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New research published in the Journal of Leukocyte Biology suggests that these changes to the behaviour of the immune system are persistent and can continue even after your diet has improved.[1] It is fairly universally understood that improving your food behaviour and choice will most likely improve your health. However, less well understood or known is that the effects of poor eating habits persist long after dietary habits are improved. In a new report appearing in the November 2014 issue of the Journal of Leukocyte Biology, scientists use mice to show that even after successful treatment of atherosclerosis (including lowering of blood cholesterol and a change in dietary habits) the effects of an unhealthy lifestyle still impact upon the way the immune system functions. This change in function occurs largely because poor eating habits alter the way genes express themselves, including genes related to immunity which make up the largest collection of specific genes in the human structure. This change in gene expression (epigenetics) ultimately maintains the risk of cardiovascular disorders at a level far higher than it would be had there been no exposure to unhealthy foods in the first place.

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A recent article in Medscape (Expert Rev Clin Immunol. 2013;9(8):735-747.) looked at the role of foods in the management of IBD. The author Lynette Ferguson summarised some of the key areas, and this summary is a synopsis of her paper.

Inflammatory bowel disease includes ulcerative colitis and Crohn’s disease, which are both inflammatory disorders of the gastrointestinal tract. Both types of inflammatory bowel disease have a complex aetiology, resulting from a genetically determined susceptibility interacting with environmental factors, including the diet and gut microbiota. Genome Wide Association Studies have implicated more than 160 single-nucleotide polymorphisms in disease susceptibility. Consideration of the different pathways suggested to be involved implies that specific dietary interventions are likely to be appropriate, dependent upon the nature of the genes involved. Epigenetics and the gut microbiota are also responsive to dietary interventions. Nutrigenetics may lead to personalized nutrition for disease prevention and treatment, while nutrigenomics may help to understand the nature of the disease and individual response to nutrients.

Nature Vs Nurture Debate Meets Godzilla

Monday, 14 June 2010 by | Comments: 1
Reading Time: 4 minutes

Nutrition, infection, experiences, the environment and genes interact to provide alterations to the phenotype. This concept is referred to as plasticity, the ability of organisms or cells to alter their phenotype in response to changes in the environment.[1]

This interaction is able to be measured at the level of the actual genome by analysing epigenetic modifications, at the individual cell and organism level by observing the effects during development of the embryo or by changes in the behaviour of adults for example.

Traditional science taught us that cells were hard wired for a lifetime and that our future was encoded in our DNA, providing a neat ‘get out of responsibility’ clause for those patients wishing to explain their lack of willingness to engage in lifestyle changes as being a pointless attempt to mitigate those genetic codes handed down from their parents.

Modern science demonstrates that cells are remarkably plastic in their ability to adapt, and epigenetics explains how these modifications impact on our future decisions concerning interventions that influence cell and gene expression.

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Folate (the naturally occurring form) and folic acid are forms of a water-soluble B vitamin (B9) that were first synthesized in 1945. Folate functions as an important cofactor in the transfer and use of 1-carbon moieties, primarily methyl groups. An important advance in understanding subclinical folate deficiency came in 1991 with the demonstration that folic acid supplementation before and during pregnancy dramatically reduced the risk of neural-tube defects in newborns. Folate supplementation of women before and during the first trimester of pregnancy has a dose-response effect in preventing neural-tube defects, ranging from a 23% reduction with 200 μg to an 85% reduction with 5000 μg of folic acid per day. The strong evidence demonstrating reduced risks of neural-tube defects led to mandatory folic acid fortification of cereal grain products in the United States by January 1, 1998. Fortification of foods with folic acid in the United States costs about $1,000 per neural-tube defect prevented. Even with all the information on the benefits of folate, many studies show inadequate folate intake among young women. Adequate folate levels have also been associated with reduced risks of coronary artery disease, colorectal cancer, and dementia.