Obesity is a growing global health challenge, closely linked to chronic low-grade inflammation. This persistent, low-intensity immune response contributes to the development of metabolic, cardiovascular, and cancer-related diseases. A key player in this process is the gut microbiota. Dysbiosis, an imbalance in gut bacterial composition, disrupts metabolic function, weakens the intestinal barrier, and promotes the production of pro-inflammatory cytokines. In people with obesity, gut microbial diversity is reduced, and the ratio of beneficial to harmful bacteria shifts, affecting lipid metabolism and immune balance. Short-chain fatty acids, produced by gut bacteria, help maintain gut integrity and reduce inflammation. Butyrate, a major SCFA, also improves insulin sensitivity and may support obesity treatment. Diet plays a central role in shaping the gut microbiome. Western diets tend to promote dysbiosis and inflammation, while Mediterranean-style diets encourage the growth of beneficial bacteria. Targeted modulation of the microbiota through diet, probiotics, or medication emerges as a promising strategy for preventing and managing obesity.

According to WHO (World Health Organization), in 2022, 43% of adults worldwide were overweight and 16% suffered from obesity. Overweight and obesity is a condition in which the body, due to the excess of consumed calories, accumulates it in the form of adipose tissue. However, this tissue is not only an energy store but also secretes numerous adipokines, mainly with pro-inflammatory effects. The mobilization of the immune system due to the accumulation of adipose tissue is called low-grade inflammation (LGI) and is a mediating factor between excess body weight and diseases such as cardiovascular disease, insulin resistance, type 2 diabetes, neurodegenerative diseases, sleep apnea, and even cancer. The aim of the review is to update reports related to dietary factors influencing the severity or alleviation of low-grade inflammation in obese people. The review used studies from PubMed and Google Scholar from the last 10 years. The results indicate that the Western diet, rich in processed foods, high levels of saturated fatty acids, simple sugars, salt, and low fiber and nutrient content (vitamins and minerals), leads to increased low-grade inflammation. On the other hand, calorie restrictions and an appropriate balance of macronutrients, fatty acids, and antioxidant or anti-inflammatory nutrients (e.g., polyphenols, vitamins A, C, and E, and selenium) may reduce the severity of LGI, reducing the risk of obesity-related diseases.

Neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis, currently represent one of the major challenges in contemporary medicine and geriatrics. Progressive degeneration of the nervous system affects not only patients’ physical functioning but also their psychosocial well-being, often leading to social isolation and disruption of interpersonal relationships. These processes are most strongly associated with individuals over 65 years of age, in whom metabolic syndrome is frequently diagnosed and constitutes a significant factor predisposing them to the exacerbation of neuropathological changes. This review analyzes the role of selected vitamins in modulating the course of neurodegenerative disorders, with particular emphasis on their neuroprotective potential. Specific attention is given to their involvement in antioxidant defense mechanisms, regulation of inflammatory pathways, prevention of abnormal protein aggregation, participation in neurotransmitter synthesis, and support of mitochondrial function and cellular energy metabolism. The review also considers key interactions between vitamins and coenzyme Q10, which synergistically enhance neuroprotective mechanisms. Deficiencies in certain vitamins may exacerbate oxidative stress, impair synaptic transmission, and intensify neuroinflammatory responses, thereby contributing to disease progression. The study analyzes the available data on therapeutic doses of vitamins and compares them with the recommended dietary intake and the upper tolerable intake levels (UL). The available evidence suggests that personalized vitamin supplementation, when integrated with a well-balanced and nutrient-dense diet, may constitute a valuable adjunctive therapeutic strategy. Such an approach may help attenuate disease progression, support neuronal integrity, and improve functional outcomes. Ultimately, targeted nutritional interventions may enhance overall well-being and quality of life in patients affected by neurodegenerative diseases.

Inflammatory bowel diseases (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), are chronic diseases with complex aetiology involving genetic, immunological, and environmental factors and intestinal microbiota disorders. Mutations in genes such as NOD2, ATG16L1, IRGM, TLR4, and IL23R disrupt the functioning of the intestinal barrier and the immune response, increasing susceptibility to chronic inflammation. Recent studies indicate that interactions between diet, gene expression, and epigenetic mechanisms play a key role in modulating the course of IBD, e.g., DNA methylation, histone modifications, and microRNA activity. The use of bioactive dietary components in combination with epigenome modulation is a promising tool in the treatment of IBD, enabling the reduction in chronic inflammation, improving intestinal barrier function, and supporting the immune response.

Obesity, type 2 diabetes mellitus (T2DM) and steatohepatitis associated with metabolic dysfunction (MASLD) are on the rise and pose serious health challenges worldwide. In recent years, researchers have gained a better understanding of the important role of the gut microbiota in the development and progression of these diseases. Intestinal dysbiosis can contribute to the occurrence of increased intestinal permeability, inflammation and reduced numbers of commensal bacteria. In obesity, these changes contribute to chronic low-grade inflammation and deregulated metabolism. In MASLD, gut microbiota dysbiosis can promote liver fibrosis and impair bile acid metabolism, while in T2DM, they are associated with impaired glycemic control and insulin resistance. Regular physical activity has a positive effect on the composition of the gut microbiota, increasing its diversity, modulating its metabolic functions, strengthening the intestinal barrier and reducing inflammation. These findings suggest that exercise and microbiota-targeted interventions may play an important role in the prevention and treatment of metabolic diseases.

Background: Atherosclerosis is a chronic inflammatory disease driven by complex interactions between lipid metabolism disorders, oxidative stress, and immune dysregulation. Despite advances in pharmacotherapy, there is growing interest in nutraceutical compounds with multi-target effects. Thymoquinone (TQ), the main bioactive constituent of Nigella sativa, has emerged as a promising candidate due to its anti-inflammatory, antioxidant, and lipid-modulating properties. This review aims to comprehensively evaluate the effects of TQ on the key pathophysiological mechanisms involved in atherosclerosis, with particular emphasis on inflammation, oxidative stress, and lipid metabolism. Methods: A narrative review of preclinical studies, including in vitro and in vivo experimental models, was conducted to assess the biological activity of TQ and its potential anti-atherosclerotic effects. Results: TQ exhibits multi-target activity by modulating several molecular pathways associated with atherogenesis. It reduces oxidative stress by enhancing antioxidant enzyme activity and decreasing reactive oxygen species production. TQ also suppresses inflammatory signaling pathways, including NF-κB, MAPK, and COX-2, leading to decreased expression of pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α. Furthermore, it influences lipid metabolism by lowering total cholesterol and LDL-C levels while improving lipid profiles. TQ has also been shown to inhibit foam cell formation, endothelial dysfunction, and vascular inflammation. Additionally, nanocarrier-based formulations of TQ may improve its bioavailability and therapeutic potential. Conclusions: Current preclinical evidence suggests that TQ may play a significant role in the prevention and modulation of atherosclerosis through its multi-mechanistic action. However, the lack of well-designed clinical trials, limited bioavailability, and insufficient data on long-term safety highlight the need for further research to establish its clinical efficacy and optimal therapeutic use.