The genetic revolution: Epistemic and technological

The genetic revolution can be described as progressing in two stages, both of which have profound implications for justice in the genomic era. The first stage of this revolution is an epistemic revolution, as we gain new and significant empirical insights into the role genes play in the development of different phenotypes (that is, observable characteristics such as health, disease, and behavior). While this dimension of the revolution does not itself directly manipulate or alter people’s genes, it can shed light on the demands of justice by revealing new insights into the nurture versus nature debate.

The second stage of the genetic revolution, which follows from the epistemic revolution, is the technological revolution that translates this new scientific knowledge into novel medical interventions (e.g., genome editing or a pill that slows the aging process or enhances cognition). At this stage in time, the specific details of the technological revolution are still speculative and unknown as the epistemic dimension of the revolution is still in its infancy.

The genetic revolution began to gain serious momentum in the mid-twentieth century after James Watson and Francis Crick (Reference Watson and Crick1953) formulated the double-helix structure of DNA in 1953. Less than 50 years later, the human genome was sequenced (International Human Genome Sequencing Consortium, 2001; Venter et al., Reference Venter, Adams, Myers, Li, Mural, Sutton, Smith, Yandell, Evans, Holt, Gocayne, Amanatides, Ballew, Huson, Wortman, Zhang, Kodira, Zheng, Chen and Xiaonong2001), identifying the approximately 20,500 protein-coding genes we have. Since the turn of the twenty-first century, the number of genetic tests available has increased significantly, from tests for just a few conditions (such as cystic fibrosis and phenylketonuria) to approximately 75,000 genetic tests on the market today (Phillips et al., Reference Phillips, Deverka, Hooker and Douglas2018).Footnote ² Over the past decade, studies have examined the role that genetics play in parental investment (Champagne & Curley, Reference Champagne, Curley, Royle, Smiseth and Köllike2012; Pérusse et al., Reference Pérusse, Neale, Heath and Eaves1994), intelligence (Benyamin et al., Reference Benyamin, Pourcain, Davis, Davies, Hansell, Brion, Kirkpatrick, Cents, Franić, Miller, Haworth, Meaburn, Pricce, Evans, Timpson, Kemp, Ring, McArdle, Medland and Visscher2014; Shakeshaft et al., Reference Shakeshaft, Trzaskowski, McMillan, Krapohl, Simpson, Cederlof, Larsson, Lichtenstein and Plomin2015), aggression (Tiihonen et al., Reference Tiihonen, Rautiainen, Ollila, Repo-Tiihonen, Virkkunen, Palotie, Pietiläinen, Kristiansson, Joukamaa, Lauerma, Saarela, Tyni, Vartiainen, Paananen, Goldman and Paunio2015), political behavior (Fowler et al., Reference Fowler, Baker and Dawes2008; Fowler & Dawes, Reference Fowler and Dawes2008), exceptional longevity (Perls et al., Reference Perls, Kunkel and Puca2002; Sebastiani et al., Reference Sebastiani, Solovieff, DeWan, Walsh, Puca, Hartley, Mellista, Andersen, Dworkis, Wilk, Myers, Steinberg, Montano, Baldwin, Hoh and Perls2012), and human happiness (Lykken & Tellegen, Reference Lykken and Tellegen1996; Okbay et al., Reference Okbay, Baselmans, De Neve, Turley, Nivard, Fontana, Meddens, Linnér, Rietveld, Derringer, Gratten, Lee, Liu, de Vlaming, Ahluwalia, Buchwald, Cavadino, Frazier-Wood, Furlotte and Cesarini2016).

The first, or epistemic, stage of the genetic revolution presents us with a more complete understanding of our biology. Therefore, it can help justice theorists transcend the simplistic “nature versus nurture” debate instigated (at least in part) by Francis Galton, who, in English Men of Science: Their Nature and Nurture (Reference Galton1874), argued that character and intelligence were heritable. We now have conclusive evidence that both genetic determinism and environmental determinism are false.

Before the sequencing of the human genome and twin studies, scholars in the humanities and social sciences theorized about ethics and justice from behind a real “veil of ignorance.” Over the past few decades, this veil has been gradually lifted. No specific scientific consensus has (at least yet) emerged, but what is certainly clear is that the debate is about nature and nurture, not nature versus nurture. Environment and heredity both play significant roles in influencing intelligence, health, happiness, and behavior. The real challenge is figuring out how the two things influence these different phenotypes. There are circumstances in which environment alone determines serious disadvantage, such as a lack of access to clean drinking water, food, adequate shelter, education, and medical care. And there are clearly cases in which possessing particular genetic mutations is sufficient for serious disadvantage, including premature death.

According to the World Health Organization ([WHO] 2020a), scientists estimate there are more than 10,000 known monogenetic diseases, meaning they are caused by an error in a single gene. “Such diseases typically can develop in practically all usual environments” (Alper, Reference Alper and Alper2002, p. 20). A child who inherits the gene implicated in a single-gene disorder, such as cystic fibrosis or Fragile X syndrome, can suffer premature death or severe cognitive impairment. The genes we inherit from our parents can also influence our risk of chronic diseases, such as cancer, heart disease, and stroke.

At the other end of the spectrum of the “genetic lottery” of life are those fortunate (and very rare) individuals who inherit the genes associated with exceptional healthy longevity. Such individuals can enjoy a century of disease-free life. The exceptionally long-lived share “longevity genes” (Sebastiani et al., Reference Sebastiani, Solovieff, DeWan, Walsh, Puca, Hartley, Mellista, Andersen, Dworkis, Wilk, Myers, Steinberg, Montano, Baldwin, Hoh and Perls2012) that can extend the “biological warranty period”Footnote ³ for humans beyond that of the average person. For the vast majority of humans, we have a biological warranty period of approximately 70 years,Footnote ⁴ and modern medicine permits us to live beyond that period by managing multimorbidity to delay death. The maximum (but not average) human lifespan, without any intentional genetic modifications, is believed to be around 125 years (Weon & Je, Reference Weon and Je2009). But the prevalence of centenarians is very low. In the United States and other industrialized nations, centenarians occur at a rate of about 1 per 6,000. Supercentenarians (aged 110 and older) occur at a rate of about 1 per 5 million (Boston University, 2020).

