A Feminist Neuroethics of Mental Health

By Ann E. Fink

Ann Fink is currently the Wittig Fellow in Feminist Biology at the University of Wisconsin–Madison, with an appointment in Gender and Women’s Studies and concurrent affiliations with Psychology and the Center for Healthy Minds. Her research in cellular and behavioral neuroscience has appeared in the Journal of Neuroscience, Journal of Neurophysiology, PNAS and other journals. Ann’s interdisciplinary work addresses the ethics of neuroscience in relation to gender, mental health and social justice. 

Emotionality and gender are tied together in the popular imagination in ways that permeate mental health research. At first glance, gender, emotion, and mental health seem like a simple equation: when populations are divided in two, women show roughly double the incidence of depression, anxiety, and stress-related disorders^1-3. Innate biological explanations are easy to produce in the form of genes or hormones. It could be tempting to conclude that being born with XX chromosomes is simply the first step into a life of troubled mood. Yet, buried in the most simplistic formulations of mental illness as chemical imbalance or mis-wiring is the knowledge that human well-being is a shifting, psychosocial phenomenon. Learning and memory research offers a treasure trove of knowledge about how the physical and social environment changes the brain. Feminist scholarship adds to this understanding through critical inquiry into gender as a mode of interaction with the world. This essay explores how a feminist neuroethics framework enriches biological research into mental health. 

Problems with “Biology-from-birth” stories 

What if understanding gender and health isn’t a tale of two gonads (or genitalia, or chromosomes)? The primary theoretical problem with applying binary biology to health is essentialism^4,5, an oversimplified view of gender as comprising two distinct groups of people separated by innate and static biological traits. Feminist neurobiology counters this view with the observation that gender, a complex biopsychosocial phenomenon, cannot be reduced to dimorphism. This is illustrated by work from neuroimager Daphna Joel indicating that brains (unlike most genitalia) live happily in the land of intersex. Joel proposes a “brain mosaic”: human brains are a hodgepodge of statistically “male”-biased, “female”-biased, and neutral characteristics, rather than reflecting two categories⁶. Similarly, psychologist Janet Hyde demonstrates that genders are more alike than different in most cognitive and behavioral characteristics⁷.

The different components of biological sex.

Image courtesy of Wikimedia Commons.

What about those characteristics that differ by crude biological measures of sex? To ignore binary health disparities could be irresponsible. This reasoning precipitated the 2015 NIH mandate to study “sex as a biological variable”⁸, a corrective for the exclusion of “female” tissues and organisms from prior biomedical research. This move has in turn raised questions about what it means to properly study sex, and what, if anything, such research has to do with gender^9,10. The problem: sex and gender represent complex, interacting outcomes of social and biological forces. The first danger of essentialism is, therefore, to scientific knowledge in its own right. Other potential forms of harm then emerge from this oversimplification.

One danger of “biology-from-birth” stories is the possibility of iatrogenic (arising from medical care) disparities in health arising from inappropriate treatment differentials. As an example^9,10 the hypnotic drug zolpidem is cleared more slowly, on average, from women’s bodies compared to men’s, leading to concerns about inappropriate dosing. This gender difference, however, is mediated by weight, which correlates with gender. Potential harm and benefit emerge from this example. Dosing by gender risks overdosing men who weigh less than average, and ineffectively dosing women who weigh more than average. To base decisions on gender, rather than directly predictive indicators, in such cases might constitute negligence. This concern is amplified for people who do not fit neatly into binary categories of sex/gender.



Mental illness labels raise unique questions about autonomy and psychological competence. Furthermore, the definition of psychological disorders is particularly entangled with gender roles. Innate biological explanations risk activating stigma¹¹ by framing mental illness as static and disqualifying, and equating susceptibility with inferiority. The interactions of gendered stigma and mental health stigma can also deliver a double-hit of marginalization¹². The medico-social risks of stigma and assessments of incompetence include undermined consent, patient autonomy, and bodily integrity, as seen, for instance, in the dismal and ongoing justification of coerced sterilizations (tellingly, first labeled “asexualization”¹³). In a more subtle example, one suspected reason for women’s disproportionate cardiovascular mortality is their more frequent referral to psychiatrists than cardiologists (e.g. [14]).

Image courtesy of Wikimedia Commons.

If essentialist categories of identity and mental illness pose a threat to the health and autonomy of pathologized groups, a related risk is the justification of ongoing inequities and violence in larger social structures. Early-life maltreatment and lifelong adversity are major additive risk factors for poor psychological and physical health^15,16; these vary by gender and other aspects of social identity^17,18. Economic instability follows suit: a 2016 study links the gender wage gap to mood disorders¹⁹. To willfully ignore gendered, racialized or otherwise targeted harm in assessing health risk is to tacitly condone such harm. A feminist neuroethics recognizes the need to address social causes of biological susceptibility. 

The future of gender, neurobiology and mental health 

Feminist neurobiology avoids the pitfalls of simple, untenable “biology-from-birth” explanations. Rippon et al.’s guidelines for sex/gender research in neuroimaging⁴ are broadly applicable: their framework takes into account gender similarities (“overlap”) and brain mosaicism, recognizing brains as the ever-changing material substrates for equally dynamic mental states and social interactions (“entanglement”). They also call for improved experimental design, analysis²⁰, and interpretation. Feminist neuroethics respects historicity in science, acknowledging prior harm and proposing restorative and protective measures²¹. Feminist ethics can also protect against other forms of biological essentialism, including deterministic concepts of mental capacity. In agreement with philosopher Helen Longino’s formulation of science as a social endeavor requiring participation by a representative community²², feminist analyses acknowledge that mental health represents a continually debated set of norms.

Finally, a feminist neuroethics incorporates social causality and responsibility into biobehavioral health. Its guiding principle is a sustained attention to the problems of power, violence, and inequality that are so readily buried in reductionist research models. This view adds to mental health research by asking: 1) what interventions curb the staggeringly gendered experience of sexual and intimate partner violence²³ or the exposure to stress and deprivation that contribute to both social stratification and mental illness?, and 2) what are the neurobiological effects of, and remedies for, marginalization and interpersonal violence? (for starters, see: 24-26). A feminist neuroethics invokes biology as an enquiry into a dynamic world, embraces ambiguity, and promises a more nuanced and valuable knowledge of human health. 

References

1. Altemus, M., N. Sarvaiya, and C.N. Epperson. 2014. Sex differences in anxiety and depression: clinical perspectives. Frontiers in Neuroendocrinology 35(3): 320-330. 

2. Steel, Z., C. Marnane, C. Iranpour, et al. 2014. The global prevalence of common mental disorders: a systematic review and meta-analysis 1980–2013. International Journal of Epidemiology 43(2): 476-93. 

3. Kessler, R. C., P. Berglund, O. Demler, et al. 2005. Lifetime Prevalence and Age-of-Onset Distributions of DSM-IV Disorders in the National Comorbidity Survey Replication. Arch Gen Psychiatry 62(6):593–602. 

4. Rippon, G., R. Jordan-Young, A. Kaiser, and C. Fine. 2014. Recommendations for sex/gender neuroimaging research: key principles and implications for research design, analysis, and interpretation. Frontiers in Human Neuroscience 8: 650. 

5. Haslam, Nick, and Jennifer Whelan. 2008. Human natures: Psychological essentialism in thinking about differences between people. Social and Personality Psychology Compass 2, no. 3 (2008): 1297-312. 

6. Joel D, Berman Z, Tavor I, et al. (2015) Sex beyond the genitalia: The human brain mosaic. PNAS 112(50): 15468-15473. 

7. Hyde, J.S. 2005. The gender similarities hypothesis. American Psychologist 60: 581-592. 

8. Clayton, J. A., and F. S. Collins. 2014. Policy: NIH to balance sex in cell and animal studies.  Nature 509 (7500):282-3. 

9. Richardson, S. S., M. Reiches, H. Shattuck-Heidorn, et al. 2015. Opinion: Focus on preclinical sex differences will not address women's and men's health disparities.  Proc Natl Acad Sci USA 112 (44):13419-20. 

