Behavioural addiction is a form of addiction that involves a compulsion to engage in a rewarding non-substance-related behaviour – sometimes called a natural reward – despite any negative consequences to the person’s physical, mental, social or financial well-being. Addiction canonically refers to substance abuse; however, the term’s connotation has been expanded to include behaviours that may lead to a reward (e.g. gambling, eating, or shopping) since the 1990s. A gene transcription factor known as ΔFosB has been identified as a necessary common factor involved in both behavioural and drug addictions, which are associated with the same set of neural adaptations in the reward system.
Psychiatric and Medical Classifications
Diagnostic models do not currently include the criteria necessary to identify behaviours as addictions in a clinical setting. Behavioural addictions have been proposed as a new class in DSM-5, but the only category included is gambling addiction. Internet gaming addiction is included in the appendix as a condition for further study.
Behavioural addictions, which are sometimes referred to as impulse control disorders, are increasingly recognised as treatable forms of addiction. The type of excessive behaviours identified as being addictive include gambling, eating, having sexual intercourses, using pornography, computers, video games, internet and digital media, physical exercise, and shopping.
In August 2011, the American Society of Addiction Medicine (ASAM) issued a public statement defining all addiction in terms of brain changes. “Addiction is a primary, chronic disease of brain reward, motivation, memory and related circuitry.”
The following excerpts are taken from the organisation’s FAQs:
The new ASAM definition makes a departure from equating addiction with just substance dependence, by describing how addiction is also related to behaviors that are rewarding. This is the first time that ASAM has taken an official position that addiction is not solely “substance dependence.” This definition says that addiction is about functioning and brain circuitry and how the structure and function of the brains of persons with addiction differ from the structure and function of the brains of persons who do not have addiction. It talks about reward circuitry in the brain and related circuitry, but the emphasis is not on the external rewards that act on the reward system. Food and sexual behaviors and gambling behaviors can be associated with the “pathological pursuit of rewards” described in this new definition of addiction.
We all have the brain reward circuitry that makes food and sex rewarding. In fact, this is a survival mechanism. In a healthy brain, these rewards have feedback mechanisms for satiety or ‘enough.’ In someone with addiction, the circuitry becomes dysfunctional such that the message to the individual becomes ‘more’, which leads to the pathological pursuit of rewards and/or relief through the use of substances and behaviors. So, anyone who has addiction is vulnerable to food and sex addiction.
Meanwhile, DSM-5 has deprecated the term “addiction”.
Behavioural addiction is a treatable condition. Treatment options include psychotherapy and psychopharmacotherapy (i.e. medications) or a combination of both. Cognitive behavioural therapy (CBT) is the most common form of psychotherapy used in treating behavioural addictions; it focuses on identifying patterns that trigger compulsive behaviour and making lifestyle changes to promote healthier behaviours. Because cognitive behavioural therapy is considered a short term therapy, the number of sessions for treatment normally ranges from five to twenty. During the session, therapists will lead patients through the topics of identifying the issue, becoming aware of one’s thoughts surrounding the issue, identifying any negative or false thinking, and reshaping said negative and false thinking. While CBT does not cure behavioural addiction, it does help with coping with the condition in a healthy way. Currently, there are no medications approved for treatment of behavioural addictions in general, but some medications used for treatment of drug addiction may also be beneficial with specific behavioural addictions. Any unrelated psychiatric disorders should be kept under control, and differentiated from the contributing factors that cause the addiction.
A recent narrative review in 2017 examined the existing literature for studies reporting associations between behavioural addictions (pathological gambling, problematic internet use, problematic online gaming, compulsive sexual behaviour disorder, compulsive buying and exercise addiction) and psychiatric disorders. Overall, there is solid evidence for associations between behavioural addictions and mood disorder, anxiety disorder as well as substance use disorders. Associations between ADHD may be specific to problematic internet use and problematic online gaming. The authors also conclude that most of current research on the association between behavioural addictions and psychiatric disorders has several limitations: they are mostly cross-sectional, are not from representative samples, and are often based on small samples, among others. Especially more longitudinal studies are needed to establish the direction of causation, i.e. whether behavioural addictions are a cause or a consequence of psychiatric disorders.
ΔFosB, a gene transcription factor, has been identified as playing a critical role in the development of addictive states in both behavioural addictions and drug addictions. Overexpression of ΔFosB in the nucleus accumbens is necessary and sufficient for many of the neural adaptations seen in drug addiction; it has been implicated in addictions to alcohol, cannabinoids, cocaine, nicotine, phenylcyclidine, and substituted amphetamines as well as addictions to natural rewards such as sex, exercise, and food. A recent study also demonstrated a cross-sensitization between drug reward (amphetamine) and a natural reward (sex) that was mediated by ΔFosB.
Besides increased ΔFosB expression in the nucleus accumbens, there are many other correlations in the neurobiology of behavioural addictions with drug addictions.
One of the most important discoveries of addictions has been the drug based reinforcement and, even more important, reward based learning processes. Several structures of the brain are important in the conditioning process of behavioural addiction; these subcortical structures form the brain regions known as the reward system. One of the major areas of study is the amygdala, a brain structure which involves emotional significance and associated learning. Research shows that dopaminergic projections from the ventral tegmental area facilitate a motivational or learned association to a specific behaviour. Dopamine neurons take a role in the learning and sustaining of many acquired behaviours. Research specific to Parkinson’s disease has led to identifying the intracellular signalling pathways that underlie the immediate actions of dopamine. The most common mechanism of dopamine is to create addictive properties along with certain behaviours. There are three stages to the dopamine reward system: bursts of dopamine, triggering of behaviour, and further impact to the behaviour. Once electronically signalled, possibly through the behaviour, dopamine neurons let out a ‘burst-fire’ of elements to stimulate areas along fast transmitting pathways. The behaviour response then perpetuates the striated neurons to further send stimuli. The fast firing of dopamine neurons can be monitored over time by evaluating the amount of extracellular concentrations of dopamine through micro dialysis and brain imaging. This monitoring can lead to a model in which one can see the multiplicity of triggering over a period of time. Once the behaviour is triggered, it is hard to work away from the dopamine reward system.
Behaviours like gambling have been linked to the newfound idea of the brain’s capacity to anticipate rewards. The reward system can be triggered by early detectors of the behaviour, and trigger dopamine neurons to begin stimulating behaviours. But in some cases, it can lead to many issues due to error, or reward-prediction errors. These errors can act as teaching signals to create a complex behaviour task over time.
The American Society of Addiction Medicine (ASAM), founded in 1954, is a professional medical society representing over 6,000 physicians, clinicians and associated professionals in the field of addiction medicine.
ASAM is dedicated to increasing access and improving the quality of addiction treatment, educating physicians and the public, supporting research and prevention, and promoting the appropriate role of physicians in the care of patients with addiction.
Addiction is a state characterised by compulsive engagement in rewarding stimuli, despite adverse consequences. The process of developing an addiction occurs through instrumental learning, which is otherwise known as operant conditioning.
Neuroscientists believe that drug addicts’ behaviour is a direct correlation to some physiological change in their brain, caused by using drugs. This view believes there is a bodily function in the brain causing the addiction. This is brought on by a change in the brain caused by brain damage or adaptation from chronic drug use.
In humans, addiction is diagnosed according to diagnostic models such as the Diagnostic and Statistical Manual of Mental Disorders, through observed behaviours. There has been significant advancement in understanding the structural changes that occur in parts of the brain involved in the reward pathway (mesolimbic system) that underlies addiction. Most research has focused on two portions of the brain: the ventral tegmental area (VTA) and the nucleus accumbens (NAc).
The VTA is the portion of the mesolimbic system responsible for spreading dopamine to the whole system. The VTA is stimulated by ″rewarding experiences″. The release of dopamine by the VTA induces pleasure, thus reinforcing behaviours that lead to the reward. Drugs of abuse increase the VTA’s ability to project dopamine to the rest of the reward circuit. These structural changes only last 7-10 days, however, indicating that the VTA cannot be the only part of the brain that is affected by drug use, and changed during the development of addiction.
The nucleus accumbens (NAc) plays an essential part in the formation of addiction. Almost every drug with addictive potential induces the release of dopamine into the NAc. In contrast to the VTA, the NAc shows long-term structural changes. Drugs of abuse weaken the connections within the NAc after habitual use, as well as after use then withdrawal.
Learning by experience occurs through modifications of the structural circuits of the brain. These circuits are composed of many neurons and their connections, called synapses, which occur between the axon of one neuron and the dendrite of another. A single neuron generally has many dendrites which are called dendritic branches, each of which can be synapsed by many axons.
Along dendritic branches there can be hundreds or even thousands of dendritic spines, structural protrusions that are sites of excitatory synapses. These spines increase the number of axons from which the dendrite can receive information. Dendritic spines are very plastic, meaning they can be formed and eliminated very quickly, in the order of a few hours. More spines grow on a dendrite when it is repetitively activated. Dendritic spine changes have been correlated with long-term potentiation (LTP) and long-term depression (LTD).
LTP is the way that connections between neurons and synapses are strengthened. LTD is the process by which synapses are weakened. For LTP to occur, NMDA receptors on the dendritic spine send intracellular signals to increase the number of AMPA receptors on the post synaptic neuron. If a spine is stabilised by repeated activation, the spine becomes mushroom shaped and acquires many more AMPA receptors. This structural change, which is the basis of LTP, persists for months and may be an explanation for some of the long-term behavioural changes that are associated with learned behaviours, including addiction.
Animal models, especially rats and mice, are used for many types of biological research. The animal models of addiction are particularly useful because animals that are addicted to a substance show behaviours similar to human addicts. This implies that the structural changes that can be observed after the animal ingests a drug can be correlated with an animal’s behavioural changes, as well as with similar changes occurring in humans.
Administration of drugs that are often abused can be done either by the experimenter (non-contingent), or by a self-administration (contingent) method. The latter usually involves the animal pressing a lever to receive a drug. Non-contingent models are generally used for convenience, being useful for examining the pharmacological and structural effects of the drugs. Contingent methods are more realistic because the animal controls when and how much of the drug it receives. This is generally considered a better method for studying the behaviours associated with addiction. Contingent administration of drugs has been shown to produce larger structural changes in certain parts of the brain, in comparison to non-contingent administration.
Types of Drugs
All abused drugs directly or indirectly promote dopamine signalling in the mesolimbic dopamine neurons which project from the ventral tegmental area to the nucleus accumbens (NAc). The types of drugs used in experimentation increase this dopamine release through different mechanisms.
Opiates are a class of sedative with the capacity for pain relief.
Morphine is an opiate that is commonly used in animal testing of addiction.
Opiates stimulate dopamine neurons in the brain indirectly by inhibiting GABA release from modulatory interneurons that synapse onto the dopamine neurons.
GABA is an inhibitory neurotransmitter that decreases the probability that the target neuron will send a subsequent signal.
Stimulants used regularly in neuroscience experimentation are cocaine and amphetamine.
These drugs induce an increase in synaptic dopamine by inhibiting the reuptake of dopamine from the synaptic cleft, effectively increasing the amount of dopamine that reaches the target neuron.
The Reward Pathway
The reward pathway, also called the mesolimbic system of the brain, is the part of the brain that registers reward and pleasure. This circuit reinforces the behaviour that leads to a positive and pleasurable outcome. In drug addiction, the drug-seeking behaviours become reinforced by the rush of dopamine that follows the administration of a drug of abuse. The effects of drugs of abuse on the ventral tegmental area (VTA) and the nucleus accumbens (NAc) have been studied extensively.
