Monday, June 23, 2014

Epigenetics: the burden of proof vs the folly of dismissal

We haven't written much about epigenetics for a while, in part because it's so trendy that it's impossible to know what much of it means or how it's all going to shake out, and in part because there are so many different interpretations of the word that it's hard to know whether everyone's talking about the same thing.  Tools to detect epigenetic changes in the genome, that is, specific locations that have been chemically modified in ways that affect nearby gene transcription, are now available.  Still, it is clearly a fad in the sense that once tools are there the scientific community seizes them in a bandwagon effect, showing up in study designs and grant applications and so on, in ways that can exceed the reality.  Everybody now simply 'has' to do an epigenetic analysis on their favorite project.  And partly for this reason, not everyone else accepts that epigenetics will prove in the long run to be a significant actor in development and disease.

Epigentics: what is it?
We've posted about epigenetics in the past (e.g., here and here).  Relevant to today's post, the idea of epigenetic changes is that DNA can be chemically modified not by changing its nucleotide sequence itself, but by altering the packaging of the chromosome near genes that are to be expressed (or repressed).  Since different cells in the body are different because of their differential use of genes (cells in your brain and your skull have the same DNA, but turn on different sets of genes to become what they are, as well as to do what they do throughout life), this is simply a statement of one of the mechanisms by which it's achieved.  That's not the controversy.

The controversy goes a bit deeper and reaction to claims of epigenetic changes are emotional and often vehement.  There are two reasons for this.  First, what causes epigenetic marking of specific chromosome regions is the state of the cell at a given time, and that can change in response to the conditions it senses--its environment.  The evidence is, further, that until active mechanisms alter the epigenetic marking of chromosomes, the gene-expression pattern of the cell is inherited when it divides.  Since the inducing mechanism is part of the environmental situation of the cell, this gets uncomfortably close to Lamarckian inheritance.  The cartoon example of Lamarck's pre-Darwinian idea is the giraffe stretching to reach high leaves and, if successful, passing on long-neck genes to its offspring.  This is the antithesis of modern Darwinian theory (though Darwin himself toyed with it in his own theory of inheritance).  That Darwinian theory has randomly arising mutation being screened by natural selection to pick the successful genes: the lucky giraffe that happened to have inherited a long-neck genetic variant ate better and had more girafflets than its shorter-necked peers.  Here, the facts speak for themselves, and nothing known suggests that striving for something can in itself engineer heritable genetic change, specific DNA mutations, to make that something happen.

Masai giraffe; Wikipedia

But the second reason that epigenetics touches raw ideological nerves, especially in regard to humans, is that one school of thought wants to see everything human as written deterministically in our genomes: you (including your behavior) are what your DNA sequences prescribes.  Anyone offering any other suggestion is by this group widely denigrated without inhibition as a soft-headed denier of the importance of heredity.  That's because if environments really do affect your achieved nature, then genetic determinism and all that goes with it are no longer biological universals set in stone.

But what if, beyond environmental effects on gene expression in an individual during its lifetime, those effects were heritable into the next and future generations?  That would suggest that we are not just dealing with a fad made possible by a fancy bit of gear that can help you get a grant, but that there are things about our achieved natures and our evolution that we don't yet really understand.  And a couple of papers, one from last year, and one more recent, struck us as worth writing about, for different reasons.

Epigenetic---and then some?
A lot of attention was paid to a December 2013 paper in Nature Neuroscience ("Parental olfactory experience influences behavior and neural structure in subsequent generations", Dias and Ressler). Their point was first to show that your experiences involving odor detection are specific and can leave a long-lasting chemical and behavioral 'memory'.  Dias and Ressler exposed mice to a particular well-studied single-molecule odor, and coupled that exposure with a shock to the mouse's foot, to condition the animals to fear the odor (a logic resembling Pavlov's famous dog experiments).  This triggered the activation of cells that express a particular odor-detection (olfactory receptor, or OR) gene, out of the repertoire of about 1000 such genes, as well as the conditioned fear response upon smelling the odor, even absent the shock. But the authors reported something much more remarkable, and challenging to understand.

