Alchemica

Mesembryanthemum cordifolium L.f. (syn. Aptenia cordifolia) Think there's some variety in colour

I've just mashed it and put it in a jar, sun fermented then oven dried (smells a bit...) before to get a usable powder as per herbalistics DIY Sceletium fermentation page. Bigger batches including roots were problematic with mold. I needed high doses to get effects but I'm a bit of a serotonergic hard head. I personally don't think you'd get enough of a dose via insufflation.

One I've heard of and seems to be very otherwise benign is Hibiscus/Rosella Rosella appears to be a safe and well-tolerated treatment option, which may have a place in the treatment of mild-to-moderate essential hypertension. Data suggests that it may provide comparable effectiveness to some pharmaceutical antihypertensive medications. [1]

Looking for various Tabernaemontana - divaricata, pandacaqui etc. Any that may be phytochemically interesting Message me if you have surplus Many thanks in advance

There may possibly be if someone has cancers etc, BDNF participates in the process of metastasis and in the migration of cancer cells . That said, exercise induces similar sorts of elevations of BDNF and it's generally considered wholesomely healthy

There'd likely be BDNF elevations [seen in animal studies here] and enhanced neurogenesis on chronic dosing (in line with the therapeutic activity seen in depression where case-studies note delayed improvements, eg 1-2 weeks, 10 days etc) from both the serotonergic effects and PDE4 inhibition

Trying to root up cuttings at the moment, if I have success I'll be in touch It's really annoying as it's a potent therapeutic and it would be good to have it remain therapeutically appreciated, rather than abused. It's made the list of the United Nations “plants of concern.” and features in some drug testing/analysis papers so probably be an issue soon [1].

"Based on the venation type, the species is mainly classified as either emarcidum or tortuosum types. In the emarcidum type, the leaf is more flat and the dried leaf venation pattern shows a central main vein with the curved secondary vein which branches off the main vein, reaching the leaf margins. In plants of the tortuosum type, the dry leaves are more concave and usually show about three to five or sometimes up to seven major parallel veins. The secondary veins run straight up to the apex on both sides of the middle vein." https://www.intechopen.com/chapters/53426 While the emarcidum is much easier to grow it seems to be devoid of mesembrine and instead comprised of 4'-O-demethylated mesembrine-type alkaloids [1, 2] which are poorly characterised pharmacologically. S. strictum seems to again have a different alkaloid profile centred on mesembrine and mesembrenone and is proposed to be useful based on that [1] https://doi.org/10.3389%2Ffnut.2022.819753 [2] https://www.intechopen.com/chapters/53426 Pretty sure the first one I have is emarcidum-type and the second tortuosum if that helps you ID.

