Luckily, there are things we can do to limit the risk posed by pathogenic E. coli and other pathogens.
Smoking, stress and high-fat diets are lifestyle factors that contribute to increased risk. Changing to a healthier, high-fibre diet can help to limit your bowel cancer risk and the impact of pathogenic bacteria. This is known as a “prebiotic” effect where dietary fibres produce a substance called butyrate. Butyrate has natural anti-inflammatory properties and can help replenish probiotic bacteria too.
Also, dietary fibres from plantains, bananas and broccoli can block harmful bacteria from sticking to your gut cells and promote their passage out of the gut. This is known as a “contrabiotic” effect and was recently shown to be effective against bacteria such as E. coli and Salmonella.
Vitamin D has been shown to help kill pathogenic bacteria, particularly E. coli, even when they are already inside our cells. Vitamin D deficiency is now associated with colon cancer, so maintaining healthy levels of vitamin D could further reduce your risk.
Foods such as almonds, red onions and chives are high in molecules known as flavonoids that have antibacterial properties and could help limit the effects of pathogenic bacteria.
Regular exercise helps maintain a normal bacterial diversity in the gut and could reduce your risk of bowel cancer by up to 50%.
Anti-inflammatory drugs such as aspirin have been shown to reduce the risk of bowel cancer. It is highly possible that future studies could find anti-inflammatory drugs reduce the inflammation caused by infections and hence your bowel cancer risk.
In the coming years we are likely to see both drug-based and natural treatments that specifically target E. coli and other bacteria associated with bowel cancer risk.
With researchers looking for more of these types of answers we are being enabled to fight bowel cancer in different ways. Therefore, it is becoming more necessary for us to be proactive and increase our awareness of the impact we can have before cancers can even develop.