Pereise1

The Cure For Narcolepsy

94 posts in this topic

@Pereise1 bright light may increase orexin expression as well. Testosterone in men too seems to influence orexin expression in certain areas on the brain. Bright light = more orexin + more testosterone so there might be a double benefit. Same with exercise. I'll put the links when I dig them up. 

Also regarding exercise, it upregulates D2 receptors, doesn't it? Is there any difference in forms of exercise as to neurogenesis, receptor expression, etc? For instance sustained cardio, high intensity interval training, or resistance training? I haven't looked into it yet.

I've been forcing my ass out of bed each morning for about a week instead of taking medication and then laying in bed for it to kick in. I've been alternating between high intensity interval training, and a brisk walk. Both are 1.4 miles. I'll wake up, take medication and have some coffee. 15 minutes after waking I'm out the door it's 7am and I'm walking. Admittedly I'd gotten in terrible cardiovascular shape. But just within the week I've noticed daily improvement in EDS each morning, motivation, and feel happier. The view doesn't hurt either lol

 

img_20170514_085326__GnUn2.jpg

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Jasonm, re exercise, I don't know the reason, but exercise helped me a lot. Before diagnosis, it was one of the main ways I managed.

For me, it worked best at the end of a work day. I always felt best after a run. And it helped my night time sleep for sure. Eventually, I pushed myself way too hard with "trying to feel better" through exercise and did a sprint triathlon. I was mistaking cataplexy for being out of shape and pushed myself waaaay too hard.

So, I would say that moderation is key. You have a level head and you know what works for you.

I've let myself get out of shape and am just trying to start back. But when I do, it will be much more moderate.

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I stand with Hank on the moderation. I can tell you that I was in the best shape of my life when I was diagnosed. I biked, I hiked and I skied. But diagnosis explained why I skied so well in the morning and fell down the mountain by 1 p.m.... in other words, enjoy the exercise but don't push yourself to exertion.

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@Hank3326 I've had the same experience with exercise. I'm not sure about the exact mechanism of its effectiveness. I was hoping Pereise would do the leg work lol and see if there are different benefits to the various forms.

I'm doing some high intensity interval training, which is like 40 second sprints then moderate/low aerobic for a couple minutes, then sprint.. and so on for 10-15 minutes, which is supposedly substantially better for rapid cardiovascular fitness improvement. Well that is assuming you don't have a heart attack lol. I hate jogging but don't mind sprints. I don't know if it's any better for EDS though. It does obliterate the I don't have time excuse though. I'm absolutely not built for extended jogging. I know myself and I'll never do it. It's all about what works for you. I've just been walking the last couple days because my legs are too sore to run lol. 

Just getting up and forcing myself out the door in the morning for a little over a mile walk, which takes about 30 mins, is way more helpful than just taking medication and laying around until it kicks in. It takes a lot more willpower though. It took a lot for me to do it the first day. But the reward was so quick, now I look forward to it. Getting my heart rate up seems to produce better results.

@Ferret believe me I'm not lol. I sit at a desk most of the day.. it's so damned hard to get motivated when you're sleepy.

 

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On 5/18/2017 at 8:08 AM, Jasonm said:

@Hank3326 I've had the same experience with exercise. I'm not sure about the exact mechanism of it's effectiveness. I was hoping Pereise would do the leg work lol and see if there are different benefits to the various forms.

I'm doing some high intensity interval training, which is like 40 second sprints then moderate/low aerobic for a couple minutes, then sprint.. and so on for 10-15 minutes, which is supposedly substantially better for rapid cardiovascular fitness improvement. Well that is assuming you don't have a heart attack lol. I hate jogging but don't mind sprints. I don't know if it's any better for EDS though. It does obliterate the I don't have time excuse though. I'm absolutely not built for extended jogging. I know myself and I'll never do it. It's all about what works for you. I've just been walking the last couple days because my legs are too sore to run lol. 

