Lets Pray

[Nightingale 0]

By evolved, I mean that, for example, the different species of cat, such as lions, lynx, bobcat, housecat, and cheetah have their origin in a pre-existing common ancestor and gradually changed over time into the animals we know today.

[pajarito 0]

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By evolved, I mean that, for example, the different species of cat, such as lions, lynx, bobcat, housecat, and cheetah have their origin in a pre-existing common ancestor and gradually changed over time into the animals we know today.

Variation.

[Nightingale 0]

Okay... now you've got me confused.

Doesn't Genesis 2:19-20 say "God formed every beast of the field, and every fowl of the air; and brought them unto Adam to see what he would call them: and whatsoever Adam called every living creature, that was the name thereof."

Genesis says that God created EVERY beast and EVERY fowl, and then brought them to Adam. Wouldn't that mean that every beast and fowl was at existence at the time of Adam, and therefore would need to be on the ark at the time of Noah?

[pajarito 0]

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Okay... now you've got me confused.

Doesn't Genesis 2:19-20 say "God formed every beast of the field, and every fowl of the air; and brought them unto Adam to see what he would call them: and whatsoever Adam called every living creature, that was the name thereof."

Genesis says that God created EVERY beast and EVERY fowl, and then brought them to Adam. Wouldn't that mean that every beast and fowl was at existence at the time of Adam, and therefore would need to be on the ark at the time of Noah?

That's some pretty bad heurmaneutics.

[Nightingale 0]

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That's some pretty bad heurmaneutics.

Well, as hermeneutics and scriptural interpretation go, I'm trying to figure out where exactly in the Bible you're getting this theory of "variations" of "kinds" of animals. Is it actually there in scripture, or is it something that people are theorizing to explain the million plus species of animals that we have today in light of the ark story?

[pajarito 0]

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Well, as hermeneutics and scriptural interpretation go, I'm trying to figure out where exactly in the Bible you're getting this theory of "variations" of "kinds" of animals. Is it actually there in scripture, or is it something that people are theorizing to explain the million plus species of animals that we have today in light of the ark story?

Because the Bible explains that each animal was created according to its kind and variation within those kinds is what we actually observe in science.

[billvon 2,991]

>It's the difference between observational science, what we can observe
>and test with repeatable results and historical science, based on a belief
>about our origins.

You have left out extrapolation, which is why it is possible for us to do things like predict weather, design airplanes that will actually fly and create drugs to cure disease.

>Adding the "magic ingredient" of "millions" or even "billions" of years . . .

Time really isn't a magic ingredient. Engineers use it all the time when designing something that has to last a long time. Even though (for example) they may never seen a major bridge rust all the way through, they can check the rate of rusting on an existing bridge and determine how to make it last a "magically" long time. They do this by extrapolation. If you lose X inches of a beam to rust every year, and it seems constant over 10 years, it's a good bet that you will continue to lose X inches of a beam every year thereafter unless you change something.

Likewise, if evolution can change wolves to chihuahuas in 6000 years, then through extrapolation, it can make significantly greater changes in 60,000, 600,000, 6,000,000 or 60,000,000 years. Take the difference between a wolf and a chihuahua, then imagine an animal that is 10,000 times the difference. It is indeed hard to do, but those are the scales we're talking about.

[pajarito 0]

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Likewise, if evolution variation through natural selection can change wolves to chihuahuas in 6000 years, then through extrapolation, it can make significantly greater changes in 60,000, 600,000, 6,000,000 or 60,000,000 years.

Only within the limitations of the finite amount of information possessed in its genes (regardless of the time frame we're talking about)

[Lindsey 0]

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Likewise, if evolution variation through natural selection can change wolves to chihuahuas in 6000 years, then through extrapolation, it can make significantly greater changes in 60,000, 600,000, 6,000,000 or 60,000,000 years.

Only within the limitations of the finite amount of information possessed in its genes (regardless of the time frame we're talking about)

Given that genes are just sequences of nucleotides, and we know that mutations happen all the time in these sequences, I guess the "variations" that could occur over time could lead to a pretty incredible bit of diversity, even if you don't want to use the word evolution.

--
A conservative is just a liberal who's been mugged. A liberal is just a conservative who's been to jail

[Nightingale 0]

Since genus and species are latin based words, I looked up the latin.

