Why do some catholics believe in evolution?

[xixxvmcm85]

I’m not a DNA specialist, but this doesn’t ring true to me.

You’re correct. At least you have the intellectual humility to admit when you lack the expertise to answer a question.

 

[kalt]

You’re correct. At least you have the intellectual humility to admit when you lack the expertise to answer a question.

The thing is, you don’t have to be a specialist to see that statement as “funny”. Don’t a few human genetic problems result when errors result in “extra stuff”?

 

[kalt]

I do not think that one can prove a transition from fossils. No more than you can go into an automobile junk yard and prove from car parts from old cars give birth to each other.

Can you explain how I can examine a fossil and prove that it is a transition?

In terms like someone like me (who can’t find his way through a library) can understand?

Your analogy doesn’t work, but let’s use it anyway.

You find an horse-drawn coach in an old forgotten barn. In a 1920’s garage you find a Model T. In someone’s 1950’s garage you find a Desoto. In a 1970’s backyard you find a Mustang. In a 1980’s carport you find a Mustang GT. In a 1990’s lot you find a Honda Accord. In your driveway is a 2008 Honda Accord.

Gee that Model T looks an awful lot like an old coach. The Desoto still has similar lines, but it’s not quite as much like the coach. The Mustang is a real departure, and the newer Mustang resembles the older, but it has modifications that make it faster, more aerodynamic. The 2008 Honda looks a lot rounder than the older one, and it has a bunch of modifications under the hood.

Of course one never gave birth to the another, but it’s clear that even the genius auto engineers didn’t jump from the horse-drawn coach to the 2008 Honda in one leap. There were definite transitional models. At first there were only horsedrawn coaches. From that “idea” came several “kinds” of cars–more or fewer “kinds” as the market (environment) allows. Only the fittest (most well-adapted to the the environment) survive, but all change over time. Those that don’t change w/ the market (environment), or that are poorly designed for the existing environment (market) die.

RIP Edsel.

As another poster said, living things do pass down information to the new generation. Changes happen. Transitional forms exist.

 

[KingAlfred]

“Why do some catholics believe in evolution?”

I believe in Intelligent Design. Creationism is simply too much of a *stretch *for me.

 

[kalt]

“Why do some catholics believe in evolution?”

I believe in Intelligent Design. Creationism is simply too much of a *stretch *for me.

ID is creationism pretending to be scientific.

 

[Pixie_Dust]

ID is creationism pretending to be scientific.

ID allows for evolution where creationism does not.

 

[StAnastasia]

ID is creationism pretending to be scientific.

Yes, and they were convicted of this in court!

 

[ralphinal]

It was once hypothesized, and I believe there are still a handful of biologists that hold on to this hypothesis, but I believe it has been well repudiated by most of the scientific community. When I took a few evo clases, I was instructed that H. neaderthalis is currently hypothesized to have bifurcated from a common ancestor of ours (H. sapien) indicating that H. neaderthalis is not a transition from the common ancestor to us, rather a “distant cousin”.

I’m not certain though as my credentials are in molecular biology, not evolutionary biology.

It was passe when I was in college in the early 1990s. Lately, I have seen hypothoses that they bred back into our line, giving us about 5-10% of our code. I am not sure how much i accept that. Although I have known some guys who look just like the drawings, and I am not talking about the Geico cavemen.

 

[jimmy]

Well, if we believe that God inspired scripture, God defined a day as the passing of an evening, and then a morning.

“And there was evening, and there was morning—the second day”.

You must pay attention to the literary genre of each part of scripture. Genesis1 and 2 are not necessarily meant to be understood in a literalistic way. Just like the parable of the sower is not a story of a historical event, it is a parable.

 

[xixxvmcm85]

“Why do some catholics believe in evolution?”

I believe in Intelligent Design. Creationism is simply too much of a *stretch *for me.

It’s posts like these that lead me to believe that it would be most conducive to the discussion if we all define our terms. “Intelligent Design” may perfectly mean (to you) a form of what many call “theistic evolution” (which is where I stand, in most respects) namely that macroevolution indeed occurs, yet the ultimate goal is slowly directed by some sentient source. Notice the bolded words, they all imply design but not necessarily in the instantaneous fashion as actual creationists believe.

“Intelligent Design”, however, is used by the majority to simply mean “strict creationism with all the explicit references to God being removed as to be palpable to secular educational institutions.” I’ve read two ID text books and both made it very clear that contemporary species and genera are fixed, rigid, and static since the day they were “designed”. In other words, ID is really just bleached creationism.

