Eggs for Choline & Brain Function

Table of Contents

1. What Is Choline and Why Eggs?
2. The Three Biochemical Roles of Choline
3. Fetal Brain Development
4. The Caudill 930 mg Trial
5. Neural Tube Defects and Choline
6. Adult Cognition and the Framingham Data
7. Choline Deficiency and Non-Alcoholic Fatty Liver
8. Practical Dosing — How Many Eggs?
9. If You Don't Eat Eggs: Alternative Sources
10. Cautions (Trimethylamine N-Oxide, Genetic Variants, Upper Limit)
11. Key Research Papers
12. Connections
13. Featured Videos

What Is Choline and Why Eggs?

Choline is a quaternary ammonium compound — a small water-soluble molecule that the body uses to build cell membranes (as phosphatidylcholine), to synthesize the neurotransmitter acetylcholine, and to donate methyl groups (via betaine) in the one-carbon metabolism cycle that handles DNA methylation and homocysteine recycling. The liver can synthesize a small amount of choline de novo by methylating phosphatidylethanolamine using S-adenosylmethionine, but this endogenous synthesis covers nowhere near the body's total requirement — choline must come from food.

For most of human evolutionary history, choline was abundant in the diet because organ meats, egg yolks, and animal fat were daily staples. The 20th-century shift away from these foods (driven first by the lipid hypothesis and then by industrial food economics) coincided with a measurable population-level drop in choline intake. The 1998 Institute of Medicine panel set the infant adequate intake from the choline content of human breast milk, the adult figure from the dose that prevented a liver-enzyme (alanine aminotransferase) abnormality in a single volunteer feeding study of healthy men (Zeisel et al., 1991), and the pregnancy figure by adding the amount needed for the fetus and placenta. The panel itself called the adult estimate uncertain because it was based on a single published study. Steven Zeisel was a member of that panel, which was chaired by Roy M. Pitkin; a later feeding study from his group (Fischer et al., 2007) found that an intake at the Adequate Intake did not prevent organ dysfunction in 19 of its 57 participants.

Eggs are uniquely effective at delivering choline because:

1. The yolk is concentrated. One large egg yolk (~17 g) contains roughly 139 mg of choline, and a whole large egg about 147 mg (USDA FoodData Central). Beef liver is denser (~420 mg per 100 g serving) but most Americans never eat liver. Eggs are eaten by nearly everyone.
2. The form is phosphatidylcholine, not free choline. Roughly 80% of egg-yolk choline is bound into phosphatidylcholine, the same form used by the body's own cell membranes. Phosphatidylcholine is absorbed more efficiently than free choline chloride or choline bitartrate (the typical supplement forms), but it is not exempt from the gut-microbiome conversion that produces trimethylamine (TMA), the precursor of the controversial cardiovascular biomarker trimethylamine N-oxide (TMAO): Wang et al. (2011) linked gut-flora metabolism of dietary phosphatidylcholine to TMAO production.
3. The cost is trivial. At ~30 US cents per egg, two eggs per day delivers ~300 mg of choline for ~60 cents. Equivalent choline from a supplement costs roughly the same per dose but lacks the additional protein, vitamins, lutein, and zeaxanthin you get from the whole food.

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The Three Biochemical Roles of Choline

Choline functions in three distinct biochemical roles, and each maps to a different category of clinical effect when intake is inadequate.

