Leading behavior geneticist Robert Plomin is publishing “Blueprint: How DNA Makes Us Who We Are” in October of 2018. I, of course, have not read the book yet. But if the main thesis of the book is that DNA is a “code”, “recipe”, or “blueprint”, then that is already wrong. This is because presuming that DNA is any of the three aforementioned things marries one to certain ideas, even if they themselves do not explicitly state them. Nevertheless, Robert Plomin is what one would term a “hereditarian”, meaning that he believes that genes—more than environment—shape an individual’s psychological and other traits. (That’s a false dichotomy, though.) In the preview for the book at MIT Press, they write:
In Blueprint, behavioral geneticist Robert Plomin describes how the DNA revolution has made DNA personal by giving us the power to predict our psychological strengths and weaknesses from birth. A century of genetic research shows that DNA differences inherited from our parents are the consistent life-long sources of our psychological individuality—the blueprint that makes us who we are. This, says Plomin, is a game-changer. It calls for a radical rethinking of what makes us who were are.
Genetics accounts for fifty percent of psychological differences—not just mental health and school achievement, but all psychological traits, from personality to intellectual abilities. Nature defeats nurture by a landslide.
Plomin explores the implications of this, drawing some provocative conclusions—among them that parenting styles don’t really affect children’s outcomes once genetics is taken into effect. Neither tiger mothers nor attachment parenting affects children’s ability to get into Harvard. After describing why DNA matters, Plomin explains what DNA does, offering readers a unique insider’s view of the exciting synergies that came from combining genetics and psychology.
I won’t get into most of these things today (I will wait until I read the book for that), but this will be just an article showing that DNA is, in fact, not a blueprint, and DNA is not a “code” or “recipe” for the organism.
It’s funny that the little blurb says that “Nature defeats nurture by a landslide“, because, as I have argued at length, nature vs nurture is a false dichotomy (See Oyama, 1985, 2000, 1999; Moore, 2002; Schneider, 2007; Moore, 2017). Nature vs nurture is the battleground that the false dichotomy of genes vs environment is fought on. However, it makes no sense to partition heritability estimates if it is indeed true that genes interact with environment—that is, if nature interacts with nurture.
DNA is also called “the book of life”. For example, in her book The Epigenetics Revolution: How Modern Biology Is Rewriting Our Understanding of Genetics, Disease, and Inheritance, Nessa Carey writes that “There’s no debate that the DNA blueprint is a starting point” (pg 16). This, though, can be contested. “But the promise of a peep into the ‘book of life’ leading to a cure for all diseases was a mistake” (Noble, 2017: 161).
Developmental psychologist and cognitive scientist David S. Moore concurs. In his book The Developing Genome: An Introduction to Behavioral Epigenetics, he writes (pg 45):
So, although I will talk about genes repeatedly in this book, it is only because there is no other convenient way to communicate about contemporary ideas in molecular biology. And when I refer to gebe, I will be talking about a segment or segments of DNA containing sequence information that is used to help construct a protein (or some other product that performs a biological function). But it is worth remembering that contemporary biologists do not mean any one thing when they talk about “genes”; the gene remains a fundementally hypothetical concept to this day. The common belief that there are things inside of us that constitute a set of instructions for building bodies and minds—things that are analogous to “blueprings” or “recipes”—is undoubedtly false. Instead, DNA segements often contain information that is ambiguous, and that must be edited or arranged in context-dependent ways before it can be used.
Still, other may use terms like “genes for” trait T. This, too, is incorrect. In his outstanding book Making Sense of Genes, Kostas Kamporakis writes (pg 19):
I also explain why the notion of “genes for,” in the vernacular sense, is not only misleading but also entirely inaccurate and scientifcally illegitamate.
First, I show that genes “operate” in the context of development only. This means that genes are impllicated in the development of characters but do not determine them. Second, I explain why single genes do not alone produce characters or disease but contribute to their variation. This means that genes can account for variation in characters but cannot alone explain their origin. Third, I show that genes are not the masters of the game but are subject to complex regulatory processes.
Genes can only be seen as passive templates, not ultimate causes (Noble, 2011), and they cannot explain the origin of different characters but can account for variation in physical characters. Genes only “do” something in the context of development; they are inert molecules and thusly cannot “cause” anything on their own.
Genes are not ‘for’ traits, but they are difference-makers for traits. Sterelny and Griffiths (1999: 102), in their book Sex and Death: An Introduction to Philosophy of Biology write:
Sterelny and Griffiths (1988) responded to the idea that genes are invisible to selection by treating genes as difference makers, and as visible to selection by virtue of the differences they make. In doing so, they provided a formal reconstruction of the “gene for” locution. The details are complex, but the basic intent of the reconstruction is simple. A certain allele in humans is an “allele for brown eyes” because, in standard environments, having that allele rather than alternatives typically available in the population means that your eyes will be brown rather than blue. This is the concpet of a gene as a difference maker. It is very important to note, however, that genes are context-sensitive difference makers. Their effects depend on the genetic, cellular, and other features of their environment.