What they found was that the behavioral response to that same odor is activated in at least two future generations that had not been exposed to the fear-conditioning.
We subjected FO mice to odor fear conditioning before conception and found that subsequently conceived F1 and F2 generations had an increased behavioral sensitivity to the FO-conditioned odor, but not to other odors... Bisulfite sequencing of sperm DNA from conditioned F0 males and F1 naive offspring revealed CpG hypomethylation in the Olfr151 gene.  In addition, in vitro fertilization, F2 inheritance and cross-fostering revealed that these transgenerational effects are inherited via parental gametes.  Our findings provide a framework for addressing how environmental information may be inherited transgenerationally at behavioral, neuroanatomical and epigenetic levels.
A very important part of this is that the transmission was by males who had been conditioned, via their sperm, to females who had no such experience....and then to their sons' offspring (that is, the marking was present on the sons' sperm cells, directing hyper-expression of the OR gene in the grandchild-mice).

Reaction to this paper seemed to fall along party lines, with determinists doubting that the results could be real, and others intrigued.  Indeed, this is curious because the experience affects not just the startled males' odor-detecting mechanism in its nose cells where odors are detected, and fear response, but seems to imprint the specific effect on sperm cells.  There is no means known (to us, at least) by which this could occur, unless all cells' OR genes are affected during the F0 males' conditioning, nor are we qualified or patient enough to judge whether the study, or its set-up in some way has led to a misleading result.  To be fair, while the authors didn't demur to send their paper to a Nature journal, nor (in expected fashion) did the Nature journal demur from publishing without requiring such a mechanism to be shown, the authors themselves in fact did not venture a mechanism and recognized the issue in the Discussion.

If this sort of specific epigenetic mechanism does in fact persist across generations, without further conditioning, many questions are raised.  Not only is the targeting mechanism important to know, but since every generation has different experiences, what sort of expression mishmash would new pups have after millions of years of evolution in all sorts of environments?  Nonetheless, mice (and we, and trees, and even bacteria) are differentiating organisms that respond to environmental conditions in ways that certainly include altered gene expression.  So being skeptical may be fully justified, and this is not in any sense an "Aha!" moment for Lamarckians.  But its strangeness to what is currently known is also no reason to dismiss it because it doesn't fit your, say, genomic determinist or selectionist predilections. This is especially so because there is in fact a lot of evidence for environmentally induced changes in gene usage, and hence in the traits, of organisms including humans.  And that brings us to the other, more recent paper.

Do big bodies mean big epigenetic news?
The other paper is a recent report in The Lancet ("DNA methylation and body-mass index: a genome-wide analysis," Dick et al., 2014), which describes the results of a genome-wide analysis of methylation at CpG sites and its association with obesity, measured by BMI.  CpG refers to a C nucleotide being next to a G nucleotide along a DNA strand.  Methylation is a way of chemically attaching a small tag to that CpG in gene regulating areas of a chromosome, that makes it hard for the proteins that are needed to express a nearby gene to bind to the DNA to do their job.  That is, the expression of methylated genes is repressed.

A commentary in the June 7 Lancet applauds the work of Dick et al., and heralds the beginning of the "EWAS [epigenome-wide association study] era."  Of course, one's first reaction might be a sigh of 'here we go again!' in regard to hype far out-performing hope, a new fad for rescuing hopeless non-replicable findings, and journals having to sell copy and holding no standards of circumspection. But how should one react?

The possible significance of epigenetics to disease has not been lost on epidemiologists, and a new field called epigenetic epidemiology is abornin', counting on the importance of non-sequence modifications of DNA, in particular methylation and acetylation patterns, to (finally!) explain patterns of disease.  In that sense EWAS may be important, or may to a cynic just be an E-for-G swap to keep the GWAS funding flowing.

The Dick et al. paper is from this burgeoning field.  Epidemiology had many successes in the last century identifying environmental causes of disease, but when complex chronic diseases overtook infectious diseases as leading causes of death, the field had a much rougher time finding the causes of major diseases, and predicting who would get them.  So, epidemiology turned to genetics, but ran into the same problem genetics itself was up against -- complexity.  But if specific epigenetic changes can now be attributed in a useful way to environmental factors, on say the McFood-O-Meter scale, the claim will be that reductionist science has found the mechanism that shows that new epidemiological studies will have to be funded to focus on the risk factor that causes the epigenetic change.

