Physical exertion at work and addictive behaviors: tobacco, cannabis, alcohol, sugar and fat consumption: longitudinal analyses in the CONSTANCES cohort

We examined the prospective association of physical exertion at work with subsequent tobacco, cannabis, alcohol use, and sugar and fat consumption. Volunteers of the French population-based CONSTANCES cohort currently employed were included from 2012 to 2017 for tobacco and cannabis outcomes (n = 100,612), and from 2012 to 2016 for alcohol and sugar and fat outcomes (n = 75,414). High level of physical exertion at work was defined as a score ≥ 12 at the Rating Perceived Exertion Borg scale. Substance use was self-reported and diet rich in sugar and fat was obtained from principal component analysis and analyzed as quartiles. Generalized linear models computed odds of substance use and sugar and fat consumption at follow-up according to baseline physical exertion at work, while adjusting for sociodemographic factors, depressive symptoms and baseline level of consumption. High physical exertion was associated with tobacco use with dose-dependent relationships. It was also associated with increased odds of cannabis use at least once per month compared to no use in the past and with increased odds of diet rich in sugar and fat. Hence, the role of physical exertion at work on tobacco and cannabis use and diet rich in sugar and fat should be tackled for information and prevention strategies.

Food addiction and lifetime alcohol and illicit drugs use in specific eating disorders

Background and aims Food addiction (FA) and substance use (SU) have frequently been reported in patients with eating disorders (EDs). Our study aimed to assess the prevalence rates of FA and/or lifetime problematic alcohol and illicit drug use among patients with specific ED, such as: bulimia nervosa (BN), binge eating disorder (BED), and other specified feeding and eating disorder (OSFED). We sought to identify clinical, psychopathological, and personality profiles involved in these addictive behavior-based phenotypes. Methods The total sample was 527 patients (176 BN, 115 BED, and 236 OSFED). FA was assessed through the Yale Food Addiction Scale 2.0. To determine lifetime SU, a semi-structured clinical interview was carried out. Results Patients with BN had the highest rates of FA both with and without SU. No gender differences were obtained for the prevalence of current FA and/or lifetime SU. Patients reporting at least one addictive-related behavior exhibited increased clinical severity compared to those who reported none. Increased impulsivity (such as high lack of premeditation, sensation seeking, and positive urgency) and low self-directedness were differentiating factors for presenting one or two addictive behaviors. Discussion and Conclusions Overall, patients presenting with at least one addictive-like behavior reported a poorer clinical status than those without. Also, patients with FA and SU exhibited a more dysfunctional profile characterized by high impulsivity and low self-directedness. These findings would support the need for targeted treatments to reduce impulsivity and increase self-directedness, especially in patients with any addictive-related behavior, as a step towards improving their treatment outcome.

Current Status of Evidence for a New Diagnosis: Food Addiction-A Literature Review

Food addiction is considered an important link for a better understanding of psychiatric and medical problems triggered by dysfunctions of eating behaviors, e. g., obesity, metabolic syndrome, binge eating disorder, or bulimia nervosa. At behavioral level, food addiction has high degrees of similarity with other eating disorders, a phenomenon that creates difficulties in finding specific diagnostic criteria. Food addiction has been also described as “eating addiction” or “eating dependence” by several researchers, who placed the emphasis on the behavior and not on the food itself. High-sodium foods, artificially flavored-foods, rich carbohydrate- and saturated fats-containing foods are triggers for the activation of the same neural pathways, therefore they act similarly to any drug of abuse. Food addiction is considered a disorder based on functional negative consequences, associated distress and potential risks to both psychological well-being and physical health. A clinical scale was validated for the quantification of the eating addiction severity, namely the Yale Food Addiction Severity Scale (YFAS), constructed to match DSM IV criteria for substance dependence. Using this instrument, a high prevalence of food addiction was found in the general population, up to 20% according to a meta-analytic research. The pathogenesis of this entity is still uncertain, but reward dysfunction, impulsivity and emotion dysregulation have been considered basic mechanisms that trigger both eating dysfunctions and addictive behaviors. Genetic factors may be involved in this dependence, as modulators of higher carbohydrate and saturate fat craving. Regarding the existence of potential therapeutic solutions, lorcaserin, antiepileptic drugs, opioid antagonists, antiaddictive agents are recommended for obesity and eating disorders, and they may be intuitively used in food addiction, but clinical trials are necessary to confirm their efficacy. In conclusion, a better understanding of food addiction's clinical profile and pathogenesis may help clinicians in finding prevention- and therapeutic-focused interventions in the near future.

