Dysmenorrhea refers to pain and cramping during menses that, when severe, may interfere with normal functioning. It is the most common menstrual complaint, with 50%-90% of women worldwide reporting painful menstruation. Severe, sometimes incapacitating, symptoms occur in 2%-29% of studied populations.
Primary dysmenorrhea (menstrual pain that occurs in the absence of underlying pelvic pathology) is thought to be related to the release of prostaglandins during menstruation, which can cause excessive and prolonged uterine contractions. These contractions can lead to myometrial ischemia. The pain begins 24-48 hours before menses and then subsides within 12-72 hours. The pain is typically midline but may also radiate to the back or thighs. Accompanying symptoms (related to prostaglandin-induced sequelae) may include nausea, vomiting, diarrhea, fatigue, headache, and respiratory difficulties. The symptoms of dysmenorrhea typically begin within 2 years of menarche, and prevalence diminishes with age.
Secondary dysmenorrhea is caused by pelvic disease such as endometriosis, uterine fibroids, adenomyosis, pelvic inflammatory disease, pelvic adhesions, and cervical stenosis. The pain of secondary dysmenorrhea usually begins earlier in the menstrual cycle and continues beyond the end of menses. Further symptoms may be present depending on the underlying pathology. While secondary causes can manifest at any age, they typically present well after menarche, often as late as the fourth or fifth decade of life.
The following factors are associated with risk for primary dysmenorrhea. Due to the presence of confounding variables and possible selection bias, further studies are needed to firmly establish these risk factors. Risk factors for secondary dysmenorrhea depend on the underlying pelvic pathology.
Age. The most intense symptoms occur during adolescence and typically decrease with age.
Body mass index less than 20 or greater than 25, along with attempts to lose weight.
History of sexual abuse or assault.
Prolonged, irregular or heavy menses.
Family history of dysmenorrhea.
In addition to the above factors, psychological factors, miscarriage, pelvic inflammatory disease, premenstrual syndrome, sterilization, female genital cutting (“female circumcision”), and work in cold environments, may also be associated with risk. Oral contraceptives, previous pregnancy and younger age at first birth are considered protective.
Primary dysmenorrhea is a diagnosis of exclusion. A complete history including menstrual, gynecologic, psychosocial, and dietary factors and physical examination are necessary for all patients. Abdominal, pelvic, and rectal examinations may reveal underlying disorders. More extensive evaluation may not be necessary in many cases, particularly when the history and physical support the diagnosis of primary dysmenorrhea and the pain responds to nonsteroidal anti-inflammatory drugs or oral contraceptives.
Laboratory testing may include pregnancy testing, sexually transmitted disease evaluation, urinalysis, and complete blood count.
Cultures for gonorrhea and chlamydia are generally indicated, but negative cultures do not exclude pelvic infection.
Imaging studies may include pelvic and vaginal ultrasound.
Laparoscopy is not typically indicated, as the history, examination, and imaging typically identify the cause of pain. However, this procedure may be indicated for the diagnosis of and treatment of endometriosis and as therapy for fibroids, adhesions, ovarian cysts, and other abdominal or pelvic pathologies.
Primary dysmenorrhea is best treated with a multidisciplinary approach that may include medical, lifestyle, and nutritional interventions.
Nutritional interventions, such as a low-fat, vegan diet, are described below (see Nutritional Considerations).
Regular exercise may be helpful. In unblinded trials, women who exercise appear to have less severe menstrual symptoms, compared with women who do not exercise. The regular practice of yoga may also reduce cramps and improve distress. Physical activity decreases blood estrogen concentrations, which would be expected to decrease the risk of dysmenorrhea. The effects of exercise on stress level and weight are also plausible mechanisms for decreased pain.
Smoking cessation may be helpful.
Acupuncture and transcutaneous electrical nerve stimulation (TENS) may be beneficial. Limited evidence from controlled trials indicates that acupuncture produces significantly better pain relief compared with sham acupuncture and decreases the use of pain medications. Acupressure provides pain relief similar to that of nonsteroidal anti-inflammatory drugs (NSAIDs) when compared with sham acupressure treatment.
