The thyroid gland is an endocrine organ whose hormones enable the proper functioning of the organism. The normal function of this organ is influenced by internal and external factors. One of the external factors is trace elements. Trace elements in appropriate concentrations are necessary for the proper functioning of the thyroid. Fe, Cu, Mn, I, Zn, and Se are part of the enzymes involved in oxidative stress reduction, while Cd, Hg, and Pb can increase ROS production. Cu and Fe are necessary for the correct TPO synthesis. An imbalance in the concentration of trace elements such as Fe, Cu, Co, I, Mn, Zn, Ag, Cd, Hg, Pb, and Se in thyroid cells can lead to thyroid diseases such as Graves’ disease, Hashimoto’s thyroiditis, hypothyroidism, autoimmune thyroiditis, thyroid nodules, thyroid cancer, and postpartum thyroiditis. Lack of adequate Fe levels may lead to hypothyroidism and cancer development. The thyroid gland’s ability to absorb I is reversibly reduced by Co. Adequate levels of I are required for correct thyroid function; both deficiency and excess can predispose to the development of thyroid disorders. High concentrations of Mn may lead to hypothyroidism. Furthermore, Mn may cause cancer development and progression. Insufficient Zn supplementation causes hypothyroidism and thyroid nodule development. Cd affecting molecular mechanisms may also lead to thyroid disorders. Hg accumulating in the thyroid may interfere with hormone secretion and stimulate cancer cell proliferation. A higher risk of thyroid nodules, cancer, autoimmune thyroiditis, and hypothyroidism were linked to elevated Pb levels. Se deficiency disrupts thyroid cell function and may lead to several thyroid disorders. On the other hand, some of the trace elements may be useful in the treatment of thyroid diseases. Therefore, the effects of trace elements on the thyroid require further research.

Proper joint function has a significant impact on people’s quality of life. Joints are the point of connection between two or more bones and consist of at least three elements: joint surfaces, the joint capsule, and the joint cavity. Joint diseases are a serious social problem. Risk factors for the development of these diseases include overweight and obesity, gender, and intestinal microbiome disorders. Another factor that is considered to influence joint diseases is trace elements. Under normal conditions, elements such as iron (Fe), copper (Cu), cobalt (Co), iodine (I), manganese (Mn), zinc (Zn), silver (Ag), cadmium (Cd), mercury (Hg), lead (Pb), nickel (Ni) selenium (Se), boron (B), and silicon (Si) are part of enzymes involved in reactions that determine the proper functioning of cells, regulate redox metabolism, and determine the maturation of cells that build joint components. However, when the normal concentration of the above-mentioned elements is disturbed and toxic elements are present, dangerous joint diseases can develop. In this article, we focus on the role of trace elements in joint function. We describe the molecular mechanisms that explain their interaction with chondrocytes, osteocytes, osteoblasts, osteoclasts, and synoviocytes, as well as their proliferation, apoptosis, and extracellular matrix synthesis. We also focus on the role of these trace elements in the pathogenesis of joint diseases: rheumatoid arthritis (RA), osteoarthritis (OA), psoriatic arthritis (PsA), ankylosing spondylitis (AS), and systemic lupus erythematosus (SLE). We describe the roles of increased or decreased concentrations of individual elements in the pathogenesis and development of joint diseases and their impact on inflammation and disease progression, referring to molecular mechanisms. We also discuss their potential application in the treatment of joint diseases.

Gastric cancer (GC) ranks third in terms of cancer-related deaths and is the fifth most commonly diagnosed type of cancer. Its risk factors include Helicobacter pylori infection, Epstein–Barr virus infection, the consumption of broiled and charbroiled animal meats, salt-preserved and smoke-enhanced foods, alcohol drinking, tobacco smoking, exposure to ionizing radiation, and positive family history. The limited effectiveness of conventional therapies and the widespread risk factors of GC encourage the search for new methods of treatment and prevention. In the quest for cheap and commonly available medications, numerous studies focus on herbal medicine, traditional brews, and spices. In this review, we outline the potential use of spices, including turmeric, ginger, garlic, black cumin, chili pepper, saffron, black pepper, rosemary, galangal, coriander, wasabi, cinnamon, oregano, cardamom, fenugreek, caraway, clove, dill, thyme, Piper sarmentosum, basil, as well as the compounds they contain, in the prevention and treatment of GC. We present the potential molecular mechanisms responsible for the effectivity of a given seasoning substance and their impact on GC cells. We discuss their potential effects on proliferation, apoptosis, and migration. For most of the spices discussed, we also outline the unavailability and side effects of their use.

