June 5, 2006
From the desk of Jane Galt:Department of missing data
A ways back, I meditated on the awfulness of the data available on the mechanism by which the morning-after pill (and by extension, the ordinary birth-control pill), prevents pregnancy.
Now, data on this sort of thing is hard to get. But it's not impossible to get; how come we don't have any?Well, nobody wants to provide it, that's why. Pharmaceutical companies manufacturing birth control sure don't want a study indicating that taking the pill causes fertilized embryos to slip the womb, since that would limit the market for their products. They don't have to do such studies--so why do it?
Now, a number of my liberal readers are no doubt rubbing their hands right now, saying "See! We can't leave research in the hands of private companies! The profit motive distorts it."
Um . . . yeah. So where are all the government studies on the numbers of abortions, the reasons women have them, the biochemical effects of hormonal contraception?
Why, we don't have them, do we? Because the government sure as hell doesn't want to put out a study that will make millions of women at least think twice about their so-easy, so-convenient, so-effective birth control. Why, they'd be storming Capitol Hill with pitchforks!
I had a chance to air this theory at a dinner party this weekend with some science-y types, where a throwaway remark about the birth control pill preventing ovulation led to an intense discussion over whether or not this was true. A British woman who had in a previous life done a graduate degree in biochemistry was stonkered by my casual assertion that the pill prevented ovulation; she had always heard that it worked by preventing implantation, and said that believing otherwise went against everything she knew about biochemistry. I was reduced to arguing that if the Pro-Life Physicians of America believe it prevents ovulation in most cases, it probably does.
But this launched us into a broader discussion of why, exactly, the matter is uncertain. It should not, said the other people at the party, be that hard to figure out. Having read how some of these tests are done on rabbits and rats, I wasn't so sure, but they maintained that it should be easy to discover whether or not a woman is ovulating without cutting her open to check.
My first theory was the one I stated above: we don't know because no one funding studies wants to know. Even European pharmaceutical companies are, AFAIK, doing research primarily for the lucrative (read free) US market; they certainly cannot have much interest in funding research that might cause millions of American women to stop using their product.
But what about European governments? They pointed out. They have no political worries, since no one (okay, almost no one) in Europe cares. Why haven't they done good studies to find out whether the pill suppresses ovulation?
Theories that have been advanced, some of which are mutually exclusive, and none of which have been even cursorily checked:
1) They have, and I didn't find them, because American pro-lifers can't read French, German, or Italian, and neither can American journalists looking for studies on how birth control pills work.2) The state of European financing for research is apalling, and this subject falls quite a ways down the list of topics their governments are willing to fund.
3) The only way to tell is to do microscopic analysis of a woman's fallopian tubes, which ain't going to happen
4) One sciency guy suggested that you could get around above by injecting some sort of tracer dye into a woman's ovaries and seeing whether it comes out in menstruation. My guess was that given that we already know that the pill is safe, and it works, an experiment that involved injecting anything into a woman's ovaries would never pass human subject review, or its European equivalent. Especially since I don't see how you'd find a single human cell 100 micrometers in diameter in several ounces of non-homongenous liquid without using something radioactive. But I have no idea what I'm talking about.
5) Human ovaries are too variable--or the fraction of total available eggs actually released over an average woman's lifetime too small--to discover whether a woman ovulates simply by totting up the number of eggs in the ovaries of longtime pill users
6) The average woman is on the pill for too short a time to have a statistically significant number of eggs suppressed from ovulating.
7) There are enough women on the pill long term that it would be possible to tot them up, but no one is interested enough in the topic to do a study which involves waiting for a bunch of young pill users to die of natural causes so you can take out their ovaries and have a look.
8) Someone is willing to do such a study, but the eggs in the ovaries disappear between menopause and death, and no one would sign up for a study that involved having your ovaries taken out as soon as you hit menopause.
