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

Abstract

Women's evolution for nurturing and fat accumulation, which historically yielded health and longevity advantages against scarcity, may now be counteracted by increasing risks in the obesogenic environment, recently shown by narrowing gender health gap. Women's differential metabolism/disease risks, i.e. in fat accumulation/distribution, exemplified during puberty/adolescence, suggest gender dimorphism with obesity outcomes. Women's higher body fat percentage than men, even with equal body mass index, may be a better risk predictor. Differential metabolic responses to weight-reduction diets, with women's lower abdominal fat loss, better response to high-protein vs. high-carbohydrate diets, higher risks with sedentariness vs. exercise benefits, and tendency toward delayed manifestation of central obesity, metabolic syndrome, diabetes, cardiovascular disease, and certain cancers until menopause-but accelerated thereafter-suggest a need for differing metabolic and chronological perspectives for prevention/intervention. These perspectives, including women's differential responses to lifestyle changes, strongly support further research with a gender nutrition emphasis within predictive, preventive, and personalized medicine.

Figure 1

Prevalence of morbid obesity among adults aged 16+ years: Health Survey for England 1993–2010 [13]. The rise of morbid obesity (≥40 kg/m²) has been led by women in developed, high-income countries, i.e. in the UK where between 1993 and 2010, the prevalence of morbid obesity was consistently higher among women (increasing from 1.5% in 1993 to 3.8% in 2010) than among men (increasing from 0.3% in 1993 to 1.6% in 2010).

Figure 2

Gender-environment interaction effect on obesity, health risks, life expectancy (LE), and healthy life expectancy (HLE). Obesogenic (increased calories and reduced mobility) conditions in Western lifestyles, compared to historically restrictive dietary conditions and high mobility, have conferred a great burden of overconsumption and obesity. Women's innate tendency toward fat accumulation and higher lifelong body fat percentage could make them more vulnerable and have contributed to the recent decline in the gender gap (females-males, years) of life expectancy (LE) and healthy LE (HLE) years.

Figure 3

Life expectancy at age 55 with/without disability in activities of daily living (univariate analysis). Error bars represent 95% confidence intervals of disability-free and total life expectancy [31]. The average LE at 55 years of age is 24.0 years for men and 28.2 years for women (excluding underweight individuals). The longest disability-free LE was found with a BMI between 18.5 and 22.9 for women and 25.0 and 29.9 for men. Mild obesity (BMI 30–34.9) did not shorten total LE, but at age 55, it shortened disability-free life to 2.9 years for males and 4.3 years for females compared to high normal weight (BMI 23–24.9). Severely obese men live an average of 6.0 years less free from ADL disability and women for 8.4 less years. For men, low normal weight (BMI 18.5-22.9) lowers both total and disability-free LE.

Figure 4

Overview of insulin resistance induced by estrogen deficiency, and subsequent disturbances in metabolic tissues [54]. As estrogen participates in the regulation of glucose homeostasis, estrogen deficiency, like that seen in post menopausal women, is strongly linked to the development of insulin resistance and subsequent impairments manifested in the pancreas, liver, and muscle and adipose tissue, key organs influencing risk of chronic metabolic disease.