Text Size

Site Search powered by Ajax




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:

Egg yolk1490Split peas201
Liver 550Rice bran170
Whole egg 162Roasted peanuts162
Wheat germ 406Oatmeal156
Soybeans 340Peanut butter145
Rice germ 300Bran143
Barley 139Blackeye peas257
Ham 122Garbanzo beans245
Brown rice 112Brewer's yeast240
Veal 104Rice polishings102

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.

Therapeutic Approaches

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.

Alcoholic Cirrhosis

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.

Tardive Dyskinesia

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.

Toxicity Factors

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.

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.

Soy lecithin has approval status as an herb by the German Commission E.


Blumenthal, M (Ed.): The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. American Botanical Council. Austin, TX. 1998.



Anonymous. Editorial. Drugs and memory. Lancet. 1982. II; 474-476.

Artom, C. & M.A. Swanson. On absorption of phospholipids. J Biol Chem. 1948. 175; 871-881.

Baraona, E. & C.S. Lieber. Effects of ethanol on lipid metabolism. J Lipid Res. 1979. 20; 289-315.

Bartus, RT et al., The cholinergic hypothesis of geriatric memory dysfunction. Sci. 1982. 217; 408-417.

Berg-A; Frey-I; Baumstark-MW; Halle-M; Keul-J: Physical activity and lipoprotein lipid disorders. Sports-Med. 1994 Jan; 17(1): 6-21.

Blomstrand, R. Intestinal absorption of phospholipids in rat. Acta Physiol Scand. 1955. 34; 147-157.

Bowen, D.M., C.B. Smith, P. White & N. Dawson. Neurotransmitter-related enzymes and indices of hypoxia in senile dementia and other abiotrophies. Brain. 1976. 99; 459-456.

Bowen D., J. Spillane, G. Curzon, et al. Accelerated aging or selective neuronal loss as an important cause of dementia. Lancet. 1979. 1; 11-14.

Bowen, D.M., J.S. Benton, J.A. Spillane, C.T.T. Smith & S.J. Allen. Cholineacetyltransferase activity and histopathology of frontal neocortex from biopsies of demented patients. J Neurol Sci. 1982. 57; 191-202.

Boyd, W.D., J. Graham-White, G. Blackwood, I. Glen & J. McQueen. Clinical effects of choline in Alzheimer senile dementia. Lancet. 1977. II; 711.

Brinkman, S.D., R.C. Smith, J.S. Meyer, et al. Lecithin and memory training in suspected Alzheimer's disease. J Gerontol. 1982. 37; 4-9.

Canty-DJ; Zeisel-SH: Lecithin and choline in human health and disease. Nutr-Rev. 1994 Oct; 52(10): 327-39.

Childs, M.T. et al. The contrasting effects of a dietary soya-lecithin product and corn oil on lipoprotein lipids in normolipidemic and familial hypercholesterolemic subjects. Athero. 1981. 38;217-228.

Davies, P. & A.J. Maloney. Selective loss of central cholinergic neurons in Alzheimer's disease. Lancet. 1976. II; 1403.

Davies, P. & A.H. Verth. Regional distribution of muscarinic acetylcholine receptor in normal and Alzheimer's-type dementia brains. Brain Res. 1978. 138; 385-392.

Davis, K.L., L.E. Hollister, J.D. Barchas & P.A. Berger. Choline in tardive dyskinesia and Huntington's disease. Life Sci. 1976. 19; 1507.

Davis, K.L., P.A. Berger & L.E. Hollister. Lecithin - Nutrition and the Brain. Volume 5. Raven Press. New York. 1979. pp. 305-315.

Drachman, D.A., G. Glosser, P. Flemming & G. Longenecker. Memory decline in the aged: treatment with high dose lecithin. Neurology. 1981. 31; 101.

