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Who's had good experiences with probiotics/prebiotics in relation to their mental health?

A randomized controlled trial to test the effect of multispecies probiotics on cognitive reactivity to sad mood

Background: Recent insights into the role of the human microbiota in cognitive and affective functioning have led to the hypothesis that probiotic supplementation may act as an adjuvant strategy to ameliorate or prevent depression. Objective: Heightened cognitive reactivity to normal, transient changes in sad mood is an established marker of vulnerability to depression and is considered an important target for interventions. The present study aimed to test if a multispecies probiotic containing Bifidobacterium bifidum W23, Bifidobacterium lactis W52, Lactobacillus acidophilus W37, Lactobacillus brevis W63, Lactobacillus casei W56, Lactobacillus salivarius W24, and Lactococcus lactis (W19 and W58) may reduce cognitive reactivity in non-depressed individuals. Design: In a triple-blind, placebo-controlled, randomized, pre- and post-intervention assessment design, 20 healthy participants without current mood disorder received a 4-week probiotic food-supplement intervention with the multispecies probiotics, while 20 control participants received an inert placebo for the same period. In the pre- and post-intervention assessment, cognitive reactivity to sad mood was assessed using the revised Leiden index of depression sensitivity scale. Results: Compared to participants who received the placebo intervention, participants who received the 4-week multispecies probiotics intervention showed a significantly reduced overall cognitive reactivity to sad mood, which was largely accounted for by reduced rumination and aggressive thoughts. Conclusion: These results provide the first evidence that the intake of probiotics may help reduce negative thoughts associated with sad mood. Probiotics supplementation warrants further research as a potential preventive strategy for depression

Magnetic resonance spectroscopy reveals oral Lactobacillus promotion of increases in brain GABA, N-acetyl aspartate and glutamate.

The gut microbiome has been shown to regulate the development and functions of the enteric and central nervous systems. Its involvement in the regulation of behavior has attracted particular attention because of its potential translational importance in clinical disorders, however little is known about the pathways involved. We previously have demonstrated that administration of Lactobacillus rhamnosus (JB-1) to healthy male BALB/c mice, promotes consistent changes in GABA-A and -B receptor sub-types in specific brain regions, accompanied by reductions in anxiety and depression-related behaviors. In the present study, using magnetic resonance spectroscopy (MRS), we quantitatively assessed two clinically validated biomarkers of brain activity and function, glutamate+glutamine (Glx) and total N-acetyl aspartate+N-acetylaspartylglutamic acid (tNAA), as well as GABA, the chief brain inhibitory neurotransmitter. Mice received 10(9) JB-1 per day for 28days and were subjected to MRS weekly and again 4weeks after cessation of treatment to ascertain temporal changes in these neurometabolites. Baseline concentrations for Glx, tNAA and GABA were equal to 10.4±0.3mM, 8.7±0.1mM, and 1.2±0.1mM, respectively. Delayed increases were first seen for Glx (~10%) and NAA (~37%) at 2weeks which persisted only to the end of treatment. However, Glx was still elevated 4weeks after treatment had ceased. Significantly elevated GABA (~25%) was only seen at 4weeks. These results suggest specific metabolic pathways in our pursuit of mechanisms of action of psychoactive bacteria. They also offer through application of standard clinical neurodiagnostic techniques, translational opportunities to assess biomarkers accompanying behavioral changes induced by alterations in the gut microbiome.

Psychotropic effects of Lactobacillus plantarum PS128 in early life-stressed and naïve adult mice.

Ingestion of specific probiotics, namely “psychobiotics”, produces psychotropic effects on behavior and affects the hypothalamic-pituitary-adrenal axis and neurochemicals in the brain. We examined the psychotropic effects of a potential psychobiotic bacterium, Lactobacillus plantarum strain PS128 (PS128), on mice subjected to early life stress (ELS) and on naïve adult mice. Behavioral tests revealed that chronic ingestion of PS128 increased the locomotor activities in both ELS and naïve adult mice in the open field test. In the elevated plus maze, PS128 significantly reduced the anxiety-like behaviors in naïve adult mice but not in the ELS mice; whereas the depression-like behaviors were reduced in ELS mice but not in naïve mice in forced swimming test and sucrose preference test. PS128 administration also reduced ELS-induced elevation of serum corticosterone under both basal and stressed states but had no effect on naïve mice. In addition, PS128 reduced inflammatory cytokine levels and increased anti-inflammatory cytokine level in the serum of ELS mice. Furthermore, the dopamine level in the prefrontal cortex (PFC) was significantly increased in PS128 treated ELS and naïve adult mice whereas serotonin (5-HT) level was increased only in the naïve adult mice. These results suggest that chronic ingestion of PS128 could ameliorate anxiety- and depression-like behaviors and modulate neurochemicals related to affective disorders. Thus PS128 shows psychotropic properties and has great potential for improving stress-related symptoms

