The perspective examines two recently introduced products that exemplify the trend. The first, Puffpaw, is a nicotine vaping device that has been marketed, remarkably, as an aid for quitting e-cigarettes, even as it ties rewards to continued use. The second, Gudtrip, is a cannabis vaping device that explicitly positions itself at the intersection of artificial intelligence, cryptocurrency, and cannabis culture. Both products pair the physical device with a smartphone app that monitors user behavior and converts vaping activity into redeemable value. What struck the researchers most forcefully was the fundamental inversion of established addiction treatment principles embedded in this design. In evidence-based substance use treatment, clinicians work to help patients discover sources of reward that are not connected to drug use. These devices do precisely the opposite, layering additional reward onto a behavior that is already powerfully rewarding at the neurochemical level.

The neuroscience underlying this concern is straightforward but sobering. Nicotine and cannabis both activate the brain’s reward circuitry, reinforcing the desire to use them repeatedly. Vaping may intensify this reinforcement loop because, unlike smoking a cigarette from start to finish, vaping allows users to take individual puffs scattered throughout the day. Each puff is another opportunity for the drug to engage the reward system, and each engagement is another chance for the behavior to be woven into daily routines and habitual patterns. Amanda Palmer, a Hollings researcher and lead author of the perspective, noted that the products reward people for engaging in an already rewarding behavior, a combination she described as standing out sharply against the logic of treatment. Tracy Smith, an addiction scientist who co-leads the Cancer Prevention and Control Research Program at Hollings, was blunter, saying that the idea of financially incentivizing nicotine use is genuinely frightening given how addictive nicotine is.

Critically, the reward structures of these devices do not incentivize quitting. Points accumulated through vaping can be exchanged for cryptocurrency or used to purchase refill cartridges, which means the rewards feed directly back into further consumption. Palmer described this as a self-sustaining system with no incentive for abstaining, one that keeps users continuously engaged with the product. The concept of rewarding tobacco use is not entirely new, of course. Tobacco companies spent decades cultivating brand loyalty through rewards programs and promotional giveaways, most famously schemes like Camel Cash and Marlboro Miles, which allowed smokers to collect coupons redeemable for merchandise. What distinguishes the current generation of smart vapes is the technological amplification of that old playbook. By combining classic tobacco marketing tactics with smartphone connectivity, cryptocurrency, and game-like mechanics that monitor behavior and reward persistence, these devices achieve a degree of behavioral engineering that earlier loyalty programs could never approach.

The researchers emphasize that this approach diverges fundamentally from evidence-based cessation science. Financial incentives do have a legitimate and well-documented role in helping people quit tobacco, but only when those incentives reward abstinence or healthy behaviors rather than continued substance use. Contingency management programs, for example, have repeatedly demonstrated effectiveness by paying people for verified periods of not using drugs. The vape-to-earn model inverts this architecture entirely, converting each puff into a microtransaction and each session into an earning opportunity. In doing so, it weaponizes one of the most reliable tools in behavioral medicine against the very populations that tool was designed to help, and it does so with a consumer product that requires no prescription, no oversight, and no clinical framing whatsoever.

Perhaps the most acute concern raised in the perspective is the likely appeal of these products to adolescents and young adults. The marketing of smart vapes resembles that of a technology or gaming platform far more than a traditional vaping device, and the deliberate use of artificial intelligence, mobile apps, financial rewards, and game-like features is intended to maximize user engagement. Benjamin Toll, co-director of the Lung Cancer Screening Program and director of the Tobacco Treatment Program at Hollings, expressed particular alarm about the cannabis product, observing that its positioning at the intersection of AI, cryptocurrency, and cannabis produces features that are highly engaging for young people and deeply concerning given the vulnerability of children, adolescents, and young adults whose brains are still developing and especially sensitive to rewarding experiences. The researchers also worry about people experiencing financial hardship, who may be drawn by the promise of earning money or digital assets through vaping, and about individuals with substance use disorders, for whom reward-based recovery programs could be dangerously confused with products that reward the opposite behavior.

Regulation, the paper argues, has failed to keep pace with the technology. In the United States, manufacturers of nicotine vaping products must demonstrate to the Food and Drug Administration that their products are appropriate for the protection of public health before they can be legally marketed. Neither of the smart vaping products examined in the perspective has received FDA authorization, which means they are not legally authorized for sale, yet unauthorized vaping products remain widely available across the country. Smith described the agency’s dilemma bluntly: thousands of unauthorized vaping products are flooding the market, and while the FDA can pursue enforcement against specific companies, it cannot match the sheer scale of the current influx. The FDA has previously prioritized enforcement against products designed to appeal to youth, including devices resembling toys or gaming hardware, and the researchers contend that nicotine products rewarding vaping through cryptocurrency and gamification deserve precisely the same scrutiny.

Cannabis products present an even thornier regulatory problem. Unlike tobacco, there is no federal agency charged with overseeing cannabis products nationwide. Regulation instead varies from state to state, and existing frameworks tend to concentrate on how cannabis products are manufactured and sold rather than on how they are marketed or designed. Palmer noted that there is no equivalent federal oversight system for cannabis and that cannabis regulatory science is not as mature as tobacco regulatory science, which makes emerging technologies of this kind especially difficult to address. The devices raise a further concern that sits outside traditional drug regulation altogether: because they connect to smartphone apps, they collect detailed data about user behavior, and it remains unclear how that information could ultimately be used, monetized, or shared. A device that logs when, where, and how often a person consumes nicotine or cannabis is also a device holding a granular behavioral profile of a potentially vulnerable consumer.

