Fermented dairy, lactic acid, and CLA: a response to James

James left a good comment on the Fermented dairy, lactic aicd, and CLA post. I started to reply as a comment but then it I felt it should be in a post as it was getting rather long.

James I always appreciate your comments.

There are reliable reports on the Maasai/Masai. For further exploration: Peter Dobromylskyj, Stephan Guyenet, Chris Masterjohn have all written on the Maasai. Ray Peat has also commented on the health of the Maasai:

“Many people advocate a low protein diet, specifically to prevent or treat osteoporosis, but the cultures that traditionally have had extremely high protein diets, such as the Masai, are very healthy.” (Peat, n.d.)

There are also interesting studies isolating the impacts of different types of fat in mice (Horn, Laver, & Wood, 1981; MacQueen, 2011).

The question of healthy, healthier, and healthiest is relative. There are many optimums in health and there is plenty of observational evidence to support this position; in the literature and anecdotal.

If I am in Europe and then go to the United States and see that the average population of Europe is healthier than the average population of the United States-clearly Europe is doing something different to achieve those results. Is Europe’s approach optimal, not necessarily, but one could argue that it is a step towards something better (a degree of improvement towards something optimal). If I am in an area of the world that has a high concentration of 90+ year old inhabitants and then move to an area where the phenomena is absent–regardless of the factors–if longevity is your goal, then in my opinion it is worth further exploration.

Another example: If I look at the longest lived and see that sucrose is relatively low, and I see evidence in the literature that sucrose is healthful, then the next question to be asked is if sucrose is a negative, neutral, or positive contributing factor to longevity and good health. If I see that some people who live a long time eat relatively little sugar and I see that some people also live long lives eating more sucrose, then I can see that there are apparently two different paradigms at work that perhaps achieve the same results. You can look at a pattern and develop a theory, but as soon as the pattern is broken it means the foundation on which the theory is based is flawed.

A comical example is if someone tells me that bacon is unhealthful and that industrial bacon is even more unhealthful. We walk away thinking bacon is unhealthful but industrial bacon is worse. But then we find a woman who is 100+ years old who gives responsibility of her longevity to the high quantities of bacon she eats that is more than likely less than pastured. So not only is she eating “harmful” bacon,  she is eating the worst of the worst. Is there a protective factor that protects from the negative factors of bacon? Or is it such that bacon, regardless of the source, is either a neutral or positive factor towards longevity?

Good health is usually a balance between the concepts of security and freedom.

I agree:

“I’m a bit skeptic about inferring that a habit or food is good based upon the apparent health of a population.”

However, the question I am raising is not a matter of health, it is a matter of toxicity. When a food dominates a particular diet and the population is in good health and it is claimed that same food is harmful, there is an irregularity. For example, if smoking is harmful and/or toxic, and the oldest person on earth smoked (as well as others in the record books) there is an irregularity. Either the toxin is indeed harmful and there is a protective factor or the toxin is not harmful; or the mechanism for harmfulness is incorrect or there are contextual considerations. A further example would be fatty acids such as those found in breast milk and coconut oil that are ketogenic. These fatty acids are ketogenic in their nature. If we agree that breast milk and coconut oil are good even though they produce ketones (or in the case of breast milk which enhances ketogenesis) then there are now at least two contexts for ketosis. One that is stimulated by metabolic substrates, and one that is produced in certain physiological situations (self-induced or as a result of disease). In a baby who is in ketosis we do not say that ketones are harmful, yet ketoacidosis in a diabetic is harmful. Clearly ketones are protective. But the context (physiological states) in which they are measured might lead some people to throw out the baby with the bath water. My opinion is that lactic acid and lactate have different contexts as well.

Your last question:

“But Ray Peat seems to think carb (esp. sugar – but let’s leave alone the debate on starch and endotoxin for now) is needed for good thyroid even once in good health – do you disagree and if so why?”

I think glucose is probably wise. How much is required for good health and stress resistance? I don’t know, but I think the requirement is rather low. I have a post on this topic that I have not yet had a chance to finish. Fresh meat contains glycogen which indeed is a source of glucose. That is something that I think is important which most miss when gauging carbohydrate requirements. Even then I have no idea how much glycogen is available in fresh meat.

Personally I recovered predominately on a high saturated fat diet similar to the Maasai pattern (I suppose a “what do I eat?” type of post is overdue). In my toolbox, however, were varying amounts of sugars and thyroid along the way (Cynoplus and Cynomel I no longer need, and my CO2 always falls somewhere between 29-32 mEq/L). Another kind of quirky thing about me is that the only carbohydrates I trust are those produced from animals. Namely those found in milk and honey. Maybe that is silly, maybe not. How much of the sugars we actually use after gut fermentation from milk is questionable. How much sugar? I have no idea but overall rather low, sometimes I put sucrose or honey in my coffee or tea sometimes I don’t. I like the occasional scoop of vanilla ice cream with bits of chocolate or if I’m feeling wild chocolate syrup. I also like cheesecake. I usually have absolutely no sweet cravings. But there were periods where I attempted to force feed myself large amounts of fruit. Virgin coconut oil was useful for slimming down at some points but refined was not. Sometimes I gently melt the coconut oil down and pour it over a bit of ice cream to make the chocolate syrup I make crispy.

