Craigo

"The pilot ‘Psilocybin Efficacy and Acceptability on Cluster Headache Episodes’ (PEACE) pilot trial will assess whether 10 mg of psilocybin once a week for four weeks compared to placebo can prevent cluster headache attacks. The study builds on early patient reports and small-scale trials that indicate its potential benefits." So that's 1g dried cubensis give or take (0.8 - 1.2g) depending potency every 7 days for 4 weeks, in sort parallels the community busting protocol. I hope they are able to recruit the numbers. I had recently read one of his articles on migraine: Migraine management: Non-pharmacological points for patients and health care professionals He is also the recipient of the 2025 Peter Goadsby Award for Best Scientific Oral Abstract presentation at the Australian and New Zealand Headache Society Annual Scientific Meeting in Sydney on 30–31 August. His presentation, “Gaps in Research and Management of Cluster Headache Through Patient Perspectives,” underscored the need to listen to patient voices and address the gaps that remain in both clinical care and research.

A new clinical trial in Australia has funding approved to test psilocybin as a preventive treatment for cluster headache. The PEACE Trial (Psilocybin Efficacy and Acceptability on Cluster headache Episodes), led by Faraidoon Haghdoost and supported by the The George Institute for Global Health and the University of New South Wales under the Medical Research Future Fund (MRFF), aims to evaluate whether weekly low-dose psilocybin can safely reduce the frequency or severity of cluster attacks. There is also a survey on Faraidoon's page assessing the cluster headache research gaps based on the patients perspectives. https://www.faraidoonhaghdoost.com/post/cluster-headache-trial-got-funded-in-australia https://www.georgeinstitute.org/news-and-media/news/hope-for-cluster-headache-community-as-psilocybin-trial-funded

Greetings and sorry they are back - it sucks. My one fall from remission whilst using the D3 regimen saw me find o2 and the cluster o2 kit for the first time - I was getting o2 slap backs but as Bejeeber said that’s not bad to have several hours in between nocturnal attacks, I was aborting in 6 minutes or so and getting a slap back an hour later. An amazing advocate in our community Pete McCormick suggested to try staying on the oxygen for the same amount of time it took to abort the attack but at a lower flow rate, when I did that I found an immediate improvement back to my normal 2-3 attacks per night, aborted and back to bed in around the 15-20 minute mark which was an amazing improvement on previous abortives. I only needed the o2 setup for a total of four days before higher levels of vitamin D3 put me back into remission, thank God. Can’t add much about caffeine suffice to say some warriors use a strong black coffee rather than energy drinks and report it works, if concerned / wary about energy drinks, I know I am. I’d just straight hit up the oxygen upon waking rather than caffeine and save a strong black coffee or otherwise for shadows during the day. All that being said and in lieu of challenges obtaining Emgality, is the vitamin D3 regimen an option for you as another tool to add in the kit?

Another review on this subject published a few days back.. A review on gut microbiota and migraine severity: a complex relationship Noha M. Gamil, Rana M. Ghorab, Reham Z. Elsadawy, Nada M. Khadrawy, Mohamed Abdelhamid, Khalid A. Ismael, Omar A. Mohamed, Mohamed M. Ata, Habiba T. Jalal, Joumana E. Zeidan, Reem T. Rashed & Riham A. El-Shiekh Springer Nature Inflammopharmacology Published: 27 November 2025 The gut-brain axis plays a vital role in migraine pathophysiology. Studies highlight reciprocal interactions between the central nervous system and the gastrointestinal tract. Previous research suggests that factors such as gut microbiota profiles, inflammatory mediators, neuropeptides, serotonin pathways, stress hormones, and nutritional substances influence this interaction. The pathophysiology of migraine has been linked to changes in the gut-brain axis, which affects migraine severity and frequency. Additionally, dietary approaches, including the ketogenic diet, vitamin D supplementation, omega-3 intake, probiotics, and weight loss plans, have shown promising effects in reducing migraine symptoms by positively impacting the gut microbiota and the gut-brain axis. Understanding these connections could lead to novel therapeutic strategies for effectively managing migraines. It is worth noting that research highlights several innovative treatments for migraine, such as Zelirex and Cevimide, implantable devices like Cefaly and Revilion, and new effective routes of administration for Sumatriptan. Finally, patients’ perspectives and concerns were thoroughly discussed, with a focus on future directions in the migraine-gut axis research.

Notebook LM Audio Summary Podcast Generation (AI generated). Cluster_Headaches_Solved_Dual-Target_Neuromodulation.m4a

Update of Seven Cases of Refractory Cluster Headache Treated with Combined Occipital Nerve and Sphenopalatine Ganglion Stimulation with Good Mean Outcome in a Long Term Follow Up Juan Carlos Mario Andreani, Fabián Piedimonte, Osvaldo Bruera, Marco Lisicki, Diego Bashkansky Published Vol. 19 in NeuroTarget 2025 Link: https://doi.org/10.47924/neurotarget2025549 Abstract: Cluster headache (CH) is an extremely debilitating and often difficult-to-treat headache disorder characterized by recurrent attacks of excruciating pain associated with cranial autonomic symptoms. Several invasive neuromodulation procedures have been evaluated in the past, but the combination of these procedures to maximize response has not been studied in groups of patients. This presentation aims to describe an update on the evolution of cases based on a recent publication of ours. This single-center, retrospective, observational study included seven patients (3F/4M) suffering from CCH, according to the diagnostic criteria of the current International Classification of Headache Disorders, and considered refractory based on the Consensus Statement of the European Headache Federation. Between February 2010 and March 2021, these patients underwent implantation of electrodes for SPG and greater occipital nerve (GON) stimulation ipsilateral to the side of the pain. The mean follow-up time was 6.38 years ± 3.6. Six out of the seven patients (86%) experienced good-to-excellent initial pain relief, defined as ≥50% reduction in VAS scores compared to baseline, with marked improvement in attack severity and functional impact. Almost complete remission of symptoms was achieved in most cases. Multiple techniques have been proposed to control CH symptoms. Here we report, for the first time, that combined invasive SPG and GON neurostimulation significantly and enduringly improves CCH symptoms in a series of refractory patients. The relatively low number and severity of complications suggest a favorable risk-benefit profile. Synergistic invasive SPG-GON stimulation appears to be a relatively safe and promising alternative for effective and long-lasting control of CCH.

