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Acetylcholine in food: Acetylcholine – Receptors, Foods & Supplements


Acetylcholine – Receptors, Foods & Supplements

Diet might play a role in the production of acetylcholine and a decreased risk of certain diseases.

Acetylcholine is a neurotransmitter produced in the brain that plays an important role in muscle movements, thinking, and working memory.

Working memory is the brain’s ability to hold information in the mind temporarily.

Problems with the production and use of acetylcholine are hallmarks of diseases such as dementia and myasthenia gravis (an autoimmune disease that weakens the muscles).

Acetylcholine Receptors

Acetylcholine receptors are proteins to which acetylcholine binds, allowing signals to flow from one nerve cell to another.

Drugs that work on the acetylcholine receptors have many medical uses, including the treatment of Alzheimer’s disease and myasthenia gravis.

Medications that stimulate acetylcholine receptors are called agonists, while those that inhibit receptors are called antagonists.

Acetylcholine and Alzheimer’s Disease

People with Alzheimer’s disease produce less acetylcholine.

Medications that stop the breakdown of acetylcholine in the brain, called cholinesterase inhibitors, may be prescribed to people with mild to moderate Alzheimer’s symptoms.

These drugs may help delay or prevent behavioral symptoms such as agitation, delusions, or sundowning (a state of confusion and distress late in the day) from becoming worse for a limited period of time.

However, they may lose their effectiveness as the brain produces less and less acetylcholine.

Acetylcholine Foods and Supplements

There are no foods or supplements that contain the chemical acetylcholine, though some foods and supplements may contain the building blocks of acetylcholine.

Choline is an essential nutrient and a building block of acetylcholine. Foods that are naturally high in choline include whole eggs, meats and fish, and whole grains.

Studies in laboratory animals and humans suggest that consuming foods or supplements rich in choline may elevate levels of acetylcholine in the brain.

This means that choline could potentially have a protective effect against certain types of dementia, including Alzheimer’s disease.

However, more research is needed to tease out the complicated relationship between dietary choline and brain function.

Current State of Knowledge Across the Life Cycle

2.1. Choline Metabolism

Choline metabolism can be divided into four main pathways which are involved in the synthesis of acetylcholine, trimethylamine (TMA), betaine, and phospholipids (). Choline is used as the precursor for the synthesis of the neurotransmitter, acetylcholine, by choline acyltransferase in the cytosol of pre-synaptic cholinergic neurons [16]. Acetylcholine is subsequently packaged into vesicles and released into the synaptic cleft, where it binds to receptors of the post-synaptic neuron in the central and peripheral nervous systems [17]. Acetylcholine synthesis has also been reported in tissues, including placenta, muscle, intestine, and lymphocytes [18,19]. In the large intestine, choline is metabolized to TMA by the gut microbiota prior to absorption [20,21]. After absorption, TMA is metabolized to trimethylamine-N-oxide (TMAO) by flavin monooxygenases in the liver [22].

Simplified overview of choline metabolism. Abbreviations: SAM, S-adenosylmethionine; SAH, S-adenosylhomocysteine; TMA, trimethylamine; TMAO, trimethylamine-N-oxide.

Choline can be irreversibly oxidized to yield betaine in a two-step process catalyzed by choline dehydrogenase and betaine aldehyde dehydrogenase mainly in the liver and kidney [23,24]. Betaine is an important osmolyte and a methyl group donor. As a methyl group donor, betaine participates in the re-methylation of homocysteine to methionine by betaine-homocysteine S-methyltransferase (BHMT), also producing dimethylglycine [25,26]. This reaction is an alternative pathway, parallel to the ubiquitous vitamin B12-folate-dependent pathway for homocysteine re-methylation [27]. The BHMT accounts for up to half of the hepatic homocysteine re-methylation activity [28]. Methionine is the precursor of the universal methyl donor, S-adenosyl methionine (SAM), which is involved in several methylation reactions, such as epigenetic regulation of DNA as well as the synthesis of phosphatidylcholine [29,30]. As for betaine, dimethylglycine synthesis occurs primarily in the liver and kidney [31,32,33], and further demethylation of dimethylglycine produces sarcosine, which is subsequently metabolized to glycine, resulting in a carbon unit transferred to the folate pool [34].

Finally, choline is a precursor for the synthesis of phosphatidylcholine, the most abundant form of phospholipid in the body. Phosphatidylcholine is synthesized through the cytidine diphosphate (CDP)-choline pathway, which occurs in all nucleated cells [35]. It has been estimated that 70% of total phosphatidylcholine in the liver is synthesized by this pathway [36,37,38]. Alternatively, phosphatidylcholine can be generated by the de novo synthesis pathway by the sequential methylation of phosphatidylethanolamine by phosphatidylethanolamine N-methyltransferase (PEMT) [39,40,41]. This reaction consumes three molecules of SAM, which in turn generate three molecules of S-adenosyl homocysteine (SAH), a precursor of homocysteine [1,42]. It has been estimated that up to 50% of homocysteine production may originate from PEMT activity, with the highest activity being detected in the liver (although activity is also observed in other tissues, such as the mammary gland) [1,37,39,43,44,45,46]. In humans, this is the only known endogenous de novo pathway for choline synthesis. Recently, it has been reported that phosphatidylcholine produced by the PEMT pathway differs from that originating from the CDP-choline pathway, particularly in the fatty acid composition, with the first characterized by having a higher composition of long-chain fatty acids, such as docosahexaenoic acid [47,48].

2.2. Biological Functions of Choline

Choline has received considerable attention due to its inverse association with adverse health outcomes that can occur across the life cycle, including birth defects, neurodevelopment and cognition alterations, hepatic steatosis, cardiovascular disease (CVD), and cancer [5,7,49,50,51,52,53,54,55,56,57,58,59]. Oxidation of choline to betaine and subsequent SAM synthesis are critical methylation reactions that represent a cornerstone for epigenetic regulation of gene expression [60,61]. In rodents, maternal choline-deficient diets during the perinatal period altered DNA and histone methylation in the offspring [62,63,64]. In humans, low maternal choline intake during pregnancy can alter DNA methylation in the placenta and cord blood [65]. Notably, there is an inverse relationship between the risk of neural tube defects and maternal choline intake or plasma choline concentrations, independent of dietary folate or supplemental folic acid intakes [49,52]; to some extent, this is analogous to that reported for folate. In addition, other birth defects associated with choline deficiency include cleft lip, hypospadias, and cardiac defects [66,67,68,69].

The role of choline in neurodevelopment and cognition involves not only the synthesis of acetylcholine and components of cellular membranes, but also gene expression. In rodents, maternal choline intake during the perinatal period impacts both anatomical and biochemical aspects of cognitive function, along with lifelong effects, including memory decline in the offspring as they age [70]. The neuroprotection effect of choline observed in animal studies has also been studied in humans; however, results are inconclusive [53,54,71,72,73]. In children, only two studies have been published, and no association was found between plasma free choline concentrations and child cognition, albeit plasma betaine concentrations were positively associated with language [55,74]. In adults, positive associations between cognition and plasma free choline concentrations, and between dietary choline intake and better cognitive performance, have been described [75,76]. However, other researchers examining choline supplementation, in adults, have reported inconsistent results [77,78,79,80,81,82]. Therefore, more research is required to clarify the relationship between choline and cognitive function in different age groups.

In humans, liver damage (e.g., elevated serum alanine aminotransferase concentration) occurred in healthy men after only three weeks of dietary choline restriction (n = 7, 0.42 to 0.62 µkat/L), which was not observed in the control group (n = 8, 0.40 to 0.32 µkat/L) [7]. In the same study, a 30% decrease in plasma free choline concentration was observed in the choline-deficient group. Similarly, muscular damage (e.g., elevated serum creatine phosphokinase concentration) was reported after three weeks of dietary choline restriction [83]. These examples of tissue damage were attributed to altered structural integrity and increased cellular membrane permeability that arises due to a decreased phosphatidylcholine to phosphatidylethanolamine ratio [84,85,86,87]. In addition, the production of very low-density lipoproteins requires phosphatidylcholine synthesis in the liver [88,89]. Without an adequate supply of choline for phosphatidylcholine synthesis, triacylglycerides will accumulate, which leads to fatty liver condition [90,91]. Similar alterations have been reported in patients receiving long-term total parenteral nutrition devoid of choline [92,93]. These data supported the classification of choline as an essential nutrient by indicating that de novo synthesis of choline is not sufficient to meet the body’s requirements in some instances.

The reported association between choline status and CVD risk is linked to homocysteine and TMAO concentrations; however, this area is not fully understood, and that evidence exists for pathways that could, at least in theory, either increase or decrease CVD risk. Elevated homocysteine concentrations have been positively associated with a risk of CVD [94,95]. In prospective cohort studies, dietary choline intakes were negatively associated with homocysteine concentrations, and plasma betaine concentrations were also negatively associated with risk of CVD [96,97]. In contrast, a recent meta-analysis reported no evidence of a positive association between dietary choline or betaine and CVD incidence [98]. Intervention studies, with betaine or phosphatidylcholine supplementation, have reported a reduction in homocysteine concentrations [99,100,101]. However, lowering homocysteine concentrations with B-vitamins, such as folate and B12, does not reduce CVD risk [102,103]. Furthermore, a concern about choline intake and CVD is related to a possible increase in TMAO concentration, which has been positively associated with CVD risk [104,105,106]. It has also been reported that only a low proportion of choline intake derived from eggs is converted to TMAO [107], which is then excreted and does not accumulate in the blood [108]. In addition to choline intake and gut microbiota, TMAO levels are also controlled by renal excretion [109]. To date, the mechanisms by which TMAO increases CVD risk and the identification of the type of bacteria involved in TMA synthesis are now becoming understood [21,110]. However, it is important to recognize that TMAO content is high in seafood [111], and only a small variation of TMAO concentrations can be explained by dietary intake [112].

Choline | The Nutrition Source

Choline is an essential nutrient that is naturally present in certain foods and available as a supplement. The body can also produce small amounts on its own in the liver, but not enough to meet daily needs. Choline is converted into a neurotransmitter called acetylcholine, which helps muscles to contract, activates pain responses, and plays a role in brain functions of memory and thinking. Most choline is metabolized in the liver where it is converted into phosphatidylcholine, which assists in building fat-carrying proteins and breaking down cholesterol. It is also “food” for beneficial gut bacteria. [1]

Recommended Amounts

There is not enough data to establish a Recommended Dietary Allowance for choline. [2] The Food and Nutrition Board established an Adequate Intake (AI) for choline based on the prevention of liver damage.

AI: The Adequate Intake for men and women ages 19+ years is 550 mg and 425 mg daily, respectively. For pregnancy and lactation, the AI is 450 mg and 550 mg daily, respectively.

UL: A Tolerable Upper Intake Level (UL) is the maximum daily dose unlikely to cause adverse side effects in the general population. A UL has not been established for choline, because a toxic level has not been observed from food sources or from longer-term intakes of high-dose supplements.

