Sugar, CO2, and You
Sugar & Lactic AcidYour body needing sugar is no joke.Low carb, fasting, and keto all simulate the metabolism of a cancer cell. Characterized by fatty acid oxidation, and excess lactic acid production.Anything that interferes with the cells ability to oxidize glucose (sugar) will contribute to this effect.According to 'The Randle Cycle', the cell will either preferentially use sugar, or fat for fuel, depending on which one it is given more of. The Randle Cycle can be competed for, and will choose fat in the context of a high fat:carb ratio in the diet or meal, and will choose sugar in the opposite scenario. You want it choosing sugar.In the early 1900s, Otto Warburg observed that a key marker of cancer proliferation was high levels of lactic acid. What produces excess lactic acid? Fatty acid metabolism. What drives fatty acid metabolism? Low blood sugar. How to remedy that? By stabilizing blood sugar through eating sugar and protein, throughout the day.I use the term sugar synonymously with carbohydrate, sucrose (white sugar), glucose, and fructose.Starches like potato and rice are converted entirely into glucose when metabolized. Simple sugars typically are broken into a combination of glucose and fructose. Fructose does not require insulin in order to be used to make energy in the cell. Glucose does.White sugar (sucrose) is just a 50/50 split of pure glucose/fructose. It is one of the easiest substances for the body to metabolize as energy. Demonizing it is completely misguided, and lacks basic understanding of physiology.Having said that, there are no vitamins or minerals in white sugar, so it needs to be consumed in the context of a nutrient dense diet, as anything that raises energy metabolism, also raises vitamin and mineral requirements."... because 'sugar feeds cancer.' This is often, incorrectly, said to be the meaning of Warburg's demonstration that cancer cells have a respiratory defect that causes them to produce lactic acid from glucose even in the presence of oxygen. Cancer cells use glucose and the amino acid glutamine primarily for synthetic purposes, and use fats as their energy source; the growth stimulating effect of the ‘essential fatty acids' (Sueyoshi and Nagao, 1962a; Holley, et al.,1974) shows that depriving a tumor of those fats retards its growth (Omega 3)." - Ray Peat PhD - Cancer: Disorder and EnergyCarbon DioxideCO2 - a result of oxygen consuming, sugar burning energy production in the cell.If excess lactic acid is implicated in pathology like the cancer metabolism, how do we keep it under control?The answer is carbon dioxide. And how do we create more carbon dioxide? By eating carbohydrates.Carbon dioxide, along with ATP (the energy/heat molecule, must be bound to Magnesium), and water, are all the result of efficient energy metabolism of glucose.Carbon dioxide is what allows hemoglobin to release oxygen to the cells. This is called the Bohr Effect. No carbon dioxide = no oxygen utilization.When you have less oxygen utilization, from less co2, you get an anaerobic fermentation style of metabolism. What does this produce? Lactic acid. Its a slippery slope.The best way to produce more CO2 is by eating a diet that supports the metabolism, with sugar and protein throughout the day.Other great tips for CO2 production/lactic acid reduction are: 1. Magnesium Bicarbonate - Bicarbonate will actually dissociate into CO2 in the body. So along with being the most effective way to take Magnesium, Mg Bicarb is also a great CO2 supplement.2. Methylene Blue - Methylene Blue has a strong ability to reduce lactic acid, by reducing the ability of enzyme Lactate Dehydrogenase (LDH), and increasing oxidative metabolism. 3. Sodium Bicarbonate Baths - adding baking soda to a bath will increase the amount of CO2 in the water, and can be delivered to your tissues through the skin. References:1. Ray Peat Phd. Cancer: Disorder and Energyhttp://raypeat.com/articles/articles/cancer-disorder-energy.shtml2. Combining lipoic acid to methylene blue reduces the Warburg effect in CHO cells: From TCA cycle activation to enhancing monoclonal antibody production.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7162497/3. The Randle cycle revisited: a new head for an old hat.https://journals.physiology.org/doi/full/10.1152/ajpendo.00093.2009
Meat in Context
