Rebecca M. Allen, MD, MPH

Genetic information is slowly working its way into psychiatric practice and our patients’ daily lives.

 Pharmacogenomic panels can be ordered by psychiatrists, and genetic testing is being sold to the general public without any involvement of physicians or genetic counselors. The practicing psychiatrist needs to be informed about both of these types of services.

When pharmacogenomic panels started to hit the market about 5 years ago, most general psychiatrists greeted this option with understandable skepticism. Now the use of these tests is growing, both in numbers of genes tested and in the number of psychiatrists utilizing them.

According to Daniel Dowd, PharmD, Vice President of Medical Affairs at Genomind, one of the two leading commercial pharmacogenomic services, close to 5000 clinicians are currently using Genomind’s panel, and the company has recently logged its 100,000th test. “What we’re actually seeing in practice is most psychiatrists are ordering this for the treatment-resistant patients with 2 or more treatment failures,” says Dr. Dowd. “But in the pediatric patient population, they’re more likely to order it for treatment-naive patients.”

John A. R. Grimaldi Jr, MD, Instructor at Harvard Medical School (HMS) and attending outpatient psychiatrist at Brigham and Women’s Hospital (BWH), says he has had many patients ask about these genetic panels, and 2 patients brought in genetic panels ordered by their previous psychiatrist. “There is a real need for guidance about the use of these ‘assays’,” says Dr. Grimaldi. “I can imagine that ‘genetic assays’ would be useful with treatment-resistant patients, if the assay were paid for by insurance and if there were an evidence base to support interpretation.”

As a new neuropsychiatry fellow, I started to use pharmacogenomic testing for some of my patients last year when I inherited and started to collect a patient caseload filled with very complicated people. Some had tried many different psychiatric medications with little effect, or with significant and sometimes surprising adverse effects.

My supervisor and mentor, Barry Fogel, MD, Professor of Psychiatry at HMS and staff neurologist and psychiatrist at BWH, had asked me if I had considered pharmacogenomic testing. I objected that I did not know anyone who had ever used this testing, and that I did not know how to order it or how much this would cost my patients. Dr. Fogel gently pointed out that these were not insurmountable barriers.

When I looked into the options for pharmacogenomic testing, I found multiple companies offering similar panels, some of which had booths at the American Psychiatric Association meeting in May 2017. The biggest and most well-established providers of pharmacogenomic testing are GeneSight and Genomind.

GeneSight currently offers 4 panels: psychotropic, analgesic, ADHD, and methylene tetrahydrofolate reductase (MTHFR). The GeneSight website states that its “Psychotropic laboratory developed test analyzes how patients’ genes may affect his/her metabolism and response to FDA-approved medicines . . . .”

The psychotropic panel looks at genes for liver enzymes that are responsible for the metabolism of most neuropsychiatric medications. It tests for various gene alleles and classifies the possible phenotypes as ultra-rapid, extensive, intermediate, or poor metabolizers. The panel also tests for a few genes not related to hepatic metabolism of psychotropic drugs, which are receptor polymorphisms with potential pharmacodynamic implications.

Genomind has one panel, the “Genecept Assay.” The assay includes genes encoding the serotonin transporter, calcium channel, sodium channel, serotonin receptor 2C, melanocortin 4 receptor, dopamine 2 receptor, catechol-O-methyltransferase, alpha-2A adrenergic receptor, MTHFR, brain-derived neurotrophic factor, Î¼-opioid receptor, and glutamate receptor, as well as a number of the hepatic cytochromes. According to Dr. Dowd, Genomind has received the most positive feedback from clinicians regarding the serotonin transporter gene (

) and the 2 weight-gain–related genes on the panel (

). Dr. Dowd asserts that certain serotonin transporter gene alleles identify people with lower response and remission rates and more adverse effects when treated for depression with SSRIs and that certain alleles of 

 imply a significantly higher risk of weight gain if the patient is treated with an atypical antipsychotic drug.

Shaun Purcell, PhD, Associate Professor of Psychiatry at HMS and a genetic epidemiologist who was involved in some of the studies to identify genes as risk factors for mental disorders, believes psychiatrists have ample cause to be cautious about using genetic testing. “To me, the evidence is underwhelming to say the least. It’s definitely concerning that these kinds of tests are being pushed prematurely.”

For the non-metabolic genes on the panel, Dr. Purcell says, “I’d question the basic assumptions and science behind the panel. As far as I’m aware, these genes are coming from studies of disease risk.” He adds, “It’s a different thing to have an association in the literature and to have it be clinically meaningful.”

Dr. Purcell continues: “The associations of major psychiatric illness with common variants in 

 are unambiguously sound. They say nothing about what implications these variants have, if any, for guiding treatment.” He adds, “There is a fundamental disconnect between what is being claimed and the extant evidence base for 

.” He also questions the premise that any of the other non-metabolic genes tested on the GeneSight and Genomind panels have clinical utility. “There’s no evidence that these variants are going to be clinically actionable in terms of guiding treatment.”

Dr. Fogel, who is generally in favor of clinicians considering pharmacogenomic testing for difficult-to-treat patients, agrees with Dr. Purcell that the clinical relevance of some of the genes on the panels is questionable. He says, “Will getting a gene associated with BDNF actually make more of a difference than getting a BDNF level? I don’t think so.” Regarding Genomind’s listed “treatment impacts” for the 

 genes, Dr. Fogel says, “A methylfolate supplement and exercise would usually be good for a patient no matter what their genotype.”

Of course, the evidence is different for each gene on the panels. For example, take the serotonin transporter gene, 

, which is heavily studied. The short form of the serotonin transporter-linked polymorphic region is associated with reduced activity of the serotonin transporter (low expression) and with higher levels of intrasynaptic serotonin. The long form (high expression) is associated with increased activity of the serotonin transporter and lower levels of intrasynaptic serotonin.

This variation has been associated with affective disorders and with pathological behaviors and personality traits related to anxiety, impulsivity, and stress.

 For example, those with a low-expression form of the 

 serotonin transporter gene have a bias to pay attention to both negative and positive affective pictures.

 This suggests that the serotonin transporter gene might be a plasticity gene rather than a vulnerability gene-the low-expressing form allowing people to tune in to the affective significance of their surroundings.

More relevant to pharmacogenetic testing is the question of whether variations in the serotonin transporter gene can guide prescribing. The literature on this is fairly robust, with 33 studies included in the most recent meta-analysis in 2012. Of 3 meta-analyses published between 2007 and 2012, 2 found that the long/long (

) genotype in Caucasians was associated with response to antidepressants, mostly SSRIs, and all 3 found that carrying the l allele was associated with remission.

 genotype predicts antidepressant response in Asians is less clear.

A 2016 pilot study of 35 patients showed that the 

 allele was associated with better response to desvenlafaxine.

 The genetic connection to treatment response may not only differ by ethnicity, but by age. A 2015 study of 234 patients with late-life depression showed that at least one 

 allele was associated with about a 2-fold probability of having a good SSRI response.

 Although the serotonin transporter gene has literature supporting its clinical relevance, there does not seem to be a clear, simple connection between genotype and treatment response.

But what about the CYP liver enzyme gene variations? The relationship of these liver enzymes to drug metabolism is not in question. “We cannot say who is going to respond to what,” Dr. Fogel says. “But the drug metabolism is pretty well established, and there are genotypes that imply someone is going to be a slower or faster metabolizer of certain drugs. That may be relevant in clinical situations where getting to a therapeutic drug level or avoiding a drug interaction or an unintentional overdose is really going to be a problem for the patient.” He adds, “You have some very specific situations where you can say it really makes sense to have advance intelligence on what sort of metabolizer this person with this drug will be.”

For my patients, getting information about drug metabolism from the genetic panels helped me build a therapeutic alliance and/or choose which drug to try next when the first drug I prescribed was not effective. One patient’s results showed slow metabolism for every psychotropic she had ever tried. She found this validating, as she had experienced an unusual amount of adverse effects, and we were able to pick a new option from the short list of medications she metabolizes well. Another patient felt reassured when his panel indicated that his metabolism was normal for almost everything. Thereafter, he expressed fewer concerns about trying new medications. A third patient felt validated that her testing supported her intolerance of and lack of response to SSRIs, and she was more willing to try other classes of antidepressants.

John F. Sullivan, MD, Instructor at HMS and neuropsychiatrist at BWH, has ordered GeneSight panels for 3 of his patients who “would have dramatic adverse reactions to tiny doses of anything, regardless of the medication’s mechanism. One of these patients had panic attacks to his multivitamin.” Dr. Sullivan found the results of the genetic testing useful to demonstrate that the severe adverse reactions his patients had to a multitude of medications were not related to a biologic process.

