Intergenerational continuity in substance use and parental beliefs

The intergenerational continuity of substance use is well established [5,6,7] with multiple prospective longitudinal studies demonstrating the continuity of SUD across three generations [8]. Research on the intergenerational transmission of SUD focuses on teasing out the mechanisms and associations that underlie intergenerational continuity [4, 9, 10]. While the etiology of SUD is multi-determined, an example of developmental equifinality, heritability estimates suggest genetic factors account for approximately 50% of the risk for SUDs [11]. There has been increasing emphasis on the genetic and/or neurobiological basis of addictive behaviors in research [12], the popular press, and in many interventions as the primary explanatory model underlying SUD. A recent meta-analysis of genome-wide association (GWAS) studies involving over one million participants, has underscored the complex, probabilistic and polygenic nature of risk across SUDs and for substance specific pathways [13]. More limited, however, has been research considering how parents with SUDs understand and respond to the risk of the intergenerational transmission of SUD [11], particularly in the context of epidemiological and clinical-intervention models that emphasize genetic vulnerabilities.

Parents’ sense-making around the information they receive about addiction and its intergenerational transmission is as important as it is poorly understood. If parents come to view their children’s risk as linear, deterministic, and inevitable (e.g., ‘in their genes’), a self-fulfilling prophecy may be set in motion with the power to shape their investment in and motivation for treatment, parenting behavior and, in a transactional manner, parent-child relationship patterns across a child’s development [14, 15, 16]. Linear and deterministic beliefs may then impact parental mental models of their child’s future and contribute to negative perceptions and downstream effects on parenting behaviour. Conversely, parents who understand their children’s risk for later addiction to be probabilistic, and modifiable may actively seek intervention, be more engaged in treatment, or attend to environmental and parenting factors that may be more amenable to treatment and also influence substance use, in order to prevent future addiction for their children.

Whichever the case, we have relatively little empirical knowledge about how parents with SUD conceptualize the impact of their ‘personal histories of inheritance’ on their young children’s future risk of developing a SUD. Although many studies examine the etiology of continuity of SUD within families [4, 8,9,10, 17], there is less research that examines how parents with a SUD understand and respond to the risk of intergenerational transmission [14, 18, 19]. This work seeks to fill this gap, building a theory about parents’ understanding of their children’s risk for the later development of a SUD. Examining the sense-making [17] of parents in SUD treatment about the risk of intergenerational transmission of SUD helps identify how families interpret and then respond to risk for conditions that have complex etiological origins.

Explanations for the intergenerational transmission of substance use

Explanations for the intergenerational transmission of SUD are multi-factorial. Decades of research point to contributions of genetics [9, 12], family interaction patterns [20,21,22,23] and family and community norms [24,25,26] as influencing the continuity of SUD in families. These different explanatory factors are examined in more detail below.

Briefly, twin studies demonstrate genetic links related to the quantity and use of specific substances. More recent research considers the genetic risk of SUD to be linked to sensitivities in the Brain Reward Cascade, which controls the release of dopamine [24]. Deficiencies or variations in this system of neurochemicals may heighten the individual risk of SUD. While some studies have not shown an association between specific genes or neurochemical clusters, others assert that anywhere between 25 and 75% of risk for the development of SUD is attributable to these genetic causes [4, 24]. Research in genetics and neurobiology suggests strong associations between neurochemical vulnerabilities and later development of SUD. These associations, however, are probabilistic with great variation in the strength of the associations and genetic researchers employing GWAS strategies to identify loci probabilistically important to SUDs, have highlighted the challenge and limitations of the polygenic nature of substance use disorders [27]. For example, the Virginia Twin study demonstrated that while genetic vulnerabilities were a factor in the development of adolescent SUD, familial and peer-related factors were more likely to influence later use than genetic vulnerabilities [25]. Similarly, a Swedish study examining adopted and non-adopted children of parents with SUD found that adopted children who received sensitive and consistent care were less likely to develop a SUD than children raised by their biological parents [26]. These studies make a strong case for how environmental influences transact with genetic vulnerabilities to shape later development of a SUD. Genetic predispositions to SUD are, therefore, probably best understood in dynamic relation to their environmental and other contextual factors.

