Obesity complications and overweight problems
Obesity is a serious chronic disease associated with complications and comorbidities that involve most systems of the body. The common factor in all obese people is the presence of excess adipose tissue stores and an increased percentage of body fat. Even in the absence of complications and comorbidities, obesity increases the risk of early mortality. It has been estimated that there are 300 000 obesity related deaths in the United States each year. In addition to medical complications, obesity is associated with psychological and social problems that may overshadow the medical problems in the quality of life for many obese people. Here is a list with the possible complications of obesity:
- Metabolic complications - type 2 diabetes, insulin resistance and hyperinsulinemia, dyslipidemia, gout.
- Abnormalities of hormones - growth hormone, hypothalamic-pituitary-adrenal axis, cytokines, renin-angiotensin system, leptin, ghrelin.
- Cardiac and vascular diseases - coronary heart disease, hypertension, congestive heart failure, cerebrovascular disease, thromboembolic disease.
- Respiratory system abnormalities - obesity-hypoventilation syndrome, sleep apnea.
- Digestive system abnormalities - gallbladder disease, hepatic disease.
- Nervous system - pseudotumor cerebri, adiposis dolorosa, alzheimer's disease.
- Mechanical complications - arthritis, increased intra-abdominal pressure.
- Other complications - immune system dysfunction, skin disease, eye disease, cancer, social complications.
Distribution of body fat and its role in obesity complications
1. - Intramuscular fat 2. - Intrahepatic fat
3. - Abdominal (visceral) fat 4. - Subcutaneous fat
The distribution of excess adipose tissue contributes to the complications of obesity. Obese individuals may be classified as those whose excess fat is deposited in the upper body versus those with increased lower body obesity. Upper body obesity may be localized to the subcutaneous space versus the abdominal space (visceral fat). Waist circumference and the ratio of waist to hip circumferences correlate with the morbidity and mortality of obesity. Individuals with increased visceral fat are at greater risk for systemic complications of obesity compared to people with fat localized to subcutaneous depots or to the lower body. The mechanisms of these differences are not clear, but research has shown that visceral fat has a higher triglyceride turnover rate and releases greater amounts of fatty acids into the circulation than do other adipose tissue depots. Since blood vessels from the visceral fat drain into the portal vein, some investigators postulate that exposure of the liver to high levels of free fatty acids produces insulin resistance, which is known to be correlated with many of the complications of obesity described here. There are significant racial differences in deposition of visceral fat. Asians and Hispanics tend to selectively deposit fat in the abdominal cavity with excess energy intake, whereas blacks have less visceral fat than other groups.
Type 2 diabetes
A strong association of obesity with the prevalence of type 2 diabetes mellitus (DM) is well documented. The US National Diabetes Commission reported that the risk of diabetes doubles for every 20% of excess body weight. The risk of type 2 DM is greater with visceral obesity. Weight loss is a very effective treatment for type 2 DM and can prevent the onset of type 2 DM in susceptible individuals. Type 2 DM, once very rare in children, has increased greatly in prevalence with the obesity epidemic.
Insulin resistance and hyperinsulinemia
"Insulin resistance" refers to the phenomenon of insensitivity of the cells of the body to insulin's actions. Different tissues may have different insulin sensitivities. For example, adipose tissue may be more sensitive to insulin than muscle tissue, thus favoring the deposition of fatty acids in adipose tissue and diminished fatty acid oxidation in muscle. Insulin resistance is usually associated with hyperinsulinemia. Hyperinsulinemia is an independent marker that predicts the development of atherosclerosis.
Obesity, particularly visceral obesity, is associated with increased serum levels of cholesterol, triglycerides, low-density lipoproteins (LDL), very low-density lipoproteins (VLDL), apolipoprotein B, and reduced levels of high-density lipoprotein (HDL) cholesterol. Every 10% increase in relative body weight is associated with a 12 mg/dl increase in serum cholesterol concentration.
