OBESITY

OBESITY: History and its Consequences

Chronic food shortage and malnutrition have been the scourge of humankind from the dawn of history. The current worldwide epidemic of obesity, now recognized as a public health crisis, is barely a few decades old. Only after the technological advances of the eighteenth century did a gradual increase in food supply became available.
 The initial effect of these advances in improved public health and amount, quality, and variety of food was increased longevity and body size. These early favorable outcomes of technological advances notwithstanding, their incremental effect since the Second World War has been an overabundance of easily accessible food, coupled with reduced physical activity, that accounts for the recent increased prevalence of obesity.

 Obesity as a chronic disease with well-defined pathologic consequences is less than a century old. The scarcity of food throughout most of history had led to connotations that being fat was good, and that corpulence and increased “flesh” were desirable as reflected in the arts, literature, and medical opinion of the times. 
Only in the latter half of the nineteenth century did being fat begin to be stigmatized for aesthetic reasons, and in the twentieth century, its association with increased mortality was recognized. Whereas early reports listed obesity as a risk factor for mortality from “chronic nephritis,” the subsequent recognition of the more common association of obesity with diabetes, hypertension, and heart disease altered the listings and questioned its being a risk factor for kidney disease. An enlarging body of evidence, accrued over the past decade, now indicates a direct association of obesity with chronic kidney disease and its outcomes.

Much like other killer diseases (cardiac, vascular, and respiratory) that have emerged as the scourge of humankind over the same period of time, obesity is a chronic disease. As a chronic disease, the indolent onset of its complications (diabetes, hypertension, and atherosclerosis) account for its morbidity and mortality.

 Unlike the other chronic diseases, however, it is not a silent killer, but one whose external manifestations are evident to afflicted individuals from its outset as weight gain and increased girth. As a public-health problem, therefore, this externally manifest disease is one that is easy to detect, which allows for potentially considerable time to prevent its complications. Prevention is not an easy task at best, and complications remain “a bomb awaiting to be defused.”

Pathology of excess fat

Each disease whose risk is increased by overweight can be classified into one of two pathophysiological categories. The first category of disabilities arises from the increased mass of fat itself. These include the stigma of obesity and the behavioral responses it produces, osteoarthritis, and sleep apnea. The second category is risks that result from the metabolic changes associated with excess fat. These include diabetes mellitus, gallbladder disease, hypertension, cardiovascular disease, and some forms of cancer associated with overweight.

The fat cell can be viewed as a type of endocrine cell, and adipose tissue as an endocrine organ. It is the hypertrophy and/or hyperplasia of this organ that is the pathologic lesion in obesity. After the identification of adipsin or complement D in the fat cell, a number of other secretory peptides were found. Leptin clearly is the most important and secures the role of the adipocyte as an endocrine cell and fat as an endocrine organ. From the pathophysiological perspective, however, the release of free fatty acids may be the most important.

Hypertension.

Blood pressure often is increased in overweight individuals In the Swedish Obesity Study, hypertension was present at baseline in 44–51% of the subjects. One estimate suggests that control of overweight would eliminate 48% of the hypertension in whites and 28% in blacks. For each decline of 1 mm Hg in diastolic blood pressure, the risk of myocardial infarction decreases an estimated 2–3%.

Overweight and hypertension interact with cardiac function. Hypertension in normal weight people produces concentric hypertrophy of the heart, with thickening of the ventricular walls. In overweight individuals, eccentric dilatation occurs. Increased preload and stroke work are associated with hypertension. The combination of overweight and hypertension leads to thickening of the ventricular wall and larger heart volume, and thus to a greater likelihood of cardiac failure.

The hypertension of overweight people appears strongly related to altered sympathetic activity. During insulin infusion, overweight subjects have a much greater increase in the muscle sympathetic nerve firing rate than do normal weight subjects, but the altered activity is associated with a lesser change in the vascular resistance of calf muscles.

Hypertension is strongly associated with type II diabetes, impaired glucose tolerance, hypertriglyceridemia, and hypercholesterolemia, as noted above in the discussion of the metabolic syndrome. Hyperinsulinemia in overweight and hypertensive patients suggests insulin resistance and the metabolic syndrome. An analysis of the factors that predict blood pressure and changes in peripheral vascular resistance in response to body weight gain showed that a key determinant of the weight-induced increases in blood pressure was a disproportionate increase in cardiac output that could not be fully accounted for by the hemodynamic contribution of new tissue. This hemodynamic change may be attributable to a disproportionate increase in cardiac output related to an increase in sympathetic activity.

Obesity may also affect the kidney. Glomerulopathy was significantly increased in pathological specimens compared with other forms of end-stage renal disease.