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Common Name(s): Granulestin, Kelecin, Lecithin, Lecithol, Phosphatidylcholine, Vitellin

Medically reviewed by Last updated on Jan 23, 2023.

Clinical Overview


Lecithin is used for its emulsifying properties in the food, pharmaceutical, and cosmetic industries. Clinical data are available from 2 studies (N=216) that support use in patients with active ulcerative colitis; however, robust study data are lacking to support use for any other condition.


Delayed-release phosphatidylcholine 3.2 to 6 g/day for 3 months has been used in studies of patients with active ulcerative colitis.


Contraindications have not been identified.


Information regarding safety and efficacy in pregnancy and lactation is lacking.


None well documented.

Adverse Reactions

Adverse effects are usually not associated with lecithin. However, there have been reports of anorexia, nausea, sweating, increased salivation, other GI effects, and hepatitis.


Information regarding toxicity with the use of lecithin is limited.


Lecithin is found in many animal and vegetable sources, including beef liver, steak, eggs, peanuts, cauliflower, and oranges.(Murray 1996) Commercial lecithin products may be derived from plant sources (eg, soybeans, sunflower seeds) and animal sources (eg, egg yolk, bovine brain).(Budavari 1989, Crebelli 2017, Venturella 1995) Some commercial lecithin and lecithin supplements contain between 10% and 35% phosphatidylcholine.(Murray 1996)


The word lecithin originated from the Greek lekithos, referring to egg yolk.(Murray 1996, Reynolds 1996) Lecithin was discovered in 1805 by the French scientist Maurice Gobley(Potter 2009) and has been proposed for use in treating liver ailments, hypercholesterolemia, and neurologic diseases,(Murray 1996, Reynolds 1996) as well as in the food processing industry.(Budavari 1989, Crebelli 2017) Lecithin is required for proper biological function and is a common compound found in cells of all living organisms.(Saba 1978)


Lecithin is a phospholipid mixture of acetone-insoluble phosphatides consisting mainly of phosphatidylcholine, phosphatidyl ethanolamine, phosphatidyl serine, and phosphatidyl inositol combined with various other substances, including fatty acids and carbohydrates.(Reynolds 1996) Phosphatidylcholines are the main compounds of lecithin; chemically lecithin is a mixture of diglycerides of fatty acids linked to the choline ester of phosphoric acid (ie, soybean lecithin contains 4% stearic, 18.4% palmitic, and 10.7% oleic acids, among others). Lecithin also contains phosphorous and nitrogenous (eg, choline) compounds.(Crebelli 2017) Lecithin is also known as 1,2-diacyl-sn-glycero-3-phosphocholine.

Physical properties of lecithin can vary depending on acid value. Lecithin is a waxy mass at acid value 20 and a thick pourable fluid at acid value 30. It is white when freshly made but turns yellow to brown when exposed to air. It is an edible and digestible surfactant and emulsifier.(Budavari 1989)

Uses and Pharmacology

Lecithin is used as an emulsifying and stabilizing agent in the food (eg, margarine, chocolate production), pharmaceutical, and cosmetic (eg, creams, lipsticks, conditioners) industries.(Budavari 1989, Crebelli 2017, Reynolds 1996) Lecithin has also been used in development of nanoemulsions and nanoparticles to improve drug delivery to targets; this method has been studied alone and in combination with ultrasound.(Dong 2020, Prasad 2020)

Athletic performance

Clinical data

A study in triathletes and adolescent runners found that lecithin supplementation could help prevent the reduction in plasma choline levels that occurs under physical stress, suggesting a possible impact on athletic performance.(von Allworden 1993)

CNS disorders

Variable results have been reported regarding use of lecithin supplementation for treatment of neurologic disorders. Evidence-based Canadian guidelines for pharmacotherapy of tic disorders (2012) determined that there was insufficient evidence to make a formal recommendation regarding lecithin for the treatment of tics. Although limited studies are available, it was determined that further research is unwarranted per group consensus.(Pringsheim 2012)

