Heart Disease In Later Life Research Articles

Characteristics of Premature Myocardial Infarction Among Women With Prior Adverse Pregnancy Outcomes

BackgroundAdverse pregnancy outcomes (APOs), hypertensive disorders of pregnancy, gestational diabetes mellitus, and preterm birth are associated with ischemic heart disease in later life. ObjectivesThe authors aimed to study the features of premature myocardial infarction (MI) among women with and without prior APOs. MethodsWe performed a retrospective analysis of women with premature MI (<65 years of age) referred for left heart catheterization matched with a database of abstracted pregnancy data. We compared MI characteristics and epicardial coronary anatomy between women with and without APOs during their index pregnancy and evaluated time from delivery to MI. ResultsOf 391 women with premature MI and associated coronary angiography (age: 49 ± 8 years), 154 (39%) had a prior APO (hypertensive disorders of pregnancy n = 78, preeclampsia n = 35, gestational diabetes mellitus n = 28, and preterm birth n = 48). Women with APO history had a higher prevalence of diabetes (33% vs 16% without APO; P = 0.001) and presented earlier with MI following delivery (19.6 [IQR: 14.3-23.5] years vs those without APO 21.5 [IQR: 17.0-25.4] years; P = 0.012), driven by preeclampsia (17.1 [IQR: 12.7-22.4] years, P = 0.010). Women with and without APOs had similar MI features including rates of ST-segment elevation MI, obstructive and multi-vessel coronary artery disease, percutaneous coronary intervention, and shock. ConclusionsAmong women with premature MIs, 39% had a history of an APO. Women with APO history presented sooner after pregnancy but had similar MI characteristics vs those without APOs. Pregnancy history may identify women who warrant early, aggressive cardiovascular disease prevention.

Childhood household dysfunction is associated with reduced left ventricular mass in young adulthood.

The effect of adverse childhood experiences (ACEs) on left ventricular mass (LVM) and left ventricular function remains largely unknown across the lifespan. This study investigated the influence of ACEs on LVM and left ventricular function and whether inflammation influences this relationship. Two hundred forty-eight healthy young adults participated and a final sample of 217 (age, 22.6 ± 0.1 yr; females, 114) had complete data. Echocardiographic assessment of LVM was indexed to height2.7 (LVMHT) and body surface area (LVMBSA). Ejection fraction (EF) and fractional shortening were also assessed. Interleukin-6 (IL-6), C-reactive protein, tumor necrosis factor-α, and matrix metalloproteinase (MMP) 1-3 were measured and ACEs exposures were assessed based on exposure and nonexposure to childhood household dysfunction and maltreatment, and quantity of adversity, (i.e., <4 ACEs and ≥4 ACEs). Individuals who experienced household dysfunction demonstrated lower LVM, LVMHT, and LVMBSA (P < 0.01) and greater IL-6 (P < 0.05) than those who did not experience household dysfunction. Reduced MMP3 was present in individuals who experienced maltreatment (P < 0.05) and ≥4 ACEs (P < 0.01) compared with no maltreatment and <4 ACEs, respectively. After controlling for covariates (i.e., sex, recent life stress, height, body mass index, smoking, physical activity, and inflammation), a significant negative effect of household dysfunction on LVM, LVMHT, and LVMBSA persisted. Likewise, a negative effect on EF independent of covariates was observed in individuals who experienced ≥4 ACEs. As such, alterations in LVM and EF may be perpetuated through a toxic home environment, promoting left ventricular underdevelopment in young adulthood. The effect of which in midlife and beyond requires additional investigation.NEW & NOTEWORTHY This is the first study to investigate the influence of adverse childhood experiences (ACEs) on left ventricular mass (LVM) and function. We identified experiencing any childhood household dysfunction was associated with lower LVM in young adults independent of sex, recent life stress, BMI and height, smoking, physical activity, and inflammation. We speculate an inflection point in LVM occurs in midlife predisposing these individuals toward a hypertrophic profile and elevated risk of heart disease in later life, although this requires longitudinal investigation.

