pattismith
Senior Member
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ME/CFS patients should pay attention to everything that can disrupt their thyroid hormons.
Some of my symptoms were worse with antibiotics (metronidazole, doxycycline, azithromcine, clarythromycine), and I thought for sometime that it was related to mitochondrial toxicity, or even to microbiome toxicity....
I finally tested for a full thyroid panel and discovered I had a Low T3 syndrome.
I started to supplement with T3 and I improved quickly for Head pressure/muscle burning and pain and weakness and walking difficulties.
I realized that the side effects I had from these ATB was related to my Low T3 syndrome, which means that they all had a worsening effect on my syndrome.
I only found a confirmation that Macrolides can do such a thing in the article below, but Tetra are also known to have some thyroid impact.
@heapsreal
"Drug Effects
A large number of drugs is known to influence thyroid function interfering with various mechanisms of thyroid hormone metabolism (363).
Lithium and aminoglutethimide decrease thyroid hormone secretion.
A high iodine load, as it ensues from amiodarone and/or radiocontrast dye application, decreases both central and peripheral deiodinases activity (364–368).
In addition to causing hypodeiodination, amiodarone has antagonistic actions on T3 signaling, presumably due to its molecular similarity to thyroid hormones (369, 370).
Dopamine, glucocorticoids, and somatostatin analogs suppress TSH release (371).
Thyroxine absorption is altered by multiple substances including caffeine, bile acid sequestrants, sucralfate, ferrous sulfate, and aluminum hydroxide (372). This results in disruption of the enterohepatic circulation of thyroid hormones, thus contributing to reduced half-life.
Moreover, many drugs alter thyroxine and triiodothyronine transport in serum such as estrogens, tamoxifen, heroin, methadone, mitotane, androgens, anabolic steroids, furosemide, NSAIDs, and salicylates by either increasing or decreasing TBG concentration or displacing them from protein-binding sites (363, 373).
Antiepileptic drugs such as phenobarbital, phenytoin, and carbamazepine increase hepatic metabolism of thyroxine and triiodothyronine.
In addition to amiodarone propylthiouracil, macrolides, and unselective beta-adrenergic blockers inhibit the activity of type 1 deiodinase (374), while sorafenib is able to increase D3 activity (375)."
Some of my symptoms were worse with antibiotics (metronidazole, doxycycline, azithromcine, clarythromycine), and I thought for sometime that it was related to mitochondrial toxicity, or even to microbiome toxicity....
I finally tested for a full thyroid panel and discovered I had a Low T3 syndrome.
I started to supplement with T3 and I improved quickly for Head pressure/muscle burning and pain and weakness and walking difficulties.
I realized that the side effects I had from these ATB was related to my Low T3 syndrome, which means that they all had a worsening effect on my syndrome.
I only found a confirmation that Macrolides can do such a thing in the article below, but Tetra are also known to have some thyroid impact.
@heapsreal
"Drug Effects
A large number of drugs is known to influence thyroid function interfering with various mechanisms of thyroid hormone metabolism (363).
Lithium and aminoglutethimide decrease thyroid hormone secretion.
A high iodine load, as it ensues from amiodarone and/or radiocontrast dye application, decreases both central and peripheral deiodinases activity (364–368).
In addition to causing hypodeiodination, amiodarone has antagonistic actions on T3 signaling, presumably due to its molecular similarity to thyroid hormones (369, 370).
Dopamine, glucocorticoids, and somatostatin analogs suppress TSH release (371).
Thyroxine absorption is altered by multiple substances including caffeine, bile acid sequestrants, sucralfate, ferrous sulfate, and aluminum hydroxide (372). This results in disruption of the enterohepatic circulation of thyroid hormones, thus contributing to reduced half-life.
Moreover, many drugs alter thyroxine and triiodothyronine transport in serum such as estrogens, tamoxifen, heroin, methadone, mitotane, androgens, anabolic steroids, furosemide, NSAIDs, and salicylates by either increasing or decreasing TBG concentration or displacing them from protein-binding sites (363, 373).
Antiepileptic drugs such as phenobarbital, phenytoin, and carbamazepine increase hepatic metabolism of thyroxine and triiodothyronine.
In addition to amiodarone propylthiouracil, macrolides, and unselective beta-adrenergic blockers inhibit the activity of type 1 deiodinase (374), while sorafenib is able to increase D3 activity (375)."