Showing papers on "Addiction published in 2011"
TL;DR: Functional neuroimaging studies conducted in the past decade that have expanded the understanding of the involvement of the PFC in drug addiction are focused on.
Abstract: The loss of control over drug intake that occurs in addiction was initially believed to result from disruption of subcortical reward circuits. However, imaging studies in addictive behaviours have identified a key involvement of the prefrontal cortex (PFC) both through its regulation of limbic reward regions and its involvement in higher-order executive function (for example, self-control, salience attribution and awareness). This Review focuses on functional neuroimaging studies conducted in the past decade that have expanded our understanding of the involvement of the PFC in drug addiction. Disruption of the PFC in addiction underlies not only compulsive drug taking but also accounts for the disadvantageous behaviours that are associated with addiction and the erosion of free will.
2,008 citations
TL;DR: The findings indicate that SNSs are predominantly used for social purposes, mostly related to the maintenance of established offline networks, and extraverts appear to use social networking sites for social enhancement, whereas introverts use it for social compensation.
Abstract: Social Networking Sites (SNSs) are virtual communities where users can create individual public profiles, interact with real-life friends, and meet other people based on shared interests. They are seen as a 'global consumer phenomenon' with an exponential rise in usage within the last few years. Anecdotal case study evidence suggests that 'addiction' to social networks on the Internet may be a potential mental health problem for some users. However, the contemporary scientific literature addressing the addictive qualities of social networks on the Internet is scarce. Therefore, this literature review is intended to provide empirical and conceptual insight into the emerging phenomenon of addiction to SNSs by: (1) outlining SNS usage patterns, (2) examining motivations for SNS usage, (3) examining personalities of SNS users, (4) examining negative consequences of SNS usage, (5) exploring potential SNS addiction, and (6) exploring SNS addiction specificity and comorbidity. The findings indicate that SNSs are predominantly used for social purposes, mostly related to the maintenance of established offline networks. Moreover, extraverts appear to use social networking sites for social enhancement, whereas introverts use it for social compensation, each of which appears to be related to greater usage, as does low conscientiousness and high narcissism. Negative correlates of SNS usage include the decrease in real life social community participation and academic achievement, as well as relationship problems, each of which may be indicative of potential addiction.
1,427 citations
TL;DR: The results indicate that the vulnerability to stimulant addiction may depend on an impulsivity endophenotype, and characterize in neurobehavioral and neurochemical terms a rodent model of impulsivity based on premature responding in an attentional task.
1,334 citations
TL;DR: Results point to an imbalance between dopaminergic circuits that underlie reward and conditioning and those thatUnderlie executive function (emotional control and decision making), which contributes to the compulsive drug use and loss of control in addiction.
Abstract: Dopamine (DA) is considered crucial for the rewarding effects of drugs of abuse, but its role in addiction is much less clear. This review focuses on studies that used PET to characterize the brain DA system in addicted subjects. These studies have corroborated in humans the relevance of drug-induced fast DA increases in striatum [including nucleus accumbens (NAc)] in their rewarding effects but have unexpectedly shown that in addicted subjects, drug-induced DA increases (as well as their subjective reinforcing effects) are markedly blunted compared with controls. In contrast, addicted subjects show significant DA increases in striatum in response to drug-conditioned cues that are associated with self-reports of drug craving and appear to be of a greater magnitude than the DA responses to the drug. We postulate that the discrepancy between the expectation for the drug effects (conditioned responses) and the blunted pharmacological effects maintains drug taking in an attempt to achieve the expected reward. Also, whether tested during early or protracted withdrawal, addicted subjects show lower levels of D2 receptors in striatum (including NAc), which are associated with decreases in baseline activity in frontal brain regions implicated in salience attribution (orbitofrontal cortex) and inhibitory control (anterior cingulate gyrus), whose disruption results in compulsivity and impulsivity. These results point to an imbalance between dopaminergic circuits that underlie reward and conditioning and those that underlie executive function (emotional control and decision making), which we postulate contributes to the compulsive drug use and loss of control in addiction.
