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NOTE: None of the following was written or edited by AI. All of this
material was copy and pasted by me from diverse articles and studies,
search engine results, Facebook or YouTube posts and comments, and then
summarized, combined, and edited by me together with a few comments and
thoughts of my own. At the time it was not practical to record every
citation for every phrase or sentence or paragraph. I did not plan on
or realize early on that this would be so wide-ranging as it has turned out
to be. A fair amount of original source materials is in the
Documentations on or videos listed throughout the Carnivore section of this
website. Thank-you.
ANTI-NUTRIENTS Many of the nutrients in plants are blocked from being absorbed by humans because of numerous compounds also in plants which are labeled as anti-nutrients. Some of these have been/are used by humans for their anti-oxidant, anti-bacterial, anti-fungal, and other medical properties for millennia, as well as for culinary and industrial (i.e., tanning) purposes. Anti-nutrients are self-protective chemicals or defensive compounds in plants, and also some of the resulting metabolites created in animals when the plants are ingested. Many plants contain more than one of these and they may serve to regulate processes in plants in addition to being protective. "Anti-nutrients" include such things as alkaloids [at least seven broad categories for hundreds of thousands of these nitrogen-containing compounds: human reactions include drug and mushroom toxicities, hypoglycemia, hyperthyroidism, acute tetanus], amylase inhibitors [block up to half of carb-digesting enzymes leading to GI discomforts], coumarins [over 1,000 naturally-occurring compounds: increase bleeding and bruising, respiratory and GI discomforts and skin reactions], cyanogenic glycosides [90% of known cyanogens: acute cyanide intoxication], FODMAPS [fermentable oligosaccharides, disaccharides, monosaccharides, and polyols: can cause GI discomforts], furanocoumarins [at least two dozen types of photosensitizers: pigment-stimulating and GI issues; mostly from the Apiaceae, Rutaceae, Moraceae, Polygonaceae, and Hypericaceae families, and to a lesser extent the Amaranthaceae, Anacardiaceae, Fabaceae, Rosaceae, and Asteraceae families among others: primarily celery, carrots, dill, fennel, parsley, parsnip, anise seed, citrus (orange, grapefruit, lemon, lime, kumquat, mandarin, bergamot, etc.), rue, fig, mulberry, breadfruit, buckwheat, St. John's Wort, spinach, aloe, chickpea, soybean, pea, clove, coffee, chili pepper, turmeric. (Seed oils have also been implicated as well.)], glucosinolates [about 132 types that cause GI discomforts and are degraded by gut microflora to form nitriles, isothiocyanates, and sulforaphane, which are then metabolized to goitrin and thiocyanate which interfere with the uptake of iodine by the thyroid gland and block the synthesis of the thyroid hormones T3 (thyroxine) and T4 (triiodothyronine) increasing the risk of thyroid diseases, such as goiter and hypothyroidism], goitrogens [mainly goitrins, thiocyanates and flavonoids which affect the thyroid gland and block cellular uptake of iodine], hemaglutinins and lectins [over 500 identified and isolated types: interfere with mineral absorption, bind to intestinal cells causing autoimmune issues, GI discomforts], lipase inhibitors [interfere with absorption of fat and fat-soluble vitamins], oxalates [mineral binders producing crystals and about 75% of all kidney stones], phytates and phytic acid [in the bran of grains and outer layer of legumes and some vegetables, these chelate minerals (P, Zn, Mg, Cu, Fe) into insoluble complexes which then starve our cells no matter how much we consume], phytoestrogens [endocrine disruptors], polyphenols [8K compounds including flavonoids (60%), phenolic acids (30%), isoflavones, and lignans, some are recommended for their antioxidant and anti-inflammatory that may lower blood sugar, blood pressure, heart disease and certain cancers' risk: they also inhibit iron absorption and digestive enzymes], protease inhibitors [read halfway down this page, https://my.clevelandclinic.org/health/treatments/24937-protease-inhibitors], resins [allergic reactions, GI discomforts, bruising or bleeding], salicylates [respiratory and intestinal tract and skin reactions], saponins [over 500 known types: block nutrient absorption, damage fat metabolism, and disrupt endocrine function], tannins [interfere with iron absorption and cause GI discomforts], terpenoids [bruising or bleeding, anemia, GI discomforts, peripheral neuropathy, headaches, mouth sores and ulcers], toxalbumins [GI discomforts and skin reactions], trypsin inhibitors [impede protein and nutrient absorption, GI discomforts, impair thyroid function, damage the pancreas, skin reactions] and indigestible fiber [GI discomforts]. Therefore the amounts of nutrients technically noted in plants are not very bioavailable to us -- even if the plants are soaked or cooked. Plus the Omega-3 fatty acid we can get from plants is not in a form we can use, and there is all that gas-producing indigestible fiber they have. And many commercially-grown food plants have pesticide and herbicide residues these days which are not only on the surfaces but are often taken up and incorporated into the plant itself and thus cannot simply be washed off. Drinking plant juices and smoothies, specifically, give our guts very concentrated amounts of the antinutrients in a very short time. Seaweeds contain various anti-nutrient compounds -- and heavy metals -- that can reduce their nutritional quality and hinder the absorption of essential nutrients. These compounds can negatively affect human and animal health by decreasing the availability of vital nutrients, leading to deficiencies and related disorders. These compounds include trypsin and α-amylase inhibitors, polyphenol compounds such as tannins, lectins, phytates, saponins, alkaloids, terpenoids, oxalates, and cyanogenic glycosides. Seaweed polysaccharides are also regarded as an antinutritional factor that limits the action of human digestive enzymes, for example, pepsin activity. The presence of anionic polysaccharides (e.g., alginates or carrageenans) and neutral polysaccharides (e.g., xylanes and cellulose) in large quantities in seaweed cell walls can limit the availability of biologically active compounds (e.g., proteins) not only during enzyme digestion, but also during extraction procedures that aim at the isolation of bioactive compounds from algal biomass. Therefore, the presence of a large polysaccharide fraction (e.g., cellulose) in seaweeds can limit their use as a source of proteins for humans or