Meat can be both extremely medicinal, anabolic, and beneficial for someone's health, or inflammatory and potentially harmful. It all depends on how you use it, and how you source it. For reference - meat in this context means muscle meat. Such as: chicken breast, steaks, chops, roasts, ground, and so forth. Meat, and especially grass-fed or wild red meat such as beef, bison, buffalo, elk, and venison are amazing sources of bioavailable protein (amino acids), B vitamins(B12, B6, B3, B2), Zinc, Choline, Selenium, Betaine, Potassium, and peptides carnosine and carnitine, and even plant phytonutrients like terpenes, depending on the type of grass and pasture the animal has access to. But - meat is very high in a few things that must be balanced out, and not over-consumed in order to achieve a long term, sustainable health benefit from it. Meat Drawbacks - high amounts of:1. Phosphorous 2. The amino acids: tryptophan, cysteine, methionine3. Iron **Important note: Many grains, legumes vegetables, nuts, and seeds have the same drawbacks. 1. In 8 ounces, or about 225g of beef - there is about 500mg of Phosphorous. This needs to be balanced by Calcium intake with at least a 1:1 ratio. If Phosphorous (P) intake is high with unmatched Calcium (Ca) intake - the following happens:- Parathyroid Hormone (PTH) rises- PTH pulls calcium out of the bone into the blood to balance out Ca:P; resulting in soft tissue calcification, and bone density loss (think stiff muscles/tissues and osteo- conditions, arterial calcium buildup, kidney stones)- Active 1,25(OH)D (calcitriol) form of Vitamin D rises, to which the storage 25(OH)D (cholecalciferol) is a precursor, and therefore it is not surprising that this value could fall when all of this is happening. The latter is the only Vitamin D molecule that 'Doc' tests you for, and then tells you that you have low Vitamin D and need to take more D3 (cholecalciferol) 2. Amino acids are the chemicals that make up 'protein'. All protein is a collection of varying amino acids, in various amounts.Tryptophan and Methionine are essential amino acids (EAAs), meaning the body cannot produce them, and must be supplied by the diet. Non-essential amino acids can be produced by the body, when all the EAAs are present. Meat has all of the EAAs, but is especially high in tryptophan, methionine, and cysteine.When consumed in high amounts, unbalanced by a wider variety of amino acids, these three can be inflammatory, stressful, anti-metabolic, anti-thyroid, and eventually toxic. Under stress, or carbohydrate depletion, the body releases tryptophan and cysteine from our tissues into the bloodstream as part of a 'backup' energy production system. Tryptophan specifically - is the precursor to serotonin. When elevated beyond baseline, serotonin is inflammatory, immunosuppressive, and promotes cortisol production.Eating meat or other food high in these amino acids has a similar effect as it floods the bloodstream with them. The greatest way to restore balance is by returning to a more traditional "nose-to-tail" eating style, as roughly 50% of the protein in an animal is gelatin. Gelatin is void of the inflammatory amino acids, and high in glycine, proline, and alanine.Glycine itself is anti-fibrotic, anti-inflammatory, anti-stress, and overall protective. It's closely connected to the neurotransmitter GABA, which is responsible for relaxation, reducing stress, and other inhibitory type function. 3. Iron is a long story. But as a basic overview it's important to know the following:- Iron is an essential mineral- However, Iron is in just about everything you eat- Copper, and the other trace minerals such as selenium, zinc, iodine etc have influence in the balance and regulation of iron- Vitamin A (retinol) helps play a role, along with the trace minerals, to form mineral binding proteins that allow the mineral balance to take place- Iron overload can cause or exacerbate many forms of disease and dysfunction- Iron combines with Polyunsaturated Fatty Acids (PUFA) to create lipofuscin (see "Omega 3s are Toxic blog post) All humans have an iron recycling system, called the "reticuloendothelial system (RES)"Because of this recycling system, although the body uses around 24mg of Iron per day - it only loses 1mg, the rest is recycled. That means we only need 1mg by absorbed consumption at most - which may mean 5-15mg depending on how much is absorbed (many variables there). So, whether it is through meat or not, iron intake is unavoidable. Its in grains, its in legumes, eggs, meat, vegetables, you name it. What happens when you have too much iron? Iron oxidizes, and turns into what is basically rust in our body. This suffocates our cells, and prevents proper energy, tissue, and organ function. It could be the cause of any condition. The best way to mitigate the damages of iron overload is through the consumption of trace mineral rich foods, and Vitamin A rich foods. With all the above said, here are the best ways to mitigate and balance out the downsides of meat consumption, so that it can be a massively valuable part of your diet. Simple solutions:1. Increase Calcium intake from dairy foods, especially on days of eating meat. Milk, cheese, yogurt, and so forth. 2. Consume collagen/gelatin sources alongside meat. Bone broth (homemade or store-bought, or bone broth concentrate found online), gelatinous cuts of meat like oxtail and shank, grass-fed bovine gelatin powder, collagen. 