9) Another possible means of detecting it--studying human ovaries in vats--is unfeasible, either because it's not possible to replicate the complex hormonal balance of the human body, or because the process requires a physical environment (such as proximate fallopian tubes) that cannot be realistically reproduced.
10) James Dobson's stealth operatives have infiltrated the EU.
All of which is a long-winded way of asking my readers (particularly the amazing Derek Lowe) to weigh in with any theories or knowlege they may have: why can't I find any solid studies to tell me whether the Pill works by supressing ovulation, or preventing implantation, or both?
Posted by Jane Galt at June 5, 2006 4:38 PM | TrackBack | Technorati inbound linksNow, these are by no means accurate studies...but...
Googling "pill ovulation" brings up:
http://www.wdxcyber.com/bcp.htm
http://www.womhealth.org.au/healthjourney/pill_myths_misconceptions.htm
http://www.ovulation-calculator.com/pregnancy/thepill.htm
http://www.studenthealth.ucla.edu/healthed/faq-contraception.html
And several thousand other pages which mention in passing that the pill prevents ovulation. No idea if these pages are correct though, but I'd assume this was the cause.
Which is funny, because I have a sister in-law who would never think of getting an abortion but is stuck in the "right to choose, it's my body" mindset, and uses the argument on me before that the pill prevents implantation, not ovulation.
Could it be possible that the reason is that the studies all pre-date the internet and have never been added to it? Remember, the pill came into common use in the 60's. I'm old enough to be aware of many facts that are old enough never to have made it to the internet. As much as tech savy people would like you to believe that the internet is the font of all knowledge, it just ain't so.
I think the reason the studies don't exist is because by the way the pill works, no study is required to check it. The pill tricks the body into thinking it is pregnant, thereby preventing ovulation. Wikipedia doesn't explain why, but it does mention that the pill works primarily by preventing ovulation (See Mechanism of action section).
Well, if the morning-after pill is really highly effective even taken five days after coitus (as you claim in the previous post) it can't possibly work by preventing ovulation can it? Sounds like it is preventing implantation to me.
From their website (FAQs):
ORTHO TRI-CYCLEN LO inhibits ovulation—the most fertile stage in a woman's cycle. Once a month, usually in mid-cycle, a mature egg is released from a woman's ovary into the fallopian tube. Once in the tube, the egg is ready to be fertilized by a man's sperm. While ovulation is occurring, the lining of the uterus begins to thicken in preparation to receive and nourish a fertilized egg.
If ovulation does not occur, your egg is not released, it can't be fertilized by sperm, and you can't get pregnant. By delivering an adequate amount of progestin and estrogen throughout your body, ORTHO TRI-CYCLEN LO stops ovulation from occurring. ORTHO TRI-CYCLEN LO also thickens the cervical mucus, making it difficult for sperm to enter the uterus, and changes the lining of the uterus to reduce the likelihood of implantation.
The above-post is for regular birth control pills. I'll keep looking for morning after pills. Seems they should work similarly, unless its more of a spermicide.
The pill works by calling Cthulu just enough that it can take weak souls within the body.
(This is a joke,obviously)
While not specifically about oral contraceptives of the combined or progestrogen only varieties, the quote from the textbook on this link suggests that 20 years ago it was not a major technical feat to recover ova (both fertilized and unfertilized) from menses:
http://www.managingcontraception.com/QA/show_item.php?item=672&type=qna
In two studies, researchers recovered ova from 14 women using four types of copper IUDs and from a control group of 20 women not using any contraception. [Alvarez - 1988][Ortiz - 1987] All women had intercourse close to the time of ovulation. Clear signs of fertilization were apparent in half of the ova recovered from the controls but none of the ova recovered from IUD users.
Bloody mess though it may seem to the casual eye, it's my recollection that as cells' go, an ovum is giant and has relatively distinct surface chemistry. Just on a mass basis there may be some simple kind of centrifuge extraction.