ID is creationism pretending to be scientific.

Indeed. I repeat, ID is simply repackaged creationism conveniently disguised to make its way into secular institutions (hence the removal of any proper nouns that are definitively Judeo-Christian).

ID allows for evolution where creationism does not.

Again, this depends on your definition of what “intelligent design” is. It’s perfectly permissible to use it to mean “theistic evolution”, however the majority take it to be synonymous to “strict creationism”, so I’d kindly suggest to you to use “theistic evolution”.

Those high up in the ID movement themselves have stated that macroevolution has no place in the ID “hypothesis” (see Dr. Michael Behe).

Yes, and they were convicted of this in court!

Ah yes! The Kitzmiller V. Dover Area School District

It was passe when I was in college in the early 1990s. Lately, I have seen hypothoses that they bred back into our line, giving us about 5-10% of our code. I am not sure how much i accept that. Although I have known some guys who look just like the drawings, and I am not talking about the Geico cavemen.

You know, come to think of it I remember one of my professors a few years back touching base on this with me during an office hour of hers. Interesting information, and not really all that out there.

I can’t remember if it was H. erectus or H. neanderthalis that buried their dead (and specifically with artifacts implying that they believed in an afterlife).

As I said before, my specialty is in molecular biology, so I’m obviously going to have a bias toward genetic evidence. For me, I drop my skepticism to an evolutionary hypothesis as soon as they provide DNA evidence, which as anyone could imagine is hard to do with fossils.

I’d be interested in any information concerning recent developments in the H. neanderthalis (or H. erectus) genome projects. Last I heard only a sliver of the genome has been reconstructed (and this includes multiple parts from all over the karyotype).

 

[xixxvmcm85]

The thing is, you don’t have to be a specialist to see that statement as “funny”. Don’t a few human genetic problems result when errors result in “extra stuff”?

“Advantageous” and “Disadvantageous” are not static terms. They depend on the environment of the population (ecological niche), the population’s relationship with other populations (symbiosis), and the rise to increased reproduction (fecundity). Something advantageous to average American humans today in 2008 may not be advantageous to the same population 100 years from now.

The OP seems to be thinking too much in black & white terms (possibly due to his/her experience as an engineer and thus subsequently a mathematician). For him/her it’s an either/or “mutations are either harmful or helpful” when there are indeed cases of them being BOTH.

Take the gene the predisposes one to sickle-cell anemia. If a westerner (someone in Europe or the Americas) inherits such a gene (obviously a destructive mutation) it is damn near certain a death certificate (even in cases where the individual has only one copy of the gene compared to two), yet in sub-Saharan Africa, we find the majority of the population having the heterozygous condition for this gene (having one copy of it while the other copy is normal), why is this if it produces such a horrible condition?

The answer turns out to be a sort of “dual product” scenario. The heterozygous condition for sickle-cell anemia seems to also give RESISTANCE TO MALARIA (something that would be EXTREMELY advantageous to areas such as Africa) whereas populations such as those in the US have no need for it, and therefore natural selection does not select for it.

It’s hard to rid ourselves of our homocentric biases, but its important when trying to study something like biology in as much a quantitative manner as possible. “Good” “bad”, “unfortunate” etc are emotional terms that may or may not have a place in evolution. Natural selection is blind, and only if a mutation is NOT disadvantageous will the gene be radiated through the population. Claiming that there are never any advantageous mutations wreaks of hindsight bias.

 

[kalt]

“When DNA mutates, it always loses information, never gains new information out of nothing. If anything, devolution, not evolution happens.”

“I’m not a DNA specialist, but this doesn’t ring true to me.”

This is what I was talking about.

"Down syndrome occurs when an individual has three, rather than two, copies of the 21st chromosome. This additional genetic material alters the course of development and causes the characteristics associated with Down syndrome. "

And aren’t there other conditions that result from “extra” genetic material?

BTW, no one is claiming that something comes from nothing–species or DNA. Evolution isn’t about “new information out of nothing.”

 

[xixxvmcm85]

"Down syndrome occurs when an individual has three, rather than two, copies of the 21st chromosome. This additional genetic material alters the course of development and causes the characteristics associated with Down syndrome. "

And aren’t there other conditions that result from “extra” genetic material?

Trisomy 21 (AKA Down Syndrome) along with all other conditions that we call “aneuploidy” are not due to mutations. Mutations are pin-point alterations, deletions, or insertions into the nucleotide base sequence of the DNA itself. Aneuploidy conditions are ones in which entire chromosomes (with billions of nucleotide base sequences and thousands of genes) are increased in number in an individual.

