Genetic and Brain Mechanisms of Addictive Behavior and Neuroadaptation

Genetic differences play a role in the susceptibility to addictive drug use, the probability that the use of these drugs will escalate and result in a drug use disorder, and whether relapse to use will occur during or after treatment [...]

Adolescent Cannabis Users Who Have Never Smoked A Combustible Cigarette: Trends and Level of Addictive Drug Use from 1976 to 2020

Background. Adolescents cannabis users are at a substantially elevated risk for use of highly addictive drugs such as cocaine, heroin, and nonmedical use of prescription drugs. Unknown is whether this elevated risk applies to adolescent cannabis users who have never smoked a combustible cigarette, a group that has grown considerably in size in recent years. This study documents the recent growth in the proportion of adolescent cannabis users who abstain from combustible cigarette use, and examines their probability for use of addictive drugs. Methods. Data are annual, cross-sectional, nationally-representative Monitoring the Future surveys of 607,932 U.S. 12th grade students from 1976-2020. Results. Among ever cannabis users, the percentage who had never smoked a combustible cigarette grew from 11% in 2000 to 58% in 2020. This group had levels of addictive drug use that were 8% higher than their peers. In comparison, adolescents who had ever used cannabis – regardless of whether they had ever smoked a cigarette – had levels of addictive drug use 500% higher than their peers.Conclusions. Adolescent cannabis users who have not smoked a combustible cigarette have much lower levels of addictive drug use than the group of cannabis users as a whole. These results suggest policies and laws aimed at reducing adolescent prevalence of addictive drugs may do better to focus on cigarette use of adolescent cannabis users rather than cannabis use per se.

The patterns and burden of multimorbidity in geriatric patients with prolonged use of addictive medications

Background Multimorbidity and prolonged use of addictive medications are prevalent among older patients, and known to increase the risk of adverse drug events. Yet, the relationship between these two entities has remained understudied. Aims This study explored the association between multimorbidity burden and prolonged use of addictive medications in geriatric patients, adjusted for clinically important covariates. Furthermore, we identified comorbidity patterns in prolonged users. Methods We conducted a cross-sectional study on a consecutive sample of 246 patients, aged 65–90 years, admitted to a large public university hospital in Norway. We defined prolonged use of addictive medications as using benzodiazepines, opioids and/or z-hypnotics beyond the duration recommended by clinical guidelines (≥ 4 weeks). Multimorbidity was assessed with the Cumulative Illness Rating Scale for Geriatrics (CIRS-G), based on diagnoses made by independent physicians. Results Compared to non-prolonged use, prolonged use was significantly more common among patients who had psychiatric (19/27, 70%), liver (19/22, 86%), upper gastrointestinal tract (21/32, 66%), musculoskeletal (52/96, 54%), or nervous system disorders (46/92, 50%). Patients with prolonged use had a higher multimorbidity burden than those without such use (CIRS-G score, mean = 7.7, SD = 2.7 versus mean = 4.6, SD = 2.2, p < 0.001). Multivariable logistic regression indicated a significant association between multimorbidity burden and prolonged addictive medication use (OR = 1.72, 95% CI 1.42–2.08). Predictive margins postestimation showed a systematic increase in the predicted CIRS-G scores when the number of addictive drug used increases. Conclusions Multimorbidity is strongly associated with prolonged use of addictive medications. Multiple substance use may aggravate disease burden of older patients.

Exploration of Epigenetic State Hyperdopaminergia (Surfeit) and Genetic Trait Hypodopaminergia (Deficit) During Adolescent Brain Development

