onelovez

We Dronowo.pl​ (https://www.facebook.com/dronowopl?fref=ts) are taking a part in a competition for a best photo. Please click on the photo, then like it and share it, if you would like to support us!! Link: https://www.facebook.com/akademicki.szczecin/photos/a.826445897423628.1073741832.680017122066507/826446004090284/?type=1&theater The prize is a camera that will be used to record landscapes of Brazil with a drone and to make a blog about it. I am sorry for the off-topic - but I need you guys on this one - This camera, will give me something to do here in Brazil, which in a way will help me and may stabilize my financial situation, which in turn hopefully will contribute to improving my situation of HPPD. Thank you all !!

I played fallout 1 and 2 . Fallout 2 is one of the greatest games of all times I didn't get a chance to play the fallout 3 too much. But I got an impression it takes a lot of time to travel everywhere in it..

I think you can eat this much no problem, the question is will you body/stomach handle this much coconut oil Try it and see if you are comfortable with it. Confused.. not really. I was feeling kind of heavy to move around or to get up and do some things, thats about it. Ok when I was playing battlefield 4 id get little slower reaction - all the above just for the first few days... The good thing about it was when I went for a massage it was much more pleasurable.

They say ketogenic diet is supposed to be 60-65% calories in fat, 30-35% calories in protein and 5% in carbs. 1 g of carbs and protein are equal to 4kcal while 1 g of fat is equal to 9kcal. I calculated my daily intake of those assuming that I need 2500 calories everyday. 2500 calories * 60% = 1500 calories / 9 calories = 166 grams of fat 2500 * 35% = 875 / 4 = 220 grams of protein 2500 * 5%= 125 / 4 calories = 30 grams of carbs lol Keep in mind that beef / chicken and whatever do not contain 100% protiens. They have maybe 15-30 grams of protein per 100g of weight. According to this I was eating 300g of meat twice a day, in between some polish sausages (replacement of snacks), 4 eggs scrumble egg everyday. I had to be careful not to eat like more than one onion and some other veg's a day. Also as I say I was eating bit more carbs, around 50-60 (but everyone is different). Buy ketones urine test sticks - as long as you mantain traces amount of ketones in your urine (you are in ketosis), your good. I have seen some interviews where they say when you are in ketosis you can eat as much fat as you want and you will still burn it all. Some keto veterans eat few % less proteins for the sake of few % of extra fat. By the above calculations I came up with 5 big spoons of coconat oil a day (and that should be your minimum I believe). If theres anything else you wanna know, shoot.

When I do ketogenic diet, what I do is I eat not 0 or 5 grams but around 50 grams or even little more of carbs a day. They recommend less, I think like between 0-30 grams at the beginnning of the diet, but everybody has different treshold of ketosis. If you stuff yourself with coconut oil (eg 5 spoons a day) which delivers ketones to your system immidiately, you can then allow yourself eat more carbs and mantain ketosis. The best thing to do is buy ketosticks , (test for ketosis) and with their help you can find your sweet spot. First few days on ketosis I tend to be very flegmatic/slow to move (but also relaxed), prob I get lower pressure. After few days it gets much better. They say the first 2 or 4 weeks are hard. I think first few days because of energy levels and later, when that gets better, because of cravings. I crave too much for sweet things and I have a feeling if I had 0-5 grams of carbs a day I would turn depressed and unbearably fatigued.. Also the increased cravings would also increase the chance of breaking the diet faster. So, I advice to balance it for yourself too, maybe then you are not gonna suffer drastic worsening of energy levels/mood etc. Im trying it again, hopefuly I will go pass 2-4 weeks this time and to see how it supposed to make me feel. (day 4 now) Good luck!

