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Off to bloggier pastures: bringing ladybusiness to the SciAm Network

If you’re on Twitter or read any other science blogs, by now you know that the Scientific American Blog Network has launched. And, I’m pleased to say that I am a part of it! Context and Variation has moved to new digs, surrounded by a network full of bright, interesting people with great communities and great things to say.

But of course, while I encourage you to check out Bora’s post where he introduces every one of us, I have to plug a few bloggers in particular.

First, the University of Illinois is the only university to be represented by three bloggers on this new network (yeah, we totally did a press release for it). Alex Wild of Myrmecos (you know, the guy who comes up if you just google insect photography) has created a blog called Compound Eye that will cover science photography. What’s exciting about this blog is that Alex, true to his nature, will be very generous with his space and will showcase the work of many other photographers.

Joanne Manaster, who you may know as sciencegoddess on Twitter, hosts the blog JoanneLovesScience.com. Joanne is a truly exceptional science educator and puts great attention on reaching young audiences, from exploding gummy bears, the science of makeup, and Kids Read Science programs. On the SciAm blog network, Joanne will be co-hosting a new blog PsiVid with Carin Bondar. This blog will continue Joanne’s work of thinking about engaging audiences and getting them interesting in science in new ways.

In addition to these great U of I bloggers, I also have to mention my fellow anthropologists. Krystal D’Costa is moving her fantastic blog Anthropology in Practice to SciAm. You can expect more thoughtful, detailed, yet readable and fun posts from Krystal. She is a wonderful observer of human nature, and I love how she forces me to be an anthropologist at all sorts of casual moments when I usually take my academic lenses off.

Then there is Eric Michael Johnson’s blog The Primate Diaries. Eric is another very talented writer, sharing insights from a great mind. I have enjoyed his posts on sexuality, primatology, sexism, and human evolution.

Oh, and need I even mention? There are lots of female bloggers on this new, kickass network. Check out The Mary Sue’s coverage. They’re right. The SciAm Blog Network does introduce us to about a zillion new women in the sciences. Incidentally, it does a pretty decent job of introducing readers to people of varying sexualities and ethnicities as well. We can always do better, but it is a strong start.

The people of this network have exceptional voices and important perspectives. And now more people will see what they have to offer. I hope you’ll all join me over at my new place, that you’ll check out the rest of my network peeps, and that you will enjoy helping me bring the ladybusiness to Scientific American.

Summer of the pill: Will the pill mess up my ability to detect my One True Love?

Should I advise recently single ScarJo to stay
off the pill to find her next beau? From here.

Imagine you are a single, heterosexual woman. You meet a nice man at the driving range, or on a blind date. You like him and he likes you. You date, you get engaged, you get married. You decide to have a child together, so you go off the pill. One morning you wake up and look at your husband, and it’s like seeing him through new eyes. Who is this stranger you married, and what did you ever see in him?

After some articles made the news when they suggested mate preferences change on hormonal contraception, this seemed to be the scenario in the heads of many women. Is my pill deceiving me? What if my birth control is making me date the wrong man?

Several articles over the years have demonstrated that women prefer men with more masculine features at midcycle, or ovulation, and more feminine features in less fertile periods. Based on body odor, women and men also often prefer individuals with MHC (major histocompatibility complex) that are different from theirs, which may be a way for them to select mates that will give their offspring an immunological advantage. These findings have been replicated a few times, looking at a few different gendered traits. And as I suggested above, other work has suggested that the birth control pill, which in some ways mimics pregnancy, may mask our natural tendency to make these distinctions and preferences, regarding both masculinity and MHC (Little et al. 2002; Roberts et al. 2008; Wedekind et al. 1995).

On the one hand, I think it’s both interesting and important to consider the implications of the birth control pill beyond just contraception. Hormones are messages, so any cells that have receptors for these messages, like specialized mailboxes, can receive them. The pill is made of synthetic versions of estradiol and progesterone, and there are estradiol and progesterone receptors in your brain. And yes, these hormones do change your brain, both during the natural cycle and on hormonal contraception; Scicurious has written well on this in the past.

Jolie, had she been on the pill and chosen her mate
differently. From here. Yes, looks to be a real pic.

On the other hand, I have a lot of questions: First and most important to me, how does any of this translate to non-straight women? I find the constant focus on mate choice between men and women a bit exhausting, and am not sure we can assume non-straight relationships to work the same way. Next, how well do preferences over the cycle map on to actual choices for mates, short term or long term? If we happen to find Brad Pitt more attractive than Justin Bieber at midcycle, does that mean no one will do but Brad Pitt? And finally, what are all the factors that we need to consider in mate choice besides a deep voice or square jawline (again, especially if you try to expand your thinking beyond straight relationships)?

I’ll start with the last two questions that deal with mate preference versus ultimate mate selection. As you all might expect, women and men choose mates for lots of reasons, not just masculinity or complementary immune systems. Bereczkei et al (1997) looked at singles ads and found women often sought mates with high parental care. In a separate singles ad evaluation, Pawlowski and Dunbar (1999) found that women mostly selected men of high resource potential who were interested in long-term relationships (either unlikely to divorce or unlikely to die within twenty years), where men selected women by markers of fecundity (ability to have babies). In a sample of 18-24 year old straight people in the US, Buston and Emlen (2003) found that most people selected mates who had similar characteristics to themselves. And a speed dating sample showed that people under those conditions selected dates based on easily observable traits, like physical attractiveness (Kurzban and Weeden 2005).

Now on to the fact that all of this research is on straight people. I found very little on lesbian women and the menstrual cycle… but what I found was very cool! Brinsmead-Stockham et al (2008) found that, like heterosexual women, lesbian women are quicker to identify unknown faces at midcycle, as long as they were the faces of the sex they preferred. So straight women were good at identifying male faces, lesbian women good at identifying female faces. Burleson et al (2002) found that sexual behavior in lesbian and straight women was mostly similar through the menstrual cycle, with both peaking at midcycle.

So, mate preference may be about telling a research assistant who is the hottest to you at a particular point in your cycle. And it is a fairly robust and consistent finding. However, when it comes to ultimate mate selection the most important thing to consider is a great point made by Pawlowski and Dunbar: finding a mate is about advertising what you have to offer while making known what you want in a mate. Then it’s all about finding some kind of compromise through a series of trade-offs based on what the individual wants, what they can offer, and what’s available in the dating pool. (So, since neither Brad Pitt nor Justin Bieber are currently in the dating pool, my previous comparison was pointless.)