The researchers are careful to draw a distinction between their concerns about vape-to-earn products and opposition to harm reduction or technological innovation more broadly. Electronic cigarettes do expose users to fewer harmful chemicals than combustible cigarettes, and vaping cannabis may reduce exposure to toxins compared with smoking it. The problem is not the hardware but the incentive architecture layered on top of it, which threatens to make addictive substances harder to quit precisely when cessation support is most needed. Palmer explained that the team published the perspective now because researchers and regulators have a rare window to act before these products become commonplace, adding that the vaping marketplace changes incredibly quickly and that careful thought is needed about how such technologies are designed and marketed. The authors hope the paper raises awareness among clinicians and parents about the changing nature of vaping products, encouraging clinicians in particular to stay informed about emerging devices their adolescent and young adult patients may be using. At a minimum, they believe vape-to-earn products should undergo careful review by federal and state regulators, and they hope to spark a broader conversation about how emerging technologies, financial incentives, and addictive substances intersect, and about the need for policy to evolve quickly enough to protect public health. For anyone seeking to quit nicotine, evidence-based tobacco cessation treatments remain highly effective, and comprehensive programs such as MUSC Health’s Tobacco Treatment Program continue to offer support grounded in science rather than in cryptocurrency payouts.

Subject of Research: Smart vaping devices that reward use with cryptocurrency and gamification and their public health risks

Article Title: Getting paid to vape? Researchers say that’s a dangerous combination

Article References: Getting paid to vape? Researchers say that’s a dangerous combination. (n.d.). Original publication

Image Credits: AI Generated

DOI: Not provided

Keywords: vaping, e-cigarettes, nicotine, cryptocurrency, gamification, addiction, cannabis, FDA regulation, public health, smart devices, smoking cessation, adolescent health

May, who died in 2005 and spent much of his career at the Shalem Institute for Spiritual Formation, drew a famous distinction in his 1982 book Will and Spirit between two postures of the human will. Willfulness, in his account, is the ego’s insistence on consenting to reality only on its own terms, a posture of control that resists surrender. Willingness is its opposite: an unforced, open consent to what is, including the presence of God, other people, and one’s own inner life. May, who also wrote influentially about addiction and grace, saw willfulness not as simple defiance but as a deep structure of attachment and avoidance. Lee’s central move is to argue that digital environments do not merely distract young people; they actively train willfulness, making the ego’s demand for control feel effortless and natural.

The article coins the term “digital willfulness” to name this pattern. Drawing on what Lee calls pastoral thick description, an approach indebted to anthropologist Clifford Geertz’s method of interpreting cultures from within, the paper describes three reinforcing mechanisms. First, digital environments encourage affect regulation through immediate mediation: uncomfortable feelings are met not by sitting with them but by opening an app, scrolling, gaming, or messaging until the emotion is buffered. Second, platforms reward self-curation on strictly egoic terms, since profiles, feeds, and algorithmic mirrors invite users to present and even perceive themselves only as they wish to be seen. Third, and most theologically significant, digital life trains avoidance of unmediated presence before God, self, and others, because every moment of silence, boredom, or face-to-face exposure can be escaped with a screen.

The technical vocabulary Lee deploys here comes from several converging literatures. Emotion-regulation research, notably the work summarized by psychologist James Gross, distinguishes strategies that modify an emotional situation from strategies that avoid it altogether, and experiential avoidance has long been implicated in behavioral disorders by acceptance and commitment therapy researchers such as Steven Hayes and colleagues. The digital world, Lee suggests, industrializes avoidance. The paper also situates itself amid the heated empirical debate over social media and youth mental health, citing systematic reviews linking heavy use to depression, anxiety, and disturbed sleep, cohort studies connecting online experience to loneliness among young adults, and high-profile interventions from the American Psychological Association and the U.S. Surgeon General. Lee is careful, however, not to reduce the problem to screen-time arithmetic; the point is formational, not merely quantitative.

That formational framing draws on a lineage of pastoral theology that treats digital technology as an environment shaping desire, not just a tool. Scholars such as Kylie Agnew-Bingaman have argued that neuroplasticity itself makes contemplative practice pastorally relevant, since repeated practices physically reshape attentional circuits, while James K. A. Smith’s account of habit and liturgy argues that humans are formed by what they repeatedly love. Sherry Turkle’s studies of conversation and solitude, Shoshana Zuboff’s analysis of the attention economy, and Tristan Harris’s critiques of platform design all appear in the paper’s evidentiary spine. What these sources share, in Lee’s reading, is the insight that digital systems are not neutral containers of content; they are training regimes for the will.

Against this diagnosis, Lee proposes willingness as the central aim of spiritual formation in the digital age, and he argues that two classical practices together form what he calls a pastoral ecology of counter-formation. The first is Centering Prayer, the silent, wordless prayer form renewed by Trappist monks Thomas Keating, M. Basil Pennington, and William Meninger from sources such as The Cloud of Unknowing. In Centering Prayer, a practitioner settles into silence, consents to God’s presence, and when thoughts arise, gently returns to a sacred word. Lee reads the practice technically: it retrains attention, decouples affective reactivity from immediate soothing, and rehearses embodied consent, the very capacity that digital willfulness erodes. Empirical work gives the proposal some grounding, including a pilot study by Andres Eros and Thomas Plante on Centering Prayer and well-being in undergraduates, an intervention study by Johannes Rohde and colleagues on contemplative practice and flourishing, and earlier process research by Jason Ferguson and colleagues on prayer and everyday stress.

The second practice is spiritual direction, the ancient accompaniment described by May himself in Care of Mind, Care of Spirit and by William Barry and William Connolly. Where Centering Prayer works on attention from the inside, Lee argues, spiritual direction provides relational containment and theological discernment from the outside: a regular, unhurried, human relationship in which a digitally saturated young adult can narrate experience, notice patterns of avoidance, and interpret them theologically rather than morally. The pairing matters because neither practice alone suffices; silent prayer without discernment can become private technique, and conversation without contemplative depth can dissolve into advice. Together, Lee contends, they counter-form the will that platforms have colonized.

