People who are overweight or obese are at higher risk of developing one or more serious medical conditions, and obesity is associated with increases in deaths from all causes. Overweight and obesity significantly increase the risk for Type 2 diabetes; hypercholesterolemia (high cholesterol), hypertension, heart disease, and stroke; gallbladder disease; osteoarthritis, chronic joint pain, and back injury; sleep apnea and other respiratory problems; and several cancers. According to the American Obesity Association, obesity is a contributing cause in at least 400,000 deaths per year. Approximately sixty-two million visits to the physician's office are usually due to obesity-related problems.
FIGURE 2.4 Age-adjusted prevalence of low HDL-cholesterol* according to BMI
Hypercholesterolemia, Hypertension, Heart Disease, and Stroke
Overweight, obesity, and excess abdominal fat are directly related to cardiovascular risk factors, including high levels of total serum cholesterol, LDL-cholesterol (a fat-like substance often termed "bad cholesterol" because high levels increase risk for heart disease), triglycerides, blood pressure, fibrinogen, and insulin, and low levels of HDL-cholesterol (often termed "good cholesterol" because high levels appear to protect against heart disease). The association between total serum cholesterol and coronary heart disease is largely due to low-density lipoprotein (LDL). A high-risk LDL-cholesterol is greater than or equal to 160 mg/dL with a 10 mg/dL rise in LDL-cholesterol corresponding to approximately a 10% increase in risk. The relationship of the age-adjusted prevalence of high total cholesterol (defined as greater than or equal to 240 mg/dL) to BMI is shown Figure 2.3. The age-adjusted prevalence of low HDL-cholesterol (defined as less than 35 mg/dL in men and less than 45 mg/dL in women) is shown in Figure 2.4. The percent of the population suffering from high serum cholesterol levels fell from 19.7% between 1988 to 1994 to 17% during the years 1999 to 2002. (See Table 2.6.) The overall decline in high TABLE 2.6 Serum cholesterol levels among persons 20 years of age and over, by demographic characteristics, selected years 1960–2002serum cholesterol occurred in response to the increasing use of effective cholesterol-lowering statin drugs. Figure 2.5 shows the steady rise in medical office visits to obtain cholesterol-lowering statin drugs from 1995 through 2002—a 200% increase among adults age forty-five-sixty-four—and the even sharper increase among men age sixty-five and older (250%) and women age sixty-five and older (180%) from 1999 to 2002.
| TABLE 2.6 | |||||
|---|---|---|---|---|---|
| Serum cholesterol levels among persons 20 years of age and over, by demographic characteristics, selected years 1960–2002 | |||||
| [Data are based on physical examinations of a sample of the civilian noninstitutionalized population] | |||||
| Sex, age, race and Hispanic origina, and poverty status | 1960–62 | 1971–74 | 1976–80b | 1988–94 | 1999–2002 |
| 20-74 years, age adjustedc | Percent of population with high serum cholesterol | ||||
| Both sexesd | 33.3 | 28.6 | 27.8 | 19.7 | 17.0 |
| Male | 30.6 | 27.9 | 26.4 | 18.8 | 16.9 |
| Female | 35.6 | 29.1 | 28.8 | 20.5 | 17.0 |
| Not Hispanic or Latino: | |||||
| White only, male | — | — | 26.4 | 18.7 | 17.0 |
| White only, female | — | — | 29.6 | 20.7 | 17.4 |
| Black or African American only, male | — | — | 25.5 | 16.4 | 12.5 |
| Black or African American only, female | — | — | 26.3 | 19.9 | 16.6 |
| Mexican male | — | — | 20.3 | 18.7 | 17.6 |
| Mexican female | — | — | 20.5 | 17.7 | 12.7 |
| Poverty status:e | |||||
| Poor | — | 24.4 | 23.5 | 19.3 | 17.8 |
| Near poor | — | 28.9 | 26.5 | 19.4 | 18.8 |
| Nonpoor | — | 28.9 | 29.0 | 19.6 | 16.5 |
| 20 years and over, age adjustedc | |||||
| Both sexesd | — | — | — | 20.8 | 17.3 |
| Male | — | — | — | 19.0 | 16.4 |
| Female | — | — | — | 22.0 | 17.8 |
| Not Hispanic or Latino: | |||||
| White only, male | — | — | — | 18.8 | 16.5 |
| White only, female | — | — | — | 22.2 | 18.1 |
| Black or African American only, male | — | — | — | 16.9 | 12.4 |
| Black or African American only, female | — | — | — | 21.4 | 17.7 |
| Mexican male | — | — | — | 18.5 | 17.4 |
| Mexican female | — | — | — | 18.7 | 13.8 |
| Poverty status:e | |||||
| Poor | — | — | — | 20.6 | 18.3 |
| Near poor | — | — | — | 20.6 | 19.1 |
| Nonpoor | — | — | — | 20.4 | 16.5 |
| 20 years and over, crude | |||||
| Both sexesd | — | — | — | 19.6 | 17.3 |
| Male | — | — | — | 17.7 | 16.6 |
| Female | — | — | — | 21.3 | 18.0 |
| Not Hispanic or Latino: | |||||
| White only, male | — | — | — | 18.0 | 16.9 |
| White only, female | — | — | — | 22.5 | 19.1 |
| Black or African American only, male | — | — | — | 14.7 | 12.2 |
| Black or African American only, female | — | — | — | 18.2 | 16.1 |
| Mexican male | — | — | — | 15.4 | 15.0 |
| Mexican female | — | — | — | 14.3 | 10.7 |
| Poverty status:e | — | ||||
| Poor | — | — | — | 17.6 | 16.4 |
| Near poor | — | — | — | 19.8 | 18.2 |
| Nonpoor | — | — | — | 19.5 | 16.9 |
| Male | — | ||||
| 20-34 years | 15.1 | 12.4 | 11.9 | 8.2 | 9.8 |
| 35-44 years | 33.9 | 31.8 | 27.9 | 19.4 | 19.8 |
| 45-54 years | 39.2 | 37.5 | 36.9 | 26.6 | 23.6 |
| 55-64 years | 41.6 | 36.2 | 36.8 | 28.0 | 19.9 |
| 65-74 years | 38.0 | 34.7 | 31.7 | 21.9 | 13.7 |
| 75 years and over | — | — | — | 20.4 | 10.2 |
| Female | |||||
| 20-34 years | 12.4 | 10.9 | 9.8 | 7.3 | 8.9 |
| 35-44 years | 23.1 | 19.3 | 20.7 | 12.3 | 12.4 |
| 45-54 years | 46.9 | 38.7 | 40.5 | 26.7 | 21.4 |
| 55-64 years | 70.1 | 53.1 | 52.9 | 40.9 | 25.6 |
| 65-74 years | 68.5 | 57.7 | 51.6 | 41.3 | 32.3 |
| 75 years and over | — | — | — | 38.2 | 26.5 |
TABLE 2.6 Serum cholesterol levels among persons 20 years of age and over, by demographic characteristics, selected years 1960–2002 [CONTINUED]
| TABLE 2.6 | |||||
|---|---|---|---|---|---|
| Serum cholesterol levels among persons 20 years of age and over, by demographic characteristics, selected years 1960–2002 [CONTINUED] | |||||
| [Data are based on physical examinations of a sample of the civilian noninstitutionalized population] | |||||
| Sex, age, race and Hispanic origina, and poverty status | 1960–62 | 1971–74 | 1976–80b | 1988–94 | 1999–2002 |
| 20-74 years, age adjustedc | Mean serum cholesterol level, mg/dL | ||||
| Both sexesd | 222 | 216 | 215 | 205 | 203 |
| Male | 220 | 216 | 213 | 204 | 203 |
| Female | 224 | 217 | 216 | 205 | 202 |
| Not Hispanic or Latino: | |||||
| White only, male | — | — | 213 | 204 | 202 |
| White only, female | — | — | 216 | 206 | 204 |
| Black or African American only, male | — | — | 211 | 201 | 195 |
| Black or African American only, female | — | — | 216 | 204 | 200 |
| Mexican male | — | — | 209 | 206 | 205 |
| Mexican female | — | — | 209 | 204 | 198 |
| Poverty status:e | |||||
| Poor | — | 211 | 211 | 203 | 200 |
| Near poor | — | 217 | 213 | 203 | 203 |
| Nonpoor | — | 217 | 216 | 206 | 203 |
| 20 years and over, age adjustedc | |||||
| Both sexesd | — | — | — | 206 | 203 |
| Male | — | — | — | 204 | 202 |
