A Review of Treatment approaches to Pre-Menstrual
Syndrome- What do British women perceive to be effective
for their symptoms?
By Jo George BSc (Hons) Acupuncture
Since 1995 many women have sought my help for symptoms related to premenstrual
syndrome (PMS). It was clear through clinical and personal experience that it was
usual for symptoms to vary in severity and type, from woman to woman, month to
month, and that lifestyle adjustments, complementary therapies, and some drugs had
Pre-menstrual syndromes (PMS) are a group of menstrually related, chronic, cyclical
disorders manifested by emotional and physical symptoms in the second part of the
menstrual cycle, which subside after the beginning of the menstrual period. (1)
Many doctors do not believe there is such condition as PMS and, consequently, fail to
recognise and treat it. Of 482 women who called the National Association for
Premenstrual Syndrome (NAPS) helpline last year, 42% said that their GPs were
unsympathetic or did not seem to know much about PMS. (2)
Over the last 60 years, research has been directed towards establishing the causes and
generating effective treatments for PMS. The lack of agreement about premenstrual
problems as a syndrome, and its diagnosis has contributed greatly to GP’s disbelief.
Its recognition is a twentieth century event, reflecting changes in our social structure
and lifestyle. In the past the time between puberty and the menopause was filled with
many pregnancies when PMS disappears. Each was followed by the cessation of
ovulation caused by prolonged breastfeeding. Nowadays with fewer pregnancies the
effects of the menstrual cycle are more apparent. (3) Incidence
Most women experience premenstrual symptoms during their reproductive years, but
not all perceive PMS as debilitating or distressing. However between 5-10% of
women- approximately 1.5m women in the UK, suffer from such severe premenstrual
symptoms (PMDD Premenstrual Dysphoric Disorder) that it impairs their work,
relationships and social lives. Severe PMS is more common between 30-40 years; and
in women with young children. (4) Certain hormonal events may be linked with the
onset of PMS, for instance, childbirth (particularly if followed by postnatal illness),
cessation of oral contraception use, or sterilisation. There is also evidence to suggest
significant symptom exacerbation due to stress. (5)
The aetiology of PMS is unknown. Hormonal causes such as excessive circulating
oestrogen, increased or decreased levels of progesterone, or imbalance between
oestrogen and progesterone have been proposed.(6) Other theories include:
• Prolactin (direct influence on breast tissue, association with stress, and
indirect relationship with dopamine and nervous pathways)
• Prostaglandin imbalance (effect of sex hormones on their synthesis)
Because PMS continues after hysterectomy if the ovaries are conserved, but
disappears during pregnancy, drug suppressed ovulation, and after the menopause
when the ovaries are removed, gonadal hormones seem to be causal. (7) However no
significant hormonal differences between those with PMS and those without the
disorder have been found (8).
The current consensus is that PMS is the result of reaction to normal hormonal,
biological and environmental change in susceptible women. The pathogenesis is said
to involve altered central neuroregulation and disordered homeostasis. This viewpoint
has encouraged the investigation of neuro-endocrine modulated central
neurotransmitters and the role of the hypothalamic-pituitary-gonadal axis in PMDD.
The absence of specific tests, and inconsistent acknowledgement of over 150
symptoms contribute to the difficulty in diagnosis, which relies on charting the timing
of symptoms and menstruation. Symptoms arise during the luteal phase of the
menstrual cycle. If behavioural symptoms persist throughout the menstrual cycle then
the disorder might be psychological or psychiatric. (11,12) Symptoms
Psychological and behavioural symptoms Physical symptoms
Mood swings and depression
Exacerbation of epilepsy, migraine, asthma, rhinitis or urticaria.
While the literature contains many rational arguments and trials for treatment, only
three recent studies (13,14,15) explored women’s
perception of their effectiveness.
