Evidence for creationism, Part 2.

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If God created us in his image why are there harmful mutations? Does God have bad genes?
 
I think one can make the argument that it was the apple eaten by Adam & Eve that cursed us with that.

Not that I'm making said argument.
 
What about vestigial organs? We and other organisms are riddled with those purposeless things. Why?
 
I think one can make the argument that it was the apple eaten by Adam & Eve that cursed us with that.

Not that I'm making said argument.

You think something called the Tree of Knowledge of Good and Evil would just give you knowledge.

Edit: Also Magicfan you still haven't named those 15 defects that fit my criteria I've made couple posts back.
 
Seems as if Court is in Session.


Have you proven this yet?
yes! please provide a mutation in humans that does not cause an information lost.


Do you understand this thing called reproductive science? Phenotypes? Crossing Over? Cellular Reproduction? Gametes? Meiosis?
answered in post above. evolution depends on "good" mutations but mutations are bad or neutral and natural selection can not remove them.





This article does not disprove pizza's assertion that most mutations are neutral in effect.
The only reason mutations are neutral because we dont know the full functionality of the genome. so they are labeled neutral because no apparent damage is found based on our knowledge. when mutations happen they are overwhelmingly bad or neutral not "good".



what does this mean?
sorry i meant to say that it was from the nature article
 
Preemptive creationist response:

1) Satan
2) Mark of Cain
3) Banished from Eden --> Painful childbirth, sickness, hunger, etc.
 
Here's two - the coccyx and the appendix.
 
please provide an example of an vestigial organ in humans. all organs have a functions in the body

Vermiform appendix, coccyx, tailbone, muscles in the ear, and Plica semilunaris of conjunctiva. Now where is my 15 negative mutations that fit the criteria I gave you early in this thread?
 
Maybe not vestigial, but just as perplexing: male nipples

And wisdom teeth.
 
Here's two - the coccyx and the appendix.

coccyx: it is an important attachment for various muscles, tendons and ligaments — which makes it necessary for physicians and patients to pay special attention to these attachments when considering surgical removal of the coccyx. Additionally, it is also part of the weight-bearing tripod structure which act as a support for a sitting person

appendix: Loren G. Martin, a professor of physiology at Oklahoma State University, argues that the appendix has a function in fetuses and adults.[7] Endocrine cells have been found in the appendix of 11-week-old fetuses that contribute to "biological control (homeostatic) mechanisms." In adults, Martin argues that the appendix acts as a lymphatic organ. The appendix is experimentally verified as being rich in infection-fighting lymphoid cells, suggesting that it might play a role in the immune system. Zahid[8] suggests that it plays a role in both manufacturing hormones in fetal development as well as functioning to "train" the immune system, exposing the body to antigens so that it can produce antibodies. He notes that doctors in the last decade have stopped removing the appendix during other surgical procedures as a routine precaution, because it can be successfully transplanted into the urinary tract to rebuild a sphincter muscle and reconstruct a functional bladder.
 
Do the tiny webs between our fingers/toes represent a vestigial trait also?
 
perfect answer to your statement, mutations are adding up in the gene pool



http://www.newton.dep.anl.gov/askasci/mole00/mole00460.htm

iirc sickle cell anemia actually has uses. I remember learning in a health class that SCA, which is more common among Africans, makes them more resistant to malaria or something like that, which would probably better explain why it is still persistent in the human genome.

I was right, and here's the proof:
source: http://sickle.bwh.harvard.edu/malaria_sickle.html
At the red cell membrane, the Duffy antigen is the molecule used by the parasite P. vivax to enter the red cell. The high association of Duffy antigen null rell cells in some groups of people with sickle cell trait suggested that the Duffy antigen might provide some protection against malaria (Gelpi and King, 1976). Later investigations showed the Duffy antigen to be the receptor by which the merozoites of P. vivax enter red cells. People who lack the Duffy antigen (FY*O allele) are resistant to P. vivax (Hamblin and Di Rienzo, 2000). The Duffy null phenotype is most common in people whose ancestors derive from regions in Africa where vivax malaria is endemic.