Presumably, one would have to track down the methods section of those Alvarez and Ortiz papers to assess things like error rates and so on. Either tracers were unproblematic or other ova recovery mechanisms aren't hard (and don't discount flourescing tracers that are inert until lit up with UV to pick out your ova). The small sample sizes of 14 and 20 and such suggest that either ova recovery failure rates are tiny or the referenced studies are some kind of embarassment to the peer review system. (for if the recovery failure rate is very high relative to 1/14 you wouldn't be able to conclude much at all.)
As a scientist, who makes the radioactive in radioactive drugs, I can see a few issues, practical and ethical, with a radiotracer-based experiment. To list the first of each type:
1) First, you want a chemist to spend his time making a tracer ligand which will target egg cells, when he could be targeting cancer?
(Yes, I know, you put that out as a straw-man knockdown arguement, I just thought I'd give it some substance before knocking it down.)
2) Granted, that could likely be done, eventually. Not sure how, but I spend my time on the physics side of the street, not doing chemistry/biology. So great, you can radiolabel eggs with great efficiency (hypothetically speaking, of course.) What does this mean? It means, most of your radioactivity is being focused on the one spot where it has the most potential to harm the next generation. This is where the ethics review board steps in. Even if the woman in question swears off kids forever, you have to give her the right to change her mind.
Trust me, a method to test this hypothesis with radiotracers is not viable. You won't get anybody to ask permission to pursue it, which is good, because they would never get that permission. So they can go back to looking for the next Prozac, which pays much better anyway.
James, sperm can remain alive for up to five days (I think in rare cases it's even been a few more), waiting for that egg to appear. I think that's what explains why Plan B is much less likely to work after three days, presumably because at that time the egg might have already appeared.
I don't think that there's any particular conspiracy going on. This information is actually pretty well worked out, and had to be before the pills could be marketed. My best guess on why this information seems hard to obtain is that it's contained in medical texts and journals, which aren't widely available in full text on the internet.
But PubMed has a good supply of them. In one of their online endocrinology texts, we have:
"The underlying principle of the combined estrogen/progesterone contraceptives is to suppress ovulation by negative feedback. Additionally, progesterone can exert direct anti-fertility effects on the female genital tract hence inhibiting implantation. Progesterone-only pills, which are taken continuously, or subcutaneous depot injections that release the steroid over a period of 8 weeks to 5 years, work principally by their effect on the cervical mucus and perhaps the endometrium preventing fertilization and implantation. Ovulation is also suppressed in about 20% of women taking progesterone-only contraception. Compliance is important for women taking oral progesterone-only contraception because its effects on the cervical mucus only last for about 22–26 hours, after which time fertility returns."
So both mechanisms you mention are correct - just for different types of steroid hormone contraceptives. The chapter goes on to say:
"Finally there are the post-coital contraceptives (inappropriately named ‘the morning after pill’) in which high doses of estrogenic contraceptives in combination with a progestagen, are given within 72 hours of unprotected sex and in two doses 12 hours apart. Their action is to interfere with the transport and implantation of a possible conceptus."
"Conceptus" is a word that I'm surprised isn't in greater use, given the sorts of arguments people have about this subject.
Those are the basics, but that brings up another possible reason that this information isn't found everywhere you look. Like most parts of endocrinology (as a guy, I'm tempted to say "like most things having to do with the female reproductive system"), the subject gets more complex as you go into detail. For that, here's a good overview from another PubMed textbook (FSH is follicle-stimulating hormone, and LH is luteinizing hormone):
"Oral contraceptives provide two hormones. The estrogens in birth control pills inhibit ovulation via the effect on the hypothalamus and the subsequent suppression of pituitary FSH and LH; inhibit implantation of the fertilized egg; accelerate ovum transport; and cause luteolysis, or degeneration of the corpus luteum, thereby causing the fall of serum progesterone levels, which prevents normal implantation and placental attachment. The progestins in birth control pills create a thick cervical mucus that hampers the transport of sperm; inhibit capacitation required for sperm to penetrate the cells and macromolecular investments surrounding the ovum; inhibit implantation; and inhibit ovulation by a subtle disturbance in the hypothalamic–pituitary–ovarian functions and by modification of the midcycle surge of FSH and LH."
