Table 1.
CVD risk factor | Men | Women | Evidence/potential mechanisms |
---|---|---|---|
Impaired glucose regulationA |
↑ Incidence of impaired fasting glucose ↑ Incidence of diabetes at earlier ages ↓ Insulin sensitivity |
↑ Incidence of impaired glucose tolerance ↓ Incidence of diabetes ↑ Insulin sensitivity |
Estrogens may confer a protective effect on insulin-glucose homeostasis [172–178]: - Reduction in inflammation, reactive oxygen species, hepatic glucose production, and central and visceral adiposity. - Improves glucose uptake by skeletal muscle via activation of PPAR-γ. Testosterone appears to exhibit a U-shaped association with insulin resistance [179–183]: - Excess testosterone in both sexes is associated with dysglycemia and inhibits myocyte, adipocyte insulin in women. - Testosterone associates with reduced visceral and central adiposity, as well as decreased waist-to-hip ratio in men. |
DyslipidemiaB |
↓ HDL-C ↑ LDL-C ↑ VLDL ↑ Total plasma TG ↑ FFA oxidation at rest |
↑ HDL-C ↓ LDL-C ↓ VLDL ↓ Total plasma TG ↑ FFA storage at rest |
Sexual dimorphism is observed in lipid profiles of premenopausal women compared to men [184–187] |
HypertensionC |
↑ Systolic BP ↑ Incident hypertension ↓ Salt sensitivity Older ages ↓ Incident hypertension All ages ↑ Diastolic BP ↓ Survival with hypertension |
Younger ages ↓ Systolic BP ↓ Incident hypertension ↑ Salt sensitivity Older ages (postmenopausal) ↑ Incident hypertension All ages ↓ Diastolic BP ↑ Survival with hypertension |
Endogenous estrogen has a BP lowering effect [118, 191–194]. - Possible mechanisms include RAAS and endothelin system, oxidative stress, nitric oxide production, and salt sensitivity. Androgens (testosterone) have pro-hypertensive properties. - Possible mechanisms include blunting of the pressure-natriuresis relationship, RAAS, and oxidative stress. |
ObesityD |
↓ Obesity [195] ↑ Lean tissue; ↓ Total fat ↑ Visceral adipose tissue |
↑ Obesity [195] ↓ Lean tissue; ↑ Total fat ↑ Subcutaneous adipose tissue |
Estrogen and androgens impact energy utilization, storage, and fat distribution [196–199]. |
ABroad category of prediabetic syndromes, including impaired fasting glucose (WHO criteria, > 110 mg/dL; ADA criteria, > 100 mg/dL) as well as impaired glucose tolerance, a condition in which a given concentration of insulin, endogenous or exogenous, is accompanied by an inadequate glucose response
BAn elevation in circulating total cholesterol, low-density lipoprotein, high-density lipoprotein, and/or triglycerides
CDefined by ACC/AHA 2017 guidelines: systolic blood pressure ≥ 130 mmHg or diastolic blood pressure ≥ 80 mmHg
DDefined by a body mass index ≥ 30 kg/m2
BP blood pressure, FFA free fatty acids, HDL-C high-density lipoprotein cholesterol, LDL-C low-density lipoprotein cholesterol, PPAR-γ peroxisome proliferator-activator gamma, RAAS renin-angiotensin-aldosterone system, VLDL-C very low-density lipoprotein cholesterol