## 1 Background  
The global rise in obesity is linked to a concurrent increase in the prevalence of metabolic syndrome and its cardiovascular sequelae [1]. This trend is particularly pronounced among post-menopausal women [2], who exhibit a higher prevalence of obesity due to menopause-related shifts in energy metabolism, including diminished fat oxidation and decreased spontaneous physical activity [3; 4], leading to a decline in overall energy expenditure [3]. Additionally, the deficiency in estrogen production during menopause contributes to the loss of muscle mass and the increase in fat mass, particularly in central areas of the body, such as the abdomen and visceral regions. Consequently, this redistribution of body fat increases the risk of cardiovascular diseases [5; 6].  
Thyroid hormones play a pivotal role in governing metabolic processes, encompassing energy expenditure and thermogenesis, as well as the regulation of protein, carbohydrate, and lipid metabolism, and thyroid dysfunction has the potential to precipitate obesity or give rise to conditions associated with it [7]. Thyroid impairment or dysfunction, such as hypothyroidism, can mimic metabolic syndrome characteristics, including weight gain and altered body composition, and can potentially elevate cardiovascular risk through associations with insulin resistance and dyslipidemia [7; 8].  
Focusing on thyroid function, total and free thyroid hormones, (including free-triiodothyonine (FT3) and free-thyroxine (FT4) levels and the FT3/FT4 ratio) higher serum thyroid-stimulating hormone (TSH) concentrations and low serum FT4 levels were reported in obese individuals in comparison to non-obese ones. Observational studies reported abnormal thyroid hormone levels in obesity, suggesting increased deiodinase activity and a compensatory mechanism in total triiodothyonine (TT3) levels to counteract obesity-related fat accumulation [7]. It should be noted that the observed increase in FT3 levels among obese individuals, which govern both resting metabolic rate and thermogenesis, could potentially represent a compensatory mechanism aimed at addressing the heightened central fat accumulation associated with this condition [9; 10]: to facilitate fat-burning through the elevation of basal metabolic rate and the stimulation of brown adipose tissue production [7]. However, the interplay between thyroid function and age-related hormonal and adipose changes, particularly at a time when women are undergoing a transition towards an increased cardiovascular risk, such as during menopause, remains inadequately understood [7; 9].  
The relative inconsistency of research findings necessitates further exploration into how societal and health factors can influence fat remodeling and cardiovascular risk mitigation in post-menopausal women. This has been recently reaffirmed in a milestone article published in _The Lancet_[11]. Based on these considerations, our study aimed to conduct a detailed metabolic assessment of post-menopausal women within 2 to 8 years post-menopausal, focusing on thyroid function, blood pressure (BP), arterial stiffness, body composition, and cardiovascular risk. Our population sample was stratified into two groups, comparing those who have gained weight (menopausal weight gain group--MWGG) to those who have maintained weight (menopausal weight maintenance group--MWMG).  
We further explored the potential correlation between cardiovascular parameters and physical and metabolic changes in our selected menopausal women with arterial hypertension.