Friday, June 24th 2011
|Found here. IUDs are back in style.
Neon sunglasses? Not so much.
What is used by 20-26% of European, 30% of Israeli, 34% of Chinese, 34% of Egyptian, and 49% of Korean women… but only 1-2% of US women (Harper et al. 2008)? The intrauterine device, or IUD! The IUD is found in two forms: the copper IUD, and the hormone-releasing IUD that releases a tiny amount of progesterone. Both make the uterus inhospitable to pregnancy.
The modern incarnation of the IUD is possibly safer and more effective than oral contraception. Chances of pregnancy on the IUD range from 0-1.1 per 100 woman-years of use, and they get lower with each year you use it (Prager and Darney 2007). That is far better than your chances on the pill.
The IUD suffers from a bad reputation, in part due to misinformation or misunderstanding on the part of medical providers. Harper et al (2008) surveyed 816 physicians, nurse practitioners and physician assistants who each serve more than 100 contraceptive patients per year in the California State family planning program. They found that 40% of medical providers didn’t offer IUDs to patients, 36% provided infrequent counseling. Further, 46% thought nulliparous women, and 39% thought postabortion women were good candidates for the IUDs. Younger physicians were more likely than older physicians to recommend the IUD (Harper et al. 2008), which suggests a generational gap due to the overinflated descriptions of the dangers of early IUDs.
So let’s go through the actual pros and cons of this form of contraception, so that over the course of the summer you can compare this information to what you’ll be learning about the pill.
Remember, I’m just an anthropologist who studies this stuff. I am not a medical doctor.
Danger danger! Or not
The biggest danger from an IUD is that it could perforate the uterus, or be expelled from it. And that can certainly be painful, reduce fertility, or get you pregnant when you think you are protected. So let’s look at how often this happens.
Prager and Darney (2007) wrote a review on the levonorgestrel IUD (hormone-releasing, like Mirena) in nulliparous (that means no parity, or no children) women. This is important because many still carry the misconception that nulliparous women shouldn’t use IUDs, because of an increased risk of perforation, infertility, pelvic inflammatory disease risk, and difficulty in placement.
There are notable differences between the parous (has had children) and nulliparous (no kids) uterus. The parous uterus is a little bigger, and the cervix dilates a bit more easily. However, it turns out that for the most part these differences are not great enough to produce any differences in side effects or danger to the woman using it.
Prager and Darney (2007) found six studies on perforation or expulsion rates for IUDs (some copper, some hormone-releasing, which are made of plastic and are flexible). They did not find enough data to support a link either way for nulliparity and perforation, because the studies they found had anywhere from zero to two nulliparous women in them. That said, the perforation rates for each study ranged from 0-1.3% in one study, and 2.6 out of 1000 in another (Prager and Darney 2007).
Expulsion rates do not seem to differ between parous and nulliparous women, and again, are very low for all women. The annual expulsion rate among cited studies was 0-4.2 per 100, 0-1.2% per year, and 0-0.2% per year (Prager and Darney 2007). The one important point they do make is that there is a very slightly increased risk of expulsion for lactating women – perhaps this is due to the oxytocin released during nipple stimulation, which could contract muscle?
The other concern sometimes mentioned is that of pelvic inflammatory disease. PID is an infection of the uterus and is usually associated with a sexually transmitted disease. PID can increase the risk of infertility. So for women who haven’t had a kid, but want to some day, the concern about getting PID can loom large.
However, Prager and Darney (2007) surveyed the literature and found that the only studies that support a link between PID and IUDs involves an IUD no longer on the market, or was associated with high-risk sexual behavior.
In some women, copper IUDs can increase menstruation. However, the hormone-releasing IUDs tend to decrease menstruation, and many women stop getting periods altogether. Hormone-releasing IUDs can be prescribed to women with menorrhagia, or pathologically heavy menstruation, too.
Prager and Darney (2007) describe a study in which hormone-releasing IUD users were compared to oral contraceptive users. These IUD users had less dysmenorrhea (painful periods), less spotting, fewer days of bleeding, fewer cycles. Further, 88% of the IUD users wanted to continue with that method of contraception after a year, compared to 68% of pill users, and this difference was statistically significant (p = 0.003).
