In Mendels Mirror: Philosophical Reflections on Biology
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Despite these brief remarks, a full account of why we concentrate so much on genes has to wait for another occasion. The story goes much deeper: into epistemological, ontological, anthropological, ethical, as well as historical matters. However, the aim here is simply to make explicit in which sense interactionism goes together with the increase of genetic diseases.
The answer is: genes are increasingly taken to be easily tractable causes necessary conditions or probabilistic causes of diseases. Even though the interactionist consensus does not assume that there is a dichotomous partitioning between innate and acquired traits, as illustrated above, it does assume that there is a continuum of traits with two poles: ranging from monogenetic diseases, such as Huntington chorea or phenylketonuria, to largely acquired impairments, such as the loss of an arm due to a car accident.
In between these poles, the realm of complexity reigns: many genes interact with each other and with environmental factors in complex ways. Scientific progress in this area is still quite tentative. If we sort diseases along this simple continuum, we already refuse to take part in any debates that ask whether genes are in principle more determining than other factors. Debates over whether genes act as informational, or programming, or have any other property that makes them special, vivid until today in philosophy of biology, become pointless from this perspective.
First of all, whether genes are more determining than other factors depends on the case in point and is a matter of degree. Second, the interactionist consensus i. Third, nobody in medicine is interested in an answer to in-principle debates. The patients as well as the physicians want to know where on the continuum a disease resides and whether it is possible to prevent it, but they do not want an answer to one of the in-principle debates.
This is understandable, since only the former questions touch the issue of fatalism, an important issue, if prevention is one of your goals. In-principle debates only tackle philosophical in-house problems about ontology, causation, information, and so on: important topics, certainly, but not for the patient or physician. In addition to the continuum, and partly constituting it, the interactionist consensus rests on a further nondichotomizing way of putting the issue: genes have specific norms of reaction that differ in various ways, defining the kind of determination at issue.
It has a flat form. A hypothetical flat norm of reaction Kitcher , p. Such a flat norm of reaction shows that changes in the value of the environmental variable horizontal axis do not make a difference to the level of expression of a trait vertical axis , given a specific genotype. Deterministic themes Kitcher , p. A flat norm of reaction means that the level of expression for a trait is constant across all the measured environments. The other kinds of genetic determination also express kinds of constancy. As Kitcher , p. An example should suffice to illustrate why mentioning these kinds of genetic determination is important.
With this, he wants, as everybody today, to escape the charge of ignoring nurture.
In order to illustrate explicitly why he does so is intriguing. Fukuyama not only assumes the determinist theme c , but he also changes, in between, the explanandum. He started with the individual level of development of the token trait height and ends with talking about the interindividual level of differences in the expression of this trait as a type. This change, inscribed in any move from a developmental context to norms of reaction, is not illegitimate, but it is important to make clear what the move means, since it includes not only a change from an individual to an interindividual level, but also a change of explanandum , and thus a change in the type of answer, and probably a change in the concept of causation involved e.
Finally, the move includes a change of perspective—from looking at the complex developmental process to looking at simple correlations between genotypes and phenotypes. It is a change to a perspective that black-boxes the developmental process. When we do not have means to understand the complex actual developmental process, we look at the termini only, as Kitcher , p. In order to investigate genotype—phenotype correlations, plotting a norm of reaction, despite its simplifying nature, is nonetheless fruitful, at least for practical contexts such as medicine, as, for instance, Lewontin , pp.
The concept of norms of reaction shows, as the simple continuum view already did, that the nature—nurture issue is a matter of degree and that the answers depend on the case in point. In-principle debates are out of place. A norm of reaction also allows us to clearly distinguish between the different kinds of genetic determination depicted by Kitcher, something we could not do if we only had a simple continuum.
Knowing the norm of reaction for a trait, given a specific gene, is thus much more informative than locating a disease at a certain position on the simple continuum. In addition, a norm of reaction clearly shows how society determines whether a trait is considered as innate i. Each genotype has a specific and context-dependent norm of reaction, specific for each gene and dependent on a given range of environments.
