The Interplay between Social Pain and Addiction

A spectre is haunting North America—the spectre of addiction. Newspaper articles and journal cover pages proclaim the era of the “Opioid epidemic.” Depositaries for used needle tips have become ubiquitous within gas station bathrooms, and naloxone kits adorn the walls of all workplaces. A crisis that originated with standard prescription pain medication, such as Vicodin and Oxycodone, has metamorphosed into a catastrophe with the rise of fentanyl. Because of its sheer potency—roughly 50 to 100 times that of morphine—fentanyl has become quasi-metonymic for overdose. Indeed, Christie (2021) reports that in 2018, an average of 130 people died from opioid overdose in the United States alone, which represents an astronomical increase of 400% from 1999. Addiction, however, is not confined solely to opioids, as the prevalence of alcohol, cocaine, methamphetamines, or benzodiazepines can attest. Nor is it limited to foreign substances, given the rates of gambling, sex, and work addiction within our societies. In what follows, we will argue that addiction is deeply intertwined with the experience of social pain and that substance use often functions as a compensatory mechanism for disrupted attachment and trauma-induced dysregulation of our endogenous opioid systems.

Any such investigation must begin by attending to the human condition. Ever since our primordial ancestors emerged from the forests and banded together as hunter-gatherers, the importance of social bonds has been paramount to us. Our descent from a world wherein exile from one’s tribe effectively constituted a death sentence has left us evolutionarily predisposed for relationality. Taylor and Gonzago (2007) posit, therefore, that while stress is commonly construed as causing a fight or flight response in humans, it may be that stress predominantly engenders us to “come together as a group” (p. 456-457). They claim that human beings have neural circuitry that intrinsically motivates us to maintain at least a baseline level of social relationships (Taylor and Gonzago, 2007). If affiliations fall below that threshold, oxytocin acts as a biological signal that prompts social behaviour aimed at resolving the tension; when such social behaviour is rebuffed, however, stress becomes heightened (Taylor & Gonzago, 2007). This notion that social pain serves as a “call to action” is corroborated by the work of Naomi Eisenberger.

In their groundbreaking study, Moieni and Eisenberger conclude that physical and social pain share a neural correlation. They begin by observing the plethora of figures of speech that connect the two experiences. For instance, a broken heart is used to signify tremendous emotional pain, yet it is a physical metaphor: the same is true of hurt feelings; one cannot literally “hurt” feelings as one might a finger (Moieni & Eisenberger, 2016, p. 204). Yet, as there is no specific word that designates social pain in the English language, metaphors are all that is available to us (Moieni & Eisenberger, 2016).

Moieni and Eisenberger (2016) divide pain into two subcomponents: the sensory component, which is involved in the identification of “discriminative aspects of pain such as location, quality, and intensity,” and the affective component, which “is associated with detecting the subjective experience of pain,” such as how upsetting or aggravating the pain is (p. 205). Each subcomponent has its corresponding neural network responsible for processing it. In the case of sensory pain, processing is mainly performed by the primary and secondary somatosensory cortex and the posterior insula, as made evident via human lesion studies (Moieni & Eisenberger, 2016). Meanwhile, affective pain is computed by the dorsal anterior cingulate cortex and the anterior insula, as activity in both regions “correlates with the self-reported unpleasantness of pain” (Moieni & Eisenberger, 2016, p. 206). Because dACC and AI activity have been linked to behaviour motivated to escape pain, Moieni and Eisenberger posit that these neural networks also underlie “the experience of social pain in order to prevent the dangers that may result from social exclusion” (2016, p. 207).

