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The evidence for the beneficial effects of drinking hydrogen-water (HW) is rare. We aimed to investigate the effects of HW consumption on oxidative stress and immune functions in healthy adults using systemic approaches of biochemical, cellular, and molecular nutrition. In a randomized, double-blind, placebo-controlled study, healthy adults (20–59 y) consumed either 1.5 L/d of HW ( n  = 20) or plain water (PW, n  = 18) for 4 weeks. The changes from baseline to the 4th week in serum biological antioxidant potential (BAP), derivatives of reactive oxygen, and 8-Oxo-2′-deoxyguanosine did not differ between groups; however, in those aged ≥ 30 y, BAP increased greater in the HW group than the PW group. Apoptosis of peripheral blood mononuclear cells (PBMCs) was significantly less in the HW group. Flow cytometry analysis of CD4 + , CD8 + , CD20 + , CD14 + and CD11b + cells showed that the frequency of CD14 + cells decreased in the HW group. RNA-sequencing analysis of PBMCs demonstrated that the transcriptomes of the HW group were clearly distinguished from those of the PW group. Most notably, transcriptional networks of inflammatory responses and NF-κB signaling were significantly down-regulated in the HW group. These finding suggest HW increases antioxidant capacity thereby reducing inflammatory responses in healthy adults.

Not only the water quantity consumed but also the source of drinking water has been considered for their health benefits, but there is limited evidence. We aimed to determine whether the amount and type of drinking water affect physiological and biological functions, including brain function, by confirming how it affects gut microbiota which has an important regulatory role in host physiology. Three-week-old infant mice were subjected to 1) a water restriction experiment (control group, ad libitum consumption of distilled water; dehydration group, time-limited access to distilled water [15 min/day]) and 2) different water source experiment (distilled water, purified water, spring water, and tap water groups). The gut microbiota and cognitive development were analyzed using the 16S ribosomal ribonucleic acid sequencing method and the Barnes maze, respectively. The relative abundance of Firmicutes and Bacteroidetes and the Firmicutes-to-Bacteroidetes ratio (F/B ratio) changed depending on age (juveniles vs. infants). Insufficient water intake reversed these developmental changes, showing that the relative abundances of Bacteroidetes and Firmicutes and the F/B ratio in dehydrated juvenile mice were similar to those in normal infant mice. Additionally, clustering analysis revealed no significant differences in the intestinal flora in the mice from the different drinking water sources; however, dehydration significantly altered the composition of the genera compared to the other water source groups wherein water was provided ad libitum . Moreover, cognitive development was significantly disrupted by insufficient water intake, although the type of drinking water had no significant influence. Cognitive decline, measured by relative latency, was positively associated with the relative abundance of unclassified Erysipelotrichaceae that were in significantly high relative abundance in the dehydration group. These results suggest that the water quantity consumed, rather than the mineral content of drinking water, is imperative for shaping the early gut microbiota associated with cognitive development during infancy.

PurposeWe aimed to investigate the link of vitamin C status with vitality and psychological functions in a cross-sectional study, and examine their causal relationship through a randomized controlled trial (RCT).MethodsWe first conducted a population-based cross-sectional investigation of healthy young adults (n = 214, 20–39 years), and analyzed the associations of serum vitamin C concentrations with vitality (fatigue and attention) and mood status (stress, depression, and positive and negative affect) using Pearson’s correlation and multiple linear regression analyses. Next, we performed a double-blind RCT in healthy subjects whose serum vitamin C concentrations were inadequate (< 50 μmol/L). Subjects were randomly allocated to receive 500 mg of vitamin C twice a day for 4 weeks (n = 24) or a placebo (n = 22). We assessed vitality, which included fatigue, attention, work engagement, and self-control resources, and measured mood status, including stress, depression, positive and negative affect, and anxiety. ELISA determined serum brain-derived neurotrophic factor (BDNF), and a Stroop color–word test evaluated attention capacity and processing speed.ResultsIn the cross-sectional data, the serum vitamin C concentration was positively associated with the level of attention (r = 0.16, p = 0.02; standardized β = 0.21, p = 0.003), while no significant associations with the levels of fatigue and mood variables being found. In the RCT, compared to the placebo, the vitamin C supplementation significantly increased attention (p = 0.03) and work absorption (p = 0.03) with distinct tendency of improvement on fatigue (p = 0.06) and comprehensive work engagement (p = 0.07). The vitamin C supplementation did not affect mood and serum concentrations of BDNF. However, in the Stroop color–word test, the subjects supplemented with vitamin C showed better performance than those in the placebo group (p = 0.04).ConclusionInadequate vitamin C status is related to a low level of mental vitality. Vitamin C supplementation effectively increased work motivation and attentional focus and contributed to better performance on cognitive tasks requiring sustained attention.Trial registration number and date of registrationCross-sectional study: KCT0005074 (cris.nih.go.kr)/1 June, 2020 (retrospectively registered). Intervention study: KCT0004276 (cris.nih.go.kr)/4 September, 2019.

