One of things that many find difficult with Dr. Peat is that you can read pages and pages of his ideas and at the end of it you basically are left guessing what it is that you are going to eat. Never mind the inaccuracies. People like Danny Roddy and forums like Peatarian, Ray Peat forum and Co. have attempted to make recommendations through their interpretations. There are some interesting graphics and the sort all around the web, based on those ideas.
I’m all for theory and all that jazz and cool diagrams and inverted pyramids, but really, like I have written before in various places, most people are interested in nutrition because they are sick, not because they want to become nutritionists. They just want to get better and get on with their lives. In that sense I believe in something practical.
My unimpressive advice is to source your diet from cattle. This means eating things like steaks, roasted bones (the marrow), liver, oxtails, suet, tallow, (insert whatever part of the cow you fancy here). Those things are good to eat cooked however you like. This also means that all dairy such as cheese (fresh or aged), yogurt of any type e.g. Kefir, FAGE, (insert any type of plain full fat yogurt here), sour cream, whole milk, cream, half and half, butter, etc. Although I’m using the cow here, as a specific example, really, any ruminant animal and their milk and milk products are good to eat e.g. sheep, bison, goat, etc.
Eat till you are full and drink as much milk as you like. Suet is useful for a lot of things, a lot of people like to use coconut oil, but suet is cheaper in most cases and I think it is better to use along with butter. I don’t recommend coconut oil.
There is no doubt that you can carve out a fine existence living off of those things.
Things to minimize: starch and sugar. Non-starchy vegetables are a fine and welcome addition to any stew as well as whatever spices and seasonings you like. For example, carrots, celery, leek, garlic, onion, (those are just random vegetables, no, there is no reason for me mentioning them, and no they do not hold magical power), all of these things you will find in hearty stews, as well as seasonings for your meat which adds wonderful flavor. Boiled greens are also good to eat, they can be boiled in water with a pinch of salt, cooked until they have a pleasant taste, drained, and then covered with a bit of cream or butter.
The major source of CHO will be coming from dairy. There is no magic number of carbohydrates I recommend I just recommend that you drink a fair amount of milk something like 1.5-2+ quarts per day. Lactose in milk is sufficient to supply the amount of glucose you need. Galactose is also unique in that it enhances OXPHOS and reverses the inhibitive effect on respiration caused by glucose and fructose (Aguer et al., 2011; Chico, Olavarría, & de Castro, 1978; Diaz-Ruiz, Rigoulet, & Devin, 2011; Dott, Mistry, Wright, Cain, & Herbert, 2014; Marroquin, Hynes, Dykens, Jamieson, & Will, 2007; Sussman, Erecińska, & Wilson, 1980).
Eat till you feel satisfied, eat when you are hungry, and don’t count anything, don’t worry about phosphate (Hettleman, Sabina, Drezner, Holmes, & Swain, 1983), don’t worry about trying to get a certain number of this or that. Focus on getting creative with the infinite amount of dishes you can prepare with these rich ingredients.
Coffee, chocolate, beer, wine, and tea, are always welcome, and I think nicotine is useful.
Salt your food to taste (MENEELY, TUCKER, & DARBY, 1952; MENEELY, TUCKER, DARBY, & AUERBACH, 1953).
