an international and interdisciplinary journal of postmodern cultural sound, text and image
Volume 7, March-April 2010, ISSN
1552-5112
Towards a Philosophical Account of Explanation in Behavioral
Genetics
I.
Introduction
On one level of generality the topic of behavioral
genetics seems relatively uncontroversial; but at another level behavioral
genetics is much more contentious. If we
ask whether genes are central to the development of basic capacities for
behavior, then it will widely be agreed that of course genes are very
important; change or delete certain key genes early on and certain behavioral
capacities simply will not develop.[1] But, if we
ask about the role of specific genes in determining the appearance of specific
behavioral traits, then things are much less clear. In spite of significant media hype over the
past several decades regarding the alleged discovery of particular genetic
structures for very particular behaviors, to judge by the meager list on
certain government run web-sites[2], we are not in a position to have much confidence in
progress towards accumulating significant information about simple direct
connections between the presence of specific genes and the appearance of
specific behaviors. This, in turn, has
led to significant pessimism about the whole behavioral genetics project.[3] It has prompted
others to suggest that a more nuanced approach to behavioral genetics is
needed, and to propose certain revisions.[4] I fall into
the latter category. If the behavioral
genetics project is to continue to be viewed as a viable scientific project,
then it is in need of clarification and modification as well as support. In
this presentation I will offer a philosophical case for a revised behavioral
genetics, building on important work of others.[5]
For an exploration of a revised version of behavioral
genetics to be worthwhile, we must first make sure that the basic elements of
such a view do not face serious problems.
But, the very concepts that constitute any form of behavioral genetics,
namely those of genes and behavior, are far from enjoying unproblematic
status. The continued use of a
gene-centered approach to scientific investigation has been severely critiqued;
while the gene-centered approach has been ably defended methodologically[6], there are other important arguments that demand the
attention of defenders of behavioral genetics.
In this paper I begin by examining a particularly
disturbing eliminativist argument from Evelyn Fox Keller against the continued
use of the very concept of the gene. If
Fox Keller’s argument were to work, then any attempt to continue with or
attempt to revise behavioral genetics would be doomed. In the course of replying to Fox Keller’s
argument a revised, functional concept of the gene is presented and defending. Using this revised conception of the gene I
then consider how appeal to a functional approach to the gene can itself lead
to a more general functionalist revision of the basic behavioral genetics
project. In the third part of the paper I then turn to examining the advantages
with respect to scientific explanation that such a functionalist account can
provide. And, I end by considering how
such an account might provide some help in dealing with additional ethical
worries, including additional ethical arguments from Fox Keller against the
continued use of the concept of the gene as well as ethical concerns that have
been raised regarding behaviorally designed babies.
II.
Keller’s Herculean Burden Argument
Evelyn Fox Keller comments in her 2000 book, The Century of the Gene as follows:
…Johannsen’s little word [gene], so innocently conceived in the early days of this century,
had had to bear a load that was veritably Herculean. One single entity was taken to be the
guarantor of intergenerational stability, the factor responsible for individual
traits, and, at the same time, the agent directing the organism’s
development. Indeed, one might say that
no load seemed too great—as long, that is, as the gene was seen as a
quasi-mythical entity. But by the middle
part of the century, the gene had come to be recognized as a real physical
molecule…just a bit of DNA …and here…the history of genetics takes its most
surprising turn. Both the excitement and
the triumph of the new science of molecular biology came from the remarkable
evidence it provided suggesting that, incredibly enough, the gene, now
understood as a self-replicating molecule of DNA, was a structure equal to its
task. Yet, with the maturation of
molecular biology, the impracticality…that load has become steadily easier to
discern.
New kinds of data gathered
over the last few decades have dramatically fleshed out our understanding of
the parts played by genes in cellular and organismic processes, and in doing so
they have made it increasingly apparent how far the weight of such a load
exceeds what any one single entity can reasonably be expected to bear, and
hence, how appropriate that it be distributed among many different players in
the game of life. [145]
From this extended comment we can derive an
interesting eliminativist argument[7] that I will refer to as Fox Keller’s
Herculean Burden Argument:
1.
Genes are
required to [a] be the sole guarantor of intergenerational stability, [b] the
sole factor responsible for all individual traits, and [c] the agent that
directs the organisms development.
2.
Genes are
identical with sequences of DNA.
3.
Research results
establish that mere sequences of DNA cannot by themselves perform the three
required tasks of maintaining intergenerational stability, trait fixity and
organismic developmental.
4.
Thus, mere DNA
sequences cannot perform the tasks required of DNA.
5.
Thus, genes
cannot perform the tasks required to be genes.
6.
Thus, talk of
genes should be eliminated in favor of different concepts.
I will assume that there are some here who will find
Fox Keller’s argument controversial.[8] My suggestion
is that friends of genes, when faced with Keller’s claims, should not only
reject the second premise, arguing that genes were something more than mere DNA
sequences; they should also reject the first premise as being too strong a
requirement for genes. While some
purists may be horrified, I will argue that as long as the elements discussed
are significant or major determining elements in development, composed of DNA
and combined with perhaps something else, relatively stable and significantly
involved in trait fixity, then, they could still count as genes. The specific objections I propose to Fox
Keller’s argument are the following:
Objections to Fox Keller’s Herculean Burden Argument
1.