None was in this country. However, it was clear from personal clinical experience that
women had a lot to say on the subject. Therefore questionnaires were sent to members
of the National Association for Premenstrual Syndrome (NAPS) in England, to find
out women’s assessment of the treatments they had tried. Conventional Treatments
Between the 1950’s and 1980’s progesterone deficiency was thought to
underlie PMS and was a popular therapy. The consensus in the literature to date
suggests there is no direct evidence to support this aetiology, nor its use as a
treatment, although 4 out of 12 Trials showed some benefit. Side effects included
alteration in length of menstrual cycle. (16)
Progestogen(synthetic progesterone like drugs)
-Seven reviewed RCT’s in 1999,
found three of these reported significant improvements with the drug, and the
remaining four showed no therapeutic benefit. Paradoxically, progestogens have been
shown to induce PMS symptoms. (16) Combined Oral Contraceptives-
Oral contraceptives (OC) continue to be widely used
to suppress ovulation; despite this only four RCTs have investigated their
effectiveness. Limited evidence suggests some women may find OC’s effective for
some physical symptoms, however for others they intensify mood symptoms. Daily
progestogen may produce PMS like side effects and a seven-day break may allow
symptom relapse, in addition to a higher risk of thromboembolic disorder in
This is also true for oestrogen, danazol and GnRH analogues.
(16) Oestrogen patches/ Implants-
Ablates the menstrual cycle. In addition Progesterone
or progestogen is needed to prevent endometrial hyperplasia in non-hysterectomised
women. Side effects include breast pain, nausea, weight gain, and skin patches may
irritate the skin. (5) Bromocriptine-
Inhibits the release of prolactin; used for treating breast tenderness or
mastalgia. Not widely prescribed. Side effects include nausea, constipation, headache
and dizziness. (17) Danazol-
Is a synthetic androgen used for the relief of mastalgia. It suppresses
ovulation, but long-term cardiovascular consequences and masculinisation outweigh
the benefits. (16) GnRH analogues-
Another drug that suppresses ovulation, found to have benefits.
However maximum treatment period is 6 months, and hormone replacement therapy
has to be given to prevent symptoms commonly seen in the menopause including
bone loss. (18).
Diuretics (e.g. Spironolactone)-
Usually used for weight gain, which includes water
retention. Long-term use not recommended. Side effects include potassium depletion
(not Spironolactone). (16,19) Selective Serotonin Re-uptake Inhibitors (SSRI’s)-
Used for psychological and
behavioural symptoms. 14 RCT’s showed improvements compared to placebo. Side
effects include nausea, vomiting, diarrhoea, dry mouth, anxiety, headache,
palpitations, dizziness and reduction in libido. Research is presently focussing on
using low doses in the luteal phase to reduce side effects. (10,16)
Mefenamic acid (Non-steroidal anti-inflammatory drugs)-
Current consensus in the
literature suggests is of benefit in somatic symptoms- headache and general aches and
pains but not for breast pain. Side effects include gastrointestinal problems. (16,20) Lifestyle Treatments
Frequent intake of carbohydrates
- Tryptophan levels in the brain are associated with
serotonin synthesis. Carbohydrates are said to raise these levels with a positive effect
on mood and cognition. Some women with PMS eat more carbohydrate during the
luteal phase, which may be an attempt at self-regulation of mood changes. (21) Other
research has shown no differences between glucose levels in PMS and control
subjects. (7) Caffeine and fluid intake
- A strong concordance between consumption of caffeine
beverages and PMS symptoms has been found. (22) However, the evidence from the
limited number of RCT’s does not convincingly support advice to reduce caffeine
intake and increase fluid intake. Alcohol-
Promotes a distinct fall in plasma glucose. One study found women with
PMS more likely to consume more alcohol in the symptom free period of the
menstrual cycle (22), which is in direct opposition to an earlier study which proposed
increased consumption of alcohol was a self-medicated attempt to alleviate PMS
symptoms. (23) However, the limited research in this area has focused mainly on
alcoholic women. Sugary foods-
Simulate insulin release, but differences in glucose levels between
PMS patients and control subjects have not been found; although it has been reported
that increased consumption of sugar, dairy, and refined carbohydrates have been
observed in PMS patients (25). Another study found that chocolate, beer, and fruit
juice had a strong association with more severe PMS. (26) B6 (Pyroxitine)-
Vitamin B6, may affect the liver clearance of oestrogen thereby
relieving premenstrual symptoms, and is widely used. Conclusions drawn from an
extensive review were that B6 was more effective than placebo in relieving overall