Those of you who met your mate while on the pill: not to fear. I don’t think that the possibility that you may have some suppression of masculinized preferences at one point in your cycle means you’ve chosen the wrong person.

Who knows, it could have opened you up to the Mr. or Ms. Right.

References
Bereczkei T, Voros S, Gal A, & Bernath L (1997). Resources, attractiveness, family commitment; reproductive decisions in human mate choice. Ethology : formerly Zeitschrift fur Tierpsychologie, 103 (8), 681-99 PMID: 12293453

Brinsmead-Stockham K, Johnston L, Miles L, & Neil Macrae C (2008). Female sexual orientation and menstrual influences on person perception Journal of Experimental Social Psychology, 44 (3), 729-734 DOI: 10.1016/j.jesp.2007.05.003

Burleson MH, Trevathan WR, & Gregory WL (2002). Sexual behavior in lesbian and heterosexual women: relations with menstrual cycle phase and partner availability. Psychoneuroendocrinology, 27 (4), 489-503 PMID: 11912001

Buston PM, & Emlen ST (2003). Cognitive processes underlying human mate choice: The relationship between self-perception and mate preference in Western society. Proceedings of the National Academy of Sciences of the United States of America, 100 (15), 8805-10 PMID: 12843405

Kurzban R, & Weeden J (2005). HurryDate: Mate preferences in action Evolution and Human Behavior, 26 (3), 227-244 DOI: 10.1016/j.evolhumbehav.2004.08.012

Little AC, Jones BC, Penton-Voak IS, Burt DM, and Perrett DI. 2002. Partnership status and the temporal context of relationships influence human female preferences for sexual dimorphism in male face shape. Proceedings of the Royal Society of London Series B: Biological Sciences 269(1496):1095-1100.

Pawłowski B, & Dunbar RI (1999). Impact of market value on human mate choice decisions. Proceedings. Biological sciences / The Royal Society, 266 (1416), 281-5 PMID: 10081164

Roberts SC, Gosling LM, Carter V, & Petrie M (2008). MHC-correlated odour preferences in humans and the use of oral contraceptives. Proceedings. Biological sciences / The Royal Society, 275 (1652), 2715-22 PMID: 18700206

Wedekind C, Seebeck T, Bettens F, & Paepke AJ (1995). MHC-Dependent Mate Preferences in Humans Proceedings: Biological Sciences, 260 (1359), 245-249 DOI: 10.1098/rspb.1995.0087

Summer of the Pill: The latest fashion accessory to hit your uterus: the IUD!

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.

Hidden benefits

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.

References

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

C&V Shorts: Make the most of your time and energy

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.

References

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

Summer of the Pill: Why do we menstruate?

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?

Found here.

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.

References

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

Summer of the Pill

It’s summertime, and as we shed our winter layers thoughts turn not only to love and sex, but also regulating menstrual cycles, understanding premenstrual syndrome, and potential population variation in the pharmacokinetics of hormonal contraception. Or is that just me, as a ladybusiness anthropologist?

If my inbox is a clue I am not the only person who wants good information on hormonal contraception. Many women are on the pill, and they use it for many reasons, only one of them contraception. Remembering to take the pill or get a new prescription, deciding on the relative impact of the current side effects versus new ones one might get from switching, wondering if it’s really doing its job, wondering if it’s increasing or decreasing breast cancer risk… these questions are like a buzzing in the back of the head at all times for many reproductively-aged women and their partners. And they want the buzzing to stop.

Let me see if I can help. Let’s make the summer of 2011 the Summer of the Pill. Every week I will cover a different topic or answer a different question on the subject of hormonal contraception, in addition to my usual posts.

Want to suggest a topic or ask a question? Comment on this post, email me, or @ me on Twitter.

The first post should appear by this Friday.

Why it’s cool to be a scientist (especially an anthropologist)

From here.

This month, I am taking part in I’m a Scientist, Get Me Out of Here! which is a program that links up teenage students with scientists all over the world. We put together bios, answer questions, and do live chats with them. I am looking forward to the chance to share my vast knowledge of ladybusiness anthropology — and biological anthropology more generally — with students who are looking to find out whether science is boring or fun.

The way this project is set up is that, over the course of the few weeks we interact with the students, they vote us off one by one; the last person left wins 500 pounds to use towards a science outreach project. If I win, I hope to put these funds towards a project that will link young people together to share their stories of how their lives vary, and what impact that has on their biology. My hope is that this project will achieve two goals: first, to get young people to observe their own bodies and biology in order to be more aware of the science that surrounds them, and second, to show them that variation is what is normal. In the teenage years (and even earlier), there is often a lot of peer pressure to fit some culturally-sanctioned definition of “normal.” But what is normal, really, when we all come from such different places and lead such different lives? When we can directly observe how our lifestyle and environment impact our biology, it becomes clear that difference, not similarity, is the true normal.

As a companion piece to my bio, I would like to share why I think it’s cool to study and enjoy science.

Science is fun

Found here.

I first got really interested in science because of my AP Biology teacher. Mr. Cabral demonstrated his excitement and zest for biology every day. One day I got so caught up in what he was talking about — the potential impact of genetically modified corn on crops throughout the country — that as soon as I got home, I got on our AOL dial-up internet and started digging (this would have been the fall of 1996). I used AOL’s clunky search engine and managed to find several interesting websites that talked about Archer Daniels Midland. I printed it out on three ring binder paper — I think we were out of regular printer paper — and brought it to him the next day. I remember how motivated I was to learn about ADM, and then how that internal motivation was reinforced by how excited Mr. Cabral was by my find.

This was my first experience with the kind of detective work science can entail. Yes you do experiments, you do labwork or fieldwork, you collect samples or make things blow up or work with stuff that smells. And there is a sense in adventure to that. But another important piece of the work of science is setting out with a question, and doing the sleuthing necessary to find out the answer for yourself.

That will never stop being fun for me.

Science is logical
Fun is what got me started on science, the constant sense of discovery and the enjoyment of developing expertise where no one else has it. But what has kept me in science has been an increasing love, even total devotion, to the idea of the scientific method.

Castle and Beckett, from one of my
favorite detective shows, Castle.

The scientific method is another place where the metaphor of the detective is useful. A detective has a question: “Who dunnit?” And then, if she’s a good detective, she develops a hypothesis about who she thinks did it, then methodically tests her hypothesis. If she finds her hypothesis is not supported, she produces a new hypothesis to try again, based on what she has learned. If her hypothesis is supported, she likely will want more evidence to continue to better support her hypothesis.