1. Phosphatidylcholine for cell membranes. Roughly 30% of all phospholipids in human cell membranes are phosphatidylcholine. The brain is the most lipid-dense organ in the body (roughly 60% lipid by dry weight), and a developing fetal brain requires enormous quantities of phosphatidylcholine to construct new neuronal membranes during the rapid third-trimester growth spurt. Adult brain membrane turnover is slower but ongoing, and inadequate choline impairs membrane repair and remyelination.
2. Acetylcholine for neurotransmission. Acetylcholine is the neurotransmitter of the parasympathetic nervous system, the neuromuscular junction, and the cognitive cholinergic pathways from the basal forebrain (nucleus basalis of Meynert) that project to the cortex and hippocampus. The basal forebrain cholinergic system is the first system damaged in Alzheimer's disease, which is why the first-line Alzheimer's drugs (donepezil, rivastigmine, galantamine) are cholinesterase inhibitors that boost acetylcholine levels. Adequate dietary choline supports the synthesis of acetylcholine in these neurons.
3. Betaine as a methyl donor in one-carbon metabolism. Choline is oxidized to betaine in the liver and kidney. Betaine then donates a methyl group to homocysteine, regenerating methionine and reducing homocysteine accumulation. This methyl-donor function overlaps with folate and Vitamin B12, and adequate choline can partially compensate for low folate intake (though not fully). Inadequate methyl donors lead to elevated homocysteine, hypomethylation of DNA, and dysregulation of gene expression.

The clinical effects of choline deficiency therefore span three organ systems: brain (cognitive impairment, neural tube defects), liver (steatosis from inability to package triglycerides into very-low-density lipoprotein (VLDL)), and DNA methylation (epigenetic dysregulation, potentially relevant to cancer risk and fetal programming).

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Fetal Brain Development

The fetal brain undergoes its most rapid growth in the third trimester. Between weeks 28 and 40, the brain triples in weight, the cortex undergoes dramatic gyrification, and synaptogenesis begins in earnest. This growth phase requires enormous quantities of phosphatidylcholine to build new neuronal membranes, choline for acetylcholine synthesis in developing cholinergic pathways, and methyl donors for the DNA methylation events that regulate neurogenesis.

The placenta actively transports choline from maternal blood to the fetus, with cord-blood choline concentrations roughly 3× maternal concentrations at term. This active transport explains why the maternal Adequate Intake rises from 425 mg/day pre-pregnancy to 450 mg/day during pregnancy and 550 mg/day during lactation — the fetus and nursing infant are pulling choline directly out of maternal stores.

Rodent models established the developmental choline story first. Pregnant rats fed choline-supplemented diets gave birth to offspring with measurably enhanced hippocampal-dependent memory function that persisted into adulthood. Conversely, choline-deficient maternal diets produced offspring with permanent deficits in attention and visuospatial memory. The effect was both prenatal (third trimester equivalent) and postnatal (early lactation equivalent), and the mechanism appeared to involve permanent changes in hippocampal neurogenesis and in the epigenetic state of genes involved in synaptic plasticity.

The human translation took decades to demonstrate. Observational cohort studies gave mixed results. In Project Viva, Boeke et al. (2013) found that the top quartile of second-trimester maternal choline intake was associated with modestly better child visual memory at age 7 than the bottom quartile. In the Seychelles, Strain et al. (2013), who measured the children's own plasma choline at age 5, found no indication that choline or its metabolites within the normal range were associated with neurodevelopmental outcomes. Observational data are also vulnerable to confounding by overall maternal nutrition, education, and socioeconomic factors. Randomized trials have differed too: a 2012 trial (Cheatham et al.) found that 750 mg/day of supplemental phosphatidylcholine in pregnancy did not enhance infant cognitive function, while the 2018 Caudill trial described below reported faster infant information processing; the Caudill authors described the two earlier human experimental studies as having produced inconsistent results.

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The Caudill 930 mg Trial

In 2018, Marie Caudill and colleagues at Cornell published the most important choline trial in pregnancy to date. The design was a randomized, double-blind, controlled feeding study. Twenty-six women entering their third trimester were randomized to consume, until delivery, a controlled diet providing a total of either 480 mg/day of choline (13 women; close to the pregnancy Adequate Intake of 450 mg/day) or 930 mg/day (13 women; roughly twice the Adequate Intake), and 24 of their infants were tested. Outcomes were measured in the infants at 4, 7, 10, and 13 months using a standardized infant information-processing-speed task (color-change visual paired-comparison paradigm).

