This was my EE that I wrote in 2018 which is why I'm still using American spelling... fun fact I think I switched to British spelling end 2018 right before IB.
Introduction
Attention-Deficit Hyperactivity Disorder (ADHD) is a “neurodevelopmental disorder of behavioral inhibition interfering with self-regulation and organization of behaviour” (Barkley, 1997). Emerging in early childhood, ADHD features “developmentally inappropriate inattention, aggression, hyperactivity and impulsivity” (Matson, 1993) that significantly hinders academic, social and work performance.
For diagnosis, symptoms must occur often and be incongruent or maladaptive (Curatolo P., 2010), “persisting for at least 6 months to a degree inconsistent with development level, negatively impacting social and academic/occupational activities” (DSM V, 2013). Thomas et al.’s (2015) analysis found global prevalence of ADHD in children 18 and younger at an estimated 7.2%. There are plausibly some advantageous aspects to certain ADHD characteristics (Jensen, 1997) that result in the adaptive development of the disorder. These symptoms seem to have held some adaptive survival value during evolutionary history (Shelley-Tremblay, J.F., 1996).
Although functional aspects of cortical development and neuronal activity are impacted by early experiences (Nelson and Bloom, 1997), certain DSM-defined disorders may have arisen as adaptive responses to early pathogenic environments, (e.g. trauma and neglect), while others originate from neural adjustment to early environments inconsistent with future demands the child must meet (Jensen and Hoagwood, 1997). The straightforward DSM-5 criteria disregard the fundamental adaptation of human beings, ignoring brain plasticity in response to environmental stimuli (Depue et al., 1996; Greenough and Black, 1992).
This essay aims to discover how ADHD may be an adaptive result to adverse and pathogenic environments, holding importance to clinicians seeking to treat ADHD. Understanding its adaptiveness, and thus origin, is fundamental and may aid further research into ADHD to better treatment efficacy. It is important for children with ADHD to understand how to handle their disorder. I will show that, while ADHD traits may not be ideal in some settings, they may be adaptive and advantageous in others, thus leading me to investigate “To what extent is ADHD an adaptive response to early pathogenic environments?”.
Approaching the topic in contexts of trauma, parental neglect, harsh and migratory environments to evaluate the adaptiveness of ADHD in response to pathogenic environments, this essay seeks to counter the American Psychological Association’s (APA, 2017) claim that those with ADHD adapt poorly by showing how ADHD may be an adaptive response to early pathogenic environments, while demonstrating how the adaptiveness of the disorder may lead to success in later life. ________________________________________________________________________________
Deconstruction of Research Question
For purposes of this essay, ‘pathogenic environments’ refers to domains where factors that would affect ADHD were present. This will encompass:
early traumatic nicotine-saturated environments
environments of parental neglect
harsh prehistoric environments where natural selection and adaptive evolution took place
environments where migration is necessary
‘Early’ is defined as:
early developmental stages of one’s life
primitive periods of history
‘Adaptive responses’ define behaviour increasing survival and/or reproductive opportunities of an individual. Accepting the genetic predisposition of some behaviour, it is expected that natural selection favours adaptive behaviours. ________________________________________________________________________________
Main body
1. Origins of ADHD
Typical symptoms, including characteristic impulsivity, inattention and hyperactivity of modern ADHD were described by physician Heinrich Hoffman as early as 1846 (Thome, J. & J.K.A., 2004). In 1923, these traits were collectively recognized in the Diagnostic and Statistic Manual of Mental Disorders, DSM-II, under “Hyperkinetic Reaction of Childhood”, whose name itself alludes to the disorder being one of an adaptive nature. The word ‘reaction’ suggests that these traits occurred in response to a stimuli.
DSM-III only proposed the term “Attention-Deficit Disorder with or without Hyperactivity” (ADD) in 1980. This title no longer viewed the disorder simply as a behavioural reaction of childhood, instead focusing on its cognitive, developmental nature, prompting the creation of more explicit criteria to define and diagnose the disorder. Recognizing problems associated with hyperactivity and impulse control were critical to distinguishing between the two types of ADD and thus the prediction of later developmental risks, resulting in another disorder classified under Attention-Deficit/Hyperactivity Disorder in DSM-III (APA, 1987).