Bipolar disorder

Clinical data

In a small study of patients with bipolar disorder, lecithin 10 mg 3 times daily decreased hallucinations and delusions, and improved incoherent speech, as noted by changes in Brief Psychiatric Rating Scale and Global Assessment Scale scores.(Cohen 1982)

Memory disorders

Lecithin is a good source of choline, and may be beneficial in treatment of dementias.(Reynolds 1996) Phosphatidylcholine is thought to be a precursor of choline for acetylcholine (ACh) synthesis.(Blusztajn 1987) Choline increases the accumulation of ACh within the brain. ACh is important for many brain functions, including memory; therefore, increasing the concentration of this neurotransmitter can result in improved memory.(Murray 1996)

Clinical data

A report showed no improvement with lecithin in memory disorders when taken in 30 mg/day dosages.(Caine 1980) Lecithin supplementation has been studied in Alzheimer disease to improve memory difficulties. In a long-term, double-blind, placebo-controlled trial of high-dose lecithin in senile dementia of the Alzheimer type, 51 subjects were given 20 to 25 g/day of purified soya lecithin (containing 90% phosphatidyl plus lysophosphatidyl choline) for 6 months and followed for at least another 6 months. Plasma choline levels were monitored throughout the treatment period. There were no differences between the placebo group and the lecithin group but there was an improvement in a subgroup of relatively poor compliers who were older and had intermediate levels of plasma choline. It is suggested that the effects of lecithin are complex but that there may be a "therapeutic window" for the effects of lecithin in Alzheimer disease and that this may be more evident in older patients.(Little 1985) Combination tacrine and lecithin therapy administered in a 32-patient, double-blind trial yielded poor results.(Maltby 1994) In a multicenter study, this combination did not improve mental status in 67 Alzheimer patients.(Chatellier 1990) Evidence from a 2003 meta-analysis does not support the use of lecithin for dementias.(Higgins 2003)

Movement disorders

ACh deficiencies are associated with other neurological disorders, including tardive dyskinesia, Huntington chorea, Friedreich ataxia, myasthenia gravis, and other brain atrophies.

Clinical data

In 2 patients with tardive dyskinesia, lecithin administration reduced abnormal movements. Ten cases of Friedreich ataxia were also improved with lecithin supplementation.(Barbeau 1978) One study failed to show any beneficial response in 12 patients with Friedreich ataxia who were taking lecithin 25 g daily.(Pentland 1981)

In a Cochrane review and meta-analysis of placebo-controlled studies of patients with schizophrenia or other chronic mental illness (4 studies consisting of a lecithin subgroup; n=115), effects of newer and older cholinergic drugs (including lecithin) were no different than placebo in the management of antipsychotic-induced tardive dyskinesia. The study populations ranged from 6 to 50 participants, with treatment groups receiving lecithin 50 to 60 g/day (20 to 35 g/day of phosphatidylcholine) for a duration of 11 days to 8 weeks.(Tammenmaa-Aho 2018)

Contact lenses

Clinical data

A double-blind, randomized, crossover trial in 40 soft contact lens wearers evaluated effects of ocular lipid-based supplements on ocular comfort. Phosphatidylcholine liposomal eye spray and phosphatidylglycerol emulsion eye drops were compared with saline-based placebo spray and drops. After 2 weeks of intervention and placebo, no correlation was found between ocular comfort and lipid layer patterns, but a weak significant correlation between ocular comfort and tear evaporation rate and noninvasive surface drying time was observed. The latter was demonstrated with lipid drops and placebo, specifically in asymptomatic participants. Visual disturbance, including temporary blurred vision, was reported in approximately 40% of participants during lipid drop use.(Rohit 2017)


Clinical data

During a 19-year follow-up, higher dietary intake of phosphatidylcholine was associated with a 41% lower relative risk of development of type 2 diabetes in men, compared to the lowest intake quartile.(Virtanen 2020)

Gallstone treatment

Due to the high concentration of phospholipids, lecithin may decrease the lithogenicity of bile through increases in phospholipid concentrations.(Gaby 2009)