Result: mean reaction time, averaged across the four test ages, was significantly faster for infants of mothers in the 930 mg/day arm. The difference appeared even though the comparator arm was consuming roughly the Adequate Intake (not zero choline). The authors concluded that maternal consumption of approximately twice the recommended amount of choline during the last trimester improves infant information processing speed.

The Caudill trial has not yet led to a change in official prenatal recommendations, but it has shifted clinical thinking. Many obstetricians and dietitians now suggest pregnant women aim for at least 550 mg/day of choline (the lactation Adequate Intake) and ideally 900-1000 mg/day during the third trimester. This is achievable with three eggs per day plus typical background diet, or with prenatal vitamin supplementation that includes 500+ mg of phosphatidylcholine. Most prenatal vitamins, notably, contain little to no choline — a striking gap given the strength of the evidence.

For an earlier 2012 Caudill trial that pre-dated this work, see the Yan et al. paper on maternal and fetal choline biomarkers. The pre-2018 literature established that dietary choline alters fetal biomarker status; the 2018 trial established that it alters fetal cognitive outcomes.

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Neural Tube Defects and Choline

Folate is the famous nutrient for preventing neural tube defects (anencephaly, spina bifida) — the United States has fortified the grain supply with folic acid since 1998 specifically to reduce NTD incidence, with dramatic success. Less well-known is that choline has a parallel and independent protective effect against NTDs, operating through the same one-carbon-metabolism pathway that folate occupies.

The pivotal observational study was Shaw et al. (2004), which used data from the California Birth Defects Monitoring Program to compare periconceptional dietary choline intake in the mothers of 424 NTD-affected pregnancies and 440 controls (California births, 1989–1991). Higher dietary choline was associated with a lower risk of an NTD-affected pregnancy, and controlling for supplemental folic acid, dietary folate, methionine and other factors did not substantially change that result — so the choline signal was not simply a marker for folate. Risk was lowest for women whose diets were rich in choline, betaine and methionine together: above the 75th percentile for all three, compared with below the 25th, the odds of an NTD-affected pregnancy were about one-sixth (odds ratio 0.17).

The mechanism: NTDs occur when the neural tube fails to close completely during weeks 3-4 post-conception. Neural tube closure requires extensive DNA methylation events (controlled by methyl donors, which include both folate and choline via betaine), rapid membrane lipid synthesis (driven by phosphatidylcholine), and acetylcholine signaling in the early neuroectoderm. Folate handles the methylation arm. Choline handles the membrane lipid arm and provides additional methyl donor capacity. Both are necessary; neither alone is fully sufficient.

Because the neural tube closes in weeks 3-4 after conception, these findings concern periconceptional choline intake — the intake around the time of conception, which is what Shaw et al. measured. Three eggs per day combined with a typical background diet supply roughly the Adequate Intake, by the arithmetic in the dosing section below. For vegetarian women relying on plant choline sources (cruciferous vegetables, lentils, soybeans), total intake is harder to reach because plant choline densities are lower than egg yolk by 5-10×.

For more on neural tube defect prevention, see our Folate page.

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Adult Cognition and the Framingham Data

The Framingham Offspring Cohort — a multi-generational US epidemiological study originally launched in 1948 in the town of Framingham, Massachusetts — provided the most important adult-cognition data on choline through the Poly et al. (2011) analysis. Among 1,391 dementia-free participants aged 36 to 83, dietary choline intake (assessed by food frequency questionnaire in 1991-1995, “remote” intake, and again in 1998-2001, “concurrent” intake) was associated with:

• Better performance on verbal memory and visual memory tests with higher concurrent intake. Effect sizes were modest but statistically robust.
• Lower volume of white matter hyperintensities on magnetic resonance imaging (MRI) — white matter hyperintensities are small areas of demyelination and ischemic damage visible on T2-weighted magnetic resonance imaging that accumulate with age and correlate with cognitive decline. This association was with remote (earlier) intake rather than concurrent intake: higher remote choline intake was linked to lower white-matter hyperintensity volume and to lower odds of a large hyperintensity volume (odds ratio 0.56).
• Effects persisted after adjustment for age, education, total energy intake, B vitamins (folate, B6, B12), and other potential confounders.

