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The Genetic Insertion Event

We were therefore interested in examining the gene content of the intra- and inter-chromosomal duplications involving 2qFus-related sequence. Because these duplications took place during hominid evolution, resulting variation in gene number and function might contribute to phenotypic differences among primates.

YUXIN FAN, TERA NEWMAN, ELENA LINARDOPOULOU, AND BARBARA J. TRASK, “GENE CONTENT AND FUNCTION OF THE ANCESTRAL CHROMOSOME FUSION SITE IN HUMAN CHROMOSOME 2Q13–2Q14.1 AND PARALOGOUS REGIONS”

As we saw in prior chapters, chromosomes compose the primary difference, in genetic terms, between humans and chimpanzees: humans have one fewer pair of chromosomes than do the great apes.

Evolutionary geneticists believe that in the human lineage, two ancestral ape chromosomes fused at their ends, which produced human chromosome 2.

According to the conclusions of the Chimpanzee Genome Project:

The results of the chimpanzee genome project suggest that when ancestral chromosomes 2A and 2B fused to produce human chromosome 2, no genes were lost from the fused ends of 2A and 2B. At the site of fusion, there are about 150,000 base pairs of sequence not found in chimpanzee chromosomes 2A and 2B.¹

That is a very odd state of affairs. Logic would suggest that a fusion event would not add new base pairs that were lacking in the ancestor and the other great apes. In fact, we would expect to see a conservation or even a loss of pairs as complexity was shed in favor of simplification (i.e., two fewer chromosomes).

(Does not the theory of evolution argue for simplification and conservation?)

It is this chromosomal difference that prevents humans and the great apes from breeding and producing viable offspring. The entire “fusion” scenario is questionable. For the sake of argument, we will assume that the first protohuman mutant was born from the alleged common ancestral lineage, millions of years ago.

Question: Who would this mutant, with differing chromosomes, mate with to perpetuate this new genetic assembly?

It could not have been with the forty-eight-chromosome ancestral line, as the forty-six-chromosome mutation (fusion) represented a complete genetic departure. Additionally, are we to also assume that another member of the opposite sex—who had also mutated—was born at the same time? That seems quite improbable.

So how did we get from forty-eight down to forty-six chromosomes since there is a genetic wall preventing a reproductive union? Next, since mutations are rare and seldom successful, what gave a survival advantage to the mutant forty-six-chromosome individuals (our theoretical ancestors)?

This is where the external manipulation of the human genome appears to have occurred. While humans and chimpanzees have similar genomes to a point, they are not as similar as horse and donkey or lion and tiger genomes, as we have seen.

As we noted previously, those animals can mate and produce viable, if sterile, offspring. It is more accurate to say that these species are very similar genetically than it is to say that humans and chimps are.

The gene transfer that took place, via bioengineering by the Genesis Race, added new information that did not exist in the ancestral lineage. The added (inserted) genes reveal another key difference that separates humans and the great apes.

An important feature of the human genome is a substance called cobalamin synthetase, a bacterial enzyme that makes cobalamin, also known as vitamin B₁₂. We humans are unusual in that we have several copies of cobalamin synthetase–like genes, including the one on chromosome 2. Chimpanzees only have one.

Why is cobalamin such a critical factor? It is vital for brain development in children and for energy and red blood cell production, as well as the all-critical effective DNA replication process.

The cobalamin synthetase gene in modern humans is inactive, which is an enigmatic fact.

Since plants do not contain cobalamin and the human B₁₂ gene to synthesize it is inactive, we have to obtain it from various animal sources. (This is why strict vegans are warned to take a B₁₂ supplement.)

Low cobalamin levels in the blood serum can lead to pernicious anemia and a host of other complications, including chronic fatigue.

In fact, vitamin B₁₂ is important for brain development, and a deficiency during pregnancy or early childhood results in severe neurological defects in human children. Humans can survive on a vegetarian diet; however, we are not genetically programmed to function at an optimal level without cobalamin (B12).

Note that in Genesis, the people after Adam and Eve are told they can eat meat; the reason for that was this genetic change, starting with Adam and Eve, that deactivated the cobalamin synthetase gene. In reality, they had to eat meat.

On the other hand, both chimpanzees and gorillas are largely vegetarians, the latter exclusively so. Chimpanzees primarily subsist on fruits, nuts, seeds, leaves, and insects and, on rare occasions, meat. The differences between human and great ape cobalamin metabolism are largely responsible for our greater postnatal brain growth, which is lacking in the great apes.

The only way we are able to import cobalamin into our human metabolism is by having the right bacteria in our guts; bacterial flora break down the cobalamin for us. While plants and fungi do not contain B12, some bacteria and yeasts do.

I posit that the cobalamin difference, which stimulates brain growth in a way that does not occur in the great apes, was also the outcome of genetic engineering.

I make this claim because of the fact that it is in the fusion region where we find the inactivated cobalamin synthetase gene. The inactivation of this gene is curious because it does not appear to confer any kind of survival advantage; quite the opposite.

Obviously, it would be better if we could synthesize cobalamin without depending on external sources in the bacteria family. Nonetheless, we have to import the bacteria into the gut first, and the bacteria then extracts the B12, which we can get only from animal sources.

When we add the fact that the major human ABO blood group is type O positive, which both chimpanzees and gorillas lack, it becomes clear that we humans are unique, outliers so to speak..

Taken as a whole, the chromosomal, cobalamin metabolism, and blood group data suggest that we modern humans were a fairly recent insertion into the mammal and primate genome mix. But that does not mean that we are not ancient in cosmic terms. Our genes tie back to the extraterrestrial planet that our progenitors came from.

How else could type O positive, which is recessive to both A and B blood types, still exist as the majority blood group if we have been evolving together with the great apes for millions of years?

Though scientists claim that the other primates also have ABO blood groups, the distribution is totally different; none but humans have the O positive predominance or the Rh negative blood type. (So where did that come from?)

Therefore, human beings represent an outlier species, a hybrid that was produced using the same genetic material that other animals display (up to a point) due to the relative uniformity of DNA.

The reason that evolutionists were confounded by our human shortage of genes, 23,000 compared with the 145,000 of the wheat genome, is because we have not been in the mix that long on Earth. They expected the human genome to be five times that large and much more complex than that of a supposedly simple plant, but that did not turn out to be the case.

The constant focus on our supposed close genetic relationship with chimpanzees hides the fact that most animals and even plants have many similarities in their genomes. How else could we create cross-species hybrids?

If a corn plant was entirely different from a bacterium, then it would not be possible to insert the bacteria into the corn germ to produce Bt corn, a hybrid of the two. However, Bt corn exists, proving that most of the genomes are very compatible.

We should be very careful about how we interpret these emerging new genetic data. It was not that long ago those geneticists talked about large segments of the genome housing junk DNA. That has since been proven to have been a false interpretation of the data.

How many more misinterpretations have been made?

CONCLUSION

The alleged fusion event, the mutation that supposedly occurred in the ancestral ape population that gave rise to modern humans, presents anomalies. At the fusion site, we find an insertion of new genetic information that appears to be pivotal in distinguishing humans from the great apes.

It is curious to explain the two-chromosome human difference from apes by positing that a loss or subtraction of genes produced additional DNA, making the human genome more complex.