Confused About Thyroid And How It Works

[Johhny Tazzle]

So i have been reading up on how the thyroid works, and am confused about how the thyroid gets moving if tsh is low. Peat recommends keeping the tsh low, but then does the thyroid just produce t4 and send it to the liver to be made into t3 automatically, what keeps the thyroid moving and functioning if tsh is low? I guess im wondering how the thyroid works, I haven't been able to find an explanation other than when thyroid hormone is low in the blood tsh is made to signal thyroid to make t4.

 

[Mito]

when thyroid hormone is low in the blood tsh is made to signal thyroid to make t4.

I think you answered your own question. The pituitary decreases TSH as it senses adequate thyroid hormone. So the lower the TSH level that produces adequate thyroid hormone the better.

 

[meatbag]

I learned a ton from this interview, probably one of my favs

 

[Travis]

I learned a ton from this interview, probably one of my favs

Wow. I never thought that Ray Peat had spoken with Gary Null. I like both of these people, Gary Null being a fairly serious investigator himself.

 

[Johhny Tazzle]

So are most people are in a state where their tsh is chronically elevated, you would think tsh would rise then go back to normal after it did its function of telling the thyroid to produce t4. So is tsh a safety mechanism? Like its not needed unless your thyroid is suboptimal, or is tsh part of what makes your thyroid function? Im going to listem to tgat interview thanks for the recommemdation

 

[Johhny Tazzle]

I like this gary null guy already

 

[meatbag]

So are most people are in a state where their tsh is chronically elevated, you would think tsh would rise then go back to normal after it did its function of telling the thyroid to produce t4. So is tsh a safety mechanism? Like its not needed unless your thyroid is suboptimal, or is tsh part of what makes your thyroid function? Im going to listem to tgat interview thanks for the recommemdation

I think the tsh is about more than just whats going on with the thyroid gland, since as Peat points out in his article "Increasingly, TSH (the pituitary thyroid stimulating hormone) has been treated as if it meant something independently; however, it can be brought down into the normal range, or lower, by substances other than the thyroid hormones."

So it is like a signal from the pituitary in cases of a failure in the oxidation/ thyroid activities systemically, so operate using this other method.

"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.


TSH has direct actions on many cell types other than the thyroid, and probably contributes directly to edema (Wheatley and Edwards, 1983), fibrosis, and mastocytosis. If people are concerned about the effects of a TSH “deficiency,” then I think they have to explain the remarkable longevity of the animals lacking pituitaries in W.D. Denckla's experiments, or of the naturally pituitary deficient dwarf mice that lack TSH, prolactin, and growth hormone, but live about a year longer than normal mice (Heiman, et al., 2003). Until there is evidence that very low TSH is somehow harmful, there is no basis for setting a lower limit to the normal range.


Some types of thyroid cancer can usually be controlled by keeping TSH completely suppressed. Since TSH produces reactions in cells as different as fibroblasts and fat cells, pigment cells in the skin, mast cells and bone marrow cells (Whetsell, et al., 1999), it won't be surprising if it turns out to have a role in the development of a variety of cancers, including melanoma.


Many things, including the liver and the senses, regulate the function of the thyroid system, and the pituitary is just one of the factors affecting the synthesis and secretion of the thyroid hormones.


A few people who had extremely low levels of pituitary hormones, and were told that they must take several hormone supplements for the rest of their life, began producing normal amounts of those hormones within a few days of eating more protein and fruit. Their endocrinologist described them as, effectively, having no pituitary gland. Extreme malnutrition in Africa has been described as creating “. . . a condition resembling hypophysectomy,” (Ingenbleek and Beckers, 1975) but the people I talked to in Oregon were just following what they thought were healthful nutritional policies, avoiding eggs and sugars, and eating soy products.


Occasionally, a small supplement of thyroid in addition to a good diet is needed to quickly escape from the stress-induced “hypophysectomized” condition.


Aging, infection, trauma, prolonged cortisol excess, somatostatin, dopamine or L-dopa, adrenaline (sometimes; Mannisto, et al., 1979), amphetamine, caffeine and fever can lower TSH, apart from the effect of feedback by the thyroid hormones, creating a situation in which TSH can appear normal or low, at the same time that there is a real hypothyroidism."

As is also discussed in the article the TSH seems to relate more to energy states than necessarily glandular secretions;

"
The stress-induced suppression of TSH and other pituitary hormones is reminiscent of the protective inhibition that occurs in individual nerve fibers during dangerously intense stress, and might involve such a “parabiotic” process in the nerves of the hypothalamus or other brain region. The relative disappearance of the pituitary hormones when the organism is in very good condition (for example, the suppression of ACTH and cortisol by sugar or pregnenolone) is parallel to the high energy quiescence of individual nerve fibers.