10. Ritz, S.A., D.M. Antle, J. Cote, et al. 2014. First steps for integrating sex and gender considerations into basic experimental biomedical research. The FASEB Journal 28: 4-13. 

11. Rusch, N., A. R. Todd, G. V. Bodenhausen, and P. W. Corrigan. 2010. Biogenetic models of psychopathology, implicit guilt, and mental illness stigma. Psychiatry Research 179(3): 328 – 332. 

12. Koenig, Anne M., and Alice H. Eagly. 2014. Extending Role Congruity Theory of Prejudice to Men and Women With Sex-Typed Mental Illnesses. Basic & Applied Social Psychology 36 (1):70-82. 

13. Stern, A. M. 2005. Sterilized in the name of public health: race, immigration, and reproductive control in modern California.  Am J Public Health 95 (7):1128-38. 

14. Maserejian, N. N., C. L. Link, K. L. Lutfey, et al. 2009. Disparities in physicians' interpretations of heart disease symptoms by patient gender: results of a video vignette factorial experiment.  J Womens Health (Larchmt) 18 (10):1661-7. 

15. Cohen, S., D. Janicki-Deverts, and G. E. Miller. 2007. Psychological stress and disease.  JAMA 298 (14):1685-7. 

16. Felitti, V. J., R. F. Anda, D. Nordenberg, D. F., et al. 1998. Relationship of childhood abuse and household dysfunction to many of the leading causes of death in adults. The Adverse Childhood Experiences (ACE) Study.  Am J Prev Med 14 (4):245-58. 

17. Berger, M., and Z. Sarnyai. 2015. "More than skin deep": stress neurobiology and mental health consequences of racial discrimination.  Stress 18 (1):1-10.  

18. Westfall, N. C., and C. B. Nemeroff. 2015. The Preeminence of Early Life Trauma as a Risk Factor for Worsened Long-Term Health Outcomes in Women.  Curr Psychiatry Rep 17 (11):90. 

19. Platt, J., S. Prins, L. Bates, and K. Keyes. 2016. Unequal depression for equal work? How the wage gap explains gendered disparities in mood disorders.  Soc Sci Med 149:1-8. 

20. Fine, Cordelia, and Fiona Fidler. 2015. Sex and Power: Why Sex/Gender Neuroscience Should Motivate Statistical Reform. In Handbook of Neuroethics, ed. Jens Clausen and Neil Levy, 1447-1462. 

21. Chalfin, M. C., E. R. Murphy, and K. A. Karkazis. 2008. "Women's neuroethics? Why sex matters for neuroethics."  Am J Bioeth 8 (1):1-2. 

22. Longino, Helen E. 1990. Science as social knowledge : values and objectivity in scientific inquiry: Princeton, N.J. : Princeton University Press. 

23. Smith, S.G., J. Chen, K.C. Basile, L.K., et al. (2017). The National Intimate Partner and Sexual Violence Survey (NISVS): 2010-2012 State Report. Atlanta, GA: National Center for Injury Prevention and Control, Centers for Disease Control and Prevention. Downloaded on 8/4/2017 from https://www.cdc.gov/violenceprevention/nisvs/summaryreports.html 

24. Sapolsky, R.M. (2005) The Influence of Social Hierarchy on Primate Health. Science 308 (5722):648-52.  

25. Cacioppo, JT et al. (2011) Social isolation. Annals of the New York Academy of Sciences, 1231: 17–22. 

26. Hackman, DA et al. (2010) Socioeconomic Status and the brain: mechanistic insights from human and animal research. Nat Rev Neurosci 11(9): 651 – 659.

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Fink, A. (2017). A Feminist Neuroethics of Mental Health. The Neuroethics Blog. Retrieved on , from http://www.theneuroethicsblog.com/2017/08/a-feminist-neuroethics-of-mental-health.html

Primordial soup to nuts: are some men naturally selected to be better dads?

Children are the future. So “why do some men choose not to invest in their children?” This was the question that Dr. James Rilling set out to answer over the last few years. Dr. Rilling is the head of the Laboratory for Darwinian Neuroscience in the Anthropology Department at Emory University and states one of the lab’s aims is “exploring the neural basis of human social cognition and behavior, particularly those aspects that have been under strong evolutionary selection pressure.” But are absent fathers the result of natural selection?



In the last half-century, the basic structure of American families has been changing. Within two-parent households, fathers are spending more time with their children than they used to as more mothers work outside the home. However, there are also many more single mothers raising children without any paternal help and roughly half of all American children are raised by a single parent at some point during childhood [1].



These changes have occurred far too rapidly to be the result of natural selection, but this trend compels additional study into the factors underlying paternal commitment. It is not known if there may in fact be an evolutionary explanation for why some men are more committed fathers than others. More to the point, do biological differences between men influence behavioral variation? Life History Theory posits that natural selection shapes the allocation of finite resources toward aspects of growth, survivorship, and reproduction. Within reproduction, there is arguably a trade-off in this zero-sum game between parenting and mating activities, and natural selection shapes phenotypes to support optimal strategies.

In the non-human world, there is evidence for a connection between mating strategy and testicular size in males. For example, gorillas, who typically live in harem-like situations with little competition from other males have rather small testes for their body weight whereas chimpanzees, who typically face much more mating rivalry are much better-endowed [2]. Other studies have found a relationship between testicular volume and mating success within species [3,4].



Dr. Rilling’s group reasoned that perhaps testicular volume would also be indicative of mating investment within a species (ours) and tested whether testicular size or testosterone levels correlated with measures of paternal involvement. To take it a step further, they also used fMRI to examine the activation of reward pathways in fathers’ brains while viewing photographs of their children. The researchers recruited fathers of children (age 1-2) in Atlanta, GA who were co-habitating with their partner and child. They then asked the fathers – and also the mothers – to come into the lab and answer a series of questions designed to gauge the fathers’ involvement and parenting responsibilities, and also their desired level of involvement.



They then asked the fathers – and also the mothers – to come into the lab and answer a series of questions designed to gauge the fathers’ involvement and parenting responsibilities, and also their desired level of involvement. The survey assessed involvement by asking who is responsible for the child on a 1 – 5 scale (1 being mother almost always to 5 father almost always) in 24 different tasks and situations like bathing the baby or getting up at night to attend to waking. The mothers’ ratings served to corroborate the fathers’ self-reported involvement and supplemental information showed that there was in fact a very high level of agreement. The fathers then provided blood samples for hormonal measures and received structural and functional MRI scans. In the fMRI scanner, they were shown pictures of their own child, an unknown child, and an unknown adult with neutral, happy, or sad facial expressions. Finally, testicular volume was measured by structural MRI.



They hypothesized that the more invested fathers would have lower testosterone levels and smaller testes – reflecting more of an energetic investment in parenting than in mating behavior. Furthermore, they reasoned that this behavior may be related to activity in the ventral tegmental area – a part of brain’s reward system – because more involved fathers may find interaction with their children more rewarding. Indeed, this is what they found.



Mascaro and colleagues published the results of their study entitled “Testicular volume is inversely correlated with nurturing-related brain activity in human fathers” in PNAS [5]. As one might expect, headline writers (this one included) made the most of this opportunity: “Men with smaller gonads are better dads”, “Have you got the balls to be a good dad?”, “How your big balls lead to bad parenting”, etc., etc.

From The Onion

Some Internet commenters and science bloggers who, admittedly, are not by-and-large known for their levelheadedness and foresight, found the study pointless or a waste of money. These remarks may reflect a public attitude that scientific research reported by the mainstream press needs to have some impact on our daily life. They also reflect a lack of understanding of the way science funding works, as this finding was a small piece of a larger study that examined the more general biological influences on paternal behavior and which has resulted in multiple non-testes related publications. This quick-trigger dismissal of science as a waste of money is worrisome given the current state of science funding.



One couldn’t be faulted for asking, “what am I supposed to do with this information?” Does this mean that deadbeat dads should be excused for their irresponsibility so long as they are well-endowed? Not so fast. The authors were careful to note that this study does not establish causality: “it remains unclear whether greater testes volume is a cause or a consequence of male life-history strategies.” In other words, it might also be the case that fathers who choose to be more invested in child rearing experience a drop in testosterone and mating drive (but this doesn’t mean that changing diapers will shrink your manhood!). One limitation of this study is that it confined its analysis to the heteronormative parenting model. An interesting next step could be to determine if these correlations also hold in same-sex male couples.



