Gender and scientific success

I didn't want to write this post.  I really don't want to touch this with a ten foot pole. What follows is messy and complicated and guaranteed to make everyone mad at least some of the time. (Ask Larry Summers).

We need a sane approach to how we deal with gender in the sciences.

Women are making measurable representation gains in the sciences. This is an undisputed good. Everyone benefits when the right people are doing the right job. However, despite the fact that the majority of bachelor's degrees are now being awarded to women, women only make up about 20% of professorships in math and the sciences. Why?

The three basic alternative answers: 1.) women tend not to choose careers in math or science (either willingly or due to life/family circumstances); 2.) women are barred from achievement in math and science through acts of willful discrimination; or 3.) women do not have the same aptitude for achievement in math and sciences as men.

This is a difficult issue to study as people's careers cannot be manipulated experimentally, and we are left to mostly correlational evidence. An exception are CV studies where identical CVs are given to judges with either a woman or man's name on the top. Judges are asked to determine the competence of the candidates. These studies typically find that the "male candidates" are judged to be more competent than the "female candidates". As no objective differences exist between them, this is a measure of sex discrimination.

Reviewing the correlational evidence for gender discrimination in the sciences, Ceci and Williams find that when examining researchers with equal access to resources (lab space, teaching loads, etc), that no productivity difference is found between male and female scientists. Female scientists are, on average, less likely to have as many resources as male scientists as they are more likely to take positions with heavier teaching loads. How to reconcile the CV studies showing discrimination and the correlational evidence suggesting none? In an excellent analysis of the Ceci and Williams paper, Alison Gopnik asserts a possible hypothesis: "Women, knowing that they are subject to discrimination, may work twice as hard to produce high-quality grants and papers, so that the high quality offsets the influence of discrimination".

It's possible. But Gopnik also admits that it is also possible that policy changes could be responsible. In other words, that affirmative action-style policies that give women advantages could counteract the subconscious gender discrimination seen in the CV studies.

There's a darker side to these policies, though. Some worry about the discounting of a female professor's abilities, assuming she rose to the position via policy rather than talent. Furthermore, some policies designed to given women more voice actually end up give them more work - if a certain number of women need to be on a committee, then female professors are doing more service work than their male counterparts.

And then there's the matter of why female faculty find themselves in low-resource situations to begin with. Stated eloquently by Gopnik, "the conflict between female fertility and the typical tenure process is one important factor in women's access to resources. You could say that universities don't discriminate against women, they just discriminate against people whose fertility declines rapidly after 35."


And well-meaning policies also interact with the fertility issue in insidious ways. For example, many universities offer to "pause" the tenure clock for a year for a faculty member who gives birth before tenure. Sounds great, right?  It could be, except that there is a tremendous amount of pressure to not take this credit for fear of seeming weak. This is especially true in departments that have faculty members who have already chosen not to take the time.

So... we have unconscious discrimination, conscious policies to counter said unconscious discrimination, conscious and unconscious backlash against the policies, and a structural problem for female fertility. In other words, it's a complicated picture and I don't know what the answer is. I do, however agree with Shankar Vedantam's assessment: "It is true that fewer women than men break into science and engineering careers today because they do not choose such careers. What isn't true is that those choices are truly "free.""

Getting Savage on evolutionary psychology

Now, I love sex advice columnist Dan Savage. I have been a faithful purveyor of his columns, podcasts and blogs for some time now. And sure, I don’t agree with him on every bit of advice, but he bats a solid .900 and articulately calls out many forms of B.S. But right now, I have a beef with Mr. Savage over his love affair with the new evolutionary psychology-inspired book Sex at Dawn by Christopher Ryan and Cacilda Jethá. This is an example of the all-too-common use of science-y thinking as justification for a particular belief, in this case, the use of evolutionary psychology to endorse the “naturalness” of polyamory.

My contentions are the following: 1. while I am all for the promotion of reading and scientific literacy, we need to be especially vigilant against accepting poor science that confirms what we already believe; 2. that we need to critically examine whether science can inform social policy discussions; and 3. we need to divorce the notion that the “naturalness” of an act means that the act is desirable.

