Biology, Philosophy of
BIOLOGY, PHILOSOPHY OF•••
While it may seem that the philosophy of biology, a field known for its focus on metaphysical, epistemological, and conceptual issues in biology, is far removed from the concerns of bioethics, there is a trend in philosophy of biology towards descriptivism that paradoxically allows for significant bridges with the predominantly normative concerns of bioethics.
About the same time that bioethics was born (the 1960s), the field of philosophy of biology took its first steps. Initially, it looked a lot like the rest of philosophy of science, which often meant focusing on the kinds of concerns that had their roots in physics. David Hull, Michael Ruse (1973) and others created a field that was dominated by formal concerns in evolutionary biology, including the nature and structure of its theories. Questions for the field included the nature of any reductions from the theories of Mendelian and transmission genetics to molecular genetics, whether it was possible to axiomatize evolutionary theory, how to account for the apparent teleology of evolutionary explanations, whether species are classes or individuals, and what the units of selection are. Many of these topics have remained active sub-fields to the present day.
Over time, philosophy of biology came to include much richer and detailed involvement with both current biology and the history of biology. Many philosophers came to ground their philosophical insights in rich historical accounts of various periods in the history of biology or in contemporary debates of active concern to practicing biologists. This naturalistic turn occurred in many parts of philosophy of science, but seems to have been most acute in philosophy of biology, at least partly for institutional reasons, including the creation of the International Society for the History, Philosophy, and Social Studies of Biology (Callebaut).
Through these developments, the field still largely avoided normative issues and focused on evolutionary biology. Recently several attempts have been made to move the field to other parts of biology. There are a number of philosophers working on developmental biology and using it as an alternative for framing traditional issues (Oyama, Griffiths, and Gray). Kenneth Schaffner has made a notable and unusual attempt to discuss the more medical parts of biology. Paul Thagard has similarly attempted to use work in the biomedical sciences (attempts at explaining the causes of ulcers) to address general philosophical issues in the nature of explanation.
There are a number of topics within philosophy of biology that especially bear on issues within bioethics.
One of the central concepts in the more medical parts of biology, particularly physiology, is the concept of function. It is impossible to understand the way we classify organ systems without this concept. The function of the heart is to pump blood. Hence any blood pump is a heart—even if there are some structural differences between the hearts of different species or (as mechanical hearts demonstrate) differences in the material makeup of the heart. So, what makes something a heart is fundamentally its function or purpose. This poses a philosophical problem, because the concept of function is a teleological notion. The function of the heart is to pump blood is simply another way of saying that the heart is designed to pump blood. But, who is the designer? Prior to Darwin the answer would have been an appeal to God.
Philosophers have attempted to account for the apparent goal-directed nature of biological science in two different ways. One solution is to accept that functions are goal directed, but to appeal to natural selection. Rather than a conscious designer, natural selection designed the heart to pump blood. The etiological view of functions (sometimes called Wright functions) gives an explanation of why a function is there in historical terms. More precisely, "The function of X is Z means (a) X is there because it does Z and(b) Z is a consequence (or result) of X's being there" (Wright, p. 139–168). To Larry Wright, "a heart beats because its beating pumps blood" (p. 40).
In contrast, in 1975 Robert Cummins rejected the goal-directed, historical approach to functions. What matters in thinking of functions is the contribution it makes to a whole system, the role that it plays in bringing about the performance of that system.
Early-twenty-first-century commentators have concluded that each approach captures a different notion of function. Where Larry Wright attempts to account for why a function is there (a function as opposed to an accident), Cummins explains what a function does, what it is good for (whether it is an accident or not). Continued debate over whether an etiological account can be developed in the Wright mode and how to overcome various problems continues (Cummins and Perlman).
The concept of function plays an especially important role in medicine since health and disease are often understood as normal (species typical) functioning or dysfunction respectively.