The latin text states:

1:24 "et bestias terræ secundum species suas"

which translates to: "beasts of the earth, according to their species."

What's really interesting is that earlier, the text states: "et omne volatile secundum genus suum."

which translates to: all the flying creatures, according to their genus (kind)

The latin text differentiates specifically between genus and species, while the English translation does not.

So, were birds created according to their kind or genus, and land mammals according to their species? or is the latin text just wrong?

[billvon 2,991]

>Only within the limitations of the finite amount of information
>possessed in its genes (regardless of the time frame we're talking about)

Agreed. Within a human genome, we have about 3 billion base pairs - which means there are only 4^3000000000 possibilities based on rearrangement of our current DNA. Of course, that number can easily change - even within a few generations, the length of people's chromosomes (and sometimes even the number of chromosomes) changes.

But for now we're limited to approximately that number. Of course, that means that you could have one of each and easily fill the entire volume of the solar system with human variants - and we easily have enough genetic material to code for every living creature on the planet.

So the argument "we are limited in what we can evolve to" is indeed true, but the entire sequence of evolution is easily covered by even the potential variations within our genome (which isn't all that big by terran standards.)

[NJSkydiver 0]

George Bush is the . hahaha really....who cares. he's done good with my tax returns so he's okay in book adn he's our president so let him finish out his term and let's respect that.

- What do I owe beer for this time?

[pajarito 0]

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Given that genes are just sequences of nucleotides, and we know that mutations happen all the time in these sequences, I guess the "variations" that could occur over time could lead to a pretty incredible bit of diversity, even if you don't want to use the word evolution.

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Mutation leads to better survival in beach mice

by Dr. Georgia Purdom
August 23, 2006

According to a recent news article released by Howard Hughes Medical Institute (HHMI) based on an article released in the July 7th Science magazine, a single mutation in mouse DNA is a major contributor to the light coat color seen in beach mice leading to better survival in a sandy environment. The news article states that this “provides evidence that evolution can occur in big leaps.”

Beach mice and coat color

Beach mice, Peromyscus polionotus, vary widely in color. The particular mice studied in this research live on the Gulf coast of Florida’s barrier islands. It had been noted in previous research that some mice were very light colored but the underlying molecular mechanism was not known. The researchers found that these mice have a mutation in the melanocortin-1 receptor gene (Mc1r). A single base change in the DNA led to an amino acid change in the protein; an arginine was replaced with a cysteine. Arginine is a charged amino acid and cysteine is not, and cysteine can form special disulfide bonds in the protein that arginine cannot. This causes the two amino acids to have a different physical behavior in a protein, thereby probably altering the structure of the mutant protein (although this was not directly addressed in the Science article). As a result, the mutant Mc1r protein has a reduced affinity for the melanocyte stimulating hormone (MSH) that binds to it. This receptor–hormone interaction is important in mammals for the production of melanin, which is responsible for pigmentation. (In humans, a dysfunctional Mc1r gene can be responsible for red hair and fair skin.) It would thus be assumed that since this interaction is weakened in the light-colored mice, the mice’s melanin production is decreased, resulting in the lighter-colored fur.

Evolution or adaptation

To creationists, the authors’ explanations of their findings seem paradoxical. “This is a striking example of how protein-coding changes can play a role in adaptation and divergence in population, and ultimately species.” I agree. “Identification of a single mutation that contributes to the color change that has arisen in these animals argues for a model of evolution in which populations diverge in big steps” (in a short time, as the researchers believe this happened in less than 6,000 years). Hoekstra contrasts this with the popular evolution mechanism of “small changes accumulated over long periods of time”. I disagree. Once again, adaptation / natural selection is being extrapolated to explain molecules-to-man evolution. I also question whether a change of coat color is really relevant to this form of evolution. If the mice had a mutation that somehow (even though a mutation could never do this) allowed the growth of a useful appendage, that might provide some movement in the right direction! What scientists must demonstrate for molecules-to-man evolution to be plausible is the genetic mechanism to account for the origin of the melanin gene, pigmentation, etc. Clearly a mutation in a pigmentation gene causing less of the pigment to be made does not provide that kind of example. Directional evolution cannot be achieved by reduction/elimination of pre-existing genetic information.