The reason I love this method is that, if you are willing to really become a good detective, you can detect unintentional and intentional bias. Some conclusions in science, especially the older stuff, and especially stuff on humans that is related to sex or race, was biased by the preconceptions of who performed and interpreted the work. The entire field of women’s reproductive physiology is tainted by early, false observations by a twelfth century monk that women are not human, that they have a seven chambered uterus, that women can decide on the sex of their babies by lying down a certain way, and wicked women will choose to have girls (Rodnite Lemay 1992). Even research in the twentieth century indicated that the sweat of menstruating women makes babies die and flowers wilt (Bryant et al. 1977; Freeman et al. 1934; Macht 1924). And of course, none of these things are true.

I believe that reality of science always wins. We are constantly becoming more aware of implicit bias and honest mistakes, we are constantly developing new methodologies to test our questions. My students, or my students’ students, will probably find things wrong with my own work and modify or correct it some day. This is very exciting to me!

Science solves important problems
I am a biological anthropologist. That means that I am interested in human evolutionary biology, and in understanding the interaction of biology and culture in the production of a human being. I think we can all come up with problems science helps solve, from making cars and homes more energy efficient, to saving endangered species. Biological anthropology can help answer these from the perspective of human ancestry, evolution and behavior. For instance, it’s great that we are making cars more energy efficient, but how do we change usage patterns? How do we get people to drive less? Really, how do we get a species that evolved to consider short and medium term problems and be selfish, to think altruistically and really long term?

In my corner of the field, bio anthro can help answer the following (and more):

  • How does environment and lifestyle impact our hormones?
  • Why do some people have a harder time having babies than others?
  • What is the impact of our changing environment, to one where we are sitting around more and eating more, on our health?
  • Does psychological stress impact our physical health? Can sexism or racism have real effects on the body?
  • How does moving from one country to another change your hormones?
  • Is taking the pill good for you?
  • Does what you do as a pregnant woman really matter that much to the health of your baby?

And that’s just the beginning.


Anyone can love science
I want more people, and more different kinds of people, to do science. But I also just want more people to realize how exciting it is to read and learn science. Becoming an engaged science reader, even as someone who already is a scientist, has been a wonderful experience for me. I have developed an appreciation for insects, found out about variation in circadian rhythms, and fallen in love with rivers.

I have realized that there is a lot of great science out there, not just biological anthropology, and it’s all worth fighting for. I have taught a lot of non-science majors since becoming a professor – literally hundreds and hundreds. And when I talk to them, many of them explain that the reason they hate science is that someone made them feel stupid: a teacher, a fellow student, sometimes a relative. I’ve heard several explicit stories where a student was told by a teacher that they weren’t good at science. I’ve had students break down in tears as they describe the sexism and racism that has made them decide science wasn’t for them.

And so, because of the rudeness of another person, the oppression of a system, or a series of incidents that just become too much to bear, they turned away from one of the most logical, exciting, and natural ways of thinking about the world. And many began to dislike it, then mistrust it, then not believe anything they heard about it. And who can blame a young person for turning away from a field, if that is what they are up against?

Nothing, and no one, should turn people away from science, because anyone can love science. Even if you never take another class on it or pick up a single textbook, even if you don’t become a scientist or educator or writer or any of the many jobs where you can use science, you can revel in the beauty of a photograph, the stories of triumph over adversity, the excitement of discovery. You miss out on the simple human pleasure of satisfying curiosity about the natural world if you don’t read science. In addition to improving access and eliminating oppression so that more people can excel in science, we need to make it possible for people to just learn and love it.

One of my favorite things about being a scientist is that I get to hang out with other scientists. At conferences, other scientists present talks or posters to talk about their latest research. If you listen closely to these conversations, along with the jargon, and the statistics, and the graphs and tables and lightning-fast discussions of various technical methodologies, you will also hear people abruptly and delightedly exclaim: “Isn’t this just so cool?”

Yes. Yes, it is.


References
Bryant, J., Heathcote, D., & Pickles, V. (1977). THE SEARCH FOR “MENOTOXIN” The Lancet, 309 (8014) DOI: 10.1016/S0140-6736(77)92199-7
Freeman W, Looney JM, and Small RR. 1934. Studies on the phytotoxic index II. Menstrual toxin (“menotoxin”). Journal of Pharmacology and Experimental Therapeutics 52(2):179-183.
Macht D. 1924. Influence of menotoxin on the coagulation of blood. Journal of Pharmacology and Experimental Therapeutics 24(3):213-220.
Rodnite Lemay H. 1992. Womens Secrets: A Translation of Pseudo-Albertus Magnus’ de Secretis Mulierum with Commentaries: State University of New York Press.

Do girls steal some of their mother’s beauty? Sex bias in parental investment

Sons and daughters and differential parental investment

One of my favorite rhetorical tricks is asking my students a question that has an obvious answer based on cultural expectations, but is wrong. So every year, when I start to teach my students about parental investment, I ask:

Who is harder to raise, sons or daughters?

I’ve asked by a show of hands and with iClickers, over the years, and the room of 750 is almost unanimous: daughters are harder to raise. So, then I get off the stage and walk around a bit. What do you mean by that? I ask.

Girls cause more gray hairs.
Girls cause more trouble when they start to like boys.
Girls are more work, and cost more money, since they shop all the time.
Girls talk back more.

And of course, there is always the saying that girls steal some of their mother’s beauty.
So then I show them this:

From Helle et al 2002.

Here is a graph of maternal longevity based on the number of sons or daughters they have. This data was based on a historical population from Finland from 1640-1870 using church records (Helle et al 2002). As you can see, the more sons mothers bear, the shorter their lifespans. You see the opposite for daughters. So sons have a negative impact, and daughters have a positive impact. This same trend has been found in records from a Flemish village (van de Putte et al 2003, 2004), where sons negatively impact lifespan but not daughters. Interestingly, data from church records from the field site where I work in rural Poland provides a slightly different picture: every offspring of either sex reduced lifespan by about 95 weeks (Jasienska et al 2006).

From Jasienska et al 2006.

Once students see these graphs, they quickly realize what is going on. Generally speaking, girls help mothers more at home in terms of chores and alloparenting. And in many cultures, particularly the historical ones studied so far, sons are costly because parents invest more in them, to help launch their own families. Daughters, not so much. In the Polish population, there may be other factors where daughter investment is important, or it is just costly to have so many offspring and you have maternal depletion regardless of daughter help.