An Investigation of the Acute Effects of Oligofructose-Enriched Inulin on Subjective Wellbeing, Mood and Cognitive Performance

Inulin is a natural food component found in many plants that are part of the human diet (e.g., leeks, onions, wheat, garlic, chicory and artichokes). It is added to many foods and is used to increase dietary fibre, replace fats or carbohydrates, and as a prebiotic (a stimulant of beneficial bacteria in the colon). Oligofructose, which is also present in these foods, produces similar effects and most research has used a combination of these products. A previous study (Smith, 2005) investigated the effects of regular consumption of oligofructose-enriched inulin on wellbeing, mood, and cognitive performance in humans. The results showed that oligofructose-enriched inulin had no negative effects but that it did not improve wellbeing, mood, or performance. The aim of the present study was to examine the acute effects of oligofructose-enriched inulin (5 g) over a 4 h period during which the participants remained in the laboratory. A double blind placebo (maltodextrin) controlled study (N = 47) was carried out with the order of conditions being counterbalanced and the two sessions a week apart. On each test day mood and cognitive performance were assessed at baseline (at 8:00) and then following inulin or placebo (at 11:00). Prior to the second test session (at 10:30) participants completed a questionnaire assessing their physical symptoms and mental health during the test morning. The inulin and placebo were provided in powder form in 5 g sachets. Volunteers consumed one sachet in decaffeinated tea or decaffeinated coffee with breakfast (9:00). Questionnaire results showed that on the day that the inulin was consumed, participants felt happier, had less indigestion and were less hungry than when they consumed the placebo. As for performance and mood tasks, the most consistent effects were on the episodic memory tasks where consumption of inulin was associated with greater accuracy on a recognition memory task, and improved recall performance (immediate and delayed). Further research is required to identify the mechanisms that underlie this effect with glucose metabolism being one candidate.

diet.jpg?w=700

This schematic represents the putative modulatory capability of diet, especially dietary extremes, represented by the Mediterranean-style diet, rich in components which support the gut microbiota, and the Western-style diet, with high fat and animal protein which mediate a detrimental impact on the gut microbiota and their metabolic output, on the gut:brain axis. Key intermediaries in this communication highway are the metabolites produced/regulated by the gut microbiota [e.g., serotonin/5-hydroxytryptamine (5-HT), gamma-amino butyric acid (GABA), glutamate (Glu), Phenylalanine (Phe), Tryptophan (Trp), tyrosine (Tyr), Carnosine, short-chain fatty acids (SCFA), Threonine (Thr), Alanine (Ala), Lysine (Lys), Glycine (Gly), Serine (Ser), aspartic acid (Asp), Ammonia, gut hormone/incretin production], microbial regulation of barrier integrity (both within the gut and at the blood brain barrier, BBB), and nutrient absorption at the mucosal surface, which is itself controlled in part by gut bacteria. These activities have the potential to impact on neurotransmission, inflammation, redox potential and epigenetic regulation of developmental processes, as well as neurological function, probably through the vagus nerve or in certain cases, may mediate direct effects on the brain [Source]

