Issue 6: Lack of referral to an endocrinologist who understands

Doctor
If you are lucky enough to get referred to an endocrinologist, will they understand the importance of T3? Image: “Doctor Hand,” by Truthout.org, September 8, 2009, from https://flic.kr/p/6WMPmu

This series of 6 blog posts tells my story and outlines the six challenges I’ve faced.

This post focuses on the fact that most family doctors are not equipped to test for or treat underlying hormonal thyroid dysfunction that may occur despite “normal” TSH and T4 levels.

Unfortunately, it also describes a disappointing consultation with an endocrinologist.

It is important for thyroid patients to have access to a specialist who can interpret abberant thyroid test data and manage conditions such as chronic Low-T3 in patients treated with Synthroid.

At almost every turning point in my experience with Hashimoto’s thyroiditis, I have had to do my own research and take initiative to ask my doctors for tests that should have been done years earlier.

On top of my hypothyroid symptoms (during treatment as well as pre-treatment) and the fact that chronic hypothyroidism increases risk for other health issues (such as heart problems), I have struggled with systemic barriers in the health care system:

  1. Delayed diagnosis of hypothyroidism
  2. Misdiagnosis of thyroid-related depression
  3. Ignorance of Hashimoto’s autoimmunity
  4. Lack of regular (or any!) thyroid ultrasound testing
  5. Lack of testing for Free T3 and Reverse T3 levels
  6. Lack of referral to an endocrinologist who understands

Issue 6: Lack of referral to an endocrinologist who understands

I was treated with Synthroid since I was diagnosed with hypothyroidism in 2003. For more than 13 years, I had never seen an endocrinologist.

This is normal state of things, since it is assumed that treating hypothyroidism is as simple as adjusting synthroid dosage to TSH lab results, something well within the function of a family physician.

However, hormonal dysfunction can occur undetected for years under the level of TSH test results.  TSH may be within the lab reference range, but only T4 and T3 testing may reveal insufficient production of and conversion to T3, the essential thyroid hormone that every cell of our body requires.

Why was it not puzzling to see such a high-normal T4 consistently hand-in-hand with too low T3?  Would that not make a physician wonder about an underlying T4-T3 conversion dysfunction?

Even TSH and T4 testing alone, when viewed over the long term, could have showed signs of dysfunction that prompted a referral.  It would take a long-term perspective to see that it was beyond the control of mere adjustments to T4 dosage to get my TSH into the “normal” lab range in the first place, and then get it to stay there for more than a year.

Some cases are beyond the expertise of the average family doctor… a specialist like an endocrinologist is needed to troubleshoot and fix the many problems that can occur to disrupt the usual hormonal chain of events between T4 medication ingestion and T3 secretion/production and T3 cellular reception.

If it has been so difficult for my regular family doctor to find the right dosage to treat my symptoms and get my TSH and T3 into a normal range, why was I not referred to an endocrinologist earlier?

The need for an endocrinologist who actually understands

I recently received a referral to an endocrinologist through a roundabout fashion.  I went to Emergency with suspected heart problems. Only a small anomaly appeared on my ECG and my troponin levels were detectable but low in the reference range, so I was referred to a heart clinic.

Luckily the heart clinic physician heard my concerns about my thyroid and referred me to an endocrinologist.

My first-ever visit to an endocrinologist was filled with such high hopes. Finally I would get to talk to an expert. Would they put me on T4-T3 combination therapy to address my low T3 levels?  I hoped they would look at the lab test data I presented and instantly see the logic of doing this.

What a disappointment.  At every turn, she proved that she was ruled by dogma and was treating as irrelevant the medical evidence and arguments I provided:

  • On my explaining that I wanted to bring her advice back to another doctor I’m consulting on my thyroid, she said that her approach was “evidence based” and was therefore likely to conflict with any “naturopath” I consulted on my thyroid.  I said no, he’s not a “naturopath.” He’s an MD.  He specializes in hormones.  Unfortunately the doctor was quick to judge me and any other doctor I was consulting as being less “evidence based” than herself.  This was not an auspicious beginning to our meeting.
  • She said I was only “mildly hypothyroid,” a diagnosis made by looking only at my current Synthroid dose of 110/112 per day and my TSH and T4 levels. My recent lab tests showed a high TSH of 10.27 (lab ref 0.20-4.00), fT4 of 18.3 (lab ref 10.0-25.0), and a fT3 of 2.9 (lab ref 3.5-6.5).  Not only were my TSH and fT3 significantly out of range, but she made this statement before hearing any of my symptoms, or hearing me say I had reduced my Synthroid dose even further since the lab test. Nor did she ask me why I (in consultation with other doctors) had been reducing my Synthroid dose despite knowing this would make my hypothyroidism worse.
  • I showed her my graph of thyroid lab test results since Fall of 2013.  She interpreted my erratic thyroid lab results history over 3+ years as a problem with stabilizing my T4 dose and normalizing the TSH.  However, normalizing TSH had always been the target of my thyroid therapy, and of course I and my doctor wanted a stable T4 dose.
  • She did not ask why the dosing had changed at all from 2013 to 2015—or why the graph began with a TSH of 0.08 that then swung up to a TSH of 18. It was because I had lost a lot of weight over the preceding year not shown on the graph. My doctor and I were trying to readjust the dosage to my new body weight by getting my TSH back into range.
  • She did not ask why I was being tested monthly five times since November 2015—I was having very distressing symptoms that could not be traced to any other likely condition than thyroid, since I was otherwise very healthy.  I had many tests because I was seeing many doctors and changing dosages while dealing with extreme symptoms.
  • She considered it irrelevant or unimportant that my T3 was always below range over 3+ years. She did not think it suspicious that T3 was consistently low regardless of whether the TSH was too high or too low. Her attention was only on the fluctuation of TSH and change in thyroid dose. She was not interested in the levels of the essential thyroid hormone, T3.
  • She then explained that T3 levels were not important to test because they varied so much and the half-life of T3 is very short. She said she would not even consider looking at my T3 or T4 results until my TSH was normalized.
  • She said that I was changing doses and testing too quickly and explained that it took about two months to stabilize on a new dose. I explained that my TSH and Synthroid dose had actually been stable for 11 months over several tests shown on my graph, and it was near the end of that time on a stable dose that my TSH and T3 results had unexpectedly worsened in December.
  • She did not ask why the dosing changed from 2013 to 2015—it was because I had lost a lot of weight over the preceding year and we were trying to readjust the dosage to my new lower, stable body weight by getting my TSH back into range.
  • She did not ask why I was being tested 5 times in five months since November 2015—the testing became more frequent because I was having very distressing symptoms that could not be traced to any other likely condition than thyroid, since I was otherwise very healthy.  In February I started to have cardiovascular problems that seemed to respond directly to different T4 dosages.
  • She refused to look at the official Reverse T3 lab test results that I put on the examining table.  If she had looked, she would have seen that my most recent RT3 level, measured a month ago, was 33 ng/dL, when the lab range was 8-25.  But without looking at the paper, she said that Reverse T3 results were “irrelevant.”
  • She dismissed my question about the relevance of recent endocrinology research. When I brought out of my bag a printout of “a 2015 article on people with reduced T4-T3 conversion rates” she said, refusing to look at it, “you can find anything on Google.”  I immediately interjected, “It’s from an endocrinology journal.” She then said “T4-T3 conversion is a controversial area in endocrinology” and “you don’t fit within the populations studied in the research because their TSH was normal.”
  • She said it was “not indicated” that I have a thyroid ultrasound, when I told her that another doctor had ordered one for me and the test was going to happen the day after our appointment. I had never had a thyroid ultrasound before, and I had been feeling inflammation in the region of my thyroid.  She palpated my thyroid and had me drink a small cup of water as she watched the movement of my thyroid.  She said my thyroid appeared to be “normal.” The next day, the ultrasound showed I had a severely atrophied gland, about 1/2 the size of a normal adult female gland. Research says that an atrophic gland is confirmation that I have autoimmune thyroiditis, and that this means I am more likely to get thyroid cancer. This means that it is important to check for thyroid nodules via ultrasound.
  • I had told her that I found that slight increases in my T4 doses resulted in increasing my cardiovascular pain within 8-30 hours of increase. She considered it merely coincidental and “unlikely” that there was any correlation between my T4 dose and my cardiovascular symptoms. Apparently she was unaware of all the research that showed how serum T3 levels, and reverse T3, affect blood vessels and heart directly, and was not considering that higher T4 levels were being converted into higher Reverse T3 levels instantly upon being ingested. Apparently she did not consider my dosing/symptom correlation to make any logical sense given her knowledge of the thyroid. I did not have time to explain the additional confirmation in my N=1 experiment, that each time I reduced my dose by 6.5 mcg it alleviated my symptoms for 3-5 days following, and that the three times I tried to raise it to go back to an optimal dose and TSH, I had ended up in Emergency.
  • She recommended that I gradually increase my Synthroid dose back to normal in order to “normalize the TSH” over the next few months. I thanked her for her professional advice, since this is exactly what I wanted from her: her honest professional opinion on what I should do with my thyroid medication given the data. However, I explained that I was not willing to take the risk of raising my T4 Synthroid dose levels while I continued to have cardiovascular symptoms, given my recent experience with it worsening those symptoms.

