5: Dysmenorrhoea

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Case 5 Dysmenorrhoea

Description of dysmenorrhoea

Definition

Dysmenorrhoea is defined as cyclic lower abdominal pain that occurs with, or precedes, menstruation.¹ Depending on the aetiology of the condition, dysmenorrhoea may be classified as either primary or secondary. Primary dysmenorrhoea is a functional disorder that has no identifiable pathological aetiology and is typically associated with ovulation. Pain caused by a demonstrable pathology to the pelvic or reproductive structures, however, is referred to as secondary dysmenorrhoea.¹

Epidemiology

The prevalence of dysmenorrhoea varies across the globe, affecting between 16.8 and 81 per cent of women.² Of the two categories of menstrual pain, primary dysmenorrhoea is the most common, contributing to around ninety per cent of dysmenorrhoeic cases.³ Primary dysmenorrhoea usually begins during adolescence or the early twenties, generally after regular ovulation is established, and usually after the first three to six menstrual cycles.⁴ Unlike the prevalence of secondary dysmenorrhoea, which increases with advancing age, the prevalence of primary dysmenorrhoea diminishes with age and, in some cases, following pregnancy.⁴

Aetiology and pathophysiology

Primary dysmenorrhoea is caused by abnormal eicosanoid production, specifically, an abnormal increase in endometrium-derived prostaglandin (PG) F_2α and PGE₂. These proinflammatory compounds are formed under the influence of progesterone, but can also rise following endometrial shedding, endometrial cell necrosis,⁴ excess omega 6 fatty acid intake, low omega 3 fatty acid consumption and/or abnormal fatty acid metabolism.^3,^5,⁶ The PGs implicated in the pathogenesis of dysmenorrhoea exhibit a wide range of effects. PGF_2α, for instance, affects the gastrointestinal (GI) tract, causing nausea, vomiting and diarrhoea.⁴ PGF_2α is also a potent smooth muscle stimulant and vasoconstrictor, which, in sufficient quantities, can cause uterine ischaemia, myometrial contractions and uterine pain.³ In contrast, PGE₂ is a potent vasodilator and a possible contributor to excessive menstrual bleeding.⁴ While the cytokine hypothesis of dysmenorrhoea is theoretically plausible, evidence from clinical studies is mixed.^7,⁸

As opposed to the proinflammatory state of primary dysmenorrhoea, the cause of secondary dysmenorrhoea is primarily pathological. Conditions usually associated with secondary dysmenorrhoea include endometriosis, uterine adenomycosis, leiomyomata or fibroids, pelvic adhesions, cervical stenosis, pelvic inflammatory disease, in situ intrauterine device and endometrial polyps.^1,⁴

Other factors that may increase the severity or duration of dysmenorrhoea are anxiety, low levels of exercise, low fish consumption and cigarette smoking.^1,³ Several studies also report a higher risk of dysmenorrhoea among women with high stress (i.e. occupational or perceived stress) compared to those with low stress.^9,¹⁰

Clinical manifestations

Dysmenorrhoea typically presents as recurrent, spasmodic lower abdominal or suprapubic pain that is sharp or dull in quality.⁴ In many cases, the pain radiates to the lower back or thighs. Some women also report symptomatic improvement following the application of heat to the abdomen or by assuming the fetal position.⁴ In primary dysmenorrhoea symptoms usually begin 1–3 days before menses, peak 24 hours after the onset of menstruation and subside 2–3 days later. In secondary dysmenorrhoea, menstrual pain may commence long before menses begins and continue well after menstruation has ceased.¹ It is not uncommon for women with either type of dysmenorrhoea to also experience concomitant nausea, vomiting, diarrhoea, constipation, headache, fatigue, irritability, nervousness, urinary frequency, dizziness, sleeplessness and depression.^1,³

Clinical case

23-year-old woman with primary dysmenorrhoea

Rapport

Adopt the practitioner strategies and behaviours highlighted in Table 2.1 (chapter 2) to improve client trust, communication and rapport, as well as the accuracy and comprehensiveness of the clinical assessment.

Assessment

Once measures have been put into place to build client–practitioner rapport, the clinician can begin the clinical assessment.

