At the end is one of Peat’s articles on the thyroid in its entirety. There are more Peat thyroid articles and other Peat articles online here under Supplements – Peat Category, and at his site.
All discussions above Peat’s are based on my own opinions and interpretations and what I have found useful for my own use as well as from feedback from many, many, many, many others.
See Books and Newsletters, Ray Peat for additional detailed discussion about thyroid.
Thyroid supplements, and the medical thyroid industry itself, are mostly based on a fraudulent, wrong-science, misunderstood physiology industry. Many of the tests are interpreted incorrectly, and many popular thyroid meds are compounded and manufactured around the corruption and fraud. They can be ineffective at the least, and damaging at the worst.
The supplement I have used for decades is CynoPlus (T4 120 mcg/T3 30 mcg combo product) and/or CynoMel (T3 only product).
The NovoTiral version I found will also work if CynoPlus is unavailable (which sometimes it has been).
In addition, I have found it very useful to ALSO take 200 mcg of selenium with the first dose in the morning.
CynoPlus (levothyroxine sodium and liothyronine in a particular ratio)is manufactured by GROSSMAN® SA pharmaceuticals in Mexico. This is true T3 + T4 respectively.
This is considered a prescription drug but is unavailable in the US. I found it can easily be ordered without prescription from Mexican pharmacies as below:
I order from this online Mexican pharmacy and it’s easy to get a good quantity for a lot less $ (about 1/4 the price!) and I have ordered multiple times from them with no problems in the past.
I pay easily through their “Mercado Pago” portal (or Bitcoin) with a credit card. The portal offers PayPal but if you use that choice the payment will currently be rejected for orders going through the US.
However, using their portal is easy. You do NOT need to verify email or identity or other as some of the portal leads to do. Choose the “Nueva Tarjeta” button right under the Paypal choice and you can enter your card info.
If you have any trouble, email them directly from your order email you receive. Their customer service is fabulous and depending on the time of day, they will respond nearly immediately.
They sell other supplements and health products too.
Or I have also purchased from this Mexican company online with a credit card, also from an invoice they generate to me, but they are very expensive.
Natural thyroid products such as “glandular” types (the prescription Armour brand, or health food store brands) can vary dramatically in potency even from pill to pill.
They can make monitoring change and working for effective thyroid healing even more difficult because of this.
I wasted more than a year experimenting with the glandular, sometimes taking up to 12 tablets of it per day over long stretches with no effect. Other times my heart would be racing with just one or two tabs after a couple of days.
I kept charts on myself and really could not figure out how much to take. I heard there is no way to manufacture these products with a consistent ingredient amount of what’s needed.
Physicians like Broda Barnes, MD. and scientists like Ray Peat, PhD., have suggested the best way to regulate the thyroid taking supplements is by charting 3 simple things of yourself– by yourself. Pulse. Temperature. Symptoms.
Blood tests that are taken will only measure that one pinpoint in time and the results are usually interpreted to recommend expensive prescription drugs.
It would be impractical to have a physician test your basal body temperature upon awaking and your temps again after eating, and your heart beats per minute at various times of day.
So the most recommended supplement I found where I could take responsibility for this myself, is to use the CynoPlus, which is a stable formulation, and to keep charts on myself– myself.
As well, there is the T3 version, called CynoMEL from both these locations.
Peat talks about how it would be helpful to use both the CynoPlus (T4/T3) in combination with the CynoMel (T3 only) product. See his newsletter here for more about that, scroll down to the middle of his newsletter about it.
If CynoPlus is unavailable, a type called Novotiral is very similar, also from Mexico only.
HOW I WORK WITH IT:
I CHART THIS for optimal dosing.
I would START LOW, like a 1/4th tab of a standard dose 120/30 mcg tablet per day or 1/4 tablet every 2-3 hours starting in the morning to take up to a whole tablet (4 doses of 1/4th tab).
But I started LOW first to see what I needed (I use a pill splitter).
I might ONLY NEED the 1/4th tab ONLY per day, which is the most common.
Other people, including Peat, including me, report overheating if taking one full tab of 120/30 (the standard CynoPlus brand tablet dose).
