Coronary heart disease (CHD) kills more individuals and impinges on society’s productivity and economics more than any other disease in the United States.1 Evidence accumulated from various autopsy studies, animal experimentation, and long-term epidemiologic studies supports the concept that atherosclerosis has its inception in childhood, and it has also been shown that risk factors which accelerate it originate in the same age group.2
There are studies which have shown that large geographical variations in cardiovascular disease (CVD) morbidity and mortality are influenced even by factors acting prenatally and in early life, or by a combination of factors present throughout the course of life.3
In Norway in the 1970s, Forsdahl3 put forward the hypothesis that geographical differences in CVD mortality might not be related to contemporary circumstances, but to poverty or deprivation in early life. Barker et al.4developed a new hypothesis in the 1980s based on the relationship between areas with the highest CVD and infant mortality rates, and lower birth weight and increased risk of CVD mortality.5 The suggestion drawn from these historical cohort studies was that chronic diseases are biologically programmed in utero or in early infancy. In the case of heart disease, it is hypothesized that fetal undernutrition, during middle gestation in particular, raises the risk of later disease by the programming of blood pressure, cholesterol metabolism, blood coagulation and hormonal settings.6 Yajnik et al.7 found that children with low birth weight have insulin resistance as early as 4 years of life. Weight at 1 year has also been found to be inverselyrelatedto the prevalence of CHD.8
A more clear and positive correlation between childhood risk factors andcoronary artery lesions has been shown in a study carried out by Newman et al.9 Thus, pediatric prevention of CHD is strongly recommended.10 It nevertheless remains unclear as to who should do the counseling in the pediatric age group. Pediatricians are high on the list of suitable candidates for implementing CHD preventive measures in children, and the intended message for the general pediatrician is that the current knowledge on the prevention of CHD no longer justifies neutrality; rather, it calls for an active and calculated role to be played by the pediatrician.
Although there is a general trend towards focusing on the importance of pediatric prevention, yet a lack of clear guidelines and commitment hamper the application of these measures. There is hesitation on the part of some epidemiologists to recommend lifestyle changes for children, mainly due to a lack of solid pediatric data and longitudinal studies extending from infancy to adulthood, and for fear of compromising childhood nutrition. Thus, there is a clear-cut need to formulate guidelines for an effective and specific, yet harmless and cost-effective, approach. The aim of this article is to review CHD risk factors and their pertinence to children, and to recommend general guidelines for the prevention of CHD in children.
Natural History of Coronary Artery Disease
The development of coronary artery disease can be divided into the following periods.11,12
1. Incubation period: which begins in infancy and probably continues into adolescence.
2. Preclinical and latent period: when the disease is present in varying degrees of severity but the patient is asymptomatic.
3. Clinical period: when signs and symptoms appear.
The earliest recognizable pathologic lesions are the fatty streaks, which make their appearance in the aorta of most children even before 3 years of age.13 The fatty streaks are composed of deposits of lipid within the cells of both the intima and inner media of the vessel. The lipid is associated with elastin and other fiber protein. In general, during the second decade, the fatty streaks increase in number, size, and distribution, and become evident in the coronary arteries.13 The progression of the fatty streaks to fibrous plaques begins in the third decade.11 The fibrous plaque is a firm, raised lesion which contains increased amounts of lipid, collagen, and mucopolysaccharides, as well as fibrin and red cells. Despite the lack of longitudinal studies, it appears evident that precursors of CHD begin in early childhood and advance into later life. Extensive post- mortem analysis on the hearts of young US casualties (mean age 22 years) in the Korean and Viet Nam conflicts showed the incidence of coronary atherosclerotic lesions to be 77% and 45%, respectively.14,15
Thus, given our current knowledge of the accelerating effects of the risk factors for CHD as well as their prevalence in childhood, it seems reasonable to conclude that by modifying risk factors in the pediatric population, we can prevent or delay the ultimate disease process.9
Risk Factors
Risk factors fitting into the realm of pediatric counseling are: hypercholesterolemia, hypertension, smoking, diabetes, obesity, and physical inactivity.
