Skip to main content
  • More from ADA
    • Diabetes
    • Diabetes Care
    • Clinical Diabetes
    • ADA Standards of Medical Care
    • ADA Standards of Medical Care, abridged
    • ADA Scientific Sessions Abstracts
    • BMJ Open Diabetes Research & Care
  • Subscribe
  • Log in
  • My Cart
  • Follow ada on Twitter
  • RSS
  • Visit ada on Facebook
Diabetes Spectrum

Advanced Search

Main menu

  • Home
  • Current
    • Current Issue
    • Online Ahead of Print
    • ADA Standards of Medical Care
    • ADA Standards of Medical Care, Abridged
  • Browse
    • Issue Archive
    • Saved Searches
    • COVID-19 Article Collection
    • ADA Standards of Medical Care
    • ADA Standards of Medical Care, Abridged
  • Info
    • About the Journal
    • About the Editors
    • ADA Journal Policies
    • Instructions for Authors
    • Guidance for Reviewers
  • Reprints/Reuse
  • Advertising
  • Subscriptions
    • Individual Subscriptions
    • Institutional Subscriptions and Site Licenses
    • Access Institutional Usage Reports
    • Purchase Single Issues
  • Alerts
    • E­mail Alerts
    • RSS Feeds
  • Podcasts
    • Diabetes Core Update
    • Special Podcast Series: Therapeutic Inertia
    • Special Podcast Series: Influenza Podcasts
    • Special Podcast Series: SGLT2 Inhibitors
    • Special Podcast Series: COVID-19
  • Submit
    • Submit a Manuscript
    • Journal Policies
    • Instructions for Authors
  • More from ADA
    • Diabetes
    • Diabetes Care
    • Clinical Diabetes
    • ADA Standards of Medical Care
    • ADA Standards of Medical Care, abridged
    • ADA Scientific Sessions Abstracts
    • BMJ Open Diabetes Research & Care

User menu

  • Subscribe
  • Log in
  • My Cart

Search

  • Advanced search
Diabetes Spectrum
  • Home
  • Current
    • Current Issue
    • Online Ahead of Print
    • ADA Standards of Medical Care
    • ADA Standards of Medical Care, Abridged
  • Browse
    • Issue Archive
    • Saved Searches
    • COVID-19 Article Collection
    • ADA Standards of Medical Care
    • ADA Standards of Medical Care, Abridged
  • Info
    • About the Journal
    • About the Editors
    • ADA Journal Policies
    • Instructions for Authors
    • Guidance for Reviewers
  • Reprints/Reuse
  • Advertising
  • Subscriptions
    • Individual Subscriptions
    • Institutional Subscriptions and Site Licenses
    • Access Institutional Usage Reports
    • Purchase Single Issues
  • Alerts
    • E­mail Alerts
    • RSS Feeds
  • Podcasts
    • Diabetes Core Update
    • Special Podcast Series: Therapeutic Inertia
    • Special Podcast Series: Influenza Podcasts
    • Special Podcast Series: SGLT2 Inhibitors
    • Special Podcast Series: COVID-19
  • Submit
    • Submit a Manuscript
    • Journal Policies
    • Instructions for Authors
Departments

The Role of Polycystic Ovary Syndrome in Reproductive and Metabolic Health: Overview and Approaches for Treatment

  1. Carrie C. Dennett1 and
  2. Judy Simon2,3
  1. 1Northwest Natural Health, Seattle, WA
  2. 2University of Washington Department of Medicine Roosevelt Clinic, Seattle, WA
  3. 3Mind Body Nutrition, Bellevue, WA
  1. Corresponding author: Judy Simon, judy{at}mind-body-nutrition.com
Diabetes Spectrum 2015 May; 28(2): 116-120. https://doi.org/10.2337/diaspect.28.2.116
Next
  • Article
  • Figures & Tables
  • Info & Metrics
  • PDF
Loading

Polycystic ovary syndrome (PCOS) is a condition with a range of reproductive and metabolic features that affects 4–18% of reproductive-age women, depending on the diagnostic criteria used (1,2). PCOS typically involves hormonal imbalances, insulin resistance, and metabolic abnormalities, which significantly increase the risk of infertility, type 2 diabetes, and cardiovascular disease (CVD) (3) and affect quality of life (4). Women with PCOS suffer from greater body dissatisfaction and are also at increased risk of mood, generalized anxiety, and eating disorders (2,5,6). Despite its prevalence and implications for reproductive, metabolic, and psychological health, PCOS is underdiagnosed, in part because of the diversity of phenotypes manifested by this condition.

