M. J. Behe , in Philosophy of Biology : An Anthology, A. Rosenberg, R. Arp, Eds. (Wiley-Blackwell, 2004), pp. 427–438 .
where he says
But Russell Doolittle – an eminent protein biochemist, a professor of biochemistry at the University of California–San Diego, a member of the National Academy of Sciences, and a lifelong student of the blood clotting system – disagreed
and goes on to cite and gives a more detailed explanation, why Russell Doolittle case does not refute him
Even in Darwin Devolves Behe wrote
I argued in the book that a major part of the blood-clotting cascade was irreducibly complex…However, a man named Russell Doolittle (a distant relative of W. Ford Doolittle) disagreed…Russell Doolittle is one of the very top researchers in the area of blood clotting. Yet, as his essay clearly shows, he himself did not know how the clotting cascade could have arisen by Darwinian processes.Nor did he know of any papers in which an explanation had been given. If he had, he simply would have cited them.Instead, he cited a paper about dying mice. So the second important lesson from the affair is this: if Russell Doolittle himself cannot account for a system of the complexity of the clotting cascade by Darwinian processes, nobody can—nobody in the whole world….In 2013 Russell Doolittle published a book, The Evolution of Vertebrate Blood Clotting, which summarized his findings and other work…But virtually no experimental work was done, even on how the systems themselves work in the respective species, let alone on how they might change under selective pressure
This is off-topic. It will be moved soon. Then we can discuss. You the focus is not Behe though, but how you have come to the conclusion he has been mistreated.
It needs to be said that having some sort of disease or disorder does not equal having lower reproductive fitness.
Some neurodegenerative diseases (iirc some types of frontotemporal dementia caused by mutations in the ataxin-2 gene) cause patients to have less social inhibitions, are more likely to instigate and respond to advances from potential sexual partners, and therefore generally have more children on average, than people without the disease.
So strictly speaking these people have higher reproductive fitness, despite them also experiencing higher early cognitive decline and higher mortality.
I suggest a change of topic and to focus now on the woolly mammoth instead of the polar bear.
An interesting article published in Cell Reports in 2015 entitled « Elephantid genomes reveal the molecular bases of wholly mammoth adaptations to the artic » seems to bring support to Behe’s view that adaptation most often arise by damaging mutations. For example , here is what the authors say about TRPV3 : « these data suggest that the hypomorphic mammoth TRPV3 may have phenocopied TRPV3-null mice and contributed to evolution of cold tolerance, long haïr, and large adipose stores in mammoths »
The hypomorphic version of mammoth TRPV3 clearly isn’t the same as TRPV3-null mice - the mammoth TRPV3 is still quite functional (see figure 6F), just at a slightly lower level than before (without the mutation).
This is a good example of the problem with Behe’s definition of “damaging” though. In this instance he calls the mutation “damaging” because it results in the channel not opening quite as much upon activation, but in another instance where the opposite happens - the channel opens wider upon activation - Behe would probably also call this “damaging” because it “damaged” the original opening width.