Background Long-term intake of a Western diet (WD), characterized by a high-fat content and sugary drinks, is hypothesized to contribute to the development of inflammatory bowel disease (IBD). Despite the identified clinical association, the molecular mechanisms by which dietary changes contribute to IBD development remain unknown. Therefore, we examined the influence of long-term intake of a WD on intestinal inflammation and the mechanisms by which WD intake affects IBD development. Methods Mice fed normal diet or WD for 10 weeks, and bowel inflammation was evaluated through pathohistological and infiltrated inflammatory cell assessments. To understand the role of intestinal taste receptor type 1 member 3 (TAS1R3) in WD-induced intestinal inflammation, cultured enteroendocrine cells harboring TAS1R3, subjected to RNA interference or antagonist treatment, and Tas1r3 -deficient mice were used. RNA-sequencing, flow cytometry, 16S metagenomic sequencing, and bioinformatics analyses were performed to examine the involved mechanisms. To demonstrate their clinical relevance, intestinal biopsies from patients with IBD and mice with dextran sulfate sodium-induced colitis were analyzed. Results Our study revealed for the first time that intestinal TAS1R3 is a critical mediator of WD-induced intestinal inflammation. WD-fed mice showed marked TAS1R3 overexpression with hallmarks of serious bowel inflammation. Conversely, mice lacking TAS1R3 failed to exhibit inflammatory responses to WD. Mechanistically, intestinal transcriptome analysis revealed that Tas1r3 deficiency suppressed mTOR signaling, significantly increasing the expression of PPARγ (a major mucosal defense enhancer) and upregulating the expression of PPARγ target-gene (tight junction protein and antimicrobial peptide). The gut microbiota of Tas1r3 -deficient mice showed expansion of butyrate-producing Clostridia. Moreover, an increased expression of host PPARγ-signaling pathway proteins was positively correlated with butyrate-producing microbes, suggesting that intestinal TAS1R3 regulates the relationship between host metabolism and gut microflora in response to dietary factors. In cultured intestinal cells, regulation of the TAS1R3–mTOR–PPARγ axis was critical for triggering an inflammatory response via proinflammatory cytokine production and secretion. Abnormal regulation of the axis was observed in patients with IBD. Conclusions Our findings suggest that the TAS1R3–mTOR–PPARγ axis in the gut links Western diet consumption with intestinal inflammation and is a potential therapeutic target for IBD.

The Westernized diet has been associated with the pathogenesis of metabolic diseases, whereas a Korean diet has been reported to exert beneficial effects on health in several studies. However, the effects of Western and Korean diets on the gut microbiome and host metabolome are unclear. To examine the diet-specific effects on microbiome and metabolome, we conducted a randomized crossover clinical trial of typical Korean diet (TKD), typical American diet (TAD), and recommended American diet (RAD). The trial involved a 4-week consumption of an experimental diet followed by a 2-week interval before diet crossover. 16S rRNA sequencing analysis identified 16, 10, and 14 differential bacteria genera specific to TKD, RAD, and TAD, respectively. The Firmucutes-Bacteroidetes ratio was increased by TKD. Nuclear magnetic resonance metabolome profiling revealed that TKD enriched branched chain amino acid metabolism, whereas ketone body metabolism was evident in RAD and TAD. Microbiome and metabolome responses to the experimental diets varied with individual enterotypes. These findings provide evidence that the gut microbiome and host metabolome rapidly respond to different cultural diets. The findings will inform clarification of the diet-related communication networks of the gut microbiome and host metabolome in humans.

