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Probiotic turmerics for mental health and pro-inflammatory CNS conditions

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I put myself on daily probiotic turmeric. Been doing that for a while now. Anyone use it as a brain tonic?



I whip up a couple of strong (20g)  turmeric, ginger, black pepper and occasionally saffron probiotic sludges a day


The more probiotic turmeric combos I get into me, the more I see how much I was probably running on likely extreme neuroinflammation. It's a robust shift, some really positive glimpses at something when I mega dose, some days not always feeling wonderful but on the whole small steps that are generally positive, using pretty much all the polyphenol classes and including the turmeric concoctions at a high dose in a good diet. I'm sticking with this, hoping an antidepressant effect becomes apparent..


So far, the most robust improvement I've had is in self-regulation (which was in tatters) buffering to better levels, along with getting sleep (quite a bit of sleep debt built up), more so than mood.


Quite profound is the way these probiotic turmeric combos seem to be modulating aberrant reward related stuff. It's very anti-addictive but at the same time I'm stopping so many locked in behavioural loops that nothing at all left seems rewarding anymore. Push through it, hope I can write some new eudaimonic pathways

Inflammation and mental health:


Research indicates that mood disturbances and psychiatric disorders are closely related to CNS or whole body inflammation [1]. The prevalence of inflammation, measured by one marker only, in the diagnostic groups of psychotic disorders, mood disorders, neurotic disorders and personality disorders was 32%, 21%, 22% and 42%, respectively [2].


Inflammation was consistently found to affect basal ganglia and cortical reward and motor circuits to drive reduced motivation and motor activity, as well as anxiety-related brain regions including amygdala, insula and anterior cingulate cortex, which may result from cytokine effects on monoamines and glutamate [3].


Higher levels of inflammation are associated with longitudinal changes in brain function in regions important for cognition [4]. Increasing evidence points toward an involvement of the immune system in MDD pathogenesis. Inflammation can affect monoaminergic and glutamatergic neurotransmission [5]. Negative symptoms of schizophrenia are associated with increased inflammation [6].


Inflammation may at least partly mediate resting state functional connectivity via effects on mesolimbic and mesocortical dopaminergic systems [7]. Inflammatory measures were positively related to striatolimbic resting-state functional connectivity but negatively related to corticostriatal resting-state functional connectivity

Chronically elevated levels of inflammatory markers, for example, are associated with clinical depression, post-traumatic stress disorder (PTSD) and many other psychological and behavioral issues and likewise these conditions often have elevated impulsivity. Inflammatory mediators promote a general trade-off towards focusing on immediate versus delayed outcomes. Inflammation is particularly influential on impulsivity - higher active inflammation – as quantified by plasma levels of IL-6, TNF-α, and white blood cell count – predicted more impulsivity. The relationship remained significant when controlling for factors known to covary with both inflammation and impulsivity [8]


"Better understanding of the outcomes associated with impulsivity of inflammatory origins may yield low-cost interventions that can ameliorate behavioral problems notoriously resistant to current treatment strategies. For example, anti-inflammatory medications may be helpful as adjunct treatments for behavioral disorders related to impulsivity, such as substance abuse or certain mental illnesses."


[1] http://www.dailymail.co.uk/…/Cambridge-psychiatrist-claims-…
[2] https://www.ncbi.nlm.nih.gov/pubmed/29544672
[3] https://www.ncbi.nlm.nih.gov/pubmed/29173175
[4] https://www.ncbi.nlm.nih.gov/pubmed/29304217
[5] https://www.ncbi.nlm.nih.gov/pubmed/29604382
[6] https://www.ncbi.nlm.nih.gov/pubmed/29499967
[7] https://www.ncbi.nlm.nih.gov/pubmed/29689344

[8] https://repository.tcu.edu/handle/116099117/20630


More on neuroinflammation

 Mental illnesses and ASD seem to be strongly related to neuroinflammation, activation of inflammation in animal models leads to behavioural abnormalities. That said, it is suggested to be at best one cause of depression [1]. Schizophrenia and autism spectrum disorders share core symptoms and overlap in many ways pathologically, mainly by extensive microglial activation and similar behavioural attributes, this microglial activation also extends to brain injuries. The neuroprotective effect of curcumin is mainly mediated by blockade of microglial cell activation [2].


Psychological stress activates inflammation and that this activation would be found to predict the later development of pathology. Social isolation/feeling lonely is associated with systemic inflammation. There is evidence that a range of psychosocial stressors lead to elevated microglial activity [3]. Neuroticism has also been associated with higher levels of inflammatory markers while conscientiousness has been associated with lower inflammatory markers [4].


