Hyperthyroidism (1) is chronic systemic hypoxia

A member of my Discord server asked a very good question that I haven’t really addressed, here is part of the answer.

I think the speculation that there is a sweet spot is correct as at either extreme of temperature ATP production becomes unstable.

I do remember seeing posts of people claiming they were hypothyroid right around the time Paul Jaminet introduced the Perfect Health Diet. I also remember some of the more extreme people saying the chilliness people where experiencing was a sign that they were doing things right. LOL.

I’m not sure who originated the idea that ketosis was causal in thyroid dysfunction/low T3 except that, very consistently, lower T3 is associated ketosis type diets and starvation and further I’m not quite sure where the idea even comes from as far as being “harmful” as the effect ON SERUM is expected. Not very many of them provided evidence for this, so I’m not sure if it was based on signs and symptoms or symptoms alone. But the effect is physiological not pathological; at least initially.

Regardless, across species there is an inverse correlation between T3 and longevity and like with temperature there probably is a sweet spot for T3 as well but serum measurements are highly variable. What is important is local tissue levels which we don’t have commercial tests for; but we can do this in the lab with PCR, which I have done when I was researching the effects that viruses have on cellular thyroid hormone metabolism.

I’ve mentioned in the past that when cells are provided with the correct energy substrates that hormones are background. There is normal circadian oscillation for catabolic and anabolic processes but in a situation where appropriate energy substrates are used hormones remain in the background.

Lifecycle oscillations of thyroid hormone are also orchestrated by physiological processes such as in utero and during birth, stress, cold, the death of a family member or a bad breakup. In healthy adults, there also is an postive association between T3 and waist size that nobody seems to want to address. Indeed, T3 administration above physiological amounts causes diabetes to develop.

As well, during illness thyroid hormone levels decrease, adjuvant therapy with thyroid hormone during these situations tends to exacerbate the illness pointing in the direction that fluctuation in thyroid hormones is an adaptive process.

Thyroid hormones are catabolic, sometimes they appear anabolic but this is only because during catabolism, anabolic parameters also increase.

Increased T3 is a symptom of hypoxia both at the cellular, tissue, and organism level and the level of hypoxia in vivo is largely an effect of 2 things 1) the predominant metabolic substrates being provided to your cells and 2) the external availability of oxygen.

When does thyroid hormone increase? Under carbohydrate load and under anaerobic/hypoxic conditions. Given that thyroid hormone is catabolic this makes sense, as the increased local thyroid hormone concentration is secondary symptom of anaerobic/carbohydrate metabolism.

But why?

Excess carbohydrates in a normoxic environment is maladaptive, as I’ve pointed out in the past in my energy and structure blog posts, carbohydrates are a primitive fuel source this is why high-level organisms utilize fatty acids for their basal metabolism unless the situation is such that they are in a hypoxic environment. Even in naked mole rats although serum levels of thyroid hormones are low, ultrastructurally (cellular and tissue level) there is increased secretion of the hormones.

One of the functions of thyroid hormones is to orchestrate “form”, what this means is that through very carefully controlled fluctuations in cellular respiration you can change the phenotype of a cell, you can also kill cells with thyroid hormones which is part of their function as well in organisms that go through metamorphosis. For example, in tadpoles as the frog develops thyroid hormones increase to supraphysiological levels at the posterior-proximal junction of the tadpole tail, ROS and autophagy increases and the tail essentially cauterizes off.

Thyroid hormones are a necessary to “keep form”, thyroid hormones activate during carbohydrate/hypoxic situations in order to keep the cells utilizing carbohydrates from degenerating into more primitive cell types, for example, cancer. When this mechanism fails, for any number of reasons, whether it be fueling the basal metabolism with primitive energy substrates, external hypoxia, internal hypoxia from antimetabolic compounds, at the end of the day thyroid hormones help to maintain “form”, structure, and function. In a very real sense not only is thyroid hormone catabolic, it is protective and can be better classified as a stress hormone. It is an organizer.

One of the things that happens during Paleo style diets with all the PUFA, nuts, antinutrients, excess protein, etc., is that all of these things have an inhibiting effect on respiration. While serum levels of thyroid hormones fall, it is only because ultrastructural levels of thyroid hormone increase, that is, more is being used than can be produced, hence the nuclear blast of unsavory symptoms.

So your last point:

“This was the main reason I always steered clear of ketogenic diets. What do you make of that? Could it be simply the cumulative inhibitory effect of PUFA, since these people were probably not discriminating againsts those fat sources? Could it be the compounding of these diets + exercise that causes this? Excessive protein elevating cortisol and that in turn suppressing thyroid function?”

You hit the nail on the head exactly. Lower serum = higher ultrastructural levels = emergency = maintaining form because of the hypoxia induced from Paleo style diets is more important than thermoregulation. Your physiology is redirecting ATP and H+ pools to maintain form to survive verses cozy metabolically generated warmth.

Saturated fat does not do this. I steer clear of ketosis. Ketones are a symptom of hypoxia. We are indeed omnivores, glucose is essential for optimal health, people who say well, we have gluconeogenesis and ketones aren’t thinking about things in the broader context. It’s like, we have those pathways as evidence that yes, some glucose is required and probably optimal, we do not have the high output gluconeogenic pathways that true carnivores have. And when are those pathways active? Hmmm.

I hope that that answers at least part of your question. Ask any follow up questions and I’ll be sure to address them. This is a good topic.

Aside: One of the interesting things to look at is that RPF folks can sometimes initially loose weight, that is a function of elevated thyroid hormones trying to rescue the metabolism, but if they continue and ignore all shitty symptoms all of the sudden they blow the fuck up whether it is weight gain or worsening problems such as panic attacks, helplessness, social avoidance, etc. These of course are all symptoms of hypoxia … unless they start taking thyroid hormone. I prefer the advice “… let us avoid the problem to begin with …” the situation with the folks on the RPF is first physiological then pathological. Yikes.

1 Comment Hyperthyroidism (1) is chronic systemic hypoxia

  1. Adam

    I’m new and a little curious. So I know you and Peter at Hyperlipid recommend high fat diets that produce some level of ketones. Peter seems bigger on restricting protein and carbs like traditional keto diets, and you seem not to restrict glucose, but you do restrict fructose. I could be wrong but I also haven’t gathered that you restrict protein either. So I guess my question would be, how do we continue to run a predominantly SFA metabolism while taking in glucose, and not restricting protein. And secondly, why not then have fructose instead of the glucose, which is what Ray Peat might recommend, or is this one of the areas where you and him are split?
    Would really appreciate a reply.
    Thanks so much.

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