Dysmenorrhea, also called menstrual cramps is one of the most common problems in menstruating women. There are two types of dysmenorrhea: Primary and secondary. Primary dysmenorrhea includes lower abdominal/uterus/pelvic pain during the menses and in the absence of any known pelvic pathology. On the other hand, secondary dysmenorrhea is caused by a disorder in the pelvic area (uterus, ovaries). The pain tends to get worse over time and it often lasts longer than normal menstrual cramps. Examples of causes of secondary dysmenorrhea include endometriosis and adenomyosis. The mechanisms of primary dysmenorrhea are thought to be due to an increase in the production of prostaglandins and leukotrienes from the myometrium. At the end of the ovulation phase of the cycle, fatty acids are produced and accumulated in the cell membrane of the myometrium. At the end of the ovulation phase, just before menses, the now decreased progesterone levels send signals for the onset of menstruation and the release of these fatty acids including arachidonic acid, prostaglandin F2alpha and leukotrienes. These substances cause the uterine muscular contractions and induce the menstrual pain. If there is an excess of these prostaglandins, then there is too much cramping pelvic pain.
The current systematic review was performed to investigate the role of calcium and vitamin D in the relief of primary dysmenorrhea. A systematic literature search covered publications from 2010 to 2020. Two or four studies did not show any relationship between serum vitamin D levels and the intensity of primary dysmenorrhea. On the other hand, 2 studies reported that there was a diverse relationship between serum vitamin D levels and the pain intensity. As the severity of pain increases, there was an associated decreasing serum vitamin D level. Six clinical trial studies showed that vitamin D intake in supplemental form, reduced the severity of primary dysmenorrhea. Another study compared the effects of vitamin D and vitamin E and found that Vitamin D was more effective in reducing the severity than vitamin E. One study found that vitamin D was associated with a need for fewer pain relieving medications.
Other studies have shown that metabolism and absorption of vitamins and mineral may play a role in the development of and treatment of primary dysmenorrhea. Two studies report an association between low calcium intake or vitamin D deficiency in primary dysmenorrhea of adolescents and young women. The benefit of supplemental calcium has been shown to reduce the severity of menstrual cramps and menstrual back pain in some studies and in one study, supplementing 1,200 mg/day of calcium carbonate reduced menstrual back pain and abdominal cramps. While the current review supports the efficacy of vitamin D, oddly, one study found that calcium intake alone was more effective than calcium along with vitamin D supplementation in reducing the severity of primary dysmenorrhea.
Commentary: The systematic review in total, concluded that low calcium levels increase uterine muscle contraction and can cause pain following decreased uterine blood flow. Low serum levels of vitamin D can also increase primary dysmenorrhea by increasing prostaglandin production or decreasing calcium intestinal absorption. In the end, consider calcium and vitamin D supplementation daily, to reduce the severity of menstrual pain. Dosing is variable but consider calcium supplement of 500 mg/day in those who eat a diet that includes about 500 mg/day-600 mg/day from food and consider vitamin D dosing based on serum testing. Not everyone will need the high dose of 50,000 IU per week.
Reference: Abdi F, Amjadi M, Zaheri F, Rahnemaei F. Role of vitamin D and calcium in the relief of primary dysmenorrhea: a systematic review. Obstet Gynecol Sci 2021;64(1):13-26
