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- 1. Management of Obesity in Women: Current Strategies Robert Kushner, MD Professor of Medicine Northwestern University Feinberg School of Medicine Clinical Director, Northwestern Comprehensive Center on Obesity rkushner@northwestern.edu
- 2. Disclosures • Dr. Kushner has served on the Medical Advisory Boards for Amylin, Vivus, Orexigen and Allergan. • He is the author of Dr. Kushner’s Personality Type Diet and Counseling Overweight Adults: The Lifestyle Patterns Approach and Toolkit
- 3. Multiple Determinants of Obesity • Genetics Health care • Biology Economics • Environment Ecology • Society Diet • Personal Physical activity responsibility Social networks • Weight gaining Stress and emotion medications
- 4. Life cycle
- 5. Weight-Life Events Graph Your Weight Gain Your eight Gain Weight Time
- 6. Weight Gain – Life Events Graph: Childhood and Adolescence
- 7. Childhood & Adolescent Obesity • Screen time (TV, computer, video games, smart phone) • Less exercise time during school • Liquid calories (colas, juices) • More meals eaten away from home • Snacking • Parenting and role modeling
- 8. Portion Sizes out of Control
- 9. ‘Let’s Move’ • Nationwide campaign targeting childhood obesity – Getting parents more informed about nutrition and exercise – Improving quality of food in schools – Making healthy foods more affordable and accessible for families – Focusing more on physical education
- 11. The Pressure of Beauty Ideals
- 12. The Stigma of Obesity
- 14. Obesity and Infertility Relative Risks by BMI at Age 18 Menstrual Cycle Irregularity Primary Ovulatory Infertility 2 4 1.75 3.5 3 1.5 2.5 Relative Relative Risk 1.25 Risk 2 1 1.5 Reference 1 0.75 Reference 0.5 0.5 0 15 20 25 30 35 15 20 25 30 35 BMI at Age 18 BMI at Age 18 pted from Rich-Edwards et al. Am J Obstet Gynecol. 1994;171:171-177.
- 15. Weight Gain – Life Events Graph Pregnancy
- 16. Weight Gain – Life Events Graph Pregnancy
- 17. Weight Gain – Life Events Graph Pregnancy
- 19. Consequences of Maternal Weight Gain • Postpartum weight • Stillbirth retention • Shoulder dystocia • Obstetric • Large baby complications • Shorter breast feeding – Gestational • Fetal imprinting diabetes – Developmental- – Hypertension origins for long-term – Eclampsia risk – Caesarean delivery • Offspring obesity
- 20. Relationship Between Mother’s Weight and Child’s Risk of Obesity % Children Obese Maternal BMI 2-yr olds 3-yr olds 4-yr olds < 18.5 2.5 4.4 4.7 18.5 – 24.9 6.4 7.5 9.0 25 – 29.9 9.0 12.0 14.5 30 – 30.9 13.9 19.7 22.8 ≥ 40 19.4 24.0 28.8 Maternal BMI measured in the first trimester of child’s gestation Whitaker RC. Pediatrics 2004;114(1): e29-e36
- 21. (25 – 35 lbs) (15 – 25 lbs) (11 – 20 lbs) JAMA 2009;302:241
- 23. Weight Gain – Life Events Graph Midlife
- 24. Weight Gain – Life Events Graph Midlife
- 25. Impairment of Health and Quality of Life Women BMI n=7018 <25 >30 Proportions of subjects, % Shortness of breath walking upstairs 18.4 46.4 Chronic low back pain 17.8 24.7 Poor QOL: Moderate activities 18.4 36.0 Bending, kneeling 20.7 48.3 Walking 1 block 4.5 15.4 Lean et al, Arch Intern Med 1999
- 26. Prevalence (%) of Comorbidity Among Women by Obesity Class* Weight Status Category (%)† Health Condition Under- Normal Over- Obesity Obesity Obesity weight weight Class 1 Class 2 Class 3 Type 2 diabetes mellitus 4.76 2.38 7.12 7.24 13.1 19.8 Gallbladder disease 6.42 6.29 11.8 15.99 19.1 23.4 Coronary heart disease 12.0 6.87 11.1 12.56 12.3 19.2 High blood cholesterol 13.3 26.89 45.5 40.37 40.9 36.3 High blood pressure 19.8 23.26 38.7 47.95 54.5 63.1 Osteoarthritis 7.79 5.22 8.51 9.94 10.3 17.1 *N = 7,689. † Estimates are weighted to account for the sample design. Weight categories are based on the NHLBI classification. (Must A, et al. JAMA. 1999)
- 27. Relationship Between BMI and Risk of Type 2 Diabetes Mellitus 100 93.2 90 Age-Adjusted Relative Risk 80 70 ■ Men ● Women 60 54.0 50 42.1 40.3 40 27.6 30 21.3 8.1 15.8 20 5.0 11.6 2.9 4.3 2.2 6.7 1.0 1.5 4.4 10 1.0 1.0 0 <22 <23 23-23.9 24-24.9 25-26.9 27-28.9 29-30.9 31-32.9 33-34.9 35+ Body Mass Index (kg/m2) Chan J, et al. Diabetes Care. 1994;17:961-969. Colditz G, et al. Ann Intern Med. 1995;122:481-486.