Just getting up and forcing myself out the door in the morning for a little over a mile walk, which takes about 30 mins, is way more helpful than just taking medication and laying around until it kicks in. It takes a lot more willpower though. It took a lot for me to do it the first day. But the reward was so quick, now I look forward to it. Getting my heart rate up seems to produce better results.

@Ferret believe me I'm not lol. I sit at a desk most of the day.. it's so damned hard to get motivated when you're sleepy.

 

I'm quite interested in reading about the bright light link, I certainly feel better being in bright areas, indoors or out, so it'd be nice to know exactly why that is lol. The testosterone thing makes perfect sense, seeing as they've found orexin binding sites in the genitals of several mammals so a healthy hormonal balance should be a priority too.

And yes, exercise is quite the challenge despite being one of the best possible treatments. I'm curious how everyone else feels because personally, it's not even about really being "in shape". I only get benefits from exercise when I do it 3+ times a week. I surprised myself a few months ago when my wife and I went to Redwood National Park and, despite not exercising regularly, we were still more than able to do a 14 mile hike over a few ridges including 2 miles of walking on the beach. I still seem to have my pre-narcolepsy endurance but unless I exercise at least 3 times a week, I might as well be a couch potato. 

The only study I could find on exercise and the D2 receptors was this rat one: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3273304/

Also, LOL, yes I'll probably spend a portion of this work day today looking up the best form of exercise :lol:. I do find that, again, in my case, enjoying the form of exercise is more therapeutic than the amount of exertion. I get more out of volleyball with friends than a solid hour at the gym. Maybe the anti-stress aspect? The brain is so complicated and overfocusing on every variable just adds to the EDS so I got to take it slowly sometimes.

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@Jasonm So I snooped around a bit for studies but I had a number of urgent surgery bookings today :wacko:. That said, I found an interesting study, in Narcoleptic dogs, that showed that exercise only upped Orexin when the animals enjoyed it:

Quote

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3535459/

In a previous study we reported that Hcrt-1 levels in dogs were significantly increased by yard play (Wu et al., 2002), suggesting that the hypocretin system might be activated by motor activity. In the present study, however, we found that intense locomotor activity alone on a treadmill did not change CSF Hcrt-1 level compared to the control condition of simply standing on the treadmill, despite major changes in activity level, respiration, HR and body temperature. Clearly, changes in Hcrt release, as assessed by CSF level, are not required to mediate these phenomena. This contrasts with prior studies implicating Hcrt in mediating cardiovascular changes. However, these prior conclusions were all based on manipulations of the Hcrt system or examination of mutants rather than recordings of Hcrt release. Our results do not rule out the possibility of smaller changes that might not be detectable in the CSF. But they indicate that the magnitude of any such changes are significantly less than those produced by yard play. Furthermore our results show that great differences in locomotor speed, and the associated correlated changes in respiratory and cardiovascular activity during treadmill locomotion, produce no detectable change in CSF Hcrt level.

The emotional excitement that comes with social interaction with other dogs in the yard contrasts with the monotonous physical movement on the treadmill. Hypocretin neurons are heavily innervated by the amygdala and cholinergic arousal-related basal forebrain (Sakurai et al., 2005; Yoshida et al., 2006). They are activated by anticipation of positive reinforcements, such as food and opiate drugs (Boutrel et al., 2005; Harris et al., 2005; Mileykovskiy et al., 2005; Borgland et al., 2006), and during spontaneous wheel running (Anaclet et al., 2009; Furlong et al., 2009).

Heightened, and most often positive, emotions trigger cataplexy in Hcrt-deficient narcoleptic humans and animals (Guilleminault, 1976; Lin et al., 1999; Mitler et al., 1976). In humans, laughter is the most common trigger. During the yard play period, the dogs were free to engage in any activity, including digging holes in the grass, playing with toys and interacting with other dogs. When cages were opened for the daily exercise period, the dogs would run to the yard. In contrast, they generally had to be coaxed to go to the treadmill room. This behavior suggests that they enjoyed the free play more than the treadmill locomotion. However, once they were on the treadmill, they ran and elevated autonomic measures to levels comparable to those achieved during the yard play.

