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Every
winter, as the influenza (flu) season spreads, people
flock to stores to get vitamin C tablets to deliver them
from the symptoms of the common cold. Vitamin C, or
ascorbic acid, is an important cofactor that stimulates
the immune system and apparently assists in shortening
the length of illness and the severity of flu symptoms
(although the exact effects of vitamin C on the flu are
still debated).

In addition to stimulating the immune system, vitamin C
has been identified with several other functions in the
human body including production of an important protein,
collagen, found in several types of connective tissue
including bone and cartilage (Garrett 1999). A
deficiency in vitamin C can cause scurvy, a disease that
results from deterioration of connective tissue, and
prolonged lack of vitamin C can even lead to death (Marieb
1998).
Humans are unable to synthesize vitamin C, but are able
to store a 30-day supply of this important nutrient. To
maintain this supply, a person must ingest about 60 mg
of vitamin C each day, or approximately the amount of
vitamin C in an average size orange. Although humans,
apes, monkeys, fruit bats, and several species of fish
(including trout and salmon) are unable to synthesize
vitamin C, many other animals are quite capable of
making their own vitamin C and do not need to eat fruit
and vegetables to acquire this nutrient (Garrett 1999).
Many people, especially in northern climates during the
winter, have suffered from a lack of vitamin C
throughout history. It’s very likely that many people
have died from scurvy as a result of being unable to
provide themselves with fresh fruit and vegetables
during the winter months. If vitamin C is such an
important nutrient, and many other animals possess the
ability to synthesize it, why didn’t God give humans the
biochemical pathways to synthesize vitamin C? There are
two obvious possibilities why people today cannot
synthesize vitamin C: (1) Humans were created without
the ability to synthesize vitamin C, or (2) they lost
the information from genes that code for the proteins
necessary to synthesize vitamin C.
The first possibility is very simple and there is
logical Biblical and scientific support for this
scenario. From the beginning, Adam and Eve were not
created with a biochemical pathway for making vitamin C
and were dependent on eating fruit, the best source of
vitamin C. We know they were instructed to eat any fruit
in the Garden of Eden except fruit from the Tree of the
Knowledge of Good and Evil, and yet had access to the
Tree of Life. Adam and Eve lived in an environment with
many similarities to heaven. However, unlike those in
heaven, Adam and Eve were commanded to be fruitful and
multiply, and produce little Adams and Eves.
Human reproduction would require nutrients to build
tissues for the child during and after pregnancy, an
indication that Adam and Eve had to eat to provide for
their developing children and also for the maintenance
of their own bodies. Furthermore, today nutritionists
recommend a diet high in fruit and vegetables as being
the healthiest source of nutrients, which is consistent
with what God instructed Adam and Eve to eat. It is
possible that God made Adam and Eve (and us) dependent
on fruit as a source of vitamin C as a reminder that
they were dependent on Him for food that must be eaten
to stay healthy.
Is it possible that Adam and Eve did have the
information in their genes to produce the enzymes
necessary for synthesizing vitamin C? Are there any
remnants of those genes that can be identified in the
human genome today? What would a non-functioning remnant
of a gene look like if scientists found one? One thing
is sure today — if Adam and Eve did have the information
in their genes to make vitamin C, health problems with
scurvy recorded as far back as the Roman Empire (Davies
1970) indicate this information disappeared long ago
from the human genome.
There are sequences of DNA (in the genome) that are
claimed to be non-functional remnants of presently
functional genes. These sequences of DNA are called
pseudo-genes, and there are several criteria used to
distinguish pseudo-genes from functional genes. A
pseudo-gene DNA sequence typically is greater than 70%
similar (homologous) to a functional gene but lacks a
promoter that would enable the sequence to be
transcribed into RNA and finally a protein (Zhang et al.
2003). Pseudo-genes also typically have disruptions to
the “coding region,” such as stop codons that
prematurely end the translation of the gene into a
protein (Zhang et al. 2003). Pseudo-genes are believed
to vary significantly from the original functioning gene
because they are no longer under selective constraints.
In other words, since the cell is no longer using this
stretch of DNA, it accumulates mutations at a fast rate
— degrading the original functional gene sequence into a
pseudo-gene (Karp 2002). Many pseudo-genes are
identified by comparing similar sequences in the genome
to functional genes within an organism.
