Carbohydrate Restriction as an Adjunct Treatment for Hypothyroidism

by Sam Knox

One of the functions of T3, the active thyroid hormone, is metabolizing blood sugar. Other things equal, the higher the carbohydrate content of a diet the higher the average levels of blood sugar.

Sure enough, the isocaloric addition of carbohydrate to a diet elevates blood levels of T3.

This is not good news.

While adding carbohydrate to a diet increases blood levels of T3, it does not also increase basal metabolism. This suggests that the additional T3 is used exclusively to metabolize higher levels of blood sugar.

The implications for hypothyroidism should be obvious: The smaller the amount of T3 required to process blood sugar, the greater the amount available to perform more important metabolic functions.

It follows that if high-carbohydrate diets require higher levels of thyroid hormones, they also require higher levels of their dietary precursors, especially iodine. A persuasive case has already been made that, perhaps in most instances, a high level of dietary carbohydrate, not a lack of iodine in the environment, causes iodine-deficiency diseases.

Hypothyroidism is a distressingly common condition, one from which I suffer myself. My diet includes sufficient amounts of the dietary precursors of thyroid hormones, avoids goitrogens (substances in food that inhibit the production of thyroid hormones) and restricts carbohydrate.


1. Colorado State Online Textbooks: Mechanism of Action and Physiologic Effects of Thyroid Hormones

“Thyroid hormones stimulate almost all aspects of carbohydrate metabolism, including enhancement of insulin-dependent entry of glucose into cells …”

2. Kim, et al: A hypothesis of synergism: the interrelationship of T3 and insulin to disturbances in metabolic homeostasis; Med Hypotheses, 2002 Dec;59(6):660-6.

“In summary, the synergism between T3 and insulin appears to be responsible for the expression of the enzymes required for the entire process of metabolism of glucose…”

3. Spaulding, et al: Effect of caloric restriction and dietary composition of serum T3 and reverse T3 in man; Journal of Clinical Endocrinology & Metabolism, Jan, 1976; 42 (1): 197–200

“We conclude that dietary carbohydrate is an important regulatory factor in T3 production in man.”

4. Danforth, et al: Dietary-induced Alterations in Thyroid Hormone Metabolism during Overnutrition, Clin Invest. 1979 November; 64(5): 1336–1347

“During the weight-maintenance phases of the long-term overfeeding studies, concentrations of T3 were increased when carbohydrate was isocalorically substituted for fat in the diet.”

5. Bisschop PH, et al: Isocaloric carbohydrate deprivation induces protein catabolism despite a low T3-syndrome in healthy men; Clinical Endocrinology, 2001; 54: 75-80

“…dietary carbohydrate content did not influence resting energy expenditure.”

6. Kopp W.: Nutrition, evolution and thyroid hormone levels – a link to iodine deficiency disorders?; Med Hypotheses. 2004;62(6):871-5.

Abstract: An increased iodine requirement as a result of significant changes in human nutrition rather than a decreased environmental iodine supply is suggested to represent the main cause of the iodine deficiency disorders (IDD). The pathomechanism proposed is based on the fact that serum concentrations of thyroid hormones, especially of trijodothyronine (T3), are dependent on the amount of dietary carbohydrate. High-carbohydrate diets are associated with significantly higher serum T3 concentrations, compared with very low-carbohydrate diets. While our Paleolithic ancestors subsisted on a very low carbohydrate/high protein diet, the agricultural revolution about 10,000 years ago brought about a significant increase in dietary carbohydrate. These nutritional changes have increased T3 levels significantly. Higher T3 levels are associated with an enhanced T3 production and an increased iodine requirement. The higher iodine requirement exceeds the availability of iodine from environmental sources in many regions of the world, resulting in the development of IDD.