Questions flooded in for the 12/29/10 teleseminar with Dr. John C. Lowe (http://budurl.com/2z7d, and the time ran out before the questions did.
Dr. Lowe very graciously agreed to answer the remaining questions in writing–and here they are. Great stuff!
1. What triggers hypothyroidism, is it genetic etc…… AND why do we get and have thyroid problems
We have two classes of thyroid hormone disorders that lead to the need for people to take thyroid hormone. One disorder is hypothyroidism, or a thyroid hormone deficiency. The other is partial cellular resistance to thyroid hormone. In this latter disorder, cells respond only sluggishly to normal amounts of thyroid hormone. The two disorders have different causes.
Iodine deficiency was once thought to be the most common cause of deficiency production of thyroid hormone by the thyroid gland. In geographical regions where there is too little iodine, iodine deficiency may still be the most common trigger. However, in areas where iodine is plentiful, autoimmune thyroid disease is the most common cause of hypothyroidism.
But iodine deficiency and autoimmune disease are far from the only causes of hypothyroidism. Many people develop thyroid hormone deficiencies because of infections of the thyroid gland, thiocyanide in cigarette smoke, trauma to the gland as in whiplash injuries, and radiation exposure. We’re subjected to a lot of x-rays, as when we travel inside airliners. I’m convinced that going through screening x-ray fields in airports will increase the incidence of hypothyroidism. I’ve talked to too many x-ray researchers to trust our government’s reassurances that those x-ray fields are virtually harmless.
Other people are hypothyroid because of damage of the pituitary gland or hypothalamus. Pituitary damage can result from interference with the nerve supply to the gland from the upper cervical spine in the neck. And a wide array of chemicals can cause mutations in cells of the pituitary and hypothalamus. The hypothalamus and pituitary secrete hormones that regulate the thyroid gland. These are, respectively, TRH and TSH. When too little of one or both of these hormones is produced, or if they are mutated, then the thyroid gland doesn’t produce enough thyroid hormone.
We’re not as sure about the various causes of partial cellular resistance to thyroid hormone. In the form of resistance called “peripheral,” the pituitary gland isn’t resistant. Because of that, the people have in-range TSH and thyroid hormone levels. Nonetheless, they have symptoms characteristic of hypothyroidism. In the late 1990s, a member of my research and treatment team, Richard L. Garrison, MD, designated resistance “type 2 hypothyroidism.” In 2000, I published this in my book The Metabolic Treatment of Fibromyalgia. Several years later, Mark Starr, MD published a book titled Hypothyroidism Type 2: The Epidemic. I think the term helps some people understand thyroid hormone resistance. Dr. Garrison’s reason for inventing the term was that resistance is somewhat analogous to type 2 diabetes. But I still use the traditionally term “thyroid hormone resistance.”
People with resistance have hypothyroid-like symptoms because of one or more glitches in the person’s cellular use of thyroid hormone. Most of them can recover, but they have to use fairly high doses of T3. The high doses override the resistance. As a result, cell function and metabolism become normal and the symptoms are relieved.
The first unequivocally proven cause of thyroid hormone resistance was mutations in the c-erbA-beta gene on chromosome 3. This gene codes for the beta-thyroid hormone receptor. This is the main receptor by which thyroid hormone regulates the function of cell. When the gene has a mutation, it causes one amino acid in the receptor, which is a protein, to be substituted by another amino acid. This causes the receptor to have a low affinity for thyroid hormone; the hormone doesn’t readily bind to the receptor. More than a hundred mutations have been identified in the gene. These can be caused by radiation, some chemicals in cigarette smoke, and many of the vast array of chlorinated chemical contaminants that industry saturated us with during the 20th and 21st centuries.
2. Did Dr Lowe suffer cognitive problems as a child?
Yes, I suffered from severe cognitive dysfunction. I especially remember how tough it was to comprehend when I read. If a sentence had, say, ten words, by the time I reached the last five words, I’d forgotten what the first five words were. I’d have to read the sentence over-and-over again. Eventually I might grasp what the meaning of the sentence was. It seemed to me that when I tried to hold the meaning in my mind, holes would spontaneously appear and some of the meaning would evaporate from my mind. Then I had to read the sentence again, may be several times. I struggled with this from elementary school through college.
In school, I was passed by what was known as “social promotion.” This meant that I had failing grades, but for social reasons, they passed me anyway. I sneaked into the back door of junior college. You could do this in Florida by signing up for nighttime classes. For some reason, if one did this, he or she didn’t have to go through the application process that would’ve caused a refusal of admission to the college. I learned some memory techniques. With those, I could at least scratch my way through most courses. I failed others more than once, such as English.
