Adult Obesity and Metabolic Syndrome Flashcards

1
Q

How do we diagnose overweight and obesity?

A

Body Mass Index= Body weight (kg)/ Height (m^2)

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2
Q

Who and When to Treat? Assessing Obesity in Clinical Practice

A

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

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3
Q

BMI-Associated Disease Risk

A

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.

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4
Q

Are you measuring BMI?

A

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.

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5
Q

Relationship Between BMI and Percent

Body Fat in Men and Women

A

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.

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6
Q

BMI may not be the whole story…

A

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
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7
Q

Waist Circumference

Memorize these waist circumferences

A

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.

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8
Q

Waist Circumference is NOT Belt Size

A

WC is measured 2 inches above iliac crest

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9
Q

Abdominal Fat Distribution Increases the Risk of Coronary Heart Disease

A

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.

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10
Q

Why is Abdominal Obesity Bad?

A

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

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11
Q

The Metabolically Healthy Obese

A

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.

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12
Q

Evidence for Racial-Ethnic Differences in Weight: AA and Latino

AA= african american

A

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

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13
Q

Relationship Between BMI and

Risk of Type 2 Diabetes Mellitus

A

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

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14
Q

Weight gain in adulthood and risk of type 2 diabetes mellitus

A

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.

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15
Q

Hypertension

A

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

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16
Q

Stroke

A

Asia-Pacific Cohort Collaboration Study: each unit change in BMI 8% increase in hypertensive death and ischemic stroke

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17
Q

Obstructive Sleep Apnea

A

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.

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18
Q

Cancer and Obesity

A
Overweight and obesity associated with ↑ risk of:  
Post-menopausal breast 
Colon
Endometrial
Renal cell
Esophageal
Pancreatic
Prostate
Cervical
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19
Q

Characteristics of the Metabolic Syndrome: NCEP-ATP III

A

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”

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20
Q

ATP III: the metabolic syndrome

A

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).

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21
Q

Metabolic Syndrome: Impact on Cardiovascular Health

A

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

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22
Q

Metabolic Syndrome: Impact on Mortality

A

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].

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23
Q

Elevated Risk of CVD Prior to Clinical Diagnosis of Type 2 Diabetes

A

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

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24
Q

Obesity Is Caused by Long-Term Positive Energy Balance

A

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

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25
Q

Gene–Environment Interaction in the

Pathogenesis of Obesity

A

a. Although genetics is an important factor in the pathogenesis of obesity, the recent increase in obesity cannot be attributed to genetics alone and must be a result of alterations in environmental influences.
b. However, people with certain genetic backgrounds are particularly predisposed to weight gain and obesity-related diseases, especially when they are exposed to a precipitating lifestyle.
c. A striking example of this is given by the Pima Indians of Arizona. Lifestyle changes have resulted in an epidemic of obesity and diabetes within this population during the last 50 years
d. Today, the Pimas of Arizona consume a high-fat diet (50% of energy as fat) provided by government surplus commodities rather than their traditional low-fat diet (15% of energy as fat), and they are much more sedentary than when they were farmers. In contrast, Pima Indians who live in the Sierra Madre mountains of Northern Mexico, and consequently who have been isolated from Western influences, eat a traditional Pima diet and are physically active as farmers and sawmill workers.
e. The Pimas of Mexico have a much lower incidence of obesity and diabetes than their genetic kindred in Arizona.

26
Q

Changing Our Obesigenic

Environment

A
a. Energy Intake:
Portion size
High energy density
High glycemic index
Soft drinks/”junk food In schools
Added sugar
Easy food access
Low cost
Variety
Convenience
Great taste
Ads/marketing
b. Energy Expenditure:
Sedentary workplaces
Sedentary schools
Activity “unfriendly” community design
Automobiles
Drive-through conveniences
Elevators/escalators
Remote controls
Sedentary entertainment
Labor saving devices
Television/computer
27
Q