old-friends-inflammation.jpg?w=700

Loss of contact with “old friends” and increased inflammatory conditions in the modern world. In populations adequately exposed to old friends, such as many societies in the developing world, priming of regulatory T cells (Treg) is sufficient to maintain an appropriate balance of Treg to effector T cells (Teff), with the result that inappropriate inflammation is generally constrained. When contact with the old friends is disrupted as a result of modern cultural practices (e.g. sanitation, water and food treatment, modern medicines), priming of Treg is inadequate, with the result that the ratio of Treg to Teff is low. In this situation, the population as a whole is at risk for a variety of syndromes attributable to inadequate termination of inflammatory responses to any of a range of environmental stimuli. Consistent with this, although the prevalence of serious infections is significantly reduced in the industrialized world, rates of chronic inflammatory conditions (e.g. autoimmune diseases, allergies, asthma, and cardiovascular disease) have been shown in many studies to be much higher than in the developing world. Some individuals have a genetic background and/or immunological history that places them at risk for disorders, such as multiple sclerosis (MS), inflammatory bowel disease (IBD) and type 1 diabetes mellitus (DM), characterized by overactive/uncontrolled T helper (Th) type 1 and/or Th17 activity. In other individuals, Th2 responses are more liable to inadequate control, resulting in asthma and allergic disorders. While not developing gross immune-related pathology, a further group of individuals with inadequate termination of either Th1 or Th2 inflammatory responses is susceptible to CNS effects of cytokines, including major depressive disorder (MDD). It should be noted, however, that conditions associated with Th1/Th17 and Th2 dysregulation are highly comorbid with MDD. IL-10: interleukin-10; TGF-β: transforming growth factor-β [source]

The ‘‘psychomicrobiotic’’: Targeting microbiota in major psychiatric disorders: A systematic review.:

The term ‘‘dysbiosis’’ refers to situations where microbial composition and functions are shifted from their normal beneficial state to another that is deleterious to the host’s health. The microbiota dysbiosis may negatively impact CNS functioning through various intertwined pathways that collectively form the ‘‘brain-gut axis’’. These pathways can be described as follows:
  • modification of intestinal permeability that allows entry of endotoxins in the systemic blood flow. The lipopolysaccharide (LPS) is a potent pro-inflammatory endotoxin of the cell walls of gram-negative bacteria that can alter neuronal activity in the limbic system (e.g. increased amygdala activity) and also activate microglia, thus potentially contributing to chronic inflammation in the host’s CNS. Leakage of LPS from the intestine might be a trigger for peripheral inflammatory responses that lead to de novo production of cytokines in the brain. Improving the epithelial barrier may reduce traffic of bacteria and their byproducts and hence be a way to stop the inflammatory response;
  • neuropeptides synthesis;
  • modulation of local and peripheral inflammation. The gut microbiota regulates the development of lymphoid structures and modulates the differentiation of immune cell subsets thus maintaining homeostatic interactions between the host and the gut microbiota. Certain specific bacteria, including members of the Enterobacteriaceae family, appear to be better equipped for survival under the prevailing conditions in the inflamed gut than are the anaerobic commensals dominant in healthy individuals. Given the postulated anti-inflammatory effects of butyrate, it is possible that depletion in butyrate producing bacteria in dysbiosis may contribute to inflammation. Major depressive disorder, bipolar disorder and schizophrenia are associated with a dysregulation of immune responses as reflected by the observed abnormal profiles of circulating pro- and anti-inflammatory cytokines in affected subjects;
  • decrease in absorption of beneficial and essential nutrients (e.g. essential amino acids, vitamins, polyunsaturated fatty acids), increase of deleterious compound synthesis (ammonia, phenols, indoles, sulphide and amines), reduction of the antioxidant status and increase in lipid peroxidation, increase of carbohydrate malabsorption;
  • activation/deactivation of the autonomic nervous system that is directly connected to the nucleus tractus solitarius. This nucleus in turn issues direct noradrenergic ascending projections to brain areas involved in anxiety regulation (namely amygdala, basal forebrain cholinergic system and cortex);
  • modulation of brain-derived neurotrophic factor;
  • increase of small intestinal bacterial overgrowth and/or gastric/instestinal pathogens (e.g. Helicobacter pylori)