animals. (https://www.sciencedirect.com/science/article/abs/pii/S0889157525000973; https://pmc.ncbi.nlm.nih.gov/articles/PMC6891420/) We individually do have different sensitivities to these substances, and that is what we need to personally discover if we want to continue including plants in our diets. How do we react to even small amounts of each of these plants? The dose makes the poison: each of us has different allergies and sensitivities. One meal may not harm us, but chronic consumption does add up and the body cannot always protect us from accumulated substances that are not simply flushed out after every meal. What are the most common worst anti-nutrients? Oxalates, lectins, and goitregens. THE BRAIN Note VITAMIN C Vitamin C and glucose -- which share a similar molecular structure -- share similar receptors/transporters into our cells, such as GLUT1, GLUT3, and GLUT4, with glucose out-competing vitamin C and having higher uptake. Therefore, with a high carb diet which produces a lot of glucose, much more vitamin C is needed. (The hexoses glucose, galactose and fructose serve as important dietary energy sources in animals and glucose plays a central role in energy homeostasis within eucaryotic cells. Eukaryotic cells are defined by the presence of a membrane-bound nucleus and various organelles, which allow for compartmentalization of cellular functions. They can be unicellular or multicellular and include organisms such as animals, plants, fungi, and protists. These molecules are unable to diffuse passively across cellular membranes, and require transporter proteins for entry into and exit from cells.) On a low or zero carb diet, the amount of vitamin C present in meat can be sufficient for bodily needs -- including preventing scurvy. However, many analyses of vitamin C in meat lazily ASSUMED that there was not any in there, so they said that the vitamin C content was zero. (Technically if the amount of vitamin C in a food is below the threshold of 0.5 mg/100 gm then it can be legally claimed that the amount is zero.) If there is less glucose circulating there are fewer free radicals causing oxidative stress and, therefore, we don't need nearly as much C as someone on the standard diet. When ketogenesis occurs in the liver, mitochondrial glutathione levels are increased. More glutathione means more enzyme glutathione reductase to recycle dehydroascorbic acid (oxidized vitamin C) in the body into ascorbic acid (reduced vitamin C). (Glutathione is an organic compound made of the amino acids glutamate, cysteine and glycine and is an antioxidant in almost every known life form.) Ketogenic diets can also increase uric acid, the major antioxidant in human serum, believed to spare vitamin C in its antioxidant capacity, and conserving it for other tasks. Animal foods also provide generous amounts of carnitine, meaning that less vitamin C is needed to synthesize carnitine (a process to which vitamin C is crucial). Collagen, a group of about 28 types of the complex triple helix and most abundant (25-35%) protein in mammals, is part of the carnivore intake and provides the amino acids (about 33% glycine and 17% proline) which otherwise would require more vitamin C co-factor for their synthesis in the human body. (Zinc, copper and manganese are the other co-factors.) (https://tools.myfooddata.com/nutrient-ranking-tool/vitamin-c/meats/highest/household/common+sr/no ; https://www.youtube.com/watch?v=_jvcWrYqEL4) Vitamin C is accumulated in mammalian cells by two types of proteins: sodium-ascorbate co-transporters (SVCTs) and hexose transporters (GLUTs); in particular, SVCTs actively import ascorbate, the reduced form of this vitamin. SVCTs are surface glycoproteins encoded by two different genes, very similar in structure. They show distinct tissue distribution and functional characteristics, which indicate different physiological roles. SVCT1 is involved in whole-body homeostasis of vitamin C, while SVCT2 protects metabolically active cells against oxidative stress. (https://pubmed.ncbi.nlm.nih.gov/17541511/) The Inuits have gone for lifetimes with very little plant matter in their diets -- some seasonal berries and definitely no citrus -- and there are no recorded cases of scurvy among them. One addition: fresh and frozen meat contains enough vitamin C, but canned or dehydrated meat does not. Old time sailors had barrels of dried meat to eat (along with large quantities of often moldy hardtack bread). Hardtack is a type of dense cracker made from flour, water, and sometimes salt which was then, for long voyages, baked four times rather than the more common two and prepared six months before sailing. Hardtack is very inexpensive and long-lasting if kept dry, allowing it to be used for sustenance in the absence of perishable foods. Crushing or dampening the biscuits made them edible. Sailors whose rations included up to a pound daily of hardtack and some salt pork did get scurvy. Their officers who could dine on fresh meat did not come down with this often 50% fatal malady. (It is also worth noting that higher levels of vitamin C are often found in fruits which have higher levels of sugars.) The name "vitamin C" always refers to the l-enantiomer of ascorbic acid and its oxidized form, dehydroascorbate (DHAA, aka DHA). Therefore, unless written otherwise, "ascorbate" and "ascorbic acid" refer in the nutritional literature to l-ascorbate and l-ascorbic acid respectively. Most animals are able to synthesize their own vitamin C. However, apes (including humans) and monkeys (but not all primates), most bats, most fish, some rodents, and certain other animals must acquire it from dietary sources because a gene for a synthesis enzyme has mutations that render it dysfunctional. (https://en.wikipedia.org/wiki/Vitamin_C) The global human metabolism of ascorbic acid differs from that of animal species in several respects. Firstly, the half-life of ascorbate was shown to be ~4 to 5 times longer in man than in guinea pigs and rats. Second, in guinea pigs and rats, radiolabelled CO2 is produced from ascorbate labelled on C1. Third, whereas in humans DHA is almost completely converted to ascorbate, this process is less efficient in other animals where DHA is rapidly catabolized. Finally, on virtually vitamin C-free diet, the onset of scurvy is less rapid in man than in guinea pigs. These findings indicate that humans are better able than rodents to save vitamin C, probably because of both a better ability to reduce DHA to ascorbate and a lower dehydroascorbatase activity. It is speculated that this also applies to bats, which are unable to synthesize ascorbic acid and some of which have a low supply of this vitamin in their food. Glucose provides a key supply of energy and carbon for all living organisms and its transport is a