Drugs of abuse change the complexity of dendritic branching as well as the number and size of the branches in both the VTA and the NAc. By correlation, these structural changes have been linked to addictive behaviours. The effect of these structural changes on behaviour is uncertain and studies have produced conflicting results. Two studies have shown that an increase in dendritic spine density due to cocaine exposure facilitates behavioural sensitisation, while two other studies produce contradicting evidence.
In response to drugs of abuse, structural changes can be observed in the size of neurons and the shape and number of the synapses between them. The nature of the structural changes is specific to the type of drug used in the experiment. Opiates and stimulants produce opposite effects in structural plasticity in the reward pathway. It is not expected that these drugs would induce opposing structural changes in the brain because these two classes of drugs, opiates and stimulants, both cause similar behavioural phenotypes.
Both of these drugs induce increased locomotor activity acutely, escalated self-administration chronically, and dysphoria when the drug is taken away. Although their effects on structural plasticity are opposite, there are two possible explanations as to why these drugs still produce the same indicators of addiction: Either these changes produce the same behavioural phenotype when any change from baseline is produced, or the critical changes that cause the addictive behaviour cannot be quantified by measuring dendritic spine density.
Opiates decrease spine density and dendrite complexity in the nucleus accumbens (NAc). Morphine decreases spine density regardless of the treatment paradigm. Either chronic or intermittent administration of morphine will produce the same effect. The only case where opiates increase dendritic density is with chronic morphine exposure, which increases spine density on pyramidal neurons in the orbitofrontal cortex. Stimulants increase spinal density and dendritic complexity in the nucleus accumbens (NAc), ventral tegmental area (VTA), and other structures in the reward circuit.
Ventral Tegmental Area
There are neurons with cell bodies in the VTA that release dopamine onto specific parts of the brain, including many of the limbic regions such as the NAc, the medial prefrontal cortex (mPFC), dorsal striatum, amygdala, and the hippocampus. The VTA has both dopaminergic and GABAergic neurons that both project to the NAc and mPFC. GABAergic neurons in the VTA also synapse on local dopamine cells. In non-drug models, the VTA dopamine neurons are stimulated by rewarding experiences. A release of dopamine from the VTA neurons seems to be the driving action behind drug-induced pleasure and reward.
Exposure to drugs of abuse elicits LTP at excitatory synapses on VTA dopamine neurons. Excitatory synapses in brain slices from the VTA taken 24 hours after a single cocaine exposure showed an increase in AMPA receptors in comparison to a saline control. Additional LTP could not be induced in these synapses. This is thought to be because the maximal amount of LTP had already been induced by the administration of cocaine. LTP is only seen on the dopamine neurons, not on neighbouring GABAergic neurons. This is of interest because the administration of drugs of abuse increases the excitation of VTA dopamine neurons, but does not increase inhibition. Excitatory inputs into the VTA will activate the dopamine neurons 200%, but do not increase activation of GABA neurons which are important in local inhibition.
This effect of inducing LTP in VTA slices 24 hours after drug exposure has been shown using morphine, nicotine, ethanol, cocaine, and amphetamines. These drugs have very little in common except that they are all potentially addictive. This is evidence supporting a link between structural changes in the VTA and the development of addiction.
Changes other than LTP have been observed in the VTA after treatment with drugs of abuse. For example, neuronal body size decreased in response to opiates.
Although the structural changes in the VTA invoked by exposure to an addictive drug generally disappear after a week or two, the target regions of the VTA, including the NAc, may be where the longer-term changes associated with addiction occur during the development of the addiction.
The nucleus accumbens plays an integral role in addiction. Almost every addictive drug of abuse induces the release of dopamine into the nucleus accumbens. The NAc is particularly important for instrumental learning, including cue-induced reinstatement of drug-seeking behaviour. It is also involved in mediating the initial reinforcing effects of addictive drugs. The most common cell type in the NAc is the GABAergic medium spiny neuron. These neurons project inhibitory connections to the VTA and receive excitatory input from various other structures in the limbic system. Changes in the excitatory synaptic inputs into these neurons have been shown to be important in mediating addiction-related behaviours. It has been shown that LTP and LTD occurs at NAc excitatory synapses.
Unlike the VTA, a single dose of cocaine induces no change in potentiation in the excitatory synapses of the NAc. LTD was observed in the medium spiny neurons in the NAc following two different protocols: a daily cocaine administration for five days or a single dose followed by 10-14 days of withdrawal. This suggests that the structural changes in the NAc are associated with long-term behaviours (rather than acute responses) associated with addiction such as drug seeking.
Neuroscientists studying addiction define relapse as the reinstatement of drug-seeking behaviour after a period of abstinence. The structural changes in the VTA are hypothesized to contribute to relapse. Once the molecular mechanisms of relapse are better understood, a pharmacological treatment may be developed to prevent it.
Relapse is the biggest problem for recovering addicts; an addict can be forced to abstain from using drugs while they are admitted in a treatment clinic, but once they leave the clinic they are at risk of relapse. Relapse can be triggered by stress, cues associated with past drug use, or re-exposure to the substance. Animal models of relapse can be triggered in the same way.
Search for a Cure for Addiction
The goal of addiction research is to find ways to prevent and reverse the effects of addiction on the brain. Theoretically, if the structural changes in the brain associated with addiction can be blocked, then the negative behaviours associated with the disease should never develop.
Structural changes associated with addiction can be inhibited by NMDA receptor antagonists which block the activity of NMDA receptors. NMDA receptors are essential in the process of LTP and LTD. Drugs of this class are unlikely candidates for pharmacological prevention of addiction because these drugs themselves are used recreationally. Examples of NMDAR antagonists are ketamine, dextromethorphan (DXM), phencyclidine (PCP).