We get too hot off and on during the day taking too high a dose.
My current dose is only 1/2 tab per day, split into two 1/4th tabs, and both taken in the morning but 2 hours apart.
Someone else might need a higher dose, maybe one whole tab split into 1/4th pieces you take every two hours, of a dose for a couple weeks, for a month or 3 while they are also getting there food right, but most people feel more comfortable with about one-quarter to one-half of this tablet max during the day (taken as two quarters) once all begins to even out.
Temperature is taken first thing upon waking up before moving in any way out of bed when I would wake up, and then again during the day.
The easiest thermometer I found to use is one of those forehead/infrared for body temps electronic ones– just from a drugstore. These devices take a temp in just seconds, and I can take several measurements right in a row to get the accurate one, I point it right in my underarm arm pit.
These are the recommended levels I found from those I trust:
Temp upon waking and before getting up: 98
Temp after eating breakfast: 98.6
Temp during day: 98.6 (about 1/2 hour after eating, before 3 pm)
Pulse, sitting/resting: 80-85
I found keeping a regular chart on myself was highly recommended and beneficial, since doses and symptoms change and vary over time for each person.
Per Peat: “Keeping a chart of temperature and pulse rate is important, since T4 accumulates in the body, and takes about two weeks to reach equilibrium for a given dose”.
Most people will show lower temps and pulse and lots of symptoms than above and are clearly low thyroid.
However, those with severe low thyroid can also present with very high temps, and racing pulses because of high adrenaline.
Look to your lifestyle, diet, environment, and of course symptoms, symptoms, symptoms.
By the way, heating blankets will artificially raise the temps. Be sure the temp is still 98.6 after morning breakfast.
If a person’s waking temperature is “high” (98.6 or more) and falls after breakfast, cause could be from intense adrenal and cortisone hypoglycemic nocturnal stress.
This is often the case with lactic acid toxic athletes, and other severe low thyroid cases.
Diet is usually the problem.
My notes with Peat suggest thyroid supplementation is often needed, with high protein, salty broth (melted, dissolved, warm gelatin with a bit of salt), a bit of sugar (or orange juice with a bit of salt) before going to bed. I note that if you are getting up during the night with insomnia, eating a bit of these foods can help correct this.
When people begin to take the thyroid supplement, sometimes they might experience flushing, and pounding heartbeats just by walking up stairs, etc.
This is often because the adrenal glands are taking the place of an exhausted thyroid.
Now the thyroid supplement is present, helping and doing what it’s supposed to, but so is still an overflow of adrenaline.
It could take weeks or months to heal all, and for the adrenals and thyroid to settle down.
I was advised by a professional NOT TO STOP taking the thyroid supplement if this happens.
“Drinking orange juice [from Eileen–only fresh-pressed, not masticated and not frozen or bottled fresh from any source, even organic (damaging enzymes are used in the processing) and self-pulp-free it by straining through a fine mesh strainer] 3 or 4 times a day mixed with 1/4 teaspoon magnesium carbonate [from Eileen–magnesium supplements are not for long term use, it will irritate the intestines], and eating salty foods will help lower the adrenaline if you have the flushing, pounding, etc.”–Ray Peat
I found I needed to push through this uncomfortable period by continuing with the CynoPlus or CynoMel and orange juice/salt, or I wouldn’t heal.
This happened with me, this happened with other clients.
Many people do come out well on the other side, continuing to take the CynoPlus or CynoMel, perhaps in lessening quantities, but experiencing no more flushing, and with strong muscles and stable emotions.
Many believe a low pulse of 50 or 60 beats per minute is “relaxed”, or an “excellent meditative state”.
Read Ray Peat books and newsletters, and general physiology to understand the incorrect thinking about this vital indicator.
Meditations and relaxation are far easier to achieve when the thyroid and hormones are in good working order.