It's not an entirely new idea.  For some years, George Davey Smith, an epidemiologist at the University of Bristol, has been advocating the use of 'Mendelian randomisation ', a strategy to see whether a variant in a gene whose function relates to processing some environmental factor has the same effect in people not exposed to that factor as those who are.  Maybe someone will cook up other prevention or treatment strategies if epigenetic mechanisms prove important.  

Dick et al. identified five methylation sites in the genome that in their sample were associated with being overweight by the Body Mass Index (BMI) criterion: three were in intron 1 of the HIF3A gene. HIF3A is a gene that regulates response to reduced oxygen levels.  The authors note that "Although the main focus on HIF has been its role in cellular and vascular response to changes in oxygen tension during normal development or pathological processes (eg, cardiovascular disease and cancer), compelling and increasing experimental data suggest that the HIF system also plays a key part in metabolism, energy expenditure, and obesity."

Have Dick et al. found the cause of obesity?  Well, no.  As the Lancet commentary points out, there are numerous difficulties in epigenetic research, a primary one being that a gene won't be modified in every tissue, nor all the time, nor even necessarily in every cell of the appropriate type in a given tissue.  That means that the choice of tissues in which to search for methylation and when to look are crucially important considerations.  Dick et al. did test various tissues, and found that methylation varied.

Another important issue in epigenetic studies is determining the order of events -- which came first, the disorder or the DNA modification?  That is, does the disorder lead to methylation of genes involved, or does methylation of related genes cause the disorder?
Dick and colleagues attempt to address the issue of causality by applying a mendelian randomisation approach to interrogate the causal relation between HIF3A methylation and BMI. This approach uses a genetic proxy for DNA methylation (namely, methylation quantitative trait loci) to identify a causal relation between an exposure or trait and epigenetic variation, assuming that genetic associations are largely immune to residual confounding and reverse causation. Dick and colleagues identified two upstream single nucleotide polymorphisms that were independently associated with DNA methylation at a HIF3A locus in both the discovery and replication cohorts. However, these single nucleotide polymorphisms were not associated with BMI in the study cohorts or the high-powered GIANT consortium dataset, suggesting that hypermethylation at the HIF3A locus is likely to be a result of increased BMI rather than a causal association between increased methylation and BMI.
So, apparently the obesity came first, methylation later, and has nothing necessarily to do with the cause of obesity. Interestingly, The Lancet still describes this as an important study. "Dick and colleagues’ study represents an important advance for both obesity-related research and the specialty of epigenetic epidemiology." Why? "The widespread uptake of instruments such as the Illumina 450K HumanMethylation array means that large collaborative EWAS meta-analyses can be done, building on the success of similar approaches in genetics."

Have instrument, will use it.

The burden of proof vs the folly of dismissal
It's early days yet in the understanding of the role of epigenetics in disease and behavior, and there's a lot left to be learned.  There is now a wealth of experimental literature on cells as well as a variety of laboratory species, demonstrating some of the mechanisms of gene regulation that involve epigenetic changes of DNA.  There are carefully done experimental studies that show multi-generational transmission of such changes. There have also been epidemiological and even experimental studies of intra-uterine or maternal experience affecting things like body weight in offspring.  Thus, even without specific epigenetic data at the genome level we have every reason to expect that life experience at any age could affect even complex traits.  And what would be more likely than some sort of epigenetic mechanism to be responsible?

One should also keep in mind that trans-generational correlation can look very much like regular genetic transmission and make a trait look 'genetic' in the classical sense, rather than in the epigenetic sense.

It clearly befalls those advocating, and those dismissing, epigenetic inheritance to keep their powder dry until we can see more clearly into the whites of the genome's eyes.  In fact, since we are obviously differentiated organisms descended from a single cell, who respond in all sorts of physical and behavioral ways to our internal and external environments, it seems obvious that some such mechanisms are fundamental to genome function, as experience clearly suggests.  But how well complex traits like body shape or odor detection would be transmitted not just across cell divisions in specific types of responding cells, but also across generations, is far from clear.