Fortunately, I’d become an extremely good and showy drummer in popular local bands, such as the Laymen, and this brought me intelligent lady friends. They kindly taught me some study methods, and they tutored me in English grammar and other subjects. They also got me to study junior high and high school books. This enabled me to catch up on my huge educational deficits. So through their generous help, I compensated for a mind that still had spontaneously forming holes like Swiss cheese. I compensated well enough to move along through college. A turning point was toward the end of junior college. That was when I discovered Adelle Davis’ books on nutrition and began taking mega doses of nutritional supplements. This didn’t cure my cognitive dysfunction, but it improved it enough so that I did better in college.
When I transferred to the University of West Florida, I also sort of sneaked in. Because of my poor grades in junior college, they weren’t going to allow me in. But then it was discovered that my father died in the Air Force, and because of some strange provision, that qualified me to be accepted.
I didn’t acquire what I consider normal cognitive function until I learned that I was thyroid hormone resistant. That was when I began taking Cytomel in my late thirties. Afterward, I didn’t have to compensate for poor mental function, but my compensatory methods (such as memory techniques) had become habit by then. I still use them. With a normally functioning brain, if I’m going to give a presentation at a conference, I use those memory techniques so that I don’t have to use notes during my presentations.
3. Was Dr. Lowe’s condition caused by Hashimoto?
No, I never had anti-thyroid antibodies. I also had reference range TSH and thyroid hormone levels. Even my TRH-stimulation test results were in range.
3. Does your current dose of T3 fluctuate?
Mine doesn’t very often nowadays. In years passed, I occasionally felt like I should slightly decrease my usual 150 mcg of T3. At other times, I felt I should increase it slightly. I typically decreased or increased it by 12.5 mcg.
However, years ago, the new instruments called “indirect calorimeters” became available for measuring the basal metabolic rate (BMR). Since I began using these instruments, if I feel I need to alter my dose, I measure my basal metabolic rate. I also run an ECG/EKG and measure the voltage of my heart’s R waves. When I see that my BMR is exactly where it’s supposed to be, and my R-wave voltage is where it’s supposed to be, I leave my T3 dose where it is. I wait, and usually within a few days, I’ve lost the feeling that I need to decrease or increase my dose. This has kept me from altering my dosage very often. I rarely do, and only briefly, in the course of a couple of years. I think my feeling that I need to alter my dosage was usually due to some other factor, such as insufficient sleep, allergy-induced fatigue, or a phase in my “chronobiology.”
The term chronobiology refers to the biological and psychological cycles of living organisms as they adapt to the rhythms of the sun and moon. The cycles are probably a source of much confusion over whether one is on the right dose of thyroid hormone, or the right product for the individual. It’s important to consider that a phase of your chronobiological cycles may account for your feeling that you need more or less thyroid hormone. Sometimes it’s best just to wait and see whether the perception changes over time.
4. How useful is a reverse T3 test in diagnosing HYPOTHYROIDISM?
I believe the test is of virtually no value in diagnosing hypothyroidism, if by hypothyroidism we mean a thyroid hormone deficiency. When the thyroid gland produces too little T4 and T3, less of these two hormones are available. The vast bulk of what the thyroid gland produces and releases into the blood is T4. With a lower-than-usual amount of T4 available, it’s likely that more of it will be converted to T3 rather than reverse T3. This presumably results from a need to keep the T3 high enough to maintain effective cell function. Also presumably, reverse T3 production from T4 will decrease to some degree. As a result, in moderate-to-severe hypothyroidism we might find low T4, low-to-mid-range T3, and a low reverse T3. However, as far as I know, no researchers have shown that this lab result pattern is useful for diagnosing hypothyroidism.
This pattern in hypothyroidism is only a conception based on principles. But in actual practice, I’ve rarely seen this pattern in hypothyroid patients. I believe the reason is that when the TSH and thyroid hormone levels are in range, their levels vary (as Japanese researchers say) “dramatically every thirty minutes or so.” There is no correlation from thirty-minute period to thirty-minute period, day-to-day, and week-to-week.
In my opinion, the reverse T3 has served us best in diagnosing a condition that has a variety of names: “euthyroid sick syndrome,” “low T3 syndrome,” and “non-thyroidal illness syndrome.” The word “euthyroid,” of course, means that the person has in-range TSH, T4, and T3 levels. In this condition, the hypothalamus secretes less TRH, the pituitary secretes less TSH, and less thyroid hormone is transported into cells. Also, the enzyme called “5-prime deiodinase,” which converts T4 to T3, becomes far less active. Another enzyme, “5 deiodinase” (no “prime” as a modifier) becomes more active and converts more T4 to reverse T3.
The words “sick syndrome” is somewhat misleading. That term is used presumably because the condition was first identified in sick people, such as anorexics and hospitalized patients in critical condition. Studies showed that the patients had steeply raised cortisol levels. It’s their high cortisol levels that inhibit the enzyme (5-prime deiodinase) that converts T4 to T3.
