2. Common Descent Explains the Vagus Nerve

With Evo, we don't end up with perfect solutions. There are strange anomalies that are explicable only because we have shared ancestors.

The vagus nerve that controls our voice box runs from the brain, right past the larynx, down to the top of the heart where it runs round an artery, then comes back up your neck to the larynx. It is the same in all mammals. In the giraffe it's the same. The distance from the brain to the larynx is about 2 inches, but the nerve connecting them does the same thing as it does in all mammals - down to the heart, round the artery, and back up the neck again - in an adult giraffe, a distance of about 15 feet.

Obvious question - how incompetent would a designer have to be to use the same design even when a better way is so obvious.

A detailed explanation here of how the Giraffe illustartes Evo and contradicts idea of an intelligent designer

3. Evo Explains Why Humans Don't Make Vitamin C

• All animals need Vitamin C to live. But, dogs and cats, mice and rats, most birds and fish, horses and donkeys, oxen and cattle, sheep and goats, hogs and hippos, rabbits and hares, hamsters and gerbils, elephants and rhinos, gators and crocs, lizards and llamas, coyotes and foxes, the buffalo that roam, the deer and the antelope that play, lions, tigers, and bears (oh my!), among many, many others, all get along just fine without having to eat Vitamin C. Why not, if they need it to live?
  
  Because, all of those other animals make their own Vitamin C! But how? We know how. We know exactly how they do it. We know every step involved. They make it within their livers. Tiny factories located deep within certain liver cells produce enzymes, under the control of DNA.
  
  Four different enzymes are produced. The first one takes ordinary, everyday water (an extremely simple inorganic molecule necessary for life, and partly for this very reason) and glucose (a slightly more complex organic molecule found in all living things and obtained from nearly all foods) and turns it into a more complex intermediate organic molecule. The second enzyme takes the resulting intermediate molecules formed by the first and assembles it with others to form an even more complex intermediate molecules. The third does likewise with the results of the second, producing a chemical called "D-glucuronolactone" aka "L-gulono-1,4-lactone".
  
  The fourth enzyme takes that D-glucuronolactone aka "L-gulono-1,4-lactone" produced by the third, and combines it with oxygen (with flavin adenine dinucleotide [FAD] as a co-factor) to form "L-xylo-hex-3-gulonolactone" aka "2-keto-gulono-γ-lactone" (that's a Greek lowercase gamma [uppercase: "Γ"], not an English/Latin lowercase "Y" or "y") which then, without enzymatic action, spontaneously converts to hexuronic acid aka ascorbic acid, aka Vitamin C!
  
  Think of it as like a modern factory robotic assembly line with four stages, and each cellular factory is a factory robot, with the enzymes being materials that the robots make and use to do their tasks. Just as factory robots are programmed, each of these cellular "factory robots" is programmed by a DNA enzyme-encoding gene sequence to perform a specific task in a specific way. The first "robot" starts with common raw materials found in all living things (water and glucose), and the remaining "robots" each take the output of the preceding "robot" and further build onto it.
  
  The fourth and final enzyme in this process is called "L-gulonolactone oxidase" (aka "L-gulono-γ-lactone oxidase"). Like the other three enzymes, it's produced by a cellular factory programmed by a specific DNA sequence, or gene. In this case, the gene is called "GULO." We know exactly where it is on the genomes of animals that we've mapped so far (for instance, in various species of hogs, it's on either Chromosome #4 or #14). We also know where it is on the genomes of haplorrhini primates, including tarsiers and simians (the latter including apes, and thus us). For us, it's on the shorter arm of Chromosome #8 (8p), at location 8p21.
  
  Or, at least, that's where the erroneous version is for humans. We have an error in our DNA at that spot! We have everything we need to make our own Vitamin C, just like all those other animals. We have livers, just like they do. Our livers have cells, just as theirs do. Those cells have microscopic enzyme factories, just like theirs. Ours produce the first three enzymes just fine, just like theirs do.
  
  We have everything we need, but it all fails at the final stage because our GULO gene is faulty and prevents the final enzyme of the four from being produced correctly! The erroneous version is called a "pseudogene" ("GULOP" in this case - the "P" suffix appended to "GULO" stands for "pseudogene") since it doesn't actually work. It doesn't program the production of L-gulonolactone oxidase. And without that, the D-glucuronolactone produced by the third enzyme in the process never gets converted into L-xylo-hex-3-gulonolactone and thus into hexuronic/ascorbic acid, aka Vitamin C.
  
  Do you realize what this means? It means that our so-called "Creator" or "Intelligent" Designer would've had to've gone to all the extra work to give us everything we need to make our own Vitamin C, just like all those other animals have: the same sorts of liver cells, the same complex tiny enzyme factories within those liver cells, producing the same first three enzymes, which take the water and glucose and use it to produce the same intermediate-stage complex organic molecules, only to have the whole thing fail at the very last stage because of this error in the GULO gene (making it a GULOP psuedogene instead), aborting the Vitamin C-making process at the very last stage! Gee, that's not such an "Intelligent Design," now, is it?
  
  But wait, it gets even better! Did you notice a whole class of animals was missing from my list of Vitamin C-making animals above? Not just us humans. What else?
  
  Apes & monkeys! Collectively, they (and us - we are apes) are the Class of simian primates. And not just them, but the tarsiers, too. The tarsiers and simian primates together form the Sub-Order of haplorhinni ("dry-nosed") primates. None of them can make their own Vitamin C, either, and for the same reason!
  