Schizophrenia and bipolar disorders

Severance et al. recently measured serological surrogate markers of bacterial translocation (soluble CD14 (sCD14) and lipopolysaccharide binding protein (LBP)) in bipolar subjects (n = 38) and schizophrenia subjects (n = 141) compared to controls. sCD14 seropositivity conferred a 3.1-fold increased odds of association with schizophrenia (OR = 3.09, P < 0.0001) compared to controls. Case–control differences in sCD14 were not matched by LBP. Quantitative levels of LBP, but not sCD14, correlated with BMI in schizophrenia (r2 = 0.21, P < 0.0001). sCD14 and LBP also exhibited some congruency in schizophrenia with both significantly correlated with CRP (P < 0.0001). Antipsychotic treatment generally did not impact sCD14 or LBP levels except for significant correlations, especially sCD14, with gluten antibodies in antipsychotic-naıve schizophrenia (r2 = 0.27, P < 0.0001). In bipolar disorder, sCD14 levels were significantly correlated with anti-tissue transglutaminase IgG (r2 = 0.37, P < 0.001). The authors concluded that these bacterial translocation markers produced discordant patterns of activity that may reflect an imbalanced, activated innate immune state. Whereas both markers may upregulate following systemic exposure to Gram-negative bacteria, autoimmunity, non-lipopolysaccharide-based monocyte activation and metabolic dysfunction may also contribute to the observed marker profiles.

Conclusion

Research on the role of the human intestinal microbiota in the genesis and/or maintenance of psychiatric disorders is in its infancy but appears as one of the most promising avenues of research in psychiatry. While rodent models suggest that the microbiota plays a fundamental role in the genesis of the HPA axis, the serotoninergic system and the immuno-inflammatory system, and that the microbiota can affect the CNS through multiple pathways, few studies have been carried out on humans. Today, autism is the psychiatric disorder in which the role of the microbiota has been the most studied. Some therapeutic opportunities targeting potential microbiota dysbiosis have already been explored such as probiotic administration or diet modifications, with inconsistent results. Further studies are warranted to determine which patients may benefit from microbiota-oriented therapies.

Microbiota Regulation of the Mammalian Gut–Brain Axis

“The findings from clinical studies demonstrate an upregulated immune and inflammatory status in patients with schizophrenia (
Song et al., 2013
) and a correlation between the level of inflammatory markers and severity of clinical symptoms (
Hope et al., 2013
). It has been suggested that the uncontrolled neuroinflammation by proinflammatory cytokines is involved in the pathogenesis of schizophrenia (Dennison et al., 2012 and Nemani et al., 2014). Chronic macrophage activation and secretion of interleukin-2 and interleukin-2 receptors has been proposed as the basic biological mechanism of schizophrenia in earlier papers (Smith, 1991 and Smith, 1992). For example, the protozoa
Toxoplasma gondii
is known to cause major perturbation to the gut microbiota and is a recognized environmental risk factor for schizophrenia ( Bhadra et al., 2013 and Molloy et al., 2013). More recently a chlorovirus (family Phycodnaviridae) has been identified in humans that affects cognitive function relevant to schizophrenia in animal models (
Yolken et al., 2014
).

NMDA receptor hypofunction is believed to be central to the pathophysiology of schizophrenia, as NMDA receptor antagonists produce schizophrenia-like symptoms while agents that enhance NMDA receptor function reduce negative symptoms and improve cognition (
Coyle, 2012
). Variation in BDNF expression is believed to play a role in the molecular mechanism underlying cognitive dysfunction in schizophrenia (
Nieto, Kukuljan, & Silva, 2013
). Given that normal development of the microbiota is necessary to stimulate brain plasticity through the appropriate expression of BDNF and NMDA receptors, it is possible that altered microbiota may contribute to the NMDA receptor dysfunction seen in schizophrenia (Dinan et al., 2014 and Nemani et al., 2015). In animal model of schizophrenia (chronic NMDA antagonist treatment), it has been shown that the gut microbiota profile correlated to memory performance, suggesting an influence of the microbiota on cognition in the model, which was supported by restoration of cognition through oral ampicillin administration (
Pyndt Jorgensen et al., 2014
).

Evidence showing possible microbiota alteration in schizophrenia includes structural damage to the GI tract, a heightened immune response to infectious pathogens and food antigens, and known differences in the microbiome in other neuropsychiatric disorders (
Nemani et al., 2014
). Further investigation into the microbiota and how the gut–brain axis may mediate the link between neuropsychiatric disease and the immune system is needed.