Serum uric acid and the prevalence of gout correlate positively with BMI. High serum uric acid levels correlate with insulin resistance and an increased risk of atherosclerotic cardiovascular disease in obesity. Serum uric acid levels may temporarily increase with acute weight loss, but they usually decrease with large amounts of weight loss. The lower uric acid levels are maintained with continued weight loss.
Obesity is typically accompanied by a decrease in growth hormone (GH) levels and an increase in growth hormone binding protein levels. An inverse relation exists between GH levels and percentage fat mass.
Coronary heart disease
Longitudinal studies show a positive correlation of BMI with coronary heart disease (CHD), and obesity is an independent predictor of CHD. However, in the presence of other risk factors, such as hypertension, high serum cholesterol and triglycerides levels, low serum HDL cholesterol levels, and insulin resistance, all of which are increased by obesity, the risk of atherosclerotic CHD increases dramatically. Weight loss reduces all of these risk factors associated with cardiovascular disease, but because long-term reductions in body weight have been difficult to achieve, there are few long-term studies of changes in cardiovascular mortality due to weight loss. A very low-fat diet (10% of total calories as fat) has been shown to reduce the size of atherosclerotic plaques in coronary arteries. Such low-fat diets almost invariably produce weight loss.
The prevalence of hypertension among overweight adults in the United States is 2.9 times higher than that of non-overweight individuals. Every 10 kg increase in body weight is associated with an increase of 3 and 2 mmHg in systolic and diastolic blood pressures, respectively. Except in long-standing cases, weight reduction is usually accompanied by a decrease in blood pressure. The reductions in blood pressure with weight loss are not dependent on decreases in salt intake. Many studies have shown that even modest weight losses, in the range of 5-10% of initial body weight, may produce reductions or even normalization of blood pressure in obese individuals.
Congestive heart failure
Total blood volume increases with excess body weight. Higher oxygen consumption in obesity and increased blood flow to the splanchnic bed and adipose tissue increase cardiac output. Also, the transverse diameter of heart, thickness of the posterior wall, and thickness of the interventricular septum increase with body weight. Left ventricular mass is a stronger predictor of morbidity and mortality than blood pressure. A combination of these factors may result in the congestive heart failure seen in severely obese people. The heart rate, stroke volume, blood volume, cardiac output, and left ventricular work return to normal with weight reduction. One study that compared weight loss by dieting to treatment with antihypertensive drugs demonstrated a greater improvement in cardiac hypertrophy with weight loss, despite similar reductions in blood pressure.
Obesity related atherosclerosis and arteriosclerosis increase the risk of cerebrovascular disease and strokes. Obesity is an independent risk factor for strokes, even in the absence of other comorbidities.
The risks of venous stasis, deep vein thrombosis, and pulmonary embolism are increased in obesity, particularly in people with abdominal obesity. Lower extremity venous disease may result from increased intra-abdominal pressure, impaired fibrinolysis, and the increase in inflammatory mediators described previously.
Respiratory system abnormalities
Obesity is associated with reduced lung volume, altered respiratory patterns, and an overall reduction in the compliance of the respiratory system, including a diminished vital capacity and total lung capacity. More severe obesity is associated with the "obesity-hypoventilation syndrome", which is characterized by excessive daytime sleepiness and hypoventilation. The increased work required to move the chest wall, a decrease in arterial oxygenation in the lungs, and a diminished sensitivity of the respiratory center to the stimulatory effect of carbon dioxide are postulated to contribute to the obesity-hypoventilation syndrome.
The obesity-hypoventilation syndrome may be associated with, or exacerbated by, obstructive sleep apnea, a syndrome characterized by repeated collapse of the upper airway and cessation of breathing with sleep. Obstructive sleep apnea occurs when the tongue obstructs the glottis and prevents entry of air into the trachea. Up to 50% of massively obese people have sleep apnea. The risk of arrhythmias and sudden death increases during apneic episodes. Weight reduction usually reduces the severity of sleep apnea, and massive weight reduction, such as that after gastric bypass surgery, eliminates the disease in most patients.
