Let’s Talk About Goiters (cont’d)
06/07/10 18:52
Let’s recap a little—
We know that T-4, or thyroxine, is the “signal” that “tells” the pituitary gland to lower the amount of TSH it is releasing. So, you lower T-4, you increase TSH, and you increase T4 and this results in a decrease of TSH. It’s an inverse relationship between T-4 and TSH. And, it’s the elevated TSH that causes goiter. And, in much simpler terms, if you have enough T-4, you don’t get goiters.
But whether you have enough thyroxine (T-4) or not depends not just on how much iodine you have in the system. More specifically, it depends on how much iodine the thyroid can absorb from the system. That’s where isothiocyanates (and thiocyanates) poke their noses into this system. Both the isothiocyanates and the thiocyanates inhibit iodine uptake by the thyroid, which leads to decreased production of thyroxine.
Now, I’m going to be a little redundant here, but I want you to remember something: The level of T-4, or thyroxine, has an effect on whether or not you get a goiter (it’s actually a persistently high level of TSH that causes goiter, but this is caused by a persistently low level of thyroxine).
So, we can look at thyroxine and say what effects the levels of thyroxine? You’ve already got:
1. Iodine deficiency
2. Interference with the thyroid’s ability to absorb iodine
But just thinking about this logically, without referring to the research, there’s something else that would effect levels of thyroxine, isn’t there? Remember that thyroxine is changed into T-3 (tri-iodothyronine), the active form of the protein. What IF you were changing too much thyroxine too quickly, into tri-iodothyronine? You’d have less thyroxine, wouldn’t you?
Well, guess what happens in the case of zinc deficiency? Yep. Exactly. Here an abstract to peruse, on this topic:
Drug Nutr Interact. 1987;5(2):113-24. Effects of zinc deficiency on thyroid function.
Oliver JW, Sachan DS, Su P, Applehans FM.
Abstract
Interactive combinations of altered zinc and thyroid states were studied in rats to assess pathophysiologic effects. Clinical signs of zinc deficiency or thyroid alteration were limited to effects on growth rate. Changes in organ and glandular weights and serum thyrotropin levels reflected changes in serum thyroid hormone concentrations. Significantly (probability less than .001), zinc-deficient rats had enhanced hepatic thyroxine-5'-monodeiodinase activity. In addition, the zinc-deficient state was found to be protective against thiouracil-induced suppression of the microsomal-monooxygenase and thyroxine-5'-monodeiodinase enzyme complex. This protective effect was evident by greater thyroxine-5'-monodeiodinase and reduced nicotinamide-adenine dinucleotide phosphate cytochrome c reductase activities, as well as cytochrome P-450 content, in zinc-deficient/thiouracil-treated animals. Thus, the enzyme complex had increased triiodothyronine-generating capacity in conditions of zinc deficiency, which may be important because of the greater biological reactivity of triiodothyronine. Primary zinc deficiency conditions of the magnitude seen in this study and in this-age rat did not appear to alter serum thyroid hormone levels or organ/glandular function. However, concurrent zinc deficiency and altered thyroid status did change thyroid hormone response and disposition, which may be important to populations at risk because of thyroid dysfunctional states.
Here are a couple more you might want to look up, on your own:
1. Fujimoto S, Indo Y, Higashi A, et al. Conversion of thyroxine into tri-iodothyronine in zinc deficient rat liver. J Pediatr Gastroenterol Nutr 1986;5:799-805.
2. Hartoma TR, Sotaniemi EA, Maattanen J. Effect of zinc on some biochemical indices of metabolism. Nutr Metab 1979;23:294-300.
Now, keep in mind that I’m not saying that this is exactly what is happening. I don’t know for sure. But I do know that zinc deficiency, in case after case, in research article after research article, lowers thyroxine levels. So, it is not only iodine, or the lack of it, that is linked to the formation of goiters. Zinc plays a large role in that system.
And, in the case of CF, you have MAJOR problems with zinc homeostasis. And, please, PLEASE do NOT go out and buy some zinc supplements and start eating them like candy. The problem is with zinc HOMEOSTASIS. Zinc delivery and the uptake of zinc by various enzymes and proteins is what is screwed up in CF, and if you take too much zinc, you’re only going to exacerbate the problem, not help anything.
Zinc is REQUIRED for maintenance of the proper level of thyroxine. Look it up.
I’m going to end this blog post with yet another apology. I’ve been working on this post and left it on my computer, open, for the last several days, because I could not get back to it. I’ve been traveling, which is a large part of my job.
But I am here, now, for a few days, and I intend to finish up some of my other blog posts, and get them on here. I’ve also answered a couple of comments in the blog, from Francesco and Paul. Please see my answers there.
