Polycystic Ovary Syndrome: An Evolutionary Adaptation to Lifestyle and the Environment

Abstract

Polycystic ovary syndrome (PCOS) is increasingly recognized as a complex metabolic disorder that manifests in genetically susceptible women following a range of negative exposures to nutritional and environmental factors related to contemporary lifestyle. The hypothesis that PCOS phenotypes are derived from a mismatch between ancient genetic survival mechanisms and modern lifestyle practices is supported by a diversity of research findings. The proposed evolutionary model of the pathogenesis of PCOS incorporates evidence related to evolutionary theory, genetic studies, in utero developmental epigenetic programming, transgenerational inheritance, metabolic features including insulin resistance, obesity and the apparent paradox of lean phenotypes, reproductive effects and subfertility, the impact of the microbiome and dysbiosis, endocrine-disrupting chemical exposure, and the influence of lifestyle factors such as poor-quality diet and physical inactivity. Based on these premises, the diverse lines of research are synthesized into a composite evolutionary model of the pathogenesis of PCOS. It is hoped that this model will assist clinicians and patients to understand the importance of lifestyle interventions in the prevention and management of PCOS and provide a conceptual framework for future research. It is appreciated that this theory represents a synthesis of the current evidence and that it is expected to evolve and change over time.

Positive Effects of α-Lactalbumin in the Management of Symptoms of Polycystic Ovary Syndrome

“…In particular, as neonates largely acquire their microbiota from their mothers, one could argue that neonates from mothers with PCOS acquire an altered microbiota which reflects the maternal composition [ 88 ]. The prenatal exposure to maternal hyperandrogenic milieu in pregnant women with PCOS results in increased androgen secretion, insulin resistance and weight gain at birth, supporting the hypothesis of a transmission of PCOS dysbiotic microbiota from the mother to neonates [ 89 , 90 ]. Gulan and colleagues came up with the same findings using a rat model of PCOS.…”

Therapy of obesity in women with PCOS using GLP-1 analogues — benefits and limitations [Terapia otyłości u kobiet z PCOS przy zastosowaniu analogów GLP-1 — korzyści i ograniczenia]

“…According to the literature, the aetiology of PCOS is a combination that involves an interaction between developmental, environmental, genetic, and epigenetic mechanisms [3]. Non-genetic conditions that are supposed to be involved in PCOS are prenatal androgen exposure related to maternal, foetal, or placental sources, lifestyle factors including poor-quality diet and physical inactivity, endocrine-disrupting chemicals (EDC), altered light exposure, sleep disturbance, heightened levels of stress, lifestyle-induced changes in the gastrointestinal tract microbiome, and others [7]. Extensive evidence indicates that foetal genomic programming of metabolic and endocrine pathways can increase the further susceptibility to develop PCOS following exposure to specific nutritional and environmental factors.…”

“…Interestingly, there is a theory that PCOS is a result of an evolutionary adaptation to lifestyle and the environment. It seems highly reasonable that, in the past, specific features (IR, hyperandrogenism, adiposity, and subfertility) were metabolic survival responses to food shortages [7].…”

The role of Sirtuin 1 in the pathophysiology of polycystic ovary syndrome

“…Multiple lines of evidence now suggest that in the modern world, there are maladaptive reactions in humans to rapidly changing nutritional, physiological, psychological and cultural environments, which lead to pathological responses to IR, hyperandrogens, enhanced energy storage and ovulation [ 66 , 67 ]. SIRT1 is conserved throughout evolutionary history, as a cellular metabolic energy sensor, right back to the beginning of eukaryotic organisms.…”