Chronic neuroinflammation and the loss of neurotrophic factors promotes 'locked in' behavioural inflexibility and promotes the pathogenesis of disorders such as addictions and feeds antisocial personality traits [5]. A multitude of studies support the notion that inflammatory processes form an integral part of the mechanisms precipitating addictions [6].


It appears elevated neuroinflammation is important throughout the cortico-striato-thalamo-cortical circuit of obsessive compulsive disorder, too [7]


See Resident evil: Inflammation and depression

[1] http://www.psychiatrictimes.com/special-reports/introduction-inflammation-connection
[2] https://www.ncbi.nlm.nih.gov/pubmed/18214347
[3] https://www.ncbi.nlm.nih.gov/pubmed/26847047
[4] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4544833/
[5] https://www.ncbi.nlm.nih.gov/pubmed/28810156
[6] https://www.ncbi.nlm.nih.gov/pubmed/29054292
[7] https://www.ncbi.nlm.nih.gov/pubmed/28636705


Microglial activation - a pathological player?


Activated pro-inflammatory microglia trigger anxiety- and depressive-like behaviours, mainly by increasing the expression of pro-inflammatory mediators and neurotoxins in stress-sensitive brain regions. Injury, stress, toxic exposures and social stress can induce microglial over-activation [1]


It is proposed M1 and M2 microglia are related to relapse and remission, respectively in psychiatric disorders and diseases [2]. While activated M1 microglia may exacerbate injury by producing neurotoxic substances when overactivated for prolonged times, activated M2 microglia (the anti-inflammatory and tissue-reparative phenotype) protect neighboring cells by removing cell debris and releasing trophic factors for brain repair. Curcumin promoted microglial M2 polarisation and inhibited M1 polarisation.


Long-term depression is a progressive disease and elevated microglial activation and inflammation play a role, it is suggested targeting the inflammatory process is needed to prevent neuroprogression [3].


Our gut microbiota is critical for modulation of the HPA axis and thus the stress response and brain processes such as myelination, neurogenesis and microglial activation and can effectively modulate behaviour and influence psychological processes such as mood and cognition. The gut microbiota is essential for the maintenance of microglia in a healthy functional state, which is necessary for the prevention of neurodevelopmental and neurodegenerative disorders [4].


Microglia have more recently emerged as key players in regulating neuronal network excitability [5] and reward. Activated microglia within reward circuitry result in disruption of dopaminergic signaling and reward behaviour. Activation of microglia by addictive drugs or other causes results in a proinflammatory dominance of the innate immune system, which is then critically synergise on the neurocircuit of reward and dependence [6]. Repeated drug-induced microglial activation produces progressive increases in microglial reactivity, further potentiating the neurobiological consequences of chronic drug use [7]


Even acute inflammation impairs 'theory of mind' (ToM) explaining social-cognitive deficits in people that exhibit low-grade inflammation [8].


Inflammation, Self-Regulation, and Health: An Immunologic Model of Self-Regulatory Failure


Exposure to stress, infection, and disease in early life increases proinflammatory cytokine activity, which decreases an individual’s self-regulatory ability. Poor self-regulation and poor health behaviours, which lead to greater exposure to stress and disease. As these dynamics continue over childhood and adolescence, compounded by social stressors, more stable differences in brain structure and function can develop that ultimately produce persistent impairments in self-regulation in adulthood.


Dysregulated or enhanced neuroinflammation is argued to facilitate the etiology of mental disorders. Immune system activity — especially components of the immune system involved in inflammation — appear to impair numerous facets of self-regulation: inflammatory activity can impair both cognitive and emotional self-regulation. Markers of systemic inflammation have been associated with brain alterations that negatively impact executive function in humans: higher levels of proinflammatory cytokines at baseline predict lower executive function.


Acute inflammatory challenges alter DLPFC response when individuals engage in tasks that require self-control, reduces resting glucose metabolism in the ACC in humans, which is a brain region critically important in self-regulation and reduces functional connectivity between the medial PFC (mPFC) and brain regions involved in mood and emotion. Inflammatory activity impairs sensitivity to reward. Inflammatory activity may impair self-regulation by reducing motivation and may either help or hinder self-regulation by decreasing sensitivity to reward. Inflammation may modulate mesolimbic and mesocortical dopaminergic systems.