A fictionalized composite vignette, a recognized method in pastoral theology as practiced by researchers such as Mary Clark Moschella, illustrates the movement from digital willfulness toward willingness in a plausible pastoral case. Lee also extends the argument into territory where technology and theology collide most dramatically: the discourse of “techno sapiens” and the suggestion, surfacing in works by Yuval Noah Harari, Max Tegmark, and others, that artificial intelligence might function as a kind of deity. Recent contributions from the Vatican’s Dicastery for the Doctrine of the Faith, the theologian Noreen Herzfeld, Marius Dorobantu, and Benjamin Singler have explored whether AI can bear or mediate the divine. Lee responds by defining re-formation as the graced redirection of an ongoing formation process, and by interpreting willingness as an enacted expression of a relational imago Dei, the image of God understood not as a capacity that machines might replicate but as a mode of relation that only creatures capable of consent can live.

The paper’s constructive method means it advances proposals rather than testable hypotheses, and readers expecting new survey data will not find them; the author notes that no datasets were generated or analyzed. Yet the essay lands at a moment when both church and clinic are searching for language beyond the addiction frame. By relocating the problem from behavior to the will, Lee offers pastoral caregivers a non-shaming diagnosis: digital natives are not simply broken or addicted, but trained into a posture of control that contemplative practice can patiently unlearn. Whether the prescription of silence, consent, and unhurried spiritual friendship can compete with an economy engineered to capture attention remains the open question, and it is precisely the one this paper is designed to provoke.

Subject of Research: Gerald May's contemplative psychology applied to pastoral and spiritual care of digital natives

Article Title: From Digital Willfulness to Willingness: Gerald May’s Contemplative Psychology for Pastoral and Spiritual Care of Digital Natives

Article References: Lee, J. H. (2026). From Digital Willfulness to Willingness: Gerald May’s Contemplative Psychology for Pastoral and Spiritual Care of Digital Natives. Pastoral Psychology. https://doi.org/10.1007/s11089-026-01378-9

Image Credits: AI Generated

DOI: 10.1007/s11089-026-01378-9

Keywords: pastoral psychology, digital natives, Gerald May, willfulness, willingness, Centering Prayer, spiritual direction, spiritual formation, digital willfulness, contemplative practice, imago Dei, attention economy

The researchers set out to answer a question that has shadowed addiction neuroscience for decades: what allows drugs to drive dopamine release at intensities that ordinary rewards never reach? Their hypothesis centered on energy. Dopamine terminals in the nucleus accumbens are extraordinarily metabolically demanding structures, packed with mitochondria positioned near active zones where vesicles of dopamine await release signals. When dopaminergic neurons fire at high frequency, the energy demands of packaging, mobilizing, and releasing vesicles can outstrip local ATP supplies. Previous work had established that presynaptic mitochondria buffer calcium and synthesize ATP on demand, but whether this mitochondrial machinery was specifically recruited during drug reward—rather than reward in general—remained unknown.

To watch mitochondrial calcium in real time, the team used a genetically encoded fluorescent indicator called 4mt-jGCaMP8s, targeted to the mitochondrial matrix, expressed selectively in dopaminergic neurons of mice. Using fiber photometry, they monitored calcium signals from dopaminergic terminals in the nucleus accumbens while animals received heroin, morphine, methamphetamine, or cocaine. The results were unambiguous: heroin and methamphetamine produced robust, rapid mitochondrial calcium transients in accumbal dopamine terminals, while cocaine did not. This selectivity held up under two-photon imaging with a head-mounted microscope in freely moving animals, and the signal was strongest in the core of the nucleus accumbens, a subregion closely tied to drug seeking. Critically, when animals consumed natural rewards such as sucrose, the same terminals showed no comparable mitochondrial calcium influx.

The gateway for this calcium was identified as the mitochondrial calcium uniporter, or MCU, a channel in the inner mitochondrial membrane that was molecularly identified more than a decade ago. MCU allows calcium to flow down its steep concentration gradient into the mitochondrial matrix, where it activates calcium-sensitive enzymes of the tricarboxylic acid cycle and stimulates oxidative phosphorylation. In essence, mitochondrial calcium influx is how a mitochondrion learns that its host cell is working hard and needs more fuel. The Beijing team confirmed that the drug-evoked signals depended on MCU: in dopaminergic neurons lacking the uniporter, or in neurons treated with the MCU inhibitors Ru360 and berberine, the drug-induced mitochondrial calcium rise was abolished, while cytoplasmic calcium responses to the drugs remained intact.

Why would drugs, but not natural rewards, engage this pathway? The answer emerged from optogenetic experiments in which the researchers artificially drove dopaminergic terminals at defined frequencies. At low stimulation frequencies of around 4 hertz, mimicking the modest firing rates associated with physiological rewards, mitochondrial calcium barely moved, and deleting MCU had no effect on evoked dopamine release. But at 20 and 40 hertz—intensities characteristic of drug-evoked activation—mitochondrial calcium influx became prominent, and its absence sharply reduced dopamine release measured with the GRAB_DA2m fluorescent sensor. The conclusion is elegant: MCU-mediated mitochondrial calcium is recruited only when dopaminergic neurons are pushed beyond their normal metabolic comfort zone, which is precisely the regime that addictive drugs occupy and that natural rewards do not.