Problems with evolutionary psychology

I need to point out in the spirit of full-disclosure that I have not read Sex at Dawn. However, from Mr. Savage’s multiple interviews with Dr. Ryan, it is evident that the apple of this book does not fall far from the tree of Buss and Baker.

Evolutionary psychology offers only post-hoc fits of theory to data

            In evolutionary psychology, one asks how human evolutionary history can explain aspects of current human behavior. Functionally, it amounts to doing thought experiments on questions such as “how did a cave man’s life influence the shape of the human penis”? The problem with this kind of problem statement is that you are looking at some data (in this case the shape of human penises) and looking for a model that fits this data. You can come up with many such models, because you are fitting the data after the fact, but you have no guarantee that your model is correct.

Let’s take a case in point of an issue brought up in the latest interview with Dr. Ryan on the Savage Lovecast. The question: why are human penises larger than gorilla penises when gorillas are larger than men? The given answer: because they were designed as plungers to remove the semen of rival males from the reproductive tract of a female. The larger theory behind this answer lies in the idea of sperm competition, the notion that females practice selective non-monogamy as a means of maximizing genetic quality in the offspring. The male, worried that he might be cuckolded into investing resources into offspring not genetically related to him needs adaptations to keep his partner from being impregnated by rivals. Therefore, it is to his advantage to have a “plunger penis” that will reduce the probability of pregnancy from a rival.

           

It’s kind of like an intellectual Rube-Goldberg machine, isn’t it? Or perhaps more fittingly, like one of Kipling’s “just-so stories”.

The “scientific data” for this claim come from this paper, which might be the most hilarious scientific study I’ve ever read (and this includes the smoking pot in the fMRI scanner study). From the abstract:

Inanimate models were used to assess the possibility that certain features of the human penis evolved to displace semen left by other males in the female reproductive tract. Displacement of artificial semen in simulated vaginas varied as a function of glans/coronal ridge morphology, semen viscosity, and depth of thrusting. Results obtained by modifying an artificial penis suggest that the coronal ridge is an important morphological feature mediating semen displacement.

 

Yes, kids… this is research with dildos and masturbation sleeves. Other great sound bites from the article include the “recipe” for artificial semen: 

Simulated semen was created by mixing 7 ml of water at room temperature with 7.16 g of cornstarch and stirring for 5 min. After trying different mixtures of cornstarch and water, this recipe was judged by three sexually experienced males to best approximate the viscosity and texture of human seminal fluid.

And in addressing limitations of the current paradigm:

A limitation of our attempts to model semen displacement was the greater rigidity of the prosthetic as compared to real genitals. The artificial vaginas did not expand as readily as real vaginal tissue nor did the phalluses compress, and, as a result, semen displacement was assessed on the basis of a single insertion. The effects, however, were robust and generalized across different artificial phalluses, different artificial vaginas, different types of simulated semen, and different semen viscosities.

…Sigh…. My own research seems so vanilla in comparison! But in all seriousness, extraordinary claims require extraordinary evidence, and this is not that evidence.

 

Evolutionary psychology does not make uniquely falsifiable claims

The hallmark of actual science is that it makes predictions that can be falsified and separated from other possible explanations. Evolutionary psychology does not do this. For example, the fact that men who have spent more time away from their partners find their partners more attractive and desirable, and ejaculate semen with higher sperm counts during copulation are taken as evidence for the sperm competition hypothesis. The argument is that as the man has not observed his partner, he is threatened by sperm competition, so it is to his advantage to copulate often and with… uh, greater virility. Although these studies control for time since last copulation, it doesn’t take much creativity to come up with alternative explanations.

Another example: the sperm competition hypothesis would predict that men would be more concerned with sexual infidelities of a partner (as this could result in cuckoldry) and women would be more concerned with emotional infidelities (as this could result in him leaving her without resources, or diverting resources into another partner). To test this prediction, David Buss conducted many surveys with many different groups asking them whether they would theoretically be more upset by a sexual or emotional infidelity. As nicely shown in David Buller’s critique of evolutionary psychology, although more men than women say that sexual infidelity is more upsetting, half of the men are still choosing emotional infidelity as more upsetting, so this model is far from complete.

