Synthetic Biology: Creating New Life Forms by Rearranging DNA
$this->bbcode_second_pass_quote('Lew Rockwell', '[')b]Two courses
Consider two courses for synthetic biology. One is the current prevailing agenda to limit the size of human populations. Another is the prolongation of life. Let's consider the second use of synthetic biology first - to prolong the human life span. One way biologists could do this is to introduce into human fertilized ova the gene sequence for synthesis of an enzyme called gulonolactone oxidase (GLO), so that human offspring can continually synthesize vitamin C as most other mammals do.
This should be a priority among biologists since humans carry a dysfunctional gene for this enzyme, which disables the synthesis of vitamin C in the liver, making humans totally reliant upon paltry dietary doses of vitamin C to prevent scurvy. Surprisingly, there are only 142 published reports on GLO in the expansive and growing National Library of Medicine database. Biologists have demonstrated little interest in this topic.
Humans have been described as a mutant species because of their inability to produce vitamin C. Most mammals have the intact gene for GLO synthesis and produce generous daily amounts of the liver metabolite ascorbate (vitamin C), about 20 milligrams per pound of body weight (equivalent to 3200 milligrams for a 160-pound/70-kilogram human). The restoration of this missing hormone/vitamin was proposed by Irwin Stone in the 1970s to create "a new and more robust, longer-living, tough human sub-species." [Medical Hypotheses 5: 711–21, 1979]
Four enzymes are required for the conversion of blood sugar into ascorbate (vitamin C). Long ago in human history the gene that controls the fourth enzyme, gulonolactone oxidase, fell into disrepair. The injection of the GLO enzyme into guinea pigs, which suffer the same predicament as humans and cannot synthesize ascorbate, produces vitamin C. [Nutrition Reviews 1982 Oct; 40(10): 310–1] The effects of this mutation and vitamin deficiency are not solely limited to symptoms of overt scurvy (bleeding gums, sore joints, fatigue, poor wound healing). For example, without the provision of supplemental vitamin C, ~800 milligram human equivalent in a guinea pig, this animal will invariably develop cardiovascular disease and die prematurely.
The whole structure of the human GLO gene, which is similar in structure and origin to a gene in another species, has been disclosed by a computer-assisted search. Geneticists at Wakayama University in Japan know how to correct this genetic error.
Here is their description of the problem:
Only five exons (the protein coding DNA sequence of a gene), as compared to 12 exons constituting the functional rat GLO gene, remain in the human genome. A comparison of these exons with those of their functional counterparts in rats shows that there are two single nucleotide deletions (a nucleotide is a subunit of DNA as adenine, guanine, thymine, or cytosine), one triple nucleotide deletion, and one single nucleotide insertion in the human sequence. When compared in terms of codons (a specific sequence of three DNA bases within a gene), the human sequence has a deletion of a single amino acid, two stop codons, and two aberrant codons missing one nucleotide besides many amino acid substitutions. [Journal Nutrition Science Vitaminology 49: 315–19, 2003]
Furthermore, researchers at Kyoto University in Japan have successfully inserted the missing or dysfunctional GLO gene into fertilized eggs of scurvy-prone medaka fish, producing offspring that can synthesize vitamin C. [Biochemical Biophysical Research Communications 223: 650–53, 1996]
So why is there no priority among synthetic biologists to restore the major human biological flaw that has plagued mankind for centuries? The lack of expressed enthusiasm for the re-insertion of a functional GLO gene into the human genome goes unexplained. Maybe it’s because the loss of the GLO gene does not fit preconceived Darwinian theories, that mankind progressively evolved from lower species. This gene mutation would have made Homo sapiens less able to survive. Who really knows why this main concern hasn’t taken precedence within the ranks of synthetic biologists? It is believed the restoration of the GLO gene would prolong human life by many decades over and above current life expectancy. Possibly the prevailing agenda to control the size of the world’s human population would explain the absence of a GLO gene insertion project from the drawing boards of biologists.





