In Plomin’s case, his fanaticism for polygenic scores could be written off as wishful thinking for a man at the end of his career, touting a perceived future of ever improving polygenic prediction. Harden, on the other hand, has had a few years to see the hype dwindle, with study after study noting the limitations of such scores.
Harden’s primary focus is what is referred to as “educational attainment,” basically a simple measurement of how far someone goes in school, viewing it as a trait with some genetic basis. In truth, this “trait” is a bit of subterfuge, serving as a proxy for intelligence, while avoiding some of the controversy surrounding genetic studies of IQ (and their association with books like Charles Murray’s, “The Bell Curve”).
Harden's writing style at times involves condescending oversimplification through analogy: “If a gene is a recipe, then your genome - all the DNA contained in all of your cells - is a large collection of recipes, an enormous cookbook.” This quaint presentation of the subject suggests that she is targeting a lay audience, but I question whether those not already familiar with this kind of research would find this book engaging and these analogies do not appear to clarify the subject in a more comprehensible manner.
Books of this nature generally have the same two issues to tackle and Harden’s is no exception. The first is to sell the scientific evidence related to claims of a genetic basis for educational attainment and other behavioral traits. The second relates to the ethical and practical implications of this research. I will address her treatment of both issues here, beginning with the latter.
As Harden notes: “When people hear ‘genes’ or ‘intelligence’ - particularly in the United States - they cannot help but hear ‘race.’” I’m not sure this is what comes to mind for me, but it’s certainly true for many of those touting these types of genetic studies, often using them as fodder for eugenic, classist and racist ideas, thinly disguised as science. Harden addresses the historical relationship between behavioral genetics and eugenics head on, but this leaves her trying to push largely hypothetical “benefits” of genetic studies, with a reframing of the ideas as egalitarian.
“What I am aiming to do in this book is re-envision the relationship between genetic science and equality… Can we imagine a new synthesis? And can this new synthesis broaden our understanding of what equality looks like and how to achieve it?”
I think that this falls flat and demonstrates a naive understanding of just what she is up against. Rather than admit that these studies feed fascistic and racist ideas, she attempts to “both-sides” the issues, focusing on leftists, for whom she appears to have some disdain, fancying herself as some kind of sensible centrist, by contrast. Case in point is her interpretation of a study related to bias towards genetic determinists:
“... a scientist who reported genetic influence on intelligence was also perceived as less objective, more motivated to prove a particular hypothesis, and more likely to hold non-egalitarian beliefs that predated their scientific research career…people who described themselves as politically liberal were particularly likely to doubt the scientist’s objectivity when she reported genetic influences on intelligence.”
Her point here is to paint the left as hopelessly biased on this subject, but despite Harden’s dubious effort to paint herself as a leftist, many individuals touting genetic determinist views also harbor racist and classist views that are hardly egalitarian. There are obvious reasons for this and it doesn’t take a leftist to distrust their motives, nor should one expect leftists to embrace a sugar-coated version of genetic determinism.
As Harden acknowledges, the field of behavioral genetics was largely founded on the backs of racist eugenicists such as Francis Galton and Karl Pearson. We still see this today, perhaps in a more attenuated form, both from scientific poseurs like Charles Murray, as well as renowned scientists, such as James Watson. Imagine expecting them to “re-envision” their view of the world. This demonstrates a real inability to read the room and, if there was any doubt about that, we already have race-oriented “scientists” embracing aspects of Harden’s book.
Nonetheless, what matters in the end is the validity of the science and the book is written under the presumption that the science is settled. This couldn’t be further from the truth. Books of this nature can’t rely solely on actual scientific evidence, because there isn’t much there. Their acceptance relies on decades of hyperbole, ingraining the psyche of society, at large. Even those having little familiarity with the subject have been exposed to enough headlines in news media suggesting genes have been “found” for intelligence, schizophrenia, personality traits or your favorite flavor of ice cream. This is bolstered by futuristic books and movies, presenting a mythology, dystopic or otherwise, of genetic deification.