739 citations
TL;DR: Recent advances in the understanding of the brain circuitries that regulate hedonic aspects of feeding behavior will be reviewed and emerging evidence suggesting that obesity and drug addiction may share commonHedonic mechanisms will also be considered.
645 citations
TL;DR: It is argued that sensitization remains a useful model for determining the neural basis of addiction, and an example is provided in which data from sensitization studies led to potential pharmacotherapies that have been tested in animal models of relapse and in human addicts.
Abstract: Repeated exposure to drugs of abuse enhances the motor-stimulant response to these drugs, a phenomenon termed behavioral sensitization. Animals that are extinguished from self-administration training readily relapse to drug, conditioned cue, or stress priming. The involvement of sensitization in reinstated drug-seeking behavior remains controversial. This review describes sensitization and reinstated drug seeking as behavioral events, and the neural circuitry, neurochemistry, and neuropharmacology underlying both behavioral models will be described, compared, and contrasted. It seems that although sensitization and reinstatement involve overlapping circuitry and neurotransmitter and receptor systems, the role of sensitization in reinstatement remains ill-defined. Nevertheless, it is argued that sensitization remains a useful model for determining the neural basis of addiction, and an example is provided in which data from sensitization studies led to potential pharmacotherapies that have been tested in animal models of relapse and in human addicts.
584 citations
TL;DR: Similar patterns of neural activation are implicated in addictive-like eating behavior and substance dependence: elevated activation in reward circuitry in response to food cues and reduced activation of inhibitory regions in responseto food intake.
Abstract: Context Research has implicated an addictive process in the development and maintenance of obesity. Although parallels in neural functioning between obesity and substance dependence have been found, to our knowledge, no studies have examined the neural correlates of addictive-like eating behavior. Objective To test the hypothesis that elevated“food addiction” scores are associated with similar patterns of neural activation as substance dependence. Design Between-subjects functional magnetic resonance imaging study. Setting A university neuroimaging center. Participants Forty-eight healthy young women ranging from lean to obese recruited for a healthy weight maintenance trial. Main Outcome Measure The relation between elevated food addiction scores and blood oxygen level–dependent functional magnetic resonance imaging activation in response to receipt and anticipated receipt of palatable food (chocolate milkshake). Results Food addiction scores (N = 39) correlated with greater activation in the anterior cingulate cortex, medial orbitofrontal cortex, and amygdala in response to anticipated receipt of food (P Conclusions Similar patterns of neural activation are implicated in addictive-like eating behavior and substance dependence: elevated activation in reward circuitry in response to food cues and reduced activation of inhibitory regions in response to food intake.
572 citations
TL;DR: There appears to be a direct pathway from chronic stress exposure in pre-pubertal children via adolescent problem drinking to alcohol and drug dependence in early adulthood, however, this route can be moderated by genetic and environmental factors.
Abstract: Rationale
Genetic and environmental influences on the development of alcohol and drug dependence are equally important. Exposure to early life stress, that is unfortunately common in the general population, has been shown to predict a wide range of psychopathology, including addiction.
499 citations
TL;DR: The authors assert that it is most plausible that 47% of the U.S. adult population suffers from maladaptive signs of an addictive disorder over a 12-month period and that it may be useful to think of addictions as due to problems of lifestyle as well as to person-level factors.
Abstract: An increasing number of research studies over the last three decades suggest that a wide range of substance and process addictions may serve similar functions. The current article considers 11 such potential addictions (tobacco, alcohol, illicit drugs, eating, gambling, Internet, love, sex, exercise, work, and shopping), their prevalence, and co-occurrence, based on a systematic review of the literature. Data from 83 studies (each study n = at least 500 subjects) were presented and supplemented with small-scale data. Depending on which assumptions are made, overall 12-month prevalence of an addiction among U.S. adults varies from 15% to 61%. The authors assert that it is most plausible that 47% of the U.S. adult population suffers from maladaptive signs of an addictive disorder over a 12-month period and that it may be useful to think of addictions as due to problems of lifestyle as well as to person-level factors.
