With the rising epidemic of obesity, metabolic syndrome, and type 2 diabetes mellitus in China, metabolic dysfunction-associated non-alcoholic fatty liver disease has become the most prevalent chronic liver disease. This condition frequently occurs in Chinese patients with alcoholic liver disease and chronic hepatitis B. To address the impending public health crisis of non-alcoholic fatty liver disease and its underlying metabolic issues, the Chinese Society of Hepatology and the Chinese Medical Association convened a panel of clinical experts to revise and update the “Guideline of prevention and treatment of non-alcoholic fatty liver disease (2018, China)”. The new edition, titled “Guideline for the prevention and treatment of metabolic dysfunction-associated fatty liver disease (Version 2024)”, offers comprehensive recommendations on key clinical issues, including screening and monitoring, diagnosis and evaluation, treatment, and follow-up for metabolic dysfunction-associated fatty liver disease and metabolic dysfunction-associated steatotic liver disease. Metabolic dysfunction-associated fatty liver disease is now the preferred English term and is used interchangeably with metabolic dysfunction-associated steatotic liver disease. Additionally, the guideline emphasizes the importance of multidisciplinary collaboration among hepatologists and other specialists to manage cardiometabolic disorders and liver disease effectively.

Aging is an intricate process driven by various factors, including the dynamic interplay between the host microbiome and aging. The gut microbiome undergoes several changes throughout the entire lifespan of a healthy human. Numerous factors, ranging from the mode of childbirth and sex differences to lifestyle, are known to impact the gut microbiome in healthy individuals. As a result, the gut microbiome varies widely among individuals and exhibits robustness after early childhood. However, as one ages, the human body undergoes several important changes, and so does the gut microbiome. This review addresses the relationship between aging and the dynamics of the host microbiome from in utero to over 100 years of age. Additionally, we attempted to untangle this intricate relationship between the gut microbiome and aging by presenting various microbiota-dependent mechanisms involving intrinsic and extrinsic factors such as metabolic, neurological, immunological, dietary, and lifestyle factors that potentially regulate aging. Furthermore, we aimed to highlight microbiome-based aging intervention studies focused on modulating or rejuvenating the microbiota for healthy aging and longevity.

Gluten has multiple harmful effects that compromise human health, not only in gluten-dependent diseases but also in non-gluten-affected chronic inflammatory conditions. After consumption, the indigestible gluten peptides are modified by luminal microbial transglutaminase or transported through the gut epithelium to interact with the highly populated mucosal immune cells. As a disruptor of gut permeability, gluten peptides compromise tight junction integrity, allowing foreign immunogenic molecules to reach internal compartments. Gliadin peptides are distributed systemically to remote organs, where they encounter endogenous tissue transglutaminase. Following post-translational deamidation or transamidation, the peptides become immunogenic and pro-inflammatory, inducing organ dysfunction and pathology. Cross-reactivity and sequence homology between gluten/gliadin peptides and human epitopes may contribute to molecular mimicry in autoimmunity induction. A gluten-free diet can prevent these phenomena through various mechanisms. As proof of concept, gluten withdrawal alleviates disease activity in chronic inflammatory, metabolic, and autoimmune conditions, and even in neurodegeneration. We recommend combining the gluten-free and Mediterranean diets to leverage the advantages of both. Before recommending gluten withdrawal for non-gluten-dependent conditions, patients should be asked about gut symptomatology and screened for celiac-associated antibodies. The current list of gluten-induced diseases includes celiac disease, dermatitis herpetiformis, gluten ataxia, gluten allergy, and non-celiac gluten sensitivity. In view of gluten being a universal pro-inflammatory molecule, other non-celiac autoinflammatory and neurodegenerative conditions should be investigated for potential gluten avoidance.

In recent years, there has been a notable shift towards a holistic approach to human health, recognizing the importance of integrating essential nutrients with traditional natural medicines. This review article examines the potential synergy between nutrition and traditional healing practices in promoting well-being and disease prevention. It explores the diverse landscape of traditional medicine systems worldwide, highlighting their cultural significance and accumulated wisdom over generations. Moreover, it sheds light on the scientific foundations of these traditional remedies, showcasing their relevance in modern healthcare. Traditional natural medicines, often sourced from plants, animals, or minerals, offer a wide array of therapeutic options addressing root causes rather than symptoms alone. This enduring wisdom has sparked interest in complementing modern healthcare with traditional practices, aiming for a harmonious integration of tradition and evidence-based medicine. Furthermore, the article underscores the critical role of nutrients in maintaining overall health and preventing chronic diseases. It emphasizes the holistic perspective of health, encompassing mental, emotional, and physical well-being. The relationship between nutrition and health is also explored, emphasizing the importance of a balanced diet. The synergy between traditional natural medicines and nutritional interventions presents a promising avenue for a comprehensive approach to healthcare. The article advocates for collaborative research, interdisciplinary dialogue, and cross-cultural exchanges to harness the collective wisdom of the past and present. By embracing both nutrients and traditional medicines, we can move towards achieving optimal health and wellness, recognizing the profound interconnectedness between humans and the natural world.

