Diet and the gut microbiota-immune axis in the context of perinatal mental health: Protocol for a prospective cohort study.

Background: Physiological and psychosocial changes experienced by women during the perinatal period may put them at risk for postpartum mental health disturbances. Accumulating evidence suggests that dietary patterns may influence mental health through the modulation of the gut microbiota and its effects on host immune activity. Thus, targeting the gut microbiota via dietary intake could serve as both a preventative and therapeutic strategy in improving perinatal mental health.

Sex-specific effects of voluntary wheel running on behavior and the gut microbiota-immune-brain axis in mice.

Physical exercise has been positioned as a promising strategy to prevent and/or alleviate anxiety and depression, but the biological processes associated with its effects on mental health have yet to be entirely determined. Although the prevalence of depression and anxiety in women is about twice that of men, very few studies have examined whether physical exercise could affect mental health differently according to sex. This study examined, in singly-housed mice, the sex-specific effects of voluntary exercise on depressive- and anxiety-like behaviors as well as on different markers along the gut microbiota-immune-brain axis.

Understanding the impact of radical changes in diet and the gut microbiota on brain function and structure: rationale and design of the EMBRACE study.

Background: Bariatric surgery leads to profound changes in gut microbiota and dietary patterns, both of which may interact to impact gut-brain communication. Though cognitive function improves postsurgery, there is a large variability in outcomes. How bariatric surgery-induced modifications in the gut microbiota and dietary patterns influence the variability in cognitive function is still unclear.

Survival and Interplay of γ-Aminobutyric Acid-Producing Psychobiotic Candidates with the Gut Microbiota in a Continuous Model of the Human Colon.

Over decades, probiotic research has focused on their benefits to gut health. Recently, the gut microbiota has been proven to share bidirectional connections with the brain through the gut-brain axis. Therefore, the manipulation of this axis via probiotics has garnered interest.

Screening, characterization and growth of γ-aminobutyric acid-producing probiotic candidates from food origin under simulated colonic conditions.

Aims: This study aims to isolate probiotic bacteria candidates from various starter cultures and fermented foods and characterize their ability to produce γ-aminobutyric acid (GABA). GABA is a major inhibitory neuromediator of the central and enteric nervous systems with a role in several health disorders.

Methods And Results: Fourteen strains of lactic acid bacteria were isolated from food environment and screened for the presence of the glutamate decarboxylase (gadB) gene using PCR and GAD enzymatic assay.

Fracture Risk Following an Atypical Femoral Fracture.

Atypical femoral fractures (AFFs) occurring during the course of osteoporosis treatment usually lead to discontinuation of anti-resorptive (AR) drugs. However, the risk of fracture after an AFF is unknown. We conducted a follow-up study of patients with AFF matched 1:3 for age and gender with patients with a peripheral major osteoporotic fracture (pMOF), in the setting of a fracture liaison service, to investigate the incidence of subsequent low-trauma fractures.

Beyond the neuro-immune interplay in depression: Could gut microbes be the missing link?

Accumulating evidence have positioned inflammatory signaling pathways as crucial routes by which microbes inhabiting the gastrointestinal tract (the gut microbiota) communicate with the host brain to influence behavior, with impacts on mental illnesses. In this short review, an overview of inflammatory and gut microbiota status in human depression and in rodent models of the illness are provided. Next, potential inflammatory pathways mediating the communications between the gut and the brain under stressful conditions are described.

Stress-induced disturbances along the gut microbiota-immune-brain axis and implications for mental health: Does sex matter?

Women are roughly twice as likely as men to suffer from stress-related disorders, especially major depression and generalized anxiety. Accumulating evidence suggest that microbes inhabiting the gastrointestinal tract (the gut microbiota) interact with the host brain and may play a key role in the pathogenesis of mental illnesses. Here, the possibility that sexually dimorphic alterations along the gut microbiota-immune-brain axis could play a role in promoting this female bias of mood and anxiety disorders will be discussed.

Mindfulness and psychoeducation to manage stress in amnestic mild cognitive impairment: A pilot study.

