Risk Of Disease In Later Life Research Articles

Prenatal Alcohol Exposure and Metabolic Disorders in Pediatrics: The Role of the Oxidative Stress-A Review of the Literature.

Prenatal alcohol exposure is responsible for increasing chronic disease risk in later life, including obesity and metabolic syndrome. Alcohol drinking may compromise endogenous antioxidant capacity, causing an increase in free radicals and reactive oxygen species in the newborn. Excessive reactive oxygen species could attack the cellular proteins, lipids, and nucleic acids, leading to cellular dysfunction. Moreover, oxidative stress could play a crucial role in the altered synthesis and release of neurotrophins and progressive mitochondrial modifications with uncontrolled apoptosis. This narrative review aims to underline the important role of alcohol abuse in oxidative stress events and consequent metabolic and neurocognitive impairments in children exposed to alcohol during gestational life.

On the importance of birth weight in relation to disease risk in later life.

On the importance of birth weight in relation to disease risk in later life.

Prenatal Exposure to Multiple Endocrine-Disrupting Chemicals and Childhood BMI Trajectories in the INMA Cohort Study.

Prenatal exposure to endocrine-disrupting chemicals (EDCs) may disrupt normal fetal and postnatal growth. Studies have mainly focused on individual aspects of growth at specific time points using single chemical exposure models. However, humans are exposed to multiple EDCs simultaneously, and growth is a dynamic process. The objective of this study was to evaluate the associations between prenatal exposure to EDCs and children's body mass index (BMI) growth trajectories using single exposure and mixture modeling approaches. Using data from the INfancia y Medio Ambiente (INMA) Spanish birth cohort (), prenatal exposure to persistent chemicals [hexachlorobenzene (HCB), 4-4'-dichlorodiphenyldichloroethylene (DDE), polychlorinated biphenyls (PCB-138, -150, and -180), 4 perfluoroalkyl substances (PFAS)] and nonpersistent chemicals (8 phthalate metabolites, 7 phenols) was assessed using blood and spot urine concentrations. BMI growth trajectories were calculated from birth to 9 years of age using latent class growth analysis. Multinomial regression was used to assess associations for single exposures, and Bayesian weighted quantile sum (BWQS) regression was used to evaluate the EDC mixture's association with child growth trajectories. In single exposure models exposure to HCB, DDE, PCBs, and perfluorononanoic acid (PFNA) were associated with increased risk of belonging to a trajectory of lower birth size followed by accelerated BMI gain by 19%-32%, compared with a trajectory of average birth size and subsequent slower BMI gain [e.g., relative risk ratio (RRR) per doubling in DDE (95% CI: 1.05, 1.35); RRR for (95% CI: 1.05, 1.66)]. HCB and DDE exposure were also associated with higher probability of belonging to a trajectory of higher birth size and accelerated BMI gain. Results from the BWQS regression showed the mixture was positively associated with increased odds of belonging to a BMI trajectory of lower birth size and accelerated BMI gain (odds ratio per 1-quantile increase of the ; credible interval: 1.03, 2.61), with HCB, DDE, and PCBs contributing the most. This study provides evidence that prenatal EDC exposure, particularly persistent EDCs, may lead to BMI trajectories in childhood characterized by accelerated BMI gain. Given that accelerated growth is linked to a higher disease risk in later life, continued research is important. https://doi.org/10.1289/EHP11103.