Sex bias in parental investment is an important part of understanding both the biology and culture of parenting, and the developmental trajectories of children. The Trivers-Willard hypothesis, which has been tested many times in humans and animals, suggests that parents should invest more in sons when conditions are good, and more in daughters when conditions are bad. That is, when you have lots of resource you should put it towards a son in order to increase the chances he will have high reproductive success, since his is assumed to be more variable and high effort could lead to high reward. But in periods of low resource, daughters are a good bet because they are more likely to have at least some reproductive success no matter what.

From Hrdy 1990.

Of course, differential investment based on resources is further conflated in humans due to culture and, I would contend, our almost universal favor for patriarchy (Smuts 1995). Here is an image of an Indian family waiting at a clinic. There is a mother, an older son, and a twin boy and girl. Notice the extreme difference in health between the infant boy and girl – they are twins, yet the infant girl is emaciated. This is because in this population sons are always fed and cared for first, and whatever is left over, if there’s anything, is given to daughters.

So, parental investment can have real effects on the parent in terms of lifespan, and perhaps also their own future reproductive capabilities. Further, the conditions under which you may have children can vary, but how much a parent chooses to invest in their children varies too.

The piece of this that may be toughest to parse out, particularly in humans, is how the condition of the mother (or parents) can vary, and how that variation impacts the sex ratio of their children. In some species, like red deer, it is easier to imagine a mechanism: these animals have diapause, a period where their embryos are dormant until it is a good time to gestate and bear them. It is easier to insert some kind of selection process into a period where several embryos are all “frozen” and sex has been determined. But what about humans that produce singletons and invest huge, overlapping amounts of support to their children over decades? How would a sex bias based on maternal condition operate? And is there anything the offspring can do about it?

Changes in maternal breast size during pregnancy

It turns out that measurements as easy as stepping on a scale, and knowing your bra size, can begin to unpack the answer. First, a confession: I consider the author of this paper Andrzej Galbarczyk more than a colleague, but a friend. Andrzej is the graduate student who oversaw my Polish field site last season (Mogielica Human Ecology Study Site, director Dr. Grazyna Jasienska). He has translated consent forms and surveys for me and we’ve had many valuable and important conversations about my fieldwork. He is a smart, kind and thoughtful person and scholar. So, I let him see an early draft of this post to make sure I understood his point of view.

Galbarczyk performed an internet survey in Poland with 120 women, where he asked them to report their pre-pregnancy weight and bra size, their bra size directly after giving birth, and the sex of their offspring. He found two notable differences in these women: mothers of daughters weighed less before pregnancy, but had a greater changes in breast size during pregnancy.

The evidence about maternal pre-pregnancy weight is consistent with the Trivers-Willard hypothesis, as mothers who had sons were more likely to be heavier, and thus have more resource to invest. The second significant difference, that mothers with daughters had larger breasts after pregnancy, seems could be argued either way: Galbarczyk argues that it supports Trivers-Willard because mothers of sons could have been devoting more resource to growing their offspring rather than their breasts.

In other animals and primates particularly, mothers of male infants produce more energy-dense milk, yet mothers of female infants may produce a greater quantity of milk (Hinde 2009). And breast size is a pretty noisy signal of milk quality or quantity. So, what is the meaning of this difference in breast size?

Adaptation or physiological inevitability?

Galbarczyk suggests the difference is related to the evolutionary underpinnings of human female breasts. Women develop breasts around puberty, and though they certainly change in size and shape over time, keep them their whole lives. Other animals develop their mammary glands only shortly before lactating and then they regress again. Many contend that human breasts are an honest signal of fertility. This is at least partially confirmed by the correlation between breast size and estradiol concentrations (Jasienska et al 2006).

Galbarczyk thinks that the larger breasts seen in postpartum mothers to daughters may be a way to attract a mate for parental care. Perhaps this would help where she has given birth to the less-favored sex and needs to really convince him to participate; this could be a signal from the mother or the female fetus. Or maybe by appearing more attractive, she can have another reproductive opportunity, which would give her a chance to have a son.

You all know how I feel about evolutionary storytelling. In certain ways I do find this particular argument compelling, from the perspective of the Trivers-Willard hypothesis. But the evidence for the adaptive scenario around breast size is circumstantial.

Also, I don’t want this story to detract from some very interesting data: remember that Galbarczyk found that in this population, mothers of daughters weigh less before pregnancy, and develop larger breasts afterwards. Very cool. So perhaps we should consider a mechanistic, rather than adaptive explanation?

I have two thoughts about this, both related to androgens (androgens are the class of hormone that testosterone falls under). First, I wonder if there is an effect of fetal androgens from a male fetus on breast size. If so, mothers of daughters would have larger breasts simply because they aren’t having their breast tissue growth or density suppressed by androgens. It could simply be physiology that doesn’t have adaptive meaning.

Second, the mothers of sons were heavier before pregnancy. Heavier individuals tend to have higher circulating insulin levels, and the ovary can respond to higher insulin by producing more androgens (Poretsky 1991, Dimitrakakis et al 2004). So you could have a suppressive effect on breast size from that avenue as well. You don’t need an adaptive scenario for either of these mechanisms, just a consequence of how hormones work.

I would love to see Galbarczyk or someone else follow up on these thought-provoking results by measuring women, rather than relying on self-report, and by measuring their estradiol, progesterone and androgens. Understanding the different factors and motivations that lead to sex differential investment and outcome is a great field of study, and this work gets us thinking in a new direction.

References

Dimitrakakis C, Jones RA, Liu A, & Bondy CA (2004). Breast cancer incidence in postmenopausal women using testosterone in addition to usual hormone therapy. Menopause (New York, N.Y.), 11 (5), 531-5 PMID: 15356405

Galbarczyk A (2011). Unexpected changes in maternal breast size during pregnancy in relation to infant sex: An evolutionary interpretation. American journal of human biology : the official journal of the Human Biology Council PMID: 21544894

Helle, S. (2002). Sons Reduced Maternal Longevity in Preindustrial Humans Science, 296 (5570), 1085-1085 DOI: 10.1126/science.1070106

Hinde K (2009). Richer milk for sons but more milk for daughters: Sex-biased investment during lactation varies with maternal life history in rhesus macaques. American journal of human biology : the official journal of the Human Biology Council, 21 (4), 512-9 PMID: 19384860

Hrdy, S. (1990). Sex bias in nature and in history: A late 1980s reexamination of the “biological origins” argument American Journal of Physical Anthropology, 33 (S11), 25-37 DOI: 10.1002/ajpa.1330330504

Jasienska G, Nenko I, & Jasienski M (2006). Daughters increase longevity of fathers, but daughters and sons equally reduce longevity of mothers. American journal of human biology : the official journal of the Human Biology Council, 18 (3), 422-5 PMID: 16634019