Here's an interesting paper and some research I compiled: Essential Oils and Their Constituents: An Alternative Source for Novel Antidepressants Calamus oil: β-asarone produces an antidepressant effect, increases TH and could promote expression of GDNF, BDNF, and CNTF genes. β-Asarone functions as a neuroprotective effect in both in vivo and in vitro models of PD. α-asarone or β-asarone potentiated the NGF-induced neuronal differentiation. The antidepressant-like effect of α-asarone could be mediated through both noradrenergic (α1 and α2 adrenoceptors) and serotonergic (particularly, 5-HT1A receptors) systems. α-asarone effectively modulates microglial morphological dynamics, this effect of α-asarone may functionally relate to its influence on neurogenesis. α-asarone improved m1 mAChR expression and ACh levels, and attenuated the increased AChE activity in a mouse model of FXS. β-asarone antagonised Aβ neurotoxicity in vivo and improved the learning and memory ability. β-asarone might be effective for the treatment of AD Chamomile - anxiolytic: Bisabolol (α-(-)-bisabolol) is a sesquiterpene which is a part of the essential oil of a variety of plants, but its common source is German chamomile. It is a potent GABAAR modulator at the BZD site - the anxiolytic-like activity of bisabolol occurs via the GABAergic but not serotonergic transmission Copaiba oil: Anti-inflammatory, analgesic, anti-addictive, antidepressant etc. ~50% β-caryophyllene. CB2 agonist, PPARγ modulator. Regulates μ opioid receptors increasing analgesic effects, alters expression of 5-HT2ARs, activates TrkA receptors mimicking NGF exerting antidepressant effects. Frankincense: Contains significant quantities of α-pinine which is anxiolytic via GABAA BZD site modulation, antiinflammatory (PGE2) and memory enhancing via AChE. Also in rosemary EO. Also contains the psychoactive incensole acetate which is a potent TRPV3 agonist that causes anxiolytic-like and antidepressive-like effects. Jasmine: Contains methyl jasmonate. Antidepressant effects, established in animals, may be related to suppression of oxidative stress and release of TNFα. Recently, it has been discovered to have anti-psychotic activity, suppressing pro-psychotic activity of dopaminergics and NMDA antagonists: MJ demonstrated antipsychotic-like property via mechanism related to its antioxidant property and interference with dopaminergic neurotransmission It has strong anti-neuroinflammatory activity and suppresses memory dysfunction in mice. MJ also suppressed the expression of COX2, iNOS and NFκB. It has anti-amyloidogenesis-like effects. Lavender - contains linalool and linalyl acetate etc: Anti-convulsant, analgesic, potent anxiolytic. VDCC blocker, GABAA modulator, DAergic, glutamate/ NMDAR modulator, 5-HT modulator (particularly altering 5-HT1AR binding). 80mg orally as efficacious as lorazepam and paroxetine for GAD. (-)-linalool to stimulates opioidergic, cholinergic M2 and dopaminergic D2 systems, as well as interacts with potassium ion (K+)-channels. The effects of (-)-linalool on pain responses are mediated, at least in part, by the activity of adenosine A1 and A2A receptors and by the reduction of nitric oxide (NO) production/release, probably through mechanisms involving opioidergic, cholinergic and/or glutamatergic systems. Reverses the effects of stress at the transcriptional level on inhalation, increasing things like oxytocin. Lemon - limonene reversed increased immobility time in the FST induced by neuropathic pain in rats. The putative mechanism by which lemon oil produces antidepressant-like effects seems to be mediated by 5-HT and dopamine neurotransmission. The pretreatment with buspirone (5-HT1A partial agonist), DOI (5-HT2A receptor agonist), miaserin (5-HT2A/C receptor agonist), apomorphin (nonselective dopamine receptor agonist) and haloperidol (nonselective dopamine receptor antagonist), blocked the antidepressant effects of lemon oil. Moreover, the acute inhalation of this oil significantly increased dopamine contents in the hippocampus and 5-HT in the prefrontal cortex and hippocampus. As commented before, dopamine and 5-HT are intrinsically involved in the modulation of mood states, and hippocampus and prefrontal cortex are the main stages of this action. Thus, the antidepressant-like effects of Citrus limon oil might be mediated by limonene. Indeed, modulation of 5-HT and dopamine neurotransmission in brain areas highly involved with mood states could be on the basis of the antidepressant effects of lemon oil. Limonene also seems to have effects on adenosine receptors. Oregano - contains carvacrol - antidepressant and antiinflammatory/ PPARα/γ dual agonist, TRPV3 agonist, modulates DA and 5-HT, decreases COX expression Patchouli: Antidepressant. This aroma oil exposure may modulate the blood platelet serotonergic regulation through MAOA depending on the dose, duration, and conditions of exposure. Patchouli alcohol exerts antidepressant effects orally. Piper: Piper species are considered to play a role in alleviating neuronal ailments that are associated with inhibition of acetylcholinesterase (AChE). Sesquiterpenes and phenylpropanoids were found to be rich in these EOs, of which asaricin, caryophyllene, caryophyllene oxide, isospathulenol, (+)-spathulenol, and β-bisabolene are the major constituents. The EOs from the leaves and stems of Piper austrosinense, P. puberulum, P. flaviflorum, P. betle, and P. hispidimervium showed strong AChE inhibitory activity with IC50 values in the range of 1.51 to 13.9 mg/mL. A thin-layer chromatography (TLC) bioautography assay was employed to identify active compound(s) in the most active EO from P. hispidimervium. The active compound was isolated and identified as asaricin, which gave an IC50 value of 0.44 ± 0.02 mg/mL against AChE, comparable to galantamine with an IC50 0.15 ± 0.01 mg/mL. Spearmint (Mentha spicata) and caraway (Carum carvi) essential oils - sodium channel antimanics: Contain ®-(-)-carvone and (S)-(+)-carvone which prevent mania in animal models. (S)-(+)-carvone decreased spontaneous locomotor activity in sleep deprivation experiment, indicating a sedative effect while ®-(-)-carvone is not sedating Some Australian Natives I love:

I used to think more was better particularly as there seems to be dose-dependent increases in DA levels but then noticed low doses cumulatively ie a pinch seems better... and likely safer as increased doses seem to come with notable toxicity. Not sure where the cut off for CNS toxicity is but considering the clinically used doses are low and they seem effective, maybe wise to keep to lower doses? " saffron constituents such as crocin, crocetin and safranal can exert antioxidant or toxic effects depending on their endogenous concentration. " [1]

I made lavender + chocolate once... the taste was intense! (questionably tolerable, I wouldn't want to make an oral spray with it!) 80gm raw cacao butter, 1 tablespoon virgin coconut oil, 3 tablespoons raw agave nectar, 800mg Lavandula angustifolia EO, 55 g Criollo (organic) cacao powder, 4g L-theanine, 2g L-tryptophan. The last three mixed well together until homogenous prior to addition. Melt the cacao butter, coconut oil over a pot of boiling water, stirring all the time, add agave and stir in to combine, add lavender oil and then add cacao powder + L-theanine + L-tryptophan stirring till lovely and smooth and shiny. Allow to set 20 x serves. each providing 200mg L-theanine. 40mg L. angustifolia EO* and 100mg L-tryptophan. 1-2 should calm a stressed body *80mg is as efficacious as paroxetine and lorazepam for generalised anxiety in some studies. I'd probably just try lavender first and skip the calamus and add some other calming stuff but up to you! I'd just try saffron gummies, the alcohol will evaporate off which is good and I'd guess it could survive 100deg C for a bit. Play around with the mint geranium. I like glycerites as I avoid alcohol, maybe you could mash up some leaves in some glycerine and pour off?

You're correct on anions being negatively charged ions, while cations are positively charged ions. Air Purifiers: Ionic and Ionizers, Are They Bad for You? - Molekule Blog It seems ozone might have some detrimental effects on plant growth see: CO2 Science Do Air Purifiers Help Plants Grow? Can They Be Bad For Plants? (ionizerhub.com)

Not sure if Adelaide is what you're after location wise. I haven't personally noted it dying down except if it got sunburnt then it stunts. I tend to get plants like this: I keep the leaf as it seems useful (but tastes horrible) - I make a glycerite to cover the taste a bit The leaves possess higher content of active withanolides, Withaferin-A and Withanone, as compared to the roots [1]. Nootropic and CNS therapeutic properties of the leaf have been claimed [2]. Withaferin-A is a potent leptin sensitiser with additional antidiabetic actions and resulted in a 20-25% reduction of body weight in overweight mice [3]. It improves insulin sensitivity [4]. Anti-neuroinflammatory properties have been ascribed to the leaf [5] along with neuroprotective properties [6] Withaferin-A shows anti-neuroinflammatory [7] anti-Aβ properties [8] and dopamine-restoring [9] properties. Improvement of cognitive dysfunction has been ascribed to Withanone [10] including inhibition of AChE, anti-Aβ, protection against oxidative stress and anti-inflammatory effects. Many toxicological studies have demonstrated that Ashwagandha, in its reasonable dose, is a non-toxic, safe and edible herb - despite that, there is sometimes movement away from the cytotoxic constituents towards root extracts which may be less effective [1] https://www.ncbi.nlm.nih.gov/pubmed/27936030 [2] https://www.ncbi.nlm.nih.gov/pubmed/26361721 [3] https://www.ncbi.nlm.nih.gov/pubmed/27479085 [4] https://www.ncbi.nlm.nih.gov/pubmed/30417321 [5] https://www.ncbi.nlm.nih.gov/pubmed/27550017 [6] https://www.ncbi.nlm.nih.gov/pubmed/25789768 [7] https://www.ncbi.nlm.nih.gov/pubmed/26266054 [8] https://www.ncbi.nlm.nih.gov/pubmed/30356847 [9] https://www.ncbi.nlm.nih.gov/pubmed/30544122 [10] https://www.ncbi.nlm.nih.gov/pubmed/29108796

Either they had it in a sealed vessel under pressure, or were using a different solvent. I'd personally suggest, if you want to explore, just downing a few high α-acid hop pellets and seeing if it's your thing. I used about 3g dried pellets, not sure the best dose to use but you want to skull them down to avoid tasting them at all personally I was just giving you my notes, I was interested in the iso-α-acids for a bit for their different CNS profile but they are SO BITTER at the required doses you'd have to be really masochistic. The brew was horridly hard to drink! Maybe if you isomerised them, dried it out and capped it up it would be ok

The main actives are normally considered to be withanolides which are steroidal lactones ie more fat soluble so it's likely to primarily be the ethanol that extracts them. For a very crude extraction: Drying and powdering the root first helps. I'd do alcohol first as that's likely to be the best solvent and maybe the only one needed? Sit the dry, powdered root (weigh it first) in sufficient warm ethanol and leave to extract. As for how much, depends how much you have to spare! Pour off the ethanol filtering through something - I use a hop brew straining bag to filter it, if you fold it over itself a few times you get a good filter for bulk herbs -saving the filtrate and repeat again, extracting the root material, if possible with a second lot of alcohol. Wash the material in the filter with some alcohol too. Carefully evaporate it and dry to resin/powder. You could repeat using boiling water to extract (boil it in water, filter, evaporate to leave resin, dehydrate to powder) Filter bag: That said, it seems the best solvent is 50:50 alcohol:water as a single extraction solvent: "The maximum extract yield and the total withanolide and phenolic content were obtained from aqueous alcoholic compositions at 50:50 (v/v), 70:30 (v/v), and 100:0 (v/v), respectively" so maybe a single extraction with 50% ethanol is better than doing two separate extractions! On Ashwagandha, if you're not averse to alcohol, you could also try an ashwagandharishtha-style preparation [1]. It's a really pleasant way to take the medicine, if you don't mind the interesting flavour. "Emerging evidence suggests the ability of fermentation to enhance the bioactivity and therapeutic potential of traditional medicines. Indeed, the fermentation was shown to increase the availability of the active molecules and to eliminate the undesired compounds." Ashwagandharishtha is a liquid polyherbal formulation traditionally prepared by fermentation process using the flowers of Woodfordia fruticosa. It contains roots of Withania somnifera as a major crude drug. Alcohol generated during the fermentation causes the extraction of water insoluble phytoconstituents. Yeasts present on the flowers are responsible for this fermentation. I simply fermented ashwagandha root etc with added yeast and sugar. [1] https://doi.org/10.1016/j.imr.2013.04.002 [2] https://www.ayurmedinfo.com/2011/06/27/ashwagandharishta-uses-ingredients-dose-and-side-effects/