Cohort Profile: The Xiamen Pubertal Growth Cohort Longitudinal Study

This cohort was set up to capture pubertal onset among children in China and to analyze how timing of pubertal onset would influence cardiovascular disease risk in later life. Pubertal onset was defined as secondary sexual characteristics (SSC) attained Tanner II stage, which was breast development for girls and testis of 4 mL for boys. Meanwhile, height growth spurt, defined as age of take-off and age of peak height velocity, were also involved to observe the consistency between the three indicators in discriminating pubertal onset. The study was conducted in Xiamen, China from November 2017 to November 2020 with 6-month gaps. One thousand, four hundred and sixteen children from four project schools who had not yet started puberty were involved at baseline. By November 2020, 1272 children were still under follow-up, with 945 (74.3%) of them reaching Tanner II stage. We would continue to follow the pubertal development, as well as change in crucial risk factors for cardiovascular disease in these participants. Evidence from the present cohort study would help to reveal the influence of pubertal growth on long-term cardiovascular health and would be one of the very first studies to provide such evidence from Asian countries.

Physical Activity Interventions to Reduce Metabolic Risk Factors to Cognitive Health

Physical activity is a health-protective factor that can reduce disease risk in later life. Designing interventions that increase physical activity participation are paramount but need to increase potency and reduce the time to effectiveness. This paper aims to outline one transdisciplinary, team science effort to increase behavioral intervention potency through the integration of the autonomous cognition model whereby data guide each decision in developing a school-based physical activity intervention. Examples of data collected by stage and a summary of potential action steps are provided.

Scientific Analysis of Garbhini Ahar as Epigenetics Modifier of Offspring Genetics - A Critical Review

Reproduction is a bliss that aids in transferring genes from one generation to another. Every prospective parent desire procreation of progeny endowed with supreme health throughout whole life. But, in today’ s era due to faulty dietary and lifestyle habits people are not paying attention to their health resulting in rising incidence of chronic health related hazards like, NCD, DM, HTN, Dyslipidemia, allergies in later life. In last few decades, growing number of epidemiological studies provide evidence for association between nutrition during intrauterine life and major risk factors for CVS disorders and metabolic syndrome in adult life known as fetal origin of adult disease. The notion that intrauterine environmental factors can reset physiological parameters and the resetting can endure into adulthood and can even affect the following generation is known as fetal programming Ayurveda is far advanced as the concept of Garbhini paricharya particularly concept of month wise dietary regime is highly scientific and practical in terms of modern scientific knowledge. On screening the dietary articles mentioned for pregnant lady, it was found that every single fact pertaining to maternal diet mentioned in Ayurvedic text is scientific and has potential to modify the genome/phenotypic expression. Although these ancient dietary approaches have been successfully practiced from millennia but in present era elucidation of these approaches will improve the fidelity of Ayurvedic antenatal care as well as pave the way for future disease prevention. By focusing on Garbhini swasthavritta (pregnancy diet and lifestyle regimens) mentioned in Ayurveda we can reprogram the epigenetic modifications associated with increased disease risk in later life. Ghrita, milk and honey are very essential component of diet during pregnancy and should be consumed regularly. These dietary guidelines should be inoculated into general public for future imprinting of our next generation.

The Role of Human Milk Lipids and Lipid Metabolites in Protecting the Infant against Non-Communicable Disease.

Non-communicable diseases continue to increase globally and have their origins early in life. Early life obesity tracks from childhood to adulthood, is associated with obesity, inflammation, and metabolic dysfunction, and predicts non-communicable disease risk in later life. There is mounting evidence that these factors are more prevalent in infants who are formula-fed compared to those who are breastfed. Human milk provides the infant with a complex formulation of lipids, many of which are not present in infant formula, or are present in markedly different concentrations, and the plasma lipidome of breastfed infants differs significantly from that of formula-fed infants. With this knowledge, and the knowledge that lipids have critical implications in human health, the lipid composition of human milk is a promising approach to understanding how breastfeeding protects against obesity, inflammation, and subsequent cardiovascular disease risk. Here we review bioactive human milk lipids and lipid metabolites that may play a protective role against obesity and inflammation in later life. We identify key knowledge gaps and highlight priorities for future research.