Evolutionary psychology assumes that we know what psychological pressures existed for our ancestors in the Pleistocene.

We don’t. 

A closely related problem is that evolutionary psychology assumes that the mind evolved to the problems of the Pleistocene and then remained static for over 12,000 years. This seems implausible as large species-wide shifts have been observed in as little as 18 generations (less than 500 years for human generations).

However, many people who hate evolutionary psychology do so for irrational reasons

Evolutionary psychology is fine for intellectual masturbation, but we should strongly question its place as an actual science. However, many of its loudest critiques are based on emotional and political responses, rather than on the quality of the academic content.

Consider Megan McArdle’s critique of Sex at Dawn for The Atlantic. She writes:

“For example, like a lot of evolutionary biology critiques, this one leans heavily on bonobos (at least so far).  Here's the thing:  humans aren't like bonobos. And do you know how I know that we are not like bonobos?  Because we're not like bonobos.”

(Emphasis in original). 

Although I am sure Ms. McArdle is more articulate in other matters, it is true that when our beliefs are challenged, we are quick to say that scientific inquiry into the matter in question is useless.

Evolutionary psychology stirs up a political hornet’s nest. If we believe that our minds evolved to solve problems of the Pleistocene and have remained largely unchanged, this suggests that our minds have little capacity to change. Therefore, we can do little about real social problems such as war, racism and rape.

As Steven Pinker points out, ignoble tendencies do not have to lead to ignoble behavior. In other words, what “is” is not the same as what “ought”. The confusion between these two concepts comes from a fallacy confounding what is natural with what is good. Which leads me to my last problem with Dan Savage’s promotion of this book…..

Things that are natural are not necessarily desirable

Let’s step back and assume for a moment that the science of evolutionary psychology was solid, and that Ryan’s hypothesis about the polyamorous nature of humans was true. There would still be a major problem with Dan Savage’s use of this book to endorse polyamorous relationships: just because some behavior is fundamental to the nature of human beings does not mean that it’s a desirable state for current human beings.

Let me be clear on this point - I am not saying that humans shouldn’t be polyamorous. I believe consenting adults should do whatever they like. However, I am saying that the “naturalness” of polyamory does not inform its desirability.

Savage and Ryan are implicitly stating that since polyamory occurs throughout animal species and in human evolutionary history, it is natural. OK, but so are war, conquest, exploitation and rape and we do not condone these.

Dan, you are a smart guy…. Don’t get sucked in to poor science just because it tells a compelling story that you want to believe!

So, what makes you happy?

Research on the factors increasing or decreasing happiness has been of interest to psychologists and economists alike. Early research indicated that, contrary to our intuition, that major life events such as winning the lottery did not change our long-term ratings of our happiness. In other words, after a major life change, you will experience a temporary change in your happiness, but will return to being as happy as before the event. Such findings led to the set-point hypothesis that stated that each of us has an innate level of happiness, and that outside events, even large ones, don’t have a major influence on that set point.

 

Evidence for the set point hypothesis typically comes from longitudinal studies in which the same people rate their happiness each year, and report any major life events that occurred between surveys. From these data, you can correlate happiness as a function of the event by time-locking a sample population’s happiness the year an event occurs, and then seeing how it changes later. Let’s take marriage for example. Although each person in the sample gets married at a different time, the researcher can define year 0 to be the year of marriage for each person. Then, the researcher can look at this person’s happiness ratings both before and after marriage to determine the impact of marriage on happiness rankings. Below is the kind of graph that you get: planning and getting married makes people happy, and this happiness lasts for a couple of years, but after this, people go back to being however happy they were before.

 

Interestingly, although people hedonically adapt to marriage, they do not hedonically adapt to divorce. In other words, although marriage will not cause a permanent change in your happiness, getting a divorce will make you sadder in the long-term. Even more interesting is looking at the initial happiness ratings of people who marry and eventually divorce, and compare them to people who marry and stay married. It turns out that people who stay married were happier than their to-be-married-then-divorced friends even five years before marriage! This can be even before these people met their spouse.