Romer and Linsberger (2009) also looked at satisfaction with the hormone-releasing IUD in a sample of 8680 women across 18 countries: 95% were satisfied with their method of contraception.
The fine print
Insertion of the IUD can be a little more painful in a nulliparous woman, since her cervix has not dilated before. Also, a minority of women may spot for a while after insertion of the IUD… and by a while, I mean a few months. But once those few months of light spotting are over, they often don’t get a period again until removing the IUD. And of course, the IUD is not conducive to sudden desires to start the babymaking process: you will need to schedule its removal first.
However, with the number of women who are ambivalent at best about birth control pills, but do not want to use a barrier method, the IUD offers a lot in the way of safety, efficacy and ease of use.
Harper CC, Blum M, de Bocanegra HT, Darney PD, Speidel JJ, Policar M, & Drey EA (2008). Challenges in translating evidence to practice: the provision of intrauterine contraception. Obstetrics and gynecology, 111 (6), 1359-69 PMID: 18515520
Prager, S., & Darney, P. (2007). The levonorgestrel intrauterine system in nulliparous women Contraception, 75 (6) DOI: 10.1016/j.contraception.2007.01.018
Römer, T., & Linsberger, D. (2009). User satisfaction with a levonorgestrel-releasing intrauterine system (LNG-IUS): Data from an international survey The European Journal of Contraception and Reproductive Health Care, 14 (6), 391-398 DOI: 10.3109/13625180903203154
Friday, June 17th 2011
This is part of my Summer of the Pill series, where I will answer a question about the birth control pill every week for the summer. I will try and make them shorter than my usual posts. Please remember that I am not a medical doctor, so do not use this material to diagnose or treat any condition. I still hope you find these posts informative and useful.
One of the questions I got on my inaugural Summer of the Pill post is one that I have been asked many times over the years: Why do we menstruate, and is it even necessary while on the pill?
So first, let me back up and explain the modern birth control pill. Most of the standard, monthly pill packs have three weeks of synthetic hormones that you take daily. These hormones out-compete your natural ones, which is how they suppress ovulation. Over the course of these three weeks your endometrial lining is also building up some in response to these hormones. For many adult women in urban, or industrialized environments, the amount of synthetic hormone is lower than what their body would naturally produce, so the lining of the uterus is less thick than it would usually be.
The fourth week is a placebo week – you don’t have to take these pills, but you are usually encouraged to just so that you keep up the habit of taking a pill every day – and the absence of the synthetic hormones in your body triggers menstruation. Then you slough off the endometrial lining that was thickening and again, if you are one of the many adult industrialized women for whom the pill is designed, then you should actually have a lighter period than what you have in a natural cycle.
The placebo week in your standard pill pack is there because the original maker of the pill thought women would be disturbed by the absence of a period. And there are still many women who would prefer to get their period than not. But what about the women who would just as gladly stop menstruating at the end of each cycle or pill pack? Would this be a safe decision?
In order to get at these questions, I will answer three different ones for you: Why do we menstruate? What did we do back in the day? and What is appropriate today?
Why do we menstruate?
|Adapted from Fleagle 1999 by me.
Humans are not the only animals to undergo cycles of growth and regression in our endometrial lining. Yet, only a few animals actually menstruate. Menstruation has occasionally been observed in other great apes (this is the primate group where humans belong, with the chimps, bonobos, gorillas and orangs), and a few other animals. As far as we can tell, everyone else resorbs the lining before growing a new one. It seems to be that those animals who menstruate, do so because the amount of lining they have is greater than what they are able to resorb.
Then, even among those few other animals who have been occasionally observed to menstruate, only humans are copious menstruators. That is, we’re the only ones who seem to do it every time a cycle ends, in a large enough quantity that it is visible (and those of us in industrialized environments know it’s more than just visible – there is a whole section of the drugstore devoted entirely to pads, tampons and cups to help us dispose of it).
Most people seem to think that the reason humans have such thick endometria, that produce the byproduct of copious menstruation, is that we have big-brained babies with high oxygen and glucose needs. We have the most invasive trophoblast of all animals, where the selfish little bugger burrows its way right through the endometrium in order to set up shop and start making the placenta. And so the thickness and differentiation of the endometrium, as well as the precise timing of its readiness for implantation and network of blood vessels at the ready to feed that fetus, make it a highly specialized tissue of a rather significant quantity!
