There is a relatively new, and very exciting area in Nutritional Therapy called nutrigenomics. Nutrigenomics explores the relationship between your diet and your genes. Whether we eat, drink, move or breathe, we initiate interactions between our genes (nature) and their environment (nurture). This is nutrigenomics in actions, every minute of every day.
Nutrigenomics is often used interchangeably with nutrigenetics however there is a difference. Nutrigenetics refers to the effect of genetic variation on a dietary response. Examples could be the LCT gene on lactose tolerance. Nutrigenomics is more systemic, describing the impact of nutrients and foods on gene expression. An example might be the effect grapefruit juice has on detoxification pathways and vitamins such as folate and B12 has on the Folate and Methionine Cycles, equating to methylation.
Nutrigenomics as a far-reaching effect and potential when it comes to preventing diet-related diseases.
Nutrigenomics is far from straight-forward when providing a linear perspective on anyone give SNP (single nucleotide polymorphism), or enzyme deletion. Since nature has always provided multiple pathways to arrive at any one end result. Therefore when considering the health of each organ and system, there will be many complexes, and interrelated factors to be considered With rarely one single gene that inevitably leads to any given result.
Single Gene Impacts
BCO1 is the gene responsible for the conversion of beta-carotene to vitamin A, its biologically active form. When there are two BCO1 SNP’s, this can reduce the gene activity by as much as 69%. BCO1 is then further reduced by each variant, Someone with no variants would expect to have hi conversion activity, whereas variants on both BCO1 SNP’s would expect low conversion. Other genotypes would be somewhere in the middle.
This expressivity is the key, which links the gene activity to an observable trait or disease. Not necessarily directly, as there are multiple and bio-directional downstream consequences with every SNP’s deletion.
Another example of variable expressivity is eye colour. Whereby the extent to which the gene for brown pigment is expressed on a sliding scale in the eyes.
Those with low expressivity should look to food with sufficient vitamin A, such as liver, fish oil and egg yolk, rather than relying on carrots, and beta carotene in its unconverted form.
The HLA gene family and coeliac disease
HLA means the Human Leukocyte Antigen family of genes, that help the immune system to distinguish our own proteins in the body from those made by foreign invaders; such as viruses and bacteria.
Those people who have dysfunctional HLA genes, due to genetic variance are more likely to develop autoimmune diseases from cross-reactivity between viruses and food. Diseases such as coeliac, but also type 1 diabetes, RA other autoimmune conditions.
Coeliac results from an immune response to gluten in those who are genetically predisposed, with 90% of those with Coeliac Disease having the HLA-DQA1 gene and about 8% on the HLA-DQB1 gene. The level of risk is highest with the two variants on the HLA-DQA1 gene.
However, a positive DQ gene on its own does not mean that a person has coeliac. It just means there is a likelihood that they will develop it, given the wrong food and pathogenic environment. But having negative HLA DQ test result can be, and is used to rule out coeliac disease.
the infamous MTHFR gene, playing out a key role in the conversion of 5,10-MTHF to 5-MTHF.
Arguably the most impactful SNP of the MTHFR gene is C677T, reducing activity by up to 35% in a heterozygous genotype and 70% for a homozygous genotype. Ultimately generating less 5-MTHF, and reduced homocysteine recycling, reduced glutathione ad a myriad of detrimental health outcomes. The C677T SNP is however very common with about 10% of people homozygous, and 30% heterozygous.
Once again, it’s vital to look to the bigger picture!
Diet, lifestyle, health history, environmental influences. Gut health, pregnancies, stress, exercise, and family history of diseases all play their part in the potential outcomes of this deletion.
Many people with the MTHF SNP’s are healthy, as they have instinctively selected a diet high in folate and other B vitamins and cofactors as well as a lifestyle that is supportive of their genetic make-up.
However there is also hyper-methylation as well as hypo-methylation, which can occur when those who have not bee tested self-diagnose, and self prescribe with B-vitamins especially. For the sensitive individual, this can be just as damaging as hypo-methylation.
Nutrigenomics is both insightful and incredibly powerful when used in context, by an experienced health practitioner. It can also be motivational and empowering
When a client presents one or more complex health symptom I recommend that they work closely with an experienced Genetic Nutritionist and complete a comprehensive genetic report that looks at the folate, methionine, transulphoration, BH4, acetylation cycles. With the addition of other specific genes.