by Carl Wieland

Headlines have screamed that fish in New York’s Hudson River have ‘evolved’ into ‘super mutants’, able to resist the toxic effects of PCBs (polychlorinated biphenyls) in that heavily polluted waterway. And all this ‘evolution’ has happened in less than 50 years.1

As reported in the respected journal Science,2 researchers have indeed shown that some 95% of the Hudson’s bottom-feeding Atlantic tomcod have become resistant to these poisons. It is the first recorded case of poison resistance (similar to antibiotic resistance or pesticide resistance) developing in vertebrates (creatures with backbones). And this is almost certainly via mutation, which is then favoured by natural selection.

So the fish have adapted to this new environment by a Darwinian mechanism. But as we have already extensively shown in detail (for example, in this article on supergerms), such resistance to poisons in bacteria, for instance, most definitely does not demonstrate the sort of biological change required to have turned microbes into magnolias, mosquitoes and microbiologists. It is in fact demonstrating the opposite, if anything, especially in those cases of antibiotic resistance where mutations have generated the resistance.

This is something that is simple to understand and demonstrate; the germs become resistant due to various forms of damage (which is what mutations—inherited genetic copying mistakes—mostly do) to their internal engineering. A good example is where a germ that uses biological pumps to draw in its nutrition has a mutation that damages the pumps. That makes it harder for it to pump in not just nutrients, but also antibiotics when these are in its environment—in short, it is no longer as good at sucking in the poison that kills it….

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