Midlife Fitness Predicts Less Burden of Chronic Disease in Later Life

2013 ◽  
Vol 23 (6) ◽  
pp. 499-500 ◽  
Author(s):  
Taina Rantanen
Keyword(s):  
Chronic Disease ◽  
Later Life

scholarly journals Epigenetics and DOHaD: from basics to birth and beyond

2017 ◽  
Vol 8 (5) ◽  
pp. 513-519 ◽  
Author(s):  
T. Bianco-Miotto ◽  
J. M. Craig ◽  
Y. P. Gasser ◽  
S. J. van Dijk ◽  
S. E. Ozanne
Keyword(s):  
Dna Methylation ◽  
Chronic Disease ◽  
Chronic Diseases ◽  
Early Life ◽  
Later Life ◽  
Metabolic Health ◽  
Number Of Children ◽  
Early Life Environment ◽  
Increased Risk ◽  
Early Life Exposures

Developmental origins of health and disease (DOHaD) is the study of how the early life environment can impact the risk of chronic diseases from childhood to adulthood and the mechanisms involved. Epigenetic modifications such as DNA methylation, histone modifications and non-coding RNAs are involved in mediating how early life environment impacts later health. This review is a summary of the Epigenetics and DOHaD workshop held at the 2016 DOHaD Society of Australia and New Zealand Conference. Our extensive knowledge of how the early life environment impacts later risk for chronic disease would not have been possible without animal models. In this review we highlight some animal model examples that demonstrate how an adverse early life exposure results in epigenetic and gene expression changes that may contribute to increased risk of chronic disease later in life. Type 2 diabetes and cardiovascular disease are chronic diseases with an increasing incidence due to the increased number of children and adults that are obese. Epigenetic changes such as DNA methylation have been shown to be associated with metabolic health measures and potentially predict future metabolic health status. Although more difficult to elucidate in humans, recent studies suggest that DNA methylation may be one of the epigenetic mechanisms that mediates the effects of early life exposures on later life risk of obesity and obesity related diseases. Finally, we discuss the role of the microbiome and how it is a new player in developmental programming and mediating early life exposures on later risk of chronic disease.

scholarly journals Association Between Speed of Multimorbidity Accumulation in Old Age and Life Experiences: A Cohort Study

2019 ◽  
Vol 188 (9) ◽  
pp. 1627-1636 ◽  
Author(s):  
Serhiy Dekhtyar ◽  
Davide Liborio Vetrano ◽  
Alessandra Marengoni ◽  
Hui-Xin Wang ◽  
Kuan-Yu Pan ◽  
...  
Keyword(s):  
Chronic Disease ◽  
Elementary Education ◽  
Chronic Conditions ◽  
Life Experiences ◽  
Laboratory Data ◽  
Later Life ◽  
Adverse Outcomes ◽  
National Study ◽  
Multiple Chronic Conditions ◽  
Medical Histories

Abstract Rapidly accumulating multiple chronic conditions (multimorbidity) during aging are associated with many adverse outcomes. We explored the association between 4 experiences throughout life—childhood socioeconomic circumstances, early-adulthood education, midlife occupational stress, and late-life social network—and the speed of chronic disease accumulation. We followed 2,589 individuals aged ≥60 years from the Swedish National Study on Aging and Care in Kungsholmen for 9 years (2001–2013). Information on life experiences was collected from detailed life-history interviews. Speed of disease accumulation was operationalized as the change in the count of chronic conditions obtained from clinical examinations, medical histories, laboratory data, drug use, and register linkages over 9 years. Linear mixed models were used to analyze the data. Speed of disease accumulation was lower in individuals with more than elementary education (for secondary, β × time = −0.065, 95% CI: −0.126, −0.004; for university, β × time = −0.118, 95% CI: −0.185, −0.050); for active occupations compared with high-strain jobs (β × time = −0.078, 95% CI: −0.138, −0.017); and for richer social networks (for moderate tertile, β × time = −0.102, 95% CI: −0.149, −0.055; for highest tertile, β × time = −0.135, 95% CI: −0.182, −0.088). The association between childhood circumstances and speed of disease accumulation was attenuated by later-life experiences. Diverse experiences throughout life might decelerate chronic disease accumulation during aging.

