The official definition of genetic drift says that it is a change, not by natural selection, but rather by a chance fluctuation of different characteristics in the gene pool (the set of all of genes in a species) of a particular small population. Considerably large populations will not experience genetic drift, contrary to the small ones in which genetic drift might become not only the driving force of evolutionary change but also the cause of complete loss of certain alleles (variant forms of the same gene).

Evolutionists suggest that genetic drift, through the mutation process, increases genetic variability. It reverses the decrease of variability in a population’s gene pool, caused by the selective pressure of speciation. Genetic drift is thought to even reverse the increase of entropy, expected in closed systems. haldanes However, the problem of this hypothesis is the lack of evidence, namely, that new genes do arise from genetic drift to such an extent that the increase of entropy is reversed.

Scientific reports describe random genetic drift in small populations to be so strong that it can override the effects of even substantial mutations. According to population geneticists, apart from effective selection, in a population of 10,000 the new mutant has only one chance in 20,000 (the total number of non-mutant nucleotides present in the population) of not being lost via drift. Even with some modest level of selection operating, there is a very high probability of random loss, especially if the mutant is recessive or is weakly expressed. (Stanford) [1]. Briefly, genetic drift can eliminate gene polymorphisms and thereby erode genetic variability. Because its effects are the greatest in populations of small size, they are always subject to ‘mutational meltdown’ or accumulating deleterious mutations resulting in the decrease of the fitness of the population and thus even further accumulating more deleterious mutations. Such a mutational meltdown most of the time ends in the extinction of the species. Here are a few supporting quotes from these claims.

When selection is unable to counter the loss of information caused by mutations, a situation arises called ‘error catastrophe.’ If not rapidly corrected, this situation leads to the eventual death of the species – extinction. In its final stages, genomic degeneration leads to declining fertility, which curtails further selection (selection always requires a surplus population, some of which can then be eliminated each generation). Inbreeding and genetic drift must then take over entirely, rapidly finishing off the genome. When this point is reached, the process becomes an irreversible downward spiral. This advanced stage of genomic degeneration is called ‘mutational meltdown’ (Bernardes, 1996).

Many scientists agree that in the past, human species went through population bottlenecks and thus also through genetic drift. If, for the sake of argument, we accept that the human species had non-human ancestors, according to the above reasoning, this would mean that human beings should have significantly degenerated downward from our ape-like ancestors. This is already obvious from the fact that Neanderthals were bigger than modern humans and had larger brains.

Actually, now there is an arising doubt whether Neanderthals and humans are evolutionarily related species because of the great difference in the mtDNA sequence and genetic diversity among them.

The Neanderthal mtDNA sequence from the Scladina cave (Belgium) confirms that Neanderthals and modern humans were only distant relatives. Neanderthal sequences are all closer to each other than to any known human sequence. But the study also reveals that the genetic diversity of Neanderthals has been underestimated. Indeed, the mtDNA from the Scladina sample is a more divergent relative to modern humans than is mtDNA from recent Neanderthals. This suggests that Neanderthals were a more genetically diverse group than previously thought. (Orlando et al.: “Correspondence: Revisiting Neanderthal diversity with a 100,000 year old mtDNA sequence.” Current Biology 16, R400-402, June 6, 2006.)

Now, let us make a small genetic calculation to determine whether it was really possible for us human beings to evolve from a common ancestor.

A famous geneticist, Haldane (1957), calculated that, given what he considered a ‘reasonable’ mixture of recessive and dominant mutations, it would take (on average) 300 generations (at least 6,000 years) to select a single new mutation to fixation. Selection at this rate is so very slow; it is essentially the same as no selection at all. This problem has classically been called ‘Haldane’s dilemma.’ At this rate of selection, one could fix only 1,000 beneficial nucleotide mutations within the whole genome, in the time since we supposedly evolved from chimps (6 million years). This simple fact has been confirmed independently by Crow and Kimura (1970), and ReMine (1993, 2005).

Man and chimp differ by at least 150 million nucleotides, representing at least 40 million hypothetical mutations (Britten, 2002). So if man evolved from a chimp-like creature, then during that process there were at least 20 million mutations fixed within the human lineage (40 million divided by 2), yet natural selection could only have selected for 1,000 of those. All the rest would have had to have been fixed by random drift – creating millions of nearly-neutral deleterious mutations. This would not just have made us inferior to our chimp-like ancestors – it would surely have killed us. (Stanford, 2005).

