These arguments then rest on the disputable assumption that one’s genetic endowments completely determine one’s physical, psychological, and intellectual characteristics. It presupposes that a simple correlation between genotype and phenotype exists for what undeniably are very complex human traits. But such an assumption has no scientific basis. It simply ignores that genotypes have a range of phenotypic expression, overlooks the importance of the environment, and disregards the significance of one’s choices in building a unique and distinctive life. It seems that unless we incorrectly assume that our genome completely determines who we will be, then there are no reasons to believe that genetic manipulation by itself would interfere with human dignity or human freedom, or that it will be able to create creatures so smart, talented, sensitive, or imaginative as to make them unrecognizably human or post-human. Contrary to these ideas, the evidence that we have about the feasibility of using genetic engineering to change or influence these or similar characteristics significantly is that human biology is far more complex than it might appear by reading discussions of human genetic enhancement.
Think of a relatively “simple” characteristic such as, for example, being healthier. We have good evidence that most diseases affecting humans are multifactorial (Weiss, 2005; Becker, 2004; Cummings, 2003; Wilkie, 2001; Risch, 2002). Unlike Mendelian diseases, the transmission of these diseases is governed by multiple factors, and familial patterns of inheritance do not follow a strictly Mendelian mode. Alleles contributing to these complex diseases are neither necessary nor sufficient to cause the particular disease; that is, some people might suffer the disease without having the related mutations, and some people might carry the mutations but might not have the disease in question. For many of these complex diseases, more than one gene at different loci contribute to the disease, and those loci might interact with each other. Depending on their roles on the pathogenesis of diseases, these interactions might be additive, multiplicative, or might have no additional effect. Modifier genes can also interact with mutations involved in the production of some diseases. The effects of interaction between an allele that might predispose to a particular disease and a protective allele might be especially difficult to predict with any accuracy. Similarly, epigenetic factors can modify the expression patterns of genes without altering the DNA sequence (Jiang et al., 2004; Dennis, 2003). The expression of most human diseases also involves the relations of multiple genetic and environmental factors. Additionally, cases of incomplete penetrance and variable expressivity introduce even more difficulties in our ability to predict the risks of developing a particular disease and thus of preventing it (Wilkie, 2001; Risch, 2002). The different penetrance of mutations is not entirely an intrinsic character (Veneis et al., 2001). On the contrary, it appears to depend on several factors such as the importance of the function of the protein encoded by the gene, the functional importance of the mutation, the interactions with other genes, the interactions with the environment, the onset of the disease, and the existence of alternative pathways that can substitute for the lost function. What is more, some of these factors can vary between individuals. Things are then not as simple as sometimes they are made to appear. So, making people healthier by tinkering with their DNA does not seem that easy: and, where there is the possibility of doing so, it does not seem that the changes would be significant enough to talk about a different species of post-humans.
Consider another characteristic often mentioned in the debates on human enhancement: longer life spans by slowing the aging process. Presumably, our first concern would be to ask how much longer a human would need to live to become a post-human. Advances in public health care and in medical technologies have certainly increased average human life spans considerably during the last few centuries (Wilmoth, 2000). These increases, however, have not been taken to mean that we are on the path to becoming post-humans. Thus, it seems that the increase needs to be more significant. Obviously, immortality would be a candidate. Indeed for some (Kass, 2001; Harris, 2004; Fukuyama, 2002) there is a scientific race to achieve human immortality. Such speculations include claims about whether immortality would produce boredom, how it would affect our, already depleted, economic and environmental resources, whether there will be a loss of personal identity, whether it would make people happier, and about the consequences of having parallel populations of mortals and immortals existing alongside one another (Kass, 2001; Harris, 2004, 2000; Fukuyama, 2002; Glannon, 2002). Yet it hardly seems necessary to say that no evidence whatsoever exists that manipulating human DNA can attain such a goal. Also, longer lives filled with the manifestations of old age would hardly be desirable. Thus, those desiring longer lives for humans also desire to slow the aging process. But, there is no empirical evidence to support the claim that aging in humans has been modified by any means, nor is there any evidence that it is possible to measure biological age (Hayflick, 2004; Turner, 2004; Olshansky et al., 2004; Miller, 2002). It appears then that discussions about changing human life spans and aging processes in ways significant enough to create post-humans are no more than wishful thinking (Turner, 2004, 19-21). Nothing in current biological knowledge suggests that genes alone are responsible for controlling these traits.
The misunderstandings about human biology are not limited only to the incorrect assumption that genes control most human traits and behaviors (or at least that they control those traits that we think represent the “essence” of humanity,) and that thus, other aspects of humans’ biology, environmental factors, and social arrangements and institutions are irrelevant as causal contributors to such traits or behaviors. Proponents and opponents of genetic enhancement also err by presupposing that our social environment is immaterial as a causal contributor to the judgments about such traits. That is, these arguments commit the error of assuming that our biological traits and behaviors can be evaluated outside of the environmental, social, and political contexts in which such traits and behaviors are expressed. Genetic predispositions have to be expressed as phenotypic traits, i.e., observable physical or behavioral characteristics that result from the interplay of genes and environments, before we can evaluate whether these characteristics are good or bad things. And, many human phenotypic attributes diverge in value according to the social and environmental contexts in which they are expressed. For instance, homosexuality, assuming for the sake of this argument that this is a genetically determined trait, can be very problematic in societies that place great value on the connection between sexual acts and reproduction, but it would be unlikely to raise much concern in social environments where such a connection is irrelevant.
Let us go back to our interest in making “healthier” humans. As the recent debate on obesity indicates the concepts of “heath” and “disease” as applied to humans are far from uncontroversial (Kaplan, 2000, ch. 8; Mokdad et al., 2004; Flegal et al., 2005; Gard, 2005; Oliver, 2005). It is clear, however, that health and disease cannot be assessed by simply looking at genes, not even at genes in the context of whole organisms. Consider, for example, the case of allergic reactions to a substance that is only present, and in great quantities, in highly industrialized societies. Even if such allergic reactions were mainly determined by having certain genetic material, we would be hard pressed to call this a disease or disorder, indeed, we would be hard pressed to be concerned with it at all were we living in a nonindustrial society. Or, take the case of some Italian speakers who have neurological markers for dyslexia, but show no learning impairment, as compared with Englishspeaking dyslexics who have a much more difficult time learning to read because of the complexity of their language (Paulesu et al., 2001). It seems then, that to evaluate human diseases, disabilities, or disorders and their effects, one must take into account the ecological and social environment in which human beings grow and develop. Human biology is not independent of where we live and how we live. Most human traits and behaviors need to be evaluated in social contexts. Such social contexts are not fixed. They have changed over human history, and there seem to be no reasons to believe that we cannot change them again to pursue worthy moral goals such as, for example, equality or fairness. Judgments about the desirability of traits such as beauty, health, weight, strength, or life span depend on the environmental context in which they are expressed, which in the case of humans includes social and political contexts. If the value of these traits is not determined by the fact that they are genetic traits or behaviors, then to assume that these traits will be valued by future generations as we now value them presupposes that we must believe that the social and political context will not change. Nothing in human history warrants such a belief.