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6 Cardiovascular Health Promotion Early in Life The risk factors for cardiovascular disease (CVD) in adults are now well established. However, emerging evidence highlights the importance of exposures and experiences throughout the life course, beginning as early as the prenatal period, on the subsequent development of CVD. As a result, there are opportunities for intervention during the early years of life that can form a crucial component of the global effort to reduce the burden of CVD. This chapter describes the determinants of CVD that have origins early in life, followed by a discussion of the effects of childhood health promotion and prevention initiatives on later CVD risk. This chapter, consistent with the scope of this report as described in Chapter 1, focuses on the accumulation starting early in life of risk for coronary heart disease and stroke This is not intended to underemphasize the importance of treating and preventing congenital heart diseases and other cardiovascular diseases in childhood, including prevention and treatment of streptococcal infections to prevent rheumatic heart disease, which exacts a high toll on children in low and middle income countries and was discussed in more detail in Chapter 2. In addition, although the emerging epidemiological evidence is compelling for the importance of childhood and adolescence in the development of risk for CVD, this chapter is not intended to imply that attention should be drawn away from much-needed intervention approaches to reduce risk in adults. Indeed, there is not sufficient low and middle income country evidence on intervention effectiveness, health impact, or cost-effectiveness analyses to conclude that childhood prevention alone is a top priority for widespread implementation.
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Rather, the aim of this chapter is to highlight several important messages. First, although evidence has not fully elucidated the onset of risk in early childhood, well-documented trends on youth tobacco use and childhood obesity present an immediate obstacle to achieving future reductions in CVD disease burden. Second, those already working in child health globally should take chronic disease prevention into consideration where there are relatively feasible and evidence-based interventions available in order to achieve not only short-term child outcomes but also to promote lifelong health. Third, the impact of health promotion and health education in children on adult CVD outcomes as well as the effectiveness of active CVD prevention programs in early childhood, youth, and adolescence in low and middle income countries are areas to be emphasized for further intervention research. A summary framework of opportunities to promote lifelong heart health during development and to engage the next generation in the fight against CVD and related chronic diseases is illustrated in Figure 6.1. FIGURE 6.1 Growing toward heart health: Influences and opportunities into adulthood.
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ASSOCIATION BETWEEN EARLY LIFE FACTORS AND SUBSEQUENT RISK FOR CVD Prenatal, Infancy, and Early Childhood There is growing recognition in developing and developed countries, based on recent data emanating from prospective cohort studies, of the importance of the fetal and early childhood periods in the onset of CVD later in life (Aboderin et al., 2002; Victora et al., 2008; Walker and George, 2007; WHO, 2009). The influences during this period include maternal factors during pregnancy, such as smoking, obesity, and malnutrition, and factors in infancy and early childhood, such as breastfeeding, low birth weight, and undernutrition, especially when coupled with rapid weight gain later in childhood. Maternal smoking during pregnancy has been linked to CVD-related risk factors. It has been consistently associated with increased childhood obesity independent of other risk factors (Oken et al., 2008). This raises the concern that the increasing trend of smoking among young women in the developing world, described in Chapter 2, could contribute to increased prevalence of childhood obesity and obesity-related diseases in those populations. A number of studies have examined the effects of maternal obesity on the body weight of their children; however, the evidence is inconsistent. Two