第６弾　MEとホルモン

broadcast on December 7th, 2012

In general, we can say that the hormonal changes in ME are probably fully secondary. In other words, the result of an underlying mechanism, rather than being primarily at the core of the disease.

I very much want to argue against those colleagues who only treat the hormonal abnormalities. Because that way you don't actually treat the core of the disease, and you can also cause a lot of damage.

Having said this, the problem of hormonal abnormalities is probably rooted in what we call the hypothalamus. Due to various reasons, such as blood flow, neurotoxins and inflammation, the hypothalamus is in a kind of hibernation state. Like a bear in winter. Who also reverses his hypothalamus. And we know that the function of the hypothalamus can be reduced in different ways. The question is whether this is a protective mechanism or just the result of a number of underlying mechanisms. But if the hypothalamus does not function normally, neither will the pituitary. This is the gland situated at the lower end of the brain and that produces hormones, which control a lot of the organs in the body.

So we are looking at three levels here. But I think the problem is mainly situated at the first level. Because when we look at other organs producing hormones, we don’t always see intrinsic problems there.

The problem has mainly to do with the hypothalamus. To illustrate this I can say that there are two hormones that are produced directly in the hypothalamus, and nowhere else within the body. The most important one is ADH, the antidiuretic hormone, the hormone that is needed to concentrate urine. We observe the activity of ADH becoming very low at a certain point during the disease. That’s why people have to get up four or five times a night to urinate. Because there is too little of this hormone to be able to concentrate the urine. Consequently, patients’ concentration of urine is very low. Normally, urine is four times more concentrated in the morning than during the day, which is when you drink a lot. This is then already an indirect indication that there is a problem at the level of the hypothalamus.

The other hormone that is produced by the hypothalamus, oxytocin, seems to be present in a reduced quantity too and seems partly responsible for a change in the behaviour of some patients. They are more introspective, which is sometimes described as being autistic. That may be linked to a reduced production of oxytocin. Quite a few doctors prescribe standard nasal sprays containing ADH and oxytocin. These are extremely small molecules that can easily be administered as a medication; as a nasal spray to prevent having to get up at night to urinate. In other words, a substitute is administered.

Moreover, we know that ME patients suffer from many thyroid problems. These are also concerned with hypothalamic abnormalities; but also with the auto-immune phenomena that occur in ME patients. The adrenal gland produces too little cortisol, so we’re not dealing here with Addison’s disease – an autoimmune disease of the adrenal gland itself. The adrenal gland is probably poorly stimulated by the pituitary gland, which in its turn is controlled by the hypothalamus. This has been demonstrated in a number of studies.

We also see significant changes in ME patients in terms of the male and female hormones. Often, with men there is a progressive decrease of testosterone that doesn't correspond with aging, but develops much faster. In women all sorts of cycle disorders arise, which has to do with changes of pulsation. The hormone in the brain that is responsible for regulating the menstrual cycle no longer has its normal pulsations. That’s because it is not produced in a constant stream. It comes in pulses and if an abnormality occurs in those pulses, we also see changes in progesterone and oestrogen occurring during the menstrual cycle.

Additionally, inflammation plays a role here. Many of our patients suffer from a very intense PMS, premenstrual syndrome. This has to do with changes in the prostaglandin metabolism.

And then there’s also the question of why more women than men suffer from ME. My experience is that gender makes no difference, and in my practice we have at least 400 children under the age of 12. Up to the age of approximately 12 or 13, the ratio is one to one. After that the difference progressively extends to about four to one. Four women appear for consultation for every man. This is probably caused by various factors.

The immune system plays an important part in this, because oestrogens weaken a certain part of the immune system. Which is precisely the part that is essential to control bacteria living within the cells, the so-called intracellular bacteria, and to control parasites and viruses, like herpes viruses, which are already present within our body. That is what we call the Th1 immunity. Testosterone stimulates Th1 immunity. Oestrogens, however, weaken the Th1 immunity, so that the T-helpers – the type 2 cells – eventually become more prominently active. We know that there is a very clear effect on the immunity. This is also a known fact outside ME research.

We see this deviation quite clearly, in such a way that predominantly from the age of 12 to 13, we see more and more women with this condition. So the type of person that we see during the consultations is a woman of an average age of 37. Because the strongest oestrogen activity occurs in the ages between 12 and 50.

An additional argument for example is pregnancy. During pregnancy, HCG is released, which is a hormone that testosterone. Many women with ME feel somewhat better during pregnancy, but immediately after pregnancy we notice a strong relapse. And as with MS, we see that three to six months after pregnancy spells of the disease occur (and this has not yet been reported but it’s an observation we have made). And that too is most probably multifactorial. But hormones play a part in this too.