Philip S. Kitcher | ekevibukuw.gq
Extrapolation to and thus prediction of the expression of the trait in environments not covered in the norm of reaction is not possible. This point, stressed already by Hogben and pushed again forcefully by Lewontin , adds another dimension to the case dependency already evident in the continuum view. There simply is no general answer to whether genes or environmental factors are more important. It depends not only on the trait but also on the environments considered. Whether a gene determines in one of the above-mentioned ways a specific trait depends on the environments we single out for consideration.
Since it will always be hard to epistemically single out the most relevant environments, the value of a norm of reaction is limited, as Kitcher , pp. Since it is our society that determines which environments are available at all for consideration, our society strongly influences whether a trait is considered as genetically determined or not. As long as we do not provide equal education, for instance, we will not be able to make a reliable statement about the development of individuals in such an equal environment.
Last but not least, that norms of reaction can take different shapes illustrates that genetic determination does not always support fatalism. Something can be genetically determined, even if it can be prevented from occurring. Phenylketonuria PKU seems to be the single most often-cited example for this in the literature on genetic determinism. It is conventionally treated as a monogenetic disorder. As Huntington chorea, it is at the hereditary extreme of the continuum of traits, with severe effects on neural development, among other things. Even if the case of PKU shows that no fatalism is implied in our talk of genetic diseases, the just-given picture of PKU is still a simplified one.
There is a considerable amount of clinical heterogeneity i. The more knowledge we get, the more complex the picture of the etiology and nature of PKU becomes. However, the point I want to make here is independent of these complications, since the simple as well as the complex picture support the point about the difference between genetic determination and fatalism, and that is the important point in this article. In addition, the complex picture seems not to disturb the bias towards geneticization.
There is a gene, the PAH gene, at which mutations correlated with PKU have been identified; there is relative developmental stability over a specific range of environments; and the physiological mechanism is understood quite well. Be that as it may, PKU is a telling example for this study, since it shows how society enters the connection between genetic determination and fatalism.
In a possible world that does, contrary to our world, not allow for any environment without phenylalanine, PKU would probably have a flat norm of reaction.
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It would be a fatal destiny. However, the following also holds, and that is the important aspect. If we currently regard a genetic disease, or such Mendelian traits as sex or blood group, as having a flat norm of reaction, we might ignore a socially possible world, in which a different set of environments would destroy the flatness of the norm of reaction and allow modification of the trait. The untried possible worlds are always bountiful. If they are untried, we should not forget to ask who gains by leaving them untried. The important conclusion from considering norms of reaction as part of our interactionist consensus is thus: whatever the scientific, and often mere statistical, measure with which we try to express that environment does not influence a trait be it Mendelian segregation, a flat norm of reaction, positive predictive value, penetrance, heritability, expressivity, concordance rate, etc.
It is dependent on the environments considered in the measure. Which environments are considered is a choice, and the choice depends on which environments are considered as practically possible and desirable in this world. It depends on our socially determined preferences about how the world should look, especially with respect to war, crime, poverty, education, and so on. It is time to summarize the account of interactionism given here: a rigid genetic determinism has largely been replaced by an interactionist consensus. This consensus nonetheless embraces the above-mentioned deterministic themes, i.
The innate—acquired distinction appears in a nondichotomous, nongeneralizing, and nonfatalistic manner: first, there is no dichotomous partitioning of traits but a continuum of traits, ranging from genetic diseases to acquired traits; second, where we put a trait along this axis cannot be generalized since it depends on the environments considered; finally, if a disease such as PKU is considered as a genetic disease, it does not imply fatalism.
In sum, there is no simple dichotomy between innate and acquired traits in our contemporary interactionist concept of genetic determination. At the level of causal factors rather than traits , however, we have a very clearcut partitioning, as the concept of norms of reaction shows, which depends on the exclusive and exhaustive distinction between genetic factors on the one hand and nongenetic factors on the other. As mentioned in the beginning, the nongenetic factors include everything except DNA i.