Laura Safar, MD, also an Instructor at HMS and neuropsychiatrist at BWH, has ordered panels for several patients and found that the information helped her understand patients’ response to medication adverse effects. The panels either validated patient concerns or, in one of her cases, supported her impression that the patient’s high levels of adverse effects to very low doses of medications were due to anxiety

Do genetic panels change patient outcomes? The largest GeneSight study was conducted in 2013, when the company had only a 5-gene pharmacogenomics test. This open-label study compared 114 patients whose clinicians had access to the GeneSight report (“guided”) with 113 patients whose clinician could not see the report (“unguided”). After 8 weeks, the guided group had a 70% greater improvement in depression scores, as well as better remission rates. Participants in the unguided group who at baseline were prescribed a medication that was “most discordant with their genotype” experienced the least improvement.

Genomind did an unblinded study of its 10-gene panel in 2013, with 685 patients and a variety of diagnoses. The study showed that 91% of patients with 2 or more prior treatment failures had clinically measurable improvement, but the study was limited by having no treatment-as-usual comparison group.

It is fair to say that there is not a large body of evidence to prove that ordering genetic panels affects treatment decisions or the course of disease.

Jane Erb, MD, Assistant Professor at HMS and Clinical Director of the Brigham Depression Center, has not incorporated genetic testing into her practice because “as of a couple of years ago, the data were not convincing that the information improved outcomes.” She says, “I have seen a handful or two of patients who have had testing run by others, and I’ve reviewed the results, which did not seem to explain the patients’ medication responses.”

Gaston Baslet, MD, Assistant Professor at HMS and attending neuropsychiatrist at BWH, says genetic testing “needs to be put in context with many other clinical factors that are usually going to be the ones directing my decision, such as factors obtained from a detailed med history.” He adds, “I therefore don’t think that the amount of time and effort in getting these results would be contributing enough to my decision-making to justify their regular use. Of course, there are exceptions to every rule.”

Putting the genetic information into clinical context is very important. A study published in January 2017 showed that less-experienced psychiatrists tended to be more influenced by genetic information than older psychiatrists.

 The study presented 67 psychiatrists with patients’ pre- or post-treatment scores on the Positive and Negative Syndrome Scale for 2 hypothetical treatments for schizophrenia. Psychiatrists were also informed whether the patient possessed a genotype linked to hyper-responsiveness to one of the treatments, and they were asked to recommend one of these two treatments. Less-experienced psychiatrists were inclined to believe the genetic information more than the clinical report of how patients responded to different drugs in the past, and to recommend treatment based on the genotype. McMichael and colleagues concluded that “psychiatrists and other clinicians should be cautious about allowing a patient’s genetic information to carry unnecessary weight in their clinical decision-making.”

Barriers to adoption of pharmacogenomics include changes in workflow and the time and effort involved in signing up at the company’s website, ordering test kits, obtaining cheek swabs, and sending in the samples. However, for both GeneSight and Genomind panels, collecting the samples was easy-a quick cheek swab in the office-and results were back within 2 weeks. Cost is also a major concern. Both companies do their best to get insurance companies to pay and promise that the most a patient will ever be charged (even with no insurance coverage) is in the low $300s.

In the future, we should expect expansion of the use of pharmacogenomic testing. The industry is growing rapidly, and in the next year or two the panels are expected to have more variants. There may be information on the genetic panels that can help determine how likely a patient is to respond to ECT or transcranial magnetic stimulation, but so far these are relatively small studies and need to be replicated.

With GeneSight and Genomind, the business model is for physicians to order the panels. But, there are services that offer direct-to-consumer genetic testing, such as 23andMe.

Last year, 23andMe was like fast food: fairly quick, kind of fun, and with little substance. It provided carrier status for 39 genetic diseases and not much else in the way of health information.

Before 2013, 23andMe used to provide a lot of clinical data, from carrier status for hereditary cancers to information about drug metabolism. Dr. Purcell comments that the original 23andMe genetic testing “included some patently bogus reports for psychiatric diseases including schizophrenia.”

In 2013, the FDA cracked down on the company for not getting proper approval to market what the FDA considered to be a medical device. 23andMe responded by significantly slimming down their panel. Now, they are building it back up. This year, 23andMe has a few new “Genetic Health Risk Reports”: the 

 genes for hereditary thrombophilia, and the 

 gene for alpha-1 antitrypsin deficiency. As a physician who treats dementia, I was surprised and dismayed to see that the 

 Alzheimer risk gene has returned to 23andMe after being removed in 2013. In general, though, health information is limited.