The LifeCycle Project-EU Child Cohort Network: a federated analysis infrastructure and harmonized data of more than 250,000 children and parents

Early life is an important window of opportunity to improve health across the full lifecycle. An accumulating body of evidence suggests that exposure to adverse stressors during early life leads to developmental adaptations, which subsequently affect disease risk in later life. Also, geographical, socio-economic, and ethnic differences are related to health inequalities from early life onwards. To address these important public health challenges, many European pregnancy and childhood cohorts have been established over the last 30 years. The enormous wealth of data of these cohorts has led to important new biological insights and important impact for health from early life onwards. The impact of these cohorts and their data could be further increased by combining data from different cohorts. Combining data will lead to the possibility of identifying smaller effect estimates, and the opportunity to better identify risk groups and risk factors leading to disease across the lifecycle across countries. Also, it enables research on better causal understanding and modelling of life course health trajectories. The EU Child Cohort Network, established by the Horizon2020-funded LifeCycle Project, brings together nineteen pregnancy and childhood cohorts, together including more than 250,000 children and their parents. A large set of variables has been harmonised and standardized across these cohorts. The harmonized data are kept within each institution and can be accessed by external researchers through a shared federated data analysis platform using the R-based platform DataSHIELD, which takes relevant national and international data regulations into account. The EU Child Cohort Network has an open character. All protocols for data harmonization and setting up the data analysis platform are available online. The EU Child Cohort Network creates great opportunities for researchers to use data from different cohorts, during and beyond the LifeCycle Project duration. It also provides a novel model for collaborative research in large research infrastructures with individual-level data. The LifeCycle Project will translate results from research using the EU Child Cohort Network into recommendations for targeted prevention strategies to improve health trajectories for current and future generations by optimizing their earliest phases of life.

DNA methylation loci in placenta associated with birthweight and expression of genes relevant for early development and adult diseases

BackgroundBirthweight marks an important milestone of health across the lifespan, including cardiometabolic disease risk in later life. The placenta, a transient organ at the maternal-fetal interface, regulates fetal growth. Identifying genetic loci where DNA methylation in placenta is associated with birthweight can unravel genomic pathways that are dysregulated in aberrant fetal growth and cardiometabolic diseases in later life.ResultsWe performed placental epigenome-wide association study (EWAS) of birthweight in an ethnic diverse cohort of pregnant women (n = 301). Methylation at 15 cytosine-(phosphate)-guanine sites (CpGs) was associated with birthweight (false discovery rate (FDR) < 0.05). Methylation at four (26.7%) CpG sites was associated with placental transcript levels of 15 genes (FDR < 0.05), including genes known to be associated with adult lipid traits, inflammation and oxidative stress. Increased methylation at cg06155341 was associated with higher birthweight and lower FOSL1 expression, and lower FOSL1 expression was correlated with higher birthweight. Given the role of the FOSL1 transcription factor in regulating developmental processes at the maternal-fetal interface, epigenetic mechanisms at this locus may regulate fetal development. We demonstrated trans-tissue portability of methylation at four genes (MLLT1, PDE9A, ASAP2, and SLC20A2) implicated in birthweight by a previous study in cord blood. We also found that methylation changes known to be related to maternal underweight, preeclampsia and adult type 2 diabetes were associated with lower birthweight in placenta.ConclusionWe identified novel placental DNA methylation changes associated with birthweight. Placental epigenetic mechanisms may underlie dysregulated fetal development and early origins of adult cardiometabolic diseases.Clinical trial registrationClinicalTrials.gov, NCT00912132

Phthalate Exposure During the Prenatal and Lactational Period Increases the Susceptibility to Rheumatoid Arthritis in Mice.

