Type 2 Diabetes and Hyper- versus Hypothyroidism

T2diabetes-hyper-hypoSurprise surprise. Having less thyroid hormone makes you more susceptible to Type 2 Diabetes.

How does it work? Quote from Dr. Chaker, lead author: “Thyroid hormone is also directly involved in the control of insulin secretion and glucose homeostasis. Hypothyroidism is associated with decreased insulin sensitivity and glucose tolerance and treatment of hypothyroidism has shown to improve these effects. The exact mechanism or mechanisms that are involved in the association need to be investigated.” (1)

This is an apparent paradox for people who assume (incorrectly) that the body always responds in opposite ways to hyper- and hypothyroidism. In the case of insulin sensitivity, the response at both ends of the hypo-hyper spectrum can be the same.

For those who are not well-versed in diabetes, here is an explanation in layman’s terms, from a Healthline website: “Being insulin resistant is a bad thing, while being insulin sensitive is good.” “Insulin resistance” means exactly the same thing as “decreased insulin sensitivity.” (6)

In insulin resistance, they explain, “the pancreas start producing even more insulin to bring the blood sugar levels down. This leads to high insulin levels in the blood, termed hyperinsulinemia.” As a result, “both insulin and blood sugar levels go up. Eventually, the pancreas may not be able to keep up anymore and the cells in the pancreas may become damaged. This leads to decreased insulin production, so now there are low amounts of insulin and cells that don’t respond to the little insulin that is available. This can lead to skyrocketing blood sugar levels. When blood sugar levels exceed a certain threshold, a diagnosis of type 2 diabetes is made. In fact, this is a simplified version of how type 2 diabetes develops.” (6)

Okay, so if lower T4 and higher TSH even within reference can increase risk of Type 2 diabetes by 35% (according to the article), shouldn’t people at risk for Type 2 diabetes should be checked for this pattern?

But of course, right away, people look to the bottom line of costs for testing among the undiagnosed. “it’s too soon to recommend thyroid screening tests for people with prediabetes. ” — of course screening, prior to diagnosis, means the TSH test.

But what about people known to be on thyroid hormone medication who have low, or low-normal T3? How much of a difference does low T3 make in people with higher T4 levels?

Was T3 included in their study?

No. The methods and results do not mention it. This is disappointing.

For one thing, every time people look at “low thyroid function” they mean assessing gland function. They tend to take a narrow look at the organ health, not the bigger picture of T3 hormone metabolism. They make statements that omit T3, such as “Elevated TSH and reduced T4 indicate low thyroid function.”

Dear researchers of hypothyroidism, as your treated thyroid patients, we’re sick and tired of people talking about the gland all the time.

Folks, stop focusing on just the gland…. the poor thyroid gland.

The gland is the victim here, not the ultimate cause of other diseases like type 2 diabetes. Even people with healthy thyroids can suffer thyroid hormone _metabolism_ dysfunction.

In thyroid disease and therapy, the thyroid gland fades out of the picture to the degree that it has been killed off by antibodies, anti-thyroid meds, or removed by a thyroidectomy.

So the more important question is, which thyroid hormone is the one that puts us at the most increased risk of type 2 diabetes, T4 or T3?

In thyroid therapy, patients without thyroid tissue have significantly less Free T3 hormone and more Free T4 than the average untreated healthy patient throughout the TSH reference range (2). We have a relative T3 deficit and T4 excess that is artificially induced by our medication.

Are we at increased risk from our lower T3?

I place my bets on lower T3 increasing the risk more than lower T4. Here’s why.

For those people on therapy (and people who are not on therapy), neither Low T4 nor high TSH are capable of causing the ultimate harm to organs and tissues.

Statistical associations with TSH or T4 hormones are not likely to bring us close enough to the cause-effect relationship.

T3 is the hormone with the most powerful effects on all cells and organs throughout the body. (3) T4 has very limited effects on the integrin receptors on cell walls. (4)

The main role of T4 hormone is to float around as raw material to potentially convert to T3 or RT3.

The main role of TSH in a person with a healthy thyroid is to regulate T4 production and secretion, and secondarily to adjust the rate and ratio of T3 production and secretion, as T3 from a thyroid increases in relation to T4 at higher levels of TSH.

T4-T3 conversion is not completely controlled by TSH, although a higher TSH enhances conversion in various organs. Nobody can correctly estimate how much T4 has become the active hormone T3 or the (relatively) inactive hormone Reverse T3 throughout the body until we measure T3 in blood.

Why do blood levels of T3 matter so much?

Research has proven that blood levels of T3 are sensitively controlled in health to remain very constant even within the reference range. See Abdalla & Bianco’s 2014 article titled “Defending plasma T3 is a biological priority.”

A healthy body maintains steady blood T3 levels.

A healthy body maintains steady blood sugar levels.

The parallel between blood T3 and blood sugar should be of interest.

All humans, with thyroid disease or not, on therapy or not, can be harmed by low T3 or excess T3. (When I say “low” or “excess” I mean in relation to the individual human body’s metabolic range in health, not in relation to the wider statistical population reference range.)