The mechanism linking calcium to release proved to be energy. Using the genetically encoded ATP sensor ATeam1.03 targeted to mitochondria, the researchers showed that drug-like high-intensity stimulation drove a rapid rise in mitochondrial ATP production that required MCU. When they blocked ATP synthesis with oligomycin, or supplied exogenous ATP to neurons lacking MCU, the picture sharpened further: ATP replenishment rescued the vesicle release deficit in MCU-deficient neurons, while ATP depletion mimicked it. Probing the vesicle machinery directly with a pHluorin-tagged vesicular monoamine transporter, the team found that the readily releasable pool of dopamine vesicles was depleted in MCU knockout neurons, and that this deficit was restored by ATP supplementation. In other words, the mitochondrial calcium influx does not directly trigger release; it manufactures the ATP that keeps the release machinery stocked during metabolically punishing bursts of activity.

The behavioral consequences were decisive. Mice engineered to lack MCU specifically in dopaminergic neurons showed dramatically reduced locomotor responses to heroin and morphine, blunted conditioned place preference for opioids, and diminished cue-induced reinstatement of cocaine seeking after extinction—a laboratory model of relapse. Circuit-specific deletion confirmed the anatomy: removing MCU only from dopaminergic neurons projecting from the ventral tegmental area to the nucleus accumbens impaired heroin reward, whereas deletion in the projection to the prefrontal cortex did not. Pharmacological validation followed. Berberine, a natural compound recently characterized as an MCU inhibitor that disrupts the channel’s assembly with its regulatory partner EMRE, reduced mitochondrial calcium uptake in cultured dopaminergic neurons, attenuated heroin conditioned place preference when microinjected into the nucleus accumbens, and suppressed cue-induced reinstatement of cocaine seeking when given systemically.

Perhaps most striking is what did not happen. Mice lacking MCU in dopaminergic neurons performed indistinguishably from controls across a battery of tests probing dopamine-dependent physiology: spontaneous locomotion, working memory in the Y-maze, anxiety-like behavior, despair-related immobility, sucrose preference, motor coordination on the rotarod, and spatial learning in the Morris water maze. Food-conditioned place preference, a model of natural reward learning, was preserved. Whole-brain MCU knockout mice, generated with Nestin-Cre, developed normally with expected Mendelian ratios and showed no deficits in dopamine-related behaviors. The therapeutic window implied by these results is unusually wide: the bioenergetic pathway appears to be dispensable for everyday reward processing yet essential for the supraphysiological dopamine output that drugs commandeer.

The study reframes addiction as, in part, a metabolic disease of synapses. Drugs of abuse differ in their molecular targets—opioids bind receptors, methamphetamine reverses transporters, cocaine blocks reuptake—but they converge on a common output: high-intensity dopaminergic activation in the accumbens. This work shows that convergence extends to the mitochondria, which are forced into emergency ATP production to sustain the pathological signal. By targeting MCU, or the calcium-driven bioenergetics it enables, it may be possible to starve the addictive circuitry of its energy supply while leaving the mitochondria of ordinary reward signaling untouched. Considerable distance remains between mouse models and human therapy, and berberine’s properties as a drug candidate will need rigorous evaluation. But the identification of a drug-selective mitochondrial mechanism offers something addiction research has rarely possessed: a molecular distinction between the dopamine that fuels compulsion and the dopamine that fuels life.

Subject of Research: Mitochondrial calcium uniporter-mediated bioenergetics in dopaminergic terminals that selectively enable drug-induced dopamine release and addictive behavior

Article Title: Mitochondrial calcium influx-driven bioenergetics selectively enable drug addiction

Article References: Gao, J., Zhao, H., Han, X., Zeng, L., Pan, J., Liu, G., Wei, X., Liu, C., Wu, W., Chen, S., Chen, J., Li, T., Yin, J., Zhou, T., Zhang, X.-M., Li, A.-L., Li, T., & Pan, X. (2026). Mitochondrial calcium influx-driven bioenergetics selectively enable drug addiction. Nature Neuroscience. https://doi.org/10.1038/s41593-026-02421-x

Image Credits: AI Generated

DOI: 10.1038/s41593-026-02421-x

Keywords: addiction, mitochondria, mitochondrial calcium uniporter, dopamine, nucleus accumbens, reward, MCU, bioenergetics, opioids, methamphetamine, ATP, berberine

The research, conducted by Joaquín Rodríguez-Ruiz of the University of Huelva along with Raquel Espejo-Siles and Izabela Zych of the University of Córdoba, appears in the International Journal of Mental Health and Addiction. It draws on the psychological concept of moral disengagement, first described by Albert Bandura and colleagues in the 1990s. Moral disengagement is the process by which people switch off their internal moral sanctions, allowing themselves to commit acts that violate their own ethical standards without feeling remorse. Mechanisms include moral justification, euphemistic labeling, advantageous comparison, and diffusion of responsibility.

Decades of research have linked moral disengagement to aggression, bullying, cyberbullying, and violence in adolescents. Evidence connecting it to substance use has been sparser. Cross-sectional studies in Australia found that moral disengagement was associated with underage drinking, heavy episodic drinking, and cannabis use among secondary school students. Research with British college athletes linked the construct to doping attitudes, and an online survey of British adults found that high moral disengagement predicted cocaine use. But cross-sectional designs cannot establish which comes first, leaving a crucial gap in understanding.

To address this, the Spanish team followed 533 adolescents, 48.1 percent female and 51.9 percent male, across three consecutive school years starting in fall 2020. Participants were on average 12.46 years old at the first assessment. The researchers measured perceived parental moral disengagement using a questionnaire asking adolescents how often their parents justified immoral behavior, with items such as my parents think it is fine to treat certain people badly. They also administered a short version of Bandura’s Moral Disengagement Scale and a substance use subscale covering legal substances like beer, wine, spirits, and tobacco, as well as illegal ones including cannabis, cocaine, and amphetamines.