cohort studies in the United States found that excessive weight gain or maternal obesity during pregnancy was associated with overweight and obesity in the children at ages 3 and 4 years (Gillman et al., 2008; Whitaker, 2004). Similarly, a cohort study in Finland found that mothers’ body mass index (BMI) was positively associated with their sons’ BMI in childhood (Eriksson et al., 1999). However, the recent Avon Longitudinal Study of Parents and Children (ALSPAC) study in the United Kingdom found no association between maternal BMI and child BMI (Davey Smith, 2008; Davey Smith et al., 2007). Furthermore, several researchers have expressed methodological concerns about the retrospective cohort studies that have been used thus far to assess the relationship between maternal and child BMI, asserting that such studies cannot account for confounding variables such as postnatal eating habits of children with obese parents (Davey Smith, 2008). Another factor that appears to influence risk for long-term cardiovascular health is breastfeeding. Breastfeeding has been found to not only reduce childhood morbidity and mortality but also to be weakly protective against obesity later in life (Bhutta et al., 2008; Gluckman et al., 2008). However, the promotion of breastfeeding must be considered in coordination with other global health efforts so as not to encourage the spread of
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some infectious diseases, including HIV, which can be transmitted through breast milk. A link to adult CVD risk has also been made for maternal malnutrition, low birth weight, and undernutrition in infancy, especially when followed by rapid weight gain. These have been associated with increased risk of CVD and diabetes in adulthood (Barker and Bagby, 2005; Caballero, 2005; Gluckman et al., 2008; Prentice and Moore, 2005). In what is known as the developmental origins theory of CVD, disruptions to the nutritional, metabolic, and hormonal environment at critical stages of development (in utero and in the first years of life) are hypothesized to lead to permanent “programming” of the body’s structure, physiology, and metabolism that translate into pathology and disease, including CVD, later in life (Barker, 1997, 1998, 2007). The exact physiological mechanisms through which this programming occurs are not yet fully elucidated; however, there is evidence that fetal and early postnatal undernutrition can cause metabolic, anatomic, and endocrine adaptations that affect the hypothalamic-pituitary-adrenal axis, lipoprotein profiles, and end organ glucose uptake, among other processes (Prentice and Moore, 2005). Support for the developmental origins theory of CVD comes from a number of retrospective, and more recently prospective, cohort studies in various populations. Studies in the United Kingdom, the United States, Finland, and India found that fetal undernutrition (as measured by low birth weight, small birth size, ratio of birth length to weight, or ratio of head circumference to weight at birth), followed by a rapid catch-up growth from childhood to early adolescence was significantly associated with the later development of CVD in both men and women (Barker et al., 2005; Eriksson et al., 1999; Forsen et al., 1999; Osmond and Barker, 2000; Stein et al., 1996). Early undernutrition followed by catch-up growth during childhood has also been associated with subsequent hypertension and type 2 diabetes (Barker, 1998; Osmond and Barker, 2000). More recently, Stein et al. (2005) reviewed nutritional studies from China, India, Guatemala, Brazil, and the Philippines and found that growth failure between conception and age 2 years and accelerated weight gain from childhood to adolescence were associated with significantly increased risk of diabetes and CVD in adulthood. In another developing country cohort, a longitudinal study of more than 3,000 children in South Africa also found that the combination of low birth weight and rapid growth in childhood was associated with an increased risk of obesity and risk factors for type 2 diabetes (Crowther et al., 1998; Richter et al., 2007). This emerging data on the effects of rapid weight gain after early undernutrition have prompted some researchers to suggest a shift from the original “fetal origins” hypothesis to an “accelerated postnatal growth hypothesis” of CVD (Singhal et al., 2003, 2004).
