- Open Access
Impact of nutrition since early life on cardiovascular prevention
Italian Journal of Pediatrics volume 38, Article number: 73 (2012)
The cardiovascular disease represents the leading cause of morbidity and mortality in Western countries and it is related to the atherosclerotic process. Cardiovascular disease risk factors, such as dyslipidemia, hypertension, insulin resistance, obesity, accelerate the atherosclerotic process which begins in childhood and progresses throughout the life span. The cardiovascular disease risk factor detection and management through prevention delays the atherosclerotic progression towards clinical cardiovascular disease. Dietary habits, from prenatal nutrition, breastfeeding, complementary feeding to childhood and adolescence nutrition play a basic role for this topic.
The metabolic and neuroendocrine environment of the fetus is fundamental in the body’s “metabolic programming”. Further several studies have demonstrated the beneficial effects of breastfeeding on cardiovascular risk factors reduction. Moreover the introduction of complementary foods represents another important step, with particular regard to protein intake. An adequate distribution between macronutrients (lipids, proteins and carbohydrates) is required for correct growth development from infancy throughout adolescence and for prevention of several cardiovascular disease risk determinants in adulthood.
The purpose of this review is to examine the impact of nutrition since early life on disease.
La malattia cardiovascolare rappresenta la principale causa di morbilità e mortalità dei paesi occidentali ed è correlata a degenerazione vascolare aterosclerotica. I fattori di rischio cardiovascolari quali dislipidemia, ipertensione, insulino resistenza e obesità accelerano tale processo il cui esordio è noto sin dell’età pediatrica ed evolve nel corso della vita. L’individuazione e la cura dei fattori di rischio cardiovascolari mediante la prevenzione dei fattori causali ritardano la progressione dell’aterosclerosi e l’insorgenza dei sintomi cardiovascolari. La nutrizione svolge un ruolo preventivo fondamentale sin dall’epoca prenatale e nelle diverse età della crescita.
La condizione metabolica e neuro-endocrino cui è sottoposto il feto è rilevante per la “programmazione metabolica”. E’ dimostrata inoltre l’importanza delle modalità di allattamento e divezzamento con particolare interesse per l’assunzione di proteine nel controllo dei fattori di rischio cardiovascolari. La corretta distribuzione di macronutrienti (lipidi, proteine e carboidrati) dall’infanzia all’adolescenza favorisce una crescita corretta e risulta utile a prevenire l’insorgenza dei determinanti di rischio di malattia cardiovascolare in età adulta.
Nella presente review verrà esaminato l’impatto della nutrizione dalle più precoci fasi delle vita sul rischio cardiovascolare.
Cardiovascular diseases (CVD) represent the leading cause of morbidity and mortality in Western countries. It has been demonstrated that atherosclerosis begins early in life and progresses throughout life span [1, 2]. Risk factors, such as dyslipidemia (including high levels of low-density lipoprotein cholesterol [LDL-C], high levels of triglycerides [TG] and low levels of high-density lipoprotein cholesterol [HDL-C]), hypertension, obesity, insulin resistance (IR), accelerate the atherosclerotic process and increase CVD risk. Several studies in children and adolescents have demonstrated that risk factors may be present since childhood, tracking into adult life, so an early identification is necessary to establish a primary prevention approach . Recent evidences from population-based and clinical studies have emphasized the importance of primordial prevention, aimed to avoid risk factors development [3, 4].
Several epidemiological studies across a wide range of countries and ethnicities have demonstrated that nutrition, from fetal life ongoing and early human development, exert a profound impact on risk development of adult disease. The theory of the “fetal origins of adult disease” (FOAD) [5–7], as coronary artery disease (CAD) , diabetes mellitus (DM) , as well as cancer and others pathologies, was formulated. The FOAD hypothesis is based on the premise of “developmental plasticity”: it is the phenomenon by which one genotype can produce different phenotypes in response to different environmental factors. In particular there are specific “critical” periods whereby the organs and systems of the human body are plastic and sensitive to the environment [6, 10]. During intrauterine life, nutrition plays an important role for the so called “metabolic programming”: several different stimuli produce permanent changes which persist throughout life span and have long-term implications for later development of metabolic diseases. This programming extends also into early life and childhood .
Recent evidences have demonstrated that environmental factors can interact with fetal genome through epigenetic processes, without altering it. Epigenetic mechanisms, comprising DNA methylation and de-methylation, post-transcriptional processes as methylation, phosphorylation and acetylation of core histones, produce heritable changes resulting in phenotype variations [11–13]. These emerging findings can offer opportunities for novel risk biomarkers and for interventions to promote health across the life course . Other mechanisms involved in early life programming are represented by permanent structural changes (eg, the permanent reduction of renal glomeruli or β-cell mass in the endocrine pancreas) and permanent effects on cellular aging regulation (eg, oxidative stress processes) .
This review examines the impact of nutrition since early life on CVD risk.
Maternal nutritional status influences the quantity and quality of nutrients reaching the fetus, thus representing a potential determinant of metabolic programming and body composition.
Data from several human studies on early-life CVD risk determinants have been primarily focused on birthweight. An inverse association between CVD mortality and birthweight was identified [5, 15, 16]. Further epidemiological studies have been conducted over the last decades in attempt to determine a possible correlation between birthweight and CVD risk factors. Most of these studies were retrospective and involved adult populations, while few prospective studies were conducted in children. It has been showed that subjects with low birthweight (LBW), especially as a result of intrauterine growth restriction, presented a higher prevalence of arterial hypertension [17–19], IR , T2DM [9, 20] and metabolic syndrome (MS) . Among birthweight determinants, the mother size and the intrauterine nutrient supply are the most important. In particular intrauterine growth retardation can be induced by prolonged but modest changes in maternal diet or by more severe changes in uterine blood supply near to the pregnancy term.
In relation to nutrients’ quantity, many studies examined the impact of maternal undernutrition on offspring phenotype [22, 23] and CVD outcome [24, 25]. Hales et al. formulated the hypotheses of “thrifty phenotype” which suggested that, when exposed to conditions of deprivation during fetal life, subjects developed metabolic, endocrine and/or anatomical adaptations aimed to immediate survival . The “thrifty phenotype” is characterized by a condition of IR which may be considered as the persistence of fetal response in order to facilitate energy serving and maintain an adequate concentration of glucose for vital organs, particularly the brain. This results in a state of hyperglicemia and increases de novo lipogenesis. The latter is responsible for later disease as IR and diabetes because of the “mismatch” between intra- and extra-uterine environment [27, 28]. Further it has been demonstrated that fetal growth restriction alters adipose tissue development. Subjects born small for gestational age have greater body fat percentage than subjects born appropriate for gestational age, and difference in fat distribution track to adulthood .
Furthermore another relevant consequence of undernutrition during fetal life is represented by the reduced cell number and growth in many organs, such as kidney. A reduced number of glomeruli, associated with the development of glomerulo-sclerosis, consequent to an increased blood flow over time, favours the development of hypertension in adult life .
In the last years a dramatic worldwide increase in overweight and obesity has occurred. This condition of overnutrition had in turn led to a relevant number of pregnant women with gestational obesity and gestational diabetes mellitus thus promoting fetal hyperinsulinemia. These conditions are related to adulthood overweight, obesity, impaired glucose tolerance and MS [31, 32].
