Using genes to prevent disease

When the Human Genome Project was launched it was hoped that we would identify signature genes for each of the many types of cancer that would in turn lead to targeted treatments. By the time the project was wound up those hopes were dashed. Cancer mutations are diverse and confusing and have not led to the solutions we were hoping for. Cancer, it turns out, is a multifactorial disease that cannot be explained by a single gene.

Apart from Mendelian (or single gene) diseases most genes don’t actually cause disease – they are merely ‘associated’ with a disease. That means that even if you have ‘the Alzheimer’s gene’ or the ‘breast cancer gene’ you have a predisposition – but the outcome is much more in your hands than you may think – especially in the early stages.

For example, we have discovered that the infamous BRCA1 gene mutation that ‘causes’ about 10% of breast cancers, drives oxidative stress and glycolysis in the cell. In the process it causes damage to delicate cellular structures, including DNA, and upregulates the use of sugar by the cell.

Pharmaceutical companies use this sort of information to develop drugs to target the aberrant pathways. Nutritional Therapists look at nutrients that work in similar ways. For example we may look to reduce sugar availability, and provide more of the nutrients that can protect against oxidative stress.

At the time of writing there are no pharmaceutical treatments for BRCA, the best we can do is offer surgery to remove hormone sensitive tissues that may be prone to damage. Nutritionally the best hope lies in the fact that many women who carry the BRCA gene do not go on to develop breast cancer so we know it’s not inevitable. There may be several reasons for this (including the potential for another unknown protective gene combination) but it’s likely that diet and lifestyle and toxic exposure play a key role. The genes that control antioxidant enzymes and the metabolic factors that drive glycolysis are sensitive to dietary inputs. By using our understanding of the way the gene works we can focus on related diet and lifestyle areas, and manage the relevant SNPs.

In future we may be able to offer BRCA carriers more palatable options than prophylactic surgery or genetic modification, and right now we can take diet and lifestyle steps to avoid the sort of damage that BRCA can cause, supported by insights provided by SNPs. So a diet that minimises glycolysis and maximises antioxidant status can be seen not just an ‘alternative’ way to support people with cancer and BRCA, it’s a fundamental part of an integrated cancer prevention strategy.