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Onemorestep

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Everything posted by Onemorestep

  1. I wouldn’t be surprised if your glutamate/gaba ratio is out of whack. Kava helped me with this but it’s not a perfect solution. I used root of happiness kava. i would experiment with naltrexone. When I drink, I get rebound anxiety even after one heavy night. Naltrexone takes care of 80-90 percent of that anxiety. Why? Who knows. Opioid receptors play an important role in disassociation and thus anxiety. also, I would take DHM when you drink. It will help with your hangovers and help prevent your gaba receptors from getting fucked.
  2. I too have had feeling of being “cured” by valerian. What I did not know is that valerian is just a benzodiazepine drug that occurs in nature. Keep us updated on how you’re faring! Would love to see this as a success story
  3. Ambien is in a class of non-benzodiazepine drugs colloquially know as “z-drugs”. It works through positive allosteric modulation of gaba-a receptors just as benzodiazepines do. Remember, just because something cannot technically be called a benzodiazepine drug due to its structure, does not mean it isn’t, for all intents and purposes, a benzodiazepine drug. Ambien comes with all the same nasty withdrawal effects that normal benzodiazepines do. And, like many benzodiazepines, it will drastically increase the likelyhood you will experience some form of dementia later in life if taken for an extended period of time into old age. Hell, even if started in old age it will do this. Seniors who start any benzodiazepine drug have a 50% high chance of developing dementia within 3 years of starting the drug. So that’s how ambien is really just a benzo... and here’s how it’s waaaaay different from one: 1) ambien is one of e few benzodiazepine-like drugs that can cause hppd. Due to this, I would be incredibly careful with this drug. It is possible it will not trigger this in you the first time you take it, or the second, the 30th time, or at all. But, like hppd, you don’t always get the trigger on the first try. 2) Ambien has also been known to bring some people in semi vegetative states back to consciousness while they are on the drug. Why this happens? Who knows. But it certainly doesn’t happen with Ativan or clonazepam. Im certainly happy that you have found relief from a condition that has been ailing you. I too have had issues with insomnia and it can be very aggravating. I do recommend that people try more natural remedies to their insomnia before chemical ones. The brain is particularly good at instigating tolerance in the face of chemical sleep aids. It is inevitable and something I have seen with ambien frequently. It is not fun to have to take ambien or you won’t sleep for days until you do. if you are looking for ways to improve your sleep quality, these are the most important things I have found: 1) buy a blue light box for seasonal depression and use it year round. They are available on Amazon for very cheap. They are also lightweight, small, and portable. You need a box that creates 10,000 lux. If you use it for at least an hour before 11 am, you will receive an “melatonin dump” from your pineal gland in the evening of that day. It’s going to make you feel quite tired and you will want to sleep. The more you do this, the more reliable this effect becomes. Humans were meant to be outside in the mornings, and we rely on the angle of the sun hitting the atmosphere to produce blue light for our circadian rhythms.... but only in the morning. This is why people say screens are so bad for your sleep. It tells your brain it’s morning and to not release melatonin. 2) only use your bed for sleeping. If you can, only use your ROOM for sleeping. Do not watch television in bed. Create a habit where the second you get into bed, your brain knows it’s time to sleep. 3) try to fall asleep by 10pm. Your brain receives its deepest sleep between the hours of 10pm and 2am. This sleep can not be made up by extra hours at different times. 10 hours of sleep between 10pm and 8 am is infinitely superior to 10 hours form 2 am to 12pm. There are plenty more things that can help you sleep better that will not harm you! These are the three most important things for me though. hope this helps oms
  4. Definitely do not want to overdue it! I find if I do a dose of 20,000 every week or so I’m fine. Or max 5,000 a day. I may be able to/need to take more though because I have a VDR mutation. I mainly posted this because I, like many Americans, do not get enough sunlight. I started to exhibit some pretty intense D deficiency symptoms very rapidly a few weeks ago. Extreme depression, anxiety, lethargy, orthostatic hypertension, shortness of breath you name it. 20,000 units of D later I felt like a human again. I do get bit by seasonal depression every winter no matter what. It’s never gotten this bad before though.... might have something to do with the 300,000mcg of methyl b12 I took one day
