MetabolicDisease Risk in Children
MetabolicDisease Risk in Children
Themetabolic process allows the breakdown of foods into small compounds.It is essential to note that disorder in the normal metabolism of thebody normally leads to metabolic disease. Disruptions orabnormalities in the biochemical reactions lead to metabolism errorshence, it is important to determine the exact cause of metabolicdisease. Most people construe that hereditary factors cause metabolicdisease in children alone, but the fact is wrong since obesity andinsulin resistance also cause the disease. The metabolic disease isusually inherited as an autosomal condition, which means that twocopies of defective genes from both parents must exist for thedisease to develop. Hoffmann (2002) contends that there is always a25 percent chance that will inherit two defective gene copies fromthe carrier parents. It is also important to note that the hereditaryargument is inconclusive since studies have shown that other factorssuch as mitochondrial overload, insulin resistance, and accumulationof fats also lead to a metabolic disorder. Insulin resistance leadsto metabolic disease because the human body responds to physiologicalinsulin level through the reduction of glucose uptake. The primarytarget of insulin action is the liver because it plays a major rolewhen it comes to substrate metabolism. On the other hand, globalconcerns about the increase in metabolic dysregulation among childrenhave increased lately especially after some studies illustrated thatthere exist a positive correlation between metabolic disease andobesity. A recent survey has revealed that pediatric obesity is theleading risk factor for metabolic disease contrary to earlierassertions that the metabolic disease is purely hereditary. Obesechildren have a high chance of developing the metabolic disease ascompared to other children.
Metabolismis a very important process in the human body because the biochemicalreactions and interconversions produce energy and other importantcompounds for the body. For the body to take up food, the food mustbe broken down into simple compounds through the metabolic process.Therefore, a disruption in the normal metabolism of the body is whatnormally leads to metabolic disease. According toChen, Srinivasan, and Berenson (2008), enzymesplay a critical role in the metabolic process because they speed upthe biochemical reactions taking place at the cellular level. Anyabnormality or disruption in the biochemical reactions andinterconversions leads to metabolism errors. Enzymes normally controlthe rate of chemical reactions and therefore, any defects in theenzyme structure can affect the metabolic process(Twitter, 2016).Thus, although metabolic disease in children is to some extent causedby hereditary factors, the argument that the disease is purelyhereditary is not true.
Therehas been an increasing global concern about the increase in metabolicdysregulation among children, and this is largely caused by theprevalence of pediatric obesity (Symplur, 2016). In addition,different scholars continue to argue whether the metabolic disease isonly caused by genetic mutations or can also be caused by other riskfactors. Obese children have a high chance of developing themetabolic disease as compared to children that are not obese(Symplur, 2016). A recent survey also indicates that obese childrenare also associated with cardiovascular risk factors associated withmetabolic diseases such as abdominal obesity, glucose metabolism, andhypertension. The racial and pubertal differences among children makeit difficult to define the metabolic disease (Twitter,2016).Enzyme deficiency can lead to the production of toxic products, thebuild-up of toxic intermediate and a reduction of essential productsin the body.
Themetabolic disease is normally inherited as an autosomal condition.For the disease to develop there must be two copies of defectivegenes 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 todevelop the disease but they are categorized as carries as long aseach has one defective gene copy. According to Hoffmann (2002), thereis always a 25 percent chance that will inherit two defective genecopies from the carrier parents. The disease cannot develop whenthere is only one copy of a defective gene. One working copy canmaintain sufficient levels of the enzyme because of the recessivenature of the metabolic disease.
Thehereditary argument makes some sense, but it is not a good idea toconfine the disease to hereditary factors because research has shownthat other factors such as mitochondrial overload, insulinresistance, and accumulation of fats can also lead to a metabolicdisorder (Weiss, Bremer, & Lustig, 2013). As such, the hereditaryargument is not conclusive thus, should not be taken as scientificfact.
Geneticmutations lead to enzyme defects through binding of cofactors,creation of problems with transportation apart from affecting enzymestructure and regulation(Clarke,2005). The metabolic disease is always inherited, and the conditionis known to cause enzyme deficiency.
