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date: 08 August 2020

Neuroethics: Cognitive Enhancement

Abstract and Keywords

This article describes how psychostimulants and other drugs can enhance cognitive capacities and explores the ethical implications of this form of enhancement. Focusing mainly on methylphenidate, dextroamphetamine, and modafinil, the article cites scientific studies indicating that those with a lower baseline of working memory tend to benefit more from cognitive enhancement than those with a higher baseline. Enhancing some cognitive capacities through neurotransmitters may come at the cost of diminishing others and may result in addiction or other pathological behavior. This suggests that an unlimited augmentative conception of enhancement needs to be replaced by one that that involves optimal levels of cognitive capacities to improve performance on specific tasks in promoting flexible behavior and adaptability to the environment. Cognitive enhancement would not likely increase social inequality and would be consistent with authenticity, excellence, and achievement. How cognitive enhancement could be one component of moral enhancement is also discussed.

Keywords: adaptability, authenticity, cognitive enhancement, dextroamphetamine, methylphenidate, modafinil, moral enhancement, pathology, risks, social inequality

Introduction

Cognitive enhancement refers to interventions in the brain that improve attention, concentration, and information processing in executive functions such as reasoning and decision-making. There are three main conceptions of cognitive enhancement: augmenting, diminishing, and optimizing. The first conception considers interventions in the brain as enhancements when they improve some function by increasing its ability to do what it normally does (Harris, 2007; Bostrom and Sandberg, 2009). An enhancement is an intervention “designed to improve human form or function beyond what is necessary to restore or sustain good human health” (Juengst, 1998). The second conception claims that some functions can be improved by diminishing the extent of what they do and their effects. It is a welfarist view of enhancement. “Sometimes the diminishment of a capacity or function, under the right set of circumstances, could plausibly contribute to an individual’s overall well-being: more is not always better, and sometimes less is more” (Earp et al., 2014; See also Savulescu et al., 2011). For example, methylphenidate (Ritalin) may help some people to perform better on a certain cognitive task because the drug diminishes the content of their thought, enabling them to avoid distracting stimuli and focus on that task. The third conception takes enhancement to be any intervention that “aims at optimizing a specific class of information-processing functions; cognitive functions, physically realized by the human brain” (Metzinger and Hildt, 2011, p. 245.)

A broad, optimizing conception is probably the most consistent with people’s intuitions about cognitive enhancement. The goal of altering cognitive functions is not just to improve performance on a particular task but also to promote flexible behavior and adaptability to the environment. This is more likely to occur when neural and mental processes are neither underactive nor overactive. Optimal levels of cognitive functions can be produced by augmenting or diminishing certain aspects of them. However, “optimal” suggests that there are limits to the extent to which we can improve these functions (Agar, 2014b).

While there has been speculation on the possibility of enhancing neural and mental functions through genetic modification, this type of intervention is still unproven. Noninvasive brain manipulation such as transcranial magnetic stimulation and transcranial direct current stimulation has enhanced the performance of a small number of healthy research subjects on some cognitive tasks. But psychopharmacology has been and likely will continue to be the most common means of cognitive enhancement. Many people have enhanced mental functions in this way for generations, and this practice is becoming more pervasive especially among adolescent and young adult populations. Some studies estimate that approximately 25 percent of American secondary school students use psychostimulants such as dextroamphetamine (Adderall), methylphenidate, and the wakefulness-promoting drug modafinil (Provigil) for nontherapeutic purposes (Wilens et al., 2008). Earlier studies estimated that roughly 7 percent of university students in the United States with no psychiatric or neurological disorder used these drugs (McCabe et al., 2005). Roughly 5 percent of the working population in Germany uses psychotropic drugs to enhance their cognitive functions (Heinz et al., 2012). In 2008, the journal Nature published the results of an informal survey of its readers (Maher, 2008). One-third of the 1,400 readers who responded said that they had used these drugs for off-label nontherapeutic reasons. The use of these drugs to perform better on exams, write more successful grant applications, or improve work performance is likely to increase (Sahakian and Morein-Zamir, 2007, 2011)

I describe how psychostimulants and other drugs can enhance cognitive capacities and explore the ethical implications of this form of enhancement. Studies of the drugs’ effects on neurotransmitters indicate that enhancing some cognitive capacities may come at the cost of diminishing others. More significant, trying to improve cognitive functions by increasing concentrations of the relevant neurotransmitters could unwittingly result in pathological behavior. This suggests that an unlimited augmentative conception of enhancement is flawed and needs to be replaced by a conception of enhancement as an intervention that produces optimal levels of cognitive functions. Some types of enhancement are conducive to improving performance of certain tasks but not others, which is why the value of enhancing cognitive functions should be assessed in terms of the overall effects it has on a person’s behavior. Insofar as the aim of enhancement should be to promote individual and collective well-being, it should be construed not as an empirical or descriptive concept but as a normative, welfarist one (Savulescu et al., 2011). Empirical evidence of the effects of cognition-enhancing drugs suggests that they would not increase social inequality. In addition, enhancement could be consistent with authenticity (living according to one’s own values), excellence (exercising one’s natural capacities at the highest level), and achievement (attaining goals through one’s own efforts). This rejects the claim that a drug rather than the person whose capacities were enhanced would be the real agent of this change. By increasing the capacity to imagine or foresee possible outcomes of our actions and to recognize reasons for social cooperation, cognitive enhancement could be a critical component of moral enhancement. Yet a number of questions, including whether this type of enhancement would be voluntary or mandatory, would have to be addressed and resolved before such a project could be accepted and developed on any scale.

Neurobiological Mechanisms and Enhancing Effects

For those whose cognitive functions fall within a species-normal range, drugs such as methylphenidate, dextroamphetamine, and modafinil may improve attention, concentration, and other functions associated with working memory. This involves the capacity to hold and use information for brief periods and is critical for decision-making. Scientific experiments have shown that methylphenidate generally has moderate enhancing effects on these functions by increasing levels of dopamine in the brain. Short-term studies indicate that people with a lower baseline of working memory on an absolute scale tend to benefit more from this drug, while those with a higher baseline tend to benefit less (Farah et al., 2004; de Jongh et al., 2008). In some instances, the latter experience impairment in some cognitive functions. Children with attention deficit hyperactivity disorder tend to do better academically when taking methylphenidate and other stimulant medications than those with the same disorder who do not take the medications (Scheffler et al., 2009). But there is no evidence that these drugs significantly improve the academic performance of children who do not have these disorders.

