What to eat?

7-SAV137-perfectroast-400x330One 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.

40 Comments What to eat?

  1. James

    Suet? This blog has quite a few cooking ideas…

    I’m a bit undecided on the theoretical differences between ideas found here and the Peat inspired ones. I’m waiting to grasp where the fundamental difference lies. I’m a bit puzzled because both you and Peat look at cellular energy and have access to the same sources of information, yet the assumptions and conclusions differ.

    On the practical level there’s a pretty big convergence with the heavy milk consumption, ensuring high amounts of calcium and protein, but divergence on fruit and lactic acid. From my experience, I would say fruit is not essential, and that going low fat high carb is not great. There is also potential divergence on issues like iron overload and inflammatory amino acids, but not necessarily if one is drinking that much milk, coffee and the other things.

  2. Edward

    Nat Sherman, Dunhill (I prefer to import from the EU), American Spirit (if there was an apocalypse I’d settle). When I can import it, General Snus.

  3. erik

    Why import dunhill and general snus? You can’t find it locally?

    Also are nat sherman cigarettes fsc?

  4. Edward

    I do not think the Dunhill Internationals taste as good as what is distributed in the EU. In Europe there is also a difference between what is distributed to the Western and Eastern European nations even though the boxes are the same the taste is different.

    I do not know what you mean by “fsc”.

  5. Edward

    I’ve used tobacco since I was 18 years old. The frequency has varied over the years, I chain smoked while in the military, probably close to a pack a day for over 6 years. After I got out of the military I tapered off to probably half a pack a day. As the years have gone by I’ve smoked less and less on average because I enjoy Snus more so than anything else. There was a 2 year period where I didn’t use tobacco at all, I think I was 25 or 26 when that started. I honestly wasn’t trying to quit I just didn’t have a desire for it. I’ve always had a positive opinion on tobacco. These past two years I’ve probably averaged 5 or 6 a day. But I do on occasion, especially on weekends, enjoy a pack or two. I don’t know, there really is no formula or counting going on, I use tobacco when I desire it and don’t when I don’t desire it. Does that make sense?

    I’ve never had any respiratory issues, in fact, compared to when I was younger (I had chronic asthma, allergies, etc.) I have zero problems with asthma since I started using tobacco, and I don’t get sick when bugs are going around while everybody else does. Diet plays a role in that obviously, but I think tobacco aids in immunity. I’ve never had any cough that is typically associated with smoking or crap in my throat. But to be fair I know people who do that are the same age and have smoked just as long. I think there are a few factors that come into play there. Or I could just be a freak. It’s never affected any of my athletic pursuits as well even when I was running marathons.

    I think tobacco could help a lot of people, nicotine in a of itself has numerous studies documenting a protective effect. I think it’s primary mechanism of action is by inhibiting Complex I. Which protects you from glucose toxicity.

  6. James

    “I think tobacco could help a lot of people, nicotine in a of itself has numerous studies documenting a protective effect.”

    It seems to protect the brain at old age. I’m not too surprised that positive results exists, since it seems to help reduce anxiety and that points to at least something good. However, I also see those studies about weaker bone healing (non-unions), so I wonder if its not also doing fundamentally bad, so a possible trade-off overall. As to its effect on lung health, carbon monoxide, nitric oxide…maybe a healthy immune system can deal with those, just not sure if its good for healing is one is weaker to start with.

  7. Jake

    Hi Edward, thanks for the post.

    I was browsing your site in an attempt to find a post on alcohol/beer but cannot find one. I’m interested in such a post if you have the time to research/write one. What sort of alcohol/beer do you suggest? I am also curious as to why you suggest it? Dr.Peat seems to think that alcohol is estrogenic and is to be avoided, but also speaks about drinking alcohol in an interview (I am too lazy to track it down at the moment).

    Blessings, Jake

  8. Edward

    Galactose is metabolized in the liver via the Leloir pathway and ultimately catabolized to UDP-glucose, UDP-glucose is also a glycogen precursor.

    Drinking milk and the liver metabolizing galactose is something quite different then an intravenous injection. All carbohydrates are worse for you when injected intravenously.

  9. Viny

    I could use some input on Mg deficiency. I have been on a fairly high dairy low starch diet for sometime. The higher the sat fat the more huff and puff I have hiking. Not so much, if any, biking. I also tend to get muscle cramps a lot after biking and ingesting milk. There seem to be an awful lot of ways to mess up the Ca:Mg ratio with diets, especially ones high in fat:

    Do you take Mg supplements on a high dairy diet? Have you been high dairy for sometime with no adverse effects?

  10. Edward

    Viny, I don’t take any supplements. Have been eating a high dairy diet since around 2005. Obviously the Massai did not take any supplements and were active. I’ve not had any adverse symptoms and I’m active.

    Stimulants like coffee/caffeine can cause muscle cramping by causing cells to take up more calcium. That would prevent the muscles from relaxing.

  11. Shane

    Edward, I assume “don’t count anything” also includes the ‘stay under 4g of PUFA/day’ the you-know-who’s insist on?

    I’ve never understood how that could be practically (ie. real-world) possible unless one subsisted on skim milk, low fat cheese and fruit juices along with some other Peaty type things (liver, gelatin, etc), and yet there are so many examples of indigenous populations who thrived despite not having access to such a diet.

  12. Isaac

    Apparently there is a brand of cigarettes that doesn’t use flame retardants, is naturally grown, doesn’t bleach the paper, and tastes and smells a lot better than American Spirit called Hestia Tobacco.

  13. Isaac

    Hey, about nicotine and aldosterone, apparently nicotine inhibits aldosterone secretion, does this mean that nicotine could predispose to hyperkalemia or some other arrhythmia producing electrolyte abnormalities? Anxiety’s acting up again.

  14. Edward

    Be careful when using the word “inhibit”, there are usually degrees of inhibition, not “on” and “off”. It would probably be more precise to say that nicotine can attenuate aldosterone secretion. I mention that because although nicotine seemingly attenuates aldosterone secrection that effect seems to occur in the context of certain types of stress. Which I wouldn’t necessary consider a bad thing but that is another can of worms. I don’t know what the effect of nicotine is on baseline aldosterone. I’ve never gone balls deep into the subject of aldosterone to know for certain but it is an interesting question. Plus I really am the wrong guy to ask. I’m so beyond biased on this topic. Nonetheless if you have a study in mind send it my way I’d be interested in taking a look.

  15. Matt

    I saw above you mentioned choosing to import general snus. Is it because you like the blend more, or for a superior product health- wise? Like EU standards being more strict or something.

  16. Edward

    Yeah, I like the blend more, and from what I’ve read Snus is regulated like a food product and so the manufacturers are limited in what they can put in it. Most seem to be a blend of water, salt, and some type of flavoring if you go that route. Myself, I’ve always preferred the earthy taste of tobacco. Snus is really fine so you either have to get the individual portions that are wrapped in some type of tea bag material or get a press which allows you to portion it into controlled amounts.

  17. James

    I find Snus to make my extremities extremely cold, probably vasoconstriction because in the case of smoking tobacco I can feel constriction in my fingers tips almost while smoking (sharper but less long lived effect than with Snus). Although I read that it is a studied side effect of nicotine, I am puzzled as to why it happens to me to this degree, I don’t think nicotine has much of that effects on others.

  18. Edward

    James, for sure that would be vasoconstriction. And that can be a side effect of nicotine. Why it occurs in some and not others I can only speculate. My feeling is that it probably has something to do with baseline stress. I’ve never had that particular issue with nicotine, but I have had it with coffee.

  19. Matt

    I notice a pretty big variation in how I react to nicotine based on diet. If I’m eating well [high sfa – low carb/pufa/sugar] I get a mild buzz. If I’m eating poorly, I get “high”, like a really floaty feeling in my head, from cigarettes or snus.

    As far as cold hands and feet go, I think Edward is right, in the sense that nicotine is a mild stressor that tests your homeostatic balance. If you are healthy, well slept, have had enough calories, etc., you will probably handle it well. If you are physiologically taxed in some way, the mild stressor of nicotine might throw you off even more.