It is also worth noting that one of the most important side effects of treatments for schizophrenia is weight gain and metabolic syndrome. We have recently shown that the microbiota plays a critical role in olanzapine-induced weight gain in rats (Davey et al., 2013 and Davey et al., 2012) which has been confirmed in germ-free mice study (
Morgan et al., 2014
)”

“Considering the gut’s multifaceted capacity to communicate with the CNS, it is plausible that the gut and its components are playing a crucial role in resultant mood and behaviors. Some therapeutic opportunities targeting potential microbiota dysbiosis have already been explored such as probiotic administration, fecal transplantation, or diet modifications, with inconsistent results. Exciting evidence from animal studies has provided the rationale to warrant further exploration in humans, both in health and disease. Future research should focus on delineating the relative contributions of immune, neural, and endocrine pathways through which the gut microbiota communicates with the brain. A better understanding of these pathways will improve our knowledge about the role of gut microbiota play in a range of neurological disorders, including neuropsychiatric diseases”

Schizophrenia and the gut–brain axis

Potential novel therapeutics for schizophrenia

“The composition of the microbiome in schizophrenia has yet to be investigated, but there are several therapeutic interventions on the horizon which have less potential for toxicity than traditional treatment and may exert their influence through altering the microbiota.

Dietary interventions

Dietary changes affect both the composition and function of the gut microbial communities, which in turn can alter the innate and adaptive immune system (Vieira et al., 2014). Seven clinical trials have been published that examine the effects of a gluten-free diet on schizophrenia symptoms (Kalaydjian et al., 2006). These early studies included schizophrenia patients not tested for antibodies and had variable results. The resolution of schizophrenia symptoms after initiation of a gluten-free diet has been described in case reports (De Santis et al., 1997, Jackson et al., 2012, Jansson et al., 1984 and Kraft and Westman, 2009), and there are at least two current trials underway that are investigating the effects of gluten removal on schizophrenia symptoms in AGA-positive individuals. Data from these trials and future studies are needed to determine the impact of gluten-free diet on the subpopulation of people with schizophrenia who are sensitive to gluten.

While a study conducted in 1973 showed earlier discharge from the hospital in relapsed schizophrenia patients after a cereal-free, milk-free diet (Dohan and Grasberger, 1973), the impact of a casein-free diet in isolation on schizophrenia has yet to be investigated.

Antimicrobials

Alteration of the gut commensal microbiota with antibiotics has been shown to modify the susceptibility to autoimmune demyelinating processes of the central nervous system, such as that seen in multiple sclerosis (Ochoa-Repáraz et al., 2009). The protection afforded antimicrobials is associated with a shift in the immune response from Th1/Th17 toward anti-inflammatory Th2-type responses (Ochoa-Repáraz et al., 2010). Minocycline, a second generation tetracycline, is currently under investigation as an adjunct treatment in schizophrenia and there has been some early evidence of its efficacy in treating negative symptoms (Jhamnani et al., 2013, Khodaie-Ardakani et al., 2014 and Liu et al., 2014) and treatment-resistant schizophrenia (Qurashi et al., 2014). While tetracycline is believed to have a neuroprotective effect due to its anti-inflammatory action and ability to enhance glutamate neurotransmission (Liu et al., 2014), its immunomodulatory properties as mediated by gut microbiota have yet to be investigated and may play a role.

Probiotics

There is promising clinical evidence to support a role of probiotic interventions in reducing anxiety, decreasing the stress response, and improving mood in both animals (Arseneault-Bréard et al., 2012, Bravo et al., 2011 and Messaoudi et al., 2011) and humans (Logan and Katzman, 2005, Messaoudi et al., 2011 and Rao et al., 2009). The mechanism responsible for these effects is not known, but it has been hypothesized that it may be related to a reduction in the effects of pro-inflammatory cytokines as well as modification in nutritional status through direct effects on B vitamins, omega-3 fatty acids, and minerals (Cryan and O’Mahony, 2011 and Logan and Katzman, 2005). Probiotics have also been found to improve lactose digestion and potentially reduce the interference that high intestinal lactose concentration may have with serotonin availability through l-tryptophan metabolism (Ledochowski et al., 1998). As patients with schizophrenia often suffer from an increased stress response, compromised nutritional status, increased inflammatory status, and lactose sensitivity, probiotic interventions have promising therapeutic potential.

