Temperature and Pulse Basics & Monthly Log
The Cholesterol and Thyroid Connection
Inflammation from Decrease in Body Temperature
High Cholesterol and Metabolism
The Truth about Low Cholesterol
Thyroid Status and Oxidized LDL
“Normal” TSH: Marker for Increased Risk of Fatal Coronary Heart Disease
Thyroid Status and Cardiovascular Disease
High Blood Pressure and Hypothyroidism
A Cure for Heart Disease
Hypothyroidism and A Shift in Death Patterns
Is 98.6 Really Normal?
“Measuring the amount of thyroid in the blood isn’t a good way to evaluate adequacy of thyroid function, since the response of tissues to the hormone can be suppressed (for example, by unsaturated fats).
In the 1930′s accurate diagnosis was made by evaluating a variety of indications, including basal oxygen consumption, serum cholesterol level, pulse rate, temperature, carotenemia, bowel function, and quality of hair and skin. A good estimate can be made using only the temperature and pulse rate.
Oral or armpit temperature, in the morning before getting out of bed, should be around 98F, and it should rise to 98.6F by mid-morning. This is not valid if you sleep under and electric blanket, or is the weather is hot and humid. A person who is hypothyroid produces heat at a low rate, but doesn’t lose it at a normal rate, since there is less sweating, and the skin is relatively cool. Many hypothyroid people compensate with high adrenalin production (sometimes 40 times higher than normal), and this tends to keep the skin cook, especially on the hands, feet, and nose. The high adrenalin is the consequence of low blood glucose, so a feeding of carbohydrate, such as a glass of orange juice, will sometimes lower the pulse rate momentarily. Healthy populations have an average resting pulse of about 85 per minute. Especially in hot weather it is useful to consider both temperature and pulse rate.”
“The thyroid gland secretes about 3 parts thyroxin to one part triiodothyronine, and this allows the liver to regulate thyroid function, by converting more of the T4 to the active T3 when there is an abundance of energy. Glucose is essential for the conversion, so during fasting there is a sharp decrease in metabolic rate, and in experiments, 200 to 300 calories of carbohydrate can be added to the diet diet without causing fat storage.
When the liver is the main cause of hypothyroidism, your temperature (and especially the temperature of your nose, hands and feet) will fall when hungry, and will rise when you eat carbohydrates. If a hypothyroid person has a very slow pulse, and feels lethargic, it seems that there is little adrenalin; in this case, a feeding of carbohydrate is likely to increase both the pulse rate and the temperature, as the liver is permitted to form the active T3 hormone.
Women often have above-average thyroxin, with symptoms of hypothyroidism. This is apparently because it isn’t being converted to the active form (T3). Before using a Cytomel (T3) supplement, it might be possible to solve the problem with diet alone. A piece of fruit or glass of juice or milk between meals, and adequate animal protein (or potato protein) in the diet is sometimes enough to allow the liver to produce the hormone. If Cytomel is used, it is efficient to approximate the physiological rate of T3 formation, by nibbling one (10 to 25 mcg) tablet during the day. When a large amount is taken at one time, the liver is likely to convert much of it to the inactive reverse T3 form, in a normal defensive response.
Women normally have less active livers than men do. Estrogen can have a directly toxic effect on the liver, but the normal reason for the difference is probably that temperature and thyroid function strongly influence the liver, and are generally lower in women than in men. Estrogen inhibits the secretion of hormone by the thyroid gland itself, probably by inhibiting the proteolytic enzymes which dissolves the colloid. Progesterone has the opposite effect, promoting the release of the hormones from the gland. At puberty, in pregnancy, and at menopause, the thyroid gland often enlarges, probably as a result of estrogen dominance.
