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I'm getting pretty bad CHs. My GP has - yesterday - prescribed 40mg Verapimil twice a day. Having read up on this, 40mg seems like a very low dose, and I'm wondering how effective it's likely to be. I could myself increase it to 80mg by taking two tablets morning and night. What do people think?

Yeah it's a long similar story as what im finding out through reading various accounts and explanations that other cluster survivors describe. The undiagnosed ADHD is the big key for me because the cluster headaches started for me in May 2025, 2 days after starting vraylor which was not something I easily agreed on but since id spent over 25 years treating anxiety with SSRI, SNRI, Benzos and counseling, I decided last year to talk to my providers about treating the ADHD that has always been crazy noticeable about me(not in a bad way I swear lol) that maybe that might actually cure the anxiety and it did. But not before a provider wanted to rule out one more mood disorder before moving on to treating the ADHD. I felt at the time that medical history should matter more because honestly it felt like mine was worth nothing. But I'm a good patient. So I started vraylor and day 2 the clusters hit. Day 3 I easily decided that vraylor was never going to enter my body again. Days 3, 4 and 5 were bad. The clusters started around midnight each night. Than started progressing to earlier, than more, than earlier, than more and eventually 8 weeks later July 24th was my last one. I started ADHD meds the following month and realized or felt that Dopamine was something worth looking into but not for treatment for CH but more like there is a link between dopamine, serotonin and CH. That led me to find many published research papers on dopamine, serotonin, mast cell(this one hurt to learn the wheels of profit because of the results of triptan were widely accepted that mast cell research has been dormant ever since as far as I can tell) that was around late 80s early 90s when triptons came out. This ties directly into my first couple forum reads on here where some of us guys use cialis and apparently I am the oddball of the general consensus of it being agreed on as a trigger for CH(thankfully) because ive taken it for years. Sometimes everyday, sometimes weekly but that led me to search why the heck something that is like 50 to 1 on triggering vs has never triggered me could be. Dopamine deficiency or untreated ADHD effects the way vitamin D(d3 reg) will work in us. D3 works because it boosts dopamine production in the hypothalamus, the clock,and not just because it's anti-inflammatory. The people it doesn't work for probably have dopamine low enough that D3 alone can't get them above the tipping point. I've not found any research that connects these but the individual researches we see all touch on it in some fashion or another. I have been hesitant to comment and share these findings because as CH survivors we know. We know that the pain of the beast is more than any one person should have to suffer through and I see a loving community here. I'm not trying to burst any bubbles of comfort for anyone. I'd love to hear about or find more on CH->NO->DOPAMINE(both in terms of ADHD and the traceable chemical pipeline)->D3->hypothalamus. Please keep in mind I am not saying take speed. I'm just saying why isn't neuroscience, immunology, psychiatry and pharmacology not communicating their findings from decades of research because between the 4 of those fields I see plenty of I dividual bits and pieces of everything we say clusters are and feel like. For me mentally, I had to investigate this because once I got through the clusters, and started ADHD meds for the first time in my entire life, the anxiety stopped. Like really stopped and that in itself is huge for me. But having to go through the clusters first, like directly before it. Just to rule a mood disorder out that 25 years worth of that same thought already ruled out and vraylor being the trigger to the worst pain and experience I've ever endured? The convergence of all of this is why I probably spent the first week of the clusters not understanding how such a simple decision with a med triggered it. Took me several weeks to mentally get past that fully. I haven't done the D3 regimen, or mushrooms or the other stuff I'm reading about on here not because I'm anti any of it but because im new to this still. They haven't returned yet for me. I'm assuming the shadow I keep reading about on here is lingering around though. Sorry for the longwinded read folks.

What a great post. Thank you. I'm looking forward to perhaps a follow-up from @Craigo This seems possibly valid to me. I'm just wondering how you reached the conclusion, and why "undiagnosed." In Rozen's big 2011 study of people with CH, he asked about other medical conditions that people with CH have, but it doesn't seem that ADHD was among the possible answers. Someone at ClusterBusters might know whether another big study is planned (there was another one, after Rozen's, by Larry Schor), since CB is a source for research subjects. It seems like this is a question that might be asked (at least about diagnosed ADHD). Also, regarding dopamine, I admit to not having studied the two reports I posted in the research/scientific news section below, but I guess I could imagine that increased dopamine production accounts in part for the effect of D3 on mood.