"Prolonged or severe stress exposure disrupts homeostatic or ‘healthy’ communication between the CNS and peripheral immune system, shifting immune signaling toward a proinflammatory state. Part of this response includes elevated and prolonged proinflammatory signaling in the CNS that is argued to be linked with stress-related psychiatric disorders."


There is mounting evidence that social stress activates microglial cells in the central nervous system. Microglial activation is positively correlated with psychiatric disorders. Pro-inflammatory cytokines including IL-1β and TNF-α, can reduce the availability of serotonin, dopamine and noradrenaline by increasing the expression and function of reuptake transporters, reducing synthesis or decreasing monoamine precursors and also act on the glutamate pathway and together with astrocytes stimulate the increased release of this neurotransmitter and decreased brain-derived neurotrophic factor, which ultimately leads to excitotoxicity [9]


Elevated pro-inflammatory cytokine levels caused by microglia activation, often induced by social stress, contributes to the development and persistent anxiety-like behaviour [10]

[1] https://www.frontiersin.org/articles/10.3389/fnbeh.2017.00207/full
[2] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4276905/
[3] https://www.karger.com/Article/Abstract/470805.
[4] https://www.wjgnet.com/1007-9327/full/v23/i30/5486.htm
[5] https://www.hindawi.com/journals/np/2013/429815/
[6] https://www.ncbi.nlm.nih.gov/pubmed/22707932
[7] https://www.colorado.edu/lab/bachtell/research/neuroinflammation-and-addiction
[8] https://www.ncbi.nlm.nih.gov/pubmed/29742460
[9] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5660717/
[10] https://www.nature.com/articles/npp2016102


Why turmeric?


Turmeric, a source of curcuminoids, including the essential oil containing ar-turmerone [1] is a neuroprotective and neuropharmacological drug. It may be used in neurodegenerative disorders [2] including MS [3], depression etc. Curcumin may be used as an effective and safe modality for treatment in patients with depression, with a better tolerability profile and safety than SSRIs [4]. Patients receiving curcumin showed increased levels of BDNF relative to baseline, whereas patients receiving placebo showed declines relative to baseline but results did not show more distal effects on cognition or clinical symptoms for patients with schizophrenia [5]


Curcumin may increase the concentration of monoamines available to interact with receptors, alleviating depression
Curcumin strongly inhibits inflammatory cytokines like nuclear factor-kappa B, NLRP3 inflammasome, and interleukin-1B. this may help explain its antidepressant activity.


There's suggestion that  curcumin may be useful for treating human motivational symptoms


The study findings that epigenetically, cooking with/using whole turmeric is superior to using turmeric extract preparations seem to match my experiences - those 'bioavailability enhanced commercial products' or curcumin extracts (even with piperine) just don't personally compare to solid dose of whole turmeric etc IMO. Something about it fermenting in the gut, activity of the volatiles, or high volume of dispersion/absorption of the curcuminoids through using the actual powder, I'm not sure? Particularly fermented with quality probiotics.


Even a curcumin free water turmeric extract has effects on mood . At least 235 compounds, primarily phenolic compounds and terpenoids, have been identified from C. longa. What's interesting about using whole turmeric is curcumin-free turmeric components such as those in a possess numerous biological activities, including neuroprotective, anti-inflammatory, anticancer, and antidiabetic activities. Volatiles like aromatic-turmerone exerts beneficial effects on the brain - inhibiting microglial activation, preventing brain damage caused by neuroinflammation and increasing neural stem cell proliferation . Bisacurone has been identified as another of these components, also with anti-inflammatory effects.


[1] a) https://www.ncbi.nlm.nih.gov/pubmed/28849618
b ) https://www.ncbi.nlm.nih.gov/pubmed/25928248
[2] https://www.ncbi.nlm.nih.gov/pubmed/22742420
[3] https://www.ncbi.nlm.nih.gov/pubmed/29079885
[4] https://www.ncbi.nlm.nih.gov/pubmed/23832433
[5] https://doi.org/10.1016/j.schres.2017.09.046


The effect of curcumin on serotonin appeared to be dose-dependent, at high doses curcumin also increased dopamine and to a lesser extent noradrenaline. Additionally, the effect of curcumin on the serotonergic system was possibly related to its interaction with 5-HT1A/1B and 5-HT2C receptors. In studies, regarding behavioural changes; the effect of curcumin was more pronounced than fluoxetine. Curcumin raised brain GSH and reduced brain MDA, TNF-α and IL-6 contents


Importantly, curcumin normalises the levels of dopamine in the frontal cortex of rats and exerts biochemical and morphological effects of the on the PFC and hippocampus. Curcumin enhances the level of neurotrophic factors such as brain derived neurotrophic factor (BDNF)


There have been signs of antidepressant properties through an interaction of curcumin with dopamine receptors and an increase in brain dopamine levels.


