Cognitive Distortions Associated with Alcohol and Marijuana Use in Uruguayan Citizens.

Background: Psychological distress (i.e., incipient symptoms of anxiety, stress, and depression) may promote substance use through increased emission of cognitive distortions. These are automatic irrational thoughts that can promote distress, which in turn increases substance use. Aim: This study analyzed, in a sample of Uruguayan citizens, the unique contribution of cognitive distortions on the frequency and quantity of alcohol or marijuana use, over and above the contribution of psychological distress or the use of emotion regulation strategies. We also assessed whether these variables were associated with having initiated or resumed the use of a substance. Methods: A survey asked about alcohol and marijuana use, psychological distress, emotion regulation strategies, and cognitive distortions. The study comprised a convenience sample of 1132 participants (Mean age = 29.07 ± 8.19 years, 72.26% women). Separate hierarchical linear regression analyses were conducted on the frequency and quantity of alcohol or marijuana use, whereas a logistic regression was applied on having initiated or resumed the use of a substance. Results: Several cognitive distortions were significant predictors of frequency and quantity of alcohol consumption or frequency of marijuana use, over and above psychological distress. Differential emission of automatic thoughts was also associated, along with higher scores of psychological distress, with a significantly higher probability of having initiated the use of a new substance or having resumed the use of a substance. Conclusions: Cognitive distortions may promote alcohol and marijuana use. Interventions aimed at modifying these distortions should be considered to reduce the emission of these behaviors.

Juvenile variable stress modulates, in female but not in male Wistar rats, ethanol intake in adulthood.

Early stress can increase vulnerability to psychopathological disorders, including substance use disorders. The effects of stress in the juvenile period of the rat, that extends between weaning and the onset of adolescence (equivalent to late human childhood), have received little attention. This study assessed short and long-term behavioral effects of juvenile stress, with a focus on effects on ethanol intake. Male and female Wistar rats were exposed to variable stress (restraint, elevated platform, forced swimming, and social instability) or to restraint stress only, between postnatal days 26 to 29 (PDs 26-29). During adolescence, patterns of anxiety (PD 31) and depression (PD 33), ethanol intake (PDs 36-45) and behavioral sensitivity to the effects of acute stress (PD 47) were evaluated. In adulthood, alcohol ingestion was assessed through two-bottle ethanol intake tests (PDs 75-85). An additional experiment measured blood ethanol levels after a limited access intake session in adolescence. Exposure to juvenile variable stress exerted very mild effects in adolescence, but reduced ethanol ingestion in adulthood, in females only. Ethanol intake during the limited access session was significantly correlated to blood alcohol levels. The results indicate that a schedule of juvenile variable stress that did not significantly alter anxiety-related behaviors induced, nonetheless, sexually dimorphic effects on ethanol intake in adulthood. Early stress exposure that reduced alcohol intake in Wistar rats has been associated with changes on brain opioid and dopamine receptors. These results highlight the impact of early stress exposure on adult female ethanol consumption and its possible underlying neurobiological changes, involving opioid and dopamine receptors.

Neurobehavioral alterations induced by third-trimester gestation-equivalent ethanol exposure are inhibited by folate administration.

Prenatal ethanol exposure (PEE) causes several neurobehavioral impairments in the fetus. Postnatal days (PDs) 4-9 in rodents are considered equivalent to the third trimester of gestation in humans. This period is characterized by high rates of synaptogenesis and myelination and the maturation of key structures and transmitter systems. Nutritional supplements, such as folate, have gained attention as putative treatments to mitigate detrimental effects of PEE. Folate is crucial for DNA synthesis and amino acid metabolism and heightens antioxidant defenses. The present study examined neurobehavioral effects of the concurrent administration of folate (20 mg/kg/day) and ethanol (5 g/kg/day) during PDs 4-9 in male and female Wistar rats. During PDs 16-18, the rat pups were tested for anxiety-like and exploratory activity in the light-dark box (LDB), open field (OF), and concentric square field (CSF) tests. After weaning, they were tested for sucrose preference and ethanol intake. Neonatal ethanol exposure reduced body weight in infancy but did not enhance ethanol self-administration or significantly affect performance in the OF or LDB. Neonatal ethanol exposure also reduced sucrose intake in the preference test and increased shelter-seeking in the CSF, and folate significantly inhibited these effects. The present findings suggest that folate, a treatment that is devoid of serious side effects, can ameliorate some neurobehavioral effects of PEE.