How can iodine decrease the vascularity of thyroid gland?

[scilearner]

Hi,

If you give high doses of iodine thyroid hormone synthesis decreases. This means TSH level must increase. TSH function is to cause hyperplasia of the gland and increase vascularity of the gland. So how can iodine decrease vasculariy, when TSH is there to counter it. Thanks

[CharonY]

I think you got the effect of TSH wrong. As its name (thyroid stimulating hormone) implies, it induces production of thyroid hormones. However the hormones themselves inhibit TSH production and thus limit their own production. Hyperplasia happens if regulation is disrupted.

[scilearner]

Thanks for the reply CharonY, but I still don't understand where I went wrong. I understand the feedback system

 

1) I know iodine is needed for thyroxine production, but according to "wolf-chaikoff" effect, iodine in high doses actually deplete the production of thyroxine

2) This means we give high doses of iodine, free T4 would decrease, this mean due to feedback TSH would increase.

3) Now high TSH increases the vascularity of the gland. But high iodine concentration is given before thyroid surgery to decrease vascularity of the gland. Now how can high iodine do that in presence of high TSH?

 

I get the feeling you know all this, and I may have misunderstood what you are saying. So please explain again where I went wrong. Thanks

Edited May 26, 2013 by scilearner

[CharonY]

OK in order to explain that one has to be careful from which viewpoint you start the discussion. As such we cannot e.g. state that the role of TSH is to cause hyperplasia, for example. Its production is altered involved, but only under extreme conditions.

So again the baseline is the regulation of T3/T4 via inhibitions of TSH. So normally higher iodine concentration would tend to increase baseline T3/T4 up to the point where the levels of their level would inhibit further production.

The Wolf-Chaikoff again is a phenomenon happening under conditions when the regulatory system is overloaded but involves a different regulatory circuit. While the circuit itself affects TSH and T3/4 levels, the mechanisms are independent.

In fact, the mechanisms have not been completely elucidated. What is known is that organification of iodide is inhibited at this point it depends on how high the actualy thyroid hormone levels are how TSH is getting affected, how long the inhibition is maintained. Often Wolf-Chaikoff can continue for up to a few days, before the escape mechanism kicks in (basically reduction in iodine uptake due to inhibition of transporters). During this time thyroid hormone levels may become depleted and then TSH rises. If the effect is shorter it may not happen (but usually a short inhibition would not be noticed clinically, anyway).

 

Now finally to the point of vascularity. The link between TSH, and iodide treatment to vascularity are much more vague than the OP indicates. I.e. it is not a straightforwarded regulatory control or link between these items. In fact there are studies indicating that iodide treatment has little to no effect on vascularity on Grave's disease patients, whereas other found them to be beneficial, for example. Likewise (at least to my knowledge) it has not been shown with absolute certainty whether TSH or actually TSH receptor antibodies are responsible for changes in vascularity.

Finally you have to remember that in cases when iodide therapy is indicated, parts of the usual regulatory control is messed up (which actually leads to e.g. hyperthyroidism). So again using the example of Grave, here we have a case where T3/4 are high, TSH is low whereas TSH receptor as well as antibodies against these receptors are elevated (the primary cause of the condition).

 

I.e. the assumptions in OP are too simplified to explain occurrences (which are not terribly well understood, unless there is some very current literature that I may have not seen).

[EdEarl]

Is there any indication that eating either angeogenic or antiangeogenic foods affect vascularity of the gland, and if so what are the affects?

Edited May 27, 2013 by EdEarl

[scilearner]

Thanks CharonY again I think I got it this time, tell me if I misunderstood again.

 

1) Ok so I give iodine, T4 production increases'

2) I give lots of iodine, lots of T4 produced.

3) This increase in T4, leads to feedback control and low level of TSH

4) Now less TSH mean less proliferation and less vascularity--- purpose served

5) Mean time high iodinee also inhibits organification of idoine, which is not related to the feedback system, but another protective measure

 

I know it is not clear cut like this, but for basic understanding is this right

 

My question then is if iodine is given before surgery to decrease vascularity and the way iodine does that is by increasing production of thyroxine, isn't that bad for patient who has hyperthyroidism wouldn't it exacerbate the symptoms. If u have hypothyroidism this seems like a good methods. But as CharonY mentioned it makes me think since so many thyroid disorders mess up the feedback system, why is iodine given at all before surgery to reduce vascularity, it might have no effect at all. Also how long does it take for iodine to produce high levels of thyroxine to decrease TSH?

Edited May 27, 2013 by scilearner