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Natural Treatment That Works (For Me)


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#1 ronny

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Posted 04 November 2013 - 11:08 AM

Hi,

 

I would like to share some personal experience and discoveries that has helped me a lot in managing my narcolepsy symptoms. I have been following the latest research regarding narcolepsy treatment and experimented with a lot of different natural supplements. Most of what I have tried had little or no effect, however there are a couple of things that actually works for me. Hopefully this can help some of you as well.

 

I have noticed a dramatical improvement of symptoms after taking Kutaj (Holarrhena antidysenterica). I did some research into patent applications for narcolepsy drugs and found that several drugs affecting the H3 receptor s now under development. Scientific background: http://www.hal.inser...nserm-00150083/ . Not wanting to wait years for these drugs to be approved and put on the market, I tried to find a natural supplement working as a H3 receptor antagonist and I found Kutaj (Holarrhena antidysenterica) that has this effect  because of its natural content of Conessine ( http://en.wikipedia.org/wiki/Conessine ). Kutaj is used in Indian Ayurvedic Medicines for a totally different purpose, but I found it to be very effective for managing daytime sleepiness.

Another supplement that has helped me as well is  Ginko Biloba that work as a GABA Receptor Antagonist,  Glycine Regulator and enhances dopaminergic neurotransmission:

http://www.ncbi.nlm....pubmed/12600688
http://www.ncbi.nlm....pubmed/18325484
http://www.ncbi.nlm....pubmed/19427589

 

Lastly I'm using L-tyrosine that affect dopamine and noradrealine levels and therfore activating orexin nevrons.

 

http://deepblue.lib.....pdf?sequence=1

http://www.earthsfin...y-research.html

 

These three all natural supplements has improved my daytime sleepiness a lot. I hope they can be of use to you as well :)

 

 

 

 



#2 Kimpossible

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Posted 06 November 2013 - 10:55 AM

Chemist - if you're out there, I'm interested to see what you think about this.



#3 b.chrissie@yahoo.com

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Posted 15 November 2013 - 11:30 AM

Thank you so much for sharing this Ronny. I tried a bevy of natural supplements to no avail, perhaps this Kutaj (Holarrhena antidysenterica) will help! Thanks again.



#4 Ferret

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Posted 15 November 2013 - 01:57 PM

Please check the entire pathways for different supplements...MOST REQUIRE THE B VITAMINS to work in the body.
I'll have to come back to this later...I just lost an entire post complete with numerous links explaining and detailing the pathway for Serotonin...and, sorry, but now it's nap time. Catch ya later.

#5 Chemist

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Posted 15 November 2013 - 07:51 PM

Chemist - if you're out there, I'm interested to see what you think about this.

 

Well first I think it's important to note that just because a chemical compound comes directly from nature does not make it any more safer, effective, or tolerable than man-made drugs. An overwhelming number of them cause serious illness, permanent disability, or death. So I would advise people not to automatically associate "natural" with "good for you" and man-made with "bad for you." Where science has taken naturally occurring chemical compounds and turned them into drugs in the past, they're usually "tweaked" to make them much safer and tolerable for humans.

As far as the potential use of the chemical compounds suggested by ronny, I'll say this:

Conessine from Kutaj (Holarrhena antidysenterica) - This chemical compound is in fact a potent and specific H3 antagonist, and H3 antagonists are being studied for the treatment of Excessive Daytime Sleepiness. However, conessine in particular is considered to have no medicinal value due to its exceptionally long half life in the body and its binding to alpha-2 adrenoreceptors. The reason this makes it thoroughly unusable is because H3 antagonists are expected to act as stimulants, and stimulants must have a half-life short enough to allow the majority of the drug to be gone by bed time to prevent interference with sleep and development of chronic tolerance. The half-life of conessine is so long that it would disrupt sleep for a few days until tolerance was established, and thereafter it would have little to no effect on energy levels whatsoever. I found no mention of whether conessine acts as an agonist/antagonist/inverse agonist at the alpha-2 adrenoreceptor, but presumably it acts as an antagonist there as well. This would cause an increase in adrenaline and noradrenaline neurotransmission which could lead to numerous side effects with the most serious being anxiety, rapid heart rate, hypertension, and palpitations.