Itis a fact that genetic mutations can lead to enzyme errors, but thisdoes not necessary means that it is the only cause of such errors.Other factors such as mitochondrial overload as well as insulinresistance can lead to enzyme errors that can disrupt the metabolicprocess. It is also important to point out that hereditary factors donot cause dysfunctional cellular, and yet it can lead to thedisruption of the normal functioning of enzymes (Weiss et al., 2013).There are many instances where parents may not have the defectivegene copies and yet their children end up developing the metabolicdisease. Moreover, obesity is among the leading risk factors formetabolic disease, and yet it is just a lifestyle condition. Enzymedeficiency may be caused by other factors apart from mutations.
Moststudies and diagnosis have shown that obesity is a major cause ofmetabolic disease in children. Although the disease can also occuramong lean children, it is important to point out that obesity is aserious marker for the cardiovascular disease. The various elementsof the metabolic disease can be caused by dysfunctional subcellularenergy and mitochondrial overload that result from lipid partitioningof specific fat deposits. Mitochondrial overload is normally causedby various factors such as the propensity of food intake, an increasein insulin resistance, as well as sleep and stress deprivation (Weisset al., 2013). It is this mitochondrial that eventually leads toearly atherogenesis during childhood as well as altered glucosemetabolism. This type of overload also causes the adverse biochemicalphenotype. Obesity leads to a higher level of risk factors formetabolic disease among children as a compared to other major causes(Weiss et al., 2013). It is essential to note that obesity is a majorcause of metabolic disease hence, the diagnosis should remaincognizant of obesity’s implications.
Insulinresistance is another leading cause of metabolic disease because thehuman body responds to physiological insulin level through thereduction of glucose uptake. Insulin driven metabolic pathways areaffected by the body response to insulin levels (Weiss et al., 2013). There are up to three categories of insulin resistance that can leadto and these include hepatic insulin resistance, muscle insulinresistance as well as adipose tissue insulin resistance. The primarytarget of insulin action is the liver because it plays a major rolewhen it comes to substrate metabolism. Moreover, increased plasma FFAlevels, as well as the downstream of an insulin resistant liver,disrupt the skeletal muscle uptake of insulin-mediated glucose. Inaddition to that, the lipolysis process is also accelerated by theinsulin resistant state and in the process increasing the release ofFFA into circulation.
Thisarticle has discussed metabolic risk factors from all sides with themain issue being the argument that the metabolic disease is purelyhereditary. However, research findings have revealed that metabolicdisease is not purely a hereditary condition but can be caused byother non-hereditary factors such as obesity, insulin resistance, andmitochondrial overload. The fact that here are varieties of riskfactors for metabolic disease among children means that itsdefinition cannot be limited to genetics. Obese children are normallyat a high risk of developing the metabolic disease as compared tochildren with normal weight. It is therefore very difficult to comeup with a definite conclusion on the cause of metabolic disease amongchildren because the disease is known to manifest itself in differentforms.
Chen,W., Srinivasan, S. R., & Berenson, G. S. (2008). Path analysis ofmetabolic syndrome components in black versus white children,adolescents, and adults: the Bogalusa Heart Study. Annalsof epidemiology,18(2),85-91.
Clarke,J. (2005). Aclinical guide to inherited metabolic diseases.Cambridge: Cambridge University Press. 60Hoffmann,G. (2002). Inheritedmetabolic diseases.New York: Lippincott Williams & Wilkins. 209-215
Sympler.(2016). #ChildhoodObesity? Retrieved 18, May 2015 fromhttp://www.symplur.com/healthcare-hashtags/childhoodobesity/.
Twitter.(2016). #metabolicdisorders.Retrieved 18, May 2015 from https://twitter.com/hashtag/metabolic.2016
Weiss,R., Bremer, A. A., & Lustig, R. H. (2013). What is metabolicsyndrome, and why are children getting it?. Annalsof the New York Academy of Sciences, 1281(1),123-140.