Dietary Choline

pboy

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so a Peat diet is probably one of the more adequate in choline relative to RDA and pregnant mother reccomendations and things...it seems an average diet provides maybe even half or around there choline, depending on factors. Apparently its a methyl/methionine kind of thing which you hear to keep down for long life and less aging and things (its apparently the true cause of low calorie extending lifespan) and Ray warms agains over methylation (yet advocates coffee which has caffeine which is trimethyl xanthine). Basically I find it strange that I never crave eggs though the diet I consume is probably half to 70% of what is recommended for choline dietarily, so perhaps de novo synthesis is taking place from proteins...but I was wondering if Peat has commented on this or if anyone has any info. I also do consume xanthines...used to in huge amounts theobromine, caffeine, theophylline, the whole gambit...now still some but more moderate maybe anywhere from little to none to 700ish mg a day varied sources depending on things...I don't know if other methyl donors would vastly aid in de novo choline synthesis and maybe this is behind caffeins aid in liver clearing and lipid clearing propensity, as methyl donors would be a limiting factor in choline synthesis and the dietary folate, b6, and b12 are basically in micrograms or at most a milligram or 2 so that is kind of an irrelivent factor as far as synthesizing 300+ for example mg of choline would need...something like spinach, beets, or even quinoa has a lot of betaine which could spare choline and potentially provide methyl donors though I think, not sure, but think it might be an irreversible thing (once the methyls are in betaine). So basically does anyone have any Peat info, or actual info, on choline that's not maybe so common that maybe people could already have read on the first page of google for example, and do you think providing methyl donors via xanthine sources is a good thing for liver clearance, potential choline synthesis, and where is that line between the 'dangers of overmethylation', what you hear about methyl and or methionine being bad, and yet the profound or perported benefits they also can have...is it maybe a metabolic thing related in the direction your metabolism is going so to speak...hibernation or growth? Basically personally I don't care that much cause I haven't craved eggs or anything high in choline for years so I think milk + whatever else I consume is providing enough but I'm interested in the whole process of xanthines, methyls, ect...and for a while I didn't need any xanthines...didn't have for basically a year to year and a half any, but then as stress went up the desire came back and its good, so in a sense im glad I recovered them they are enjoyable, its not really true stress though its basic authoritative stuff environment stress not really personal or dietary, but in that case a bit of extra fire helps...when life is on own path thyroid alone covers easily energy but when 'combatting' so to speak not physically obviously but when being challenged for time and usage of energy by outside forces somehow xanthines seem to be useful...anyways more interested in methyls, methionine, and choline mostly..any info would be cool
 

Parsifal

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Have you tried Mitolipin? I guet bad reactions with things relating to choline even though I am homozygous on some methylation genes.
 

Amazoniac

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The gurus provide valuable labs to detect any liver dysfunction*, variability in choline requirements (some reaching good blood markers ingesting little, whereas others needing a lot during repletion), and they likely observed the opposing effects of pboysterone and progesterone on estrogen.

Sex and menopausal status influence human dietary requirements for the nutrient choline

"We found that most men and postmenopausal women developed organ dysfunction when deprived of choline, whereas most premenopausal women did not."

"The glomerulus of the kidney uses 2 metabolites of choline (betaine and glycerophosphocholine) as osmolytes (41, 42), and choline-deficient rodents have renal dysfunction (1, 43). We did not observe dietary choline-related changes in urinalysis or urine-specific gravity in our subjects (data not shown)."

"Choline is derived not only from the diet but from de novo synthesis of phosphatidylcholine catalyzed by PEMT. As discussed earlier, PEMT activity is increased by estrogen in animal models. We hypothesize that this is the reason why premenopausal women were more resistant to developing signs of organ dysfunction when fed a low-choline diet." :ss

"The requirement for choline in the diet is quite variable. A portion of the men and women we studied required more than the recommended AI for choline, whereas others required <50 mg choline · 70 kg−1 · d−1. Some subjects became deplete quickly and some took almost 7 wk to develop organ dysfunction when fed a low-choline diet. Estrogen status accounts for much of this variability."

"We previously published that choline metabolism is interrelated to homocysteine metabolism (18). It is interesting that premenopausal women, whatever the response group, had a lower plasma homocysteine concentration at baseline (with signs: 5.7 ± 0.4 nmol/mL; without signs: 4.6 ± 0.2 nmol/mL) than did men (with signs: 7.4 ± 0.3 nmol/mL; without signs: 6.9 ± 0.6 nmol/mL); however, when subjects were fed the low-choline diet, homocysteine concentrations uniformly increased 20% in men (with signs: 8.8 ± 0.6 nmol/mL; without signs: 8.6 ± 0.7 nmol/mL), premenopausal women (with signs: 6.9 ± 0.6 nmol/mL; without signs: 5.8 ± 0.2 nmol/mL), and postmenopausal women (data not shown). Also, we report that plasma concentrations of methylated end products of choline and methionine metabolism changed in predicted directions (Table 4)."