The risk of gallbladder disease, particularly gallstone formation, is increased in obesity and occurs with greater frequency in women. The prevalence of gallbladder disease in obese individuals increases with age, body weight, and parity. The etiology of increased gallstones is unclear, but genetic factors play a role. Increased cholesterol production, which leads to increased excretion of cholesterol in bile, is known to occur in obesity and correlates with increases in body weight. Many obese people skip meals and the reduced number of meals may result in less frequent emptying of the gallbladder. The resulting bile stasis may contribute to gallstone formation. Although long-term weight loss and maintenance may reduce the occurrence of gallbladder disease, the risk of gallstone formation actually increases during the active weight loss phase. The etiology of this increase is thought to be the mobilization of cholesterol from adipose tissue during rapid weight loss. This increased load of cholesterol in the circulation produces supersaturation of the bile, leading to gallbladder sludge in approximately 25% of patients and to symptomatic disease in approximately 1-3%. Treatment with ursodeoxycholic acid reduces or eliminates the risk of gallstone formation during weight loss.
Abnormalities in hepatic function are commonly reported in obese people. Fatty liver, due to increased concentrations of fatty acids, diglycerides, and triglycerides in hepatocytes, is reported in obese people. The frequency of fatty liver has been reported to be as high as 94% in very obese subjects. A small number of very obese subjects will develop micronodular cirrhosis. Abnormal liver enzymes on laboratory screening are very common in obese people and do not require further evaluation unless they are markedly elevated. Weight loss results in disappearance of the excess fat and normalization of the liver function tests.
Obesity is frequently complicated by degenerative arthritis (DJD). Increased body weight leads to trauma of the weight-bearing joints and speeds the development of osteoarthritis in obesity. Knee and hip joints are particularly affected. However, obese patients have increased DJD of the hands, perhaps due to cytokines produced by adipose tissue, which may damage the cartilage in joints. Flattening of the arc of the planter surface of the feet (flat feet) occurs more frequently in obese people, presumably due to the stress of carrying excess body weight. Flat feet may lead to unsteady gait and aches and pains after walking. Increased fat deposition, particularly in the abdominal region, can change the natural curvature of the spine, causing lordosis and resulting in backache in obese people.
In severely obese people, the excess visceral fat is thought to increase intra-abdominal pressure. Animal research shows that experimentally induced acute increases in intra-abdominal pressure to the levels seen in the abdomens of very obese people cause increases in pleural pressure, intracranial pressure, and central venous pressure. The investigators postulated that in humans, increased intra-abdominal pressure may contribute to hypertension, insulin resistance and type 2 DM, obesity-hypoventilation syndrome, pseudotumor cerebri, incisional hernia, and urinary incontinence. Massive weight loss following obesity surgery normalizes the increased intra-abdominal pressure and reduces or eliminates all the symptoms listed previously.
Obese people may have several disorders of the skin. The most common is stasis changes of the skin of the lower legs in massively obese people. The etiology of this finding is venous stasis, edema, and breakdown of the skin. Fragilitas cutis inguinalis is a condition of fragile skin in the inguinal area of obese people. This condition is diagnosed by stretching the skin of the inguinal area. A linear tear appears at right angles to an applied force that is insufficient to tear the skin of a normal person. This condition is unrelated to the sex and age of the person.
Obesity is associated with an increased prevalence of cataracts. People with abdominal obesity are at greater risk than those with lower body obesity, insulin resistance may be involved in the pathogenesis of cataract formation, and diabetes is a well-known risk factor.
Obesity increases the risk of cancers of the breast, colon, prostate, endometrium, cervix, ovary, kidney, and gallbladder. Studies have also found a somewhat increased risk for cancers of the liver, pancreas, rectum, brain, esophagus, and non-Hodgkin's lymphoma. Although there are many theories about how obesity increases cancer risk, the exact mechanisms are not known. The mechanisms may be different for different types of cancer. Also, because obesity develops through a complex interaction of heredity and lifestyle factors, researchers may not be able to determine whether the obesity or other factors led to the development of cancer.