These associations between energy state and cellular activity can be used for evaluating the thyroid state, as in measuring nerve and muscle reaction times and relaxation rates. For example, relaxation which is retarded, because of slow restoration of the energy needed for cellular “repolarization,” is the basis for the traditional use of the Achilles tendon reflex relaxation test for diagnosing hypothyroidism. The speed of relaxation of the heart muscle also indicates thyroid status (Mohr-Kahaly, et al., 1996).


Stress, besides suppressing the TSH, acts in other ways to suppress the real thyroid function. Cortisol, for example, inhibits the conversion of T4 to T3, which is responsible for the respiratory production of energy and carbon dioxide. Adrenaline, besides leading to increased production of cortisol, is lipolytic, releasing the fatty acids which, if they are polyunsaturated, inhibit the production and transport of thyroid hormone, and also interfere directly with the respiratory functions of the mitochondria. Adrenaline decreases the conversion to T4 to T3, and increases the formation of the antagonistic reverse T3 (Nauman, et al., 1980, 1984).


During the night, at the time adrenaline and free fatty acids are at their highest, TSH usually reaches its peak. TSH itself can produce lipolysis, raising the level of circulating free fatty acids. This suggests that a high level of TSH could sometimes contribute to functional hypothyroidism, because of the antimetabolic effects of the unsaturated fatty acids.


These are the basic reasons for thinking that the TSH tests should be given only moderate weight in interpreting thyroid function.


The metabolic rate is very closely related to thyroid hormone function, but defining it and measuring it have to be done with awareness of its complexity.


The basal metabolic rate that was commonly used in the 1930s for diagnosing thyroid disorders was usually a measurement of the rate of oxygen consumption, made while lying quietly early in the morning without having eaten anything for several hours. When carbon dioxide production can be measured at the same time as oxygen consumption, it's possible to estimate the proportion of energy that is being derived from glucose, rather than fat or protein, since oxidation of glucose produces more carbon dioxide than oxidation of fat does. Glucose oxidation is efficient, and suggests a state of low stress.


The very high adrenaline that sometimes occurs in hypothyroidism will increase the metabolic rate in several ways, but it tends to increase the oxidation of fat. If the production of carbon dioxide is measured, the adrenaline/stress component of metabolism will be minimized in the measurement. When polyunsaturated fats are mobilized, their spontaneous peroxidation consumes some oxygen, without producing any usable energy or carbon dioxide, so this is another reason that the production of carbon dioxide is a very good indicator of thyroid hormone activity. The measurement of oxygen consumption was usually done for two minutes, and carbon dioxide production could be accurately measured in a similarly short time. Even a measurement of the percentage of carbon dioxide at the end of a single breath can give an indication of the stress-free, thyroid hormone stimulated rate of metabolism (it should approach five or six percent of the expired air).


Increasingly in the last several years, people who have many of the standard symptoms of hypothyroidism have told me that they are hyperthyroid, and that they have to decide whether to have surgery or radiation to destroy their thyroid gland. They have told me that their symptoms of “hyperthyroidism,” according to their physicians, were fatigue, weakness, irritability, poor memory, and insomnia.


They didn't eat very much. They didn't sweat noticeably, and they drank a moderate amount of fluids. Their pulse rates and body temperature were normal, or a little low.


Simply on the basis of some laboratory tests, they were going to have their thyroid gland destroyed. But on the basis of all of the traditional ways of judging thyroid function, they were hypothyroid.
"
~http://raypeat.com/articles/articles/hypothyroidism.shtml

 

[Johhny Tazzle]

Thanks there are some real gems in there

 

[Johhny Tazzle]

Also im just thinking if you see a low t4 and high t3 does that tell you the liver is working well? Bare with me im just diving into the details of this stuff, also what would be a possible cause for high rt3 versus high t3. Would the vause if this be the cells inability to utilize t3?

 

[meatbag]

Also im just thinking if you see a low t4 and high t3 does that tell you the liver is working well? Bare with me im just diving into the details of this stuff, also what would be a possible cause for high rt3 versus high t3. Would the vause if this be the cells inability to utilize t3?

I believe rt3 is due to overwhelming t4 which is converted to rt3 as a protective measure. I'm not sure about what exactly would cause too much t3 besides over supplementation due to how it is secreted and converted but I could be very wrong.