PMS symptoms and in depression associated with PMS, but it was not dose
dependant. There is no evidence to suggest that women with PMS have a lower
vitamin B6 status than do others (27). Magnesium (Mg)-
Different groups have reported lowered magnesium levels in the
blood cells of women affected by PMS (28,29). Dairy products and sugar, which are
taken excessively by some PMS patients, have been shown to interfere with
magnesium absorption and excretion (25). However the different doses used in trials
and inadequate information about absorption rates in humans, make interpretation of
results difficult. Zinc-
While studies have indicated lower zinc levels in PMS patients (29), none have
measured its effectiveness as a treatment for the symptoms. Calcium-
Has also been postulated to be the root of the pathophysiological
changes in PMS. A rigorous, well designed study of 441 patients, found that 55% of
women given calcium had a 50% global symptom improvement and suggests that
calcium may effect the monoamine metabolism, reversing serotonin dysregulation.
However another study did not reveal any significant differences in the concentration
of calcium in PMS and control subjects (7). Evening Primrose Oil (EPO)-
Women with PMS may have a deficiency of gamma-
linoleic acid (found in EPO), a precursor of prostaglandin E1 which may lead to
sensitivity to luteal phase prolactin and steroids (30). The current limited evidence
suggests EPO is of little therapeutic value in PMS. Exercise-
Although a clear physiological explanation is lacking, three RCT’s have
found that moderate aerobic exercise reduces negative mood states and pain, (16,31).
Hence there is more agreement here but there are methodological problems with the
Stress may exacerbate PMS. One RCT found a 58% improvement in the
relaxation response group in 46 women with PMS. (32) However another study found
no overall benefit.(33) Further research is needed. Complementary and Alternative Treatments
Proposes that spinal misalignment can produce neurological
interference, which can affect the health of the innervated part e.g. reproductive
structures. One case study reported a universal decrease in PMS symptoms, but is not
as reliable as a trial. (34) Acupuncture-
PMS is defined both aetiologically and patho-physiologically within
Traditional Chinese Medicine (TCM), which recognises groups of signs and
symptoms as a pattern of disharmony. The basic imbalance that causes PMS
according to TCM is Liver Qi Stagnation. The liver in TCM is responsible for the
smooth flow of Qi, and reflects the rise and fall of hormones in the endocrine system.
Diet, relaxation, and exercise are also said to benefit the liver and release stuck Qi,
hence they are included in this therapeutic model. Similarly Chinese Herbs are
administered according to the energetic imbalance in TCM theory. Many different
herbs may be used, and no one individual is likely to receive the same prescription
(35). Specific research measuring TCM’s effectiveness in PMS is lacking. Homoeopathy-
Many homoeopathic remedies for PMS have been listed, but although
homoeopathic physicians report success, there is little scientific evidence. One
placebo controlled double blind study failed to demonstrate the efficacy of
homoeopathic remedies. (36). Light Therapy
- Melotonin concentrations may represent a vulnerability factor for
depressive symptoms during the menstrual cycle and patients with PMS experience
substantial seasonal patterns in mood and premenstrual symptoms. A promising
preliminary study showed bright light therapy to have beneficial responses in patients
with PMDD. (37) Cognitive behavioural therapy (CBT)-
Five RCT’s measured its efficacy in treating
premenstrual dysphoric changes. One study found it more useful for symptom relief
than dydrogesterone, or relaxation therapy. A later study found cognitive therapy and
information regarding diet, rest and exercise given to the control group were equally
effective. Two other RCT’s, reported its effectiveness, whereas one found no benefit
A study of women’s perceptions
found that some types of massage therapy
were the most effective self help treatment for mood /anxiety, pain and water
retention. (15) However, no RCT’s have specifically investigated this area. Osteopathy-
Treatment of PMS includes manipulation of facilitated segments, at the
same level of innervation in visceral segments (reproductive organs). The
normalisation of musculoskeletal function is said to restore normal physiology
through reflex actions (38). Although there are no trials assess its effectiveness in
PMS Nutrition therapy-
Its efficacy in PMS has not been proven despite years of
research into individual nutrients, and the nutritional status of PMS patients.(25)
At present no specific research exists which examines the usefulness of individual
nutrition schedules created by nutritionists for PMS patients. What treatments did British Women use for their PMS and how
effective did they perceive them to be?
