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Phosphatidylcholine

Date: 03/30/2003

 

Phosphatidylcholine (derived from lecithin), a primary dietary source of choline, is composed of a phosphate group, 2 fatty acids, and choline. The composition of essential fatty acids in phosphatidylcholine determines its value in promoting health. When phosphatidylcholine is ingested, most of it is broken down into choline, glycerol free fatty acids, and the phosphate group, rather than being incorporated intact into cellular membranes.

• Although choline can be manufactured in humans from either methionine or serine, it has recently been designated an essential nutrient.

 

Function

• Choline is required for the proper metabolism of fats; it facilitates the movement of fats in and out of cells. Like Vitamin B12, 5-adenosylmethionine, and Folic Acid, choline acts in the human body as a methyl donor. As such, choline is essential for proper liver function due to its key role in the lipotropic effect, i.e., the export of fat from the liver. In the absence of adequate choline, fats become trapped in the liver, where they block metabolism. Stagnation of fat and bile eventually leads to the development of more serious liver disorders such as cirrhosis.

• Choline is needed for cell membrane integrity because of the critical role it plays in the manufacture of primary components of cell membranes, such as phosphatidylcholine and sphingomyelin.

• Choline is essential in the synthesis of acetylcholine. Choline supplementation increases the accumulation of acetylcholine which plays a crucial role in many brain processes, including memory. (Canty, DJ and Zeisel, SH. Nutr Reviews. 52;327-339, 1994)

• Phosphatidylcholine increases the solubility of cholesterol and thereby decreases cholesterol‘s ability to induce atherosclerosis. Phosphatidylcholine aids in lowering cholesterol levels, removing cholesterol from tissue deposits, and inhibiting platelet aggregation. (Brook, JG, Linn, S, and Aviram, M. Biochem Med Metabol Biol. 35;31-39, 1986.) The high content of linoleic acid in phosphatidylcholine may be responsible for much of the benefit derived from supplementation.

 

Mode of Action

• Choline acts as a methyl donor, especially in liver function.

• Choline enables synthesis of acetylcholine, phosphatidylcholine and sphingomyelin.

 

Requirements

• Choline has recently been designated as an essential nutrient.

• RDA:

Infants and children: 125 to 375 mg/day

Women: 425 mg/day; Pregnant women: 450 mg/day; Breast-feeding women: 500 mg/day

Men: 500 mg/day

• Average intake in the U.S.: Approximately 6 g per day as phosphatidylcholine

 

Food sources

• As free choline in vegetables (especially cauliflower and lettuce), whole grains, liver, and soy.

• As lecithin (containing 10-20% phosphatidylcholine) in grains, legumes, meat and egg yolks.

 

Deficiency

• True choline deficiency appears to be rare or non-existent and has only been induced in a research setting.

• Deficiencies typically present as muscle weakness, tingling in the fingers and toes, weight loss or fatigue.

• Liver and kidney disorders develop when animals are fed a choline-deficient diet.

• Fatty infiltration of the liver and other signs of liver dysfunction develops in humans fed a choline-deficient diet.

• Choline is an essential nutrient for human cells in cell cultures, and humans receiving intravenous feeding with solutions low in choline develop signs of choline deficiency.

(Canty, DJ and Zeisel, SH. Nutr Reviews. 52;327-339, 1994; Zeisel, SH, et al. FASEB J 5;2093-2098, 1991)

 

Therapeutic Uses

Liver Disorders

Phosphatidylcholine is used in the treatment of a variety of liver disorders, including:

  • Acute & Chronic Viral Hepatitis: Chronic viral manifestations severely challenge the liver yet numerous controlled trials have established PC as a safe and potent intervention for infection (Mueting 1972, Hirayama 1980, Yamo1978, Kosina 1981, Jenkins 1982, Visco 1985, Hantak 1990, Ilic and Begic-Janev 1991). Optimal results were achieved in these studies when subjects were maintained on a combination of oral and infused PC utilizing higher doses. Once clinical indicators began returning to normal subjects were maintained on oral doses of PC. In addition to decreases in liver enzymes, serum lipids, immune markers and bilirubin, subjects experienced reversal of fatty degeneration, inflammation, jaundice, liver swelling and fibrosis, per liver biopsy.
  • Cirrhosis of the liver
  • Decreased bile solubility
  • Diabetic fatty liver
  • Drug-induced liver damage: The use of anticonvulsant drugs often leads to liver toxicity. Subjects who had received anticonvulsants for an average of five years were assessed by GGT elevation (Hisanaga 1980) and given PC for six months. Positive outcome was consistently achieved in subjects in addition to a decrease in GGT levels.
  • Toxic liver damage: (Kuntz 1965) reported remarkable effects with PC in subjects with chemical poisoning and Esslinger (1966) with plant toxin.
  • Fatty liver: 650 subjects with varying degrees of liver damage were followed for 5 years. Subjects received intravenous PC at 950 mg along with oral PC (450- 700 mg). When blood parameters returned to normal subjects were shifted to oral PC only. Subjects were categorized as to severity of liver damage: fatty degeneration, acute inflammation, chronic aggressive inflammation, and advanced fibrotic damage. All groups in the study had marked benefit. There was reversal of fatty degeneration in many subjects and in those with acute inflammation PC accelerated recovery by an average of ten days. (Wallnoefer and Hanusch 1973).
  • Alcohol-induced liver disease: Studies with baboons have found that phosphatidylcholine supplementation protects against alcohol-induced liver abnormalities and cirrhosis; presumably some of these same effects will be present in humans. Nevertheless, choline salts do not seem to be of any value in the treatment of alcohol-induced liver disease in humans but may be useful in general liver support. (Lieber,CS and Rubin, E. N Engl J Med 280;705-708, 1969)

 

Detoxification

The health of the membrane is synonymous with the health of the entire organism. Toxins have an affinity for fatty acids; they literally take up residence in the lipid environment and in so doing, weaken and disrupt. The probable result is early apoptosis, premature death of the cell. Generally, normal mitosis provides for new cellular growth to maintain the health of the body, i.e. the previous discussion on photo receptors. However, toxicity's affinity for lipids can easily redistribute toxins and diseased toxic lipids into the new growth. In a healthy state with adequate glutathione and ascorbate to bind the toxins before they take up new residence, the body can keep the bad guys under control. However, if defenses are weak, toxins can continually be redistributed and eventually hide in the CNS and bone where the regeneration process is at a slower pace. The goal of detoxification is to 1) encourage regrowth with a renewed effort at the correct balancing of the essential nutrients, with the exchange of high energy lipids (PUPA and HUP A) to fuel regeneration and the eventual detoxification process; and 2) at the correct time, the inclusion of the toxin removal specialists, ascorbate, chlorella, and if possible IV glutathione.

 

Detoxification of neurotoxins requires that the cell membrane is nourished with balanced essential fatty acids (4:1, plus HUFAs) and supportive phospholipids. Phosphatidylcholine (PC) is the most abundant phospholipid of the cell membrane and protects the liver, with its 33,000 square meters of membrane, against toxicity and infection. The liver plays a pivotal role in detoxification but due to its fatty acid content and the lipid soluble characteristics of neurotoxins, lipid based interventions are required to impact toxic burdens. Once the liver has been damaged it can no longer metabolize fats normally. Pools of lipids are then deposited within hepatocytes throughout the liver. Beta oxidation of fatty acids is suppressed impairing detoxification and prostaglandin production. Extensive research with PC has revealed that it protects the liver against damage from alcohol, pharmaceuticals, environmental pollutants, xenobiotics and infection due to viral, bacterial and fungal manifestations (Lieber 1994a, 1994b, 1995, 2001a, 2001b).

 

Hypercholesterolemia and Atherosclerosis

Phosphatidylcholine increases the solubility of cholesterol and thereby decreases its ability to induce atherosclerosis. Phosphatidylcholine also aids in lowering cholesterol levels, removing cholesterol from tissue deposits, and inhibiting platelet aggregation. (Brook, JG, Linn, S, and Aviram, M. Biochem Med Metabol Biol. 35;31-39, 1986.) Here some of the beneficial effects may be attributable to the high content of linoleic acid in phosphatidylcholine.