The actual science is far less impressive, and for those not familiar, it essentially relies on establishing genetic “correlations,” without defining what or how these genes might influence a particular trait. The principle behind the studies is not much different than what commercial genealogy sites like Ancestry.com do, but instead of establishing ethnicity or ancestry, they correlate the genetic variants that are more common in one group than another for a particular behavioral trait, or just about anything that can be designated on a questionnaire. Then they score the total number of these correlated variants a person has for a “polygenic score,” the idea being that a higher score makes it more likely you will have the trait. This is based on the hypothesis that traits are “polygenic,” consisting of hundreds or thousands of genetic variants. It is a probabilistic assessment, with no definitive set of genetic variants that would confer a trait or explanation of how any of these variants would contribute to the trait, nor explain why many with high scores do not have the trait and many with low scores do.
In truth, applying a polygenic score for a trait isn’t a whole lot different than commercial genealogy sites assessing whether someone has genetic variation that is more common for, say, Italian or Korean people. The difference is that Ancestry.com is not absurdly claiming that these genetic variations are causing Italians to like pizza or Koreans to use chopsticks. That, however, is essentially what behavioral geneticists are trying to claim, but instead of pizza or chopsticks, Harden is focused largely on so-called “educational attainment.”
Much of the genetic variation we find in people is due to genetic drift, where populations in historically isolated parts of the world randomly acquire different genetic variants over generations, that will be more common among people in a particular region. These genetic variations generally have little or no known functional difference, but can serve as genealogy identifiers. Geography is probably the most important aspect in looking at ancestry, although individuals of different ethnicity, living in the same region might also acquire common, distinguishing variants due to marrying within their own group (a form of assortative mating). In either case, these phenomena create what is called “population stratification” and allow you to distinguish populations via their genetics.
It’s not difficult to see how a trait like educational attainment would be subject to population stratification. People of one social class will marry others in the same class and highly educated individuals will tend to marry others in that social class and push their children in that direction for successive generations. Harden is arguing that these people have, at least in part, won the genetic lottery and that the genes they have in common confer some abilities that allow them to achieve higher education over those who are more, say, blue collar. To assume this up front, in my view, is an aristocratic way of thinking.
The problem here is that you add nothing to the argument by pedantically looking at the genetic variants that are found in different social classes. Of course you will find genetic variants that are more or less frequent due to long-standing population stratification, but are you really doing anything more than correlating Italians to pizza and Koreans to chopsticks? I contend that you are not and Harden and others in the field, all highly educated, and mostly from privileged backgrounds, should be wary of doing such self-affirming research on educational attainment. Believing that people within these privileged classes have actual genetic variants that allow them to be “... smart and curious and hard-working,” in some way that confers educational attainment is blind to both common sense and the obvious realities of the society we (and the UK, where many of these studies arise) live in. Although Harden does acknowledge some of the factors leading to this kind of confounding in genetic studies, she tries to make the case that these factors can be weeded out, leaving us with only the good stuff.
There are a number of problems with this claim. The first is that the claimed high heritability of a trait like “educational attainment,” like other behavioral traits, was divined by twin studies, which Harden defends, but these studies are simply not confirmed by actual genetic studies, which find miniscule heritability by comparison. This leaves behavioral geneticists to flailingly suggest that there is “missing heritability” still to be found. Harden attempts to explain this as being due to “...particularly rare genetic variants which might have especially large effects.” In other words, the genetic variants that aren’t common enough to be picked up in a GWAS genetic study just happen to have all the missing heritability. There is no evidence to support this and, frankly, it smacks of desperation.
Thus, we have the circular argument that keeps the field of behavioral genetics alive: The heritability of a trait seen in twin studies proves there is a genetic basis for that trait, and the fact that we are not able to confirm twin studies via genetic studies shows only that we haven’t found the genes we expected yet, but we know must exist because of twin studies. Such circular assumptions are then presented as established science. For example, Harden claims as fact that behavioral traits are “polygenic”:
“Schizophrenia and autism and depression and obesity and educational attainment are not associated with one gene. They are not associated with even a dozen different SNPs. They are polygenic - associated with thousands upon thousands of SNP’s [genetic variants] scattered all throughout a person’s genome.”
These contradictory assumptions leave us with a “polygenic” model with thousands of genetic variants adding up to a tiny bit of heritability, and unidentified “rare variants,” to be found at a later date, accounting for the remaining huge chunks of missing heritability. This is simply wishful thinking.