Hypercholesterolemia: Several studies have now documented that elevated blood cholesterol is one of the major causes of CHD.9 Extrapolation of several studies in adults has shown that a 1% reduction in blood cholesterol level yields an approximately 2% reduction in CHD rates.16
Further research has documented that cholesterol levels track well from childhood to adulthood.12,17 This association permits identification of hypercholesterolemia, and warrants appropriate intervention during the pre-adult years. Adolescence is an appropriate time period for such an evaluation. During adolescence, teenagers start to make individual choices and develop personal lifestyles.18 Many of these lifestyle choices are related to risk factors for CHD, such as diet patterns and the development o obesity, physical activity, cigarette smoking, and the use of oral contraceptives.17,19 Therefore, appropriate intervention has the potential for lifetime effectiveness. Despite the potential usefulness of such early identification, evaluation is not uniform because the guidelines for pediatric cholesterol screening remain controversial. Many such guidelines suggest only targeted screening, i.e. screening specific highrisk individuals.10,12,20
One such guideline for the screening of hypercholesterolemic children has been framed by the American Academy of Pediatrics (AAP) in 1985. This was further expanded slightly by the AAP in 1988. It proposes targeted screening based on family history and individual risk factors21,22 (Tables 1 and 2).
However, some studies, particularly those carried out by Dennison et al.,23 Griffin et al.,24 and Garcia and Moodie25 presented data to demonstrate that a parental history of hypercholesterolemia had poor sensitivity as a screening criterion.
In another study, Steiner et al.26 evaluated the efficacy of the AAP criteria for identifying hypercholesterolemia in teenagers. This study demonstrated that despite the utilization of the 1985, 1988, or a combination of both AAP criteria for hypercholesterolemia screening, a substantial portion of adolescents with abnormal cholesterol levels would not be identified (Table3).
Thus, the conclusion drawn from these studies is that targeted screening is insufficient to adequately identify adolescents with hypercholesterolemia. These studies further proposed that until questions such as the ideal time for cholesterol testing in childhood, and the cut-off point for hypercholesterolemia in teenagers are more clearly understood, all adolescents must be screened to accurately identify those with hypercholesterolemia.
It has been demonstrated that 2 factors—composition of dietary lipids and genetics—influence serum lipid levels, and thus subsequently affect atherosclerotic lesions. People with familial hyperlipoproteinemia are particularly prone to CHD. This trait, apparently transmitted as an autosomal dominant, has been provisionally estimated to be present in as many as 1 in 200 newborn infants.27,28 It has also been estimated that among male heterozygotes with this trait, the chances of developing ischemic heart disease are 5% by the age of 30 years, 51% by the age of 50 years, and 85% by the age of 60 years.29 Disability among presumed homozygotes with this defect is still greater and occurs earlier. Homozygotes may have xanthomas and vascular disease before the age of 10 years.29
Based on the statistical association of diet with the development of atherosclerosis, the Atherosclerosis Study Group and Epidemiology Study Group30 have proposed the following recommendations for the general public from infancy through childhood: (i) caloric intake should be adjusted to achieve and maintain optimal weight; (ii) dietary cholesterol should be reduced to less than 300 mg per day; and (iii) substantial reduction in the intake of dietary saturated fats—dietary fats should contribute less than 35% of total calories, and fat calories should be equally distributed among saturated, monounsaturated and polyunsaturated sources. The Atherosclerosis Study Group and Epidemiology Study Group stated that with these dietary principles, the requirements for optimal nutrition can be met for all sections of the population including infants, children, and adolescents.30 In another research, it has been shown that children who consume low-fatmilk are at a slightly higher risk for gastrointestinal disease,31 although the risk of gastrointestinal disease in children over 2 years of age is negligible. Therefore, consumption of milk with 2% fat in children >2 years of age belonging to a family at high risk for CHD may well be recommended, whereas evidence does not favor this approach in infants (<1 year).32
However, the lack of data has created a difference of opinion regarding the efficacy of dietary modifications on the rates of premature atherosclerotic disease. Severalauthorities do not recommend such early dietary alterations for all children.33,34 Potential detrimental consequences of such dietary changes have been hypothesized by many researchers.28,35,36 The committee on nutrition of the AAP stressed that these dietary interventions were experimental and recommended against dietary changes for all children.2
In conclusion, despite the lack of longitudinal studies in the pediatric age group, based on the extrapolations of available data, efforts to reduce the saturated fat intake of children to 10% of calories37 and to reduce cholesterol intake to <300 mg/day or ideally to100 mg/1000 calories/ day seem justified.