Thyroid function stimulates the liver to inactivate estrogen for secretion, so estrogen dominance can create a viscous circle, in which estrogen (or deficient progesterone) blocks thyroid secretion, causing the liver to allow estrogen to accumulate to even higher levels. Progesterone (even one dose, in some cases) can break the cycle. However, if the gland is very big, one person can experience a few months of hyperthyroidism, as the gland returns to normal. It is better to allow the enlarged gland to shrink more slowly by using a thyroid supplement. If an enlarged gland does begin to secrete too much thyroid hormone, it can be controlled with tablets of propylthiouracil, or even raw cabbage or cabbage juice, and cysteine rich meats, including liver.
Besides fasting, or chronic protein deficiency, the common causes of hypothyroidism are excessive stress or “aerobic” (i.e., anaerobic) exercise, and diets containing beans, lentils, nuts, unsaturated fats (including carotene), and undercooked broccoli, cauliflower, cabbage, and mustard greens. Many health conscious people become hypothyroid with a synergistic program of undercooked vegetables, legumes instead of animal proteins, oils instead of butter, carotene instead of vitamin A, and breathless exercise instead of stimulating life.”
“Each of the indicators of thyroid function can be useful, but has to be interpreted in relation to the physiological state.
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.
“Basal” body temperature is influenced by many things besides thyroid. The resting heart rate helps to interpret the temperature. In a cool environment, the temperature of the extremities is sometimes a better indicator than the oral or eardrum temperature.”
“Unless someone can demonstrate the scientific invalidity of the methods used to diagnose hypothyroidism up to 1945, then they constitute the best present evidence for evaluating hypothyroidism, because all of the blood tests that have been used since 1950 have been shown to be, at best, very crude and conceptually inappropriate methods.
Thomas H. McGavack’s 1951 book, The Thyroid, was representative of the earlier approach to the study of thyroid physiology. Familiarity with the different effects of abnormal thyroid function under different conditions, at different ages, and the effects of gender, were standard parts of medical education that had disappeared by the end of the century. Arthritis, irregularities of growth, wasting, obesity, a variety of abnormalities of the hair and skin, carotenemia, amenorrhea, tendency to miscarry, infertility in males and females, insomnia or somnolence, emphysema, various heart diseases, psychosis, dementia, poor memory, anxiety, cold extremities, anemia, and many other problems were known reasons to suspect hypothyroidism. If the physician didn’t have a device for measuring oxygen consumption, estimated calorie intake could provide supporting evidence. The Achilles’ tendon reflex was another simple objective measurement with a very strong correlation to the basal metabolic rate. Skin electrical resistance, or whole body impedance wasn’t widely accepted, though it had considerable scientific validity.
A therapeutic trial was the final test of the validity of the diagnosis: If the patient’s symptoms disappeared as his temperature and pulse rate and food intake were normalized, the diagnostic hypothesis was confirmed. It was common to begin therapy with one or two grains of thyroid, and to adjust the dose according to the patient’s response. Whatever objective indicator was used, whether it was basal metabolic rate, or serum cholesterol, or core temperature, or reflex relaxation rate, a simple chart would graphically indicate the rate of recovery toward normal health.”
“Since I have been interested in the way that hypothyroidism, a T3 deficiency, causes sleep problems, I have seen similar patterns in several seemingly different conditions. At menopause, insomnia, hypothyroidism, and diabetes are like to develop along with hot flashes. Although hypothyroidism often causes the temperature to be subnormal, I saw many women whose temperature before breakfast was normal, but then fell after breakfast, usually following some hot flashes and sweats. Gradually, I began to realize that this corresponded to extremely high adrenaline and cortisol in the morning, and that high morning temperature was sometimes the first sing of the developing “hyper-alert” state, though most often it just represented the stress and exhaustion that result from disturbed, inefficient sleep.
Using a small does of T3 normally causes an increase of temperature and pulse rate, but in these people who are in an extremely adrenergic state, the T3 causes both the temperature and heart rate to decrease, as it restores metabolic efficiency. Then, as the stress state disappears, the thyroid supplements will gradually begin to bring the metabolic rate, temperature, and pulse up to normal. When the body temperature is maintained by thyroid-supported respiration, rather than by stress hormones, the sleep is efficient.