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Uncovering the neurological substrates underlying restlessness in cluster headache - A functional MRI study Shu-Ting Chen, Chia-Chun Chiang, Yung-Lin Chen, Shin-Yi Tseng, Mei-Chun Chen, Chi-ieong David Lau & Jr-Wei Wu Published in The Journal of Headache and Pain on November 25, 2025 Link: https://doi.org/10.1186/s10194-025-02209-7 Abstract: Restlessness or agitation is one of the core symptoms of cluster headache (CH). However, the neurological substrate underlying this phenomenon has not been thoroughly analyzed. Whether they are attributed to the core aggression circuit or other CH-related structures remains unclear. The aim of this study is to use functional neuroimaging to elucidate the underlying mechanism of restlessness or agitation in CH. We prospectively recruited consecutive patients with CH from the Headache Clinic of Taipei Veterans General Hospital between Jan 2022 and July 2025. Patients who consistently reported either the presence or absence of restlessness during CH attacks were enrolled and categorized into two groups: restlessness and non-restlessness. All enrolled patients underwent a functional magnetic resonance imaging (fMRI) scan. In the restlessness group, patients were required to exhibit restlessness during the fMRI scan, whereas those in the non-restlessness group showed no restlessness at the time of scanning. In this study, 32 regions of interest (ROIs) relevant to CH pathophysiology and the core aggression circuit were selected. To identify restlessness-related networks, ROI-to-ROI functional connectivity was compared between the restlessness and non-restlessness groups. To investigate downstream network for restlessness, ROI-to-voxel analyses were conducted using a general linear model, with ROIs showing significant differences in the initial ROI-to-ROI analysis as seeds. Multiple comparisons were corrected using both the false discovery rate (FDR) and family-wise error (FWE) methods. A total of 24 patients with CH were recruited and categorized into two groups: restlessness (N = 14) and non-restlessness (N = 10). The ROI-to-ROI functional connectivity analysis of CH patients with restlessness revealed a significant connection between the non-pain side locus coeruleus (LC) and the pain-side substantia nigra pars compacta (SNpc), which survived FDR correction (p-FDR = 0.016). Seed-based general linear model analysis further revealed decreased connectivity between the pain-side SNpc and pain-side superior frontal gyrus, which survived FWE correction (p = 0.037). However, there were no significant cortical connectivity from the LC survived the FDR correction. Our fMRI findings suggest that the neurological substrates of restlessness in CH involve the LC and SNpc rather than the core aggression network. Weakened connectivity from the SNpc to the superior frontal cortex may represent the downstream pathway contributing to restlessness in CH.

Notebook LLM Audio Summary Podcast Generation (AI generated). Leaky_Gut_Causes_Chronic_Migraines_and_Pain.m4a

In lieu of a recent article I wrote exploring the literature that may support dysbiosis in cluster headache (check general board), a number of parallels were cautiously drawn from emerging migraine literature, which I thought worth sharing in one place here on the migraine board. These recent studies explore the emerging role of dysbiosis as a causative factor in migraine pathogenesis, exploring potential links via the gut-brain axis, microbial imbalance and therapeutic interventions like probiotics or faecal microbiota transplantation (FMT). Whilst I don’t suffer from migraine myself, having read this body of work, if I did I think it would be a fair and reasonable question to be asking: “Do I have dysbiosis, and if so, what can I do about it?” None of the papers below explore the role of optimised nutrition in detail, nor do they touch on two of my favourite patient-led protocols that are known to reshape the gastrointestinal environment and microbiome - high-dose vitamin D and psilocybin - but the door remains open for those avenues to be investigated (and hopefully discussed here). Happy reading – welcome your comment and you’ll find a NotebookLM audio summary generation below if you’d rather listen to a podcast rather than read studies. I have offered the links to the articles and a short generated summary snippet - any of the articles are behind a paywall and you’d like me to shoot you off a copy please reach out via DM. Gut microbiota dysbiosis enhances migraine-like pain via TNFα upregulation Published January 2020 https://doi.org/10.1007/s12035-019-01721-7 Yuanyuan Tang, Sufang Liu, Hui Shu, Lora Yanagisawa, Feng Tao Key finding: Antibiotic-induced dysbiosis and germ-free status markedly worsen nitroglycerin-triggered migraine-like pain in mice through TNFα-mediated trigeminal sensitisation; probiotics reverse the effect. The association between migraine and gut microbiota: a systematic review Published April 2023 https://doi.org/10.1007/s13760-025-02779-y Alon Gorenshtein, Kamel Shihada, Liron Leibovitch, Tom Liba, Avner Goren Key finding: Consistent reduction in anti-inflammatory genera (especially Faecalibacterium) and increased Veillonella in migraineurs; overall picture of dysbiosis and reduced diversity. A causal effect of gut microbiota in the development of migraine Published July 2023 https://doi.org/10.1186/s10194-023-01609-x Qiang He, Wenjing Wang, Yang Xiong, Chuanyuan Tao, Lu Ma, Junpeng Ma, Chao You, and The International Headache Genetics Consortium Key finding: Mendelian randomisation evidence of causal links from multiple bacterial taxa (including Bifidobacteriaceae) to migraine, migraine with aura, and migraine without aura. Making migraine easier to stomach: the role of the gut–brain–immune axis in headache disorders Published 2023 https://doi.org/10.1111/ene.15934 Marissa Sgro, Jason Ray, Emma Foster, Richelle Mychasiuk Key finding: Narrative review emphasising that a diverse, healthy microbiome is required for optimal brain health and that dietary manipulation is a logical therapeutic lever. Migraine as a Disease Associated with Dysbiosis and Possible Therapy with Fecal Microbiota Transplantation Published 14 August 2023 https://doi.org/10.3390/microorganisms11082083 Ágnes Kappéter, Dávid Sipos, Adorján Varga, Szabolcs Vigvári, Bernadett Halda-Kiss, Zoltán Péterfi Key finding: Explicitly proposes fecal microbiota transplantation as a future therapeutic option for migraine on the basis of restored serotonin signalling and reduced neuroinflammation. Linking Migraine to Gut Dysbiosis and Chronic Non-Communicable Diseases Published 11 October 2023 https://doi.org/10.3390/nu15204327 Manuela Di Lauro, Cristina Guerriero, Kevin Cornali, Maria Albanese, Micaela Costacurta, Nicola Biagio Mercuri, Nicola Di Daniele, Annalisa Noce Key finding: Places gut dysbiosis at the centre of a bidirectional relationship between migraine and cardiometabolic disorders; advocates nutritional and lifestyle approaches to restore eubiosis. Lipopolysaccharide, VE-cadherin, HMGB1, and HIF-1α levels are elevated in the systemic circulation in chronic migraine patients with medication overuse headache: evidence of leaky gut and inflammation Published 2024 https://doi.org/10.1186/s10194-024-01730-5 Doga Vuralli, Merve Ceren Akgor, Hale Gok Dagidir, Ozlem Gulbahar, Meltem Yalinay, Hayrunnisa Bolay Key finding: First human evidence of raised circulating LPS and leaky-gut markers in chronic migraine + medication-overuse headache, directly implicating intestinal hyperpermeability. The Brain, the Eating Plate, and the Gut Microbiome: Partners in Migraine Pathogenesis Published 11 July 2024 https://doi.org/10.3390/nu16142222 Parisa Gazerani, Laura Papetti, Turgay Dalkara, Calli Leighann Cook, Caitlin Webster, Jinbing Bai Key finding: Strong call for personalised dietary and pre/probiotic interventions; highlights bidirectional influence between diet, microbiome, and migraine susceptibility. Oral and Gut Dysbiosis in Migraine: Oral Microbial Signatures as Biomarkers of Migraine Published 2025 https://doi.org/10.1212/NXI.0000000000200437 Soomi Cho, Yeonjae Jung, Hyun-Seok Oh, Jungyon Yum, Seungwon Song, JaeWook Jeong, Woo-Seok Ha, Kyung Min Kim, Won-Joo Kim, Min Kyung Chu Key finding: Oral dysbiosis is even more pronounced than gut dysbiosis in migraine; specific oral microbial clusters predict migraine status with high accuracy and correlate with headache frequency. Unravelling the gut–brain connection: a systematic review of migraine and the gut microbiome Published 3 April 2025 https://doi.org/10.1186/s10194-025-02039-7 Caroline W Mugo, Ella Church, Richard D Horniblow, Susan P Mollan, Hannah Botfield, Lisa J Hill, Alexandra J Sinclair, Olivia Grech Key finding: Synbiotic and combined probiotic–synbiotic regimens consistently reduce attack frequency, severity, duration, and analgesic consumption in randomised trials. Gut microbiota, probiotics, and migraine: a clinical review and meta-analysis Published 12 September 2025 https://doi.org/10.22514/jofph.2025.043 Olga Grodzka, Izabela Domitrz Key finding: Meta-analysis of RCTs confirms probiotics significantly lower migraine frequency; effect on severity approaches significance despite limited trials.

