| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Center for Human Nutrition, University of Colorado School of Medicine, Denver, CO 80262
* To whom correspondence should be addressed. E-mail: James.hill{at}uchsc.edu.
The intent of this paper is to address the obesity epidemic which is a term used to describe the sudden and rapid increase in obesity rates that began in the 1980s and continue unabated today. Since 1980, the entire population, regardless of starting weight, is gradually gaining weight. This has led to escalating obesity rates and to obesity being considered one of the most serious public health challenges facing the world. At one level, the obesity epidemic is a classic gene-environment interaction where the human genotype is susceptible to environmental influences that affect energy intake and energy expenditure. It is also a problem of energy balance. Understanding the etiology of obesity requires the study of how behavioral and environmental factors have interacted to produce positive energy balance and weight gain. Reversing the epidemic of obesity will require modifying some combination of these factors to help the population achieve energy balance at a healthy body weight. While body weight is strongly influenced by biological and behavioral factors, it has been changes in the environment promoting positive energy balance that is most responsible for the obesity epidemic. Our best strategy for reversing the obesity epidemic is to focus on preventing positive energy balance in the population through small changes in diet and physical activity that take advantage of our biological systems for regulating energy balance. Simultaneously we must address the environment to make it easier to make better food and physical activity choices. This is a very long-term strategy for first stopping and then reversing the escalating obesity rates, but one than can, over time, return obesity rates to pre 1980 s levels.
This article has been cited by other articles:
![]() |
R. Stienstra, C. Duval, S. Keshtkar, J. van der Laak, S. Kersten, and M. Muller Peroxisome Proliferator-activated Receptor {gamma} Activation Promotes Infiltration of Alternatively Activated Macrophages into Adipose Tissue J. Biol. Chem., August 15, 2008; 283(33): 22620 - 22627. [Abstract] [Full Text] [PDF] |
||||
![]() |
I. Murano, G. Barbatelli, V. Parisani, C. Latini, G. Muzzonigro, M. Castellucci, and S. Cinti Dead adipocytes, detected as crown-like structures, are prevalent in visceral fat depots of genetically obese mice J. Lipid Res., July 1, 2008; 49(7): 1562 - 1568. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. L. Mark Dietary Therapy for Obesity: An Emperor With No Clothes Hypertension, June 1, 2008; 51(6): 1426 - 1434. [Full Text] [PDF] |
||||
![]() |
D. L. Eizirik, A. K. Cardozo, and M. Cnop The Role for Endoplasmic Reticulum Stress in Diabetes Mellitus Endocr. Rev., February 1, 2008; 29(1): 42 - 61. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Siervo, G. Fruhbeck, A. Dixon, G. R. Goldberg, W. A. Coward, P. R. Murgatroyd, A. M. Prentice, and S. A. Jebb Efficiency of autoregulatory homeostatic responses to imposed caloric excess in lean men Am J Physiol Endocrinol Metab, February 1, 2008; 294(2): E416 - E424. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |