Low T3 thyroid hormone, insomnia, and sleep apnea

Hypothyroidism and SLEEP-apnea

Hypothyroidism and SLEEP2Have you struggled with sleep disorders, whether insomina or sleep apnea? Apparently it’s associated with hypothyroidism. Even if it’s true that people with untreated hypo sleep a LOT.

My mother has agonized over her chronic insomnia. She had been on low dose Synthroid for decades before she was diagnosed with a serious case of sleep apnea in her 80s. Since finding out her FT3 was chronically below range on Synthroid, switching to desiccated thyroid and being on CPAP therapy have been helping.

A doctor I know who treats hypothyroidism has said this about insomnia:

“Although hypothyroid patients are thought of as sleeping, sleeping, sleeping, they often do not fit this classic concept of hypothyroidism.

Yes, hypothyroid patients may not want to get out of bed, but, most of them have insomnia, and, as a consequence, fail to get restful sleep. Those who have difficulty sleeping appreciate the curse of insomnia. For some, the curse is so bad that they do not want to live.

Insomnia is like a heavy weight that these patients carry every day. And, the burden gets worse and worse. The fatigue of insomnia added to the fatigue of hypothyroidism itself can become unbearable for some patients.

But, when these desperate patients seek help and are dismissed because they do not have hypothyroidism, on the basis of TSH, this response can be horribly deflating and abandoning.

No-one likes the feeling of being alone, but, many hypothyroid patients, unable to find help, feel hopelessly alone.”

WHAT DOES THE SCIENCE SAY?

I recently came across one of the very first studies on insomnia and hypothyroidism. It has been sitting on the dusty shelves of university libraries since … wow… 1967!

Title: “All Night Sleep Studies in Hypothyroid Patients, Before and After Treatment” (Kales et al).

The 4 young patients had a significant decrease in stage 3 sleep compared to euthyroid.

In the four “elderly” hypothyroid patients (aged only 55, 56, 64, and 65), even more extreme results:

NO stage 3 or stage 4 sleep was present!

The article also includes interesting clinical descriptions of several individual patients, like this one that revealed high doses and many tests of thyroid hormone sufficiency (before the TSH test became commonly adopted) —

“J.F. was a 21-year-old female who was diagnosed as being hypothyroid during childhood. She had taken 5 grains of [desiccated] thyroid daily [note: equal to 300mg ERFA Thyroid] until she was referred to UCLA for evaluation.

Two months after WITHDRAWAL of [desiccated] thyroid medication,

  • The patient had gained 10 pounds in weight, was clinically hypothyroid and had
  • a PBI [protein-based iodine, the old measure of thyroid hormones] of 1.2 mcg/100ml,
  • a cholesterol of 259 mg/100 ml,
  • a radioactive iodine uptake [how much iodine enters the thyroid gland] of 0% in 6 hr, 0% in 24 hr
  • and a half relaxation time of the Achilles tendon reflex (photomotogram) [a technical measuring device for reflex response] of 460 msec (upper limit of normal: 380 msec).”

“After our sleep study was completed the patient was put back on her previous thyroid medication.

Four months later, she was clinically euthyroid, had returned to her original weight and had a PBI of 7.2 mcg/100ml, cholesterol of 130 mg/100ml, half relaxation time in the photomotogram of 260 msec.”

This was Patient #1 in the younger group of patients studied. Her sleep was like night and day, on and off desiccated thyroid therapy.

Bottom line:

The patients when hypothyroid had less stage 3 and 4 sleep (and a slew of other disorders and aberrant test results).

When these same patients were clinically euthyroid (on desiccated thyroid therapy), they had increases in these very same stages of sleep.

WHY STAGE 3 SLEEP MATTERS

Naska and Goldberg, writing on the blog of the American Sleep Apnea Association, say “Stage N3” sleep is “sometimes referred to as Delta Sleep or slow wave sleep, because of the slow delta brain waves, which have been recorded during this sleep stage.”

They explain the importance of stage 3 sleep to health. “N3 sleep is a regenerative period where your body heals and repairs itself.”

But getting enough stage 3 sleep is not about sleeping more hours. That’s why hypo oversleepers can still be poor sleepers.

They say “The first episode of Stage N3 lasts from 45-90 minutes.  Subsequent episodes of N3 sleep have shorter and shorter time periods as the night progresses.”

