Women's higher health risks in the obesogenic environment: a gender nutrition approach to metabolic dimorphism with predictive, preventive, and personalised medicine

Women's evolution vs. food scarcity, which necessitated effective fat accumulation for preparing available energy and nutrients for fertility and feeding/caring of offspring, has long translated to a health and longevity advantage. However, this may now be counteracted by the ‘obesogenic’ environment.Pubertal gender dichotomy of girls accumulating fat vs. boys losing fat and growing muscles and height [1,2] illustrates an obesity-related aspect of gender differential adaptation to scarcity and women's advantage. However, extreme changes in the environment, particularly increasing food availability/accessibility and reduced mobility, as well as increased calories and reduced nutrient density in processed foods—together defined as an obesogenic environment—have conferred a great burden of overconsumption and obesity (Figure 1), unrelated to nutritional sufficiency/deficiency [3]. This may be especially critical in females, given their innate tendency toward fat accumulation and risks from nutrient-exhausting pregnancy/lactation, and resultant deficiency disorders [4-6]. This new metabolic ‘mismatch’ in women could greatly contribute to the recent decline in the gender gap in life expectancy (LE) and in healthy LE (HLE), associated with a slowed increase in female LE and HLE compared to males [7-10] (Figure 2), that is gradually narrowing the gender gap [11,12] resulting from increases in the environmental burden on women's health and consequently on the healthcare system.Beyond the general perspective that the declining gender LE gap was associated primarily with changes in smoking and alcohol use [14], a new perspective on women's health should include their specific metabolic risks and differing timetables, i.e. earlier and higher risk of lifelong obesity, differential fat distribution and risk measures, i.e. body mass index (BMI), waist circumference (WC), and delayed risk manifestation to postmenopausal age, which is associated with reduced estrogen protection. He