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WHAT CAUSES THE PMS?

I well remember one evening in the country town of Grafton, NSW, relating the Hippocrates theory on the causation of PMS to an entirely male audience who had come to listen to my after-dinner talk about "How To Be A Perfect Husband''. My mother had got me into this rather sticky situation as she had delighted in 1 'setting me up'' when the Lions Club had requested my presence.
As I related that Hippocrates had blamed a wandering uterus that travelled up to the brain and disturbed the emotions, a little man at the back of the audience became wide-eyed and intrigued. I further related that Hippocrates' treatment for PMS was to entice the wayward uterus back into its rightful position in the pelvis by burning aromatic incense at the vaginal opening. At this juncture the same man's jaw fell open and he looked relieved. After my light-hearted dissertation, he came to me and whispered in my ear saying that he had problems at home and did I have any incense for sale!
After Hippocrates, it took until 1931 for doctors to realize that hormones had something to do with PMS and a certain Dr. Franks preached the theory that too much oestrogen caused PMS. His treatment was more drastic than that of Hippocrates as he recommended large doses of laxatives to flush the demon hormones out of the body. Dr. Franks claimed great success with this treatment which is little wonder as the violence of the resulting diarrhea was enough to drown out all the other woes of the PMS victim.
Some women even had their ovaries subjected to radiation and consequent destruction in a desperate attempt to end their PMS
There is no doubt that the cyclical fluctuations in the levels of the sex hormones oestrogen and progesterone manufactured by the sex glands (ovaries) play a large role in causing PMS. This is supported by the observation that PMS begins only after puberty, recurs on a monthly basis and disappears during pregnancy and after the menopause. You will see that the pituitary gland situated at the base of the brain controls and speaks to the ovaries by sending chemical messengers called Follicle Stimulating Hormone (FSH) and Luteinising Hormone (LH) via the blood stream to the ovaries. FSH and LH stimulate the ovaries to manufacture both oestrogen and progesterone. Ovulation occurs when an ovary releases a mature egg and the cells left behind in the ovary then form a small yellow gland called the corpus lustrum which sets to work and pumps out progesterone. It is after ovulation in PMS sufferers that the fireworks begin. In a woman without PMS, the levels of oestrogen and progesterone remain in sufficient and balanced amounts between ovulation and menstrual bleeding. In a woman with PMS, the levels of oestrogen and progesterone are out of balance with insufficient oestrogen and/or progesterone between ovulation and bleeding.
Some researchers believe that it is the ratio of oestrogen to progesterone that is more important than the absolute amounts of these hormones. They have found that women who have too much oestrogen compared to progesterone have anxiety, while women with too little oestrogen compared to progesterone complain of depression during the premenstrual phase.
Indeed, there are many subtle variations in the levels of sex hormones produced from the ovaries and a whole range of imbalances in all three ovarian sex hormones, oestrogen, progesterone and testosterone are probably involved. This accounts for the variation in PMS symptoms between different women and between different cycles in the same woman.
The study of female sex hormones is called gynaecological endocrinology and it is a relatively new medical specialty with still much to explore and learn. We stand at the frontier of an explosion in the understanding and scientific discovery of how imbalances in sex hormones influence our mind and bodies. PMS is truly a Pandora's box and we have now dared to lift the lid so that one by one the hormonal demons will be tamed and controlled.
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EPILEPSY AND PREGNANCY

Women with epilepsy are quite often concerned about getting pregnant. There appear to be five reasons for this concern. They wish to know:
if they are likely to hand their epilepsy on to their children;
whether their fits will get worse during pregnancy;
whether it is safe for the baby that the mother should take anticonvulsants drugs during pregnancy;
if there will be any problems in the newborn baby from these drugs;
if they can safely breast feed the baby.
With regard to handing on epilepsy to one’s children – as mentioned earlier, if one parent has epilepsy, the chances of one of the children having epilepsy are no greater than in the population at large. If both parents have epilepsy, it would appear that the risk of a child having epilepsy is about 10 per cent. So in fact the chance of a child inheriting epilepsy, particularly idiopathic epilepsy, is negligible.
As far as seizures during pregnancy are concerned, the situation is not as clear as it might be. There is evidence that for some women, seizure control may deteriorate, while for others there may in fact be no change or even an improvement. A patient told me recently that “she would like to remain pregnant forever” as she had not had a single fit during her pregnancy, compared with six fits in the preceding nine months!
As a general working rule, it is suggested that people who have more than one grand mal fit a month are those who are most likely to have a deterioration in seizure control during pregnancy. The deterioration, if it occurs, is most likely during the first three months of pregnancy. There are a number of theories why this may happen, but none has been proved. It may be of value to check the blood anticonvulsant levels during pregnancy, especially if there is a deterioration in seizure control. The blood levels may fall, necessitating an increase in dosage during the pregnancy.
The main concern for parents is whether the anticonvulsants can harm the unborn baby (foetus). It is known by most people with epilepsy that this is a potential hazard. The effects include physical abnormalities in the baby, a process known as teratogenesis. Abnormalities have been reported in the offspring of mothers on all the commonly used anticonvulsants with the exception of carbamazepine. This is particularly applicable to phenytoin, barbiturates and sodium valproate. Babies born to mothers who have been on carbamazepine have not been shown to have any physical abnormalities, but have a smaller head size than other babies. This has not been shown to be any handicap to the babies who have been followed up for five years.
The risk of abnormalities in the baby is difficult to assess, but it seems to be most common in mothers on polytherapy (receiving numerous drugs), especially if they are on three or more anticonvulsants. The risk in mothers on phenytoin, with or without other medications, appears to be about a 10% chance of the baby showing features of the ‘foetal hydantoin’ syndrome. This syndrome consists of cleft palate, abnormalities of the fingers, possible heart abnormalities and mild mental retardation. Thus, at present, if it is possible, it would seem wise to try to change patients over to carbamazepine before conception. This may not be possible in all patients and, of course, many women will first visit their doctor when already pregnant, at which time there is no purpose in making the change.
Anticonvulsants taken by the mother during pregnancy may have some effects on the baby immediately after birth, as they are transmitted to the baby across the placenta. These include the possibility of a mild bleeding tendency and some drowsiness. In mothers who have been taking barbiturates, the infant may occasionally show features of a withdrawal reaction with irritability, jitteriness and poor sucking. None of these features is [...]

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ERECTILE DYSFUNCTION SYMPTOMS

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