vendredi 23 août 2013

Gut feelings

It would appear that the saying "gut feeling" has some validity.

Recent research, see below, is indicating the relationship between gut health and mental health.

Probiotics have been indicated as contribution to gut health.

So does anyone have any anecdotal evidence of their experience with probiotics and mental health?



I have collected a few interesting studies on the subject.



Postnatal microbial colonization programs the hypothalamic–pituitary–adrenal system or stress response in mice



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Indigenous microbiota have several beneficial effects on host physiological functions; however, little is known about whether or not postnatal microbial colonization can affect the development of brain plasticity and a subsequent physiological system response. To test

the idea that such microbes may affect the development of neural systems that govern the endocrine response to stress, we investigated hypothalamic–pituitary–adrenal (HPA) reaction to stress by comparing germfree (GF), specific pathogen free (SPF) and gnotobiotic mice. Plasma ACTH and corticosterone elevation in response to restraint stress was substantially

higher in GF mice than in SPF mice, but not in response to stimulation with ether. Moreover, GF mice also exhibited reduced brain-derived neurotrophic factor expression levels in the cortex and hippocampus relative to SPF mice. The exaggerated HPA stress response by GF mice was reversed by reconstitution with Bifidobacterium infantis. In contrast, monoassociation with enteropathogenic Escherichia coli , but not with its mutant strain devoid

of the translocated intimin receptor gene, enhanced the response to stress. Importantly, the enhanced HPA response of GF mice was partly corrected by reconstitution with SPF faeces at an early stage, but not by any reconstitution exerted at a later stage, which therefore indicates that exposure to microbes at an early developmental stage is required for the HPA system to become fully susceptible to inhibitory neural regulation. These results suggest that commensal microbiota can affect the postnatal development of the HPA stress response in mice.



http://onlinelibrary.wiley.com/doi/1...004.063388/pdf



Effects of gut microbiota on the brain: implications for psychiatry


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It may be surprising to learn that the human gastrointestinal tract is home to 1014 bacterial organisms.1 In fact, there are more bacteria in the gut than there are somatic cells in the body. These resident bacteria are referred to as commensal microbiota, and their arrival during the first few postnatal days sets up a symbiotic association that is necessary and crucial to normal physiology. This lifelong association is essential to host pathogen defence and plays an important role in nutrient uptake and metabolism.2 Immunologists have been aware of this system and its importance to the development of the muscosal and systemic immune systems for a long time.3,4 What is new and noteworthy is emerging evidence that gut microbiota influence behaviour and central nervous system (CNS) function.5 This commentary provides a brief overview of research related to gut–brain communication in a context that allows neuroscientists and psychiatrists to take note and consider the role of microbiota in their research related to CNS function and behaviour.



http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2674977/



Reduced anxiety-like behavior and central neurochemical

change in germ-free mice



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There is increasing interest in the gut-brain axis and the role intestinal microbiota may play in communication between these two systems.

Acquisition of intestinal microbiota in the immediate postnatal period has a defining impact on the develop- ment and function of the gastrointestinal, immune, neuroendocrine and metabolic systems. For example, the presence of gut microbiota regulates the set point for hypothalamic-pituitary-adrenal (HPA) axis activity. Methods We investigated basal behavior of adult

germ-free (GF), Swiss Webster female mice in the elevated plus maze (EPM) and compared this to conventionally reared specific pathogen free(SPF)mice.

Additionally, we measured brain mRNA expression of genes implicated in anxiety and stress-reactivity. Key Results Germ-free mice, compared to SPF mice, exhibited basal behavior in the EPM that can be inter-preted as anxiolytic. Altered GF behavior was accom- panied by a decrease in the N-methyl-D-aspartate receptor subunit NR2BmRNA expression in thecentral

amygdala, increased brain-derived neurotrophic factor expression and decreased serotonin receptor 1A (5HT1A) expression in the dentate granule layer of the hippocampus. Conclusions & Inferences We conclude

that the presence or absence of conventional intestinal microbiota influences the development of behavior, and is accompanied by neurochemical changes in the brain.



