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

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

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.

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.

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


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.

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.

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?

psychological evolution! what about the clock effect?

Quote:
And we know this how?

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