ketogenic diet increases serotonin and dopamine activity if I remember right Im trying to mantaing it but I its hard for me for few reasons I keep breaking the diet by stuffing myself with sweet things between day 5-11.. But lets keep trying. It would be easier to mantain if I was living on my own, not seeing other people eating tasty carbs I have some feeling that long-term keto diet could be good for HPPD (calming the overexcited brain etc). In our project's notes, if you scroll down, you will find some good studies about keto and intermittent fasting. http://www.evernote.com/l/AbRsTAeTpEdAK4WUDtw86U-VLIzve9l_4Ks/ I gonna paste it here: Study: The ketogenic diet and brain metabolism of amino acids: relationship to the anticonvulsant effect. http://www.ncbi.nlm.nih.gov/pubmed/17444813 Study: Ketogenic diet alters dopaminergic activity in the mouse cortex http://www.sciencedirect.com/science/article/pii/S030439401400319X Study: The effect of fasting on 5-hydroxytryptamine metabolism in brain regions of the albino rat. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1987105/ Study: The effects of the ketogenic diet on behavior and cognition. http://europepmc.org/articles/PMC4112040;jsessionid=B9oUAx0Z2pEpp22vSWUq.41 https://www.ncbi.nlm.nih.gov/pubmed/21872440 Study: Caloric restriction and intermittent fasting: Two potential diets for successful brain aging. http://www.zentrum-der-gesundheit.de/pdf/intermittierendes-fasten-ia-04.pdf Article: Ketosis: anti-brain fog. Neurotransmitters, dietary protein, and the gut microbiome. http://caloriesproper.com/ketosis-anti-brain-fog-neurotransmitters-dietary-protein-and-the-gut-microbiome/ Article: Your Brain on Ketones http://evolutionarypsychiatry.blogspot.com.br/2010/08/your-brain-on-ketones.html Article: Fasting can help protect against brain diseases, scientists say http://www.theguardian.com/society/2012/feb/18/fasting-protect-brain-diseases-scientists My conclusion - keto is worth of try at least for few weeks. If you are a vegan and can't do keto diet, DO INTERMITTENT FASTING! I like 2 protocols - either one 24h fast a week (two are ideal, but extremely hard in longer terms, makes you think about food all the time). OR eating in 8h time frame everyday and then having 16h fast. Warriors diet is more advanced 4h and 20h of eating and fasting. here is more about one guys experiences with intermittent fasting. its highly recommended if you attempt to try it. Article/home-made experiment: Experiments with fasting https://www.dropbox.com/s/nmc83ca61i31tkm/202534335-IntermittentFasting.pdf?dl=0 i will be making a separate post about this in future

In the past when I smoked weed, took xanaxes or valium I would experience some auditory hallucinations the NEXT day (when not taking anything again), while falling asleep.. By auditory hallucinations I mean some sounds that my brains imagines and hm... they seem to be on the edge of "a thought of a sound" and "a sound" - but as I fall asleep/drift away it closer the sound than just a thought of it. Last time I had something similar to a clock ticking - im sure you know what i mean, but I am giving a description for those who don't. I took clonazepam/clonopine twice recently and same thing happened to me. It gives me the auditory visuals + some random thoughts, that I don't experience so much anymore on a regular basis (there was a time I did when taking different drugs occasionally). I don't intend to take it anymore as clonazepam makes me amnestic (spaced out), whats the point of being relaxed if you have nothing there to talk about. It wonders me a bit is it just HPPD related and what mechanisms cause it, since agonising GABA, I GUESS, should be good for temporary calming of HPPD if the GABA receptors were downregulated, but it seems that it kind of exacerbate the hallucinatory symptom of HPPD. Does anybody experience similar from clonazepam or other medicines? cheers

We have limited resources so we should focus on the most important things first. Right now I would focus on brain scans together with genetic tests.. the genetic tests seem to be even more important - they may give us great insight into what study we should do next - am I right? I think we should hold on for a while with trial studies, until we gather more evidences. This is completely random example - what if the genetic tests shows that none of us need supplementation of Methylfolate - the missing enzyme in depressed patients. In this case there would be no point doing a Methylfolate trial - we save up time and resources. Also we should write down more medicines to choose from and then think about which ones we want to try. (eg. There are some medicines that seem to be helpful in controlling tinnitus - would they help in controlling other HPPD symptoms? eg Acamprosate. http://www.evernote.com/l/AbSdQyCG9BtFxbgUH-dPZ2vaP_wp2E0MhAI/ ) We can try some of the new drugs ourselves to see if we think they may have any potential. The studies I support in the order of highest to lowest priority: 5 - Genetic vulnerability Yes, yes, yes. 6 - Recovery rate Only if it could give some insight into possible cures - then yes. I have a feeling it could. 1 - Brain imaging study using MRI of patients with HPPD and people with no HPPD Yes. What about other tests though? like PET/SPECT? or would MRI be totally sufficient? qEEG - i guess its not needed since there is enough study on it already right? 3 - Study 3: PPI If it can give insight into cures then yes. 2 - Pupil dilation testStudy 2 Shouldn't waste much of our resources - we can do it on the side together with some other study maybe. 7 - Open-label study on the effectiveness of treatments for HPPD Festidalcholine which improves the eye - in my opinion we should focus on cognition (would you rather think clearly or see clearly ;p) - unless festidacholine can affect cognition. Methylfolate - like I said above, lets do genetic tests first Little doubts about this one: 4 - CFF and dark adaption What if we spend time doing it and the answer will be "yes". Does that info matters a lot to us and would it be worth the time?

