Genetics News

Gene previously linked to obesity is unrelated

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From ScienceDaily:

A gene previously suspected of wielding the single greatest genetic influence on human obesity actually has nothing to do with body weight, according to a new study led by researchers at Harvard Medical School and Boston Children’s Hospital.

The work not only overturns a major finding about the genetics of obesity but also provides the first effective ways to analyze “particularly ornery and confusing” parts of the genome, such as the locus of this gene, said the study’s co-senior author, Steven McCarroll, assistant professor of genetics at HMS.

He analyzed genome-wide association data collected by the GIANT Consortium and found no association between AMY1 and body mass index, a measure of a person’s weight relative to their height. But because that region of the genome was so complicated, with AMY1 varying so widely (from two to 14 or more copies per person), he wasn’t sure his data told the whole story.

“There are hundreds of loci in the human genome with this kind of complexity. They have been like black holes in our knowledge of the human genome,” said McCarroll. “I think this is the beginning of a playbook for making sense of those regions.”

“If AMY1 had been a simple variant, it would have been really surprising to see opposite results like this,” said Hirschhorn. “We’ve established best practices for identifying and confirming simple variants, but complex variants are not at that stage yet. This is a younger field having its birth pangs.” More.

Of course, before we heard that, we had heard, in “Starchy Dangers in Human Evolution”:

Furthermore, variation in AMY1 copies may account for somewhere between 2.5% and 20% of all variation in risk of besity among people. Prior to this study, all of the hundreds of genetic variants found to be associated with obesity accounted together for only 2-4% of the genetic risk of obesity, or less than 3% of the overall risk of obesity.

Note that little damage is done to the overall credibility of human evolution claims that so many are shown to be incorrect. However inevitable, that outcome should detract from their credibility, not provide an excuse for lack thereof. But it doesn’t, because they are not really science claims in the first place.

See also: There’s a gene for that… or is there?:

… 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. …

Here’s the abstract:

Hundreds of genes reside in structurally complex, poorly understood regions of the human genome1, 2, 3. One such region contains the three amylase genes (AMY2B, AMY2A and AMY1) responsible for digesting starch into sugar. Copy number of AMY1 is reported to be the largest genomic influence on obesity4, although genome-wide association studies for obesity have found this locus unremarkable. Using whole-genome sequence analysis3, 5, droplet digital PCR6 and genome mapping7, we identified eight common structural haplotypes of the amylase locus that suggest its mutational history. We found that the AMY1 copy number in an individual’s genome is generally even (rather than odd) and partially correlates with nearby SNPs, which do not associate with body mass index (BMI). We measured amylase gene copy number in 1,000 obese or lean Estonians and in 2 other cohorts totaling ~3,500 individuals. We had 99% power to detect the lower bound of the reported effects on BMI4, yet found no association. (paywall) – Christina L Usher, Robert E Handsaker, Tõnu Esko, Marcus A Tuke, Michael N Weedon, Alex R Hastie, Han Cao, Jennifer E Moon, Seva Kashin, Christian Fuchsberger, Andres Metspalu, Carlos N Pato, Michele T Pato, Mark I McCarthy, Michael Boehnke, David M Altshuler, Timothy M Frayling, Joel N Hirschhorn, Steven A McCarroll. Structural forms of the human amylase locus and their relationships to SNPs, haplotypes and obesity. Nature Genetics, 2015; DOI: 10.1038/ng.3340

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3 Replies to “Gene previously linked to obesity is unrelated

  1. 1
    Mung says:

    That’s why studies like this should be done on cats. No such thing as a fat cat!

  2. 2
    bb says:

    I always liked this bit about genes by John Cleese: https://www.youtube.com/watch?v=-M-vnmejwXo

  3. 3
    bornagain77 says:

    Before neo-Darwinists claim that there is a particular gene FOR some particular trait, would it not help if they could define exactly what a gene actually is in the first place?

    Why the ‘Gene’ Concept Holds Back Evolutionary Thinking – James Shapiro – 11/30/2012
    Excerpt: The Century of the Gene. In a 1948 Scientific American article, soon-to-be Nobel Laureate George Beadle wrote: “genes are the basic units of all living things.”,,,
    This notion of the genome as a collection of discrete gene units prevailed when the neo-Darwinian “Modern Synthesis” emerged in the pre-DNA 1940s. Some prominent theorists even proposed that evolution could be defined simply as a change over time in the frequencies of different gene forms in a population.,,,
    The basic issue is that molecular genetics has made it impossible to provide a consistent, or even useful, definition of the term “gene.” In March 2009, I attended a workshop at the Santa Fe Institute entitled “Complexity of the Gene Concept.” Although we had a lot of smart people around the table, we failed as a group to agree on a clear meaning for the term.
    The modern concept of the genome has no basic units. It has literally become “systems all the way down.” There are piecemeal coding sequences, expression signals, splicing signals, regulatory signals, epigenetic formatting signals, and many other “DNA elements” (to use the neutral ENCODE terminology) that participate in the multiple functions involved in genome expression, replication, transmission, repair and evolution.,,,
    Conventional thinkers may claim that molecular data only add details to a well-established evolutionary paradigm. But the diehard defenders of orthodoxy in evolutionary biology are grievously mistaken in their stubbornness. DNA and molecular genetics have brought us to a fundamentally new conceptual understanding of genomes, how they are organized and how they function.
    http://www.huffingtonpost.com/.....07245.html