Choline and Health

Cardiovascular disease

Choline has been suggested to both protect and increase the risk of cardiovascular disease (CVD). Choline, along with the B vitamin folate, helps to lower blood levels of homocysteine by converting it to methionine. High homocysteine levels are a risk factor for CVD. Choline may also help to reduce blood pressure and stroke. In a study of almost 4,000 African-American participants followed for 9 years, higher choline intakes were associated with a lower risk of ischemic strokes. [3]

But choline may also act negatively toward the heart. Choline is converted by gut bacteria into a byproduct called trimethylamine (TMA), which is then converted in the liver to trimethylamine-N-oxide (TMAO). Higher blood levels of TMAO have been associated with a higher risk of CVD in animal studies. [4,5] However, it is unclear what is TMAO’s relationship to CVD, or if it is just a marker of an underlying disease process that leads to CVD. A large cohort of men and women from the Nurses’ Health Study and Health Professionals Follow-up Study, followed for 20-25 years, found that higher phosphatidylcholine intakes were associated with an increased risk of deaths from CVD and other causes. [6] There was a 26% increased risk of CVD deaths when combining data from both cohorts comparing the highest intakes of phosphatidylcholine with the lowest. Furthermore, having diabetes heightened that risk. It is believed that circulating TMAO may promote atherosclerosis by preventing the removal of cholesterol in the liver. However, it was noted that TMAO blood levels were not measured in this study, only choline from foods reported in diet questionnaires.

Other earlier, large epidemiological studies found the contrary, with no association of high choline intakes with a higher risk of cardiovascular diseases, though these studies also did not specifically measure TMAO blood levels. [7,8]

There appears to be an association with diets high in choline-rich foods and cardiovascular disease, but the reasons for this link need further study.

Type 2 diabetes

In three large cohorts of men and women, higher intakes of phosphatidylcholine were associated with an increased risk of type 2 diabetes mellitus (T2DM). [9] Those who had the highest dietary intakes of choline showed a 34% increased risk of T2DM compared with the lowest intakes. The exact mechanism of this association is unclear and warrants further research.

Nonalcoholic fatty liver disease

There is a link between choline deficiency and liver disease. Phosphatidylcholine carries fats away from the liver, so a choline deficiency can cause the liver to store too much fat. This increases the risk for nonalcoholic fatty liver disease (NAFLD), which may then progress to cirrhosis (an inflammation of liver cells, followed by thickening and hardening of liver tissue), liver cancer, or liver failure. This ultimately interferes with normal liver function. Changes in the metabolism of choline or phosphatidylcholine can also negatively impact certain biochemical pathways that lead to NAFLD. [10] NAFLD occurs most often in  individuals with excess weight or obesity, and the main treatment is to reduce body fat with calorie restriction and exercise. Although a choline deficiency can lead to liver dysfunction, it is not yet clear if dietary choline or choline supplementation can treat NAFLD. 

Cognitive function

Choline is associated with brain health because it is converted into acetylcholine, which plays a role in memory and thinking. Studies have found that people with Alzheimer’s disease have lower levels of an enzyme that converts choline into acetylcholine, and therefore theorize that higher dietary intakes of choline may prevent cognitive decline. [11] Although some  observational studies have found that higher intakes of choline are associated with higher levels of cognitive function like memory, clinical trials have not found that choline supplementation significantly improves these cognitive measures. [1]

Food Sources

Choline is found in a variety of foods. The richest sources are meat, fish, poultry, dairy, and eggs.

Signs of Deficiency and Toxicity


Most Americans eat less than the AI for choline but a deficiency is very rare in healthy persons, as the body can make some choline on its own. Also, the amount of dietary choline an individual needs can vary widely and depends on various factors. For example, premenopausal women may have lower requirements for dietary choline because higher estrogen levels stimulate the creation of choline in the body. A higher choline requirement may be needed in persons who have a genetic variation that interferes with the normal metabolism of choline. [10] A true choline deficiency can lead to muscle or liver damage, and nonalcoholic fatty liver disease. [12]

Groups at higher risk of deficiency:

  • Pregnant women—In addition to low average dietary intakes in the general public, prenatal supplements do not typically contain choline.
  • Patients dependent on intravenous nutrition—Total parenteral nutrition (TPN) is administered through a vein to people whose digestive tracts cannot tolerate solid food due to disease, surgery, or other digestive conditions. Choline is not typically included in TPN formulas unless specified. [13] NAFLD has been observed in long-term TPN patients. [1]


Very high intakes of choline can lead to low blood pressure (hypotension) and liver toxicity. It may also lead to the excess production of TMAO, which is associated with a higher risk of cardiovascular disease. Other symptoms include excessive sweating, fishy body odor, or nausea/vomiting. The Tolerable Upper Intake Level (UL) for choline for adults 19 years and older is 3,500 mg daily and is based on the amount that has been shown to produce these side effects. [1] Reaching this high amount would most likely be caused by taking very high dose supplements rather than from diet alone.

Did You Know?

  • Multivitamins do not typically contain choline.
  • Although foods rich in choline—liver, egg yolks, and red meat—tend to be higher in saturated fat, choline can also be found in foods lower in saturated fat including salmon, cod, tilapia, chicken breast, and legumes.


B Vitamins
Vitamins and Minerals


  1. S. Department of Health and Human Services. Vitamin B2 Fact Sheet for Health Professionals. https://ods.od.nih.gov/factsheets/Choline-HealthProfessional/ Accessed 2/9/20.
  2. Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes: Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline. Washington, DC: National Academy Press; 1998.
  3. Millard HR, Musani SK, Dibaba DT, Talegawkar SA, Taylor HA, Tucker KL, Bidulescu A. Dietary choline and betaine; associations with subclinical markers of cardiovascular disease risk and incidence of CVD, coronary heart disease and stroke: the Jackson Heart Study. European journal of nutrition. 2018 Feb 1;57(1):51-60.
  4. Wang Z, Klipfell E, Bennett BJ, Koeth R, Levison BS, DuGar B, Feldstein AE, Britt EB, Fu X, Chung YM, Wu Y. Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease. Nature. 2011 Apr;472(7341):57-63.
  5. Tang WW, Wang Z, Levison BS, Koeth RA, Britt EB, Fu X, Wu Y, Hazen SL. Intestinal microbial metabolism of phosphatidylcholine and cardiovascular risk. New England Journal of Medicine. 2013 Apr 25;368(17):1575-84.
  6. Zheng Y, Li Y, Rimm EB, Hu FB, Albert CM, Rexrode KM, Manson JE, Qi L. Dietary phosphatidylcholine and risk of all-cause and cardiovascular-specific mortality among US women and men. The American journal of clinical nutrition. 2016 Jul 1;104(1):173-80.
  7. Bidulescu A, Chambless LE, Siega-Riz AM, Zeisel SH, Heiss G. Usual choline and betaine dietary intake and incident coronary heart disease: the Atherosclerosis Risk in Communities (ARIC) study. BMC cardiovascular disorders. 2007 Dec 1;7(1):20.
  8. Dalmeijer GW, Olthof MR, Verhoef P, Bots ML, Van der Schouw YT. Prospective study on dietary intakes of folate, betaine, and choline and cardiovascular disease risk in women. European Journal of Clinical Nutrition. 2008 Mar;62(3):386-94.
  9. Li Y, Wang DD, Chiuve SE, Manson JE, Willett WC, Hu FB, Qi L. Dietary phosphatidylcholine intake and type 2 diabetes in men and women. Diabetes Care. 2015 Feb 1;38(2):e13-4.
  10. Sherriff JL, O’Sullivan TA, Properzi C, Oddo JL, Adams LA. Choline, its potential role in nonalcoholic fatty liver disease, and the case for human and bacterial genes. Advances in nutrition. 2016 Jan;7(1):5-13.
  11. Sharma K. Cholinesterase inhibitors as Alzheimer’s therapeutics. Molecular medicine reports. 2019 Aug 1;20(2):1479-87.
  12. Corbin KD, Zeisel SH. Choline metabolism provides novel insights into non-alcoholic fatty liver disease and its progression. Current opinion in gastroenterology. 2012 Mar;28(2):159.
  13. Vanek VW, Borum P, Buchman A, Fessler TA, Howard L, Jeejeebhoy K, Kochevar M, Shenkin A, Valentine CJ, Novel Nutrient Task Force, Parenteral Multi‐Vitamin and Multi–Trace Element Working Group, American Society for Parenteral and Enteral Nutrition (ASPEN) Board of Directors. ASPEN position paper: recommendations for changes in commercially available parenteral multivitamin and multi–trace element products. Nutrition in Clinical Practice. 2012 Aug;27(4):440-91.

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The secret ingredient to keeping your mind and muscles young

See the important neurotransmitter for memory, learning and movement that can keep you slim and energized.


Though it sounds like a mouthful, acetylcholine is important for many of the body’s key functions. Healthy acetylcholine levels are important for strong, healthy, metabolically active muscles and it improves tissue health, muscle growth, skin tone, bone density and fat loss.

Low levels of acetylcholine are often a result of aging, over-exercising, poor nutrition as well as Alzheimer’s and other memory disorders. It can present itself in the form of attention problems, loss of creativity, sluggish bowel function (constipation) and poor reflexes.

In order to keep your mind and muscles young here are my suggestions for keeping your acetylcholine levels in check:

1. Don’t over exercise
The more we exercise, the more acetylcholine we use up. That’s not to say that couch potatoes are brimming with high acetycholine levels, but athletes often have significant reductions in acetylcholine levels following strenuous activities such as running, cycling and swimming. A study on marathon runners published in the International Journal of Sports Medicine found that choline stores dropped 40 percent at the end of the race.

We can use natural supplements and foods that stimulate the production of choline — the building block of acetylcholine — to vastly improve stamina and even reduce post-exercise fatigue. This may be particularly important if you’re training for an athletic competition.

Although you usually have enough acetycholine to get you through a workout, lengthy endurance sessions will definitely leave you feeling depleted.

Bottom line: Since keeping acetylcholine levels high is one of the secrets to healthy muscles I recommend short but intense cardio and strength training sessions 30 minutes, three times a week.

2. Reach for l-carnitine
Acetyl-l-carnitine is a potent antioxidant for the brain. It’s an anti-inflammatory that provides a source of the acetyl group needed to make acetylcholine, as well as l-carnitine, which assists with fat burning. It’s my favourite choice for boosting acetylcholine, aiding weight loss and slowing aging of the brain. As an added bonus, it can improve your weight loss results.

One study found that 1000 mg of l-carnitine taken three times daily over 12 weeks significantly lowered fasting blood sugar in middle-aged adults with type 2 diabetes. Remember, an imbalance of blood sugar and insulin will have you battling the scale.

Bottom line: For the ultimate duo I recommend pairing 2-4 capsules (1 tsp) of extra strength fish oil with 500-1000 mg of l-carnitine twice daily.

3. Get PC
Phosphatidylcholine (PC) provides choline, which is needed to make acetylcholine. Another great option is GPC choline, a more expensive but better absorbed version of phosphatidylcholine.

A study by Italian researchers found that young adults who were given alpha-GPC for 10 days prevented a decline in their memory and attention after they were given scopolamine, a drug that depletes acetylcholine in the brain and causes mild, temporary amnesia. Not convinced yet? It’s also been shown to boost growth hormone levels – your fountain of youth.

Bottom line: Take 1,200-2,400 mg per day of PC with food. Or, if you’re using GPC, take 500-2,000 mg daily broken up into two doses; one before breakfast and one before lunch.

If you prefer food sources of choline try a three ounce serving of beef liver (355 mg), three ounces of cod (71 mg), a large egg (126 mg), broccoli or a glass of milk (38 mg).