I got Astragalus root 200mg pills from Thompson company. It says its an standardized extract, but doesn't state any concentration, so I don't know how much it compares to of the pure herb. I have been taking 2 pills a day for last few days and it has no effect on me. I am thinking to increase it to 4 in a week time and see if anything happens, although it says only to take one pill a day. Chesterfool you only took 1 g a day of the dried root ya? PS. also im going to eat 1-2 raw garlic cloves a day as recommended here: http://puu.sh/hPKXr/fa6261dbe2.png Have to buy curcumin (i used to bomb 1-2 grams of it everyday mixed with a drop of water).. This combo has to help ;d

Try eating healthy - some high fat low carb diet (ketogenic) is good for your brain. do use some good probiotics - they can't do harm. You can continue to do intermittent fasting by eating only in an 8 hour frame window everyday (16h of fast then) - apparently that can put you in ketosis everyday, which is good for the brain. For me eating carbs especially a lot of carbs - makes me lazy to go excercise etc. let us know of the effects of hwatever you end up doing. goo dluck!

How long have you been on Sertraline / Zoloft? Apparently the visuals (ghosting etc) increase at the beginning of taking Zoloft, but maybe they will go away? I wonder if they go away later.. update us if you see any improvement.

Hi. Id like to move this project forward - if we want to figure out the solutions, we need to work together. Its not a one man operation, hence I am asking everybody who is interested in seeing it progressing to participate. I will be creating posts with specific subjects and then we can work on it together. Anybody can submit an article, study, anecdote and I will be pasting everything relevant into the top post. This way we will build our small 'encyclopedia' of the desired subjects, which hopefully will give us better insight into solutions for hppd. In this particular post I want to focus on finding out everything on how exercise affect us but also how does different types of exercise influence us. I have seen one guy reporting that his hppd got better after doing particularly sprints! Now I am wondering how sprints affect the brain. From what I have read, lifting weights upregulates dopamine and its receptors. Is that the case for jogging too though? these are the kind of questions id like to get answer to. So let me start with what I found on exercise: Source: http://serendip.brynmawr.edu/bb/neuro/neuro05/web2/mmcgovern.html The Effects of Exercise on the Brain MK McGovern Exercise has been touted to do everything from treat depression to improve memory, with the power to cure a host of problems while preventing even more. In particular, exercise leads to the release of certain neurotransmitters in the brain that alleviate pain, both physical and mental. Additionally, it is one of the few ways scientists have found to generate new neurons. Much of the research done in this area has focused on running, but all types of aerobic exercise provide benefits. Although the exact nature of these benefits is still being determined, enough research has been done to provide even skeptics with a motivation to take up exercise. Exercise exerts its effects on the brain through several mechanisms, including neurogenesis, mood enhancement, and endorphin release. This paper not only examines how these mechanisms improve cognitive functioning and elevate mood states, but also proposes potential directions for future research. Furthermore, it provides an explanation for exercise's generally non-habit forming nature, despite effects on the reward centers of the brain that mimic those of highly addictive drugs like morphine. One of the most exciting changes that exercise causes is neurogenesis, or the creation of new neurons. The new neurons are created in the hippocampus, the center of learning and memory in the brain (1), however the exact mechanism behind this neurogenesis is still being explored. At a cellular level, it is possible that the mild stress generated by exercise stimulates an influx of calcium, which activates transcription factors in existing hippocampus neurons. The transcription factors initiate the expression of the BDNF (Brain-Derived Neurotrophic Factor) gene, creating BDNF proteins that act to promote neurogenesis (17). Thus the generation of BDNF is a protective response to stress, and BDNF acts not only to generate new neurons, but also to protect existing neurons and to promote synaptic plasticity (the efficiency of signal transmission across the synaptic cleft between neurons, generally considered the basis of learning and memory) (1, 3, 17). However, BDNF's effects are more than protective, they are reparative. For example, in a comparison between sedentary and active mice, scientists found that active mice regenerated more sciatic axons post-injury than sedentary mice. This effect was not observed when the active mice were injected with a neurotrophin-blocking agent, indicating that exercise stimulates injured neurons to regenerate axons via neurotrophin-signaling mechanisms (3). This reparative effect is particularly relevant to humans because the brain starts to lose nerve tissue beginning at age 30. Aerobic exercise reinforces neural connections by increasing the number of dendrite connections between neurons, creating a denser network, which is then better able to process and