Aguer, C., Gambarotta, D., Mailloux, R. J., Moffat, C., Dent, R., McPherson, R., & Harper, M.-E. (2011). Galactose enhances oxidative metabolism and reveals mitochondrial dysfunction in human primary muscle cells. PloS one, 6(12), e28536. doi:10.1371/journal.pone.0028536
BACKGROUND: Human primary myotubes are highly glycolytic when cultured in high glucose medium rendering it difficult to study mitochondrial dysfunction. Galactose is known to enhance mitochondrial metabolism and could be an excellent model to study mitochondrial dysfunction in human primary myotubes. The aim of the present study was to 1) characterize the effect of differentiating healthy human myoblasts in galactose on oxidative metabolism and 2) determine whether galactose can pinpoint a mitochondrial malfunction in post-diabetic myotubes. METHODOLOGY/PRINCIPAL FINDINGS: Oxygen consumption rate (OCR), lactate levels, mitochondrial content, citrate synthase and cytochrome C oxidase activities, and AMPK phosphorylation were determined in healthy myotubes differentiated in different sources/concentrations of carbohydrates: 25 mM glucose (high glucose (HG)), 5 mM glucose (low glucose (LG)) or 10 mM galactose (GAL). Effect of carbohydrates on OCR was also determined in myotubes derived from post-diabetic patients and matched obese non-diabetic subjects. OCR was significantly increased whereas anaerobic glycolysis was significantly decreased in GAL myotubes compared to LG or HG myotubes. This increased OCR in GAL myotubes occurred in conjunction with increased cytochrome C oxidase activity and expression, as well as increased AMPK phosphorylation. OCR of post-diabetic myotubes was not different than that of obese non-diabetic myotubes when differentiated in LG or HG. However, whereas GAL increased OCR in obese non-diabetic myotubes, it did not affect OCR in post-diabetic myotubes, leading to a significant difference in OCR between groups. The lack of an increase in OCR in post-diabetic myotubes differentiated in GAL was in relation with unaltered cytochrome C oxidase activity levels or AMPK phosphorylation. CONCLUSIONS/SIGNIFICANCE: Our results indicate that differentiating human primary myoblasts in GAL enhances aerobic metabolism. Because this cell culture model elicited an abnormal response in cells from post-diabetic patients, it may be useful in further studies of the molecular mechanisms of mitochondrial dysfunction.
Chico, E., Olavarría, J. S., & de Castro, I. N. (1978). Crabtree effect induced by fructose in isolated hepatocytes from fed rats. Biochemical and biophysical research communications, 83(4), 1422–9. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/29632
Diaz-Ruiz, R., Rigoulet, M., & Devin, A. (2011). The Warburg and Crabtree effects: On the origin of cancer cell energy metabolism and of yeast glucose repression. Biochimica et biophysica acta, 1807(6), 568–76. doi:10.1016/j.bbabio.2010.08.010
During the last decades a considerable amount of research has been focused on cancer. Recently, tumor cell metabolism has been considered as a possible target for cancer therapy. It is widely accepted that tumors display enhanced glycolytic activity and impaired oxidative phosphorylation (Warburg effect). Therefore, it seems reasonable that disruption of glycolysis might be a promising candidate for specific anti-cancer therapy. Nevertheless, the concept of aerobic glycolysis as the paradigm of tumor cell metabolism has been challenged, as some tumor cells exhibit high rates of oxidative phosphorylation. Mitochondrial physiology in cancer cells is linked to the Warburg effect. Besides, its central role in apoptosis makes this organelle a promising “dual hit target” to selectively eliminate tumor cells. From a metabolic point of view, the fermenting yeast Saccharomyces cerevisiae and tumor cells share several features. In this paper we will review these common metabolic properties as well as the possible origins of the Crabtree and Warburg effects.