  How very interesting! Not only do the Creationists / IDers have to explain why their Creator / Designer made such a mistake with us, they also have to explain why He made the exact same mistake in almost the exact same way in all of the other animals, but only those other animals, that science places in the same Sub-Order as us! (There are some other animals that cannot make Vitamin C [prairie dogs, all bats, and some birds, among a few others], but mostly for differing reasons, and for those that are due to a GULOP, theirs are faulty in a different way than the GULOP of the haplorhinni primates.)
  
  But what if, oh, about 63 million years ago (give or take), some common ancestor of all the haplorrhini primates, itself a primate, had its GULO gene mutated into a GULOP pseudogene, and passed that on to all of its descendants, all the way down to and including us? Why, that would explain it quite nicely, thenkyewverramuch! This common ancestor would've been related to, but not descended from, the common ancestors of another sub-order of primates, namely, the strepsirrhini ("wet-nosed") primates (lorises, galagos, pottos, and lemurs) who do have a functioning GULO gene and thus can and do make their own Vitamin C.
  
  Evolution by descent from common ancestors through mutation selected by natural selection, aka Darwinism. That explains it. Neither Creationism nor "Intelligent" Design can, unless the Creator / "Intelligent Designer" were utterly incompetent, or else willfully, maliciously, and very deliberately deceptive.
  
  But wait, it gets even better! You see, there are in fact some slight differences in the GULOP pseudogenes of the various haplorrhini primate species (that have nothing to do with how they're broken). The extent of those differences differs exactly according to how closely or distantly related they are. For instance, using ours as the base for comparison, the GULOP of a bonobo (so-called pygmy chimpanzee, our closest surviving relative) is very slightly different. Those of the other chimpanzee species are a bit more different. Those of other Great Ape species (e.g. gorillas, orangutans, etc.) are a bit more different still, while those of lesser apes and monkeys (both simians) are even more different, and those of the tarsiers are the most different of all from ours among the haplorrhini primates. The same thing happens when you compare any other haplorrhini species's GULOP as the base of comparison against the others.
  
  Not only does the mere presence of those differences utterly demolish the "Same Designer re-using Common DNA Building Blocks" excuse, do you have any idea what the odds of this would be for them to work out that way if it happened any other way than by evolution through common descent from a common ancestor!?
  
  

Elephants and Cancer

Elephants have evolved extra copies of a gene that fights tumour cells, according to two independent studies, offering an explanation for why the animals so rarely develop cancer.

Why elephants do not get cancer is a famous conundrum that was posed — in a different form — by epidemiologist Richard Peto of the University of Oxford, UK, in the 1970s. Peto noted that, in general, there is little relationship between cancer rates and the body size or age of animals. That is surprising: the cells of large-bodied or older animals should have divided many more times than those of smaller or younger ones, so should possess more random mutations predisposing them to cancer. Peto speculated that there might be an intrinsic biological mechanism that protects cells from cancer as they age and expand.

At least one solution to Peto's paradox may now have been found, according to a pair of papers independently published this week. Elephants have 20 copies of a gene called p53 (or, more properly, TP53), in their genome, where humans and other mammals have only one. The gene is known as a tumour suppressor, and it snaps to action when cells suffer DNA damage, churning out copies of its associated p53 protein and either repairing the damage or killing off the cell.

The elephant's tale

Uncovering TP53's role has taken a few years. Joshua Schiffman, a paediatric oncologist and scientist at the University of Utah in Salt Lake City, first heard about Peto’s paradox three years ago at an evolution conference, when Carlo Maley, an evolutionary biologist now at Arizona State University in Tempe, revealed he had found multiple copies of TP53 in the African elephant's genome.

Schiffman specializes in treating children missing one of their TP53 gene's two alleles, which leads them to develop cancer. So after hearing Maley's talk, he wondered whether elephants held some biological insight that could help his patients. He teamed up with Maley, who had not yet published his work, and asked elephant keepers at Salt Lake City’s zoo whether they could spare some elephant blood so that he could test how the p53 protein works in the mammals' white blood cells.

At about the same time, in mid-2012, Vincent Lynch, an evolutionary geneticist at the University of Chicago in Illinois, was preparing for a lecture on Peto’s paradox, and wondered about mechanisms that could explain it. “Right before I gave the lecture, I searched the elephant genome for p53, and 20 hits came up,” says Lynch.

Schiffman and Lynch’s teams have now independently revealed their findings — Schiffman's in the Journal of the American Medical Association, and Lynch's in a paper posted to the bioRxiv.org preprint site, but which is in review at the journal eLife.

Using zoo autopsy records for 36 mammals — from striped grass mice to elephants — Schiffman’s team recorded no relationship between body size and cancer rate. (Around 3% of elephants get cancer, according to the team’s analysis of hundreds of captive-elephant deaths).

The researchers found that elephants produce extra copies of the p53 protein, and that elephant blood cells seem exquisitely sensitive to DNA damage from ionizing radiation. The animals' cells carry out a controlled self-destruction called apoptosis in response to DNA damage at much higher rates than do human cells. Schiffman suggests that, instead of repairing the DNA damage, compromised elephant cells have evolved to kill themselves to nip nascent tumours in the bud. “This is a brilliant solution to Peto’s paradox,” he says.

Mammoth set

Lynch’s team — working with African and Asian elephant skin cells from the San Diego Zoo in California — found similar results. They also discovered more than a dozen TP53 copies in two extinct species of mammoth, but just one copy in elephants’ close living relatives, manatees and hyraxes (a small, furry mammal). Lynch thinks that the extra copies evolved as the lineage that led to elephants expanded in size. But he thinks that other biological mechanisms are involved too.