Clinical data

In 2 of 7 patients with radiolucent stones of the gallbladder or biliary tree, gallstone dissolution occurred with lecithin and oral cholic acid treatment for 6 months. One patient experienced a reduction in stone size.(Toouli 1975)

GI conditions

Phosphatidylcholine exhibits anti-inflammatory and antioxidant properties. It is considered an essential protective component of colonic mucus that increases the intestinal hydrophobic barrier function, which is reduced in ulcerative colitis patients. Such a loss in intestinal integrity can facilitate inflammation and ulceration.(Karner 2014)


Clinical data

In a case series of adults (mean age, 80 years) hospitalized for percutaneous endoscopic gastrostomy (N=13), egg yolk lecithin was used as an emulsifier in an enteral nutrition formula to offset the complication of diarrhea commonly associated with enteral nutrition therapy. Lecithin enteral formula was administered 3 times daily. After a mean observation period of 5.5 days, no diarrhea or vomiting occurred, and enteral nutrition could be continued in all cases. An increase in nonwatery stools was documented following a dose increase in 1 patient from 200 to 300 mL/hour, but resolved when the dose was reduced to 200 mL/hour.(Akashi 2018)

Ulcerative colitis

Clinical data

A double-blind, randomized, placebo-controlled trial in 156 patients refractory to mesalazine (ie, mesalamine in the United States) with moderately active ulcerative colitis (bloody diarrhea for at least 6 weeks despite treatment with mesalazine 3 g/day or more) demonstrated significantly improved disease activity scores with the use of a delayed-release formulation of phosphatidylcholine (more than 94% soy lecithin). Disease activity was assessed using the Simple Clinical Colitis Activity Index (SCCAI) (score of 0 to 19, with the low end indicating less disease activity), which assesses stool frequency (day and night), defecation urgency, blood in the stool, general wellbeing, abdominal pain, and extra-intestinal manifestations. Phosphatidylcholine was dosed at 0.8, 1.6, and 3.2 g/day for 12 weeks. High-dose phosphatidylcholine (3.2 g/day) reduced baseline disease activity scores by 51.7% compared to 33.3% for placebo (P=0.03) and also increased rates of clinical response (defined as SCCAI reduction of at least 2 points) significantly (83% and 60%, respectively; P=0.03). Overall, patients treated with phosphatidylcholine experienced complete symptom resolution almost twice as often and approximately 2 weeks sooner than those treated with placebo. The numbers needed to treat to reach clinical response and for complete remission (mean SCCAI score less than 3 with no blood in the stool) with phosphatidylcholine were 4.3 and 6.1, respectively. After treatment discontinuation, responders from all arms were followed for 8 weeks. Relapse-free periods occurred in a higher percentage of patients and for longer periods of time in those who had been treated with phosphatidylcholine compared to those treated with placebo (P=0.02). No treatment-related adverse events were observed among the groups.(Karner 2014) These results build upon earlier studies, including a phase 2, double-blind, randomized, placebo-controlled study (N=60) conducted in adults with long-term, steroid- and immunosuppressant-independent active ulcerative colitis. Compared to placebo, administration of a delayed-release phosphatidylcholine-rich phospholipid mixture 1.5 g given 4 times daily for 3 months was significantly better regarding rate of clinical remission (clinical activity index [CAI] less than 3) (53% vs 10% of placebo patients; P=0.00063), CAI improvement of at least 50% (3 of 30 phosphatidylcholine patients vs 27 of 30 placebo patients; P<0.0001), and magnitude of CAI change over the study period (−7 [P<0.0001] vs +2 [P<0.139], respectively). Endoscopic and histologic measures supported these findings.(Stremmel 2005)

Hearing impairment

Animal and in vitro data

Experimental and animal studies suggest that lecithin supplementation may improve hearing and lessen age-related hearing impairment via antioxidant effects that protect cochlear mitochondria and the auditory nerve.(Tang 2019)


Lecithin may reduce cholesterol levels and control or prevent atherosclerosis. However, studies conducted in the late 1970s to early 1980s provide insufficient clinical or epidemiologic evidence to definitively support a positive effect in atherosclerosis.

