Craigo

I heard a similar story from a CHer in Canada last week whom once a year picks up everyone’s fav coffee, tea or whatever (he has it written down) along with some deluxe pastries and donuts and puts on a morning tea for his oxygen hero’s at the store. They appreciate it and I know he appreciates their very efficient assistance. Love it.

No, I'm just saying in the years I have helped people around the world with Pete Batcheller's regimen I have found often times they buy a magnesium supplement whereby the 400mg dose is x3 capsules daily, rather than one capsule being 400mg so I considered worth a note - never know whom else may read this, wander over to their supplement box and find - wullah, indeed they had been taking too little. As I found the regimen kept me in remission so long and certainly believe the attacks during this cycle mild to the brain bruising experience of full kip-10's, I decided to throw everything but the kitchen sink so I am on 800mg magnesium per day, one capsule in AM and one with dinner - no stomach upset but also have added inulin as part of an OMG can't believe I found myself in cycle for so long - what can I do to improve my overall health (knowing full well that all the recent literature suggests there is never really a return to normal post an episodic cycle ending). Just to be pain free again anyway - for today, I'll take that. And I wish for you the same streak of luck to continue friend. I'll try and swing back here in a couple months and share with ya'll my updated 25(OH)D, calcium and PTH labs when I get around to taking them. I don't think I want to allow my level to drop to 78ng/mL again, which I'm not attributing to the cause of the cycle (frankly I reackon it was a good dose of life stress in Feb). It was surprising to me that it had dropped that low considering it's only the rare occasion I get lazy and flag the vitamins for the day.

Not a doctor, not medical advice. First, celebrate the win, it’s great to hear you have found it has reduced the intensity of the attacks, hopefully the cycle is short lived. You are correct in principle. With rising 25(OH)D, PTH trends downward due to improved calcium homeostasis however a couple thoughts for you and your lab values. 1. PTH is not a static marker and fluctuates based on circadian rhythm, dietary calcium intake, hydration status, assay variability and even lab timing. I would think a shift from 46 to 55 is fairly small and within normal variability. 2. If dietary calcium is inconsistent or on the lower side, PTH may rise slightly to maintain serum calcium, even in the presence of higher levels of vitamin D. Are you taking a men’s multi with calcium? Any of the doctors at my clinic don’t know much about vitamin D3 apart from that it’s important - they will order the lab tests for me, even right a script for subsidized D3 capsules but I understand they can’t get on board given it isn’t in their practice guidelines. I wouldn’t worry too much about your level, my own would be slightly higher having taken a loading dose with a baseline of 78ng/mL of 800,000iu and anticipate hovering around this level for a wee bit longer (I think I am one week or so out of this unexpected cycle that started mid-March having added MM this time round with success, it seems). Look after your kidneys, hydrate well and ensure you are taking the adequate amount magnesium (often times people miss to get the required magnesium dose often requires 3x capsules per day). Hope it helps, just my 2 cents. PFW - hope cycle ends soon mate. Craig.

Hey Mike, what size tanks do you have and do you have the Cluster O2 Kit for your breathing apparatus? Using that kit and the mouthpiece at 15lpm I am able to abort an attack in about 3-5 minutes, making a point to fully exhale before drawing back the full bag of 02. Once I have aborted the attack I step the reg down to 10lpm, slowing down my breathing but following the same technique and then down to 8 or 6lpm, again using the same technique, in order to conserve oxygen. You may find that others, and I will attest to this myself, say that if you don’t stay on the o2 for a minimum of as long as it took to abort and maybe a few more mins so for me that’s 10-12 mins, then they experience rebound attacks an hour later, staying on the o2 at the lower flow rate may be worth a shot to see if this results in fewer slap backs for you (although I get the feeling of it being counterintuitive as you want to conserve 02 if it’s arduous to replenish or a weekend etc). I also suggest having an easy to use timer, I hate fidgeting with my phone to reset timers during an attack etc, an analog one means I can easily keep an eye on the timer. Is your o2 covered or are you paying for it? I know one or two warriors that have purchased an Invacare o2 concentrator and tank filler unit so they can refill their own tanks and not worry about having to go to suppliers etc, I was and maybe still will consider this. It’s said that the purity is above 90 but less than 100% - from my conversations with those that use it with the Cluster 02 Kit mention it works for them just fine to abort attacks, albeit a bit of a costly setup to get initially. I’m sorry if I missed any other posts but I would ask what preventative meds you are taking? I find the D3 regimen has really helped reduce intensity of the attacks (when it hasn’t kept me pain free completely) and it was originally designed by Batch in an effort to improve his 02 abort times. Hope that helps, we in it together, keep us posted.

