| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Circulation. 2007;116:973-974.)
© 2007 American Heart Association, Inc.
Editorial |
From the Department of Pediatrics, University of Colorado, School of Medicine, Denver.
Correspondence to Dr Stephen R. Daniels, University of Colorado at Denver and Health Science Center, Department of Pediatrics, 1056 E 19th Ave, B065, Denver, CO 80218. E-mail daniels.Stephen{at}tchden.org
Key Words: Editorials atherosclerosis diet fatty acids pediatrics prevention
It is now clear that the process of atherosclerosis begins in childhood. A series of pathology studies, starting with autopsy examination of young soldiers killed in combat in the Korean War1 and the war in Vietnam2 to more recent studies such as the Pathobiologic Determinants of Atherosclerosis in Youth (PDAY) study3 and the Bogalusa study,4,5 have demonstrated that fatty streaks in the aorta and coronary arteries develop early in life and that even the more advanced and more concerning fibrous plaques are present in a proportion of adolescents and young adults. The PDAY and Bogalusa studies also have demonstrated that the traditional risk factors such as high body mass index, high blood pressure, and dyslipidemia are strongly associated with the presence and extent of arterial lesions.3,4 The Bogalusa cohort also has demonstrated that the presence of multiple risk factors is associated with an even higher risk for atherosclerotic lesions.5
Article p 1032
It is also well known that atherosclerotic cardiovascular disease is the most common cause of death in developed countries.6 Not uncommonly, the first clinical episode related to atherosclerosis is sudden cardiac death.7 Taken together, these data argue very strongly for the prevention of atherosclerosis and for prevention efforts to begin early in life. This might best be labeled primordial prevention because it is aimed at the prevention of development of risk factors in the first place. However, pediatric prevention of cardiovascular disease also includes primary prevention that focuses on control of cardiovascular disease risk factors once they are present to prevent overt clinical disease in adulthood.
Dietary intervention is a key component of primordial prevention of dyslipidemia. Reduced intake of saturated fat and cholesterol in the diet has been shown in numerous studies to be associated with lower total and low-density lipoprotein cholesterol.8 Overall control of calories and restriction of added sugar also are important in the prevention of hypertriglyceridemia.9 However, implementing diet changes in infants, children, and adolescents has not been without controversy. The central nervous system develops rapidly during the first 2 years of life. This includes the process of myelination, which is thought to depend to some extent on the intake of fats in the diet. There also has been concern that a diet lower in saturated fat might interfere with normal growth and development. This concern was based on case reports of infants and children who developed failure to thrive as a result of the misguided overrestriction of calories from fat by parents.10 There also has been concern that a diet lower in saturated fat and cholesterol might interfere with normal sexual maturation. This concern is based in part on the concept that cholesterol is an important building block of sex steroid hormones. This tension between a desire to prevent dyslipidemia and atherosclerosis and a concern that some dietary interventions might be disadvantageous has been heightened by a dearth of scientific evidence. Thus, the optimum diet for infants, children, and adolescents that would be useful in the prevention of atherosclerosis and also free of unwanted side effects has remained obscure.
Fortunately, the special Turku Coronary Risk Factor Intervention Project (STRIP) has been able to provide important information on diet throughout childhood and its role in the primordial prevention of atherosclerosis.11 The STRIP study is a prospective randomized controlled clinical trial of diet carried out in Turku, Finland. In this study, infants were recruited from well-baby clinics from 1990 to 1997. At 7 months of age, infants were randomly assigned either to receive counseling aimed at controlling environmental factors related to cardiovascular disease risk or to a control group. The intervention families had intensive diet counseling; the control families were seen by the same team and received standard advice but without intensive dietary counseling. Dietary counseling for the intervention was supervised by a dietitian, and the aim was to keep the total intake of fat at 30% to 35% of daily energy, the ratio of saturated fat to monounsaturated plus polyunsaturated fatty acid at 1:2, and the cholesterol intake at <200 mg/d. Breastfeeding was encouraged for the first year of life in both groups. When infants in the intervention group reached 1 year of age, skim milk was recommended. Parents in the intervention group were counseled to include increased fruits, vegetables, and whole grain products in the diet. Food records were used as an important part of the dietary counseling. During the early years of the study, diet counseling was directed at the parents. As the study subjects reached 7 years of age and older, progressively more dietary counseling was directed at the child. The control group received the standard health education that would be routinely given at Finnish well-baby and well-child visits. At 12 months of age, cow milk with 1.9% fat was recommended for daily use. Thus, the control group recommendations paralleled the kind of diet information that has been most frequently provided to parents in the United States.