(Genes can be difference makers for physical traits, but not for psychological traits because no psychophysical laws exist, but I’ll get to that in the future.)
Note how the terms “context-sensitive” and “context-dependent” continue to appear. The DNA-as-blueprint statement presumes that DNA is context-independent, but we cannot divorce genes—whatever they are—from their context, since genes and environment, nature and nurture, are intertwined. (And it is even questioned if ‘genes’ are truly units of inheritance, see Fogle, 1990. Fogle, 2000 also argues to dispense with the concept of “gene” and that biologists should be using terms like intron, promoter region, and exon. Nevertheless, there is a huge disconnect with the term “gene” in molecular biology and classical genetics. Keller 2000 argues that there are still uses for the term “gene” and that we should not dispense with the term. I believe we should dispense with it.)
Susan Oyama (2000: 77) writes in her book The Ontogeny of Information:
“Though a plan implies action, it does not itself act, so if the genes are a blueprint, something else is the constructor-construction worker. Though blueprints are usually contrasted with building materials, the genes are quite easily conceptualized as templates for building tools and materials; once so utilized, of course, they enter the developmental process and influence its course. The point of the blueprint analogy, though, does not seem to be to illuminate developmental processes, but rather to assume them and, in celebrating their regularity, to impute cognitive functions to genes. How these functions are exercised is left unclear in this type of metaphor, except that the genetic plan is seen in some peculiar way to carry itself out, generating all the necessary steps in the necessary sequence. No light is shed on multiple developmental possibilities, species-typical or atypical.“
The Modern Synthesis is one of the causes for the genes-as-blueprints thinking; the Modern Synthesis has causation in biology wrong. Genes are not active causes, but they are passive templates, as argued by many authors. They, thus, cannot “cause” anything on their own.
In his 2017 book Dance to the Tune of Life: Biological Relativity, Denis Noble writes (pg 157):
As we saw earlier in this chapter, these triplet sequences are formed from any combination of the four bases U, C, A and G in RNA and T, C, A and G in DNA. They are often described as a genetic ‘code’, but it is important to understand that this usage of the word ‘code’ carries overtones that can be confusing.
A code was originally an intentional encryption used by humans to communicate. The genetic ‘code’ is not intentional in that sense. The word ‘code’ has unfortunately reinforced the idea that genes are active and even complete causes, in much the same was as a computer is caused to follow the instructions of a computer program. The more nuetral word ‘template’ would be better. Templates are used only when required (activated); they are not themselves active causes. The active causes lie within the cells themselves since they determine the expression patterns for the different cell types and states. These patterns are comminicated to the DNA by transcrption factors, by methylation patterns and by binding to the tails of histones, all of which influence the pattern and speed of transcription of different parts of the genome. If the word ‘instruction’ is useful here at all, it is rather that the cell instructs the genome. As Barbara McClintock wrote in 1984 after receiving her Nobel Prize, the genome is an ‘organ of the cell’, not the other way around.
Realising that DNA is under the control of the system has been reinforced by the discovery that cells use different start, stop and splice sites for producing different messenger RNAs from a single DNA sequence. This enables the same sequence to code different proteins in different cell types and under different conditions [here’s where context-dependency comes into play again].
Representing the direction of causality in biology the wrong way round is therefore confusing and has far-reaching conseqeunces. The causality is circular, acting both ways: passive causality by DNA sequences acting as otherwise inert templates, and active causality by the functional networks of interactions that determine how the genome is activated.
This takes care of the idea that DNA is a ‘code’. But what about DNA being a ‘blueprint’, that all of the information is contained in the DNA of the organism before conception? DNA is clearly not a ‘program’, in the sense that all of the information to construct the organism exists already in DNA. The complete cell is also needed, and its “complex structures are inherited by self-templating” (Noble, 2017: 161). Thus, the “blueprint” is the whole cell, not just the genome itself (remember that the genome is an organ of the cell).
Lastly, GWA studies have been all the rage recently. However, there is only so much we can learn just from association studies, before we need to turn to the physiological sciences for functional analyses. Indeed, Denis Noble (2018) writes in a new editorial:
As with the results of GWAS (genome-wide association studies) generally, the associations at the genome sequence level are remarkably weak and, with the exception of certain rare genetic diseases, may even be meaningless (13, 21). The reason is that if you gather a sufficiently large data set, it is a mathematical necessity that you will find correlations, even if the data set was generated randomly so that the correlations must be spurious. The bigger the data set, the more spurious correlations will be found (3).
