Two foundational developments of modern biology—the theories of evolution by natural selection and the genetic basis of heredity—were built from the language, arguments, evidence, and practices of controlled breeding in agriculture and the laboratory. The genotype-phenotype distinction—or, rather, a series of different meanings of those terms—provides an entry point into the implications of that genesis and subsequent developments. Complexities get suppressed, which engenders new problems and complexity-recovering responses. Many of these are raised or implied by Johannsen (1911), where the terms genotype and phenotype were introduced to English-language readers. Continue reading
This 23-minute youtube video is a practice run of a talk with the following abstract:
How difficult is it to change the typical distributions of a trait, such as aggression, substance abuse, suicide attempts, as they differ between males and females? This can be construed as a matter of fixity versus flexibility in the development of traits in individuals over their life course or of the relative degrees of hereditary versus environmental influences on the variation between versus within groups. This paper contrasts the conceptual critiques of research of the two construals with a view to clarifying how they address practical concerns about the development of gendered individuals, as raised especially by feminist scholars. Drawing on my book, Nature-Nurture? No (2014), I argue that inattention to heterogeneity has limited critique as well as research under both construals.
The three take home messages are that: conceptual critique (of the forms I describe) clears space for focusing on the development of gendered individuals; this counters a persistent essentialism about gender; and these first two messages have implications well beyond issues raised by feminist scholars.
See http://bit.ly/ishpssb15 for text of talk and references
A previous post considered the connection between two different Nature-Nurture issues: the matter of fixity versus flexibility in the development of traits in individuals over their life course and the relative degrees of hereditary versus environmental influences on the variation of the trait between versus within groups? (“Groups” here refers to males or females, but the question might be extended to socially defined racial or socio-economic groups.) Continue reading
Kendler and colleagues examine behavioral traits in relation to a wealth of environmental factors over the life course as well as to the relatedness of the individuals (Kendler and Prescott 2006). In Kendler et al. (2002), for example, data on over 1,900 twins are used to fit the incidence of major depression to an additive model that incorporates many environmental factors and a “genetic risk” factor. This last factor is derived from the incidence of major depression in the co-twin and parents, with adjustments made for the degree of relatedness of the twins (monozygotic versus dizygotic). The model accounts for 52% of the variance in the trait and provides a picture of development that is rich and plausible (see figure below).
Why nature versus nurture? Surely it must be nature and nurture—we all know that traits develop over time through the interaction of the organism with genetic or hereditary and environmental or social influences. Indeed, the modern science of epigenetics, building on ever-increasing information about DNA sequences and how genes function, now shows us how chemicals from outside the cell can modify the activity of genes for the rest of an organism’s life and sometimes even into subsequent generations. Moreover, since the late 1800s—well before advances in molecular biology—developmental biologists have been studying the mechanisms through which a single cell divides into multiple cell types and gets arranged into tissues, organs, and the organism’s overall form (Gilbert 2013). The nature versus nurture in this book [Taylor 2014] is not, however, a matter of development of traits over time. A sketch of the history and current state of the study of heredity, development, and variation is needed to set the scene.
Various groups co-sponsored a presentation by my road trip co-driver, Raúl García Barrios, on his various ecological and social restoration and conservation projects around Cuernavaca, México. My role was to lead a 30-minute discussion.
The contradiction referred to in the title has three main parts:
- the monetary value that can be placed on ecosystem services in some of the watersheds near Cuernavaca is 1000 times less than the value that would follow from proposed housing developments (and freeways to serve those developments);
- the campaign to preserve the undeveloped system might succeed by appealing to legal and constitutional procedures (“defending the wall”), not market comparisons (i.e., economic valuations);
- the high economic values for development are based on government subsidies for home buyers and on a bubble, so blocking development is also a chance to save people from suffering when the bubble bursts, as it would eventually do.
The paper generated discussion on its own and I stepped back and let that happen. However, as an experiment I had asked the audience to do a notecard exercise before the talk started, so I got them to do part 2 at the end. The exercise was designed to explore how the audience view the three related questions (to follow) before versus after the presentation.
