Incomprehensive/ble Notes On Choline

raypeatclips

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I'm too poor at the moment to be picky, so I had to fire my chicken-masseuse. The look on his henpecked face was heartbreaking.

I don't think I've ever heard Peat address MTHFR. If nobody else has either, maybe I'll e-mail him to ask about it.

Please post the response you get, he usually has fascinating takes on things. (Rays response not your chicken masseuse.)

I'd definitely say kale is a very good addition to a diet, maybe cooked carrots too, I wonder about yolks and cholesterol, over time I saw z few people report high testosterone while eating 6+ yolks a day.

Normal Plasma Cholesterol in an 88-Year-Old Man Who Eats 25 Eggs a Day — Mechanisms of Adaptation
Fred Kern, Jr., M.D.

"The data obtained were compared with those obtained in a study currently in progress. Eleven volunteers, 10 women and 1 man, ranging in age from 30 to 60 years, were studied similarly while following their usual diet and again after 16 to 18 days during which their diets were supplemented with five eggs a day, representing approximately 2590 μmol (1000 mg) of additional cholesterol. The mean daily dietary cholesterol intake was 567 μmol (219 mg) during the low-cholesterol period and 2995 μmol (1156 mg) during the high-cholesterol period. All the subjects were healthy, except that eight had asymptomatic radiolucent gallstones."

"The mean amount of cholesterol absorbed was 54.6 percent in the subjects on the low-cholesterol diet (300 of the 567 μmol of cholesterol ingested per day) and 46.4 percent on the high-cholesterol diet (1390 of the 2995 μmol in the daily diet) (P<0.001 by paired t-test)."


https://www.annualreviews.org/doi/10.1146/annurev.nu.03.070183.000443

Effects of dietary cholesterol on the regulation of total body cholesterol in man. - PubMed - NCBI

Abstract
Studies on the interaction of cholesterol absorption, synthesis, and excretion were carried out in eight patients using sterol balance techniques. Absorption of dietary cholesterol was found to increase with intake; up to 1 g of cholesterol was absorbed in patients fed as much as 3 g per day. In most patients, increased absorption of cholesterol evoked two compensatory mechanisms: (a) increased reexcretion of cholesterol (but not of bile acids), and (b) decrease in total body synthesis. However, the amount of suppression in synthesis was extremely variable from one patient to another; one patient had no decrease in synthesis despite a large increment in absorption of dietary cholesterol, and two patients showed a complete suppression of synthesis. In the majority of cases the accumulation of cholesterol in body pools was small because of adequate compensation by reexcretion plus reduced synthesis, but in a few patients large accumulations occurred on high cholesterol diets when absorption exceeded the compensatory mechanisms. These accumulations were not necessarily reflected in plasma cholesterol levels; these increased only slightly or not at all.​

This is an interesting aspect to consider, I wonder what could be spared when cholesterol is provided by the diet.

Very interesting thanks for posting these.
 
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Changes of Vitamin A Distribution in Choline Deficiency

"Summary. Rats on a choline-poor diet containing liberal supplements of carotene develop fatty livers poor in vitamin A. The kidneys of these animals are extremely rich in vitamin A."

"Choline-deficient diets produce fatty livers (Best1). Griffith2 demonstrated that in addition to the liver changes, young rats develop an acute syndrome with hemorrhagic renal degeneration, splenic enlargement, ocular hemorrhage and thymic involution. Livers of experimental animals made fatty by diets3 or toxic agents4 ordinarily are rich in vitamin A which can be seen histologically in the fat droplets.5 Choline feeding stimulates the removal of vitamin A [accumulation?] as well as fat from the liver.3 It seemed important, therefore, to determine whether a choline deficiency reveals a similar dependence of the vitamin A storage upon fat deposition in the liver. Since fatty livers may be either rich or poor in vitamin A,6 this question assumes clinical significance."

"Fourteen rats on the deficient diet showed fatty livers of varying degrees within 2 to 10 days. The vitamin A fluorescence at first increased over the low levels in the newly weaned animals. After the third day, however, the fluorescence diminished steadily as the liver fat accumulated. Only in irregular patches, did Kupffer cells and large fat droplets of surrounding liver cells show appreciable vitamin A fluorescence. This fluorescence diminished towards the periphery of the patches. Outside of these areas, the fluorescence was completely absent. Shortly before death of the rats, such patches were very small and the Kupffer cells free from vitamin A. Thus, the total vitamin A in the liver at this time, was much less than at the start of the experiment, despite liberal carotene supplements. Liver of control animals receiving choline daily were rich in vitamin A. About the sixth day, the rats showed the characteristic hemorrhagic renal changes.8 Marked vitamin A fluorescence appeared in the interstitium of the renal cortex in a distribution following the nephron. The adrenals were hemorrhagic in some animals, vitamin A-free in all. Ocular hemorrhage was occasionally seen in rats displaying the most severe changes. No sex difference in vitamin A distribution was apparent.
Ten rats which either spontaneously had survived the critical period of choline deficiency (10 days) or had received subnormal choline supplements were sacrificed after 20 to 90 days on the diet. Their livers were fatty with no vitamin A in Kupffer cells and only patchy traces or none at all in fat droplets. By chemical analysis, from 1.3 to 19 International Units of vitamin A per gram were found, in contrast to the normal value of over 200 I.U. Male animals showed much less vitamin A than females both chemically and histologically. The kidneys seemed normal upon routine histological examination except for scars indicating some past injury. With the fluorescence microscope, however, the cortical interstitium appeared extremely rich in vitamin A in a nephron-bound distribution.

