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Omar Abdulrahim
order_4948638.docxRunning head: METABOLIC DISEASE RISK 1
METABOLIC DISEASE RISK 8
Metabolic Disease Risk in Children
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Metabolic Disease Risk in Children
Summary
The metabolic process allows the breakdown of foods into small compounds. It is essential to note that disorder in the normal metabolism of the body normally leads to metabolic disease. Moreover, disruptions or abnormalities in the biochemical reactions lead to metabolism errors; hence, it is important to determine the exact cause of metabolic disease. Most people construe that hereditary factors cause metabolic disease in children alone, but the fact is wrong since other factors such as obesity and insulin resistance also cause the disease. The metabolic disease is usually inherited as an autosomal condition, which means that two copies of defective genes from both parents must exist for the disease to develop. Hoffmann (2002) contends that there is always a 25 percent chance that will inherit two defective gene copies from the carrier parents. It is also important to note that the hereditary argument is inconclusive since studies have shown that other factors such as mitochondrial overload, insulin resistance, and accumulation of fats also lead to a metabolic disorder. Insulin resistance leads to metabolic disease because the human body responds to physiological insulin level through the reduction of glucose uptake. The primary target of insulin action is the liver because it plays a major role when it comes to substrate metabolism. On the other hand, global concern about the increase in metabolic dysregulation among children has increased lately especially after some studies illustrated that there exists a positive correlation between metabolic disease and obesity. A recent survey has revealed that pediatric obesity is the leading risk factor for metabolic disease contrary to earlier assertions that the metabolic disease is purely hereditary. Obese children have a high chance of developing the metabolic disease as compared to other children.
Introduction
Metabolism is a very important process in the human body because the biochemical reactions and interconversions are what produce energy and other important compounds for the body. For the body to take up food, the food must be broken down into simple compounds through the metabolic process. Therefore, a disruption in the normal metabolism of the body is what normally leads to metabolic disease. According to Chen, Srinivasan, and Berenson (2008), enzymes play a critical role in the metabolic process because they speed up the biochemical reactions taking place at the cellular level. Any abnormality or disruption in the biochemical reactions and interconversions leads to metabolism errors. Enzymes normally control the rate of chemical reactions and therefore, any defects in the enzyme structure can affect the metabolic process (Twitter, 2016). Thus, although metabolic disease in children is to some extent caused by hereditary factors, the argument that the disease is purely hereditary is not true.
Background of Issue
There has been an increasing global concern about the increase in metabolic dysregulation among children, and this is largely caused by the prevalence of pediatric obesity (Symplur, 2016). In addition to that, different scholars continue to argue whether the metabolic disease is only caused by genetic mutations or can also be caused by other risk factors. A recent survey has revealed that pediatric obesity is the leading risk factor for metabolic disease, and this is contrary to assertions that the metabolic disease is purely hereditary. Obese children have a high chance of developing the metabolic disease as compared to children that are not obese (Symplur, 2016). A recent survey also indicates that obese children are also associated with cardiovascular risk factors associated with metabolic diseases such as abdominal obesity, glucose metabolism, and hypertension. The racial and pubertal differences among children make it difficult to define the metabolic disease (Twitter, 2016). Enzyme deficiency can lead to the production of toxic products, the build-up of toxic intermediate and a reduction of essential products in the body.
Counter-claim 1
The metabolic disease is normally inherited as an autosomal condition. For the disease to develop there must be two copies of defective genes from both parents (Hoffmann, 2002). Thus, the condition occurs as a kind of inheritance pattern. It is not necessary for parents to have the disease for the child to develop the disease but they are categorized as carries as long as each has one defective gene copy. According to Hoffmann (2002), there is always a 25 percent chance that will inherit two defective gene copies from the carrier parents. The disease cannot develop when there is only one copy of a defective gene. One working copy can maintain sufficient levels of the enzyme because of the recessive nature of the metabolic disease.