First objection:
Genes need not be the sole determining elements in development
2.
Second
objection: Genes need not be solely responsible for trait fixity
3.
Third objection:
Genes need not be completely stable
4.
Fourth
objection: Genes could be something over and above [or other than mere] DNA
Before specifically considering these objections I
would like to motivate my response to Fox Keller’s argument by considering an
analogy between genes and another important concept from the history of
science, namely, the concept of ‘atom’.
When we compare what we currently say about atoms with what was once
said about atoms we find significant change.
Originally conceived as smallest unit of matter, of radically different
kinds, as not transformable into another kind … all of these claims about atoms
have gone away over time. Still, we
continue to talk about atoms. Atoms are a terribly small unit of matter, and
the smallest of an important way of distinguishing an important set of kinds of
matter from one another, namely elements, they represent kinds that have
radically different properties, even if they are composed of very similar
parts, and they are transformable into another kind, but the method of
transformation is theoretically well understood, and poses no serious conceptual
problem for the current conception of atoms and their parts. Thus, from the case of atoms we see that
requirements originally associated with a scientific term can be revised as
greater theoretical understanding is gained, as major changes in theory occur
and are incorporated, and that the term can remain, and can continue to play a
useful if somewhat changed--but still importantly related--role. This is the alternative message we should
take from Fox Keller’s discussion concerning the concept of genes. Why so?
Let us now consider each of her specific complaints in turn.
First, Fox Keller’s developmental requirement seems
too strong. While genes are typically
thought of as important in determining how an organism develops, one need not
assign all developmental responsibility for development to genes. Genes are now thought of as working in normal
biological contexts; these contexts are now recognized as providing much that
is needed to enable the organism to develop.[9] Further, one
might decide to think of genes as being more passive than in the common lay
interpretation. But, partially passive
genes would still seem to count as genes.
One need not think of genes as little omni-causal agents telling other
parts of the cell what to do, where to go, what to make, etc.
While casual discussion of genes does often refer to
causal activities that genes initiate, as in, “his alcoholism gene switched on
and caused him to start hitting the bottle pretty hard”, it is not clear at all
that gene talk must take causal agency as an absolutely essential, necessary
condition of gene-hood. Whether genes
have agency or not, their being background conditions that help serve to lead
to particular courses of development, suffices for their having causal
influence. Further, there is no clear
contradiction in claiming that certain genes do not causally initiate any
activities, but take part in causal activities initiated elsewhere. What is crucial is that genes continue to
figure causally in the biological explanation of inheritance.[10] To construct
a serious objection to genes based on causality, one would need evidence that
putative “genes” play no discernable causal role in adequate discussions of
inheritance, a more difficulty task.
With respect to stability of gene structure, Fox
Keller makes the following claim:
The stability of gene structure thus appears not as a
starting point but as an end-product-as the result of a highly orchestrated
dynamic process requiring the participation of a large number of enzymes
organized into complex metabolic networks that regulate and ensure both the
stability of the DNA molecule and its fidelity in replication….Moreover, not
only are the mechanisms controlling stability and mutability held in a delicate
balance, but that very balance is under cellular regular, and it shifts in
response to the particular environment in which the cell finds itself. All this is a far cry from the traditional
view of DNA as an inherently stable molecule subject to occasional random
errors, and it suggests an even further departure from the traditional view of
evolution as a process of cumulative selection of those exceedingly rare
mutations that happen to result in increased fitness…. [31, 34-35]
Fox Keller makes the point that the stability of DNA,
which had previously been taken for granted by most, is not something DNA is
responsible for but is something it owes to cell activities. DNA cannot by itself provide the stability
required for genetic transmission. Since
genes are sequences of DNA, genes cannot by themselves provide the stability
required for genetic transmission. But,
we can grant this point and still continue to talk sensibly of genes. If we can accept passive genes, it should not
be too far fetched to think of genetic stability as a product of other forces,
not something that genes are able to achieve for themselves on their own.
The important point concerning stability is not
really who or what is important for genetic stability, but what genetic
stability is for. There are good reasons
for maintaining genetic stability that concern with how species are able to
survive in particular niches for which they have evolved specific adaptations. How the stability of factors responsible for
these adaptations is maintained does not seem to be of importance in
determining whether these factors are genes.
The most serious worry Fox Keller presents concerns
genetic fixity: how to determine what a gene actually is. Problems arose when it was discovered that
gene splicing could produce a variety of products. Why does this worry demand our
attention? When the structure of DNA was
discovered and the putative identification of genes with sequences of DNA
advanced, the alleged payoff was that structural identity conditions of genes
could be given. As philosophers know,
one way of securing an item’s existence is to provide clear identity
conditions; structural chemical identity conditions seemed an excellent way to
solidify this worry about gene identity.