- 28. Abdominal Obesity Is Associated with Increased Risk of Developing Diabetes 24 20 Relative Risk 16 12 8 4 0 <71 71–75.9 76–81 81.1–86 86.1–91 91.1–96.3 >96.3 [<27.9 in.] [27.9–29.8 in.] [29.9–31.9 in.] [32–33.9 in.] [34–35.8 in.] [35.9–37.9 in.] [>38 in.] Waist Circumference (cm) Carey VJ, et al. Am J Epidemiol. 1997;145:614-619.
- 30. 20-yr Changes in BMI and Waist Circumference Among Women Body Mass Index (BMI) Waist Circumference (cm) Black White Total Hispanic Data from NHANES completed during yrs 1976 - 2006 Kramer H, et al. J Diabetes Complications 2010;24:368-74
- 32. Changes in Weight and Body Composition Through the Menopausal Transition Lovejoy JC et al. International J Obesity 2008;32:949-58
- 33. Changes in Hormones and Calories Through the Menopausal Transition Lovejoy JC et al. International J Obesity 2008;32:949-58
- 34. Importance of Measuring Waist Circumference: BMI 25-29.9 (Overweight) Men (n=3081) Women (n=2606) Prevalence, % Nl WC High WC Nl WC High WC Hypertension 23.0 44.8 12.3 37.5 Type 2 DM 2.7 10.6 1.6 10.0 Hyper-chol 17.2 26.2 19.4 35.2 High LDL-C 19.3 27.2 13.6 26.6 Low HDL-C 35.3 49.0 10.0 15.0 Hyper-TG 21.7 36.3 10.6 21.8 Janssen et al. Arch Intern Med 2002;162:2074-9
- 35. Abdominal Fat Distribution Increases the Risk of Coronary Heart Disease The Iowa Women’s Health Study 2.5 2.0 Relative Risk 1.5 1.0 3 t io 0.5 2 Ra p t- Hi tile 0.0 1 a is Ter 3 2 1 W Body Mass Index Tertile Folsom AR et al. Arch Intern Med. 2000;160:2117-2128.
- 36. Gastroesophageal Reflux and Obese Women 4 Association between body mass index 3.5 and the risk of frequent symptoms of GERD frequency of GERD symptoms Multivariate odds ratio for 3 P < 0.001 ● ● 2.93 (2.24-3.85) 2.92 2.5 ● (2.35-3.62) 2 ● 2.43 (1.96-3.01) 2.20 (1.81-2.66) 1.5 ●1.38 (1.13-1.67) 1 ● ● 0.67 (0.48-0.93) 0.5 0 <20.0 20.0-22.4 22.5-24.9 25.0-27.4 27.5-29.9 30.0-34.9 ≥35 Body mass index n = 2306 women with symptoms of heartburn, acid regurgitation, or both Jacobson BC, et al. N Engl J Med. 2006;354:2340-2348.
- 37. Obesity and Cancer Mortality Women Uterus (≥40) 6.25 Kidney (≥40) 4.75 Cervix (≥35) 3.20 Pancreas (≥40) 2.76 Esophagus (≥30) 1.88* Type of All other cancers (≥40) 2.51 cancer Gallbladder (≥30) 2.13 (highest Breast (≥40) 2.12 BMI Non-Hodgkin lymphoma (≥35) 2.51* category) All cancers (≥40) 2.64* Liver (≥35) 1.68 Ovary (≥35) 1.51 Colon and rectum (≥40) 1.46 Multiple myeloma (≥35) 1.44 0 1 2 3 4 5 6 7 P≤.05, *relative risk for women who never smoked Relative Risk For each relative risk, the comparison was between women in the highest BMI category and men in the reference category (BMI 18.5 to 24.9) Calle EE et al. N Engl J Med. 2003;348:1625-1638.
- 38. Current Approaches to Treating Obesity ● Diet, exercise, and behavioral therapy continue to be the mainstays of obesity treatment ● There is limited pharmacotherapy available. When possible, use weight-losing medications when treating co-morbidities ● A 5 – 10% weight loss improves many of the obesity-related metabolic ● Active weight loss and maintenance of lost weight requires ongoing support and use of resources
- 39. Macronutrients To Address Individual Risk Factors Waist circumference Caloric Reduction Blood pressure DASH Metabolic Blood glucose Carbohydrate controlled Syndrome Triglycerides HDL-cholesterol Mediterranean, TLC LDL-cholesterol Insulin resistance Mediterranean Thrombotic risk Omega–3 Fatty acids
- 40. Manson JE et al. Arch Intern Med 2004;164:249-58
- 41. Summary • There are multiple events in a woman’s life that predispose her to weight gain • The reasons for weight gain at each time point differ – a combination of changing biology, hormonal status and life events • It is important to implement preventive and treatment strategies to halt further weight gain and the development of ill health
- 42. Thank you!