universally conserved property. Vertebrate glucose transporters belong to the Glut family of multimembrane-spanning facilitative transporters. The first identified protein of this family, Glut1, is a type 2 integral membrane protein composed of 12 transmembrane domains that delineate six extracellular loops. Fourteen Glut isoforms have now been identified in the human genome but Glut1 is the main functional transporter of glucose in most transformed cells as well as in various hematopoietic cell lineages. The Glut1 transporter is also crucial for facilitating glucose transport in the brain; a haploinsufficiency of Glut1 results in infantile seizures, delayed development, and microcephaly. Glut1 also transports L-dehydroascorbic acid (DHAA, aka DHA), an oxidized intermediate of ascorbic acid (AA). DHA entry via Glut family transporters was initially investigated because of the structural similarities between DHAA and glucose. Once transported into the cell, DHAA is immediately reduced to AA allowing a recycling of ascorbate. The uptake of AA into cells is mediated by a distinct class of transporters; sodium-dependent vitamin C transporters (SVCT1 and SVCT2) whose expression profiles differ from those of Glut family members. AA is essential for maintaining plasma and tissue reductive capacity, removing superoxide via its own oxidation into DHAA. CALORIES Note CANCER AND TST Note FRUCTOSE Fructose spillover is where a quantity of fructose, which the intestines cannot breakdown into glucose and organic acids, then enters the liver. High fructose corn syrup in beverages and foods is the chief way we have fructose spillover, which is the quantity of fructose that exceeds what the intestines can filter and transform to glucose. (Glucose measurement in the blood does not measure fructose.) Fructose has six to seven times the glycation effects as glucose. Glycation is when a carbohydrate molecule fuses to other molecules such as proteins and permanently damages them. The carbohydrate combines with protein under body heat and causes the Maillard reaction which makes tissues stiffer and inflamed. Poorly controlled elevated blood glucose does this every day. This is measured with HbA1c, an advanced glycation end product (AGEs) of glucose with hemoglobin, a specific oxygen-transport metalloprotein in your red blood cells. HbA1c shows what your average blood sugar levels have been for the past two or three months. These glucose molecules can also glycate the insides of your arteries and cause damage to the arteries resulting in atherosclerosis, heart disease, and joint damage including in the spine. Fructose has not been a main focus of glycation research because of the difficulty in measuring its adducts (products formed by an addition reaction), and, more importantly, because although it is 10 times more reactive than glucose, its plasma concentration is only 1% of that of glucose. Fructose is elevated in several tissues of diabetic patients where the polyol pathway is active, reaching the same order of magnitude as glucose. It is plausible that the high reactivity of fructose, directly or via its metabolites, may contribute to the formation of intracellular AGEs and to vascular complications. The evidence, however, is still unconvincing. ApoB is a tag on lipoproteins, not an inflammatory marker. Fructose generates more oxidative damage to the body than glucose or galactose. It is primarily/preferentially processed by the liver, the main detoxifying organ. Fructose is rapidly converted by the body into fat through the normal process of de novo lipogenesis (DNL). [When saturated fats are not available, the body has a backup plan -- it makes saturated fats out of carbohydrates, especially refined carbohydrates like sugar or white flour. This process is called de novo lipogenesis (DNL). A high-carbohydrate diet is thus a high-fat diet! In fact, avoiding saturated fat is a recipe for creating carb cravings. The body needs saturated fats so fundamentally, that it will get them one way or another. And while the body can make saturated fat by DNL, it is better to get it from the diet. To create saturated fats including palmitic acid, DNL uses up the hydrogen ions and electrons carried by niacin (vitamin B3), making this essential nutrient much less effective. When niacin levels are depleted for DNL, it is no longer available to defend against antioxidants and recycle folate and vitamin K, processes that protect us against heart disease. The brain making cholesterol also occurs due to DNL.] Glut5 is a fructose transporter. The brain, heart, muscle, arteries do not express this transporter, but only the liver and cancer cells do. Excessive dietary fructose can thus do six to seven times as much damage as glucose. Fructose causes the development of insulin resistance in the muscle and liver, stimulates the secretion of ghrelin (which contributes to the hunger sensation), inhibits the satiety effect of leptin on the brain, causes an alcohol pathway resulting in lethargy, and also partially breaks-down to form uric acid. [Sleep deprivation makes leptin lower and ghrelin higher.] Excess fructose intake equals larger amounts of uric acid for the body to metabolize -- including through the development of gout and the inhibition of the production of nitric oxide for our cells. Nitric oxide maintains brain blood supply, it keeps the endothelium (the lining under arteries) smooth, which helps keep our blood vessels "toned," and it enables our white blood cells to move around the body to fight infection. Fructose is implicated in the increased production of small dense LDL particles, "the worst of the bad cholestrol," which result from glycation and when oxidized play out in the current society's cardiovascular catastrophe. There is also a polyol pathway that converts up to 30% of ingested glucose into fructose. However, gout is not due to a high purine or high fat diet, as is commonly believed. The metabolism of fructose causes depletion of phosphate in the body, which results in the production of more uric acid, which then turns into the uric acid crystals of gout. Gout is a joint inflammation, not because of uric acid but because of high insulin in the blood. Stop drinking fructose or sucrose drinks, fruit juices or large amounts of whole fruit, alcohol (especially beer), sugars and grains. Coffee is O.K. Stop using inflammatory industrial seed oils. Go on a low carb diet. Obesity is directly related to gout attacks also. (Resources: https://www.youtube.com/watch?v=95mhn0ry2LY ; uric acid, https://www.youtube.com/watch?v=cmW01owq9fU , https://www.youtube.com/watch?v=Eh6pg3jBPEk) [The polyol pathway is a negative cycle and two-step process that converts glucose to fructose. In this pathway glucose is reduced to