Hi folks!

So a question on vasoconstriction!

As I understand it that's why oxygen and imitrex work well to help reduce clusters. I've read Batch's regimen and have been taking D3 and magnesium, but was surprised to find that magnesium is a vasodilator. I'm sure there's a good reason for that, but would love to hear about the underlying mechanisms.

I regularly take caffeine to help with vasoconstriction, and have been curious about other things I can do to help support that. Right now I do lots of O2, 480mg of verapamil, and finally imitrex should all else fail.

But as always it seems there are other factors that might help keep the pain away, since I'm still getting hit two or three times a night. Salt is in theory a vasoconstrictor too, for example. And if potassium plays a strong role in vasodilation, wouldn't it be best to avoid it?

Any thoughts or explanations would be much appreciated. I know there are thousands of variables that go into clusters, but am trying to figure out how to make the best choices possible. It drives me crazy trying to figure out why some days are better than others (though one can never really isolate individual variables very well).

Thanks!

Hey Batch! I'm glad you weighed in, I was hoping you would!

I follow for sure! What's so difficult in dealing with clusters is trying to identify causality as opposed to correlation. Every cycle over the years I try something new to try and find a "helper" mechanism to aid D3/O2/Verapamil/Imitrex.

In the past I was all about an anti-inflammation diet and eating and drinking the most alkaline friendly foods possible and had little success. My thought being, if O2 caused rapid alkatosis, perhaps I could get some relief by reducing inflammation however I could.

This year I've been pushing caffeine hard (unfortunately can't do energy drinks because of the verapamil). But it's maddening trying to figure out why some days are better or worse than others. We naturally want to try and find the variable responsible!

My thought on vasodilation stems from a neuro who said plainly that, "you have to treat these like a vascular headache." That got me thinking- reading through the medical literature it's my best guess that vasodilation is perhaps a resultant cause of the pain, but not the originating event or triggering mechanism. Therefore, if your blood vessels were constricted sufficiently, that triggering mechanism wouldn't be able to start the secondary process (vasodilation) that caused the pain.

To put it another way- there are perhaps two (of probably many more) ways to treat the mechanisms of CH pain. To reduce, change, or eliminate the triggering or maladapted mechanisms that can eventually lead to vasodilation, or to reduce the vasodilation itself and let the triggers continue to fire blindly.

A lot of the literature kind of writes off vasodilation as a "cause" since people were able to get relief using mechanisms that were unrelated (ie taking care of the primary triggers / brain chemistry). But it seems to me that they are two separate approaches that both might work in their own ways.

I'd love to hear your thoughts on this, Batch! Also, some quick questions for you:

1. After extensive googling of vasoconstrictors I've been surprised by some interesting findings. Nearly every drug listed on the wikipedia page has been linked with successful treatment of CH. Adderall, for example, seems to be a wonder drug of sorts for some folks, but it seems very uncommon for CH treatment. Ritalin is more common as another wonder drug, but is often "unreliable". I wonder if this is because it has a short half-life, (ie "the headaches came back several hours later, so it doesn't work") and people were unaware of the vasoconstriction mechanism potentially being the primary mechanism of relief.

I then looked and found that two of the largest triggers, alcohol and smoking, are both vasodilators. Psilocybin is suprisingly a vasoconstrictor. So this is all correlation, mind you, but the significance of the correlation is pretty staggering. Is a treatment plan potentially as simple as avoiding dilators and using constrictors when needed?

2. Any thoughts on potassium? Potassium rich foods seem to cause problems for me. I know this is one of the main channels involved in vasodilation.

3. How about sodium? Theoretically it would vasoconstrict blood vessels, and I'm not finding much from folks about it being a trigger. I feel like this is one of the holdovers from migraine / tension treatments that people often try to eliminate. But perhaps we should do the opposite? Also, maybe this is coincidentally why baking soda helps some folks?

4. Any dietary or lifestyle changes that you're aware of that would promote vasoconstriction?