September 7, 2004 | David F. Coppedge

Natural Selection Demonstrated in European Heart-Disease Gene?

Stephen Wooding (U. of Utah) is elated.  He sees an “exciting trend” in genetic research that might, finally, demonstrate positive natural selection acting on a gene with a clear phenotypic effect (measurable outward benefit).  Writing in the Sept. 7 Current Biology,1 he mentions a few recent papers suggesting this connection, but focuses particularly on one study by Rockman et al. in the same issue.2  This UK/American team claims to have identified a gene that has been positively selected to shape heart disease risk among Europeans.  The story was summarized by EurekAlert.
    The gene under investigation is named MMP3, a regulator of a substance that builds coronary artery walls.  The amount of up- or down-regulation of this gene affects their elasticity and thickness.  The researchers compared this gene and its surrounding DNA between nine kinds of monkeys and apes, and between six human populations.  They claim to have found a trend among Europeans to possess a certain mutation that up-regulates the products of MMP3 (because it inhibits repressive factors).  This leads to less hardening of the arteries but more risk of blood clot induced heart attack or stroke (myocardial infarction).  The mutation changes one T to a C at a certain position on the gene.  Using molecular phylogenetic techniques, they estimated the mutation might have occurred in the European line anywhere from 36,600 to 2,200 years ago.  Maybe it came about in the Ice Age, they surmise, and natural selection acting on this mutation may have given Europeans dining on animal fat some protection from atherosclerosis.  Whatever, the selection probably did not act alone on that one gene, which only regulates other genes, but on a suite of genes due to pleiotropic effects (i.e., when one gene evolves, other unrelated phenotypic effects can result).
    The authors seemed happy to be able to provide an example of natural selection acting positively on a gene for a beneficial physiological effect: “The evolutionary forces of mutation, natural selection, and genetic drift shape the pattern of phenotypic variation in nature, but the roles of these forces in defining the distributions of particular traits have been hard to disentangle.”  (Emphasis added in all quotes.) 

Natural selection is an important factor influencing variation in the human genome, but most genetic studies of natural selection have focused on variants with unknown phenotypic associations.  This trend is changing.  New studies are rapidly revealing the effects of natural selection on genetic variants of known or likely functional importance….
These [studies on] variants [on genes with known phenotypic effects] are particularly interesting from an evolutionary standpoint because they are where the phenotypic rubber meets the road of natural selection – variants upon which natural selection could be having particularly direct effects.

Those assuming this was old news since Darwin’s day might be surprised at this admission that studies have rarely connected a mutation to an actual physical benefit.  Analyses at the molecular level of the gene, to be fair, have only recently become possible.  Stephen Wooding is greatly encouraged by this study.  He thinks it represents not only an exciting trend, but a new means of paving “an unusually direct path between ancient human history and modern human health.”  Rockman’s team claims that British men would have 43% more heart attacks had this mutation not occurred among their distant ancestors.  But then, since hardening of the arteries seems to be a recent malady among humans, he admitted that maybe the natural selection at the time was for something else “and the heart disease effect was incidental.”
    One other benefit Rockman claims for this study is that it shows natural selection can act not only on the genes the make proteins, but on the genes that regulate other genes– a factor he claims “traditional evolutionary biology has all but ignored.”  Considering the evolution of regulatory factors extends natural selection theory to the level of the “wiring diagram,” he says.  No longer should we just consider good genes and bad genes.  “Rather, there is a complex set of interactions” such that certain combinations might be best in one environment, others better in another.  “So we’re advocating a more nuanced view of how we view the genetic bases of disease,” he said in the press release from Duke University.

1Stephen Wooding, “Natural Selection: Sign, Sign, Everywhere a Sign,” Current Biology, Volume 14, Issue 17, 7 September 2004, Pages R700-R701, doi:10.1016/j.cub.2004.08.041.
2Rockman et al., “Positive Selection on MMP3 Regulation Has Shaped Heart Disease Risk,” Current Biology, Volume 14, Issue 17, 7 September 2004, Pages 1531-1539, doi:10.1016/j.cub.2004.08.051.

Remember the old moron jokes?  “How do you keep a moron busy for an hour?  Put him in a round room and tell him there’s a penny in the corner.”  It doesn’t take much to amuse Darwinists.  Tell them there’s a hint of natural selection in the human genome, and it is incredible the amount of work they will do to find it.  You can bet any claims will be ambiguous, hazy, uncertain, questionable and open to different interpretations, but if they can be offered in homage to buddha Charlie, it’s worth it to them to run in logical circles and keep up the candles of hope burning.  (For another example, look at this story on EurekAlert, about Penn State scientists “hunting illusive signs of natural selection” between Europeans and Africans, and finding only ambiguous signs of differing susceptibility to disease or milk intolerance.)
    What did these guys find, really?  One single-nucleotide polymorphism in just one gene out of hundreds that regulate heart health.  Sure, tweaking the regulation of this gene might put a person at risk for hardening of the arteries, but is Darwinian evolution the only explanation?  The Europeans could have descended from a clan whose grandpappy had the mutation at the Tower of Babel, for that matter; how could they prove otherwise?  The monkeys they studied had very different polymorphisms of these genes, and you don’t see them all keeling over from heart attacks.  If natural selection acted on this gene, why didn’t it act on Siberians or Eskimos or Australians or others at similar latitudes?  Did this mutation lead to a new organ or function or add to the genetic information?  No, it only tweaked the existing information.  And some evolution!  Pick your poison: increased risk of atherosclerosis, or increased risk of myocardial infarction.  Is this one of the finest examples they can find of the miracle-working mechanism of natural selection, the discovery that made Chairman Charlie famous, so powerful that during the same period of time it turned monkeys swinging from trees into humans writing books?
    The line about Ice Age men benefiting from the mutation because of their mammal-fat diet is comical.  How could that help the population genetics, if the individuals most likely got their heart attacks after having children?  The error bars on their dates are huge, even if one were to swallow the highly questionable phylogenetic techniques they used, and the evolution-based assumptions about mutation rates.  A chain of reasoning is only as strong as its weakest link: e.g., “if there was water on Mars, there might have been life, therefore there might have been intelligent life, therefore there might have been lawyers.”  Evolutionists get away with stacked assumptions only because they have ruled out anything other than naturalistic explanations.  Since the only contender is something akin to Darwinism, it’s the best they can offer (see Best-in-Field Fallacy).
    Why are we the only ones questioning the Darwinist spin on this paper, and asking the hard questions while the other science outlets mindlessly inherit the wind and parrot the spin with lines like “Heart gene yields insights into evolution”?  Why not consider the obvious, that a functioning circulatory system is a tremendous example of interrelated, functional design?  The diagnosis is simple.  It is that ancient human malady, hardness of heart.

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Categories: Human Body

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