took part in the study.
• The five most commonly tried orthodox treatments were selective
serotonin re-uptake inhibitors (SSRI’s), progesterone, oral contraceptives, paracetamol, and progestrogen.
• The five most commonly tried lifestyle treatments were evening primrose
oil (EPO), less caffeine, B6, frequent starchy food, and exercise.
• The five most commonly tried non-orthodox treatments were massage,
osteopathy, homoeopathy, acupuncture, and cognitive behaviour therapy (CBT).
Table shows treatments perceived effective in the relief of PMS symptoms in over 60% of women who tried them.
CBT =cognitive behaviour therapy.
GnRH=Gonadotrophin releasing hormone. Overall rest, exercise, and massage were preferred to prescribed medication. In
addition women who tried complementary therapies perceived them to be
Where 50% of the women reported relief for a particular symptom it was recorded.
• EPO for painful tender or swollen breasts.
• Mefanamic acid or paracetamol for abdominal heaviness, discomfort or pain.
• Osteopathy and mefenamic acid for backache, joint or muscle pains, or
• Diuretics for feeling bloated, oedema and puffiness or water retention.
• SSRI’s, progestogen, and acupuncture for feeling under stress/ like you just
• SSRI’s, cognitive behaviour therapy and progesterone for feeling sad or
• Frequent starchy food, progestogen and a reduction of sugar for outbursts of
PMS is probably the consequence of numerous physiological changes involving
ovarian hormones, mineralocorticoids, prolactin, androgens, prostaglandins,
nutritional factors, hypoglycaemia, endorphins and other central nervous system
changes. As symptoms vary so much from woman to woman, it is likely that each has a different aetiology and all may be influenced by emotional factors. The findings of this study largely confirm previous research except for greater use of SSRI’s by women in this group. Despite this trend, a high proportion of these women perceived lifestyle adjustments- rest, exercise, less caffeine/ alcohol/ sugar, increase fluid intake, frequent starchy food, and evening primrose oil (EPO ),plus complementary therapies- massage, acupuncture, cognitive behaviour therapy (CBT), osteopathy, and light therapy as effective. It seems important from these results that more RCT’s are designed to isolate the effects of lifestyle adjustments and complimentary therapies on PMS symptoms. This future research is important due to questions raised about the long-term use of SSRI’s, such as whether efficacy is maintained, the emergence of side effects, or the re-emergence of symptoms, given the assumption that PMS is a long-term, cyclic and episodic disorder.
About the Researcher/ Author
Jo George. BSc (Hons) Acupuncture, Dip. Clin. Acu. (China), ICHT, Dip TTM
(Thailand), is an Acupuncturist, Aromatherapist, Reflexologist, Thai / Remedial
massage therapist, Reiki Master and assistant Swedish remedial massage tutor at The
University of Westminster. Gynaecology and obstetrics are areas of particular interest
for Jo. She runs a busy private practice in North London.
The Highgate Village Osteopathy Clinic. Tel: 020 8347 6160/ 020 8348 1777.