Two useful tools I wanted to share for anyone here who keenly follows research on cluster headaches, migraine or anything for that matter. The first is Harzing’s Publish or Perish. It is a free citation analysis program that lets you easily search scientific literature across a range of journal sources. Link: https://harzing.com/resources/publish-or-perish The second that I am really loving at the moment is Google’s NotebookLM. It allows you to upload papers, PDFs, and links, then ask structured questions and generate summaries, comparisons and notes directly from your sources. For anyone trying to understand mechanisms, track themes across papers or just stay organised while reading, it is extremely handy. Link: https://notebooklm.google Both tools make it easier for patients who like to follow the science closely to evaluate studies and stay on top of emerging research. If anyone wants a quick explanation of how to use either tool for cluster headache-related topics, I am happy to share examples. The last tool - bonus lol, I went looking for something to match CHFathers cat picture in a recent AI post - found another Google tool. An experimental tool for visual exploration: you input images for subject, scene, style and the system remixes them into new visuals - here's what I got for my new CH Forums profile pic - I am here to stay now! https://labs.google/fx/tools/whisk

Hey Kevin. To my knowledge there is no specific migraine busting protocol. FunTimes offered a solid reply to your earlier post on the general board and the key information regarding the process is on the following page. https://clusterbusters.org/resource/alternative-treatments/#busting You might find the Yale psilocybin migraine study useful to look at as the dose they used somewhat correlates to the Cluster Busters range, if I am correct They gave 0.143 mg/kg of pure psilocybin and when you apply a conversion factor for Psilocybe cubensis potency (roughly 0.8 percent psilocybin by dry weight with variance as to strain, when it was picked and even which part of the fruit) that works out to the same content found in about 1.5 g of dried cubensis - give or take, maybe a little less. The key difference is that the study used one single dose followed by a two-week observation period whereas cluster warriors traditionally repeat doses every five to seven days. https://www.sciencedirect.com/science/article/pii/S187874792301214X My personal thoughts - start a bit lower than the typical 1.5g dried cubensis mushroom to get accustomed to the feeling, I quite enjoy the euphoria and introspection and find it doesn’t last too long before I’m hungry and tired. For what it’s worth a quick scour of the literature found the most recent paper with title including "migraine" "psilocybin" - a case report of a single male migraineur in his 30s whom used psilocybin alongside otc pain relief at 1.2g dried as an acute treatment with greater reported efficacy than pain relief alone. https://pmc.ncbi.nlm.nih.gov/articles/PMC10561985/ You may find another popular treatment option used by members of the CH community worth a look-in whilst you are here, the Vitamin D3 Anti-Inflammatory Regimen. You’ll find the information here or collated by myself and Pete Batcheller over at www.vitamindregimen.com I would say that given a sensible approach and applying the protocols as per the guides, IMHO both of these patient led avenues are generally safe and worth investigating - in any event a walk down the unknown path can cause a bit of anxiety so good luck as you navigate - I remember being nervous as heck in 2015 when I started the D3 regimen against my Doctors best recommendations and yet 8 days later things took a turn for me, I cried like baby, hugged wifey and got my life back - 10 years later I think there is still a part of me that is in disbelief that it actually worked and I only wish that could be the same for everyone. Whilst I have had success with D3, I found a penchant in the hobby of mycology, I have a wonderful big laminar flow hood that takes up our spare room and all the mycological tools to grow wild and wonderful varieties from "cubes" to turkey tails and beyond - and have done so over the years with great success, it is a fascinating and wildly fulfilling hobby with lots of highs (no pun intended) and lows of the process. It isn't a fast thing either and after weeks, sometimes months of cultivation to have a fruiting body appear overnight is awesome or to awake one morning after the same period to find dreaded trichoderma has destroyed all your hard work is devastating! Still, well worth it for the journey and knowledge learned! Were there any specific questions you wanted answers to, I’m sure we will do our best to help. Best wishes to you. Cheers, Craig.

Hi Nut cluster. I’m clearly not female (I missed the social cues upon joining the forum regarding using a cat as my profile picture), I don’t have much to add regarding estrogen but I have always been intrigued with vitamin D biology during pregnancy and your post captured my interest so please excuse me if this is a little off topic but wanted to share. Cholecalciferol / vitamin D3 is converted via hydroxylation into the blood storage form calcifediol which is then further converted into its hormonal form, calcitriol, mostly (but not exclusively) by the kidneys. The blood level of calcitriol is maintained in a strict range to maintain calcium homeostasis and is regulated by parathyroid hormone. During pregnancy the levels of calcitriol, the hormonal form, increases by double or triple to levels you’d see in granulomatous disease or intoxication but without hypercalcemia. The body deliberately raises both calcitriol and binding proteins in order to support placental development, immuno-regulation and fetal skeletal growth. The levels then fall back into normal range 2-6 weeks postpartum. There is still much we don’t understand about this intriguing process. It’s interesting that many female warriors report skipping cycles during pregnancy and to also consider why they return postpartum (and perhaps also why MS relapse may occur postpartum), and although tempting to speculate it may have something to do with the increase in calcitriol and its immuno-modulatory properties, probably an oversimplification - the body is just so complex. Dr. Hollis & Dr. Wagner have a combined century or so of research looking at vitamin D and reproductive outcomes, this was a great talk from last year although can’t recall if they cover the specifics of the points above.

