Source and amount of carbohydrate in the diet and inflammation in women with polycystic ovary syndrome

Abstract

High carbohydrate intake and low-grade inflammation cooperate with insulin resistance and hyperandrogenism to constitute an interactive continuum acting on the pathophysiology of polycystic ovary syndrome (PCOS), the most common endocrine disorder in women of reproductive age characterised by oligo-anovulatory infertility and cardiometabolic disorders. The role of insulin in PCOS is pivotal both in regulating the activity of ovarian and liver enzymes, respectively involved in androgen production and in triggering low-grade inflammation usually reported to be associated with an insulin resistance, dyslipidaemia and cardiometabolic diseases. Although an acute hyperglycaemia induced by oral glucose loading may increase inflammation and oxidative stress by generating reactive oxygen species through different mechanisms, the postprandial glucose increment, commonly associated with the Western diet, represents the major contributor of chronic sustained hyperglycaemia and pro-inflammatory state. Together with hyperinsulinaemia, hyperandrogenism and low-grade inflammation, unhealthy diet should be viewed as a key component of the 'deadly quartet' of metabolic risk factors associated with PCOS pathophysiology. The identification of a tight diet-inflammation-health association makes the adoption of healthy nutritional approaches a primary preventive and therapeutic tool in women with PCOS, weakening insulin resistance and eventually promoting improvements of reproductive life and endocrine outcomes. The intriguing nutritional-endocrine connections operating in PCOS underline the role of expert nutritionists in the management of this syndrome. The aim of the present review is to provide an at-a-glance overview of the possible bi-directional mechanisms linking inflammation, androgen excess and carbohydrate intake in women with PCOS.

Role of gut microbiota in the development of insulin resistance and the mechanism underlying polycystic ovary syndrome: a review

“…Such a sequence of events can ultimately form a vicious cycle between hyperandrogenemia and IR in PCOS, thus promoting the occurrence and development of PCOS. Barre et al suggested that high intake of carbohydrate, hyperinsulinemia, hyperandrogenemia, and chronic low-grade inflammation are the four vital factors of pathophysiological changes in PCOS [80]. A metabolic dysfunction occuring predominantly in women diagnosed with hyperandrogenism and ovulatory dysfunction [81,82].…”

Changes in Metabolic Profile in the Women with a History of PCOS—A Long-Term Follow-Up Study

“…The nature of PCOS is multifactorial and heterogeneous. Environmental factors such as prenatal androgen exposure, poor fetal growth, high carbohydrate consumption and acquired obesity interact with genetic origins and contribute to PCOS pathogenesis [ 5 , 6 , 7 , 8 , 9 ]. It is well established that insulin resistance (IR) and compensatory hyperinsulinaemia are central aetiological abnormalities in women with PCOS which lead to the overproduction of ovarian and adrenal androgens and an increase in androgen bioavailability through inhibition of sex hormone-binding globulin (SHBG) secretion [ 10 ].…”

Effects of a ketogenic diet in overweight women with polycystic ovary syndrome

“…Interestingly, excess carbohydrate intake and low-grade inflammation mutually interact with insulin resistance and hyperandrogenism to reinforce the metabolic phenotype of PCOS [9]. In fact, acute hyperglycaemia is known to increase inflammation and oxidative stress through generation of reactive oxygen species (ROS) [10].…”