For example, in humans there are many functional genes
for ribosomal proteins, and there are several human
ribosomal pseudo-genes that meet the criteria mentioned
above (Zhang et al. 2003). To find a pseudo-gene for
vitamin C in the human genome, a comparison would have
to be made between the human genome and the genome of an
organism that had a functional gene for synthesizing
vitamin C.
In 1994, a group of Japanese scientists identified a DNA
sequence in humans that had many similarities to the rat
gene that codes for the enzyme (L-gulono-ã-lactone) that
catalyzes the last step of vitamin C synthesis (Nishikimi
et al. 1994). The human pseudo-gene sequence discovered
has four of these 12 exons. (Exons are the modular
coding regions of a gene.) These four human exon
sequences have many characteristics of a pseudo-gene.
There is a 70-80% sequence homology between the rat and
human sequences depending on the exon, and two stop
codons. Later analysis confirmed that these four exons
are present in other primates as well (Inai, Ohta, and
Nishikimi 2003). Humans are missing only the final
enzyme for the last step in synthesizing vitamin C, but
have all of the other enzymes necessary to convert
glucose into vitamin C.
It would seem from the evidence of a potential human
pseudogene for L-gulono-ã-lactone and the presence of
the other enzymes necessary for synthesizing vitamin C
that humans have lost the ability to make vitamin C.
However, there is more to this story. There are only
four exons for the gene encoding L-gulono-ã-lactone in
humans. Two-thirds of the homologous rat gene is
completely missing. Most pseudogenes represent 90% of
the entire functional gene. This DNA sequence, labeled
as a pseudogene, might have an entirely different
function than the rat gene.
Stating that only the last enzyme is missing for the
pathway to convert glucose to vitamin C might imply to
the untrained individual that there is a biochemical
pathway that leads to a dead end. Actually, the
biochemical pathway that leads to the synthesis of
vitamin C in rats also leads to the formation of
five-carbon sugars in the pentose phosphate pathway
present in virtually all animals (Linster and Van
Schaftingen 2007).
There are several metabolic intermediates in this
pathway illustrating that these substances can be used
as precursors for many compounds in the cell. In the
pentose phosphate pathway, five-carbon sugars are made
from glucose (a six-carbon sugar) to be used in the
synthesis of DNA, RNA, and many energy producing
substances such as ATP and NADPH (Garrett 1999). Animals
that synthesize vitamin C can use both pathways
illustrated in the simplified diagram below. Humans and
the other animals “less fortunate” than rats only use
the pentose phosphate pathway.
There is no dead end or wasted metabolic intermediates,
and there is no need to have the enzyme to make vitamin
C since humans are able to get all of the vitamin C they
need from food substances.
Thousands of human pseudo-genes have been catalogued,
but in spite of the similarities to functional genes,
the exact role of pseudogene sequences in the genome are
not known by any scientist. It is not necessary to
assume that pseudo-genes are remnants of once
functioning genes that have been lost and now clutter
the genome like junk in a rubbish heap. It is possible
that these regions of DNA do have a role in human and
animal genomes and this role has not been discovered
yet.
Over 100 years ago, Robert Wiedersheim hypothesized that
the human body had more than 80 organs that lacked any
function simply because it was unknown at the time what
these organs did (Wiedersheim 1895). They were assumed
to be vestigial or “junk” leftovers from evolutionary
history and several of these organs are still presented
this way in biology textbooks today. The science of
genomics is in the same position today. Just because
scientists do not currently know the function of a
portion of DNA does not mean that it does not have any
function and therefore it is an evolutionary leftover.
It has been reported that pseudo-genes play a regulatory
role in yeast for the functional genes that they share
sequence homology with (Hirotsune et al. 2003). There
needs to be more research in this area to verify these
claims, but at least there are some indications of a
functional role for pseudo-genes in the human genome.
So, did Adam and Eve have a gene to code for an enzyme
that would synthesize vitamin C and was this information
eventually lost as a result of the curse, or were they
simply created without this information in their
genomes? That question might not get answered until
Christ returns. But in the meantime, humans require
plenty of vitamin C in their diet — so have an orange!
Courtesy:
(© 2009 Institute of Creation Research. All rights
reserved. www.icr.org )
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