Excess ProteinEnergy Intake

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these individuals die from secondary infections, rather than from the starvation itself.
The most common form of PEM seen in the United States occurs in the hospital setting. A typical course of events is as follows: The patient has not been eating well for several weeks or months prior to entering the hospital due to chronic or debilitating illness. He/she enters the hospital with major trauma, severe infection, or for major surgery, all of which cause a large negative nitrogen balance. This is often compounded by difficulties in feeding the patient or by the necessity of fasting in preparation for surgery or diagnostic tests. The net result is PEM as measured by low levels of serum albumin and other serum proteins or by decreased cellular immunity tests. Recent studies have shown that hospitalized patients with demonstrable PEM have delayed wound healing, decreased resistance to infection, increased mortality, and increased length of hospitalization. Most major hospitals have programs to monitor the nutritional status of their patients and to intervene where necessary to maintain a positive nitrogen and energy balance (see Clin. Corr. 27.3).
27.5— Excess Protein–Energy Intake
Much has been said in recent years about the large amount of protein that the average American consumes. Certainly most consume far more than needed to maintain positive nitrogen balance. An average American currently consumes 99 g of protein, 68% from animal sources. However, most studies show that a healthy adult can consume that amount of protein with no apparent harm. Concern has been raised about possible effects of high­protein intake on calcium requirements. Some studies suggest that high­protein intake increases urinary loss of calcium and may accelerate bone demineralization associated with aging. However, this issue is far from settled.
Obesity Has Dietary and Genetic Components
Perhaps the more serious nutritional problem is excessive energy consumption. In fact, obesity is the most frequent nutritional disorder in the United States. It would, however, be unfair to label obesity as simply a problem of excess consumption. Overeating plays an important role in many individuals, as does inadequate exercise, but there is also a strong genetic component as well. While the biochemical mechanisms for this genetic predisposition are unclear, investigators have recently identified an obesity gene in mice that appears to regulate obesity through effects on both appetite and deposition of fat. A similar gene exists in humans, but its metabolic function is still not known (see p. 378). Detailed characterization of this and other genes that predispose to obesity in animals may yield valuable clues to the causes and treatment of obesity in humans.
Metabolic Consequences of Obesity Have Significant Health Implications
A discussion of the treatment of obesity is clearly beyond the scope of this chapter, but it is worthwhile to consider some of the metabolic consequences of obesity. One striking clinical feature of overweight individuals is a marked elevation of serum free fatty acids, cholesterol, and triacylglycerols irrespective of the dietary intake of fat. Why is this? Obesity is obviously associated with an increased number and/or size of adipose cells. These cells contain fewer Insulin receptors and thus respond more poorly to insulin, resulting in increased activity of the hormone­sensitive lipase. The increased lipase activity