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Hypolipidemia, Low Cholesterol, And The Art Of Being Hormoneless

  1. Great thread, thanks!
  2. Question: what are the best ways to get more cholesterol? Say I get sick of egg yolks for a while. Are there any reasonable supplements, or other foods that come close to eggs?
  3. @AnonE
    -Saturated fat (beef tallow, cocoa butter, butter, coconut oil)
    -sugars (fruit, juice, honey)
    -organ meats
    -dairy if tolerated
  4. Thank you for these postings. My husband recently had a stent put in, was placed on statin drugs that lowered his LDL cholesterol from a normal 161 to 61 and HDL lowered to <27. He was also placed on digoxin for heart racing and thyroxine for hypothyroidism. That is a contradiction in application for sure. One slows the heart rate and the other increases it..... ? He also has been diagnosed with MDS and CMML leukemias. Only from reading this forum and Dr Peat have I been informed enough to know that low cholesterol isn't a good thing if one expects protective hormones to be formed, and thyroid meds given to someone with extremely low cholesterol has detrimental effects. We stopped the statin drugs and the digoxin, and cut the thyroid med in half. In later tests he was found to be low in magnesium. He has no racing heart since stopping the digoxin. It is scary to go against mainstream doctoring but it can be life altering negatively to blindly allow another human being to dictate one's health future. I appreciate all of the postings on this forum as they allow one to examine evidence and form opinion as relating to the persons' individuality.
  5. - Hypocholesterolemia in clinically serious conditions - review

    "Cholesterol is an inevitable component of almost all phospholipid membranes in the human organism. It occurs in both the free and ester form of cholesterol and fatty acids. Free cholesterol is a component of cell membranes. In plasma, about one third of cholesterol is free, and two thirds exist as esters containing linoleic and oleic acids[1]. [We can infer that Diokine wasn't the subject in question] Intracellularly, the stockpool of cholesterol is formed by its esters with oleic, palmitic and linoleic acids in some cells. Cholesterol in the organism originates both from the external environment by absorption from the digestive tract and by synthesis de novo from acetyl-CoA. Under normal circumstances, a significant portion of the required amount of cholesterol is obtained from food."

    "Absorption of cholesterol is a complex process performed by specific carriers on the brush border of enterocytes in the jejunum."

    "Cholesterol absorption effectiveness ranges around 50-60% depending on the kind of diet and its cholesterol content. During the day, on average about 250-500 mg of cholesterol is absorbed in this way, and this amount is regulated by enterocyte nuclear receptors."

    "Under physiological conditions, de novo synthesis in the whole body exceeds absorption of cholesterol from food several times. All cells of the human body except nucleus-free erythrocytes are able to synthesize cholesterol de novo and the product is dedicated for intracellular use. Cholesterol dedicated for plasma lipoproteins (additional supply for many types of cells) is synthesized in the liver and in the distal part of the small intestine[10]."

    "Complete biosynthesis (Fig. 1) of cholesterol amounts to nearly 200 enzymatic processes, and thus it is not surprising that higher organisms at the top of the food pyramid make use of cholesterol synthesized by lower organisms, thus saving the load connected with the hugely complicated and energy-demanding cholesterol synthesis. Thus, many tissues prefer cholesterol from plasma lipoproteins rather than their own intracellular synthesis. Also from this viewpoint it is logical that cholesterol synthesis, because of its energy demands, takes place mainly in the night between 2 and 4 a.m., in the period of physical rest of the organism. The maximal synthesis of cholesterol in a healthy human being varies in the range of 500-1000 mg a day."

    "The major excretory pathway for cholesterol is bile formation. Cholesterol is a substrate for bile acid formation. There are two major pathways of bile acid synthesis – neutral (“classic”) and acidic (“alternative”). In the neutral, or “classic” pathway, synthesis begins with hydroxylation of the cholesterol molecule in the 7α position by microsomal cholesterol 7α-hydroxylase (CYP7α1); in the acidic, or “alternative” pathway, bile acids are hydroxylated in position 27 by cholesterol 27-hydroxylase (CYP-27) (ref.15). While people with inborn errors in the CYP7α1 pathway display a hypercholesterolemic phenotype and resistance to cholesterol lowering agents, CYP-27 deficiency is responsible for a severe clinical picture, characterized by neurological impairment and accelerated atherosclerosis[15]. Bile acids achieve multiple physiological functions: they are mandatory for lipid digestion and absorption in the intestine; they represent the end product of cholesterol catabolism; they constitute the most important molecules to drive bile formation and flow, a property otherwise termed “choleretic activity”. Cholesterol itself is also secreted in bile, stored in the gallbladder and expelled in the intestine upon feeding. Thus, intraluminally there is almost always more cholesterol from bile than from the diet[10]. At present, the only recognized disposal mechanism of body cholesterol is through biliary excretion. The liver is thereby the main source of both cholesterol synthesis and disposal."