Health history

History of presenting condition

A 23-year-old woman presents to the clinic complaining of dull, spasmodic menstrual pain. The pain is located over the suprapubic region primarily, but at times can radiate to the lower back and is often accompanied by mild nausea, bloating, fatigue and irritability. The pain and concomitant symptoms have been present for the past 7 years and typically follow the same pattern – begin 1 day before menstruation, peak on the first day of menses (pain score = 7/10) and subside 2 days later. The menstrual cycle is regular (cycling every 28–30 days), menstruation volume is moderate and menses duration is generally 4–5 days. There is no mid-cycle bleeding or pain, nor abnormal vaginal or urethral discharge, dyspareunia, altered libido or dysuria. Fatigue generally aggravates the symptoms; paracetamol and hot packs to the abdomen provide moderate relief of pain.

Lifestyle history

Diet and fluid intake
Breakfast	White toast with butter, coffee.
Morning tea	Coffee, banana or carrot cake.
Lunch	Leftover dinner, sandwich with white bread, ham, tomato, lettuce and pickles.
Afternoon tea	Coffee.
Dinner	Chicken or beef and vegetable stirfry with white rice, penne carbonara with mushrooms, focaccia with grilled chicken or roast beef, eggplant, capsicum and lettuce.
Fluid intake	3–4 cups of instant coffee a day, 2–3 cups of water a day.
Food frequency
Fruit	0–1 serve daily
Vegetables	2–3 serves daily
Dairy	0–1 serve daily
Cereals	5–6 serves daily
Red meat	6–7 serves a week
Chicken	1–2 serves a week
Fish	0 serves a week
Takeaway/fast food	twice a week

Quality and duration of sleep

Difficulty falling asleep (sleep latency of approximately 1 hour). Continuous sleep; average duration is 6 hours.

Frequency and duration of exercise

Has little time for a dedicated exercise program. Drives to work. Engages in incidental exercise (i.e. work-related walking) less than 2 hours a day. Engages in sedentary activities (i.e. desk duties) more than 8 hours a day.

Socioeconomic background

The client and both parents were born in the US. Since completing her law degree 3 years ago, the client has been employed as a full-time lawyer in a busy law firm in the central business district (CBD), which the client states is very stressful and often requires overtime. The client and her supportive same-sex partner reside in a privately rented apartment in the CBD. This same-sex relationship has led to some hostility between the client and her parents and two siblings. The client has no religious or cultural affiliations.

Physical examination

Clinical examination of the reproductive system is outside the scope of practice for most CAM practitioners. Thus, the following five elements represent a summary of the clinical examination conducted by the client’s physician.

Inspection

Both breasts are symmetrical, with no visible masses, lesions or discharge. The abdomen is flat. The labia, clitoris, urethral meatus, vaginal orifice, perineum and cervix are unremarkable.

Olfaction

There are no abnormal odours present.

Palpation

Both breasts are non-tender, with no palpable masses. The abdomen is soft and non-tender, with no palpable masses. Labia, clitoris, urethral meatus, vagina, perineum and cervix are non-tender. Bimanual examination revealed that the uterus is of normal size, shape and contour, and is non-tender. Rectovaginal examination is unremarkable.

Percussion

Not applicable.

Auscultation

Bowel sounds are normoactive in all four quadrants.

Additional signs

Client is afebrile (36.7°C, per oral). Blood pressure is 118/64. Client is of normal weight (BMI is 24.1 kg/m², waist circumference is 71 cm).

Clinical assessment tools

The menstrual symptom questionnaire (MSQ) provided an overall score of 72/120, where a score of zero represents no menstrual symptoms and a score of 120 represents frequent and intense menstrual symptoms. The menstrual pain ‘often’ experienced before and during menses and the concomitant symptoms ‘sometimes’ experienced during menstruation corroborate the type, frequency and intensity of symptoms reported in the client’s history.

Diagnostics

CAM practitioners may request, perform and/or interpret findings from a range of diagnostic tests in order to add valuable data to the pool of clinical information. While several investigations are pertinent to this case (as described below), the decision to use these tests should be considered alongside factors such as cost, convenience, comfort, turnaround time, access, practitioner competence and scope of practice, and history of previous investigations.

Pathology tests

Fatty acids

Plasma or red cell fatty acid analysis assesses the concentration of fatty acids within the plasma or erythrocyte, including omega 3, omega 6 and omega 9 polyunsaturated fatty acids, saturated fatty acids and trans fatty acids. Given that the fatty acid composition of plasma and erythrocytes is correlated with the dietary intake of fatty acids,¹¹ this test can help to determine whether excess omega 6 fatty acid intake and/or low omega 3 fatty acid consumption are contributing factors in dysmenorrhoea.^3,⁵

Hormones and eicosanoids

Several small studies have compared the plasma concentrations of oxytocin, follicle-stimulating hormone, 17β-estradiol, vasopressin, luteinising hormone, progesterone and PGF_2α in healthy controls to women with primary dysmenorrhoea.^7,^12,¹³ However, findings from these studies have been inconsistent, rendering questionable the value of hormone testing in women with dysmenorrhoea.

