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My Diet Study: protocol for a two-part observational, longitudinal, psycho-biological study of dieting in Australian youth.
INTRODUCTION: Self-directed dieting (i.e., unsupervised) is very common among adolescents and young adults but has had almost no direct research. This paper describes the protocol for the My Diet Study, a two-arm observational investigation of the natural progression of dieting among young people over a period of 6-months. The study aims to examine the links between self-directed dieting, general physiological and psychological metrics of wellbeing (e.g., depressive symptoms) and biomarkers of gut-brain axis functions (e.g., microbiome and hormones) that are predicted to influence diet adherence through appetite, mood and metabolism regulation. METHODS: Young people aged 16-25, intending to start a diet will be invited to participate in this observational study. For Part 1 (psychological arm), participants will be asked to complete a set of questionnaires and diaries at the beginning of every month for 6 months, to assess overall mental (e.g., psychological distress, disordered eating) and physical (e.g., weight) health, perceived diet success, food intake and gastrointestinal movements. For Part 2 (biological arm), a subsample of 50 participants will be asked to provide feces, blood and saliva for bio-sampling each month for the first 3-months of their participation in Part 1. DISCUSSION: The My Diet Study will be the first longitudinal, observational study of dieting in young people combining in-depth psychological and biological data. It is anticipated that the findings will yield psychological & biological information about the impacts and effectiveness of self-directed dieting in young people, inform a framework for advice on safety in dieting among young people and help to establish the potential for biomarkers for risk management and improvement of diet-based lifestyle interventions.
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Platelets bridging the gap between gut dysbiosis and neuroinflammation in stress-linked disorders: A narrative review.
In this narrative review, we examine the association between gut dysbiosis, neuroinflammation, and stress-linked disorders, including depression, anxiety, and post-traumatic stress disorder (PTSD), and investigate whether tryptophan (TRP) metabolism and platelets play a role in this association. The mechanisms underlying the aetiology of stress-linked disorders are complex and not yet completely understood. However, a potential link between chronic inflammation and these disorders may potentially be found in TRP metabolism and platelets. By critically analysing existing literature on platelets, the gut microbiome, and stress-linked disorders, we hope to elicit the role of platelets in mediating the effects on serotonin (5-HT) levels and neuroinflammation. We have included studies specifically investigating platelets and TRP metabolism in relation to inflammation, neuroinflammation and neuropsychiatric disorders. Alteration in microbial composition due to stress could contribute to increased intestinal permeability, facilitating the translocation of microbial products, and triggering the release of pro-inflammatory cytokines. This causes platelets to become hyperactive and secrete 5-HT into the plasma. Increased levels of pro-inflammatory cytokines may also lead to increased permeability of the blood-brain barrier (BBB), allowing inflammatory mediators entry into the brain, affecting the balance of TRP metabolism products, such as 5-HT, kynurenic acid (KYNA), and quinolinic acid (QUIN). These alterations may contribute to neuroinflammation and possible neurological damage. Furthermore, platelets can cross the compromised BBB and interact with astrocytes and neurons, leading to the secretion of 5-HT and pro-inflammatory factors, exacerbating inflammatory conditions in the brain. The mechanisms underlying neuroinflammation resulting from peripheral inflammation are still unclear, but the connection between the brain and gut through the bloodstream could be significant. Identifying peripheral biomarkers and mechanisms in the plasma that reflect neuroinflammation may be important. This review serves as a foundation for further research on the association between the gut microbiome, blood microbiome, and neuropsychiatric disorders. The integration of these findings with protein and metabolite markers in the blood may expand our understanding of the subject.
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Biopsychosocial Influences on the Gut Microbiome in Women's Health: Moving Towards Eubiosis.
Research on the human microbiome, particularly the gut microbiome, has expanded rapidly as its influence on health and behavior becomes increasingly evident. Once understood primarily in terms of digestion and immune function, the microbiome is now recognized as a key contributor to brain function, mood regulation, and social behavior. Emerging evidence links microbial dysbiosis to the onset and persistence of mood disorders, opening new pathways for mental health research and intervention. This paper challenges reductionist biomedical models by advancing a biopsychosocial framework for interpreting health outcomes related to microbiome dynamics. The gut-brain axis illustrates the biological complexity of these interactions, with microbial communities shaping neurodevelopment and neurotransmitter production. Psychologically, alterations in microbial composition have been associated with depression, anxiety, and stress responsivity, while social determinants-including early-life environments, socioeconomic conditions, and relationships-structure microbial variation in ways that may reinforce existing health inequities. Focusing on women's health, this narrative review examines how microbial states both influence and are shaped by interconnected biological, psychological, and social factors. Interdisciplinary implications of microbiome research for understanding and achieving eubiosis and holistic models care in both research and clinical practice are discussed.