In conclusion, the present experiments show that motor activity and the associated autonomic and respiratory changes do not alter Hcrt level. We hypothesize that activity during positive emotions, of the sort that the dogs experienced during play behavior, is responsible for the increased Hcrt release we observed.

 

So basically any physical activity that we actually enjoy would be the best kind in our specific circumstances. However, I'm still not 100% sure because in non-narcoleptic humans, exercise did increase plasma orexin although that's not always the best measurement: https://www.degruyter.com/view/j/jbcpp.2016.27.issue-6/jbcpp-2015-0133/jbcpp-2015-0133.xml?format=INT

So yeah, wasn't able to dig up too much today but hopefully it's a step in the right direction.

 

 

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Will continue to try to motivate my 13yr old to exercise - not easy!

We're in the UK, and the BBC are currently running some health promoting programmes.  Last week it was 'The Truth about Sleep' Michael Mosley http://www.bbc.co.uk/programmes/b05p5v5f   It wasn't about N&C but a couple of interesting items that backup the 'life style' modifications that can help:

natural daylight can help to reset the body clock - can't find anything published - but this is the project: http://cphpost.dk/news/oxford-university-moves-unique-research-project-to-bornholm.html

prebiotic helps improve sleep: http://journal.frontiersin.org/article/10.3389/fnbeh.2016.00240/full

 

 

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Does anyone have a reliable link for a supplier of Centella Asiatica (Gotu Kola) and Acetyl L-Carnitine?
I am based in Spain and can have things shipped but looking for low cost shipping, so probably not from the US.

Thanks
 

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@Pereise1 there's not tons of research on the subject but here's what I found. 

Cardiovascular fitness in narcolepsy is inversely related to sleepiness and the number of cataplexy episodes. This is just an association. 

Exercise Influence on Hippocampal Function: Possible Involvement of Orexin-A this article has a bunch of information you may find interesting since it also goes into neurogenesis.

In men with severe sleepiness, regular exercise was associated with a reduction of sleepiness by nearly 41%. It's unclear if this only applies to sleep apnea. 

Bright light soon after waking in the morning, preferably outdoor sunlight, seems to be beneficial as well. 

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Another option for accessing research material is to visit your closest state college. They usually have access to research study papers, journals, and such. Since they are state colleges, their library facilities are accessible to individuals who can prove they live in the state. Most people aren't aware they can check out books and materials from not only their public library, but these facilities, too. Sometimes they do inter-library loans with your local libraries, as well.

Happy hunting!

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Has anyone looked at the relevancy of stem cell activation via the fasting mimicking diet?

http://sci-hub.ac/10.1016/j.mce.2017.01.042  Nutrition and fasting mimicking diets in the prevention and treatment of autoimmune diseases and immunosenescence

CD8 T cell-mediated killing of orexinergic neurons induces a narcolepsy-like phenotype in mice.  http://sci-hub.ac/10.1073/pnas.1603325113

 

Thanks @Jasonmfor the sci-hub info - opened up a whole new world!

On 12/04/2017 at 4:41 PM, Jasonm said:

For anyone that is or is interested in being a fellow with too much time on their hands@Pereise1 @HBr (jk) like me and thought man that abstract sounds interesting and want the full article, try:

www.sci-hub.ac

It doesn't work for pubmed links but it does for just about every other one. I've always been able to get the full article using it. It was started by a renegade scientist that thought research shouldn't be restricted. It's pretty ridiculous that research mostly funded by tax money costs $30-40 an article. Enjoy. 

 

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On 5/28/2017 at 9:29 AM, Jasonm said:

@Pereise1 there's not tons of research on the subject but here's what I found. 

Cardiovascular fitness in narcolepsy is inversely related to sleepiness and the number of cataplexy episodes. This is just an association. 

Exercise Influence on Hippocampal Function: Possible Involvement of Orexin-A this article has a bunch of information you may find interesting since it also goes into neurogenesis.