Children’s exposure to parental substance use can occur in multiple forms in addition to genetics: children can be exposed chemically to substance in utero and exposed socially through parental use at any stage in the life course [28, 29]. The impact of prenatal exposure to substances varies depending on the substance, dose, frequency, and timing of use during pregnancy [30]. However, research suggests that social conditions, particularly socio-economic status, parental mental health, and parenting style, are more likely to influence child outcomes than chemical exposure to substances itself [31,32,33]. Therefore, the impact of prenatal chemical exposure on negative child outcomes cannot be attributed solely to neurobiology and varies widely.

Adult SUD often co-occurs with trauma, mental health challenges, family stress, and poverty [34] which can also underlie the development of a SUD. Trauma, mental health, poverty, and addiction are often chronic, cumulative, and reciprocally reinforcing. When trauma, mental health challenges, poverty and parental SUD co-occur, risks for negative child outcomes, such as the later development of a SUD, increase [35]. Teasing out the relationship between genetics and environmental influences is particularly complicated because parental trauma, mental health challenges and SUD independently, and interactively, can create challenges in the caregiving environment that shape children’s development, which, in turn, can influence their later development of SUD.

There is a robust body of research that considers parenting behaviors among caregivers with a SUD. Parents with a SUD who have young children are more likely to struggle to provide sensitive and consistent care, have inappropriate developmental expectations of their child(ren), have inconsistent rules or limits, be reactive, and engage in harsh parenting [36,37,38,39,40,41,42]. Each of these parenting behaviors are associated with poorer quality parent-child relationships and poorer child outcomes [43,44,45,46,47]. Parents with older children who have SUD are less likely to monitor their older children, are more likely to struggle with limit setting, and are more likely to have lower levels of positive interactions [48]. These parenting behaviors create relational vulnerabilities that make the future development of a SUD more likely for a child.

The association between the caregiving environment and the later development of a SUD is born out in the extensive literature linking parental SUD to negative child outcomes. Having a parent with a SUD is associated with poorer outcomes for children and youth across the life course [5, 49]. The risk of intergenerational transmission of SUD, and of adverse childhood experiences and later outcomes increase when both parents have a SUD [50,51,52]. Young children whose parents have a SUD are more likely to have behavioral difficulties, poorer physical health, and developmental delays [53]. Youth who have a caregiver with a SUD are more likely to have symptoms of internalizing [54] or externalizing mental health disorders [54, 55, 56]. Viewed from a transactional perspective, these poorer outcomes become risks for the later development of a SUD as youth may be more likely to engage in risky behaviors or seek relief from negative feeling states that result from early childhood trauma and/or family dysfunction [28, 57,58,59,60]. Challenging parenting behaviors and impingements in the caregiving environment may create relational vulnerabilities that make the development of a SUD more likely. Therefore, the emotional legacy of challenging parent-child relationships is another mechanism by which the intergenerational continuity of SUD takes place.

Primacy of brain disease model of addiction (BMDA) in treatment and support programs

Even as studies focus on the interplay between neurobiological, familial, social, and structural factors that underlie the development of a SUD, there has been an increasing focus on the Brain Disease Model of Addiction [61,62,63,64] as the primary explanatory model for addiction in public-facing treatment and support program offerings. This etiological explanation was reinforced by its association with researchers at the National Institute on Drug Abuse and by the American Society for Addiction Medicine, which set research and funding priorities related to examining addiction as a chronic brain disease [4, 36, 63].

