Laboratory for Evolutionary Endocrinology

LabEvoEndo Journal Club: Dana Ahern presents on PMDD

2011-04-11T18:22:00.000-05:00

This is the third guest post of the LabEvoEndo Journal Club, a new series for the LabEvoEndo blog meant to highlight student contributions to the lab (first post here, second post here). The author is Honors Anthropology Junior Dana Ahern. Dana has been in my lab since her sophomore year.

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I’d like to start this blog post with a little background on progesterone. Progesterone is fascinating and it affects a lot more than just the menstrual cycle. We are starting to understand just how big of an impact progesterone has, and the research project I am working on is beginning to show some of the potential applications of progesterone in medicine. These applications include improving recovery time after traumatic brain injury and strokes, as well as helping us understand postpartum depression (PPD) and premenstrual dysphoric disorder (PMDD).

PMDD is similar in mechanism with postpartum depression, although the exact mechanism is still being researched. Some research suggests a hormonal influence, as allopregnanolone, an offshoot neuroregulator of progesterone, modulates GABA, which is a neurotransmitter related to mood and anxiety. Too much GABA results in increased anxiety and mood related issues, so it is a logical conclusion that the drop in progesterone during the late luteal phase of the menstrual cycle would result in excess GABA and therefore symptoms of PMDD.

The article we discussed looked at PET scans of 12 women with and 12 women without a diagnosis of PMDD, taking scans during the follicular phase and the late luteal phase of their menstrual cycles. The women in the study were screened for two months with mood surveys and then taken in for a day of PET scans and blood/urine samples, once during the follicular phase and once during the late luteal phase, when the symptoms of PMDD would have begun. PMDD can affect certain brain functions, so they were using the PET scan to detect brain dysfunction, such as one study the article looked at that showed frontal lobe dysfunction associated with PMDD.

The hormone measurements didn’t show anything significant and PET scans showed increased cerebellum activity from follicular to late luteal phase in PMDD women only. The cerebellum has many GABA receptors, which is a possible explanation of this, but in journal club, we wondered if it is the lack of modulation after a drop in the progesterone, or if there is something going on with the number of receptors, such as perhaps some sort of diminished sensitivity to allopregnanolone.

In journal club, we discussed some of the problems we had with this study. Someone brought up the small sample size and too few collection times for samples and scan. The fact that only one cycle was measured impacted the study. Kate also mentioned that blood hormones are a less useful measure than salivary hormone measurements. Finally, while the article states that the cause of PMDD is an overactive cerebellum in women suffering from PMDD, they never really reach a definite reason for what is causing the increased action. Ultimately, the article would have benefitted from examining the hormones more closely and more often.

Reference

Rapkin AJ, Berman SM, Mandelkern MA, Silverman DH, Morgan M, & London ED (2011). Neuroimaging evidence of cerebellar involvement in premenstrual dysphoric disorder. Biological psychiatry, 69 (4), 374-80 PMID: 21092938

LabEvoEndo Journal Club: Sophia Bodnar presents on cervical cancer

2011-04-04T12:03:00.000-05:00

This is the second guest post of the LabEvoEndo Journal Club, a new series for the LabEvoEndo blog meant to highlight student contributions to the lab (first post here). The author is Anthropology Junior Sophia Bodnar. Sophia has been in my lab since her sophomore year.

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In light of recent acceptance to a summer program where I will be working in immunology, I wanted to choose an article relevant to reproductive health and immunology. The first place I turned to was the Journal of Reproductive Immunology. This seems like a copout, but I found a very interesting and recent article for the lab meeting entitled "Higher levels of cervicovaginal inflammatory and regulatory cytokines and chemokines in healthy young women with immature cervical epithelium" by Hwang et al in 2011.

It would be wonderful if human variation was always taken into account, particularly when discussing reproductive health. This is exactly what the researchers from UCSF aimed to do and why this article was a refreshing read. It is known that women aged 15-24 have the highest rates of Sexually Transmitted Infections (STIs) and is commonplace in the medical community to associate STIs with risky sexual behavior. The study looked at cervical epithelium, tissue that lines the cervix, and accompanying levels of cytokines and chemokines in order to show basic biological differences in immune function of the cervix between adults and adolescents to account for the predominance of STIs in younger women.

Thirty-two women aged 13-21 were selected. The women were placed in the immature group (>50% columnar epithelium) or mature cervical group (<5% columnar epithelium). In order to help you envision these epithelial cells, think of a single line of figure skaters (fragile, columnar cells) versus a stack of sumo wrestlers (strong, squamous cells). Younger women have more columnar cells and throughout development the columnar cells become squamous cells. This is why it is extremely important to take variation into account, because at any given point in a woman’s development the ratio of squamous to columnar cells varies.

Participants were excluded for pregnancy, surgery on the cervix, cervical dysplasia (grades above 1), taking immunosuppressive agents, or being symptomatic for genital complaints such as yeast. However, women were not excluded for having HPV because the researchers consider it a very common infection. The women filled out surveys detailing sexual and nonsexual behavior (number of partners, contraception, substance abuse, etc) and reproductive health history (previous pregnancies, menarche, etc). Colpophotagraphs were taken of the cervical epithelium and the researchers measured and rated maturity by counting pixels from the photograph. Women were evaluated only once, a strong drawback to this study as they are interested in the variation of the epithelium.

They found that ten of the cytokines and chemokine levels were higher in the immature group (one cytokine was excluded). Although other studies have previously looked at cervical levels of cytokines and chemokines, this study looked at levels of these cell-signaling protein molecules in relation to type of cervical epithelium. The authors note that having more columnar cells may be considered beneficial for young women as these cells are more easily damaged and likely to initiate an immune response, but this would mean that younger women are less prone toward infection. The researchers then go on to conclude that because these columnar cells are more prone to damage and thus immune response, chronic inflammation is more likely which could lead to greater rates of infection. This study only looked at the epithelium of healthy women, so it is important to examine women with various infections in the future. The epithelium and levels of cytokines/chemokines in women with STIs could lead to a better understanding or correlation between type of epithelium and its subsequent immune response and risk rate.

In our discussion of the article, it was mentioned that there are no “normal” levels of cytokine and chemokine levels with which to compare the researcher’s values. In the study this was referred to as a challenge. Perhaps there will never be established normative levels of these protein molecules, but so what? Our lab group concluded that this should not be considered a challenge and may be beneficial as we will simply have to take variation into account which is strongly lacking in the medical realm of reproductive health! We all agreed that this study should have been conducted over a longer period of time, and that the women should have had their epithelium photographed and correlating levels of cytokines/chemokines measured far more often. Because this study’s main focus was variation of the epithilium, it would make sense for these women to contribute visits over the course of their entire menstrual cycle whereas this study simply adjusted for days since last menstrual cycle. We also discussed that this study may be perceived as far more qualitative than quantitative. However, we acknowledged that the clarity of the cervical photos was great so quantitative measurements of the pixels could be taken seriously. It was also noted that these findings were not all that surprising. It seems commonsense that younger women have cells that are more easily damaged and that this could lead to chronic inflammation that poses negative risks. Although this may be true, I think that we should still applaud these authors for acknowledging variation throughout their research.

I also find it interesting that the most common cervical cancer is squamous cell carcinoma. Columnar cells may be damaged more easily, but it seems that squamous cells are more prone towards division and supporting abnormal growth. Most cases of cervical cancer are due in part to HPV infection, which in going along with the findings of this article, is more common in younger women with immature columnar cells. It would be interesting to see how the squamous cells in women with cervical cancer compare to the columnar cells of women with HPV. Perhaps cervical cancer, as a result of HPV, is more common in women who have more columnar cells than squamous cells, but the cancer arises in and prefers the squamous cells because they are less likely to initiate a strong immune response. In general, I appreciate how easy and enjoyable this article is to read. Hopefully more articles acknowledging variation, particularly when it comes to reproductive health, will be published as a result of this interesting finding.

Reference

Hwang LY, Scott ME, Ma Y, & Moscicki AB (2011). Higher levels of cervicovaginal inflammatory and regulatory cytokines and chemokines in healthy young women with immature cervical epithelium. Journal of reproductive immunology, 88 (1), 66-71 PMID: 21051089

LabEvoEndo Journal Club: Laura Klein presents on food allergies

2011-03-24T15:22:00.000-05:00

This semester I'm trying out something a bit new -- I've encouraged my students to do quick write-ups of the papers they present in journal club in a way they think would be suitable for a blog post. This is to share what we're up to and give my brilliant students a chance to show their stuff.

This first guest post of the LabEvoEndo Journal Club is by Integrative Biology Honors Senior Laura Klein. Laura's been in my lab since her sophomore year.

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Welcome, readers! This blog post will start a series of posts by undergraduate lab members about the topics that LabEvoEndo currently finds interesting and are discussing in our weekly lab meetings. Usually, these will be related to our own current research projects and will somehow tie into the broader goals of the lab.

The other week, I spent a lot of time looking at some Polish survey data related to food allergies and food intolerances that Dr. Clancy and I collected last summer. This led me to thinking about the health implications of food allergies, so this week’s lab meeting article is "Food allergies in children affect nutrient intake and growth” by Christie et al from 2002. As the authors from this article are all medical professionals, I also wanted to supplement this article with some information about the daily social stressors that food allergies can have on individuals or families, so we also read excerpts about The Impacts of Food Allergies on the Quality of Life’ from Fernandez-Rivas and Miles “Food allergies: clinical and psychosocial perspectives.”

