James K. Rone, MD, FACP, FACE

Hypothyroidism & Chronic Fatigue Syndrome

July 26, 2012

Tags: Thyroid, Chronic fatigue syndrome, Myalgic encephalomyelitis

Ms. Hagerty:

I appreciate your kind words about the book.

My father, who was a newspaper editor, was fond of saying that the British and Americans were two peoples separated by a common language. We have an example of that here: Upon my first reading of you email I’m embarrassed to say I had no clue what “ME” was. However, a brief Google search indicates to me that it is the same thing as what the US medical community calls chronic fatigue syndrome (CFS). I’ll preface my further comments by stating that I am no expert on true CFS, which (you know all this better than I, I’m sure) has very specific diagnostic criteria, and is of unknown etiology, but infectious and/or neurological causes are suspected. It is also a diagnosis of exclusion in that part of diagnosing CFS is ruling out everything else, including hypothyroidism—which can be problematic as you discovered and I discuss at length in "The Thyroid Paradox."

I agree with your statement that the list of symptoms of CFS and hypothyroidism are virtually identical, and I have no doubt that there is a subpopulation of CFS patients that are in truth undiagnosed or under-treated hypothyroidism sufferers, and that that is the cause of or at least a contributor to the fatigue. The trick of course is identifying that subpopulation—that might be done in some cases with a more open-minded interpretation of the lab work (not ruling out hypothyroidism, for example, on the basis of a TSH of 5.0, just because the lab says 5.0 is “normal”), and in other cases it might take a trial of thyroid supplementation. When we do the latter it is of course very important to stop the thyroid treatment if no clear benefit is noted after a sufficient time on a sufficient dose—which is of course evidence in favor of some non-thyroid cause of chronic fatigue.

As an aside, I also believe that a subpopulation of patients who get labeled with “fibromyalgia”—a similarly frustrating, chronic debilitating illness to CFS—actually have hypothyroidism.

Your experience wherein you felt better on an extra 12 mcg LT4 illustrates the need for careful titration of dosing, often with very small adjustments, and supports the avoidance of generic thyroid hormone replacement products, which opens us up to unacceptable variations in bioavailability. That your dose was dropped on the basis, it sounds like, of a low TSH only, resulting in a deterioration of symptom control, is alas typical on both sides of the Atlantic. As you know from the book, I believe that such determinations must be made on the basis of TSH and FT4 and FT3 and perhaps most importantly on symptoms. And I don’t mean to overstate the problem—there are experts out there besides me who recognize that there are clinical situations where it is okay to leave a patient with a low or even undetectable TSH—unfortunately, whether you’re dealing with a primary-care doc, or even a “consultant of flavour,” such willingness to look past a low TSH is, in the real world, very very rare. I smack my head against that wall every day practically.

I did not know, and thank you for telling me, that the availability of LT4 dose strengths in the UK is so limited (at most, just 25, 50, and 100 mcg tabs based on my brief online search). Fortunately, using various tricks (mixing and match full and ½ tablets of different strengths, or skipping days, or taking extra periodically) there is no dose that we have that you can’t mimic, as long as the prescribing healthcare provider bothers. Even here, with those 12 tablet sizes available, there are a lot of primary care providers who adjust (incorrectly in most cases) in 50mcg increments or the like.

Lastly, to address your main question of modulating LT4 doses based on physical activity—I do touch on this in the book as you know. What you propose is interesting, that is, upping the LT4 dose proactively in anticipation of a period of increased physical training/activity. I have never done that, but let me outline of what I can definitively say about thyroid and physical activity, most or all of which is covered in the book, I believe:

(1) Twenty years ago I published data (in a UK medical journal, by the way) that indicated an increase in thyroid hormone utilization (and thus presumably an increased LT4 dose requirement) in triathletes compared to sedentary controls (“couch potatoes”). The study could not distinguish between the observed differences being a cause of or a consequence of the improved physical conditioning—my speculation in the paper being that the alteration of thyroid hormone metabolism was what led to the improved athletic performance and endurance. To my knowledge no further research has been to settle that question. Either way though, theoretically, increased exertion might demand increased LT4 dosing. However, it is not certain that the results of this study are relevant to the “ME patient” gradually speeding up his or her life. There is a big difference between that kind of physical exertion and the running of a triathlon.

(2) I have observed that my thyroid dose has needed to be increased (based mostly on my lab results) when I am more physically active. It is possible that there were other factors—such as reflux medicine. And of course weight loss, which might result from increased activity, would tend to decrease dose requirements. So, I think the effects of increased exercise on thyroid requirements depends on the interaction of many factors—amount and type of activity (weight-lifting vs. running, for instance), duration, the conditioning of the person, diet, weight changes)

(3) I have also observed patients feeling better on LT4 and becoming more active as a result, and then seemingly having a relapse of the fatigue as a result at that increased activity—this is essentially the scenario you are painting. My interpretation of that scenario is that the patient lost musculoskeletal and cardiovascular conditioning during their period of inactivity when they were hypothyroid, and that it will take time to restore that conditioning through gradually increasing frequency and duration and intensity of exercise. It has been my feeling that no amount of thyroid hormone would solve this problem.

Might, as you suggest, the answer be a proactive increase in LT4 to stave off the renewed fatigue. I don’t know. I kind of doubt it, but I haven’t tried it, so I don’t know. Were it to be tried, I would advise no more than an increase of 12.5 mcg at a time with close monitoring of signs, symptoms, and blood tests.

I hope that helps and if you wish please feel free to share this with and recommend the book to your ME patient organizations. And put a good review of the book on Amazon if you are so inclined.

Best,
jkr

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