Regulation of food intake

A

a. The regulation of food intake involves a complex interaction of systems that determine the size, content, and frequency of feedings.
b. Presumably, the brain is the final processing center that translates central and peripheral signals to initiate or stop feeding.
c. Neuronal circuits have been identified in the hypothalamus that affect satiation (level of fullness during a meal which regulates the amount of food consumed) and satiety (level of hunger after a meal is consumed which regulates the frequency of eating).
d. Regulatory mechanisms also must be present that integrate determinants of short-term energy intake with long-term energy requirements

28
Q

Foot Intake and Chemical Messangers

A

a. The discovery of leptin, the protein product of the ob/ob gene, in 1995 led to a marked increase in our understanding of the regulation of food intake.
b. Leptin is produced by fat cells, released into the circulation, and it crosses the blood-brain barrier to bind to its receptor in the hypothalamus, which stimulates the expression of neuropeptides and neurotransmitters that inhibit food intake.
c. Therefore, leptin provides a unique feedback signaling system that transmits information regarding adipose tissue energy stores to the central nervous system.
d. Other peripheral organs also communicate with the brain about energy intake through neural signaling and endocrine pathways. The gastrointestinal system, which is responsible for digesting and absorbing ingested nutrients, is particularly involved.
e. The gastrointestinal tract produces cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1), apolipoprotein A-IV (apo A-IV), ghrelin, insulin, and glucose, which are likely involved in short-term, and possibly long-term, regulation of food intake.
f. Central neuropeptides and neurotransmitter signals produced in hypothalamic nuclei stimulate 1) neuropeptide Y (NPY), 2) agouti-related protein (AGRP), 3) galanin, 4) orexin-A, and 5) dynorphin, or inhibit 1) a-melanocyte-stimulating hormone (a-MSH), a peptide derived from proopiomelanocortin (POMC), 2) corticotropin-releasing hormone/urocortin (CRH/UCN), 3) glucagon-like peptide-1 (GLP-1), 4) cocaine- and amphetamine-regulated transcript (CART), 5) norepinephrine (NE), and 5) serotonin (5-HT) [2].
g. The redundancy of these complex signaling pathways tend to defend food intake and provides a formidable barrier to treating obesity. Therefore, a clear understanding of the factors involved in regulating food intake has important implications in designing therapeutic agents for obesity management

29
Q

Initial Office Visit

A

a. Include evaluation of potential obesity related diseases within history, physical examination, and laboratory tests
b. Obtain weight and weight loss history, eating, and activity behaviors
c. Search for triggering factors, including medications
d. Measure weight, height, and calculate body mass index
e. Categorize obesity classification and health risk

f. Determine readiness to lose weight
Initiate treatment plan (involve other professionals if needed)

g. Discuss goals and expectations
h. Arrange follow-up and support

30
Q

Rule out other Medical Causes for Obesity

A

a. Drug Classes Associated with Weight Gain
i. Steroids (glucocorticoids, progestins)
ii. Anti-psychotics (olanzapine, clozapine)
iii. Anti-epileptics (gabapentin, VPA, carbemazapine)
iv. Anti-depressants (some SSRIs, TCA)
v. Mood stabilizing agents (lithium)
vi Insulin, TZD, sulfonylureas, thiazolidinediones
vii. HAART
viii. Hormonal agents (progestins, tamoxifen)
ix. Beta blockers

b. Secondary Causes of Obesity
i. Hypothyroidism: wt gain modest, can impede weight loss efforts.
ii. Cushing’s Syndrome (1/1,000,000) screen only if hx/PE findings suggestive.
iii. Congenital: Prader Willi, Down’s
iv. Hypothalamic disorders: trauma, tumor, surgery

31
Q

Assessing weight loss readiness

A

a. Motivation: Patient seeks weight reduction
b. Stress level: Free of major life crises
c. Psychiatric issues: Free of severe depression, substance abuse, bulimia nervosa
d. Time availability: Patient can devote 15-30 min/d to weight control for next 26 weeks

32
Q

Appropriate Office Environment for Obese Patients

A

a. Waiting room chairs without arms
b. Step stools next to examination tables
c. Large gowns and blood pressure cuffs
d. Scale that can weigh extremely obese patients, located in a private area
e. Appropriate obesity educational materials, handouts, and treatment protocols
f. Empathetic, respectful, and supportive office staff

