Category: Mental Health

Psychologists Reveal Magicians’ Secret Trick: A Low Risk of Depression

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Magicians are less likely to suffer from the mental health challenges faced by other creative people, like musicians and comedians, according to a new study published in the journal BJPsych Open. From comedians like Robin Williams, to poets and painters like Sylvia Plath and Van Gogh, many famous names have had well-publicised mental health disorders.

While not fully understood, there is growing evidence of a link between these health challenges and creativity. This new research led by Aberystwyth University shows that on some key measures, magicians are apparently an exception to this trend.

The study measured the psychological traits of 195 magicians and 233 people from the general population and compared with data from other creative groups. The academics’ work shows that on three key measures of psychosis or degrees of losing contact with reality, magicians are significantly less likely to suffer than artists, musicians and comedians. Magicians were less likely than all other creatives to have unusual experiences, such as hallucinations or cognitive disorganisation, which can make it hard to concentrate. Indeed, on many measures magicians appear to be less prone to these conditions than the general population. Their mental health profiles are most similar to those of mathematicians and scientists.

Dr Gil Greengross from the Department of Psychology at Aberystwyth University commented: “There is a common perception that many creative people have mental illnesses, and such illnesses make them more creative. This is the first study to show a creative group with lower scores on psychotic traits than the general population. Our research shows that members of at least one creative group, magicians, do not exhibit higher levels of mental disorders. The results demonstrate that the association between creativity and psychopathology is more complex than previously thought, and different kinds of creative work could be associated with either high or low psychoticism or autistic traits.

“The study highlights the unique characteristics of magicians, and the possible myriad associations between creativity and mental disorders among creative groups. One thing that distinguishes magicians from most other performing artists is the precision required in their performances. So, compared to other performers, it is more difficult to overcome errors. Magic tricks are largely ‘all or nothing’ acts that culminate in an ‘aha’ moment of surprise and awe. Failed magic tricks leave a greater impact than unfunny jokes, and are harder to compensate for, as they are few and far between. So, in addition to requiring highly technical skills, regardless of the type of magic performed, the high stakes of magic performances make magicians a unique creative group to study amongst all artistic professions.”

Dr Greengross from Aberystwyth University added: “What distinguishes magicians from most other creative people is that they not only create their own magic tricks but also perform them, while most creative groups are either creators or performers. For example, poets, writers, composers and choreographers create something that will be consumed or performed by others. In contrast, actors, musicians and dancers perform and interpret the creation of others. Magicians, like comedians and singer-songwriters, are one of the rare groups that do both.

“Magicians scored low on impulsive nonconformity, a trait that is associated with anti-social behaviour and lower self-control. These traits are valuable for many creative groups such as writers, poets and comedians whose creative acts are often edgy and challenge conventional wisdom. Magicians can also be equally innovative and push the limits of what is thought to be possible in magic, such as David Copperfield’s famous flying illusion. However, many magicians perform familiar tricks or some variations of them without feeling the need to innovate.”

Source: Aberystwyth University

Having Pets did not Result in Better Well-being During COVID

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Although pets are generally perceived as having a positive impact on well-being, a new study has found that there was no association between well-being and owning a pet during the COVID pandemic. This finding, published in the Personality and Social Psychology Bulletin, was in spite of pets owners reporting that pet ownership improved their lives.

There is a general understanding that pets have a positive impact on one’s well-being. A new study by Michigan State University found that although pet owners reported pets improving their lives, there was not a reliable association between pet ownership and well-being during the COVID-19 pandemic.

The study assessed 767 people over three periods in May 2020. The researchers took a mixed-method approach that allowed them to look at several indicators of well-being while also asking people in an open-ended question to reflect on the role of pets from their point of view. Pet owners reported that pets made them happy. They claimed pets helped them feel more positive emotions and provided affection and companionship. They also reported negative aspects of pet ownership like being worried about their pet’s well-being and having their pets interfere with working remotely.

However, when their happiness was compared to nonpet owners, the data showed no difference in the well-being of pet owners and nonpet owners over time. The researchers found that it did not matter what type of pet was owned, how many pets were owned or how close they were with their pet. The personalities of the owners were not a factor.

“People say that pets make them happy, but when we actually measure happiness, that doesn’t appear to be the case,” said William Chopik, an associate professor in MSU’s Department of Psychology and co-author of the study. “People see friends as lonely or wanting companionship, and they recommend getting a pet. But it’s unlikely that it’ll be as transformative as people think.”

The researchers explored several reasons why there is not a difference between the well-being of pet owners and nonpet owners. One of them being that nonpet owners may have filled their lives with a variety of other things that make them happy.