Methylphenidate appears to produce an inverted dose–response curve in experiments with healthy subjects. Moderate doses improve performance on mental tasks, while higher doses impair or do not affect performance (de Jong et al., 2008). Some studies suggest that methylphenidate enhances executive functions on novel tasks but impairs these functions on tasks that have been learned (de Jongh et al., 2008). In a recent experiment using transcranial electrical stimulation to test the learning and application of mathematical information, researchers found that stimulating an area of the subject’s prefrontal cortex impaired learning new information but enhanced the application of what was learned. Stimulating an area of the parietal cortex had the opposite effect in enhancing learning while impairing the ability to apply the new information (Iuculano and Cohen Kadosh, 2013).

The upshot of these studies is that enhancing certain mental functions through drugs or electrical stimulation may come at the cost of other mental functions. There may be cognitive trade-offs that one would have to weigh in deciding on enhancement. The results of the studies illustrate problems with an augmentative conception of enhancement. They suggest that there are optimal levels of cognitive functions and limits to the extent to which they can be improved.

Modafinil activates dopamine, which then activates norepinephrine and histamine in a process that blocks the hypothalamus from promoting sleep. This enables people taking the drug to be more alert and focused, even when they are sleep-deprived. Although it is prescribed for sleep disorders, it has been used by airline pilots with normal sleep–wake cycles to remain alert on transcontinental flights. It can also enable students studying for exams or writing papers or researchers writing grant applications to forego sleep and thus allow more time for these activities. In one study of healthy young human volunteers, 100 to 200 mg doses of modafinil improved attention and alertness, as well as spatial planning and visual pattern recognition (Muller et al., 2004). These effects improve decision-making by enabling careful evaluation of a problem before initiating a response. As in the studies of methylphenidate, the effects of modafinil on working memory in this study were more pronounced in subjects with a lower baseline of cognitive capacities. It improved accuracy in a sustained attention task for those with a lower (but still above-average) IQ and a lower baseline of working memory. Those with a higher IQ and a higher baseline of working memory were either unaffected or worse in performing this task on modafinil. So, like other psychostimulants, the effects of modafinil are limited to certain cognitive functions, can vary among persons, and may not always be beneficial.

Propranolol (Inderal) is a drug that can have indirect enhancing effects on cognition. This beta-adrenergic receptor antagonist, or beta-blocker, reduces the cardiovascular response to adrenaline and noradrenaline. By reducing the response of receptors in the body and brain to these hormones, propranolol can prevent or attenuate symptoms associated with a fearful or anxious response to stimuli. It can enable those anxious about musical performance or public speaking to avoid being distracted by awareness of a rapid heartbeat, sweating, or other manifestations of the stress response. In this way, the drug can improve focus on the task at hand and facilitate more effective execution of it.

There can also be trade-offs in taking drugs to be more focused on a specific task. One study comparing cognitive responses from older and younger subjects on a number of cognitive tests suggests that a broad attention span and less focus on a specific task over time may make a person more able to transfer information from one situation to another (Carson et al., 2003). This can facilitate more creative thinking and effective problem-solving. Chronic use of methylphenidate and similar-acting drugs may improve some cognitive functions but decrease the ability to flexibly alter behavior and adapt to changing circumstances. Whether or to what extent there are trade-offs from continued use of the drugs could depend on the dosage and whether they were used chronically or intermittently. Although the results of the transcranial electrical stimulation study on mathematical information might suggest otherwise, for many people occasional use of psychostimulants or noninvasive brain stimulation might enhance some functions without impairing others. But this is an open empirical question that can only be answered after a sufficient number of controlled studies of the drugs’ or techniques’ effects on cognition have been conducted.

One cognitive capacity that many have discussed in the context of enhancement is memory. While there are different types of memory, one particularly interesting possibility is enhancing the capacity to store and retrieve more episodic memories of events and semantic memories of facts, concepts, and general knowledge about the world. Protein synthesis in the hippocampus and adjacent structures in the medial temporal lobes of the brain is necessary for the encoding and consolidation of these memories. Drugs that increased the rate of protein synthesis and long-term potentiation by strengthening synapses regulating memory could in theory increase our capacity to recall more facts and events. This is speculative, but one class of drugs that might do this is ampakines, which interact with glutaminergic AMPA and NMDA receptors that have a critical role in learning. Some might think that increasing storage and retrieval of episodic and semantic memories would give us access to more information and enable us to use working memory more effectively, but there are limits to enhancing memory. Indeed, beyond a certain level, storing and retrieving details from past experience can be pathological. Adding to them would not enhance but inhibit one’s ability to form and execute action plans (Hauskeller, 2013, Ch. 2).

Solomon Shereshevskii, a patient of the Russian neuropsychologist Alexander Luria, had what some might describe as a “perfect memory.” He had the exceptional ability to recall a wealth of facts. Yet he was unable to express the gist of these memories, to conceptually unify them into a coherent and meaningful whole. His inability to forget trivial facts severely impaired his ability to learn new information and cognitive skills. The only job he was able to hold was that of a traveling mnemonist (Luria, 1969). Shereshevskii’s pathology was similar to that of the fictional character Ireneo Funes in Borges’ short story, “Funes the Memorious.” Funes remembers every detail of everything he experiences. Borges writes that he “was not very capable of thought. To think is to forget a difference, to generalize, to abstract. In the overly replete world of Funes, there was nothing but details, almost contiguous details” (Borges, 1962, p. 115). An actual case of hyperthymesia, or autobiographical memory syndrome, has afflicted American Jill Price since her late teens. Price cannot control the retrieval of a large volume of episodic memories, which she finds intrusive and calls a “horrible distraction” (Price and Davis, 2008, p. 38; Parker et al., 2006). She has commented on the “real value in being able to forget a good deal about our lives.” Instead, “I remember all the clutter” (p. 45). Her memory is more of a burden than a blessing. As in the case of Shereshevskii, Price’s inability to forget trivial details from her past impairs her ability to learn new things. These cases underscore the importance of optimal levels of memory storage and retrieval and the adaptive value of a balance between learning and forgetting. Any form of memory enhancement would have to be consistent with this balance.

