DNA Deniers


From Michael Pollan:


Michael Pollan and his flock became all aerated the other day when Michael tweeted this tidbit. It links to a story with quite the title:

The Great DNA Data Deficit: Are Genes for Disease a Mirage?

Srsly. That’s what it says.

What do I think this is? The second case of gene denialism that I have observed. (The first was a group disputing autism genes.)

I knew that after the genome came along there would be woo. I knew that snake-oil salesmen would be pitching purchases that would work with your skin genes. I knew there would be anti-aging compounds that work with your genes. I know there’s already a DNA diet, and vitamins sold to you based on your DNA. I’ve seen DNA dating. But honestly, I didn’t expect the DNA deniers.

Probably I should have seen it coming. I’ve followed a couple of different topics that flow with anti-science woo: anti-vaxxers and anti-GMOsters. There is overlap between these groups, but it’s not complete. But there is remarkable coincidence between their argument styles. Both groups make big claims, mostly unsourced–or if sourced are cherry-picked points or entirely misused. And when the science isn’t going their way, they deny the science, and then they move the goal posts.

This article–which purportedly blows away the connection between genes and disease–is appallingly mistaken. Let me be clear: genes can influence disease risk. Period. Of course environment may influence biology. Diet and exercise can affect health, certainly. Exposure to natural or man-made carcinogens can trigger cancer. And even the hardest core gene jocks know this.  But this desire to sever the connection between genes and diabetes–or prostate cancer, or Crohn’s disease–because they haven’t found a single smoking gun gene yet, using one kind of study?  That’s just bizarre and twisted. There are numerous examples of leads on complex disorders that are quite strong, insights into disease pathways and mechanisms, and we’ve really just started. And new technologies are opening new paths as well. A nice article on this was in Nature this fall: Genomics: The search for association.

Sure, we’ve wanted more data and stronger signals from GWAS (genome-wide association studies). But it turns out humans are inveterate outbreeders and it’s hard to tease out strong pointers from them.

Probably if you are a regular reader of this blog I don’t need to convince you of that. But for anyone else who stumbles across this let me offer some resources:

What I can’t quite figure out is why the authors of that post attempt to discredit all the work and all of the discoveries that have been made so far–and those we are going to unearth. As a relatively new strategy, and as we refine the tools, the populations study groups, and build on new knowledge, we are going to find more. And much had been done–check out the GWAS Catalog for an overview. Scroll down. And keep scrolling. As it says on that page: “As of 12/09/10, this table includes 725 publications and 3606 SNPs.

And I also can’t figure out why Pollan’s minions are celebrating this. Here are samples of the responses to this:

If this was true (which it certainly isn’t), why would this be a reason to chuckle? Why celebrate? I honestly don’t get it. The actual emotion ought to be embarrassment for the credulity.

But ok, you aren’t down with the human GWAS data right now–let’s look at other GWAS and see what’s coming out of that. There have been some really stunning examples of these studies in dogs. There was a talk a couple of years back that we watched: Genes for Complex Traits in the Domestic Dog. You can watch that online to learn more. An advantage of working with dogs is that they are highly inbred. A professor of mine in grad school once snarked that we can’t do that with humans–although that was part of the purpose of the Ivy League, he claimed–a couple of hundred years of intensive breeding and good pedigree records make gene hunting in the canine genome somewhat easier than it is in the messy human populations. Here’s another recent article on dog traits in NatureIf you think that genes don’t cause complex disorders, you have to dispute that some dog breeds are prone to anxiety due to their genes. And that some are prone to deafness–it’s clearly the Dalmatian lifestyle, right? Or that dobermans are bringing their narcolepsy on themselves somehow. [Seriously--they are narcoleptic? Who knew....]

Clearly the authors have an agenda. At the end they make their case:

Nevertheless, most governments cooperate far more, for example, with their food industries than with those who wish to eat a healthy diet. The laying to rest of genetic determinism for disease, however, provides an opportunity to shift this cynical political calculus. It raises the stakes by confronting policy-makers as never before with the fact that they have every opportunity, through promoting food labeling, taxing junk food, or funding unbiased research, to help their electorates make enormously positive lifestyle choices.