Real problems

A major surprise for the researchers was that the mutation they found would had to have occurred fairly rapidly, as the islands on which P. polionotus lives are considered to be less than 6,000 years old. This is no surprise to creationists, as such processes (and perhaps other factors affecting the genome) would have occurred rapidly after the Flood, producing variation within the animal kinds (in addition to their already created diversity). Such effects are largely responsible for generating the tremendous diversity seen in the living world. In addition, there are many other modern-day examples of adaptation that has occurred quickly.

Another important point is that most mutations in DNA are not selectable even though they seem to be making a big deal out of one that is. In order for a mutation to be selected for or against, it must make some change in the organism at the phenotypic, whole-organism level. The change must be large enough to give the organism an increased or decreased fitness in its environment. Most mutations in the DNA are either silent (leading to no change at the phenotypic level), lethal (leading to death of the organism), or slightly deleterious (not altering phenotype sufficiently to be specifically detected by any selection process). It is unusual to find one mutation that leads directly to a selectable trait in a higher organism (although this does happen commonly in bacteria, as is seen in antibiotic-resistant bacteria).

The mutation, although beneficial to the beach mice, still leads to a loss of genetic information. The mutant Mc1r protein does not bind as well to MSH and thus, the mice have decreased melanin production leading to lighter fur color. Although this is an advantage in the beach environment, it may not be an advantage should the mice change geographic location, e.g., to a forest, where darker fur color would be preferred. In addition, molecules-to-man evolution must account for the origin of melanin and pigmentation, not the loss of it. Mutations that decrease melanin production and cause lighter pigmentation are contrary to directional evolution but fully consistent with the effects of living in a post-Fall world. Evolutionists tend to assume that anything that is positively selected is “evolution” in action, and that is simply not the case. The news article also states that because this mutation was found in a protein-coding region of the DNA, the differences between humans and chimps and other organisms may not be in the regulatory regions as suspected. This is a big assumption based on the discovery of only one mutation. The affectionately called “junk” DNA is being discovered as highly functional (including being involved in controlling protein expression), to the point that eventually all of our genome may be found to be greater than 100% functional!

Another striking reality is that light-colored mice on the Atlantic coast have a different mechanism for developing their coat color, as they do not possess a mutation in the melanocortin-1 receptor. So even though the mice share a similar coloration they have different mechanisms for achieving it. The origin and development of one mechanism for coat color variation is difficult enough for evolution to explain—try explaining two!

Conclusion

From a creationist perspective, this research provides us with yet another example of a beneficial outcome of a mutation in a given environment allowing an organism a selectable advantage. Mutations lead to loss of information, and while the organism may be more well suited for its current environment, it may have lost the ability to adapt to other environments. The mutation described in this Science paper does not address the origin of the melanin gene or pigmentation, only the loss of them, thus it is not relevant mutation to the discussion of molecules-to-man evolution.

[pajarito 0]

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Agreed. Within a human genome, we have about 3 billion base pairs - which means there are only 4^3000000000 possibilities based on rearrangement of our current DNA. Of course, that number can easily change - even within a few generations, the length of people's chromosomes (and sometimes even the number of chromosomes) changes.

The number of chromosomes is not an accurate way of measuring quantities of information. They are just the containers. Some bacteria have many more chromosomes that we do. Would you argue that those bacteria have all the genetic information they need to account for all of the diversity of life we see today? What about that first organism which developed from the supposed primordial goo?

[jakee 1,490]

I'm going to bring up two simple points which I very much hope aren't too 'Awkward' for you to answer this time.

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A major surprise for the researchers was that the mutation they found would had to have occurred fairly rapidly,

A single mutation will occur over a single generation. How can any point mutation be classed as either rapid or gradual?

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The mutation, although beneficial to the beach mice, still leads to a loss of genetic information.

Can you please point me to any scientist who can quantify genetic information? What method do they use to measure genetic information? What units do they use to quantify the exact amount of information in a genome?

Do you want to have an ideagasm?

[jakee 1,490]

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Some bacteria have many more chromosomes that we do. Would you argue that those bacteria have all the genetic information they need to account for all of the diversity of life we see today?