What did we do back in the day?
These days the average industrialized woman menstruates about 400 times in her life, and like I said, that menses is copious. Average menstrual blood loss is around 30mL, but anything below about 120mL is considered normal.
However, women in more traditional environments, particularly those who are foragers or pastoralists, menstruate far less frequently, only around 50 times (Strassmann 1997). Part of the reason for this is that their first period is much later in life, say around seventeen years old rather than twelve or thirteen, and that they expend a lot more energy and eat fewer calories each day (Strassmann 1997).
But there is another reason that the traditional environment, the one we assume humans evolved in, leads to far frequent menstruation: these women usually don’t have access to contraception, and thus practice what is called natural fertility. So the average number of live births for these women can be as many as eight, and even with high infant mortality that’s a lot of babies. Add to that the fact that these women will breastfeed through toddlerhood, and you have several menstruation-free years.
|Figure 1. The industrial (top) versus nonindustrial (bottom) pattern of menstruation through the reproductive life span. The pink bars represent infrequent menses, the red bars represent frequent menses; breaks indicate no menses due to pregnancy and lactation. Note that the first period begins earlier in the industrialized pattern, and that fewer births, less breastfeeding, and more calories lead to more frequent menses across the reproductive years.
So the industrial pattern doesn’t look anything like the nonindustrial, or traditional pattern. But the pill doesn’t necessarily look like either pattern – in terms of the number of menstruations it is like the industrial pattern, but in terms of ovulations it’s likely closer to the traditional pattern. The question is whether one of these patterns is necessarily healthier. I will partially answer this today.
What is appropriate today?
The placebo week of the pill is not necessary for contraceptive purposes, and the menstruation that occurs during this time may not be important for most women either. The two things worth talking to your doctor about are breakthrough bleeding, and the additional week of hormone exposure per month.
Breakthrough bleeding is when you have some kind of blood discharge at a time other than when you would expect to menstruate: when on the pill this would be any other time than the placebo week. And this can be very common in some populations even when using the normal pill preparations with the placebo week (Bentley 1996, Vitzthum et al 2001, Vitzthum and Ringheim 2005). Young users of the pill (say under 25 years old), athletes, and users from nonindustrial populations may be especially at risk.
If you have breast cancer or other reproductive cancers in your family history that are of the hormone-responsive variety, you may not want to expose yourself to any more hormone than you have to. The amount of hormone exposure in one’s life is correlated with risk of breast cancer (Jasienska and Thune 2001). However, the question of whether taking the pill helps or hurts your breast cancer risk is a very murky issue, and one that I will try to address in its own post later this summer.
Something you’ll read in this Summer of the Pill series is that making decisions about reproduction is about understanding trade-offs. You need to weigh the reasons you take the pill with the side-effects or negative impact of the pill, if you experience any. And many women out there could make up a pro/con list for taking the pill, or changing preparations, or skipping the placebo week, or changing to an IUD, and find that they weight each item very differently. There is rarely a single right answer.
Bentley, GR. (1996) “Evidence for interpopulation variation in normal ovarian function and consequences for hormonal contraception” in Variability in human fertility, eds L. a. M.-T. Rosetta, C.G.N. (Cambridge University Press, Cambridge, UK), pp 46-65.
Jasienska, G., & Thune, I. (2001). Research pointers: Lifestyle, hormones, and risk of breast cancer BMJ, 322 (7286), 586-587 DOI: 10.1136/bmj.322.7286.586
Strassmann, B. (1997). The Biology of Menstruation in Homo Sapiens: Total Lifetime Menses, Fecundity, and Nonsynchrony in a Natural-Fertility Population Current Anthropology, 38 (1) DOI: 10.1086/204592
Vitzthum VJ, Spielvogel H, Caceres E, & Miller A (2001). Vaginal bleeding patterns among rural highland Bolivian women: relationship to fecundity and fetal loss. Contraception, 64 (5), 319-25 PMID: 11777494
Vitzthum VJ, & Ringheim K (2005). Hormonal contraception and physiology: a research-based theory of discontinuation due to side effects. Studies in family planning, 36 (1), 13-32 PMID: 15828522
Wednesday, March 16th 2011
My blogging mojo has been channeled almost entirely towards a book project I’ve undertaken with Julienne Rutherford of UIC and Katie Hinde of UCLA (though shortly to be of Harvard). The book is called Building Babies: Primate Development in Proximate and Ultimate Perspective and it will be published by Springer in 2012. Each co-editor has a chapter in there, and then we have a number of other rather fancy-pants contributors as well.