The D3 regimen works for a lot of us, and the usual explanation is 'anti-inflammatory.' That's part of it, but there's actually a deeper reason. Vitamin D3 at high doses upregulates an enzyme called tyrosine hydroxylase, which is the rate-limiting step in making dopamine. And it does this specifically in the hypothalamus, which is the clock that runs our cycles. So when you're loading D3, you're not just fighting inflammation, you're helping your brain make more of the chemical that keeps the beast on its leash. That's also probably why it doesn't work for everyone. If your baseline dopamine is already really low for other reasons (like undiagnosed ADHD, which is way more common in CH than anyone's studied), the D3 boost might not be enough on its own to keep you above the tipping point. Doesn't mean it's not doing something it just means some of us need more than one thing pushing dopamine in the right direction. For me I have already found huge connections between ADHD and CH and I am greatful that this community is here because the suffering is too much for any one person to try to navigate alone.

Hallo! Currently operating on an available budget of £5K, but aiming for £15-20 total, to cover the full process including post-prod, and festival submission etc... Initially, we were planning to run it on the shoestring/low budget end of things, but my new director is keen on securing proper funding so we're not compromising on quality or fees. We have a possible producer on board now and links to a few potential backers, but all interest is good interest! The script is currently 14 pages and we'll be aiming at 10-12minutes or so Cheers!

What’s ur expected budget and running time?

Hi folks! I'm an actor and writer living in London, and I have written a short film about living with Cluster headaches. It's based entirely on my own experiences, though descends into some more abstract representations of the pain, for which I've taken inspiration from forums and conversations with other sufferers. Currently it doesn't delve into 'busting' though if I can get it made, I may well pitch for a second or a series. It's called 'Clusterfu*k,' and I have a director on board and the beginnings of a budget as well as some locations and talent. Basically, I'm wondering if anybody knows of any organisations or individuals who would be interested in helping support, endorse and/or finance the film? I have a number of contacts in the screen industry and my new director is very well connected, but as with all arts at the moment, funding is going to be the sticking point. For me the film is an attempt to visually communicate the difficulties, pain, and sometimes amusing quirks of living with this illness and trying to get on with life. Overall, I've been relatively fortunate in my response to medications (verap, O2, Triptans etc), while living in the UK means I have access to NHS oxygen, which is a gamechanger. I guess I'm hoping to raise some awareness, communicate the actual experience of the headaches (which often feels near-impossible and a stumbling block for future engagement/research) and create a platform for myself as an artist. Let me know if anything jumps to mind, or if anyone is particularly interested in talking about it further. Enormous thanks and solidarity, Angus

I'm not sure how a PPI would help for CHs. In fact, one of the common side effects is severe headaches. https://www.nyheadache.com/blog-posts/ppis-are-the-worst-but-all-heartburn-drugs-increase-the-risk-of-severe-headaches#:~:text=A new study just published,having migraines or severe headaches. "A new study just published in Neurology showed that people taking proton pump inhibitors (PPIs) such as omeprazole (Prilosec) and esomeprazole (Nexium) have a 70% higher risk of having migraines or severe headaches." I take rabeprazole, for GERD; but, started taking it after successfully busting. So, I can't say whether it has had any effect on my CHs. But, I just don't see how it would help.