New evidences from epidemiological and experimental studies have provided data about the impact of maternal diet quality on long-term implications for their offsprings thus supporting the concept of gene–diet interactions modulating CVD risk factors. The modulation by a genetic polymorphism of a dietary component effect on a specific phenotype (e.g., cholesterol levels and obesity), can interact increasing the risk for developing chronic disease. Maternal dietary fat composition is the most important determinant of the quality of fatty acids which are transferred across the placenta . Maternal dietary lipids, including fatty acids, have demonstrated effects on different tissues and metabolic systems: adipose tissue, muscle, liver, pancreas, intestine and hypothalamic appetite/energy sensing pathways. Dietary fatty acids composition can regulate gene expression, inter-cellular communications, metabolic and neuroendocrine networks . Besides the relevance of nutrition itself attention should be paid to the concept of gene–diet interactions and its impact on the clinical outcome. The modulation by a genetic polymorphism of a dietary component effect on a specific phenotype (e.g., cholesterol levels, obesity, hypertension), can interact increasing the risk for developing chronic disease. A body of studies focus on concentrations of specific plasma fatty acids which may interact with genes and are determined by both intake and metabolism. An example is represented by the activity of key enzymes desaturases. The latter are encoded by genes in the FADs cluster that contribute to PUFA concentrations. A genome-wide association study applied to the Italian InCHIANTI population described strong associations for the FADS1, FADS2, and FASD3 variants and PUFA levels. This study identifies sites at which the genetic variability in enzymes metabolizing essential fatty acids interacts with diet thus changing plasma fatty acid concentrations and potentially modulating the genetic risk related to metabolic pathways . Anyway, despite the fact that multiple studies have shown statistically significant interactions between n-3 fatty acids and genetic variants on intermediate and disease phenotypes, the individual level of evidence is very low and recommendations cannot be made on increasing or reducing the intake of n-3 fatty acids based on each individual’s genotype . In the last half-century changes in dietary lipid intake are represented by an excess of ω-6 fatty acids (eg. linoleic acid [LA], arachidonic acid [ARA]), inadequate ω-3 fatty acids (including linolenic acid [ALA], docosahexaenoic acid [DHA] and eicosapentaenoic acid [EPA]) and monounsaturated oleic acid consumption, and high intake of fat from refined triacylglycerols . LA and ALA are mainly derived from vegetable fats and oils while ARA, DHA and EPA are present only in animal tissue lipids, thus meaning that their intake depends mainly on protein dietary sources. Among fatty acids, the role of DHA with regard to brain and retina development is well known . Beside this property, Weisenger et al. highlighted the possible effect of DHA on blood pressure (BP) control because they observed that DHA deficiency in the perinatal period resulted in increased BP later in life . So these results suggest that perinatal supplementation of long chain polyunsaturated fatty acids (LCPUFA) could prevent hypertension in adulthood .
Heerwagen et al. have suggested that maternal-to-fetal fatty acid transfer depends on elevated maternal body and plasma TG concentration producing increased birthweight, body fat composition and elevated inflammatory cytokines . Oxidative stress and inflammation are particularly influenced by trans fatty acids derived from partially hydrogenated vegetable oils. These conditions during fetal life predispose to hyperphagia, obesity, IR and diabetes .
Finally it should be mentioned that air and food pollutants may impact on fetal development as demonstrated benzopyrene exposure that may impair fetal growth, particularly in genetically susceptible populations carrying the variant Val allele on the GSTP1 gene .
Several studies and statements have demonstrated the potential benefits of breastfeeding on CVD risk reduction.
Human milk is a complex fluid secreted by the mammary gland, containing carbohydrates and salts in solution, casein in colloidal dispersion, cells and cellular debris, and lipids mostly in emulsified globules . In addition human milk contains essential fatty acids, hormones, growth factors, immune-related components, enzymes, polyamines and other biologically active compounds, which may play a relevant role in the health benefits associated with breastfeeding .
Concerning human milk lipids (which content is around 50%), they are represented by triacylglycerols (98%), phospholipids (0.8%), cholesterol (0.5%) and many others. The major monounsaturated fatty acid (MUFA), the oleic acid, in addition to the usual role of energy source and structural components, facilitates triacylglycerols metabolism of milk fat globules. Nowadays fatty acids trans-isomers represent a hot topic: they originate from the maternal diet, are secreted into human milk and exert damaging effects on infant development, as previous reported by Carlson et al..
Exclusive breastfeeding for at least 6 months has been recommended by the European Society of Pediatric Gastroenterology Hepatology and Nutrition (ESPGHAN) because human milk properties are important in promoting optimal growth, neurocognitive development, resistance to infections and cardiovascular health [47, 49, 50]. Several studies have reported beneficial effects on dyslipidemia, hypertension, reduced glucose tolerance, overweight/obesity prevention.
Data accumulated over the last years have suggested that breastfeeding influences lipid metabolism, determining lower levels of total cholesterol (TC) in adulthood. Owen et al. in a systematic review observed higher TC concentrations in breast-fed than in formula-fed infants (<12 months), because of an higher cholesterol content in human milk than in infant formulae (mean TC difference 0.64, 95% CI 0.50 to 0.79 mmol/L), while adulthood TC levels resulted lower in those breast-fed in infancy (mean TC difference −0.18, 95% CI −0.30 to −0.06 mmol/L) . These data were further confirmed by a meta-analysis conducted by the World Health Organization (WHO) .
These results suggest a possible effect of breast milk on lipid metabolism by a “nutritional programming” consequent to an early exposure to human milk high cholesterol content. This stimulus may modulate cholesterol metabolism by regulating hydroxymethylglutaril coenzyme A (HMG-CoA) reductase activity or by increasing LDL-receptor activity .
The impact of breastfeeding on BP is controversial. In a meta-analysis by Owen et al. a slight mean difference in systolic BP (SBP) of −1.10 mmHg (95% CI −1.79 to −0.42) was found in subjects breast-fed while no difference was observed for diastolic BP (DBP) later in life. A subsequent meta-analysis in 2005, including approximately 10.000 subjects from 3 studies, demonstrated a difference in SBP of −1.4 mmHg (95% CI −2.2 to −0.6) and in DBP of −0.5 mmHg (95% CI −0.9 to −0.04) in adults previously breast-fed . These data were confirmed by a meta-analysis conducted by WHO . Martin et al. reported that breastfeeding was associated with a lower BP at the age of 7.5 years in children born at term , but contrasted with PROBIT study results which did not demonstrate any effect of breastfeeding on BP in children 6.5 years aged . Further a negative association between breastfeeding duration and later BP was observed [55, 57].
A possible explanation of the role of human milk in reducing BP is represented by the low sodium content [57, 58] associated with the LCPUFA high concentration. LCPUFA are incorporated into cell membranes of the vascular endothelium and increase endothelial nitric oxide synthesis . Further it has been demonstrated that the dietary supplementation with LCPUFA, from birth to 6 months, is associated with a significant reduction in mean BP and DBP at the age of 6 years . Another possible relevant effect can be exerted by human milk lower protein amount compared to infant formulae. The latter higher protein intake could stimulate insulin secretion, thus promoting IR which in turn may increase BP via several mechanisms as stimulation of the sympathetic nervous system, smooth muscle hypertrophy and increased renal sodium retention .