NSAIDs (ibuprofen, naproxen) are often effective in treating the pain of primary (and occasionally secondary) dysmenorrhea. Treatment is more effective if begun prior to the expected onset of symptoms and continued throughout menses.
Oral contraceptives are often effective and are commonly used for pain that is refractory to NSAID therapy. Other forms of contraceptives (patches, vaginal ring, and injectable medroxyprogesterone) may also provide symptom relief. Oral contraceptives and an NSAID may be combined if monotherapy with each of these is not effective.
Intrauterine devices with levonorgestrel are also helpful, although devices without hormones may aggravate symptoms.
Calcium channel blockers, nitroglycerin, and nitric oxide, agents that block uterine contractions and other pharmaceuticals are under investigation for their role in treating dysmenorrhea.
Women who do not respond to therapy (including the nutritional steps described below) within 3-4 cycles should undergo reevaluation for the cause of symptoms. This next step typically includes diagnostic laparoscopy.
Treatment is based on the underlying pathology. NSAIDs and oral contraceptive pills may be useful in some patients.
The rationale for dietary changes in dysmenorrhea comes from the observation that diets that are low in fat or high in fiber reduce plasma estrogen concentrations and estrogen activity. Under controlled conditions high-fiber, low-fat diets have been shown to reduce estradiol levels by 10%-25%. A meta-analysis of intervention studies suggested that, overall, studies reducing dietary fat have reduced serum estradiol concentrations by 7.4% in premenopausal women and 23% in postmenopausal women, but that greater reductions in dietary fat were associated with greater reductions in estradiol. Similar findings were evident in a randomized trial of women previously treated for breast cancer. A high-fiber, low fat diet significantly reduced plasma estradiol concentrations.
Fiber’s ability to reduce plasma estrogens is explained by its ability to interrupt enterohepatic circulation. That is, as estrogens are filtered from the blood by the liver and pass through the bile duct into the intestinal tract, fiber carries them away with the wastes. In the absence of fiber, estrogens can be reabsorbed back into circulation. The mechanism by which lower-fat diets reduce estrogens is not clear.
Reduced estrogen concentrations presumably reduce endometrial thickening. In turn, reduced endometrial thickening may reduce the production of prostaglandins (e.g., PGE2) that cause the uterine muscle contraction and ischemia. Diet can also play a role by helping to suppress the inflammation that contributes to pain perception in patients with dysmenorrhea.
A low-fat, vegan diet has been shown to reduce dysmenorrhea symptoms. In a placebo-controlled, crossover trial, a low-fat, vegan diet was shown to increase serum concentrations of sex-hormone-binding globulin and reduce dysmenorrhea symptoms. Prior to the diet change, volunteers reported an average of 3.9 days of pain in each cycle, which fell to 2.7 days on a low-fat vegan diet. In addition, the severity of pain was significantly reduced.
Animal products increase estrogen concentrations, and the arachidonic acid and saturated fat they contain activate inflammatory pathways through upregulating NFκB. Patients with dysmenorrhea have also been found to have higher blood levels of arachidonic acid-derived prostaglandins such as PGE2 and PGF2α. A systematic review of studies on diet and dysmenorrhea concluded from observational and clinical trials that a higher dietary ratio of omega-3 to omega-6 fatty acids and supplementation with omega-3 fatty acids are protective against dysmenorrhea by reducing pro-inflammatory prostaglandin formation.,,,
Maintain a healthy weight. Although mixed, research has revealed that being underweight or overweight increases the risk for dysmenorrhea. In a study including 9,688 women, underweight women were at 34% increased risk of dysmenorrhea, and obese women were at 22% increased risk, compared with women with normal weight. Obese women who lost weight reduced their risk of dysmenorrhea. Researchers speculate that under- and overweight status lead to menstrual irregularities, which, in turn, increase the risk of dysmenorrhea.
Low-fat, vegan diet. See Basic Diet Orders.
Counseling on stress reduction techniques.
A patient making diet changes to improve symptoms of dysmenorrhea will benefit from the support of family members, who are likely to find that the same diet changes help them with weight control and other health issues.