This chapter sets the scene for the subsequent philosophical discussions by surveying a number of biological interventions that have been used, or might in the future be used, for the purposes of crime prevention. These interventions are pharmaceutical interventions intended to suppress libido, treat substance abuse or attention deficit-hyperactivity disorder (ADHD), or modulate serotonin activity; nutritional interventions; and electrical and magnetic brain stimulation. Where applicable, we briefly comment on the historical use of these interventions, and in each case we (...) discuss the evidence that they are effective, or might become so with further refinement. The chapter concludes with a comment on some potentially significant differences between the varieties of intervention that we canvass. (shrink)

The purpose of this paper is to discuss the biological plausibility of the pace of creation written in the genesis. A fascinating hypothesis is made on the central role of serotonin as a guide, as the director of the phenomena that enable the best use of light by the plant world, the growth, the regulation of mood in the complex molecular interactions that characterize the varying levels of consciousness. This hypothesis provides biological interpretations of the c.

In recent years, the scientific study of meditation and psychedelic drugs has seen remarkable developments. The increased focus on meditation in cognitive neuroscience has led to a cross-cultural classification of standard meditation styles validated by functional and structural neuroanatomical data. Meanwhile, the renaissance of psychedelic research has shed light on the neurophysiology of altered states of consciousness induced by classical psychedelics, such as psilocybin and LSD, whose effects are mainly mediated by agonism of serotonin receptors. Few attempts have been (...) made at bridging these two domains of inquiry, despite intriguing evidence of overlap between the phenomenology and neurophysiology of meditation practice and psychedelic states. In particular, many contemplative traditions explicitly aim at dissolving the sense of self by eliciting altered states of consciousness through meditation, while classical psychedelics are known to produce significant disruptions of self-consciousness, a phenomenon known as drug-induced ego dissolution. In this article, we discuss available evidence regarding convergences and differences between phenomenological and neurophysiological data on meditation practice and psychedelic drug-induced states, with a particular emphasis on alterations of self-experience. While both meditation and psychedelics may disrupt self-consciousness and underlying neural processes, we emphasize that neither meditation nor psychedelic states can be conceived as simple, uniform categories. Moreover, we suggest that there are important phenomenological differences even between conscious states described as experiences of self-loss. As a result, we propose that self-consciousness may be best construed as a multidimensional construct, and that “self-loss,” far from being an unequivocal phenomenon, can take several forms. Indeed, various aspects of self-consciousness, including narrative aspects linked to autobiographical memory, self-related thoughts and mental time travel, and embodied aspects rooted in multisensory processes, may be differently affected by psychedelics and meditation practices. Finally, we consider long-term outcomes of experiences of self-loss induced by meditation and psychedelics on individual traits and prosocial behavior. We call for caution regarding the problematic conflation of temporary states of self-loss with “selflessness” as a behavioral or social trait, although there is preliminary evidence that correlations between short-term experiences of self-loss and long-term trait alterations may exist. (shrink)

A number of concerns have been raised about the possible future use of pharmaceuticals designed to enhance cognitive, affective, and motivational processes, particularly where the aim is to produce morally better decisions or behavior. In this article, we draw attention to what is arguably a more worrying possibility: that pharmaceuticals currently in widespread therapeutic use are already having unintended effects on these processes, and thus on moral decision making and morally significant behavior. We review current evidence on the moral effects (...) of three widely used drugs or drug types: propranolol, selective serotonin reuptake inhibitors, and drugs that effect oxytocin physiology. This evidence suggests that the alterations to moral decision making and behavior caused by these agents may have important and difficult-to-evaluate consequences, at least at the population level. We argue that the moral effects of these and other widely used pharmaceuticals warrant further empirical research and ethical analysis. (shrink)

Studies have shown that both serotonin and glutamate receptor systems play a crucial role in the mechanisms underlying drug-induced synesthesia. The specific nature of these mechanisms, however, continues to remain elusive. Here we propose two distinct hypotheses for how synesthesia triggered by hallucinogens in the serotonin-agonist family may occur. One hypothesis is that the drug-induced destabilization of thalamic projections via GABAergic neuronal circuits from sensory areas leads to a disruption of low-level, spontaneous integration of multisensory stimuli. This sort (...) of integration regularly occurs when spatial and temporal attributes match. Destabilization of feedback loops, however, can result in incongruent experiences or binding of random thalamus activation with sensory input in a particular sensory modality. The second hypothesis builds on embodied cognition, cases in which visual images of external stimuli activate task-related neural regions. On this proposal, binding processes that do not normally generate awareness become accessible to consciousness as a result of decreased attentional discrimination among incoming stimuli. (shrink)