Response
The hereditary argument makes some sense, but it is not a good idea to confine the disease to hereditary factors because research has shown that other factors such as mitochondrial overload, insulin resistance, and accumulation of fats can also lead to a metabolic disorder (Weiss, Bremer, & Lustig, 2013). As such, the hereditary argument is not conclusive; thus, should not be taken as scientific fact.
Counter-claim 2
Genetic mutations lead to enzyme defects through binding of cofactors, creation of problems with transportation apart from affecting enzyme structure and regulation (Clarke, 2005). The metabolic disease is always inherited, and the condition is known to cause enzyme deficiency.
Response
It is a fact that genetic mutations can lead to enzyme errors, but this does not necessary means that it is the only cause of such errors. Other factors such as mitochondrial overload as well as insulin resistance can lead to enzyme errors that can disrupt the metabolic process. It is also important to point out that hereditary factors do not cause dysfunctional cellular, and yet it can lead to the disruption of the normal functioning of enzymes (Weiss et al., 2013). There are many instances where parents may not have the defective gene copies and yet their children end up developing the metabolic disease. Moreover, obesity is among the leading risk factors for metabolic disease, and yet it is just a lifestyle condition. Enzyme deficiency may be caused by other factors apart from mutations.
Unique point 1
Most studies and diagnosis have shown that obesity is a major cause of metabolic disease in children. Although the disease can also occur among lean children, it is important to point out that obesity is a serious marker for the cardiovascular disease. The various elements of the metabolic disease can be caused by dysfunctional subcellular energy and mitochondrial overload that result from lipid partitioning of specific fat deposits. Mitochondrial overload is normally caused by various factors such as the propensity of food intake, an increase in insulin resistance, as well as sleep and stress deprivation (Weiss et al., 2013). It is this mitochondrial that eventually leads to early atherogenesis during childhood as well as altered glucose metabolism. This type of overload also causes the adverse biochemical phenotype. Obesity leads to a higher level of risk factors for metabolic disease among children as a compared to other major causes (Weiss et al., 2013). It is essential to note that obesity is a major cause of metabolic disease; hence, the diagnosis should remain cognizant of obesity’s implications.
Unique point 2
Insulin resistance is another leading cause of metabolic disease because the human body responds to physiological insulin level through the reduction of glucose uptake. Insulin driven metabolic pathways are affected by the body response to insulin levels (Weiss et al., 2013). There are up to three categories of insulin resistance that can lead to and these include hepatic insulin resistance, muscle insulin resistance as well as adipose tissue insulin resistance. The primary target of insulin action is the liver because it plays a major role when it comes to substrate metabolism. Moreover, increased plasma FFA levels, as well as the downstream of an insulin resistant liver, disrupt the skeletal muscle uptake of insulin-mediated glucose. In addition to that, the lipolysis process is also accelerated by the insulin resistant state and in the process increasing the release of FFA into circulation.
Conclusion
References
Chen, W., Srinivasan, S. R., & Berenson, G. S. (2008). Path analysis of metabolic syndrome components in black versus white children, adolescents, and adults: the Bogalusa Heart Study. Annals of epidemiology,18(2), 85-91.
Clarke, J. (2005). A clinical guide to inherited metabolic diseases. Cambridge: Cambridge University Press. 60
Hoffmann, G. (2002). Inherited metabolic diseases. New York: Lippincott Williams & Wilkins. 209-215
Sympler. (2016). #ChildhoodObesity ? Retrieved 18, May 2015 from http://www.symplur.com/healthcare-hashtags/childhoodobesity/.
Twitter. (2016). #metabolic disorders. Retrieved 18, May 2015 from https://twitter.com/hashtag/metabolic. 2016
Weiss, R., Bremer, A. A., & Lustig, R. H. (2013). What is metabolic syndrome, and why are children getting it?. Annals of the New York Academy of Sciences, 1281(1), 123-140.