Poretsky L, Seto-Young D, Shrestha A, Dhillon S, Mirjany M, Liu HC, Yih MC, & Rosenwaks Z (2001). Phosphatidyl-inositol-3 kinase-independent insulin action pathway(s) in the human ovary. The Journal of clinical endocrinology and metabolism, 86 (7), 3115-9 PMID: 11443175

AAPA symposium on Evolution through the Life Course: Why we shouldn’t prescribe hormonal contraception to twelve year olds

When Dr. Grażyna Jasieńska invited me to give a talk on my thoughts around adolescents and hormonal contraceptives as part of an invited symposium on “Evolution through the Life Course,” I thought it was going to be an embarrassing experience, because I would not be presenting the quantitative data more common at the American Association of Physical Anthropology meetings. But I can’t say no to Grażyna, who has served as a wonderful mentor and cheerleader for almost ten years. Besides, if I can rant on a blog, surely I can let myself rant in a talk every now and then.

What follows is a bloggy version of the talk I gave Thursday the 14th, at the meetings in Minneapolis. Writing this post will, I hope, help me begin to turn this into a manuscript. Normally I wouldn’t dare write something on a blog that I would eventually want to publish. However, this is a piece that would benefit enormously from the kinds of conversations that happen in the science blogosphere. Further, I hope to publish it as an opinion piece well-studded with evidence. I think that by sharing my early thoughts now, my later thoughts will be more sophisticated.

* * *

Variation in adolescent menstrual cycles, doctor-patient relationships, and why we shouldn’t prescribe hormonal contraceptives to twelve year olds

From Vihko and Apter (1984).

Vihko and Apter (1984) showed that there is variation in age at menarche, and that that variation tells us something about how long it should take an adolescent to start to achieve regular ovulatory cycles. The later your age at menarche, the longer you will experience irregular cycles. However, even in girls with ages at menarche twelve and under, it still took on average five years to achieve regular cycles. This indicates that, in adolescents, irregularity is in fact regular.

Lipson and Ellison (1992) have also looked at age-related variation in progesterone concentrations. Progesterone is the sex steroid hormone secreted by the ovary after ovulation, which is in the luteal phase. Luteal phase function is the one that seems to be the most variable within and between populations, and so progesterone is a great way to understand how female bodies vary. They found that those with the lowest hormone concentrations were on the extreme ends of their sample – 18-19 year olds, and 40-44 year olds and, as you might expect, hormone concentrations were higher as you moved towards the middle of that age range. So both younger and older women have low hormone concentrations relative to women in their reproductive prime, which is 25-35 years of age. But of course, this means that low hormone concentrations when you are in those early or late age ranges means that you are normal for your age.

From Lipson and Ellison (1992).

Now, the United States has the highest rate of unintended teen pregnancy among industrialized nations. So I can understand why there are so many papers, and such a great effort, to get young girls on hormonal contraception (Clark et al. 2004; Clark 2001; Gerschultz et al. 2007; Gupta et al. 2008; Krishnamoorthy et al. 2008; Ott et al. 2002; Roye 1998; Roye and Seals 2001; Sayegh et al. 2006; Zibners et al. 1999).

But I’ve noticed two things: first, that hormonal contraception is used imperfectly in this population, with some estimates that 10-15% of adolescents on hormonal contraception still get pregnant (Gupta et al. 2008). Second, discontinuation rates for hormonal contraception in young girls are high, with many girls complaining about side effects, particularly breakthrough bleeding (Clark et al. 2004; Gupta et al. 2008; Zibners et al. 1999). I have to admit some concern over the fact that many of the papers I read that mentioned these discontinuation rates and side effects were almost condescending in their tone. The implication was that the side effects weren’t a big deal.

One of the ways clinicians and sexual health educators are trying to improve hormonal contraceptive use in adolescents is to emphasize their off-label use as a “regulator” – that is, the pill can regulate your cycle, regulate your mood, regulate your skin. The idea is to emphasize the positive effects of hormonal contraception to combat the side effects young girls both worry about, and actually experience. This also tends to produce campaigns and commercials with images of idealized young women that young girls would want to model themselves after – skinny, confident, and of course very feminine.

From here

Despite the criticisms I’ve begun to name, there are substantial benefits to hormonal contraception in adult women. When women take hormonal contraception in adulthood, particularly in the 25-35 year range, they are very effective contraception. The pill also may reduce risk of reproductive cancers, though results are mixed (Collaborative Group 1996; Collaborative Group 2008; Kahlenborn et al. 2006; Marchbanks et al. 2002; Modan et al. 2001; Narod et al. 1998; Smith et al. 2003). And of course, off-label use to treat painful periods or premenstrual syndrome can be beneficial for many (Fraser and Kovacs 2003).

However, the benefits of hormonal contraception in adults seems to be limited to more industrialized populations. Bentley (1994; 1996) first raised these concerns. She discussed the possible genetic, ethnic and developmental differences between women that could produce variation in pharmacokinetics, which could in turn vastly change the experience and efficacy of hormonal contraception in a global context. Virginia Vitzthum and others have also shown that there are high discontinuation rates and complaints of breakthrough bleeding in rural Bolivian women on hormonal contraception (Vitzthum and Ringheim 2005; Vitzthum et al. 2001). Other studies have shown similar discontinuation rates and side effects in other non-industrial populations (de Oliveira D’Antona et al. 2009; Gubhaju 2009).

You might notice that the issues in non-industrial populations mirror what has been seen in industrial adolescent girls. This isn’t surprising, given that they also have in common fewer ovulatory cycles and lower hormone concentrations.

So, I worry about whether the clear benefits of hormonal contraception in adulthood can be applied to adolescent girls, some as young as eleven or twelve years old. With the imperfect administration and high discontinuation rates, they aren’t that great as contraception. But there are additional, physiological concerns. What are the effects of giving doses of hormones to young girls with newly developing hypothalamic-pituitary-ovarian axes? The variation I mentioned before, where irregularity is regular in adolescence, is because the feedback loop between the brain and the gonads is priming and developing in this period, and this takes time. The sensitivity of the feedback loop is being set. If we flood this feedback loop with extra hormone, does this alter its sensitivity? It is a question worth testing.

Further, if we flood this immature system that normally has irregular cycles and low hormones, are we increasing lifetime estrogen exposure? High lifetime estrogen exposure is a risk factor for breast cancer and other reproductive cancers. Is it possible that hormonal contraception in adolescence could have the opposite effect of hormonal contraception in adulthood? Again, we need to test this hypothesis.