scholarly journals Neighborhoods and Chronic Disease Onset in Later Life

2011 ◽  
Vol 101 (1) ◽  
pp. 79-86 ◽  
Author(s):  
Vicki A. Freedman ◽  
Irina B. Grafova ◽  
Jeannette Rogowski
Keyword(s):  
Chronic Disease ◽  
Disease Onset ◽  
Later Life

scholarly journals Pre-eclampsia and long-term maternal health

2012 ◽  
Vol 5 (3) ◽  
pp. 98-104 ◽  
Author(s):  
David Williams
Keyword(s):  
Chronic Disease ◽  
Endothelial Dysfunction ◽  
Later Life ◽  
Hepatic Necrosis ◽  
Chronic Hypertension ◽  
Maternal Circulation ◽  
Single Episode ◽  
Impaired Memory ◽  
Increased Risk

Pre-eclampsia is a syndrome of pregnancy, defined by the gestational-onset of hypertension and proteinuria, which resolves postpartum. This definition does not consider the variable multiorgan involvement of a syndrome that can include seizures, fulminating hepatic necrosis and a consumptive coagulopathy. These disparate clinical features are a consequence of an accelerated but transient metabolic syndrome with widespread maternal endothelial dysfunction and inflammation. A trigger to this maternal state is the relatively ischaemic placenta. As pregnancy progresses, the concentration of vaso-toxic factors released by the relatively ischaemic placenta gradually builds up in the maternal circulation. Those predisposed to endothelial dysfunction, e.g. women with risk factors for cardiovascular disease, are more sensitive to these placental derived factors and will develop pre-eclampsia before natural onset of labour. A woman's vulnerability to pre-eclampsia is therefore composed of a unique balance between her pre-existing maternal endothelial and metabolic health and the concentration of placental derived factors toxic to maternal endothelium. Delivery of the placenta remains the only cure. Years later, women who had pre-eclampsia are at increased risk of chronic hypertension, ischaemic heart disease, cerebrovascular disease, kidney disease, diabetes mellitus, thromboembolism, hypothyroidism and even impaired memory. This article describes how a brief, usually single episode of this acute pregnancy syndrome might both identify those vulnerable to chronic disease in later life and in some cases initiate chronic disease.

Fetal programming: the perspective of single and twin pregnancies

2005 ◽  
Vol 17 (3) ◽  
pp. 379 ◽  
Author(s):  
Michael J. Davies
Keyword(s):  
Chronic Disease ◽  
Fetal Growth ◽  
Low Birthweight ◽  
Multiple Pregnancy ◽  
Experimental Studies ◽  
Later Life ◽  
Growth Restriction ◽  
Physiological Adaptation ◽  
Increased Risk ◽  
Twin Pregnancies

Multiple pregnancy is associated with increased risk of adverse consequences for both mother and fetus(es), including increased rates of maternal hypertension and pre-eclampsia, spontaneous abortion, Caesarean delivery, low birthweight, birth prematurity, perinatal mortality, admission to neonatal intensive care and extended length of care, respiratory distress, cerebral palsy, developmental delay, contact with disability services and mortality to age 5 years. Premature birth, which affects 97% of triplets and 53.3% of twins in Australia, is not the sole factor involved. The rate of multiple pregnancy in Australia is 1.7%. This compares to 22.1% for pregnancies resulting from assisted reproduction technology (ART). As a result, 21.8% of babies born from ART are from a multiple pregnancy, in comparison to the USA where the majority of babies born from ART are from a multiple pregnancy. Additionally, the population rate of multiple births is rising due to the more frequent use of ART and continued multi-embryo transfers, which is operating against a background of rising implantation rates within ART clinics. Twins have been of interest from a programming perspective. However, analysis of associations between crude birthweight and subsequent metabolic risk factors or mortality in adulthood from chronic disease indicate that adaptations in pregnancy to support multi-fetal growth are not identical to fetal growth restriction in singleton pregnancies. Indeed, the process of ‘maternal constraint’ is incompletely understood and confounds such comparisons. From a programming perspective, it is a challenge to identify in twin pregnancies the transition from physiological adaptation to pathological growth restriction. Growth disparity between twins has been more illuminating of subtle adverse effects for the smaller of twin pairs in both blood pressure and insulin resistance in adulthood. Interestingly, these effects can be observed in both dizygotic and to a lesser degree in monozygotic twins, which indicates a role for both genetic and environmental factors in these measures. This suggests that, consistent with experimental studies in other species, the relationship between impaired growth in utero and chronic disease in later life is not simply mediated by a common genetic pathway.

scholarly journals Chronic disease and infant nutrition: is it significant to public health?