Drugs or techniques would enhance memory not by increasing the storage and retrieval capacity of memories in the brain but by facilitating more efficient retrieval of relevant information in working memory. Making working memory more efficient would be preferable to adding episodic memories because the purpose of enhancing this cognitive function would be to improve the execution of immediate cognitive tasks. Although currently there are no drugs that can do this in humans, they would target the neurotransmitters glutamate and acetylcholine. In addition, manipulating episodic memory to ensure the right balance between learning and forgetting could also improve the capacity to deliberate and plan for actions at later times. This would involve not only processing new information and applying it in the execution of familiar and novel tasks but also the capacity to imagine and project oneself into the future. This is supported by research showing that episodic memory is useful because it provides a cognitive basis on which to consider hypothetical courses of action. It is useful not because of what it tells us about the past but because it enables us to plan for the future (De Brigard, 2014; Schacter and Addis, 2007). Solomon Shereshevskii and Jill Price were impaired in this capacity because their brains were overloaded with a large body of useless memories of episodes they were unable to forget.

Risks

Methylphenidate stimulates the central nervous system and inhibits excessive reuptake of dopamine in the brain. Increasing concentrations of this neurotransmitter in normally functioning brains could disrupt the reward system and make one susceptible to addictive behavior such as gambling and hypersexuality (Volkow et al., 2009). This has occurred in some patients taking dopamine agonists for Parkinson’s disease, where an overactivated reward system interferes with the deliberative and inhibitory functions of the prefrontal cortex. Chronic use of methylphenidate or dextroamphetamine could have the same side effects as any drug in the class of amphetamines. These include hypertension, increased risk of stroke and myocardial infarction, insomnia, psychosis, and in some cases death. In a recently reported case, a university student in the United States died from complications associated with chronic use of Adderall to enhance his capacity to concentrate while studying (Schwarz, 2013). Any adverse effects from using methylphenidate for cognitive enhancement intuitively would be less acceptable than using it therapeutically for a disorder such as attention deficit hyperactivity disorder on the grounds that enhancement is not necessary to sustain a normal range of cognitive functions. Some might question this claim, given that attention falls along a spectrum and that some interventions described as treatments for attention deficit may also be described as enhancements. The distinction between treatment and enhancement is not always clear-cut. Still, in cases where there is evidence that individuals have dopamine dysfunction and moderately severe to severe impairment in behavior control associated with attention, the use of methylphenidate would appropriately be described as treatment. In contrast, for those whose behavior shows no such impairment, using this drug could appropriately be described as enhancement.

As with methylphenidate, occasional use of modafinil may not have any untoward effects on those who use it to stay awake and remain alert and focused, but chronic use could be problematic. If one used modafinil repeatedly to forego sleep and remain alert over long periods, then prolonged sleep deprivation could be a risk factor for metabolic and endocrine disorders such as obesity and diabetes, as well as cardiovascular disease. These conditions are more common among the chronically sleep-deprived. Being alert and attentive for a short period when we need to perform a cognitively demanding task can be adaptive, but being constantly alert and attentive could cause hyperactivation of the stress response and disturb the feedback loop that regulates stress and relaxation responses in the sympathetic and parasympathetic arms of the autonomic nervous system. This imbalance could cause one to develop the metabolic and endocrine disorders just mentioned. Alterations between sleep and attention are adaptations to the environment. If the brain senses that constant attention is a sign of constant demand, then this could overload it. Unnecessary wakefulness can be more problematic than unnecessary sleep. Constant manipulation of sleep–wake cycles with modafinil may cause them to become dysfunctional because the perceived demands of the moment, such as studying for an exam or completing a grant application, may be at odds with more important demands of one’s natural and social context.

Some people can sleep for only 4 hours a night and function well physically and cognitively. For those who sleep for 7 or 8 hours but could function well on much less than this, modafinil could enable them to gain the additional 3 or 4 hours without wasting time on unnecessary sleep. It would allow them to spend more time on research, writing and with family and friends. Yet this assumes that the drug would only prevent the unnecessary sleep and not have any other effects on brain and body metabolism. Most drugs, especially psychotropic drugs, have at least some adverse effects. It may be assuming too much to say that, for the 4-hour group, modafinil would have only salutary metabolic effects limited to sleeping and waking cycles. Studies to determine the safety and efficacy of modafinil in promoting wakefulness could expose research subjects to risks, a point that I will elaborate shortly.

As noted, propranolol can dampen adrenergic and noradrenergic mechanisms in the body and brain-regulating responses to anxiety-inducing stimuli. It can prevent these responses from interfering with concentration in performing certain actions. Depending on the dose and frequency of use, however, this drug could interfere with natural neural and psychological responses to fear-inducing stimuli and put one at risk of harm by failing to respond appropriately to real threats. For example, diminishing these responses could cause a pedestrian to be less cautious when crossing streets in heavy traffic. Also, by taking some of the edge off the anxiety that one may experience in musical performance or public speaking, the drug could weaken the emotional response associated with audience interaction and detract from the meaning and positive feeling they ordinarily produce. Propranolol could blunt the “adrenaline rush” that can produce a salutary emotional response in such a context. The drug might also threaten authenticity and excellence in the sense that performance anxiety is a state that one should encounter and overcome through one’s own efforts rather than prevent or eliminate pharmacologically. Not all performers who took an anxiety-blunting drug would have these qualms. They could point out that the drug only removed an obstacle to exercising their capacities and did not provide a boost to these capacities themselves. But for those with such qualms, there would be two senses of emotional cost from engaging in this type of indirect enhancement.