| Female | — | — | — | 207 | 204 |
| Not Hispanic or Latino: | |||||
| White only, male | — | — | — | 205 | 202 |
| White only, female | — | — | — | 208 | 205 |
| Black or African American only, male | — | — | — | 202 | 195 |
| Black or African American only, female | — | — | — | 207 | 202 |
| Mexican male | — | — | — | 206 | 204 |
| Mexican female | — | — | — | 206 | 199 |
| Poverty status:e | |||||
| Poor | — | — | — | 205 | 201 |
| Near poor | — | — | — | 205 | 204 |
| Nonpoor | — | — | — | 207 | 203 |
| 20 years and over, crude | |||||
| Both sexesd | — | — | — | 204 | 203 |
| Male | — | — | — | 202 | 202 |
| Female | — | — | — | 206 | 204 |
| Not Hispanic or Latino: | |||||
| White only, male | — | — | — | 203 | 203 |
| White only, female | — | — | — | 208 | 206 |
| Black or African American only, male | — | — | — | 198 | 194 |
| Black or African American only, female | — | — | — | 201 | 199 |
| Mexican male | — | — | — | 199 | 200 |
| Mexican female | — | — | — | 198 | 194 |
| Poverty status:e | |||||
| Poor | — | — | — | 200 | 198 |
| Near poor | — | — | — | 202 | 202 |
| Nonpoor | — | — | — | 205 | 204 |
| Male | |||||
| 20-34 years | 198 | 194 | 192 | 186 | 188 |
| 35-44 years | 227 | 221 | 217 | 206 | 207 |
| 45-54 years | 231 | 229 | 227 | 216 | 215 |
| 55-64 years | 233 | 229 | 229 | 216 | 212 |
| 65-74 years | 230 | 226 | 221 | 212 | 202 |
| 75 years and over | — | — | — | 205 | 195 |
The percent of the population suffering from hypertension increased between the periods 1988 to 1994 and 1999 to 2002, from 21.7% of the population to 25.5%. The highest rates for those aged twenty to seventy-four during the 1999–2002 period were reported among African-American females (39.4%). Both men and women were increasingly likely to have hypertension as they aged. (See Table 2.7.) The American Heart Association estimates that more than 75% of hypertension is directly attributable to obesity. Hypertension is approximately three times more common in obese than in normal-weight people, and the relationship between weight and blood pressure is clearly one of cause and effect because when weight increases, so does blood pressure, and when weight decreases, blood pressure falls. Data from the National Health and Nutrition Examination Surveys (NHANES III 1988–1994) revealed that the age-adjusted prevalence of high blood pressure increases progressively with higher levels of BMI in men and women. (See Figure 2.6.) The prevalence of high blood pressure
TABLE 2.6 Serum cholesterol levels among persons 20 years of age and over, by demographic characteristics, selected years 1960–2002 [CONTINUED]
| TABLE 2.6 | |||||
|---|---|---|---|---|---|
| Serum cholesterol levels among persons 20 years of age and over, by demographic characteristics, selected years 1960–2002 [CONTINUED] | |||||
| [Data are based on physical examinations of a sample of the civilian noninstitutionalized population] | |||||
| Sex, age, race and Hispanic origina, and poverty status | 1960–62 | 1971–74 | 1976–80b | 1988–94 | 1999–2002 |
| Notes:—= Data not available. High serum cholesterol is defined as greater than or equal to 240 mg/dL (6.20 mmol/L). | |||||
| aPersons of Mexican origin may be of any race. Starting with data year 1999 race-specific estimates are tabulated according to 1997 Standards for Federal Data on Race and Ethnicity and are not strictly comparable with estimates for earlier years. The two non-Hispanic race categories shown in the table conform to 1997 standards. The 1999–2002 race-specific estimates are for persons who reported only one racial group. Prior to data year 1999, data were tabulated according to 1977 standards. Estimates for single race categories prior to 1999 included persons who reported one race or, if they reported more than one race, identified one race as best representing their race. | |||||
| bData for Mexicans are for 1982–84. | |||||
| cAge adjusted to the 2000 standard population using five age groups. Age-adjusted estimates may differ from other age-adjusted estimates based on the same data and presented elsewhere if different age groups are used in the adjustment procedure. | |||||
| dIncludes persons of all races and Hispanic origins, not just those shown separately. | |||||
| ePoor persons are defined as below the poverty threshold. Near poor persons have incomes of 100 percent to less than 200 percent of the poverty threshold. Nonpoor persons have incomes of 200 percent or greater than the poverty threshold. Persons with unknown poverty status are excluded. | |||||
| SOURCE: "Table 70. Serum Cholesterol Levels among Persons 20 Years of Age and Over, According to Sex, Age, Race and Hispanic Origin, and Poverty Status: United States, 1960–62, 1971–74, 1976–1980, 1988–1994, and 1999–2002," in Health, United States, 2005, Centers for Disease Control and Prevention, National Center for Health Statistics, December 8, 2005, http://www.cdc.gov/nchs/data/hus/hus05.pdf#chartbookontrendsinthe (accessed January 8, 2006) | |||||
| Female | |||||
| 20-34 years | 194 | 191 | 189 | 184 | 185 |
| 35-44 years | 214 | 207 | 207 | 195 | 198 |
| 45-54 years | 237 | 232 | 232 | 217 | 211 |
| 55-64 years | 262 | 245 | 249 | 235 | 221 |
| 65-74 years | 266 | 250 | 246 | 233 | 224 |
| 75 years and over | — | — | — | 229 | 217 |
The physiological processes that produce the hypertension associated with obesity include sodium retention and increases in vascular resistance, blood volume, and cardiac output (the volume of blood pumped, measured in liters per minute). While it is not known precisely how weight loss results in a decrease in blood pressure, it is known that weight loss is associated with a reduction in vascular resistance and total blood volume and cardiac output. Weight loss also results in improvement in insulin resistance, a reduction in sympathetic nervous system activity, and suppression of the rennin-angiotensin-aldosterone system. (The rennin-angiotensin-aldosterone system is a group of hormones that are responsible for the opening and narrowing of blood vessels and retention of fluids.)
Obesity increases risk for coronary artery disease, which in turn increases risk for future heart failure. Congestive heart failure is not a disease but a condition that occurs when the heart is unable to pump enough blood to meet the needs of the body's tissues. When the heart fails, it is unable to pump out all the blood that enters its chambers. Congestive heart failure is a frequent complication of severe obesity and a major cause of death. The duration of the obesity is a strong predictor of congestive heart failure because over time elevated total blood volume and high cardiac output cause the left ventricle of the heart to increase in size (known as left ventricular hypertrophy) beyond that expected from normal growth. Although left ventricular hypertrophy is frequently identified in cardiac patients with obesity and in part results from hypertension, abnormalities in left ventricular mass and function also occur in the absence of hypertension and may be related to the severity of obesity.