In a situation that concerns you:
- what do you know?
- what can be done on the basis of that knowledge?
- what more do you need to inquire into in order to have the knowledge you need to see or show what is to be done.
Part 2 was to repeat this after the talk.
My review of the Before vs. After did not in most cases show the influence of the presentation, but the result was a rich set of issues that could be pursued in an environmental education curriculum, e.g.,
- How to prioritize scale of response & target actors
- Relationship between: quest to understand complexity vs. need to act
- Are there certain incentives that can increase good composting?
- Look into financial structure of the tourism industry; Tourism income doesn’t directly support conservation practices; long term residents get little income
- If sustainable development in subject to market rules, and thus to ethical and practical limitations therein, what are alternative pathways?
- Low participation by minority students in environmental studies
- Inquire into historical examples of defending the wall vs. state supported market forces
- Delegitimation of state support for market
In a 2011 graduate course on “Gender, Race, and the Complexities of Science and Technology,” students were asked to add an annotated reference or resource (=person, organization…) to the evolving googledocs bibliography each week. (Annotations were to convey the article’s key points as well as its connection to the student’s own inquiries and interests.) The result is as follows: Continue reading
Heterogeneous construction is a variant of the idea of intersecting processes, which, in turn, is an attempt to discipline without suppressing the unruliness of complexity. The concept of heterogeneous construction can be illustrated by reference to the previous post on the Brown and Harris/Bowlby account of class, family, and psychology combining to explain the onset of serious depression.
As stated in the previous post, the factors are not separate contributing causes, like spokes on a wheel, but take their place in the multistranded life course of the individual [i.e., in the intersecting processes]. Each line should be interpreted as one contributing causal link in the construction of the behavior. The lines are dashed, however, to moderate any determinism implied in presenting a smoothed out or averaged schema; the links, while common, do not apply to all women at all times, and are contingent on background conditions not shown in the diagram.
For example, in a society in which women are expected to be the primary caregivers for children (a background condition), the loss of a mother increases the chances of, or is linked to, the child’s lacking consistent, reliable support for at least some period. Given the dominance of men over women and the social ideal of a heterosexual nuclear family, an adolescent girl in a disrupted family or custodial institution would be likely to see a marriage or partnership with a man as a positive alternative, even though early marriages tend to break up more easily. In a society of restricted class mobility, working-class origins tend to lead to working-class adulthood, in which living conditions are more difficult, especially if a woman has children to look after and provide for on her own. In many such ways these family, class, and psychological strands of the woman’s life build on each other. Let us also note that, as an unavoidable side effect, the pathways to an individual’s depression intersect with and influence other phenomena, such as the state’s changing role in providing welfare and custodial institutions, and these other phenomena continue even after the end point, namely, depression, has been arrived at.
Suppose now, quite hypothetically, that certain genes, expressed in the body’s chemistry, increase a child’s susceptibility to anxiousness in attachment compared to other children, even those within the same family. Suppose also that this inborn biochemistry, or the subsequent biochemical changes corresponding to the anxiety, rendered the child more susceptible to the biochemical shifts that are associated with depression. It is conceivable that early genetic or biochemical diagnosis followed by lifelong treatment with prophylactic antidepressants could reduce the chances of onset of severe depression. This might be true without any other action to ameliorate the effects of loss of mother, working-class living conditions, and so on. There are, however, many other readily conceivable engagements to reduce the chances of onset of depression, for example, counseling adolescent girls with low self-esteem, quickly acting to ensure a reliable caregiver when a mother dies or is hospitalized, making custodial institutions or foster care arrangements more humane, increasing the availability of contraceptives for adolescents, increasing state support for single mothers, and so on. If the goal is reduction in depression for working-class women, the unchangeability of the hypothetical inherited genes says nothing about the most effective, economical, or otherwise socially desirable engagement—or combinations of engagements—to pursue. Notice also that many of these engagements have their downstream effect on depression via pathways that cross between the different strands. For example, if self-esteem counseling were somewhat effective then fewer unwanted pregnancies and unsupportive partnerships might be initiated; both effects could, in turn, reduce the incidence of single parenthood and difficult living conditions.