The progeny of females on the deficient diet showed fatty livers with little vitamin A. This condition was accentuated if mother and litter were further maintained on the choline-free ration. Liver vitamin A values as low as 0.5 I.U. per gram were observed.

Liver storage of vitamin A thus depends not only upon dietary ingestion and fat deposition, but also upon choline intake. The disappearance of vitamin A from the fatty livers of choline-deficient rats is not related to the acute stage with "hemorrhagic degeneration" since it is even more marked in the chronic experiments. Nor is inability of the liver to convert carotene into vitamin A a major factor, since preliminary experiments replacing carotene by vitamin A in the diet reveal the same picture. The excessive vitamin A of the kidneys, never seen normally,9 excludes an absorption difficulty. Furthermore, the wealth of vitamin A histologically normal as well as hemorrhagic kidneys would seem to exclude renal pathology as a fundamental cause. Whether the vitamin A deposits in the kidney are due to compensatory storage or urinary excretion cannot yet be answered."​

But please don't be too alarmed because there are conflicting outcomes here:
Vitamin A Storage and Factors That Affect the Liver: One Figure | The Journal of Nutrition | Oxford Academic

These two studies weren't much different in terms of diet, but the first used synthetic vitamins, and the second used yeast. I doubt yeast supplied enough choline because the animals were showing degenerative problems related to its deficiency.
Both diets were low in protein but with extra cystine added.

Maybe it was the combination of vitamin A being supplied daily (contrary to the second) and a severe deficiency (synthetic vs yeast).

It's impossible to get to that state on a natural diet, but I have the impression that a chronic choline insufficiency impairs vitamin A metabolism, even if it's in an indirect way by impairing the liver first.
 

Mossy

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Changes of Vitamin A Distribution in Choline Deficiency

"Summary. Rats on a choline-poor diet containing liberal supplements of carotene develop fatty livers poor in vitamin A. The kidneys of these animals are extremely rich in vitamin A."

"Choline-deficient diets produce fatty livers (Best1). Griffith2 demonstrated that in addition to the liver changes, young rats develop an acute syndrome with hemorrhagic renal degeneration, splenic enlargement, ocular hemorrhage and thymic involution. Livers of experimental animals made fatty by diets3 or toxic agents4 ordinarily are rich in vitamin A which can be seen histologically in the fat droplets.5 Choline feeding stimulates the removal of vitamin A [accumulation?] as well as fat from the liver.3 It seemed important, therefore, to determine whether a choline deficiency reveals a similar dependence of the vitamin A storage upon fat deposition in the liver. Since fatty livers may be either rich or poor in vitamin A,6 this question assumes clinical significance."

"Fourteen rats on the deficient diet showed fatty livers of varying degrees within 2 to 10 days. The vitamin A fluorescence at first increased over the low levels in the newly weaned animals. After the third day, however, the fluorescence diminished steadily as the liver fat accumulated. Only in irregular patches, did Kupffer cells and large fat droplets of surrounding liver cells show appreciable vitamin A fluorescence. This fluorescence diminished towards the periphery of the patches. Outside of these areas, the fluorescence was completely absent. Shortly before death of the rats, such patches were very small and the Kupffer cells free from vitamin A. Thus, the total vitamin A in the liver at this time, was much less than at the start of the experiment, despite liberal carotene supplements. Liver of control animals receiving choline daily were rich in vitamin A. About the sixth day, the rats showed the characteristic hemorrhagic renal changes.8 Marked vitamin A fluorescence appeared in the interstitium of the renal cortex in a distribution following the nephron. The adrenals were hemorrhagic in some animals, vitamin A-free in all. Ocular hemorrhage was occasionally seen in rats displaying the most severe changes. No sex difference in vitamin A distribution was apparent.
Ten rats which either spontaneously had survived the critical period of choline deficiency (10 days) or had received subnormal choline supplements were sacrificed after 20 to 90 days on the diet. Their livers were fatty with no vitamin A in Kupffer cells and only patchy traces or none at all in fat droplets. By chemical analysis, from 1.3 to 19 International Units of vitamin A per gram were found, in contrast to the normal value of over 200 I.U. Male animals showed much less vitamin A than females both chemically and histologically. The kidneys seemed normal upon routine histological examination except for scars indicating some past injury. With the fluorescence microscope, however, the cortical interstitium appeared extremely rich in vitamin A in a nephron-bound distribution.