Inflammation in blood vessels and throughout the body is thought to increase risk for heart disease and stroke. People with more body fat have higher blood levels of substances such as plasminogen activator inhibitor-1—an enzyme produced in the kidneys that inhibits conversion of plasminogen to plasmin and initiates fibrinolysis. Fibrinolysis leads to the breakdown of fibrin, which is responsible for the semisolid character of a blood clot that can occlude (block) blood vessels. This is the mechanism believed to account for the finding that obesity is associated with an increased risk of blood clot formation. Occluded arteries may produce myocardial infarction (heart attack) or stroke (sudden injury to the brain due to compromised blood and oxygen supply). Overweight increases risk for ischemic stroke—resulting from a clot or blockage—but does not appear to increase risk for hemorrhagic stroke (bleeding inside the brain), which, in general, is associated with more fatality. According to the National Heart, Lung, and Blood Institute in
FIGURE 2.5 Cholesterol-lowering statin drug visits among adults 45 years of age and over by sex and age, selected years 1995–2002
Even when there are no other risk factors present, such as smoking or elevated cholesterol levels, obesity by itself increases the risk of heart disease. Modest elevations in BMI are associated with increased risk for nonfatal myocardial infarction and coronary heart disease. Data from the Framingham Heart Study (a landmark study of fifty years of data from residents of Framingham, Massachusetts, that significantly contributed to understanding the development and progression of heart disease and its risk factors) indicated that being overweight might contribute to the risk of stroke, independent of the known association of hypertension and diabetes with stroke.
Figure 2.7 shows the process, known as a treatment algorithm, used to assess and treat overweight individuals, based on their body weight, abdominal fat, and the risk factors for cardiovascular morbidity and mortality.
Type 2 Diabetes
Diabetes is a disease that affects the body's use of food, causing blood glucose (sugar levels in the blood) to become too high. Normally, the body converts sugars, starches, and proteins into a form of sugar called glucose. The blood then carries glucose to all cells throughout the body. In the cells, with the help of the hormone insulin, the glucose is either converted into energy for use immediately or stored for the future. Beta cells of the pancreas, a small organ located behind the stomach, manufacture the insulin. The process of turning food into energy via glucose (blood sugar) is important because the body depends on glucose for every function.
In diabetes, the body can convert food to glucose, but there is a problem with insulin. In one type of diabetes (insulin-dependent diabetes or Type 1), the pancreas does not manufacture enough insulin, and in another type (non-insulin dependent or Type 2), the body has insulin but cannot use the insulin effectively (this latter condition is called insulin resistance). When insulin is either absent or ineffective, glucose cannot get into the cells to be used for energy. Instead, the unused glucose builds up in the bloodstream and circulates through the kidneys. If a person's blood-glucose level rises high enough, the excess glucose "spills" over into the urine, causing frequent urination. This, in turn, leads to an increased feeling of thirst as the body tries to compensate for the fluid lost through urination.
Non-insulin-dependent diabetes (also known as Type 2) is most often seen in adults and is the most common type of diabetes in the United States. In this type, the pancreas produces insulin, but it is not used effectively, and the body resists responding to it. Heredity may be a predisposing factor in the genesis of Type 2 diabetes, but since the pancreas continues to produce insulin, the disease is considered more of a problem of insulin-resistance, in which the body is not using the hormone efficiently.
Because diabetes deprives body cells of the glucose needed to function properly, several complications can develop to threaten the lives of diabetics further. The healing process of the body is slowed or impaired, and the risk of infection increases. Complications of diabetes include: higher risk and rates of heart disease; circulatory problems, especially in the legs, are often severe enough to require surgery or even amputation; diabetic retinopathy, a condition that can cause blindness; kidney disease that may require dialysis; dental problems; and problems with pregnancy. Close attention to preventive health care TABLE 2.7 Hypertension among persons 20 years of age and over, by demographic characteristics, 1988–94 and 1999–2002such as regular eye, dental, and foot examinations and tight control of blood sugar levels have been shown to prevent some of the consequences of diabetes.
| TABLE 2.7 | ||||
|---|---|---|---|---|
| Hypertension among persons 20 years of age and over, by demographic characteristics, 1988–94 and 1999–2002 | ||||
| [Data are based on physical examinations of a sample of the civilian noninstitutionalized population] | ||||
| Sex, age, race and Hispanic origina, and poverty status | Elevated blood pressure or taking antihypertensive medicationb,c | Elevated blood pressureb | ||
| 1988–94 | 1999–2002 | 1988–94 | 1999–2002 | |
| 20-74 years, age adjustedd | Percent of population | |||
| Both sexese,f | 21.7 | 25.6 | 15.4 | 16.4 |
| Male | 23.4 | 25.2 | 18.2 | 16.3 |
| Femalee | 20.0 | 25.7 | 12.6 | 16.1 |
| Not Hispanic or Latino: | ||||
| White only, male | 22.6 | 24.0 | 17.3 | 14.8 |
| White only, femalee | 18.4 | 23.3 | 11.2 | 14.1 |
| Black or African American only, male | 34.3 | 36.9 | 27.9 | 25.6 |
| Black or African American only, femalee | 35.0 | 39.5 | 23.5 | 25.7 |
| Mexican male | 23.4 | 22.6 | 19.1 | 18.2 |
| Mexican femalee | 21.0 | 23.4 | 16.5 | 17.2 |
| Poverty status:g | ||||
| Poor | 27.5 | 29.0 | 19.0 | 19.3 |
| Near poor | 22.6 | 29.3 | 15.8 | 19.5 |
| Nonpoor | 20.4 | 24.1 | 14.6 | 14.9 |
| 20 years and over, age adjustedd | ||||
| Both sexese,f | 25.5 | 30.0 | 18.5 | 19.9 |
| Male | 26.4 | 28.8 | 20.6 | 19.1 |
| Femalee | 24.4 | 30.6 | 16.4 | 20.2 |
| Not Hispanic or Latino: | ||||
| White only, male | 25.6 | 27.6 | 19.7 | 17.6 |
| White only, femalee | 23.0 | 28.5 | 15.1 | 18.5 |
| Black or African American only, male | 37.5 | 40.6 | 30.3 | 28.2 |
| Black or African American only, femalee | 38.3 | 43.5 | 26.4 | 28.9 |
| Mexican male | 26.9 | 26.8 | 22.2 | 21.5 |
| Mexican femalee | 25.0 | 27.9 | 20.4 | 21.2 |
| Poverty status:g | ||||
| Poor | 31.7 | 33.9 | 22.5 | 23.3 |
| Near poor | 26.6 | 33.5 | 19.3 | 23.0 |
| Nonpoor | 23.9 | 28.2 | 17.5 | 18.2 |
| 20 years and over, crude | ||||
| Both sexese,f | 24.1 | 30.2 | 17.6 | 19.9 |
| Male | 23.8 | 27.6 | 18.7 | 18.2 |
| Femalee | 24.4 | 32.7 | 16.5 | 21.6 |
| Not Hispanic or Latino: | ||||
| White only, male | 24.3 | 28.3 | 18.7 | 17.8 |
| White only, femalee | 24.6 | 32.9 | 16.4 | 21.6 |
| Black or African American only, male | 31.1 | 35.9 | 25.5 | 25.2 |
| Black or African American only, femalee | 32.5 | 42.1 | 22.2 | 27.3 |
| Mexican male | 16.4 | 16.5 | 13.9 | 14.1 |
| Mexican femalee | 15.9 | 18.8 | 12.7 | 13.8 |
| Poverty status:g | ||||
| Poor | 25.7 | 30.3 | 18.7 | 21.1 |
| Near poor | 26.7 | 34.8 | 19.8 | 24.1 |
| Nonpoor | 22.2 | 28.2 | 16.2 | 17.8 |
More than 80% of people with Type 2 diabetes are overweight, and in people prone to Type 2 diabetes becoming overweight can trigger onset of the disease. It is not known precisely how overweight contributes to causation of this disease. One hypothesis is that being overweight causes cells to change, making them less effective at using sugar from the blood. This then stresses the cells that produce insulin, causing them gradually to fail. Maintaining a healthy weight and keeping physically fit can usually prevent diabetes.
