Primary dysmenorrhea, which is defined as painful menses in women with normal pelvic anatomy, usually begins during adolescence. It is characterized by crampy pelvic pain beginning shortly before or at the onset of menses and lasting one to three days. It is often accompanied by other symptoms, such as heavy menstrual flow, sweating, headache, nausea, vomiting, diarrhea, irritability, and fatigue. It can cause a significantly reduced quality of life. Dysmenorrhea may be more common than we think; it is, in fact, the leading cause of short-term school absenteeism among adolescents.[1] However, only about 15% of sufferers consult a physician for it.[2] Many may feel it is just what happens with their cycle, but it is not a normal condition, and intervention can be successful.
Estimates of its prevalence world-wide vary wildly, ranging from 16% to 93%.[3] Risk factors for dysmenorrhea include earlier age at menarche, long menstrual periods, heavy menstrual flow, smoking and positive family history. It is estimated that about 10% of dysmenorrhea cases may be secondary to pelvic organ pathologies[4], such as endometriosis, ovarian cysts, pelvic inflammatory disease (PID), or lumbrosacral spine disorders.[5]
Overproduction of potent uterine prostaglandins plays an important role in generating primary dysmenorrhea symptoms.[6] Prostaglandins (PGs) E2 and PGF2α are localized hormone-like substances normally produced in the endometrium, and are important for menstruation and fertility. However, dysmenorrhea is associated with increased production of PGF2α relative to PGE2.[7] Dysmenorrhea may also be associated with increased vasopressin, a pituitary hormone that vasoconstricts and regulates water retention.[8],[9] Together with vasopressin, PGs induce arterial vasoconstriction and uterine wall hyper-contractility, leading to painful cramping, as well as many other symptoms (headache, nausea, vomiting, diarrhea, etc).[10],[11],[12] Vasoconstriction is an ischemic process—temporarily reducing or stopping blood supply to the uterus. This deprives the uterus of oxygen, resulting in contractions and pain.[13]
The main, first-line therapy prescribed for dysmenorrhea remains NSAIDs, following closely by oral contraceptives. This approach does suppress PGE2 and PGF2α, thereby relieving the pain and discomfort, but not without the side effects of these pharmaceuticals. Researchers have also reported that the failure rate for the medicines is between 20% and 25%.[14]
More natural approaches to treatment have been investigated. Perhaps the most important nutraceutical to employ is fish oil.[15] Zafari and colleagues found that moderate doses of fish oil reduced dysmenorrhea pain even better than Ibuprofen.[16] Fish oil modifies the PG system toward a less inflammatory profile. Krill oil may be used instead of fish oil, as it has also been found efficacious. Other treatments include vitamin D (50,000 IU once a week),[17] acupuncture,[18] heat application,[19] and vitamin B1 (100 mg/day).[20] It is important to continue natural treatments for at least three months for full benefit.
References
[1] French L. (2005). Dysmenorrhea. Am Fam Physician. Jan 15;71(2):285-91.
[2] Sultan C, Gaspari L, Paris F. (2012). Adolescent dysmenorrhea. Endocr Dev. 2012;22:171-80.
[3] De Sanctis V, Soliman A, Bernasconi S, et al. (2015). Primary Dysmenorrhea in Adolescents: Prevalence, Impact and Recent Knowledge. Pediatr Endocrinol Rev. Dec;13(2):512-20.
[4] Drosdzol A, Skrzypulec V. (2008). [Dysmenorrhea in pediatric and adolescent gynaecology]. [Article in Polish]. Ginekol Pol. Jul;79(7):499-503.
[5] Grgić V. (2009). [Dysmenorrhea induced by lumbosacral spine disorders. Pathogenesis, diagnosis and therapy with special emphasis on spinal manipulative therapy].
[Article in Croatian]. Lijec Vjesn. Sep-Oct;131(9-10):275-9.
[6] Harel Z. (2012). Dysmenorrhea in adolescents and young adults: an update on pharmacological treatments and management strategies. Expert Opin Pharmacother. Oct;13(15):2157-70.
[7] Bresson E, Boucher-Kovalik S, Chapdelaine P, et al. (2011). The human aldose reductase AKR1B1 qualifies as the primary prostaglandin F synthase in the endometrium. J Clin Endocrinol Metab. Jan;96(1):210-9.
[8] Tzafettas J. (2006). Painful menstruation. Pediatr Endocrinol Rev. Jan;3 Suppl 1:160-3.
[9] French, op. cit.
[10] Sultan, op. cit.
[11] Grgić, op. cit.
[12] French, op. cit.
[13] Eby GA. (2007). Zinc treatment prevents dysmenorrhea. Med Hypotheses. 69(2):297-301.
[14] De Sanctis, op. cit.
[15] Rahbar N, Asgharzadeh N, Ghorbani R. (2012). Effect of omega-3 fatty acids on intensity of primary dysmenorrhea. Int J Gynaecol Obstet. Apr;117(1):45-7.
[16] Zafari M, Behmanesh F, Agha Mohammadi A. (2011). Comparison of the effect of fish oil and ibuprofen on treatment of severe pain in primary dysmenorrhea. Caspian J Intern Med. Summer;2(3):279-82.
[17] Moini A, Ebrahimi T, Shirzad N, et al. (2016). The effect of vitamin D on primary dysmenorrhea with vitamin D deficiency: a randomized double-blind controlled clinical trial. Gynecol Endocrinol. Jun;32(6):502-5.
[18] Sriprasert I, Suerungruang S, Athilarp P, et al. (2015). Efficacy of Acupuncture versus Combined Oral Contraceptive Pill in Treatment of Moderate-to-SevereDysmenorrhea: A Randomized Controlled Trial. Evid Based Complement Alternat Med. 2015:735690.
[19] Aktaş D. (2015). Dysmenorrhea in Female University Students: Effect on General Comfort Level. Pain Manag Nurs. Aug;16(4):534-43.
[20] Hosseinlou A, Alinejad V, Alinejad M, et al. (2014). The effects of fish oil capsules and vitamin B1 tablets on duration and severity of dysmenorrhea in students of high school in Urmia-Iran. Glob J Health Sci. Sep 18;6(7 Spec No):124-9.