In men with severe sleepiness, regular exercise was associated with a reduction of sleepiness by nearly 41%. It's unclear if this only applies to sleep apnea. 

Bright light soon after waking in the morning, preferably outdoor sunlight, seems to be beneficial as well. 

Sorry for the delay in responding, just came back from the sister-in-law's wedding in Peru. The 1st and 3rd studies are mainly correlations, although I can think of a few reasons why exercise would help with sleepiness and cataplexy. I found the 2nd study highly interesting. I would have guessed that orexin would improve hippocampal neurogenesis as orexin has an antidepressant effect and its activation is necessary to the addiction process as well as simply feeling joy from life. But per that study, it directly enhanced neuron growth. I'm curious if my current orexin-a dosing is helping in this way. Certainly feels like it but I can't say for sure.

As for one of the main mechanisms behind the benefits of exercise in Narcolepsy, the serotonin 5-HT1A receptor plays a big role. The presynaptic 5-ht1a receptor, heavily localized in the raphe nuclei, is an autoreceptor which decreases serotonin in other parts of the brain. This is good for us, as the hypothalamus almost exclusively expresses postsynaptic 5-ht1a receptors, which strongly antagonize orexin. For reference, check out the following 2 studies:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3738049/ ("Influence of Inhibitory Serotonergic Inputs to Orexin/Hypocretin Neurons on the Diurnal Rhythm of Sleep and Wakefulness")

http://www.jneurosci.org/content/24/32/7159 ("Serotonergic Regulation of the Orexin/Hypocretin Neurons through the 5-HT1A Receptor")

Exercise upregulates the 5-HT1A receptor in the Raphe Nuclei (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4386483/), which is a major site of presynaptic receptors and reduces the binding of serotonin to other sites in the brain, particularly the postsynaptic 5-HT1A receptors in the hypothalamus where they release stress hormones and are anxiety inducing (http://www.jneurosci.org/content/16/15/4810.full and https://www.ncbi.nlm.nih.gov/pubmed/8199791). 

Just for that reason alone I'd recommend exercise to each and every PwN. Depression is a massive obstacle to healing a glial scar and to any kind of neurogenesis. In addition, the Raphe Nuclei (presynaptic 5-ht1a) is a major target for orexin, so anything increasing it's function is a step in the right direction:

Quote

The hypothalamus plays a critical role in maintaining energy homeostasis by coordinating behavioral, metabolic, and neuroendocrine responses (Bernardis and Bellinger, 1996). Within this region, the lateral hypothalamic area (LHA) has been regarded as an important center for feeding and arousal because animal models with LHA lesions exhibit hypophagia and decreased arousal that frequently leads to death. Orexin A and orexin B (also known as hypocretin 1 and hypocretin 2) are neuropeptides expressed exclusively by LHA neurons. Orexin-producing neurons (orexin neurons) project their axons throughout the brain (Peyron et al., 1998; Nambu et al., 1999), which suggests that their functions are varied. Remarkably, dense projections of orexin neurons are observed in the serotonergic dorsal raphe nucleus (DR), noradrenergic locus coeruleus (LC), and histaminergic tuberomammillary nucleus (TMN); and all of these nuclei are involved in promoting arousal (Saper et al., 2005). Prepro-orexin knockout mice, orexin receptor knockout mice, and orexin neuron-ablated transgenic mice all show severely defective sleep/wakefulness cycles (Chemelli et al., 1999; Hara et al., 2001; Willie et al., 2003). Consistently, deficiencies of orexin function were found in human narcolepsy (Nishino et al., 2000; Peyron et al., 2000; Thannickal et al., 2000). These findings clearly show the importance of the orexin system in the regulation of sleep/wakefulness. Past studies also revealed roles for orexin neurons beyond feeding and arousal, including autonomic nervous system control (Sellayah et al., 2011; Tupone et al., 2011) and in reward and stress systems (Boutrel et al., 2005; Harris et al., 2005).