To give you some background for the study, 6-8% of American children will develop food allergies in the first 3 years of life, which also happens to be a critical period for growth. Of children with food allergies, most will have a single allergy to cow’s milk, eggs, peanuts, what, soy, tree nuts, or fish. Previous studies have found that children with cow’s milk allergies have a lower height/age ratio, though they did not propose a mechanism for this trend. One possibility is that elimination diets in general may reduce the amount of macro or micro nutrients available in the diet.

In this study, Christie et al. compared 98 children with and 99 children without food allergies (all about age 4) to determine if food allergies and elimination diets impact the growth and nutrient intake of children with food allergies. All children who were diagnosed with an allergy had been following a food elimination diet. The BMI, height-for-age, and weight-for-age for all children was compared to the CDC’s Health Statistics Growth Charts, and individuals were classified as having ‘potential undernutrition’ (<25th percentile), ‘adequate nutrition’ (25th-75th percentile), and ‘potential overnutrition’ (>75th percentile). Parents also completed three days of dietary intake records, which were compared with recommended dietary allowances.

The authors found that more children with allergies were categorized as having ‘potential undernutrition’ as determined by height-for-age than children without allergies. Additionally, a large number of these children had two or more allergies. Because the article only focused on height-for-age despite collecting many other measurements, we were skeptical that food allergies were the sole cause having low height-for-age. Some possibilities that we discussed but the study did not control for included premature birth and genetic influences on height or growth rates.

Another study result that generated much discussion was that more than 25% of the children in both the control and allergy groups were not getting the recommended daily intake levels of calcium and Vitamins D & E. We thought this was problematic, not necessarily for the health of the children, but for how recommended daily intake levels are defined. Children with milk allergies who consumed supplementary fortified beverages were more likely to be meeting all of the intake recommendations than even children without any dietary restrictions. Considering this, are the current guidelines a reflection of realistic intake for small children?

In the discussion, the authors introduce the possibility that ‘catch-up’ growth during puberty. They suggest that this could be many food allergies disappear as children mature, so foods can be reintroduced into the diet. However, we also suggested that early teenagers are usually simply hungrier than toddlers (as anyone who has been in a high school cafeteria knows). Greater consumption of calories may provide greater energy sources for growth. Also, by puberty, people usually have more access to food because they are able to prepare it themselves. Both of these situations could contribute to more available energy that could be used for growth.

Finally, we wrapped up our discussion talking about how different kinds of elimination diets have biological and social impacts. For members of our group with food allergies and intolerances, especially ones like nuts or gluten, group dinners can be a challenge because hosts can be unsure what to prepare and may only have one or two ‘safe’ dishes. This related to a problem brought up in both articles- that parents with children newly diagnosed with food allergies may unnecessarily restrict many foods because they are unsure what will cause an allergic reaction. This could cause an artificially limited availability or nutrients or calories. And, to tie this back to an earlier point, as children grow up and learn what foods to avoid, their teachers and friends’ parents may give them more freedom to choose a range of foods that are acceptable, instead of limiting them to one or two ‘safe’ foods.

A good analogy to this situation might be someone who has just decided to adopt a vegetarian diet. Younger people may at first be so focused on avoiding meat that they don’t pay attention to the nutrition content of their food. For example, cheese pizza and grilled cheese are meat-free, but don’t provide all protein, vitamins, and minerals needed for a complete diet. Also, young people who still live at home may have less control over the types of food bought or prepared. As one former vegetarian in the group told us, to balance all the portions of your diet takes a lot of effort and planning. She said she had never been more aware of what she was eating, but that it took time to figure out how to achieve a good balance of nutrients.

Stay tuned for updates and about brains and hormones!

References

Christie L, Hine RJ, Parker JG, & Burks W (2002). Food allergies in children affect nutrient intake and growth. Journal of the American Dietetic Association, 102 (11), 1648-51 PMID: 12449289

Fernandez-Rivas, M, & Miles, S (2007). Chapter 1. Food allergies: Clinical and Psychosocial Perspectives Plant Food Allergens DOI: 10.1002/9780470995174.ch1

Join me in a conversation about hormonal contraceptives! Eat free food!

2011-02-22T11:03:00.002-06:00

Women in the United States use hormonal contraceptives more than any other nation in the world. Doctors and patients in other countries report a hesitance to prescribe hormonal contraceptives for off-label use (to improve the skin, or regulate the cycle) where most pharmaceutical advertisements in the US celebrate exactly those uses.

Why do women in the US use hormonal contraceptives more frequently? How did you and your doctor decide that this prescription was right for you?

If you live in or near Champaign-Urbana, we would like to have you come participate in a focus group on exactly this topic! We would like to validate a survey that will be used online, but also get freeform responses from real women about their real experiences.

Please email us to participate! We can answer any questions you may have. You must be:

Over eighteen years old
Female
Have been prescribed hormonal contraceptives at least once

Participation involves:

Filling out an eligibility survey and indicating your time preference for the focus group (5 minutes)
Attending a focus group, where you will fill out a survey and discuss your broader experiences with hormonal contraceptives (90 minutes)

We will provide you with some tasty snacks during the focus group. So far we have found that participants have really loved being a part of this, because it’s given them a chance to reflect on their own contraceptive choices. Join us! Email us today! You will be helping us put together a comprehensive research program to understand why US women take hormonal contraceptives far more than women from other developed countries.

IRB approval for this message: #12269, amendment 02/22/2010

An embarrassment of riches

2011-02-07T13:09:00.000-06:00

Cross-posted at Context and Variation.

I have been quite the fancypants lately. In addition to the flood of new traffic from Science Online 2011, and in particular my post on the women scienceblogging panel, folks have been heading here to talk about broader issues of underrepresentation and racism, and, of course, iron-deficiency and the ladybusiness.

Then, because of a happy accident and the fact that Laura Weisskopf Bleill of Chambanamoms.com wanted to help me promote some focus groups I am running for a study on doctor-patient relationships around hormonal contraceptives,* I became a Chambana Mom to Know. At the same time I was recruited by the ever-clever John Hawks to do a bloggingheads.tv diavlog where we discuss women in science, blogging in academia, my fieldwork, the ladybusiness, #aaafail, and lots of other stuff.

I am feeling quite overwhelmed by the fact that I have a lot of new readers, and this is no longer the intimate space it once was (usually when I write, I imagine myself to be talking to a group of female friends while we sit on the couch and hang out - it now feels like giving a seminar to a medium-sized room full of people, where we are somehow still able to manage cool sidebar conversations). This is new and exciting, and while there is a part of me that will grieve for that little space where I knew most of the people who read me, I am delighted to bring anthropology to more people and keep pushing myself to write more accessibly for more people.

So, I am trying to think of next steps in terms of my writing. I still owe you all a summary of the survey I did on my readers a few weeks ago: given my day job commitments, that is the plan for what will probably be my single big post of the week.

However, I also want to continue to do two things: shorter researchblogging posts on articles I find interesting, and longer posts on specific issues around women's health, anthropology and medicine. So if there are particular papers you want me to read, particular topics you want me to cover... head over there to say so in the comments!

*I need to double-check with the IRB about whether I have approval to advertise this on the blog. If it turns out I do, expect a post on it this week!

LEE folks in the news

2011-01-18T12:30:00.001-06:00

Dr. Clancy was mentioned by Robin Lloyd in Scientific American today regarding the panel she co-chaired with Anne Jefferson, Sheril Kirschenbaum and Joanne Manaster at Science Online 2011 this past weekend on the Perils of Blogging as a Woman under her Real Name.

A quick highlight:

The entire concept of a woman science blogger overturns various long-held assumptions about science and gender. Kirshenbaum urged the session audience to bring important science and health information to women readers even at old guard, mass-media "women's" magazines such as Redbook. "I am adamantly a believer that we have to reach beyond [conventional science news outlets]," she said. "Science is not addressed to women. It's written for men and marketed to men even if men at the magazines don't claim that it is."
A face-palm reaction rippled among the 20 or so mostly female attendees of the session when "Not exactly rocket science" blogger Ed Yong (@edyong209) said, "I suspect there is a bias in terms of what is pushed to me through Twitter." He explained that, although other male writers often ask him to retweet links to their latest blog posts, not a single such request has ever come from a woman writer. Women in the room immediately broke into laughter, and commented about the novelty and presumptuousness to them of such a practice. Said Yong, "The fact that people haven't done this speaks volumes."

Check it out!

Cross-posted at Context and Variation

Dr. Clancy's post at Scientific American

2010-12-23T11:13:00.000-06:00

Head on over to the Scientific American Guest Blog for my post: "I don't have a twenty eight day menstrual cycle, and neither should you."

Enjoy and Happy Holidays!

What are some of the cool things happening in our lab?

2010-11-17T09:30:00.000-06:00

Despite a few efforts to get others to write in this space, my face from that CNN.com article is still at the top of the page a month and a half later. So I decided to share some of the cool things happening in the lab right now as a way to bump it down and highlight the hard work of my students and colleagues.

Dana Ahern and Antoine Dejong are both becoming mouse experts: they are working on my collaboration with Dr. Gregory Freund, Head of Pathology here at Illinois, looking at behavioral effects of progesterone.

Sophia Bodnar and Emily Marzolph, with Laura Klein, are starting to get together the resources we will need to run a large study in the spring to look at differences in circulating and excreted C-reactive protein.

Theresa Emmerling and Ashley Higgins, both graduates of LEE but still members of our lab group, have been working with me to develop a project to collect narratives from women about their experiences with hormonal contraceptives.