495 citations
TL;DR: The findings contribute to the discussion on the inclusion of non-substance addictions in the proposed unified concept of 'Addiction and Related Disorders' for the DSM-V by providing indirect identification and validation of a group of suspected online video game addicts.
Abstract: Aims To provide empirical data-driven identification of a group of addicted online gamers. Design Repeated cross-sectional survey study, comprising a longitudinal cohort, conducted in 2008 and 2009. Setting Secondary schools in the Netherlands. Participants Two large samples of Dutch schoolchildren (aged 13-16 years). Measurements Compulsive internet use scale, weekly hours of online gaming and psychosocial variables. Findings Thisstudyconfirmstheexistenceof asmallgroupof addictedonlinegamers(3%),representingabout1.5% of all children aged 13-16 years in the Netherlands. Although these gamers report addiction-like problems, relation- ships with decreased psychosocial health were less evident. Conclusions The identification of a small group of addicted online gamers supports efforts to develop and validate questionnaire scales aimed at measuring the phenom- enon of online video game addiction. The findings contribute to the discussion on the inclusion of non-substance addictions in the proposed unified concept of 'Addiction and Related Disorders' for the DSM-V by providing indirect identification and validation of a group of suspected online video game addicts.
TL;DR: Those who met the diagnostic criteria for FA had a significantly greater co-morbidity with Binge Eating Disorder, depression, and attention-deficit/hyperactivity disorder compared to their age- and weight-equivalent counterparts.
TL;DR: Results suggest that both obese and drug-addicted individuals suffer from impairments in dopaminergic pathways that regulate neuronal systems associated not only with reward sensitivity and incentive motivation, but also with conditioning, impulse control, stress reactivity, and interoceptive awareness.
Abstract: Both drug addiction and obesity can be defined as disorders in which the saliency value of one type of reward (drugs and food, respectively) becomes abnormally enhanced relative to, and at the expense of others. This model is consistent with the fact that both drugs and food have powerful reinforcing effects—partly mediated by dopamine increases in the limbic system—that, under certain circumstances or in vulnerable individuals, could overwhelm the brain’s homeostatic control mechanisms. Such parallels have generated significant interest in understanding the shared vulnerabilities and trajectories between addiction and obesity. Now, brain imaging discoveries have started to uncover common features between these two conditions and to delineate some of the overlapping brain circuits whose dysfunctions may explain stereotypic and related behavioral deficits in human subjects. These results suggest that both obese and drug-addicted individuals suffer from impairments in dopaminergic pathways that regulate neuronal systems associated not only with reward sensitivity and incentive motivation, but also with conditioning (memory/learning), impulse control (behavioural inhibition), stress reactivity, and interoceptive awareness. Here, we integrate findings predominantly derived from positron emission tomography that shed light on the role of dopamine in drug addiction and in obesity, and propose an updated working model to help identify treatment strategies that may benefit both of these conditions.
TL;DR: It is argued that opiate addiction and psychostimulant addiction are behaviourally and neurobiologically distinct and that the differences have important implications for addiction treatment, addiction theories and future research.
Abstract: The publication of the psychomotor stimulant theory of addiction in 1987 and the finding that addictive drugs increase dopamine concentrations in the rat mesolimbic system in 1988 have led to a predominance of psychobiological theories that consider addiction to opiates and addiction to psychostimulants as essentially identical phenomena. Indeed, current theories of addiction - hedonic allostasis, incentive sensitization, aberrant learning and frontostriatal dysfunction - all argue for a unitary account of drug addiction. This view is challenged by behavioural, cognitive and neurobiological findings in laboratory animals and humans. Here, we argue that opiate addiction and psychostimulant addiction are behaviourally and neurobiologically distinct and that the differences have important implications for addiction treatment, addiction theories and future research.
