[_ Old Earth _] Five Pillars of Evolution Compared with Creation

[Charlie Hatchett]

Slevin:

There is no law that life comes from life.

Charlie:

How about the rule of cause and effect and repeated observations. Also consider the lack of observations to the contrary. The idea that life came from purely naturalistic causes is pure conjecture and lacks observability, repeatability, and violates the rule of cause and effect and the Second Law. In my opinion, in the face of observations and hard facts, accepting purely naturalistic causes for the origins of life requires the believer to exhibit an inordinate amount of faith, well outside the bounds of science.

Charlie Hatchett wrote:

How about the rule of cause and effect and repeated observations.


Slevin:

What about it?


Charlie:
Also consider the lack of observations to the contrary. The idea that life came from purely naturalistic causes is pure conjecture and lacks observability, repeatability, and violates the rule of cause and effect and the Second Law. In my opinion, in the face of observations and hard facts, accepting purely naturalistic causes for the origins of life requires the believer to exhibit an inordinate amount of faith, well outside the bounds of science.

Slevin:
1. It is speculation, but like all sciences, they start out with speculation and then we go from there.
2. We have observation to the contrary to support the idea, they are basic experiments but they indicate slight possibilities.
3. All life is composed of non-life, so it's not that huge of a step.
4. How does it violate the rule of cause and effect?
5. How does it violate the Second Lw?
6. Your opinion is irrelevant then, because it doesn't.

Charlie:
#1. Your hypothesis, then, is life comes from non-life.

#2 And your arguement is there are "basic" experiments that indicate "slight possibilities".

#3 You strengthen your arguement above by claiming that subatomic particles randomly organizing themselves into information bearing, self-replicating DNA is not a huge step.

#4 and 5 The Cause has less entropy than the effect

#6 Brilliant response :P

Charlie:
#1. Your hypothesis, then, is life comes from non-life.

Slevin:
No it isn't.

Charlie:
#2 And your arguement is there are "basic" experiments that indicate "slight possibilities".

Slevin:
No it isn't.

Charlie:
#3 You strengthen your arguement above by claiming that subatomic particles randomly organizing themselves into information bearing, self-replicating DNA is not a huge step.

Slevin:
No I didn't.

Charlie:
#4 and 5 The Cause has less entropy than the effect

Slevin:
No I didn't.

Charlie:
#6 Brilliant response

Slevin:
Brilliant strawman.

 

[Slevin]

Quote:
1. It is speculation, but like all sciences, they start out with speculation and then we go from there.
2. We have observation to the contrary to support the idea, they are basic experiments but they indicate slight possibilities.
3. All life is composed of non-life, so it's not that huge of a step.
4. How does it violate the rule of cause and effect?
5. How does it violate the Second Lw?
6. Your opinion is irrelevant then, because it doesn't.


#1. Your hypothesis, then, is life comes from non-life.

#2 And your arguement is there are "basic" experiments that indicate "slight possibilities".

#3 You strengthen your arguement above by claiming that subatomic particles randomly organizing themselves into information bearing, self-replicating DNA is not a huge step.

#4 and 5 The Cause has less entropy than the effect

#6 Brilliant response

Repeating it doesn't make anything you said less of a strawman.

 

[Solo]