    "[..]important by-products of the cholesterol synthetic pathway are ubiquinones, which play a decisive role in the maintenance of reduction-oxidation balance and oxidative phosphorylation in cells and, dolichols which are essential in the process of glycoprotein synthesis[1]."

    "The hypocholesterolemia of acute illness is associated with a moderate increase in triacylglyceride levels caused by an increase in VLDL. The increase in triacylglycerides is a consequence of both decreased clearance and increased hepatic lipogenesis. Animal studies have shown that the hepatic triacylglycerol output can increase by 50% within 2 hours of endotoxin challenge and that both TNF-α and IL-6 increase hepatic lipogenesis[57, 58]. Increased adipose tissue lipolysis in response to endotoxin and cytokines provides increased quantities of fatty acid for triacylglycerol synthesis. Muscle and adipose tissue biopsies taken from patients with sepsis have shown reduced lipoprotein lipase activity, and animals with sepsis have shown decreased triacylglycerol clearance when exogenous lipid is infused[59]. In vitro studies have shown that TNF-α suppresses lipoprotein lipase activity[60]."

    "In pathological processes connected with pus formation, there are very large losses of cholesterol, which is eliminated from the organism in the form of disintegrated white blood cells, and this cholesterol cannot be reutilized. The need for cholesterol for cell division and reparative processes may exceed by 5 to 6 times the maximum endogenous cholesterol synthesis[32, 61]. In gastroenterological patients in critical conditions with large losses of enteric material from fistulae or ileostomies, a large loss of cholesterol may occur in the form of bile acids, due to interruption of the enterohepatic cycle."

    "At the other end of the causes of hypocholesterolemia there is a decrease in cholesterol supply. Critically ill patients naturally do not receive peroral food, an important external source of cholesterol. The only possible nutritional support for these patients is parenteral or enteral nutrition. Only some parenteral fat emulsions contain trace amounts of cholesterol (the source of cholesterol is lecithin from the egg yolk used as the stabilizer and emulsifier of intravenously administered fat emulsions). The amount of cholesterol in parenteral nutrition, however, does not exceed 25 mg per day (65 mmol per day) even when fat emulsions with the highest cholesterol content are employed. Undoubtedly, this does not suffice to cover even a fraction of the requirements of the organism in critically ill patients."

    "Hypocholesterolemia is common in critically ill patients. Lipids have been found to play an important rôle in the reaction of the organism to inflammation and generally in immune functions. Their role in neutralization of lipopolysaccharides, i.e., endotoxins, is of particular importance."

    "Hypolipidemia reduces competition for binding of lipopolysaccharide (LPS) to lipopolysaccharide-binding protein (LBP), leading to ligation of the CD14 complex and activation of mononuclear cells[62-64]. Conversely, binding of LPS to lipoproteins facilitates delivery of LPS to hepatocytes for detoxification, which if insufficient may lead to increased mononuclear cell activation[65]."

    "Lipoproteins, especially HDL, bind to and neutralize lipopolysaccharide (LPS). Reconstituted HDL (rHDL), which consists of purified apolipoprotein A1 and phosphatidylcholine is even more eff ective in neutralizing endotoxin toxicity[66]. In rabbits, administration of rHDL reduced TNF production in response to LPS (ref. [67, 68]) and reduced TNF production and acidosis after E. coli, but not S. aureus bacteremia[69, 70]."

    "The degree of hypocholesterolemia reproduces, in a parallel manner, the seriousness of the inflammatory response and metabolic dysregulation, abnormalities in cytokine level, gravity of illness and organ dysfunction, and it has a negative predictive value[35, 61, 79-86]."

    "An important clinical observation has been that in critically ill patients with hypocholesterolemia there is progressive increase in cholesterol concomitantly with the general improvement of the clinical condition; therefore repeated cholesterol determinations may provide useful information on the course of the disease[35]."

    "In patients with prolonged septic shock, absolute or relative adrenal insufficiency is found[80]. This phenomenon can be explained by the central role of cholesterol in the production of adrenal hormones, primarily cortisol."

