Dysmenorrhea simply means painful menstrual cramps, which are experienced by 90 percent of women. It is primarily caused by inflammatory prostaglandins (PGF) that are released from the uterine lining. This PGF release is involved in initiating menstruation as it stimulates contraction of the uterus, cuts off the blood supply to the uterus tissue, and enhances nerve sensitivity. The severity of dysmenorrhea is directly related to the amount of PGF in menstrual fluid, which typically peaks during the first two days of the menses.To treat the symptoms of PGF activity on the uterus, physicians typically prescribe oral contraceptive pills (OCPs) tor nonsteroidal anti-inflammatory (NSAIDs) such as aspirin and ibuprofen. NSAIDs essentially inhibit prostaglandin synthesis, lowering the release of inflammatory prostaglandins that cause the cramping. This is also why you may notice a decrease in flow of menstrual blood if you take an NSAID to relive your cramps. In recent studies it has been found that 10 percent of women do not response to either treatment. Yet in a healthy cycle with balanced hormones and a diet rich in omega fats, there are no cramps, breast tenderness, or PMS! 

You are not alone…
Dysmenorrhea significantly interrupts the lives of women, keeping them from work, school, and general life activities. Absenteeism is an unappreciated problem among 34 to 50 percent of women, tallying up to an annual 600 million lost work hours and $2 billion lost productivity.

How do good fats help relieve menstrual cramps?
Omega-3 fatty acids make up the membranes of all cells in the body. They are also responsible for producing eicosanoids, a key part of fighting inflammation that plays a role in the prevention and treatment of various diseases. Dysmenorrhea is a disturbed balance between anti-inflammatory, vasodilator eicosanoids (derived from Omega-3) and pro-inflammatory, vasoconstrictor eicosanoids (derived from omega-6). By increasing the intake of Omega-3, painful cramping symptoms can be reversed, decreasing the amount of Omega-6 in cell membranes.

Nutrient Deficiency 
Linolenic acid (Omega-3) and linoleic acid (Omega-6) are precursors to muscle-relaxing prostaglandins. PgE1 prostaglandins are responsible for the antispasmodic and anti-inflammatory effect. It is essential for the body to use linoleic acid in order to convert gamma linolenic acids (GLA), which produces PgE1 prostaglandins. The conversion pathway of linoleic acid to GLA requires magnesium, vitamin B6, zinc, vitamin C, and niacin. It is commonly seen among nutrient deficient women to have more cramping because they cannot properly make this conversion.

Balancing through Diet
There are several ways to naturopathically treat these symptoms of dysmenorrhea. Linolenic acids and linoleic acids are found in fatty acids, such as seeds (pumpkin and flaxseeds). Supplementing with flax oil (high in Omega-3 FA) or borage oil, black current oil, and evening primrose oil are other excellent in promoting the synthesis of the beneficial prostaglandins and fewer uterine contractions and menstrual pains. Top three foods rich in nutrients needed for proper linoleic acid conversion are: papaya (rich in vitamin C), spinach (rich in magnesium), and lentils (rich in thiamine).


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Coco, Andrews S. “Primary Dysmenorrhea.” American Family Physician. American Academy of Family Physicians, 1 Aug. 1999. Web. 01 Aug. 2012.           .
Deutch, Bente, Eva Bonefeld Jorgenson, and Jens C. Hansen. “Menstrual discomfort in Danishwomen Reduced by Dietary Supplements of Omega-3 PUFA and B12 (fish   Oil or Seal Oil Capsules).” Nutrition Research. Elservier, Inc., 6 July 2000. Web.           01 Aug. 2012.
Proctor, Michelle, and Patricia A. Murphy. “Herbal and Dietary Therapies for Primary and Secondary Dysmenorrhoea.” The Cochrane Library. John Wiley & Sons, Inc,   21 Jan. 2009. Web. 01 Aug. 2012.             .
Saldeen, Pia, and Tom Saldeen. “Women and Omega-3 Fatty Acids.” Obstetrical & Gynecological Survey. Lippincott Williams and Wilkins, Inc., Oct. 2004. Web. 01 Aug. 2012.