4. Load up on DMAE
Dimethylaminoethanol (DMAE) is an anti-inflammatory and antioxidant that increases the production of acetylcholine. It’s useful for cognitive function and improving muscle contractions. It can also be used topically to improve skin tone and firmness.

Bottom line: Take 100-300 mg per day with food. If you don’t feel like adding to your supplement arsenal it’s also found in sardines, anchovies, squid and salmon.

5. Reach for something new in the morning
Ever wonder why you need a morning cup of coffee to get you going each morning? Along with foods containing sugar, coffee wakes up your neurotransmitters —  especially acetylcholine — that plays an important role in your sensory perception upon waking. It also sustains your attention and helps get you through the morning.

If you’re trying to wean yourself off of coffee, and/or other morning stimulants, alpha-GPC can help. It’s also known for maintaining neurological health and enhancing growth hormone.

Bottom line: The standard dose is one to two 500 mg capsules per day, away from food. Avoid taking it late in the day as it may keep you awake (much like that cup of coffee).

Natasha Turner, N. D. is a naturopathic doctor, Chatelaine magazine columnist, and author of the bestselling books The Hormone Diet and The Supercharged Hormone Diet. Her newest release, The Carb Sensitivity Program, is now available across Canada. She is also the founder of the Toronto-based Clear Medicine Wellness Boutique. For more wellness advice from Natasha Turner, click here. 

Natural Stacks Acetylcholine Brain Food 60 vcaps

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Acetylcholine Brain Food™ is designed to promote the production of acetylcholine, a neurotransmitter essential to mental processing. Research suggests that the natural compounds in Acetylcholine Brain Food™ are associated with memory and cognitive function.†

  • Improved attention to detail†
  • Better mental clarity†
  • Faster thinking†
  • Cuts through brain fog†

To make acetylcholine, the brain needs two elements: an acetyl group and a choline molecule.

An acetyl group is a type of simple molecular building block of organic chemistry with a chemical formula of C2h40. The acetyl group is usually present in the brain as Acetyl-CoA. Choline and the acetyl group are grouped together by the enzyme Choline Acetyltransferase (ChAT). They are both stored in neurons, released, and then broken down by another enzyme called acetylcholinesterase (AchE). To increase levels of acetylcholine, we use the following approach:

  • Create more acetyl-CoA molecules to provide acetyl groups to ChAT for acetylcholine production.
  • Provide more choline in choline producing (cholinergic) neurons for use by ChAT.
  • Increase or upregulate the activity of ChAT.
  • Decrease the activity of AchE.

Acetylcholine Brain Food™ contains the essential raw materials for the brain to increase production, achieve balance, and maintain prolonged activity of the neurotransmitter acetylcholine — the Learning Molecule.


Take a serving of 2-4 capsules to support mental processing speed, or as directed by a healthcare practitioner. Do not exceed 8 capsules per day.

Acetylcholine: What Is It and What Are Its Functions?

Egg yolks are rich in brain-boosting choline, which your body converts into acetylcholine.

Image Credit: Alexander Spatari/Moment/GettyImages

Acetylcholine is the most abundant neurotransmitter in the human body, primarily found in the hippocampus. It’s integral for memory, mood, muscle control, and other nervous system and brain functions.

Read more: 19 Best Brain Superfoods

If you’ve never heard of acetylcholine, you’ve likely heard of choline. Choline, found in many animal products, is the precursor to acetylcholine that’s synthesized through a chemical reaction where acetic acid is esterified from acetyl-CoA and choline. Having sufficient amounts of choline is necessary for the production of acetylcholine. Adult women need 425 milligrams per day while adult men need 550 milligrams per day.

An August 2017 paper published in Nutrients examined the neuroprotective qualities of choline and found that the nutrient is essential for brain development, cognitive performance and resistance to cognitive decline associated with aging and neurodegenerative diseases. While acetylcholine cannot be ingested through dietary sources, choline is found in food sources and can be synthesized to acetylcholine in the body. Rich sources of dietary choline include:

  • Egg yolks
  • Turkey
  • Beef
  • Green split peas
  • Liver
  • Salmon
  • Soybeans
  • Mung beans
  • Lentils

Because acetylcholine is an important neurotransmitter involved in both brain function and health, low levels have been associated with neurological dysfunction. A small clinical trial published in May 2019 in BMC Neurology showed that acetylcholine may slow down the pathogenesis of Alzheimer’s disease while a November 2018 study pubished in the journal of Aging Clinical and Experimental Research found that low levels of acetylcholine in elderly individuals was a contributor to postoperative delirium, marked by notable changes in consciousness, inattention and disordered thinking.

Contrastingly, a December 2015 human imaging study published in the journal of Current Opinion in Neurobiology, suggested that individuals major depressive disorder or bipolar disorder have higher levels of acetylcholine throughout multiple regions of the brain in comparison to healthy subjects.

Accumulation of acetylcholine can cause cramping, increased salivation, exessive tear production, weak muscles, paralysis, diarrhea and blurry vision. The mechanisms behind acetylcholine imbalances are not well understood and continue to be studied.

Other effects of high levels of acetylcholine have been reported after the use of acetylcholinesterase inhibitors, medications that block the breakdown of acetylcholine. In fact, a July 2016 paper published in BioMed Research International documented the use of acetylcholinesterase inhibitors as a protocol for the symptomatic treatment of Alzheimer’s — showing promise for the neurotransmitter.


While eating foods rich in choline doesn’t have adverse reactions, using supplements to boost acetylcholine production is not indicated nor is it safe for everyone. In fact, it may even do more harm than good when contraindications are present. All diagnosing of acetylcholine deficiency or toxicity and subsequent supplementation should only be done under the care of a qualified healthcare provider.

Read more: How Aerobic Exercise Improves Brain Health

Choline | Linus Pauling Institute



  • Choline is a vitamin-like essential nutrient and a methyl donor involved in many physiological processes, including normal metabolism and transport of lipids, methylation reactions, and neurotransmitter synthesis. (More information)
  • Choline deficiency causes muscle damage and abnormal deposition of fat in the liver, which results in a condition called nonalcoholic fatty liver disease. Genetic predispositions and gender can influence individual variation in choline requirements and thus the susceptibility to choline deficiency-induced fatty liver disease. (More information)
  • The recommended adequate intake (AI) of choline is set at 425 milligrams (mg)/day for women and 550 mg/day for men. (More information)
  • Choline is involved in the regulation of homocysteine concentration in the blood through its metabolite betaine. There is currently no convincing evidence that high choline intakes could benefit cardiovascular health through lowering blood homocysteine. Besides, elevated blood concentrations of trimethylamine N-oxide (TMAO), generated from choline, may increase the risk of cardiovascular events. (More information)
  • The need for choline is probably increased during pregnancy. Case-control studies examining the relationship between maternal choline status and risk of neural tube defects (NTDs) have given inconsistent results. It is not yet known whether periconceptual choline supplementation could confer protection against NTDs. (More information)
  • Animal studies have shown that choline is essential for optimal brain development and influences cognitive function in later life. However, in humans, there is not enough evidence to assert that choline supplementation during pregnancy improves offspring’s cognitive performance or that it helps prevent cognitive decline in older people. (More information)
  • Recent intervention studies have found that supplementation with citicoline (a choline derivative) may be useful to limit neurologic damage in stroke patients and improve retinal function in some glaucoma patients. It remains unclear whether citicoline could be used in the treatment of dementias and in head trauma patients. (More information) 
  • De novo choline synthesis in humans is not sufficient to meet their metabolic needs. Good dietary sources of choline include eggs, meat, poultry, fish, cruciferous vegetables, peanuts, and dairy products. (More information)
  • Excessive consumption of choline (≥7,500 mg) has been associated with blood pressure lowering, sweating, fishy body odor, and gastrointestinal side effects. The tolerable upper intake level (UL) for adults is 3,500 mg/day. (More information)

Although choline is not by strict definition a vitamin, it is an essential nutrient. Despite the fact that humans can synthesize it in small amounts, choline must be consumed in the diet to maintain health. The majority of the body’s choline is found in specialized fat molecules known as phospholipids, the most common of which is called phosphatidylcholine (1).


Choline and compounds derived from choline (i.e., metabolites) serve a number of vital biological functions (Figure 1) (1).

Structural integrity of cell membranes

Choline is used in the synthesis of certain phospholipids (phosphatidylcholine and sphingomyelin) that are essential structural components of cell membranes. Phosphatidylcholine accounts for about 95% of total choline in tissues (2). This phospholipid can be synthesized from dietary choline via the cytidine diphosphocholine (CDP-choline) pathway or through the methylation of another phospholipid, phosphatidylethanolamine (Figure 2) (3). Sphingomyelin is a type of sphingosine-containing phospholipid (sphingolipid) that is synthesized by the transfer of a phosphocholine residue from a phosphatidylcholine to a ceramide (Figure 3). Sphingomyelin is found in cell membranes and in the fatty sheath that envelops myelinated nerve fibers. 

Cell signaling

The choline-containing phospholipids, phosphatidylcholine and sphingomyelin, are precursors for the intracellular messenger molecules, diacylglycerol and ceramide. Specifically, sphingomyelinases (also known as sphingomyelin phosphodiestarases) catalyze the cleavage of sphingomyelin, generating phosphocholine and ceramide. Diacylglycerol is released by the degradation of phosphatidylcholine by phospholipases. Other choline metabolites known to be cell-signaling molecules include platelet activating factor (PAF) and sphingophosphocholine. 

Nerve impulse transmission

Choline is a precursor for acetylcholine, an important neurotransmitter synthesized by cholinergic neurons and involved in muscle control, circadian rhythm, memory, and many other neuronal functions. Choline acetyltransferase catalyzes the acetylation of choline to acetylcholine, and acetylcholine esterase hydrolyzes acetylcholine to choline and acetate (4). CDP-choline administration was also found to stimulate the synthesis and release of a family of neurotransmitters derived from tyrosine (i.e., the catecholamines, including noradrenaline, adrenaline, and dopamine) (5). Of note, non-neuronal cells of various tissues and organ systems also synthesize and release acetylcholine, which then binds and stimulates cholinergic receptors on target cells (reviewed in 6).

Lipid (fat) transport and metabolism

Fat and cholesterol consumed in the diet are transported to the liver by lipoproteins called chylomicrons. In the liver, fat and cholesterol are packaged into lipoproteins called very-low-density lipoproteins (VLDL) for transport in the bloodstream to extrahepatic tissues. Phosphatidylcholine synthesis by the phosphatidylethanolamine N-methyltransferase (PEMT) pathway is required for VLDL assembly and secretion from the liver (7, 8). Without adequate phosphatidylcholine, fat and cholesterol accumulate in the liver (see Deficiency). 

Major source of methyl groups

Choline may be oxidized in the liver and kidney to form a metabolite called betaine via a two-step enzymatic reaction. In the mitochondrial inner membrane, flavin adenine dinucleotide (FAD)-dependent choline oxidase catalyzes the conversion of choline to betaine aldehyde, which is then converted to betaine by betaine aldehyde dehydrogenase in either the mitochondrial matrix or the cytosol (2). Betaine is a source of up to 60% of the methyl (CH3) groups required for the methylation of homocysteine (9). Betaine homocysteine methyltransferase (BHMT) uses betaine as a methyl donor to convert homocysteine to methionine in one-carbon metabolism (Figure 4). The ubiquitous vitamin B12-dependent methionine synthase (MS) enzyme also catalyzes the re-methylation of homocysteine, using the folate derivative, 5-methyltetrahydrofolate, as a methyl donor (see Nutrient interactions). Elevated concentrations of homocysteine in the blood have been associated with increased risk of cardiovascular disease (10).


