Adult Obesity and Metabolic Syndrome Flashcards
How do we diagnose overweight and obesity?
Body Mass Index= Body weight (kg)/ Height (m^2)
Who and When to Treat? Assessing Obesity in Clinical Practice
Body Mass Index (BMI) = weight(kg)/height (m2)
a. Surrogate measurement for body fat content
b. Same calculation for men and women
c. No frame adjustments like “insurance tables”
d. BMI allows classification of patients as to degree of obesity
e. BMI correlates with adverse health affects from excess body fat
BMI-Associated Disease Risk
The use of body mass index (BMI) has been proposed by the National Institutes of Health and the World Health Organization as a method for defining overweight and obesity.
b. This classification system is based on epidemiologic data indicating that the risk of premature mortality usually begins to increase at a BMI of 25 to 29.9 kg/m2, and increases further at a BMI of 30 kg/m2.
c. Other factors, such as waist circumference, weight gain since young adulthood, fitness level, and ethnic or racial background, also influence the relationship between BMI and overall disease risk.
Are you measuring BMI?
Several ways to measure BMI, with charts like these or with calculators online or available for palm pilot. BMI is a vital sign. It should be recorded as routinely as blood pressure or pulse.
BMI can be easily determined with a chart such as this one.
BMI, although invaluable for evaluating obesity, is not the only tool available. Fat mass and the distribution of body fat are also important, and no measurement can be a substitute for the clinician’s judgment.
Relationship Between BMI and Percent
Body Fat in Men and Women
a. The relationship between BMI and percent body fat is sex- and age-dependent. At an equivalent BMI, women and older persons have a higher percent body fat than men and younger persons.
b. In addition, persons who have a large muscle mass can have an “obese” BMI despite having a normal amount of body fat, while those with excess adiposity and reduced muscle mass can have a “normal” BMI.
BMI may not be the whole story…
a. BMI is a measure of weight for height, cannot distinguish between lean and fat mass.
b. BMI may be less accurate in certain populations: elderly, certain ethnic groups, large muscle mass.
c. Some "obese" people according to BMI: Tom Cruise (5'7 201 lbs) = 31 Sylvester Stallone (5'9 228 lbs) = 33 Arnold Schwarzenegger (6'2 257 lbs) = 32
Waist Circumference
Memorize these waist circumferences
a. Health risks of obesity influenced by BMI AND by the way body fat is distributed:
b. Abdominal adiposity: independent predictor of risk for DM, HTN, CAD, and dyslipidemia. 1
c. WC: correlated w/ abdominal fat mass.
d. Used w/ BMI: to identify those at increased risk of obesity related complications. 2
e. Increased risk: ♀ ≥ 35 in, ♂ ≥ 40.
Waist Circumference is NOT Belt Size
WC is measured 2 inches above iliac crest
Abdominal Fat Distribution Increases the Risk of Coronary Heart Disease
a. Abdominal fat distribution increases the risk for coronary heart disease (CHD) among lean, overweight, and obese persons.
b. The risk of CHD begins to increase at a normal BMI, which is 23 kg/m2 for men and 22 kg/m2 for women.
c. 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.
Why is Abdominal Obesity Bad?
a. Proposed mechanism: release of free fatty acids into the blood stream into liver, causing insulin resistance
i. Free fatty acids from intra-peritoneal fat
b. Increased VAT correlates with insulin resistance only if there are increased intrahepatic triglycerides
i. Neither omentectomy nor liposuction in humans seems to improve insulin sensitivity
The Metabolically Healthy Obese
These are epidemiologic data from a study of 5440 participants in the National Health and Nutrition Examination Survey (NHANES).
Metabolic risk factors in this study were: 1) blood pressure >130/85 or on medication; 2) triglycerides ≥150 mg/dl; 3) HDL < 40 (women) or < 50 (men); 4) fasting glucose ≥ 100 mg/dl or on medication; 5) insulin resistance (HOMA > 5.13, 90th percentile); or 6) systemic inflammation (hsCRP > 0.1, which was 90th percentile).
Metabolically abnormal was having 2 or more of these risk factors. INTERESTINGLY, WAIST CIRCUMFERENCE WAS NOT COUNTED IN THIS, ONLY BMI.
Evidence for Racial-Ethnic Differences in Weight: AA and Latino
AA= african american
a. AA women have REE 100 kcal lower than white women, even after adjusting for body weight and fat free mass
b. Some metabolic improvements after diet are seen less in AA patients compared to white and Latino patients
c. After adjusting for BMI, AA patients are less likely than white patients to have low HDL and high TG3
d. Waist circumference cutoffs that correlated with presence of CV risk factors were 5-6 cm greater in AA men compared to white men, with Mexican-American men intermediate
Relationship Between BMI and
Risk of Type 2 Diabetes Mellitus
a. The risk of diabetes increases with increasing BMI values in men and women
b. Moreover, the age-adjusted relative risk for diabetes begins to increase at BMI values that are considered normal for men (24 kg/m2) and women (22 kg/m2) based on mortality risk.
c. The marked increase in the prevalence of obesity is an important contributor to the 25% increase in the prevalence of diabetes in the United States over the last 20 years
d. Increases in abdominal fat mass, weight gain since young adulthood, and a sedentary lifestyle are additional obesity-related risk factors for diabetes
Weight gain in adulthood and risk of type 2 diabetes mellitus
a. An increase in weight since young adulthood (18–20 years of age) in men and women is associated with increased risk of developing type 2 diabetes.
b. A weight gain of 10 kg, which is the average amount of weight gained by US adults from 20 to 50 years of age, is associated with a two- to threefold increase in the risk of diabetes.
c. Weight gain during adulthood is also associated with an increased risk of coronary heart disease, hypertension, and cholelithiasis compared with those who maintain their weight after 18 to 20 years of age.