So let us briefly repeat a few important points:

* Deleterious mutations become fixed by genetic drift. (Kondrashov, 1995; Crow, 1997; Eyre-Walker and Keightley, 1999; Higgins and Lynch, 2001).

* Genetic drift has the potential to prevent the accumulation of advantageous changes at the population level. (Rambaut A, Posada D, Crandall KA, Holmes EC: The causes and consequences of HIV evolution. Nat Rev Genet 2004, 5:52-61.)

* When genetic drift is strong, deleterious mutations may accumulate, leading to an irreversible decline in population fitness. (Muller HJ: The Relation of Recombination to Mutational Advance. Mutat Res 1964, 106:2-9.)

In conclusion, we can see that genetic drift produces more harmful effects than beneficial; it degenerates the species more than it evolves. This situation is just like the wheel that is horizontally rotating backward and the ants on it going in opposite direction. In other words, although the ants are going forward they are actually moving more backward. Similarly, the devolution is always greater than the tiny micro-evolutionary adaptation to the new environments or the limited bodily changes of the species.

Discussion:

Objection: The main problem with Haldane’s calculations is that it assumes that beneficial mutations are fixed consecutively, i.e. 2 mutations take twice as long to fix as one mutation. This is not the case, since many genes would be linked with genes which are selected, so would hitch-hike with them to fixation.

Answer: The nature of selection is such that selecting for one nucleotide always reduces our ability to select for other nucleotides (selection interference) – therefore simultaneous selection does not hasten this process.

Objection: Haldane also did not think about crossing-over during meiosis, which can bring favorable genes together.

Answer: What is mostly called ‘evolution,’ is nothing more than just the arising of new variations by the mechanism of natural variety (that is the sexual reproduction with recombination as its most important part). But everything else, e.g. the above mentioned genetic drift, results not in evolution but degeneration.

Many genes work well in certain combinations, but are undesirable all by themselves (this would be true wherever there is heterosis or epistasis). Selecting for such gene combinations is really ‘false selection,’ because it does no good – the gene combinations are broken up in meiosis, and are not passed on to the offspring. Yet such ‘false selection’ must still be paid for, requiring still more reproduction.

Additional comment: At a first glance, the above calculation seems to suggest that one might at least be able to select for the creation of one small gene (of up to 1,000 nucleotides) in the time since we reputedly diverged from chimpanzee. There are two reasons why this is not true. First, Haldane’s calculations were only for independent, unlinked mutations. Selection for 1,000 specific and adjacent mutations could not happen in 6 million years – because that specific sequence of adjacent mutations would never arise – not even in 6 billion years. One cannot select mutations that have not happened. Secondly, the vast bulk of a gene’s nucleotides are near-neutral and cannot be selected at all – not in any length of time. The bottom line of Haldane’s dilemma is that selection to fix new beneficial mutations occurs at glacial speeds, and the more nucleotides which are under selection, the slower the progress. This severely limits progressive selection. Within reasonable evolutionary timeframes, we can only select for an extremely limited number of unlinked nucleotides. In the last 6 million years, selection could maximally fix 1,000 unlinked beneficial mutations – creating less new information than is on this page of text. There is no way that such a small amount of information could transform an ape into a human. (Stanford, 2005)

So, as it was above mentioned, many thousands of harmful mutations should have been also fixed, via genetic drift what logically leads us to conclude that human species degenerated due to deleterious fixations greatly outnumbering beneficial fixations. Thus evolution is a myth and design followed by devolution is a fact. Or in the words of Neil A. Campbell: “a random change (genetic drift) is not likely to improve the genome (genetic code) any more than firing a gunshot blindly through the hood of a car is likely to improve engine performance.”[2]

References

[1] John Stanford, GENETIC ENTROPY & The Mystery Of The GENOME (2005) p. 40-41.

[2] Neil A. Campbell, Biology, 4th Edition (Menlo Park, CA: University of California, The Benjamin/Cummings Publishing Company, Inc., 1996).

For further information on simplar topics visit: “The Hare Krishna Views On science” at www.krishnascience.com [http://www.krishnascience.com] Nitai is the member of the Bhaktivedanta Research Institute in Amsterdam – Netherlands. In his research, the main inspiration is from the ancient Vedic literature that impressed many great thinkers like Einstein, Eugen Wigner, Brian Josepson etc..