Some online surveys indicate that the perceived probability and extent of side effects from cognition-enhancing drugs reduces the willingness among students and university teachers to use them (Sattler et al., 2013). A higher perceived probability of enhancing effects increases it. However, many individuals who take these drugs for enhancement purposes are not aware of the risks associated with them. Younger potential and actual users may know of these risks but ignore or discount them and focus instead on the potential benefit. Older potential users may be more risk-averse and more inclined not to enhance. The problem is that the long-term risks of chronic use of these drugs may not be known for some time. Until this knowledge is available, as a matter of autonomy individuals should have the right to use these drugs if they so choose. To be sure, marketing strategies by the pharmaceutical industry touting the “benefits” of the drugs could distort the information available to those considering using them. It might be paternalistic to suggest that these strategies would justify denying people the opportunity to enhance, since not all of the information about the drugs would come from the pharmaceutical industry, but considering that a significant amount of the information about the benefits and side effects of drugs does come from it and that this information reflects the industry’s self-interest, it might not be paternalistic to ban enhancement drugs on that account—or at least there would be reasons for regulating pharmaceutical companies’ statements about the benefits of enhancement. This would be more difficult to do than regulating statements about the beneficial effects of drugs for diagnosed diseases because data on the long-term effects of enhancers are not yet available. The data would be necessary to justify any form of regulation. The influence of the pharmaceutical industry alone would not be sufficient grounds for prohibiting people from using the drugs. Clear evidence of adverse effects would be the strongest reason for limiting or prohibiting them. One could argue that those who used the drugs should take responsibility for any untoward consequences and be accountable for any social costs associated with them. This might involve paying for medical care necessary to treat conditions resulting from using the drugs. This may strike some as too harsh. Alternatively, those who take enhancing drugs could be required to pay higher medical insurance premiums given the possibility of adverse outcomes. But justification for such action would depend on a better understanding of the drugs’ risk.

The short-term and suspected long-term risks of these drugs arguably may be enough to prohibit physicians from prescribing them to individuals with normal cognitive functions. Consistent with the professional obligation to benefit and not harm patients by preventing or treating disease, there would be no compelling reason to prescribe a drug to enhance cognitive functions if there were no disease to prevent or treat and some risk in taking it. Prohibiting this practice might be justified on the grounds that prescribing cognition-enhancing drugs to healthy people with normal cognitive functions would not be an efficient use of limited resources in a publicly funded health care system. (Merkel et al., 2007, p. 37; cf. Synofzik, 2009). Individuals may and indeed do often acquire cognition-enhancing drugs from acquaintances or the Internet, but professional obligation could prevent physicians from being an additional source of the drugs. Some might question why we should allow access to cognition-enhancing drugs outside of the doctor–patient relationship if physicians were prohibited from prescribing the drugs because of the potential harm to those who used them. One response is that as yet there is no definitive answer to the question of whether the drugs are harmful, or how harmful they might be, and such an answer would be necessary to defend prohibition. Despite the one documented death from the use of a stimulant for cognitive enhancement, more data are needed to support the claim that the medical profession or the state should prohibit or limit enhancement. For the principled reason against interfering with individual liberty and the practical difficulty in deciding which drugs posed the greatest risk of harm, state prohibition of enhancement would be difficult to justify.

Some might claim that there are no significant differences between the cognition-enhancing effects of psychostimulants and those of substances in certain foods and drinks, such as caffeine. Yet Andreas Heinz and coauthors point out that “there is a substantial difference between dopamine release caused by a particular experience of food without addiction potential and one resulting from psychotropic substances used for the purpose of neuroenhancement with respect to the extent and the habituation of dopamine release” (Heinz et al., 2012, p. 373). Heinz et al. add: “Dopamine concentrations, which are triggered by food, sex, and human communication, increase by approximately 50 percent to 100 percent, while drugs that directly affect dopamine transporter function (e.g., amphetamine, cocaine, and the psychostimulants methylphenidate and modafinil) induce dopamine releases ranging from 175 percent to 1000 percent. As a result, subjects learn to crave for the ‘more effective’ drugs of misuse and lose interest in non-drug-associated stimuli.” (p. 373). Repeated use of these drugs can cause dysregulation of dopaminergic mechanisms in the brain. In addition, caffeine appears to stimulate dopamine release in the prefrontal cortex but not also in the ventral striatum, which is a component of the reward system. The effects of psychotropic drugs in the brain are more direct and pronounced than those of substances in our food and drink. If chronic use of these drugs inclined some people to addictive behavior, then we could question whether cognitive enhancement had a favorable benefit–risk ratio.

Research into the addictive potential of cognitive enhancement may pose an ethical problem regarding the determination of acceptable risk and the safety of the drugs. Participants in prospective studies of the drugs would be healthy subjects with no history of addiction. Those in the experimental arm of a clinical trial receiving regular doses of a psychostimulant and experiencing heightened dopaminergic effects in their brains’ reward system would be exposed to a potentially addictive substance. Proving that chronic use of a drug was in fact addictive could mean causing previously healthy individuals to become addicted. Heinz et al. say that “to date no single variable has been identified that reliably predicts addiction to neuroenhancers. To identify such predictive factors, a substantial number of subjects would have to be exposed to potentially addictive drugs in prospective studies. Since these healthy volunteers do not have a disease, the risk-benefit ratio for such exposures remains rather unfavorable” (p. 374). Subjects should retain the right to participate in these studies if they are capable of giving informed consent to participate in them, and this would include being informed of any risks. But some may cite researchers’ duty of nonmaleficence and question whether exposing healthy subjects to potentially addictive behavior would be consistent with this duty. In some respects, this would be similar to enrolling healthy subjects in a trial testing the anxiolytic effects of benzodiazepines, which are known to be addictive.

With careful design and monitoring of effects in subjects, studies that quantified the risks associated with chronic use of cognition-enhancing drugs would be both empirically and ethically justified. Nevertheless, this research would require resources from public health systems. Because health resources are scarce, many would argue that research into the effects of cognitive enhancement should receive lower funding priority than research into developing preventive and therapeutic treatments for neuropsychiatric and other diseases. There is a more urgent need to generate scientific knowledge of the causes and possible treatments for these diseases than to generate knowledge of the effects of trying to improve normal brain function. Indeed, because it does not involve disease, some might argue that research into the effects of cognitive enhancement should not be publicly funded at all. This raises the more fundamental question of what a just society should pay for in providing health resources to citizens. A just society is one in which institutions ensure that all citizens have adequate access to health care for a decent minimum level of physical and cognitive functions. These are necessary for equal opportunity to achieve a decent minimum level of well-being (Daniels, 2008). Insofar as enhancement involves raising these functions above a decent minimum, it is questionable whether the state would be obligated to provide resources necessary for enhancement, even if it could afford to pay for them.

