Fact or Fiction? Is a Low Glycemic Index Diet the Best Choice for your PCOS Patients?
Abstract & Commentary
By Bridget S. Bongaard, MD, FACP. Dr. Bongaard is the Director of the Integrative Medicine Service Line at CMC-NorthEast Medical Center; she reports no financial relationship to this field of study.
Synopsis: In addition to metformin, dietary therapy is the cornerstone of conventional treatment recommendations for polycystic ovary syndrome (PCOS) to prevent the development of related comorbidities such as type 2 diabetes, heart disease, menstrual irregularities, and infertility. This randomized controlled study is the first to drill down to the specific question of whether type of carbohydrate during dietary therapy actually makes a clinical difference, while holding the other macronutrients and fiber content constant. Insulin resistance, glucose tolerance, body composition, plasma lipids, reproductive hormones, health-related quality of life, and menstrual cycle abnormalities were followed in both groups. On final comparison, there was a remarkable improvement in insulin sensitivity in the cohort with low-glycemic vs. moderate- to high-glycemic carbohydrates and notation that the effect was amplified for those patients also taking metformin. The benefit translated clinically to improved menstrual function and lower plasma fibrinogen concentrations, while there was no change in the other parameters.
Source: Marsh KA, et al. Effect of a low glycemic index compared with a conventional healthy diet on polycystic ovary syndrome. Am J Clin Nutr 2010;92:83-92.
Women with polycystic ovary syndrome (pcos) are a challenging group of patients who have significant metabolic disease in addition to infertility and hyperandrogenism. Approximately 6%-10% of reproductive-age women is affected (totaling 6.8 million women).1 This constitutes a large group that is at high risk for the development of type 2 diabetes, hypertension, and heart disease, creating enormous personal, public health, and economic impact. The underlying sinister abnormality in the complex process of the syndrome is that of insulin resistance. Indeed, approximately 50% of all PCOS patients meets the criteria for metabolic syndrome, and thus has increased risk for developing cardiovascular disease due to the resulting hyperinsulinemia, hyperlipidemia, and elevated inflammatory markers. The risk of gestational diabetes may also be increased, though evidence is not conclusive at this point. The effect of the PCOS disease process may also extend beyond an increase in endometrial cancer, fibroids, and infertility for the individual, and pose risk for offspring. Sons of women with PCOS have early onset of obesity, insulin resistance, and hypercholesterolemia, observable even in infancy.2
Dietary education is the cornerstone of therapy. Many studies focus on the importance of energy restriction to engender weight loss, as it is known that even achieving a modest 10% reduction can significantly reduce hyperlipidemia, hyperglycemia, and insulin resistance, while increasing frequency of ovulation and conception.3 Others look at the manipulation of macronutrients to achieve a therapeutic clinical outcome, as weight loss is very difficult to achieve in this population.
Though a low-fat/high-carbohydrate diet traditionally was thought to aid in weight loss and improve clinical outcome, there has been a change to now recommending a high-protein/low-carbohydrate diet due to the increased satiating power of protein compared with carbohydrate or fat.4 Fiber and fat content make a difference in postprandial glucose and insulin levels. In a study by Katcher et al, 15 PCOS patients were placed on a high-fat/low-carbohydrate/low-fiber Western diet (62% fat, 24% carbs, 1% fiber) vs. a low-fat/high-carbohydrate/high-fiber diet (6% fat, 81% carbs, and 27 g fiber).5 It was noted that the low-fat/high-fiber diet worsened postprandial glucose and insulin levels (two times higher than the high-fat Western diet). This suggests that the carbohydrate portion of meals may be more influential than their fat content.
Kasim-Karakas et al looked specifically at the effect of manipulating protein vs. carbohydrate intake on hyperinsulinemia.6 They showed that when PCOS patients were placed on a fixed hypocaloric diet, which was then supplemented by either whey protein or simple sugars, the protein-supplemented group had significantly reduced body weight, fat mass, and serum cholesterol, compared with the simple sugars group. Diets rich in simple sugars (high-glycemic index) not only increase postprandial hyperglycemia, but also increase levels of ghrelin, leading to prolonged hunger, and rebound eating. Complex carbohydrates experience slower breakdown and absorption, hence a lower compensatory postprandial insulin output, and thus are deemed to have a low-glycemic index. The type of carbohydrate makes a critical difference, but no study to date has adequately and objectively compared the effectiveness of this strategy to a conventional healthy diet in the PCOS population.
The study by Marsh et al set out to answer just this question. They randomly assigned overweight and obese premenopausal women with documented PCOS to consumption of either a low-fat, low-glycemic index (GI) or a low-fat conventional healthy diet on the basis of high-fiber and moderate- to high-GI breads and cereal foods. Both diets were designed to contain reduced energy, low fat, low saturated fat, and moderate-to-high fiber content. They also had a similar macronutrient distribution, so that only the quality of the carbohydrate varied between the two study groups. There was no energy restriction, but portion control was implemented so that there would be a progressive weight loss. They were also encouraged to do 30 minutes of moderate-intensity exercise daily, or 10,000 steps measured by pedometer
Women who were diabetic or with other endocrine disorders, pregnant, on oral contraceptives, or using antidepressants or lipid-lowering medications were excluded. Those with depression or an eating disorder were also culled from the candidate pool. The groups were matched for age, weight (BMI > 30 kg/m2 and BMI < 30 kg/m2), and whether they were currently utilizing metformin therapy (1,000-1,500 mg daily). Of the 280 that were screened, only 96 met the inclusion criteria.