I’ve found no evidence that this condition becomes chronic, as Dr. Dennis Wilson proposed. Instead, the research literature shows that within a week or two, TSH secretion increases and 5-prime deiodinase escapes the inhibition by cortisol. This happens even though the person’s cortisol levels remain high. For example, if the person undergoes prolonged treatment with prednisone, within a week or two, the TSH level returns to its previous level and 5-prime deiodinase becomes normally active again.
Old studies show that on average, most people convert more than 50% of their T4 to reverse T3; correspondingly, they convert less than 50% of T4 to the metabolically active hormone T3. And the levels of reverse T3 fluctuate up and down through the day. Because of this, I’m never confident of coming to a conclusion that someone has a problem with high reverse T3, not unless the person has had multiple measures of the reverse T3 over a 24-hour period. Like the TSH, free T4, free T3, reverse T3 levels vary dramatically every 30 minutes or so. Depending on when a person’s blood is drawn or saliva taken. Sometimes the levels will vary enough so that a clinician will give the patient a different diagnosis from the one that he or she would have given 30-minutes before or after the blood or saliva sample was taken.
So blood levels vary rapidly. Because of this, I don’t believe the reverse T3 or the other lab tests in general are very useful. However, I do believe the reverse T3 is useful under one circumstance: when we have enough measures to get averages over time, and when the levels are regularly way out of range. So, in my view, the reverse T3 can be useful, but I think its usefulness is limited, which is true of the TSH and other thyroid hormone levels. >>>
5. What is thyroid resistance and how is it treated? I cannot tolerate T4 or natural dessicated thyroid, only cytomel, but my doctor doesn’t know how much T3 to give me. I don’t seem to get hyperthyroid at all with 100 mcg, but it seems like a lot. I’m a 62 yr old female, 140#. I have been diagnosed with “low voltage”, by a cardiologist, but never knew until hearing you tonight that this was connected. People say too much T3 will cause heart problems. I would like to hear what you have to say on this. Thanks!
Unless a person takes a daily dose of T3 that is too high for him or her, then it’s highly unlikely that the T3 will cause any heart problems. The same is true, however, of T4. Keep in mind that T4 is not a hormone; it’s a prohormone and is metabolically inert until it’s converted to T3. So, if it were true that taking too much T3 causes heart problems, the same would be true of taking too much T4, it that some of it will be converted to T3.
The only person for whom a small dose of T3 would be harmful would be someone with an extremely fragile heart. Among ambulatory people, this is extremely rare. When a person begins to take an effective dose of T3, his or her previously under-stimulated heart beats more forcibly. The person isn’t used to feeling the vibrations produced by the more forceful projection of blood out of the left large heart chamber (ventricle) against the inner wall of the aorta. Because of this, the person perceives the pounding. Many people misinterpret the pounding as overstimulation of the heart. In fact, it’s just a normal occurrence, as in people who haven’t been hypothyroid. Perception of the pounding is usually enhanced if the person lies on a bed. The bed acts as a sounding board, and this amplifies the perception of pounding and may frighten the person. But if the person understands that the pounding is a harmless phenomenon, he or she will become desensitized to it after a week or two. The pounding from vibrations continue, but the person then isn’t aware of it.
Of course, if the heart beats too rapidly, say more than 90-to-100 beats per minute at rest, there are possible explanations other than too much T3. If the person’s dose is below, say, 90-to-100 mcg per day, chances are the problem is something related to over-activity of the sympathetic nervous system. Low or high blood sugar is a common cause of the over-activity. B complex vitamin deficiencies, such as a B1 and B12, may also be the cause of the rapid heart rate. When such other factors are interacting with T3 to cause a rapid heart rate, the proper way to relieve the problem isn’t to stop the T3 altogether. It’s proper to reduce the dose low enough to relieve the rapid heart rate, and then identify and correct the other problem. Then the person should be able to use a dose of T3 high enough to be fully effective without causing the heart to beat too fast.
Incidentally, before the TSH scourge came to afflict patients some forty years ago, the Physicians’ Desk Reference specified what a full replacement dose of T3 was for a person who has no thyroid gland. The dosage range was 75-to-100 mcg. So your 100 mcg wouldn’t necessarily be considered too high. Dosing is always highly individual, though. Because of that, the question to ask is whether that amount is too high, just enough, or too little for you as an individual.
In your question you wrote, “People say too much T3 will cause heart problems.” (Italics mine.) I would rephrase the statement to read, “Too much T3 for a particular individual may cause heart problems.” I’ve seen many patients who were thyrotoxic from T4 alone, T4/T3 products, and T3 alone who had no adverse heart effects. It’s safest, of course, to avoid anything more than mild and brief overstimulation by thyroid hormone, although the endocrinology specialty has grossly exaggerated the potential for harm.
Dr. Lowe, I really appreciate your help. My subscribers love you.
Thank you, Bette. You’re so kind to me. I very much appreciate both you and your Subscribers.