Given that people do not strictly have one happiness set-point, what factors account for long-term changes in happiness? A new study in PNAS examines this question using 25 year longitudinal data from Germany. What I particularly enjoy about this study is that they focused on factors that people can control: although becoming disabled in an accident will likely lead to a long-term change in happiness, it is not something you can readily control. However, you do have control over things like your choice of romantic partner, your degree of religious involvement, your life priorities, whether you exercise, etc. Here is what they found:

-         Focusing on money can’t buy you happiness. People who rated the acquisition of material goods as very important were less happy than people focused on family or volunteerism. Women whose partners were materially focused were particularly sad.

-         You are less happy when you work more or (in particular) less than you would prefer to work.

-         Being with friends and exercising regularly can make you happy.

-         If you are a man, don’t be underweight. If you are a woman, don’t be obese.

-         Choose a partner who is not neurotic.

-         Although the study found a positive effect of religious participation, this is also correlated with altruism, family focus, and social participation, all of which independently increase happiness.

Although each of these factors had a small effect on happiness, all of them seem like good, common sense. I’ll go out for a run now.

Headey B, Muffels R, & Wagner GG (2010). Long-running German panel survey shows that personal and economic choices, not just genes, matter for happiness. Proceedings of the National Academy of Sciences of the United States of America, 107 (42), 17922-6 PMID: 20921399

Did my brain make me do it?

Our first case is from a 40-year old man who developed a new and intense interest in child pornography.  His sexuality also generally increased, and he found himself frequenting prostitutes even though he never had before.  He was ashamed of his behavior and went to lengths to hide it, and could communicate that it was morally wrong.  However, he then began making sexual advances on his pre-pubescent step-daughter and spoke of raping his landlady.  He was removed from his home, but failed a 12 step sexual addiction program as he could not restrain himself from soliciting sexual favors from the staff and fellow group members.  As he failed the program, he was sentenced to prison, but developed debilitating headaches and balance problems shortly before admission.  An MRI revealed a large tumor in his orbitofrontal lobe, an area associated with self control, executive function and the regulation of social behavior.  Following surgical removal of the tumor, the man was able to successfully complete the sexual addition course, successfully moved back in with his family and no longer had pedophilic or other deviant urges.

Consider, then our second case: the 1992 trial of Herbert Weinstein, a 65-year-old advertising executive who was charged with strangling his wife to death and then, in an effort to make the murder look like a suicide, throwing her body out the window of their Manhattan apartment.  At his neuropsychiatric evaluation, it was found that Mr. Weinstein had a small, subarachnoid cyst in his brain. The defense moved to use this cyst as evidence of Mr. Weinstein’s inability to control, or be responsible for, his behavior. The cyst in Weinstein’s brain has never been linked to mental illness or violent behavior. After a contentious pre-trial hearing about using this evidence, Mr. Weinstein accepted a plea bargain.

Are both of these men equally responsible for their own behavior?

A central tenet of neuroscience is that all behavior is caused by the brain. This sounds simple enough, but given our long intellectual history of separating the mind from brain, we hold very dear to the idea of an “I”, separate from the 3 pounds of electrical meat that is our brain, calling the shots. After all, “I” feel like “I” make decisions that shape my life. If “I” wasn’t responsible for these decisions, if the decisions instead came from the electrical meat, which is determined by the laws of physics, then how is it that “I” decided to wear a blue shirt instead of the red one? More troubling, if “I” am just my brain, and my brain is malfunctioning, am “I” still responsible for my behavior?

People are remarkably consistent in their moral judgments. Therefore, with some confidence, I can predict that you feel that the man from case 1 is less responsible for his behavior than Mr. Weinstein from case 2.  Is this gut-level feeling rational? After all, both men had damage to their brains, and their brains govern their behavior.