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Modulatory Effects of Gut Microbiota on the Central Nervous System: How Gut Could Play a Role in Neuropsychiatric Health and Diseases.
Gut microbiome is an integral part of the Gut-Brain axis. It is becoming increasingly recognized that the presence of a healthy and diverse gut microbiota is important to normal cognitive and emotional processing. It was known that altered emotional state and chronic stress can change the composition of gut microbiome, but it is becoming more evident that interaction between gut microbiome and central nervous system is bidirectional. Alteration in the composition of the gut microbiome can potentially lead to increased intestinal permeability and impair the function of the intestinal barrier. Subsequently, neuro-active compounds and metabolites can gain access to the areas within the central nervous system that regulate cognition and emotional responses. Deregulated inflammatory response, promoted by harmful microbiota, can activate the vagal system and impact neuropsychological functions. Some bacteria can produce peptides or short chain fatty acids that can affect gene expression and inflammation within the central nervous system. In this review, we summarize the evidence supporting the role of gut microbiota in modulating neuropsychological functions of the central nervous system and exploring the potential underlying mechanisms.
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Regulation of the stress response by the gut microbiota: implications for psychoneuroendocrinology.
There is now an expanding volume of evidence to support the view that commensal organisms within the gut play a role in early programming and later responsivity of the stress system. The gut is inhabited by 10¹³-10¹⁴ micro-organisms, which is ten times the number of cells in the human body and contains 150 times as many genes as our genome. It has long been recognised that gut pathogens such as Escherichia coli, if they enter the gut can activate the HPA. However, animals raised in a germ-free environment show exaggerated HPA responses to psychological stress, which normalises with monocolonisation by certain bacterial species including Bifidobacterium infantis. Moreover, increased evidence suggests that animals treated with probiotics have a blunted HPA response. Stress induces increased permeability of the gut allowing bacteria and bacterial antigens to cross the epithelial barrier and activate a mucosal immune response, which in turn alters the composition of the microbiome and leads to enhanced HPA drive. Increasing data from patients with irritable bowel syndrome and major depression indicate that in these syndromes alteration of the HPA may be induced by increased gut permeability. In the case of irritable bowel syndrome the increased permeability can respond to probiotic therapy. Detailed prospective studies in patients with mood disorders examining the gut microbiota, immune parameters and HPA activity are required to throw further light on this emerging area. It is however clear that the gut microbiota must be taken into account when considering the factors regulating the HPA.
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Polycystic Ovary Syndrome Pathophysiology: Integrating Systemic, CNS and Circadian Processes.
The conceptualization of polycystic ovary syndrome (PCOS) has primarily focused on hormonal alterations driven by changes within the hypothalamus and ovarian granulosa cells, with treatment by the contraceptive pill and weight loss. However, a growing body of data implicates wider systemic and central nervous system (CNS) changes in the pathoetiology and pathophysiology of PCOS, with consequent implications for targeted treatments. It is proposed that there is a significant role for night-time interactions of factors acting to regulate whether the rising level of cortisol over the night and during the morning cortisol awakening response (CAR) is able to induce the nuclear translocation of the glucocorticoid receptor (GR), thereby influencing how the immune and glial systems regulate cellular function in preparation for the coming day. Factors affording protection in PCOS also inhibit GR nuclear translocation including gut microbiome-derived butyrate, and pineal/local melatonin as well as melatonin regulated bcl2-associated athanogene (BAG)-1. A significant pathophysiological role in PCOS is attributed to the aryl hydrocarbon receptor (AhR), which shows heightened levels and activity in PCOS. The AhR is activated by ligands of many systemic processes, including white adipocyte-derived kynurenine, implicating obesity in the pathophysiological changes occurring in the hypothalamus and ovaries. AhR activation has consequences for the physiological function in the hypothalamic paraventricular nucleus, granulosa cells and adipocytes, partly mediated by AhR upregulation of the mitochondrial N-acetylserotonin/melatonin ratio, thereby decreasing melatonin availability whilst increasing local stress plasticity in the paraventricular nucleus. This article reviews in detail the wider systemic and CNS changes in PCOS highlighting interactions of local and pineal melatonergic pathway, gut microbiome-derived butyrate, white adipocyte-derived kynurenine, the hypothalamic paraventricular nucleus tanycytes/astrocytes, and the hypothalamus-pituitary-adrenal (HPA) axis driven glucocorticoid receptor activation in PCOS pathophysiology. This integrates a wide array of previously disparate data on the biological underpinnings of PCOS, including how PCOS associates with many other currently classified medical conditions, such as depression, bipolar disorder, type 1 diabetes mellitus and the autism spectrum. Numerous future research and treatment implications are detailed.
