Menstrual Irregularities: Dysmenorrhea

What is Dysmenorrhea?

Dysmenorrhea is the medical term for painful menstrual periods. Dysmenorrhea is common, and in about 20% of women it can be severe enough to interfere with daily functioning. Dysmenorrhea is not only associated with cramping, but also with other symptoms like low back and leg pain, bloating, nausea, diarrhea, and fatigue. Dysmenorrhea is classified as primary or secondary. Primary dysmenorrhea occurs due to prostaglandins in the uterus. During menses, prostaglandins are responsible for causing contractions in the uterus, which expel the uterine lining. Ideally the contractions would be small enough to not cause significant discomfort. Some women, however, produce high amounts of prostaglandins or have an increased sensitivity to them. Women with dysmenorrhea have increased uterine activity, which results in increased contractility and increased frequency of contractions. In primary dysmenorrhea, there is no underlying condition or structural abnormality contributing to the pain. In secondary dysmenorrhea, the pain is due to medical conditions or structural abnormalities. Common secondary causes include endometriosis, pelvic inflammatory disease, and fibroids. Secondary causes of dysmenorrhea can be ruled out or diagnosed by your gynecologist. Today, we will be focusing on primary dysmenorrhea and strategies to reduce symptoms.

Gambone, J. C., & Raskin, A. J. (2010). Pelvic Pain. N. F. Hacker, J. C. Gambone, C. J. Hobel, & G. J. Moore (Authors), Hacker and Moore’s essentials of obstetrics and gynecology (pp. 256-264). Philadelphia, PA: Saunders/Elsevier.


We mentioned above that prostaglandins are responsible for primary dysmenorrhea. What are prostaglandins? Prostaglandins are hormone-like chemicals. Unlike most hormones, which are made by particular glands and then transported to other areas of the body via the blood stream,  prostaglandins are produced in almost all cells as they are needed. They are often made at sites of tissue damage or infection to stimulate healing. All of our cell membranes are composed of a phospholipid bilayer. Phospholipids consist of fatty acids and alcohol. When needed, enzymes can release certain fatty acids from the cell membrane to make prostaglandins. To release prostaglandin E2 (PGE2), the primary prostaglandin responsible for dysmenorrhea,  the enzyme phospholipase A2 (PLA2) releases the fatty acid arachidonic acid (AA) from the cell membrane. Then cyclooxygenase enzymes and prostaglandin synthase enzymes are responsible for further transforming that AA into PGE2. I am explaining this process now so the treatments and recommendations can be better understood.

After ovulation, early in the luteal phase, the ruptured follicle transforms into the corpus luteum, which produces progesterone as the primary hormone. The higher levels of progesterone help to prepare the endometrial lining for possible implantation. The LH surge prior to ovulation also stimulates an elevation of PGE2 in the follicle. If there is no implantation of a fertilized egg, there is a drop in progesterone as the corpus luteum fails. This rapid drop in progesterone signals a number of events and changes within the endometrium including the release of enzymes that digest cells, releasing prostaglandins. Prostaglandins cause narrowing of the blood vessels supplying the endometrium and contractile activity in the uterus, which leads to ischemia of the uterus and increased sensitivity of the nerve endings. These mechanisms lead to the expulsion of the uterine lining, but can also trigger the pain experienced during menses.

There is significant evidence pointing to prostaglandins as primary culprits in dysmenorrhea. Menstrual fluid from women with dysmenorrhea shows higher amounts of prostaglandins, especially prostaglandin E2. Women with primary dysmenorrhea also have upregulated cyclooxygenase (COX) enzyme activity, which is an enzyme involved in prostaglandin production.  Anovulatory endometrium without progesterone (endometrium during a cycle without ovulation) contains little prostaglandin, and these menses are usually painless.


Allopathic Treatments for Dysmenorrhea

Nonsteroid anti-Inflammatory drugs (NSAIDs) are a first line treatment for primary dysmenorrhea. They should be started 1-2 days prior to the anticipated start date of menses and continued on a set schedule for 2-3 days. They work by inhibiting COX enzymes, reducing prostaglandin production. Celecoxib, Ibuprofen, and Naproxen are common examples.

Oral contraceptive pills can also be used for women with primary dysmenorrhea who are also interested in contraception. The synthetic hormones in oral contraceptive pills suppress ovulation, reducing the amount of prostaglandin produced.