Clinical data

Four months of soybean lecithin administration reduced total serum lipids, cholesterol, and triglycerides in 21 hyperlipidemic patients.(Saba 1978) The mechanism appeared to be enhanced cholesterol metabolism in the digestive system.

Immunomodulatory effects

Clinical data

Lecithin has been used for immune modulation, activating specific and nonspecific defense systems in 20 patients receiving 1 tsp 3 times daily for 30 days.(Pawlik 1996)


Clinical data

Case reports of breastfeeding women and anecdotal evidence from practicing lactation consultants have documented the benefit of lecithin supplements for managing nipple bleb/blisters in some women.(McGuire 2015)

Liver disease

In Germany, phosphatidylcholine (Essentiale) is marketed for liver disorders, including acute and chronic hepatitis, cirrhosis, diabetic fatty liver, and toxic liver damage. Documentation supporting these claims has been authorized by the British-German Association, the German equivalent of the US Food and Drug and Administration.

Animal data

One report described supplementation with phosphatidylcholine and protection against alcoholic cirrhosis in baboons.(Murray 1996) Another study in rats suggests that lecithin may counteract changes in body weight and biochemical parameters caused by alcohol. Specifically, enzyme markers such as glutathione reductase and glutathione peroxidase levels were improved with lecithin.(Das 2006) Lecithin plus vitamin B complex reduced AST, ALT, interleukin 10, interferon gamma, and thiobarbituric acid reactive substance level in mice with long-term alcohol ingestion. The combination was also effective in increasing superoxide dismutase activity and glutathione levels.(Das 2007)

In a study of mice with mutations in the multidrug resistance 3 gene ABCB4, lecithin decreased liver damage caused by dietary supplementation with cholic acid, which accelerates development of hepatic lesions. Bilirubin and gamma-glutamyltransferase (GGT) levels were higher in mice receiving a cholic acid–supplemented diet. Lecithin in combination with a cholic acid–supplemented diet yielded bilirubin and GGT levels similar to mice receiving lecithin only. Results suggest a potential role in patients with mutations in the ABCB4 gene, which are thought to underlie progressive familial intrahepatic cholestasis type 3, a severe pediatric liver disease progressing to cirrhosis.(Lamireau 2007)

In freshly isolated rat hepatocytes exposed to D-galactosamine and in rats administered D-galactosamine to induce hepatotoxicity, lecithin administration was found to exert hepatoprotective effects similar to those noted with silymarin.(Raj 2010)


Clinical data

An 8-week, double-blind, randomized, placebo-controlled study in 96 middle-aged Japanese women with fatigue investigated the effects of high-dose (1,200 mg/day) and low-dose (600 mg/day) soy lecithin compared to placebo. The women were 40 to 59 years of age and the majority were either naturally postmenopausal (45.7%) or premenopausal (35.7%). Various parameters were evaluated (eg, age, menopausal status, lifestyle factors, physical and psychological symptoms of menopause, subjective symptoms of insomnia and fatigue, cardiovascular parameters, body composition, physical activities and objective sleep states before and at 4 and 8 weeks after treatment). Limited information was reported by the authors for outcomes, and no mention was made regarding adjustments to results for the significantly higher weight, body mass index (BMI), and body fat mass at baseline in the high-dose group. There was no significant difference among groups for fatigue based on one of the scales used, the scores for which improved significantly in all 3 groups. Results were provided for only 1 of the 6 major mood domains on the Profile of Mood States-brief scale: Vigor scores improved significantly in the high-dose group compared to placebo (mean, 1.9 vs 0.2, respectively; P=0.02). Additionally, mean diastolic blood pressure and cardioankle vascular index improved in the high-dose group compared with placebo (P=0.05 and P=0.03, respectively). No adverse events were reported.(Hirose 2018)

