Incomprehensive/ble Notes On Choline

Discussion in 'Vitamins' started by Amazoniac, Apr 7, 2018.

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  1. Amazoniac

    Amazoniac Member

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    ..and why avoiding eggs due to a couple grams of PUFAs might not be a good idea. They're not the only source, but are by far the best since livers aren't ideal for regular consumption.
    Finding pastured eggs locally and online - Toxinless

    These were all over of the places. I figured it could be helpful to collect them here.

    - A Cancer Therapy By Max Gerson - Selected Parts

    [..]effects of choline and methionine [in protecting the liver] can be reversed by excess fat supplements.

    With the tremendous amount of experimental work done on lipotropic agents, and their effectiveness in dietary fatty liver in animals, it is only natural that clinicians should turn to these substances in the treatment of fatty liver; however, the only type of fatty liver that choline (the most important of the lipotropic substances) can cure is the one due to a choline deficiency. It is likely that at least some of the fatty livers in man are due to choline deficiency, but in fatty livers of prolonged infection or those due to toxins, no deficiency of choline in the diet can be postulated, and therefore, no beneficial effect from choline can be expected.
    Mitchell A. Spellberg, Diseases of the Liver, p. 309.​

    - A Cancer Therapy By Max Gerson - Selected Parts

    "Choline has much to do with the oxidation of fats. That it prevents the conversion of amino acids and of sugars to fats under the influence of cholesterol, it seems there is sufficient evidence when the rest of the oxidation mechanism is normal. It does not aid the burning of aceto-acetic acid [acetylsucholine], but where the rest of the oxidation mechanism is sound, its presence favors the burning of fats or their precursors by another route. It is, therefore, an important link in the oxidation mechanism, but of course where the oxidation process is otherwise impaired we must assume that it not only fails to function and therefore accumulates [again] or is formed in greater quantity for compensation than normally occurs; and worst of all it is not burned itself and produces its toxic effects. Thus one might well assume that it is a factor in coronary disease, much like cholesterol is in other vascular degeneration that are so well known. In fact they both accumulate where the normal catalysis of oxidation is broken, and therefore both coronary disease and atheromatous degeneration and arterial sclerosis depend upon one basic deficiency, a crippled oxidation catalysis [also known as hypotravisism]." "Vascular normalcy is important to tissue function and obliterative vascular disease so often the cause of tissue degeneration that one might say that all disease shows its marks on the vascular system early or late. The infectious granulomata all start out with an obliterative endarteritis. Cancer does also, and cancer should be classified with the granulomata. They are all based upon toxic activity that destroys oxidation catalysis. They are all curable by restoration of the oxidation catalysis to normal or to better than normal."

    "Through an over-active nervous system, therefore, in the presence of deficient oxidation catalysis, an accumulation of metabolites to toxic concentration, be it sucholine, neurine, cholesterol or some other, is possible whereby disease is produced in a similar way to that caused by disease germ poisons where the oxidation catalysis is insufficient to destroy them. The various allergies including cancer possess in this way an additional mechanism for being brought about and being maintained. Again let me repeat that the restoration of a vigorous oxidation catalysis removes the offending substance, no matter what its origin may be, and thus establishes the basis for recovery."​

    - "I Have Liver Issues And I Am Not Making Progress"

    It only takes an inability to digest casein or insufficient protein to make the stereotyped diet associated with our domesticator similar to a diet that is used to fatten up lab animals' livers: plenty of fructose, coconut oil, not enough methionine, not enough choline, but also sedentarism. High-protein and eggs are two important aspects unless the intuition tells not to do so.
    There are people that thrive on variations of it, but they don't seem to be pushing it in attempt to make it work.

    Search for "lipotropic factors/agents"

    Wolters Kluwer - Modern Nutrition in Health and Disease

    "For nonruminant animals, a diet deficient in choline has major consequences including hepatic, renal, pancreatic, memory, and growth disorders (8). In most animals, choline deficiency results in liver dysfunction. Large amounts of lipid (mainly triglycerides) can accumulate in liver and eventually fill the entire hepatocyte. Fatty infiltration of the liver starts in the central area of the lobule and spreads peripherally. This process is different from that occurring in kwashiorkor or essential amino acid deficiency, in which fatty infiltration usually begins in the portal area of the lobule. Lipid accumulation within hepatocytes begins within hours after rats are started on a choline-deficient diet, peaks within the first 6 months, and then diminishes as liver becomes fibrotic (120). Fatty liver occurs because triacylglycerol must be packaged as very-low-density lipoprotein (VLDL) to be exported from liver, and phosphatidylcholine is required for VLDL formation (121–123). Activation of proliferator-activated receptor Diokine (PPARcharlie) receptors decreased the severity of choline deficiency–induced steatosis (124). Choline-deficient humans have diminished plasma low-density lipoprotein cholesterol (derived from VLDL) (125) and elevated plasma homocysteine concentrations when they are challenged with a methionine load (82). This observation is consistent with the hypothesis that in humans, as in other species, choline is required for VLDL secretion."

    "In animals, renal function is also compromised by choline deficiency (8); abnormal concentrating ability, free water reabsorption, sodium excretion, glomerular filtration rate, renal plasma flow, and gross renal hemorrhage are noted. Infertility, growth impairment, bony abnormalities, decreased hematopoiesis, and hypertension have also been reported to be associated with diets low in choline content (8). In addition, pancreatic function can be compromised in animals fed methyl-donor–deficient diets (126). Choline appears to be needed for normal carnitine transport into tissues (127–130), and choline deficiency is associated with decreased serum and urinary carnitine concentrations (131, 132)."