Supplementation of curcuminoids to standard antidepressants showed a significant reduction of anxiety and depression in patients with major depressive disorder Moreover, curcumin extracts significantly improved depressive symptoms and demonstrated anxiolytic effects in patients with atypical depression.


There was a significant improvement of sustained attention, working memory tasks, and mood after curcumin treatment.

Curcumin showed a significant reduction in SGA‑induced body weight gain on the rats. It exerts hypoglycemic, antioxidant, antitumor, and anticarcinogenic activities. It also prevents tardive dyskinesia

Why probiotic?


Influence of gut microbiota on neuropsychiatric disorders


Got a broad spectrum of probiotics gong on. Along with things like L. plantarum which significantly reduced anxiety-related behaviour and altered GABAergic and serotonergic signaling in the brain, it also ameliorated cognition deficits but also restored ACh and the histopathological features to control group in an AD model, I'm using a lot of L. rhamnosus rich food which has anxiolytic and mood effects: Lactobacillus rhamnosus, can dramatically alter GABA activity in the brains of mice. It reduces stress-induced elevation in stress hormones. Enriching food with Bifidobacterium longum which decreases anxiety and may improve mood among anxious animal models. Lactobacillus casei which cultures appeared to improve mood among those only with a low/depressive mood at baseline. Bifidobacterium animalis which scavenged free radicals and decreased MAO activity.


"The development of the forebrain, esp. the neocortex, in social mammals and ultimately primates and humans depends on correct and timely signals from microbial symbionts—which is disturbed, when the microbiota is absent or disturbed. Likewise when the microbiome is disturbed, there is evidence of increased hypothalamic–pituitary–adrenal (HPA) axis activity in response to acute stress. The immune pathway within the brain–gut–microbiome axis may be a plausible mediator of the effects of this axis on social behaviour"


Recent data provide evidence that related bacterial species can interact specifically with a variety of different neuronal populations. For example some bacteria affects the functioning of CNS neurons in the hippocampus and amygdala, and alter PFC funtioning. They can alter vagal tone, HPA axis activity, neuroinflammation/microglial activation, alter serotonergic transmission, levels of brain-derived neurotrophic factor, NMDA receptor subunit expression, GABAergic signalling and receptor expression etc [ref] There are also links to a role for oxytocin.


Altering the microbiome has been shown to do things like:
-improve mood, but only in those who have poorer mood at baseline and alter anxiety related measures
-reduce cortisol output in response to an acute stressor
-alter brain activity when processing information related to emotional facial expressions
-improvement in sustained attention in healthy older adults

The first clinical trial of probiotics in bipolar disorder found probiotics lowered the rate of rehospitalisation, building on previous research that has found promise for these in depression, anxiety, cognition, and autism

Supplemental probiotics to combat brain-related dysfunction offers a promising approach [1]. Evidence suggests [2] that chronic administration of Lactobacilli and Bifidobacteria strains can have effects on areas of the brain related to emotion, mood, memory, and somatosensory processing - probiotic ingestion attenuates emotional reactions and decreases activity of certain brain regions when measuring brain responses to emotional stimuli


Along with improved depression, anxiety, anger, and anxiety in adults [3], probiotic intake for 4-6 weeks altered neural activity in brain regions that control central processing of emotion and sensation in healthy women but no change in gut microbial composition was detected [4].


In a more recent study, a slight change was detected in the microbiome and [5]:


Probiotics improved self-reported behavioural measures of positive affect and cognitive reactivity

Probiotic administration influenced the behavioral scores for depression and anxiety questionnaires, significantly increasing positive affect and blunting vulnerability to depression in terms of hopelessness and risk aversion

Probiotics improved memory performance and altered brain activation patterns

Probiotic administration for 4 weeks was associated with changes in brain activation patterns in response to emotional memory and emotional decision-making tasks


In major depression, probiotic (Lactobacillus helveticus and Bifidobacterium longum) resulted in an improvement in BDI score compared with placebo whereas no significant effect of prebiotic supplementation (galactooligosaccharide) was seen [6]