The prenatal and early postnatal period is highly sensitive to environmental exposures that may interfere with the developmental programming of the immune system leading to an altered disease risk in later life. To clarify the role of early influences in activation or exacerbation of autoimmune diseases like rheumatoid arthritis (RA) we investigated the effect of maternal exposure during the prenatal and lactational period of DBA/1 mice to the plasticizer benzyl butyl phthalate (BBP) on the development of RA in the offspring. Using a mild collagen-induced arthritis (CIA) model, maternal BBP-exposure increased both the prevalence and the severity of RA in the progeny compared to un-exposed dams. Additionally, maternal BBP exposure led to elevated serum IgG1 and IgG2a level in the offspring and increased the IFN-γ and IL-17 release from collagen-re-stimulated spleen cells. Transcriptome analysis of splenocytes isolated from 3-week-old pups before RA-induction revealed considerable changes in gene expression in the offspring from BBP-exposed dams. Among them were regulator of G-protein signaling 1 (rgs1), interleukin-7 receptor (il-7r) and CXC chemokine 4 (cxcr4), all genes that have previously been described as associated with RA pathology. In summary, our results demonstrate that perinatal exposure to BBP increases the susceptibility of the offspring to RA, probably via a phthalate-induced disturbed regulation of RA-relevant genes or signaling pathways.

The Gut Microbiome in Child Malnutrition.

Undernutrition affects almost 25% of all children under the age of 5 worldwide and underlies almost half of all child deaths. Child undernutrition is also associated with long-term growth deficits, in addition to reduced cognitive potential, reduced economic potential, and elevated chronic disease risk in later life. Dietary interventions alone are insufficient to comprehensively reduce the burden of child undernutrition and fail to address the persistent infectious burden of the disease. Although the role of infections is well recognized in the pathogenesis of undernutrition, an emerging body of evidence suggests that commensal microbial communities, known as the microbiome, also play an important role. The gut microbiome regulates energy harvesting from nutrients, growth hormone signaling, colonization resistance, and immune tolerance against pathogens, amongst other pathways critically associated with healthy child growth. Hence, disturbance of the normal gut microbial ecosystem via undernourished diets or unhygienic environments, especially in the early phases of life, may perturb these critical pathways associated with child growth, thereby contributing to child undernutrition. Here we discuss the emerging evidence for the role of the gut microbiome in child undernutrition and the potential for novel gut microbiota-targeted treatments to restore healthy child growth.

Expression of cholesterol packaging and transport genes in human and rat placenta: impact of obesity and a high-fat diet.

Evidence suggests that sub-optimal maternal nutrition has implications for the developing offspring. We have previously shown that exposure to a low-protein diet during gestation was associated with upregulation of genes associated with cholesterol transport and packaging within the placenta. This study aimed to elucidate the effect of altering maternal dietary linoleic acid (LA; omega-6) to alpha-linolenic acid (ALA; omega-6) ratios as well as total fat content on placental expression of genes associated with cholesterol transport. The potential for maternal body mass index (BMI) to be associated with expression of these genes in human placental samples was also evaluated. Placentas were collected from 24 Wistar rats at 20-day gestation (term = 21-22-day gestation) that had been fed one of four diets containing varying fatty acid compositions during pregnancy, and from 62 women at the time of delivery. Expression of 14 placental genes associated with cholesterol packaging and transfer was assessed in rodent and human samples by quantitative real time polymerase chain reaction. In rats, placental mRNA expression of ApoA2, ApoC2, Cubn, Fgg, Mttp and Ttr was significantly elevated (3-30 fold) in animals fed a high LA (36% fat) diet, suggesting increased cholesterol transport across the placenta in this group. In women, maternal BMI was associated with fewer inconsistent alterations in gene expression. In summary, sub-optimal maternal nutrition is associated with alterations in the expression of genes associated with cholesterol transport in a rat model. This may contribute to altered fetal development and potentially programme disease risk in later life. Further investigation of human placenta in response to specific dietary interventions is required.