sorbitol, which is subsequently oxidized to fructose. It is also called the sorbitol-aldose reductase pathway. The pathway is implicated in diabetic complications, especially in microvascular damage to the retina, kidneys, and nerves. Sorbitol cannot cross cell membranes. When it accumulates it produces osmotic stresses on cells by drawing water into the insulin-independent tissues. Activation of the polyol pathway results in a decrease of reduced NADPH (Nicotinamide adenine dinucleotide phosphate) and oxidized NAD+ (Nicotinamide adenine dinucleotide which has a positive formal charge on one of its nitrogen atoms); these are necessary co-factors in redox reactions throughout the body, and under normal conditions they are not interchangeable. The decreased concentration of these NADPH leads to decreased synthesis of reduced glutathione, nitric oxide, myo-inositol, and taurine. Myo-inositol is particularly required for the normal function of nerves. Sorbitol may also glycate nitrogens on proteins, such as collagen, and the products of these glycations are referred-to as AGEs -- advanced glycation end-products. AGEs are thought to cause disease in the human body, one effect of which is mediated by RAGE (receptor for advanced glycation end-products) and the ensuing inflammatory responses induced.] To protect the body from glycation damage the insulin levels are raised. Insulin drives energy into cells, but also is an anabolic steroid that when elevated tells tissues to grow: muscles, fat, prostate, skin tags, rectal polyps, uterine fibroids, and thickens the smooth muscle layer in your arteries. Excess insulin also holds in too much sodium from the urine and that can raise blood pressure as well. Increased insulin blocks estrogen production in women, testosterone production in men, and blocks the production and action of growth hormone in both men and women resulting in premature aging because growth hormone is very important for tissue healing, building and repairing and also for fat loss. A rule of thumb for fructose intake would be 0.25g/kg of body weight for persons on a low carb diet (which for my 69 kg weight is about 17g of fructose per day), and 0.5 g/kg of body weight for persons on a more Standard Western Diet. Fructose is not measured in the glycemic index. Now, unfortunately, fructose is actually proven to be more deleterious to our health than glucose. And this is the big failing of the glycemic index as a measure. Fructose rich foods simply don't get measured in the glycemic index. Thus, fructose-rich foods and drinks become invisible to everyday dietary considerations. The liver uses a lot of copper to metabolize fructose. (A diet high in zinc can also result in low copper absorption. However, a diet heavy on corn can block 100% of zinc absorption and beans cause slightly less blocking...) Less copper available means less ceruloplasmin, the major (95%) copper-carrying enzymic protein in the blood which maintains the status of copper in the mitochondria. Ceruloplasmin also transports iron in the body. Less iron transported means a build-up in the liver which oxidizes and results in fatty liver disease. Vitamin A (retinol) is also needed for the liver to be able to synthesize ceruloplasmin, which also maintains the status of copper in the mitochondria. And we cannot metabolize fat without copper. The liver is supposed to store copper and Vitamin A (retinol) in the presence of copper and magnesium. In the presence of low copper, the liver gets filled with iron instead, which causes oxidative stress which then depletes magnesium first. Vitamin A (retinol) makes copper bioavailable. An iron deficiency results in a decrease in the production of dopamine and serotonin -- neurotransmitters the brain needs for optimal functioning. And a magnesium deficiency shuts down the Vitamin D synthesis and metabolism pathway. The presence of excess fructose has a domino-effect. Foods fortified with non-heme iron is toxic (and when eaten with fruit or another vitamin C bearer even more of this iron is absorbed). No iron overload from meat; yes from plants and definitely from iron supplements (many of which, as in fortified cereal, are basically fine iron shavings). GLUCONEOGENSIS If energy demand is not significantly increased during either a high-carbohydrate or very high fat loading in order to use up these excess fuel sources, damage to the mitochondria can be induced. What is termed gluconeogenesis (GNG) is the conversion of pyruvate into glucose in a nine-step process. Pyruvate can be generated from the degradation of lactate, fatty acids, certain amino acids, and glycerol (which comes from the break down of triglycerides to form fatty acids into ketones and the remaining glycerol molecule backbone into glucose). GNG is also one of the body's main clearing mechanisms for the muscle and red blood cell metabolite, lactic acid. The pancreatic alpha cells secrete the hormone glucagon in response to falling blood glucose levels in hypoglycemia, heavy exercise, infection, or starvation. Glucagon is a peptide hormone produced by the alpha cells of the pancreatic islets and whose effects are the opposite of those of insulin -- with which glucagon works for homeostasis. Glucagon is the most important promoter of GNG. Secondary ones include the catecholamines, growth hormone, cortisol, and gluconeogenic substrates. The liver mostly makes all the glucose the body normally needs beginning 4 to 6 hours after fasting begins, with up to 20% also being made in the kidneys after 18 to 28 hours of fasting when stored liver glucose (a carbohydrate called glycogen) is depleted. (Glycogen found in muscle stores is primarily used by the muscles themselves. Which also points to having more muscle means being able to hold more reserves for that amount of muscle.) Only about 4-5 grams or one teaspoon per hour of glucose is said to be needed from GNG. That is the amount of glucose in the blood normally. This metabolic pathway is important because the brain depends on glucose as its primary fuel. Ketone bodies can serve as the brain's alternative fuel source; however, the testes, innermost part of the kidneys (renal medulla), and red blood cells cannot survive long periods without glucose. What the optimum fuel is for the eyes, and perhaps other organs, has not been settled. [Exogenous glucose is used at the rate of <40 g/hr and then plummeting sharply to zero grams by about the first 4 to 6 hours after a meal. From about hour 4 through 28, glycogen is used with a maximum of about 8 g/hr reached at about hour 6. At about hour 16, active GNG surpasses stored glycogen as the source of glucose at about 4 g/hr of each. Between 12 and 18 hours, insulin levels drop, giving the digestive system a break and allowing