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Exploring the mechanisms of action of the antidepressant effect of the ketogenic diet.
The ketogenic diet (KD) is characterized by a diet ratio of 4:1 fat to non-fat energy sources. For decades KD has been successfully used to control seizures in epilepsy patients. Investigations into its mechanism of action suggest that it may have an effect on the metabolic, nervous, immune, and digestive systems. In this review, we postulate that KD may also improve depressive symptoms - for that, we highlight the similarities between depression and epilepsy, describe the extent to which body systems involved in both conditions are affected by the KD, and ultimately hypothesize how KD could improve MDD outcomes. Research into animal models and human patients have reported that KD can increase mitochondrial biogenesis and increase cellular resistance to oxidative stress both at the mitochondrial and genetic levels. Its effect on neurotransmitters alters cell-to-cell communication in the brain and may decrease hyperexcitability by increasing Gamma Aminobutyric Acid (GABA) and decreasing excitatory neurotransmitter levels. Its anti-inflammatory effects are mediated by decreasing chemo- and cytokine levels, including TNF-alpha and IL-1 levels. Finally, KD can alter gut microbiota (GM). Certain strains of microbiota predominate in major depressive disorder (MDD) when compared to healthy individuals. Recent evidence points to Bacteroidetes as a potential treatment predictor as it seems to increase in KD treatment responders for epilepsy. Each of these observations contributes to the presumed modulatory effects of KD on mood and supports its potential role as antidepressant.
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Gut microbiota and inflammatory factor characteristics in major depressive disorder patients with anorexia.
BACKGROUND: This study aimed to explore the gut microbiota and inflammatory factor characteristics in major depressive disorder (MDD) patients with anorexia and to analyze the correlation between gut microbiota and inflammatory factors, anorexia, and HAMD scores. METHODS: 46 MDD patients and 46 healthy controls (HC) were included in the study. The 46 MDD patients were divided into two groups according to whether they had anorexia:20 MDD without anorexia (MDA0 group) and 26 MDD with anorexia (MDA1 group). We used the Hamilton Depression Scale-24 (HAMD-24) to evaluate the depression status of all participants and 16 S ribosomal RNA (16 S rRNA)sequencing to evaluate the composition of the gut microbiota. Inflammatory factors in peripheral blood such as C-reactive protein (CRP) were detected using enzyme-linked immunosorbent assay (ELISA). Spearman's correlation analysis was used to evaluate the correlation between gut microbiota and inflammatory factors, HAMD scores, and anorexia. RESULTS: 1). CRP was significantly higher in the MDA0, MDA1, than HC. 2). An analysis of α-diversity shows: the Simpson and Pielou indices of the HC group are higher than the MDA1 group (P < 0.05). 3). The β-diversity analysis shows differences in the composition of microbial communities between the MDA0, MDA1, and HC group. 4). A correlation analysis showed that Blautia positively correlated with anorexia, HAMD scores, and CRP level, whereas Faecalibacterium, Bacteroides, Roseburia, and Parabacteroides negatively correlated with anorexia, HAMD scores, and CRP level. 5). The receiver operating characteristic (ROC) curve was drawn using the differential bacterial genera between MDD patients with or without anorexia as biomarkers to identify whether MDD patients were accompanied with anorexia, and its area under curve (AUC) was 0.85. The ROC curve was drawn using the differential bacterial genera between MDD patients with anorexia and healthy controls as biomarkers to diagnose MDD patients with anorexia, with its AUC was 0.97. CONCLUSION: This study suggested that MDD patients with anorexia had a distinct gut microbiota compared to healthy individuals, with higher level of CRP. Blautia was more abundant in MDD patients with anorexia and positively correlated with CRP, HAMD scores, and anorexia. The gut microbiota might have influenced MDD and anorexia through the inflammatory factor CRP.
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Probiotics as an Adjuvant Therapy in Major Depressive Disorder.