Nonetheless, Harden embraces the idea that these genetic studies will someday close the gap on this missing heritability, touting a recent study for educational attainment in which she claims, “You can account for 13% of the variance.” Although this is not anywhere near what one would expect from twin studies, on the surface it is significantly better than the usual 2 to 3% that such studies generally yield. It is a bit of sleight hand, however, for Harden to tout this figure, when she also touts within family studies (comparing the genetics of siblings and their parents and then assessing their educational attainment polygenic score), as a way to strip down to the actual causal genes, and such a study was conducted and brought this figure back down to 2 or 3%. Such decreases are merely a flesh wound for Harden, though, who notes that, “... the heritability of educational attainment is still not zero.”
However, that’s not really certain, for a couple of reasons. The first is that when you are at such a low percentage, you could be merely talking about statistical aberrations. As one recent study describing such “measurement errors” notes: “We find that sibling models, in general, fail to uncover direct genetic effects… Our findings suggest that interpreting results from sibling analysis aimed at uncovering direct genetic effects should be treated with caution.”
Secondly, we have no idea what most of the genes in question actually do, so even if you argue that these genetic variants are causal, you haven’t ruled out physical causation to explain this small percentage. Traits that Harden herself notes such as “pretty, tall, skinny, light-colored,” which would hardly convey a meritorious advantage towards educational attainment might be all that we are really seeing. Perhaps that is the true “genetic lottery.” Thus, arguably, when talking about miniscule results like this, you might, indeed, truly be at zero genetic influence, leaving her entire book promoting a faulty premise.
Moreover, there is another significant problem with these genetic studies and the derived polygenic scores: They are largely useless outside of the ancestry group being studied, which is usually those of white European ancestry. Harden addresses this to an extent:
“I anticipate that scientists will have developed a polygenic score that is as strongly related statistically to academic achievement in Black students as it is in White students.”
There are a number of difficulties with this statement. The first is that it is probably not going to be the case. The polygenic score for educational “achievement” relies on population stratification that has probably not had as much time to develop in the West for those of African ancestry. Moreover, there is an assumption underlying that, which is that what would constitute genetics of educational attainment would involve entirely different genes for Black students than those used to assess White students. This should reinforce the fact that these scores are based largely on population stratification, and should make it clear that the genetic variants have no real function. There is simply no reason to believe that a collection of genetic variants would be entirely different from one ancestral group to another and still confer the same behavioral trait. Despite her attempt at logical extension, you can’t just make this assumption because you believe it to be true for a person’s height or milk production in cows (which have their own problems).
If this isn’t obvious for a singularly numeric trait like educational attainment, consider a trait that is not as easily quantifiable, like schizophrenia. Like educational attainment, a polygenic score for schizophrenia based on a white European population, would not be useful for an African American population. So again you would be forced to surmise that Black and White people who get schizophrenia have an entirely different collection of genetic variants that "cause" schizophrenia. Yet, schizophrenia has about the same prevalence in African Americans and those of White European descent, and it presents in the same manner. This is not consistent with separate genetic mechanisms and should lead to the conclusion that genetics are not the primary mechanism behind it. The same could be said for depression, bipolar disorder, personality disorders or just about any behavioral trait. No one is claiming a significant difference in the presentation of these traits or the general prevalence in different ancestral populations, which one would expect from separate polygenic influences.
Another obvious concern with such separate but equal polygenic mechanisms, is that it will fuel the very racists Harden denounces. Harden is careful to make the distinction between ancestry and race and, while the distinction is important, for those engaging in “race science,” referring to individuals as African ancestry is hardly going to dissuade them from extending this to racist conclusions.
It’s also worth pointing out that, like most books related to this subject, Harden presents, at best, a sophomoric understanding of human psychology. There is no theory or dynamic formulation to be found. There is no debate to be had, other than statistical sophistry, to argue that schizophrenia, depression, educational achievement, or other traits are “partly genetic.” With that called into question, you are left with little else, but “bluster and bluff and empty show.” It’s shocking that the bulk of resources for psychology research are being poured into this pedantic shell game. It has contributed nothing to the field after decades of this research, has historically caused a lot of harm, and probably will continue to do so. Harden cannot hope to “re-envision” the field, because it has no validity and too many of those who embrace it have dubious motives. Her book, like those preceding it, props up a field that is apparently too big to fail.
My review of Kevin Mitchell’s, “Innate” available here: http://unwashedgenes.blogspot.com/2023/05/review-of-innate-by-kevin-mitchell.html
I think the really, really high hill for skeptics like yourself to climb is this: essentially no one serious disputes the fact that our genomes influence literally every element of our physiological selves, but have in turn literally no influence on behavior. That seems utterly fanciful to me, just beyond the realm of possibility. But it lurks in the background of what you've said here.