All Variety of Life Came From One Original, Single Cell

1. This is illustrated with a "tree of life" pattern.
   Although it can be illustrated in theory, it cannot be documented in practice. No one claims to "see" evolution happening today -- it takes too long. (Fruit fly and pepper moth experiments are irrelevant. Although changes occur within the species, the species do not change at all -- and the latter is what evolution is supposed to be all about.]
   [/*:m:70a87]
2. Originally it was presumed that "missing links" would appear in the fossil record, the geological column. Charles Darwin said in Origin of Species (Collier, 1962, p. 168), "As by this theory innumerable transitional forms must have existed, why do we not find them imbedded in countless numbers in the crust of the earth? . . . I will here only state that I believe the answer mainly lies in the record being incomparably less perfect than is generally supposed (i.e., not enough fossils have been studied yet)." To continue (Ibid, p.308), "Why then is not every geological formation and every stratum full of such intermediate links? . . . this, perhaps, is the most serious and obvious objection which can be urged against the theory."
   [/*:m:70a87]
3. Now it is crystal clear there are NO intermediate fossils.
   "Despite the bright promise that paleontology provides a means of 'seeing' evolution, it has presented some nasty difficulties for evolutionists, the most notorious of which is the presence of 'gaps' In the fossil record. Evolution requires intermediate forms between species and paleontology does not provide them." (D. B. Kitts, Evolution, Vol.28, 1974, p.467)
   [/*:m:70a87]
4. Thus there is a new theory of evolution recently.
   Because Darwinism (slow, gradual evolution) has completely failed to explain how evolution occurred, a new theory was suggested. Instead of rejecting evolution because of a lack of evidence for it, evolutionary philosophers still "believe" in it and proposed that it happened in "quantum leaps". They call it "punctuated equilibrium". In an incredible forsaking of logic, they say that the lack of evidence IS the evidence for it!!
   "Evidence from the fossil record now points overwhelmingly away from the classical Darwinism which most Americans learned in high school. . . . scientists now believe that species change little for millions of years and then evolve quickly, in a kind of quantum leap." (Newsweek, 11/3/80.)[/*:m:70a87]

 

[blunthitta4life]

Why do people attack darwin and expect that to somehow debunk evolution.... theories change in light of new data.

While, the theory of evolution has changed, it has not been debunked. It has stood up to 150 years of scrutiny. If anyone could actually disprove the theory of evolution, that would be one of the biggest discoveries since basically all of modern biology depends on it.

 

[Barbarian]

I don't see a mutation as necessarily an increase in thermodynamical entropy, whereas a true mutation is necessarily an increase in informational entropy.

All new mutations provide an decrease in informational entropy.


Would you like to see the numbers on that?

 

[Solo]

Great Stretches of Time Are Required for Evolution To Occur

1. Evolutionists claim the earth is 4.5 billion years old.
   Since evolutionists have insisted evolution occurs over vast stretches of time, time is extremely important to them. Creationists make a mistake trying to sidestep that issue. A little over 100 years ago it was no issue since all scientists felt the earth was relatively young. A chart in the American Museum of Natural History (in NYC) says, "The earth increased in age 40 million years each year between 1868 and 1968." Of course it did not really increase in age. Scientists simply say it did to accomodate the evolution theory. And therefore, now some dating methods seem to support the idea of a very old earth.
   [/*:m:32f9b]
2. Many evolutionists feel the universe is eternal.
   This is a logical corollary to the belief of evolutionists that God is not necessary. If there is no eternal God, then there must be an eternal universe.
   [/*:m:32f9b]
3. However, 4.5 billion years is not enough.
   Four of the world's best mathematicians met with geneticists to discuss the probabilities of Darwinism. They were asked, "Has there been enough time for natural selection . . . to operate and give rise to the observed phenomena of nature? No. Is it likely that the superbly ordered biochemistry which we see now could have evolved ...? Again, no. The probability is virtually zero." (Scientific Research, 11/67, pp. 59-60.)
   [/*:m:32f9b]
4. On the other hand, many factors limit the age of the earth/universe:[list:32f9b]
5. Rapid fossil formation [/*:m:32f9b]
6. Shrinking sun [/*:m:32f9b]
7. Decay of earth's magnetic field [/*:m:32f9b]
8. Recession of moon [/*:m:32f9b]
9. Formation of river deltas [/*:m:32f9b]
10. Earth's rotation speed [/*:m:32f9b]
11. Moon dust accumulation [/*:m:32f9b]
12. Atmospheric oxygen/helium[/*:m:32f9b]

If enough factors limit the earth (and universe) to relative youth, then all indicators for long ages must be re-examined as to their validity.[/*:m:32f9b][/list:o:32f9b]

 

[jwu]

Evolutionists claim the earth is 4.5 billion years old.
Since evolutionists have insisted evolution occurs over vast stretches of time, time is extremely important to them. Creationists make a mistake trying to sidestep that issue. A little over 100 years ago it was no issue since all scientists felt the earth was relatively young. A chart in the American Museum of Natural History (in NYC) says, "The earth increased in age 40 million years each year between 1868 and 1968." Of course it did not really increase in age. Scientists simply say it did to accomodate the evolution theory. And therefore, now some dating methods seem to support the idea of a very old earth.

Actually it's not said to accomodate the theory of evolution, but because of independent evidence.