The first drafts of the chapters were due yesterday. I did not submit my chapter (er, to myself). I’m running about a week late. I thought I would come clean with this, because there are a number of elements of the writing process that I think remain obscure for students and other junior scholars. And after I share a few thoughts about academic writing, I thought I would show you some of the draft I’m working on.
First drafts suck
They really, really do. If you think your first draft is amazing, give it to someone else, and that someone else can’t be a pet, spouse or parent. First drafts suck because we write the most obvious things in them, the most vague. First drafts don’t have enough context. First drafts are where you use cliches because you haven’t figured out how to say what you’re saying in a sophisticated way. They are often under-cited. They are out of order. And, they aren’t that compelling.
This is why so much student writing is bad — but it’s not their fault. Close together deadlines, ones that align with other projects, and little teaching of time management means most students start writing projects just before they are due. So they essentially submit first drafts of papers, with a little copyediting if you’re lucky. Plus, somehow a lot of students have picked up this idea that first drafts are better or more authentic than revisions. This is patently false. They are simply the place our favorite worst stuff goes to die (this is why revision is so often called killing our darlings, to use a term from scio11, though its origin is much older).
But everyone has bad first drafts, so it is absolutely useless to feel bad about them. Give them to your advisor or your colleague if they have said they will read a first draft (otherwise, revise it after consulting with someone else first). They write bad first drafts too. You have to write a first draft in order to get to the revision, and to me, this was a liberating realization. Get it all out now! Don’t worry about using the right word! Just get the words on the page, get about the right content in about the right order, and if something is repetitive, just leave it for now. Because after a little breather away from it, or a look from a trusted colleague or advisor, you will hack it up and remake it into something far better.
Revising only sucks sometimes
Revising sucks when you get your first comments back from a colleague, because it is terrifying to share that vulnerable, bad first draft with another person (ever had that moment after you print it out or hit send when you realize your prized metaphor was a trembling nod to your failed attempt as a fiction writer?). It sucks at those moments when you feel at cross-purposes with the thesis of your paper. And it’s frustrating, also, that revising is the most important yet under-taught skill in academic writing.
But here’s the thing. Revising can be glorious. If you abandon any sense that you own your words, and remember only to own your mind, it allows you to be merciless in cutting out all the badness of that first draft: the cliches, the vague repetition, the jargon. If you return again and again to your outline, or abstract, or data, or whatever materials you keep to help you remember what the paper is about, you will start to see the right shape of the piece. And then you can also build in the context.
The best moments of revision are when you remember why you were writing the piece in the first place. Do you want to produce a fundamental review that will be useful to other practitioners in your field? Do you have an amazing piece of data to share? A well-grounded hypothesis that you want to articulate? What was surprising or compelling about that work when you first set fingers to keyboard?
One last thing I’ll say about revising is that owning your mind is not the same as owning your ideas. You need to be willing to let go of being right, and you need to be willing to change if the evidence is against you. Accepting reality and working with it in an interesting way is the mark of a good scientist, and a good revision.
My first drafts suck
The title of my chapter is: “Inflammatory factors that produce variation in ovarian and endometrial functioning” (eventually, I think, I will need to change the title to better reflect the manuscript). I thought this would be an easy piece for me, since I have been doing a lot of work on C-reactive protein, a biomarker for systemic inflammation, and I have been studying the endometrium and ovaries for many years.
I was wrong. Oh, so wrong.
A few quick searches pulled up an embarrassingly large number of citations for chemokines and cytokines, for toll-like receptors, natural killer cells, and other immunological terms I barely remembered from high school and college. So I re-drafted my outline, set aside a lot of time for reading (as in, several days straight), and then finally set to work.