Duffy, F.H., G. McAnulty, M. Albert, H. Durwen & S. Weintraub. Lecithin - absence of neurophysiologic effect in Alzheimer's disease by EEG topography. Neurology. 1987. 37; 1015-1019.

Dullaart-RP; Hoogenberg-K; Dikkeschei-BD; van-Tol-A: Higher plasma lipid transfer protein activities and unfavorable lipoprotein changes in cigarette-smoking men. Arterioscler-Thromb. 1994 Oct; 14(10): 1581-5.

Elble, R., E. Giacobini & C. Higgins. Choline levels are increased in cerebrospinal fluid of Alzheimer's patients. Neurobiol Aging. 1989. 10; 45-50.

Etienne, P., S. Gauthier, G. Johnson, et al. Clinical effects of choline in Alzheimer's disease. Lancet. 1987. I; 508-509.

Etienne, P., D. Dastoor, S. Gauthier, S. et al. Alzheimer's disease - lack of effect of lecithin treatment for 3 months. Neurology. 1981. 31; 1552-1554.

Federal Register. 1979. 44; 16144-16147.

Fisman, M., H. Merskey, E. Helmes, J. McCready, E.H. Coulhon & B.J. Rylett. Double-blind study of lecithin in patients with Alzheimer's disease. Can J Psychiatry. 1981. 26; 426-428.

Gauthier, S., P. Etienne, D. Dastoor, B. Collier & R. Ludwick. Lack of an effect of a 3 month treatment with lecithin in Alzheimer's disease. Neurology. 1981. 31; 1552-1554.

Gelenberg. A.J. et al. Choline and lecithin in the treatment of tardive dyskinesia - preliminary results from a pilot study. Am J Psychiatry. 1979. 136; 772-776.

Heyman, A., D. Schmechel, W. Wilkinson, H. Rogers, R. Krishna, D. Holloway, K. Schultz, L. Gwyther, R. Peoples, et al. Failure of long term high dose lecithin to retard progression of early-onset Alzheimer's disease. J Neural Trans Supplemental. 1987. 24; 279-286.

Hoff er, A. & M. Walker. Nutrients to Age Without Senility. Keats Pub. New Canaan, CT. 1980, p. 166-167.

Hunt, C. et al. Hyperlipoproteinaemia and atherosclerosis in rabbits fed low-level cholesterol and lecithin. Brit J Exp Pathol. 1985. 66; 35-46.

Hunt, S.M. & J.L. Groff. Advanced Nutrition and Human Metabolism. St. Paul: West Publishing Co. 1990.

Imdizumi, K. The contrasting effect of dietary phosphatidylethanolamine and phosphatidyl-choline on serum lipoproteins and liver lipids in rats. J Nutr. 1983. 113; 2403-2411.

Kanfer, J.N. & D.G. McCartney. Phosphatase and phospholipase activity in Alzheimer brain tissue. J Neural Transmission. Supplemental. 1987. 24; 183-188.

Kinoshita-M: Familial LCAT deficiency. Nippon-Rinsho. 1994 Dec; 52(12): 3210-5.

Knebl-J; DeFazio-P; Clearfield-MB; Little-L; McConathy-WJ; McPherson-R; Lacko-AG: Plasma lipids and cholesterol esterification in Alzheimer's disease. Mech-Ageing-Dev. 1994 Jan; 73(1): 69-77.

Lavaud-F; Perdu-D; Prevost-A; Vallerand-H; Cossart-C; Passemard-F: Baker's asthma related to soybean lecithin exposure. Allergy. 1994 Mar; 49(3): 159-62

Lawson, H.W. Standards for Fats & Oils. AVI Publishing. Westport, CT. 1985. p. 25.

Lieber, C.S. & L.M. DeCarli. Study of agents for the prevention of fatty liver produced by prolonged alcohol intake. Gastroenterol. 1966. 50; 316-322.

Little, A et al., A double-blind, placebo controlled trial of high-dose lecithin in Alzheimer's disease. J Neurol Neurosurg Psychiatry. 1985. 48; 736-742.