E.g. before there was knowledge of nuclear fusion it was thought that the sun burns because of gravitational collapse, which sets an upper limit to its age of several million years.
Then nuclear fusion was discovered as the source of energy of the sun, and this indicated a way older sun.

# Many evolutionists feel the universe is eternal.
This is a logical corollary to the belief of evolutionists that God is not necessary. If there is no eternal God, then there must be an eternal universe.

That doesn*t make any sense, non sequitur...it has nothing to do with the validity of the theory of evolution either, and i'd like to know how many these "many" evolutionists actually are.

However, 4.5 billion years is not enough.
Four of the world's best mathematicians met with geneticists to discuss the probabilities of Darwinism. They were asked, "Has there been enough time for natural selection . . . to operate and give rise to the observed phenomena of nature? No. Is it likely that the superbly ordered biochemistry which we see now could have evolved ...? Again, no. The probability is virtually zero." (Scientific Research, 11/67, pp. 59-60.)

A priori probabiities for getting the exact thing which we have now mean nothing.

Rapid fossil formation

Could you elaborate how this is supposed to liomit the age of the earth?

Shrinking sun

The sun oscillates, it does not shrink at the rate which is proposed in this common creationist claim.

Decay of earth's magnetic field

Same here, this argument is based on an invalid exponential extrapolation of a short part of a graph which - if extended based on actual hard evidence - actually shows an oscillation

Recession of moon

Actually that is slow enough not to pose any problems for an old earth.

Formation of river deltas

...is rather evidence for an old earth, as massive deltas and canyons take longer than the 6000 years of young earth creation to form.

Earth's rotation speed

Not a problem either...4.5 billion years ago one day took about 5 hours if i recall correctly what i read somewhere. Since then it has slowed down to 24 hours.
If you have different numbers, let's see them.

Moon dust accumulation

Oh my...even creationist organizations like Answers In Genesis say this doesn't hold any water, it's based on faulty estimations of the influx of dust from the early 60ies...meanwhile actual measurements say something else.
http://www.answersingenesis.org/home/ar ... nt_use.asp

Atmospheric oxygen/helium

Not a problem at all either if ionization is considered:
http://www.talkorigins.org/indexcc/CE/CE001.html

 

[Solo]

http://www.ancientdays.net/geotime.htm

 

[jwu]

Oh, great...another link dropping debate. It takes you a few second to copy and paste a link, but you apparently expect me to invest much more time to write a lengthy response about why that is not a valid argument.

Why don't you argue that case with your own words? You might even learn something from that, instead of just forgetting things again that you merely skimmed over.

But ok, from that site:

If the coelacanth. is used as an index fossil it must have died out entirely 300 million years ago (or 150 or 75 million, whichever is felt to be the most likely). Thus it should be impossible to find any living on the earth at the present time.

Note the "if". The coelacant is not used as an index fossil for exactly these reasons.
Basically the reasoning on that website is "some species are unsuitable as index fossils, therefore the whole geological column is wrong". That's just incredibly weak. Absolutely laughable.

But, LIVING COELACANTH. HAVE BEEN FOUND IN MADAGASCAR and they are EXACTLY THE SAME as the fossils!

...and there we even have an outright lie. Today's coelacanths are not even the same family. They are deepwater fish, while the ancient ones lived in shallow water.
Today's coelacanths are Latimeriidae, the ancient ones are part of the family Coelacanthidae.

And besides, the ToE does not require things to change anyway, so even if they were the same, that wouldn't be a problem.

 

[Barbarian]

I don't see a mutation as necessarily an increase in thermodynamical entropy, whereas a true mutation is necessarily an increase in informational entropy.

Barbarian observes:
All new mutations provide an increase in informational entropy.

Would you like to see the numbers on that?

(crickets chirp quietliy)

Guess not. Is anyone surprised?

 

[Charlie Hatchett]

Barbarian observes:
All new mutations provide an increase in informational entropy.

I agree. What are the numbers you have?

 

[Charlie Hatchett]

And what is informational entropy anyway?
In Shannon's terms it is just the degree of alteration of the original message. Evolution actually requires an increase of Shannon entropy.
In K/C terms it's the frequency of letters compared to the overall size of the alphabet. This is completely neutral in terms of evolution, and K/C entropy explicitly is allowed to decrease.

