Integrative perspectives on dysmenorrhea

Photo Cred: silviarita/Pixabay

By Gary Goldman

Menstrual cramps, also known as dysmenorrhea, are experienced by more than 50 percent of women. The degree of pain is variable and can be described in a bell curve distribution—for some the pain is hardly noticeable, for others it is severe, and for the majority the pain is somewhere in between.

The constellation of symptoms can include focal cramping or pain in the lower abdomen, pelvis, lower back, and legs. Gastro-enterologic symptoms include nausea, vomiting, and diarrhea. Generalized somatic symptoms such as fatigue or weakness can also be problematic.

Primary dysmenorrhea is the pain produced directly from the uterus and not from other pathology. This pain usually lasts one to three days, starting just before menstrual flow begins. Cramps are usually worse as an adolescent and lessen with time, especially after childbirth. Pain is caused by uterine contractions, relative hypoxemia, and prostaglandin release.

Prostaglandins PGE2 and PGF2 alpha are released by the breakdown of endometrial cells, and cause pain by inducing vasoconstriction and local hypoxia, through directly irritating nerves, and via stimulating uterine contractions. Prostaglandin inhibitors are an important option in treating dysmenorrhea.

The hormone vasopressin has also been implicated. It works similarly by causing contractions and vasoconstriction. Through the action of leukotrienes, vasopressin also causes increased sensitivity of neural pain fibers in the myometrium. Unfortunately, trials of vasopressin antagonists have proved disappointing in the treatment of dysmenorrhea.

Risk factors of primary dysmenorrhea include:

• Getting your first period (menarche) earlier than age 11
• Smoking
• High levels of stress
• Increased body mass
• Depression, anxiety and poor support networks

Secondary dysmenorrhea occurs due to causes other than ordinary menstruation. This pain usually arises years after menarche and tends to worsen over time if left untreated. Causes can include:

• Endometriosis
• Adenomyosis
• Pelvic inflammatory disease and other sexually transmitted infections (STIs)
• Fibroids (myomata uteri)
• Ovarian cysts
• Cervical stenosis, imperforate hymen, and other congenital anomalies

An initial evaluation of dysmenorrhea should include a thorough personal and family health history. A physical exam and sonogram can help to exclude many types of pathology. Cervical cultures for gonorrhea and chlamydia are also performed. In some cases, a laparoscopy is performed to directly visualize the pelvic organs to better evaluate the etiology of pain. In select cases, an MRI or hysteroscopy might also be indicated.

Therapy is based on the suspected etiology. The American College of Obstetrics and Gynecology (ACOG) recommends an initial therapy for presumptive primary dysmenorrhea of a three- to six-month trial of the oral contraceptive pill (OCP) as well as non-steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen. OCPs and NSAIDs independently reduce menstrual volume, prostaglandin formation, and pain. Other options for long term hormonal therapy are a levonorgestrel containing intrauterine device (IUD), oral or intramuscular progestins, and medications that prevent ovulation by modifying the action of gonadotropin releasing hormone (GnRH).

Other commonly recommended measures to mitigate menstrual pain include:

• Avoid smoking
• Increase aerobic exercise
• Use a heating pad across the pelvis or lower back
• Avoid caffeine, sugar and alcohol
• Massage

For secondary dysmenorrhea, the underlying cause should be treated. For instance, some functional ovarian cysts will respond to hormonal therapy such as OCPs, while other cysts such as endometriomas may require surgical excision. Chlamydia and gonorrhea require antibiotic therapy for both the patient and any potentially exposed partners. In the most extreme cases, removal of the uterus, fallopian tubes and/or ovaries is usually an effective option.

Complementary and alternative options for the treatment of dysmenorrhea in general have not been as extensively studied. The ACOG mentions though does not endorse various alternative medicine options, such as acupuncture, vitamin B1, magnesium, fenugreek, ginger, valerian, zataria, zinc sulphate, transcutaneous electrical nerve stimulation (TENS), and yoga.

A review of the literature allows us to explore many additional options. Vitamin B1 (thiamine) at a dose of 100 milligrams daily has been shown to be effective in a randomized controlled study in a group of 500 Indian women. Vitamin E 2,500 international units (IUs) daily for five days, overlapping the time of pain, has also been shown to be effective. High dose vitamin D (50,000 IUs weekly) has been shown to be useful in treating dysmenorrhea, but additional studies evaluating the efficacy of vitamin D have not been as convincing.

In 2001, a Cochrane review found that magnesium was more effective than placebo for dysmenorrhea. Magnesium is a muscle relaxant, helping to diminish uterine contractility as a source of pain, as well as improving vascular flow. Magnesium glycinate at 400 milligrams is helpful when taken once to twice daily starting several days before menses starts through the end of flow. 