Author Latham goes further at HuffPo (home to mucho woo of many stripes) emphasis mine:

­That means environment must be the entire cause of ill health, i.e. junk food, pollution, lack of exercise, etc. The reason we wrote an article about human genetics (when we are a food and agricultur­e website) is that we believe that if people live right, agricultur­e and therefore the planet will more or less fix itself.

I don’t care if you want to discredit the food industry and if you hate Big Ag and want to say so on your own blog. But misusing and discrediting science and the efforts of scientists that have nothing to do with that is a stupid and flawed strategy. And Michael Pollan: please use better judgment before hitching your agenda to deniers.

This piece of tripe is one of those sorts of sciency-ness things that Mike the Mad Biologist once hailed as having The Asymmetric Advantage of Bullsh-t.  It has multiple levels of crap. And there isn’t a comment feature on it, so you can’t discuss it over at their site. I will look for other responses to this item and collect them here if I find them, or add them in the comments if you have them.  Anyway, I’m sure someone will take on the #FAIL in other parts of that post–there are plenty of opportunities. I wanted to address the denial aspect.  I agree with Deanna–wow–and I’d love to see a good Fisking by Genomes Unzipped–and it may be coming.

Top tweet on this so far goes to @emmecola:

But scientists, my plea to you: don’t let the DNA deniers get a foothold on this topic. We’ve seen what happened with anti-vaxxers. Like that group, this could affect the public health if people start dismissing real risks of colon cancer and subsequent screenings, or forgoing treatment for their psychiatric disorders because someone told them they could fix it with an organic carrot. There are real consequences to this.

Baker, M. (2010). Genomics: The search for association Nature, 467 (7319), 1135-1138 DOI: 10.1038/4671135a

Cyranoski, D. (2010). Genetics: Pet project Nature, 466 (7310), 1036-1038 DOI: 10.1038/4661036a

1. Here’s a take on it from Genomes Unzipped: Estimating Heritability Using Twins

2. Here’s a take at HuffPo–fount of crap science: Is There a Genie in the Genome? I am embarrassed to link to it, but did think this bit was funny: “suggests that genomics is one part boondoggle, one part conspiracy by the military-industrial establishment.” Snorf.

3. Oh, my–look what the twitter fairies just dropped on my desk. An evidence-based review of diabetes:  Genomics, Type 2 Diabetes, and Obesity and be sure to look especially at Table 1.

4. Another discussion of it from Mike at ScienceBlogs: GWAS FIGHT! (Hiss! Snarl!): Déja Vu All Over Again and check out Daniel MacArthur’s comment over there #FTW.  (Hat tip to GenomeWeb).

5. Oh, FFS: Marion Nestle catches teh stupid too. And Marion–this is not a “study”. It’s a polemic. You should know better than that. You have an appropriate degree. Pollan I can sorta cut some slack–he’s got an English art degree. 6. And Daniel brings the shredder. This is great: Bioscience Resource Project critique of modern genomics: a missed opportunity

7. ROFL: Keith snarks it up with this title: The Great Health Data Deficit: Are Environmental causes for Disease a Mirage? That was a fun start to my day.

8. my GenomiX summarizes the conflama with La complessità dei viventi è un dato di fatto. Teh Google tells me this says “The complexity of living beings is a fact”. Sì. (By the way, translators are getting much better–I think. That looked great to me.)

9. Mary Carmichael #FTW–she does a multi-media smackdown of “environmental determinism” with a great essay and accompanying video.

10. Mike the Mad Biologist weighs in with: On Genetic Denialism

33 thoughts on “DNA Deniers

  1. Moreno

    Hey thanks for giving the “Top Tweet” to me! :-) (By the way, Homer Simpson is really cited there!)

    The fact that diet and lifestyle have a strong influence is true, everybody knows that. But we don’t have to choose genetic determinism OR genetic denialism: the truth is somewhere between the two.

  2. Mary Post author

    That cracked me up.

    People want simple answers, unfortunately. A lot of people aren’t willing or able to deal with complexity.

    I just hate that someone with a megaphone the size of Michael Pollan’s is spreading this.

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  4. Keith Grimaldi

    Congrats to @emmecola – truly deserved!

    re the article, it’s too too long and it reminds me of the streets of Napoli, near where I live, as the world will know, they are full of rubbish.