Keeping our powder dry should be automatic for scientists, as this is a very important question well worthy of careful investigation.  But whether we can keep obfuscation by ideology and equipment salesmen at bay is just as serious a question.


Holly Dunsworth said...

Thank you for this review, Anne.

Just wanted to note how I've gotten the impression from some who resist epigenetics that they assume that things like fear are experienced only in the head/mind/brain/whatever. With that kind of thinking, I suppose it would seem ludicrous that fear could affect the sperm!

Anne Buchanan said...

Yes, epigenetics seems to be a Rohrshach test at the moment, with reactions revealing one's politics perhaps even more than one's knowledge of the biology...

Ken Weiss said...

There is a lot of processing of epigenetic modification (such as 'imprinting') that goes on, differently, in sperm or egg cells, so that one has to be very circumspect about how the report could be true. Still, there are so many reports that one has to keep an open mind.
Even if it seems strangely perplexing.

Holly Dunsworth said...

That's not the only study to find that fear response is passed on to offspring without mutating the genome itself.

Holly Dunsworth said...

For me, it's just as awe-some to imagine that DNA molecules affect behaviors as it is for epigenetic molecular effects to do the same. And something on that unimaginable scale has to be guiding, if not 100% determining (from birth and then with conditioning and learning through life) much animal behavior given how little evidence there is that they're thinking and making decisions about how to behave and in which situations. Humans included in that, to a potentially lesser degree ;).

Ken Weiss said...

It's so tempting to think in a Lamarckian way, that it would be evolutionarily useful to transmit to our offspring what we learn in life. It seems so obvious. But the separation of germ and somatic cell lines, an important at-least-apparent understanding that goes back to Weismann in the 19th century, is a pillar of our understanding of multicellular organismal inheritance and evolution.

So it will be very interesting to see if there really is such somatic-germline communication. If so, it will just force us to redefine what is 'inherited'. A mechanism for imprinting experience onto genomes will then need to be found.....but then it could just be added to the repertoire of 'traits' that evolved by Darwinian means.

Holly Dunsworth said...

What's funny is how people accept that they'll break out in a sweat from merely remembering something embarrassing they said, and these sweaty places are not the places that we imbue with the ability to remember, and yet somehow we assume that our gonads are hermetically sealed from such moments?

Holly Dunsworth said...

How much mind/body dualism is at play in the dismissal of "lamarckian" inheritance? There's got to be a philosopher who's already written about this.

Ken Weiss said...

Yes, it was Weismann who, iconically at least, sealed the deal for Darwin vs Lamarck with his experiments such as (if I recall correctly) snipping mouse tails and showing that it did not lead to shorter tails in the next generations. But it may then have become the dogma that installed Darwin as dogma.

Another problem is how we want to (or, that is, choose to) define inheritance. In some ways, as we wrote in our Mermaid's Tale (the book), songbird nests are inherited. So, recent work shows, are aspects of our 'microbiome'.

Dogma is bad for science even if it may be needed for people to design studies etc. at any given stage of knowledge. But whether these issues are semantic (what is 'inheritance') or more substantive is also debatable (and semantic).

Ken Weiss said...

How much dualism is involved is a good question. Genetic dogmatists don't want to open the door for any immaterial aspect to function, including extending this to 'behavior'. That view resists acknowledging the effects of non-behavioral traits being inherited.

But behavior is itself inherently related to environment, so epigenetic inheritance of the results of experience need not imply any dualism at all. But again I agree that this may be part of the essentially sociopolitical resistance.

Holly Dunsworth said...

Did you mean to write "non-genetic" rather than "non-behavioral" in the first graf?

Ken Weiss said...

No, I mean to deny epigenetic effects because they go against a genetic deterministic dogma because one doesn't want any soft-headedness regarding behavior, means one must also deny that the same could apply to non-behavioral traits. Because if it can affect physical traits like, say, ear shape, why not behavioral ones? In other words, the genetic dogma wants to keep the door entirely closed, not opening Pandora's box.

Holly Dunsworth said...

Okay, so, for example, inherited epigenetic effects on obesity or stature.

Ken Weiss said...