Just a simple extraction using both alcohol and boiling water as two different solvents (ie doing the extraction once with alcohol, then following up repeating with water). Most of the constituents in things like Passiflora and Skullcap seem to be flavonoids so it seems to suit such. Only do it if you like the effect of the particular herb - try it in unextracted form as a higher dose first - just makes dosing more convenient. Hops I used to just eat the hop brewing pellets, either as is or boil them for awhile to isomerise it Here are some of my notes, sorry for the over-detail. Hops increases GABA levels. The typical use for hops is for sleep disturbances and mood disorders, such as anxiety and restlessness. Data from in vivo studies in rats have shown that a hops extract and its fraction containing alpha-bitter acids (humulones) exert significant sedative and antidepressant effects, whilst hops beta-acids (lupulones) appear to also exhibit antidepressant activity with fewer sedative effects, probably by affecting gamma-aminobutyric acid (GABA) neurotransmission activity. Moreover, in vitro binding experiments have shown that hops interact with certain serotonin (5-HT6) and melatonin (ML1) receptor subtypes, which are involved in various CNS functions related to stress activity, relaxation, circadian rhythms and sleep. Zanoli et al. have investigated the in vivo and in vitro effect of hop beta-acids on central nervous system function and suggested an antidepressant-like activity. Behavioral effects of beta-acids fraction were explained by a modification in the GABAergic activity. That said it contains a highly potent phytoestrogen 8-prenylnaringenin)]. Terpenes likely add to the effect eg myrcenol, which is produced from myrcene during boiling hops Iso-α-acids Iso-α-acids prevented hippocampal inflammation and cognitive impairment and seem particularly effective for the suppression of inflammation-induced depression-like behaviour and appear to do this in part via activation of the vagus nerve, which can in turn improve depression-like behaviour, as a safe and novel approach for treating depression Generally the bitterness induced by effective doses of iso-α-acids precludes their acceptance but they have been shown to a) safely reduce body fat b) improve cognition in metabolically induced cognitive impairment and c) improve working memory I used Galaxy 15.7% α-acids "The rate of conversion of α-acids to iso-α-acids was highly dependent on temperature. For typical 100°C boiling conditions, 77% of alpha acids were isomerized within 120 min. Temperatures of 130 °C isomerized 100% of alpha acids within 30 min of heating. A 90 min boil at 100 °C corresponded to a final iso-alpha acid concentration equal to 60% of the starting alpha acid concentration" The α-acids fraction can be considered as the major responsible constituent for the enhanced GABAergic action and for the antidepressant property The bitter iso-α-acids: - improve health by influencing lipid metabolism, glucose tolerance, and body weight - could be effective for improvement of working memory potentially through enhancement of dopamine release - consumption prevents inflammation in the hippocampus and ameliorates age-related cognitive decline - can suppress hippocampal inflammation and improve hyper neural activity - suppress neuronal damage and depression-like behaviour induced by inflammation Hop β-bitter acids (lupulones) also show antidepressant-like effects. Lupulones are activators of TRPC6, which mediates antidepressant activity The fraction containing β-acids needed a dosage approximately 6 times higher than that of α-acids for sedative effects

Agreed, there's wild variability. For herbs, I settled on doing very simple alcohol/water extracts on raw herbs as it provided a more reliable effect outcome. Even simple water/alcohol dual extracts reduced to a resin then oven dried/dehydrator at lowish temps often leave generally effective extracts, often found they reduced to around 7X extracts after filtering all solids out and evaporating. It's easy to get imported extracts that are super questionably even what they say they are As far as kava, for the better one I've found at chemists (it's not great but find it better than others) is 'Bioglan' capsules that contain an extract powder that is better than nothing and can add to herbal synergies when better stuff isn't available. Another one I've explored in the past but forgot to mention is Californian Poppy root. "...rather than disorientating the user, it tends to normalise psychological function" Both aerial parts and roots contain alkaloids, the latter being MUCH richer (1.6-2.7%) Traditionally used for several disorders “Reactive, agitated and masked depressions, melancholy, neurasthenia, neuropathy, organ neurosis, vegetative-dystonic disturbances, imbalances, constitutional lability of the nervous system”, as well as a sleep-inducer and sedative tea. Relative safety is evidenced by traditional use of the plant, which can be found in the European market for more than 30 years without any safety concern. Affinity for the benzodiazepine receptors and alkaloids increase the binding of GABA to GABA receptors Binding to 5-HT1A and 5-HT7 receptors