A protective role of breastfeeding against glucose intolerance and T2DM development has been demonstrated in several studies. Owen et al. highlighted, in a review including results from 7 studies, the possible preventive effect of breastfeeding on T2DM development (OR 0.61, 95% CI 0.41-0.85). These results evidenced lower blood glucose and serum insulin levels in infancy and lower insulin levels later in life . Similar results were also reported in the WHO meta-analysis . These effects can be attributed to human milk components, in particular to hormones such as leptin, adiponectin, resistin and ghrelin . Considering leptin, it plays a fundamental role in glucose metabolism regulation since early life. This hormone, particularly, improves insulin sensitivity by reducing intracellular lipid levels in liver, skeletal muscle and pancreatic β-cells . Also adiponectin contributes to regulate glucose homeostasis: it increases insulin action in the liver as well as glucose metabolism in the skeletal muscle . It should be remarked that adiponectin correlates with neonatal growth parameters and adiposity. Further resistin shows a role in maintaining metabolic neonatal homeostasis and it may exert little or no contribution to IR . Considering ghrelin, there are contrasting data about its influence on insulin secretion .
Breastfeeding could play a key role in preventing overweight/obesity across the life course as reported by numerous systematic reviews and reports [67–71]. But how breastfeeding exert these effects? Breastfeeding potential benefits on body composition may be due to the slower pattern of growth, in particular related to the weight gain, in breastfed compared with formula-fed infants , so the former show a lower risk of obesity. These outcome difference could be explained by human and formula milk composition and by infants’ nutritional behaviour.
About formula and human milk composition, the latter has a lower protein and a slightly lower energy content. It has been demonstrated that a high protein intake in infancy enhances the secretion of insulin and insulin growth factor 1 (IGF-1) thus stimulating cell proliferation, accelerating growth and increasing adipose tissue deposition, with an early occurrence of adiposity rebound . These evidences have been confirmed in a randomized clinical trial, by Koletzko et al., who found a positive association between infant formula protein content and higher weight gain in the first 2 years of life . Further in recent years it has been better understood the role of breast milk hormones on obesity prevention: leptin, adiponectin, IGF-1, ghrelin, obestatin and resistin regulate energy balance and food intake and modulate neuroendocrine mechanism involved in body weight regulation .
From a behavioural point of view a possible explanation could be the self regulation achieved by breast-fed babies that persist later in life .
Introduction of complementary foods
Recommendations by ESPGHAN Committee on Nutrition have suggested that exclusive breastfeeding should be pursued for around 6 months to achieve optimal growth, development and health  and complementary foods could be introduced between 17 and 26 weeks . At this time human milk would be insufficient to satisfy energy, protein, some fat-soluble vitamins and micronutrients requirements. Among weaning timing determinants, it has been observed that infant weight plays an important role as heavier infants tended to be weaned earlier than age-matched lighter infants . About the relationship between new food introduction and infant growth, Wilson et al. demonstrated a higher prevalence of obese children at 7 years of age among those who were given solid food before 12 weeks of age .
Several studies evaluated the relationship between protein intake from complementary foods and obesity risk. Some data have demonstrated that a protein intake of 4–5 g/kg wt per day (corresponding to 16-20% of total energy intake) at the age of 8–24 months is associated to an overweight higher risk later in life . This association was not observed when a dietary protein intake was limited to 3.75 g/kg wt per day (corresponding to 15% of total energy intake) . The association between high-protein intake and early adiposity rebound has been explained by Agostoni et al. and Ketelslegers et al.: dietary protein could stimulate the activity of IGF-1, determining both adipocyte differentiation and adipogenesis [73, 79]. About the relationship between protein intake during the complementary period and BP, no definitive conclusions are available at present. Infancy may be a greater salt sensitive period than later life  and it has been demonstrated that an excess of dietary sodium intake in newborns and young infants could raise BP  while a salt restriction during the first year of life significantly slows down the BP rise in childhood . Furthermore the effect of LCPUFA intake during the complementary feeding period on later BP was considered by a trial in which 9-month-old infants were randomized to receive a fish oil supplement for 3 months or no supplement . At 12 months a lower SBP (−6 mmHg) was reported in those children who received fish oil supplementation. These results are in accordance with the follow-up study by Forsyth et al..
Concerning the fat intake during the weaning period, several studies did not found any association with subsequent weight or fatness in infants and children [84, 85]. In the DONALD Study Karaolis et al. demonstrated that, among normal growers, a high fat intake at both 12 and 18–24 months resulted in a normal decrease in body fat composition between 2 and 5 years, on the contrary to rapid growers . Further a significant association between fat intake and subsequent weight and body fat mass was observed after 2 years of age. So these evidences suggest that fat intake should not be restricted during the first 2 years of life, except for rare lipid disorders which require fat restriction since early infancy. The ESPGHAN Committee on Nutrition has recommended that fat content should provide at least 25% of the total energy intake in order to guarantee a correct growth and neurocognitive development . It has been demonstrated that overconsumption of energy-dense complementary foods could induce excessive weight gain in infancy, with an higher risk of obesity in childhood and adulthood [86, 87].So the quantity and the quality of foods given during the weaning period are fundamental, in particular as feeding practices during the first year of life provide the basis for food habits in childhood and impact on later health in adulthood.
Nutrition in childhood and adolescence
Nutrition in childhood and adolescence may play a relevant role in the development of CVD in adulthood. The National Cholesterol Education Program Pediatric Panel Report provided dietary recommendations for all children as part of a population-based approach to reduce CVD risk for the first time in 1992 . These recommendations were revised in 1998  and 2008 . In addition in 2011 the Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents published a Summary Report which provided evidences regarding the efficacy of specific dietary intervention to reduce CVD risk .
It has been suggested that the total fat intake should be limited to 30% of daily calories, saturated fat intake limited to 7-10% of calories and dietary cholesterol limited to 200–300 mg/day. The remaining fat intake should derived from MUFA (10%) and polyunsaturated fatty acids (PUFA) (10%); further trans fatty acids should be avoided. Protein and carbohydrate intakes should account for 15-20% and 50-55% of daily calories, respectively. These dietary indications, concerning in particular daily fat intake, are recommended for children older than 2 years .
In the prospective Special Turku Coronary Risk Factor Intervention Project (STRIP), over than 1.000 infants 7 months aged, recruited from the general population, were randomized to receive a low-saturated-fat, low-cholesterol diet (total fat of 30-35% of calories, saturated fat/MUFA+PUFA ratio of 1:2 and cholesterol intake < 200 mg/day) or an unrestricted diet . These subjects were followed up during childhood and adolescence, and parameters including dietary intakes, serum lipids, BP, somatic growth and sexual maturation were monitored. It was demonstrated that intervention boy group had lower cholesterol values than controls between 13 and 60 months of age, while a slightly but no significant difference was found in females. TG concentration instead was similar in the 2 groups . The difference in TC levels was further confirmed in boys at the age of 7 years, together with slightly larger LDL particles in the intervention group , and persisted through at least the first 14 years of life . The effect on LDL particles should be underlined because large LDL are demonstrated to be less atherogenic than small dense LDL. Another significant observation was represented by a lower prevalence of obesity in girls in the intervention group, compared with controls .