These sequences of multiple causes, building on each other over the individual’s life history, permit a number of conclusions about the nature-nurture debate:
1. Neither the unchangeability of genes nor the reliability of some gene- or biochemistry-based intervention, such as the hypothetical prophylactic antidepressants, would prove that the genes are the most significant cause of the acute depression that has been occurring in the absence of such treatment.
2. Critics of genetic explanations could dismiss the attribution of an individual’s behavior to genes (or 50% or 80% to genes) as a technically meaningless partitioning of causes without placing themselves at the other pole from genetic determination.[i] That is, they would not have to make the counterclaim that the environment determines behavior or that, if the right environment were found, any desired behavior could be elicited. The Brown-Harris-Bowlby (BHB) account addresses malleability or immalleability of behavioral outcomes without ruling out genetic contributions.
3. Similarly, critics would not need to rest their case on demonstrations that behavioral genetics has been or still is methodologically flawed (Lewontin et al. 1984), on textual deconstructions of the categories and rhetoric employed (Lewontin 1979), or on attributions of political bias to the supporters of behavioral geneticists. These are all interesting, but, in light of the BHB account of the behavior, not necessary for a conceptual critique of genetic determinism.
Over and above these conclusions, the BHB account of the origins of acute depression in working-class women also displays the following features that I associate with the idea that something is “heterogeneously constructed,” or an outcome of “intersecting processes.”
a) Without any superintending constructor or outcome-directed agent,
b) many heterogeneous components are linked together, which implies that
c) the outcome has multiple contributing causes, and thus
d) there are multiple points of intervention or engagement that could modify the course of development. In short,
e) causality and agency are distributed, not localized. Moreover,
f) construction is a process, that is, the components are linked over time,
g) building on what has already been constructed, so that
h) it is not the components, but the components in linkage that constitute the causes. Points c) and f–h) together ensure that
i) it is difficult to partition relative importance or responsibility for an outcome among the different types of cause (e.g., 80% genetic vs. 20% environmental). Generally,
j) there are alternative routes to the same end, and
k) construction is “polypotent” (Sclove 1995), that is, things involved in one construction process are implicated in many others. Engaging in a construction process, even in very focused interventions, will have side effects. Finally, points f) and k) mean that
l) construction never stops; completed outcomes are less end points than snapshots taken of ongoing, intersecting processes.
I am aware that there may be objections to the case I have chosen to make the preceeding points. In discussing depression among working class women, rather than in other groups, I could be seen as perpetuating a male, professional class perspective. However, the politics of the case can be viewed quite differently. Although depressed working class women are the focus, the intersecting processes account brings a range of other agents into the picture. While the account does not identify ways to cure the women studied, other girls and women that follow them might seek support from, or find themselves supported by—to pick up on the potential engagements mentioned earlier—counsellors, hospital social workers, people reforming custodial institutions, family planning workers, social policy makers, and so on. Moreover, these agents can view their engagement as linked with others, not as a solution on its own. For example, when women’s movement activists create women’s refuges as a step away from living in unsupportive households, this makes it possible for therapists who specialize in the psychological dynamics of the woman in her family to consider referring women to refuges as a critical disruption to the family’s dynamic. The politics of highlighting different kinds of causes and their interlinkages can be seen as promoting such exchange among the distributed set of agents and contributing to the potential re-formation of the social worlds intersecting around the development of any given focal individual or outcome.
Extracted from Taylor, P.J., “Distributed agency within intersecting ecological, social, and scientific processes,” pp. 313-332 in S. Oyama, P. Griffiths and R. Gray (Eds.), Cycles of Contingency: Developmental Systems and Evolution. Cambridge, MA: MIT Press, 2001.