 

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@Pereise1 interesting. Hope you had a pleasant trip! I've heard the opposite about postsynaptic 5ht1a. For instance, I've read presynaptic agonism is what causes the initial side effects from SSRIs and that the efficacy of SSRIs is largely dependent on the eventual down regulation of the receptor. 

Serotonin is obnoxiously complicated however. From my rudimentary understanding it's true postsynaptic 5ht1a agonism hyperpolarizes orexin neurons. However orexin activates postsynaptic 5ht1a, and that lack of activation in orexin deficiency may be a large contributing factor to EDS. It could be an autoregulatory response. Obviously if you have N+C and no orexin neurons to hyperpolarize 5ht1a post synaptic agonism isn't going to hyperpolarize them. SSRIs made me so lethargic I could barely move. Selective post synaptic 5ht1a agonists are in development for the improved treatment of depression. 

A 5ht1a postsynaptic agonist returned orexin knockout nice to control levels of activity in one study. Obviously this might not work for non orexin deficient N. That or it's just giving them serotonin syndrome lol. 

Narcolepsy-like sleep disturbance in orexin knockout mice are normalized by the 5-HT1A receptor agonist 8-OH-DPAT


If anyone is really bored this is a good video on postsynaptic vs presynaptic 5ht1a.

@Jacky happy to help! Just be careful. A lot of the research out there is bad or biased. The bigger very selective journals tend to be more reliable. 

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On 6/10/2017 at 6:47 AM, Jasonm said:

@Pereise1 interesting. Hope you had a pleasant trip! I've heard the opposite about postsynaptic 5ht1a. For instance, I've read presynaptic agonism is what causes the initial side effects from SSRIs and that the efficacy of SSRIs is largely dependent on the eventual down regulation of the receptor. 

Serotonin is obnoxiously complicated however. From my rudimentary understanding it's true postsynaptic 5ht1a agonism hyperpolarizes orexin neurons. However orexin activates postsynaptic 5ht1a, and that lack of activation in orexin deficiency may be a large contributing factor to EDS. It could be an autoregulatory response. Obviously if you have N+C and no orexin neurons to hyperpolarize 5ht1a post synaptic agonism isn't going to hyperpolarize them. SSRIs made me so lethargic I could barely move. Selective post synaptic 5ht1a agonists are in development for the improved treatment of depression. 

A 5ht1a postsynaptic agonist returned orexin knockout nice to control levels of activity in one study. Obviously this might not work for non orexin deficient N. That or it's just giving them serotonin syndrome lol. 

Narcolepsy-like sleep disturbance in orexin knockout mice are normalized by the 5-HT1A receptor agonist 8-OH-DPAT


If anyone is really bored this is a good video on postsynaptic vs presynaptic 5ht1a.

@Jacky happy to help! Just be careful. A lot of the research out there is bad or biased. The bigger very selective journals tend to be more reliable. 

I've spent a lot of my free time the last 3 days trying to come up with an adequate, yet brief, response lol. To put it briefly, the therapeutic lag in SSRIs seems to have a lot to do with post-synaptic 5-HT1A downregulation, as opposed to the somatodendritic receptor. The post-synaptic receptor is heavily expressed in the hypothalamus, which is why most of it's function is mainly neuroendocrine, which would obviously increase activity due to it's cortisol releasing properties.

As you said though, with serotonin, nothing is that simple. Activation of the presynaptic receptors in certain brain regions can have a positive effect by inducing oxytocin or by inhibiting the stress response. Of course, activation of the post-synaptic receptors can also have a positive effect on low cortisol/hypoactive individuals, however, this apparently has a lot to do with the ratio of presynaptic vs postsynaptic 5-HT1A receptors. I found the following review interesting:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2736801/ ("5-HT1A Receptor Function in Major Depressive Disorder")