There's a lot more where that came from. I've always been amazed that the human race reproduces as successfully as it does, personally.
RU486, the 'morning after pill': "A progestational and glucocorticoid hormone antagonist. Its inhibition of progesterone induces bleeding during the luteal phase and in early pregnancy by releasing endogenous prostaglandins from the endometrium or decidua..," its definition in Pubmed, the nlm or National Library of Medicine site, which has been indexing the medical literature for over 50 years. A recent American journal of Obstetrics and Gynecology article reports uterine 'collagen (connective tisue) breakdown in the uterus of rats' from its use. Reasonable to assume interference with implantation. It was synthesized by the Frenchman Etienne Emile Baulieu who still writes on it. BCP contain estrogen and progesterone, not a (-) progesterone. The chemistry or physiological effects do not suggest a similar mechanism of action. I was interested in the physiology of DHEA, another interest of Baulieu's.
Who _really_ cares?
If "the pill causes fertilized embryos to slip the womb", do you really think that millions of women are going to change their minds?
The pill is inexpensive, convenient and relatively harmless. The alternatives are all worse (from my male perspective).
I just don't understand your position on this issue...
Are you concerned about the millions of Catholics who may be committing 'murder' and not knowing about it? Do you see yourself as the one who is going to reveal the truth? Despite the Catholic Church's opposition to contraception, it is still being practised by millions of Catholics.
Or is this just curiosity about the mechanics of birth control?
I'm not Catholic, and I don't care _how_ it works, as long as it does. I can ask my wife, but I don't think that she cares, either.
The pill prevents ovulation as shown by the fact that you don't have a true "period" while using it, rather just breakthrough bleeding from stopping the chemical hormone. If you take the pill constantly, not using the one week of dummy pills but continue on immediately to the next pack, no period because no ovulation.
Depo Provera, Seasonale, et al., are the same hormone as the pill and work the same way--stopping ovulation, but because it's constant release, there's no fake periods.
Speaking of information that is hard to get, I'm having trouble finding fuel consumption and torque curves and data.
Anyone?
Ok...I didn't have such a hard time tracking down some things.
First, ovulation is prevented by the pill, "almost always", meaning >90% of the time. I could find no real studies by doctors to support those 60% figures.
Second, body temperature and hormone spikes as popularized by the rhythm method continue to be signs of ovulation, though the spike may be rounded out by the prescribed hormones.
Third, if that weren't enough, you can prevent cutting and get super high-res images with transvaginal ultrasonography -- though one might quip about how "invasive" that is, I think some kind of local cervical relaxant is all that's needed. (Wands need to be close to the target to get high-res the way ultrasound works.) These can at least be used to really test the hormone/temperature probes for ovulation in the presence of conceivably confusing hormones.
Fourth, the reasons for innacuracy are probably due to both diversity of prescriptions (some being below measurement threshold and some being order 10%).
Fifth, (due to 2nd) if Catholics/etc. care enough, they can check their own personal case and prescription via body temperature methods and follow up with blood samples, and if they're super sweet to the knowledge gathering industry report these to the drug companies or their doctor. That they don't but rather whine like wankers probably pertains to the question as to why there isn't "good data" here. Who's going to trust that? Still, it was a Catholic guy who developed the original pill. So, maybe.
