rice 112 Brewer's yeast 240 Veal 104 Rice polishings 102
Milligrams per 100 g edible portion (100 g = 3 1/2 oz)
Lecithin is used as an emulsifying agent in processed foods such as chocolate and margarine, and as confectionary coatings. Lecithin is used in chocolate as a fat extender, replacing in part the more expensive cocoa butter. It has been found 0.5% to 0.7% of lecithin can reduce the cocoa butter content of chocolate by up to 7%, reducing the total fat from 37% to 30% without changing the blend's viscosity.
Method of Action
The phosphatidyl choline (PC) functions structurally as a component of the cell membrane. PC also occurs in plasma lipoprotein complexes where it assists in the transport of lipids throughout the bloodstream.
In bile PC acts as an emulsifier while aiding in fat transport from the gastrointestinal tract.
While some dietary lecithin is absorbed directly by the gastrointestinal system, most of it is hydrolyzed, absorbed as individual components, then resynthesized in the intestinal mucosa.
Dietary phospholipids increase the fecal excretion of neutral sterols. This may reduce the absorption of dietary cholesterol from the intestinal contents, while restricting the reabsorption of endogenously-produced cholesterol into the bloodstream. This reduction may account for lecithin's ability to lower serum cholesterol.
In relation to the cholinergic hypothesis and its application to Alzheimer's disease, circulating choline, the precursor of the neurotransmitter acetylcholine, affects brain choline content and the release of acetycholine in the central nervous system.
Disaturated phosphatidylcholine, from the synthesis of lecithin, is also required for lung function. It is a major pulmonary surfactant lowering surface tension of the lung thereby allowing for the appropriate exchange of of oxygen and carbon dioxide.
A deficiency of this surfactant may play a major role in the pathogensis of respiratory distress syndrome in premature human infants.
There remains some debate about the choice between animal (egg) or vegetable (soy) versions of lecithin. Some authorities specify a particular form, such as animal for viruses e.g. AIDS or Epstein Barr patients.
Supplementation is usually one capsule before meals.
Because dietary lecithin yields comparable increases in blood choline levels and possibly brain acetylcholine levels, lecithin is currently preferred in clinical use, when the two choices are given.
Recent reviews on the possible benefits of lecithin or choline in the treatment of alcoholic cirrhosis have concluded that neither is of any benefit, even in rats given massive doses of pure choline.
Since 1951, lecithin has been known to increase the capacity of the bile to solubilize cholesterol. Lecithin supplementation of at least 2 to 10 grams per day may normalize the abnormally low phospholipid : cholesterol ratio associated with gallstones in some patients. In one study, only 1 in 8 patients demonstrated a decrease in the size of the stones, as well as in their shape over an 18 to 34 month period. In a second study, gallstones in 2 of 9 patients completely disappeared with lecithin supplementation. In in yet another patient, the stones had significantly decreased in size.
Clinical studies have shown lecithin may reduce serum lipid levels, particularly cholesterol. This reduction could decrease the risk for coronary artery disease.
Phosphatylethanolamine (PE) in lecithin is effective in lowering serum cholesterol while increasing bile acid excretion. However, phosphatidylcholine (PC) also has this effect, although to a lesser degree than PE. Hence, the composition and potency of lecithin's phosphatides is important. Although concentrates of PE and PC are on the market, PE and PC taken together seem to have better corresponding effects on lowering cholesterol levels than either alone.
This was demonstrated in a study showing no decrease in serum lipoproteins or liver lipids when rats were fed only PC derived from soybeans. However, when the same strain of rats were fed egg yolks containing both PE and PC, serum cholesterol and apolipoprotein A-1 declined, while serum apolipoprotein B and liver cholesterol increased.
In these studies 35 grams of lecithin (53% PC) a day was required to significantly lower total cholesterol and LDL cholesterol, while raising HDL cholesterol. This is a considerable amount of lecithin. Nevertheless these results are supported by studies on patients with familial hypercholesterolemia and rabbits with modified arterial lesions due to cholesterol-induced atherogenesis.
Mental Function in Healthy Older Adults
Preliminary work reported in 1989 by Florida International University and the Baumel-Eisner Neuromedical Institute, suggests dietary lecithin supplements may have a beneficial effect on the mental function of healthy older adults.
The double-blind placebo study involved 89 "healthy" older adults, ages 50 to 80 years of age. Forty-one subjects received two tablespoons daily of lecithin providing 500 milligrams of choline, while the remaining controls received a placebo. The subjects were supplemented over a five week period.
Memory lapses diminished significantly in the lecithin group. Further the lecithin users reported improvements in mood and reduced stress.
Long term studies supporting these findings are yet to be completed. Additionally, studies, using a new lecithin-like product seven times purer than traditional lecithin to test these results at lower daily intakes, have already been proposed.
Senile Dementia (Alzheimer Type)
In Alzheimer's disease, choline levels in particular regions of the brain are lower than normal. In addition, patients with senile dementia of the Alzheimer type (SDAT) have been found to have diminished levels of brain choline acetyltransferase and decreased acetylcholine biosynthesis in the cerebral cortex and hippocampus.
The cholinergic dysfunction appears to be largely presynaptic, since most investigators have found either normal, or minimally decreased, numbers of muscarine receptors in brains of patients with SDAT.