TL;DR: In this article, the authors examined how user cognition and ultimately usage intentions toward an information technology are distorted by addiction to the technology, and found that addiction to online auctions augments user perceptions of enjoyment, usefulness, and ease of use attributed to the information technology, which in turn influence usage intentions.
Abstract: Technology addiction is a relatively new mental condition that has not yet been well integrated into mainstream MIS models. This study bridges this gap and incorporates technology addiction into technology use processes in the context of online auctions. It examines how user cognition and ultimately usage intentions toward an information technology are distorted by addiction to the technology. The findings from two empirical studies of 132 and 223 eBay users, using three different operationalizations of addiction, indicate that the level of online auction addiction distorts the way the IT artifact is perceived. Informing a range of cognitionmodification processes, addiction to online auctions augments user perceptions of enjoyment, usefulness, and ease of use attributed to the technology, which in turn influence usage intentions. Overall, consistent with behavioral addiction models, the findings indicate that users' levels of online auction addiction influence their reasoned IT usage decisions by altering users' belief systems. The formation of maladaptive perceptions is driven by a combination of memory-, learning-, and bias-based cognition modification processes. Implications of the findings are discussed.
TL;DR: The ACC, right pallidum and ventral striatum were related to drug cue reactivity as well as self‐reported craving, suggesting that this set of brain regions constitutes the core circuit of drug craving in nicotine and alcohol addiction.
Abstract: The present quantitative meta-analysis set out to test whether cue-reactivity responses in humans differ across drugs of abuse and whether these responses constitute the biological basis of drug craving as a core psychopathology of addiction. By means of activation likelihood estimation, we investigated the concurrence of brain regions activated by cue-induced craving paradigms across studies on nicotine, alcohol and cocaine addicts. Furthermore, we analysed the concurrence of brain regions positively correlated with self-reported craving in nicotine and alcohol studies. We found direct overlap between nicotine, alcohol and cocaine cue reactivity in the ventral striatum. In addition, regions of close proximity were observed in the anterior cingulate cortex (ACC; nicotine and cocaine) and amygdala (alcohol, nicotine and cocaine). Brain regions of concurrence in drug cue-reactivity paradigms that overlapped with brain regions of concurrence in self-reported craving correlations were found in the ACC, ventral striatum and right pallidum (for alcohol). This first quantitative meta-analysis on drug cue reactivity identifies brain regions underlying nicotine, alcohol and cocaine dependency, i.e. the ventral striatum. The ACC, right pallidum and ventral striatum were related to drug cue reactivity as well as self-reported craving, suggesting that this set of brain regions constitutes the core circuit of drug craving in nicotine and alcohol addiction.
TL;DR: Evidence suggesting that obesity and drug addiction may share common molecular, cellular and systems-level mechanisms is reviewed.
Abstract: The hedonic properties of food can stimulate feeding behaviour even when energy requirements have been met, contributing to weight gain and obesity. Similarly, the hedonic effects of drugs of abuse can motivate their excessive intake, culminating in addiction. Common brain substrates regulate the hedonic properties of palatable food and addictive drugs, and recent reports suggest that excessive consumption of food or drugs of abuse induces similar neuroadaptive responses in brain reward circuitries. Here, we review evidence suggesting that obesity and drug addiction may share common molecular, cellular and systems-level mechanisms.
TL;DR: Nicotine taps into diverse neural systems and an array of nicotinic acetylcholine receptor (nAChR) subtypes to influence reward, addiction, and withdrawal.
