Quality Control the Gold Standard

Evopeach, I'm sorry for your loss--cancer has visited tragedy on so many of our families. It killed my father, grandfather, and other family members; it nearly killed older brother, and, based on my family history and other risk factors, will probably kill me.Please note, however, that:1) The P53 mutation does not stand accused of causing all breast cancers.2) Mutations are neither good nor bad; mutations are random, and they may have deleterious or advantageous effects for survival and, potentially, reproductive fitness. 3) Many cancers occur later in life, as do many other debilitating and fatal diseases. If a disease has a genetic component, but the disease does not strike until after the reproductive years, then it will not be subject to natural selection, and thus would not be eliminated.Even if the genes are expressed early enough in life to affect reproductive fitness, there is no reason to expect natural selection to eliminnate or reduce its occurrence in the human genome in only a few thousand years, the time since the invention of writing. Evolution works on a much large time scale. Oncologists have noted that if we lived long enough, we would all die from cancer; they also suggest our lengthening life spans account for some portion of rising cancer rates.I don't see any consistency in this message, though. Do you deny that cancer has a genetic component? If it does, how does the occurrence of cancer support intelligent design rather than evolution, and how would the occurrence of cancer support the notion of a perfect, all-powerful creator rather than an error-ridden, "just good enough" process of evolution?*P.S. Please note that "baited" breath is a common mutation of language usage: "bated" is the correct term. One waits with breath held (i.e., "abated"), not with breath become a lure.

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The mutation may be advantageous or deleterious depending on the environment in which it is expressed. For example, sickle cell anemia can equip a carrier of one sickle cell gene and one normal hemoglobin gene to survive malaria, which is both deleterious and advantageous in malaria-ridden areas--because while the sickle cell gene will almost certainly shorten the individual lifespan, it also allows the individual to survive long enough to reproduce.This phenomenon is not "unknown, undefined, unquantifiable, unmeasureable." Do your own homework if you want the statistical analysis of variance between malaria-ridden and malaria-free regions of the world.Of course, in a malaria-free environment, it serves no useful purpose at all and could be called purely deleterious in that environment. Here's some basic info from Harvard: search for "balanced polymorphism" or "heterozygote" if you want to zoom in on more details. Sickle Cell Anemia and Malaria. Selection works on the individual; evolution occurs in the population.Ubiquitous? Not all cancers are caused by the P53 mutation, so if the incidence of breast cancer in women by the age of 70 is 16%, the subset of cases caused by P53 is lower than that, hardly what I would describe as "existing or being everywhere at the same time." Most incidents of breast cancer are not caused by DNA mutations but by environmental or lifestyle factors--unlike the sickle cell allele, there are no benefits that would cause the gene to be selected for in the population.So, do we see this pattern elsewhere in DNA mutation linked breast cancers? Note the ages highlighted in the BRCA1 mutation breakdown: The phenomenon was precisely described, EP, however much you wave your rhetorical hands or seek to create strawmen. How many young girls die of breast cancer? Very, very few. Why? Because genes which kill before the individual carrying them reaches reproductive age are not conserved in the genome, since they cannot be passed by that individual to the next generation. Well, I know it's hard--hang in there, though, you'll get it eventually.

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"Dost thou think because thou art virtuous there shall be no more cakes and ale?"
-Sir Toby Belch, Twelfth Night Save lives! Click here!
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If I understand the question correctly, it is a tautology. What does the constancy or inconstancy of the mutational rate have to do with the expression of the mutation and the contingency of its "reception" by the environments in which it occurs?Here's another example for your amusement. Red-green color blindness is awkward for the men who have it in our stoplight world, though not a serious hindrance. However, in a rain forest environment, male hunters with red-green color blindness reap a benefit from their altered vision: they enjoy a much finer discrimination in the green-brown (khaki range), useful for distinguishing prey camouflaged in branches and leaves.This perceptual advantage has been recently confirmed by studies comparing the ability of such color blind men in khaki shade discrimination, and at last explains why red-green color blindness has persisted in the genome. Not very useful at traffic lights, is it? But it's just killer in the hunter-gatherer environment.What difference would the mutational rate make in the scenario above? Red-green color blindness is inheritable. It runs in families. It does not occur de novo with each individual.By the way, some controversial research has suggested that, in fact, the mutational rate is not indifferent to the environment, but it is not definitive. Interestingly, that research is most often cited here by opponents of the theory of evolution. I haven't suggested the mutational rate changed over time, nor is it a logical implication of any assertion of mine. Do you believe it did? That would make an interesting topic. I have not posited any effects that vary mutational rates. I have pointed out that some mutations confer benefit, some confer harm, and some confer both, all of these conferrals contingent upon the environment in which the mutation is expressed. The sickle cell gene persists in the human genome because, in the heterozygotic form, it confers sufficient benefit to allow reproduction. The red-green color blindness persists because it conferred exactly the color acuity a hunter needed in one of our ancestral environments. If that were not so, if the sickle cell gene invariably caused death before reproductive age, there would be far fewer individuals carrying the gene, and red-green color blindness would not have become so common. What does any of that have to do with mutational rates?Are you supposing that the sickle cell mutation, or the P53 mutation, or color blindness, are in each case de novo events? They are certainly not--they are inheritable changes in DNA, which is why family histories of illness are useful indicators of risk, allowing for DNA tests which yield information useful for treatment.Perhaps you could quote the passages in my message that seem to suggest my point was about mutational rates. I know that makes it more difficult to construct and burn a strawman, but I've found quotes are conducive to honest debate. Apparently, you didn't understand it then, either.This message has been edited by Omnivorous, 02-08-2006 08:43 PM

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"Dost thou think because thou art virtuous there shall be no more cakes and ale?"
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Well, here's one part of the answer:

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"Dost thou think because thou art virtuous there shall be no more cakes and ale?"
-Sir Toby Belch, Twelfth Night Save lives! Click here!
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Do you actually believe Newton formulated a mathematical expression before he made any observations of gravity at work?The tale of the falling apple may be apocryphal, but it serves very well as an exemplar of naturalistic observation.Scientific hypotheses are made to explain observed phenomena. Then the hypothesis is used to make predictions, and the predictions are tested.Darwin made observations, then formulated his hypothesis. The modern synthesis has made predictions, both with and without mathematical tools, and the success of those predictions has strongly confirmed the theory.Most "great science" did not first pop into existence as formulae.

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"Dost thou think because thou art virtuous there shall be no more cakes and ale?"
-Sir Toby Belch, Twelfth Night Save lives! Click here!
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There is one factor we can get a numerical handle on:The rate of spontaneous abortions (miscarriages) in detected pregnancies is 15-20% (about 1 in 6). Some studies suggest the overall rate may be as high as 50% (with many miscarriages so early as to have not been clinically confirmed), with the mother experiencing only a "late period." The underlying cause is overwhelmingly fetal chromosomal abnormality; consequently, human births with chromosomal abnormalities are rare. The risk of a second miscarriage is no higher; i.e., the risk remains at 15-20%, suggesting an error in the genetic process itself, not in the parental material. More info here.

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"Dost thou think because thou art virtuous there shall be no more cakes and ale?"
-Sir Toby Belch, Twelfth Night Save lives! Click here!
Join the World Community Grid with Team EvC!
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