33
Q

Obese Patients Have Unrealistic Weight Loss Goals

A

a. Most obese patients have unrealistic weight loss goals. In patients seeking weight loss therapy, there is considerable disparity between weight loss expectations and weight loss that can be reasonably achieved.

b. This table shows data from a study of obese women who were about to start a weight loss program
i. On average, they reported their goal was to lose 32% of their weight.
ii. These women also reported that their “dream” was to lose 38% of their weight, they would be “happy” with a 31% weight loss, they would “accept” a 25% weight loss, but they would be “disappointed” with a 17% weight loss

c. Therefore, an acceptable weight loss for most patients is 2 to 3 times more than that achieved with current behavioral and pharmacologic treatments.
d. After 48 weeks of intensive diet and exercise therapy, subjects participating in this study lost an average of 16% of their initial weight, and end-of-treatment weights for 47% of patients were lower than that defined as disappointing. Patients who seek bariatric surgery also have unrealistically high weight loss expectations

e. These studies illustrate the need to help patients accept more modest, but clinically important, weight loss outcomes.
i. This can be done by redefining success as an improvement in health and quality of life, discussing limits to weight loss, congratulating patients on weight that has been lost, and empathizing with their disappointment if they do not reach their goal weight.

34
Q

Impact of weight loss on risk factors

A

a. Weight losses of 5%-10% have been shown to have a significant impact on several aspects of the metabolic syndrome, including well-recognized risk factors for cardiovascular disease and diabetes.

b. For example:
Wing and colleagues at Brown University evaluated the effect of modest weight loss in 114 patients with type 2 diabetes. Those who lost 5% or more of their baseline weight showed statistically significant decreases in serum HbA1c levels

c. The Trial of Antihypertensive Interventions and Management Study found that weight losses of 5% or more produced reductions in diastolic pressure that were equivalent to those produced by a single dose of antihypertensive medication
d. Numerous studies have shown that weight losses of 5%-10% improve total cholesterol, LDL-to-HDL ratio, and the ratio of total-to-HDL cholesterol [1]. In one study, weight reduction of just 5.8% was associated with a 16% reduction in total cholesterol, an 18% increase in HDL cholesterol, and a 12% decrease in LDL cholesterol
e. More recently, Ditschunheit and colleagues documented significant decreases in total cholesterol, triglycerides, and VLDL in obese patients with baseline hyperlipidemia who maintained a weight loss of 7.6%

35
Q

Health Effects of Weight Loss in Look AHEAD

A

These two figures show the health benefits of the moderate weight losses achieved in Look AHEAD. Participants in ILI had greater reductions in hemoglobin A1c and in systolic blood pressure at one year, and these differences are maintained out to year 4 even though the differences have narrowed (due to weight regain).

Not shown in this figure are the significant reductions in medication use in the ILI arm for diabetes, blood pressure, and lipids, most of which were maintained at Year 4.

36
Q

Assessing Obesity: BMI, Waist Circumference, and Disease Risk*

A

WC is most helpful in the BMI range between 25 and 35, where an elevated WC confers an increased risk of DM2, HTN and CAD.

37
Q

Race/ethnicity specific cutoffs for

waist circumference

A

a. Although we use the same cutoffs for all patients, increasingly we recognize that there are racial and ethnic differences in disease risk for BMI and waist circumference.
b. These are data from 10,969 participants in NHANES (National Health and Nutrition Examination Survey) III, carried out from 1988-1994.
c. They show that the odds of having a cardiovascular disease risk factor (blood glucose > 125, blood pressure >140/90, or high cholesterol [LDL > 160 or low HDL]) was lowest for African-Americans.
d. For men, it was highest for Hispanic/Latinos, and for women, it was highest for whites.