Sixth, good data on a) ovulation is just an upper bound to the "chemical abortion" rate. You need good data on both b) the ultimate pregnancy rate [ not trivial to get in itself and the primary benchmark everyone really cares about like "fuel consumption and torque curves and data" (that made me chuckle). ] and c) inhibition of sperm by extra cervical mucus to back out an estimate for d) chemical abortions. (Effects a, c, and d are all thought to influence b from basic physiological observations, but a detailed quantitative breakdown is tricky, especially if c and d are low probability events...Imagine tracking the 1000 ovulations of 100 women looking for changes by 3 or 4 and ascribing meaning to the non-pregnancies of 3 or 4 ovulations.)
Often pregnancy is only about a 10..20% chance given no prevention anyway and may be less due to a muckier cervix. If there's even a factor of two reduction in this, and breakthrough ovulation is rare, then you might need thousands of women (per prescription) to even come close to a good estimate and then you start getting into tricky parts of scaling studies and having them all stay strict about the regimens and so on.
So, the full, detailed breakdown across a wide range of prescriptions and demographics might be exorbitantly expensive and blocked less by political will and more by practica extreme expense or impracticality kinds of issues. Maybe still related to economic incentives, but not so requiring artificial inflation due to the politicization of reproductive rights...explaining why Europeans haven't tracked it down in spite of a not completely infirmed (thank you) medical research community.
Seventh, I'd bet some drug companies do work on c) just for background knowledge related to new methods of contraception which given how lucrative they might be could be kept as proprietary information. Also, they're incentivized to, ahem, represent as generously as possible overall pregnancy stats, but there's probably some kind of watchdog/liability mechanism if they'e really bad.
So, the real reason for the estimate being a wide range is probably either the 4th or 6th points here unless people are specifically quoting particular prescriptions...they'll pick the "best" and "worst" overall kinds of strategy which misrepresents "uncertainty" anyway. But if you're worried about huge breakthrough rates you should be able to assess that personally. Ironic that only if the "scare mongering" scenario is false that the religious right would have to rely on the medical community here, no? That being said, even tiny .5% breakthrough rates that would probably be very hard to eliminate would correspond to about as many "chemical abortions" as surgical abortions. So, the personal monitoring can only really disprove the "nightmare scenario" of 95+% of abortions in the US being chemical. But if you're really a life-at-conception-er then you will almost surely have a problem with all hormonal contraceptives for the foreseeable future. Just seems hard to really get a bound dramatically less than 1/200 ovulations (once per most of the fertile lifetime of a woman...big variety of women, etc.) Just my own "foresight", of course. In any event -- since the really high breakthrough rate is easily detectable and not being reported (in my searches) in medical journals, it is probably safe to assume that it's on the lower side of the range for most women, but I bet you can check yourself, though you may need some period when you're off the pill to properly map out how your body responds to ovulation.
Oh, and eighth, "low dose" prescriptions are not necessarily more prone to breakthrough ovulation as is often assumed. I found a study which found "orthotricyclin lo" to be much better than ordinary orthotricyclin. At least, I assume "lo" means lower dosage. So, such comparative studies of ovulation, anyway, (just one piece to the chemical abortion estimate puzzle) do seem common enough in the literature. At least I found one in just a little bit of searching and I knew embarrassingly little about the whole issue to begin with. It's on a commercial site, so I can't link to it. 0/41 women had a breakthrough ovulation for o-lo and 3/36 for regular otc. Not sure how many cycles as I could only read the abstract. And that's percentages of women, not cycles, too. The per cycle rate is surely lower unless it just totally failed for some women.
Oh, and ninth, morning-after pill-wise, the presumption by most is that it works like the ordinary pill by blocking ovulation and there is some evidence for that in terms of the timing of its efficacy (you are behind the curve for cervical mucus and ahead of the curve for endometrial blockage, after all). It's probably pretty hard to get meaningful sample sizes there, too, though I didn't look for research in this vein. So, what happens with most such cases in medicine is that you get some half-assed sample size to compute some bound your customers and/or patients are happy enough with. If they start freaking out on you, it changes the incentive and that determines the size of the market and accuracy of the result. But constantly shifting prescriptions/sands/variety of women/a whole complex of physiological mechanisms also inhibits a super great answer.