Probiotic interventions have also been shown to improve obesity-associated dyslipidemia and insulin resistance in animal models (Yu et al., 2013) and reduce weight gain and fat mass (Ji et al., 2012). Oral administration of Lactobacillus gasseri SBT2055 in healthy overweight humans has been found to reduce abdominal visceral and subcutaneous fat ( Kadooka et al., 2010). The anti-obesity effects of probiotics may have therapeutic potential for patients with schizophrenia given their higher risk metabolic profile. A recent study in rats reported that co-administration of antibiotics attenuated olanzapine-induced alteration in microbiota, as well as olanzapine-induced metabolic disturbances including weight gain, visceral fat deposition, elevated plasma free fatty acids, and macrophage infiltration of adipose tissue ( Davey et al., 2013). These findings suggest that microbiota might be a novel treatment target for metabolic comorbidity in patients with schizophrenia.

Fecal microbiota transplantation

While probiotics and antibiotics may be the best known and commercially available options to treat gastrointestinal dysbiosis, fecal microbiota transplantation is an old procedure that has been rediscovered as a cutting-edge option for the restoration of gut microbiota. There has been growing interest in the use of fecal microbiota for the treatment of patients with chronic gastrointestinal infections and inflammatory bowel diseases. Lately, there has also been interest in its therapeutic potential for extraintestinal conditions including cardiometabolic disease and autoimmune disorders (Smits et al., 2013). A better understanding of the microbiome in schizophrenia needs to be gained before the therapeutic potential of fecal transplantation can be explored.”

Evidence that patients with schizophrenia may have altered microbiota:

1. Changes in the microbiota seen in neuropsychiatric disorders

2. Structural damage to the GI tract in schizophrenia

3. Abnormal response to infectious pathogens in schizophrenia

4. Abnormal response to food antigens in schizophrenia

5. Sensitivity to gluten and bovine casein

“Several risk factors for the development of schizophrenia can be linked through a common pathway in the intestinal tract. A growing body of research emphasizes the role of the microbiota in regulating brain development, immune function, and metabolism but the composition of the microbiome in individuals with schizophrenia has yet to be investigated. Evidence that indicates possible microbiota alteration in schizophrenia includes structural damage to the GI tract, a heightened immune response to infectious pathogens and food antigens, and known differences in the microbiome in other neuropsychiatric disorders. A significant subgroup of patients may benefit from the initiation of a gluten and casein-free diet, and the therapeutic potential of antimicrobial and probiotic interventions will be elucidated by further research. Further investigation into the microbiome and how the gut may mediate the link between neuropsychiatric disease and the immune system is needed.”

Immunomodulatory Effects of Probiotic Supplementation in Schizophrenia Patients: A Randomized, Placebo-Controlled Trial.

Although peripheral immune system abnormalities have been linked to schizophrenia pathophysiology, standard antipsychotic drugs show limited immunological effects. Thus, more effective treatment approaches are required. Probiotics are microorganisms that modulate the immune response of the host and, therefore, may be beneficial to schizophrenia patients. The aim of this study was to examine the possible immunomodulatory effects of probiotic supplementation in chronic schizophrenia patients. The concentrations of 47 immune-related serum proteins were measured using multiplexed immunoassays in samples collected from patients before and after 14 weeks of adjuvant treatment with probiotics (Lactobacillus rhamnosus strain GG and Bifidobacterium animalis subsp. lactis strain Bb12; n = 31) or placebo (n = 27). Probiotic add-on treatment significantly reduced levels of von Willebrand factor (vWF) and increased levels of monocyte chemotactic protein-1 (MCP-1), brain-derived neurotrophic factor (BDNF), RANTES, and macrophage inflammatory protein-1 beta (MIP-1) beta with borderline significance (P ≤ 0.08). In silico pathway analysis revealed that probiotic-induced alterations are related to regulation of immune and intestinal epithelial cells through the IL-17 family of cytokines. We hypothesize that supplementation of probiotics to schizophrenia patients may improve control of gastrointestinal leakage.

brain-gut.jpg?w=700

Bidirectional brain gut microbial interactions

For more information:

The gut microbiota and inflammatory noncommunicable diseases: Associations and potentials for gut microbiota therapies

Gut microbiota modulation and implications for host health: Dietary strategies to influence the gut–brain axis

Host microbiota constantly control maturation and function of microglia in the CNS

Serotonin, tryptophan metabolism and the brain-gut-microbiome axis

Diet-Microbe Interactions in the Gut

Collective unconscious: How gut microbes shape human behavior.

Adult Hippocampal Neurogenesis Is Regulated by the Microbiome

Prebiotic feeding elevates central brain derived neurotrophic factor, N-methyl-D-aspartate receptor subunits and D-serine.