There are numerous reasons to connect the dACC and AI to the experience of affective pain, several of which originate within lesion studies. As Moieni and Eisenberger (2016) observe, infants within mammalian species are dependent on maternal care for survival; thus, any estrangement from their caregiver results in separation anxiety and distress vocalizations on the part of the infant. These vocalizations may not reflect social pain per se, but they stem from social separation and are, therefore, directly related to ACC activity (Moieni & Eisenberger, 2016). Brain lesions of the dACC and vACC in monkeys have been linked to a reduction in such distress vocalizations, whereas exogenous electrical stimulation of the dACC and vACC prompted vocalizations (Moieni & Eisenberger, 2016). Furthermore, in humans, Moieni and Eisenberger note that people who have undergone cingulotomy (a surgical procedure that lesions a section of the Anterior Cingulate Gyrus) are less self-conscious and less concerned about social judgment, suggesting that the ACC plays an active role in human social experience (2016). Due to this multitude of circumstantial evidence, Eisenberger sought to conduct a study to precisely measure the neurological effect of social pain.

Eisenberger conducted her study by having participants play a simulated game of cyberball, wherein players toss a ball back and forth to one another (Moieni & Eisenberger, 2016). Although the participants believed that they were playing with two other participants, they actually played against pre-programmed avatars. The avatars were set to include the human participant at the beginning of the game, but then to exclude them entirely by tossing the ball only between themselves (Moieni & Eisenberger, 2016). Eisenberger had her participants fill out self-reports regarding their social distress while also monitoring their brain response during the cyberball game and found that greater dACC activity was predictive of higher reported distress (Moieni & Eisenberger, 2016). Eisenberger also focused specifically on participants who had either undergone a recent romantic breakup or who had suffered the loss of a loved one, and in both cases, viewing context relevant photos (i.e. of their romantic rejector or deceased loved one) initiated greater dACC activity than did viewing randomized stranger photos (Moieni & Eisenberger, 2016).

Of those participants who were socially excluded in cyberball, Moeini and Eisenberger report that the participants with more social support showed less dACC activation (2016). Moeini and Eisenberger (2016) observe, however, that “factors thought to increase sensitivity to social exclusion are associated with increased activity in the dACC and AI” (p. 209). These factors included socially isolated participants, those with greater “interpersonal sensitivity,” individuals with lower self-esteem, and participants with anxious attachment styles (Moieni & Eisenberger, 2016, p. 209-210). Given that the affective component of physical pain and social pain are both correlated with dACC and AI activity, Moieni and Eisenberger hypothesize that “factors that decrease physical pain” (i.e. opiates) ought to also relieve social pain: they cite a 2010 study by DeWall et al. that showed that participants taking only over-the-counter Tylenol had lower self-reported distress and less dACC and AI activation in response to social exclusion (2016, p. 216). Moreover, Moieni and Eisenberger demonstrate that factors that perpetuate physical pain also engender social pain: inflammation is tied to both increased physical pain and “feelings of social disconnection,” and participants who were socially excluded at cyberball reported exaggerated feelings of physical pain when exposed to painful stimuli (2016, p. 216).

I find the correlation that Moieni and Eisenberger unearth between social maladaptation and heightened sensitivity to social exclusion to be particularly salient to the field of addiction studies, as there is a multifaceted history of research into the negative effects of trauma and adversity on one’s propensity for addiction. This scholarship is a great aid to comprehending the propensity of addiction among the Indigenous peoples of North America. As stated in a 2021 paper by Julie Gameon and Monica Skewes, “American Indians and Alaska Natives have… disproportionately high rates of substance use disorders” (p. 295). It cannot be argued that Indigenous peoples simply suffer from a greater innate propensity for addiction, as there is no evidence to suggest that Indigenous peoples ever struggled with addiction pre-colonization. It is only post-colonization, in a society where Indigenous peoples have been forcibly removed from their ancestral homelands, shunted onto reserves, and have had their traditions, cultures, and languages systematically attacked in order to force them to assimilate, that addiction has become a widespread problem. Their situation can only be understood when one considers the immeasurable pain and chaos that such social dislocation must have and still does entail. Gameon and Skewes report that “psychological and physical health problems” are common within “historically oppressed groups.” This phenomenon is referred to as a “historical trauma response” that is derived through “intergenerational transmission of trauma” (2021, p. 296).