The BDMA holds that addiction is an unwanted condition where initial, voluntary substance use gradually becomes involuntary as the brain’s reward system becomes ‘hijacked’ [65] via a set of neurochemical processes. In this ‘hijacking,’ a negative feedback loop occurs where increased exposure to substances and their associated positive feelings (reward) becomes dulled after repeated exposure. Conditioned to receive a positive response, people seek higher doses of a substance and use substances more frequently when the expected reward is not received. Increasing the quantity and frequency use of substances also produces changes in the stress response system through alterations to the amygdala. The stress-response system becomes highly reactive, which in turn, can make it harder to manage day to day challenges. Not only does the process of addiction decrease the release of dopamine in relation to the use of the targeted substance, over time the brain becomes less sensitive to any experience that releases dopamine) and the pleasures associated with it [66]. The impaired reward and stress systems interact, producing ever-increasing triggers for use as people become conditioned to seek an increasingly difficult to obtain reward [66]. This occurs while the pleasures of everyday life become more attenuated and stress and negative experiences increase, creating a greater need to use substances [66].

Changes in the neural reward and stress response circuitry combine with changes in the neural regulatory circuitry to create the basis for addiction. According to the BDMA, addiction overwhelms areas of the brain related to executive control which governs decision-making, inhibitory control and self-regulation. Disruptions in the prefrontal cortex make it difficult for an individual to exercise choice in their use and achieve or maintain sobriety [57, 60].

The social, practical, and scientific consequences of the BDMA as an explanatory model have been widely debated [4, 30, 58]. Proponents contend that a neurobiological explanation of addiction will decrease stigma, create treatment options through the development of medications to block cravings, and offer a clear scientific explanation for why people continue to use drugs when the effects are no longer pleasurable and the consequences of use severe [63, 66]. Critics argue that the BDMA model may lead people to believe that addiction is intractable, and the unintended consequence of this framing is that it will decrease interest in treatment and impede self-efficacy [67, 68]. Further, the static presentation of the brain in the BMDA model, critics assert, is contradicted by more recent understandings of neuroplasticity and the adaptability of the brain [36]. Critics also contend that there is very little empirical evidence to support the BMDA as an explanatory model, noting that in practice, BMDA has not led to significant policy or treatment interventions that alleviate addiction [69].

Despite the substantive disagreements about the empirical basis and utility of the BMDA there is little disagreement over whether this model of addiction holds primacy both scientifically and in the popular imagination. Research examining the impact of the BMDA on doctors, addiction treatment providers, and the public suggests that neither the most positive or negative impacts predicted by proponents or opponents have come to pass [4, 64, 68]. The explanatory dominance of the BDMA makes it important to examine its implications for personal decision-making and sense-making related to the intergenerational continuity of SUD. As demonstrated above there are multiple contributions to the intergenerational transmission of use. How people understand these contributions is likely to matter for how they approach the intersection of SUD and parenting.

Lay understandings of genetics and stigma

Social science examinations of lay people’s meaning-making of genetics and disease makes clear that interpretations of the scientific literature are not monolithic and often do not show concordance with expert theories [4, 67]. Rather, how people make sense of disease, genetics, and risk varies by person and the social acceptability of the disease itself [70,71,72,73,74,75]. People demonstrate a profound capacity to hold complex and contradictory views as they interpret and then apply scientific literature to their own lives and decision-making. Often these applications belie the more concrete presentations in the research as people adapt neuroscientific or biological understandings of disease to fit within their other understandings of themselves in dynamic and nonlinear ways [68, 70, 76].

Personal narratives about genetic inheritance and addiction complicate academic debates between BDMA proponents and opponents as predictions about the promises and the pitfalls of the BDMA are not always borne out. Research on public understanding of the BDMA model suggests varying degree of acceptance and reduction of stigma. In one study, while half of the participants accepted a brain disease explanation of addiction, only a small fraction then linked this etiology to a reduction in moral judgement [68]. Dingel and colleagues found that among participants in an addiction treatment program, most did not find the genetic conception of addiction etiology helpful, but a minority of participants reported that it released them from feelings of shame and guilt related to their substance use [4]. Dingel’s research demonstrates that there is not a singular response to genetic or biological narratives about addiction.

Attribution theory describes one rationale for asserting that a neurobiological conception of addiction will reduce stigma. Attribution theory suggests that “low causal responsibility for a stigmatized characteristic […] is associated with less blame and more positive emotions” [77]. In other words, the blame for an outcome (for example, having a SUD) will decrease if the behavior is attributed to a cause over which a person has little to no control [75]. However, when the behavior is seen as untreatable and