store information (4). This suggests possible preventative and therapeutic effects for diseases such as Alzheimer's and Parkinson's that progress via the loss of neurons. Indeed, a correlation between lifestyle and Alzheimer's has already been demonstrated (6). In addition, exercise has been shown to decrease the loss of dopamine-containing neurons in mice with Parkinson's (2). There is a limit to the positive effects of neurotrophic factors, however. Mice bred to overexercise actually showed an inability to learn. A possible cause for this inability is the disruption of cognitive function by a preoccupation with exercise. The overexercising mice had elevated BDNF and neurogenesis, but the levels reached a plateau that did not increase with more exercise (14). This limitation is further illustrated by a study of exercise effects on a group of 60- to 75-year-olds versus a group of 18- to 24-year-olds. Sedentary 60- to 75-year-olds who began aerobic exercise demonstrated an improvement in executive cognitive functions, e.g. planning, scheduling, and working memory, while the group of 18- 24-year-olds did not. Brain-wave analysis showed a 35-millisecond faster brain response time post-exercise versus pre-exercise in the 18- to 24-year-olds. Essentially, less cognitive function was lost in 18- to 24-year-olds than in 60- to 75-year-olds, so there is less room for improvement, and that improvement will be less obvious (4). Apparently it is not possible to exercise to brilliance. Fortunately, it may be possible to exercise to happiness. It has been shown that physically active people recover from mild depression more quickly, and physical activity is strongly correlated with good mental health as people age (7). Depression is related to low levels of certain neurotransmitters like serotonin and norepinephrine. Exercise increases concentrations of these neurotransmitters by stimulating the sympathetic nervous system (12). In addition, serotonin has a reciprocal relationship with BDNF, i.e. BDNF boosts serotonin production and serotonergic signaling stimulates BDNF expression (17). Since exercise also increases BDNF production directly, there is a reinforcement of the serotonin-BDNF loop, indicating exercise's significant potential as a mood-enhancer. In fact, a combination of exercise and antidepressants (which increase BDNF via the serotonin-BDNF loop) has been particularly effective in treating depressive behaviors in rats. The BDNF gene can be expressed in multiple forms, and physical activity increases the expression of two forms: one with fast but short antidepressive effects, and one with slow but longer antidepressive effects. By combining exercise with antidepressants (which increase the expression of the long-lasting form), scientists were able to both increase and accelerate the production of BDNF. The rats showed a decrease in depressive behaviors in two days instead of the two weeks experienced by those given antidepressants alone, indicating a potential therapy for depressed patients that produces almost immediate results (13). There also seems to be a role for neurogenesis in the treatment of depression. Studies show that the hippocampus of depressed women can be up to 15% smaller than normal. In addition, there is a correlation between the decrease in size and the length of the depression. This damage may be reversed by BDNF-stimulated neurogenesis. Interestingly, the time it took for antidepressants to take effect is equal to the time needed to induce neurogenesis (16). All of these facts seem to point back to BDNF as the key chemical underlying exercise's impact on the brain. Perhaps it is not exercise that has the curative power, but rather BDNF, and exercise is only the trigger. Another factor to consider is endorphins, the chemicals released by the pituitary gland in response to stress or pain. They bind to opioid receptors in neurons, blocking the release of neurotransmitters and thus interfering with the transmission of pain impulses to the brain (12). Exercise stimulates the release of endorphins within approximately 30 minutes from the start of activity. These endorphins tend to minimize the discomfort of exercise and are even associated with a feeling of euphoria. There is some uncertainty around the cause of this euphoria since it's not clear if endorphins are directly responsible for it, or if they just block pain and allow the pleasure associated with neurotransmitters such as serotonin and dopamine to be more apparent (15). If the latter is true, this would indicate a connection to BDNF via the serotonin-BDNF loop. In this case, BDNF is again the underlying chemical providing the benefits of exercise, and endorphins act in a supporting role by blocking pain and reducing the cost associated with acquiring the benefits of exercise. The release of endorphins has an addictive effect, and more exercise is needed to achieve the same level of euphoria over time. In fact, endorphins attach to the same neuron receptors as opiates such as morphine and heroin (12). Yet, exercise is not nearly as addictive as these opiates; it's not even as addictive as milder substances such as nicotine. It seems strange that an activity as beneficial as exercise, with a built-in mechanism for addiction, is so easy to give up. According to some polls, only about 15% of Americans say they exercise regularly (18). The key to this seeming contradiction may lie in