3. Incorporate high copper, selenium, zinc and Vitamin A foods in the diet as much as possible. This includes beef liver, shellfish, fruit, and bee pollen for copper. Liver, butter, eggs, whole milk, and other dairy fat sources for Vitamin A. 4. Final note: Protein has a blood sugar lowering effect, so always consume it paired with a carbohydrate source, which will raise and help stabilize blood sugar. Fruit, honey, squash, potatoes, white rice, craft soda, etc. This is another point for learning to get back to balance, and the harmony that exists within nature and all of the foods we have available. Consuming the whole animal, nose-to-tail, organs and all, dairy, fruits and vegetables, will ensure we get lots of trace minerals, Vitamin A, the right amount of iron (accounting for intake and inhibitors), Calcium to balance phosphorous, gelatin to balance muscle, and protein to balance carb. How great is that. References:1. Rodriguez, et al (2012). FGF23 and mineral metabolism, implications in CKD-MBD.https://www.researchgate.net/publication/224971667_FGF23_and_mineral_metabolism_implications_in_CKD-MBD 2. Root, A. W., (2018). Genetic disorders of calcium, phosphorus, and bone homeostasishttps://www.researchgate.net/publication/324509706_Genetic_disorders_of_calcium_phosphorus_and_bone_homeostasis3. Peat, R. (2009). Gelatin, stress, longevity. http://raypeat.com/articles/articles/gelatin.shtml4. Knutson, M., & Wessling-Resnick, M. (2003). Iron Metabolism in the Reticuloendothelial System. Critical Reviews in Biochemistry and Molecular Biology, 38(1), 61–88. doi:10.1080/713609210 https://sci-hub.st/10.1080/713609210
Methylene Blue: Swiss Army Knife
Methylene Blue is not meant for internal consumption and is intended for research purposes only. Made in 1876, Methylene Blue (MB) became the first ever fully synthetic material to be used in medicine. Initially, Methylene Blue was used as a treatment for malaria in WWII by Allied Forces, and for psychiatric disorders such as schizophrenia. But as the research continued, it was realized that MB has a seriously broad spectrum of action and benefit. What does Methylene Blue actually do? Methylene Blue (MB) has the fantastic ability of being able to repair damaged tissue, cells and mitochondria, allowing them to restore proper energy function. It restores the most proper, organized, and efficient pathway of energy production in the mitochondria, where oxygen and carbohydrate are consumed, and ATP, CO2, and water are created. It specifically has its effect in the electron transport chain (ETC), where it can act as a redox agent, meaning it can reduce itself, or oxidize itself wherever necessary. This means that it can donate electrons in the ETC where more electrons are needed, and can receive electrons when there are too many. This is a large component of its reparative effect. The paper Neurometabolic mechanisms for memory enhancement and neuroprotection of methylene blue by Rojas et. al provides a really great description of MB's action from a biological and mechanistic perspective, summarizing how we achieve so much systemic benefit from it."Methylene blue’s action is unique because its neurobiological effects are not determined by regular drug-receptor interactions or drug-response paradigms. Methylene blue shows a hormetic dose-response, with opposite effects at low and high doses. At low doses, methylene blue is an electron cycler in the mitochondrial electron transport chain, with unparalleled antioxidant and cell respiration-enhancing properties that affect the function of the nervous system in a versatile manner. A major role of the respiratory enzyme cytochrome oxidase on the memory-enhancing effects of methylene blue is supported by available data. The memory-enhancing effects have been associated with improvement of memory consolidation in a network-specific and use-dependent fashion. In addition, low doses of methylene blue have also been used for neuroprotection against mitochondrial dysfunction in humans and experimental models of disease. The unique auto-oxidizing property of methylene blue and its pleiotropic effects on a number of tissue oxidases explain its potent neuroprotective effects at low doses."By 2010, a total of 11,000 studies on MB had been published on PubMed, and the therapeutic effects are well known in the medical research community. Still, the FDA has only recognized the use of MB for treatment of methemoglobinemia, urinary tract infection prevention, cyanide and carbon monoxide poisoning, and treatment of septic shock. For that reason, this product is available to purchase for research purposes only. I'll provide a brief list of the things that I would consider to be the marquee benefits of Methylene Blue, as well as some of the conditions it has had a positive effect on in research. After