Fertility Histories and Heart Disease in Later Life in China.

PurposeBased on life course theories, health among older people is driven by a continuous and cumulative process that develops over the life course. To better understand the aging process, it is important to assess associations between parity and heart disease in older people of China.MethodThe associations between heart disease prevalence and number of births, number of boys or girls ever born were evaluated among 5,990 samples (mean age 64.1 years) using the Probit regression model based on the data from China Health and Retirement Longitudinal Study (CHARLS) conducted in 2013 and 2018. The model was adjusted only for rural or urban residents, and multivariate regression models were run separately by gender.ResultsOur results showed that more than three children or more than two boys ever born were associated with a higher risk of heart disease. However, the number of girls ever born had no significant effect on heart disease in the elderly. We further analyzed the group difference between urban and rural residents using the regression model. More than three children or more than two boys ever born were associated with a high risk of heart disease in rural areas. Compared to urban residents, rural residents were more likely to be suffering from heart disease due to high parity. When considering the digender difference the paper found that more than three children ever born were associated with a high risk of heart disease in the female group. Late age at the time of giving birth for the first time was associated with a poorer risk level of heart disease in the rural residents, because the phenomenon of early childbearing was serious in the rural residents. But after considering the impact on the physical health of using chronic diseases, the first birth and the last birth both increased the risk of heart disease.ConclusionsSome policy implications were being put forward. Firstly, parents who were ready to give birth should be aware of the possible health loss of high parity. Postpartum nutrition supplements and chronic disease prevention were suggested to prevent heart disease in later life. Secondly, the elderly in rural areas should pay more attention to heart diseases. Participating in more daily exercise and physical examinations was a good choice to reduce the risk of heart disease. Thirdly, women who give birth prematurely have a higher risk of CVD. Based on our results, age at entry to parenthood was closely related to the risk of heart disease in later life.

Harnessing Whole Genome Polygenic Risk Scores to Stratify Individuals Based on Cardiometabolic Risk Factors and Biomarkers at Age 10 in the Lifecourse-Brief Report.

In this study, we investigated the capability of polygenic risk scores to stratify a cohort of young individuals into risk deciles based on 10 different cardiovascular traits and circulating biomarkers. We first conducted large-scale genome-wide association studies using data on adults (mean age 56.5 years) enrolled in the UK Biobank study (n=393 193 to n=461 460). Traits and biomarkers analyzed were body mass index, systolic blood pressure, diastolic blood pressure, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, triglycerides, apolipoprotein B, apolipoprotein A-I, C-reactive protein and vitamin D. Findings were then leveraged to build whole genome polygenic risk scores in participants from the Avon Longitudinal Study of Parents and Children (mean age, 9.9 years) which were used to stratify this cohort into deciles in turn and analyzed against their respective traits. For each of the 10 different traits assessed, we found strong evidence of an incremental trend across deciles (all P<0.0001). Large differences were identified when comparing top and bottom deciles; for example, using the apolipoprotein B polygenic risk scores there was a mean difference of 13.2 mg/dL for this established risk factor of coronary heart disease in later life. Although the use of polygenic prediction in a clinical setting may currently be premature, our findings suggest they are becoming increasingly powerful as a means of predicting complex trait variation at an early stage in the lifecourse.