Several studies have demonstrated the efficacy of omega-3 fish oil at a dose of 2 grams per day. Omega-3 fatty acids are the precursor of the potent anti-inflammatory and vasodilating eicosanoids. This conversion requires niacin, magnesium, vitamin B6, vitamin C, and zinc. Omega-6 fatty acids are the basis for producing pro-inflammatory vasoconstrictor eicosanoids. Increasing the proportion of omega-3 to omega-6 reduces inflammation and improves vascular flow, reducing tissue hypoxia. Beneficial eicosanoid precursors can be found in black current oil, evening primrose oil, pumpkin, and flax seeds.

Cinnamon acts in a multitude of beneficial ways to reduce dysmenorrhea. It increases insulin sensitivity, thus reducing inflammation. It reduces the volume of menstrual flow. It is an anti-spasmodic. It also improves circulation, thus reducing tissue hypoxia.

Many studies have evaluated ginger which has been found to have a substantial impact on menstrual pain. Two components in ginger, the gingerols and gingerdiones, inhibit leukotriene and prostaglandin synthesis, thus decreasing pain. One study evaluated a dose of 500 milligrams three times daily for five days, beginning two days prior to the onset of flow. Another study used 250 milligrams four times daily for three days beginning on the first day of flow. Ginger was as effective or more effective than placebo or NSAIDs and had the bonus of diminishing nausea.

Cannabidiol (CBD) oil is an anti-inflammatory agent as well as an analgesic when taken systemically. Both effects are very useful in the treatment of dysmenorrhea. CBD is also an anxiolytic. Anxiety is a risk factor for primary dysmenorrhea, and is also a result of cyclic pain, the anticipation of pain produces anxiety.

The role of essential oils in the treating of menstrual pain has not been well studied. One 2013 report found that a blend of cinnamon, clove, lavender, and rose in an almond base was superior to sham or placebo when applied via abdominal massage. A May 2012 study demonstrated benefits from massage using lavender, clary sage, or marjoram essential oils.

Of course, supplementals are only supplemental to diet. A healthy diet has far-reaching benefits, one of which is reduction of menstrual pain. A low-fat vegan diet study published in Obstetrics & Gynecology in February 2000 showed significantly reduced pain for many women. The diet eliminated all animal fats and nearly all vegetable oils. It also emphasized plant-based foods, rich in fiber.

The authors conjecture that a low-fat, high-fiber diet can reduce estrogen levels by about 20 percent. Since estrogen is responsible for growth of endometrium, less estrogen equates with less endometrium, less menstrual flow and less prostaglandin production. The high amount of vegetable fibers assists in estrogen metabolite elimination. Improved bowel elimination also prevents reabsorption via the enterohepatic circulation.

Others point out that inflammation is the hallmark of dysmenorrhea and recommend an anti-inflammatory diet. Typically found in a Paleo or Mediterranean diet, this consists of high amounts of vegetables, low sugars and other carbohydrates, reduced or eliminated dairy and gluten, use of healthy oils such as avocado and olive oils, and use of nuts and seeds. These foods yield a higher omeg-3 and omega-6 ratio than the standard American diet.

Aerobic exercise is anti-inflammatory, improves circulation, improves anxiety and depression, improves bowel function and estrogen metabolite elimination, and results in an outpouring of endogenous endorphins, our own natural pain relievers. Similarly, orgasms have been promoted to have similar effects with the added benefit of directly increasing uterine circulation.

Lastly, stress contributes to poor mood, increased inflammation, and poor sleep. Stress management is an integral part of treating women with dysmenorrhea, as their cyclic pain will surely contribute to angst and further dysfunction. Meditation, yoga, prayer, mindful awareness, and other stress-reduction efforts are an essential part of caring for women in pain.

Case Study

Carol is a 27-year-old nulliparous woman with a lengthy history of dysmenorrhea. She underwent menarche at age 11 and experienced periods every 24 to 26 days with heavy flow for six to seven days. This required changing tampons plus pads every two hours over the first four days of her period. By age 15, she missed two to three days of school each month due to pain. She consulted with her pediatrician and then a gynecologist who advised ibuprofen 600 milligrams every six hours plus the OCP.

Her period flow and pain initially improved, but over the next two years recurred and began to progress. Carol’s gynecologist encouraged her to join the track team and improve her diet, avoiding sweets and gluten, and her period pain improved.

Unfortunately, by age 25, her period pain again had progressed to the point where she missed at least one day of work each month. She underwent testing, which included a normal pelvic exam, a normal transvaginal sonogram, and no evidence of STIs. Her doctor recommended and performed a laparoscopy which demonstrated mild endometriosis, which was excised sharply. She was put back on OCPs post-operatively.

Carol felt well for about 18 months, and then her dysmenorrhea returned. Her gynecologist recommended a six-month long course of Lupron. Carol was concerned about the side effects, plus the risk of bone loss, especially since her mother had osteoporosis. She then presented to my office seeking non-traditional alternatives to her care.