    "The adrenal gland does not store cortisol: increased secretion occurs because of increased synthesis controlled by adrenocorticotropin (ACTH). Cholesterol is the principal precursor for steroid biosynthesis in steroidogenic tissue. In a number of sequential enzymatic steps, cholesterol is metabolized by P450 cytochromes to aldosterone, dehydroepiandrosterone, androstenedione, and cortisol. The first and rate-limiting step is the formation of pregnenolone from cholesterol. At rest and during stress about 80% of circulating cortisol is derived from plasma cholesterol: the remaining 20% is synthesized in situ from acetate and other precursors[91]. Experimental studies suggest that HDL is the preferred cholesterol source of steroidogenic substrate in the adrenal gland[92]."

    "Besides the reparative role in the restoration of damaged cell membranes, cholesterol also plays an important role in organization and development of tissues and organs."

    "Hypocholesterolemia is also related to decreases in some plasma proteins. Direct relationships between cholesterol and albumin, total protein, prealbumin, retinol-binding protein, transferrin, iron binding capacity, cholinesterase, and prothrombin activity have recently been confirmed[34, 82, 84, 94, 95]."

    "It is worth noting that the degree of hypocholesterolemia may be moderated by the simultaneous presence of cholestasis."

    "There is a well-known relationship between hypocholesterolemia and undernourishment. Hypocholesterolemia was experimentally induced by a low-protein diet, and on the other hand, alleviated by parenteral supplementation of amino acids, mainly branched-chain amino acids[82]."

    "Cholesterol seems to be a potentially essential component of nutrition, particularly in critically ill patients, where, due to the absence of cholesterol in parenteral nutrition, its exogenous supply is discontinued."​

    - Chris Masterjohn — My Experience With Vegetarianism
  6. - Revisiting Human Cholesterol Synthesis and Absorption: The Reciprocity Paradigm and its Key Regulators (!)


    "Cholesterol biosynthesis is regulated through a system of feedback inhibition where the intracellular cholesterol levels are sensed, resulting in the modulation of the expression of key proteins that control cholesterol homeostasis [18]."

    "Increasing the meal frequency reduces cholesterogenesis [20, 25, 26]."

    "Dietary cholesterol is thought to modulate the cholesterol synthesis, and in humans, dietary cholesterol provided at different levels in various studies either modestly altered or suppressed [31, 33–36] or did not have any effect at all [12, 37–39] on cholesterol synthesis. However, in some studies, an almost equal decrease in synthesis per increase in absorbed cholesterol was observed [40, 41]. Jones et al. [36] measured DI and mevalonic acid excretion in individuals and found modest decreases in synthesis when dietary cholesterol was provided in a stepwise incremental fashion from 50 to 650 mg/day. However, the cholesterol-absorbing and cholesterol-synthesizing ability of each individual could heavily influence this push–pull mechanism, accounting for a wide inter-individual variability in responsiveness to dietary cholesterol."

    "One of the key factors that must be taken into account is overweight and especially abdominal obesity [42–44] which have larger effects on cholesterol synthesis. The rate of synthesis is estimated to range between 11 and 13 mg/ kg/day at an ideal weight, whereas with increasing adiposity and weight gain, the synthesis rates could rise up to 20 mg/kg/day [45]. Such an increase is often associated with a suppression of cholesterol absorption [13, 46]. Conversely, weight loss of 3–8 kg in overweight and obese men resulted in a decline in whole body cholesterol synthesis [47], which corroborates the existence of body weightdependent reciprocity between cholesterol synthesis and cholesterol absorption."

    "In humans, circadian rhythm is thought to play an important rôle in cholesterol synthesis. Fractional synthesis rates (FSR) were found to peak at 06:00 h and reach a nadir at 14:00–18:00 h [48]. Delaying meal times altered maximum and minimum cholesterol synthesis rates [49]."

    "In humans, cholic acid supplementation enhances cholesterol absorption and suppresses cholesterol synthesis, indicating the influence of circadian rhythm [54, 55]."

    "Intriguing evidence suggests that adult blood cholesterol, and thus CVD risk, may be influenced by feeding practices in early life [82–84]. The importance of the cholesterol content of early nutrition and its possible imprinting of later cholesterol metabolism was first hypothesized by Reiser and Sidelmen [85]. These authors concluded that serum cholesterol homeostasis undergoes canalization on the basis of the cholesterol content of milk [85]. Cholesterol content of human milk (90–150 mg/L) is greater than that of regular cow’s milk formulas (10–40 mg/L) or soy milk-based formulas which contain no cholesterol [86]. The lower plasma cholesterol concentrations observed in adults who had been breast-fed in infancy raise the possibility that exposure to high cholesterol-containing breast milk may have long-term effects on processes controlling sterol trafficking and thus plasma cholesterol concentrations in later life [87–89]."