    "Rats and mice fed a choline-deficient (and methyl-deficient) diet first accumulate large amounts of lipid in the liver that diminish as the liver becomes fibrotic, followed by foci of enzyme-altered hepatocytes that are similar to those induced during initiation of cancer with one of many different chemical carcinogens (120, 202–205). In choline deficiency, these altered foci of hepatocytes, which express y-glutamyltranspeptidase (206) and the placental form of glutathione S-transferase (207), precede the formation of adenomas and hepatocellular carcinomas (208). A diet containing 0.8% added choline completely prevented the development of cancer in experimental animals (209). Choline deficiency also sensitizes to hepatic carcinogens such as aflatoxin B1 (210), and it sensitizes to breast carcinogens such as dimethylbenz[a]anthracene (DMBA) (210), or DMBA and medroxyprogesterone acetate (MPA) (211), as well as procarbazine (212). For example, after treatment with procarbazine, mammary tumor incidence increased by more than 50% in male rats fed a choline-deficient diet compared with rats on a choline-adequate diet and treated with the drug (212)."​
    https://www.researchgate.net/profil..._Nutrition/links/00463522603a36807a000000.pdf

    "Total hepatic folate content decreased 31% after rats were 2 weeks on a choline-deficient diet, and an elongation of the glutamate chains of the folates was observed, which suggests prolonged retention time within liver (152). Rats fed diets deficient in both methionine and choline for five weeks had hepatic folate concentrations half those of controls (83). During choline deficiency, hepatic S-adenosyl-methionine concentrations also decreased as much as 50% (7, 135, 155, 190)."

    "In the human (187), rat (106), hamster (70), guinea pig (161), pig (17, 54), dog (13, 14, 79), and monkey (81), choline deficiency results in liver dysfunction owing to massive accumulation of triacylglycerol within the hepatocyte (21, 106, 107, 178, 179). In rats, fatty liver begins within hours to days after initiation of a choline-deficient diet (43)"

    "Choline-deficient humans have diminished plasma LDL cholesterol (187). This observation is consistent with the hypothesis that in humans, as in other species, choline is required for VLDL secretion."

    "Choline is the only single nutrient for which dietary deficiency causes development of hepatocarcinomas without any known carcinogen (121). Interestingly, choline-deficient rats not only have a higher incidence of spontaneous hepatocarcinoma, but they are markedly sensitized to the effects of administered carcinogens (121). Choline deficiency is therefore considered to stimulate both cancer-initiating and cancer-promoting activities. Several mechanisms have been suggested for the cancer-promoting effect of a diet devoid of choline. In the choline-deficient liver, a progressive increase in cell proliferation occurs that is related to regeneration of liver after parenchymal cell death (32, 33, 121). Cell proliferation (with an associated increasedrate of DNA synthesis) could be responsible for the greater sensitivity to chemical carcinogens (64). Stimuli for increased DNA synthesis, e.g. hepatectomy and necrogenic chemicals, increase carcinogenesis. However, the overall rate of liver cell proliferation could be dissociated from the rate at which preneoplastic lesions form during choline deficiency (154). This possibility suggests that cell proliferation is not the sole condition acting as a promoter of liver cancer. Methylation of DNA is important for the normal expression of genetic information. Undermethylation of DNA, observed during choline deficiency (despite adequate dietary methionine), may be responsible for carcinogenesis (48, 105). Another proposed mechanism derives from the observation that when rats eat a choline-deficient diet, increased lipid peroxidation occurs within liver (148). Lipid peroxides in the nucleus may be a source of free radicals that could modify DNA and cause carcinogenesis. Recently, we proposed that choline deficiency perturbs PKC signal transduction, thereby promoting carcinogenesis. As discussed above, choline deficiency causes massive fatty liver (see section entitled "Hepatic Secretion of Very Low-Density Lipoprotein")."

    "Malnourished humans, in whom stores of choline, methionine, and folate have been depleted (37, 153), also appear to need more dietary choline than did our healthy adult subjects. The liver is the primary site for endogenous synthesis of choline. Alcoholics with liver cirrhosis have diminished plasma choline concentration and fatty liver, which resolves when patients are supplemented with choline (37)."

    "Conditions that enhance hepatic triglyceride synthesis (such as carbohydrate loading) increase the requirement for choline needed for export of triglyceride from liver (31). Thus, treatment of malnourished patients with high-calorie parenteral nutrition solutions at a time of depleted choline stores might enhance the likelihood of hepatic dysfunction."​

    - "I Have Liver Issues And I Am Not Making Progress"


    3:51 - "if you accumulate fat in your liver cells, that in itself is associated with metabolic dysregulation and cardiovascular disease. And since the liver is the metabolic hub of the body, the central organ of detoxification, playing so many central roles, there are probably many reasons for why fat accumulation in liver would be associated with disease risk." "if you look at liver cells under a microscope, when they've accumulated triglycerides, the nuclei of those cells are flattened. That's because the triglycerides take up so much room, but there's not even room left for the nuclei of those cells. Imagine what that does to your glycogen storage. Those are the cells that you stored glycogen in. So if the fat is taking up so much room in the hepatocytes that it's smooshing and flattening the nuclei, you can bet your bottom dollar that that cell doesn't have room for glycogen storage. And if you are decreasing your ability to store glycogen, how are you going to maintain stable blood sugar through the course of the day and overnight, when your primary means of maintaining stable blood sugar in between meals is to access your hepatic glycogen?"

