While not specific to Cluster, there is some insight into an old question which we often discuss. [BJ}
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Headache. 2010 Jun 10.

A History of Cigarette Smoking Is Associated With the Development of Cranial Autonomic Symptoms With Migraine Headaches.
Rozen TD.

From the Geisinger Wyoming Valley, Department of Neurology, Wilkes-Barre, PA, USA.

Abstract
(Headache 2010;**:**-**) Objective.- To look at the smoking history of migraine patients and to determine if a history of cigarette smoking is associated with the development of cranial autonomic symptoms with migraine headaches. Background.- It has recently been noted that a significant number of migraine patients may develop autonomic symptoms during their attacks of headache. Why some headache patients activate the trigeminal autonomic reflex and develop cranial autonomic symptoms while others do not is unknown. CLUSTER HEADACHE OCCURS MORE OFTEN IN PATIENTS WITH A HISTORY OF CIGARETTE SMOKING, SUGGESTING A LINK BETWEEN TOBACCO EXPOSURE AND CLUSTER HEADACHE PATHOGENESIS. COULD CIGARETTE SMOKING IN SOME MANNER LEAD TO ACTIVATION OF THE TRIGEMINAL-AUTONOMIC REFLEX IN HEADACHE PATIENTS? If cigarette smoking does lower the threshold for activation of the trigeminal autonomic reflex then do migraine patients who have a history of cigarette smoking more often develop cranial autonomic symptoms than migraineurs who have never smoked? Methods.- Consecutive patients diagnosed with migraine (episodic or chronic) who were seen over a 7-month time period at a newly established headache center were asked about the presence of cranial autonomic symptoms during an attack of head pain. Patients were deemed to have positive autonomic symptoms along with headache if they experienced at least one of the following symptoms: eyelid ptosis or droop, eyelid or orbital swelling, conjunctival injection, lacrimation, or nasal congestion/rhinorrhea. A smoking history was determined for each patient including was the patient a current smoker, past smoker, or had never smoked. Patients were deemed to have a positive history of cigarette smoking if they had smoked continuously during their lifetime for at least at 1 year. Results.- A total of 117 migraine patients were included in the analysis (96 female, 21 male). Forty-six patients had a positive smoking history, while 71 patients had no smoking history. Some 70% (32/46) of migraineurs with a positive history of cigarette smoking had cranial autonomic symptoms along with their headaches, while only 42% (30/71) of the nonsmoking patients experienced at least 1 autonomic symptom along with headaches and this was a statistically significant difference (P < .005). In total, 74% of current smokers had autonomic symptoms with their headaches compared with 61% of past smokers and this was not a statistically significant difference. There was a statistically significant difference between the number of current smokers who had autonomic symptoms with their headaches compared with the number of patients who never smoked and had autonomic symptoms (P < .05). Overall, 52% of the studied migraineurs had autonomic symptoms. THERE WAS A STATISTICALLY SIGNIFICANT DIFFERENCE BETWEEN AUTONOMIC SYMPTOM OCCURRENCE IN MALE AND FEMALE SMOKERS VS MALE AND FEMALE NONSMOKERS. EACH SUBTYPE OF CRANIAL AUTONOMIC SYMPTOMS WAS ALL MORE FREQUENT IN SMOKERS. CONCLUSION.- A HISTORY OF CIGARETTE SMOKING APPEARS TO BE ASSOCIATED WITH THE DEVELOPMENT OF CRANIAL AUTONOMIC SYMPTOMS WITH MIGRAINE HEADACHES.

PMID: 20553330 [PubMed]

Chicken vs. egg.

Modern medical research still refuses (or doesn't know how) to consider the possibility that CH sufferers, because of a defective hypothalamus, may be more prone to addictive behaviors.

And these people call themselves scientists.

interesting study on a subject that definitely needs more evaluation.
One point I find particularly interesting is that there was no statistical difference in occurrence of autonomic sx between current and past smokers - to imply that quitting smoking did not change the autonomic responses of these patients. 

Question - then is it as Brew suggests - there is an inherent issue with those with CH that predisposes to behaviors such as smoking? 
Or, did the smoking (however distant in the past) change the structure and composition of neurotransmitters/arteries/veins/whatever in such a permanent way as to continue to have effects long after the exposure?

I also noticed (as it is only an abstract) that while the definition of smokers is outlined, there is no similar definition of an ex-smoker.  How long much one have quit to be considered an ex-smoker - 1day, 1 month, 1 year?  The time of last exposure may make a difference.

Also brings up the question, is it nicotine - i.e. chewers, pipe smokers - or is it cigarettes?

You might think I'm crazy, but I believe it's more of the sucking motion of the mouth and facial movements from smoking that bring on the attacks. I have periods of no attacks for up to 2 years and smoke through that, but during active cycles, I think moving my face to smoke can trigger an attack. Eating hard foods can trigger an attack for me or squinting my face. So now they think I might have TMJ on top of this. But reading, being in hot sun, stress and even trying to get on here with the computer are triggers. One forgotten dose of verapamil=attack. And why can I have an attack and when it's done-that I can chainsmoke and another attack doesn't happen for days? Maybe none of them are triggers, maybe it comes and goes as it wants and I associate whatever I was doing at the moment as the reason. It really is driving me out of my mind.

Cause and effect........vs simple coincidence! CH will drive you batty trying to figure out that one! What seems like a guaranteed trigger one cycle will have absolutely no effect in the next cycle. Like we need anything else about this condition to give us more frustration. Hoping you catch a break soon. [smiley=hug.gif]

Joe

Is tobacco innocent until proven guilty? Sure, and so is Joran Van Der Sloot.

I think the convergence of evidence points to smoking being a causal factor/risk factor, but some people will not be satisfied until we do an experiment where 1000 young people with the right genetics and a history of traumatic head injuries are split into two groups and one is made to smoke for a decade or two while the other is prevented from smoking at all. That experiment would put all controversy to rest, but it ain't gonna happen.

There is huge pile of info that shows that smoking and nicotine can cause or aggravate several brain disturbances (including schizophrenia, depression, OCD, etc) in people that are susceptible to those conditions... a decade ago, it was an open question of whether it was a spurious correlation, or what was causing what. Today, it is pretty clear that tobacco use does contribute to those diseases. And each year, the evidence keeps piling up that smoking can push people closer to the glitched-brain state known as cluster headaches.



Lettucehead wrote on Jun 22^nd, 2010 at 6:06pm:

Also brings up the question, is it nicotine - i.e. chewers, pipe smokers - or is it cigarettes?

Good question - my guess is both, but that smoking is probably somewhat worse. Nicotine itself disturbs autonomic nervous function, but the carbon monoxide, tar and particulates from smoking also affect the autonomic system, and by a different path.

Quote:

And each year, the evidence keeps piling up that smoking can push people closer to the glitched-brain state known as cluster headaches.

No it doesn't. That's pure conjecture.

I must have missed that pile of evidence Monty. Can you link me to some of it?

Brew wrote on Jun 23^rd, 2010 at 1:15pm:

No it doesn't. That's pure conjecture.

If by conjecture, you mean "A proposition that is unproven but appears correct and has not been disproven" then I would agree it is conjecture. As I said in my original statement, no one has done the type of experiment that would conclusively prove or disprove the idea, and no one is likely to do so.

Given incomplete information, scientists and doctors can only rely on concepts like 'likely', 'convergence of evidence' and 'precautionary principle'. Given all that we know about how smoking affects neurotransmitters (not to mention health in general), old fashioned ideas of 'prudence' dictates that the habit should be avoided, not embraced.

Jimi wrote on Jun 23^rd, 2010 at 2:23pm:

I must have missed that pile of evidence Monty. Can you link me to some of it?

I would like to see that pile.

       Potter

Jimi wrote on Jun 23^rd, 2010 at 2:23pm:

I must have missed that pile of evidence Monty. Can you link me to some of it?

Sure - to get started, go to PubMed, and look up the research that shows that nicotine up-regulates the serotonin-2 receptors.  This is the opposite of things like the clusterbusters, olanzapine and kudzu, which abort or prevent by reducing the activity of serotonin-2 receptors.

Hmm interesting bit of 'research' and done where I live no less.  :D

But... I still have to agree with Brew here.


Brew wrote on Jun 22^nd, 2010 at 3:14pm:

Chicken vs. egg. Modern medical research still refuses (or doesn't know how) to consider the possibility that CH sufferers, because of a defective hypothalamus, may be more prone to addictive behaviors. And these people call themselves scientists.

Correlation is not causation, and shouldn't be assumed to be such.

Mosaicwench wrote on Jun 23^rd, 2010 at 8:17pm:

Correlation is not causation, and shouldn't be assumed to be such.

LOL ok sorry Brew Mosaic said it better!!!  ^5

Hello,

I write this with full knowledge that it is anecdotal and therefore the equivalent of an opinion....and everyone has got one of those...and you know what is said about those.

I grew up in a home where my Father smoked. Never bothered me....and no ch.

At age 22 I started smoking myself...no ch for the next 4 yrs.

At age 26, ch hit me like a 2 x 4 to the head. Over the years I have "quit".... for sometimes months at a time. Whether smoking or not....no effect on the ch.
Couldn't smoke DURING a hit...made it MUCH worse...but AFTER a hit....a desperate need that helped the "come down".

Recently had to quit (3-30-10) for the "long term" due to other concerns. Have been in a low cycle since...but now ramping back up....I KNOW what's coming.

SO...was it a history of exposure? Dunno.

My personal belief is that a "cracked" hypothalamus is contributory to an addictive personality. What smoking has to do with cause or effect re ch...I have no idea.

Best,

Jon

No wonder it's driving me out of my mind, I have a glitched brain! Oh, just kidding, needed a laugh. Thanks for all the information.

It's why you like us all so much....you're as defective as we are! ;D

Joe

what about people who use a Personal Electronic Nicotine Inhalation System  ;)

But seriously E Cigeretts should be in here too

Headache Boy uk wrote on Jun 23^rd, 2010 at 10:02pm:

what about people who use a Personal Electronic Nicotine Inhalation System  ;) But seriously E Cigeretts should be in here too

No. Not that. Anything but that.

Not the dreaded P.E.N.I.S. suckers....

Headache Boy uk wrote on Jun 23^rd, 2010 at 10:02pm:

what about people who use a Personal Electronic Nicotine Inhalation System  ;) But seriously E Cigeretts should be in here too

[smiley=crackup.gif]  [smiley=crackup.gif]  [smiley=crackup.gif]  [smiley=crackup.gif]

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Hay just leave us P.E.N.I.S. user out of this.

We are not bothering anyone :D.
There is no smell, no second hand smoke - NO tobacco and most important NO SIN TAX!!!!! :P

You...you...you P.E.N.I.S. user, you.

Brew wrote on Jun 23^rd, 2010 at 10:35pm:

You...you...you P.E.N.I.S. user, you.

and proud of it  :-?

;D

monty wrote on Jun 23^rd, 2010 at 7:17pm:

Sure - to get started, go to PubMed, and look up the research that shows that nicotine up-regulates the serotonin-2 receptors.  This is the opposite of things like the clusterbusters, olanzapine and kudzu, which abort or prevent by reducing the activity of serotonin-2 receptors.

And some CH medications are agonists and some are antagonists.  Go figure.

They also said o2 therapy seems to work better on smokers than non.

Bob P wrote on Jun 24^th, 2010 at 8:13am:

And some CH medications are agonists and some are antagonists.  Go figure.

I have figured: All the effective CH meds that interact with serotonin either boost 5-HT1 activity OR they reduce 5-HT2 activity (or both). This is not a random pattern (as you suggest) - there is a very specific pattern that points to a causal mechanism.

These two types of receptors are very different from each other, and they often work in opposition to each other. I am not aware of any case where decreasing the activity of 5-HT1B/D or increasing the activity of the 5-HT2 receptors (as nicotine does) is good for treating cluster headaches.

But the real question is how does smoking effect the "cause" of CH, not how does it effect the symptoms.

on a more serious note... about about the e-cigarette or personal vaporizer. I have used it for over a year now I have not touched a tobacco product and this has been the easiest cycle that I have ever had.  Could it be a coincidence maybe only time will tell. I do know that I enjoy not smoking anymore, but having a back up for when I am feeling weak.

edit to add : I guess my point is I am not sure that nicotine is the culprit - I think all the additives and chemicals in tobacco are a problem.

Despite sporatically sprinkled mention and whatever discussion of brought about, I've yet to be convinced or a fan of the idea.  CH indisposes both despite. 

Yeah, many may smoke, but Bob's had previously reasonable input tending to be palatable that inspecting deeper doesn't jibe with what is happening. 

I've made mention also of an unrelated mechanism operating similar to an episodic cycle of CH.  An opinion unsubstantuated, yet interesting.  There may yet be a discovering link working of this nature, but smoking may not be antagonistic enough to create a prevailing process to contribute.  That's a good observation though, Jon. 

Kilroy 2.0 wrote on Jun 25^th, 2010 at 8:45am:

on a more serious note... about about the e-cigarette or personal vaporizer. I have used it for over a year now I have not touched a tobacco product and this has been the easiest cycle that I have ever had.  Could it be a coincidence maybe only time will tell. I do know that I enjoy not smoking anymore, but having a back up for when I am feeling weak. edit to add : I guess my point is I am not sure that nicotine is the culprit - I think all the additives and chemicals in tobacco are a problem.

Gee, I have this same coincidence.  Since I quit 5 years ago, my cycles are shorter, duration shorter, intensity shorter.  This could be my rc seeds working as well, but before I used seeds, the cycles were cut in half or more.  I guess I owe some of that to not smoking...

Sensing what seemed apparently less need, I began to decrease my verap back in February, completely eliminatiing all meds without a single hit since.  This is the longest pf ever time since the early 90's and unusual since being chronic since 2004.  Any change of smoking or non-smoking wasn't to bear.  Just another side of the coin.

As I said, I do not want to calm it does have anything to do with it until I know for awhile. I may never know for sure. I do know that for me changing from smoking to vaping has made a difference in my life in many ways, my CH may or may not be one. It really does not matter because I am happy with the over all health changes I have seen, like not having bronchitis this winter for the first time since I can remember. Walking up stairs without losing my breath etc.

Bob P wrote on Jun 25^th, 2010 at 8:07am:

But the real question is how does smoking effect the "cause" of CH, not how does it effect the symptoms.

There are many therapies, but the one that has the longest impact (and which has the greatest influence on the underlying causes of CH, IMO) is the clusterbusting approach. All clusterbusters share one thing: a medium to long-term down regulation of the 5-HT2 receptors. These type 2 receptors stimulate calcium release (an effect opposite to verapamil) and lead to particular activity in the IP3 pathway, an increase in certain phospholipases, the release of Substance P, etc. etc. These are not merely symptoms, they are part of the mechanism of disorder and disease. To the degree that nicotine increases the number, density and activity of 5-HT2 receptors, it is strengthening the cause of CH.

First pharmaceutical nicotine and nicotine derived from tobacco use are two different things and work in different ways. There are other chemicals at work with the nicotine in the brain to produce the effect that most tobacco users are looking for and crave. Why do think most nicotine replacement therapies fail? If it were the same most people would just have to pop a piece of gum and be done with it. Why do you think the commercials say quitting sucks but (insert whatever here) makes it suck just a little less.

You have to look at more then just smoking – Just nicotine etc.

Not to mention the whole human nature factor.

I agree that a smoke free form of nicotine (be it electronic cigarettes, gum, or whatever) may be beneficial for clusters compared to smoking. The tar, for example, contains compounds that have an effect similar to perfume, gasoline, and alcohol and may increase headache frequency or intensity in some.  The particulates and carbon monoxide may also give strength to the beast.  And the risk of other diseases (heart disease, cancer, emphysema, etc) seem to be less or much less if the tar, particulates, and carbon monoxide are eliminated. These alternative sources of nicotine may result in significant risk reduction, and are generally a good idea.

"Pharmaceutical" nicotine is not that different than any other form. It may be in a slow-release complex, but when it gets into the blood, it is nicotine. I have met people who have switched from cigarettes to gum or lozenges for several years - not much interest in smoking again, no intention of quitting the alternative form of nicotine.

Nicotine substitution itself does not fail; neither does it offer any real advantage to people who want to quit. When someone tapers off or quits nicotine gum or lozenges, they go through the same withdrawal symptoms that smokers do when they taper off or quit. The fact that these gums are packaged as a 'quit smoking' program is merely a marketing ploy ... they are simply a form of chewing tobacco that has a controlled dose of clean nicotine.

It sure gives your lungs a break though huh.

Well Monty I can't really talk for a lot of other people but I can talk for a few. I know that I do not have the cravings I use to with cigarettes. When I drink, eat or do any of the other activities that used to trigger the urge to smoke. It did take several months of being off cigs before that happened. Yes the e-cig help A LOT but it was not a cigarette. I do not have the same cravings or urges for the e-cig as I did the real ones, and I am involved in a forum with a whole lot of people from all over the world that feel the same way so I know it is not just me. 

I guess it just leave me wondering why? 

Kilroy

I am thinking of trying the E Cig and I was wondering about how much you pay for yours and where you order from, would prefer a reputable company if you get my drift.  I have been doing some research on it but would like a reference to a reliable company to order from if I choose to do so.  Any suggestions?

If you don't want to put it here feel free to pm me on it. 

Thanks!

psychological evolution! what about the clock effect?

rare ? wrote on Jun 28^th, 2010 at 7:09pm:

psychological evolution! what about the clock effect?

Thought this was interesting...per the above.

See Page 6 for circadian periodicity:
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Of course to most of us this just states what we already know...you can pretty much set your clock by us.

Edited to add Note:
Also see page 11.

Quote:

All clusterbusters share one thing: a medium to long-term down regulation of the 5-HT2 receptors.

And we know this how?

We know it from research, including studies like these:

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So what you meant to say is rats have a 2 day down regulation of the 5-HT2 receptors with LSD?

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