Depression: Does psychotherapy make new nerve cells grow?

According to a study at the University of Halle-Wittenberg, the effect of psychotherapy has now been “medically and scientifically” proven

Depression is increasingly becoming a widespread disorder. Despite ongoing criticism of the effectiveness of so-called antidepressants, enough of them are now prescribed in Germany to treat five million people every day. Many people seek psychotherapeutic help. For those with statutory health insurance, waiting times are painfully long, while psychology associations are calling for more treatment places and funding has remained unclear since the reform of training to become a psychotherapist. (Incidentally, Germany also has a private healthcare system with better services for those who can afford it and for civil servants.) That alone could make you depressed.

A research group led by Ronny Redlich, Professor of Biological and Clinical Psychology at the University of Halle-Wittenberg, has now investigated the possible effects of psychotherapy on the brain in more detail. “More gray matter through psychotherapy,” commented the university’s press release on August 27. It sounds like a breakthrough: “Now, for the first time, we have a valid biomarker for the effect of psychotherapy on brain structure,” explains the professor. “To put it simply: psychotherapy changes the brain.”

Well. Reading this article changes your brain (hopefully in a positive way). Walks in nature change the brain. Throughout our lives, everything we do and perceive changes the brain. It is a plastic organ with around 86 billion nerve cells that still hides many secrets of its functioning from us. Let’s take a closer look at the new study.

The study

For the study now published in the journal Translational Psychiatry 30 people with an average age of 28 and a diagnosis of depression were examined (Zwiky et al., 2025). Their brain structure was recorded twice using magnetic resonance imaging (MRI): once shortly before the start of cognitive behavioral therapy and then after around 22 therapy sessions or 40 weeks later. According to the researchers, the focus of the brain examinations was on structures of the limbic system such as the amygdalae or hippocampi. These are often associated with emotion processing.

By the way: What exactly belongs to the “limbic system” is not so clear, Latin limbus simply means “hem”. In addition, the explanatory power of the brain model, which assigns mental processes to specific brain regions, has faced increasing opposition in recent years (Noble et al., 2024). However, the alternative view that the brain is a holistic network does not explain much—and above all does not justify the use of scanners costing millions. As is so often the case in science: “It’s complex!”

First of all, the study showed that psychotherapy helped: various questionnaires measuring depressive symptoms showed a decrease. These effects were strong and statistically very significant. In 19 of the 30 people, depression was partially or completely improved after the 40 weeks. And what did the brain show?

The volume of gray matter had increased in both amygdalae as well as in the right hippocampus. However, this was only evident in a targeted search in these regions and not when looking at the whole brain. The so-called “region of interest” analyses can circumvent the problem of having to control more for random hits.

If you examine the entire brain, you calculate tens of thousands of statistical tests, all of which have a certain probability of error. As a rule, however, the alternative procedure indicates smaller effects. And in fact, the brain result was weaker than the evaluation of the questionnaires.

Brain findings

So let’s take a look at the brain findings:

Figure 1: The figure on the right shows a positive statistical finding for the two amygdalae. On the left is a correlation of the change in the right amygdala (y-axis) and a measure of emotion identification (x-axis). This correlation was just so significant at the p < 0.05 level. Source: Zwiky et al, 2025; License: CC BY 4.0

However, there was no direct correlation between the measured values for the depressive symptoms and the brain changes. Only when evaluating a questionnaire for alexithymia—a technical term for problems perceiving and describing feelings—was there a hit. And then only for the sub-item “Difficulty describing feelings”.

The publication was built around this theme, as the researchers put it in their second hypothesis: “We further hypothesize regional volumetric changes to be related to improvements in alexithymia rather than declines in overall depressive symptom severity” (Zwiky et al., 2025, p. 2).

It is a pity that the researchers did not register their study in advance. This is common practice in drug research, with which they compared their results in the press release. And in the course of the crisis in psychology over the last ten to 15 years, the importance of this procedure has been emphasized time and again: without registration, researchers can knit a story around a chance finding afterwards as if that was exactly what they were looking for.

