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

Antonio Paoli,Maria Cristina Giacona,Antonino Bianco,Massimiliano Caprio,Laura Mancin

doi:10.1186/s12967-020-02277-0

Abstract

BackgroundPolycystic ovary syndrome (PCOS) is the most common endocrine disorder in women during reproductive age. It is characterised clinically by oligo-ovulation or anovulation, hyper-androgenism, and the presence of polycystic ovaries. It is associated with an increased prevalence of metabolic syndrome, cardiovascular disease and type 2 diabetes. The onset of PCOS has been associated to several hereditary and environmental factors, but insulin resistance plays a key pathogenetic role. We sought to investigate the effects of a ketogenic diet (KD) on women of childbearing age with a diagnosis of PCOS.MethodsFourteen overweight women with diagnosis of PCOS underwent to a ketogenic Mediterranean diet with phyoextracts (KEMEPHY) for 12 week. Changes in body weight, body mass index (BMI), fat body mass (FBM), lean body mass (LBM), visceral adipose tissue (VAT), insulin, glucose, HOMA-IR, total cholesterol, low density lipoprotein (LDL), high density lipoprotein (HDL), triglycerides (TGs), total and free testosterone, luteinizing hormone (LH), follicle stimulating hormone (FSH); dehydroepiandrosterone sulfate (DHEAs), estradiol, progesterone, sex hormone binding globulin (SHBG) and Ferriman Gallwey score were evaluated.ResultsAfter 12 weeks, anthropometric and body composition measurements revealed a significant reduction of body weight (− 9.43 kg), BMI (− 3.35), FBM (8.29 kg) and VAT. There was a significant, slightly decrease of LBM. A significant decrease in glucose and insulin blood levels were observed, together with a significant improvement of HOMA-IR. A significant decrease of triglycerides, total cholesterol and LDL were observed along with a rise in HDL levels. The LH/FSH ratio, LH total and free testosterone, and DHEAS blood levels were also significantly reduced. Estradiol, progesterone and SHBG increased. The Ferriman Gallwey Score was slightly, although not significantly, reduced.ConclusionsOur results suggest that a KD may be considered as a valuable non pharmacological treatment for PCOS. Longer treatment periods should be tested to verify the effect of a KD on the dermatological aspects of PCOS.Trial registration Clinicaltrial.gov, NCT04163120, registrered 10 November 2019, retrospectively registered, https://clinicaltrials.gov.

Highlights

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women during reproductive age
Abdominal obesity could be linked to PCOS by a relationship in which it performs the double role of cause and effect: on the one hand, the increase in visceral fat is favored by Glucose Insulin Homeostasis model assessment–insulin-resistance (HOMA-IR) Triglycerides Total cholesterol low density lipoprotein (LDL) high density lipoprotein (HDL)
Abdominal adipocytes are more active as endocrine cells than adipocytes of the lower portion of the body, which define gynoid obesity: they are more sensitive to catecholamines and less to insulin, with the end result of a hyperinsulinemia compensatory with lowgrade inflammation, altered lipid profile, increased production of androgens and low levels of sex hormone binding globulin (SHBG), which overall favor anovulation

Summary

Introduction

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women during reproductive age. It is characterised clinically by oligo-ovulation or anovulation, hyper-androgenism, and the presence of polycystic ovaries. It is associated with an increased prevalence of metabolic syndrome, cardiovascular disease and type 2 diabetes. Polycystic ovarian syndrome (PCOS) is considered the most common endocrine disorder in women in the reproductive age, with an estimated prevalence ranging from 6 to 15%, depending on the diagnostic criteria used. A partial elucidation of this mechanism is explained by the action of insulin on the ovary through the IGF-1 receptor This binding occurs when insulin reaches high concentrations, as in compensatory hyperinsulinemia. High insulin levels inhibit both the production of sex hormone binding globulin (SHBG) by the liver, causing increased levels of free testosterone [7], and the synthesis of IGF-BP1, increasing level of free IGF-1 [8]

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