Notebook LLM Audio Summary Podcast Generation (AI generated). Vitamin_D_deficiency_linked_to_migraine_treatment.m4a

Vitamin D Deficiency and Supplementation in Migraine: A Scoping Review of Clinical Efficacy, Evidence Gaps, and Research Priorities Amey Marathe, Shailly Vaghasiya, Arth Shah, Soaham Desai Published in Annals of Indian Academy of Neurology on November 12, 2025 Link: https://doi.org/10.4103/aian.aian_417_25 Abstract: Background and Objectives: Migraine is a debilitating neurological disorder affecting 10%–20% of the global population, with significant socioeconomic burdens. Vitamin D deficiency, prevalent in over 1 billion individuals, has been proposed as a modifiable risk factor in migraine management due to its potential role in pain modulation and neuroinflammation. This scoping review aimed to map global vitamin D deficiency prevalence across migraine subtypes and geographic regions, synthesize clinical correlations between vitamin D status and migraine characteristics, and explore heterogeneity in therapeutic evidence across paediatric, chronic, and refractory migraine subgroups. Methods: A systematic search of PubMed, Scopus, and Embase was conducted, identifying 3,447 records initially. After screening and eligibility assessment, 30 studies were included. These encompassed observational studies (n = 14), randomized controlled trials (n = 9), and systematic reviews (n = 7). Data were synthesized narratively due to clinical heterogeneity and the predominance of cross sectional evidence. Results: Vitamin D deficiency (serum 25 hydroxyvitamin D [25(OH) D] <20 ng/mL) was highly prevalent among migraine patients (65%–88%), particularly in chronic migraine (80%–92%) and high latitude populations (>40°N: 75%–90%). Inverse correlations were observed between vitamin D levels and headache frequency and disability scores. High dose vitamin D supplementation (≥50,000 IU/week) reduced migraine attacks by 50%–72% in deficient adults, while minimal benefit was seen in replete individuals. Single trials revealed enhanced efficacy when combined with probiotics or topiramate in refractory and paediatric cases, respectively, but this requires further validation. Conclusion: Vitamin D deficiency is consistently associated with increased migraine burden. Supplementation shows context dependent efficacy, particularly in deficient individuals and specific subgroups. Future research should focus on mechanistic trials, global standardization of assays, and comprehensive outcome assessments. Clinically, baseline 25(OH)D testing is recommended to guide targeted supplementation strategies.

This is a new and highly relevant study for anyone with CH considering or already following the Vitamin D3 Anti-Inflammatory Regimen. In participants with baseline 25(OH)D3 levels below 20ng/mL, researchers used the same loading dose of 600,000 IU that the regimen recommends. What makes this particularly interesting is that their maintenance doses were substantially higher than the standard 10,000 IU per day typically required to sustain serum levels in the 80–100 ng/mL range. Across roughly ninety patients these higher doses were well tolerated, with no evidence of renal impairment or disturbances in calcium homeostasis. This offers compelling reassurance for CH'ers who may feel uneasy about achieving or maintaining the regimen’s target vitamin D levels. Regular monitoring remains essential, but this study reinforces that the dosing strategy is safe when managed appropriately. It also suggests that if some CH'ers fail to achieve a therapeutic response with the base regimen they may entertain elevating their 25(OH)D3 level higher in order to reach a therapeutic threshold (again with close monitoring of labs).

Notebook LLM Audio Summary Podcast Generation (AI generated). Unlocking_Remission__How_High-Dose,_Monitored_Vitamin_D3_Safely.m4a

Prolonged high dose daily oral vitamin D3 in the management of psoriasis: A retrospective chart analysis Renu Mahtani, Sudhir Singh, Pradeep MK Nair, Satya Prakash Singh & Mankul Goyal Published in IP Indian Journal of Clinical and Experimental Dermatology on 26 September 2025 Link: https://doi.org/10.18231/j.ijced.89447.1758864688 Abstract: Background: Autoimmune disorders, particularly psoriasis, are often associated with vitamin D deficiency and vitamin D resistance. Higher daily doses of vitamin D3 are considered effective in overcoming vitamin D resistance and reversing psoriasis symptoms. This study was conducted to evaluate the safety and efficacy of individualized, prolonged high‑dose daily oral vitamin D3 therapy in patients with moderate‑to‑severe psoriasis. Materials and Methods: In this study, we present data from 95 patients with moderate‑to‑severe psoriasis who underwent individualized high‑dose daily oral vitamin D3 (cholecalciferol) therapy. From this cohort, six representative cases are described in detail to illustrate the approach to personalized dosing and the monitoring process using biochemical markers such as parathyroid hormone (PTH) and ionized calcium. The efficacy of the intervention was assessed using Psoriasis Area and Severity Index (PASI) scores, while safety was evaluated through regular monitoring of serum creatinine and ionized calcium levels. Statistical analyses were conducted to examine the relationship between vitamin D3 dosage, serum 25(OH)D levels, PTH suppression, and clinical improvement. Results: Significant clinical improvement or remission was noted, without hypercalcemia or toxicity. PTH levels consistently declined in parallel with clinical response, suggesting vitamin D action. Conclusion: Monitored oral vitamin D3 therapy in higher than supplemental dose, can be a safe and effective treatment for psoriasis.

Hey Erick. It's not strange at all - I get it, we get it - I actually travelled from New Zealand to Dallas this September just to meet other cluster headache patients. We hear you, we see you. Welcome and I am sorry that you find yourself in the midst of a particularly tough cycle. 1-2 a week would be nice, 3-7 a day is more in tune with my cycles which run annually Nov-Mar. I would say this isn't your life now and there are options available to you and you are in the right place to learn about those. There are 3 types of therapies for CH, abortive, bridging and preventative. For the abortive I hear your thoughts re triptans, they come with side effects, you can only use so many within a 24 period and they can cause rebound attacks. I would recommend investigating high flow oxygen via a non-rebreathable mask like the cluster o2 kit or looking into a DMT vape pen (there is a recent thread on this from one of our active members maybe worth checking out). Once you find you are able to abort effectively and quickly you'll hopefully find you get a bit less dread and anxiety for the next attack. Bridging therapies are used temporarily to offer relief whilst you wait for a preventative therapy to start working, sometimes a short tapered course of prednisone is enough to break a cycle or buy you 10-14 days pain free bliss and hopefully when you taper off, a preventative medication has started to work. You haven't mentioned what preventative meds have tried, you could share that info - perhaps we could offer our thoughts. I would just leave you with my experience being that I am now in the 10th season of successfully preventing my CH using the patient led treatment protocol the Vitamin D3 Anti-Inflammatory Regimen for Cluster Headache. If you immediately thought yeah, right - tell me another one then I'd encourage you to put that preconception to the side and just learn a little more to see if it resonates with you. It has been so effective for me I consider myself lucky but I am one of thousands since circa 2011 that has seen similar benefit. I also like that it is natural, safe (when followed as documented), accessible and affordable - I buy the supplements for less than $1 USD per day. www.vitamindregimen.com or I am sure you will find the protocol here on this site as well. There is the option of busting and I am sure others would be able to offer solid advice over and above the resources available on this amazing website. Importantly hang in there man, I hope pain free days are around the corner for you - this will pass. PFW, Craig.