Reproduction, critical to survival, deals with replication of information in the form of DNA and minimizing the amount of Shannon entropy of the replicated information. Minimizing Shannon entropy is paramount to reproductive success.
There are many feedback loops in the transcription, splicing and translation processes that play the role of conserving the information. If the feedback loops were not in place, the rate of mutations would increase to the point the species would have no chance of survival. Alot of things would go "haywire" at once. Also, Shannon's theory deals with information after receipt, whereas KC theory deals with randomness prior to receipt. Applying KC theory in this context is, in my opinion, a misapplication.

A priori probabiities for getting the exact thing which we have now mean nothing.

They are, however, useful in the context of comparing the most probable scenario, out of multiple, hypothesized scenarios.

For example, is it more probable that random matter organized itself into information bearing DNA by natural laws, or that the information bearing DNA matter is the result of intelligent activity...say aliens for example? If you were on, say, one of Jupiter’s moons, and you found a computer, would you feel it was more probablistic that the computer’s existence is due matter randomly combining over eons of time, our perhaps, would the odds be on other intellectual beings visiting the moon prior to us?

 

[jwu]

If the feedback loops were not in place, the rate of mutations would increase to the point the species would have no chance of survival.

Excessive mutation rates would be bad - because then too many changes happen at once for a proper genetic drift. I don't think anyone in my camp claims anything to the contrary.

However, a simple question:
What effect would a beneficial mutation have on the shannon entropy of the genome, and why is that so?

Also, Shannon's theory deals with information after receipt, whereas KC theory deals with randomness prior to receipt. Applying KC theory in this context is, in my opinion, a misapplication.

K/C information theory however is the one that is used for compression algorithms and so on, when the actual content is relevant.

 

[Charlie Hatchett]

oops...jwu...I edited one more time while you were posting. Would you like to re-post below.

Sorry, the server was taking a while to accept my edits.

 

[jwu]

I'll just address the new part. However, please don't forget to answer my question, it's crucial.

For example, is it more probable that random matter organized itself into information bearing DNA by natural laws, or that the information bearing DNA matter is the result of intelligent activity...say aliens for example? If you were on, say, one of Jupiter’s moons, and you found a computer, would you feel it was more probablistic that the computer’s existence is due matter randomly combining over eons of time, our perhaps, would the odds be on other intellectual beings visiting the moon prior to us?

That's against abiogenesis, not evolution. The analogy is also lacking as we know computers purely as a product of humans, while this can't be said about DNA. Moreover, one visits other planets or moons with the explicit expectation to find no such thing there, while there was no human to formulate such an expectation when there was no life yet.

 

[Charlie Hatchett]

What effect would a beneficial mutation have on the shannon entropy of the genome, and why is that so?

I'm trying to envision an example. Have you got one in mind, other than obvious, built in variations?

 

[jwu]

E.g. this:

Plasminogen activator inhibitor-1 (PAI-1) plasma levels have been consistently related to a polymorphism (4G/5G) of the PAI-1 gene. The renin-angiotensin pathway plays a role in the regulation of PAI-1 plasma levels. An insertion (I)/deletion (D) polymorphism of the angiotensin-converting enzyme (ACE) gene has been related to plasma and cellular ACE levels. In 1032 employees (446 men and 586 women; 22 to 66 years old) of a hospital in southern Italy, we investigated the association between PAI-1 4G/5G and the ACE I/D gene variants and plasma PAI-1 antigen levels. None of the individuals enrolled had clinical evidence of atherosclerosis. In univariate analysis, PAI-1 levels were significantly higher in men (P<.001), alcohol drinkers (P<.001), smokers (P=.009), and homozygotes for the PAI-1 gene deletion allele(4G/4G) (P=.012). Multivariate analysis documented the independent effect on PAI-1 plasma levels of body mass index (P<.001), triglycerides (P<.001), sex (P<.001), PAI-1 4G/5G polymorphism (P=.019), smoking habit (P=.041), and ACE I/D genotype (P=.042). Thus, in addition to the markers of insulin resistance and smoking habit, gene variants of PAI-1 and ACE account for a significant portion of the between-individual variability of circulating PAI-1 antigen concentrations in a general population without clinical evidence of atherosclerosis.

A mutation which confers resistance or even immunity to atherosclerosis. Even the individual who first had that mutation has been identified.

