With the rate of obesity among children increasing by the day, there is an urgent need to determine the root cause of the problem with the end goal of establishing viable, permanent solutions. Considering that the prevalence of childhood obesity is high in developed countries and low in poor and developing nations, obesity in children has been generally associated with lifestyle. However, recent research in the context of twins, family, and adoption has suggested that inheritance plays an important role in determining the susceptibility of individuals to become obese. Considering that dietary intake has also been proven to determine obese outcomes, it emerges that the interaction of nurture and nature causes obesity. In this discussion, the genetic contribution to obesity will be compared with environmental factors in causing obesity. The arguments presented will be based on the proposition that – while nature (primarily inherited conditions) significantly determine individuals’ susceptibility to obesity, nurture (environmental influences) play a more influential role in causing obesity among children.
Traditionally, it was difficult to determine the role of genetics in causing obesity in children. More recently, however, family, twin, and adoption studies have been used to find this association, with findings suggesting that up to 70% variation of weight between children could be linked to genetic factors (Lopomo et al. 152). In one twin study, it was observed that up to 90% of the variance in weight could be associated with genetic factors (Dubois 480). This study further suggested that the genetic influence on obesity declines with age. In a separate twin study, it was observed that, while environmental conditions were important in determining a child’s likelihood to become obese, genetics significantly determined this outcome for up to 18 years of the child’s life. This is evidence suggests that even if environmental conditions are kept constant, it is possible for some children to become obese as the result of inherited genes.
The evidence from twin studies is supported by evidence from adoption and family studies. Family studies have revealed that children born into families with obese parents or obese families are up to five times more likely to become obese than those born into families with normal-weight individuals. One such study was conducted by Claude Bouchard, who suggested that the prevalence of childhood obesity may be growing as the result of preferential mating among obese parents contributing to more obese parents, compared to normal weight parents (1501). This study falls short of determining whether obese parents’ dietary habits play a significant role in determining their children’s weight status at an early age. However, the author finds that obese parents have a higher likelihood of birthing overweight infants who are, in turn, more susceptible to becoming obese, compared to babies born with normal weight (Bouchard 1500). The idea that infants born to obese parents have a higher likelihood to become obese suggests that obesity has a genetic basis.
Studies in gene mutation have been used to determine the genetic causes of obesity. Such studies have primarily concentrated on the role of genes in controlling leptin production. Leptin, the hormone produced by fatty tissues in the body, influences body weight by stimulating the release of hormones that decrease appetite and increase the body’s energy expenditure. In turn, the individual’s food intake is controlled, thus averting obesity. In the event of mutations in the genes controlling leptin production, one possible outcome is increased appetite, decreased energy expenditure in the body, excessive food intake, and in turn, obesity. Limited studies have explored the role of genetic mutation in causing childhood obesity. Bouchard, however, established that genetic mutation accounts for up to 5% of cases of child obesity. Therefore, in the effort to resolve the crisis of childhood obesity, it is important to consider the genetic factors that could stimulate the condition.
In spite of the substantial evidence linking obesity with genetic factors, the role of nurture in promoting of obesity is still significant. Nurture, in this regard, refers to food intake, food quality, and energy expenditure. There is substantial evidence to suggest that obesity is the outcome of an imbalance of food consumed and energy expended. Mothers play a crucial role in determining their children’s dietary intake, with one study suggesting that overweight mothers are more likely to offer their children larger servings and more fatty foods. While consuming large quantities of low-fat foods may not cause obese conditions, frequent intake of large quantities of fatty foods has been associated with obesity in children (Patro‐Gołąb 1247). This evidence has also been supported by adoptive studies, which reveal that adopted children are more likely to become obese when they join families with improper dietary habits that are likely to cause obesity, regardless of the children’s genetic conditions (Kmietowicz 817). Indeed, Kmietowicz’s study boldly concludes that nurture is more important than nature as far as obesity is concerned. From these studies, it emerges that, regardless of an individual’s genetic susceptibility to obesity, the importance of proper dietary intake cannot be overlooked.
The role of the quality of food consumed in yielding obese outcomes is significant. Fatty foods are energy-dense and are more likely to be stored in the child’s body. The nature of these foods demands that parents are aware of the calories they contain as they are closely linked with obesity. Fatty foods are reported to be palatable and to provide weak satiety signals compared to carbohydrates (Cawley 937). They are also more easily accessible and one can easily form the habit of consuming fatty foods while avoiding low-fat nutritious foods such as fruits and vegetables. Obese individuals have been found to replace fruits and vegetables with soft drinks, which provide extra calories, leading to weight gain (Cawley 938). The tendency by overweight mothers to fail to keep a record of the calories consumed by their children has been found to contribute to childhood obesity. This factor is particularly significant when eating patterns lead to uneven energy distribution during the day. These findings suggest that dietary intake is of primary significance in controlling weight gain in children.
Conclusion
As this analysis reveals, obesity in children is the outcome of an interplay between nurture and nature. Nature determines children’s susceptibility to obesity as some individuals have genes that encourage the early onset of overweight conditions. Genes could also control the production of leptin, the hormone that controls a person’s appetite, thus leading to the early onset of obesity. However, nurture has an even more crucial role in yielding obesity. The frequent intake of fatty foods has been found to cause obese conditions, which explains why the children of mothers with poor dietary habits are likely to become obese. In the effort to resolve childhood obesity, it is relevant to understand the interplay between nurture and nature in promoting obesity.
Work Cited
Bouchard, Claude. “Childhood obesity: are genetic differences involved?” The American Journal of Clinical Nutrition 89.5 (2009): 1494S-1501S.
Cawley, John, et al. “Testing For Family Influences On Obesity: The Role Of Genetic Nurture.” Health Economics 28.7 (2019): 937-952.
Dubois, Lise, et al. “Genetic and environmental influences on body size in early childhood: a twin birth-cohort study.” Twin Research and Human Genetics 10.3 (2007): 479-485.
Kmietowicz, Zosia. “Nurture is More Important than Nature in Childhood Obesity, Study Finds.” BMJ 350 (2015): h817.
Lopomo, Angela, E. Burgio, and Lucia Migliore. “Epigenetics of Obesity.” Progress in Molecular Biology and Translational Science. Vol. 140. Academic Press, 2016. 151-184.
Patro‐Gołąb, Bernadeta, et al. “Nutritional Interventions or Exposures in Infants and Children Aged Up To 3 years and Their Effects on Subsequent Risk of Overweight, Obesity, and Body Fat: A Systematic Review of Systematic Reviews.” Obesity Reviews 17.12 (2016): 1245-1257.