Nutrigenetics, Nutrigenomics and Inflammatory Bowel Diseases
Nutrigenetics, Nutrigenomics and Inflammatory Bowel Diseases
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 etiology, 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.
The field of nutrigenetics recognizes the effect of genetic variation on nutrient requirements, while nutrigenomics covers the nutrient regulation of gene expression. Inflammatory bowel diseases (IBDs) fall into one of two main groups: Crohn's disease (CD) or ulcerative colitis (UC). Both are chronic inflammatory disorders of the gastrointestinal tract, involving dysregulation of the immune system. It has also been suggested that both of these forms of IBD are excellent examples for which both nutrigenetics and nutrigenomics are relevant.
The author previously reviewed this field in 2010. It is still true that nutrigenomic approaches are appropriate to maintaining disease remission, but that the current situation regarding detection of disease susceptibility and early disease development remains largely unchanged from that in 2010 (Figure 1).
(Enlarge Image)
Figure 1.
Current situation in respect to detection of inflammatory bowel disease susceptibility. Currently, when people (often teenagers) are diagnosed with inflammatory bowel disease, they are given an elemental diet and/or pharmaceutical assistance. Very often, despite these measures, people with the disease will require ongoing clinical and surgical interventions.Reproduced with permission from [1].
More recently published studies emphasize the importance, not only of genetic susceptibility to disease and of gene–diet interactions, but also of epigenetics and the gut microbiota, which are equally susceptible to dietary manipulation.
Epigenetics provides a mechanism for regulating otherwise heritable changes in gene expression, but without changes to the coding DNA sequence. The importance of this field in IBD has become increasingly recognized in recent years. In the current review, epigenetics appears in two sections. The first section provides key principles including epigenetic mechanisms and the role of epigenetics in IBD symptoms and progression. The second part of the work on epigenetics appears in the section on diet, where some of the publications specifically consider the role of specific nutrients in modulating epigenetic status.
The gut microbiota is also proving important to IBD initiation and progression. A less variable gut microbial ecosystem as compared with normal individuals is common in both forms of IBD. Baker et al. discussed how mucosal lesions in IBD may be the result of a dysregulated immune response that is caused by aberrant microbial colonization of the gastrointestinal tract. This would be especially true where individuals are genetically susceptible to IBD, through carrying variants in immune response or autophagy. However, whether this distinctive gut microbiome is a cause or an effect of the disease is unclear at present.
This update primarily considers new data published between 2011 and 2013.
Abstract and Introduction
Abstract
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 etiology, 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.
Introduction
The field of nutrigenetics recognizes the effect of genetic variation on nutrient requirements, while nutrigenomics covers the nutrient regulation of gene expression. Inflammatory bowel diseases (IBDs) fall into one of two main groups: Crohn's disease (CD) or ulcerative colitis (UC). Both are chronic inflammatory disorders of the gastrointestinal tract, involving dysregulation of the immune system. It has also been suggested that both of these forms of IBD are excellent examples for which both nutrigenetics and nutrigenomics are relevant.
The author previously reviewed this field in 2010. It is still true that nutrigenomic approaches are appropriate to maintaining disease remission, but that the current situation regarding detection of disease susceptibility and early disease development remains largely unchanged from that in 2010 (Figure 1).
(Enlarge Image)
Figure 1.
Current situation in respect to detection of inflammatory bowel disease susceptibility. Currently, when people (often teenagers) are diagnosed with inflammatory bowel disease, they are given an elemental diet and/or pharmaceutical assistance. Very often, despite these measures, people with the disease will require ongoing clinical and surgical interventions.Reproduced with permission from [1].
More recently published studies emphasize the importance, not only of genetic susceptibility to disease and of gene–diet interactions, but also of epigenetics and the gut microbiota, which are equally susceptible to dietary manipulation.
Epigenetics provides a mechanism for regulating otherwise heritable changes in gene expression, but without changes to the coding DNA sequence. The importance of this field in IBD has become increasingly recognized in recent years. In the current review, epigenetics appears in two sections. The first section provides key principles including epigenetic mechanisms and the role of epigenetics in IBD symptoms and progression. The second part of the work on epigenetics appears in the section on diet, where some of the publications specifically consider the role of specific nutrients in modulating epigenetic status.
The gut microbiota is also proving important to IBD initiation and progression. A less variable gut microbial ecosystem as compared with normal individuals is common in both forms of IBD. Baker et al. discussed how mucosal lesions in IBD may be the result of a dysregulated immune response that is caused by aberrant microbial colonization of the gastrointestinal tract. This would be especially true where individuals are genetically susceptible to IBD, through carrying variants in immune response or autophagy. However, whether this distinctive gut microbiome is a cause or an effect of the disease is unclear at present.
This update primarily considers new data published between 2011 and 2013.