Amnestic mild cognitive impairment (aMCI) often corresponds to the prodromal stage of Alzheimer disease (AD). The aMCI stage represents a crucial time window to apply preventive interventions in an attempt to delay cognitive decline. Stress, one of AD's modifiable risk factors frequently co-occurring with aMCI, stands out as a key intervention target.

Palatable Food Dampens the Long-Term Behavioral and Endocrine Effects of Juvenile Stressor Exposure but May Also Provoke Metabolic Syndrome in Rats.

The juvenile period is marked by a reorganization and growth of important brain regions including structures associating with reward seeking behaviors such as the nucleus accumbens (NA) and prefrontal cortex (PFC). These changes are impacted by stressors during the juvenile period and may lead to a predisposition to stress induced psychopathology and abnormal development of brain reward systems. Like in humans, adult rodents engage certain coping mechanisms such as increases in the consumption of calorie-rich palatable foods to reduce stress, but this behavior can lead to obesity and metabolic disorders.

Post-weaning Environmental Enrichment in Male CD-1 Mice: Impact on Social Behaviors, Corticosterone Levels and Prefrontal Cytokine Expression in Adulthood.

Environmental enrichment is typically associated with enhanced well-being, improved cognitive function and stress resilience. However, in some instances grouping adult male mice in enriched conditions promoted a stressful environment, which resulted in elevated endocrine, monoamine and inflammatory outcomes in response to subsequent stressor exposure. The current investigation examined whether raising male mice in an enriched environment (EE) would modulate social and anxiety-like behaviors in early adulthood and influence brain expression of pro-inflammatory cytokines and brain-derived neurotrophic factor (BDNF).

Functional Performances on Admission Predict In-Hospital Falls, Injurious Falls, and Fractures in Older Patients: A Prospective Study.

Falls are common among older inpatients and remain a great challenge for hospitals. Despite the relevance of physical impairments to falls, the prognostic value of performance-based functional measures for in-hospital falls and injurious falls remains unknown. This study aimed to determine the predictive ability and accuracy of various functional tests administered at or close to admission in a geriatric hospital to identify in-hospital fallers and injurious fallers.

Implications of the gut microbiota in vulnerability to the social avoidance effects of chronic social defeat in male mice.

Appreciable evidence suggests that perturbations within the gut microbiome and the immune system may play a key role in the pathogenesis of depression stemming from earlier stressful experiences. In the present investigation we examined whether microbial changes in cecum contents were associated with social avoidance behaviors, a feature of depression, and pro-inflammatory variations among socially stressed mice. Male C57BL/6 mice experienced social defeat or a control condition once a day for 10 consecutive days.

Fracture Prospectively Recorded From Prepuberty to Young Adulthood: Are They Markers of Peak Bone Mass and Strength in Males?

Fractures are common in otherwise healthy children and adolescents. They result from trauma of varying severity. Some reflect a greater skeletal fragility.

Environmental factors associated with familial or non-familial forms of Paget's disease of bone.

Objectives: The most frequent mutation linked to Paget's disease of bone (PDB), p.Pro392Leu within SQSTM1 gene, leads to phenotypic characteristics of PDB, but this mutation is seemingly insufficient to result in complete pagetic osteoclast phenotype, suggesting that possible environmental factors play a role in PDB pathogenesis. We performed an exploratory study to identify environmental factors potentially associated with familial or non-familial form of PDB in the French-Canadian population.

Prepubertal Impact of Protein Intake and Physical Activity on Weight-Bearing Peak Bone Mass and Strength in Males.

Context: Peak bone mass (PBM) and strength are important determinants of fracture risk in later life. During growth, bone is responsive to changes in nutrition and physical activity (PA), particularly before pubertal maturation.

Objective: In prepubertal healthy boys, protein intake (Prot-Int) enhances the impact of PA on weight-bearing bone.

Inflammation and the microbiome: implications for depressive disorders.

Inflammatory processes have been linked to depressive illness, possibly being driven by stressful experiences. As well changes in the balance between microbial species compromising the microbiome could be important in precipitating cytokines and other inflammatory factors that, in turn, influence several pathways leading to depression. In particular, hormonal (e.