“The Social Network” – How the Gut Microbiome Governs Our Social Behaviour


[1] https://www.ncbi.nlm.nih.gov/pubmed/29701810
[2] https://www.ncbi.nlm.nih.gov/pubmed/29698377
[3] https://www.ncbi.nlm.nih.gov/pubmed/20974015
[4] https://www.ncbi.nlm.nih.gov/pubmed/23474283
[5] https://www.tandfonline.com/doi/abs/10.1080/19490976.2018.1460015
[6] https://doi.org/10.1016/j.clnu.2018.04.010



There seem to be changes in the microbiota that are associated with substance use [1] across an array of SUDs and eating disorders [2]

Ethanol drastically changes the microbiome and increase in gut permeability and induces a pro-inflammatory responses. Microbiome alterations were shown to be correlated with alcohol use disorder-related symptoms, i.e. craving, depression and anxiety and manipulations in the gut microbiota may affect cocaine-related behaviors (Animals with reduced gut bacteria showed an enhanced sensitivity to cocaine reward and enhanced sensitivity to the locomotor-sensitising effects of repeated cocaine administration [3]) and methamphetamine [4].

There is a strong negative influence of alcohol dependence on gut microbiota [5] and "Intestinal flora between cocaine users and non-cocaine users and have found that cocaine users have a higher mean relative abundance of Bacteroidetes and a lower abundance of Firmicutes than non-users; are more likely to smoke; have a lower mean percentage of body fat; and consume more alcohol than non-users."

Phytonutrients impact the microbiome “eat the rainbow” AND eat prebiotic and probiotic foods" so to do omega-3's: Some of the health-related benefits of omega-3 may be due, in part, to increases in butyrate-producing bacteria.

You can shift the microbiome with probiotics. Some of the other non-LAB are also now available as supplements. Probiotic intake induced an increase in Proteobacteria and in the Clostridiales spp. Patients taking probiotics had an increased numbers of butyrate-producing bacteria, especially Faecalibacterium and Clostridiales spp. Probiotic intervention modulated the fecal concentrations of butyrate in a manner dependent on the initial levels of short-chain fatty acids (SCFAs) [things like live B. bifidum cells affected the relative abundance of dominant taxa in the fecal microbiota and modulated fecal butyrate levels]

[1] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5472629/
[2] https://www.ncbi.nlm.nih.gov/pubmed/28482009
[3] https://www.ncbi.nlm.nih.gov/pubmed/27752130
[4] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5575146/
[5] https://microbiomejournal.biomedcentral.com/.../s40168...


 Black pepper - more than a spice and bioavailability enhancer...


"During the time of Hippocrates the pepper was used as both a spice for food and as a medicine. The Asian world has long considered black pepper to be an important spice for detoxifying and as an anti-aging compound. It is widely used in different traditional systems of medicine like Ayurvedic and Unani System of medicines"


Black pepper is itself used as an analgesic, antiinflammatory, anticonvulsant, antioxidant, antidepressant and cognitive-enhancing agent. It contains 5-10% pungent acid-amides, with piperine as its main compound and several others, such as the N-isobutylamide guineensine which is a nanomolar inhibitor of cellular uptake of the endocannabinoid anandamide.


Recent studies on the pharmacological actions of piperine have demonstrated its antioxidant activity, antiinflammatory [1] and cognitive-enhancing effect following long-term oral administration. It performed as well as memantine in an Alzheimer's model [2]. It reduces cholinesterase levels and amyloidal plaque formation [3].

It is a potent anti-inflammatory [4].


The antidepressant-like effects might depend on the augmentation of the neurotransmitter synthesis or the reduction of the neurotransmitter reuptake, along with inducing BDNF promoter, increasing brain-derived neurotrophic factor expression in the hippocampus and promoting neurite outgrowth [5,6]. It predominately seems to be mediated via the serotonergic system by enhancing 5-HT content [7]


It exerts anxiolytic effects by GABAergic and nitrergic systems [8]


It exerts anticonvulsant effects [9] due to antioxidant actions, as well as TNF-α reduction, along with effects on inhibitory amino acids and on the GABAergic system [10] and analgesic properties dependent on the opioid system [11]


Piperine pre-treatment time-dependently improves the bioavailability of poylphenols, including flavonoids/green tea catechins and curcumin, through the reversible and selective inhibition of UGTs and SULTs. It also increases the bioavailability of things like ashwagandha, rosmarinic acid and a variety of drugs [12]. Enzymatic inhibition by piperine resulted in increased bioavailability of many drugs and nutrients e.g. amoxicillin, ampicillin, acefotaxime, carbamazepine, ciprofloxacin, norfloxacin, metronidazole, oxytetracyclin, nimesulide, pentobarbitone, phenytoin, resveratrol, beta-carotene, curcumin, gallic acid, tiferron, nevirapine, and sparteine by different types of mechanisms.


