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
Tuesday, June 21st 2011
This is the first in a new series at Context and Variation where I will attempt to be more concise. As I continue along the Summer of the Pill series I want to make sure I still put some attention on other topics within biological anthropology. C&V shorts allows me to share something I find cool, in half the words I usually do.
What would you do if you knew you had eighty years to live? What if you knew you only had forty?
Life history theory is the idea that the timing of major life events is adaptive. That is, when to be born, when to wean, when to grow, and when to reproduce are dependent on selection pressures in the environment. The most important concept within life history theory, then, is that of tradeoffs, because when you time these events is based off how you want to allocate your resources. In your environment, would it be best to grow right now? Should you grow under the care of your mother, or should you be independent? Is it time to have a child? How about your second, or third, or fourth child?
For this reason, many people study life history transitions, which means the critical yet variable period when people move from one state to another: from growing to reproductive cycling, from cycling to gestating, gestating to lactating, even lactating back to cycling. And much of what governs these transitions has to do with energy, because energy is finite: energy you use towards one purpose, like growing, cannot be used for another, like reproducing. This is especially true in humans because we permanently transition from allocating to growth to reproduction at puberty, unlike other species that keep growing throughout their reproductive years.
But energy isn’t the only factor that enters into our physiological decision-making: time is also important. And as I hinted in the first paragraph, if you have some sense that your time on this earth will be short or long, you might make different decisions about when to do what.
|Found here. Perhaps part of a
modern menarche ceremony?
A few years ago, Walker et al (2006) looked at all the available data on growth and development in small-scale societies – that means foragers and agrarian populations. They found that girls with a later age at menarche – that is the first menstrual period – are shorter in stature. If we consider only energy, this makes no sense! The later you wait to start reproducing should mean you had more time to grow, so why did Walker et al (2006) find the opposite?
The answer is timing. It turns out that mortality rates tell us something about growth and development: the higher the mortality in a population, the earlier their age at menarche and age at first reproduction. So, the higher your chances of being offed at any given moment, the more likely you are to favor reproduction over growth so you can move ahead with the whole reproductive success thing. So, constraints on time and energy affect our physiology differently, and mean we may have to make different predictions about life history transitions that are dependent on human societies. Predation or access to health care impact mortality, but so do homicide or war.
In 2011, McIntyre and Kacerosky performed a similar analysis, only this time they compared small-scale societies with industrialized ones – industrialized societies are those that are more urban, technology-driven, with greater access to modern health care, like the USA. Their analysis of small-scale societies confirmed Walker et al’s (2006) results.
But McIntyre and Kacerosky (2011) found the opposite relationship in industrialized societies: there, the later you hit menarche, the taller you were. And this makes sense if we think we can assume most industrialized populations have lower mortality than the foragers: within the industrialized pops, those who had the time and energy to grow big by holding off on menarche, did.
McIntyre and Kacerosky (2011) are hesitant to be full adaptationists in their paper, which I appreciate. So, they offer two hypotheses and suggestions for future testing. The first hypothesis falls in line with the life history theory described in this post, though their focus is more on parental investment than mortality. But still, environment, and access to time and energy, set life history trajectories for different populations. However they are also careful to point out a nonadaptive hypothesis: it could be that variability in stature is decreasing as heritability is increasing, meaning we are hitting up against biological constraints for size.
Genes and environment interact to produce phenotype, and this is something most people remember from high school biology. But sometimes it’s nice to peek under the hood and learn a little something about the life history mechanisms that are set into motion by this interaction. Early life events, perhaps even life events of our mothers and grandmothers, start our life history trajectories. Then tradeoffs at certain important transition periods nudge us a little further one way or another for the rest of our lives.
McIntyre MH, & Kacerosky PM (2011). Age and size at maturity in women: a norm of reaction? American journal of human biology : the official journal of the Human Biology Council, 23 (3), 305-12 PMID: 21484909
Walker, R., Gurven, M., Hill, K., Migliano, A., Chagnon, N., De Souza, R., Djurovic, G., Hames, R., Hurtado, A., Kaplan, H., Kramer, K., Oliver, W., Valeggia, C., & Yamauchi, T. (2006). Growth rates and life histories in twenty-two small-scale societies American Journal of Human Biology, 18 (3), 295-311 DOI: 10.1002/ajhb.20510
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