Two studies (bold and italics are added by me) 2024: The effect of vitamin D supplementation on depression: a systematic review and dose–response meta-analysis of randomized controlled trials | Psychological Medicine | Cambridge Core The impact of vitamin D supplementation on depressive symptoms remains uncertain. This study aimed to investigate the dose-dependent effects of vitamin D supplementation on depressive and anxiety symptoms in adults. We systematically searched PubMed, Scopus, and Web of Science up to December 2022 to identify randomized controlled trials evaluating the effects of vitamin D3 supplementation on depression and anxiety symptoms in adults. Using a random-effects model, we calculated the standardized mean difference (SMD) for each 1000 IU/day vitamin D3 supplementation. The GRADE tool assessed the certainty of evidence. Our analysis included 31 trials with 24189 participants. Each 1000 IU/day vitamin D3 supplementation slightly reduced depressive symptoms in individuals with and without depression (SMD: −0.32, 95% CI −0.43 to −0.22; GEADE = moderate). The effect was more pronounced in those with depressive symptoms (SMD: −0.57, 95% CI −0.69 to −0.44; n = 15). The greatest reduction occurred at 8000 IU/day (SMD: −2.04, 95% CI −3.77 to −0.31). Trials with follow-up ⩽8 weeks (SMD: −0.45, 95% CI −0.70 to −0.20; n = 8) and 8 to ⩽24 weeks (SMD: −0.47, 95% CI −0.70 to −0.24; n = 15) showed stronger effects compared to those lasting 24 to ⩽52 weeks (SMD: −0.13, 95% CI −0.28 to 0.02; n = 5) or longer than 52 weeks (SMD: 0.14, 95% CI −0.16 to 0.44; n = 3) (p group difference <0.001). Vitamin D3 supplementation had no significant effects on anxiety symptoms. In summary, this study suggests that vitamin D3 supplementation may effectively reduce depressive symptoms in short term. Further high-quality trials are warranted for a conclusive assessment of its impact on anxiety. 2025: https://www.frontiersin.org/journals/psychiatry/articles/10.3389/fpsyt.2025.1622796/full Our findings indicate that vitamin D supplementation is associated with a moderate but statistically significant improvement in depressive symptoms..... This meta-analysis demonstrates that vitamin D supplementation significantly alleviates depressive symptoms (SMD = -0.36), particularly in subgroups with baseline deficiency (<20 ng/mL) and comorbid chronic inflammatory conditions.

I'm launching a new zoom support group for Illinois- everyone is welcome, though being able to connect to people in the area will be the main goal. Nearby areas are most welcome as the resources will be helpful to you as well. To get an invite you can message me your email address or fill out this form: https://forms.gle/kNpeB678DQzNyW9G7 The group will meet the 3rd Thursday of every month at 7pm CT. Feel free to drop in anytime!

Faraidoon is the headache researcher whom is leading the Psilocybin Efficacy and Acceptability on Cluster headache Episodes (PEACE) Trial.

Patient perspectives on research gaps in cluster headache Faraidoon Haghdoost, Dilara Bahceci, Candice Delcourt, Tissa Wijeratne, Rigmor H Jensen, Carl Cincinnato, Susan Tomlinson, Bob Wold, Vince Polito, Cheryl Carcel, Usman Ashraf, Bronwyn Jenkins, Anja Sofie Petersen, Jason C Ray, Emmanuelle A D Schindler, Benjamin Tsang, Chris Gianacas, Anthony Rodgers Published in Headache on January 21, 2026 Link: https://doi.org/10.1111/head.70031 Abstract: Objective: This study was undertaken to identify gaps in cluster headache management, highlight patient-prioritized research needs, and assess patient interest in, and preferences for, clinical trial participation.

Most of these studies were posted here on the forum, study by study over the course of 2025. For those wanting to look at some of the studies mentioned they are in my 2025 CH Research Notebook.

2025 Highlights in cluster headache Roemer B. Brandt, Rolf Fronczek Published in Cephalalgia on January 2026 Link: https://doi.org/10.1177/03331024251411870 Abstract: Cluster headache remains enigmatic with a significant unmet treatment need, especially in the chronic form. The steps made in 2025 have taken us further along the road to a true understanding of the still unknown pathophysiology, hopefully leading to a causal treatment.

(via google trad) When I see certain neurologists in France openly advising their patients to overdose on sumatripatan, some even administering up to 10 doses a day if necessary... And when we explain to them that their neurologist is wrong, we are generally insulted...

He might be more likely to see this if we include his handle here, @xxx.

Batch - I’m a 20-year episodic CH sufferer, and I’ve been following the anti-inflammatory regimen for several years now. Thanks to it, my CH had been in remission for the last 2–3 years. A couple of weeks ago, it came back - possibly triggered by a virus, a stretch of bad eating habits, or a combination of both. I immediately started the loading dose for both the anti-inflammatory regimen and the “Full Monty,” and I’m happy to report that my attacks only lasted about 12 days. Normally, my cycles last several weeks, so this was a huge improvement. I just wanted to say thank you for everything you do. Your work has truly made a difference in my life, and I’m incredibly grateful.