Hypothesizing in the Face of the Opioid Crisis Coupling Genetic Addiction Risk Severity (GARS) Testing with Electrotherapeutic Nonopioid Modalities Such as H-Wave Could Attenuate Both Pain and Hedonic Addictive Behaviors

In the United States, amid the opioid overdose epidemic, nonaddicting/nonpharmacological proven strategies are available to treat pain and manage chronic pain effectively without opioids. Evidence supporting the long-term use of opioids for pain is lacking, as is the will to alter the drug-embracing culture in American chronic pain management. Some pain clinicians seem to prefer classical analgesic agents that promote unwanted tolerance to analgesics and subsequent biological induction of the “addictive brain”. Reward genes play a vital part in modulation of nociception and adaptations in the dopaminergic circuitry. They may affect various sensory and affective components of the chronic pain syndromes. The Genetic Addiction Risk Severity (GARS) test coupled with the H-Wave at entry in pain clinics could attenuate pain and help prevent addiction. The GARS test results identify high-risk for both drug and alcohol, and H-Wave can be initiated to treat pain instead of opioids. The utilization of H-Wave to aid in pain reduction and mitigation of hedonic addictive behaviors is recommended, notwithstanding required randomized control studies. This frontline approach would reduce the possibility of long-term neurobiological deficits and fatalities associated with potent opioid analgesics.

The Use of Motivational Interviewing (Mi) in Preventing Relapse on Methamphetamine Drug User

Methamphetamine (MA) is a potent stimulant with a high potential for abuse that can be smoked, inhaled, injected or taken orally. It is easily being relapse among drug abuse. Thus, this study aims to investigate the impact of drug addiction therapy utilizing the Motivational Interviewing (MI) approach. This is a qualitative study using interview sessions as a study design. The subject is a drug misuse client undergoing imprisonment in Kajang Prison, Selangor. Client’s progression was assessed through direct observations using the Mental State Examination (MSE), client records, and client speech changes. The study revealed that client has gained mental literacy and the client needs to change his behaviors so that the misery does not recur. The use of MI strategies in treatment sessions has been able to help clients eliminate ambiguities related to addictive behaviors, clients are confident to stay recovering and now have concrete plans to not re -addict in the future. The implications of the findings of this case study suggest the MI strategy is a treatment option that counselors can use in assisting drug abuse clients.

Linking Ethanol-Addictive Behaviors With Brain Catecholamines: Release Pattern Matters

Using a variety of animal models that simulate key features of the alcohol use disorder (AUD), remarkable progress has been made in identifying neurochemical targets that may contribute to the development of alcohol addiction. In this search, the dopamine (DA) and norepinephrine (NE) systems have been long thought to play a leading role in comparison with other brain systems. However, just recent development and application of optogenetic approaches into the alcohol research field provided opportunity to identify neuronal circuits and specific patterns of neurotransmission that govern the key components of ethanol-addictive behaviors. This critical review summarizes earlier findings, which initially disclosed catecholamine substrates of ethanol actions in the brain and shows how the latest methodologies help us to reveal the significance of DA and NE release changes. Specifically, we focused on recent optogenetic investigations aimed to reveal cause-effect relationships between ethanol-drinking (seeking and taking) behaviors and catecholamine dynamics in distinct brain pathways. These studies gain the knowledge that is needed for the better understanding addiction mechanisms and, therefore, for development of more effective AUD treatments. Based on the reviewed findings, new messages for researches were indicated, which may have broad applications beyond the field of alcohol addiction.

Dorsal Bed Nucleus of the Stria Terminalis-Subcortical Output Circuits Encode Positive Bias in Pavlovian Fear and Reward

Opposite emotions like fear and reward states often utilize the same brain regions. The bed nucleus of the stria terminalis (BNST) comprises one hub for processing fear and reward processes. However, it remains unknown how dorsal BNST (dBNST) circuits process these antagonistic behaviors. Here, we exploited a combined Pavlovian fear and reward conditioning task that exposed mice to conditioned tone stimuli (CS)s, either paired with sucrose delivery or footshock unconditioned stimuli (US). Pharmacological inactivation identified the dorsal BNST as a crucial element for both fear and reward behavior. Deep brain calcium imaging revealed opposite roles of two distinct dBNST neuronal output pathways to the periaqueductal gray (PAG) or paraventricular hypothalamus (PVH). dBNST neural activity profiles differentially process valence and Pavlovian behavior components: dBNST-PAG neurons encode fear CS, whereas dBNST-PVH neurons encode reward responding. Optogenetic activation of BNST-PVH neurons increased reward seeking, whereas dBNST-PAG neurons attenuated freezing. Thus, dBNST-PVH or dBNST-PAG circuitry encodes oppositely valenced fear and reward states, while simultaneously triggering an overall positive affective response bias (increased reward seeking while reducing fear responses). We speculate that this mechanism amplifies reward responding and suppresses fear responses linked to BNST dysfunction in stress and addictive behaviors.