 

  • The phospholipid preparation Lipostabil has been researched for use in the treatment of high cholesterol levels and atherosclerosis. In several trials evaluating this 70% phosphatidylcholine content lecithin product from Germany, total serum cholesterol and triglyceride levels dropped significantly and HDL cholesterol levels improved using dosage ranging from 1.5 g once daily to 3.5 g three timed per day. (Lipostabil. Natterman International GMBH,1990; Wojcicki, J, et al. Phytotherapy Res. 9;597-599, 1995)
  • A high-concentration phosphatidylcholine preparation, marketed in Germany under the trade name "Essentiale", has produced clinical results consistent enough to gain authorization from the BGA, the German equivalent of the FDA. This form contains 90% phosphatidylcholine, with 50% of the molecule having linoleic acid, the essential fatty acid, bound at the proper position; i.e., the first and second carbon of the glycerol molecule. Using this preparation the standard dosage recommendation is 350 mg three times per day with meals. (Essentiale, Natterman International GMBH, 1989.) 

 

Bipolar Depression

  • There is evidence that mania is associated with a reduced brain cholinergic activity. Phosphatidylcholine supplementation at levels of 15-30 g/day has been found to exert beneficial effects in the treatment of bipolar depression. (Wutman, R, et al. Nutrition and the Brain. Vol. 5. Raven Press: New York, 1979; Cohen, B, et al. Am J Psychiat 137:242-243, 1980; Cohen, B, et al. Am J Psychiat 139;1162-1164, 1982.)

·        The use of phosphatidylcholine may result in significant improvement or amelioration of symptoms in some patients suffering from bipolar depression by increasing brain choline levels. Some researchers believe that one effect of Lithium carbonate, the standard pharmaceutical treatment for bipolar depression, is the promotion of increased acetylcholine activity in the brain. (Jope, R, et al. Am J Psychiat 142;356-358,1985)

 

Alzheimer’s Disease

  • Choline supplementation increases the accumulation of acetylcholine within the brain in normal patients so many researchers hypothesized that phosphatidylcholine supplementation would benefit Alzheimer patients. Some research has indicated that increasing acetylcholine content in the brain through supplemental choline might result in improved memory. However, clinical trials using phosphatidylcholine have not produced significant benefits. Studies revealed inconsistent improvements in memory from choline supplementation in both normal and Alzheimer’s patients. Nevertheless, criticisms of these studies and their interpretations have been raised on the grounds that sample size was too small, the dosage of phosphatidylcholine used was too low, and the studies themselves were poorly designed. (Rosenberg, G and Davis, KL. Am J Clin Nutr. 36; 709-720, 1982; Levy, R, et al. Lancet 1;474-476,1982; Sitaram, N, et al. Life Sci 22;1555-1560, 1978.)
  • Alzheimer’s disease is characterized by a decrease in cholinergic transmission, but the basic defect in cholinergic transmission in Alzheimer’s disease relates to impaired activity of the enzyme acetylcholine transferase, not to a deficiency of choline. Acetylcholine transferase combines choline with an acetyl molecule to form acetylcholine. However, since increased levels of choline do not necessarily increase the activity of this critical enzyme, phosphatidylcholine supplementation will probably not prove efficacious in the majority of patients with Alzheimer’s disease.
  • In a patient with mild to moderate dementia, the use of a high-quality phosphatidylcholine preparation at a dosage level of 15 to 25 g/day may be beneficial. (Murray, M. p. 140, 1996.)

 

Forms

• Choline is available as a soluble salt, most commonly as either choline bitartrate, citrate, or chloride, or as phosphatidylcholine in lecithin.

• Most commercial forms of lecithin contains only 10-20% phosphatidylcholine.

• Most supplements labeled as "phosphatidylcholine" contain only 35 percent.

