It’s starting. With the approaching 50th anniversary of the birth control pill, there will be a flood of anniversary celebrations and reviews of birth control methods. Which is good. We should have those discussions more often. Just say “no” (on the part of parents who don’t want to hear about it) is a big contributor to unwanted teen pregnancy.
Today’s Wall Street Journal is running an article called The Birth-Control Riddle. The riddle is apparently the high rate of unwanted pregnancy, despite the availability of a range of effective birth control methods. And, as befits the Wall Street Journal, each birth control method is accompanied by a price tag, so you can make an informed consumer decision.
But what I noticed was that there is no real awareness of what we at SMCR feel is an important consideration: Does your birth control method stop your cycle?
Some methods do – they deliver progestins and/or estradiol in high enough doses to act on the parts of the brain that normally make the hormones that talk to the ovaries that stimulate growth of a follicle, then trigger its release. This is a complex, whole body system, that normally we only notice because of uterine effects (that would be menstrual bleeding or pregnancy). And as a culture we have fairly casually accepted the idea that it is optional, and perhaps even optimally replaced by a pill made by a drug company.
When addressing the (no longer so) new extended use cycle-stopping contraceptive options, the WSJ glibly explains that “Experts say there is no health reason that women need to have a period if they are not ovulating or building up uterine lining each month.” In other words, so long as your uterus is not endangered (by pregnancy or endometrial cancer), there is no worry. Never mind that both estrogen and progesterone act on receptors throughout the body (bone, skin, blood vessels, brain, gut, breast), or that the synthetic estrogens and progestins don’t quite act in the same way, and we don’t quite completely understand how yet. And it’s just a change of schedule, so what difference can it make that your tissues are stimulated for 12 (or 52) weeks at a time instead of 3 before they get a break?
The problem is, with changes in the schedule of delivery and the reduction in hormone-free time, we really won’t know whether there are any consequences for a while. Oral contraceptives are taken by healthy young women, so the base rate of problems is low, and you need large numbers to measure the rates of serious side effects. I haven’t heard any further about the post-marketing surveillance studies for blood clots (venous thromboembolism) that the FDA asked Lybrel to conduct following its 2007 approval. But those 5-year followup data should be out around 2013. It will be interesting to see whether they are published, or just submitted as a report to the FDA. I’m guessing that will depend on whether the company likes the story they tell.
In addition, there’s increasing evidence that the effects of the pill vary with your age and the maturity of your hormonal system. So, for young women, it is looking more and more as though the pill is bad for bones, slowing or stopping the accumulation of bone mineral during teens and twenties. And maybe you can make that up after you come off. But many women never come off, replace their hormonal cycle with a pharmaceutical cycle for literally decades. And shouldn’t we be a bit concerned about that? At the other end of the reproductive life cycle, it’s important to know that the large safety trials exclude older women. Regulators want contraceptives tested on fertile women (which makes sense), but that means that safety trials usually cut off at 35 or 40. And as you get older, your chances of blood clots and strokes goes up anyway, so even if the relative risk were the same, the absolute risk (the number of new events) is going to go up with age. We do know that smokers who are over 35 are at very high risk. Continue reading...