The association between childhood conditions and heart disease among middle-aged and older population in China: a life course perspective

BackgroundHeart disease is a severe health problem among adult populations in China. The prevalence rates of heart disease increase with age. The pathogenic causes of heart disease are often related to conditions in early life. Using a nationally representative sample of adults aged 45 or older in China, we examined the association between childhood conditions and heart disease in later life from a life course perspective.MethodsThe data used in this study were derived from the life history module and 2015 wave of China Health and Retirement Longitudinal Study (CHARLS). Missingness were handled by multiple imputation, generating 20 complete datasets with a final sample of 19,800. Doctor-diagnosed heart disease was the main dependent variable. Respondents’ conditions in childhood, adulthood, and older age were the independent variables (e.g., socioeconomic status, health, and health resources). Random-effects logistic regression models were conducted to test the hypotheses.ResultsA total of 16.6% respondents reported being diagnosed with heart disease by doctors. Regarding childhood socioeconomic status, 8.2% of the respondents considered that they were (a lot) better off than their neighbors, and 31.1% considered that their health status in childhood was better than their peers. More than 90% of respondents did not have severe illnesses during their childhood, and around 80.3% had access to health resources nearby in childhood. Lower socioeconomic status and poorer health conditions in childhood were associated with a greater likelihood of reporting doctor-diagnosed heart diseases, even after controlling for conditions in adulthood and older age (socioeconomic status: odds ratio (OR) = 0.947; self-rated health: OR = 0.917; severe illnesses: OR = 1.196).ConclusionsAlong with chronic diseases (e.g., hypertension, diabetes, and dyslipidemia), unhealthy behaviors, overweight and obesity, poor childhood conditions should be considered as screening criteria to identify populations at risk of heart disease. Relevant preventive strategies and interventions should be developed from a life course perspective and conducted in communities by providing health education program among older population with low socioeconomic status, and encouraging early detection and treatment.

The pandemic of 1918 and the heart disease epidemic in middle-aged men and women in the United States

ABSTRACT Members of birth cohorts who were alive in 1918 and survived the influenza pandemic were likely to have been “primed” for heart disease in later life. We examine the hypothesis that the twentieth-century heart disease epidemic was a cohort effect reflecting the changing susceptibility composition of the population. We estimated heart disease death rates by single years of age for cohorts born in 1860–1949. We prepared age-specific rates for calendar years 1900–2016, as well as age-standardized cohort and calendar year rates. Males born in 1880–1919 contributed 90 per cent to 100 per cent of all heart disease deaths among males aged 40–64 from 1940 to 1959, when the heart disease epidemic was at its peak. There was no heart disease epidemic among females aged 40–64. Death from heart disease in females tends to occur at older ages. Cigarette smoking, unemployment, and other factors may have played a role in the heart disease epidemic in men and would have interacted with injury from influenza, but our results suggest that having been alive at the time of the 1918 influenza pandemic probably played an important role.

Exercise: A Free Medicine of All Time

Dear Editor, Exercise is good to the well-being of people. Older people are susceptible to numerous chronic diseases. From a cardiovascular health data it was discovered that people with the best exercise test scores were less likely to die within the next 30 years than their counterpart. A research stated that as little as 15 minutes of exercise almost daily can help to lower the risk of cardiovascular diseases (1-3). Another study reveals that the physical inactivity is the primary cause of most chronic diseases across the globe (2, 4). It was evident that regular exercise can improve the brain functions as well as physical and mental functions (5). Strong and consistent evidence reveals that exercise has a significant impact in preventing symptoms and reducing back pain (6). An overview research conducted in United Kingdom reveals that exercise may have specific benefits in reducing the severity of chronic pain (7). The eye health of more than 40,000 men and women runners has been reviewed over several years and they had significantly lower rates of eye diseases than the general public. Each year in the US thousands of people are diagnosed with colon cancer. Many studies found that those that engaged in high intensity activities were less likely to develop colon cancer than others that had minimal workouts (8). A new study involving thousands participants found that people with high fitness during their middle age were significantly less likely to die from heart disease in later life. Professionals recommends that starting to exercise early in life and continuing to do it often could protect both the mental and physical health of patients battling depression and facing heart disease risks. According to new research taking up a daily run could lower heart disease risks by almost 56 percent, and working out could be particularly good medicine for those with depression (9). A study reported that a moderate-intensity activities are so vital to our own health and can reduce the risk of death in older women. Health professional should be suggesting exercise for older women, in addition to other conventional treatments. Many studies reveals that intensity activity can have mental and physical health benefits (10). Everyone should stay active in order to stay healthy.