  5. Thought I should share this here: reduction in autoimmune disease via testosterone. There is some thought that HPPD could be immune related in some way. " In our study, we substituted testosterone levels in experimental autoimmune orchitis (EAO) in rat by s.c. testosterone implants. EAO development was reduced to 17% when animals were treated with low-dose testosterone implants (3 cm long, EAO+T3) and to 33% when rats were supplied with high-dose testosterone implants (24 cm, EAO+T24) compared with 80% of animals developing disease in the EAO control group. In the testis, testosterone replacement in EAO animals prevented the accumulation of macrophages and significantly reduced the number of CD4+ T cells with a strong concomitant increase in the number of regulatory T cells (CD4+CD25+Foxp3+) compared with EAO control. In vitro testosterone treatment of naive T cells led to an expansion of the regulatory T cell subset with suppressive activity and ameliorated MCP-1–stimulated chemotaxis of T lymphocytes in a Transwell assay. Moreover, expression of proinflammatory mediators such as MCP-1, TNF-α, and IL-6 in the testis and secretion of Th1 cytokines such as IFN-γ and IL-2 by mononuclear cells isolated from testicular draining lymph nodes were decreased in the EAO+T3 and EAO+T24 groups. Thus, our study shows an immunomodulatory and protective effect of testosterone substitution in the pathogenesis of EAO and suggests androgens as a new factor in the differentiation of regulatory T cells." https://www.jimmunol.org/content/186/9/5162
  6. Thought I should share this here: reduction in autoimmune disease via testosterone " In our study, we substituted testosterone levels in experimental autoimmune orchitis (EAO) in rat by s.c. testosterone implants. EAO development was reduced to 17% when animals were treated with low-dose testosterone implants (3 cm long, EAO+T3) and to 33% when rats were supplied with high-dose testosterone implants (24 cm, EAO+T24) compared with 80% of animals developing disease in the EAO control group. In the testis, testosterone replacement in EAO animals prevented the accumulation of macrophages and significantly reduced the number of CD4+ T cells with a strong concomitant increase in the number of regulatory T cells (CD4+CD25+Foxp3+) compared with EAO control. In vitro testosterone treatment of naive T cells led to an expansion of the regulatory T cell subset with suppressive activity and ameliorated MCP-1–stimulated chemotaxis of T lymphocytes in a Transwell assay. Moreover, expression of proinflammatory mediators such as MCP-1, TNF-α, and IL-6 in the testis and secretion of Th1 cytokines such as IFN-γ and IL-2 by mononuclear cells isolated from testicular draining lymph nodes were decreased in the EAO+T3 and EAO+T24 groups. Thus, our study shows an immunomodulatory and protective effect of testosterone substitution in the pathogenesis of EAO and suggests androgens as a new factor in the differentiation of regulatory T cells." https://www.jimmunol.org/content/186/9/5162
  7. Just a reminder to take your vitamin D! Almost have the population is deficient in the US and it’s hard to be happy without remember you need D + K2 at the same time for absorption and to make sure the calcium in your body goes into your bones and not your arteries. I use metagenics brand but there are plenty of others I’m sure are fine. https://www.amazon.com/Metagenics-D3-5000-120-Count/dp/B002D64I98 “Berridge conducted a study in 2017 which have evidenced that depression caused by an imbalance between excitatory and inhibitory pathways in the brain. Hypothesis argues that vitamin D reduces the increase in neuronal levels of calcium (CA +2) that are driving depression. Vitamin D plays a role in maintaining the expression of the CA 2+ pumps and buffers that reduce CA 2+ levels, which may explain how it acts to reduce the onset of depression [21]. In 2014, Gezen-AK et al. conducted a study which shows that vitamin D regulates the release of nerve growth factor (NGF), an essential molecule for the neuronal survival of hippocampal neurons as well as cortical neurons [22]. Di Somma et al., in a study, shows optimal levels of vitamin D in the bloodstream are necessary to preserve the neurological development and protect the adult brain [27]. Balanced dietary intake is a well-established lifestyle factor in maintaining cognition during ageing. A recent study shows that vitamin D helps in keeping cognitive function in older adults [28]. An interesting study conducted by Harrison et al. shows the association of vitamin D deficiency and the development of diabetes mellitus through paraventricular hypothalamic nuclei. It shows the positive relationships between them [29]. In November 2017, Kesby JP et al. conducted a study showing the effect of vitamin D on both widespread neurotransmitter changes (glutamine/noradrenaline) and regionally selective neurotransmitter changes (dopamine/serotonin). It concluded that developmental vitamin D deficiency leads to these brain changes [30-31]. Due to its effect on dopamine pathway in the brain, vitamin D can be a useful therapeutic agent used as an intervention therapy to be combined with existing treatments for Parkinson’s disease [32]. Staphylococcal enterotoxin B (SEB) is a superantigen and can initiate inflammation. Microglial cells in brain fight against these types of inflammation. Vitamin D deficiency affects the inflammatory process in the brain causing exposure of the brain to these vulnerable pathogens” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6132681/
  8. https://www.physiology.org/doi/full/10.1152/ajpheart.00683.2017 ”Minoxidil improves vascular compliance, restores cerebral blood flow, and alters extracellular matrix gene expression in a model of chronic vascular stiffness” interesting at the least. I’ve been helped by drugs that increase blood flow to the brain before. I used to take low dose coal is daily just because it made me feel better.