Hydration status plays a critical role in modulating oxidative stress during exercise, which can influence physical performance and recovery. While the acute effects of hydration on exercise-induced oxidative stress are well-documented, the long-term impact of chronic water intake remains poorly understood. Therefore, this study aimed to investigate the relationship between chronic low water intake and exercise-induced oxidative stress, as well as changes in the phenotypic composition of peripheral immune cells. We assessed the usual plain water intake of the participants (  = 26; 19-29 years) using a questionnaire and classified them as habitually high-water drinkers (HIGH;  = 16; mean plain water intake = 1.22 ± 0.19 L/d) or low-water drinkers (LOW;  = 10; 0.41 ± 0.10 L/d). We conducted a maximal graded exercise test and investigated whether the extent of exercise-induced oxidative stress and immunological changes differed depending on the habitual water intake. Free radical production before and after the exercise test was assessed using serum concentrations of reactive oxygen metabolites (ROMs). The antioxidant capacity to eliminate free radicals was assessed using the serum biological antioxidant potential (BAP). We profiled peripheral blood mononuclear cells (PBMCs; CD4 , CD8 , CD20 , CD14 , CD11b , and Annexin V ) using fluorescence-activated cell sorting. At baseline, the LOW group showed higher concentrations of serum ROMs than the HIGH group (  = 0.033). In a maximal graded exercise test, both groups showed comparable performance parameters including peak heart rate, VO max, and exercise duration. However, the biochemical responses differed markedly: serum BAP significantly increased in the HIGH group but remained unchanged in the LOW group ( = 0.030). Furthermore, the LOW group showed a larger increase in PBMC apoptosis than the HIGH group, both in absolute cell number and percentage (  = 0.031 and = 0.034, respectively). The LOW group also showed differential PBMC subset frequencies, with greater CD11b cell recruitment (  = 0.015) and less pronounced CD14 cell reduction compared to the HIGH group (  = 0.050). Habitual low water intake was associated with elevated concentrations of free radical by-products in the resting state and impaired antioxidant capacity during acute exercise stress. In response to exercise stress, impaired redox balance in low-water drinkers resulted in accelerated cellular damage and increased myeloid cell recruitment. These findings highlight the importance of maintaining adequate habitual water intake to cope with exercise-induced oxidative stress and prevent excessive cellular stress responses. Registered at the Clinical Research Information Service (CRIS) on 12 April 2019 (Registry No. KCT0003763).

Gut microbiota is suggested to regulate the host’s mental health via the gut-brain axis. In this study, we investigated the relationship between the microbiome and psychological pain due to social exclusion. Adult individuals with ( n  = 14) and without ( n  = 25) social exclusion experience were assessed for the psychological status using self-reported questionnaires: Beck Anxiety Inventory (BAI), Beck Depression Inventory, and the UCLA Loneliness Scale. The gut microbiota was analyzed by 16 S rRNA gene sequencing and bioinformatics. The exclusion group had a 1.70-fold higher total BAI score and 2.16-fold higher levels of anxiety-related physical symptoms ( p  < 0.05). The gut microbial profiles also differed between the two groups. The exclusion group showed higher probability of having Prevotella -enriched microbiome (odds ratio, 2.29; 95% confidence interval, 1.65–2.75; p  < 0.05), a significantly reduced Firmicutes/Bacteroidetes ratio, and decreased abundance of Faecalibacterium spp. ( p  < 0.05) which was associated with the duration and intensity of social exclusion ( p  < 0.05). Our results indicate that the psychological pain due to social exclusion is correlated with the gut microbiota composition, suggesting that targeting social exclusion-related microorganisms can be a new approach to solving psychological problems and related social issues.

This study sought to characterize the impact of long-term dehydration in terms of physiological and biochemical parameters, as well as renal transcriptomes. Furthermore, we assessed whether consumption of specific types of water elicit more beneficial effects on these health parameters. To this end, C57BL/6 mice were either provided water for 15 min/day over 2 and 4 weeks (water restricted; RES), or ad libitum access to distilled (CON), tap, spring, or purified water. Results show that water restriction decreases urine output and hematocrit levels while increasing brain vasopressin mRNA levels in RES mice compared to control mice (CON). Meanwhile, blood urea nitrogen and creatinine levels were higher in the RES group compared to the CON group. Kidney transcriptome analysis further identified kidney damage as the most significant biological process modulated by dehydration. Mechanistically, prolonged dehydration induces kidney damage by suppressing the NRF2-signaling pathway, which targets the cytoprotective defense system. However, type of drinking water does not appear to impact physiological or blood biochemical parameters, nor the renal transcriptome profile, suggesting that sufficient water consumption is critical, irrespective of the water type. Importantly, these findings also inform practical action for environmental sustainability by providing a theoretical basis for reducing bottled water consumption.