Gameon and Skewes (2021) note that such a response culminates in intense feelings of “grief, anger, depression, and anxiety,” especially in conjunction with reflecting on collective cultural suffering (p. 296). Greater historical trauma rumination has been correlated with increased “depressive symptoms, suicidal ideation, and substance use,” suggesting that substance usage may be an attempt at alleviating psychological distress (Gameon & Skewes, 2021, p. 297). That substance abuse is interpreted as a coping mechanism would come as no surprise to Gabor Maté. The Canadian psychologist has long been at the forefront of addiction studies, his interest stemming from the effect that his experience as a Jewish infant born in 1944 in Eastern Europe had on him, as well as his 12 years of service at a methadone clinic in Eastern Vancouver.

Maté believes that addiction’s root is primarily in early childhood adversity and negative attachment styles. He notes (2012) that healthy interactions between caregivers and infants stimulate natural opioid production within the infants. It is these endogenous endorphins that facilitate the establishment of a secure attachment relationship as well as assist proper development of the infant’s opioid and dopamine neural circuitry (Maté, 2012). Given that the mammalian infant is utterly dependent on its caregivers for survival, the actualization of secure attachment is imperative. The secure infant internalizes that the external world is safe, loving, and caring, while the insecure infant becomes convinced of the precise antithesis. Maté argues that absentee or inadequate caregiving prompts a stress response in the infant, causing the maldevelopment of opioid and dopamine circuitry directly linked to addiction (2012). This effect has been observed in rat pups, who, when separated from their mothers in early infancy, “displayed permanent disruption” within midbrain dopamine circuitry that plays “a key role in the onset of addiction and craving” (Maté, 2012, p. 57). Maté (2012) also reports that monkeys separated from their mothers and raised amongst peer groups exhibit far greater levels of aggression and alcohol consumption than control groups: he summarizes, “Children who suffer disruptions in their attachment relationships will not have the same biochemical milieu in their brains as their well-attached and well-nurtured peers. As a result, their experiences and interpretations of their environment, and their responses to it, will be less flexible, less adaptive, and less conducive to health and maturity” (p. 58).

In short, the insecurely attached infant internalizes a mental framework of a hostile world, which subsequently clouds their interactions with it and leaves them more vulnerable to socio-emotional pain. What also cannot be discounted, Maté (2012) notes, is the damage wrought by childhood trauma, which the renowned CDC study on Adverse Childhood Experience, running from 1995-1997, helped illuminate. The ACE study examined ten disparate categories of potential trauma that might occur in a child’s life (e.g. divorce, sexual abuse, the death of a parent) and then investigated whether a correlation between the frequency of such events and later substance abuse exists (Maté, 2012). The study revealed that any such traumatic instance culminated in an approximate 200-400% increased likelihood of addiction (Maté, 2012). If one considers that a child experiencing one such event has a much-increased probability of experiencing more such events (if a child is sexually abused, for example, the odds are that there is more nefarious activity at play), the implications are shocking. Indeed, Mate (2012) cites a study by Dube et al. that posits over 60% of “injection drug use can be attributed to abusive and traumatic childhood experience” (p. 59). Trauma impacts such children, Mate says, by establishing a “lower set point” for stress, resulting in enhanced anxiety within adulthood (2012, p. 60). Mate (2012) concludes, “Not all addicts were subjected to childhood trauma, just as not all severely abused children grow up to be addicts. However, clinical experience has shown that a majority of hardcore injection users were subjected to childhood trauma” (p. 59).