2. Pathogenic Environments
A: Nicotine can create traumatic environments resulting in synaptic pruning in fetuses that culminate in ADHD
Overwhelming stress can challenge immature stress systems which often rely on external regulation by a primary caregiver in infants. Trauma and stress can adversely impact developmental processes, leading to abnormal adaptations in the form of overactive stress systems (Loman and Gunnar, 2010).
The expression of ADHD-behaviour is associated with pathogenic environments, which may exist as the traumatic environment created by prenatal smoke exposure. Nicotine is a toxic substance in cigarettes detrimental to foetus growth, readily crossing the placenta, resulting in concentrations up to 15% higher in the foetus than in the mother (Huizink and Mulder, 2006). However, many studies in their literature review used participants’ retrospective self-report of prenatal exposure in their methodology. This increased vulnerabilities in underreporting smoking during pregnancy by participants given the stigma attached to this behaviour. Consequently skewed data could demarcate accuracy, but was mitigated through the use of a large sample size entailing 6356 participants.
Causal data revealed that prenatal nicotine exposure accounts for 270,000 excess ADHD cases in the USA (Braun, 2006). This exposure may create a traumatic environment for fetuses still sharing their mother’s blood (Nigg and Breslau, 2007), a finding elucidated by studies demonstrating that prenatal exposure to nicotine increased risks for ADHD (Linnet et al., 2003). Neuman’s (2007) biological study confirmed that ADHD diagnosis was 2.9 times higher in twins exposed to prenatal smoking than in those unexposed, establishing the correlation between genetically predisposed children of smokers and susceptibility to ADHD-traits of impaired attention and poor impulse control (Eppolito and Smith, 2006). Furthermore, since postnatal smoke exposure was not associated with ADHD (Braun, 2006), the causal relationship between prenatal smoke exposure and resultant ADHD is substantiated.
Nicotine disrupts interactions with neurotransmitter acetylcholine (Eriksson et al. 2000), which plays an active role in mediating motor control, attention, learning and memory (English, B.A., 2009), as well as brain development (Pugh et al. 2000). Obstructing acetylcholine can lead to constricted uterine arteries, decreasing oxygen supply and the flow of essential nutrients across the placenta to the foetus (Lambers and Clark, 1996).
Greater prenatal exposure to nicotine could result in the up-regulation of genes that code for formation of nicotine receptors which may hamper cognitive developmental systems. If present during the first trimester in the fetal brain, these receptors can disrupt other neural development. This subsequent predisposition to hindered development results in poor impulse control, attention deficits and aggression, distinctive ADHD-traits (Kandel et al. 1994).
Environmental sensory information is imperative in shaping and refining synaptic connections, meaning that pathogenic environments can result in maladaptive developmental disorders like ADHD (De Felice, 2015) which occurs as a result of impaired neurodevelopmental pathway function. Because nicotine desensitizes neurotransmitter functions related to modulating environmental stimuli in prenatally exposed children, the high levels of toxin to which the foetus is exposed create dangerous, pathogenic environments. Synaptic pruning may then occur as “experience-dependent strengthening of frequently activated [nicotine] connections in response to [the pathogenic] environment” (Rakic et al., 1994), eliminating less utilized connections. Since nicotine receptors in highly-exposed fetuses would be used significantly more relative to others, synaptic pruning could increase the number of nicotine receptors in an attempt to mitigate unusually high nicotine levels. Frequently activated nicotine receptors are thus strengthened while others that could be essential for development are neglected or eliminated.
In this situation, the adaptive response is the synaptic pruning in the foetus’ brain that mitigates high nicotine levels. Synaptic pruning can increase vulnerability to developmental deficits (e.g. ADHD) because of insufficient connections. Thus, the predisposition of an individual to ADHD is not an adaptive response to high nicotine levels, but simply results from adverse synaptic pruning, rendering ADHD unaccountable as an adaptive response to an early pathogenic environment. If this response to a nicotine-saturated environment is extrapolated to other equally traumatic domains, ADHD can be regarded as a consequence of the brain’s adaptive response to early pathogenic environments of trauma. In this context, ADHD is not a direct result, but instead a verbatim repercussion of, synaptic pruning in response to nicotine exposure.
Another possibility could simply be that irresponsible parents who smoke during pregnancy are poorer guardians, leading to the exploration of how ADHD may be an adaptive response to the pathogenic environment of neglect.