that I will leave several fascinating studies linked with a brief quote to summarize, for your own exploration and interest. Methylene Blue: Broad spectrum anti-inflammatory Antioxidant capable of lowering oxidative stress and markers of aging Repairs cellular mitochondrial energy production Improves cellular ability to use oxygen (oxidative phosphorylation) Short-term, long-term and working memory improvement Neuroprotective Shown to improve depression, anxiety, psychosis, schizophrenia Shown to improve Alzheimer's, dementia, Parkinson's Promotes autophagy (the cell's garbage removal system) Reduces harmful Nitric Oxide Metabolic enhancer Please feel free, as always, to go through the research yourself and come to your own conclusions.Research: 1. Common antioxidant could slow symptoms of aging in human skinhttps://www.sciencedaily.com/releases/2017/05/170530140701.htm"Methylene blue improved physical, biochemical and genetic aging markers in experiments with human skin cells and simulated skin tissues" 2. Methylene blue is more toxic to erythroleukemic cells than to normal peripheral blood mononuclear cells: a possible use in chemotherapyhttps://pubmed.ncbi.nlm.nih.gov/16052340/ "Our group has shown that MB was capable of inhibiting the in vitro growth of erythroleukemic cells with multidrug resistance (MDR). " 3. Methylene blue protects dopaminergic neurons against MPTP-induced neurotoxicity by upregulating brain-derived neurotrophic factorhttps://pubmed.ncbi.nlm.nih.gov/29882218/ "...methylene blue (MB) is known to possess neuroprotective properties by reducing aggregated proteins, augmenting the antioxidant response, and enhancing mitochondrial function and survival in various models of neurodegenerative diseases." "Our results indicate that pretreatment with MB significantly attenuated MPTP-induced loss of dopaminergic neurons, glial cell activation, and depletion of dopamine. We also found that MB upregulated brain-derived neurotrophic factor (BDNF) and activated its downstream signaling pathways, suggesting that BDNF might be a contributor to MB-associated neuroprotection" 4. Methylene blue and its analogues as antidepressant compoundshttps://pubmed.ncbi.nlm.nih.gov/28762173/ "...these disorders are also characterised by mitochondrial dysfunction and redox imbalance. By acting as an alternative electron acceptor/donor MB restores mitochondrial function, improves neuronal energy production and inhibits the formation of superoxide, effects that also may contribute to its therapeutic activity. 5. A controlled trial of methylene blue in severe depressive illnesshttps://pubmed.ncbi.nlm.nih.gov/3555627/ "Improvement in patients receiving methylene blue was significantly greater than in those receiving placebo. Methylene blue at a dose of 15 mg/day (3 week trial) appears to be a potent antidepressant, and further clinical evaluation is essential." 6. Methylene blue. A possible treatment for manic depressive psychosis https://pubmed.ncbi.nlm.nih.gov/6222095/"Methylene blue was given to patients who had failed to respond to standard therapies. Of the 19 manic depressives who received oral methylene blue, 14 were judged to show definite improvement, 3 patients in whom the diagnosis was uncertain showed no beneficial response." 7. A two-year double-blind crossover trial of the prophylactic effect of methylene blue in manic-depressive psychosishttps://pubmed.ncbi.nlm.nih.gov/3091097/ "The results of the present study suggest that methylene blue (at a dose of 300 mg/day) is a useful therapeutic addition to prophylactic lithium in bipolar manic-depresive patients, reducing the amount of illness by almost half" (this is an extremely high dose - research setting only) 8. Neuroprotective actions of methylene blue and its derivativeshttps://pubmed.ncbi.nlm.nih.gov/23118969/"MB retains its protective activity in in vivo models of stroke, Parkinson’s disease, and optic neuropathy""MB causes an increase in cellular oxygen consumption and a corresponding decrease in anaerobic glycolysis (fermentation) in vitro and in vivo""Our study demonstrated that MB has a distinct action as an alternative mitochondrial electron transfer carrier and a re-generable anti-oxidant in the mitochondria and hence may provide neuroprotective effects for various neurological disorders."9. Methylene Blue in the Treatment of Neuropsychiatric Disordershttps://pubmed.ncbi.nlm.nih.gov/31144270/" Of interest to psychiatrists, methylene blue has antidepressant, anxiolytic, and neuroprotective properties.. Long-term use of methylene blue in bipolar disorder led to a better stabilization and a reduction in residual symptoms of the illness."10. Methylene blue exerts a neuroprotective effect against traumatic brain injury by promoting autophagy and inhibiting microglial activationhttps://pubmed.ncbi.nlm.nih.gov/26572258/"Neurological