I obtained a Dutch test, which demonstrated excessive degradation of estradiol via the 16-hydroxy-estrone pathway. She had a normal degree of 2-hydroxy- and 4-hydroxy-estrone, but a low 2-methoxy-estrone and a high methyl malonate, both suggestive of poor 2-hydroxy-estrone clearance via methylation in general and via vitamin B-12 in particular. Follow-up testing revealed a high homocysteine, and an MTHFR analysis demonstrated she was a double heterozygote carrier, one for C677T and one for A1298C. This is consistent with a 70 percent decrease in methylation, vital for clearing the predominant 2-hydroxy metabolite. Her 16-hydroxy-estrone is also a potent estrogen. My conclusion was that this was a contributory root cause of her dysmenorrhea and endometriosis, as well as an important risk for breast cancer.

I placed her on a methylated B12 and folate supplement as well as S-Adenosyl methionine to improve her methylation and clearance of 2-hydroxy estrone. I also added magnesium to improve 2-hydroxy clearance, relax the uterine musculature, help her to absorb dietary calcium, and improve bowel clearance. I also added diindolylmethane to clear the 2-hydroxy metabolites. We inhibited synthesis of the 16-hydoxy- moiety by supplementing with grapefruit, pomegranate, and valerian.

I took Carol off the birth control pill and placed her on a six-month course of low-dose Orilissa, a GnRH antagonist, at 150mg/day. This medication is given orally, has a fast half-life, a quick onset of action, and is highly effective in the treatment of dysmenorrhea secondary to endometriosis, and has far less adverse metabolic impact than Lupron.

To help protect her bones, I encouraged an anti-inflammatory diet, and both aerobic and weight training exercises five times weekly. She stays at the gym after her workouts to attend yoga classes. I added vitamin D3, vitamin K2, calcium, and boron to her daily regimen. Lastly, I added CBD oil to help with pain and inflammation, as well as her anxiety due to the recurring concerns of debilitating dysmenorrhea. We obtained a baseline DEXA bone density study and a urinary NTX study to follow bone turnover.

Carol’s progress has been nothing short of remarkable. Her menstrual pain is entirely gone. Her exercise program has improved her mood, her anxiety, and her body strength. Her labs have normalized, her NTX studies remain reassuringly stable, and for the first time she is not fearing the future.

References

The American College of Obstetrics and Gynecology (2018). ACOG Committee Opinion. Retrieved from: https://www.acog.org/Clinical-Guidance-and-Publications/Committee-Opinions/Committee-on-Adolescent-Health-Care/Dysmenorrhea-and-Endometriosis-in-the-Adolescent?IsMobileSet=false#30

The American College of Obstetrics and Gynecology (2015). Dysmenorrhea: Painful Periods. Retrieved from:  https://www.acog.org/-/media/For-Patients/faq046.pdf?dmc=1&ts=20191103T1642016457

Bagga, D., Ashley, J.M., and Geffrey, S.P., et al. (1995) Effects of a very low fat, high fiber diet on serum hormones and menstrual function. Implications for breast cancer prevention. Cancer. Retrieved from: https://www.ncbi.nlm.nih.gov/pubmed/8625075

Barnard, N.D., Scialli, A.R., Hurlock, D., and Bertron, P. (2000) Diet and sex-hormone binding globulin, dysmenorrhea, and premenstrual symptoms. Obstetrics & Gynecology. Retrieved from: https://www.ncbi.nlm.nih.gov/pubmed/10674588

Cleveland Clinic (2014) Dysmenorrhea. Retrieved from: https://my.clevelandclinic.org/health/diseases/4148-dysmenorrhea/management-and-treatment

DiPasquale, R. (2014) Dysmenorrhea: It Isn’t Normal. Naturopathic Doctor News and Review. Retrieved from: https://ndnr.com/botanical-medicine/dysmenorrhea-it-isnt-normal/

French, L. (2005) Dysmenorrhea. American Family Physician. Retrieved from: https://www.ncbi.nlm.nih.gov/pubmed/15686299

Prentice, R., Thompson, D., Clifford, C., Gorbach, S., Goldin, B., and Byar, D. (1990) Dietary fat reduction and plasma estradiol concentration in healthy postmenopausal women Journal of the National Cancer Institute. Retrieved from: https://www.ncbi.nlm.nih.gov/pubmed/2294222

Proctor, M. and Farquhar, C. (2006) Diagnosis and management of dysmenorrhoea. Clinical Evidence. Retrieved from: ncbi.nlm.nih.gov/pmc/articles/PMC1459624/

U.S. Department of Health and Human Services, Office on Women’s Health. (2018) Period Problems. Retrieved from: https://www.womenshealth.gov/menstrual-cycle/period-problems

Wu, A.H., Pike, M.C., and Stram, D.O. Meta-analysis: dietary fat intake, serum estrogen levels, and the risk of breast cancer. Journal of the National Cancer Institute. Retrieved from: https://www.ncbi.nlm.nih.gov/pubmed/10088623