Mark Grabowski is RAing for me this semester and has been plugging away at the University of Saskatchewan collaboration analyses. He has been using some statistical methods with which I am completely unfamiliar, so I am glad to be learning a lot from him. He has already begun to find some very interesting relationships between C-peptide and endometrial thickness -- stay tuned as we figure out more!

Laura Klein is working away at graduate school and NSF GRF applications. Of course, she is also starting to get together the materials necessary for our study of cortisol, stress, and sonography. We are re-running some samples from my dissertation to see if cortisol is elevated on the days women had transvaginal ultrasounds, to test the assumption that these ultrasound are stressful.

Talia Melber is working on grant applications and her dissertation proposal. She is also looking at some archived data to see if she can come up with a useful proxy for hormones she is interested in.

Katie Tribble is experiencing a minor setback with a broken wrist, but will soon be able to run some tests on blood spots to make sure that medium will work with our assay kits. She is also applying to med school. For anyone reading: this is a young woman you would be lucky to have as a doctor!

Ashley Voigt has been doing some great work curating my current project files. She is also applying to pharmacy school and has been getting acceptances and interviews galore.

Dr. Clancy's IVF story, now on CNN.com

2010-10-04T18:26:00.001-05:00

I'm in a bragging mood, because it's not every day your face is on the front page of CNN.com. And the only reason why is because I jabbed some needles into my leg to help me have a baby!

Here's the permalink. And don't read the comments; they are mean.

I'm a bit bummed they didn't cover what, at least to navel-gazing me, is the cool part: the fact that I study women's reproductive biology and there are some interesting intersections between my experience and my research. The reporter Elizabeth Landau seemed quite interested in this and asked a lot of questions about it, so my guess is just that that part of the story ended up on the cutting room floor.

Anyway, I have been meaning to post this whole story to the blog, so consider this just a teaser for when I find more time later this week.

Adolescent Menstrual Variation and Oral Contraceptives

2010-08-31T13:47:00.000-05:00

The guest post below is by LEE alums Theresa and Ashley (currently skilled lab technicians planning their next steps in life!), with minimal editing by me. They did some fantastic research in their senior year and put together this blog post to teach the world about menstrual cycling in young girls. It's worth a read, and please comment with your thoughts!

Adolescent Menstrual Variation and Oral Contraceptives
By: Theresa Emmerling, Ashley Higgins and Kathryn Clancy

Many informational videos and documentaries have been produced to inform young women on the changes that they will experience during puberty and upon first menstruation, also called menarche. Unfortunately, these explanations are quite often generalizations that can lead to misrepresentations of what is normal. The information available to young women today stresses normative values for menstrual cycle length rather than the wide degree of variation characteristic of their cycles and may have an impact on adolescents’ future choices concerning oral contraceptives.

Figure 1 from Vihko and Apter 1984

Most women are taught that the menstrual cycle is twenty-eight days long, with ovulation occurring at day 14, and that only tiny deviations from this are healthy. Teens are taught to expect that every month after first menses they will experience menstruation for about 5 days; however, most adolescents do not experience the average menstrual cycle. Many adolescents experience longer menstrual cycles, with the luteal phase lasting anywhere between four to thirteen days (Apter, 1978), and anovulation, where an egg is not released from the ovary, is the primary characteristic of their cycles (Figure 1, Vihko and Apter 1984). The HPO axis is not an “on/off” switch that commences a string of twenty-eight day menstrual cycles at menarche. Rather, it takes time for the pituitary to respond to LH surges, which occurs only after multiple exposures to GnRH and estrogen (Apter et al, 1978; Apter, 1997). Therefore, it can take an adolescent up to five years to begin seeing something closer to the average twenty-eight day cycle (Figures 1 and 2, Vihko and Apter 1984).

Figure 2 from Vihko and Apter 1984

To be fair, the challenge is determining what the normal variation in an adolescent’s cycle is and what is due to pathology: environmental factors and pathologies may influence the menstrual cycle during development of the HPO axis. Numerous studies have tried to pathologize what we believe is normal variation in adolescent menstrual cycles, calling them “menstrual disturbances” or characterizing them as some level of amenorrhea (Morimatsu et al, 2009). As of yet, there is no conclusive evidence. Many studies find correlations between irregular menstrual cycles and pathology (Singer et al, 2009), but do not control for oral contraceptives (i.e., van Hoof et al, 2004), other environmental factors that may influence the HPO axis (Christo et al, 2008), or the study consists of adolescents with an already known pathology (El-Khayat, 2008). The American Academy of Pediatrics published a paper in 2006 stating that while the definition of amenorrhea is the absence of menses for six or more months, adolescents should be examined after only three months and "not reassured that it is 'normal' to have irregular periods in the first gynecological years" (p. 2247).

Given that it is more common, even normal, for adolescents to have very long menstrual cycles, we are concerned with what looks like stronger criteria for amenorrhea in exactly the population where it is expected (though the AAP paper discusses the low frequency of very long cycles, it also fails to mention the frequency of the pathology they worry is hidden in these long cycles). Further, more stringent criteria that misrepresents normal variation in this group of women serves only to frighten a population already concerned about normality and fitting in. For many, the teenage years are a time when standing out is to be avoided, and anything that makes one seem abnormal – an early or late age at menarche, long or short menstrual cycles – can be a stigma and cause stress. Educating young women on the reality, that this variation is what is normal, and that if anything the 28-day cycle is abnormal at this life stage, may prevent some of the considerable misunderstandings they have about their health. Understanding one's own body is an important step in making educated, healthy choices in the future. If most young women do not actually experience what they are taught is the average menstrual cycle, despite the fact that the reality is that wide variation in menstrual cycle length is the primary characteristic of post-menarcheal cycling, we are providing information that could lead them to feel abnormal and want to treat what is likely healthy variation.

A source of serious concern stems from what’s happening in the doctor’s office. Doctors, particularly in the United States, prescribe oral contraceptives at the slightest mention of deviation from the norm or evidence of a “menstrual disturbance.” In 79% of cases, health care providers will prescribe OCs at the patient’s request (Andrista et al, 2004). Less than 5% of doctors offer alternative forms of contraception to their patients in the US (Gerschultz, 2007), despite the fact that intrauterine devices, or IUDs, are more widely prescribed globally, and are both safe and effective. Future research questions should address whether doctors believe OCs are the best choice for women or that they the easiest method to prescribe; further, it is important to understand the decisions involved in prescribing these hormone treatments to adolescents. We have found evidence of doctors prescribing oral contraceptives to girls as young as twelve years of age (Cromer et al., 2008). Additionally, doctors prescribe OCs for adolescents who do not “live a lifestyle conducive to menstruation” (Sucato, 2002). We worry that ingesting cocktails of exogenous hormones have become a tool of convenience without regard to the possible trade-offs in their consumption. There is a large gap in the literature concerning adolescents and the long-term effects of OCs, yet doctors’ primary concern is that adolescents will accidentally skip a couple pills every pack (Omar et al, 2005).

Natural variation in adolescent hormone levels is a largely unexplored realm of science, with the same handful of decades-old articles cited repeatedly. Further research will yield not only a better understanding of this "time of change" but also less pathologizing of natural variation. However, until that research is published and generally accepted in the scientific and medical communities, the prescription of OCs for adolescents should weighted against the possible long-term impacts of priming an immature HPO axis with hormones.

References

American Academy of Pediatrics Committee on Adolescence, American College of Obstetricians and Gynecologists Committee on Adolescent Health Care, Diaz A, Laufer MR, & Breech LL (2006). Menstruation in girls and adolescents: using the menstrual cycle as a vital sign. Pediatrics, 118 (5), 2245-50 PMID: 17079600

Andrist LC, Arias RD, Nucatola D, Kaunitz AM, Musselman BL, Reiter S, Boulanger J, Dominguez L, & Emmert S (2004). Women's and providers' attitudes toward menstrual suppression with extended use of oral contraceptives. Contraception, 70 (5), 359-63 PMID: 15504373

Apter, D, Viinikka, L, Vihko, R. (1978). Hormonal pattern of adolescent menstrual cycles. J of Clin Endocrinol Metab 47: 944-954.

APTER, D. (1997). Development of the Hypothalamic-Pituitary-Ovarian Axis Annals of the New York Academy of Sciences, 816 (1 Adolescent Gy), 9-21 DOI: 10.1111/j.1749-6632.1997.tb52125.x

Christo, K., Cord, J., Mendes, N., Miller, K., Goldstein, M., Klibanski, A., & Misra, M. (2008). Acylated ghrelin and leptin in adolescent athletes with amenorrhea, eumenorrheic athletes and controls: a cross-sectional study Clinical Endocrinology, 69 (4), 628-633 DOI: 10.1111/j.1365-2265.2008.03237.x

Cromer BA, Bonny AE, Stager M, Lazebnik R, Rome E, Ziegler J, Camlin-Shingler K, & Secic M (2008). Bone mineral density in adolescent females using injectable or oral contraceptives: a 24-month prospective study. Fertility and sterility, 90 (6), 2060-7 PMID: 18222431

El-Khayat, H., Soliman, N., Tomoum, H., Omran, M., El-Wakad, A., & Shatla, R. (2008). Reproductive hormonal changes and catamenial pattern in adolescent females with epilepsy Epilepsia, 49 (9), 1619-1626 DOI: 10.1111/j.1528-1167.2008.01622.x

GERSCHULTZ, K., SUCATO, G., HENNON, T., MURRAY, P., & GOLD, M. (2007). Extended Cycling of Combined Hormonal Contraceptives in Adolescents: Physician Views and Prescribing Practices Journal of Adolescent Health, 40 (2), 151-157 DOI: 10.1016/j.jadohealth.2006.09.013

Morimatsu, Y., Matsubara, S., Watanabe, T., Hashimoto, Y., Matsui, T., Asada, K., & Suzuki, M. (2009). Future recovery of the normal menstrual cycle in adolescent patients with secondary amenorrhea Journal of Obstetrics and Gynaecology Research, 35 (3), 545-550 DOI: 10.1111/j.1447-0756.2009.01014.x

Omar H, Kives S, & Allen L (2005). Extended use of the oral contraceptive pill--is it an acceptable option for the adolescent? Journal of pediatric and adolescent gynecology, 18 (4), 285-8 PMID: 16171734

Singer, K., Rosenthal, A., & Kasa-Vubu, J. (2009). Elevated Testosterone and Hypergonadotropism in Active Adolescents of Normal Weight with Oligomenorrhea Journal of Pediatric and Adolescent Gynecology, 22 (5), 323-327 DOI: 10.1016/j.jpag.2008.12.010

Check out my new blog!