the delayed gratification experienced during exercise. Exercise differs from other addictions in that there is an initial amount of pain to endure before the euphoric payoff. The approximate 30-minute delay in the release of endorphins requires a certain level of fortitude that has not been cultivated by the American culture of video games, 30-second commercials, and various timesaving devices. In addition, exercising is made up of several tasks— putting on correct clothing, deciding on a form of exercise, maintaining adequate hydration, etc. Though each task may be mundane enough to form a habit, putting all the tasks together requires too much attention for exercise to be experienced entirely as a habit, which associates the reward or pleasure of completing a particular task with the first step of that task. In addition, the subconscious brain may use the feeling of fatigue as a regulated, anticipatory response to exercise in order to preserve homeostasis (8), possibly discouraging the continuance of exercise before the addictive euphoria is attained. If future research could find a way to trigger the release of endorphins at the start of physical activity, exercise might become more popular. Another possibility would be research around the synthesis of BDNF. If it really is the underlying chemical for all of exercise's nervous system benefits, then making it safely and readily accessible could allow people to circumvent exercise altogether, at least in terms of the nervous system. While exercise is attractive in theory, it can often be rather painful in actuality, and the discomfort of exercise is more immediately felt than its benefits. The delayed release of endorphins creates a lapse between the pain and the pleasure elements of physical activity. The next area for research could be finding ways to make the benefits of exercise more apparent while the exercise is actually occurring, thus satisfying the need for instant gratification and tipping the scales in favor of exercise. ReferencesNote that starred (*) sources are accessible only to Bryn Mawr, Haverford, and Swarthmore students through Tripod and double-starred (**) sources are informational, but not directly cited resources 1) Modie, Jonathan. (2003). "'Good' Chemical, Neurons in Brain Elevated Among Exercise Addicts." OHSU, online. 2) "Exercise protects brain cells affected by Parkinson's." (2004). Medical Research News, online. 3) "Exercise can help brain healing process." (2004). Medical Research News, online. 4) Chaudhry, Laura. (2004). "Brain Workout." South China Morning Post, online. 5) "Controlling Brain Wiring With the Flick of a Chemical Switch." (2005). AScribe Newswire, online.** 6) Kotulak, Ronald. (2005). "Exercise, education found to supercharge genes, reduce Alzheimer's." Chicago Tribune, online. 7) McKimmie, Marnie. (2005). "Walk away from depression." The West Australian (Perth), online. 8) "Exercise fatigue may be part of a response coordinated in the subconscious brain." (2004). Obesity, Fitness & Wellness Week, online. 9) "Keep Your Noggin Fit With Brain Exercise." (2003). Southern Illinois Healthcare, online.** 10) Francis, Lori. "The Biology of Pleasure." online.** 11) "How to Maintain Brain Power." (2005). Help the Aged, online.** 12) "How Does Exercise Affect Our Mood?" online. 13) Russo-Neustadt, A.A., R.C. Beard, Y.M. Huang, and C.W. Cotman. (2000). "Physical Activity and Antidepressant Treatment Potentiate the Expression of Specific Brain-Derived Neurotrophic Factor Transcripts in the Rat Hippocampus." Neuroscience, 101, 305-312.* 14) Rhodes, Justin S., Susan Jeffrey, Isabelle Girard, Gordon S. Mitchell, Henriette van Praag, Theodore Garland, Jr., and Fred H. Gage. (2003). "Exercise Increases Hippocampal Neurogenesis to High Levels but Does Not Improve Spatial Learning in Mice Bred for Increased Voluntary Wheel Running." Behavioral Neuroscience, 117, 1006-1016.* 15) "The Antidepressive Effects of Exercise." online. 16) Sanders, Jenny. "Brain Physiology." online. 17) Mattson, Mark P., Wenzhen Duan, Ruqian Wan, and Zhihong Guo. (2004). "Prophylactic Activation of Neuroprotective Stress Response Pathways by Dietary and Behavioral Manipulations." NeuroRx, 111-116, online. 18) Farley, Tom, and Deborah Cohen. (2001). "Fixing a Fat Nation." Washington Monthly, online. Comments: "Exercise increases concentrations of these neurotransmitters by stimulating the sympathetic nervous system (12). In addition, serotonin has a reciprocal relationship with BDNF, i.e. BDNF boosts serotonin production and serotonergic signaling stimulates BDNF expression (17). Since exercise also increases BDNF production directly, there is a reinforcement of the serotonin-BDNF loop, indicating exercise's significant potential as a mood-enhancer." This is the most important fact out of the article - i really like the idea of serotonin-BDNF loop .. Same way as depression can be caused by some a viscous cycle, the same way mood can be enhanced by this positive feedback loop. good thing to keep in mind while jogging Also worth of noting sugar suppresses BDNF. So please, post whatever you would like to this article. I will be updating it with useful info. It will be also available to view at http://www.evernote.com/l/AbR5gZan_09HNIDCi2mL_z2kpDML41ynXiA/ Later I will get all the good links together in one place and make a website out of it. Hopefully this will inspire others to do more research. Cheers!

