- Email: [email protected]
Higher levels of inflammation in obese children
EDITORIAL OPINIONS
Higher Levels of Inflammation in Obese Children INTRODUCTION The prevalence of obesity is increasing in Western countries. A similar trend is being observed for children.1 In the United States, the prevalence of overweight has increased from 5.0% between 1963 and 1965 to 13.6% between 1988 and 1994 among children 6 to 11 y. In adolescents, these numbers are 5.0% and 11.4%, respectively.2 Even in preschool children aged 4 to 5 y, an increasing prevalence of overweight was observed between 1971 and 1974 (5.8%) and between 1988 and 1994 (10%).3 Although the health risks of obesity in adulthood are well characterized, much less is known about the (long-term) health risks of obesity at young ages.
METABOLIC CORRELATES OF CHILDHOOD OBESITY Obesity in children has been associated with the presence of the metabolic cardiovascular syndrome.4,5 Compared with leaner children, fatter children have higher systolic and diastolic blood pressures, higher fasting levels of glucose and insulin, higher total and low-density lipoprotein cholesterol, lower high-density lipoprotein cholesterol, and higher factor VIIc.6,7 Further, prospective research has shown that increases in adiposity at a young age are associated with increases in total and low-density lipoprotein cholesterol and decreases in high-density lipoprotein cholesterol, suggesting an increasingly atherogenic lipoprotein profile.8
INFLAMMATION AND CHILDHOOD OBESITY Recent studies have found that overweight and obesity in children also is associated with higher levels of inflammation. In these studies, the serum concentration of acute-phase proteins such as C-reactive protein (CRP) and fibrinogen were used as sensitive markers of inflammation status. My colleagues and I reported a strong association between overweight and inflammation in children.9 Serum CRP levels were collected from 3512 children aged 8 to 16 y who were participants in the third National Health and Nutrition Examination Study and a representative sample of the U.S. population. Overweight was defined as having a body mass index or a sum of three skinfolds above the sex-specific 85th percentile. After adjustment for potential confounders including smoking and health status, overweight boys were 3.7 to 5.1 times more likely to have elevated CRP (ⱖ0.22 mg/dL) and overweight girls were 2.9 to 3.2 times more likely to have elevated CRP. Moreover, the overweight children had higher white blood cell counts than normal-weight children, indicating a higher inflammation status.
The research of Dr. Visser was made possible by a fellowship from the Royal Netherlands Academy of Arts and Sciences. Correspondence to: Marjolein Visser, MD, Institute for Research in Extramural Medicine, Faculty of Medicine, Vrije Universiteit, Van der Boechorststraat 7, 1081 BT Amsterdam, Netherlands. E-mail: m.visser.emgo@ med.vu.nl Nutrition 17:480 – 484, 2001 ©Elsevier Science Inc., 2001. Printed in the United States. All rights reserved.
Results from the Ten Towns Children’s Study, which used data from 699 children aged 10 to 11 y, support our findings.7 A positive relationship between the Ponderal index (weight/height3) and CRP was found. CRP levels were 270% higher in the top quintile of Ponderal index than in the lowest quintile. Adiposity at 10 to 11 y (current age) was a stronger determinant of CRP levels than obesity at 5 to 7 y, suggesting that the effect on CRP is due to current adiposity. Further, obesity was a stronger determinant of CRP levels than other factors that increase CRP levels such as Helicobacter pylori infection and environmental exposure to tobacco smoke as measured by salivary cotinine levels. A positive association between body mass index or Ponderal index and fibrinogen levels also was found in children, indicating low-grade systemic inflammation in obese children.10,11
OBESITY AND INFLAMMATION: A CAUSAL RELATIONSHIP? Obesity has been repeatedly associated with higher inflammation levels in adults.12–14 However, many factors correlated with obesity can cause higher inflammation levels, including smoking, arthritis, cardiovascular disease, and diabetes mellitus. Whether obesity and inflammation are causally related or whether the association is indirect through other obesity-related factors is not clear. The recent findings of an association between obesity and inflammation in children support a direct relationship because the prevalence of smoking, atherosclerosis,15 and preexisting disease is low in children and is unlikely to confound the relationship. However, more research is warranted to test whether the association between obesity and inflammation is causal.