Notes de l'éditeur
- 16
- 1. Colditz GA, Willett WC, Rotnitzky A, Manson JE. Weight gain as a risk factor for clinical diabetes mellitus in women. Ann Intern Med 1995;122:481-486. 2. Chan JM, Rimm EB, Colditz GA, et al. Obesity, fat distribution, and weight gain as risk factors for clinical diabetes in men. Diabetes Care 1994;17:961-969. 3. Harris MI, Flegal KM, Cowie CC, et al. Prevalence of diabetes, impaired fasting glucose, and impaired glucose tolerance in U.S. adults. The Third National Health and Nutrition Examination Survey, 1988-1994. Diabetes Care 1998;21:518-524. 4. Ohlson LO, Larsson B, Svardsudd K, et al. The influence of body fat distribution on the incidence of diabetes mellitus. Diabetes 1985;34:1055-1058. 5. Helmrich SP, Ragland DR, Leung RW, Paffenbarger Jr RS. Physical activity and reduced occurrence of non-insulin-dependent diabetes mellitus. N Engl J Med 1991;325:147-152.
- >96.3 cm = >37.9 inches 91.1 - 96.3 cm = 35.8- 37.9 inches 86.1 – 91.0 cm = 33.9 – 35.8 inches 81.1 – 86.0 cm = 31.9 – 33.9 inches 76.0 – 81.0 cm = 29.9 – 31.9 inches 71.0 – 75.9 cm = 27.9 – 29.8 inches <71 cm =<27.9 inches Increased abdominal adiposity is highly correlated with insulin resistance, and ultimately T2 DM Carey VJ, et al. Am J Epidemiol . 1997;145:614-619.
- In 1947 Jean Vague a French physician made the association of the apple shape (i.e., android obesity or male patterned obesity of central abdominal obesity) with increased risk for CVD. Likewise, Vague noted that the pear shape (i.e., gynoid obesity or female pattern obesity) was associated with a lower risk for CVD. Notice in gynoid obesity the weight is carried below the waist in the hips and thighs. Why worry about Central Obesity versus BMI? The deep abdominal fat cells that lie in the visceral area below the omental membrane have been found to be metabolically active. {The Visceral Adipose Tissue (VAT)} The superfical fat tissue of Superfical Adipose Tissue (SAT) is believed to be less atherogenic. Why should we worry more about deep VAT versus SAT! The deep visceral adipose tissue or fat cells (under the omental membrane) called abdominal adipocytes are metabolically active and excrete substrates that are deleterious to the CV system. Visceral Adipose Tissue (VAT) As the adipocytes increase or enlarge macrophages or white blood cells are drawn to the abdominal fat cells in increased numbers. These macrophages reside in between abdominal adipose cells and release abnormal substrates called cytokines etc. (i.e., IL-6, Tumor necrosis factor etc) Central Obesity is the cornerstone of a group of abnormalities associated with development of Type 2 Diabetes (T2D) and CVD . There is a predictable pathway known as the “ Metabolic Syndrome ,” that imposes increased risk, as much as a decade prior to diagnosis of frank pathology.
- Abdominal fat distribution increases the risk for coronary heart disease (CHD) among lean, overweight, and obese persons. The risk of CHD begins to increase at a normal BMI, which is 23 kg/m 2 for men and 22 kg/m 2 for women [1]. Data from both the Iowa Women’s Health Study [2] (shown on this figure) and the Nurses’ Health Study [3] found that women in the lowest BMI but highest waist-to-hip circumference ratio tertiles (a measure of abdominal adiposity) had a greater risk of fatal and nonfatal myocardial infarctions than women in the highest BMI but lowest waist-to-hip circumference ratio tertiles. Reference 1. Stamler J et al. Is relationship between serum cholesterol and risk of premature death from coronary disease continuous or graded? Findings in 356,222 primary screenees of the Multiple Risk Factor Intervention Trial (MRFIT). JAMA . 1986;256:2823-2828. 2. Folsom AR et al. Associations of general and abdominal obesity with multiple health outcomes in older women. Arch Intern Med . 2000;160:2117-2128. 3. Rexrode KM et al. Abdominal adiposity and coronary heart disease in women. JAMA . 1998;280:1843-1848.
- Diet, exercise, and behavioral therapy continue to be the mainstays of obesity treatment. Short-term efficacy of pharmacotherapy has been noted in clinical trials. Side effects of pharmacologic therapy vary and may impact administration. Surgery is reserved for morbidly obese patients with comorbidities.
- Current interventions for preventing metabolic syndrome often are insufficient, being directed to CVD risk factors instead of a significant root cause—ie, visceral fat as evidenced by increased weight circumference. Dyslipidemia and metabolic abnormalities often persist. Patients continue to be placed at increased risk for CVD and diabetes.