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

@Ron:

I do see evolution happening in many places by many mechanisms. I can list a few, but before I do, let me ask you, what is your definition of evolution. I keep offering examples looking for some common ground from which to start a discussion. If you don’t accept the examples that Darwin himself used, like the finches, then it seems to me that you must be talking about something other than Darwinian evolution.

The Darwinian mechanism for evolution is random genetic mutations combined with mindless natural selection that only acts at the phenotypic level – whereby novel genetic information is added or removed from a given gene pool over time. This mechanism (RM/NS) is real and does produced measurable, but very limited, changes over time. While it can easily remove information from the gene pool, as Sanford describes, and can add novel forms of low-level genetic information, it is unable to produce qualitatively novel systems that require a minimum of more than 1000 specifically arranged amino acid residues (single or multi-protein systems).

Ironically, many of the examples Darwin himself attributed to his RM/NS mechanism were not really the result of random mutations or anything functionally new being added to the gene pool over time. As already explained for you, Darwin didn’t know about Mendelian variation – a different form of “change over time” that is based on pre-programmed information that already exists within the gene pool which allows for high level variability in different environments. Nothing new is evolved into or out of the gene pool via Mendelian variation. In other words, during Mendelian variation the qualitative information and potential of the gene pool itself does not change at all. It is for this reason that multiple children born to the very same parents (from the very same gene pool) can look very different from their siblings or their parents… not based on any mutational changes to their own genome vs. that of their parents.

For example, my own brother and I look quite different. He has dark skin and I have light skin. He is very hairy while I am not. He has dark eyes while I have light green eyes. etc. None of these differences between us were the result of mutational changes. They were simply the result of Mendelian variations among the pre-established genetic options within our parental gene pool.

1. The HIV virus evolves through a sloppy reverse transcriptase that has an extremely high rate of error. Again, without trying to get into your argument, to a non-mathematician this seems like an example that would disprove Dr. Sanford’s theory, since HIV’s mutation rate is exceedingly high, and so far we see no sign of a genetic meltdown.

You’re forgetting about the reproductive rate aspect of the problem (no doubt because you haven’t really considered the statistics or math involved). Science is based on statistics – on determining the odds that a particular hypothesis is or isn’t correct compared to the null hypothesis. This is why your hunches or “face tests” really aren’t scientific.

So, even though you don’t seem to like statistics, consider that the HIV virus has an extremely high reproductive rate. It is this very high reproductive rate that allows the HIV population to keep up with its high detrimental mutation rate. The same is not true for slowly reproducing creatures – like humans and all other mammals who do no reproduce remotely fast enough to produce the minimum required per generation death rate needed by natural selection to remove the detrimental mutations as fast as they are entering the gene pool.

One other caveat here is that not all of the regions of the HIV virus mutate at the same rate. There are certain specific hyper-variable regions that are targeted by antigens that mutate much faster than other regions, but have little to do with the structure and overall function of the HIV virus.

2. Antibodies in the blood are created by the generation of random segments on the variable chain, then the thymus exerts a selective pressure by killing all the lymphocytes that produce antibodies that happen to match the HLA antigens.

What is evolving in the immune system? The overall structure and function of the immune cells does not evolve over time and neither do the types of antibodies that are produced. All the major types of immune cells and antibodies are produced before any functional selection takes place. Only after the T-cells are formed do they go to school to be “selected”. Also, this selection process only selects for a very limited ability – the ability to recognize and refrain from attacking self antigens. This particular selection process is very specific and it does not change over time to produce anything new. So, the major differences in antibody specificity that are maintained were all made before any selection process took place.

As far as the immune system is concerned, the initial action of “selection” and survival of the fittest only narrows the field. It reduces the antibody diversity that was initially created before selection came along.

This is different from Darwinian-style evolution where the Darwinian mechanism is supposed to create diversity. Selection, in the case of the immune system, does not expand or create more diversity – at least not in the initial steps of immune system education.