B: ADHD can be a consequence of parental neglect of children
Early pathogenic care, characterized by disregarding a child’s basic emotional needs (Dahmen, 2012), is care from a primary caretaker that can manifest as frequent changes in caregivers or neglect. This can lead to children exhibiting externalizing ADHD-like behaviours of impulsivity and hyperactivity.
Fair et al. (2009) combined theoretic graph analyses to examine dynamic multi-neural relationships during cognitive development, proposing that certain cognitive functions develop tremendously over the initial developmental stages of life, making them especially susceptible to external influences (Davidson et al., 2006). This finding (Fair et al., 2009) remained consistent with Johnson et al.’s (2005), who attest that cortical connections have biased information processing properties at birth, but are much less selective than in adults, emphasizing the susceptibility of the infant brain reacting to pathogenic environmental stimulus. Accordingly, interactive specialization predicts that many of these pathways still exist shortly after birth but specific regions will be activated, maintained, or eliminated during development as connections interact with sensory stimuli.
Every child has needs which pathogenic care seems to ignore, adversely impacting cognitive and physical childhood development (Loman et al., 2009). The effects of childhood environment interact with neurodevelopmental processes. When these needs remain unmet, children become especially vulnerable to developmental deficits that manifest as ADHD (Perry, 2002). Meanwhile, cross-referenced human and animal studies substantiate that caring socio-emotional environments adequate to a child’s needs are essential for appropriate brain development.
Children in orphanages deprived of emotional contact appear to also lack developmentally congruent cortical connections, which disrupt brain development of both “caring behaviour and cognitive capacities” (Perry, 2002). When deprived of a caring familial environment, Perry (2002) found children without experiences which promote positive developmental and caring cognitive growth processes, perhaps explaining the manifestation of externalizing aggressive ADHD-like behaviour.
The 30% of children in foster care placed there because of parental neglect suffer elevated mental health risk (Oswald et al., 2010). Four times as many foster children were found to have ADHD than the general population (McMillen et al., 2005). The extensive scope of Oswald et al.’s (2010) literature review concluded that children with ADHD in foster care was around 10-12% while only 3-7% in the general population, reinforcing that the less an individual’s childhood environment corresponds to a natural family setting, the more prevalent ADHD-symptoms were (Dahmen, 2012). Oswald et al. (2010), however, could not associate development of symptoms to the foster children’s pathogenic background of neglect due to an absence of valid retrospective information regarding past events, decreasing the validity of their results since the link between parental neglect and development of ADHD remained unclear.
Troutman (2011) explains this link, suggesting that constant changes in caregivers can result in behavioural and emotional disruptions that lead to the observed disruptive ADHD-like behaviours. Regardless of how caring a foster family is, constantly shifting a child’s home or school environment increases the risk of externalizing behaviours like ADHD by severely obstructing the formation of emotional attachments between child and suitable caregiver (Wolfe and Jaffe, 1991). These are imperative in proper maturation of neurodevelopment processes, rendering the lack of such cumulating in an environment of neglect. This is corroborated by how foster children’s ADHD-inattentive symptoms seemed to ameliorate once they were permanently adopted from institutions into particularly caring families (that removed the pathogenic neglectful environment) (Ghera et al., 2009), demonstrating that once allowed to settle down into an environment representative of a natural family setting, foster children’s ADHD-symptoms were alleviated.
Besides foster care, children may come from difficult or unstable family backgrounds. Parental neglect may encompass abuse (cause of institutionalization of 25% of the 749 children in San Francisco’s Child Protection Center) (Oswald et al., 2010). Disruptive home environments have been associated with higher levels of externalizing behaviour in children (Wolfe and Jaffe, 1991), some of which manifests as hyperactivity and violence that may be misinterpreted as symptoms of ADHD (Evans, S.E., 20018).
Not all children with early pathogenic care develop ADHD-symptoms; those who do may simply be externalizing ADHD-like behaviour without actually having the disorder. ADHD-traits developed from neglectful and unstable early pathogenic environments can be extenuated with the introduction of an environment of proper care. Thus, these traits symptomatic of ADHD develop as a means to mitigate the emotional disregard a child experiences, acting as an adaptive response to the early pathogenic environment of neglect.
C: Harsh environments can trigger ADHD as an adaptive response
“An evolutionary approach to the issue of ADHD derives from the assumption that what is regarded as a pathological phenomenon today was once an adaptive response to conditions of life in ancestral stages of human development.” (Matejcek, 2003).
