Goiters AGAIN?
09/08/10 20:02
Even those of you who mentioned goiters are probably sick of this topic by now, but it’s still not complete.
I’ll recap a little here and boil it down to just a couple of things:
1. Higher levels of TSH make your thyroid swell and this is a goiter.
2. Levels of TSH go down when there are high enough levels of T4 (thyroxine).
Now, when we see that abstract on those CF kids who took iodine therapy for goiters, we see that those who took the iodine therapy developed goiters and those that didn’t take the therapy, didn’t develop goiters, right? Can we say that iodine causes goiters in CF patients? Or is it more likely that there is a relationship between zinc levels and iodine levels that affects the levels of thyroxine?
The latter is probably the case here. If it were simply a problem with a lack of iodine, you would not see goiters in those CF patients that got the iodine therapy [in the abstract, below] and if there were not a relationship between zinc and iodine, in terms of goiters, you would not see the kids NOT having the iodine therapy NOT developing the goiters.
But there is something else here, too—there is a relationship between zinc, selenium, iodine, and manganese—a balance that, if perturbed, will affect thyroid function in a very fundamental way. And, if you have an imbalance in ALL of them, and you add one of those components, such as iodine, you’ve not solved the imbalance, and you might have exacerbated it to the point where you actually have a pathology (goiter). It is like the B vitamins, where if you have a low amount of two and you supplement one of them, the one that you didn’t supplement is more out of whack than ever.
Now, I’m not saying that BITC or any other isothiocyanate won’t interfere with thyroid hormone levels. I don’t study the thyroid. I don’t intend to. And although I’ve got one person who used this compound who had high TSH levels, and they went down to normal, that one person isn’t enough to make a case for BITC’s ability (or rather, it’s induction of the expression of a functionally redundant protein to the CFTR) to restore that balance.
And if you know that you have a perturbation of the homeostasis in ALL of these compounds, what do you do? Do you try to guess at the amount you should supplement each one? And, what if supplementation doesn’t help? What if homeostasis is determined by the DELIVERY or the CHELATION (opposite of delivery—it means the pick up, or taking away) of one of these elements to an enzyme, or an expression factor, and not simply by levels in the serum? Wouldn’t you think you would fare better, overall, by restoring that SYSTEM of homeostasis, instead of a single element in it?
Volume 79, Issue 4, Pages 684-687 (October 1971)
Complications of iodide therapy in patients with cystic fibrosis**
William L. Nyhan (Editor), Harry C. Shirkey (Consultant), M.D. Thomas F. Dolan Jr., M.D. Lewis E. Gibson
Forty-seven of 55 patients receiving long-term daily iodile therapy as part of the therapeutic regimen for cystic fibrosis of the pancreas developed goiters. Goiters usually appeared 2 to 3 years after onset of therapy, with a range of 3 months to 12 years. Fourteen patients receiving iodides had laboratory or clinical evidence of hypothyroidism; 2 of these 14 did not have a goiter. No goiters were observed among 55 patients with cystic fibrosis not receiving iodides. Fourteen of 55 children receiving iodide therapy developed nasal polyposis whereas no polyps were seen in 40 patients not receiving iodide. This may be due to the age distribution of patients studied, since most children in the 5 to 15 year age range received iodide therapy.
I’ll recap a little here and boil it down to just a couple of things:
1. Higher levels of TSH make your thyroid swell and this is a goiter.
2. Levels of TSH go down when there are high enough levels of T4 (thyroxine).
Now, when we see that abstract on those CF kids who took iodine therapy for goiters, we see that those who took the iodine therapy developed goiters and those that didn’t take the therapy, didn’t develop goiters, right? Can we say that iodine causes goiters in CF patients? Or is it more likely that there is a relationship between zinc levels and iodine levels that affects the levels of thyroxine?
The latter is probably the case here. If it were simply a problem with a lack of iodine, you would not see goiters in those CF patients that got the iodine therapy [in the abstract, below] and if there were not a relationship between zinc and iodine, in terms of goiters, you would not see the kids NOT having the iodine therapy NOT developing the goiters.
But there is something else here, too—there is a relationship between zinc, selenium, iodine, and manganese—a balance that, if perturbed, will affect thyroid function in a very fundamental way. And, if you have an imbalance in ALL of them, and you add one of those components, such as iodine, you’ve not solved the imbalance, and you might have exacerbated it to the point where you actually have a pathology (goiter). It is like the B vitamins, where if you have a low amount of two and you supplement one of them, the one that you didn’t supplement is more out of whack than ever.
Now, I’m not saying that BITC or any other isothiocyanate won’t interfere with thyroid hormone levels. I don’t study the thyroid. I don’t intend to. And although I’ve got one person who used this compound who had high TSH levels, and they went down to normal, that one person isn’t enough to make a case for BITC’s ability (or rather, it’s induction of the expression of a functionally redundant protein to the CFTR) to restore that balance.
And if you know that you have a perturbation of the homeostasis in ALL of these compounds, what do you do? Do you try to guess at the amount you should supplement each one? And, what if supplementation doesn’t help? What if homeostasis is determined by the DELIVERY or the CHELATION (opposite of delivery—it means the pick up, or taking away) of one of these elements to an enzyme, or an expression factor, and not simply by levels in the serum? Wouldn’t you think you would fare better, overall, by restoring that SYSTEM of homeostasis, instead of a single element in it?
Volume 79, Issue 4, Pages 684-687 (October 1971)
Complications of iodide therapy in patients with cystic fibrosis**
William L. Nyhan (Editor), Harry C. Shirkey (Consultant), M.D. Thomas F. Dolan Jr., M.D. Lewis E. Gibson
Forty-seven of 55 patients receiving long-term daily iodile therapy as part of the therapeutic regimen for cystic fibrosis of the pancreas developed goiters. Goiters usually appeared 2 to 3 years after onset of therapy, with a range of 3 months to 12 years. Fourteen patients receiving iodides had laboratory or clinical evidence of hypothyroidism; 2 of these 14 did not have a goiter. No goiters were observed among 55 patients with cystic fibrosis not receiving iodides. Fourteen of 55 children receiving iodide therapy developed nasal polyposis whereas no polyps were seen in 40 patients not receiving iodide. This may be due to the age distribution of patients studied, since most children in the 5 to 15 year age range received iodide therapy.