Contributors to Wisconsin\u2019s persistent black-white gap in life expectancy

BackgroundAlthough the black-white gap in life expectancy has narrowed in the U.S., there is considerable variability across states. In Wisconsin, the black-white gap exceeds 6 years, well above the national average. Reducing this disparity is an urgent public health priority, but there is limited understanding of what contributes to Wisconsin’s racial gap in longevity. Our investigation identifies causes of death that contribute most to Wisconsin’s black-white gap in life expectancy among males and females, and highlights specific ages where each cause of death contributes most to the gap.MethodsOur study employs 1999–2016 restricted-use mortality data provided by the National Center for Health Statistics. After generating race- and sex-specific life tables for each 3-year period of observation (e.g., 1999–2001), we trace recent trends in the black-white life expectancy gap in Wisconsin. We subsequently conduct a series of analyses to decompose the black-white gap in three time periods into 13 separate causes and 19 different age groups.ResultsIn 2014–16, Wisconsin’s black-white gap in life expectancy was 7.34 years for males (67% larger than the national gap), and 5.61 years for females (115% larger than the national gap). Among males, homicide was the single largest contributor, accounting for 1.56 years of the total gap. Heart disease and cancer followed, contributing 1.43 and 1.42 years, respectively. Among females, heart disease and cancer were the two leading contributors to the gap, accounting for 1.12 and 1.00 years, respectively. Whereas homicide contributed most to the racial gap in male longevity during late adolescence and early adulthood, heart disease and cancer exerted most of their influence between ages 50–70 for both males and females. Other notable contributors were unintentional injuries (males), diabetes and cerebrovascular disease (females), and perinatal conditions (males and females).ConclusionsOur study identifies targets for future policy interventions that could substantially reduce Wisconsin’s racial gap in life expectancy. Concerted efforts to eliminate racial disparities in perinatal mortality and homicide early in the life course, and chronic conditions such as cancer and heart disease in later life, promise to help Wisconsin achieve the public health objective of racial parity in longevity.

The highs and lows of programmed cardiovascular disease by developmental hypoxia: studies in the chicken embryo.

It is now established that adverse conditions during pregnancy can trigger a fetal origin of cardiovascular dysfunction and/or increase the risk of heart disease in later life. Suboptimal environmental conditions during early life that may promote the development of cardiovascular dysfunction in the offspring include alterations in fetal oxygenation and nutrition as well as fetal exposure to stress hormones, such as glucocorticoids. There has been growing interest in identifying the partial contributions of each of these stressors to programming of cardiovascular dysfunction. However, in humans and in many animal models this is difficult, as the challenges cannot be disentangled. By using the chicken embryo as an animal model, science has been able to circumvent a number of problems. In contrast to mammals, in the chicken embryo the effects on the developing cardiovascular system of changes in oxygenation, nutrition or stress hormones can be isolated and determined directly, independent of changes in the maternal or placental physiology. In this review, we summarise studies that have exploited the chicken embryo model to determine the effects on prenatal growth, cardiovascular development and pituitary-adrenal function of isolated chronic developmental hypoxia.

Membrane potential, serum calcium and serum selenium decrease in preeclampsia subjects in Owerri