Awesome I am happy for you to get pain free and hopefully have broken the cycle. Woohoo. That must feel great! I yearn for the same, I think I’m nearly there with this cycle. For others curious and I am sure it is recorded in other threads on the forum but immediate release melatonin at 10mg before bed has been studied in a small cohort in the 90’s, 10 with and 10 without, of the 10 in the intervention arm, 5 got into remission within a week (all episodic patients). https://pubmed.ncbi.nlm.nih.gov/8933994/ There have been some other case reports of efficacy in chronic CHers as well. Here is a case series of two that was published a few years after the above study and they saw benefit in 48 hours. https://pubmed.ncbi.nlm.nih.gov/11843873/ That being said, a recent thread on Reddit had a similar report of efficacy with melatonin at this dosage but I also noted a number of replies from others that said they found it triggered attacks, so there is that - who knows if those that reported it triggered used immediate release and/or a dose close to 10mg. For the CHer at home considering it, it’s relatively safe - could be something to ask your doctor about. I’d love to see more literature as to its mechanism. I believe whilst it is produced by the pineal gland for sleep, it is also produced directly in mitochondria and scavenges free radicals, up-regulates antioxidant enzymes and stabilizes mitochondrial membranes. Based on a Mendelian randomization study earlier this year which found a number of metabolites elevated in CH patients that showed a causative risk factor for CH, those metabolites are involved in ATP production, both the electron transport chain and the glutathione cycle, and suggests to me that a feature of CH may be disruption / inefficiency in how we produce ATP, the cells energy currency. https://pmc.ncbi.nlm.nih.gov/articles/PMC12988619/ I am curious if this results in a metabolic crisis where, as the body moves from wakefulness into sleep and the energy requirements of cells change, the mitochondria are unable to meet the energy demands for the processes involved in sleep, triggering an attack. I am also curious as to why / how DMT is able to arrest this crisis - is it temporarily boosting ATP production via calcium flux at the endoplasmic reticulum via chaperone receptor S1R - Sigma 1? These are findings they are now investigating in the context of Alzheimer’s. My mind is also curious as to the 2024 thought piece of Jonathan Borkum whom suggests Lee Kudrow's earlier hypothesis of hypoxia in CH may indeed hold some relevance when considered in this context, however as the author suggests, it may not be low oxygen that triggers the crisis (as researchers were able to show and thus the theory was largely left in the 90’s), more rather an issue in the way in which cells sense subtle changes in o2 levels during the sleep / wakefulness cycles and, if I follow his hypothesis correctly, suggests the accumulation of hypoxic inducible factors (HIFs), which are normally continually degraded in the presence of oxygen by enzymes, as somehow being related to this metabolic crisis. https://pubmed.ncbi.nlm.nih.gov/39728749/ There is a PhD that talks about this in a roundabout sort of a way, Chris Masterjohn. Well worth a watch of his presentation on SSRI’s and ATP. Whilst unrelated to CH, many of the aspects touched on above are discussed in more detail in this presentation including melatonin, serotonin, DMT and ATP. He suggests that when we sleep our mitochondrial energy production drops, as does the energy requirements of the cell so that there is always an excess of ATP to meet metabolic demands. https://youtu.be/lkPUHw1oPd8?si=UjadSDEym-V3dAA1 I am sorry I have hijacked this post. Just thought it’d be worth sharing that insight but notwithstanding, long may your remission period continue!

Hi everyone. Dr. Haghdoosts presentation from Sunday evening is below. If you had any questions or insights you'd like to share that may assist in their study design, you'd be welcome to place them as a reply below and I could email them once collated. Thankyou.