Addiction vulnerability is an individual’s risk of developing an addiction during his or her lifetime. There are a range of genetic and environmental risk factors for developing an addiction that vary across the population.
Genetic and environmental risk factors each account for roughly half of an individual’s risk for developing an addiction; the contribution from epigenetic (inheritable traits) risk factors to the total risk is unknown. Even in individuals with a relatively low genetic risk, exposure to sufficiently high doses of an addictive drug for a long period of time (e.g. weeks-months) can result in an addiction. In other words, anyone can become an addict under particular circumstances. Research is working toward establishing a comprehensive picture of the neurobiology of addiction vulnerability, including all factors at work in propensity for addiction.
Accepted research now shows that some people have vulnerabilities to addiction and has established a three-factor standard for vulnerability to drug addiction: genetic factors, environmental factors, and repeated exposure to drugs of abuse. Being vulnerable to addiction means that there exists some factor which makes one individual more likely to develop an addiction than another individual. Additionally, many in the science community agree that addiction is not simply just a result of desensitised neural receptors but also a corollary of long-term associated memories (or cues) of substance use and self-administration. Vulnerability to addiction has both physiological and biological components.
Contemporary research in neurobiology (a branch of science that deals with the anatomy, physiology, and pathology of nervous system) of addiction points to genetics as a major contributing factor to addiction vulnerability. It has been estimated that 40-60% of the vulnerability to developing an addiction is due to genetics. One gene in particular, the D2 subtype of dopamine receptor, has been studied at length in association to substance addiction. The D2 receptor responds to the chemical dopamine which produces rewarding and pleasurable feelings in the brain. Through mice studies, agreeing contemporary research has shown that individuals with a deficiency in this dopamine receptor exhibit not only a preference for and increased consumption of alcohol over their genetically normal peers, but also compensated levels of the cannabinoid receptor type CB1.
This suggests that both of these genetic factors work together in the regulation of alcohol and cocaine in the brain and in the normal regulation of dopamine. Individuals with this genetic deficiency in the D2 dopamine receptor may be more likely to seek out these recreational pleasure/reward producing substances as they are less receptive to the natural “feel good’’ effects of dopamine. This naturally occurring deficiency is one of the most studied genetic vulnerabilities to substance abuse across the field. Recent studies show that GABA also plays a role in vulnerability to addiction. When alcohol is consumed it affects GABA by mimicking its effects on the brain, such as basic motor functions.
Additionally, genetics play a role on individual traits, which may put one at increased risk for experimentation with drugs, continued use of drugs, addictions, and potential for relapse. Some of these individual personality traits, such as impulsivity, reward-seeking, and response to stress, may lead to increased vulnerability to addiction.
A major environmental factor that increases vulnerability to developing addiction is availability of drugs. Additionally, other environmental factors come into play, such as socioeconomic status and poor familial relationships, and have been shown to be contributing factors in the initiation (and continued use) of drug abuse. Neurobiology again plays a role in addiction vulnerability when in combination with environmental factors. The main risk of chronic stressors contributing to vulnerability is that they can put the brain in a compromised state. External stressors (such as financial concerns and family problems) can, after repeated exposure, affect the physiology of the brain.
Chronic stress or trauma has been shown to have neuroadaptive effects such that the brain can essentially physically “rewire” itself to accommodate for the increase in cortisol produced by the stressors. Evidence has also shown that a great amount of stress hinders your prefrontal functioning as well causes an increased limbic-stratal level responding. This can lead to low behavioural and cognitive control. Additionally, when the brain is put under severe stress due to repeated drug use, it has been shown to be physiologically altered. This compromised neural state plays a large role in perpetuating addiction and in making recovery more difficult.
Repeated exposure to a drug is one of the determining factors in distinguishing recreational substance use from chronic abuse. Many neurobiological theories of addiction place repeated or continued use of the drug in the path of addiction development. For example, researchers have theorized that addiction is the result of the shift from goal-directed actions to habits and ultimately, to compulsive drug-seeking and taking.
In other words, repeated, deliberate use of the drug plays a role in the eventual compulsory drug-taking and/or habitual drug-taking associated with addiction. Another theory suggests that through repeated use of the drug, individuals become sensitised to drug-associated stimuli which may result in compulsive motivation and desire for the drug.
Additionally, a third neurobiological theory highlights the changes in brain reward circuitry following repeated drug use that contributes to the development of addiction such that addiction is conceptualised as being a progression of allostatic changes in which the addicted individual is able to maintain stability but at a pathological set point. Experience-dependent neural plasticity is a hallmark of repeated drug exposure and refers to the adaptation of the brain due to increased levels of the drug in the body. In this sense, repeated exposure falls under the both physiological vulnerability and behavioural/psychological vulnerability to addiction.
Although many variables individually contribute to an increased risk of developing a substance use disorder, no single vulnerability guarantees the development of addiction. It is the combination of many factors (e.g. genetics, environmental stressors, initiation and continued use of the drug) that culminates in the development of this disorder.
Previous research has examined the increased risk of substance use initiation during adolescence. Many factors have been identified as being associated with increased risk of substance use during this period of development including individual differences (e.g. negative affect, decreased harm avoidance, and low motivation for achievement), biological (e.g., genetic predisposition and neurological development), and environmental factors (e.g. high levels of stress, peer influences, availability of substances, etc.). Rat studies provide behavioural evidence that adolescence is a period of increased vulnerability to drug-seeking behaviour and onset addiction.
