Skip to content


A later age at menopause onset has been associated with presenting a higher blood pressure (BP) value, although the mediation pathways remain unclear. Recently Wu et al. [1] examined in quantitative manner the mediation effects of various obesity indicators using baseline data from the Guangzhou Biobank Cohort Study (Phase 4). Authors used product of coefficients approach and bootstrapping procedures to assess the mediation effects of body mass index (BMI), waist circumference (WC), waist-to-hip ratio (WHR) and waist-to-height ratio (WHtR) on the association between age at menopause and BP values. They adjusted for various co-variates such as age, education, occupation, family income, smoking, drinking, diet, physical activity, age at menarche, number of births, fasting glucose, triglycerides, and HDL-C. Of a total of 5,429 women with natural menopause, the mean age and mean age at menopause were 60.0 ± 5.8 and 50.3 ± 3.1 years, respectively. The prevalence of hypertension was 29.6%. In women with an age at menopause onset of ≥ 50 years, BMI, WC, WHR and WHtR showed significant mediation effects on the positive association between menopausal age and BP. The adjusted proportion (95% confidence interval) of the mediation effects for those variables were 26.04% (10.40-116.82%), 25.92% (10.19-108.57%), 14.11% (3.59-62.78%), and 23.17% (8.70-95.81%), respectively, for systolic BP values and 22.59% (10.72-53.60%), 20.67% (9.83-49.31%), 9.21% (2.73-23.92%), and 17.19% (7.56-41.31%) for diastolic BP values. In women with a menopausal age of <50 years, no significant association between age at menopause and systolic/diastolic BP values was found. The authors conclude that obesity indicators showed significant mediating effects on the association between having a later age at menopause (50 years or more) and having a higher BP value. They recommend that further longitudinal studies with detailed and accurate measurements of metabolic changes after menopause and sufficient follow-up are needed to confirm these results.


Obesity is a global health problem that increases the morbidity and mortality of patients [2]. The World Health Organization (WHO) defines overweight as a body mass index (BMI) equal to or greater than 25 kg/m2 and obesity as a BMI equal to or greater than 30 kg/m2. Obesity can be classified into class I (BMI 30 to < 35 kg/m2), class II (BMI 35 to < 40 kg/m2) and class III (BMI ≥ 40 kg/m2). An abdominal perimeter is also considered a sign of obesity when it greater than or equal to 102 cm in men and greater than or equal to 88 cm in women [3]. Among the main causes of obesity is the increased consumption of hypercaloric foods and less physical activity. In fact, as a consequence of both quantitative and qualitative changes in diet that have occurred in recent years, related to economic, social, demographic changes and health factors, traditional diets have been replaced by others with a higher energetic density, with a higher consumption of animal fat, more sugar in food and a decrease in the consumption of complex carbohydrates and fiber. These dietary changes, together with a reduction in physical activity at work and during leisure time, have led to a significant increase in the incidence of obesity [4].

Obesity is associated with various disorders, such as diabetes mellitus, hypertension, hypercholesterolemia, heart disease, obstructive sleep apnea, asthma, and arthritis, which contribute to increased morbidity and mortality in patients. In addition, in women obesity is a factor that increases the risk of certain gynecological disorders, such as menstrual disorders, infertility, prolapse and urinary incontinence. Obese women are also at increased risk of endometrial and breast cancer [5]. In the present discussed cohort study of more than 5,000 women with natural menopause, Wu et al. [1] point out that there is a relationship between obesity, later menopause, and hypertension. Their results support what is already known that obesity, especially when associated with excess visceral adiposity, is an important risk factor for arterial hypertension [6]. High blood pressure and obesity, as well as multiple metabolic disorders and inflammation, are highly prevalent in postmenopausal women [7]. Obesity-induced arterial hypertension is characterized by excessive activation of the renin-angiotensin-aldosterone system and the sympathetic nervous system due, in part, to changes in circulating adipokines such as leptin [8]. On the other hand, the results of this study show that obesity is associated with a later menopause, probably due to a longer maintenance of blood estradiol levels. The positive association of BMI and estradiol in obese postmenopausal women has already been clearly demonstrated [9].

It has been hypothesized that the association between obesity and hormones is related to resistance to insulin or other substances derived from the adipose tissue such as adiponectin or leptin [10]. However, it is still a field under intensive research. There is no doubt that the increase in obesity throughout the world population, and especially in postmenopausal women, makes it a subject of special attention and reminds us of the importance of preventing and treating obesity.

Santiago Palacios, MD
Instituto Palacios, Salud y Medicina de la Mujer
Madrid Spain


  1. Wu YJ, Jiang CQ, Zhu T, et al. Obesity indicators as mediators of the association between age at menopause and blood pressure values. Hypertens Res. 2023 Jan 26. doi: 10.1038/s41440-023-01184-3
  2. World Health Organization. Global status report on noncommunicable diseases 2014.
  3. World Health Organization. Obesity and overweight.
  4. Estrategia NAOS (Nutrición, Actividad Física y Prevención de la Obesidad).
  5. Palacios S. Obesity in women’s life: role of GLP-1 agonists. Gynecol Endocrinol. 2022;38(11):889-890.
  6. Borlaug BA. The pathophysiology of heart failure with preserved ejection fraction. Nat Rev Cardiol. 2014;11(9):507-515.
  7. Hall JE, do Carmo JM, da Silva AA, Wang Z, Hall ME. Obesity-induced hypertension: interaction of neurohumoral and renal mechanisms. Circ Res. 2015;116(6):991-1006.
  8. da Silva AA, do Carmo JM, Wang Z, Hall JE. Melanocortin-4 Receptors and Sympathetic Nervous System Activation in Hypertension. Curr Hypertens Rep. 2019;21(6):46.
  9. Santoro N, Crawford SL, Lasley WL, et al. Factors related to declining luteal function in women during the menopausal transition. J Clin Endocrinol Metab. 2008;93(5):1711-1721.
  10. Garaulet M, Pérez-Llamas F, Baraza JC, et al. Body fat distribution in pre-and post-menopausal women: metabolic and anthropometric variables. J Nutr Health Aging. 2002;6(2):123-126.

If you would like to add a comment or contribute to a discussion based on this issue, please contact Menopause Live Editor, Peter Chedraui, at

Having trouble opening PDFs? Download Adobe Reader here.

International Menopause Society

Install International Menopause Society - DEV

Install this application on your home screen for quick and easy access when you’re on the go.

Just tap then “Add to Home Screen”