Background Pre-eclampsia is a serious hypertensive condition of pregnancy associated with high maternal and fetal morbidity and mortality. Women who have had pre-eclampsia have a greater risk of developing hypertension, stroke and ischemic heart disease in later life. The etiology of pre-eclampsia remains unclear. Placental insufficiency plays a key role in the progression of this disease. The aim of this study was to determine membrane potential, serum calcium and serum selenium levels in preeclampsia subjects in Owerri. MethodsA case control study involving 200 primigravida (100 preeclamptic and 100 apparently healthy) between the ages of 20 and 32 years attending General Hospital Owerri. Fasting venous blood was collected for the determination of serum selenium and serum calcium while membrane potential was calculated using the Nernst equation. The serum calcium was estimated using Randox Kit and serum selenium by atomic absorption spectrophotometry. The Independent Student t test was used for statistical analysis. ResultsThe results revealed that membrane potential and serum selenium as well as serum calcium were significantly decreased in preeclampsia when compared with the controls, at p&lt;0.05. ConclusionOur study demonstrated that the decrease in membrane potential, serum calcium and serum selenium levels may play a critical role in the pathogenesis of pre-eclampsia. There may be a need for increasing the dietary intake of these essential trace metals during pregnancy to prevent pre-eclampsia in Owerri.

Deranged Serum Fasting Lipid Profile in Children and Adolescent with Thalassemia Major

Introduction: Serum fasting lipid profile has been studied in various clinical spectrum of β-thalassemia syndrome. Premature cardiac impairment in thalassemia major (TM) appears primarily due to iron accumulation and oxidative injury; however it might be a sequel of abnormal lipoprotein concentrations. Recent studies revealed impaired lipid profile and atherosclerosis in TM as an emerging complication in patients with prolonged survival. As these children are at risk of premature atherosclerosis, sub clinical atherosclerosis probably begins early in their life might evolve into coronary heart diseases in later life.The rational of this prospective cross sectional study is to analyze the serum fasting lipid profile in cardiovascular disease free thalassemia major patients and to establish any correlation with age, gender, hematological parameters, liver enzymes and serum ferritin.Method: The study group comprises of thirty six patients with β-thalassemia major, who were enrolled from March 2012 to March 2014. Fasting blood lipid levels (total lipid, cholesterol, triglycerides, HDL and LDL-cholesterol), liver function test and serum ferritin were measured in all study participants on Hitachi 912 through photometric assay (for lipid profile and liver function test) and by immunoturbidity methodology for serumferritin. Hematological parameters were determined by Cell Dyne Ruby (Abbot, Architect, USA). Patients were stratified in two groups, age ≤ 15 years and >15 years, to determine the possible lipid profile distinction in relation to increasing age.Results: Of the 36 patients, 17 were males (15.5±5.9 years) and 19 were females (10.1±4.5 years) with the mean age of 12.69±5.85 (range 5-24) years. Mean hemoglobin was 7.4±1.9gm/dl with the hematocrit of 23.1±5.7% while serum ferritin was markedly elevated 4699.7±3089ng/ml. The mean total lipid, cholesterol and triglycerides levels were 494.7 ± 114.5, 90.3 ±23.9 and 150.5±95.1 mg/dl respectively. High triglycerides were detected in 36.1%. While HDL cholesterol and LDL cholesterol were markedly low 17.7±9.2 and 42.3±22.0 mg/dl respectively. The mean total cholesterol to HDL ratio was significantly elevated, 6.21± 3.06 (normal <5.0). In addition, total-cholesterol to HDL-cholesterol ratios were increased irrespective of gender, that is 6.0±2.0 and 6.4± 3.8 in males and females respectively (P=0.6). Data analysis revealed that 22.2% females and 13.8% males had high triglyceride levels (P=0.05). No statistically significant difference was noted in two stratified age groups in respect to lipid profile (table-1).We established positive correlation of elevated total bilirubin with cholesterol, HDL and LDL cholesterol (P<0.05). Cholesterol ratio was also significantly high in patients with hemoglobin > 8gm/dl (P<0.05). Low HDL cholesterol was correlated positively with LDL cholesterol levels. While no significant correlation of serum lipid could be established with age, gender, high ferritins and with liver enzymes.Conclusion: Our study revealed that lipid profile impairment is not unusual in β-thalassemia major patients irrespective of age. Considerable deficiency of high density cholesterol and significantly high total-cholesterol to HDL-cholesterol ratio may strongly be associated with occurrence of coronary heart disease in later life. We propose that lipid profile should be regularly done in these patients particularly those with hemoglobin > 8gm/dl and high total bilirubin levels. Whilst total to HDL ratio, underlines as a significant diagnostic marker for future cardiac events in these patients.Keywords: β-thalassemia major, triglyceride, HDL-cholesterol, LDL-cholesterol.Table 1:Comparative analysis of serum lipid profile in relation to ageParametersAge ≤15 yearsn= 24Age >15 yearsn= 12P- valueTotal lipid515.7± 121.1452.9 ±90.60.1 *Cholesterol95.0±17.680.9±32.10.09 *Serum triglyceride168.1 ± 109.7115.2± 40.10.1 *HDL cholesterol19.4±10.214.4± 5.90.1 *LDL cholesterol43.1±19.940.9±26.60.7 *Cholesterol ratio6.3± 3.46.0 ±2.10.8 **Not significant DisclosuresNo relevant conflicts of interest to declare.