The mesolimbic dopamine system of the brain is undergoing reorganisation and functional changes during adolescence. Rat studies have demonstrated that adolescents have tendencies and abilities to drink more than adults due to minimal disruption to their motor functions and also due to minimal sensitivity to sedation. As a result, it is more susceptible to become addicted in the wake of drug use during this developmental period. Overall, social, behavioural and developmental factors in adolescence make individuals more liable to drug seeking behaviour, and as a result, addiction.
Transgenerational Epigenetic Inheritance
Epigenetic genes and their products (e.g. proteins) are the key components through which environmental influences can affect the genes of an individual; they also serve as the mechanism responsible for transgenerational epigenetic inheritance, a phenomenon in which environmental influences on the genes of a parent can affect the associated traits and behavioural phenotypes of their offspring (e.g. behavioural responses to environmental stimuli). In addiction, epigenetic mechanisms play a central role in the pathophysiology of the disease; it has been noted that some of the alterations to the epigenome which arise through chronic exposure to addictive stimuli during an addiction can be transmitted across generations, in turn affecting the behaviour of one’s children (e.g. the child’s behavioural responses to addictive drugs and natural rewards).
The general classes of epigenetic alterations that have been implicated in transgenerational epigenetic inheritance include DNA methylation, histone modifications, and downregulation or upregulation of microRNAs. With respect to addiction, more research is needed to determine the specific heritable epigenetic alterations that arise from various forms of addiction in humans and the corresponding behavioural phenotypes from these epigenetic alterations that occur in human offspring. Based upon preclinical evidence from animal research, certain addiction-induced epigenetic alterations in rats can be transmitted from parent to offspring and produce behavioural phenotypes that decrease the offspring’s risk of developing an addiction [note 1]. More generally, the heritable behavioural phenotypes that are derived from addiction-induced epigenetic alterations and transmitted from parent to offspring may serve to either increase or decrease the offspring’s risk of developing an addiction.
According to a review of experimental animal models that examined the transgenerational epigenetic inheritance of epigenetic marks that occur in addiction, alterations in histone acetylation – specifically, di-acetylation of lysine residues 9 and 14 on histone 3 (i.e. H3K9ac2 and H3K14ac2) in association with BDNF gene promoters – have been shown to occur within the medial prefrontal cortex (mPFC), testes, and sperm of cocaine-addicted male rats.
These epigenetic alterations in the rat mPFC result in increased BDNF gene expression within the mPFC, which in turn blunts the rewarding properties of cocaine and reduces cocaine self-administration.
The male but not female offspring of these cocaine-exposed rats inherited both epigenetic marks (i.e. di-acetylation of lysine residues 9 and 14 on histone 3) within mPFC neurons, the corresponding increase in BDNF expression within mPFC neurons, and the behavioural phenotype associated with these effects (i.e. a reduction in cocaine reward, resulting in reduced cocaine-seeking by these male offspring).
Consequently, the transmission of these two cocaine-induced epigenetic alterations (i.e. H3K9ac2 and H3K14ac2) in rats from male fathers to male offspring served to reduce the offspring’s risk of developing an addiction to cocaine.
As of 2018, neither the heritability of these epigenetic marks in humans nor the behavioural effects of the marks within human mPFC neurons has been established.
An addictive personality refers to a hypothesized set of personality traits that make an individual predisposed to developing addictions.
This hypothesis states that there may be common personality traits observable in people suffering from addiction; however, the lack of a universally agreed upon definition has marked the research surrounding addictive personality. Addiction is a fairly broad term; it is most often associated with substance abuse, but it can also be extended to cover a number of other compulsive behaviours, including sex, internet, television, gambling, food, and shopping. Within these categories of addiction a common diagnostic scale involves tolerance, withdraw, and cravings.
This is a fairly contentious topic, with many experts suggesting the term be retired due to a lack of cumulative evidence supporting the existence of addictive personality. Stating that characteristics of personality attributed to addictive personality do not predict addiction, but can result from addiction. However, different personality traits have been linked to various types of addictive behaviours, suggesting that individual addictions may be associated with different personality profiles. The strongest consensus is that genetic factors play the largest role in determining a predisposition for addictive behaviours. Even then, however, genes play different roles in different types of addictions. Forty to seventy percent of the population variance in the expression of addictions can be explained by genetic factors.
The following factors are believed to influence addiction susceptibility.
Nonconformity combined with weak commitment to socially valued goals for achievement.
Social alienation and tolerance for deviance.
Heightened stress coupled with lack of coping skills.
Some claim the existence of “addictive beliefs” in people more likely to develop addictions, such as “I cannot make an impact on my world” or “I am not good enough”, which may lead to developing traits associated with addiction, such as depression and emotional insecurity. People who strongly believe that they control their own lives and are mostly self-reliant in learning information (rather than relying on others) are less likely to become addicted. However, it is unclear whether these traits are causes, results or merely associated coincidentally. For example, depression due to physical disease can cause feelings of hopelessness that are mitigated after successful treatment of the underlying condition, and addiction can increase dependence on others. Certain psychological disorders such as panic attacks, depressive disorders, and generalized anxiety disorder have been related to addiction. The addict, who struggles with reality and feels negative feelings, such as anxiety and depression, will seek out ways to help them avoid such feelings.
Overeating due to food addiction has not yet ben recognized as a medical disorder under the Diagnostic and Statistical Manual of Mental Disorders despite its prevalence in the general population. A study based on social cognitive theories, included a personality-targeted intervention that was shown to help treat substance addiction. It is feasible that by changing certain elements of one’s personality, one can gain a step in the right direction towards changing their addictive personality.