Social Inequality

Let us assume that cognition-enhancing drugs would be safe. Some opponents of cognitive neuroenhancement might claim that it would exacerbate unjust social inequalities if it were practiced on a broad scale. Although people decide to take cognition-enhancing drugs for many reasons, one is to give them a competitive edge over others in obtaining such positional goods as an elite education or lucrative jobs. It may seem unfair that some who are cognitively better off than others could use psychopharmacology to improve their cognitive capacities. But these capacities are already enhanced when parents arrange for private tutors for their children or send them to private schools. They are also enhanced when students and athletes employ private trainers. So we should not focus entirely on drug-induced cognitive enhancement. Still, these examples of enhancement often reflect income inequalities between the socially better off and worse off, which suggests that it may be unfair to those who lack the financial means to have these same opportunities. If cognition-enhancing drugs were available to all and not prohibitively expensive, and if the positive effects of these drugs were stronger among the cognitively worse off and weaker among the cognitively better off, then wider use of the drugs by more people would probably not increase inequality. The enhanced cognitive functions could generate more opportunities for the worse off. There would be no leveling down among the cognitively better off, whose capacities would remain relatively unchanged, and there would be some improvement among the cognitively worse off. Thus there may be social reasons for cognitive enhancement.

Some will take issue with these claims. For those who cannot afford prescription drugs needed for treatment of disease, cognition-enhancing drugs might not be within their means. Also, access to the drugs through prescriptions or the online market would require a certain degree of sophistication in persuading physicians to prescribe or navigating the Internet. This could correlate with income, impede access to the drugs, and sustain rather than reduce inequality between the cognitively better and worse off. (Bostrom and Sandberg, 2009). Moreover, given that enhancers improve some but not all cognitive functions and may involve trade-offs between them, the cognitively worse off may “level up” in some respects but not others. Because differences in cognitive ability are only one aspect of social inequality, the different effects of enhancing drugs on the cognitively better and worse off could support the weaker claim that they would not increase inequality but not the stronger claim that they would reduce it. Besides, most of those who enhance are secondary school and university students, who can be quite sophisticated in obtaining whatever will give them a competitive edge. They will prioritize their spending practices to purchase the drugs, which for them may not be prohibitively expensive.

In light of scientific studies demonstrating positive effects of the drugs on executive functions, some students, university teachers, and other workers might feel coerced into taking the drugs just to keep up with their cognitively enhanced peers. Employers might pressure employees to take the drugs in order to work more efficiently and productively. This already occurs to some extent in the military. Some personnel are encouraged or required by their superiors to take modafinil or other stimulants in order to perform certain tasks over long periods without the need for sleep. Some workers might decline to take the drugs out of concern about potential deleterious effects on their bodies and brains. This could put them at a competitive disadvantage compared with those who took the drugs. Whether these concerns were warranted would depend on the actual effects on neural and cognitive functions, which have often been exaggerated. On the basis of meta-analyses of the effects of methylphenidate and modafinil in healthy individuals, psychopharmacologist Reinoud de Jongh and coauthors state: “High expectations regarding the effects of enhancement drugs are not warranted. However, societal pressure may occur with respect to drugs that are ineffective or only slightly effective simply because people believe these drugs improve performance, as the illicit use of methylphenidate and modafinil shows. Creating realistic expectations appears to be very hard to accomplish” (de Jongh et al., 2008, pp. 771–772; see also Repantis et al., 2010; and Lucke et al., 2011).

Coercion can result from unreasonable expectations imposed by some on others, forcing them to accept situations that are worse for them than any alternatives. But if everyone were suitably informed of the generally modest effects of psychostimulants on cognition and of studies showing that these effects primarily benefit the cognitively worse off, then expectations about these effects would adjust accordingly. Consequently, the incidence of real or perceived coercion or unfairness regarding the use of these drugs would diminish. An additional factor to consider is that enhancing cognitive capacities by itself would not necessarily make our lives better on the whole, since well-being is more than a function of the extent to which we have and exercise these capacities (Tannsjo, 2009). But cognitive capacities are an important component of human welfare in enabling us to formulate and execute action plans that reflect our interests and values, and enhancing them could contribute to a higher level of well-being.

Inauthenticity and Alienation

Another concern about enhancing normal cognitive functions with drugs is that it would undermine our authenticity. Our selves consist of a unified set of mental states generated and sustained by normal functions in the brain. We come to have authentic selves by identifying with our mental states. This identification results from a process of critical reflection on our desires, beliefs, intentions, and emotions. It is through this reflective process that we endorse them as our own and make them the springs of our actions (Frankfurt, 1988; Taylor, 1991). Being a free and authentic agent consists in the general capacity to control which of these states issue in our actions. Insofar as agency is a necessary condition of selfhood, being an authentic agent is a necessary condition of having an authentic self.

Altering our mental states with psychotropic drugs presumably would alienate us from our true selves. Leon Kass notes this as a potential consequence of cognitive enhancement: “As the power to transform our native powers increases, both in magnitude and refinement, so does the possibility for self-alienation—for losing, confounding, or abandoning our identity” (Kass, 2003, p. 294). Kass claims that the difference between enhancement through drugs and enhancement through one’s own effort is that the drugs “make improvements to our performance less intelligible… On the plane of human experience and understanding, there is a difference between changes in our body that proceed through self-direction and those that do not” (Kass, 2003, p. 294). Kass seems to be saying that what leads to alienation and inauthenticity is that drugs undermine the very meaning of performance and achievement by undermining human agency. “Biomedical interventions act directly on the human body and mind to bring about their effects on a subject who is not merely passive but who plays no role at all. In addition, he can at best feel their effects without understanding their meaning in human terms” (p. 295) Enhancing drugs disrupt the relation between the subject and his or her activities and their fulfillment. Kass is not so much defending the idea of authenticity conceived of as a process of self-discovery rather than self-creation (De Grazia, 2000; Elliott, 2003; Parens, 2005; Levy, 2011). Instead, Kass’s point is that “the lack of ‘authenticity’ sometimes complained of in these discussions… is a departure from ‘genuine,’ unmediated, and (in principle) self-transparent human activity” (p. 295). Some might also cite Jurgen Habermas’ claim that a genetically enhanced person would not be “the sole author of their own life history” in arguing that cognitive enhancement would undermine individual autonomy and authenticity (Habermas, 2003, p. 80). One could not identify with the altered mental states because their source or author would not be the person but the drugs and their effects on his or her brain.