In the STRIP study follow-up Niinikoski et al. reported the positive effect of the restriction of saturated fat from infancy until 15 years of age on BP. SBP and DBP resulted 1.0 mm Hg lower (95% CI for systolic: -1.7 to −0.2; 95% CI for diastolic: -1.5 to −0.4) in children receiving low-saturated-fat counselling than in control children . The explanation of these BP variations in the intervention group can be partly attributed to the quality of fats assumed, rather than the quantity, as saturated fat intake can determine central obesity, related to insulin sensitivity. The latter resulted improved during the intervention period, thus contributing to lower BP . Other variables such as a higher intake of PUFA, a higher protein intake, fibers amount, or a combination of all of these, can exert a significant effect on BP. Overall it should be underlined that STRIP supervised dietary regimen reduces the exposure to cardiovascular risks without any adverse effects on growth, cognitive and pubertal development.
The relationship between BP and dietary macronutrients in children have been estimated by other studies, with contrasting findings. Boulton J. observed that greater intakes of energy, fats, and carbohydrates were associated with lower BP in 2 years old children while no any association with protein intake was detected . On the contrary, Ulbak et al. did not found any association between BP and intakes of fats, saturated fatty acids, PUFA, while a negative association between MUFA intake (daily energy percentage and g per day) and SBP was reported. This study also demonstrated that protein intake, expressed as daily energy percentage and as g per day, was significantly associated with lower SBP and DBP in 2.5 years old children . Concerning gender, Jenner DA et al. observed in 9 years old Australian children that SBP was negatively associated to calorie-adjusted protein intake in girls, while no detectable relationships between BP and calorie-adjusted intakes of fats, carbohydrates, sodium, potassium, calcium, magnesium was reported . The possible effect of protein on BP could be explained by the vasodilating properties of certain amino acids, which determine an increased production of nitric oxide . Fiber intake might also influence children’s BP [99, 102].
It has been reported by many studies that BP tracks from early childhood into adulthood . Recent data from the Cardiovascular Risk in Young Finns Study have been published about the relationship between childhood diet, with particular regard to fatty acids quality, and BP in adulthood in more than 800 individuals who participate in the 27 years follow-up. Kaikkonen et al. have highlighted the positive independent association between childhood serum cholesterol ester fatty acid (CEFA) proportion and SBP and DBP in adolescence and adulthood . These results were stronger in men than in women and stronger for SBP than for DBP. In particular fatty acids derived from animal fats of dietary origin seemed to be linked with higher BP in adulthood, while fatty acids derived from vegetable oils and margarine appeared to be associated with lower BP. Looking at fatty acids fractions, in men the proportions of saturated fatty acids, MUFA and ω-3 PUFA were positively associated with BP while ω-6 PUFA were negatively associated with BP. In women weaker associations between CEFA proportions and BP were reported.
A dietary intervention is mandatory when CVD risk factors are present since childhood. The Dietary Intervention Study in Children (DISC) evaluated the effect of a restricted saturated fat and cholesterol diet in a cohort of 663 children affected by elevated LDL-C levels, aged 8 to 11 years, with a mean of 7.5 years follow up . It was found that the dietary intervention could improve lipid profile over 3 years with intensive adherence, although not significantly over 5 years, probably as a consequence of a lower-intensity maintenance intervention. In the DISC study the relationship between dietary nutrients and BP was also investigated . Controlling for all nutrients, total fats were significantly directly associated with both SBP and DBP, and fiber was significantly inversely associated with DBP. So these results provide evidence of the potential role of dietary fats, and possibly fiber, on BP levels in children. Further studies are required to provide conclusive findings.
Other dietary measures useful for CVD prevention such as to encourage high dietary fiber intake from food, to avoid sugar-sweetened beverage intake, and to limit sodium intake were suggested by the Expert Panel . Dietary fiber is an important constituent of diet: it promotes gastrointestinal function and helps to prevent CVD risk factors by lowering serum total and LDL-C  and serum insulin concentrations and by reducing the risk of obesity as demonstrated in young adults . Dietary fiber intake is inversely associated with energy density and with increased levels of body fat and is positively associated with nutrient density. A daily dietary fiber intake of at least age plus 5 g for young children up to 14 g/1.000 kcal for older children and adolescents is recommended.
Several evidences have demonstrated that high added sugar consumption, in particular in the form of sugar-sweetened beverages, is associated with cardiovascular risk factors, both independently and through the development of obesity [109, 110].
A healthy dietary model widely recognized is represented by the Mediterranean diet. The beneficial effects of this food intake regimen on CVD and other major chronic diseases have been demonstrated by several studies in different populations, in epidemiological, population based and randomised clinical trials [111–113]. The traditional components of this dietary pattern are represented by whole cereals (complex carbohydrates), vegetables and fruits (fiber, vitamins, antioxidants), nuts (PUFA), legumes (vegetal proteins), fish (proteins and PUFA) and virgin olive oil (MUFA and antioxidants). Serra-Majem et al. demonstrated in a cohort of more than 3.000 Spanish subjects, aged 6–24 years, the high nutritional quality of the Mediterranean diet, particularly in children and adolescents . In a recent meta-analysis by Nordmann et al. considering overweight/obese adults with at least one additional cardiovascular risk factor, the Mediterranean diet appeared to be more effective than low-fat diets in inducing clinically relevant long-term changes in CVD risk factors and inflammatory markers . Thus this dietary pattern should be promoted since childhood and adolescence in order to prevent CVD later in life.
This review highlights several evidences from epidemiological, population based and randomized clinical trials taking in account the nutrition impact on CVD burden.
Maternal nutritional status represents a potential determinant of metabolic programming and body composition affecting fetal life ongoing. This programming extends also into infancy and childhood: the quantity of energy intake and particularly the quality of macronutrients influence growth and CVD risk factor development.
Finally this relevant body of knowledge should be considered in the clinical practice, since prenatal life, in order to develop preventive and intervention strategies to promote health across life course, aimed to CVD prevention.
Coronary artery disease
Cholesterol ester fatty acid
Dietary interventio dietary intervention study in children
European society of pediatric gastroenterology hepatology and nutrition
Fetal origins of adult disease
High-density lipoprotein cholesterol
Hydroxymethylglutaril coenzyme A
Insulin growth factor 1
Long chain polyunsaturated fatty acids
Low-density lipoprotein cholesterol
Monounsaturated fatty acid
Polyunsaturated fatty acids
Special turku coronary risk factor intervention project
Type 2 diabetes mellitus
World health organization.
McGill HC, McMahan CA, Zieske AW, Sloop GD, Walcott JV, Troxclair DA, Malcom GT, Tracy RE, Oalmann MC, Strong JP: Associations of coronary heart disease risk factors with the intermediate lesion of atherosclerosis in youth. The Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Research Group. Arterioscler Thromb Vasc Biol. 2000, 20: 1998-2004. 10.1161/01.ATV.20.8.1998.
Berenson GS, Srinivasan SR, Bao W, Newman WP, 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. 10.1056/NEJM199806043382302.
Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents: Summary Report. 2011, available online http://www.nhlbi.nih.gov/guidelines/cvd_ped/index.htm
Weintraub WS, Daniels SR, Burke LE, Franklin BA, Goff DC, Hayman LL, Lloyd-Jones D, Pandey DK, Sanchez EJ, Schram AP, Whitsel LP, American Heart Association Advocacy Coordinating Committee; Council on Cardiovascular Disease in the Young; Council on the Kidney in Cardiovascular Disease; Council on Epidemiology and Prevention; Council on Cardiovascular Nursing; Council on Arteriosclerosis; Thrombosis and Vascular Biology; Council on Clinical Cardiology, and Stroke Council: Value of primordial and primary prevention for cardiovascular disease: a policy statement from the American Heart Association. Circulation. 2011, 124: 967-990. 10.1161/CIR.0b013e3182285a81.
Barker DJP: Mothers, Babies and Health in Later Life. 1998, London, UK: Churchill Livingstone
Barker DJP: The developmental origins of adult disease. J Am Col. Nutr. 2004, 23: 588S-595S.
Barker DJP: The origins of the developmental origins theory. J Intern Med. 2007, 261: 412-417. 10.1111/j.1365-2796.2007.01809.x.
Barker DJP: Fetal origins of coronary artery disease. BMJ. 1995, 311: 171-174. 10.1136/bmj.311.6998.171.
Barker DJ, Hales CN, Fall CH, Osmond C, Phipps K, Clark PM: Type 2 (non-insulin-dependent) diabetes mellitus, hypertension and hyperlipidaemia (syndrome X): relation to reduced fetal growth. Diabetologia. 1993, 36: 62-67. 10.1007/BF00399095.
Calkins K, Devaskar SU: Fetal origins of adult disease. Curr Probl Pediatr Adolesc Health Care. 2011, 41: 158-176. 10.1016/j.cppeds.2011.01.001.
Hanson MA, Low FM, Gluckman PD: Epigenetic epidemiology: the rebirth of soft inheritance. Ann Nutr Metab. 2011, 58: 8-15.
Handel AE, Ebers GC, Ramagopalan SV: Epigenetics: molecular mechanisms and implications for disease. Trends Mol Med. 2009, 16: 7-16.
Sebert S, Sharkey D, Budge H, Symonds ME: The early programming of metabolic health: is epigenetic setting the missing link?. Am J Clin Nutr. 2011, 94: 1953S-1958S. 10.3945/ajcn.110.001040.
Tarry-Adkins JL, Ozane SE: Mechanism of early life programming: current knowledge and future directions. Am J Clin Nutr. 2011, 94: 1765S-1771S. 10.3945/ajcn.110.000620.
Kajantie E, Osmond C, Barker DJ, Forsén T, Phillips DI, Eriksson JG: Size at birth as a predictor of mortality in adulthood: a follow-up of 350 000 person-years. Int J Epidemiol. 2005, 34: 655-663.
Leon DA, Lithell HO, Vagero D, Koupilová I, Mohsen R, Berglund L, Lithell UB, McKeigue PM: Reduced fetal growth rate and increased risk of death from ischaemic heart disease: cohort study of 15 000 Swedish men and women born 1915–29. Br J Med. 1998, 317: 241-245. 10.1136/bmj.317.7153.241.
Barker DJP, Osmond C, Golding J, Kuh D, Wadsworth ME: Growth in utero, blood pressure in childhood and adult life, and mortality from cardiovascular disease. BMJ. 1989, 298: 564-567. 10.1136/bmj.298.6673.564.
Pereira JA, Rondo PHC, Lemos JO, de Pacheco SJM, Dias RSC: The influence of birthweight on arterial blood pressure of children. Clin Nutr. 2010, 29: 337-340. 10.1016/j.clnu.2010.01.005.
Norman M: Low birth weight and the developing vascular tree: a systematic review. Acta Paediatr. 2008, 97: 1165-1172. 10.1111/j.1651-2227.2008.00904.x.
Chiavaroli V, Giannini C, D’Adamo E, de Giorgis T, Chiarelli F, Mohn A: Insulin resistance and oxidative stress in children born small and large for gestational age. Pediatrics. 2009, 124 (2): 695-702. 10.1542/peds.2008-3056.
Meas T: Fetal origins of insulin resistance and the metabolic syndrome: A key role for adipose tissue?. Diabetes Metab. 2010, 36: 11-20. 10.1016/j.diabet.2009.09.001.
de Rooij SR, Painter RC, Philips DI, Osmond C, Michels RP, Godsland IF, Bossuyt PM, Bleker OP, Roseboom TJ: Impaired insulin secretion after prenatal exposure to the Dutch famine. Diabetes Care. 2006, 29: 1897-1901. 10.2337/dc06-0460.
Ravelli AC, van der Meulen JH, Osmond C, Barker DJ, Bleker OP: Obesity at the age of 50 y in men and women exposed to famine prenatally. Am J Clin Nutr. 1999, 70: 811-816.
Painter RC, de Rooij SR, Bossuyt PM, Simmers TA, Osmond C, Barker DJ, Bleker OP, Roseboom TJ: Early onset of coronary artery disease after prenatal exposure to the Dutch famine. Am J Clin Nutr. 2006, 84: 322-327.
Roseboom T, de Rooij S, Painter R: The Dutch famine and its long-term consequences for adult health. Early Hum Dev. 2006, 82: 485-491. 10.1016/j.earlhumdev.2006.07.001.
Hales CN, Barker DJ: The thrifty phenotype hypothesis. Br Med Bull. 2001, 60: 5-20. 10.1093/bmb/60.1.5.
Phillips DIW: Insulin resistance as a programmed response to fetal undernutrition. Diabetologia. 1996, 39: 1119-1122. 10.1007/BF00400663.
Lithell HO, McKeigue PM, Berglund L, Mohsen R, Lithell UB, Leon DA: Relation of size at birth to non-insulin dependent diabetes and insulin concentrations in men aged 50–60 years. BMJ. 1996, 312: 406-410. 10.1136/bmj.312.7028.406.
Kensara OA, Wootton SA, Phillips DI, Patel M, Jackson AA, Elia M, Hertfordshire Study Group: Programming of body composition: relation between birth weight and body composition measured with dual-energy X-ray absorptiometry and anthropometric methods in older Englishmen. Am J Clin Nutr. 2005, 82: 980-987.
Brenner BM, Chertow GM: Congenital oligonephropathy: an inborn cause of adult hypertension and progressive renal injury?. Curr Opin Nephrol Hypertens. 1993, 2: 691-695. 10.1097/00041552-199309000-00001.
Poston L, Harthoorn LF, Van Der Beek EM: Contributors to the ILSI Europe Workshop: obesity in pregnancy: implications for the mother and lifelong health of the child. A consensus statement. Pediatr Res. 2011, 69: 175-180. 10.1203/PDR.0b013e3182055ede.
Tam WH, Ma RC, Yang X, Li AM, Ko GT, Kong AP, Lao TT, Chan MH, Lam CW, Chan JC: Glucose intolerance and cardiometabolic risk in adolescents exposed to maternal gestational diabetes: a 15-year follow-up study. Diabetes Care. 2010, 33: 382-384.