  9. I have taken Gaba before and noticed a slight effect--but I have a very permeable Blood Brain Barrier due to a slew of TBI's. There are gaba receptors in the body, but tbh i didnt notice much. It may increase growth hormone though. For normal people, Gaba is unable to enter the brain because it cannot pass through the protective barrier that separates the brain from the body. Thank god for that... else msg would kill you. Gaba would make you overdose. It would be very bad. The reason we develop drugs such as clonazepam is because they can get to the brain and increase gaba functioning. There are thousands of molecules that can work at receptor sites but only a few can get into the brain in the first place.
  10. "Furthermore, LEV restored the Glu/GABA ratio to approximately the control level and significantly increased the GABA concentration after the initiation of high-K+ conditions. Based on these data, LEV treatment restored the lost balance between the excitatory and inhibitory systems under basal conditions. Moreover, LEV showed a selective effect by preferentially increasing vesicular release of GABA, a mechanism by which LEV could reduce epileptic seizures." https://www.ncbi.nlm.nih.gov/pubmed/29331845 This isn't the first time i've come across data that shows Keppra is able to restore homeostasis to brain systems. I'm still searching for the other article I read about restoration of other systems besides inhibitory/excitatory balance. Since many people here appear to be in some sort of pre-epileptic state, this may be good to show your doctor if you are trying to get a prescription for keppra.
  11. I have read that taking b6 can help with the Keppra rage. I had a bit of it myself on keppra and regular old b6 basically made it go away.
  12. Good to hear it’s working out. You should look into antioxidants for the 6 hydroxydopamine metabolite. This is what causes the damage from amps. running cycles of bpc-157 while taking breaks from the amphetamines should help with any weird DAWS effects. memantine should help prevent tolerance. Can have side effects tho but not for all.
  13. The main issue I see with this is the effect doesn’t seem to be any different from taking a non gaba Maoi and adding gabapentin, which also works through inhibiting gabaT. Unfortunately, gabapentin comes with a slew of side effects for some and a pretty nasty withdrawal. From personal experience, I can say I never want to withdraw from it again. The relief it provides pretty much stopped after 8 months and it took me about a year to get off of it this was longer than I think most patients, but I was already working with a very screwed up gaba system from hppd and benzo withdrawal. This was a drug I looked into though and it is cool in my mind from a pharmacological aspect if it can be used short term or cycled it would be pretty sweet I think
  14. I can now handle some caffeine after about 6 years of healing and it is pleasurable/not anxiety inducing. If I smoke marijuana, this threshold decreases over time until it is no longer pleasurable and just causes anxiety. Being able to handle a small amount of things that I couldn’t at the onset of hppd took a LONG TIME OF ABSTINENCE. Your brain needs time to heal. Diego is correct that the general consensus is that it is bad. If you overdo it early on it can put you back several steps in healing.
