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Just thinking about this subject this morning. And people can think what they want regarding the connection with thyroid (sluggish) and depression and anxiety , but in the years when I was struggling with 10 yrs of depression and my "gut" was telling me it was thyroid but the doc's numbers ruled.
I did not have a home computer so I could not go on line to seek info for myself. I depended totally on the doctors. Today everyone has computers and we can do so much work for ourselves.
Thinking now, there are MANY companies who produce thyroid support products and one I've talked to when my med was in short temporary supply was Nutri Med...they have consultants for their adrenal and thyroid products.
Anyway, keep thinking about solutions..
Last edited by jaminhealth; 02-19-2018 at 11:04 AM..
True, those are causes. But I doubt they are the only cause. There's a part of your quote that echos my main point. High rT3 results in "sick euthyroid syndrome". Meaning that the rest of the thyroid panel can look normal (euthyroid), but the patients can still exhibit symptoms of hypothyroidism, hence "sick euthyroid", which is pretty much a misnomer. rT3 competitively inhibits thyroid receptor activation. Thus, I believe it is foolish to not test rT3 in light of this.
No, just the opposite. "Sick euthyroid" patients have abnormal thyroid function studies but no clinical symptoms of thyroid disease.
"Euthyroid sick syndrome is low serum levels of thyroid hormones in clinically euthyroid patients with nonthyroidal systemic illness. Diagnosis is based on excluding hypothyroidism. Treatment is of the underlying illness; thyroid hormone replacement is not indicated."
It's not directly relevant, but it's relevant because we don't know how receptors work on a fundamental level. There is a glaring possibility that these "resistance" syndromes are a receptor problem, not a problem with the level of circulating hormones. What does a thyroid panel tell us about the functioning of the receptor? Next to zero, for now.
How receptors work is known at the molecular level. Could there be a receptor problem? Sure, but that is not what is going on with 99.9999% of hypothyroidism.
Last edited by suzy_q2010; 02-19-2018 at 12:42 PM..
"Euthyroid sick syndrome is low serum levels of thyroid hormones in clinically euthyroid patients with nonthyroidal systemic illness. Diagnosis is based on excluding hypothyroidism. Treatment is of the underlying illness; thyroid hormone replacement is not indicated."
And I learned a lot from those links, thanks for that!
Quote:
Originally Posted by suzy_q2010
How receptors work is known at the molecular level. Could there be a receptor problem? Sure, but that is not what is going on with 99.9999% of hypothyroidism.
I still disagree with the notion that we truly know how receptors work. But I do agree with your notion (or the notion of your cites) that hypothyroidism is more of a symptom of something greater.
Still, I think that rT3 needs to be tested in virtually all cases. It inhibits thyroid function, and can point to other causes of illness. Do you agree with that? Also, any idea why they don't test for it?
And I learned a lot from those links, thanks for that!
You're welcome.
Quote:
I still disagree with the notion that we truly know how receptors work. But I do agree with your notion (or the notion of your cites) that hypothyroidism is more of a symptom of something greater.
Still, I think that rT3 needs to be tested in virtually all cases. It inhibits thyroid function, and can point to other causes of illness. Do you agree with that? Also, any idea why they don't test for it?
But rT3 does not inhibit thyroid function.
How receptors work is well understood. In fact, what we know about receptors would make it unlikely that T3 and rT3 could bind to the same receptor, because the physical shape of the molecules is different.
As the links I gave you showed, rT3 is tested for in the context of conditions that can cause it to be elevated, such as euthyroid sick syndrome. Elevations are not indicative of actual thyroid disease.
How receptors work is well understood. In fact, what we know about receptors would make it unlikely that T3 and rT3 could bind to the same receptor, because the physical shape of the molecules is different.
As the links I gave you showed, rT3 is tested for in the context of conditions that can cause it to be elevated, such as euthyroid sick syndrome. Elevations are not indicative of actual thyroid disease.
I see what you're saying. So what does rT3 do? I couldn't find definite proof that rT3 is either inhibitive, inactive, or active. But it appears at least inactive. Could it be a reduction of metabolism (thyroid action) via elimination of T4? rT3 appears to be hypometabolic. It also appears that the causes of euthyroid sick syndrome are highly stressful events (burns, infection, liver problems).
