Summary: Researchers report estrogen and other sex hormones may be responsible for the higher prevalence of migraines in women.
Research published today reveals a potential mechanism for migraine causation which could explain why women get more migraines than men. The study, in Frontiers in Molecular Biosciences, suggests that sex hormones affect cells around the trigeminal nerve and connected blood vessels in the head, with estrogens — at their highest levels in women of reproductive age — being particularly important for sensitizing these cells to migraine triggers. The finding provides scientists with a promising new route to personalized treatments for migraine patients.
“We can observe significant differences in our experimental migraine model between males and females and are trying to understand the molecular correlates responsible for these differences,” explains Professor Antonio Ferrer-Montiel from the Universitas Miguel Hernández, Spain. “Although this is a complex process, we believe that modulation of the trigeminovascular system by sex hormones plays an important role that has not been properly addressed.”
Ferrer-Montiel and his team reviewed decades of literature on sex hormones, migraine sensitivity and cells’ responses to migraine triggers to identify the role of specific hormones. Some (like testosterone) seem to protect against migraines, while others (like prolactin) appear to make migraines worse. They do this by making the cells’ ion channels, which control the cells’ reactions to outside stimuli, more or less vulnerable to migraine triggers.
Some hormones need much more research to determine their role. However, estrogen stands out as a key candidate for understanding migraine occurrence. It was first identified as a factor by the greater prevalence of migraine in menstruating women and the association of some types of migraine with period-related changes in hormone levels. The research team’s evidence now suggests that estrogen and changes in estrogen levels sensitize cells around the trigeminal nerve to stimuli. That makes it easier to trigger a migraine attack.
However, Ferrer-Montiel cautions that their work is preliminary. The role of estrogen and other hormones in migraine is complex and much more research is needed to understand it. The authors emphasize the need for longitudinal studies focusing on the relationship between menstrual hormones and migraines. Their current work relies on in vitro and animal models, which aren’t easy to translate to human migraine sufferers.
Nonetheless, Ferrer-Montiel and his colleagues see a promising future for migraine medication in their current findings. They intend to continue their research using pre-clinical, human-based models which better reflect real patients.
“If successful, we will contribute to better personalized medicine for migraine therapy,” he says.
The research is part of a special article collection on cell membrane proteins as targets for drugs.
Funding: AEI-MINECO, PROMETEO, FEDER funded this study.
Source: Emma Duncan – Frontiers
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Open access research for “TRP Channels as Potential Targets for Sex-Related Differences in Migraine Pain” by Maite Artero-Morales, Sara González-Rodríguez and Antonio Ferrer-Montiel in Frontiers in Molecular Biosciences Published August 14 2018.
[cbtabs][cbtab title=”MLA”]Frontiers”Why Do Women Get More Migraines?.” NeuroscienceNews. NeuroscienceNews, 14 August 2018.
<https://neurosciencenews.com/migraine-women-9696/>.[/cbtab][cbtab title=”APA”]Frontiers(2018, August 14). Why Do Women Get More Migraines?. NeuroscienceNews. Retrieved August 14, 2018 from https://neurosciencenews.com/migraine-women-9696/[/cbtab][cbtab title=”Chicago”]Frontiers”Why Do Women Get More Migraines?.” https://neurosciencenews.com/migraine-women-9696/ (accessed August 14, 2018).[/cbtab][/cbtabs]
TRP Channels as Potential Targets for Sex-Related Differences in Migraine Pain
Chronic pain is one of the most debilitating human diseases and represents a social and economic burden for our society. Great efforts are being made to understand the molecular and cellular mechanisms underlying the pathophysiology of pain transduction. It is particularly noteworthy that some types of chronic pain, such as migraine, display a remarkable sex dimorphism, being up to three times more prevalent in women than in men. This gender prevalence in migraine appears to be related to sex differences arising from both gonadal and genetic factors. Indeed, the functionality of the somatosensory, immune, and endothelial systems seems modulated by sex hormones, as well as by X-linked genes differentially expressed during development. Here, we review the current data on the modulation of the somatosensory system functionality by gonadal hormones. Although this is still an area that requires intense investigation, there is evidence suggesting a direct regulation of nociceptor activity by sex hormones at the transcriptional, translational, and functional levels. Data are being accumulated on the effect of sex hormones on TRP channels such as TRPV1 that make pivotal contributions to nociceptor excitability and sensitization in migraine and other chronic pain syndromes. These data suggest that modulation of TRP channels’ expression and/or activity by gonadal hormones provide novel pathways for drug intervention that may be useful for targeting the sex dimorphism observed in migraine.