The statistical strategy was rigorous. Because the data were non-normal, the team used bootstrapping with 1,000 resamples to estimate robust standard errors and compute bias-corrected 95 percent confidence intervals for indirect effects. If the confidence interval for an indirect effect excludes zero, that effect is considered statistically significant. This approach allows researchers to formally test mediation, meaning whether a third variable explains the pathway between a cause and an outcome.

The results were strikingly specific. Parental moral disengagement at the first wave showed no significant direct effect on licit substance use at the third wave. But the indirect pathway was significant. Parents who morally disengaged had adolescents who themselves scored higher on moral disengagement a year later, and those adolescents went on to report more alcohol and tobacco use the following year. The indirect effect was statistically significant with a 95 percent confidence interval that did not include zero.

Why the asymmetry between legal and illegal substances? The authors point to accessibility and perceived risk. Alcohol and tobacco are easy to obtain, widely consumed, and sometimes even reported in childhood, so parental justification may readily extend to them. Illegal drugs, by contrast, are more harmful, harder to access, and often tied to criminal settings. That severity may keep both parents and adolescents from morally excusing their use, explaining why parental moral disengagement at baseline did not predict later illicit substance use.

The theoretical framework combines Bandura’s Social Learning Theory with Robert Putnam’s Social Capital Theory. Social learning holds that children acquire attitudes and behavioral scripts from their social environment, most powerfully from parents. When a parent routinely justifies harmful behavior, the child learns a cognitive style, not just a specific attitude. Social Capital Theory adds that healthy social relationships protect against problem behavior, so a family environment saturated with moral excuses erodes one of the strongest protective resources an adolescent has.

The study has limitations worth noting. Data came from self-reports, which can be shaped by social desirability, although self-reports remain the standard tool for measuring problem behavior in adolescents. The sample was selected by convenience from 16 schools in the province of Córdoba rather than being nationally representative, and attrition from the first to third wave was 38.28 percent, mostly due to absences, school changes, and unusable codes. The authors also call for future models that account for confounders such as availability, peer pressure, and comorbid psychiatric conditions.

The practical implications are nonetheless compelling. Because the pathway from parents to substance use runs through the adolescents’ own moral disengagement, programs that strengthen adolescents’ moral competencies could interrupt the chain even when parents continue to model moral shortcuts. Schools, the authors argue, could play a central role in such efforts. And since parental involvement boosts the effectiveness of adolescent psychosocial interventions, prevention programs may need to target parents’ moral reasoning as well. This research, the first to link parental moral disengagement prospectively to substance use, suggests that the fight against adolescent drinking and smoking may begin not with the substances themselves, but with the everyday excuses families make.

Subject of Research: Intergenerational transmission of moral disengagement and its longitudinal mediation of adolescent licit substance use

Article Title: Parental Moral Disengagement and Adolescent Substance Use: The Mediating Role of Adolescents’ Moral Disengagement in a Three-Wave Longitudinal Study

Article References: Rodríguez-Ruiz, J., Espejo-Siles, R., & Zych, I. (2026). Parental Moral Disengagement and Adolescent Substance Use: The Mediating Role of Adolescents’ Moral Disengagement in a Three-Wave Longitudinal Study. International Journal of Mental Health and Addiction. https://doi.org/10.1007/s11469-026-01730-3

Image Credits: AI Generated

DOI: 10.1007/s11469-026-01730-3

Keywords: moral disengagement, parenting, adolescence, substance use, alcohol, tobacco, Social Learning Theory, longitudinal study, mediation analysis, prevention, moral development, addiction

The research, published in the International Journal of Mental Health and Addiction, draws on terror management theory, a framework inspired by the cultural anthropologist Ernest Becker. According to this theory, humans cope with the terror of mortality by embedding themselves in cultural worldviews, cultivating self-esteem, and forming secure attachments to others. These psychological buffers give people a sense that they are meaningful, valued, and connected to something larger and more lasting than their individual lives. Among the most important of these defenses is symbolic immortality: the conviction that one’s name, accomplishments, or legacy will persist in the memories of others after death.

Despite the theoretical prominence of symbolic immortality, no study had ever tested whether it is systematically linked to mental health and addictive behavior. To fill this gap, a team led by Uri Lifshin of the Hebrew University of Jerusalem and the Israel Center for Addiction and Mental Health analyzed data from 2,912 Jewish Israeli adults. The sample was quasi-representative of the adult Jewish population in terms of gender, age, religiosity, and area of residence, and the data were collected in February 2025, during the Swords of Iron war—a period of acute collective threat in which mortality was anything but abstract.

Participants completed a comprehensive battery of validated instruments. Problematic substance use was assessed with the World Health Organization’s ASSIST screening test, covering alcohol, cannabis, sedatives, prescription stimulants, and opioid painkillers. Behavioral addictions were measured with established scales for gambling, problematic pornography use, sex addiction, gaming, social media, and internet use. Psychological problems were captured through the PCL-5 for post-traumatic stress, the GAD-7 for anxiety, the PHQ-9 for depression, the Pittsburgh Sleep Quality Index, and the Difficulties in Emotion Regulation Scale. Crucially, symbolic immortality was measured with a single, deceptively simple question: do you think you will be remembered by other people after you die, for example through your accomplishments or legacy?

The results were strikingly consistent. People who believed they would be remembered reported significantly higher self-esteem, greater perceived social support, stronger national identification, stronger belief in God, and a greater sense of meaning in life. They also reported lower attachment anxiety and avoidance, the two insecure dimensions of close relationships. In other words, symbolic immortality behaved exactly as terror management theory predicts a successful anxiety buffer should: it traveled alongside every major psychological resource theorized to protect people from death-related fear.