2010-08-25T10:53:00.000-05:00

Context and Variation won out as the blog title, because it seemed the most adaptable to the many purposes of the blog. Please check out the first post of my new blog and let me know what you think!

Help me choose a blog title

2010-08-15T14:14:00.000-05:00

I have been thinking a lot about this space on the Laboratory for Evolutionary Endocrinology blog. I want this blog to be a place for research blogging, announcements about the lab, and where other voices from the lab besides me are heard. I will start to set this up by encouraging others in the group to write. I'd like to have a separate space for my own musings; many things will be cross-posted, but that way I won't feel like I'm hogging the front page of the lab's website and you all can come to this site to appreciate the awesomeness of the whole lab group and what we're up to.

My own blog will be a science blog, mostly on reproductive ecology, human biological variation, and evolutionary medicine. I will occasionally mix personal, political and academic, but a lot of what I'll do there will be research blogging. I have strong points of view that I want to advance about science communication and literacy, women's reproductive health, and higher education, and I want to start to engage not just regular readers of science blogs, like other science bloggers, academics, and layfolk interested in science (though that whole audience is definitely important to me), but also my past and current students, and women who google their way to me because they want to learn more about things like PMS.

But my new blog will need a name. It could certainly just be MY name. But it would be nice to have it mean something, either by saying something about what is important to me as an academic, or specifically as an anthropologist. I'll offer a few ideas I'm kicking around for titles, but would also love to hear either votes of confidence in what I've thought of, or a few ideas of your own.

My current favorite:
"Context and variation" (I'm really leaning towards this one because it so nicely defines what I think is important in women's reproductive biology AND scientific literacy)

Runner up:
"Ladybusiness Anthropology" (because it makes me laugh every time)

Others I like:
"Rosie the Pipettor"
"Anthropology for the ladies"
"Fertile Anthropology"
"We can observe it!"
"Spit Jockey"
"Proximate causation"

So... what do you think?

Which is more safe: home birth or hospital birth?

2010-08-03T16:50:00.002-05:00

You have probably seen the buzz about the recent American Journal of Obstetrics and Gynecology article (Wax et al 2010) on home birth safety, and the editorial in the Lancet that took the article’s shaky meta-analysis to crazytown: “Women have the right to choose how and where to give birth, but they do not have the right to put their baby at risk,” they write.

I have a lot of thoughts about this study and how it has been covered, by medical doctors and by the media. My main issues revolve around: 1) what these statistics mean from a personal versus a public health perspective, 2) maternal recovery and mortality, 3) the problem with criminalizing home birth, 4) the literature around birth experiences and the process of birth and resources for women, and 5) how we should look at this topic in the future.

What do these statistics mean?

According to the Wax et al (2010) meta-analysis, the difference in infant mortality between hospital births and home births is 0.2% versus 0.9% (other people have already done a nice take-down of the cherry-picking of older studies that have received significant criticism, yet were included). While headlines have screamed that this is a three-fold difference, it makes sense for us to pay attention to the absolute values. Infant mortality, in hospital or home births, is under one percent. We can’t even say that one in one hundred babies die in childbirth in developed countries any more (at least not as a whole – for now I’ll side-step some major differences relating to social disparities and race). If you are pregnant and considering where you want to give birth, I’m not sure how this slight difference could really sway you one way or the other. The problem is that the editors of the Lancet (and others) are conflating public health recommendations with personal recommendations… and shaming women in the process.

From a public health perspective, I suppose I can grudgingly understand why the difference in infant mortality in home versus hospital births matters. But you cannot take population-wide statistics and apply them to individuals. To do so is to ignore inter and intrapopulational variation, and to take a women’s decision about her body out of the context in which it should be understood.

Another thing to notice, Wax et al (2010) found that “neonatal outcomes of planned home births revealed less frequent prematurity, low birthweight, and assisted newborn ventilation.” So of the more than 99% of babies who were fine, home birth babies tended to be healthier. This of course could be a bias of who chooses a planned home birth versus someone who does not, so I am not assuming the directionality to be that the home birth predicts healthier kids. But I wouldn’t be surprised if further analysis showed both directions to be causal; that is, that women more likely to have healthier kids choose to plan a home birth, but also that because home births have fewer interventions those kids are more likely to be healthy.

What about maternal health?

What the Lancet editorial and Wax et al (2010) mention only briefly, is that for maternal mortality and morbidity in low-risk births, to me, home births (and, I would contend, birth center births) are the clear winner. By not being in the same room as epidural medicine (it’s right behind you in big cabinets, just waiting for you to say “ow”*), single beds with little room to maneuver, continuous fetal monitoring and an IV under your skin as soon as you’re admitted, you avoid interventions that often carry their own significant risks and precipitate a cascade of other interventions.

Many women in the US don’t want to give birth in hospitals because being in a hospital increases the risk of maternal mortality and morbidity and, perhaps more importantly, slows recovery time. I say the recovery time issue may be more important, because while the US is embarrassingly bad at keeping mothers alive, the numbers are still better than in infant mortality (though, obviously, this makes sense from a life history perspective). The US is ranked 40^th in the world in terms of maternal mortality – that means 39 countries do a better job keeping women alive during childbirth. Our incidence of maternal mortality is increasing, not decreasing, with the latest figures for 2008 being 17 deaths out of 100,000 births (Canada, for instance, has 7/100,000). Developed countries with higher rates of home birth have lower rates of maternal mortality.

Criminalizing home birth

Another problem I have is that part of the reason they cite home births as unsafe is that so few of them are staffed by certified midwives (only one third according to the Lancet editorial). The only reason more home births are not staffed by certified midwives is that organizations like the American Medical Association and others have lobbied to keep home births illegal in many states. Midwives cannot legally help a family give birth at home where I now live, in Illinois. Instead, I have been told by local homebirth supporters that there is an underground movement of lay midwives who try to help women stay out of hospitals, if it’s what they want. Is this a safe way to give birth if you are low-risk? Maybe, maybe not. I’m not sure I would be keen on a home birth that did not have a Certified Professional Midwife or Certified Nurse Midwife attending, who also had a good relationship to a doctor at the nearest hospital. But I also would not want to give low-risk birth in a hospital, even if I had a midwife, because of the major risks you incur just by stepping into a hospital (like infection). Women in states like mine are stuck between a rock and a hard place: give birth at home and risk not having someone with the right qualifications (and potentially face legal action), or risk giving birth under conditions where you may have interventions you don't want, and treated like something less than human (which I'll get to more in the next section).

By criminalizing home birth, medical doctors and their lobbyists force women who don’t want a medical birth to find less-than-perfect alternatives. So when Lancet editors and others criticize US women for not having the right people at their home births, I call shenanigans: they were complicit in making the laws that prohibit it in the first place.

Birth experiences in hospitals, birth centers and the home

There is a huge literature already on the medicalization and pathologization of femaleness, and I encourage you to devour it all, from Emily Martin’s The Woman in the Body to Robbie Davis-Floyd’s Birth as an American Rite of Passage.

So the other issue I want to make sure to include here is that pregnant patients don’t have the same rights as non-pregnant patients in a hospital (link to pdf), to refuse treatment, to leave, to contest a decision; hospitals can and do get court orders to force pregnant women to receive treatments they have refused. On the one hand, I can understand that sometimes decisions need to be made quickly during labor. On the other hand, I think there is a problem when we place a fetus’s rights above that of its mother’s. This recent story of police violence against a pregnant woman links to several problems with pregnant patient rights. Here are examples of court-ordered interventions. And here is more information on pregnant patient rights.

These are other reasons many women find the idea of a hospital birth frightening, and thus choose home birth or a birthing center. And if you read Davis-Floyd and others, you will see the interviews of women who have had hospital births how they were disempowered by the experience. This isn’t to say there aren’t many, many women who aren’t totally satisfied with hospital births, and would never consider home birth. It’s just to say that to acknowledge differences in infant mortality risk that are not necessarily meaningful to an individual making a decision about this, in the absence of all this other information, is disingenuous on the part of the editorial writers at the Lancet.

Future work on this topic


My daughter, just born at the birth center.