Dott, W., Mistry, P., Wright, J., Cain, K., & Herbert, K. E. (2014). Modulation of mitochondrial bioenergetics in a skeletal muscle cell line model of mitochondrial toxicity. Redox biology, 2, 224–33. doi:10.1016/j.redox.2013.12.028
Mitochondrial toxicity is increasingly being implicated as a contributing factor to many xenobiotic-induced organ toxicities, including skeletal muscle toxicity. This has necessitated the need for predictive in vitro models that are able to sensitively detect mitochondrial toxicity of chemical entities early in the research and development process. One such cell model involves substituting galactose for glucose in the culture media. Since cells cultured in galactose are unable to generate sufficient ATP from glycolysis they are forced to rely on mitochondrial oxidative phosphorylation for ATP generation and consequently are more sensitive to mitochondrial perturbation than cells grown in glucose. The aim of this study was to characterise cellular growth, bioenergetics and mitochondrial toxicity of the L6 rat skeletal muscle cell line cultured in either high glucose or galactose media. L6 myoblasts proliferated more slowly when cultured in galactose media, although they maintained similar levels of ATP. Galactose cultured L6 cells were significantly more sensitive to classical mitochondrial toxicants than glucose-cultured cells, confirming the cells had adapted to galactose media. Analysis of bioenergetic function with the XF Seahorse extracellular flux analyser demonstrated that oxygen consumption rate (OCR) was significantly increased whereas extracellular acidification rate (ECAR), a measure of glycolysis, was decreased in cells grown in galactose. Mitochondria operated closer to state 3 respiration and had a lower mitochondrial membrane potential and basal mitochondrial O2 (•-) level compared to cells in the glucose model. An antimycin A (AA) dose response revealed that there was no difference in the sensitivity of OCR to AA inhibition between glucose and galactose cells. Importantly, cells in glucose were able to up-regulate glycolysis, while galactose cells were not. These results confirm that L6 cells are able to adapt to growth in a galactose media model and are consequently more susceptible to mitochondrial toxicants.
Hettleman, B. D., Sabina, R. L., Drezner, M. K., Holmes, E. W., & Swain, J. L. (1983). Defective adenosine triphosphate synthesis. An explanation for skeletal muscle dysfunction in phosphate-deficient mice. The Journal of clinical investigation, 72(2), 582–9. doi:10.1172/JCI111006
The basis for skeletal muscle dysfunction in phosphate-deficient patients and animals is not known, but it is hypothesized that intracellular phosphate deficiency leads to a defect in ATP synthesis. To test this hypothesis, changes in muscle function and nucleotide metabolism were studied in an animal model of hypophosphatemia. Mice were made hypophosphatemic through restriction of dietary phosphate intake. Gastrocnemius function was assessed in situ by recording isometric tension developed after stimulation of the nerve innervating this muscle. Changes in purine nucleotide, nucleoside, and base content of the muscle were quantitated at several time points during stimulation and recovery. Serum concentration and skeletal muscle content of phosphorous are reduced by 55 and 45%, respectively, in the dietary restricted animals. The gastrocnemius muscle of the phosphate-deficient mice fatigues more rapidly compared with control mice. ATP and creatine phosphate content fall to a comparable extent during fatigue in the muscle from both groups of animals; AMP, inosine, and hypoxanthine (indices of ATP catabolism) appear in higher concentration in the muscle of phosphate-deficient animals. Since total ATP use in contracting muscle is closely linked to total developed tension, we conclude that the comparable drop in ATP content in association with a more rapid loss of tension is best explained by a slower rate of ATP synthesis in the muscle of phosphate-deficient animals. During the period of recovery after muscle stimulation, ATP use for contraction is minimal, since the muscle is at rest. In the recovery period, ATP content returns to resting levels more slowly in the phosphate-deficient than in the control animals. In association with the slower rate of ATP repletion, the precursors inosine monophosphate and AMP remain elevated for a longer period of time in the muscle of phosphate-deficient animals. The slower rate of ATP repletion correlates with delayed return of normal muscle contractility in the phosphate-deficient mice. These studies suggest that the slower rate of repletion of the ATP pool may be the consequence of a slower rate of ATP synthesis and this is in part responsible for the delayed recovery of normal muscle contractility.