The interactionist consensus, with its three conceptual levels i. This is also mirrored in the practical context of treatment of diseases as well as in our folk concept of innateness. The innate—acquired distinction is quite tenacious, at least in medicine. Taking the latter for granted, it is not clear at least not to me why drugs count as biologized treatment and why environmental treatments do not. The boundary between the second and third kinds of treatment drugs and environmental intervention, respectively is fuzzy.
The boundary between the first, i. Giving someone a pill is surely a different treatment than introducing a diet, as in the case of the genetic disorder PKU, and it certainly makes a difference for our vision of health whether we choose the second or the third kind of treatment, but what exactly accounts for the difference between them seems to be not very clear, at least not to me.
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The difference between giving a pill and keeping a diet on the one hand and eliminating the respective allele on the other hand, is, however, very clear: one is eliminating bits of DNA, the other is eliminating or changing the usual consequences of these hereditary factors by changing other factors. The clearcut dichotomous distinction between factors, which we found already inscribed in the norms of reaction, is thus reappearing in the context of treatment. Furthermore, it is also constitutive for the concept of innateness, a concept that has recently been at issue in a vivid debate in the philosophy of biology.
Each of the finalists of these candidates refers to only one aspect of the complex and fuzzy folk concept of innateness, e. I cannot go into the details of the debate. Space would not suffice to do so, and it is not necessary for the purpose of this article. I thus regard the following as a good approximation of the folk concept of innateness:. X is innate if and only if it is present at the moment of birth or, if that is not the case, at least inevitably appearing during development at a certain age, relative to a given range of environments , and does so because of causal factors present at the moment of conception.
The exclusion of acquired diseases is part of the folk concept of innateness, and this is the important point for this article. Their example is the acquisition of the bacterium Clostridium difficile C. Wendler , pp. Humans normally get clostridia via nutrition, without negative effects. When, however, sick people are treated with antibiotics, then C. Usually, the reaction to such an example is that such infectious dispositions should be excluded from being innate, even though they are, relative to a specific set of environments, inevitably acquired during development.
Certainly, this folk concept has a history and could be further questioned philosophically. The brief account just given will neither satisfy the historian nor the usual demands of philosophers with enough perseverance for infinite conceptual analysis. Many aspects of the situation I described were certainly different in the past and are certainly different in many other contexts in which the innate—acquired distinction is used as well.
However, I merely claim that there are contexts in which there is such a clear division: the conceptual context of the interactionist consensus, the practical context of treatment, and the conceptual context of the folk concept of innateness. This holds even if there are other contexts where there is no such division.
Philosophers, on the other hand, would object that the above reconstruction fails. Given the reconstruction, we still can, in fact, count the possession of C. Our interactionist consensus enables us to see that it is always genes with stress on the plural and environmental factors that are involved in the development of a specific trait. Thus, the acquisition of C. If we had different genes, e. I cannot here offer a final solution to whether we should, or how we could, consistently distinguish between innate and acquired diseases, given our interactionist consensus.
As already mentioned in Part 1, such a solution would require a clear account of what causation in developmental contexts means and whether the individual is the level of analysis that we should concentrate on.
The tentative reconstruction of the folk concept of innateness was merely intended to show that we intuitively want the definition of innateness to reflect a rigid innate—acquired distinction. In other words, our implicit assumption seems to be that there are two kinds of diseases: innate and acquired ones. This is not in contradiction to the continuum view. On the contrary, it is the foundation for it, defining the poles of the nondichotomous distinction. The continuum view only adds the realm of complexity for the cases in between the two extremes.
In other words, we want to distinguish between diseases such as PKU and things like car accidents, despite the interactionist consensus. And we accept that there are myriads of cases that are hard to classify. In other words, we accept that the bipolar distinction between innate and acquired is vague. We accept this as we accept that the bipolar distinction between white and black is vague, i.