The progeny of females on the deficient diet showed fatty livers with little vitamin A. This condition was accentuated if mother and litter were further maintained on the choline-free ration. Liver vitamin A values as low as 0.5 I.U. per gram were observed.

Liver storage of vitamin A thus depends not only upon dietary ingestion and fat deposition, but also upon choline intake. The disappearance of vitamin A from the fatty livers of choline-deficient rats is not related to the acute stage with "hemorrhagic degeneration" since it is even more marked in the chronic experiments. Nor is inability of the liver to convert carotene into vitamin A a major factor, since preliminary experiments replacing carotene by vitamin A in the diet reveal the same picture. The excessive vitamin A of the kidneys, never seen normally,9 excludes an absorption difficulty. Furthermore, the wealth of vitamin A histologically normal as well as hemorrhagic kidneys would seem to exclude renal pathology as a fundamental cause. Whether the vitamin A deposits in the kidney are due to compensatory storage or urinary excretion cannot yet be answered."​

But please don't be too alarmed because there are conflicting outcomes here:
Vitamin A Storage and Factors That Affect the Liver: One Figure | The Journal of Nutrition | Oxford Academic

These two studies weren't much different in terms of diet, but the first used synthetic vitamins, and the second used yeast. I doubt yeast supplied enough choline because the animals were showing degenerative problems related to its deficiency.
Both diets were low in protein but with extra cystine added.

Maybe it was the combination of vitamin A being supplied daily (contrary to the second) and a severe deficiency (synthetic vs yeast).

It's impossible to get to that state on a natural diet, but I have the impression that a chronic choline insufficiency impairs vitamin A metabolism, even if it's in an indirect way by impairing the liver first.
Thanks for sharing the info.

My response doesn't necessitate a reply, I'm just thinking out loud (kind of lamely). My health state is such an enigma, wrapped in a riddle, wrapped in a corn dog, but I think choline deficiency may be an area worth looking into. You mention the need for choline when taking thiamine; well, if there's any correlation, I don't feel well on thiamine, but I do remember feeling well on choline (supplement). And, that's saying a lot, considering I feel worse with most supplements. Also, I don't do well with vitamin A supplements--maybe choline is the missing link there. Maybe choline is needed for assimilation, if I'm allowed to use that kind of language.

So, in these coming days, I'll be experimenting to see if choline is the balance needed for these supplements, let alone just on its own. If I don't do well with just the choline, I won't even go to the other supplements.

P.S. I forgot to mention, I've purchased MitoLipin, to get what I understand to be the higher quality saturated choline.
 
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- Choline’s role in maintaining liver function: new evidence for epigenetic mechanisms

"[Cholin's] metabolite betaine is needed for normal kidney glomerular function, and perhaps for mitochondrial function"
@Jennifer

"Half of the methionine coming from diets is utilized by the liver for forming SAM that is needed for methylation reactions and more than 85% of methylation reactions take place in liver. Interestingly, the critical genes for controlling methyl metabolism and DNA methylation capacity are themselves regulated by methylation. For example, MAT1A (forms SAM) is underexpressed when it is hypermethylated [44], and the expression of the DNA methyltransferases DNMT1 AND DNMT3A are controlled by methylation of specific CpG sites [21,45▪,46]. The expression of G9a histone methylase is also decreased when CpGs at specific sites in the gene are methylated [47,48]. Thus, rodents fed diets low in choline and methionine undermethylate these methyltransferase genes and therefore overexpress these methyltransferases [21,45▪,46–48]. This explains why some genes are paradoxically overmethylated despite methyl-donor deficiency [46]."​

- The Metabolic Burden of Methyl Donor Deficiency with Focus on the Betaine Homocysteine Methyltransferase Pathway

"Betaine is the methyl donor in the BHMT pathway and is a methylamine as it contains three chemically reactive methyl groups linked to a nitrogen atom. Wheat bran, wheat germ, spinach, and beets are rich sources of betaine in the human diet." "In addition to dietary sources, betaine can be produced through the irreversible oxidation of choline via choline dehydrogenase and betaine aldehyde dehydrogenase."

It might be relevant for those supplementing wheat germ pboyl and not eating enough choline/betaine.​

"Choline generation via PEMT consumes a significant amount of SAM (3 mole SAM to produce 1 mole choline) and produces homocysteine."

"A choline-deficient diet lowered methionine formation in animal livers by 20%–25% [22], probably because less choline was available for conversion into betaine. However, the effects of choline deficiency on reducing liver SAM (by 60%) and increasing liver SAH (by 50%) were impressive [22]. Therefore, the effect of choline deficiency on lowering SAM is probably not solely mediated by lowering methionine. A choline-deficient diet may increase SAM utilization in the liver, to convert phosphatidylethanolamine into phosphatidylcholine via PEMT."

