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 http://ajcn.nutrition.org/content/28/8/800.short
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 http://www.ncbi.nlm.nih.gov/pubmed/8873290
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 http://www.ncbi.nlm.nih.gov/pubmed/4539646