functional deficits, measured using the modified neurological severity score, were significantly lower in the acute phase in the MB‑treated animals and cerebral lesion volumes in the MB‑treated animals were significantly lower, compared with the other groups at all time‑points... These results indicated that MB exerts a neuroprotective effect by increasing autophagy, decreasing brain edema and inhibiting microglial activation."11. Alternative mitochondrial electron transfer for the treatment of neurodegenerative diseases and cancers: Methylene blue connects the dotshttps://pubmed.ncbi.nlm.nih.gov/26603930/ "...cancers, including glioblastoma, have increased glucose uptake and rely on aerobic glycolysis for energy metabolism. The switch of high efficient oxidative phosphorylation to low efficient aerobic glycolysis pathway (Warburg effect) provides macromolecule for biosynthesis and proliferation (pathological). Current research indicates that methylene blue, a century old drug, can receive electron from NADH in the presence of complex I and donates it to cytochrome c, providing an alternative electron transfer pathway." "In summary, there is accumulating evidence providing a proof of concept that enhancement of mitochondrial oxidative phosphorylation via alternative mitochondrial electron transfer may offer protective action against neurodegenerative diseases and inhibit cancers proliferation."12. Methylene blue photodynamic therapy induces selective and massive cell death in human breast cancer cellshttps://bmccancer.biomedcentral.com/articles/10.1186/s12885-017-3179-7"..our observations underscore the potential of MB-PDT as a highly efficient strategy which could use as a powerful adjunct therapy to surgery of breast tumours, and possibly other types of tumours, to safely increase the eradication rate of microscopic residual disease and thus minimizing the chance of both local and metastatic recurrence." 13. Inactivation of dengue virus by methylene blue/narrow bandwidth light systemhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7129913/"Dengue virus could be completely inactivated at 2.5 m in 5 min when MB ⩾ 1.0 μg/ml. However, when the distance reached 3.0 m, only greater concentrations of MB (2.0 μg/ml) could completely inactivate virus in a reasonably short time (20 min), and smaller concentrations of MB (1.0 μg/ml) could only completely inactivate virus using longer times (25 min). The results of this virus inactivation model indicate that our MB/narrow bandwidth light system provides a powerful, easy way to inactivate dengue viruses." 14. The measurement of bioreductive capacity of tumor cells using methylene bluehttps://pubmed.ncbi.nlm.nih.gov/26603930/ "The unique property of this drug to affect the major intracellular reductant NAD(P)H provides a mechanism for nearly total removal of cellular reducing equivalents... Therefore MB may be used for the determination of the total bioreductive capacity of cells."15. Neurometabolic mechanisms for memory enhancement and neuroprotection of methylene bluehttps://pmc.ncbi.nlm.nih.gov/articles/PMC3265679/ This information is meant for educational purposes only.
Omega-3s are Toxic
"The economy of fish oil is a very essential consideration. When a manufacturer is forced to use less oil, such as the condition we have recently experienced, he cannot make as much paint--or profit." - Mattil, W. H., Oil & Soap (July, 1944). In 1940, unsaturated oils like fish oil, soy oil, safflower oil, and linseed (flaxseed) oil were used to make paints, varnishes, and various other wood oil finish products. Once chemists figured out how to make the same products using petroleum, but for much cheaper, these well established oil farming and processing industries had to find another way to sustain profits and repurpose the oils.Around the same time, farmers began to experiment with feeding livestock with these crops from the paint industry, and found that the animals were fattened up much easier using less food. This was the beginning of how these foods began to be marketed towards humans. Distracting from the fattening effects of these foods and oils, the marketing slogan of "no cholesterol" was promoted, under the false pretense that dietary cholesterol is harmful for human health, and it still exists to this day.In the article "Fish oil in the protective coating field" (Mattil, 1944) quoted above, the author explains how they would use the most unsaturated oils as "fast drying" finishes that solidified into plastic like coatings that were more weather resistant. The chemical reaction he was referring to is called lipid peroxidation, which is the oxidation, or the rancidification of a fatty acid, when it is exposed to oxygen, heat, and/or light. The susceptibility of a fatty acid to lipid peroxidation is dependent on how many double bonds the fatty acid has. In this diagram, you can see that the saturated fatty acid molecule is fully saturated with Hydrogen, with no double bonds (open spaces) for oxygen, heat, light, and free radicals to attach and degrade the molecule. When these things react with the double bonds in the monounsaturated (MUFA) and polyunsaturated fatty acids (PUFA), lipid peroxidation is the result. So, the same transformation from oil to plastic-like coating in the paints and varnishes, happens in our heat and oxygen filled body when we consume these types of fats. This is called lipofuscin. Excess iron also combines with this product to make it more progressive and harmful. Once you understand this, in combination with mineral balance, you're well on your way to understanding the main drivers of biological aging. When lipofuscin accumulates from a lifetime of consuming PUFAs from:- fried foods- fast food - oils added to just about every grocery store food product (cereals, breads, snack bars, chips, dips, spreads, granola etc.) - nut butters - nuts/seeds- cooking in vegetable/seed oils,- cold-water fish - iron fortified foods (every wheat product in North America)it can progress to the point where it is visible on the skin. Often called "liver spots", "age spots", or "age pigment", what you're seeing on the person's hand is exactly lipofuscin [16]. Once it gets to this point, you can bet that the person's insides are caked in it, from the cells, to the heart, liver, arteries, and more. This disease has many names in the medical literature: yellow fat disease, steatitis, fatty liver disease, fatty liver, age 50 effect, black kidney, blue kidney, bovine renal lipofuscinosis (BRL), brown atrophy of neuronia, brown atrophy of the heart, brown atrophy of the liver, brown fat disease, brown heart disease, cardiac necrosis, cumulative lipofuscinosis, embryonic death syndrome (from mom’s use of omega 3s), fatty necrosis, granulomatous steatitis, hepatic dietetica, hepatic steatosis, lipofuscinosis, necrotizing granulomatous steatitis, nonalcoholic fatty liver disease, non-suppurative pansteatitis, nutritional fat necrosis, nutritional muscular dystrophy, nutritional myodegeneration (NMD), nutritional myopathy, osteohaematochromatosis, pansteatitis, pansteatosis, pigmentary atrophy of the heart, progressive lipofuscinosis, shrunken heart disease, steatosis, stiff calf disease, stiff lamb disease, watery hide disease, waxy liver disease, waxy yellow fat disease, white fat disease, white muscle disease, xanthomatosis, xanthosis, atherosclerosis.But its all the same thing. Singh, et al, (2010) says that "Lipid peroxidation leads to the formation of a number of aldehydes by-products, including malondialdehyde (MDA), 4-hydroxy-2-nonenal (HNE), and acrolein". These are the breakdown products of oxidized unsaturated fats, and they increase the susceptibility of oxidative stress, inflammation, diabetes, Alzheimer's, dementia, cancer, aging, cardiovascular disease, and autoimmune conditions [2-6]. Omega 3 and 6s also have a well documented carcinogenic and tumorigenic role in animal studies [5, 11-14]. What can we do about it? Even though most of us have consumed PUFAs in high amounts for our entire lives, and supplemented with Omega 3 in the name of 'health', not all hope is lost. Vitamin E is our primary defense against the oxidation of these fats. Raederstorff, et al, (2015) say "the vitamin E requirement increases almost linearly with the degree of unsaturation of the PUFA" and "It will be prudent to assure an adequate vitamin E intake to match the increased PUFA intake, especially as vitamin E intake is already below recommendations in many populations worldwide.". Valk and Hornstra (2000) add that "The antioxidant function of vitamin E is critical for the prevention of oxidation of tissue PUFA". In reference to Vitamin E, Weglicki et al., (1968) state "Deficiencies of this vitamin promote accumulation of lipofuscin in a variety of tissues". So not only can we take away that Vitamin E is our first line of defense, but also that the more PUFA we consume, and have consumed for our entire lives, the higher our Vitamin E requirements will be. What are the safest fats to consume?The safest fats to consume would be the ones that have the highest levels of saturation. Saturated fat, and MUFA, from foods such as:- Coconut/coconut oil/MCT oil- Grass fed dairy products (butter, ghee, milk, cream, etc)- Grass-fed ruminant meat (beef, buffalo, bison, elk, venison)- Pasture raised eggsIn moderation:- Olives, Olive/oil- Pasture-raised poultry- Pasture-raised pork- AvocadoI don't recommend conventionally raised meat, especially fatty chicken or pork. These cheaply raised animals are typically fed very high PUFA diets in order to fatten them up at a low cost, mainly consisting of soy and corn. Ruminant animals like cows have four stomach chambers to ferment their food and convert these PUFAs into saturated fat, but chickens and pigs do not have the same biological filtration systems. Therefore, the end product will have much more of that PUFA in it. What else can we do?The liver plays a huge role in detoxing PUFAs with a process called glucuronidation. So how do we support the liver?