Denis Noble goes after Darwinian evolution again, scores own goal

August 7, 2022 • 11:00 am

Denis Noble (born 1936) is a British physiologist highly regarded for his work in that field (he has an FRS). Wikipedia notes his accomplishments:

He is one of the pioneers of systems biology and developed the first viable mathematical model of the working heart in 1960.

What the article doesn’t discuss is that Noble has spent the last period of his life attacking neo-Darwinism, asserting that its most important foundations are either wrong or overemphasized. Noble is regarded by colleagues I respect as a bit of an enthusiast, bordering on an unhealthy obsession, though he’s much admired by the “Third Way of Evolution” group who argue that neo-Darwinism either needs a serious revision or a trip to the garbage can.  Noble shows us that you can be a great physiologist but a lousy evolutionary biologist.

In an earlier post I wrote, “Famous physiologist embarrasses himself by claiming that the modern theory of evolution is in tatters“, I emphasized five assertions Noble made in a 2013 paper in Experimental Physiology, and then I criticized them as being either deeply misguided or flat wrong. Noble’s claims:

  1. Mutations are not random
  2. Acquired characteristics can be inherited
  3. The gene-centered view of evolution is wrong [This is connected with #2.]
  4. Evolution is not a gradual gene-by-gene process but is macromutational.
  5. Scientists have not been able to create new species in the lab or greenhouse, and we haven’t seen speciation occurring in nature.

Wrong, partly right but irrrelevant, wrong, almost completely wrong, and totally wrong (speciation is my own area).

And yet Noble continues to bang on about “the broken paradigm of Neo-Darwinism,” which happens to be the subtitle of his new article (below) in IAI News, usually a respectable website run by the Institute of Art and Ideas.

Noble is especially excited because he sees himself in a war for the soul of biology, a soul currently occupied by the modern theory of evolution. And so, in this article (see below), Noble once again raises the specter of Lamarckian evolution: the idea—which he sees as both very important and unduly neglected—that adaptations can arise from modifications of an organism’s heredity directly by the environment. (The classic example is a giraffe stretching its neck to reach leaves on trees, and that usage elongates the neck, an environmentally-induced change that somehow worms its way into the mechanism of inheritance so that giraffes eventually evolve long necks)

Darwin himself held a form of Lamarckism, positing that cells of organism, induced by the environment, could feed “pangenes” thoughout the body in a way that could modify its inheritance. That’s why Darwin was always emphasizing “changed conditions” as a source of heritable variation. The problem with this view is that tests of environmental modification as a source of inherited variation have almost never succeeded, and even when they do, they have not created adaptations. The idea that Lamarckian inheritance is an important cause of adaptation is, to put it mildly, ridiculous. (I note here that DARWIN WAS WRONG about inheritance.)

Nevertheless, Noble persists—in the face of all the facts—to make the same tired old assertions. Click to read, and shame on IAI!

First Noble argues that environmental modifications can produce traits that become inherited, though only for a short while. This is true, but the phenomenon is rare.


Modern physiology has vindicated Darwin’s idea. The small vesicles, called exosomes or extracellular vesicles, poured out by all cells of the body can function precisely as Darwin’s idea proposed. They have now been proven to communicate such acquired characteristics as metabolic disorders, and sexual preferences, to the germ-line via small regulatory RNA molecules. We can therefore be sure that Lamarckian use-disuse memory can be passed across generations. Weismann’s assertion that the inheritance of acquired characteristics is impossible was therefore incorrect. The debate now centres on two questions: “how often this happens and, when it does, for how many generations do the changes persist?”

The standard neo-Darwinist defense against this clear break of the Weismann Barrier has been to suggest that it only happens in unimportant circumstances and persists for very few generations. There is assumed to be no permanent transmission. The DNA continues “hard” transmission while “soft” inheritance inevitably dies away.