You seem very confused. Are you saying that it's impossible for an organism to have more gentic information than a human unless it has enough information to code for every species in existence? Are you therefore saying that the human genome could code for every species in existence? If not, just what the fuck is your point?

Do you want to have an ideagasm?

[billvon 2,991]

>They are just the containers.

More like the letters and words that make up our genetic 'story.'

>Some bacteria have many more chromosomes that we do.

Right. Indeed, most of our DNA is junk that does not encode for anything (but often plays ancillary roles, like creating 'buffers' on telomeres.)

>Would you argue that those bacteria have all the genetic information they
> need to account for all of the diversity of life we see today?

Those bacteria have all the equipment they need to account for all of the diversity of life we see today. In terms of the english analogy, they have all the words they need and many of the sentences - those words and sentences have not yet been combined into a story that describes a mouse (for example.) But the basics are all there.

>What about that first organism which developed from the supposed
>primordial goo?

Depends how you define "organism." All life on earth shares the same basic codons, so if you define "first organism" as the first organism to possess our method of genetic reproduction - then that one organism had all the TOOLS needed to account for all the diversity of life we see today, just as an english dictionary contains all the words needed to account for all the english literature we see today.

[pajarito 0]

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If not, just what the fuck is your point?

Does the use of profanity indicate an element of hostility and, therefore, closed mindedness?

Have a good day Jakee.

[jakee 1,490]

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If not, just what the fuck is your point?

Does the use of profanity indicate an element of hostility and, therefore, closed mindedness?

Have a good day Jakee.

No, it indicates a level of exasperation with the intellectual dishonesty of your posts.

I notice you were unable to provide any kind of answer to my questions by the way. Telling, is it not?

Do you want to have an ideagasm?

[pajarito 0]

How is Information Content Measured

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In my book [Not by Chance], I did not quantify the information gain or loss in a mutation. I didn’t do it mainly because I was reluctant to introduce equations and scare off the average reader. And anyway, I thought it rather obvious that a mutation that destroys the functionality of a gene (such as a repressor gene) is a loss of information. I also thought it rather obvious that a mutation that reduces the specificity of an enzyme is also a loss of information. But I shall take this opportunity to quantify the information difference before and after mutation in an important special case, which I described in my book.

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The information content of the genome is difficult to evaluate with any precision. Fortunately, for my purposes, I need only consider the change in the information in an enzyme caused by a mutation. The information content of an enzyme is the sum of many parts, among which are:

- Level of catalytic activity
- Specificity with respect to the substrate
- Strength of binding to cell structure
- Specificity of binding to cell structure
- Specificity of the amino-acid sequence devoted to specifying the enzyme for degradation

These are all difficult to evaluate, but the easiest to get a handle on is the information in the substrate specificity.
To estimate the information in an enzyme I shall assume that the information content of the enzyme itself is at least the maximum information gained in transforming the substrate distribution into the product distribution. (I think this assumption is reasonable, but to be rigorous it should really be proved.) We can think of the substrate specificity of the enzyme as a kind of filter. The entropy of the ensemble of substances separated after filtration is less than the entropy of the original ensemble of the mixture. We can therefore say that the filtration process results in an information gain equal to the decrease in entropy. Let’s imagine a uniform distribution of substrates presented to many copies of an enzyme. I choose a uniform distribution of substrates because that will permit the enzyme to express its maximum information gain. The substrates considered here are restricted to a set of similar molecules on which the enzyme has the same metabolic effect. This restriction not only simplifies our exercise but it applies to the case I discussed in my book.
The products of a substrate on which the enzyme has a higher activity will be more numerous than those of a substrate on which the enzyme has a lower activity. Because of the filtering, the distribution of concentrations of products will have a lower entropy than that of substrates. Note that we are neglecting whatever entropy change stems from the chemical changes of the substrates into products, and we are focusing on the entropy change reflected in the distributions of the products of the substrates acted upon by the enzyme.

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Although these simplifications prevent us from calculating the total entropy decrease achieved by action of the enzyme, we are able to calculate the entropy change due to enzyme specificity alone.