    7:00 - "The more fat you have circulating in the blood, the more exposure the liver has to that fat."

    7:28 - "out of [dietary fat, fructose, and ethanol], dietary fat is much more important simply because de novo lipogenesis, the synthesis of fat from nonfat precursors is a minor pathway in humans. De novo lipogenesis is increased threefold in people who have fatty liver disease, but its contribution to the hepatic fat pool is estimated to increase from about 5 to 15%. So it's still minor compared to dietary fat and circulating fat that's entering the liver because it's not being stored in adipose tissue [insulin resistance cycle]."

    10:42 - Lipid peroxidation leads to the oxidative destruction of hepatic ApoB [responsible for exporting fats from the liver]. Iron chelator or vit E, both normalize the inflammation that occurs when PUFA is present. They also almost normalize the secretion of the exporting protein in the presence of PUFA. "Oxidative stress in the liver causes a massive decrement in ApoB secretion."

    13:15 - Coconut oil abolishes inflammation as if animals weren't deficient (choline and methionine), quite remarkable. It also spares glutathione, again, as if animals weren't deficient. PUFA had the opposite effect.

    Coconut Oil
    The unsaturated oils in some cooked foods become rancid in just a few hours, even at refrigerator temperatures, and are responsible for the stale taste of left-over foods. (Eating slightly stale food isn't particularly harmful, since the same oils, even when eaten absolutely fresh, will oxidize at a much higher rate once they are in the body, where they are heated and thoroughly mixed with an abundance of oxygen.) Coconut oil that has been kept at room temperature for a year has been tested for rancidity, and showed no evidence of it. Since we would expect the small percentage of unsaturated oils naturally contained in coconut oil to become rancid, it seems that the other (saturated) oils have an antioxidative effect: I suspect that the dilution keeps the unstable unsaturated fat molecules spatially separated from each other, so they can't interact in the destructive chain reactions that occur in other oils. To interrupt chain-reactions of oxidation is one of the functions of antioxidants, and it is possible that a sufficient quantity of coconut oil in the body has this function. It is well established that dietary coconut oil reduces our need for vitamin E, but I think its antioxidant role is more general than that, and that it has both direct and indirect antioxidant activities.​
    15:35 - A low-fat diet is similar to coconut oil when it comes to inflammation. Ironically, consuming a low-fat diet rendered even worse accumulation of fat in the liver in comparison to coconut oil. However I opened the study a long time ago, and if I remember correctly, what they refer to as low-fat is questionable (and it was actually less PUFA than normal). So, all dietary fats tend to accumulate, including coconut oil and cause the mentioned problems at the begining, regardless of how safe they are. On the bigger picture, it can have a slightly negative effect. If you have too much stored PUFA, I would go the coconut oil route, with plenty of it. Rayzord mentioned that saturated fats can be curative in liver problems: if it's already turned to burning fats, it's better that you supply saturated ones to protect the organ anyway. But if you don't have excess of PUFA, it's better to go the low-fat route, and of course prioritizing coconut oil or butter as fats, just not so in great amounts. In both cases some vit E and iron chelators are probably helpful as well.

    17:08 - Green tea mimics fasting/caloric restriction. Since it all comes down to excess of what you can handle, minimizing energy intake will reduce the damage. There are many discussions on the forum about fasting defattening organs. It's stressful, but possibly less than the current overloaded state.[/QUOTE]​
    - "I Have Liver Issues And I Am Not Making Progress"

    "Increasing choline intake is not often mentioned for someone that needs to improve liver glycogen storage."​

    - "I Have Liver Issues And I Am Not Making Progress"

    Manganese in Health and Disease - Dorothy Klimis-Zacas

    "In vivo studies by Baquer et al.[22] have shown that Mn2+ given to young male rats in conjunction with a fat-rich diet stimulated lipogenesis. A lipotropic effect of manganese on the rat liver was reported by Amdur et al.[23] from experiments attempting to determine the effects of manganese and choline on bone formation in rats. The authors observed that manganese as well as choline prevented deposition of excess fat in the livers of manganese-deficient rats than in the livers of rats receiving adequate manganese. When level of choline in the diet was low, the lipotropic action of manganese was greater, indicating a manganese-choline interaction. Rats placed on a choline-deficient diet for 25 days exhibited lower hepatic manganese levels than those of controls.[24] The authors suggested that this was due to reduced intestinal transport of the metal. Barak et al.[25] also reported that a choline deficiency increased liver fat and reduced hepatic manganese content in rats. Moorkerjea[26] et no one else has shown that during the 5- and 21-day period of choline deficiency there was no lipid release from the liver concomitant with a reduced hepatic manganese content. An increase in hepatic manganese together with elevated hepatic lipid transport seemed to implicate manganese in the transport mechanism. Furthermore, the changes in liver ultrastructure that arose in choline deficiency were very similar to those observed in manganese deficiency.[27,28] These investigators reported that when mice were fed a manganese-deficient diet, ultrastructural changes were observed in their livers. Changes in the integrity of cell membranes were observed such as swollen and irregular endoplasmic reticulum and elongated and stacked cristae of the mitochondria in liver, heart, and kidney cells. Accumulation of large lipid droplets free of membranes, considered to be triglycerides, was observed in liver parenchymal and kidney tubule cells."