ReplyDeleteLurks in the background, that is, because though you've mocked Paige for failing to advance a coherent vision of human psychology, you haven't advanced any of your own, at least in any way that responsibly integrates even a modicum of genetic influence into our understanding of behavior. For example, that smarter biological parents have smarter biological children is not a matter of dispute - we cannot prove that this is causally true, but we know for a fact that it is summatively true, as vast datasets have demonstrated for decades. So, what's your version of how this came to be? I don't see one; I just see bluster. So you're asking me to compare your lack of any coherent story about the relationship between genes and behavior to Paige's (in my opinion, careful and compelling) story. It's a common tactic in these debates and indicative of the denialist failure to advance the outstanding questions in any way.
I have severe bipolar disorder; when unmedicated my condition reliably produces psychosis, which is to say severely alters my behavior. Essentially no one in the relevant fields disputes that there is a strong genetic component to bipolar disorder. So there's widespread acceptance that my genes could influence my behavior thanks to bipolar disorder, but absolute refusal to consider that other genes could influence my academic behaviors, my social behaviors. But... why?
Hmm sorry first sentence should be more like "I think the really, really high hill for skeptics like yourself to climb is this: essentially no one seriously disputes the fact that our genomes influence literally every element of our physiological selves, but people believe that this physiological influence has in turn literally no influence on behavior"
DeleteI don’t think the hill to be climbed is mine, my friend. 30 years of genetic studies have produced nothing. You can’t just keep saying Sisyphus will get to the top of the hill this time. At some point, you have to give up the genetic snipe hunt.
DeleteI am a board certified psychiatrist and I do not think that Bipolar Disorder is significantly related to genetic variants among individuals. Please read through my blog, if you want to understand my reasoning and my direct critiques of genetic studies of bipolar disorder.
DeleteFreddie,
Delete"essentially no one serious disputes the fact that our genomes influence literally every element of our physiological selves, but have in turn literally no influence on behavior."
It depends what you mean by "influence" here. In my view, this debate is about necessary vs sufficient causation. Genes are necessary causes - they, along with other developmental resources, influence a trait but you can't then say that genes are sufficient causes since there is no privileged level of causation when it comes to developmental systems (see eg Denis Noble's Genes and Causation and A Theory of Biological Relativity).
When it comes to advancing an alternative view of what Paige discusses, we don't need to do that. We only need to show how their arguments fail - and this has been done for decades except Paige attempts to dress up an old argument with new clothes.
This is what needs to be addressed: How do genes cause "behavior"? From what I've seen in all my years reading behavioral genetics, they have not distinguished between "action" and "behavior" and this is to their downfall.
When you say that "smarter biological parents have smarter biological children", you're accepting the (unargued) claim that IQ tests are a measure without articulating the specified measured object, the object of measurement and the measurement unit for IQ. There also needs to be a theory and definition of the construct and we need to know that it exists. So, where has this been done? It hasn't been done anywhere yet, to the best of my knowledge, and because of this, claims like Paige's will always fail.
Your comment here rests on what you mean by "influence" - are genes necessary or sufficient causes? I agree genes are necessary but I disagree that genes are sufficient causes. You'd need to provide an argument that genes are sufficient causes and you also need an argument that defeats Noble's Biological Relativity argument.
Freddie,
Delete1) Most of the most thoughtful critiques have been from geneticists themselves. Behavioral genetics almost never deals with the causal mechanisms wherein genes operate to build mRNAs, ncRNAs and proteins. The last 30 years of molecular genetics, and its failure to explain significant amounts of complex behavior have resulted in nuance and caution that is completely absent from your own and Hardens discussions. I myself have spent many years attempting to change behavior through experimental means of actually manipulating genetic variants in the brains of animals. So, your comment that we need to climb a “really high hill” is misplaced. We have already climbed it, we have a decent understanding (as much as one can) about how genes operate, and that understanding allows us to better critique claims of genetic causality where causality is conspicuously absent. Filling your own misunderstandings of genetic causes and functions with some sort of black-box-causal-manifold based on correlative data isn’t how to make progress on understanding the role genes play.
