Thyroid function and saturated fat

A few years ago I came across this letter (Kasper, Schonborn, & Rabast, 1975). I was still in Germany at the time and still fiddling with carbohydrates. I knew at the time that saturated fat increased thyroid hormone production and promoted an optimal metabolism because I was outside in the cold doing a lot of running and when my carbohydrates got a bit higher than normal I wouldn’t be able to run in freezing weather with shorts, no I’d have to put the thermal tights on thus reducing me to a grade B bad ass instead of grade A.

I remember this bit catching my attention at the time:


I filed it away in my brain.

Shortly after I remember coming across this paper that proposed that iodine deficiency may be caused by an increase in carbohydrates (Kopp, 2004). This seemed to fit in with the theme: those energy substrates that are efficient AND optimal are so because they require less overall cofactors to be oxidized and because they are the exact type of resource “desired” by the mitochondria. Typically efficiency is the ratio of useful output to the total input in a system. Sure mitochondria can oxidize other substrates, however, what you find is that those substrates namely the polyunsaturated fats and carbohydrates tax the entire organism bringing into the picture those hormones that otherwise would be background which typically increase the need for more energy. That bit there—that hormones are background until undesirable energy substrates are brought into the picture—is a key point to remember for future posts.

Recently I came across this paper (Yoshimura, Hori, & Yoshimura, 1972):


I’ve come across several papers looking at the effects of macronutrients on thyroid hormones. The pattern is that fat has the greatest impact on thyroid hormone production and that carbohydrate while it can temporarily increase T3; the increase in T3 caused by increased carbohydrate consumption is actually a protective measure, a symptom. A symptom that I think is best to avoid. Interestingly fat reduces anxiety when compared to the other macronutrients which in my opinion points to stable thyroid hormone production (Prasad & Prasad, 1996).

It has been shown that carbohydrate can increase RQ. Though this is often not clear cut it is the general trend that RQ increases with carbohydrate consumption. This is in my opinion a result of the Crabtree effect.

When carbohydrates are consumed T3 increases which results in an increase in fatty acid oxidation. This is curious because one might be so inclined to expect an increase in glucose oxidation. Instead what happens is that fatty acid oxidation increases and so does DNL. Essentially carbohydrates are being converted to fatty acids, insulin is raised and the surplus of fatty acids is being stored, T3 if it can stay elevated long enough tries to bring back energy balance by burning fatty acids. Of course overtime this breaks (pathological insulin resistance coupled with thyroid disorder probably leads to ketoacidosis) and results in metabolic derangement not unlike how the pancreas breaks after a few decades of hyperglycemia. The solution to this problem is to eat in a way that prevents the problem in the first place.

T3 also happens to stimulate mitochondrial uncoupling, the uncoupling effect is partially indirect and the result of burning fatty acids. Uncoupling is for another time.

I think that when you base your diet off of saturated fat that ketones and glucose are spared in the right amounts for the tissues that desire them, much like in neonates. I think that aging is mainly a defect in fatty acid metabolism not glucose metabolism. I think this is why our risk for cancer increases as we age, again Crabtree effect. Thyroid hormones keep the body organized i.e. saturated fat as the predominate energy substrate keeps the body functioning properly, carbohydrates cause disorganization. For the most part people who live a long time like their fat, and when you see an exception my opinion is that they are going the naked mole rat route, they are eating carbohydrate but are actually fermenting it all to fatty acids and like the naked mole rat are physiologically insulin resistant.


Kasper, H., Schonborn, J., & Rabast, U. (1975). Letter: Behavior of body weight under a low carbohydrate, high fat diet. The American Journal of …, 28(8), 800–801. Retrieved from

Kopp, W. (2004). Nutrition, evolution and thyroid hormone levels – a link to iodine deficiency disorders? Medical Hypotheses, 62(6), 871–5. doi:10.1016/j.mehy.2004.02.033

Prasad, A., & Prasad, C. (1996). Short-term consumption of a diet rich in fat decreases anxiety response in adult male rats. Physiology & Behavior, 60(3), 1039–42. Retrieved from

Yoshimura, M., Hori, S., & Yoshimura, H. (1972). Effect of high-fat diet on thermal acclimation with special reference to thyroid activity. The Japanese Journal of Physiology, 22(5), 517–31. Retrieved from


28 Comments Thyroid function and saturated fat

  1. VoS

    Looking forward to your post on uncoupling as it relates to therapeutic CO2-producing uncoupling across all tissues. Are saturated fats (C:12-C:16) therapeutic uncouplers? How about T3? Aspirin? DNP? Any other therapeutic uncouplers that increase CO2 production in all tissues? Thanks for writing!

