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Premenstrual Syndrome – A Proposed Explanation

The premenstrual syndrome and ovarian dysfunction is a subject that has defied clear explanation for many years and at least well antedating the efforts of Dr Katherine Dalton, who treated the condition in the 1950s in London. The treatment was with progesterone that was subsequently shown to be ineffective in double-blind trials. Nonetheless, Dr Dalton achieved a certain reputation, if not notoriety, for her efforts and I think probably demonstrated the power of placebo response in attending to this vexed question. The secret, of course, to detecting a placebo response is whether or not the treatment benefit extends beyond the six months that usually is the time within which the placebo effect expires. Hence, naturopaths are wont to say that they administer “courses of treatment” and that when one “course of treatment” becomes ineffective, then they set up a second course of treatment and everybody benefits from the placebo results.

I used to hate dealing with premenstrual syndrome, simply because I didn’t understand it and I didn’t have a suitable treatment available for something I didn’t understand. In due course, I took time out to consider the symptoms and clinical signs at my leisure and evolved what I termed a “model of understanding” of the condition on which I then instigated a treatment schedule. My model of understanding was that the mid-cycle ovulation was either absent or impaired, so that luteinisation of the follicle does not occur effectively: and so the follicle simply keeps on growing and the oestradiol secretion level does not undergo the characteristic mid-cycle decline, as would be the case in a normal cycle: either that or there may be the development of multiple follicles again with impaired luteinisation. The oestrogen level, therefore, continues to climb through the menstrual month, until the end, at which time the oestrogen levels may achieve toxic levels. Since the length of the month is not regulated by ovulation, it can be a variable length, both short and long and because there is no luteinisation of the endometrium the blood loss can be very heavy and prolonged. The excess oestrogen in the last seven to ten days of the month is characterised by a series of symptoms, which I will describe below.  

At the same time that the oestrogen production is excessive, the progesterone disappears entirely and so does the testosterone, both in terms of production and availability that is controlled by the oestrogen stimulation of the sex hormone binding globulin. So the woman has oestrogen toxicity with progesterone and testosterone deficiency. Replacement of progesterone, as I have already indicated, has historically been shown to be ineffective. The use of the oral contraceptive pill, to some extent, can be effective, but adds more oestrogen to a situation that is already oestrogen replete. Administration of testosterone, however, I believe, dampens the rate of follicular growth by direct suppression of the ovary and, at the same time, and most usefully, replaces that testosterone which has been lost and a deficiency that can be shown to be clearly symptomatic. As the hormonal status returns to normal, the degree of bleeding is reduced, both in duration and in volume, and allows the woman to avoid the hysterectomy that is so often done for this condition on indications that are contrived and not truly causative. It is all very well undertaking the hysterectomy to stop troublesome bleeding and pain, but the symptoms of ovarian dysfunction continue post-operatively.

The symptoms of the ovarian dysfunction and premenstrual syndrome, are those of abdominal bloating, swelling of the hands and feet, temporary weight gain and menstrual diuresis, menstrual headache/migraine, enlarged sore breasts, and significant mood upset. The mood upset can be towards anger or tears or both. The number of these symptoms that a woman may experience and express may not be a complete list of symptoms but may be some of them, with others absent. For example, there seem to be some women who are subject, particularly, to fluid retention, in which they give evidence of swelling in the hands and feet, abdominal bloating and facial swelling. Others have none of that at all and don’t even have a menstrual diuresis. One woman at least had trembling with her cycle at the time of menstruation that was labelled as “orthostatic tremor”; she was also prone to anxiety.

At the same time, the symptoms of testosterone deficiency are quite pronounced and in the order of priority, as decided by the patients (not the doctors!), both male and female are as follows. Mood upset to a variable status with tears and/or anger, loss of energy, poor stamina, impaired concentration, deteriorating memory, lack of decisiveness, enlargement and soreness of the breasts, loss of libido, loss of clitoridal sensitivity, dry and irritated vulval skin, dry facial skin, loss of muscle strength, and soreness in the neck and shoulders. These are highly characteristic testosterone deficiency symptoms and the order of priority should be noted, particularly as most doctors perceive testosterone deficiency to be intimately, if not exclusively, related to the loss of sexual drive. While this does occur, it is not by any means the most important symptom.

The glitch about this idea is that the pathology doesn’t support it. Very frequently the testosterone levels are gratifyingly suppressed with a raised SHBG but the oestrogens are normal or low even when taken late in the cycle. Maybe the excess oestrogen is not inevitably oestradiol that we conventionally measure.

What is worrying about the premenstrual syndrome is that recurrent stimulation of the breasts, to the point of soreness, and leads one on to wonder whether these women are being set up for the hormonal instigation of breast cancer. These cancers in younger women are so characteristically likely to occur in excessively stressed individuals leading a frenetic existence, who are more likely to develop ovarian dysfunction that is so simply treated.

Certainly, in my publications and now others, I have shown in a modest manner that testosterone appears to reduce the breast cancer incidence to below normal. This, I hasten to say, is very far from proven and is based simply on retrospective observational studies. The reference to those studies is as follows.

http://menopause.com.au/files/ABC_Study.pdf
http://menopause.com.au/files/ABC_Study_Editorial.pdf
http://www.ncbi.nlm.nih.gov/pubmed/19453875

The thought occurs as to whether mammographic density studies may be a discriminatory investigation in terms of both diagnosis and a measure of the success of treatment

The other thought that comes to mind is the question of endometrial cancer (cancer of the lining of the womb). This is a hormonally dependent cancer just as the prostate in men is a hormonally dependent cancer. If a doctor was unwise enough to give hormone replacement in the menopause with oestrogen but no progestogen then the incidence of endometrial cancer rises steeply. In PMS/ovarian dysfunction it may be assumed that ovulation fails and that there is no normal production of progesterone. It could be worth enquiring into whether the incidence of endometrial cancers is increased in this condition. Certainly the menstrual loss may be irregular, prolonged and heavy.

With the administration of testosterone in whatever dose that is required to be effective, the syndrome comes under control, the symptoms all but disappear and the cycle becomes regulated with a shorter, lighter bleed. As the administered testosterone level begins to decline at the four months following implantation, the symptoms tend to start to recur; a further testosterone implant can then be administered and suppression of the ovarian dysfunction may continue. At least in the untreated state the premenstrual syndrome may improve, as a woman travels through her late 40s, since during those years ovarian function may start to fail and with that failure there comes a failure of the ovarian dysfunction as well, with some amelioration of symptoms. The woman becomes quite joyous at the prospect of becoming well again, only to be downcast when the menopause arrives and she may then be troubled with menopausal symptoms.

This condition is not insignificant, in that I meet women who have had the problem for 30 years, perhaps, and who have exhausted the doctors in their attempts to find a solution. Whether it goes so far as for the woman to commit suicide, I am uncertain but I am well aware that the woman suffering the premenstrual syndrome may be provoked into homicide, or at least attempted murder of her partner. These were the sort of women whom Katherine Dalton was defending in court when they became arraigned.

Some of these women say that the problem started after the birth of their last child. That is too common a history to be ignored but, as yet, I have no clear understanding of what event might have occurred in a final pregnancy to set the ovary off on its miscreant course. A proven understanding of the original cause could be useful in contributing to a more complete understanding of the whole condition. In some ways, I believe there is more that I don’t understand about the condition than I do understand but that status, I believe, is the mark of an educated woman.

Guest post by Dr Rosemary A. JONES
Adelaide, South Australia