Cytokine variations and mood disorders: influence of social stressors and social support.

Stressful events have been implicated in the evolution of mood disorders. In addition to brain neurotransmitters and growth factors, the view has been offered that these disorders might be provoked by the activation of the inflammatory immune system as well as by de novo changes of inflammatory cytokines within the brain. The present review describes the impact of social stressors in animals and in humans on behavioral changes reminiscent of depressive states as well as on cytokine functioning.

Interplay between pro-inflammatory cytokines and growth factors in depressive illnesses.

The development of depressive disorders had long been attributed to monoamine variations, and pharmacological treatment strategies likewise focused on methods of altering monoamine availability. However, the limited success achieved by treatments that altered these processes spurred the search for alternative mechanisms and treatments. Here we provide a brief overview concerning a possible role for pro-inflammatory cytokines and growth factors in major depression, as well as the possibility of targeting these factors in treating this disorder.

Social agonistic distress in male and female mice: changes of behavior and brain monoamine functioning in relation to acute and chronic challenges.

Stressful events promote several neuroendocrine and neurotransmitter changes that might contribute to the provocation of psychological and physical pathologies. Perhaps, because of its apparent ecological validity and its simple application, there has been increasing use of social defeat (resident-intruder) paradigms as a stressor. The frequency of stress-related psychopathology is much greater in females than in males, but the typical resident-intruder paradigm is less useful in assessing stressor effects in females.

Environmental enrichment influences brain cytokine variations elicited by social defeat in mice.

Environmental enrichment may protect against some of the adverse behavioural and biological effects of stressors. However, unlike the effects seen in some species, among male mice housed in groups, enrichment may alter social stability, encourage competition and aggression, and thus promote the establishment of a stressful environment. A potent psychosocial stressor such as social defeat in mice promotes brain neurochemical changes as well as pro-inflammatory cytokine variations in the prefrontal cortex (PFC) and hippocampus.

The differential impact of social defeat on mice living in isolation or groups in an enriched environment: plasma corticosterone and monoamine variations.

Social defeat in mice is a potent stressor that promotes the development of depressive- and anxiety-like behaviours, as well as variations of neuroendocrine and brain neurotransmitter activity. Although environmental enrichment may protect against some of the adverse behavioural and biological effects of social defeat, it seems that, among male group-housed mice maintained in an enriched environment (EE), aggressive behaviours may be more readily instigated, thus promoting distress and exacerbating psychopathological features. Thus, although an EE can potentially have numerous beneficial effects, these may depend on the general conditions in which mice were raised.

Environmental enrichment in male CD-1 mice promotes aggressive behaviors and elevated corticosterone and brain norepinephrine activity in response to a mild stressor.

Housing rodents in an enriched environment (EE) has been typically considered to have positive effects on well-being and cognitive functioning of the animals. However, in some strains of mice, EEs have also been reported to elicit aggression and to promote stress-related outcomes. In the current investigation, we examined whether environmental enrichment would elicit aggression among CD-1 male mice and thus sensitize responses to a subsequent mild stressor.

Social defeat promotes specific cytokine variations within the prefrontal cortex upon subsequent aggressive or endotoxin challenges.

Stressful experiences typically have short-lived neuroendocrine and neurochemical effects, but the processes leading to these biological alterations may be sensitized so that later challenges promote exaggerated responses. As stressors and immunogenic insults have both been associated with inflammatory immune variations within the brain, we assessed whether a social defeat stressor would result in augmented corticosterone release and mRNA expression of pro-inflammatory cytokines within the prefrontal cortex (PFC) upon later social defeat (sensitization) or endotoxin (lipopolysaccharide: LPS) challenges (cross-sensitization). In the absence of a prior stressor experience, the social defeat challenge did not affect prefrontal interleukin (IL)-1β or tumor necrosis factor (TNF)-α mRNA expression, but increased that of IL-6, whereas LPS increased the expression of each cytokine.