I don’t want to accuse this research group of anything. I can only say that this doesn’t make sense to me: If you know about the positive effect of cognitive behavioral therapy on depressive symptoms and want to pin this down in the brain, why do you narrow your focus to alexithymia? And why then only on the aspect of describing feelings?

At the end of the article, I will discuss another reason why I think the correlation in Figure 1 is problematic. But that will be a bit more complex. At this point, I would like to address two important points of criticism that should be understandable to laypeople.

Lack of controls

We remember the core message: psychotherapy changes the brain structure. However, I fear that the study cannot support this result—due to fundamental flaws in the study design:

According to the study, the gray matter—on average of the 30 people—was slightly more pronounced in some brain regions after 40 weeks or 22 therapy sessions. This is initially only a correlation. How do we know that there really is a causal connection, that it was really the psychotherapy that brought about the brain changes?

To make this conclusion at least plausible, the researchers would have had to compare these 30 people with a control group that did not differ from the target group in any way—except for therapy. Ideally, there would have been two additional groups with a diagnosis of depression: one that went for regular walks in nature, for example, and one that did nothing at all while waiting for a place in therapy. There are (unfortunately) more than enough of these. That would have been important because, firstly, going for walks also changes the brain and, secondly, a depressive episode often passes on its own after four to nine months, even without treatment.

Admittedly, making people in the control group wait for a place in therapy is not without its problems. Nevertheless, there are always control groups in good psychotherapy research (e.g. Cuijpers et al., 2023). Without these, it is impossible to interpret a result causally. For comparison: you may have good reasons for not having any money with you when you come back from sport and want to buy some apple juice, but it is still not right to take it with you without paying. Similarly, you cannot do without the control group if you specifically want to investigate the effect of psychotherapy, even if you have good reasons for doing so.

But even that would not be the biggest problem. We’ll come to that now.

Medication

However, a second problem is even more serious: Of the 30 people, nine—almost a third—were taking so-called antidepressants; seven of these nine were even taking high doses. However, it has long been known that in people with depression but without medication smaller amygdalae and in those with medication larger ones were measured. This was shown, for example, in a much-cited meta-analysis from 2008 (Hamilton et al., 2008). With this in mind, let’s take a closer look at the correlation in Figure 1:

Figure 2: The figure again shows the change in the volume of the right amygdala (y-axis) in relation to the measured value for the identification of feelings (x-axis). The blue circle in the middle shows nine people for whom, roughly, nothing has changed and the orange rectangle in the top right shows six people who, as it were, “pull up” the result—the dashed straight line below. Source: adapted from Zwiky et al., 2025; License: CC BY 4.0

We can see from the figure that for some people in the study—those in the blue circle—neither the volume in the right amygdala nor the identification of feelings changed significantly. The already small effect is mainly pulled upwards by the six people in the orange rectangle.

If some of them took medication, this could better explain the change in brain volume, while the researchers attribute the result to psychotherapy. That would be a gross mistake. Therefore, in my opinion, they should definitely repeat the analysis again without the antidepressant group.

Old wine

We remember that the press release presented the result as new: “For the first time, the researchers have also documented concrete anatomical changes.” And study leader Redlich added: “Now, for the first time, we have a valid biomarker for the effect of psychotherapy on brain structure. To put it simply: psychotherapy changes the brain.”

This presentation is very strange for two reasons: Firstly, no one seriously doubts that psychotherapy changes the brain. Just learning anything, say the melody of “All My Ducklings” on the piano, changes something in the body and especially in the brain. Secondly, brain changes have often been reported in connection with psychotherapy.

For example, back in 2012, the Bremen “Hanse-Neuropsychoanalysis Study” by Anna Buchheim and with the participation of the now deceased German “brain guru” Gerhard Roth (1942-2023) traced brain changes over the course of 15 months of psychoanalytic psychotherapy. At that time, too, the main focus was on the limbic system and differences in the right amygdala. This study is not even mentioned by the researchers from Halle-Wittenberg.