The relatively recent rise in Type 2 diabetes in the United States is in part attributed to rising obesity among adults, and overweight among children and adolescents. A CDC study found that 54.8% of diabetics over age nineteen were obese between 1999 and 2002 compared with 45.7% in the same age group between 1988 and 1994. When the category was expanded to include diabetics who were obese or overweight, the percentage escalated to 85.2% in 1999–2002 compared with 78.5% in the earlier period.
TABLE 2.7 Hypertension among persons 20 years of age and over, by demographic characteristics, 1988–94 and 1999–2002 [CONTINUED]
| TABLE 2.7 | ||||
|---|---|---|---|---|
| Hypertension among persons 20 years of age and over, by demographic characteristics, 1988–94 and 1999–2002 [CONTINUED] | ||||
| [Data are based on physical examinations of a sample of the civilian noninstitutionalized population] | ||||
| Sex, age, race and Hispanic origina, and poverty status | Elevated blood pressure or taking antihypertensive medicationb, c | Elevated blood pressureb | ||
| 1988–94 | 1999–2002 | 1988–94 | 1999–2002 | |
| Note: Percents are based on the average of blood pressure measurements taken. In 1999–2002, 78 percent of participants had 3 blood pressure readings. | ||||
| aPersons of Mexican origin may be of any race. Starting with data year 1999 race-specific estimates are tabulated according to 1997 Standards for Federal Data on Race and Ethnicity and are not strictly comparable with estimates for earlier years. The two non-Hispanic race categories shown in the table conform to 1997 standards. The 1999–2002 race-specific estimates are for persons who reported only one racial group. Prior to data year 1999, data were tabulated according to 1977 standards. Estimates for single race categories prior to 1999 included persons who reported one race or, if they reported more than one race, identified one race as best representing their race. | ||||
| bElevated blood pressure is defined as having systolic pressure of at least 140 mmHg or diastolic pressure of at least 90 mmHg. Those with elevated blood pressure may be taking prescribed medicine for high blood pressure. | ||||
| cRespondents were asked, "Are you now taking prescribed medicine for your high blood pressure?" | ||||
| dAge adjusted to the 2000 standard population using five age groups. Age-adjusted estimates may differ from other age-adjusted estimates based on the same data and presented elsewhere if different age groups are used in the adjustment procedure. | ||||
| eExcludes pregnant women. | ||||
| fIncludes persons of all races and Hispanic origins, not just those shown separately. | ||||
| gPoor persons are defined as below the poverty threshold. Near poor persons have incomes of 100 percent to less than 200 percent of the poverty threshold. Nonpoor persons have incomes of 200 percent or greater than the poverty threshold. Persons with unknown poverty status are excluded. | ||||
| hEstimates are considered unreliable. | ||||
| SOURCE: "Table 69. Hypertension among Persons 20 Years of Age and Over, According to Sex, Age, Race, and Hispanic Origin, and Poverty Status: United States, 1988–1994 and 1999–2002," in Health, United States, 2005, Centers for Disease Control and Prevention, National Center for Health Statistics, December 8, 2005, http://www.cdc.gov/nchs/data/hus/hus05.pdf#chartbookontrendsinthe (accessed January 8, 2006) | ||||
| Male | ||||
| 20-34 years | 7.1 | 8.1h | 6.6 | 7.3h |
| 35-44 years | 17.1 | 17.1 | 15.2 | 12.1 |
| 45-54 years | 29.2 | 31.0 | 21.9 | 20.4 |
| 55-64 years | 40.6 | 45.0 | 28.4 | 24.8 |
| 65-74 years | 54.4 | 59.6 | 39.9 | 34.9 |
| 75 years and over | 60.4 | 69.0 | 49.7 | 50.6 |
| Femalee | ||||
| 20-34 years | 2.9 | 2.7h | 2.4h | 1.4h |
| 35-44 years | 11.2 | 15.1 | 6.4 | 8.5 |
| 45-54 years | 23.9 | 31.8 | 13.7 | 19.1 |
| 55-64 years | 42.6 | 53.9 | 27.0 | 31.9 |
| 65-74 years | 56.2 | 72.7 | 38.2 | 53.0 |
| 75 years and over | 73.6 | 83.1 | 59.9 | 64.4 |
In 2002, 18.2 million people, more than 6% of the adult population suffered from diabetes. Among people age twenty and older, 8.7% have diabetes and among those age 60 or older 18.3% suffer from the disease. (See Figure 2.8.) Between 1997 and 2002 the percent of adults diagnosed with diabetes increased for all age groups. Worse still, these numbers may significantly underestimate the true prevalence of diabetes in the United States in view of National Health and Nutrition Surveys findings that showed sizeable numbers of adults have undiagnosed diabetes.
"DIABESITY" AND "DOUBLE DIABETES"
Recognition of obesity-dependent diabetes prompted scientists and physicians to coin a new term to describe this condition—diabesity. The term was first used in the 1990s and has gained widespread acceptance. Although diabesity is attributed to the same causes as Type 2 diabetes—insulin resistance and pancreatic cell dysfunction, researchers are beginning to link the inflammation associated with obesity to the development of diabetes and cardiovascular disease.
Pediatric endocrinologist Francine R. Kaufman, who served as president of the American Diabetes Association, contends that the diabesity epidemic "imperils human existence as we now know it" in Diabesity: The Obesity-Diabetes Epidemic That Threatens America—And What We Must Do to Stop It (New York: Bantam, 2005) and observes that more than one-third of American children born in 2000 will develop diabetes in their lifetime. Kaufman warns that unless drastic measures are taken, by 2020 there will be a 72% increase in the number of diabetics in America.
Another recent phenomenon is patients diagnosed with both Type 1 and type 2 diabetes simultaneously. Dubbed "double diabetes," it has been reported in children and adults. Among children it often results when children with Type 1 diabetes who rely on insulin injections to control their diabetes gain weight and develop the insulin resistance that characterizes Type 2 diabetes. Adults who have been diagnosed with Type 2 diabetes, but fail to respond to treatment have been found to also suffer from the Type 1, insulin-dependent form of the disease.
FIGURE 2.6 Age-adjusted prevalence of hypertension* according to BMI
Although there are no reliable statistics about the prevalence of double diabetes, in a July 19, 2005 interview, Dr. Dorothy Becker, a pediatric endocrinologist and leading double-diabetes researcher at Children's Hospital of Pittsburgh, estimated that 25% of children with Type 1 diabetes who are overweight also have symptoms of Type 2 diabetes. Dr. Becker theorizes that overweight people require more insulin to process glucose regardless of whether they are insulin-resistant. It may be that obesity overworks the pancreas until it wears out. It also is possible that obesity triggers or hastens the autoimmune destruction, which implies that individuals genetically predisposed to Type 1 diabetes might not develop the disease if they maintained a healthy weight (Lauran Neergaard, "'Double Diabetes' Harder to Detect, Treat," Associated Press, July 19, 2005).
Osteoarthritis and Joint Injury
Being only ten pounds overweight increases the force on the knee by thirty-sixty pounds with each step. Even small amounts of weight loss reduce the risk of developing knee OA. Preliminary studies suggest weight loss decreases pain substantially in those with knee OA.