The problem with many cases of “my brain made me do it” arguments is that the association between a brain injury and a behavioral problem is not causal evidence that the injury caused the behavior. Another way of saying this is that “correlation does not imply causation”. We are quick to call B.S. on associations that don’t seem to have plausible causal connections: although drowning is associated with ice cream consumption, we do not guess that ice cream causes drowning. In the criminal realm, we are also likely to see through a Twinkie defense, even if “neuro-babble” makes for a more compelling case.

However, in the case of the first man, we are able to establish a causal connection between his brain injury and his bad behavior: he had “normal” behavior (presumably) before and after the tumor. Unfortunately, we cannot surgically repair most malfunctioning brains, so most connections between behavior and brain are speculative.

Beyond the problem of causality is the problem of will. How can we establish that someone absolutely cannot control his behavior? People can exhibit a certain degree of regulation over even autonomic functions using biofeedback or certain styles of meditation. In the lab, feedback from fMRI has been used to train subjects to willfully activate and de-activate a region involved in the perception of pain. However, it is incredibly difficult to willfully change most behaviors. It takes many days of consistent effort to form new habits. Many ex-smokers report that the physical withdrawal from nicotine was much easier to deal with than the reprogramming of one’s automatic response to grab a cigarette in various contexts. Although the politics of how we frame addiction is a larger topic for another post, suffice it to say that there is no consistent agreement what behaviors we expect people to be able to control, and those we don’t.

So, did my brain make me do it? Well, yes, of course it caused my behavior. Am I to be held responsible for this behavior? Given the above difficulties, I have to agree with Michael Gazzaniga who states that this question is to be left to the legal scholar and not the neuroscientist.

Against simple determinants of complex behavior: the case of oxytocin

Earlier, I argued against the view that complex behaviors and psychiatric diagnoses were caused by single genes. (In other words, that we will not find a gene for altruism, schizophrenia, or the propensity to drive slowly in the left lane).

A shy reader sent me the following private message:

“However, I have been amazed by the more I dig into the literature the more you find ‘one protein’ being responsible for very complex traits, one example is bonding and vasopressin and oxytocin.”

Oxytocin is a hormone produced in the brain by the posterior pituitary gland. It is released in quantity during child-birth to trigger lactation. Smaller amounts are released in both males and females following orgasm.

In sheep, the oxytocin released at birth seems necessary for bonding between a ewe and her lamb. In the absence of oxytocin release, the ewe is repelled by the odor of amniotic fluid, and will reject lambs approaching her.  However, the mechanism behind this hormonal influence on behavior is unknown.

However, the most famous case study for the striking behavioral effects of oxytocin comes from the prairie vole.  Prairie voles form strong and long-lasting bonds with single partners, typically following the first mating event. If a female vole is given oxytocin and then placed in the presence of a male she has not mated with, she will bond to him as if she had. Conversely, if oxytocin is blocked in the female after mating, she will not bond with the male. A similar pattern is shown in the male for the hormone vasopressin.

Different interests have capitalized on this data, calling oxytocin the “cuddle drug” and selling it for romantic courtship, curing social phobias, or by the military for interrogation enhancement.

But does oxytocin have such a clear role in changing the behavior of humans?  It is neither feasible nor ethical to manipulate the bonding between human parents and partners, so there is still much we don’t know. In a recent study, either oxytocin or placebo was given to participants playing an economic game requiring the trust of an unseen other player. Participants who received oxytocin demonstrated more trust in their partner, but only when the partner was behaving in a trustworthy way. In other words, oxytocin does facilitate trust, but not over-ride common sense.

 

It seems most likely that human behaviors are too complex to be completely modulated by ocytocin. However, I should also note in closing that even in animal models, the association between oxytocin and behavior is not 1:1. In the prairie vole, a strong pair bond can occur in the absence of mating (and hence an absence of oxytocin). And interestingly, genetically mutated mice without an oxytocin receptor gene have no trouble giving birth or lactating.

So, even in “textbook” cases of a single neurotransmitter causing a complex set of behaviors, we can have the following take-home messages:

1. Even in animal models, the neurotransmitter might not be necessary and sufficient (e.g. the voles still forming pair bonds in the absence of mating).
2. Cases of behavioral modification, in both humans and animals, cannot be divorced from context. Context can be biological (e.g. birth, mating) or social (the humans who were not gullible with oxytocin).

