Female pain is one of the most poorly-understood phenomena in medicine.
At least 30 percent of women suffer pain during sex, and one in five have menstrual cramps as agonizing as heart attacks – and yet, there is no solution beyond popping some more Advil.
Now, a team at the University of Texas at Dallas has found the clearest evidence that pain manifests itself differently in the cells of women than it does in those of men.
In other words, we do not know much about women’s pain because, until now, our pain research has been done on male cells, with the assumption that their ‘extraordinarily specific’ results are applicable to females too.
The finding adds to a growing body of research that certain drugs may work for men and not for women, and vice versa.
Unfortunately, the researchers lament, in making this discovery they have found a novel way to treat male pain – but we are still in the dark when it comes to a cure for women, who suffer more chronic pain.
Most scientific studies only used male models to avoid fluctuating hormones tarring results, until the NIH made a mandate to test both genders. Now researchers at the University of Texas at Dallas have found the latest evidence that female cells react differently to male cells
The new study began in 2014, after the National Institutes of Health ordered all pre-clinical trials to include both male and female data.
Prior to that, scientists tended to avoid tests on female models, since the menstrual cycle and fluctuating hormones made for less consistent results.
‘We’ve been overlooking a key variable for a long time, and I’m as guilty as everyone else,’ lead author Dr Ted Price, of the Pain Neurobiology Research Group, admitted.
‘Professionally, we saw no reason to do it until 2014. But we’re discovering that the NIH’s decision was the right thing. Everyone I know doing these studies is finding new and interesting mechanisms that we’ve simply overlooked.’
He added: ‘[I]t’s another very clear indication that there are extraordinarily strong mechanistic sex differences in how pain becomes chronic.
‘When you take what everybody has done in the field, that theme is really something that we have to pay very close attention to, and I feel like it’s going to lead to the breakthrough we all really want.’
To assess the differences, Dr Price and his colleague Dr Salim Megat manipulated the receptors for the neurotransmitter dopamine in both male and female mice.
Dopamine is a type of molecule which is released from nerve cells to signal to other nerves. It can induce a wave of happiness, and is generally held to offer an antidote to pain.
However, Drs Price and Megat found that manipulating these receptors only impaired chronic pain in male mice, yet had no effect on females.
‘It leads me to believe that it’s fairly likely we’ll want to make male- and female-specific drugs for chronic pain,’ Dr Price said.
‘If not that, we may need to develop diagnostics to look at an individual’s cell types that are prolonging pain, so we can tailor the therapeutic based on the underlying mechanism. We just don’t do that right now.’
To his disappointment, we are no closer to a gender-specific drug for women, only for men.
‘Discovering D5 receptors as a pain relief target upsets me in a way,’ he said.
‘Most chronic pain patients are women, not men, so I would prefer to develop something that was certain to work in females.’
The findings could explain why scores of scientists have found their preclinical results on (all male) lab mice completely contradict their results among (mainly female) human participants.
‘Those running clinical trials for the last five years have been frustrated because the preclinical results don’t come through in the clinical studies,’ Dr Price explained.
‘The cause of this problem, potentially, is that up until recently, many of the preclinical investigators were just using males.
‘Then, in the clinical trials, human participants are primarily female, because more women suffer chronic pain than men.’