  20. Isaac

    Yep, was finally able to smoke nearly a whole bowl (the bottom tastes bad anyway) of tobacco from my pipe, because I finally was able to keep it lit for more than 30 seconds and my hands are now rather cold. I thought maybe the buccal absorption from pipe smoking would produce less of a stress reaction, but it’s possible it results in a higher total nicotine exposure compared to a cigarette.

  21. Arborescence


    Why would someone eating a lot of saturated fat get a running nose?

    I’ve read that fat increases serotonin, are you aware of that?

  22. Edward

    Good morning Isaac, interesting find. Here is the citation that corresponds with the news release:

    Leitzman, P., Narayanapillai, S. C., Balbo, S., Zhou, B., Upadhyaya, P., Shaik, A. A., … Xing, C. (2014). Kava blocks 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced lung tumorigenesis in association with reducing O6-methylguanine DNA adduct in A/J mice. Cancer Prevention Research , 7(1), 86–96. http://doi.org/10.1158/1940-6207.CAPR-13-0301

    A quick browse on Google Scholar revealed a bit of pharmacological research on Kava. I’ve never heard of it. Along similar lines here is a Nature review paper on other chemopreventive compounds, there is a mention of Kava in there as well:

    Hecht, S. S., Kassie, F., & Hatsukami, D. K. (2009). Chemoprevention of lung carcinogenesis in addicted smokers and ex-smokers. Nature Reviews. Cancer, 9(7), 476–488. http://doi.org/10.1038/nrc2674

  23. Isaac

    Kava is pretty effective for anxiety, studies say that it’s just about as effective as benzodiazepines. It also comes as a nice euphoriant, so that’s a good deal, heh heh. Interestingly no tolerance is developed, and you get no withdrawals if you stop drinking it.

  24. James

    I do not know many things as powerful as kava for anxiety. But intuitively, for something so good I would expect a price not just monetary (it costs a fortune) but something in terms of addiction, I tend to think that if a plant or pill is more effective at solving a problem than food or lifestyle then there is trade-off behind the scenes because a random chemical can’t solve a fundamental energy problem.

  25. Jacob D.

    The reason snus is vasoconstrictive vs cigarette which don’t seem to have that problem is probably because when you smoke a cigarette you inhale a good amount of carbon monoxide. Nitric oxide also has a part to play with cigarettes.

    I have noticed that when I smoke normally, I generally get warm and blow flow usually increases. But when I have methylene blue in my system, which is an inhibitor of nitric oxide at many levels, I actually get cold and feel stiff when I smoke. I think I’m done with methylene blue. I want some cascara or thymoquinone.

    This is a great thread on Longecity.org


    Ignore the moderators saying that the thread has been debunked, it hasn’t.

    That thread is actually the reason I started smoking in the first place. Nightlight, the OP, cites study after study showing that animals and people who smoke are generally healthier than their matched peers. Anti-smoking is pretty similar to anti-salt, or anti-fat, or anti-cholesterol, or anti-sugar, the similarity being that the conclusion of what’s good or bad for humans is based on epidemiology and correlation, which is poor science.

    Nightlight actually has a theory that the reason anti-smoking was pushed s heavily by the American government was because they were testing so many nuclear weapons at the time, and they needed a scapegoat for when people started getting cancer. Based on how the U.S. government has operated before, it doesn’t make sense that they would try to persuade people to stop smoking. Basically what I’m saying is that the U.S. government wouldn’t invest money into advertising anti-smoking campaigns, unless it had an ulterior motive separate from trying to help people.

  26. Edward

    Jacob, thanks for your comment. I have no doubt that the nuclear testing in Nevada had an impact on the health of the people living in the United States. When I look at pictures from that era people seem to be more symmetrical. I also found it interesting that overseas in Europe the people there too are generally more symmetrical. I’ve often wondered if one of the consequences of that testing is a partial cause of the loss of symmetry that is typical of Americans.

    In the past when I’ve looked at rates of lung cancer by state it’s interesting that areas with higher rates of lung cancer seem to be associated with states that at one point in time (or still are) engaged in industrial mining operations. According to USGS data those states also tend to have higher levels of arsenic among other things.

