Maybe the microbiome is our puppet master.
Is eating behavior manipulated by the gastrointestinal microbiota? Evolutionary pressures and potential mechanisms BioEssaysThe potential for Microbial Psychiatry previously
Microbes in the gastrointestinal tract are under selective pressure to manipulate host eating behavior to increase their fitness, sometimes at the expense of host fitness. Microbes may do this through two potential strategies: (i) generating cravings for foods that they specialize on or foods that suppress their competitors, or (ii) inducing dysphoria until we eat foods that enhance their fitness. We review several potential mechanisms for microbial control over eating behavior including microbial influence on reward and satiety pathways, production of toxins that alter mood, changes to receptors including taste receptors, and hijacking of the vagus nerve, the neural axis between the gut and the brain. We also review the evidence for alternative explanations for cravings and unhealthy eating behavior. Because microbiota are easily manipulatable by prebiotics, probiotics, antibiotics, fecal transplants, and dietary changes, altering our microbiota offers a tractable approach to otherwise intractable problems of obesity and unhealthy eating.
Microbial genes, brain & behaviour 每 epigenetic regulation of the gut每brain axis Genes, Brain and Behavior
To date, there is rapidly increasing evidence for host每microbe interaction at virtually all levels of complexity, ranging from direct cell-to-cell communication to extensive systemic signalling, and involving various organs and organ systems, including the central nervous system. As such, the discovery that differential microbial composition is associated with alterations in behaviour and cognition has significantly contributed to establishing the microbiota每gut每brain axis as an extension of the well-accepted gut每brain axis concept. Many efforts have been focused on delineating a role for this axis in health and disease, ranging from stress-related disorders such as depression, anxiety and irritable bowel syndrome to neurodevelopmental disorders such as autism. There is also a growing appreciation of the role of epigenetic mechanisms in shaping brain and behaviour. However, the role of epigenetics in informing host每microbe interactions has received little attention to date. This is despite the fact that there are many plausible routes of interaction between epigenetic mechanisms and the host-microbiota dialogue. From this new perspective we put forward novel, yet testable, hypotheses. Firstly, we suggest that gut-microbial products can affect chromatin plasticity within their host's brain that in turn leads to changes in neuronal transcription and eventually alters host behaviour. Secondly, we argue that the microbiota is an important mediator of gene-environment interactions. Finally, we reason that the microbiota itself may be viewed as an epigenetic entity. In conclusion, the fields of (neuro)epigenetics and microbiology are converging at many levels and more interdisciplinary studies are necessary to unravel the full range of this interaction.
Ingestion of Lactobacillus strain regulates emotional behavior and central GABA receptor expression in a mouse via the vagus nerve PNAS
There is increasing, but largely indirect, evidence pointing to an effect of commensal gut microbiota on the central nervous system (CNS). However, it is unknown whether lactic acid bacteria such as Lactobacillus rhamnosus could have a direct effect on neurotransmitter receptors in the CNS in normal, healthy animals. GABA is the main CNS inhibitory neurotransmitter and is significantly involved in regulating many physiological and psychological processes. Alterations in central GABA receptor expression are implicated in the pathogenesis of anxiety and depression, which are highly comorbid with functional bowel disorders. In this work, we show that chronic treatment with L. rhamnosus (JB-1) induced region-dependent alterations in GABAB1b mRNA in the brain with increases in cortical regions (cingulate and prelimbic) and concomitant reductions in expression in the hippocampus, amygdala, and locus coeruleus, in comparison with control-fed mice. In addition, L. rhamnosus (JB-1) reduced GABAA汐2 mRNA expression in the prefrontal cortex and amygdala, but increased GABAA汐2 in the hippocampus. Importantly, L. rhamnosus (JB-1) reduced stress-induced corticosterone and anxiety- and depression-related behavior. Moreover, the neurochemical and behavioral effects were not found in vagotomized mice, identifying the vagus as a major modulatory constitutive communication pathway between the bacteria exposed to the gut and the brain. Together, these findings highlight the important role of bacteria in the bidirectional communication of the gut每brain axis and suggest that certain organisms may prove to be useful therapeutic adjuncts in stress-related disorders such as anxiety and depression.
The adoptive transfer of behavioral phenotype via the intestinal microbiota: experimental evidence and clinical implications Current Opinion in Microbiology
Intestinal commensal bacteria or their products may be used to treat CNS disorders.