Or this:

Z Gastroenterol 1996 Jun;34 Suppl 3:56-8

Identification of putative beneficial mutations for lipid transport.

Galton DJ, Mattu R, Needham EW, Cavanna J

Medical Professorial Unit, St Bartholomew's Hospital, London, U.K.

To determine the effect of a common mutation (Ser447-Ter) of the human LPL gene upon serum lipid and lipoprotein levels and coronary artery disease (CAD) within a representative adult male population, we analyzed subjects from the Caerphilly Prospective Heart Disease Study (n = 1273). The possession of this mutation associates with protective lipid and lipoprotein profiles. Subjects possessing the mutation have significantly higher HDL-C (p = 0.002) and apo AI (p < 0.04) levels, lower triglycerides (p = < 0.04) and total cholesterol/HDL-C ratios (p < 0.02); all established previously to reduce risk of CAD. We also find that this mutation is significantly less frequent amongst CAD subjects (p < 0.05). These associations provide evidence for a common mutation that appears to confer beneficial lipid and lipoprotein profiles amongst an adult male population with regard to risk of CAD.

Have you got one in mind, other than obvious, built in variations?

Umm...how does one distinguish those from what you would consider "the real thing"? And why would there be "built in variation" anyway, and where are its limits?

 

[Charlie Hatchett]

E.g. this:
Quote:
Plasminogen activator inhibitor-1 (PAI-1) plasma levels have been consistently related to a polymorphism (4G/5G) of the PAI-1 gene. The renin-angiotensin pathway plays a role in the regulation of PAI-1 plasma levels. An insertion (I)/deletion (D) polymorphism of the angiotensin-converting enzyme (ACE) gene has been related to plasma and cellular ACE levels. In 1032 employees (446 men and 586 women; 22 to 66 years old) of a hospital in southern Italy, we investigated the association between PAI-1 4G/5G and the ACE I/D gene variants and plasma PAI-1 antigen levels. None of the individuals enrolled had clinical evidence of atherosclerosis. In univariate analysis, PAI-1 levels were significantly higher in men (P<.001), alcohol drinkers (P<.001), smokers (P=.009), and homozygotes for the PAI-1 gene deletion allele(4G/4G) (P=.012). Multivariate analysis documented the independent effect on PAI-1 plasma levels of body mass index (P<.001), triglycerides (P<.001), sex (P<.001), PAI-1 4G/5G polymorphism (P=.019), smoking habit (P=.041), and ACE I/D genotype (P=.042). Thus, in addition to the markers of insulin resistance and smoking habit, gene variants of PAI-1 and ACE account for a significant portion of the between-individual variability of circulating PAI-1 antigen concentrations in a general population without clinical evidence of atherosclerosis.


A mutation which confers resistance or even immunity to atherosclerosis. Even the individual who first had that mutation has been identified.

Or this:
Quote:
Z Gastroenterol 1996 Jun;34 Suppl 3:56-8

Identification of putative beneficial mutations for lipid transport.

Galton DJ, Mattu R, Needham EW, Cavanna J

Medical Professorial Unit, St Bartholomew's Hospital, London, U.K.

To determine the effect of a common mutation (Ser447-Ter) of the human LPL gene upon serum lipid and lipoprotein levels and coronary artery disease (CAD) within a representative adult male population, we analyzed subjects from the Caerphilly Prospective Heart Disease Study (n = 1273). The possession of this mutation associates with protective lipid and lipoprotein profiles. Subjects possessing the mutation have significantly higher HDL-C (p = 0.002) and apo AI (p < 0.04) levels, lower triglycerides (p = < 0.04) and total cholesterol/HDL-C ratios (p < 0.02); all established previously to reduce risk of CAD. We also find that this mutation is significantly less frequent amongst CAD subjects (p < 0.05). These associations provide evidence for a common mutation that appears to confer beneficial lipid and lipoprotein profiles amongst an adult male population with regard to risk of CAD.

_________________
Proud to be on ikester7579's ignore list.

How do we know these are novel traits? How long have these traits been observed? These examples only speak to current observations. Extrapolating or interpolating is only conjecture, taking into account the relatively short observation period.

jwu:

Umm...how does one distinguish those from what you would consider "the real thing"? And why would there be "built in variation" anyway, and where are its limits?

charlie:
Reproduction, critical to survival, deals with replication of information in the form of DNA and minimizing the amount of Shannon entropy of the replicated information. Minimizing Shannon entropy is paramount to reproductive success.
There are many feedback loops in the transcription, splicing and translation processes that play the role of conserving the information. If the feedback loops were not in place, the rate of mutations would increase to the point the species would have no chance of survival.

jwu:

And why would there be "built in variation" anyway

Adaptation in varying conditions.

