0 registered members (),
1,128
guests, and 16
spiders. |
Key:
Admin,
Global Mod,
Mod
|
|
S |
M |
T |
W |
T |
F |
S |
|
|
|
1
|
2
|
3
|
4
|
5
|
6
|
7
|
8
|
9
|
10
|
11
|
12
|
13
|
14
|
15
|
16
|
17
|
18
|
19
|
20
|
21
|
22
|
23
|
24
|
25
|
26
|
27
|
28
|
29
|
30
|
31
|
|
|
Only The Best Herbs!
Your best source of world-class herbal information! More... |
#1 Book We've Found!
"Silver" fillings, mercury detox, & much more. More... |
For Mercury Detox
Prevent mercury reabsorption in the colon during detox. More... |
Softcover & Kindle
Excellent resource for mercury detox. More... |
For Mercury Chelation
For calcium chelation and heart health. More... |
Must for Every Parent
The most complete vaccine info on the planet. More... |
Finally.
Relief! More... |
Dr. Sherri Tenpenny
Get the info you need to protect yourself. More... |
What everyone's talking about!
Safe, powerful, timely! More... |
There is a difference!
A powerful brain antioxidant for use during Hg detox. More... |
This changed my life!
This book convinced me remove my fillings. More... |
This is what we use!
The only multi where you feel the difference. More... |
Hair Tests Explained!
Discover hidden toxicities, easily. More... |
Have Racing Thoughts?
Many use GABA for anxiety and better sleep. More... |
Help Them!
Natural health for pets. More... |
The Bible We Use!
King James with study notes by Bullinger. More... |
The Bible We Use!
King James with study notes by Bullinger. More... |
Food Additives
Protect your family from toxic food! More... |
|
|
|
|
AIN'T NO GOOD MUTATIONS HERE
#69511
12/20/12 07:27 PM
12/20/12 07:27 PM
|
OP
Master Elite Member
|
Joined: Dec 1999
Posts: 30,797
Maine, USA
|
|
AIN'T
NO GOOD MUTATIONS HERE - (Print)
Most of the mutations in our DNA are only 5,000-10,000 years old, according
to a study by the Exome Sequencing Project at the National Institutes of Health.
That's a good thing, then, because a recent article in the American Journal
of Human Genetics says we're all rife with genetic mistakes, and it's hard
to find any that have benefited us at all. We might not have been able to handle
many more years of DNA deterioration.
Researchers on the 1000 Genome
Project used genetic data from 179 individuals and found that all had between 40
and 110 potentially disease-causing mutations in their DNA. The individuals had
281-515 actual substitutions each, but the trouble only really started when
both parents had passed on a mutation in the same gene. The
researchers, estimated, "(about)400 damaging variants and (about)2 bona
fide disease mutations per individual."
Not every damaging mutation
shows up immediately. Some might increase one's chances for heart disease.
Another might simply weaken the kidneys or slow the production of insulin. The
body is also good at covering for an improperly functioning gene, using backup
systems or compensating in some way when a gene isn't doing its job right. When
all else fails, though, mutations tend to cause disease.
The researchers
have been working to develop and fill out the Human Gene Mutation Database with
the more dangerous genetic defects, giving doctors a tool in diagnosing
inherited diseases. It is distinctly noticeable that while some mutations are
not as destructive as others, the researchers are not developing a database of
all the improvements made by random changes in the genetic code.
Mutations and Evolution: In order for evolution to
work on a grand scale, changing one family of creatures into another family of
creatures, beneficial mutations must appear to add new information to the
genetic code. Without mutations, there are no major evolutionary steps.
Yes, the genetic information already existing within a species can
vary due to natural selection, but this always strains out information; it
never adds new, previously non-existent coding to the genome. Yet,
while Darwinists claim that rare, beneficial mutations do
exist, the math shows that random mutations result in the net removal
of functional programming from the genetic code rather than adding to it.
Beneficial Mutations? Beneficial mutations in any
sense are extremely rare in our world today. Those that can be
considered "beneficial" in specific situations always involve the loss
of some function and generally result in the deterioration of the
creature's overall health. For instance, sickle-cell anemia is considered a
beneficial mutation because it protects many Africans against
malaria, yet sickle-cell anemia itself is a very serious
disease.
Sickle cell anemia is a genetic disorder in which the red
blood cells take a long, thin, sickle-like shape instead of the round donut
shape of a healthy red blood cell. While this deformity prevents the
body from carrying malaria, protecting people in high-malaria areas from dying
from the disease, the sickle cell anemia is itself dangerous. Sickle cell
blood cells carry less oxygen than normal cells. The misshapen cells also tend
to clump up and get stuck in blood vessels, leading to infection and organ
damage. Sickle-shaped cells often die after only 10-20 days,
while healthy red blood cells live an average of 120 days before they
die.
People with the mutation from only one parent can live
normally because they have the genes from the other parent still producing
correctly-shaped blood cells. The sickle-shaped cells are also produced, but the
body doesn't have to depend on them. Those with the sickle cell mutation from
both parents, however, have a problem. Their body functions in a state of
constant oxygen deprivation, and it struggles to produce enough red blood cells
to replace the dying ones, greatly reducing general health. The life
expectancy for men with sickle-cell anemia is only 42 years.