But, as Fox Keller’s comments indicate, mere structure is not
necessarily enough in all cases. Since
the same structure can apparently sometimes give rise to different elements
which produce a variety of different proteins, it is no longer clear how to
account for the identity conditions of genes.
Without identity conditions Quineans[11] among us urge that no entity will be found,
either.
Fox Keller rejects the attempt to try to found
identity conditions for genes functionally:
Fifteen years ago Richard Burian observed…’There is a
fact of the matter about the structure of DNA, but there is no single fact of
the matter about what the gene is.’ In
the interim, things have only gotten worse….The complications brought by the
new data are vast…Taken together, they threaten to throw the very concept of
“the gene”—either as a unit of structure or as a unit of function—into blatant
disarray.
Techniques
and data from sequence analysis have lead to the identification not only of
split genes but also of repeated genes, overlapping genes, cryptic DNA,
antisense transcription, nested genes, and multiple promoters (allowing
transcription to be initiated at alternative sites and according to variable
criteria). All of these variations
immeasurably confound the task of defining the gene as a structural unit.
Similarly,
discovery of the extensive editorial process to which the primary transcript is
subject, of regulatory mechanisms operating on the level of protein synthesis,
and others operating even on the level of protein function confound our efforts
to give a clear-cut functional definition of the gene.” [66-67]
Since neither functional nor structural criteria will
work, and since these two criteria exhaust the sources for identity conditions,
Fox Keller concludes that the gene is a concept in trouble.
While we should admit that this is an interesting
worry, rather than wring our hands and hold out for future discovery of a
hidden novel purely structural feature to solve the identity conditions problem,
there is a more promising present strategy.
While waiting we can suggest, instead, that a combination of structural
and functional elements might work. That
is, suppose we propose to identify a gene as a particular DNA sequence of DNA
typically assembled in a particular way in certain typical contexts and
typically produces specific protein/s.[12]
That is, let us seriously consider a functional role
identity for the gene:
The functional role approach to gene identity:
Identify a gene as a specific DNA sequence, S, that
plays a typical functional role, R, of typically producing protein P in context
C in an organism O.
This approach has several virtues. First, it can accommodate the aberrant
findings to which Fox Keller refers above.
Second, it is consistent with what we should have been expecting
regarding the notion of the gene. After
all, the gene was originally conceived teleologically, as an item with certain
functions. While some may have assumed
that the teleological stage was eliminable upon the discovery of DNA, as Fox
Keller has admirably demonstrated, this assumption has been short lived. If we re-introduce teleology into our account
of the gene, we are really just returning to our honest biological roots[13], and are no longer pretending that chemistry all by
itself can completely explain living phenomena.
In reply, one may, of course, pose skeptical worries about how likely we
are to find functional roles for DNA sequences, fears of multiple sequences
with the same role, qualms about cases lacking characteristic functional roles,
etc. But, none of this shows that no
such functional roles are to be found.[14]
The sketch of what constitutes a gene will only work
if characteristic activities and characteristic outputs can be shown to account
for regularities of inheritance that must be explained. If these regularities can not be tied to
similar internal regularities of the sort mentioned above, where there is
sufficient differentiation between genes in terms of constituents, relationships
and outputs, there would no longer be any need for talk of individual genes but
of the general, undifferentiated mechanism of inheritance. If any blob of DNA whatsoever could produce
any particular feature you choose, then there would be no need to postulate
specific individual elements of difference-makers and similarity-makers, which
is an important part of what genes have always done.[15]
III. The
Causal Role Account of the Path from Gene to Behavior
In the previous section I proposed a rough functional
role notion of identity for the gene as a way to avoid certain conceptual
worries. While this proposal does not
make explicit mention of behavior, once we have agreed to consider implementing
the functional role approach with respect to gene identity, we are then in an
interesting position with respect to asking about the biological explanation of
behavior. For the functional role
approach to genes naturally invites consideration of relevance of the nature of
functional roles that we have inherited from work in the last century in the
philosophy of mind on the mind-body problem.
But this raises a number of questions: How is such an approach to be
construed? What elements should it
contain? How are the elements to be
related? What can we learn from this approach?
