Friday, October 22, 2010

Consequences of Malnutrition, Fasting, Stress and Disease - Nutrition Partner B. Braun

Consequences of Malnutrition, Fasting, Stress and Disease - Nutrition Partner B. Braun

4. Consequences of fasting, stress and disease

Fasting and stress have opposite influences on the energy expenditure of the human organism. The healthy human body is capable of passing from a state involving three regular food intakes to a state of short-term fasting and even prolonged fasting, as a result of precise metabolic regulation. In these cases, the organism will save as much energy as possible, thus reducing energy expenditure.

However, in stress conditions, energy expenditure is markedly increased. As a result, the body´s metabolism will be converted into a catabolic state, the gravity of which is determined by the nature and degree of the injury and type and severity of underlying disease.

These and other processes will be developed in the following chapters.

[Table of contents]

4.1 Effects of fasting

In theory, if a person having 15 kg of adipose triglycerides — i.e. 140.000 kcal of reserves in the form of fats (Cahill, 1970)— and energy requirements of 1800 kcal/day, begins to fast, he should be capable of withstanding 75 days of total fasting. In practice, an abstinence from feeding leads to death after about 50 days of total fasting. In other words, the theoretical value of the energy reserves can not be used in its entirety, because death intervenes beforehand due to partial depletion of functional tissue proteins.

In the case of abstinence or fasting, endogenous energy stores are used for metabolic processes. Fat, stored in indifferent fat tissue, is the major source of energy. Energy can also be derived from protein; however, there is no indifferent protein tissue and as a consequence the loss of protein always leads to a loss of organ function.

Hence, in the case of fasting in healthy persons, the metabolism is aimed at keeping the loss of protein as low as possible by lowering the metabolism and the gluconeogenesis. The loss of nitrogen is reduced in the case of complete fasting from 10 g per day to 4 - 5 g a day after 3 weeks. Fat stores are depleted faster with the purpose of providing energy.

Many organs including the heart, kidneys and muscles, can use either fatty acids or ketone bodies, derived from partial oxidation of fatty acids, directly as energy substrates. The central nervous system, on the other hand, and the red blood cells can only use glucose as an energy substrate. For example, during a 24 hour fast, the brain will consume 150 g of glucose and the other organs about 36 g, i.e. a total of 186 g of glucose per day. Since the body is incapable of synthesizing glucose from fat, it uses other substrates for gluconeogenesis. In fact, the glycogen reserves are insufficient to cover the requirements for more than 1 day. The most important substrate for gluconeogenesis is provided by amino acids and, to a minor extent, by glycerol derived from the triglycerides.
Metabolism of short-term fasting
Fig. 8: Metabolism of short-term fasting

In short-term fasting, some of the glucose required by the brain is provided by liver glycogen, the reserve being exhausted within 48 hours. If the human body is to withstand fasting, it must mobilize 1800 kcal/day and produce 186 g of glucose mainly for the central nervous system. Eighty percent of the energy requirements are provided by lipolysis of adipose tissue where 160 g of triglycerides are split into fatty acids and glycerol. Approximately 75 g of muscle proteins, i.e. nearly 300 g of muscle, per day are mobilized to provide the substrate for gluconeogenesis. If protein breakdown were to continue at the initial rate, roughly one-third of the total body proteins would be exhausted in 3 weeks, which is incompatible with survival.

So, if fasting is prolonged, a major metabolic adaptation occurs. The central nervous system begins to use ketone bodies as an energy substrate, thereby reducing glucose requirements. Therefore, in prolonged fasting, there is a shift from the use of protein as an energy source towards the use of fats (in the form of ketone bodies). This adaptation permits protein sparing and preserves the proteins' functional role. Nevertheless, obligatory proteolysis always persists, amounting in the foregoing example to at least 20 g of protein daily.
Metabolism of short-term fasting
Fig. 9: Metabolism of prolonged fasting

Metabolic processes respond to internal signals. During fasting, blood glucose levels fall with a consequent reduction in the secretion of insulin and an increase in glucagon, two hormones with antagonistic actions on energy metabolism. As a result of the decrease in the circulating insulin level, triglyceride catabolism increases, causing the release of free fatty acids and glycerol. The raised glucagon levels lead initially to a distinct increase in liver glycogenolysis. Further, gluconeogenesis is stimulated by glucagon, which inhibits protein synthesis and stimulates muscular proteolysis, thereby furnishing the amino acid substrate.

There is therefore a metabolic adaptation to prolonged fasting, resulting in a reduction of energy expenditure of up to 40% (Goldstein and Elwyn, 1989; Kinney, 1970). These mechanisms, which tend to limit proteolysis in the healthy person, are defective or non-operative in cases of severe disease or stress, as will be discussed in the next chapter.

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