I don’t know what to title this post: follow-up

This post is going to serve as a sort of summary for the posts that I will be writing on the relationship between thyroid hormones and saturated fat. I’ve been working on ways to make things understandable and trying to develop some analogies so we can get a visual in the brain.

The first concepts I will be covering is the behavior of T3 alone, what it does to your metabolism and how it functions. I hope to dissolve some myths concerning the type of metabolism T3 promotes and why perhaps taking T3 on a low fat diet might be a mistake which can increase stress as well as making one more sensitive to stress.

From there I will work into the behavior of saturated fat alone, what it does to your metabolism, and how it functions. I hope to dissolve some myths concerning the type of metabolism that saturated fat promotes. I also hope to make it perfectly clear that there is a difference between a high saturated fat diet and a high fat diet that is high in polyunsaturated fats. And I also hope to make clear the difference between free saturated fatty acids and free polyunsaturated fatty acids.

At that point some light bulbs should be turning on and I will compare the similarities between the thyroid hormones and saturated fat. I will use that post as a jumping off point to make some predictions about things we should see in reality and the literature if this concept is true which I will follow up with examples and supporting literature.

Then I will write posts on longevity, metabolic rate, disease, and dovetail all of these concepts together. I was struggling with either wanting to write one large article or a series. I decided on writing a series because it will allow me to manage my time a little better with my work schedule. Plus I am getting ready to transfer to a hospital in Connecticut so with that pending move there might be some delays here and there. But the delays will give you a chance to start digging around yourself and poke holes in things that I may have overlooked. It is important to be vigilant. I have been very thorough in looking to find exceptions but I am only one person, and the literature is massive, and maybe you will look  at things a little differently. And that is o.k., all we are after is answers to questions, and questioning assumptions.

Finally, always look for exceptions. It leads to great questions.

6 Comments I don’t know what to title this post: follow-up

  1. JJ Andrade

    Hi Edward, I was reading a bunch of your posts over at the raypeatforum a while ago and I couldn’t figure out why your info stopped coming. Having just discovered your blog, I now understand. To clarify your opinion towards Ray Peat’s work, are you critical of his promotion of sugar to sustain oxidative metabolism? Do you go so far as to suggest a ketogenic diet with essentially no carbs? Or do you still eat a significant amount of sugar and get your ketones from coconut oil and things?

  2. Edward

    Oxidative metabolism (oxidative phoshorylation or OXPHOS) is the the use of energy substrates in the presence of oxygen. Oxidative metabolism is not specific to carbohydrate (CH2O). All energy substrates that enter the mitochondria are going through oxidative phosphorylation. Different energy substrates have different consequences on the mitochondria, the cell, and the organism as well as reactive oxygen species (ROS) production and resting metabolic rate (RMR) and respiratory quotient (RQ).

    The answers to the rest of your questions will be addressed in future posts.

  3. shtove

    Hi. Interesting blog – I found it through the endless debate over keto and safe carbs.
    Maybe it’s just my browser, but I can’t see how to navigate topics, tags etc. Would be helpful.

  4. George Henderson

    T3 on a low-fat diet, or indeed a high-fat vegan diet, might not be optimal because of the interaction between retinol and thyroxine. They are transported on the same protein http://en.wikipedia.org/wiki/Transthyretin
    and retinol products activated by thyroxine go on to upregulate mitochondria.
    “After mitochondrial import and binding to specific sequences of the organelle genome, mt-RXR induces a ligand-dependent increase in mitochondrial RNA levels. mt-RXR physically interacts with p43 and acts alone or through a heterodimerical complex activated by 9-cis-retinoic acid and T3 to increase RNA levels. These data indicate that hormonal regulation of mitochondrial transcription occurs through pathways similar to those that take place in the nucleus and open a new way to better understand hormone and vitamin action at the cellular level.”

  5. Edward


    Going to speculate a bit here. In the PUFA post I mentioned how unsaturated fatty acids displace thyroid hormones and over time essentially block the use of thyroid hormones. Linoleic acid et al. binds to transthyretin (or prealbumin for those of you wanting to a comprehensive search into older literature) whereas the saturated fats are neutral. If transthyretin is imported into the cell nucleus and mitochondria with linoleic acid still bound to it, I would guess this would eventually have the effect of interfering with respiration and DNA synthesis.

    Interesting that lithium binds to transthyretin as well. I would guess that if lithium can cause symptoms of thyroid disorder that what ever happens to be bound to transthyretin gets groupie access to the VIP areas of the cell.

  6. Edward


    What is also fascinating is TTR involvement with Alzheimer’s and the ability of a ketogenic diet (high in saturated fats) to reduce Amyloid-beta. As well, nicotine seems to serve well in those situations partially due to increased synthesis of TTR. Besides the mitochondrial effects, or, maybe it is mediated by some sort of feedback.

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