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The Dangers of Conclusion Jumping

Spetner: As a final example let me take part of a series of experiments I discussed in my book, which demonstrate the dangers of conclusion jumping. This subject bears emphasis because evolutionists from Darwin on have been guilty of jumping to unwarranted conclusions from inadequate data. I shall here take only a portion of the discussion in my book, namely, what I took from a paper by Burleigh et al. (1974, Biochem. J. 143:341) to illustrate my point.

Ribitol is a naturally occurring sugar that some soil bacteria can normally metabolize, and ribitol dehydrogenase is the enzyme that catalyzes the first step in its metabolism. Xylitol is a sugar very similar in structure to ribitol, but does not occur in nature. Bacteria cannot normally live on xylitol, but when a large population of them were cultured on only xylitol, mutants appeared that were able to metabolize it. The wild-type enzyme was found to have a small activity on xylitol, but not large enough for the bacteria to live on xylitol alone.

The mutant enzyme had an activity large enough to permit the bacterium to live on xylitol alone. Fig. 1 shows the activity of the wild-type enzyme and the mutant enzyme on both ribitol and xylitol. Note that the mutant enzyme has a lower activity on ribitol and a higher activity on xylitol than does the wild-type enzyme. An evolutionist would be tempted to see here the beginning of a trend. He might be inclined to jump to the conclusion that with a series of many mutations of this kind, one after another, evolution could produce an enzyme that would have a high activity on xylitol and a low, or zero, activity on ribitol. Now wouldn’t that be a useful thing for a bacterium that had only xylitol available and no ribitol? Such a series would produce the kind of evolutionary change NDT calls for. It would be an example of the kind of series that would support NDT. The series would have to consist of mutations that would, step by step, lower the activity of the enzyme on the first substrate while increasing it on the second. But Fig. 1 is misleading in this regard because it provides only a restricted view of the story. Burleigh and his colleagues also measured the activities of the two enzymes on another similar sugar, L-arabitol, and the results of these measurements are shown in Fig. 2. With the additional data on L-arabitol, a different picture emerges. No longer do we see the mutation just swinging the activity away from ribitol and toward xylitol. We see instead a general lowering of the selectivity of the enzyme over the set of substrates. The activity profiles in Fig.2 show that the wild-type enzyme is more selective than is the mutant enzyme.

In Fig. 1 alone, there appears to be a trend evolving an enzyme with a high activity on xylitol and a low activity on ribitol. But Fig. 2 shows that such an extrapolation is unwarranted. It shows instead a much different trend. An extrapolation of the trend that appears in Fig. 2 would indicate that a series of such mutations could result in an enzyme that had no selectivity at all, but exhibited the same low activity on a wide set of substrates.

The point to be made from this example is that conclusion jumping from the observation of an apparent trend is a risky business. From a little data, the mutation appears to add information to the enzyme. From a little more data, the mutation appears to be degrading the enzyme’s specificity and losing information. Just as we calculated information in the two special cases above, we can calculate the information in the enzyme acting on a uniform mixture of the three substrates for both the wild type and the mutant enzyme. Using the measured activity values reported by Burleigh et al. we find the information in the specificities of the two enzymes to be 0.74 and 0.38 bits respectively. The information in the wild-type enzyme then turns out to be about twice that of the mutant.

The evolutionist community, from Darwin to today, has based its major claims on unwarranted conclusion jumping. Darwin saw that pigeon breeders could achieve a wide variety of forms in their pigeons by selection, and he assumed that the reach of selection was unlimited. Evolutionists, who have seen crops and farm animals bred to have many commercially desirable features, have jumped to the conclusion that natural selection, in the course of millions of years, could achieve many-fold greater adaptive changes than artificial selection has achieved in only tens of years. I have shown in my book that such extrapolations are ill founded because breeding experiments, such as those giving wheat greater protein content or vegetables greater size, result from mutations that disable repressor genes. The conclusions jumped to were false because they were based on data that could not be extrapolated to long sequences. One cannot gain information from a long sequence of steps that all lose information. As I noted in my book, that would be like the merchant who lost a little money on each sale, but thought he could make it up on volume.

