Glad you liked my comment, I usually don’t post them I too agree with the notion of quantum drivers involved in biodiversity. There is a lot of emerging work about how quantum processes are involved with mutations, DNA structure, photosynthesis etc. This is quite an interesting time for the field.

I am currently working in science but just wanted to point out that mutations on their own are not sole drivers for “classical” diversity. For example, large sections of chromosomes are usually “swapped” by bacteria and equivalently “shuffled” by eukaryotes during meiosis; transposable elements which are regions of genomes that copy and insert themselves at other positions in the same genome also increases an organisms phenotype diversity. Viral DNA (reverse transcribed from RNA to DNA) litters most eukaryotic genomes again adding to the hosts diversity. There are epigenetic factors where the environment is said to shape the structure of DNA packaging restricting or enhancing gene expression. We must therefore see all these processes in terms of their quantum driving properties e.g. how does QM influence double strand break and recombination, viral RNA mutation rates such as with HIV and so on.

The phrase “goes about its business via it’s host slaves with confident arrogance” is very befitting. I think as the two disciplines of QM physics finally merges with biology that we can finally put ‘life’ whatever it is or is not, into some context.

Whilst I accept the notion that decoherence and coupling to the environment may play a key role in biology, is it fair to say that just because mutations in oncogenes and tumour suppressors are rare that classical mechanics cannot account for them? Even without quantum mechanics, due to the population of cells and resulting Darwinian selection means that cancer is, or should be, a common or at least expected phenotype.

I refer you to: Nature 458, 719-724 (9 April 2009) | doi:10.1038/nature07943

“All cancers are thought to share a common pathogenesis. Each is the outcome of a process of Darwinian evolution occurring among cell populations within the microenvironments provided by the tissues of a multicellular organism. Analogous to Darwinian evolution occurring in the origins of species, cancer development is based on two constituent processes, the continuous acquisition of heritable genetic variation in individual cells by more-or-less random mutation and natural selection acting on the resultant phenotypic diversity. The selection may weed out cells that have acquired deleterious mutations or it may foster cells carrying alterations that confer the capability to proliferate and survive more effectively than their neighbours. Within an adult human there are probably thousands of minor winners of this ongoing competition, most of which have limited abnormal growth potential and are invisible or manifest as common benign growths such as skin moles. Occasionally, however, a single cell acquires a set of sufficiently advantageous mutations that allows it to proliferate autonomously, invade tissues and metastasize.”

Is your suggestion more related to the role of “quantum Darwinism” [ Nature | doi:10.1038/news041220-12], whereby a superposition of mutations occurs and eigenstates and eigenvalues that result or favour mutations of cancer genes further enhance the cancer cells’ ability to proliferate?

p.s. Like your book “Quantum Aspects Of Life” – quick plug for you there!