Curcuminoids and piperine could inhibit drug metabolism but is "unlikely to result in a clinically significant interaction involving CYP3A, CYP2C9 or the paracetamol conjugation enzymes."


[1] https://www.ncbi.nlm.nih.gov/pubmed/28185326
[2] https://www.ncbi.nlm.nih.gov/pubmed/28939403
[3] https://www.ncbi.nlm.nih.gov/pubmed/26023568
[4] https://www.ncbi.nlm.nih.gov/pubmed/28185326
[5] https://www.ncbi.nlm.nih.gov/pubmed/29063362
[6] https://www.ncbi.nlm.nih.gov/pubmed/17701559
[7] https://www.ncbi.nlm.nih.gov/pubmed/21477634
[8] https://www.ncbi.nlm.nih.gov/pubmed/25149996
[9] https://www.ncbi.nlm.nih.gov/pubmed/28352353
[10] https://www.ncbi.nlm.nih.gov/pubmed/23313550
[11] https://www.ncbi.nlm.nih.gov/pubmed/24388894
[12] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3458266/




This itself functions as a bioavailability enhancer.


Ginger has also a broad anti-inflammatory properties and may be useful in auto-immune conditions including MS. Ginger and its constituents, such as 6-gingerol, 6-shogaol, 6-paradol, zingerone, and dehydrozingerone, are effective for ameliorating the neurological symptoms of neurodegenerative conditions.

Ginger and neurodegenerative disorders:



Edited by Alchemica
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I started growing turmeric for this reason, The plants are still taking off so i'll be interested to know/ notice some effects.

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Same here. I bought a few small pieces of rhizome from the local green grocer. (wasn't cheap!)

I broke it up and planted it all in spring,  and all but one of the 8 sprouted. 

It's going well now,  probably ready to dig some up. 


Anyone got any favourite recipes? Preferably quick and easy B)

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I've been continuing this quite awhile hoping it would make a standalone anti-depressant option for me. The seasonal shift has been intense for me. If anything, it's brought some stability but actually confronted me with new levels of existential distress


That classic K10 question "how often did you feel worthless" so pressing... this scary crushing sense of my mortality imbuing this impetus to do things worthwhile and positive even when things are a struggle. Normally, I'd be in quite a suicidal state, where you're actually encouraging that process of death to hurry up but when you start seeing the bigger picture, in a more clear-headed and less pathological state of mind...


Coming out of that seemingly super-inflammatory state - I strongly believe inflammatory mediators, as research suggests, strongly promote a general trade-off towards focusing on immediate (often maladaptive) versus delayed (often more eudaimonic) outcomes while leading from everything to mood issues, anger problems to impulsivity - has been strange, not being pepped pathologically, forcing me to be reconsidering what the hell I'm doing with life. It's not easy finding that meaning, purpose and contribution when you're not feeling the greatest but I'm trying to make small positive vibrational shifts.

Probiotic turmerics, even with saffron, is not providing good stable uplift - Been sticking with it, hoping the mood support would be adequate.. It's easing some symptoms but the mood has been incredibly 'sanely depressing'. Been trying to give the anhedonic, anergic, apathetic moods a kick in the arse by keeping up exercise (it's reduced in vigour as I'm just so drained), gardening and exerting meaning and purpose but it's not working very well.


 Been chipping away at incremental meaningful stuff but plagued by quite an intense and anergic dysphoria, at best anhedonia - what I was trying to keep on top of and had slight success for a bit... Been painfully fighting the inner death drive with lots of potting up plants for others and propagating things that will hopefully cope with the weather, sounds small but all I can manage. The "life output" trays are filling up again, trying to give the barrage of morbid looping thoughts the finger but it's a battle.


Trying to assert some simple meaning and break my mind from the loops of depressogenic thoughts, maintain some behavioural activation even though it's so energetically hard, haven't had a energetic shift like this in a long time. Been a long time without my serotonin transporters occupied and continual serotonergics... finding aiming for the social can amplify things the wrong way at the moment, yet trying to not get extra disconnected.