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Economic Impact of a Precision Nutrition Digital Therapeutic on Employer Health Costs: A Multi-Employer and Multi-Year Claims Analysis.
Background: Obesity, gastrointestinal disorders, and mental health conditions are major drivers of employer healthcare expenditures, yet nutrition-focused interventions are infrequently reimbursed by health insurance. Precision nutrition, which integrates genetic, gut microbiome, biometric, and behavioral data to guide personalized dietary and lifestyle changes, may offer a scalable approach to reducing costs associated with diet-responsive conditions. Objectives: To evaluate the impact of a precision nutrition digital therapeutic on employer medical spending for diet-responsive conditions in self-insured U.S. health plans. Methods: We conducted a retrospective cohort study of medical claims from January 2022 to December 2024 across seven U.S. self-insured employers. Employees enrolled in a precision nutrition digital therapeutic (n = 258) were compared with never-enrolled peers (n = 8268). We estimated treatment effects using a two-stage difference-in-differences model with member and calendar-month fixed effects and clustered standard errors, focusing on per-member-per-year (PMPY) employer-paid medical spending overall and for predefined diet-responsive condition categories. PMPY estimates were defined conditional on months with positive employer-paid spending and therefore reflect changes in the intensity of spending among members generating claims rather than unconditional per-capita costs. Results: Enrollment in the precision nutrition digital therapeutic was associated with a -$3012 PMPY reduction in diet-responsive medical spending (p = 0.021) relative to non-enrolled peers on this conditional basis. The largest relative reductions were observed for digestive disorders (-$9240 PMPY; p = 0.029) and obesity (-$4884 PMPY; p = 0.007), with a smaller reduction for anxiety-related conditions (-$1356 PMPY; p = 0.043). Total medical spending decreased by -$4044 PMPY but this change did not reach statistical significance (p = 0.09). Conclusions: In this multi-employer claims analysis, participation in a precision nutrition digital therapeutic was associated with lower employer-paid medical expenditures for diet-responsive conditions, particularly digestive disorders and obesity. These findings suggest that precision nutrition digital therapeutics may represent a scalable strategy for employers to address the economic burden of chronic disease within self-insured health plans by reducing the intensity of medical spending among members.
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Jia Wei Xiao Yao San ameliorates chronic stress-induced depression-like behaviors in mice by regulating the gut microbiome and brain metabolome in relation to purine metabolism.
BACKGROUND: The pathogenesis of depression remains largely unknown. Accumulating evidence demonstrates the existence of a complex relationship between gut microbiome composition and brain functions. Jia Wei Xiao Yao San (JWXYS) is considered a potential antidepressant. However, the pharmacological mechanisms of JWXYS have not yet been clarified. PURPOSE: This study aimed to explore the effects of JWXYS on chronic stress-induced depression-like behaviors in mice. METHODS: A chronic restraint stress mouse model of depression was established. JWXYS was administered, and the responses of these mice to treatment were evaluated through several behavioral tests. The activity of astrocytes and microglia was detected by specific fluorescent labels. Inflammatory cytokines were quantified in intestinal and cerebral tissues. An integrated approach with full-length 16S rRNA sequencing and different types of untargeted metabolomics was conducted to investigate the relationship between the gut microbiome at the species level, metabolic brain functions, and JWXYS. RESULTS: We found that behavioral symptoms were associated with the relative abundance of Lactobacillus animalis. After JWXYS treatment, the relative abundance of Ileibacterium valens with enzymes potentially involved in purine metabolism was also described. The activation of astrocytes and microglia was negatively correlated with the relative abundance of L. animalis. Combined with network pharmacological analysis, several targets predicted based on JWXYS treatment focused on purine metabolism, which was also enriched from cerebral metabolites regulated by JWXYS. CONCLUSION: Our study suggests that L. animalis is involved in depression-like behaviors in mice. JWXYS increases the abundance of I. valens with potential enzymes in relation to cerebral purine metabolism, which is positively correlated with the activation of astrocytes in the amygdala.