hey guys i updated the post with some studies above, check it out !

I am after seeing few studies/private reports where people got long-term remission/improvement of symptoms after doing some drug treatments. eg. in this study http://www.ncbi.nlm.nih.gov/pubmed/12598822?dopt=Abstract Clonazepam treatment of lysergic acid diethylamide-induced hallucinogen persisting perception disorder with anxiety features. AbstractAn unique and intriguing characteristic of lysergic acid diethylamide (LSD) and LSD-like substances is the recurrence of some of the symptoms which appear during the intoxication, in the absence of recent intake of hallucinogens. Hallucinogen persisting perception disorder (HPPD) is a condition in which the re-experiencing of one or more perceptual symptoms causes significant distress or impairment in social, occupational or other important areas of functioning and may be extremely debilitating. Benzodiazepines are one of the recommended agents for the treatment of HPPD but it is unclear which of them may be more helpful. The goal of our investigation was to assess the efficacy of clonazepam in the treatment of LSD-induced HPPD. Sixteen patients fulfilled entrance criteria. All complained of HPPD with anxiety features for at least 3 months and were drug free at least 3 months. They received clonazepam 2 mg/day for 2 months. Follow-up was continued for 6 months. They were weekly evaluated during the 2 months of clonazepam administration and monthly during the follow-up period using the Clinical Global Impression Scale, a Self-report Scale and Hamilton Anxiety Rating Scale. Patients reported a significant relief and the presence of only mild symptomatology during the clonazepam administration. This improvement was clearly sustained and persisted during a 6-month follow-up period. This study suggests that high potency benzodiazepines like clonazepam, which has serotonergic properties, may be more effective than low-potency benzodiazepines in the treatment of some patients with LSD-induced HPPD. Yet many people on this forum say that drugs are not a cure to HPPD. I hope by curing they mean completely getting rid of the root cause and if thats not the case Id like to ask you guys what do you think: Which drugs can improve the symptoms in long-terms and which drugs would rather alleviate the symptoms, only while taking them? Thanks in advance.

Thanks for posting it Brake. Can anybody here view full text of the studies? This study looks interesting.. Let me quote it. Yokukansan, a traditional Japanese medicine, decreases head-twitch behaviors and serotonin 2A receptors in the prefrontal cortex of isolation-stressed mice: "ETHNOPHARMACOLOGICAL RELEVANCE:Yokukansan, a traditional Japanese (Kampo) medicine, has recently been used to treat the behavioral and psychological symptoms of dementia (BPSD), including aggressiveness, excitability, and hallucination. The present study was designed to investigate the mechanisms underlying the ameliorative effects of yokukansan on BPSD using animals exhibiting hallucination-like behaviors. For this purpose, we initially examined whether chronic isolation stress increases the frequency of hallucination in response to a psychedelic drug. Using this animal model, we next examined the effects of yokukansan on drug-induced hallucination-like behaviors. Finally, we examined the density and mRNA levels of serotonin 2A (5-HT2A) receptors. MATERIALS AND METHODS:Male mice were subjected to isolation stress for six weeks. Yokukansan was incorporated into food pellets, and administered to the mice for six weeks. In some experiments, yokukansan and each of seven constituent herbs were administered orally to the mice for the last two weeks during the six-week period of isolation stress. A 5-HT2A receptor agonist, 2,5-dimethoxy-4-iodoamphetamine (DOI, 2.5mg/kg), was injected into the mice, and head-twitch behaviors were quantified. The binding sites of 5-HT2A receptors on the plasma membrane of the prefrontal cortex (PFC) were assessed by a receptor-binding assay using tritium-labeled ketanserin, and the density and affinity were calculated from a Scatchard plot. The level of mRNAs was measured by PCR analyses. RESULTS:Isolation stress enhanced the frequency of the DOI-induced head-twitch response, and yokukansan treatment by feeding significantly reduced this enhancement. Isolation stress significantly increased the 5-HT2A receptor density in the PFC, and yokukansan treatment by feeding as well as administration significantly down-regulated this increase. Isolation stress and yokukansan did not affect the affinity. Among seven constituent herbs, Bupleurum Root, Uncaria Hook, Japanese Angelica Root, and Glycyrrhiza down-regulated the increase, but statistically not significant, in which their efficacies were over 50% relative to yokukansan. Neither isolation stress nor yokukansan affected mRNA levels of 5-HT2A receptors. CONCLUSION:Yokukansan attenuated drug-induced hallucination-like behaviors in isolated mice, which is suggested to be mediated by 5-HT2A receptor down-regulation in the PFC. This mechanism may underlie the ameliorative effects of yokukansan on hallucination." My question is .. could that be anyhow relevant to HPPD? The common theory is that HPPD is caused by downregulation of the receptors, but could it be the case that they become upregulated? another study that Brake passed on to me says something that supports the above thesis Flashbacks and HPPD: A Clinical-oriented Concise Review (2014) http://doctorsonly.co.il/wp-content/uploads/2015/01/13_Flashbacks-and-HPPD.pdf "...There are controversial reports regarding SSRIs like Sertraline which has been reported to worsen (41) as well as improve (18) visual disturbances. Alleviation after long-term administration of SSRIs was attributed to the down regulation of 5-HT2 receptors, adding further evidence to support the serotonergic mechanisms underlying this syndrome (18)...." . ref 18: Young CR. Sertraline treatment of hallucinogen persisting perception http://www.ncbi.nlm.nih.gov/pubmed/9062378?dopt=Abstract (why is there no abstract though?) ref 41: LSD flashback syndrome exacerbated by selective serotonin reuptake inhibitor antidepressants in adolescents. http://www.ncbi.nlm.nih.gov/pubmed/7965440 (no info about duration of the treatment .. )