Rather than blaming the women who are trying to make the best decisions for themselves and their families and fetuses, medical doctors should be doing more to make different kinds of birth options available for women. In 2008, I gave birth in a birth center that was across the street from a hospital – the Cambridge Birth Center in Cambridge, MA. I had midwives, doulas, a labor and delivery nurse, my husband and sister to help me. I had a nice big king-size bed, a big tub to labor in, and just about every device you can think of to help me labor and push out the baby, from floating noodles for the tub, to a yoga ball, to a birthing stool. The time to get from the birth center to operating room if there was a complication was 4 minutes – the same amount of time had I been in the delivery room at the same hospital. This option is not available to me now, as a resident of the state of Illinois.

I’d like to see is re-analysis of the literature, where only home births with a certified midwife are analyzed. This is what is possible if we allow women more choices in where they give birth, so this is what we should examine. When we decriminalize women who don’t want the higher risk of epidurals or cesareans or infections, when we provide women more options for how and when to labor and give birth to their babies, and when we are honest with the failings of the medical system towards pregnant women and women in general, we’ll be heading in the right direction.

References

Wax, J., Lucas, F., Lamont, M., Pinette, M., Cartin, A., & Blackstone, J. (2010). Maternal and newborn outcomes in planned home birth vs planned hospital births: a metaanalysis American Journal of Obstetrics and Gynecology DOI: 10.1016/j.ajog.2010.05.028

Editorial staff (2010). Home birth--proceed with caution. Lancet, 376 (9738) PMID: 20674705

*What bothers me about epidurals and narcotics is not that women choose to use them during birth. I have given birth, I know how much it hurts and how it feels like the pain will never, ever end. I would never, ever begrudge a woman for choosing pain relief under those circumstances. What bothers me is that it is presented almost as a given in most hospital settings these days, since the medicine is already in the mother’s hospital room. There are many interventions one can give for pain that are not pharmaceutical, but few doctors are trained in these interventions. My midwives and doulas had so many tricks up their sleeves that even though I was in excruciating pain, I was able to remain in the birth center and have a totally normal, natural childbirth. I also want to be clear that if I hadn’t clearly stated I wanted this in my birth plan, they would not have worked so hard to make this possible. I wanted to be kept out of the hospital, kept away from the risk of infection and the risk of narcotics and the risk of cesareans and episiotomies, so they helped facilitate that within what was safe for me and my baby.

So, why did you become an anthropologist? (Part 3 of 3)

2010-07-22T10:04:00.005-05:00

This is the third and final part of the series “So, why did you become an anthropologist?” based on the AAPA plenary talk I gave in 2010 alongside many other wonderful and interesting anthropologists (Parts 1 and 2). The question that frames this final part is, How did you get a freaking job?

How did you get a freaking job?

How I survived graduate school
For most of my time in graduate school, I was a union organizer for the Graduate Employees and Students Organization at Yale University. Most semesters the hours I put in were equivalent to a full-time job, sometimes more. My last semester of graduate school I worked full time as expository writing faculty at Harvard. Yet I finished in six years, which was shorter than average in my department. How did I do this?

Well, first, I was lucky enough that my family was able to supply extra funding (like a car and car insurance) that my small stipend couldn’t cover, so I didn’t need to work. I didn’t have any dependents like I do now, unless you count my needy cat. I was and am able-bodied, so the university and surrounding area was set up well for me. And because I didn’t mind the occasional cockroach (well, I minded, but I was willing to tolerate them and several health and safety violations because my apartment was so airy and pretty), I was able to afford living less than a mile from campus.

Then, two things helped me be successful: I worked my ass off, and I had a community of people who were able to contradict the oppression and isolation of graduate school.

I’ll explain the easy part first. There has to be some tiny part of you that is crazily passionate about the work you do in order to be successful in graduate school. If not, you will not put in the necessary hours, you will not feel compelled to go to the library on a Saturday morning, you will not go back into lab in the evening after three hours of house visits and an intense two-hour staff meeting.
But really, that’s the easy part. Because if you’re considering graduate school, you are or shortly will become intensely interested in your discipline, you will think about it all the time, you will read about it just to learn more. Being an academic doesn’t require that this be constant; if anything, I think the more sane and more successful academics I know get periodically exhausted by their jobs and know when to put a project or manuscript down for a while. But you probably do need that occasionally manic buzzing in your ear that makes you spend three extra hours reading up and teaching yourself about inflammosomes when you could be watching an NCIS marathon.

The harder part is finding a way to contradict isolation and oppression. I think we need to be honest with ourselves that graduate school is incredibly oppressive, not necessarily by individuals, but certainly as a system. I don’t think I need to explain myself here, but if you are not in academia, as one example, find a graduate student and talk to her before and after her qualifying exams. Her feelings of isolation, stupidity, confusion, anger, self-blame will be incredibly high in your first interview compared to your second! And this is independent of the bread-and-butter issues that also promote stress during graduate school, like pay and benefits.

Being in GESO made me part of a collective of women and men that were able to identify the source of their oppression as external – the system of higher education – rather than internal. Not blaming yourself for feeling crazy all the time goes a long way towards feeling better during graduate school. Being a union organizer also meant I was creating social change on a daily basis. I got people to join the union, sometimes after months of conversations, and many of these people became lifelong friends. I helped write reports that showed the university’s true commitments to gender equality and other issues. I was arrested in civil disobedience and I went on strike, two times each. These were personally meaningful moments just as much as they contributed positively to the climate at Yale.

To me, being part of a movement to change the system of higher education is a necessary component of graduate school. This isn’t just selfishly to find friends to help you through graduate school and it’s not playing at union organizing. It is serious, it is real, and it is how we start our stewardship of higher education. If you are going to be an academic, you need to understand the workings and failings of academia, and you need to have experience working to improve it. Otherwise, the feelings of powerlessness that one can feel over qualifying exams, grantwriting, dissertation research, mentor relationships and the job market can overwhelm.

Myths and meritocracies
Academia is not a meritocracy. There, I said it! Many of the best scholars and intellectuals I have known quit graduate school, or left academia after getting a PhD. Many other excellent academics took years to find the magical tenure-track job. Still others are still looking. I think that many excellent scholars do tend to eventually find a home in academia, but I am also saying that while sitting comfortably in a tenure-track position at an R1 institution.

Academia is not a meritocracy. Racism, sexism and classism, to name just a few, still run rampant. A lot of this is built into the institution: for instance, many places are improving their recruitment of people of color, but are still poor at retention. On-site childcare that is nonexistent or has too few slots is a disincentive for people with dependents or those who shoulder a greater proportion of childcare; these tend to be women. Departmental culture can discourage people from varying backgrounds to express themselves, or even survive in that world: I know male faculty who feel they can’t express themselves as parents in their departments because the other fathers work all the time and never see their children. I know a woman who quit graduate school in the physical sciences because of objectionable images of women plastered in the halls to advertise social events in her department; her work to have the images taken down ended in a meeting with a Dean who told her she was ruining her career by speaking up.

Academia is not a meritocracy. I am a spousal hire. I know that some people view spousal hires as second class citizens (I also know that those people don’t happen to reside in my department). I think this view originates in the fact that we want to believe academia is a meritocracy and that only the best get in, and that somehow dual hires get around that. There are two problems with this: first, spousal hires do not get around meritocracy, because they are as rigorously evaluated as other hires and are rejected as often as accepted (at least at R1s; I do know occasionally this happens differently at other types of institutions). The other dual hires I know on this campus are inspiring, intelligent, and major players in their departments. Second, since the idea of a meritocracy is a myth anyway, it is silly to pick on one group of people when we are all struggling to find work in the discipline we love.

The idea that academia is a meritocracy is a myth that keeps people who have not been successful in finishing their degrees/finding jobs/getting tenure/etc from speaking up about larger inequalities and issues in higher education. It’s time we discarded this in favor of an honest appraisal of what is wonderful and problematic about academia.

What now?
I finished my degree, then spent a year as a faculty preceptor at Harvard University teaching expository writing (that is a grueling job to cut your teaching chops, but has good pay, benefits and job security). Then I had a baby and a semester of maternity leave (sort of, but we’ll leave FMLA gripes for another day), then in the fall of 2008 moved to Illinois to begin my position here with a five month old in tow and only twenty hours a week of childcare because it was so hard to come by. We wouldn’t get to full time childcare until the beginning of my second year. This meant even less sleep than usual for young parents, as my husband and I had to work nights and weekends to make up for the childcare deficit.

In my work, I take a holistic approach to ecology and women’s reproductive functioning. While my dissertation was on the endometrium and that is still a major interest, some of the mechanisms for variation in endometrial functioning, and a little navel gazing from my experience of pregnancy and a recent diagnosis of gluten intolerance, led me towards immune health and inflammation. I have a few projects nearing completion (if you were at the AAPAs/HBAs and saw my talks you heard about one of them on ovarian follicular waves) and a few others in the mix (a departure from my human snobbery to work with mice?!).

All criticism of the system of higher education aside, and all paperwork and bureaucracy and grading and meetings aside, this is the most stimulating, interesting and fun job I could have ever hoped to have. I get to spend my day using my mind, interrogating ideas, and learning new things. If I have an idea for a project, it’s on me to do the legwork and on me if it fails… but how cool is it that I get to go after the idea in the first place? I love that if I get excited about something, I can explore it further. I can do a literature review, or write a grant, or find a collaborator in another discipline. One of my most interesting collaborations so far came from emailing the authors of an article I found interesting out of the blue.

I can teach women that what they learned about their bodies was reductive, that they aren’t diseased simply by being female. I can mentor undergraduates and graduates, make them critical thinkers, and help them get grants and get jobs and get into graduate school. I can work with non-science majors and make them less afraid of science. I can promote different kinds of pedagogy and increase access to education using online learning technologies.