There is growing interest in the ability of the intestinal microbiome to influence host function within and beyond the gastrointestinal tract. Here we review evidence of microbiome每brain interactions in mice and focus on the ability to transfer behavioral traits between mouse strains using fecal microbiota transplantation (FMT). Transplantation alters brain chemistry and behavior in recipient ex-germ free mice, raising the possibility of using FMT for disorders of the central nervous system, and prompting caution in the selection of FMT donors for conditions that may include refractory Clostridium difficile infection, diabetes and inflammatory bowel disease in humans.?Behavioral phenotype can be transferred via the intestinal microbiota in mice.
?Changes in behavior in recipient mice are accompanied by changes in brain chemistry.
?Investigation of the intestinal microbiome in central nervous system (CNS) disorders is warranted.
?Donor screening for fecal transplants should exclude CNS and psychiatric illness.
"I'm impatient to see treatment methodologies come from bettering our understanding of our interdependence, but greater knowled ge of our mutual interdependence should make us even more cautious about the little bitty "others" we may tread upon."There is a lot of crazy and woo around all of this, like how the modern anti-vaxx movement is built around Wakefield's clearly fraudulent connection between the gut and the MMR vaccine, as well as various diets that all lack clear evidence. However, as this shows, the basic idea that some neurological disorders can be positively or negatively affected by the microbial composition of the gut has been very plausible for a while - even if there is no clear evidence pointing to any particular neurological disorder being affected this way, or microbial composition that can have such an effect, or treatment that can cause that composition. The effects of something like that being found are kind of fun to think about though, psychiatric facilities would need to get a lot more particular about poop, the ethics and logistics of fecal transplants for both C. difficile problems and psychiatric/neurological disorders would get really weird really fast, and "splashback" would turn into a simultaneously dead serious, disorienting, and hilarious epidemiological concern.
"So the new and easier way to deal with intractable problems of obesity and unhealthy eating may involve dietary change? Hmm."While I get the appeal of reasoning that you has been right about whatever all along, our models for understanding obesity, much less its relationship to diet or the food choices that create diets, remain wildly inadequate to the task of effectively treating it.
Adding certain species of bacteria to a normal mouse＊s microbiome can reveal other ways in which they can influence behavior. Some bacteria lower stress levels in the mouse. When scientists sever the nerve relaying signals from the gut to the brain, this stress-reducing effect disappears.So, yeah, the microbes "take care of themselves", but in many cases it's "enlightened self interest". Keeping their environment healthy is good for them!
Some experiments suggest that bacteria also can influence the way their hosts eat. Germ-free mice develop more receptors for sweet flavors in their intestines, for example. They also prefer to drink sweeter drinks than normal mice do.
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Research by Dr. Cryan and others suggests that a healthy microbiome helps mammals develop socially. Germ-free mice, for example, tend to avoid contact with other mice.
Commensal bacteria protect against food allergen sensitization PNASposted by Blasdelb at 5:42 AM on August 27, 2014 [2 favorites]
Abstract
Environmentally induced alterations in the commensal microbiota have been implicated in the increasing prevalence of food allergy. We show here that sensitization to a food allergen is increased in mice that have been treated with antibiotics or are devoid of a commensal microbiota. By selectively colonizing gnotobiotic mice, we demonstrate that the allergy-protective capacity is conferred by a Clostridia-containing microbiota. Microarray analysis of intestinal epithelial cells from gnotobiotic mice revealed a previously unidentified mechanism by which Clostridia regulate innate lymphoid cell function and intestinal epithelial permeability to protect against allergen sensitization. Our findings will inform the development of novel approaches to prevent or treat food allergy based on modulating the composition of the intestinal microbiota.
Significance
The prevalence of food allergy is rising at an alarming rate; the US Centers for Disease Control and Prevention documented an 18% increase among children in the United States between 1997 and 2007. Twenty-first century environmental interventions are implicated by this dramatic generational increase. In this report we examine how alterations in the trillions of commensal bacteria that normally populate the gastrointestinal tract influence allergic responses to food. We identify a bacterial community that protects against sensitization and describe the mechanism by which these bacteria regulate epithelial permeability to food allergens. Our data support the development of novel adjunctive probiotic therapies to potentiate the induction of tolerance to dietary allergens.
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posted by LogicalDash at 5:08 AM on August 18, 2014 [16 favorites]