However, B-cell evolution is a bit different. Once a particular B-cell is selected for mass replication, the offspring of that parent cell are not exactly the same. The antibodies that are produced by the offspring B-cells are slightly different – usually in their “hypervariable regions”. These changes are indeed random changes that were not present in the original pool of immune system options. In other words, they are truly new sequences. When the same foreign antigen is encountered again, those slightly different clones of the original B-cell that recognize the antigen better will be preferentially selected, over the siblings that do not have as close a match, to be cloned and produce the offspring of the next generation. In this manner the specificity of immunity will indeed evolve in a stepwise truly Darwinian-style fashion of improvement over time.

The only difference here is that the antigen template the B-cells are looking to attack, like a specific type of lock, is limited in size and the number of key-code options, if you will. Also, with each additional correct match to a particular antigen code, the B-cell that produces this enhanced matched with be given increased survivability. Very quickly, then, random antibody changes over a few generations of B-cells will come up with an excellent match to the antibody sequence.

So, yes, this is evolution via RM/NS, but in a very limited restricted sense. For a more detailed discussion of antibody evolution see:

http://www.detectingdesign.com/immunesystem.html

3. Large mammals of different species can pass genes between species through hybrids. For example the horse and the donkey. They have a common hybrid in the mule. Generally mules are sterile, but occasionally one is fertile. When a Mule is fertile, then it can randomly pass whole chromosomes between species just like any other pairing within a species.

Species that can produce viable and/or verile hybrids are actually part of the same gene pool. There are no qualitative functional differences between the gene pools of a horse or a donkey or a mule. The phenotypic differences are the result of differences in the chromosomal arrangements – not in the information carried by the chromosomes.

As already noted for you, please do read more about this topic at:

http://www.detectingdesign.com/donkeyshorsesmules.html

4. Ideas in my shop evolve through a process of intelligent design. (At least I hope there is some intelligence.) I come up with a solution to a problem, I build something that I think will work, and as I am in the process of building it, I often get ideas about how to make it better, so over time, it continues to evolve to be more functional and higher quality.

Stepwise creation isn’t in question here. Obviously intelligence can create in a stepwise manner. However, such intelligent creativity is not based on random mutations and mindless natural selection… which is the basis of neo-Darwinism.

5. Nylonase Gene, I’m not sure, I think the bacteria copied and combined nonfunctional gene fragments.

The nylonase enzyme was originally thought to have evolved via a frameshift mutation in a stretch of DNA coding for a 472aa protein. This frameshift mutation was thought to have been caused by the insertion of a single thymine nucleotide at just the right spot to create a “start codon” and produce an entirely new protein sequence of 392aa (6-aminohexanoic acid linear oligomer hydrolase). Other nylonase proteins have been coded for by as few as 355aa with what seems to be fairly loose minimum sequence specificity. Then, a series of more recent studies by a team led by Seiji Negoro, of the University of Hyogo, Japan, suggest that in fact no frameshift mutation was involved in the evolution of the 6-aminohexanoic acid hydrolase (i.e., Nylonase). However, many other genes have been discovered which did evolve by gene duplication followed by a frameshift mutation affecting at least part of the gene. A 2006 study found 470 examples in humans alone. Scientists have also been able to induce another species of bacteria, Pseudomonas aeruginosa, to evolve the capability to break down the same nylon byproducts in a laboratory by forcing them to live in an environment with no other source of nutrients – using different enzymes than had been utilized by the original Flavobacterium strain.

In short, there are thousands of such examples of evolution in action published in literature. However, as already explained for you, these are all low levels examples of evolution in action. None of these examples get remotely close to the level of 1000 specifically arranged amino acid residues.

It is easy to evolve novel single protein enzymes at such low levels of functional complexity because potentially beneficial sequences at such low levels are much more common within low-level sequence space.