PCOS and Reproductive Health

PCOS is the most common cause of anovulatory infertility; ∼ 90–95% of anovulatory women seeking treatment for infertility have PCOS (7). Women may learn they have PCOS only after seeking infertility treatment. Most women with PCOS have elevated levels of luteinizing hormone and reduced levels of follicle-stimulating hormone (FSH), coupled with elevated levels of androgens and insulin (8). These imbalances can manifest as oligomenorrhea or amenorrhea (infrequent or lack of menstruation). Underproduction of estrogen and overproduction of androgens (testosterone, dehydroepiandrosterone, and androstenedione) by the ovaries can result in a number of additional clinical features, including tiny cysts on the surface of the ovaries (polycysts) and hair and skin symptoms (9). Women with PCOS who become pregnant are at higher risk than those without PCOS of developing gestational diabetes mellitus or suffering a first-trimester spontaneous abortion (2,9).

PCOS and Metabolic Health

Insulin resistance with compensatory hyperinsulinemia affects ∼ 65–70% of women with PCOS (10). An estimated 30–40% of PCOS patients have impaired glucose tolerance (IGT), and 7.5–10% have type 2 diabetes (7,9). Conversely, the prevalence of PCOS is elevated among women who have already been diagnosed with type 1 or type 2 diabetes (2). Studies suggest that the annual progression rate from normal glucose tolerance to IGT and from IGT to type 2 diabetes in women is substantially enhanced among women with PCOS, with the highest risk in women who are also obese and have a family history of type 2 diabetes (9,11). A 2010 systematic review and meta-analysis (12) of 35 studies found that PCOS is associated with a 2.5-fold increased prevalence of IGT and a fourfold increased prevalence of type 2 diabetes. Insulin resistance, which occurs independently of obesity in PCOS (2), may affect ovulation and fertility by interfering with hepatic production of sex hormone–binding globulin (SHBG) (13). Reduced SHBG levels lead to an increase in free testosterone levels (14). Women with PCOS who have chronic anovulation but normal androgen levels tend to not be insulin resistant (15). The combination of anovulation and hyperinsulinemia can promote endometrial cell proliferation, increasing the risk of endometrial carcinomas and other abnormalities (16).

In addition to glucose and insulin abnormalities, CVD risk factors (hypertension, hyperlipidemia, impaired blood vessel function) often accompany PCOS (1,2). In the United States, 33–47% of women with PCOS have metabolic syndrome, a rate two to three times higher than that of age-matched healthy women without PCOS (16). Women with PCOS also have a four- to sevenfold higher risk of having a heart attack than women of the same age who do not have PCOS (17). Between 35 and 60% of women with PCOS are obese (15), which appears to worsen both the metabolic and reproductive features of the condition, particularly in cases of visceral adiposity (18). PCOS and metabolic syndrome have many anthropometric and metabolic abnormalities in common, and hyperinsulinemia may be a crucial link between the two conditions (14). Women who have PCOS and metabolic syndrome or type 2 diabetes are at the highest risk of CVD (19). Production of androgens tends to decrease in the years leading to menopause, so the menstrual cycles of women with PCOS often become more regular, with corresponding improvement in reproductive functioning (20,21). However, research on the impact of PCOS on cardiovascular risk in the postmenopausal years is inconclusive and lacking (22,23).

Etiology of PCOS

Although the exact cause of PCOS is unknown, it is understood to be a multifactorial condition with a genetic component. Approximately 20–40% of first-degree female relatives of women with PCOS go on to develop PCOS themselves, compared to an estimated 4–6% prevalence in the general population (16). Many women with PCOS have female relatives with PCOS, even if it was never diagnosed (2). As with type 2 diabetes, it is likely that numerous genes each make a small contribution to the etiology of PCOS; and recent genome-wide association studies have identified candidate genes (2,3,16). Any underlying genetic predisposition is likely complicated by epigenetic and environmental factors such as an unhealthy diet and lack of physical activity (3,16).