38
Q

The metabolic syndrome: current perspective

A

a. Since the 1998 Banting lecture, a number of new candidates have been recognized for the metabolic syndrome/insulin resistance syndrome/syndrome “X”.
b. These additional candidates have included small dense LDL and a group of novel risk factors including elevated CRP levels, PAI-1 and fibrinogen.

c. Other investigators have noted that insulin resistance occurs in women with polycystic ovarian syndrome and some authors are now making an association of insulin resistance with non-alcoholic fatty liver disease.
i. Note that in this more recent review, Professor Reaven acknowledges the importance of visceral adiposity.

39
Q

Modest Weight Loss Prevents Diabetes in Overweight and Obese Persons With Impaired Glucose Tolerance

A

a. Summary: Both lifestyle changes and metformin treatment produced significant reductions in the incidence of diabetes, although the lifestyle intervention was more effective
b. Type 2 diabetes affects 8% of the U.S. population. Significant reversible risk factors are associated with this disease (eg, elevated plasma glucose in the fasting state and after oral glucose load, overweight, and a sedentary lifestyle).
c. The above study randomized 3234 nondiabetic individuals (mean age = 51 y) to placebo, metformin (850 mg BID) or a lifestyle modification program with the goals of at least a 7% weight loss and at least 150 minutes of exercise per week.
d. Using criteria of the ADA, the cumulative incidence of diabetes was significant between each treatment group and placebo, as well as between treatment groups.
e. Both lifestyle changes and metformin treatment produced significant reductions in the incidence of diabetes, although the lifestyle intervention was more effective

40
Q

Relationship Between BMI and Cardiovascular Disease Mortality

A

a. Several large epidemiologic studies have found that increasing BMI is associated with an increased risk of mortality.
b. This figure shows an increased risk of cardiovascular death with increasing BMI in adults who never smoked and who had no history of disease at enrollment.
c. The mortality curves represent a continuum, which begins to increase at a BMI of 25 kg/m2.
d. A BMI between 23.5 and 24.9 kg/m2 had the lowest risk of cardiovascular death and was used as the reference BMI category

41
Q

Selecting a Treatment

A
  1. BMI 25-26.9—> Diet, physical activity,
    and behavior therapy
  2. BMI 27- 29.9—->
    i. Diet, physical activity, and behavior therapy
    ii. Pharmcotherapy
  3. BMI 30-34.9
    i. Diet, physical activity, and behavior therapy
    ii. Pharmcotherapy
  4. BMI 35 and higher
    i. Diet, physical activity, and behavior therapy
    ii. Pharmcotherapy
    iii. Surgery
42
Q

In general, the care of overweight and obese patients requires a two-step process.

A

a. Step 1 is an office assessment or evaluation, and Step 2 is long-term treatment plan.

b. A major goal of the evaluation is to determine the patient’s relative weight and how that weight affects their overall health risk. The management plan is then based on this assessment.
i. The higher the overall health risk, the more aggressive the treatment options that may be considered.

43
Q

Defining Obesity and Risk Status using BMI and Waist Circumference

Summary

A

a. Obesity is characterized by the accumulation of excess body fat.
b. Although accurate methods to measure body fat do exist, they are expensive and impractical for general use.

c. Body mass index (BMI) has become the recommended method to estimate the extent to which body weight may negatively impact health.
i. The physician should think of the BMI as a routine vital sign, particularly in the care of outpatients.

d. Height and weight should be accurately measured on all patients wearing without shoes and a BMI calculated from these measures.

e. BMI is determined by weight in kilograms divided by height in meters squared (BMI = kg/m2).
i. Alternatively, pre-calculated charts and BMI wheels are available that can be used to determine a patient’s BMI.
ii. Most current electronic medical records systems now automatically compute a patient’s BMI.

44
Q

However, BMI does have some limitations

Important Summary

A

a. In persons who are very muscular such as elite athletes, BMI may overestimate the health risk.
b. However, in health care settings it is much more common for BMI to underestimate health risk in persons who have lost large amounts of muscle mass, but who have clinically important obesity, such as the elderly (“sarcopenic obesity”).
c. Many patients with a BMI of 25-29.9 kg/m2 are not obese by BMI but have abdominal obesity and thus are at increased risk of health complications.
d. Thus, the interpretation of BMI must be supplemented with clinical judgment on a case by case basis.