Yes but even that gets dangerously close to opening the behavior-environmentalist's box! That's because how tall or fat you are is clearly related to what you eat, clearly, and those are behavioral traits that are not built into the genome (or these traits wouldn't change so rapidly)

Holly Dunsworth said...

I have been thinking for a while now that our imaginations are quite limited about DNA as a result, perhaps, of how it's almost always drawn in a vacuum!

Anne Buchanan said...

Indeed! Plus, we tend to think of DNA as linear, which can stifle thinking about it in context, as a 3-dimensional, folding, complex molecule. And a lot of what happens to it depends on its 3D structure.

Ken Weiss said...

That is exactly the issue with reductionism as the main scientific tactic in the last 400 years. Other approaches (referred to by terms like 'systems', 'holism', 'emergence', and 'complexity' are harder to deal with operationally, often seem like mysticism or vagueness, and threaten hard-nosed real-politik in science. On the other hand, reductionism has been spectacularly successful, hence its defendants.

Anonymous said...

one school of thought wants to see everything human as written deterministically in our genomes: you (including your behavior) are what your DNA sequences prescribes. Anyone offering any other suggestion is by this group widely denigrated without inhibition as a soft-headed denier of the importance of heredity.

Who are these people? I have read widely in behavioral genetics, evolutionary psychology, sociobiology, etc., but I have never encountered researchers claiming that "everything human [is] written deterministically in our genomes." You claim that there is in fact a whole group of such researchers, so you could you please name some of them.

Anne Buchanan said...

Indeed, I've never seen such a claim either, and if you will note, that's not what we said. What we said is that there are people who prefer to believe that behavioral traits will turn out to be genetically determined. And this colors their view of, say, epigenetics. And blog posts about epigenetics.

Anne Buchanan said...

Our friend Charlie, a human geneticist (though not exclusively -- he also grows amazing popcorn) who has thought long and hard about complexity and causation, sent us the following comment this morning. He has agreed to let me post it here; I think it adds further appreciation of complexity to the discussion.

"It seems to me that the devotees of epigenetic causation are gripped with the same reductionists insanity when they are looking for a particular site that is methylated in a particular gene when they should be recognizing that the possibilities for interactions between agents is now more than ever apparent with copious variation in the code (and the DNA modifiers of the code) and variation in the widespread modifications of the code by the environment among people, tissues and cells. They (we) should be asking whether it is possible (design an experiment?) to separate out changes in the base sequence and changes in the methylation of the sequence at any site, or the genome at large, when the quantitative phenotype of interest depends on the input of both AND the effects of the environment that do not influence the behavior of the DNA molecule. It should be apparent to all but the most adamant reductionists that we are dealing with at least four non independent domains of material causes. On the positive side, the new epigenetic measurement tools have helped to expose and validate our ignorance about how genes and environments function.

I think that there must be information in the pattern of methylation that influences domains of the sequence, beyond the influences of a particular CpG methylations, that influence folding and hence transcription. The attached paper gives evidence (in at least one dataset on one tissue) that the pattern of methylation in the reference genome is not random and may be fractal as suggested by a power law. Pattern as well as position may have influence on function, making the situation about as complex as life itself. And, how can science separate the effects of pattern from the effects of particular base changes and particular methylated bases? What scientist involved in unraveling this hairball would say that it is the gas pedal below your right foot that makes the car go?"

Tabitha Powledge said...

OK then, name some of *those* people. I want to make sure we're not in a wrestling match between straw men.

Tabitha Powledge said...

This is a reply specifically to Ken Weiss's first comment above. We've really got to stop tossing "Lamarckian" around so sloppily when talking about epigenetics. No, I repeat no, transgenerational epigenetic phenomenon has been shown to persist beyond 3 or 4 generations. These changes peter out. This is *not* evolution (and not Lamarckian neck-stretching) because it doesn't involve permanent inherited changes.
Also, on the utility of being able to pass on epigenetic changes to future generations: Maybe not. The point seems to be to help an organism cope with what's going on in its environment. But that environment could well be different by the time subsequent generations come along. Better to remain flexible.

Anne Buchanan said...

Nope, no names. There is an extensive literature attributing behavioral traits to genes.

We happen to think that biology is more complex.

Ken Weiss said...

