Non-Alcoholic Fatty Liver Disease (NAFLD) emerged as the most prevalent liver disorder contributing significantly to disease burden worldwide. It manifests as a broad spectrum of hepatic damage with varying severity ranging from less serious steatosis to a more severe Non-Alcoholic Steatohepatitis (NASH), with or without fibrosis, cirrhosis, and hepatocellular carcinoma. Vitamins, on the other hand, are micronutrients that are vital for healthy well-being. Some studies have linked liver diseases with hypovitaminosis; however, there are still some gaps about the basis of their correlation. Hence, this systematic review aims to discuss the role of vitamins in the pathogenesis of NAFLD and explore their hepatoprotective potential that may benefit clinicians in managing this condition. This systematic review searched for studies indexed in the PubMed, PubMed Central, Medline, Google Scholar, and ScienceDirect databases. Inclusion and exclusion criteria were applied, duplicates were removed, and meticulous screening of articles was done systematically. Out of 729 unique studies generated using the search strategy, 17 were finally included after thorough review and quality appraisal. NAFLD is not simply an outcome of insulin resistance and metabolic derangements; instead, it is a disease with complex underlying pathogenesis. Moreover, vitamin deficiency has been associated with NAFLD development and increased susceptibility to more severe liver damage. Derangement in vitamins correlates to the lipotoxic hepatic environment, altered immune system, unwarranted inflammation, oxidative stress, gene mutations, epigenetic modification, and gut dysbiosis seen in NAFLD. As they influence several pathophysiologic processes in the liver, vitamins A, B3, B6, B9, B12, C, D, and E are promising potential options that can impact NAFLD management. However, more well-designed studies conducted in the human population are still necessary to establish their efficacy and safety as therapeutic agents.

Parkinson’s disease (PD) is a neurodegenerative disease caused due to the destruction of dopaminergic neurons and the deposition of α-synuclein proteins, known as Lewy bodies. Generally, the diagnosis of PD is centered around motor symptoms. However, the early recognition of non-motor symptoms such as autonomic dysfunction, sleep disturbances, and cognitive and psychiatric disturbances are gaining increased attention for the early diagnosis of PD. Rapid eye movement (REM) sleep behavior disorder or REM sleep behavior disorder (RBD) is described as parasomnia, which is a condition of loss of normal muscle atonia causing the person to act out vivid dreams and it has been seen to be associated with the misprocessing of intercellular α-synuclein leading to neurodegenerative diseases such as PD. This review’s objective is to highlight the significance of RBD as a prodromal premotor marker for the early detection of PD. We used PubMed as our primary database to search for articles on May 2, 2021, and a total of 1849 articles were found in our initial search using keywords and medical subject heading (MeSH) keywords. Thereafter, we removed the duplicates, applied the inclusion/exclusion criteria, and did a quality appraisal to include 10 articles in this study. We concluded that the recognition and diagnosis of RBD are of paramount importance to detect early PD, and further longitudinal studies and clinical trials are of utmost importance to understand their correlation; also, treatment trials are needed to prevent the phenoconversion of RBD into PD.

Individuals with schizophrenia are particularly vulnerable to substance abuse problems. Comorbidity with substance use disorders (SUDs) frequently results in early death and increased dysfunction observed in schizophrenia. This dual diagnosis can be explained through multiple general mechanisms. Tobacco, alcohol, cannabis, and cocaine are substances widely used by individuals with schizophrenia. This study highlights the predictors, mechanisms responsible for the relationship between substance use disorder and schizophrenia and how it can help with the treatment of both disorders. The publications were rigorously reviewed after being found in multiple databases. The study's inclusion criteria were research published within the last five years, publications written in English, full-text availability, and human studies. A total of ten papers were selected for examination from a total of 9,106 articles found using the search method across several databases. This study follows the rules listed within the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) checklist 2009. The information gathered from these published studies was used to investigate the elements that contribute to the link between schizophrenia and substance abuse. Here, we evaluate a close relationship between schizophrenia and substance use disorders. The articles studied exhibit a bidirectional association between the two disorders in most individuals. From our analysis, the comorbidity between the two disorders is partially due to shared polygenic liability. Individuals with schizophrenia have dysfunctional Mesocorticolimbic brain reward circuits indicating a history of substance use. An underlying genetic vulnerability to schizophrenia may be triggered by extensive cannabis usage at a young age. A combination of psychological and pharmacological interventions for both disorders can significantly improve the outcome.

Celiac disease (CD) and type 1 diabetes mellitus (T1DM) are autoimmune diseases that coexist frequently. These illnesses share a common genetic background. This study aims to review the different pathophysiologic mechanisms that have been studied about the coexistence of CD and T1DM, to contrast them, and to summarize their specific role in these autoimmune diseases. We conducted a systematic review following the Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) checklist and used the Medical Subject Headings (MeSH) search strategy to obtain relevant articles. We found 585 papers which were reduced to 355 after removing duplicates. Later, the filters and inclusion/exclusion criteria were applied which ended the search with 78 articles. Finally, we reviewed the articles that contained information about the pathogenesis of CD and T1DM, their coexistence, and how the pathogenesis impacts clinical outcomes. The reviewed studies strongly conclude that the presence of human leukocyte antigen (HLA) genes DQ2 and DQ8 are high-risk for developing the coexistence of CD and T1DM. We found that killer immunoglobulin-like receptor (KIR) genes, enterovirus infection in gut cells, and gut microbiota dysbiosis with the predominance of Bacteroides spp. also play a role in the pathogenesis and development of symptoms of CD in patients with the previous diagnosis of T1DM. CD4+ and CD8+ cell levels vary among patients and studies, consequently, more study on this topic is needed.

Type 2 diabetes mellitus has been on the rise in recent years. A major cause of death in the United States is myocardial infarction with underlying coronary artery disease. Impairment of tissue insulin sensitivity in type 2 diabetes is a significant factor for sudden cardiac death. The complex pathophysiology stems from coexisting cardiovascular disease and complications of impaired tissue sensitivity to insulin. Long-term diabetics with underlying kidney disease and those requiring dialysis have systemic inflammation that adds to an increased risk of death. During times of pathological stress, myocardial tissue will express substrates and growth factors that cause conduction disequilibrium and predispose to sudden cardiac death. Diabetes is a modifiable risk factor in the prevention of sudden cardiac arrest. Specific prevention measures aimed towards lifestyle modification and medications are important to prevent diabetes and decrease mortality of future cardiac death. In recent times, drugs that compete with glucose in the proximal convoluted tubule of the nephron have clinical significance in lowering the risk of sudden cardiac arrest.