the body to switch from burning glucose to burning fat. By the second day of fasting or no carbs, the brain starts using ketone bodies also, and the body begins a process called autophagy -- literally "self-cleaning" or "self-eating." Damaged cells are broken down and recycled, supporting immune function and longevity. Between 36 and 48 hours, inflammation markers drop, gut bacteria rebalance, and growth hormone rises, helping repair tissues and strengthen the body. After about the 24th day ketones are up to 75% of the fuel used by the brain.] The daily glucose requirement of the brain in a typical adult human being is about 120 g, which accounts for most of the 160-190 g of glucose needed daily by the whole body. The amount of glucose present in body fluids is about 20 g, and that readily available from the liver's glycogen is approximately 190 g. Thus, the direct glucose reserves are sufficient to meet glucose needs for about a day. While the brain can use 100-130 g of glucose a day, that does not mean the brain needs that from external sources. GNG and internally generated ketones are all that is needed. A larger amount of circulating glucose than what a cell can utilize will effectively lock out additional glucose and also fat from entering the cell, so these cannot be utilized until the amount in the cell returns to a lower level. "Insulin resistance" means that cells have locked out more glucose so additional insulin cannot put any more glucose into the cells. (At least one out of three Americans is estimated to be "insulin resistant.") Once cells are topped off with glucose fuel, the liver transforms additional carbs into fat. Carbohydrate intake via diet has very little effect on the amount of glucose made in GNG. And therefore, despite what some influencers may say, the body is NOT stressed out by GNG if one doesn't consume a certain amount of carbohydrates. Essentially no cortisol is needed for the glycerol metabolism of GNG, the predominant pathway. The amount of cortisol required for the much less important protein metabolism pathway of GNG (from muscle and tissues which kicks in when our fat stores have been nearly exhausted) is not any higher than what our bodies already make. Insulin handles, in order, alcohol (ethanol) and then sugar (carbohydrates), which spike insulin whose elevation then crashes blood sugar resulting in hunger for more carbs; next comes fat (some of which is changed to ketones), and, finally, ketones themselves (stable, clean and efficient). Insulin is a type of insurance or safety mechanism so that in short seasons we can eat a large amount of berries/carbs and not be endangered. However, modern diets have large amounts of carbs day in and day out, and this is not what our bodies are supposed to be able to safely handle. The body is designed to manufacture glucose from fat and use it accordingly. The level of blood glucose will be kept steady as it is monitored by cells and controlled through genetic expression. If we start supplying the body with undisclosed levels of glucose through the digestive tract, genetic expression shifts on many levels, cells cannot calibrate production, and are forced to burn the glucose to lower its content in the blood. Instead of producing glucose from fat, the liver has to reverse the process and convert the excess glucose into fat. GROUNDING/EARTHING Note KETO FLU Note LYMPH Note MITOCHONDRIA/ATP Note OXALATES Per Sally Norton (with other source inputs), the body -- the liver, some red blood cells, possibly the kidneys, or connective tissues (including bone broth that gels in the refrigerator) -- normally produces 12 mg of oxalates every day, and the kidneys can handle up to 26 mg per day. This means that oxalates as such are not inherently foreign or toxic. When someone becomes highly sensitive to oxalate-rich foods, the more meaningful question is not are oxalates toxic or poisonous but what reduced this person's adaptive capacity? It is no longer that a simple removal/elimination of oxalates from one's diet will fix everything. The oxalic acid is derived from the metabolism of ascorbic acid (present especially in high doses of vitamin C supplementation) and glyoxylate. (The glyoxylate cycle is important for the survival of organisms that rely on lipids as their primary energy source.) Oxalate is the ionized form of oxalic acid, which means it carries a negative charge. In contrast, oxalic acid is less commonly found in its free form in nature. However, it is a metabolic byproduct in some organisms, including certain fungi and bacteria. Oxalate is naturally present in many plant-based foods, including spinach, beet greens, rhubarb, whole grains, almonds, cashews, swiss chard, navy beans, baked potato w/skin, seeds and nuts, soy, raspberries, chocolate. There are about 4 mg of oxalate, for example, in one almond. So the naturally produced amount of oxalate in your body plus 4 almonds is above what your body can easily handle on any given day with excretion through the kidneys. One half cup of either cultivated blueberries or blackberries contain about 2 mg of oxalates. Apricots have less than 1 mg of oxalate per fruit. Macadamia nuts contain about 5 - 12 mg of oxalates per 1 oz which is about 10-12 nuts. Our depleted, inorganic soil deposits are what create such high amounts of oxalates in plant foods. Plenty of research shows that plants grow these inflammatory compounds in response to unhealthy soil with microbial overgrowth. It makes sense, a plant that is in a healthy, diverse microbiome wouldn't need to defend against microorganisms nearly as much as those grown in unhealthy ones. How much oxalate food is someone eating? How often? For how many years? Are they absorbing those oxalates efficiently? Are they excreting them normally? Do they have a history of kidney stones? Do they have underlying gastrointestinal issues that alter oxalate absorption? Do they have symptoms that actually point toward oxalate accumulation, or are we simply looking for an explanation because we've heard oxalates discussed online? The 10 Worst Oxalate Foods, https://www.youtube.com/watch?v=Gt3ZkvMPKc8. See also oxalate, https://en.wikipedia.org/wiki/Oxalate, and oxaloacetic_acid, https://en.wikipedia.org/wiki/Oxaloacetic_acid. RANDLE CYCLE Except for galactose and lactose plus fat in milk, there are no natural sources of sugar carbs with fats that would throw off the Randle Cycle, the metabolic process involving the competition of glucose and fatty-acids for their oxidation and uptake in muscle and adipose tissue. (This is not an all-or-nothing process: the state of each individual cell as far as its amount of glucose already stored determines how and when the Randle Cycle comes into play for each cell.) Man-made sources are