This study, presented by lead author Dr. Jenny Mascaro at the Emory Neuroethics Program’s monthly Neuroscience, Ethics, and the News Journal Club, is exactly the type of article that this forum was created to discuss. It was published in a high-impact journal and distributed to a wide audience in many fields. The press immediately pounced on it and broadly disseminated the main findings, which is understandable due to how the topic is relatable and digestible (not to mention provocative). In addition, these findings raise interesting questions about biological reductionism and what it means for individual responsibility.



It is difficult to communicate findings such as these – which shed light on our nature and tendencies but do not necessarily explain any single individual’s behavior – to the general public without misinterpretation. Still, it is relatable, fascinating studies like this one that can keep the public engaged with scientific research and help all of us understand a little more about the complexity of human nature.



References



1. Cabrera, Natasha J., Catherine S. Tamis-LeMonda, Robert H. Bradley, Sandra Hofferth, and Michael E. Lamb. “Fatherhood in the Twenty-First Century.” Child Development 71, no. 1 (January 1, 2000): 127–36.



2. Harcourt, A.H., P.H. Harvey, S.G. Larson, and R.V. Short. “Testis Weight, Body Weight and Breeding System in Primates.” Nature 293, no. 3 (September 3, 1981): 55–57.



3. Schulte-Hostedde, Albrecht I., and John S. Millar. “Intraspecific Variation of Testis Size and Sperm Length in the Yellow-Pine Chipmunk (Tamias Amoenus): Implications for Sperm Competition and Reproductive Success.” Behavioral Ecology and Sociobiology 55, no. 3 (October 31, 2003): 272–77.



4. Preston, B. T., I. R. Stevenson, J. M. Pemberton, D. W. Coltman, and K. Wilson. “Overt and Covert Competition in a Promiscuous Mammal: The Importance of Weaponry and Testes Size to Male Reproductive Success.” Proceedings of the Royal Society of London B: Biological Sciences 270, no. 1515 (March 22, 2003): 633–40.



5. Mascaro, Jennifer S., Patrick D. Hackett, and James K. Rilling. “Testicular Volume Is Inversely Correlated with Nurturing-Related Brain Activity in Human Fathers.” Proceedings of the National Academy of Sciences of the United States of America 110, no. 39 (September 24, 2013): 15746–51.





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Purcell, R. (2015). Primordial soup to nuts: are some men naturally selected to be better dads? Retrieved on , from http://www.theneuroethicsblog.com/2015/03/primordial-soup-to-nuts-are-some-men.html

Can Neuroscience Validate the Excuse “Not Tonight, Dear, I have a Headache?"

Men
and women experience fluctuations in sexual motivation over a lifetime. Whether
sexual desire is enhanced or diminished at any particular time can depend on a
number of factors and circumstances, but researchers from McGill University
recently set out to determine specifically how pain impacts sexual behavior.¹ Results from this study, published in The Journal of Neuroscience earlier this
year, were the topic of the most recent “Neuroethics and Neuroscience in the
News” discussion facilitated by Emory Women’s
Gender and Sexuality graduate student Natalie Turrin and Neuroscience
graduate student Mallory Bowers.




To study how pain impacts sexual
motivation, researchers used a partitioned Plexiglas chamber where the
partition contained small, semi-circular openings only large enough for the
female mice to pass through (this study required that male mice be greater than
45 g and female mice smaller than 25 g). In this set-up, the females were free
to either cross the partition and engage in sexual activity with the male mice
or “escape” to the side where the males were unable to follow. Sexual
motivation in this study was measured by how many total mounts occurred, and since
mounting involves male participation, time spent on the male side of the
chamber was also a measure of female sexual motivation. When researchers
injected female mice with inflammatory agents in the vulva, hind paw, tail, or
cheek to induce pain, female mice consistently participated in less mounting
behavior and spent less time on the male side of the cage compared to no
injections. Males, on the other hand, when injected with the same inflammatory
agents in either the penis, hind paw, tail, or cheek, experienced unimpeded
sexual activity (total number of mounts did not decrease compared to controls) in
an open field paradigm where the males had unrestricted access to the females. Although
it has been observed that female mice can have a higher sensitivity to pain
than male mice,² researchers observed that male and female
mice exhibited the same level of sensitivity towards inflammation to the hind
leg according to the mouse grimace scale (MGS), a visual observation of a mouse’s facial
features to determine pain levels.




The final experiments to study sexual
activity involved rescuing the lack of sexual motivation from female mice using
either an antinflammatory agent or two different prosexual drugs. The analgesic
pregabalin reversed the reduction of total mounts that resulted from inducing
pain in females, and according to the MGS, also reduced the level of pain. “Prosexual”
drugs, apomorphine (APO) and melanotan-II (MT-II), had the same rescuing effect,
but based on the MGS, did not have the ability to relieve pain from the
inflammatory injections. It should be noted though that APO increases
locomotion³ in mice, which may partially account for
the females moving towards the male side of the cage more often.




From these experiments, researchers
concluded that female mice have lower levels of sexual motivation when in pain,
but even in penile pain, male mice maintain a desire to participate in sexual
activity. However, the decrease in sexual motivation can be rescued in females
by either pain reduction or aphrodisiacs,
in this case a dopamine agonist (APO) or an α-melanocyte-stimulating hormone
analog (MT-II). Perhaps these claims made regarding mice are reasonable, but it
is even more problematic that the authors confidently extrapolate the results
to humans. The final line of the abstract reads “These findings suggest that the well known context sensitivity of the
human female libido can be explained by evolutionary rather than sociocultural
factors, as female mice can be similarly affected.”




Of course, media outlets ran with this
conclusion and multiple articles were published with definitive titles like “Women ARE more likely to go off sex when
they are in pain” and “That headache excuse is real: For females,
pain kills sexual desire.”
The authors of this paper perpetrated the idea that a woman’s lack of sexual
motivation at any given moment is
either a biological or
a sociocultural one. In the press release and the paper, the authors refer to the
apparently common aphorism “Not tonight, dear, I have a headache,” and mention
that this would be evidence that sometimes wives are in too much pain to have
sex that has been initiated by their husbands. But sexual relations are so much
more complicated than just a simple relationship such as a pain from a headache
equals lack of sexual motivation. What if the woman (or man, for that matter)
doesn’t really have a headache, but there is another underlying reason that a
partner is too embarrassed to share? Or, what if pain from a headache makes you
feel less sexy, and that feeling is the sexual deterrent, not the pain alone? Pain,
either directly or indirectly, would most likely make a person feel less
sexual, but why does is take a study with mice (who aren’t insecure about love
handles or annoyed with a spouse due to an insensitive comment) to validate
this thought? It is reminiscent of neuro-realism, the
idea that attaching a brain scan to any study or correlation suddenly qualifies
the findings as real or more true.⁴ While this study only involved mice,
researchers did use fMRI to study the difference between the brains of women
with and without acquired hypoactive sexual desire disorder (HSDD) in this paper.⁵ But no one - including females, their sexual
partners, researchers, or doctors - really wins when it is being advertised
that the female libido is something that can be can characterized as either
biologically or socioculturally driven. 

Via The Telegraph

One reason for ascribing a biological reason
to the lack of sexual motivation could involve drug development; if a
biological target can be found that is responsible for diminishing sex drive,
then perhaps there is a pill to fix that. The work in the paper was supported
by a Pfizer Pain Research Award from Pfizer Canada, and Pfizer Canada did
kindly provide the pregabalin that was used in the sexual recovery research. There
have been a number of pharmaceutical companies that have sought FDA approval
for low female sexual desire,⁶ even when the diagnosis of disorders such as
HSDD and female sexual dysfunction (FSD) are controversial. One example though
is Lybrido, a drug meant to treat HSDD. (Mallory actually gave a journal club talk last year about the implications of pharmaceutical
companies targeting the female sex drive with a focus on Lybrido). Lybrido
is interesting because it was ineffective in a cohort of women who “suffer from
HSDD as a result of inhibitory mechanisms,” resulting from negative
associations with sex and for that reason Lybridos was developed.⁷ Lybidos has an additional
component that targets the prefrontal cortex areas of the brain and is meant to
alleviate these inhibitory mechanisms.⁸ A discussion of drug
development for women that have negative associations with sex is beyond the
scope of this post, but the mentality that this could be relieved with only a
pill is grossly overly simplifying the complexities of the female libido and
how this affects relationships women have with their sexual partners. If
researchers in academia though are willing to commit to the idea that female
sexuality can be classified as solely biologically determined, then can we
really expect that pharmaceutical companies, marketing campaigns, and sensationalized
news articles won’t try to capitalize on that idea?