Abstract: Nicotine is the principal addictive component that drives continued tobacco use despite users' knowledge of the harmful consequences. The initiation of addiction involves the mesocorticolimbic dopamine system, which contributes to the processing of rewarding sensory stimuli during the overall shaping of successful behaviors. Acting mainly through nicotinic receptors containing the α4 and β2 subunits, often in combination with the α6 subunit, nicotine increases the firing rate and the phasic bursts by midbrain dopamine neurons. Neuroadaptations arise during chronic exposure to nicotine, producing an altered brain condition that requires the continued presence of nicotine to be maintained. When nicotine is removed, a withdrawal syndrome develops. The expression of somatic withdrawal symptoms depends mainly on the α5, α2, and β4 (and likely α3) nicotinic subunits involving the epithalamic habenular complex and its targets. Thus, nicotine taps into diverse neural systems and an array of nicotinic acetylcholine receptor (nAChR) subtypes to influence reward, addiction, and withdrawal.
TL;DR: It is argued for a concerted effort to clinically evaluate the hypothesis that targeting glial and neuronal proteins regulating excitatory synaptic plasticity may prove beneficial in treating addiction.
Abstract: The repeated use of drugs that directly or indirectly stimulate dopamine transmission carry addiction liability and produce enduring pathological changes in the brain circuitry that normally regulates adaptive behavioral responding to a changing environment. This circuitry is rich in glutamatergic projections, and addiction-related behaviors in animal models have been linked to impairments in excitatory synaptic plasticity. Among the best-characterized glutamatergic projection in this circuit is the prefrontal efferent to the nucleus accumbens. A variety of molecular adaptations have been identified in the prefrontal glutamate synapses in the accumbens, many of which are induced by different classes of addictive drugs. Based largely on work with cocaine, we hypothesize that the drug-induced adaptations impair synaptic plasticity in the cortico-accumbens projection, and thereby dysregulate the ability of addicts to control their drug-taking habits. Accordingly, we go on to describe the literature implicating the drug-induced changes in protein content or function that impinge upon synaptic plasticity and have been targeted in preclinical models of relapse and, in some cases, in pilot clinical trials. Based upon modeling drug-induced impairments in neuroplasticity in the cortico-accumbens pathway, we argue for a concerted effort to clinically evaluate the hypothesis that targeting glial and neuronal proteins regulating excitatory synaptic plasticity may prove beneficial in treating addiction.
TL;DR: Progress in defining the distinct molecular and functional contributions of the two MSN subtypes in mediating addiction is reviewed.
Abstract: The striatum plays a key role in mediating the acute and chronic effects of addictive drugs, with drugs of abuse causing long-lasting molecular and cellular alterations in both dorsal striatum and nucleus accumbens (ventral striatum). Despite the wealth of research on the biological actions of abused drugs in striatum, until recently, the distinct roles of the striatum’s two major subtypes of medium spiny neuron (MSN) in drug addiction remained elusive. Recent advances in cell-type specific technologies, including fluorescent reporter mice, transgenic or knockout mice, and viral-mediated gene transfer, have advanced the field toward a more comprehensive understanding of the two MSN subtypes in the long-term actions of drugs of abuse. Here we review progress in defining the distinct molecular and functional contributions of the two MSN subtypes in mediating addiction.
TL;DR: It seems that adding any psychosocial support to standard maintenance treatments do not add additional benefits, and data do not show differences also for contingency approaches, contrary to all expectations.