To get an idea of what these genetic tests provide, I decided to try 23andMe. What did I learn? I have fewer Neanderthal variants than 88% of customers. I am genetically more likely to have a “photic sneeze,” or sneeze in the sunlight (and I do). I am less likely to be a deep sleeper and am more likely to move in my sleep.

I was not surprised to find out that I am 63.2% British and Irish; a slow coffee metabolizer; unlikely to have a cleft chin, unibrow, dimples, or a widow’s peak (indeed, I don’t); and that my earlobes are likely to be detached (they are). I was very surprised to learn that I am more likely than others to be able to smell the asparagus metabolite in urine, though I can say with complete honesty that my curiosity about myself had never once strayed toward that question.

There is a way around the limitations of 23andMe: download your raw data, then upload it to another program to tease out the health information. The program I used is Promethease, which costs $5 to $10 depending on the source of the DNA. Promethease describes itself as “a literature retrieval system that builds a personal DNA report based on connecting a file of DNA genotypes to the scientific findings cited in SNPedia.”

The Promethease report is a far cry from the simplistic, jargon-free, and sparsely populated pages of the 23andMe website. For each gene variant, Promethease provides information about the frequency of that genotype in your population (eg, Caucasian), the location of the gene, and the number of papers published.

As with 23andMe, the information in Promethease was often amusing. For example, I have an allele that was associated with good memory in a Swiss cohort. I unfortunately do not have a gene associated with longevity in Japanese men. Some of the “genos” were helpful or enlightening: my single copy of the C677T allele of 

 puts me at some risk of having low vitamin B

 and folic acid. Of course, some were anxiety-provoking, like risk factors for cardiovascular disease, diabetes, and various inflammatory and neurological diseases.

Although I am of the general persuasion that knowledge is power, I find it reassuring that, even as a doctor with some (albeit limited) knowledge of genetics, it was not a simple process for me to find my own genetic risk factors. While some patients could certainly wade through their own Promethease data and glean appropriate or useful information, most people will likely not go beyond the information available on the 23andMe website.

Dr. Allen is a Clinical Fellow in Neuropsychiatry, Brigham and Women’s Hospital, Boston, MA. 

Dr. Allen reports no conflicts of interest concerning the subject matter of this article.

 Serretti A, Calati R, Mandelli L, et al. Serotonin transporter gene variants and behavior: a comprehensive review. 

 Fox E, Zougkou K, Ridgewell A, Garner K. The serotonin transporter gene alters sensitivity to attention bias modification: evidence for a plasticity gene. 

 Porcelli S, Fabbri C, Serretti A. Meta-analysis of serotonin transporter gene promoter polymorphism (5-HTTLPR) association with antidepressant efficacy. 

 Ng CH, Bousman C, Smith DJ, et al. A prospective study of serotonin and norepinephrine transporter genes and the response to desvenlafaxine over 8 weeks in major depressive disorder. 

 Seripa D, Pilotto A, Paroni G, et al. Role of the serotonin transporter gene locus in the response to SSRI treatment of major depressive disorder in late life. 

 Hall-Flavin DK, Winner JG, Allen JD, et al. Utility of integrated pharmacogenomic testing to support the treatment of major depressive disorder in a psychiatric outpatient setting. 

 Brennan FX, Gardner KR, Lombard J, et al. A naturalistic study of the effectiveness of pharmacogenetic testing to guide treatment in psychiatric patients with mood and anxiety disorders. 

 McMichael AJ, Boeri M, Rolison JJ, et al. The influence of genotype information on psychiatrists’ treatment recommendations: more experienced clinicians know better what to ignore. 

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Have you considered using pharmacogenomic testing in your practice?

Weighing the Benefits of Genetic Information in Clinical Psychiatry

We have long known-based on research from social psychology, political science, and business-that men and women are perceived and treated unequally in our work environments. The difference this year is that we are talking about it much more than usual. Nothing brings gender quite to the forefront of one’s thoughts like the intersection of-in my case-being pregnant most of last year, applying for a job, and following the news coverage of the election. In the wake of our first-ever major party female candidate for US President, there has been a remarkable amount of news coverage on sexism.

