drob31
Senior Member
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- 1,487
I've been doing a little research because I wanted to find the mechanism behind the water retention for when your cells aren't getting adequate t3.
This could be because you have low t3, or because of sick euthyroid syndrome, where you have enough serum free t3, but your receptors are resistant. This is usually because of high cortisol. We know low cortisol can cause hypothyroidism because cortisol is required for the t3 to enter the cell. There are allot of possible reasons for this, but I'm not focusing on this here. We're assuming the actual water retention itself is mediated by either high aldosterone/cortisol or hypothyroid (celluar thyroid resistance due to high cortisol, with normal free t3).
Judging by the renin-angiotensin system ( http://upload.wikimedia.org/wikiped...24px-Renin-angiotensin-aldosterone_system.png ), I could see two places where it could be mitigated, either at the step where ACE converts Angiotensin I to Angiotensin II. I think that would call for an ACE inhibitor.
Also I noticed if it was strictly caused by ADH, it could be mitigated with a vasopressin antagonist.
This would be treating a symptom instead of the root cause, but it would be interesting to find out if using one of these would work. It would prove the hypothesis correct.
"...hypothyroidism causes a reversible increase in vasopressin (antidiuretic hormone or ADH) sensitivity of the collecting ducts, thus increasing free water reabsorption. The increased fluid retention, however, is unable to maximally suppress ADH in hypothyroidism.[45] The resistance of pituitary response to increased fluid retention leads to continued ADH activity and further free water retention."
My doc is on board with letting me start with an ACEi to test this hypothesis.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3313737/
Also, thyroid receptor resistance:
http://www.ncbi.nlm.nih.gov/pubmed/2574767
This could be because you have low t3, or because of sick euthyroid syndrome, where you have enough serum free t3, but your receptors are resistant. This is usually because of high cortisol. We know low cortisol can cause hypothyroidism because cortisol is required for the t3 to enter the cell. There are allot of possible reasons for this, but I'm not focusing on this here. We're assuming the actual water retention itself is mediated by either high aldosterone/cortisol or hypothyroid (celluar thyroid resistance due to high cortisol, with normal free t3).
Judging by the renin-angiotensin system ( http://upload.wikimedia.org/wikiped...24px-Renin-angiotensin-aldosterone_system.png ), I could see two places where it could be mitigated, either at the step where ACE converts Angiotensin I to Angiotensin II. I think that would call for an ACE inhibitor.
Also I noticed if it was strictly caused by ADH, it could be mitigated with a vasopressin antagonist.
This would be treating a symptom instead of the root cause, but it would be interesting to find out if using one of these would work. It would prove the hypothesis correct.
"...hypothyroidism causes a reversible increase in vasopressin (antidiuretic hormone or ADH) sensitivity of the collecting ducts, thus increasing free water reabsorption. The increased fluid retention, however, is unable to maximally suppress ADH in hypothyroidism.[45] The resistance of pituitary response to increased fluid retention leads to continued ADH activity and further free water retention."
My doc is on board with letting me start with an ACEi to test this hypothesis.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3313737/
Also, thyroid receptor resistance:
http://www.ncbi.nlm.nih.gov/pubmed/2574767