Diagnosing PCOS

Diagnosing and treating PCOS is important to preserve or restore fertility, reduce symptoms, and prevent complications that can develop in women with PCOS from adolescence to the postmenopausal period. Obstacles to timely diagnosis include the presence of multiple PCOS phenotypes and significant individual variation in clinical features, as well as competing diagnostic criteria from the National Institutes of Health (NIH), the European Society for Human Reproduction and Embryology and American Society for Reproductive Medicine (ESHRE/ASRM Rotterdam), and the Androgen Excess and PCOS Society (AE-PCOS) (Table 1) (3,15). To be diagnosed with PCOS under the ESHRE/ASRM Rotterdam criteria, which are considered to be a compromise between those of NIH and AE-PCOS, a woman must have at least two of three criteria after other related health conditions are ruled out: oligo-ovulation and/or anovulation, clinical and/or biochemical signs of hyperandrogenism, and polycystic ovaries visible by ultrasound (24,25). Although approximately three out of four women with PCOS have polycysts on their ovaries, this clinical feature is no longer deemed necessary or sufficient for diagnosis. One recommendation from the NIH Evidence-Based Methodology Workshop on Polycystic Ovary Syndrome held in December 2012 was that PCOS be renamed to more accurately reflect the complex nature of this syndrome and its implications for women’s reproductive and metabolic health (3).

View this table:
  • View inline
  • View popup
TABLE 1.

Diagnostic Criteria for PCOS

Clinically, PCOS may manifest as a mild menstrual disorder or a severe disturbance of reproductive and metabolic functions (15). Most visible signs are caused by excessive production of insulin or androgens. Hirsutism (excess hair growth on the face and body) is present in ∼ 70% of women with PCOS and is considered to be a good marker for hyperandrogenism but should be evaluated biochemically (20). Alopecia (thinning scalp hair), acne, and other skin symptoms are less common and are not good markers (20). Oral contraceptive use can temporarily “hide” PCOS by lowering androgen levels, preventing visual signs, and helping to regulate the menstrual cycle, and some women with PCOS have normal androgen levels. Because acne is common in adolescence and the menstrual cycle is often irregular for the first few years of menstruation, progressive hirsutism may be the most consistent marker for PCOS in the teenage years (20,21). It has been suggested that a definitive diagnosis be deferred until at least 2 years after onset of menstruation to assess whether other diagnostic criteria are met (26,27). As with adult PCOS phenotypes, obesity can exacerbate symptoms of hyperandrogenism and hyperinsulinemia in the adolescent phenotypes, and these issues can be treated before a PCOS diagnosis is confirmed (16,26,27).

Insulin resistance can cause acanthosis nigricans, which presents as “dirty looking” raised velvety areas on the skin, often in body folds around the neck, armpits, groin, and breasts. It can also cause skin tags, rough elbows, and rough, reddened hair follicles on the upper arms. Women with PCOS who have insulin resistance may experience hyperglycemia and hypoglycemia and report having intense cravings for carbohydrates. The AE-PCOS Society recommends that all women with PCOS be screened for IGT with a 2-hour oral glucose tolerance test and that women with normal glucose tolerance at baseline be screened at least once every 2 years, or earlier if they have additional risk factors for type 2 diabetes such as obesity or family history of diabetes or metabolic syndrome (9,11).

Other important information to aid diagnosis include weight history, results of previous blood tests and ultrasounds, and menstrual history. Prolonged anovulation may lead to dysfunctional uterine bleeding that mimics menstrual bleeding, and women with oligo-ovulation may experience heavy bleeding when they do menstruate (24). Patients may not know if they have a family history of PCOS; asking about a history of irregular periods or infertility among first-degree female family members can be useful.

Treating PCOS: Lifestyle Interventions

Because the underlying pathophysiology of PCOS has not been fully determined yet, treatment plans typically focus on specific symptoms. Lifestyle change (dietary, exercise, or behavioral interventions) is considered the first-line treatment for management of infertility and metabolic complications in women with PCOS, including reduction of the conversion rate from IGT to type 2 diabetes (2,9,28) and CVD risk (19). Intensive lifestyle modification and weight reduction has been shown to reduce circulating insulin and androgen levels and improve lipid and FSH levels, which can reduce many of the physical symptoms, normalize menstrual cycles, induce ovulation, and improve general health (1,8,15,16). For women with PCOS who are overweight or obese, weight loss of as little as 5–10% has been associated with significant clinical benefits in improving reproductive, metabolic, and psychological features of the condition (2,7).