Abstract: Objective: To evaluate the effectiveness of any psychosocial plus any agonist maintenance treatment versus standard agonist treatment for opiate dependence in respect of retention in treatment, use of substances, health and social status. The abuse of opioid drugs and drug dependency are major health and social issues. Maintenance treatments with pharmacological agents can help to reduce the risks associated with the use of street drugs for drug addicts who are unable to abstain from drug use. Methadone is effective in retaining patients in treatment and reducing heroin use but re-addiction remains as a substantial challenge. Opiate addicts often have psychiatric problems such as anxiety and depression and may not be able to cope with stress. Psychosocial interventions including psychiatric care, psychotherapy, counselling, and social work services are commonly offered as part of the maintenance programs. Psychological support varies from structured psychotherapies such as cognitive behavioural therapy and supportive-expressive therapy to behavioural interventions and contingency management. This review addressed whether a specific psychosocial intervention provides any additional benefit to pharmacological maintenance treatment. The control intervention was a maintenance program, which routinely offers counselling sessions in addition to pharmacological treatment. Present evidence suggests that adding psychosocial support does not change the effectiveness of retention in treatment and opiate use during treatment. Findings on retention in treatment were for 12 different psychosocial interventions including contingency management. These conclusions are based on 34 randomised trials involving 3777 opiate addicts, some 73% of whom were male. All but three studies were conducted in the USA. The previous version of this review showed a reduction in opiate use during treatment that was no longer the case with the addition of new studies and the same is for the number of participants abstinent at the end of follow up. The psychosocial interventions are likely to require rigorous assessment of any changes in emotional, interpersonal, vocational and physical health areas of life functioning that may indirectly reduce drug use over longer periods of time.
TL;DR: The 'bio-psycho-social' model of etiology holds very well for addiction, and addiction appears to correlate with a hypodopaminergic dysfunctional state within the reward circuitry of the brain.
Abstract: Addictive drugs have in common that they are voluntarily self-administered by laboratory animals (usually avidly), and that they enhance the functioning of the reward circuitry of the brain (producing the 'high' that the drug user seeks). The core reward circuitry consists of an 'in-series' circuit linking the ventral tegmental area, nucleus accumbens and ventral pallidum via the medial forebrain bundle. Although originally believed to simply encode the set point of hedonic tone, these circuits are now believed to be functionally far more complex, also encoding attention, expectancy of reward, disconfirmation of reward expectancy, and incentive motivation. 'Hedonic dysregulation' within these circuits may lead to addiction. The 'second-stage' dopaminergic component in this reward circuitry is the crucial addictive-drug-sensitive component. All addictive drugs have in common that they enhance (directly or indirectly or even transsynaptically) dop-aminergic reward synaptic function in the nucleus accumbens. Drug self-administration is regulated by nucleus accumbens dopamine levels, and is done to keep nucleus accumbens dopamine within a specific elevated range (to maintain a desired hedonic level). For some classes of addictive drugs (e.g. opiates), tolerance to the euphoric effects develops with chronic use. Postuse dysphoria then comes to dominate reward circuit hedonic tone, and addicts no longer use drugs to get high, but simply to get back to normal ('get straight'). The brain circuits mediating the pleasurable effects of addictive drugs are anatomically, neurophysiologically and neurochemically different from those mediating physical dependence, and from those mediating craving and relapse. There are important genetic variations in vulnerability to drug addiction, yet environmental factors such as stress and social defeat also alter brain-reward mechanisms in such a manner as to impart vulnerability to addiction. In short, the 'bio-psycho-social' model of etiology holds very well for addiction. Addiction appears to correlate with a hypodopaminergic dysfunctional state within the reward circuitry of the brain. Neuroimaging studies in humans add credence to this hypothesis. Credible evidence also implicates serotonergic, opioid, endocannabinoid, GABAergic and glutamatergic mechanisms in addiction. Critically, drug addiction progresses from occasional recreational use to impulsive use to habitual compulsive use. This correlates with a progression from reward-driven to habit-driven drug-seeking behavior. This behavioral progression correlates with a neuroanatomical progression from ventral striatal (nucleus accumbens) to dorsal striatal control over drug-seeking behavior. The three classical sets of craving and relapse triggers are (a) reexposure to addictive drugs, (b) stress, and (c) reexposure to environmental cues (people, places, things) previously associated with drug-taking behavior. Drug-triggered relapse involves the nucleus accumbens and the neurotransmitter dopamine. Stress-triggered relapse involves (a) the central nucleus of the amygdala, the bed nucleus of the stria terminalis, and the neurotransmitter corticotrophin-releasing factor, and (b) the lateral tegmental noradrenergic nuclei of the brain stem and the neurotransmitter norepinephrine. Cue-triggered relapse involves the basolateral nucleus of the amygdala, the hippocampus and the neurotransmitter glutamate. Knowledge of the neuroanatomy, neurophysiology, neurochemistry and neuropharmacology of addictive drug action in the brain is currently producing a variety of strategies for pharmacotherapeutic treatment of drug addiction, some of which appear promising.