Extreme prehistoric conditions in which evolution is assumed to have taken place could have resulted in development of adaptive ADHD. These dangerous environments allude to human survival being largely dependent on ‘response-readiness’ (Jensen, 1997), or hyper-vigilance (i.e. inattention: rapidly-shifting attention consistently monitoring dangers; inattention to single stimuli, allowing constant awareness of surroundings). ‘Response-readiness’ encompasses the ability to rapidly process environmental stimuli using all senses, to be motorically-hyperactive (i.e. hyperactivity: foraging for food, moving as seasons shift), and to have quick flight (i.e. impulsive) or fight (i.e. aggression) instincts.
Evolutionarily, individuals lacking quick responses adapt and react to surrounding environments more poorly, lending themselves particularly vulnerable to early deaths. Milliken (2016) suggested in ‘PlayDHD’ that ADHD-impulsivity was historically genetically advantageous; the ADHD-associated gene remains in today’s society. Because natural selection occurs to remove disadvantageous or maladaptive genes from the genetic makeup of subsequent generations, ADHD’s beneficiality allowing its natural selection is highlighted. To reinforce, Thom Hartmann’s hunter-farmer theory suggests that ADHD-traits were favourable to pre-agricultural humans in hunter societies, proposing that ADHD-traits were naturally selected for their adaptive value. Hartmann’s (1993) theory, however, makes assumptions about cultural milieu in which primitive humans lived (Shelley-Tremblay, J.F., 1996), raising concerns about his generalization of ancestral populations and the environment in which evolution took place. Nonetheless, the theory will still be utilized for its elucidation of how selective pressures of past domains shaped behavioural functions to develop as adaptations to the harsh pathogenic ancestral environment.
Contrary to the Hunter-Farmer theory, Desmond Morris (1967) indicated that primitive hunters must exhibit stealth, concentration, silence and an acute awareness of their environment. This is juxtaposed with the inattentive, hyperactive and impulsive aspects of ADHD that lead to lack of self-control and regulation. In conjunction with Morris (1967), the beneficial defensive impulsivity Milliken (2016) proposed could be outweighed by the negative effect it has may have in resource-scarce environments, such as missing critical environmental cues (e.g. mistaking poisonous food from physically similar edible ones).
Impulsivity in evolutionary contexts can be defined as “an organism’s quick response to environmental cues while not considering alternative reactions” (Jensen, 1997). Though likened to response-readiness, a lucrative survival characteristic under harsh conditions (Matejcek, 2003), those with ADHD-impulsivity and hyperactivity may find it difficult to remain quiet and motionless in situations where they need to hide from threats. An impulsive-hyperactive child would attract greater attention from their surroundings or predator, instead being a burden on their tribe, increasing vulnerability to exposure or predation (Matejcek, 2003). Additionally, impulsivity can lead to indifferences to danger. ADHD-children may rush towards unknown situations without considering possible risks, making them troublesome to look after. While Jensen (1997) suggested that impulsivity is adaptive behaviour allowing for hyper-vigilance, Matejcek (2003) disagrees; impulsive ADHD-children habitually “act before thinking”, leading to failures in distinguishing dangerous from safe situations. This lack of consideration may render impulsivity a maladaptive feature decreasing the chance of survival of ADHD-children who become especially susceptible to engaging in dangerous situations. Thus, ADHD-children’s survival could simply result from exceptionally protective parental care offered throughout evolution instead of being an adaptive response to their environments.
Humans in more dangerous environments were found more likely to have rapidly-shifting attentions that permitted constant vigilance (Jensen, 1997), demonstrating inattention’s adaptivity and vitality to survival. Highlighting the importance of ADHD in early pathogenic environments is the nomadic Ariaal tribe, whose ADHD-behaviour bettered their ability to survive harsh conditions (Chen et al., 1999). Chen et al. (1999) established that nomadic Ariaal have higher frequencies with the DRD4-7R, ADHD-associated allele than sedentary Ariaal. Similarly, nomads were found better nourished than sedentary Ariaal without DRD4-7R, insinuating that harsher contexts allow people with DRD4-7R and the subsequent manifestation of ADHD-behaviour to be more evolutionarily successful (Chen et al., 1999). The comparison between nomadic and sedentary Ariaal in this study allowed testing of the ADHD-allele across environments inhabited by genetically and culturally similar people. This ecological validity means that the better nutrition and consequent survival in nomadic Ariaal with DRD4-7R could account for its apparent natural selection as a result of the adaptive advantage of ADHD-traits is a reasonable conclusion. Conversely, increased hyperactivity could instead result in greater caloric-usage and resultant decreases in nutritional stores, suggesting ADHD’s contextual adaptivity.