"The liver and the muscles are the major sites of choline metabolism. Choline deficiency caused fatty liver and muscle damage in humans and increased hepatic carcinogenesis in rodents exposed to alcohol [23]."

"Studies simulating methyl-deficient diets have reported disorders in protein synthesis in the liver and fatty liver as well as muscle disturbances [24,25,26]. Betaine [27,28,29,30], choline, or folate [31] were able to reverse alcohol-related or non-alcohol related liver disturbances, probably via epigenetic regulation [32] or lipid-related mechanisms."

"folate supplementation causes a dose-dependent increase in plasma betaine [42]" "Supplementing folic acid 400–800 µg/day for 12 weeks caused a 15% increase in plasma betaine levels"
@Travis

"Changes in tHcy concentrations reflect only one side of the metabolic burden of methyl group deficiency or nutrient supplementation. Folate [16], betaine [16,33,44], and choline [45] are significant determinants of the fasting plasma concentrations of tHcy."
@gilson d dantas

"Betaine is a major osmolyte in the cell [52]; it regulates the cell volume and stabilizes proteins. It is stored at high amounts in the liver and the kidney. Betaine levels in skeletal muscles are similar to those in the plasma and brain [35]. Betaine prevents osmolytic stress when added to farmed fish upon transfer from low to high salinity. Moreover, in cells exposed to hyperosmotic conditions, choline uptake is enhanced in mitochondria in order to resist volume reduction and osmotic water loss. Choline is converted into betaine under these conditions [53]."

"The methionine-sparing effect of betaine makes methionine more available for protein synthesis, and the choline-sparing effect makes choline more available for lipid metabolism. The role of betaine in energy metabolism appears to be effective at low total energy intake. Betaine is useful as a partitioning agent under low amino acid and energy intake situations in animals [56,57]; thus, it has the potential to solve public health problems related to excess fat in meat products."

"Löest et al. found that betaine may decrease the demand for choline methyl groups, thus increasing choline availability for lipid metabolism [59]. This was supported by the findings of Yao and Vance [60] showing that betaine can correct very low density lipoprotein (VLDL) secretion from hepatocytes grown in a choline deficient medium."

"Folate and choline can prevent disorders in brain development and function, at least in part by supplementing methyl groups."​

- Adult emotionality and neural plasticity as a function of adolescent nutrient supplementation in male rats
 
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To make the complementings on post #22, the interaction with vitamin A works both ways:

Vitamin A-Choline Interrelationship

"Abels. Gorham, Pack. and Rhoads (1) found that levels of vit. A in plasma of patients with malignant disease, particularly of the gastrointestinal tract, were below the normal range in 86% of cases examined. No response was obtained after vit. A administration, but feeding of yeast or pancreatic extracts, themselves free of carotenoids, raised the reduced plasma levels of vit. A. That this property in yeast or pancreas may be due to choline content has become apparent from later experiments. There was an average rise of 73% in plasma levels of vit. A in patients who were fed 1.5 g of choline chloride each day for 3 days. Popper and Chinn (2) showed that rats on a choline-poor diet containing liberal supplements of carotene developed fatty livers poor in vit. A."

upload_2018-7-2_16-51-31.png

"Animals of the supplemented group received an additional 5,000 International Units of vit. A orally each day for one week before sacrifice."
Diet provided "Vit. A oactivity-1100 I.U., Carotene 0.14 mg"

"The results indicate that there is some vit. A-choline interrelationship. The total choline concentration was highest in the 3 normal groups, but this concentration was reduced when an excessive amount or a deficient amount of vit. A was stored in the liver. Since the phospholipid choline content showed little variation under these experimental conditions, it appears that total choline variation is on the basis of a change in the free choline content. It is interesting to note that the maximum level of free choline is related to the normal level of vit. A.

This relationship between vit. A and choline has been further substantiated by the work of Thorbjarnarson and Drummond (7), who found that choline feeding stimulated removal of vit. A as well as fat from the liver. Popper and Chinn(2) also reported that a choline-poor diet revealed a similar dependence upon vit. A storage in the liver.

The low vit. A blood levels found in patients with malignant disease of the gastrointestinal tract may in some way be tied up with a disturbance of this vit. A-choline relationship in the liver."
Effects of Choline From Eggs vs. Supplements on the Generation of TMAO in Humans - Full Text View - ClinicalTrials.gov
"The investigators have also recently shown a 10-fold increase in plasma TMAO levels following supplementation with choline bitartrate supplements [to amount 450mg of sucholine a day (original post above)]. However, another pilot study by a collaborator (unpublished) did not show the same increase in plasma TMAO levels following the ingestion of whole eggs, a major dietary source of choline. Therefore, with this study the investigators wish to examine the differences, if any, between the ingestion of an equivalent mass of total choline in the free form (as bitartrate salt) as a supplement vs. within whole eggs."