I'm not sure exactly what 'first comment' of mine you are objecting to. However, we did not in any way say otherwise about Lamarck. We did not suggest that actual Lamarckian evolution occurs. In fact, however, no inherited change is 'permanent'. Mutation will come along and change it. It's just a different mechanism. So 'evolution' becomes somewhat semantic, because you are using the word in its long-term sense. We would not disagree in the sense that you use it, nor do I think we said anything to the contrary.

But this is, in fact, a semantic and/or numbers game. You say no, and repeat no trans-generational epigenetic phenomenon has lasted more than 3 or 4 generations (I think one has been reported in C. elegans that lasted 7, if I remember, but that makes no difference to the point). And if 4, how do you know there can't be such things that do last many generations? I would not argue for that, and of course we have no such evidence.

The energetic opposition to epigenetic change is generally not about these phenomena which aren't really a threat to current evolutionary genetics. It's because a polarized fraction of people want to deny the importance of experience-based traits, because they want to stress how much they see traits as being programmed by the genome. Naturally, in our view, this is for sociopolitical reasons having to do with race, inequity and things of that sort. You may or may not agree, but you don't see the kind of trash mail comments that we get when we suggest that environment might affect traits of this sort. That view is in part a reaction to the strong denial of genomic determinism by what one might call hyper-environmentalists. This has to do with social inequality, and the nature-nurture cycle of explanations that seems to occur.

Nobody we know seriously thinks evolution is Lamarckian in the literal sense (nor is it Darwinian in the literal sense, and maybe we should be more careful throwing that around, because it implies that basically every variation no matter how small is detected by selection, as Darwin repeatedly stressed (and he also toyed with the inheritance of acquired characters not all that far from Lamarck's ideas except for the latter's notion of 'striving')).

The relevant point is not a rehash of Lamarckian vs Darwinian processes. But the mal-yclept 'Central Dogma' long held, and yes dogmatically, that genetic causation went from genome to RNA to protein and not the other way. But epigenetics, among other things, shows that influences do go the other way.

[because of a blogspot length limit, this will continue in a second reply]

Ken Weiss said...

[Response continued]

There's much more to that story, but the point I would say is that we should move away from dogmas and on to science, where we are learning that there are many more things going on than a mid-20th century doctrine held.

As to your last comment, we say exactly the same thing in tomorrow's post, which has already been written in response to a tweeted comment we received on this post today. So we agree with you on that. In fact, in my own view, the burden of proof should be on the shoulders of anyone who would argue too strenuously that all that we are is inscribed in our genomes.

We have many times here argued that behavior and brain function would, in principle, be more 'adaptive' if it were about assessing conditions and making context-specific rather than hard-wired decisions. In our book Mermaid's Tale and elsewhere, we have used the world 'facultative' for this property. That would seem, to us, more important than hard-wiring in regard to human behavior. And last week we wrote about animal behavioral abilities in the context of what should be called 'intelligent'.

Part of the problem, I think, is that it is easy to think of a 'mechanism' for behaviors resident in DNA, since DNA is a molecule. That point of view tends to view facultative ability as verging on the immaterial, mind rather than matter dualism, or mystically vague since it is harder to imagine a molecular mechanism for such thinking phenomena. But there were a lot of things we once didn't understand that we now do, and the opposition to flexibility isn't on any particularly more solid ground.

Steve Sailer said...

I have to say that I've never quite gotten the excitement over epigenetics as a revolutionizing nature-nurture debates. This is not to say that the study of epigenetics isn't valuable in and of itself, it just seems to have less implication for the kind of arguments that people really care about than its publicists assume. I'm not saying that it isn't valuable to know that one way the environment affects traits is through sending a message to the genes to turn themselves on or off, but that that doesn't tell us anything terribly significantly new about what people get hot under the collar about: the limits of environmental influence.

If I say, "Twin studies, adoption studies, and so forth suggest that for a lot of traits, there's roughly a 50-50 breakdown between the effects of heredity and environment," over the last few years, I constantly get told that: "Oh, no, that's so 20th Century. You see, some of the genes are also being affected by the environment."

Me: "Okay, but that still leaves us with the results of twin and adoption studies. So, what it sounds like you are saying is that genes aren't just 50% of the importance, they're something like 75%, but maybe 1/3rd of the genes are influenced by the environment, right? So we're back to 50-50, right?"

