Genetics Human evolution Intelligent Design

Do all genes affect every complex trait?

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The more closely geneticists look at complex traits and diseases, the harder it gets to find active genes that don’t influence them.

From Veronique Greenwood at Quanta:

Mutations of a single gene are behind sickle cell anemia, for instance, and mutations in another are behind cystic fibrosis.
But unfortunately for those who like things simple, these conditions are the exceptions. The roots of many traits, from how tall you are to your susceptibility to schizophrenia, are far more tangled. In fact, they may be so complex that almost the entire genome may be involved in some way…

One very early genetic mapping study in 1999 suggested that “a large number of loci (perhaps > than 15)” might contribute to autism risk, recalled Jonathan Pritchard, now a geneticist at Stanford University. “That’s a lot!” he remembered thinking when the paper came out.

Over the years, however, what scientists might consider “a lot” in this context has quietly inflated. Last June, Pritchard and his Stanford colleagues Evan Boyle and Yang Li (now at the University of Chicago) published a paper about this in Cell that immediately sparked controversy, although it also had many people nodding in cautious agreement. The authors described what they called the “omnigenic” model of complex traits. Drawing on GWAS analyses of three diseases, they concluded that in the cell types that are relevant to a disease, it appears that not 15, not 100, but essentially all genes contribute to the condition. The authors suggested that for some traits, “multiple” loci could mean more than 100,000. More.

This isn’t the Darwinism we were promised.

Hat tip: Philip Cunningham

See also: New book from Michael Behe on how today’s DNA findings “devolve” Darwin. Devolution… at last, something Darwinism really explains! How odd that genome mapper and theistic evolutionist Francis Collins should have helped kill Darwinism before he got most Christians to buy into it.

4 Replies to “Do all genes affect every complex trait?

  1. 1
    bornagain77 says:

    The article News highlighted in the OP makes the genotype-phenotype mapping problem that much worse for neo-Darwinists. Here are few notes to that throw a little light on just how bad the genotype-phenotype mapping problem now is for Darwinists:

    The next evolutionary synthesis: from Lamarck and Darwin to genomic variation and systems biology – Bard – 2011
    Excerpt: If more than about three genes (nature unspecified) underpin a phenotype, the mathematics of population genetics, while qualitatively analyzable, requires too many unknown parameters to make quantitatively testable predictions [6]. The inadequacy of this approach is demonstrated by illustrations of the molecular pathways that generates traits [7]: the network underpinning something as simple as growth may have forty or fifty participating proteins whose production involves perhaps twice as many DNA sequences, if one includes enhancers, splice variants etc. Theoretical genetics simply cannot handle this level of complexity, let alone analyse the effects of mutation..
    http://www.biosignaling.com/co.....X-9-30.pdf

    With a Startling Candor, Oxford Scientist Admits a Gaping Hole in Evolutionary Theory – November 2011
    Excerpt: As of now, we have no good theory of how to read [genetic] networks, how to model them mathematically or how one network meshes with another; worse, we have no obvious experimental lines of investigation for studying these areas. There is a great deal for systems biology to do in order to produce a full explanation of how genotypes generate phenotypes,,,
    http://www.evolutionnews.org/2.....52821.html

    Not Junk After All—Conclusion – August 29, 2013
    Excerpt: Many scientists have pointed out that the relationship between the genome and the organism — the genotype-phenotype mapping — cannot be reduced to a genetic program encoded in DNA sequences. Atlan and Koppel wrote in 1990 that advances in artificial intelligence showed that cellular operations are not controlled by a linear sequence of instructions in DNA but by a “distributed multilayer network” [150]. According to Denton and his co-workers, protein folding appears to involve formal causes that transcend material mechanisms [151], and according to Sternberg this is even more evident at higher levels of the genotype-phenotype mapping [152]
    http://www.uncommondescent.com.....onclusion/

    The Fairyland of Evolutionary Modeling – May 7, 2013
    Excerpt: Salazar-Ciudad and Marín-Riera have shown that not only are suboptimal dead ends an evolutionary possibility, but they are also exceedingly likely to occur in real, developmentally complex structures when fitness is determined by the exact form of the phenotype.
    http://www.evolutionnews.org/2.....71901.html

    As the preceding articles strongly indicated, phenotypic traits in general, and Biological Form in particular, simply are not reducible to Darwinian explanations

    Darwinism vs Biological Form – video
    https://www.youtube.com/watch?v=JyNzNPgjM4w
    Excerpt: to state what should be glaringly obvious, since neo-Darwinian explanations are grossly inadequate for explaining how any particular organism might achieve its basic form, then neo-Darwinian speculations for how one type of organism might transform into another type of organism are based on pure fantasy and have no discernible experimental basis in reality.

    And here are a few more references that further back up the claim made in the OP:

    Gene previously linked to obesity is unrelated – June 29, 2015
    Excerpt: … in the real world of careful analysis, scientists are just not finding the “genes” that the headline writers need. British geneticist Steve Jones points out that most human traits are influenced by so many genes that there is no likely systematic cause and effect:
    “We know of more than 50 different genes associated with height … That has not percolated into the public mind, as the Google search for “scientists find the gene for” shows. The three letter word for — the gene FOR something — is the most dangerous word in genetics.”
    And the craze is not harmless, he warns. …
    http://www.uncommondescent.com.....unrelated/

    What If (Almost) Every Gene Affects (Almost) Everything? – JUN 16, 2017
    Excerpt: If you told a modern geneticist that a complex trait—whether a physical characteristic like height or weight, or the risk of a disease like cancer or schizophrenia—was the work of just 15 genes, they’d probably laugh. It’s now thought that such traits are the work of thousands of genetic variants, working in concert. The vast majority of them have only tiny effects, but together, they can dramatically shape our bodies and our health. They’re weak individually, but powerful en masse.
    https://www.theatlantic.com/science/archive/2017/06/its-like-all-connected-man/530532/

  2. 2
    Bob O'H says:

    This isn’t the Darwinism we were promised.