No specific dietary composition has been demonstrated to be most beneficial, in part because of clinical heterogeneity and methodological problems with the current body of research (29,30). A recent systematic review (30) found that subtle but inconclusive improvements were observed with a low-glycemic diet but that further research is needed. This review did find that a nutritionally adequate weight loss diet based on healthy food choices was of clinical benefit in overweight and obese women with PCOS regardless of the diet composition.

Along with a healthful eating plan, regular physical activity can help with many of the issues and health concerns that surround PCOS by increasing SHBG and decreasing androgen levels, improving insulin sensitivity, assisting with weight management, improving lipid levels, and lowering blood pressure (31). Regular physical activity can also improve mood and body image and help reduce chronic stress and stress-related eating, although women with PCOS should also be screened for mood and anxiety disorders and treated using established therapies (6). Vitamin D deficiency is common in women with PCOS, and there is limited evidence that vitamin D supplementation may improve reproductive function and insulin sensitivity (32). Although more randomized controlled trials are needed, vitamin D levels should be tested, and supplementation may be warranted to increase low levels, especially in women undergoing in vitro fertilization (33).

Medical nutrition therapy (MNT) can help women with PCOS make and maintain the lifestyle changes needed to help reduce symptoms and prevent complications. MNT is based on an assessment of lifestyle changes that would help a patient with PCOS achieve and maintain clinical goals. The Academy of Nutrition and Dietetics’ evidence-based nutrition practice guidelines (34) recommend the following structure for the implementation of MNT for adults with PCOS:

  • Thorough nutrition assessment to help prioritize MNT

  • Nutrition diagnosis, which includes the presence of, risk of, or potential for developing a nutritional deficit that can be addressed by nutrition therapy

  • Nutrition interventions, which are specific actions to remedy the nutrition diagnosis; these can include clinical and behavioral goals collaboratively agreed upon with the patient, as well as specific nutrition interventions such as selecting a meal-planning strategy or education on controlling portion sizes or making healthy choices when dining out

  • Nutrition monitoring and evaluation with ongoing follow-up to support long-term lifestyle changes, evaluate outcomes, and modify interventions as needed

The following case study demonstrates how MNT can effectively facilitate lifestyle changes that lead to improved health outcomes.

Case Study: MNT in PCOS

Patient

The patient, Gita, is a 27-year-old South-Asian female referred for MNT with diagnoses of PCOS and infertility.

Food- and Nutrition-Related History

Gita is a lacto-vegetarian who consumes no eggs because of her religious beliefs. She typically skips breakfast; eats a granola bar or orange juice for lunch; snacks on chocolate candy bars, juice, or fruit smoothies; and then enjoys a full supper of vegetarian curry, basmati rice, vegetables, and lentils. She reports having gained 20 lb since moving to the United States from India 1 year ago.

Nutrient Intake

  • Most calories consumed at night

  • Diet high in carbohydrates

Activity

  • Very minimal physical activity

Anthropometrics

  • Height: 5 feet, 3 inches

  • Weight: 162 lb

  • BMI: 28.7 kg/m2

  • Waist circumference: 38.4 inches

Biochemical Data

  • A1C: 5.5% (normal 4.5–6%) (1)

  • Fasting blood glucose: 90 mg/dL (normal 70–100 mg/dL)

  • Vitamin D: 6 ng/mL (normal 30.0–74.0 ng/mL)

  • Cholesterol: 188 mg/dL (normal <200 mg/dL)

  • HDL cholesterol: 34 mg/dL (normal ≥60 mg/dL)

Nutrition Diagnoses

  • Diagnosis 1: Excessive carbohydrate intake related to knowledge deficit as evidenced by diet history and BMI

  • Diagnosis 2: Physical inactivity related to knowledge deficit as evidenced by current physical activity level

Nutrition Intervention

Gita agreed to eat three meals and two snacks daily, distributing carbohydrates with fat and protein throughout the day. She can now identify the carbohydrate content of Indian dishes and knows how to balance carbohydrate portions. She understands how to add protein sources to meals and snacks by adding servings of soy milk and yogurt and by using lentils, beans, edamame, and quinoa to provide protein and low-glycemic carbohydrates. She will increase her intake of omega-3 fatty acids through food sources such as nuts, flax, and chia seeds. She also agreed to include the following supplements in her routine: vitamin D (50,000 IU weekly for 8 weeks), ground flax, and a prenatal multivitamin and mineral. In terms of physical activity, she will begin with 15 minutes of walking daily and gradually work up to 45 minutes daily.