ADIPOSE TISSUE AS AN ENDOCRINE ORGAN Results of several (experimental) studies have suggested that interleukin-6 is the link between obesity and inflammation. Interleukin-6 is expressed in adipose tissue16 –18 and released into the circulation.18,19 Proinflammatory cytokines, including interleukin-6, stimulate the production of acute-phase proteins in the liver.20,21 Further, higher adipose-tissue content of interleukin-6 has been associated with higher serum CRP concentrations in obese persons.22 Moreover, a decrease in serum and adipose-tissue interleukin-6 was found after weight loss in 14 obese non-diabetic women.23 The release of interleukin-6 from adipose tissue might induce elevated levels of acute-phase proteins in persons with excess body fat, leading to low-grade systemic inflammation.
CHILDHOOD OBESITY, INFLAMMATION, AND HEALTH RISKS In adults, higher CRP or fibrinogen levels are predictive of future myocardial infarction, peripheral arterial disease, ischemic stroke, and diabetes mellitus.24,25 Whether higher inflammation levels in overweight and obese children predispose them to disease at older ages is not known. However, body weight and weight gain during childhood are related to adult cardiovascular risk and mortality risk.26,27 Obese children at 7 y are four times more likely to have metabolic syndrome in adulthood.28 The risk for this syndrome is still twice as high after adjustment for body weight in adulthood. Similar results were obtained in the Harvard Growth Study in 0899-9007/01/$20.00
Nutrition Volume 17, Number 6, 2001 which adolescents were followed for 55 y. Overweight at adolescence was a strong predictor of coronary heart disease and atherosclerosis during adulthood, independent of body weight during adulthood.29 The presence of higher inflammation levels during childhood might in part explain the increased risk for cardiovascular disease in adulthood among obese children. Because overweight is associated with various risk factors among children, successful prevention and treatment of obesity in childhood might reduce the adult incidence of cardiovascular disease. Because obese children as young as 5 to 8 y already have higher inflammation levels and several risk factors for cardiovascular disease, efforts to prevent overweight should begin in early childhood.
Marjolein Visser, PhD Institute for Research in Extramural Medicine Vrije Universiteit Amsterdam Netherlands
Editorial Opinions
20. 21.
22.
23.
24.
25.
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27.
REFERENCES 1. Chinn S, Rona RJ. Prevalence and trends in overweight and obesity in three cross sectional studies of British children, 1974 –94. BMJ 2001;322:24 2. MacKay AP, Fingerhut LA, Duran CR. Adolescent health chartbook. Health, United States, 2000. Hyattsville, MD: National Center for Health Statistics, 2000 3. Ogden CL, Troiano RP, Briefel RR, et al. Prevalence of overweight among preschool children in the United States, 1971 through 1994. Pediatrics 1997; 99(4). Available from: http://www.pediatrics.org/cgi/content/full/99/4/e1 4. Morrison JA, Sprecher DL, Barton BA, Waclawiw MA, Daniels SR. Overweight, fat patterning, and cardiovascular disease risk factors in black and white girls: the National Heart, Lung, and Blood Institute Growth and Health Study. J Pediatr 1999;135:458 5. Csabi G, Torok K, Jeges S, Molnar D. Presence of metabolic cardiovascular syndrome in obese children. Eur J Pediatr 2000;159:91 6. Freedman DS, Dietz WH, Srinivasan SR, Berenson GS. The relation of overweight to cardiovascular risk factors among children and adolescents: the Bogalusa Heart Study. Pediatrics 1999;103:1175 7. Cook DG, Mendall MA, Whincup PH, et al. C-reactive protein concentration in children: relationship to adiposity and other cardiovascular risk factors. Atherosclerosis 2000;149:139 8. Freedman DS, Burke GL, Harsha DW, et al. Relationship of changes in obesity to serum lipid and lipoprotein changes in childhood and adolescence. JAMA 1985;254:515 9. Visser M, Bouter LM, McQuillan GM, Wener MH, Harris TB. Low-grade systemic inflammation in overweight children. Pediatrics 2000;107(1). Available from: http://www/pediatrics.org/cgi/content/full/107/1/e13 10. Cook DG, Whincup PH, Miller G, et al. Fibrinogen and factor VII levels are related to adiposity but not fetal growth or social class in children aged 10 –11 years. Am J Epidemiol 1999;150:727 11. Shea S, Isasi CR, Couch S, et al. Relations of plasma fibrinogen level in children to measures of obesity, the (G⫺4553 A) mutation in the -fibrinogen promotor gene, and family history of ischemic heart disease. Am J Epidemiol 1999;150:737 12. Mendall MA, Patel P, Ballam L, Strachan D, Northfield TC. C reactive protein and its relation to cardiovascular risk factors: a population based cross-sectional study. Br Med J 1996;312:1061 13. Visser M, Bouter LM, McQuillan GM, Wener MH, Harris TB. Elevated C-reactive protein levels in overweight and obese adults. JAMA 1999;282:2131 14. Hak AE, Stehouwer CD, Bots ML, et al. Associations of C-reactive protein with measures of obesity, insulin resistance, and subclinical atherosclerosis in healthy, middle-aged women. Arterioscler Thromb Vasc Biol 1999;19:1986 15. Stary HC. Lipid and macrophage accumulations in arteries of children and the development of atherosclerosis. Am J Clin Nutr 2000;72(suppl):1297S 16. Purohit A, Ghilchik MW, Duncan L, et al. Aromatase activity and interleukin-6 production by normal and malignant breast tissues. J Clin Endocrinol Metab 1995;80:3052 17. Crichton MB, Nichols JE, Zhao Y, Bulun SE, Simpson ER. Expression of transcripts of interleukin-6 and related cytokines by human breast tumors, breast cancer cells, and adipose stromal cells. Mol Cell Endocrinol 1996;118:215 18. Mohamed-Ali V, Goodrick S, Rawesh A, et al. Subcutaneous adipose tissue releases interleukin-6, but not tumor necrosis factor-␣, in vivo. J Clin Endocrinol Metab 1997;82:4196 19. Fried SK, Bunkin DA, Greenberg AS. Omental and subcutaneous adipose tissues
28.
29.
481
of obese subjects release interleukin-6: depot difference and regulation by glucocorticoid. J Clin Endocrinol Metab 1998;83:847 Banks RE, Forbes MA, Shorr M, et al. The acute phase response in patients receiving subcutaneous IL-6. Clin Exp Immunol 1995;102:217 Papanicolaou DA, Wilder RL, Manolagas SC, Chrousos GP. The pathophysiologic roles of interleukin-6 in human disease. Ann Intern Med 1998;128: 127 Bastard JP, Jardel C, Delattre J, et al. Evidence for a link between adipose tissue interleukin-6 content and serum C-reactive protein concentrations in obese subjects. Circulation 1999;99:2221 Bastard JP, Jardel C, Bruckert E, et al. Elevated levels of interleukin 6 are reduced in serum and subcutaneous adipose tissue of obese women after weight loss. J Clin Endocrinol Metab 2000;85:3338 Danesh J, Collins R, Appleby P, Peto R. Association of fibrinogen, C-reactive protein, albumin, or leukocyte count with coronary heart disease. JAMA 1998; 279:1477 Schmidt MI, Duncan BB, Sharrett AR, et al. Markers of inflammation and prediction of diabetes mellitus in adults (Atherosclerosis Risk in Communities study): a cohort study. Lancet 1999;353:1649 DiPietro L, Mossberg HO, Stunkard AJ. A 40-year history of overweight children in Stockholm: life-time overweight, morbidity, and mortality. Int J Obes Rel Metab Disord 1994;18:585 Sinaiko AR, Donahue RP, Jacobs DR Jr, Prineas RJ. Relation of weight and rate of increase in weight during childhood and adolescence to body size, blood pressure, fasting insulin, and lipids in young adults. The Minneapolis Children’s Blood Pressure Study. Circulation 1999;99:1471 Vanhala MJ, Vanhala PT, Keina¨nen-Kiukaanniemi SM, Kumpusalo EA, Takala JK. Relative weight gain and obesity as a child predict metabolic syndrome as an adult. Int J Obes 1999;23:656 Must A, Jacques PF, Dallal GE, Bajema CJ, Dietz WH. Long-term morbidity and mortality of overweight adolescents. A follow-up of the Harvard Growth Study of 1922 to 1935. N Engl J Med 1992;327:1350
PII S00899-9007(01)00509-3