- Eating carbohydrates and (animal) protein frequently - Not skipping breakfast- Choline (Vitamin J) from egg yolks- Fructose from fruit- Not fasting/intermittent fasting- Not restricting carbohydrates (SUGAR)- Limit PUFAs as much as possible (full avoidance is impossible) Lastly, throw the Omega 3 supplement in the trash, or use it to finish your latest woodworking piece. References:1. Mattil, W. H. (1944). Fish oil in the protective coating field. Oil & Soap, 21(7), 197–201. https://sci-hub.se/10.1007/bf025441712. Wang Y, Cui P. Reactive Carbonyl Species Derived from Omega-3 and Omega-6 Fatty Acids. J Agric Food Chem. 2015 Jul 22;63(28):6293-6. Epub 2015 Jul 9.https://sci-hub.se/10.1021/acs.jafc.5b023763. Singh M, Dang TN, Arseneault M, Ramassamy C. Role of by-products of lipid oxidation in Alzheimer's disease brain: a focus on acrolein. J Alzheimers Dis. 2010;21(3):741-56. https://sci-hub.se/10.3233/jad-2010-100405 4. Glauber H, Wallace P, Griver K, Brechtel G. Adverse metabolic effect of omega-3 fatty acids in non-insulin-dependent diabetes mellitus. Ann Intern Med. 1988 May;108(5):663-8. https://sci-hub.se/10.7326/0003-4819-108-5-6635. Olivo SE, Hilakivi-Clarke L. Opposing effects of prepubertal low- and high-fat n-3 polyunsaturated fatty acid diets on rat mammary tumorigenesis. Carcinogenesis. 2005 Sep;26(9):1563-72. Epub 2005 May 11. https://sci-hub.se/10.1093/carcin/bgi1186. Nicholls SJ, Lincoff AM, Garcia M, et al. Effect of High-Dose Omega-3 Fatty Acids vs Corn Oil on Major Adverse Cardiovascular Events in Patients at High Cardiovascular Risk: The STRENGTH Randomized Clinical Trial. JAMA. November, 2020. https://jamanetwork.com/journals/jama/article-abstract/27731207. Csallany AS, Ayaz KL, Su LC. Effect of dietary vitamin E and aging on tissue lipofuscin pigment concentration in mice. J Nutr. 1977 Oct;107(10):1792-9. https://pubmed.ncbi.nlm.nih.gov/903824/8. E.K. Winstanley, V.W. Pentreath. Lipofuscin accumulation and its prevention by vitamin E in nervous tissue: Quantitative analysis using snail buccal ganglia as a simple model system, Mechanisms of Ageing and Development. Volume 29, Issue 3,1985, 299 307. https://pubmed.ncbi.nlm.nih.gov/3990384/9. Weglicki, W. B., Reichel, W. and Nair, P. M. (1968)J. Gerontol. 23,469-475. 10. Davies I, Fotheringham AP. Lipofuscin--does it affect cellular performance? Exp Gerontol. 1981;16(2):119-25. sci-hub.se/10.1016/0531-5565(81)90034-611. Noguchi M, Rose DP, Earashi M, Miyazaki I. The role of fatty acids and eicosanoid synthesis inhibitors in breast carcinoma. Oncology. 1995 Jul-Aug;52(4):265-71. sci-hub.se/10.1159/00022747112. Sasaki T, Kobayashi Y, Shimizu J, Wada M, In'nami S, Kanke Y, Takita T. Effects of dietary n-3-to-n-6 polyunsaturated fatty acid ratio on mammary carcinogenesis in rats. Nutr Cancer. 1998;30(2):137-43. Erratum in: Nutr Cancer 1998;31(2):151. sci-hub.se/10.1080/0163558980951465313. Carroll KK. Dietary fat in relation to mammary carcinogenesis. Princess Takamatsu Symp. 1985;16:255-63. https://pubmed.ncbi.nlm.nih.gov/3916197/14. Cave WT Jr. Dietary n-3 (omega-3) polyunsaturated fatty acid effects on animal tumorigenesis. FASEB J. 1991 May;5(8):2160-6. sci-hub.se/10.1096/fasebj.5.8.167366415. Carroll, K K et al. “Dietary fat and mammary cancer.” Canadian Medical Association journal vol. 98,12 (1968): 590-4.16. Danse LH, Steenbergen-Botterweg WA. Enzyme histochemical studies of adipose tissue in porcine yellow fat disease. Vet Pathol. 1974;11(6):465-76. doi: 10.1177/030098587401100601. PMID: 4156983.17. Danse LH, Verschuren PM. Fish oil-induced yellow fat disease in rats. I. Histological changes. Vet Pathol. 1978 Jan;15(1):114-24. sci-hub.se/10.1177/030098587801500113 18. Raederstorff D, Wyss A, Calder PC, Weber P, Eggersdorfer M. Vitamin E function and requirements in relation to PUFA. Br J Nutr. 2015 Oct 28;114(8):1113-22. Epub 2015 Aug 21. sci-hub.se/10.1017/S000711451500272X19. Valk EE, Hornstra G. Relationship between vitamin E requirement and polyunsaturated fatty acid intake in man: a review. Int J Vitam Nutr Res. 2000 Mar;70(2):31-42. sci-hub.se/10.1024/0300-9831.70.2.31. 20. Bässler KH. On the problematic nature of vitamin E requirements: net vitamin E. Z Ernahrungswiss. 1991 Sep;30(3):174-80. https://sci-hub.se/10.1007/BF0161034021. Villaverde C, Cortinas L, Barroeta AC, Martín-Orúe SM, Baucells MD. Relationship between dietary unsaturation and vitamin E in poultry. J Anim Physiol Anim Nutr (Berl). 2004 Apr;88(3-4):143-9. sci-hub.se/10.1111/j.1439-0396.2003.00471.x
What is Magnesium and Why Do You Need It?