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No Guts About It: Captivity, But Not Neophobia Phenotype, Influences the Cloacal Microbiome of House Sparrows (Passer domesticus).
Behavioral traits such as anxiety and depression have been linked to diversity of the gut microbiome in humans, domesticated animals, and lab-bred model species, but the extent to which this link exists in wild animals, and thus its ecological relevance, is poorly understood. We examined the relationship between a behavioral trait (neophobia) and the cloacal microbiome in wild house sparrows (Passer domesticus, n = 22) to determine whether gut microbial diversity is related to personality in a wild animal. We swabbed the cloaca immediately upon capture, assessed neophobia phenotypes in the lab, and then swabbed the cloaca again after several weeks in captivity to additionally test whether the microbiome of different personality types is affected disparately by captivity, and characterized gut microbiomes using 16S rRNA gene amplicon sequencing. We did not detect differences in cloacal alpha or beta microbial diversity between neophobic and non-neophobic house sparrows, and diversity for both phenotypes was negatively impacted by captivity. Although our results suggest that the adult cloacal microbiome and neophobia are not strongly linked in wild sparrows, we did detect specific OTUs that appeared more frequently and at higher abundances in neophobic sparrows, suggesting that links between the gut microbiome and behavior may occur at the level of specific taxa. Further investigations of personality and the gut microbiome are needed in more wild species to reveal how the microbiome-gut-brain axis and behavior interact in an ecological context.
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Increased Oxidative Stress in the Prefrontal Cortex as a Shared Feature of Depressive- and PTSD-Like Syndromes: Effects of a Standardized Herbal Antioxidant.
Major depression (MD) and posttraumatic stress disorder (PTSD) share common brain mechanisms and treatment strategies. Nowadays, the dramatically developing COVID-19 situation unavoidably results in stress, psychological trauma, and high incidence of MD and PTSD. Hence, the importance of the development of new treatments for these disorders cannot be overstated. Herbal medicine appears to be an effective and safe treatment with fewer side effects than classic pharmaca and that is affordable in low-income countries. Currently, oxidative stress and neuroinflammation attract increasing attention as important mechanisms of MD and PTSD. We investigated the effects of a standardized herbal cocktail (SHC), an extract of clove, bell pepper, basil, pomegranate, nettle, and other plants, that was designed as an antioxidant treatment in mouse models of MD and PTSD. In the MD model of "emotional" ultrasound stress (US), mice were subjected to ultrasound frequencies of 16-20 kHz, mimicking rodent sounds of anxiety/despair and "neutral" frequencies of 25-45 kHz, for three weeks and concomitantly treated with SHC. US-exposed mice showed elevated concentrations of oxidative stress markers malondialdehyde and protein carbonyl, increased gene and protein expression of pro-inflammatory cytokines interleukin (IL)-1β and IL-6 and other molecular changes in the prefrontal cortex as well as weight loss, helplessness, anxiety-like behavior, and neophobia that were ameliorated by the SHC treatment. In the PTSD model of the modified forced swim test (modFST), in which a 2-day swim is followed by an additional swim on day 5, mice were pretreated with SHC for 16 days. Increases in the floating behavior and oxidative stress markers malondialdehyde and protein carbonyl in the prefrontal cortex of modFST-mice were prevented by the administration of SHC. Chromatography mass spectrometry revealed bioactive constituents of SHC, including D-ribofuranose, beta-D-lactose, malic, glyceric, and citric acids that can modulate oxidative stress, immunity, and gut and microbiome functions and, thus, are likely to be active antistress elements underlying the beneficial effects of SHC. Significant correlations of malondialdehyde concentration in the prefrontal cortex with altered measures of behavioral despair and anxiety-like behavior suggest that the accumulation of oxidative stress markers are a common biological feature of MD and PTSD that can be equally effectively targeted therapeutically with antioxidant therapy, such as the SHC investigated here.