2) You seem to be almost wholly unfamiliar with the assumptions of GWAS and heritability estimates: The partitioning of variance into independent and additive genetic factors. makes developmental assumptions that the causal contribution of genes and environments can be independent and additive. This means that regardless of other organismal considerations any mix of gene/PSG/whatever-the-unit-is-now X with any other function Y, Z, U, ect, will always result in functional outcome X, or more of X, or a slight variant of X. However, research in developmental genetics and developmental psychobiology has unequivocally demonstrated that independence and additivity conflict with the very process that genes operate in developmental systems. It always dependent and often multiplicative. This means if you have gene/PSG X and context Y you get function L, wherein in context B you get function R. This basic fact is a huge upset for application of heritability estimates in uncontrolled settings, as it makes it impossible outside a lab to know what factor “difference that is making a difference”. Harden completely ignored this in her book, as you did in your book. Thus, behavioral genetics has not lived up to its name, it's not genetics, indeed it is little more than “family studies” and the core finding in the last 30 years has been the banal point that some things “run in families”.
Thanks,
Greg
Also,
Delete3) In lack of the actual synthesis with biology, behavioral genetics has had a history of generating controversies in lieu of meaningful findings. This was covered expertly in Panofsky’s book “Misbehaving Science”. Early in the history of behavioral genetic there were many animal researchers investigating the processes wherein genes cause behaviors. Their findings were nuanced, with direct behavioral measurements, and left open the door for more careful consideration of developmental processes. The adoption of heritability estimates as the fields zeitgeist led to a mass exodus of these researchers to animal behavior and behavioral neuroscience. They were appalled at the methods being used to assess genetic causality. Jerry Hirsch, one of the very founders of the field of behavioral genetics even wrote a paper calling it “The Bankruptcy of “Science“ Without Scholarship.” It’s a great formula, publish something that purposefully controversial and based on flimsy enough evidence that it will cause enough outrage (see our comments here as an example) to get a lot of eyeballs, attention, and discussion. When this gets to hot, the field simply change the tune (Hardens book here is basically the field attempting to change tune from Jensen by moving it to a more manageable controversy) and move onto another controversy without changing methodologies (Jensen to Harden use almost identical assumptions in their methods). The attention this brings can then be used to secure enough funding to keep the field going for a while. Meanwhile the only thing that truly suffers is public understanding of how genes actually operate in the development of abilities, behaviors, and traits.
Greg,
DeleteYour second point seems quite important, particularly because it is a methodological critique and so argues against Harden's position on her own terms. Can you link to the papers that best articulate these findings about context dependence? I'm also curious about which of your papers regarding behavioral change through genetic manipulation are most relevant to this discussion. Thank you.
I will do so.
ReplyDeleteI have tried to understand supposed benefit of studies like Harden's and have come up empty. Even if some set of 1000 SNPs makes one better at an IQ test or more likely to earn a PhD, this seems a most pointless discovery. In what way should should this knowledge inform the society we create? Do the "smart" people need larger houses or fancier cars? Should they be encouraged to have more children to improve the human race? Should they necessarily be relieved of toil and hard work that might dirty their hands or cause their muscles pain?
ReplyDeleteIf we really believe that those with more education or higher IQ are better than others, from whatever cause, then it would seem to me that they have an obligation to others less wonderful than themselves. But even when such people talk of creating a more egalitarian society, it's almost always just that -- talk. Which makes me question their actual superiority given what I view as an important moral failing.
What we can do is stop punishing smarter jews asians and whites for having the crime of larger brains, consistently better test scores and observable mental aptitude from childhood, the gaps between them and black children not even changing with adoption, stereotype threat having totally failed to prove anything etc etc
DeleteI mean hereditarians can literally predict the outcomes on average of 100 Asian 100 white and 100 black kids whether adopted or otherwise, regardless of their SES or school type etc.
Same gap always occurs.
You have no recourse to anything but a mystical kind of racism you almost never explain how it causaly causes such persistent gaps. You can't explain why the white supremacists who control our society conspired to get asians and jews to do better, even if they're adopted by whites, TO THE SAME DEGREE. The larger brain size which correlates to IQ is just a coincidence
All these billions of coincidences. Hereditarians have a causal explanation and the power of prediction
You have nothing but just added attempts to oppress asians.