The conversion of choline to betaine is irreversible. Betaine is an osmolyte that regulates cell volume and protect cell integrity against osmotic stress (especially in the kidney). Osmotic stress has been associated with a reduced BHMT expression such that the role of betaine in osmoregulation may be temporarily prioritized over its function as a methyl donor (2).



Men and women fed intravenously (IV) with solutions that contained adequate methionine and folate but lacked choline have been found to develop a condition called nonalcoholic fatty liver disease (NAFLD) and signs of liver damage that resolved when choline was provided (11). The occurrence of NAFLD is usually associated with the co-presentation of metabolic disorders, including obesity, dyslipidemia, insulin resistance, and hypertension, in subjects with metabolic syndrome. NAFLD is estimated to progress to a more severe condition called nonalcoholic steatohepatitis (NASH) in about one-third of NAFLD patients, as well as to increase the risk of cirrhosis and liver cancer (12). 

Because phosphatidylcholine is required in the synthesis of very-low-density lipoprotein (VLDL) particles (see Function), choline deficiency results in impaired VLDL secretion and accumulation of fat in the liver (steatosis), ultimately leading to liver damage. Because low-density lipoprotein (LDL) particles are formed from VLDL particles, choline-deficient individuals also show reduced blood concentrations of LDL-cholesterol (13). Abnormally elevated biomarkers of organ dysfunction in the blood, including creatine phosphokinase, aspartate aminotransferase, and alanine aminotransferase, are corrected upon choline repletion. Choline deficiency-induced organ dysfunction has also been associated with increased DNA damage and apoptosis in circulating lymphocytes (14). In the liver, the accumulation of lipids is thought to impair mitochondrial function, thus reducing fatty acid oxidation and increasing the production of reactive oxygen species (ROS) that trigger lipid peroxidation, DNA damage, and apoptosis. Further, oxidative stress is thought to be responsible for prompting inflammatory processes that can lead to the progression of NAFLD to NASH and cirrhosis (end-stage liver disease) (15). 

An intervention study in 57 healthy adults who were fed choline-deficient diets under controlled conditions found that 77% of men, 80% of postmenopausal women, and 44% of premenopausal women developed fatty liver, liver damage, and/or muscle damage (16). These signs of organ dysfunction resolved upon choline reintroduction in the diet. Because estrogen stimulates the endogenous synthesis of phosphatidylcholine via the phosphatidylethanolamine N-methyltransferase (PEMT) pathway, premenopausal women may be less likely to develop signs of choline deficiency in response to a low-choline diet compared to postmenopausal women (17, 18). Further, a notable single nucleotide polymorphism (SNP; rs12325817) of the PEMT gene, which may affect the expression and/or activity of the PEMT enzyme, is thought to increase the susceptibility to choline deficiency-induced organ dysfunction (17). Additional genetic polymorphisms occurring in choline and one-carbon metabolic pathways may alter the dietary requirement for choline and thus increase the likelihood of developing signs of deficiency when choline intake is inadequate (19-21). The composition of one’s intestinal microbiota has been recently identified as another potential predictor of susceptibility to choline deficiency-induced NAFLD (22). Of note, intestinal microbiota-dependent metabolism of dietary phosphatidylcholine might also be involved in the pathogenesis of cardiovascular disease (see Safety) (23, 24).  

See Disease Prevention for more information on fatty liver diseases.

Nutrient interactions

Together with several B-vitamins (i.e., folate, vitamin B12, vitamin B6, and riboflavin), choline is required for the metabolism of nucleic acids and amino acids, and for the generation of the universal methyl group donor, S-adenosylmethionine (SAM) (see Figure 4 above). SAM is synthesized from the essential amino acid, methionine. Three molecules of SAM are required for the methylation reaction that converts phosphatidylethanolamine into phosphatidylcholine (see Figure 2 above). Once SAM donates a methyl group it becomes S-adenosylhomocysteine (SAH), which is then metabolized to homocysteine. Homocysteine can be converted back to methionine in a reaction catalyzed by vitamin B12-dependent methionine synthase, which requires 5-methyltetrahydrofolate (5-meTHF) as a methyl donor. Alternately, betaine (a metabolite of choline) is used as the methyl donor for the methylation of homocysteine to methionine by the enzyme, betaine-homocysteine methyltransferase (BHMT) (1). Homocysteine can also be metabolized to cysteine via the vitamin B6-dependent transsulfuration pathway (see Figure 4 above). 

Thus, the human requirement for choline is especially influenced by the relationship between choline and other methyl group donors such as folate and S-adenosylmethionine. A low intake of folate leads to an increased demand for choline-derived metabolite, betaine. Moreover, the de novo synthesis of phosphatidylcholine is not sufficient to maintain adequate choline nutritional status when dietary intakes of folate and choline are low (25). Conversely, the demand for folate is increased when dietary supply for choline is limited (26). 

The Adequate Intake (AI)

In 1998, the Food and Nutrition Board (FNB) of the Institute of Medicine established a dietary reference intake (DRI) for choline (27). The FNB felt the existing scientific evidence was insufficient to calculate an RDA for choline, so they set an Adequate Intake (AI; Table 1). The main criterion for establishing the AI for choline was the prevention of liver damage. Yet, common polymorphisms in genes involved in choline or folate metabolism alter one’s susceptibility to choline deficiency and thus may affect dietary requirements for choline (see Deficiency) (17, 19).

Table 1. Adequate Intake (AI) for Choline
Life Stage Age Males
Infants 0-6 months 125 125
Infants 7-12 months 150 150
Children 1-3 years 200 200
Children 4-8 years 250 250
Children 9-13 years 375 375
Adolescents 14-18 years 550 400
Adults 19 years and older 550 425
Pregnancy all ages 450
Breast-feeding all ages 550

Disease Prevention

Cardiovascular disease

Choline and homocysteine

A large body of research indicates that even moderately elevated levels of homocysteine in the blood increase the risk of cardiovascular disease (CVD) (10). The most common cause of a myocardial infarction or a stroke is the rupture of atherosclerotic plaques in arterial walls causing blood clot formation (thrombogenesis). High homocysteine concentrations may promote the development of atherosclerosis (atherogenesis) and thrombogenesis via mechanisms involving oxidative stress and endothelial dysfunction, inflammation, abnormal blood coagulation, and disordered lipid metabolism (reviewed in 28). 

Once formed from dietary methionine, homocysteine can be catabolized to cysteine via the transsulfuration pathway or re-methylated to methionine (see Figure 4 above). Folate and choline are involved in alternate pathways that catalyze the re-methylation of homocysteine (see Nutrient interactions). Specifically, choline is the precursor of betaine, which provides a methyl group for the conversion of homocysteine to methionine via the enzyme, betaine-homocysteine methyltransferase (BHMT). While the amount of homocysteine in the blood is regulated by several nutrients, including folate and choline, conditions that cause damage to the liver like nonalcoholic steatohepatitis (NASH) may also affect homocysteine metabolism (29).  

Dietary intakes of choline and betaine and CVD

Because both folate- and choline-dependent metabolic pathways catalyze the re-methylation of homocysteine, dietary intakes of both nutrients need to be considered when the association between homocysteine concentrations and cardiovascular disease is assessed. Yet, despite its relevance, the relationship of betaine and choline to homocysteine metabolism has been only lightly investigated in humans, essentially because the choline content of foods could not be accurately measured until recently. In preliminary intervention studies, pharmacologic doses of betaine (1,500 to 6,000 mg/day) were found to reduce blood homocysteine concentrations in a small number of volunteers with normal-to-mildly elevated homocysteine concentrations (30-33). Yet, in a cross-sectional analysis of a large cohort of 16,165 women (ages, 49-79 years), lower betaine doses in the range of dietary intakes were not found to be correlated with homocysteine concentrations (34). This study also showed that levels of choline intake were inversely associated with homocysteine concentrations in the blood. However, an eight-year follow-up study of the cohort failed to show any difference in cardiovascular risk between women in the upper versus bottom quartile of dietary choline intakes (>329 mg/day vs. ≤266 mg/day) (34). The prospective study of the Atherosclerosis Risk in Communities (ARIC) cohort found that the highest vs. lowest quartile (>486 mg/day vs. <298 mg/day) of total choline intakes from food was not significantly associated with the incidence of coronary artery disease in 14,430 middle-aged participants (35). Also, in a recent analysis of the Health Professionals Follow-up Study (HPFS) that enrolled 44,504 men for a period of 24 years, the risk of peripheral artery disease was positively correlated with homocysteine concentrations but neither with betaine nor choline levels of intake (36).

While further research is indicated, convincing evidence that increased dietary intake of choline or betaine could benefit cardiovascular health through lowering homocysteine concentrations in the blood is presently lacking.

Circulating concentrations of choline and betaine and CVD risk

A 1995 study had found that elevated blood homocysteine concentrations in patients who experienced a vascular occlusion were associated with higher urinary excretion of betaine, rather than with reduced intake of choline or betaine or diminished activity of BHMT (37). In a recent prospective study, high urinary betaine excretion was also associated with increased risk of heart failure in 325 nondiabetic subjects who have been hospitalized for acute coronary syndrome (38). In the same study, both top and bottom quintiles of plasma betaine concentrations were associated with an increased risk of secondary acute myocardial infarction. The findings of another prospective study (the Hordaland Health Study) that followed 7,045 healthy adults (ages, 47-49 years and 71-74 years) suggested that high choline and low betaine plasma concentrations were associated with an unfavorable cardiovascular risk profile (39). Indeed, plasma choline was positively associated with a number of cardiovascular risk factors, such as BMI, percentage body fat, waist circumference, and serum triglycerides, and inversely associated with HDL-cholesterol. On the contrary, plasma betaine was positively correlated to HDL-cholesterol and inversely associated with the above-mentioned risk factors as well as with systolic and diastolic blood pressure. More recent studies now suggest that the blood concentration of trimethylamine N-oxide (TMAO), generated from trimethylamine-containing nutrients like dietary choline, rather than that of choline, might influence the risk of cardiovascular events (see Safety).

It is not yet clear whether concentrations of choline, betaine, and/or TMAO in the blood can predict the risk for cardiovascular disease.

Liver diseases

Fatty liver diseases

While a choline-deficient diet results in organ dysfunction and nonalcoholic fatty liver disease (NAFLD) (see Deficiency; 16), it is not known whether suboptimal dietary choline intakes in healthy subjects may contribute to an increased risk for NAFLD. A cross-sectional analysis of two large prospective studies conducted in China – the Shanghai Women’s Health Study and the Shanghai Men’s Health Study – including 56,195 people (ages, 40-75 years), was recently conducted to assess the association between dietary choline intakes and self-reported diagnosis of fatty liver disease (40). The highest versus lowest quintile of choline intake (412 mg/day vs. 179 mg/day) was associated with a 28% lower risk of fatty liver disease in normal-weight women, but no association was found in overweight or obese women or in men. Another cross-sectional study of 664 individuals with NAFLD or nonalcoholic steatohepatitis (NASH) also reported that disease severity was inversely correlated with dietary choline intakes in postmenopausal women, but not in premenopausal women, men, or children (41). 