—Susan Bartlett, "Osteoarthritis and Body Weight," Johns Hopkins University, 2005
The word "arthritis" literally means joint inflammation. The name applies to more than 100 related diseases known as rheumatic diseases. A joint is any point where two bones meet. When a joint becomes inflamed, swelling, redness, pain, and loss of motion occur. In the most serious forms of the disease, the loss of motion can be physically disabling. Arthritis is the leading cause of disability and the leading cause of limitation of activity among working-age adults in the United States. (See Figure 2.9.)
People who are overweight or obese are at increased risk for osteoarthritis, which is not an inflammatory arthritis. Osteoarthritis, sometimes called degenerative arthritis, causes the breakdown of bones and cartilage (connective tissue attached to bones), and usually causes pain and stiffness in the fingers, knees, feet, hips, and back. Extra weight places extra pressure on joints and cartilage, causing them to erode. Further, people with more body fat may have higher blood levels of substances that cause inflammation. Inflammation at the joints may increase the risk for osteoarthritis.
Osteoarthritis affects about twenty million Americans, usually after age forty-five. The association between overweight and the risk for development of knee osteoarthritis is stronger in women than in men, but for both men and women an increase in weight is significantly associated with increased pain in weight-bearing joints. Data from the National Health and Nutrition Examination Survey revealed that obese women had about four times the risk of knee osteoarthritis compared with women of healthy weight and for obese men, the risk was nearly five times greater. People with clinically severe obesity—those in the highest fifth of body weight have a tenfold risk of developing knee osteoarthritis compared with those in the lowest fifth.
Weight loss may decrease the likelihood of developing osteoarthritis in the knees, hips, and lower back and has been shown to relieve the symptoms of osteoarthritis. The National Heart, Lung, and Blood Institute reported research findings that a decrease in BMI of two units or greater during a ten-year period decreased the risk of developing knee osteoarthritis by more than 50%. Another study found that people with osteoarthritis who lost weight had improved range of motion and less joint pain.
Research conducted by Gary M. Ford and his colleagues at the University of Utah's Rocky Mountain Center for Occupational Environmental Health found that overweight also is linked to cartilage tears in the knee. The investigators studied 544 patients who had surgical cartilage tears repaired between 1996 and 2000. The patients were men and women aged fifty-seventy-nine who had surgery to repair the meniscus, the shock-absorbing cartilage in the knee. The study found that people with BMI
FIGURE 2.7 Treatment algorithm
Gallbladder Disease
Gallstones are small, hard pellets that can form when bile in the gallbladder—a muscular sac-like organ that lies under the liver in the right side of the abdomen—precipitates (becomes solid out of the bile solution). Bile contains water, cholesterol, fats, bile salts, proteins, and bilirubin. The gallbladder stores and concentrates the bile produced in the liver that is not immediately needed for digestion. Bile is released from the gallbladder into the small intestine in response to food. The pancreatic duct joins the common bile duct at the small intestine, adding enzymes to aid in digestion. (See Figure 2.10.) If the liquid bile contains too much cholesterol, bile salts, or bilirubin, under certain conditions it can harden
FIGURE 2.8 Total prevalence of diabetes in people aged 20 years or older, by age group, 2005
People who are overweight are at higher risk for developing gallstones because the liver overproduces cholesterol and delivers it into the bile, which then becomes supersaturated. According to the National Heart, Lung, and Blood Institute in Guidelines on Overweight and Obesity: Electronic Textbook http://www.nhlbi.nih. gov/guidelines/obesity/e_txtbk/ratnl/2217.htm, the risk of gallstones is as high as twenty per 1,000 women per year when BMI is above 40, compared with three per 1,000 among women with BMI less than 24.
Analysis of data from the third National Health and Nutrition Examination Survey, conducted between 1988 and 1994 (NHANES III), revealed that the prevalence of gallstone disease among women increased from 9.4% in the first quartile of BMI to 25.5% in the fourth quartile of BMI. Among men, the prevalence of gallstone disease increased from 4.6% in the first quartile of BMI to 10.8% in the fourth quartile of BMI. Rapid weight loss or weight cycling—dieting, losing weight, and regaining weight lost—further increase cholesterol production in the liver, with resulting supersaturation and risk for gallstone formation.
Jarl Torgerson and his colleagues at the Department of Body Composition and Metabolism, Sahlgrenska University Hospital in Göteborg, Sweden, examined the relationship between gallstones and pancreatitis (inflammation of the pancreas, a large elongated gland located
FIGURE 2.9 Selected chronic health conditions causing limitation of activity among working-age adults by age, 2002–03
FIGURE 2.10 The biliary system
Fatty Liver Disease
Fatty liver is defined as an excess accumulation of fat in the liver, usually exceeding 5% of the total liver weight. More than 50% of the excess fat deposit in the liver is triglyceride. The enlargement of the liver is caused by the reduction of fatty acid oxidation in the liver, resulting in excess accumulation of fat. It causes injury and inflammation in the liver and may lead to severe liver damage, cirrhosis (build-up of scar tissue that blocks proper blood flow in the liver), or liver failure. An estimated nine million individuals in the United States suffer from nonalcoholic fatty liver disease.
People with diabetes or with higher than normal blood sugar levels (but not yet in the diabetic range) are more likely to have fatty liver disease than those with normal blood sugar levels. It is not known why some people who are overweight or diabetic get fatty liver and others do not. Losing weight reduces the buildup of fat in the liver and prevents further injury; however, weight loss should not exceed 1 kg (2.2 pounds) per week because more rapid weight loss may exacerbate the disease.
Cancer
Cancer is a large group of diseases characterized by the uncontrolled growth and spread of abnormal cells. These cells may grow into masses of tissue called tumors. Tumors consisting of cancer cells are called malignant tumors. The dangerous aspect of cancer is that cancer cells invade and destroy normal tissue.
The spread of cancer cells occurs either by local growth of the tumor or by some of the cells becoming detached and traveling through the blood and lymph systems to start additional tumors in other parts of the body. Metastasis (the spread of cancer cells) may be confined to a region of the body, but left untreated (and often despite treatment), the cancer cells can spread throughout the entire body, causing death. It is perhaps the rapid, invasive, and destructive nature of cancer that makes it, arguably, the most feared of all diseases, even though it is second to heart disease as the leading cause of death in the United States.
Overweight increases the risk of developing several types of cancer, including cancers of the colon, esophagus, gallbladder, kidney, liver and prostate, as well as uterine (specifically cancer of the lining of the uterus) and postmenopausal breast cancer. Excessive weight gain during adult life increases the risk for several of these cancers. For example, according to the National Heart, Lung, and Blood Institute, a gain of more than twenty pounds from age eighteen to midlife doubles a woman's risk of breast cancer, and even more modest weight gains are associated with increased risk. In 2005 researchers from International Agency for Research on Cancer (IARC) estimated that 40% of uterine cancers, up to 25% of kidney cancers, and about 10% of breast and colon cancers would not develop if people avoided gaining excess weight. The IARC also asserted that obesity increases the risk of breast cancer in postmenopausal women by as much as 40%.
Investigators at the Albert Einstein College of Medicine in New York found a relationship between obesity and colorectal cancer. In "Obesity and Colorectal Cancer Risk in Women" (Gut: An International Journal of Gastroenterology and Hepatology, vol. 51, no. 2, August 2002), the authors reported that obesity (BMI of 30 or more) was associated with a nearly twofold increased risk of colorectal cancer in premenopausal women. The investigators hypothesized that the biological mechanism underlying their findings was the positive relationship between adiposity (fatness) and blood insulin levels. An increase in blood insulin levels lowers insulin-like growth factor (IGF) binding protein 1 and may lead to increased levels of free IGF-1, which has been linked to increased risk of colorectal cancer in men and women.