For a more detailed explanation of this topic see:

http://www.detectingdesign.com/kennethmiller.html#Nylonase

6. Sickle Cell trait. It was a single base transcription error. I think there are lots of mechanisms that can do such a thing. I don’t know if we know which one was the actual one. Maybe ionizing radiation?

Sickle cell anemia is the result of a single point mutation in the hemoglobin molecule that cases it to polymerize and become extremely rigid. This is caused by a point mutation in the beta globin gene at position six. As a result of this mutation, valine (a non-polar amino acid) is inserted into the b-globin chain instead of glutamic acid (an electrically charged amino acid). This mutation produces a “sticky” patch on the surface of the b-chains when they are not complexed with oxygen. Because other molecules of sickle cell hemoglobin also develop the sticky patch, they adhere to each other and polymerize into long fibers that distort the RBC into a sickle shape.

In short, this mutation produces a loss of functionality, not a novel gain in functionality. This loss of functionality is so severe that not even the malaria parasite can live in such conditions (even in individuals with the heterozygous form of this mutation – i.e., those with sickle cell trait).

This is a classic example of devolution, not evolution, within a gene pool. While a loss of information can sometimes be selectively beneficial in certain environments (as is also true for CCR5 mutations in the environment of HIV), it is still based on a loss of genetic information…

7. Cars and other transportation devices evolve through a process of intelligent design responding to the selection pressures of the market.

Again, this is not a form of Darwinian-style evolution since intelligence is involved. Stepwise creation is not the same thing as random genetic mutations and non-intelligent phenotypic selection.

8. The shape of the tree out front evolves each year based on selective growth as each leaf tries to optimize it’s sun exposure. Limbs that get more sun grow better.

Nothing new is produced at the genotypic level here. We are talking about functional changes to the gene pool over time…

9. I heard on the radio today that violent men tend to have higher testosterone levels, and tend to father a higher ratio of males to females, so that creates a selection bias in favor of violent men. I have no idea how accurate the statement is, but it is an example of how pervasive evolutionary principles are.

Scientists first became aware of this unusual fact – curiously enough – when they began to study men suffering from prostatic cancer. They noticed that individuals with prostate cancer, which itself is strongly linked with high testosterone levels (don’t forget that testosterone is the KEY androgen), tended to have many more male than female children. In whites, men who develop prostate cancer have about 4 per cent more male children, compared to men without prostatic tumours; in blacks, the increase amounts to more than 12 per cent (‘The Hypothesized Hormonal Control of Human Sex Ratio at Birth – an Update,’ Journal of Theoretical Biology, vol. 143, pp. 555-564, 1990).

So, while testosterone levels do seem to affect the chances of fathering male vs. female children, this is not an example of anything other than increased production of something that already exists within the gene pool. It is not an example of the novel evolution of something qualitatively new within the gene pool.

10. Relative HIV resistance in humans is conferred on Europeans, compared to Africans, by an increased prevalence of the CCR5 allele which most likely entered the Northern population through a plague, probably viral.

CCR5 is the main coreceptor on white blood cells targeted by the HIV virus. CCR5 is mainly expressed in memory T-cells, macrophages, and immature dendritic cells, and is upregulated by proinflammatory cytokines. It is coupled to the Gi class of heterotrimeric G-proteins, and inhibits cAMP production, stimulates Ca2+ release, and activates PI3-kinase and MAP kinases, as well as other tyrosine kinase cascades. A mutant allele of CCR5, CCR5 delta 32 is frequent in populations of European origin, and encodes a nonfunctional truncated protein that is not transported to the cell surface. Homozygotes for the delta 32 allele exhibit a strong, although incomplete, resistance to HIV infection, whereas heterozygotes display delayed progression to acquired immunodeficiency syndrome (AIDS).

This mutant form of CCR5 is the result of a random germline mutation, not the result of transmission via a viral plague. It has been hypothesized that this allele was favored by natural selection during outbreaks of smallpox (not the Black Death).