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Good work man, i drink turmeric tea most everyday as well, The thoughts of death are not morbid in my view, i say embrace who you are whatever that is, by frequently embracing the strong emotion of death i feel i am gifted with courage to do anything that i will, to explore deeply and look deeply, face all things in waking life and the dream space.Gardening is good and  I find Buddhist books give me some grounding, its good to learn some simple bar chords on the guitar and scream with them lol, or listen to this -

I have learned to embrace how i feel but at the same time not attaching to them, knowing the emotions and thoughts are not what or who i am but what i am internally experiencing, that experiencing is not what you think it is, it just is, if you think what it is then you are condensing the experience down to a thought. All is transient so when feeling super low or dark remember you are not that feeling and the feeling no matter how long or persistent is still transient there for not really anything to worry much about, even if you worry you are not worry but experiencing worry, i think this way or view is very convenient for deep thinkers. No need to rush to something that is inevitable, take it easy and take a good proper look around you, look at your hands, take it all in deeply, this shit is hardcore awesome, so don't you clock off on us ya bastard : ) Keep up the good work ma brother




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I needed a bit of extra help with my mood over winter so went back on a minimal SSRI dose. Recently, I've been cautiously exploring how things like turmeric and saffron to go with that SSRI, which I don't find alone effective. The spices etc seem quite tailorable to be used to 'level up' when mood needs a more acute lift.


. I've explored conventional pharmacotherapy extensively, shifting thinking/psychological stuff and other strategies, with little sustained benefits, at many times the side-effects of conventional pharmacotherapy caused more problems than solutions and sent me off dangerously self-medicating. Also I've explored herbal options too, finding some that some helped somewhat with excellent side-effect profiles.


I'm currently giving the synergy of healthy dietary phytochemicals and minimal Western medicine a go. Does it hold promise, the best of both worlds for treatment resistant conditions? I still side with improvements being bio-psychosocial-spiritual but if you're biologically bed-ridden/housebound with debilitating symptoms, you can't tackle the other dimensions properly.


One thing I'll say, is conventional pharmacotherapy as a standalone for mental illness is poorly effective for MANY people. Even coupled with psychological stuff. That said, our plant medicines aren't panaceas. Diet doesn't cure everything.


The medicinal spices had enough potential merit, tolerability, evidence-base and safety to make it something worth considering as continued tools, especially useful for milder symptoms but efficacy waned relying on it as standalone for myself, as things like my fermented turmeric concoctions. While curcumin alone shows antidepressant efficacy, supplementary administration of curcumin to antidepressant therapy may reverse the development of depression and enhance the outcome of antidepressant treatment, also offering more rapid relief of depressive symptoms [1]. Same with saffron, it's got me through some really dark times off antidepressants but once again, efficacy waned for mood. Saffron did seem unique for psychotic spectrum stuff, crocins not only modulate the HPA axis and NMDARs but the DAergic system in a way that may be of relevance for schizophrenia-like behavioural deficits. These spices are useful tools and seem to have limited potential for interactions with SSRIs. While saffron is useful alone, showing efficacy equal to SSRIs [2], saffron could effectively prevent reaching the criteria of metabolic syndrome [3] and it significantly augmented SSRIs, both reducing side effects [4,5] and augmenting efficacy [6]


I normally use bulk Iranian saffron but spotted a cheap Saffron + Curcumin (BCM-95, which is turmeric volatiles enhancing the bioavailability of curcumin, so piperine interactions with pharmaceuticals aren't problematic). I found I could kind of chase a saffron buzz a bit, as this product, I might be more sparing.


[1] https://www.ncbi.nlm.nih.gov/pubmed/26066335
[2] https://www.ncbi.nlm.nih.gov/pubmed/27701683
[3] https://www.ncbi.nlm.nih.gov/pubmed/24955550
[4,5] https://www.ncbi.nlm.nih.gov/pubmed/23280545 https://www.ncbi.nlm.nih.gov/pubmed/22552758
[6] https://www.ncbi.nlm.nih.gov/pubmed/25484177


My mood has been so pathological, absolutely crap, so I'm trying a few things at once. Got into waking early (partial sleep deprivation as needed), keeping up exercise and skipping breakfast and having ALCAR as a meal replacement.


have to tackle my body and brain at the same time particularly before they get even more out of whack, the two are linked. Things like saffron are established as being useful preventing metabolic abnormalities but ALCAR is cheap.


"Scientists have noted a connection between depressive disorders, primarily seen as brain-based, and, insulin resistance (IR), a modifiable metabolic pro-inflammatory state that is typically seen as peripheral. Treating IR can with drugs or behavioural interventions can ameliorate, or possibly prevent, depressive disorder and its long-term consequences including dementia at various stages of the life course.