Researchers from the American Cancer Society and the Department of Preventive Medicine, University of Southern California School of Medicine found a relationship between obesity and pancreatic cancer. In 1992 the researchers obtained information on current weight and weight at age eighteen, location of weight gain, and recreational physical activity were obtained at baseline using a self-administered questionnaire for 145,627 men and women who were cancer-free at the start of the study. During seven years of follow-up, 242 cases of pancreatic cancer were diagnosed in the research subjects. Analysis of these data revealed an increased risk of pancreatic cancer among obese men and women compared with men and women of normal weight. The risk of pancreatic cancer was also higher among men and women who reported a tendency for central (abdominal) weight gain compared with subjects who reported a tendency for peripheral weight gain (Alpa V. Patel et al., "Obesity, Recreational Physical Activity, and Risk of Pancreatic Cancer in a Large U.S. Cohort," Cancer Epidemiology Biomarkers & Prevention, vol. 14, February 2005).
Another study suggested that about 30% of cases of acute myelogenous leukemia (AML) in older women might be linked to overweight or obesity. An analysis of data from the Iowa Women's Health Study, which gathered data from more than 40,000 Iowa women ages fifty-five to sixty-nine from 1986–2001 found that the risk for AML was 90% higher among women fifty-five and older who were overweight (BMI 25-29). The risk was 140% higher among obese (BMI of 30 or greater) women in this age group (Julie A. Ross et al., "Body Mass Index and Risk of Leukemia in Older Women," Cancer Epidemiology Biomarkers & Prevention, vol. 13, November 2004).
Overweight also may increase the risk of dying from some cancers. In "Weight Loss in Breast Cancer Patient Management" (Journal of Clinical Oncology, vol. 20, no. 4, February 15, 2002), researchers Rowan Chlebowski, Erin Aiello, and Anne McTiernan concluded that "women with breast cancer who are overweight or gain weight after diagnosis are found to be at greater risk for breast cancer recurrence and death compared with lighter women. Obesity is also associated with hormonal profiles likely to stimulate breast cancer growth."
It is not known exactly how being overweight increases cancer risk, recurrence, or mortality. It may be that fat cells make or influence hormones that affect cell growth and lead to cancer. It also is possible that eating habits—such as a high-fat, high-calorie diet—or physical inactivity that promote overweight contribute to cancer risk.
Sleep Apnea and Sleep Disorders
Sleep apnea is a condition in which breathing becomes very shallow or stops completely for short periods during sleep. Each pause lasts about ten to twenty seconds or longer and pauses can occur twenty times or more an hour. Sleep apnea can increase the risk of developing high blood pressure, heart attack, or stroke. Untreated sleep apnea can increase the risk of diabetes and daytime sleepiness and difficulty concentrating can increase the risk for work-related accidents and automobile accidents.
The most common type of sleep apnea, and the type that is linked to overweight and obesity, is obstructive sleep apnea (OSA). During sleep there is insufficient airflow into the lungs through the mouth and nose, and the amount of oxygen in the blood may drop because the airway is transiently occluded (blocked). According to the National Heart, Lung, and Blood Institute, more than twelve million Americans have OSA, and one in twenty-five men over age forty and one in fifty women over age forty have debilitating sleep apnea that causes them to be very sleepy during the day. The condition is more common in men, African-Americans, Hispanics, and Pacific Islanders.
Obesity, particularly upper body obesity, is a risk factor for sleep apnea and is related to its severity. Most people with sleep apnea have a BMI greater than 30. In general, men whose neck circumference is seventeen inches or greater and women with neck circumference of sixteen inches or greater are at higher risk for sleep apnea. Large neck girth in both men and women who snore is highly predictive of sleep apnea because people with large neck girth store more fat around their necks, which may compromise their airways. A smaller airway can make breathing difficult or stop it altogether. In addition, fat stored in the neck and throughout the body can produce substances that cause inflammation, and inflammation in the neck may be a risk factor for sleep apnea. Weight loss usually resolves or significantly improves sleep apnea by decreasing neck size and reducing inflammation.
Anatomic risk factors for obstructive sleep apnea run in families—the volume of upper-airway soft tissue structures, including the lateral pharyngeal walls and tongue, is greater in individuals with OSA than in healthy control subjects. In "Familial Link Seen in Obstructive Sleep Apnea" (Journal of the American Medical Association, vol. 290, no. 22, December 10, 2003), author Lynne Lamberg observes that family history of OSA explains about 30% of the variability of OSA in the general population and that an individual with a first-degree relative with OSA has a 50% to 75% higher risk of having the condition than an individual with no known affected relatives. Lamberg reported that researchers postulate the existence of a syndrome involving obesity, high blood pressure, and diabetes, in which OSA exacerbates the other traits, generating a vicious cycle.
The results of a large, long-term, prospective controlled study of untreated men with severe obstructive sleep apnea were published in The Lancet in March 2005. Investigators at the Hospital Universitatio Miguel Servet in Spain followed 264 healthy men, 377 men who simply snored, 403 with untreated mild-to-moderate severe OSA, 235 with severe OSA, and 372 with treated severe OSA for about ten years. Treated subjects with OSA had fatal and non-fatal cardiovascular event rates that were closer to those seen in healthy subjects than the other subjects with severe OSA. Subjects with untreated severe OSA had two to three times the risk of fatal and non-fatal cardiovascular events compared with healthy subjects. The investigators concluded that there is a relation between the severity of OSA and cardiovascular risk, but effective treatment with continuous positive airway pressure (CPAP) seems to cut this risk and significantly reduce the cardiovascular illness associated with OSA (J. M. Marin et al., "Long-term Cardiovascular Outcomes in Men with Obstructive Sleep Apnea-Hypopnoea with or without Treatment with Continuous Positive Airway Pressure: An Observational Study," Lancet, vol. 365, March 19, 2005).
Too little sleep is also linked to obesity. A study presented at the November 2004 meeting of the North American Association for the Study of Obesity found that people who got less than four hours of sleep a night were 73% more likely to be obese than those who got the recommended seven to nine hours of rest. People who averaged five hours of sleep had 50% greater risk, and those who got six hours had 23% greater risk of obesity ("Lack of Sleep May Lead to Excess Weight," http://www.naaso.org/news/20041116.asp, November 16, 2004).
Dr. Robert D. Vorona and his colleagues at Eastern Virginia Medical School found that people who were overweight or obese reported that they slept less per week than their normal-weight counterparts. Total sleep time decreased as BMI increased except in the extremely obese group. The difference averaged sixteen minutes per day between normal weight and overweight subjects totaling nearly two hours per week. The researchers speculated that lost sleep might have metabolic and hormonal consequences. For example, sleep restriction may reduce levels of leptin, a hormone involved in appetite regulation, which could account for the relationship between diminished sleep and obesity. They observed that their findings did not establish a cause-and-effect relationship between sleep and obesity; however, they "suggest that an extra twenty minutes of sleep per night seems to be associated with a lower BMI" (Robert D. Vorona et al., "Overweight and Obese Patients in a Primary Care Population Report Less Sleep than Patients with a Normal Body Mass Index" Archives of Internal Medicine, vol. 165, no. 1, January 10, 2005).
Women's Reproductive Health
In addition to increased risk of breast and endometrial cancers (the endometrium is the lining of the uterus), women who are overweight or obese may suffer from infertility (difficulty or inability to conceive a child), and other gynecological or pregnancy-related medical problems. Obesity is associated with such menstrual irregularities as abnormally heavy menstrual periods and amenorrhea (cessation of menstruation), and has been found to affect ovulation, response to fertility treatment, pregnancy rates, and pregnancy outcomes.
