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.
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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.
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.
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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.
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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
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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
Panel today, 11am: "The Scorpion and the Frog, How Journalists and Scientists Can Learn To Trust Each Other (though occasionally they shouldn’t)."
Come see me blather on about how social media can bring the scorpions and frogs together. The main speaker is Matt Richtel, New York Times science journalist.
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Matt Richtel, Pulitzer Price winning journalist from the New York Times, will present a special lecture on Thursday, April 7 at 11:00 a.m. in the Beckman Auditorium. His talk is entitled “The Scorpion and the Frog, How Journalists and Scientists Can Learn To Trust Each Other (though occasionally they shouldn’t).”
Matt’s talk (about 30 minutes) will be followed by a discussion of Science and Journalism with a small panel of colleagues from science and the media (Kathryn Clancy, Diana Yates, Brant Houston, Dan Simons & Scott White).
Abstract for Matt Richtel’s presentation:
More so than ever, journalists and scientists need to be great partners in disseminating discovery and truth. But they need to learn to better understand each other’s needs and methods. Here are some concrete tips for so doing, told through war stories (some personally embarrassing to the speaker, some to the scientists), and as told too through the examples from the Pulitzer Prize winning series “Driven to Distraction” about the risks of multitasking behind the wheel.
Matt Richtel’s Bio:
Matt Richtel is a Pulitzer-prize winning journalist and novelist. Since
2000, he has worked in the San Francisco bureau of the New York Times, covering technology and its impact on society. His recent series “Your Brain On Computers,” focuses on how heavy technology use impacts behavior and the brain. His series about distracted driving won the 2010 Pulitzer Prize for National Reporting. His first novel, Hooked, was a critically-acclaimed tech-centric thriller. The sequel, Devil’s Plaything, hits bookstores in May, 2011.
If I objectify you, will it make you feel bad enough to objectify yourself? On shopping, sexiness and hormones.
When I was younger, periods were not a fun time, and I was plagued with dysmenorrhea, which is a fancy term for really bad cramps. In high school, I would often take 1000 mg of ibuprofen every four hours to alleviate symptoms to get through all my classes, band, sports practice, and homework (what, it took you this long to realize I was, and am, a dork?).
After having my daughter in 2008, and the thirteen months of lactational amenorrhea that followed it (lactational amenorrhea means absence of periods due to lactation), my periods resumed. Pain during my periods has almost totally ceased, but I have noticed more cycle-related variation in emotion. In particular, my patience and tolerance for rude behavior, and my tendency to cry sentimentally at even the lamest greeting card, skyrocket in my premenstrual phase. I already have low tolerance for rudeness, and I already cry easily. But something about progesterone decline — which is a normal process towards the end of ovulatory cycles — seems to make it harder for me to repress these behaviors in order to fit in culturally with those around me.
I tell this to you to say, I don’t doubt that hormones, and hormonal variation through the cycle, plays some role in variation in female behavior and emotion. And I find this kind of work inherently interesting. I hate to repeat myself, but you will find echoes of my structural and methodological concerns with evolutionary psychology in this post as well.
Durante et al (2011) observe that women spend more money on their appearance than men, and claim that this sex difference is cross-culturally consistent (I wonder, is this consistent across cultures without money?). In order to understand this sex difference, they wish to see whether spending or shopping behavior is dependent on cycle phase. Therefore the authors hypothesize that women choose sexier clothing during ovulation — “even if the women themselves are not consciously aware of this biological fact” (Durante et al 2011: 922), a problematic turn of phase if I ever saw one, but I’ll get to that later. They also consider the effects of priming a shopping woman with images of attractive women and hypothesize there is a greater effect of this priming on high-fertility women.
The participants were female undergraduates and were compensated with course credit or money. The authors claim the participants had no idea the study had anything to do with the menstrual cycle, but the participants had to use LH strips at midcycle to see when she was ovulating (this is a urine test to check for a luteinizing hormone peak, which comes before ovulation).
Here’s the important part, for me:
“The first urine test was scheduled 2 days before the expected day of ovulation. If an LH surge was not detected, women came back each day until an LH surge was detected or six tests had been completed, whichever came first” (Durante et al 2011: 924).
Here are my questions: what is 2 days before the expected day of ovulation? The follicular phase — that’s from menstruation to ovulation — is the most variable phase of the menstrual cycle (Fehring et al. 2006; Lenton et al. 1984). I wonder how many ovulations they missed because of this. Perhaps even worse, how many participants had six LH tests and didn’t have a detectable LH surge? It sounds like they were included in the project. But, they either ovulated before the authors started testing, or they had an anovulatory cycle. That means the authors were including participants in their study that weren’t ovulating… in a study of behavior during ovulation.
Participants viewed a made-up shopping website on a high-fertility (near the LH surge) and low-fertility (about eight days later) day, where they had to select ten items they would like to buy that day. They were randomized into two groups: one shown a site featuring casual clothes, the other featuring clothes and accessories. The clothing on these made-up sites were “pretested to be sexy” (Durante et al 2011: 925). While that is a phrase I never expected to write on this blog, the separate validation they did to determine sexy versus nonsexy clothing seems fine.
Hypothesis 1: Near ovulation, women should be more likely to choose sexier and revealing clothing and other fashion items rather than items that are less revealing and sexy (Durante et al 2011: 923).
Women chose a greater percentage of sexy clothing and accessory items near ovulation: 59.8% ± 21.6 during ovulation, 51.3% ± 22.4 during low fertility. This was a statistically significant difference, but they did a repeated measures ANOVA, and I don’t understand why they didn’t do a paired t-test. Further, statistically significant or not, I question how meaningful it is when the averages are so close and the standard deviations almost completely overlap.