Hypertension: The role of hypertension as a risk factor is clear, and familial aggregation of blood pressure and the tracking phenomenon support the concept that children with hypertension will most likely be adult hypertensives, and will surely be at risk for early CHD.38,39 In a study of healthy school-going children from northern India between 5 and 14 years of age, the prevalence of hypertension was found to be 11.7%.40
There is no doubt that excessive salt intake, particularly in salt-sensitive or geneticallypredisposed individuals who often have a family history of essential hypertension, is an important risk factor.39,41 Obesity is also a contributing factor.
The role of dietary sodium has been extended into infancy, and infants fed formulas with a sodium content similar to that of breast milk have been shown to have lower blood pressure after 6 months,42 thereby justifying the recommendation of breast milk and formulas with a similar sodium content as the choice foods in the first year of life. Also, as infants are indifferent to the taste of salt,43 and naturally occurring sodium is sufficient to meet their recommended daily intake,44 adding salt to their food is unnecessary.
Smoking: According to an estimate, about 3000 adolescents in the USA become smokers each day, and the rise in the number of young female smokers in recent years has been particularly noteworthy.45 The incidence of CHD and hypertension is higher in those who begin smoking before 20 years of age.46 The need for pediatricians’ intervention regarding this risk factor is unequivocal and absolutely justified. Educating young children and adolescents about the hazards of smoking should become a part of pediatric counseling.
Obesity: Obesity is associated with high blood pressure and abnormalities of serum lipids and carbohydrate metabolism, and no one can rationally state that the obese individual has good physical health. The vast majority of programs attacking obesity have met with failure. Therefore, the only sensible way to reduce the incidence of obesity is to prevent it. Mayer47 has concluded that the first one to two years of life are the only times fat cells can multiply. It thus appears that early infancy may be the most important period for weight control on a permanent basis. Because obese infants have larger and more fat cells than nonobese infants, they are apparently more prone to becoming obese adolescents and obese adults.48
To reduce obesity and its concomitants, Smith49 proposed the limiting of high-calorie food, the use of ironfortified formulas, and avoidance of homogenized whole milk in infancy. He also suggested that there should be no place for junk food in a well-supervised program of infant nutrition. Consumption of salted snacks and junk foods, especially those with a high calorie content, should be discouraged.
Physical activity: Physical activity in moderation is important for the normal growth and development of children. It has also been suggested that physical activity may enhance their academic performance.50 There is no direct link between physical activity and CHD, although lack of physical activity is often seen in obese children. Persuading children to develop appropriate exercise habits, which can continue into later life is justified, and should have a definite place in pediatric counseling.
Thus, in general, based on various hypotheses and research data, the following recommendations can be formulated:
1. Proper maternal nutrition should be instituted and maintained during pregnancy.
2. Mother’s milk, because of its low sodium content, is the best food for all infants and should be strongly recommended. What should be stressed is that breastfed infants may in fact have a lower risk of coronary artery disease in future life. However, if breastfeeding is not possible due to any cause, parents should be encouraged to use a formula similar to breast milk with respect to sodium content.
3. A healthy lifestyle should be encouraged for all children:
(i)
overeating should be discouraged;
(ii) consumption of salted snacks should be discouraged;
(iii)intake of food rich in cholesterol, saturated fat and sodium should be
discouraged.
In predisposed children (overweight or with a strong family history of a lipid disorder), these measures should be more judiciously applied. In the diet recommended for these children, 50% of their daily calories should come from complex carbohydrates and natural sugars (whole grains, fruits, vegetables), fat consumption should be decreased so that it comprises less than 30% of their daily calories (10% from saturated fats and 20% from polyunsaturated fats), cholesterol intake should also be decreased to less than 300 mg/day or 100 mg/1000 kcal.
4. Children should be encouraged to start and maintain a regular daily exercise program under parental supervision.
5. Antismoking counseling and education should begin in childhood. In view of children following parental footsteps, parents should also be strongly discouraged to smoke.
In conclusion, the available data strongly emphasize the role of pediatricians and pediatric cardiologists in delivering the preventive message to parents and in applying these lifestyle and dietary modifications to all children. These measures should be very aggressively instituted, specifically for Indian children in whom coronary artery disease is assuming epidemic proportions. Every child who is properly counseled may, in addition to living a healthier life, become an effective future advocate of CHD prevention.