The second stage of the genetic revolution is the technological revolution, which involves increasing the power that humans have to directly and purposively shape our biology by making changes at the genetic level. This is often referred to as “genetically engineering” humans. A clear example that this revolution is underway is the first officially sanctioned gene therapy experiment in 1990. The subjects of the earliest gene therapy experiments were children who suffered from a rare genetic disease called adenosine deaminase deficiency. Today, almost 3,000 gene therapy clinical trials have been approved and are either ongoing or completed worldwide.Footnote ⁵

With gene therapy, genetic material is inserted into the cells to correct the effect of a mutated gene that is causing disease. Genome editing is a much more recent, and precise, technique of genetic manipulation. It involves adding, removing, or altering DNA in the genome. CRISPR-Cas9 is a technique that offers scientists a simpler method of manipulating genes; CRISPR was approved for human clinical trials in the United States in 2016. In November 2018, the first (alleged) genetically edited babies (twins) were born in China.Footnote ⁶ The lead scientist who conducted the experiment, He Jiankui, claimed that he and his colleagues utilized the genome-editing tool CRISPR-Cas9 to modify the embryos to disable the gene CCR5, which is “a key player in HIV infection due to its major involvement in the infection process” (Lopalco, Reference Lopalco2010). Applying experimental genome editing to healthy embryos in the hopes of creating people who are HIV-resistant is ethically dubious given the current risks involved with genome editing, especially on healthy embryos that do not face a high risk of developing disease. Scientists from around the world, including Chinese HIV professionals (Zhang et al., Reference Zhang, Zhong, Zhai, Shao and Lu2018), were quick to condemn He’s experiment as ethically unsound.

Such rapid and profound scientific developments make it clear that we are living in the midst of an epistemic and technological “genetic revolution.” This revolution raises significant challenges for theories of justice. Should we aspire to purposely alter our biology via genetic modification? And if so, how do we avoid repeating the injustices of the eugenics movement? Should we pursue only genetic therapy (e.g., treating disease) but not “enhancement” (going beyond “normal species functioning”)? And is the therapy/enhancement distinction even tenable (Resnick, Reference Resnick2000)?

In our haste to try to answer these questions, I believe moral and political philosophers have missed a unique opportunity to critically reflect on how the genetic revolution ought to change the way we theorize about ethics and justice. In this article, my central concern is with this methodological issue rather than positing and defending any substantive conclusions concerning what the specific demands of justice ought to be in the genomic era.

For the sake of simplicity, I will refer here to “ideal theorizing” about justice in the genomic era as the methodological approach in which one applies/extends to the genomic era a distributive principle (e.g., “liberty upsets patterns”) or value (e.g., autonomy) or theory of justice (e.g., “luck egalitarianism” or Rawls’s “justice as fairness”) that was initially invoked or derived to apply in a simplified and/or idealized pre-genomic era. This mode of theorizing (typically, but not always) makes the distribution of wealth and income the locus of our normative theorizing. But this is precisely the issue that the genetic revolution requires us to radically reevaluate—to conceptualize the demands of justice far beyond the distribution of wealth and income, to the distribution of natural endowments themselves. A comprehensive examination of such ideal-level analyses would be too burdensome to undertake in detail here, but I shall briefly survey a few such approaches, covering a wide spectrum of theories. These include liberal egalitarianism, Kantianism, perfectionism, libertarianism, and consequentialism.

Ideal theorizing about genomic justice

My goal in this article is not to refute or undermine the value of ideal theorizing about justice. I have a more modest and specific claim in mind: namely, when it comes to theorizing about justice in the genomic era, we should turn to non-ideal (rather than ideal) theory. Earlier, I noted that Valentini (Reference Valentini2009) characterized ideal theory as theorizing that makes “social reality appear significantly ‘simpler and better’ than it actually is” (p. 332). By contrast, non-ideal theory, especially when it is extended to the genomic era, takes seriously the complexity and vulnerability of human biology. In this section, I shall briefly highlight some of the non-ideal considerations ignored by ideal theorists.

To date, manyFootnote ⁷ of the emerging debates concerning genetics and justice promote the type of normative analysis that is typical of debates concerning the ideal distribution of wealth and income spurred by Rawls’s original account of ideal justice. For example, Norman Daniels (Reference Daniels1985), who initially relaxed the Rawlsian assumption that everyone is healthy (one of Rawls’s “idealizing” assumptions) so that the principle of fair equality of opportunity could form the basis of an account of just health care, extended this line of argument to the topic of genetics and justice in From Chance to Choice: Genetics and Justice (Buchanan et al., Reference Buchanan, Brock, Daniels and Wikler2000). Daniels, together with Allen Buchanan, Dan Brock, and Daniel Wikler, endorses two specific conclusions that they believe should guide public policy choices in the age of genetic intervention. The first is that there is a principled presumption that genetic intervention to prevent or ameliorate serious limitations caused by disease is a requirement of justice, and second, that justice may require regulating conditions of access to genetic enhancements to prevent exacerbating existing unjust inequalities.

A foundational premise of Daniels’s argument is the idea that justice requires that we restore people to “normal species functioning.” But John Harris (Reference Harris2007) nicely captures the deficiency of utilizing “normal species functioning” as some moral baseline in theorizing about the ethics of genetic intervention in an aging world:

Noting the problem inherent in invoking the ideal of “normal species functioning” is critical given the rapid rise of chronic disease in the world as populations age. To claim that there is a “principled presumption that genetic intervention to prevent or ameliorate serious limitations caused by disease is a requirement of justice” would mean spending more and more research dollars on searching for treatments for specific diseases of aging.Footnote ⁸ This costly endeavor can delay death and increase life expectancy, but at the cost of increasing the human frailspan versus the human healthspan. This means that “further life extension in an aging world will expose the saved population to an elevated risk for all other aging-related diseases” (Olshansky, Reference Olshansky2018, p. 1323). This is a reality that a non-ideal analysis of the justice in the genomic era takes seriously.

Furthermore, utilizing the idea of “normal species functioning,” or what is “natural” with respect to our genetic endowments, is misguided because, as noted in a recent National Academies of Sciences, Engineering, and Medicine (2017) report on the ethics and governance of genome editing, “there is no single ‘normal’ human genome sequence; rather, there are multiple variant human genomic sequences … all of which occur in the worldwide human gene pool and, in that sense, are ‘natural,’ and all of which can be either advantageous or disadvantageous” (p. 106).

Bioconservatives opposed to the genetic engineering of humans have also invoked “idealized” moral sensibilities in their arguments against going down the path of genetic interventions. In his short book on the subject, The Case against Perfection: Ethics in the Age of Genetic Engineering, Michael Sandel (Reference Sandel2007) argues that the quest to perfect our biology “threatens to banish our appreciation of life as a gift, and to leave us with nothing to affirm or behold outside of our own will” (pp. 99–100). Life may very well be a gift, but it is not clear why utilizing the knowledge and innovation of the genetic revolution to reduce our susceptibility to disease, or to improve our cognition and happiness, is any different from pursuing environmental interventions (e.g., access to medical expertise, healthy diet, education, fulfilling leisure activities, and relationships) for the same purpose. It is precisely because life is a gift, one might argue, that we ought to utilize all possible scientific innovations, including genome editing, to promote more health and happiness. Sandel does not adequately explain why genetic engineering is any different from other forms of social engineering (e.g., the family, the political economy, the Constitution, and public health measures such as immunizations) that we believe justice requires but are not typically considered a threat to the idea that life is a gift. In Beyond Humanity? Buchanan (Reference Buchanan2011) criticizes Sandel’s sweeping generalization of enhancements, describing such an argument as “a priori psychology and sociology … [positing] controversial generalizations about human behavior or the workings of human society from the armchair” (p. 9).