Concepts of Disease and Health
This is perhaps the most important area of research in philosophy of biology for bioethics. Arthur Caplan explains it as follows:
It may strain credulity to believe that the analysis of concepts such as health, disease, or normality can shed light on the ethical and policy issues associated with the vast amounts of new knowledge being generated by the human genome project and related inquiries in biomedicine. However credulity must be strained. The focus of attention qua philosophy tends to be on who owns the genome or whether an insurance company can boot you off the rolls if you are at risk of succumbing to a costly disease. But this is not really where the ethical and philosophical action is with respect to the ongoing revolution in genetics. (p. 128)
There are two important distinctions that must be understood in the debates over concepts of disease. First, there is a distinction between ontological and nominalist concepts of disease. On the ontological (realist) view of disease, diseases are real entities that exist in the world. Nosologies represent a true classification of the world—they carve nature at the joints. The paradigm diseases on this view would be either discrete disease causing agents that are at the same time identified as the diseases themselves or as discrete lesions. Thus, poliovirus is not the cause of poliomyelitis, it is poliomyelitis.
In contrast, the nominalist about disease would appeal to the old saying, "there are no diseases, only sick people." On this view, nosologies are merely conventional systems of classification. They may have a great deal of practical value, but they are not in any meaningful sense true descriptions of reality. In some cases we classify diseases based on the pathogen that causes the disease. In other cases we classify based on the signs and symptoms. In others we focus on the organ system that is damaged, regardless of the causes or the symptoms. Thus, the nominalist would use the current lack of unity in the organization of our taxonomy of diseases as support for the view that it is merely a conventional (and somewhat arbitrary) system. Realists would respond by appealing to the role of disease in medical science and point to similar problems with other taxonomic systems in science that are nonetheless regarded as capturing reality.
One of the arenas where this debate has been most heated has been over the issue of the status of the Diagnostic and Statistical Manual of Mental Disorders (DSM) in all of its versions. The fact that there are so many changes in the different versions of the DSM can be interpreted either as an indication that the classification scheme is merely a convention, or that the science of psychiatry is progressing (as any science does).
The second related distinction in debates over the concept of disease is over the role of values in the development of the nosologies. For the non-normativist, the starting point for understanding disease is to understand species typical functioning. Disease is malfunction of the organism, a failure to function as organisms are designed to do. To understand disease, one needs only to understand physiology. The concepts are the same in humans as in understanding disease in nonhuman organisms. Therefore, (non-scientific or epistemological) values play no role in the development of the classification and understanding of disease (Boorse).
In contrast, normativists believe that identifying a condition as a disease is a value-laden exercise. To say that a condition is a disease is to say something about what we value. Labeling something as a disease is a way of signaling the undesirability of the state. Normativists appeal to many examples that illustrate the way social values seem to permeate nosology. The early versions of the DSM identified homosexuality as a disease. The tendency of some slaves to attempt to escape was identified as a disease in the United States in the nineteenth century. Foot binding in Japan produces a condition that would be recognized as a disease in many parts of the world, but is seen as normal in Japan. Normativists deny that an account of disease solely in terms of species typical functioning can work. It is normal in some sense for humans to develop osteoarthritis in old age, normal for teeth to decay, normal to develop many ailments at advanced age. Yet medicine is committed to these things as disease. In fact age itself may be conceived of as both normal and a disease (Caplan et al.).
Finally, there is a dispute over the meaning of health. Non-normativists tend to think of health as the absence of disease. In that case, an organism is functioning within the normal parameters of its species at its age. In contrast there are those who adopt a much broader concept of health. On this view health is not the mere absence of disease, but is the full flourishing of a person in multiple dimensions, including psychological, economic, physical, and social well being. These different conceptions of health and disease lead to very different views about the obligations of medicine towards society, the scope of the medical field, and the nature of medical care.
What Counts as a Genetic Trait?