The relationship between umbilical cord length and chronic rheumatic heart disease: a prospective cohort study.

One previous, preliminary study reported that the length of the umbilical cord at birth is related to the risk of developing chronic rheumatic heart disease in later life. We sought to replicate this finding. Prospective, population-based birth cohort. We traced 11,580 individuals born between 1915 and 1929 in Uppsala, Sweden. We identified cases with a main or secondary diagnosis of chronic rheumatic heart disease in the Swedish national inpatient, outpatient or death registers. Archived obstetric records provided data on umbilical cord length, gestational age, birthweight and placental weight. There were 136 patients with chronic rheumatic heart disease (72 men and 64 women) with a mean age at first hospital admission of 68years (range 36-92). There was evidence of a positive association between umbilical cord length and risk of subsequent chronic rheumatic heart disease. The overall hazard ratio in the Swedish study (1.13, 95% confidence interval 1.01 to 1.27) was similar to that of the previous study, with some suggestion of larger effect in men than in women. No other birth characteristics were predictive except for weak evidence of a protective effect of higher birthweight in men. People with longer umbilical cords at birth are more likely to develop chronic rheumatic heart disease in later life. As longer umbilical cords have more spiral arteries and a higher vascular resistance, we hypothesize that the increased pressure load on the heart leads to changes in endothelial biology and increased vulnerability to the autoimmune process initiated by infection with β-haemolytic streptococci.

Preterm Birth

See related article, pp 226–234 There is compelling epidemiological and experimental data that suggest that blood pressure in later life can be programmed by adverse influences during fetal life.1 Evidence for the theory of developmental programming of adult health and disease was first based on the geographical association of deaths from heart disease to death rates among newborn infants. This observation led to the hypothesis that undernutrition during fetal life permanently alters the physiology, structure, and metabolism of an individual leading to heart disease in later life.2 Poor fetal growth, the link to infant mortality, was also associated with systolic blood pressure (SBP), a known risk factor for heart disease; however, this association was independent of gestational age.3 In this issue of Hypertension , de Jong et al4 present their findings from a thorough and systematic review of the literature followed by a meta-analysis to determine whether preterm birth predicts a higher SBP in later life. Their results indicate that individuals born preterm have a higher SBP in later life than infants born at term (2.5 mm Hg).4 Although this difference in SBP is small, it is similar to the increase observed in studies linking birth weight and SBP,5 indicating that preterm birth, not unlike poor fetal growth with birth at term, may also …

Prenatal exposure to wartime stress – long-term effect on coronary heart disease in later life

Background. Increased rates of coronary heart disease (CHD) and cerebrovascular disease in later life have been repeatedly observed in subjects with low birth-weight. One possible reason for low birth-weight is prenatal stress. Little is known about the influence of prenatal stress on lifelong health outcomes.Aims. In this study we investigate the influence of prenatal stress on CHD and cerebrovascular disease incidence in adult life.Methods. We analysed data originating from the Helsinki Birth Cohort Study including hospital data from all men and women born between 1934 and 1944 (n = 13,039) in two hospitals of Helsinki. We estimated the hazard function based on Weibull distribution. We compared those exposed and unexposed to bombings while in utero in terms of lifelong CHD and cerebrovascular disease hazard.Results. In women exposed to bombings while in utero, we observed higher survival rates of both CHD and cerebrovascular disease than in those unexposed. In men, the results were ambiguous.Conclusions. Our findings suggest that prenatal exposure to severe stress may be associated with protective effects on the development of CHD in later life.