Why scientists aren’t going to find my neurotic gene any time soon

There has been some talk lately about a recent study that found that no robust statistical relations could be found between the whole genome and a standard personality test.

Seem surprising? Not so much.

So, a gene codes a protein. What does the protein do? Such a great number of things that it’s difficult to even list: a protein can become a structural element of a cell (such as actin or myosin that make up muscle tissue), or they can become neurotransmitters or other messengers in a complicated cascade of signaling events. For example, the PubMed description of the protein neuregulin 1 (statistically associated with schizophrenia, and high creativity) starts with “The protein encoded by this gene was originally identified as a 44-kD glycoprotein that interacts with the NEU/ERBB2 receptor tyrosine kinase to increase its phosphorylation on tyrosine residues.” Aside from the technical language, the first description of this protein is the relationship that it has to another protein, to provide a specific biochemical context (phosphorylation).

Alright. So a gene codes a protein, and this protein is a widget that works in concert with other such widgets in a particular biochemical and environmental context.  Does it even make sense to say that there is a gene for a complex behavioral phenomenon such as schizophrenia, depression, or a neurotic personality?  Not very much, really. Not at least in the sense of “I have this computer for writing this blog post”. Kenneth Kendler points out the lack of causal link further by making the following analogy:

“A jumbo jet contains about as many parts as there are genes in the human genome. If someone went into the fuselage and removed a 2-foot length of hydraulic cable connecting the cockpit to the wing flaps, the plane could not take off. Is this piece of equipment then a cable for flying?”

While most people would answer that no, the tube does not directly cause the jet to fly, this is the exact same logic that is used when we try to find a gene for X.

The issue is that we expect genes to have very lawful 1:1 correspondences with specific traits because in school we learned about Mendel’s pea pods, or cystic fibrosis, or Huntington’s disease that show such a relationship. This type of inheritance seems to be the exception, rather than the rule. There exists a wide distribution of association strengths between a single gene and a particular outcome. Scientists express this strength using a statistic called the odds ratio. Briefly, this is the odds that someone with gene A will have disease X, versus the odds that someone without gene A will have disease X. For a completely Mendelian disease (one like cystic fibrosis that cannot be contracted through the environment), the odds ratio is infinite because if you have the gene, you will always have the disease, and if you don’t have the gene, you never will. Statistical associations that we perceive as strong (such as the link between heavy smoking and lung cancer) have an odds ratio of about 20.  Psychiatric associations, on the other hand have an odds ratio of 1-2.  In other words, don’t go rush out to get genetically tested for depression. It won’t do you much good.

 

Partially, this lack of association is due to complex interactions between genes and the environments. For example, people with a particular variant of a serotonin transporter are more likely to experience depression, but only in the context of having experienced a stressful life event. 

A possible exception to the single-genes-don’t-change-behavior-in-isolation rule might be the COMT gene. This gene makes the enzyme that breaks down several neurotransmitters in the brain, including dopamine.  Like many genes, individuals may have different variations (or alleles) of the gene.  However, unlike alleles that change an individual’s hair color, different alleles in the COMT gene have been associated with striking differences in cognitive function.  Incredibly, these differences arise due to a single amino acid difference in the enzyme!  Substituting valine for methionine at position 158 in the gene is associated with a host of poorer psychological outcomes.  As each person inherits one copy of the gene from each of his parents, individuals can either have two valines, two methionines, or one of each.  Interestingly enough, the number of valines correlates with the degree of negative outcome.  For example, a 2008 study was conducted in which people recorded the events that were taking place in their lives, and rated how positive these events were.  The authors found that valine-valine individuals found a very pleasant event only as positive and methionine-methionine people found a sort-of positive event.  Given these results, it is easy to see how these individuals have difficulties with major depression and addiction.

 

So, genes code proteins which work together in an incredibly complex biochemical context created by other genes, the environment, and interactions of the genes, the biochemical milieu and the environment. Instead of asking ourselves why we haven’t found the gene for X, we should really be asking ourselves why we keep asking that question.