Radiology tests

Medical imaging, such as CT, MRI, ultrasound and uterosalpingography, may be requested if secondary dysmenorrhoea is suspected, particularly if it is attributed to uterine fibroids, tumours, pelvic inflammatory disease, adhesions or the presence of foreign objects.

Functional tests

A female hormone profile measures salivary levels of oestradiol, progesterone, testosterone and dehydroepiandrosterone (DHEA) over a single 28-day menstrual cycle. While saliva is a valid and reliable sample source for hormone analysis,¹⁴ the value of hormone testing in women with dysmenorrhoea is questionable as female hormones appear to play little to no role in the pathogenesis of the condition.

Invasive tests

Invasive tests may be required if secondary dysmenorrhoea is suspected. Hysteroscopy, laparoscopy and, in few cases, Papanicolaou testing, can be useful in detecting conditions associated with secondary dysmenorrhoea, such as endometriosis, uterine fibroids, pelvic adhesions and pelvic inflammatory disease.

Miscellaneous tests

Not applicable.

Diagnosis

Clusters of data extracted from the health history, clinical examination and pertinent diagnostic test results point towards the following differential CAM diagnosis.

• Menstrual pain (actual), related to emotional stress (client works in a stressful occupation, and has reported unresolved family conflict), high omega 6:omega 3 fatty acid intake (dietary intake of foods containing omega 3 fatty acid is minimal and the intake of omega 6 fatty acids is relatively high), and sedentary lifestyle (client’s occupation is largely desk-bound and client engages in very little physical exercise).

Planning

The goals and expected outcomes that best serve the client’s needs, and are most relevant to the case (as determined by the clinical assessment and CAM diagnoses), are as follows.

Goal

1. Client will demonstrate an improvement in menstrual pain (client’s primary concern is menstrual pain).

Expected outcomes

Based on the degree of improvement reported in clinical studies that have used CAM interventions for the management of dysmenorrhoea,¹⁵^–¹⁸ the following are anticipated:

1. Client will demonstrate a fifty per cent reduction in baseline severity of menstrual pain in 7 weeks or by dd/mm/yyyy (measured by 0–10 visual analogue scale).

2. Client will report a thirty per cent decrease in baseline duration of menstrual pain in 8 weeks or by dd/mm/yyyy (measured by symptom diary).

3. Client will demonstrate a fifty per cent reduction in baseline intensity and frequency of menstrual symptoms in 12 weeks or by dd/mm/yyyy (measured by MSQ).

Application

The range of interventions reported in the CAM literature that may be used in the treatment of dysmenorrhoea are appraised below.

Diet

Miscellaneous diets (Level I, Strength B, Direction + (low-fat vegetarian diet only))

According to results from several cross-sectional studies, the dietary consumption of particular foods and nutrients may influence the manifestation of dysmenorrhoea. Low intake of fruit, fish and fibre, for instance, was found to be inversely related to menstrual pain, as was a low omega 3:omega 6 fatty acid intake. The association between egg consumption and dysmenorrhoea was inconsistent, while soy and fat intake were found to have no effect on menstrual symptoms.¹⁹ Some of these findings have been corroborated by data from RCTs.¹⁹ In terms of fat intake, for instance, one trial (n = 30 adults) found neither low dietary fat intake nor a low polyunsaturated fatty acid:saturated fatty acid (P:S) ratio to have an effect on menstrual pain when compared with a high-fat diet or high P:S ratio at 4 months.²⁰ In a trial of 33 women with moderate to severe dysmenorrhoea, consumption of a low-fat vegetarian diet significantly reduced the duration and intensity of menstrual pain when compared with a normal diet and placebo supplement after two menstrual cycles.¹⁸ Collectively, what these findings suggest is that a low-fat vegetarian diet, an increase in dietary fibre consumption and an increase in omega 3:omega 6 fatty acid intake may be beneficial in alleviating the symptoms of dysmenorrhoea. Further investigation is required to assess the validity of this claim.