 

[jwu]

How do we know these are novel traits? How long have these traits been observed?

We know it because e.g. in case of the artheriosclerosis example we even identified the individual who first had that mutation.

And in the other case it's limited to a small population.

I can get you plenty more examples. And keep in mind, even creationist organizations like AiG concede that beneficial mutations happen, so i don't really understand what you are trying to achieve with this...they are indisputable.

Adaptation in varying conditions.

Resistance to artheriosclerosis is pretty much beneficial under any condition, there is no reason why this should be subject of variation as a response towards differnet conditions. In case of creationism humans should always have had this trait, right from the start.

I don't understand how the text about entropy is supposed to answer these questions:

Umm...how does one distinguish those from what you would consider "the real thing"? And why would there be "built in variation" anyway, and where are its limits?

Please explain it, or post a real answer to them. And please don't forget the above question about the effect on shannon entropy of a beneficial mutation, it's really important.

 

[Charlie Hatchett]

We know it because e.g. in case of the artheriosclerosis example we even identified the individual who first had that mutation.

And in the other case it's limited to a small population.

I can get you plenty more examples. And keep in mind, even creationist organizations like AiG concede that beneficial mutations happen, so i don't really understand what you are trying to achieve with this...they are indisputable.

How do we know the one individual or group of individuals were the first to express these traits? How long have these studies been going on?

Any kind of so called "beneficial mutations" are actually a loss of genetic information, not an increase.

I think what we're having here is semantical arguement between mutation and built in variation. Just because a trait may seem novel in the short term, doesn't mean the trait is actually novel. We may be just now observing them. As we both know, the human genome is quite complex, and we are just "scraping the surface" of understanding it's complexity and how it relates to physical expression.

Argument: Some mutations are beneficial

Evolutionists say, ‘Mutations and other biological mechanisms have been observed to produce new features in organisms.’

by Jonathan Sarfati, with Michael Matthews (AIG)

First published in Refuting Evolution 2
Chapter 5

When they begin to talk about mutations, evolutionists tacitly acknowledge that natural selection, by itself, cannot explain the rise of new genetic information. Somehow they have to explain the introduction of completely new genetic instructions for feathers and other wonders that never existed in ‘simpler’ life forms. So they place their faith in mutations.

In the process of defending mutations as a mechanism for creating new genetic code, they attack a straw-man version of the creationist model, and they have no answer for the creationists’ real scientific objections. Scientific American states this common straw-man position and their answer to it.

10. Mutations are essential to evolution theory, but mutations can only eliminate traits. They cannot produce new features.

[quote:2a32b] On the contrary, biology has catalogued many traits produced by point mutations (changes at precise positions in an organism’s DNA)â€â€bacterial resistance to antibiotics, for example. [SA 82]

This is a serious misstatement of the creationist argument. The issue is not new traits, but new genetic information. In no known case is antibiotic resistance the result of new information. There are several ways that an information loss can confer resistance, as already discussed. We have also pointed out in various ways how new traits, even helpful, adaptive traits, can arise through loss of genetic information (which is to be expected from mutations).

Mutations that arise in the homeobox (Hox) family of development-regulating genes in animals can also have complex effects. Hox genes direct where legs, wings, antennae, and body segments should grow. In fruit flies, for instance, the mutation called Antennapedia causes legs to sprout where antennae should grow. [SA 82]

Once again, there is no new information! Rather, a mutation in the hox gene (see next section) results in already-existing information being switched on in the wrong place.1 The hox gene merely moved legs to the wrong place; it did not produce any of the information that actually constructs the legs, which in ants and bees include a wondrously complex mechanical and hydraulic mechanism that enables these insects to stick to surfaces.2

These abnormal limbs are not functional, but their existence demonstrates that genetic mistakes can produce complex structures, which natural selection can then test for possible uses. [SA 82]

Amazingâ€â€natural selection can ‘test for possible uses’ of ‘non-functional’ (i.e., useless!) limbs in the wrong place. Such deformities would be active hindrances to survival.
Gene switches: means of evolution?