Yes, and soft inheritance can also be mediated by epigenetic (environmentally induced) modification of the DNA, usually by putting methyl groups (−CH3) onto the DNA bases.  As Noble admits, these forms of inheritance gradually go away, with nearly all epigenetic modifications erased during the process of reproduction.  That’s one reason why this kind of inheritance can’t be the basis of long-term adaptation. But wait! Noble says that short-term adaptation is of great value!

This defence fails to recognise the great virtue of “soft” inheritance, which is precisely the possibility that it can be temporary.

Yes, and so can adaptation based on genes (think of the increase in beak size of the Galápagos finches, which was reversed in a single generation when the size-inducing drought went away). If there’s substantial variation, these reversals can be fast. But Noble fails to recognize that most adaptations hang around for many generations, and those cannot be based on “Lamarckian” inheritance. It’s almost as if Noble is claiming that this form of inheritance, by some kind of group selection, has been installed in the organism to facilitate short term adaptation!

Here’s one example that people like Noble trot out when attacking modern evolutionary theory:

Consider a species under extreme environmental stress, such as the Dutch population during the starvation winter of the 1940s in the Second World War. The inherited signs of that stress have now been passed down three generations, to the great-grandchildren of the 1940s population. The chances are that it will progressively die out as the later generations experience good nutrition. And so it should!

The “Dutch famine syndrome” was caused by epigenetic modification of fetuses in utero when their mothers were starving during the Dutch “hunger winter” of 1944-1945. I’m not sure about the three generations, but I’ll let that pass. What we know for sure is that these offspring show DNA methylation changes probably due to starvation.

BUT this was not adaptive! The epigenetic changes reduced the health of their carriers, as this article shows. From its abstract (my emphasis):

This paper describes the findings from a cohort study of 2414 people born around the time of the Dutch famine. Exposure to famine during any stage of gestation was associated with glucose intolerance. We found more coronary heart disease, a more atherogenic lipid profile, disturbed blood coagulation, increased stress responsiveness and more obesity among those exposed to famine in early gestation. Women exposed to famine in early gestation also had an increased risk of breast cancer. People exposed to famine in mid gestation had more microalbuminuria and obstructive airways disease. These findings show that maternal undernutrition during gestation has important effects on health in later life, but that the effects on health depend on its timing during gestation. Especially early gestation seems to be a vulnerable period. Adequate dietary advice to women before and during pregnancy seems a promising strategy in preventing chronic diseases in future generations.

Now is that, on top of the inherited stress, an adaptive change? I think not.

It is intellectually irresponsible for Noble to suggest that the Dutch Famine syndrome has anything to do with adaptive change, much less evolution. In fact, I know of not a single adaptation that rests on epigenetic modification. I may have missed one or two, but when adaptive genetic changes in animals (including humans) are localized, they invariably are found to rest on base-pair changes in the DNA. When you map adaptations in humans, like changes in lactase persistence or adaptive skin color, you find that they are based not on methylation or episomes or micro-RNAs, but on good old-fashioned mutations that change the sequence of DNA. And so they must be, because these changes have lasted for many generations.

It’s intellectually irresponsible of Noble not to mention that, too.

Further, Noble cites the well-known phenomenon of “genetic assimilation,” in which an environmental change exposes genetic variation that can then be subject to selection, as if this were some kind of refutation of neo-Darwinism. (One hypothetical example: if you starve plants, it may, by stunting them al, hide genetic variation for height.) Noble says that studies of genetic assimilation, which are in all the textbooks, are actually discouraged by evolutionists who don’t like their non-Darwinian implications:

Given the importance of the question, why have so few attempts been made on the genetic assimilation of “soft” inheritance since Waddington’s work? The answer is that funding organisations would not be willing to support such work. If you submit a Lamarckian inheritance project to standard grant bodies, you will be almost certain to receive a firm rejection. Such is the hold of the Neo-Darwinian paradigm on innovative ideas in evolutionary biology.

Get this straight, Dr. Noble: GENETIC ASSIMILATION IS NOT LAMARCKIAN INHERITANCE! As every evolutionist with more than a handful of neurons knows, in these cases the environment exposes standard DNA mutations, allowing them to be selected in the classical neo-Darwinian fashion.