45
Q

Important Summary of Different levels of BMI

A

a. Both the National Institutes of Health and the World Health Organization have defined overweight as a BMI of 25.0 to 29.9 kg/m2, and obesity as a BMI of 30 kg/m2 or greater.
b. Severe (formerly referred to as “morbid”) obesity, which in the United States generally qualifies an individual for weight loss surgery, is defined as a BMI of 40 kg/m2 or greater, or as a BMI of 35 kg/m2 or higher with a weight-related medical complication (e.g., diabetes).
c. These BMI cutoffs were determined using studies evaluating the relationship between BMI and mortality and morbidity risk. In general, morbidity and mortality risk increases as BMI rises.
d. A recent meta-analysis of studies concluded that overweight (BMI of 25-29.9 kg/m2) was associated with slightly lower mortality and that stage I obesity (BMI of 30-34.9 kg/m2) had similar mortality, compared with “normal” BMI (BMI 18.5-24.9 kg/m2).

e. Thus, a BMI of 25-29.9 kg/m2 is associated with increased morbidity but not with increased mortality.
i. The relationship between BMI and total mortality and morbidity rises more steeply at cutoffs of 35 kg/m2 and 40 kg/m2.

46
Q

Gender, Age, and Ethnicity of BMI

A

a. Gender does not substantially alter the relationship between obesity and health risk.
i. Therefore, the same cutoff points are used to define overweight (BMI 25-29.9 kg/m2), obesity (BMI ≥ 30 kg/m2), and severe obesity (BMI ≥ 40 kg/m2), and in both men and women.

b. Age does modify this relationship to some extent, with studies showing that the lowest mortality in older individuals may be a BMI of 25-29.9 kg/m2.

c. Ethnic differences exist in disease risk at a given degree of obesity.
i. For example, the International Diabetes Federation recommends a lower waist circumference cutoff for east Asian and south Asian patient to define abdominal obesity, as compared to white populations.
ii. Some studies suggest that weight-related disease risk is lower in African-American populations, compared to whites.

d. However, in the U.S., elevated waist circumference definitions currently are the same for all ethnic groups (≥ 35 inches for women, ≥ 40 inches for men

47
Q

Waist Circumference and patient risk

A

a, A waist circumference measurement can be used in “intermediate risk patients” (BMI of 25-34.9 kg/m2) to assess risk status.

b. Waist circumference is best used in conjunction with body mass index and will provide additional information on the location of the patient’s excess adiposity (i.e., body fat distribution).
c. The reason to measure waist circumference is that excess abdominal fat is associated with greater risk than fat located in other areas (buttocks, thighs).

d. Abdominal fat is associated with fat deposition in internal organs (visceral fat).
i. Thus, abdominal obesity is an independent risk factor for cardiovascular disease, type 2 diabetes, hypertension, hypercholesterolemia and even mortality, even when BMI is not elevated.

e. Measurements of waist circumference can provide useful information about health risk, especially for adults with an intermediate BMI of 25-35 kg/m2

48
Q

Why to use waist circumferance

A

a. The reason to measure waist circumference is that excess abdominal fat is associated with greater risk than fat located in other areas (buttocks, thighs).
b. Abdominal fat is associated with fat deposition in internal organs (visceral fat).
c. Thus, abdominal obesity is an independent risk factor for cardiovascular disease, type 2 diabetes, hypertension, hypercholesterolemia and even mortality, even when BMI is not elevated.
d. Measurements of waist circumference can provide useful information about health risk, especially for adults with an intermediate BMI of 25-35 kg/m2

49
Q

How to measure weight circumferance correctly

A

a. To measure waist circumference, locate the top of the iliac crest.
i. Place a measuring tape in a horizontal plane around the abdomen at the level of the superior border of the iliac crest.
ii. The measurement should be made at the end of a normal expiration and should not compress the skin.

b. An alternative but accepted method to measure waist circumference is to mark a point halfway between the iliac crests and the lower border of the ribs.
i. This alternative method is somewhat more difficult, and thus, used less frequently.