Monitoring/Evaluation

  • Record dietary intake, including carbohydrate servings, and e-mail them directly to the registered dietitian every week

  • Meet for in-person MNT sessions every 3–4 weeks

Outcomes

Gita lost 12 lb (8% of baseline body weight) over 6 months and successfully conceived a healthy son through the use of timed intercourse. She met with the dietitian for an additional nutrition session during pregnancy, and her glucose tolerance test result was normal.

Treating PCOS: Pharmaceutical Interventions

When lifestyle treatment does not result in desired outcomes, pharmacotherapy may be added. In premenopausal patients not currently trying to become pregnant, the Endocrine Society recommends hormonal contraceptives as the first-line therapy to manage menstrual abnormalities and reduce hirsutism and acne (2,35). Metformin helps to improve insulin sensitivity in both women and adolescents with PCOS, which in turn can decrease circulating androgen levels and normalize the menstrual cycle and ovulation (2,15,36). Clomiphene citrate, an estrogen receptor antagonist, is the drug of first choice for induction of ovulation in women with PCOS (2). However, most published, randomized, controlled trials that used medications such as clomiphene citrate or metformin failed to find significant differences in menstrual function between lifestyle intervention and pharmacotherapy. For that reason, in infertile overweight or obese adults with PCOS, evidence does not support treatment with these drugs ahead of either lifestyle intervention alone or starting lifestyle treatment in combination with these drugs (29,37,38). The Endocrine Society recommends metformin for adult PCOS patients with IGT or type 2 diabetes when lifestyle interventions alone are not sufficient and for adolescent patients who have IGT or metabolic syndrome (35).

Summary

Although PCOS is treatable with lifestyle changes and medication, many of the estimated 1 in 10 women with this condition go without adequate treatment because of underdiagnosis. To facilitate accurate diagnosis and timely treatment, clinicians who see female patients need to be familiar with the diversity of PCOS phenotypes that may be encountered in a clinical setting. The adverse effects of PCOS on ovulation and fertility understandably garner much attention, but this condition has broader implications for a woman’s metabolic and psychological health before, during, and after her reproductive years, and treatment interventions should reflect that fact.

Duality of Interest

No potential conflicts of interest relevant to this article were reported.

  • © 2015 by the American Diabetes Association.

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0 for details.