• Some newer and more potent preparations contains up to 98 percent phosphatidylcholine. These more pure forms of phosphatidylcholine are preferred since they are associated with fewer gastrointestinal side effects. This is particularly true in the treatment of those conditions that require large doses of phosphatidylcholine (i.e., 15 to 30 grams) because low-concentration forms such as lecithin would be required in such large amounts that side effects would be nearly inevitable.

Intravenous form is also available. The liver is the largest organ of the body and receives the first flush of PC from an infusion. However an exchange of lipids is systemic with every organ, every neuron, every cell sharing the increased PC and the higher performing lipids (HUFAs). It should be expected that improved metabolic performance would also be systemic.

 

Dosage

• Using lecithin, the most common form of choline supplementation, with 90 percent phosphatidylcholine, the dosage (three times daily with meals) is:

• 350-500 mg t.i.d. for the treatment of liver disorders;

• 500-900 mg t.i.d. for lowering cholesterol;

• 5,000-10,000 mg q.d. for the treatment of Alzheimer’s disease and bipolar depression.

(Murray, M. p. 141, 1996) 

 

Side Effects

• Choline and phosphatidylcholine are generally well tolerated.

• At doses over 20grams daily, pure choline, but not phosphatidylcholine, will produce a "fishy" odor.

• High doses of lecithin, several grams per day, will produce reduced appetite, nausea, abdominal bloating, gastrointestinal pain and/or diarrhea in some people. 

Toxicity

• No toxicity beyond the side effects mentioned above were found in any of the sources cited. 

 

Contraindications

• Phosphatidylcholine is not indicated in patients with depression (unipolar or clinical depression) unless under the supervision of a physician because high-dosage phosphatidylcholine supplementation can worsen depression in some cases.

 

Interactions

• Choline works together with other methyl donors and helps the body conserve carnitine and folic acid. (Daily, JW and Sachan, DS. J Nutr 125;1938-1944, 1995; Varela-Mreiras, G, et al. J Nutr Biochem 3;519-522, 1992.)

• Phosphatidylcholine and pantothenic acid are used to form acetylcholine.

 

Phosphatidylcholine
“Technical Version”

Alternative Medicine Review, Vol 7, #2, April, 2002

 

Introduction

Phosphatidylcholine (PC) is a phospholipid, one of a primal class of substances ubiquitous among life fonns.1 PC is the predominant phospholipid of all cell membranes and of the circulating blood lipoproteins. It is the main functional constituent of the natural surfactants, and the body's foremost reservoir of choline, an essential nutrient.2 PC is a normal constituent of the bile that facilitates fat emulsification, absorption, and transport, and is recycled via entero-hepatic circulation. Until recently the nomenclature of PC was confused with lecithin, a complex mixture of phospholipids and other lipids. Lecithin preparations enriched in PC at or above 30 percent by weight are considered PC concentrates.

 

Pharmacokinetics and Metabolism

·        Chemically, PC is a glycerophospholipid,3 built on glycerol (CH2OH-CHOH-CH2OH) and substituted at all three carbons. Carbons I and 2 are substituted by fatty acids and carbon 3 by phosphorylcholine. Simplistically, the PC molecule consists of a head-group (phosphorylcholine), a middle piece (glycerol), and two tails (the fatty acids, which vary). Variations in the fatty acids in the tails account for the great variety of PC molecular species in human tissues.

·        In vivo, PC is produced via two major pathways.4 In the predominant pathway, two fatty acids (acyl "tails") are added to glycerol phosphate (the "middle piece"), to generate phosphatidic acid (PA). Next, PA is converted to diacylglycerol, after which phosphocholine (the "head-group") is added on from CDP-choline. The second, minor pathway is phosphatidylethanolamine (PE) methylation, in which the phospholipid PE has three methyl groups added to its ethanolamine head-group, thereby converting it into PC.

·        Taken orally PC is very well absorbed, up to 90% per 24 hrs when take with meals.