Via The Neurocritic

References 

(1)  Farmer, M. A.; Leja, A.; Foxen-Craft,
E.; Chan, L.; MacIntyre, L. C.; Niaki, T.; Chen, M.; Mapplebeck, J. C. S.;
Tabry, V.; Topham, L.; Sukosd, M.; Binik, Y. M.; Pfaus, J. G.; Mogil, J. S.
Pain Reduces Sexual Motivation in Female But Not Male Mice. J. Neurosci.
2014, 34, 5747–5753.

(2)  Mogil, J. S. Sex
Differences in Pain and Pain Inhibition: Multiple Explanations of a
Controversial Phenomenon. Nat. Rev. Neurosci. 2012, 13,
859–866.

(3)  Horn, C. C.;
Kimball, B. A.; Wang, H.; Kaus, J.; Dienel, S.; Nagy, A.; Gathright, G. R.;
Yates, B. J.; Andrews, P. L. R. Why Can’t Rodents Vomit? A Comparative
Behavioral, Anatomical, and Physiological Study. PLoS ONE 2013, 8,
e60537.

(4)  Racine, E.; Bar-Ilan,
O.; Illes, J. fMRI in the Public Eye. Nat. Rev. Neurosci. 2005, 6,
159–164.

(5)  Woodard, T. L.;
Nowak, N. T.; Balon, R.; Tancer, M.; Diamond, M. P. Brain Activation Patterns
in Women with Acquired Hypoactive Sexual Desire Disorder and Women with Normal
Sexual Function: A Cross-Sectional Pilot Study. Fertil. Steril. 2013,
100, 1068–1076.e5.

(6)  Shames, D.; Monroe,
S. E.; Davis, D.; Soule, L. Regulatory Perspective on Clinical Trials and End
Points for Female Sexual Dysfunction, in Particular, Hypoactive Sexual Desire
Disorder: Formulating Recommendations in an Environment of Evolving Clinical
Science. Int. J. Impot. Res. 2006, 19, 30–36.

(7)  Lybrido
http://www.emotionalbrain.nl/lybrido (accessed Oct 30, 2014).

(8)  Lybridos
http://www.emotionalbrain.nl/lybridos (accessed Oct 30, 2014).

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Strong, K. (2014). Can Neuroscience Validate the Excuse “Not Tonight, Dear, I have a Headache?" The Neuroethics Blog. Retrieved on

, from http://www.theneuroethicsblog.com/2014/11/can-neuroscience-validate-excuse-not.html

(en)Gendering psychiatric disease: what does sex/gender have to do with posttraumatic stress disorder (PTSD)?

Mallory Bowers is a 5th year Neuroscience doctoral candidate working with Dr. Kerry Ressler at Emory University. Prior to graduate school, Mallory received her Bachelor of Arts from the University of Pennsylvania. Mallory is interested in behavioral neuroscience, with a particular focus on how neural plasticity contributes to learning. With Dr. Ressler, Mallory is using a mouse model of exposure-based psychotherapy to better understand the neurobiology of learned fear. Specifically, her research focuses on a potential interaction between the cholecystokinin and endogenous cannabinoid systems that may underlie extinction of cued fear. Mallory was on the organizing committee for the 2013 “Bias in the Academy” Conference and is President of Emory Women in Neuroscience (E-WIN).



As I’ve become more entrenched in the PTSD field, I’ve been struck by the prominent sex/gender difference in the prevalence of PTSD (among many other psychiatric disorders) and the categorical use of male animal models. As researchers begin to explore sex differences in animal models of stress, anxiety, and fear, evidence suggests that male animals are more vulnerable to acute and chronic stress, while females appear to be more resilient (Cohen and Yehuda 2011). The results of these animal studies contradict the human epidemiological data, with lifetime prevalence of PTSD at 10-14% in women and 5-6% in men in the United States (Breslau, Davis, et al. 1991, Breslau, Davis, et al. 1997, Kessler, Sonnega, et al. 1995, Resnick, Kilpatrick, et al. 1993). In this post, I’d like to explore the ways in which socio-cultural conditioning genders an individual’s sense of self, influences definitions and language surrounding mental health, and supports frameworks of gender bias (a putative low-grade, chronic stressor) - potentially contributing to sex/gender differences observed in the prevalence of certain psychiatric disorders, specifically PTSD.



Sex and Gender Primer



Sex refers to the biological and physiological characteristics that define men and women, including sex chromosomes, gonads, and hormones. The definition of gender is more complicated, but generally refers to socially and culturally endorsed roles, behaviors, and activities for men and women. Gender can describe the relationship between one’s traits and one’s sense of self as male, female, or somewhere in between. Social and cultural influences promote gender scripts from infancy throughout adulthood. For the purposes of this post, I use the term sex/gender to acknowledge the importance of both physical and cultural features, particularly in describing the interpretations of data from human research.

Via BigStockPhoto.com

Importance of self-definition



Consistently, evidence from psychology research suggests that sense of self and self-definition (also referred to as self-construal) can function as a lens through which individuals can interpret information (Wyer and Srull 1984). Rigid gender roles in Western cultures, some have suggested, could differentially impact the development of self-construal (Cross and Madson 1997, Cross, Bacon, et al. 2000). In considering sex/gender differences in prevalence of PTSD, could a gendered self-construal precipitate risk for PTSD by influencing interpretation of trauma? In fact, trauma severity is thought to contribute to prevalence of PTSD, where trauma severity is defined by subjective emotional response that varies based on individual perception (Foa, Zinbarg, et al. 1992, Kessler, Sonnega, et al. 1995, Yehuda 2002, Yehuda 2004).



Interestingly, analysis of US epidemiological data reveals sex/gender differences in PTSD for certain types of trauma – specifically, trauma that involves interpersonal conflict. Kessler et al. find significant sex/gender differences in rates of PTSD when trauma involves molestation, physical attack, combat, shock, threat with a weapon, physical abuse, or witnessing injury or death (Breslau, Davis, et al. 1991, Kessler, Sonnega, et al. 1995). Men and women develop PTSD at comparable rates when trauma involves sudden injury, accident, natural disaster with fire, or witnessing injury or death (Breslau, Davis, et al. 1991, Kessler, Sonnega, et al. 1995). This suggests that it is not merely the presence of trauma, but the interpretation of a specific trauma that results in sex/gender differences in the prevalence of PTSD. If trauma severity - shaped by an individual’s subjective perception - influences risk for PTSD and perception (or self-construal) is gendered according to socio-cultural conditioning, then researchers need to address whether strict gender binaries influence self-construal and/or traits that differentially precipitate risk for PTSD.



Gendered representations of PTSD



Although I propose that gendered self-construals could interact with particular types of trauma, manifesting in differential rates of PTSD among men and women, this is likely not the sole mechanism contributing to sex/gender differences in rates of PTSD. One possibility is that sex/gender specific presentations of PTSD in men leads to “misdiagnosis”. Young girls who are exposed to trauma are more likely to report “internalizing” symptoms - depression, anxiety, and hyperarousal, whereas boys more often report “externalizing” symptoms, such as aggression and conduct problems (Buckner, Beardslee, et al. 2004, Gustafsson, Larsson, et al. 2009). Men present with more denial, emotion control, behavioral problems, suicidality, violence, and substance abuse following sexual trauma (Darves-Bornoz, Choquet, et al. 1998, Kaufman, Divasto, et al. 1980). These externalizing versus internalizing symptoms, some have posited, contribute to sex/gender differences in the diagnosis of antisocial personality disorder (ASPD) and borderline personality disorder (BPD) – which some have suggested are the same disorder with gender specific presentations (Hudziak, Boffeli, et al. 1996, Lobbestael, Arntz, et al. 2005). With differential rates of PTSD among men and women, potentially derived from differences in symptomatology, one reasonable question to ask is - are there gender essential psychiatric disorders? This is particularly interesting, as most psychiatric disorders are not diagnosed by “objective” measures, such as biomarkers, but by suites of symptoms characterized in the Diagnostic and Statistical Manual of Mental Disorders (DSM-V). This question might be clarified by comparing the symptomatology of psychiatric disorders that present with sex/gender differences.