Anna Buchheim, Gerhard Roth and two colleagues published a commentary on this in 2012 in the German Gehirn&Geist with the title “The brain also heals“. In it, they wrote that there had been around 15 neuroscientific studies on the effectiveness of psychotherapy in 2005 and 40 in 2012. How can such results still be considered new in 2025?

Caution

These and a number of other problems should make us cautious when interpreting the results. In the new publication, the researchers themselves referred to the small group size. The fact that there was no control group without treatment was also acknowledged as a limiting factor. And in particular: “As correlations between gray matter volume increases and enhancements in specific psychological functions … were only small, they need to be interpreted with caution” (Zwiky et al., 2025, p. 5).

How does this fit in with presenting the study to the media as a major breakthrough? Incidentally, the claim that psychotherapy has proven the development of new “gray cells” is nonsense: You can’t even determine this with such a crude MRI measurement in the living brain.

Whether new neurons are created in the brain at all after the age of around 14 is a matter of debate among experts. This would actually require a biopsy and even then it is not trivial to distinguish new from old neurons among billions of cells. For ethical reasons, this is of course forbidden in living people and the interpretation of the results from dead bodies is still being debated. Recently, a research group concluded that the significance of this phenomenon should not be overestimated, even if it occurs in adults (Duque et al., 2022).

I find this conclusion by study leader Redlich particularly problematic: “It is therefore all the more encouraging that we were able to show in our study that psychotherapy is an equally effective alternative from a medical and scientific standpoint.” This expresses the old trauma of psychology and psychiatry: Something can only be true if it is neurologically proven. Is that what you do when someone says, “I am your friend” or “I love you”, that you then ask for a brain scan as proof instead of looking at the person’s behavior?

But of course, exaggerations—where all criticism, restrictions and restraint are forgotten—are a feast for the media. So it rustled through the press at the speed of light: “Depression: More grey cells through psychotherapy” (Deutschlandfunk), “Depression: Psychotherapy builds up grey cells” (Scinexx), “Psychotherapy changes the brain” (wissenschaft.de), “More grey cells through psychotherapy” (Ärztenachrichtendienst) or “Depression: How psychotherapy strengthens the brain” (MDR)—to name just the first few online hits.

Biological Psychiatry

I’ll take it a little further. Let’s remember what the statistically strongest finding of the study was: Of the 30 people, 19 had experienced a moderate or strong improvement after 22 psychotherapy sessions. But what the media are jumping on is the brain finding, which is neither new nor surprising, but very speculative in this study.

The head of the study, Ronny Redlich, was also involved in a more recent study that allows us to look deep into the soul of biological psychiatry. In it, dozens of authors, including many big names in psychiatric research in Germany today, searched for a biomarker for depression (Winter et al., 2024). Despite all the brain talk, many laypeople are unaware that neither depression nor any of the other hundreds of psychological and psychiatric disorders can be diagnosed neuroscientifically. In the new study, the experts tried artificial intelligence.

The sobering result surprised them: “Despite the improved predictive capability … no informative individual-level major depressive disorder biomarker—even under extensive machine learning optimization in a large sample of diagnosed patients—could be identified” (Winter et al., 2024, E1). Since at least the early 1800s, biological psychiatrists have tried every trick in the book to find the organic cause of depression and other disorders. With rare exceptions, all of which have long since migrated to neurology—think neurosyphilis, epilepsy, multiple sclerosis, Parkinson’s disease, Alzheimer’s dementia is still a borderline case—, these attempts have been unsuccessful for over 200 years.

Give us more money!

But instead of finally abandoning the brain ideology with its molecules, genes, neuronal circuits and laboratory animals after so many falsifications and instead working mainly on and with people, these researchers concluded: “It is imperative for researchers, journals and funding agencies to reflect on the next steps in advancing biological psychiatry”(ibid., p. E8).

You have to let this logical short-circuit melt in your mouth: Our approach fails time and time again, and just failed again; you need to give us more money! In the interests of patients and society, however, this research project should not be developed further, but finally abandoned.