TL;DR: It is reported that a functional OPRM1 A118G polymorphism is a major determinant of striatal dopamine responses to alcohol, a mechanism by which it likely modulates alcohol reward.
Abstract: Excessive alcohol use, a major cause of morbidity and mortality, is less well understood than other addictive disorders. Dopamine release in ventral striatum is a common element of drug reward, but alcohol has an unusually complex pharmacology, and humans vary greatly in their alcohol responses. This variation is related to genetic susceptibility for alcoholism, which contributes more than half of alcoholism risk. Here, we report that a functional OPRM1 A118G polymorphism is a major determinant of striatal dopamine responses to alcohol. Social drinkers recruited based on OPRM1 genotype were challenged in separate sessions with alcohol and placebo under pharmacokinetically controlled conditions, and examined for striatal dopamine release using positron emission tomography and [11C]-raclopride displacement. A striatal dopamine response to alcohol was restricted to carriers of the minor 118G allele. To directly establish the causal role of OPRM1 A118G variation, we generated two humanized mouse lines, carrying the respective human sequence variant. Brain microdialysis showed a fourfold greater peak dopamine response to an alcohol challenge in h/mOPRM1-118GG than in h/mOPRM1-118AA mice. OPRM1 A118G variation is a genetic determinant of dopamine responses to alcohol, a mechanism by which it likely modulates alcohol reward.
TL;DR: Exposure to non-drug rewards can alter neural plasticity in regions of the brain that are affected by drugs of abuse, and repeated exposure to natural rewards might induce neuroplasticity that either promotes or counteracts addictive behavior.
TL;DR: The heightened response of striatal reward circuitry to heterogeneous reward-related visual cues among a group of patients with different impulsive-compulsive behaviours is consistent with a global sensitization to appetitive behaviours with dopaminergic therapy in vulnerable individuals.
Abstract: Impulsive-compulsive behaviours are a significant source of morbidity for patients with Parkinson’s disease receiving dopaminergic therapy. The development of these behaviours may reflect sensitization of the neural response to non-drug rewards, similar to that proposed for sensitization to drug rewards in addiction. Here, by using 11C-raclopride positron emission tomography imaging, we investigated the effects of reward-related cues and l-dopa challenge in patients with Parkinson’s disease with and without impulsive-compulsive behaviours on striatal levels of synaptic dopamine. Eighteen patients (11 with and seven without impulsive-compulsive behaviours) underwent three 11C-raclopride positron emission tomography scans. The impulsive-compulsive behaviours included hypersexuality, binge eating, punding, compulsive use of dopamine replacement therapy, compulsive buying and pathological gambling, with eight patients exhibiting more than one impulsive-compulsive behaviour. There were no significant differences in baseline dopamine D2 receptor availability between the Parkinson’s disease groups. No differences were found when comparing the percentage change of raclopride binding potential between the two Parkinson’s disease groups following l-dopa challenge with neutral cues. The group with Parkinson’s disease with impulsive-compulsive behaviours had a greater reduction of ventral striatum 11C-raclopride binding potential following reward-related cue exposure, relative to neutral cue exposure, following l-dopa challenge (16.3% compared with 5.8% in Parkinson’s disease controls, P = 0.016). The heightened response of striatal reward circuitry to heterogeneous reward-related visual cues among a group of patients with different impulsive-compulsive behaviours is consistent with a global sensitization to appetitive behaviours with dopaminergic therapy in vulnerable individuals. Our findings are relevant for the broader debate on the relation between impulsive-compulsive behaviours and addictions and may have important implications with regards to advertisement legislation in an effort to prevent the onset of behavioural addictions.