Let us briefly recall some basic Post-Identity-Theory
philosophy of mind. Mind-Body
Functionalism, the currently reigning orthodoxy on the nature of the relation
of the mind to the body for at least the past two decades[16], is the view that mental states are to be defined,
not in terms of specific physical substances or specific physical properties,
but in terms of the causal role played by an item, such as a neural state, in
terms of responding to specific typical inputs and in terms of generating
specific typical outputs, and, importantly, also in terms of relations to other
such states. Specific cases of mental
states are items, of whatever sort, that instance the right sort of causal
role. The earliest versions of the view[17] were concerned to account for the possibility of
artificial intelligence, and hence made reference to machine states as
definitive. But, while finding machine
states for machines was obvious, it has always been difficult to imagine
clearly how a machine state characterization of human mental states would
suffice to distinguish mental states from other, non-mental activities. Some early causal role theorists seemed to
think that reflective common sense was sufficient to determine the causal roles
of such states.[18] Other
theorists held out for the contrasting view that it will be future science that
will reveal to us the specific elements that make up the causal roles that
characterize specific mental states.[19] While this
latter approach might strike some of the scientific pluralists here present as
being rooted too firmly in scientific monist commitments, I think one can
interpret scientific functionalism so as not to require commitment either to
monism or pluralism in science. This
said, it should also be noted that some functionalists explicitly utilize
specifically biological notions, such as function or teleology, to provide
guidance for determining the nature of specific causal roles[20]. And, I would
suggest, given that specifically teleological biological concepts, such as
hearts, livers, etc, are defined specifically in terms of function and not
structure, this last approach is most appropriate for understanding a
biological concept, such as the gene, which was hypothesized initially as a
functional item before any inkling of its structure was known. The key notion that all of these versions of
functionalism have in common is a rejection of a simplistic type-type identity
approach to the relation between mental and physical state and its replacement
with a functional-role/realization model of this relation.[21]
While the notion of function is not sufficient to
show how a revised behavioral genetics should go and how one can derive
explanatory power from it once so conceived, as it is not plausible to
attribute enough individual functions to all genes, it is a good start.[22] We attribute
heart status to diverse items, earthworm hearts, Jarvik-7’s, etc. It is not the material used to construct the
item or the exact design, but what the item could be reasonably said to do in
the right circumstances, the rest of the body behaving appropriately, the
environment cooperating, etc. This
broader characterization helps us see how appropriately to relate genes to
behavior.
It should be noted in passing is that an appeal to
functional characterization should also make it easy for us to see the
connection between traditional Mendelian genes and molecular genes. Mendelian genes are defined in terms of the
typical phenotypic results whereas molecular genes are defined in terms of
their chemical structures and their biochemical products. Given the functional
characterization of genes we see that phenotypic results are simply a later
stage in the causal role that includes, as an earlier stage, the chemical
production of appropriate proteins.
Thus, the molecular genes may be seen as more specific “realizations” of
items playing general causal roles that also include their Mendelian
counterparts. Given my commitment above
to genes as functionally defined in a broad enough sense to include both the
Mendelian and molecular varieties, there are additional consequences that also
follow when we attempt to impose a functionalist account on genetic
activity.
First, functional causal role accounts can include
typical causes as well as typical effects.
When it comes to genes, there seem to be relatively limited or standard
typical causes, including the basic inheritance facts of meiosis which, in
turn, requires a sufficient number of parents behaving appropriately[23], and, more unusually, environmental mutational
forces. In addition, as Fox Keller notes
above, there are important cellular sustaining forces that come into play.
Second, functional role accounts typically recognize
the need to accommodate interconnections between functionally characterized
items. Standard mind-body functionalists
recognize important interconnections in their causal roles between mental
states such as beliefs and desires; it is certainly also the case that we need
to account for the polygenic contributing causes of complex behavioral in
addition to most other complex traits.
Thus, the same gene could operate with a potentially wide variety of
other sets of genes to produce an equal variety of different items.[24] This, in
turn, would demonstrate that one also needs to think of diverse functional
roles for diverse sets of genes of genes!
Third, functional accounts importantly emphasize
typical effects. And, as we note that
other items defined in terms of causal roles, such as hearts and livers, it is
the typical effects that are the most prominent. It is with trying to enumerate typical
effects involving genes, however, that we find a more elaborate series of items
that will help carry us toward behaviors.
The first effect, with the discovery of the molecular
phase of gene activity we are now aware of the production of proteins as being
a crucial activity for genes to perform.
It is via protein production
that we can hope to fill in the otherwise strange and apparently magical gap[25] from postulated special item in the body to
phenotypic element observed in the progeny.
Protein production is relatively unimportant unless it can be shown to
lead, under normal circumstances, to typical effects in the body. But, a second effect factor, the body itself,
must be characterized in such a way as contributing significantly to the
particular effects in question. In
addition, as a third factor, it is widely agreed to be equally of importance
that the organism’s environment provide significant items for the production of
states of the body that would make it possible for behaviors to be manifested
when appropriately stimulated. A fourth,
and for the purposes of this session, the importantly relevant effect, is the
manifestations of typical behaviors, which again depend on either internal and
external stimuli or both. It is with the
addition of this last factor, combined importantly with the other three factors
that we can see what an improved and revised approach to behavioral genetics
would look like, though I shall consider below whether it is still appropriate
to treat the view that I shall propose as a version of behavioral genetics.
A rough picture of this causal role involving genes
as well as other factors may be represented as follows:
Rough Schematic Model of a Causal Role account of
Genes leading to Behavior
ES…. EF
ES
↓ ↓ ↓
RC → G
→ MP → IS → DB → B
→….
↑ ↑ ↑ ↑
IF ISC…. IF IS
ES = environmental support DB = Dispositions to behave
RC = reproductive causes IF = internal forces
ISC = sustaining causes EF = external environmental forces
G = genes ES
= external stimuli
MP = molecular products IS = internal stimuli
IS = internal states MB
= manifestations of behavior
[…. = continued!]
