Abstract
The concept is emerging that low-normal thyroid function, i.e., either higher thyroid-stimulating hormone or lower free thyroxine levels within the euthyroid reference range, could contribute to the development of atherosclerotic cardiovascular disease. It is possible that adverse effects of low-normal thyroid function on cardiovascular outcome may be particularly relevant for specific populations, such as younger people and subjects with high cardiovascular risk. Low-normal thyroid function probably relates to modest increases in plasma total cholesterol, low density lipoprotein cholesterol, triglycerides and insulin resistance, but effects on high density lipoprotein (HDL) cholesterol and non-alcoholic fatty liver disease are inconsistent. Low-normal thyroid function may enhance plasma cholesteryl ester transfer, and contribute to an impaired ability of HDL to inhibit oxidative modification of LDL, reflecting pro-atherogenic alterations in lipoprotein metabolism and HDL function, respectively. Low-normal thyroid function also confers lower levels of bilirubin, a strong natural anti-oxidant. Remarkably, all these effects of low-normal thyroid functional status appear to be more outspoken in the context of chronic hyperglycemia and/or insulin resistance. Collectively, these data support the concept that low-normal thyroid function may adversely affect several processes which conceivably contribute to the pathogenesis of atherosclerotic cardiovascular disease, beyond effects on conventional lipoprotein measures.
Highlights
It is widely appreciated that overt hypothyroidism adversely affects cardiovascular morbidity and mortality [1,2]
We have delineated accumulating evidence which supports the concept that low-normal thyroid function, i.e., either higher thyroidstimulating hormone (TSH) or lower FT4 levels within the euthyroid range, may play a pathogenetic role in the development of atherosclerotic cardiovascular disease
The extent to which low-normal thyroid function impacts on cardiovascular outcome is still unclear. It is unknown whether possible adverse effects of low-normal thyroid function on cardiovascular outcome may be relevant for specific populations, such as younger people and subjects at high cardiovascular risk
Summary
It is widely appreciated that overt hypothyroidism adversely affects cardiovascular morbidity and mortality [1,2]. This report showed that SCH is associated with higher systolic blood pressure, higher plasma total cholesterol, low density lipoprotein (LDL) cholesterol and triglycerides [22] It remains to be established in how far greater cIMT in SCH is attributable to these cardiovascular risk factors. Women with higher TSH levels within the normal range were positively and linearly associated with mortality from CHD (hazard ratio upper vs lower tertile, 1.69) This association remained significant after adjustment for conventional cardiovascular risk factors, and was only present in non-smokers. The relationship of lipoprotein measures with TSH and/or FT4 were rather low (correlation coefficients < 0.12) Taken together, these studies suggests that low-normal thyroid function may give rise to small increases in plasma levels of apoB-containing lipoproteins, in keeping with qualitatively comparable lipoprotein alterations in SCH. Thyroid hormones have multifaceted and crucial roles in intracellular lipid homeostasis, as well as in plasma lipoprotein metabolism [30,31,33,44]
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