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Some researchers have expressed reservations about interpreting the available data in this area due to concerns that much of the research to date has not sufficiently accounted for the confounding impact of the social and economic environment during early childhood (Davey Smith, 2007, 2008). In addition, although there is a growing body of evidence exploring the effects of undernutrition in infancy followed by rapid catch-up growth later in childhood on CVD, diabetes, obesity, and metabolic disease in adulthood, evidence is mixed on the effects of rapid growth between birth and age 2 years (Victora et al., 2008). Singhal et al. (2004) found that rapid weight gain within the first 2 weeks after birth was associated with adverse cardiovascular effects later in life. On the other hand, several recent reviews and meta-analyses of studies examining early undernutrition found rapid weight gain between birth and age 2 years was associated with lower morbidity and mortality in low and middle income countries (Black et al., 2008; Victora et al., 2008). The emerging evidence on the association between low birth weight followed by rapid growth in childhood and subsequent risk for CVD raises important considerations for addressing global CVD because low birth weight and exposure to undernutrition in utero and in infancy are common in many developing countries (Caballero, 2009; Kelishadi, 2007). For example, the 2005-2006 National Family Health International Survey in India found that more than 40 percent of children under age 3 were underweight (International Institute of Population Studies, 2005-2006). In addition, the coexistence of these high rates of undernutrition in utero and early childhood with the potential for overnutrition in later childhood and adulthood may accelerate the epidemics of obesity and CVD in populations that undergo rapid nutrition transitions (Victora et al., 2008). Identifying the most prudent strategy for nourishing low birth weight and stunted infants while neither compromising their childhood health nor increasing their risk for cardiovascular and metabolic complications later in life will be an important area of future research. Childhood and Adolescence The acquisition and accumulation of risk for CVD continues in childhood and adolescence (Celermajer and Ayer, 2006; Freedman et al., 2001; Strong et al., 1999). Unhealthful lifestyle practices such as consumption of high calorie and high fat foods, tobacco use, and physical inactivity begin in childhood, introducing major behavioral risks for CVD. Childhood adversity also influences adult cardiovascular health. In addition, there is also an emerging body of evidence on the presence of biological risk factors in children and youth, including pathophysiological processes associated with heart disease that can be seen as early as childhood.
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Childhood Obesity and CVD Risk Childhood obesity is associated with multiple risk factors for CVD, which are amplified in the presence of overweight and persist from childhood into adulthood. These risk factors include hyperlipidemia, high blood pressure, impaired glucose tolerance and high insulin levels, as well as metabolic syndrome. It has been estimated that 60 percent of overweight children possess at least one of these risk factors that can lead to CVD in adulthood (Freedman et al., 1999). This is especially important in terms of implications for global CVD because, as will be described later in this chapter, the prevalence of childhood obesity is increasing in developing countries (WHO, 2008b). The Bogalusa Heart Study, conducted in the United States in a community near New Orleans, examined the natural history of CVD among children and young adults (Berenson, 2002; Freedman et al., 2001). Repeated cross-sectional and longitudinal studies with participants aged 5 to 38 years suggested that overweight children and adolescents are more likely to become obese adults. A large prospective cohort study from Denmark also found that higher BMI during childhood is associated with an increased risk of coronary heart disease (CHD) in adulthood and that the elevated risk associated with childhood obesity increases with the age of the child (Baker et al., 2007). Several studies in developed countries have reported that the prevalence of hypertension is significantly higher in obese children as compared to normal-weight children (Guillaume et al., 1996; Rosner et al., 2000; Sorof and Daniels, 2002). Obese children are at a three-fold higher risk of developing hypertension compared to nonobese children, and the risk continues to increase with higher BMI values (Sorof and Daniels, 2002). Similar findings have been reported in studies across developing countries. Verma et al. (1994) found that the prevalence of hypertension was 13.7 percent in obese children as compared to 0.4 percent in nonobese children in Punjab, India. Childhood obesity is associated with impaired glucose tolerance (Sinaiko et al., 2001) and diabetes mellitus (Rocchini, 2002; Sinha et al., 2002) among children and adolescents. Over the years it has been observed that the upsurge in the prevalence of obesity among children and adolescents has been paralleled by an increasing prevalence of diabetes mellitus. This finding is significant, especially in developing countries such as India and China, which have the highest number of persons with diabetes in the world (Hossain et al., 2007). Sinha et al. (2002) found 25 percent of children (4-10 years) and 21 percent of adolescents (11-18 years) to have impaired glucose tolerance in the United States. Metabolic syndrome is associated with childhood obesity, as estab-