Background: Tocotrienols, lesser-studied members of the vitamin E family, have gained attention because of their pleiotropic biological activities and potential role in cardiometabolic disease. Recent randomized controlled trials (RCTs) indicate benefits beyond α-tocopherol, including antioxidant, anti-inflammatory, and metabolic effects. Aim: To summarize RCT evidence published between 2020 and 2025 on the effects of tocotrienol supplementation in metabolic syndrome, type 2 diabetes (T2D), non-alcoholic fatty liver disease (NAFLD), and diabetic complications. Methods: This narrative review included RCTs evaluating tocotrienol supplementation in adults with metabolic disorders. Outcomes included oxidative stress, inflammation, glycaemic control, lipid metabolism, vascular and neural function, and liver injury. Owing to heterogeneity in formulations, doses, and study designs, findings were synthesized narratively. Results: Tocotrienol supplementation improved biomarkers of oxidative stress, inflammation, and metabolic regulation. In metabolic syndrome, it modulated microRNAs associated with insulin resistance and inflammation. In T2D, δ-tocotrienol reduced HbA1c, fasting glucose, insulin resistance, and malondialdehyde while increasing antioxidant capacity. In NAFLD, δ-tocotrienol reduced inflammatory cytokines and liver injury markers more effectively than α-tocopherol. Tocotrienol-rich vitamin E also improved nerve conduction in diabetic neuropathy and supported renal function in diabetic kidney disease. Supplementation was well tolerated. Conclusions: Tocotrienols show promising metabolic, anti-inflammatory, and organ-protective effects, particularly in T2D and NAFLD. However, heterogeneity, small sample sizes, and short intervention periods limit definitive conclusions. Larger, standardized, long-term RCTs are needed to confirm their role as adjunctive therapy in cardiometabolic disease.

The pancreas is an organ with two functions: endocrine and exocrine. The proper functioning of the pancreas depends on many factors. One of these is trace elements—precise control of trace element homeostasis is important for both the endocrine and exocrine parts. This review provides a comprehensive summary of current knowledge regarding the role of trace elements: iron (Fe), copper (Cu), cobalt (Co), iodine (I), manganese (Mn), zinc (Zn), silver (Ag), cadmium (Cd), mercury (Hg), lead (Pb), and selenium (Se) in pancreatic physiology and their influence on the pathogenesis of key diseases of this organ, such as diabetes (DM), acute (AP) and chronic pancreatitis (CP), autoimmune pancreatitis (AIP), and pancreatic cancer (PC). Trace elements, including Fe, Cu, Zn, Se, and Mn, play a fundamental role in maintaining endocrine and exocrine homeostasis, participating in insulin synthesis, stabilizing digestive enzymes, and the functioning of antioxidant systems. It has been demonstrated that disturbances in their concentrations lead to the activation of pathological molecular pathways, including oxidative stress, chronic inflammation, and beta-cell apoptosis. In the context of diabetes, excess Fe promotes ferroptosis, whilst exposure to heavy metals such as Cd, Pb, and Hg induces insulin resistance and pancreatic islet dysfunction. In the course of pancreatitis, elements such as Zn and Se exhibit protective potential by stabilizing tissue barriers, whereas toxic metals impair ion transport, exacerbating fibrotic processes. Furthermore, analysis of available data indicates a significant association between heavy metal accumulation and pancreatic carcinogenesis, driven by DNA damage and oncogene modulation. Understanding pancreatic metallomics opens new prospects for early diagnosis, environmental prevention, and the development of targeted therapeutic strategies that restore the body’s micronutrient balance.

Haglund’s disease is a significant cause of posterior heel pain, particularly among physically active individuals. It is associated with a posterosuperior calcaneal prominence leading to irritation of the retrocalcaneal bursa and Achilles tendon. The condition has a multifactorial etiology, including anatomical, biomechanical, and environmental factors. Diagnosis is based on clinical examination and imaging modalities such as X-ray, MRI, and ultrasound. Treatment includes both conservative and surgical approaches depending on symptom severity.