Liver cancer

In animal models, dietary choline deficiency has been associated with an increased incidence of spontaneous liver cancer (hepatocellular carcinoma) and increased sensitivity to carcinogenic chemicals (9). A number of mechanisms have been proposed to contribute to the cancer-promoting effects of choline deficiency: (1) enhanced liver cell regeneration and tissue sensitivity to chemical insults; (2) altered expression of numerous genes regulating cell proliferation, differentiation, DNA repair, and apoptosis due to improper DNA methylation; (3) increased likelihood of DNA damage caused by mitochondrial dysfunction-induced oxidative stress; and (4) activated protein kinase C-mediated cell-signaling cascade, eventually leading to an increase in liver cell apoptosis (2). Yet, it is not known whether choline deficiency can increase the susceptibility to cancer in humans (2).

Neural tube defects

It is known that folate is critical for normal embryonic development, and maternal supplementation with folic acid decreases the incidence of neural tube defects (NTDs) (42). NTDs include various malformations, such as lesions of the brain (e.g., anencephaly, encephalocele) or lesions of the spine (spina bifida), which are devastating and usually incompatible with life (43). These defects occur between the 21st and 28th days after conception, a time when many women do not realize that they are pregnant (44). While the protective effect of folate against NTD is well established, only a few studies have investigated the role of other methyl group donors, including choline and betaine, in the occurrence of NTDs. A case-control study (424 NTD cases and 440 controls) found that women in the highest versus lowest quartile of periconceptual choline intake (>498.46 mg/day vs. ≤290.41 mg/day) had a 51% lower risk of an NTD-affected pregnancy (45). However, more recent studies failed to find an inverse relationship between maternal choline intake and risk of NTDs (46, 47). Another case-control study (80 NTD-affected pregnancy and 409 controls) in US women found that the lowest concentrations of serum choline (<2.49 mmol/L) during mid-pregnancy were associated with a 2.4-fold higher risk of NTDs (48). Finally, a more recent study, including 71 NTD-affected pregnancies, 214 pregnancies with non NTD malformations, 98 normal pregnancies in women with prior NTD-affected pregnancies, and 386 normal pregnancies, found no associations between maternal blood concentrations of choline during pregnancy, choline- and folate-related genetic variants, and risk of NTDs (49). However, it is important to note that circulating choline concentrations do not accurately reflect dietary intake of choline.

More research is needed to determine whether supplemental choline could add to the protective effect currently being achieved by periconceptual folic acid supplementation.

Cognitive health

Neuro-cognitive development

Increased dietary intake of cytidine 5’-diphosphocholine (CDP-choline or citicoline, a precursor of phosphatidylcholine; see Figure 2 above) very early in life can diminish the severity of memory deficits in aged rats (50). Choline supplementation of the mothers of unborn rats, as well as rat pups during the first month of life, led to improved performance in spatial memory tests months after choline supplementation had been discontinued (51). A review by McCann et al. discusses the experimental evidence from rodent studies regarding the availability of choline during prenatal development and cognitive function in the offspring (52).  

Because of the importance of DNA methylation in normal brain development, neuronal functions, and cognitive processes (53), methyl donor nutrients like choline are essential for optimal brain functioning. However, clinical evidence to determine whether findings in rodent studies are applicable to humans is currently limited. Recently, the analysis of the Seychelles Child Development Nutrition Cohort study reported a lack of an association between plasma concentrations of choline and its related metabolites and cognitive abilities in 256 five-year-old children. Only plasma betaine concentrations were found to be positively correlated with preschool language test scores (54). Yet, because circulating concentrations of choline are not directly related to dietary choline intakes, the study could not evaluate whether maternal choline intakes influence children’s brain development. 

Project Viva is an ongoing prospective study that has examined the relationship between daily intakes of methyl donor nutrients in 1,210 women during pregnancy and child cognition at three and seven years postpartum. Maternal intake of choline during the first and/or second trimester of pregnancy was not correlated with measures of cognitive performance in children at age 3 years (55). Another report of the study indicated that upper vs. lower quartile of maternal choline intakes during the second trimester of pregnancy (median intakes, 392 mg/day vs. 260 mg/day) was significantly associated with higher visual memory scores in children aged 7 years old (56). Recently, a small randomized, double-blind, placebo-controlled trial in 99 pregnant women (ages, 21-41 years old) evaluated the effect of choline supplementation during pregnancy and lactation on infants’ cognitive function at ages 10 and 12 months (57). The results indicated that maternal choline supplementation (750 mg/day of choline in the form of phosphatidylcholine) from 18 weeks of gestation to 3 months’ postpartum provided no cognitive benefits in children regarding short-term visio-spatial memory, long-term episodic memory, and language and global development.  

Cognitive function in older adults

Cognitive function, including the domains of memory, speed, and executive function, decline gradually with increasing age. The rate of cognitive decline is also influenced by modifiable risk factors like dietary habits. Deficiency in B-vitamins and elevated homocysteine concentrations in the blood have been associated with cognitive impairments in the elderly. Yet, a recent meta-analysis of 11 trials indicated that homocysteine lowering using B-vitamin supplementation fails to limit cognitive decline or improve cognitive performance in older adults (58). The cross-sectional data analysis of a subgroup of 1,391 volunteers (ages, 36-83 years) from the large Framingham Heart Study Offspring cohort has indicated that dietary choline intake was positively associated with specific cognitive functions, namely verbal memory and visual memory (59). Another cross-sectional study of 2,195 individuals (ages, 70-74 years) from the Hordaland Health Study examined cognitive abilities and blood concentrations of various determinants of circulating homocysteine, including choline and betaine (60). Unlike betaine, high vs. low plasma concentrations of free choline (>8.36 mcmol/L vs. ≤8.36 mcmol/L) were found to be significantly associated with a greater performance at cognitive tests assessing sensory motor speed, perceptual speed, executive function, and global cognition. However, in an earlier intervention study that enrolled 235 elderly individuals (mean age, 81 years old) with or without mild vitamin B12 deficiency, baseline concentrations of betaine − but not choline − were found to be positively correlated to test scores evaluating the cognitive domains of construction, sensory motor speed, and executive function (61). 

More research is needed to determine the effect of choline on the developing brain and whether choline intakes above the RDA may be useful in the prevention of memory loss or dementia in humans.

Disease Treatment

Cerebrovascular diseases

Cerebrovascular diseases (including stroke and sub-acute ischemic cerebrovascular disease) are the main cause of cognitive impairments in older people. Results from experimental studies have suggested that pharmacological doses of citicoline (CDP-choline) could enhance the metabolism of glucose and the biosynthesis of phospholipids and neurotransmitters, while limiting the degradation of phospholipids in neuronal membranes in models of ischemia and neurodegenerative diseases (reviewed in 62). Many short-term intervention studies in older individuals with vascular diseases have found that therapeutic doses of citicoline given either orally, by intramuscular injection, or by intravenous infusion, resulted in improvements in neuropsychological functions, including cognitive, emotional, and behavioral functions (reviewed in 5).

A six-month, multicenter observational study enrolled 197 stroke subjects (mean age, 81.5 years) with a progressive decline of their mental health and general confusion and/or stupor who were initially administered citicoline for 5 or 10 days (2,000 mg/day, by intravenous infusion) within a four-month period, and then for 21 days (1,000 mg/day, by intramuscular injection), repeated once after a seven-day washout period (63). Citicoline treatment was found to be associated with higher scores on cognitive and functional evaluation scales when compared to baseline measurements. However, only randomized controlled trials would be able to assess whether citicoline is protective against vascular damage and cognitive impairment in elderly adults with complex geriatric symptoms. 

The International Citicoline Trial on acUte Stroke (ICTUS) is a multicenter and double-blind study that assessed the effect of supplementing 2,298 patients with acute ischemic stroke with citicoline (2,000 mg/day) or a placebo for six weeks on several functional and neurologic outcomes and on mortality rate (64). The results showed no difference between treatment groups after a 90-day follow-up period. Only subgroup analyses found significant benefits of citicoline in patients older than 70 years, in those with moderate rather than severe strokes, and in those not treated with recombinant tissue plasminogen activator (rtPA; standard-of-care treatment). An earlier meta-analysis of small randomized, placebo-controlled trials had reported a positive impact of citicoline (1,000 mg/day, administered for 28 days to 12 months) on memory and behavior in subjects with cognitive deficits associated with cerebrovascular disorders (65). The effect of citicoline was also evaluated in a recent multicenter, open-label, controlled trial (IDEALE trial) in Italian elderly adults (ages, 65-94 years) with evidence of vascular lesions on neuroradiology and mild-to-moderate cognitive deficits, as assessed by Mini-Mental State Examination (MMSE; scores ≥21) (66). Three hundred and forty-nine participants received oral citicoline (1,000 mg/day) or no treatment for nine months. MMSE scores in citicoline-treated individuals remained unchanged while they significantly deteriorated in untreated patients such that MMSE scores between groups were found to be significantly different after three and nine months of treatment. No significant effect was reported in measures of functional autonomy, mood, and behavioral disorders. Another recent open-label, randomized, controlled trial evaluated the effect of citicoline (1,000 mg/day for 12 months) in 347 subjects (mean age, 67.2 years) who suffered an acute stroke. The results demonstrated that citicoline significantly limited cognitive impairments in the domains of attention and executive functions and temporal orientation at 6 and 12 months post-stroke in treated compared to untreated patients (67).

Neurodegenerative diseases


Neurodegenerative diseases, such as Alzheimer’s disease (AD) and Parkinson’s disease (PD), are characterized by progressive cognitive decline and dementia. Dysfunctions in neurotransmitter signaling, affecting cholinergic and dopaminergic pathways in particular, have been involved in the occurrence of cognitive impairments. Deficits in acetylcholine and abnormal phospholipid metabolism have been reported in postmortem studies of the brains of AD patients (11). For these reasons, inhibitors of (acetyl) cholinesterase (which catalyzes the breakdown of acetylcholine) and large doses of lecithin (phosphatidylcholine) have been used to treat patients with dementia due to AD in hopes of raising the amount of acetylcholine available in the brain. While cholinesterase inhibitors have shown positive effects on cognitive functions and measures of clinical global state (68), a systematic review of randomized controlled trials did not find lecithin to be more beneficial than placebo in the treatment of patients with cognitive impairment, vascular dementia, AD, or mixed dementia (69). Limited data are available to assess whether citicoline (CDP-choline) might improve cognitive performance in subjects with AD (70). No recent trial has investigated the effect of citicoline in PD patients.


Optic neuropathies, including glaucoma, are associated with damage of the optic nerve and loss of visual function. In glaucoma, the progressive deterioration of the optic nerve is caused by loss of a specific neuronal population known as retinal ganglion cells (RGC), such that the condition has been classified as a neurodegenerative disease (71). In a small, double-blind, placebo-controlled study, the effect of citicoline was assessed in 24 subjects affected by open-angle glaucoma and treated with β-blockers. Patients were randomized to follow a therapeutic cycle for a total period of eight years: citicoline (1,000 mg/day, by intramuscular injection) or placebo (β-blockers alone) for a two-month period followed by a four-month washout period (72). Electrophysiological examinations were used to assess the extent of visual dysfunctions, including the simultaneous recordings of Pattern ElectroRetinoGrams (PERG) and Visual Evoked Potentials (VEP). Citicoline was found to enhance retinal function and neural conduction along post-retinal visual pathways, such that responses of the visual cortex to stimuli were significantly improved compared to placebo. 

