Warning: verbose!
On his website he writes of himself in the third person:
He postulates that cancer killed uncountable numbers of immature animals and concludes that the resulting accumulation of defenses against the disease enabled the emergence of complexity. In all evolving animal lineages selection favored utmost precision in the construction of all cells in order to avoid death of the organism from imprecision in a single cell. This imperative of exactness at the level of individual somatic cells permitted the emergence of complex tissue, organs and organisms.Geoff Watts tells the story of a senior executive in a large multinational corporation who in a flash of inspiration turned himself into an evolutionary biologist. His idea was this.
Cancer is a common occurrence, and certainly a life-threatening one. But biologists generally regard it as having no effect on evolutionary change because it mostly afflicts people beyond their child-bearing years. As a result, cancer cannot affect their chances of passing on any protective genes they may possess to the next generation.I agree that cancer is not without effect. Cancer kills the baby; baby doesn't get to reproduce. But that this should be a driving factor in the evolution of complex tissue etc. needs further elucidation. I have not read his book, and I shall not promise to do so, either. But kick me if Graham has scientifically assessed his hypothesis, you know, like a proper scientist. I mean, if he wants to be taken seriously, this is what he has to do. (Scroll down to learn what he thinks of that idea.)
It could serve to eliminate those individuals who inherited a genetic programme unable to cope with any damaging side-effects associated with change. Cancer, in other words, is evolution's method of quality control.But organisms don't need anything to kill them in order to make sure that they don't mature and reproduce. The damaging side-effects - whatever they may be - are enough in themselves. The damaging side-effects is already quality control. Either you make or you don't. In that light there is nothing special about cancer. If your developmental program fail and you get cancer, then you will be selected against. If, say, your immune system fails, then you will be selected against. There is no difference.
Childhood cancer kills before the age of reproduction, and is therefore amenable to selection. Yet it continues to exist. Why? Because natural selection has not yet had the time to deal with it.No. Cancer is not one disease. The phenomenon of uncontrolled cell-growth is incredibly varied and thus very, very difficult to evolve resistance to. That alone is a far more parsimonious explanation for the persistence of cancer in children, and thus preferred over Graham's hypothesis.
And hypothesis is apparently all we get, because Graham is outright against testing his idea scientifically:
Graham claims that cancer selection is not a but the driving force in the emergence of complex animal life. "He believes that with good, clear thinking one can arrive at an answer," Leroi says. "But this isn't enough.Exactly!
Because something could be a certain way doesn't mean that it actually is that way. All those biologists who spend their time trying to test evolutionary theory - well, he thinks they're just number-crunchers who can't see the big picture." (My emphasis.)
Graham has also written a document listing twenty-five problems not solved by conventional evolutionary theory (tl;dr). One of the points goes as follows:
5. There is on display at the American Museum of Natural History in New York a fossil of a small disk-shaped jellyfish which is more than 500 million years old. A specialist might detect differences between this fossilized organism and modern specimens, but even experts would agree that the primordial jellyfish looks substantively like today's jellyfish. It seems that, compared to bilaterians, there has been little organismic transformation in the cnidarians (and in the Porifera). What is the mechanistic explanation for this, as some might call it, unpunctuated equilibrium?This "unpuctuated equilibrium" goes under the name of stasis, and has several good explanations. For example, if a species' local environment is unchanged, then all or almost all mutations are harmful, causing natural selection to eliminate variation. The coelacanth is another organism that is unchanged for millions of years in this way. The exact nature of stasis is debated, but there is certainly no lack of hypotheses, as Graham seemingly would have us believe.
In 2005 two scientists published a paper titled Adaptive evolution of the human fatty acid synthase gene: Support for the cancer selection and fat utilization hypotheses? To Graham's stated chagrin there is no reference to his work in any form, even though "cancer selection" appears both in title and body of the paper. The authors analyzed how selection has acted on a gene (FAS) involved in both cancer and human brain development, and conclude that the most they can do is speculate that the role played by FAS in one of these two has created a selective pressure for the gene (positive selection), although they can't rule out the various other functions of FAS. In other words, nothing to indicate that cancer selection drives the evolution of complex features. No evidence that Graham's idea has any merit.
As a bonus we are told that Graham has these delusions of grandeur. What can you say? Well you can snort and chuckle, I say.
Graham goes on to compare himself to Darwin (neither had been educated as a scientist) and Friedrich Wegener of continental drift fame (as a meteorologist not a geologist, Wegener too was an outsider). Thomas Kuhn's classic The Nature of Scientific Revolutions is wheeled out to remind us that people responsible for the "fundamental inventions of a new paradigm have been either very young or very new to the field whose paradigm they change". (The italics are Graham's.) He even compares his method of work to Albert Einstein's.Goodnight.
M OCONNELL, J MCINERNEY (2005). Adaptive evolution of the human fatty acid synthase gene: Support for the cancer selection and fat utilization hypotheses? Gene, 360 (2), 151-159 DOI: 10.1016/j.gene.2005.06.020
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