    "Maternal nutrition during pregnancy plays a major role in determining the health of the offspring as well as lipid metabolism through fetal programming [105]. Protein and folic acid content of the diet are found to impart a programming effect on the offspring’s lipid metabolism which was also dependent on the fat content of the diet [105]. These findings suggest that maternal undernutrition could result in long-term dysregulation of cholesterol metabolism in the offspring through epigenetic mechanisms."

    "[..]of noteworthy importance is the short chain fatty acid (SCFA) production and metabolizing functions of the gut microbiome [111]. SCFA are known to modulate various physiological functions in the host and serve as substrates in the cholesterogenesis pathways [111]. Hence, the role of SCFA-enhancing substrates such as dietary fibres and their contribution towards cholesterol homeostasis require further research."

    "Environmental pollutants are one of the major emerging factors that result in significant negative health outcomes because of their purported disruptive effects on endocrinal physiology and metabolism of humans [115]. Chronic exposure to organic pollutants has been established to result in insulin resistance [116]. It has also been shown that pollutants such as phthalates, organophosphates, and fibrates modulate liver X receptors (LXR), which play an essential role in cholesterol homeostasis and bile acid, triglyceride, and carbohydrate metabolism [117, 118]."

    "Decreased size of the biliary bile salt pool and output and biliary phospholipid output reduces the proportion of cholesterol absorbed [119, 142–144]. Also, factors such as increased cholesterol content of bile, hydrophilic-hydrophobic index of bile salt pool, and biliary cholesterol output suppress absorption [145, 146]. Such a suppression of absorption can be expected to result in a corresponding elevation in synthesis. Conversely, when dietary cholesterol intake is increased, the push–pull mechanism starts to suppress cholesterol synthesis through the SREBP1 pathway, triggering an enhanced secretion of cholesterol into bile and bile acids synthesis from cholesterol [147]."

    "Luminal factors such as increased gastric emptying and small intestinal transit times are known to increase absorption [119, 148, 149]. Reduced mucin production, especially Mucin1, has been identified to reduce absorption as well [119, 148]. Knockout studies in mice with deficient activities of enzymes CEL and pancreatic triglyceride lipase have shown reduced cholesterol absorption in the intestine [119, 128, 150]. These factors could potentially induce the cholesterol synthetic machinery and compensate for the reduced absorption."

    "Dietary fibres are known to have an impact on cholesterol absorption, because of their ability to sequester bile acids affecting the enterohepatic bile acid cycle [157]. Another potential possibility by which dietary fibres could directly affect cholesterol synthesis is by lowering postprandial glucose levels, resulting in a decline in insulin levels and consequently suppressing hepatic cholesterol synthesis by inhibition of HMGCR [158]. However, these suggestions need further exploration in the direction as to what degree the push–pull function is altered. Also, a bidirectional physiological association between dietary fibres (prebiotics) and their metabolizing gut microbiome is known."

    The guru needs to be more careful with roughage when dealing with fairly low cholesterol.​

    "The normal dietary intake of phospholipids is 2–8 g/day from foods such as eggs, organ and lean meats, fish, shellfish, cereal grains, and oilseeds [159]. Higher amounts of dietary phospholipids lead to decreased cholesterol absorption as demonstrated consistently in animal and human studies [160, 161]."

    "Plant sterols significantly inhibit intestinal cholesterol absorption with an efficacy of 5–15% from dietary and biliary sources [140, 164]."

    "The role of the gut microbiome in cholesterol absorption originates from the fact that the bile acid metabolism is affected by the gut microbiome. Recent studies show that the microbiome not only controls the composition of the bile pool but also affects the expression of genes controlled by FXR [211]. In the small intestine, bile salt hydrolaseactive bacteria in the gut microbiota perform bile acid deconjugation and aid in the maintenance of normal levels of circulating deconjugated bile acids and cholesterol [211, 212]. These studies therefore suggest that the gut microbiome could potentially affect intestinal cholesterol absorption and also result in a corresponding alteration of cholesterol synthesis."
  7. In the article below, Mito discussed how fatty liver induced by choline/methionine deficiency in lab animals can lower their circulating cholesterol and providing those again normalizes it. Fucose and saturated fats indeed increase its synthesis in liver, but to show up in blood, fats has to be export'd. It might not be as simple as having adequate methyl donors in the diet because some other factor can leave them stuck, such lack of enough magnesium, poor metabolism, inflammation and other good stuff.
    - Why Is My Cholesterol So High On This Diet? (check out comments)

    - Cholesterol - Wikipedia

    "All animal cells manufacture cholesterol, for both membrane structure and other uses, with relative production rates varying by cell type and organ function. About 80% of total daily cholesterol production occurs in the liver and the intestines;[25] other sites of higher synthesis rates include adrenal glands, and reproductive organs."​

    Not sure if bacterial overgrowth can interfere with the production at the distal small intestine, it might given that the region starts to harbor a lot of microbes but is more susceptible than the colon to their toxins.

