1. Summer 2012 Seminar Marie Gorski-Mahne

2. What is PCOS? PCOS is the most common endocrine disorder affecting women (1, 5). Symptoms of PCOS include: - Oligomenorrhea or amenorrhoea - Hyperandrogenaemia - Ovarian cysts - Acne - Weight gain - Alopecia - Skin tags - Pelvic pain - Anxiety or depression - Sleep apnea - acanthosis nigricans

3. What is PCOS?  Characteristic biochemical abnormalities of PCOS include (9): - elevated serum androgen concentrations - elevated luteinizing hormone (LH) concentrations - with normal levels of follicle-stimulating hormone (FSH)

4. Causes of PCOS

5. What is PCOS?  There is a strong association between PCOS and abnormalities of metabolic syndrome including (1): - central obesity - dyslipidemia - hypertension - insulin resistance

6. What is PCOS?

7. Occurrence of PCOS  Between 1 in 10 and 1 in 20 women of childbearing age have PCOS affecting nearly 5 million women in the United States alone, and can occur in girls as young as 11 years old (4).

8. Causes of PCOS  While there are no specific known causes of PCOS, there are several factors which may be involved including genetics. Women are more likely to develop PCOS if a mother or sister is already affected (4).

9. Causes of PCOS  Symptoms of PCOS are related to the underlying hormonal imbalance where ovaries produce excessive amounts of the male hormone – androgen.  Excess androgen affects the development and release of eggs during ovulation (4).

10. Causes of PCOS  While it is widely thought that PCOS develops from a genetic dysfunction involving likely more than one gene (11), research shows that obese women are more at risk for hirsutism and ovulatory dysfunction than their lean counterparts (12).

11. Medical Intervention  While there is no known cure for PCOS, medical interventions target increasing ovulation and improving insulin resistance.  Metformin has been used successfully to control blood sugar and lower the production of testosterone (4).  Bariatric surgery has also resulted in increased fertility in morbidly obese women (BMI >40) with PCOS.

12. Medical Intervention  Women with PCOS who also face infertility may benefit from fertility medications to stimulate ovulation including: - Clomiphene (oral medication) - Metformin with Clomiphene - Gonadotropins (injections) - IVF (in vitro fertilization)

13. Nutrition Intervention  Insulin resistance and lipid disorders are noted in women with PCOS independent of body mass however, obesity in PCOS is shown to have a greater incidence of diabetes and dyslipidemia (5).  At least 50% of women with PCOS are obese (5).  70% of lean women with PCOS have android fat distribution (6).

14. Nutrition Intervention  A recent study from Corton et al., showed an “increased expression of pro- inflammatory genes, as well as those involved in regulating immune function, oxidative stress, lipid metabolism, and insulin signaling” (7) from gene expression profiling of visceral fat in women with PCOS.

15. Nutrition Intervention  Reducing the glycemic load by consuming foods with a lower glycemic index (GI) appears to have a tri-fold affect on women with PCOS including: - improved insulin sensitivity - decrease in post prandial hyperglycemia - decease in triglycerides and increase in HDL-cholesterol (8)

16. Nutrition Intervention  1. Daily energy requirement of 2,000 – 2,400 kcal for patient of average build who is not too active.  2. Exercise regularly: 30 min of moderate exercise daily will help to maintain body weight. More prolonged or vigorous exercise may  be needed to produce weight loss.  3. Eat no more than 30% of daily calories as fat, restricting saturated fat to 5-10% total calories. Use low fat spreads and dairy products.  4. Carbohydrate should count for 45 – 55% of the diet initially. Keep intake of refined carbohydrate down. Concentrate on low  glycemic index (GI) foods, those high in fiber and wholegrain foods.  5. Diet of higher protein content may improve satiety and insulin sensitivity. Start with 20% of daily energy as protein, but this may be  increased by substituting for carbohydrate in those who have difficulty controlling eating or maintaining weight. (1)

17. Nutrition Intervention  6. Avoid too much red meat. Eat oily fish at least once per week to supply long-chain essential fatty acids (omega-3, polyunsaturated  fatty acids).  7. Eat at least five portions of fruit or vegetable per day. This promotes satiety, supplies fiber and maintains the micronutrient content  of the diet.  8. Eat regularly and focus food intake on three meals per day (with snacks). Breakfast is an important meal.  9. Avoid calorie-dense snacks as they promote hyperinsulinemia and drive hunger. Make sure that drinks are counted in daily  calorie intake estimated – fruit juices and alcoholic drinks are often forgotten but are rich in calories and carbohydrates.  10. Even modest weight loss has health benefits. Achieving this requires energy restriction – modest 200 kcal deficit (decreased  intake or increased utilization will lead to 5% weight loss in 6 months for many. A 500 kcal per day energy deficit usually equates  to weight loss of up to 0.5 kg/week. (1)

18. Nutrition Intervention

19. References 1. FarshchiI H., Rane A., Love A., Kennedy R. Diet and nutrition in polycystic ovary syndrome (PCOS): Pointers for nutritional management. J of Obst and Gyn. 2007;27(8)762-773. 2. Ehrmann DA. 2005. Polycystic ovary syndrome. New England Journal of Medicine 352:1223 – 1236. 3. Sartor BM, Dickey RP. 2005. Polycystic ovarian syndrome and the metabolic syndrome. American Journal of the Medical Sciences 330:336 – 342. 4. Department of Health and Human Services, Office on Women’s Health. Polycystic Ovarian Syndrome (PCOS) fact sheet [internet]. 2012 [retrieved on Jul 5, 2012] from: http://www.womenshealth.gov/publications/our-publications/fact-sheet/polycystic-ovary- syndrome.cfm#a http://www.womenshealth.gov/publications/our-publications/fact-sheet/polycystic-ovary- syndrome.cfm#a 5. Gambineri A, Pelusi C, Vicennati V, Pagotto U, Pasquali R. 2002.Obesity and the Polycystic Ovary Syndrome. International Journal of Obesity 26:883 – 896. 6. Kirchengast S, Huber J. 2001. Body composition characteristics and body fat distribution in lean women with polycystic ovary syndrome. Human Reproduction 16:1255 – 1260. 7. Corton M, Botella-Carretero JI, Benguria A, Villuendas G, Zaballos A, San Millan JL et al. 2007. Differential gene expression profile in omental adipose tissue in women with polycystic ovary syndrome. Journal of Clinical Endocrinology and Metabolism 92:328 – 337. 8. Marsh K, Brand-Miller J. 2005. The optimal diet for women with polycystic ovary syndrome? British Journal of Nutrition 94:154 –165. 9. Franks S. Polycystic ovarian syndrome in adolecents. Intl J of Obesity. 2008;32,1035-1041. 10. Rotterdam 1. Revised 2003 consensus on diagnostic criteria and ong-term health risks related to polycystic ovary syndrome (PCOS). Hum Reprod 2004; 19: 41–47. 11. Franks S, Gharani N,Waterworth D, Batty S, White D,Williamson R et al. The genetic basis of polycystic ovary syndrome.Hum Reprod 1997; 12: 2641–2648. 12. Kiddy DS, Sharp PS, White DM, Scanlon MF, Mason HD, Bray CS et al. Differences in clinical and endocrine features between obese and non-obese subjects with polycystic ovary syndrome: an analysis of 263 consecutive cases. Clin Endocrinol (Oxf) 1990; 32:213–220.