Effect of a low glycemic index compared with a conventional healthy diet on polycystic ovary syndrome.
BACKGROUND
Women with polycystic ovarian syndrome (PCOS) are intrinsically insulin resistant and have a high risk of cardiovascular disease and type 2 diabetes. Weight loss improves risk factors, but the optimal diet composition is unknown. Low-glycemic index (low-GI) diets are recommended without evidence of their clinical effectiveness.


OBJECTIVE
We compared changes in insulin sensitivity and clinical outcomes after similar weight losses after consumption of a low-GI diet compared with a conventional healthy diet in women with PCOS.


METHODS
We assigned overweight and obese premenopausal women with PCOS (n = 96) to consume either an ad libitum low-GI diet or a macronutrient-matched healthy diet and followed the women for 12 mo or until they achieved a 7% weight loss. We compared changes in whole-body insulin sensitivity, which we assessed using the insulin sensitivity index derived from the oral-glucose-tolerance test (ISI(OGTT)); glucose tolerance; body composition; plasma lipids; reproductive hormones; health-related quality of life; and menstrual cycle regularity.


RESULTS
The attrition rate was high in both groups (49%). Among completers, ISI(OGTT) improved more with the low-GI diet than with the conventional healthy diet (mean +/- SEM: 2.2 +/- 0.7 compared with 0.7 +/- 0.6, respectively; P = 0.03). There was a significant diet-metformin interaction (P = 0.048), with greater improvement in ISI(OGTT) among women prescribed both metformin and the low-GI diet. Compared with women who consumed the conventional healthy diet, more women who consumed the low-GI diet showed improved menstrual cyclicity (95% compared with 63%, respectively; P = 0.03). Among the biochemical measures, only serum fibrinogen concentrations showed significant differences between diets (P < 0.05).


CONCLUSIONS
To the best of our knowledge, this study provides the first objective evidence to justify the use of low-GI diets in the management of PCOS.
Marsh
Kate A
KA
School of Molecular Bioscience, University of Sydney, Sydney, Australia.
Steinbeck
Katharine S
KS
Atkinson
Fiona S
FS
Petocz
Peter
P
Brand-Miller
Jennie C
JC
D000293:Adolescent; D000328:Adult; D001786:Blood Glucose / Q000378:metabolism*; D001823:Body Composition; D015992:Body Mass Index; D002318:Cardiovascular Diseases / Q000453:epidemiology / Q000209:etiology; D004032:Diet; D005260:Female; D005307:Fertilization in Vitro; D038321:Glycemic Index; D006801:Humans; D007003:Hypoglycemia; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D008687:Metformin / Q000627:therapeutic use; D050177:Overweight / Q000097:blood* / Q000178:diet therapy; D011085:Polycystic Ovary Syndrome / Q000097:blood* / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology; D011247:Pregnancy; D040242:Risk Reduction Behavior; D015431:Weight Loss
D001786:Blood Glucose; D007004:Hypoglycemic Agents; D008687:Metformin