In a similar pilot trial, citicoline efficacy was assessed in 26 volunteers (mean age, 65.4 years) affected by another type of optic neuropathy known as non-arteritic anterior ischemic optic neuropathy (NAION). Oral citicoline (1,600 mg/day) was given for 60 days followed by 60 days of washout, and the therapeutic cycle was repeated once. Compared to placebo, citicoline was found to improve retinal function and post-retinal neural conduction, evidenced by PERG and VEP measures (73). Oral citicoline (four cycles of 500 mg/day for four months followed by a two-month washout period) was also found to significantly reduce the rate of visual field loss and the level of intraocular pressure in 41 patients with progressive glaucoma (74). Larger randomized controlled trials are needed to establish whether citicoline supplementation could be included in the medical treatment of glaucoma. 

Traumatic brain injury

For decades, pre-clinical and small clinical studies have investigated the effect of citicoline in the management of patients sustaining a traumatic brain injury (TBI). A systematic review of clinical data suggested that citicoline could hasten the resorption of cerebral edema and improve the recovery of consciousness and neurologic disorders in severe TBI cases (classified by Glasgow Coma Scale [GCS] scores of ≤8). Citicoline also appeared to limit memory deficits and the duration and severity of other post-traumatic symptoms (e.g., headache, dizziness, attention disorder) in TBI patients with mild-to-moderate injuries (GCS scores, 9-15) (reviewed in 5). Although citicoline is currently included in TBI therapeutic regimen in 59 countries, only one multicenter, randomized, double-blind, placebo-controlled trial has recently been conducted in the US. The CiticOline Brain Injury Trial (COBRIT) has enrolled 1,213 patients with mild-to-severe TBI and assessed the effect of enteral or oral citicoline (2,000 mg/day, for 90 days) on functional and cognitive outcomes (measured by components of the TBI Clinical Trials Network Care Battery) (75). No significant benefits of citicoline supplementation over placebo were found at 90 days (end of treatment period) and 180 days. A Cochrane review of the effect of citicoline in the treatment of TBI should be available soon (76).


De novo synthesis (biosynthesis)

Humans can synthesize choline moieties in small amounts by converting phosphatidylethanolamine into phosphatidylcholine (see Figure 2 above). Three methylation reactions catalyzed by phosphatidylethanolamine N-methyltransferase (PEMT) are required, each using S-adenosylmethionine (SAM) as a methyl group donor. Choline is generated endogenously when the methylation of phosphatidylethanolamine is coupled with the catabolism of newly formed phosphatidylcholine by phospholipases. This is referred to as de novo synthesis of choline. The substitution of choline by serine in the synthesis of phosphatidylserine from phosphatidylcholine by phosphatidylserine synthase-1 also releases choline (4). Because phosphatidylcholine metabolism is a source of endogenous choline, the nutrient was not initially classified as essential (1). Yet, de novo choline synthesis in humans is not sufficient to meet their metabolic needs such that healthy humans fed choline-deficient diets develop fatty liver, liver damage, and/or muscle damage (see Deficiency). 

Food sources

In the US, mean dietary intakes of choline are well below the recommended AI. According to a US national survey, NHANES 2007-2008, mean dietary intakes of choline were approximately 260 mg/day for women and 396 mg/day for men (77). In a 14-year US prospective study, including over 14,000 middle-aged participants, mean daily intakes of choline were 294 mg and 332 mg in women and men, respectively (35). Eggs, liver, and peanuts, are especially rich in choline (27). Major contributors to choline in the American diet are meat, poultry, fish, dairy foods, pasta, rice, and egg-based dishes (77). Spinach, beets, wheat, and shellfish are also good sources of the choline metabolite, betaine (78). Betaine cannot be converted back to choline but can spare some choline requirements for homocysteine remethylation (1). Phosphatidylcholine, which contains about 13% choline by weight, is the main form of choline in dietary products (79). Lecithin extracts, which comprise a mixture of phosphatidylcholine and other phospholipids, are often added during food processing. Lecithins in processed food have been estimated to increase the daily consumption of phosphatidylcholine by about 1.5 mg/kg of body weight for adults (27). 

Strict vegetarians, who consume no meat, milk, or eggs, may be at risk for inadequate choline intake. The total choline contents of some choline-containing foods are listed in milligrams (mg) in Table 2. For more information on the nutrient content of specific foods, search the USDA food composition website or the USDA documentation on the choline content of common foods.

Table 2. Some Food Sources of Choline
Food Serving Total Choline (mg)
Beef liver, pan fried 3 ounces* 356
Wheat germ, toasted 1 cup 202
Egg 1 large 147
Beef, trim cut, cooked 3 ounces 97
Scallop, cooked, steamed 3 ounces 94
Salmon, pink, canned 3 ounces 75
Chicken, breast, cooked, roasted 3 ounces 73
Atlantic cod, cooked 3 ounces 71
Shrimp, canned 3 ounces 69
Brussel sprouts, cooked, boiled 1 cup 63
Broccoli, cooked, boiled 1 cup, chopped 63
Milk, skim 8 fluid ounces 38
Peanut butter, smooth 2 tablespoons 20
Milk chocolate 1.5-ounce bar 20
Peanuts 1 ounce 15
*A three-ounce serving of meat or fish is about the size of a deck of cards.


CDP-choline (citicoline) and choline salts, such as choline chloride and choline bitartrate, are available as supplements. Phosphatidylcholine supplements also provide choline; however, choline comprises only about 13% of the weight of phosphatidylcholine (79). Therefore, a supplement containing 4,230 mg (4.23 grams) of phosphatidylcholine would provide 550 mg of choline. Although the term “lecithin” is synonymous with phosphatidylcholine when used in chemistry, commercial lecithins are usually prepared from soybean, sunflower, and rapeseed, and may contain anywhere from 20%-90% of phosphatidylcholine. Egg yolk lecithin is a more unlikely source of lecithin in dietary supplements. Moreover, the nature of phosphatidylcholine-containing fatty acids depends on whether lecithin is produced from vegetable, animal, or microbial sources. In particular, soybean lecithin is richer in polyunsaturated fatty acids than egg yolk lecithin (80).



High doses (10,000 to 16,000 mg/day) of choline have been associated with a fishy body odor, vomiting, salivation, and increased sweating. The fishy body odor results from excessive production and excretion of trimethylamine, a metabolite of choline. In the inherited condition, primary trimethylaminuria (also known as “fish odor syndrome”; see the article on Riboflavin), a defective flavin containing monooxygenase 3 (FMO3) enzyme results in impaired oxidation of trimethylamine in the liver. Disease management includes the use of choline-restricted diets in affected individuals (81).

Taking large doses of choline in the form of phosphatidylcholine (lecithin) does not generally result in fishy body odor, because its metabolism results in little trimethylamine. A dose of 7,500 mg/day of choline was found to have a slight blood pressure lowering (hypotensive) effect, which could result in dizziness or fainting. Choline magnesium trisalicylate at doses of 3,000 mg/day has resulted in impaired liver function, generalized itching, and ringing of the ears (tinnitus). However, it is likely that these effects were caused by the salicylate, rather than the choline in the preparation (27).

In 1998, the Food and Nutrition Board (FNB) of the Institute of Medicine established the tolerable upper intake level (UL) for choline at 3,500 mg/day for adults (Table 3). This recommendation was based primarily on preventing hypotension (low blood pressure), and secondarily, on preventing the fishy body odor due to increased excretion of trimethylamine. The UL was established for generally healthy people, and the FNB noted that individuals with liver or kidney disease, Parkinson’s disease, depression, or inherited trimethylaminuria might be at increased risk of adverse effects when consuming choline at levels near the UL (27).

Table 3. Tolerable Upper Intake Level (UL) for Choline
Age Group UL (mg/day)
Infants 0-12 months Not possible to establish*
Children 1-8 years 1,000
Children 9-13 years 2,000
Adolescents 14-18 years 3,000
Adults 19 years and older 3,500
*Source of intake should be food and formula only.
Do high choline intakes and/or phosphatidylcholine supplements increase the risk for cardiovascular disease?

Oral supplementation with phosphatidylcholine (250 mg of total choline from food plus 250 mg of supplemental phosphatidylcholine) has been found to result in detectable concentrations of trimethylamine and trimethylamine N-oxide (TMAO) in the blood (23). The intestinal microbiota is directly implicated in the generation of trimethylamine from dietary choline, phosphatidylcholine, and carnitine. Trimethylamine is subsequently converted into TMAO by flavin-containing monooxygenases in the liver. The prospective study that followed 4,007 individuals,with or without cardiovascular disease (CVD) for a three-year period found baseline concentrations of circulating TMAO to be positively correlated with incidence of death, nonfatal myocardial infarction, and stroke − described as major adverse cardiac events (MACE) (23). In the same cohort, MACE risk was found to be about 30% higher in individuals in the highest vs. lowest quartile of choline or betaine plasma concentrations (82). However, depending on gut microbiota composition, the risk of having an adverse cardiovascular event may be lower in individuals with low vs. high circulating TMAO even though choline and/or betaine concentrations in the blood are elevated (82). 

Elevated TMAO concentrations have been reported in subjects at increased risk of CVD, such as those with diabetes mellitus (83) or end-stage renal disease (chronic kidney failure) (84), and in patients with cardiac insufficiency (chronic heart failure) (85). Yet, in the latter patients, high plasma concentrations of choline, betaine, and TMAO were not associated with a poorer survival rate after five years of follow-up (85). Finally, supplementation with choline, TMAO, or betaine was found to result in the formation of macrophage-derived foam cells in atherosclerosis-prone mice (24). Foam cells are known to contribute to the development of atherosclerotic lesions (i.e., atherogenesis) by accumulating excessive amounts of lipids within the arterial walls and triggering the secretion of pro-inflammatory cytokines. 

Further research is needed to understand how the composition of intestinal microbiota influences the metabolic fate of ingested choline. At present, there is no evidence that dietary choline increases the risk of cardiovascular events.

Drug interactions

Methotrexate, a medication used in the treatment of cancer, psoriasis, and rheumatoid arthritis, inhibits the enzyme dihydrofolate reductase and therefore limits the availability of methyl groups donated from folate derivatives. Rats given methotrexate have shown evidence of diminished nutritional status of choline and greater drug adverse reactions due to liver dysfunction (11, 86). Thus, individuals taking methotrexate may have an increased choline requirement. Treatments with a family of lipid-lowering drugs known as fibrates (e.g., fenofibrate, bezofibrate) have been associated with an increased excretion of betaine in the urine and a rise in homocysteine concentration in the blood of patients with diabetes mellitus or metabolic syndrome (87, 88). If the benefits of fibrate therapy are indeed mitigated by fibrate-induced betaine deficiency, the use and safety of supplementing patients with betaine would need to be considered (89).

Linus Pauling Institute Recommendation

Little is known regarding the amount of dietary choline required to promote optimum health or prevent chronic diseases in humans. The Linus Pauling Institute supports the recommendation by the Food and Nutrition Board of 550 mg/day for adult men and 425 mg/day for adult women. A varied diet should provide enough choline for most people, but strict vegetarians who consume no milk or eggs may be at risk of inadequate choline intake. 

