Right. The "scientific method" is to skip debate and go straight to ad hominems. That's ok. I'm used to fools like you. Some of them are neocons who support the war for no rational reason. Some are liberals who hate Ron Paul because they think he was destroy civilization as they know it. And some are evolutionazis such as yourself.
What's the funniest is that the facts you give actually support my arguments. I clearly said that most people who run for office claim to be Christian. You point that out as if it was some kind of revelation. But notice that the media isn't running Hillary Clinton, Barack Obama, John McCain or Mitt Romney to get them to either affirm or deny evolution and if they do affirm it to explain how they rationalize their belief in Christianity. Only Ron Paul.
Quick question. Do you hate Dr. Paul as much as you hate Christians in general? I suspect not since you are posting on a Ron Paul forum. Ultimately our purpose is to help him to become president. But some people like yourself feel it's more important to attack your fellow supporters and force them to adopt your world view. Why is that? This is a movement about freedom. If someone wants to believe that we were created by space aliens then that's their belief. Ron Paul is an avowed Christian which means he believes we were created by God. Deal with it. And God bless you.
Regards,
John M. Drake
Alright, I went slightly out of my way to help you...This is from another forum, a very brilliant young woman wrote this:
"Much verifiable, valid, scientific evidence came to light at the conclusion of The Human Genome project. We now know that humans and chimpanzees are 96% identical at the DNA level, but that is not what is so fascinating.
For that, you need to look at the chromosomes. Humans have 23 pairs of chromosomes; the chimp has 24 (gorillas and orangutans also have 24 pairs like the chimp). The difference in the number appears to be the consequence of two ancestral chromosomes fusing together to form chromosome number 2 in humans.
To review, chromosomes are made up of two parts called arms. They are joined by something called a centromere, which is the pinched or narrow area between the arms. The short arm of the chromosome is called p (petite or small); the long arm is called q because q follows p. The p arm is always on top and the arms are what contain the genes.
At the end of the Human Genome Project they were able to pinpoint the exact location where the fusion occurred. Special sequences occur at the tips of all primate chromosomes and those sequences do not occur elsewhere. Now where we have chromosome number 2, primates have one extra chromosome (for clarity’s sake we will call them chromosome 2a and 2b). They have proof that 2a and 2b fused together to make chromosome 2 in humans because that special primate sequence (remember, it occurs at the tips of the primate chromosomes) is found along the long arm (q) of chromosome number 2 in humans (which is right in the middle of chromosome number 2, remember the short arm p, is on top, comes first, then it is joined by the q arm at the centromere).
So, this special sequence, which is only found on the tips of primate chromosomes, is found right in the middle of our fused second chromosome!!!!
Irrefutable proof that we both shared a common ancestor in the distant past.
The Human Genome Study showed inexorably that humans share a common ancestor with other living things.
Take for example, the human and mouse genomes, I’ll use these two genomes as an example due to the fact that they both have been determined now at a very high rate of accuracy. No way they could be similar right? Or if they are, it is only because God used successful design principles over and over again, right? WRONG.
The size of these two genomes is roughly similar and the inventory of protein coding genes is amazingly similar. The exact same order of genes along both the human and mouse chromosome is found/maintained over very substantial stretches of DNA. If you find say, human genes A, B, and C, in that order on the human genome, you will also find that the mouse has the counterparts of A, B, and C, placed in the same order although the spacing between the genes may have varied a bit. In some instances, the correlation extends over substantial distances; for example, all the genes on human chromosome 17 are also found on mouse chromosome 11.
Even more compelling evidence for a common ancestor has been achieved through the study of the ancient repetitive elements or ARE’s, which arise from “jumping genes” which are capable of copying and inserting themselves at random in various locations on the genome usually without any functional consequences. It is now possible to identify in the spaces between the genes the remnants of many jumping genes. Some of these elements have acquired many mutations compared to the original jumping gene and appear to be very old, hence the name, ARE’s.
Interestingly, these ancient elements are found in the exact same position (say between gene A and B) on both the human and mouse genome, even more interestingly was the finding of truncated ARE’s (truncated at a precise base pair at the time of insertion, losing part of its DNA sequence and all possibility of future function) in the EXACT same place on the mouse and human genome.
Finding a precisely truncated ARE in the exact same place on the mouse and human genome is evidence that the insertion event occurred in an ancestor that was common to both the mouse and human.
This is consistent with the ARE having arrived in a common mammalian ancestor and then carried along ever since.
Mammal genomes are littered with ARE’s and just about 45% of the human genome is made up of ARE’s. And remember the process of transposition often damages the jumping gene and there are ARE’s throughout the human and mouse genome that were truncated when they landed, removing all possibility of function and over and over again ( as stated above) you find a defunct ARE in parallel positions on the mouse and human genome.
God didn’t place defunct ARE’s in the exact same position to confuse or mislead us. The God that I believe in is neither a trickster nor a magician.
These truncated ARE’s are OVERWHELMING EVIDENCE for a COMMON ANCESTOR for humans and mice.
Random mutation of the gene for the jaw muscle protein MYH16 in humans led to a beneficial reduction in the mass of the human jaw muscle. This is beneficial because in humans the development of the weaker jaw led to the upward expansion of our skulls to accommodate our expanding brains. Multiple genetic changes then occurred leading to the development of the larger brain cortex.
