Coronary Heart Disease In Adult Life Research Articles

Prenatal and maternal characteristics and later risk for coronary heart disease among women.

The pace and pathways of early growth have major influences on later health. Coronary heart disease (CHD) is a major killer and kills more women than men, but usually manifests about 10 years later in women. Therefore there are fewer studies of early growth and CHD amongst women than men. The Helsinki Birth Cohort Study includes 9817 women born during 1924-1944. We used national registers to identify hospital admissions and deaths from CHD during 1971-2010. We used a Cox model to obtain hazard ratios (HRs) for CHD. Altogether 967 women (9.9%) developed CHD. Socioeconomic factors were strongly and inversely associated with CHD. Neither maternal age nor body mass index (BMI) was associated with CHD in the daughters. There were inverse associations of birth weight (p = 0.07) and length (p = 0.02) with CHD in adult life. We divided the mothers according to parity. Daughters of primiparous women had lower birth weight and shorter birth length than the offspring of multiparous women (both p-values < 0.001). Birth weight (p = 0.008), birth length (p = 0.05) and birth BMI (p = 0.02) were all inversely associated with CHD. Among first-born women, a 1 kg increase in birth weight was associated with a 25% lower risk for CHD (HR 0.75, 95% confidence interval (CI) 0.60-0.93). The findings changed little after adjustment for socioeconomic factors. Among later-born women none of the birth characteristics was associated with CHD. Small birth size is associated with CHD among women. First-born women with high birth weight appear to be at lower risk for CHD compared with later born women.

Epidemiology, genes and the environment: lessons learned from the Helsinki Birth Cohort Study

Nonoptimal growth during fetal life and infancy is associated with an increased risk of coronary heart disease and type 2 diabetes later in life. This early pattern of growth is associated with an increased disease risk especially when followed by a relative gain in body size later in childhood. Genetic factors are closely involved in growth and disease pathogenesis and gene-early life environmental interactions will be described affecting adult health outcomes. This overview will primarily focus upon findings from the Helsinki Birth Cohort Study consisting of 15846 subjects born 1924-1944 on whom growth data and information on adult health are available.

A perinatal strategy to prevent coronary heart disease

Objectives I investigated whether metabolism of essential fatty acids and the concentrations of their long-chain metabolites (long-chain polyunsaturated fatty acids [LCPUFAs]) are altered in fetal or perinatal growth retardation, maternal hypercholesterolemia, low-grade systemic inflammation, insulin resistance, and atherosclerosis, conditions that predispose to the development of coronary heart disease (CHD). Methods I critically reviewed the literature pertaining to the metabolism of essential fatty acids in CHD and conditions that predispose to it. Results LCPUFAs enhance endothelial nitric oxide synthesis, suppress the production of the proinflammatory cytokines tumor necrosis factor and interleukin-6, attenuate insulin resistance, and have antiatherosclerotic properties. Low-birthweight infants have decreased concentrations of LCPUFAs, especially arachidonic acid. Neonatal arachidonic acid status is related to intrauterine growth, and LCPUFAs improve fetal and postnatal growth. LCPUFAs are useful in the management of hyperlipidemia, inhibit 3-hydroxy-3-methylglutaryl coenzyme A reductase activity, and may mediate the beneficial actions of statins. Plasma concentrations of various LCPUFAs are low in diabetes mellitus, hypertension, and CHD and in populations at high risk of CHD. Breast milk is rich in LCPUFAs, and this may explain why and how adequate (6 mo to 1 y) breast feeding protects against the development of obesity, hypertension, insulin resistance, and CHD. Conclusions LCPUFAs are essential for the growth and development of the fetus and infant. LCPUFAs can prevent various conditions that predispose to the development of CHD. The low incidence of CHD seen in adequately breast-fed infants can be linked to the LCPUFA content of breast milk. Based on this evidence, I suggest that provision of LCPUFAs during critical periods of growth, especially from the second trimester of pregnancy to age 5 y, prevents CHD in adult life.

Preventing coronary heart disease: the implementation of healthy lifestyle strategies for children and adolescents.

Extensive epidemiologic, clinical, and laboratory data accumulated over the past 3 decades provide convincing rationale for primary prevention of coronary heart disease (CHD) beginning early in life. This article focuses on evidence-based strategies designed to promote cardiovascular health in children and adolescents and reduce the risk and burden of CHD in adult life. Emphasis is placed on healthful lifestyle training and behavioral change interventions applicable in health care and school-based and community-based settings.

Childhood growth and coronary heart disease in later life

Coronary heart disease (CHD) originates early in life and numerous studies have shown inverse associations between body size at birth and CHD in adult life. Recently it has been shown that the increased risk for CHD associated with a small body size at birth is modified by growth during childhood. The greatest risk for CHD is noted in individuals with small body size at birth and who 'catch-up' in weight and body size during childhood. An increase in body weight and body mass index during the first year of life is however associated with a reduced risk of CHD. These recent findings add to the evidence that optimizing early growth is an important area in primary prevention of CHD. There are several potential mechanisms explaining the association between a non-optimal early growth and CHD. Behavioral, physiological, hormonal and genetic factors influence growth. Although socio-economic factors influence the risk of CHD, the association between slow fetal growth and CHD is not caused by confounding socio-economic factors. Biological programming -- the process whereby a stimulus during critical periods of development has long lasting or lifelong effects on metabolism -- is proposed to mediate the effects between early growth and adult diseases.

Childhood growth and coronary heart disease in later life

Coronary heart disease (CHD) originates early in life and numerous studies have shown inverse associations between body size at birth and CHD in adult life. Recently it has been shown that the increased risk for CHD associated with a small body size at birth is modified by growth during childhood. The greatest risk for CHD is noted in individuals with small body size at birth and who 'catch-up' in weight and body size during childhood. An increase in body weight and body mass index during the first year of life is however associated with a reduced risk of CHD. These recent findings add to the evidence that optimizing early growth is an important area in primary prevention of CHD. There are several potential mechanisms explaining the association between a non-optimal early growth and CHD. Behavioral, physiological, hormonal and genetic factors influence growth. Although socio-economic factors influence the risk of CHD, the association between slow fetal growth and CHD is not caused by confounding socio-economic factors. Biological programming -- the process whereby a stimulus during critical periods of development has long lasting or lifelong effects on metabolism -- is proposed to mediate the effects between early growth and adult diseases.