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Hashimoto's mechanism explained by Dr. Nguyen
"Let's Talk A Little Bit About Your Immune System..."
The immune system has two sides like a teeter-totter. The first side, called our "T"-Helper 1 System (TH-1 System), is our immediate immune system. It is responsible for an immediate attack against foreign invaders like bacteria or parasites. The cells involved in the TH-1 system are called macrophages, natural killer cells, and cytotoxic T Cells. It is our front line defense.
The other side of our immune teeter-totter is our T-Helper 2 (TH-2) system. It involves the production of antibodies to "tag" onto invaders so our TH-1 system can more easily destroy the invaders. It is our B cells that are responsible for producing the antibodies.
Most of the time our TH-1 system will successfully destroy invaders, before antibodies are ever produced. If the invader is not destroyed by the TH-1 system immediately, the TH-2 antibody system gets involved and produces antibodies. These antibodies are like attaching strobe lights to the foreign invaders. It makes it extremely easy for the TH-1 cells to find and kill the foreign invaders. .
In order for the various immune cells of the TH-1 and TH-2 system to communicate and coordinate their function they produce little messenger proteins called cytokines.
"In an autoimmune condition, like Hashimoto's Autoimmune Thyroid, the two sides of the immune teeter-totter get terribly imbalanced..."
It is almost like there is a person on only one side, which if you've ever seen a teeter-totter, you know that this does not work. It is this dysregulation in the immune system, the imbalance between the two systems, that tricks your body into attacking its own tissue.
This "dominance" on one side of the immune system is also why the hormone replacement model as the sole treatment source doesn't always result in patients feeling better, even though lab markers may look normal for a time. (Remember I told you I would get to this)
The cytokines that are produced in the autoimmune attack actually interfere with the thyroid receptor sites from producing normal responses. This means even if you have an adequate amount of thyroid hormone in the blood stream, the hormones won't necessarily bind to your cells and create a normal metabolic response. Which means...you still have thyroid symptoms even with normal levels of hormones circulating in your blood stream.
Normally when a thyroid hormone binds to a cell it causes the cell to increase it's metabolism and this increases the production of certain proteins inside the cell. This is called a "proteomic response." In Hashimoto's the proteomic response is diminished by the inflammatory cytokines that are produced from the autoimmune attack.
So even when the thyroid hormones bind to cell receptors their isn't a very strong proteomic response. This is exactly why the replacement mode only of thyroid management can result in continuing thyroid symptoms.
Most doctors don't acknowledge this concept. They will try to make your lab panels look "normal" with replacement hormones and when you tell them you still have the same symptoms they are going to assume that you are depressed, or that it is "all in your head." Not a lot of credence is paid to how you as the patient feel.. what your everyday experience is.
Or if you are continually gaining weight, without ANY change in diet, they will assume you are just overeating...that you need to exercise.
The immune system has two sides like a teeter-totter. The first side, called our "T"-Helper 1 System (TH-1 System), is our immediate immune system. It is responsible for an immediate attack against foreign invaders like bacteria or parasites. The cells involved in the TH-1 system are called macrophages, natural killer cells, and cytotoxic T Cells. It is our front line defense.
The other side of our immune teeter-totter is our T-Helper 2 (TH-2) system. It involves the production of antibodies to "tag" onto invaders so our TH-1 system can more easily destroy the invaders. It is our B cells that are responsible for producing the antibodies.
Most of the time our TH-1 system will successfully destroy invaders, before antibodies are ever produced. If the invader is not destroyed by the TH-1 system immediately, the TH-2 antibody system gets involved and produces antibodies. These antibodies are like attaching strobe lights to the foreign invaders. It makes it extremely easy for the TH-1 cells to find and kill the foreign invaders. .
In order for the various immune cells of the TH-1 and TH-2 system to communicate and coordinate their function they produce little messenger proteins called cytokines.
"In an autoimmune condition, like Hashimoto's Autoimmune Thyroid, the two sides of the immune teeter-totter get terribly imbalanced..."
It is almost like there is a person on only one side, which if you've ever seen a teeter-totter, you know that this does not work. It is this dysregulation in the immune system, the imbalance between the two systems, that tricks your body into attacking its own tissue.
This "dominance" on one side of the immune system is also why the hormone replacement model as the sole treatment source doesn't always result in patients feeling better, even though lab markers may look normal for a time. (Remember I told you I would get to this)
The cytokines that are produced in the autoimmune attack actually interfere with the thyroid receptor sites from producing normal responses. This means even if you have an adequate amount of thyroid hormone in the blood stream, the hormones won't necessarily bind to your cells and create a normal metabolic response. Which means...you still have thyroid symptoms even with normal levels of hormones circulating in your blood stream.
Normally when a thyroid hormone binds to a cell it causes the cell to increase it's metabolism and this increases the production of certain proteins inside the cell. This is called a "proteomic response." In Hashimoto's the proteomic response is diminished by the inflammatory cytokines that are produced from the autoimmune attack.