Lifestyle

Relaxation therapy (Level I, Strength C, Direction o)

Relaxation therapy (RT) describes myriad mind–body techniques that facilitate the relaxation response and moderate sympathetic nervous system activity. In doing so, RT might attenuate the effect of stress on menstrual pain, thereby providing theoretical justification for the use of RT in dysmenorrhoea. Nevertheless, a Cochrane review of three small RCTs (n = 175) of variable duration (i.e. 5–20 weeks) found that RT alone, with biofeedback or with imagery to be no more effective than waiting list controls at improving dysmenorrhoea symptoms (as measured by symptom severity scale), yet when descriptive data were analysed results were mixed.²¹ Since these trials are more than 20 years old and the diagnostic criteria and outcome measures are no longer widely used, the validity of these findings is uncertain. Further research in this area is warranted.

Nutritional supplementation

Calcium (Level I, Strength B, Direction +)

A 10-year case–control study (n = 3025) nested within the prospective Nurses’ Health Study II cohort has shown that women in the highest quintile of dietary calcium intake have a thirty per cent lower risk of developing menstrual symptoms than women in the lowest quintile (p = 0.02).²² Even though this study is unable to establish a causal relationship between calcium intake and dysmenorrhoea specifically, and mechanistic data explaining this relationship is lacking, evidence from clinical studies is promising.²³ Two RCTs, one using a parallel group design (n = 466)¹⁸ and one a crossover approach (n = 33)¹⁷ found oral calcium carbonate (1.0–1.2 g daily) administered over a period of three menstrual cycles to be significantly superior to placebo in reducing premenstrual and menstrual pain. Research examining the clinical efficacy of other formulations and dosages of supplemental calcium in dysmenorrhoea is now warranted.

Magnesium (Level I, Strength C, Direction + (pain reduction only))

Magnesium is involved in many enzymatic reactions and physiological processes throughout the body. Low serum magnesium levels have been shown to intensify neuromuscular cell excitability, resulting in increased smooth muscle contractility. High serum levels of magnesium cause smooth muscle relaxation.²⁴ By decreasing myometrial spasm, magnesium could potentially reduce menstrual pain. A Cochrane review of three small, double-blind, controlled clinical trials (n = 117) has reported mixed results, with two of three trials showing magnesium (variable dosage for 5–6 months) to be more effective than placebo and as effective as vitamin B₆ in reducing menstrual pain.²¹ Between-group differences in the need for analgesia were inconsistent. While the best available evidence appears to favour the use of magnesium for dysmenorrhoea, the evidence is not strong, suggesting that further investigation is needed.

Omega 3 fatty acids (Level I, Strength C, Direction o)

The anti-inflammatory effects of essential fatty acids have been reported in numerous populations and clinical studies.²⁵ Given that heightened inflammatory activity is implicated in the pathogenesis of dysmenorrhoea, it is theoretically plausible that omega 3 fatty acids could attenuate menstrual pain. A Cochrane review of one small double-blind RCT (n = 42 adolescents with dysmenorrhoea) supports this premise; it found fish oil (dose unknown, but containing 1080 mg EPA + 720 mg DHA daily) to be statistically significantly superior to placebo in reducing the Cox menstrual symptom score, a non-standardised aggregate score of the frequency and severity of multiple menstrual symptoms, and analgesic use after 8 weeks of treatment.²⁶ While the fish oil group reported significantly more adverse effects than the placebo group, only four effects (e.g. nausea, acne exacerbation) were reported in the fish oil group in total, all of which were mild. A more recent, larger and longer double-blind RCT involving 78 adolescents and women with dysmenorrhoea found neither fish oil (2.5 g daily, EPA/DHA content unknown) nor seal oil (2.5 g daily) to be superior to placebo (2.5 g mixed fatty acids daily) in reducing menstrual pain scores at 12 weeks. In the group receiving fish oil (2.5 g daily) and vitamin B₁₂ (dose unknown), a statistically significant reduction in menstrual pain was observed when compared with placebo.²⁷ It must be said, then, that the best available evidence for omega 3 fatty acid supplementation and dysmenorrhoea is inconclusive.