A correction: RU 486 (Mifepristone) is NOT the "Morning After Pill" -- it is used for up to 49 days into pregnancy to cause a chemical abortion.
I think nobody's studying it because the primary mechanism of the Pill is so well-understood, and it's just not interesting for researchers.
In the normal female, ovulation is initiated by the release of a hormone called GnRH (Gonadotropin-Releasing Hormone) from the hypothalamus, which tells the pituitary to produce FSH (Follicle Stimulating Hormone) and LH (luteinizing hormone). FSH tells the ovary to start growing a follicle containing an ovum, and the follicle produces E2 (estradiol, a form of estrogen) as it grows. E2 stimulates the thickening of the uterine lining, and the rise in E2 levels tells the pituitary to step up output of LH, which causes the ovum to mature and release. LH also turns the remnants of the follicle into the corpus luteum, which produces progesterone (P4), the job of which is to transform the thickened endometrium slightly so that it's suitable for implantation of the fertilized ovum. If the ovum implants into the lining, it begins to produce Human Chorionic Gonadotropin, which tells the corpus luteum to stick around and keep spitting out P4; but without HCG, the corpus luteum dies, and the fall in P4 causes the endometrium to break down, and the woman menstruates.
A negative feedback loop exists between P4 (progesterone) and GnRH/FSH/LH production. As long as P4 is suitably high (and that there's nothing wrong with the receptors in the hypothalamus, or the pituitary, or anything else along that chain), the brain won't produce enough FSH to cause follicles to grow. Thus, the primary ingredient in hormonal birth control is progesterone, usually a synthetic form. The "mini-pill" is a progesterone-only pill, although combo pills containing estrogen are more commonly used, as the latter are protective of bone mass and more comfortable for many women, as well as being slightly more effective at squashing GnRH production (as E2 also plays a part in that negative feedback loop). Depo-Provera is a long-acting injection of medroxyprogesterone acetate, and modern IUDs usually also release progesterone to suppress ovulation.
A lot of things can go wrong with that feedback loop -- some women's ovaries are highly responsive to even small amounts of FSH, others still produce some GnRH unless progesterone levels are higher than caused by hormonal contraception -- and so it's not perfectly 100% effective. However, that's pretty much how it works, and it's reliable enough that further study probably won't produce more effective hormonal birth control, just different delivery mechanisms. There just aren't enough fascinating unknowns for reproductive endocrinologists to want to run studies, not when there are so many other mysteries in human reproduction. The only circumstances in which the Pill is interesting are: 1) political debates over abortion, which nobody wants to touch unless there's an ideological driving factor to begin with; and 2) determining whether the Pill reliably suppresses ovulation for usage in the context of in-vitro fertilization.
The morning-after pill is a little different -- all it does is artificially elevate P4 for a short period of time, and the subsequent drop in P4 levels initiates endometrial breakdown. It has to be done in a certain time frame after ovulation, because if the fertilized embryo implants (which usually happens 5 to 7 days after fertilization), the corpus luteum will be producing P4 in response to HCG, and thus the lining isn't shed and the embryo grows. This, too, is a pretty well-understood process, because we've been initiating periods for 30 years in women who don't have regular cycles by giving them oral or injected medroxyprogesterone acetate. It's one of the most routine things in gynecology, and the only thing new about it at all is the political aspect.
If you search Pubmed on "oral contraceptive ivf", you may find some studies which interest you. It probably won't be 100% clear-cut, because most IVF protocols use a GnRH agonist like Lupron to aid in suppression, but it might help.