Holly Dunsworth said...

This isn't directed at any one comment here, it's just some thoughts that arose as a result...

Although no one with any cred puts in writing that all traits are determined by genes, one could say that it is the majority default view in the evolutionary sciences and it has broad reach into other disciplines and into the popular zeitgeist as well. That's because the default for any given trait of study has been, and seems to continue to be, that it is mostly genetic and/or that it exists due to natural selection.

What astounds me is how people can get so defensive about how much they certainly *do* appreciate that biology's usually a lot more complicated than a single or a few inherited genes while they cling to a definition of evolution that is just dominated by natural selection, prefering adaptive stories for the evolution of traits and for why they vary. How does one reconcile biological complexity with simple story-telling about why it is so?

Apparently reconciliation between what we see and the theory we use to explain it isn't required to continue doing evolutionary research or thinking about it, but it's very difficult for me to understand why that is. Hopefully things are changing and I'll be able to see that change in my lifetime. It would be very exciting.

Ken Weiss said...

Any science has its tribes and food fights, but usually they stay within the science itself, I think. But when it comes to the study of humans, it so often seems inextricably connected to peoples' personal views of society and its structures, inequities or not, and the behavior of others. Group categorization is a common, perhaps natural, way of thinking, but becomes destructive when applied too casually to humans. The web, of course, has engendered snarkiness and worse far beyond what usually went down in public discussion.

Even the idea that there is a 'balance' of contributing causation doesn't bear much scrutiny. We have too much trouble knowing even what 'causation' is, or what 'balance' would mean, or whether it matters whether that is (as a prior comment notes) 50-50 or 70-30 or 30-70, etc.

The issues put in this way are basically silly if they weren't so potentially damaging to people when this sort of science affects policy. Each side of the nature-nurture divide has its innings. Right now the self-confident trumpeting is mainly coming from the nature side. When people get bored with that, or a new generation has to prove how wise and deep-seeing it is, nurture will rise again.

Holly Dunsworth said...

I see this issue of ever-increasing understanding of complexity yet clinging to adaptationism as being the trend across evolutionary biology, beyond that of humans. Maybe I just don't understand what about my comment tripped your particular thoughts in your reply to it. I see this discussion as remaining more like nature vs. nurture than it should be, as long as there are people who know how to study the nature (and not the nurture) and people who know how to study the nurture (and not the nature)... don't you think?

I just saw Colbert interview two authors of a book on female confidence on his show. These women said confidence "is genetic" and that they've been genotyped for confidence. What the hell are they talking about? Colbert didn't ask, but I wish he had. Are they talking about all the genes that contribute to height? Because being tall helps with confidence. Etc etc etc.

Ken Weiss said...

I do agree, and my comments above weren't intended to say otherwise. It's a strange division of thought, akin to the proverbial 'bicameral mind'.

Holly Dunsworth said...

In case anyone's interested in the genes for confidence stuff.

Here's the Colbert interview.

Here's an except from their book.

Holly Dunsworth said...

No accounting for how genes contribute to your looks, which I'd assume go a long way to affect how others shape your behavior.

Anne Buchanan said...

Here's a lovely example of developmental plasticity that someone mentioned on Twitter. "Temperature dependent plasticity of segment number in an arthropod species: the centipede Strigamia maritime", 2008, Vedel et al. With higher temperatures during embryogenesis, centipedes develop more segments. This isn't the same as facultativeness during life, which is built-in adaptability on the fly, but it's adaptability all the same.

Holly Dunsworth said...

(and Colbert did ask, whoops!)

Ken Weiss said...

This epigenetic response seems built-in to the developmental plan, and in that sense also genetic. In principle, given its distribution and apparent stability, it must be consistent with the adaptive environments of these various species. And it seems to cross the apparent species distinctions (if those are accurate in this case), showing that epigenetic mechanisms can indeed have evolutionary relevance. At the same time, one might expect genetic assimilation to have occurred (see June 24 post), but whether it has in any species probably isn't known--or maintaining flexibility could be what's going on.

Anne Buchanan said...

Colbert was right on target here!