ABSTRACT
Background: Metabolic syndrome is characterized by a cluster-like occurrence of conditions such as hypertension, hyperglycaemia, elevated low-density lipoprotein (LDL) cholesterol or triglycerides (TG) and high visceral fat. Metabolic syndrome is linked to the build-up of plaque within the artery, which leads to disorders of the circulatory, nervous and immune systems. A variety of treatments target the regulation of these conditions; nevertheless, they remain dominant risk factors for the development of type 2 diabetes (T2DM) and cardiovascular disease (CVD), which affect 26.9% of the US population. Management and intervention strategies for improving cholesterol and/or TG are worthwhile, and recent studies on hydrogen treatment are promising, particularly as molecular hydrogen is easily ingested. This study aimed to investigate the lipid-lowering effects and quality of life (QOL) improvement of hydrogen-rich coral calcium (HRCC) in patients with metabolic syndrome. Methods: The patients, all Taiwanese, were randomly assigned to 3 different doses (low, medium, and high) of HRCC capsules. The primary outcome was the adverse effects/symptoms during this 4-week use of HRCC capsules. The secondary outcome was lipid profile changes. Complete blood count, inflammatory biomarkers, and QOL were also measured before and after the course of HRCC. Results: Sixteen patients with metabolic syndrome completed this study (7 males, 9 females; mean age: 62 years; range: 32-80). No obvious adverse effects were recorded. Only changes in blood TG reached significance. The baseline TG value was 193.19 µL (SD = 107.44), which decreased to 151.75 µL (SD = 45.27) after 4 weeks of HRCC (p = 0.04). QOL showed no significant changes. Conclusion: This study is the first human clinical trial evaluating HRCC capsules in patients with metabolic syndrome. Based on the safety and potential TG-lowering effects of short-term HRCC, further long-term investigations of HRCC are warranted. Clinical trial registration: [ClinicalTrials.gov], identifier [NCT05196295].
ABSTRACT
Background: Molecular hydrogen, with its antioxidant and anti-inflammatory properties, may be suitable for the prevention and treatment of chronic obstructive pulmonary disease (COPD). This study aims to investigate the therapeutic efficacy of hydrogen-oxygen (H2/O2) treatment in cigarette smoke solution (CSS)-induced COPD-like injury in a female BALB/c mouse model. Methods: Thirty mice were randomly assigned to three groups: Control (n=8), COPD (n=10), and COPD + H2/O2 (n=12). CSS was administered by intraperitoneal (IP) injection twice weekly for 6 weeks during the COPD induction phase. Simultaneously, the COPD + H2/O2 group started received 75 minutes of inhalation therapy (42% H2) delivered by the Oxy-Hydrogen Generator twice daily for 9 weeks. Mice body weights and survival were measured throughout the study period. Neutrophil elastase (NE) activity and lung histopathological changes were also evaluated. Results: The results showed a higher survival rate in the COPD + H2/O2 group compared to the COPD group (100% vs. 80%) during the induction phase. Slight decreases in body weight gains were observed in the COPD and COPD + H2/O2 groups during the first 15 days of the induction phase, but there was no significant difference in mean body weights among the three groups throughout the study period. NE activity was numerically lower in the COPD + H2/O2 group compared to the COPD group. The histopathological evaluation showed significant improvements in the H2/O2-treated mice with respect to mean linear intercept (MLI) and lesion (inflammation and emphysema) scores. Improvements in goblet cell hypertrophy and hyperplasia of airway epithelium were not significant. Conclusions: A 9-week H2/O2 inhalation therapy delivered by the Oxy-Hydrogen Generator to CSS-induced COPD-like injury in mice showed improvement in survival rate, alveolar structural changes, and histopathological lesion scores of the lung.
ABSTRACT
Interleukin 1A (IL-1A), a potent proinflammatory cytokine, has been implicated in the pathogenesis of Alzheimer's disease (AD). Several recent studies have shown that a polymorphism in the IL-1A locus -889 was associated with AD risk and onset age, however, other studies were not able to replicate these findings. In this investigation, the IL-1A C(-889)T polymorphism has been analyzed for a Chinese population of 234 AD patients and 170 controls. There were no significance differences in IL-1A genotype or allele frequencies comparing the AD cases and controls, even after stratification for age of onset and adjustment for apolipoprotein E genotype. The results reveal that it is not likely that the IL-1A C(-889)T polymorphism is involved in AD pathogenesis in the Chinese population. Further studies of the associations between other IL-1A genetic polymorphisms and AD are needed to fully elaborate the involvement of this gene in AD.