Prevalence of Metabolic Syndrome and Its Components among Saudi Young Adults 18 - 30 Years of Age

Background: Metabolic syndrome (MS) is a cluster of established cardiovascular risk factors that collectively increase predisposition to major chronic diseases, including heart diseases and diabetes mellitus. Young adults can be affected by MS or any of its components which predispose them to its complications later in their life. Hence early detection of MS and its components can be of help in preventing or controlling its adverse consequences among young adults. Materials and Methods: A total of 1354 Saudis aged 18 - 30 was randomly selected from 20 regions in the Kingdom of Saudi Arabia (KSA). Anthropometrics were collected, and fasting blood samples were collected to ascertain fasting blood glucose and lipid profile. Components of full MS and its components according to the International Diabetes Federation (IDF) were used in this study. Results: Metabolic syndrome prevalence was 12% and was significantly higher among males, advancing age and government employees and unemployed subjects but not according to income or education levels MS was significantly higher among current smokers, subjects with low physical activity level, but not significant according to dietary habits in terms of combined fruits and vegetables consumption. Low levels of High Density Lipoprotein (HDL) were the most frequent component in both males and females. Both waist circumference (WC) and low levels of HDL were much higher among females. Significant predictors included male gender, advancing age, lower level of physical activity and current smoking. Conclusion: The prevalence of MS is 12% in young adults. Low HDL is the most prevalent component of MS in young adults and thus may also be the first detectable component of MS in many young adults. Early identification of MS components could lead to targeted interventions to prevent the development of the syndrome, and thus reduce cardiovascular disease risk in later life.

Investigating the impact of cigarette smoking behaviours on DNA methylation patterns in adolescence.

Smoking usually begins in adolescence, and early onset of smoking has been linked to increased risk of later life disease. There is a need to better understand the biological impact of cigarette smoking behaviours in adolescence. DNA methylation profiles related to smoking behaviours and cessation in adulthood have been previously identified, but alterations arising from smoking initiation have not been thoroughly investigated. We aimed to investigate DNA methylation in the Avon Longitudinal Study of Parents and Children in relation to (1) different smoking measures, (2) time since smoking initiation and frequency of smoke exposure and (3) latent classes of smoking behaviour. Using 2620 CpG sites previously associated with cigarette smoking, we investigated DNA methylation change in relation to own smoking measures, smoke exposure duration and frequency, and using longitudinal latent class analysis of different smoking behaviour patterns in 968 adolescents. Eleven CpG sites located in seven gene regions were differentially methylated in relation to smoking in adolescence. While only AHRR (cg05575921) showed a robust pattern of methylation in relation to weekly smoking, several CpGs showed differences in methylation among individuals who had tried smoking compared with non-smokers. In relation to smoke exposure duration and frequency, cg05575921 showed a strong dose–response relationship, while there was evidence for more immediate methylation change at other sites. Our findings illustrate the impact of cigarette smoking behaviours on DNA methylation at some smoking-responsive CpG sites, even among individuals with a short smoking history.

Cord blood leptin and insulin levels in association with mitochondrial DNA content

BackgroundThe developmental origins of health and disease theory states that a disturbance in the early life environment can contribute to disease risk in later life. Leptin and insulin are anorectic hormones involved in energy homeostasis and are crucial for foetal growth. Disturbances in the levels of these hormones contribute to obesity and diabetes. In adults, altered mitochondrial function is an important hallmark of metabolic disorders, including obesity and diabetes. However, the mitochondrial effects of early life metabolic variation are unexplored. We investigated whether there is an association between metabolic hormones and mitochondrial DNA (mtDNA) content in early life.MethodsThe study included 236 newborns from the FLEHS III birth cohort, Flanders (Belgium). Relative mtDNA content of cord blood leukocytes was determined using quantitative PCR. Cord blood levels of leptin and insulin were determined using immunoassays. We studied the association between these metabolic hormones and mtDNA content using multiple linear regression models, while accounting for covariates and potential confounders.ResultsLeptin and insulin levels were positively associated with cord blood mtDNA content. mtDNA content was respectively 4.49% (95% CI 1.15–7.93; p = 0.008) and 1.60% (95% CI 0.31–2.91; p = 0.02) higher for a interquartile range increase of respectively cord blood leptin and insulin levels. In a sensitivity analysis, we observed that insulin and leptin were independently associated to mtDNA content and that insulin was stronger associated to mtDNA content in boys than in girls.ConclusionNeonatal metabolic hormones were associated with cord blood mtDNA content, which suggests that in early life the variation of mtDNA content might accommodate or reflect changes in the metabolic status.

