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Does thyroid function have relationship with the overweight/obesity of post-menopause?

Today, more than 1.4 billion adults aged 20 and older are overweight. Of these, over 200 million men and nearly 300 million women are obese. The prevalence of obesity is even more severe in post-menopausal women, due to declining estrogen levels, increased FSH hormone, and reduced energy expenditure. Furthermore, other endogenous hormones, such as thyroid hormones, may contribute to post-menopausal obesity. However, it has been challenging to evaluate the effect of thyroid hormones on weight gain in the post-menopausal state, especially when using traditional indicators of fat mass such as body mass index (BMI) and waist circumference. First, serum thyroid-stimulating hormone (TSH) concentrations and the prevalence of thyroid dysfunction increase along with menopause and aging due to decreased iodine absorption capacity and daily production of triiodothyroxine (T3) and thyroxine (T4).

Second, post-menopausal women experienced changes in body fat characterized by increased weight gain in overall fat mass and, primarily, central adiposity. Body mass index and waist circumference, used as common indicators of obesity, could hardly distinguish body fat distribution in post-menopausal women. For the reasons stated above, the relationship between thyroid hormones and general obesity as well as regional adiposity indicated as the area of visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) remains at the center of the debate both in subjects with dysfunction thyroid than in euthyroid individuals. Since obesity is known as a risk factor for cardiovascular disease, determining potential risk factors for anatomical fat accumulation during this period of women’s lives represents an important health objective.

To solve this puzzle, scientists at Chengdu Hospital in Sichuan, China, explored the relationship between serum thyroid hormones and MRI-determined obesity in a sample of euthyroid post-menopausal women. In this cross-sectional study of 540 euthyroid postmenopausal women, they demonstrated that VAT rather than SAT was negatively correlated with free hormone (fT4) and positively correlated with fT3 and fT3/fT4. However, common parameters of obesity assessed by BMI and waist circumferences were not associated with thyroid hormones. Furthermore, we found no relationship between body fat distribution and TSH. Furthermore, in agreement with previous investigations, the researchers found that fT3 and fT4 levels were inversely correlated with VAT in euthyroid post-menopausal women. Interestingly, scientists have found no correlation between SAT and thyroid hormones.

Alevizaki’s results showed that SAT was negatively associated with fT4 and positively associated with TSH among overweight euthyroid individuals. Westerink et al., however, observed that TSH levels in the normal range were associated with increased VAT in patients with vascular disease older than 66 years. This could be partially explained by the different functional characteristics of abdominal VAT and SAT with different physiological and metabolic responses in managing excess fat. The strengths of this study are that the quantitative determination of VAT and SAT was precisely assessed by magnetic resonance imaging (MRI), which more accurately described the distribution of body fat in postmenopausal women. The data collectively suggest that slight differences in thyroid function parameters may reflect increased intra-abdominal fat.

Further longitudinal studies are needed to better understand the causality between serum fT4 or fT3 levels and regional adiposity in post-menopausal women with regular thyroid function. Until further confirmatory results, it is possible that the contribution of the thyroid to overweight or becoming obese for menopausal women is not as stringent or conditioning.

  • Edited by Dr. Gianfrancesco Cormaci, PhD, specialist in Clinical Biochemistry.

Scientific references

Yang Q et al. Endokrynol Pol. 2020; 71(4):229-305.

Siemińska L et al. Endokrynol Pol. 2015; 66(5):394.

Roef G et al. Eur J Endocrinol. 2012; 167(5):719–726.

Westerink J et al. Eur J Clin Invest. 2011; 41(2):159-66.

Alevizaki M et al. Eur J Endocrinol. 2009; 161(3):459.

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Dott. Gianfrancesco Cormaci
Dott. Gianfrancesco Cormaci
Laurea in Medicina e Chirurgia nel 1998, specialista in Biochimica Clinica dal 2002, ha conseguito dottorato in Neurobiologia nel 2006. Ex-ricercatore, ha trascorso 5 anni negli USA alle dipendenze dell' NIH/NIDA e poi della Johns Hopkins University. Guardia medica presso la casa di Cura Sant'Agata a Catania. In libera professione, si occupa di Medicina Preventiva personalizzata e intolleranze alimentari. Detentore di un brevetto per la fabbricazione di sfarinati gluten-free a partire da regolare farina di grano. Responsabile della sezione R&D della CoFood s.r.l. per la ricerca e sviluppo di nuovi prodotti alimentari, inclusi quelli a fini medici speciali.

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