  15. dopamine deficits are commonly seen in patients with hppd and may be an underlying influence in the symptomatology of the disorder. I have had extensive correspondence with a member of this website who has experimented with the pde7 inhibitor S14, which induce dopaminergic neurogenisis and reduces inflammation, to great success. I was wondering if anyone else here has tried this too? It isn’t exactly the easiest drug to acquire unfortunately. I do, however, have the source for synth that they used and am considering trying some. I had great benefit from bpc-157 on my dopamine system and believe that s14 could push that healing farther. I used a lot of amphetamines throughout my childhood an adult life as treatment for adhd. I noticed, after taking 2 years off them when I was 17 and then returning to them for 2 years, that I felt very different. Less able to get pleasure or motivation from the things pre amphetamine. This never really went away. Bpc helped, but I’d like to see if it can’t improve more. I’ve taken a big break from trying new things the last year and a half so I’m not sure I’m ready to jump in yet, but I am interested in people’s thoughts and opinions. below is a link about s14 cheers, oms https://www.researchgate.net/publication/312578151_Targeting_PDE7_by_the_small_molecule_S14_a_potential_disease-modifying_Parkinson's_disease_therapy_ready_to_start_clinical_trials and links about PDE7 inhibition: References/studies regarding PDE7 Targeting PDE7 by the small molecule S14: a potential disease-modifying Parkinson's disease therapy ready to start clinical trials https://www.research...clinical_trials PDE7 inhibitors as new drugs for neurological and inflammatory disorders https://www.research...atory_disorders Amyloid β-induced impairments on mitochondrial dynamics, hippocampal neurogenesis, and memory are restored by phosphodiesterase 7 inhibition https://alzres.biome...3195-018-0352-4 Phosphodiesterase 7 Inhibition Induces Dopaminergic Neurogenesis in Hemiparkinsonian Rats https://www.ncbi.nlm...les/PMC4449102/ Omeros Elucidates Mechanism of its PDE7 Inhibitors in Addiction https://www.prnewswi...-198935981.html Dual inhibitor of PDE7 and GSK-3-VP1.15 acts as antipsychotic and cognitive enhancer in C57BL/6J mice. https://www.ncbi.nlm...pubmed/22749842
  16. A patient died by they “think” titrating too fast? Jesus...
  17. Most add meds can cause a temporary (As long as used in small doses) spike in hppd symptoms. I found I had to stop the add meds I had been on my whole life because that spike was uncomfortable and anxiety inducing enough that my attention was worse on them than off. ritalin, however, is another beast altogether. It is the only ADD med on the market, as far as I know, that can CAUSE hppd. This has to do with Ritalin effect on the serotonin pool IMO. It is remarkably close in structure to cocaine, which caused a mild increase in hppd for me back in 2016. I have tried Ritalin once since getting hppd, and it really screwed up my brain chemistry permanently. I was doing great at the time and on Keppra (which was working better than I could have imagined; hppd was essentially gone). After a single 10mg dose of Ritalin the keppra no longer worked and I had an extreme relapse into hppd. interestingly, the Ritalin followed the same schedule as when I took lsd for onset of symptoms. I felt a little weird the following day but it wasn’t until day 3 that I had the return of hppd. It was the same with lsd for me and my onset. As for focusing, I’ve found a few things that help me. selegiline: 1-3mg per day orally. An MAOI that only effects mao-b when under 10mg. This drug attaches to the enzyme that “digests” dopamine which leaves more in the synapse. And since that digestion process is how you make norepinephrine and 5-hydroxydopamine (a toxic metabolite of dopamine) the effect is a smooth increase in dopamine and antioxidant effect without traditional adrenaline based anxiety. After 10mg, selegiline completely attaches to all mao-b enzymes to achieve full inhibition and then they start to attach to the less preferred mao-a. 10mg is a LOT Though and not comfortable to get to. Hell 5mg is too much for me. Too much dopamine which leads to anxiety. You will never need to go to a point where mao-a in being inhibited. mao-b inhibition, which provides dopamine, comes with none of the traditional dangers and food sensitivities you see with mao-a inhibition. You will not need to avoid foods on selegiline as you would with normal Maois on the market. the best (and worst) part about selegiline is there isn’t a comedown: your brain is constantly manufacturing the enzyme that breaks down dopamine. But selegiline binds to this enzyme PERMANENTLY. You will eventually excrete the inhibited enzyme and replace it with a normal one but this takes 2 weeks to do so fully. this sounds like a bad thing because who wants to be on an add med for two weeks straight? But that’s not what this is. Selegiline is prescribed as an antidepressant and doesn’t feel like a traditional add med. it has been the closest thing I have found to fixing the hypothesized dopamine deficit in add people instead of just doing a bandaid with harmful (and neurotoxic) amphetamines/amphetamine analogues. In fact it’s a healthy alternative; selegiline has been shown to increase lifespan when taken at 1mg daily due to its antioxidant effect on the dopamine system. selegiline builds up in your system because of what I explained about the enzyme inhibition. It took a few days of dosing for me to notice it. If you don’t like the medication in the early stages, you simply stop taking it and within 24 hours. If you stop after prolonged use, it can take a few days to lower. I have been on selegiline for 1 year to date as of thanksgiving. source: prescribed by doctor. You can however find it online in liquid forms but I have not looked. bpc-157: this has been the most important part of my recovery from a lifetime of add medication use. It is starting to look more and more like there is a semi permanent (and maybe permanent) post acute withdrawal syndrome associated with the use of ADD medication. Bpc has been shown to positively influence the