Comments

First, I’m always surprised that people read my blog, I don’t get a lot of traffic and there are a lot of people who are smarter than me and have fascinating ideas. True, I only read their blogs because they happen to draw similar conclusions or confirm my own ideas but they are miles ahead in their concrete understanding while I’m left to daydream and theorize.

I thank those who have commented and asked questions it only goes further to deepen all of our understandings, both directions.

I respect your privacy, however, I dislike anonymous comments or comments with your name as an organization or business and comments with fake email addresses and websites. I give you my name and details of my personal experiences (see “About” page) and you can freely contact me. I dislike off point comments or comments that don’t contribute. I dislike argumentative claims that aren’t cited.

I want to encourage “realness” here. Use your name (capitalize the first letter), you only need your first, I want a more personal experience. I want you to be an individual and stand by your comments or expressions or questions. I want to know the people who read here. I want as human an experience as possible while masked behind fancy studies and carefully thought out words and phrases. Take pride in your comment, stand by it, cite it if it is needed, punctuate and use the spell checker, make your ideas and comments accessible to everyone. Cumulative knowledge.

A person I deeply respect once said in so many words “information is information good or bad, both sets help you to draw meaningful conclusions”. You know who you are.

Edward

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:

clip

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):

thyroid

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.

References

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

 

What do I eat (2014)?

It’s been a while, I do have a back log of posts waiting to be finished on mitochondrial uncoupling, hormones, ketones, and diatomic hydrogen, they are all separate posts but they fit together.

Work has been busy, so has life, but thinking about what I think about never stops. And I constantly flagellate myself for not keeping up with writing.

Since I have limited time I thought I’d write a bit about what I eat for those that are curious or confused by some previous posts.

In the mornings I usually have about half a pint of cream (which is pastured), there is coffee somewhere in there (a French roast made in the press). I do drink this throughout the morning, it’s not a contest.

For lunch or somewhere around that time I like cream cheese which is imported from France (hat tip to Whole Foods for managing that one), cream cheese is made from cream not milk, so it has tiny amounts of protein and although the label says there are no carbohydrates I bet there are a few molecules in there somewhere.

After lunch I usually have a cup or two of Bulgarian yogurt which is made from whole milk.  I sometimes have that in the morning as well. It’s pretty common for me to go through at least 3 cups of that a day.

Dinner is usually beef (which is pastured and I go very very out of my way to get it from a specific farmer… the fat still tastes sweet… that’s fresh), although I don’t always eat meat every day, when I do I make up for it. I like beef short ribs, beef shank, marrow bones, oxtails, and that sort of thing. Love roasts. I don’t know how much beef I eat but probably approaching 1 pound or so on average which sometimes includes the weight of the bones other times not.

Somewhere between lunch and dinner I usually work in the other half pint of cream, and in the evenings I’ve been known to have up to 2 quarts of milk accompanied with cream cheese. But that is rare.

I rarely use anything more but salt, and even then I usually don’t use it, I salt to taste when needed. Needless to say I have no problem with using spices and the like and/or veggies when I have a hankering for them. My taste buds are unspoiled I guess.

I do lift heavy weights every single day, not for health reasons but because I enjoy that type of thing, much like the other things I do in my life.

That’s about it. Some days I have only cream and yogurt, some days I’m not hungry in the morning and don’t eat till dinner, you get the picture.

Edward

Oh, I do have butter milk on occasion or mix it with my milk, I like the sour taste.

Pastured verses standard dairy cream

“Dairy products derived from the milk of cows fed in pastures are characterised by higher amounts of conjugated linoleic acid and α-linolenic acid (ALA), and several studies have shown their ability to reduce cardiovascular risk. However, their specific metabolic effects compared with standard dairy in a high-fat diet (HFD) context remain largely unknown; this is what we determined in the present study with a focus on the metabolic and intestinal parameters. The experimental animals were fed for 12 weeks a HFD containing 20 % fat in the form of a pasture dairy cream (PDC) or a standard dairy cream (SDC). Samples of plasma, liver, white adipose tissue, duodenum, jejunum and colon were analysed. The PDC mice, despite a higher food intake, exhibited lower fat mass, plasma and hepatic TAG concentrations, and inflammation in the adipose tissue than the SDC mice. Furthermore, they exhibited a higher expression of hepatic PPARα mRNA and adipose tissue uncoupling protein 2 mRNA, suggesting an enhanced oxidative activity of the tissues. These results might be explained, in part, by the higher amounts of ALA in the PDC diet and in the liver and adipose tissue of the PDC mice. Moreover, the PDC diet was found to increase the proportions of two strategic cell populations involved in the protective function of the intestinal epithelium, namely Paneth and goblet cells in the small intestine and colon, compared with the SDC diet. In conclusion, a PDC HFD leads to improved metabolic outcomes and to a stronger gut barrier compared with a SDC HFD. This may be due, at least in part, to the protective mechanisms induced by specific lipids.”

Benoit, B., Plaisancié, P., Géloën, A., Estienne, M., Debard, C., Meugnier, E., … Michalski, M.-C. (2014). Pasture v. standard dairy cream in high-fat diet-fed mice: improved metabolic outcomes and stronger intestinal barrier. The British Journal of Nutrition, 112(4), 520–35. doi:10.1017/S0007114514001172