It will be nice to compare if eggs fare better..
:sleeping
 
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https://onlinelibrary.wiley.com/doi/pdf/10.1002/14356007.a07_039

"Choline is a strong base (pk = 5.06) which absorbs carbon dioxide and water from the air." "Choline reacts with acids to form stable salts. Most of the choline salts except the chloride, bitartrate and dihydrogen citrate are difficult to crystallize. Choline also reacts with acids to form esters."

Choline bicarbonate and gluconate forms exist:

"Choline bicarbonate [78-73-9], C6H15NO4, Mr 165.2, its solution is a clear liquid, colorless to slightly yellow with a characteristic amine-like odor. An aqueous solution containing about 75% choline bicarbonate has a pH between 9.0 and 11.5. Besides being very soluble in water, choline bicarbonate is freely soluble in alcohol and slightly soluble in benzene."

"Choline gluconate [608-59-3], C11H25O8N, Mr 299.33, is a hygroscopic yellow mass, soluble in water and slightly soluble in ethanol."

"Choline salts, such as the chloride, hydrogen tartrate, dihydrogen citrate and gluconate are used therapeutically for patients with liver cirrhosis that has not advanced to the irreversible fibrous stage. Oral choline does appear to be effective in reversing fatty infiltration and arresting the cirrhosis process."
 
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Amazoniac

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Koch was a beast. His work is really impressive.

http://www.williamfkoch.com/pages/natural/?pID=1&pID2=27

"It is found that acetyl choline produced at the parasympathetic nerve endings during their function, prevents the accumulation of fat in the liver on heavy fat and cholesterol feeding, when injected into the body in such minute dosage as one to ten million. One is inclined to look upon an exhaustion or fatigue and insufficiency in its production as a cause of cholesterol deposition and of the changes that regularly follow in the degeneration of the vessel wall; whereas an overproduction, with consequent vessel spasm and impoverished circulation in the wall, accounts for the coronary spasm and ultimately occlusion with the changes that are consequent. Since the excess acetyl choline is normally burned and destroyed by a normal oxidation mechanism, no harm can come in the presence of good oxidation catalysis, which burns up the acetyl choline not used.

Acetyl choline cannot be held to be the only, or even the major factor in vascular disease, however, for the injured oxidation catalysis that permits cholesterol excess and deposition in the absence of normal acetyl choline production, is also responsible for the failure to burn other toxic agents that injure the tissues. The failure of sufficient oxidation catalysis may be of the degree that does not supply the energy for acetyl choline production, on the one hand, and thus be fundamental to atheromatous change; or, on the other hand, it may be insufficient to destroy toxic agents actively producing lesions in the vessel wall that result in thrombosis and occlusion.

Even though acetyl choline spasm may prove injurious to the coronary vessels, it is not the only substance that behaves so, nor is its action nearly as destructive as the Benzopyrene type of compounds or the dihydroxybenzenes and quinones that have allergenic and carcinogenic action. These substances are destroyed by the oxidation catalysts we have introduced quite like the toxic structures that cause coronary lesions and occlusion. The etiology of both types of vascular disease may thus be regarded as producible by one type of poison. The same structural type causes cancer and the other allergies, and the same structural arrangement is essential to the curative substance."
 
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- The Interrelationship Between Methionine, Choline, and Sulfate in Broiler Diets

"Balnave (1981), working with a semipurified diet, pointed out that high concentrations of choline in diets with suboptimal concentrations of sulfur amino acids reduced growth and feed efficiency due to an induced pyridoxine deficiency. However, Gordon and Sizer (1955) obtained a growth response when chicks were fed purified diets deficient in cystine and supplemented with inorganic sulfate. These results were confirmed by Machlin and Pearson (1956) and Sasse and Baker (1974a) working under similar experimental conditions. Ross and Harms (1970) also reported a growth response in broiler chicks fed a high energy corn-soy diet deficient in methionine."

"[..]supplementation of choline in the presence of methionine did not give a further response. Therefore, the growth response obtained by the addition of choline may be attributed to its function as a labile methyl donor (Pesti et al, 1979), but because methionine was deficient per se, the addition of the latter resulted in the higher response. However, supplementation of the basal diet with inorganic sulfate alone resulted in a significant growth depression at 2 weeks of age and a numerical depression at 3 weeks. Supplementation with sulfate in the presence of choline resulted in a greater growth response than when either was supplemented alone, indicating a sparing action of SAA by sulfate or a requirement of inorganic sulfate per se. The absence of a response from the addition of choline when methionine and sulfate were both added indicates again that the diet was not deficient in choline."