One clue that genetic assimilation depends on genetic variation and not changes in the environment becoming genetic variation is this: Conrad Waddington, who popularized the phenomenon of genetic assimilation using experiments in Drosophila, had a student repeat those experiments with an inbred strain of flies, a strain that had almost no genetic variation. Voilà: no genetic assimilation, no change in the trait. If the Lamarckian theory were correct, there should still have been changes in the character in inbred lines.

Once again we smell the odor of intellectual mendacity in Noble’s prose.

At the end, Noble beefs about how a 2016 Royal Society symposium he organized, on “New trends in evolutionary biology: biological, philosophical, and social science perspectives,” was protested by 20 other fellows of the Royal Society.  He couches this as censorship against discussing new ideas, but he’s wrong. Many of the speakers at the symposium were touting ideas that had already been already refuted, and the purpose of the meeting was to show that neo-Darwinism is dead. It’s as if there were to be a Royal Society symposium on Intelligent Design (the ID people, by the way, loved that symposium). Of course one would object if someone who knows jack about evolutionary biology organizes a symposium designed to dismantle its modern form. It’s like a fox organizing a symposium on how to breed chickens.

I’m not saying that Noble has no right to weigh in on modern evolutionary biology simply because he was a physiologist. No, I’m asserting that Noble’s claims about the death of modern evolutionary biology should be ignored because there is virtually no data to support them.  His claims should be ignored because he is ignorant, and willfully so. (Others have corrected him many times.)

I’m through with Noble; he says the same thing over and over again, tilting at the windmill of modern evolutionary biology with a soda straw. I probably should have ignored Noble’s mush, but the laws of physics compelled me to write. At least the readers here can be aware of his numerous errors and misstatements, even if Noble plays the same tune until he’s underground.

h/t: Daniel

27 thoughts on “Denis Noble goes after Darwinian evolution again, scores own goal

  1. Good post. I did not know about “Third Way of Evolution”

    Attention seekers, it seems, rather than lucid thinkiers

    1. As are creationists, holocaust deniers, climate change deniers, flat earthers, anti-vaxxers, conspiracy theorists, ad nauseam…

    2. Attention seekers and the other term for then is careerists. They want to do something really big and become famous.

  2. The form of “Dutch Famine Syndrome” I regularly run up against on the internet is the claim that the trauma is passed down through the generations because it changes the brain. This means that a grandparent (usually grandmother) who went through the Holocaust can have a daughter, granddaughter, etc etc who feels anxious, uneasy, depressed, etc. It’s evolution, it’s epigenetics, and it’s science.

    I don’t think so. It sounds more like either parenting styles being passed down or yet another easy explanation for mental distress.

    1. Presumably as eggs are formed while a female child is gestating, in a sense we were partly formed at that time, so for a Dutch woman born in 1945 who had a child 30 years later in 1975, that child would be from an egg formed 30 years before, subject to starvation conditions.

  3. Interesting article – thank you! What possible mechanism is suggested for non-random mutations? What exactly does the term mean? Is it possible that environmental circumstances can increase the *rate* of mutations?

      1. “My friend Paul Sniegowski, a professor at Penn, uses the term “indifferent” instead of “random,” and I think that’s a better way to describe the neo-Darwinian view of mutations.”

        That’s perfect, thanks. And clearly environmental factors can increase the rate of mutation, e.g., radioactivity. If somehow the “need” to change increased the rate of mutation, that would be huge, but I think the process would still be unambiguously Darwinian.

