Insulin is commonly discussed as a blood sugar regulating hormone, but it is deeply integrated with the sex hormone system. Elevated insulin stimulates androgen production in the ovaries in women with insulin resistance, contributing to conditions such as polycystic ovarian syndrome and elevated testosterone with unfavourable oestrogen ratios. In men, insulin resistance drives the conversion of testosterone to oestrogen via aromatase, reduces sex hormone-binding globulin, and creates a low-testosterone, high-oestrogen state associated with central fat gain and muscle loss.
The Thyroid Connection
Insulin resistance impairs the conversion of T4 to the active T3 thyroid hormone, effectively reducing the amount of active thyroid hormone available to cells even when TSH and T4 levels appear normal. This is one of the mechanisms behind the common clinical picture of normal thyroid function tests alongside persistent hypothyroid symptoms in adults who are also insulin resistant. Resolving the insulin resistance often partially or fully resolves the thyroid symptoms without any thyroid-specific treatment.
The Interventions With the Best Evidence
- Reducing refined carbohydrate intake: the most direct intervention for lowering fasting insulin and improving insulin sensitivity
- Resistance training: improves insulin sensitivity via GLUT-4 transporter upregulation in muscle independently of weight loss
- Losing visceral fat: reduces the inflammatory signalling that drives insulin resistance
- Time-restricted eating: reduces the number of daily insulin spikes even without changing total calorie intake
- Aerobic exercise: zone 2 cardio specifically improves mitochondrial function and insulin sensitivity in muscle cells
Sources
- Diamanti-Kandarakis, E., & Dunaif, A. (2012). Insulin resistance and the polycystic ovary syndrome revisited. Endocrine Reviews, 33(6), 981-1030.
- Livingstone, C., & Collison, M. (2002). Sex steroids and insulin resistance. Clinical Science, 102(2), 151-166.
- Sandhu, M.S., et al. (2002). Insulin, insulin-like growth factor-I (IGF-I), IGF binding proteins, their biologic interactions, and colorectal cancer. Journal of the National Cancer Institute, 94(13), 972-980.