    This short quote from the article says most of what needs saying: “genetic predispositions (i.e. causes)”

    Melanoma is a complex disease, it’s caused by UV from the sun isn’t it? But why don’t all those Africans and Australian aborigines get it then? Ah yes, it’s caused by those white skin genes, sorry. Hang on maybe it involves both, maybe white skin is a genetic predisposition (bravo Homer…)

    It’s a totally stupid article and the authors must surely know it. I believe that they do have an agenda rather than being totally stupid themselves. Maybe they are quite aware of the distortions and plain untruths but they justify it to themselves because they think genetic determinism is too strong. Indeed some scientists and many journalists are guilty of exaggerating the role of genes but that’s no excuse.

    In their resources section they link to the UK’s Genewatch – now they are gene deniers par excellence, have been for a decade or so. I guarantee that in almost all their comments on commercial genetics there will be the phrase “the marketing of fear”

    So NO their mission is not: “To provide the highest quality scientific information and analysis to enable a healthy food system and a healthy world.” http://bit.ly/f4q0Mq

    It’s something else

  5. Trey

    You know, I loved Omnivore’s Dilemma and In Defense of Food. I think he describes well how our food system and our diet affect our health. I actually agree with the mantra “eat (whole/minimally-processed) food, less of it, mostly plants” and that this way of eating is the healthiest for the vast majority of people.

    So it’s sad that he’s decided to jump of the woo cliff and extrapolate what is basically true into some denial of science in toto.

  6. Mary Post author

    @Keith: that’s a good example too. I decided to use the dog ones because sometimes I find that people are able to separate out what they know about dogs rather than what they want to think about themselves. And I hope the idea that Dalmatians are causing their own deafness with lifestyle (what, are they going to loud concerts on the weekends??) would be absurd enough to stick with people.

    Yeah, it was full of rubbish. But it had a veneer of science to it, and I was worried that people would be taken in by it. And clearly Pollan was.

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  8. JRLatham

    I am struggling to understand your comments which are long on insults “faux science”; “full of rubbish”; “distortions and plain untruths” and “multiple levels of crap” for a science blog. I had hoped for more constructive points but I suspect that your comments will just put curious people off from reading what is a serious contribution. That would be a pity.

    Re your scientific comments. The article cites the Lucia Hindorff paper announcing the catalogue of GWA studies, though not the website. There is no need to impute ignorance on our part. Certainly, there are lots of studies. Our point is they are not finding either the individual major genes or the total genetic contribution predicted. This is undeniably a big problem for medicine, personalised genomics and explaining disease in general as a genetic phenomenon.

    Secondly, the insights into disease mechanisms only may turn out to be valuable. Many people think they are of NO value. The companies consider they have more than enough drug targets already.

    Lastly, when you propose this is about denying DNA you are misrepresenting the article. The article is very clearly about “COMMON DISEASES” and not monogenic or rare disorders, NOR is it denying genetic variation for other traits, like behaviour in dogs.


  9. Mary Post author

    @JRLatham: Wrong. Again. Your title belies you. Your conclusions about the “laying to rest” and the laughable press release claims:

    The case for a substantial role of genes in susceptibility to the major human diseases is now scientifically refuted argues a groundbreaking new analysis published by the public interest science organization, The Bioscience Resource Project.

    Major. Human. Diseases.

    and this:

    “to find important human disease genes”.

    We see what you are trying to do. And you might be able to pull the wool over on Pollan and GeneWatch, but you can’t do it to us.

  10. Trey


    The dog study, as with many similar organismal studies, do not point to just ‘behavior’ but to other complex traits like diseases and conditions (deafness?). And that’s an important scientific point you have glossed over. Model organisms are pointing to information we can not yet get yet from GWAS in humans because human populations and genomics are much more complex. The lack of evidence to date (and it’s not near the paucity you suggest) does not suggest no evidence.

    Environment does indeed play a huge part in common human disease, but to suggest it is the only player is to misunderstand science and to fall into the false dichotomy of nature vs. nurture.

    I’d like to suggest family health pedigrees which have been used for a long time for their predictive value as a strong indication that many common diseases are indeed genetic in basis, while at the same time having large environmental influences.