Older adults (>50 years)

Little is known regarding the amount of dietary choline most likely to promote optimum health or prevent chronic diseases in older adults. At present, there is no evidence to support a different recommended intake of choline from that of younger adults (550 mg/day for men and 425 mg/day for women).

Authors and Reviewers

Originally written in 2000 by:
Jane Higdon, Ph.D.
Linus Pauling Institute
Oregon State University

Updated in May 2003 by:
Jane Higdon, Ph.D.
Linus Pauling Institute
Oregon State University

Updated in January 2008 by:
Victoria J. Drake, Ph.D.
Linus Pauling Institute
Oregon State University

Updated in August 2009 by:
Victoria J. Drake, Ph.D.
Linus Pauling Institute
Oregon State University

Updated in January 2015 by: 
Barbara Delage, Ph.D. 
Linus Pauling Institute 
Oregon State University

Reviewed in February 2015 by:
Steven H. Zeisel, M.D., Ph.D.
Professor and Chair of Nutrition
School of Public Health
The University of North Carolina, Chapel Hill

Copyright 2000-2021  Linus Pauling Institute


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Choline (vitamin B4)

Chemical structure and properties

Choline – aminoethyl alcohol containing 3 methyl groups at the nitrogen atom.

Choline is a syrupy liquid with strong alkaline properties.


Choline comes from food. It is partially destroyed by the intestinal microflora (with the formation of trimethylamine). With a high content of choline in the diet, it is absorbed by diffusion, with a low content, by active transport. In enterocytes, choline is phosphorylated.

From the intestine, phosphocholine (and partially free choline) in the composition of lipoproteins with the blood is carried to the tissues, where it is included in the metabolism.

Biochemical functions:

  • Choline is the metabolic precursor of the important neurotransmitter acetylcholine.

  • Phosphocholine, activated by CDP, is used to synthesize phosphatidylcholine (lecithin). In addition to participating in the synthesis of lecithin, choline is required for the synthesis of another lipid – sphingomyelin, which is formed by the transfer of choline from phosphatidylcholine to ceramide.

  • Choline is a donor of methyl groups in transmethylation reactions (for example, betaine formed during the oxidation of choline serves as a source of methyl groups in methionine synthesis reactions).


The manifestation of choline deficiency in humans has not been described. In animals, fatty liver infiltration, renal hemorrhages and damage to blood (especially coronary) vessels are noted.

Food Sources

Dietary sources of choline are meat and grains.

T.S. Morozkina, A.G. Moiseyonok Vitamins. A short guide for physicians and students of medical, pharmaceutical and biological specialties.

Cholinesterase (S-Pseudocholinesterase, cholinesterase II, S-ChE, acylcholine acylhydrolase, Cholinesterase)

Method of determination

Kinetic colorimetric method.

Study material
Blood serum

The study of cholinesterase in blood serum is used to assess liver function, diagnose poisoning with organophosphate insecticides, identify congenital deficiency to assess the risk of using certain drugs.

Synonyms: Serum cholinesterase; Cholinesterase II; Butyrylcholinesterase;


Brief characteristics of the analyte Cholinesterase

Cholinesterase is an enzyme of the hydrolase class that catalyzes the cleavage of the acyl group from various choline esters, including acetylcholine.

There are two related species of cholinesterase that have the ability to hydrolyze acetylcholine.

The first type is acetylcholinesterase, also called “true cholinesterase”, or cholinesterase I. True cholinesterase is found in erythrocytes, lungs and spleen, in nerve endings and gray matter of the brain.Rapid hydrolysis of acetylcholine by true cholinesterase is an important stage in the transmission of nerve impulses through the synapse.

The second type of enzyme (synonyms: pseudocholinesterase, serum cholinesterase, cholinesterase II) is found in the liver, pancreas, heart, white matter of the brain and blood serum (where it significantly predominates over cholinesterase I). Pseudocholinesterase hydrolyzes acetylcholine less efficiently than type 1 cholinesterase; the exact physiological role of this enzyme is still not well understood.Among the clinical manifestations of the rare deficiency of pseudocholinesterase in the blood plasma due to abnormal genetic variants of this enzyme, only hypersensitivity to some medicinal substances is noted. The source of serum cholinesterase is the liver.

Under what conditions can the level of cholinesterase decrease

Serum cholinesterase is used in clinical diagnostics. Serum cholinesterase is produced in the liver and can be considered as one of the markers of its protein-synthesizing function in dystrophic and cytolytic changes (similar to albumin and prothrombin).Cholinesterase activity is reduced in hepatitis, cirrhosis, liver metastases, liver damage in heart failure, hepatic amebiasis. The degree of decrease in cholinesterase activity correlates with the severity of the disease, which makes it possible to use the test as a prognostic test in patients with liver pathologies and to monitor the effectiveness of treatment.

Organophosphorus compounds (for example, chlorophos, dichlorvos, parathion, tetraethyl pyrophosphate) inhibit serum cholinesterase.Decreased cholinesterase activity is an indicator of insecticide poisoning.

Of clinical interest are atypical (genetic) variants of cholinesterase with reduced activity against acetylcholine and other substrates. Cholinesterase normally hydrolyzes some muscle relaxants used during surgery. In patients with an atypical variant of cholinesterase, due to its low activity, the destruction of muscle relaxants takes a long time and a period of prolonged paralysis of the respiratory muscles may occur, requiring mechanical ventilation.

For what purpose is the level of cholinesterase in serum determined?

Measurement of serum cholinesterase activity is used to assess liver function, as an indicator of possible insecticide poisoning, and to identify patients with atypical forms of the enzyme who are at risk of prolonged exposure to muscle relaxants used in surgical procedures.

What else can affect the result of a blood test for cholinesterase

The activity of the enzyme is reduced in late pregnancy, in conditions with a low level of serum albumin (for example, with malabsorption syndrome), the effect of the drugs used is possible (see.(See Interpretation section.)

Taking medications from the group of cholinesterase inhibitors.

Acetylcholine “brought to clean water”

Scientists of the Institute of Chemistry of Solutions of the Russian Academy of Sciences and the Institute of Theoretical and Experimental Biophysics of the Russian Academy of Sciences have modeled what role water can play in the biological activity of acetylcholine, the first open neurotransmitter. The research results are published in the Journal of Molecular Liquids.

The human brain consists of hundreds of billions of neurons, each of which interacts with thousands of similar ones.There are about a trillion such connections in total. Thanks to them, we think and learn, rejoice and sad, move and fall asleep. Communication of nerve cells with each other is provided by mediators – neurotransmitters (neurotransmitters). Through special communication nodes – synapses – they transmit nerve impulses from neuron to neuron. And if these “couriers” for some reason lose their activity, the person immediately feels it. It is known, in particular, that disruptions in the work of acetylcholine – a neurotransmitter involved in the transmission of nervous excitation in the central and peripheral nervous system (also called a memory molecule) – can lead to the development of Alzheimer’s disease.If science answers the questions why this neurotransmitter sometimes loses its working form and how to make it perform its functions, the key will be found to control its behavior, and therefore, to control the development of neurodegenerative diseases.

A group of scientists from the Institute of Chemistry of Solutions of the Russian Academy of Sciences, together with colleagues from the Institute of Theoretical and Experimental Biophysics of the Russian Academy of Sciences, have found new opportunities for studying the structural environment of acetylcholine in water. To do this, they used the methods of statistical mechanics.

What role does water play in the biological activity of neurotransmitters? The fact is that these “agents” begin to act after they bind to cellular targets – receptors. Before that can happen, however, neurotransmitters enter the synaptic cleft, the water-filled space within the synapse. There they interact with water molecules, that is, they enter the process of hydration, as a result of which they can change their spatial structure. This presumably affects their biological activity.In recent works by Canadian scientists, it is suggested that hydration affects the rapid metabolism of neurotransmitters in the synaptic cleft and their reuptake by nerve endings.

However, until now the hydration of neurotransmitters has been little studied, no calculations have been presented to prove its effect on the behavior of acetylcholine. For the first time, Russian researchers investigated the hydration environment of various conformers of the memory neurotransmitter in water and showed that the difference in their hydration is determined by their spatial configuration.The neurotransmitter, like most biomolecules, does not have a solidified form. Depending on what conformation it takes, its capabilities also change. So, the acetylcholine molecule can be “unfolded” – in this form it easily penetrates into the membrane area and binds to the muscarinic receptor transmitting impulses, and “folded”, capable of penetrating only to the extracellular site of the nicotinic receptor binding without interacting with the membrane itself. Prior to the study by scientists from the Institute of Chemical Chemistry of the Russian Academy of Sciences and ITEB RAS, it was not known why the neurotransmitter approaches receptors in one form or another.His results showed that the main role in its transformation is played by hydration – the interaction of a neurotransmitter with water molecules.

“You can run towards another person with outstretched arms or clenched fists. Naturally, the result of the meeting will be different depending on your “conformation”. However, your behavior and condition will be very different from where you meet, in a crowd or in a forest. It is the same with hydration, it may not allow you to open your arms wide, ”explains Gennady Chuev, one of the authors of the study, a leading researcher at the Laboratory of Excitable Media at the Institute of Theoretical and Experimental Biophysics of the Russian Academy of Sciences.

Scientists believe that the results obtained help to understand the molecular mechanisms of binding of neurotransmitters to receptors on the membrane and, ultimately, will make it possible to identify ways of controlling this process.

Dietary supplement to food, royal jelly with ginseng

Dietary supplement to food, royal jelly with ginseng

Especially revered product in China. Strengthens the body, improves blood circulation.Effective for the prevention of inflammatory and malignant functions of the liver and spleen. Reduces the risk of cancer. Softens the effects of radiation, improves metabolism.
Royal jelly: the secret of the allotropic glands of worker bees. For the normal growth and development of the human body, essential amino acids are needed, which our body cannot synthesize itself and must receive ready-made. Royal jelly contains these essential acids (arginine, histidine, valine, methionine, tryptophan, etc.)). Contains biologically active substances (acetylcholine, cholinesterase, etc.), vitamins B1, B2, B3, B6, B12, Sun, C, H, PP, E, folic acid, biotin, etc. Of the microelements contained in milk, of particular interest represents iron, manganese, zinc, cobalt, necessary for normal blood flow (promotes the regeneration of red blood cells).
Royal jelly has a bacteriostatic and bactericidal effect. It contains 40-45% protein, 20% free amino acids, 20% carbohydrates, 13-15% fats.

Ingredients: ginseng extract, fresh royal jelly, Chinese magnolia vine, honey.

Indications for use: high quality tonic preparation. It strengthens the immune system and body resistance, is effective in the treatment of poor appetite, insomnia, dystrophy and neurasthenia, rheumatoid arthritis. Has a particularly effective result in the treatment of fatigue, increases sexual, anti-cancer and anti-radiation function. Recommended for the treatment of hepatitis, anemia, stomach ulcers, asthma.Promotes strengthening of the body and good spirits, especially for people who have had an illness, in the postpartum period, with senile weakness.

Action: tones up the activity of the central nervous system (increases mental performance, regulates the processes of excitation and inhibition in the cerebral cortex, increases resistance to stress, improves blood supply to the brain), improves appetite.

Contraindications: not identified.

Method of administration and dosage: is most effective when taken in the cold season in long courses (3 courses of 10 days with 10-day breaks).The recommended dose is 10 ml each. a day, twice a day before breakfast and bedtime. Shake well before use!

Storage conditions: Store in a cool dry place.

