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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
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
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
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.
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
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
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.