Psychiatry should be 80 percent psychosocial and a maximum of 20 percent biological. Incidentally, this new study with artificial intelligence has also shown what has been repeatedly confirmed for decades: The greatest influence on depression is the environment, expressed here as social support and experienced child abuse. Nobody was interested in this because they were doing real “medical and scientific” research. The social aspect then disappears from the radar, although it is much more important.

Below, I provide a brief historical overview of how psychiatry became so obsessed with the brain since the early 1800s, the era of phrenology. Based on this and some remarkable quotations from leading psychiatrists of our time, which they made only after their retirement, it should become clearer why I feel entitled to call this “brain ideology.” I should note that I myself worked in that field of research for my PhD, but left it in 2009 because I didn’t find it promising.

The dogma of biological psychiatry in historical perspective

The disorders simply cannot be detected in the brain. What conclusions can be drawn from this?

Biological psychiatry’s attempts to prove the existence of hundreds of disorders such as depression or anxiety and attention disorders in the brain fail time and again. Nevertheless, these researchers have been demanding more and more money for decades. And they usually get it. This has devastating consequences for other areas of research, clinical practice and therefore the well-being of patients.

In economic terms, this is called “opportunity costs”. What else do you lose if one branch of research dominates like that?

Opportunity costs

The distribution of funds is not as innocent as it may seem at first glance. And it is by no means a purely scientific dispute. As a number of American and British psychiatrists pointed out a few years ago, every euro, pound or dollar can only be spent once. Due to the strong dominance of neuro-research, there is a lack of projects to prevent psychological and psychiatric problems, to support families who are having a hard time and to prevent suicides (Lewis-Fernández et al., 2016).

However, the situation in 2025 is that billions of research dollars worldwide—shown here using the example of the largest psychiatric research institution, the National Institute of Mental Health (NIMH) in the USA (Zilberstein et al., 2025)—are still being spent primarily on the search for neuronal causes. According to the most common official criteria, there are 227 valid symptom combinations for depression, and as many as 116,220 for attention deficit disorder (ADHD; Schleim, 2022). This complexity and vagueness, as determined by leading experts around the conference table, cannot be overcome with neuroscientific research.

In my German book The Neurosociety from 2011, I debunked some neuromyths. Ironically, it was reviewed by the leading European neuropsychologist in the Journal of Neuropsychology very favorably. Another institute director wrote to me that he largely agreed with me, but that he would not recommend the book to his staff. Otherwise he would have to fear that they would stop working. But that would have been the best conclusion.

In 2021, I called for the medical model in psychiatry to finally be abandoned and to return to people and their psychosocial needs. This would have saved many billions in research and could have been invested not only in prevention, but also in better training for clinical psychologists and psychiatrists. Anyone who thinks my criticism is exaggerated can take a look at a quote from Thomas Insel. He was director of the NIMH from 2002 to 2015 and decided on a budget worth billions every year. Amazingly, he, the “star neuroscientist”, told Wired:

“I spent 13 years at NIMH really pushing on the neuroscience and genetics of mental disorders, and when I look back on that I realize that while I think I succeeded at getting lots of really cool papers published by cool scientists at fairly large costs—I think $20 billion—I don’t think we moved the needle in reducing suicide, reducing hospitalizations, improving recovery for the tens of millions of people who have mental illness.” (Thomas Insel in Wired, 2017)

History

A brief historical overview illustrates how this “cool research by cool scientists” has become the dominant trend in psychiatry.

The 19th century saw major upheavals in medicine. Inspired by scientific advances—associated with names that are still well-known today, such as Rudolf Virchow (1821-1902), Robert Koch (1843-1910) and Paul Ehrlich (1854-1915)—more and more bacteria, viruses and organic abnormalities were discovered as sources of disease. Psychiatry and psychotherapy in the modern sense were not yet known. There was pastoral care and prisons for the poor. The wealthy were sent to sanatoriums. Those who could really afford it hired a personal physician as a traveling companion to get a breath of fresh air and change their thoughts.

In the big cities, the misery of the poor was also great. Eventually, they—especially the elderly, beggars, people with dementia, epileptics and prostitutes who had nowhere else to go—were admitted to hospitals. Examples include the Salpêtrière in Paris, which was taken over by the psychiatric reformer Philippe Pinel (1745-1826) in 1795; the young Sigmund Freud (1856-1939) would later study here and be initiated into hypnosis. Or the Bethlem Hospital in London, which still exists today, where the doctor and pharmacist John Haslam (1764-1844) searched for the seat of depression in the brains of deceased patients around 1800—and even believed he had found it!

Psychiatry needed an organic cause for the “mental illnesses” in order to be perceived not just as pastors or “lunatic doctors”, but as real physicians. Fittingly, the doctor and anatomist Franz Joseph Gall (1758-1828) developed phrenology at the time. The medical profession was critical of the later popularization by Gall’s assistant, Johann Gaspar Spurzheim (1776-1832), and others. However, the view that “mental illnesses” had to be brain diseases fitted in with the spirit of the times. It solved the embarrassing dilemma of having no organ to point to.

Figure 3: The idea of the functional specialization of the brain, indicated on the left by the phrenologists Gall and Spurzheim in an anatomical drawing from 1810, has inspired psychiatry and psychology to this day. However, the later popularization of the idea that personality traits can be recognized by the shape of the head, shown here in a book from 1859, brought phrenology into lasting disrepute.

The hypothesis of brain disorders finally became dogma in the course of the 19th century. Ronny Redlich’s statement above that his—on closer inspection rather modest—study had shown the equivalence of psychotherapy “from a scientific-medical point of view” illustrates the effect this still has today. Equivalent to what, actually? He meant psychopharmacological drugs.

This is an interesting example because, according to new epidemiological studies, they hardly work better than placebo for depression. The perhaps still somewhat optimistic finding that they help about 15 percent of those affected, but then intensively (Stone et al., 2022), has just been further relativized by a brand new study: If you don’t just research this, funded by the pharmaceutical industry, in carefully selected patient groups, but in representative groups like those actually found in clinics, then the effectiveness is even lower (Xu et al., 2025).

Broken brains?

It is well known that people with psychological and psychiatric problems fear that they will not be taken seriously. However, it is astonishing that so many experts in the field still cling to the 200-year-old dogma, even persistently ignoring the genetic consensus since the 1970s. As they fail to reduce their disorder categories to gene variations time and again, they are now chasing “hidden heritability” instead.

This is the “dark energy” of psychiatry, whereby physics is perhaps even more forgiven for assuming unobserved entities in order to maintain the otherwise very well-functioning standard model. But what could a “well-functioning standard model” of biological psychiatry be? That they can control some symptoms with psychoactive drugs or electrical current? This is also already known since the 19th century. And it leaves too many patients helpless and, in the worst case, with new problems because of severe side effects and drug dependence.

The wave of biological psychiatry that continues today emerged in the 1980s. At that time, the era of “neuro” and “gene” began. Thomas Insel’s pre-pre-pre-pre-predecessor as director at the NIMH, Alan Leshner, explained after his retirement how this worked: “Mental health advocates started referring to schizophrenia as a ‘brain disease’ and showing brain scans to members of congress to get them to increase funding for research. It really worked” (cited in Satel & Lilienfeld, 2014, p. 4).

Leshner was in office from 1990 to 1992, just at the beginning of the “Decade of the Brain”—exceptionally as a neuropsychologist, not as a biological psychiatrist. Today, 30 years later, psychiatrists want to replace the concept of “schizophrenia” (Böge et al., 2025), partly because it can cause more suffering in patients than it helps.

Leshner was rewarded for his commitment to psychiatry by being appointed the first director of the newly founded National Institute on Drug Abuse (NIDA). One of his major achievements was to present addiction as a brain disease (Leshner, 1997). If it worked in the time of the phrenologists, why not in the late 1990s? A good 25 years later, the USA has an unprecedented addiction problem with many deaths and even more misery.

But for the researchers, the math worked out: In the words of Thomas Insel, they had great opportunities for “cool careers with cool papers”. There was no shortage of research billions. A neuropsychiatrist I hold in high esteem once said in an interview: “At scientific congresses, you don’t go down so well with social psychiatric presentations in this day and age. And people also want to make a career.” I agree.

Present

What matters most to human beings is hardly respected in research, which obsessively wants to be “medical and scientific” but is in reality primarily ideology. One could smile about the coup if there wasn’t so much at stake: The anti-addiction drugs promised by Leshner and many others, for example, have largely remained a dream, while today many millions of people are living an addictive nightmare.

The better therapies promised in the German 2004 “Manifesto of Leading Brain Researchers” still do not exist. And all of the advances in biological psychiatry promised by Thomas Insel in 2010 for the year 2020—including diagnostic biomarkers, better therapies and even vaccinations against mental disorders—are still missing today (Insel, 2010). A decade after he vacated his billion-dollar director’s chair at the NIMH, Insel explained the issue of “faulty brain circuits” as a metaphor. We still don’t know enough about the brain. Ah, I see.

With Leshner, you could say: “It really worked.” In his new book Healing: Our Path from Mental Illness to Mental Health Insel explained that solving the mental health crisis might require solving social-institutional problems after all (Insel, 2022). Ah, I see. Biological psychiatry, which mainly wants to push molecules around, has no answer to that.

Hypes

When I was doing my doctorate in this field, “personalized medicine” was in vogue. In the biomedical paradigm, however, this was just a cipher for even more biotechnological medicine. Because that didn’t help many patients, the next thing they came up with was “translational medicine”: As if medical research didn’t always have to be practical, application-oriented and in the interests of those affected. They now call the latest hype “precision medicine”.

I didn’t like the idea of always having to sell something preliminary and hypothetical as a major breakthrough. That’s why I stopped doing this research in 2010. Since then, I’ve been surprised more than once by researchers with great careers who acknowledge criticism in personal conversations—only to tell the something completely different in research proposals, public lectures or media interviews. Is this just functional optimism or is it already a psychological-psychiatric disorder, keyword “loss of reality”?

For the publication criticized above under the leadership of Ronny Redlich in the journal Translational Psychiatry the publisher paid 4000 euros in publication costs according to the price list. I would have to pay 1300 euros to publish my criticism. So it will just be a LinkedIn article. However, it should have become clear that those seeking help are not served by tracing the neuronal imprints of psychosocial therapy.

The future

Swiss psychiatry professor Matthias Jäger recently criticized the flood of patients following the many destigmatization campaigns in society: “[The social aspect of psychiatry] does not mean that psychiatry is responsible for remedying social problems and socially undesirable behavior of any kind” (Jäger, 2025; transl.). This brings us back to the early 19th century, to a certain extent before the medical professionalization of the discipline, to the time of poorhouses and asylums.

Thanks to tight budgets, a lack of prevention and the prospect of further welfare cuts for national defense, we cannot assume a decrease in psychological and psychiatric disorders. In the UK, however, where social cuts are already one or two steps further and people’s need is correspondingly great, new solutions are also emerging:

There is a ministry against loneliness. A network of critical psychiatrists including Joanna Moncrieff, a professor of psychiatry in London, helps people to stop taking antidepressants. The fact that patients can become dependent on them has long been denied. And local community help should be available to people where they live and navigate the challenges of their everyday lives.

Here in my article, a possibility was identified where a few billion could be saved immediately (globally) and still hundreds of millions in Europe. And if psychology (literally: the study of the soul) and psychiatry (literally: the healing of the soul) overcome their lack of soul and once again appreciate people as the biopsychosocial beings that they are, perhaps problems will be solved again and not just symptoms treated. Decades of psychotherapy research have also come to the conclusion that relationships and the environment are the key factors.

Nevertheless, I would like to express my sincere respect for all psychiatrists who, despite the difficult conditions, face the challenges of their work, often day and night. My criticism is not directed at them, but at the biological dogma that restricts research and practice.

This shows us alternatives. Whether we pursue them depends on our decisions, both individually and collectively.