what the SAD consists of: bread and butter, bagels and cream cheese, macaroni or crackers with cheese, grilled cheese sandwiches, frosted cake, potatoes or breaded foods that are fried, potatoes with butter and sour cream, pasta and oil, pizza, burgers or hot dogs on buns, cereal or cookies with milk, chips and dip, pork and beans, tuna casserole, etc. Any of those combinations will shut down fat/ketone fueling of the cells in lieu of burning glucose to clear the bloodstream of excessive sugar. If there is too much glucose in the cells, fatty acids are prevented from getting into the cell to be used as the ideal fuel source by the mitochondria (which are up to 400% more efficient on ketones rather than on glucose). "Insulin resistance" is not the cause of Type 2 diabetes. Excess blood glucose/sugar is the cause. The reason we mistakenly say "insulin resistance" is because in the presence of large amounts of both fatty acids and carbs/glucose, the Randle Cycle mechanism will suppress uptake of glucose into the cells. Then insulin can not metabolize the glucose from carbs. That leaves an excess of glucose in the blood stream (high blood sugar). Too much glucose will lock out glucose or fat being utilized by cells for fuel; too much fat will lock out fat or glcuose being utilized by cells for fuel. A carbohydrate+protein diet will let you subsist for 3 to 5 years before deficiencies cause you to quit like 84% of all vegans. The mixed macronutrient standard of carbohydrate+protein+fat does not do well long-term for most humans either. Of fats or carbohydrates, the human body will be running on one or the other primarily based on what is provided chronically. The body will set up its enzymes, its pathways optimally for the predominant intake; the other one will be discouraged/locked out to some degree from flowing through the metabolic pathway. Carbohydrates will make you inefficient at using fats; if you're running on fats, you are not efficient on running on carbohydrates and you are actually locked out from using carbohydrates. Raising the blood glucose above its homeostatic level, its sit point, that is toxic and will damage the physical structure of your cells. Stable isotope testing of bones from 11,000 to 350,000 years prove within 5% that humans have always been obligate hypercarnivores. Three excellent Randle Cycle Presentations are here: https://www.youtube.com/watch?v=5DKAfhrpSUk , https://www.youtube.com/watch?v=qaW1n0HAi2w , and https://www.youtube.com/watch?v=OlsjnLMANDQ. It is at least 72 hours after eating carbohydrates before they have been metabolized and the Randle Cycle can then switch over to metabolize fat. It is not just a matter of every other meal or every other day eating carbs and then fats. If a balanced diet is consumed which contains fairly equal proportions of fats and carbohydrates, then the Randle Cycle is constantly activated. What will actually occur will be a build-up in the cell fluid of a thing called inorganic phosphate, which binds to the pro-inflammatory cytokines, which thus initiates chronic systemic inflammation. NOTE: Per https://www.sciencedaily.com/releases/2026/10/261005012444.htm "Scientists reveal what seven days of fasting does to the human body": Benefits only start after day 3. That is the 72 hour window before the Randal Cycle switches over, isn't it? RED BLOOD CELLS "Red blood cells (RBCs) rely heavily on glucose for energy since they lack mitochondria, which means they cannot utilize fatty acids or other substrates effectively. Instead, they primarily rely on anaerobic glycolysis to produce ATP (adenosine triphosphate), the energy currency of cells. This dependence highlights how critical glucose is to red blood cell functionality. Low glucose levels can lead to insufficient energy production within RBCs. This condition can impair their ability to transport oxygen effectively, potentially leading to symptoms like fatigue and weakness. On the other hand, excessively high glucose levels can also have detrimental effects.7nbsp; When there's too much glucose in the bloodstream, it can lead to glycation -- a process where sugar molecules bind to proteins without enzymes. This reaction alters protein structure and function and can affect hemoglobin in RBCs. The formation of glycated hemoglobin (HbA1c) is a common marker used in diabetes management, indicating prolonged elevated glucose levels. Glycation affects not just hemoglobin but also other proteins throughout the body, including collagen and elastin in the skin. When proteins become glycated, they may lose their normal function or become less effective at what they do. In RBCs, this can lead to decreased oxygen-carrying capacity and impaired circulation. Moreover, elevated glycation products contribute to oxidative stress -- a condition where there's an imbalance between free radicals and antioxidants in the body. Oxidative stress can damage RBC membranes, making them more fragile and susceptible to rupture. This fragility can lead to anemia or reduced red blood cell lifespan." (https://wellwisp.com/effect-of-glucose-on-red-blood-cells/) RBCs lack mitochondria, the power plants that use oxygen and nutrients to power the cell. As such, despite carrying a lot of oxygen, red blood cells don't use any of it themselves. This constant presence of large amounts of oxygen leads to some oxidative stress -- oxygen reacts to form reactive oxygen species (ROS), highly reactive molecules that damage the cell over time. In the average person, RBCs are produced in the bone marrow of the long bones and then live for about 115 to 120 days, during which time these flexible, biconcave cells travel roughly 300 miles (480 km) through the circulatory system, delivering vital oxygen to tissues before being systematically retired and recycled by the spleen and liver. The measured range is 70 to 140 days. Reduced RBC lifespan can be due to autoimmune disorders, hemolytic anemia (with a significantly shortened lifespan for the RBCs, often less than 30 days), hereditary conditions like thalassemia or sickle cell disease (the latter with the reduced lifespan of its crescent-shaped cells often less than 20 days), Vitamin B deficiency (resulting in pernicious anemia), folate deficiency (resulting in megaloblastic anemia), malaria, or else adverse reactions to certain medications. Your Hba1c shows how much glycation has happened to these cells. Recent studies have shown that in patients with Iron-Deficiency Anemia (IDA), RBCs actually have longer lifespans than those in healthy individuals. Iron deficiency, the most common micronutrient deficiency worldwide, is a pathophysiological state characterized by insufficient iron storage due to inadequate iron intake, impaired utilization, or excess loss. Although the