Dr. Allen is a graduate of the Harvard Longwood Psychiatry Residency Training Program.  She is currently in her second year of the Harvard Medical School affiliated Fellowship in Behavioral Neurology/Neuropsychiatry at Brigham and Women’s Hospital in Boston, Massachusetts. She reports no conflicts of interest concerning the subject matter of this article.

The 2016 election highlighted the difference in standards for male and female leaders. During the election, many journalists discussed how voters viewed Hillary Clinton and how her opponents treated her. Her opponents carefully questioned her health, “stamina,” presidential “look,” and 

 She was scrutinized for every aspect of her appearance, especially her clothes, bringing to mind the 

 of sexism by a male television reporter in Australia who wore the same suit every day for a year-and nobody noticed.

 Hillary Clinton was perceived by some as cold or aloof. As 

, “I had to learn as a young woman to control my emotions. And that’s a hard path to walk. Because you need to protect yourself, you need to keep steady, but at the same time you don’t want to seem ‘walled off.’”

 Post-election coverage has largely focused on how the current President treats women-given the lack of female cabinet members, this comes as no surprise.

Gender inequality at work is well supported by data. Women tend to be interrupted much more often than men

 and, despite the perception that women talk excessively, men actually do about 

 A Yale series of studies on “volubility” (total amount of time spent talking) cheerily concludes that “though men primed with power talk more, women show no effect of power on volubility” and “powerful women are in fact correct in assuming that they will incur backlash as a result of talking more than others-an effect that is observed among both male and female perceivers.”

 In other words, women who speak up suffer consequences.

Women also get judged more harshly for ethical violations. A recent study that analyzed American Bar Association data found that female attorneys were more than twice as likely to be disbarred as males, despite having identical ethical infractions.

, volunteers were asked to recommend a jail sentence for a hospital administrator who unethically filed a false Medicare claim. If the administrator was named Jack, the jail sentence was 80 days, but if the name was Jane, the sentence was 130 days.

In academic science, perceptions of scientific achievement and potential are also affected by gender. A 2012 study asked a broad, nationwide sample of biology, chemistry, and physics professors to evaluate the identical application materials of either a male or a female undergraduate science student who had ostensibly applied for a science laboratory manager position. Both male and female faculty judged a female student to be less competent and less worthy of being hired than an identical male student-and also offered her a smaller starting salary and less career mentoring.

Compared with men, women in academic medicine perceive lower gender equity, are less likely to believe their institutions are making changes to address diversity goals, are less likely to consider their workplace family-friendly, and report less congruence between their own values and those of their institutions.

 The 2013-2014 American Association of Medical Colleges’ report on the state of women in academic medicine found that while 46% of all residents are female, this number drops rapidly up the academic hierarchy: only 38% of faculty, 21% of full professors, and 16% of deans are female. The report concluded that “the proportion of full-time full professors who are women has increased since 2003–04, but the percentage of new tenures who are women remains unchanged since 2008–09. Although the percentages have slowly increased over the past 10 years, women continue to hold a 

 of key leadership positions (department chair, dean) than do men.”

In psychiatry, as in every field of medicine, there is gender disparity in salary and promotion. A 2016 study that looked at academic physician salaries showed that even after accounting for physician age, experience, faculty rank, specialty, scientific authorship, National Institutes of Health funding, clinical trial participation, and Medicare reimbursements, female physicians still earn less than males in every field with the exception of radiology.

 In psychiatry, after adjusting for all of these factors, men earn an average of $211,709, while women earn $14,799 less per year, or $196,909.

Although the numbers of women and men who enter psychiatry have been equal since 1999, a recent demographic study showed only 12 of 118 psychiatry departments have female chairs.

 Male chairs are much more likely to be in charge of large departments and are more likely to be married. Women psychiatry chairs report barriers to career development such as little or no mentorship, gender discrimination, and family obligations.

In reflecting on these data, a woman who receives a job offer may wonder if the proposed salary is lower than would be offered to a man-but there is no way to know for sure. She then may have a difficult time negotiating her salary without being seen in a negative light. A 2013 series of studies on salary negotiation and backlash concluded:

Assertive, self-advocating female negotiators suffer backlash consistent with negative masculine characterizations. They are seen as dominant and arrogant, and people do not want to interact on a peer level with them. Non-assertive, other-advocating female negotiators suffer a different backlash consistent with negative feminine characterizations. They are seen as weak and gullible, and people do not want to be led by them.