Folks, I have drunk the kool-aid. This is a great job. But I don’t want to keep it to myself; I want more people to have access to academia and secure jobs and to just having a more intellectual life. That is why the institution and culture of higher education needs to change, and why I become an academic anthropologist. I like to think about women, I like to think about biology and medicine, but I also like to share my excitement. I hope you’ll join me in working towards positive change so that anthropology can continue to grow and have a positive influence on society.

So, why did you become an anthropologist? (Part 2 of 3)

2010-06-30T14:41:00.003-05:00

This is the second post in a three-part series on why I became an anthropologist. I was invited to answer this question in the Plenary Session of the 2010 American Association of Physical Anthropology Meetings in Albuquerque this past April. You can find part 1 of the series here.

As I mentioned in the first post, I feel like this question has several parts. The first, answered already, is Why did I fall in love with anthropology? The one I'll answer today is Why did I pursue academia? And the last part of the series will answer How did I get a freaking job?

Why did I pursue academia?

Public school kids are intelligent too
As I finished my senior year in college, I considered my options. I could become a consultant, like many of my friends. I could become an investment banker, another popular option. I was strongly considering becoming a massage therapist or yoga instructor, or getting an MFA in creative writing to become a fiction writer (no, I'm not joking). I had looked into programs for all three of these options, because I felt adrift when I tried to sit down and consider what I wanted to do for a career. Consulting and investment banking just seemed like more of the same Harvard competitiveness, rather than a career I'd want to do for my whole life, where my other ideas had at least some appeal. I didn't know if I was smart enough for much else, quite frankly, which speaks to the hard time I had being a kid from a poor public school (actually, I think fiction writing may take a lot more intelligence than I have, but I told myself I could be a Starbucks barista as my day job).

Part of this can be blamed on a higher education system that doesn't support or think about the preparation of its variable students before arrival on campus -- that is, the culture of elite institutions like Harvard are not inclusive of people like me whose high school calculus teacher didn't actually know calculus, or even show up to teach most of class that year. I often received really good training and advice from people that I could not absorb because of my different background or lack of preparation. But if people like me either didn't know how to ask the right questions, or couldn't understand what was offered, then it's not really good advice, is it?

At the same time, part of what happened can be blamed on the lens through which I was seeing everything, which was tinted by resentfulness and frustration due to sexism and classism -- that is, even when I was given good advice or good training in a way that should have been accessible to me, I was too mad (or sometimes immature) to do anything with it. I did not take or understand criticism well, and now realize how much good raw material and real help I messed up for this reason.

All of that said, at some point I finally realized that public school kids are not dumb. I could keep being mad about being underprepared, I could lament my lack of boarding school experience, or I could suck it up and figure out how to do my work. This really didn't happen until I wrote my senior thesis, and if you are ever unfortunate enough to read the thesis you will see that it was too little, too late. But as I mentioned in part 1, even though my knowledge, skill set and writing bloomed late and incompletely, this allowed me to begin to love learning anthropology for its own sake, to learn to ask good questions and design good projects, and continue to bloom into graduate school.

Somebody has to believe in you
Please allow me to briefly wax cheesy. I think at least one of the major factors that made it possible for me to realize that I was not dumb involved dating my boyfriend, now husband. He too was a public school kid, albeit from a rich Boston suburb. What amazed me from the first day I met him was how committed he was to working hard to solve problems and do his academic work. He was curious and intellectual, yes, but he also knew that you had to put in a lot of time and that the qualities necessary to become a scholar were not something you already had (or didn't have) going into college. You had to work for it.

Inspired by him, I finally started to work hard. I had avoided working hard – doing all the readings, studying for exams – throughout college so that I could avoid feeling bad when I didn't perform well. I could always tell myself if I got a B (or worse, as I did spectacularly fail one test in a course by my own thesis advisor) on something that it was because I didn't study. I didn't work hard on everything, only on what I cared about, but that work became all-consuming. I spent entire days in the Currier House dining hall near a power outlet with my laptop (my first ever! and it didn't have internet at first!), writing and writing away on my thesis. I spent hours most nights there, drinking far too many cups of hot chocolate. It was exhilarating to put so much attention on one thing.

I discovered two things: first, that I was smarter than I thought, and second, that when you work hard on something you care about, it only leads you to care even more. Working hard on my senior thesis led me to fall in love with anthropology all over again, and re-commit myself to the beauty of the physiology, as well as the political nature of women's reproductive health. After that, I couldn't imagine being happy teaching sun salutations or massaging someone's wonky shoulder because what I really loved was learning about the way environmental variation impacts reproductive functioning, and how our incorrect medical understanding of that variation led to overpathologizing an entire gender.

So, why did you become an anthropologist? The white female early career parent weighs in (Part 1 of 3)

2010-04-26T17:00:00.007-05:00

For the American Association of Physical Anthropology meetings this year in Albuquerque, six anthropologists were asked to answer the question: "So, why did YOU become an anthropologist?" in the AAPA Plenary Session. The other participants, who had some amazing and wonderful stories to share, were Kaye Reed, Karen Strier, Mark Zlojutro, Alan Swedlund and Jim Calcagno. Lorena Madrigal organized and chaired the session. I decided to turn my talk into a three-part series for the blog, because I think it's fun to hear the backgrounds of academics, and important to hear where things were hard for us. So here is part one.

* * * * *
I am an Assistant Professor in biological anthropology at the University of Illinois in Urbana-Champaign. I am in my second year there, but took a tenure rollback because of the birth of my child, so really it’s like I’m repeating my freshman year. I wanted to tell the story of not only how I became an anthropologist, but why I persist in being one today.

For me, this breaks down into three questions: 1) Why did I fall in love with anthropology? 2) Why did I pursue academia? And 3) How did I get a freaking job? And of course, I really lied, because there is also a fourth question in the mix here: What am I doing now?

Why did I fall in love with anthropology?

When I was a freshman at Harvard University, I spent a lot of time being angry. I was angry at large lectures, at being an underprepared public school student, at sexism, at feeling like I didn’t particularly belong. I took Science B-29: Human Behavioral Biology to meet a core requirement, but also because it fulfilled a bio requirement I would need if I ended up going into biology like I had been planning when I first got there. My abysmal performance in math and chemistry – prereqs for the bio courses I wanted to take – and my abysmal performance in Expository Writing – which was not easy to swallow since I thought I also wanted to be a writer – had me feeling pretty horrible going into my second semester of college. Then this one class that I thought sounded interesting had 500 students in it and was nicknamed “Sex.” I took B-29 despite my growing concerns about my placement at that university and my ability to do science.

The course was okay. It would have been exceptional to me if I was into behavior, because Professors Marc Hauser and Irven Devore are engaging, interesting and thoughtful speakers. But for most of the class, I only became more convinced that I wasn’t biology material. I didn’t like learning about mating strategies in lizards and felt like my fellow students were making pretty problematic conclusions based off what we were learning. It seemed like I was getting into the kind of problematic, reductionist material that only triggered my righteous sexist anger. If it isn’t obvious already, I do want to be clear that my perceptions of that class were tinted by my experiences as a kid from a poor public school who was having a pretty crappy time in an elite college that didn’t acknowledge her different experience of high school and lack of preparation, and that I was going to be angry about that class even if they had handed us all copies of the Feminine Mystique along with Sex, Evolution and Behavior.

Then, on the last day of class, Irv Devore gave a rousing speech that, to me, was on cultural sexism and its incompatibility with biology. I will never forget how angry he looked when he talked about academic science: the glass ceiling for female academic scientists, he said, is reinforced with concrete. He continued, It is a sad day when a man who has written three books but spent little time with his children is given tenure over an equally talented woman who has produced two but been involved in her family’s life, especially given the nature of the imbalance of physiological investment in parenting. Devore also spoke eloquently about the ridiculousness of laws that prevent women from breastfeeding publicly, when she is only feeding her child, and the wellbeing of her child should not be threatened because we have decided to sexualize breasts.

I don’t know that I can really describe what it was like to have an older man stand in front of five hundred college students and speak so strongly as an ally to women against sexism. I was also amazed and excited by the idea that science could be political, that I could work to eliminate sexism as an anthropologist. I had been invalidated in my anger for so many years, that all I could do in response to this lecture was cry. So cry I did, all the way back to my dorm room, where I proceeded to write the dorkiest letter of my life to Devore, praising his talk, admitting my tears, and proclaiming that I would become a joint Biological Anthropology and Women’s Studies major.

Soon after sending the email – just a day or two later if I remember correctly – Professor Devore called me up on the phone. Mind you, this means he had to look me up in the directory and dial a number to talk to the weepy, dorky girl who had changed her major based on a fifty minute lecture. I nearly fell on the floor when my roommate handed me the phone! He said he appreciated my email, and thought Biological Anthropology was a good major, but that I should skip the Women’s Studies thing because I could just take Women’s Studies classes as electives.

So of course I became a joint major in Biological Anthropology and Women’s Studies.

I took some lovely courses in both majors, and having feminist theory on one side, and bio anthro on the other, provided me with the necessary foundation to think well about the meaning behind my work. While an undergrad, despite good training, I was not good at articulating all of this, and yet over the years I have realized that this coursework was essential in my personal and professional development, and I draw from this training every day in my job as an academic. In particular, I had a tutorial in Women’s Studies led by Lauren Korfine (the one wearing her baby in the picture) that provided me with the support I needed to write my honors thesis. My work as an undergrad was probably pretty unremarkable, and my thesis isn’t something I pass around for kicks, but sometimes it’s less about the work you produce and more about the way to learn to think and the relationships you build. It is because of my peers and mentors in both majors that I love anthropology as much as I do today.