Can we identify potential long-term consequences of digitalisation on public health? Environmental studies, metabolic research, and state of the art research in neurobiology point towards the reduced amount of natural day and sunlight exposure of the developing child, as a consequence of increasingly long hours spent indoors online, as the single unifying source of a whole set of health risks identified worldwide, as is made clear in this review of currently available literature. Over exposure to digital environments, from abuse to (...) addiction, now concerns even the youngest (ages 0 to 2) and triggers, as argued on the basis of clear examples herein, a chain of interdependent negative and potentially long-term metabolic changes. This leads to a deregulation of the serotonin and dopamine neurotransmitter pathways in the developing brain, currently associated with online activity abuse and/or internet addiction, and akin to that found in severe substance abuse syndromes. A general functional working model is proposed under the light of evidence brought to the forefront in this review. (shrink)

In this article, I argue that depression and suicide are natural kinds insofar as they are classes of abnormal behavior underwritten by sets of stable biological mechanisms. In particular, depression and suicide are neurobiological kinds characterized by disturbances in serotonin functioning that affect various brain areas (i.e., the amygdala, anterior cingulate, prefrontal cortex, and hippocampus). The significance of this argument is that the natural (biological) basis of depression and suicide allows for reliable projectable inferences (i.e., predictions) to be made (...) about individual members of a kind. In the context of assisted suicide, inferences about the decision-making capacity of depressed individuals seeking physician-assisted suicide are of special interest. I examine evidence that depression can hamper the decision-making capacity of individuals seeking assisted suicide and discuss some implications. (shrink)

Located within the ascending reticular activating system are nuclei which release neurotransmitters such as acetylcholine, serotonin, dopamine, and norepinephrine. These nuclei have widespread projections that extend into the limbic system and throughout cortex. Activation of these neurotransmitters during awake states leads to arousal, while inhibition leads to the loss of consciousness experienced during slow-wave sleep. Previously, we proposed a mechanism in which cardiorespiratory synchronization may underlie the widespread hyperpolarization that occurs throughout the brain during slow-wave sleep. We further propose (...) that a similar homeostatic mechanism may be involved in sleep-wake transitions and maintaining various arousal states including rapid eye movement sleep, waking, and anxiety. Widespread depolarization associated with more rapid, shallow breathing and desynchronized cardiorespiratory oscillatory activity may underlie waking, anxiety, and rapid eye movement sleep states. The exact voltage values of these widespread membrane potential changes remain unknown and possibly highly variable between different neural areas and cell types. Here, we place these consciousness states on a spectrum of approximated widespread membrane potential values with anxiety states being the most depolarized, followed by waking states, and rapid eye movement sleep. We propose that although these widespread membrane potential changes are minor, they may underlie transitions between and maintenance of varying levels of arousal. Further research on these mechanisms could provide insights into how the brain functions. This homeodynamic arousal mechanism involves the established feed-forward and feedback signaling between the ascending reticular activating system and the hypothalamus, as well as the modulation by cardiorespiratory oscillatory feedback from the body. Understanding the basic mechanisms responsible for the states of sleep, waking, and anxiety could lead to better treatment options in health and disease. (shrink)

Background: The complexity of diagnostic presentations of an inpatient psychiatry population requires an integrative approach to health and well-being. In this sense, the primary need of this research aims at developing clinical strategies and healthier coping skills for anger, anxiety, and depression; promoting self-esteem, healthier sleep, and anxiety reduction; as well as enhancing mood and emotional–behavioral regulation via exercise and nutrition education. Objectives: The primary objective is to promote exercise, fitness, and physical health in inpatient psychiatry patients. The secondary objective (...) includes therapeutic management of depressive symptoms and patient-centered approach to mania, angry outbursts, and generalized disruptive behavior. The tertiary objective is promoting research in the psychophysiological effectors of exercise and nutrition education in combination with psychotherapy. Method: Monitoring self-reported changes in mood and general well-being via administration of surveys and questionnaires pre- and postexercise sessions. Results: The research yielded positive outcomes in all areas investigated, suggesting the positive effects of exercise and mind–body strategies in the context of psychotherapy in inpatient psychiatry. Conclusion: Physical exercise may be a helpful way to reduce mental health disorders in the context of inpatient psychiatry by targeting anxiety, depression, anger, psychomotor agitation, and muscle tension and addressing stressors and triggers and to develop a more balanced and integrated sense of self. (shrink)