It has been reported increased PC plasma levels raise brain choline levels and, consequently, neuronal acetylcholine synthesis. If the converse were true, dietary deficiencies of choline or PC would result in the decreased biosynthesis of acetylcholine and a reduction in the neurotransmission of electrical impulses across synapses. The relationship between choline levels in the brain to brain function and the ability of choline and its precursor, lecithin, to raise brain choline levels form the basis for the "cholinergic hypothesis".
Numerous clinical studies have attempted to determine the benefit of choline or its precursor, lecithin, in SDAT. Until 1985, most trials with choline or lecithin were disappointing. Frequently these studies were criticized because low doses or impure lecithin were used.
In 1985, a double-blind placebo-controlled trial of high-dose lecithin of patients with advanced Alzheimer's disease was reported. Unlike earlier trials which had numerous methodological weaknesses, this study tested the hypothesis that high doses of purified lecithin might slow down the deterioration of SDAT.
The purified lecithin came from soya and contained 90% phosphatidyl- and lysophosphatidyl-choline. Patients received 20 to 25 grams a day of this purified soya lecithin. Plasma choline levels were monitored throughout the study.
The study found a limited number of patients benefited from high dose supplementation, especially "poor-compliers." The latter group showed moderate improvements in orientation, learning and memory within four months. However, these improvements did not last past six months, probably owing to the patients discontinuing lecithin supplementation after conclusion of the study.
Overall, there was no difference between the placebo group and the lecithin group at the end of the study, with the exception of the improvement of the poor complier subgroup.
In 1987, a carefully conducted double-blind placebo controlled crossover study examined the possible role of lecithin in retarding the progression of Alzheimer's disease from its onset. In this study, patients with nearly identical scores on the Clinical Dementia Rating Scale (1.6) were given either lecithin therapy or a placebo for three months, then crossed-over to the other treatment. Neuropsychological scores showed no differences in the dementia process over time between the lecithin-treated or placebo groups, in spite of significant raises in plasma choline levels (from 15.9 to 28.8 nanomols/milliliter) in the lecithin group.
In another study, homogenates of brain tissue from patients with Alzheimer's disease were shown to have a reduced ability to release choline from either lecithin or PC. The inability to obtain choline from its precursors may account for the disappointing results seen in the above trial.
Favorable results were reported in 1989 by a Canadian collaborative clinical study of lecithin and tetrahydroaminoacridine (THA), an acetylcholinesterase inhibitor. Alzheimer's patients were given 25 and 50 milligram capsules of THA orally. Doses were increased in 50 milligram increments every two weeks, to a maximum daily dose of 200 milligrams. However, gastrointestinal intolerance and evidence of hepatoxicity appeared at these high doses, so the dose was reduced to a maximum of 100 milligrams daily. These subjects were also given 1.2 grams of lecithin, consisting of 12% phosporylcholine, at mealtime. Results from THA + lecithin administration were clinically modest but statistically significant, especially for cognitive function.
By contrast, a 1989 report indicated physostigmine, another cholinesterase inhibitor, improved the selective reminding task, a test of verbal memory, with no improvement in cognition. This finding is interesting, as it indicates these inhibitors may be effective in and of themselves. Even when lecithin is added as a supplement to physostigmine, any improvement in memory occurs only for a brief period of time.
Further data showing a lack of support for long term benefits from ordinary lecithin supplementation comes from an electroencephalo-graphic (EEG) study of Alzheimer's patients given either lecithin or placebo. In a 26 week double-blind trial, topographic maps of EEG spectra were compared between the two groups. No difference could be found between the two treatments, confirming the findings of earlier studies.
Recently, highly purified lecithin with concentrated PC has become commercially available. It has the ability to increase blood choline levels at lower doses than plain lecithin.
Supplementation with three grams of this purified product, rather than with 20-25 grams of ordinary lecithin, can raise blood choline levels by 50% in just two hours. Nine grams of the purified product successfully doubled the blood levels. Purified lecithin accomplishes this rapid increase by reducing other phosphatides that ordinarily impede choline absorption.
Preliminary reports suggest some patients with tardive dyskinesia may benefit from large doses of either lecithin or choline. The responders seem to have a deficiency of cholinergic transmission in the brain. Further work in this area seems warranted.
There is presently no evidence lecithin, choline chloride, choline bitartrate, or choline dihydrogen citrate is toxic to humans. Doses as high as 100 grams per day for up to four months have been reported, with no evidence of ill effects. However, theoretically, there is the possibility of choline and possibly lecithin, causing clinical depression, as would be consistent with the dopamine-acetylcholine balance theory.Abstracts
Lecithin has low toxicity potential and is favored over choline chloride since the latter has a tendency to induce gastrointestinal irritation and a "fishy" odor.
Gastrointestinal intolerance to lecithin taken with any of the acetylcholinesterase inhibitors (e.g. tetrahydroaminoacridine; physostigmine) has been reported by several investigators treating Alzheimer's disease.
As in the case of the Canadian collaborative study of THA and lecithin, peripheral cholinergic side-effects were treated with 6 milligrams a day of propantheline bromide up to 30 milligrams per day at the discretion of the treating physician.
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