A Good Start in Life: Breast Is Best, but Complementary Foods Should Not Be Worse Optimum nutrition and feeding of infants and young children are among the most important determinants of their health, growth, and development. They can prevent malnutrition and early growth retardation, which are common in many parts of the world.1 Poorly fed children have higher rates and severity of enteric and other infections, and they are at greater risk of dying prematurely. There is evidence that poor fetal and infant nutrition have long-term health consequences and play a role in the genesis of some chronic non-communicable diseases in adults. Furthermore, micronutrient deficiencies, especially of iron and iodine, might be associated with delayed motor development and impaired cognitive function. Thus, improvements in the nutrition of young children are desirable, not only for their positive effects on physical health and growth but also to reduce the risk of infection, ensure optimal psychomotor development and school performance and, in the long-term, improve adult life opportunities, health, and productivity. The period of transition, from an exclusively milk diet to one in which an increasing variety of foods is required to satisfy nutritional needs, is a particularly vulnerable time. Despite recognition of the public-health importance of infant and young-child nutrition and feeding practices, there are few guidelines based on scientific evidence for this critical weaning period.2,3 The World Health Organization (WHO) is aiming to reach consensus on the optimum duration of exclusive breast feeding and age of introduction of complementary feeds and, with UNICEF, to develop a global strategy for infant and young-child feeding.4
Correspondence to: Lawrence Weaver, MD, Department of Child Health, University of Glasgow, Royal Hospital for Sick Children, Yorkhill, Glasgow G3 8SJ, UK. E-mail: [email protected]
Higher Levels of Inflammation in Obese Children INTRODUCTION The prevalence of obesity is increasing in Western countries. A similar trend is being observed for children.1 In the United States, the prevalence of overweight has increased from 5.0% between 1963 and 1965 to 13.6% between 1988 and 1994 among children 6 to 11 y. In adolescents, these numbers are 5.0% and 11.4%, respectively.2 Even in preschool children aged 4 to 5 y, an increasing prevalence of overweight was observed between 1971 and 1974 (5.8%) and between 1988 and 1994 (10%).3 Although the health risks of obesity in adulthood are well characterized, much less is known about the (long-term) health risks of obesity at young ages.
METABOLIC CORRELATES OF CHILDHOOD OBESITY Obesity in children has been associated with the presence of the metabolic cardiovascular syndrome.4,5 Compared with leaner children, fatter children have higher systolic and diastolic blood pressures, higher fasting levels of glucose and insulin, higher total and low-density lipoprotein cholesterol, lower high-density lipoprotein cholesterol, and higher factor VIIc.6,7 Further, prospective research has shown that increases in adiposity at a young age are associated with increases in total and low-density lipoprotein cholesterol and decreases in high-density lipoprotein cholesterol, suggesting an increasingly atherogenic lipoprotein profile.8
INFLAMMATION AND CHILDHOOD OBESITY Recent studies have found that overweight and obesity in children also is associated with higher levels of inflammation. In these studies, the serum concentration of acute-phase proteins such as C-reactive protein (CRP) and fibrinogen were used as sensitive markers of inflammation status. My colleagues and I reported a strong association between overweight and inflammation in children.9 Serum CRP levels were collected from 3512 children aged 8 to 16 y who were participants in the third National Health and Nutrition Examination Study and a representative sample of the U.S. population. Overweight was defined as having a body mass index or a sum of three skinfolds above the sex-specific 85th percentile. After adjustment for potential confounders including smoking and health status, overweight boys were 3.7 to 5.1 times more likely to have elevated CRP (ⱖ0.22 mg/dL) and overweight girls were 2.9 to 3.2 times more likely to have elevated CRP. Moreover, the overweight children had higher white blood cell counts than normal-weight children, indicating a higher inflammation status.