My body temperatures are rock solid stable on high saturated fat 98.6-99 F. If I get a little wild with the sugars my body temperatures get wild as well which tends to agree with this.

On another note:

There is also another post I have in the pipes about mucin deficiency, which some have said is a lack of glucose in certain low carbohydrate promoting circles, whereas I believe it to be a deficiency of certain amino acids in the context of a diet that is high in muscle meats-namely glycine, which mucin is partly made up of.

Another topic I plan on writing about is methionine restriction. Obviously in some animals methionine restriction leads to increased lifespan, but I haven’t seen anything that would convince me that outright restriction in humans would have the same effect, and I think it is because there are certain species of gut bacteria that digest methionine. In fact there is some evidence to suggest that methionine deficiency causes gray hair. Anecdotally when I was in Santa Fe, NM at altitude there is a large vegetarian population there, and I noticed that a lot of young vegetarians 30-50 years old had rich gray hair.


Horn, P. L., Laver, J. J., & Wood, J. T. (1981). Changes of aging parameters among rats on diets differing in fat quantity and quality. Journal of Gerontology, 36(3), 285–93. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/7229275

MacQueen, H. A. (2011). Age-Related Biomarkers Can be Modulated by Diet in the Rat. Food and Nutrition Sciences, 02(08), 884–890. doi:10.4236/fns.2011.28120

Peat, R. (n.d.). Calcium and Disease: Hypertension, organ calcification, & shock, vs. respiratory energy. Retrieved March 29, 2014, from http://raypeat.com/articles/articles/calcium.shtml

10 Comments Fermented dairy, lactic acid, and CLA: a response to James

  1. James

    Thanks for the detailed comments! I will read more about the Masai. My initial thought about them was that their health could simply be explained by a high (quality) protein diet with ample calcium and nutrients (products from grass fed happy cows). That alone is a feat at the population level. But the fact that a lot of their dairy was fermented warrants the observations you made.

    It’s interesting that you show preference for some foods (sugar from animal not from fruit, virgin not refined coconut oil…) that seem only slightly different from others. Is that due to different nutrients, or to different digestion/absorption? Either could have physiological effects, though I’m not sure why virgin coconut oil would make a difference other than by providing more nutrients.

    When I read Peat, my understanding is that a high carb diet is better as I assume that using fat rather for energy is more likely to be associated with stress hormones. In particular, the liver needs to be kept happy with glycogen, so why not directly feed it with sugar instead of waiting for fat to be converted in gluconeogenesis? This seems more indirect and leaves more opportunities for a deplete liver and stress.

    That argument does not necessarily imply low dietary fat however. For example fat as additional energy source would be useful during sleep if the initial liver glycogen doesn’t last all night. Muscles would come in handy for their fat storage capacity. I personally haven’t benefited from this in practice, as although my body expanded from skinny to athletic (maybe simply due to just milk/protein rather than sugar), I haven’t noticed any improved ability to retain energy (for a long time).

  2. Edward

    James, your last paragraph, could you clarify a bit more. I’m not sure if I’m understanding you correctly that you are saying that when you eat low-fat you haven’t noticed increased ability to retain energy and with more fat you do or don’t or it (fat) doesn’t seem to make a difference?

  3. James

    I just meant that I haven’t noticed a difference with varying dietary fat amount. That said, I don’t think I’ve experimented with huge amounts of fat. I’m probably not eating enough of something, as I systematically get the so-called “delayed onset muscle soreness” (there’s even a Wikipedia page on that!) when I occasionally do press-ups.

  4. Edward

    Aoi, W., Naito, Y., Nakamura, T., Akagiri, S., Masuyama, A., Takano, T., … Yoshikawa, T. (2007). Inhibitory effect of fermented milk on delayed-onset muscle damage after exercise. The Journal of nutritional biochemistry, 18(2), 140–5. doi:10.1016/j.jnutbio.2006.05.002

    Milk fermented with a starter containing Lactobacillus helveticus and Saccharomyces cerevisiae is drunk on a daily basis by many people in Japan and has several beneficial effects. We studied the influence of this fermented milk product on muscle damage after prolonged exercise in rats. Wistar rats were divided into four groups: rested controls, rested rats given fermented milk diet, exercised rats and exercised rats given fermented milk diet. After 3 weeks of acclimatization, both exercise groups were made to run on a treadmill at 26 m/min for 60 min. Exercise increased the serum creatine kinase level, as well as myeloperoxidase activity and the level of thiobarbituric-acid-reactive substances in the gastrocnemius muscle after 24 h. These changes were ameliorated by intake of fermented milk. An increase of CINC-1 was also ameliorated by fermented milk. Furthermore, milk diet increased the mRNA and protein levels of protective proteins such as antioxidants and chaperone proteins. These results indicate that fermented milk can ameliorate delayed-onset muscle damage after prolonged exercise, which is associated with an increased antioxidant capacity of muscles.