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lished by several studies in developed (Cook et al., 2003; Cruz et al., 2004) as well as developing countries (Agirbasli et al., 2006; Csabi et al., 2000; Kelishadi, 2007). Singh et al. (2007) estimated the prevalence of metabolic syndrome using the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) criterion in adolescents aged 12-17 years in Chandigarh, India, to be 4.2 percent with no gender differences. Moreover, the study also estimated that 11.5 percent of the overweight adolescents and 1.9 percent of those who were of normal weight met the criterion of metabolic syndrome, suggesting a significant difference. Similar findings have been noted in studies conducted in other low and middle income countries (Agirbasli et al., 2006; Csabi et al., 2000; Kelishadi, 2007). Childhood Adversity and CVD Risk Stressful or traumatic circumstances in childhood also appear to increase the risk of CVD later in life. The Adverse Childhood Experiences study found that adults exposed to adversities such as abuse, household dysfunction (defined as the presence of alcohol or substance abuse, mental illness, or criminal behavior in the house), or neglect during childhood were significantly more likely to smoke, be physically inactive, be severely obese, and be depressed or angry, all risk factors for CVD. There was a dose–response relationship between the number of childhood exposures to adverse experiences and the number of risk factors for chronic disease later in life (Dong et al., 2004; Felitti et al., 1998). In a further analysis of the study data, Dong et al. (2004) found a similar graded relationship between the number of childhood adverse experiences and risk of ischemic heart disease in adulthood. In addition to adverse experiences, growing up poor has also been linked to an increased risk of developing and dying from CVD. A review of prospective and cross-sectional studies in high income countries reported that the vast majority found an association between poor socioeconomic circumstances in childhood and greater risk of CHD, angina, stroke, and atherosclerosis in adulthood. This association was independent of the economic circumstances of study participants in adulthood (Galobardes et al., 2006). Initiation of Tobacco Use Tobacco use initiated in childhood or adolescence is another factor that leads to early vascular dysfunction and later adult CVD. There are an array of biological, social, environmental, and interpersonal factors that influence experimentation and maintenance of tobacco use among youth. Nicotine is a highly addictive substance. Cigarettes and other forms of tobacco act as
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carriers of nicotine, which affects the brain by reinforcing behavior, altering mood and creating a need that did not exist prior to drug exposure (Oates et al., 1988). Once youth start using tobacco, many of them become addicted to nicotine. After reaching the brain, nicotine stimulates the reward pathways in the brain and stimulates the release of dopamine, which is a neurotransmitter associated with addiction (Glover et al., 2003). The brains of children and adolescents, which are still in developmental stages, are highly susceptible to nicotine addiction (Difranza et al., 2002). The number of cigarettes and the duration of smoking that is necessary for making a person addicted are lower in adolescents than in adults. A study by Difranza et al. (2002) showed that some adolescents begin to experience loss of control over their smoking within weeks of smoking the first cigarette. The U.S. Surgeon General’s report of 1994, Preventing Tobacco Use Among Young People, described four broad categories of psychosocial risk factors that are linked to the initiation of the habit of smoking: sociodemographic, behavioral, personal, and environmental (U.S. Department of Health and Human Services, 1994). The specific sociodemographic factors associated with tobacco use are low socioeconomic status, male gender, low parental education, and single-parent households (Buttross and Kastner, 2003; Tyas and Pederson, 1998). Various behavioral and personal factors are poor academic achievement, low self-esteem, and peer influences (Buttross and Kastner, 2003; Tyas and Pederson, 1998). Environmental influences include smoking by parents, siblings, and peers; absence of rules prohibiting smoking at home (Buttross and Kastner, 2003; Tyas and Pederson, 1998); and the influence of films, television, and media campaigns (Prokhorov et al., 