Symptoms of a hypothyroid (too low) thyroid can include, but are not limited to:
- Allergies
- Arthritis
- Asthma
- Attention Deficit Disorder (ADD)
- Bedwetting (children)
- Cholesterol, high serum
- Chronic fatigue
- Chronic infections, especially of the lungs, and other
- Constipation and other colon problems including chronic or acute appendicitis
- Coarse hair (men and women)
- Cold, sensitive to
- Depression
- Digestive problems
- Edema
- Fatigue
- Female problems (PMS, fibroids, miscarriage, infertility, tumors)
- Gallbladder attacks
- Hair loss (women and men)
- Headaches
- Hearing, Impaired
- Heart problems
- Hyperactivity
- Hypertension
- Hypoglycemia
- Insomnia
- Mental problems
- Migraines
- Mitral valve prolapse
- Mood Swings/Irritability
- Multiple sclerosis
- Skin problems (dry skin, acne, psoriasis, eczema)
- Tumors, breast, pelvic or otherwise
- Weight, Increase or decrease
CAUTION: No other brands/types of thyroid supplementation except the CynoPlus and NovoTiral were ever recommended to me in any way.
Ingredients and processes of thyroid supplements are often linked to a highly fraudulent industry.
What might well be labeled “T3” might be an incorrect definition based on the fraud, etc.
Set up your chart with days, temps, pulse rates and symptoms.
I have found the process of using thyroid, and healing in general involves a very unique and individual regime involving several factors.
Using a chart can help calculate how much to supplement.
Unless someone can hire a full-time, live-in endocrinologist, I don’t think any professional can do this for you, since it involves all day, daily monitoring of yourself.
I’ll give the directions I have used again with a little different words so this is clear:
CynoPlus, (T3 and T4) I would start with one tab or less, depending on my private situation, broken into 4 pieces– I use a pill splitter and spread out that one tab or less throughout a day. I start with no more that 1/2 tab anyway per day for the first week.
I take one of these quarter pieces no closer together than every 2 to 3 hours.
The liver can not process any more than that.
I can break these into even smaller pieces and take some every hour if my symptoms are severe.
The T4 helps the liver to heal and begin to make it’s own again. I have been advised by professionals that those diagnosed with signs of Addison’s disease need to start slowly, and will want to consult with their physician to monitor any adverse effects.
I would keep taking the CynoPlus and charting temps/pulse.
After a couple of weeks, if my temps are not up to the above ranges, I begin to add 1/4 tab per day every 5 days until the temps get up there to normal.
Once I reach normal, if I stay at whatever dose got me there, that might be too much thyroid to supplement.
So with my chart, I will notice if I need to begin to then decrease by 1/4 tab per day every 5 days.
Once I am stabilized with the thyroid supplements and protocols (this can go quickly for me or sometimes it can take months), I then experiment with decreasing my use of CynoPlus to 1/2 of one tab per day or so.
I need to always use my charting. See Ray Peat’s newsletters and books.
NOTE:
Thyroid tests of THS which you can test here or here without a doctor’s office visit or prescription, and other thyroid components can sometimes be useful.
Some people who have a healthy amount of good cholesterol from now long-time eating the correct and real foods, have a healthy amount of natural pregnenolone forming from the natural cholesterol, and a healthy amount of progesterone, and with the correct dose of thyroid supplement meds, their THS is often lower than the medical industry’s recommended amount after having corrected the food and supplements.
Thyroid specializing physicians are still using incorrect information to read and interpret the diagnosis and tests. With a lower test result than what the mainstream considers normal, some people could be told they are now hyper instead of steady.
I learned that the better test is to know my body, know my own normal pulse; my own temps per the suggestions above AFTER I have spent the time getting my other synergy items in place like a clean environment and air, clean water, clean and correct food and clean and correct supplements.
And then I read my tests with my own eye and own critical thinking.
A R T I C L E
TSH, temperature, pulse rate, and other indicators in hypothyroidism
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.
The “basal” metabolic rate, especially if the rate of carbon dioxide production is measured, is very useful. The amount of water and calories disposed of in a day can give a rough idea of the metabolic rate.
The T wave on the electrocardiogram, and the relaxation rate on the Achilles reflex test are useful.
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.
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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.
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.