The research of Dr. Visser was made possible by a fellowship from the Royal Netherlands Academy of Arts and Sciences. Correspondence to: Marjolein Visser, MD, Institute for Research in Extramural Medicine, Faculty of Medicine, Vrije Universiteit, Van der Boechorststraat 7, 1081 BT Amsterdam, Netherlands. E-mail: m.visser.emgo@ med.vu.nl Nutrition 17:480 – 484, 2001 ©Elsevier Science Inc., 2001. Printed in the United States. All rights reserved.
Results from the Ten Towns Children’s Study, which used data from 699 children aged 10 to 11 y, support our findings.7 A positive relationship between the Ponderal index (weight/height3) and CRP was found. CRP levels were 270% higher in the top quintile of Ponderal index than in the lowest quintile. Adiposity at 10 to 11 y (current age) was a stronger determinant of CRP levels than obesity at 5 to 7 y, suggesting that the effect on CRP is due to current adiposity. Further, obesity was a stronger determinant of CRP levels than other factors that increase CRP levels such as Helicobacter pylori infection and environmental exposure to tobacco smoke as measured by salivary cotinine levels. A positive association between body mass index or Ponderal index and fibrinogen levels also was found in children, indicating low-grade systemic inflammation in obese children.10,11
OBESITY AND INFLAMMATION: A CAUSAL RELATIONSHIP? Obesity has been repeatedly associated with higher inflammation levels in adults.12–14 However, many factors correlated with obesity can cause higher inflammation levels, including smoking, arthritis, cardiovascular disease, and diabetes mellitus. Whether obesity and inflammation are causally related or whether the association is indirect through other obesity-related factors is not clear. The recent findings of an association between obesity and inflammation in children support a direct relationship because the prevalence of smoking, atherosclerosis,15 and preexisting disease is low in children and is unlikely to confound the relationship. However, more research is warranted to test whether the association between obesity and inflammation is causal.
ADIPOSE TISSUE AS AN ENDOCRINE ORGAN Results of several (experimental) studies have suggested that interleukin-6 is the link between obesity and inflammation. Interleukin-6 is expressed in adipose tissue16 –18 and released into the circulation.18,19 Proinflammatory cytokines, including interleukin-6, stimulate the production of acute-phase proteins in the liver.20,21 Further, higher adipose-tissue content of interleukin-6 has been associated with higher serum CRP concentrations in obese persons.22 Moreover, a decrease in serum and adipose-tissue interleukin-6 was found after weight loss in 14 obese non-diabetic women.23 The release of interleukin-6 from adipose tissue might induce elevated levels of acute-phase proteins in persons with excess body fat, leading to low-grade systemic inflammation.
CHILDHOOD OBESITY, INFLAMMATION, AND HEALTH RISKS In adults, higher CRP or fibrinogen levels are predictive of future myocardial infarction, peripheral arterial disease, ischemic stroke, and diabetes mellitus.24,25 Whether higher inflammation levels in overweight and obese children predispose them to disease at older ages is not known. However, body weight and weight gain during childhood are related to adult cardiovascular risk and mortality risk.26,27 Obese children at 7 y are four times more likely to have metabolic syndrome in adulthood.28 The risk for this syndrome is still twice as high after adjustment for body weight in adulthood. Similar results were obtained in the Harvard Growth Study in 0899-9007/01/$20.00
Nutrition Volume 17, Number 6, 2001 which adolescents were followed for 55 y. Overweight at adolescence was a strong predictor of coronary heart disease and atherosclerosis during adulthood, independent of body weight during adulthood.29 The presence of higher inflammation levels during childhood might in part explain the increased risk for cardiovascular disease in adulthood among obese children. Because overweight is associated with various risk factors among children, successful prevention and treatment of obesity in childhood might reduce the adult incidence of cardiovascular disease. Because obese children as young as 5 to 8 y already have higher inflammation levels and several risk factors for cardiovascular disease, efforts to prevent overweight should begin in early childhood.