Jürgen Habermas claims that parents selecting the genetic constitutions of their offspring threaten the self-understanding of the affected person as an autonomous and responsible agent. Eugenic practices, he argues, “might well harm the status of the future person as a member of the universe of moral beings” (Habermas, Reference Habermas2003, p. 79). Like Sandel’s invocation of the sentiment that life is a gift, it is difficult to see how Habermas’s vague appeal to the autonomy of future potential people can inspire instructive and helpful debate on the ethics of pursing genetic engineering. Rather than clarifying the moral stakes at issue with genetic engineering, the Habermasian strategy sidetracks the discussion and debate into the metaphysics of the Kantian account of ideal autonomy.

The left libertarian Hillel Steiner (Reference Steiner1994) proposed, in his book An Essay on Rights, that germline genetic information is a natural resource that could help achieve luck egalitarian equality by mitigating genetic inequalities (which are unchosen). While such a proposal is insightful and provocative, the catalyst for Steiner’s theorizing about genetics comes not from a recognition of the potentially profound implications of the epistemic and technological advances of the genetic revolution, but rather from a desire to resolve a paradox in libertarian political thought. Namely, the tension between the libertarian belief that we own the fruits of our labor but are also the result of our parent’s labor. Steiner posits the paradox as follows:

1. 1. It is logically possible that all persons are self-owners.

2. 2. All self-owners own the products of their labor.

3. 3. All persons are the product of other persons’ labor.

4. 4. Therefore it is logically impossible that all persons are self-owners. (Steiner, Reference Steiner, Burley and Harris2002, p. 321)

By invoking the proposal that we treat germline genetic information as natural resources that are owned equally, Steiner argues that a solution can be found to what he calls the “paradox of universal self-ownership.”

Steiner’s argument has been criticized by others elsewhere (Curchin, Reference Curchin2007; Shnayderman, Reference Shnayderman2019), so I will not go into the details of the potential problems with his suggestion to treat germline genetic information as a natural resource that could help achieve a luck egalitarian distribution. But I think his extension of the domain of libertarian justice to include genetic endowments is telling, in that what drives the intellectual move to do so is his prior theoretical commitment to the two premises of libertarianism. Justice is extended to germline genetic information because it potentially helps solve the conceptual tension within libertarianism. Steiner’s approach is paradigmatic of ideal theorizing, starting with the idealized commitment to self-ownership, rather than theorizing the non-ideal realities of genetic disadvantage and complexity in the world today and permitting those realities to help the theorist determine which normative sensibilities are appropriate for helping us address those predicaments.

Finally, Julian Savulescu (Reference Savulescu2001) is a “pro-enhancement” consequentialist who champions the principle that he calls “procreative beneficence” (PB). PB prescribes that “couples (or single reproducers) should select the child, of the possible children they could have, who is expected to have the best life, or at least as good a life as the others, based on the relevant, available information” (Savulescu, Reference Savulescu2001, p. 415). The principle applies to screening embryos at the pre-implantation stage of in-vitro fertilization (IVF). PB instructs prospective parents to use all the available information (not limited to just screening against disease) and choose the embryo that is expected to have the best life. For example, when utilizing IVF, more eggs may be fertilized than will be implanted in a woman’s uterus. Pre-implantation genetic diagnosis can be utilized to screen those embryos for information about the likelihood of disease and nondisease traits developing in the potential offspring. When selecting which of the embryos to implant during IVF, PB prescribes that parents should utilize all available information on the potential for health and other characteristics relevant to the future well-being of their potential offspring.

Perhaps the most pressing objection to PB is the non-ideal reality that it imposes extra procreative burdens on women. As the feminist bioethicist Christine Overall (Reference Overall2012) notes, “any discussion of the ethics of procreation must include feminist perspectives because choosing whether to have children is gendered; it cannot be discussed as if men’s and women’s very different roles are irrelevant to the issue” (p. 8). Prescribing that prospective parents must select “the best” imposes an expectation that children will be conceived via IVF rather than naturally (de Melo-Martin, Reference de Melo-Martin2004, p. 73). Prospective fathers pursuing IVF need only provide a sperm sample. But prospective mothers will first begin to take hormone treatments to control egg production. Mature eggs are then collected via needle aspiration, a procedure that is typically undertaken with pain medicine and sedation. While this surgery is minor, it and the anesthesia carry potential risks (see de Melo-Martin [Reference de Melo-Martin2004, pp. 75–78] for an elaboration of this line of objection).

Furthermore, the fixation of PB on “selecting the genetic best” neglects other important moral and prudential considerations. For example, if prospective parents are intent on spending thousands of dollars (thousands more—parenthood is extremely expensive as it is) to improve the opportunities their offspring have to flourish, perhaps that money would be better spent on environmental interventions (e.g., extra tutoring) rather than screening the genes of embryos. So there is a risk that PB fetishes genetic information, in addition to adding yet more procreative burdens on potential mothers.

As ideologically diverse as all these authors are, from Rawlsian liberalism, perfectionism, and Kantianism to libertarianism and consequentialism, what they share is a commitment to theorizing about justice in the genomic era with some pre-genomic era moral ideals or normative theories. Whether it be a principle of sufficiency, or a desire to conserve what has been the historical “biological norm,” or autonomy, luck egalitarianism, or beneficence, the central methodological assumption of such theorizing is that the best strategy for addressing the topic of justice in the genomic era is to simply extend one’s favored conception of morality/justice from the pre-genomic area to the genomic era. I will now detail what I take to be an attractive alternative to such ideal theorizing—namely, to develop an account of justice in the genomic era that begins by theorizing the “non-ideal.”

There are, of course, a plurality of non-ideal realities concerning human biology. We die. We frequently get sick, even the healthiest among us. Many people suffer permanent disability. Some suffer severe cognitive limitations. Others suffer dementia. And when it comes to our personalities, some people are more prone to addiction (Bevilacqua & Goldman, Reference Bevilacqua and Goldman2009, p. 359) and impulsive behavior. One cannot start by theorizing all of the non-ideal, so where to begin? I propose keeping the initial focus of theorizing the non-ideal realities of justice in the genomic era on the concerns that arise in the two stages of the genetic revolution. The first stage of this revolution is primarily epistemic. That is, it has led to new knowledge: knowledge about the role that genes play in the development of different phenotypes and the ability to identify the likelihood of particular phenotypes developing (e.g., genetic disease) via genetic testing. Such knowledge raises concerns about (1) repeating the injustices of past eugenics (e.g., sterilization of the “unfit”) and (2) exacerbating inequalities (e.g., genetic discrimination or increasing the reproductive burdens on prospective mothers). A non-ideal analysis of justice in the genomic era will diagnose the injustices of past eugenic practices and prescribe appropriate precautions to avoid exacerbating inequalities through discrimination or imposing unfair burdens on prospective mothers.