More remarkable were the associations with clinical outcomes. Stronger belief in symbolic immortality correlated with lower levels of depression, anxiety, and post-traumatic stress symptoms, as well as fewer sleep disturbances and emotion-regulation difficulties. It was also linked to less problematic use of alcohol, cannabis, and prescription drugs, and to lower severity of gambling, pornography, sex, gaming, social media, and internet addictions. These relationships held even after the researchers statistically controlled for gender, education, political orientation, military service, relationship status, parental status, and—importantly—belief in an afterlife.

That last control proved theoretically decisive. Belief in literal immortality, such as faith in heaven or reincarnation, is the religious cousin of symbolic immortality, and the two constructs were moderately correlated in the sample. Yet their psychological profiles diverged sharply. Afterlife belief was strongly tied to religiosity and belief in God but only weakly related to self-esteem, unrelated to attachment anxiety, and essentially unrelated to any measure of psychological distress. It showed only scattered negative associations with addictions and was even positively associated with problematic internet use. Symbolic immortality, by contrast, was consistently and broadly protective. Being remembered by others, it seems, does psychological work that merely believing in heaven does not.

The authors interpret these findings through the lens of anxiety buffer disruption theory, an extension of terror management theory focused on psychopathology. When core death-anxiety buffers—attachment security, self-esteem, worldview connection, and meaning in life—are chronically or acutely shattered, death-related concerns intrude into consciousness and destabilize emotional life, producing symptoms of trauma, depression, and anxiety. Addictions, in this view, can emerge as maladaptive compensatory defenses: substances and compulsive behaviors that temporarily numb existential distress when healthier buffers have failed. Prior work by the same group found that combat soldiers exposed to life-threatening situations showed more post-traumatic stress and more problematic substance use when attachment anxiety was high and ideological identification was weak. A recent meta-analysis of 104 studies likewise found moderate associations between death anxiety and a broad range of psychiatric symptoms.

Within this framework, symbolic immortality emerges as something like the positive face of a transdiagnostic risk factor. Where fragile or broken anxiety buffers leave people exposed to death anxiety and its downstream disorders, a robust sense of symbolic immortality signals that the buffering system is functioning—loved, esteemed, meaningful, and woven into a collective story that will outlast the self. The researchers are careful to note that the study does not establish symbolic immortality as an independent causal predictor separate from the other buffers; rather, it appears to be a broad indicator that multiple protective processes are operating together.

The study has clear limitations. It is correlational, so the arrows could point in either direction or both: poor mental health and addiction may erode the social bonds, self-worth, and meaning that make people feel remembered, just as much as the reverse. Symbolic immortality was captured with a single item, and future work should develop multi-item scales that distinguish immortality beliefs across life domains, from creative legacy to descendants to national belonging. The setting is also distinctive: data were gathered in Israel during an active multifront war, when mortality salience, national identity, and collective trauma were all unusually heightened, potentially amplifying the observed associations. Cross-cultural replications, ideally in peacetime populations and clinical samples, remain necessary.

Even so, the implications are provocative. Addictive behaviors of the kind studied here rarely appear in wild animals, and the authors suggest a reason: addiction may be partly rooted in the existential problems that only humans face—awareness of death, meaninglessness, and uncertainty—and in the fragile cultural technologies we use to manage them. If the sense of being remembered is one of those technologies, then interventions that strengthen legacy, belonging, and meaning may do more than comfort the dying. They may help protect the living from despair and compulsion, offering a scientifically grounded answer to a question as old as Jimi Hendrix’s castles made of sand: what, exactly, keeps the sea at bay?

Subject of Research: The association between belief in symbolic immortality and mental health problems and addictions, examined through terror management theory

Article Title: Symbolic Immortality, Mental Health, and Addictions: A Terror Management Perspective

Article References: Lifshin, U., Shmulewitz, D., Levitin, M. D., Skvirsky, V., Cherniak, A. D., & Mikulincer, M. (2026). Symbolic Immortality, Mental Health, and Addictions: A Terror Management Perspective. International Journal of Mental Health and Addiction. https://doi.org/10.1007/s11469-026-01720-5

Image Credits: AI Generated

DOI: 10.1007/s11469-026-01720-5

Keywords: symbolic immortality, terror management theory, death anxiety, mental health, addiction, substance use, behavioral addictions, anxiety buffer disruption, depression, PTSD, meaning in life, existential psychology

The scale of the problem is staggering. According to the review, an estimated 4.3 million people in the United States meet diagnostic criteria for stimulant use disorder, nearly a quarter of them aged 25 or younger. National overdose deaths involving stimulants rose nearly 34-fold between 2002 and 2022, and 182,502 stimulant-related overdose deaths were reported between 2021 and 2024. More than 60,000 stimulant-related overdose deaths have been recorded annually in recent years, with 43.1 percent of stimulant-involved deaths between January 2021 and June 2024 also involving opioids. Black or African American and American Indian or Alaska Native communities have experienced disproportionately steep increases in stimulant-involved deaths, adding an urgent health equity dimension to the crisis.

Yet while medications exist for opioid, alcohol, and tobacco use disorders, stimulant use disorder remains one of the few major substance use disorders with no FDA-approved drug therapy, leaving clinicians dependent on behavioral interventions with limited long-term efficacy. It is against this backdrop that the LSU team examined the theoretical potential of Brixadi. Brixadi is an extended-release injectable buprenorphine that uses a fluid-crystal depot delivery system: after subcutaneous injection, the solution solidifies into a viscous crystalline gel that gradually releases the drug over one week or one month, producing stable plasma concentrations and sustained receptor occupancy. Peak plasma levels occur roughly 20 hours after injection, and steady state is reached by the fourth dose, with half-lives ranging from 3 to 5 days for weekly injections and 19 to 26 days for monthly ones.