1. McPherson A, Waller D. Women’s Health. Oxford University Press.
2. Sadler D. A GP’s Perspective of PMS. NAPS. 31:4 . Summer 2000. 3. Steiner M. Premenstrual syndromes. Annual Review in Medicine. 48: 447-445. 1997. 4. Freeman E, Rickels K, Schweizer E, Ting T. Relationships Between Age and Symptom Severity Among Women Seeking Medical Treatment for Premenstrual Symptoms. Psychological Medicine. 25: 309-315. 1995. 5. Panay N et al. Premenstrual Syndrome- A Clinical Review. NAPS. 1-6. 1999. 6. Redei E, Freeman EW. Daily Plasma Estradiol and Progesterone Levels Over the Menstrual Cycle and Their Relationship to Premenstrual Symptoms. Psychoneuroendocrinology. 20 (3): 259-267. 1995. 7. Roca CA, Schmidt et al. Implications of Endocrine Studies of Premenstrual Syndrome. Annals of Psychiatry. 26: 576-580. 1996.
8. Cerin A, Colilins A et al. Hormonal and Biochemical Profiles of Premenstrual Syndrome. Acta Obstetrica et Gyneclogica Scandinavica. 72: 337-343. 1993. 9. Rubinow DR, Schmidt PJ. The Neuroendocrinlogy of Menstrual Cycle Disorders. NY Academic Science. 26: 576-580. 1995. 10. Halbreich U, Smoller JW. Intermittent Luteal Phase Sertaline Treatment of Dysphoric Premenstrual Syndrome. Journal of Clinical Psychiatry. 58: 399-402.1997. 11. Mortola JF. Issues in the Diagnosis and Research of Premenstrual Syndrome. Clinical Obstetrics and Gynecology. 35 (3): 587-600. 1992. 12. Gehlert S, Chang C. Symptom Patterns of Premenstrual Dysphoric Disorder as Defined in the Diagnostic and Statistical Manual of Mental Disorders-IV. Journal of Women’s Health. 8 (1): 75-85. 1999. 13. Campbell, EM, Peterkin DRN, O’Grady K, Fisher- Sanson R. Premenstrual Symptoms in General Practice Patients: Prevalence and Treatment. The Journal of Reproductive Medicine. 42 (10): 637-645. 1997. 14. Singh BB, Simpson RL. Incidence of Premenstrual Syndrome and Remedy Usage: A National Probability Sample Study. Alternative Therapies in Health and Medicine. 3: 75-79. 1998. 15. Pullon SR, Reinken JA, Sparrow MJ. Treatment of Premenstrual Symptoms in Wellington Women. New Zealand Medical Journal. 102:72-4. 1989. 16. Wyatt KM, Dimmock PW, O’Brien PMS. Premenstrual Syndrome. Clinical Evidence. 1: 286-297. 1999. 17. Andersch B. Bromocriptine and Premenstrual Symptoms: A Survey of Double Blind Trials. Obstetrical and Gynecological Survey. 38(11): 643-646. 1983. 18. West CP, Hillier H. Ovarian Suppression with the Gonadotrophin-releasing Hormone Agonist Goserelin (Zoladex) in the Management of the Premenstrual Tension Syndrome. Human Reproduction. 9 (6): 1058-1063. 1994. 19. Wang M, Hammarback S, Lindhe BA, Backstrom T. Treatment of Premenstrual Syndrome by Spironolactone: A Double Blind, Placebo controlled Trial. Acta Obstetricia et Gyneclogica Scandinavica. 74: 803-808. 1995. 20. Budoff PW. Use of Prostaglandin Inhibitors in the Treatment of PMS. Clinical Obstetrics and Gynecology. 30:453-464. 1987. 21. Christensen L. Effects of Eating Behaviour on Mood: A Review of the Literature. International Journal of Eating Disorders. 14 (2): 171-183. 1993. 22. Rossignol AM, Bonnlander H. Prevalence and severity of the premenstrual syndrome: Effects of food and beverages that are sweet or high in sugar content. Journal of Reproductive Medicine. 36: 131-139. 1991.
