Tuesday, May 17th 2011
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.
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
Wednesday, April 20th 2011
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.
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.
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//0022-3522.214.171.1243
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
Saturday, April 16th 2011
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.