·        Postprandially, PC enters the blood gradually and its levels peak over 8-12 hours. During the digestive process, the position-2 fatty acid becomes detached (de-acylation) in the majority of the PC molecules.5 The resulting lyso-PC readily enters intestinal lining cells, and is subsequently re-acylated at position 2. The position-2 fatty acid contributes to membrane fluidity (along with position I), but is preferentially available for eicosanoid generation and signal transduction. The omega-6/omega-3 balance of the PC fatty acids is subject to adjustment via dietary fatty acid intake.6,7

·        Choline is most likely an essential nutrient for humans,8 and dietary choline is ingested predominantly as PC. Greater than 98 percent of blood and tissue choline is sequestered in PC, 2 and dietary PC serves as a "slow-release" blood choline source.9 Malnourished individuals with lowered blood choline frequently display liver steatosis and related dysfunctions; these often respond favorably to PC supplementation10.

·        Methyl group (-CH3) availability is crucial for protein and nucleic acid synthesis and regulation, phase-two hepatic detoxification, and numerous other biochemical processes involving methyl donation.

·        Methyl deficiency induced by restricted choline intake is linked to liver steatosis in humans, and to increased cancer risk in many mammals. PC is an excellent source of methyl groups, supplying up to three per PC molecule.

 

Mechanisms of Action

  • PC is the main structural support of cell membranes, the dynamic molecular sheets on which most life processes occur.1 Comprising 40 percent of total membrane phospholipids, PC's presence is important for homeostatic regulation of membrane fluidity. The PC molecules of the outermost cell membrane deliver fatty acids on demand for prostaglandin/eicosanoid cellular messenger functions, and support signal transduction from the cell's exterior to its interior6.
  • PC is the main lipid constituent of the lipoprotein particles circulating in the blood. The amphipathic properties of PC render it an obligatory micellizing constituent of bile.12,13 PC has surfactant (surface-active) properties that substantially protect the epithelial-luminal interfaces of the lungs and GI tract14,15.
  • Biochemically, PC is the preferred precursor for certain phospholipids and other biologically important molecules.4 PC also provides antioxidant protection in vivo.16 In animal and human studies, PC protected against a variety of chemical toxins and pharmaceutical adverse effects1.

 

Clinical Indications

The best-documented clinical success with PC to date is its significant amelioration of liver damage, probably because liver recovery following damage requires substantial replacement of cell membrane mass. The findings from eight double-blind trials and numerous other clinical reports 1,7 indicate consistently significant clinical benefit, including improvement of enzymatic and other biochemical indicators, faster functional and structural rebuilding of liver tissue, accelerated restoration of subjects' overall well-being, and improved survival following PC treatment.

 

Alcoholic Hepatic Steatosis and Inflammation

  • Knuechel conducted a double-blind trial on 40 male subjects with hepatic steatosis (fatty liver) and inflammation linked to alcohol intake.17 Subjects were taken off pharmaceuticals and randomized into two groups; one group received placebo, the other 1,350 mg PC per day by mouth (fortified with B vitamins). Benefits from PC were evident at two weeks, and by the eighth week a wide variety of biochemical liver function measures were significantly improved over placebo.
  • Three subsequent double-blind trials corroborated these findings. Schuller Perez and San Martin concluded, "It is our view that the use of highly-unsaturated phosphatidylcholine for therapy of alcohol-dependent steatoses is very productive."18 Buchman et al administered PC double-blind to 15 subjects with fatty liver as part of a total parenteral nutrition intravenous feeding regimen, and also obtained significant benefit.19 Other researchers report that subjects with mild to moderate hepatic inflammation benefit the most from PC supplementation.20
  • In an animal study, baboons were placed on a daily alcohol regimen for up to eight years. Following a blinded trial design, PC was added to the diet of some of the animals. After several years, baboons fed alcohol without PC had progressed to advanced fibrosis, while the PC-supplemented baboons developed fatty liver and mild fibrosis, but did not progress further. After three of the animals were taken off PC and kept on alcohol, they rapidly progressed to extensive; life-terminating liver fibrosis.21

 

Drug-Induced Liver Damage

  • In a double-blind trial, 101 tuberculous subjects who had suffered liver damage from rifampin and two other anti-tuberculosis pharmaceuticals received placebo or 1,350 mg of fortified PC daily. After three months, the PC group had significantly lower SGOT and SGPT enzyme levels.22