    1. Is it possible that environmental circumstances can increase the *rate* of mutations?

      Trivially, yes. We wouldn’t have whole classes of chemicals considered as “teratogenic” or “carcinogenic” if they didn’t increase the rate of mutations when introduced into the environment of people or animals.
      It’s not just “artificial” chemicals ; infections with some organisms are also teratogenic/ carcinogenic. (I’m thinking Wolbachia in lots of species/ genera/ orders, and maybe some of the fungi fingered for blame in the “amphibian crisis”. There are human pathogens with this property too – Human Papilloma Virus, for example is quite strongly linked with cervical cancers.)
      Less trivially, the natural dose rate of radiation onto organisms from both terrestrial sources (minerals containing radionuclides, from potassium to uranium, via polonium) and cosmic sources varies with time as radionuclides decay into daughter nuclides, eventually stable ones. But that’s likely to be a slow change, hard to pick out from the noise in all biological systems.

      1. Right, but (correct me if I’m wrong) these aren’t the kinds of mutations that get passed down to the next generation. I’m wondering if the rate of mutant offspring can increase due to environmental factors that “stress” the species.

        1. I’ll remind you about the Roolz regarding frequency of posting. To answer your comment, mutation rates can be increased by selection, but only under very specific conditions involving rates of environmental change and linkage of the “mutator” locus to the loci causing adaptation. Remember, the vast majority of mutations are maladaptive or neutral, so it would be hard to select for a general increase in mutations.

  4. Loquacious cranks are not unknown in the academic world, and their freedom to crankify is one of its
    strong points. During my year at the University of Sussex, I observed a different crank grouplet, one that was opposed to molecular biology. A small clique around a clever theoretical biologist (a disciple of Waddington’s who later moved to the Open University) liked to intone that DNA was the merest side-issue in regard to the deeper questions in biology. Another even tinier groupuscule liked to amalgamate molecular biology with vulgar Marxism, arriving at this wonderful formulation: DNA as the ruling class, ribosomes as the exploited proletariat. No kidding. This lot is still not quite extinct.

    1. There’s a long tradition of British eccentrics that believe strongly in odd theories outside their own field of expertise. It’s particularly common among engineers and definitely a non-adaptive trait. There is some evidence it can be passed by means of the epigenome to male offspring. 🙂

  5. I am sure it is tiresome to keep on trotting out rebuttals to this kind of cranky anti-Darwinism but it is a useful service because there are plenty of outlets – the popular press etc – that are all too keen to lap it up. The uniformed reader then sees these sorts of claims and assumes that there is a widespread consensus amongst scientists that Darwin’s theories are discredited.

  6. Hi Jerry, You were enquring the other day about the type of posts people like. I can’t speak for anyone else, but this is a perfect example of my favourite type of post: one in which you deal with and take down silly ideas around evolution and the silly people that purvey them.

    I find it bonkers that these non specialists have the arrogance to tell the real experts that they’re wrong. What’s most surprising is that it often comes from excellent scientists. Freeman Dyson was another in the long line of otherwise accomplished people who nevertheless think they know better than the experts. In fact, you couldn’t wish for a better real-world embodiment of the Dunning-Kruger effect. That such clever people can’t see this in themselves is very revealing.

    As you’ve said before, it happens in virtually no other scientific area. This must be infuriating for you, but personally I find it perplexing too. Religion is no doubt the main reason for these ideas in non-scientists, but it doesn’t seem sufficient to explain the prevalence of silly ideas among scientists. I don’t get why so many non-religious scientists have such a bee in their bonnet about Darwin and Darwinism. Fortunately, you have real expertise and authority in the field of evolutionary biology, and deal with them perfectly. I think it’s important that people such as yourself tackle these crackpots.

    Not only do I thoroughly enjoy these posts, I learn so much compared to other articles. I think it’s because the subjects are often small, easily understood, and presented as claim then rebuttal.

    Anyway, it’s great that you are able and willing to stand up for the real science. Keeping the Dunning-Kruger evolutionists in their place is important, long may it continue!


        1. Thanks Stephen, that’s a short account of what I was referring to.

          And sorry Jerry – it looks like I replied to you in a new comment (below) by mistake. I’ve taken liberty of pasting a couple of questions that Dyson answered at that link. He actually pronounces on speciation too, which must be infuriating. The arrogance to think he was better than the specialists is just appalling.