However, I will also say that there is no medical difficulty in determining whether follicular growth and ovulation is occurring -- it's done every day in IVF clinics across the country. Transvaginal ultrasound is used to measure follicles, E2 levels are assessed to confirm follicle growth, and a P4 level of >5 on the 21st day of the menstrual cycle is accepted as the standard level for determining that ovulation occurred. (Also, contrary to CB's assertion, you don't to relax the cervix or anything, just stick the probe in and start counting follicles. It takes about 10 minutes, start-to-finish, and while I wouldn't exactly call it fun, it's a lot less bad than, say, egg retrieval for IVF.) Transvaginal ultrasound can also used to measure the corpus luteum and provide confirmation of ovulation. This is accepted methodology for confirmation of ovulation, and has been done in many, many studies.
(No, I'm not a reproductive endocrinologist -- I've just spent the last year going through infertility treatment of various sorts, thanks to some hypothlamaic/pituitary axis disturbances. It's amazing how much you can learn about reproductive biology when you're REALLY motivated.)
Perhaps you should consider option 11: You don't know where to look to find the relevant research.
Two minute of searching on Pubmed (I started with "hormonal contraception ovulation" as my search terms, and then clicked on the related articles link for the two or three most promising articles) turned up a good dozen articles addressing the mechanism by which both emergency contraception and birth control pills prevent pregnancy.
If you're really serious about engaging this issue, why don't you try familiarizing yourself with the scientific literature? It's not that hard to understand - a year of college-level introductory biology, and the willingness to take the time and effort to understand the technical terms being used will be enough to get you through the material.
Oh, I should have specified that what I said about the morning-after pill applies if it's taken AFTER ovulation. If it's taken before ovulation, then yes, it may disrupt the GnRH feedback loop and disrupt or delay ovulation, or it may not, depending on whether the LH surge is already in progress.
However, if ovulation has already occurred, the only way it can function is by preventing a fertilized ovum from implanting in the endometrium. The cervical mucus question isn't relevant in such a case, as sperm have already penetrated deeper into the reproductive tract before the hormones in the Pill begin to take effect.
Contrary to the link in Derek's post, it's now thought that P4 does indeed prevent ovulation from occurring, which is why I specified that P4 disrupts the *GnRH* feedback loop. E2 specifically inhibits FSH, yes (as E2 rises, FSH drops and LH increases), but P4 does inhibit LH, without which the final maturation and release of the ovum does not occur.
I'm rather certain that the hormonal interactions of the combined (estrogen/progesterone) BCP were part of my high school sex ed class. I think the mechanism by which it works has been fairly well understood since the late 50's.
The progestin only pills were relatively new and I don't recall them in the curriculum. However, many readers had much to say on them in the comments above. Learn something new every day. :)
One of the most interesting, and to me recently least known effects of the pill is that it kills libido!
http://www.guardian.co.uk/medicine/story/0,11381,1492378,00.html
Taking the pill could reduce women's libido, US scientists claim
Ian Sample, science correspondent
Thursday May 26, 2005
The Guardian
Women who take the contraceptive pill are in danger of permanently dampening their libido, according to a team of American scientists.
Researchers at Boston University Medical College found that women who take the pill regularly have much lower levels of the hormone that drives sexual desire. The hormone remains suppressed even when they come off the pill.
The scientists behind the study called on GPs to warn women of the potential danger before prescribing the pill and criticised the medical profession for handing out oral contraceptives "like candy". But the Royal College of General Practitioners moved to reassure women that the pill was safe and encouraged them not to shun the pill in light of the findings.
Taking the pill could reduce women's libido, US scientists claim
Ian Sample, science correspondent
Thursday May 26, 2005
The Guardian
Women who take the contraceptive pill are in danger of permanently dampening their libido, according to a team of American scientists.
Researchers at Boston University Medical College found that women who take the pill regularly have much lower levels of the hormone that drives sexual desire. The hormone remains suppressed even when they come off the pill.
The scientists behind the study called on GPs to warn women of the potential danger before prescribing the pill and criticised the medical profession for handing out oral contraceptives "like candy". But the Royal College of General Practitioners moved to reassure women that the pill was safe and encouraged them not to shun the pill in light of the findings.