The problem with the literature on this topic is that it is wholly mechanistic. I can now tell you what interleukins are expressed in the periovulatory phase versus the implantation window, or which ones are suppressed or overexpressed for certain pathologies, but I can’t tell you what that means in a broader sense, or what produces variation in any of these immunological factors in a systemic way that might impact local inflammation in the female reproductive system.
Here is my section on normal endometrial functioning (alas, given the literature, the section on pathology in the endometrium is far, far longer). First draft ahead! Remember, I am sharing this embarrassingly bad prose for the good of SCIENCE.
The endometrium is composed of the functionalis and basalis layers; the functionalis comprises two thirds of the endometrium and is the part that proliferates and sheds each reproductive cycle. The basalis is adjacent to the myometrium, and is the place from which the endometrium regenerates after menses. The proliferative (also known as follicular) phase is when estradiol promotes proliferation of endometrial tissue, where the secretory (also known as luteal) phase is characterized by progesterone control of decidualization and menstruation. The endometrium typically proliferates with narrow, straight glands and a thin surface epithelium, and angiongenesis continues as ovulation nears (King and Critchley 2010). After ovulation and during the secretory phase, the endometrium differentiates: endometrial glands become increasingly secretory, and by the late secretory phase spiral arterioles form. If implantation does not occur, the corpus luteum degrades, progesterone declines, and this triggers a cascade of events to produce menstruation.
Menstruation is a key inflammatory process of the endometrium. Menstruation is when the functionalis are shed at the end of the human reproductive cycle. The basalis regenerates over the course of the next cycle. The demise of the corpus luteum and the associated withdrawal of progesterone precipitate inflammatory mediators that cause tissue degradation. For instance, progesterone inhibits nuclear factor κ B (NF-κB), which increases the expression of inflammatory cytokines like IL-1 and IL-6 (Maybin et al. 2011). The withdrawal of progesterone is also associated with an increase in endometrial leukocytes and IL-8, which regulate the repair process (Maybin et al. 2011). At this time other inflammatory factors promote MMP production to break down endometrial tissue (Maybin et al. 2011). Further, it is thought that progesterone withdrawal, not an increase in estradiol concentrations, leads to the repair of the endometrium so that it can resume activity for the next cycle (Maybin et al. 2011). Thus, variation in progesterone concentrations may lead to variation in inflammatory activity, degradation, repair and cycling in the endometrium.
First question: why should I care about any of the above? So what if any of this happens? Then, you might not know this, but I do: the only two citations in these two paragraphs are both review papers, and one of the authors overlap between them. Therefore, it’s quite under-cited. To be fair, in this section it is less important that I demonstrate the depth of the literature, but a review that only cites two other reviews isn’t doing its job.
Do I inspire excitement in my field? No. Do I provide an appropriate context for this material in order to situate the reader? Not so much. Right now, these two paragraphs contain the exact information I wanted them to contain, based on what was in my outline. That is, I’ve described the basic functioning of the endometrium, and menstruation. It’s flat because that’s all that I did.
My job in this chapter is to take this vast reproductive immunological literature, pair it with what little we have in anthropology and ecology that helps us understand the way genes and environment might produce this variation, and then describe the necessary context in future work to understand these mechanisms. In some places, a lack of context may help me make my case, because it will demonstrate why anthropologists need to be in the field. But if my whole manuscript looks like the two paragraphs above, it will be an unreadable yawnfest that doesn’t contribute a thing to anthropology.
So, I guess I would expand the “kill your darlings” advice. First, accept your darlings. Accept that you have them like everyone else, and that darlings aren’t just turns of phrase but entire ideas, hypotheses, fields of thought. Then, once you have accepted that your darlings make you just like every other academic writer out there, from the middle schooler to the full professor, kill them. With fire. Finally, make sure you provide what is left with context or else there is no reason to read what you wrote.
And now, I have been sufficiently inspired to go finish my bad first draft.
King, A., & Critchley, H. (2010). Oestrogen and progesterone regulation of inflammatory processes in the human endometrium The Journal of Steroid Biochemistry and Molecular Biology, 120 (2-3), 116-126 DOI: 10.1016/j.jsbmb.2010.01.003
Maybin JA, Critchley HO, & Jabbour HN (2011). Inflammatory pathways in endometrial disorders. Molecular and cellular endocrinology, 335 (1), 42-51 PMID: 20723578