Buprenorphine’s pharmacology is what makes the hypothesis plausible. The drug is a partial agonist at the mu-opioid receptor and an antagonist at the kappa-opioid receptor, binding with exceptionally high affinity—reported inhibition constants of approximately 0.2 nanomolar at the mu receptor and 0.07 nanomolar at the kappa receptor—and dissociating slowly. That ceiling effect on respiratory depression and euphoria underpins its favorable safety profile, while its high affinity allows it to displace full agonists such as fentanyl and heroin from receptors. But for stimulant addiction, the kappa receptor is the critical piece. Kappa-opioid receptors respond to dynorphins, endogenous peptides that suppress dopamine signaling in the mesolimbic reward pathway and generate dysphoria, stress responses, and drug craving. Chronic stimulant use upregulates prodynorphin transcription, elevating dynorphin levels and pushing the brain into a low-dopamine state that drives further drug seeking in a self-reinforcing loop.

Animal research supports this framework. Methamphetamine exposure increases dynorphin expression in the nucleus accumbens and preclinical cortex, and in mouse studies by Whitfield and colleagues, kappa receptor activation during abstinence appeared to create neuroadaptations that made methamphetamine more appealing, essentially fueling relapse through negative reinforcement. Conversely, pharmacologic blockade of the kappa receptor has, in some animal models, reduced drug-seeking behavior or methamphetamine self-administration, although the effects have not been uniform across species and paradigms. In rodents and rhesus monkeys, buprenorphine has also been shown to decrease cocaine self-administration and cocaine-seeking behavior, and rodent studies suggest buprenorphine reduces methamphetamine consumption and drug seeking partly through activation of the nociceptin/orphanin FQ peptide receptor.

Human evidence remains thin but intriguing. A double-blind randomized clinical trial by Ahmadi and Razeghian Jahromi found that buprenorphine reduced methamphetamine craving during withdrawal more effectively than methadone, though the 17-day trial could not determine whether the effect persisted or prevented relapse. Trials of concurrent opioid and cocaine dependence have reported reductions in cocaine use and craving with buprenorphine, and a combination of buprenorphine and naltrexone blocked compulsive cocaine intake in rodents without producing opioid dependence. Buprenorphine’s antidepressant-like effects in animal models—mediated through kappa receptors and stress modulation—further suggest it may blunt the hyperkatifeia, the intensified negative emotional state, that fuels relapse during stimulant withdrawal.

The strongest practical argument, however, may lie in polysubstance use. Toxicologic data show that 89.6 percent of individuals presenting for opioid use disorder treatment test positive for more than one substance, with a mean of 3.3 substances per person and up to 11 detected in some cases. Approximately one-third of individuals with opioid use disorder use stimulants concurrently, methamphetamine use in this population has risen by more than 80 percent, and over half of US overdose deaths from 2018 to 2024 involved concurrent opioid and stimulant use. Because opioid and stimulant use disorders converge on overlapping dopamine, reward, and stress circuitry—psychostimulants acting directly on dopaminergic transporters and opioids disinhibiting dopamine release indirectly—stabilizing the opioid component may disrupt the reinforcing environment sustaining stimulant use. Notably, when patients remained in buprenorphine treatment, one study found a 15 percent absolute reduction in methamphetamine use at six months, even though methamphetamine use predicted lower treatment retention overall.

Brixadi’s depot formulation may add distinct advantages in this population. Long-acting buprenorphine formulations have achieved treatment retention rates above 60 to 70 percent at six months, and maintenance on buprenorphine is associated with a greater than 50 percent reduction in all-cause mortality compared with no treatment. Monthly or weekly injections remove the daily adherence burden that trips up patients experiencing housing instability or limited transportation, minimize peak-to-trough fluctuations, and keep patients engaged in care long enough to benefit from behavioral therapies such as contingency management, the intervention with the best evidence for stimulant use disorder. The authors frame this as harm reduction: buprenorphine does not directly treat stimulant craving, but stabilizing opioid dependence may reduce chaotic polysubstance patterns, lower overdose risk, and create openings for broader therapeutic engagement.

The review is candid about its limitations. Brixadi is not approved for any stimulant use disorder, no clinical trial has demonstrated that buprenorphine reduces methamphetamine or cocaine use as a primary outcome, and much of the kappa-antagonism rationale rests on preclinical models and neurobiologic theory. Larger, well-controlled clinical trials are needed to determine whether the proposed mechanisms translate into meaningful reductions in stimulant use, craving, and relapse. Still, the convergence of an unmet clinical need, a well-characterized safety profile, plausible stress-and-craving pharmacology, and enormous polysubstance overlap makes the proposition difficult to ignore. With more than 60,000 stimulant-related deaths each year and no approved medication in sight, the authors argue that Brixadi’s extended-release profile and potential to counter withdrawal-related dysphoria and stress-induced drug seeking present a compelling case for accelerated clinical investigation.

Subject of Research: Evaluation of extended-release injectable buprenorphine (Brixadi) as a potential pharmacotherapy for stimulant use disorder

Article Title: Brixadi for Stimulant Use Disorder: Evolving Pharmacologic Considerations and Clinical Implications

Article References: Brixadi for Stimulant Use Disorder: Evolving Pharmacologic Considerations and Clinical Implications. (n.d.). https://doi.org/10.1007/s12325-026-03772-4

Image Credits: AI Generated

DOI: 10.1007/s12325-026-03772-4

Keywords: Brixadi, buprenorphine, stimulant use disorder, methamphetamine, cocaine, kappa-opioid receptor, dynorphin, polysubstance use, opioid use disorder, harm reduction, pharmacotherapy, addiction

Theory of Mind, often abbreviated as ToM, is the cognitive machinery that allows humans to attribute mental states to others and to predict behavior on that basis. First described in the landmark 1978 question of whether chimpanzees possess a theory of mind, the capacity depends on a distributed network of cortical regions, particularly the prefrontal, insular and cingulate areas. Those same regions are among the most consistently altered in people with substance use disorder, whether through reduced cortical volume, disrupted connectivity or changes in neurochemistry. This anatomical overlap is one reason researchers have long suspected that psychoactive substances could compromise the ability to understand other people.