Elucidating Adverse Nutritional Implications of Exposure to Endocrine-Disrupting Chemicals and Mycotoxins through Stable Isotope Techniques.

Multiple drivers of the double burden of malnutrition (DBM) include a rapid shift from predominantly plant-based diets to energy-dense foods based on meats, milk, animal fats and vegetable oils. The shift to overweight and obesity is driven by increased exposure to mass media, urbanization, technological advances in food processing, rising income and increased population density associated with increased access to cheap foods. At the same time, undernutrition persists mainly due to food insecurity and lack of access to safe water, sanitation and adequate health care. All known nutrition interventions result in only one third reduction in stunting. Little consideration has been given to hazardous exposure to endocrine disrupting chemicals (EDCs) and microbial toxins as major components of the malnutrition-causal framework. These hazards include microbial toxins, for example, mycotoxins, and environmental pollutants such as persistent organic pollutants (POPs), some of which are known to disrupt the endocrine system. These hazards sit at the cross road of undernutrition and overweight and obesity since the exposure cuts across the critical window of opportunity (the first 1000 days). In this review, we update on the role of food and environmental contaminants, especially EDCs and aflatoxins, in child growth and on the implications for metabolic dysfunction and disease risk in later life, and discuss potential applications of nuclear and isotopic techniques to elucidate the underlying biological mechanisms, outcome indicators, as well as occurrence levels.

Maternal Metabolic Health Parameters During Pregnancy in Relation to Early Childhood BMI Trajectories.

The objective of this study was to evaluate the associations between maternal metabolic parameters and early childhood BMI trajectories. Two thousand two hundred fifty-one children born in Spain between 2004 and 2008 were analyzed. Five BMI z score trajectories from birth to age 4 years were identified by using latent class growth analysis. Multinomial regression assessed the associations between maternal metabolic parameters and offspring's BMI trajectories. Children in the reference BMI trajectory had average size at birth followed by a slower BMI gain. Maternal prepregnancy obesity was associated with trajectories of accelerated BMI gain departing from either higher (relative risk ratio [RRR] = 1.77; 95% CI: 1.07-2.91) or lower size at birth (RRR = 1.91; 95% CI: 1.17-3.12). Gestational weight gain (GWG) above clinical guidelines was associated with a trajectory of higher birth size followed by accelerated BMI gain (RRR = 2.14; 95% CI: 1.53-2.97). Maternal serum triglycerides were negatively associated with BMI trajectories departing from lower birth sizes. Gestational diabetes, maternal serum cholesterol, and C-reactive protein were unrelated to children's BMI trajectories. Maternal prepregnancy obesity, GWG, and serum triglycerides are associated with longitudinal BMI trajectories in early childhood that may increase disease risk in later life. Health initiatives should promote healthy weight status before and during pregnancy to improve maternal and child health.

Maternal nutrient restriction in guinea pigs as an animal model for studying growth-restricted offspring with postnatal catch-up growth.