    From CDC data it is interesting that there is no data for rates of lung cancer but there is data for deaths from lung cancer in the state of Nevada. Why that single state would not have data for rates is beyond me. But certainly lung cancer in Nevada is lethal but there is no rate data. However, considering the nuclear testing in Nevada the overall death rate from lung cancer assuming there is a strong correlation between lung cancer and nuclear testing, is not as high compared to other states which also have or did have big mining operations.

    Then when you compare smoking rates by state against rates of lung cancer and then again with deaths from lung cancer there are interesting paradoxes that create doubt about the association between smoking and lung cancer. There are very good loose associations with a lot of states, but then when you factor in industry one has to wonder whether or not the association is real.

    And it is those anomalies in the data that remind me of the controversies such as the cholesterol hypothesis and it’s own set of “paradoxes”, etc. Which you mentioned.

    Whether or not it is a conspiracy I don’t know. Uncle Sam does some shady shit sometimes.

    As I’ve mentioned in the past in other comments, at the end of the day, I’m the wrong guy to comment on these issues as I’m beyond biased. It doesn’t mean I can’t look at the data honestly it just means when I look at lung cancer the first thing I consider is not smoking, of course, if the first thing you do consider is smoking, then I guess that makes them just as biased! For me there are just more blatantly obvious potential causes of lung cancer to consider.

  27. Jacob D.

    Yeah I’ve noticed both of those things too. People from old pictures seem to generally look a lot healthier, though maybe that’s the camera quality lol. But I completely relate to European people looking healthier. I had some friends who were foreign exchange students, one from Spain, the other from Denmark, and they both looked extremely healthy. The Spanish one had never done serious swimming in his life, but when he joined the swim team, he was absolutely amazing at it, in fact our coach told him that he could go to the Olympics for Spain if he practiced. My Spanish friend had flawless teeth and extremely smooth skin, his hairline was very straight. Girls thought he was hot hahah. My Denmark friend was a rich kid, he looked a bit unhealthier than the Spanish one, but he still had great skin and teeth, two indicators of health that I think are very important. They both look far more symmetrical and healthier than most people in the school. And they grew up eating all kinds of food. I think the food quality is far better in Europe than the U.S., though I think we all know that. Air quality is prob better too. My Spanish friend also at a big dinner at 10:00-11:00 (IIRC) growing up, which goes against so many health theories on the internet. It’s interesting thinking about them now. This tells me that many health theories are completely missing the things that actually matter. I think living in the U.S. is generally incompatible with maximized health, though that’s a huge generalization.

    Dude that’s crazy that there’s no data for Nevada. That’s very creepy actually. Your mining theory is interesting. I think people, like I said earlier, focus on the stuff that doesn’t matter. People care about smoking but don’t care about how they’re downwind of a nuclear reactor or mining operation. Odd.

    In nightlights thread, people were saying that maybe so many centenarians smoke, is because they have genes good enough to handle the stress of smoking. That reminds me of people on the RayPeatForum saying that babies are in ketosis because it’s stressful. I feel as though they are missing the point. But hey maybe I’m missing the point.

    And I concur. I am biased, but I consider myself less biased than other smokers, because I chose to smoke for health benefits, rather than because it felt good. And yes, I am aware of how ridiculous that sounds hahaha.

    “if the first thing you do consider is smoking, then I guess that makes them just as biased! For me there are just more blatantly obvious potential causes of lung cancer to consider.” hahah yes I agree.

  28. AK

    I don’t know, but does it just break your heart that you write these incredibly liberating posts, and the comments you get back are along the lines of, “So, what kind of flour do you use?”

    Our national eating disorder is the thing. I hope we get beyond it, and I am grateful for your contribution to letting go of it (difficult as these things may be).

    Having said that–what cigs do you smoke that are not killing you? :)

  29. Edward

    First choice is Dunhill Blue (the European version), second choice is Nat Sherman Red, third choice is American Spirit Black.

Leave a Reply

Your email address will not be published. Required fields are marked *