Marjolein Visser, PhD Institute for Research in Extramural Medicine Vrije Universiteit Amsterdam Netherlands
Editorial Opinions
20. 21.
22.
23.
24.
25.
26.
27.
REFERENCES 1. Chinn S, Rona RJ. Prevalence and trends in overweight and obesity in three cross sectional studies of British children, 1974 –94. BMJ 2001;322:24 2. MacKay AP, Fingerhut LA, Duran CR. Adolescent health chartbook. Health, United States, 2000. Hyattsville, MD: National Center for Health Statistics, 2000 3. Ogden CL, Troiano RP, Briefel RR, et al. Prevalence of overweight among preschool children in the United States, 1971 through 1994. Pediatrics 1997; 99(4). Available from: http://www.pediatrics.org/cgi/content/full/99/4/e1 4. Morrison JA, Sprecher DL, Barton BA, Waclawiw MA, Daniels SR. Overweight, fat patterning, and cardiovascular disease risk factors in black and white girls: the National Heart, Lung, and Blood Institute Growth and Health Study. J Pediatr 1999;135:458 5. Csabi G, Torok K, Jeges S, Molnar D. Presence of metabolic cardiovascular syndrome in obese children. Eur J Pediatr 2000;159:91 6. Freedman DS, Dietz WH, Srinivasan SR, Berenson GS. The relation of overweight to cardiovascular risk factors among children and adolescents: the Bogalusa Heart Study. Pediatrics 1999;103:1175 7. Cook DG, Mendall MA, Whincup PH, et al. C-reactive protein concentration in children: relationship to adiposity and other cardiovascular risk factors. Atherosclerosis 2000;149:139 8. Freedman DS, Burke GL, Harsha DW, et al. Relationship of changes in obesity to serum lipid and lipoprotein changes in childhood and adolescence. JAMA 1985;254:515 9. Visser M, Bouter LM, McQuillan GM, Wener MH, Harris TB. Low-grade systemic inflammation in overweight children. Pediatrics 2000;107(1). Available from: http://www/pediatrics.org/cgi/content/full/107/1/e13 10. Cook DG, Whincup PH, Miller G, et al. Fibrinogen and factor VII levels are related to adiposity but not fetal growth or social class in children aged 10 –11 years. Am J Epidemiol 1999;150:727 11. Shea S, Isasi CR, Couch S, et al. Relations of plasma fibrinogen level in children to measures of obesity, the (G⫺4553 A) mutation in the -fibrinogen promotor gene, and family history of ischemic heart disease. Am J Epidemiol 1999;150:737 12. Mendall MA, Patel P, Ballam L, Strachan D, Northfield TC. C reactive protein and its relation to cardiovascular risk factors: a population based cross-sectional study. Br Med J 1996;312:1061 13. Visser M, Bouter LM, McQuillan GM, Wener MH, Harris TB. Elevated C-reactive protein levels in overweight and obese adults. JAMA 1999;282:2131 14. Hak AE, Stehouwer CD, Bots ML, et al. Associations of C-reactive protein with measures of obesity, insulin resistance, and subclinical atherosclerosis in healthy, middle-aged women. Arterioscler Thromb Vasc Biol 1999;19:1986 15. Stary HC. Lipid and macrophage accumulations in arteries of children and the development of atherosclerosis. Am J Clin Nutr 2000;72(suppl):1297S 16. Purohit A, Ghilchik MW, Duncan L, et al. Aromatase activity and interleukin-6 production by normal and malignant breast tissues. J Clin Endocrinol Metab 1995;80:3052 17. Crichton MB, Nichols JE, Zhao Y, Bulun SE, Simpson ER. Expression of transcripts of interleukin-6 and related cytokines by human breast tumors, breast cancer cells, and adipose stromal cells. Mol Cell Endocrinol 1996;118:215 18. Mohamed-Ali V, Goodrick S, Rawesh A, et al. Subcutaneous adipose tissue releases interleukin-6, but not tumor necrosis factor-␣, in vivo. J Clin Endocrinol Metab 1997;82:4196 19. Fried SK, Bunkin DA, Greenberg AS. Omental and subcutaneous adipose tissues
28.