We determined the impact of moderate maternal nutrient restriction (MNR) in guinea pigs with fetal growth restriction (FGR) on offspring body and organ weights, hypothesizing that FGR-MNR animals will show catch-up growth but with organ-specific differences. Guinea pig sows were fed ad libitum (Control) or 70% of the control diet from 4 weeks preconception, switching to 90% at midpregnancy (MNR). Control newborns >95 g [appropriate for gestational age (AGA); n = 37] and MNR newborns <85 g (FGR; n = 37) were monitored until neonatal (~25 days) or adult (~110 days) necropsy. Birth weights and body/organ weights at necropsy were used to calculate absolute and fractional growth rates (FRs). FGR-MNR birth weights were decreased ~32% compared with the AGA-Controls. FGR-MNR neonatal whole body FRs were increased ~36% compared with Controls indicating catch-up growth, with values negatively correlated to birth weights indicating the degree of FGR leads to greater catch-up growth. However, the increase in organ FRs in the FGR-MNR neonates compared with Controls was variable, being similar for the brain and kidneys indicating comparable catch-up growth to that of the whole body and twofold increased for the liver but negligible for the heart indicating markedly increased and absent catch-up growth, respectively. While FGR-MNR body and organ weights were unchanged from the AGA-Controls by adulthood, whole body growth rates were increased. These findings confirm early catch-up growth in FGR-MNR guinea pigs but with organ-specific differences and enhanced growth rates by adulthood, which are likely to have implications for structural alterations and disease risk in later life.

A longitudinal study of the associations of children's body mass index and physical activity with blood pressure.

Childhood blood pressure is a marker of cardiovascular disease risk in later life. We examined how body mass index (BMI) and physical activity, and changes in these, are associated with blood pressure in primary school-aged children. Data are from 1223 children aged 9 years (Year 4) in Bristol, UK, 685 of whom had been assessed at 6 years (Year 1). Child height and weight were measured, and children wore accelerometers for five days, from which average counts per minute, and moderate-to-vigorous-intensity physical activity and sedentary minutes per day were derived. At age 9 years, blood pressure was measured. Multiple imputation of missing data and adjusted linear regression models were used to examine associations. Child BMI at 9 years was cross-sectionally associated with higher systolic (SBP) and diastolic (DBP) blood pressure (mean difference [95% CI]: 1.10 [0.34, 1.87] mmHg and 0.86 [0.13, 1.60] mmHg, respectively, per SD of BMI). Prospective associations of BMI at age 6 with blood pressure at age 9 were consistent with these cross-sectional associations. However, change in BMI between 6 and 9 years was not strongly associated with subsequent SBP or DBP (0.68 [-0.61, 1.98] mmHg and 1.23 [-0.09, 2.54] mmHg, respectively). There was little evidence that physical activity or sedentary time were associated with blood pressure in either cross-sectional or prospective analyses. Greater childhood BMI is associated with higher blood pressure, and this association persists over several years. Prevention of excessive bodyweight from early childhood may be important in stemming the development of cardiovascular risk.

Influence of early feeding practices on biomarkers of cardiovascular disease risk in later life

BackgroundAn analysis of risk factors linked to ischemic heart disease (IHD) shows a strong link between these risk factors and early feeding practices. Aim of the workThe aim of this study was to evaluate cardiac biomarkers that could predict cardiovascular disease (lipid profile and highly sensitive C-reactive protein (hs-CRP) for both mothers and their children and demonstrate their associations with early feeding practices. MethodsThis was a cross-sectional study comprising one hundred twenty pairs of mother and their children, one half of whom were exclusively breastfed for 6 months, the other half their children were formula fed from birth. The groups were matched for age and sex. Full feeding history was taken for children and assessments of risk behaviour of cardiovascular disease including Anthropometric measurements to assess Body Mass Index, blood pressures and blood samples for lipid profile and hs-CRP for both mothers and children. ResultsThere was a statistically significant difference between the two groups regarding hs-CRP as it was higher in mothers and their children who were artificially feed than mothers and their children who were breastfeed (m = 3.3 + 2.2–1.72 ± 1.96, 2.08 ± 1.64–0.84 ± 1.09 respectively), however there was no a statistically significant difference for both mothers and their children regarding lipid profile. ConclusionEarly feeding practices can influence the development of cardiovascular diseases as breast fed infants and their mothers had lower hs- CRP levels which is considered as a biomarker of CVD risk.