So if rT3 is correlated with stressful events, wouldn't it be a good indicator of non-thyroid-related problems being the root cause of depression?
Boy, just glad the D.O. back when he put me on a theraputic dose of Armour didn't try to tell me all the "scientific" stuff in the last couple postings. What he did, worked for me and got rid of the depression. This was T3/T4.
I see what you're saying. So what does rT3 do? I couldn't find definite proof that rT3 is either inhibitive, inactive, or active. But it appears at least inactive. Could it be a reduction of metabolism (thyroid action) via elimination of T4? rT3 appears to be hypometabolic. It also appears that the causes of euthyroid sick syndrome are highly stressful events (burns, infection, liver problems).
So if rT3 is correlated with stressful events, wouldn't it be a good indicator of non-thyroid-related problems being the root cause of depression?
"There is no credible scientific evidence that rT3 enters the nucleus of the cell at all, and the bulk of the scientific literature states clearly that rT3 does not bind to, and has no known transcriptional activity at, the thyroid receptor. It is, however, known to have potent activity in the cytoplasm as an initiator of actin polymerization in astrocytes in the brain [7]. This is mediated in a non-genomic manner by its binding to a very specific thyroid receptor that exists only in the extranuclear compartment. Actin polymerization is important to cell structure and motility, and particularly important to normal brain development."
So it does have an effect in certain brain cells.
Keep in mind that with the euthyroid sick syndrome, the thyroid numbers are affected but there are no symptoms of hypothyroidism. If the underlying illness gets better, so do the thyroid numbers. It is not necessary to use any thyroid medication at all.
"There is no credible scientific evidence that rT3 enters the nucleus of the cell at all, and the bulk of the scientific literature states clearly that rT3 does not bind to, and has no known transcriptional activity at, the thyroid receptor. It is, however, known to have potent activity in the cytoplasm as an initiator of actin polymerization in astrocytes in the brain [7]. This is mediated in a non-genomic manner by its binding to a very specific thyroid receptor that exists only in the extranuclear compartment. Actin polymerization is important to cell structure and motility, and particularly important to normal brain development."
So it does have an effect in certain brain cells.
Keep in mind that with the euthyroid sick syndrome, the thyroid numbers are affected but there are no symptoms of hypothyroidism. If the underlying illness gets better, so do the thyroid numbers. It is not necessary to use any thyroid medication at all.
I saw that. So yes, technically rT3 does not enter the nucleus of the cell to activate the main thyroid receptor that regulates gene transcription, but it still does have a receptor.
But his original question (and mine) was, does rT3 really slow metabolism? Actually, there's still moderate evidence that exogenous rT3 has a hypometabolic effect.
Boy, just glad the D.O. back when he put me on a theraputic dose of Armour didn't try to tell me all the "scientific" stuff in the last couple postings. What he did, worked for me and got rid of the depression. This was T3/T4.
That's what I need! I can't figure it out myself. I've been doing okay for the last twenty years. I changed to a mail order pharmacy and the generic levothyroxine is not having the same effect. I finally got a thyroid test but not before my doctor offered me Prozac. I feel like she really dropped the ball and I know longer have faith in her.
Should I have asked for the test? Yes. Should I have had to ask? No. We have both got complacent.
I had forgotten how bad being under medicated feels.
That's what I need! I can't figure it out myself. I've been doing okay for the last twenty years. I changed to a mail order pharmacy and the generic levothyroxine is not having the same effect. I finally got a thyroid test but not before my doctor offered me Prozac. I feel like she really dropped the ball and I know longer have faith in her.
Should I have asked for the test? Yes. Should I have had to ask? No. We have both got complacent.
I had forgotten how bad being under medicated feels.
I was SO SO fortunate to have this D.O. in my life as he took care of my back for years..never thought to ask him about the thyroid, which I saw the "experts" who did squat but give me A/D drugs. To get it "right" it seems today to find a conventional MD who works with ALL thyroid supports or an N.D. or Integrative MD...conventional MD's as a whole go with levo family etc. My thinking is they are brainwashed by the manufacturer, I've read plenty on that issue as I've been on thyroid support groups.
As I said maybe a little earlier here, a friend switched to Kaiser and they took her off her long time thyroid med that was working good for years...now she is full of anxiety and depression.
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