[Ski]

#1075060

One note to kimmie: NO, we do not all have TSH levels in the .001 range any more. Only hyperthyroid patients have TSH levels that low (well, and perhaps with some other conditions there may be a measurement like this, but let’s stick with the Graves’ patients for clarity’s sake right now…).

Once we go hypothyroid, our TSH rises (it has an inverse relationship with our thyroid hormone levels). When we are on replacement hormone (or effectively managed on ATDs), our TSH levels should be inside the normal range, hopefully at OUR normal point.

We’ve all HAD TSH levels in the .001 range, but we are treated specifically to correct that.

[kimmie]

#1075061

I cannot thank the people on this site enough. What clear, easily understood answers you’ve given me. Doctorspeak is so much harder to understand and retain. Again, thanks to all for your help, and bless this site.

[DianneW]

#1075062

Regarding a low TSH with normal thyroid levels:

Scientists in the Netherlands (Brokken,Wiersinga, & Prummel) discovered that in Graves’ Disease, TBII antibodies suppress TSH secretion independently of thyroid levels, even when thyroid levels have returned to normal. Furthermore, they found that patients who are positive for TBII antibodies have a lower TSH following treatment for similar Free T3 and Free T4 levels than do patients with negative TBII levels, and that the TSH correlated only with TBII titres and not with Free T3 or Free T4 levels.

Many doctors aren’t aware of this. For this reason it’s important for patients to be seen by an endocrinologist who is familiar with the latest research. The bottom line is that for patients with Graves’ Disease, the TSH isn’t always a reliable indicator of thyroid hormone status.

Of possible interest to RAI patients: a recent study has shown that RAI causes thyroid stimulating antibodies (including TBII) to elevate, and that they remain slightly elevated even five years following treatment. In comparison, the antibody levels of patients who had surgery or were treated with antithyroid drugs usually return to normal. There are several possible implications of this. One is a possible explanation for why the eye disease develops or worsens temporarily in some RAI patients. Another is that TSH levels in some RAI patients might be lower than they should be long after treatment, leading to a possibility of slightly inadequate thyroid replacement; a possible explanation for why some patients still feel hypo with a normal TSH?

About Armour thyroid and T3 supplementation:

Many patients on thyroid replacement hormone still have some of their own thyroid still functioning and therefore are still receiving adequate T3. Most of the studies that have been done recently have concluded that patients don’t need T3 supplementation, but so far none of these studies have been done exclusively on patients who have virtually no thyroid tissue remaining. I’d like to see if the results of the studies change if they separate the patient groups. I hope future studies do this, and make another important change. In the studies done so far, T3 was given once a day, which will give the patient too much T3 initially and the patient will run out the rest of the day (Bobbi explained the half life of T3 in an earlier post). Until time-release technology for T3 can be perfected, T3 studies should be done with split-dose therapy, giving the T3 three times per day. That’s the easiest way to keep T3 levels constant in the serum (blood).

I take Armour thyroid, and split it into three daily doses. Since it’s difficult enough to remember one pill daily, I have to put it in a pill box that has room for three daily pills, or I’d never remember for certain if I took each dose or not. It’s very difficult to find a time during each day to separate pill times from meals that might inhibit absorption, but I do my best.

My thyroid is pretty much gone. How does one know? It’s difficult. One way to tell is by how much thyroid replacement you’re taking, but that too can vary from person to person. Still, I have a friend who thinks she has no thyroid left but she’s only on 50 mcg Synthroid, so I know she’s wrong about that. I’m taking the equivalent of 225 mcg Synthroid, and she and I are about the same size. I’m 5’7" and about 135. My guess is that unless a person is on at least 175-200 mcg of T4, a reasonable amount of thyroid remains and is functioning still.

Recent studies have shown that most people on thyroid replacement have normal T3 levels on T4 supplementation alone. I’m one who didn’t, even though my Free T4 was above normal, and being on Armour made a world of difference in how I felt. It’s a good idea to make certain your T3 levels really need supplementation before you worry about getting it done, mainly because the risks of too much T3 all at once are real. Taking T3 in a pill doesn’t allow it to be distributed gradually the way your own thyroid can do. It’s different with T4, which has a long half-life and can be stored in the organs for a week or so and used as needed. One study was done showing that while not ideal, it’s even possible to give patients T4 replacement all in a weekly dose.