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CD39+ CD4+ T cells influence cluster headache risk via ADP/N-acetylneuraminate and choline metabolic pathways: evidence from Mendelian Randomization Jingshan Zeng, Ying Yi, Hu Xie & Yun Zhu Published in International Journal of Neuroscience on October 30, 2025 Link: https://doi.org/10.1080/00207454.2025.2580332 Abstract: This study employs the Mendelian randomization (MR) approach to investigate the causal relationships among immune cells, cluster headache (CH), and potential mediation by serum metabolites. Using genome-wide association study (GWAS) data, MR analyses were conducted on 731 immune cell phenotypes, 1400 serum metabolites, and CH. The inverse variance weighted (IVW) method was employed as the primary analytical approach, supplemented by MR-Egger and weighted median analyses. Stability of results was assessed using Cochran’s Q and other statistical tests. The analysis identified a negative causal relationship between CD39+ CD4+ %T cells and CH, supported by sensitivity analyses. Reverse MR analysis showed no effect of CH on CD39+ CD4+ T cells, suggesting a unidirectional role of these cells in reducing CH risk. Further mediation MR analysis indicated that CD39+ CD4+ T cells may influence CH risk through the regulation of either the adenosine 5′-diphosphate (ADP) to N-acetylneuraminate ratio or the choline phosphate to phosphoethanolamine ratio, with mediation effect ratios of 12.4% and 12.5%, respectively. CD39+ CD4+ T cells may reduce CH risk by increasing the adenosine 5′-diphosphate (ADP) to N-acetylneuraminate ratio or the choline phosphate to phosphoethanolamine ratio. These findings provide novel insights into potential targets for the prevention and treatment of CH.

Thank-you for reading and for sharing your kind feedback, I appreciate it. I believe everything I have offered is factual and surmises the research findings correctly although I admit its shortcomings being there is no hard evidence right now linking dysbiosis in pathogenesis of CH. Hopefully it stimulates a further conversation or inspires someone to further investigate. I guess if I gave up my job today and went back to university, I might have a degree in immunology and microbiology in another decade and a more meaty take on the matter for you. In respect of your thoughts around a therapeutic protocol, I like your thought process and when I look at the case report by Beltran and having further read his other case reports and presentations, the diagnostic work-up usually includes the GI Map (here's a sample report) & SIFO/SIBO breath test. The treatment protocol he uses employs what he refers the Microbiome Concordance Index Score to assess microbiome dysfunction and inform a tailored treatment protocol, specifically the selection of dietary intervention and use of herbal antimicrobials alongside high dose vitamin D3. If anything, if I found myself falling from remission whilst maintaining a vitamin D3 level of 100ng/mL I would take another loading dose and add the full monty supplements as well as starting a ketogenic diet with a 24 hour fast. It's worked for me once before, I am confident it would do again, it is just a bit nerve racking taking your 25(OH)D3 up close to the 200ng/mL range. Beyond that ordering a GI map and navigating the complexities of selecting the appropriate herbals and diet based on the results is probably beyond my level of comfort, I'd seek the advice of a functional doctor. Thanks again for your reply.

An Exploration of the Psychological Aspects of Cluster Headache Helena Whitley Published by University of East Anglia on October 30, 2025 Link: https://ueaeprints.uea.ac.uk/id/eprint/100852 Abstract: Cluster Headache (CH) is cited as one of the most painful experiences known to humankind. This thesis portfolio aimed to provide a greater insight into the psychological aspects of CH. A systematic review accumulated evidence of rates of depression and suicidality in individuals living with CH and an empirical paper explored the psychological experience of living with CH. A systematic review and meta-analysis was conducted to determine rates of depression and suicidality amongst individuals with CH compared to non-headache controls and individuals with other primary headache conditions (Migraine or Tension-Type Headache (TTH)). Secondly, 13 interviews were conducted with individuals living with CH and this data was analysed using Reflexive Thematic Analysis. Meta-analyses of 20 studies showed that compared to non-headache controls, adults with CH had much higher levels of depression and suicidality. However, there was no significant difference in depression levels between CH and Migraine individuals. Comparing individuals with CH and TTH, the initial meta-analysis found no significant difference in depression levels, but a sensitivity analysis showed TTH individuals having higher levels of depression. Considerable heterogeneity and publication bias were present. Reflective Thematic Analysis identified five themes relevant to the CH experience: “Darkness”, “Battling”, “Shifting”, “Control”, and “Despair”. There were differences within these themes based on whether a person was in the moment of pain or between attacks, whether they had the chronic or episodic form of CH, and how long they had lived with CH. This portfolio highlighted that psychological aspects of CH include increased depression and suicidality. Increased depression was also present for the other primary headache disorders. The empirical paper identified various psychological processes important in the experience of CH which could be the target of psychological treatment. Transcription.m4a

Non-Invasive Vagus Nerve Stimulation in Cluster Headache: A Clinical Practice Guideline Peter J. Goadsby, Alexander Feoktistov, Magdalena Anitescu, Miles Day, Peter Staats Published in Pain Practice on October 6, 2025 Link: https://doi.org/10.1111/papr.70084 Abstract: Cluster headache (CH) is a rare but severe primary headache disorder characterized by recurrent attacks of unilateral, typically periocular pain lasting 15 min to 3 h, accompanied by ipsilateral autonomic symptoms and restlessness or agitation. Attacks may occur multiple times daily and present in clusters lasting weeks to months, interspersed with remission periods in episodic CH, or without remission in chronic CH. This review summarizes the clinical evidence supporting the use of transcutaneous cervical vagus nerve stimulation (tcVNS) for both the acute and preventive treatment of CH. Relevant clinical trials, real-world studies, and guideline recommendations are discussed. Pharmacological therapy for CH includes triptans and high-flow oxygen for acute management, and verapamil, corticosteroids, or galcanezumab for prevention. For patients with inadequate response or intolerance to these options, neuromodulation may be required. TcVNS has emerged as a noninvasive, safe, and effective alternative to invasive neuromodulation. Clinical trials have demonstrated significant reductions in attack frequency and intensity, leading to U.S. Food and Drug Administration (FDA) clearance and UK National Institute for Health and Care Excellence (NICE) approval for both acute and preventive treatment of CH. TcVNS represents a well-tolerated, noninvasive neuromodulatory option for patients with cluster headache, offering both acute and preventive benefits. This paper provides an overview of the current evidence, mechanisms of action, and practical guidelines for incorporating tcVNS into clinical management.