As a female physician, I fortunately have difficulty thinking of examples of overt sexism. I do not have war stories like those told by Dr. Frances K. Conley, the first female tenured professor of neurosurgery in the US, in her book 

But one incident does come to mind. When I was a 4th-year medical student, the neurosurgery residency program had just been shaken up by matching not 1, but 2 female neurosurgery interns, filling both available slots after several years of no women matching. I did not hear physicians say anything negative about this change, but staff in the operating rooms, both male and female, were shockingly non-subtle in declaring their fear of facing 6 years of working with female doctors. “Neurosurgery is not a good field for women,” one surgical technician declared, while another told me that women in neurosurgery are unhappy and mean. They anticipated future conflict and possibly verbal abuse. The basis for this concern? They saw the single woman who had completed the program as exemplifying all women in neurosurgery.

Anecdotally and experientially as a medical student rotating on different services, I found that overt sexism varies among the specialties in medicine. A 

 on sexism in medicine by an Emory medicine resident cited examples of 

–style misogyny from a surgical service.

But subtle gender differences are still noticeable in psychiatry, despite the 

 of women in our field than in most other specialties.

 The leadership in my department is largely male. Most meetings I attend are dominated by male voices, even if the absolute number of women and men in the room is fairly balanced. Women speak less, and their comments are noticeably shorter, prefaced by more uncertainty, and more often interrupted than male contributions. Other examples of subtle sexism include patients and staff mistaking me for a nurse or non-physician, patients defaulting to calling me by my first name, and both male and female nurses treating me somewhat differently than male residents when on call.

Women physicians and childcare responsibilities

In a medical world where we are exposed to subtle gender discrimination that, although measurable, is hard to see on a day-to-day basis, maybe it is not so surprising that younger women physicians are rather complacent. My female medical school classmates and co-residents were hesitant to describe themselves as “feminist” and rarely complained about sexism. Many of my female classmates in medical school and residency followed the cultural norm of marrying men a few years older and potentially higher earning or farther along in their careers (and most women also changed their names). This tends to perpetuate a system in which women take on more of the childcare responsibility than men by choosing less demanding specialties or working fewer hours.

The choice to prioritize childcare is one that every person, male or female, should be able to make. However, our current culture leads to women doing this much more often than men. Indeed, although many male and female medical school faculty members in the US work part-time, men more often work part-time to accommodate their work at another practice site or in another professional position, while women work part-time to provide care for dependent children.

Because women are more likely than men to make career changes after having children, patients and colleagues may, consciously or not, perceive a pregnant physician differently. There is no equivalent experience for male physicians. Pregnancy puts one’s private family life on display, and dodging patient questions about family can be just as awkward as answering them. Many patients asked me not when, but if I planned to return to work after having a baby-a question they likely would not ask men who go on paternity leave.

As a third-year resident pregnant with my first child, I was very concerned about how my colleagues and superiors would view me and how much my mentors would want to invest in my career. I had no intention of altering my career goals after having a baby, but I felt (correctly or not) that I had to work hard after returning from leave to show that I was the same committed physician as before I became a mother. Now, having my second child at the same time as applying for a job, I have similar concerns. I had to disclose that I was pregnant to avoid scheduling the interviews during a time when I could not travel, and I also feared that if I were visibly pregnant during a job interview, it would be an unwelcome distraction.

Substantial progress-but still a long way to go

While it is important to recognize how gender greatly affects our lives in the personal, professional, and political spheres, and to work to eliminate subtle sexism in our culture, it is also important not to become demoralized in the process. Despite recent events-both personal and political-I recognize the substantial progress women have made and hope we keep up the momentum. In our field, we have strong women role models, including many recent American Psychiatric Association presidents, and I have had the pleasure of working with female psychiatrists who have successfully pursued ambitious work goals while also raising children.

But we still have a long way to go: expectations for women leaders are both high and narrow, while male leaders do well with a variety of personality types and styles. A rise in the number of strong women in power would help foster broader and more positive public perceptions. For our cultural expectation of women to change, we have to start by putting women in leadership positions.

 This piece was adapted from Dr. Allen’s article “Enjoy Being a Girl?” which appeared in the November/December 2016 issue of the 

This article was originally posted on 3/9/2017 and has since been updated.

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In psychiatry, as in every field of medicine, there is still gender disparity in salary and promotion. 

Author | Rebecca M. Allen, MD, MPH

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