BACKGROUND: Major depressive disorder is a common, debilitating psychiatric disorder, which originates from the interaction of susceptibility genes and noxious environmental events, in particular stressful events. It has been shown that dysregulation of hypothalamus-pituitary-adrenal (HPA) axis, imbalance between anti- and pro-inflammatory cytokines, depletion of neurotransmitters (serotonin, norepinephrine and/or dopamine) in the central nervous system, altered glutamatergic and GABAergic transmission have an important role in the pathogenesis of depression. Due to numerous diverse biological events included in the pathophysiology of depression a large number of antidepressant drugs exerting distinct pharmacological effects have been developed. Nevertheless, clinical needs are still not solved. RESULTS: Relatively new research strategies advanced the understanding of psychiatric illness and their connections with disturbances in gastrointestinal tract. The existence of bidirectional communication between the brain and the gut has been proven, and an increasing body of evidence supports the hypothesis that cognitive and emotional processes are influenced through the brain-gut axis. On the other hand, microbiome may influence brain function and even behavior giving to the specific microorganisms a psychobiotic potential. CONCLUSIONS: In this review we discuss the possibilities of classical antidepressant drug treatment being supported with the psychobiotics/probiotic bacteria in patients suffering from major depressive disorder.
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The Tryptophan-Kynurenine Pathway as a Key Mediator of the Gut-Brain Axis in Depression and Alzheimer's Disease.
Depression and Alzheimer's disease are among the most prevalent and disabling disorders worldwide, imposing a substantial social, economic, and healthcare burden. Increasing evidence suggests that these conditions share several pathophysiological mechanisms, including chronic inflammation, oxidative stress, mitochondrial dysfunction, altered neurotransmission, and gut microbiota dysbiosis. In recent years, the microbiota-gut-brain axis has emerged as a key regulatory system linking gastrointestinal, immune, metabolic, and neural functions. Within this complex network, the tryptophan-kynurenine pathway has gained considerable attention as a critical mediator connecting gut microbial activity, immune responses, and central nervous system function. This review examines the role of the microbiota-gut-brain axis and the tryptophan-kynurenine pathway in the development and progression of depression and Alzheimer's disease. Particular emphasis is placed on the regulation of tryptophan metabolism by gut microbiota, the inflammatory activation of indoleamine 2,3-dioxygenase, and the generation of neuroactive kynurenine metabolites. Dysregulation of these processes may reduce serotonin synthesis while promoting the accumulation of neurotoxic compounds such as quinolinic acid and 3-hydroxykynurenine, thereby contributing to neuroinflammation, excitotoxicity, cognitive decline, and depressive symptoms. Current evidence also highlights the therapeutic potential of interventions targeting gut microbiota composition and kynurenine pathway activity. A better understanding of these interconnected mechanisms may facilitate the identification of novel biomarkers and the development of personalized strategies for the prevention and treatment of both psychiatric and neurodegenerative disorders.
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The use of diet for preventing and treating depression in young men: current evidence and existing challenges.
Emerging evidence suggests that diet therapy (nutrients, foods and dietary patterns) could be effective as a potential adjunctive treatment option for major depressive disorder. Numerous mechanisms have been proposed, including the role inflammation, oxidative stress, brain-derived neurotrophic factor, the gastrointestinal tract microbiome and tryptophan/serotonin metabolism. Despite known differences in depression characteristics and treatment responses between males and females, there are limited sex-specific studies examining the role of diet in young men specifically. This is important as young men are often reluctant to seek mental health support, so finding treatment strategies which appeal to this demographic is crucial. This brief report provides an overview of the most recent advances in the use of diet for preventing and treating depression in young men, highlighting existing challenges and opportunities for future research. We recommend that clinicians discuss the role of diet with depressed young men, so that diet may be used alongside current treatment options.
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Fecal Microbiota Changes in Patients With Postpartum Depressive Disorder.
