Phosphatidylcholine (PC) is a phospholipid, one of a primal class of substances ubiquitous among life forms.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 enterohepatic 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.

 

Chemically, PC is a glycerophospholipid,³ built on glycerol (CH₂OH-CHOH-CH₂OH) and substituted at all three carbons. Carbons 1 and 2 are substituted by fatty acids and carbon 3 by phosphorylcholine. Simplistically, the PC molecule consists of a head-group (phosphoryl- choline), 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 CDPcholine. The second, minor pathway is hosphatidylethanola- mine (PE) methylation, in which the phospholipid PE has three methyl groups added to its ethanola- mine head-group, thereby converting it into PC.

 

 

 

 

磷脂酰胆碱（PC）是一种磷脂，而磷脂是一类在各种生命形式中广泛存在基本物质类型。在所有细胞膜和循环血脂蛋白的脂质成分中，PC是占大多数的一种磷脂。PC是天然表面活性物质中的主要功能成分，是机体胆碱的主要储存形式，是一种必需的营养物质。PC是胆汁中的一种成分，可以使食物中的脂肪得以乳化，进而被机体吸收和转运。而其中的PC通过肠肝循环得以循环利用。

 

直至最近，磷脂酰胆碱的命名还和卵磷脂相混淆。实质上，卵磷脂是一种磷脂和其它脂类的混合物质。卵磷脂的生成过程中PC被富集，在卵磷脂的各种成分中，按重量计算PC占30%或以上。

 

 

从化学角度上看，PC是一种甘油磷脂，在甘油骨架上构建而成，并在三个碳原子上都有取代基团。在1位和2位碳原子上的羟基被脂肪酸取代，3位碳原子上的羟基被磷酸胆碱取代。简单的说，PC分子包括一个头部（磷酸胆碱），一个中间体（甘油骨架），两个尾部（各种脂肪酸）。尾部脂肪酸的多样性决定了人体不同组织中PC分子的多样性。

 

在体内，PC主要通过两条途径产生。一条是占主导地位的途径，过程如下：两个脂肪酸（酰化，形成尾部）被结合到甘油磷酸盐上（中间部分），产生磷脂酸(phosphatidic acid, PA)，PA转化成为二酯酰甘油，二酯酰甘油与CDP-choline反应，得到磷酸胆碱（头部），产生PC。而数量较少的PC通过另一条途径产生，这是由磷脂酰乙醇胺（PE）甲基化实现的。在这条途径中，PE（一种磷脂）的乙醇胺头部与三个甲基基团结合，从而形成PC。

 

 

 

Taken orally, PC is very well absorbed, up to 90 percent per 24 hours when taken 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 1), 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 supplementation.¹⁰

 

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.¹¹ Methyl deficiency induced by restricted cholineintake 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.

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 interior.⁶

 

通过口服途径进入的PC能很好的得到吸收，食物所含PC中的90%能在24小时内被吸收。进食后，PC逐渐进入血液循环，峰值出现在进食后8-12小时。在消化过程中，大部分PC分子2位上的脂肪酸被分解出去（去酰基化），产生溶解性磷脂酰胆碱。后者很容易进入肠壁内层细胞，然后在2位上再重新酰化产生PC。PC分子2位上的脂肪酸与1位上脂肪酸一同使细胞膜具有流动性。但是它们更重要的作用是产生二十碳脂肪酸衍生物并参与信号转导。PC所含脂肪酸中omega-6和omega-3脂肪酸的比例平衡可以由饮食中脂肪酸的摄入来调整。

 

胆碱是人类的一种必需营养物质，而通过食物摄入的胆碱大部分是以PC的形式实现的。血液和组织中超过98%的胆碱是作为一种组成部分被包含在PC分子中，同时食物中的PC成为血液中胆碱来源的一种“缓释”形式。营养不良患者如果血液中胆碱含量较低，常常表现为肝脏的脂肪变性和与此相关的功能不全。而这些症状在给与补充PC后往往能够得到改善。

甲基集团(–CH3)最重要的功效，是参与蛋白质与核算的生物合成和调节，此外肝脏解毒的第二阶段以及其它许多生化过程中都有甲基供体参与。通过限制PC的摄取，造成甲基不足可以引起人类肝脏脂肪变性；对许多哺乳动物来说，增加了罹患癌症的危险。PC是甲基集团的良好来源，因为每个PC分子中包括三个甲基。

 

PC是细胞膜的主要支撑结构，许多生物进程依赖这一流动性的薄片状分子而得以发生。膜磷脂成分中40%是PC，而PC的存在对膜流动性的稳态调节来说是至关重要的。按需递送细胞膜最外层PC分子中的脂肪酸，作为前列腺素/二十碳脂肪酸细胞信使功能，将信号由细胞外转导致细胞内。

 

 

 

 

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 tract.^14,15

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 effects.¹

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.

