Sunday, June 27, 2010

Low T3 Level: An Indication for Treatment? (revisited)

Three years ago I posted this and today I ran into it again and found that someone had actually responded to it.  Even though I haven't posted a response to the comment, I am going to post the whole thing here today. 

In the past three years my dealing with T3 has changed a lot.

Consultations & Comments
Reader Reaction and Timely answers from Experts 

Low T3 Level: An Indication for Treatment?

http://www.consultantlive.com/display/article/10162/37329


June 1, 2007


I am an adult psychiatric nurse practitioner, and a significant part of my practice has been the treatment of subclinical hypothyroidism. Whenever a patient has depression and low energy, I measure free T4, free T3, and thyroid-stimulating hormone (TSH) levels. In most of the subclinical hypothyroidism I have detected, the TSH level is normal. In many cases, the only level that is low is the free T3. When liothyronine is prescribed for these patients, their symptoms of depression and tiredness decrease and their need for antidepressants has, in a few cases, been eliminated.
My goal is to get patients' levels to the middle of the normal ranges for free T4 (1.1 ng/dL) and free T3 (3.3 pmol/L). I have found that a free T3 level of less than 2.7 pmol/L is significant and that supplementation makes a difference. A free T4 level of less than 1.0 ng/dL with a corresponding free T3 level of less than 2.8 pmol/L is significant enough to treat, and I have not been disappointed in the results of treatment.
My experience is all anecdotal, and these tests do cost more than a standard approach. However, I believe that the end result is cost-effective when one considers the number of failed trials with medications, continuation of depression, and patient nonproductivity seen with more standard therapy. I would be interested to hear what an expert thinks of this approach.
—John V. Billings, MS, ARNP
  Spokane, Wash





First, the definition of subclinical hypothyroidism is an elevated serum TSH level with normal free T4 and T3 levels, so the approach you describe is not a treatment for subclinical hypothyroidism. Second, free T3 assays are notoriously variable. Third, non-thyroidal illness, including depression, may suppress serum T3 and free T3 levels; only in severe cases, in which TSH levels are also suppressed, could one argue that these patients have acquired central hypothyroidism. However, even in cases in which T3, free T3, and TSH levels are all suppressed, most experts do not recommend treatment. Finally, liothyronine (T3) treatment should increase T3 levels but reduce T4 levels, because of negative feedback on pituitary TSH; this effect should make it difficult to maintain a free T4 level of 1.1 ng/dL unless only tiny doses of liothyronine are administered.
A large body of literature suggests that liothyronine may be of benefit in depression; however, in most studies, liothyronine was used pharmacologically to cause mild hyperthyroidism, with its associated risks to the heart (atrial arrhythmias) and bone (osteoporosis). Experts have long argued that patients feel better when given a little more thyroid hormone, based on anecdotal experience similar to yours, as well as non-blind trials. Hypothyroid symptoms were recently the subject of double-blind, randomized controlled studies. In one study, patients could not distinguish their usual dose of thyroxine from doses that were 25 to 50 µg/d higher. In other studies, up to 40% of patients given placebo had improved symptom scores. Because hypothyroid symptoms are so nonspecific and because overzealous treatment with thyroid hormone can be dangerous, I do not think that empiric treatment of low free T3 levels with liothyronine is appropriate in the absence of benefit demonstrated in a blind trial.
— Douglas S. Ross, MD
  Associate Professor of Medicine
  Harvard Medical School
  Cambridge, Mass



Thank you Dr. Ross for your comment.  I wrote this three years ago and since then I have

I do respect the medical profession because of the vast background of clinical experience and research that makes the treatments rendered by practitioners, using medical standards, safe and effective. 

I found your response in compliance with all of the myriad of articles and textbooks and professionals which I have read and consulted.  And should I conform to the medical standards I would not find myself crosswise with the medical community in which I work.

Up until last September, and for the previous 12 years, I have practiced within that standard.  The only exception being that when I started practicing in Spokane Washington, my two mentors, who are respected professionals, teachers and researchers, taught me about T3.  I had been informed that the free T3 should be between 3.0 and 3.5.  Since that first year, whenever I have found a free T3 less than 2.8, and I have treated it to raise the free T3 to 3.0 or above, I have been rewarded with improvement in psychiatric symptoms and even a decrease in medications needed to treat the conditions.

What is most interesting to me is that about 20% of my clientele have had a free T3 below 2.8.  And all of my clientele for the past 13 years, except a few dozen at most, have had a free T3  below 3.6.  My whole practice is full of people that have low T3 levels.  I believe that this is so because the majority of my clientele have failed psychiatric treatment in two or more settings and have been labeled treatment resistant.  I do not have a typical practice, and if I use the same standards to treat my clients I will have the same results.  I have had to look for reasons why they are treatment resistant, and treating low T3 has been a fruitful avenue.

Because of what I learned last September, I have been trying to find out as much as I can.  The process has produced more questions than answers.  My clinical experience has not coincided with the medical research I have read.  And this dissonance, along with the resistance from the medical community, has fueled my desire to understand why.

As I read your response I came up with questions that arise from my experiences.

First, the definition of subclinical hypothyroidism is an elevated serum TSH level with normal free T4 and T3 levels
Are there symptoms of hypothyroidism in sub-clinical hypothyroidism?

Are TSH levels effected by the total or the free fraction of T4 and T3?

To what extent do each, the T4 and T3, have on the TSH level?

If the free T4 and free T3 levels are normal when the TSH is elevated, wouldn't the individual be in a condition that didn't require treatment, especially if there were no symptoms of hypothyroidism? 

If the individual were treated, wouldn't the goal of treatment be to simply get the TSH within the reference range? 