Postpartum depressive disorder (PPD) is a unique subtype of major depressive disorder and a substantial contributor to maternal morbidity and mortality. However, the pathogenesis of PPD has still remained elusive, and it may associate with genetic and environmental factors. Gut microbiota has already been proved to be associated with depression; however, a limited number of studies have concentrated on PPD. The present study aimed to explore the potential correlations between gut microbiota and PPD. In this study, 57 participants were enrolled, in which fecal samples of 28 patients with PPD and 16 healthy controls (HCs) were collected and then analyzed by high-throughput sequencing of the 16S ribosomal RNA (rRNA) gene. The results showed that diversity and composition of gut microbial communities were partly different between PPD patients and HCs. The relative abundance of Firmicutes phyla was lower in PPD patients. The levels of several predominant genera were significantly different between PPD patients and HCs. More importantly, the PPD patients experienced reduced levels of Faecalibacterium, Phascolarctobacterium, Butyricicoccus, and Lachnospiraceae, as well as increased levels of Enterobacteriaceae family. In addition, a correlation was observed between levels of Phascolarctobacterium, Lachnospiraceae, Faecalibacterium, and Tyzzerella.3 and the severity of depressive symptoms. Various kinds of bacteria, such as Lachnospiraceae and Faecalibacterium, were found to be associated with levels of sex hormones. This study indicated the correlation between gut microbiota and PPD, and gut microbiota-based biomarkers may be helpful for the diagnosis and treatment of PPD patients. However, further studies need to be conducted to clarify the cause-effect relationship between PPD patients and gut microbiota and to highlight the suitability of gut microbiome as a biomarker.
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Association between major depressive disorder and gut microbiota dysbiosis.
OBJECTIVE: Major depressive disorder (MDD) affects 300 million people globally. Because dysbiosis may alter the central nervous system, it plays a potential role in this disorder. Dysbiosis is characterized by a decrease in microbial diversity and an increase in proinflammatory species. The human gut microbiota refers to the trillions of microbes, such as bacteria, that live in the human gut. The purpose of this study was to compare the gut microbiota of patients with MDD with that of healthy controls. METHODS: This case-control study involved 35 MDD cases and 35 healthy age- and sex-matched controls. Stool samples were collected and subjected to quantitative real-time PCR. Four intestinal bacterial phyla (firmicutes, bacteroidetes, actinobacteria, and proteobacteria) were investigated by 16SrRNA analysis. RESULTS: The findings indicated a relative abundance of bacteroidetes to firmicutes in the control and case groups was 0.66 vs. 1.33, respectively (p < .05). There were no significant differences in actinobacteria or proteobacteria among those in the MDD group compared to the healthy control group. CONCLUSIONS: Gut microbiota dysbiosis may contribute to the onset of depression, underscoring the importance of understanding the relationship between MDD and gut microbiota. Firmicutes, which produce short-chain fatty acids, are crucial for intestinal health. However, dysbiosis can disrupt the gut microbiota, impacting the central nervous system and contributing to the onset of depression.
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Inflammasome signaling affects anxiety- and depressive-like behavior and gut microbiome composition.