Its miserable because you could just face the brutal reality that there's inequality in this, like height and like appearance and like physical strength. All the evidence is there-you try to suppress the research because you can't disprove it and you don't have any alternatives that withstand scrutiny.
Imagine the amount of progress you've impeded. The lives and careers you've sabotaged. All to hide from the average black kid, that he doesn't have the same odds of being an astrophysicist that his Jewish classmate like the latter doesn't have the same odds as making it to the NBA
No, we've got to just oppress and sabotage jews and asians for the greater intelligence they inherited
Cruel, inhumane and not even benefiting black children.
I'm the same commenter as a second ago-
DeleteTo be more direct in response, you could just help the more talented, typically more Asian and Jewish kids be economically productive and then tax that to the benefit of everyone. Universal Healthcare including for blacks who mostly won't be economically pulling their weight relative to jewish or Asian kids.
Instead of endlessly trying to sabotage asians and watch the country descend into a libertarian hellhole
I’m going to leave these idiotic comments on here, because it makes my point about the what Harden is fostering.
DeleteI'm really disappointed in Harden. Whenever racist bigots start defending you, it's because you're producing material they value.
DeleteYeah, you hate unpleasant empirical reality because it's just really bad. I won't even say because it conflicts with your ideology. Any human of normal compassion should not be happy with this kind of inequality. But it simply is there and she is not the criminal here for investigating it. Jts just s brutal horrifying but also true reality.
DeleteDr. Pittelli - "Yet, schizophrenia has about the same prevalence in African Americans and those of White European descent, ..."
ReplyDelete--NAH, NOT ACTUALLY TRUE!!
Published research says schizophrenia is about 3 to 4 times more prevalent in African Americans compared to White European descent Americans.
https://link.springer.com/article/10.1007%2Fs00127-004-0824-7
https://academic.oup.com/ije/article/36/4/751/665657
Furthermore the population average polygenic score for schizophrenia risk is much higher in Blacks compared to Whites.
So the research pretty much validates the Hereditarian/Behavioral Genetics/scientific racism viewpoint, and indicates that although you might be politically/morally correct--you are probably scientifically incorrect.
You are misreading the studies, which note that African Americans are far more likely to be given the diagnosis of schizophrenia when they have the same symptoms compared to whites.
ReplyDeleteGreat review.
ReplyDeleteThank you for your excellent review & critique! I had a difficult time locating anything near a critical analysis of Harden's "publication".
ReplyDeleteI find her work an astonishingly irrelevant exercise in reductionism in extremis.
From hypothesis->methodology->"findings"
<>
You say "the claimed high heritability of a trait like “educational attainment,” like other behavioral traits, was divined by twin studies, which Harden defends, but these studies are simply not confirmed by actual genetic studies, which find miniscule heritability by comparison."
ReplyDeleteCould I have some example citations? I don't understand the difference between twin studies and "actual genetic studies" in this context, and in general would like to get a sense of how the studies are performed.
Hi Kz. Actual genetic studies refers to studies that look directly at the genes of individuals. Google Genome-wide association studies (GWAS). The polygenic scores are derived from the results of these studies. Twin studies merely compare whether two identical twins are more likely to have a trait than two non-identical twins. The assumption is that if the identical twins are more alike, they have some genes that make it so. Twins studies will show that identical twins are more alike than fraternal twins, leading researchers to claim that their are genes that make them alike for a trait, but when they look at the genes in a population from one of GWAS, they can’t find specific genes that would account for such a similarity. So they call that “missing heritablility.”
ReplyDeleteThank you for a good discussion.
ReplyDeleteBut after reading through these and half-way through the book, I think Harden is basically right.
Genes do influence our life development, attainments and failures. Polygenetic scores seem valid. And are only claimed to provide an influence, not deterministic.
If she says it, then that’s better than actual evidence…
DeleteEverything influences. Everything.
DeleteThe question is what you're gonna do about all those influential factors. Focusing on genes when you can absolutely *zero* about them, no matter their influence, should make you wonder what people's true interest in genetics is when it comes to life outcomes. Personally, I think people are looking for excuses to claim superiority over others and while suggesting that *zero* can be done about it. Of course, a living thing's outcome *always* depends on the environment into which it's placed, as should be obvious to everyone, and humans have shown great capacity for changing the environments in which they live. So perhaps talking about genes is just cover for ignoring the created environment.
madremía no has entendido nada del libro...
ReplyDelete