In recent years, cases of liver damage caused by ashwagandha herbal supplements have been reported from different parts of the world (Japan, Iceland, India, and the USA). Here, we describe the clinical phenotype of suspected ashwagandha-induced liver injury and the potential causative mechanism. The patient was admitted to the hospital because of jaundice. In the interview, it was reported that he had been taking ashwagandha for a year. Laboratory results showed an increase in total bilirubin, alanine transaminase (ALT), aspartate transaminase (AST), (gamma-glutamyl transpherase (GGT), alkaline phosphatase (ALP), total cholesterol, triglycerides, and ferritin. Based on clinical symptoms and additional tests, the patient was diagnosed with acute hepatitis and referred to a facility with a higher reference rate to exclude drug-induced liver injury. An R-value was assessed, indicative of hepatocellular injury. The result of the 24 h urine collection exceeded the upper limit of normal for copper excretion in urine twice. The clinical condition improved after intensive pharmacological treatment and four plasmapheresis treatments. This case is another showing the hepatotoxic potential of ashwagandha to cause cholestatic liver damage mixed with severe jaundice. In view of several documented cases of liver damage caused by ashwagandha and the unknown metabolic molecular mechanisms of substances contained in it, attention should be paid to patients reporting the use of these products in the past and presenting symptoms of liver damage.

Decreased bone mass in patients with inflammatory bowel diseases (IBD) is a clinical problem with extremely severe consequences of osteoporotic fractures. Despite its increasing prevalence and the need for mandatory intervention and monitoring, it is often ignored in IBD patients’ care. Determining the biomarkers of susceptibility to bone mineral density disorder in IBD patients appears to be indispensable. We aim to investigate the impact of estrogen receptor gene (ESR1) gene polymorphisms on bone mineral density (BMD) in patients with ulcerative colitis (UC) and Crohn’s disease (CD), as they may contribute both, to osteoporosis and inflammatory processes. We characterised 197 patients with IBD (97 with UC, 100 with CD), and 41 controls carrying out vitamin D, calcium and phosphorus serum levels, and bone mineral density assessment at the lumbar spine and the femoral neck by dual-energy X-ray absorptiometry (DXA), ESR1 genotyping and haplotype analysis. We observed that women with CD showed the lowest bone density parameters, which corresponded to the ESR1 c.454-397T and c.454-351A allele dose. The ESR1 gene PvuII and XbaI TA (px) haplotype correlated with decreased femoral neck T-score (OR = 2.75, CI = [1.21–6.27], P-value = 0.016) and may be predictive of osteoporosis in female patients with CD.

Inflammatory bowel disease (IBD) arises from the interplay between genetic susceptibility, immune dysregulation, microbiota, and environmental exposures, with diet potentially contributing to both pathogenesis and management. Patients frequently modify their diet independently, often using different strategies during remission and active symptoms. This narrative review synthesises evidence on patient-accessible dietary patterns and selected structured nutritional therapies across five domains: incident IBD, objective intestinal inflammation, gastrointestinal symptoms and quality of life, nutritional safety, and real-world feasibility. Mediterranean and other minimally processed plant-forward patterns are associated with higher diet quality and potentially favourable microbial and metabolic profiles; however, current trials do not demonstrate consistent superiority for objective remission or mucosal healing. Western and ultra-processed food-rich patterns are associated with incident IBD, whereas evidence for relapse in established disease is less consistent. Low-FODMAP approaches may improve selected symptoms but should not be interpreted as anti-inflammatory therapy. Evidence for ketogenic and intentional carnivore diets remains insufficient for routine use. Exclusive enteral nutrition and the Crohn’s Disease Exclusion Diet have distinct, protocolised therapeutic roles, particularly in Crohn’s disease. Across strategies, affordability, food security, cooking resources, disease phenotype, nutritional risk, and access to specialist dietetic care determine safe and equitable implementation.