Background: Understanding the risk for all addictive drug and non-drug behaviors, especially, in the unmyelinated Prefrontal Cortex (PFC) of adolescents, is important and complex. Many animal and human studies show the epigenetic impact on the developing brain in adolescents, compared to adults. Some reveal an underlying hyperdopaminergia that seems to set our youth up for risky behaviors by inducing high quanta pre-synaptic dopamine release at reward site neurons. In addition, altered reward gene expression in adolescents caused epigenetically by social defeat, like bullying, can continue into adulthood. In contrast, there is also evidence that epigenetic events can elicit adolescent hypodopaminergia. This complexity suggests that neuroscience cannot make a definitive claim that all adolescents carry a hyperdopaminergia trait. Objective: The primary issue involves the question of whether there exists a mixed hypo or hyper –dopaminergia in this population. Method: Genetic Addiction Risk Score (GARS®) testing of 24 Caucasians, ages 12-19 derived from families with RDS. Results: We have found that adolescents from this cohort, derived from RDS parents, displays a high risk for any addictive behavior (a hypodopaminergia), especially, drug-seeking (95%) and alcohol-seeking (64 %). Conclusion: The adolescents in our study, although more work is required, show a hypodopaminergic trait, derived from a family with Reward Deficiency Syndrome (RDS). Certainly in future studies we will analyze GARS in non-RDS Caucasians between the ages of 12-19. The suggestion is first to identify risk alleles with the GARS test and, then, use well-researched precision, pro-dopamine neutraceutical regulation. This “two-hit” approach might prevent tragic fatalities among adolescents, in the face of the American opioid/psychostimulant, epidemic.

Rare cause of acute abdomen–cocaine-induced small intestinal perforation with coexisting lower gastrointestinal bleed: an unusual presentation

Cocaine, an alkaloid, is an addictive drug and its abuse as a recreational drug is on the increasing side with its associated complications. Gastrointestinal complications, after cocaine abuse, are less known and need to be addressed since the abuse is on the rise and the existing evidence is scarce. We report a case of a 22-year-old male patient who presented with abdominal pain following a cocaine injection. On examination, signs of peritonitis were noted and laparotomy revealed a 2×1 cm perforation in the distal ileum. The unhealthy intestinal segment was resected and taken out as a double-barrel ileostomy. The patient had an episode of severe lower gastrointestinal bleeding on postoperative day 6. CT and colonoscopy revealed signs of ischaemic bowel and tissue biopsy showed oedematous, inflamed and haemorrhagic bowel mucosa. The patient was managed conservatively and is doing well under follow-up in a de-addiction centre.

Addiction of drugs like Cocaine and Opium - A Review

Cocaine is an addictive drug. Thousands of years ago it made by South America from leaves of coca plant. It is also known as a coke. It appears as a fine white crystalline powder. Surgeons used it to block pain, before the development of synthetic local aesthetic. There is no pharmacological treatment for that addiction. It impact on a genetic factor and brain. It also consists as a brain disease, which effects directly on a neuropath ways of brain and it modified the various enviourment factors like; epigenetic, hinges, mentality, social influences, etc. its addiction can developed quickly even after trying a few times. These drugs quickly affected health like; psychological effects, physical effects and mentally effects or any other diseases. All stimulants function as an extracellular concentration of dopamine, norpinephirine and serotonin which can induce symptoms such; paranoia, panic, hallucination, aggression, irritability, anxiety, depression, poor judgement, repeated or aberrant behaviour. Some physical effects of this medication are harmful weight loss; raise heart rate, nausea, abdomen pain, headaches, chest discomfort, heart arrhythmia, heart attack, seizure, stroke and many more such ailments. These drugs can block the transport of these neurotransmitters.

Acute and delayed nephropathy due to methamphetamine abuse

Methamphetamine is a highly addictive drug that acts as a stimulant for the central nervous system. It increases alertness and physical activity but can cause cardiac dysrhythmias, hypertension, hallucinations and violent behavior. The excretion rate of methamphetamine by the kidney can be seriously altered by urinary pH. Methamphetamine is a weak base, consequently, the proportion of the excreted amount of unchanged drug can vary from as little as 2% in alkaline (pH ≥8.0) to 76% in acidic urine (pH ≤5.0). Methamphetamine is metabolized by hepatic metabolism and renal excretion via cytochrome P450 2D6 (CYP2D6). The effects of methamphetamine on the kidneys can be divided into the following sub-groups: vascular effects, non-traumatic rhabdomyolysis and direct nephrotoxicity. Additionally, methamphetamine directly stimulates the release of ET-1, a potent vasoconstrictor. ET-1 stimulates vasoconstriction, inflammation and fibrosis in kidney, thus promoting hypertension, atherosclerosis and chronic kidney disease.