I’d like to offer a contemporary perspective on recent patient reports from the cluster headache (CH) community alongside my own experience regarding the treatment of CH with nutritional interventions. This draws on a range of emerging research to explore how modulation of the gut microbiota more so than any one diet may present as a novel future therapeutic target in CH. As best I can as a CH patient, I will attempt to integrate the converging lines of evidence that support this hypothesis including a case report, drawn from the grey literature, illustrating the clinical application of such a targeted microbiome-based approach and conclude with some final thoughts on what really is a fascinating subject. More bacteria than we are human... The human genome encodes for between 20,000 and 25,000 genes. In remarkable comparison our collective microbial genome, comprised of trillions of microbes that inhabit our bodies, contains an estimated 3,000,000 to 4,000,000 million genes. The gut microbiota is a vast community of bacteria, fungi, viruses and archaea that inhabit the gastrointestinal tract, with the highest density of microbes anywhere in the body found in the colon. The diversity of this community is influenced by a number of factors including diet, environment, motility, autonomic tone, antibiotic exposure, previous infection, vitamin D3 and psychedelics (more on the vitamin D3 and psychedelics later). Their primary energy source is dietary fibre and other non-digestible carbohydrates of which they ferment into short-chain fatty acids (SCFA’s) such as acetate, propionate and butyrate. They also synthesize vitamins such as vitamin K and several B-group vitamins, amino acid derivatives like indole and GABA and secondary bile acids that in turn regulate metabolism and immune function. Together these microbes and their metabolites play an existential role in maintaining gut integrity, modulating inflammation and supporting our overall health. Balance is the key to life... that sentiment resonates with me... When this community of microbes is balanced, or in eubiosis, the relationship is mutually beneficial. We nourish the microbes and they nourish us. When the balance of this community is disrupted, disease may follow through a process referred to as dysbiosis. Imbalance of the microbiota may degrade the mucin layer, a protective layer of mucous that protects the epithelial lining of the gut. When the mucosal layer is degraded, disruption may occur at the level of the epithelium where the tight junctions that maintain integrity of permeable membranes are compromised, increasing the translocation of toxins from the gut into blood and lymph where they invoke an immune response. An example of this is lipopolysaccharide (LPS), a structural component of the outer membrane of gram-negative bacteria. LPS engages the toll like receptor 4 (TLR4) complex on innate immune cells, activating the transcription factor nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), which translocates to the nucleus and upregulates the expression of pro-inflammatory cytokines such as interleukin-1β (IL-1β) and tumor necrosis factor-alpha (TNF-α). This cascade contributes to a process commonly referred to as “leaky gut” syndrome. Emerging Migraine Research... Whilst CH and migraine are clinically distinct disorders they do share several overlapping mechanisms including activation of the trigeminovascular system and neurogenic inflammation, as well as responsiveness to medications such as triptans and anti-CGRP monoclonal antibodies such as Emgality. Both conditions also exhibit cyclical patterns and hypersensitivity within pain processing networks. Given the larger body of research on migraine, it is useful to cautiously draw insights from migraine studies given they may reveal potential pathophysiological processes and therapeutic targets relevant to CH. In my view recent literature seems to have shifted the understanding of migraine from a neurovascular disorder toward a systemic inflammatory condition modulated by the gut-brain-immune axis. Multiple independent studies now converge on the idea that gut dysbiosis and intestinal permeability are central to migraine pathophysiology. A study by He et al. (2023) confirmed a causal relationship between gut microbial composition and migraine risk, identifying protective taxa such as Bifidobacteriales and pathogenic associations with Anaerotruncus and Clostridium genera, providing what I believe was the first robust evidence that microbiota composition can directly influence migraine susceptibility. In a 2024 study, Vuralli et al. found elevated serum LPS, VE-cadherin, HMGB1 and IL-6 in chronic migraine patients with medication overuse, supporting a “leaky-gut” inflammatory phenotype linked to trigeminal sensitization. Recent reviews and meta-analyses converge on much the same theme; migraineurs show lower microbial diversity, depletion of SCFA producing species such as Faecalibacterium and Roseburia and a relative overgrowth of pro-inflammatory species. Emerging clinical research supports therapeutic modulation of the microbiota. Grodzka and Domitrz (2025) conducted a meta-analysis that showed probiotic supplementation reduced migraine frequency with mixed effects on severity whilst Kappéter et al. (2023) proposed fecal microbiota transplantation (FMT) as a means of microbial restoration and normalizing the inflammatory mediators implicated in migraine chronification. What does the CH literature say? Comparable findings in CH are absent however new evidence does show an emerging persistent inflammatory signature. In peripheral blood, Lund et al. (2025) found distinct cytokine profiles across all CH types with oncostatin M (OSM), an IL-6 family cytokine, elevated in cCH, eCH in-cycle and eCH in remission groups. In cerebrospinal fluid, Ran et al. (2024) demonstrated higher chemokine concentrations with a serum-to-CSF gradient, concentrating inflammation within the central nervous system (CNS) and present both during active cycle and remission periods. More recently, PACAP-38 has also been found to be elevated in CH compared with controls, further supporting the presence of sustained neuroimmune activation involving vasoactive peptides even during remission periods. And whilst an underlying inflammatory signature has now been identified, the upstream driver of these elevated markers remains unlinked to dysbiosis. Taken together however these new findings point to CH as a condition underpinned by ongoing inflammation within the CNS rather than a series of isolated pain events attributed to dysfunction of the hypothalamus. So, what was this about a diet? Sign me up! What has recently been referenced by myself and others in the CH community is a 2018 case-control study by Di Lorenzo et al. that examined the effects of a ketogenic diet in a small cohort of 18 chronic CH patients refractory to standard preventive treatments. The authors reported that 15 participants responded favorably, with 11 achieving sustained pain-free remission and 12 choosing to remain on the intervention even after the study concluded. Although the mechanism of action was not explored, it is my view that the therapeutic benefit of the ketogenic diet likely extends beyond the metabolic effects of ketone production to include modulation of the gut microbiota and its associated inflammatory milieu. To my knowledge, this remains the only dietary intervention in CH and while the sample size was small the findings were nonetheless remarkable. Here warrior – I recommend giving this a try... Consider this a brief pause, a half-time reflection, before moving into the following sections. Few examples illustrate the power of patient-led initiatives better than what the CH community has been able to achieve. Out of necessity and sheer persistence, patients have effectively conducted some of the most successful citizen science projects in existence. From the early work exploring psychedelic therapy to the development of the vitamin D3 anti-inflammatory regimen, each step has been driven by individuals determined to find solutions where few existed. These remarkable efforts have