What does it mean to call something a genetic trait or disease? Clearly, at least part of that judgment rests on some kind of causal assessment. If a disease is genetic, then it is caused by one or more of an organism's genes. Indeed, this seems to fit a more general concept of disease, in which the causal basis of disease is incorporated into our nosologies. As Richard Hull has explained:
In its efforts to understand, control, and avoid disease, modern medicine has incorporated into the very identification of a disease the notion of the cause of the syndrome. This permits the individuation of similar syndromes with distinct causes into different diseases. (p. 61)
There is a fairly obvious problem with this as a way of distinguishing between genetic and epigenetic diseases. That is because there are genetic and nongenetic factors which are causally relevant to every trait, a fact recognized by virtually all commentators on the concept of genetic disease (see Gifford; Hull, 1979). So the real issue in deciding that something is a genetic disease, is whether the causal factors which are genetic are the most important causes. How do we decide whether genetic factors or environmental factors are more important in the production of various diseases? In response to the selection problem, a number of solutions have been proposed. These can be grouped into a few major categories.
One approach is to try to tease out a notion of genes as direct causes of disease. In 1990 Fred Gifford tried to capture this notion in one of his two definitions:
…the trait must be the specific effect of some genetic cause, that the trait must be described or individuated in such a way that it is properly matched to what the gene causes specifically. (p. 329)
However, this approach seems hopeless in the face of the actual complexity of development. Quite simply, this definition probably does not identify any diseases or traits as genetic. As Kelly Smith argued in 1990, "genes do not directly cause anything of immediate phenotypic significance" (p. 338).
Perhaps the most obvious and promising approach to the selection problems is to try a statistical approach. A number of variants on this have been attempted.
The first and central sense of genetic is this: a trait is genetic if genetic differences in a given population account for the phenotypic differences in the trait-variable amongst members of that population. (Gifford, p. 334)
This seems to exactly capture at least something important about society's concept of genetic disease. It can be put perhaps more precisely in terms of covariance. When some trait is identified as genetic, it can be argued that (in that population) the covariance of the trait with some genetic factor(s) is greater than the covariance of the trait with other (nongenetic) factors. This solves the selection problem neatly by allowing us to pick out which causal factors are irrelevant (the ones which are fixed) and highlight the important ones (the ones that make the difference ). In one of the canonical examples of causality, one is inclined to say that the lighting of a match (under normal circumstances) was the cause of the fire, while the presence of oxygen (while a contributing causal factor) was not. In contrast, in an environment where fire was normally present and oxygen was not, one might well pick out the (unusual) presence of oxygen as the cause of a fire.
There are several advantages to this approach to the selection problem. First, it corresponds to the use of analysis of variance that is used by biologists to measure the causal contribution of hereditary and environmental factors in a population. Second, it is capable of clear explication. Third, it has at least some intuitive support. However, this account seems to conflict with common usage in cases where pathogens typically identified as the cause of disease are nearly ubiquitous (so that, for example, genetic factors may make the difference between which people exposed to the pathogen become ill).
In spite of its advantages, the statistical approach fails to capture all of the myriad uses of the concept of genetic disease. Another approach has been developed from the way the most important causal factor in an explanation is picked out.
Philosophers have claimed on quite general grounds that the most important cause is chosen in terms of the manipulability of the various factors. Whatever the general virtues of this approach, it is promising when it comes to medicine. In the natural sciences, it could be argued that there is a strong interest in prediction and explanation. In contrast it has been argued that the medical realm is more concerned with the prevention and treatment of disease than with explanation (Wulff; Engelhardt). Instrumentalist interests play a much more central role in medical practice than in science. Hence, the appropriate solution to the selection problem can be formulated in terms of manipulability. The most important cause is the one that is identified as the most easily manipulated to prevent or treat disease. A disease is genetic if it is genes that play this role and epigenetic if it is non-genetic factors that are most easily manipulated.
Like the statistical definition, the manipulability definition captures something important about our usage of the term. In addition it is often an implicit aspect of the justification for the extension of the concept of genetic disease to new cases. However there are some problems with this approach as well. The obvious problem seems to be that on this analysis, no disease could be classified as genetic. Many of the paradigm genetic diseases (phenylketonuria [PKU], cystic fibrosis [CF]) involve treatments that are not molecular. Indeed, in the case of PKU, the standard treatment involves a change in diet. At the same time the tests for PKU were developed before the actual mutation responsible for the disease had been identified. It is impossible to adhere to the manipulability definition and accept that PKU is a genetic disease. This seems to be a fatal flaw in the manipulability definition. In addition, it is not true that biomedical science is always instrumentally oriented. A great deal of effort is aimed not just at treating and preventing disease, but at understanding it. This may lead to a conflict over which causal factor is most important (the factor most easily manipulated for treating or preventing a disease may not be the most revealing for the purposes of understanding a disease).