    It’s just not good science to declare ‘victory’ in the nature vs. nurture debate when there is no victory ever to be had.

  11. Moreno


    In my humble opinion you’re wrong because you come to your conclusions too fast. GWAS can be seen as a Yes/No question, and obviously we cannot expect to find simple answers when instead the answers are complex. But this doesn’t mean that genes have not a role at all.

    What you call “unlikely places” to find missing heritability (gene-gene interactions, rare variants, CNVs, epigenetics..) are in my opinion quite likely instead, and since we are studying them seriously only recently we would rather wait these new results before denying the role of genetics in common diseases.

  12. Keith Grimaldi

    @JRLatham – you are wrong in many places. To say”genetic predispositions (i.e. causes)” is inexcusable in an article that pretends to be an expert commentary on genetics and disease causation.

    “Our point is they are not finding either the individual major genes or the total genetic contribution predicted”

    Predicted by only some people… you ignore the many who predicted that pure genetic/disease association studies, without any measure of the environment (especially diet and lifestyle) would not yield strong risk associations. For very good logical reasons. GWAS has nevertheless done pretty well at sorting out many of the genes involved in many of the pathways implicated in the complex diseases. Next level studies have been are are ongoing where the environmental effects TOGETHER with genetics are being measured.

    Common complex diseases – they are not just environmental nor are they just genetic. I don’t recall seeing articles or blogs proposing the latter, yours though proposes the former but offers no evidence for it and ignores all the evidence against it.

  13. Keith Grimaldi

    @JRLatham I just said you are wrong in many places, well you’re wrong here too: http://huff.to/gU5qAd

    “The ‘one health’ concept is an excellent one. All things are indeed connected…We have just reported that genetics now demonstrat­es that genes cannot be the cause of common disease…That means environmen­t must be the entire cause of ill health”

    The ENTIRE cause? really, that’s what you want to say? Genes have no role at all in the common diseases? Certainly there is NO evidence presented by you for that claim. None. Also you never reference in your article where anyone has actually said that genes (alone) cause common disease.

    Genes x Environment, you can’t choose one or the other

  14. Anastasia

    @Keith Grimaldi

    The authors of The Bioscience Resource Project certainly do fail at their mission “To provide the highest quality scientific information and analysis to enable a healthy food system and a healthy world.”

    Their articles contain just enough legitimate information to get you to let your guard down and then they slip in some nonsense.

    An example I found recently is “The AquaBounty Salmon: Will the World’s First Commercial GE Animal Be an Albatross?” where they freak out about multiple insertions of the transgene and all the unintended consequences and then at the bottom in a little footnote, way after most people who were just there to confirm their own preconceived notions had stopped reading, they put “There is unlikely to be an unlinked transgene since the AquAdvantage salmon has been backcrossed six times.”

    The problem isn’t that they make mistakes – we all do. It’s that they make mistakes and then don’t have a comment section so no one can offer corrections. To me, that’s making mistakes and then being cocky about it. Some of the “mistakes” have me wondering if they’re intentionally trying to mislead because the authors have enough training so that they should know better. Not cool.

    @ Mary

    Thanks very much for writing this post. I saw Pollan’s tweet, read the article, thought, “woah, that’s a pile of ****” but haven’t had time to write anything about it. This is a a great take down!

  15. Mary Post author

    @Anastasia: I had seen the other dross over there and have also looked up comments by JRLatham elsewhere on the web. And you have pinged the strategy exactly–enough legit information with some references to look sciency, and then nonsense and malformed conclusions.

    There are a couple of options:
    1) That everyone is misreading this post. If everyone is coming to the conclusion that “human disease is primarily of environmental and not inherited origin” (which comes straight out of the press release, and has been repeated around the web) and that the “the gene-disease paradigm appears to be collapsing” or that people are now under the impression that brown rice can determine whether or not you get schizophrenia, and that’s not what these authors intended–then they suck as communicators.


    2) That’s exactly the conclusion that they wanted the naive and non-science-based folks to come to. That makes them deceptive and manipulative.