Later, I will turn to a non-ideal analysis of the technological aspect of the genetic revolution. A non-ideal analysis of our susceptibility to early and late-onset morbidity reveals the moral urgency of shifting from what Russell Powell and Allen Buchanan (Reference Buchanan2011) call “unintentional genetic modification” to “intentional genetic modification.”

Theorizing the non-ideal aspects of the epistemic revolution

An account of justice that addresses the significance of the genetic revolution would be remiss if it did not consider the injustices of past eugenic movements. So perhaps the first non-ideal consideration to theorize (with our vulnerability to morbidity a close second) is the injustices of past eugenic practices. Justice in the genomic era of the twenty-first century must not repeat the mistakes of the past. What were the mistakes of the eugenic practices from 1880 to 1945? And how can we best avoid repeating those same mistakes now?

In Reference Russell1924, Bertrand Russell defined eugenics as a social movement, characterizing it as “the attempt to improve the biological character of a breed by deliberate methods adopted to that end” (p. 255). Stated in this general way, one can appreciate the point that calling a public policy or moral aspiration “eugenic” does not convey sufficient information concerning its potential injustice or immorality. Some have argued that we would be better off without “eugenics talk” because of the emotive power it invokes, which can circumvent people’s critical-rational faculties (see Wilkinson, Reference Wilkinson2008). But Russell’s definition is useful as it can help the non-ideal theorist pinpoint two significant issues that must be addressed: the “ends” and the “means” of any potential screening/genetic intervention.

Striving to improve our biological character by immunizing a population to help protect it from infectious disease (such as COVID-19) is not morally objectionable. Indeed, one could reasonably argue that there is a pressing moral duty to make such interventions widely accessible. Russell’s definition identifies both an end—“the improvement of our biological character”—and a means—“the methods adopted to that end.” A non-ideal analysis of justice in the genomic era will pay attention to both the means and the ends of any proposed use of genetic information and technologies. Ends such as “racial hygiene” are predicated on prejudice and thus fail the test of being aims that can be reasonably justified in a free and democratic society. Similarly, coercion and punitive means, such as sterilization of those deemed “unfit,” are unjust as they violate the equality of all persons. Violations of individual rights, in the name of morally dubious collective aims, ought not to be permitted.

Unlike past eugenics movements, which were informed by pseudo-scientific “hunches” about heredity, the sequencing of the human genome and the identification of genes implicated in single-gene disorders and complex diseases are on much more credible empirical grounds. Does this mean that justice in the genomic era might permit, or even require, some goals that can be considered “eugenic”? For example, encouraging prospective parents to make use of genetic testing to identify embryos and fetuses that might be at risk of serious genetic disorders?

To answer this question, the non-ideal theorist could make some comparisons with existing public health measures where similar concerns arise.Footnote ⁹ For example, in the United States, the Centers for Disease Control and Prevention (2019) recommends that women of childbearing age (ages 15–45) consume 0.4 milligrams of folic acid daily. This daily recommendation applies to all women in this age group, not only those planning to get pregnant, because nearly half of all pregnancies in the United States are unplanned (Finer & Zolna, Reference Finer and Zolna2016). The goal of having folic acid taken en masse is intended to prevent two common and serious birth defects: spina bifida and anencephaly. Such a measure could be described as being “eugenics.” But the aim is to prevent serious birth defects, and the means invoked (encouraging the consumption of folic acid) is empirically credible and noncoercive.

The example of considering past and present eugenic practices is illustrative of the importance of undertaking a non-ideal analysis of the demands of justice in the genomic era. Consideration must be given to not only how scientifically credible and morally defensible such aims are, but also how morally defensible the means of achieving those aims are. To start at the level of ideal theory, theorizing an account of the aims of a perfectly just society with new genetic information and technologies risks relegating the question of how such goals could be fairly achieved to the background of our attention. Given the mistakes of past eugenics movements, it would be imprudent of philosophers not to keep such non-ideal realities at the forefront of their normative theorizing.

A second non-ideal reality of the epistemic dimension of the genetic revolution is that new genetic information about our risks of disease could lead to new inequalities—for example, genetic discrimination in employment and health insurance (in a country that does not provide universal health care). In 2008, the United States passed the Genetic Information Nondiscrimination Act to address this worry. A non-ideal analysis of justice in the genomic era can help reinforce the importance of the traditional demands of socioeconomic justice, such as equality of opportunity in employment, health insurance, and education. Having access to education, employment, and health care are extremely important determinates of how well a person fares in life. If the genetic revolution were to reduce, or threaten to reduce, the opportunities that the “genetically disadvantaged” have to access these goods and services, it would exacerbate inequality and thus possibly create new injustices.

The encouraging news is that findings from large genomic studies on educational attainment can actually help strengthen, rather than undermine, arguments for equality of opportunity in education. A recent large-scale genetic association analysis of educational attainment in a sample of approximately 1.1 million individuals found that the polygenic scores that the study employed explained only 11%–13% and 7%–10% of the variance in educational attainment and cognitive performance, respectively (Lee et al., Reference Lee, Wedow, Okbay, Kong, Maghzian, Zacher, Kguyen-Viet, Bowers, Sidorenko, Linner, Fontana, Kundu, Lee, Li, Li, Royer, Timshel, Walters, Willoughby and Cesarini2018). This means that environment, such as parental investment and affluence (rather than genes), is the main determinate of educational attainment. Thus the traditional concerns of social justice ought to remain at the forefront of an account of justice in the genomic era. Starting with non-ideal (rather than ideal) theory, which compels the theorist to compare how both nature and nurture influence our life prospects, will bring such findings to the fore of our theorizing because non-ideal theory does not employ idealizations (such as environmental or genetic determinism).

Access to new genetic information might also impose unequal burdens on men and women, and this is another inequality that non-ideal theory should be cognizant of. As noted earlier, Savulescu’s (Reference Savulescu2001) principle of procreative beneficence prescribes the following:

The principle applies to screening embryos at the pre-implantation stage of IVF. However, Savulescu does not consider the implicit requirement that conception be done artificially, if one is to screen an embryo for the best genetic lineage. This imposes extra burdens on women. Rather than invoke PB as a procreative moral principle for the genomic era, a non-ideal normative analysis will pay attention to the different burdens that arise in different types of cases—for example, for a couple that intends on conceiving naturally versus a couple that is already undergoing IVF because of fertility reasons or because of the risks of genetic disease. Non-ideal theory prescribes that the theorist start by recognizing that the process of reproduction imposes different types of burdens on men and women. Those burdens must be factored into any account of what justice requires in the genomic era.