I tried to rank some subjectively on potency once recently and came up with this list: Lemon balm < Lower dose Passiflora < Lower dose skullcap < Zizyphus seed < Hops = Valerian < Oral lavender oil 80-160mg = lower dose kava = low dose CBD < Erythrina mulungu < Higher dose 25g+ Passiflora < CBD 600mg + < Higher dose skullcap < High dose kava. Some I haven't found overly notable despite evidence base eg Galphimia glauca Things like saffron, lavender, passionflower etc appear to be worthy of consideration for the treatment of depression and anxiety with minimal risk of serious side effects. Even years after abstinence from alcohol etc, still find the Passionflower comparatively mild unless the dose is high. The skullcap seems more notably anxiolytic but I still require higher doses than normal. As my 'chill' blend I used 300mg kavalactones + Skullcap and Passiflora [both dual alcohol/water extract] In a study of herbalist preferences for anxiety reduction, the overall the herb of choice was S. lateriflora It had notable effects in reducing subjective anxiety scores [1] S. lateriflora may be superior to pharmaceutical anxiolytics in its ability to produce mood enhancing effects without side-effects such as a reduction in energy or cognition or causing fatigue [2] [1] https://pubmed.ncbi.nlm.nih.gov/12652886/ [2] https://pubmed.ncbi.nlm.nih.gov/23878109/ If it's OCD-like you might consider saffron: Saffron (Crocus sativus L.) has demonstrated antidepressant effects in clinical studies and extensive anxiolytic effects in experimental animal models. It reputedly has acute effects. Saffron is a potential efficacious and tolerable treatment for major depressive disorder with anxious distress. It increased mood, reduced anxiety and managed stress without side effects, offering a natural alternative to standard treatments and likewise has effects comparable to conventional pharmacotherapy for OCD. It has been used to augment and reduce side effects of SSRIs. .

Thought I'd share how Eremophila are currently being studied Biodiscoveries within the Australian plant genus Eremophila based on international and interdisciplinary collaboration: the results and perspectives on outstanding ethical dilemmas Personally, the most interesting finding was DAT modulating compounds from E. oppositifolia The latest (unpublished) results comprise the identification of compounds isolated from Eremophila species, capable of both potentiating and inhibiting the transport of dopamine The search for novel ligands from Eremophila species targeting neurotransmitter:sodium symporters Abstract: The family of neurotransmitter:sodium symporters (NSSs) mediate rapid re-uptake of neurotransmitters released to the synaptic cleft making them important determinants of neuronal communication. Accordingly, drugs that modulate their activity are central for the treatment of many neuropsychiatric diseases, such as depression, attention deficit hyperactivity disorder (ADHD), anxiety and narcolepsy. However, many patients do not respond adequately to the current drugs. Others stop the treatment due to severe side effects. In addition, high-affinity inhibitors for many NSS proteins are still to be found. Here, we present results from purified compounds and extracts from Eremorphila species for their activity towards the dopamine transporter (DAT). We find that the addition of the branched chain fatty acid KU030-14 potentiated DAT transport of dopamine. We also found several extracts that inhibited DAT activity. Taken together, we find it possible that Eremorphila species contain one or more active compounds towards DAT and possibly also other NSS proteins. https://synbio.ku.dk/calendar/2019/1st-cross-continent-eremophila-conference/speaker-information/

New Discoveries in Magic Mushroom Enzymes - Psychedelic Science Review (psychedelicreview.com) Fungi seem to have different enzymes that hydroxylate the indoleamines at the 4 position (tryptamine-4-monooxygenase), whereas other metabolic pathways lead to 5-OH (eg enzymes like tryptophan-5-hydroxylase) If you consider the numbering on the indole nucleus that might help you get an idea of the way it's numbered Consider changing the hydroxyl position from 4-OH to 5-OH changes a major part of the molecular structure that allows different binding characteristics to different receptors Take for example serotonin (5-OH-tryptamine) binds something like this to 5-HT2ARs Psilocybin binds more like this Consider how it changes the location of the hydroxyl group to allow different strength intermolecular forces with receptor proteins causing different binding profiles An important determinant of the neurobehavioral responses induced by a drug is its relative receptor selectivity. These different molecular structures allow different receptor binding profiles eg Psilocin: 4.00 5ht2b, 3.40 5ht1d, 3.37 D1, 3.03 5ht1e, 2.88 5ht1a, 2.83 5ht5a, 2.82 5ht7, 2.82 5ht6, 2.67 D3, 2.52 5ht2c, 2.19 5ht1b, 2.14 5ht2a, 1.77 Imidazoline1, 1.74 SERT, 1.57 Alpha2B, 1.36 Alpha2A, 1.03 Alpha2C where higher numbers mean higher binding. A 5-OH vs a 4-OH will change the profile of receptor binding

