Yes, it could be that it downregulated your Histamine H3-receptors; leaving you with more histamine and yet less "partial agonism" at the H1 receptor which may be that your body has been put back into homeostasis.ErgogenicHealth wrote: ↑Mon Nov 15, 2021 8:09 pmI did Betahistine 16mg twice daily for like 4-5 days. It felt BAD on the drug, but I think it has left my brain in a positive place.Imeniaan wrote: ↑Fri Oct 08, 2021 1:40 amLucas, what is your EXACT protocol please?ErgogenicHealth wrote: ↑Thu Oct 07, 2021 3:26 am I have been adhering to Area1255 suggestions, with Betahistine, and it is now day 9 and something may have flipped the switch. I have been in 4 day window now, don't want to speak to soon, but FU** I am feeling like my young self again. FULL sensation, full body orgasm and libido so strong that staring at hot girls easily gets me hard.
Thank you.
Eur J Pharmacol
. 2002 Jun 20;446(1-3):63-73. doi: 10.1016/s0014-2999(02)01795-8.
Betahistine dihydrochloride interaction with the histaminergic system in the cat: neurochemical and molecular mechanisms
Brahim Tighilet 1, Suzanne Trottier, Christiane Mourre, Carole Chotard, Michel Lacour
Affiliations expand
PMID: 12098586 DOI: 10.1016/s0014-2999(02)01795-8
Abstract
Drugs interfering with the histaminergic system facilitate behavioral recovery after vestibular lesion, likely by increasing histamine turnover and release. The effects of betahistine (structural analogue of histamine) on the histaminergic system were tested by quantifying messenger RNA for histidine decarboxylase (enzyme synthesizing histamine) by in situ hybridization and binding to histamine H(3) receptors (mediating, namely, histamine autoinhibition) using a histamine H(3) receptor agonist ([(3)H]N-alpha-methylhistamine) and radioautography methods. Experiments were done in brain sections of control cats (N=6) and cats treated with betahistine for 1 (N=6) or 3 (N=6) weeks. Betahistine treatment induced symmetrical changes with up-regulation of histidine decarboxylase mRNA in the tuberomammillary nucleus and reduction of [(3)H]N-alpha-methylhistamine labeling in both the tuberomammillary nucleus, the vestibular nuclei complex and nuclei of the inferior olive. These findings suggest that betahistine upregulates histamine turnover and release, very likely by blocking presynaptic histamine H(3) receptors, and induces histamine H(3) receptor downregulation. This action on the histaminergic system could explain the effectiveness of betahistine in the treatment of vertigo and vestibular disease.