Relationship between complexity and number of genes contained in DNA

There is of course a rough relationship between the number of proteins coded for by a DNA sequence and the level of specified complexity. But “number of genes” is very approximate. For example, the human DNA supposedly contains some 35,000 “genes” and yet the human cell can produce over 100,000 proteins (estimates range up to 150,000 or even more). Obviously, there is much that is not known about how 35,000 “genes” can produce so many different proteins. A more accurate measure of the specified complexity of a given genome would be the number of proteins coded. However, there is also much information not involved directly in protein production—for example, in chromosome structure. And there is probably a huge amount of information present that determines developmental sequences, for example—none of this is really understood. There is also the possibility of error-checking sequences, etc., etc. There is just not enough known yet about the functions of all the DNA sequences to meaningfully quantify the information properly.

If mutation causes single amino acid substitution or causes duplication of DNA, why is this a reduction of information content?

See Spetner for an example that explains the principles involved (above). However, a mutation does not necessarily reduce specified complexity—just that it is so likely to do so that it cannot be the mechanism for generating the huge amount of specified complexity that we see in living things. That mutations are known primarily by the defects they cause testifies to the overwhelming tendency for them to reduce the information in living things (just like a mistake on my computer keyboard will decrease the information content of what I am typing). Spetner also discusses gene duplication at the above URL. However, just think: if you buy two copies of the newspaper, do you buy twice as much information? Of course not. Duplication of anything does not constitute an increase of information. Random mutations to change the duplicated gene would not add information unless the mutated sequence coded for some new, useful protein (no one has demonstrated such a thing happening; there have only been imaginative scenarios proposed). To illustrate: if “superman” were the duplicated “gene”, and mutations in the letters changed it to “sxyxvawtu ”, you have clearly lost information, although you have a new sequence. This is the difference between complexity and specified complexity. A pile of sand is complex , but is information-poor, because it specifies nothing.

[pajarito 0]

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Since genus and species are latin based words, I looked up the latin.

The latin text states:

1:24 "et bestias terræ secundum species suas"

which translates to: "beasts of the earth, according to their species."

What's really interesting is that earlier, the text states: "et omne volatile secundum genus suum."

which translates to: all the flying creatures, according to their genus (kind)

The latin text differentiates specifically between genus and species, while the English translation does not.

So, were birds created according to their kind or genus, and land mammals according to their species? or is the latin text just wrong?

Genesis was written in Hebrew.

[Nightingale 0]

Many of the translations of the Hebrew language Torah also translate the word as "species" rather than "kind."

http://bible.ort.org/intro1.asp
The Living Torah

That's the problem with translation. Words don't always translate straight from one language to the next. The translator is the lens that focuses in on the appropriate word in the new language, and different people interpret the texts in different ways. Some say "species" others say "kind."

[pajarito 0]

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Many of the translations of the Hebrew language Torah also translate the word as "species" rather than "kind."

http://bible.ort.org/intro1.asp

The Living Torah

That's the problem with translation. Words don't always translate straight from one language to the next. The translator is the lens that focuses in on the appropriate word in the new language, and different people interpret the texts in different ways. Some say "species" others say "kind."

…Hence the need for good methodology in biblical interpretation. One of the principles of hermeneutics includes looking at the text in historical context in order to better understand what the writer was trying to convey. A word may have a broader or narrower meaning depending on when it was used. In this case…

***Genesis chapter 1 says that the animals were created according to their kinds, rather than according to their species—the phrase ‘after his/their kind’ occurs 10 times in this chapter (referring to both plants and animals). Exactly what the term ‘kind’ (Hebrew min) corresponds to in terms of the modern Linnaean classification system is not clear, but it appears that sometimes the min corresponds to today’s species, sometimes to the genus, and sometimes to the family. It indicates the limitations of variation. What is clear is that numerically there must have been fewer kinds in Adam’s day than the number of species we count today. [Ed. note: for more information, see Ligers and wholphins? What next?]

For example, it is more than likely that there would have been no domestic dogs, coyotes, and wolves as such, but rather one ancestral kind containing the genetic information for all of these to appear under natural selection pressures.

This is not evolution, because no new information is added. In the same way, the mongrel dog population of a few hundred years back was able to give rise (under human [artificial] selection) to the various modern breeds of dog—because the information was already there in that population, much more than in today’s specialized, genetically depleted breeds. That’s why you can’t start with a chihuahua population, and expect that breeding/selection will eventually produce Great Danes.

Naming the animals