Can chuck some blue corn and Glass Gem Rayaa in an envelope no cost just PM me. Also Oaxacan Green Can't guarantee viability but chuck it in the ground and see I'll have more purple corn soon hopefully as a late crop is almost nearly done. Also have maybe 10 Glass Gem Rayaa corns I picked slightly too early, you're welcome to them if you can use them experimentally for your bourbon

I can give you Centella asiatica [1] (what I was sold as C. asiatica) and what I think is Centella cordifolia (Swamp pennywort) [2] Let me know if they're suitable 1. 2.

I'd suggest Sacred and herbal healing beers: the secrets of ancient fermentation as a starting point. I've PM'd the link If you wanted to get technical, I tried to brew with things early in the mix if I wanted to encourage potential bioconversion of actives, or add them later if the actives were likely to be degraded to less active metabolites. You could consider if the actives are likely to be destroyed, or bioconverted to more potent ones with a bit of research "...fermentation could be considered as a potential technology for releasing phenolic compounds from natural resources, as well as for producing new bioactive compounds. The ability of fermentation to improve the yield and to change the profile of phenolic compounds is mainly due to the release of bound phenolic compounds, as a consequence of the degradation of the cell wall structure by enzymes produced during fermentation." [1] The simple recipes simply use things like: Lemon BaIm AIe 4 pounds dark brown sugar 3 gallons water 1/2 pound dried lemon balm herb yeast Boil 3 gallons water with 8 ounces dried lemon balm herb and 4 pounds sugar for one hour; skim off scum. Let cool and strain into fermenter. Add yeast. Ferment until complete; 7 to 10 days. Prime bottles, fill with beer, and cap. Ready to drink in one to two weeks.

Back to playing with essential oils... There's some new papers Exploring Pharmacological Mechanisms of Essential Oils on the Central Nervous System A Review of the Potential Use of Pinene and Linalool as Terpene-Based Medicines for Brain Health The main oil I've been diffusing is Eucalyptus because it's not only cheap but it seems to have some neat benefits on paper. Also fond of lavender still. 1,8-cineole can elevate synaptic 5-HT levels by increasing the releasable synaptic pools of 5-HT, exocytosis and levels in the synapse and is a novel therapy for treating depression [1] It has anti-inflammatory and antioxidant effects. It is proposed to be a NMDA antagonist and AChE inhibitor [2] with plasma 1,8-cineole concentrations correlated with cognitive performance [3] Increases in dopamine release with exposure to 1,8-cineole and eucalyptus oil were 241 ± 29% and 182 ± 16%, respectively [4]

There's initial human studies on some of the probiotic strains used in commercial kombucha's eg Bacillus coagulans GBI-30, 6086 Clinical studies showed that consuming BC30 helped alter the gut microbiome by increasing the numbers of beneficial bacteria, and ex vivo testing of blood from elderly humans who had consumed BC30 for 28 days showed increased anti-inflammatory cytokine responses. Results from a recent clinical trial suggest that the consumption of BC30 supports exercise performance and helps reduce exercise-induced muscle damage. Cell walls from the live B. coagulans GBI-30, 6086 strain have demonstrated immune modulating and anti-inflammatory effects in vitro. The immune-modulating effects of the BC30 strain were associated both with the cell wall fraction and with the metabolites produced by the live bacteria in vitro. It has shown benefit in IBS and rheumatoid arthritis