In my opinion, the fact that replacing T4 and T3 in a pill can’t be done in the same manner our healthy thyroid was able to do is central to the question that was originally being discussed in this thread. It’s not just that doctors can’t replace the substances that a healthy thyroid used to produce, because they can. The trouble is, they can’t replace it in the same manner, or when it’s needed, or in an amount that our body knows is correct for us. Once our thyroid is gone, we’re at the mercy of whatever TSH number our particular endocrinologist decides is his favorite number, regardless of what our body used to find optimum. At that, it will be a number that can’t change for changing conditions. So while I’m thankful we have the treatments we do have, I don’t think that the idea of destroying a thyroid "because hypothyroidism is easily treatable" is something that should be done lightly, as if taking this T4 pill was exactly the same thing as our thyroid gland.

Yes, we can be for the most part healthy again, but scores of hypothyroid patients have ongoing symptoms, for which the cause hasn’t been determined. Unless a better answer is found, some aspect of the inadequacy of replacement hormone has to remain the major suspect. Researchers are still debating all these issues. Many have hard set opinions one way or another. A prominent thyroid researcher actually told me the reason I felt better on T3 because it was like taking speed. That answer left me speechless! How does bringing my T3 into normal ranges become taking speed when his thyroid producing T3 is not? I could understand that view if I was raising my T3 above normal, but I fail to see the problem with wanting to have a normal level and feel like myself again!

The bottom line is that all the current studies show there is no role for T3 supplementation, so most endos are moving away from this. Current thought is that most people will have a normal Free T3 level if their Free T4 level is brought high enough, and that it’s acceptable for it to be brought slightly above normal if necessary to bring Free T3 high enough as long as the TSH doesn’t go too low. This is considered safer for the patient than risking spikes of T3 that are way too high, with once-daily doses of T3 supplementation, which can be dangerous for the heart.

T1 and T2 are produced when iodine molecules are removed from T3, and as such if the body had use for them, they’d still be available with T4 supplementation. As I understand it, most researchers believe there is no use for them.

Bobbi has discussed Calcitonin, but I’d like to add a few things:

Its actions are to work against parathyroid hormone to:

1) Regulate bone mineral metabolism (protection against calcium loss). It is currently used as a treatment for osteoporosis.

2) Regulate serum (blood) calcium level

3) Act as a satiety hormone: May have CNS (central nervous system) action involving the regulation of feeding and appetite

Still, the way calcitonin works in the human body is much less well-understood than is the way it works in animals, and we seem to do well without it.

My personal view is that there’s a reason for everything (it wasn’t that long ago when doctors believed the tonsils weren’t needed). The miraculous way our bodies function has no substitute.

For all these reasons, I really think it’s reasonable for people who want to try antithyroid drug therapy to give that a go before doing something more permanent, as long as there isn’t a medical reason not to. It seems that an overwhelming number of doctors in the US now are convinced that RAI is the way to go, and they steer people in that direction many times without giving much serious consideration to other options. Reasons I hear for that include the justification that many Graves’ patients will become hypothyroid eventually anyway, but becoming hypothyroid is a lot different than destroying an entire gland. More importantly, many patients will NOT become hypothyroid, and will live their lives with normal thyroid function. Others will live many more years before relapsing.

Maybe some doctors don’t want to take the time to explain to their patients the implications of all the treatment choices. That makes it easier to recommend RAI to all patients. There’s no question that some patients might have a difficult time with compliance with antithyroid drugs, and that not only might be dangerous, but won’t give the desired results.

I think an important function of the Graves’ Disease Foundation is to help people learn about ALL the options, and to know the entire range of implications contained in those options. We all have different wants, needs, and plans going on, and not all of us are in the same life stage. I love it that we can learn from what others have actually experienced, and not have to rely only on the particular prejudice of the endo we happened to be referred to. (I guarantee you that even they disagree on these issues a lot.) So in most cases it’s fine to make up our own minds about treatment issues and then find a doctor who will support that.

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