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Developmental origins of health and disease: reducing the burden of chronic disease in the next generation
Peter D Gluckman, Mark A Hanson, Murray D Mitchell
Genome Medicine , 2010, DOI: 10.1186/gm135
Abstract: The concept of developmental origins of health and disease is predicated upon the assumption that environmental factors acting early in life (usually in fetal life) have profound effects on vulnerability to disease later in life, often in adulthood. The range of experimental, clinical and epidemiological data linking conditions in early life to later health is now overwhelming [1]. Initially, the focus was on a small fraction of children -those who were born small - but it is now clear that the environment impacts on the development of every child [2]. Observations and experimental approaches have generally considered nutritional changes or, classically, alterations in glucocorticosteroid exposure, reflecting the critical maturational events linked to such events. Indeed, the placenta is in a critical position to cause or modify such challenges by altering nutritional transport functions or the pattern and nature of endocrine signals impacting the fetus. Nor does the story end at birth, because epigenetic development can be influenced by how the infant is fed, and perhaps how its gut is colonized with commensal bacteria.Yet there has been considerable resistance to these ideas. Medicine is replete with reductionist biomedical thinking and this has, in some ways, limited not only our understanding but also our ability to address the challenge of some contemporary health problems. Nowhere is this clearer than in the outcomes of genome-wide association studies where, despite substantial investment, only a relatively small proportion of risk of common non-communicable diseases (NCDs) - such as cardiovascular disease and diabetes - is explained [3]. The economic and humanitarian costs of NCDs are enormous in both the developed and the developing world, and indeed they may destabilize the economies of low-income countries where recent data show that risk markers for these diseases become evident early in the process of socioeconomic improvement, and well below the level o
Health Promotion and Disease Prevention Strategies in Older Adults with Intellectual and Developmental Disabilities  [PDF]
Eli Carmeli
Frontiers in Public Health , 2014, DOI: 10.3389/fpubh.2014.00031
Abstract: The rapid growth in the number of individuals living with intellectual and developmental disabilities (IDD) along with their increased longevity present challenges to those concerned about health and well-being of this unique population. While much is known about health promotion and disease prevention in the general geriatric population, far less is known about those in older adults with IDD. Effective and efficient health promotion and disease prevention strategies need to be developed and implemented for improving the health and quality of life of older adults living with IDD. This is considered to be challenging given the continued shrinkage in the overall health care and welfare system services due to the cut in the governmental budget in some of the western countries. The ideal health promotion and disease prevention strategies for older adults with IDD should be tailored to the individuals’ health risks, address primary and secondary disease prevention, and prevent avoidable impairments that cause premature institutionalization. Domains of intervention should include cognitive, mental and physical health, accommodations, workplace considerations, assistive technology, recreational activities, and nutrition.
Developmental origins of non-communicable disease: Implications for research and public health
Robert Barouki, Peter D Gluckman, Philippe Grandjean, Mark Hanson, Jerrold J Heindel
Environmental Health , 2012, DOI: 10.1186/1476-069x-11-42
Abstract: For many years biologists considered the developmental period to be controlled by a strict, hard-wired genetic program, and thus it was uncertain how it could be influenced by the environment. It is now clear that development is plastic, and that it allows the organism to respond to the surrounding environment, especially during early development when cells are differentiating and tissues are developing. This capacity is based on molecular pathways that lead to control of gene expression and induction of specific phenotypes in the absence of DNA sequence modification [1]. These pathways, as currently understood, include DNA methylation, histone covalent modification, and noncoding RNA expression. Such epigenetic modifications can be passed from one cell generation to the next and, in some cases, when germ cells are targeted, can be transgenerationally transmitted [2]. Furthermore, these changes can be cell, tissue, and sex specific, and time dependent. In many cases they may not be apparent during a latent period which may last from months to years or decades. Thus, each individual has one genome, but will hold multiple epigenomes.The ability to