50
Q

Comparing BMI and waist circumference

A

a. While the primary classification of overweight and obesity is based on BMI, waist circumference adds additional information about the location of the excess fat and is particularly useful in patients who are categorized as normal weight, overweight, or mildly obese (BMI 30-34.9 kg/m2) by BMI.
b. A patient with a BMI of 28 kg/m2 and who has a high waist circumference is at a higher health risk than a patient with the same BMI but who has a normal waist circumference.
c. In addition, if it is suspected that the BMI might not be an accurate surrogate measurement of body fat (for example, a very muscular patient), waist circumference can be very useful to determine if the patient is at risk.
d. Nearly all individuals with a BMI of ≥ 35 kg/m2 have an elevated waist circumference.
e. Thus, measurement of waist circumference in these individuals does not provide additional information and it is not necessary to measure waist circumference in these patients.

51
Q

Lists the symptoms and diseases that are directly or indirectly related to obesity

Large Summary

A

Type 2 Diabetes and Impaired Glucose Tolerance: BMI, abdominal fat distribution and weight gain are important risk factors for the development of type 2 diabetes. Data from NHANES III found that almost 70% of adult men and women in the U.S. with type 2 diabetes have a BMI of 27 or greater, and the risk of diabetes increases linearly with BMI. Data from 8 years of follow up of a cohort of over 113,000 US women aged 30-55 in the Nurses’ Health Study found that, among women of BMI 23-23.9 kg/m2, the relative risk of diabetes was 3.6 times that of women having a body mass index less than 22 kg/m2.

Dyslipidemia: Visceral obesity is associated with elevated triglycerides, low HDL cholesterol, and increased small, dense LDL particles. Data from NHANES III suggest that prevalence of hypercholesterolemia (total cholesterol > 240 mg/dl) increased progressively with BMI in men. In women, the prevalence was highest at a BMI of 25-27 kg/m2, and did not increase further with increasing BMI.

Coronary Artery Disease (CAD). Obese persons, particularly those with abdominal fat distribution, are at increased risk for CAD. The risk of CAD begins to increase at a BMI of 23 kg/m2 for men and 22 kg/m2 for women. It was previously thought that most of the increased risk was mediated by obesity related increases in risk factors, particularly hypertension, dyslipidemia, impaired glucose tolerance/diabetes, and the metabolic syndrome. However, several long term epidemiologic studies including the Nurses’ Health Study and the Framingham Study have shown that overweight and obesity increased the risk for CAD even after correction for other known risk factors. The American Heart Association has added obesity to its list of major risk factors for CAD.

Sleep Apnea: Obese men and women are also at high risk for sleep apnea, in which partial or complete upper airway obstruction during sleep leads to episodes of apnea or hypopnea. The interruption in nighttime sleep and repeated episodes of hypoxemia lead to daytime somnolence, morning headache, systemic hypertension, and can eventually result in pulmonary hypertension and right heart failure. In a study of two hundred obese women and 50 obese men (mean BMI 45.3 kg/m2) and 128 controls matched for age and sex, 40% of obese men and 3% of obese women demonstrated sleep apnea warranting therapeutic intervention. Another 8% of men and 5.5% of women showed apneic activity that warranted recommendation for evaluation in the sleep laboratory. In contrast, none of the 128 controls demonstrated sleep apneic activity severe enough for therapeutic intervention.

Non-Alcoholic Fatty Liver Disease: Obesity is associated with a spectrum of liver disease known as non-alcoholic fatty liver disease (NAFLD) or non-alcoholic steatohepatitis (NASH). Manifestations of this disorder include hepatomegaly, abnormal liver associated enzyme tests, and abnormal liver histology including macrovesicular steatosis, steatohepatitis, fibrosis, and in a worst case scenario, cirrhosis. NAFLD/NASH has become a common cause of cirrhosis in the U.S., along with viral hepatitis and alcohol use. The exact prevalence of NAFLD/NASH in obese patients is not fully known. However data, from autopsy studies suggest that steatohepatitis occurs in approximately 20% of obese patients.