"[..]the consistent sulfate response in the diet containing supplemental choline and no supplemental methionine was an unexpected finding and has not been reported in the literature. If, in fact, a choline-S04 interrelationship exists per se this would explain the growth depression that occurred when sulfate was supplemented alone to the basal diet but not when supplemented in the presence of choline. Further studies are required in order to understand the interrelationship between choline and inorganic sulfate that would result in a growth response as seen in this study. Martin et al. (1966) demonstrated the ability of the chick to synthesize taurine from sulfate, and it has been suggested diat this could account for at least part of the beneficial response to dietary sulfate. However, the addition of taurine to a diet that would respond to sulfate supplementation does not enhance chick performance (Martin, 1972; Sasse and Baker, 1974b)."

"Results indicated that the 2-week data were more sensitive than the 3-week data. The chick's ability to synthesize choline may be age dependent (Nesheim et al, 1971) or the response at 3 weeks may have differed because as the chick increased in weight the choline intake per gram body weight decreased."​

- Isolated sulfite oxidase deficiency: Review of two cases in one family - ScienceDirect

1-s2.0-S0161642099904086-gr6.gif

- https://raypeatforum.com/community/...rd-to-pronounce-harder-still-to-obtain.12466/ ))

@whit
 

ddjd

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@Amazoniac thanks for all these notes you've pulled together on choline. I myself have the PEMT dysfunction-homozygous, and i notice whenever I take phosphatidylcholine in the form of sunflower lecithin, my chronically bloated stomach, shrinks and becomes flat, so its definitely having a very positive effect on the liver and gallbladder without a doubt. Long term, I'm looking to get hold of a saturated form of Phosphatidyl choline, similar to what haidut sells in Mitolipin, but i need it in much bigger doses. I was wondering what do you think about the saturated PC option? do you supplement choline?
 

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I don’t mess with extra Choline, it can aggravate depression and agitated states via acetylcholine in the brain
 

ddjd

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I don’t mess with extra Choline, it can aggravate depression and agitated states via acetylcholine in the brain
this is fine for someone who has a fully functioning PEMT gene but i can guarantee you someone like myself with PEMT dysfunction definitely needs to supplement choline. I just wish there was a cheap saturated PC option
 
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@Amazoniac thanks for all these notes you've pulled together on choline. I myself have the PEMT dysfunction-homozygous, and i notice whenever I take phosphatidylcholine in the form of sunflower lecithin, my chronically bloated stomach, shrinks and becomes flat, so its definitely having a very positive effect on the liver and gallbladder without a doubt. Long term, I'm looking to get hold of a saturated form of Phosphatidyl choline, similar to what haidut sells in Mitolipin, but i need it in much bigger doses. I was wondering what do you think about the saturated PC option? do you supplement choline?
Shalom,

Not long ago I read your thread on citicoline supplementation and found it interesting. I assume you can't find reliable eggs or don't like them, right?

I don't supplement because I ***t my pants about it. I've been encouraging our supplement vendors to supply some sort of desiccated liver (extract?). It can take care of B12, vitamin A, choline, folate, riboflavin, selenium, copper and other trace minerals all at once, which can be very useful.

It's relatively easy to find reliable sources of ruminant liver, but they're impractical due to their limiting copper and maybe vitamin A. You probably read the other thread: poultry liver can solve that. Unfortunately it's more difficult to find reliable ones. And this is where gurus that sell supplements can help.

Usual Choline Intakes Are Associated with Egg and Protein Food Consumption in the United States
"Adults 19+ y had a usual intake of 338 ± 1.86 mg/d (males: 405 ± 3.30 mg/d; females: 273 ± 2.13 mg/d)."
This vvas authored by someone involved in the egg industry, if anything, they would've decreased the estimated intakes to inspire more consumption.

100 g of whole chicken liver provides about 300 mg of cholin. 2/3 of that is enough to supplement to an amount that normalizes blood markers of organs functions in most people.

Premenopausal women are remarkable in terms of being resistant to depletion (from a link on the previous of the pages):
Sex and menopausal status influence human dietary requirements for the nutrient choline

Apparently estrogen and progesterone are involved in the functioning of the enzyme that you mentioned for the synthesis of cholin when the diet isn't providing enough. I haven't read about it in details but it makes you wonder what happens when you're deficient in cholin and the hormones are lowered.
An example is taking these during a deficiency.
 

Mossy

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I don’t mess with extra Choline, it can aggravate depression and agitated states via acetylcholine in the brain
I can attest to the agitated state, with my recent small doses of topical choline. To be fair, I was using a homemade topical that had caffeine in it, at the same time. Even so, the topical choline was definitely agitating/stimulating, which I’ve read could be the case. In the past, oral supplementation had made me feel good, so, maybe that is what is needed. I still haven’t had the courage to try it orally, since a bad agitation episode, but I’ll have to at some point.
 