Participants were instructed to follow the diet until they had lost either 7% of body weight or completed 12 months of the study. Dietitians monitored the food intake at a weekly or biweekly meeting with the patients and monitored food journals kept by the patients. At study onset, blood was drawn for baseline total cholesterol, HDL cholesterol, triglycerides, apolipoprotein B, C-reactive protein (CRP), fibrinogen, plasminogen activator inhibitor 1 (PAI-1), testosterone, sex hormone-binding globulin, luteinizing hormone, and follicle-stimulating hormone concentrations. At baseline and completion, an oral glucose tolerance test with plasma insulin and glucose was performed. Subjects using metformin stopped the medication 2 weeks prior to this test to have an adequate washout time and allow authentic values to be obtained. The patients also kept menstrual charts from 6 months prior to the study through the end to accurately determine improvements or worsening of function. The Polycystic Ovary Syndrome Questionnaire was administered to determine changes in quality of life before and after treatment.
The findings of the study were a bit surprising in that very few participants actually achieved the intended 7% weight loss within the 12-month time. In addition, there was a large dropout rate for both groups, such that 21 in the low-GI group and 26 in the moderate-GI group failed to complete the study. The subjects who dropped out had a higher BMI and were more insulin-resistant. Of those who did complete the study, there was no statistically significant difference between the two groups for weight loss, body fat, fat mass, PAI-1, CRP, testosterone, sex hormone-binding globulin, free androgen index, luteinizing hormone, or follicle-stimulating hormone. The only parameters that did improve with the change in dietary carbohydrate composition were menstrual cycle irregularities. In those women with abnormalities at baseline, 95% in the low-GI group showed improvement in regularity, while only 63% in the moderate-GI arm did. Both diet groups showed an improvement in quality-of-life scores, with a significant improvement in the "emotion" category for the low-GI patients. For those patients taking metformin, there was significant improvement in insulin sensitivity with the addition of a low-GI diet change vs. those with low-GI diet alone, or compared with the moderate-GI diet with or without metformin.
Commentary
While this study was well-designed to exclusively separate out the difference obtained in recommending a low- vs. moderate-GI carbohydrate content, while holding exercise, energy expenditure, and macronutrients stable, there was little fanfare at the end for all the work. Happily, there was improvement in quality-of-life scores, and "improvement of menstrual irregularities," but surprisingly there was not the expected improvement in other parameters related to improved insulin sensitivity: lipid analysis (triglycerides, HDL, total cholesterol), inflammatory agents (CRP, PAI-1), sex hormone levels (testosterone, or sex hormone-binding globulin, luteinizing hormone, follicle-stimulating hormone), or weight (BMI).
Some of the disparities noted may have been due to the select patient population that excluded type 2 diabetics, and those with BMIs > 30 kg/m2, which put the patient at much more risk for the metabolically induced diseases mentioned. This created a more homogenous population with fewer variables. The high dropout rate figured into the problem as most of these women had the higher BMI and insulin resistance scores, which could have given the study more contrast and potency if they had completed the course of therapy. In addition, the select population had normal plasma lipid analyses at baseline, so it would be difficult to achieve a large or significant therapeutic excursion in this population. The authors conceded that the study was sufficiently powered to evaluate primary outcomes of determining insulin sensitivity and menstrual irregularity, but not the secondary outcomes (lipid, sex hormone, and inflammation parameters). The study did control for weight loss and allowed the dietary composition to be evaluated independently of weight loss. Part of the problem may have been the lack of significant difference between the low-glycemic and moderate-glycemic foods. Perhaps they should have utilized a high-glycemic load to be able to show more variance, and more semblance of the real life high-glycemic carbohydrate intake of most of these patients.
References
1. Alexander CJ, et al. Polycystic ovary syndrome: A major unrecognized cardiovascular risk factor in women. Rev Obstet Gynecol 2009;2:232-239.
2. Azziz R. Polycystic ovary syndrome is a family affair. J Clin Endocrinol Metab 2008;93:1579-1581.
3. Kasim-Karakas SE, et al. Relation of nutrients and hormones in polycystic ovary syndrome. Am J Clin Nutr 2007;85:688-694.
4. Moran LJ, et al. Dietary composition in restoring reproductive and metabolic physiology in overweight women with polycystic ovary syndrome. J Clin Endocrinol Metab 2003;88:812-819.
5. Katcher HI, et al. Comparison of hormonal and metabolic markers after a high-fat, Western meal versus a low-fat, high-fiber meal in women with polycystic ovary syndrome. Fertil Steril 2009;91:1175-1182.
6. Kasim-Karakas SE, et al. Effects of protein versus simple sugar intake on weight loss in polycystic ovary syndrome (according to the National Institutes of Health criteria). Fertil Steril 2009;92:262-270.
In addition to metformin, dietary therapy is the cornerstone of conventional treatment recommendations for polycystic ovary syndrome (PCOS) to prevent the development of related comorbidities such as type 2 diabetes, heart disease, menstrual irregularities, and infertility.You have reached your article limit for the month. Subscribe now to access this article plus other member-only content.
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