Ginkgo biloba - There are at least four different biologically active compounds in ginkgo biloba and there has been a lot of research into gingko biloba. The reason for the research is that it does appear to have some weak but interesting medicinal properties and if we can figure out what is responsible for those effects, we may be able to make a man-made drug that acts in a similar fashion but is many times stronger, safer, and tolerable in humans. At present, the only significant properties we find that ginkgo biloba has when taken for more than a few days is some improvement in blood flow, mainly due to its effect on platelets, and moderate norepinephrine reuptake inhibition. Any effects upon GABA(A) receptors are likely to be very weak and essentially of no significance.

Note that generally drugs acting upon GABA either as agonists or antagonists are not very desirable due to the widespread prevalence of GABA receptors in the brain. This means drugs acting on GABA typically cause global effects on the entire CNS as opposed to affecting a small number of functions or pathways in the brain. With GABA agonists like ethanol or benzodiazepines you get sedation, confusion, impaired memory and with GABA antagonists you get hyperexcitability, seizures, and potentially brain damage. Tolerance also builds rapidly to these types of drugs, and the withdrawal from them can cause life threatening complications.

L-Tyrosine is just an amino acid we all produce in our bodies from the essential amino acid L-Phenylalanine that we get in our diets. It is used in our bodies to generate dopamine, epinephrine, norepinephrine, and the thyroid hormones T3 and T4. Using L-Tyrosine supplements does increase its concentration in the blood and does in fact increase the plasma concentrations of the neurotransmitters it's a precursor to, but it has little if any effect on mood or energy. Typically people take the supplement L-DOPA instead of L-Tyrosine, because the rate-limiting step in the biosynthesis of dopamine from L-Phenylalanine is the conversion of L-Tyrosine into L-DOPA. L-DOPA itself is then rapidly converted into dopamine and immediately available for use. Even so, L-DOPA is not typically considered a stimulant and in fact large doses of L-DOPA or certain drugs in the dopamine agonist class actually cause narcolepsy-like sleep attacks. Most of the studies referenced by ronny are those that were conducted before it was known that orexin and histamine were the major players in regulating arousal and not dopamine.

As far as dopamine and norepinephrine activating orexinergic neurons, that's not true. In fact, it's the opposite. Orexinergic neurons have receptors for several neurotransmitters and neuropeptides, all of which can be excitatory or inhibitory and thus increase or decrease the likelihood that the neuron will fire and release orexin. When orexin is released onto catecholaminergic neurons it is extremely excitatory and promotes dopamine and norepinephrine mediated neurotransmission. However, when those catecholamines flood back onto the orexinergic neurons they produce an inhibitory action and provide negative feedback to the orexinergic neuron. The study that ronny referenced had shown that dopamine and norepinephrine INDIRECTLY activate orexinergic neurons, and ONLY when the animals were not anesthetized. When the animals were anesthetized, dopamine and norepinephrine did not activate the orexinergic neurons.

Another important thing to note is that in classic narcolepsy where there is a loss of orexinergic neurons and cataplexy, trying to activate orexinergic neurons is an exercise in futility, because those neurons have physically been destroyed and their debris mopped up. There's no neuron physically present which can release orexin anymore. In other forms of narcolepsy and hypersomnia exciting the remaining healthy orexin producing neurons may prove useful, but orexin agonists will probably be the most useful tool in treating excessive daytime sleepiness (EDS.)
 

So essentially, and here comes the much shorter answer, the suggested combination of supplements would not be expected to have any significant impact on excessive daytime sleepiness.



