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Here's something from 2019: https://pmc.ncbi.nlm.nih.gov/articles/PMC7802413/ "As previously mentioned, it is still unclear why oxygen exhibits such good efficacy in the treatment of CH. The vasoconstrictive theory was prevalent in the early 20th century until Wolff et al. found that ergotamine constricted external carotid arteries and simultaneously relieved migrainous headaches.20 Therefore, they proposed that headache is caused by vasodilation rather than vasoconstriction. The study was published in 1938 and overturned the past theory.20 In 1961, Horton7 proposed that histamine cephalalgia was caused by the vasodilatation of extracranial vessels, and that oxygen was a vasoconstriction factor. If the vasoconstrictive effect of oxygen exists, oxygen therapy should be effective for both migraine and CH. However, the oxygen treatment is only effective for CH. In the 1980s, some studies reported a decrease of cerebrospinal flui in patients after breathing 100% oxygen as compared to breathing room air.21 Since then, animal model studies have demonstrated the protective, anti-inflammatory role of hyperoxia in microcirculatory inflammation. In 2006, Schuh-Hofer et al.11 demonstrated that hyperoxia can inhibit dural plasma protein extravasation in rats. Recent studies have suggested that CH is associated with some brain structures, including the trigeminovascular system, the cranial autonomic system, and the hypothalamus. The activation of the trigeminovascular system is thought to play an important role in the pathophysiology of CH. Goadsby and Edvinsson22 attempted to demonstrate the associations between hyperoxia and neuropeptides, and the results indicated that a significant reduction of calcitonin gene related peptide concentration in the jugular vein after oxygen treatment occurred, which suggests a possible effect of hyperoxia on trigeminal afferents. However, animal experiments have shown that oxygen does not directly act on trigeminal afferents, but appears to play a key role at the parasympathetic pathways.23 At present, studies assume that oxygen may act as a terminating factor in CH attacks. More research is needed to clarify the specific mechanisms of oxygen treatment for CH. Table 1. The history of oxygen used for cluster headache Study Year Findings Alvarez et al.15 1940 First use of oxygen for headache at a flow rate between 6 and 8 L/min. Horton16 1952 First description of oxygen used for histamine cephalalgia. Horton17 1955 Oxygen treatment in 1176 patients with histamine cephalalgia. Horton7 1961 He raised the vasoconstrictive effect of oxygen in histamine cephalalgia. Kudrow et al.18 1981 First systematic study on oxygen used for cluster headache. Fogan et al.12 1985 Crossover study found that oxygen was more effective than room air. Cohen et al.19 2009 Oxygen at 12 L/min, as well as at 7 L/min, was effective. Open in a new tab Figure 1. Open in a new tab The possible mechanism of oxygen in cluster headache. Note: TCC: Trigeminal cervical complex.

1. Alcohol consumption increases adenosine. https://pmc.ncbi.nlm.nih.gov/articles/PMC6826818/ 2. High-flow oxygen reduces adenosine. https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2020.00097/full 3. Caffeine blocks adenosine. https://pubmed.ncbi.nlm.nih.gov/20164566/ 4. Adenosine has been associated with cluster headaches. https://pubmed.ncbi.nlm.nih.gov/38127692/ Therefore, I think I'll try reducing adenosine. Coffee is not the only thing that is supposed to work for that. https://selfhacked.com/blog/adenosine-risks/

Very interesting line of thought, are you planning a trial of one of the supplements listed in the selfhacked article? Please keep us posted.