The voluntary use of a drug or brain stimulation to enhance cognition would not necessarily make us inauthentic, nor would it replace the person who uses them as the author of his or her actions. If an individual with the capacity for critical self-reflection freely decides to take a cognition-enhancing drug, then he or she is the agent of any change in mental states. The drug or stimulating device is merely the means through which the change is produced. Provided that the individual has the capacity to weigh the reasons for and against these interventions in his or her brain and mind and to act on these reasons, enhancement would not result in an inauthentic or alien self. Improving one’s cognitive capacities by manipulating the brain could be an expression of autonomy and authenticity if it resulted from a deliberated and informed decision consistent with one’s considered desires and values. Enhancement would not undermine the capacity to judge what was in one’s best interests and could very well be in line with these interests. (De Grazia, 2000) So claims about the presumed adverse effects of cognitive enhancement on the source and nature of our mental states are unsupported.

Michael Sandel claims that the desire to enhance our natural cognitive and physical capacities is driven by the more fundamental desire for perfection and absolute control of our lives (Sandel, 2007). He says that we should welcome rather than try to alter these capacities, imperfect as they are. Sandel is particularly concerned about the harmful effects enhancement might have on our character. The drive to master our human capacities could destroy what Sandel calls the “giftedness of life” (p. 96). This includes an appreciation of what is good in what we have and do in an absolute and objective rather than relative and subjective sense. Without this appreciation, we cannot flourish and be truly happy, because happiness needs to be grounded in some sense of objective good. The drive for mastery, or the desire for complete control over nature through biomedical enhancement, denies absolute value to things, including human excellence and achievement. Sandel’s concern is not about the permissibility of enhancement. He does not claim that it is immoral but instead unwise to enhance because it makes us lose our understanding of what makes a good life. Defending an Aristotelian view of the virtue of wisdom, Sandel claims that an appreciation of the giftedness of life is a precondition for a good life and that enhancement precludes this appreciation. In addition, he is critical of the drive to mastery because he believes that it could weaken social solidarity and remove moral and aesthetic qualities from our appreciation of excellence.

But the desire to improve the capacities and dispositions that constitute our character does not imply a desire to master or perfect them. It does not reflect a hubristic wish to completely control our lives. As Allen Buchanan points out: “Even in a world of pervasive and powerful biomedical enhancements, we’d still have plenty of opportunities for appreciating that many of the good things in our lives are not our accomplishments, not subject to our wills” (Buchanan, 2011, p. 134). Enhancement could have unintended bad effects on a person’s character if, for example, too high a dose of a drug increased dopamine levels to the point of causing addictive behavior. Yet is it is not the idea of enhancement as such but its positive or negative effects on our cognitive and emotional capacities that would determine its value or disvalue. It would be difficult to find anything morally objectionable about improving one’s character by pharmacological or other means, especially if that character consists entirely in self-interest and ignores the interests of others. Sandel also fails to fully appreciate inequalities in people’s natural cognitive abilities. As the empirical data cited earlier suggest, improving these abilities among the worse off with enhancers may not lead to a more egalitarian society but at least would not exacerbate social inequality.

Another concern that Sandel and others have is that enhancements would undermine our conception of excellence. This suggests that excellence in achieving goals is entirely the result of one’s own efforts in exercising one’s natural capacities. There is considerable variation among people in the cognitive capacities that enable them to undertake and complete projects. Some are naturally more cognitively endowed than others because of the different ways in which their brains are wired, and this may give some an advantage over others in undertaking and completing projects. In addition to neurobiological luck, parental support and other social factors beyond our control influence how successful we are in achieving them. For those who have not fared as well as others in the biological and social lottery, a cognition-enhancing drug combined with effort and cultivation of certain skills could be a way of compensating for what they naturally lack in pursuing and achieving goals. In fact, insofar as the positive effects of enhancement are modest, concern about its potential impact on performance and excellence may be out of proportion to its actual impact on them. This may deflate worry about drugs affecting our understanding of and the value we attribute to excellence. Sandel’s critique may have some force against an augmentative conception of enhancement insofar as it is associated with the idea of mastery, but it has less force against an optimizing conception of enhancement insofar as it is associated with the idea of improvement.

Still, taking a cognition-enhancing drug does not guarantee outcomes superior to those that would have obtained without the drugs. Whether the drugs improve the relevant functions in performing actions and lead to better outcomes depends on how we make use of any cognitive boost they provide. Many of our achievements result from the combination of personal effort and enhancements. These include not only drugs that improve attention, focus, and working memory but also private tutors and trainers. The enhancing agent alone will not produce the desired result. A procrastinating student who has to submit a research paper for a class the next day has to decide how much time to devote to the research and how much time to actually write the paper. Modafinil may enable the student to remain awake, and methylphenidate may help him sharpen his focus, but the drugs will not help him to make this decision, nor would they necessarily enable him to write a better paper than what he would have written without them. The outcome depends on more than the enhancer. Journalist Margaret Talbot writes: “Even with the aid of a neuroenhancer, you still have to write the essay, conceive the screenplay, or finish the grant proposal, and if you can take credit for what you’ve done on caffeine or nicotine, then you can take credit for work produced on Provigil” (Talbot, 2009, p. 40).

Moral Enhancement

Enhancing cognitive capacities associated with reasoning could be one component of enhancing moral sensitivity in recognizing and responding to the rights, needs, and interests of others. The other component would involve enhancing affective capacities such as empathy and trust. Enhanced cognitive and affective capacities could result in moral progress by promoting behavior that would reduce the incidence of humans harming other humans and result in greater well-being for all (Douglas, 2008; Chan and Harris, 2011; Harris, 2011; Metzinger, 2011). The moral problem is one of both ignorance and motivation, and the purpose of enhancing the relevant capacities would be to strengthen the ability to recognize and respond to reasons for or against actions that affect others.