If you don't want to meet brilliant young biological anthropologists, you can ignore this post

2010-04-22T14:26:00.003-05:00

Which is exactly why you are reading. Who wouldn't want to meet the coolest cohort in the AAPAs?

Plenty of us young biological anthropology folk are struggling in isolation at an important point in our careers: we may be writing up our dissertations, defending, starting our first postdoc, contingent faculty or tenure-line faculty gig, or we may be otherwise looking at the established folk and thinking, "How in heck did they get there, and will I ever get there too?"

Enter BANDIT, the brainchild of brilliant and eminently likable Assistant Professor Julienne Rutherford of the University of Illinois, Chicago (full disclosure: I am completely biased because we are collaborators and friends). BANDIT, or Biological ANthropology Developing Investigators Troop, is a loose collective of young anthropologists sharing information, insight, and support. Check it out, contribute, and appreciate the early career anthropologist in your life by supporting this site. Go to http://aapabandit.blogspot.com for more information, and check back in as it grows.

Premenstrual syndrome: understanding origin and variation

2010-02-26T16:14:00.014-06:00

If you are female and post-menarcheal (that is, you’ve had your first period), you have probably had at least one person tell you that you are PMSing – either jokingly, or with an unpleasant edge. You may have expressed anger or irritability; you may have simply stood up for yourself. Or, you may have no idea what prompted the statement.

Maybe you were angered further by this comment, because you have never experienced any shifts in mood in your premenstrual phase (the several days leading up to your period). Maybe you were embarrassed because, whether or not the comment was at the time accurate, you do feel different right before your period. There is a lot of variation in the emotional experience of the premenstrual phase, from no changes, to dysphoria (that’s mild depression) or anger and irritability, increased creativity, well-being and happiness, to a whole host of other feelings. Part of this variation is a small minority of women who do experience negative symptoms strong enough to interfere with their daily lives, often called premenstrual syndrome. A syndrome refers to the association of symptoms and/or signs that often occur together, but that does not mean the etiology, or origin, of this syndrome is the same for everybody, and that does not mean everyone has the same disease if they have the same set of symptoms. This distinction is important because there are several syndromes out there relevant to women’s health (polycystic ovary syndrome and chronic fatigue syndrome come to mind), yet it is a classification that says, to me, “hey, we don’t know what causes this and in fact it may be a whole bunch of different things going on for different people, but this is what we have so far.”

Despite the fact that the experience of the premenstrual phase is varied, and the negative symptoms some number of women experience are categorized by a syndrome which does nothing to explain its etiology, there appear to be only two games in town in treating PMS: hormonal contraceptives (HCs) and selective serotonin reuptake inhibitors (SSRIs). And the most studied potential origin of PMS is progesterone withdrawal.

Now, a twenty-eight day, ovulatory menstrual cycle looks like this:

Notice the estradiol (that’s a kind of estrogen) peak just before ovulation, and the swell of progesterone (pro-gest, so supporting gestation should you conceive) in the second half of the cycle. Progesterone is secreted by the corpus luteum, which is left behind by the follicle that erupts from your ovary when you ovulate. If that egg is not fertilized, to wend its way through the fallopian tube and invasively implant its way through your endometrium, then that corpus luteum and progesterone doesn’t have much of a purpose. Without a signal that pregnancy has occurred, the corpus luteum degrades, progesterone concentrations decline, and your nicely primed endometrium sloughs off to be able to make another plush surface for the next attempt.

Allow me to briefly wax anthropological before moving on in my discussion of these premenstrual symptoms. This twenty eight day cycle with its nice estradiol peak and progesterone swell and ovulation smack dab in the middle? It’s pretty much a farce.

Those are real luteal progesterone concentrations from healthy, normal, reproductively-aged women from past studies of mine in one population of women in rural Poland (the follicular phase is the first half of your cycle, luteal phase the second). And the next image is from a whole bunch of other studies showing population variation in progesterone. Regular menstrual cycles, and yet luteal phases that range from 9-17 days. Mid-luteal progesterone concentrations varying by several orders of magnitude. You are looking at data ONLY of healthy women, in a homogenous rural environment, and ONLY cycles where they ovulated. And yet, look at all that variation.

So hormone concentrations, menstrual cycle lengths, experiences of the menstrual cycle and menses themselves, vary so much so that the idea that there is such a thing as one normal cycle for everyone is patently false. Women’s reproductive functioning only makes sense in the context of its environment, and if it is responding logically (high stress, low function, and vice versa), it’s pretty safe to say that woman is normal.

Okay, so back to PMS and progesterone withdrawal. You may have noticed something in the preceding images: progesterone concentrations decline in the days leading up to menses in all ovulatory cycles. In a physiological process with so much variation it’s hard to determine universals, this is one of them. So I suppose it makes sense, then, that researchers think progesterone withdrawal has something to do with premenstrual symptoms. Further, post-partum depression or the maternity blues occurs soon after parturition, when a mother goes from having huge quantities of progesterone (orders of magnitude higher than in a regular menstrual cycle) to zero, once that placenta that was making all that yummy progesterone is birthed.

At the same time, if these symptoms are not universal, if in fact some women have positive experiences of their premenstrual phase (and post-partum period), and to top it off progesterone withdrawal is a major feature of the menstrual cycle for most women… then perhaps the idea that progesterone withdrawal is the trigger only serves to further pathologize a population that is historically overpathologized and understudied. That is, does it make sense to consider a universal feature of the menstrual cycle the culprit for a set of symptoms that affect about five percent of the population?

Let’s unpack the data a bit more, then, and cut these folks some slack… at least to start. There are two kinds of work going on in the literature: the first is the identification of the mechanism of how progesterone withdrawal could be producing effects in the brain, and what most folks are focusing on is the fact that progesterone concentrations are tied to allopregnanalone (ALLO) concentrations in the brain (this makes sense, since ALLO is a kind of progestin and progesterone is its precursor). The second is to identify whether it is how rapidly progesterone declines that produces negative symptoms (this certainly does vary, if you look at how different women’s mid-luteal progesterone concentrations are), the overall concentration, or the estradiol to progesterone ratio.

Several studies indicate an association between decreased ALLO concentrations and premenstrual syndrome and post-partum depression [1-6]. Gracia et al [3] also note lower ALLO concentrations in those individuals suffering from PMS who are responsive to SSRI treatment, versus unresponsive individuals. So it does seem like those with lower concentrations of ALLO (and thus lower progesterone at that time as well) are perhaps more likely to have PMS. However, it also looks like reduced ALLO isn’t the only explanation for PMS: 1) only 63% saw improvement with SSRI treatment, and 2) the women in this study (n = 46) were grouped into tertiles by their ALLO concentrations, and the highest tertile (the women with the highest ALLO concentrations) did not show improvement. So it seems it is possible to have PMS without low ALLO relative to your population.

The second issue, that it may not be total levels of progesterone/ALLO triggering PMS symptoms but rather something about the rapidity of decline (an understandable hypothesis to start from given what we know of post-partum depression) is not as frequently studied. But I did find one study that examined this and managed to review a few articles I hadn’t yet found: Beckley and Finn [1] described work that suggested more rapid decline in progesterone concentrations was associated with depression-like behaviors in rodents, and themselves found similar results both when creating progesterone withdrawal conditions with supplementation, and when using finasteride (which inhibits progesterone metabolism; also known as Propecia).

I think the idea here and the results are tantalizing, but I am not yet confident in the mechanism. Part of the reason for this is that in human studies women were only sampled once per cycle in the luteal phase; often something like five plus or minus three days before menses. If you look at the graph above (this is the same as the second figure, just the mean and standard deviation instead of the concentrations of each individual), that six day spread (-8 to -2) shows a significant amount of time-dependent variation in progesterone concentrations. Further, progesterone is strongly influenced by age, energy balance, energy expenditure, and population (developmental conditions) [7-14], and I am unclear whether this variation has an impact on these results or can be controlled for in future work. One last point to consider is that social influences on perceptions of menstruation, as well as degree of social support, urban versus rural setting, and level of education, predict premenstrual syndrome and post-partum depression quite strongly [15-18]. We need to be careful when examining something that is a product of the interaction between biology and culture not to simply look at the concentration of a hormone to explain its etiology.

