Herbal Medicine: Expanded Commission E
Soy Phospholipid
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Latin Name: Glycine max
Pharmacopeial Name: ojae Lecithinum
Other Names: lecithin enriched extract from soybean
Overview
The Commission E has published two positive monographs (in 1988 and in 1994) on soy lecithin, which consists of soybean phospholipids, and soy phospholipid containing 7379% (3-sn-phosphatidyl)choline. The monographs differ in that the former refers to phospholipids extracted from soybeans, while the latter pertains to preparations consisting of a specific concentration of those phospholipids: 7379%. Generally, lecithin removed from soybeans contains about 76% phosphatidylcholine (Schulz et al., 1998). Phospholipids contain mostly linoleic acid (LA), a fatty acid essential to cell membrane formation. Linoleic acid is obtained primarily from food; a small amount is synthesized in the liver. When liver function is compromised, linoleic acid is deficient. Dietary supplementation with soy phospholipids may help patients with liver disease, alcoholism, or chronic parenteral nutrition reduce their risk of LA deficiency. Soy phospholipid 7379% (3-sn-phosphatydyl)choline products, in addition, are reported to reduce symptoms of liver disease, chronic hepatitis, or liver dysfunction due to malnutrition, such as loss of appetite and abdominal pain (Schulz et al., 1998). Soy may also lower blood lipids. Soy is recommended for hypercholesteremia in patients whose cholesterol levels do not respond to exercise or weight loss regimens. A recent meta-analysis of 38 studies noted that when dietary meat protein was supplanted with vegetable protein, risks for coronary artery disease were reduced (Anderson et al., 1995). The soy-based diets reduced serum levels of total cholesterol, LDL cholesterol, and triglyceride, without affecting HDL cholesterol (Manson et al., 1992; Anderson et al., 1995). The full extent of soy phospholipid effects has not been determined. Published studies suggest that phospholipids may be useful in the treatment of menopause and post-menopausal conditions, cancer, hypertension, aging, and benign prostatic hyperplasia (Holt, 1996). Soy cultivation is believed to have begun in China; the emperor Shen-nong, who compiled the Medical Bible of the Yellow Emperor (Huang-di nei jing) sometime between 2967 and 2597 B.C.E., counted soybean among the five sacred crops. Since then, both ancient Chinese and contemporary Chinese medical literature have claimed health benefits from soy. During the Ming Dynasty (13681644 B.C.E.), in his 52-volume Chinese Materia Medica, Li-Shi Zhen recommended soybeans for the treatment of kidney disease, edema, and poisoning. Today soy may be recommended for skin diseases, gastrointestinal disorders, leg ulcer, vitamin deficiency, and pregnancy toxemia (Holt, 1996).
Description
Lecithinum ex soja, lecithin from soybean, extracted from Glycine max (L.) Merrill [Fam. Fabaceae], enriched extract with 7379% (3-sn-phosphatidyl)choline. The extract also includes phosphatidylethanolamine (maximum 7%), phosphatidylinositic acid (less than 0.5%), oil (26%), and vitamin E (0.20.5%). The range includes both production and analytical variances.