Most injected drugs are species of the opioid family, and Williams, Cole, Girdler, and Cromeens (2022) also explicitly connect opioid abuse with trauma. Commenting on the approximately 50,000 annual fatalities from opioid overdose in the United States, Williams et al. (2022) postulate that such mortality is surely correlated with the widespread experience of interpersonal trauma. Williams et al. (2022) report that 60% of individuals suffer interpersonal trauma and that such individuals “experience disproportionately high rates of adverse health and social outcomes, including opioid misuse” (p. 120). Victims of trauma are more likely to be prescribed and to abuse opioids than people lacking a traumatic background (Williams et al. 2022). What appears to be crucial vis-à-vis resisting opioid addiction is what Williams et al. (2022) define as personal resources (i.e. “coping strategies, self-efficacy, [and] social support”) (p. 120). What is meant by social support is the support available to an individual in the form of friends, family, community, and social groups (Williams et al., 2022). Williams et al. (2022) observe similar findings to Moieni and Eisenberger (2016), noting that social connection ameliorates chronic pain, benefits physical functioning, and aids health outcomes for individuals addicted to opioids (p. 120).

Such an effect is precisely what the work of Kyte, Jerram, and Dibase would predict. They remark that what compels people to engage in maladaptive behaviour (e.g. addiction) is that such behaviour serves “the basic survival function of quelling physical or emotional distress” (2020, p. 12). Ktye et al. (2020) claim that although other neurotransmitters are also implicated in social connection (e.g. dopamine, oxytocin, serotonin), the human endogenous opiate system is vital for all our “relational processes” (p. 12). Christie (2021) echoes this sentiment, conceding that while oxytocin is critical to the initial formation of social bonds, the role of oxytocin in the maintenance of said bonds is exaggerated due to an over-reliance on rodent studies. Humans are among some primates that contain the capacity for life-long bonds “between non-kin individuals,” and Christie (2021) posits that this capacity is attributable to our endogenous opioid system (p. 651). As evidence for the connection between internal opioids and social bonding, Christie (2021) submits the fact that the administration of exogenous opioids reduces maternal care within rat populations. If endorphins reinforce maternal care, then a reduction in such care due to compensatory external opioids is logical. Moreover, social touch has been directly linked to endorphin production, which is why parents are encouraged to maximize skin-to-skin contact with newborns (Christie, 2021). Animals engaging in rough social play with one another show elevated levels of internal opioid production, as do animals exhibiting grooming behaviour (Christie, 2021). Indeed, grooming behaviour can be eliminated through the application of external opioids and also increased through administering the opioid counteragent naloxone, which suggests that when grooming behaviour does not result in the typical endorphin reward due to naloxone blockage, animals demonstrate greater urgency to groom in order to generate endogenous opioid production (Christie, 2021).

Evidence for the interplay between opioids and social connection extends beyond animal studies to anecdotal human reports. Christie (2021) recounts that opioid users frequently describe the drug in loving terms, as their language conveys a sense of “social warmth and connection” (p. 651). Several examples of this are the comparison of being high on heroin to being held by your mother, of it being the intimate hug you have ever experienced, or “[it being] like a hug from your grandma” (Christie, 2021, p. 651). Even the English author Thomas De Quincey, writing several centuries previously in Confessions of an English Opium-Eater (1821), puts it similarly: “Oh just, subtle, and mighty Opium! That to the hearts of poor and rich alike, for the wounds that never heal… bringst an assuaging balm… to the guilty man for one night givest back the hopes of his youth, and hands washed free from blood… Thou only givest these gifts to man and thou hast the keys to Paradise” (no page number). That opium—a narcotic and opiate—provides solace to never-healing wounds is particularly telling. It illuminates why those of us with a history of trauma are more obedient to addiction’s siren call: their wounds are greater, seemingly unhealed.

