Neuroethical issues in cognitive enhancement: Modafinil as the example of a workplace drug?

Abstract

The use of cognitive-enhancing drugs by healthy individuals has been a feature for much of recorded history. Cocaine and amphetamine are modern cases of drugs initially enthusiastically acclaimed for enhancing cognition and mood. Today, an increasing number of healthy people are reported to use cognitive-enhancing drugs, as well as other interventions, such as non-invasive brain stimulation, to maintain or improve work performance. Cognitive-enhancing drugs, such as methylphenidate and modafinil, which were developed as treatments, are increasingly being used by healthy people. Modafinil not only affects 'cold' cognition, but also improves 'hot' cognition, such as emotion recognition and task-related motivation. The lifestyle use of 'smart drugs' raises both safety concerns as well as ethical issues, including coercion and increasing disparity in society. As a society, we need to consider which forms of cognitive enhancement (e.g. pharmacological, exercise, lifelong learning) are acceptable and for which groups under what conditions and by what methods we would wish to improve and flourish.

Keywords: Cognitive-enhancing drugs; hot and cold cognition; improved task-related motivation; modafinil; neuroethics; workplace enhancement.

Figure 1.

Normal ‘cold’ cognition in non-depressed individuals. ‘Cold’ (emotion-independent) cognition is instantiated via a complex set of circuits, including interactions (blue arrows) between the dorsolateral prefrontal cortex (DLPFC), the dorsal anterior cingulate cortex (ACC), and the hippocampus (H). Limbic structures connected to DLPFC, ACC, and H, such as the amygdala (A), the nucleus accumbens (NAcc), and the subgenual portion of the ACC (sgACC) may also be activated during cold cognition, but are more strongly engaged during ‘hot’ (emotion-laden) cognition (Figure 2). Monoamine neurotransmitter (NT) projections (purple arrows) emanating from the brainstem, including serotonin (5-HT), norepinephrine (NE), and dopamine (DA), may influence cold cognition via modulatory actions in cortical and subcortical regions. Note that most circuit nodes and connections are excluded in this and later figures for clarity, and that some connections may be indirect.

Figure 2.

Normal positively biased ‘hot’ (emotion-laden) cognition in non-depressed individuals. Hot cognition is instantiated by circuits including interactions (green arrows) between limbic regions including A, NAcc, and sgACC, the activity which is profoundly modulated by 5-HT, NE, and DA. These regions share reciprocal connections with DLPFC, ACC, and H, and consequently hot and ‘cold’ (emotion-independent) cognition necessarily interact (for example, motivation alters ostensibly cold cognitive test performance). Non-depressed individuals exhibit positive (green arrows) bottom-up (perceptions/experience) and top-down (expectation) biases, providing resilience to adverse events. Abbreviations and indications to colour as in Figure 1.