    I’m leaning to option 2. But if they wanted to correct the impressions they’ve given people all over the intertubz I’d be willing to look at that. I would expect it to be full of weasel-wording and more half-assed sleights of hand.

  16. Anastasia

    Mary, there is an option 3!

    It is possible that they just don’t know what they’re talking about so make gross errors despite being good communicators and having good intentions*.

    *Of course, one hopes this isn’t the case because the 2 main contributors to the site do have PhDs in relevant subjects.

  17. Mary Post author

    @Anastasia: How generous of you. But ok–if they want to correct errors I’d have a look at the corrections.

    Maybe they could use this as an example. I happen to be working on our update for the dbGaP tutorial today (I should have listed dbGaP in the resources– http://www.ncbi.nlm.nih.gov/gap ). The example we use is Crohn’s disease.

    Here’s a page about that GWAS study:

    You can see right on that page some publications. If the BSR team would like to show me where these researchers are wrong, I’d look. Of course, they’d also have to explore the subsequent confirmations of this result. A search of Pubmed.gov with the search terms “il23r[All Fields] AND crohn’s[All Fields]” leads us to a number of additional papers. But here are 2 particularly recent and useful ones:

    Replication and meta-analysis of 13,000 cases defines the risk for interleukin-23 receptor and autophagy-related 16-like 1 variants in Crohn’s disease.


    Pathway analysis comparison using Crohn’s disease genome wide association studies.

    All of these papers are freely available, so there’s no excuse of behind a firewall.

    If Pollan or Philpott would want to take those on too, I’d be happy to look.

  18. Karl Haro von Mogel

    “That means environmen­t must be the entire cause of ill health, i.e. junk food, pollution, lack of exercise, etc. The reason we wrote an article about human genetics (when we are a food and agricultur­e website) is that we believe that if people live right, agricultur­e and therefore the planet will more or less fix itself. Because there is indeed only ‘one health’. Bravo!”

    There is only One True Health and Jonathan Latham is his Prophet. One more reason why the Bioscience Resource Project should be doubted. Its really not about resources, but a weird narrow advocacy using science as a mantle. This comment of his is very easily debunked, and you don’t even have to go into discussions of allelic variation as contributing factors with additive effects that influence disease. All you need are two words: Muscular Dystrophy. Done.

    I’m not sure if Latham is still in Ithaca, NY, but he should meet up with John Sanford, also from that area. They’ve got a lot in common.

  19. JRLatham

    Hi Moreno
    We can indeed have legitimately different opinions on how unlikely are the what we call “unlikely places” to be hiding genetic variation but the fact that until recently we were hardly studying these alternative places much at all suggests strongly that until the GWA studies delivered their negative results ”highly unlikely” was everyone else’s view too. Our inference is that the push to study epigenetics, CNVs, rare variants etc. is being driven not by scientific rigour but by the need to keep the genetic bandwagon on the road.

  20. Mary Post author

    @JRLatham: Please see everyone’s smack-downs of your work around the web. Your errors and misrepresentations are all addressed somewhere. The updates I have provided (and will continue to add as I find them) offer you more opportunity to flail if that’s what you want.

    But that said, as I wrote over at Genetic Future–you are a classic denier:

    He’s doing the classic “god of the gaps” strategy: when science hasn’t found the answer I want, I get to make up the gap-filler! It’s precisely what the anti-vax/autism argument does: science refuses to find my pet cause, so I’m going assert what I want anyway!

    I know this is part of a broader effort by folks who share your anti-science views who want to interfere with biotech funding and what might lead to wider acceptance of GMOs. It’s an attempt to undermine the consensus view of the science. We have your number, dude.

  21. Keith Grimaldi

    @JRLatham – it would be good for you to correct your most basic errors before carrying on with your denial

    you say … ”genetic predispositions (i.e. causes)”

    This is a howler. Genes are not causes. we can agree that environment causes all common complex diseases – genes actually cause nothing, they code for (mainly) proteins. Common complex diseases are the result of environmental causes in genetically pre-disposed individuals – that’s the simplest theory that fits with the evidence and is a long way from being refuted.

    What GWAs and all the rest of the genetic “bandwagon” is trying to identify is the genetics of the predispositions.