Thyroid, especially T3, has been commonly used in the treatment of depression, and there are many indications that, as it relieves the depression, it is also correcting a state of stress, lowering the cortisol which is typically chronically increased in depression, making sleep restful, rather than debilitating.”
“Blood tests for cholesterol, albumin, glucose, sodium, lactate, total thyroxine and total T3 are useful to know, because they help to evaluate the present thyroid status, and sometimes they can suggest ways to correct the problem.
Less common blood or urine tests (adrenaline, cortisol, ammonium, free fatty acids), if they are available, can help to understand compensatory reactions to hypothyroidism.
A book such as McGavack’s The Thyroid, that provides traditional medical knowledge about thyroid physiology, can help to dispel some of the current dogmas about the thyroid.
Using more physiologically relevant methods to diagnose hypothyroidism will contribute to understanding its role in many problems now considered to be unrelated to the thyroid.”
“Years ago it was reported that Armour thyroid, U.S.P., released T3 and T4, when digested, in a ratio of 1:3, and that people who used it had much higher ratios of T3 to T4 in their serum, than people who took only thyroxine. The argument was made that thyroxine was superior to thyroid U.S.P., without explaining the significance of the fact that healthy people who weren’t taking any thyroid supplement had higher T3:T4 ratios than the people who took thyroxine, or that our own thyroid gland releases a high ratio of T3 to T4. The fact that the T3 is being used faster than T4, removing it from the blood more quickly than it enters from the thyroid gland itself, hasn’t been discussed in the journals, possibly because it would support the view that a natural glandular balance was more appropriate to supplement than pure thyroxine.
The serum’s high ratio of T4 to T3 is a pitifully poor argument to justify the use of thyroxine instead of a product that resembles the proportion of these substances secreted by a healthy thyroid gland, or maintained inside cells. About 30 years ago, when many people still thought of thyroxine as “the thryoid hormone,” someone was making the argument that “the thyroid hormone” must work exclusively as an activator of genes, since most of the organ slices he tested didn’t increase their oxygen consumption when it was added. In fact, the addition of thyroxine to brain slices suppressed their respiration by 6% during the experiment. Since most T3 is produced from T4 in the liver, not in the brain, I think that experiment had great significance, despite the ignorant interpretation of the author. An excess of thyroxine, in a tissue that doesn’t convert it rapidly to T3, has an antithyroid action. (See Goumaz, et al, 1987.) This happens in many women who are given thyroxine; as their dose is increased, their symptoms get worse.
The brain concentrates T3 from the serum, and may have a concentration 6 times higher than the serum (Goumaz, et al., 1987), and it can achieve a higher concentration of T3 than T4. It takes up and concentrates T3, while tending to expel T4. Reverse T3 (rT3) doesn’t have much ability to enter the brain, but increased T4 can cause it to be produced in the brain. These observations suggest to me that the blood’s T3:T4 ratio would be very “brain favorable” if it approached more closely to the ratio formed in the thyroid gland, and secreted into the blood. Although most synthetic combination thyroid products now use a ratio of four T4 to one T3, many people feel that their memory and thinking are clearer when they take a ratio of about three to one. More active metabolism probably keeps the blood ratio of T3 to T4 relatively high, with the liver consuming T4 at about the same rate that T3 is used.
Since T3 has a short half life, it should be taken frequently. If the liver isn’t producing a noticeable amount of T3, it is usually helpful to take a few micorgrams per hour. Since it restores respiration and metabolic efficiency very quickly, it isn’t usually necessary to take it every hour or two, but until normal temperature and pulse have been achieved and stabilized, sometimes it’s necessary to take it four or more times during the day. T4 acts by being changed to T3, so it tends to accumulate in the body, and on a given dose, usually reaches a steady concentration after about two weeks.