Individual traits can share common underlying factors or interact. For example, depression, poor self-control, and compulsive behaviour are linked to neurotransmitter abnormalities, i.e., biological mechanisms. In laboratory studies with rats only some rats develop a pattern of self-administration of stimulant drugs, supporting the existence of some inherent propensity for addictive tendencies. In these rats, a positive correlation was found between locomotor response to novel stimuli and the amount of amphetamine self-administered during the first few days of testing. Twin and adoption studies have shown genetic factors account for 50-60% of the risk for alcoholism. In early adolescence, social and familial factors play a more important role in the initiation of drug use but their importance fades with progression into adulthood. The gene CHRNA5 has been heavily linked to the addictions of cigarettes. Researchers discovered that the CHRNA5 variant creates a less nauseating experience for a first time smoker. The gene is active in the region of the brain called the Habenula. Research showed that frequent smoking might damage the neurons within the Habenula that inhibit its role in aversion and avoidance which might cause the smoker to then use more nicotine to feel relief from resulting distressful and negative feelings.
Studies have found numerous environmental factors that correlate with addiction. Exposure to sustained stress in childhood, such as physical or sexual abuse, especially accompanied by unpredictable parental behaviour strongly correlates with drug addiction and overeating in adulthood. Children who tend to react to distress in a more rash way have been linked to becoming more likely to drink and smoke in their adolescence. Results from this research found that this was because the reaction to distress affected psychosocial learning, which led to increased expectancy to drink or smoke. A lack of social interaction has also been shown to correlate with addictive tendencies; rats reared in isolation were quicker to develop a pattern of cocaine self-administration than rats reared in groups. There is a gene/environment connection in that individuals with particular personality traits may self-select into different environments, e.g. they may seek out work environments where addictive substances are more readily available.
People who suffer from an addictive personality spend excessive time on a behaviour or with an item, not as a hobby but because they feel they have to. Addiction can be defined when the engagement in the activity or experience affects the person’s quality of life in some way. In this way, many people who maintain an addictive personality isolate themselves from social situations in order to mask their addiction.
People that face this issue are currently defined to have a brain disease as promoted by the National Institute on Drug Abuse and other authorities. People who experience addictive personality disorders typically act on impulses and cannot deal with delayed gratification. At the same time, people with this type of personality tend to believe that they do not fit into societal norms and therefore, acting on impulses, deviate from conformity to rebel. People with addictive personalities are very sensitive to emotional stress. They have trouble handling situations that they deem frustrating, even if the event is for a very short duration. The combination of low self-esteem, impulsivity and low tolerance for stress causes these individuals to have frequent mood swings and often suffer from some sort of depression. A coping mechanism to deal with their conflicting personality becomes their addiction and the addiction acts as something that the person can control when they find it difficult to control their personality traits.
People with addictive personalities typically switch from one addiction to the next. These individuals may show impulsive behaviour such as excessive caffeine consumption, Internet use, eating chocolate or other sugar-laden foods, television watching, or even running.
Extraversion, self-monitoring, and loneliness are also common characteristics found in those who suffer from addiction. Individuals who score high on self-monitoring are more prone to developing an addiction. High self-monitors are sensitive to social situations; they act how they think others expect them to act. They wish to fit in, hence they are very easily influenced by others. Likewise, those who have low self-esteem also seek peer approval; therefore, they participate in “attractive” activities such as smoking or drinking to try to fit in.
People with addictive personalities find it difficult to manage their stress levels. In fact, lack of stress tolerance is a telltale sign of the disorder. They find it difficult to face stressful situations and fight hard to get out of such conditions. Long-term goals prove difficult to achieve because people with addictive personalities usually focus on the stress that comes with getting through the short-term goals. Such personalities will often switch to other enjoyable activities the moment that they are deprived of enjoyment in their previous addiction.
Addictive individuals feel highly insecure when it comes to relationships. They may often find it difficult to make commitments in relationships or trust their beloved because of the difficulty they find in achieving long-term goals. They constantly seek approval of others and as a result, these misunderstandings may contribute to the destruction of relationships. People suffering from addictive personality disorder usually undergo depression and anxiety, managing their emotions by developing addiction to alcohol, other types of drugs, or other pleasurable activities.
An addict is more prone to depression, anxiety, and anger. Both the addict’s environment, genetics and biological tendency contribute to their addiction. People with very severe personality disorders are more likely to become addicts. Addictive substances usually stop primary and secondary neuroses, meaning people with personality disorders like the relief from their pain.
Personality Traits and Addiction
Addiction is defined by scholars as “a biopsychosocial disorder characterised by persistent use of drugs (including alcohol) despite substantial harm and adverse consequences”. Substance-based addictions are those based upon the release of dopamine in the brain, upon which the range of sensations produced by the euphoric event in the brain changes the brain’s immediate behaviour, causing more susceptibility for future addictions. Behaviour-based addictions, on the other hand, are those that are not linked to neurological behaviour as much and are thus thought to be linked to personality traits; it is this type of addiction that combines a behaviour with a mental state and the repeated routine is therefore associated with the mental state.
A group of British forensic psychologists and data scientists analysed a new large database of users of psychoactive substances. To analyse the predisposition to drug use, they utilised 7 psychological traits, the Five Factor Model supplemented by Impulsivity and Sensation seeking:
Neuroticism is a long-term tendency to experience negative emotions such as nervousness, tension, anxiety and depression (associated adjectives: anxious, self-pitying, tense, touchy, unstable, and worrying);
Extraversion is manifested in outgoing, warm, active, assertive, talkative, cheerful characters, often in search of stimulation (associated adjectives: active, assertive, energetic, enthusiastic, outgoing, and talkative);
Openness to experience is a general appreciation for art, unusual ideas, and imaginative, creative, unconventional, and wide interests (associated adjectives: artistic, curious, imaginative, insightful, original, and wide interest);
Agreeableness is a dimension of interpersonal relations, characterized by altruism, trust, modesty, kindness, compassion and cooperativeness (associated adjectives: appreciative, forgiving, generous, kind, sympathetic, and trusting);
Conscientiousness is a tendency to be organized and dependable, strong-willed, persistent, reliable, and efficient (associated adjectives: efficient, organised, reliable, responsible, and thorough);
Impulsivity is defined as a tendency to act without adequate forethought;
Sensation Seeking is defined by the search for experiences and feelings, that are varied, novel, complex and intense, and by the readiness to take risks for the sake of such experiences.
