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Drugs of Abuse and Addiction
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Shalini Mani, Chahat Kubba, Aarushi Singh
Few studies suggest that genetic factors account for 50% of this individual variability in addiction vulnerability and this heritability is true for mostly all drugs (Kandel et al., 2006; Nestler, 2013). Hundreds of genetic variations have been a great setback in recognizing the exact genes involved in these addicition vulnerabilities. The other 50% of addiction is presumed to be from environmental factors which secondarily influence on the genetic composition of an individual (as per the epigenetic mechanisms discussed above) (Kalivas and O'Brien, 2008). Many of the “gateway” drugs like nicotine have been considered to impact upon the vulnerability (increase) of an individual to another drug. There is also increasing evidence that sufficiently high portions of a drug for longer time can transform an individual with lower genetic loading into an addict (Wang et al., 2012; Kandel et al., 2006; Kalivas and O'Brien, 2008).
Clinical and Neuroscience Basis for the 2 × 4 Model
Published in R. Andrew Chambers, The 2 × 4 Model, 2017
Our own lab and others around the world had by 2012 conducted research consistent with Dual Diagnosis Neuroscience Experiment #2, and this research has shown that addiction vulnerability does generalize to different addictive drug types and different forms of mental illness. For example, it turns out that the NVHL model of schizophrenia causes rats to show addiction vulnerability not only to cocaine but also to nicotine and alcohol, which agrees exactly with our clinical knowledge: People with schizophrenia have much higher rates of addiction (compared to the general population) spanning several different addictive drug types, including nicotine, alcohol, and cocaine. Of note, this is one example of the phenomena of multifinality in the pathogenesis of dual diagnosis; one biological context (e.g., the NVHL model) sets the brain up for multiple psychiatric symptoms and even different types of drug addictions.
Stress and Addiction
Published in Hanna Pickard, Serge H. Ahmed, The Routledge Handbook of Philosophy and Science of Addiction, 2019
This chapter focuses on the accumulating evidence from preclinical, clinical and population studies that highly stressful situations and chronic stress increases addiction vulnerability, facilitating continued drug use and abuse and ultimately chronicity of addiction severity and relapse risk. The types of stressors that increase addiction risk are identified in Table 24.1. These tend to be highly emotionally distressing events that are uncontrollable and unpredictable. The themes range from loss, violence and aggression, poor support, interpersonal conflict, and isolation and trauma. There is also evidence for a dose-dependent relationship between accumulated adversity and addiction risk, with the greater the number of stressors an individual is exposed to, the higher the risk of developing substance use disorders. Work-related stressors have weaker support but individual level variables such as trait negative emotionality and poor self-control (possibly similar to poor executive function) appear to also contribute uniquely to addiction risk. Exposure to such stressors early in life and accumulation of stress (chronicity) results in neuroendocrine, physiological, behavioral and subjective changes that tend to be long lasting and adversely affect development of brain systems involved in learning and motivation and stress-related adaptive behaviors. Research that directly addresses stress-related neurobiological changes and its association with behavioral outcomes is sorely needed. Evidence to clarify the contribution of stress on alterations in mesolimbic dopamine activity and its association to drug use is also needed.