I was honestly puzzled about why she felt I should repeat, for her sake, the effort to normalize my TSH, although the same efforts had largely failed over the past 4 years and left me with continually low T3 regardless of whether TSH was too high or too low.

I did not tell her that I believed I needed a T3 prescription (though she might have surmised this from our conversation).  I had plans to begin T3 therapy as soon as possible.  If she was not willing to prescribe it, luckily I had already found a hormone-specialist MD who would be willing to do so.

My guess is that perhaps the endocrinologist would ONLY have considered an alternative treatment if she had personally been involved long-term in my treatment over the past 4 years and had been unsuccessful in normalizing my TSH.

However, I could not submit to being a guinea pig and re-doing any of those 4 years of experimentation. I was not willing to submit to what I saw as a clear cardiovascular risk of increasing my reverse T3 levels and further reducing T3 access to my arteries. This is exactly what would have happened if I had tried to bring my  T4 dose back up to what should be an adequate physiological replacement.

It is highly likely that even after years of working with someone like me, instead of releasing hold on her tightly-held dogma, she would have decided that my hormone lab test anomalies and symptoms were caused by some other health condition that was beyond her specialization to treat (i.e. cardiovascular, rheumatological, neurological). By then, who knows how far further my cardiovascular health would have deteriorated? Research has shown repeatedly that low-T3 is independently associated with morbidity and mortality in many chronic illnesses, and especially cardiovascular illness.

In conclusion

Regular family physicians cannot be relied upon to treat the thyroid when there is an underlying dysfunction in hormone conversion and/or continued symptoms in the presence of “normal” TSH and T4.

Referral to an endocrinologist seems like a logical path in such cases where there seems to be a dysfunction in the normal feedback loop of TSH and it is difficult to interpret aberrant lab results.

However, not every endocrinologist is willing to consider data and evidence from a patient’s history of lab tests, endocrinology journal articles, and patient reports of symptoms that correlate with dosages and lab results.

Endocrinologists as a community are very, VERY reluctant to consider any “controversial” treatment (i.e. anything other than T4-only therapy) … even in clear-cut cases of poor T4-T3 conversion and chronically low-T3.

This is unacceptable. What about patients who don’t do as much research as I do? What about patients who are not as lucky as I was to find an MD who truly understands how to interpret and treat T3 levels?

  • Endocrinologists and family doctors, should become more aware of the physiological NEED for minimal levels of T3.
  • Endocrinologists and family doctors should be taught about the serious health problems and prognoses that are associated with (especially cardiovascular problems) insufficient levels of T3 in serum. They should understand how T3 impacts important organs such as the heart, brain, kidney, and bones. They should not prescribe non-thyroidal treatments, such as antidepressants, if there is a high likelihood that the health problem could be caused by T3 hormone insufficiency and resolved by increasing T3 levels.
  • Endocrinologists and family doctors should know that many things can go wrong with hormone metabolism and secretion that break down the feedback loop and make TSH levels alone unreliable.  TSH cannot be the sole goal of thyroid therapy.  Every cell in the human body requires adequate T3, not merely a TSH within lab range.
  • Endocrinologists and family doctors should test for T3 levels. If T3 levels remain low regardless of increasing T4 dose, they should investigate further and try to increase T3 levels by various means to achieve optimal hormonal health. Even if the patient is not currently experiencing hypothyroid symptoms, they should use healthy T3 levels as a goal of therapy in order to reduce risk to the patient’s long term health.

I agree that research is not yet conclusive about low T3 by itself causing health problems. However, thyroid disease research has focused too exclusively on TSH and T4, and therefore honest endocrinologists should confess ignorance until their researchers do more studies on the impact of chronically low T3 on various organs and bodily systems.  There is enough research evidence now—much of it published in fields beyond endocrinology—that casts strong doubt on the idea that a long-term Low-T3 state could ever be an “adaptive” or “benign” state, or that an increasing Reverse T3 level could be “irrelevant” in light of low T3.

After seeing the endocrinologist

I closed the door on my high hopes that an endocrinologist would understand. I had been experiencing distressing cardiovascular symptoms for 3 months, and I knew the association between low T3 and cardiovascular problems was NOT controversial.  Recent randomized controlled research studies on heart patients had shown T3 therapy helped them considerably.  I was becoming increasingly hypothyroid because reducing T4 helped and increasing T4 caused problems. In this scenario T3 treatment was a logical alternative that offered hope. I could not wait any longer to try T3.

I began T4-T3 therapy on April 7, under the guidance of my hormone MD, with a 2-month programme that gradually weaned me off of T4 and gradually increased T3 levels. Every two weeks I am reducing T4 dosage by 25mcg and replacing it with 5mcg of T3 (since T3 is about 5x as potent as T4).  My cardiovascular symptoms have improved with each reduction in T4 and increase in T3.

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