52
Q

Obesity: Type 2 Diabetes and your blood cholesterol

A

Type 2 Diabetes and Impaired Glucose Tolerance: BMI, abdominal fat distribution and weight gain are important risk factors for the development of type 2 diabetes. Data from NHANES III found that almost 70% of adult men and women in the U.S. with type 2 diabetes have a BMI of 27 or greater, and the risk of diabetes increases linearly with BMI. Data from 8 years of follow up of a cohort of over 113,000 US women aged 30-55 in the Nurses’ Health Study found that, among women of BMI 23-23.9 kg/m2, the relative risk of diabetes was 3.6 times that of women having a body mass index less than 22 kg/m2.

Dyslipidemia: Visceral obesity is associated with elevated triglycerides, low HDL cholesterol, and increased small, dense LDL particles. Data from NHANES III suggest that prevalence of hypercholesterolemia (total cholesterol > 240 mg/dl) increased progressively with BMI in men. In women, the prevalence was highest at a BMI of 25-27 kg/m2, and did not increase further with increasing BMI.

53
Q

Coronary Artery Disease and Obesity

A

Coronary Artery Disease (CAD). Obese persons, particularly those with abdominal fat distribution, are at increased risk for CAD. The risk of CAD begins to increase at a BMI of 23 kg/m2 for men and 22 kg/m2 for women. It was previously thought that most of the increased risk was mediated by obesity related increases in risk factors, particularly hypertension, dyslipidemia, impaired glucose tolerance/diabetes, and the metabolic syndrome. However, several long term epidemiologic studies including the Nurses’ Health Study and the Framingham Study have shown that overweight and obesity increased the risk for CAD even after correction for other known risk factors. The American Heart Association has added obesity to its list of major risk factors for CAD.

54
Q

Obesity: Fatty Liver disease and Sleep Apnea

A

Sleep Apnea: Obese men and women are also at high risk for sleep apnea, in which partial or complete upper airway obstruction during sleep leads to episodes of apnea or hypopnea. The interruption in nighttime sleep and repeated episodes of hypoxemia lead to daytime somnolence, morning headache, systemic hypertension, and can eventually result in pulmonary hypertension and right heart failure. In a study of two hundred obese women and 50 obese men (mean BMI 45.3 kg/m2) and 128 controls matched for age and sex, 40% of obese men and 3% of obese women demonstrated sleep apnea warranting therapeutic intervention. Another 8% of men and 5.5% of women showed apneic activity that warranted recommendation for evaluation in the sleep laboratory. In contrast, none of the 128 controls demonstrated sleep apneic activity severe enough for therapeutic intervention.

Non-Alcoholic Fatty Liver Disease: Obesity is associated with a spectrum of liver disease known as non-alcoholic fatty liver disease (NAFLD) or non-alcoholic steatohepatitis (NASH). Manifestations of this disorder include hepatomegaly, abnormal liver associated enzyme tests, and abnormal liver histology including macrovesicular steatosis, steatohepatitis, fibrosis, and in a worst case scenario, cirrhosis. NAFLD/NASH has become a common cause of cirrhosis in the U.S., along with viral hepatitis and alcohol use. The exact prevalence of NAFLD/NASH in obese patients is not fully known. However data, from autopsy studies suggest that steatohepatitis occurs in approximately 20% of obese patients.

55
Q

TABLE 2: COMORBIDITIES AND COMPLICATIONS OF OBESITY

A
Cardiovascular
	Coronary artery disease
	Hyperlipidemia
	Hypertension
	Congestive heart failure
	Stroke
	Venous thromboembolism
	Premature death

Pulmonary
 Obstructive Sleep Apnea
 Obesity-hypoventilation syndrome
 Asthma

Psychological
	Depression
	Social stigmatization 
	Low self-esteem
	Distorted body image

Gastrointestinal
 Cholelithiasis
 Gastroesophageal reflux disease
 Nonalcoholic fatty liver disease

Dermatological
	Acanthosis nigricans
	Cellulitis
	Striae
	Lymphedema
	Venous stasis