References

  1. ↵
    1. Moran LJ,
    2. Hutchison SK,
    3. Norman RJ,
    4. Teed HJ
    . Lifestyle changes in women with polycystic ovary syndrome (review). Cochrane Database Syst Rev 2011, CD007506]
  2. ↵
    1. Sirmans SM,
    2. Pate KA
    . Epidemiology, diagnosis, and management of polycystic ovary syndrome. Clin Epidemiol 2014;6:1–13
    OpenUrl
  3. ↵
    1. National Institutes of Health
    . NIH Evidence-Based Methodology Workshop on Polycystic Ovary Syndrome: executive summary, 2012. https://prevention.nih.gov/docs/programs/pcos/FinalReport.pdf. Accessed 23 February 2015
  4. ↵
    1. Cinar N,
    2. Kizilarslanoglu MC,
    3. Harmanci A, et al
    . Depression, anxiety and cardiometabolic risk in polycystic ovary syndrome. Hum Reprod 2011;26:3339–3345
    OpenUrlAbstract/FREE Full Text
  5. ↵
    1. Himelein MJ,
    2. Thatcher SS
    . Depression and body image among women with polycystic ovary syndrome. J Health Psychol 2006;11:616–625
    OpenUrl
  6. ↵
    1. Dokras A
    . Mood and anxiety disorders in women with PCOS. Steroids 2012;77:338–341
    OpenUrlPubMed
  7. ↵
    1. Teede H,
    2. Deeks A,
    3. Moran L
    . Polycystic ovary syndrome: a complex condition with psychological, reproductive and metabolic manifestations that impacts health across the lifespan. BMC Medicine 2010;8:41
    OpenUrlPubMed
  8. ↵
    1. Haqq L,
    2. McFarlane J,
    3. Dieberg G,
    4. Smart N
    . Effect of lifestyle intervention on the reproductive endocrine profile in women with polycystic ovarian syndrome: a systematic review and meta-analysis. Endocr Connect 2014;3:36–46
    OpenUrlAbstract/FREE Full Text
  9. ↵
    1. Salley KES,
    2. Wickham EP,
    3. Cheang KI,
    4. Essah PA,
    5. Kargane NW,
    6. Nestler JE
    . Glucose intolerance in polycystic ovary syndrome: a position statement of the Androgen Excess Society. J Clin Endocrinol Metab 2007;92:4546–4556
    OpenUrlCrossRefPubMedWeb of Science
  10. ↵
    1. DeUgarte CM,
    2. Bartolucci AA,
    3. Azziz R
    . Prevalence of insulin resistance in the polycystic ovary syndrome using the homeostatis model assessment. Fertil Steril 2005;83:1454–1460
    OpenUrlCrossRefPubMedWeb of Science
  11. ↵
    1. Tomlinson J,
    2. Millward A,
    3. Stenhouse E,
    4. Pinkney J
    . Type 2 diabetes and cardiovascular disease in polycystic ovary syndrome: what are the risks and can they be reduced? Diabet Med 2010;27:498–514
    OpenUrlCrossRefPubMed
  12. ↵
    1. Moran LJ,
    2. Misso ML,
    3. Wild RA,
    4. Norman RJ
    . Impaired glucose tolerance, type 2 diabetes and metabolic syndrome in polycystic ovary syndrome: a systematic review and meta-analysis. Hum Reprod Update 2010;16:347–363
    OpenUrlAbstract/FREE Full Text
  13. ↵
    1. Martinez-Garcia MA,
    2. Gambineri A,
    3. Alpañés M,
    4. Sanchón R,
    5. Pasquali R,
    6. Escobar-Morreale HF
    . Common variants in the sex hormone-binding globulin gene (SHBG) and polycystic ovary syndrome (PCOS) in Mediterranean women. Hum Reprod 2012;27:3569–3576
    OpenUrlAbstract/FREE Full Text
  14. ↵
    1. Ehrmann DA,
    2. Liljenquist DR,
    3. Kasza K,
    4. Azziz R,
    5. Legro RS,
    6. Ghazzi MN
    . Prevalence and predictors of the metabolic syndrome in women with polycystic ovary syndrome. J Clin Endocrinol Metab 2006;91:48–53
    OpenUrlCrossRefPubMedWeb of Science
  15. ↵
    1. Badawy A,
    2. Elnashar A
    . Treatment options for polycystic ovary syndrome. Int J Women’s Health 2011;3:25–35
    OpenUrlPubMed
  16. ↵
    1. Goodarzi MO,
    2. Dumesic DA,
    3. Chazenbalk G,
    4. Azziz R
    . Polycystic ovary syndrome: etiology, pathogenesis and diagnosis. Nat Rev Endocrinol 2011;7:219–2311
    OpenUrlCrossRefPubMed
  17. ↵
    1. Office on Women’s Health, U.S. Department of Health and Human Services
    . Polycystic ovary syndrome (PCOS) fact sheet. Available from https://www.womenshealth.gov/publications/our-publications/fact-sheet/polycystic-ovary-syndrome.pdf Accessed 23 February 2015
  18. ↵
    1. Teede HJ,
    2. Joham AE,
    3. Paul E, et al
    . Longitudinal weight gain in women identified with polycystic ovary syndrome: Results of an observational study in young women. Obesity 2013;21:1526–1532