An effective way to use supplements is to take a combination T4-T3 dose, e.g., 40 mcg of T4 and 10 mcg of T3 once a day, and to use a few mcg of T3 at other times in the day. Keeping a 14-day chart of pulse rate and temperature allows you to see whether the dose is producing the desired response. If the figures aren’t increasing at all after a few days, the dose can be increased, until a gradual daily increment can be seen, moving toward the goal at the rate of about 1/14 per day.”
“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.
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.
A disease or its treatment can obscure the presence of hypothyroidism. Parkinson’s disease is a clear example of this. (Garcia-Moreno and Chacon, 2002: “… in the same way hypothyroidism can simulate Parkinson’s disease, the latter can also conceal hypothyroidism.”)
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.
Broda Barnes, who worked mostly in Fort Collins, Colorado, argued that the body temperature, measured before getting out of bed in the morning, was the best basis for diagnosing thyroid function.
Fort Collins, at a high altitude, has a cool climate most of the year. The altitude itself helps the thyroid to function normally. For example, one study (Savourey, et al., 1998) showed an 18% increase in T3 at a high altitude, and mitochondria become more numerous and are more efficient at preventing lactic acid production, capillary leakiness, etc.
In Eugene during a hot and humid summer, I saw several obviously hypothyroid people whose temperature seemed perfectly normal, euthyroid by Barnes’ standards. But I noticed that their pulse rates were, in several cases, very low. It takes very little metabolic energy to keep the body at 98.6 degrees when the air temperature is in the nineties. In cooler weather, I began asking people whether they used electric blankets, and ignored their temperature measurements if they did.
The combination of pulse rate and temperature is much better than either one alone. I happened to see two people whose resting pulse rates were chronically extremely high, despite their hypothyroid symptoms. When they took a thyroid supplement, their pulse rates came down to normal. (Healthy and intelligent groups of people have been found to have an average resting pulse rate of 85/minute, while less healthy groups average close to 70/minute.)
The speed of the pulse is partly determined by adrenaline, and many hypothyroid people compensate with very high adrenaline production. Knowing that hypothyroid people are susceptible to hypoglycemia, and that hypoglycemia increases adrenaline, I found that many people had normal (and sometimes faster than average) pulse rates when they woke up in the morning, and when they got hungry. Salt, which helps to maintain blood sugar, also tends to lower adrenalin, and hypothyroid people often lose salt too easily in their urine and sweat. Measuring the pulse rate before and after breakfast, and in the afternoon, can give a good impression of the variations in adrenalin. (The blood pressure, too, will show the effects of adrenaline in hypothyroid people. Hypothyroidism is a major cause of hypertension.)
But hypoglycemia also tends to decrease the conversion of T4 to T3, so heat production often decreases when a person is hungry. First, their fingers, toes, and nose will get cold, because adrenalin, or adrenergic sympathetic nervous activity, will increase to keep the brain and heart at a normal temperature, by reducing circulation to the skin and extremities. Despite the temperature-regulating effect of adrenalin, the reduced heat production resulting from decreased T3 will make a person susceptible to hypothermia if the environment is cool.
Since food, especially carbohydrate and protein, will increase blood sugar and T3 production, eating is “thermogenic,” and the oral (or eardrum) temperature is likely to rise after eating.
Blood sugar falls at night, and the body relies on the glucose stored in the liver as glycogen for energy, and hypothyroid people store very little sugar. As a result, adrenalin and cortisol begin to rise almost as soon as a person goes to bed, and in hypothyroid people, they rise very high, with the adrenalin usually peaking around 1 or 2 A.M., and the cortisol peaking around dawn; the high cortisol raises blood sugar as morning approaches, and allows adrenalin to decline. Some people wake up during the adrenalin peak with a pounding heart, and have trouble getting back to sleep unless they eat something.
If the night-time stress is very high, the adrenalin will still be high until breakfast, increasing both temperature and pulse rate. The cortisol stimulates the breakdown of muscle tissue and its conversion to energy, so it is thermogenic, for some of the same reasons that food is thermogenic.