Correspondence:
Dr Savitri
Shrivastava,
Senior Consultant,
Escorts Heart Institute and Research Centre,
Okhla Road, New Delhi 110025
References
1. Health United States 1989. Hyattsville, MD: US Department of Health and Human Services 1989; 21,104, DHHS Publication 90-1232
2. American Academy of Pediatrics. Committee on Nutrition: childhood diet and coronary heart disease. Pediatrics 1972; 49: 305–307
3. Forsdahl A. Are poor living conditions in childhood and adolescence an important risk factor for arteriosclerotic heart disease? Br J Prev Soc Med 1977; 31: 91–95
4. Barker DJP, Osmond C. Infant mortality, childhood nutrition, and ischaemic heart disease in England and Wales. Lancet 1986; 1: 1077– 1081
5. Barker DJ, Winter PD, Osmond C, Margetts B, Simmonds SJ. Weight in infancy and death from ischaemic heart disease. Lancet 1989; 2: 577–580
6. Barker DJ. Fetal origins of coronary heart disease. BMJ 1995; 311:171–174
7. Yajnik CS, Fall CH, Vaidya U, Pandit AN, Bavdekar A, Bhat DS, et al.Fetal growth and glucose and insulin metabolism in four-year-old Indian children. Diabet Med 1995; 12: 330–336
8. Vijayakumar M, Fall CH, Osmond C, Barker DJ. Birth weight, weight at one year, and left ventricular mass in adult life. Br Heart J 1995; 73: 363–367
9. Newman WP 3rd, Freedman DS, Voors AW, Gard PD, Srinivasan SR, Cresanta JL, et al. Relation of serum lipoprotein levels and systolic blood pressure to early atherosclerosis. The Bogalusa Heart Study.New Engl J Med 1986; 314: 138–144
10. Glueck CJ. Pediatric primary prevention of atherosclerosis. N Engl J Med 1986; 314: 175–177
11. Neufeld NH, Wagenvoort GA, Edward JE. Coronary arteries in fetuses, infants, juveniles and young adults. Lab Invest 1962; 11: 837
12. Orchard TJ, Donahue RP, Kuller LH, Hodge PN, Drash AL. Cholesterol screening in childhood: does it predict adult hypercholesterolemia? The Beaver County experience. J Pediatr 1983; 103: 687–691
13. McGill HC. Fatty streaks in coronary arteries and aorta. Lab Invest 1968; 18: 560
14. Enos WF, Holmes RH, Beyer J. Coronary disease among United States soldiers killed in action in Korea. Preliminary report. JAMA 1953; 152: 1090–1093
15. McNamara JJ, Molot MA, Stremple JF, Cutting RT. Coronary artery disease in combat casualties in Vietnam. JAMA 1971; 216: 1185– 1187
16. The Lipid Research Clinics Coronary Primary Prevention Trial results. I. Reduction in incidence of coronary heart disease. JAMA 1984; 251: 351–364
17. Lauer RM, Lee J, Clarke WR. Factors affecting the relationship between childhood and adult cholesterol levels: the Muscatine Study. Pediatrics 1988; 82: 309–318 18.