Despite the 30+ hours of reading I've done on the serotonin system to try to understand why the paxil I was put on effected me so negatively long term, it's still one of the most complicated subjects of neurology for me. That's why the only times I'll mess with serotonin is with herbal stuff, as the pharmaceuticals have too many risks IMO. The 8-OH-DPAT from that Narcolepsy is a little flawed, mainly in that the study makes the theory that only the 5-HT1A receptor was involved when it's been discovered that 8-OH-DPAT also has significant actions at 5-HT7 and is also a SSRI/SRA (https://en.wikipedia.org/wiki/8-OH-DPAT)

Finally, the "antidepressant" effect of many SSRIs is thought now to have more to do with the conversion of serotonin to N-Acetylserotonin, which, as opposed to serotonin itself, is a strong antidepressant which increases BDNF + other neat stuff: https://en.wikipedia.org/wiki/N-Acetylserotonin

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4 hours ago, Pereise1 said:

to try to understand why the paxil I was put on effected me so negatively long term

Tends to rot your liver leading to possible death.

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@Pereise1 oh believe me I was skeptical of the 8-OH-DPAT study. Serotonin syndrome will cause increased activity too. It's too simple of a model and sounds too good to be true. 

Not surprising that we've come to the opposite conclusion on presynaptic vs post. Unfortunately the literature is all over the place. It's definitely not settled how SSRIs, depression, etc relate. I kind of feel like they just chose a random neurotransmitter, in this case serotonin, and decided it was the most important factor in depression. Definitely an interesting topic. 

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On 6/13/2017 at 11:02 PM, HBr said:

Tends to rot your liver leading to possible death.

I wouldn't doubt it, that stuff is garbage even among SSRIs. I've noticed that I can't take anything serotoninergic or any MAOAIs. I feel that I may have an impaired SERT (Serotonin transporter) even 7 years after discontinuing the Paxil. I'm curious if I can join some class action lawsuit, as I was a minor when it was prescribed. Something to look into.

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On 6/14/2017 at 5:41 AM, Jasonm said:

@Pereise1 oh believe me I was skeptical of the 8-OH-DPAT study. Serotonin syndrome will cause increased activity too. It's too simple of a model and sounds too good to be true. 

Not surprising that we've come to the opposite conclusion on presynaptic vs post. Unfortunately the literature is all over the place. It's definitely not settled how SSRIs, depression, etc relate. I kind of feel like they just chose a random neurotransmitter, in this case serotonin, and decided it was the most important factor in depression. Definitely an interesting topic. 

Yes, that's why I tend to prefer clinical reviews to the odd, pharmaceutical company funded study. As for the presynaptic vs postsynaptic, I'm not sure that we disagree. I'm against the notion of touching that receptor with any high affinity pharmaceuticals because, as you mentioned, the literature is all over the place. The neuroendocrine and anti-orexin effects of the postsynaptic receptor definitely make me more wary of activating it in general. In these cases, I strongly prefer even anecdotal reports to flawed pharmaceutical studies. For example, it's well documented that exercise is an effective antidepressant. It's also known that it increases the 5-HT1A receptor in certain parts of the brain and that this effect is what is possibly behind it's help in stress management and fatigue. So increasing the 5-HT1A receptor in this way has solid anecdotal proof that it helps with fatigue and stress management, therefore, I'm on board with it. Otherwise, I prefer leaving the serotonin system alone, aside from trying to lower general levels of it in my personal case as this subjectively helps with my symptoms.

And yes, the serotonin system is far too complicated to just wantonly say low serotonin = depression. I remember reading in a study one time that even the researchers came to the conclusion that "As time goes on, it has become clear that the serotonin system is one of the most exceedingly complicated aspects of neurobiology". :wacko:

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47 minutes ago, Pereise1 said:

I wouldn't doubt it, that stuff is garbage even among SSRIs. I've noticed that I can't take anything serotoninergic or any MAOAIs. I feel that I may have an impaired SERT (Serotonin transporter) even 7 years after discontinuing the Paxil. I'm curious if I can join some class action lawsuit, as I was a minor when it was prescribed. Something to look into.

It was pulled off the market north of 49 ages ago, although the druggist did say they hadn't done the same for the generic version. There was associated deaths. I'm surprised to hear it was still available 7 years ago!? The stuff made me extremely tired and I'm glad I discontinued it quickly.