2010 ◽  
Vol 14 (2) ◽  
pp. 279-289 ◽  
Author(s):  
Julie P Smith ◽  
Peta J Harvey
Keyword(s):  
Public Health ◽  
Chronic Disease ◽  
Breast Milk ◽  
Breast Feeding ◽  
Disease Risk ◽  
Later Life ◽  
Chronic Disease Risk ◽  
Public Health Significance ◽  
Health Significance ◽  
Breast Fed

AbstractObjectiveTo assess the public health significance of premature weaning of infants from breast milk on later-life risk of chronic illness.DesignA review and summary of recent meta-analyses of studies linking premature weaning from breast milk with later-life chronic disease risk is presented followed by an estimation of the approximate exposure in a developed Western country, based on historical breast-feeding prevalence data for Australia since 1927. The population-attributable proportion of chronic disease associated with current patterns of artificial feeding in infancy is estimated.ResultsAfter adjustment for major confounding variables, current research suggests that the risks of chronic disease are 30–200 % higher in those who were not breast-fed compared to those who were breast-fed in infancy. Exposure to premature weaning ranges from 20 % to 90 % in post-World War II age cohorts. Overall, the attributable proportion of chronic disease in the population is estimated at 6–24 % for a 30 % exposure to premature weaning.ConclusionsBreast-feeding is of public health significance in preventing chronic disease. There is a small but consistent effect of premature weaning from breast milk in increasing later-life chronic disease risk. Risk exposure in the Australian population is substantial. Approximately 90 % of current 35–45-year-olds were weaned from breast-feeding by 6 months of age. Encouraging greater duration and exclusivity of breast-feeding is a potential avenue for reducing future chronic disease burden and health system costs.

scholarly journals Physical activity throughout pregnancy is key to preventing chronic disease

Reproduction ◽  
2020 ◽  
Vol 160 (5) ◽  
pp. R111-R118 ◽  
Author(s):  
Taniya S Nagpal ◽  
Michelle F Mottola
Keyword(s):  
Physical Activity ◽  
Chronic Disease ◽  
Chronic Diseases ◽  
Physiological Response ◽  
Exercise Intervention ◽  
Disease Risk ◽  
Later Life ◽  
Intrauterine Environment ◽  
Chronic Disease Risk ◽  
Maternal Exposures

According to The Developmental Origins of Health and Disease theory, the intrauterine environment of the developing fetus may impact later life physiology, including susceptibility to chronic disease conditions. Maternal exposures during pregnancy can affect the intrauterine environment and result in fetal programming for chronic diseases through changes in the structure or function of specific organs. Negative maternal exposures, such as poor nutrition intake, have been shown to increase the risk for later life chronic diseases. On the contrary, healthful behaviors, such as physical activity, may have a positive and protective effect against chronic disease risk. This narrative review summarizes literature to discuss the potential preventative role prenatal physical activity may have on prevalent chronic diseases: obesity, type 2 diabetes, and cardiovascular disease. We describe the natural physiological response to pregnancy that may increase the risk for complications and consequently later life disease for both mother and baby. We then present evidence highlighting the role prenatal exercise may have in preventing pregnancy complications and downstream chronic disease development, as well as proposing potential mechanisms that may explain the protective maternal and fetal physiological response to exercise. As the prevalence of these non-communicable diseases increase globally, intervening during pregnancy with an effective exercise intervention may be the key to preventing chronic disease risk in more than one generation.

In utero programming of chronic disease

1998 ◽  
Vol 95 (2) ◽  
pp. 115-128 ◽  
Author(s):  
D. J. P. BARKER
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Chronic Disease ◽  
Later Life ◽  
In Utero ◽  
Human Fetuses ◽  
Limited Supply ◽  
Structure And Metabolism

1.Many human fetuses have to adapt to a limited supply of nutrients. In doing so they permanently change their structure and metabolism. 2.These ‘programmed' changes may be the origins of a number of diseases in later life, including coronary heart disease and the related disorders stroke, diabetes and hypertension. 3.This review examines the evidence linking these diseases to fetal undernutrition and provides an overview of previous studies in this area.

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