Acetyl-L-Carnitine (LAC) is an endogenous molecule that regulates glutamate homeostasis and promotes healthy mitochondrial function, among other actions.


Acetyl-L-carnitine presents a significant link between altered peripheral and neural function in the context of stress and depression.

It has epigenetic action in reactivating neuroplasticity by restoring an inhibitory tone upon the release of glutamate driven by elevation of a stress-induced decrease in histone acetylation.


Administration is also known to ameliorate insulin sensitivity in patients with type 2 diabetes


Disruption of LAC function is an example of a molecular mediator that indicates a lack of resilience leading to negative outcomes. Indeed, epigenetic alteration of LAC is a marker of IR. Importantly, modulation of LAC levels is an example of capacity for flexible adaptation—thus LAC function can be reinstated and result in amelioration of changes associated with glutamatergic damage.


LAC supplementation while targeting IR (i.e., reducing peripheral hyperglycemia, hyperinsulinemia, and hypertriglyceridemia) leads to antidepressant-like responses seen after few days of administration, while responses to standard antidepressant medications require repeated weeks of administration in the same animal models"



Full text: http://sci-hub.tw/10.1016/j.neuropharm.2017.11.038


Quickly, that combination resulted in a good mood improvement and symptom reduction.

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Hey @Alchemica, good to see you here and posting - I'd been wondering how you'd been getting along. 

I have a little bit to share with regard to these topics but can't seem to put the words together right now.

Anyway, I didn't want to just "like" your post and leave it at that.


Take care

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Thanks for the kind words @Xperiment Likewise, had been wondering how you were traveling. Hope things are OK, feel free to chat with a message if ever needed. It's nice to not be in the continued pep of mixed weird moods, which turned into a bit of a nose dive, driven by grief and anger and other emotions I was struggling with in part but it's nice to get a day like today where I had the balance of positive mood, social contact, meaningful activity all working etc.

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Thanks,  yeah I managed to get some home grown turmeric out to a fellow member who was after some. I still have some in the ground if anyone here would like a few pieces. 


I've also been giving the herbal tea a good go. Mostly chamomile before bedtime,  with good results,  but also passion flower and others. I have developed a bedtime ritual in my head to get to sleep and so far so good at that end,  but still waking up exhausted!

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On 27/05/2018 at 7:25 AM, Alchemica said:

 - has been strange, not being pepped pathologically, forcing me to be reconsidering what the hell I'm doing with life. It's not easy finding that meaning, purpose and contribution when you're not feeling the greatest but I'm trying to make small positive vibrational shifts.


 ... finding aiming for the social can amplify things the wrong way at the moment, yet trying to not get extra disconnected.


Damn, I'd been struggling with this exact issue - knowing that I should be socialising, but finding the negatives (mostly from my own anxiety) keep outweighing the positive & so I can't escape the idea that I'm just making things worse for myself long-term, by creating/reinforcing all these negative associations... not sure how to break the cycle.


I'm even aware of the huge body of research into how social isolation impacts mental health, but a little voice inside keeps pointing out the flaws & blind spots of those studies, & insisting that they don't apply to *me*...:rolleyes:


Real health bullshit not helping - when I don't have the energy to even do basic chores, it's too easy to say "oh but of course I should postpone social activities until I'm feeling better" - but when that happens for 3 months straight it kinda starts to feel like an excuse no matter how serious the illness is.


I came here because I remembered you writing about overcoming anxieties to do social stuff & wanted to ask for some tips... sorry to hear you've been struggling too mate - happy the meds are a help for you.

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Da Fuck I miss this..... Excellent info


It's hard to be on top of your game when ya feel in shit. Sometimes your gotta go with it and at other times grasp it and say Fuck it and take it back.....no matter how Rinse and repeat. 


Keep the fire burning.... 

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Yeah, feel you on that, sorry to hear things are a struggle for you. I got disconnected again and the only way I've recently been able to reconnect is through plants. It takes my head off the social situation which is hard to manage with anxiety, social anhedonia and not finding common ground etc.

Churned out a bunch of Ashwagandha tubestocks through winter that did well in the greenhouse, ready for spring. Joined the local grow free group. I've been forcing myself to connect with new people, even strangers, by giving the plants away. It just makes an awkward social encounter more positive. A reason to try.

Just breaking that pattern of isolation through a plant can be potent. You can rebuild some social skills etc. Transfer interests from one domain to another etc

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