These factors are not statistically independent but the condition number of the correlation matrix is less than 10 and the multicollinearity effects are not expected to be strong.
The results of the detailed analysis of modern data support partially the hypothesis about psychological predisposition to addiction. The group of users of illicit drugs differs from the group of non-users for N, O, A, C, Imp, and SS. Symbolically, this difference can be illustrated as follows:
(N, O, Imp, and SS scores are higher for users; A and C scores are lower for users).
The hypothesis about importance of E for addiction was not supported by this aggregated analysis of use of all illicit drugs.
Analysis of consumption of different drugs separately demonstrated that predisposition to use of different drugs is different. For all illicit drugs groups of their users have the following common properties:
(O, Imp, and SS scores are higher for users and C score is lower for users).
Deviation of N, E, and A scores for users of different drugs can be different. For example, heroin users have average profile
whereas for LSD and Ecstasy (the latter being a so-called “Party drug”) users N has no significant deviation from the population level and E can be higher.
Several personality profiles of risky behaviour were identified by various researchers, for example (Insecures) and (Impulsives, Hedonists). Various types of addictive personality have in common low C.
Internet addiction is associated with higher scores in neuroticism and lower scores in extraversion and conscientiousness. One explanation for the association with high neuroticism is that virtual environments may be regarded as more safe and comfortable by individuals with lower self-esteem and increased negative emotion (traits associated with high neuroticism) compared to real-life environments. Similarly, individuals with low extraversion that desire social interaction but are averse to face-to-face interaction may find the opportunity for online communication attractive.
There is an ongoing debate about the question of whether an addictive personality really exists. The assumption that personality might be to blame for an addicted person, who is in need of rehabilitation due to drug and alcohol addictions, can have great negative impacts from its supporting a homogeneous answer to a heterogeneous issue in question. These people run the risk of being labelled as stigmas and become incorrectly marginalised, and these misjudgements of personality may then lead to poor mental, medical, and social health practices. There are two sides of this argument, each with many levels and variations. One side believes that there are certain traits and dimensions of personality that, if existent in a person, cause the person to be more prone to developing addictions throughout their life. The other side argues that addiction is in chemistry, as in how the brain’s synapses respond to neurotransmitters and is therefore not affected by personality. A major argument in favour of defining and labelling an addictive personality has to do with the human ability to make decisions and the notion of free will. This argument suggests human beings are aware of their actions and what the consequences of their own actions are and many choose against certain things because of this. This can be seen in that people are not forced to drink excessively or smoke every day, but it is within the reach of their own free will that some may choose to do so. Therefore, those with addictive personalities are high in neuroticism and hence choose to engage in riskier behaviours. The theory of addictive personalities agrees that there are two types of people: risk-takers and risk-averse. Risk-takers enjoy challenges, new experiences and want instant gratification. These people enjoy the excitement of danger and trying new things. On the other hand, risk-averse are those who are by nature cautious in what they do and the activities they involve themselves in. It is the personality traits of individuals that combine to create either a risk-taker or risk-averse person.
Another important concern is the lack of evidence supporting the addictive personality label and the possibility of stigma. While there is a medical consensus surrounding the genetic components of addiction, there is no such consensus supporting the idea that specific personality types have a tendency towards addictive behaviours. In fact, continued use of this term in the absence of clear evidence could be damaging to the people who believe they have an addictive personality.
1946 – Claude Steele, American social psychologist and academic.
Claude Mason Steele (born January 1, 1946) is a social psychologist and emeritus professor at Stanford University, where he is the I. James Quillen Endowed Dean, Emeritus at the Stanford Graduate School of Education, and Lucie Stern Professor in the Social Sciences, Emeritus.
Formerly he was the executive vice chancellor and provost at the University of California, Berkeley. He also served as the 21st provost of Columbia University for two years. Before that, he had been a professor of psychology at various institutions for almost 40 years.
He is best known for his work on stereotype threat and its application to minority student academic performance. His earlier work dealt with research on the self (like self-image and self-affirmation) as well as the role of self-regulation in addictive behaviours.
In 2010, he released his book, Whistling Vivaldi and Other Clues to How Stereotypes Affect Us, summarising years of research on stereotype threat and the underperformance of minority students in higher education.
He enrolled at Hiram College in Hiram, Ohio, where he earned a B.A. in psychology in 1967.
At Hiram College, Steele’s passion for reading novels led to an interest in how the individual faces the social world. After being fully immersed in the Civil Rights Movement and the issues of racial equality, rights, and the nature of prejudice as a child, Steele formed a desire to study the topics in a scientific manner. He was especially keen to discover their effects on social relationships and quality of life. Steele was inspired by African-American social psychologist Kenneth Clark’s TV appearance discussing the psychological implications of the 1964 race riots in Harlem, New York City, which led to doing behavioural research. Steele conducted early experimental research at Hiram College in physiological psychology (looking at behavioural motives in Siamese fighting fish) and social psychology (studying how African-American dialect among kids maintains ethnic/racial identity), where he worked under the mentorship of social psychologist, Ralph Cebulla.
In graduate school, he studied social psychology, earning an M.A. in 1969 and a Ph.D. in 1971 at Ohio State University, with a minor in statistical psychology. His dissertation work, with faculty adviser Tom Ostrom at Ohio State, focused on attitude measurement and attitude change.
Throughout his academic career, his work fell into three main domains of research under the broad subject area of social psychology: stereotype threat, self-affirmation, and addictive behaviours. Although separate and distinct, the three lines of research are linked by their shared focus on self-evaluation and how people cope with threats to their self-image and self-identities.
