In recent decades, the mental health and sleep quality of populations have worsened globally, leading healthcare professionals and researchers to seek new, safe therapies that extend beyond traditional pharmacological treatments. Withania somnifera, commonly known as ashwagandha, appears to be a valuable element for improving overall quality of life due to its abundance of active substances and known multidirectional effects on the human body. This review aims to critically evaluate the available literature on ashwagandha extract and its potential roles in enhancing well-being, with a focus on reducing stress, fatigue, anxiety, and depressive disorders; improving sleep quality; and enhancing cognitive function. Furthermore, an attempt has also been made to highlight the limitations associated with the use of this plant extract in clinical practice and indicate directions for future research.

Ferroptosis, a form of regulated cell death driven by iron-dependent lipid peroxidation, has emerged as a key player in the pathogenesis of gastrointestinal (GI) diseases. Unlike apoptosis or necrosis, ferroptosis is characterized by distinctive metabolic and molecular pathways, including dysregulated iron metabolism, oxidative stress, and impaired antioxidant defenses. This review explores the complex role of ferroptosis in conditions such as inflammatory bowel disease (IBD), non-alcoholic steatohepatitis (NASH), and gastrointestinal cancers. Special attention is given to the molecular mechanisms underlying ferroptosis, including the Xc−/GSH/GPX4 axis, ferritinophagy, ACSL4/LPCAT3-mediated lipid remodeling, and the influence of the gut microbiota. Therapeutic strategies targeting ferroptosis—including pharmacological inhibitors, iron chelators, and microbiota-based interventions—are evaluated for their translational potential, underscoring ferroptosis as a promising target for precision therapies in gastroenterology and highlighting the need for further clinical studies to validate its diagnostic and therapeutic implications.

Growing evidence indicates that the gut microbiota is a central regulator of systemic immunity, acting through epithelial barrier integrity, microbial metabolites, and bidirectional signaling with innate and adaptive immune cells. Within this framework, probiotics have attracted substantial interest as tools for immune modulation; however, their effects are not uniform and should not be generalized across species or formulations. This review synthesizes current evidence on the gut microbiota–immune axis and examines how defined probiotic strains influence immune homeostasis, inflammation, and clinical outcomes. Particular emphasis is placed on strain-specific effects among lactic acid bacteria, bifidobacteria, yeast probiotics, and emerging nontraditional candidates, with attention to mechanisms involving cytokine signaling, regulatory T-cell induction, nuclear factor kappa B (NF-κB) modulation, toll-like receptor (TLR) pathways, short-chain fatty acids (SCFAs), tryptophan metabolites, and bile-acid-dependent signaling. The available literature indicates that the most meaningful immunological effects arise from precisely characterized strains acting in specific host contexts, whereas inconsistent trial design, small sample sizes, variable dosing, and poor strain resolution continue to limit translation. Overall, current data support a shift from generic probiotic use toward mechanism-based, strain-specific, and increasingly personalized strategies for immune modulation.

Migraine, with a prevalence of 14–15% in the world population, is one of the diseases that markedly reduce patients’ quality of life. Despite extensive therapeutic tools, the search for substances that may have potential therapeutic properties in migraine patients is still ongoing. Coenzyme Q10 (CoQ10), as a natural and potent antioxidant, appears to be a valuable adjunct in treating and preventing many conditions, such as cardiovascular, metabolic, autoimmune, or neurodegenerative diseases. This review aims to evaluate if CoQ10 can be a potential therapeutic agent in the treatment of migraine. Based on the studies discussed, CoQ10 may have applications in migraine therapy due to its potent anti-inflammatory and oxidative stress-reducing properties. Furthermore, by improving mitochondrial function, CoQ10 can contribute to the energy supply to brain cells, which is particularly important in migraine. Supplementation with CoQ10 in a wide range of doses has resulted in many therapeutic benefits in subjects, including a decrease in the frequency and duration of migraine attacks, a reduction in nausea, a lower maximum pain during an attack, and fewer days with migraine. Therefore, it seems that CoQ10 may be a relevant therapeutic supplement for the treatment and prevention of migraine.