Institute for Creation Research } Vitamin C (deficiency vit. c; scurvy

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Adam and Eve, Vitamin C, and Pseudogenes by Daniel Criswell, Ph.D.*

Every winter, as the influenza (flu) season spreads across America,

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

nonfunctional remnants of presently functional genes. These sequences of

DNA are called pseudogenes, and there are several criteria used to

distinguish pseudogenes from functional genes. A pseudogene 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). Pseudogenes 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). Pseudogenes 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 pseudogene (Karp 2002). Many

pseudogenes 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 pseudogenes that meet the criteria mentioned above

(Zhang et al. 2003). To find a pseudogene 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 pseudogene 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 pseudogene. 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.

 

[http://static.icr.org/i/articles/imp/imp-407-arrows.jpg]

 

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 pseudogenes 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 pseudogenes 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 pseudogenes 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 pseudogenes 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!

 

References

 

1. Davies, R. W. 1970. Some Roman medicine. Med Hist 14 (1):101-6.

2. Garrett, R. H., and C. M. Grisham, 1999. Biochemistry. 2nd ed. New

York: Saunders College Publishing. 3. Hirotsune, S., N. Yoshida, A.

Chen, L. Garrett, F. Sugiyama, S. Takahashi, K. Yagami, A.

Wynshaw-Boris, and A. Yoshiki. 2003. An expressed pseudogene regulates

the messenger-RNA stability of its homologous coding gene. Nature 423

(6935):91-6. 4. Inai, Y., Y. Ohta, and M. Nishikimi. 2003. The whole

structure of the human nonfunctional L-gulono-gamma-lactone oxidase gene

-- the gene responsible for scurvy -- and the evolution of repetitive

sequences thereon. J Nutr Sci Vitaminol (Tokyo) 49 (5):315-9. 5.

Karp, G. 2002. Cell and Molecular Biology. 3rd ed. New York: John Wiley

and Sons. 6. Linster, C. L., and E. Van Schaftingen. 2007. Vitamin C

Biosynthesis, Recycling and Degradation in Mammals. Febs J 274 (1):1-22.

7. Marieb, E. N. 1998. Human anatomy and physiology. 4th ed. Menlo Park:

Benjamin Cummings. 8. Nishikimi, M., R. Fukuyama, S. Minoshima, N.

Shimizu, and K. Yagi. 1994. Cloning and chromosomal mapping of the human

nonfunctional gene for L-gulono-gamma-lactone oxidase, the enzyme for

L-ascorbic acid biosynthesis missing in man. J Biol Chem 269

(18):13685-8. 9. Wiedersheim, Robert. 1895. The structure of man: An

index to his past history. 2nd ed. Translated by H. and M. Bernard.

London: Macmillan and Co. 10. Zhang, Z., P. M. Harrison, Y. Liu, and

M. Gerstein. 2003. Millions of years of evolution preserved: a

comprehensive catalog of the processed pseudogenes in the human genome.

Genome Res 13 (12):2541-58.

 

*Daniel Criswell has a Ph.D. in molecular biology and is a biology

professor at the ICR Graduate School.

 

Cite this article: Criswell, D. 2007. Adam and Eve, Vitamin C, and

Pseudogenes. Acts & Facts. 36 (5).

 

This article was originally published May, 2007. " Adam and Eve, Vitamin

C, and Pseudogenes " , Institute for Creation Research,

http://www.icr.org/article/adam-eve-vitamin-c-pseudogenes (accessed

February 11, 2009).

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