Although many people primarily associate Steele with his significant contributions in the development of stereotype threat research, the 14 years of his post-doctoral academic career that he spent at the University of Washington were focused on addictive behaviours and the social psychology behind alcohol use and addiction.
He was interested in the role of alcohol and drug use in self-regulation processes and social behaviour.
Among his major findings were that alcohol myopia, the cognitive impairment by alcohol use, reduces cognitive dissonance, leads to more extreme social responses, increases helping behaviour, reduces anxiety when it is combined with a distracting activity, and enhances important self-evaluations.
While studying the effects of alcohol use on social behaviour, Steele was formulating a theory about the effects of self-affirmation.
Developed in the 1980s, self-affirmational processes referred to the ability to reduce threats to self-image by stepping back and affirming a value that is important to self-concept.
Steele often uses the example of smokers who are told that smoking will lead to significant negative health outcomes.
The perception that they may be evaluated negatively by their willingness to engage in negative behaviours threatens their self-image.
However, affirming a value in a domain completely unrelated to smoking but important to one’s self-concept: joining a valued cause, or accomplishing more at work, will counter the negative effects of the self-image threat and re-establish self-integrity.
Self-affirmation theory was originally formulated as an alternative motivational explanation for cognitive dissonance theory that threats to the self led to a change in attitudes rather than psychologically inconsistent ideas, and self-affirmational strategies can reduce dissonance as effectively as attitude change.
His research on self-affirmation and its effects demonstrated the power of self-affirmation to reduce biased attitudes, lead to positive health behaviours, and even improve the academic performance of minority students.
Steele is best known for his work on stereotype threat and its application to explain real-world problems such as the underperformance of female students in mathematics and science classes as well as Black students in academic contexts.
Steele first began to explore the issues surrounding stereotype threat at the University of Michigan, when his membership on a university committee called for him to tackle the problem of academic underachievement of minority students at the university.
He discovered that the dropout rate for Black students was much higher than for their white peers even though they were good students and had received excellent SAT scores.
That led him to form a hypothesis involving stereotype threat.
Stereotype threat refers to the threat felt in particular situations in which stereotypes relevant to one’s collective identity exist, and the mere knowledge of the stereotypes can be distracting enough to negatively affect performance in a domain related to the stereotype.
Steele has demonstrated the far-reaching implications of stereotype threat by showing that it is more likely to undermine the performance of individuals highly invested in the domain being threatened and that stereotype threat can even lead to Black people having significant negative health outcomes.
The theories of stereotype threat can be applied for better understanding group differences in performance not only in intellectual situations but also in athletics.
Steele has spearheaded many successful interventions aimed at reducing the negative effects of stereotype threat, including how to provide critical feedback effectively to a student under the effects of stereotype threat, inspired by the motivating style of feedback of his graduate school adviser, Ostrom, and how teacher practices can foster a feeling of identity safety.
That would improve performance outcomes by elementary school minority students.
The Addiction Treatment Planner: Includes DSM-5 Updates.
Author(s): Robert R. Perkinson, Arthur E. Jongsma, and Timothy J. Bruce.
Edition: Fifth (5th).
Type(s): Paperback and Kindle.
The Addiction Treatment Planner, Fifth Edition provides all the elements necessary to quickly and easily develop formal treatment plans that satisfy the demands of HMOs, managed care companies, third-party payors, and state and federal agencies.
New edition features empirically supported, evidence-based treatment interventions.
Organised around 43 behaviourally based presenting problems, including substance use, eating disorders, schizoid traits, and others.
Over 1,000 prewritten treatment goals, objectives, and interventions – plus space to record your own treatment plan options.
Easy-to-use reference format helps locate treatment plan components by behavioural problem.
Includes a sample treatment plan that conforms to the requirements of most third-party payors and accrediting agencies including CARF, The Joint Commission (TJC), COA, and the NCQA.
Internet Addiction in Children and Adolescents: Risk Factors, Assessment, and Treatment.
Author(s): Kimberly S. Young and Cristiano Nabuco de Abreu (Editors).
Edition: First (1st).
Publisher: Springer Publishing Co Inc.
Type(s): Paperback and Kindle.
This is the first book to thoroughly examine how early and easy access to the Internet and digital technologies impacts children and adolescents. Experts in the field examine the research that shows the social, cognitive, developmental, and academic problems that can result when children spend excessive time in front of screens. As a whole, the book provides an invaluable resource for those who need to assess, treat, and prevent Internet addiction in children and adolescents.
Internet Addiction in Children and Adolescents:
Provides tools that help predict a child’s level of risk for media-related problems.
Examines how to diagnose and differentiate Internet addiction from other psychiatric conditions.
Explores evidence-based treatment approaches and how to distinguish pathology from normal development.
Shows how to create inpatient treatment programs and therapies to address media addiction.
Highlights the psychological, social, and family conditions for those most at risk.
Evaluates the effects of the excessive use of electronic games and the Internet on brain development.
Explores the physical risks that result from excessive media use and strategies for combating the problem.
Examines school-based initiatives that employ policies and procedures designed to increase awareness of excessive media use and help educators identify students who misuse technology, and that provide strategies of intervention and communication with parents.
Identifies signs of problem Internet behavior such as aggressive behavior, lying about screen use, and a preference for screen time over social interactions.
Outlines the risk factors for developing Internet addiction.
Provides strategies for treatment and prevention in family, school, and community settings.
Practitioners and researchers in psychology, social work, school counseling, child and family therapy, and nursing will appreciate this book’s thorough review of Internet addiction among children and adolescents. The book also serves as an engaging supplement in courses on media psychology, addiction counseling, abnormal psychology, school counseling, social issues, and more.
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