In this issue of Circulation, Niinikoski et al12 present the most up-to-date findings from the Special Turku Coronary Risk Factor Intervention Project (STRIP). This report focuses on results from the subjects in the study at 14 years of age. Thus, we now have data across many dimensions in which concerns have been raised about diet, lipids, and lipoproteins in infancy, childhood, and adolescence. In this report, the STRIP investigators demonstrate that ongoing dietary intervention has resulted in significantly lower total and low-density lipoprotein cholesterol at 14 years of age. High-density lipoprotein cholesterol remained similar between the 2 groups. As important as those results is the fact that no significant differences existed between the dietary intervention and the control groups in growth, body mass index, pubertal development, or age at menarche for girls. This means that the STRIP dietary intervention is both safe and effective when applied from 7 months to 14 years of age. The results of this study are consistent with those of the Dietary Intervention Study in Children (DISC), which was a shorter-term study done in school-age children in the United States.13
The results of the STRIP study have important clinical and public health implications. Evidence is mounting that we should be implementing a diet similar to the one used by the STRIP investigators in infants, children, and adolescents in the United States. This includes supporting breastfeeding and introducing low-fat dairy products at 1 year of age. However, it also is important that ongoing, appropriate counseling on diet be provided to parents during primary pediatric care. This will help to minimize any misguided attempts of some parents to use a very-low-fat, low-calorie diet, which can result in failure to thrive. Recently, Ford et al14 reported that approximately half of the decline in deaths resulting from coronary artery disease in the United States from 1980 to 2000 was attributable to a reduction in major risk factors for cardiovascular disease. It is possible that more widespread adoption of a STRIP-type diet in childhood could lead to a further reduction in low-density lipoprotein cholesterol and ultimately death resulting from coronary artery disease.
| Acknowledgments |
|---|
None.
| Footnotes |
|---|
| References |
|---|
|
|
|---|
2. McNamara JJ, Molot MA, Stremple JF, Cutting RT. Coronary artery disease in combat casualties in Vietnam. JAMA. 1971; 216: 1185–1887.
3. Relationship of atherosclerosis in young men to serum lipoprotein cholesterol concentrations and smoking: a preliminary report from the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Research Group. JAMA. 1990; 264: 3018–3024.
4. Newman WP, Freedman DS, Voors AW, Gard PD, Srinivasan SR, Cresanta JL, Williamson GD, Webber LS, Berenson GS. Relation of serum lipoprotein levels and systolic blood pressure to early atherosclerosis: the Bogalusa Heart Study. N Engl J Med. 1986; 3124: 138–144.
5. Berenson GS, Srinivasan SR, Bao W, Newman WP 3rd, Tracy RE, Wattigney WA. Association between multiple cardiovascular risk factors and atherosclerosis in children and young adults: the Bogalusa Heart Study. N Engl J Med. 1998; 338: 1650–1656.
6. Rosamond W, Flegal K, Friday G, Furie K, Go A, Greenlund K, Haase N, Ho M, Howard V, Kissela B, Kittner S, Lloyd-Jones D, McDermott M, Meigs J, Moy C, Nichol G, ODonnell CJ, Roger V, Rumsfeld J, Sorlie P, Steinberger J, Thom T, Wasserthiel-Smoller S, Hong Y, for the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics: 2007 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation. 2007; 115: e69–e171.
7. Kaikkonen KS, Kortelainen ML, Linna E, Huikuri HV. Family history and the risk of sudden cardiac death as a manifestation of an acute coronary event. Circulation. 2006; 114: 1462–1467.
8. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive summary of the third report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA. 2001; 285: 2508–2509.
9. Schulze MB, Manson JE, Ludwig DS, Colditz GA, Stampfer MJ, Willett WC, Hu FB. Sugar-sweetened beverages, weight gain, and incidence of type 2 diabetes in young and middle-aged women. JAMA. 2004; 292: 927–934.
10. Lifshitz F, Moses N. Growth failure: a complication of dietary treatment of hypercholesterolemia. Am J Dis Child. 1989; 143: 537–542.
11. Lapinleimu H, Viikari J, Jokinen E, Salo P, Routi T, Leino A, Ronnemaa T, Seppanen R, Valimaki I, Simell O. Prospective randomized trial in 1,062 infants of diet low in saturated fat and cholesterol. Lancet. 1995: 345: 471–476.[CrossRef][Medline] [Order article via Infotrieve]
12. Niinikoski H, Lagström H, Jokinen E, Siltala M, Rönnemaa T, Viikari J, Raitakari OT, Jula A, Marniemi J, Näntö-Salonen K, Simell O. Impact of repeated dietary counseling between infancy and 14 years of age on dietary intakes and serum lipids and lipoproteins: the STRIP study. Circulation. 2007; 116: 1032–1041.
13. Writing Group for the DISC Collaborative Research Group. Efficacy and safety of lowering dietary intake of fat and cholesterol in children with elevated low-density lipoprotein cholesterol. JAMA. 1995; 273: 1429–1435.
14. Ford E, Ajani U, Croft J, Critchley JA, Phil D, Labarthe DR, Kottke TE, Giles WH, Capewell S. Explaining the decrease in U.S. deaths from coronary disease, 1980–2000. N Engl J Med. 2007; 356: 2388–2398.
This article has been cited by other articles:
![]() |
O. Simell, H. Niinikoski, T. Ronnemaa, O. T Raitakari, H. Lagstrom, M. Laurinen, M. Aromaa, P. Hakala, A. Jula, E. Jokinen, et al. Cohort Profile: The STRIP Study (Special Turku Coronary Risk Factor Intervention Project), an Infancy-onset Dietary and Life-style Intervention Trial Int. J. Epidemiol., June 1, 2009; 38(3): 650 - 655. [Full Text] [PDF] |
||||
![]() |
D. Steinberg, C. K. Glass, and J. L. Witztum Evidence Mandating Earlier and More Aggressive Treatment of Hypercholesterolemia Circulation, August 5, 2008; 118(6): 672 - 677. [Full Text] [PDF] |
||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
Circulation Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2007 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |