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The recent pandemic SARS-CoV-2 outbreak affects all kinds of individuals worldwide. The health, social, and economic impacts of the pandemic are dramatic, and vaccines or specific treatment options are not yet available. The only approaches that we currently have available to stop the epidemic are those of classical epidemic control, such as case isolation, contact tracing and quarantine, physical distancing, and hygiene measures. It is therefore essential to find further preventive measures and possible interventions that can slow down the number of infected individuals and decrease the severity of disease when affected by SARS-CoV-2. It seems that epigenetic mechanisms are an important part of the pathophysiology and illness severity of COVID-19. These mechanisms have been identified in SARS-CoV-2 but also in other viral infections. If and when these mechanisms are confirmed, then epigenetic interventions influencing DNA methylation could be indicated as primary and/or secondary preventive options.

Chronic non-communicable diseases (NCDs) are the leading causes of work absence, disability, and mortality worldwide. Most of these diseases are associated with low-grade inflammation. Here, we hypothesize that stresses (defined as homeostatic disturbances) can induce low-grade inflammation by increasing the availability of water, sodium, and energy-rich substances to meet the increased metabolic demand induced by the stressor. One way of triggering low-grade inflammation is by increasing intestinal barrier permeability through activation of various components of the stress system. Although beneficial to meet the demands necessary during stress, increased intestinal barrier permeability also raises the possibility of the translocation of bacteria and their toxins across the intestinal lumen into the blood circulation. In combination with modern life-style factors, the increase in bacteria/bacterial toxin translocation arising from a more permeable intestinal wall causes a low-grade inflammatory state. We support this hypothesis with numerous studies finding associations with NCDs and markers of endotoxemia, suggesting that this process plays a pivotal and perhaps even a causal role in the development of low-grade inflammation and its related diseases.

Type 2 diabetes mellitus (T2DM) is a global health burden characterized by hyperglycemia, oxidative stress, and systemic inflammation, which leads to complications that remain insufficiently managed by standard therapies. Photobiomodulation therapy (PBMT) has been proposed to be a complementary approach, but its effects in T2DM are unclear. We conducted a systematic review and meta-analysis of randomized controlled trials to evaluate the effects of PBMT on metabolic, inflammatory, and neurological outcomes in adults with T2DM. Five databases were searched until June 2025 (PROSPERO CRD420251083550) for relevant studies. Metabolic, inflammatory, and neurological outcomes were defined a priori as primary outcomes and were synthesized narratively due to substantial heterogeneity and incomplete reporting that precluded valid quantitative pooling. Although periodontal outcomes were not predefined as primary outcomes, they were reported in multiple trials; thus, these were analyzed quantitatively as secondary outcomes where sufficient homogeneity enabled meta-analysis. The narrative synthesis of primary outcomes showed inconsistent and largely short-term effects on glycemic control, systemic inflammation, and neurological function. In contrast, meta-analysis of secondary periodontal outcomes demonstrated modest but statistically significant improvements in clinical attachment level (−0.21 mm) and probing depth (−0.25 mm), with no effect on plaque index. Overall, the certainty of the evidence was low. PBMT may offer statistically significant but small adjunctive periodontal effects in adults with T2DM. However, the certainty of evidence is low, and these effects are unlikely to be clinically meaningful in isolation. Evidence for systemic metabolic, inflammatory, and neurological outcomes is preliminary and requires confirmation in larger, standardized RCTs.

Background Frozen Shoulder (FS), also known as adhesive shoulder capsulitis, is characterized by a fibrotic inflammatory process of unknown origin, with the most prominent symptoms being pain, stiffness, and reduced joint mobility. Methods The systematic review and meta-analysis presented herein provide insights into the pathogenesis of this condition, as well as common metabolic biomarkers potentially implicated in FS, such as glycated hemoglobin (HbA1c), and inflammatory biomarkers, including interleukins (IL-1, IL-6) and tumor necrosis factor alpha (TNF-α). Dyslipidemia and hormonal factors, such as thyroid dysfunctions, are also examined. Results A total of 7,499 individuals were included in the meta-analysis, and one additional study collected 28,416 blood samples from individuals with FS from biobanks. The meta-analysis of metabolic variables showed that HbA1c was the most significantly elevated marker in FS, with a standardized mean difference (SMD) of μ^ = 0.3970 (95% CI: 0.0998 to 0.6943), indicating a moderate effect. Glucose showed a mean difference of -0.28 (95% CI: -0.60 to 0.05), which was not statistically significant, suggesting that short-term fluctuations in glucose levels may not be as relevant as long-term metabolic control. Cholesterol had a standardized difference of 0.278 (95% CI: 0.171 to 0.385), being significantly higher in FS. For triglycerides, the SMD was μ^ = 1.0318 (95% CI: -1.0027 to 3.0664), indicating high heterogeneity and preventing a clear conclusion. Hypothyroidism was also evaluated, with a total SMD of 0.067, a total variance of 0.0021, and a 95% confidence interval of -0.024 to 0.158, confirming no association between FS and thyroid function. Regarding inflammatory biomarkers, IL-1β was the most predominant, showing significantly higher levels in FS, with an SMD of μ^ = 2.2671 (95% CI: 0.5750 to 3.9591). TNF-α had a mean difference of μ^ = 0.7814 (95% CI: 0.1013 to 1.4615), reflecting a significant difference from zero (z = 2.2520, p  = 0.0243). Finally, IL-6 did not show a significant association, with an SMD of μ^ = 1.6721 (95% CI: -0.9368 to 4.2810). Conclusion This meta-analysis highlights the role of metabolic dysfunction and chronic inflammation in the pathogenesis of FS. HbA1c and cholesterol were the most associated metabolic biomarkers, while IL-1β and TNF-α showed a strong link to inflammation and fibrosis. The heterogeneity in triglycerides and IL-6 underscores the need for studies with standardized methodologies and subgroup analyses. Future research should focus on biomarker progression, patient stratification, and new therapeutic strategies targeting metabolic and immune modulation, considering FS within a broader metabolic-inflammatory framework to improve its classification and treatment.

Aging can result in major changes in the composition and metabolic activities of bacterial populations in the gastrointestinal system and result in impaired function of the immune system. We assessed the efficacy of prebiotic Darmocare Pre® (Bonusan Besloten Vennootschap (BV), Numansdorp, The Netherlands) to evaluate whether the regular intake of this product can improve frailty criteria, functional status and response of the immune system in elderly people affected by the frailty syndrome. The study was a placebo-controlled, randomized, double blind design in sixty older participants aged 65 and over. The prebiotic product was composed of a mixture of inulin plus fructooligosaccharides and was compared with placebo (maltodextrin). Participants were randomized to a parallel group intervention of 13 weeks’ duration with a daily intake of Darmocare Pre® or placebo. Either prebiotic or placebo were administered after breakfast (between 9–10 a.m.) dissolved in a glass of water carefully stirred just before drinking. The primary outcome was to study the effect on frailty syndrome. The secondary outcomes were effect on functional and cognitive behavior and sleep quality. Moreover, we evaluated whether prebiotic administration alters blood parameters (haemogram and biochemical analysis). The overall rate of frailty was not significantly modified by Darmocare Pre® administration. Nevertheless, prebiotic administration compared with placebo significantly improved two frailty criteria, e.g., exhaustion and handgrip strength (p < 0.01 and p < 0.05, respectively). No significant effects were observed in functional and cognitive behavior or sleep quality. The use of novel therapeutic approaches influencing the gut microbiota–muscle–brain axis could be considered for treatment of the frailty syndrome.

Treating sarcopenia in older individuals remains a challenge, and nutritional interventions present promising approaches in individuals that perform limited physical exercise. We assessed the efficacy of leucine administration to evaluate whether the regular intake of this essential amino acid can improve muscle mass, muscle strength and functional performance and respiratory muscle function in institutionalized older individuals. The study was a placebo-controlled, randomized, double-blind design in fifty participants aged 65 and over (ClinicalTrials.gov identifier NCT03831399). The participants were randomized to a parallel group intervention of 13 weeks’ duration with a daily intake of leucine (6 g/day) or placebo (lactose, 6 g/day). The primary outcome was to study the effect on sarcopenia and respiratory muscle function. The secondary outcomes were changes in the geriatric evaluation scales, such as cognitive function, functional impairment and nutritional assessments. We also evaluated whether leucine administration alters blood analytical parameters and inflammatory markers. Administration of leucine was well-tolerated and significantly improves some criteria of sarcopenia in elderly individuals such as functional performance measured by walking time (p = 0.011), and improved lean mass index. For respiratory muscle function, the leucine-treated group improved significantly (p = 0.026) in maximum static expiratory force compared to the placebo. No significant effects on functional impairment, cognitive function or nutritional assessment, inflammatory cytokines IL-6, TNF-alpha were observed after leucine administration compared to the placebo. The use of l-leucine supplementation can have some beneficial effects on sarcopenia and could be considered for the treatment of sarcopenia in older individuals.

Obesity, and obesity-associated conditions such as hypertension, chronic kidney disease, type 2 diabetes, and cardiovascular disease, are important risk factors for severe Coronavirus disease-2019 (COVID-19). The common denominator is metaflammation, a portmanteau of metabolism and inflammation, which is characterized by chronically elevated levels of leptin and pro-inflammatory cytokines. These induce the “Suppressor Of Cytokine Signaling 1 and 3” (SOCS1/3), which deactivates the leptin receptor and also other SOCS1/3 sensitive cytokine receptors in immune cells, impairing the type I and III interferon early responses. By also upregulating SOCS1/3, Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV)-2 adds a significant boost to this. The ensuing consequence is a delayed but over-reactive immune response, characterized by high-grade inflammation (e.g., cytokine storm), endothelial damage, and hypercoagulation, thus leading to severe COVID-19. Superimposing an acute disturbance, such as a SARS-CoV-2 infection, on metaflammation severely tests resilience. In the long run, metaflammation causes the “typical western” conditions associated with metabolic syndrome. Severe COVID-19 and other serious infectious diseases can be added to the list of its short-term consequences. Therefore, preventive measures should include not only vaccination and the well-established actions intended to avoid infection, but also dietary and lifestyle interventions aimed at improving body composition and preventing or reversing metaflammation.

Frozen shoulder is a common epidemiological affliction. Data acquired from people who suffer from this type of damage in other joints such as the hip, wrist and ankle also exist; although these syndromes are less common. Treatment for frozen shoulder is primarily physical (physiotherapy, manual therapy), secondary medical (corticosteroid injections) and finally surgical but with limited success. The difficulty in treating this type of condition successfully lies in the lack of knowledge about the risk factors involved and the pathophysiology underlying this mysterious syndrome. This review gives an overview of the current scientific position of frozen shoulder in terms of evolutionary factors, etiology, the different mechanisms of action involved, current treatment options and other possible interventions based on recent discoveries of pathophysiological mechanisms. The overall objective is to clarify several unknown aspects of a syndrome that affects up to 5% of the world's population.