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Dr. Tori Hudson, Portland, Oregon, Blog Healthline Blog

Menstrual cramps are one of the most common gynecological problems in reproductive aged women. Menstrual cramps due to primary dysmenorrhea (the type of menstrual cramps that are due to a physiological problem, rather than a medical condition such as endometriosis). Primary dysmenorrhea starts after the release of prostaglandins from endometrial cells (those cells that line the inside of the uterus). The target of treatment of acute primary dysmenorrhea has focused on the suppression of the synthesis or function of these prostaglandins. These treatments include non-steroidal anti-inflammatory drugs (NSAIDS), herbal extracts, nutritional supplements and hormonal contraceptives. Most of us are familiar with the role of vitamin D in calcium homeostasis, bone mineralization and immune function. But, vitamin D reduces the expression of cyclooxygenase-2 and thus reduces prostaglandin production, increases prostaglandin inactivation, regulates the expression of prostaglandin receptors, targets the endometrium and thus reduces the intensity of pain as well as possibly has anti-inflammatory effects.

Vitamin DWith the prevalence of primary dysmenorrhea (between 45% and 95%), the prevalence of vitamin D insufficiency, and the influence of vitamin D on prostaglandins, it seems logical that someone would choose to evaluate the effect of vitamin D supplementation on primary dysmenorrhea in women with a vitamin D deficiency.

This randomized double-blind placebo-controlled clinical trial was conducted on 60 Iranian with primary dysmenorrhea and vitamin D deficiency. Women had to have at least four recent consecutive menstrual cycles with painful cramps during the previous 6 months. Women also had to have a serum vitamin D level < 50 ng/ml. (Severe deficiency = < 10 ng/mL; moderate deficiency = 10-19 ng/mL and mild or insufficient = 20-29 ng/mL.) Women in the treatment group (n=30) received 50,000 oral vitamin D once per week for 8 weeks and 30 women received a placebo once weekly for 8 weeks. In the end, 23 women remained in the vitamin D group and 27 women in the placebo group. Among these 50 women, 31 had severe vitamin D deficiency and the remaining 19 had moderate vitamin D deficiency.

After 2 months of treatment, those in the vitamin D group had significant increases in serum levels of vitamin D and none in the placebo group. In the vitamin D treatment group prior to treatment, pain was mild in 3 (13%), moderate in 16 (69.6%) and severe in 4 (17.4%) of the women. After treatment, 22 (95.7%) had mild pain, 1 (4.3%) had moderate pain and none had severe pain. In the placebo group, after the two months of no treatment, 4 (14.8%) had mild pain, 17 (63%) had moderate pain and 6 (22.2%) had severe pain. Pain intensity significantly decreased in the treatment group after 8 weeks of treatment with a significant difference in pain intensity between the two groups after the 8 weeks of treatment and one month after the end of treatment.

Commentary: A weekly dose of 50,000 IU Vitamin D for 8 weeks in women with primary dysmenorrhea and recently determined vitamin D deficiency is a safe, simple, inexpensive strategy to reduce mild, moderate and severe menstrual pains. In a previous 2012 study (Lasco et al.) on vitamin D for primary dysmenorrhea, women received a single dose of 300,000 IU Vitamin D before the beginning of their menstrual cycle and was done in women with low normal vitamin D levels but not deficiency. In the current study, the serum levels of vitamin D increased to sufficient levels (approx. 55 ng/mL). This approach with vitamin D could go a long way to decreasing the need for NSAIDS or even prescription pain pills for women with acute primary dysmenorrhea and a vitamin D deficiency.

Reference: Moini A, Ebrahimi T, Shirzad N, et al. The effect of vitamin D on primary dysmenorrhea with vitamin D deficiency: a randomized double-blind controlled clinical trial. Gynecological Endocrinology 2016, Early Online: 1-4

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