GlaxoSmithKline has paid substantial fines, paid settlements in class action lawsuits, and become the subject of several highly critical books in relation to its marketing of paroxetine, in particular the off-label marketing of paroxetine for children, the suppression of negative research results relating to its use in children, and allegations that it failed to warn consumers of substantial withdrawal effects associated with use of the drug.[12][13][14]

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@Pereise1 you took an maoi? 

My only real interest in serotonin is that 5ht2a antagonism has shown promising results on increasing sws and decreasing awakenings. 

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4 hours ago, HBr said:

Good thing you discontinued it quickly, I discontinued it cold turkey as soon as I started getting suicidal thoughts. Right after that my anxiety got strangely better but the dreaded brain zaps and irritability continued for quite some time. My OCD and anxiety is mainly gone, except for the ruminating thoughts part, but the trade off is most definitely not worth it. I used to really be into art, since then, for some reason both my desire and my base skill have never been the same. I've done a lot of research into how to gain this aspect of myself back but it eludes me unfortunately. Ah... to be 16 again :P

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1 hour ago, Jasonm said:

@Pereise1 you took an maoi? 

My only real interest in serotonin is that 5ht2a antagonism has shown promising results on increasing sws and decreasing awakenings. 

A few of the herbals I've taken have MAO-A inhibiting activity. Some, like Rhodiola and Turmeric, are tolerable. Others, like Polygala Tenuifolia, can sometimes cause a little dysphoria, which is unfortunate as Polygala's one of the best herbs out there and has a really positive effect on my cognitive dysfunction.

Also, there's a number of good results from manipulating certain well understood serotonin receptors. 5-HT3 is one I try blocking every day as Armodafinil agonizes it and I feel like that's behind my strong loss of appetite during the last couple of months. Well that and mold exposure.

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Hi guys, new here

Seriously interesting research going on here. I've been trying to document everything I can find on the subject ever since my MSLT. 

Some questions regarding to the subject matter above:

1. Regarding to the interaction of Orexin and Histamine and water/electrolyte intake: ever since the symptoms worsened somewhat during the past two years, my skin and body seem to show what I would call symptoms of dehydration. (red indentations when leaning on things that don't disappear). Is there any research on this interaction? (both histamine and orexin are also involved in water/hydration of the body). While my wakefulness in general hass increased, I notice that my body produces much more histamine, or at least symptoms thereof: I somehow have the skin-writing thing now (a form of urticaria) which also increases a lot just before a sleep attack. Also the body temperature rises a lot in that period and blood-flow seems to become stagnant. (tingling hands, feet)

2. Is there any research on airway-function during the day (and leading upto a sleep-attack)? I'm a singer and swimmer, and in both my airway and long-function seem to change drastically when on the verge of a sleep or cataplexy attack. Also bodily posture and muscle activity seems to lower a lot in general. (in particular skeletal muscles seem to relax, the throat becomes narrow and particularly the exhale part of breathing is virtually non-existent or very passive). 

3. I somehow have lost a lot of my sense of smell and taste during the past 1,5 year. Which is also pretty annoying and perhaps tied into the dehydration symptoms (nasal irrigiation is pretty much non-existent). 

The body gets used to cataplexy somehow (it seems to become much more rigid when the symptom arises). But I'm trying to find ways to optimize my productivity inbetween sleep and cataplexy episodes. 

I'm a fulltime artist, and one way I've found to deal with the crazy dreams and hallucinations, is by documenting them to use for my work. This makes you more curious as to what is going to happen, rather than afraid. But there are certain places where I had bad experiences that seem to take my mind immediatly to the spooky stuff. 

 

Thanks for this interesting forum, I now have a place to read up on research en try to explain what I've found so far myself.

 

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@Nocturne: I think we would need to know what meds you are on to offer better insight. You say your wakefulness has improved - what has made that happen? 

Regarding the dehydration issues: have you tried increasing your daily fluid intake?

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