#6 Ferret

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Posted 15 November 2013 - 11:38 PM

I experimented with the Serotonin pathway way back in '89. There was no internet (for the general public) and I was limited to medical texts. Much more is known today including info about Serotonin Syndrome...which is TOO MUCH Serotonin...whereas I made the assumption that I had TOO LITTLE Serotonin because I wasn't getting the restful stage of sleep. I could not, at that time, find any info on what the precursor substances were for Norepinephrine which was also stated to be responsible for the restful stage of sleep. This all took place four years after diagnosis of N&C and after my disaster with Ritalin and Tofranil. Not taking any meds and I was a zombie.
Taking supplements without checking whether you need those supplements can be detrimental to your health...more is not necessarily better. Be warned! AND TAKE THE WARNING SERIOUSLY! You wouldn't even attempt what I did IF you were taking antidepressants (SSRI's)
Trytophan plus vitamin B6 converts to Serotonin...caffeine interferes with the conversion.
1) B6 + Tryptophan naturally (almonds, milk, bananas) and no caffeine = no change
2) B6 + Tryptophan supplement and no caffeine = improvement in mood and EDS
3) Tryptophan supplement and no caffeine = back to square one
Each test was done for one month. I was about to go back to doing test #2 when Tryptophan was pulled off the market.
It did work for me and I did feel better but I think I was really lucky that I really did need those supplements because I could have really done some damage to myself.
More information is available now...and probably much more to come. We have very complicated bodies.
FYI...
edited to add... http://www.livestron...n-affect-sleep/  (can't believe I forgot this one)

http://www.livestron...tonin-produced/
http://www.lef.org/m...&key=Tryptophan
http://www.livestron...ease-serotonin/
http://www.livestron...b-12-serotonin/
http://www.livestron...in-c-serotonin/

So, I'm still a believer...and have often wondered why the tryptophan supplement worked but I seemed to be unable to get the tryptophan out of the food...missing enzymes? or?...whatever.
I also wonder if chronic bowel inflammation ends up affecting the amount of serotonin produced in the brain 'cuz the gut is swiping all the tryptophan for the serotonin produced in the enterochromaffin cells of the gut.
http://robbwolf.com/...inal-disorders/

Lots of questions...even after all these years.



#7 Chemist

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Posted 16 November 2013 - 05:09 AM

Re: Serotonin

 

L-Tryptophan supplements were pulled off the market after contaminants in some batches were causing irreversible neurological damage in people taking it. However, it's back on the market now, along with 5-HTP which is one step closer to serotonin in the biosynthesis pathway. You can easily find them online or in most shops these days. The supplements offer much higher concentrations than what you would get out of a meal. Plus when you eat a meal most of the various amino acids are in competition with one another for absorption. When you take a large dose of pure amino acid, there's no competition and a huge amount of it gets absorbed, and quickly. That's the major difference between getting an amino acid from a meal and getting it from a supplement.

 

The precursors for norepinephrine are L-phenylalanine -> L-tyrosine -> L-DOPA -> Dopamine -> Norepinephrine with L-tyrosine -> L-DOPA being the rate limiting step. However, you cannot expect to get improved sleep by causing a general increase in the concentrations of dopamine and norepinephrine because that would cause arousal and insomnia in most cases. During sleep only specific circuits in the brain that signal through norepinephrine and dopamine are active and regulating sleep, the others transition through no-low periods of activity and periods of high activity. Unfortunately you can't specifically target the circuits that are actually responsible for regulating portions of sleep without also affecting all the others that have nothing to do with it. At least, not through any conventional therapeutic means.

 

In any event, the effect of serotonin on suppressing REM and promoting SWS, along with helping to reduce insomnia in general, is well known. That's one reason, beyond the frequent comorbidity of anxiety/depression and narcolepsy, you see PWN having been prescribed an SSRI at one point or another.



#8 Kimpossible

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Posted 16 November 2013 - 09:45 AM

How do people know if they have any orexin receptors left or if they are all gone?



