Malnutrition and starvation

Malnutrition is a condition that happens due to sub-optimal intake of the necessary nutrients. Even malnutrition can attack those animals that intake surmountable amount of food, but they are incapable to ingest, digest, absorb or utilize the food. Therefore, malnutrition arises prior to starvation, i.e. long-term deprival of food and its unpleasant effects (Boullatta & Armenti 2010). Causes for malnutrition are parasitism, presence of antibodies in the digestive tract, injuries, disease, poor teeth, and amplified motility of the digestive tract or tumor.

Some symptoms of malnutrition and starvation include:

Bones of the rib, hip, shoulder, and back-bone starts to protrude.

Eyes become drowned, and abdomen appears as if stuck-up.

Little or poor quality food maybe traced in the alimentary canal.

Fatty tissues are absent around the kidney, heart, in the bone marrow, under the skin, and other organs.

Organs and muscle mass may well decrease in size (Malnutrition- what to look for).

Metabolic adaption expresses the change in the nature of a biological system in reaction to alteration, in external or internal environment. Starvation can induce several behavioral and psychological alterations in the human body. For instance, take the case of Boitel, who starved for 53 days before dying. However, before he died he had to undergo several metabolic adaptations due to starvation as discussed below.

Early Stages of starvation

At the beginning, his body became endogenous i.e. utilized stored calories to manufacture energy for essential functions. At first, glucose was the primary energy substrate for the CNS, leading to metabolism of 100 to 150g/day absolutely in to water and carbon (iv) oxide. As he went on with starvation, glucose continued to be unavailable, leading to rapid change in neuronal activity, marked by personality alteration, coma, lethargy and confusion (Shils 2005 pp. 741-742).

His system recycled lactase in Cori cycle in the liver and kidney, back to glucose. The process used energy obtained from oxidation of fatty acids. Pyruvate may be used as a substrate for gluconeogenesis in the liver, or underwent oxidation to form ATP. Phagocytes and fibroblasts obtain their energy from anaerobic metabolism of glucose to lactate (Freeman, 2002). The oxidation of free fatty acids to acetoacetate, ketone and acetone was to suppliy energy to the liver, heart, renal cortex, and skeletal muscle. The branched-chain amino acid was also oxidized in the skeletal muscle to provide energy. In addition to this, gastrointestinal tract oxidized glutamine to water and carbon (iv) oxide (Payne, Grimble & A Silk 2001pp. 3-4).

His body depended on gluconeogenesis to stabilize glucose requirements. This was due to little preservation of glucose in extracellular glucose and liver glycogen. Also, the inability to convert muscle glycogen to blood glucose was due to the absence of glucose-6-phosphate in muscle contributed to dependency on gluconeogenesis (Metabolic effects of starvation).

His kidneys supplied approximately a half of the total glucose manufactured as the starvation continued. During his early starvation, gluconeogenesis took place majorly in the liver with alanine as the substrate. Production of pyruvate in the muscle was through anaerobic metabolism of glucose. The nitrogen moiety was conveyed to pyruvate to produce alanine that was discharged in to blood. In the muscle, the branch-chain amino acid carbon skeleton was totally oxidized to water, and carbon (iv) oxide to supply extra ATP for the body usage (Payne, Grimble, & A Silk 2001).

The alanine was later absorbed by the liver, where nitrogen was split-off. The consequential pyruvate was reprocessed to glucose through gluconeogenesis. Not all nitrogen is excreted in the urine as urea, but also some are reused in protein synthesis. Glutamine form the principal substrate for gluconeogenesis in the kidney, and numerous amino acids are changed in to glutamine through transamination. Ammonia, which is a crucial nitrogenous by-product, is partially reutilized in protein synthesis and partially discharged in urine (Peitzman et al 2007 pp. 469-470).

Late stages of Starvation

As his body mass fell metabolism decreased to preserve resources and energy. The consequences were increased sleep, lessening muscle activity and reduced interior temperature. Furthermore, the requirement for gluconeogenesis decreases due to conversion of the central nervous system (CNS) to use ketone bodies for energy other than glucose. The stimulus for this adaptation was partly attributed to increase in ketone body or serum alanine concentration or by reduction in serum molar ratio of insulin to glucagon. Consequently, there was a drop of 75 to 20g/day in protein catabolism, followed drop of 3 to 5g/day in urea nitrogen excretion (Metabolic effects of starvation).

As he continued with starvation, about 5% of the total daily calories were produced by the protein catabolism. With a reduction in gluconeogenesis, adipose became significant energy substrate with metabolism of fat, conversion of free fatty acids to ketone bodies, and metabolism of ketone bodies by peripheral tissues producing approximately 60%, 10% and 25% of total daily calories spending (Metabolic effects of starvation). Rise in fat metabolism stimulated an increase in serum ketone body concentration, which finally surpasses the renal threshold. The physiological reaction towards prolong starvation is characterized by the availability of ketone bodies in urine. It is in this modification state that enable him survive for 53 days before he died (metabolic effects of starvation).

Conclusion

About 160g of adipose tissue and 75g of the body are metabolizing daily for every 1800kcal used during early stages of starvation. Every endogenous protein is used-up, even those with crucial tasks in metabolism, like digestive enzymes and organ and plasma proteins (Metabolic effects of starvation). Clinical evidence indicates that a majority of protein loss is traced from skeletal muscles. Lipolysis produces glycerol and free fatty acids, and it rose as concentration of serum insulin dropped with an increase in starvation. Although, free fatty acids were crucial energy source in the liver for Cori cycle, they were not directly involved in gluconeogenesis. The Cori cycle facilitated the transformation of pyruvate to oxaloacetate. Finally, to survive a prolonged starvation, depends one’s body preservation, the age and the ruthlessness of the Caloric deficit (Peitzman et al 2007 pp. 469-470). Studies indicate that nitrogen-sparing is effective when used with water solutions or glucose-free salt, permitting complete adaptation to starvation.

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