Mycotoxins and cancer risk

    While some mycotoxins have been definitively associated with cancer risk in human studies, other mycotoxins still require further human studies to firmly establish cancer risks. As persistent mycotoxin exposures do result in chronic inflammation, which is an established cancer risk, any mold exposures may indeed contribute to overall risk. Therefore, any action that reduces such toxic exposures, promotes healthy antioxidant status, or supports detoxification pathways is likely to reduce overall cancer risks. Almost 20% of human cancers and infections have been associated with chronic inflammation. Cancer risks increase further increase if comorbid infections are present, such as Helicobacter pylori (stomach cancer), hepatitis B or C (hepatocellular carcinoma), and human papilloma virus (cervical cancer).

    Mycotoxins contribute to cancer induction by damaging cellular DNA. Mitochondrial DNA or proteins may also be damaged and affect cellular energy status. If the DNA is not properly repaired, then cellular proteins and signaling may change from homeostasis to inflammation. If these damaged, inflammatory cells are not detected or destroyed by the immune system, they will continue to promote local and systemic inflammation. Metabolomics tests  evaluates two analytes associated with DNA repair:

- Methylmalonate is a precursor for DNA building blocks. Low levels of methylmalonate may prevent or delay DNA synthesis or repair.

- Orotate is metabolized into uridine, another DNA building block. A high orotate level, with low levels of other protein status markers (alpha-ketoglutarate, fumarate, branch-chain amino acids, etc.) may indicate a blockage in the DNA repair pathway.

    Toxic exposures are now known to be cumulative and synergistic in their impact on human health. Adult disorders associated with plastics exposure include obesity, heart disease and cancers.