 

Hepatitis B

  • In a double-blind trial on 30 subjects with progressing liver damage from chronic hepatitis B virus infection (negative for HBsAg), standard immunosuppressive therapy was retained and subjects received either PC (2,300 mg per day) or pla- cebo. At one year, the PC group had clinically stabilized, with significant improvement of liver structure, whereas the placebo group had worsened.23
  • Sixty subjects positive for hepatitis B (HBsAg-positive) were placed in a fortified PC group (1,350mg per day) or a placebo group for 60 days. From 30 days onward the PC group was clinically improved over placebo, with 50 percent becoming HbsAg-negative, compared to 25 percent of the placebo group.24
  • In a double-blind trial of 50 subjects, all HBsAg-positive and manifesting extremely severe liver damage verified by biopsy and immunologic testing, the PC group (1,350 mg fortified PC per day) benefited considerably more (p<0.001) than placebo. In the PC group, 80 percent (20 of 25) were judged greatly improved, while 24 percent (6 of 25) moderately improved in the placebo group. Cell-structure, biochemical, immunologic, and hematologic parameters were significantly improved over placebo. Clinical improvement continued well past the end of the one-year trial.25

 

Hepatitis C

  • In a multicenter, double-blind trial, 176 patients with chronic viral hepatitis (B or C) were begun on interferon alpha for 24 weeks then randomized to PC (1.8 g/day) or placebo for 24 weeks. Significantly more patients responded to PC, particularly in the hepatitis C subgroup. In addition, PC supplementation sustained a longer term improvement from hepatitis C over another 24 weeks.26
  • A long-term, multicenter, double-blind trial of PC for liver disease is ongoing; its results could signal a breakthrough in nutritional management of this life-threatening disease.27

 

Respiratory Distress Syndrome

  • The surfactant of premature babies is abnormally low in PC. Treatment with exogenous, mature-profile surfactant (with PC 70-80% of the total phospholipids) is the standard therapy for infants with, or at risk of having, respiratory distress syndrome (RDS). A meta-analysis of clinical trials suggests improved survival and overall better outcome from natural surfactant over synthetic forms.28  In another randomized trial with 78 RDS babies, natural surfactant proved superior after six hours, and by 24 hours normalized the surfactant PC profile.14

 

Necrotizing Enterocolitis, Gastrointestinal Protection

·        As the major intrinsic surfactant of the gastrointestinal tract, PC helps maintain the acid barrier properties of the gastric epithelium. Animal research suggests PC helps protect against the adverse GI effects of aspirin and other non-steroidal anti-inflammatory drugs without blocking their efficacy. 25,29,30 Carlson et al reported a lower incidence of necrotizing enterocolitis in pre-term infants fed with formula high in PC and other phospholipids.31

 

Central Nervous System Cholinergic Imbalances

  • In contrast to persistent anecdotal claims, PC failed to benefit cognition in ten double-blind, placebo-controlled trials.32 There are indications the "therapeutic window" for PC might be very narrow,33 which could also explain the disappointing trial results against ataxias, tardive dyskinesia, and other CNS conditions that feature cholinergic imbalances.

 

Toxicity and Side Effects

PC is freely compatible with other nutrients, and when co-administered may enhance their absorption. Standard toxicological assessments indicate no significant acute or chronic toxicity from PC, as well as no mutagenicity and no teratogenicity. PC is well tolerated at daily intakes of up to 18 grams} Symptoms of intolerance are almost exclusively restricted to GI discomfort - diarrhea, excessive fullness, and nausea.

 

Dosage

The therapeutic range of intake is 800- 2,400 mg daily, and 4-6 grams or higher for liver salvage. For subjects with severe liver damage, best results may be obtained by initiating therapy with intravenous and oral PC, then maintaining on oral supplementation after improvement has begun. In cases of liver damage from deathcap mushroom poisoning this procedure has proved lifesaving.34

 

References

1.        Kidd PM. Dietary phospholipids as anti-aging nutraceuticals. In: Klatz RA, Goldman R, eds. Anti-Aging Medical Therapeutics. Chicago, IL: Health Quest Publications; 2000:283-301.