The stress of gender bias



Moreover, is gender inequality generally stressful – possibly contributing to higher rates of PTSD and other psychiatric disorders in women? Notably, several international studies (conducted in Canada, Australia, Germany, and Switzerland) have not found significant sex/gender differences in the prevalence of PTSD (Creamer, Burgess, et al. 2001, Lukaschek, Kruse, et al. 2013, Maercker, Forstmeier, et al. 2008, Stein, Walker, et al. 1997). According to the 2013 Global Gender Gap report, these countries rank equal to or higher than the United States on an index measuring the percentage of inequality between men and women that has been closed (meaning, these countries have lower rates of sex/gender inequality than the United States). The stress of microaggressions (Sue 2010) related to gender bias and discrimination is likely to exert long-term ramifications, potentially contributing to rates of psychiatric disease like PTSD, as research demonstrates that pre-trauma risk factors like life stress predict PTSD (Brewin, Andrews, et al. 2000).



Interestingly, researchers have begun to uncover links between chronic stress - which often precipitates psychiatric disease - and rates of cellular aging. Cellular environment, which can be regulated by perceived stress via oxidative stress, plays an important role in controlling telomere length (Epel, Blackburn, et al. 2004). Telomeres are regions of repetitive nucleotide sequences that protect the end of chromosomes. Telomeres protect gene truncation during DNA replication, as DNA polymerases are unable to continue DNA duplication through the end of chromosomes (Blackburn and Gall 1978). Studies suggest that oxidative stress shortens telomeres, and that antioxidants can decrease the rate of shortening (von Zglinicki 2002). African-Americans who are subject to significant racial discrimination, due to “weathering” or higher psychosocial stress, exhibit greater rates of telomere shortening compared to Caucasians (Rewak, Buka, et al. 2014). Further, African-Americans who report more interpersonal experiences of racial discrimination and have greater internalized negative racial bias have shorter telomere lengths compared to other African-Americans (Chae, Nuru-Jeter, et al. 2014). Some researchers report higher rates of PTSD among African-Americans compared to other races, although the literature is mixed, potentially due to problems of underreporting of psychiatric disease in African-Americans (Breslau and Anthony 2007, Kessler, Sonnega, et al. 1995). As in African-Americans, telomere length could provide a biological correlate of psychosocial stress due to gender bias, which could, in part, offer an explanation as to why women are more likely to develop PTSD. Addressing the question of whether the stress of gender inequality contributes to higher rates of PTSD and other psychiatric disorders is likely to be extremely complicated. However, the results of these studies could be transformative in how we think about psychiatric disease and how we might design and conduct future research to identify novel targets for treating and preventing PTSD.

Telomere Shortening (via nia.nih.gov)

Future directions and recommendations



By exclusively focusing on animal studies, or worse – conflating sex and gender in human research, researchers may accidentally disregard an important source of influence on neurobiology – society and culture. To avoid this ambiguity, scientists are advised to be discerning when referring to “sex” and “gender” in the interpretation of data (e.g. gender may not be appropriate when discussing a mouse model). As most human research is correlative, researchers will be unable to tease apart whether differences are attributed to sex or gender (to state otherwise would be un-scientific). Additionally, sex and gender influences are not necessarily mutually exclusive. Therefore, data interpretations should acknowledge as much.



Future scientific endeavors, particularly in the investigation of sex/gender differences in the prevalence of PTSD, will benefit from an alliance with the humanities who can provide a rich knowledge on how sociocultural factors shape conceptions of not only gender, but also illness. In this way, researchers can more thoroughly parse through risk factors for PTSD, such as differences in self-construal and gender bias. Furthermore, cross disciplinary, collaborative dialogue between the sciences would create more inclusive definitions of mental illness, as outlined by the DSM-V.



In highlighting the ways that society and culture influence the etiology and definition of PTSD, I hope I’ve underlined the work that needs to be done in order to bridge the gap in our understanding of psychiatric disease.





References



Blackburn, E.H. and J.G. Gall (1978). A tandemly repeated sequence at the termini of the extrachromosomal ribosomal RNA genes in Tetrahymena. J Mol Biol 120 (1): p. 33-53.

Breslau, N., G.C. Davis, P. Andreski, and E. Peterson (1991). Traumatic events and posttraumatic stress disorder in an urban population of young adults. Arch Gen Psychiatry 48 (3): p. 216-22.

Breslau, N., G.C. Davis, P. Andreski, E.L. Peterson, and L.R. Schultz (1997). Sex differences in posttraumatic stress disorder. Arch Gen Psychiatry 54 (11): p. 1044-8.

Breslau, N. and J.C. Anthony (2007). Gender differences in the sensitivity to posttraumatic stress disorder: An epidemiological study of urban young adults. J Abnorm Psychol 116 (3): p. 607-11.

Brewin, C.R., B. Andrews, and J.D. Valentine (2000). Meta-analysis of risk factors for posttraumatic stress disorder in trauma-exposed adults. J Consult Clin Psychol 68 (5): p. 748-66.

Buckner, J.C., W.R. Beardslee, and E.L. Bassuk (2004). Exposure to violence and low-income children's mental health: direct, moderated, and mediated relations. Am J Orthopsychiatry 74 (4): p. 413-23.

Chae, D.H., A.M. Nuru-Jeter, N.E. Adler, G.H. Brody, J. Lin, E.H. Blackburn, et al. (2014). Discrimination, racial bias, and telomere length in African-American men. Am J Prev Med 46 (2): p. 103-11.

Cohen, H. and R. Yehuda (2011). Gender differences in animal models of posttraumatic stress disorder. Dis Markers 30 (2-3): p. 141-50.

Creamer, M., P. Burgess, and A.C. McFarlane (2001). Post-traumatic stress disorder: findings from the Australian National Survey of Mental Health and Well-being. Psychol Med 31 (7): p. 1237-47.

Cross, S.E. and L. Madson (1997). Models of the self: self-construals and gender. Psychol Bull 122 (1): p. 5-37.

Cross, S.E., P.L. Bacon, and M.L. Morris (2000). The relational-interdependent self-construal and relationships. J Pers Soc Psychol 78 (4): p. 791-808.

Darves-Bornoz, J.M., M. Choquet, S. Ledoux, I. Gasquet, and R. Manfredi (1998). Gender differences in symptoms of adolescents reporting sexual assault. Soc Psychiatry Psychiatr Epidemiol 33 (3): p. 111-7.

Epel, E.S., E.H. Blackburn, J. Lin, F.S. Dhabhar, N.E. Adler, J.D. Morrow, et al. (2004). Accelerated telomere shortening in response to life stress. Proc Natl Acad Sci U S A 101 (49): p. 17312-5.

Foa, E.B., R. Zinbarg, and B.O. Rothbaum (1992). Uncontrollability and unpredictability in post-traumatic stress disorder: an animal model. Psychol Bull 112 (2): p. 218-38.

Gustafsson, P.E., I. Larsson, N. Nelson, and P.A. Gustafsson (2009). Sociocultural disadvantage, traumatic life events, and psychiatric symptoms in preadolescent children. Am J Orthopsychiatry 79 (3): p. 387-97.

Hudziak, J.J., T.J. Boffeli, J.J. Kreisman, M.M. Battaglia, C. Stanger, and S.B. Guze (1996). Clinical study of the relation of borderline personality disorder to Briquet's syndrome (hysteria), somatization disorder, antisocial personality disorder, and substance abuse disorders. Am J Psychiatry 153 (12): p. 1598-606.