Why might this be? Well, the mutation(s) that disrupt normal CCR5 functionality, while having a negative effect upon overall T cell function, appear to protect against smallpox and HIV. Yersinia pestis (the bubonic plague bacterium) was demonstrated in the laboratory not to associate with CCR5. Individuals with the non-functional Δ32 allele of CCR5 are disproportionately at higher risk of contracting the West Nile virus.

In any case, like the evolution of antibiotic resistance, the evolution of viral resistance is relatively easy to achieve in a short amount of time because such forms of evolution are based on the disruption of a pre-established interaction. It is much easier to break something that was previously working just fine (like the CCR5 co-receptor protein) via a random mutation(s) compared to trying to evolve a novel system of function.

This is what makes the evolution of antiviral and antibiotic resistance such a problem in the medical community.

For more information on this topic see:

http://www.detectingdesign.com/antibioticresistance.html

11. I read recently that there have been identified 38 specific mutations in the Tibetan population that has occurred in the last 3000 years that has allowed their population to escape pressure from the Han Chinese by moving to higher altitudes. I don’t know the mechanisms. But, are you denying that this is evolution?

As I’ve already explained to you in this very same thread, it seems that a modification of just one gene is primarily responsible for the enhanced ability of Tibetans to tolerate high altitudes (EPAS1). This EPAS1 gene is thought to affect red blood cell production. It happens to be present in both the Han (low altitude) as well as the Tibetan (high altitude) populations. It is just that this gene is present in only 9% of the Han population, but is found in 87% of the Tibetan population.

“It is the fastest change in the frequency of a mutation described in humans,” said Professor Nielsen.

So, the evolution responsible for this particular effect is two fold. First, it involved a mutation that enhanced a pre-existing function of red blood cell production. It did not produce a novel type of function that did not already exist. It just increased the amount of what already existed. Such mutations are quite common and are very rapidly evolved via random mutations to pre-existing systems.

Once realized, this beneficial mutation will indeed spread fairly rapidly throughout the population… as is clearly evident in many such examples.

None of this, however, discounts or significantly mitigates the reality that detrimental mutations are still building up in all human populations far far faster than they can be removed by natural selection – even in Tibetans. The reason for this is that detrimental mutations greatly outpace the rate of such beneficial mutations (to include reversion mutations). We are all, therefore, rapidly heading downhill toward the eventual and inevitable extinction of the entire human race.

12. At one point, humans had the same number of Chromosomes as the chimps, but two of the chromosomes combined into one chromosome, so now Humans have one less chromosome than chimps do. How do you fit that fact into the Biblical narrative? Do you think that the chromosome combination took place some time after creation? I have a hard time imagining God creating us originally with a chromosome with double centrameres and telemeres.

Sure. This mutation could easily have taken place during a population bottleneck – as is the case for donkeys vs. horses. It is really functionally irrelevant as it does not add or take away any functional element from the gene pool.

For more information on this topic see:

http://www.detectingdesign.com/pseudogenes.html#Fusion

I would note however that the presence of evolution does not necessarily imply an improvement. Let’s go back to Darwin’s finches. We could imagine an island that had both finches and gross beaks on it at the start. Then some catastrophe destroys all of the gross beaks. Those finches who have larger bills may be more successful at taking advantage of the new ecological niche that opened up, so the finch population evolves toward larger beaks. But that doesn’t mean that the finches are better than the gross beaks were. This would be an example of “devolution” on the larger, island scale, with positive evolution on the smaller, finch, scale. I suspect we will see more and more of this kind of evolution as we kill off more and more of our highly specialized species.

This isn’t an example of the evolution of anything new within gene pools at all (neither a gain or a loss). The extinction of one gene pool did not add or take away genetic information from the other gene pool. Again, this illustration of yours would be an example of Mendelian variation – not the same thing as Darwinian evolution.

Sean Pitman
www.DetectingDesign.com

Sean Pitman Also Commented

Recent Comments by Sean Pitman