Unjust eugenic practices, genetic discrimination, and unfair reproductive burdens on women are just some of the potential non-ideal realities of the genomic era. Such considerations should not be bracketed while ideal theorists determine what perfect justice looks like in the genomic era. Instead, normative theorists should advance moral analyses that seek to address the new inequalities that might arise as a result of the epistemic dimension of the genetic revolution.

Theorizing the non-ideal aspects of our biological vulnerabilities

The genetic revolution offers scholars in the humanities and social sciences a unique opportunity not only to revisit the nature versus nurture debate with fresh empirical insights, but also to entertain the prospect of how future technologies might be employed to directly influence our biology in novel ways that have significance for both clinical medicine (e.g., treatment of specific diseases) and public health (preventive medicine).

One significant “non-ideal” reality to theorize with respect to the technological dimension of the genetic revolution is our vulnerability to disease, both early- and late-onset disease. Early-onset genetic disorders (such as cystic fibrosis) are very rare, while most people suffer multimorbidity (e.g., cancer and heart disease) in late life. To understand why some diseases are rare while others are very common, we must understand how our species’ evolved biology has brought the health vulnerabilities we currently face. Framing things in this way will help provide the justificatory framework needed to urge that, especially with today’s aging populations, justice requires we shift from what Powell and Buchanan (Reference Powell and Buchanan2011) call unintentional genetic modification to intentional genetic modification.

Unintentional genetic modification is how human biology was shaped historically, through the process of evolution by natural selection. The potential benefits of shifting to intentional genetic modification could be framed in terms of clinical medicine (e.g., treatment for specific disorders) and public health (e.g., preventive medicine). Theorizing the non-ideal will involve examining the implications of the technological aspect of the genomic revolution for both clinical medicine and public health. Before doing so, I will bring to the fore the health vulnerabilities that evolution by natural selection has left us with.

Charles Darwin’s idea of evolution by natural selection is one of the most significant scientific insights in human history. Evolution by natural selection occurs in a population when there is (1) a variation in a trait (e.g., height, resistance to local pathogens, length of a beak, aggression), (2) differential reproduction (e.g., some individuals have greater reproductive success than others), and (3) heredity (e.g., genes that influence height, immunity, a long beak, aggression). Over time, the traits that are advantageous (in terms of reproductive fitness) become more common.

A non-ideal theory of justice in the genomic era contemplating the prospect of “genetically engineering humans” will aspire to understand the history of our biology, in particular the reality that our biology has been shaped by the extrinsic risks of the external world. Historically, life for humans was, as Thomas Hobbes so eloquently phrased it, “nasty, brutish and short.”Footnote ¹⁰ Life on this planet is inhospitable to all forms of life, including human life. Starting with this reality (rather than an idealized hypothetical in which all are healthy) helps us understand why unintentional genetic modification is a morally deficient “biological baseline” for humanity in the twenty-first century.

Evolution cares for nothing, and it certainly does not care about human health. We are susceptible to many infectious diseases, such as the flu (influenza), HIV, malaria, hepatitis, and cholera. A population’s susceptibility to infectious disease is influenced by many factors, including its geography (e.g., latitude) and medical knowledge, as well as affluence and technology (e.g., sanitation). More than 1,000 infectious organisms have been identified as causing disease in humans. Pathogens are arguably the strongest selective pressure driving the evolution of modern humans (Karlsson et al., Reference Karlsson, Kwiatkowski and Sabeti2014, p. 390).

Contemplating justice in the genomic era, which ought to highlight the important (and yet complex) interplay between genes and environment, can help reframe and amplify duties of justice to address poverty and climate change. One obvious (and important) dimension to theorize when contemplating justice in the genomic era concerns the duty to prevent and treat early-onset genetic conditions via gene therapy or genome editing. This is the focus of clinical medicine, and what justice requires is often characterized as treatments for specific diseases. But rather than starting with an idealized distributive principle, such as a genetic decent minimum (as Buchanan et al. [Reference Buchanan, Brock, Daniels and Wikler2000] endorse), the non-ideal realities of genomic justice today entail addressing the realities that gene therapy and genomic editing are (at this stage) still experimental (risky) and costly medical procedures.

Consideration must also be given to the different moral stakes involved in redressing rare versus more common types of disadvantage. When it comes to preventing and treating early-onset death and disadvantage, the case for pursuing intentional genetic modification as a pressing demand of justice must be weighed against the reality that most causes of early mortality in the world today are nongenetic. Lack of access to improved sanitation, food, peace, and immunizations, for instance, are the kinds of factors that have prevented us from making the world a more equal place in terms of a child’s likelihood of making it to midlife. Genetic technologies to treat rare, early-onset disorders can help us redress the genetic inequalities that people are born with. But from a population health perspective, if we want to save the young, then the empirically valid and cost-effective ways that have helped developed countries enjoy low child mortality must be diffused more equitably to developing countries.

There is another intriguing, and timely (as the COVID-19 pandemic has made clear), task facing normative theorists this century: we must theorize what should be done to improve health in late life. The normative grounds for aspiring to move from unintentional genetic modification to intentional genetic modification go much further than simply wanting to find novel ways to mitigate early-onset genetic diseases, many of which are very rare. A public health framework can help justice theorists articulate the potential magnitude of the benefits of technologies that can help keep populations (and not just individuals) healthy. Age is one of the biggest risk factors for the most common diseases and disabilities.

Evolution by natural selection has given us a biology that is not only susceptible to more than 10,000 single-gene disorders (many of which are early-onset disorders), but also makes us very susceptible to multimorbidity in the postreproductive stage of life. Sixty-two percent of Americans over age 65 have multiple chronic conditions (Vogeli et al., Reference Vogeli, Shields, Lee, Gibson, Marder, Weiss and Blumenthal2007, p. 392). Robert Butler (1927–2010), the first director of the National Institute on Aging, coined the term “ageism” in 1969. Butler, along with many prominent aging researchers (Butler et al., Reference Butler, Miller, Perry, Carnes, Williams, Kirkwood, Martin and Olshansky2008; Kaeberlein et al., Reference Kaeberlein, Rabinovitch and Martin2015; Olshansky, Reference Olshansky2018; Rae et al., Reference Rae, Butler, Campisi, de Gray, Finch, Gough, Martin, Vjig, Perrott and Logan2010), has called for a concerted effort to slow down the rate of human aging as a form of preventive medicine. According to such researchers, age retardation would be among one of the most significant advances in public health this century. Such a goal aspires to increase the healthspan, rather than simply extend the lifespan by permitting people to live longer in a frail state while managing multimorbidity (which is what is occurring with the strategy of tackling each specific chronic disease, one at a time).

The COVID-19 pandemic has revealed the health vulnerabilities of today’s aging populations, as the virus is significantly more lethal for older persons than children or young adults. The Centers for Disease Control and Prevention (2020a) estimates that the rate of death from the virus for persons ages 75–84 is 220 times that for persons ages 18–29. And for persons over age 85, the death rate is 630 times higher. Promoting health in late life is a significant, complex, and novel aspiration that no previous generations had to undertake given the historically high prevalence of early and midlife mortality.

