Pediatric Annals

CME Article 

Epidemiology of Pediatric Obesity

Michael Rosenbaum, MD

  • Pediatric Annals. 2007;36(2)
  • Posted February 1, 2007

Abstract

The ability to store calories as fat would have helped our ancestors to survive periods of prolonged caloric restriction, and would have enhanced the ability of women to breast feed their offspring and provide greater energy stores to nourish mother and fetus during pregnancy. Thus, it is likely that the human genome is enriched with genes favoring the storage of calories as adipose tissue. In contrast, there would have been little evolutionary pressure to favor genotypes that are defending body thinness prior to the industrial revolution. Our ancestors rarely had the opportunity to consume calories to the point that they experienced significant adiposity-related morbidity, nor did they frequently survive to an age when the cumulative effects of morbidities, such as diabetes and cardiovascular disease, would have a significant effect on their health or reproductive capacity. In an environment that favors the consumption of calorically dense foods and a sedentary lifestyle, any “defense” against further weight gain is stretched to the limit, while opposition to sustaining weight loss remains potent and viable. Thus, we are confronted with a tendency for our own metabolic systems to be “biased” toward further weight gain and biased against attempts to sustain weight loss.

ABOUT THE AUTHOR

Michael Rosenbaum, MD, is with New York Presbyterian Hospital, Columbia University College of Physicians and Surgeons, New York, NY.

Address correspondence to: Michael Rosenbaum, MD, Russ Berrie Medical Science Pavilion, Sixth Floor, 1150 St. Nicholas Avenue, New York, NY 10032; or email: mr475@columbia.edu.

Dr. Rosenbaum disclosed no relevant financial interest.

EDUCATIONAL OBJECTIVES

  1. Develop an understanding of the changing demographics of pediatric obesity.
  2. Demonstrate an understanding of these changing demographics as the product of genetic and environmental interactions.
  3. Develop an understanding of pediatric obesity as a risk factor for adult obesity and its comorbidities.

Abstract

The ability to store calories as fat would have helped our ancestors to survive periods of prolonged caloric restriction, and would have enhanced the ability of women to breast feed their offspring and provide greater energy stores to nourish mother and fetus during pregnancy. Thus, it is likely that the human genome is enriched with genes favoring the storage of calories as adipose tissue. In contrast, there would have been little evolutionary pressure to favor genotypes that are defending body thinness prior to the industrial revolution. Our ancestors rarely had the opportunity to consume calories to the point that they experienced significant adiposity-related morbidity, nor did they frequently survive to an age when the cumulative effects of morbidities, such as diabetes and cardiovascular disease, would have a significant effect on their health or reproductive capacity. In an environment that favors the consumption of calorically dense foods and a sedentary lifestyle, any “defense” against further weight gain is stretched to the limit, while opposition to sustaining weight loss remains potent and viable. Thus, we are confronted with a tendency for our own metabolic systems to be “biased” toward further weight gain and biased against attempts to sustain weight loss.

ABOUT THE AUTHOR

Michael Rosenbaum, MD, is with New York Presbyterian Hospital, Columbia University College of Physicians and Surgeons, New York, NY.

Address correspondence to: Michael Rosenbaum, MD, Russ Berrie Medical Science Pavilion, Sixth Floor, 1150 St. Nicholas Avenue, New York, NY 10032; or email: mr475@columbia.edu.

Dr. Rosenbaum disclosed no relevant financial interest.

EDUCATIONAL OBJECTIVES

  1. Develop an understanding of the changing demographics of pediatric obesity.
  2. Demonstrate an understanding of these changing demographics as the product of genetic and environmental interactions.
  3. Develop an understanding of pediatric obesity as a risk factor for adult obesity and its comorbidities.

The ability to store calories as fat would have helped our ancestors to survive periods of prolonged caloric restriction, and would have enhanced the ability of women to breast feed their offspring and provide greater energy stores to nourish mother and fetus during pregnancy. Thus, it is likely that the human genome is enriched with genes favoring the storage of calories as adipose tissue. In contrast, there would have been little evolutionary pressure to favor genotypes that are defending body thinness prior to the industrial revolution. Our ancestors rarely had the opportunity to consume calories to the point that they experienced significant adiposity-related morbidity, nor did they frequently survive to an age when the cumulative effects of morbidities, such as diabetes and cardiovascular disease, would have a significant effect on their health or reproductive capacity. In an environment that favors the consumption of calorically dense foods and a sedentary lifestyle, any “defense” against further weight gain is stretched to the limit, while opposition to sustaining weight loss remains potent and viable. Thus, we are confronted with a tendency for our own metabolic systems to be “biased” toward further weight gain and biased against attempts to sustain weight loss.

ABOUT THE AUTHOR

Michael Rosenbaum, MD, is with New York Presbyterian Hospital, Columbia University College of Physicians and Surgeons, New York, NY.

Address correspondence to: Michael Rosenbaum, MD, Russ Berrie Medical Science Pavilion, Sixth Floor, 1150 St. Nicholas Avenue, New York, NY 10032; or email: mr475@columbia.edu.

Dr. Rosenbaum disclosed no relevant financial interest.

EDUCATIONAL OBJECTIVES

  1. Develop an understanding of the changing demographics of pediatric obesity.
  2. Demonstrate an understanding of these changing demographics as the product of genetic and environmental interactions.
  3. Develop an understanding of pediatric obesity as a risk factor for adult obesity and its comorbidities.

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