TL;DR: Recent observations from animal models reveal how benzodiazepines, acting through specific GABA(A) receptor subtypes, activate midbrain dopamine neurons, and how this could hijack the mesolimbic reward system, and have important implications for the future design of benzidiazepines with reduced or even absent addiction liability.
TL;DR: Two of the most used Internet addiction research measures are compared, the Internet Addiction Test (IAT) and the Internet-Related Problem Scale (IRPS), along with a self-diagnostic question simply asking Internet users if they thought they were addicted to the Internet.
Abstract: One of the more prominent issues in the field of Internet addiction is the validity of the instrument used to assess users' level of Internet involvement. Many of the instruments used to assess Internet addiction have high face validity but have yet to be tested psychometrically. The aim of this study is to compare two of the most used Internet addiction research measures, the Internet Addiction Test (IAT) and the Internet-Related Problem Scale (IRPS), along with a self-diagnostic question simply asking Internet users if they thought they were addicted to the Internet. A total of 225 Internet users participated in the study (69 males and 156 females). Participants who defined themselves as Internet addicts had higher scores on both the IAT and IRPS, and the three different Internet addiction measures were strongly correlated to each other. For the IAT, factor analysis generated three factors (emotional/psychological conflict; time management issues; mood modification) explaining 56.3% of the vari...
TL;DR: This first functional imaging study to investigate explicitly reward circuitry in OCD shows attenuated reward anticipation activity in the nucleus accumbens compared with healthy control subjects, and supports the conceptualization of OCD as a disorder of reward processing and behavioral addiction.
TL;DR: The hypothesis that innate immune gene induction underlies addiction and affective disorders creates new targets for therapy.
Abstract: Addiction occurs through repeated abuse of drugs that progressively reduce behavioral control and cognitive flexibility while increasing limbic negative emotion Recent discoveries indicate neuroimmune signaling underlies addiction and co-morbid depression Low threshold microglia undergo progressive stages of innate immune activation involving astrocytes and neurons with repeated drug abuse, stress, and/or cell damage signals Increased brain NF-κB transcription of proinflammatory chemokines, cytokines, oxidases, proteases, TLR and other genes create loops amplifying NF-κB transcription and innate immune target gene expression Human post-mortem alcoholic brain has increased NF-κB and NF-κB target gene message, increased microglial markers and chemokine-MCP1 Polymorphisms of human NF-κB1 and other innate immune genes contribute to genetic risk for alcoholism Animal transgenic and genetic studies link NF-κB innate immune gene expression to alcohol drinking Human drug addicts show deficits in behavioral flexibility modeled pre-clinically using reversal learning Binge alcohol, chronic cocaine, and lesions link addiction neurobiology to frontal cortex, neuroimmune signaling and loss of behavioral flexibility Addiction also involves increasing limbic negative emotion and depression-like behavior that is reflected in hippocampal neurogenesis Innate immune activation parallels loss of neurogenesis and increased depression-like behavior Protection against loss of neurogenesis and negative affect by anti-oxidant, anti-inflammatory, anti-depressant, opiate antagonist and abstinence from ethanol dependence link limbic affect to changes in innate immune signaling The hypothesis that innate immune gene induction underlies addiction and affective disorders creates new targets for therapy
TL;DR: Addiction-related changes in the modern food environment are explored, the historical and modern understanding of addictive substances as applied to hyperpalatable foods are examined, and shared factors that increase the public health costs of both addictive drugs and certain foods are outlined.
Abstract: Scientific interest in "food addiction" continues to grow due both to neurobiological and behavioral similarities between substance dependence and excessive food consumption. An important next step is to examine the addictive potential of highly processed foods. In this paper, we explore addiction-related changes in the modern food environment (e.g., increased potency, elevated speed of absorption), examine the historical and modern understanding of addictive substances as applied to hyperpalatable foods, and outline shared factors that increase the public health costs of both addictive drugs and certain foods.