    Shameless plug:
    Manganese And Its Unimportance In Health

    - Dietary Choline

    "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"​

    - Dietary Choline

    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.​

    - "I Have Liver Issues And I Am Not Making Progress"

    Association between composition of the human gastrointestinal microbiome and development of fatty liver with choline deficiency

    "common single nucleotide polymorphisms (SNPs) in several genes have been shown to affect choline production and metabolism.16-17 One notable example is the gene, PEMT, which is important in the endogenous de novo synthesis of phosphatidylcholine. A common haplotype associated with a defective estrogen response element in PEMT's promoter region disrupts this critical process.16-17"

    "Previous literature suggests that changes associated with menopause in women, particularly when combined with relevant SNPs, may disrupt endogenous choline production, increase a subject's need for dietary choline and predispose post-menopausal women to developing fatty liver.16-17,
    51-52 If this model is correct, the subjects who deplete most on a choline deficient diet are those who are least efficient at endogenous choline production and are, therefore, the most dependent on obtaining needed choline from their normal diets."

    "Combining the SNP status of PEMT with the abundance of the two taxa produces a correlation with essentially no outliers (Figure 5D). These data support a model in which subjects with the ability to endogenously produce phosphatidycholine are less dependent on the composition of the microbial community. While such a model will need further validation, the observation that Gammaproteobacteria abundance went to zero in all but two of our patients when dietary choline levels were high (Figure 4) lends further support to the assertion that members of this taxa are involved in choline-sensitive pathways that have implications for host health."
    That's the common cascade of stress; disrupted balance; vulnerabilized, inflammed and less efficient organs; liver and intestines being no different.

    "Animal models have also suggested a relationship between choline deficiency induced fatty liver and the gut microbiome. Dumas et al. described a microbiota-mediated mechanism underlying the development of fatty liver that mimicked choline deficiency in mice fed high fat diets and was also associated with insulin resistance.29 This mechanism was explained by microbial flora that disrupt choline bioavailability to the host by converting choline to methylamines, although no specific taxa were named. Increases in Proteobacteria, the phylum that includes Gammaproteobacteria, were also observed in mice that were fed high fat diets and that exhibited increased obesity.12 A study of metabolic endotoxemia, high-fat diets and obesity identified lipopolysaccharide (LPS), a phospholipid in the outer membrane of most gram-negative bacteria53, as a possible culprit in the chronic inflammation that accompanies metabolic dysfunction, insulin resistance and diabetes.28 Recent work by Kudo et al. implicated gut-derived bacterial endotoxin in up-regulation of TNF-Waynish, apoptosis of primary hepatocytes and development of liver injury in a murine model of non-alcoholic steatohepatitis.54 Taken together, these studies provide support for the assertion that nutrient imbalance may trigger a bloom of inflammation-producing bacteria and concurrent metabolic dysfunction."
    There should be no doubt that emotional stress can initiate problems.

    __
    Thematic Review Series: Glycerolipids. Phosphatidylcholine and choline homeostasis

    "Recent studies indicate that choline is recycled in the liver and redistributed from kidney, lung, and intestine to liver and brain when choline supply is attenuated."​

    - Glycine Is An Endotoxin (TLR4) Antagonist

    "The biochemical studies on rats proved that glycine is synthesized from threonine (through threonine dehydrogenase pathway), choline (via formation of sarcosine), and serine (through serine hydroxymethyltransferase [SHMT]). Later on, in other investigations it was proved that the glycine synthesis in pigs, humans, and other mammals is through the abovementioned three pathways [8]. From the recent studies it was stated that hydroxyproline and glyoxylate are substrates for glycine synthesis in humans and mammals [9, 10]." [?]

    "Methyl groups are generated in the mammalian tissues during degradation of choline to glycine. Generally in adult rats around 40– 45% of the choline uptake is converted to glycine and this value can sometimes increases up to 70% when the choline uptake is very low." @Mito

    "The reactions involving the transfer of methyl group in cells are largely affected by S-adenosylhomocysteine to S-adenosylmethionine. If the content of choline in diet is very low, then glycine synthesis is quantitatively very low in mammals."​

    - Creatine


    - Folate And Other B's

    https://www.researchgate.net/publication/279402461_Folate_and_Choline_Interrelationships

    "It is likely that the dietary requirement for choline is affected by folate and possibly the intake of other methyl donors. The interrelationship between choline and folate arises from the participation of these nutrients in one-carbon metabolism (Figure 18.2). In liver and kidney tissue, either folate or betaine may serve as methyl donors for the conversion of Hcy [non-burtlancysteine] to methionine. Thus, deficiency of one nutrient may increase the demand for the other. Further, hepatic biosynthesis of phosphatidylcholine through the PEMT pathway is a major consumer of one-carbon units [18,56]. Thus, 5-methyl-THF, as a primary source of methyl groups for PEMT, is integral to de novo biosynthesis of choline. Finally, the catabolism of choline provides one-carbon units that ultimately feed into folate-mediated one-carbon metabolism as formate [57,58]. However, the quantitative signifi cance of the choline oxidation pathway to one-carbon metabolism is uncertain."