Kaufman, A., P. Divasto, R. Jackson, D. Voorhees, and J. Christy (1980). Male rape victims: noninstitutionalized assault. Am J Psychiatry 137 (2): p. 221-3.

Kessler, R.C., A. Sonnega, E. Bromet, M. Hughes, and C.B. Nelson (1995). Posttraumatic stress disorder in the National Comorbidity Survey. Arch Gen Psychiatry 52 (12): p. 1048-60.

Lobbestael, J., A. Arntz, and S. Sieswerda (2005). Schema modes and childhood abuse in borderline and antisocial personality disorders. J Behav Ther Exp Psychiatry 36 (3): p. 240-53.

Lukaschek, K., J. Kruse, R.T. Emeny, M.E. Lacruz, A. von Eisenhart Rothe, and K.H. Ladwig (2013). Lifetime traumatic experiences and their impact on PTSD: a general population study. Soc Psychiatry Psychiatr Epidemiol 48 (4): p. 525-32.

Maercker, A., S. Forstmeier, A. Enzler, G. Krusi, E. Horler, C. Maier, et al. (2008). Adjustment disorders, posttraumatic stress disorder, and depressive disorders in old age: findings from a community survey. Compr Psychiatry 49 (2): p. 113-20.

Resnick, H.S., D.G. Kilpatrick, B.S. Dansky, B.E. Saunders, and C.L. Best (1993). Prevalence of civilian trauma and posttraumatic stress disorder in a representative national sample of women. J Consult Clin Psychol 61 (6): p. 984-91.

Rewak, M., S. Buka, J. Prescott, I. De Vivo, E.B. Loucks, I. Kawachi, et al. (2014). Race-related health disparities and biological aging: Does rate of telomere shortening differ across blacks and whites? Biol Psychol 99C: p. 92-99.

Stein, M.B., J.R. Walker, A.L. Hazen, and D.R. Forde (1997). Full and partial posttraumatic stress disorder: findings from a community survey. Am J Psychiatry 154 (8): p. 1114-9.

Sue, D.W. (2010) Microaggressions in everyday life : race, gender, and sexual orientation. Series2010, Hoboken, N.J.: Wiley. xxiii, 328 p.

von Zglinicki, T. (2002). Oxidative stress shortens telomeres. Trends Biochem Sci 27 (7): p. 339-44.

Wyer, R.S. and T.K. Srull (1984) Handbook of social cognition. Series1984, Hillsdale, N.J.: L. Erlbaum Associates. v. <1>.

Yehuda, R. (2002). Post-traumatic stress disorder. N Engl J Med 346 (2): p. 108-14.

Yehuda, R. (2004). Risk and resilience in posttraumatic stress disorder. J Clin Psychiatry 65 Suppl 1: p. 29-36.







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Bowers, M. (2014). (en)Gendering psychiatric disease: what does sex/gender have to do with posttraumatic stress disorder (PTSD)? The Neuroethics Blog. Retrieved on , from http://www.theneuroethicsblog.com/2014/05/engendering-psychiatric-disease-what.html

Doing Feminist Science/Feminists Doing Science: An interview with Dr. Sari van Anders, Founder of Gap Junction Science Part II

Continued from Part I. In Part II, Dr. van Anders discusses her website, www.gapjunctionscience.org.



How did Gap Junction Science come about? Prior to Gap Junction, how did you find and network with feminist scientists?



I became really interested in the doing of feminist science – it felt very hard for me to figure things out, and there wasn’t that much community of actual feminist scientists. I wanted to develop a place where feminist science could be discussed – both practice and theory. I sometimes hear people talk about the theory as if it is practice. Of course it’s relevant, but you know what they say about theory and practice: in theory, they’re the same, in practice, they’re not. I was lucky that while I was thinking about these things, there was a call for grants at UM from our ADVANCE program for online networks in science that promote diversity. Feminism isn’t necessarily diverse, but the feminist science I envision at its heart attends to diversity. So, I wanted a space where scientists didn’t have to defend their very identity, and where feminist beliefs were a starting point, not a debate. I hoped that Gap Junction Science could be a space where feminist scientists could challenge ourselves, learn more, develop methods, and engage in a shared project. Prior to Gap Junction Science, and still, I do a lot of grassroots networking – emailing, meeting, etc. I like that ‘bottom-up’ approach and I like that now I also have a ‘top-down’ source too.

Via OffWorld Designs

How do you see visitors to the site using Gap Junction?



At first, I thought of it more as a social networking site, and this was influenced by colleagues who led other sites where the social networking features were predominant. But, visitors to Gap Junction Science seem to be doing a lot more reading than engaging, from our statistics. I think people are using it to learn more about feminism and how feminism and science could come together. After all, almost all scientific training explicitly or implicitly teaches that the two cannot come together, so I think it has more of an educational component than I first anticipated. People are reading it to try to flesh out their own understanding of feminist science and how to talk about it, explain and ‘defend’ their own passions to others, and incorporate new ways of seeing and doing into their own science.



Do you think it’s important to have female mentors? Do you see Gap Junction fostering mentorship?



I usually say that what matters is having feminist mentors. I find the point in Donna Haraway’s Cyborg manifesto as really useful here: she calls for alliances based on affinities rather than identities. So, choosing a mentor based on gender is choosing based on identity, but what does that identity represent? I don’t think all women are one unified essential group. Neither are feminists! But at least with feminism you have an inkling of the politics and sympathies and beliefs. That said, sometimes you really need identity-specific advice, and that can be hard to get from someone who doesn’t share your social location. But a good feminist mentor should be able to guide you to someone who can give you what they can’t. I will also say that I have repeatedly seen a very special bitterness reserved for mentors who share a social location but not an affinity; there’s an expectation that the mentor will ‘get’ the mentee and, when they don’t, it feels like way more of a violation. There’s nothing worse than not finding a home where you thought one would be. So, I recommend a feminist mentor and, for identity-related issues, going to someone with ‘epistemic privilege.’ That is someone who has critically engaged with their social location and positionality. In other words, find someone who has insights about the lived experiences you share, not just someone who shares the social location itself. So find someone who understands the issues you’re facing, when you can. That person is going be able to help you navigate difference in some remarkable ways. I think that Gap Junction Science kind of acts as impersonal indirect mentorship, especially about topics where local knowledge and expertise might be missing. For example, I’ve had a few colleagues now tell me that they’ve frantically read the site before teaching or giving a talk on issues around gender, sex, feminism, and science. That did my heart good! Knowing that it could be useful in that way makes me realize how much more useful I could make it to that end.

Courtesy of Indiana University

What is your vision for the future of Gap Junction Science?



Well, definitely world domination, first. After that, milkshake machines for everyone! Then, who knows?! Just kidding (never about milkshakes). We’re in the process of thinking more about this, now that we see how the site is being used in the world. We’d like to make it much more of a resource, now that I know that it’s being used that way. I’d like to see more involvement of trainees – grad students especially. I’d love to have more people involved in posting, and invested in the site. Finally, I think a major goal is to be a ‘third space’ for exploring and how-to’s of creating feminist science knowledge. My vision for Gap Junction Science is to be a place where scientists can ‘catch up’ on feminist science and where feminist scholars can engage with the day-to-day issues of feminist science as well.







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Bowers, M. (2014). Doing Feminist Science/Feminists Doing Science: An interview with Dr. Sari van Anders, Founder of Gap Junction Science Part II. The Neuroethics Blog. Retrieved on , from http://www.theneuroethicsblog.com/2014/03/doing-feminist-sciencefeminists-doing_4175.html

Doing Feminist Science/Feminists Doing Science: An interview with Dr. Sari van Anders, Founder of Gap Junction Science Part I

Dr. van Anders

*Editor's note. The title of this post is the title of Sari van Anders' talk sponsored by Emory Women in Neuroscience on March 20th. This post is the first of a two-part series.



