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.

Breast cancer (BC), the leading cancer in women, is increasing in prevalence worldwide, concurrent with western metabolic epidemics, that is, obesity, metabolic syndrome, and diabetes, and shares major risk factors with these diseases. The corresponding potential for nutritional contributions toward BC prevention is reviewed and related to critical stages in the life cycle and their implications for carcinogenic and pathometabolic trajectories. BC initiation potentially involves diet-related pro-oxidative, inflammatory, and procarcinogenic processes, that interact through combined lipid/fatty acid peroxidation, estrogen metabolism, and related DNA-adduct/depurination/mutation formation. The pathometabolic trajectory is affected by high estrogen, insulin, and growth factor cascades and resultant accelerated proliferation/progression. Anthropometric risk factors – high birth weight, adult tallness, adiposity/BMI, and weight gain – are often reflective of these trends. A sex-based nutritional approach targets women’s specific risk in western obesogenic environments, associated with increasing fatness, estrogen metabolism, n-6 : n-3 polyunsaturated fatty acid ratio, and n-6 polyunsaturated fatty acid conversion to proinflammatory/carcinogenic eicosanoids, and effects of timing of life events, for example, ages at menarche, full-term pregnancy, and menopause. Recent large-scale studies have confirmed the effectiveness of the evidence-based recommendations against BC risk, emphasizing low-energy density diets, highly nutritious plant-based regimes, physical activity, and body/abdominal adiposity management. Better understanding of dietary inter-relationships with BC, as applied to food intake, selection, combination, and processing/preparation, and recommended patterns, for example, Mediterranean, DASH, plant-based, low energy density, and low glycemic load, with high nutrient/phytonutrient density, would increase public motivation and authoritative support for early/timely prevention, optimally merging with other dietary/health goals, for lifelong BC prevention.

The prenatal period encompasses a critical window for future health and functioning of mother and child. Attention previously focused on undernutrition risk (i.e., in developing countries and famine conditions) shifted to mismatch between prenatal ‘programming’ by undernutrition and postnatal overconsumption (i.e., low birthweight vs rapid postnatal growth), now to overconsumption/overweight throughout the reproductive cycle and short- and long-term health risks, including obesity, diabetes, dyslipidemia and cardiovascular disease. Moreover, overconsumption/overweight do not guarantee adequacy of critical nutrients (i.e., against birth defects or for brain development). Multinutrient supplementation – including zinc, iodine, choline and long-chain polyunsaturated fatty acids, especially n-3 – may have advantages over single-nutrient supplements, for example, iron or folate. Future nutritional care for healthy in utero programming may necessitate individual assessment and follow-up, including preconception nutritional preparation, appropriate weight gain, metabolic balance and food-based regimens enhanced by key nutrient fortification and/or supplementation, warranting further research into nutritional optimization of pregnancy outcomes.

My hypothesis is that higher female sensitivity to increased n-6 polyunsaturated fatty acids and their carcinogenic effect may contribute to the recent Israeli ‘cancer shift’ over heart disease mortality (23.1 vs. 22.3%, 1999). High n-6 polyunsaturated fatty acid intake was the presumed dietary risk underlying the ‘Israeli paradox’, the unexpected gap between ‘ill’ health and ‘good’ diet. Scientific literature and population health surveillance reports were reviewed. Cancer death rates for Israeli Arabs, who consumed a more traditional Mediterranean diet – more monounsaturated fatty acids, mostly olive oil, and less n-6 polyunsaturated fatty acids – are still 1.1–1.7 times (men–women) lower than in Israeli Jews, but are increasing faster (23.6 and 5.1% vs. 5.3 and −3.3%, 1980–2000), concurrently with dietary ‘Israelization’ – specifically, increased intake of n-6 polyunsaturated fatty acids. Israeli-Jewish women attained an earlier, much larger (29 vs. 7%, 1999) ‘cancer : heart disease mortality shift’ (ratio >1.0), ranked much worse for cancer (15th/44 European countries) than men (37th) and heart disease (38th and 34th, respectively), and had much higher cancer prevalence (1 : 3) than Israeli-Arab women (1 : 6), though dietary compositions were similar, save for higher n-6 polyunsaturated fatty acid and polyunsaturated fatty acid : monounsaturated fatty acid ratio. Population studies of Israeli Jews, Arabs, and women support the association of high n-6 polyunsaturated fatty acid intake with increased cancer risk and higher female sensitivity. Research findings suggest that gender and sex hormones may influence n-6 polyunsaturated fatty acid metabolism and carcinogenesis. This appears to be the first time gender has been proposed to modulate national cancer epidemiology, suggesting implications for differential nutritional prevention, warranting further research.

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