But after all that about Stage 3 for healing, this is what the experts paradoxically conclude:

“N3 sleep decreases with age such that elderly people may have no measured N3 sleep at night.  This occurs in healthy sleepers and does not indicate a disorder or disease state in itself.”

Loss of stage 3 sleep is just naturally part of aging and it does not indicated a disorder or a disease! What?

If that’s true, then why is …

STAGE 3 ASSOCIATED WITH SLEEP APNEA

Nasca and Goldberg go on to explain later in their article that sleep apnea, yes, a disease, is directly related to Stage 3 sleep loss.

According to Naska and Goldberg, again, “People with apnea may have reduced stages N3 and REM when their interrupted breathing causes sleep to be fragmented, possibly alternating between stages N1 and N2 over and over all night.”

Let’s connect one more dot to this constellation.  My favorite topic: T3 hormone.

SLEEP APNEA AND LOWER FREE T3

A 2015 study (Takeuchi et al) found that higher TSH (in untreated patients) and lower Free T3 correlated with sleep apnea.

Takeuchi was very interested in the FT3 data:

“Subjects with lower FT3 (≤3.75 pg/ml) showed longer mean apnea time compared to those with higher FT3 (>3.75 pg/ml)”

Their reference range for FT3 was 2.47–4.34 pg/ml

A Free T3 of 3.75 is 68% of reference range.

Even more interesting is that sleep apnea and hypothyroidism are both often associated with obesity, but in this study, low FT3 was not related to obesity; patients with lower Free T3 tended to have low BMI. You can’t blame obesity. It’s about Free T3.

The article reviews many other studies of sleep and thyroid hormones, but they all suffered from the late 1970s recategorization of patients as “hypothyroid” based on TSH alone rather than a host of other tests including ankle reflex and cholesterol.

Takeuchi pointed out that research has discovered standard T4 (thyroxine) therapy does not resolve sleep apnea for the majority of patients merely by normalizing TSH:

“Grunstein et al. [3] demonstrated that 75% of patients showed persistent sleep apnea after an euthyroid status [normal TSH] had been achieved.”

The authors mention that not measuring Free T3 has been a major oversight in past research:

“Most of them measured TSH only [8, 15], or at most, FT4 in addition to TSH [6, 7, 11], to diagnose hypothyroidism; the measurement of FT3 was not included in their screening.”

They go on to make this profound statement: “In other words, clinical significance of FT3 and various indices of sleep apnea other than AHI and RDI may have been overlooked until now in the management of patients with sleep apnea.”

How exciting!  Maybe more researchers will measure FT3 and sleep!

But no…

A PUZZLING RESPONSE TO TAKEUCHI

After all the emphasis Takeuchi et al placed on Free T3, Aaron B. Holley, the editor of the journal issue in which it was published, focused on [TSH] screening and [standard] thyroid therapy.

His title responded directly to the article by Takeuchi.

But he takes it in a completely different direction. Back to the well-traveled road, or should I say the ruts, of TSH and T4. Here we go.

He focuses instead on “screening” and “thyroid disease”: “Should you screen all your sleep apnea patients for thyroid disease?”

His answer is no.

His overall response is a medical researcher’s equivalent of “Yawn. so what?” (It put him to sleep, maybe a good thing.)

He writes, “Takeuchi et al. found that thyroid levels were not related to AHI but TSH and FT3 were weakly associated with apnea duration. This fits with what we already know—hypothyroidism blunts the ventilatory response to hypoxia and hypercapnia [6].”

In other words, it is well understood that when you are hypothyroid and you run out of oxygen and have too much carbon dioxide while sleeping, you don’t respond normally by breathing in more oxygen.

That’s nothing to laugh at. So why be apathetic then?

His apathy toward TSH and Free T3 alike in sleep apnea appears to be born of the limitations of standard [TSH] “screening” and standard [T4] “thyroid therapy.”

He is indirectly expressing a reasonable sense of futility in a person trained to heal:

Why bother screening for thyroid disease in sleep apnea if today’s therapy for thyroid disease is largely ineffective in resolving sleep apnea?

He knows that there’s a cause-effect relationship between hypothyroidism and sleep apnea. But he also knows that the standard therapy used today is not going to fix the problem. Recall that Takeuchi mentioned that standard thyroid therapy was found to be ineffective in resolving sleep apnea in 75% of cases.