Given the global prevalence and rising incidence of metabolic dysfunction-associated steatotic liver disease (MASLD), the absence of licensed medications is striking. A deeper understanding of the heterogeneous nature of MASLD has recently contributed to the discovery of novel groups of agents and the potential repurposing of currently available medications. MASLD therapies center on four major pathways. Considering the close relationship between MASLD and type 2 diabetes, the first approach involves antidiabetic medications, including incretins, thiazolidinedione insulin sensitizers, and sodium-glucose cotransporter 2 inhibitors. The second approach targets hepatic lipid accumulation and the resultant metabolic stress. Agents in this group include peroxisome proliferator-activated receptor agonists (e.g., pioglitazone, elafibranor, saroglitazar), bile acid-farnesoid X receptor axis regulators (obeticholic acid), de novo lipogenesis inhibitors (aramchol, NDI-010976), and fibroblast growth factor 21/19 analogs. The third approach focuses on targeting oxidative stress, inflammation, and fibrosis. Agents in this group include antioxidants (vitamin E), tumor necrosis factor α pathway regulators (emricasan, pentoxifylline, ZSP1601), and immune modulators (cenicriviroc, belapectin). The final group targets the gut (IMM-124e, solithromycin). Combination therapies targeting different pathogenetic pathways may provide an alternative to MASLD treatment with higher efficacy and fewer side effects. This review aimed to provide an update on these medications.

Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as non-alcoholic fatty liver disease, has a high global prevalence and can progress to metabolic dysfunction-associated steatohepatitis, cirrhosis, and hepatocellular carcinoma. The pathogenesis of MASLD is primarily driven by disturbances in hepatic lipid metabolism, involving six key processes: increased hepatic fatty acid uptake, enhanced fatty acid synthesis, reduced oxidative degradation of fatty acids, increased cholesterol uptake, elevated cholesterol synthesis, and increased bile acid synthesis. Consequently, maintaining hepatic lipid metabolic homeostasis is essential for effective MASLD management. Numerous novel molecules and Chinese proprietary medicines have demonstrated promising therapeutic potential in treating MASLD, primarily by inhibiting lipid synthesis and promoting lipid oxidation. In this review, we summarized recent research on MASLD, elucidated the molecular mechanisms by which lipid metabolism disorders contribute to MASLD pathogenesis, and discussed various lipid metabolism-targeted therapeutic approaches for MASLD.

Natural products have been used effectively to treat different ailments since the advent of human history. Angiosperms contain numerous bioactive molecules that have been applied as medicines to treat various human diseases, including cancer. Jamun (Syzygium cumini) is an angiosperm belonging to the Myrtaceae family. This comprehensive review on Jamun includes information collected from Google Scholar, SciFinder, PubMed, ScienceDirect, and other websites on the internet, giving an account of its botanical profile, chemical composition, and medicinal properties. Ethnomedicinally, various parts of Jamun are used to treat various conditions and have been administered since ancient times in Ayurveda to treat arthritis, obesity, urinary diseases, asthma, bowel spasms, stomach pain, flatulence, diabetes, and dysentery. Several scientific studies also have demonstrated the pluripotent medicinal properties of Jamun, including anti-oxidant, anti-allergic, antiretinitis, antipyretic, antidiarrheal, antinociceptive, anticancer, antidiabetic, anti-obesity, antihyperlipidemic, anti-inflammatory, antimicrobial, diuretic, cardioprotective, chemopreventive, gastroprotective, immunomodulatory, hepatoprotective, wound healing, anthelmintic, and radioprotective. Jamun contains alkaloids, anthraquinones, catechins, cardiac glycosides, flavonoids, glycosides, steroids, phenols, tannins, and saponins. Numerous active phytochemicals have been isolated from its roots, stems, leaves, flowers, fruits, and seeds. Jamun increases glutathione, glutathione peroxidase, catalase, and superoxide dismutase expression and reduces lipid peroxidation levels to exert its beneficial effects on important organs and tissues. Jamun also protects against DNA damage induced by toxic agents including metals, chemicals and ionizing radiation. Jamun activates peroxisome proliferator-activated receptors alpha and gamma and increases fatty acid and glucose metabolism. Additionally, Jamun suppresses various genes at the molecular level. Thus, the scientific evaluation of Jamun is a step forward in validating its traditional use to treat various disorders and may pave the way for translational research for its medicinal use.

Bilirubin, the primary breakdown product of hemoproteins, particularly hemoglobin, plays a key role in the diagnosis, prognosis, and monitoring of liver diseases. In acute liver diseases, such as acute liver failure, drug-induced liver injury, and viral hepatitis, bilirubin serves as a biomarker reflecting the extent of hepatocyte loss and liver damage. Chronic liver diseases, including alcohol-related liver disease, chronic hepatitis C virus infection, metabolic dysfunction-associated fatty liver disease, and autoimmune liver diseases, are marked by persistent liver injury and inflammation. Bilirubin levels in chronic liver diseases provide insight into liver function, disease severity, and prognosis. As a versatile biomarker, bilirubin offers valuable information on the pathophysiology of liver diseases and aids in guiding clinical decision-making regarding the treatment of liver diseases and their complications. This review aimed to explore the multifunctional role of bilirubin in liver diseases by analyzing its biological functions beyond its role as a biomarker of liver damage.