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Worldwide, the high prevalence of the Polycystic Ovary Syndrome (PCOS), a heritable cause of ovarian infertility, is an evolutionary paradox, which provides insight into the susceptibility of well-fed human populations to cardiovascular disease and diabetes. We propose that PCOS, Type 2 diabetes (T2D) and the Metabolic Syndrome are modern phenotypic expressions of a metabolic genotype attuned to the dietary and energetic conditions of the Pleistocene. This metabolic "Fertility First" rather than "Thrifty" genotype persisted at high prevalence throughout the entire agrarian period-from around 12,000 years ago until 1800 AD-primarily, we contend, because it conferred a fertility advantage in an environment defined by chronic and often severe seasonal food shortage. Conversely, we argue that genetic adaptations to a high carbohydrate, low protein agrarian diet, with increased sensitivity to insulin action, were constrained because these adaptations compromised fertility by raising the lower bound of body weight and energy intake optimal for ovulation and reproduction. After 1800, the progressive attainment of dietary energy sufficiency released human populations from this constraint. This release, through the powerful mechanism of fertility selection, increased, in decades rather than centuries, the prevalence of a genotype better suited to carbohydrate metabolism. This putative mechanism for rapid and recent human evolution can explain the lower susceptibility to T2D of today's Europid populations. This hypothesis predicts that the increasing rates of diabetes and cardiovascular disease, which typically accompany economic development, will be tempered by natural, but particularly fertility, selection against the conserved ancestral genotypes that currently underpin them.

There are no reported studies on the effects of ambient air pollution on emergency department (ED) attendances in Sydney, Australia. This study aimed to determine associations between ambient air pollutants and ED attendances for cardiovascular disease (CVD) in those aged 65+ years. We constructed daily time series of hospital ED attendances, air pollutants and meteorological factors for the Sydney metropolitan area from 1 January 1997 to 31 December 2001. We used generalised linear models to determine associations between daily air pollution and daily ED attendances and controlled for the effects of long-term trends, seasonality, weather and other potential confounders. Increased ED attendances for all CVD, cardiac disease and ischaemic heart disease were seen with 24-h particulate pollution, 1-h NO(2), 8-h CO and 24-h SO(2). Air pollutants were associated with decreased ED attendances for stroke. The effects of air pollutants on CVD, cardiac disease and stroke attendances were generally greater in the cool period compared to the warm period. The single-pollutant effects of CO, O(3), NO(2) and SO(2) were essentially unchanged in two-pollutant models. Although air pollution levels in Sydney are relatively low compared to similar cities, we have demonstrated associations between ambient air pollutants and ED attendances for CVD in people aged 65+ years. Our study adds to the growing evidence for the effects of ambient air pollution on CVD outcomes even at relatively low ambient concentrations.