See also Fetal origins of adult disease-the hypothesis revisited.
Thus, the fetal origins hypothesis has not only survived contact with economics, but has flourished.
Origins of Cystic Fibrosis Lung Disease — NEJM
Obviously, we disagree. We take no comfort in the fact that a person, as demonstrated in case reports, can accidentally take several thousand times the recommended dose of vitamin D and still seem healthy after only several months â which is the only data Dr. Vieth provided. Our attention is directed towards long-term outcomes, time windows which correspond to the slow growth of chronic bacteria and other pathogens that may play a role in causing chronic disease. Also, the full negative effect of immunosuppressants (recall that we have found that 25-D acts as an immunosuppressant) can often only be noted after decades.
“The fetal origins hypothesis states that fetal undernutrition in middle to late gestation, which leads to disproportionate fetal growth, programmes later coronary heart disease.”
PPT - Fetal Origins Hypothesis: Pros and Cons …
Positioning the FOAD-hypothesis within the broader life course perspective in line with the suggestion of Ben-Shlomo and Kuh, fetal growth becomes merely one out of many periods of development, which cannot be assessed independently and detached from other periods. Without incorporation into a more comprehensive scope of theorizing and investigation – supportive evidence of the fetal origins hypothesis are bound to be merely scientific fragments. This insight was exemplified by a study on blood pressure based on the ‘Barry Caerphilly Growth Study’. This study investigates the comparative predictive value of fetal growth versus early childhood growth for blood pressure in early adulthood. According to the authors, it was the first study with sufficiently detailed data on growth trajectories over the first five years of life, and also follow-up in adulthood (age ≈25). By modelling growth trajectories before and after birth, they concluded that both prenatal and postnatal developmental factors are important determinants for blood pressure in early adulthood – indicating more than one early critical period for the development of hypertension. Studies that include fetal growth as part of a life-course perspective can help identify the relative importance of fetal growth against other factors, and further refine our insights into the aetiology of diseases in adulthood.
The FOAD-hypothesis has expanded greatly during the past decades, and is influential in medicine and epidemiology. Recently, the World Health Organization included low birthweight as a risk for factor for cardiovascular disease. The heart of the hypothesis – that environmental influences during gestation have an effect on later development – is a major insight and constitutes a complement to genetic and more proximal factors (such as adult lifestyle) as causes of adult disease. Whether there is an independent and direct public health impact of the associations reported within the FOAD-framework is however still unclear, even for outcomes such as blood pressure, non-insulin dependent diabetes mellitus and heart disease. As the search for determinants for disease and health continues, the FOAD-hypothesis is likely to remain an important perspective. It may however be better positioned as part of a life course epidemiology, than as an independent hypothesis.
Fetal Origins Hypothesis: Pros and Cons
The effects of impaired fetal growth are modified by subsequent growth: the highest risks of heart disease and of type 2 diabetes, the insulin resistance syndrome, or impaired glucose tolerance (collectively referred to below as impaired glucose tolerance) are in those who were small at birth but became overweight adults. This led to the second part of the hypothesis proposed by Barker and Hales: the idea of the “thrifty phenotype.” As an adaptation to undernutrition in fetal life permanent metabolic and endocrine changes occur which would be beneficial if nutrition remained scarce after birth. If nutrition becomes plentiful, however, these changes predispose to obesity and impaired glucose tolerance.
The congress heard a wide range of research that these hypotheses have stimulated. The patterns of prenatal and postnatal growth that predispose to the two major disease outcomes—ischaemic heart disease and impaired glucose tolerance—are complex (D J P Barker; J Eriksson and C Osmond). In general the most unfavourable growth pattern is smallness and thinness at birth, continued slow growth in early childhood, then acceleration of growth so that height and weight approach the population means. A continuing rise in body mass index above the mean is associated with impaired glucose tolerance. However, the patterns differ by sex and also by ponderal index (a rough measure of fatness) at birth. Whether or not the thrifty phenotype is the mechanism, low birth weight and high body mass index undoubtedly interact: their effects on blood pressure and impaired glucose tolerance are multiplicative ( D Leon).Birth weight and ponderal index (as well as body mass index) are crude measures of how fetal nutrition has affected body composition and of the balance between lean body mass and fat, so the true size of the effect of fetal growth on later disease is hard to measure.
The fetal and infant origins of adult disease
Fetal Origins Hypothesis: Mother’s Environment May …
Women are at a higher risk for heart disease than men because of a lack of knowledge and information.
See also Fetal origins of adult disease-the hypothesis ..
Unprotected sex, smoking, and obesity are not the disease; they are the cause of disease.
Fetal origins of disease hypothesis by Wendy Demelo - …
Christina Kanaka-Gantenbein Fetal origins of adult diabetes. Ann. N. Y. Acad. Sci.: 2010, 1205;99-105
Fetal Origins of Disease Hypothesis
Crucial when considering the origin of common diseases!
coronary heart disease + related disorders (hypertension, adult on-set diabetes, stroke) occur because of maladaptations that occur when a fetus in under-nourished.
1. Evidence for fetal origins of adult disease
The framework originally labelled ‘the Barker hypothesis’ has become among the more important frameworks on distal temporal determinants, suggesting that chronic illness is initiated by processes at prenatal stages. The main feature of the model is that intrauterine environmental exposures and events affect the fetus' development, and thereby increases the risk of specific diseases in adult life. Initially, the potential intrauterine environmental exposures of interest were both malnutrition and infections, but subsequent epidemiological studies have mainly focused on intrauterine nutrition. Support for the general hypothesis was first documented for coronary heart disease, but the framework has now been expanded to include a range of chronic conditions. Following the expansion, the hypothesis has been dubbed the fetal origins of adult disease (FOAD), and an increased focus on the mechanisms behind the observed associations has entailed. This narrative review will discuss the epidemiological evidence for the FOAD-hypothesis, and suggest future research directions within a broader framework of life course epidemiology.
Evidence for fetal origins of adult disease
The fetal origins of adult disease (FOAD) hypothesis suggests that risk factors from intrauterine environmental exposures affect the fetus' development during sensitive periods, and increases the risk of specific diseases in adult life. This link was initially observed between prenatal exposures and adult coronary heart disease, but corresponding observations have later been published for a range of chronic conditions. Although the hypothesis has been praised as an essential shift in our understanding of determinants for health, the hypothesis has also been criticized on a number of accounts, both methodologically and theoretically. The aim of this paper is to critically discuss the FOAD-hypothesis, in relation to the epidemiological evidence. We conclude that much of the research literature on the FOAD-hypothesis finds support for the hypothesis. Despite this, it is still unclear if the effects are independent and what the public health relevance is. Notwithstanding the heart of the hypothesis – that environmental influences during gestation have an effect on later development – should be considered a major insight and constitutes a complement to a focus on genetic and more proximal factors (such as adult lifestyle) as causes of adult disease. As the search for determinants for disease and health continues, the FOAD-hypothesis is likely to remain an important perspective. It may however be better positioned as part of a broader life course perspective, rather than as an independent hypothesis.
PPT – Fetal Origins Hypothesis: Pros and Cons …
This narrative review is based on a series of literature searches carried out over time during a PhD-project on associations between fetal and early life factors, and adult disease. The searches were done using several databases, including PubMed, Google Scholar and ISI Web of science. The reference lists of the identified research papers were inspected for further relevant literature (ancestry approach). The identified studies were read and assessed in accordance with the aims of the study.
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