Depression and biomarker blues

It’s been an eventful week for depression research. That’s because a recent study raises hopes for a biological test to predict which young men are most vulnerable to depression. The problem is, based on early reports on this study, it’s not clear that this biomarker offers any information we can’t get from asking people about their experiences and emotional states.

The study — set to be published in the PNAS journal but not yet available to the public — measured the levels of the stress hormone cortisol in the saliva of hundreds of teenagers. Researchers also asked the teens to report on symptoms of depression over a 12-month period. Based on this information, the teenagers were divided into four groups based on whether they had high or low levels of cortisol and high or low levels of depressive symptoms. After tracking these teens for another four years, the researchers found that boys (but not girls) who initially showed both high levels of cortisol and more depressive symptoms were most likely to develop clinical depression.

A quick note about sex: it’s not clear why this pattern showed up for boys but not girls. The BBC article on this study mentions a theory that women naturally have higher cortisol levels (perhaps because high concentrations of estrogen in the body can lead to increased cortisol). Whatever the reason, it doesn’t look like cortisol can work as a biomarker among girls.

I’m just also not clear whether it would be a helpful biomarker among boys. For me, the key point here is that a combination of reported depressive symptoms and high cortisol levels predicted the highest rates of depression. That combination of hormone levels and symptoms raises questions about what really drives the depression. Perhaps the boys in the high cortisol/many symptoms group had higher cortisol levels precisely because their experienced symptoms — which can include everything from chronic fatigue to feelings of emptiness or trouble concentrating — were more frequent, or more strongly felt.

In that case, the cortisol levels would basically reflect the information we get from surveying young men about the symptoms they may be experiencing. Intense symptoms would correspond with higher cortisol levels, and also with higher rates of depression.

To tease out whether cortisol levels offer truly unique information, it would be helpful to compare the frequency and intensity of symptoms reported by the boys in the high and low cortisol groups. If both groups reported equally frequent, equally intense symptoms regardless of their cortisol levels, and the high cortisol group still went on to show higher rates of depression, that would answer some of my concerns. It would suggest that cortisol by itself contributes to the likelihood of depression, independent of the information we get from the boys’ self-reported symptoms.

It’s hard to get to the bottom of this issue since PNAS hasn’t yet published the study. I’m only writing about it now because the study is already being reported as a breakthrough, and that seems a bit premature. I can understand the general excitement — researchers have struggled to identify clear-cut biological bases for depression, so this finding must feel like a sudden light appearing in the dark. But I wonder whether the hype reflects a tendency to privilege biological information over other kinds of information about mental health disorders, even when there’s no compelling reason to do so.

One point I’ve seen clearly in my recent exposure to the history of psychology: both scientists and non-scientists often assume that physical and measurable information — like cortisol levels — is automatically useful because physical stuff is just, well, “real.” But just because you can touch something (or in this case, extract it from teenage boys’ saliva) doesn’t necessarily mean it tells you more than you’d learn from asking those boys whether they’ve been sleeping too much or feeling hopeless.

To paraphrase the German psychologist Wolfgang Köhler, when we want to know if someone’s angry, we don’t prick his finger to measure the adrenaline levels in his blood. We’ll ask him, or observe for ourselves whether the veins in his forehead are throbbing, whether his voice sounds heated, and so forth. While common sense doesn’t always get us the right answers, in that kind of situation it tends to work well enough.

Insofar as we’re hoping for magic biomarkers that make it easier to predict depression, I’m curious as to how screenings would work. Let’s say more evidence comes out to support cortisol as a biomarker, so we screen a bunch of young men for their cortisol levels. If those teens report high depressive symptoms but low amounts of cortisol, do we dismissively tell them and their families not to worry so much about the risk of depression? If teens report medium depressive symptoms but high levels of cortisol, do we scare them by saying their hormonal levels point to a high likelihood of depression? Even if those scenarios are a bit caricatured, they draw out real questions about how biomarkers for depression could be implemented in healthcare.

If all this reads as my being a wet blanket about this research, I’d say it’s just the opposite. For one thing, I think it’s clear that we can benefit from more information on the biological correlates of depression, even if that information does not translate to biomarkers. For another, I don’t think we should feel so desperate for biological correlates when it looks like we quite accurately identify depression by asking people what their lives are like and how they feel.

That doesn’t mean we do a great job of treating or preventing depression. But since depression seems to result from combinations of many factors, it’s not an issue that can be solved by any single approach, biological or otherwise.


3 thoughts on “Depression and biomarker blues

  1. I agree with your sentiments entirely. People place a very high value on quantifiable data. Another example of this is the focus on the cognitive to the detriment of the affective in preferred treatment modalities for depression. For example, short-term therapies such as CBT which focus on the “thoughts cause mood” link are preferred to long-term psychoanalysis which paints on a broader canvas. While I believe CBT skills are excellent, I do not believe they are a complete treatment for depression and other mood disorders, because they neglect the “moods generate thoughts” side of the equation. Unfortunately, therapies such as psychodynamic psychotherapy are harder to complete randomized clinical trials on, because the process is prolonged and not as proscribed as CBT. This leads to a tendency among clinical psychologists – at least where I live in Australia – to look down their nose at therapies which deal with the affect.
    Of course, there’s always an exception, and dialectical behaviour therapy is a modality which seems to address both cognition and affect. I’m still only learning about DBT, though.

    • Interesting point about CBT. I think categorizing symptoms, or even behaviors generally, as either “cognitive” OR “affective” is sometimes just a tempting oversimplification. Emotional and cognitive factors presumably have a lot of overlap. And I know very little about DBT, but you’ve encouraged me to learn more!

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