The DNA code of the FOXP2 gene on chromosome 7 is stable in all mammals with the exception of the homosapien mammal, two significant changes occurred in the coding region of the FOXP2 gene 100,000 years ago, that led to the development of speech/language. It has been studied in multiple generational families that have severe difficulties in speaking, struggling to process words, understand complex sentence structure and the inability to move the muscles of their mouths, faces and larynx to articulate sounds, their DNA code in the FOXP2 gene is misspelled.
All organisms live in an oxygen rich environment, most of the time that is a good thing, but it causes serious problems at the cellular level, oxygen is highly reactive and with other compounds can produce H2O2 and an even more reactive compound called **** This damages DNA and proteins, and once the protein is so damaged by oxidation, the cell’s only solution is to junk the damaged macromolecule and make a new one.
So, what makes a protein susceptible to damage? Well the folks at Harvard took a bacterial protein and set up the conditions favorable to the evolution of a new protein resistant to such damage. Those smart cookies chose a protein enzyme that normally was produced only by fermentation in the absence of O2, I’d give you its name, but it is very long, so we will use the nickname that the scientists gave it, ProNADO, it is generally not around when O2 is present, so it is easily damaged by O2.
They grew these bacteria in the presence of O2 but supplied propanediol as a food source. Now, the only way for the bacterium to use propanediol as a food source is to convert it to other compounds, and to do that it must produce ProNADO, even though O2 is present. And guess what? Sure enough, in two separate experiments, mutants appeared in which the gene for ProNADO was switched on all the time, EVEN in the presence of O2, SCORE ONE FOR EVOLUTION, thank you very much.
Part Two:
Because ProNADO was not adapted to work in an O2 rich environment it was easily damaged by the **** radicals (and other oxidizing compounds). Now the researchers didn’t know enough on how to engineer the protein to make it resistant, so they sat back and thought,“We’ll let evolution teach us.”
So, they simply grew the mutant bacteria in plenty of O2, figuring that those chance random mechanisms of mutations (that the Creationists scorn) would come up with an oxygen-resistant form of ProNADO.
Sure enough, mutation and natural selection did the trick. It produced two mutants, each which were resistant to oxidative damage. In the first mutant, a single amino acid (the seventh in the chain) had been changed from an isoleucine to a leucine, and in the other a leucine in the eighth position was changed to a valine.
In fewer than 200 bacterial generations, the mechanism of random, undirected mutation had taken the gene for an oxygen sensitive protein produced only during fermentation and changed it into one that switched on all the time and was highly resistant to O2 damage.
E.C.C. Lin, et al.,“Evolution of an E. Coli Protein with Increased Resistance to Oxidative Stress”, Journal of Biological Chemistry 273,(1998): 8308-8316.
Benefits of lactose tolerance mutation and natural selection.
Got lactase?
April 2007
Quote:
In the US and many other countries, we've certainly "got milk," but not everyone can enjoy it. For around 10% of Americans, 10% of Africa's Tutsi tribe, 50% of Spanish and French people, and 99% of Chinese, a tall cold glass of milk means an upset stomach and other unpleasant digestive side effects. In fact, most adults in the world are lactose intolerant and cannot digest lactose, the primary sugar in milk. And yet, regardless of our ancestry, most of us began our lives happily drinking milk from a bottle or breast — so what happened in the intervening time? Why do so many babies enjoy lactose and so many adults avoid it? Lactose is broken down by a protein called lactase, which acts as a pair of molecular scissors, snipping the lactose molecule in two. Anyone who drank milk as a baby carries a working version of the gene that codes for lactase. In lactose tolerant individuals, that gene keeps working into adulthood, producing the protein that digests lactose and makes eating ice cream a pleasant experience. But in people who are lactose intolerant, that lactase gene is switched off after weaning. Now, new research reveals that the Stone Age ancestors of European dairy-lovers probably couldn't digest milk either. So how did they get from bellyaches to milk mustaches? The answer is an evolutionary story that takes us from the milkmaids of the Alps to the Maasai herdsmen of Africa.
Where's the evolution?
Mutations that keep the lactase gene permanently switched on are common among modern Europeans — but not among their ancestors. In March 2007, a team of German and British researchers announced that they went looking for that mutation in the 7000-year-old fossils of ancient Europeans and came up empty-handed. The researchers managed to extract the length of DNA corresponding to the lactose tolerance mutation from eight Neolithic human fossils and one Mesolithic fossil, but those DNA sequences did not carry the telltale mutation. The results suggest that as late as 5000 BC most ancient Europeans could not have digested milk as adults — and that they only later evolved into milk-drinking societies.
Today, the ability to digest milk as an adult seems like a clear benefit, but that wasn't always the case. Lactose tolerance is only advantageous in environments and cultures where humans have access to domesticated dairy animals. Multiple lines of evidence from human genetics, cattle genetics, and archaeological records suggest that Middle Eastern and North Africans populations domesticated cattle between 7500 and 9000 years ago, and that these animals were later brought into Europe. In that cow-friendly environment, being able to drink milk directly (instead of having to process it into lower-lactose cheese) would have been advantageous, providing additional sustenance and, during droughts, a source of water. The lactose tolerance mutation arose randomly (as all mutations do), but once it arose, it had a distinct advantage in these populations. Natural selection would have favored individuals carrying the lactose tolerance mutation, spreading it through ancient European populations that depended on dairying. Many thousands of years later, we see the indirect (but delicious) effects of this mutation's success in European cuisines: oozing French cheeses, Swiss milk chocolate, and creamy Italian gelatos."
Unquote
Work cited:
http://evolution.berkeley.edu/evolibrary/