wow, thanks for pointing out this study. this could be huge for us Biological Mechanisms Implicated The study points to several pathways: Oxidative Stress Impaired antioxidant defenses (5-oxoproline) May damage brain cells Mitochondrial Dysfunction Energy production problems (orotate, 3-hydroxy-3-methylglutarate) Brain can't generate enough energy Neurotransmitter Imbalance Dopamine and glutamate pathway disruptions Lipid Metabolism & Inflammation Membrane signaling problems Inflammatory responses Methylation Pathways Betaine involvement suggests epigenetic mechanis Clinical Implications Potential Future Applications: Biomarker Development Could identify people at risk (though CSF collection is impractical) Need to find blood-based correlates New Treatment Targets Antioxidant therapies Mitochondrial support supplements Methylation pathway modulators Mechanistic Understanding Helps explain why cluster headaches occur Could lead to more targeted therapies

I am getting better at turning to AI for questions like this. I asked ChatGPT (which probably isn't even the best AI engine for this kind of thing): "What does this mean: In the forward MR analysis, 11 CSF metabolites were significantly associated with CH risk (P<0.05). The strongest associations were observed for orotate (β = 0.53, 95% CI: 0.23–0.82, P = 0.0006), betaine (β = 0.47, 95% CI: 0.16–0.79, P = 0.0035), and 5-oxoproline (β = 0.57, 95% CI: 0.17–0.97, P = 0.0053). In the reverse MR analysis, eight metabolites, including lysine (β = 0.015, P = 0.029) and kynurenine (β = 0.025, P = 0.020), were nominally associated with genetic liability to CH. Sensitivity analyses showed no evidence of directional pleiotropy or heterogeneity (all P > 0.05). This bidirectional MR study provides the first genetic evidence linking central metabolic alterations to CH susceptibility. While these results highlight potential metabolic biomarkers and mechanistic pathways, the findings remain preliminary due to modest statistical power and should be replicated in larger and ethnically diverse cohorts." In the blink of an eye, the answer that came was (formatting is much clearer in the Chat version; I have just pasted it here as plain text). NOTE that at the end it offers to go deeper: Maybe some of your other questions could be asked there. Well, I tried pasting it. I get an error message that says, The value entered includes a character that is not allowed such as an Emoji. Since I have no idea what that character might be, I guess you'll have to do the exercise yourself. I don't think you will be disappointed.

This is a pretty epic study and I have a lot of questions. I am not even sure I fully understand all of it yet, so I want to check that I am interpreting it correctly. Anyone else have any thoughts, please share. In their bidirectional Mendelian randomization analysis, are they essentially saying that they identified 11 cerebrospinal fluid metabolites that are associated with increased risk of cluster headache, and that among those, three showed the strongest associations, and these key metabolites are involved in pathways linked to mitochondrial energy metabolism and ATP production? Rather than mitochondria in cluster headache fail to produce enough ATP, it appears they are suggesting that ATP production is inefficient and metabolically costly. Do these findings help explain the small ketogenic diet study from 2018, where 11 of 18 refractory chronic cluster headache patients became pain free? There is often discussion about ketone bodies being a more efficient fuel source than glucose metabolism. In the context of this paper, could ketosis be improving ATP yield per unit of oxygen or reducing oxidative and redox burden on already stressed mitochondria, thereby raising the threshold for attack generation? What do these results suggest about the role of the “Full Monty” supplements that are recommended for non-responders to the base Vitamin D regimen? Many of those supplements have antioxidant or reactive oxygen species scavenging properties. Does this metabolite profile support the idea that reducing oxidative stress and the ATP cost of redox maintenance could improve mitochondrial efficiency and help explain why some non-responders improve when these additional supplements are introduced? The paper also references the glutathione cycle. Does the signal around 5-oxoproline and glutathione metabolism suggest that supplementing glutathione might be beneficial in this context? Or is the implication more that excessive glutathione turnover reflects an upstream oxidative burden that needs to be addressed rather than simply supplying more? What do these findings imply about the role of melatonin? Melatonin is synthesized within mitochondria and is known to improve mitochondrial efficiency, reduce oxidative stress, and support electron transport chain function. Could impaired or mistimed melatonin signaling be one of the factors that lowers energetic resilience during vulnerable circadian windows in cluster headache? Finally, do these findings offer any insight into a potential abortive mechanism for DMT? Anyone have any insight in this regard?