After eating breakfast, the cortisol (and adrenalin, if it stayed high despite the increased cortisol) will start returning to a more normal, lower level, as the blood sugar is sustained by food, instead of by the stress hormones. In some hypothyroid people, this is a good time to measure the temperature and pulse rate. In a normal person, both temperature and pulse rate rise after breakfast, but in very hypothyroid people either, or both, might fall.
Some hypothyroid people have a very slow pulse, apparently because they aren’t compensating with a large production of adrenalin. When they eat, the liver’s increased production of T3 is likely to increase both their temperature and their pulse rate.
By watching the temperature and pulse rate at different times of day, especially before and after meals, it’s possible to separate some of the effects of stress from the thyroid-dependent, relatively “basal” metabolic rate. When beginning to take a thyroid supplement, it’s important to keep a chart of these measurements for at least two weeks, since that’s roughly the half-life of thyroxine in the body. When the body has accumulated a steady level of the hormones, and begun to function more fully, the factors such as adrenaline that have been chronically distorted to compensate for hypothyroidism will have begun to normalize, and the early effects of the supplementary thyroid will in many cases seem to disappear, with heart rate and temperature declining. The daily dose of thyroid often has to be increased several times, as the state of stress and the adrenaline and cortisol production decrease.
Counting calories achieves approximately the same thing as measuring oxygen consumption, and is something that will allow people to evaluate the various thyroid tests they may be given by their doctor. Although food intake and metabolic rate vary from day to day, an approximate calorie count for several days can often make it clear that a diagnosis of hyperthyroidism is mistaken. If a person is eating only about 1800 calories per day, and has a steady and normal body weight, any “hyperthyroidism” is strictly metaphysical, or as they say, “clinical.”
When the humidity and temperature are normal, a person evaporates about a liter of water for every 1000 calories metabolized. Eating 2000 calories per day, a normal person will take in about four liters of liquid, and form about two liters of urine. A hyperthyroid person will invisibly lose several quarts of water in a day, and a hypothyroid person may evaporate a quart or less.
When cells, because of a low metabolic rate, don’t easily return to their thoroughly energized state after they have been stimulated, they tend to take up water, or, in the case of blood vessels, to become excessively permeable. Fatigued muscles swell noticeably, and chronically fatigued nerves can swell enough to cause them to be compressed by the surrounding connective tissues. The energy and hydration state of cells can be detected in various ways, including magnetic resonance, and electrical impedance, but functional tests are easy and practical.
With suitable measuring instruments, the effects of hypothyroidism can be seen as slowed conduction along nerves, and slowed recovery and readiness for new responses. Slow reaction time is associated with slowed memory, perception, and other mental processes. Some of these nervous deficits can be remedied slightly just by raising the core temperature and providing suitable nutrients, but the active thyroid hormone, T3 is mainly responsible for maintaining the temperature, the nutrients, and the intracellular respiratory energy production.
In nerves, as in other cells, the ability to rest and repair themselves increases with the proper level of thyroid hormone. In some cells, the energized stability produced by the thyroid hormones prevents inflammation or an immunological hyperactivity. In the 1950s, shortly after it was identified as a distinct substance, T3 was found to be anti-inflammatory, and both T4 and T3 have a variety of anti-inflammatory actions, besides the suppression of the pro-inflammatory TSH.
Because the actions of T3 can be inhibited by many factors, including polyunsaturated fatty acids, reverse T3, and excess thyroxine, the absolute level of T3 can’t be used by itself for diagnosis. “Free T3” or “free T4” is a laboratory concept, and the biological activity of T3 doesn’t necessarily correspond to its “freedom” in the test. T3 bound to its transport proteins can be demonstrated to enter cells, mitochondria, and nuclei. Transthyretin, which carries both vitamin A and thyroid hormones, is sharply decreased by stress, and should probably be regularly measured as part of the thyroid examination.
