Search

Eating is necessary for survival, but it is also one of the great pleasures enjoyed by human beings. Research to date shows that palatable food can be rewarding in a similar way to drugs of abuse, indicating considerable comorbidity between eating disorders and substance-use disorders. Analysis of the common characteristics of both types of disorder has led to a new wave of studies proposing a Gateway Theory of food as a vulnerability factor that modulates the development of drug addiction. The homeostatic and hedonic mechanisms of feeding overlap with some of the mechanisms implicated in drug abuse and their interaction plays a crucial role in the development of drug addiction. Studies in animal models have shown how palatable food sensitizes the reward circuit and makes individuals more sensitive to other substances of abuse, such as cocaine or alcohol. However, when palatable food is administered continuously as a model of obesity, the consequences are different, and studies provide controversial data. In the present review, we will cover the main homeostatic and hedonic mechanisms that regulate palatable food intake behavior and will explain, using animal models, how different types of diet and their intake patterns have direct consequences on the rewarding effects of psychostimulants and ethanol.

Mindfulness-based interventions (MBI) have been shown to be effective in increasing empathy in health professionals. Yet, more research is needed to analyse the specific influence of mindfulness exercises on biological variables involved in empathy, such as the biological system of oxytocin activity. In this study, we analyse the effects of a brief mindfulness session on positive and negative affect, state anxiety and salivary oxytocin (sOXT) in psychology students (N = 68). In the experimental group (n = 42), a mindfulness session was performed that included different guided meditation exercises. In the control group (n = 26), an emotion recognition exercise was carried out, along with a series of creative activities. Results showed that the mindfulness session was effective, because there was a significant reduction in negative affect (d = -.56, p < .001) and state anxiety (d = -.54, p = .007) in the experimental group. Likewise, there was an increase in sOXT (d = .99, p < .001) in this group, compared with the control group. Guided mindfulness meditation practice could be useful to reach an emotional and biological state that facilitates empathy. In this regard, the increase in sOXT after the mindfulness session adds further evidence about the biological mechanisms underlying the benefits of MBI on empathy.

Numerosos estudios preclínicos han demostrado que el estrés social incrementa la vulnerabilidad a los efectos reforzantes de la cocaína. Sin embargo, los resultados obtenidos no son homogéneos, observándose siempre una subpoblación que no muestra dicho incremento. Utilizando el modelo de derrota social (DS) repetida en ratones, en este trabajo hemos querido caracterizar conductualmente a los ratones resilientes al incremento de los efectos reforzantes de la cocaína inducido por el estrés social. Utilizamos ratones adultos macho de la cepa C57/BL6 a los que sometimos al protocolo de DS repetida y tres semanas más tarde, realizamos el Condicionamiento de Preferencia de Lugar (CPL) inducido por una dosis no efectiva de cocaína (1mg/kg). Una vez finalizado este procedimiento se midieron los niveles estriatales de interleucina 6, ya que el estrés social produce una respuesta de neuroinflamación. No se observó CPL en los ratones controles, pero los animales derrotados tomados en conjunto desarrollaron preferencia. Sin embargo, esta muestra se pudo dividir en ratones resilientes (no desarrollaron preferencia) y susceptibles (presentaron CPL). Durante las derrotas sociales, los animales resilientes pasaron menos tiempo en las conductas de huida y sumisión que los catalogados como susceptible y presentaron conductas de ataque hacia el ratón residente, manifestando por tanto resistencia a ser derrotados. No se observaron diferencias en la respuesta de neuroinflamación, probablemente debido al largo periodo de tiempo trascurrido desde la última derrota social. Nuestros resultados sugieren que un estilo de afrontamiento activo al estrés social va a ser determinante en la protección del sujeto a desarrollar un trastorno por uso de drogas. Preclinical studies have shown that social stress increases vulnerability to the reinforcing effects of cocaine. However, the results are not always homogeneous, revealing a subpopulation that does not show a preference for cocaine. Thus, the main aim of the present study was to characterize the behavioral profile of resilient mice to the stress-induced rewarding effects of cocaine using an animal model of repeated social defeat stress (SD). To this end, male adult mice of the C57/BL6 strain were exposed to SD and, three weeks later, assessed using the Conditioned Place Preference paradigm induced by an ineffective dose of cocaine (1mg/kg). Afterwards, the striatal levels of interleukin 6 were measured, as social stress usually induces a neuroinflammatory response. Control mice did not develop CPP, while defeated mice did overall develop a preference for the drug-paired compartment. Based on the conditioning score that they exhibited, the SD sample was subdivided into resilient (did not develop preference) and susceptible mice (developed preference). During the SD sessions, resilient animals showed less flight and submission behaviors than susceptible mice and they presented attack behaviors towards the residents, thereby showing their resistance to being defeated. There were no differences in the neuroinflammatory response, probably due to the long time elapsed after the last SD session. These results suggest that an active coping style to social stress may be decisive in protecting the individual from developing an addiction. © 2021, Edita Socidrogalcohol. All rights reserved.

Psychiatric eating disorders (ED) and substance use disorder (SUD) are frequent comorbidities and negatively affect evaluation, treatment, and prognosis of both pathologies. The aim of the present study was to determine the prevalence of eating disorders amongst patients seeking treatment for SUD, mainly alcohol, cocaine, and cannabis, and the modulating role of impulsivity and the presence of the eating restriction disorder. We employed the following evaluation instruments: the Barratt impulsivity scale, the eating disorder inventory (EDI), and the Valencia Addiction to Eating Restriction Questionnaire (CVAR). The results showed that patients with a SUD had higher levels of impulsivity and higher restriction scores. In terms of eating disorders, patients with SUD had a higher prevalence than the control group, with women presenting significantly higher scores than men. These results confirm that eating disorders have a very high prevalence in the population with addictions; especially, women present eating disorders that are more serious and higher impulsivity rates.