The Framingham data are observational and cannot establish causation, but they are consistent with the mechanistic story: choline supports cholinergic neurotransmission (which underlies attention and memory), membrane lipid maintenance (which protects against demyelination), and methyl donor capacity (which supports DNA repair and homocysteine clearance, both linked to cognitive resilience).

The clinical translation for adults concerned about cognitive aging is straightforward. Achieving and maintaining adequate choline intake (550 mg/day for men, 425 mg/day for women, more if pregnant or lactating) is part of the same general nutritional pattern that supports brain health in aging: adequate omega-3 fatty acids (docosahexaenoic acid, DHA), B vitamins, antioxidants, and protein. Two to three eggs per day is one of the simplest ways to ensure choline adequacy.

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Choline Deficiency and Non-Alcoholic Fatty Liver

Non-alcoholic fatty liver disease (NAFLD) is now the most common chronic liver disease in the developed world, affecting roughly 25-30% of adults in the United States. The disease begins as benign hepatic steatosis (fat accumulation in liver cells) and progresses in a subset to non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and hepatocellular carcinoma.

Choline deficiency is a well-established cause of hepatic steatosis. The mechanism: the liver packages triglycerides for export to the bloodstream by wrapping them in very-low-density lipoprotein (VLDL) particles. The protein scaffold of a very-low-density lipoprotein particle is apolipoprotein B-100, and its outer phospholipid monolayer is primarily phosphatidylcholine. Without adequate phosphatidylcholine (which requires adequate dietary choline as the rate-limiting substrate), the liver cannot construct very-low-density lipoprotein fast enough to export the triglycerides it synthesizes. Triglycerides accumulate in hepatocytes — this is steatosis.

Volunteer feeding studies tested this directly. In a 1991 study (Zeisel et al.), healthy men fed a choline-deficient diet for three weeks showed a steady rise in the liver enzyme alanine aminotransferase while other tests of liver and kidney function were unchanged — signs the authors described as incipient liver dysfunction. A later study that measured liver fat by magnetic resonance imaging (Fischer et al., 2007) found that 77% of men, 80% of postmenopausal women and 44% of premenopausal women deprived of choline for up to 42 days developed fatty liver or muscle damage, and normal organ function was restored when choline was added back. The IOM 1998 panel based the adult Adequate Intake on the 1991 study: 500 mg/day (about 7 mg/kg/day) was the dose that prevented alanine aminotransferase abnormalities in healthy men, which for a 76 kg reference man the panel rounded to 550 mg/day, and it called the estimate uncertain because it rested on a single published study.

For patients with established non-alcoholic fatty liver disease, choline adequacy is part of the nutritional management. The standard treatment is weight loss, the Mediterranean dietary pattern, and treatment of insulin resistance, but adequate choline intake removes one of the contributing mechanisms. Two to three eggs per day in a non-alcoholic fatty liver disease patient is generally fine (it does not worsen the disease) and may modestly improve very-low-density lipoprotein export capacity. For more on non-alcoholic fatty liver disease, see our Fatty Liver Disease page.

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Practical Dosing — How Many Eggs?