Innis SM: Essential fatty acid transfer and fetal development. Placenta. 2005, 26: S70-S75.
Innis SM: Metabolic programming of long-term outcomes due to fatty acid nutrition in early life. Matern Child Nutr. 2011, 7: 112-123.
Smith CE, Ordovás JM: Fatty acid interactions with genetic polymorphisms for cardiovascular disease. Curr Opin Clin Nutr Metab Care. 2010, 13 (2): 139-144. 10.1097/MCO.0b013e3283357287.
Corella D, Ordovás JM: Interactions between dietary n-3 fatty acids and genetic variants and risk of disease. Br J Nutr. 2012, 107 (Suppl 2): S271-283.
Hadders-Algra M: Prenatal long-chain polyunsaturated fatty acid status: the importance of a balanced intake of docosahexaenoic acid and arachidonic acid. J Perinat Med. 2008, 36: 101-109.
Weisinger HS, Armitage JA, Sinclair AJ, Vingrys AJ, Burns PL, Weisinger RS: Perinatal omega-3 deficiency affects blood pressure in later in life. Nat Med. 2001, 7: 258-259. 10.1038/85354.
Das UN: Can perinatal supplementation of long-chain polyunsaturated fatty acids prevent hypertension in adult life?. Hypertension. 2001, 38: E6-E8. 10.1161/01.HYP.38.1.6.
Heerwagen MJ, Miller MR, Barbour LA, Friedman JE: Maternal obesity and fetal metabolic programming: a fertile epigenetic soil. Am J Physiol Regul Integr Comp Physiol. 2010, 299: R711-R722. 10.1152/ajpregu.00310.2010.
Campbell DM, Hall MH, Barker DJ, Cross J, Shiell AW, Godfrey KM: Diet in pregnancy and the offspring’s blood pressure 40 years later. Br J Obstet Gynaecol. 1996, 103: 273-280. 10.1111/j.1471-0528.1996.tb09718.x.
Adair LS, Kuzawa CW, Borja J: Maternal energy stores and diet composition during pregnancy program adolescent blood pressure. Circulation. 2001, 104: 1034-1039. 10.1161/hc3401.095037.
Leary SD, Ness AR, Emmett PM, Davey SG, Headley JE: Maternal diet in pregnancy and offspring blood pressure. Arch Dis Child. 2005, 90: 492-493. 10.1136/adc.2004.070698.
Huh SY, Rifas-Shiman SL, Kleinman KP, Rich-Edwards JW, Lipshultz SE, Gillman MW: Maternal protein intake is not associated with infant blood pressure. Int J Epidemiol. 2005, 34: 378-384. 10.1093/ije/dyh373.
Duarte-Salles T, Mendez MA, Morales E, Bustamante M, Rodríguez-Vicente A, Kogevinas M, Sunyer J: Dietary benzo(a)pyrene and fetal growth: Effect modification by vitamin C intake and glutathione S-transferase P1 polymorphism. Environ Int. 2012, 45: 1-8.
Jensen RG: Lipids in human milk. Lipids. 1999, 34: 1243-1271. 10.1007/s11745-999-0477-2.
Agostoni C, Braegger C, Decsi T, Kolacek S, Koletzko B, Fleischer Michaelsen K, Mihatsch W, Moreno LA, Puntis J, Shamir R, Szajewska H, Turck D, van Goudoever J, ESPGHAN Committee on Nutrition: Breast-feeding: a commentary by the ESPGHAN committee on nutrition. J Pediatr Gastroenterol Nutr. 2009, 49: 112-125. 10.1097/MPG.0b013e31819f1e05.
Carlson SE, Clandinin MT, Cook HW, Emken EA, Filer LJ: Trans fatty acids: infant and fetal development. Am J Clin Nutr. 1997, 66: 717S-736S.
Agostoni C, Baselli L, Mazzoni MB: Early nutrition patterns and diseases of adulthood: a plausible link?. Eur J Intern Med. 2012, in press
Owen CG, Whincup PH, Odoki K, Gilg JA, Cook DG: Infant feeding and blood cholesterol: a study in adolescents and a systematic review. Pediatrics. 2002, 110: 597-608. 10.1542/peds.110.3.597.
World Health Organization: Evidence on the long-term effects of breastfeeding. Systematic reviews and meta-analyses. 2007, Geneva, Switzerland: WHO Press, World Health Organization, Available at http://whqlibdoc.who.int/publications/2007/
Wong WW, Hachey DL, Insull W, Opekun AR, Klein PD: Effect of dietary cholesterol on cholesterol synthesis in breast-fed and formula-fed infants. J Lipid Res. 1993, 34: 1403-1411.
Owen CG, Whincup PH, Gilg JA, Cook DG: Effect of breast feeding in infancy on blood pressure in later life: systematic review and meta-analysis. BMJ. 2003, 327: 1189-1195. 10.1136/bmj.327.7425.1189.
Martin RM, Gunnell D, Davey SG: Breastfeeding in infancy and blood pressure in later life: systematic review and meta-analysis. Am J Epidemiol. 2005, 161: 15-26. 10.1093/aje/kwh338.
Martin RM, Ness AR, Gunnell D, Emmet P, Davey SG: Does breastfeeding in infancy lower blood pressure in childhood? the Avon longitudinal study of parents and children (ALSPAC). Circulation. 2004, 109: 1259-1266. 10.1161/01.CIR.0000118468.76447.CE.
Kramer MS, Matush L, Vanilovich I, Platt RW, Bogdanovich N, Sevkovskaya Z, Dzikovich I, Shishko G, Collet JP, Martin RM, Davey Smith G, Gillman MW, Chalmers B, Hodnett E, Shapiro S, PROBIT Study Group: Effects of prolonged and exclusive breastfeeding on child height, weight, adiposity, and blood pressure at age 6.5 y: evidence from a large randomized trial. Am J Clin Nutr. 2007, 86: 1717-1721.
Wilson AC, Forsyth JS, Greene SA, Irvine L, Hau C, Howie PW: Relation of infant diet to childhood health: 7 year follow up of cohort children in Dundee infant feeding study. BMJ. 1998, 316: 21-25. 10.1136/bmj.316.7124.21.
Taittonen L, Nuutinen M, Turtinen J, Uhari M: Prenatal and postnatal factors in predicting later blood pressure among children: cardiovascular risk in young Finns. Pediatr Res. 1996, 40: 627-632. 10.1203/00006450-199610000-00019.
Das UN: A perinatal strategy to prevent coronary heart disease. Nutrition. 2003, 19: 1022-1027. 10.1016/j.nut.2003.08.002.
Forsyth JS, Willatts P, Agostoni C, Bissenden J, Casaer P, Boehm G: Long chain polyunsaturated fatty acid supplementation in infant formula and blood pressure in later childhood: follow-up of a randomised controlled trial. BMJ. 2003, 326: 953-959. 10.1136/bmj.326.7396.953.
Axelsson IE, Ivarsson SA, Raiha NC: Protein intake in early infancy: effects on plasma amino acid concentrations, insulin metabolism, and growth. Pediatr Res. 1989, 26: 614-617.
Owen CG, Martin RM, Whincup PH, Smith GD, Cook DG: Does breastfeeding influence risk of type 2 diabetes in later life? a quantitative analysis of published evidence. Am J Clin Nutr. 2006, 84: 1043-1054.
