Is there connection between thyroid hormones and insulin? by Connie b. Dellobuono
Thyroid hormones are necessary for the body to metabolize carbohydrates, as well as for the pancreas to properly function (the organ producing insulin). Low thyroid hormones cause a drop in insulin levels — insulin is a hormone needed to take sugar from the blood to different cells throughout the body.
Hypothyroid patients show a reduced glucose tolerance test because of a decrease in intestinal glucose absorption and a sometimes reduced glucose turnover.
- Studies have found that diabetes and thyroid disorders tend to coexist in patients. Both conditions involve a dysfunction of the endocrine system.
- Hypothyroidism caused by pituitary dysfunction
This pattern is caused by high cortisol. Cortisol, in turn, is elevated in response to active infection; (1) blood sugar dysregulation, hypoglycemia, insulin resistance, or chronic stress; (2) or pregnancy. These stressors fatigue the pituitary gland; as a result, it can’t release enough thyroid-stimulating hormone (TSH) to stimulate the thyroid gland to produce T4 and T3. In other words, there is nothing wrong with the thyroid gland itself; the problem lies with the pituitary gland. The key to correcting this pattern is to resolve the underlying causes of pituitary dysfunction by treating infection, balancing blood sugar, improving insulin sensitivity, and helping patients find ways to reduce their stress levels.
Answer by Connie b. Dellobuono:
Thyroid hormones affect all cells in the body and is part of the hypothalamic–pituitary–thyroid axis (HPT axis for short, aka thyroid homeostasis or thyrotropic feedback control) which is a part of the neuroendocrine system responsible for the regulation of metabolism.
From the American Diabetes Association:
The relationship between the levels of circulating thyroid hormones and the action of insulin on adipose tissue was investigated in 6 hypothyroid patients and 6 hyperthyroid patients, all untreated, and 8 healthy control subjects. All were matched for age, body weight, and fat cell size. Gluteal s.c. adipose tissue was used. The insulin receptor number in isolated adipocytes was increased by 70% in hypothyroldism and decreased by 40% in hyperthyroidism. The sensitivities of the effects of insulin on lipolysis and glucose oxidation were increased fourfold in hypothyroidism and decreased fivefold in hyperthyroidism. The maximum insulin-induced glucose oxidation (insulin responsiveness) was inhibited by 60% in hypothyroidism and enhanced by 180% in hyperthyroidism. The thyroid hormone concentration was significantly correlated with insulin receptor number (r = −0.72), insulin responsiveness (r = 0.71), and insulin sensitivity (r = −0.75). It is suggested that thyroid hormones regulate the effect of insulin on adipose tissue, which occurs at the receptor and postreceptor levels of insulin action.
Received April 5, 1983.
I would help my body achieve balance in all these hormones by eating selenium rich foods (seafood), avoiding toxins and eating whole foods.
Where does intestinal sulfatase come from? You guessed it: healthy gut bacteria. Intestinal dysbiosis, an imbalance between pathogenic and beneficial bacteria in the gut, significantly reducesthe conversion of T3S and T3AC to T3. This is one reason why people with poor gut function may have thyroid symptoms but normal lab results.
Inflammation in the gut also reduces T3 by raising cortisol. Cortisol decreases active T3 levels while increasing levels of inactive T3. 1
Studies have also shown that cell walls of intestinal bacteria, called lipopolysaccharides (LPS), negatively effect thyroid metabolism in several ways. LPS:
- reduce thyroid hormone levels;
- dull thyroid hormone receptor sites;
- increase amounts of inactive T3;
- decrease TSH; and
- promote autoimmune thyroid disease (AITD).