    "The choline-sparing effect and the lipotropic properties of folate depend on its possession of biologically labile methyl groups that may be used for the biosynthesis of choline (i.e., phosphatidylcholine) through the PEMT pathway. Evidence of interplay between folate and choline was demonstrated by showing perturbed choline metabolism, as assessed by abnormalities in hepatic betaine concentrations, in rats following the administration of the folate antagonist methotrexate [59]. Subsequent work showed that rats made severely folate deficient had 65% to 80% lower hepatic choline and phosphocholine concentrations than did folate-adequate controls; moderately folate-deficient rats had a 36% (P < .09) reduction in hepatic choline [60]. Investigations with healthy male [61] and female [62–64] study participants have also demonstrated an effect of folate intake on biomarkers of choline status. In premenopausal Mexican American (MA) women consuming a constant intake of choline (i.e., 349 mg/day), plasma phosphatidylcholine decreased in response to folate restriction (i.e., 135 μg of dietary folate equivalents [DFE]/day) and increased in response to folate treatment with 800 μg of DFE/day [62] (Figure 18.3). These findings are consistent with the important role of folate in providing labile methyl groups required for de novo biosynthesis of phosphatidylcholine through the PEMT pathway."

    "The interplay between folate and choline was recognized more than 50 years ago when the choline-sparing effect of folate was noted in animal models of fatty liver."​

    - Treatment Of Cirrhosis Of The Liver By A Nutritious Diet And Supplements Rich In Vitamin B Complex

    "In recent years a number of reports have suggested that the administration of choline or methionine may produce effects apart from that provided by diet. For reasons stated, it is not easy to evaluate these reports. It is far more difficult to establish controls and to determine the role of a specific dietary factor in studies of human beings than in experiments with animals. Our own limited experience does not suggest that choline and methionine exert a specific effect in the late stage of hepatic failure. It would seem that their field of greatest usefulness might be in the precirrhotic fatty stage of the disease, since they are lipotropic agents. There appears to be no danger in administering these substances, but there may be harm in stressing their importance to the extent that other factors are neglected. Although observations on laboratory animals have established that choline and methionine protect against experimental cirrhosis produced by diets low in protein, the evidence for their curative effect has been less conclusive. Certainly, it has not been shown that these substances alone are adequate for repair or regeneration of the cirrhotic liver. It is possible that several factors may facilitate repair of the liver and restoration of function."

    "In view of the experimental work on the lipotropic action and protective effects exerted by choline on the liver, it seemed plausible to Wintrobe and the writer to administer this substance to patients with cirrhosis as an additional supplement to the measures already outlined. At least ten patients have now received choline chloride, 1.5 gm. a day, administered in the form of a 10 per cent elixir prepared by the hospital pharmacy, in doses of 5 cc. after each meal. No untoward effects have been noted after the continued administration of choline for weeks or even months. It is as yet too early to speculate upon the possible merits of choline therapy in cirrhosis."

    - Pantothenic Acid Helped With Gut Troubles

    Acetylcholine comes from acetyl CoA (pantothenic acid) and choline. As suspected at this point, a chronic insufficiency in any of them can be involved in constipation:
    https://www.researchgate.net/profil...idiopathic-slow-transit-type-constipation.pdf

    Role of presynaptic nicotinic acetylcholine receptors in the regulation of gastrointestinal motility. - PubMed - NCBI

    Our emancipator wrote about this system and how problems arise when there's an excess of acetylcholine or not enough cholinesterase.
    New Page Title Here

    But the problem here is being managed by increasing acetylcholine.
    A choline deficiency is a possibility despite a normal intake:
    Supplementary Choline Raises Risk Of Blood Clots; Aspirin To The Rescue
    Now that is a good reason to consider a topical supplement. #Zeus

    Manganese involvement:
    The inhibitory effect of manganese on acetylcholinesterase activity enhances oxidative stress and neuroinflammation in the rat brain
    http://www.neurotoxicology.org.il/wp-content/uploads/2016/02/Mn_ACh_2007_NeuroToxicology.pdf

    Caffeine:
    Inhibition of acetylcholinesterase by caffeine, anabasine, methyl pyrrolidine and their derivatives - ScienceDirect
    Caffeine Inhibits Acetylcholinesterase, But Not Butyrylcholinesterase

    - Supplementary Choline Raises Risk Of Blood Clots; Aspirin To The Rescue

    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..​

    - "I Have Liver Issues And I Am Not Making Progress"

    Here's the problem that was mentioned a few pages back:
    https://www.preprints.org/manuscript/201709.0040/v1/download
    "Choline not only is an indispensable component of cell membrane phospholipids, but also plays important role in lipids metabolism. Choline facilitates the lipids transport in hepatocytes and prevents the abnormal accumulation of lipids in liver, while choline deficiency usually leads to hepatic steatosis [35, 36]. Gut microbiota also involve in choline metabolism by converting it into toxic dimethylamine and trimethylamine, which are transported to liver and converted into trimethylamine oxide (TMAO) that causes liver inflammation and damage [37]. The increased production of TMAO is also the culprit for cardiovascular disease [37-39]. On the other hand, the content of dietary choline influences the composition and abundance of gut microbiota that are associated with the development of NAFLD [40]. The close relationship between gut microbiota and choline metabolism provides important rationale for gut microbiota-targeted therapy for NAFLD.
    Bile acids are synthesized from cholesterol with a wide range of physiological functions. Bile acids can not only facilitate digestion and absorption of fat-soluble food, but also preserve the intestinal barrier and preventing bacterial translocation [41, 42]. Moreover, bile acids could function as signaling molecules that modulate the balance of bile acids metabolism by activating farnesoid X receptor (FXR) and G protein-coupled receptor (TGR5)[43-46]. Study reveals that antibiotics could attenuate the high-fat diet-induced NAFLD development by altering the composition of bile acids and inhibiting FXR signaling pathway, whereas mice with intestine-specific Fxr disruption have reduced triglyceride accumulation in the liver compared with control mice [47]. Bile acids usually have strong anti-microbial property and gut microbiota can also influence the homeostasis of bile acids pool by deconjugating and metabolizing the primary bile acids into secondary bile acids in intestinal tract, which are involved in modulating lipids and energy metabolism pathways during NAFLD formation[44]. The crosstalk between gut microbiota and bile acids provides fundamental evidence for gut microbiota-targeted therapy of NAFLD."