  2. erik

    Carbs deplete iodine? Maybe that’s why japanese have sea weed with their rice?

  3. Edward

    Indirectly yes. Carbohydrate temporarily increases the need for thyroid hormones to control the Crabtree effect which increases the need for iodine.

  4. Edward

    I do not think all uncoupling is positive. Often uncoupling can be indicative of stress. For example fish oil as well other PUFA are potent uncouplers. There is quite a difference in context there much like there is a difference between the ketosis produced by stress and the ketosis that occurs in neonates. I’m just after the mild uncoupling induced by the saturated fats. Not all chain lengths of the saturated fats uncouple respiration. You need some superoxide production for general health. Estrogen couples the mitochondria. In the future I will probably write on the stress response as it relates to the mitochondria and uncoupling.

  5. James

    Now that you have mentioned a traditional culture (Japanese) eating a high carbohydrate diet and its possibly deleterious effect on BMR, I wonder what about the existence of any positive effects. Unless the tradition is irrational, there must be something. I don’t see why they can’t have a high dairy/beef diet with their land resources.

  6. Edward

    Shibata, H., Nagai, H., Haga, H., Yasumura, S., Suzuki, T., & Suyama, Y. (1992). Nutrition for the Japanese elderly. Nutrition and Health, 8(2-3), 165–75. Retrieved from

    The present paper examines the relationship of nutritional status to further life expectancy and health status in the Japanese elderly based on 3 epidemiological studies. 1. Nutrient intakes in 94 Japanese centenarians investigated between 1972 and 1973 showed a higher proportion of animal protein to total proteins than in contemporary average Japanese. 2. High intakes of milk and fats and oils had favorable effects on 10-year (1976-1986) survivorship in 422 urban residents aged 69-71. The survivors revealed a longitudinal increase in intakes of animal foods such as eggs, milk, fish and meat over the 10 years. 3. Nutrient intakes were compared, based on 24-hour dietary records, between a sample from Okinawa Prefecture where life expectancies at birth and 65 were the longest in Japan, and a sample from Akita Prefecture where the life expectancies were much shorter. Intakes of Ca, Fe, vitamins A, B1, B2, C, and the proportion of energy from proteins and fats were significantly higher in the former than in the latter. Intakes of carbohydrates and NaCl were lower.

  7. Edward

    I’m Okinawan, it’s important to point out the diet of mainland Japan is different than the traditional Okinawan diet which is high in pork fat. Okinawans are boar hunters. I believe that Kobe beef (from Wagyu cattle, a Japanese breed) has taken hold in Okinawa as well.

  8. Edward

    I think stressful ketosis occurs during pathological insulin resistance e.g. diabetes, during a ketogenic diet where the fat is primarily from unsaturated fatty acids, in hyperthyroidism, in a high sugar diet (, during extreme fasting, caloric restriction, and fructose/sucrose induced hyperinsulinemia.

    Regarding the polyunsaturated fats, I should point out that a ketogenic diet based on those fats does seem to outperform low fat diets when it comes to aging and bone density. Of course “ketogenic” diets based on saturated fats are superior in regards to disease and aging among other things.

  9. James

    “Essentially carbohydrates are being converted to fatty acids, insulin is raised and the surplus of fatty acids is being stored, T3 if it can stay elevated long enough tries to bring back energy balance by burning fatty acids”

    Why is it a problem that a surplus is being stored? I had a vague understanding that if you eat a reasonable amount of carbs, maybe 50g for a single meal, then some of it gets used immediately while the rest goes to the liver. And that a well stored liver is a good thing, at least that hypoglycemia would be a worse thing than an excess and the resulting storage. I had the picture that fats may fail to prevent the hypoglycemia because it digests more slowly (a burden) and doesn’t get released out of its stores efficiently or without stress. In that picture, it makes sense to eat a small amount of carbs regularly, maybe not very convenient in practice, but at least effective as preventing hypoglycemia. I don’t think its true anymore from experience, but I think its easy to be thinking that sort of “fat is greasy and heavy, so its painful to digest and use”.