Muscle atrophy

Clinical data

Lecithin provided no protective effect against atrophic muscle changes during a short-term arm immobilization study in healthy young adults.(Bostock 2017a, Bostock 2017b) Soya lecithin 2,400 mg/day was administered as placebo in a 2-week double-blind, randomized, controlled trial (N=24) investigating the effects of omega-3 fatty acids (eicosapentaenoic acid 1,770 mg/day, docosahexaenoic acid 390 mg/day) and vitamin D3 (1,000 units/day) on muscle composition after short-term arm immobilization. The lecithin and vitamin D3 groups experienced significantly greater subcutaneous adipose thickness in the biceps than the omega-3 group (P<0.05 for both); however, no significant differences were observed in bicep or tricep muscle thickness. Although a significant decrease in bone mineral content and arm girth was observed in the lecithin group compared with baseline, the differences among groups for body composition (ie, fat mass, fat percentage, bone mineral density, bone mineral content) and arm girth were not significant among the 3 groups.(Bostock 2017a) Similarly, no significant differences were observed among lecithin, vitamin D3, or omega-3 fatty acids on bicep or tricep muscle function (ie, isometric or isokinetic torque, cocontraction, fatigue contractions) or arterial resting blood flow.(Bostock 2017b)


Ulcerative colitis: Delayed-release phosphatidylcholine 3.2 to 6 g/day for 3 months has been studied in clinical trials.(Karner 2014, Stremmel 2005)

Pregnancy / Lactation

Information regarding safety and efficacy in pregnancy and lactation is lacking.

One report in rats showed biochemical alterations and impaired sensorimotor development in offspring of rats exposed to a 2% or 5% soy lecithin preparation, suggesting lecithin consumption is inadvisable during pregnancy.(Bell 1985)


None well documented.

Adverse Reactions

Adverse reactions generally have not been associated with lecithin nutritional supplementation,(Bell 1985) with some studies reporting no observable adverse reactions.(Barbeau 1978, Budavari 1989, Saba 1978) Large intakes of lecithin (ie, more than 25 g/day) may cause short-term GI distress, sweating, increased salivation, or anorexia(Potter 2009); higher long-term consumption has been associated with an increase in all-cause or cardiovascular disease (CVD) mortality, particularly in diabetic patients.(Zheng 2016) GI adverse effects and hepatitis were reported in a study in Alzheimer patients taking both tacrine and lecithin.(Chatellier 1990)

Allergy to soy and egg lecithin has been documented in children and adults via positive prick tests and oral provocation tests conducted subsequent to reactions to pharmaceuticals (ie, propofol, intralipid parenteral nutrition, benzathine benzylpenicillin). Residual immunoglobulin E–binding activity has been observed with soy lecithin, which is often likely due to soy or egg proteins that contaminate the lecithin.(Barni 2015, Richard 2016)


One report in rats showed biochemical alterations and impaired sensorimotor development in offspring of rats exposed to a 2% or 5% soy lecithin preparation, suggesting lecithin consumption is inadvisable during pregnancy.(Bell 1985)

The potential association between dietary intake of phosphatidylcholine and all-cause or CVD mortality was assessed in an analysis of data collected over 25 to 35 years from more than 120,000 participants from the Nurses' Health Study and the Health Professionals Follow-up Study. Overall, higher dietary intake of phosphatidylcholine was correlated with increased all-cause and CVD mortality risk, a finding confirmed during all multivariate adjustments (eg, age, major foods, nutrients, smoking, menopausal status) except for diabetes status, which was the primary variable that modified the risk of all-cause and CVD-related mortality. Diabetic and nondiabetic participants in the top quintile of phosphatidylcholine intake experienced a 67% and 19% increase, respectively, in CVD-related mortality risk, whereas rates for all-cause mortality were increased 24% and 9%, respectively. CVD-related mortality risk increased by a mean of 13% for each increase of 100 mg/day in dietary phosphatidylcholine intake.(Zheng 2016)



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