The arithmetic is straightforward. One large whole egg delivers about 147 mg of choline; USDA lists about 139 mg for a large yolk on its own and about 0.4 mg for a large egg white (negligible). Therefore:

• Adult man (Adequate Intake 550 mg/day): 3 eggs supply ~441 mg (80% of Adequate Intake); 4 eggs supply ~588 mg (107% of Adequate Intake). Background diet typically provides 100-200 mg additional from grains, vegetables, meat, and dairy. Two to three eggs per day is sufficient for most men.
• Adult woman (Adequate Intake 425 mg/day): 2 eggs supply ~294 mg (69% of Adequate Intake); 3 eggs supply ~441 mg (104% of Adequate Intake). Two eggs per day with normal background diet is sufficient for most women.
• Pregnant woman (Adequate Intake 450 mg/day, but Caudill data suggest 900 mg/day for optimal fetal brain development): 3 eggs per day plus background diet hits the Adequate Intake; reaching the Caudill 930 mg/day target requires 3 eggs plus an additional 400-500 mg from supplemental phosphatidylcholine or sunflower lecithin, since reaching that dose from food alone requires 5-6 eggs/day or 3-4 oz of beef liver weekly.
• Lactating woman (Adequate Intake 550 mg/day): Same as adult man — 3 eggs per day is sufficient.
• Children: Adequate Intake scales by age (200 mg/day at 1-3 years, 250 mg/day at 4-8, 375 mg/day at 9-13). One to two eggs per day is appropriate for most school-age children.

The Tolerable Upper Intake Level (UL) for choline is 3,500 mg/day in adults, set primarily based on fishy body odor and hypotension reported at doses above 7 g/day. Reaching the Tolerable Upper Intake Level from food alone is essentially impossible — you would need to eat ~24 eggs per day. The Tolerable Upper Intake Level is a safeguard against high-dose supplementation, not a concern for whole-food intake.

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If You Don't Eat Eggs: Alternative Sources

Egg-free individuals (vegan, allergic, ethically opposed, or simply egg-averse) need to assemble their choline intake from a wider mix of sources. The densest non-egg sources are:

• Beef liver, 100 g serving: ~420 mg choline — the densest single source after egg yolk. One small serving per week meets a meaningful fraction of the weekly requirement.
• Salmon, 100 g serving: ~95 mg choline. See our Salmon page.
• Chicken breast, 100 g serving: ~73 mg choline.
• Beef, 100 g serving: ~70 mg choline. See our Beef page.
• Cod, 100 g serving: ~71 mg choline. See our Cod page.
• Soybeans, 1 cup cooked: ~82 mg choline (USDA).
• Quinoa, 1 cup cooked: ~43 mg choline.
• Lentils, 1 cup cooked: ~65 mg choline. See our Lentils page.
• Cruciferous vegetables (broccoli, Brussels sprouts, cauliflower), 1 cup cooked: 30-60 mg choline.
• Sunflower lecithin supplement: ~250-500 mg phosphatidylcholine per 1 tablespoon. The most efficient supplemental source for vegans and pregnant women aiming for the Caudill 930 mg/day target.
• Pure choline bitartrate or alpha-GPC supplements: 250-500 mg per capsule. More efficient than lecithin but lacks the additional phosphatidylcholine structure.

Vegan choline intake is typically half to one-third of omnivore intake without active attention. For pregnant or lactating vegans, supplemental phosphatidylcholine and sunflower lecithin are the concentrated non-food sources. For nonpregnant vegan adults, combining soybeans, lentils, quinoa, and cruciferous vegetables daily can approach the Adequate Intake, though reaching it consistently usually requires some supplementation or particularly thoughtful menu planning.