Probiotic gut effect prevents the chronic psychological stress-induced brain activity abnormality in mice.

Commentary: Gut Microbiota and Brain Function: A New Target for Brain Diseases?

Probiotic ‘glow of health’: it’s more than skin deep.

Dietary magnesium deficiency alters gut microbiota and leads to depressive-like behaviour.

The prebiotics 3'Sialyllactose and 6'Sialyllactose diminish stressor-induced anxiety-like behavior and colonic microbiota alterations: Evidence for effects on the gut-brain axis.

Relationships between diet-related changes in the gut microbiome and cognitive flexibility.

Edited by Alchemica
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i smash down resistant starch in the form of potato starch. you can also cook then cool meals of potato as the fattening starches of hot potato transform into (zero calorie, bacteria-feeding) resistant starch when cold.

green bananas are the other option. same concept, resistant starches have not yet fully transformed into carbs that your body can utilise.

i didn't read any of the material you posted because it's lengthy and i'm satisfied with how my lifestyle is adjusted based on my meager understanding.

Edited by ThunderIdeal
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Nice!

I'm trying ~20g inulin and a broad spectrum probiotic http://www.healthy-lifespace.com/. Gets me gassy and coupled with my high protein diet and poor bowel movement frequency, the flatulence is REALLY bad. Have to put more thought into a good way to get my guts back in order...

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most weeks i will be on a baby dose or no dose but one or two days a week is when i shovel it down.

i can't speak for inulin. even though resistant starch in a prebiotic i'm not sure it works the same way as other prebiotics. with RS though, i read that you should (as with any major change to the diet) ease your way up to the higher doses and unpleasant symptoms like farting twice for every breath you take should eventually abate. i have found that to be true :D although i don't understand why? it seems to counter reason.

at least you know its working right?

your knowledge of probiotic strains etc probably dwarfs mine if you've read half of those links but i'd suggest instead of relying on lab grown strains you can also supplement fermented foods (small amounts but frequently). cavemen used to eat with dirty hands!

i'm not sure i've ever encountered a claim that protein far in excess if your bodies needs is a good thing.

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Thanks TI,

i can't speak for inulin. even though resistant starch in a prebiotic i'm not sure it works the same way as other prebiotics. with RS though, i read that you should (as with any major change to the diet) ease your way up to the higher doses and unpleasant symptoms like farting twice for every breath you take should eventually abate. i have found that to be true :D although i don't understand why? it seems to counter reason.

Yeah, I should probably stick with 5g (recommended dose) which wasn't quite as gassy. Tend to do things to excess...

i'm not sure i've ever encountered a claim that protein far in excess if your bodies needs is a good thing.

Very true. I have this issue where I get up at night and 'sleep eat'. It's really weird. Started when I was on a potent antipsychotic and seems to have become habit worsened by another antipsychotic I use for sleep. I turn into a 'zombie' craving carbs so I've put on quite a bit of weight with that, hence me trying to use high protein diet during the day to counter the weight gain. I have some self-control during the day but this sleep eating is just so impulsive. The Drs aren't sure what to do, the only options in the literature are antiparkinson medications apparently.

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^ I also "pray to the fridge gods" at night with little recollection. Its a grazing more than a gorging.

The Mrs has found me many times naked, legs crossed sitting in the dark in front of the fridge being bathed by the fridge light.

She has had apparently reasonably coherent conversations that I cannot remember. Only do it at home thankfully.

I have "awoken" in the position mentioned above with that WTF feeling

No antipsych usage, but have run a few things through me over the years...lol...been doing it for decades.

I was known for epic sleep walking as a kid....

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feel you on that ,...

not just the fridge/kitchen but particularly the bathroom floor , does the bathroom monster get ya too?

- just found self there a bit ago after a stupid 40hour pain sesh wondering how id gotten there again and its a totally different property and only been here a few days .. but identical to the last home in bathroom floorings ...

-just glad its a wet room now.. which was much nicer than cold tiles ..

-edit- just bought some raw saurkraut now you mention it TI

will report back at some point if benefits felt

-edit 2- Alchemica your write ups are seriously world class !

Edited by ☽Ţ ҉ĥϋηϠ₡яღ☯ॐ€ðяئॐ♡Pϟiℓℴϟℴ
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Only the kitchen/fridge for me horsey, but have done it at every place I've lived at.