23. Caan B, Duncan D et al. Association between alcoholic and caffeinated Beverages and Premenstrual syndrome. The Journal of Reproductive Medicine. 38 (8): 630-636. 1993. 24. Halliday A, Bush B, Cleary P. Alcohol Abuse in Women Seeking Gynecological Care. Obstetrics and Gynecology. 68:322. 1986. 25. Goei, GS. Dietary Patterns of Patients with Premenstrual Tension. Journal of Applied Nutrition. 34: 4-11.1982. 26. Rossignol, AM, Bonnlander, H. Prevalence and severity of the premenstrual syndrome: Effects of food and beverages that are sweet or high in sugar content. Journal of Reproductive Medicine. 36: 131-139. 1991. 27. Wyatt K M, Dimmock, PW et al. Efficacy of Vitamin B6 in the Treatment of Premenstrual Syndrome: Systematic Review. British Medical Journal. 318:1375-1381.1999. 28. Rosenstein, DL, Elin RJ et al. Magnesium Measures Across the Menstrual Cycle in Premenstrual Syndrome. Journal of Biological Psychiatry. 35:557-565. 1994. 29. Posaci C, Erten O, Uren A, Acar B. Plasma copper Zinc and Magnesium Levels in Patients With Premenstrual Tension Syndrome. Acta Obstetricia et Gyneclogica Scandinavica. 73: 452-454. 1994. 30. Horrobin DF. The Role of Essential Fatty Acids and Prostaglandin’s in the Premenstrual Syndrome. Journal of Reproductive Medicine. 28:465-468. 1983. 31. Aganoff JA, Boyle GJ. Aerobic Exercise, Mood States and Menstrual Cycle Symptoms. Journal of Psychosomatic Research. 38:183-192. 1994. 32. Goodale IL, Domar AD, Benson H. Alleviation of Premenstrual Syndrome Symptoms with the Relaxation Response. Obstetrics and Gynecology. 75:649-655. 1990. 33. Kirkby RJ. Changes in Premenstrual Symptoms and Irrational Thinking Following Cognitive Behavioural Coping Skills Training. Journal of Consulting and Clinical Psychology. 62(5): 1026-1032. 1994. 34. Stude DE. The Management of Symptoms Associated with Premenstrual Syndrome. Journal of Manipulative and Physiological Therapeutics. 14(3): 209-216. 1991. 35. Deadman P. Acupuncture in the Treatment of Premenstrual Syndrome. Journal of Chinese Medicine. 48: 5-14. 1995. 36. Chapman EH, Angelica J et al. Results of the Homeopathic Treatment of PMS. Journal of The American Institute of Homoeopaths. 87(1): 14-21. 1994.
37. Anderson DJ, Legg NJ, Ridout DA. Preliminary Trial of Photic Stimulation for Premenstrual Syndrome. Journal of Obstetrics and Gynaecology. 17(1): 76-79. 1997. 38. Giovanna D, Eileen L, Schiovitz S. (eds) An Osteopathic Approach to Diagnosis and Treatment. 2nd Edition. Philadelphia: Lippincoh-Raven. Pgs 454-459. 1997.
Toronto Police Association (TPA) Toronto Police Services (TPS) AND IN THE MATTER OF AN ACCOMMODATION GRIEVANCE DATED DECEMBER 4, 2003 OF Tim Hill Kevin Whitaker, Sole Arbitrator Appearances for the TPA Beth Symes, Counsel Tim Hill, grievor Appearances for the TPS Glenn Christie, Counsel and others Hearings were held in Toronto commencing on January 31, 2006 and completed on May 16, 20
Unit 3A & 3B: Study Guide Compiled by your Table Captains Chapter 3A: The Neuron: Cell body -the cell life's support center Dendrites - received messages from other cells Axon - passes messages away from the cell body to other neurons, muscles, or glands Myelin Sheath- covers the axon of some neurons and helps speed neural impulses Terminal Branches - form junction with other ce