Diet Recommendations for Dysmenorrhea

Prostaglandins are derived from the fatty acids in our cell membranes. Dietary fatty acids affect the composition of our cell membranes. In general, omega 6 fatty acids are precursors to pro-inflammatory prostaglandins and omega 3 fatty acids are precursors are precursors to anti-inflammatory prostaglandins. Both omega 6 and omega 3 fatty acids are important, but, in general, the standard American diet is much higher in omega 6 fatty acids than omega 3 fatty acids. The body uses a particular omega-6 fatty acid, arachidonic acid, to create prostaglandin E2 – the one responsible for uterine contractions. Egg yolks, red meat, and poultry are significant sources of arachidonic acid. Decreasing these foods in the diet can help to rebalance the omega 6:omega 3 ratio. We can also try to increase the fatty acids that promote anti-spasmodic prostaglandins E1 & E3. These include omega 3 fatty acids like EPA found in fatty fish like sardines and salmon. Increasing omega 3 fatty acids in the diet is another strategy to balance the omega 6:omega 3 ratio and reduce excess prostaglandin production.

Alpha-linolenic acid is a vegetarian source of omega-3 fatty acids found in foods like walnuts, flax, chia and hemp. EPA and DHA however are more active forms of omega 3 fatty acids. There is poor conversion of ALA to EPA and DHA in the body. Algae based DHA supplements can be given to vegans as there is retro-conversion from DHA to EPA.

Sugar and alcohol do not directly affect prostaglandin E2 production, but they can affect the metabolism of important B vitamins and minerals that play a role in dysmenorrhea. Therefore, avoiding high sugar foods and alcohol can be helpful.


Important Nutrients in Dysmenorrhea

Some dietary nutrient insufficiencies have been associated with dysmenorrhea and supplementation with certain nutrients has been shown to help in symptom reduction.

  • B vitamins: Both B1 & B3 have been shown to help reduce dysmenorrhea in clinical studies
  • Magnesium: Magnesium has also been shown to help reduce dysmenorrhea in some women. Its mechanism of action is thought to be due to its smooth muscle relaxation effects and its inhibition of prostaglandin E2.
  • Calcium: Muscles need calcium to maintain their normal tone. If deficient in calcium, they are more likely to cramp. Low calcium has been associated with greater pain during menses.
  • Iron: An association between iron deficiency and dysmenorrhea has been identified.
  • Omega 3 fatty acids: The American diet tends to be much higher in omega 6 fatty acids than omega 3 fatty acids. As we discussed, having much higher amounts of omega 6 fatty acids, predisposes us to produce more prostaglandin E2 (the spasmodic prostaglandin) than prostaglandins E1 and E3 (the antispasmodic prostaglandins).


Other Recommendations

Stress Reduction
Stress not only contributes to pain, but also affects our perception of/ability to deal with that pain. A study demonstrated that women with high stress were more likely to experience dysmenorrhea in the following menstrual cycle. There are few hypotheses for how stress might affect dysmenorrhea. First, cortisol (a stress hormone) interacts with our pituitary gland, which regulates ovarian hormone release. Downstream ovarian hormone imbalances could increase pain at menses. Stress also modulates pain perception and can increase pain sensitivity. We see maladaptive changes in the pathways that process pain in individuals under stress. Finally, stress can also affect inflammation and prostaglandin synthesis. Biofeedback with relaxation practices and/or acupuncture can be particularly helpful tools in cases where women with dysmenorrhea are under stress.

Acupuncture can be an effective treatment modality for reducing menstrual pain. According to TCM theory, there are three primary etiologies in dysmenorrhea: liver qi stagnation, cold accumulation, and qi and blood deficiency. Working with a licensed acupuncturist can help to identify your particular imbalances and  restore balance in the body. Possible mechanisms of action include restoring optimal blood flow in the reproductive organs, reducing chronic inflammation and stress reduction (it has been shown to stimulate the vagus nerve and cause a rise in dopamine).

Both aerobic exercise and targeted isometric exercises have been shown to be effective in the prevention and reduction of dysmenorrhea. Exercise can increase pelvic blood flow, help to transfer waste and prostaglandins from the uterus, reduce stress, and increase levels of endorphins. All of these mechanisms can help to reduce severity of menstrual pain.