dopamine sustem and being it back to its natural homeostasis. It’s so does this with the gaba system. this drug is responsible for a huge part of my recovery and has allowed me to regain motivation and even surpass that which I had before add medications. It has a remarkably safe profile and very few anecdotal negative reports with thousands and thousands of users. Unfortunately, One of the three serious negative reports I have come across is one this website. As far as I know, only myself and two others here have tried it. One of them had an extreme anhedonic reaction that has taken a lot of time to get better. I have some theories about what happened, but what will caution is that you SOURCE YOUR BPC CAREFULLY. The peptide industry is unregulated and anything that’s made in China is not to be trusted. I use American research labs for mine and have taken probably 10 vials worth from them, so take that for what you will. I’m actually on a cycle of theirs right now. I created a thread about bpc, where to find it, and how to use it on this website. Just search for it. source: American research labs nsi-189: this is an experimental antidepressant made by neural stem that failed its phase II (III?) clinical trials but only because they couldn’t prove it more effective than placebo, which is bullshit seeing as the placebo effect is very strong. And so is this stuff. I can’t tell you what the mechanism of action is since it’s proprietary, but it has had a very positive effect on my ability to experience pleasure and reward. This is a risk though, as nsi is not without risks and side effects for some. This medication requires a lot of research before taking so you know what to do if anything goes wrong. Through my own experience it feels excitatory but I do not know through which system. I do not take this everyday, as I am one of the unfortunate people that get anxiety through prolonged usage. I am still able to take it once a week in low dose however and have for about 18 months. source: originally online nootropics website that has since closed. I bought several years worth and have yet to put a dent in it. memantine: acts as an nmda antagonist and dopamine agonist. Can be used to reduce/delay the increase in tolerance to drugs. I use this for NMDA rebound about once a month. I started at once every two weeks, 3 mg. Now I do once every month at 3-10mg. This is primarily to boost glutamate signaling in the NAC (reward center of the brain) reward circuit which leads to more sensitized pleasure response. source: originally online nootropics website that has since closed; now I get it prescribed from doctor low dose naltrexone: I take 5mg of naltrexone daily to upregulate my opioid system and increase pleasure. Any more than this causes depression for me. I started this initially to reduce microglial based inflammation to great success and kept it in for the mood enhancement. source: originally online nootropics website that has since closed; now I get it prescribed from doctor dl-phenylalanine: increases dopamine and natural endorphins. Can be used in conjunction with selegiline to great effect. Needs to be cycled as tolerance builds rapidly. No withdrawal to speak of only diminishing returns. Source: amazon; bulk supplements all of these drugs are available to buy OTC but not in store (maybe do-phenylalanine). I do recommend you do your own research and consult with your physician. I’m not a doctor and can only say what has worked for me backed by scientific/anecdotal research. Ymmv as always. cheers, oms
  18. I had many qEEGs done and a Tailored form of TMS. The doctor said my qEEG was unusual and not only that but a Or today my brain was hyper resistant to the therapy which he had not seen in any patients and he was doing a clinical trial along with treating thousands of patients. He also said that depending on the time of day, my scan looked completely different. He said one scan looked okay and I complained about how TERRIBLE I felt so he did another at a time of day we didn’t normally do, not with any time theory in mind, and it looked completely different. He said it was highly unusual. I just said “yea don’t take lsd”
  19. I am male and have taken testosterone in the past, which mad me feel better, but I am unable to get that from a doctor now. Feel free to pm me if you know a source! I know many people use in conjunction with testosterone when they have low t. I figured it would not be as effective as both but still might show me something. i have a pituitary micro are adenoma which the doctor said is “probably benign” since my hormones are “within range” but the thing about ranges... they are only helpful if you have a baseline in good health. I need to pull up my numbers but because I don’t remember them specifically, but 4 things give me pause: 1. many males my age have higher levels than me even if I am within normal range. 2. I’ve had MANY head injuries, which has been known to effect hormone production. 3. I had a bad experience with oxiracetam and coluracetam which damaged my hypothalamus. I suspect this has screwed up my hpa axis somewhat. When I first began my long road to recovery in the end of 2015, I was unable to experience hunger, thirst, or sexual lust. I still have basically no circadian rhythm anymore... it’s quite taxing. 4. before starting testosterone the first time, I was 23 and completely unable to grow any facial hair. My body hair was also sparse, and I looked probably 6 years younger than I was. Within a few months I started to grow facial hair etc. I remember being on a lowing dose of testim to try and negate the halting you mention. Not sure how well that worked. I went off of it very rapidly and was suffering from a doctor induced overdose of thyroid medication... real bad juju. I do remember feeling like utter shit but there was so much going on medically it was hard to pinpoint what was what. your story is quite remarkable— and not the first tile I’ve heard tell of testosterone improving symptoms. Im so happy you’ve found some relief we all deserve a bit of luck Id say. It’s a tough gig dealing with hppd. Thank you so much for sharing your experience; It’s so important that we do.