Humans in higher-threat environments may be more likely to display ADHD-traits which, being adaptive and advantageous, will be naturally selected for. Even though ADHD-behaviour may embody elements of maladaptation emanating from hyperactivity and impulsivity (increased vulnerability of exposure to dangers), the larger implications of ADHD’s evolutionary advantages ensured its continued prevalence. Resultantly, ADHD-traits are retained through generations even when no longer necessary. For instance, nomadic Ariaal children have short-attention spans originating from DRD4-7R, allowing effective learning in early dynamic environments without schools (Chen et al. 1999) and rapid understanding of survival means in harsh environments. However, this same attention span will interfere in learning if the same children with linked ADHD-traits were placed in today’s classroom environments. Therefore, ADHD and its likened behaviour are adaptive responses to early pathogenic environments where quick modifications to environmental stimuli were necessary for survival, but is less so in modern contexts.
The proposition of ADHD as an adaptive response to early prehistoric environments is better substantiated than its alternative by the fact that children with ADHD still exist, and are even appearing to increase. Primitive environments shaped the tendencies of particular humans in that time period to express hyper-vigilant, impulsive behaviours, traits which proved to be useful, were naturally selected for, and are still prevalent today. Thus, from this evolutionary perspective, it can be surmised that ADHD is largely an adaptive response to the pathogenic environment of prehistoric domains.
D: ADHD can be an adaptive response to regular inevitable migration
Expressions of genetic tendencies are influenced by one’s environmental stimuli. Genetic variants associated with ADHD are found at higher frequencies in populations with histories of migration (Milliken, 2016), implying ADHD’s adaptive nature to constantly changing environmental stimuli. Recognizing genetic variants can predispose ADHD, patterns of natural selection can be associated with the fact that this behavioral trait provides evolutionary advantage (Arcos-Burgos, M.,2007).
The DRD4 ADHD-associated gene is linked to “novelty-seeking personality, hyperactivity, and risk-taking behaviours”, featuring more in populations with greater migratory histories (Eisenberg and Campbell, 2011). People with DRD4 relocate more frequently as a result of their need for constant environmental shifts. This could stem from impulsivity (increased exploration) and inattention (boredom in unchanging environments), ADHD-traits linked to DRD4-7R, compelling greater movement (hyperactivity), increasing the likelihood of varied environmental stimulus.
Instead of resulting from ADHD-traits that promote constant movement, migration could simply be determined by pathogenic situational factors like war or depletion of natural resources which act as push-factors for relocation to resource-rich environments more suited to survival.
Differing frequencies of DRD4-7R between nomadic and sedentary populations could result from natural selection of the favourable gene in nomadic populations who consistently migrate to new environments, tying in with the evolutionary explanation for ADHD’s adaptiveness. Chen et al. (1999) studied migratory patterns of 2,320 individuals from 39 groups, raising the possibility that ADHD adaptive to migration processes was caused by selective migration of individuals carrying DRD4, selective favoring of those genes in the new environment, or both (Buss, 2009). Far more prevalent in nomadic populations, this evidence supports the notion that adaptive components of ADHD are useful to nomads who still retain past lifestyles.
Individuals need time to grasp essentialities of new domains. Those with ADHD may be more equipped to attune to their new environment by rapidly adapting to new requirements, such as learning new hunting methods or navigating “new sociocultural norms” (Eisenberg and Campbell, 2011). From this, it is reasonable to conclude that ADHD-traits allow better adaptation to new environments, thus showing ADHD as an adaptive response in this context.