Pyridoxine (Level I, Strength C, Direction o)

Animal studies have demonstrated enhanced inflammatory activity in the presence of vitamin B₆ deficiency.²⁸ In human studies, plasma pyridoxine and pyridoxal 5-phosphate levels are shown to be similar between women with premenstrual symptoms to those with no or mild premenstrual symptoms.²⁹^–³¹ Even though biological plausibility is lacking, this has not prevented researchers from examining the clinical efficacy of pyridoxine supplementation in dysmenorrhoea. In a systematic review of one double-blind RCT, orally administered vitamin B₆ (200 mg daily for 20 weeks) was shown to be significantly more effective than placebo at reducing menstrual pain and analgesic use in 46 women with dysmenorrhoea,²⁶ yet in two RCTs involving women with premenstrual symptoms (n = 183), vitamin B₆ (50–300 mg daily for 12 weeks) was shown to be no more effective than placebo at reducing abdominal cramping or back pain.^32,³³ While differences in patient populations and treatment durations may have contributed to these disparate findings, this may only become clearer with additional research in the area.

Thiamine (Level II, Strength B, Direction +)

Thiamine is a water-soluble vitamin that plays an important role in carbohydrate metabolism and neurotransmitter biosynthesis. Even though these actions are essential for life, neither of them justifies the use of vitamin B₁ in painful or inflammatory conditions such as dysmenorrhoea. In spite of the paucity of mechanistic data in this area, there is good evidence of effectiveness for thiamine in dysmenorrhoea. In a double-blind, randomised placebo-controlled trial involving 556 adolescent girls and young women with moderate to very severe spasmodic dysmenorrhoea, for example, 90 days of thiamine hydrochloride supplementation (100 mg daily) was found to be significantly more effective than placebo in reducing the incidence of menstrual pain.³⁴ Verification of these findings is needed.

Vitamin E (Level I, Strength B, Direction +)

Among the many functions of vitamin E, perhaps the most relevant to dysmenorrhoea is its anti-inflammatory activity; in particular, the capacity to reduce the release of proinflammatory cytokines.³⁵ This mechanism of action is distinctly different from that of the non-steroidal anti-inflammatory drugs (NSAIDs), which suggests that these two anti-inflammatory agents may complement each other in the management of dysmenorrhoea. This does not appear to be the case with an open-label, randomised crossover trial (n = 50 adolescents) that found no statistically significant difference in menstrual pain between groups receiving vitamin E (100 mg daily for 20 days per month, for 2 months) and ibuprofen (400 mg daily at onset of pain for 2 months), to ibuprofen alone (400 mg daily at onset of pain for 2 months).^26,³⁶

In two RCTs comparing vitamin E to placebo, vitamin E supplementation (200–500 IU for 5 days a month for 2–4 months) was shown to be statistically significantly superior to placebo in reducing the severity and duration of menstrual pain in adolescents with primary dysmenorrhoea (n = 378).^37,³⁸ Since both of these trials were conducted by the same principal researcher, corroboration from independent studies is warranted. In particular, the efficacy of supplemental vitamin E in women with dysmenorrhoea is an area in need of further study.

Iron, niacin and tryptophan

These minerals demonstrate an array of effects that could affect the outcomes of premenstrual syndrome, although the administration of these nutrients in dysmenorrhoea is not yet supported by rigorous clinical evidence, only by pathophysiologic rationale or experimental research findings.

Herbal medicine

Hypericum perforatum (Level IV, Strength D, Direction o)

St John’s wort demonstrates anti-inflammatory and analgesic activity in vivo.^39,⁴⁰ The administration of hypericum in painful inflammatory conditions, such as dysmenorrhoea, is therefore theoretically justified. Even though several clinical trials have investigated the clinical efficacy of H. perforatum in premenstrual syndrome,^41,⁴² only one of these studies provides sufficient data on the effectiveness of hypericum for menstrual pain.⁴³ This prospective, open, uncontrolled, observational study reported a statistically significant reduction in cramping pain after the first month of hypericum treatment (300 mg daily for two menstrual cycles) and a non-significant reduction in pain after the second month of treatment when compared with baseline. This inconsistent finding, together with the small size of the trial and the methodological limitations of the study, adds very little to the body of evidence for hypericum and dysmenorrhoea.