The inflammasome is hypothesized to be a key mediator of the response to physiological and psychological stressors, and its dysregulation may be implicated in major depressive disorder. Inflammasome activation causes the maturation of caspase-1 and activation of interleukin (IL)-1β and IL-18, two proinflammatory cytokines involved in neuroimmunomodulation, neuroinflammation and neurodegeneration. In this study, C57BL/6 mice with genetic deficiency or pharmacological inhibition of caspase-1 were screened for anxiety- and depressive-like behaviors, and locomotion at baseline and after chronic stress. We found that genetic deficiency of caspase-1 decreased depressive- and anxiety-like behaviors, and conversely increased locomotor activity and skills. Caspase-1 deficiency also prevented the exacerbation of depressive-like behaviors following chronic stress. Furthermore, pharmacological caspase-1 antagonism with minocycline ameliorated stress-induced depressive-like behavior in wild-type mice. Interestingly, chronic stress or pharmacological inhibition of caspase-1 per se altered the fecal microbiome in a very similar manner. When stressed mice were treated with minocycline, the observed gut microbiota changes included increase in relative abundance of Akkermansia spp. and Blautia spp., which are compatible with beneficial effects of attenuated inflammation and rebalance of gut microbiota, respectively, and the increment in Lachnospiracea abundance was consistent with microbiota changes of caspase-1 deficiency. Our results suggest that the protective effect of caspase-1 inhibition involves the modulation of the relationship between stress and gut microbiota composition, and establishes the basis for a gut microbiota-inflammasome-brain axis, whereby the gut microbiota via inflammasome signaling modulate pathways that will alter brain function, and affect depressive- and anxiety-like behaviors. Our data also suggest that further elucidation of the gut microbiota-inflammasome-brain axis may offer novel therapeutic targets for psychiatric disorders.
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Gut Microbiota-Related Inflammation Factors as a Potential Biomarker for Diagnosing Major Depressive Disorder.
OBJECTIVE: Although many works have been done, the objectively measured diagnostic biomarkers are not available. Thus, we conducted this study to identify potential biomarkers for objectively diagnosing depression and explore the role of gut microbiota in the onset of depression. METHODS: Major depressive disorder (MDD) patients (n=56) and demographic data-matched healthy controls (HCs) (n=56) were included in this study. The gut microbiota in fecal samples and inflammation-related factors in serum were measured. Both univariate and multivariate statistical analyses were performed to identify the differential gut microbiota and inflammation-related factors. RESULTS: Finally, 46 differential operational taxonomic units (OTUs) (60.9% OTUs belonging to Firmicutes) and ten differential inflammation-related factors were identified. Correlation analysis showed that there were significant correlations between 14 differential OTUs (9 OTUs belonging to Firmicutes and 5 OTUs belonging to family Lachnospiraceae under Firmicutes) and seven differential inflammation-related factors. Meanwhile, 14 differential OTUs (9 OTUs belonging to Firmicutes and 5 OTUs belonging to family Lachnospiraceae under Firmicutes) and five differential inflammation-related factors (adiponectin, apolipoprotein A1, alpha 1-antitrypsin, neutrophilicgranulocyte count/white blood cell count and basophil count) were significantly correlated to depression severity. A panel consisting of these five differential inflammation-related factors could effectively diagnose MDD patients from HCs. CONCLUSIONS: Our results suggested that Firmicutes, especially family Lachnospiraceae, might play a role in the onset of depression via affecting the inflammation levels of host, and these five differential inflammation-related factors could be potential biomarkers for objectively diagnosing MDD.
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Exploring the Potential of Probiotics and Prebiotics in Major Depression: From Molecular Function to Clinical Therapy.
Major depressive disorder (MDD) represents a complex and challenging mental health condition with multifaceted etiology. Recent research exploring the gut-brain axis has shed light on the potential influence of gut microbiota on mental health, offering novel avenues for therapeutic intervention. This paper reviews current evidence on the role of prebiotics and probiotics in the context of MDD treatment. Clinical studies assessing the effects of prebiotic and probiotic interventions have demonstrated promising results, showcasing improvements in depression symptoms and metabolic parameters in certain populations. Notably, prebiotics and probiotics have shown the capacity to modulate inflammatory markers, cortisol levels, and neurotransmitter pathways linked to MDD. However, existing research presents varied outcomes, underscoring the need for further investigation into specific microbial strains, dosage optimization, and long-term effects. Future research should aim at refining personalized interventions, elucidating mechanisms of action, and establishing standardized protocols to integrate these interventions into clinical practice. While prebiotics and probiotics offer potential adjunctive therapies for MDD, continued interdisciplinary efforts are vital to harnessing their full therapeutic potential and reshaping the landscape of depression treatment paradigms.