Comment on Dr. John Sanford Lectures on Inevitable Genomic Deterioration by Sean Pitman.

@pauluc:

It now appears we actually agree on most of this.

1] “The human genome/gene pool is not currently in functional “meltdown” mode.” totally agree there is no evidence for this.
2] “What I said is that it is heading toward a meltdown”. I agree if as Lynch discusses in his papers the standard selection pressures on human populations are removed by the environmental manipulations of first world technologies.

We would be heading toward a functional genetic meltdown regardless of if selection pressures are in play or not. The reason for this is that detrimental mutation rates are far too high to be compensated for even if selection pressures were maxed out. In other words, even if selection pressures were so strong that the maximum tolerable death rate were achieved in each generation, every single person in every generation would still have significantly more detrimental mutations than his/her parents had.

3] “The point is that mutational divergence over time is ongoing.” Agree entirely otherwise where is the variation on which natural selection is to act and where are the change on which Kimura model of neutral selection is based.

Kimura’s neutral theory of evolution only deals with functionally neutral mutations. We aren’t talking about neutral mutations here. We are talking about mutations that have a functional impact on the gene pool – pretty much all of which are detrimental.

4] Mutations rate are less than 100 per generation. Agree and it appears that I was wrong in suggesting you are unchanged by this dialog as you seem to have presented me again with the references I cited in July last year.

The overall mutation rate makes no real difference when it comes to the level of detrimental mutations realized which cannot be reversed by natural selection pressures in slowly reproducing populations.

5] “The fact that mutational differences build up over time is also not contested in literature – and is in fact used as a clock to measure time since the MRCA. If you compare living individuals with the DNA obtained from ancient relatives, the mutation rate can actually be calculated in a direct manner – and it is similar to the mutation rates described above.”

Sean what is happening here? Why are you talking about most recent common ancestors? Are you now accepting that hominids have been here for more than 100,000 years or 1.5 million?

All humans share a MRCA. That doesn’t mean that our MRCA lived a million years ago. In fact, fairly recent papers have been published noting that all modern humans share a common ancestor that lived no more than a few thousand years ago… right in light with the Biblical account of origins.

Is death really the only way [to remove detrimental mutations from the gene pool]?

Yes, when you’re talking about natural selection, the only way this mechanism works is through pre-mature death, before reproduction, of individuals competing in a given environment.

Are there mechanisms for removal of mutations in the germline during meitic division and cross over events?

Yes, there are. But, the average mutation rates that I’ve listed for you take these features into account. The mutation rates listed are mutations that are missed after all editing functions have taken place. Then, once these mutations are passed on to the next generation, they are no longer targeted for editing by error-detecting mechanisms within the germline cell itself.

Are there gene conversion events that favour functional genes?

Not as far as I’m aware – not outside of the effects of natural selection and premature death.

Is there selection for specific gametes during gametogenesis or embryo selection for function that would slowly remove detrimental mutations?

Yes, there is selection for specific gametes. If a spermatozoan is mutated so that it can’t swim as well, then its genetic information will be selected against. This is a form of natural selection where a form of premature death is also required. While a very high death rate is in play here, which is good to maintain appropriately functioning spermatozoa over time, the only real impact this form of selection has is on the structure and function of those genetic elements that form the structure of the spermatozoa. However, outside of a very limited number of genes that deal with the structure of the spermatozoa – there is really no effect on the genetic information of the rest of the genes that are carried within the spermatozoa. So, overall, this effect has no real impact in removing detrimental mutations from the overall gene pool faster than they are entering it.

Also, there is embryo selection as well. Up to 31% human conceptions are spontaneously aborted (taking into account both recognize and unrecognized pregnancies) due to morphologic defects that are genetically related about half the time. That’s a pretty high rate of genetically-induced abortions – even considering your cheetah example. It suggests that humans have already suffered a significant genetic insult as an overall species.

The real problem with this example of natural selection is, of course, that this death rate has already been taken into consideration within the numbers I’ve already given you. These fetal deaths have already been counted as part of the minimum number of pregnancies needed, per woman, to keep the human gene pool neutral with respect to the very high detrimental mutation rate. As already noted, no woman can have trillions of pregnancies as would be required to keep the population genetically neutral – to avoid the downhill drift toward eventual genetic meltdown. Modern women don’t even have 20 pregnancies on average. So, you see, this form of natural selection is effectively irrelevant to the problem as well.

According to your model of death as the only purifying selector the death rate would never have been able to do this and their doom is assured. As Galileo was purported to has said; “and yet they move”
Real data trumps theory every time. Particularly when that theory is based on religous wishes and statistical conjecture rather than real observation and hypothesis testing.

Your cheetah population was infused with genetic information from an outside population that had not declined as rapidly in genetic health. This doesn’t mean that the overall cheetah gene pool isn’t gradually declining as well. It just means that very small populations drift downhill at a faster rate is all – because of the increased statistical fragility of very small populations when it comes to having the time to deal with detrimental mutations that have a stronger detrimental effect.

Nothing has “trumped” or solved the problem here. Your arguments don’t remotely address the problem in play when it comes to the continued decline of the human gene pool as well as all other slowly reproducing populations of living things.

In short, we are where we started. The very best empirical evidence we currently have in hand strongly supports Sanford’s position. Your notions simply aren’t backed up by science. At best they are working hypotheses, hunches, or wishful thinking that simply aren’t testable in a potentially falsifiable manner.

Your position on this topic simply isn’t scientific. You might be proved right given future information. Unfortunately for you right now, science isn’t based on what might be discovered in the future. Science is based on the best of what is currently known.

Sean Pitman
www.DetectingDesign.com

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