Oenothera biennis (Level I, Strength C, Direction o)

Evening primrose oil (EPO) is extracted from the seed of O. biennis. The oil is a complex mixture of essential fatty acids, containing around seventy per cent cis-linolenic acid (omega 3 fatty acid), nine per cent cis-gamma-linolenic acid (omega 6 fatty acid), small amounts of oleic acid (omega 9 fatty acid), and palmitic and stearic acids (saturated fatty acids).⁴⁴ Under experimental conditions the oil has been shown to reduce cyclo-oxygenase-derived eicosanoid production, including the generation of PGE₂.⁴⁵ Thus, while it is possible that EPO could attenuate the pathogenesis of dysmenorrhoea, a systematic review of four small RCTs (n = 105) failed to find any statistically significant difference in premenstrual symptoms between EPO (3–6 g daily for 2–6 menstrual cycles) and placebo.⁴⁶ All three controlled trials excluded from the review (because of a lack of evidence of randomisation) found EPO to be superior to placebo in reducing premenstrual symptoms. But the high risk of bias in these latter studies and the uncertainty about the inclusion of pain as an outcome measure in several of these studies adds little strength to the body of evidence for EPO and dysmenorrhoea. A less detailed but more recent review of EPO concluded that the evidence for EPO and premenstrual symptoms was still unconvincing.²³

Vitex agnus castus (Level V, Strength NA, Direction NA)

Chaste tree is used in traditional Western herbal medicine as a treatment for gynaecological problems, including menstrual pain. Evidence from experimental studies suggests vitex might improve menstrual pain by stimulating mu-opiate receptors and, in doing so, may activate analgesic and mood regulatory pathways.⁴⁷ Even though many systematic reviews and clinical trials have shown chaste tree extract to be effective in alleviating a number of premenstrual symptoms,^23,^46,⁴⁸ none have presented specific data on the efficacy of vitex for menstrual pain. Thus, there is no current evidence to show that vitex is effective in treating dysmenorrhoea.

Zingiber officinale (Level III-1, Strength B, Direction +)

Ginger is used in many alternative systems of healing for its anti-inflammatory and circulatory stimulant properties. Under experimental conditions, ginger has been shown to inhibit the synthesis of PGE₄ in vivo ⁴⁹ and leukotriene B₄ in vitro,⁵⁰ which may be useful in attenuating the pain of dysmenorrhoea. This appears to be the case according to findings from a recent double-blind comparative clinical trial involving 150 university students with primary dysmenorrhoea. The trial found dried ginger rhizome powder (250 mg 4 times a day), when administered for 3 days from the start of menses, to be as effective as ibuprofen and mefenamic acid at reducing the severity of dysmenorrhoea, as well as the need for breakthrough analgesia.⁵¹ The long-term effectiveness of ginger in dysmenorrhoea now warrants further investigation.

Other herbs

Alchemilla vulgaris (ladies mantle), Angelica sinensis (dong quai), Capsella bursa-pastoris (shepherds purse), Caulophyllum thalictroides (blue cohosh), Chamaelirium luteum (false unicorn root), Cimicifuga racemosa (black cohosh), Corydalis ambigua (corydalis), Dioscorea spp. (wild yam), Glycyrrhiza glabra (licorice), Hydrastis canadensis (golden seal), Leonurus cardiaca (motherwort), Matricaria recutita (German chamomile), Mentha piperita (peppermint), Mitchella repens (squaw vine), Paeonia lactiflora (peony), Piscidia erythrina (Jamaican dogwood), Valeriana officinalis (valerian), Viburnum opulus (cramp bark) and Viburnum prunifolium (black haw)

These herbs have been traditionally used and/or tested under experimental conditions for their analgesic, antispasmodic, uterine tonic or anti-inflammatory activity. Herbs, such as Ginkgo biloba (maidenhair tree),^52,⁵³ have also been shown under clinical trial conditions to be significantly more effective than placebo in alleviating a number of menstrual symptoms. But there is still insufficient clinical data to support the use of these herbs (as monopreparations) in dysmenorrhoea specifically.

Other

Acupuncture (Level I, Strength C, Direction o)

Acupuncture originated in China more than 4000 years ago.⁵⁴ Since then, a large traditional evidence base for the therapy has been established. Positive findings from case reports and uncontrolled trials have added to this traditional knowledge, particularly in the area of dysmenorrhoea.^55,⁵⁶ However, a recent systematic review of 30 RCTs and two controlled clinical trials reported conflicting results for the effectiveness of acupuncture-related therapies in dysmenorrhoea.⁵⁷ These inconsistent findings, together with the significant heterogeneity of trials and the low methodological quality of most studies, does not enable any firm conclusions to be made. Evidence from a more recent Cochrane review in this area, which has yet to be completed, may shed further light on the effectiveness of acupuncture in dysmenorrhoea.⁵⁸