Hi guys. A heads up this Sunday I am privileged to host Dr. Faraidoon Haghdoost via live webinar who will share insights from his recent work in cluster headache research. During the session Dr. Haghdoost will discuss his recently published 2026 study exploring patient perspectives of cluster headache in Australia and provide an overview of the upcoming PEACE trial investigating psilocybin based therapy as a potential treatment for cluster headache. This is an opportunity to hear directly from a researcher studying a treatment approach long recognised by our community. Sunday 22 March New Zealand 6:00 PM NZDT Australia 1:00 PM Perth 3:00 PM Brisbane 3:30 PM Adelaide 4:00 PM Sydney / Melbourne / Canberra / Hobart Register and watch live: https://streamyard.com/watch/eRh3FsriH3x7 Pre-read the study being discussed: Patient perspectives on research gaps in cluster headache https://pubmed.ncbi.nlm.nih.gov/41562498/ More about the PEACE Trial (The Psilocybin Efficacy and Acceptability on Cluster headache Episodes) If you have a question you would like Dr. Haghdoost to answer regarding the above, or feedback, he is very receptive to input from the community. Please send your question or feedback to craigedstewart@gmail.com or submit anonymously here: https://forms.gle/k46Vz5CZigTRn8MJ8 and I will make sure he receives these ahead of time so they can be answered during the presentation. I imagine there are hoops and lengths Dr. Haghdoost and his team need to jump through to get studies like this across the line so I am doing this to help raise awareness and hopefully he will be able to recruit enough participants and garner enough insights from our community to give the study the best shot. Everyone is welcome - if you are interested but do not live in Australia or New Zealand and can accommodate the timing, you are welcome to register and join. Also I will try and make sure it is recorded and shared after. Thanks everyone.

@dhuddly and to all reading. After a sleep I feel I overstepped with my comments above so I wanted to offer an apology and make clear that's my stuff, not his and I should have chosen my words better. Sorry Dhuddly, hope you may be able to accept my apology.

I can work with truck driver vocabulary and your grammar isn't that bad. Books and written to be read and videos to be watched, I'd love to check them out, please feel free to drop links here or send me a DM so I can go check them out. I just read The Headache, Tom Zeller Jr, episodic cluster sufferer and it was an absolutely amazing read. Welcome again to the community @dhuddly, if that's what you were after then certainly you are in the right place, there are some phenomenally good people in the cluster headache community, of that I can say for sure - and the reason I reckon I will be back in Chicago come October for this years conference!

