In this article, we focus on menopause from a metabolic point of view, looking at cardiovascular health, lipid profile, diabetes, and obesity.
Menopause is the cessation of ovarian function, with loss of reproductive hormone production and irreversible loss of fertility. The physiology of menopause is complex and incompletely understood. Globally, menopause occurs around the age of 49 years. The hormonal changes of menopausal transition may result in both symptoms and long-term systemic effects, mostly adverse effects on cardiometabolic and musculoskeletal health.2
Oestrogen depletion following menopause puts women at increased risk of cardiovascular disease (CVD), mainly ischaemic heart disease. This is most common in cases of premature menopause.1 With regard to dyslipidaemia, as women enter menopause, they demonstrate a lipid profile characterised by an increase in total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), triglycerides (TG), apolipoprotein B (apoB), LDL-C/apoB ratio, as well as a decrease in high-density lipoprotein cholesterol (HDL-C) concentrations.1
The association between transition to menopause and CVD is largely evident for women with a history of early menopause (EM), which is menopause under age 45, and for those with premature ovarian insufficiency (POI), with age at menopause <40 years. EM and POI are associated with increased risk of overall coronary heart disease (CHD).1
Transition to menopause leads to metabolic issues, such as increase in abdominal obesity, atherogenic dyslipidaemia, dysregulation of glucose homeostasis and artirial hypertension (AH).
Transition to menopause leads to body fat redistribution, characterised by increased visceral adipose tissue deposit, with almost 50% greater intra-abdominal fat area. Postmenopausal women are at two-fold increased risk of non-alcoholic fatty liver disease (NAFLD).1
The presence of oestrogen receptor in the liver, skeletal muscles and adipose tissue, which affect glucose uptake, and pancreatic β-cells affecting insulin secretion, provide the basis for the impairment in glucose homeostasis during and after transition to menopause.1
“The decline in oestrogen concentrations during menopause leads to impaired endothelial and vascular function and increased systemic inflammation, further enhancing the atherosclerotic process. Moreover, transition to menopause leads to accumulation of several CVD risk factors, such as abdominal adiposity, atherogenic dyslipidaemia, insulin resistance and AH, which may be reversed after prompt administration of menopausal hormone therapy (MHT),” explained Anagnostis et al (2023).
MHT exerts many beneficial effects on lipid profile and glucose homeostasis as well as direct arterial effects and may reduce CVD risk if initiated promptly (under the age of 60 or within 10 years of the final menstrual period).
Transdermal oestradiol and micronised progesterone or dydrogesterone are the safest regimens in terms of venous thromboembolic events (VTE) and breast cancer risk.1
MHT improves most of the cardiometabolic risk factors, exerting a differential effect according to dose and route of oestrogen administration and the type of progestogen (safest with the transdermal 17β-oestradiol and micronised progesterone or dydrogesterone). MHT may reduce CVD risk if initiated promptly.1
References available on request.