  20. Hormones are something in incredibly interested in as I could believe hypothalamic/pituitary issues could easily result from the negative brain effects of hallucinogens we are experiencing. These are very sensitive brain areas, and it’s not uncommon for those suffering from tbi, a group we share a remarkable resemblance to, to have issues with. i have some Anastrozole handy and have been considering trying it. We shall se. I need to look into it more.
  21. As far as I know, they are safe. I’ve taken them plenty in the past, albeit never on a regular basis. The reason for this is if it helps—tolerance and subsequent withdrawal can be really rough. Imagine not being able to stop epinephrine from over agonizing? It’s not fun. if you have dpdr problems look into naltrexone. Low dose is easy with minimal side effects. I know one member on here took 50mg once and had a permanent decrease in his dpdr, although it was not a pleasant experience while on the drug. This is understandable as it is a opioid antagonist and will make you depressed, temporarily, in high doses.
  22. I received improvements in all of my symptoms except visual. The effects were permanent as far as I can tell. Subsequent dosing did not seem to have any effect, but I do still take it occasionally because as you say—why not. After squiring hppd I no longer responded well to add medications. I used to, but even when I was well they eventually made me burn out—hard. I’ve healed now to a point where I think I could take them again—but why? There are much better alternatives out there imo. I find therapeutic amphetamine use to be ironic. Neurotoxic compounds should not be used therapeutically in my opinion. You would not be the first, nor last, to do so however. If you do decide to take bpc, I do not recommend you take it at the same time as add medications. I am also not sure if bpc is reversing damage (unlikely) or correcting distinction at the remaining receptors. I also have a feeling that bpc may somehow be excitatory even if evidence (although scant) seems to point to gaba a function. I had a bad reaction to sarcosine while on it and while I have no way to confirm my belief it certainly felt stimulating in a way I associate with increased glutamate. all in all it’s worth a shot—especially if you have ever used ADD medication. You may even find that you don’t feel you need to use ADD meds after trying it. It supremely increases my motivation and didn’t have any crash. That felt a hell of a lot healthier to me
  23. This is a good place to start: https://www.selfdecode.com/ mthfr gene mutations (inefficient processing of folate into active form) are INCREDIBLY common (Up to 50% in some populations) and can cause a wide swath of cognitive, emotional, and physical issues. I have been a big advocate for genetic testing to, at the very least, rule out this mutation. Folate is used in 800 different bodily processes and without adequate amounts, you will think and feel like shit. if you do have it, there are fairly easy solutions. If you do not, I would be surprised if there wasn’t something having your genes tested couldn’t do to improve your state. I used 23&me for my testing as selfdecode didn’t offer any back when I had mine done (2013). I have, however, used their site and found it to be extraordinary. This is cutting edge for self care. best, oms
  24. Just wanted to post my experience with lmm. I find it to be nicely synergistic with coffee (which I can now drink again after 6 years of hppd). It’s stimulating and also relaxing for me. However, after several weeks of daily use, I will enter a BLACK depression that lasts 24-48 hours. I have screwed around with my brain chemistry probably more than most people. I think I’ve probably felt every major type of depression from a neurotransmitter standpoint.... this felt decidedly cholinergic. It’s a pretty distinct feeling, as acetylcholine is competitive with a lot of other neurotransmitters. Excess levels feels a lot like ssri withdrawal combined with too little dopamine. Terrible feeling really. tldr: lions mane is safe for me, but daily use leads to cholinergic depression
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