Abdominal obesity in women is linked to polycystic ovarian syndrome (PCOS), an endocrine condition that afflicts approximately 6%-10% of premenopausal women. PCOS is characterized by the accumulation of cysts (fluid-filled sacs) on the ovaries, chronic anovulation (absent ovulation), and other metabolic disturbances. Symptoms include excess facial and body hair, acne, obesity, irregular menstrual cycles, insulin resistance, and infertility. A key characteristic of PCOS is hyperan-drogenism—excessive production of male hormones (androgens), particularly testosterone, by the ovaries—that is responsible for the acne, male pattern hair growth, and baldness seen in women with PCOS. Hyperandrogenism has been linked with insulin resistance, the inability of the body to respond to insulin, and hyperinsulinemia (high blood insulin levels), both of which are common in PCOS. Women with PCOS have an increased risk of early-onset heart disease, hypertension, diabetes, reproductive cancers, and a higher incidence of miscarriage and infertility. In overweight women, modest weight loss (as little as 5%) through diet and exercise may correct hyperandrogenism, and restore ovulation and fertility.
Obesity during pregnancy is associated with increased morbidity for both the expectant mother and the unborn child. Obese pregnant women are significantly more likely to suffer from hypertension and gestational diabetes (glucose intolerance of variable severity that starts or is first recognized during pregnancy) than normal-weight expectant mothers. Obesity also is associated with difficulties in managing labor and delivery, leading to higher rates of Caesarean section (delivery of a fetus by surgical incision through the abdominal wall and uterus). Risks associated with anesthesia are higher in obese women, as there is greater tendency toward hypoxemia (abnormal lack of oxygen in the blood) and greater difficulty administering local or general anesthesia.
The children of women who are obese during pregnancy are at increased risk of birth defects—congenital malformations, particularly of neural tube defects. Neural tube defects are abnormalities of the brain and spinal cord resulting from the failure of the neural tube to develop properly during early pregnancy. The neural tube is the embryonic nerve tissue that eventually develops into the brain and the spinal cord. Every year, about 4,000 unborn children are affected with neural tube defects. Of these, approximately 2,500 involve infants born with the two most common neural tube defects—anencephaly (absence of a major part of the brain, skull, and scalp) and spina bifida (failure of the vertebrae (backbones) to completely cover the spinal cord early in fetal development, leaving the spinal cord exposed).
Research indicates that boys born to higher-weight mothers may be more likely to develop testicular cancer. Exposure of unborn males to high levels of estrogen is believed to be involved in the subsequent development of testicular cancer. Boys born to higher-weight mothers are more likely to have been exposed to high estrogen levels than boys born to lower-weight mothers because higher weight results in higher insulin levels and lower levels of the protein that normally binds estrogen. As a result, higher levels of estrogen are able to cross the placenta and affect the male fetus. (Elin L. Aschim et al., "Is There an Association between Maternal Weight and the Risk of Testicular Cancer? An Epidemiologic Study of Norwegian Data with an Emphasis on World War II"-International Journal of Cancer, vol. 116, no. 2, August 20, 2005)
Further, women who are obese before pregnancy appear to have a higher risk of stillbirth and of having an infant die soon after birth. A study of more than 24,000 Danish women found that compared with normal-weight women, those who were obese before pregnancy had twice the risk of stillbirth and newborn deaths. Although earlier researchers have reported comparable risks attributed in part to the higher rates of diabetes and high blood pressure observed in overweight pregnant women, this study found that diabetes and high blood pressure were not responsible for their findings. When women with diabetes or high blood pressure were excluded from their analysis, the risks of stillbirth and newborn death linked to obesity were still significantly higher than the risks for normal weight or overweight women. While it is not yet known how obesity increases the risk of stillbirth and early infant death, the Danish researchers posit that obesity influences the hormonal system and the metabolism of blood fats that in turn may compromise blood flow to the placenta (an organ that forms during pregnancy and functions as a filter between the mother and fetus) (Janni Kristensen, "Pre-pregnancy Weight and the Risk of Stillbirth and Neonatal Death," British Journal of Gynecology, vol. 112, no. 4, April 2005).
WEIGHT GAIN DURING PREGNANCY
Weight gain during pregnancy is expected and beneficial. The fetus, expanded blood volume, the enlarged uterus, breast tissue growth, and other products of conception generate approximately thirteen to seventeen pounds of extra weight. Weight gain beyond this anticipated amount is largely maternal adipose tissue that often is retained after pregnancy. The challenge health professionals face when developing recommendations about weight gain during pregnancy is achieving a balance between gains intended to produce high-birth-weight infants, who may then require delivery by Caesarean section, and low-birth-TABLE 2.8 Recommended weight gain during pregnancy
| TABLE 2.8 | ||
|---|---|---|
| Recommended weight gain during pregnancy | ||
| BMI | Kilograms | Pounds |
| SOURCE: "Weight Gain During Pregnancy," in Guidelines on Overweight and Obesity: Electronic Textbook, National Heart, Lung, and Blood Institute in cooperation with the National Institute of Diabetes and Digestive and Kidney Diseases, 1998, http://www.nhlbi.nih.gov/guidelines/obesity/e_txtbk/ratnl/22111.htm (accessed January 12, 2006) | ||
| <19.8 | 12.5 to 18 | 28 to 40 |
| >19.8 to 26 | 11.5 to 16 | 25 to 35 |
| >26 to 29 | 7 to 11.5 | 15 to 25 |
| >29 | ≤6 | ≤13 |
A 1990 report by the Institute of Medicine of the National Academy of Sciences issued recommendations about weight gain in pregnancy. The Institute of Medicine suggested that women with BMI of less than 20 should gain about 0.5 kg (1.1 lb) of weight per week during the second and third trimester. For women with BMI greater than 26, a gain of 0.3 kg (0.7 lb) per week during the last two trimesters is recommended. Women who are overweight or obese at the onset of pregnancy are advised to gain less total weight during pregnancy than women at normal weights pre-pregnancy. (See Table 2.8.)
In 2001 Cornell University professor of nutritional science Christine Olsen and her colleagues at the Research Institute of Bassett Healthcare in New York looked at weight gain in 577 pregnant women and found that more than 40% of the women gained more weight during pregnancy than is recommended by the Institute of Medicine. They also found that one-fourth of all the pregnant women studied were at least ten pounds heavier one year after giving birth. The researchers concluded that women who gain more than the amount recommended during pregnancy are four times more likely to be obese one year after giving birth compared with mothers who gain within the recommended range.
Another study conducted by Cornell University and Bassett Hospital researchers in 2001 found that normal-weight women who gained more than the twenty-four to thirty-five pounds during pregnancy recommended by the Institute of Medicine were 74% more likely to be unsuccessful at breastfeeding than mothers who observed the guidelines. The study confirmed previous findings that obese women are at higher risk for discontinuing breastfeeding than normal-weight mothers. Investigator Kathleen Rasmussen speculated that a combination of biological, mechanical, and psychosocial factors combined to make breastfeeding problematical for obese women.
Metabolic Syndrome
In 2005 an estimated 44% of Americans over age fifty exhibited a cluster of medical conditions characterized by insulin resistance and the presence of obesity, abdominal fat, high blood sugar and triglycerides, high blood cholesterol, and high blood pressure. This constellation of symptoms, termed "metabolic syndrome" was first defined in the May 15, 2001 Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (ATPIII). The report concluded that for the majority of affected people, metabolic syndrome results from poor diet and insufficient physical activity.