  22. Trey


    “…but the fact that until recently we were hardly studying these alternative places much at all suggests strongly that until the GWA studies delivered their negative results ”highly unlikely” was everyone else’s view too. Our inference is that the push to study epigenetics, CNVs, rare variants etc. is being driven not by scientific rigour but by the need to keep the genetic bandwagon on the road.”

    This comment is a clear misreading of the recent (last 50 years) history of science and misunderstanding of how science is done.

    “until recently we were hardly studying these alternative places”
    is a direct falsehood. I spent most of the decade of the 90′s studying the evolution of retrotransposable elements. We knew since the 50′s that transposable elements had a major effect on the human genome. Hundreds of scientists have been studying these “alternative places” for decades. Many (Barbara McKlintock, Andrew Zire, etc come to mind) have won Nobel prizes for research in these “alternative places”. It has been quite well known in the last few decades, and especially since the HGP, that these “alternative places” are very important in evolution and disease. So the statement you make is, to be polite, false. Some alternative places, miRNA and CNV for example, have only come to light in the last decade (after decades of research).

    But let’s look at the last part of that statement too. Science works exactly the way you try to make out to be some sort of conspiracy (at worst) or ‘bandwagon’ (at best). Science has evidences, questions and hypotheses. We attempt to find answers through several avenues. If one doesn’t pan out, we go to the other. We find new evidences and questions along the way. The research has to follow the evidence. The evidence is that our genome in all it’s complexity has a huge effect on disease. What science does _not_ do, as you have done, is make a sweeping conclusion (environment is the only source of common disease!!!) based on a lack of evidence on one line of research. You have taken a side on a false dichotomy (environment/genetics, nurture/nature), and it is a very false dichotomy, and are staking a claim to that side based on air. Believing a false dichotomy against all evidence and staking a claim to one side… it’s really bad science.

  23. JRLatham

    those people who read all the way to the footnotes will find this:
    (1) ‘Genes for’ disease is shorthand for genetic variants predisposing the carrier to disease.

    Just for your satisfaction-’gene variants’ vary in their penetrance. Some, such as the Huntington’s disease gene are more or less 100% penetrant. They are commonly held to ’cause’ the disease. Those alleles that are less than 100% penetrant predispose to disease. There is a continuum of penetrance that is not the equivalent of common definitions of the words ’cause’ or ‘predispose’.


  24. Moreno


    You say that these other variations have been hardly studied until now because they were considered highly unlikely. Maybe they were not studied deeply simply because we lacked a technology that could identify them in the same fast and straighforward way as it has been done with SNPs.

    Moreover, even if you’re right on this point, science works step by step: you have an hypothesis and you try to prove it with an experiment. The problem here is that this was a very big hypothesis and many years of experiments were needed to realize that single genes cannot cause diseases (generally). So now we should move to other hypothesis. That’s science!

    Just some examples now. This year I read a paper in which a fat diet caused an epigenetic modification in rats which was passed to the offspring, which in turn was more likely to develop diabetes. Epigenetics can also turn a bee into a queen, and queen and workers are extremely different from a phenotypic point of view. So, epigenetics is powerful. Maybe we should focus on that. It could partially “reconcile” genes and environment (diet can produce epigenetic changes).

  25. Keith Grimaldi

    @JRLatham – thanks for the genetic lesson

    So when you say that there is a “continuum of penetrance” I guess you are saying that genes are actually very important in disease after all. 100% for Huntingdon’s all the way down to a few % for infection – with the common diseases somewhere in the middle. Bravo, you’re right this time. Your previous statement elsewhere “environmen­t must be the entire cause of ill health” – was obviously some mistake on your part.

    It would be a good idea now to go back and make all the relevant corrections to your original article – especially if you want to continue to claim “To provide the highest quality scientific information and analysis”

    Also however you want to spin it to say that “genetic predispositions = causes” is completely misleading and wrong. Your article is an attempt to argue that the only important thing in common disease is environment, that genes have NO importance. That’s why you say ”genetic predispositions (i.e. causes)” because you know very well that a predisposition is not a cause but if you dress it up as the same then you can use that tactic to demonstrate that genes are not causing most disease and therefore not important. It’s a clever weaving of words to deliver the conclusion desired, whatever the evidence.

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