Essential Fatty Acids
Essential fatty acids (EFAs), such as linoleic acid (LA) and gamma-linolenic acid (GLA), are vital precursors of prostaglandins. The anti-inflammatory series 1 PGs are derived from LA, which is converted to GLA by the enzyme delta-6-desaturase (D6D), and then to dihomo-gamma-linolenic acid (DGLA). Nutrients known to increase the conversion of EFAs to the anti-inflammatory series 1 PGs include magnesium, vitamin B6, zinc, niacin, and vitamin C. Factors that interfere with the production of anti-inflammatory PGs include diets rich in saturated fats, alcohol consumption, and catecholamines released from the adrenal medulla during stress.
Arachidonic acid (AA), found in animal fats, is the precursor of the pro-inflammatory series 2 PGs. Much of the AA used for 2 series PG formation comes from dietary sources, notably meat and dairy products.7 A deficiency of EFAs, either due to inadequate intake or failure of normal conversion of linoleic acid to GLA, and a high consumption of saturated animal fats can result in overproduction of AA to the pro-inflammatory PGs.
Because there is little GLA or DGLA in the usual human diet, supplementation with GLA-rich evening primrose oil or borage seed oil may effectively reduce the production of pro-inflammatory PGs in favor of anti-inflammatory PGs.
Magnesium
Magnesium’s role in dysmenorrhea may be due to several factors:
1) magnesium has a direct effect on vascular tone and can act physiologically to control and regulate the entry of calcium into smooth muscle cells, acting as a naturally occurring calcium channel blocker. Through controlling calcium, magnesium influences the contractility, tone, and relaxation of the uterine smooth muscle;
2) magnesium is required for the synthesis of second messenger cAMP (cyclic AMP) from adenosine triphosphate (ATP).cAMP, a ubiquitous nucleotide derived from ATP through the action of the enzyme adenylate cyclase, plays a crucial role in the communication process between the gonadotropins (LH, FSH) and the ovaries
3) magnesium plays an important role in the conversion of LA to GLA, a rate limiting step in anti-inflammatory series 1 PG synthesis, and may inhibit the synthesis of PGF2α;
4) magnesium is involved in estrogen conjugation and the activation of the B vitamins, especially vitamin B6.
Large numbers of women may be at risk for magnesium deficiency. Dietary intake studies consistently show intakes of magnesium to be below the RDA in many age groups, with teenage girls and adult women among those most at risk of low intakes. Magnesium depletion can be compounded by the use of diuretics, increased alcohol and dietary fat intakes, a high intake of dairy products, stress, and malabsorption syndromes.
Vitamin B6
Vitamin B6 (pyridoxine hydrochloride) is an important cofactor for the conversion of LA to DGLA in the production of antiinflammatory PGs; for enzymes involved in estrogen conjugation in the liver; and for the synthesis of several eurotransmitters. With decreased levels of B6 in the body, the liver cannot conjugate estrogens, thus causing an increased blood level of estrogens. Vitamin B6 also stimulates cell membrane transfer of magnesium and increases intracellular magnesium, which plays a role in muscle relaxation.
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PG synthetase inhibitors (non-steroidal anti-inflammatory drugs), such as ibuprofen, mefanamic acid, naproxen, and indomethacin, have been used as analgesic treatment for dysmenorrhea since the early 1970s.1,19 Prior to their discovery, women who had dysmenorrhea were dependent largely on narcotics or oral contraceptives for pain relief.8 PG inhibitors block PG synthesis early in the inflammatory reaction by inhibiting the cyclooxygenase pathway. Once pain has become severe, relief is unlikely. However, these drugs should not be used prior to the onset of menses because of their teratogenic potential.
In a comprehensive review of clinical trials of PG inhibitors in the treatment of primary dysmenorrhea, it was found that significant pain relief was reported for each of the PG inhibitors for the majority of women.1 However, the authors concluded that 9% to 22% of dysmenorrheic women will not benefit from PG inhibitor treatment, possibly because some of these women may have secondary dysmenorrhea. While PG inhibitors are generally recognized as effective against pain, there are drawbacks. These drugs are not selective in their inhibition of PGs, translating to a reduction of all PGs, good or bad. In addition, possible side effects include dizziness, headache, nausea, vomiting, heartburn, and diarrhea, as well as GI damage with protracted use.
