Comparing the research paper to the popular press: depression

Last week an old school friend shared this article about depression, on Facebook; being me I decided to find the original paper it’s based on. Luckily, there was a link to the paper in the article itself. The article was written, or published 4th May 2016, whereas the research paper was published 30th June 2016. Reading the article made me itch at it’s stupidity, mainly because they tried to hook their ‘positive outlook’ on to a meta-analysis of brain MRI data. So, today I thought I’d read through both the paper and the article and compare the two. What I learnt was that the paper is more interesting than the article, and that people will always try to use the results to support their position, even when it doesn’t.

Lets start with the respective titles:

The paper is titled ‘Subcortical brain alterations in major depressive disorder: findings from the ENIGMA Major Depressive Disorder working group’, which is fairly descriptive, but doesn’t tell you anything about the findings. The article goes with ‘New Research Says Depression Is Not A Choice, It’s A Form Of Brain Damage’. This is fairly descriptive and purports to give you all the information in one go. The difference in form and content is the nature of the different formats. The online article is from a fairly tabloid-like website, whereas a scientific paper published by a respected journal is more formal and detailed.

What did the authors of the paper do and what did they conclude?

While the research paper very specifically discusses MDD, the article generalises to all forms of depression.

The article from suggests that the study used 9000 new samples:

Published in Molecular Psychology, the study surveyed an unprecedented 9,000 individual samples…Past studies revealed a distinct relationship is the size of the hippocampus and depression, but the testing groups were never large enough to yield definite results. No testing sample has been this large, so the results proved the theory of depression’s true cause and effect.[1]

The ENIGMA-MDD consortium used pre-existing samples of neuroimaging and clinical data from 15 different research groups:

in the current study we meta-analyzed structural magnetic resonance imaging data of a very large sample (n=8927) to identify subcortical brain volumes that robustly discriminate MDD patients from healthy controls.[2]

In total, we analyzed data from 8927 people including 1728 MDD patients and 7199 healthy controls.

That is, they engaged in meta-analysis of lots of data:

The primary aim of our ENIGMA-MDD Working Group is to identify imaging markers that robustly discriminate MDD patients from healthy controls using an individual participant data (IPD)-based meta-analysis.

The results are interesting, the ENIGMA paper concludes that ‘mean hippocampal volume was significantly lower in MDD patients compared to healthy controls (Cohen’s d (95% confidence interval):d=−0.14 (−0.22, −0.06); P-value=4.60 × 10−4, % difference=−1.25).’ That means that the mean hippocampus volume was lower in patients with MDD than those in healthy patients. In addition to comparing MDD patients and healthy people, the consortium also compared the difference in hippocampal volume between first episode and recurrent episode patients. There were no significant difference between the two groups, but between the control group and the recurrent episode group there was a difference in that recurrent episode patients showed a lower mean hippocampal volume. Age of onset of first episode had no effect on hippocampal  volume.

The higherperspective article is basically right in stating ‘patients…showed a definite shrinkage of hippocampal volume, up to 1.24 percent’. They make a small error in that 1.24% is a mean amount, not an upper limit. Thses reductions are mainly found in recurrent and early onset MDD.

These hippocampal volume reductions were mainly present in recurrent and/or early onset (less than or equal to21 years) MDD, whereas hippocampal volume reductions were absent in first episode patients and less pronounced in patients with later age of onset (>21 years) MDD.

One of the hypothesise associated with this decrease in hippocampus size is the ‘neurotrophic hypothesis of depression’. In this hypothesis, elevated glucocorticoid levels in MDD patients induces brain atrophy by remodeling and downregulation of growth factors, which may preferentially target the hippocampus. In longitudinal studies, hippocampal volume in MDD patients degrades more quickly than should be caused by age, and early onset patients showed increased likelihood of hippocampal volume reductions. These findings may support the neurotrophic hypothesis of depression, but other factors effect onset of depression, such as a family history of depression. It doesn’t tell us what triggers the first episode of depression but may suggest a reason for recurrent episodes. The authors of the paper conclude that ‘early disease onset is (in part) independently associated with lower hippocampal volumes’.

The authors give several limitations in their study: they couldn’t directly monitor the affect of remission on hippocampal volume as most of the scans were done while the patients were experiencing an episode; a second is the variety of questionnaires used to assess severity of depression; and thirdly, they restricted their analysis to subcortical grey matter, lateral ventrical and total ICV’s. Given these limitations, it is still possible to conclude that the hippocampus plays a key role in the pathophysiology of MDD, and it is a prime target region for future research to further our understanding of the pathophysiology of MDD and improving treatment.

What’s the difference between the paper and the article?

The paper’s authors concluded that the hippocampal volume reduction is involved in some way in recurring and early onset MDD; the article concludes that

the results proved the theory of depression’s true cause and effect.

This is a bit of a leap.

The hippocampus governs the formation of new memories, especially long term memory, and also in spatial navigation. It has also been shown in animal studies to be involved in behavioural inhibition[3]. It is part of the limbic system, which, among other things is associated with emotions. The quote attributed to Professor Ian Hickie, who they call a co-author of the study but I can’t find any evidence of that in the paper itself (let me know if you find any reference to him and I’ll change this bit), explains the link between the hippocampus and behaviour, but the writer of the article is adamant that it is emotions that are associated with the hippocampus. They then conclude that a shrinking hippocampus means that you only remember negative memories and leap to yoga and meditation, positive thinking and mindfulness:

As the hippocampus shrinks, your memories can become more negative, making your expectations for the future just as bleak. It becomes a cycle of self fulfillment. Not reigning in your perspective, limits the effectiveness and functionality of your brain. More research has to be done to examine the reversibility of this particular kind of damage.

There has been concrete experimentation revealing how mediation and yoga can thicken brain tissue and develop new neural connections. While positive thinking and mindful living has been acknowledged as vital for mental and spiritual health, now it has been proven to be necessary for your physical self as well. Just one more reason to change your perspective and brighten your outlook!

None of these things have been proven to be ‘necessary to your physical self’. There is some evidence that by helping people to relax mindfulness and meditation may help reduce stress but positive thinking won’t fix your depression. The article uses a legitimate paper than gives a concrete conclusion and uses it to advance their own agenda by slightly twisting the facts. They’ve taken the association of the hippocampus with the limbic system, and the volume loss in the hippocampus associated with MDD, as definitive proof that positive thinking fixes depression. The article itself is jumbled and needs the work of a dedicated editor. In addition the initial claim in the title, that depression is caused by brain damage, isn’t supported by the paper or even by their own commentary. I’d also like to point out that depression is not a choice, we don’t choose to be depressed, and the title’s suggestion that it is is insulting to people with various types of depression and mental health conditions.






In other news, I’ve heard back from the admissions department at Lincoln, the course leader wants to discuss my options with me and I’ve booked myself on an informal open day in June.


One thought on “Comparing the research paper to the popular press: depression

  1. I get so frustrated with the way the popular press reports on science. I don’t think they do this maliciously, but their misinterpretations and oversimplifications lead the public to believe some very strange ideas are “proven” scientific facts.

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