Frankdee20

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I can attest to the agitated state, with my recent small doses of topical choline. To be fair, I was using a homemade topical that had caffeine in it, at the same time. Even so, the topical choline was definitely agitating/stimulating, which I’ve read could be the case. In the past, oral supplementation had made me feel good, so, maybe that is what is needed. I still haven’t had the courage to try it orally, since a bad agitation episode, but I’ll have to at some point.

Yeah, I don’t know if things like GPC Choline or CDP Choline yield smoother results than plain phosphatidyl Choline in food, or Choline Bitartrate in supplemented form. There’s going to be new antidepressants that target the Choline system via attenuation. Perhaps this is why drugs like Chantix (agonize acetylcholine) can cause agitated states, nightmares and suicide.
 

Frankdee20

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Can you elaborate more on this @Frankdee20?

So yeah, we always hear about acetylcholine being the neurotransmitter of intelligence, or brain speed. Look at all the Nootropics that target this system. I’ve increased my Choline intake from food many times (which gets acetylated to form the neurotransmitter) to see what’s all the rage. Profoundly severe melancholia and agitation ensued with a sort of brain dampening dumbness from it. I also added Asparagus (acetylcholinesterase inhibitor) to that mix, just absolutely awful. Perhaps this is also why Nicotine has paradoxical effects depending upon dosage. Higher doses are almost dumbing, and low doses act as a stimulant and enhancer. All I know is acetylcholine can inhibit dopamine projections indirectly, and maybe that’s why I get depressed from it.
 
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So yeah, we always hear about acetylcholine being the neurotransmitter of intelligence, or brain speed. Look at all the Nootropics that target this system. I’ve increased my Choline intake from food many times (which gets acetylated to form the neurotransmitter) to see what’s all the rage. Profoundly severe melancholia and agitation ensued with a sort of brain dampening dumbness from it. I also added Asparagus (acetylcholinesterase inhibitor) to that mix, just absolutely awful. Perhaps this is also why Nicotine has paradoxical effects depending upon dosage. Higher doses are almost dumbing, and low doses act as a stimulant and enhancer. All I know is acetylcholine can inhibit dopamine projections indirectly, and maybe that’s why I get depressed from it.
Very Interesting. Thank you. Definitely something to think about...
 
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Amazoniac

Amazoniac

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I find it a bit mind bottling when people are concerned with supplementation of choline to complement diet until repletion for fear of potential problems with methylation, but at the same time consume something like 2.5 g of methionine a day through cheese.

This is the quote that often appears:

Protective CO2 and aging
"Methionine and choline are the main dietary sources of methyl donors. Restriction of methionine has many protective effects, including increased average (42%) and maximum (44%) longevity in rats (Richie, et al., 1994). Restriction of methyl donors causes demethylation of DNA (Epner, 2001). The age accelerating effect of methionine might be related to disturbing the methylation balance, inappropriately suppressing cellular activity. Besides its effect on the methyl pool, methionine inhibits thyroid function and damages mitochondria."​

From what I read, methionine restriction can be harmful and producing the counters if there's a choline deficiency.

I'm not disregarding that it can be indeed an issue, especially when you supplement in the adsense of other vitamins or a lot. I also might be missing something, such as choline providing more methyl groups per molecule, or turnover rates of each, but perhaps a greater concern than too much, is too little of it. With excess you're able to control it, niacin is one of the ways. But what can the body do in a deficiency? Chronic insufficieny is quite stressful and you can confirm it through the fast elevation in liver enzyms that happen in choline experiments in a matter of days/weeks. How is this not carcinogenic?
 
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- Should the forms of dietary choline also be considered when estimating dietary intake and the implications for health?

"Dietary choline can be provided as aqueous forms (free (unesterified) choline, phosphocholine and glycerophosphocholine (GPC)), and lipid-soluble forms (PC, lysophosphatyidylcholine (lysoPC) and sphingomyelin). In the APrON cohort, consistent with other studies, PC was the major choline form consumed, contributing 48 ± 2% of total intake. Free choline was the second most commonly form, comprising 23 ± 2% of total choline. GPC contributed 19 ± 2%, followed by sphingomyelin (5 ± 3%) and phosphoscholine (5 ± 1%). Dietary intake of lysoPC was not assessed because the content in foods is not included in the USDA Database for the Choline Content of Common Foods. Approximately 6% of the cohort consumed a supplement that contained choline, which was most frequently a choline salt (free choline). When a supplement was used, it only made a minor (6%) contribution to total intake [3]."

"The metabolism and functions of choline is complex and has been reviewed by Li et al., 2008 [4] and others [1, 2], with the main functions of each form of choline summarized in Table 1. Each choline molecule has unique roles and differences in absorption and metabolism within the body [5]."