#9 Ferret

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Posted 16 November 2013 - 10:09 AM

How do people know if they have any orexin receptors left or if they are all gone?

I plugged your question into google...

https://www.google.c...ey are all gone

 

The first link shown is from the Stanford Sleep Centre (which hosts this forum)...Hypocretin 1 is measured in the Cerebrospinal Fluid.

 

That only tells you if the Neurons producing Hypocretin 1 are toast. I don't believe there is a way to measure hypocretin receptors...yet. And, the possibility exists that those receptors are not specific to just hypocretin...just like a parking space will accept an SUV or a Mini Cooper. Complicated.



#10 Ferret

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Posted 16 November 2013 - 10:37 AM

L-Tryptophan supplements were pulled off the market after contaminants in some batches were causing irreversible neurological damage in people taking it. However, it's back on the market now, along with 5-HTP which is one step closer to serotonin in the biosynthesis pathway. You can easily find them online or in most shops these days. The supplements offer much higher concentrations than what you would get out of a meal. Plus when you eat a meal most of the various amino acids are in competition with one another for absorption. When you take a large dose of pure amino acid, there's no competition and a huge amount of it gets absorbed, and quickly. That's the major difference between getting an amino acid from a meal and getting it from a supplement.

 

The precursors for norepinephrine are L-phenylalanine -> L-tyrosine -> L-DOPA -> Dopamine -> Norepinephrine with L-tyrosine -> L-DOPA being the rate limiting step. However, you cannot expect to get improved sleep by causing a general increase in the concentrations of dopamine and norepinephrine because that would cause arousal and insomnia in most cases. During sleep only specific circuits in the brain that signal through norepinephrine and dopamine are active and regulating sleep, the others transition through no-low periods of activity and periods of high activity. Unfortunately you can't specifically target the circuits that are actually responsible for regulating portions of sleep without also affecting all the others that have nothing to do with it. At least, not through any conventional therapeutic means.

 

In any event, the effect of serotonin on suppressing REM and promoting SWS, along with helping to reduce insomnia in general, is well known. That's one reason, beyond the frequent comorbidity of anxiety/depression and narcolepsy, you see PWN having been prescribed an SSRI at one point or another.

 

If you read my post again, I said "AT THE TIME" which was '89 and the precursors for norepinephrine were not well known.

And the common prescription for SSRI as sleep aids were not well known because the ONLY one (at that time) that was allowed to be prescribed for Cataplexy was Tofranil. Period. End Story.

 

Much has been learned and discovered and there is much more to learn.

BTW, there are still warnings, even for 5-HTP, that it can still cause Eosinophilia Myalgia...and the thought is now that it may possibly not have been a contaminant at all. Who knows.

Perhaps those who got the E.M. already had sufficient Serotonin in their system and the extra produced tipped them over the edge.

It's a slippery slope taking ANY supplement that has not been PROVEN that you lack it. Be sure to also discuss it with your Doctor AND understand what the medicines that you're already taking do to your body.

UNDER NO CIRCUMSTANCES TAKE A TRYPTOPHAN OR 5-HTP SUPPLEMENT IF YOU'RE ALREADY ON AN ANTIDEPRESSANT THAT AFFECTS SEROTONIN LEVELS.



#11 Chemist

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Posted 16 November 2013 - 03:01 PM

If you read my post again, I said "AT THE TIME" which was '89 and the precursors for norepinephrine were not well known.

And the common prescription for SSRI as sleep aids were not well known because the ONLY one (at that time) that was allowed to be prescribed for Cataplexy was Tofranil. Period. End Story.

 

[...]

 

I read your post correctly the first time and just wanted to provide more information in the event that you, or more importantly others who might read this thread, weren't already aware of it. My reply was intended to be informative, not argumentative, so I apologize if it came across as such.



