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The findings appear to indicate that females exhibited an increase in their pain tolerance when given the expectation that women would tolerate the pain for a longer time, whereas males showed similar pain tolerance regardless of expected tolerance time. Another study examined the effects of high versus low monetary incentives on pain tolerance among females and males, anticipating that high external incentives would produce stronger effects among females, because males possess higher endogenous motivation to tolerate pain.257 However, the incentive manipulation had no effect on pain tolerance for females or males. In addition to the above findings addressing sex differences in responses to μ-opioid agonists, others have investigated analgesic responses to mixed-action opioid agonist-antagonists among women relative to men.

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One could argue that such pain assays, including temporal summation of pain and tonic pain induced via intramuscular administration of chemical stimuli, may provide more clinically relevant information. These studies generally support the conclusion that sex differences will be more robust with a painful stimulus that produces a deep, tonic sensation of pain.127 Given the recency of these studies, they were not included in the previous meta-analysis327 but will be reviewed below. Headache is one of the most common pain conditions.308 Unruh418 reviewed findings from over 60 studies and concluded that the prevalence of headaches and migraines is higher for women than men. Migraine is a severe recurring vascular headache and can occur with and without aura.

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• The majority of these studies (5/6, 81%) indicate that females exhibit more efficient pain inhibitory responses compared with males.
• The 46,XX testicular disorder of sex development (DSD), also known as 46,XX male syndrome, is a rare condition with an estimated prevalence of one in 20,000 males1).
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The SRY gene plays a critical role in the initiation of testicular differentiation in males18). In XY embryos, SRY, which is normally located on the Y chromosome, induces the gonadal primordia to develop into testes. If a fetus is conceived from a sperm with an SRY-bearing X chromosome, it will develop as a male despite not having a Y chromosome.

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This section was not included in Table 10 since only a limited number of studies have addressed this issue. Experimental manipulations have also been used to examine the influence of gender roles on pain perception. Levine and DeSimone248 reported that men reported less cold pressor pain in the presence of a female versus a male experimenter, whereas pain ratings for females were not influenced by experimenter sex. Similar findings were reported by Gijsbers and colleagues,160 who found that males showed a higher pressure pain threshold when tested by a female versus a male experimenter, whereas females’ pain threshold was not influenced by the sex of the experimenter. In addition to those alluded to above, several subsequent reviews of this rapidly expanding literature have been provided, often focusing on particular segments of research regarding sex, gender, and pain. We will conclude with a synopsis of the current state of the literature followed by a discussion of important issues to be addressed in future research.

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• We have also discussed multiple “biological” and “psychosocial” mechanisms that may contribute to sex differences in pain and analgesic responses, including gonadal hormones, endogenous pain modulatory systems, gender roles, and cognitive/affective factors.

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In this era of translational science, an important goal for future research in this area is to generate information that will enhance pain treatment for both sexes. Despite the challenges of translational research, several opportunities that could be exploited to enhance translation have previously been suggested.118 For example, human laboratory pain models and genetic research could both serve as translational bridges between laboratory findings from nonhuman animals and clinical populations. For example, Mogil and colleagues284 successfully translated a novel sex-related genetic association (ie, the melanocortin-1-receptor gene, MC1R) with analgesic responses across species using experimental pain models in both mice and humans.