Natal Factors Causing Childhood Obesity


Childhood Obesity

Infant or childhood obesity is a growing problem across the world today. The prevalence, causes, risks, prevention, diagnosis, treatment, and psychology of childhood obesity is a hot topic in research (Phyllis,2004).The  gestational and infancy factors that influence the risk of overweight in childhood obesity include maternal lifestyle ,  infant feeding transitions, and  environmental factors. (Julia, 2007).Further, birth weight and parental obesity also play a role in childhood obesity.Thus, childhood obesity seems to be influenced by intrauterinelife, postnatal life, feeding, childhood and genetic factors. Obese children are at risk of being overweight throughout their adulthood. They are more prone to health problems like sleep apnea, asthma, fatty liver disease, type II diabetes , cardiovascular complications, early and delayed puberty (Srinivasan,1996). Obese children have been found to have a lower self-esteem and academic achievement (Freedman, 2002).

Maternal Life style:

A recent cohort study has revealed that maternal smoking during pregnancy causes childhood obesity (Rüdiger, 2002). Obesity defined by a body mass index was observed in a dose-dependent association. Maternal smoking and alcohol consumption seem to induce mutations that cause childhood obesity. A recent research work has already implicated smoking in pregnancy in mutagenic effects on the fetus (DeMarini DM, 2005). Abby C. Collier (2002) have also proved that the metabolism of human placenta in the first trimester may be affected by maternal intake of alcohol altering the constitutive enzyme system of the placenta. Thus, maternal life style is a definite causative factor in childhood obesity.

Feeding Transitions:

Low protein intake during gestation often results in low birth weight and subsequently leads to various metabolic disturbances (Cornelia, 2001). Studies in developed countries suggest that breastfeeding has a protective effect against childhood obesity (Reynaldo et al, 2001). Children seem to have a functional preference to sweet intake because breast milk is predominantly sweet in taste. Thus, natal feeding has a strong influence on the feeding preferences of the child. But, unfortunately highly sweetened foods and beverages available today have a higher Dietary Energy Density (DED). High Dietary Energy Density seems to have strong correlations with childhood obesity(Jason et al, 2006). Thus, infant feeding practices, the transition between breastfeeding and formula feeding are important factors that influences childhood obesity. The modern day weight trends in children of course show that energy intake and expenditure are often out of balance. It has been reported that an excess 65 KJ per day can result in 8 lb weight gain in 8 years.  

Environmental Factors:

Excessive watching of television greatly reduces physical activity in children causing an energy imbalance leading to wait gain. Computer games have substituted other outdoor games resulting in reduced physical activity. Further use of strollers by parents has greatly reduced the child’s walking activity. Environmental factors acting on human beings over a period definitely lead to inherited changes in phenotype in descendant generations. Ecological pollution is one of the vital factors causing genomic changes or mutation, which is being carried through the generations. Thus, it is important to understand and study the role of this environmental factor in altering this genomic structure of an individual to actually see if it contributes to obesity. A recent study of 265 pairs of nonsmoking African-American and Latina mothers and newborns in New York City at the time of delivery have shown that mothers and newborns had the same level of DNA damage from pollutants. It is possible to measure the level of DNA damage from air pollutants in mothers and newborns by analyzing stretches of mutated DNA, called biomarkers that have been associated with exposure to diesel emissions and other air pollutants. (Pereira, et al., 2004). Further, childhood obesity seems to be associated with heterozygous coding mutations in the melanocortin 4 receptor. Cecile lubrano (2003), have demonstrated that over 54% of the obesity-associated MC4R mutations impair the membrane expression of MC4R resulting in a decrease in MC4R activity causing childhood obesity. Foetal amniotic cells have been marked as potential sites of expression of nicotine induced mutations (Rosa Ana de la Chica, 2005). Thomas (2006), have reported higher rates of overweight and obesity in children with Congenital Adrenal hyperplasia (CAH.). A high serum leptin levels have been reported in patients with CAH and seems to be involved in the development of obesity in CAH patients. The study has substantiated that children with CAH have a higher risk of obesity as evidenced by an elevated BMI SDS values.


Current data suggest that 20% of US children are overweight and show a clear upward trend in body weight in children of 0.2 kg/year since 1973 (Michael, 2001). Maternal education on life style, feeding, diet transition, activity and various other preventive measures will contribute towards reduction in child obesity.


  • Cecile Lubrano-Berthelier (2003). Molecular Genetics of Human Obesity-Associated MC4R Mutations. Annals of the New YorkAcademy of Sciences 994:49-57.

  • Cornelia C. Metges (2001). Does Dietary Protein in Early Life Affect the Development of Adiposity in Mammals? Journal of Nutrition.131: 2062-2066.

  • Douglas Willms (2004). Early childhood obesity: a call for early surveillance and preventive measures. CMAJ; 171 (3).

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  • Rüdiger Von Kries, André Michael Toschke, Berthold
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  • Sally Ann Lederman,, Sharon R. Akabas, and Barbara J. Moore.(2004). Editors’ Overview of the Conference on Preventing Childhood Obesity. PEDIATRICS  114 (4); 1139-1145.

  • Srinivasan SR, Bao W, Wattigney WA, Bereson GS(1996). Adolescent overweight is associated with adult overweight and related multiple cardiovascular risk factors: the Bogalusa Heart Study. Metabolism 45:235-40.

  • Thomas M. K. Völkl, Diemud Simm, Christoph Beier and Helmuth G. Dörr (2006). Obesity Among Children and Adolescents With Classic Congenital Adrenal Hyperplasia Due to 21-Hydroxylase Deficiency. PEDIATRICS 117(1), 98-105.
  • Copyright 2007- American Society of Registered Nurses (ASRN.ORG)-All Rights Reserved


Articles in this issue:


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    Stan Kenyon
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