#12 browndog319

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Posted 03 December 2013 - 11:44 PM

Here is a dumb/maybe not such a dumb question: in my research, I found that when they injected monkeys who had been sleep deprived for 36-42 hours with orexin,  the neurochemical alleviated the cognitive deficiencies normally seen with such amount of sleep loss. This to me signals that there should be a way to create a synthetic orexin (it's a neurochemical, why can't they make that???) to inject into us and cure us. I'm going to talk to my sleep doctor about it. He's the chief of his sleep center at an academic/research hospital.

 

Does this seem insane? Or like a plausible hypothesis?



#13 Ferret

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Posted 04 December 2013 - 12:46 AM

It's not dumb at all...but can they reproduce it? How much Orexin to inject? A or B? When? Where? and How often? Because just injecting the Orexin won't cure...it would have to be maintained.

Personally, I would like to have a transplant of Orexin producing neurons from a tissue matched donor. But, the possibility exists that whatever killed mine will also kill theirs. And then you get into brain surgery to do the transplant...sigh. Risky business. Maybe I'll just make do with what I've got :)



#14 Chemist

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Posted 04 December 2013 - 01:09 AM

Here is a dumb/maybe not such a dumb question: in my research, I found that when they injected monkeys who had been sleep deprived for 36-42 hours with orexin,  the neurochemical alleviated the cognitive deficiencies normally seen with such amount of sleep loss. This to me signals that there should be a way to create a synthetic orexin (it's a neurochemical, why can't they make that???) to inject into us and cure us. I'm going to talk to my sleep doctor about it. He's the chief of his sleep center at an academic/research hospital.

 

Does this seem insane? Or like a plausible hypothesis?

 

Producing synthetic orexin on an industrial scale would be feasible, sure. The problem is it's a peptide (small chain of amino acids) so you can't just take it in pill form because your digestive system will destroy it. You would have to be injecting it intravenously, which isn't all that efficient as it still has to cross the blood-brain barrier to have any effect. In the studies they did they used a nasal spray as a more effective delivery method, since this concentrates orexin in the blood near the blood-brain barrier, allowing more of it to get through. There's no mention of how long the effects lasted, but I imagine orexin is degraded quickly enough that you would need to be squirting this nasal spray up your nose quite often.

 

Orexin agonists would be just as if not more effective, and I believe they're already being worked on. They would have the added benefit of being in pill form and lasting all day long. Orexin antagonists,which have the opposite effect, have already been created. The idea is to use them as a sleep aid in people with insomnia. Those are in testing now.

 

While it's anticipated that orexin agonists will be highly effective as wakefulness promoting drugs, it doesn't seem likely that they will restore persons with narcolepsy to perfect health. This is because treating the excessive daytime sleepiness associated with narcolepsy does not solve the problems with deranged sleep architecture, and while destruction of orexin neurons may be the cause of that issue, you wouldn't be able to solve it with orexin or orexin agonists because you would be waking the whole brain up instead of powering the specific circuit that helps maintain a proper sleep architecture. Even so, they will likely be much more effective than the drugs we have available today.



#15 Adrian Patterson

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Posted 27 June 2014 - 07:16 AM

Hi guys, I don't have Narcolepsy, so feel a bit of an impostor- and feel free to banish me from your discussions if my presence offends you. I had an operation to remove a colloid cyst from the third ventricle, which borders the hypocretin neurons which you guys have in short supply. I have reason to believe the cyst or the operation to remove it has either destroyed some of the hypocretin neurons, or at least the connection the hypocretin nuclei make with other brain mechanisms. My symptoms are hyper-arousal, erectile dysfunction- from a failure to arouse, and broken sleep- I rarely get a full nights sleep without some form of self medication. My GP's have shown no interest in my symptoms and say it is just the "New Normal" that my brain has to put up with. I do occasionally have periods when I will have trouble staying switched on, and I take copious amounts of coffee on car journey to prevent me keeling over. My circadian rhythyms are also up the left- if I get up at a new rising time, say to start a new job, it is like the worst jet lag, with tremendous anxiety thrown in.