“About 96% of infants born in developed nations today will live to age 50 years or older, more than 84% will survive to age 65 years or older, and 75% to 77% of all deaths will predictably occur between age 65 and 95 years” (Olshansky, Reference Olshansky2018, p. 1323). Developing countries are still lagging developed countries in this respect. However, life expectancy for a baby born in the world today is now 72 (WHO, 2020b), and it is expected to rise to age 81 by the end of this century (United Nations, 2011, p. xviii). This means that most people born today can expect to live long enough to become a senior and will most likely die (despite the prevalence of COVID-19) from one of the chronic diseases of aging. This shift from the historical norm, where most death and disease occurred early in life, to the predicament today, where most disease occurs in late life, amplifies the importance of theorizing about justice in the genomic era. The dominant theories of justice developed in the past (such as “justice as fairness” and luck egalitarianism) presumed there were no feasible alternatives to unintentional genetic modification. Now that this prospect is upon us, we must rethink the foundational assumptions of what justice requires in the genomic era.

Aging populations are vulnerable to chronic disease and disability because the force of evolution by natural selection declines in late life. This means that genes that cause deleterious mutations that lead to cancer, heart disease, and stroke after age 70 are passed on without being weeded out by Darwinian selection. The evolutionary biologist Michael Rose (Reference Rose2005) explained this “evolutionary neglect” as follows:

To remain committed to unintentional genetic manipulation, despite the sharp rise in chronic disease in late life (in both developing and developed countries), is to ignore the pressing moral demands to prevent disease and disability across the complete lifespan. “As risk of death from infectious and parasitic diseases diminish, the degenerative diseases associated with ageing, such as heart disease, stroke and cancer, become much more important” (Olshansky et al., Reference Olshansky, Carnes and Cassel1993, p. 47). In the past decade or so, a new interdisciplinary field of inquiry known as “geroscience” has emerged. Geroscience “strives to understand how aging enables chronic disease and seeks to develop novel multi-disease preventative and therapeutic approaches” (Kennedy et al., Reference Kennedy, Berger, Brunet, Campisi, Cuervo, Epel, Franceschi, Lithgow, Morimoto, Pessin, Rando, Richardson, Schadt, Wyss-Coray and Sierra2014, p. 709). This represents a novel and distinctive approach to health promotion compared with the disease-specific approach. Instead of simply postponing human death by treating or preventing a specific disease of aging, geroscience promises to increase the number of healthy years humans can live. Extending the healthspan, and compressing the frailspan, is a much more novel, and morally laudable goal, than the current aspirations of the costly, disease-specific approach to medical research.

The COVID-19 pandemic effectively illustrates the significance of adopting a preventive health approach to aging and disease. Age is the most significant risk factor for hospitalization and death from the virus. The health vulnerabilities revealed by the pandemic are not unique to infectious diseases. They are linked to our intrinsic vulnerability to chronic diseases in late life. In addition to advancing the science that will make a COVID-19 vaccine a reality, we must also prioritize the science that will yield interventions into the aging process, enabling us to increase the human healthspan and compress morbidity in the final stages of life.

In a recent editorial in the journal Aging and Disease, many prominent aging researchers noted that the death and economic toll of the COVID-19 pandemic amplified the urgency of the strategy to health research they have been advocating for many years:

It is too early in the COVID-19 pandemic to ascertain precisely what role genetic inheritance plays in both the severity of symptoms of the virus and resistance to the virus. But what is clear is that biological aging is the most significant risk factor for death, as it is for chronic disease. This risk factor trumps the affluence of a country (indeed, developed countries with older populations have among the highest mortality rates), gender, and race. The wealth of the richest countries does not immunize them from the chronic diseases of cancer, heart disease, and stroke or from an infectious disease like COVID-19. This reinforces the point that it is imperative to extend the scope of justice beyond the traditional concern for material wealth and prosperity, to also include the distribution of genes for health and disease. The 1918 influenza pandemic killed an estimated 50 million people worldwide (Watanabe et al., Reference Watanabe, Watanabe, Shinya, Kim, Hatta and Kawaoka2008). What made the 1918 virus particularly devastating was the fact that nearly half of the influenza-related deaths occurred among young adults (20–40 years of age) (Simonsen et al., Reference Simonsen, Clarke, Schnberger, Arden, Cox and Fukuda1998, p. 53). This was surprising because typically it is those with less immunity (e.g., the very young or elderly) who are most at risk of death from influenza. When the 1918 virus was reconstructed, researchers found that particular genes may have played an important role in the virus’s ability to obstruct airway cells. HA, NA, and PB1 genes, for example, have been identified as the genes most optimal for virus replication and virulence (Pappas et al., Reference Pappas, Aguilar, Basler, Solorazano, Zeng, Perrone, Palese, Garcia-Sastre, Katz and Tumpey2008). “Understanding the molecular basis of the high-virulence phenotype of the 1918 pandemic virus is important, as it could identify useful targets for drug intervention when new pandemic viruses begin to emerge” (Watanabe et al., Reference Watanabe, Watanabe, Shinya, Kim, Hatta and Kawaoka2008, p. 590).

The COVID Human Genetic Effort is an international consortium comprising more than 50 genetic sequencing hubs. The consortium has two principal aims. The first aim is to study the pathogenesis of severe COVID-19. This involves the consortium undertaking the following three more specific aims (Covid Human Genetic Effort, 2020):

1. 1. Recruit otherwise healthy young patients with severe COVID-19 (and their family members, and seropositive individuals who had remained asymptomatic, when available, as controls).

2. 2. Search for candidate disease-causing variants by whole-exome sequencing/whole-genome sequencing of patients and controls (including asymptomatic infected subjects).

3. 3. Perform functional studies to characterize the products of the candidate variants biochemically, and to analyze the corresponding patients’ cells immunologically.

The second principal aim of the COVID Human Genetic Effort is to study individuals who have demonstrated a high resistance to infection by SARS-CoV-2. Such persons have not been infected by the virus despite repeated exposure. For example, they might live in the household of a patient with the virus but lack both the disease and antibodies against the virus.