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"The absorption and metabolic functions of lipid-soluble forms of choline differ from aqueous forms. As illustrated in Figure 1, lipid-soluble PC is first hydrolyzed by phospholipase A2 to form lysoPC in order to be absorbed by the enterocyte. LysoPC can then be reacetylated to PC or it can be further broken down to form GPC, then free choline. Although the aqueous forms of choline are transported directly to the liver, the lipid-soluble forms are secreted into chylomicrons in the enterocyte and enter the bloodstream through the thoracic duct. Dietary lipid-soluble forms of choline are thereby delivered directly to peripheral organs (adipose and muscle) en route to the liver (Figure 1) [5]. In the liver, dietary (like endogenously synthesized) PC can then be utilized in the synthesis of lipoproteins. It has been estimated that approximately 30% of PC synthesized by the liver occurs via phosphatidylethanolamine N-methyltransferase (PEMT) [4]. The functions of the lipid forms of choline have been summarized in Table 1, and have unique functions as structural components, signaling molecules and precursors for other metabolites."

"Consumption of the forms of choline is dependent on individual dietary patterns. An individual consuming a diet high in animal products is likely to consume higher amounts of lipid-soluble forms of choline. In the APrON cohort, consistent with other Western populations, approximately 50% of total dietary choline was from animal products (dairy, eggs and meat). The top individual dietary sources of PC (based on the amount in food and the quantity of food consumed) included eggs, chicken and turkey, ground beef, pork loin/chops, ham and salmon. Conversely, consumption of a diet consisting of more vegetable-based protein sources such as grains, legumes and pulses, may result in higher intake of water-soluble choline forms. Top food sources of free choline in the APrON cohort were bread (wheat, rye or rice), milk (1% or skim), instant coffee, bananas, orange juice and peanut butter. This is consistent with known sources of these forms of choline as free choline and other aqueous forms are found in a higher proportion in grain and legume products, whereas lipid-soluble forms of choline are found in a higher proportion in animal products."

"Eggs are one of the most concentrated dietary sources of choline, with an average whole medium egg containing approximately 130 mg of choline, with the majority of choline as PC. It was found in the APrON cohort that egg consumption significantly altered the amount and form of choline in the diet. Egg consumers (women who reported consuming at least one egg in the 24-h period) had significantly higher total choline and intakes of lipid-soluble forms of choline (PC and sphingomyelin) compared to non-egg consumers. Egg consumers had PC intakes approximately 150% greater than non-egg consumers [3]."

"Dietary intake of the forms of choline during pregnancy and lactation was also influenced by whether a woman chose to drink milk or soy beverage, a milk alternative. Although the total amount in a serving is similar, milk contains a high proportion of GPC, comprising 60% of total choline, and sphingomyelin. Conversely, soy beverage contains a high proportion of choline from free choline (55%) and PC (24%), and contains no sphingomyelin. Consistent with the composition of the different beverages, soy beverage consumers had higher intake of free choline and milk consumers had higher intake of GPC and sphingomyelin (P < 0.05 [])."

"Total choline concentrations of human milk is approximately 160 mg/L (1.5 mmol/L) and contains a significantly higher concentration of phosphocholine compared to cow or soy-derived formulas [6]. Although cow-milk-derived formula contains similar amounts of lipid-soluble forms of choline, soy-based formulas are higher in PC while containing lower amounts of sphingomyelin compared to human milk [6]. Additionally, human milk contains 30–80% less free choline compared to both cow and soy-derived formulas [6]."

"An additional factor that influences the forms of dietary choline is food preparation method. Cooking of vegetables [7] and most pulse varieties [8] significantly reduces the amount of water-soluble choline compounds, and for pulses, increases PC content. Therefore consumption of raw vegetables or pulses could result in higher intake of aqueous forms of choline, compared to consumption of cooked vegetables. Less is known about the effect of cooking on other plant sources of choline but preparation method and the length of cooking may also affect the amount of free choline and PC in foods."

"[..]in rodents, feeding high amounts of aqueous choline, or feeding of the same amount of choline as PC, differentially affected growth and development and function of the immune system in both lactating rats [9] and their offspring (unpublished results). Additionally, in lactating rat dams, very high intake of free choline (6 times recommendations for rodents) had negative effects on offspring and dams growth, and increased activation of T cells (suggesting immune system disruption) in the dams [9]. Free choline and PC have been reported to have different effects on serum and plasma cholesterol levels, suggesting that PC has antihypercholesterolemic effects compared to feeding free choline in rodents [10]. It has also been hypothesized that the variability in results between rodent and human research examining the role of choline in infant brain development may be due to the different choline forms supplemented or fed in the studies. Standard rodent diets provide a choline salt (free choline), but in humans, maternal supplementation of choline as PC during pregnancy did not enhance infant cognitive function. Due to the differences in bioavailability between forms, different biological effects may have been observed if free choline was supplemented instead."

[2]
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- Choline and Its Products Acetylcholine and Phosphatidylcholine (!)
 

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