We know that T-4, or thyroxine, is the “signal” that “tells” the pituitary gland to lower the amount of TSH it is releasing. So, you lower T-4, you increase TSH, and you increase T4 and this results in a decrease of TSH. It’s an inverse relationship between T-4 and TSH. And, it’s the elevated TSH that causes goiter. And, in much simpler terms, if you have enough T-4, you don’t get goiters.
But whether you have enough thyroxine (T-4) or not depends not just on how much iodine you have in the system. More specifically, it depends on how much iodine the thyroid can absorb from the system. That’s where isothiocyanates (and thiocyanates) poke their noses into this system. Both the isothiocyanates and the thiocyanates inhibit iodine uptake by the thyroid, which leads to decreased production of thyroxine.
Now, I’m going to be a little redundant here, but I want you to remember something: The level of T-4, or thyroxine, has an effect on whether or not you get a goiter (it’s actually a persistently high level of TSH that causes goiter, but this is caused by a persistently low level of thyroxine).
So, we can look at thyroxine and say what effects the levels of thyroxine? You’ve already got:
1. Iodine deficiency
2. Interference with the thyroid’s ability to absorb iodine
But just thinking about this logically, without referring to the research, there’s something else that would effect levels of thyroxine, isn’t there? Remember that thyroxine is changed into T-3 (tri-iodothyronine), the active form of the protein. What IF you were changing too much thyroxine too quickly, into tri-iodothyronine? You’d have less thyroxine, wouldn’t you?
Well, guess what happens in the case of zinc deficiency? Yep. Exactly. Here an abstract to peruse, on this topic:
Drug Nutr Interact. 1987;5(2):113-24. Effects of zinc deficiency on thyroid function.
Oliver JW, Sachan DS, Su P, Applehans FM.
Abstract
Interactive combinations of altered zinc and thyroid states were studied in rats to assess pathophysiologic effects. Clinical signs of zinc deficiency or thyroid alteration were limited to effects on growth rate. Changes in organ and glandular weights and serum thyrotropin levels reflected changes in serum thyroid hormone concentrations. Significantly (probability less than .001), zinc-deficient rats had enhanced hepatic thyroxine-5'-monodeiodinase activity. In addition, the zinc-deficient state was found to be protective against thiouracil-induced suppression of the microsomal-monooxygenase and thyroxine-5'-monodeiodinase enzyme complex. This protective effect was evident by greater thyroxine-5'-monodeiodinase and reduced nicotinamide-adenine dinucleotide phosphate cytochrome c reductase activities, as well as cytochrome P-450 content, in zinc-deficient/thiouracil-treated animals. Thus, the enzyme complex had increased triiodothyronine-generating capacity in conditions of zinc deficiency, which may be important because of the greater biological reactivity of triiodothyronine. Primary zinc deficiency conditions of the magnitude seen in this study and in this-age rat did not appear to alter serum thyroid hormone levels or organ/glandular function. However, concurrent zinc deficiency and altered thyroid status did change thyroid hormone response and disposition, which may be important to populations at risk because of thyroid dysfunctional states.
Here are a couple more you might want to look up, on your own:
1. Fujimoto S, Indo Y, Higashi A, et al. Conversion of thyroxine into tri-iodothyronine in zinc deficient rat liver. J Pediatr Gastroenterol Nutr 1986;5:799-805.
2. Hartoma TR, Sotaniemi EA, Maattanen J. Effect of zinc on some biochemical indices of metabolism. Nutr Metab 1979;23:294-300.
Now, keep in mind that I’m not saying that this is exactly what is happening. I don’t know for sure. But I do know that zinc deficiency, in case after case, in research article after research article, lowers thyroxine levels. So, it is not only iodine, or the lack of it, that is linked to the formation of goiters. Zinc plays a large role in that system.
And, in the case of CF, you have MAJOR problems with zinc homeostasis. And, please, PLEASE do NOT go out and buy some zinc supplements and start eating them like candy. The problem is with zinc HOMEOSTASIS. Zinc delivery and the uptake of zinc by various enzymes and proteins is what is screwed up in CF, and if you take too much zinc, you’re only going to exacerbate the problem, not help anything.
Zinc is REQUIRED for maintenance of the proper level of thyroxine. Look it up.
I’m going to end this blog post with yet another apology. I’ve been working on this post and left it on my computer, open, for the last several days, because I could not get back to it. I’ve been traveling, which is a large part of my job.
But I am here, now, for a few days, and I intend to finish up some of my other blog posts, and get them on here. I’ve also answered a couple of comments in the blog, from Francesco and Paul. Please see my answers there.