Article continues
Claudia Panzer and Irwin Goldstein tested 124 women being treated for sexual dysfunction. Half used the pill regularly, 39 had just come off the pill and 23 had never used oral contraceptives.
The scientists analysed blood samples from all the women for traces of a substance called sex hormone binding globulin (SHBG). The pill makes the body over-produce SHBG, which mops up testosterone, the hormone that drives sexual desire.
The blood tests showed that women who regularly used the pill had very low levels of testosterone, but four times as much SHBG than women who had never been on the pill.
Further blood samples from the women who had come off the pill revealed that four months later, levels of SHBG had dropped but were still nearly double that found in women who had never taken oral contraceptives.
"What concerns us most is that the levels of SHBG show no sign of dropping any further in those who came off the pill," said Dr Panzer.
"You would expect levels to drop back to normal after about six weeks, but the worry is that these women will always have more. That means they will have very low testosterone, which has huge implications for their sexual function."
The researchers fear that levels of SHBG, which is produced by the liver, might be permanently raised in women who go on the pill, regardless of whether they later stop.
"I find this scary. Birth control pills are handed out like candy, but no one is told what the pill might do for a woman's sexual function," said Dr Panzer. "Doctors who prescribe the pill should tell women about the effect it might have."
The pill is the most common contraceptive used in Britain, with 26% of women between the ages of 16 and 49. The study, which is reported in New Scientist today, was presented at the American Association of Clinical Endocrinologists in Washington DC last week.
Dr Mayur Lakhani, chairman of the Royal College of General Practitioners, said: "I want to reassure women about the safety and efficacy of the contraceptive pill and to stress that there's no need to stop taking the pill as a result of this study. Loss of libido is a recognised side effect but in the experience of GPs and practice nurses this is uncommon among most women.
"I am unconvinced by this study; there is no cause for alarm. Women receive counselling as a matter of course when prescribed the pill."
Dr Lakhani added that anyone worried should discuss their concerns with their practice nurse or GP.
'Warn women of the potential danger before prescribing the pill and criticised the medical profession for handing out oral contraceptives "like candy"'
My wire stopped takening birth control after we realized it's probably not a good thing to be unnecessarily subjecting your body to daily bombardments of chemicals. Just because there's not a bunch of women running around with cancer as a result of the pill doesn't mean it's not affecting you in subtle ways that don't have any strong cause & effect link.
You brought that up at a dinner party? Yikes.
How very scientific of you. Are you agin it er fer it?
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Similar ideas re: the rhythm method....
http://www.futurepundit.com/archives/003496.html#003496
Researchers at Boston University Medical College found that women who take the pill regularly have much lower levels of the hormone that drives sexual desire. The hormone remains suppressed even when they come off the pill.
So...as a form of birth control, it's even more effective than we thought!
We already know how morning after pills work. Here's a simplified explanation.
First, the morning after pills often do nothing. That's because the woman taking them was not actually in the phase of her menstrual cycle where pregnancy can occur.
In a woman who could become pregnant, the morning after pills affect the endometrium in the uterus. The endometrium is the inner layer of the uterus that thickens and develops a rich blood supply in anticipation of successful implantation of a fertilized ovum. The cycle of endometrial development, thickening, breakdown, and shedding (menstruation) is controlled by a mix of hormones. Morning after pills contain huge amounts of hormones that disrupt the normal cycle and trigger endometrial breakdown even if a fertilized egg is available for implantation. The fertilized egg does not find a favorable environment for implantation and dies. (An event that normally happens to ~50% of fertilized eggs without any pharmacologic intervention.)
Pills that only prevent ovulation can not work as morning after pills, because in most pregnancies ovulation preceded intercourse. The sperm meets the already released egg (usually in a uterine tube). Anyone who claims that morning after pills work by preventing ovulation is mistaken or lying.
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