Psychotropic drugs could modulate concentrations of neurotransmitters such as serotonin and might incline people to be more cooperative by increasing harm aversion (Crockett et al., 2010; Crockett, 2014). Impulsivity has been associated with excess dopamine in the brain. Although the capacity for self-control is mediated by a number of neuromodulating factors, lowering concentrations of dopamine and increasing concentrations of serotonin could in theory reduce impulsivity and also promote cooperative behavior. The selective serotonin reuptake inhibitor citalopram (Celexa) has been shown to promote prosocial behavior by enhancing harm aversion in healthy volunteers. However, there are multiple receptors for serotonin mediating multiple functions in the brain beyond those associated with this type of behavior. Further research is needed to know how serotonin interventions to enhance moral sensitivity and moral motivation might influence these other functions. Fear and the feeling of being threatened by others can be an impetus to immoral behavior. By reducing the fear response, propranolol might also increase aversion to harming others and incline people to act morally (Terbeck et al., 2012, 2013). Again, though, this effect could make one vulnerable to life-threatening situations by inhibiting a normal fear response to them. So moral reasons for using the drug would have to be weighed against prudential reasons against using it. For those who are deficient in the affective capacities of empathy and trust, remorse, and regret, strengthening the cognitive capacity to imagine counterfactual situations and foresee the probable consequences of one’s actions and how they affect others could make one more cautious in deliberating about which actions to perform.

While in principle there are good reasons to enhance people’s capacity to recognize and respond to prudential and moral reasons, in practice it would be difficult to enhance this capacity with drugs. It is an oversimplification to think that a drug targeting certain chemical receptors or circuits in the brain will transforms people’s behavior. This is a function of a complex set of factors including distributed and interacting neural circuits and pathways, genetics, and the natural and social environment. It is a much more complicated process than one involving a direct causal relation between pharmacological inputs and behavioral outputs.

Suppose that drugs or other interventions in the brain had the desired effect of moral enhancement, The aim of l this enhancement would not be to get people to recognize moral principles or truths or to construct a more convincing argument for why one moral theory is superior to others (Parfit, 2011). Rather, its aim would be to motivate people to act morally. This would not have to be cashed out specifically in Kantian terms as enhancing the capacity to respect people’s rational nature or in consequentialist terms as enhancing the capacity to bring about the best outcomes. It would mean enhancing the cognitive and emotional capacity to recognize that other people have the same rights, needs, and interests as ourselves and for this recognition to move us to act accordingly (Scanlon, 1998).

In the respects I have outlined, drugs or other means of cognitive enhancement could promote moral behavior. This need not involve the motivation to act altruistically. More pragmatically, it could involve a lower common behavioral denominator and aim at strengthening the rational capacity of individuals to realize that they would be better off cooperating and abiding by socially constructed rules of behavior than by pursuing pure self-interest (Gauthier, 1986). Cognitive enhancement as moral enhancement would be based on the idea that morality is grounded in rational choice. John Harris claims that “there are good reasons… to believe moral enhancement must, in large part, consist of cognitive enhancement” (Harris, 2011, p. 106). This would involve strengthening the capacity to imagine different possible circumstances and outcomes as a way of making one more responsive to reasons for and against different actions. Insofar as this is consistent with the idea of improving the capacity to make rational choices about mutually beneficial social behavior, moral enhancement would not necessarily involve strengthening the desire to act from altruistic motives. A constructivist model of moral enhancement based on rational choice would not necessarily involve enhancing the capacity for empathy, at least not the affective (as distinct from the cognitive) component of empathy. Although empathy plays an important role in moral behavior, the affective aspect of empathy would not be the core mental component of rational choice.

Some authors have argued that the affective or emotional component of empathy is less important in moral behavior than has been assumed (Bloom, 2014). Peter Singer has stated that cognitive empathy could be the basis of what he calls “effective altruism,” which would motivate individuals to donate money to organizations dealing with poverty and famine by recognizing impartial reasons for helping those in greatest need (Singer, 2014). If a drug or other intervention in the brain could strengthen the capacity to recognize and act on these reasons, then it might also reduce the potential for partiality and group-identification caused or exacerbated by a drug like oxytocin. Enhancing cognitive empathy for effective altruism would be one way of doing good. A more compelling reason for moral enhancement would be to prevent or reduce harm, and inducing a type of cognitive empathy involving less than an altruistic disposition may be a more realistic goal. Psychopaths commit many harmful acts, and all psychological and neuroscientific accounts attribute their antisocial and immoral behavior to a lack of empathy. Psychoactive interventions would have to target brain regions that mediate cognitive empathy, such as the ventral anterior cingulate cortex. Yet the success of the intervention would depend on how it modulated the anterior cingulate and how it affected its connections with other brain regions mediating rational and emotional capacities. Currently, there is no evidence of a drug or technique that could have these effects on the brain and mind.

Among others things, enhanced moral behavior could defuse what Ingmar Persson and Julian Savulescu (2012, 2013) identify as the most pressing threats to human survival: environmental degradation and the potential use of weapons of mass destruction. Given the extent of actual and potential future harm resulting from the failure to recognize and respond appropriately to the rights, needs, and interests of others, there appear to be compelling reasons for developing and implementing safe and effective psychopharmacological interventions to enhance our cognitive capacity to respond to reasons for cooperating with them. However, at least four issues would have to be addressed and resolved first.

First, extensive research would have to be conducted to identify a drug or drugs that would safely and effectively alter neurobiological mechanisms and enhance the relevant cognitive capacities. This would be costly, and it raises the same question regarding research on cognition-enhancing drugs: Should research into psychopharmacological agents designed to enhance our rational and moral behavior be treated on a par with research designed to prevent or find treatments for neuropsychiatric and other diseases? Some would argue that the harm resulting from actions symptomatic of our limited moral compass is as significant as the harm from disease. The immediacy and salience of the latter appear to give it more weight. Yet as Elizabeth Fenton points out, “if we do not continue scientific research into enhancement, if we halt it out of concern for the consequences, then we have no hope of achieving the great moral progress that will ensure our survival of the species” (Fenton, 2010, p. 148). But this raises the question of whether a sufficient number of research subjects could be recruited for this research, given that this would involve healthy individuals exposing themselves to the known risks of psychoactive drugs. For this same reason, it also generates doubts about whether there could be an obligation to participate in the research. What complicates drawing accurate comparisons between them is that knowing how to enhance moral cognition and how to prevent or control disease are distinct types of research with distinct aims. Professional and public debate will be necessary to decide whether priority in resource allocation should go to research aimed at ameliorating flaws in our bodies and brains or to research aimed at ameliorating flaws in our character and behavior.

