Polycystic ovary disease.
This is a condition that is poorly understood and not
well treated, if one is to believe the 'net chat'. There
are some fresh concepts that assist in the efficient
treatment of this condition. These women inevitably
suffer 'insulin resistance' and dietary modification
with adequate exercise results in the eventual
control of symptoms. Sometimes there may
be the need for diabetic like medication or indeed ovarian
stimulation drugs for the woman seeking pregnancy.
To make the diagnosis there may be a need for
MiniSite* laparoscopy. This is a 2mm telescope that
allows a good view of your organs with no more than a
needle prick puncture. Using the same instrument,
the abnormal cysts in the ovary may be punctured and drained.
Pelvic pain including Endometriosis.
This requires meticulous evaluation including the
use of ultrasound imaging and diagnostic
laparoscopy. This laparoscopy can be achieved by
the use of the MiniSite* which is a new scope no
wider than a broad bore needle, resulting in
minimal post-operative discomfort. Endometriosis is
a common cause of pain. This is a damaging
disease and the earlier dealt with the better. It can
result in damage to your fertility, chronic sexual
difficulties and upset to bladder and bowel function.
It is more common in a woman who has never given birth
but it is a disease that can persist after pregnancy
and indeed into later life when it may start to cause
serious damage. Widespread endometriosis can be
very difficult to deal with surgically and is
optimally approached with the laparoscope.
An proposed explanation of the ovarian dysfunction state, giving rise to the premenstrual syndrome.
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. That 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. 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 one 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, 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, 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.
At the same time, the symptoms of testosterone deficiency are quite pronounced and in the order of priority, as decided by the patients, 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 at the most likely time in cycle. Maybe the excess oestrogen is not 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 in excessively stressed individuals leading a frenetic existence. Who is more likely to develop ovarian dysfunction and yet 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.
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 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. 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 that 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.
Dr Rosemary A. JONES
10th March, 2009
edited 10th May 2011