          He performed the merest pondering and made a fundamental discovery, yet the silly biologists have studied for years and never realised! The world biology community must have been deliriously happy that the big physicist shared some of his great intellect to give ’em a hand.

          Here it is (sorry if it’s a bit long):

          Just to clarify here for our readers, obviously, you’re poking holes in Darwin’s Theory of Evolution but you’re saying it only tells the story up to a certain point. What do you mean by that?

          Well that he believed that evolution was driven by selection. That’s essentially Darwin’s contribution. And it’s true for big populations, but it has limits.

          The limits are you need big populations in order for selection to be dominant. If you have small populations, then random drift is actually more important than selection. That’s the Kimura theory. Kimura called it the neutral theory of evolution and he wrote a book about it which was widely ignored by all the orthodox biologists.

          But I think he was right. And in fact, it happens that small populations are very important in evolution. In fact, you have to have a small population to start a new species, almost by definition. So small populations have a controlling effect on starting new species and also in the extension of old species.

          So this neutral regime where the selection is not important may, in fact, be the real driving force of evolution when you come to a new species. And of course, if that’s true, it changes the picture in many ways.

          What do you think Richard Dawkins would make of this?
          I mean let him speak for himself, but he is generally very dogmatic that selection dominates, and he talked about the selfish gene which is correct of course if you have a big population. If you have small populations, not so much, genes come and go mostly by random chance.

          Darwin understood the difficulty. He asked the question “why is nature so diverse?”, he asked, “why do we have millions of species?” Darwin asked the question, in a beautiful way, “why did God love beetles? There are half a million species of beetles, why did God make so many?”

          And it’s hard to understand that on the basis of selection. If selection were dominant, then you’d expect that there would be a few species of beetle which would prevail. They would be the best adapted and the others would disappear.

          But in the real world, you have this enormous richness of species, many kinds of beetle and there are birds of paradise and there are all sorts of weird peacocks with peacock feathers which seem to be peculiarly unfit. And all those weird creatures which have prevailed for reasons that Darwin couldn’t explain. He understood that there was a problem and I think that the neutral theory of Kimura really does help a lot to understand that.

  7. I think he was making the usual type of pronouncements about Darwinism being only partly right. His basic thesis was that drift is much more important than we think and that selection is unable to explain the variety of adaptations we see in nature. He reckoned you need huge populations for selection to become important, and in smaller populations, evolution is driven by drift!

    He used birds of paradise and peacocks feathers as examples of features that aren’t adaptive and therefore came about by drift. I don’t think he understood sexual selection!

    I’d have to check up to make sure, but that’s what I can recall off the top of my head. I also remember he slagged of Richard Dawkins, but that’s to be expected, he’s (inexplicably) public enemy number one for many these days.

  8. Thanks for laboring through this, Jerry. Much justified, unfortunately. My problem with Noble is that I do think his introduction of systems biology thinking was important. And that his 2006 book “The Music of Life” was, in my eyes, a beautiful culmination of this. It’s core point is a critique of a naive understanding of Dawkins’ “selfish gene” metaphor. This, however, expands into a productive and enlightening discussion of the relationship between genes and phenotype, and how that informs our understanding of the actual units of selection. He also devotes a helpful chapter to the importance of metaphors in scientific communication/conceptualization. Overall, I consider him pretty masterful in developing effective metaphors, which is part of his recipe for delivering clear, engaging presentations:
    That may be just me. Curious what others are thinking of “Music of Life”…?

  9. It’s not very Noble for a scientist to keep repeating the same fallacies even after they have been pointed out.

  10. I was at that 2016 symposium. There were lots of mainstream evolutionary biologists speaking there, like Russ Lande and Doug Futuyma, and mostly the attitude is “what’s all the fuss about, we already know all about this??”. Yes, the DI had a “presence” there, inasmuch as they attended. Did they actively participate, say, by asking questions? No, they did not.

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