2.        Zeisel SH, Blusztajn JK. Choline and human nutrition. Annu Rev Nutr 1994;14:269-296.

3.        Schneider M. Phospholipids. In: Gunstone FD, Padley FB, eds. Lipid Technologies and Applications. New York, NY: Marcel Dekker; 1997:15-30.

4.        Kent C. Eukaryotic phospholipid biosynthesis. Annu Rev Biochem 1995;64:315-343.

5.        Zierenberg 0, Grundy SM. Intestinal absorption of polyenephosphatidylcholine in man. J Lipid Res 1982;23:1136-1142.

6.        Kidd PM. Cell membranes, endothelia, and atherosclerosis -the importance of dietary fatty acid balance. Altern Med Rev 1996;1:148-167.

7.        Kidd PM. Phosphatidylcholine, a superior protectant against liver damage. Altern Med Rev 1996;1:258-274.

8.        Zeisel SH, Da Costa K, Franklin PD, et al. Choline, an essential nutrient for humans. FASEB 1991;5:2093-2098.

9.        Wurtman RJ , Hirsch MI, Growdon JH. Lecithin consumption raises serum free choline levels. Lancet 1977;ii: 68-69.

10.     Buchman AL, Dubin MD, Moukarzel AA, et al. Choline deficiency: a cause of hepatic steatosis during parenteral nutrition that can be reversed with intravenous choline supplementation. Hepatology 1995;22:1399-1403.

11.     Ghyczy M, Boros M. Electrophilic methyl groups present in the diet ameliorate pathological states induced by reductive and oxidative stress: a hypothesis. Brit J Nutr 2001;85:409-414.

12.     Thistle JL, Schoenfield LJ. Bile acid, lecithin, and cholesterol in repeated human duodenal biliary drainage: effect of lecithin feeding. Clin Res 1968;16:450.

13.     Toouli J, Jablonski P, Watts JM. Gallstone dissolution in man using cholic acid and lecithin. Lancet 1975;ii: 1124-1126.

14.     Lloyd J, Todd DA, John E. Serial phospholipid analysis in pre term infants: comparison of Exosurf and Survanta. Early Human Dev 1999;54:157-168.

15.     Dunjic BS, Axelson J. Gastroprotective capability of exogenous phosphatidylcholine in experimentally induced chronic gastric ulcers in rats. Scand J Gastroenterol 1993;28:89-94.

16.     Lieber CS, Leo MA. Polyenylphosphatidylcholine decreases alcohol-induced oxidative stress in the baboon. Alcoholism Clin Exp Res 1997;21:375-379.

17.     Knuchel F. Double blind study in patients with alcohol-toxic fatty liver. Med Welt 1979;30:411-416.

18.     Schuller-Perez A, San Martin FG. Controlled study using multiply-unsaturated phosphatidylcholine in comparison with placebo in the case of alcoholic liver steatosis. Med Welt 1985;72:517~521.

19.     Buchman AL, Dubin M, Jenden D, et al. Lecithin increases plasma free choline and decreases hepatic steatosis in long-term total parenteral nutrition patients. Gastroenterology 1992;102:1363-1370.

20.     Panos MZ, PoIson R, Johnson R, et al. Activity of polyunsaturated phosphatidylcholine in HBsAg negative (autoimmune) chronic active hepatitis and in acute alcoholic hepatitis. In: Gundermann KJ, SchQmacher R, eds. 50th Anniversary of Phosp*lipid Research (EPL). Bingin-Rhein, Germany: wbn- Verlag; 1990: 103-110.

21.     Lieber CS, Robins SJ, Li J, et al. Phosphatidylcholine protects against fibrosis and cirrhosis in the baboon. Gastroenterology 1994;106:152-159.

22.     Marpaung H, Tarigan P, Zein LH, et al. Tuberkulostatische kombinations therapie aus INH, RMP und EMH. Therapiewoche 1988;38:734- 740.