Marroquin, L. D., Hynes, J., Dykens, J. A., Jamieson, J. D., & Will, Y. (2007). Circumventing the Crabtree effect: replacing media glucose with galactose increases susceptibility of HepG2 cells to mitochondrial toxicants. Toxicological sciences : an official journal of the Society of Toxicology, 97(2), 539–47. doi:10.1093/toxsci/kfm052
Many highly proliferative cells generate almost all ATP via glycolysis despite abundant O(2) and a normal complement of fully functional mitochondria, a circumstance known as the Crabtree effect. Such anaerobically poised cells are resistant to xenobiotics that impair mitochondrial function, such as the inhibitors rotenone, antimycin, oligomycin, and compounds like carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone (FCCP), that uncouple the respiratory electron transfer system from phosphorylation. These cells are also resistant to the toxicity of many drugs whose deleterious side effect profiles are either caused, or exacerbated, by impairment of mitochondrial function. Drug-induced mitochondrial toxicity is shown by members of important drug classes, including the thiazolidinediones, statins, fibrates, antivirals, antibiotics, and anticancer agents. To increase detection of drug-induced mitochondrial effects in a preclinical cell-based assay, HepG2 cells were forced to rely on mitochondrial oxidative phosphorylation rather than glycolysis by substituting galactose for glucose in the growth media. Oxygen consumption doubles in galactose-grown HepG2 cells and their susceptibility to canonical mitochondrial toxicants correspondingly increases. Similarly, toxicity of several drugs with known mitochondrial liabilities is more readily apparent in aerobically poised HepG2 cells compared to glucose-grown cells. Some drugs were equally toxic to both glucose- and galactose-grown cells, suggesting that mitochondrial impairment is likely secondary to other cytotoxic mechanisms.
MENEELY, G. R., TUCKER, R. G., & DARBY, W. J. (1952). Chronic sodium chloride toxicity in the albino rat. I. Growth on a purified diet containing various levels of sodium chloride. The Journal of nutrition, 48(4), 489–98. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/13000527
MENEELY, G. R., TUCKER, R. G., DARBY, W. J., & AUERBACH, S. H. (1953). Chronic sodium chloride toxicity in the albino rat. II. Occurrence of hypertension and of a syndrome of edema and renal failure. The Journal of experimental medicine, 98(1), 71–80. Retrieved from http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2136278&tool=pmcentrez&rendertype=abstract
Sustained arterial hypertension developed in male, albino rats chronically fed diets rich in sodium chloride with demineralized drinking water available ad libitum. After 12 months of the experimental regimen a positive, linear correlation (r = 0.91) was found between the systolic blood pressure and the concentration of sodium chloride in the diet. A syndrome of edema and renal failure was observed in 18 per cent of the group fed at the level of 7.0 to 9.8 per cent of sodium chloride. Significant histologic changes occurred in the kidneys and certain other organs in rats consuming rations containing these levels of NaCl. The relative volume of the radiosodium space was increased in the rat by high dietary sodium chloride.
Sussman, I., Erecińska, M., & Wilson, D. F. (1980). Regulation of cellular energy metabolism: the Crabtree effect. Biochimica et biophysica acta, 591(2), 209–23. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/7397121
The Crabtree effect (inhibition of respiration by glycolysis) is observed in cells with approximately equal glycolytic and respiratory capacities for ATP synthesis. Addition of glucose to aerobic suspensions of glucose-starved cells (Sarcoma 180 ascites tumor cells) causes a burst of respiration and lactate production due to ATP utilization for glucose phosphorylation by hexokinase and phosphofructokinase. This burst of activity is followed by inhibition of both respiration and glycolysis, the former to below the value before glucose addition (Crabtree effect). Both the respiratory rate and the glycolytic flux appear to be regulated by the cytosolic [ATP]/[ADP][Pi] albeit by completely different mechanisms. Respiration is regulated by the free energy of hydrolysis of ATP, such that the rate increases as the [ATP]/[ADP][Pi] decreases and decreases as the [ATP]/[adp][Pi] increases. The regulatory enzymes of glycolysis are activated by ADP (AMP) and Pi and inhibited by ATP. Thus both respiration and glycolysis increase or decrease as the [ATP]/[ADP][Pi] decreases or increases. The parallel regulation of both ATP-producing pathways by this common metabolite ratio is consistent with the cytoplasmic [ATP]/[ADP][Pi] being an important determinant of homeostatic regulation of cellular energy metabolism.