    OpenUrlCrossRefPubMedWeb of Science
  19. ↵
    1. Wild RA,
    2. Carmina E,
    3. Diamanti-Kandarakis E, et al
    . Assessment of cardiovascular risk and prevention of cardiovascular disease in women with the polycystic ovary syndrome: a consensus statement by the Androgen Excess and Polycystic Ovary Syndrome (AE-PCOS) Society. J Clin Endocrinol Metab 2010;95:2038–2049
    OpenUrlCrossRefPubMedWeb of Science
  20. ↵
    1. Fauser BCJM,
    2. Tarlatzis BC,
    3. Rebar RW, et al
    . Consensus on women’s health aspects of polycystic ovary syndrome (PCOS): the Amsterdam ESHRE/ASRM-Sponsored 3rd PCOS Consensus Workshop Group. Fertil Steril 2012;97:28–38
    OpenUrlCrossRefPubMed
  21. ↵
    1. Hsu MI
    . Changes in the PCOS phenotype with age. Steroids 2013;78:761–766
    OpenUrlCrossRefPubMedWeb of Science
  22. ↵
    1. Bates GW,
    2. Legro RS
    . Long-term management of polycystic ovarian syndrome (PCOS). Mol Cell Endocrinol 2013;373:91–97
    OpenUrlPubMed
  23. ↵
    1. Brown ZA,
    2. Louwers YV,
    3. Lie Fong S, et al
    . The phenotype of polycystic ovary syndrome ameliorates with aging. Fertil Steril 2011;96:1259–1265
    OpenUrlCrossRefPubMed
  24. ↵
    1. Broekmans FJ,
    2. Fauser BCJM
    . Diagnostic criteria for polycystic ovarian syndrome. Endocrine 2006;30:3–11
    OpenUrlCrossRefPubMedWeb of Science
  25. ↵
    1. Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group
    . Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome (PCOS). Hum Reprod 2004;19:41–474
    OpenUrlAbstract/FREE Full Text
  26. ↵
    1. Roe AH,
    2. Prochaska E,
    3. Smith M,
    4. Sammel M,
    5. Dokras A
    . Using the Androgen Excess-PCOS Society criteria to diagnose polycystic ovary syndrome and the risk of metabolic syndrome in adolescents. J Pediatr 2013;162:937–941
    OpenUrlPubMed
  27. ↵
    1. Carmina E,
    2. Oberfield SE,
    3. Lobo RA
    . The diagnosis of polycystic ovary syndrome in adolescents. Am J Obstet Gynecol 2010;203:201.e1–5
    OpenUrlPubMed
  28. ↵
    1. Randeva HS,
    2. Tan BK,
    3. Weickert MO, et al
    . Cardiometabolic aspects of the polycystic ovary syndrome. Endocr Rev 2012;33:812–841
    OpenUrlCrossRefPubMedWeb of Science
  29. ↵
    1. American College of Obstetricians and Gynecologists
    . ACOG practice bulletin No. 108: polycystic ovary syndrome. Obstet Gynecol 2009;114:936–949
    OpenUrlCrossRefPubMed
  30. ↵
    1. Moran LJ,
    2. Ko H,
    3. Misso M, et al
    . Dietary composition in the treatment of polycystic ovary syndrome: a systematic review to inform evidence-based guidelines. J Acad Nutr Diet 2013;113:520–545
    OpenUrlCrossRefPubMed
  31. ↵
    1. Giallauria F,
    2. Palomba S,
    3. Vigorito C, et al
    . Androgens in polycystic ovary syndrome: the role of exercise and diet. Semin Reprod Med 2009;27:306–315
    OpenUrlCrossRefPubMed
  32. ↵
    1. Thomson RL,
    2. Spedding S,
    3. Buckley JD
    . Vitamin D in the aetiology and management of polycystic ovary syndrome. Clin Endocrinol 012;77:343–350
  33. ↵
    1. Lerchbaum E,
    2. Rabe T
    . Vitamin D and female fertility. Curr Opin Obstet Gynecol 2014;26:145–150
    OpenUrlPubMed
  34. ↵
    1. Writing Group of the Nutrition Care Process/Standardized Language Committee
    . Nutrition care process and model, part I: the 2008 update. J Am Diet Assoc 2008;108:1113–1117
    OpenUrlCrossRefPubMed
  35. ↵
    1. Legro RS,
    2. Arslanian SA,
    3. Ehrmann DA, et al
    . Diagnosis and treatment of polycystic ovary syndrome: an Endocrine Society clinical practice guideline. J Clin Endoncrinol Metab 2013;98:4565–4592
    OpenUrl
  36. ↵
    1. Diamanti-Kandarakis E
    . PCOS in adolescents. Best Pract Res Clin Obstet Gynaecol 2010;24:173–183
    OpenUrlCrossRefPubMed
  37. ↵
    1. Costello MF,
    2. Ledger WL
    . Evidence-based lifestyle and pharmacological management of infertility in women with polycystic ovary syndrome. Women’s Health 2012;8:277–290
    OpenUrl
  38. ↵
    1. Thessaloniki ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group
    . Consensus on infertility treatment related to polycystic ovary syndrome. Hum Reprod 2008;23:462–477
    OpenUrlAbstract/FREE Full Text
Next
Back to top
Diabetes Spectrum: 28 (2)

