Part 2 in this series
Research has been busy studying sex hormones and their effects on Parkinson’s disease for a long time now but the impact PD has on menstruation, menopause, HRT treatment and pregnancy is very much an unknown factor for most people (including me!) so here we go trying to find scientific study results to inform and educate us.
Hold on a minute! Parkinson’s is an old person’s disease so there won’t be any problems such as those above. The truth is yes, it is predominantly an old person’s affliction but between 3 and 5 percent of women diagnosed with PD are below 50 years of age and their monthly cycle is still regular or they are experiencing peri-menopause or menopause. It is these women that struggle to cope for 1 week or so every month as their PD medications fail to control their symptoms.
Typically, during their periods women have described an increase in Parkinsonian symptoms with a noticeable drop off in the ability of their medicine to control their symptoms. Off spells last longer, cramps are severely painful and the loss of blood increases. Sleep disturbances are worse, bloating and weight gain are more problematic and fatigue feels more ‘ground in to their bones’ than usual. To have to go through this year-in and year-out for up to 30 years or more of their life is not a prospect that women would see as having any redeeming features at all.
The problem seems to be the outcome of hormonal levels changing gradually for 3 weeks then much more so for the week where a period takes place. If these fluctuations could be smoothed out it seems obvious that the PD drugs would work better. But is it obvious? We know PD is often contradictory and even when we stick to our times to take our medications we cannot guarantee consistency of effects from day to day.
Going back to the PD study above, a few of the women involved were using contraceptive pills which work by altering the hormonal environment internally so that pregnancy becomes well-nigh impossible. These women still experienced variations in their bodies similar to the group not using contraceptives but the intensity of the fluctuations were significantly reduced.
The use of regular exercise and relaxation techniques can be of help to decrease symptoms and improve the ability to cope.
Parkinson’s Disease and Pregnancy
Compared to the studies on PD that are piling up at the rate of 100-PLUS PAPERS PER WEEK (!) there are only a very limited number of studies on pregnancies in women with Parkinson’s (remember only 3 to 5 percent of women with PD are below the age of 50) and that seems unlikely to change.
Okay, what these studies have shown can be summarized below: During pregnancy both motor and non-motor symptoms become more severe but rarely bad enough to spoil life. Non-motor symptoms such as constipation, fatigue and depression seem to improve after giving birth but motor symptoms (rigidity, tremor and slow movement) continue to progress downhill as before.
Data analyses show that the more time estrogen levels are elevated between puberty and menopause, the greater the decrease in risk of actually getting PD becomes. In its customary contradictory form PD studies on pregnancy indicate the opposite; more time pregnant increases PD risk! The guess at the moment is that estriol (estrogen in its pregnancy state) is different from estradiol (the menstrual form of estrogen). For many women the use of anti-Parkinson’s drugs when pregnant is a potentially damaging situation for the foetus. What does the evidence show?
Some dopamine agonists seem to be safe for the unborn child but block milk production so the mother is unable to breastfeed. Other Parkinson’s drugs have a category C rating which is given when animal experiments suggest some risk but no human studies have been done or published which would confirm or refute that risk. Amantadine is the only PD medicine that caused heart malformations in babies that were exposed to it during the first trimester of pregnancy.
Women with PD generally are as fertile as those without PD but many suffer self consciousness that leads them to avoid going out or mixing in social occasions and also makes sexual intimacy very difficult to deal with.
It was previously noted that women usually develop PD later than men so most women with PD are post-menopausal. Research using a rat model of PD has shown a slow decline in dopamine cells that matches losses during menopause. The answer to that is HRT (Hormone Replacement Therapy) as rats with their ovaries removed improve considerably on HRT. But NO! The contradictory nature of PD has women in studies showing only some or even no benefit from hormone replacement. This is a timing problem as rats given HRT within 10 days of losing their ovaries saw no increase in the rate of loss of dopamine cells. Rats that started on estrogen therapy after 30 days suffered more rapid loss of cells and the hormonal therapy did not benefit them.
The few studies that compared the impact of HRT on Parkinson’s disease progression have been mildly positive. Women using hormone replacement reported more “on” time and lower UPDRS functionality scores than non-estrogen users. Unfortunately the number of women tested is too low to make a solid case for hormone replacement in women with PD.
In summary, we have a better understanding of the impact of sex hormones on the development and progression of Parkinson’s disease. Recent studies suggest that there is an inverse relationship (i.e. more estrogen equals less risk of PD) between lifetime estrogen exposure and the risk of developing Parkinson’s disease. It has also been shown that fluctuations in hormone levels will result in changes in disease control and result in the need for changes in symptom management during menstruation, pregnancy and menopause.
Hopefully, I will be able to find more research that could lead to new treatment options for women with Parkinson’s disease.