Effects of Dietary Glycemic Index and Glycemic Load on Cardiometabolic and Reproductive Profiles in Women with Polycystic Ovary Syndrome: A Systematic Review and Meta-analysis of Randomized Controlled Trials

Abstract

Women with polycystic ovary syndrome (PCOS) exhibit cardiometabolic (e.g., insulin resistance) and associated reproductive disruptions. Lifestyle modification (e.g., diet) is recommended as the first-line therapy to manage PCOS; however, a favorable dietary regimen remains unclear beyond energy restriction. We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) to summarize evidence on impacts of dietary glycemic index (GI) or glycemic load (GL) on cardiometabolic and reproductive profiles to update the International Evidence-based Guideline for the Assessment and Management of PCOS. Databases of MEDLINE, Cochrane, Web of Science, and Scopus were searched through 30 October 2019, and confirmed on 25 March 2020, to identify RCTs (≥8 wk) comparing the effects of diets with lower (LGI/LGL) and higher (HGI/HGL) GI/GL on glucoregulatory outcomes, lipid profile, anthropometrics, and androgen status in PCOS. The primary outcome was HOMA-IR. Data were pooled by random-effects models and expressed as weighted mean differences and 95% CIs. The risk of bias was assessed by the Cochrane tool. Ten RCTs (n = 403) were eligible. Eight evaluated LGI and 2 LGL diets. LGI diets decreased HOMA-IR (-0.78; -1.20, -0.37; I2 = 86.6%), fasting insulin (-2.39; -4.78, 0.00 μIU/mL; I2 = 76.8%), total cholesterol (-11.13; -18.23, -4.04 mg/dL; I2 = 0.0%), LDL cholesterol (-6.27; -12.01, -0.53 mg/dL; I2 = 0.0%), triglycerides (-14.85; -28.75, -0.95 mg/dL; I2 = 31.0%), waist circumference (-2.81; -4.40, -1.23 cm; I2 = 53.9%), and total testosterone (-0.21; -0.32, -0.09 nmol/L; I2 = 8.6%) compared with HGI diets (all: P ≤ 0.05) without affecting fasting glucose, HDL cholesterol, weight, or free androgen index (all: P ≥ 0.07). Some results were contradictory and only described narratively for 2 RCTs that evaluated LGL diets, since inclusion in meta-analyses was not possible. LGI diets improved glucoregulatory outcomes (HOMA-IR, insulin), lipid profiles, abdominal adiposity, and androgen status, conceivably supporting their inclusion for dietary management of PCOS. Further RCTs should confirm these observations and address whether LGI diets improve more patient-pressing complications, including ovulatory cyclicity, infertility, and cardiovascular disease risk in this high-risk population. This review was registered at www.crd.york.ac.uk/PROSPERO as CRD42020175300.

Keywords: cardiovascular diseases; diet; dyslipidemias; glucose; hyperandrogenism; insulin; metabolic diseases; obesity; polycystic ovary syndrome.

FIGURE 1

Intersection of diet with the etiological and pathophysiological theories of PCOS. Black lines represent the mechanisms of developing PCOS in direct (solid lines) and feedback loops (dotted lines). Green lines represent the proposed mechanism that diet, as a modifiable environmental factor, can positively affect the clinical and biochemical aberrations of PCOS. FSH, follicle-stimulating hormone; GnRH, gonadotropin-releasing hormone; LH, luteinizing hormone; PCOS, polycystic ovary syndrome; SHBG, sex hormone–binding globulin.

FIGURE 2

Flow diagram of study selection. GI, glycemic index; GL, glycemic load; PCOS, polycystic ovary syndrome; RCT, randomized controlled trial(s).