Irresistible to the opposite sex? Histamine could be why!
Histamine-induced responses shown in this study indicate a possible mechanism through which the generalized arousal factor (histamine) can affect neurons in a local brain area (VMH), which is crucial for a specific motivated behavior (lordosis). Furthermore, we addressed this question by examining whether a general arousal modulator, histamine, interacts with a hormonal modulator, estrogen, in VMH neurons. Our results are remarkable in the sense that they show a possible pivotal point where generalized arousal influences and supports a specific (sexual) arousal state. As a generalized arousal neurotransmitter, histamine’s excitatory impact on VMH neurons was further potentiated by estrogen. Thus the interaction between histamine and estrogen might be a key mechanism linking generalized arousal with specific (sexual) arousal. Read the full study here.
In plain English: this study showed that estrogen supplementation (or natural fluctuations) caused the neurotransmitter histamine be released, making female rats stick out their butts so males could mount them. Luckily as human beings we’re (mostly) able to control who mounts us!
This study explains a few things I noticed these last two years: that my symptoms fluctuate with the menstrual cycle (more on that in an upcoming post), that birth control pills made me lose my mind, but that there’s no way I could out crazy estrogen flushed high histamine pregnant friends!
The study went on to touch on my favourite subject: histamine as as weight loss and appetite control mechanism…
Histamine also modulated feeding behavior through its receptors in the VMH. As shown by Sakata (Sakata and Yoshimatsu 1995), food intake was suppressed and drinking was accelerated by either activation of H1 receptors or inhibition of H3receptors in the VMH. Pharmacological blockage of both H1 and H2 VMH receptors significantly increased overnight food intake and decreased water intake, which may be specifically attributed to the set of histaminergic receptors situated within the VMH (Magrani et al. 2004
Read the full study here.
And then of course you have the fact that histamine’s H1 receptor itself releases estrogen…
In the female genital tract, histamine is produced mainly by mast cells, endothelial and epithelial cells in the uterus and ovary. Women with histamine intolerance often suffer cyclical headache and dysmenorrhea. In addition to a contraction promoting effect, this is attributable to the fact that histamine, via the H1 receptors, increases estradiol production markedly, but progesterone production only mildly (e1). The painful uterine contractions associated with dysmenorrhea are caused by an increased production of prostaglandin F2a in the endometrium, which is promoted by estrogens and inhibited by progesterone. Histamine can therefore intensify dysmenorrhea via an increase in estrogen production. Conversely, estrogen can affect histamine activity: the cyclical rise in plasma estrogen was shown to be associated with a larger skin weal in skin prick tests (e2). Read more from the seminal histamine study by Maintz & Novak here.