I think it would be good to have subjects with variety of causes by which they excebarated hppd, not just lsd.

Odisa, could you tell me more about upregulation by this lesser know process of shor-term or intermittent agonism? It got me really interested.

how did afobazole go for you within that 3 months?

eh.. the way everybody always boasts about what they have ordered and says they will inform of the results.. and the results never come

Guys I need some advice. I really need something that will help me slightly, repair a bit my 'thoughts processing', cause I really have to get a job, but nobody is gonna hire such a spacer.. I tried flunarizinium and lamotrigine - both gave me a stingy/burning sensation in my head since day 1-2, that was getting bigger, so I stopped taking them soon after. Same as lion's mane did and some other things would too. I can't even drink few spoons of most herbs cause they affect me somehow. I haven't tried keppra yet - but Im thinking maybe I should try something else - I feel like my thought process is disrupted, especially when I undersleep. The thoughts sometimes don't seem to "make it through" the neuronal pathways.. im missing words, have problem with thoughts associations etc. Don't know lack of which neurotransmitters/receptors could be responsible for it.. I would like to try Sinemet, with COMT inhibitor? could that help my cognition? My main question is though - would it downregulate my dopamine receptors a lot - as in.. let say later, when side effects became a problem for me or id like to stop the drug when I feel little better I guess - would not the symptoms come back stronger? Due to downregulation of dopamine receptors? Would it take much time for them to come about to their baseline? 1) im little affraid cause I am a kind of a person that after quitting coffee that I used to need (1 cup a day) - It takes me 2-3 days if not longer to be able to jumpstart again and not be a zombie through the whole day.. im also sensitive to drugs etc. I have a bad feeling, that it could take months if not years for my receptors to "recover". 2) Is it not the case with people with HPPD that our brains are hmm.. neuroplasticity comes to my head, but with a negative effect. that our brains get altered easily (receptors up / down regulate fast due to drugs etc. leaving their "imprint") and then it takes long time for them to return to their old "shape"? hence we are the ones who get HPPD. I know people that do not suffer from HPPD that after smoking too much weed even, get some HPPD symptom like "framed vision".. so their brain chemistry goes to a similar state needed for that symptom to happen and then it seems their brain is flexible enough to bounce back. Our brains, like I said already, once they get "deshaped" they can't restore themselfs to their old shape (number of receptors etc). Also some people report some HPPD symptoms when coming down from extasy.. and i don't have to mention LSD. for majority of people they seem to disappear after good sleep, as like their receptors come back to the baseline.. so i don't know if we can call it a receptor damage - unless, they have some gene that lets them repair the damaged receptors, that we don't..