Future work on this topic includes asking whether adolescent menstrual cycle variation is any different today than twenty to thirty years ago. The only data we have (at least that I know of) are from the aforementioned 1984 and 1992 papers, and maybe some derivative papers using the same datasets. But we all know there have been massive changes in body composition, diet and health in the last few decades that deserve consideration. So, this work needs to be re-done on a current population.

We also need to ask how adolescent reproductive functioning varies within and between populations. While this has been studied extensively in adult women, we don’t have a sense of adolescent population variation. This will give us a sense of what ecological variables produce variation not only in age at menarche, but in how long cycle irregularity persists and reproductive hormone concentrations.

Some additional, provocative, post-meeting thoughts

Bristol Palin. Image from here.

In this symposium, Karen Kramer delivered a beautiful paper just before mine on teen pregnancy, and I had some great conversation with session participants and attendees, that has further evolved my own thinking on this issue. I want to say something just a little provocative:

While I think teen pregnancy should be avoided, culturally we overstate its dangers and consequences because we have a real problem with young people reproducing. This can lead young girls to overlook potentially more serious issues like sexually transmitted infections, HIV, and cervical cancer, all of which girls and women are at risk for if they use only hormonal contraception and have otherwise unprotected sex.

Let me explain two important points here. First, in most industrialized nations we are not set up well to support young mothers because of the way families are isolated, yet social support is a strong predictor of birth weight, postpartum depression, and labor progression (Collins et al. 1993; Feldman et al. 2000; Turner et al. 1990). So there are very strong and obvious reasons why teen pregnancy and motherhood can be incredibly challenging in industrialized environments. I wonder sometimes if that lack of cultural support is related to a fear that more young girls will get pregnant if they feel they have permission to procreate. This is similar to the argument in favor of abstinence-only sex ed: if they don’t know their options, or are shamed into believing this option is the worst possible one, then of course they won’t make them. But adults aren’t rational. I’m unsure why we expect adolescents to be.

We also need to consider population variation in adolescence and pregnancy. Variation in age at first birth in traditional populations is quite wide, from sixteen to almost twenty six years of age (Walker et al. 2006). In more traditional populations you see a lot of allomothering and grandmothering to support first time mothers, who are often teenagers (Hawkes 2003; Hrdy 2009; Kramer 2005; Kramer 2008). So, support systems are built in, and it does not alter the trajectory of your life in the same way teen pregnancy does in an industrialized population.

This range of variation in age at first birth, and the fact that most of those young mothers do just fine, perhaps even end up with higher reproductive success, leads me to my second point: the physiological evidence against teen pregnancy might be overstated. In her talk, Karen discussed a paper of hers in the American Journal of Physical Anthropology that described the negative health outcomes of teen pregnancy (Kramer 2008). In it, she reviewed literature that suggests that when you control for lack of prenatal care, first pregnancy, and low socioeconomic status, the common assumption that pregnancy is harmful to teens is significantly weakened.

Further, in her own work with Pumé foragers in Venezuela, mothers under the age of fourteen were the only group to have greater infant mortality than the referent group of late reproducers (Kramer 2008). Yet when we teach young girls about their bodies, we tell them that their bodies are not equipped to have babies in their teens and that there are extreme consequences (in fact, I have said exactly this in the past). The reality is that those consequences are worst for very young teens, and may not be as significant in older teens.

Am I advocating teenagers get pregnant? Absolutely and unequivocally no. But I think they need access to correct information, not skewed information. This means telling them the truth about our uncertainties about the health implications for hormonal contraception in adolescence, it means educating them about the importance of barrier methods, and it means making sure they understand the health risks associated with unprotected sex.

This is a nuanced issue that requires nuanced thinking. Despite my concerns about adolescent hormone contraceptive use, there are problems with barrier methods as well, particularly when there may be a cultural bias against their use, or in situations when women cannot safely use contraception in an obvious way with their partner (Gupta et al. 2008). Again, what is important here is conveying correct information, so that each individual can weigh the pros and cons as they relate to her own context. This means it could be an excellent idea for some twelve year olds to be on hormonal contraception, and a terrible one for other girls through the age of twenty. It is going to have to be up to them.

I hope this post generates some thinking and some conversation, and I welcome people who might push me in a different direction than where I’m currently thinking. I am sharing this now, before putting it together as a manuscript, to provoke thoughts and comments.

References

Bentley GR (1994). Ranging hormones: do hormonal contraceptives ignore human biological variation and evolution? Annals of the New York Academy of Sciences, 709, 201-3 PMID: 8154705

Bentley GR. 1996. Evidence for interpopulation variation in normal ovarian function and consequences for hormonal contraception. In: Rosetta LaM-T, C.G.N., editor. Variability in human fertility. Cambridge, UK: Cambridge University Press. p 46-65.

Clark, L. (2004). Menstrual irregularity from hormonal contraception triggers significant reproductive health fears in adolescent girls Journal of Adolescent Health, 34 (2), 123-124 DOI: 10.1016/j.jadohealth.2003.11.091

Clark, L. (2001). Will the Pill Make Me Sterile? Addressing Reproductive Health Concerns and Strategies to Improve Adherence to Hormonal Contraceptive Regimens in Adolescent Girls Journal of Pediatric and Adolescent Gynecology, 14 (4), 153-162 DOI: 10.1016/S1083-3188(01)00123-1

Collaborative group (1996). Breast cancer and hormonal contraceptives: collaborative reanalysis of individual data on 53 297 women with breast cancer and 100 239 women without breast cancer from 54 epidemiological studies The Lancet, 347 (9017), 1713-1727 DOI: 10.1016/S0140-6736(96)90806-5

Collaborative Group on Epidemiological Studies of Ovarian Cancer, Beral V, Doll R, Hermon C, Peto R, & Reeves G (2008). Ovarian cancer and oral contraceptives: collaborative reanalysis of data from 45 epidemiological studies including 23,257 women with ovarian cancer and 87,303 controls. Lancet, 371 (9609), 303-14 PMID: 18294997

Collins, N., Dunkel-Schetter, C., Lobel, M., & Scrimshaw, S. (1993). Social support in pregnancy: Psychosocial correlates of birth outcomes and postpartum depression. Journal of Personality and Social Psychology, 65 (6), 1243-1258 DOI: 10.1037//0022-3514.65.6.1243