    "Compared to gut microbiota modulation with antibiotic, some ingredients from herbal medicines have shown effects on gut microbiota with minor side effects [152, 153]. Berberine is a typical herbal component with potent antibacterial activity, especially bacteria in intestinal tract because berberine can hardly be absorbed in gut [154]. Currently, increasing evidence has confirmed the therapeutic effect of berberine on metabolic diseases including obesity, NAFLD, and type 2 diabetes via modulation on gut microbiota [155-157]."

    "TSG (2, 3, 5, 4’-tetrahydroxy-stilbene-2-O-β-D-glucoside) is an active component from Traditional Chinese Medicine (TCM) Polygonum multiflorum Thunb, which has shown significant effect on NAFLD prevention by modulating gut microbiota, improving the intestinal mucosal barrier and suppressing the expression of NF-κB [160]."

    "Qushi Huayu Fang (a mixture of five herbs including Artemisia capillaries Thunb, Gardenia jasminoides Ellis, Fallopia japonica, Curcuma longa L., and Hypericum japonicum Thunb) is an ancient TCM formula which has been used for NAFLD treatment. Recent studies showed that administration of Qushi Huayu Decoction (QHD) significantly decreased body weight, alleviated hepatic steatosis, and reduced the content of TG and free fatty acids in liver in HFD-induced NAFLD rats. It showed that the CHF-treated group harbored significantly different gut microbiota from that of model rats, and the bacterial profiles of NAFLD rats could be modulated by the CHF [163, 164]. Recently, the anti-obesity property of daesiho-tang (DSHT) was also investigated. It was found that DSHT treatment significantly reduced serum TC and TG and hepatic fat accumulation which were associated with the regulation on abundance of gut microbiota [165]. Although the mechanisms underlying TCM are extremely complicated and largely unknown, gut microbiota was important target for many TCM formulas because many kinds of chemicals within TCM are unabsorbable that can influence gut microbiota directly or be metabolized into active form by gut microbiota."

    In other words, it's not guaranteed, so once again cravings are more reliable.​

    - The Travis Corner

    https://chrismasterjohnphd.com/2010/12/04/meeting-choline-requirement-eggs-organs/

    "folate, vitamin B12, B6, and betaine can spare choline, but only methionine can be used to make choline. The B vitamins and betaine can thus fulfill choline's role in methylation, at least in the liver and kidney, but only methionine can provide the choline needed to export liver fat, to serve as a neurotransmitter, or to make our cell membranes work properly."

    "the PEMT enzyme actually creates homocysteine in the process of creating choline! So, if your PEMT engine is running nice and smoothly, you can make your own choline, but you still need more betaine and B vitamins to neutralize the homocysteine that’s generated in the process. If your PEMT engine is working like this, however…

    … well, then, you’ve got another problem. If PEMT isn’t using up your methionine to make choline, the methionine is just going to go further on down that pathway shown above and make more homocysteine anyway!"​

    - The Travis Corner


    -----
    When gurus start having problem with a food, they tend to isolate it from meals or eat it plain as a way to prevent ruining the entire dish or to be able to grasp the reaction better; but this is a good way to intensify the problem. If the craving and need for it exists, it should taste good in a meal and the only precaution that is useful in my opinion is to increase the amount in the gradualities of the fashions. Force-feeding rarely works.

    Eggs can be beaten, but sometimes they beat people back. Then, gurus refrain from them and reintroduce them plain, away from a variety of foods and the reactions are worsened until it becomes unmanageable and avoidance is preferable.
    When the yolk is mixed with cheese or as an ingredient of a dish, it can help to avoid becoming food for bacteria.
    Speaking of beats, our composer (the one that's in Washington, and not New Hampshire, Oregon or Wisconsin) commented that enjoys omelettes. I guess he was born right:
    Ray Peat
    "Hans Selye did experiments studying the type of lesion in the heart produced by rapeseed oil, and he found that it was the linoleic acid in it, which is still in it. They took out the peculiar unusual fatty acid but the essential fatty acid linoleic acid is heart toxic. Hans Selye showed that if you added cocoa butter, a highly saturated stearic acid to the rapeseed oil, it no longer causes the death of the heart cells."
    Omelettes are can incorporate all sorts of ingredients/spices.

    The yolk can be punctured out of its sack to prevent allergy problems. If I'm not wrong, when it's cooked to gelation (between raw and rubbery), it's in its gentlest form. There are persons who prefer it owaacooked and I never understood why but I'm sure there is a good reason for it. It might damage the lipids but reduce problems in other regards, and if it's preferred this way, there has to be net gainz involved.

    For the people that have difficulty meeting their choline needs or are in critical conditions in which egg consumption can worsen the situation, it's worth considering reducing the fat intake (as perhaps the most important factor), then ingest enough of what could help the body in sparing synthesis or make its use more efficient: glycine, creatine, a little methionine, extra B-vitamins, and some betaine.