  10. John

    “carbohydrates tax the entire organism bringing into the picture those hormones that otherwise would be background”

    Which hormones do you mean in this sentence, except i suppose insulin?
    Also, how does Sat-fat relate to cortisol? Do they lower it?

    This is interesting, looking forward to uncoupling post and more posts!!

  11. Raphael Sirtoli


    I hadn’t come across your blog before – interesting write up.

    You (rightly) mentioned that uncoupling is not always a good thing. This reminded of a point I came across when reading Thomas Seyfried’s “Cancer as a Metabolic Disease” where he states:

    “At a standard metabolic rate, a fraction of the protons pumped out across the ETC can leak back into the mitochondrial matrix without synthesizing ATP [9]. Proton leak effectively uncouples respiration from phosphorylation. Proton leak or back-decay is greater in mitochondria of tumor cells than in mitochondria of normal cells [22].”

    I’d like to know your thoughts about how thyroid hormones feed-back into the maintenance of proper cellular energy homeostasis. How does it work with the different NAD:NADH pools resulting from high-carb or ketogenic diets?


  12. Joey

    I’m just interested in what your thoughts are on a 1955 study where the ingestion of heavy cream by heart disease patients caused angia, abnormal ekg readings, and reduced tissue oxygenation. Would they adapt over time? Thanks.


    Peter T. Kuo, M.D.; Claude R. Joyner Jr., M.D.
    JAMA. 1955;158(12):1008-1013. doi:10.1001/jama.1955.02960120008004

  13. James

    This old study has humans eating 2g of fats for a few months. There doesn’t seem to be adverse symptoms. Some indicators like serum lipids are unchanged.

    It has only 1 subject who was prone to migraine (apparently improved with the diet). That’s not much. I looked a bit but couldn’t find another study with the same design. There are other studies but only lowish fat (e.g. one has 50g, but a whopping one third as pufa) and usually population level, not as controlled.

  14. Edward

    James, yes, I read that study many moons ago and found it quite interesting. I think that Peter offers good insight to what is going on in the case of zero fat or near it:

    It is interesting that the nutritional content of his diet was fairly lacking compared to orange-juice-oyster-liver slamming contestants who seem to have nothing but problems but I would also say their meat-slamming counterparts just as often have seemingly unsolvable problems as well too.

    The leukopenia would be a concern for me.

  15. Jeff

    Hello Edward
    I find that I sleep better at night and I’m stronger in the gym when I include a serving of starch (about 50-75 g carbs) with my dinner meal. The rest of the day is pretty low in carbs from a few glasses of whole milk and low sugar fruits. I typically have 1 or 2 intense workouts a week. What are your thoughts on the additional starch carbs for sleep and strength? Wouldnt carbs also be needed to refill muscle glycogen after a workout?

  16. James

    What do you think of the following study? They notice that fatty oxidation is impaired in old age and show that it could be due to low glutathione – increasing it improves the condition. They increase it by supplementing two amino acids, cysteine and glycine. I find it surprising that a broken metabolism would be more or less caused by an amino acid deficiency.

    “Impaired mitochondrial fatty acid oxidation and insulinresistance in aging: novel protective role of glutathione”

  17. James

    So, cysteine seems to be another “semi-essential” amino acid along with glycine. The body seems able to synthesise what it needs once these are provided. Since there is less deficiency in early age and the food content of these amino acids is always low, the problem seems to be a defective synthesis of these amino acids.

  18. Isaac

    Ray peat also believes saturated fat is beneficial, but what about the fact that the PUFA accumulates?

  19. Edward

    There is limited evidence to support this idea, but I think that cholesterol accelerates an EFA deficiency as well as fasting. Regarding the fasting/starvation, a lot of people during the depression era as well as holocaust survivors tended to have quite long lifespans. I would guess that this would initiate an EFA deficiency. I spoke to Dr. Peat about this recently writing: “I noticed that there were quite a few holocaust victims that lived into their nineties and were quite spry for their old age, do you think that is because perhaps they developed an “EFA” deficiency during the times they were in concentration camps?” To which Dr. Peat wrote: “That’s a very interesting thought. Prostaglandins promote DNA methylation.”

