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Re: Should obese women with polycystic ovary syndrome receive treatment for infertility?
- Sheila E. Laredo (25 February 2006)
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Lifestyle modification is central to management
- Jonathan M Lord, Robert Norman, Professor, Research Centre for Reproductive Health, Discipline of Obstetrics & Gynaecology, The University of Adelaide, The Queen Elizabeth Hospital, 28 Woodville Rd., Woodville S.A. 5011 Australia (1 March 2006)
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Increase in POCS and obesity due to young-age use of progesterones?
- Ellen C G Grant (2 March 2006)
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Sheila E. Laredo, Assistant Professor Sunnybrook & Women's College Health Sciences Centre, 790 Bay St, Ste 855 Toronto ON M5G 1N8 Canada
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To the Editor: As Balen et. al suggest in their editorial, it is apparent from epidemiologic data that obesity is associated with adverse pregnancy outcomes. However, it is also clear that the long-term maintenance of weight loss among obese populations is very low, estimated at 15% over at least 3 years of follow-up, in one systematic review.(1) Weight loss in shorter-term studies, whether of dietary or pharmacologic therapies, 6 months to 2 years in duration, does not generally exceed a mean of 5-10kg, and typically is closer to 3kg, after accounting for placebo effects. This translates to less than a 2 to 4 kg/m2 reduction (or in more typical results, just over 1 kg/m2), in body mass index (BMI) for a woman of average height. These estimates are generous, because typical lifestyle and drug trials for weight loss suffer from non-compliance or drop-out rates exceeding 30%(2-6) and participants who drop-out of weight loss trials frequently do so due to treatment failure.(7) It is unlikely that this magnitude of weight loss is sufficient to alter the decision of a clinician who has already chosen to withhold treatment due to obesity, although as the authors indicate, it may be sufficient to improve ovulatory function in women with polycystic ovary syndrome (PCOS). To therefore suggest that obese women defer treatment until they achieve a particular BMI is equivalent to refusing the majority of these women reproductive care. Women are entitled to choose a less-than-ideal treatment if they have received appropriate information regarding risks, benefits and effectiveness. A health-related quality of life measure has identified body weight, fertility and menstrual problems as 3 of the 5 most important areas of concern for women with PCOS.(8) While it is certainly reasonable and prudent to recommend weight loss for all the reasons put forth by Balen et al, suggesting that obese women with PCOS and infertility defer fertility treatment for a potentially indefinite period of time will only add to their sense of stigmatization. 1. Ayyad C, Anderson T. Long-term efficacy of dietary treatment of obesity: a systematic review of studies published between 1931-1999. Obes Rev 2000;1(2):113-9. 2. Stern L, Iqbal N, Seshadri P, Chicano KL, Daily DA, McGrory J, Williams M, Gracely EJ, Samaha F. The effects of low-carbohydrate versus conventional weight loss diets in severely obese adults: one-year follow- up of a randomized trial. Ann Intern Med 2004;140(10):778-85. 3. Samaha FF, Iqbal N, Seshadri P, Chicano KL, Daily DA, McGrory J, Williams T, Williams M, Gracely EJ, Stern L. A low-carbohydrate as compared with a low-fat diet in severe obesity. N Engl J Med 2003;348(21):2074-81. 4. Foster GD, Wyatt HR, Hill JO, McGuckin BG, Brill C, Mohammed BS, Szapary, PO, Rader DJ, Edman JS, Klein S. A randomized trial of a low- carbohydrate diet for obesity. N Engl J Med 2003;348(21):2082-90. 5. Yancy WS Jr, Olsen MK, Guyton JR, Bakst RP, Westman EC. A low- carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia: a randomized controlled trial. Ann Intern Med 2004;140(10):769-77. 6. Pi-Sunyer FX, Aronne LJ, Heshmati HM, Devin J, Rosenstock J; RIO North America Study Group. JAMA 2006;295(7):761-75. 7. Torgerson JS, Hauptman J, Boldrin MN, Sjostrom L. XENical in the prevention of diabetes in obese subjects (XENDOS) study: a randomized study of orlistat as an adjunct to lifestyle changes for the prevention of type 2 diabetes in obese patients. Diab Care 2004;27(1):155-61. 8. Cronin L, Guyatt G, Griffith L, Wong E, Azziz R, Futterweit W, Cook D, Dunaif A. Development of a health-related quality-of-life questionnaire (PCOSQ) for women with polycystic ovary syndrome. J Clin Endocrinol Metab 1998;83(6): 1976-87. Competing interests: None declared |
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Jonathan M Lord, Consultant in obstetrics and gynaecology Royal Cornwall Hospital, Truro, Cornwall TR1 3LJ. UK, Robert Norman, Professor, Research Centre for Reproductive Health, Discipline of Obstetrics & Gynaecology, The University of Adelaide, The Queen Elizabeth Hospital, 28 Woodville Rd., Woodville S.A. 5011 Australia