Second, it is doubtful that pharmacological enhancement of our cognitive capacities alone would make us more responsive to moral reasons when acting. Persson and Savulescu (2012, 2013) rightly point out the shortcomings of moral education as part of their argument for moral enhancement. Yet the right type of education could complement psychopharmacology in making us more responsive to the interests of those who exist now and those who will exist in the future. The social environment also influences brain function and provides cues that prompt us to act in different ways. Moral enhancement would thus require a full complement of education, environmental modification, and psychopharmacological intervention.

Third, just because a drug might enhance our cognitive capacity to imagine ourselves being in other people’s situations does not mean that we would exercise this capacity and be motivated to act on it. We may fail to put the necessary effort into translating receptivity to moral reasons into morally defensible actions. Factors in the social or cultural environment may incline us to self-interest and group bias. Buchanan says that “a biomedical intervention [for moral enhancement] might be one aspect of a multifaceted effort to extend concern and respect for all human beings, not just those who are like us” (2011, p. 170). Even if a model consisting of biomedical, educational, and social factors were more likely to produce the desired effects than any alternative, there is no guarantee that it would motivate people to act morally. Predicting whether enhancers could achieve this goal presupposes a near complete understanding of human moral psychology, which we currently lack and may never have (Agar, 2014a).

Fourth, reducing or averting harm from the most serious threats to our well-being and survival is a collective action problem. As such, this and related goals can only be achieved if a sufficient number of people engage in moral enhancement. Given the choice, though, many people would decide not to enhance. Those who recognized the need to voluntarily morally enhance would already be the most morally sensitive individuals. The difference between them and those who failed to recognize this need could reflect a type of moral inequality that could be an obstacle to cooperation. For those whose behavior is motivated largely by self-interest, the drugs may strengthen their capacity for instrumental reasoning and lead them to conclude that they could free ride off the cooperation of others. If a significant number of people opted out of enhancement, then it could preclude the collective effect from being achieved. There would also have to be agreement on which attitudes or virtues should be enhanced and which vices should be diminished or eliminated. Some people may use a higher common behavioral denominator and argue that drug interventions should not merely make us more inclined to cooperate or act out of a sense of duty but in a supererogatory way as “moral saints,” sacrificing self-interest for the interests of others (Wolf, 1982). This could be the consequence of augmenting the capacity for moral sensitivity. Extreme altruism would not be adaptive because it would undermine self-interest if others were not also altruistic to the same degree. The most viable moral behavior to produce would be one that promoted cooperation without completely sacrificing self-interest. It would fall between the extremes of psychopathy, or pure self-interest, and pure altruism. Still, it is unclear how there could be collective agreement on whether there would be limits to how moral we should be and how we would set these limits.

Assuming that there could be public consensus on these issues, making cognitive enhancement a mandatory rather than voluntary component of a state-sponsored program of moral enhancement would involve a more controversial problem. It could mean that individual liberty in choosing whether or not to enhance could be overridden by collective interest. This would be a violation of the presumptive right to noninterference in one’s body, including the brain and mind. Such a concern is untouched by the argument that self-prescribed enhancement would be consistent with an individual’s internal sense of freedom by inducing the right sort of moral motivation and insight (De Grazia, 2014). It would raise the question of whether improving moral behavior could be mandated externally by authoritarian means within a liberal democracy (Harris, 2011). Many would perceive this as a form of benevolent paternalism that they would unconditionally reject. Given the magnitude of the actual harm from people failing to respect others, the potential harm from the use of weapons of mass destruction and environmental degradation, and assuming that psychopharmacology could improve our moral behavior, some restrictions on individual liberty in choosing not to enhance might be justified. Even if these restrictions were justified, we would still have to identify, collectively agree on, and justify what these restrictions would be. It is not clear whether or how a general program of cognitive enhancement would enable us to achieve this goal.

Conclusion

I have considered the respects in which our cognitive capacities can be enhanced through psychopharmacology. After examining the neurobiological effects of certain drugs and how they might enhance these capacities, I cited empirical studies in pointing out that enhancing some capacities may come at the cost of diminishing others. By explaining how increasing concentrations of neurotransmitters such as dopamine could result in pathological behavior, I argued that an unlimited augmentative conception of enhancement is problematic and should be replaced by one in which the goal is to generate optimal levels of mental capacities that promote flexible behavior and adaptability to the demands of the environment. Assuming that cognitive enhancement is safe and more effective among the cognitively worse off than the better off, it would not likely increase social inequality. I also argued that claims that enhancement would alienate us from our true selves, undermine agency, or involve a hubristic pursuit of perfection have not been satisfactorily defended. Enhancement can be consistent with the ideas of authenticity, excellence, and achievement. Finally, I explained how cognitive enhancement could be one component of moral enhancement by strengthening the capacity to recognize reasons for respecting the rights, needs, and interests of others. I spelled out a number of problems that would have to be resolved before a project of moral enhancement could be implemented. The most vexing of these problems would be whether enhancing cognitive capacities to promote moral behavior would be voluntary or obligatory and whether the collective social interest could outweigh the individual right to refuse an intervention in the brain and mind.

In 2008 a group of neuroscientists and ethicists formulated a set of recommendations based on the presumption that mentally competent adults should be permitted to engage in cognitive enhancement (Greely et al., 2008). These recommendations include an evidence-based approach to the evaluation of risks and benefits and enforceable policies regarding the use of cognition-enhancing drugs to support fairness, protect individuals from coercion, and minimize enhancement-related socioeconomic disparities. Questions about the long-term risks of cognition-enhancing drugs will only be answered after a sufficient number of controlled studies of their effects have been completed. While not reducible to scientific questions about the effects of psychotropic drugs on the brain, discussion of normative questions about cognitive enhancement has to be sufficiently empirically informed. Even if the research could establish that the risks of cognitive enhancement were within reasonable limits, some may question whether funding research into improving normal neural and mental capacities could be justified in the first place. In the absence of funding and sufficient data on long-term risks, competent individuals should have the right to enhance. Yet such a right would come with the proviso that enhancing themselves did not result in any harm to others.

Acknowledgments

I am grateful to Nicholas Agar and especially an anonymous reviewer for Oxford University Press for very helpful comments on earlier versions of this chapter.

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