Less than six months after the outbreak of the COVID-19 pandemic, scientists had already identified a 3p21.31 gene cluster as a genetic susceptibility locus in patients with COVID-19 with respiratory failure and confirmed a potential involvement of the ABO blood-group system (Ellinghaus et al., Reference Ellinghaus, Degenhardt, Bujanda, Buti, Albillos, Invernizzi, Fernández, Prati, Baselli, Asselta, Marit, Grimsrud, Milani, Aziz, Kässens, May, Wendorff, Wienbrandt, Uellendahl-Werth, Zheng, Yi and Karlsen2020). Based on what scientists have already learned about other infectious diseases, such as HIV/AIDS and malaria, it is not surprising that genetics plays a significant role in our susceptibility to COVID-19 infection and mortality. This information could help with the development of new vaccines and therapies. For example, HIV can be transmitted through sexual contact (e.g., unprotected sex), through blood (e.g., sharing a needle for drug use or through blood transfusions), or through mother-to-child transmission. But some individuals who are exposed to high-risk activities, such as commercial sex workers, have remained uninfected by HIV (Fowke et al., Reference Fowke, Nagelkerke, Kimani, Simonsen, Anzala, Bwayo, MacDonald, Ngugi and Plummer1996). These (rare) individuals have a natural immunity to the disease that most of us do not have. Possession of a CCL3L1 copy number lower than the population average is associated with markedly enhanced HIV/AIDS susceptibility (Gonzalez et al., Reference Gonzalez, Kulkarni, Bolivar, Mangano, Sanchez, Catano, Nibbs, Freedman, Quinones, Bamshad, Murthy, Rovin, Bradley, Clark, Anderson, O’Connell, Agan, Ahuja, Bologna and Ahuja2005). A better understanding of how particular genes might help protect against the risks of HIV/AIDS could lead to new medicines, such as a genetic vaccine or gene therapy for HIV. The same might be true for a COVID-19 vaccine.

Malaria is transmitted via bites from infected mosquitoes. As such, malaria is a tropical disease that typically occurs in temperate regions of the world. “Malaria has been a major determinant in the evolution of several human genes, especially those involved in the constitution of red blood cells” (Guégan et al., Reference Guégan, Prugnolle, Thomas, Stearns and Koella2008, p. 25). The higher risk that African Americans face with respect to sickle cell disease, for example, stems from this fact. Sickle cell disease affects approximately 100,000 Americans and occurs in about 1 out of every 365 Black or African American births, versus 1 out of every 16,300 Hispanic American births (Centers for Disease Control and Prevention, 2020b). Individuals born with two copies of the HbS gene develop sickle cell disease because they develop distorted red blood cells; this reduced blood flow causes damage to tissues and can lead to death. But individuals born with one copy of the HbS gene and one copy of the “normal” gene variant do not typically develop any symptoms. Furthermore, having just one copy of the abnormal gene confers “significant protection against all-cause mortality, severe malarial anaemia, and high-density parasitaemia” (Aidoo et al., Reference Aidoo, Terlouw, Kolczak, McElroy, Kuile, Kariuki, Nahlen, Lal and Udhayakumar2002, p. 1311).

Within the first few months of the COVID-19 pandemic, it became apparent that the health risks of the coronavirus differed for different portions of the population. In addition to age (the largest risk factor for mortality), race and gender are other important risk factors. “Coronavirus disease 2019 (COVID-19) has disproportionately affected communities of color” (Bunyavanich et al., Reference Bunyavanich, Grant and Vicencio2020, p. 1892). To what extent do these health disparities arise from inequalities in social determinants of health (e.g., social, environmental, and geographic factors) and from genetic differences? This is a contentious, and yet important, question that must be asked and studied versus starting from an unsubstantiated commitment to either genetic or environmental determinism. In their early and provisional study of this question examining COVID-19 risk among New York–area Black individuals, Bunyavanich et al. (Reference Bunyavanich, Grant and Vicencio2020) found that nasal gene expression of TMPRSS2 was highest in Black individuals. Therefore, this might be one factor (among many) contributing to racial/ethnic differences in COVID-19 mortality. The authors note the limitations of their findings—such as the modest sample size, constraint to one metropolitan area, and participant age range of 4 to 60 years—but their study adds an important dimension to our understanding of the role that genes and environment play in our susceptibility to different types of diseases.

At the time of writing, the COVID-19 death toll in the United States exceeded 440,000 people. And yet the virus itself (in contrast with the health impact of lockdown measures) has not had a significant adverse impact on the health prospects of the young in the United States. According to the American Association of Pediatricians (2020), 624,890 total children had tested positive for COVID-19 by late September 2020, and yet children accounted for only 0%–0.26% of all COVID-19 deaths (and 17 states reported zero child deaths). In a comparative study of the health impacts of the seasonal influenza and COVID-19 in children (Song et al., Reference Song, Delaney, Shah, Campos, Wessel and DeBiasi2020), researchers found no difference in hospitalization rates, intensive care unit admission rates, and mechanical ventilator use between the two groups. This stands in sharp contrast with the health toll the virus takes on persons at the end other end of the human life span.

Before the onset of the COVID-19 pandemic, which drives home the imperative for non-ideal normative theorizing, many philosophers might have been skeptical that justice requires altering the rate of human aging. But this pandemic has made vivid the association between aging and disease, disability, and death. By emphasizing the significance of genetics in exceptional longevity and the severity of (and resistance to) COVID-19, we can begin to understand and appreciate how the genetic lottery of life influences people’s life prospects. At one end of the spectrum are children born with progeria, a very rare genetic disorder that causes accelerated aging and death, typically by age 13. The average person has a biological warranty period of about 70 years and might be able, with the help of modern medicine and a healthy lifestyle, to delay death to around age 85. And then there are the rare individuals who delay the onset of the common diseases that kill most humans in the seventh, eighth, and ninth decades of life—centenarians. These individuals have an “extended warranty,” providing some of them with a health span of more than 100 years. These exceptional success stories might hold the answers to the question of how to extend healthy human life—that would constitute one of the most significant breakthroughs of the genetic revolution.

This novel strategy of preventive medicine, which targets the largest risk factor for chronic disease (i.e., aging), is already underway with the launch of TAME (Targeting Aging with Meformin) (Barzilai et al., Reference Barzilai, Crandall, Kritchevsky and Espeland2016). TAME is a clinical trial to test the drug metformin as a safe and effective intervention against several age-related diseases. Metformin has been safely utilized as a pharmacological intervention to help control type 2 diabetes for decades. “Metformin exerts its therapeutic effects, through a number of mechanisms and physiological pathways that resemble those generated by caloric restriction (CR), an experimental model known to extend life span and health span in various organisms” (Novelle et al., Reference Novelle, Ali, Diéguez, Bernier and de Cabo2016, p. 2).