Chronic pain is something that is in part a driver for me I think, not sure why, I do know it affects me brain chemistry. I was lucky to have a very high metabolism and active and just burnt the extra calories off me. After heart surgery and getting older...lol...my fat distribution has changed (as it does) and packin on some slight love handles :o Its a change from my greyhound physique.

Might have to put a lock on the fridge...lol...don't reckon it would work though, I'd break in whilst in that state me thinks.

There is a lot we do not know about the micro-zoo that lives on and in us all, and the effects that this flora has upon us.

I found some of those links to be very interesting reading.

Sorry, no experience with probiotics Alchemica, and didnt want to digress too much - but you are not alone on the sleep eat front :wink: Wishing you well bro.

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You cant eat a medium or high carb diet without constantly craving carbs. Its really that simple imho but I welcome any counterarguments. Fuck carbs. Id rather be addicted to crack: Its far easier to kick, and it doesn't make you fat (unless you are addicted to carbs too)

Edited by ThunderIdeal

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Who's had good experiences with probiotics/prebiotics in relation to their mental health?

Me, oddly enough.

One of the old forum members here bought me round a bunch of fermented food and some water kefir after a workshop they'd run- it was a generous and thoughtful gift and the cupboards were complete bare so I ate the lot over the next month.

I felt obliged to drink the water kefir. Waste not etc.

I started to notice the mood changes ( calmer ) after the first week with the water kefir. Now, I'm absolutely mired knee deep in a town full of hippies who are prone to believing the slightest expensive shiny stupidity, so I was inclined to be sceptical. Very very skeptical. But I turned over the water kefir ( tibicos ) grains and made a few batches in a row and drank them too.

Having half-read a few of T's posts about gut bacteria before the issue started making the science blogs seriously I figured there might be something in it. Then I read a publication on the changes in gut bacteria in Parkinsons' patients.

I have Parkinsons on both sides of the family and my lifestyle years back hasn't exactly seen me avoid some of the possible elicitors. So if there is a way to slow down the progression while I'm at the age a few family members were diagnosed at it's gotta be worth a try

So I figured what the hell. Have been on it 2 years, just turning the grains over and making new batches weekly. I replaced my 2yo grains with new ones, as the old ones had slowed down, and noticed different effects- more mood smoothness than in previous six month's batches

I've been off it for a few weeks here and there while on the road, and I notice a real difference after a fortnight without water kefir, the tension starts to come back slowly, and it goes again after the new water kefir batch

Placebo? Maybe. I don't give a fuck.

I just sailed thru menopause asymptomatically. Better than pre-menopause in fact. My family has a history of menopausal cyclones which can lead to years of estrangement and unpleasantness for everyone. Not me, smooth as silk. You can hate me for it later :)

I spend about an hour a week making the drink. It is totally worth it.

Edited by Darklight
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Also, the tibicos ( water kefir ) grains are way more resilient than I'd given them credit for.

My kitchen is a disaster area, there is always some myco experiment or plant tissue culture goo around somewhere. I gave the grains six weeks til something foreign wheedled it's way in and killed them while they were fermenting.

Didn't happen. Brew performance was always standard, the grains behaved as expected, and nothing overcame them in solution

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One thing I've heard with kefir grains is they will adapt and even take on some of the good bacteria/yeast in your home. So basically every brew from every home will be a different mix of organisms (most overlapping because of the starter grains but think of it like an old fashioned sour dough). it's apparently really good for things such as sinusitis and bacterial infections as it allegedly works similar to the honey thing by introducing these foreign things into your body in a controlled way. It would be useful if you moved to a new house that gave you mouldy ears / wheezy chest etc. Sorry I can't explain it better I hope I've given an OK gist.

There's many reports of people using kefir to heal pets too.

I might reorder some grains now, mine have been stagnant since my last holiday where I fell into bad routines again lol. But yeh it definatly helps with mood I think, it's been to long to remember properly so will retry.

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yay just bought some milk kefir and some water kefir too ..

it was interesting to find they were both called kefir but seem to be completely different :)

I cant wait to feel good and healthy again ...

new house has electric heating so breathing suddenly became pretty difficult and cant stop wheezing ..

so does anyone know about this other one i came across in the hunt? ... : Organic Kombucha Scoby starter mushroom

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