mechanism remains unclear, findings suggest that in IDA the increased deformability of RBCs may reduce their likelihood of being trapped in interendothelial slits in the spleen which otherwise filter out old cells, thereby extending IDA RBCs' lifespans. This potential mechanism may compensate for the reduced hematopoietic ability in patients with IDA. Haematopoiesis is the formation of blood cellular components. Worldwide, IDA accounts for one-third of cases of anemia, is recognized as the most common type of anemia, and is a serious public health issue, particularly in developing countries. Fatigue, tachycardia, pica, and growth retardation are typical signs and symptoms of IDA. Severe IDA leads to impairment of the nervous system and prevents cognitive development among infants and children. Diabetes mellitus (DM) is a significant global health problem, currently affecting approximately 463 million individuals globally. Of these, 336 million (approximately 4/5 of the world's diabetic population) reside in low and middle-income countries. Effective diabetes monitoring is essential for the appropriate titration of medication [sic], enabling optimal glycaemic control and prevention of vascular complication. Findings suggest that in non-anaemic patients with T2D, iron deficiency does not significantly alter HbA1c levels, supporting its continued reliability as a marker of long-term glycaemic control. On a Keto / Carnivore diet, due to much better metabolic health, the RBCs can live much longer, up to 180 days. Factors that increase RBC lifespan include low oxidative stress/inflammation, stable blood sugar, and strength of your cell membranes, or specific bone marrow conditions or other underlying issues. This can give an artificially higher-looking Hba1c just because the RBCs have been around longer to absorb the effects of sugar, even though, in both examples, the rate of sugary glycation may be exactly the same. Dr. Paul Mason said there is a reticulocyte blood test that can confirm how many replacement red blood cells you are generating -- this may reveal the reason for a falsely high Hba1c. The HbA1c concentration is influenced primarily by both hemoglobin and plasma glucose concentration. However, studies have shown that factors such as race, age, diet, medication and concomitant diseases may also alter HbA1c levels. This 120-day or so RBC lifecycle is governed by the gradual exhaustion of metabolic enzymes. Because mature red blood cells lack a nucleus and ribosomes, they cannot synthesize new proteins or repair damaged membranes. Over time, oxidative stress and mechanical wear degrade the cell's structural integrity. As the cell approaches its terminal phase, its membrane becomes less flexible. The ionic pumps that maintain cellular volume begin to fail, leading to changes in shape and the exposure of specific surface markers. These signals alert the immune system that the cell is no longer fit for service. The rate of cell production is governed by the hormone erythropoietin (EPO), which is secreted by the kidneys. When oxygen levels in the blood drop, the kidneys increase EPO output to stimulate the marrow. This feedback loop ensures that the 120-day cycle is replenished by a steady stream of fresh, functional and high-capacity oxygen carriers remain in the blood. It is estimated that between 2 and 3.8 million RBCs die and are replaced every single second of the day. Every protein within the body is replaced four times per year, every 90 days or so. Every connective tissue is similarly replaced every 120 days. Protein's metabolic turnover efficiency increases with age resulting in higher amounts of muscle and bone weaknesses. "Mature red blood cells have no nucleus which is the compartment that houses the DNA and mitochondria. Immature red blood cells actually do have a nucleus but when they differentiate to become the mature red blood cells the nucleus is actually ejected, so they have no nucleus and no DNA. [These cells are primarily composed of hemoglobin and play a central role in maintaining adequate tissue oxygenation. Due to their lack of mitochondria, RBC metabolism heavily relies on anaerobic glucose fermentation for ATP production because they cannot use ketones for that. (Martí-Mateos Y, et al, "Red blood cells serve as a primary glucose sink to improve glucose tolerance at altitude," Cell Metab. 2026 Feb 19:S1550-4131(26)00018-5. doi: 10.1016/j.cmet.2026.01.019. Epub ahead of print. PMID: 41720104; PMCID: PMC12923992. (https://www.sciencedirect.com/science/article/pii/S1550413126000185?via%3Dihub)] "As to why this is and how they function, I think what the answer is really lies in what they do. Red blood cells, their only real job is to carry oxygen around the body. Not having a nucleus is actually useful for this in terms of they can have more space for hemoglobin, which is the protein which carries oxygen. And also the red blood cells need to be able to squeeze through narrow capillaries, and they have this biconcave disc shape and without a nucleus this is possible." (https://www.thenakedscientists.com/articles/questions/why-dont-red-blood-cells-have-dna) Now, during cellular senescence the cells stop dividing. There are several causes, some of which are telomere erosion, other types of DNA damage, and other factors that act independently of DNA damage. The most widely known cause of ceased cell division is telomere erosion. Telomeres are sequences of DNA that are found at each end of the chromosomes. Without DNA, the two main causes of cellular senescence do not exist in RBCs. (Per a study by Liang et al, 2023, https://pmc.ncbi.nlm.nih.gov/articles/PMC9982546/, Mature Red Blood Cells Contain Long DNA Fragments, but the existence of telomeres with those fragments is not mentioned.) SALT Note SEED OILS Derived from manufacturing waste products, especially from the cotton industry, these were originally used as mechanical lubricants which were stable under high temperatures and heating oils after whale oil became less available [in part because the American Civil War put over half the whaling vessels out of commission]. But the petroleum oil companies in the latter 1800s took over that market and then the use of candles made out of and lamps burning the vegetable seed oils was replaced with electric lights, so what could be done with all these industrial seed oils that were being produced? Why, process them further, filter and deodorize them (so you can't tell they are rancid and unstable) and they could be sold as foodstuffs which did not immediately prove toxic. The first seed oil-food chimera [oleo]margarine (1869) was a cheap and stable butter substitute, originally a jelly-like substance from beef tallow with some chopped-up pork stomach, salt, sulfate