Chemistry and Pharmacology
Lecithin extract from soybeans consists of 76% (average) phosphatidylcholine and phosphoglycerides, of which the fatty acid linoleic acid predominates. The quota of phospholipids, the chief constituents of cell membrane, is in major part obtained by eating (0.53 g per day from food) and in lesser degree from synthesis by the liver. A deficiency in phospholipids is the inevitable result of chronic parenteric nutrition. Under pharmacodynamic characteristics are 'hepatoprotective' effects in numerous experimental models, e.g., protection against ethanol, alkyl alcohols, tetrachlorides, paracetamol, and galactosamine. Furthermore, in chronic models (ethanol, thioacetamide, organic solvents), there appears to be a defense against steatosis and fibrosis of the liver. The compound works by speeding regeneration and stabilization of membranes, stopping lipid peroxidation presumably by collagen synthesis. The pharmacokinetics of orally administered lecithin have been examined in animal studies in which the phosphatidylcholine was radioactively marked, the marking on a fatty acid in position 1 or position 2, choline, or a phosphorus. The respective marker substitutions show the pharmacokinetics. Phospholipids are degraded to lyso-phosphatidylcholine in the intestine and absorbed primarily in this form. In the gut wall phospholipids are in part resynthesized, then circulated through the lymphatic system. In part, the resynthesized phosphatidylcholine is processed in the liver to form fatty acids, choline, and glycerine-3-phosphate. In plasma, phosphatidylcholine and other phosphoglycerides are tightly bound to lipoproteins or albumin, or to both. Phosphatidylcholine and other phosphoglycerides are degraded chiefly through a series of so-called phospholipases to fatty acids, choline and 'glycerin' metabolites to be in turn resynthesized in the liver and other organs. The administered metabolites integrate within a few hours into body phospholipids. Their removal corresponds to the excretion of phospholipids and their corresponding metabolites. Commission E noted the following results from toxicological studies: doses of phosphatidylcholine of up to 10 g/kg body weight in mice and rats and 4.5 g/kg body weight in rabbits given intravenously, intraperitoneally, and orally in a single dose are not toxic. The 'no-effect' dosage over 48 weeks administration to rats lies upward of 3,750 mg/kg body weight per day. Repeated intravenous application over 12 weeks places the lowest systemic toxic dosage between 0.1 and 1 g/kg body weight and lowest local toxic dosage at over 1 g/kg body weight in rats, and application over four weeks to dogs places the lowest toxic dosage at more than 0.1 g/kg body weight in dogs. Doses of up to 3,750 mg/kg body weight in pregnant animals, animal embryos, and animal neonates showed no pathology of toxicity to reproduction. The lowest teratogenic or embryo-toxic dosage in rats in oral and intravenous administration was more than 1 g/kg body weight. In rabbits teratogenic dosages were greater than 1 g/kg body weight for oral administration and greater than 0.5 g/kg body weight in intravenous administration. Various in vitro tests cannot demonstrate any mutagenic potential. Carcinogenicity has not been tested.
Uses
The Commission E approved the internal use of soy phospholipid for less severe forms of hypercholesterolemia in which diet and other non-medical interventions (e.g., exercise, weight control) have not shown results; improvement of subjective complaints, such as loss of appetite and feeling of pressure in the region of liver in toxic nutritional liver disease and chronic hepatitis; prerequisite to the therapy of chronic liver disease is the recognition and avoidance of noxious agentsin the case of alcoholic liver disease, alcohol abstinence. In chronic hepatitis adjuvant therapy with phospholipids of soybeans is only indicated when improvement of symptoms is discernible from other therapy.
Contraindications
None known.
Side Effects
Occasional gastrointestinal effects, i.e., stomach pain, loose stool, and diarrhea.
Use During Pregnancy and Lactation
No restrictions known.
Interactions with Other Drugs
None known.
Dosage and Administration
Unless otherwise prescribed: Daily dosage: 1.5-2.7 g phospholipids from soybean with 73-79% (3-sn-phosphatidyl)choline in a single dose. Duration of treatment: Medication containing arbutin should not be taken for longer than a week or more than five times a year without consulting a physician.
References
Anderson, J.W., B.M. Johnstone, M.E. Cook-Newell. 1995. Meta-analysis of the effects of soy protein intake on serum lipids. N Engl J Med 333(5):276282. Holt, S. 1996. Soya for Health: The Definitive Medical Guide. New York: Mary Ann Liebert, Inc. Manson, J.E. et al. 1992. The primary prevention of myocardial infarction. N Engl J Med 326(21):14061416. Schulz, V., R. Hnsel, V.E. Tyler. 1998. Rational Phytotherapy: A Physicians' Guide to Herbal Medicine. New York: Springer.