P.S. Deeper statistical criticism

For those who are inclined to read on, I have three statistical points here that further relativize the results of the study discussed: The first has to do with the localization of the brain structures; the second with a necessary correction for the already weak correlation; and the third with a correction for medication use.

For the study, structural brain images were taken with a spatial resolution of 1 x 1 x 1 mm³ (Zwiky et al., 2025). Such a cube is called a “voxel”, similar to the pixels on a computer screen. The amygdalae are just 1.5 cm, or 15 mm, in size (Brabec et al., 2010). In the study led by Ronny Redlich, the image data was smoothed with a size of 8 mm. In principle, this is done to improve the signal-to-noise ratio, but in this case it is already half the length of amygdala. This can blur the boundaries between the areas.

In general, I was surprised that the question of anatomical identification was not discussed in detail in the study. It has long been known that small structures such as the amygdalae and the hippocampi can be confused with each other (Ball et al., 2009). This initially referred to measurements of brain function with a poorer spatial resolution. But neuroscientists working at the microscope are regularly amazed at the ease with which anatomical regions are determined in such studies. In the present case, it appears that they relied entirely on the software to do this at the touch of a button.

But what I’m really trying to get at is how variable such measures of brain volume can be. This is shown in the following figure:

Figure 4: In this comparative study with 110 control subjects each without a psychological-psychiatric diagnosis (HC), with depression (MDD), bipolar disorder (BD) and a schizophrenia spectrum disorder (SSD), large overlaps can be seen between the groups and minimal differences in the mean value. The measure of volume change is plotted on the y-axis, here for the left hippocampus, a structure close to the amygdala. Source: adapted from Brosch et al., 2022; License: CC BY 4.0

Even the untrained eye should immediately notice the overlap between the four groups: The individual points, which represent the brain data of individual people, almost all fall within the range of -0.05 to 0.05. It goes without saying that no diagnosis is possible with such data using a brain scanner. This also illustrates how important the comparison with control groups is. Incidentally, the groups here were almost four times as large as in the psychotherapy study.

Finally, we question the correlation once again: We remember that the researchers used different questionnaires to determine depressive symptoms and alexithymia (emotional disturbance). Since they were looking at two points in time, before and after therapy, they calculated the difference (Δ, delta). They did the same for four brain regions: the two amygdalae and two parts of the right hippocampus. Correlating all questionnaires with all brain regions, we get 6 x 4 = 24 results.

Figure 5: The correlation matrix of the study. The result in bold in the eighth row, for the right amygdala, is decisive for us. The value of 0.321 is also the slope of the straight line in Figures 1 and 2. The statistical test was just significant at the usual p < 0.05 level with p = 0.042. Source: Zwiky et al., 2025; License: CC BY 4.0

Every statistical test has a certain probability of error. With the relevant calculations on the matrix, the researchers basically attempted to test the null hypothesis that there is no correlation between two variables 6 x 4, i.e. 24 times. In my opinion, the casual significance threshold of p < 0.05 is then no longer sufficient to rule out random hits.

This would eliminate the main finding of the already speculative study. Incidentally, the correlation value of 0.321 means that just 15 percent of the differences at the psychological level can be explained by differences in the right amygdala. How does this relate to the far-reaching statements in the press release?

Finally, we also remember the possibility that the result could have been pulled up by people from the patient group with the medication (Figure 2). I therefore suggested calculating the correlation without the data from these nine participants. Then it might no longer be statistically significant. But the authors would have to investigate this themselves.

In the very last sentence of the supplementary material of the study, there is a reference to the fact that the status of the medication was compared with the difference in brain volume. Apart from the fact that this effect just missed the significance threshold with p = 0.068, this is not a clean procedure in my opinion: The fact that such a test is not positive should not lead to the conclusion that there is no effect. The study could also simply have too little statistical power, for example because the group size was too small.

Compared to the far-reaching conclusions drawn from the study, the data and its interpretation seem very speculative to me.

References

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Title image after Zwiky et al., 2025, CC BY 4.0.