Holley reveals that he believes that the 25% that respond have a special sleep apnea phenotype, not that their Free T3 levels are higher.

Not a thyroid hormone specialist, Holley puts both TSH and Free T3 in the same category. But they are entirely different hormones in purpose and function. Unfortunately, your TSH level is a separate issue, especially if you are a thyroid patient taking thyroid hormones.

T3 level beyond the pituitary does not correlate with TSH.

T3 is the thyroid hormone has more direct influence over “ventilatory response” than TSH.

Not having taken T3 hormone 101, and interested in results more than molecular biology, he is not going to change anything he does.

Medical inertia:

“At our sleep center, we do not routinely draw thyroid levels on every patient diagnosed with OSA. Considering the data presented by Takeuchi et al. and the previously published
literature that they reference, I see no reason to change this practice. It is not clear that hypothyroidism occurs at a higher frequency among patients with OSA. Given the modest and variable effects that minor thyroid level abnormalities have on respiratory function during sleep, it seems unlikely that thyroid replacement will be an important part of OSA treatment in most cases.”

Zzzz. Zzzzz.

WHO IS SLEEPING AT THE WHEEL?

Patients on thyroid therapy might actually sleep better if their Free T3 were being tested. But they’re usually excluded from studies on FT3 and health.

Standard thyroid therapy won’t raise Free T3; instead, it is well known that it can often suppress FT3 to the lower half of reference range or below. How is that a helpful therapy for insomniacs and sleep apnea patients, according to Kales’ and Takeuchi’s studies?

In contrast, both desiccated thyroid therapy and synthetic T3 medication contain enough T3 to raise Free T3 levels without causing hyperthyroidism when T4 is allowed to fall lower to compensate. But our medical system has been indoctrinated by the American Thyroid Association’s relentless antagonism against desiccated thyroid therapy.

Our rigid TSH-T4 paradigm in contemporary thyroid science is stalling both inquiry and therapeutic approaches in many other fields of medicine.

Until more doctors are encouraged to raise Free T3 within range until symptoms are removed (rather than merely TSH normalized), I do not think we will see a major impact on sleep quality in thyroid patients en masse.

Doctors and researchers are not trying to optimize Free T3 whenever they require TSH to be in normal range, because research has proven that normalizing TSH can come at the expense of a patient’s individual Free T3 requirements for health.

But nobody checks FT3. They’re sleeping at the wheel.

Until the thyroid therapy paradigm and practices change, sleep doctors are not going to be interested in the thyroid hormone status of their patients. They will be apathetic about a therapy that does little to help all but overtly hypo patients with a TSH above 10.

Who will put an end to this ignorance, apathy and medical inertia regarding the relationship between T3, the most essential thyroid hormone, and health?

Who is willing to admit that historical T3-T4 combination therapies used safely and effectively for so many decades could be more effective in resolving or minimizing sleep disorders than TSH-normalized T4 monotherapy?

REFERENCES

Holley, A. B. (2015). Should you screen all your sleep apnea patients for thyroid disease? Sleep & Breathing = Schlaf & Atmung, 19(1), 21–22. https://doi.org/10.1007/s11325-014-0998-5

Kales, A., Heuser, G., Jacobson, A., Kales, J. D., Hanley, J., Zweizig, J. R., & Paulson, M. J. (1967). All Night Sleep Studies in Hypothyroid Patients, Before and After Treatment. The Journal of Clinical Endocrinology & Metabolism, 27(11), 1593–1599. https://doi.org/10.1210/jcem-27-11-1593

Nasca, T. R., Goldberg, R., & The American Sleep Apnea Association. (n.d.). The Importance of Sleep and Understanding Sleep Stages. Retrieved March 26, 2019, from SleepHealth.org website: https://www.sleephealth.org/sleep-health/importance-of-sleep-understanding-sleep-stages/

Takeuchi, S., Kitamura, T., Ohbuchi, T., Koizumi, H., Takahashi, R., Hohchi, N., & Suzuki, H. (2015). Relationship between sleep apnea and thyroid function. Sleep & Breathing = Schlaf & Atmung, 19(1), 85–89. https://doi.org/10.1007/s11325-014-0966-0

 

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