(A) The Addition of Information to the Genome
Information can be added in the following ways (but in each case, it’s only a recombination or a loss of present genetic information):
- New traits can develop. EXAMPLE: A point mutation at the receptor site of a bacteria’s ribosome can prevent an antibiotic from binding to the ribosome. This is a new trait even though it’s a loss of information that weakens the bacteria in other ways.
- Hybridized proteins, where neighboring proteins can bind together. An example is the TRIM5-CypA protein in monkeys. This is new information (that may be beneficial), but not added information.
- There is also the possibility of duplication or copy number variation where a gene is duplicated, but CNVs are typically known for the diseases they cause in the organism (e.g. Charcot-Marie-Tooth Syndrome; autism; schizophrenia).(18)(19)
- John Sanford, a population geneticist at Cornell University said, “It is widely recognized that duplication, whether within a written text or within the living genome, destroys Rare exceptions may be found where a duplication is beneficial in some minor way…but this doesn’t change the fact that random duplications overwhelmingly destroy information.” (20)
- The organism’s body may not know how to control the duplicated genes resulting in physiological imbalance. An example is when trisomy causes abnormalities such as Down syndrome. (37)
- Polyploidization, where the unreduced sperm unites with an unreduced egg resulting in ALL of the information from the parents being combined within the offspring, is common in plants, “but there is no more total information within the population.” (ibid. Sanford)(20)
- Adaptive Immunity, where changes occur in the order of a certain set of genes to create novel antibodies. Evolutionists often call these ‘mutations,’ but basically, there is a mechanism that scrambles DNA in complex ways to generate antibodies for defense against new antigens. These changes are controlled, and neither are they heritable. (37)
(B) Sequential Mutational Improbabilities & the Human Eye
The eye is a famous example of ‘irreducible complexity’ – a system where every part is necessary for function. But evolutionists posit an evolutionary path of simple steps that would have each been beneficial:
- Richard Dawkins, in his book Climbing Mount Improbable, says, “”It is grindingly, creakingly, crashingly obvious,” he writes, mixing three metaphors joyously, that the discovery by chance of a complex object is improbable; but the Darwinian mechanism, he adds, “acts by breaking the improbability up into small manageable parts, smearing out the luck needed, going round the back of Mount Improbable and crawling up the gentle slopes….” (22)
Now the eye consists of many parts: iris, cornea, pupil, lens, retina, optic nerve. There are many other parts, and each part is very complex in and of itself.
Let’s consider the possible steps: (23)(24)
- Pigment molecules that can sense light. Present in unicellular organism, Euglena. (25)
- A depression on the light-sensitive spot creating a cup eye that could sense direction. Present in Plenarian Worms. (25)
- Narrowing of the pit opening à pinhole camera. Present in Mollusk Nautilus.
- Pigment molecules à retina
- Formation of a basic lens on front of eye (what Dawkins calls a “blob of gunge” (25). Sea snails.
Not only is this a gross over-simplification, but it’s purely theoretical.
- Evolutionists have observed these different levels of “optical complexity” in nature and have theorized a step-by-step process.
- It’s worth noting that varying levels of complexity don’t equate evolution!
But let’s assume that this theoretical sequence of mutations really occurred to form our complex eye. And for the sake of argument, let’s maintain our ridiculously overly-simplified view of each mutational step:
- Mutation 1 (M1): Pigment molecules
- M2: depression à cup eye (N.S.) à pinhole eye
- M3: “blob of gunge” (lens)
- The probability of these three steps alone would be 107 x 107 x 107 = 1021 (1 in a billion trillion).
(C) Haldane’s Dilemma
Also connected here is what’s known as ‘Haldane’s Dilemma,’ posited in 1957 by evolutionary geneticist, J.B.S. Haldane, says that there is “a limit on the speed of beneficial mutation.” (34)
- In other words, not only must the organisms (with the beneficial mutation) reproduce, their reproduction rate must be high enough to spread the mutation through the population.
- This raises the question of whether or not enough time has gone by for the diversity of organisms we see today to have evolved via random mutations. 5 billion years may not be long enough!!!
- How is this relevant to the problems of genetic load and entropy? To put it simply, are beneficial mutations common enough and occurring fast enough to outpace the harmful mutations?
- According to Wikipedia, this is a valid issue: “Though the scientific community in general no longer regards Haldane’s Dilemma as a problem, there remains little clarity as to how it became dismissed, and as recently as 1992 the issue was still regarded as a challenge by evolutionary biologists.” (33)
- In 1992, George C. Williams said of Haldane’s Dilemma, “the problem was never solved.”
(35) Williams, G.C., Natural Selection: Domains, Levels, and Challenges, Oxford University Press, New York, pp. 143–148, 1992, cited in http://creation.com/images/pdfs/tj/j19_1/j19_1_113-125.pdf