I read your posts with great interest, and whilst I don't think I could describe myself as being narcoleptic, I do see paralells. I have a few questions for you. Is erectile dysfunction one of the less well known issues with narcolepsy? Is extreme anxiety linked with narcolepsy?

I had read initially that PTSD was associated with low levels of hypocretin, but subsequently read that hyperarousal is caused by producing too much hypocretin, which clearly could not be the case if you have a reduced number of hypocretin neurons.

I'm also interested in your solutions for increasing hypocretin, which is why I am replying to this post. Strikes me, and if my experience is anything to go by you can either get into the general stimulation from caffeine or other stimulants or you can work out what causes hypocretin to be secreted. The latter either can be from assisting the body to create the building blocks to make the hypocretin peptide or finding ways of causing the neurons to potentiate to fire and secrete.

Looking at the discussion so far, I am keen to get my hands on calcium lactate- pyruvate I found upset my stomach. I note also that amino acids rather than glucose also help stimulate production. A big dessert on a Sunday full of sugar, just wipes me out.  I like the idea of a herb Conessine from Kutaj (Holarrhena antidysenterica), that could help and wonder if the person who used this herb found the problems that the Chemist described?

I note for example I get an erection on strong coffee, and was going to experiment with Gurana- which had no effect- and then caffeine pills, only to realise the one I purchased also contained large amounts of glucose- which I imagine would be counterproductive. Wonder would the Conessine above help with the erections?



#16 Area-1255

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Posted 19 August 2014 - 06:28 AM

I would have to say that OP is definitely moving in a fair direction, H(3)R antagonist are being studied as Nootropic's, Vigilance Tonics and anti-depressants. As well as weight loss, obesity and for their antipsychotic profile.

 

http://area1255.blog...mine-3-h3r.html

I've outlined two different sources of Conessine in the above article.

EDIT : Btw the information on where to get these natural herbal H(3) antagonists are above in that link.

 

I plan to look into it more.

Also be aware that Green Tea/Tea extract will greatly reduce the prohistamine effects of these herbs.

The ultimate narcolepsy treatment would probably be something more like.

1.) Ginkgo

2.) Adrafanil/Modafanil

3.) Either hollarhena or Yamoa.



#17 Area-1255

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Posted 19 August 2014 - 07:32 AM

Serotonin antagonists may also be of use...specifically 5-HT1A blockers combined with 5-HT1B/D blockers. Unfortunately, there isn't any available for 5-HT1A, but Yohimbine HCL is interesting and it antagonizes 5-HT1B/C/D/F.  



#18 Sinister Hellfire

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Posted 24 August 2014 - 03:39 PM

I would have to say that OP is definitely moving in a fair direction, H(3)R antagonist are being studied as Nootropic's, Vigilance Tonics and anti-depressants. As well as weight loss, obesity and for their antipsychotic profile.

 

http://area1255.blog...mine-3-h3r.html

I've outlined two different sources of Conessine in the above article.

EDIT : Btw the information on where to get these natural herbal H(3) antagonists are above in that link.

 

I plan to look into it more.

Also be aware that Green Tea/Tea extract will greatly reduce the prohistamine effects of these herbs.

The ultimate narcolepsy treatment would probably be something more like.

1.) Ginkgo

2.) Adrafanil/Modafanil

3.) Either hollarhena or Yamoa.

wow thnx for this! i've read some of your work and i am really interested. u seem to know what you are talking about!



#19 AMxreborn

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Posted 25 August 2014 - 07:15 AM

Betahistine, Pitolisant and others have all shown promise in narcolepsy - but the one I find very interesting in particular (in regards to R&D chems) is Ciproxifan.

That's a true H(3) antagonist with extremely high BBB penetration.



#20 Area-1255

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Posted 26 August 2014 - 05:50 PM

Many of us do, I found this thread very to be very intriguing.