Hypertension
a. Epidemiologic studies document linear relationship between HTN and BMI.
b. Risk of HTN up to 5 times higher among obese than among those of normal weight.
c. 85% of HTN occurs in individuals with BMI > 25 5
Stroke
Asia-Pacific Cohort Collaboration Study: each unit change in BMI 8% increase in hypertensive death and ischemic stroke
Obstructive Sleep Apnea
a. Prevalence among obese approx 40%
b. Linked to systemic HTN and increased risk of other CVD including CAD, stroke, CHF, arrythmia, and 2° pulmonary HTN.
c. Associated with an increased risk for DM2, independent of obesity.
Cancer and Obesity
Overweight and obesity associated with ↑ risk of: Post-menopausal breast Colon Endometrial Renal cell Esophageal Pancreatic Prostate Cervical
Characteristics of the Metabolic Syndrome: NCEP-ATP III
a. The metabolic syndrome consists of a constellation of risk factors that place patients at risk for both the development of type 2 diabetes and atherosclerotic disease. The hallmarks of the syndrome are:
Abdominal obesity
Atherogenic dyslipidemia – characterized by elevated triglycerides, small LDL particles, and low HDL
Elevated blood pressure
Insulin resistance with or without glucose intolerance
A prothrombotic state
A proinflammatory state
b. These “lipid and non-lipid risk factors of metabolic origin” not only increase the risk of type 2 diabetes, but also enhance the risk for coronary heart disease “at any given cholesterol level”
ATP III: the metabolic syndrome
a. The NCEP ATP III guidelines define 5 components of the metabolic syndrome; at least 3 of the 5 criteria are required for the diagnosis of the metabolic syndrome.
i. Note that the NCEP metabolic syndrome has different criteria for triglycerides and HDL-C, unlike the WHO definition, which lists high triglycerides and/or low HDL-C as a single factor.
b. The hallmarks of the syndrome are:
1. Abdominal obesity
2. Glucose intolerance/ Insulin resistance
3. Hypertension
4. Atherogenic dyslipidemia
5. Proinflammatory/ Prothrombotic state
c. Almost all individuals in North America who have the metabolic syndrome have a high waist circumference as one of the criteria. Note also that the NCEP definition of the metabolic syndrome is more liberal than the NCEP major risk factors for blood pressure (140/90 mm Hg) and HDL-C (<40 mg/dl in both men and women).
Metabolic Syndrome: Impact on Cardiovascular Health
a. Subjects meeting the WHO definition of metabolic syndrome were significantly more likely to have a history of coronary heart disease, myocardial infarction, and stroke than those without the syndrome.
b. The presence of metabolic syndrome was associated with significantly increased risk of coronary heart disease (relative risk, 2.96, P < 0.001), myocardial infarction (RR 2.63, P < 0.001), and stroke (RR 2.27, P < 0.001)
c. Overall, the prevalence of coronary heart disease, MI, and stroke were approximately 3-fold higher in the group with metabolic syndrome
Metabolic Syndrome: Impact on Mortality
Isomaa and colleagues also evaluated differences in mortality between subjects with and without the metabolic syndrome (as defined by WHO).
The all-cause mortality rate was significantly higher in subjects with the metabolic syndrome (18.0% vs 4.6%, P < 0.001), as was cardiovascular mortality (12.0% vs 2.2%,
P < 0.001) [1].
Elevated Risk of CVD Prior to Clinical Diagnosis of Type 2 Diabetes
a. . These results suggest that aggressive management of cardiovascular risk is warranted in individuals at increased risk for type 2 diabetes.
b. This study provides strong evidence for adopting a strategy for diabetes prevention rather than just a policy screening frequently for type 2 diabetes in high-risk subjects. The latter strategy could not prevent cases of CVD that develop prior to the onset of clinical diabetes
Obesity Is Caused by Long-Term Positive Energy Balance
a. Obesity is caused by ingesting more energy than is expended over a long period of time.
b. The excess calories that are consumed lead to an accumulation of body fat either by being stored as fat or preventing the mobilization and oxidation of endogenous fat. In general, ingesting 3500 kcal more (or less) than expended will lead to a gain (or loss) of approximately 1 lb of fat. Genetic factors may influence the amount of weight gained with overfeeding.
c. In one study, weight gain varied greatly among 12 monozygotic twin pairs who were chronically overfed 1000 kcal/d
i. However, weight gains were very similar within each member of a twin pair.
d. In another study, body fat gain after 8 weeks of overfeeding also varied among study subjects but was inversely related to changes in non-volitional energy expenditure, such as fidgeting, which may be determined genetically