It is worth noting that both the statistical approaches and the manipulability approaches seem to imply a relativity in the concept of genetic disease. In the case of the statistical notion, something will count as a genetic disease or not, depending on the population it is a part of. The manipulability definition implies that technological advances will affect what counts as a genetic disease as the reach of our technology is extended. Yet, this result seems to be incompatible with an ontological conception of disease. If diseases are real entities (and independent of values) then the solution to the selection problem should not depend on factors outside of the organism (Boorse). Thus the normativist or constructivist position on disease seems to be supported by these analyses (however inadequate they are as a general account).
As philosophy has become more naturalized, it is unsurprising that philosophers (and especially philosophers of biology) would attempt to find a way to ground ethics in a biological account of human nature. Perhaps even more significantly, the development of sociobiology and its subsequent incarnation, evolutionary psychology, meant that biologists were looking to explain the origins of morality in an evolutionary account (Wilson; Farber; Wright, 1995). Michael Ruse has been perhaps the most influential voice on evolutionary ethics (1991, 1993).
Ruse argues that evolutionary theory offers the explanation of the origin of altruism and other moral sentiments. He follows the explanatory strategy of the sociobiologists (and evolutionary psychologists) by appealing to the apparent universality of cooperative behaviors and moral sentiments, combined with the obvious adaptive value that cooperative strategies represent. Indeed there are a number of game theoretic accounts to demonstrate the adaptive value of altruistic behavior in at least some circumstances (Smith, 1982).
Ruse then claims that the fact that evolution explains morality undermines moral realism. He offers two arguments. First, although human moral sentiments evolved, it is quite possible that an alternative set of sentiments could have produced the same effects. The contingency of evolution means that morality itself is contingent. Second, Ruse takes great care in dispelling any teleological interpretation of evolution. Evolution is a directionless process with no end or goal. Since morality is founded on a directionless process, it follows that realism towards ethics is undermined. Evolution is meaningless, and without value. Organisms that survived and adapted are not better in a normative sense. Hence there is no normative foundation for ethics.
Critics have attempted a number of strategies, including questioning the extent to which evolution can really account for morality (Lewontin), or denying the relevance of the facts of evolution to normative issues (Nagel). Other critics have argued that a fully naturalized ethics that accepts evolution as the foundation of morality is fully compatible with ethical realism (Maienschein and Ruse).
What Is Life?
A recently emerging research area at the intersection of philosophy of biology and bioethics is over the definition of life. This question has multiple dimensions. National Aeronautics and Space Administration (NASA) scientists wonder about the definition as they pursue research into the question of life on other planets. How will researchers know whether what they find is a living organism or a (nonliving) chemical reaction? Biologists interested in the origins of life similarly strive to understand the demarcation between the living and nonliving as they construct their models. Genomic scientists attempt to better understand gene function by trying to determine the minimal number of genes necessary for life—life's genetic essence. Public policy makers and scientists debate the moral significance of ex vivo fertilized egg cells and the stem cells that can be derived from them. Are the embryos living? Are they alive when they are frozen? Are the stem cells that can be derived from them living beings deserving of respect or are they research tools to be used to help people suffering from disease?
The process of development, from an early embryo to a fully differentiated and functioning organism is a long, complex process. Determining the moral status of that embryo at different stages of the process is a difficult task (Green). Prior to implantation, an embryo's undifferentiated blastomeres are each capable of creating separate and unique individuals (through twining). Other traits emerge later as the nervous system develops. At what point is there a (human) life? And is life (as opposed to, for instance, personhood) the right concept to be considering? And what is the status of the derived stem cells themselves? As Arthur Caplan and Glen McGee have argued, the problem of "What's in the dish?" remains one of the key concepts in this policy debate. At heart though, the issue turns on precisely the kinds of metaphysical and biological issues that philosophy of biology has been exploring for decades. Surprisingly few have weighed in (Maienschein) but more can be expected to do so in the future.