Distinct Variants at LIN28B Influence Growth in Height from Birth to Adulthood

We have studied the largely unknown genetic underpinnings of height growth by using a unique resource of longitudinal childhood height data available in Finnish population cohorts. After applying GWAS mapping of potential genes influencing pubertal height growth followed by further characterization of the genetic effects on complete postnatal growth trajectories, we have identified strong association between variants near LIN28B and pubertal growth (rs7759938; female p = 4.0 x 10(-9), male p = 1.5 x 10(-4), combined p = 5.0 x 10(-11), n = 5038). Analysis of growth during early puberty confirmed an effect on the timing of the growth spurt. Correlated SNPs have previously been implicated as influencing both adult stature and age at menarche, the same alleles associating with taller height and later age of menarche in other studies as with later pubertal growth here. Additionally, a partially correlated LIN28B SNP, rs314277, has been associated previously with final height. Testing both rs7759938 and rs314277 (pairwise r(2) = 0.29) for independent effects on postnatal growth in 8903 subjects indicated that the pubertal timing-associated marker rs7759938 affects prepubertal growth in females (p = 7 x 10(-5)) and final height in males (p = 5 x 10(-4)), whereas rs314277 has sex-specific effects on growth (p for interaction = 0.005) that were distinct from those observed at rs7759938. In conclusion, partially correlated variants at LIN28B tag distinctive, complex, and sex-specific height-growth-regulating effects, influencing the entire period of postnatal growth. These findings imply a critical role for LIN28B in the regulation of human growth.

N‐3 fatty acids on utero programming of insulin resistance, NASH and hyperlipidemia in Psammomys obesus

Nonalcoholic steatohepatitis (NASH) represents the inflammatory form of liver steatosis, which can progress to fibrosis and cirrhosis. NASH is associated with features of the insulin resistance syndrome. In view of the hypothesis that under nutrition in utero enduringly affects the function and metabolism, thereby leading to coronary heart disease in later life, we attempted to examine whether n‐3 fatty acid (FA) supplementation during pregnancy may prevent metabolic disorders and NASH in the adult period. Experiments were carried out on Psammomys obesus gerbils, a model of nutritionally induced metabolic syndrome. Pregnant females were assigned to an isocaloric control diet or a diet rich in fish oil and analyses were carried out in the offspring of diabetic mothers. Our findings could document: (1) a decrease in obesity as assessed by body weight and adipose tissue mass; (2) diminished hyperlipidemia, hyperglycemia and insulin resistance; (3) reduced amounts of lipid content in the liver; (4) lessened inflammation as reflected by the levels of TNFα; and (5) raised levels of adiponectine. Further experiments disclosed a reduced gene expression of FA synthase, malic enzyme and acetyl CoA carboxylase, emphasizing attenuation in hepatic lipogenesis. Overall, our results suggest that maternal nutrition influences fetal programming, insulin resistance and diabetes in later life. Furthermore, our works emphasizes the impact of n‐3 FA on intrauterine mechanisms regulating risk factors of cardiovascular health during adulthood.