respond to environmental conditions can be evolutionarily advantageous by allowing fine-tuning of gene expression, likely through epigenetic mechanisms [3]. Thus, developmentally plastic processes allow the organism to adapt to changing environments in order to maintain or improve reproductive capability in part by sustaining health through the reproductive period. However, interference with these developmentally-adaptive processes may also have adverse consequences on some functions and disease risks later in life. Furthermore, these mechanisms are also sensitive to environmental stimuli other than the nutrients and physiological factors that are normative, in evolutionary terms, to the human environment. Indeed, drugs, industrial chemicals, tobacco smoke, and other environmental exposures can affect these same mechanisms l
Conceptions about mental health in the field of public health
Diego A. Restrepo O,Juan C. Jaramillo E
Revista Facultad Nacional de Salud Pública , 2012,
Abstract: In the field of public health, mental health has had a great deal of relevance. This concept has been used extensively in the professional, academic, and political fields. Despite that, the different definitions of mental health face significant epistemological and practical problems. These difficulties are encountered by those who try to specify the meaning of "mental", the relationship between "health" and "mental", and, consequently, how research and intervention actions are to be carried out in the field of mental health. In practice, the orientation of actions and research involving mental health is not based on “universal” definitions in the field of public health. It is rather based on conceptions constructed from different approaches to the health-disease issue. This paper discusses the conceptions of mental health that have been configured from the biomedical, behavioral, and socio-economic approaches, the notions of "mind" underlying these conceptions, and their implications for intervention in the field of public health.
Antistreptolysin O titer in health and disease: levels and significance
Alyaa Amal Kotby,Nevin Mamdouh Habeeb,Sahar Ezz El Arab
Pediatric Reports , 2012, DOI: 10.4081/pr.2012.e8
Abstract: Over diagnosis of acute rheumatic fever (ARF) based on a raised antistreptolysin O titer (ASOT) is not uncommon in endemic areas. In this study, 660 children (aged 9.2 ±1.7 years) were recruited consecutively and classified as: G1 (control group, n=200 healthy children), G2 (n=20 with ARF 1st attack), G3 (n=40 with recurrent ARF), G4 (n=100 with rheumatic heart disease (RHD) on long acting penicillin (LAP)), G5 (n=100 with acute follicular tonsillitis), and G6 (n=200 healthy children with history of repeated follicular tonsillitis more than three times a year). Serum ASOT was measured by latex agglutination. Upper limit of normal (ULN) ASOT (80th percentile) was 400 IU in G1, 200 IU in G4, and 1600 IU in G6. Significantly high levels were seen in ARF 1st attack when compared to groups 1 and 5 (P<0.001 and P<0.05, respectively). ASOT was significantly high in children over ten years of age, during winter and in those with acute rheumatic carditis. ASOT showed significant direct correlation with the number of attacks of tonsillitis (P<0.05). Egyptian children have high ULN ASOT reaching 400 IU. This has to be taken into consideration when interpreting its values in suspected ARF. A rise in ASOT is less prominent in recurrent ARF compared to 1st attack, and acute and recurrent tonsillitis. Basal levels of ASOT increase with age but the pattern of increase during infection is not age dependent
Crying and Health: Popular and Scientific Conceptions  [PDF]
Ad J .J. M. Vingerhoets,Lauren Bylsma
Psychological Topics , 2007,
Abstract: We summarize popular and pre-scientific conceptions of the relationship between crying, well-being and health, and we review the scientific literature on this topic. First, the focus is on whether crying brings relief and facilitates emotional recovery. Next, we discuss the evidence addressing whether crying or its chronic inhibition is associated with an increased risk of developing health problems. Finally, we address crying as a signal or symptom of disease. It is concluded that the question regarding whether crying brings relief has yielded seemingly contrasting findings, dependent on the design of the study. Concerning the second and third issues, there is a lack of sound studies. Little is known about the nature of the association between depression and crying. The evidence for a relationship between neurological disorders (in particular, stroke and multiple sclerosis) appears more convincing. There is also mainly anecdotal evidence of increased crying in a wide variety of health problems, which may reflect symptoms of disease, co-morbid depression, adjustment problems, or side effects of treatment. Some recent studies further suggest a positive effect of crying on health status in certain patient groups. More systematic and well-designed studies are needed to clarify the relationship between crying and health.