"We observed no effect of folic acid supplementation on susceptibility or on mode of presentation. Previously published studies suggesting that folic acid supplementation might decrease requirements for choline used diets much higher in choline (150−300 mg choline/d) than ours (< 50 mg/d) (20, 21). Perhaps the effects of folate become apparent only when marginally adequate amounts of choline are supplied and not when diets are almost devoid of choline."

"This study, in combination with our previous work, establishes a panel of measurements that can be used to define individuals who are sufficiently deplete of choline to develop liver and muscle dysfunction[*]. Factors that we identified that increase susceptibility to developing organ dysfunction in humans fed low-choline diets, such as menopausal status and genetic polymorphisms, are likely to be of clinical importance."​

*
"The subjects were deemed to have organ dysfunction associated with choline deficiency if they had a more than 5-fold increase in serum creatine phosphokinase (CPK) activity (24); a more than 1.5-fold increase in aspartate aminotransferase (AST), alanine aminotransferase (ALT), γ-glutamyltransferase (GGT), or lactate dehydrogenase (LD); or an increase in liver fat content of >28% during the consumption of the choline-depletion diet (see later discussion) and if these elevated measures resolved when choline was returned to the diet."

"A complete panel of laboratory tests was performed on each subject at screening, on day 1, and at the end of each dietary phase. These laboratory analyses (conducted at the Mclendon Clinical Laboratory at UNC Hospitals; Clinical Laboratory Improvement Act and College of American Pathologists accredited) included measurements of sodium, potassium, magnesium, phosphorus, chloride, fasting glucose, carbon dioxide, blood urea nitrogen (BUN), creatinine, alkaline phosphatase (AP), ALT, AST, CPK, LD, total protein, albumin, uric acid, total bilirubin, calcium, GGT, amylase, lipase, complete blood count with differential (white blood cells, red blood cells, hemoglobin, hematocrit, platelet count, mean cell volume, mean cell hemoglobin, mean cell hemoglobin adjusted for cell volume, red blood cell distribution width, neutrophils, lymphocytes, monocytes, eosinophils, and basophils), prothrombin time, partial thromboplastin time, total cholesterol, triacylglycerols, and HDL and LDL cholesterol in blood drawn by venipuncture. An abbreviated toxicity panel, which included AST, ALT, GGT, AP, LD, total bilirubin, CPK, BUN, creatinine, amylase, and uric acid, was run every 3−4 d throughout the duration of the study to monitor the depletion and repletion status of subjects."​

Just like our semi-god mentioned above, coffee must reduce the requirements as it energizes the liver although I couldn't find a straight explanation yet, but the hormonal reflect is a hint along with its ability to make it lean.

@Tarmandear
 
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Amazoniac

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I later found out it was the manganese in mussels that helped, not the selenium. Tea and pineapple juice had similar effects.
Choline is derived not only from the diet but from de novo synthesis of phosphatidylcholine catalyzed by PEMT. As discussed earlier, PEMT activity is increased by estrogen in animal models.
An association between choline and Mn metabolism has been recognized for some years. In turkey poults, lack of choline has been shown to produce perosis, a Mn deficiency symptom (Jukes 1940, 1941). Choline deficient rats show lower liver Mn levels (Keefer et al., 1973). Ethanol metabolism in the gut causes an increase in hepatic Mn (Barak etal., 1971)."
"Manganese is involved in cholesterol synthesis; therefore, a deficiency can be related to a lack of this precursor for normal hormonal production. Manganese also shows a synergistic relationship with choline. A deficiency of either or both may lead to abnormal mitochondrial and cell membrane integrity.15 The liver mitochondria isolated from manganese deficient mice revealed abnormalities of the cristae and a lowered oxidation rate.16"
 

Tenacity

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Perosis in turkeys leads to cartilage deformation. Manganese deficiency would explain my pectus excavatum deformity, too...
 

Koveras

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Perosis in turkeys leads to cartilage deformation. Manganese deficiency would explain my pectus excavatum deformity, too...

Interesting, I know an individual with pectus excavatum who has several polymorphisms in the PEMT gene (reducing its activity and increasing choline requirements 3-5 fold IIRC)
 

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