    Why not? Isn’t the infinite alleles model precisely what has been modelled in quantitative genetics (e.g. by R.A.Fisher)?

  3. 3
    bornagain77 says:

    You mean the model that gave us ‘genetic load’ ‘neutral evolution’ and the now falsified ‘prediction’ of junk DNA?

    So where is the ‘real’ model of Darwinian evolution that shows us how, instead of breaking stuff, Darwinian processes can actually create genetic coding and molecular machines that far outclass anything man has yet engineered?

    The plain fact of the matter is that Darwinian Evolution does not even qualify as a real science!

    Stanford Professor Paul Ehrlich stated that the Theory of Evolution ‘cannot be refuted by any possible observations’ and is thus “outside empirical science.”

    “Our theory of evolution has become, as Popper described, one which cannot be refuted by any possible observations. Every conceivable observation can be fitted into it. It is thus “outside empirical science” but not necessarily false. No one can think of ways in which to test it. Ideas, either without basis or based on a few laboratory experiments carried out in extremely simplified systems have attained currency far beyond their validity. They have become part of an evolutionary dogma accepted by most of us as part of our training. The cure seems to us not to be a discarding of the modern synthesis of evolutionary theory, but more skepticism about many of its tenets.”
    Ehrlich, Paul and L.C. Birch (1967), “Evolutionary History and Population Biology,” Nature, 214:349-352, April 22, p. 352

    Darwin’s Theory vs Falsification – video
    https://www.youtube.com/watch?v=8rzw0JkuKuQ

    Darwinian Evolution vs Mathematics
    https://www.youtube.com/watch?v=q3gyx70BHvA

  4. 4
    bornagain77 says:

    or is that the model that Bill Basener and John Sanford recently corrected the false assumptions in?

    Defending the validity and significance of the new theorem “Fundamental Theorem of Natural Selection With Mutations, Part I: Fisher’s Impact – Bill Basener and John Sanford – February 15, 2018
    Excerpt: While Fisher’s Theorem is mathematically correct, his Corollary is false. The simple logical fallacy is that Fisher stated that mutations could effectively be treated as not impacting fitness, while it is now known that the vast majority of mutations are deleterious, providing a downward pressure on fitness. Our model and our correction of Fisher’s theorem (The Fundamental Theorem of Natural Selection with Mutations), take into account the tension between the upward force of selection with the downward force of mutations.,,,
    Our paper shows that Fisher’s corollary is clearly false, and that he misunderstood the implications of his own theorem. He (Fisher) incorrectly believed that his theorem was a mathematical proof that showed that natural selection plus mutation will necessarily and always increase fitness. He also believed his theorem was on a par with a natural law (such as entropic dissipation and the second law of thermodynamics). Because Fisher did not understand the actual fitness distribution of new mutations, his belief in the application of his “fundamental theorem of natural selection” was fundamentally and profoundly wrong – having little correspondence to biological reality. Therefore, we have reformulated Fisher’s model and have corrected his errors, thereby have established a new theorem that better describes biological reality, and allows for the specification of those key variables that will determine whether fitness will increase or decrease.
    http://theskepticalzone.com/wp.....rs-impact/

    Thus, once again, the more rigorously one tries to bring Darwinian assumptions into line with biological and physical realities, the more those biological and physical realities falsify those Darwinian assumptions.

    Of related note:

    The waiting time problem in a model hominin population – 2015 Sep 17
    John Sanford, Wesley Brewer, Franzine Smith, and John Baumgardner
    Excerpt: The program Mendel’s Accountant realistically simulates the mutation/selection process,,,
    Given optimal settings, what is the longest nucleotide string that can arise within a reasonable waiting time within a hominin population of 10,000? Arguably, the waiting time for the fixation of a “string-of-one” is by itself problematic (Table 2). Waiting a minimum of 1.5 million years (realistically, much longer), for a single point mutation is not timely adaptation in the face of any type of pressing evolutionary challenge. This is especially problematic when we consider that it is estimated that it only took six million years for the chimp and human genomes to diverge by over 5 % [1]. This represents at least 75 million nucleotide changes in the human lineage, many of which must encode new information.
    While fixing one point mutation is problematic, our simulations show that the fixation of two co-dependent mutations is extremely problematic – requiring at least 84 million years (Table 2). This is ten-fold longer than the estimated time required for ape-to-man evolution. In this light, we suggest that a string of two specific mutations is a reasonable upper limit, in terms of the longest string length that is likely to evolve within a hominin population (at least in a way that is either timely or meaningful). Certainly the creation and fixation of a string of three (requiring at least 380 million years) would be extremely untimely (and trivial in effect), in terms of the evolution of modern man.
    It is widely thought that a larger population size can eliminate the waiting time problem. If that were true, then the waiting time problem would only be meaningful within small populations. While our simulations show that larger populations do help reduce waiting time, we see that the benefit of larger population size produces rapidly diminishing returns (Table 4 and Fig. 4). When we increase the hominin population from 10,000 to 1 million (our current upper limit for these types of experiments), the waiting time for creating a string of five is only reduced from two billion to 482 million years.
    http://www.ncbi.nlm.nih.gov/pm.....MC4573302/

    Genetic Entropy – references to several peer reviewed numerical simulations analyzing and falsifying all flavors of Darwinian evolution (neutral theory included),, (via John Sanford and company)
    http://www.geneticentropy.org/#!properties/ctzx

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