    Landscape of transcription in human cells – Sept. 6, 2012
    Excerpt: Here we report evidence that three-quarters of the human genome is capable of being transcribed, as well as observations about the range and levels of expression, localization, processing fates, regulatory regions and modifications of almost all currently annotated and thousands of previously unannotated RNAs. These observations, taken together, prompt a redefinition of the concept of a gene.,,,
    Isoform expression by a gene does not follow a minimalistic expression strategy, resulting in a tendency for genes to express many isoforms simultaneously, with a plateau at about 10–12 expressed isoforms per gene per cell line.
    http://www.nature.com/nature/j.....11233.html

    Time to Redefine the Concept of a Gene? – Sept. 10, 2012
    Excerpt: As detailed in my second post on alternative splicing, there is one human gene that codes for 576 different proteins, and there is one fruit fly gene that codes for 38,016 different proteins!
    While the fact that a single gene can code for so many proteins is truly astounding, we didn’t really know how prevalent alternative splicing is. Are there only a few genes that participate in it, or do most genes engage in it? The ENCODE data presented in reference 2 indicates that at least 75% of all genes participate in alternative splicing. They also indicate that the number of different proteins each gene makes varies significantly, with most genes producing somewhere between 2 and 25.
    Based on these results, it seems clear that the RNA transcripts are the real carriers of genetic information. This is why some members of the ENCODE team are arguing that an RNA transcript, not a gene, should be considered the fundamental unit of inheritance.
    http://networkedblogs.com/BYdo8

    Towards the latter half of the following podcast, Dr Sternberg, who has a PhD in evolutionary biology, elucidates how the overturning/loss of the ‘gene’ as the central unit of inheritance turns the modern synthesis of neo-Darwinism from a science into no better than the discarded alchemy or Ptolemy astronomy of yesteryear.

    Podcast – Richard Sternberg PhD – On Human Origins: Is Our Genome Full of Junk DNA? Part 5
    (emphasis on ENCODE and the loss of the term ‘gene’ as a accurate description in biology and how that loss undermines the modern synthesis of neo-Darwinism)
    http://www.discovery.org/multi.....-dna-pt-5/

    As well, the concept of the ‘selfish gene’, which has been called Dawkins’s single most important contribution to science, is now known to be a wrong concept:

    Die, selfish gene, die – The selfish gene is one of the most successful science metaphors ever invented. Unfortunately, it’s wrong – Dec. 2013
    Excerpt: But 15 years after Hamilton and Williams kited [introduced] this idea, it was embraced and polished into gleaming form by one of the best communicators science has ever produced: the biologist Richard Dawkins. In his magnificent book The Selfish Gene (1976), Dawkins gathered all the threads of the modern synthesis — Mendel, Fisher, Haldane, Wright, Watson, Crick, Hamilton, and Williams — into a single shimmering magic carpet (called the selfish gene).
    Unfortunately, say Wray, West-Eberhard and others, it’s wrong.
    http://www.uncommondescent.com.....-heard-of/

    At the 10:30 minute mark of the following video, Dr. Trifonov states that the concept of the selfish gene ‘inflicted an immense damage to biological sciences’, for over 30 years:

    Second, third, fourth… genetic codes – One spectacular case of code crowding – Edward N. Trifonov – video
    https://vimeo.com/81930637

    Also of related interest, we are not such helpless victims of our ‘genes’ as neo-Darwinists would have us believe, but have a certain measure of control over gene expression:

    Scientists Finally Show How Your Thoughts Can Cause Specific Molecular Changes To Your Genes, – December 10, 2013
    Excerpt: “To the best of our knowledge, this is the first paper that shows rapid alterations in gene expression within subjects associated with mindfulness meditation practice,” says study author Richard J. Davidson, founder of the Center for Investigating Healthy Minds and the William James and Vilas Professor of Psychology and Psychiatry at the University of Wisconsin-Madison.
    “Most interestingly, the changes were observed in genes that are the current targets of anti-inflammatory and analgesic drugs,” says Perla Kaliman, first author of the article and a researcher at the Institute of Biomedical Research of Barcelona, Spain (IIBB-CSIC-IDIBAPS), where the molecular analyses were conducted.,,,
    the researchers say, there was no difference in the tested genes between the two groups of people at the start of the study. The observed effects were seen only in the meditators following mindfulness practice. In addition, several other DNA-modifying genes showed no differences between groups, suggesting that the mindfulness practice specifically affected certain regulatory pathways.
    http://www.tunedbody.com/scien.....ges-genes/

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