Nature vs. Nurture:
Which Accounts for Child Obesity?
Introduction
In the United States, child obesity is a serious problem because 1 in 5 children have this issue
(Centers for Disease Control and Prevention, 2021), which is associated with serious health
complications like type 2 diabetes later in life (Childhood Obesity Foundation, 2019). In terms of
its risk factors, both nature and nurture factors have been proposed. On the nature side, endocrine
genetic diseases and genetic obesity syndromes, such as congenital leptin or leptin-receptor
deficiency, pro-opiomelanocortin (POMC) deficiency, melanocortin-4 receptor (MC4R)
deficiency, congenital growth hormone deficiency (GHD), Bardet-Biedl syndrome (BBS),
Prader-Willi syndrome (PWS), have been associated with pediatric obesity (Skelton et al., 2011).
On the nurture side, environmental factors, such as diet, activity, socioeconomic status (SES),
sleep, have been linked to child obesity as well (Skelton et al., 2011).
Nature – Endocrine Genetic Diseases and Genetic Obesity Syndromes
The 2005 Human Obesity Gene Map reveals that 253 quantitative trait loci with 127
candidate genes are correlated with obesity phenotypes (Skelton et al., 2011).
Genetic mutations in the leptin-melanocortin signalling pathway can cause obesity,
accounting for about 3% of early-onset obesity (Skelton et al,, 2011). The hormone leptin is very
important in control of body weight on a long-term basis (Skelton et al., 2011). It can reduce
energy intake by down regulating arcuate neurons in the hypothalamus that increase food intake
once activated (Skelton et al., 2011). It can also promote the release of POMC from neurons in
the arcuate nucleus, and further generates α-MSH, which sends a satiety signal in the brain, after
a series of posttranslational modifications (Hill, 2010; Huvenne,2016). Congenital leptin or
, leptin-receptor deficiency caused by the mutation of the leptin or its receptor gene leads to child
obesity (Farooqi et al., 2007). Moreover, mutations in the POMC gene can cause POMC
deficiency, a condition results in early-onset severe obesity (U.S. National Library of Medicine
[NLM], 2020a). Affected individuals experience hyperphagia and obesity due to lacking central
appetite signaling (Skelton et al., 2011). In addtion, melanocortins, including
adrenocorticotropic hormone (ACTH) and MSH peptides, which are the products of POMC
posttranslational modifications, play an important role in controlling food intake and energy
expenditure too (Hill, 2010). Mutations of MC4R causing MC4R deficiency can lead to
hyperphagia and pediatric obesity (Stutzmann et al., 2008).
Mutations in genes for factors important in pituitary gland development, for receptors and
factors along the growth hormone (GH) pathway (including GH) can lead to GHD (Boston
Children’s Hospital, n.d.). GHD alone accounts for less than 2% cases of pediatric obesity
because according to the article, all endocrinologic causes account for 2-3% cases of childhood
obesity in total (Skelton et al., 2011). This disease is characterized by insufficient production of
growth hormone in the anterior pituitary gland (National Organization for Rare Disorders
[NORD], 1990/2016). As GH can help induce insulin resistance that may occur when caloric
supply exceeds demand, decreased GH secretion can prevent insulin resistance, which is an
adaptive strategy of the body for disease prevention (Salvatori, 2015). Thus fat accumulates as a
result (Salvatori, 2015). Since GH can induce adipose tissue lipolysis, decreased GH secretion
can reduce lipolysis and fat accumulation is further boosted (Kopchick et al., 2019; Salvatori,
2015). Ultimately, obesity occurs. In children, congenital GHD leads to growth retardation, short
stature, delayed lengthening of long bones and may cause truncal obesity (NORD, 1990/2016).
Which Accounts for Child Obesity?
Introduction
In the United States, child obesity is a serious problem because 1 in 5 children have this issue
(Centers for Disease Control and Prevention, 2021), which is associated with serious health
complications like type 2 diabetes later in life (Childhood Obesity Foundation, 2019). In terms of
its risk factors, both nature and nurture factors have been proposed. On the nature side, endocrine
genetic diseases and genetic obesity syndromes, such as congenital leptin or leptin-receptor
deficiency, pro-opiomelanocortin (POMC) deficiency, melanocortin-4 receptor (MC4R)
deficiency, congenital growth hormone deficiency (GHD), Bardet-Biedl syndrome (BBS),
Prader-Willi syndrome (PWS), have been associated with pediatric obesity (Skelton et al., 2011).
On the nurture side, environmental factors, such as diet, activity, socioeconomic status (SES),
sleep, have been linked to child obesity as well (Skelton et al., 2011).
Nature – Endocrine Genetic Diseases and Genetic Obesity Syndromes
The 2005 Human Obesity Gene Map reveals that 253 quantitative trait loci with 127
candidate genes are correlated with obesity phenotypes (Skelton et al., 2011).
Genetic mutations in the leptin-melanocortin signalling pathway can cause obesity,
accounting for about 3% of early-onset obesity (Skelton et al,, 2011). The hormone leptin is very
important in control of body weight on a long-term basis (Skelton et al., 2011). It can reduce
energy intake by down regulating arcuate neurons in the hypothalamus that increase food intake
once activated (Skelton et al., 2011). It can also promote the release of POMC from neurons in
the arcuate nucleus, and further generates α-MSH, which sends a satiety signal in the brain, after
a series of posttranslational modifications (Hill, 2010; Huvenne,2016). Congenital leptin or
, leptin-receptor deficiency caused by the mutation of the leptin or its receptor gene leads to child
obesity (Farooqi et al., 2007). Moreover, mutations in the POMC gene can cause POMC
deficiency, a condition results in early-onset severe obesity (U.S. National Library of Medicine
[NLM], 2020a). Affected individuals experience hyperphagia and obesity due to lacking central
appetite signaling (Skelton et al., 2011). In addtion, melanocortins, including
adrenocorticotropic hormone (ACTH) and MSH peptides, which are the products of POMC
posttranslational modifications, play an important role in controlling food intake and energy
expenditure too (Hill, 2010). Mutations of MC4R causing MC4R deficiency can lead to
hyperphagia and pediatric obesity (Stutzmann et al., 2008).
Mutations in genes for factors important in pituitary gland development, for receptors and
factors along the growth hormone (GH) pathway (including GH) can lead to GHD (Boston
Children’s Hospital, n.d.). GHD alone accounts for less than 2% cases of pediatric obesity
because according to the article, all endocrinologic causes account for 2-3% cases of childhood
obesity in total (Skelton et al., 2011). This disease is characterized by insufficient production of
growth hormone in the anterior pituitary gland (National Organization for Rare Disorders
[NORD], 1990/2016). As GH can help induce insulin resistance that may occur when caloric
supply exceeds demand, decreased GH secretion can prevent insulin resistance, which is an
adaptive strategy of the body for disease prevention (Salvatori, 2015). Thus fat accumulates as a
result (Salvatori, 2015). Since GH can induce adipose tissue lipolysis, decreased GH secretion
can reduce lipolysis and fat accumulation is further boosted (Kopchick et al., 2019; Salvatori,
2015). Ultimately, obesity occurs. In children, congenital GHD leads to growth retardation, short
stature, delayed lengthening of long bones and may cause truncal obesity (NORD, 1990/2016).