If
sickle cell anemia is the best beneficial mutation out there, our hopes for
evolving through mutations are empty and doomed to disappointment. It is true
that bacteria that develop a specific dysfunction may survive in the presence of
antibiotics, but those same bacteria are still weaker and quicker to die when
exposed to the outside world. A person with no arms may be less likely to
contract a virus, because he can't rub his nose with infected fingers, but few
people will argue that it's better to go around in life without arms. The fact
is, examples of truly beneficial mutations are massively lacking.
Loss Of Information: The real trouble with mutations
takes us down to the DNA level. We learn in high school biology that our genetic
code is made up of DNA, long strands of the nucleotide bases adenine,
guanine, thymine, and cytocine – A G T and C for short. These
four bases provide the digital code for our system, similar to the
way 0s and 1s make up binary code for computers. In the cell, during the
process of translation, these nucleotides get read in groups of three, called
codons. Each codon is like a little train car of three letters that code
for an amino acid, which go on to make up proteins. For instance, the codon AAA
codes for the amino acid lysine and TGG codes for the amino
acid tryptophan. (During transcription, thymine is replaced with
uracil - U - to make the codon UGG.)
There isn't just one code for many
amino acids, though. Lysine can also be coded by AAG. Cysteine can be coded by
both TGT and TGC, and the amino acids serine, arginine, and leucine all have six
possible codes. Other proteins on the other hand, like tryptophan, only have
that single code available to make them.
This causes a problem for the
statistics of mutations. If there are errors in the transcription process and
letters are not copied correctly (a source for mutations), certain amino acids
are going to be favored over others. For instance, if AAG is accidentally
transcribed as AAA, it won't necessarily harm the body because AAA still codes
for lysine (provided the cell has high enough levels of tRNA for the alternate
codon). If TGG for tryptophan gets changed to TTG, though, it will cause
leucine to be made. If TAA gets changed to TTA, it will also make
leucine and if CAA for Glutamine gets turned to CTA, again leucine
benefits. Statistically, an error is highly likely to accidentally make leucine
and highly unlikely to make tryptophan.
If we have been evolving for
millions of years, we would expect to see a high ratio of serine, arginine, and
leucine codes, because statistically mutations would favor making these three
amino acids. As mutations accumulated over the generations, we'd expect these
codes to dominate, making it rare to ever see tryptophan and leading to a loss
of information in the genetic code. Dr. Jerry Bergman writes:
‘This disparity would have worked against producing the code by natural
selection in the first place. An example of this method of degradation is
illustrated by the words "amino acid" which would be changed to "amano acad,"
then to "amaao aaad," and finally to "aaaaa aaaa" if the letter "a" dominated.
Another mutation can change the "a'" back to an "m" or another letter but, in
this illustration, the overall trend would be to the letter "a'" and would
eventually stabilize largely at a set of "a" letters with a few converting
back to the other letters from time to time.'
Creature Coding: There are built-in mechanisms to correct
errors, at least, and mutations do rarely slip through. The human race has
fought through the past 5,000-10,000 years of slow disintegration fairly well.
The self-correcting mechanisms would have had to have been in place at the
beginning, else the gene code's deterioration would have been rapid and
destructive before these self-correcting mechanisms evolved.
It is also
valuable to note that organisms considered closely related can favor
different codes for the same amino acid. E coli uses AAA to code for lysine 75
percent of the time, but only uses AAG one fourth of the time. Another
bacteria, Rhodobacter, uses AAG 75 percent of the time - just the
opposite. These two organisms, which are supposed to be more closely
related, don't use codes in the same proportions, while the human being and
fruit fly (not closely related) both use CTG to code for leucine just
over 40 percent of the time.
Studies have also shown there to be far more
deletions than insertions into the DNA code. In their article on the DNA loss in
Drosophila (fruit flies) in the journal Gene in 1997, Petrov
and Hartl found a "virtual absence of insertions and a remarkably high incidence
of large deletions." In their article on nucleotide substitution, insertion and
deletion in the human genome in Nucleic Acids Research in 2003, Zhang
and Gerstein found the mutational deletion rate of base pairs to be
three times as high as the insertion rate. Once again, this results in a
net loss of information rather than the net gain necessary for us to have
evolved from lower lifeforms.
Mutation Hot Spots
Mutations also do not occur randomly throughout the DNA code, but are
generally localized in certain spots. For instance, the CG dinucleotide has a
much higher chance of being involved in a mutation than any other dinucleotide –
12 times as high according to Jorde, Carey and White in Medical
Genetics(1997). Of 400 codon mutations mapped on the human tumor suppressor
antioncogene gene just over 91 percent occurred in four specific codons. Some of
these "hot spots" result from passing around the same mutation through
inheritance, but most are truly hot spots in which certain parts of the genetic
code are more prone to mutation than other parts.
The basic point
is this: mutation is not evenly, randomly distributed throughout the
genome, which we'd expect if mutations had brought about all the precise
structures in living things today.
Genome
Deterioration: Mutations are well known to cause diseases like
cystic fibrosis, hemophilia, inherited osteoporosis and literally more than 1000
others. Finding descriptions of deleterious mutations takes less than half a
minute. Finding truly beneficial mutations is a headache, and even
the so-called beneficial mutations are due to net loss of information
that, while helping an organism survive in a very specific situation, also lead
to the weakening of the organism's overall health.
If the
evolutionary model of origins were reality, we should expect to see a number of
beneficial mutations that were the result of added information. Instead, it
appears that we each receive a damaged, deteriorating version of a once
excellently engineered, fully functioning genetic code.
Related
Links:
|
|
|
|