of soda, and a little cream. (During this period, there was a great demand for butter, a product prepared with milk fat; however, its production did not meet the market demand.) Subsequent versions after 1871 were made with vegetable oils (including olive, cottonseed (1910s), peanut (1910s), palm (1920s, though very popular as stand-alone 80 years earlier), coconut (1920s), corn (1960s), safflower (1960s), soybean (1970s), canola/rapeseed (1970s), or sunflower oils) plus water, salt, colorings, emulsifiers like soybean lecithin, and other ingredients. Margarine can be hydrogenated or not. Partial hydrogenization (invented in 1897, the passing of hydrogen gas through the oil in the presence of a nickel catalyst, under controlled conditions) helped create Cottolene, a product containing 90% cotton seed fat plus some beef tallow. Later the process was used to make a beautiful white lard-substitute entirely vegetable fat competitor, Crisco (1911, bleached, deodorized and partly hydrogenated cottonseed oil, after maker Proctor & Gamble's candle business collapsed with the advent of electric lights). Both were also marketed as being used by modern, economical, and enlightened good wives and mothers. Made with cheaper ingredients, seed oil products were more profitable than natural, less-processed items and they had longer shelf-lives. There was intensive use of creative advertisements and even cookbooks were widely produced for these new "foods"with very little scientific evidence. Heart disease in 1900 usually manifested as gradual heart failure after a serious case of typhoid fever, not as sudden death by heart attack. The first recorded case of myocardial infarction (MI or "heart attack") in the U.S. occurred in 1920 [out of a U.S. population of 106 million] ; three thousand deaths from MI occurred in 1930 [out of a U.S. population of 123 million]. (Seed oils were also used again during WWII as machine lubrication. After the war, what could be done with this product still being made?) By 1960, coronary heart disease (CHD) was the leading cause of mortality in the U.S., causing more than three hundred thousand deaths annually [out of a U.S. population of 179 million]. From heart disease, there were almost seven hundred and three thousand deaths in 2022 [out of a U.S. population of 333 million]. (Keep in mind that in this brief listing, we do not have the age, gender, race, socio-economic class, co-morbidities, or use of tobacco or alcohol, among other significant variables, for these cases.) In the United States, during the 90-yr period from 1909 to 1999, a striking increase in the use of vegetable oils occurred. Specifically, per capita consumption of salad and cooking oils increased 130%, shortening consumption increased 136%, and margarine consumption increased 410%. Researchers have found that the half-life of seed oil residues in the human body is 680 days -- meaning it takes 2 years to clear out HALF of the seed oils that we have stored in our bodies from eating an average Western diet. The total amount of time it takes to remove all stored seed oils from the body is 4-7 years. This is how long it takes to rebuild every cell and mitochondria membrane that had incorporated seed oil metabolites, replacing those oxidizing polyunsaturated fatty acids (PUFAs) with stable saturated fats. This is simply how biology/biochemistry works. (https://www.youtube.com/watch?v=rD_WzormXwI See about halfway down this page, https://storables.com/garden/how-are-seed-oils-made/. Examples of seed oils commonly produced using the solvent extraction method include soybean oil, canola oil, and corn oil (the majority of seed oils used). This is followed by refining (degumming, neutralization, bleaching, and deodorizing) and then two or more filtration steps. That certainly can't be good/simple for the body to digest and absorb without effects. I prefer food ingredients that can combined at home. STOMACH ACID Gut microbiomes have a certain wide population of bacteria species no matter our diet; what we habitually eat determines the exact proportions. Collagen from a diet also feeds the microbiome. Carnivore needs much less of the bacteria which attempt to break down otherwise indigestible-to-us plant material, including "fiber." Flatulence is mostly gas from bacterial breakdown of fiber. (Carnivores pass a little gas still -- mostly from swallowed air -- but definitely nothing as loud or smelly as farts from a Standard Western Diet.) Apes and other animals have longer digestive tracts than humans do and so these other species are better suited for breaking down plant foods. Human stomach acid (baseline between pH 1.5 and 2, within the measured 0.8 to 3.5 range) is nearly as strong as that of scavengers/carrion eaters (1.1 to 1.8), so we seem to be built for eating more meat than our simian cousins (the dedicated herbivore gorillas have a 5 to 7 pH stomach acid, baboons are about 3.5). Stomach acid helps digest food, and it kills/minimizes harmful bacteria and pathogens. Studies of premature human infants and elderly persons who were also more prone to GI infections show a large percentage have stomach acid pH levels between 4 and 6.6. In gastric bypass weight loss surgery, roughly 60 percent of the stomach is removed, which results in an increase in gastric pH levels that range from 5.7 to 6.8. Your stomach juices should be very acid, almost to the point of a car battery (0.8). Their job is to break down the food you eat, assisted by the stomach muscles that pulverise the food. The acid also kills some of the bacteria that enters your body with the food, drink and air. Sphincters at either end of the stomach stop the acid escaping up through the esophagus and down into the intestines. Signals generated by the proteins, fats and the acid levels open and close these sphincters to allow food in and the, by now, largely broken down food out, in drips and drabs, into the small intestine. Carbs, especially cereals, naturally reduce the acidity of your pH, which is why on a high carb diet you tend to get stomach bugs and inflammation. With less acid to close the sphincters, acid can escape up into the esophagus, which does not have the protective lining of the stomach, causing the dreaded heart burn, which is acid burning your esophagus. Why do we still have very high acid in our stomachs if we've been eating so many carbohydrate foods for thousands of years? Maybe we really are not adapted for a high-carb diet. The clogged drain analogy is absolutely false: Kitchen pipes are not at a constant 97+ degree F temp, and the plumbing does not have muscular walls to help break down and emulsify the fats in a bath of <2 pH acid, enzymes and bile for their absorption. SUNLIGHT Note VEGAN ANIMAL DEATHS Note OTHER Note |