    Iwasa, M., Aoi, W., Mune, K., Yamauchi, H., Furuta, K., Sasaki, S., … Higashi, A. (2013). Fermented milk improves glucose metabolism in exercise-induced muscle damage in young healthy men. Nutrition journal, 12(1), 83. doi:10.1186/1475-2891-12-83

    BACKGROUND: This study investigated the effect of fermented milk supplementation on glucose metabolism associated with muscle damage after acute exercise in humans. METHODS: Eighteen healthy young men participated in each of the three trials of the study: rest, exercise with placebo, and exercise with fermented milk. In the exercise trials, subjects carried out resistance exercise consisting of five sets of leg and bench presses at 70–100% 12 repetition maximum. Examination beverage (fermented milk or placebo) was taken before and after exercise in double-blind method. On the following day, we conducted an analysis of respiratory metabolic performance, blood collection, and evaluation of muscle soreness. RESULTS: Muscle soreness was significantly suppressed by the consumption of fermented milk compared with placebo (placebo, 14.2 +/- 1.2 score vs. fermented milk, 12.6 +/- 1.1 score, p < 0.05). Serum creatine phosphokinase was significantly increased by exercise, but this increase showed a tendency of suppression after the consumption of fermented milk. Exercise significantly decreased the respiratory quotient (rest, 0.88 +/- 0.01 vs. placebo, 0.84 +/- 0.02, p < 0.05), although this decrease was negated by the consumption of fermented milk (0.88 +/- 0.01, p < 0.05). Furthermore, exercise significantly reduced the absorption capacity of serum oxygen radical (rest, 6.9 +/- 0.4 mumol TE/g vs. placebo, 6.0 +/- 0.3 mumol TE/g, p < 0.05), although this reduction was not observed with the consumption of fermented milk (6.2 +/- 0.3 mumol TE/g). CONCLUSION: These results suggest that fermented milk supplementation improves glucose metabolism and alleviates the effects of muscle soreness after high-intensity exercise, possibly associated with the regulation of antioxidant capacity.

  5. Edward

    I don’t know, I used to get DOMS all the time when I was eating a lot of carbohydrate on a regular basis (this is several years ago) and running a lot. Muscles aren’t always burning a lot of glycogen, the amount of glycogen they use during resistance exercise is actually very little. I have a study somewhere that a friend sent looking at glycogen use during some pretty exhaustive training routines and it was extremely low. It was actually surprising, I’m not sure if I still have the study on my hard drive.

    Anyway I used to think DOMS was just from a calorie deficiency because when I would eat more it would minimize it or prevent it. But then I also found that eating extra salt did the same thing. Then I found if I ate more fat I just wouldn’t get it unless I got really extreme with my activity.

    I also noticed that when I ate more carbohydrate I would get more of a “pump” when I lifted, and noticed that when I ate more fat I didn’t get the “pump” effect. It is likely that the “pump” is inflammation. Why would CHO cause a more of a “pump”? I think because CHO burning involves a higher production of ROS (reactive oxygen species) which increases calcium retention and thus inflammation and then DOMS. That idea would explain why salt worked in my case because the sodium would restore calcium balance and reduce inflammation. Saturated fat doesn’t have the ROS problem because mitochondrial complex I is inhibited.

    But those observations don’t explain why fermented dairy reduces DOMS. Fermented dairy is well known among Russian and Bulgarian Olympic lifters to be crucial during recovery. I noticed the same thing. Lactic acid bacteria are anti-inflammatory but the mechanism through which they work is complex, there are several anti-inflammatory pathways they work through. They seem to be systematically anti-inflammatory.

    Although officially I’m on the fence about lactate shuttle theory. I think it is likely the brain and CNS runs on lactate. The brain stores glycogen which is then converted locally to lactate for use by the neurons. I think one way fermented dairy reduces stress is by providing the CNS with lactate. I think that the brain and CNS use lactate because so many of the protective substances essentially are protecting the brain from ROS induced by glucose e.g. coffee. Reducing CNS stress is also going to reduce the fatigue associated with DOMS.