Additional Resources
Emmert, J.L., T.A. Garrow, D.H. Baker. 1996. Development of an experimental diet for determining bioavailable choline concentration and its application in studies with soybean lecithin. J Anim Sci 74(11):27382744. Guarini, P. et al. 1998. Effects of dietary fish oil and soy phosphatidylcholine on neutrophil fatty acid composition, superoxide release, and adhesion. Inflammation 22(4):381391. Hnsel, R., K. Keller, H. Rimpler, G. Schneider (eds.). 19921994. Hagers Handbuch der Pharmazeutischen Praxis, 5th ed. Vol. 46. Berlin-Heidelberg: Springer Verlag. Jannace, P.W., R.H. Lerman, J.I. Santos, J.J. Vitale. 1992. Effects of oral soy phosphatidylcholine on phagocytosis, arachidonate concentrations, and killing by human polymorphonuclear leukocytes. Am J Clin Nutr 56(3):599603. Oosthuizen W. et al. 1998. Lecithin has no effect on serum lipoprotein, plasma fibrinogen and macro molecular protein complex levels in hyperlipidaemic men in a double-blind controlled study. Eur J Clin Nutr 52(6):419424. Renaud, C., C. Cardiet, C. Dupont. 1996. Allergy to soy lecithin in a child. J Pediatr Gastroenterol Nutr 22(3):328329. Sirtori, C.R. et al. 1985. Cholesterol-lowering and HDL-raising properties of lecithinated soy proteins in type II hyperlipidemic patients. Ann Nutr Metab 29(6):348357. Steinegger, E. and R. Hnsel. 1992. Pharmakognosie, 5th ed. Heidelberg: Springer Verlag. Teuscher, E. 1997. Biogene Arzneimittel, 5th ed. Stuttgart: Wissenschaftliche Verlagsgesellschaft. Tompkins, R.K. and L.G. Parkin. 1980. Effects of long-term ingestion of soya phospholipids on serum lipids in humans. Am J Surg 140(3):360364. Wilson, T.A., C.M. Meservey, R.J. Nicolosi. 1998. Soy lecithin reduces plasma lipoprotein cholesterol and early atherogenesis in hypercholesterolemic monkeys and hamsters: beyond linoleate. Atherosclerosis 140(1):147153. This material was adapted from The Complete German Commission E MonographsTherapeutic Guide to Herbal Medicines. M. Blumenthal, W.R. Busse, A. Goldberg, J. Gruenwald, T. Hall, C.W. Riggins, R.S. Rister (eds.) S. Klein and R.S. Rister (trans.). 1998. Austin: American Botanical Council; Boston: Integrative Medicine Communications.
1) The Overview section is new information. 2) Description, Chemistry and Pharmacology, Uses, Contraindications, Side Effects, Interactions with Other Drugs, and Dosage sections have been drawn from the original work. Additional information has been added in some or all of these sections, as noted with references. 3) The dosage for equivalent preparations (tea infusion, fluidextract, and tincture) have been provided based on the following example: - Unless otherwise prescribed: 2 g per day of [powdered, crushed, cut or whole] [plant part]
- Infusion: 2 g in 150 ml of water
- Fluidextract 1:1 (g/ml): 2 ml
- Tincture 1:5 (g/ml): 10 ml
4) The References and Additional Resources sections are new sections. Additional Resources are not cited in the monograph but are included for research purposes. This monograph, published by the Commission E in 1994, was modified based on new scientific research. It contains more extensive pharmacological and therapeutic information taken directly from the Commission E.
Excerpt from Herbal Medicine: Expanded Commission E Monographs
Copyright 2000 American Botanical Council
Published by Integrative Medicine Communications
Available from the American Botanical Council.
This monograph, published by the Commission E in 1994, was modified based on new scientific research. It contains more extensive pharmacological and therapeutic information taken directly from the Commission E.
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