Cyclic administration of oral contraceptives, usually in the lowest dosage but occasionally with increased estrogen, is also used to alleviate pain. The mechanism of pain relief may be related to absence of ovulation or to altered endometrium resulting in decreased prostaglandin production during the luteal phase. Surgery is a rare form of intervention used in women who do not respond to medication.
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Secondary dysmenorrhea is defined as menstrual pain due to pelvic pathology. Secondary dysmenorrhea usually occurs after a woman has had normal menstrual periods for some time. It differs from primary dysmenorrhea in that the pain is caused by an abnormality or disease of the uterus, tubes or ovaries.The pain may be similar to menstrual cramps, but often lasts longer than the menses, and may also occur at other times of the month. The most common causes are infection,. adenomyosis (benign growths in the uterine walls), endometriosis (tissue from the lining of the uterus implants outside the uterus) and adhesions (scarring or adherence of two surfaces). Treatment of secondary dysmenorrhea depends on finding the cause and treating it appropriately. Medical and/or surgical treatment may be needed.
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Primary dysmenorrhea is the more common type of dysmenorrhea and is due to the production of prostaglandins. These are natural substances made by cells in the inner lining of the uterus and other parts of the body. The prostaglandins made in the uterus make the uterine muscles contract and help the uterus to shed the lining that has built up during the menstrual cycle. If excessive prostaglandins are produced, the woman may have excessive pain or dysmenorrhea with her menstrual cycle. Prostaglandins can also cause headaches, nausea, vomiting and diarrhea.
Therapies for primary dysmenorrhea include rest, heating pad to the lower abdomen or back, nutrition, aerobic exercise and medication. Nutrition. therapy includes a well-balanced diet with an adequate intake of calcium (1000 mg. per day) and a fluid intake of two quarts of water each day. Vitamin B6 , 50 to 100 mg. each day, may occasionally be helpful.
Medication for dysmenorrhea may involve two complementary strategies: decreasing prostaglandin production and hormonal alteration.
Prostaglandin production can be decreased with over-the-counter, non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen or naproxen sodium, or similar drugs that are stronger and available only by prescription. These drugs are generally well tolerated, although they can upset the stomach and are best taken with a small amount of food. Contraindications to the use of NSAIDs include pregnancy, ulcers, asthma and known allergy to this type of drug. NSAIDs are usually started with the onset of menstruation, although some women respond better if the medication is started 1-3 days prior to the onset of menstruation. It is sometimes necessary to take one of several NSAIDs until the one with the maximum efficacy for an individual woman is found.
Hormonal alteration of the menstrual cycle is usually accomplished by taking oral contraceptives (OC). OC's prevent ovulation, decrease the thickness of the uterine lining (endometrium) and as a result, fewer prostaglandins are made. The birth control shot, Depo-Provera®, 150 mg. every 10-12 weeks, can also be used to accomplish the same purpose. If Depo-Provera® is used to alter the hormones, it is extremely important that the woman obtain an adequate daily intake of calcium (1000 mg.).
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Dysmenorrhea, Greek for painful menstruation, is classified as primary (from the beginning and usually lifelong) or secondary (due to some physical cause and usually of later onset). The uterus is a muscle. Like all muscles, it contracts and relaxes. Most uterine contractions are never noticed, but strong ones are painful. During strong contractions, the uterus may contract too strongly or too frequently, causing the blood supply to the uterus to be temporarily cut off. This deprives the muscle of oxygen, causing pain. In addition to painful uterine cramping with menses, women with dysmenorrhea may experience nausea, vomiting, diarrhea, headaches, weakness, and/or fainting. Symptoms may vary in severity from cycle to cycle, but generally continue throughout the reproductive years. Dysmenorrhea can be an incapacitating problem, causing significant disruption in a woman's life each month.
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