According to this schema,[26] environmental support and internal forces lead to
reproductive causes; these reproductive causes lead to genes, which depend (for
stability, etc.) on sustaining causes and continued environmental support;
genes then lead, with continued support, to molecular products; these molecular
products, again with continued support, lead to internal states; these internal
states lead, in turn with continued support, to dispositions to behave;[27] these dispositions to behave are triggered by a
combination of internal and external stimuli, resulting in behavior.[28]
As my perspective is that of a speculative
philosopher and not a bench biologist, I would be the first to grant that the
above model is very rough indeed. There
are, undoubtedly, missing elements, such as additional feed back loops, that
either I have forgotten, of which I personally am ignorant, or perhaps remain
to be discovered. But, in one sense
concern about exact detail here is unimportant.[29] What I want
to urge is that there is a model to be found that will do what I am proposing
can be done here, namely to provide a quasi-functionalist, causal role linkage,
however complicated, between genes and behavior that reserves and important
role for genes, such that were the genetic input significantly to change, there
would also be a significant change in behavior.
It needs to be emphasized that I am proposing a
quasi-functionalist approach which emphasizes the complex causal role from
genes to behavior. I am not proposing
the apparently obviously unreasonable view (based on our present state of
knowledge) that there are distinct and specific biological functions
corresponding to each instance of the above schemata. And, I am not proposing that all stages of
the causal role sketched in the above rubric must, themselves be subject to a
functionalist definition, as philosophers of mind who embrace functionalism
urge for all mental concepts. While some
are helpfully construed functionally, such as genes, certain mental states tied
to certain behaviors, maybe even the concept of “the body”, the same does not
seem obviously to be true of certain environmental aspects of the rubric, for
example.
We need to emphasize that the rough schematic
quasi-functionalist approach, as borrowed and modified from the philosophy of
mind, stands in contrast with a standard functional analysis found typically in
biology. Functional analysis in biology
ends with identifying particular functions for biological items in specific
contexts with respect to particular goals.
In the absence of a relevant biological goal or end there cannot be a
function. The case with genes, however,
seems importantly different. While it is
reasonable to assign functions to certain activities of certain genes in terms
of bringing about certain states which would be needed to accomplish certain
biological goals, it seems most unlikely that every single human gene and every
active combination thereof equally has a function in this sense.
Thus, one can speak of the “functional role” of a set
of genes or of a “functionalist account” of some specific genetic activity
without thereby being committed to finding a corresponding distinct biological
function which that activity carries out.
For example, it seems likely that there is a set of genes which do have
the function of enabling speech, as speech is clearly an important element for
normal human functioning, and, given our evolutionary history, it has been
important for humans to have it. But,
although there also seems undoubtedly to be a genetic contribution, it also
seems, so far as we now know, unlikely that the correspondingly involved set of
genes would have the function of creating a voice of a specific quality, such
as a first tenor voice. There need not
be a specific function for every distinct functional role.[30]
This quasi-functionalist proposal is offered as an
account for showing how to amplify and incorporate current practices in
behavioral genetics within a larger philosophical framework. Let us briefly note how this proposal differs
from the four main competitors.[31] The
Quasi-Functionalist approach differs from Classical Behavioral Genetics, not in
ignoring it, but in terms of attempting to incorporate it. The same holds true for Modern Molecular
Genetics. Again, the same holds for the
Environmental Approach; it occupies a central role. The same can be said for the DST approach,
emphasizing, however, the need for a more prominent role for genes.[32]
A further
question: What is intended by the use of the arrow,
“→” in the above schema?
Nothing as strong as implication or entailment, or nomic connection can be
meant here. The relation needs to be
something much looser, something like “typically/ideally leads to”, where this is
to be understood as involving a causal contribution. The notion of a causal role seems to be just
this loose. There are many different
things that can break the chain of events in a causal role. Yet, causal roles, including those which
involve genes, still seem to be that out of which what is distinctly biological
is created and what ultimately needs to be studied if one is concerned to study
biological phenomena biologically.[33]
A final objection will end this section. Why should one consider the present
quasi-functionalist proposal as an example of Behavioral Genetics when other
significant elements are involved besides genetics and behavior? In my defense I will note that my proposal
involves a process that begins importantly with genes and ends with
behavior. It does not, however, claim
that all behavior is exclusively genetically determined. So, it is not genetic determinism. But, not all forms of behavioral genetics
need to be thought of as forms of genetic determinism. Nor does my proposal claim
that all behavior is determined by external forces. So, it is neither cultural nor environmental
determinism, either. Still, it is
conceived as a multi-factored version of behavioral determinism, one which
reaches back for explicit inspiration at least to the Enlightenment. If the term, “Behavioral Genetics” is not
sufficiently broad/flexible to include the view I propose, I welcome an alternative that would do a
better job of characterizing the present proposal, one that includes a nod to
classical behavioral genetics, which investigates the significance of genetic
input across the wide spectrum of human behaviors, as well as recognizing that
environmental and non-genetic internal factors are also importantly involved in
specific behavior production.
IV.
Philosophy of Science
Let us now consider how a broad functionalist
perspective might deal with various additional concerns from the philosophy of
science, including methodology and explanation.