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We were pleased to read the editorial by Balen et al1 and agree that lifestyle modification, including effective exercise regimes and dietary advice, should be the first line of treatment in women with PCOS. Our Cochrane review has been widely cited as supporting the use of metformin in women with PCOS, but like Balen et al we too concluded that metformin should be used as an adjuvant to general lifestyle improvements and not as a replacement for them2. An update of the Cochrane review should be available this year. The complications of obesity in both infertility treatment and in subsequent pregnancy are well known3. However lifestyle modifications can bring about beneficial metabolic changes despite only modest reductions in weight, and BMI may not be a sensitive enough measure to detect clinically significant changes in metabolic parameters, with waist circumference being a better marker in women4. More research is needed to ascertain whether the complications in pregnancy are owing to obesity per se, or to underlying insulin resistance. An additional concern that was not mentioned in the editorial is that of fetal programming. If evidence were found to support the hypothesis that insulin resistance in the mother could “programme” the fetus to become obese in later life5, then failing to treat insulin resistance in women seeking fertility treatment now may be creating problems for future generations. (1) Balen AH, Dresner M, Scott EM, Drife JO. Should obese women with polycystic ovary syndrome receive treatment for infertility? BMJ 2006; 332(7539):434-435. (2) Lord JM, Flight IHK, Norman RJ. Metformin in polycystic ovary syndrome: systematic review and meta-analysis. BMJ 2003; 327(7421):951-0. (3) Norman RJ, Noakes M, Wu R, Davies MJ, Moran L, Wang JX. Improving reproductive performance in overweight/obese women with effective weight management. Hum Reprod Update 2004; 10(3):267-280. (4) Yusuf S, Hawken S, Ounpuu S, Bautista L, Franzosi MG, Commerford P et al. Obesity and the risk of myocardial infarction in 27,000 participants from 52 countries: a case-control study. Lancet 2005; 366(9497):1640-1649. (5) Foreyt JP, Poston WS. Obesity: a never-ending cycle? Int J Fertil Womens Med 1998; 43(2):111-116. Competing interests: None declared |
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Ellen C G Grant, physican and medical gynaecologist Kingston-upon-Thames, KT2 7JU, UK
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Professor Balen and colleagues write that PCOS is increasing because more women are becoming obese.1 Progesterone use can cause rapid weight gain and many adolescent girls therefore refuse to continue taking the Pill. In an attempt to cut the numbers of unplanned teenage pregnancies more longer-acting forms of progesterone are being used. Unfortunately depo medroxyprogesterone acetate (DMPA) caused significantly greater weight gain with longer use in adolescent girls than the Pill. After 18 months obese girls gained 9 kg while non-obese girls gained 4 kg. The authors considered that the potential contribution of DMPA to severe obesity in adolescents is concerning.2 DMPA is reported to have no inherent oestrogenic or androgenic effects, which suggests that weight gain induced by DMPA is a progestogenic effect. Use of progestogens can also increase the risk of PCOS. In the Walnut Creek Contraceptive Drug Study significantly more oral contraceptive users aged 18-39 had non-functioning ovarian cysts than never users (50/7506 with 4/2556).3 Fewer functioning cysts would be expected in users of progestogens designed to stop ovaries functioning. Use of fertility drugs can also cause ovarian cysts. Progestogen use also increases the risk of diabetes. In a study of 210 women taking 150 µg levonorgestrel and 30 µg ethinyl oestradiol, 60% had stopped by 15 months and only 8% were current users at 3 years. Glucose tolerance tests deteriorated into the diabetic rangein 6 women but improved when oral contraceptives were stopped for side-effects including weight gain.4 It is reasonable that obese women with PCOS are not given fertility drugs risking more ovarian cyst development and further weight gain. Advice about weight reducing high protein/low allergy diets and life-style changes is preferable. 1 Balen AH, Dresner M, Scott EM, Drife JO. Should obese women with polycystic ovary syndrome receive treatment for infertility? BMJ 2006; 332: 434-435. 2 Bonny AE, Ziegler J, Harvey R, et al. Weight gain in obese and nonobese adolescent girls initiating depot medroxyprogesterone, oral contraceptive pills, or no hormonal contraceptive method. Arch Pediatr Adolesc Med. 2006; 160: 40-5. 3 Ramcharan S. Pellegrin RR, Hsu J-P, et al. Walnut Creek Contraceptive Drug Study 1981; Center for Population Research Monograph; Vol 111: P 162. 4 Wynn V. Effects of duration of low-dose oral contraceptive administration on carbohydrate metabolism. Am J Obstet Gynecol 1982: 142: 739-43. Competing interests: None declared |
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