The aim of this study was to undertake a prospective study of the changes in certain risk factors for cardiovascular disease occurring during menopause.
A longitudinal cohort study of 475 women was followed up for 6 years (Pizarra Study). The final menstrual period was defined after at least 6 months of amenorrhea. The women were classified into three groups: group 1, no menopause at either the first or second study; group 2, no menopause at the first study but menopause at the second study (6 y later); and group 3, menopause at the first study (and also at the second). The following are the main outcome measures used: age; body mass index; waist circumference; waist-to-hip ratio; skinfold thickness; arm circumference; intake of macronutrients (quantitative questionnaire); systolic and diastolic blood pressures; cholesterol, triglycerides; high-density lipoprotein cholesterol; uric acid; homeostasis model assessment of insulin resistance; and the prevalence of obesity, hypertension, type 2 diabetes mellitus, impaired glucose tolerance, and impaired fasting glucose.
None of the cardiovascular risk factors studied changed during the passage from premenopause to postmenopause, independently of age or physical activity.
Menopause is a biological condition of the human species, for which has recently received attempts at medicalization that were not always justified. If menopause is not accompanied by any other cardiovascular risk factor independently of age, the stigma of menopause being considered a risk factor should cease. Although the results have the strength of a prospective study, the sample size forced us to consider these findings as preliminary.
In a longitudinal cohort study, none of the cardiovascular risk factors studied changed during the passage from premenopause to postmenopause, independently of age or physical activity. If menopause is not accompanied by any other cardiovascular risk factor independently of age, the stigma of menopause being considered a risk factor should cease.
From the 1Endocrinology and Nutrition Service, Hospital Carlos Haya, Malaga, Spain; 2CIBER de Diabetes y Metabolismo (CB07/08/0019); and 3CIBER Physiopathology of Obesity and Nutrition (CB06/03/1022), Instituto de Salud Carlos III, Madrid, Spain.
Received September 26, 2008; revised and accepted December 24, 2008.
Funding/support: This work was supported by the Fondo de Investigación Sanitaria (PI041883, PI051307) and Junta de Andalucía (P06/CTS-01684).
Financial disclosure/conflicts of interest: None reported.
Address correspondence to: Federico Soriguer, PhD, Servicio de Endocrinología y Nutrición, Hospital Civil, Plaza del Hospital Civil s/n, 29009 Malaga, Spain. E-mail: email@example.com