    Interactions Of Thiamine, Riboflavin, And Other B-vitamins
    "Glycine may be metabolized via several pathways. One pathway, important in both plants and animals, involves four proteins and the interaction of pyridoxal phosphate, NAD, FAD, and tetrahydrofolic acid."​

    Oranges can contain some choline if they're good. If not, they tend to be just a bag of funky wasser.

    Some dairies (such as whole cheese) provide too much fat for less choline in comparison with some meats. And meats contain creatine.
    Fermented Dairy Has Been A Staple Of My Diet, Causing Some Issues
     
  2. ecstatichamster

    ecstatichamster Member

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    Well done and I hugely appreciate you.
     
  3. Tenacity

    Tenacity Member

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    Aren't some vegetables good choline sources too?

    Awesome thread, thank you so much.
     
  4. paymanz

    paymanz Member

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    Low fat milk also is good source of choline.

    Thanks ,i like these type of threads ,they are good reference.

    I just wish you tag them so they can be find easier.
     
  5. OP
    Amazoniac

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    Excess niacin supplementation can aggravate a lack of choline:
    "It is [] apparent that catabolism of NAD places a substantial strain on the methylating capacity of hepatocytes. If we assume that 80% of a 2 gram daily dose of time-release niacin will be methylated, this will require the methyl groups from about 2 grams of methionine (in the form of S-adenosylmethionine). Under ordinary circumstances, the lion's share of the liver's methylating capacity is used for creatine synthesis (14), since creatine turnover (in males) is about 2 grams daily (of which the diet provides a variable quantity, up to 1 gram) (15), it can be estimated that less than 2 grams of methionine are required for daily endogenous creatine production. Thus, the methylation requirements imposed by high daily doses of niacin are large compared to the liver's normal methylating activity. Fortunately, the methionine synthase reaction (in which 5-methyltetrahydrofolate donates a serine-derived methyl group to homocysteine with the assistance of vitamin B12) can 'recycle' methionine so that a limited dietary intake of methionine is often sufficient to support ordinary methylation requirements. Theoretically, when methyl group demand is high, upregulated activity of enzymes required for de-novo serine synthesis and folate pool turnover might be expected to maintain adequate methylating capacity; however, it seems likely that at least in some individuals these adaptive mechanisms would function suboptimally. Thus, the additional methyl requirements imposed by high-dose niacin therapy may have the potential to strain the capacity of the methionine synthase reaction, such that the hepatocyte pool of S-adenosylmethionine (SAM) becomes significantly depleted. As a result, other crucial methylation reactions in hepatocytes – such as synthesis of membrane phosphatidylcholine – will be underactive. I postulate that this is the chief metabolic mechanism whereby high-dose niacin therapy evokes hepatotoxicity. Furthermore, inasmuch as S-adenosylmethionine is a potent allosteric activator of the enzyme cystathioninebeta-synthase (16), required for the irreversible disposal of homocysteine, it is reasonable to expect that such therapy will tend to raise serum levels of homocysteine – a phenomenon that presumably would have a countervailing negative impact on the vascular benefits of niacin treatment."

    "The fact that methyl donors (namely choline and methionine) are reported to correct niacinamide hepatotoxicity in rats (21), can be viewed as confirmatory of the role of methyl depletion in niacin toxicity. While one could postulate that some other factor associated with accelerated NAD production was responsible for niacin/niacinamide toxicity – for example, depletion of the hepatic pool of phosphoribosylpyrophosphate or of ATP (24) – such a mechanism would appear inconsistent with the ameliorative impact of lipotropes in niacinamide-treated rats."

    "Although supplements of methionine or SAM presumably could be used to increase the hepatic SAM pool, this strategy would have the disadvantages of increasing daily homocysteine production and of promoting calciuria (38). SAM has the further drawback that it is very expensive. (However, in syndromes mediated by oxidative damage, SAM has the advantage of increasing hepatic glutathione levels) (34). With respect to choline, it is a poor source of labile methyl groups in humans owing to the fact that human hepatic choline oxidase activity is very low compared to that found in rodents (39) (in which choline is an effective lipotrope). Thus, while supplemental choline may aid phosphatidylcholine synthesis by the salvage pathway, it could not be expected to correct a deficit of SAM."
     
  6. OP
    Amazoniac

    Amazoniac Member

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    Thank you all for the kind words and encouragement above.
    I thought it was only available for threads created in the 'Scientific of the Studies' section. How can I do it?
     
  7. paymanz

    paymanz Member

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    On top of your first post, "add tags"
     
  8. Mito

    Mito Member

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    0FFC0B33-C5E8-4ABF-95B3-0AC22C430402.jpeg

    https://chrismasterjohnphd.com/2017/08/12/living-with-mthfr/
    01:08:45 Compensate with choline
    “Reason number two that this is not all about 5-methylfolate, and this reason is about choline. So normally, you get your methyl groups when you’re recycling homocysteine to methionine about 50% from folate and 50% from betaine and choline. If you deprive someone of methionine and choline and all the other sources of incoming methyl groups, you can push that up to 100% derivation of methyl groups from folate. You can likewise push it down if your MTHFR activity declines, and you ramp up the use of betaine.

    So your real problem here is not so much that you don’t have methylfolate. That is a problem when it comes to the off switch on the glycine buffering system, which we’ll talk about shortly, but in terms of having methylfolate, it is not the case that you can’t methylate if you have less methylfolate. That’s not the case at all, because you can get those methyl groups from betaine in the exact same process of regenerating homocysteine to methionine, but derived not from folate, not from B12, instead from choline or dietary betaine or supplemental trimethylglycine.