Mallory Bowers, a 5th year graduate student at Emory University and President of Emory Women in Neuroscience, interviewed Dr. Sari van Anders an Assistant Professor in the Departments of Psychology and Women’s Studies at the University of Michigan, for the Neuroethics Women Leaders group. Dr. van Anders received her Ph.D. in Biological and Cognitive Psychology from Simon Fraser University. Her current research program focuses on “social neuroendocrinology, intimacy (sexuality/pair bonding, nurturance), evolution, health, gender/sex and sexual diversity, and research and feminist science practice." The interview will be published in a two part presentation. In Part I, she discusses her path to becoming a critical feminist scientist, the pitfalls of research on sex/gender differences, and how her work fits into bioethics.



Can you talk a little bit about your evolution as a feminist scientist - who or what influenced your feminism?



A very brief selected slice: I was reading feminist science studies in undergrad, but there were no courses on it. I was also so feminist-identified that I didn’t understand the value of taking feminist courses (I thought they were to teach feminism in general, and didn’t understand what feminist scholarship was). I knew I was interested in evolution, sex, gender, and socialization, but it seemed to me that you either studied one (sex/evolution) or the other (gender/socialization). This was actually a pretty fair assumption as there were almost no places to get mentoring about how to incorporate the two into one research program. In graduate school I was doing more work on biological determinism of sex, and then moved to social modulation of hormones. It was really hard for me to see how I could bring the reading I was doing on feminist science studies into my actual science practice, and most of the scientists who were interested in feminist scholarship had left science practice, so there were no guidelines about the day-to-day of feminist science (i.e., there was lots on epistemological approaches but almost nothing on epistemic approaches to feminist science). I kept reading and thinking, noticing little things I could do and claiming them for feminist science. In graduate school, I started an interdisciplinary group at my PhD institution to bring together people interested in gender and sex. And, I started teaching courses that brought the topics together (intersexualities; biopsychological approaches to gender/sex). Slowly it came together, with many missteps and much influence from seeing important ideas in feminist science studies, realizing how I could play them out in my work, and so on. I was already doing feminist science when I took my joint position in Psychology and Women’s Studies here at the University of Michigan, but being more immersed in feminist scholarship has been a major boon to my feminist science practice.



Karen Rommelfanger and I have discussed a bit about breaking molds as it pertains to creating roles and/or careers that don’t necessarily exist. How were you able to break the mold in terms of creating your research program? What advice do you have for individuals looking to “break the mold”?



I think one key is boldness, which I also think is an important contributor to success in science in general. I think an openness to being wrong, to looking dumb, to sharing new ideas, and for learning new languages and perspectives (not just new facts) is also critical. I think being very productive is useful, because publications are the major currency of science, so that will help people overlook your ‘eccentricities’ to some extent (and being feminist and doing feminist science isn’t not seen that way). Having minor authority issues never hurts either, when it comes to breaking molds. Finally, I remember a sort of endless search for mentors and models of how to do feminist science, and I know students are still doing this same thing. There are so few, though, that a lot of it has to be experiential and learning. When you’re breaking the mold, you may want to find another mold that fits you, but that’s the whole point of mold-breaking! There is no premade mold. You have to create your space. I think I started moving forward a lot more quickly once I realized there was no one to ask permission from, no one who was going to tell me I was on the right or wrong track, and that, yes, I would sometimes make mistakes (and hopefully learn from them). So, independence is really useful. But so is collegiality, and an interest in sharing ideas and concepts and learning from others.

van Anders 2013

Your work combines methodologies from biology and the humanities, although your background is in psychology. Was it difficult becoming proficient in reading and writing from a humanities perspective? What advice do you have for someone with wet lab training that would like to become more proficient in humanities work?



It was difficult. It took a lot of time, a lot of talking, a lot of reading, and a lot of trying. Some of my initial attempts never came to fruition because I just wasn’t ready – the ideas were ready, but I wasn’t ready to articulate them yet. My colleagues at the University of Michigan in feminist scholarship have been crucial, as have others at conferences and over email. It’s kind of like learning languages – the more immersion, the better it goes (I assume). If I let my lack of language and imposter syndrome get in the way of interacting with people, I would never have been able to eventually become fluent. So, my advice would be to read, read, read, read and talk, talk, talk, without being worried about saying the wrong things. Hold onto observations and insights until you’re ready to articulate them. And interact with humanists! Unfortunately, our training as scientists generally implicitly or explicitly teaches us that science is the only valuable epistemology in town. It’s certainly the dominant one right now, but there is so much to gain from other disciplines.



What is the biggest misconception about your research?



One misconception about my research is that the biology is biologically deterministic; I work hard to separate the two and help people understand that, though the two often overlap, they don’t need to. Another misconception is that it’s about women only. That’s an interesting one because any research with women becomes known as being only about women, even when it involves men and gender-diverse people too. So I work hard to help people understand that the presence of women among my participants doesn’t somehow erase the presence of men in my studies. Another misconception is that human research is only relevant to humans – to address this, I work hard to explain how I am studying human particularities alongside comparative insights. I see humans as both specific and as another species. In other words, I have my cake (humans are unique) and eat it too (humans are animals).



What is the most common mistake researchers make in interpreting sex differences?



The most common mistake is calling these differences ‘sex’ differences in the first place! Most human behavioral science literally has nothing to say about causal routes and whether a difference reflects innate evolved factors (like sex) or social forces (like gender). Somehow, the presence of biological measures seems to muddy this, as if the mere measurement of biology somehow precludes socialization. But biological measures and biological causation have very little to say to each other. For example, if women show one behavior-hormone association and men show another, is that because these hormone-behavior associations evolved differently? Or do they reflect very different socialization histories? It could be both or either, but a biological measure does not at all point to causation even as it’s interpreted that way. This is why I use ‘gender/sex’ to help highlight that anything we study in humans is a result of a trajectory that includes biological and social influences.

Courtesy of The New York Times

How can we overcome mistakes when it comes to interpreting sex differences – should scientists be required to take a gender studies course?



Well, what’s interesting is that this mistake – mistaking biological difference for biological causation is, arguably, a scientific mistake. Scientists should be able to recognize that correlation does not imply causation without a gender studies course. But of course feminist science studies elegantly (and depressingly) demonstrate, time and time again, that when it comes to gender, sex, and biological determinism, there seems to a ‘scientific override’ button that gets pushed. I think a critical component of addressing these issues is having more feminist construction of science alongside the important pillars of feminist critiques and deconstructions of science. We need more feminists up in there (there = science). To my mind, scientists are most easily swayed by science and biolegible arguments, so changing science is something that feminist scientists can contribute to.



How do you see your research as it relates to the field of neuroethics?



I do a lot of work on testosterone and sexual desire in social context, and this is relevant to ongoing medicalization of low sexual desire and using testosterone to treat it. My work has a lot to say about this in a way that is relevant to neuroethics, because biomedical research tends to be focused on heterosexual women’s intercourse rates with male partners. No one is prescribing testosterone to increase masturbation, increase desire for hook-ups, heighten gay men’s desire, etc. So the discussion of ‘hypoactive sexual desire disorder’ is very rooted in a view of increasing married women’s desire for penile penetration. You don’t have be a critical feminist to see those problematics at all and as ripe for neuroethics investigations.



I also think that my work calls into question the assumptions of what makes for scientific methods, measures, or questions. For example, I have demonstrated that attending to social construction – typically the sine qua non of an oxymoron if paired with science! – is critical to scientific research with hormones and social behavior. I have argued that our cultural discomfort with vaginal fluid has precluded its use in science, which has limited our ability to address important theoretical and applied questions relevant to sexual health and HIV/AIDS (van Anders 2013). And, I have used qualitative work as a model of understanding phenomena relevant to bioscience. Finally, I’ve written about thinking social for bioscientific work on bisexuality (van Anders 2012). The narrowing of our methods, measures, and questions means that neuroscience has a correspondingly limited ability to answer and ask rich questions. I think that has implications for neuroethics: how do our science-culture blinders, discomforts, and pre-theoretical assumptions lead to research that may skirt the limits of ethical practice precisely because bioscientists are taught to ignore social factors?





References

van Anders SM. Nomenclature and knowledge-culture, or, we don’t call semen ‘penile mucous’. Psychology & Sexuality (2013)



van Anders SM. From one bioscientist to another: guidelines for researching and writing about bisexuality for the lab and biosciences. Journal of Bisexuality (2012), pp. 393-403.