Hi @CHfather and @dhuddly. Sorry you find yourself in our company there dhuddly, I haven't been on past couple weeks with some life changes I alluded to above and a number of projects on the go. I would appreciate links to studies you've read, always keen to expand my knowledge of the vitamin D3 literature. Here are the studies and their findings relating to the dopaminergic system in CH published last year for your reading and interest. What I would say above and beyond these studies, the work that has come out over the past number of years in CH space makes it fairly clear that between the active bout periods in episodic CH, the patient does not return to a normal baseline, the attacks may stop but there are perturbations that extend into the interictal periods that give me some level of assurance that I am doing the right thing for myself in terms of staying on the anti-inflammatory regimen 365 days of the year. I also hope that in doing so, I am providing an additional level of protection against developing other disease. I have more recently revisited Dr. Gominak's work (a contributor in part to the regimens inclusion of the B-Vitamins) and believe another reason for the regimens efficacy relates to vitamin D3's influence on the composition of the gut microbiota and the maintenance of epithelial tight junctions. Given nearly every cell expresses the VDR and the lack of formal studies in CH, it would be impossible for us to confirm Pete Batcheller's original hypothesis as to its precise mechanism of action (and as you mention, partial or non-response) but I think he is on the money with the umbrella thinking that it's underlying mechanism is the up and down regulation of genetic products which have the VDR sequence in their promoter / enhancer or silencer regions on DNA. Dysfunctional mesocorticolimbic circuitry in cluster headache. Ferraro et al. (2025) This fMRI study used a "Monetary Incentive Delay" task to probe the mesocorticolimbic dopaminergic pathways. Chronic CH (cCH): Patients exhibited blunted activity in the Ventral Tegmental Area (VTA) - a central dopaminergic hub - during reward anticipation. They also showed an imbalance in the pathway between the VTA and the medial prefrontal cortex (mPFC). Episodic CH (eCH): Patients showed intact VTA responses but abnormal mPFC activity, which the authors suggest may be an early sign of emerging dysfunction in the VTA-mPFC dopaminergic pathway. Conclusion: The study suggests an abnormal dopaminergic state in chronic patients that is distinct from affective disorders (depression/anxiety). Uncovering the neurological substrates underlying restlessness in cluster headache - A functional MRI study Chen et al. (2025) This study investigated the neural correlates of restlessness/agitation, a core clinical feature of CH. Substantia Nigra (SNpc): Patients experiencing restlessness showed increased functional connectivity between the Substantia Nigra pars compacta (SNpc) - a dopamine-producing nucleus - on the pain side and the Locus Coeruleus (noradrenergic) on the non-pain side. Frontal Inhibition: The study found decreased connectivity between the pain-side SNpc and the superior frontal gyrus, suggesting a disruption in top-down inhibitory control contributes to motor restlessness. Neurotransmitter Imbalance in Cluster Headache: A Systematic Review of Mechanisms and Therapeutic Targets Pellesi et al. (2025) This review aggregates data from multiple biochemical studies regarding dopamine levels in CH. Platelet Levels: Citing D'Andrea et al. (2006), the review notes that platelet dopamine levels were significantly higher in patients with episodic CH during both active bouts and remission compared to healthy controls. Plasma Levels: Citing D'Andrea et al. (2017), the review reports that patients with chronic CH exhibited higher plasma levels of dopamine compared to controls. Cerebrospinal Fluid (CSF): Citing Strittmatter et al. (1996), the review notes that CSF levels of dopamine were not significantly different between CH patients and controls, though norepinephrine was reduced. Autonomic dysfunction in patients with episodic cluster headache during remission period López-Bravo et al. (2025), This study summarizes previous biochemical findings in CH. It cites D'Andrea et al. (2017) regarding Abnormal Tyrosine Metabolism: Chronic CH patients show increased levels of dopamine and its precursor tyrosine in plasma. The authors interpret this anomaly in tyrosine metabolism as a potential predisposing factor for the chronification of episodic CH. Thesis: Felicia Jennysdotter Olofsgård (2025) Jennysdotter Olofsgård (Thesis) Genetics: A meta-GWAS identified WNT2 as a new risk locus for Cluster Headache. The author notes that WNT2 is known to be involved in dopaminergic neuronal development. What is seldom discussed in our community is the psychological and personality dimension of CH and how that relates to this topic. Kudrow and Graham were notably candid in the 1970s. I hesitate to be quite so direct, yet many of the personality characteristics they described feel uncomfortably familiar, as though my name might as well have been written beside them. If I may delicately say @dhuddly, from your posts and your manner of written expression, you come across as highly intelligent, thoughtful and kind. You have also mentioned being a full stack developer (I saw that response on a possible CB app - thank-you!), someone your friends describe as operating at extraordinary speed. I want to be clear that I am not attempting to analyse or explain you, rather, those observed qualities deeply resonate with me and provide a useful reference point for describing how I have come to interpret similar tendencies in my own life, over-achievement, high intelligence, tendency to work at a million miles an hour to name but a few. So... here's my story and my take on those qualities in the context of my life journey and CH. My father died before I was born. Throughout childhood I struggled to understand, let alone regulate, the emotions associated with that absence. In adolescence this unresolved grief drifted into substance abuse. Later, the same undercurrent appeared to transform into an intense drive for achievement, knowledge, and ultimately explanation. A life organised around such a pursuit rarely tolerates stillness. Pausing to enjoy simple pleasures can mean confronting emotions one has never properly learned to process. I am still learning how to do that. My sense, shaped by both experience and reading, is that unprocessed anger, grief, and guilt can sustain a chronic autonomic bias toward fight or flight, with downstream effects across our physiology. Viewed through that lens, it is perhaps unsurprising that my nervous system, which has otherwise been remarkably resilient, shows points of vulnerability. I cannot claim definitive evidence that CH, or another unique and uncommon disorder I am afflicted with - vocal cord dysfunction, arises from such experiences. This remains an interpretation, not a conclusion. The closest conceptual framework I have encountered is found in the work of Dr Allan Abbass, particularly his writing on overcoming emotional resistance through Intensive Short Term Psychodynamic Therapy. I feel his work and this topic deserves more discussion, as confronting as these topics can be. Link. Anyway, I pray I have not overstepped and I welcome you here with open arms. I am glad to connect. Craig.

See you there

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.