A lady from another state contacted me by email stating that she was diagnosed with hypothyroidism at age 13, and that she had rising thyroid peroxidase antibody (TPOAb) levels, which concern her. She is frustrated because her physicians haven’t been “interested in looking at that [the antibody levels].” I don’t have details, but she reports having been on the “gamut” standard and alternative therapies for hypothyroidism, yet her health is still not where she would like it to be—her words.
What follows is an edited, and somewhat augmented, version of my reply to her, which I prefaced with the statement that there were positives and negatives in those comments regarding whether I might be able to help her, or at least provide her what she said she was looking for—essentially a partner in holistic therapy of her thyroid condition.
My positive comments, with respect helping were as follows:
If she was diagnosed with hypothyroidism at age 13, the diagnosis was likely fairly definitive, and abnormal TPOAb’s add weight to that. My point being, if there is good hard laboratory evidence of hypothyroidism and/or Hashimoto’s thyroiditis (not the same thing: hypothyroidism is a lack of thyroid hormone, which can be due to a number of causes; Hashimoto’s is an autoimmune disorder that is an important cause of hypothyroidism, though not all Hashimoto’s patients are hypothyroid), then it is much more likely that there is some relatively straightforward therapy that will help. As opposed to: well, it sounds like hypothyroidism, but the numbers don’t clearly show it. I do treat some of those people and sometimes it helps and sometimes it doesn’t. I went on to tell her—the fact she has been on some form of thyroid therapy for over 25 years makes it likely her hypothalamic-pituitary-thyroid axis has been to some degree suppressed by outside thyroid hormone. This might result in lower TSH levels than expected for any given situation, which would lead many physicians, many endocrinologists included, to undertreat.
So there are features to this individual’s story, and I’ve heard similar ones quite often, that make me think I might be able to help her, and I told her that.
Now for the negative—and I really shouldn’t say negative, I just mean, advice, counsel, constructive criticism, disclaimers… First she mentioned as part of her plea that she had been under stress for a long time. I’m unaware that there is any general recognition that a stressful lifestyle causes or worsens Hashimoto’s or hypothyroidism, except perhaps amongst certain authors and internet “experts” who may or may not really know what they’re talking about. In fact, I might argue the opposite—that hypothyroidism, causing fatigue and depression, makes life more stressful, and lessened one’s ability to cope with the ordinary stresses of life. In other words, hypothyroidism causes stress, rather than stress causing hypothyroidism.
Having said that, I will hasten to add two points: (1) a catastrophic emotional event, like the death of a spouse, or beloved pet, is well known to trigger Graves’ disease, an autoimmune thyroid disorder causing hyperthyroidism—high thyroid levels—but that type life event is different from chronic “normal” stress; and (2) one thing I do believe stress can do is elevate cortisol (a type of steroid) release from the adrenal glands, and cortisol suppresses TSH release. If TSH is suppressed, the thyroid gland might not be properly stimulated to make thyroid hormone. This would be a form of so-called “central hypothyroidism,” in which the person is hypothyroid without the expected elevation of TSH that is usually seen. This is one of the big differences in my approach to hypothyroidism from other doctors, including endocrinologists. Nobody doubts central hypothyroidism exists, but it is felt to be rare and is seldom considered. I, on the other hand, think it might be quite common and rampantly missed. And since there is no test to confirm it (the test is the TRH stimulation test, which requires a drug that is no longer available in the United States), the only thing to do if it’s suspected is to start thyroid hormone replacement and see if it helps.
So, I should modify my above statement about stress. I doubt chronic life stress causes primary hypothyroidism due to Hashimoto’s thyroiditis, but it might cause central hypothyroidism, either as a problem by itself, or one that might further worsen existing primary hypothyroidism.
I agree therefore that stress could be part of this lady’s problem; we just need to be clear what it is or isn’t doing. Also, the very stressful, busy lifestyle she described to me, can make one feel lousy for all kinds of reasons—for example, a lack of good quality exercise leading to poor physical and cardiovascular conditioning, or lack of sleep causing fatigue during the day—the lack of sleep being due to time constraints, or inability to relax due to thinking about stressful things. The point being, all the thyroid hormone in the world won’t fix those things.
