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“Inflammation might be causing depression”: Stigma of mental illness, reductionism, and (mis-)representations of science

by Katie Givens Kime

Image courtesy of Flickr

Is depression a Kind of Allergic Reaction?” Provocative headlines like these appear throughout popular media. Besides misrepresenting scientific findings, such journalistic coverage impacts perceptions of mental illness, as well as expectations of those seeking treatment. In last month’s Neuroethics in the News talk, Dr. Jennifer Felger, from Emory’s Department of Psychiatry and Behavioral Sciences, shared her experiences and insights on the translation (and mistranslation) of research by journalists. In relating the story of her own interactions with the media, Felger emphasized the complex and varying transactional relationships between journalists and scientists. The impact of such coverage carries notable neuroethical dimensions, potentially affecting the capacity for agency and/or aspects of a sense of self for a person experiencing mental illness.

The work of Felger and others on the role of inflammation in depression emerges from widespread observations that stress and other psychological experiences, particularly chronic stress, can weaken immune responses, leaving individuals more susceptible to illness. Such vulnerability can lead to common illnesses, like colds and flus, or even contribute to major illnesses, like cardiovascular disease, cancer, and inflammatory illnesses. On the other hand, once the immune system is activated by disease, stress, trauma, or even treatments for medical illness (e.g. chemotherapy), activated immune cells can release inflammatory mediators like cytokines. These mediators, along with the immune cells, can move into the brain, affecting neurotransmitter function, leading to behavioral changes, and even causing clinical depression.

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The particular area of research for Felger and some of her colleagues involved examining the mechanisms of cytokine action on the brain, and determining how cytokine action can lead to specific depressive symptom clusters. Felger’s findings suggest that for patients with increased inflammation (including patients with depression), anti-inflammatory or pro-dopaminergic treatment strategies might target decreased corticostriatal connectivity and improve motivational and motor deficits.

In essence, Felger and her colleagues found evidence that suggests a higher level of inflammation increases the likelihood of depression. Furthermore, patients with depression who have higher levels of inflammation may experience different symptoms of depression, which are related relate to the effects of inflammation on the brain. Publication of these findings led to articles in news outlets, for example, “Inflammation may be causing depression in about one-third of patients?” Although such articles did emphasize that depression is a heterogeneous disorder with wide variations in symptoms, they often oversimplified the nuances of Felger’s research regarding the relationship between inflammation and depression. More importantly, in this particular article, unpublished observations on the frequency of depressed patients with increased inflammation, which is highly sample and study- specific, was emphasized without attention to supporting scientific literature. Promotion of oversimplified and preliminary statements by the media can bias interpretation of the findings by other scientists, health providers, and the general public alike.

During her talk, Felger shared how her recent experience with the media has changed the way in which she considers framing and phrasing her research for scientific journals. She suggested that it can be helpful to anticipate the types of quotes the press will use. Having a rough sense of the terms that journalists are likely to grab can preclude some misrepresentations, reductionisms, and reinforced stigmas of mental illness by the media. Knowing the sort of coverage a journalist is seeking is important to help a researcher determine how they should best respond. Felger noted that a piece seeking to narrate the “general movement in the field” is much harder to write well than a piece focused on a singular study or set of findings. With more general overviews, cherry-picking of particular findings or implications is more likely to happen, resulting in higher incidences of misrepresentations.

Another helpful strategy that Felger highlighted is utilizing institutional resources for communicating research. In Felger’s case, working with Emory’s Woodruff Health Sciences Center (WHSC) Office of Research Communications was highly productive. A staff member from that office collaborated with Felger on a press release, headlined “Inflammation linked to weakened reward circuits in depression.” Despite using such institutional resources, Felger is clear that she and her colleagues have no foolproof way to avoid misrepresentations of their research findings.

Fortunately, some journalists are aware of their responsibility to represent research findings accurately. In Felger’s case, some journalists shared drafts of their story before they went to press, seeking a back-and-forth collaboration to ensure ethical reporting. For example a recent article from in which Dr. Felger was interviewed, “Is this why you feel bad? 6 issues tied to inflammation.”

In Felger’s experience, emails and messages to her from members of the general public also highlighted the stakes of these matters. In the changing terrain of health information, clinicians and researchers face the inevitable complexity that most patients search the internet for information about their symptoms or diagnoses. Moreover, patients will directly contact the researchers themselves. Felger noted the difficulty and importance of crafting ethically appropriate responses when members of the public sought interaction with her on her research. Such a situation is even more ethically fraught when the researcher is an investigator and not a physician — in such cases, researchers must work with physicians to construct ethically responsible responses.

Image courtesy of Wikimedia Commons

One example of the stakes of these issues is a piece published by the BBC about three months ago: “Depression: A revolution in treatment?” The article is a relatively standard representation of how the media has covered the topic of links between depression and inflammation, though it is hardly the biggest culprit in terms of misrepresentation or distortion of research findings. Notably, the text of the piece is interrupted with a quiz titled “Could I be depressed?” and a first question, “In the last two weeks: How often have you been bothered by having little interest or pleasure in doing things?” Such interactive features are quite obvious indicators of the readership for such media pieces, and the dangers involved. The disclaimer on the quiz echoes these concerns, “If you are having trouble understanding any of these questions, or at any point you start to feel distressed, please stop and seek the advice of a medical professional. See the links below for organisations that may be able to help you.” Though such disclaimers are included, is it appropriate to be encouraging self-diagnosis through such features?

The neuroethical dimensions to these matters extend beyond clinically and ethically appropriate communications with individual members of the public, however. Perhaps the most pronounced neuroethical matters at stake are the reinforcement of stigmas and the prioritizing of biological etiology. Felger shared her experience of the rapacious hunger for biological explanations of mental illness. She received message after message from people thanking her for “finding the answer” to their depression. Similarly, in the BBC article, an individual diagnosed with severe depression is quoted as saying, “If there was a way to say depression was a physical problem, I think it would make a massive difference, I think people would treat depression as something that is not made up and going on in the head. It would be seen as a genuine condition, it would validate a lot of people’s feelings.” It is a summation of how the media’s portrayal of the connection between inflammation and depression not only implies a mechanistic solution to mental illness, but also reinforces the message that biological explanations (rather than lifting of stigma) is the way for an individual suffering mental illness to be released from blame for their illness.

The current trajectories of neuroscientific research suggest we are likely to see more and more exciting and important findings emerge as to the embodied, biological aspects of mental illness. It does not inevitably follow, however, that such findings must be interpreted and communicated in ways that split the nature of mental illness into a false binary that equates biological etiologies with release from blame, and equates psychological etiologies with blame-worthiness. Felger noted how public discourse about mental illness in the U.S. (as well as BRAIN projects on a national level) remains stuck in outdated debates about biological explanations for mental illness.

Moving forward, an important role for neuroethics is watching for how research findings communicated in the popular media contribute, for good or for ill, to the ways in which individuals understand and relate to their own health, in all its complexities.

Want to cite this post?

Kime, KG. (2016). “Inflammation might be causing depression:” Stigma of mental illness, reductionism, and (mis-)representations of science. The Neuroethics Blog. Retrieved on , from


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