Sickle hemoglobin provides the best example of a change in the hemoglobin molecule that impairs malaria growth and development. The initial hints of a relationship between the two came with the realization that the geographical distribution of the gene for hemoglobin S and the distribution of malaria in Africa virtually overlap. A further hint came with the observation that peoples indigenous to the highland regions of the continent did not display the high expression of the sickle hemoglobin gene like their lowland neighbors in the malaria belts. Malaria does not occur in the cooler, drier climates of the highlands in the tropical and subtropical regions of the world. Neither does the gene for sickle hemoglobin.

Sickle trait provides a survival advantage over people with normal hemoglobin in regions where malaria is endemic. Sickle cell trait provides neither absolute protection nor invulnerability to the disease. Rather, people (and particularly children) infected with P. falciparum are more likely to survive the acute illness if they have sickle cell trait. When these people with sickle cell trait procreate, both the gene for normal hemoglobin and that for sickle hemoglobin are transmitted into the next generation.
 
yes! please provide a mutation in humans that does not cause an information lost.

I don't see where you proved that.


answered in post above. evolution depends on "good" mutations but mutations are bad or neutral and natural selection can not remove them.

You still haven't explained anything here, proving you don't know what I was talking about. You tried to use the example that cells have DNA repair function to somehow prove that all mutations were bad.

Seriously. Do you know what happens in a meiosis, and why it is different from mitosis?

The only reason mutations are neutral because we dont know the full functionality of the genome. so they are labeled neutral because no apparent damage is found based on our knowledge. when mutations happen they are overwhelmingly bad or neutral not "good".

So in essence you failed to prove that most mutations are bad.
 
Vermiform appendix, coccyx, tailbone, muscles in the ear, and Plica semilunaris of conjunctiva. Now where is my 15 negative mutations that fit the criteria I gave you early in this thread?
genetic disorders are caused by mutations i listed them in my posting before. vestigial organs opinionated definition. if i cut off my pinky will i die? no. does that mean that my pinky is a vestigial organ. just because something has a small function does not mean it evolved over millions of years. my post was not about vestigial organs but how mutations(copying errors) do not fit the theory of evolution. mutations do not cause ape to man.
 
Magicfan101, please repeat after me: I have just been hoist by my own petard, I have no arguement whatsoever, I will stop spamming the thread with my lies and misinformation.

Spoiler :
And before you say Gotcha or anything like that I am asking for you to say this about yourself, not pretend I am talking about me.
 
iirc sickle cell anemia actually has uses. I remember learning in a health class that SCA, which is more common among Africans, makes them more resistant to malaria or something like that, which would probably better explain why it is still persistent in the human genome.

I was right, and here's the proof:
source: http://sickle.bwh.harvard.edu/malaria_sickle.html

this is from a previous post i had
Sickle-cell anemia is a disease of red blood cells. Why would anyone call that a beneficial mutation? Well, in certain parts of Africa, the death rate from malaria is quite high. Malaria is caused by a tiny, one-celled organism that gets inside the red blood cells and eats up the hemoglobin. Now, that particular germ doesn’t like sickle-cell hemoglobin. Carriers of one sickle-cell gene produce about half normal and half sickle-cell hemoglobin, and the malaria germ leaves them alone, too. So, carriers don’t get malaria. But the cost is high: 25% of the children of carriers can die of sickle-cell anemia, and another 25% are subject to malaria. If you want to call that a good mutation, you’re welcome to it! It seems doubtful to me that real improvement of human beings would result from accumulating that kind of “beneficial” mutant, and certainly hemoglobin’s ability to carry oxygen was not improved.

The gene for sickle-cell anemia has built up to high levels in certain African populations, not because it is “beneficial” in some abstract sense, but simply because the death rate from anemia in those areas is less than the death rate from malaria. Natural selection is a “blind” process that automatically accumulates genes for short-term survival, even if it reduces the long-term survival of the species. For that reason, evolutionists recognize that natural selection can occasionally lead to “mischievous results” detrimental to genetic quality. That’s the effect I think we’re seeing with sickle-cell anemia
 
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