First, let us turn to the topic of explanation. When we ask about explanation in general we
are asking, at base, for an insightful fitting together of various phenomena
within a broader context. We want to
know why we to expect particular phenomena occur instead of alternative
phenomena. While for several decades in the last century it may have been
widely accepted that all truly scientific explanation had to follow a single
pattern, this is not longer the case.[34] It is now
widely recognized that there are a variety of different sorts of explanation
that can occur in serious science. In
what senses can the proposed rubric help determine the sorts of explanation
that are possible in broad behavioral genetics appeals? There are two answers.
First, there are many opportunities for different
kinds of explanation to occur throughout the [gene → behavior] path; few
if any of the major forms of explanation are not, eventually, going to find a
place somewhere. Beginning with the
classical DN model and its causal variant,[35] we can find a place for deductive nomological
explanation in the existence of the various laws of nature that seem to govern
certain well-understood genetic combinations at the beginning of the rubric.[36] At this point
in our understanding, however, given the great complexities of relationships in
the rubric proposed, it seems unreasonable to suppose that there will be
interesting Deductive Nomological [DN] or direct causal connections, even with
generous ceteris paribus clauses,
between specific genetic states and specific behaviors. But, opportunity of possible appeal to
Inductive Statistical [IS] explanation seems much more open. Many of the connections between states of the
rubric seem to be ones where the possibility of finding a probabilistic connection
seems rather significant. But, unlike,
for example, causal appeals, many will find probabilistic connections to be
incomplete and inconclusive. Something
more closely fitting the phenomena together, more closely establishing natural
connections seems wanted. I have already
indicated that functional explanation plays a role here, both in terms
establishing the ground of all behavior and, perhaps, for a few very special
behaviors. But, I have also claimed that
the explanatory insight one can achieve by functional analysis will be limited.[37] So, we end
our discussion of the first point relating to explanation by asking: what more
helpful explanatory account can we give that is more specific to the situation
at hand?
This brings me to the second answer I want to propose
regarding explanation. How does one
typically explain the attribution of a particular trait to a member of a
particular group? While biology is one
important domain where occurs, we need to consider that something similar also
happens in a wide variety of domains, including the other natural sciences,
social sciences and studies, religious explanations, etc. How might we account for the explanation
within the context of attributing a particular feature to an item across this
wide category of items?
As a start let us consider the following outline of
an explanatory framework:
Outline of Trait Acquisition Explanation
Explaining the acquisition of a trait by an
individual item typically involves the following
stages:
1.
Identifying the
trait to be acquired
2.
Determining the origin
of the process
3.
Distinguishing
the stages in the acquisition process
4.
Discovering the
mechanisms for trait acquisition
5.
Ascertaining the
relative effectiveness of the mechanisms
6.
Establishing how
the trait acquisition process moves from one stage to another
7.
Recognizing the
internal environmental factors affecting acquisition
8.
Finding out the
external environmental factors affecting acquisition
9.
Detecting how
the various factors interact in particular contexts
10. Assessing the measure of likelihood of the process
working in a particular case
The complex form of explanation that is at work here
is not, in spite of what one might first imagine, an ad hoc invention that is limited only to cases of behavior
genetics. Instead we can view trait
acquisition in much broader framework.
We should note that this explanatory framework, while nicely fitting the
quasi-functionalist model proposed above, also can be seen to apply to a wide
variety of alternative explanatory approaches.
Such views as Special Creation Theory, Developmental Systems Theory,
Classical Lamarkianism, Evolutionary Explanations, Narrative History Accounts,
Standard Marxist Interpretations, Classical Behaviorist Explanations, even
certain fundamentalist religious accounts of trait acquisition[38], would all seem to fall nicely within this 10-stage
theory.[39]
This form of explanation, however, has several
limitations. First, it is
“mechanistic”. But the notion of
mechanism here is no more conceptually complicated than its original early
Greek sense of that which brings something about in a rather regular way. As such, it seems consistent with what we
typically require of a scientific explanation.
Second, it is also a stage based theory, which implies a development,
either of groups or individuals over time.[40] So, it is
limited in applicability to explaining items that occur historically. Still, most traits possessed by items would
seem to fall into this category, ensuring the approach wide applicability. And,
there might also be two different applications of the approach to account for
the same trait. This might occur, for
example, if we could produce both (a) a developmental account of the occurrence
of a particular behavior in an organism as well as (b) an “Evo-Devo” account of
the same behavior evolutionarily.[41] And, third,
it is aimed at attempting to account for complex phenomena, involving a variety
of different influences. This is, at the
same time, a strength of the approach, as there are numerous complex phenomena
the explanation of which seems to invite its use, as well as its most serious
challenge, as we will require, in a particular case, some way of sensibly
bringing the various diverse influences sensibly into consideration one with
another.
I want the causal role view here proposed to be
consistent with scientific pluralism.
But this interpretation is likely to lead to an initial objection: why
should scientific pluralists not oppose the present quasi-functionalist
approach, which is itself a single, comprehensive account?