produced measurable results and practical treatment tools that continue to change the lives of CH patients, indeed not all heroes wear capes. Where vitamin D3 & psilocybin converge... What I find particularly intriguing is that both of these therapies, psychedelic compounds and the Vitamin D regimen, according to emerging research, may exert part of their therapeutic effect through interactions with the gut microbiota. At the same time, their variable efficacy from one CH patient to another may be influenced by the baseline state and diversity of that patient’s microbiome. This bidirectional relationship, in which treatment both shapes and is shaped by its interaction with the microbiota, may help explain why some experience complete remission while others achieve only partial or temporary relief, or require higher or repeated doses. In the following sections, I will examine the literature that highlights the potential points of convergence between Vitamin D and psilocybin, focusing on microbiome mediated interactions. Oh vitamin D3, you have been kind to me... For almost a decade now, the Vitamin D3 anti-inflammatory regimen has kept me mostly pain-free from CH. Beyond its role in calcium homeostasis Vitamin D3 plays a key role in maintaining gastrointestinal homeostasis. The active form, 1,25-dihydroxyvitamin D3, binds to the Vitamin D receptor (VDR), which is expressed throughout the intestinal epithelium and immune cells. Through this signaling pathway Vitamin D3 influences epithelial integrity, microbial diversity and modulates the immune response (Vemulapalli et al., 2025). In refining the original regimen, Pete Batcheller included a B-complex, taking inspiration from Gominak’s work linking Vitamin D restoration to improved sleep and gut function through the microbiota’s production of B vitamins (Gominak, 2016). Gominak proposes that both Vitamin D and the microbiota exist in a symbiotic relationship, where Vitamin D supports the host environment necessary for microbial balance while a healthy microbiota contributes to the production of essential cofactors necessary for neuronal and immune health. Charoennngam et al. (2020) demonstrated that Vitamin D3 supplementation shifts the microbiota toward a less inflammatory profile, increasing beneficial commensal species such as Bacteroides while reducing pathogenic species like Porphyromonas. In regards to maintenance of the epithelial membranes, Vitamin D3 upregulates tight-junction proteins such as claudins and occludins while lowering zonulin expression, a key marker for intestinal permeability. By strengthening tight junctions Vitamin D3 may limit translocation of bacterial endotoxins such as LPS into systemic circulation (Fedele et al., 2018; Stio et al., 2016). In addition to maintaining gut barrier integrity, Vitamin D3 modulates the immune response by inhibiting NF-κB activation and reducing the production of pro-inflammatory cytokines while supporting T regulatory cell function and the production of antimicrobial peptides such as cathelicidins and beta defensins (Vemulapalli et al., 2025). Taken together these findings place Vitamin D3 as a key mediator in gut-immune homeostasis, acting at the bleeding edge between the microbial landscape and host defense. Importantly, as demonstrated by Holick and colleagues in Scientific Reports (2019), the genomic actions of Vitamin D3 are dose and blood-level responsive with higher 25-hydroxy vitamin D levels resulting in broader transcriptional changes across hundreds of genes involved in immune regulation. The fact that Pete Batcheller’s regimen has been assembled into a simple and accessible protocol with consistently impressive response rates is in itself a remarkable achievement given the devastating nature of CH. Whilst Vitamin D3 almost certainly acts on receptors within the trigeminal ganglion and hypothalamus, these recent findings suggest its actions in the periphery, particularly within the gut, may play an important role in the therapeutic efficacy of the anti-inflammatory regimen. What can mushrooms possibly have to do with any of this? Intriguing new research suggests that the therapeutic effects of psychedelics, particularly psilocybin, may in part be mediated through interactions with the gut microbiota. While its best described actions involve modulation via the serotonergic receptor, new findings reveal that psilocybin also exerts systemic effects on inflammation, immune signaling, intestinal barrier integrity as well as shaping the microbial landscape itself. Wang et al. (2025) provide an elegant synthesis of this evolving concept in a recent ACS Chemical Neuroscience viewpoint, suggesting that the therapeutic effects of psychedelics including psilocybin extend beyond cortical serotonergic circuits to modulate the gut-brain axis via interactions with the microbiome. Building on emerging evidence they position these compounds as both neuroactive and immunomodulatory agents, potentially influencing inflammation along the microbiota-gut-brain pathway via NF-κB mediated cytokine modulation as shown in complementary models like Zanikov et al., 2024. Zanikov et al. (2024) were able to show in a mouse model of colitis that psilocybin reduced gut driven neuroinflammation and lowered the expression of inflammatory cytokines IL-1β, IL-6 and COX-2 in brain parenchyma. These findings link intestinal inflammation directly to a central inflammatory response and confirm that psilocybin’s anti-inflammatory effects occur along the gut-brain axis rather than within the brain alone. Complementary in vitro work in human macrophages shows dose dependent suppression of LPS induced cytokines via modulation of NF-κB signaling, highlighting its broad immunoregulatory potential. Kelly et al. (2023) introduced the term “psilocybiome” as a framework to describe the bidirectional relationship between psychedelics and the microbiota-gut-brain axis, they propose that microbial diversity and metabolism influence every phase of psychedelic therapy from preparation and acute experience to integration. Caspani et al. (2024) build on this by exploring psychedelics potential antimicrobial effects and how they may reshape gut ecology, suggesting that microbial composition modulates psychedelic pharmacokinetics while remarkably, psychedelics, in turn, remodel the microbiota. This research suggests that psilocybin’s therapeutic benefit may indeed depend on the baseline composition and inflammatory state of the gut microbiome. This perspective offers a fresh view for the variability in dose response observed within the CH community’s collective busting experiences. It appears reasonable to suspect that interventions which restore microbial balance and support gut integrity may enhance the therapeutic window for psychedelic therapy. Although the degree to which these microbial mediated mechanisms contribute to the therapeutic benefit we see in busting for CH remains speculative, these new findings make clear that psilocybin’s actions reach beyond the mind, extending into the intricate microbial terrain in a complex dance that is beginning to be revealed. So what about that case report? Recent clinical evidence provides an example of how restoring microbial homeostasis may be achieved through an integrative approach. A 2023 case report by Beltran and Guimarães described the successful treatment of a patient with psoriasis vulgaris refractory to conventional therapies using a combined anti-inflammatory diet, high-dose vitamin D3 therapy and targeted herbal antimicrobials. The case report used a diagnostic workup that included the Gastrointestinal Microbial Assay Plus (GI-MAP), a DNA-based stool test that identifies bacterial, fungal and parasitic taxa as well as markers of gut inflammation and intestinal permeability by Quantitative PCR (qPCR). This diagnostic framework provided a precision-based view of the patient’s baseline microbial state and guided subsequent therapeutic choices. Such testing reveals that, just as no two microbiomes are identical, one size may not fit all in nutritional or supplement interventions. Importantly, dysbiosis patterns and their immunological signatures