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Even USA Today is getting into the finger measuring business, though their recommended technique is not very accurate. And some of the more recent articles on epigenetics appearing in Medline are reading like sound bites for The GenoType Diet:
Medical practice patterns which are designed to provide quick and effective amelioration of signs and symptoms are frequently not an enduring solution to many health afflictions and chronic disease states. Recent scientific discovery has rendered the drug-oriented algorithmic paradigm commonly found in contemporary evidence-based medicine to be a reductionist approach to clinical practice. Unfolding evidence appears to support a genetic predisposition model of health and illness rather than a fatalistic predestination construct - modifiable epigenetic and environmental factors have enormous potential to influence clinical outcomes. By understanding and applying fundamental clinical principles relating to the emerging fields of molecular medicine, nutrigenomics and human exposure assessment, doctors will be empowered to address causality of affliction when possible and achieve sustained reprieve for many suffering patients.
-'Our genes are not our destiny: incorporating molecular medicine into clinical practice.' J Eval Clin Pract. 2008 Feb;14(1):94-102.
A wealth of evidence points to the diet as one of the most important modifiable determinants of the risk of developing cancer, but a greater understanding of the interaction between diet and genes may help distinguish who will and will not respond to dietary interventions. The term nutrigenomics or nutritional genomics refers to the bidirectional interactions between genes and diet. Nutritional genomics encompasses an understanding about how the response to bioactive food components depends on an individual's genetic background (nutrigenetics), nutrient induced changes in DNA methylation, histone posttranslational modifications, and other chromatin alterations (nutritional epigenetics), and nutrient induced changes in gene expression (nutritional transcriptomics). These approaches to the study of nutrition will assist in understanding how genetic variation, epigenetic events, and regulation of gene expression alter requirements for, and responses to, nutrients. Recognition of the interplay between genes and diet could ultimately help identify modifiable molecular targets for preventing, delaying, or reducing the symptoms of cancer and other chronic diseases.
'Nutritional genomic approaches to cancer prevention research.' Exp Oncol. 2007 Dec;29(4):250-6
Obesity and type 2 diabetes arise from a set of complex gene-environment interactions. Explanations for the heritability of these syndromes and the environmental contribution to disease susceptibility are addressed by the "thrifty genotype" and the "thrifty phenotype" hypotheses. Here, the merits of both models are discussed and elements of them are used to synthesize a "thrifty epigenotype" hypothesis. I propose that: (1) metabolic thrift, the capacity for efficient acquisition, storage and use of energy, is an ancient, complex trait, (2) the environmentally responsive gene network encoding this trait is subject to genetic canalization and thereby has become robust against mutational perturbations, (3) DNA sequence polymorphisms play a minor role in the aetiology of obesity and type 2 diabetes-instead, disease susceptibility is predominantly determined by epigenetic variations, (4) corresponding epigenotypes have the potential to be inherited across generations, and (5) Leptin is a candidate gene for the acquisition of a thrifty epigenotype.
'The thrifty epigenotype: An acquired and heritable predisposition for obesity and diabetes?' Bioessays. 2008 Feb;30(2):156-66.
Compared to other periods of life, infancy is a period of rapid growth, but the relative relationships among rates of linear growth, weight accretion and brain growth vary greatly during the first years of life. Additionally, while the energy requirements for body tissue deposition as a fraction of daily energy needs decrease dramatically during infancy, brain energy demands, measured as the cerebral rate of glucose utilization, increase markedly during the same period. There is now substantial evidence that postnatal growth in infancy is associated with various consequences detrimental to health in adult life, particularly hypertension, cardiovascular disease, obesity and type 2 diabetes, but the relationships vary depending on whether one takes growth to mean statural growth or ponderal growth, as well as on the specific period of infant growth. Recently, several mechanisms have surfaced that might account for the relationships observed. These include epigenetic effects on gene expression, alterations in neuronal signaling because of inappropriate dendritic pruning, and gut microbiota effects on fat storage.
'Growth in the first two years of life.' Nestle Nutr Workshop Ser Pediatr Program. 2008;61:135-44.
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