William Bateson (1861–1926), who added the word ‘genetics’ to our vocabulary in 1909, found that embryos sometimes grew body parts in the wrong place. From this he theorized that there are underlying controls of certain body parts, and other controls governing where they go.

Ed Lewis investigated and won a Nobel Prize in 1995 for discovering a small set of genes that affect different body parts (Hox or Homeobox). They act like ‘architects of the body.’ Mutations in these can cause ‘dramatic’ changes. Many experiments have been performed on fruit flies (Drosophila), where poisons and radiation induced mutations.

The problem is that they are always harmful. PBS 2 showed an extra pair of wings on a fly, but failed to mention that they were a hindrance to flying because there are no accompanying muscles. Both these flies would be eliminated by natural selection.

Walter Gehring of the University of Basel (Switzerland) replaced a gene needed for eye development in a fruit fly with the corresponding gene from a mouse. The fly still developed normal fly eyes, i.e., compound eyes rather than lens/camera. This gene in both insects and mammals is called eyeless because absence of this gene means no eyes will form.

However, there is obviously more to the differences between different animals. Eyeless is a switchâ€â€it turns on the genetic information needed for eyes. But evolution requires some way of generating the new information that’s to be switched on. The information needed to build a compound eye is vastly different from that needed to build a lens/camera type of eye. By analogy, the same switch on an electric outlet/power socket can turn on a light or a laptop, but this hardly proves that a light evolved into a laptop!

All the same, the program says that eyeless is one of a small number of common genes used in the embryonic development of many animals. The program illustrated this with diagrams. Supposedly, all evolution needed to do was reshuffle packets of information into different combinations.

But as shown, known mutations in these genes cause monstrosities, and different switches are very distinct from what is switched on or off. Also, the embryo develops into its basic body plan before these genes start switchingâ€â€obviously they can’t be the cause of the plan before they are activated! But the common genes make perfect sense given the existence of a single Creator.
Increased amounts of DNA don’t mean increased function

Biologists have discovered a whole range of mechanisms that can cause radical changes in the amount of DNA possessed by an organism. Gene duplication, polyploidy, insertions, etc., do not help explain evolution, however. They represent an increase in amount of DNA, but not an increase in the amount of functional genetic informationâ€â€these mechanisms create nothing new. Macroevolution needs new genes (for making feathers on reptiles, for example), yet Scientific American completely misses this simple distinction:

Moreover, molecular biology has discovered mechanisms for genetic change that go beyond point mutations, and these expand the ways in which new traits can appear. Functional modules within genes can be spliced together in novel ways. Whole genes can be accidentally duplicated in an organism’s DNA, and the duplicates are free to mutate into genes for new, complex features. [SA 82]

In plants, but not in animals (possibly with rare exceptions), the doubling of all the chromosomes may result in an individual which can no longer interbreed with the parent typeâ€â€this is called polyploidy. Although this may technically be called a new species, because of the reproductive isolation, no new information has been produced, just repetitious doubling of existing information. If a malfunction in a printing press caused a book to be printed with every page doubled, it would not be more informative than the proper book. (Brave students of evolutionary professors might like to ask whether they would get extra marks for handing in two copies of the same assignment.)

Duplication of a single chromosome is normally harmful, as in Down’s syndrome. Insertions are a very efficient way of completely destroying the functionality of existing genes. Biophysicist Dr Lee Spetner in his book Not By Chance analyzes examples of mutational changes that evolutionists have claimed to have been increases in information, and shows that they are actually examples of loss of specificity, which means they involved loss of information (which is to be expected from information theory).

The evolutionist’s ‘gene duplication idea’ is that an existing gene may be doubled, and one copy does its normal work while the other copy is redundant and non-expressed. Therefore, it is free to mutate free of selection pressure (to get rid of it). However, such ‘neutral’ mutations are powerless to produce new genuine information. Dawkins and others point out that natural selection is the only possible naturalistic explanation for the immense design in nature (not a good one, as Spetner and others have shown). Dawkins and others propose that random changes produce a new function, then this redundant gene becomes expressed somehow and is fine-tuned under the natural selective process.