Developmental Origins of Health and Disease  [PDF]
Simon C. Langley-Evans,Barbara Alexander,Harry J. McArdle,Deborah M. Sloboda
Journal of Nutrition and Metabolism , 2012, DOI: 10.1155/2012/838640
Abstract:
Developmental Origins of Health and Disease  [PDF]
Simon C. Langley-Evans,Barbara Alexander,Harry J. McArdle,Deborah M. Sloboda
Journal of Nutrition and Metabolism , 2012, DOI: 10.1155/2012/838640
Abstract:
Theoretical conceptions on the theory on health education. Systematic review
Diaz-Valencia,Paula Andrea;
Investigación y Educación en Enfermería , 2012,
Abstract: objective. to identify the theoretical conceptions of health education (he) reported by recent scientific literature. methodology. systematic review without meta-analysis of the scientific literature published on the theory on he between 2000 and 2010 in spanish, english, and portuguese in pubmed, elsevier, and scielo. this included publications developing at least the theoretical categories on he: conceptual development, history, current situation, as discipline, teaching and research. results. some 58 articles on he were analyzed. the main categories contained in the articles were those of current situation and conceptual development. the definition and conceptualization of he are diffuse. most authors state that the term he lacks identity and that tension exists between this concept and that of healthcare promotion. conclusion. processes in he are not sufficiently qualified.
Developmental Programming of Hypertension and Kidney Disease  [PDF]
Euming Chong,Ihor V. Yosypiv
International Journal of Nephrology , 2012, DOI: 10.1155/2012/760580
Abstract: A growing body of evidence supports the concept that changes in the intrauterine milieu during “sensitive” periods of embryonic development or in infant diet after birth affect the developing individual, resulting in general health alterations later in life. This phenomenon is referred to as “developmental programming” or “developmental origins of health and disease.” The risk of developing late-onset diseases such as hypertension, chronic kidney disease (CKD), obesity or type 2 diabetes is increased in infants born prematurely at <37 weeks of gestation or in low birth weight (LBW) infants weighing <2,500?g at birth. Both genetic and environmental events contribute to the programming of subsequent risks of CKD and hypertension in premature or LBW individuals. A number of observations suggest that susceptibility to subsequent CKD and hypertension in premature or LBW infants is mediated, at least in part, by reduced nephron endowment. The major factors influencing in utero environment that are associated with a low final nephron number include uteroplacental insufficiency, maternal low-protein diet, hyperglycemia, vitamin A deficiency, exposure to or interruption of endogenous glucocorticoids, and ethanol exposure. This paper discusses the effect of premature birth, LBW, intrauterine milieu, and infant feeding on the development of hypertension and renal disease in later life as well as examines the role of the kidney in developmental programming of hypertension and CKD. 1. Introduction Despite the availability of a number of treatment options for hypertension, cardiovascular, and renal disease, the prevalence, morbidity, and mortality of these diseases in children and adults remain very high [1]. Therefore, elucidation of the causality and pathogenesis of these diseases is critical. Studies by Widdowson and McCance in the 1960s demonstrated that acceleration or retardation of the rate of growth induced by malnutrition during early postnatal life in rats led to distinct and different effects on anatomical, physiological, and chemical development [2]. In the 1980s, studies by Barker demonstrated that systolic blood pressure in older children is inversely related to their birth weight [3]. Around the same time, Brenner hypothesized that early loss of nephron mass results in hyperfiltration of remaining nephrons leading to subsequent hypertension, proteinuria, and progressive kidney injury [4]. These and subsequent studies have provided initial evidence that a suboptimal in utero environment may predispose or “program” an individual to an increased risk of
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