To Stop Obesity, Start with Toddlers
By
Aimee Angle-Zahn, Susanna Cunningham-Rundles, PhD,
and Marcus M. Reidenberg, MD, FACP
We know that being overweight or obese increases the likelihood of developing many illnesses that cause early disability and death. High blood pressure, diabetes, and coronary heart disease are among the common illnesses occurring more frequently in the overweight. According to the CDC, in 2010 69% of American adults over age 19 were overweight and 36 % of them were so overweight as to be classified as obese (1). The NIH gives the level of overweight that counts as obese. One can determine one’s own level of overweight or obesity at: http://www.nhlbi.nih.gov/guidelines/obesity/BMI/bmicalc.htm
Data from 1976 showed that overweight and obesity often starts in infancy (2). Jules Hirsch did some studies on fat cells and developed the idea that an obese individual has an excess of fat cells in the body, not just more fat in the normal number of fat cells (3). He found in animal experiments that increased feeding in infancy led to more fat cells in the body than normal feeding. This increased number of fat cells starting in infancy caused an increased amount of body fat in adult rats (4). West et al. found similar results from experimental overfeeding (5). Hirsch and others also found that markedly obese people had increased numbers of fat cells in their body (6). Spalding et al have recently shown that obese persons maintain a greater number of fat cells than lean ones even after major weight loss due to bariatric surgery. A person’s number of fat cells is likely set during childhood or adolescence (7).
‘Obese’ fat cells secrete substances different from normal fat cells. Some of these substances cause inflammation. Fat cells from obese patients, who lost weight after gastric bypass surgery, lost this abnormal substance secretion (8).
Additional recent studies add to our knowledge of the problem. Adult patients who had fat and fat cells removed from under the skin of their thighs by liposuction regained the weight lost by the end of a year. The new fat had grown in their abdomens, not from where it was removed. New fat cells replaced the ones removed (9). Thus, we seem to adapt to being overweight and restore the earlier weight with new fat cells even when the fat was removed surgically. Another study showing that 27% of kindergarten children are overweight or obese also revealed that these children were much more likely to be obese later on than children who were normal weight in kindergarten (10) Dieting causes loss of weight including fat from the fat cells but not loss of fat cells. These fat cells get abnormally smaller. They are sitting there in the body ready to suck up calories to regain their normal size (and regain the lost weight). In addition, significant weight gain can increase in the number of fat cells in the body (11).
These are reasons why it is so hard to lose weight and even harder to keep it off. To stop obesity, we must prevent it in toddlers and young children.
References:
1. CDC: Selected health conditions and risk factors: United States, selected years 1988–1994 through 2009–2010. http://www.cdc.gov/nchs/data/hus/2012/063.pdf
2. Charney E, Goodman HC, McBride M, Lyon B, Pratt R. Childhood antecedents of adult obesity. Do chubby infants become obese adults? The New England journal of medicine. 1976 Jul 1;295(1):6-9. PubMed PMID: 1272299.
3. Hirsch J. Editorial: The adipose-cell hypothesis. The New England journal of medicine. 1976 Aug 12;295(7):389-90. PubMed PMID: 934228.
4. Knittle JL, Hirsch J. Effect of early nutrition on the development of rat epididymal fat pads: cellularity and metabolism. The Journal of clinical investigation. 1968 Sep;47(9):2091-8. PubMed PMID: 5675429. Pubmed Central PMCID: 297369.
5. West DB, Diaz J, Roddy S, Woods SC. Long-term effects on adiposity after preweaning nutritional manipulations in the gastrostomy-reared rat. The Journal of nutrition. 1987 Jul;117(7):1259-64. PubMed PMID: 3112335.
6. Hirsch J, Fried SK, Edens NK, Leibel RL. The fat cell. The Medical clinics of North America. 1989 Jan;73(1):83-96. PubMed PMID: 2643010.
7. Spalding KL, Arner E, Westermark PO, Bernard S, Buchholz BA, Bergmann O, et al. Dynamics of fat cell turnover in humans. Nature. 2008 Jun 5;453(7196):783-7. PubMed PMID: 18454136.
8. Toubal A, Clement K, Fan R, Ancel P, Pelloux V, Rouault C, et al. SMRT-GPS2 corepressor pathway dysregulation coincides with obesity-linked adipocyte inflammation. The Journal of clinical investigation. 2013 Jan 2;123(1):362-79. PubMed PMID: 23221346. Pubmed Central PMCID: 3533285.
9. Hernandez TL, Kittelson JM, Law CK, Ketch LL, Stob NR, Lindstrom RC, et al. Fat redistribution following suction lipectomy: defense of body fat and patterns of restoration. Obesity. 2011 Jul;19(7):1388-95. PubMed PMID: 21475140.
10. Cunningham SA, Kramer MR, Narayan KM. Incidence of childhood obesity in the United States. The New England journal of medicine. 2014 Jan 30;370(5):403-11. PubMed PMID: 24476431.
11. Efrat M, Tepper S, Birk RZ. From fat cell biology to public health preventive strategies - pinpointing the critical period for obesity prevention. Journal of pediatric endocrinology & metabolism : JPEM. 2013;26(3-4):197-209. PubMed PMID: 23327818.
Posted 3/5/2014
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