The diagnosis of metabolic syndrome, which is also known as syndrome X, requires that people meet at least three of the following criteria:
- Waistline measurement (waist circumference) of 40 inches or more for men and 35 inches or more for women
- Blood pressure of 130/85 mm Hg or higher
- Fasting blood glucose level greater than 100 mg/dl
- Serum triglyceride level above 150 mg/dl
- High density lipoprotein level (HDL) less than 40 mg/dl for men or under 50 mg/dl for women.
According to the American Heart Association, three groups of people are most likely to be diagnosed with metabolic syndrome—diabetics, people with hypertension and hyperinsulinemia (secreting larger than normal amounts of insulin to maintain blood glucose levels), and people who have suffered heart attacks and have hyperinsulinemia without glucose intolerance.
While research has shown that the signs of metabolic syndrome are common among family members, until recently a definitive genetic link had not yet been identified. Dr. Claude Bouchard and his colleagues at the Pennington Biomedical Research Center in Baton Rouge, Louisiana, demonstrated the existence of genetic regions that may signal a predisposition to metabolic syndrome. The researchers analyzed 509 genetic markers to scan the whole genome of 456 white participants from ninety-nine families and 217 black participants from 105 families, looking for genomic regions harboring genes that could influence metabolic syndrome. In "Genome-Wide Linkage Scan for the Metabolic Syndrome in the HERITAGE Family Study" (Journal of Clinical Endocrinology and Metabolism, vol. 88, no. 12, December 2003), the researchers reported that they found evidence of genetic linkages to metabolic syndrome in both black and white patients. The researchers asserted that "Our research shows a genetic link, contributing to the clustering in families and individuals, between diabetes, cardiovascular disease, and metabolic syndrome. These findings bring us closer to discovering the actual genes that are responsible for metabolic syndrome, which puts patients at risk for so many serious health problems. This information could someday help doctors assess whether specific patients are at risk for developing the metabolic syndrome based on their genes."
Although the exact origins and mechanism of metabolic syndrome are not fully known, affected individuals experience a series of biochemical changes that, in time, lead to the development of potentially harmful medical conditions. The biochemical changes begin when insulin loses its ability to cause cells to absorb glucose from the blood (insulin resistance). As a result, glucose levels remain high after food is consumed, and the pancreas, sensing a high glucose level in the blood, continues to secrete insulin. Loss of insulin sensitivity may be genetic or may be in response to high fat levels with fatty deposits in the pancreas.
Moderate weight loss, in the range of 5% to 10% of body weight, can help restore the body's sensitivity to insulin and greatly reduce the chance that the syndrome will progress into a more serious illness. Increased activity alone also has been shown to improve insulin sensitivity.
John K. Ninomiya and his colleagues from the University of California, San Diego, investigated how each of the factors associated with metabolic syndrome influences cardiovascular risk and reported the results of their research in "Association of the Metabolic Syndrome with History of Myocardial Infarction and Stroke in the Third National Health and Nutrition Examination Survey" (Circulation, vol. 109, January 2004). Using data from 10,357 NHANES III participants, they found that having the metabolic syndrome doubled the risk. High triglycerides independently increased that risk by 66%, high blood pressure raised it by 44%, low HDL cholesterol raised it by 35%, and insulin resistance raised it by 30%. Obesity by itself did not increase the risk, but the researchers observed that obesity places people at increased risk for the other four conditions.
The researchers concluded that metabolic syndrome was significantly associated with myocardial infarction and stroke in both women and men, and asserted that "These findings re-affirm the clinical importance of the metabolic syndrome as a significant risk factor for cardiovascular disease and the need to develop strategies for controlling this syndrome and its component conditions."
Metabolic syndrome is also a risk factor for cognitive decline—loss of memory, thinking and reasoning skills. Dr. Kristine Yaffe and her colleagues at the University of California, San Francisco analyzed data from 2,632 nondemented (cognitively normal) participants in the Health, Aging and Body Composition (ABC) study. The subjects were ages seventy to seventy-nine, and were followed from 1997 through 2002. Subjects with metabolic syndrome were more likely than those without to exhibit cognitive decline. The researchers hypothesized that metabolic syndrome hastened atherosclerosis or inflammation, which led to cognitive decline (Kristine Yaffe et al., "The Metabolic Syndrome, Inflammation, and Risk of Cognitive Decline, Journal of the American Medical Association, vol. 292, no. 18, November 10, 2004).
REDEFINING THE METABOLIC SYNDROME
In an effort to standardize diagnosis, prevention, screening and treatment, on April 14, 2005, the International Diabetes Federation (IDF) presented a new worldwide definition of the metabolic syndrome. The new diagnostic criteria are central obesity, defined as waist equal to or more than 94 cm (37 inches) for males and 80 cm (31.5 inches) for females of European descent, and ethnic-specific levels in Chinese, Japanese and South Asians; along with two of the following: triglycerides of at least 1.7 mmol/L or 150 mg/dL; low HDL-cholesterol, defined as less than 1.04 mmol/L (40 mg/dL) in males and less than 1.29 mmol/L (50 mg/dL) in females; blood pressure of at least 130/85 mm Hg; and fasting hyperglycemia, defined as glucose equal to or greater than 5.6 mmol/L (100mg/dL) or previous diagnosis of diabetes or impaired glucose tolerance. The new definition of the metabolic syndrome, which includes diabetes or prediabetes, abdominal obesity, unfavorable lipid profile and hypertension, triples the risk of myocardial infarction (heart attack) or stroke and doubles mortality from these conditions. It also increases the risk of developing Type 2 diabetes, if not already present, fivefold. Using this definition, about one-quarter of the U.S. adult population may be diagnosed as having the metabolic syndrome.
SOME QUESTION THE DIAGNOSIS OF METABOLIC SYNDROME
In the fall of 2005 two leading diabetes organizations, the American Diabetes Association and European Association for the Study of Diabetes questioned the utility of the diagnosis of metabolic syndrome. Representatives of these organizations said they felt the syndrome was neither a distinct disease nor well established by scientific research. In "The Metabolic Syndrome: Time for a Critical Appraisal—Joint Statement from the American Diabetes Association and the European Association for the Study of Diabetes" (Diabetes Care, vol. 28, no. 9, September 2005), Richard Kahn of the American Diabetes Association, John Buse, of the Division of Endocrinology and of General Medicine & Clinical Epidemiology, University of North Carolina School of Medicine, and their colleagues wrote, "While there is no question that certain CVD risk factors are prone to cluster, we found that the metabolic syndrome has been imprecisely defined, there is a lack of certainty regarding its pathogenesis, and there is considerable doubt regarding its value as a cardiovascular disease (CVD) risk marker. Our analysis indicates that too much critically important information is missing to warrant its designation as a 'syndrome.'"
The authors advised physicians against diagnosing or treating patients with metabolic syndrome as a disease. Instead, they encouraged them to screen and treat high triglyceride levels, high blood pressure, low levels of HDL cholesterol, and high blood glucose as separate conditions to reduce the risk of heart disease. Their specific recommendations are that:
- Adults with any major CVD risk factor should be evaluated for the presence of other CVD risk factors.
- Patients with CVD risk variables above the cut point for normal should receive counseling for lifestyle modification, and at cut points indicative of frank disease (e.g., blood pressure >140/90 mmHg, fasting plasma glucose ≥7.0 mmol/l), treatment should correspond to established guidelines.
- Providers should avoid labeling patients with the term "metabolic syndrome," as this might create the impression that the metabolic syndrome denotes a greater risk than its components, or that it is more serious than other CVD risk factors, or that the underlying pathophysiology is clear.
- All CVD risk factors should be individually and aggressively treated.
- Until randomized controlled trials have been completed, there is no appropriate pharmacological treatment for the metabolic syndrome, nor should it be assumed that pharmacological therapy to reduce insulin resistance will be beneficial to patients with the metabolic syndrome.
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