When T3 is metabolically active, lactic acid won’t be produced unnecessarily, so the measurement of lactate in the blood is a useful test for interpreting thyroid function. Cholesterol is used rapidly under the influence of T3, and ever since the 1930s it has been clear that serum cholesterol rises in hypothyroidism, and is very useful diagnostically. Sodium, magnesium, calcium, potassium, creatinine, albumin, glucose, and other components of the serum are regulated by the thyroid hormones, and can be used along with the various functional tests for evaluating thyroid function.
Stereotypes are important. When a very thin person with high blood pressure visits a doctor, hypothyroidism isn’t likely to be considered; even high TSH and very low T4 and T3 are likely to be ignored, because of the stereotypes. (And if those tests were in the healthy range, the person would be at risk for the “hyperthyroid” diagnosis.) But remembering some of the common adaptive reactions to a thyroid deficiency, the catabolic effects of high cortisol and the circulatory disturbance caused by high adrenaline should lead to doing some of the appropriate tests, instead of treating the person’s hypertension and “under nourished” condition.”
“Using thyroid will usually reduce the amount of progesterone needed. Occasionally, a woman won’t feel any effect even from 100 mg. of progesterone; I think this indicates that they need to use thyroid and diet, to normalize their estrogen, prolactin, and cortisol.”
“Barnes experimented on rabbits, and found that when their thyroid glands were removed, they developed atherosclerosis, just as hypothyroid people did. By the mid-1930s, it was generally known that hypothyroidism causes the cholesterol level in the blood to increase; hypercholesterolemia was a diagnostic sign of hypothyroidism. Administering a thyroid supplement, blood cholesterol came down to normal exactly as the basal metabolic rate came up to the normal rate. The biology of atherosclerotic heart disease was basically solved before the second world war.”
“If a person has an enlarged thyroid gland, progesterone promotes secretion and unloading of the stored “colloid,” and can bring on a temporary hyperthyroid state. This is a corrective process, and in itself isn’t harmful. A thyroid supplement should be used to shrink the goiter before progesterone is given. Normal amounts of progesterone facilitate thyroid secretion, while a deficiency, with unopposed estrogen, causes the thyroid to enlarge.”
“When too little protein, or the wrong kind of protein, is eaten, there is a stress reaction, with thyroid suppression. Many of the people who don’t respond to a thyroid supplement are simply not eating enough good protein.”
“When a person is using a thyroid supplement, it’s common to need four times as much in December as in July.”
“..but the important point is that in normal people a totally suppressed thyroid function takes only two or three days to return to normal when the suppressive treatment is stopped. In a small percentage of a hypothyroid people, treatment for a short time with thyroid supplementation can stimulate recovery of normal thyroid function, by activating the brain-pituitary system, raising blood sugar which activates the liver enzyme system that produces T3, and by lowering the anti-thyroid stress hormones. Without using radioactive material, it is easy to visualize the process of suppression: very obvious depressions in the neck thyroid region on a thoroughly suppressive dose, and reducing the dose for a few days restores the neck contour. This very rapid adaptation of the gland’s anatomy and function to exogenous thyroid is necessary, because of the irregularity of our consumption of thyroid substance in the natural diet. Until this century, everyone ate the thyroid in various small animals, and we still get some in milk and shellfish and a few exotic foods.
The issue is different with thyroxin, T4. The bulk of our active T3 hormone is produced in the liver, as part of a quickly adaptive system for adjusting the metabolic rate in relation to nutritional status, but the pituitary is also able to convert T4 to T3 and a high level of T4 will cause suppression of TSH secretion, even if the liver is failing to produce the active T3, as in aging, stress, cirrhosis, and various other diseases. Thyroxin can literally make hypothyroidism worse. In this case you have suppression without a compensating absorption of active hormone.
Although a little thyroid substance is a normal dietary factor, and digestion of the glandular colloid converts the protein into the hormones in the same king of process that occurs in normal secretion from the living gland, I agree with Morstein that it is important to restore the gland’s normal function as far as possible.”