In Mendel's Mirror: Philosophical Reflections on Biology
The practical context has shown that we assume there are two kinds of treatments and thus two kinds of causal factors; the two conceptual contexts have shown that, based on the exclusive distinction of causal factors i. The bipolar scheme does, however, not assume two exclusive groups of diseases, since, if pressed, we admit the continuum of traits, despite the bipolar framing.
All this shows the deep entrenchment of the innate—acquired distinction. However, this entrenchment certainly did not prevent philosophers from criticizing the distinction. Let us thus enter the minefield of whether one should use the innate—acquired distinction. What follows will not do away with the pitfalls in this minefield, but it will provide a specific perspective for dealing with it and some preliminary arguments in the direction of this perspective.
Constructive interactionists or transinteractionists like Oyama , , want to establish a true causal parity of the factors involved in development. It is important to be very clear about what is actually criticized by a call for causal parity. There are two ways of giving causal priority to genes that are strawman-like, since nobody actually believes in the respective priority.
The first strawman-like claim is that genes control or determine as necessary and sufficient conditions the occurrence of a certain trait. This claim addresses the level of ontogenetic development. Part 1 illustrated that a denial of this is part of the interactionist consensus. The second strawman-like claim addresses the level of phylogenetic evolution: the claim that genes are the only hereditary elements in life i. Nobody believes in this either.
We know that cells and other organic matter as well as behavior or culture is equally transmitted down the generations, and the evidence for epigenetic inheritance reinforces this point of view. This claim is related to the evolutionary and to the developmental level but distinct from and independent of the first two ways of alleged prioritizing. I will neither discuss the pros and cons, nor take sides.
It is an in-principle debate, and, as stated above, whichever side we choose in these debates, it would not make a difference for the kinds of determination at issue here. I want to focus on something narrower: whether we have to get rid of a bipolar partitioning to prevent prioritizing of genes as it is actually practiced in the contemporary hunt for disease genes. This goal requires analyzing whether the bipolar partitioning between genes and environment, which is at the basis of and inscribed in the interactionist consensus, violates causal parity.
According to Johnston , p. Consequently, the environment, with which the organisms interact, starts outside of them. Kitcher, in other words, assumes a truly exhaustive and exclusive gene—environment distinction, i. Either something is an environmental factor or it is a genetic factor. Nothing can be both and there is no third option. Given this, the organism seems to disappear as a separate causal agency.
The organism becomes a mere effect and thus appears only as an explanandum but not as part of the explanans. Given all this, Johnston surely has a point, at least according to our folk ontology for most entities of the biotic world, since these organisms are key agents in the developmental and evolutionary processes. However, Johnston merely excludes his enemy by definition.
Whether genes interact with the environment depends on how you conceptualize environment, but defining it either way does not settle the issue of whether it makes sense to partition developmental factors dichotomously. Furthermore, partitioning life into genetic and environmental factors does not lead to organisms as mere effects, since an effect can certainly be a cause for something else e.
Fausto-Sterling provides an example of a different route. She also criticizes gene—environment interaction as ill-guided. She does so by comparing it with a similar atomistic view in neurology: it is the developmental system itself replacing the category of organism that causes something, as it is the neuronal net, and not a specific neuron or some neurons somewhere in the brain, that causes something in the brain. This is what Oyama , p.
The responses of singular neurons depend on the responses of others. However, all these pleas against atomism simply lead back to the problem of black-boxing the complex web of actual interactions during development. The atomism exists only in the simplified picture that we use and often have to use, due to the lack of anything else, and with which we obtain knowledge about the norm of reaction.
The distributed set of participants in the complex developmental process is black-boxed in the search for knowledge about the norm of reaction. However, having such knowledge, which is knowledge about what makes a difference for prevention, is quite useful, even if knowledge about the complex developmental processes, black-boxed as they are, is still missing. Trying to prevent something demands different tools than trying to understand complex holistic development. Well, this does not require it; other issues such as those standard in medicine or health care, might well.