    - The Travis Corner

  8. I appreciate the quote Amazoniac.

    After reading Masterjohn's post I get that choline deficiency causes low cholesterol; but I eat 2 eggs, a 150gr of beef and lots of low-fat milk daily, so I doubt that choline deficiency could be my issue.

    You also seem to mention how endotoxin could be interfering with cholesterol production. This is something that I was already considering, and I recently started a course of 2 weeks on Erythromycin to clean up my gut from endotoxin.

    Is there anything else that I am missing from the links and references you posted? I would appreciate if you could summarize what I am missing so I know what action to take.

  9. Yeah, it was mentioned that it might not be as simple as consuming enough because they have to be utilizable.

    - Microbial impact on cholesterol and bile acid metabolism: current status and future prospects
    There are threads on the foro discussing tests. But it's worth trying due to its safety, even if it's just for the sake of confirmation.

    These are just abstracts, but they can be a starting point for you search:
    - Lipid metabolism and magnesium
    - Vitamins and lipid metabolism

    Carotenoid-rich foods in most meals that happen to contain fat will be disrupting for someone that doesn't metabolize them properly. Raj has commented that their excess can affect hormonal functioning and the action of poisonoids. Apparently the most affected substances are lipids, their similar nature makes carotenoids prone to build up in places where they can be interfering.

    Our coach has also claimed that poison A is involved in the formation of steroids, but (at least in rats) it influences cholesterol synthesis as well:

    - Vitamin A Action on Hepatic Cholesterol Biosynthesis
    - Vitamin A Function in Ubiquinone and Cholesterol Biosynthesis

    If what was described above is happening to some extent, you'll have less active poison locally than assumed and venom D might accentuate this. But if your metabolism is sharp, this should not be an issue.

    Contrary to it, when people megadose on poison A, the excess can have a detrimental effect of lipid metabolism as well. Sometimes there can be confusing responses because the animal can be intoxicated but not being able to use, or having lower reserves and using it properly, so the activity has to be considered.

    Acetyl CoA can be formed through others means other than acetate, but it's one of the ways to obtain it and must be significant (some messages sent to a dear guru)..

    Not enough copper (whether it's due insufficient intake, functional deficiency or increased requirements from stress) is known to disturb lipid metabolism.
  10. - Fatty Acids, Gut Microbiota, and the Genesis of Obesity

    "Propionate has a role as a substrate for hepatic gluconeogenesis, in addition to inhibiting the synthesis of hepatic cholesterol. Acetate is the most abundant SCFA, being absorbed and metabolized rapidly by the liver, where it serves as a substrate for cholesterol synthesis and lipogenesis [24]. It is also involved in the satiety process by inhibiting pro-opiomelanocortin (POMC) in the hypothalamus [25]. As acetate and propionate exert opposite functions in lipid metabolism in the liver, the proportion of these two SCFAs is important to maintain lipogenic balance and cholesterol synthesis [26]. Butyrate is found in a lower quantity than the other SCFA in the blood circulation. It is the main source of energy for enterocytes. It acts mainly in cell regulation and proliferation, especially in colon intestinal cells, and plays a role in anomalous cell apoptosis. In addition, it has a function in the maintenance of tight junctions and is responsible for preserving the integrity of the intestinal barrier [27]."​
  11. - Short chain fatty acids in human large intestine, portal, hepatic and venous blood

  12. Also:

    - Colonic Health: Fermentation and Short Chain Fatty Acids

    "Various population survey data show that fecal SCFA production is in the order of acetate > propionate > butyrate[8] in a molar ratio of approximately 60:20:20, respectively.[9] The ratio seems to remain fairly constant,[10] although alterations in production and absorption may occur with dietary changes."​

    Therefore, according the figures above, already disconsidering what's not adsorbed and that acetate is the lightest of them, we may obtain 9 grams of acetate daily just from the colon.
  13. yerrag, have you read this?
    - Be Wary Of Vitamin D Supplementation
    I wasn't commenting on his case, it was in general for those who are struggling to clear the poison.
    Check out the last link of post #8.
  14. CFE11E7C-A455-4758-A96C-7384FF30F1F2.png I found this cool online tool you can use to plug in your cholesterol numbers and get a risk report.
    They site owners have a keto bent but there’s still some good information on cholesterol.