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Cautions (Trimethylamine N-Oxide, Genetic Variants, Upper Limit)

• The trimethylamine N-oxide controversy. A series of papers from Stanley Hazen's group at Cleveland Clinic (starting around 2011) reported that gut microbes convert dietary phosphatidylcholine and L-carnitine into trimethylamine (TMA), which the liver oxidizes to trimethylamine N-oxide (TMAO), and that elevated serum trimethylamine N-oxide is associated with increased cardiovascular event risk in observational cohorts. This generated alarm that eggs (and red meat) might be cardiovascularly harmful via the trimethylamine N-oxide pathway. Subsequent work has substantially walked back this concern: (1) fish contains trimethylamine N-oxide itself, and in a crossover feeding trial (Cho et al. 2017) a fish meal raised circulating trimethylamine N-oxide far more than eggs or beef, within 15 minutes of eating — suggesting it can be absorbed without processing by gut microbes; (2) the trimethylamine N-oxide-cardiovascular association in observational studies appears to be confounded by kidney function (trimethylamine N-oxide accumulates in chronic kidney disease, CKD); (3) interventional studies feeding eggs to humans do not reliably increase trimethylamine N-oxide unless the gut microbiome happens to have the relevant TMA-producing taxa; and (4) the gut-microbiome conversion can be modified by diet. Most cardiologists no longer consider trimethylamine N-oxide a clinically actionable biomarker.
• Genetic variants in PEMT (phosphatidylethanolamine N-methyltransferase). A common SNP in the PEMT gene, rs12325817, lies within 1 kb of the gene's critical estrogen response element; its risk allele fails to bind the estrogen receptor, which prevents estrogen from inducing PEMT, the enzyme of endogenous choline synthesis (Resseguie et al., 2011). Carriers may have higher dietary choline requirements than the general population, particularly in pregnancy when PEMT activity normally surges to compensate for fetal demand. Some consumer genetic-testing panels report PEMT variants.
• Fishy body odor at high doses. Choline doses above 7-10 g/day (from supplements, not realistically achievable from food) can cause fishy body odor in some individuals due to incomplete oxidation of trimethylamine. This is the basis for the IOM upper limit of 3,500 mg/day.
• Trimethylaminuria (TMAU) carriers. A rare metabolic disorder in which the FMO3 enzyme that oxidizes TMA to odorless trimethylamine N-oxide is deficient. Affected individuals develop fish-odor syndrome at much lower choline doses, which is why dietary choline restriction is part of managing the condition. Prevalence is approximately 1 in 200,000.
• Hypotension at very high doses. Doses above 7 g/day can produce mild hypotension via vagal stimulation. Not relevant for food-based intake.
• Egg allergy. Egg allergy is the second-most-common food allergy in infants and young children (after cow's milk). Most children outgrow it by school age. The 2017 STEP trial (Palmer et al.), in infants with a hereditary risk of allergy but no eczema, found no significant difference in egg allergy at age 1 between infants given daily egg powder from age 4-6 months and controls (7.0% vs 10.3%), and more infants in the egg group stopped the study powder because of an allergic reaction (6.1% vs 1.5%).