Orthopedic
 Osteoarthritis
 Restricted mobility
 Low back pain

Genitourinary
	Polycystic ovary syndrome
	Erectile dysfunction
	Benign prostatic hypertrophy
	Menstrual abnormalities
	Infertility
	Pregnancy complications
	Stress incontinence
Metabolic
	Type 2 diabetes
	Impaired glucose tolerance
	Gout
	Insulin resistance
	Metabolic syndrome
	Hyperuricemia
	Vitamin D deficiency
	Nephrolithiasis
Cancer
	Postmenopausal breast
	Colon
	Prostate
	Endometrial
	Kidney
	Gallbladder
56
Q

Define Metabolic Syndrome using the current AHA/NCEP definition

A

Metabolic syndrome is a specific body phenotype of abdominal obesity associated with a group of metabolic disorders that are risk factors for cardiovascular disease, including coronary artery disease, stroke, and congestive heart failure.

Characteristics of this syndrome include: abdominal obesity,
elevated blood pressure/hypertension,
high triglycerides, low HDL cholesterol,
and impaired glucose tolerance/type 2 diabetes

57
Q

Criteria for Diagnosis of Metabolic Syndrome

*Great slide

A

Criteria for Diagnosis of Metabolic Syndrome (Any 3 of 5 risk factors constitutes diagnosis of metabolic syndrome)

  1. Abdominal Obesity Waist Circumference
    Men ≥ 102 cm (≥ 40 inches)
    Women≥ 88 cm (≥ 35 inches)
  2. Triglycerides ≥ 150 mg/dL or on drug
    treatment for abnormal lipids
  3. HDL Cholesterol
    Men < 40 mg/dL
    Women< 50 mg/dL
  4. Blood Pressure ≥ 130 mmHg systolic or
    ≥ 85 mmHg diastolic or
    on anti-hypertensive drug
  5. *Fasting Glucose ≥ 100 mg/dL or
    on hypoglycemic drug
58
Q

How Do We Evaluate an Obese Patient?

A

List the steps in the clinical evaluation of the obese patient

1) Measure degree of adiposity
2) Assess other existing risk factors for cardiovascular disease
3) Screen for complications of obesity
4) Rule out medical causes of obesity
5) Assess readiness for treatment

59
Q

The results of the evaluation determine the overall needs of the individual and the appropriate treatment options to be considered.

Large Summary

A

a. The aggressiveness of treatment should be decided not only by the degree of obesity but also by the number of complications that the patient has.

b, In the past, clinicians mainly thought about traditional co-morbidities (e.g., type 2 diabetes).
i. Currently, we also consider other, more functional complications, such as psychosocial complications (e.g., stigma, depression, discrimination).

c. The Edmonton Obesity Staging System (EOSS) is a classification system that can be used to evaluate the impact of weight on a patient’s health.
d. In general, patients who have more complications should be treated more aggressively. However, patients who are stage 4 in the EOSS are sometimes in a palliative situation where aggressive treatment of weight will not improve survival or quality of life.
e. Patients who are not ready to make significant changes in diet and physical activity should be managed differently than patients ready to take action (e.g., the stages of change model).
f. In clinical practice, however, determining which patients are ready to change is difficult.
g. A practical way to determine which patients are ready for change is to ask patients to take some initial behavior change steps, such as self-monitoring their eating and physical activity patterns for 1 week.

60
Q

Physical Examination and Laboratory/Diagnostic tests for Obesity

A

Physical Exam:
Height, weight, body mass index
Waist circumference
Blood pressure with appropriate cuff size
Pulse rate and oxygen saturation
Signs of pulmonary hypertension/venous insufficiency (edema, skin hyperpigmentation)
Signs of thyroid disease (e.g., goiter)
Signs of insulin resistance/diabetes (acanthosis nigricans)

Laboratory/Diagnostic:
Thyroid stimulating hormone (TSH)
Diabetes screening: fasting blood glucose and/or hemoglobin A1c
Lipid panel
Liver associated enzymes
Remainder of tests determined by individual assessment and clinical suspicion (e.g., sleep study)