[i] The nonpartitionability of different kinds of biological and social causes, given the interdependence of their effects, is demonstrated well by Lewontin (1974), when he argues that statistical partitioning of effects (“analysis of variance”) does not constitute an analysis of causes. Of course, partitioning of biological and social causes does have ideological meaning (Lewontin et al. 1984).
Lewontin, R. C. (1979). Sociobiology as an adaptationist program. Behavioral Science, 24, 5-14.
Lewontin, R. C., Rose, S., & Kamin, L. J. (1984). Not in our genes: Biology, ideology and human nature. New York: Pantheon.
Sclove, R. (1995). Democracy and technology. New York: Guilford.
A line of research from England, initiated by the sociologists Brown and Harris in the late 1960s, has investigated how severe events and difficulties during people’s life course influence the onset of mental and physical illnesses (Harris 2000). This work illustrates the idea of intersecting processes in relation to development over a person’s life-course. In contrast to the dominant emphasis on genetic bases for disease, this work shows that longituidinal environmental or social exposures can be brought into the analytic picture—provided there is the will and enough effort.
Brown and Harris use wide-ranging interviews, ratings of transcripts for the significance of past events in their context (with the rating done blind, that is, without knowledge of whether the person became ill), and statistical analyses. Because what might be recorded as the same event, e.g, death of a spouse, might have very different meanings and significance for different subjects according to the context, Brown and Harris’s methods accommodate events with diverse meanings. At the same time, apparently heterogeneous events can be subsumed under one factor, such as, in explanation of depression, a severe, adverse event in the year prior to onset. In sum, the Life Events and Difficulties methodology integrates ‘the quantitative analyses of epidemiology and the [in] depth understanding of the case history approach’ (Brown and Harris 1989a, x).
The most sustained research in this tradition involves explaining depression in working-class women. For a district of London in the early 1970s, Brown and Harris identified four factors as disproportionately the case for women with severe depression: a severe, adverse event in the year prior to the onset of depression; the lack of a supportive partner; persistently difficult living conditions; and the loss of, or prolonged separation from, the mother when the woman was a child under the age of eleven (Brown and Harris 1978; 1989b). (Subsequent work has added to this picture, but that will not be taken up here; see Harris 2000.) A reconstruction of Brown and Harris’s work as it stood in the 1980s by the developmental psychologist (Bowlby 1988) suggests how the different aspects of class, family, and psychology can build on each other in the life course of the individual (Figure; see also Taylor 1995).
Figure: Life development pathways to severe depression identified in Brown and Harris’s study of working class women and reconstructed by Bowlby (1988). The dashed lines indicate that each strand tends to build on what has happened earlier in the different strands. See text for discussion and sources.
Let me give some simplified and over-generalized examples of such cross-connections: In a society in which women are expected to be the primary caregivers for children, the loss of a mother increases the chances of, or is linked to, the child lacking consistent, reliable support for at least some period. (Bowlby added his own speculation about early childhood attachment problems.) An adolescent girl in such a disrupted family or sent from such a family to a custodial institution is likely to see a marriage or partnership with a man as a positive alternative, yet such early marriages tend to break up more easily. Working-class origins tend to lead to working-class adulthood, in which living conditions are more difficult, especially if a woman has children to look after and provide for on her own. And, in these circumstances, accidents and other severe events are more likely. The consequence of a severe event is often, unless there is a supportive partner, the onset of depression (see also Brown and Moran 1997). Notice, however, that each connection in the Figure should be interpreted as one contributing causal link in the construction of the behavior. The lines are dashed to moderate any determinism implied in presenting a smoothed out or averaged schema; the links, while common, do not apply to all women at all times, and are contingent on background conditions not shown in the diagram.
In sum, longituidinal environmental or social exposures are brought into the picture, and the picture helps us think about multiple pathways to the focal endpoint of clinical depression.
