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Summary of the Biblical Chronologist Newsletter
Volume 10, Number 16 | Summary by Joshua S. Hall
Full article: A Theory of Aging 2
Part 1- The Theory
In this issue, Dr. Aardsma sets out to develop a complete theory of Aging 2. Aging 2 is the third aging disease, induced by Aging 1. A helpful analogy that Dr. Aardsma has used to explain the three aging diseases is that of a three-headed dragon. When this dragon begins growing, it sprouts two heads: Aging 0 and Aging 1 (deficiency of two previously unknown vitamins). These two heads eat away at our bodies until the dragon has grown old enough to sprout its third head, Aging 2 (a mitochondrial genetic mutation disease). This head quickly outgrows the other two, becoming the main source of destruction.
The first step in developing a complete theory of Aging 2 is to find a “biological timed switch”, which is needed to explain the form of the ancient biblical lifespan data. A biological Poisson process is also needed to provide the necessary biological timer component of the switch. However, this proves to be difficult, and the only workable candidate appears to be the shortening of telomeres. But this yields a conundrum. Dr. Aardsma’s theory of aging says that Aging 2 is a mitochondrial genetic disease. To begin to explain Aging 2 biologically seems to require that telomeres exist on human mtDNA. But human mtDNA is a circular molecule and thus has no ends and no end caps—no telomeres.
Dr. Aardsma then makes a bold postulate— he says that human mtDNA must possess “in-line telomeres.” This is considered bold because “in-line telomeres” are not known to exist, therefore making them a newly invented, purely hypothetical idea/theory.
Dr. Aardsma then goes on to show the purpose that these “in-line telomeres” would serve. He gives them the name “psephomeres”, using the Greek word “psephos” which means “pebble”. The Greek verb for the action of counting has the same root (pseph), evidently because pebbles were once used as means of counting.
The “mere” ending, which means “part”, is also used. This gives “psephomere” the meaning of “pebble/counter part”. Dr Aardsma chose this name because psephomeres are “counter-parts” that serve in counting the generation number of mtDNA copies.
Dr. Aardsma then presents an obvious question and a second bold postulate. The question is, “Why is no psephomere evident in the published map of human mtDNA?” The second bold postulate is the answer to this question: Dr. Aardsma believes that the published map of human mtDNA is for mtDNA which has already shortened its psephomere to zero. This is considered bold because it seems unlikely at first that all randomly chosen mtDNA which has been mapped out has shortened its psephomeres to zero. However, it is believed that this is because the zeroed-psephomere molecule equates to Aging 2, which is normal to the global population today for all individuals past about 10 years of age. Therefore, randomly chosen mtDNA are most likely to be of the zeroed-psephomere type.
So, Dr. Aardsma’s Theory of Aging 2 looks like this.
Due to Aging 1 (vitamin MePiA deficiency disease, which causes high free radical damage) human mitochondrial DNA (mtDNA) must frequently be replicated and replaced. However, each time this replicating takes place, there is the chance of “copy errors.” In order to reduce copy errors as much as possible, psephomeres keep track of the generation number of every mtDNA copy. (The lower the generation number, the more reliable the copy is.) This tracking is done by the successive shortening of the psephomere of each new mtDNA copy. The psephomere shortens every time a copy is made, so essentially, the longer the psephomere, the “lower” the generation number of the mtDNA copy, and therefore, the more reliable.
Due to Aging 1 (MePiA deficiency disease), the amount of mtDNA copying that goes on is extraordinarily excessive. This causes the eventual loss of psephomeres from the mtDNA copies. Copies without psephomeres are Aging 2 diseased copies. Without psephomeres, the body cannot keep track of the generation number of mtDNA, and therefore, the body cannot know which copies are the most reliable. This causes copy errors to multiply, which results in increasing mitochondrial dysfunction, which results in cellular dysfunction, which results in organ/organism dysfunction, which culminates in the death of the individual.
Part 2- Testing the Theory
If Dr. Aardsma’s theory is valid, then it ought to be able to be tested. One way of testing is looking for vestiges of psephomeres (leftover parts, inexplicable behaviors, etc) on modern maps and replication algorithms of human mtDNA.
After explaining how human mtDNA replication works, Dr. Aardsma shows that there are indeed several potential vestiges of psephomeres. These include a curious, inexplicable behavior of a part of an mtDNA copying cycle called “idling”, which happens just when and where psephomere shortening would be expected. To read more about this and several other potential vestiges within a human mtDNA copy cycle, click here.
With this, Dr. Aardsma completes his two-phase, three-disease theory of human aging. Phase I consists of Aging 0 (Vitamin MePA deficiency disease) and Aging 1 (Vitamin MePiA deficiency disease). Phase II adds Aging 2, which is a direct result of Aging 1. Aging 2 is explained as a failure of the copy error suppression mechanism for mtDNA. It works like this:
The body is deficient in vitamin MePiA (Aging 1). Free radicals are generated by normal metabolism in the body, but without the antioxidant action of MePiA to protect cells’ mitochondria, the free radicals wreak havoc on cells’ mitochondria and mitochondrial DNA (mtDNA). This creates a need for excessive amounts of mtDNA copies to be made, in order to replace the damaged ones. However, each time an mtDNA copy is made, the psephomere attached is shortened. Once the psephomere is used up, the organism can no longer keep track of which mtDNA copies are reliable, and so copy errors begin to multiply exponentially. This results in the eventual dysfunction and death of the organism.
Additional note: If Dr. Aardsma’s theory is correct, then an accurate map of a child’s mtDNA ought to show the psephomeres that Dr. Aardsma has postulated. When asked about this, Dr. Aardsma said that he does not know of any published maps of a child’s mtDNA. The reason for this, he speculates, is that mapping mtDNA is a very big job which has probably only been done by one or two labs which would have used standard cell lines originally derived from an adult.