Debates about the origins of life have produced very different approaches to the meaning of life (Rizzotti). More reductionist accounts place a heavy emphasis on genetic features—the ability to replicate is key and the genes are seen as what make cells alive. In contrast, metabolists have long focused on the interactive elements of living things. Recent attempts to define the minimal genome represent the latest in the reductionist approach to defining life (Cho et al.).
Reductionism and Genetic Determinism
One of the themes that runs through much of the intersection of philosophy of biology and bioethics is the question of reductionism and its most criticized form, genetic determinism. To what extent is behavior and character dictated by genes? Popular images in magazines hype genes as the new Rosetta stone, the key to unlocking who and what people are (Nelkin and Lindee). Many biologists have defended the view that genes are the primary determinants of key traits (Hamer; Koshland).
Philosophically there are multiple meanings of reductionism that can be distinguished. There is theory reductionism in which theories at one level are explained by other theories that are seen as more fundamental. Recent philosophy of science has moved away from traditional views about theories, requiring alternative accounts of formal reductionism that looks at models and mechanisms (Sarkar). Reductionism can be epistemological in character—it can be about what provides the epistemological force to claims at different levels. So, for example, the force of rules in psychology could be dependent on the force of genetic rules that would explain the rules in psychology. Ontological reductionism would claim in one way or another that the only real entities are those at lower levels. Ultimately, the ideal reductionist picture would show the unity of science—behavioral accounts can be reduced to population genetics, population genetics can be reduced to molecular genetics, molecular genetics reduced to chemistry, and chemistry to physics. The only real entities are the entities posited by physics.
There have been many criticisms of reductionism (Sarkar; Moss; Kaplan; Lewontin; Keller; Kitcher). These have ranged from technical difficulties with reducing theories from biology to other levels (the only plausible laws in Mendelian genetics are not only false, transmission genetics is a measure of the degree of falsity of the law of independent assortment) to criticisms of specific popular reductions which purport to demonstrate the fundamental importance of genes as the determinants of human characteristics. Reductionism (especially the popular version) is largely a promissory note, one that the critics show is virtually impossible to pay off.
Philosophy of biology continues to grapple with conceptual issues that concern bioethicists. The meaning of disease, health, genetics, and even life are all issues that are full of import for normative concerns with how research should proceed, what sorts of science and medicine should be funded, and the moral status of different entities. The turn towards thick descriptions of biology and a growing interest in parts of biomedical science beyond evolution should fuel continued overlap between philosophy of biology and bioethics.
SEE ALSO: Body: Cultural and Religious Perspectives; Healing; Life; Medicine, Philosophy of; Natural Law; Science, Philosophy of
Boorse, Christopher. 1981. "On the Distinction between Disease and Illness." Philosophy and Public Affairs 5: 49–68.
Callebaut, Werner. 1993. Taking the Naturalistic Turn. Chicago: University of Chicago Press.
Caplan, Arthur. 1992. "If Gene Therapy is the Cure, What is the Disease?" In Gene Mapping, ed. G. Annas and S. Elias. Oxford: Oxford University Press.
Caplan, Arthur; Englehardt, Tristram H.; et al., eds. 1981. Concepts of Health and Disease: Interdisciplinary Perspectives. Reading, MA: Addison-Wesley Publishing Co.
Caplan, Arthur, and McGee, Glenn. 1999. "What's in the Dish?" Hastings Center Report 29(2): 36–38.
Cho, Mildred; Magnus, David; Caplan, Arthur; et al. 1999. "Ethical Implications of Synthesizing a Minimal Genome." Science 286: 2087–2090.
Cummins Robert. 1975. "Functional Analysis." Journal of Philosophy 72: 741–765.
Cummins, Robert, and Perlman, Mark, eds. 2002. Functions: New Essays in the Philosophy of Psychology and Biology. Oxford: Oxford University Press.
