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Cluster Headache Help and Support >> Medications, Treatments, Therapies >> Niacin
(Message started by: jtt112852 on Oct 23rd, 2006, 9:46am)

Title: Niacin
Post by jtt112852 on Oct 23rd, 2006, 9:46am
New to this site but not new to clusters which I have been bleeesed with(Ha) for 22 years now. I recenty and by accident discoverd that taking at least 5000mg of niacin will stop my headache in its tracks about 80% of the time. There are twoo types of niacin(B-6) the non-flushing and regular. The non-flushing doesn't seem to work for me and if you take the regular be sure to eat something first.

Title: Re: Niacin
Post by E-Double on Oct 23rd, 2006, 9:49am
How long does it take to abort?

Title: Re: Niacin
Post by BB on Oct 23rd, 2006, 9:55am

You mean you take it at the time of the attack or regularly ?

Do you take any other meds?

Are you episodic or chronic?

Thanks for sharing the info.

Annette

Title: Re: Niacin
Post by seasonalboomer on Oct 23rd, 2006, 10:37am

on 10/23/06 at 09:46:46, jtt112852 wrote:
New to this site but not new to clusters which I have been bleeesed with(Ha) for 22 years now. I recenty and by accident discoverd that taking at least 5000mg of niacin will stop my headache in its tracks about 80% of the time. There are twoo types of niacin(B-6) the non-flushing and regular. The non-flushing doesn't seem to work for me and if you take the regular be sure to eat something first.


Niacin from my understanding is actually B-3. You need B-6 to metabolize B-3 which is the way I've read it. Hepatotoxicity (liver cell damage), including elevated liver enzymes and jaundice, has been observed at intakes as low as 750 mg of nicotinic acid/day for less than 3 months. So, be careful with that 5,000 mg dosing level eh?

Scott

Title: Re: Niacin
Post by georgej on Oct 23rd, 2006, 11:27am
I'm trying to figure out how a massive overdose of niacin might affect things for the better, but have come up empty so far.  

The amide form of nicotinic acid is a significant substructure in NAD+ and NADP+ which are implicated in the following biochemical pathways:

ALDEHYDE DEHYDROGENASE (NAD+) Available map(s): A2, D6, D8, E6, H2, I2, J10
DIHYDROURACIL DEHYDROGENASE (NAD+) Available map(s): J8
GLUTATHIONE REDUCTASE (NAD(P)H) Available map(s): H7, I7
GLYCEROL-3-PHOSPHATE DEHYDROGENASE (NAD+) Available map(s): D6
ISOCITRATE DEHYDROGENASE (NAD+) Available map(s): G6
NAD(P)+ TRANSHYDROGENASE Available map(s): J1, S10
NAD+ KINASE Available map(s): J1
NAD+ SYNTHASE Available map(s): J1
NICOTINAMIDE ADENINE DINUCLEOTIDE[NAD+] Available map(s): J1
POLYDEOXYRIBONUCLEOTIDE SYNTHASE(NAD+) [DNA LIGASE] Available map(s): O7, Q6, R6, S7
2-PROPANOL DEHYDROGENASE (NAD+)
RUBREDOXIN-NAD(+) REDUCTASE Available map(s): D8, D9
SACCHAROPINE DEHYDROGENASE (NAD+,L-GLUTAMATE-FORMING) Available map(s): J3
SACCHAROPINE DEHYDROGENASE (NAD+,L-LYSINE-FORMING) Available map(s): J3
SUCCINATE-SEMIALDEHYDE DEHYDROGENASE (NAD(P)+) Available map(s): H5

Reference:

http://www.expasy.ch/cgi-bin/search-biochem-index

(For anyone else interested in this type of thing, expasy is an excellent reference for tracing the biochemical reaction pathways for any number of compounds.)

Some references I've seen show significant VASODILATION arising from nicotinic acid and nicotinamide adenine dinucleotide (or its analog, nicotinamide guanine dinucleotide) For example:

http://hyper.ahajournals.org/cgi/content/full/35/1/397

I'll be interested to hear anything contrary to these that show how vasoconstriction might occur.  As we all know:

vasoconstriction=good
vasodilation=bad

Best wishes,

George


Title: Re: Niacin
Post by floridian on Oct 23rd, 2006, 12:57pm
There has been some interest in niacin for migraine - no good studies proving it does help, but enough anecdotal evidence to make it of interest.  

Here's' one theory: "low plasma levels of serotonin have been implicated in migraine pathogenesis, and niacin may act as a negative feedback regulator on the kynurenine pathway to shunt tryptophan into the serotonin pathway, thus increasing plasma serotonin levels."

 
Quote:
Nutr J. 2005 Jan 26;4:3.

   The treatment of migraines and tension-type headaches with intravenous and oral niacin (nicotinic acid): systematic review of the literature.

       * Prousky J,
       * Seely D.

   Department of Clinical Education, The Canadian College of Naturopathic Medicine, 1255 Sheppard Avenue East, Toronto, Ontario, M2K 1E2, Canada. jprousky@ccnm.edu

   BACKGROUND: Migraine and tension-type headaches impose a tremendous economic drain upon the healthcare system. Intravenous and oral niacin has been employed in the treatment of acute and chronic migraine and tension-type headaches, but its use has not become part of contemporary medicine, nor have there been randomized controlled trials further assessing this novel treatment. We aimed to systematically review the evidence of using intravenous and/or oral niacin as a treatment for migraine headaches, tension-type headaches, and for headaches of other etiologic types. METHODS: We searched English and non-English language articles in the following databases: MEDLINE (1966-February 2004), AMED (1995-February 2004) and Alt HealthWatch (1990-February 2004). RESULTS: Nine articles were found to meet the inclusion criteria and were included in this systematic review. Hypothetical reasons for niacin's effectiveness include its vasodilatory properties, and its ability to improve mitochondrial energy metabolism. Important side effects of niacin include flushing, nausea and fainting. CONCLUSION: Although niacin's mechanisms of action have not been substantiated from controlled clinical trials, this agent may have beneficial effects upon migraine and tension-type headaches. Adequately designed randomized trials are required to determine its clinical implications.

   PMID: 15673472 [PubMed - indexed for MEDLINE]


Yeah, the very high doses used for cholesterol control can cause liver problems, so that is a concern if you go above a multi-B supplement level (~50 mg a day).  

There are big differences between niacin, niacinamide, and  inositol hexanicotinate in terms of how they are metabolized. I have seen papers suggesting that time released niacin may be worse than regular niacin in terms of the liver.

Title: Re: Niacin
Post by jtt112852 on Oct 26th, 2006, 1:56pm

on 10/23/06 at 09:49:45, E-Double wrote:
How long does it take to abort?


for me within 15 mins

Title: Re: Niacin
Post by jtt112852 on Oct 26th, 2006, 1:58pm

on 10/23/06 at 09:55:25, BB wrote:
You mean you take it at the time of the attack or regularly ?

Do you take any other meds?

Are you episodic or chronic?

Thanks for sharing the info.

no other meds
my headaches come twice a year for 3-4 weeks at atime and always the same time of day

Annette


Title: Re: Niacin
Post by jtt112852 on Oct 26th, 2006, 1:59pm

on 10/23/06 at 10:37:02, seasonalboomer wrote:
Niacin from my understanding is actually B-3. You need B-6 to metabolize B-3 which is the way I've read it. Hepatotoxicity (liver cell damage), including elevated liver enzymes and jaundice, has been observed at intakes as low as 750 mg of nicotinic acid/day for less than 3 months. So, be careful with that 5,000 mg dosing level eh?

Scott


Your right Scott its B-3, just hit the wrong key
and liver damage is possible but rare

Title: Re: Niacin
Post by jtt112852 on Oct 26th, 2006, 2:01pm

on 10/23/06 at 11:27:04, georgej wrote:
I'm trying to figure out how a massive overdose of niacin might affect things for the better, but have come up empty so far.  

The amide form of nicotinic acid is a significant substructure in NAD+ and NADP+ which are implicated in the following biochemical pathways:

ALDEHYDE DEHYDROGENASE (NAD+) Available map(s): A2, D6, D8, E6, H2, I2, J10
DIHYDROURACIL DEHYDROGENASE (NAD+) Available map(s): J8
GLUTATHIONE REDUCTASE (NAD(P)H) Available map(s): H7, I7
GLYCEROL-3-PHOSPHATE DEHYDROGENASE (NAD+) Available map(s): D6
ISOCITRATE DEHYDROGENASE (NAD+) Available map(s): G6
NAD(P)+ TRANSHYDROGENASE Available map(s): J1, S10
NAD+ KINASE Available map(s): J1
NAD+ SYNTHASE Available map(s): J1
NICOTINAMIDE ADENINE DINUCLEOTIDE[NAD+] Available map(s): J1
POLYDEOXYRIBONUCLEOTIDE SYNTHASE(NAD+) [DNA LIGASE] Available map(s): O7, Q6, R6, S7
2-PROPANOL DEHYDROGENASE (NAD+)
RUBREDOXIN-NAD(+) REDUCTASE Available map(s): D8, D9
SACCHAROPINE DEHYDROGENASE (NAD+,L-GLUTAMATE-FORMING) Available map(s): J3
SACCHAROPINE DEHYDROGENASE (NAD+,L-LYSINE-FORMING) Available map(s): J3
SUCCINATE-SEMIALDEHYDE DEHYDROGENASE (NAD(P)+) Available map(s): H5

Reference:

http://www.expasy.ch/cgi-bin/search-biochem-index

(For anyone else interested in this type of thing, expasy is an excellent reference for tracing the biochemical reaction pathways for any number of compounds.)

Some references I've seen show significant VASODILATION arising from nicotinic acid and nicotinamide adenine dinucleotide (or its analog, nicotinamide guanine dinucleotide) For example:

http://hyper.ahajournals.org/cgi/content/full/35/1/397

I'll be interested to hear anything contrary to these that show how vasoconstriction might occur.  As we all know:

vasoconstriction=good
vasodilation=bad

Best wishes,

George

Over my head George



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