{'fraction_non_alphanumeric': 0.022581544466127684, 'fraction_numerical': 0.0036241984945637024, 'mean_word_length': 5.58348623853211, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 1, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Metabolic syndrome and cardiovascular risk factors in the menopausal transition

Alterations of the hormonal profile begin in the early 40s, before the complete cessation of menses, consequently changes in risk factors for cardiovascular disease (CVD), such as lipids and anthropometric characteristics could also be observed in this period. It has been necessary to investigate the behavior of these factors during the transition to menopause and still it is not clear when metabolic alterations occur. Some authors have found that perimenopausal women did not show more adverse alterations in lipids than premenopausal ones [1]. On the other hand, others have described an increase in atherogenic lipoproteins [2], although not always associated with hormonal status [3]. By other side, postmenopausal status is associated with an increased risk of metabolic syndrome, even after adjusting for confounding variables, such as age, body mass index, or physical inactivity [4]. Moreover, the risk of CVD attributed to the metabolic syndrome appears to be especially high in women; it is estimated that half of all cardiovascular events in women are related to this syndrome. The etiology of the metabolic syndrome is unknown, but it is thought to be a cluster of factors and its underlying pathophysiology is related to increased visceral obesity and insulin resistance. There are a few studies nowadays that investigate the behavior of the metabolic syndrome during the transition to the menopause and it is not clear when metabolic alterations begin. With regard to the standard methods of evaluating insulin resistance, such as the hyperinsulinemic euglycemic clamp technique and the intravenous glucose tolerance test, they are considered to be impractical in clinical practice and difficult to perform in population-based research studies. More simple but indirect methods have been suggested for quantification of insulin resistance, such as the homeostasis model assessment, the quantitative insulin sensitivity check index (QUICKI) and, more recently, the triglyceride/HDL-cholesterol index [5]. Some authors suggest that the latter offers a good surrogate method in the identification of insulinresistant subjects, given the well-standardized methods for the evaluation of triglycerides and HDLcholesterol, and the good correlation found with the gold standard method. On the other hand, changes in androgen levels during the menopausal transition are controversial. Although it is generally accepted that testosterone levels do not change significantly in this period of life, some authors have found a decrease in testosterone, androstenedione, and sex hormone binding globulin (SHBG) 2 years around menopause [6]. Meanwhile, other authors consider that this is a period of relative hyperandrogenism as a consequence of the greater decrease in estrogens in comparison with the decrease in androgens [7]. However, the androgenic profile in the menopausal transition has been scarcely studied. Our aim was to assess if there is a relationship between the main components of the metabolic syndrome, insulin resistance, and androgens with the menopausal status across the menopausal transition from preto postmenopausal state, including the earlier and later phases of perimenopause. In our studies, we evaluated four groups of women: premenopausal, menopausal transition women with menstrual bleeding, menopausal transition women with 3–6 months amenorrhea, and postmenopausal women. The incidence of metabolic syndrome, increased across the menopausal transition [8]. None of the