Lopez G., & I. Berry. Plasma choline levels in humans after oral adminstration of highly purified phosphatidylcholine (PC) in capsules. Alzheimer's Disease - Advances in Basic Research and Therapies. R.J. Wurtman, S.H. Corkin & J.H. Growdon. eds. Proceedings of the Fourth Meeting of the International Study Group on the Pharmacology of Memory Disorders Associated with Aging. Zurich. 1987. pp. 467-470.

Maes-M; Delanghe-J; Meltzer-HY; Scharpe-S; D'Hondt-P; Cosyns-P: Lower degree of esterification of serum cholesterol in depression: relevance for depression and suicide research. Acta-Psychiatr-Scand. 1994 Oct; 90(4): 252-8

Marchbanks, R.M. Choline, aceylcholine and dementia. Editorial Psychol Med. 1980. 10; 1-3.

Mash, D.C., D.D. Flynn & L.T. Potter. Loss of M2 muscarine receptors in the cerebral cortex in Alzheimer's disease and experimental cholinergic denervation. Science. 1985. 228; 1115-1117.

McMahon, K.E. & P.M. Farrell. The effect of choline deficiency on lung phospholipid concentrations in the rat. J Nutr. 1986. 116; 936-943.

Murata, M., K. Imaizum & M. Sugano. Effect of dietary phopholipids and their constituent bases on serum lipids and apolipoproteins in rats. J Nutr. 1982. 112; 1805-1808.

Nickless, H. & A.F. Sidaway. Use of fat in Confectionary. Fats and Oils. Chemistry and Technology. R.J. Hamilton & A. Bhati. eds. Applied Science Publishers. London. 1980, p. 171.

Perry, E.K., R.H. Perry, G. Blessed, B.E. Tomlinson. Necropsy evidence of central cholinergic defictis in senile dementia. Lancet. 1977. I; 189.

Perry, E.K., P.H. Gibson, G. Blessed, R.H. Perry & B.E. Tomlinson. Neurotransmitter enzyme abnormalities in senile dementia. J Neurol Sci. 1977. 34; 247-265.

Perry, E.K., R.H. Perry, P.H. Gibson, G. Blessed & B.E. Tomlinson. A cholinergic connection between normal aging and senile dementia in the human hippocampus. Neurosci Let. 1977. 6; 85-89.

Perry, E.K., B.E. Tomlinson, G. Blessed, K. Bergmann, P.H. Gibson & R.H. Perry. Correlation of cholinergic abnormalities with senile plaques and mental test scores in senile dementia. Br Med J. 1978. II; 1457-1459.

Qu-SJ; Fan-HZ; Blanco-Vaca-F; Pownall-HJ: Effects of site-directed mutagenesis on the serine residues of human lecithin:cholesterol acyltransferase. Lipids. 1994 Dec; 29(12): 803-9.

Renvoize, E.B. & T. Jerram. Choline in Alzheimer's disease. New Eng J Med. 1979. 301; 330.

Rinne, J.O., K. Laakso, L.T. Lonnberg, et al. Brain muscarinic receptors in senile dementia. Brain Res. 1985. 336; 19-25.

Safford, F. & B. Baumel. An exploratory study of the effects of dietary lecithin on mental function of healthy older adults. Abstract. Unpublished, 1989.

Select Committee on GRAS Substances - Evaluation of the Health Aspects of Choline Chloride and Choline Bitartrates as Food Ingredients (SCOGS-42). Life Sciences Research Office, Federation of American Societies for Experimental Biology. Bethesda, MD. 1975. pp. 1-16.

Select Committe on GRAS Substances - Evaluation of the Health Aspects of Lecithin as a Food Ingredient (SCOGS-106). Prepared for the Bureau of Foods, FDA, Contract # FDA 223-75-2004, 1979. pp. 31. Available from NTIS. Springfield, VA. PB 301 405.