REFERENCES
Clin Chem Lab Med. 2002 Dec;40(12):1344-8. Transthyretin: its response to malnutrition and stress injury. Clinical usefulness and economic implications. Bernstein LH, Ingenbleek Y.
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J Investig Med. 2002 Sep;50(5):350-4; discussion 354-5. The nocturnal serum thyrotropin surge is inhibited in patients with adrenal Incidentaloma. Coiro V, Volpi R, Capretti L, Manfredi G, Magotti MG, Bianconcini M, Cataldo S, Chiodera P.
Rev Neurol (Paris). 1992;148(5):371-3. [Hashimoto’s encephalopathy: toxic or autoimmune mechanism?] [Article in French] Ghawche F, Bordet R, Destee A. Service de Clinique Neurologique A, CHU, Lille. A 36-year-old woman presented with partial complex status epilepticus. Magnetic resonance imaging with T2-weighted sequences showed a high-intensity signal in the left posterior frontal area. Hashimoto’s thyroiditis was then discovered. The disappearance of the high-intensity signal after corticosteroid therapy was suggestive of an autoimmune mechanism. However, improvement could be obtained only with a hormonal treatment, which supports the hypothesis of a pathogenetic role of the Tyrosine-Releasing Hormone (TRH).
Am J Clin Nutr. 1986 Mar;43(3):406-13. Thyroid hormone and carrier protein interrelationships in children recovering rom kwashiorkor. Kalk WJ, Hofman KJ, Smit AM, van Drimmelen M, van der Walt LA, Moore RE. We have studied 15 infants with severe protein energy malnutrition (PEM) as a model of nutritional nonthyroidal illness. Changes in circulating thyroid hormones, binding proteins, and their interrelationships were assessed before and during recovery. Serum concentrations of total thyroxine and triiodothyronine and of thyroxine-binding proteins were extremely reduced, and increased progressively during 3 wk of refeeding. The T4:TBG molar ratio was initially 0.180 +/- 0.020, and increased progressively, parallel to the increases in TT4, to 0.344 +/- 0.038 after 21 days (p less than 0.025). The changes in free T4 estimates varied according to the methods used–FTI and analogue FT4 increased, dialysis FT4 fraction decreased. Serum TSH levels increased transiently during recovery. It is concluded 1) there is reduced binding of T4 and T3 to TBG in untreated PEM which takes 2-3 wk to recover; 2) there are methodological differences in evaluating free T4 levels in PEM; 3) increased TSH secretion appears to be an integral part of the recovery from PEM.
Neuroendocrinology. 1982;35(2):139-47. Neurotransmitter control of thyrotropin secretion. Krulich L. “The central dopaminergic system seems to have an inhibitory influence on the secretion of thyrotropin (TSH) both in humans and rats.”
Endocrinology 1972 Mar;90(3):795-801. TSH-induced release of 5-hydroxytryptamine and histamine rat thyroid mast cells. Ericson LE, Hakanson R, Melander A, Owman C, Sundler F.
Rev Neurol. 2002 Oct 16-31;35(8):741-2. [Hypothyroidism concealed by Parkinson’s disease][in Spanish] Garcia-Moreno JM, Chacon J. Servicio de Neurologia, Hospital Universitario Virgen Macarena, Sevilla, Espana. Sinue@arrakis.es AIMS: Although it is commonly recognised that diseases of the thyroids can simulate extrapyramidal disorders, a review of the causes of Parkinsonism in the neurology literature shows that they are not usually mentioned or, if so, only very briefly. The development of hypothyroidism in a patient with Parkinson s disease can go undetected, since the course of both diseases can involve similar clinical features. Generally speaking there is always an insistence on the need to conduct a thyroidal hormone study in any patient with symptoms of Parkinson, but no emphasis is put on the need to continue to rule out dysthyroidism throughout the natural course of the disease, in spite of the fact that the concurrence of both pathological conditions can be high and that, in the same way hypothyroidism can simulate Parkinson s disease, the latter can also conceal hypothyroidism. CASE REPORT: We report the case of a female patient who had been suffering from Parkinson s disease for 17 years and started to present on off fluctuations that did not respond to therapy. Hypothyroidism was observed and the hormone replacement therapy used to resolve the problem allowed the Parkinsonian fluctuations to be controlled. CONCLUSIONS: We believe that it is very wise to suspect hypothyroidism in patients known to be suffering from Parkinson s disease, and especially so in cases where the clinical condition worsens and symptoms no longer respond properly to antiparkinsonian treatment. These observations stress the possible role played by thyroid hormones in dopaminergic metabolism and vice versa.