http://onlinelibrary.wiley.com/doi/1...10.01620.x/pdf



Normal gut microbiota modulates brain development and behavior



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Microbial colonization of mammals is an evolution-driven process that modulate host physiology, many of which are associated with immunity and nutrient intake. Here, we report that colonization by gut microbiota impacts mammalian brain development and subsequent adult behavior. Using measures of motor activity and anxiety-like behavior, we demonstrate that germ free (GF) mice display increased motor activity and reduced anxiety, compared with specific pathogen free (SPF) mice with a normal gut microbiota. This behavioral phenotype is associated with altered expression of genes known to be involved in second messenger pathways and synaptic long-term potentiation in brain regions implicated in motor control and anxiety-like behavior. GF mice exposed to gut microbiota early in life display similar characteristics as SPF mice, including reduced expression of PSD-95 and synaptophysin in the striatum. Hence, our results suggest that the microbial colonization process initiates signaling mechanisms that affect neuronal circuits involved in motor control and anxiety behavior.



http://www.pnas.org/content/108/7/3047.short





The Intestinal Microbiota Affect Central Levels of Brain-Derived Neurotropic Factor and Behavior in Mice


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The intestinal microbiota influences brain chemistry and behavior independently of the autonomic nervous system, gastrointestinal-specific neurotransmitters, or inflammation. Intestinal dysbiosis might contribute to psychiatric disorders in patients with bowel disorders.



http://www.sciencedirect.com/science...1650851100607X



Regulation of the stress response by the gut microbiota: Implications for psychoneuroendocrinology


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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.



http://www.sciencedirect.com/science...06453012000935





The interplay between the intestinal microbiota and the brain


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The intestinal microbiota consists of a vast bacterial community that resides primarily in the lower gut and lives in a symbiotic relationship with the host. A bidirectional neurohumoral communication system, known as the gut–brain axis, integrates the host gut and brain activities. Here, we describe the recent advances in our understanding of how the intestinal microbiota communicates with the brain via this axis to influence brain development and behaviour. We also review how this extended communication system might influence a broad spectrum of diseases, including irritable bowel syndrome, psychiatric disorders and demyelinating conditions such as multiple sclerosis.



http://www.nature.com/nrmicro/journa...o2876.html#top



The microbiome-gut-brain axis during early life regulates the hippocampal serotonergic system in a sex-dependent manner


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Bacterial colonisation of the intestine has a major role in the post-natal development and maturation of the immune and endocrine systems. These processes are key factors underpinning central nervous system (CNS) signalling. Regulation of the microbiome–gut–brain axis is essential for maintaining homeostasis, including that of the CNS. However, there is a paucity of data pertaining to the influence of microbiome on the serotonergic system. Germ-free (GF) animals represent an effective preclinical tool to investigate such phenomena. Here we show that male GF animals have a significant elevation in the hippocampal concentration of 5-hydroxytryptamine and 5-hydroxyindoleacetic acid, its main metabolite, compared with conventionally colonised control animals. Moreover, this alteration is sex specific in contrast with the immunological and neuroendocrine effects which are evident in both sexes. Concentrations of tryptophan, the precursor of serotonin, are increased in the plasma of male GF animals, suggesting a humoral route through which the microbiota can influence CNS serotonergic neurotransmission. Interestingly, colonisation of the GF animals post weaning is insufficient to reverse the CNS neurochemical consequences in adulthood of an absent microbiota in early life despite the peripheral availability of tryptophan being restored to baseline values. In addition, reduced anxiety in GF animals is also normalised following restoration of the intestinal microbiota. These results demonstrate that CNS neurotransmission can be profoundly disturbed by the absence of a normal gut microbiota and that this aberrant neurochemical, but not behavioural, profile is resistant to restoration of a normal gut flora in later life.



http://www.nature.com/mp/journal/v18...mp201277a.html



and for those that don't like to read

http://www.radiolab.org/2012/apr/02/gut-feelings/





via JREF Forum http://forums.randi.org/showthread.php?t=264170&goto=newpost

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