This ‘idea’ is just a lot of hand-waving. It relies on a chance copying event, genes somehow being switched off, randomly mutating to something approximating a new function, then being switched on again so natural selection can tune it.

Furthermore, mutations do not occur in just the duplicated gene; they occur throughout the genome. Consequently, all the deleterious mutations in the rest of the genome have to be eliminated by the death of the unfit. Selective mutations in the target duplicate gene are extremely rareâ€â€it might represent only 1 part in 30,000 of the genome of an animal. The larger the genome, the bigger the problem, because the larger the genome, the lower the mutation rate that the creature can sustain without error catastrophe; as a result, it takes even longer for any mutation to occur, let alone a desirable one, in the duplicated gene. There just has not been enough time for such a naturalistic process to account for the amount of genetic information that we see in living things.

Dawkins and others have recognized that the ‘information space’ possible within just one gene is so huge that random changes without some guiding force could never come up with a new function. There could never be enough ‘experiments’ (mutating generations of organisms) to find anything useful by such a process. Note that an average gene of 1,000 base pairs represents 41000 possibilitiesâ€â€that is 10602 (compare this with the number of atoms in the universe estimated at ‘only’ 1080). If every atom in the universe represented an ‘experiment’ every millisecond for the supposed 15 billion years of the universe, this could only try a maximum 10100 of the possibilities for the gene. So such a ‘neutral’ process cannot possibly find any sequence with specificity (usefulness), even allowing for the fact that more than just one sequence may be functional to some extent.

So Dawkins and company have the same problem as the advocates of neutral selection theory. Increasing knowledge of the molecular basis of biological functions has exploded the known ‘information space’ so that mutations and natural selectionâ€â€with or without gene duplication, or any other known natural processâ€â€cannot account for the irreducibly complex nature of living systems.

Yet Scientific American has the impertinence to claim:

Comparisons of the DNA from a wide variety of organisms indicate that this [duplication of genes] is how the globin family of blood proteins evolved over millions of years. [SA 82]

This is about the vital red blood pigment hemoglobin that carries the oxygen. It has four polypeptide chains and iron. Evolutionists believe that this evolved from an oxygen-carrying iron-containing protein called myoglobin found in muscles, which has only one polypeptide chain. However, there is no demonstration that gene duplication plus natural selection turned the one-chained myoglobin into the four-chained hemoglobin. Nor is there any adequate explanation of how the hypothetical intermediates would have had selective advantages.

In fact, the proposed evolution of hemoglobin is far more complicated than Scientific American implies, though it requires a little advanced biology to understand. The α- and β-globin chains are encoded on genes on different chromosomes, so they are expressed independently. This expression must be controlled precisely, otherwise various types of anemia called thalassemia result. Also, there is an essential protein called AHSP (alpha hemoglobin stabilizing protein) which, as the name implies, stabilizes the α-chain, and also brings it to the β-chain. Otherwise the α-chain would precipitate and damage the red blood cells.

AHSP is one of many examples of a class of protein called chaperones which govern the folding of other proteins.3 This is yet another problem for chemical evolutionary theoriesâ€â€how did the first proteins fold correctly without chaperones? And since chaperones themselves are complex proteins, how did they fold?4

Identifying information-increasing mutations may be a small part of the whole evolutionary discussion, but it is a critical ‘weak link’ in the logical chain. PBS, Scientific American, and every other pro-evolution propaganda machine have failed to identify any evidence that might strengthen this straw link.
References and notes

1. See D. Batten, Hox (homeobox) Genesâ€â€Evolution’s Saviour? and D. DeWitt, Hox Hypeâ€â€Has Macro-evolution Been Proven?.
2. See J. Sarfati, Startling Stickiness, Creation 24(2):37 (March–May 2002).
3. A. Kihm et al., An Abundant Erythroid Protein That Stabilizes Free-haemoglobin, Nature 417(6890):758–763 (13 June 2002); comment by L. Luzzatto and R. Notaro, Haemoglobin’s Chaperone, same issue, p. 703–705.
4. See S.E. Aw, The Origin of Life: A Critique of Current Scientific Models, TJ 10(3):300–314, 1996.
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Umm...how does one distinguish those from what you would consider "the real thing"? And why would there be "built in variation" anyway, and where are its limits?

Loss of genetic information would indicate a true mutation. Built in variation ensures survivability of the species. The limit would be the creation of any new information.