Here is the answer I propose. If the “big picture” presented above is
roughly on track, then among the questions we need to ask include, most
prominently, how can we proceed to study the various aspects of this proposal so
as to make investigative “progress”? Attempting to relate all of the various
aspects of all of the various stages all at once seems like a recipe for
disaster. But, the plan of limiting our
study to attempting to determine the nature of the relations between
neighboring stages or between stages related by a gap while simultaneously
holding other stages as constant as we can makes some sense. And, this seems to be just what the various
traditional approaches to behavioral genetics do.[42]
The problem is that without a “big picture”, even one
as rough and full of flaws and limitations as the above is, one is likely to
regard the efforts of those engaged in different explanatory processes as being
hopelessly naïve or terribly misguided, instead of seeing how their various
efforts might contribute to the overall project of explaining how the process
of acquiring behavior in the largest biological sense might work.
Now, one should grant defenders of scientific
pluralism that there are serious dangers in being a slave to all big
theories. The history of science
provides many good examples of this danger.
But, it would be a mistake to regard all appeals to “big-picture”
thinking as either necessarily dangerous, or totally empty of positive value. It depends upon the specific context of
investigation and upon the shared assumptions that all researchers are willing
to make. In biology, for example, there
is a very big theory the filling in of whose many details we are all regularly
involved—and this, of course, is Darwinian Evolution. But, biological researchers are, standardly,
conscious Darwinians. If we grant that
Darwinian thinking is not dangerous thinking from a scientific perspective,
which we all should[43], then it is not mere bigness that is bad. What distinguishes Darwinian from other large
scale thinking may be the fact that Darwinian thinking is not necessarily tied
to specific mechanisms, or a fixed time-table, or a single simple way of
explaining things. So, suitably flexible
big pictures are permissible, especially if they encourage a variety of
approaches for engaging in scientific investigation. The same, I suggest, holds with regard to the
quasi-functionalist approach to connecting genetics and behavior.
There is a second likely objection from scientific
pluralists that needs to be considered.
This is the objection to a simple addition of the various diverse
features from different approaches.
Longino, for example, claims that one cannot regard the four different
standard approaches to the addressing the appearance of behaviors as being ones
that can be added. [44] For Longino
these different approaches are distinctly in conflict with each other; thus, it
is inappropriate to assume that it is meaningful to combine conflictual
elements.[45]
In response, I would point to the important
scientific pluralist claim that scientific pluralism is not reducible to an
“anything-goes” form of scientific relativism.[46] But, in order
to avoid the charge of “anything-goes” relativism there needs be a common
framework within which the players agree to participate.[47] Once the
common framework is articulated and in place, however, it is open to serious
researchers to appeal to a variety of approaches appealing to element within
the common framework to investigate the phenomena. While it is important to note that the
correct ways of currently construing certain approaches would make any current
attempts to combine data from them into single model incoherent, this by itself
does not show that future efforts, by changing particular aspects in different
approaches, could not do just that. What
would be needed, here, would be a general argument against the coherence of any
such efforts at rapprochement. And, I am
doubtful that such an argument can be given.
So, with regard to the question, “Must pluralists
oppose the combining of approaches?” I think the proper answer is, “No’; the
pluralist needs only hold that such a combination must, itself, be viewed as
yet another, separate approach. This
combination approach, moreover, should instead be viewed as conflicting with
the other current approaches.[48] Further, we
may note that a combined approach may be likely to give rise to further
alternatives with which it will conflict.[49]
I want to end this section on methodology by briefly
noting several additional objections that might be raised against the
quasi-functionalist approach here presented, objections based on concerns with
functionalism itself, which would threaten the methodological utility of the
proposed quasi-functionalist approach to behavioral genetics. First, some have worried about a certain
‘emptiness’ in the functionalist approach.
This charge is worth taking seriously so long as we have not figured out
anything about what the relevant elements in the causal role might be and how
they might be related.[50] Second, the
reliance on functionalism in the philosophy of mind, in spite of several
decades of popularity, has not actually produced significant, detailed
definitions of mental states that can withstand scrutiny. It is natural to worry whether one should
have higher expectations for behavioral genetics. Third, there is a standing worry to the
extent that qualia are implicated in
any causal role instance from genes to behavior. And, fourth, there is a related worry, namely
the problem of distinguishing standard vs. non-standard causal roles that
almost all varieties of functionalism inherit.[51] Thus, while
the functional role approach to connecting genetics and behavior is suggestive,
certain inherited worries also need to be faced.
V. An Ethical
Conclusion?
I would like to conclude with consideration of two
different ethical concerns regarding behavioral genetics. First, there are two ethical arguments
against genes from Fox Keller to consider.