    In people with MTHFR variations, what happens is that the use of betaine is increased. Now, exactly what happens to the choline depends on what study you look at, and it’s not that well-characterized. But it is clear that you use more of the betaine pathway.

    There’s a study in women that showed that when they have MTHFR polymorphisms, they are using the betaine pathway more. But surprisingly and counterintuitively, they are also taking choline and they’re shuttling it in through the CDP-choline pathway to make phosphatidylcholine.

    The reason that this is counterintuitive is that you would think that if they’re depending more on betaine, they would be trying to free choline for the choline dehydrogenase reaction to make more betaine, and they’re essentially doing the opposite. I don’t know why that is, but my suspicion is that it’s probably a way to protect the choline supply to make sure you don’t run deficient in the phosphatidylcholine that you need for your cell membranes.

    One of the reasons that—or one of the pieces of evidence that would support that is that when those women are given double the RDA for choline, that choline partitioning normalizes, so it gets rid of the shuttling of choline into phosphatidylcholine synthesis. And that seems consistent with the idea that the cell is saying, “Ah, I’m relaxed now. I’m relieved. I’m not worried that I’m gonna run out of phosphatidylcholine.”

    And the reason that that seems really significant to me is if you’re trying to minimize your free choline so that it doesn’t all get used for those reactions, you could potentially run deficient in acetylcholine, and that would affect your learning and your memory and your cognitive performance and your muscular function. It’s a speculative concern, but it’s a real one.

    There’s another study in Mexican-American men showing that the choline dehydrogenase reaction is increased and that they are oxidizing more choline to betaine. That suggests a different type of choline partitioning, but it suggests that when you have the MTHFR polymorphism, you’re depleting yourself of choline.

    Whichever study you look at, it implies that there’s a major increase in your need for choline when you have the MTHFR polymorphism. And in fact, there was a study showing that there’s DNA damage in people with the MTHFR polymorphisms that is abolished when you double the RDA for choline.”
     
  9. OP
    Amazoniac

    Amazoniac Member

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    With:
    - 8g of glycine
    Rayzord suggests 1/3 to 1/2 of gelatin. Since 60g of proteins tends to be enough to keep most people at balance (if there's not much stress present), then 20-30g of additional gelatin would help balancing them. Gelatin is about 30% glycine, so that equates to 6-9g of it.​

    - 2g of creatine
    - 150mg of taurine

    Ps.: these are just for a notion because the needs can vary a lot depending on the situation.
     
  10. OP
    Amazoniac

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    "I Have Liver Issues And I Am Not Making Progress"
    "Based on Travis' work, mature coconuts are quite nutritious, unfortunately all is lost in coconut oil. Coconut milk should be superior to the oil if you're not allergic to it. You would expect that not only the characteristic way its fatty acids are metabolized can contribute to fatty liver, but also for being an oil devoid of nutrition because all in all it always comes down to excess energy or being incapable of processing, and both should be made worse when there's not enough nutrients available."
     
  11. Dan Wich

    Dan Wich Member

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    I second this, you've really been compiling interesting stuff.

    Just a "testimonial" that this full podcast is worth a listen for anyone that suspects MTHFR issues. I'd ignored the MTHFR stuff for a long time because it was so genetic determinist-ey, but the tips from this seem to have improved my stress resistance.
     
  12. ecstatichamster

    ecstatichamster Member

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    Thanks Dan. Can you elaborate as to what it convinced you to do differently?
     
  13. Dan Wich

    Dan Wich Member

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    I've been eating more protein, egg yolks (choline), and carrots/spinach/kale (folate). I was already getting a good amount of glycine, so I didn't increase that intake.

    Granted, maybe those foods are just generally beneficial. But I'm heterozygous for C677T and A1298C (and now I'm scared to open Haidut's thread about genetic testing), so it seems reasonable that I'd benefit.
     
  14. Dan Wich

    Dan Wich Member

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    Someday I'll shell out to test my consistently high homocysteine as a more objective measure.
     
  15. OP
    Amazoniac

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    StressCholine in context: proportions of the vitamins

    upload_2018-4-14_17-27-23.png
    (colors were auto)​

    I picked beef liver because I couldn't find human. Since our reserves for these vitamins don't last long and this organ concentrates it, I figured it can be useful.

    Choline value for RDA was 400mg.

    So when supplementing something like 100mg of thiamine, even though it's safe, keep in mind it's an unusual amount, it must be good to ensure that you're getting enough choline in the diet.

    Mito, thanks for the selected parts above.
     
  16. raypeatclips

    raypeatclips Member

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    When you say you are eating more egg yolks, how many are you eating on average?
     
  17. Dan Wich

    Dan Wich Member

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    I've been having 4 on most days based on that Chris Masterjohn podcast. But now that I look at it, most sources are saying eggs yolks are down closer to 115-140mg of choline, so I'm thinking that may not actually get into the 900-1200mg range he suggests.
     
  18. raypeatclips

    raypeatclips Member

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    Do you make sure to buy eggs from pasture raised, daily massaged and bathed, individually nicknamed chickens?

    Has Peat ever commented on the MTHFR gene situation?
     
  19. Dan Wich

    Dan Wich Member

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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.
     
  20. Wagner83

    Wagner83 Member

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    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.
     
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