The developmental systems theory perspective might thus turn out to be quite useless for the pragmatics that define the clinical context of medicine and health care. First, it is not clear that we would always be equipped with better norms of reactions if we knew the whole complex developmental story. It might further our knowledge about norms of reaction, but it might also fail to do so. Second, in medicine, we often do not want to wait, if we can get some decent knowledge by black-boxing. If we admit that black-boxing can be useful, as Oyama , pp.
The following tentative arguments, certainly in need of further elaboration, shall provide a first approximation of a limited pragmatic defense of the innate—acquired distinction in medicine. These arguments are independent of the critique just discussed. Even if it were correct that the bipolar distinction leads to simplifications of the causal picture of development, this cannot prove that this simplification is necessarily something we should despise. Simplicity is an epistemic value, and in the clinical context it might well be that it pays to accept some simplicity to have some handles for prevention and treatment.
The question I thus focus on is in which sense the concept of the norm of reaction, and the underlying bipolar partitioning of causes, helps us to see that not everything is fatalistically determined by genes, despite its causally simplifying nature. The first argument, an epistemic argument, relates to knowledge about specific diseases. Without ever distinguishing in a precise way between genetic and environmental factors, it would be hard to see, for instance, that the genetic disease PKU is genetically determined in a nonfatalistic sense, i.
We could not see, at least not as easily as we pretend to, the difference between a flat norm of reaction and a punctuated one, if we were not to use the distinction between genetic and environmental factors. If we want to prevent a disease and intelligently vary the environment, then we might find a preventive effect of one of the environments, i.
Thus, from the pragmatic point of view, holding genes constant and varying other factors is not a case of giving genes priority. The bipolar partitioning of factors inscribed in the concept of the norm of reaction is therefore quite helpful, if we want to stress the importance of environment, e. This argument is similar to an early argument from Lehrman Lorenz black-boxed development and concentrated on developmental stability. Finding stability is, however, according to Lehrman, less informative than finding difference, e. Even though he criticizes the distinction between innate and acquired traits, the distinction between innate and acquired factors i.
The innate—acquired distinction thus has epistemic value in finding environmental factors that prevent diseases. Even though Lehrman , p. However, he uses it only at the level of factors and criticizes it at the level of processes maturation versus learning and of traits innate versus learned , and so do I. The second argument refers to the context of classification of diseases. Does the innate—acquired distinction have a heuristic value for this endeavor?
When you erase a bipolar distinction from a system of classification, you create a more inclusive set of things. This creates two problems. First, given our contemporary bias towards declaring more and more diseases as genetic, the elimination of the polarity will certainly further this tendency. The innate—acquired distinction constantly pulls against the contemporary bias towards calling diseases genetic. Second, erasing distinctions increases rather than decreases trivialization. The more general, i. In other words, the more you include in a class, the less it means when an element is included.
You lose depth of vision, indeed you might even literally see less. Certainly, to keep the distinction, as a bipolar but nondichotomous one, should not deter us from trying to fill out the space between the poles with ever finer categories. The third argument says that historically the distinction was necessary to keep those very factors on the table that the critics of the distinction want to give parity to.
When, at the beginning of the 20th century, American anthropology was in the process of becoming an academic discipline, Alfred L. Kroeber, one of the famous students of Franz Boas, used the opposition between nature and nurture in the form of heredity versus culture, to reach for anthropology disciplinary identity and autonomy from genetics, evolutionary theory, as well as psychology. He did so by creating an epistemic object—culture—that, as he thought, only anthropologists are able to study properly.
His making of culture as a new epistemic object was similar to the making of genes, which were postulated in the beginning of genetics as hypothetical entities and epistemic objects that can only by studied by genetics, then the new primus inter pares among the biological disciplines. Decoupling nature from culture means in this case that culture can change without a correlated change in the innate characteristics of individuals.
Culture can and did historically take off, so to say. Culture is in this sense autonomous and relies on a separate and parallel process of inheritance. There are two systems of inheritance: non-Lamarckian biological inheritance and an autonomous cultural inheritance. Historically, the innate—acquired distinction did not prevent parity of factors.
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