2006). Although these factors leading to initiation of tobacco use have been widely studied in developed countries, the evidence from youth in developing countries remains relatively sparse. Early CVD Pathology in Childhood Many of the risk factors described above have been shown to be related to surrogates for CVD pathophysiology that can already be observed in childhood, such as increased left ventricular mass, left ventricular systolic dysfunction, and higher arterial thickness in overweight children (Johnson et al., 1999; Laird and Fixler, 1981; Sorof et al., 2003). Although the predictive value of elevated C-reactive protein (CRP) and raised intima media thickness (IMT) are still under debate, it is worth noting that these have been demonstrated in obese children, along with impaired endothelial function of arteries as well as arterial stiffness and calcification (Celermajer and Ayer, 2006). BMI measured in childhood has been shown to be significantly associated with carotid IMT measured in adulthood. The Bogalusa Heart
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Study suggested that low-density lipoprotein (LDL) cholesterol and BMI in childhood are independent risk factors for increased carotid IMT in young adulthood, whereas the Cardiovascular Risk in Young Finns study suggested that systolic blood pressure, LDL cholesterol, smoking, and BMI measured at 12-18 years predict adult IMT (Li et al., 2003; Raitakari, 2003). The Pathobiological Determinants of Atherosclerosis in Youth Study study also suggested that atherosclerosis, which is a major pathological cause of coronary artery disease, has its origins in childhood (Strong et al., 1999). Fatty streaks in children are associated with risk factors such as dyslipidemia, hypertension, cigarette smoking, and diabetes mellitus (Celermajer and Ayer, 2006). Berenson (2002) suggested that fatty streaks start appearing in the aorta and other arteries as early as 3 years of age, and high maternal cholesterol levels in the ante-natal period contribute to their formation. Fatty streaks and raised lesions in the arteries, especially the aorta and coronary and carotid arteries, increase rapidly in prevalence and extent during the 15- to 34-year age span. In summary, the evidence cited here clearly suggests that the behavioral and biological risk factors for CVD in adulthood frequently start appearing in childhood and adolescence. The risk factors are genetic, environmental, and behavioral and track from childhood to adulthood leading to premature CVD in adulthood. Hence, efforts for the prevention of CVD should begin right from childhood and adolescence when lifestyle habits are being formed, especially with respect to diet and physical activity, as well as during the prenatal period with respect to maternal nutrition and health. GLOBAL TRENDS IN MAJOR DETERMINANTS OF CVD RISK EARLY IN LIFE An understanding of the trends fueling the growing burden of childhood risk factors for chronic diseases is imperative if a reversal is to be brought about through public policy and programs. The following sections offer a brief overview of the global trends in the major determinants of CVD risk in children and youth. Trends in Tobacco Use in Children and Adolescents As described in Chapter 2, tobacco use is a growing worldwide epidemic (Reddy and Gupta, 2004). It is a risk factor for many chronic diseases and is the single most important preventable cause of death in the world today (WHO, 2008a). The most susceptible time for initiating tobacco use is during adolescence and early adulthood, before the age of 18 years (U.S.
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Department of Health and Human Services, 1994), and the prevalence of tobacco use is increasing among children and adolescents. Due to this increasing prevalence, tobacco use is often referred to as a “pediatric disease” or a “pediatric epidemic” (Committee on Environmental Health et al., 2009; Perry et al., 1994). In India, for example, an estimated 5500 adolescents start using tobacco every day, joining the 4 million young people under the age of 15 years who already regularly use tobacco (Rudman, 2001). The Global Youth Tobacco Survey (GYTS) provides some insight into global trends in tobacco consumption among youth. GYTS is a school-based survey of students aged 13-15 years that was undertaken at 395 sites in 131 countries. GYTS reported that, globally, about 10 percent of adolescents currently use tobacco in any form (Asma, 2009). Nearly 25 percent of them try their first cigarette before the age of 10 years, and 19 percent are susceptible to initiating smoking during the next year (Global Youth Tobacco Survey Collaborative Group, 2002). The GYTS estimates also revealed differences within a country or a region, thereby showing how national estimates can obscure within-country differences and highlighting the need to look at subnational data. For example, India had both the highest and lowest rates of current use of any tobacco product (62.8 percent in Nagaland and 3.3 percent in Goa) (Global Youth Tobacco Survey Collaborative Group, 2002). These variations revealed by the GYTS indicate that tobacco-reduction strategies targeting youth will need to be adapted to local contexts with careful consideration paid to the unique factors influencing differential burden in each country, such as geographic regions or ethnic groups. In South Africa, for example, factors associated with race may play an important role in influencing adolescents’ decision to smoke (Panday et al., 2007a, 2007b). Adolescents in different ethnic groups had different responses to the importance of information provided on the pros and cons of smoking, contextual factors, and preexisting self-efficacy (Panday et al., 2005). More research regarding the nuances of adapting approaches to local culture and context is an important priority if the global health community hopes to reduce the startlingly high rates of tobacco use among the world’s youth. Lastly, the GYTS data provide information about the exposure of children to environmental tobacco smoke. Almost half of the students (44 percent) reported that they were exposed to tobacco smoke at home and greater than 6 in 10 students (52 percent) reported being exposed to tobacco smoke in public places (Warren et al., 2006). This is of particular concern given the causal association that has been established between exposure to secondhand smoke and the prevalence of impaired vascular function, metabolic abnormalities, and chronic debilitating conditions (Peto et al., 1996). As an example of the status of tobacco use on a national scale, the
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National Youth Risk Behavior Survey, conducted with more than 10,000 school children in South Africa in 2002, revealed that 31 percent of students had smoked, and passive tobacco smoke exposure levels ranged from 56-84 percent (Reddy et al., 2003). In addition, since the study looked at a wide variety of potential risk factors, including violence-related intentional and unintentional injuries, mental health and wellness indicators, and nutrition and physical activity levels, it provided a more complete, well-rounded picture of adolescent risk behaviors, reinforcing the need to look more closely at the complex interactions that contribute to youth health status (Reddy et al., 2003). However, as it was the first study of its kind in that country, few conclusions on temporal trends can be drawn. If the study were to be repeated regularly, it could provide information on the impact of a number of national-level policy initiatives implemented in order to bring more focus onto youth and adolescent health. Trends in Childhood Obesity The total global prevalence of overweight in children between the ages of 5 and 17 years is 10 percent, varying from under 2 percent in SubSaharan Africa to more than 30 percent in the United States (Bhardwaj et al., 2008). Although still highest in high income countries, the epidemic of childhood obesity has spread from the United States and other developed countries to low and middle income countries, especially in urban areas (Prentice, 2006). Figures 6.2 and 6.3 provide an illustration—compiled by the International Association for the Study of Obesity (IASO)—of worldwide trends in the prevalence of overweight among boys and girls, respectively, over the past two decades. While the data is not age-standardized across countries or directly comparable across years, the figures suggest a trend of growing prevalence of overweight among children in an increasing number of developing countries. For example, among school-going children and adolescents in India (rural and urban) aged 10-18 years, the prevalence of overweight was 1.7 percent in boys and 0.8 percent in girls in the year 2007 (WHO Global InfoBase, 2008). In the Middle East, Kuwait has among the highest prevalence of overweight (30 percent in boys; 31.8 percent in girls) and obesity (14.7 percent in boys; 13.1 percent in girls) among children and adolescents (10-14 years) (Al-Isa, 2004; Kelishadi, 2007). Figure 6.4 shows the prevalence of overweight and obesity among boys and girls aged 6-18 years in developing countries, demonstrating the high prevalence in the Middle East and Central and Eastern Europe. Among younger children, obesity is not a major public health issue in Asia and Sub-Saharan Africa, but in countries of Latin America, the Caribbean, the Middle East, North Africa, and Cen-
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In addition to the need for better data on CVD risk factors in children and youth, evidence from youth-focused interventions targeted at these risk factors in low and middle countries is also quite limited. There are some promising findings, especially in the area of tobacco reduction. Other intervention approaches with some success in developed countries offer models for adaptation. However, many of these possible models did not operate over long periods of time and on a large scale. The issue of what it will take to adapt, diffuse, implement, and maintain programs on a large scale in low and middle income countries needs to be addressed. One particularly important potential barrier to adopting cardiovascular health promotion programs targeting children