In experiments on animals, metformin has been shown to slow aging. And now researchers are hoping a similar effect can be shown in humans. “If TAME demonstrates that metformin modulates aging and its diseases, beyond an isolated impact on diabetes, it would pave the way for development of next-generation drugs that directly target the biology of aging” (Barzilai et al., Reference Barzilai, Crandall, Kritchevsky and Espeland2016, p. 1060). The researchers undertaking TAME describe the significance of the study as follows:

Unlike the morally suspect case of genome editing healthy embryos for HIV resistance, altering the genes of older persons to protect against chronic disease using a drug that mimics caloric restriction might constitute one of the most significant advances in public health this century. Robin Holliday (1932–2014), one of the first scientists to apply modern molecular medicine to the study of aging, had the following to say about aging 20 years ago in the journal The Lancet:

Reconciling the medical and social models of disability

Proposing to extend the purview of justice to the aspiration to prevent late-life disease and disability, by directly altering the aging process, will also compel non-ideal theorists to grapple with the potentially conflicting demands of the medical and social models of disability. According to the medical model, a disability is “a physical or mental condition we have a strong rational preference not to be in, it is, more importantly, a condition which is in some sense a ‘harmed condition’” (Harris, Reference Harris1993, p. 180). The aging process is something that should be targeted, as a matter of public health, because it harms individuals by making our bodies and minds susceptible to cancer, heart disease, dementia, arthritic pain, sleep disorders, severe COVID-19, and vision and hearing loss in the postwarranty period of the human lifespan.

In contrast with the medical model of disability, the social model emphasizes the ways in which society’s organization is itself a cause, if not the root cause, of disability. For example, Solveig Reindal (Reference Reindal2000) argues that disability “is far from merely being a medical problem that can be ‘cured,’ on the contrary it is mainly a cultural and sociopolitical problem” (p. 92). While they are often presented as rival normative lenses, I believe the medical and social models of disability can, and ought to be, considered as complementary. There is no inconsistency in asserting that justice demands we aspire to prevent the limitations aging imposes upon persons and that justice also requires we abate the discrimination and social exclusion which many older persons currently face and experience.

Adopting the lens of evolutionary biology to explain aging helps bring to the fore causal factors (such as evolutionary neglect or specific genetic mutations) that do play a significant role in our susceptibility to disease and disability in late life. But the lens of the social model of disability is also important, as it can draw attention to the fact that cultural beliefs and practices, as well as social institutions, can exacerbate these predicaments by amplifying the disadvantage individuals experience in their day-to-day lives. For example, the inborn aging process limits the mobility of persons living beyond the biological warranty period of 70 years. But the accessibility design (e.g., accessible by wheelchair or not) of movie theaters, restaurants, hospitals, and churches determines who has regular access to such services. To focus exclusively on the moral demands of prevention and treatment, but ignore concerns of inclusiveness for those who experience impairments that will not be augmentable by genetic modification, would be myopic. Theorizing about the determinants of justice in the genomic era ought to aspire to integrate, rather than bracket or obstruct, the other demands of justice that do not involve manipulating our genes.

Steering this middle ground between the medical and social models of disability has been affirmed by the WHO and its development of the International Classification of Functioning, Disability, and Health.Footnote ¹¹ In “Towards a Common Language for Functioning, Disability and Health: ICF,” the WHO (2002) notes, in reference to the medical and social models of disability,

The WHO advances a biopsychosocial model, a model in which disability and functioning are viewed as outcomes of interactions between health conditions (diseases, disorders, and injuries) and contextual factors. This permits inequalities that arise from both nature and nurture to be part of our discussions about the demands of justice in the genomic era without degrading the moral status of those living with disabilities.

Positing that justice requires that we alter our biology is perfectly compatible with the assertion that justice also requires that we modify our environments to facilitate greater inclusion for those currently living with disabilities. These two prescriptions need not be contradictory, and both are more sage when treated as complementary. Robert Butler, the first director of the National Institute on Aging, certainly believed these were complementary aspirations. Butler coined the term “ageism” in Reference Butler1969 to refer to the systematic stereotyping of, and discrimination against, people because they are old. Ageism is reflected in such colloquialisms for elders as “coot” “croon,” “geezer,” “hag,” “out to pasture,” “over the hill,” and “washed up” (Palmore, Reference Palmore1999). A champion of the rights and social needs of the elderly, Butler was also a vocal advocate of targeting the aging process as a matter of public health (Butler et al., Reference Butler, Miller, Perry, Carnes, Williams, Kirkwood, Martin and Olshansky2008). For Butler, non-ideal justice required promoting greater inclusion of those living in the postwarranty period of the human lifespan, and it required supporting science that could help extend the biological warranty period and compress the period of frailty, disease, and disability at the end of life.

In From Chance to Choice: Genetics and Justice, Buchanan and colleagues (Reference Buchanan, Brock, Daniels and Wikler2000) address the concerns that advocates of the social model of disability typically have with the medical model when they consider what they call the expressivist objection. This objection maintains that the aspiration to develop genetic interventions to prevent disabilities expresses “negative judgements about people with disabilities, and that these judgements constitute a profound injustice to those people” (Buchanan et al., Reference Buchanan, Brock, Daniels and Wikler2000, p. 272). This critique is often conjoined with what these authors call the loss of support argument: “as the application of genetic science reduces the number of persons suffering from disabilities, public support for those who have disabilities will dwindle” (Buchanan et al., Reference Buchanan, Brock, Daniels and Wikler2000, p. 266).

Critics might invoke the expressivist objection and loss of support argument to argue that aspiring to alter the rate of aging might perpetuate injustice because it expresses negative judgments about the elderly and risks diminishing the effort to combat the exclusion of those who currently have disease and disability. Buchanan et al. (Reference Buchanan, Brock, Daniels and Wikler2000) formulate a compelling reply to this type of objection by drawing a distinction between devaluing disabilities without devaluing people with disabilities. We already endorse policies and lifestyles that seek to prevent disability and chronic disease, such as requiring people to wear seat belts in automobiles, to wear safety glasses when working with hazardous materials that could cause loss of vision, to wear helmets when riding a bike, to exercise, to eat a balanced diet, and to stop smoking. Such measures are predicated on the conviction that there is a pressing moral imperative to pursue cost-effective measures that reduce disability and chronic disease. But disvaluing a disability—such as vision or cognitive impairment—does not mean that people who are visually or cognitive impaired are devalued. A society can legislate the wearing of eye protection in certain workplaces and still be committed to the equality of all persons—visually impaired or not. The latter is determined not by the extent to which a society aspires to prevent a disability or disease, but by the support it offers to those living with the disability. The same is true of disvaluing senescence itself for the way it negatively impacts our health prospects. This does not mean we ought to devalue older persons who might suffer a disability or chronic disease. Nor does it imply that people who are older and living with disability or a chronic disease do not have lives worth living.

Age is the most significant risk factor for chronic disease. The study of the biology of aging clearly establishes the fact that aging causes many “harmed conditions.” To deny this reality (which has been borne out vividly by the COVID-19 pandemic) is to remain ignorant of the biology of aging. But pointing out this reality is not an affront to the dignity of older persons, nor should it give license to discrimination against the elderly. Non-ideal theorists must ensure that they avoid the dichotomy of reducing the demands of justice to just genetic or environmental modifications. I believe justice in the twenty-first century will require a measured, informed, and humane two-pronged approach (that is, pursuing both biological and environmental interventions) to human health and well-being. The genetic revolution may soon permit us to pursue genetic interventions that would have been considered pure science fiction only a few decades ago.