D’Antona Ade O, Chelekis JA, D’Antona MF, & Siqueira AD (2009). Contraceptive discontinuation and non-use in Santarém, Brazilian Amazon. Cadernos de saude publica / Ministerio da Saude, Fundacao Oswaldo Cruz, Escola Nacional de Saude Publica, 25 (9), 2021-32 PMID: 19750389

Feldman PJ, Dunkel-Schetter C, Sandman CA, & Wadhwa PD (2000). Maternal social support predicts birth weight and fetal growth in human pregnancy. Psychosomatic medicine, 62 (5), 715-25 PMID: 11020102

Fraser IS, & Kovacs GT (2003). The efficacy of non-contraceptive uses for hormonal contraceptives. The Medical journal of Australia, 178 (12), 621-3 PMID: 12797849

Gerschultz KL, Sucato GS, Hennon TR, Murray PJ, & Gold MA (2007). Extended cycling of combined hormonal contraceptives in adolescents: physician views and prescribing practices. The Journal of adolescent health : official publication of the Society for Adolescent Medicine, 40 (2), 151-7 PMID: 17259055

Gubhaju, B. (2009). Barriers to Sustained Use of Contraception in Nepal: Quality of Care, Socioeconomic Status, and Method-Related Factors Biodemography and Social Biology, 55 (1), 52-70 DOI: 10.1080/19485560903054671

Gupta, N., Corrado, S., & Goldstein, M. (2008). Hormonal Contraception for the Adolescent Pediatrics in Review, 29 (11), 386-397 DOI: 10.1542/pir.29-11-386

Hawkes, K. (2003). Grandmothers and the evolution of human longevity American Journal of Human Biology, 15 (3), 380-400 DOI: 10.1002/ajhb.10156

Hrdy SB. 2009. Mothers and others: the evolutionary origins of mutual understanding: Belknap Press.

Kahlenborn, C., Modugno, F., Potter, D., & Severs, W. (2006). Oral Contraceptive Use as a Risk Factor for Premenopausal Breast Cancer: A Meta-analysis Mayo Clinic Proceedings, 81 (10), 1290-1302 DOI: 10.4065/81.10.1290

Kramer, K. (2005). Children’s Help and the Pace of Reproduction: Cooperative Breeding in Humans Evolutionary Anthropology: Issues, News, and Reviews, 14 (6), 224-237 DOI: 10.1002/evan.20082

Kramer KL (2008). Early sexual maturity among Pumé foragers of Venezuela: fitness implications of teen motherhood. American journal of physical anthropology, 136 (3), 338-50 PMID: 18386795

KRISHNAMOORTHY, N., SIMPSON, C., TOWNEND, J., HELMS, P., & MCLAY, J. (2008). Adolescent Females and Hormonal Contraception: A Retrospective Study in Primary Care Journal of Adolescent Health, 42 (1), 97-101 DOI: 10.1016/j.jadohealth.2007.06.016

Lipson, S., & Ellison, P. (2008). Normative study of age variation in salivary progesterone profiles Journal of Biosocial Science, 24 (02) DOI: 10.1017/S0021932000019751

Marchbanks, P., McDonald, J., Wilson, H., Folger, S., Mandel, M., Daling, J., Bernstein, L., Malone, K., Ursin, G., Strom, B., Norman, S., Wingo, P., Burkman, R., Berlin, J., Simon, M., Spirtas, R., & Weiss, L. (2002). Oral Contraceptives and the Risk of Breast Cancer New England Journal of Medicine, 346 (26), 2025-2032 DOI: 10.1056/NEJMoa013202

Modan B, Hartge P, Hirsh-Yechezkel G, Chetrit A, Lubin F, Beller U, Ben-Baruch G, Fishman A, Menczer J, Struewing JP, Tucker MA, Wacholder S, & National Israel Ovarian Cancer Study Group (2001). Parity, oral contraceptives, and the risk of ovarian cancer among carriers and noncarriers of a BRCA1 or BRCA2 mutation. The New England journal of medicine, 345 (4), 235-40 PMID: 11474660

Narod, S., Risch, H., Moslehi, R., Dørum, A., Neuhausen, S., Olsson, H., Provencher, D., Radice, P., Evans, G., Bishop, S., Brunet, J., Ponder, B., & Klijn, J. (1998). Oral Contraceptives and the Risk of Hereditary Ovarian Cancer New England Journal of Medicine, 339 (7), 424-428 DOI: 10.1056/NEJM199808133390702

Ott, M., Adler, N., Millstein, S., Tschann, J., & Ellen, J. (2002). The Trade-Off between Hormonal Contraceptives and Condoms among Adolescents Perspectives on Sexual and Reproductive Health, 34 (1) DOI: 10.2307/3030227

ROYE, C. (1998). Condom use by hispanic and african-american adolescent girls who use hormonal contraception Journal of Adolescent Health, 23 (4), 205-211 DOI: 10.1016/S1054-139X(97)00264-4

Roye CF, & Seals B (2001). A qualitative assessment of condom use decisions by female adolescents who use hormonal contraception. The Journal of the Association of Nurses in AIDS Care : JANAC, 12 (6), 78-87 PMID: 11723916

SAYEGH, M., FORTENBERRY, J., SHEW, M., & ORR, D. (2005). The developmental association of relationship quality, hormonal contraceptive choice and condom non-use among adolescent women Journal of Adolescent Health, 36 (2), 97-97 DOI: 10.1016/j.jadohealth.2004.11.009

SMITH, J., GREEN, J., DEGONZALEZ, A., APPLEBY, P., PETO, J., PLUMMER, M., FRANCESCHI, S., & BERAL, V. (2003). Cervical cancer and use of hormonal contraceptives: a systematic review The Lancet, 361 (9364), 1159-1167 DOI: 10.1016/S0140-6736(03)12949-2

Turner, R., Grindstaff, C., & Phillips, N. (1990). Social Support and Outcome in Teenage Pregnancy Journal of Health and Social Behavior, 31 (1) DOI: 10.2307/2137044

Vihko R, & Apter D (1984). Endocrine characteristics of adolescent menstrual cycles: impact of early menarche. Journal of steroid biochemistry, 20 (1), 231-6 PMID: 6231419

Vitzthum, V., & 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 DOI: 10.1111/j.1728-4465.2005.00038.x

Vitzthum, V. (2001). Vaginal bleeding patterns among rural highland Bolivian women: relationship to fecundity and fetal loss Contraception, 64 (5), 319-325 DOI: 10.1016/S0010-7824(01)00260-8

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

ZIBNERS, A., CROMER, B., & HAYES, J. (1999). Comparison of continuation rates for hormonal contraception among adolescents Journal of Pediatric and Adolescent Gynecology, 12 (2), 90-94 DOI: 10.1016/S1083-3188(00)86633-4

The Scorpion and the Frog: don’t try and tell me why I do this

On April 8th, I was fortunate to be in the company of Matt Richtel, Scott White, Diana Yates and Dan Simons as part of a talk and panel discussion sponsored by the Beckman Institute and the College of Media at the University of Illinois. Matt Richtel is a Pulitzer prize-winning journalist for the New York Times who has written on distracted driving, your brain on computers, and, as many of you know, neuroscientists on a raft. Matt also writes a comic and has published two works of fiction. It was a pleasure getting to know a journalist so committed to respecting scientists and getting the story, and the science, right.