Mallory Bowers is a 5th year Neuroscience doctoral candidate working with Dr. Kerry Ressler at Emory University. Mallory is using a mouse model of exposure-based psychotherapy to better understand the neurobiology of learned fear. Specifically, her research focuses on a putative interaction between the cholecystokinin and endogenous cannabinoid systems that may underlie the extinction of cued fear. Outside of the laboratory, Mallory is very interested in issues at the intersection of gender and neuroscience. Mallory is the current president of Emory Women in Neuroscience (E-WIN).







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Bowers, M. (2014). Doing Feminist Science/Feminists Doing Science: An interview with Dr. Sari van Anders, Founder of Gap Junction Science Part I. The Neuroethics Blog. Retrieved on , from http://www.theneuroethicsblog.com/2014/03/doing-feminist-sciencefeminists-doing_4603.html

Neuroethics Journal Club: Sexual Fantasies and Gender/Sex

In May of 2013, The
New York Times Magazine published an article
discussing the ongoing clinical trials of a unique new drug that caught the
interest of Emory University neuroscience graduate student Mallory Bowers. The drug, dubbed “Lybrido”, was being tested
for its ability to improve sexual desire in women.  However, Lybrido is not just a female
Viagra-like formulation.  That is
apparently one part of it but the other, perhaps more surprising part, is the
pill’s testosterone coating that is designed to melt away immediately in the
mouth. To better understand how testosterone (T) could modulate female desire,
and to discuss the neuroethical implications of pharmaceutically targeting it,
Ms. Bowers chose a recent paper in the Journal of Sex Research by Goldey et al. entitled “Sexual Fantasies and
Gender/Sex: A Multimethod Approach with Quantitative Content Analysis and
Hormonal Responses” for the second Neuroethics Journal Club of the year. 

In the present study, Sari van Anders’s group at the
University of Michigan designed experiments to dissect the gender differences
in testosterone’s role in sexual behavior, which has not been well-understood.  Although men have much higher levels of T, it
is secreted by the adrenal glands in both men and women.  Similarly, men have comparable levels of
circulating estradiol (E₂) to women despite that hormone being
typically associated with the female reproductive cycle.  However, according to van Anders, the
available evidence suggests that while E₂ and T are both associated
with intimacy, E₂ is more related to nurturing behavior whereas T is
more closely linked to explicit sexuality. In this study, van Anders’s group explored
these potential differences by quantifying the nurturing and explicit sexual
content of volunteers’ fantasies accompanied by hormonal measures.




The Steroid/Peptide Theory of Social Bonds (S/P Theory), as
presented by van Anders in a recent review¹,
is explained through an evolutionary perspective: explicit sexual contexts,
which support reproduction, increase T but nurturant contexts, which support
parent-offspring bonds perhaps at the energetic expense of further
reproduction, decrease T (in men). 
However, van Anders argues that social contexts strongly impact T
responses as well: men are socially discouraged from excessive nurturing and
women are socially discouraged from being overly sexual.  It is thought that perhaps due to their lower
baseline levels, women may be more sensitive to small changes in circulating
levels of T², and van Anders
hypothesized that levels of T might be differentially modulated by the content
of sexual fantasies in men and women.




In previous studies, T has been observed to increase most
consistently in the context of sexuality for physical pleasure in men and women,
but nurturing behavior has been associated with lower T in men³.  The same group found that sexual fantasy
increases T in women⁴ but not men⁵ and the authors
reasoned that sexual fantasies likely include thoughts of nurturing behaviors
in addition to those of an explicitly sexual nature which, according to S/P
Theory, would give a mixed signal in terms of T and could explain gender
differences.  These observations and
others have led van Anders to propose S/P Theory to better explain how these
hormones, in conjunction with the neuropeptides oxytocin and vasopressin,
influence social and sexual behaviors in men and women.

The Steroid/Peptide Theory of Social Bonds (van Anders et al.)

The study by Goldey et al. was designed to determine whether
fantasy content differs between genders and if the frequency of nurturing or
sexual content predicts hormonal responses. The authors report a significant
negative correlation specifically in men between change in T and frequency of
nurturant content in fantasies.  Essentially, the men who included less
nurturing images in their fantasies had larger increases in salivary T during
the test.  This was an expected result
and supports van Anders’s S/P Theory. 
However, the group also unexpectedly found no overall difference in the
amount of explicit sexual or nurturing content between male and female
fantasies.  The authors, as well as our
journal club group, thought that this might result from the volunteers being
mostly young undergraduate psychology students who are not necessarily
representative of even Western society at-large.  Moreover, it was suggested that relationship
status and history could strongly impact fantasy content and conceivably the
hormonal response to it.  An analysis of
any relationship between these variables might have been very interesting
though the sample size in this particular study might not have provided enough
statistical power to detect differences.  




So how does an individual’s hormonal profile impact fantasy
content and how do fantasies affect hormonal fluctuations?  There is still quite a lot to learn, but as exemplified by the makers of Lybrido and other potential female
libido-boosters, the impact of this research reaches well beyond academic
journal clubs and the neuroethical considerations are significant.  Another approach that this group could have
taken – which likely would have extended these findings – would be to dose
participants with placebo, T, or E₂ and then quantify sexual fantasy
narratives under each of these three conditions.  It would be very interesting to see if T and
E₂ differentially modulate narrative content in men and women but,
even if that is the case, should this be a pharmaceutical target?  Both Viagra and Lybrido essentially aim for
the same effect but the latter affects brain function as well as blood
flow.  But is lack of sexual desire
really a mood disorder or, is any uneasiness about the prospect of a female
libido-enhancer simply the result of our society being less comfortable with
women wanting to improve their sex lives? 
These questions are clearly beyond the scope of Goldey’s paper but may
be important to discuss for future basic science and clinical research.




An innovative aspect of van Anders’s study was the
integration of individual narratives as well as biological measures.  As the authors point out, biological measures
are often thought to be more valid than qualitative analyses.  In this case the narratives provided a very
useful context to understand the hormonal data and this approach will likely be
useful in future studies.  To some, the
idea of a single pill to modulate a complex mood may be offensively
reductionist but van Anders’s multi-method approach offers the possibility to
better understand the nuances of the reciprocal relationship between hormonal
fluctuations and sexual attitudes.  One
near-certainty is that a drug like Lybrido will reach the market soon and so in
the meantime, and beyond, studies and discussions such as these should
continue.






For more on Dr. van Anders check out this 2012 interview
on The Neuroethics Blog.






References

1. 
   van Anders, S. M., Goldey, K. L. & Kuo, P. X. The Steroid/Peptide Theory of
   Social Bonds: integrating testosterone and peptide responses for classifying
   social behavioral contexts. Psychoneuroendocrinology
   36, 1265-1275,
   doi:10.1016/j.psyneuen.2011.06.001 (2011).




2. 
   Sherwin,
   B. B. A Comparative-Analysis of the Role of Androgen in Human Male and Female
   Sexual Behavior - Behavioral Specificity, Critical Thresholds, and Sensitivity.
   Psychobiology 16, 416-425 (1988).
   




3. 
   S.M. van
   Anders, K. L. G., P.X. Kuo. The steroid/peptide theory of social bonds:
   Integrating testosterone and peptide responses for classifying social
   behavioral contexts. . Psychoneuroendocrinology,
   1265-1275 (2011).
   




4. 
   Goldey,
   K. L. & van Anders, S. M. Sexy thoughts: effects of sexual cognitions on
   testosterone, cortisol, and arousal in women. Hormones and behavior 59,
   754-764, doi:10.1016/j.yhbeh.2010.12.005 (2011).
   




5. 
   Goldey,
   K. L. & van Anders, S. M. Sexual thoughts: links to testosterone and
   cortisol in men. Archives of sexual
   behavior 41, 1461-1470,
   doi:10.1007/s10508-011-9858-6 (2012). 

Want to cite this post?




Ryan, P. (2013). Neuroethics Journal Club: Sexual Fantasies and Gender/Sex. Retrieved on
, from http://www.theneuroethicsblog.com/2013/11/neuroethics-journal-club-sexual.html