Endocrine. 2003 Feb-Mar;20(1-2):149-54. Body composition of prolactin-, growth hormone, and thyrotropin-deficient Ames dwarf mice. Heiman ML, Tinsley FC, Mattison JA, Hauck S, Bartke A. Lilly Research Labs, Corporate Center, Indianapolis, IN, USA. Ames dwarf mice have primary deficiency of prolactin (PRL), growth hormone (GH), and thyroid-stimulating hormone (TSH), and live considerably longer than normal animals from the same line.
(Lancet. 1975 Nov 1;2(7940):845-8.. Triiodothyronine and thyroid-stimulating hormone in protein-calorie malnutrition in infants. Ingenbleek Y, Beckers C.)
Am J Med Sci. 1995 Nov;310(5):202-5. Case report: thyrotropin-releasing hormone-induced myoclonus and tremor in a patient with Hashimoto’s encephalopathy. Ishii K, Hayashi A, Tamaoka A, Usuki S, Mizusawa H, Shoji S.
Rev Neurol (Paris). 1985;141(1):55-8. [Hashimoto’s thyroiditis and myoclonic encephalopathy. Pathogenic hypothesis] [Article in French] Latinville D, Bernardi O, Cougoule JP, Bioulac B, Henry P, Loiseau P, Mauriac L. A 49 year old caucasian female with Hashimoto thyroiditis, developed during two years a neurological disorder with tonic-clonic and myoclonic seizures and confusional states. Some attacks were followed by a transient postictal aphasia. Some parallelism was noted between the clinical state and TSH levels. Neurological events disappeared with the normalisation of thyroid functions. This association of Hashimoto thyroiditis and myoclonic encephalopathy has been rarely published. Pathogenesis could be double. Focal signs could be due to an auto-immune mechanism, perhaps through a vasculitis. A non-endocrine central action could explain diffuse signs: tonic-clonic seizures, myoclonus and confusional episodes.
J Clin Endocrinol Metab. 1992 Jun;74(6):1361-5. Fatty acid-induced increase in serum dialyzable free thyroxine after physical exercise: implication for nonthyroidal illness. Liewendahl K, Helenius T, Naveri H, Tikkanen H.
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Endocrinology 1971 Aug;89(2):528-33. TSH-induced appearance and stimulation of amine-containing mast cells in the mouse thyroid. Melander A, Owman C, Sundler F.
Epilepsy Res. 1988 Mar-Apr;2(2):102-10. Evidence of hypothyroidism in the genetically epilepsy-prone rat. Mills SA, Savage DD. Department of Pharmacology, University of New Mexico School of Medicine, Albuquerque 87131. A number of neurochemical and behavioral similarities exist between the genetically epilepsy-prone (GEPR) rat and rats made hypothyroid at birth. These similarities include lower brain monoamine levels, audiogenic seizure susceptibility and lowered electroconvulsive shock seizure threshold. Given these similarities, thyroid hormone status was examined in GEPR rats. Serum samples were collected from GEPR-9 and non-epileptic control rats at 5, 9, 13, 16, 22, 31, 45, 60, 90, 150 and 350 days of age. Serum thyroxine (T4) levels were significantly lower in GEPR-9 rats compared to control until day 22 of age. GEPR-9 thyrotropin (TSH) levels were significantly elevated during the period of diminished serum T4. GEPR-9 triiodothyronine (T3) levels were lower than control throughout the first year of life. The data indicate that the GEPR-9 rat is hypothyroid from at least the second week of life up to 1 year of age. The critical impact of neonatal hypothyroidism on brain function coupled with the development of the audiogenic seizure susceptible trait by the GEPR-9 rat during the third week after birth suggests that neonatal hypothyroidism could be one etiological factor in the development of the seizure-prone state of GEPR-9 rats.