    There is an abundant amount of evidence to support therapeutic benefits of fasting. When we are sick we naturally tend not to be hungry, I would guess that when there is less material in the colon this would lower endotoxin and any GI inflammation. As well if fasting and or starvation causes an EFA deficiency this would also have the effect of reducing inflammation. Both things in combination are probably beneficial in my opinion although Dr. Peat would probably disagree with me on that. But cultures that tend to have fasting rituals do tend to overall be healthier and that combined (depending on their dietary religious laws) is probably beneficial.

  20. Isaac

    Hmmm, I just now noticed the anxiety thing… I wish there was more definitive science on the way the brain gets “wired” to be anxious about everything, I just feel like it’s so hard to relax and I’ve had panic attacks all my life. Thanks to ray peat, I now look at the studies that say SSRI’s are HUUUGELY beneficial for Panic Disorder with extreme suspicion and it makes me wonder what, if anything, can I do? -_-

    I feel like anxiety for me is caused by low blood sugar. I’ve had some times where I woke up and was so confused and panicked, the worse type of panic is the kind that makes no freakin sense whatsoever, it basically feels like flying through space at light speed with nothing to grab (literally, I’m not sure, but I think I hallucinated that one time when this happened). I hate having something uncommon enough to be harder to solve than most things -_-

  21. Leo

    Hi, thank you for this very interesting article and I can’t wait for the one on uncoupling. But I do have one question. What do you think about all those people that go on low carb high fat diets and develop numerous thyroid problems like hypothyroidism. Do you think it might be because they eat too many PUFA? Also what do you think about Ray peat saying that you need carbs for lowering cortisol?

  22. Matt

    “I think that aging is mainly a defect in fatty acid metabolism not glucose metabolism. I think this is why our risk for cancer increases as we age, again Crabtree effect.”

    How do you repair this, though? I see James already posted a study that I’m aware of, boosting glutathione with cysteine and glycine supplementation. What if fatty acid metabolism is defective due to genetics?

    This study found that seemingly healthy relatives of type 2 diabetics had an inability to switch over to beta oxidation in response to a high fat meal, which could result in insulin resistance over time. The question is, can they adjust over time to a high fat, low carbohydrate diet without problems (rather than having to quickly make the switch after a single high fat meal in a diet that’s probably more carbcentric), or will their genetics always cause problems with fatty acid metabolism?

  23. Edward

    Hi Matt,

    I would say “seemingly healthy” would be correct, most people have some degree of IR, as most people have a hard time fasting or missing a meal and the mood swings that go along with it.

    I’ve never viewed the resistance to fatty acid oxidation as a “defect” per se. As genetic fatty acid mutations are rare for the most part. I more view the inability to switch from fasted to fed state as an inability to switch over to muscle catabolism for providing glucose as I’ve come to believe that as Chris Masterjohn says that fat burns in the flame of carbohydrate (but it doesn’t have to be exclusive but for practicalities sake and initially I think so).

    So essentially I view it as a sort of cortisol resistance or some type of cortisol deficiency which I view as maladaptive and not a good thing. Cortisol is not bad, chronically elevated cortisol is and so is a lack of cortisol.

    In the same thought I do think it is fixable or improvable depending on the degree of damage as numerous low carbohydrate studies do show improvement in IR. The amount of carbohydrate needed in the diet is probably indicative of two possible things a) you are active and need carbohydrate for lactate production during explosive movements and thus need to replenish glycogen or b) directly proportional to the degree of glycolysis going on in your cells due to a lack of or damaged mitochondria.

    Hope that makes sense.

  24. James

    “most people have a hard time fasting or missing a meal and the mood swings that go along with it”

    Health does seem intimately associated with this ability, or that of extracting value from food regardless of its quality. I notice really healthy people are able to maintain good mood and focus even when a meal is delayed or when the food is junk. In comparison I can achieve a semblance of stability (just about) but will require 3 carefully engineered meals in the day. Until the underlying metabolic problems resolve, diet is the price for an almost normal quality of living…

    On that note, I have found mood and hunger swings relatively easy to fix. I find symptoms such as subtle lightheadedness and decreased focus more difficult to tackle. Around me I notice people struggle more with the hunger swings but less with the ability to maintain a sane stable focus.

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