Using the old “letters of an alphabet” analogy, if each single nucleotide base is a letter, than a mutation will alter, add, or delete a single letter (or in other cases sets of letters if there’s some kind of chemical or quantum link between the bases). Chromosomes however are like entire multi-chapter, thousand-odd page books. Any condition that involves short-changing or increasing the number of a certain chromosome in an individual will be due to some defect during the meiotic division of sex cells called “non-disjunction”. This defect leaves a certain sperm or ovum with an extra copy of a certain chromosome and once fertilization occurs, this aneuploidy condition is then reproduced mitotically throughout every single cell that comes forth from the initial fertilized zygote.

The majority of those with aneuploidy are completely sterile (including those with trisomy 21) meaning that natural selection has no way to select for (or against) such a condition.

Now point-mutations occur in humans constantly, and the vast majority of them make absolutely no difference in the gene expression (i.e. the protein synthesis) due to the way the genetic code is read in the formation of proteins.

It takes 3 nucleotide bases to make an amino acid (the basic building block of a protein) and it’s usually only the first letter that matters, meaning that one can alter the second and third almost all s/he wants and the same amino acid will be produced.

Frame shift mutations are ones in which the entire “Reading frame” of the base sequence is disrupted resulting usually in a completely nonfunctional polypeptide.

It’s very tricky trying to find point-mutations that have occurred in humans that have given rise to something beneficial (or even neutral). I’m speaking of course about contemporary cases, not cases in which have occurred in the past over millions of years which ultimately have separated our closest primate relatives.

Though the mechanism by which both massive point-mutations over millions of years and point-mutations within individuals today is exactly the same, usually folks such as our OP tend to immediately dismiss any evidence that’s older than humanity itself.

 

[kalt]

A question. What about mosaics? When the error isn’t found in every cell? How does that happen?

This is going off topic, but it’s interesting–at least to me. I hope no one else minds.

Thanks for taking the time to inform us.

Trisomy 21 (AKA Down Syndrome) along with all other conditions that we call “aneuploidy” are not due to mutations. Mutations are pin-point alterations, deletions, or insertions into the nucleotide base sequence of the DNA itself. Aneuploidy conditions are ones in which entire chromosomes (with billions of nucleotide base sequences and thousands of genes) are increased in number in an individual.

Using the old “letters of an alphabet” analogy, if each single nucleotide base is a letter, than a mutation will alter, add, or delete a single letter (or in other cases sets of letters if there’s some kind of chemical or quantum link between the bases). Chromosomes however are like entire multi-chapter, thousand-odd page books. Any condition that involves short-changing or increasing the number of a certain chromosome in an individual will be due to some defect during the meiotic division of sex cells called “non-disjunction”. This defect leaves a certain sperm or ovum with an extra copy of a certain chromosome and once fertilization occurs, this aneuploidy condition is then reproduced mitotically throughout every single cell that comes forth from the initial fertilized zygote.

The majority of those with aneuploidy are completely sterile (including those with trisomy 21) meaning that natural selection has no way to select for (or against) such a condition.

Now point-mutations occur in humans constantly, and the vast majority of them make absolutely no difference in the gene expression (i.e. the protein synthesis) due to the way the genetic code is read in the formation of proteins.

It takes 3 nucleotide bases to make an amino acid (the basic building block of a protein) and it’s usually only the first letter that matters, meaning that one can alter the second and third almost all s/he wants and the same amino acid will be produced.

Frame shift mutations are ones in which the entire “Reading frame” of the base sequence is disrupted resulting usually in a completely nonfunctional polypeptide.

It’s very tricky trying to find point-mutations that have occurred in humans that have given rise to something beneficial (or even neutral). I’m speaking of course about contemporary cases, not cases in which have occurred in the past over millions of years which ultimately have separated our closest primate relatives.

Though the mechanism by which both massive point-mutations over millions of years and point-mutations within individuals today is exactly the same, usually folks such as our OP tend to immediately dismiss any evidence that’s older than humanity itself.

 

[xixxvmcm85]

A question. What about mosaics? When the error isn’t found in every cell? How does that happen?

This is going off topic, but it’s interesting–at least to me. I hope no one else minds.

Thanks for taking the time to inform us.

Oh it’s my pleasure! Though fair warning, this will be a bit of a long post (and may even be so off topic as to warrant the mods to delete it).

“Genetic Mosaics” is a very vague and all-encompassing term for different causes that generally lead to the same result.

Genetic Mosaics can typically take one of three forms.