Background Accumulating evidence supports that the Western diet (WD), a diet high in saturated fat and sugary drinks, contributes to the pathogenesis of anxiety disorders, which are the most prevalent mental disorders worldwide. However, the underlying mechanisms by which WD causes anxiety remain unclear. Abundant expression of taste receptor type 1 member 3 (TAS1R3) has been identified in the hypothalamus, a key brain area involved in sensing peripheral nutritional signals and regulating anxiety. Thus, we investigated the influence of excessive WD intake on anxiety and mechanisms by which WD intake affects anxiety development using wild-type (WT) and Tas1r3 deficient ( Tas1r3 −/− ) mice fed a normal diet (ND) or WD for 12 weeks. Results WD increased anxiety in male WT mice, whereas male Tas1r3 −/− mice were protected from WD-induced anxiety, as assessed by open field (OF), elevated plus maze (EPM), light–dark box (LDB), and novelty-suppressed feeding (NSF) tests. Analyzing the hypothalamic transcriptome of WD-fed WT and Tas1r3 −/− mice, we found 1,432 genes significantly up- or down-regulated as a result of Tas1r3 deficiency. Furthermore, bioinformatic analysis revealed that the CREB/BDNF signaling-mediated maintenance of neuronal regeneration, which can prevent anxiety development, was enhanced in WD-fed Tas1r3 −/− mice compared with WD-fed WT mice. Additionally, in vitro studies further confirmed that Tas1r3 knockdown prevents the suppression of Creb1 and of CREB-mediated BDNF expression caused by high levels of glucose, fructose, and palmitic acid in hypothalamic neuronal cells. Conclusions Our results imply that TAS1R3 may play a key role in WD-induced alterations in hypothalamic functions, and that inhibition of TAS1R3 overactivation in the hypothalamus could offer therapeutic targets to alleviate the effects of WD on anxiety.

Purpose Growing evidence shows that nutrient metabolism affects inflammatory bowel diseases (IBD) development. Previously, we showed that deficiency of indoleamine 2,3-dioxygenase 1 (Ido1), a tryptophan-catabolizing enzyme, reduced the severity of dextran sulfate sodium (DSS)-induced colitis in mice. However, the roles played by intestinal microbiota in generating the differences in disease progression between Ido1 + / + and Ido1 −/− mice are unknown. Therefore, we aimed to investigate the interactions between the intestinal microbiome and host IDO1 in governing intestinal inflammatory responses. Methods Microbial 16s rRNA sequencing was conducted in Ido1 + / + and Ido1 −/− mice after DSS treatment. Bacteria-derived tryptophan metabolites were measured in urine. Transcriptome analysis revealed the effects of the metabolite and IDO1 expression in HCT116 cells. Colitis severity of Ido1 + / + was compared to Ido1 −/− mice following fecal microbiota transplantation (FMT). Results Microbiome analysis through 16S-rRNA gene sequencing showed that IDO1 deficiency increased intestinal bacteria that use tryptophan preferentially to produce indolic compounds. Urinary excretion of 3-indoxyl sulfate, a metabolized form of gut bacteria-derived indole, was significantly higher in Ido1 −/− than in Ido1 + / + mice. Transcriptome analysis showed that tight junction transcripts were significantly increased by indole treatment in HCT116 cells; however, the effects were diminished by IDO1 overexpression. Using FMT experiments, we demonstrated that bacteria from Ido1 −/− mice could directly attenuate the severity of DSS-induced colitis. Conclusions Our results provide evidence that a genetic defect in utilizing tryptophan affects intestinal microbiota profiles, altering microbial metabolites, and colitis development. This suggests that the host and intestinal microbiota communicate through shared nutrient metabolic networks.