Engelhardt, T. 1981. "The Concepts of Health and Disease." In Concepts of Health and Disease: Interdisciplinary Perspectives, ed. Arthur Caplan, H. Tristram Engelhardt, and James J. McCartney. Reading, MA: Addison-Wesley Publishing Co.
Farber, Paul. 1998. The Temptations of Evolutionary Ethics. Berkeley: University of California Press.
Gifford, Fred. 1990. "Genetic Traits." Biology and Philosophy 5(3): 327–347.
Green, Ronald M. 2001. The Human Embryo Research Debates: Bioethics in the Vortex of Controversy. Oxford: Oxford University Press.
Hamer, Dean. 1998. Living with Our Genes. New York: Doubleday.
Hull, David. 1974. Philosophy of Biological Science Engelwood Cliffs, NJ: Prentice-Hall.
Hull, Richard. 1979. "Why Genetic Disease ?" In Genetic Counseling: Facts, Values and Norms, ed. Alexander Capron, Marc Lappé, Robert Murray, Jr., et al. New York: National Foundation March of Dimes Birth Defects Original Article Series.
Kaplan, Jonathan. 2000. The Limits and Lies of Human Genetic Research. New York: Routledge Press.
Keller, E. F. 1995. Refiguring Life: Metaphors of Twentieth Century Biology. New York: Columbia University Press.
Kitcher, Philip. 1984. "A Tale of Two Sciences." Philosophical Review 93: 335–373.
Koshland, Daniel. 1990. "The Rational Approach to the Irrational." Science 250: 189.
Lewontin, Richard. 1992. Biology as Ideology: The Doctrine of DNA. New York: Harper-Perennial.
Maienschein, Jane. 2003. Defining Life. Cambridge, MA: Harvard University Press.
Maienschein, Jane and Michael Ruse, eds. 1999. Biology and the Foundations of Ethics. Cambridge, Eng.: Cambridge University Press.
Moss, Lenny. 2001. What Genes Can't Do. Cambridge, MA: MIT Press.
Nagel, Thomas. 1997. The Last Word. Oxford: Oxford University Press.
Nelkin, Dorothy, and Lindee, Susan. 1995. The DNA Mystique. New York: W.H. Freeman Press.
Oyama, Susan; Griffiths, Paul; and Gray, Russell, eds. 2001. Cycles of Contingency: Developmental Systems and Evolution. Cambridge, MA: MIT Press.
Rizzotti, M, ed. 1996. Defining Life, the Central Problem in Theoretical Biology. Padova, Italy: University of Padova.
Ruse, Michael. 1973. The Philospohy of Biology. London: Hutchinson.
Ruse, Michael. 1991. "The Significance of Evolution." In A Companion to Ethics, ed. Peter Singer. Cambridge, Eng.: Blackwell.
Ruse, Michael. 1993. "The New Evolutionary Ethics." In Evolutionary Ethics, eds. Matthew Nitecki, and Doris Nitecki. Albany: State University of New York Press.
Sarkar, Sahotra. 1998. Genetics and Reductionism. Cambridge, Eng.: Cambridge University Press.
Schaffner, Kenneth. 1993. Discovery and Explanation in Biology and Medicine. Chicago: University of Chicago Press.
Smith, John Maynard. 1982. Evolution and the Theory of Games. Cambridge, Eng.: Cambridge University Press.
Smith, Kelly. 1990. "Genetic Disease, Genetic Testing, and the Clinician." Medical Student Journal of the American Medical Association 285: 327–347.
Thagard, Paul. 1999. How Scientists Explain Disease. Princeton, NJ: Princeton University Press.
Wilson, E. O. 1988. On Human Nature. Cambridge, MA: Harvard University Press.
Wright, Larry. 1973. "Functions." Philosophical Review 82: 139–168.
Wright, Robert. 1995. The Moral Animal. New York: Vintage Books.
Wulff, Henrik. 1984. "The Casual Basis of the Current Disease Classification." In Health, Disease, and Casual Explanation in Medicine, eds. Lennart Nordenfeld and Ingemar B. Lindahl. Dordrecht, The Netherlands: Reidel.