Do the free T4 and free T3 levels go up, down, or stay the same when subclinical hypothyroidism is treated, and what effect does this have on the symptoms the patient is or isn't experiencing?

What is the explanation as to why the TSH is elevated in subclinical hypothyroidism and is the condition harmful?

If hypothyroidism is always and only defined as an elevated TSH, then what do you call a normal TSH with low T3 levels?

What do you call a low TSH with low T4 and or low T3, if a person is on thyroid replacement therapy, especially when the levels of the TSH and T4 were in the normal range before treatment, but the T3 was low?

What is considered a low free T3 level?  The range of normal free T3 at one of the local laboratories is 2.3 to 4.2


Second, free T3 assays are notoriously variable.

This, in itself, is very intriguing.

Has anyone ever asked the question why free T3 levels are variable? 

Is it just the free T3 levels that are variable or does that include the total T3 levels as well, and has there been any studies done that correlate free T3 and total T3 levels?

Is it simply that the procedure is not reliable, and if it isn't reliable then why are the laboratories allowed to charge patients to pay for lab studies that are not reliable? (The laboratory I use charges less for free T3 levels than total T3)

It seems to me that the TSH and free T3 levels are independent variables and have little correlation, but which has more effect on the basal metabolism rate, or rather, which is more important?

Isn't the TSH effected by both the T3 and T4 levels, and the T3 levels have four times the effect on the TSH than the T4?

If the TSH is within normal reference range, and the free T4 is at the high end of the reference range, wouldn't the expected free T3 levels be low?

In my clinical experience, the free T3 level above 3.5 does not correlate very well with symptoms of hypothyroidism.  Why then does treatment with thyroid replacement therapy in those clients with a free T3 between 3.5 and 4.0 improve and even resolve the depressive symptoms that have been resistant to conventional treatment as well as improve other health related symptoms?


Third, non-thyroidal illness, including depression, may suppress serum T3 and free T3 levels; only in severe cases, in which TSH levels are also suppressed, could one argue that these patients have acquired central hypothyroidism.

Why does depression suppress serum T3 and free T3?

Doesn't the suppression of T3 contribute to the depression, and if not corrected wouldn't the suppressed T3 adversely effect the outcome of the treatment of the depression?

Does treatment of depression automatically correct the suppressed T3, and are there studies that show that it does?

Would it not be beneficial, if not imperative, for the approximately 4% of depressed patients that have been resistant to treatment of their depression, to at least consider treatment of  their acquired central hypothyroidism if they have it? 

However, even in cases in which T3, free T3, and TSH levels are all suppressed, most experts do not recommend treatment.

This statement includes suppressed TSH levels, and there are no experts using medical standards that would ever treat a person with a suppressed TSH with thyroid hormone replacement, because the definition of hyperthyroidism is a suppressed TSH.  However, what about a person that only had a suppressed T3 and a normal TSH?

Isn't this statement a contradiction in terms?  How can a person that has hyperthyroidism by definition essentially would express hypothyroid symptoms , and what would you diagnose such a condition?

Why does the medical profession collectively ignore T3 when it is the most important of all three of the thyroid hormones?

Finally, liothyronine (T3) treatment should increase T3 levels but reduce T4 levels, because of negative feedback on pituitary TSH; this effect should make it difficult to maintain a free T4 level of 1.1 ng/dL unless only tiny doses of liothyronine are administered.
Serum T3 is downstream of where T3 is made.  It is much more preferable for the patient to have a good free T4 level so they will make their own T3.  If the T4 is increased, the T3 is also increased.  I have recently stopped using T3 supplementation unless the patient has a free T4 that is pushed to the highest level of the reference range and continues to have a free T3 less than 4.0.

The larger issue in treating low T3 is the suppression of TSH.  Medical standards forbid the suppression of TSH except in treatment of infrequent cases of certain thyroid conditions.  And the standards absolutely forbid complete suppression of TSH when treating with thyroid replacement therapy.  However, there is no way in which you can increase a free T3 less than 3.0 up to a level of 4.0 without suppression of TSH

Does suppression of TSH make a person hyperthyroid (which would be manifested by an elevated T3 level), and does it put the person at risk for cardiac arrhythmia and bone loss due to hyperhyroidism

If the studies that were done that established the cardinal reason for not suppressing TSH, had been correlated with T3 levels, they would have found that the initial result of TSH suppression caused the suppression of T3 and not the elevation of T3.  The symptoms of cardiac arrhythmia and bone loss when the TSH is suppressed are the result of T3 suppression and it is this situation that makes suppression of TSH so dangerous. If the patient has a severe cardiac condition, especially if that condition has been undiagnosed, the result of TSH suppression can be cardiac arrest. 

Because hypothyroid symptoms are so nonspecific and because overzealous treatment with thyroid hormone can be dangerous, I do not think that empiric treatment of low free T3 levels with liothyronine is appropriate in the absence of benefit demonstrated in a blind trial.
I agree with Dr. Ross to a point.  Without studies that show the benefit of empiric treatment of low free T3 levels, such treatment can be very dangerous, and puts the practitioner using such treatment out on a limb, so to speak.  However, there are few if any studies that I have found that have pushed the envelope by suppression of TSH

There is a medical organization by the name of American Academy of Anti-Aging Medicine that are pushing the envelope.  And for this they are highly criticized by mainstream medical science.  It is only because of what I have learned through this organization that I am putting myself out on the limb.  And by so doing I have been rewarded with not a few clinical experiences that have far exceeded my expectation.  The success I have had has further encouraged me to push forward.

1 comment:

  1. The worse thing about hypothyroidism is, my hair was falling out, and I was very irritable. Good thing my aunt told me to take some desiccated porcine capsules. Now I can move faster and my hair has stopped falling.

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