Shelf life: 3 years

You can buy “Dietary supplement to food, royal jelly with ginseng” in Almaty with delivery in our Healthy Life online store. Delivery of “Biologically active food supplement, royal jelly with ginseng” to Astana. Order “Dietary supplement to food, royal jelly with ginseng” with delivery toKaraganda you can visit our online store Fitolife.com.kz. To place an order, contact us by phone +77074141124, +77076491820, +77279834270

Choline – description of the ingredient, instructions for use, indications and contraindications

Choline Description

Choline is a vitamin-like substance. It is often called vitamin B₄. The body synthesizes it on its own from methionine.

In combination with lecithin, choline provides hormone synthesis, fat and cholesterol metabolism.It is a powerful antioxidant, without which the nervous system, liver and brain cells cannot fully function.

Effects on the body and norms

Choline is essential for the proper functioning of the nervous system. It figures in the processes during which the myelinated nerve sheaths are formed. The presence of a sufficient amount of vitamin in the body prevents the destruction of the myelin layer of nerve cells.

Acetylcholine is formed from choline – an important neurotransmitter that transmits nerve impulses.Vitamin reduces the risk of nervous disorders.

Choline is an effective hepatoprotector. It stimulates regeneration processes in the liver tissue and is indicated for its damage by viruses, drugs, alcohol and drugs. Vitamin normalizes liver function and prevents the formation of gallstones.

Choline lowers blood cholesterol levels. Thanks to this component, the vascular walls are cleared of cholesterol plaques, which reduces the risk of atherosclerosis.In addition, the vitamin promotes the synthesis of methionine, which neutralizes excess homocysteine, which increases the risk of cardiovascular disorders.

Choline strengthens the membranes of insulin-producing cells, and thereby normalizes blood glucose concentration, reducing the risk of diabetes.

Vitamin B₄ participates in the synthesis of prostaglandins, ensures the prevention of disorders in the functioning of the prostate gland, increases sperm motility.

Choline is useful for mental and physical labor.It stimulates the breakdown of fats and is part of the brain.

Attention! The daily requirement for vitamin B₄ depends on age. For children under one year old, it is enough to receive 70 mg of the substance, up to 7 – 100-200 mg, up to 18 – 200-500 mg. Adults need to receive 500 mg of the vitamin per day. During pregnancy, the rate rises to 700 mg.

Signs of deficiency

Choline deficiency is indicated by arrhythmia, growth retardation, tinnitus, headache, hypertension, impaired renal and liver function, diarrhea.

Signs of oversupply

With an excess of choline, side effects are rare. Possible manifestations are nausea, hypotension, intestinal disorders, heavy sweating.

Food Sources of Choline

Choline is found in yolk, liver, kidneys, fish, cheese, meat, cottage cheese. Also, the vitamin is present in some plant foods: legumes, unrefined vegetable oils, carrots, spinach, tomatoes.

Preventive and therapeutic use

Nutritional supplements help to fill the lack of choline.Choline chloride is used for their manufacture.

Vitamin B₄ injections are indicated after strokes and heart attacks, diabetes and atherosclerosis. An encapsulated drug is prescribed to treat dementia, normalize brain activity, and improve memory. Determining the duration of the course and dosage should be entrusted to the doctor.

Contraindications for admission

Reception of choline is contraindicated in case of individual intolerance to the components of the drug.Possible side effects in this case are rashes, itching, nasal congestion, shortness of breath.

90,000 LECITHIN AND OTHER PHOSPHOLIPIDS | Republican Scientific and Practical Sports Center

Lecithi ́ n (Lecithin) – (from the Greek λέκιθος – egg yolk) is a complex of essential phospholipids (phosphatidylcholine, phosphatidylamine. Phosphatidylcholine – the main phospholipid, makes up about 50% of lecithin.The highest content of phospholipids is in the liver and brain. In addition, they are present in nerve cells.

Biological effects of lecithin

  • is the main food for the entire nervous system (part of the sheaths of nerve fibers.
  • is the most important building material for the BRAIN (increases mental activity, improves memory)
  • reduces the level of cholesterol and the concentration of fatty acids in the blood, helps to clear the walls of blood vessels from cholesterol plaques;
  • improves liver and kidney function, prevents the formation of gallstones;
  • assists in the absorption of fat-soluble vitamins A, D, E and K.

The components of lecithin – phospholipids and their constituents – themselves have significant biological activity. So, choline is considered a vitamin-like substance and must necessarily enter the human body with food. It serves as a raw material for the synthesis of one of the most important neurotransmitters (transmitters of nerve impulses) – acetylcholine.

So what happens is:

  • improvement of brain activity;
  • improves memory.

Phospholipids are an excellent solvent for cholesterol. One phospholipid molecule can bind 3 cholesterol molecules and remove them from the body, and phospholipids are able to extract cholesterol both from atherosclerotic plaques and from cell membranes in case of cholesterolosis.

According to some sources, phospholipids have an antioxidant effect, which makes them a valuable anticancer agent. According to experiments, they delay the development of cancerous tumors by 2 times (at sufficiently high dosages) even at the very last stages of cancer.This result has been confirmed in human experiments.

Lecithin plays an equally important role in improving the immune function. It helps to improve the overall defense of the whole body against viruses and bacteria. This is due to the fact that it assists in the production of antibodies and thereby improves the activity of phagocytes.

What does this give those who are actively involved in sports?

Cholesterolosis is extremely rare among active athletes.Therefore, the main use of lecithin in sports is to prevent cholesterol from high-calorie diets. The neurotropic properties of some essential phospholipids are also important, including their effect on the synthesis of acetylcholine.

In addition, the hepatoprotective effect of phospholipids can be used to protect the liver when using potent drugs, including antibiotics. Phospholipid drugs are used to correct the so-called “hepatic pain syndrome” caused by various reasons, including impaired bile flow.

Recommendations for use in sports

  • As an additional agent in combination with other drugs to protect the liver under the influence of significant physical exertion.
  • Functional disorders associated with digestion.
  • General strengthening therapy.

There are a number of phospholipid containing products on the nutritional supplement market today.As a rule, these are soy-based preparations.

Lecithin is contained in products of plant and animal origin. What foods should be eaten to replenish lecithin with food?

Egg yolk. It contains much more lecithin than cholesterol.

Lecithin is also contained in:

  • liver;
  • 90,023 caviar;

    90,023 non-fat soy products;

    90,023 olives;

  • sunflower oil;
  • 90,023 soybeans;

  • fish oil;
  • fat cottage cheese;
  • butter;
  • 90,023 beef;

    90,023 sour cream.

It is necessary to include all these products in the diet, naturally within reasonable limits. You also need to know which plant foods contain lecithin. It is:

  • green peas;
  • salad;
  • cabbage;
  • buckwheat groats;
  • carrots;
  • wheat bran;
  • 90,023 beans;

  • legumes.

The most accessible product for our consumers is unrefined sunflower oil.If possible, choose one that has not undergone any processing (even freezing – in this case, some of the phospholipids are removed) and use it in its pure form, in salads, in cereals, etc.

Special Notes

Lecithin carries no health risks, it is a completely safe substance with a lot of positive effects. During the intake of lecithin, it is required to completely eliminate the intake of alcohol, since ethyl alcohol breaks down the amino acids that make up lecithin and almost completely burns the esters of the amino alcohol choline.Side effects are rare, but they do occur. One of the rare side effects includes low blood pressure that results from high doses of choline. Other side effects that may be associated with lecithin and its main constituent choline include gastrointestinal upset. Choline in large quantities causes a fishy odor in sweat, urine and breath.

Lecithin is an active substance of hepatoprotectors. Lecithin is used to produce Essentiale Forte, Essentiale N, Esliver Forte, and a number of dietary supplements.

Neurouridin instructions for use: indications, contraindications, side effects – description Neurouridin Capsules (55641)

Neurouridin is a specially selected combination of neurotropic substances: B vitamins (B 1 , B 6 , B 9

4, B 9

4 12 ), nucleotide (uridine monophosphate) and choline, which are necessary to restore nerve fibers, improve nerve conduction, strengthen the nervous system and the general condition of the body. The properties of the product are determined by the properties of the components that make up its composition.

Uridine monophosphate – the most important nucleotide required to maintain metabolic processes (metabolism) in the nervous tissue and the formation of myelin sheaths of nerve fibers. Supports an adequate supply of enzymes to nerve cells, stimulates cell division, vital activity and regeneration of peripheral nerves. Nerve cells do not have their own energy resources for the synthesis of nucleotides; nerve cells are supplied with uridine through the blood stream from other cells, as well as with food and supplements containing uridine-5-monophosphate.Uridine monophosphate is of particular importance for accelerating the recovery of damaged nerve fibers. With lesions of the peripheral nerves, the need for pyrimidine nucleotides, such as uridine monophosphate, increases. Therefore, its entry into the body from the outside is of great importance in the course of the processes of recovery and regeneration of nerve fibers.

Vitamins of group B take an active part in biochemical processes that ensure the normal functioning of various structures of the nervous system.

Vitamin B 1 (thiamine chloride) plays a fundamental role in the production of energy in the body, necessary for the growth, development and functioning of cells. Participates in the construction of nerve cell membranes. It is necessary for the biosynthesis of acetylcholine, it is an essential component of the system for conducting excitation in nerve fibers (due to the activation of chloride ion channels in the membranes of nerve cells). Protects cells of nervous tissue from the toxic effects of peroxidation products.Helps in the regeneration of nerve tissue.

Vitamin B 6 (pyridoxine hydrochloride) is necessary for the normal functioning of the central and peripheral nervous systems. Participates in the assimilation of glucose by nerve cells. Essential for protein metabolism and amino acid transamination. Participates in the synthesis and metabolism of a number of neurotransmitters (dopamine, norepinephrine, adrenaline, histamine and GABA) and ensures the normal functioning of the nervous system, improves brain function.Accelerates regenerative processes in the nervous tissue.

Vitamin B 12 (cyanocobalamin) plays an important role in cellular metabolism, nerve function and DNA production. Vitamin B 12 is necessary for the preservation of the myelin sheath of neurons and for the synthesis of neurotransmitters. Promotes the myelination of nerve fibers, incl. in the affected areas of the nerves. Reduces the toxic effects of glutamate on nerve cells.

Folic acid (vitamin B 9 ) is critical for proper brain function and plays an important role in mental and emotional health.Participates in the production of DNA and RNA, the genetic material of the body. Folic acid is also involved in the synthesis of amino acids, myelin, and is required for the synthesis of the neurotransmitters dopamine, epinephrine, norepinephrine and serotonin. Together with vitamins B 6 and B 12 monitors the level of the amino acid homocysteine ​​in the blood.

Choline is one of the main components of the membranes of brain cells and myelin sheaths of nerve fibers. Participates in the implementation of the function of excitability and transmission of nerve impulses.Improves the transmission of neuromuscular signals, increases the speed of transmission of impulses along nerve fibers.

Neururidin components contribute to:

  • improvement of recovery processes in damaged nerve fibers;
  • Improving nerve conduction;
  • Reduction of muscle discomfort in the cervical, thoracic and lumbar spine;
  • increase in physical activity;
  • Improving metabolic processes in the brain tissue and peripheral nerves;
  • Strengthening the nervous system and improving the general condition of the body;
  • reduction of stress reactions;
  • Improve cognitive function of the brain (memory, attention).