References
1. Beckley EH, & Finn DA (2007). Inhibition of progesterone metabolism mimics the effect of progesterone withdrawal on forced swim test immobility. Pharmacology, biochemistry, and behavior, 87 (4), 412-9 PMID: 17597197
2. Brinton RD, Thompson RF, Foy MR, Baudry M, Wang J, Finch CE, Morgan TE, Pike CJ, Mack WJ, Stanczyk FZ, & Nilsen J (2008). Progesterone receptors: form and function in brain. Frontiers in neuroendocrinology, 29 (2), 313-39 PMID: 18374402
3. Gracia CR, Freeman EW, Sammel MD, Lin H, Sheng L, & Frye C (2009). Allopregnanolone levels before and after selective serotonin reuptake inhibitor treatment of premenstrual symptoms. Journal of clinical psychopharmacology, 29 (4), 403-5 PMID: 19593190
4. Maguire, J., & Mody, I. (2008). GABAAR Plasticity during Pregnancy: Relevance to Postpartum Depression Neuron, 59 (2), 207-213 DOI: 10.1016/j.neuron.2008.06.019
5. Monteleone, P. (2000). Allopregnanolone concentrations and premenstrual syndrome European Journal of Endocrinology, 142 (3), 269-273 DOI: 10.1530/eje.0.1420269
6. Nappi, R. (2001). Serum allopregnanolone in women with postpartum “blues” Obstetrics & Gynecology, 97 (1), 77-80 DOI: 10.1016/S0029-7844(00)01112-1
7. Chapman, J., McIntyre, M., Lipson, S., & Ellison, P. (2009). Weight change and ovarian steroid profiles in young women Fertility and Sterility, 91 (3), 858-861 DOI: 10.1016/j.fertnstert.2007.12.081
8. ELLISON, P. (1993). Population variation in ovarian function The Lancet, 342 (8868), 433-434 DOI: 10.1016/0140-6736(93)92845-K
9. Ellison PT, Panter-Brick C, Lipson SF, & O'Rourke MT (1993). The ecological context of human ovarian function. Human reproduction (Oxford, England), 8 (12), 2248-58 PMID: 8150934
10. Jasieńska G, & Ellison PT (1998). Physical work causes suppression of ovarian function in women. Proceedings. Biological sciences / The Royal Society, 265 (1408), 1847-51 PMID: 9802241
11. Lager, C., & Ellison, P. (1990). Effect of moderate weight loss on ovarian function assessed by salivary progesterone measurements American Journal of Human Biology, 2 (3), 303-312 DOI: 10.1002/ajhb.1310020312
12. O'Rourke, M.T., S.F. Lipson, and P.T. Ellison, Ovarian function in the latter half of the reproductive lifespan. American Journal of Human Biology, 1996. 8(6): p. 751-759.
13. Panter-Brick C, & Ellison PT (1994). Seasonality of workloads and ovarian function in Nepali women. Annals of the New York Academy of Sciences, 709, 234-5 PMID: 8154716
14. Rosetta L, Harrison GA, & Read GF (1998). Ovarian impairments of female recreational distance runners during a season of training. Annals of human biology, 25 (4), 345-57 PMID: 9667360
15. Cénac A, Maikibi DK, & Develoux M (1987). Premenstrual syndrome in Sahelian Africa. A comparative study of 400 literate and illiterate women in Niger. Transactions of the Royal Society of Tropical Medicine and Hygiene, 81 (4), 544-7 PMID: 3445335
16. Chaturvedi SK, & Chandra PS (1991). Sociocultural aspects of menstrual attitudes and premenstrual experiences in India. Social science & medicine (1982), 32 (3), 349-51 PMID: 2024146
17. Marván ML, Díaz-Erosa M, & Montesinos A (1998). Premenstrual symptoms in Mexican women with different educational levels. The Journal of psychology, 132 (5), 517-26 PMID: 9729845
18. O'hara, M., & Swain, A. (1996). Rates and risk of postpartum depression—a meta-analysis International Review of Psychiatry, 8 (1), 37-54 DOI: 10.3109/09540269609037816

A new direction

2010-01-14T08:31:00.002-06:00

One of the projects that is just getting off the ground in the Laboratory for Evolutionary Endocrinology is the study of hormonal contraception in young women. We will be exploring the science behind it -- when is it useful to young girls and women, when is it not, what future health implications does it have -- but also the relationships between health care providers and patients regarding this drug.

I am developing a hypothesis regarding when health care providers prescribe hormonal contraceptives. For now, and this is before I have delved into the literature on this, I would like to test the conditions under which it is prescribed for a health complaint, and the conditions under which the health complaint is further explored instead. My suspicion is that when a woman goes to her PCP with a reproductive health issue but is not currently interested in having children, she is often prescribed hormonal contraceptives. When a woman goes to her PCP with a reproductive health issue and is interested in having children, the possible health concern is explored.

I would like to test this hypothesis and others using an online survey in the coming months. As we work to put the survey together and obtain IRB approval, I would like to solicit your thinking. What kinds of questions should we ask? What population should we seek for answers? Should we survey doctors as well as patients? What hypotheses would you want to see tested?

Put your questions and comments in the comments section of this post. If I get a lot of clarification queries, I will post more information about what we're thinking to give you more ideas.

New Center for Gynepathology Research

2009-12-04T09:27:00.004-06:00

Linda Griffith, PhD, Professor of Biological and Mechanical Engineering at MIT, opens a new Center for Gynepathology Research today. She has paired with Padma Lakshmi of Top Chef fame to cast light on endometriosis, a condition that is said to affect 10% of women (and probably many more). You can go to the Center site here, and read the Boston Globe article about the Center here.

Dr. Griffith is doing women all over the world a service with the opening of this new Center. She is pairing up with scholars and clinicians at MIT, Vanderbilt, Harvard, Cornell and Tufts. I'm very excited by the fact that people who do basic science will be working with clinicians on a disease whose research has not advanced that much in recent years. We have a few hypotheses about why women get endometriosis -- some genetic causes, inflammatory variables, and flowback of copious menstruation -- but so far little of this research has yielded results that help prevent endometriosis, or help treat it. This Center is an important step forward.

We anthropologists and evolutionary medicine folks happen to like evidence from the angle of global and ecological variation in a condition in order to set a baseline and understand pathology better. So here are some additional questions that I think we should be asking about endometriosis:

What is the global range of variation in the presence of endometriosis in different populations? I'm not talking just about the debilitating symptoms, but the presence of endometrial tissue outside the uterus. And what is the range of variation for amount of endometrial tissue outside the uterus?
What ecological/lifestyle factors are most commonly associated with endometriosis? I'm thinking not just energetic stress, but immunological stress, psychosocial stress, diet composition, etc.
Are there less invasive ways to test for endometriosis (i.e., ultrasound) that will allow us to examine this disease in non-western or non-industrialized environments?
How do daily ovarian hormone concentrations vary with endometriosis incidence?
When and under what conditions does endometriosis co-occur with other gynepathologies, such as polycystic ovarian syndrome?

Evolution of Diseases of Modern Environments: my report now up

2009-11-17T10:15:00.002-06:00

Many of you know that I attended a conference in Berlin last month entitled "Evolution and Diseases of Modern Environments" that was convened by Randolph Nesse and dove-tailed with the 350th World Health Summit. Ben Campbell (University of Wisconsin, Milwaukee) and I were the rapporteurs for our group "Early Development and Reproductive Function." Our report is now online at The Evolution and Medicine Review and can be found here.

A highlight to get you over there:

The fertility group’s main conclusion was that we need to bring our particular approach to variability to medicine.... The main problem we note is that we are uncomfortable making strong recommendations to medicine regarding reproductive health because we do not yet have enough baseline data of the normal range of variation within and between women and within and between populations. The focus in funding mechanisms is on basic molecular science and disease-focused science, and our discipline falls between these two extremes. Thus we first propose a greater emphasis on research that assesses normal variation in the following ways: longitudinal, repetitive sampling, an assessment of lifestyle factors, documentation of ethnic and geographic variation, and a focus on the major lifestyle transitions as these can be periods of major variability.... Finally, we wanted to point out that the population that the majority of our data is western and economically developed, and that they represent the most extreme and highest concentrations of ovarian hormones (and likely other indicators of reproductive function).

Go!

Shameless self-promotion

2009-11-11T22:08:00.001-06:00

My paper in the Yearbook of Physical Anthropology is now up. You should check it out!

Expect a more substantive post next week.

The latter half of the cycle and the endometrium

2009-09-21T21:08:00.005-05:00

Because it's been a while since any of us has blogged, I thought I would post a quick teaser regarding our AAPA and HBA abstracts. Following up from a recent paper in Anthropological Science on rural Polish women, we have found in Canadian women that luteal phase length is correlated to endometrial thickness through the implantation window. The implantation window is six to twelve days after ovulation (the middle of the cycle), and the average luteal phase is twelve to sixteen days long (the second half of the menstrual cycle). Before menses endometrial thickness begins to decline, so as you might expect, those with shorter luteal phases have thinner endometria through the window of implantation.

For now this simply demonstrates variation in endometrial thickness through what has been demonstrated to be the period during which the vast majority of implantations occur. This also means that there is significant variation in luteal phase length, even in ovulatory cycles in well-fed, urban women, in a way that has the potential to be biologically meaningful. Are there factors that are producing variation in luteal phase length (timing of menstruation) that in turn impact endometrial thickness through the implantation window? Or is the endometrium breaking down early for some reason (not a timing so much as a maintenance issue), leading to the shorter luteal phase? How much of this variation is genetic?

This demonstrates that normal women are incredibly variable in their reproductive physiology. Thus, deviation from the "norm" is not immediately suggestive of pathology.

Jim is him!

2009-08-19T13:49:00.002-05:00

Here are the results of our poll:

Jim
33.3%
10

The Piddler
30%
9

G-nome
26.7%
8

Horgnome
6.7%
2

Otto Clave
3.3%
1

total votes: 30

So it looks like Jim has just barely won our little poll. Let's hope Jim keeps away the lab goblins and helps our assays run well. Already I have some hope: Laura has been messing with the concentration of some buffer components and is starting to have luck with a purification step that will help us tell a lot more about a person from their piss. This is always a good thing!

Many thanks to all who voted.

Vote for the best Lab Gnome name!

2009-08-12T09:07:00.002-05:00

Okay, we at the Laboratory for Evolutionary Endocrinology have narrowed down the excellent name suggestions to our favorite five: G-nome, Jim, Horgnome, Otto Clave, and The Piddler. You have one week to cast your votes, and you can vote as many times as you want.

Let the voting begin!