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Key Research Papers

1. Caudill MA, Strupp BJ, Muscalu L, Nevins JEH, Canfield RL (2018). Maternal choline supplementation during the third trimester of pregnancy improves infant information processing speed: a randomized, double-blind, controlled feeding study. FASEB J. 32(4):2172-2180. — PubMed PMID: 29217669
2. Shaw GM, Carmichael SL, Yang W, Selvin S, Schaffer DM (2004). Periconceptional dietary intake of choline and betaine and neural tube defects in offspring. Am J Epidemiol. 160(2):102-9. — PubMed PMID: 15234930
3. Zeisel SH, da Costa KA (2009). Choline: an essential nutrient for public health. Nutr Rev. 67(11):615-23. — PubMed PMID: 19906248
4. Wallace TC, Fulgoni VL (2017). Usual choline intakes are associated with egg and protein food consumption in the United States. Nutrients. 9(8):839. — PubMed PMID: 28783055
5. Yan J, Jiang X, West AA, Perry CA, Malysheva OV et al. (2012). Maternal choline intake modulates maternal and fetal biomarkers of choline metabolism in humans. Am J Clin Nutr. 95(5):1060-71. — PubMed PMID: 22418088
6. Poly C, Massaro JM, Seshadri S, Wolf PA, Cho E et al. (2011). The relation of dietary choline to cognitive performance and white-matter hyperintensity in the Framingham Offspring Cohort. Am J Clin Nutr. 94(6):1584-91. — PubMed PMID: 22071706
7. Boeke CE, Gillman MW, Hughes MD, Rifas-Shiman SL, Villamor E, Oken E (2013). Choline intake during pregnancy and child cognition at age 7 years. Am J Epidemiol. 177(12):1338-47. — PubMed PMID: 23425631
8. Strain JJ, McSorley EM, van Wijngaarden E, Kobrosly RW, Bonham MP et al. (2013). Choline status and neurodevelopmental outcomes at 5 years of age in the Seychelles Child Development Nutrition Study. Br J Nutr. 110(2):330-6. — PubMed PMID: 23298754
9. Cheatham CL, Goldman BD, Fischer LM, da Costa KA, Reznick JS, Zeisel SH (2012). Phosphatidylcholine supplementation in pregnant women consuming moderate-choline diets does not enhance infant cognitive function: a randomized, double-blind, placebo-controlled trial. Am J Clin Nutr. 96(6):1465-72. — PubMed PMID: 23134891
10. Zeisel SH (2006). Choline: critical role during fetal development and dietary requirements in adults. Annu Rev Nutr. 26:229-50. — PubMed PMID: 16848706
11. Institute of Medicine (1998). Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline. National Academies Press. — Search PubMed
12. Wang Z, Klipfell E, Bennett BJ, Koeth R, Levison BS et al. (2011). Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease. Nature. 472(7341):57-63. Wang TMAO Nature 2011. — PubMed PMID: 21475195
13. Cho CE, Taesuwan S, Malysheva OV, Bender E, Tulchinsky NF et al. (2017). Trimethylamine-N-oxide (TMAO) response to animal source foods varies among healthy young men and is influenced by their gut microbiota composition: a randomized controlled trial. Mol Nutr Food Res. 61(1). — PubMed PMID: 27377678
14. Resseguie M, Song J, Niculescu MD, da Costa KA, Randall TA, Zeisel SH (2007). Phosphatidylethanolamine N-methyltransferase (PEMT) gene expression is induced by estrogen in human and mouse primary hepatocytes. FASEB J. 21(10):2622-32. — PubMed PMID: 17456783
15. Resseguie ME, da Costa KA, Galanko JA, Patel M, Davis IJ, Zeisel SH (2011). Aberrant estrogen regulation of PEMT results in choline deficiency-associated liver dysfunction. J Biol Chem. 286(2):1649-58. — PubMed PMID: 21059658
16. Zeisel SH, Da Costa KA, Franklin PD, Alexander EA, Lamont JT, Sheard NF, Beiser A (1991). Choline, an essential nutrient for humans. FASEB J. 5(7):2093-8. — PubMed PMID: 2010061
17. Fischer LM, daCosta KA, Kwock L, Stewart PW, Lu TS, Stabler SP, Allen RH, Zeisel SH (2007). Sex and menopausal status influence human dietary requirements for the nutrient choline. Am J Clin Nutr. 85(5):1275-85. — PubMed PMID: 17490963

PubMed Topic Searches

1. PubMed: Choline pregnancy brain
2. PubMed: Phosphatidylcholine egg yolk
3. PubMed: Choline NTD folate
4. PubMed: TMAO cardiovascular
5. PubMed: Choline AI deficiency NHANES

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Connections

• All Food
• Eggs Overview
• Eggs Benefits Hub
• Eggs for Lutein/Zeaxanthin
• Cholesterol Myth Revisited
• Pasture vs Cage-Free Eggs
• Folate
• Vitamin B12
• Vitamin B6
• Methionine
• Organ Meats (Beef Liver)
• Salmon
• Beef
• Fatty Liver Disease
• Alzheimer's Disease
• History
• Nutrients

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