Matt began the event with a short, engaging talk on the interaction between scientists and journalists. He started with the fable of the scorpion and the frog, yet never quite resolved for the audience whether he saw the scorpion as the journalist or scientist. He shared several experiences with scientists who were uninterested in talking to the press, some who pushed him to add complexity or uncertainty to a story, and some who managed to convey simple, compelling ideas in their quotes. I want to briefly describe what he said about these three populations.

For those uninterested in talking to the press, Matt suggested that, for some, this may be due to a distrust of the press, or fear of how one will be represented to colleagues. He described a time that a female scientist agreed to talk to him, on the condition of not having her picture taken for the story. She was a former model, she explained, and didn’t want her image associated with her science, lest her colleagues take her less seriously. Unfortunately, I think there are plenty of fields where this is a legitimate issue, if past issues in the science blogosphere are any indication. That said, I think he makes a good point that while you do take a risk in talking to the press, and there may be times where your work isn’t perfectly represented (and even times where it is grossly misrepresented), most of our colleagues know not to just blame the scientist. Besides, if you have a colleague that is that punitive, they aren’t a very good colleague!

Matt told a story about a scientist who worked with him on a piece, then backed out and asked that all of his material be removed. Over the course of a difficult conversation, the scientist revealed his fear that his colleagues would judge his quotes as overstating the results of the evidence. Eventually, they worked out an alternative quote that simply added in a qualifier (I believe it was the word “almost” but I don’t remember). Keeping the qualifier, or pushing for its inclusion, can satisfy a lot of scientists talking to the press, and in doing so it adds a necessary element of uncertainty. The scientific method s not about proving things, it is about disproving them. You want to disprove the null hypothesis (an example of this would be that your hypothesis is that estrogen varies with lifestyle, and the null hypothesis is that there is no difference in estrogen based on lifestyle). And, when you get evidence that supports your hypothesis, this doesn’t prove a thing. All it does is support the hypothesis in the context of that particular study’s parameters. Given this understanding of the scientific method, perhaps journalists could see how much scientists chafe at bold conclusions or words like “proof” or “fact!”

Finally, Matt described a class of scientists who are not only good to work with, but provide statements that convey complex ideas in an engaging, easy to understand way. He calls these scientists Quote Monkeys. Quote Monkeys not only distill a difficult idea for a lay audience, yet convey excitement and delight in science. He used the example from his “your brain on computers” series where one scientist said “Bring back boredom!” This captures the idea that not multi-tasking all the time, that having downtime to process events rather than always being plugged in, is good for our brains. (So, if you’re reading this on your phone in the bathroom, put the phone down. You know who you are!)

After Matt’s wonderful talk, Scott, Diana and I served as panelists, with Dan Simons moderating. Scott White is a professor in Aerospace Engineering who has had some media attention for his supercool self-healing materials. I appreciated his approachable, dry style. Diana Yates is a journalist who covers the life science beat for the University of Illinois News Bureau, and she has done an amazing job over the years showing the rest of the world why the science that happens here at Illinois is so exciting. Dan Simons co-authored a great popular science book The Invisible Gorilla (I bought it for my brother in law this past winter before I realized Dan was on campus), and has a social media presence as well, curating interesting material mostly on cognitive psychology. We each gave a little introduction to ourselves regarding our experiences with journalists; I largely talked about how social media is what has connected me to science journalists, and my experiences with CNN.com and USA Today writers (both positive).

The questions we received were good ones, ranging from how to keep from looking like a fool while talking to journalists to how to write science stories without resorting to clichés or self-help hooks. For the first issue, we discussed the importance of asking a journalist for her/his timeline (is your story due in 20 minutes, hours or days?) and that one should request seeing the quotes that will be used before the story goes live. You also don’t have to say yes to every request; if the timeline is too short or you have looked up the journalist and they or their employer aren’t reputable, just move on. For the second question, I talked about reframing the question that captures the audience’s interest from “how does this affect me?” to “why should I care?” or “why is this cool?” I mentioned Ed Yong as an excellent example of a writer who delights the reader, regardless of whether he is discussing algae, racism, or bat fellatio. He shares his excitement and is a guide, not a sage; I think Ed’s work is compelling for the same reasons NPR’s Radiolab is so good. You get the sense the narrator is learning along with you, though in Ed’s case I think you also get the sense that he has scientific expertise to add credibility to his analysis and what he chooses to cover.

One audience member made a rather bold, critical claim that journalists and scientists were in cahoots to promote the journalists and get the scientists tenure. The other panelists handled this one delicately. I did not (what, you are surprised?). Academic readers of this blog are likely aware that writing a blog is a professional risk, as is talking to journalists, especially when one is a junior faculty member. As John Hawks said in his panel on blogging in the academy at Science Online 2011, blogging is at best a tertiary activity. But if you use your blog not only to reach out to layfolks but also to make broader claims about your field, you may have critics as well as fans. I know the risks I take every time I put up a new blog post or agree to talk to a journalist. But I have also decided that my enjoyment, and the benefits to my own goals of scientific outreach, far outweigh the risks. I want women to read my posts and pass them on to their daughters. I want readers of sites like Jezebel and Feministe getting excited about biology. And I want every person who has found evolutionary psychology claims intuitive to think on the bias that produces that false intuition.

When I was a child, my parents had the following Man of La Mancha quote in our bathroom, on a poster directly opposite the toilet:

Too much sanity
May be madness
But the maddest of all
Is to see life as it is
And not as it should be.

I learned to read with that quote. I sang it in my head. And when I was younger, it meant absolutely nothing to me. I don’t remember the moment exactly when it went from something I chanted in my head to something that defined my own outlook on the world. But I want to make this job into the job it should be, not the job it is. To me, that means blogging, talking to laypeople about science, and interacting with science communicators and journalists.

But don’t tell me I do it to get tenure.

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