The classic ketogenic diet is a diet high in fat, low in carbohydrates, and well-adjusted proteins. The reduction in glucose levels induces changes in the body’s metabolism, since the main energy source happens to be ketone bodies. Recent studies have suggested that nutritional interventions may modulate drug addiction. The present work aimed to study the potential effects of a classic ketogenic diet in modulating alcohol consumption and its rewarding effects. Two groups of adult male mice were employed in this study, one exposed to a standard diet (SD, n = 15) and the other to a ketogenic diet (KD, n = 16). When a ketotic state was stable for 7 days, animals were exposed to the oral self-administration paradigm to evaluate the reinforcing and motivating effects of ethanol. Rt-PCR analyses were performed evaluating dopamine, adenosine, CB1, and Oprm gene expression. Our results showed that animals in a ketotic state displayed an overall decrease in ethanol consumption without changes in their motivation to drink. Gene expression analyses point to several alterations in the dopamine, adenosine, and cannabinoid systems. Our results suggest that nutritional interventions may be a useful complementary tool in treating alcohol-use disorders.

Social behaviour is disturbed in many substance abuse and psychiatric disorders. Given the consensus that social behaviours of lower mammals may help to understand some human emotional reactions, the aim of the present work was to provide an up-to-date review of studies on the changes in social behaviour induced by drugs of abuse. Various animal models have been used to study the relationship between drugs of abuse and social behaviour. Herein, we describe the effects of different substances of abuse on the three most commonly used animal models of social behaviour: the social play test, the social interaction test and the resident-intruder paradigm. The first is the most widely used test to assess adolescent behaviour in rodents, the second is generally used to evaluate a wide repertoire of behaviours in adulthood and the latter is specific to aggressive behaviour. Throughout the review we will explore the most relevant studies carried out to date to evaluate the effects of alcohol, cocaine, opioids, 3,4-methylenedioxymethamphetamine (MDMA), cannabinoids, nicotine and other drugs of abuse on these three paradigms, taking into account the influence of different variables, such as social history, age and type of exposure. Drugs of diverse pharmacological classes induce alterations in social behaviour, although they can be contrasting depending on several factors (drug, individual differences and environmental conditions). Ethanol and nicotine increase social interaction at low doses but reduce it at high doses. Psychostimulants, MDMA and cannabinoids reduce social interaction, whereas opiates increase it. Ethanol and psychostimulants enhance aggression, whereas MDMA, opiates, cannabinoids and nicotine reduce it. Prenatal drug exposure alters social behaviour, whereas drug withdrawal decreases sociability and enhances aggression. As a whole, this evidence has improved our understanding of the social dimension of drug addiction.

Psychiatric disorders constitute one of the main causes of disability worldwide. During the past years, considerable research has been conducted on the genetic architecture of such diseases, although little understanding of their etiology has been achieved. The difficulty to access up-to-date, relevant genotype-phenotype information has hampered the application of this wealth of knowledge to translational research and clinical practice in order to improve diagnosis and treatment of psychiatric patients. PsyGeNET (http://www.psygenet.org/) has been developed with the aim of supporting research on the genetic architecture of psychiatric diseases, by providing integrated and structured accessibility to their genotype-phenotype association data, together with analysis and visualization tools. In this article, we describe the protocol developed for the sustainable update of this knowledge resource. It includes the recruitment of a team of domain experts in order to perform the curation of the data extracted by text mining. Annotation guidelines and a web-based annotation tool were developed to support the curators' tasks. A curation workflow was designed including a pilot phase and two rounds of curation and analysis phases. Negative evidence from the literature on gene-disease associ- ations (GDAs) was taken into account in the curation process. We report the results of the application of this workflow to the curation of GDAs for PsyGeNET, including the analysis of the inter-annotator agreement and suggest this model as a suitable approach for the sustainable development and update of knowledge resources. Database URL: http://www.psygenet.org. PsyGeNET corpus: http://www.psygenet.org/ds/PsyGeNET/results/psygenetCorpus.tar We received support from ISCIII-FEDER (PI13/00082, CP10/00524, CPII16/00026), IMI-JU under grants agreements no. 115191 (Open PHACTS)] and no. 115372 (EMIF), resources of which are composed of financial contribution from the EU-FP7 (FP7/2007-2013) and EFPIA companies in kind contribution, and the EU H2020 Programme 2014-2020 under grant agreements no. 634143 (MedBioinformatics) and no. 676559 (Elixir-Excelerate). The Research Programme on Biomedical Informatics (GRIB) is a member of the Spanish National Bioinformatics Institute (INB), PRB2-ISCIII and is supported by grant PT13/0001/0023, of the PE I + D+i 2013-2016, funded by ISCIII and FEDER. MRA, SMR and MCBG are supported RD16/0017/0007; OV, FF and MT are supported by RD16/0017/0010; and AS and FJP are supported by RD16/0017/0001, by Instituto de Salud Carlos III, Red de Trastornos Adictivos (RTA-Retics-ISCIII). AGS acknowledges financial support from the Spanish Ministry of Economy and Competitiveness, through the 'María de Maeztu' Programme for Units of Excellence in R&D (MDM-2014-0370). Funding for open access: EU H2020 Programme 2014-2020 under grant agreements no. 634143 (MedBioinformatics).