Ray Peat & Thyroid Wisdom

Hi all I've mentioned a few times on this forum that the Keto/carnivore diet is the reason for my devastating decline into overt hypothyroidism where I became unresponsive to synthetics. Since that time, I've used this forum as well as the teachings of American physiologist Ray Peat to educate myself about thyroid health. I found this, and thought it may be of interest to others about TSH. (source: raypeat.com)

I have spoken to several people who told me that their doctors had diagnosed them as “both hypothyroid and hyperthyroid.” Although physicists can believe in things which are simultaneously both particles and not particles, I think biology (and medicine, as far as it is biologically based) should occupy a world in which things are not simultaneously themselves and their opposites. Those illogical, impossible diagnoses make it clear that the rules for interpreting test results have in some situations lost touch with reality.Until the 1940s, hypothyroidism was diagnosed on the basis of signs and symptoms, and sometimes the measurement of oxygen consumption (“basal metabolic rate”) was used for confirmation.

Besides the introduction of supposedly “scientific” blood tests, such as the measurement of protein-bound iodine (PBI) in the blood, there were other motives for becoming parsimonious with the diagnosis of hypothyroidism. With the introduction of synthetic thyroxine, one of the arguments for increasing its sale was that natural Armour thyroid (which was precisely standardized by biological tests) wasn't properly standardized, and that an overdose could be fatal. A few articles in prestigious journals created a myth of the danger of thyroid, and the synthetic thyroxine was (falsely) said to be precisely standardized, and to be without the dangers of the complete glandular extract.Between 1940 and about 1950, the estimated percentage of hypothyroid Americans went from 30% or 40% to 5%, on the basis of the PBI test, and it has stayed close to that lower number (many publications claim it to be only 1% or 2%).

By the time that the measurement of PBI was shown to be only vaguely related to thyroid hormonal function, it had been in use long enough for a new generation of physicians to be taught to disregard the older ideas about diagnosing and treating hypothyroidism. They were taught to inform their patients that the traditional symptoms that were identified as hypothyroidism before 1950 were the result of the patients' own behavior (sloth and gluttony, for example, which produced fatigue, obesity, and heart disease), or that the problems were imaginary (women's hormonal and neurological problems, especially), or that they were simply mysterious diseases and defects (recurring infections, arthritis, and cancer, for example). As the newer, more direct tests became available, their meaning was defined in terms of the statistical expectation of hypothyroidism that had become an integral part of medical culture. To make the new TSH measurements fit the medical doctrine, an 8- or 10-fold variation in the hormone was defined as “normal.” With any other biological measurement, such as erythrocyte count, blood pressure, body weight, or serum sodium, calcium, chloride, or glucose, a variation of ten or 20 percent from the mean is considered to be meaningful. If the doctrine regarding the 5% prevalence of hypothyroidism hadn't been so firmly established, there would have been more interest in establishing the meaning of these great variations in TSH.In recent years the “normal range” for TSH has been decreasing.

In 2003, the American Association of Clinical Endocrinologists changed their guidelines for the normal range to 0.3 to 3.0 microIU/ml. But even though this lower range is less arbitrary than the older standards, it still isn't based on an understanding of the physiological meaning of TSH.Over a period of several years, I never saw a person whose TSH was over 2 microIU/ml who was comfortably healthy, and I formed the impression that the normal, or healthy, quantity was probably something less than 1.0. If a pathologically high TSH is defined as normal, its role in major diseases, such as breast cancer, mastalgia, MS, fibrotic diseases, and epilepsy, will simply be ignored. Even if the possibility is considered, the use of an irrational norm, instead of a proper comparison, such as the statistical difference between the mean TSH levels of cases and controls, leads to denial of an association between hypothyroidism and important diseases, despite evidence that indicates an association. Some critics have said that most physicians are “treating the TSH,” rather than the patient. If TSH is itself pathogenic, because of its pro-inflammatory actions, then that approach isn't entirely useless, even when they “treat the TSH” with only thyroxine, which often isn't well converted into the active triiodothyronine, T3. But the relief of a few symptoms in a small percentage of the population is serving to blind the medical world to the real possibilities of thyroid therapy.

[Jazzw]

I’ve read the odd bit of Ray Peat. He was one of the original “lone voices in the wilderness”.

I think I’d have bolded another part of that extract too—this bit:

They were taught to inform their patients that the traditional symptoms that were identified as hypothyroidism before 1950 were the result of the patients' own behavior (sloth and gluttony, for example, which produced fatigue, obesity, and heart disease), or that the problems were imaginary (women's hormonal and neurological problems, especially), or that they were simply mysterious diseases and defects (recurring infections, arthritis, and cancer, for example).

Fun, eh?

I go back and forth on this. The answer’s somewhere in between. I think there’s a good chance NDT was over prescribed for a while—it’s perhaps not credible that quite so many really had hypothyroidism back then (though they probably did have another hormone imbalance which hardly any doctor would have considered). Just like I think HRT is probably on the verge of being overprescribed now. Hormonal stuff is all still so much guesswork, isn’t it? And the problem with hormones is that they’re supposed to work synergistically. Mess about with one of them, mess about with several more…

For what it’s worth I do think you might be right about the detrimental effect of keto diets. Whether that’s keto itself or because we’ve already taxed our insulin feedback loops (another hormone cascade of course) by eating much higher carb loads than nature ever intended (processed foods), I’m not sure.

[MrPeaPaw]

This is the first time I've read the TSH is possibly pathogenic and a cause of inflammation. I wonder what others think.

My TSH is at the top of the "acceptable" range and my T3 only dose of 35 mcg/ day doesn't suppress it.

Everything about this condition is sometimes very confusing to me. As I am experiencing an afternoon "slump" my doctor has offered me a choice of adding Synthroid or Armour as my T4 is under range.

I take T3 only, as Synthroid made me feel ill. I'm on the horns of a dilemma here.

[Jazzw in reply to MrPeaPaw]

I’ve read that a dosage of 60mcg T3 daily is regarded as a replacement dosage for T3–what happens when you increase T3?

I’d suspect you’re simply not on enough T3.

And you’re not alone. There are several people here who just can’t tolerate taking any amount of levothyroxine. Quite why that is is unclear—but it happens.

[helvella Administrator in reply to Jazzw]

That is what is implied in the UK and Germany - when "standard" tablets are 20 micrograms are taken three times a day.

But in the USA, for. example, they say 75 micrograms. I suggest because that is three of their "standard" 25 microgram tablets.

25% more simply because of the available tablet dosages. Nothing to do with what the patient actually needs.

Shows the depth of understanding and quality of evidence that has been used.