 

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

PC是血液中脂蛋白颗粒的主要脂质组成。PC的两性分子特征使它成为胆汁中微团成分之所以产生的关键。PC的表面活性剂性质充分保护了肺和胃肠道上皮-管腔的表面。

 

 

从生物化学角度来说，PC是一些磷脂和其它重要的生物分子的良好前体。PC也是一种体内抗氧化剂，提供保护作用。在动物和人类的研究中证实，PC可以抵抗许多化学毒素和药物毒副作用。

 

 

有关PC临床应用的成功案例，资料最完善的是PC对肝损伤的改善作用。可能是由于肝脏损伤后康复需要膜物质成分的替换。从八个双盲试验和许许多多临床报道来看，PC显示出一致的显著临床效果。包括改善酶和其它生化功效、加速肝组织功能和结构的重建、促进被试全身症状的恢复以及改善未受累部分。

 

 

 

 

 

Knuechel进行了一次双盲试验，受试是40名由于饮酒造成的肝脂肪变性（脂肪肝）和肝炎患者。撤除受试的药物治疗，并随机分为两组，其中一组给予安慰剂，另一组每天给予口服1350毫克PC（由B族维生素强化）。两周后PC的效果开始显现，八周后各种生化指标检测显示，PC与安慰剂相比能显著改善肝功能。

 

 

随后的三个双盲试验证实了这些发现。Schuller Perez与San Martin得出结论“我们的观点是：使用高不饱和磷脂酰胆碱治疗酒精依赖的脂肪变性是非常有效的。”

 

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

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

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 placebo. 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 (1,350 mg 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

 

 

 

Buchman等人在15名脂肪肝患者上进行双盲试验，对患者通过静脉给予肠道外营养支持，也发现加入PC有明显优势。其他的一些研究者报道了轻度到中度肝脏炎症患者大多可以由PC补充而获益。

 

 

在一个动物实验中，狒狒每天被给予酒精，持续八年。之后的盲法试验中，在一些狒狒的饮食中加入PC。几年后，喂饲酒精而不添加PC的狒狒发展为肝纤维化，而喂饲酒精同时添加PC的狒狒，只发展为脂肪肝或有轻微纤维化而不再进展。3只狒狒被撤除PC并继续给予酒精后，它们迅速恶化成广泛的威胁生命的肝纤维化。

 

 

在一个双盲试验中，101名结核病患者由于服用利福平(rifampin)和其它两种抗结核药造成肝损伤，每天分别接受安慰剂或1350毫克强化PC治疗。三个月后，PC组SGOT和SGPT酶水平显著降低。

 

 

在一项双盲试验中，受试是30名乙型肝炎感染者（乙肝表面抗原阴性）伴有进行性肝损伤。患者在接受常规的免疫抑制治疗的同时，服用每天2300毫克PC或安慰剂。一年后，PC组临床症状稳定，肝结构明显好转，而同时安慰剂组的情况继续恶化。

 

 

60名乙肝患者（乙肝表面抗原阳性）被分为强化PC组（每天服用1350毫克）和安慰剂组，试验进行60天。30天后PC组的临床表现明显优于安慰剂组。PC组有50%的患者乙肝表面抗原转阴，而同时安慰剂组只有25%患者转阴。

 

 

 

 

 

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

 

 

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

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

 

 

 

 

 

一项在50名患者中进行的双盲试验，这些患者都是被组织活检和免疫学实验证实乙肝表面抗原阳性并有明显的严重的肝损伤的。试验中患者被分为PC组（每天服用1350毫克强化PC）和安慰剂组，结果显示PC相对与安慰剂有显著的临床疗效（P<0.001），PC组中有80%（25人中的20人）被评定为显效(greatly improved)，而安慰剂组中的24%（25人中的6人）被评定为有效(moderately improved)。细胞结构、生化、免疫学、血液指标PC组都明显优于安慰剂组，临床症状的改善在为期一年的试验结束后依然持续。

 