18. Tokuno KA. The early adult transition and friendships: mechanisms of support. Adolescence 1986; 21: 593–606
19. Nora JJ. Identifying the child at risk for coronary disease as an adult: a strategy for prevention. J Pediatr 1980; 97: 706–714
20. Weidman W, Kwiterovich P. AHA position statement of diagnosis and treatment of primary hyperlipidemia in childhood. Circulation 1986; 74: 1181A–1188A
21. American Academy of Pediatrics Committee on Nutrition. Pediatric Nutrition Handbook. 1985. pp. 236–246
22. American Academy of Pediatrics Committee on Nutrition. Indications for cholesterol testing in children. Pediatrics 1989; 83: 141–142 (Published as Policy Statement in AAP News, October, 1988)
23. Dennison BA, Kikuchi DA, Srinivasan SR, Webber LS, Berenson GS. Parental history of cardiovascular disease as an indication for screening for lipoprotein abnormalities in children. J Pediatr 1989; 115: 186–194
24. Griffin TC, Christoffel KK, Binns HJ, McGuire PA. Family history evaluation as a predictive screen for childhood hypercholesterolemia. Pediatric Practice Research Group. Pediatrics 1989; 84: 365–373
25. Garcia RE, Moodie DS. Routine cholesterol surveillance in childhood. Pediatrics 1989; 84: 751–755
26. Steiner NJ, Neinstein LS, Pennbridge J. Hypercholesterolemia in adolescents: effectiveness of screening strategies based on selected risk factors. Pediatrics 1991; 88: 269–275
27. Glueck CJ, Heckman F, Schoenfeld M, Steiner P, Pearce W. Neonatal familial type II hyperlipoproteinemia: cord blood cholesterol in 1800 births. Metabolism 1971; 20: 597–608
28. Fredrickson DS. Mutants, hyperlipoproteinaemia and coronary artery disease. Br Med J 1971; 2: 187–192
29. Slack J. Risks of ischaemic heart disease in familial hyperlipoproteinaemic states. Lancet 1969; 2: 1380–1382
30. Atherosclerosis Study Group and Epidemiology Study Group of the Inter-society Commission for Heart Disease Resources: Primary prevention of the atherosclerotic diseases. Circulation 1970; 42: A-55 –A-95
31. Koopman JS, Turkisk VJ, Monto AS, Thompson FE, Isaacson RE. Milk fat and gastrointestinal illness. Am J Public Health 1984; 74: 1371–1373
32. Cohen SA, Hendricks KM, Mathis RK, Laramee S, Walker WA. Chronic nonspecific diarrhea: dietary relationships. Pediatrics 1979; 64: 402–407
33. Mitchell S, Blount SG Jr, Blumenthal S, Jesse MJ, Weidman WH. The pediatrician and atherosclerosis. Pediatrics 1972; 49: 165–168
34. Schubert WK. Fat nutrition and diet in childhood. Am J Cardiol 1973; 31: 581–587
35. Fomon SJ. Infant nutrition. Philadelphia: W.B. Saunders Co.; 1967
36. Hofmann AF, Northfield TC, Thistle JL. Can a cholesterol-lowering diet cause gallstones? N Engl J Med 1973; 288: 46–47
37. Curtis ER, Witschi JC. Better food for American children. Pediatr Cardio Rounds 1985; 2:
38. Zinner SH, Martin LF, Sacks F, Rosner B, Kass EH. A longitudinal study of blood pressure in children. Am J Epidemiol 1974; 100: 437–442
39. Falkner B. The role of sodium in essential hypertension in genetically hypertensive adolescents. In: Gadds et al. (eds). Hypertension in young and old. Grune & Stratton; 1981. p. 29
40. Chadha SL, Tandon R, Shekhawat S, Gopinath N. An epidemiological study of blood pressure in school children (5–14 years) in Delhi. Indian Heart J 1999; 51: 178–182
41. Report of the Task Force on blood pressure control in children. Pediatrics 1977; 59 (Suppl): 5
42. Hofman A, Hazebroek A, Valkenburg HA. A randomized trial of sodium intake and blood pressure in newborn infants. JAMA 1983; 250: 370–373
43. Fomon SJ, Thomas LN, Filer LJ Jr. Acceptance of unsalted strained foods by normal infants. J Pediatr 1970; 76: 242–246
44. Yeung DL. Sodium in the infant diet and salt intake in infancy and childhood. Proceedings of a Symposium. Arraheim, CA: 1983. p. 25
45. US Department of Health, Education and Welfare, NIH 1976. Teenage smoking, national patterns of cigarette smoking ages 12 to 18 in 1972 and 1974. Publication NS (NJH). pp. 76–931
46. Borhani NO. Primary prevention of coronary heart disease: a critique. Am J Cardiol 1977; 40: 251–259
47. Mayer J. Editorial comment. Yearbook of Pediatrics. Chicago: Year Book Medical Publishers Inc; 1968. p. 72
48. Asher P. Fat babies and fat children. The prognosis of obesity in the very young. Arch Dis Child 1966; 41: 672–673
49. Smith M. Developmental nutrition: the challenge of obesity. Presented at the Maternal and Infant Nutrition Seminar; 1972; Feb 10; Atlanta, USA
50. Strong WB. Atherosclerosis: its pediatric roots. In: Kaplan NM, Stamler J (eds). Prevention of coronary heart disease. WB Saunders; 1983. pp. 20–32