Savino F, Liguori SA, Sorrenti M, Fissore MF, Oggero R: Breast milk hormones and regulation of glucose homeostasis. Int J Pediatr. 2011, 803985-
Dyck DJ: Adipokines as regulators of muscle metabolism and insulin sensitivity. Appl Physiol Nutr Metab. 2009, 34: 396-402. 10.1139/H09-037.
Pajvani UB, Du X, Combsetal TP: Structure-function studies of the adipocyte-secreted hormone Acrp30/adiponectin: implications for metabolic regulation and bioactivity. J Biol Chem. 2003, 278: 9073-9085. 10.1074/jbc.M207198200.
Owecki M, Miczke A, Nikisch E, Pupek-Musialik D, Sowiski J: Serum resistin concentrations are higher in human obesity but independent from insulin resistance. Exp Clin Endocrinol Diabetes. 2011, 119: 117-121. 10.1055/s-0030-1263111.
Evelein AMV, Geerts CC, Visseren FLJ, Bots ML, van der Ent CK, Grobbee DE, Uiterwaal CSPM: The association between breastfeeding and the cardiovascular system in early childhood. Am J Clin Nutr. 2011, 93: 712-718. 10.3945/ajcn.110.002980.
Wu TC, Chen PH: Health consequences of nutrition in childhood and early infancy. Pediatr Neonatol. 2009, 50: 135-142. 10.1016/S1875-9572(09)60051-6.
Owen CG, Martin RM, Whincup PH, Smith GD, Cook DG: Effect of infant feeding on the risk of obesity across the life course: a quantitative review of published evidence. Pediatrics. 2005, 115: 1367-1377. 10.1542/peds.2004-1176.
Harder T, Bergmann R, Kallischnigg G, Plagemann A: Duration of breastfeeding and risk of overweight: a meta- analysis. Am J Epidemiol. 2005, 162: 397-403. 10.1093/aje/kwi222.
Robinson SM, Marriott LD, Crozier SR, Harvey NC, Gale CR, Inskip HM, Baird J, Law CM, Godfrey KM, Cooper C, Southampton Women’s Survey Study Group: Variations in Infant Feeding Practice Are Associated with Body Composition in Childhood: A Prospective Cohort Study. J Clin Endocrinol Metab. 2009, 94: 2799-2805. 10.1210/jc.2009-0030.
Singhal A, Lanigan J: Breastfeeding, early growth and later obesity. Obes Rev. 2007, 8: 51-54. 10.1111/j.1467-789X.2007.00318.x.
Agostoni C, Scaglioni S, Ghisleni D, Verduci E, Giovannini M, Riva E: How much protein is safe?. Int J Obes. 2005, 29: S8-S13.
Koletzko B, von Kries R, Closa R, Escribano J, Scaglioni S, Giovannini M, Beyer J, Demmelmair H, Gruszfeld D, Dobrzanska A, Sengier A, Langhendries JP, Rolland CMF, Grote V, European Childhood Obesity Trial Study Group: Lower protein in infant formula is associated with lower weight up to age 2 y: a randomized clinical trial. Am J Clin Nutr. 2009, 89: 1836-1845. 10.3945/ajcn.2008.27091.
Savino F, Liguori SA, Fissore MF, Oggero R: Breast milk hormones and their protective effect on obesity. Int J Ped Endocr. 2009, 327505-
Agostoni C, Decsi T, Fewtrell M, Goulet O, Kolacek S, Koletzko B, Michaelsen KF, Moreno L, Puntis J, Rigo J, Shamir R, Szajewska H, Turck D, Van Goudoever J, ESPGHAN Committee on Nutrition: Complementary feeding: a commentary by the ESPGHAN Committee on Nutrition. J Pediatr Gastroenterol Nutr. 2008, 46: 99-110. 10.1097/01.mpg.0000304464.60788.bd.
Forsyth JS, Ogston SA, Clark A, Florey CD, Howie PW: Relation between early introduction of solid food to infants and their weight and illnesses during the first two years of life. BMJ. 1993, 306: 1572-1576. 10.1136/bmj.306.6892.1572.
Hoppe C, Molgaard C, Thomsen BL, Juul A, Michaelsen KF: Protein intake at 9 mo of age is associated with body size but not with body fat in 10-year-old Danish children. Am J Clin Nutr. 2004, 79: 494-501.
Ketelslegers JM, Maiter D, Maes M, Underwood LE, Thissen JP: Nutritional regulation of insulin-like growth factor-1. Metabolism. 1995, 44: 50-57.
Dahl LK, Heine M, Tassinari L: High salt content of western infant’s diet: possible relationship to hypertension in the adult. Nature. 1963, 198: 1204-1205. 10.1038/1981204a0.
Strazzullo P, Campanozzi A, Avallone S: Does salt intake in the first two years of life affect the development of cardiovascular disorders in adulthood?. Nutr Metab Cardiovasc Dis. 2012, in press
Geleijnse JM, Hofman A, Witteman JCM, Hazebroek AJM, Valkenburg HA, Grobbee DE: Long-term effects of neonatal sodium restriction on blood pressure. Hypertension. 1997, 29: 913-917. 10.1161/01.HYP.29.4.913.
Damsgaard CT, Schack-Nielsen L, Michaelsen KF, Fruekilde MB, Hels O, Lauritzen L: Fish oil affects blood pressure and the plasma lipid profile in healthy Danish infants. J Nutr. 2006, 136: 94-99.
Karaolis-Danckert N, Gunther ALB, Kroke A, Hornberg C, Buyken AE: How early dietary factors modify the effect of rapid weight gain in infancy on subsequent body-composition development in term children whose birth weight was appropriate for gestational age. Am J Clin Nutr. 2007, 86: 1700-1708.
Macé K, Shahkhalili Y, Aprikian O, Stan S: Dietary fat and fat types as early determinants of childhood obesity: a reappraisal. Int J Obes. 2006, 30: S50-S57.
Baird J, Fisher D, Lucas P, Kleijnen J, Roberts H, Law C: Being big or growing fast: systematic review of size and growth in infancy and later obesity. BMJ. 2005, 331: 929-934. 10.1136/bmj.38586.411273.E0.
Ong K, Loos R: Rapid infancy weight gain and subsequent obesity: systematic reviews and hopeful suggestions. Acta Paediatr. 2006, 95: 904-908. 10.1080/08035250600719754.
American Academy of Pediatrics: National cholesterol education program: report of the expert panel on blood cholesterol levels in children and adolescents. Pediatrics. 1992, 89: 525-584.
American Academy of Pediatrics. Committee on Nutrition: Cholesterol in Childhood. Pediatrics. 1998, 101: 141-147.
Daniels SR, Greer FR, Committee on Nutrition: Lipid Screening and Cardiovascular Health in Childhood. Pediatrics. 2008, 122: 198-208. 10.1542/peds.2008-1349.
Simell O, Niinikoski H, Rönnemaa T, Raitakari OT, Lagström H, Laurinen M, Aromaa M, Hakala P, Jula A, Jokinen E, Välimäki I, Viikari J: Cohort Profile: the STRIP Study (Special Turku Coronary Risk Factor Intervention Project), an Infancy-onset Dietary and Life-style Intervention Trial. Int J Epidemiol. 2009, 38: 650-655. 10.1093/ije/dyn072.