The results of GWAS do not reveal the secrets of life, nor have they delivered the many cures for complex diseases that society badly needs. The reason is that association studies do not reveal biological mechanisms. Physiology does. Worse still, “the more data, the more arbitrary, meaningless and useless (for future action) correlations will be found in them” is a necessary mathematical statement (3).
Nor does applying a highly restricted DNA sequence-based interpretation of evolutionary biology, and its latest manifestation in GWAS, to the social sciences augur well for society.
It is further worth noting that there is no privileged level of causation in biological systems (Noble, 2012)—a priori, there is no justification to privilege one system over another in regard to causation, so saying that one level of the organism is “higher” than another (for instance, saying that genes are, and should be, privileged over the environment or any other system in the organism regarding causation) is clearly false, since there is upwards and downwards causation, influencing all levels of the system.
In sum, it is highly misleading to refer to DNA as “blueprints”, a “code”, or a “recipe.” Referring to DNA in this way means that one presumes that DNA can be divorced from its context—that it does not work together with the environment. As I have argued in the past, association studies will not elucidate genetic mechanisms, nor will heritability estimates (Richardson, 2012). We need physiological testing for these functional analyses, and association studies like GWAS and even heritability estimates don’t tell us this type of information (Panofsky, 2014). So, it seems, that what Plomin et al are looking for that they assume are “in the genes”, are not there, because they use a false model of the gene (Burt, 2015; Richardson, 2017). Genes are resources—templates to be used by and for the system—not causes of traits and development. They can account for differences in variation, but cannot be said to be the origin of trait differences. Genes can be said to be difference makers, but knowing whether or not they are difference makers for behavior, in my opinion, cannot be known.
(For further information on genes and what they do, reach Chapters Four and Five of Ken Richardson’s book Genes, Brains, and Human Potential: The Science and Ideology of Intelligence. Plomin himself seems to be a reductionist, and Richardson took care of that paradigm in his book. Lickliter (2018) has a good review of the book, along with critiques of the reductionist paradigm that Plomin et al follow.)
i’ve been saying the same thing on all the HBD blogs for near a decade.
HBDers are incapable of understanding.
Second, I explain why single genes do not alone produce characters or disease but contribute to their variation.
they do sometimes. but genetic diseases are rare.
What’s the difference between a “passive template” and a “blueprint”? I’ve seen a few blueprints, but I’ve never seen one get up and walk.
Templates are only used when required; blueprints already have the “plan” laid out; templates are waiting to be “written on”. The context-dependency of “genes” ensures that they are not “blueprints”.
A template is rigid, and physically constrains the movement of a drawing, cutting, shaping or drilling instrument, so it is in fact more active than a blueprint, which is entirely passive, and from which a builder can (and sometimes does) deviate at will. You reject the blueprint metaphor, and naively replace it with an alternative metaphor that is even stronger than that of “blueprint”.
There is no way you can get out of the fact that DNA is AT LEAST a blueprint. If you wish to say that it is more than a blueprint, well, fine. That’s your choice.
No, I can deny that DNA is a blueprint while accepting it’s a template. Blueprints imply action, but we know they don’t act so there must be something that uses the so-called blueprints for construction of whatever is in the so-called blueprints. There is no logical reason to accept that DNA is a blueprint, code, or recipe.
Blueprints don’t imply action. Many blueprint never get turned into buildings, due to lack of money or time, or a suitable contractor, or permission from planning regulators, etc. Similarly, code doesn’t always get run, and recipes are not always followed. None of these things imply action.
And in this way, blueprints, program code and recipes are similar to DNA. Inside a cell, where it’s surrounded by RNA, DNA causes exciting things to happen, but isolated in a test tube, it does little besides adding mass and taking up space. A blueprint in the hands of a builder guides construction, but rolled up in the drawer of an architect, it does nothing.
one of the things the anti-HBDers don’t grok is that while all effects are GxE effects…
if you don’t know what the best E is for the given genome the P = G + E model is practical.
some chinese blogger made this clear to me.
so my dad did actually die last night from an unknown neurodegenerative disease his brother had died from 5 years ago. he was 73.
i’m waiting for the pathologist’s report as i arranged for his brain to be “harvested”.
rr can’t tell me what i can do to avoid the same fate. all he can tell me is neurodegenerative disease isn’t a psychological trait.
try harder paisano.
Pinpointing “one cause” in a multilevel biological system seems to me to be pointless, since every level interacts with the lower and higher levels. Gene G may be “implicated” in disease D, but only in a context-dependent manner. This is, of course, why the terminology of “genes for” is false.