3. ADHD as an Adaptive Response
Though seemingly largely largely adaptive to early pathogenic environments, allowing its continued manifestation, ADHD-inattention may be maladaptive in current society that requires analytical thinking and careful consideration. Studies, however, suggest ADHD’s usefulness and adaptivity to current societies, specifically in entrepreneurial orientation (EO), a conceptualized business characteristic composed of risk-taking (impulsive), innovative and proactive behaviour (hyperactive) proving the potential of focused and correctly managed ADHD in modern society (Thurik et al., 2016). Though modern society may not (yet) be considered a pathogenic environment, ADHD traits still seem to be adaptive and advantageous in certain contexts. Nevertheless, it is conceivable to expect massive external technological stimuli present via the rapidly expanding internet and social media to become a pathogenic environment encouraging exhibition of ADHD-inattention like symptoms. As such, ADHD as an adaptive response in acknowledging multiple stimuli in modern society could be an area for future research.
Psychiatrist Dale Archer (2014) states: “Those with ADHD traits thrive in times of crisis”. Individuals with ADHD in pre-historic times constantly searched for new hunting territory, water supplies and sites in which they could settle (Archer, 2014). While ADHD results in easy frustration with “uninteresting” and repetitive environmental stimuli, it enables those with the disorder to hyper-focus on their passions and enables them to efficiently multitask. Likewise, the DRD4 7R-allele has been linked to both ADHD and entrepreneurial tendencies.
Entrepreneurship is ideal stimulation for those with ADHD, especially playing on their willingness to take risks. Rejecting standard, logical solutions, those with ADHD are more inclined to take risks, follow their instincts and forge ahead with new, uncertain ideas. Prominent entrepreneurs even publicly credit their ADHD symptoms as the driver behind their pursuit of self-employment (Verheul et al., 2016). Coming from a humble rural background, Ingvar Kamprad, founder of IKEA, embodies the positivity of ADHD-traits, demonstrating ADHD’s risk-taking (impulsive) and hyperactive behaviors driving his entrepreneurial motivation and creative genius, highlighting ADHD’s adaptivity in current societies as well.
Children in school with the disorder must nurture strategies ensuring their focus, bypassing their ADHD-behaviour to cultivate an ability to work around their limitations and develop a resilience important in business settings. The hardships ADHD-children face during early development can result in their adopting advantageous character traits. It is further implied that ADHD may be positive for creativity (Alter, 2001), resulting in higher levels of spontaneity (Davis, 2004), leading to favourable ramifications for entrepreneurship, asserting its modern adaptive importance. The impoverished childhood of renowned rapper Eminem, who faced paternal neglect and constant migration, embodies two pathogenic environments in which this essay seeks to prove ADHD’s adaptivity to. He is acutely in touch with and open about his ADHD (Clyman, 2010), which could have manifested as a result of constant changes in environment and a parental neglect that encouraged externalizing behaviour like aggression and other ADHD-traits. Nonetheless, he channeled his impulsivity and creativity positively, inspiring the spontaneous, creative rap music enjoyed by many today.
Conclusion
Not only has ADHD been shown to provide early evolutionary advantages, it has also been correlated with the DRD4 7R-allele linked to better nutritional health and migration of nomadic populations, characteristics adaptive to early environments. Though these advantages are prevalent, ADHD holds several maladaptive traits that exist as failing to consider dangerous situations and hyperactivity that can increase vulnerability to predation and danger. Nonetheless, natural selection for ADHD and its continued manifestation in today’s general population demonstrates the overriding adaptive advantage ADHD holds even in modern society, as is shown through the examples of Ingvar Kamprad and Eminem.
Further, ADHD is a way in which children can mitigate experiences of emotional disregard or neglect, allowing them to externalize their lack of emotional regard under pathogenic care. As a result of their lack of sufficient developmental nurturing, ADHD-behaviour is an adaptive means for children suffering parental neglect to express themselves.
Opposing the Hunter-Farmer theory which suggests its lack of adaptivity in current “farmer” society, ADHD is an adaptive response that even provides advantages in today’s analytical “farmer” society. From this essay, it can be concluded that those who develop ADHD, either as a direct or indirect result of a pathogenic environment, may adapt to it, which could lead to success in later life if focused and handled properly.
In conclusion, traumatic and neglectful early developmental realms, as well as early prehistoric environments and those in which migration is a necessity constitute to areas in which ADHD-traits or ADHD itself is likely to be expressed. ADHD is an adaptive response to all the pathogenic environments evaluated in this essay with the exception of the traumatic environment of nicotine exposure to which ADHD is instead an indirect consequence of. Thus, ADHD can be considered an adaptive response to early pathogenic environments.
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