29.
481
of obese subjects release interleukin-6: depot difference and regulation by glucocorticoid. J Clin Endocrinol Metab 1998;83:847 Banks RE, Forbes MA, Shorr M, et al. The acute phase response in patients receiving subcutaneous IL-6. Clin Exp Immunol 1995;102:217 Papanicolaou DA, Wilder RL, Manolagas SC, Chrousos GP. The pathophysiologic roles of interleukin-6 in human disease. Ann Intern Med 1998;128: 127 Bastard JP, Jardel C, Delattre J, et al. Evidence for a link between adipose tissue interleukin-6 content and serum C-reactive protein concentrations in obese subjects. Circulation 1999;99:2221 Bastard JP, Jardel C, Bruckert E, et al. Elevated levels of interleukin 6 are reduced in serum and subcutaneous adipose tissue of obese women after weight loss. J Clin Endocrinol Metab 2000;85:3338 Danesh J, Collins R, Appleby P, Peto R. Association of fibrinogen, C-reactive protein, albumin, or leukocyte count with coronary heart disease. JAMA 1998; 279:1477 Schmidt MI, Duncan BB, Sharrett AR, et al. Markers of inflammation and prediction of diabetes mellitus in adults (Atherosclerosis Risk in Communities study): a cohort study. Lancet 1999;353:1649 DiPietro L, Mossberg HO, Stunkard AJ. A 40-year history of overweight children in Stockholm: life-time overweight, morbidity, and mortality. Int J Obes Rel Metab Disord 1994;18:585 Sinaiko AR, Donahue RP, Jacobs DR Jr, Prineas RJ. Relation of weight and rate of increase in weight during childhood and adolescence to body size, blood pressure, fasting insulin, and lipids in young adults. The Minneapolis Children’s Blood Pressure Study. Circulation 1999;99:1471 Vanhala MJ, Vanhala PT, Keina¨nen-Kiukaanniemi SM, Kumpusalo EA, Takala JK. Relative weight gain and obesity as a child predict metabolic syndrome as an adult. Int J Obes 1999;23:656 Must A, Jacques PF, Dallal GE, Bajema CJ, Dietz WH. Long-term morbidity and mortality of overweight adolescents. A follow-up of the Harvard Growth Study of 1922 to 1935. N Engl J Med 1992;327:1350
PII S00899-9007(01)00509-3
A Good Start in Life: Breast Is Best, but Complementary Foods Should Not Be Worse Optimum nutrition and feeding of infants and young children are among the most important determinants of their health, growth, and development. They can prevent malnutrition and early growth retardation, which are common in many parts of the world.1 Poorly fed children have higher rates and severity of enteric and other infections, and they are at greater risk of dying prematurely. There is evidence that poor fetal and infant nutrition have long-term health consequences and play a role in the genesis of some chronic non-communicable diseases in adults. Furthermore, micronutrient deficiencies, especially of iron and iodine, might be associated with delayed motor development and impaired cognitive function. Thus, improvements in the nutrition of young children are desirable, not only for their positive effects on physical health and growth but also to reduce the risk of infection, ensure optimal psychomotor development and school performance and, in the long-term, improve adult life opportunities, health, and productivity. The period of transition, from an exclusively milk diet to one in which an increasing variety of foods is required to satisfy nutritional needs, is a particularly vulnerable time. Despite recognition of the public-health importance of infant and young-child nutrition and feeding practices, there are few guidelines based on scientific evidence for this critical weaning period.2,3 The World Health Organization (WHO) is aiming to reach consensus on the optimum duration of exclusive breast feeding and age of introduction of complementary feeds and, with UNICEF, to develop a global strategy for infant and young-child feeding.4
Correspondence to: Lawrence Weaver, MD, Department of Child Health, University of Glasgow, Royal Hospital for Sick Children, Yorkhill, Glasgow G3 8SJ, UK. E-mail: [email protected]