NotebookLM Audio Summary. Cluster_Headache_s_Metabolic_Root_Cause_Found.m4a Or just check out the Notebook for yourself. https://notebooklm.google.com/notebook/27364f47-4518-433b-86d9-d3aad07c9f0e?authuser=1

Bidirectional Mendelian Randomization Analysis of 338 Cerebrospinal-Fluid Metabolites and Cluster-Headache Risk Danhua Yu, Xuewei Yang, Jinli Zhou, Weiwei Chen, Jinhui Song, Weifei Yu & Shaokang Huang Published in Journal of Pain Research on January 8, 2026 Link: https://doi.org/10.2147/JPR.S550160 Abstract: Cluster headache (CH) is a rare but highly disabling primary headache disorder characterized by severe unilateral attacks and autonomic symptoms. The metabolic mechanisms underlying CH remain poorly understood. To investigate the potential causal effects of cerebrospinal fluid (CSF) metabolite levels on CH risk, and to explore possible reverse causal effects of CH on CSF metabolites, using a bidirectional Mendelian randomization (MR) approach. We performed a bidirectional two-sample Mendelian randomization (MR) analysis integrating genome-wide association study (GWAS) data for 338 cerebrospinal fluid (CSF) metabolites and CH (1,833 cases and 498,515 controls from FinnGen release 12). Genetic instruments were selected at P < 1×10−5 (LD r2 < 0.01). The primary causal estimates were derived using the inverse-variance weighted (IVW) method under a random-effects model, complemented by MR-Egger, weighted median, and MR-PRESSO sensitivity tests. Multiple testing correction was performed using both Bonferroni and false discovery rate (FDR) approaches. In the forward MR analysis, 11 CSF metabolites were significantly associated with CH risk (P<0.05). The strongest associations were observed for orotate (β = 0.53, 95% CI: 0.23–0.82, P = 0.0006), betaine (β = 0.47, 95% CI: 0.16–0.79, P = 0.0035), and 5-oxoproline (β = 0.57, 95% CI: 0.17–0.97, P = 0.0053). In the reverse MR analysis, eight metabolites, including lysine (β = 0.015, P = 0.029) and kynurenine (β = 0.025, P = 0.020), were nominally associated with genetic liability to CH. Sensitivity analyses showed no evidence of directional pleiotropy or heterogeneity (all P > 0.05). This bidirectional MR study provides the first genetic evidence linking central metabolic alterations to CH susceptibility. While these results highlight potential metabolic biomarkers and mechanistic pathways, the findings remain preliminary due to modest statistical power and should be replicated in larger and ethnically diverse cohorts.

Your post hits me in the feels. It really does. I would say it is changing lives. I have had one of those days, your post is timely and let me be as real as I can with you on what is a topic that lies close to my heart. At least once, more often several times a week, I receive an email from someone who found www.vitamindregimen.com, come across Clusterbusters, a social site or watched one of the interviews with Pete Batcheller on YouTube. They rolled the dice on the regimen and got pain free. They write to say it changed their life. Even one of those emails is enough to justify every hour of advocacy. It’s worth it. I have spent over a decade now reading obsessively on this topic, not just to understand why and how the regimen may work, but to also understand why a percentage of people do not get fully pain free when applying it. Along the way I have interviewed some of the most amazing people in the vitamin D3 research space and with every interview, every study read, every question asked, I feel like I have moved a little closer to an answer and built upon my knowledge of the subject. I am so grateful Pete opened that door for me. That man is a global treasure. It’s also perplexing because this week alone I have seen cluster headache social media channels suggest ginger, purple cabbage, and today, chewing on a lime. I should have become a fruiterer! I understand the premise behind criticism of the regimen or pushing it to the side as a bunch of simple pills. From the outside, a handful of vitamins can look just as batshit crazy as cabbage when stacked against the sheer terror of CH. I get it. That is the real challenge. How do you communicate the regimen in a way that reaches more people, without overclaiming, without slipping into evangelism and without being lumped into the bucket of folk remedies? How do you communicate something that sits uncomfortably between patient-led discovery and clinical blind spots? I may have an opportunity to do more having just resigned my job today with no intention of continuing on the same path / career. 43, soon to be jobless - very tempting to study and see what further value I may add to this important body of work. Never too old right? Absolutely agree with you, happy for you to have found success with it and pleased to see you here on the CB forums!

So true Jeeb. Unfortunately full and continuous cessation has yet to be achieved through the D3 regimen. Less frequent attacks, regular cycles and intensity of attacks has been greatfully experience from many on the regimen making it a very useful tool for any CH sufferes toolbox.

"Completely CH free" isn't what everyone on the D3 regimen achieves, but glad you've arrived there!