Extracted from P. Taylor, “Infrastructure and Scaffolding: Interpretation and Change of Research Involving Human Genetic Information,” Science as Culture, 18(4):435-459, 2009
Bowlby, J. (1988). A Secure Base. (New York: Basic Books).
Brown, G. W. and T. Harris (1978). Social Origins of Depression. (New York: The Free Press).
Brown, G. W. and T. O. Harris (1989a). Depression in Life Events and Illness. (New York: Guilford Press).
Brown, G. W. and T. O. Harris, Eds. (1989b). Life Events and Illness. (New York: Guilford Press).
Brown, G. W. and P. M. Moran (1997). Single mothers, poverty and depression. Psychological Medicine 27: 21-33.
Harris, T., Ed. (2000). Where Inner and Outer Worlds Meet. (London: Routledge).
Taylor, P. J. (1995). Building on construction: An exploration of heterogeneous constructionism, using an analogy from psychology and a sketch from socio-economic modeling. Perspectives on Science 3(1): 66-98.
How does this happen? How often does this happen? might be a response to the earlier post citing Waddington’s experiments, in which variation that originated as an appropriate response to environmental circumstances became more or less fixed over time in a population. To answer the “how often” question, researchers have to be looking for examples, and to look for examples they not only have to be motivated but to have a model of what they are looking for, that is, an idea of how it happens. First, how it happens in my view, then in the view of Waddington and others.
Consider some acquired character, moreover one that is an appropriate response to the environmental stress. Likely there will be a range in responsiveness. Moreover, the developmental paths to the “same” response will typically differ among individuals. If there is any survival and reproductive advantage to greater responsiveness, the offspring of matings in the population will come to concentrate in a subsection of the space of developmental paths. We can expect that eventually some individuals in that subspace of responsive developmental paths will show the character in the absence of the environmental stress. That is not always a good thing, but, if it is advantageous, the subspace of responsive developmental paths will come to include ever more of those “pre-responsive” individuals. The critical part of this process—some offspring in the “concentrated” subspace of responsive developmental paths showing the character in the absence of the environmental stress—is not as a logical matter, but as a consequence of development. No reverse transcription in individual transmission is needed in this Darwinian, population-thinking version of Lamarck.
If this is how this happens, I concede that we do not have much evidence to infer that this phenomenon is widespread in nature. However, until more researchers can conceive how it can happen, they won´t be looking for it, and so evidence for it will remain slim even if it occurs often.
There are other accounts of how this happens. In Waddington´s own terms the previous environmental induction of the characters has been taken over by a genetic switch and become “genetically assimilated” (Waddington 1961). More conventional neo-Darwinists than Waddington have obscured the implications of his experiments by inventing, without further investigation, gene-centered explanations. GC Williams, in his influential book, Adaptation and Natural Selection, attributed the fixation of acquired characters in Waddington´s experiments to a change in the balance between a fixed number of suppressor alleles and a variable number of positive alleles accumulated under natural selection. (Similarly, see Mayr 1970, 361-5.) The attention is diverted away from the non-random origin of the responses and onto the postulated suppressor or positive alleles, which presumably arise randomly (that is, without reference to the environmental stress) and are then naturally selected.
The random origin of characters and the conceptual separation of origin from their change in frequency in a population makes it difficult for evolutionary theory to give significance to the structured activity of organisms during their lifetime, something that may influence the direction of change in a population. Addressing that blindspot is important whatever the answer turn out to be to the question of how often variation that originated as an appropriate response to environmental circumstances becomes more or less fixed over time in a population.
This post is adapted from P. J. Taylor, “Historical versus Selectionist Explanations in Evolutionary Theory” Cladistics 3: 1-13,1987.
Mayr, E. 1970. Population, Species, Evolution. Cambridge: Harvard University Press.
Waddington, C. H., 1961. Genetic assimilation. Advances in Genetics, 10: 257-290.
Williams, G. C. 1966. Adaptation and Natural Selection. Princeton: Princeton University Press.