and youth in schools and other settings is whether there exist reasonable incentives for non-health organizations to create and maintain such programs. For schools, the advantages of implementing such programs are not often straightforward. For example, physical activity may be central in some schools, but the engagement and participation of schools are not guaranteed, especially if there is a competition for resources that would otherwise be dedicated to their primary academic mission. They may not commit limited resources to programs over the long term if the incentives for doing so are weak and the interventions are complex to implement, manage, and maintain. Thus, it is necessary to consider the long-term viability of such efforts as the programs may dissipate even if there is early enthusiasm, especially in developing countries where resources may be limited. Additionally, in order for many school-based interventions to be implemented, especially at a large scale, there may need to be interaction and cooperation between different divisions of the national government, such as the health and education sectors. The degree to which each of these independent agents work together varies in developing countries, and thus effort may be required to assist different sectors in coordinating their actions where appropriate and feasible. This coordination with the education sector is thus a critical component of the broader messages in this report supporting intersectoral and whole-of-government approaches to address CVD and related chronic diseases. CONCLUSION Accumulation of cardiovascular risk begins early in life, and evidence on rising rates of childhood obesity and youth smoking in low and middle income countries as well as emerging evidence on the effects of early nutrition on later cardiovascular health support the value of starting cardiovascular health promotion during pregnancy and early childhood and continuing prevention efforts throughout the life course. Maternal and child health (MCH) programs offer an opportunity to provide care that takes into account not only shorter-term childhood outcomes but also
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future lifelong health. In particular, emerging evidence on the effects of early nutrition on later cardiovascular health means that the CVD and MCH communities need to work together more closely to ensure that food and nutrition programs for undernourished children do not inadvertently contribute to long-term chronic disease risk. This could be accomplished through future coordination with multinational organizations that provide both service and programmatic guidance such as the United Nations World Food Program, United States Agency for International Development, Oxfam America, and Save the Children, as well as through direct consultation with local governments where possible. Increased efforts are needed to identify ways in which emergency and long-term food provision can be accomplished without unnecessarily increasing CVD risk or significantly increasing existing program costs. The available evidence on the impact of cardiovascular health promotion and CVD prevention initiatives in childhood and adolescence is limited and of variable quality, especially in low and middle income country settings. Approaches with some success on a small scale that have emerging potential for developing countries include education initiatives targeted to children, school-based programs, and programs targeted to take advantage of the potential for adolescents and young adults to serve as powerful advocates for change. This foundation provides an opportunity to develop, evaluate, and implement child- and youth-based programs to prevent the development of CVD in later life. REFERENCES Aboderin, I., A. Kalache, Y. Ben-Shlomo, J. W. Lynch, C. S. Yajnik, D. Kuh, and D. Yach. 2002. Life course perspectives on coronary heart disease, stroke and diabetes: Key issues and implications for policy and research. Geneva: World Health Organization. Agirbasli, M., S. Cakir, S. Ozme, and G. Ciliv. 2006. Metabolic syndrome in Turkish children and adolescents. Metabolism: Clinical and Experimental 55(8):1002-1006. Al-Isa, A. N. 2004. Body mass index, overweight and obesity among Kuwaiti intermediate school adolescents aged 10-14 years. European Journal of Clinical Nutrition 58(9):1273-1277. Arnas, Y. 2006. The effects of television food advertisement on children’s food purchasing requests. Pediatrics International 48(2):138-145. Arora, M., S. Reddy, M. H. Stigler, and C. L. Perry. 2008. Associations between tobacco marketing and use among urban youth in India. American Journal of Health Behavior 32(3):283-294. Asma, S. 2009. Global tobacco surveillance system. Presentation at the Public Information Gathering Session for the Institute of Medicine Committee on Preventing the Global Epidemic of Cardiovascular Disease, Washington, DC. Baker, J. L., L. W. Olsen, and T. I. A. Sørensen. 2007. Childhood body-mass index and the risk of coronary heart disease in adulthood. New England Journal of Medicine 357(23):2329-2337.
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