1. Ploidy mosaics - Where certain cells within the organism (or colony) have an aneuploidy condition while others do not.

Unlike aneuploidy conditions such as Trisomy 21 (where the non-disjunction occurs in the sperm or egg thus affecting ALL future cells), ploidy mosaics experience the non-disjunction later on after fertilization in only one cell thus eventually affecting only whichever daughter cells arise from that single aneuploidy cell. The vast majority of intersexed conditions in humans are due to ploidy mosaic ism, like Kleinefelter’s Syndrome that results in certain tissues of cells in a male exhibiting an extra X chromosome while other are normal (i.e. XXY vs XY). Remember that most aneuploidy conditions (even mosaic ones) result in the individual being sterile. Actually, most aneuploidy conditions result in the individual dying extremely young (this is how serious the “dosage effect” is in having just the right number of chromosomes). If the individual lives to reproductive age, s/he will likely not be able to reproduce as their “library of books” (chromosomes) are just in too much disarray to be of any vitality.

Again, ALL cases of aneuploidy involve mitotic/meiotic cell division errors (i.e. non-disjunction) and not mutations.

1. Genotypic mosaics - These are where the actual genes on the chromosomes of certain cells are altered via mutation but they don’t affect the entire individual (or in the case of single celled organisms, the entire colony). Technically speaking, some cases of having moles on one’s skin, or differing eye colors from one eye to the other are cases of this genotypic mosaic (this condition is called ‘heterochromia’). The actual DNA from one cell to the other is slightly different (but not so drastically that gel electrophoresis techniques couldn’t determine to whom such a cell belonged).
2. Phenotypic mosaics - These are by far the most common type of mosaics. Here all the cells have the same DNA. No mutation has occurred, however certain cells’ genes have been “turned off” and so those individual cells do not exhibit the gene as a trait (even though the gene is still technically there).

DNA functions as the “blue-print” for making proteins. It’s the formation of the proteins that we actually experience. The most common way of turning “off” genes so that the protein for which such a gene codes will not be produced is by methylating the gene. This literally binds up the gene so tight that the enzymes that “read” the DNA cannot bind to it and so no protein is formed (or a default protein is formed instead). Again, heterochromia is an example of this in certain species (namely in humans) where the gene to produce the protein needed for melanin in the eye is so extremely methylated that no melanin can be made resulting in an iris identical to those of one who exhibits albinism. Also many intersexed conditions that don’t involve chromosome number in humans result from this:

Take AIS (Androgen Insensitivity Syndrome). Women or Men with AIS (some prefer to be called Women and other’s Men) are genotypicially male (i.e. every single cell in their body has an X and a Y chromosome) however phenotypically (the expressed trait) are WOMEN! They have female external organs (including secondary ones like breasts), they lack facial hair, are shapely like women, talk like women, etc yet they have that pesky Y chromosome and technically in lieu of ovaries have testicles (though these testicles are internal where ovaries would be). The issue arises in a certain receptor on the Y chromosome being inactivated. This one locus on the Y chromosome is essentially responsible for determining whether a fetus will continue developing as a female or become male (since all feti begin with only their X chromosome active from mom). Because this gene never gets “turned on”, testicles never drop, the clitoris never becomes a penis, testosterone production is extremely inhibited, etc.

Now most biologists exclude phenotypic mosaics as a true form of mosaicism (claiming that since the DNA is identical in all cells, it’s just a matter of chromosome inactivation, it’s best categorized in it’s own sense). I’m one of such biologists, though decided to list it here since there’s a good chance that much of the mosaicism that you likely have encountered in life is due to chromosome/gene inactivation and not cases where the DNA between cells of the same individual differs.

So, to sum up a very long post (sorry

1. The causes for genetic mosaics vary a lot be them methylation of DNA (phenotypic mosaics), actual mutations of certain cell’s DNA (genotypic mosaics), or the chromosome count of certain cells (ploidy mosaics).
2. The observed effect could be due to any of the three main causes (and may even vary from individual to individual in the same species, though usually only vary from species to species). Remember, heterochromia in humans is usually due to gene inactivation while in cats is due to genetic non-disjunction during mitosis.

 

[xixxvmcm85]

As an aside: With the advent of epigenetics, some, most, or even all of our understanding may change in the future. Epigenetics is the study of genes that are molded by experience! (Yes there actually exists evidence that something like a famine which your grandfather experienced can be imprinted on YOUR genome thus affecting YOUR metabolism some 80 years later!) How this can/will affect our understanding of replication disorders is so far unknown.