在一项多中心双盲试验中，176名慢性病毒性肝炎（乙型或丙型）在接受24周干扰素α治疗后，被随机分为PC组（每天给予1.8克）或安慰剂组，再持续24周。在PC组中有更多的患者获得疗效，尤其是丙型肝炎患者，以上差异有显著性。另外在对丙肝患者持续更长时间的试验中，继续给予PC支持24周，可以获得长期的临床效果。

另一项针对PC用于肝脏疾病的长期、多中心、双盲法试验正在进行中，这一试验的结果将对人们运用营养支持治疗这种危害人类生命的疾病产生突破性进展。

早产儿的肺泡表面活性物质中所含PC过低。治疗患有或可能有呼吸窘迫综合征（RDS）的患儿，常规的方法是运用外源性的具有成熟特性的表面活性物质（在总磷脂中PC占0-80%）。一项对临床试验的回顾性研究发现，对RDS患儿给予天然的表面活性物质，在生存率和全身症状等方面，要优于给予人工合成的表面获悉物质。在一项78名RDS患儿的随机试验中，给予天然的表面活性物质6小时后即有明显效果，而24小时后表面活性物质中的PC含量恢复正常。

 

 

 

 

 

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.15,29,30 Carlson et al reported a lower incidence of necrotizing enterocolitis in pre-term infants fed with formula high in PC and other phospholipids.³¹

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.

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.⁷ Symptoms of intolerance are almost exclusively restricted to GI discomfort –diarrhea, excessive fullness, and nausea.

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

 

 

 

作为胃肠道内生表面活性物质的主要成分，PC帮助胃粘膜上皮维持胃酸屏障。动物实验发现，PC可以在不阻断阿司匹林和其它非甾体类抗炎药物疗效的同时，防止它们对胃肠道的损伤。Carlson等报道说，对早产儿喂予高剂量的PC和其它磷脂，可以降低坏死性小肠结肠炎的发生率。

 

 

 

虽然有长期的传奇般的描述，但是在十个双盲法、安慰剂对照的试验中，PC并没有显示出疗效。有一些迹象显示PC的“治疗窗”可能非常狭窄，这也说明了对共济失调、迟缓型运动障碍和其它一些以胆碱能神经平衡失调为特征的中枢神经系统疾病，以PC为治疗措施的一些试验结果不佳的原因。

 

PC与其它营养物质有良好的兼容性，而且如果协同使用可以增强彼此的吸收。常规的毒理学试验没有发现PC有显著的长期或急性毒性，同时也没有发现PC具有致突变和致畸作用。每天给予18克PC时，仍显示有良好的耐受性。不能耐受PC的症状仅局限于一些胃肠道不适，如腹泻、腹胀和恶心。

 

 

PC的治疗剂量在800-2400毫克/每天，如针对肝脏疾病的抢救治疗可用到4.6克或更高。对于严重的肝损伤患者治疗的初期，联合运用静脉注射和口服给药，可以获得更佳疗效，在起效后可口服维持。对于一种名为“死亡之冒”（deathcap）的毒蘑菇中毒造成肝脏损伤的患者，运用上述方法可以抢救患者的生命。

 

 

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 O, 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 MJ, 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 preterm 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, Polson R, Johnson R, et al. Activity of polyunsaturated phosphatidylcholine in HBsAg negative (autoimmune) chronic active hepatitis and in acute alcoholic hepatitis. In: Gundermann KJ, Schumacher R, eds. 50^th Anniversary of Phospholipid 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 B, Tarigan P, Zein LH, et al. Tuberkulostatische kombinations therapie aus

INH, RMP und EMB. Therapiewoche 1988;38:734-740.

23. Jenkins PJ, Portmann BP. Use of polyunsaturated phosphatidyl choline 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 B-complex in the treatment of acute viral hepatitis-B. La Clinica Terapeutica 1985;114:183-188.

25. Ilic V, Begic-Janev A. Therapy for HbsAgpositive chronically active hepatitis. Med Welt 1991;42:523-525.

26. Niederau C, Strohmeyer G, Heintges T, et al. Polyunsaturated phosphatidylcholine and interferon alpha for treatment of chronic hepatitis B 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 nonsteroidal anti-inflammatory drugs by polyene phosphatidylcholine (Phospholipon 100). Eur J Pharmacol 1985;117:35-42.

30. Swarm RA, Ashley SW, Soybel DI, 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 highdose 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.