We see then that the formation of human social bonds is evolutionarily hardwired into our species and reliant upon our endogenous opioid system. We also must acknowledge that we possess neural networks that underlie our experience of social pain and are meant to facilitate our maintenance of social bonds. Lastly, we note that those of us who have been subject to more suffering and childhood adversity exhibit a greater propensity for addictive behaviour. To fully understand why this is the case, we must briefly revisit Moieni and Eisenberger’s cyberball findings, specifically their discovery that the social distress and heightened dACC and AI activity resulting from cyberball exclusion were more pronounced among socially isolated participants. Suppose it is also the case, as Christie and Kyte et al. contend, that the social relations so essential to our well-being are reinforced via internal opiates. In that case, it is perfectly logical that when our innate need for social connection remains unfulfilled, we turn to external compensatory means. Therefore, addiction acts as a pacifier for our socio-emotional pain: this explains why, as Maté highlights, trauma goes hand in hand with addiction.

Unfortunately, though, the addictive cycle is vicious and Sisyphean. Christie (2021) summarizes it well: The individual whose endogenous opiate system has become maladaptive and ineffective due to social isolation turns to external opiates in order to supplement the lacuna. However, their constant desire to acquire and use such drugs only serves to further erode their social ties, causing them to chase the drug even more, which results in even more alienation from society (Christie, 2021). Christie (2021) offers a heartbreaking encapsulation of the interplay between social isolation and addiction in a survey of opioid overdoses in West Virginia counties. West Virginia was chosen because it has the highest rate of opioid overdoses in the United States. What Christie discovered perfectly matches our theory of addiction as a pacifier. The counties with the lowest amount of social capital were also the counties with the highest rates of opioid overdoses, leading her to proclaim that “the opioid epidemic… can be viewed as an epidemic of social isolation and a lack of belongingness, which people are mitigating through the use of opioids” (Christie, 2021, p. 650-652).

How might we pull back from the brink? While it transcends the confines of this paper to propose a solution to the problem of opioid addiction, I do want to note that social support serves as a buffer against social pain. This is attested by the work of Moieni and Eisenberger (2016), who observed that participants who reported spending more time with their friends displayed less social distress from cyberball exclusion. It is also corroborated by the study performed by Williams et al. (2020), wherein they discovered that individuals with the highest number of personal resources showed the greatest resistance against opioid misuse. The data suggests, then, that to fight this spectre, we must come together. We have been wounded in relationships, but we will only find healing within relationships. Therefore, if we desire to respond meaningfully to the opioid crisis, we must reframe addiction not as a problem of character or will but instead understand it as the embodied cry of social and emotional pain—pain that demands connection, not punishment. May we all find healing.

References

Christie, N. (2021). The role of social isolation in opioid addiction. Social Cognitive and Affective Neuroscience, 16, 645-656.

DeQuincey, T. (1821). Confessions of an english opium-eater. Retrieved from Project Gutenberg website: http://www.gutenberg.org/files/2040/2040-h/2040-h.htm

Eisenberger, N., & Moieni, M. (2016). Neural correlates of social pain. In Harmon-Jones, E., & Inzlicht, M. (Eds.) Social Neuroscience: Biological approaches to social psychology. Routledge: Taylor & Francis Group.

Gameon, J. A., & Skewes, M. C. (2021). Historical trauma and substance use among american indians with current substance use problems. Psychology of Addictive Behaviours, 35, 295-309.

Kyte, D., Jerram, M., & Dibiase, R. (2020). Brain opioid theory of social attachment: A review of evidence for approach motivation to harm. Motivation Science, 6, 12-20.

Maté, G. (2012). Addiction: Childhood trauma, stress and the biology of addiction. Journal of Restorative Medicine, 1, 56-63.

Taylor, S.E., & Gonzaga, G.C. (2007). Affiliative responses to stress: A social neuroscience model. In Harmon-Jones, E., & Winkielman, P. (Eds.). Social neuroscience: Integrating biological and psychological explanations of social behaviour. Guilford Press.

Williams, J., Cole, V., Girdler, S., & Cromeens, M. (2022). Personal resource profiles of individuals with a history of interpersonal trauma and their impact on opioid misuse. Psychological Trauma: Theory, Research, Practice, and Policy, 14, 119-130.