Chronic stress in adolescence differentially affects cocaine vulnerability in adulthood in a selectively bred rat model of individual differences: role of accumbal dopamine signaling
Published in Stress, 2021
Cigdem Aydin, Karla Frohmader, Michael Emery, Peter Blandino Jr, Huda Akil
The role of dopaminergic signaling in the nucleus accumbens (Nacc) in addiction-related behaviors has been widely demonstrated (see (Chen et al., 2017) for a recent review). Notably, the Nacc is also highly susceptible to stress and is altered by stressful stimuli (Cabib and Puglisi-Allegra, 1996; Krishnan et al., 2007) due to the ability of cortisol and corticosterone to modulate dopamine release (Oswald et al., 2005; Wand et al., 2007), making it an important structure for the interaction of stress and drugs of abuse. In the Nacc, the two main dopamine receptor types, D1R and D2R, have been widely implicated in drug sensitization (Cabib et al., 1991; Kai et al., 2015) as well as in stress-related disorders (Francis and Lobo, 2017). However, their contribution to the interaction of these behaviors remain unclear. Previous studies from our laboratory have shown that the levels of D1R and D2R differ basally in the Nacc of the bHR\bLR rats (Clinton et al., 2012; Flagel et al., 2010). Specifically, lower D2R (Clinton et al., 2012; Flagel et al., 2010) but higher D1R (Clinton et al., 2012) mRNA levels are observed in the Nacc in bHRs compared to bLRs, indicating innate differences in the accumbal dopamine signaling. These differences may be associated with differences in addiction vulnerability, and possibly the differential responsivity to chronic stress observed in these animals. However, whether these differences in accumbal dopamine signaling influence the interaction of chronic stress and drugs of abuse has not been investigated.
Correlates of Concurrent Morbid Obesity and Tobacco Use Disorder Nationally in the Veterans Health Administration
Published in Journal of Dual Diagnosis, 2020
Walter Roberts, Robert A. Rosenheck
What does the seemingly counterintuitive finding that co-occurring obesity is associated with reduced risk of co-occurring substance use disorder in tobacco users indicate about the role of addiction vulnerability in obesity? One interpretation is that the presence of obesity does not signal an underlying propensity toward addiction. This interpretation challenges a body of research identifying overlap in the neurobiological pathophysiology of substance use disorder and obesity vulnerability (Volkow & Wise, 2005; Wang et al., 2001). Another interpretation is consistent with the food/drug substitution hypothesis (Kalarchian et al., 2007; Petry et al., 2008). According to this hypothesis, overconsumption of food may satisfy the underlying appetitive drive as substance use, reducing the likelihood that the individual will use substances to excess. Applying this framework to our findings, for individuals with TUD, who show a general vulnerability to addictions, overeating may fulfill similar physiological or psychological needs as substance use, such that individuals with TUD and morbid obesity are less likely to engage in other dysregulated substance use. This interpretation rests on the assumption that morbid obesity represents a pattern of dysregulated food consumption, which is likely to be the case for many but not all people with morbid obesity, since there are other causes of obesity not explained using a food addiction framework (Ziauddeen & Fletcher, 2013).
Sensorimotor Gating in Cocaine-Related Disorder with Comorbid Schizophrenia or Antisocial Personality Disorder
Published in Journal of Dual Diagnosis, 2019
Alejandro Fuertes-Saiz, Ana Benito, César Mateu, Sonia Carratalá, Isabel Almodóvar, Abel Baquero, Gonzalo Haro
Cocaine is responsible for more hospital admissions for treatment (36.5%) and emergencies (43.7%) than any other drug (Observatorio Español de la Droga y las Toxicomanías (OEDT), 2016). Schizophrenia and antisocial personality disorder (ASPD) are very prevalent in cocaine users (Araos et al., 2014; Arias et al., 2013). Prepulse inhibition (PPI; Blumenthal, Reynolds, & Spence, 2015) is a robust measure of sensorimotor gating (Kohl, Heekeren, Klosterkötter, & Kuhn, 2013), is a cross-species phenomenon (Zhang, Forkstam, Engel, & Svensson, 2000), is significantly heritable (Greenwood et al., 2016), and is a useful schizophrenia endophenotype (Siegel, Talpos, & Geyer, 2013). PPI is reduced in patients with psychiatric disorders compared with healthy controls (Arenas, Caballero-Reinaldo, Navarro-Francés, & Manzanedo, 2017). Since animal studies suggest the unitary nature of the neurocircuits that govern both major psychiatric syndromes and enhanced addiction vulnerability, it is probable that many genetic and environmental risk factors for mental illness, substance use disorders, or dual diagnosis conditions could be identical (Chambers, 2007). PPI, given its usefulness as an endophenotype, seems a good starting point to study these common etiological bases.