Two of the most well studied include an SNP in the promoter of MIF and an SNP in the tumor necrosis factor (TNF-α) gene. When a cytosine 173 base pairs upstream of macrophage migration inhibitory factor (MIF) promoter was replaced by a guanine there was an associated increase in the likelihood of the individual experiencing PD. While a CC/GG genotype led to an increase in likelihood of the individual experiencing severe menstrual pain, a CC/GC genotype led to a more significant likelihood of the disorder impacting the individual overall and increasing the likelihood of any of the three phenotypes. A second associated SNP was located 308 base pairs upstream from the start codon of the TNF-α gene, in which guanine was substituted for adenine. A GG genotype at the loci is associated with the disorder and has been proposed as a possible genetic marker to predict PD.There has also been an association with mutations in the MEFV gene and dysmenorrhea, which are considered to be causative. The phenotypes associated with these mutations in the MEFV genes have been better studied; individuals who are heterozygous for these mutations are more likely to be affected by PD which presents as a severe pain phenotype.Genes related to immunity have been identified as playing a significant role in PD as well. IL1A was found to be the gene most associated with primary dysmenorrhea in terms of its phenotypic impact.
One study indicated that in nulliparous individuals with primary dysmenorrhea, the severity of menstrual pain decreased significantly after age 40.A survey in Norway showed that 14 percent of females between the ages of 20 to 35 experience symptoms so severe that they stay home from school or work. Among adolescent girls, dysmenorrhea is the leading cause of recurrent short-term school absence. References
External links

Dysmenorrhea at Curlie