Signoret, J.L., A. Whiteley & F. L'Hermitte. Influence of choline on amnesia in early Alzheimer's disease. Lancet. 1978. II; 837.

Simms, N.R., D.M. Bowen, S.J. Allen, et al. Presynapatic cholinergic dysfunction in patients with dementia. J Neurochem. 1983. 40; 503-509.

Smith, C.M., M. Swash, A.N. Exton-Smith, et al. Choline therapy in Alzheimer's disease. Lancet. 1978. II; 318.

Smith, C.M., M. Swash & A.N. Exton-Smith. Effects of cholinergic drugs on memory in Alzhemier's disease. A.I.M. Gen & L.J. Whalley eds. Alzheimer's Disease - Early Recognition of Potentially Reversible Deficits. Churchill Livingston. Edinburgh. 1979. p.148-153.

Stein, Y. & O. Stein. Metabolism of labeled lysolecithin, lysophosphatidyl ethanolamine and lecithin in the rat. Biochim Biophys Acta. 1966. 116; 95-107.

Summers, W., L. Majorvski, G. Marsh, et al. Oral THA in long-term treatment of senile dementia, Alzheimer's type. New Eng J Med. 1986.

Tamminga, C.A., R.C. Smith, S.E. Erickson, S. Chang & J.M. Davis. Cholingeric influences in tardive dyskinesia. Am J Psychiatry. 1977. 134; 769-774.

Thal, L.J., D.M. Masur, A.D. Blau, P.A. Fuld & M.R. Klauber. Chronic oral physostigmine without lecithin improves memory in Alzheimer's disease. J Am Geriatr Soc. 1989. 37; 42-48.

Thal, L.J., D.M. Masur, N.S. Sharpless, et al. Acute and chronic effects of physostigmine and lecithin in Alzheimer's disease. Prog Neuropsychopharmcol Biol Psychiatry. 1986. 10; 627-636.

Tompkins, R.K. et al. Relationship of biliary phospholipids and cholesterol concentrations to the occurrence and dissolution of human gallstones. Ann Surg. 1970. 172; 936-945.

Tuzhilin, S.A. et al. The treatment of patients with gallstones with lecithin. Am J Gastroenterol. 1976. 65; 231.

Vida, S., L. Gauthier & S. Gauthier. Canadian collaborative study of tetrahydroaminoacridine (THA) and lecithin treatment of alzheimer's disease: effect on mood. Canad J Psychiatry. 1989. 34; 165-170.

Vroulis, G.A., R.C. Smith, S. Brinkman, J. Schoolar & J. Gordon. The effects of lecithin on memory in patients with senile dementia of the Alzheimer's type. Psychopharm Bull. 1981. 17; 127-128.

Vroulis, G., R. Smith, J. Schoolar, et al. Reduction of cholesterol risk factors by lecithin in patients with Alzheimer's disease. Am J Psychiatry. 1982. 139; 1633-1634.

White, P., M. Goodhart, J. Keet, C. Hiley, L. Carrasco & I. Williams. Neocortical cholinergic neurons in elderly people. Lancet. 1977. I; 668.

Whiteley, A., J. Signortet, Y. Agid & F. L'Hermitte. Action de la choline sur les troubles mnesiques de la maladie d'Alzheimer. Rev Neurol. Paris. 1979. 135; 565-572.

Wilcock, G.K., M.M. Esiri, D.M. Boswen & C. Smith. Alzheimer's disease. Correlation of cortical choline acetyltransferase activity with the severity of dementia and histological abnormalities. J Neurol Sci. 1982. 57; 407-417.

Williams, S., Nutrition & Diet Therapy, 5th Edition, St. Louis: Times Mirror Mosby, 1985.


Follow Applied Health on FaceBook Follow Applied Health on Twitter Follow Applied Health on Pinterest Follow Applied Health on YouTube

cruelty free - tested only on humans
We test only on humans