In this Issue

May 2015, 28(2)
  • Table of Contents
  • Table of Contents (PDF)
  • Index by Author
Sign up to receive current issue alerts
View Selected Citations (0)
Print
Download PDF
Article Alerts
Sign In to Email Alerts with your Email Address
Email Article

Thank you for your interest in spreading the word about Diabetes Spectrum.

NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.

Enter multiple addresses on separate lines or separate them with commas.
The Role of Polycystic Ovary Syndrome in Reproductive and Metabolic Health: Overview and Approaches for Treatment
(Your Name) has forwarded a page to you from Diabetes Spectrum
(Your Name) thought you would like to see this page from the Diabetes Spectrum web site.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Citation Tools
The Role of Polycystic Ovary Syndrome in Reproductive and Metabolic Health: Overview and Approaches for Treatment
Carrie C. Dennett, Judy Simon
Diabetes Spectrum May 2015, 28 (2) 116-120; DOI: 10.2337/diaspect.28.2.116

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Add to Selected Citations
Share

The Role of Polycystic Ovary Syndrome in Reproductive and Metabolic Health: Overview and Approaches for Treatment
Carrie C. Dennett, Judy Simon
Diabetes Spectrum May 2015, 28 (2) 116-120; DOI: 10.2337/diaspect.28.2.116
del.icio.us logo Digg logo Reddit logo Twitter logo CiteULike logo Facebook logo Google logo Mendeley logo
  • Tweet Widget
  • Facebook Like
  • Google Plus One

Jump to section

  • Article
    • PCOS and Reproductive Health
    • PCOS and Metabolic Health
    • Etiology of PCOS
    • Diagnosing PCOS
    • Treating PCOS: Lifestyle Interventions
    • Case Study: MNT in PCOS
    • Treating PCOS: Pharmaceutical Interventions
    • Summary
    • Duality of Interest
    • References
  • Figures & Tables
  • Info & Metrics
  • PDF

Related Articles

Cited By...

More in this TOC Section

Departments

  • Smart Connected Insulin Pens, Caps, and Attachments: A Review of the Future of Diabetes Technology
  • Brief Literature Review: The Potential of Diabetes Technology to Improve Sleep in Youth With Type 1 Diabetes and Their Parents: An Unanticipated Benefit of Hybrid Closed-Loop Insulin Delivery Systems
  • Mental Health and Behavioral Screening in Pediatric Type 1 Diabetes
Show more Departments

Nutrition FYI

  • Chrononutrition Applied to Diabetes Management: A Paradigm Shift Long Delayed
  • The Gluten-Free Diet: Fad or Necessity?
  • Nutrition Considerations for Microbiota Health in Diabetes
Show more Nutrition FYI

Similar Articles

Navigate

  • Current Issue
  • Papers in Press
  • Archives
  • Submit
  • Subscribe
  • Email Alerts
  • RSS Feeds

More Information

  • About the Journal
  • Instructions for Authors
  • Journal Policies
  • Reprints and Permissions
  • Advertising
  • Privacy Policy: ADA Journals
  • Copyright Notice/Public Access Policy
  • Contact Us

Other ADA Resources

  • Diabetes
  • Diabetes Care
  • Clinical Diabetes
  • Scientific Sessions Abstracts
  • Standards of Medical Care in Diabetes
  • BMJ Open - Diabetes Research & Care
  • Professional Books
  • Diabetes Forecast

 

  • DiabetesJournals.org
  • Diabetes Core Update
  • ADA's DiabetesPro
  • ADA Member Directory
  • Diabetes.org

© 2021 by the American Diabetes Association. Diabetes Spectrum Print ISSN: 1040-9165, Online ISSN: 1944-7353.