vary between individuals which necessitates personalized modulation of the microbiota rather than blanket probiotic or dietary advice. In the specific case testing revealed small intestinal fungal overgrowth (SIFO) driven by Candida albicans. These results informed a selection of herbal antimicrobials, notably oregano oil for its antifungal and biofilm-disruptive properties. Oregano oil’s mechanisms include membrane disruption and inhibition of fungal enzyme activity which reduce microbial burden and help restore mucosal homeostasis. To complement this, Curcumin longa (turmeric) was used for its capacity to inhibit NF-κB-mediated inflammation and upregulate VDR expression in epithelial and immune cells. Following five months of intervention immunofluorescence analysis of VDR expression in skin biopsies revealed upregulation of receptor density compared with baseline, correlating in full clinical remission. This finding parallels the discussion advanced in Beltran’s companion paper, Vitamin D Receptor Renewal Through Anti-Inflammatory Diet, which identifies the suppression of VDR by LPS, mycotoxins and inflammatory cytokines as key drivers of vitamin D resistance in chronic inflammatory and autoimmune diseases. By resolving dysbiosis and improving epithelial integrity through diet, the intervention removed the upstream inflammatory blockade to VDR transcription and restored immune tolerance. Where and how to even conclude this...? Cluster headache, long regarded as the most devastating disorder, may find part of its explanation not in the brain alone but in the microbial world that indeed sustains it. As our understanding of the gut-brain-immune axis deepens, the concept that dysbiosis and intestinal permeability may act as upstream drivers of neuroinflammation becomes increasingly difficult to ignore. While the literature in CH remains in its infancy, speculative bridges are clearly already being built with patents having been filed for microbial modulating technologies aimed at treating headache disorders, such as US9987224B2, which describes methods for altering gut microbiota composition to influence neurological outcomes including migraine and CH. Such developments are another signal of the growing recognition that modulating our microbial landscape presents as an attractive therapeutic target for disorders once considered purely neurogenic in origin. All being said, it's early days – what I think we have is an interesting hypothesis more so than settled science for CH specifically. The ketogenic results are impressive but need larger, controlled trials; vitamin D3 works for many but the anti-inflammatory regimen remains without clinical validation in CH and psilocybin's ties to the microbiome are certainly intriguing but mostly preclinical. All three treatment options are available for patients to pursue at their own discretion. I hope I have been able to articulate my take on the current literature and of course welcome your thoughts, comments and ideas. I have tried to be as accurate as possible, please point out any shortcomings. Many questions remain covering other important topics in CH such as genetics, periodicity and the role of personality; still – I feel like it is an exciting and hopeful time and look forward to seeing what future research may show in regards CH and the microbiome. References Migraine Vuralli, D., Akgör, M.C., Gök Dağıdır, H. et al. (2024) ‘Lipopolysaccharide, VE-cadherin, HMGB1 and HIF-1α are elevated in chronic migraine with MOH: evidence of leaky gut/inflammation’, J Headache Pain. Link: https://pmc.ncbi.nlm.nih.gov/articles/PMC10875763/ He, Q., Zhang, Y. and Li, R. (2023) ‘A causal effects of gut microbiota in the development of migraine’, J Headache Pain. Link: https://thejournalofheadacheandpain.biomedcentral.com/... Grodzka, O. and Domitrz, I. (2025) ‘Gut microbiota, probiotics, and migraine: a clinical review and meta-analysis’, Journal of Oral & Facial Pain and Headache. Link (journal): https://www.jofph.com/articles/10.22514/jofph.2025.043 Kappéter, Á., Zając, A., Domitrz, I. (2023) ‘Migraine as a disease associated with dysbiosis and possible therapy with fecal microbiota transplantation’, Biomedicines. Link: https://pmc.ncbi.nlm.nih.gov/articles/PMC10458656/ Cluster Headache Lund, N.L.T., Pedersen, S.H., Ashina, M. et al. (2025) ‘Distinct alterations of inflammatory biomarkers in cluster headache: a case–control study’, Annals of Neurology. Link (journal): https://onlinelibrary.wiley.com/doi/10.1002/ana.27205 Ran, C., Yang, Y., Guo, S. et al. (2024) ‘Elevated cytokine levels in the central nervous system of patients with cluster headache’, J Headache Pain. Link: https://thejournalofheadacheandpain.biomedcentral.com/... Søborg, M.L.K., Amin, F.M., Ashina, M. et al. (2025) ‘PACAP-38 in cluster headache: a prospective, case-control study of a potential treatment target’, Eur J Neurol. Link (PubMed): https://pubmed.ncbi.nlm.nih.gov/41002104/ Ketogenic Diet Di Lorenzo, C., Coppola, G., Sirianni, G. et al. (2018) ‘Efficacy of Modified Atkins Ketogenic Diet in Chronic Cluster Headache: An Open-Label, Single-Arm Clinical Trial’, Frontiers in Neurology. Link: https://www.frontiersin.org/.../10.../fneur.2018.00064/full Vitamin D3 Vemulapalli, R., Thomas, A. (2025) ‘The Role of Vitamin D in Gastrointestinal Homeostasis and Gut Inflammation.’, Int. J. Molecular Sciences Link: https://pubmed.ncbi.nlm.nih.gov/40243631/ Gominak, S.C. (2016) ‘Vitamin D deficiency changes the intestinal microbiome reducing B-vitamin production in the host: a hypothesis explaining chronic sleep disorder’, Medical Hypotheses. Link (PubMed): https://pubmed.ncbi.nlm.nih.gov/27515213/ Charoenngam, N., Shirvani, A., Holick, M.F. (2020) ‘The Effect of Various Doses of Oral Vitamin D3 Supplementation on Gut Microbiota in Healthy Adults: A Randomized, Double-blinded, Dose-response Study’, Anticancer Research. Link: https://pubmed.ncbi.nlm.nih.gov/31892611/ Stio, M. et al. (2016) ‘Vitamin D regulates the tight-junction protein expression in active ulcerative colitis’, Scand J Gastroenterol. Link (PubMed): https://pubmed.ncbi.nlm.nih.gov/27207502/ Scricciolo A, Roncoroni L, Lombardo V,Ferretti F, Doneda L,Elli L (2018) ‘Vitamin D3 Versus Gliadin: A Battle to the Last Tight Junction’, Digestive Diseases and Sciences. Link: https://pubmed.ncbi.nlm.nih.gov/29159680/ Shirvani A, Kalajian TA, Song A, Holick MF. (2019) ‘Disassociation of vitamin D’s calcemic and non-calcemic genomic activity & individual responsiveness: RCT’, Scientific Reports. Link: https://www.nature.com/articles/s41598-019-53864-1 Psychedelics Wang, X., Li, H. and Zhou, Z. (2025) ‘Psychedelics and the Gut Microbiome: Unraveling the Interplay and Therapeutic Implication’ (Viewpoint), ACS Chemical Neuroscience. Link (journal page): https://pubs.acs.org/doi/abs/10.1021/acschemneuro.5c00418 Zanikov, T., Gerasymchuk, M. and Robinson, G.I. (2024) ‘Psilocybin and eugenol prevent DSS-induced neuroinflammation in mice’, Biocatalysis and Agricultural Biotechnology. Link: https://www.sciencedirect.com/.../pii/S1878818124000161 Caspani et al. (2024) ‘Mind over matter: the microbial mindscapes of psychedelics and the gut-brain axis’, Progress in Neuro-Psychopharmacology & Biological Psychiatry. Link: https://www.sciencedirect.com/.../pii/S1043661824002834 Kelly, J.R., and Clarke, G. (2023) ‘Seeking the Psilocybiome: Psychedelics meet the microbiota-gut-brain axis’, International Journal of Psychopharmacology Link: https://pmc.ncbi.nlm.nih.gov/articles/PMC9791138/ Case Report & Other Beltran, E.P. and Guimarães, G. (2023) ‘High-dose vitamin D3, anti-inflammatory diet and targeted antimicrobials in psoriasis vulgaris: clinical case with VDR immunofluorescence’, Zenodo case report (grey literature). Link: https://zenodo.org/record/7799594 Beltran, E.P. (2023) ‘Vitamin D Receptor Renewal Through Anti-inflammatory Diet’, ResearchGate/Institutional page (grey literature). Link: https://www.researchgate.net/.../369801068_Vitamin_D... US 9,987,224 B2 (2018) ‘Method and system for preventing migraine headaches, cluster headaches and dizziness.’ Link (Google Patents): https://patents.google.com/patent/US9987224B2/en