owen06

[quote=fredfam1;920663]Sickle cell anemia reduces the fittness of the population even in some of those with the trait, or recessive gene and there for is not a positive overall trait.

Let me preface my response by saying I am not in any way trying to attack you. I simply disagree and believe there is more evidence to support my beliefs. However, I am enjoying our conversation immensely.
I am assuming the definition of fitness you are using is in reference to ones ability to pass on ones genes to the next generation (a population genetics concept central to evolutionary theory). More precisely, it is the proportion of that individuals genes that make up the sum of all the genes in the next generation. Now, if a genotype affect fitness negatively (as you claim the sickle cell trait does) then we should see this ratio become smaller and smaller; and eventually due to negative selection pressures, die out as it would not confer an advantage. HOWEVER, this is NOT the case regarding sickle cell trait.
The persistence of the sickle gene is explained by the concept of "heterozygous advantage" where in a given population; individuals who are heterozygous for a particular gene, compared to those who are homozygous, have some selective advantage. The stable frequency of the genes in question existing in areas of hyperendemic falciparum malaria, is the result of a balance between premature death of homozygotes (negative pressure) and gene selection due to the resistance of heterozygotes to death from malaria (positive pressure). Sickle cell trait is significantly associated with a decrease in all-cause mortality among children 2-16 months of age (ie most at risk of severe disease). Specifically, sickle cell trait is associated with protection against severe malarial anemia, high-density parasitemia, and cerebral malaria. As a result of the selective advantage against death from malaria conveyed by the sickle cell gene, its worldwide distribution parallels that of falciparum malaria, with its highest frequencies occurring in the "malaria belt”. [1]
I also would like to bring it to your attention that the sickle-type of hemoglobin beta chain is actually inherited in a codominant manner; not in a recessive pattern as you would suggest. Hemoglobin is a tetramer (4 proteins) of which the Beta subunit has two relevant types in this conversation (type A, and type S) which in the trait are both expressed. If it were a simple matter of dominant and recessive genes the type S gene would not be expressed except in people suffering from sickle cell disease.

The fact that a virus may not be able to live in this particular environment does not even constitute an argument for adaptation and results in an over all loss of genetic information which is not evolution or even macroevolution.

Sorry, I just wanted to let you know malaria is due to a parasite not a virus, specifically of the genus Plasmodium and of these, the most deadly is often quoted as Plasmodium falciparum and for the sake of completeness they are transmitted by female mosquitoes of the Anopheles genus. But according to your post I thought you were insinuating I must assume these binomial taxonomic classifications used and recognized globally (mostly to ensure that, when communicating with one another, scientists are talking about the same thing) are inconsequential (something to do with funding? *confused*).

"Many individuals will have decreased ability to concentrate their urine. There may be an increased incidence of urinary tract infection during pregnancy. Painless hematurea does occur in 1 to 4 % of individuals with sickle cell trait . This complication is usually not a significant problem, however, a minority of individuals may have significant problems with recurrent hematurea requiring medical intervention, transfusion, and iron therapy. Complications such as splenic infarction, pain episodes, and sudden death may be induced by severe hypoxia, severe dehydration, and exertion at the limits of human endurance."

I am not sure where this quote is from. Can I have a reference for it please? There is a large differential diagnosis for painless hematuria but in those that it is due to sickle cell trait and that it causes significant problems are truly unfortunate. It is worthwhile to note that this complication's rate is usually insignificant and that the severe problems you mentioned were associated with exertion at the limits of human endurance, a state that those who could be afflicted with sickle cell are advised to avoid.

Consider the Bard owl and the Spotted Owl, with out mans help eventually the Bard owl will win out. But they are still both owls.

I wont disagree with you on this point. They are still owls. But I was discussing how species can be genetically defined as not being able to produce viable offspring. And you stole my example! lol as mating a horse and a donkey does produce a mule but because a mule cannot successfully mate (not even with another mule) because of an abnormal number of chromosomes, this is a hybrid and NOT a separate species according to the biological definition. There are numerous kinds of hybrids and the vast majority of them run into the same problem, they are not genetically viable.


As the Bible says, they reproduce after their KIND. There is no evidence of evolution between kinds. Only adaptation, which some scientists prefer to label MICROevolution.

If you are talking about organisms that are put into categories because they are similar that’s ok. But by this argument I never stated that evolution occurs BETWEEN kinds. I would have stated that evolution leads to the production of different kinds. One kind evolves into another kind. That sorta thing.
And you seem to be saying that microevolution is possible while macroevolution is not. I am simply saying that numerous microevolutions could and do result in a macroevolution (akin to how many small steps make up a mile).

As for genetic similarity: read the following from ICR on the subject:...
[b]

With regards to the large article from the “Institute for Creation Research” (ICR) that you posted. I would just like to say the following. That nearly 10 years after decoding the human genome (which is not the same in every person) we know only the tip of the iceberg as a scientific community. It is the field of proteonomics that will start to take the lead for, as important as DNA is, it is the proteins in a cell that actually determine what happens, even so far as to whether or not cells live or die if certain pathways are activated. Most people would be surprised to learn that their DNA has, in all likelihood, changed considerably since they were born. Mutations occur on a regular basis as the mechanisms inside your cells that repair DNA have inherent error rates. There is also the problems of free-radical and radiation-induced DNA damage. Add on to this the fact that there can be spontaneous rearrangements in your DNA and that certain viruses propagate by integrating into your DNA and you may be surprised that you haven’t filled up with tumors and made it as far as you have (I am at times). However, we are lucky as, even though there are approximately 3 billion base pairs in the human genome, only approximately 1.1% of this DNA is composed of exons – the actual protein coding DNA. And of this DNA only a small percent is active at any given time (thanks to the modulating effects recently discovered in the branch of genetics known as epigenetics). Of the rest - 24% is introns, and 75% is intergenic DNA of which we are still trying to figure its purpose. However, to make a really long story short, if a mutation affects a protein that is when it matters.

How can we know that these changes in proteins are constant in time? Well, there are two possible hypotheses. One states that proteins change when DNA mutations accumulate during the process of replication (the stance taken by the ICR in the posted article). Another states that if proteins change due to random chemical degradations of DNA then the mutation rate should be constant over absolute time. To tell which is most likely we can look at the divergence of the protein cytochrome c in insects and mammals. Insects have generational times far shorter than most mammals. If it is the replication of DNA that leads to the mutations in the proteins; from the time insects and mammals split from a common ancestor insects should have evolved more differences. But, using a phylogenetic tree we can see that the average number of differences between insects and plants (45.2) and mammals and plants (45.0) is essentially the same. We must therefore conclude that cytochrome c accumulates mutations at a uniform rate. Furthermore, we must conclude that the point mutations in DNA that are accumulated in a species over time occur due to random chemical change, rather than errors in the replication process. [2]

Finally, to conclude, before you go back and read earlier in my response that DNA repair mechanisms have inherent error rates and assume this is contradicted by the above I urge you to remember that point mutations are only one type of mutation that can occur.

[1] Hoffman, Ronald, et al. Hoffman: Hematology: Basic Principles and Practice, 4th ed. 4th ed. Ed. Kimberley J. Cox. Philadelphia, Pennsylvania: Elsevier, Churchill Livingstone, 2005.
[2] Voet, Donald, and Judith G. Voet. Biochemistry. 3rd ed. Eds. David Harris and Patrick Fitzgerald. 111 River Street, Hoboken, New Jersey: John Wiley & Sons, Inc., 2004.