She said her TPOAb’s have been climbing, and her doctors aren’t interested in looking at that. Her doctors may be right. We don’t track TPOAb’s in the same way we track, say, TSHs in thyroid patients and glucoses in diabetics. The fact that TPOAb’s (a type of thyroid antibody) are elevated tells us a person is at risk of becoming hypothyroid, or in this lady’s case (having already been diagnosed) that the cause of her hypothyroidism is autoimmune. There is no advantage, however, in continuing to check it. In fact, if a person comes to me with new hypothyroidism, I hardly ever check TPOAb’s. They don’t change anything. Unless there is some other obvious cause, like thyroid surgery, most people in the United States who are hypothyroid have Hashimoto’s. I can just assume that and don’t need to do a blood test to prove it, because the treatment is the same regardless of cause. Thyroid hormone replacement.
It would be different if there were a way to stop or reverse the autoimmune destruction of the thyroid, but there isn’t. Nothing proven safe and to work, and certainly nothing anywhere near as safe and reliable and inexpensive as thyroid hormone replacement is for most people, and I’m one of those people. Steroids might shut down TPOAb production but we wouldn’t go that route because it would be a case of the cure being worse than the disease—the steroids would cause diabetes, weight gain, osteoporosis, infections, and so forth. Now, maybe there is something out there that is safe and effective, some supplement, or diet, but we don’t know what it is yet. Until we do, giving thyroid hormone is the most reliable path to feeling better.
I and most endocrinologists do know very well that many people, like this patient, on thyroid hormone for hypothyroidism don’t feel 100 percent. To that I have two comments: (1) few things in life are perfect—that’s not a cop out; it’s wisdom and truth; and (2) I believe some of those people not feeling good on thyroid hormone aren’t on enough medication. My approach to hypothyroidism is pretty standard—that is, thyroid hormone replacement, usually with Synthroid or similar products—but I often use higher doses than most doctors are comfortable with, and I think that’s why I seem to get better symptom control in some patients than they do.
Dr. Rone
What follows is an edited, and somewhat augmented, version of my reply to her, which I prefaced with the statement that there were positives and negatives in those comments regarding whether I might be able to help her, or at least provide her what she said she was looking for—essentially a partner in holistic therapy of her thyroid condition.
My positive comments, with respect helping were as follows:
If she was diagnosed with hypothyroidism at age 13, the diagnosis was likely fairly definitive, and abnormal TPOAb’s add weight to that. My point being, if there is good hard laboratory evidence of hypothyroidism and/or Hashimoto’s thyroiditis (not the same thing: hypothyroidism is a lack of thyroid hormone, which can be due to a number of causes; Hashimoto’s is an autoimmune disorder that is an important cause of hypothyroidism, though not all Hashimoto’s patients are hypothyroid), then it is much more likely that there is some relatively straightforward therapy that will help. As opposed to: well, it sounds like hypothyroidism, but the numbers don’t clearly show it. I do treat some of those people and sometimes it helps and sometimes it doesn’t. I went on to tell her—the fact she has been on some form of thyroid therapy for over 25 years makes it likely her hypothalamic-pituitary-thyroid axis has been to some degree suppressed by outside thyroid hormone. This might result in lower TSH levels than expected for any given situation, which would lead many physicians, many endocrinologists included, to undertreat.
So there are features to this individual’s story, and I’ve heard similar ones quite often, that make me think I might be able to help her, and I told her that.
Now for the negative—and I really shouldn’t say negative, I just mean, advice, counsel, constructive criticism, disclaimers… First she mentioned as part of her plea that she had been under stress for a long time. I’m unaware that there is any general recognition that a stressful lifestyle causes or worsens Hashimoto’s or hypothyroidism, except perhaps amongst certain authors and internet “experts” who may or may not really know what they’re talking about. In fact, I might argue the opposite—that hypothyroidism, causing fatigue and depression, makes life more stressful, and lessened one’s ability to cope with the ordinary stresses of life. In other words, hypothyroidism causes stress, rather than stress causing hypothyroidism.