Rask-Nissilä L, Jokinen E, Rönnemaa T, Viikari J, Tammi A, Niinikoski H, Seppänen R, Tuominen J, Simell O: Prospective, randomized, infancy-onset trial of the effects of a low-saturated-fat, low-cholesterol diet on serum lipids and lipoproteins before school age the special turku coronary risk factor intervention project (STRIP). Circulation. 2000, 102: 1477-1483. 10.1161/01.CIR.102.13.1477.
Kaitosaari T, Rönnemaa T, Raitakari O, Talvia S, Kallio K, Volanen I, Leino A, Jokinen E, Välimäki I, Viikari J, Simell O: Effect of 7-year infancy-onset dietary intervention on serum lipoproteins and lipoprotein subclasses in healthy children in the prospective, randomized special turku coronary risk factor intervention project for children (STRIP) study. Circulation. 2003, 108: 672-677. 10.1161/01.CIR.0000083723.75065.D4.
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: 1032-1040. 10.1161/CIRCULATIONAHA.107.699447.
Hakanen M, Lagström H, Kaitosaari T, Niinikoski H, Näntö-Salonen K, Jokinen E, Sillanmäki L, Viikari J, Rönnemaa T, Simell O: Development of overweight in an atherosclerosis prevention trial starting in early childhood: the STRIP study. Int J Obes. 2006, 30: 618-626. 10.1038/sj.ijo.0803249.
Niinikoski H, Jula A, Viikari J, Rönnemaa T, Heino P, Lagström H, Jokinen E, Simell O: Blood pressure is lower in children and adolescents with a low-saturated-fat diet since infancy: the special turku coronary risk factor intervention project. Hypertension. 2009, 53: 918-924. 10.1161/HYPERTENSIONAHA.109.130146.
Kaitosaari T, Ronnemaa T, Viikari J, Raitakari OT, Arffman M, Marniemi J, Kallio K, Pahkala K, Jokinen E, Simell O: Low-saturated fat dietary counselling starting in infancy improves insulin sensitivity in 9-year-old healthy children: the Special Turku Coronary Risk Factor Intervention Project for Children (STRIP) Study. Diabetes Care. 2006, 29: 781-785. 10.2337/diacare.29.04.06.dc05-1523.
Boulton J: Nutrition in childhood and its relationship to early somatic growth, body fat, blood pressure and physical fitness. Acta Paediatr Scand Suppl. 1981, 284: 68-79.
Ulbak J, Lauritzen L, Hansen HS, Michaelsen KF: Diet and blood pressure in 2.5-y-old Danish children. Am J Clin Nutr. 2004, 79: 1095-1102.
Jenner DA, English DR, Vandongen R, Beilin LJ, Armstrong BK, Miller MR, Dunbar D: Diet and blood pressure in 9-year-old Australian children. Am J Clin Nutr. 1988, 47: 1052-1059.
Preuss HG, Gondal JA, Lieberman S: Association of macronutrients and energy intake with hypertension. J Am Coll Nutr. 1996, 15: 21-35.
Vandongen R, Jenner DA, English DR: Determinants of blood pressure in childhood and adolescence. J Hypertens. 1989, 71 (suppl): S3-S5.
Elliot WJ: Blood pressure tracking. J Cardiovasc Risk. 1997, 4: 251-256. 10.1097/00043798-199708000-00003.
Kaikkonen JE, Jula A, Mikkila V, Viikari JSA, Moilanen T, Nikkari T, Kahonen M, Lehtimaki T, Raitakari OT: Childhood serum cholesterol ester fatty acids are associated with blood pressure 27 y later in the cardiovascular risk in young finns study. Am J Clin Nutr. 2012, 95: 1422-1431. 10.3945/ajcn.111.030387.
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: the dietary intervention study in children (DISC). JAMA. 1995, 273: 1429-1435. 10.1001/jama.1995.03520420045036.
Simons-Morton DG, Hunsberger SA, Van Horn L, Barton BA, Robson AM, McMahon RP, Muhonen LE, Kwiterovich PO, Lasser NL, Kimm SY, Greenlick MR: Nutrient intake and blood pressure in the Dietary Intervention Study in Children. Hypertension. 1997, 29: 930-936. 10.1161/01.HYP.29.4.930.
Ruottinen S, Lagstrom HK, Niinikoski H, Ronnemaa T, Saarinen M, Pahkala KA, Hakanen M, Viikari JSA, Simell O: Dietary fiber does not displace energy but is associated with decreased serum cholesterol concentrations in healthy children. Am J Clin Nutr. 2010, 91: 651-661. 10.3945/ajcn.2009.28461.
Ludwig DS, Pereira MA, Kroenke CH, Hilner JE, Van Horn L, Slattery ML, Jacobs DR: Dietary fiber, weight gain, and cardiovascular disease risk factors in young adults. JAMA. 1999, 282: 1539-1546. 10.1001/jama.282.16.1539.
Kavey RE: How sweet it is: sugar-sweetened beverage consumption, obesity, and cardiovascular risk in childhood. J Am Diet Assoc. 2010, 110: 1456-1460. 10.1016/j.jada.2010.07.028.
Fiorito LM, Marini M, Francis LA, Smiciklas-Wright H, Birch LL: Beverage intake of girls at age 5 y predicts adiposity and weight status in childhood and adolescence. Am J Clin Nutr. 2009, 90: 935-942. 10.3945/ajcn.2009.27623.
Trichopoulou A, Costacou T, Bamia C, Trichopoulos D: Adherence to a Mediterranean diet and survival in a Greek population. N Engl J Med. 2003, 26: 2599-2608.
Sofi F, Abbate R, Gensini GF, Casini A: Accruing evidence on benefits of adherence to the Mediterranean diet on health: an updated systematic review and meta-analysis. Am J Clin Nutr. 2010, 92: 1189-1196. 10.3945/ajcn.2010.29673.
Sofi F, Cesari F, Abbate R, Gensini GF, Casini A: Adherence to Mediterranean diet and health status: meta-analysis. BMJ. 2008, 337: 1344-1350. 10.1136/bmj.a1344.
Serra-Majem LI, Ribas L, Garcia A, Perez-Rodrigo C, Aranceta J: Nutrient adequacy and Mediterranean Diet in Spanish school children and adolescents. Eur J Clin Nutr. 2003, 57: S35-S39.
Nordmann AJ, Suter-Zimmermann K, Bucher HC, Shai I, Tuttle KR, Estruch R, Briel M: Meta-analysis comparing mediterranean to low-fat diets for modification of cardiovascular risk factors. Am J Med. 2011, 124: 841-851. 10.1016/j.amjmed.2011.04.024.
The authors declare that they have no competing interests.
All the authors contributed to the review and were involved in writing, revising and approving the final draft of the manuscript.
About this article
Cite this article
Guardamagna, O., Abello, F., Cagliero, P. et al. Impact of nutrition since early life on cardiovascular prevention. Ital J Pediatr 38, 73 (2012). https://doi.org/10.1186/1824-7288-38-73
- Prenatal nutrition
- Cardiovascular diseases