    DOMS is probably also caused partially by inorganic phosphate which is why calcium tends to also reduce DOMS and improve exercise performance. It also turns out the lactic acid bacteria can metabolize phosphate. So that may be one mechanism for the recovery powers of fermented dairy.

  6. James

    I think you were right with fat being good for muscles, I eliminated DOMS quickly by just eating more sat fat.

    On that note, do you know where muscle shaking/twitching when exercising (strenuous type eg. press-ups) could come from? Occasionally I have that, it’s a funny feeling not completely unpleasant, as if the muscles were weak and were gently giving up, almost ticklish. But when that does happen I more or less have to give up exercise. Since I’ve always had those (occasionally), I’m thinking it must be something rather fundamental. Maybe just some magnesium deficiency, but that doesn’t explain why I’d be prone to waste magnesium more than other people.

    PS. Is there a way you can also list the new comments not just new articles on your website?

  7. Edward

    Most likely a need for magnesium. Most power athletes supplement with Mg and B6. A lack of Mg alone can cause a B6 deficiency. Mg is also required for thyroid hormone production. Mg is not a surrogate nor overrated. A deficiency can cause thyroid hypertrophy. Aside: Excessive salt intake also causes thyroid hypertrophy.

    Fructose wastes Mg and also inhibits intestinal calcium absorption which depresses 1,25(OH)2D3.

    Hsu, J. M., Root, A. W., Duckett, G. E., Smith, J. C., Yunice, A. A., & Kepford, G. (1984). The effect of magnesium depletion on thyroid function in rats. The Journal of nutrition, 114(8), 1510–7. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/6747732

    Planells, E., Lerma, A., Sánchez-Morito, N., Aranda, P., & LLopis, J. (1997). Effect of magnesium deficiency on vitamin B2 and B6 status in the rat. Journal of the American College of Nutrition, 16(4), 352–6. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/9263185

    Douard, V., Patel, C., Lee, J., Tharabenjasin, P., Williams, E., Fritton, J. C., … Ferraris, R. P. (2014). Chronic High Fructose Intake Reduces Serum 1,25 (OH)2D3 Levels in Calcium-Sufficient Rodents. PloS one, 9(4), e93611. doi:10.1371/journal.pone.0093611

    Douard, V., Asgerally, A., Sabbagh, Y., Sugiura, S., Shapses, S. A., Casirola, D., & Ferraris, R. P. (2010). Dietary fructose inhibits intestinal calcium absorption and induces vitamin D insufficiency in CKD. Journal of the American Society of Nephrology : JASN, 21(2), 261–71. doi:10.1681/ASN.2009080795

  8. Edward

    Mg is a catalyst and is required for ATP synthesis and utilization i.e. Mg-ATP.

    Beard, D. A. (2005). A biophysical model of the mitochondrial respiratory system and oxidative phosphorylation. PLoS computational biology, 1(4), e36. doi:10.1371/journal.pcbi.0010036

    Beard, D. A. (2006). Correction: A Biophysical Model of the Mitochondrial Respiratory System and Oxidative Phosphorylation. PLoS Computational Biology, 2(1), e8. doi:10.1371/journal.pcbi.0020008

    Pasternak, K., Kocot, J., & Horecka, A. (2010). Biochemistry of magnesium, 15(3), 601–616.

    Magnesium is essential for biochemical functions of cells. Since Mg2+ has a relatively low ionic radius in proportion to the size of the nucleus (0.86 versus 1.14 f A for Ca2+), it shows exceptional biochemical activity. Due to its physicochemical properties, intracellular magnesium can bind to the nucleus, ribosomes, cell membranes or macromolecules occurring in the cell’s cytosol. It is indispensable for the nucleus to function as a whole and for the maintenance of physical stability as well as aggregation of rybosomes into polysomes able to initiate protein synthesis. Mg2+ can also act as a cofactor for ribonucleic acid enzymes (ribozymes) capable of specifically recognizing and cleaving the target mRNA. As an essential cofactor in NER, BER, MMR processes, Mg2+ is required for the removal of DNA damage. An activator of over 300 different enzymes, magnesium participates in many metabolic processes, such as glycolysis, Krebs cycle, β-oxidation or ion transport across cell membranes. Mg2+ plays a key role in the regulation of functions of mitochondria, including the control of their volume, composition of ions and ATP production.

  9. Matt

    Have you researched the Mongolian’s dairy consumption as well? I think they used camels, goats, sheep, horses, and cattle. Cattle for milk, sheep for meat, etc. Lots of fermented/unfermented dairy. I think vikings had a very meat dependent diet as well. I’m always interested in the diets of conquering cultures, as I think availability to superior food sources probably play a role in their ability to out-compete.

    Also, in terms of the “extended breast feeding idea”, I believe human breast milk has more sugar, more fat, and less protein than cows milk. Relevant?

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