Having said that, I will hasten to add two points: (1) a catastrophic emotional event, like the death of a spouse, or beloved pet, is well known to trigger Graves’ disease, an autoimmune thyroid disorder causing hyperthyroidism—high thyroid levels—but that type life event is different from chronic “normal” stress; and (2) one thing I do believe stress can do is elevate cortisol (a type of steroid) release from the adrenal glands, and cortisol suppresses TSH release. If TSH is suppressed, the thyroid gland might not be properly stimulated to make thyroid hormone. This would be a form of so-called “central hypothyroidism,” in which the person is hypothyroid without the expected elevation of TSH that is usually seen. This is one of the big differences in my approach to hypothyroidism from other doctors, including endocrinologists. Nobody doubts central hypothyroidism exists, but it is felt to be rare and is seldom considered. I, on the other hand, think it might be quite common and rampantly missed. And since there is no test to confirm it (the test is the TRH stimulation test, which requires a drug that is no longer available in the United States), the only thing to do if it’s suspected is to start thyroid hormone replacement and see if it helps.
So, I should modify my above statement about stress. I doubt chronic life stress causes primary hypothyroidism due to Hashimoto’s thyroiditis, but it might cause central hypothyroidism, either as a problem by itself, or one that might further worsen existing primary hypothyroidism.
I agree therefore that stress could be part of this lady’s problem; we just need to be clear what it is or isn’t doing. Also, the very stressful, busy lifestyle she described to me, can make one feel lousy for all kinds of reasons—for example, a lack of good quality exercise leading to poor physical and cardiovascular conditioning, or lack of sleep causing fatigue during the day—the lack of sleep being due to time constraints, or inability to relax due to thinking about stressful things. The point being, all the thyroid hormone in the world won’t fix those things.
She said her TPOAb’s have been climbing, and her doctors aren’t interested in looking at that. Her doctors may be right. We don’t track TPOAb’s in the same way we track, say, TSHs in thyroid patients and glucoses in diabetics. The fact that TPOAb’s (a type of thyroid antibody) are elevated tells us a person is at risk of becoming hypothyroid, or in this lady’s case (having already been diagnosed) that the cause of her hypothyroidism is autoimmune. There is no advantage, however, in continuing to check it. In fact, if a person comes to me with new hypothyroidism, I hardly ever check TPOAb’s. They don’t change anything. Unless there is some other obvious cause, like thyroid surgery, most people in the United States who are hypothyroid have Hashimoto’s. I can just assume that and don’t need to do a blood test to prove it, because the treatment is the same regardless of cause. Thyroid hormone replacement.
It would be different if there were a way to stop or reverse the autoimmune destruction of the thyroid, but there isn’t. Nothing proven safe and to work, and certainly nothing anywhere near as safe and reliable and inexpensive as thyroid hormone replacement is for most people, and I’m one of those people. Steroids might shut down TPOAb production but we wouldn’t go that route because it would be a case of the cure being worse than the disease—the steroids would cause diabetes, weight gain, osteoporosis, infections, and so forth. Now, maybe there is something out there that is safe and effective, some supplement, or diet, but we don’t know what it is yet. Until we do, giving thyroid hormone is the most reliable path to feeling better.
I and most endocrinologists do know very well that many people, like this patient, on thyroid hormone for hypothyroidism don’t feel 100 percent. To that I have two comments: (1) few things in life are perfect—that’s not a cop out; it’s wisdom and truth; and (2) I believe some of those people not feeling good on thyroid hormone aren’t on enough medication. My approach to hypothyroidism is pretty standard—that is, thyroid hormone replacement, usually with Synthroid or similar products—but I often use higher doses than most doctors are comfortable with, and I think that’s why I seem to get better symptom control in some patients than they do.
Dr. Rone