23.     Jenkins PJ, Portmann HP. Use of polyunsaturated phosphatidylcholine in HBsAg negative chronic active hepatitis: results of prospective double-blind controlled trial. Liver 1982;2:77- 81.

24.     Visco G. Polyunsaturated phosphatidylcholine (EPL) associated with vitamin H-complex in the treatment of acute viral hepatitis-H. La Clinica Terapeutica 1985;114:183-188.

25.     Ilic V, Hegic-Janev A. Therapy for HHsAg-positive chronically active hepatitis. MedWelt 1991;42:523-525.

26.     Niederau C, Strohmeyer G, Heintges T, et al. Polyunsaturated phosphatidylcholine and interferon alpha for treatment of chronic hepatitis H and C: a multicenter, double-blind, placebo-controlled trial. Hepatogastroenterol 1998;45:797-804.

27.     Schenker S. Polyunsaturated lecithin and alcoholic liver disease: a magic bullet? Alcoholism Clin Exp Res 1994;18:1286-1288.

28.    Halliday HL. Natural vs synthetic surfactants in neonatal respiratory distress syndrome. Drugs 1996;51 :226-;237.

29.     Leyck S, Dereu N, Etschenberg E, et al. Improvement of the gastric tolerance of non- steroidal anti-inflammatory drugs by polyene phosphatidylcholine (Phospholipon 100). Eur J PharmacoI1985;117:35-42.

30.     Swarm RA, Ashley SW, Soybel Dl, et al. Protective effect of exogenous phospholipid on aspirin-induced gastric mucosal injury. Am J Surg 1987;153:48-53.

31.     Carlson SE. Lower incidence of necrotizing enterocolitis in infants fed a preterm formula with egg phospholipids. Pediatr Res 1998;44:491-495.

32.     Kidd PM. Unpublished analysis. 1998; El Cerrito, California, USA: drkidd@aol.com.

33.     Little A, Levy R, Chuaqui-Kidd P, et al. A double-blind, placebo controlled trial of high- dose lecithin in Alzheimer's disease. J Neurol Neurosurg Psychiatr 1985;48:736-742.

34.     Esslinger F. Death cap mushroom poisoning: report of clinical experience. Med Welt 1966;19:1057-1063.

 

 

Appendix: Food Sources of Choline

Choline and Choline Phospholipid Content of Selected Foods, in Milligrams per Serving Free

 

Food                            Serving                         Choline             Lecithin            Total Choline

Apple                           1 medium                     0.39                 29.87               4.62

Banana                         medium                        2.85                 3.26                 3.52

Beef liver                      3.5 oz                           60.64               3362.55           532.28

Beef steak                    3.5 oz.                          0.78                 466.12             68.75

Butter                          1 tsp.                            0.02                 6.80                 1.18

Cauliflower                   1/2 cup                         6.79                 107.06             22.15

Corn oil                        1 tbsp.                          0.004               0.13                 0.03

Coffee                          6 oz.                             18.59               2.05                 19.29

Cucumber                    1/2 cup                         1.18                 3.06                 1.74

Egg                              1 large                          0.22                 2009.80           282.32

Ginger ale                     12 oz.                           0.07                 1.11                 0.34

Grape juice                   6 oz.                             8.99                 2.11                 9.37

Human milk                  1 cup                            2.10                 27.08               10.29

Iceberg lettuce 1 oz.     8.53                             2.86                 9.06

Infant formula   1 oz.     0.818                           2.97                 1.38

Lecithin supplement      1 tbsp., 7.5 g.               NA                  1725                250

(commercial, powdered)

Milk whole                   1 cup                            3.81                 27.91               9.64

Orange                         1oz.                              13.24               107.35             27.91

Potato                          1                                  5.95                 25.97               9.75

Tomato                        1v                                5.50                 4.94                 6.58

Whole wheat bread      1 slice                           2.52                 6.57                 3.43

                       

(USDA: Composition of Foods. USDA handbook # 8. Washington DC, ARS, USDA, 1976-1986)

 

 

A Healthy Approach In An Unhealthy World