So even when the thyroid hormones bind to cell receptors their isn't a very strong proteomic response. This is exactly why the replacement mode only of thyroid management can result in continuing thyroid symptoms.
Most doctors don't acknowledge this concept. They will try to make your lab panels look "normal" with replacement hormones and when you tell them you still have the same symptoms they are going to assume that you are depressed, or that it is "all in your head." Not a lot of credence is paid to how you as the patient feel.. what your everyday experience is.
Or if you are continually gaining weight, without ANY change in diet, they will assume you are just overeating...that you need to exercise.
Here's her website. I wasn't so interested in the promotional stuff but it explained a little better to me why you can have an in range TSH with Hashi's and be really hypo.
http://sacramentothyroiddoctor.com/thyroidreport.html
There are certainly lots of Docs out there ready , like this one, who want to run a gazzilion tests and get you doing all sorts of stuff, I wasn't so interested in that personally. But I thought this explanation was good. You know with receptors being bound up but having lots of T4 making it seem like you're normal but not at all. Good point though....have to look into cytokines. i had never heard of them before.
http://sacramentothyroiddoctor.com/thyroidreport.html
There are certainly lots of Docs out there ready , like this one, who want to run a gazzilion tests and get you doing all sorts of stuff, I wasn't so interested in that personally. But I thought this explanation was good. You know with receptors being bound up but having lots of T4 making it seem like you're normal but not at all. Good point though....have to look into cytokines. i had never heard of them before.
gimel makes an excellent point.
"...you still have thyroid symptoms even with normal levels of hormones circulating in your blood stream." What of those of us with Hashi's who DON'T still have thyroid symptoms? On diagnosis of Hashi's (I'd been diagnosed hypo years before), my TPOab was 900+, and my TGab was greater-than 3000, yet I was euthyroid and asymptomatic. Given Nguyen's theory, how would this be possible?
"...you still have thyroid symptoms even with normal levels of hormones circulating in your blood stream." What of those of us with Hashi's who DON'T still have thyroid symptoms? On diagnosis of Hashi's (I'd been diagnosed hypo years before), my TPOab was 900+, and my TGab was greater-than 3000, yet I was euthyroid and asymptomatic. Given Nguyen's theory, how would this be possible?
In the info you gave, "The cytokines that are produced in the autoimmune attack actually interfere with the thyroid receptor sites from producing normal responses. This means even if you have an adequate amount of thyroid hormone in the blood stream, the hormones won't necessarily bind to your cells and create a normal metabolic response. Which means...you still have thyroid symptoms even with normal levels of hormones circulating in your blood stream. "
I notice that he doesn't define what is an "adequate amount of thyroid hormone", and normal levels of hormone circulating in the blood." I expect his definition would be a test result that is anywhere within the so-called "normal" range. We all know this doesn't work, since the ranges are far too broad. But his explanation for still having symptoms is that the cytokines produced in the autoimmune attack interfere, rather than what we know about insufficient thyroid hormone due to the levels being too low in the so-called "normal" ranges.
So I would have to ask, where is the evidence that the autoimmune attack produces cytokines that "actually interfere with the thyroid receptor sites from producing normal responses"?
And if this were valid, then why do we see the same patient response when a patient having low TSH due to pituitary issues (no autoimmune attack going on), has hypo symptoms because of having low-in-the-range Free T3 and Free T4? Wouldn't be related to cytokines in that case.
I admit being cynical about this, but all this makes me somewhat suspicious that this Doctor has come up with yet another way to try to benefit from the legions of patients with hypothyroidism that are not properly diagnosed and medicated, thus still have hypo symptoms. Is there some statistically valid evidence of the validity of what the doctor is promoting?
I notice that he doesn't define what is an "adequate amount of thyroid hormone", and normal levels of hormone circulating in the blood." I expect his definition would be a test result that is anywhere within the so-called "normal" range. We all know this doesn't work, since the ranges are far too broad. But his explanation for still having symptoms is that the cytokines produced in the autoimmune attack interfere, rather than what we know about insufficient thyroid hormone due to the levels being too low in the so-called "normal" ranges.
So I would have to ask, where is the evidence that the autoimmune attack produces cytokines that "actually interfere with the thyroid receptor sites from producing normal responses"?
And if this were valid, then why do we see the same patient response when a patient having low TSH due to pituitary issues (no autoimmune attack going on), has hypo symptoms because of having low-in-the-range Free T3 and Free T4? Wouldn't be related to cytokines in that case.
I admit being cynical about this, but all this makes me somewhat suspicious that this Doctor has come up with yet another way to try to benefit from the legions of patients with hypothyroidism that are not properly diagnosed and medicated, thus still have hypo symptoms. Is there some statistically valid evidence of the validity of what the doctor is promoting?
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