Psychopharmacology & biological narcology

Despite decades of nutrition, obesity, and diabetes research, and worsening prevalences and severities of virtually every chronic metabolic disease, the scientific community remains divided over the existence and veracity of the concept of food addiction. There are numerous rationalizations — 1) you need food to survive, (of which “Food is Medicine” is the latest mantra); 2) people with obesity should not be stigmatized as “mentally ill”; 3) people with obesity should instead adhere to “personal responsibility”; 4) the data are incomplete and not strong enough; 5) it’s correlation but not causation; 6) everyone is exposed, but not everyone is addicted; 7) there is no “withdrawal” phenotype; and 8) it’s not “food addiction” but “eating addiction”. All are in play, yet more health care dollars are diverted to the treatment of food-related disease every year. While various ingestible chemicals (e.g. nicotine, cocaine, heroin, alcohol) are clearly addictive, it appears to be a stretch by some scientists to argue that individual substances found in food (e.g. sugar, caffeine), or the food itself (e.g. ultraprocessed food), rise to meet the same criteria. Symposia on food addiction proliferate and journal debates continue. The definition of addiction consists of numerous criteria, including public health demographics, biochemistry, imaging, animal trials, clinical trials, and economics. None of these have proven to be “slam dunks” to align a general consensus. But paramount for scientific acceptance is the delineation of mechanism. This article will review the history of the controversy, the data on which foods are most likely to be addictive, the two mechanisms involved in the pathogenesis of food addiction and relate it to the most likely culprits, and the role of the food industry in promulgating false narratives, in order to provide a rational way forward from this debate.

Schizophrenia is a chronic and disabling disorder that often shows limited response to standard psychopharmacotherapy. For several decades, deficiencies of various nutrients have been investigated as etiopathogenetic factors of this condition, with the hypothesis that their correction may contribute to treatment optimization. This brief review aimed to summarize existing research data on the potential synergistic effects of correcting folate metabolism disturbances, redox imbalance, and vitamin D deficiency in schizophrenia. This review examines studies demonstrating shared pathogenetic mechanisms underlying these biochemical abnormalities and their combined contribution to the etiology and pathogenesis of schizophrenia. The research data review and analysis of several points of intersection among folate metabolic pathways, vitamin D metabolism, and oxidative stress enabled the authors to propose a rationale for integrated nutrient support in schizophrenia. Hypothetically, a combined approach involving methylfolate, vitamin D, and a precursor of reduced glutathione synthesis (N-acetylcysteine) may be a more effective strategy than the use of each agent individually. However, this hypothesis requires dedicated clinical studies, as the effects of the triad have not yet been studied. Nonetheless, the combined approach may be justified based on the pathogenesis of schizophrenia, given the interrelation of metabolic pathways, shared mechanisms of action, and several potential therapeutic targets.

BACKGROUND: Substance-induced psychotic disorders constitute a heterogeneous group of psychiatric conditions that include both intoxication-related psychoses and endogenous psychoses occurring during psychoactive substance use. Selecting an optimal therapy for such psychoses remains challenging. Despite the critical importance of managing synthetic cathinone-induced psychoses, existing studies typically describe therapeutic strategies and lack a comparative analysis. This article systematizes current approaches to managing psychoses associated with the use of synthetic cathinones.

AIM: This study aimed to determine potential therapeutic strategies for cathinone-induced psychoses and to identify associations between treatment approaches, psychosis subtype, duration of psychotic symptoms, changes in positive symptoms, and severity of cognitive impairment.

METHODS: The study included 98 patients >18 years with psychotic disorders. Synthetic cathinones or their metabolites were detected in biological samples using gas chromatography–mass spectrometry. The Brief Psychiatric Rating Scale (BPRS) was used to assess the severity and trends in psychotic symptoms on days 1 and 10 of psychosis. Upon resolution of psychosis, defined as cessation of delusions and/or hallucinations, cognitive impairment was evaluated using the Mini-Mental State Examination (MMSE) scale.

RESULTS: Four principal therapeutic strategies were identified: a basic strategy incorporating infusion therapy and benzodiazepines; two strategies combining basic regimen with either typical or atypical antipsychotics; and a strategy involving forced diuresis and propofol. Psychosis duration was found to be determined primarily by psychosis subtype rather than therapeutic strategy. BPRS scores on days 1 and 10 differed significantly (F = 347.5; p_ANOVA < 0.0001). BPRS scores decreased by 52.1% with the basic strategy (q = 2.732; p_Tukey < 0.0001); by 45.0% with typical-antipsychotic strategy (q = 3.020; p_Tukey < 0.0001); by 22.2% with atypical-antipsychotic strategy (q = 3.874; p_Tukey = 0.0074); by 53.3% with the strategy combining forced diuresis and anesthetic agents (q = 3.139; p_Tukey < 0.0001). Analysis of MMSE scores showed that after the resolution of psychotic symptoms, the mean score was 25.9 ± 0.75. Between-group ANOVA revealed no significant differences (F = 0.6731; R² = 0.02060; p_ANOVA = 0.5706).

CONCLUSION: Standardizing therapeutic approaches to psychoses induced by psychoactive substances is an essential step toward establishing effective clinical pathways for these patients. This study systematizes therapeutic approaches and compares selected psychometric parameters across different treatment strategies.