Don't worry, you will get used to it and in weeks time its not gonna bother you much anymore. Maybe if you try snap out of it every time you do fixate on it, will help you a lot. But even if you woun't try, you will start to ignore it with time. about the project: http://www.evernote.com/l/AbRcywcu-55EIYDeDPUG3GLpBqsd1cRmkHc/ pm or e-mail me for more details

"i wanna get back out there and smoke again" - I was refering to this part really. I mean "I'm not asking if it is ok smoke right now that's a definite no" - its not just a no for right now, its for ever. I believe some or most of visuals stay for good. There has been people reporting being cured from HPPD (psychological aspect), with the visuals staying and there has been people reporting full recovery. Not too many unfortunately. Lets be hopefull.

If you want your symptoms back, do smoke. sorry.. I aways kept going back to weed and many other things and now I wish I was in your situation, back when I was 16 and being able to say NO, fuck this.. But I couldn't do it and hence every following year my hppd was becoming worse and worse and it had been becoming actually HARDER to stop taking drugs (when you feel more and more awfull, you just feel like saying fuck everything I gonna take it, because I just need to relax for that few moments).. This viscous cycle continues and then brings you to the point where you can't take drugs no more because suddenly instead of them relaxing you, they start to trigger your HPPD, anxiety etc. Anxiety is a big part of HPPD, which can stop you from socializing to people, friends or even talking to your own family.. your brain becomes so foggy and spaced out that you feel like there is nothing to talk about with them anymore. All this makes you feel like everything and everybody around you is dead.. and then you realize you just got yourself into hell and then you start to think about were those few good/crazy nights worth of destroying your whole world? Then you just feel like crying to your mother for what what has become of your life.. but you never actually do it. Because you know it woun't make any difference, same as 30 different vitamins/supplements/drugs/excercises you did for past few months or years, didnt do any difference - you still feel dead while being alive. I mean.. some people get better after years.. but I have a bad feeling some part of many of them remains dead forever, they just made themselfs believe its not. The sad part is that, we people are to hopefull everything will be ok, what happened to somebody else woun't happen to us. When we get warned we still don't believe and we have to.. we just really have to try it to see the consequences for ourselves.. You are probably asking if its ok for you to smoke, but at the back of your head, your mind is already rationalizing everything in his own way, making excauses to give you a permission to go and have that smoke.. can you feel it? So. Do smoke, because if I told you not to, you probably still would sooner or later.

Once you don't have your cognition completely fucked and you dont consider yourself living in hell while being alive like me, than your case may not be "that" serious. Every HPPD is a serious condition - because you basically can't take drugs, have to be carefull with drink or very often not be able to drink at all, not smoke cigs - or like me, can't even be around people who smoke cigarretes - once i smell them the day finishes for me. My visual (nevermind that) AND my cognitive reaction decreases. So, its a serious condition, but once it doesn't SERIOUSLY destroys your life/personality etc,.. if your cognition is intact, then you should be super happy. If you think your case its mild, than it probably IS mild.. unless you have some unreal methods of coping with really serious problems, but then ud probably say my problem is serious, but I learnt to cope with it. enjoy life bro and join our hppd project if you wanna improve your HPPD, no matter how serious it is

But like what tests? MRI or PET scans has been done already and showed hypermetabolism in some part of the brain. qEEG has been done, showing overactivity in the brain. Would gene testing be important? if somebody was able to separate few genes responsible for HPPD, would not that give massive insight into possible treatment no? Idk.. Im sure there are lots of things that can be tested.. eg. lets look at schizophrenia as an example: http://www.nutritional-healing.com.au/content/condition.php?condition=Schizophrenia As you see there: there is different causes/biotypes of schizophrenia. Note that each of the biotype have different substances corresponding that can be beneficial or harmful in case of schizophrenia, but whats more important sometimes they get affected by one particular substance with opposite effect! Does that reminds you of something? Like meds having different effect for different people with HPPD?. The causes of HPPD seem to be different too. (thyroid problems, stress, alcohol, drugs, ANTIBIOTICS). An anecdote: My Dad has HPPD - but he aquired it most likely from alcohol and/or stress while I did from variety of drugs (slightly different causes but same genes). (going back to DNA tests, maybe "comparing our cases with DNA of people with schizophrenia" or people in general to see if we share any common "defects"?) How many of HPPD'ers checked all different kinds of hormones? The most important are done with most basic blood tests right? should we check the ones less "popular" or the ones considered to be less important? Im sure we can think of many abnormalities that can be checked and that could turn out to be HPPD's common factor (for each different biotype ofcourse).