She concludes her 2000 discussion as follows:
….Where my own sympathies lie should now be
apparent. Genes have had a glorious run
in the twentieth century, and they have inspired incomparable and astonishing
advances in our understanding of living systems….But these very advances will
necessitate the introduction of other concepts, other terms, and other ways of
thinking about biological organization, thereby inevitably loosening the grip
that genes have had on the imagination of life scientists these many
decades. My hope is that such new
concepts and new ways of thinking will soon work to loosen the even more
powerful grip that genes have recently come to have on the popular
imagination. For if…the term gene may in fact have become a hindrance
to the understanding of biologists, it has perhaps become even more of a
hindrance to the understanding of lay readers, misleading as often as it
informs. As a consequence, it shapes
popular hopes and anxieties, in ways that are often off target and in fact
counter-productive to effective discussion of public policy even where the
issues are real and urgent. At my most
optimistic, I even imagine the possibility that new concepts can open
innovative ground where scientists and lay persons can think and act together
to develop policy that is both politically and scientifically realistic. [pp.
147-148]
I read this final comment from Fox Keller as
proposing two additional ethical arguments against continued gene talk. First, she is worried that gene talk misleads
scientists and, especially, that it causes the lay public to holding erroneous
and anxiety-producing ideas. In reply,
it should be noted that Fox Keller’s worries would be worth taking seriously if
there is no change in the current use of the concept of gene and if the public
buys into a simplistic one-gene-one-behavior view. But, if the approach I am suggesting is
accepted as a replacement for the earlier, simplistic view, it is hard to see
how gene talk embedded in a functionalist approach such as that suggested above
could have the effects Fox Keller fears.
Second, Fox Keller also seems to be claiming that
current gene talk is counter-productive to effective public policy discussion
and that there is a need for concepts which would further better public policy
discussion. Again, I would agree that a
simplistic understanding of behavioral genetics would not be useful for
meaningful public policy discussion. The
acceptance of the more nuanced account of how genes lead to behavior presented
here would have a similar salutary effect on public policy discussion without
requiring massive linguistic dislocation.
As the case of the atom considered early on
demonstrates, it is probably just too late for us to eliminate gene talk. Current evidence indicates that the brief
against the gene is just not strong enough for us to want to abandon the term
altogether.[52] A better
strategy is to improve our use of the term, make it fit better what we know
about how inheritance works and how it is effective. In this way, we can achieve the results Fox
Keller wants without having to engage in future linguistic revision. I am betting that the concept of the gene
will still be around for quite a while.
Second, given that the concept of the gene is going to
be with us for a while, there are certain aspects of the issue of behavioral
genetic engineering to which the proposals of this discussion are relevant.[53] Let us
consider that certain genetic manipulations that are likely to lead to
particular behavioral modifications are proposed. What sorts of changes should cause us
ethical concern? If one can establish
that certain genetic changes are likely to have certain negative behavioral
results in likely circumstances of development, this would seem to count
against allowing such manipulation.
Suppose, for example, that one of the behavioral effects of creating a
super-strong human through genetic manipulation would also cause the individual
also to have, given likely common environmental factors that cannot be
eliminated, dangerous aggressive tendencies.
This would create a serious ethical concern about such
manipulation. Changes that risk making
life worse, either for developing individuals or for society as a whole, will
correctly incur public moral disapproval.
(Compare with individuals whose drug or alcohol consuming behavior
during pregnancy negatively affects the developing fetus.) But, on the other hand, suppose one can establish
that certain desired behavioral modifications that can be tied effectively to
genetic manipulation within the range of “the normal”, that is, are features
that are had by healthy human beings.
And, further suppose that there are no likely negative behavioral side
effects that could be expected in those circumstances. In such a case much negative reaction to
these “normal” behavioral modifications will also be neutralized. (Compare with individuals who maintain a
healthy diet, take special vitamins, or listen to Mozart during pregnancy with
the goal of bettering fetal development.)
Both of these cases indicate how the enhanced behavioral genetics model
can be used to help us get a better ethical grip on different kinds of genetic
manipulation for the purpose of behavioral enhancement. Both rely on trying to figure out what the
normal parameters of development are.
And, as I have argued above, this is precisely what a revision of
behavioral genetics should have as its primary goal. Further, one can note that once we have a
good sense for the parameters of the system, then we will also be in a better
position to evaluate and plan against environmental threats.[54]
Let me now summarize.
In this discussion I have presented and replied to an attempt by Evelyn
Fox Keller to eliminate gene talk. The
strategy I adopted to avoid her complaint led to a functional account of
genes. This functional account, in turn,
led to my proposing a functionalist framework for doing behavioral
genetics. My attempt to account for the
specific kind of scientific explanation provided by the framework subsequently
led to my articulating a general explanatory framework for trait acquisition,
which has broad application, both inside and outside of science. I then considered two sorts of methodological
complaints: first, concerns from scientific pluralists were addressed in an
attempt to keep my functionalist proposal for behavioral genetics within the
pluralist fold; and, second, various possibly applicable traditional worries
for functionalisms that might also apply to a functionalized behavioral genetics
were noted. I concluded by showing some
ways in which this approach also helps deal with ethical arguments against
continued gene talk and with ethical worries about genetic manipulation. Thus, we have seen in this discussion that if
we rethink the behavioral genetics project, we can use it as a way to deal with
an impressive variety of problems.[55]
an international and interdisciplinary journal of postmodern cultural sound, text and image
Volume 7, March-April 2010, ISSN
1552-5112
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Notes