Przegl Lek. 1998;55(5):250-8. [Mastopathy and simple goiter–mutual relationships] [Article in Polish] Mizia-Stec K, Zych F, Widala E. “Non-toxic goitre was found in 80% patients with mastopathy, and the results of palpation examination of thyroid were confirmed by thyroid ultrasonographic examination. Non-toxic goitre was significantly more often in patients with mastopathy in comparison with healthy women, and there was found significantly higher thyroid volume in these patients.” Endocrinology. 1997 Apr;138(4):1434-9. Thyroxine administration prevents streptococcal cell wall-induced inflammatory responses. Rittenhouse PA, Redei E.
Eur J Appl Physiol Occup Physiol. 1998;77(1-2):37-43. Pre-adaptation, adaptation and de-adaptation to high altitude in humans: hormonal and biochemical changes at sea level. Savourey G, Garcia N, Caravel JP, Gharib C, Pouzeratte N, Martin S, Bittel J.
Endocrinol Jpn. 1992 Oct;39(5):445-53. Plasma free fatty acids, inhibitor of extrathyroidal conversion of T4 to T3 and thyroid hormone binding inhibitor in patients with various nonthyroidal illnesses. Suzuki Y, Nanno M, Gemma R, Yoshimi T.
Natl Med J India. 1998 Mar-Apr;11(2):62-5. Neuropsychological impairment and altered thyroid hormone levels in epilepsy. Thomas SV, Alexander A, Padmanabhan V, Sankara Sarma P. Department of Neurology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram, Kerala, India. BACKGROUND: Neuropsychological impairment is a common problem in epilepsy which interferes with the quality of life of patients. Similarly, thyroid hormone levels have been observed to be abnormal in patients with epilepsy on various treatments. This study aimed to ascertain any possible correlation between neuropsychological performance and thyroid hormone levels among epilepsy patients. METHODS: Thyroid hormone levels, indices of neuropsychological performance and social adaptation of 43 epilepsy patients were compared with those of age- and sex-matched healthy control subjects. RESULTS: Epilepsy patients exhibited significantly (p < 0.001) lower scores on attention, memory, constructional praxis, finger tapping time, and verbal intelligence quotient (i.q.) when compared with controls. Their T3, T4 and Free T3 levels were significantly lower; and TSH and Free T4 levels were significantly higher than that of controls. There was no statistically significant correlation between the indices of neuropsychological performance and thyroid hormone levels. CONCLUSION: We did not observe any correlation between neuropsychological impairment and thyroid hormone levels among patients with epilepsy.
Crit Care Med. 1994 Nov;22(11):1747-53. Dopamine suppresses pituitary function in infants and children. Van den Berghe G, de Zegher F, Lauwers P.
Ned Tijdschr Geneeskd. 2000 Jan 1;144(1):5-8. [Epilepsy, disturbances of behavior and consciousness in presence of normal thyroxine levels: still, consider the thyroid gland] [Article in Dutch] Vrancken AF, Braun KP, de Valk HW, Rinkel GJ. Afd. Neurologie, Universitair Medisch Centrum Utrecht. Three patients, one man aged 51 years, and two women aged 49 and 52 years, had severe fluctuating and progressive neurological and psychiatric symptoms. All three had normal thyroxine levels but elevated thyroid stimulating hormone levels and positive thyroid antibodies. Based on clinical, laboratory, MRI and EEG findings they were eventually diagnosed with Hashimoto’s encephalopathy, associated with Hashimoto thyroiditis. Treatment with prednisone in addition to thyroxine suppletion resulted in a remarkable remission of their neuropsychiatric symptoms. The disease is probably under-recognized.
Cell Immunol. 1999 Mar 15;192(2):159-66. Neuroendocrine-induced synthesis of bone marrow-derived cytokines with inflammatory immunomodulating properties. Whetsell M, Bagriacik EU, Seetharamaiah GS, Prabhakar BS, Klein JR.
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