The contribution of childhood obesity to adult carotid intima-media thickness: the Bogalusa Heart Study

Although obese children are at increased risk for coronary heart disease in later life, it is not clear if the association results from the persistence of childhood obesity into adulthood. We examined the relation of both childhood and adult levels of body mass index (BMI, kg m(-2)) to carotid intima-media thickness (IMT) measured at the (mean) age of 36 years. Prior to the determination of adult IMT, the 1142 participants had been examined 7 (mean) times in the Bogalusa Heart Study. In addition to BMI, levels of lipids, lipoproteins and blood pressure were measured at each examination. Cumulative levels of each risk factor were based on the areas under the individual growth curves calculated using multilevel models for repeated (BMI) measurements. We then examined the relation of these cumulative levels to adult IMT. Carotid IMT was associated with cumulative levels of BMI in both childhood and adulthood (P<0.001 for each association). Furthermore, the association between childhood BMI and adult IMT persisted, but was reduced, after controlling for adult BMI. Although childhood levels of lipids, lipoproteins and blood pressure were also associated with adult IMT, these associations were not independent of adult levels of these risk factors. These results emphasize the adverse effects of elevated childhood BMI levels. In addition to the strong tracking of BMI levels from childhood to adulthood, there appears to be a modest, independent effect of childhood BMI on adult IMT. The prevention of childhood obesity should be emphasized.

Is birth weight a risk factor for ischemic heart disease in later life?

Is birth weight a risk factor for ischemic heart disease in later life?

Can Life Before Birth Affect Health Ever After?

The environmental conditions experienced by the developing human during the peri-conceptual, embryonic, fetal, neonatal and adolescent periods, have a profound effect on the future health of that individual. Adverse early-life environmental conditions such as under or over nutrition, stress, vitamin deficiencies, drugs and alcohol exposure can permanently alter the long-term functioning of many organs. These changes significantly increase the risk of developing diseases in adult life such as cardiovascular disease, diabetes and metabolic syndrome, as well as mental health conditions such as attention deficit disorder, autism, and schizophrenia. The now widely studied, yet still mechanistically ill-defined “developmental origins of adult disease” hypothesis, was first proposed by Barker in 1986 [1]. Barker and his colleagues described an association between low birth weight and increased risk of developing ischaemic heart disease in later life. Since then, human epidemiological studies have continued to show a strong association between low birth weight and adult coronary heart disease and hypertension. This hypothesis has since been expanded to show that ‘programming’ can occur independently of low birth weight or growth retardation. Animal models are currently being used to investigate the mechanisms of the developmental origins of adult disease including maternal undernutrition, both global and nutrient specific such as low protein, uterine artery ligation to induce fetal growth restriction and maternal glucocorticoid exposure. Results vary significantly between these models depending on the type, severity and the timing of the insult. What has emerged from many of these studies is that there are key windows of development that are more susceptible to particular insults

Is birth weight a risk factor for ischemic heart disease in later life?

Background: An inverse association between birth weight and ischemic heart disease (IHD) has been seen in observational studies.Objective: We wanted to determine the strength and consistency of the association between birth weight and subsequent IHD.Design: We conducted a systematic review of observational studies.Results: Seventeen published studies of birth weight and subsequent IHD were identified that included a total of 144 794 singletons. Relative risk estimates for the association between birth weight and IHD were available from 16 of these studies. Additional data from 2 unpublished studies of 3801 persons were also included. In total, the analyses included data from 18 studies on 4210 nonfatal and 3308 fatal IHD events in 147 009 persons. The mean weighted estimate for the association between birth weight and the combined outcome of nonfatal and fatal IHD was 0.84 (95% CI: 0.81, 0.88) per kilogram of birth weight (P < 0.0001). No significant heterogeneity was observed between estimates in different studies (P = 0.09), nor was there evidence of publication bias (P = 0.3, Begg test). Neither restricting the analysis to fatal IHD events nor adjusting for socioeconomic status had any appreciable effect on the findings.Conclusions: These findings are consistent with a 1 kg higher birth weight being associated with a 10–20% lower risk of subsequent IHD. However, even if causal, interventions to increase birth weight are unlikely to reduce the incidence of IHD materially. Further studies are needed to determine whether the observed association reflects a stronger underlying association with a related exposure or is due (at least in part) to residual confounding.