Previous syntheses had already documented ToM problems among people with alcohol use disorder, with effect sizes ranging from moderate to very large. Meta-analyses of facial emotion recognition, a related social-cognitive skill, also pointed to deficits among alcohol and substance users. But evidence on substances other than alcohol remained scattered. The only earlier systematic review covering the broader landscape, published in 2016, found relatively weak evidence for ToM impairments linked to methamphetamine and no impairments among recreational cocaine users. The new study, led by José Vitor de Lima Neto and Flavia de Lima Osório of the University of São Paulo, set out to resolve that uncertainty with a formally registered, PRISMA-guided search of eight databases including Embase, Scopus, PsycINFO, Web of Science, PubMed, PsycNet, LILACS and SciELO.

The review included original quantitative studies comparing Theory of Mind performance between adult psychoactive substance users and controls. After screening, 37 studies met the criteria, and 30 of them—covering 35 distinct samples—provided data suitable for meta-analysis. Most of the research originated in Europe, with 70 percent of studies conducted there, and the field’s first study dates only to 2006, making this a young but rapidly growing literature. Alcohol was the predominant substance studied, accounting for roughly half of the samples, followed by stimulants, opioids, cannabis and a single study involving the hallucinogen MDMA. Participants were mostly men, with a mean age of about 37 years, and were largely recruited from inpatient detoxification clinics.

The pooled result was striking. Across the meta-analyzed samples, substance users showed significantly poorer Theory of Mind performance than controls, with a standardized mean difference of −0.80, a large effect by conventional statistical standards. The 95 percent confidence interval ran from −1.13 to −0.47, well clear of zero. Heterogeneity was high, at roughly 93 percent, reflecting the diversity of instruments, populations and study designs, but sensitivity analyses removing statistical outliers left the overall estimate essentially unchanged. Publication bias tests, including Begg’s rank correlation test and funnel plot inspection, found no evidence that negative findings were being suppressed.

Subgroup analyses revealed something perhaps even more consequential: the impairment did not appear to depend on which substance was used. Samples of alcohol users produced an effect size of −0.92, opioid users −1.12 and stimulant users −1.29. A formal between-group test found no statistically significant differences among these classes, with overlapping confidence intervals pointing to a common magnitude of deficit. The authors also tested whether the choice of assessment tool mattered, given ongoing debate about the Reading the Mind in the Eyes Test, the most frequently used instrument in this literature. A mixed-effects meta-regression comparing studies that used the Eyes Test with those using other measures found no significant moderating effect, suggesting the deficits are not an artifact of one particular task.

Two theoretical explanations dominate the interpretation of these findings, and they are not mutually exclusive. The first is neurotoxicity: chronic exposure to alcohol, opioids or stimulants damages or dysregulates precisely the prefrontal, insular and cingulate circuits that Theory of Mind depends upon, and decades of neuroimaging work document structural and functional changes in these regions among people with substance use disorder. The second is vulnerability: weak social cognition may predate substance use, increasing susceptibility to social stress, isolation and exclusion, and leading individuals to use substances as a way of coping with relational difficulties or of conforming to perceived social norms. Supporting the vulnerability hypothesis, a 2022 meta-analysis found an inverse relationship between alcohol-related problems and ToM performance even in non-clinical samples, where use never reached diagnostic thresholds.

The new review itself is cross-sectional in its evidence base, with 36 of the 37 included studies using cross-sectional designs, so causality cannot be established. The authors are explicit that their pooled estimate should be read as evidence of association rather than cause. They also note that the two mechanisms likely interact in a self-reinforcing loop: a primary ToM weakness predisposes someone to use substances, chronic use then intensifies the deficit through neurotoxic effects, and the deepened impairment in turn hinders therapeutic adherence and relapse control. Interestingly, one study in the review found that long-term MDMA users actually performed better on Theory of Mind tasks than non-users, a finding consistent with evidence that the pursuit of empathetic social experience motivates MDMA use—though it rests on a single study.

Important gaps remain. Evidence on cannabis, hallucinogens and nicotine is too sparse for meta-analysis; two cannabis studies found no significant differences, though the tasks used assessed affective rather than cognitive ToM, a subdomain that may be selectively vulnerable given cannabis-linked frontal reductions. Methodological quality across the field was only moderate, most samples came from high-income countries, inpatient recruitment may have inflated severity, and polysubstance use and psychiatric comorbidities were rarely controlled. Nevertheless, the authors argue the practical message is clear: sociocognitive skills deserve formal assessment in both prevention programs and addiction treatment, because deficits in reading minds can raise vulnerability to initiating use, undermine therapy and complicate recovery long after detoxification ends.

Subject of Research: Theory of Mind deficits among psychoactive substance users

Article Title: Theory of Mind in Psychoactive Substance Users: A Systematic Literature Review and Meta-analysis

Article References: Neto, J. V. D. L., & Osório, F. D. L. (2026). Theory of Mind in Psychoactive Substance Users: A Systematic Literature Review and Meta-analysis. International Journal of Mental Health and Addiction. https://doi.org/10.1007/s11469-026-01717-0

Image Credits: AI Generated

DOI: 10.1007/s11469-026-01717-0

Keywords: Theory of Mind, psychoactive substances, substance use disorder, social cognition, meta-analysis, alcohol, opioids, stimulants, addiction, prefrontal cortex, mental state attribution, systematic review