Here’s a footnote to my commentary on the House of Lords nanofood report and the government response to it. There’s a recommendation (14, para 5.32) that the definition of nanomaterials for regulatory purposes should exclude nanomaterials created from natural food substances, with which the government agrees. I accept that this distinction is a practical necessity, and I would go along with the report’s paragraph 5.31: “We acknowledge that nanomaterials created from naturally-occurring materials may pose a potential risk to human health. However, we also recognise also that it is impractical to include all natural nanomaterials present in food under the Novel Foods Regulation, and that many natural nanoscale substances have been consumed for many years with no ill effects reported.”
But I do think it is important to contest the general assertion that things that are natural are by definition harmless. There’s a long tradition of using food processing techniques to render harmless naturally occurring toxins, whether that’s simply the cooking process needed to destroy toxic lectins in kidney beans, or the more elaborate procedures needed to make some tropical tubers, like cassava, safe to eat.
There’s been a recent report of a situation where a potential link between eating naturally formed nanomaterials and disease has been identified. The nanomaterials in question are amyloid fibrils – nanoscale fibrous aggregates of misfolded proteins, of a kind that have been associated with a number of diseases, notably Alzheimer’s disease and Creutzfeldt-Jacob disease (see this earlier post for an overview of the good and bad sides of these materials – Death, life, and amyloids).
In a paper published in Proceedings of the National Academy of Sciences a couple of years ago, Solomon et al (2007) showed that foie gras – the highly fatty livers of force-fed geese – contains nanofibers (amyloid fibrils) of amyloid A protein, which when fed to mice susceptible to AA amyloidosis lead to the development of that disease.
AA amyloidosis is a chronic, incurable condition often associated with rheumatoid arthritis. The suggestion is that, if AA amyloid fibrils enter the body, they will act as “seeds” to nucleate the conversion of more AA protein into the amyloid form. A more speculative suggestion is that AA fibrils could also nucleate the formation of amyloid fibrils by other susceptible proteins, leading to other kinds of amyloid diseases. The authors of the paper draw the conclusion that “it may be hazardous for individuals who are prone to develop other types of amyloid-associated disorders, e.g., Alzheimer’s disease or type II diabetes, to consume such products” (i.e. ones contaminated with amyloid protein A fibrils). It seems to me that it is stretching what the data shows too far to come to this conclusion at the moment, but it’s an area that would bear closer investigation.