Magnesium is one of the main electrolyte minerals in the body alongside sodium, calcium, and potassium. The operation of over 40% of all enzymes in the body have magnesium as a co-factor, or are magnesium dependent. Enzymes are the catalysts of almost every function that happens within the body. Lets explore some content from "Therapeautic Uses of Magnesium" by Guerrera, M.P., M.D, Volpe, S. L., PHD, Mao, J. J., M.D. (2009) American Family Physician. 2009 Jul 15;80(2):157-162."Magnesium is an essential mineral for optimal metabolic function. Research has shown that the mineral content of magnesium in food sources is declining, and that magnesium depletion has been detected in persons with some chronic diseases... Studies have shown the effectiveness of magnesium in eclampsia and preeclampsia, arrhythmia, severe asthma, and migraine. Other areas that have shown promising results include lowering the risk of metabolic syndrome, improving glucose and insulin metabolism, relieving symptoms of dysmenorrhea, and alleviating leg cramps in women who are pregnant. Magnesium is the fourth most abundant essential mineral in the body... Studies estimate that 75 percent of Americans do not meet the recommended dietary allowance of magneisum, which has raised concern about the health effects of magnesium deficiency. Lifestyle factors (e.g., poor nutrition, excess alcohol intake), some medications (e.g., diuretics), and lower mineral content in commonly eaten foods (e.g., fruit, vegetables) have led to an increase in studies evaluating the potential link of magnesium deficiency to a number of diverse medical conditions, and magnesium's possible effectiveness in supplementation."When describing in detail some more of magnesium's roles in the body, they say "These processes include protein synthesis, cellular energy production and storage, cell growth and reproduction, DNA and RNA synthesis, and stabilization of mitochondrial membranes. Magnesium is one of the minerals responsible for managing bone metabolism, nerve transmission, cardiac excitability, neuromuscular conduction, muscular contraction, vasomotor tone, and blood pressure. Magnesium also plays a significant role in glucose and insulin metabolism, mainly through its impact on tyrosine kinase activity, phosphorylase b kinase activity, and glucose transporter protein activity. Because of these vital roles, magnesium levels may be affected by stressors to the body, such as in certain disease states. Supplementation with magnesium may have therapeutic effects in these situations."Lots to unpack here - but in simpler terms, Magnesium effects almost every physical process. It is a truly foundational piece of the biological puzzle. A large part of why the list goes on and on regarding Magnesium is because of that important enzyme concept. Enzymes facilitate most physical functions. What does that mean? To properly process carbohydrates into biological energy - there are specific enzymes required. To provide oxygen to your tissues - specific enzymes required. To produce hormones like testosterone and progesterone from cholesterol - specific enzymes. All of these enzymes require minerals to work, one of the main minerals being Magnesium. If enzymes are impaired or inhibited, then functionality suffers. When functionality suffers, you get "X" symptom, or get labeled with "Y" condition. But in reality there is a larger issue at hand that can be addressed by looking at the very foundational pieces of creating health, such as mineral balance and nutritional sufficiency. Which, along with the mitigation of physical, mental, and emotional stressors, are at the root of every issue. So if you want to rid yourself of any symptom, it's important to look at the bigger picture. Even if it's something as benign as general fatigue, lack of motivation, or mental obstacles such as anxiety, insecurity, depression, or brain fog. It may very well be that the conductors of the entire orchestra are missing, and once that is addressed a lot of these issues will go away. Of course, also done in context with a diet filled with nutrient dense foods, not restrictive of sugar/carbohydrates (the primary fuel of the cell), and animal sourced protein. In other posts I'll go more into why everyone is Magnesium deficient in the context of post-industrial revolution life, how Magnesium is required for all biological energy production (it's not ATP, it's MgATP), and what's the best way to deal with that deficiency to optimize our physical function and overall health. References:1. Guerrera, M.P., M.D, Volpe, S. L., PHD, Mao, J. J., M.D. (2009). Therapeutic Uses of Magnesium. American Family Physician. 2009 Jul 15;80(2):157-162.https://www.aafp.org/afp/2009/0715/p157.html2. J Lin, L P Pan, S I Chan. (1993). The subunit location of magnesium in cytochrome c oxidase. J Biol Chem. 1993 Oct 15;268(29):22210-4. https://pubmed.ncbi.nlm.nih.gov/8408083/3. A Panov, A Scarpa. (1996). Independent modulation of the activity of alpha-ketoglutarate dehydrogenase complex by Ca2+ and Mg2+. Biochemistry. 1996 Jan 16;35(2):427-32. doi: 10.1021/bi952101t.https://pubmed.ncbi.nlm.nih.gov/8555212/4. Martha Rodríguez-Morán, Fernando Guerrero-Romero. (2003). Oral magnesium supplementation improves insulin sensitivity and metabolic control in type 2 diabetic subjects: a randomized double-blind controlled trial. Diabetes Care. 2003 Apr;26(4):1147-52. doi: 10.2337/diacare.26.4.1147.https://pubmed.ncbi.nlm.nih.gov/12663588/