Polycystic Ovary Syndrome and Weight Management

Lisa J Moran; Catherine B Lombard; Siew Lim; Manny Noakes; Helena J Teede

Women's Health. 2010;6(2):271-283.

Polycystic Ovary Syndrome

Polycystic ovary syndrome is the most common endocrinopathy affecting reproductive-aged women, with a prevalence of approximately 11% of Australian women and 21% of Australian indigenous women.^[7–9] PCOS diagnosis is based on reproductive features, including ovulatory disturbance and hyperandrogenism. Women with PCOS present with a range of clinical reproductive features, including hyperandrogenism, hirsutism, anovulation, menstrual irregularity, infertility and the potential for increased pregnancy complications.^[10,11] Women with PCOS also present with metabolic features, such as elevated risk factors for DM2 and CVD with increased metabolic syndrome, impaired glucose tolerance and DM2 and the potential for increased risk for CVD.^[12–15] There is emerging evidence that PCOS is also associated with psychological features, including worsened quality of life and increased anxiety and depression.^[16] The etiology of PCOS is underpinned by insulin resistance.^[7,17,18] In PCOS, hyperinsulinemia augments hyperandrogenism, both through increasing ovarian androgen production in isolation^[19] and synergistically with luteinizing hormone,^[20] as well as through decreasing hepatic production of the androgen-binding protein, sex hormone-binding globulin.^[21] This worsens the clinical reproductive manifestations of PCOS, including hyperandrogenism, infertility and ovarian dysfunction.

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Table 1. Trials of modification of dietary macronutrient composition in lifestyle programs and its impact on key features in overweight/obese women with polycystic ovary syndrome.
Author (year)	Subjects	Duration	Intervention	Weight change	Hormones, metabolism and reproduction	Ref.
Moran et al. (2003)	n = 28 BMI: 37.4	4 months (3 months ER, 1 month WM)	RCT; 12 weeks: 6000 kJ/day; 4 weeks: WMD; HP: 30% P, 40% C, 30% F; HC: 15% P, 55% C, 30% F	HP: −8.5 ± 1.1 kg vs LP: −6.9 ± 0.8 kg (NS)	All subjects: IR, TC, LDL-C, TG, total T ↓ SHBG ↑ and menstrual cyclicity improved; Diet comparison, postprandial glucose ↓ for HP, HDL-C ↓ ER for LP, TC/HDL-C ↓ ER for HP and FAI ↑ during WM for LP	^[44]
Stamets et al. (2004)	n = 26 BMI: 37–38	4 weeks	RCT; Energy deficit: 4200 kJ/day; HP: 30% P, 40% C, 30% F; HC: 15% P, 55% C, 30% F	HP: 3.7 ± 1.9 kg vs LP: 4.4 ± 1.5 kg (NS)	All subjects: IR, total T and free T ↓, SHBG ↑ and menstrual cyclicity improved	^[45]
Hays et al. (2003)	n = 15 BMI: 36.1	24 weeks	Uncontrolled intervention study; High saturated fat, low starch (very low C), 7200 kJ/day; No control group comparison	-14.3% BMI: −3.7	Insulin ↓	^[68]
Mavropoulos et al. (2006)	n = 5 BMI: 38.5	6 months	Uncontrolled intervention study; Ketogenic (<20 g C/day); No control group comparison	-5 kg, 12%	Insulin and free T ↓	^[69]
Moran et al. (2006)	n = 23 BMI: 35.4	2 months ER, 6 months WM	RCT; 2 months: meal replacements: all subjects; 6 months: high GL or low GL education	High GL: 5.9 ± 2.1 kg vs low GL: 4.4 ± 0.7 kg (NS)	All subjects: insulin, total T and FAI ↓, menstrual cyclicity improved	^[72]
Kasim-Karakas et al. (2009)	n = 33 BMI: 25–40	2 months	RCT; Energy reduction of 700 kcal/day and supplement with 240 kcal whey protein or simple sugar	Protein: 3.3 ± 0.8 kg vs simple sugar: 1.1 ± 0.6 kg	All subjects: no change in glucose, insulin, IR, HBA1c, triglyceride, hsCRP, T and SHBG; Diet comparison: greater ↓ fat mass, TC, HDL-C and ApoB for protein	^[71]

C: Carbohydrate; ER: Energy restriction; F: Fat; FAI: Free adrogen index; GL: Glycemic load; HBA1c: Glycosylated hemoglobin; HC: High carbohydrate; HDL-C: High-density lipoprotein cholesterol; HOM: Homeostasis assessment of insulin resistance; HP: High protein; hsCRP: Highly sensitive C reactive protein; IR: Insulin resistance; LDL-C: Low-density lipoprotein cholesterol; NS: Nonsignificant; P: Protein; RCT: Randomized controlled trial; SHBG: Sex hormone-binding globulin; T: Testosterone; TC: Total cholesterol; TG: Triglyceride; WM: Weight maintenance; WMD: Weight maintenance diet.
Adapted with permission from ^[32].

Box 1. Lifestyle modification principles suggested for obesity management in polycystic ovary syndrome.
Guidelines for dietary and lifestyle intervention in polycystic ovary syndrome Weight management through lifestyle modification combining behavioral, dietary and exercise management can be effective in improving reproductive function, as well as metabolic and psychological parameters. Reduced-energy diets (500–1000 kcal/day reduction) are effective options for weight loss and can reduce body weight by 7–10% over a period of 6–12 months. Dietary pattern should be nutritionally complete and appropriate for each life stage. A variety of approaches, including high carbohydrate diets, high dietary protein diets, low glycemic index or load diets, as well as meal replacements, may be successful for achieving and sustaining a reduced weight. The structure and support within a weight management program is crucial and may be more important than the dietary composition. Goal setting, weight monitoring and individualization of the program, intensive follow-up and monitoring by a physician and support from a physician, family, spouse or support from peers, may assist in improving successful outcomes. Lifestyle programs need to address issues such as self-esteem, managing stress, emotional eating and time constraints. Structured exercise is an important component of a weight loss regime.

Adapted with permission from ^[112].

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