H2: Ovulation should lead women to be especially likely to choose sexier products when women are primed to compare themselves to attractive female rivals (Durante et al 2011: 924).
H3: There should be no differences in product choice between ovulating and nonovulating women when women are primed with unattractive women or men (Durante et al 2011: 924).
Follow-up studies primed sub-sets of participants (so a different cohort, same recruitment methods as above) to think about 1) attractive local women, 2) unattractive local women, 3) attractive local men, 4) unattractive local men. They did this by showing photographs of people who they claimed to be local and asking participants to rate their attractiveness.
When primed with attractive women, the percentages of sexy items chosen were 62.7% for ovulating women and 38.2% for low fertility women (I could not find standard deviations for these values so have no idea how much the two groups overlap). Priming with unattractive women, attractive men, or unattractive men produced no significant difference between low and high fertility women.
H4: Ovulation should lead women to choose sexier products when primed to think about local attractive women who constitute potential direct rivals. However, ovulation should not influence product choice when women are primed to think about women from distant locations because such women do not constitute direct rivals (Durante et al 2011: 924).
The authors used a different method for assessing fertility this time; they asked women their normal menstrual cycle length and counted back from menses to estimate when ovulation would be. So AGAIN, we don’t know how many women actually ovulated in this study, and we don’t know whether a significant portion of women were then grouped in the high-fertility group who shouldn’t have been.
This study is like the previous one in terms of photo priming, but this time the photos were said to be local or distant, and were of women only (so the four groups were local attractive, local unattractive, distant attractive, distant unattractive).
The authors claimed that the relationship between fertility, photo attractiveness and location was “marginally significant,” but the p-value was 0.09. That is, in fact, not significant, as significance is generally only considered under 0.05 unless you cheat and say your study is special and should consider a different limit (they don’t say this in their study).
That said, the only significant effect found of photo priming on high versus low fertility women was in the local attractive women group: high fertility women chose 65.8% sexy items versus low fertility’s 39.1% (I could not find standard deviations for these values so have no idea how much the two groups overlap). These results are almost identical to those found when priming women with attractive women without saying if they are local or not.
How biological are we talking here?
The authors claim a biological cause for the differences found above. And maybe there is, to some extent. But there are two major issues with the authors’ conclusions.
First, there is the major methodological flaw of including women who probably aren’t ovulating in their high-fertility group. Heads up to people who don’t study female physiology: women, even healthy women with “normal” cycle lengths, don’t ovulate every cycle. So if understanding a behavior during ovulation is important to your hypotheses, you need daily hormones on top of that LH test. Then, you know, if you can’t document ovulation, you need to exclude those women from your sample. Oh, and while we’re discussing methods, the authors don’t mention whether the participants were in a relationship or not, or what their sexualities were, or their races or socioeconomic statuses. These are all important to understanding variation in female-female competition (Campbell 2004). And since ornamentation is likely related to honest signals of health, it would be good to know waist to hip ratios, or BMI, or facial symmetry (Streeter and McBurney 2003) (hello, I’m handing someone a dissertation here! Just remember to cite me correctly).
But the second issue relates to the theme I saw throughout this paper, that changes in mood or choice behavior due to ovulation or presence of attractive women is a “biological fact.” Female-female competition is certainly found within human behavior, and behavior changes through the menstrual cycle. But is it fair to call these behaviors strictly biological, or should we have a more nuanced understanding of the interaction between biology and culture?
There are alternative cultural theories out there. Objectification theory proposes that there are consequences to living in a culture that sexually objectifies women: when women are continually appraised based on their looks, it leads to a disconnect between their body and individual (Moffitt and Szymanski 2011). This disempowers women and leads to them feeling as though their bodies exist for the pleasure of others. And if this is what women learn they have to offer others, and they seek affirmation, praise or attention from those around them, it makes sense for women to compete around attractiveness, particularly sexiness.
I would posit that shopping, particularly when primed with the image of an attractive woman, is a kind of objectification. So really, what Durante et al (2011) are measuring are the results of objectifying their study participants. Under these circumstances, a woman is more likely to start treating herself as an object to be evaluated on the basis of her appearance, so it makes sense that she would choose sexier clothing, in an effort to produce a culturally-appropriate, attractive body.
As the study stands, there is no way to parse out the impact of biology or culture — and many cultures encourage objectification, female-female competition and female attractiveness towards men. As for how that interacts with high versus low fertility samples… that’s the interesting part of this paper. If we can trust how the women are parsed. Which we can’t, since some of the high-fertility sample might not have been ovulating.
These high heels are made of deer antlers
|Antler booties from Camilla Skovgaard.|
The authors also seemed enamored with the idea of comparing their female participants to male animals. Twice they mention the idea that they want to determine whether sexy clothing is analogous to a peacock’s tail, a deer’s antlers, or a lion’s mane (really). These three examples, according to the authors, reflect a courtship function, a same-sex competition function, or both functions respectively. The authors go on to say that their results suggest that sexy dressing in women is like deer’s antlers, or, a same-sex competition function.
First, since when are a deer’s antlers only a same-sex competition function? Second, doesn’t it say something that they couldn’t find any examples of this kind of display in a female animal? This begs the question of why female humans do so much more displaying and maintenance of their appearance compared to other female animals, and again, this suggests interactions between biology and culture (Smuts 1995).
We can spin all the stories we want to explain why many human females make efforts to be physically attractive. And I do think Durante et al (2011) are on to something here as, despite methodological concerns they did find differences in high- and low-fertility choices. But if we continue to do this research on undergraduates in western contexts without sufficient hormone analysis, I’m unsure that its meaning extends beyond the participant pool.
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