Polycystic ovary syndrome
Role of diet in the treatment of polycystic ovary syndrome

Presented in part at the North American Association for the Study of Obesity meeting, Las Vegas, Nevada, November 14–18, 2004.
https://doi.org/10.1016/j.fertnstert.2005.08.045Get rights and content
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Objective

To determine whether eucaloric diets either enriched with monounsaturated fatty acids (MUFA; 17% energy) or low in carbohydrates (Low CHO; 43% energy) would increase insulin sensitivity (Si) and decrease circulating insulin concentrations, relative to a standard diet (STD; 56% CHO, 31% fat, 16% protein), among women with polycystic ovary syndrome (PCOS).

Design

Crossover.

Setting

Academic research environment.

Patient(s)

Healthy women with PCOS not on hormonal or insulin-sensitizing therapy.

Intervention(s)

Subjects consumed three, 16-day, eucaloric diets, each separated by a 3-week washout period. A frequently sampled, intravenous, glucose tolerance test was administered at baseline and following each diet.

Main Outcome Measure(s)

Fasting glucose, insulin, the acute insulin response to glucose (AIRg), Si, sex hormone-binding globulin (SHBG), dehydroepiandrosterone sulfate (DHEAS), total testosterone (T), free T, A4, total cholesterol, high-density lipoprotein cholesterol (HDL-C), tryglycerides (TG), and free fatty acids (FFA).

Result(s)

Fasting insulin was lower following the Low CHO diet relative to the STD diet; AIRg was lower following the Low CHO diet relative to the MUFA diet. Fasting glucose, Si, and the circulating concentrations of reproductive hormones were not significantly affected by the intervention.

Conclusion(s)

A moderate reduction in dietary carbohydrate reduced the fasting and postchallenge insulin concentrations among women with PCOS, which, over time, may improve reproductive/endocrine outcomes.

Key Words

Polycystic ovary syndrome
hyperandrogenism
low-carbohydrate diet
monounsaturated fat
insulin resistance
β-cell function

Cited by (0)

Supported by grants R01-HD29364 and K24-HD011346 from the National Institutes of Health; M01-RR00032 to the General Clinical Research Center, Birmingham, Alabama; P30-DK56336 to the Clinical Nutrition Research Unit, Birmingham, Alabama.