For treated thyroid patients, the T3 hormone is even more powerful and significant than TSH.

In thyroid therapy, TSH is now powerless, impotent as a controlling element of thyroid secretion, to the degree that there is a lack of living tissue or no thyroid tissue for it to stimulate.

In thyroid therapy, TSH is not the controller, but the controlled element — it is kept in chains by thyroid hormone dosing.

In thyroid therapy, T3 takes center stage as the hormone in control of health and disease … just as it is in every UNtreated human being with a healthy gland.

In certain illnesses … including the induced illnesses found in treated thyroid disease patients who are burdened with excess T4 from levothyroxine dosing … T3 could be shockingly low or it could be high. You can’t predict how well T4 is being converted because it varies widely from person to person.

In thyroid therapy, even at a completely suppressed TSH, a treated person’s Free T3 level can be below reference range, which makes them hypo, not hyper. (2)

No, neither TSH nor T4 numbers can tell anyone how much T3 is flowing through veins and getting into organs and tissues.

But research articles like these often generalize about “thyroid hormone” without specifying T3, and usually only mention T3 in the case of _excess_ T3 rather than deficiency. This passage from the Diabetes article exemplifies this, since it only mentions T3 (triiodothyronine) once, in the context of toxic high levels:


“Thyroid hormone [PLEASE SAY T3] is a major regulator of metabolism and energy expenditure, is directly involved in the control of insulin secretion and glucose homeostasis [3, 4], and has been shown to preserve beta-cell viability and proliferation [5, 6]. Hyperthyroid individuals have an increased insulin secretion [7] and higher free triiodothyronine [T3] levels are specifically associated with improved insulin secretion in individuals with prediabetes [8]. However, the deleterious effect of thyrotoxicosis on glucose metabolism has also been recognized for decades [9]. Excess thyroid hormone [PLEASE SAY EXCESS T3 AND/OR T4 SINCE EITHER OR BOTH COULD BE HIGH IN HYPER] (i.e. hyperthyroidism) causes increased liver gluconeogenesis and peripheral insulin resistance and is associated with glucose intolerance [10, 11, 12, 13]. Interestingly, lack of thyroid hormone [PLEASE SAY T4 AND/OR T3 BECAUSE EITHER OR BOTH COULD BE LOW IN HYPO] is also associated with a decrease in peripheral insulin sensitivity and glucose intolerance [14] and treatment of hypothyroidism has been shown to improve insulin sensitivity.” (5)

Please, researchers, SPECIFY the hormone that has a direct effect on a physiological parameter, instead of generalizing vaguely so that you can include the only thyroid hormone you bothered to measure (T4).

Focus on the T3 hormone that directly interacts with glucose tolerance and insulin sensitivity, since that is what your study is about.

Your study is incapacitated to the degree that it does not measure T3 and treat it like a continuous variable throughout & beyond the reference range. This crucial omission forces you to conclude with vague things like “The exact mechanism or mechanisms that are involved in the association need to be investigated.” (1)

You know that T3 is directly involved in the mechanisms.  Go measure it and investigate them.

Go to the heart of the issue for all human beings including those of us taking thyroid hormones.

T3 is the great equalizer.

T3 is relevant to all humans, including those on therapy and those not on thyroid therapy, regardless of thyroid gland status.

  • Tania S. Smith


(1) Harrar, S. (2019 January 16). Low Thyroid Hormone Raises Risk for Type 2 Diabetes. EndocrineWeb. Retrieved from https://www.endocrineweb.com/news/diabetes/55372-low-thyroid-hormone-raises-risk-type-2-diabetes

(2) Hoermann, Rudolf, Midgley, J. E. M., Giacobino, A., Eckl, W. A., Wahl, H. G., Dietrich, J. W., & Larisch, R. (2014). Homeostatic equilibria between free thyroid hormones and pituitary thyrotropin are modulated by various influences including age, body mass index and treatment. Clinical Endocrinology, 81(6), 907–915.

(3) Brent, G. A. (2012). Mechanisms of thyroid hormone action. J. Clin Invest. 122(9), 3035-3043. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3433956/

(4) Lin, H. Y., Cody, V, Davis, F.B, Hercbergs, A. A., Luidens, M. K., Mousa, S. A., & Davis, P. J. (2011). Identification and functions of the plasma membrane receptor for thyroid hormone analogues. Discov. Med. 11(59) 337-347.

(5) Chaker, L., Ligthart, S., Korevaar, T. I. M., Hofman, A., Franco, O. H., Peeters, R. P., & Dehghan, A. (2016). Thyroid function and risk of type 2 diabetes: a population-based prospective cohort study. BMC Medicine, 14. https://doi.org/10.1186/s12916-016-0693-4

(6) Healthline. (n.d.). Insulin and Insulin Resistance – The Ultimate Guide. Retrieved from https://www.healthline.com/nutrition/insulin-and-insulin-resistance

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