Source: Michigan State University

Glucocorticoid Levels Influence the Development of PTSD after Trauma

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Posttraumatic stress disorder (PTSD) is a debilitating condition that arises after experiencing traumatic events. While many people experience trauma, only about 25–35% of them develop PTSD. Understanding the factors that make certain individuals more susceptible is crucial for both prevention and treatment.

A new study led by Carmen Sandi and Simone Astori at EPFL now reveals how the development of PTSD is influenced by glucocorticoids, which are stress hormones such as cortisol. The work, which is published in Biological Psychiatry, provides significant insights into the behavioural and biological traits associated with PTSD vulnerability.

“There are considerable differences in the levels of glucocorticoids that individuals release to the bloodstream when stressed,” says Carmen Sandi. “Low glucocorticoid levels are frequently observed in PTSD patients following trauma exposure and were initially suspected to be a consequence of trauma exposure.”

She continues: “The possibility that this could be a trait constituting a pre-existing PTSD risk factor has been an outstanding open question for many years, but tackling it has been challenging due to the difficulties of both collecting biological measures before trauma exposure, and having access to relevant animal models in which the causal role of these traits can be investigated.”

To explore how a reduced hormonal response to stress might be linked to PTSD symptoms, the researchers used a genetically selected rat model that mimics people with blunted responses to cortisol. To do this, the team used MRI scans to measure the volume of different brain regions, trained rats to associate a cue with fear, recorded their sleep patterns, and measured their brain activity.

By combining these methods, the researchers discovered that a blunted responsiveness to glucocorticoids led to a “correlated multi-trait response” that includes impaired fear extinction (in males), reduced hippocampal volume, and rapid-eye movement sleep disturbances.

To explain the terms: Fear extinction is a process by which a conditioned fear response diminishes over time; problems with fear extinction are a hallmark of PTSD. Rapid-eye movement is crucial for memory consolidation, and disturbances in this type of sleep pattern have long been associated with PTSD.

But the study didn’t end there: the researchers treated the rats with the equivalent of human cognitive and behavioral therapy to reduce their learned fears. After that, they gave the rats corticosterone. As a result, both excessive fear and disturbances in rapid-eye movement sleep receded. Not only that, but the increased levels of the stress-related neurotransmitter norepinephrine in the brain also returned to normal.

“Our study provides causal evidence of a direct implication of low glucocorticoid responsiveness in the development of PTSD symptomatology following exposure to traumatic experiences, i.e., impaired fear extinction,” says Carmen Sandi. “In addition, it shows that low glucocorticoids are causally implicated in the determination of other risk factors and symptoms that were until now only independently related to PTSD.”

Silvia Monari, the study’s first author, adds: “In a nutshell, we present mechanistic evidence – previously missing – that having low glucocorticoids such as cortisol in humans is a condition for causally predisposed individuals to present all to-date vulnerability factors for developing PTSD, and causally involved in deficits to extinguish traumatic memories.”

Source: Ecole Polytechnique Fédérale de Lausanne

Scientists Identify Stress-linked Gene in Treatment-resistant Depression

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It has long been appreciated that major depressive disorder (MDD) has genetic as well as environmental influences. In a new study in Biological Psychiatry, researchers identify a gene that interacted with stress to mediate aspects of treatment-resistant MDD in an animal model.

Jing Zhang, PhD, at Fujian Medical University and senior author of the study, said, “Emerging evidence suggests that MDD is a consequence of the co-work of genetic risks and environmental factors, so it is crucial to explore how stress exposure and risk genes co-contribute to the pathogenesis of MDD.”

To do that, the authors used a mouse model of stress-induced depression called chronic social defeat stress (CSDS) in which mice are exposed to aggressor mice daily for two weeks. They focused on a gene called LHPP, which interacts with other signalling molecules at neuronal synapses. Increased expression of LHPP in the stressed mice aggravated the depression-like behaviours by decreasing expression of BDNF and PSD95 by dephosphorylating two protein kinases, CaMKIIα and ERK, under stress exposure.

Dr Zhang noted, “Interestingly, LHPP mutations (E56K, S57L) in humans can enhance CaMKIIα/ERK-BDNF/PSD95 signaling, which suggests that carrying LHPP mutations may have an antidepressant effect in the population.”

MDD is an extremely heterogeneous condition. Differences in the types of depression experienced by people influence the way they respond to treatment. A large subgroup of people with depression fail to respond to standard antidepressant medications and have “treatment-resistant” symptoms of depression. These patients often respond to different medications, such as ketamine or esketamine, or to electroconvulsive therapy. Notably, esketamine markedly alleviated LHPP-induced depression-like behaviours, whereas the traditional drug fluoxetine did not, suggesting that the mechanism might underlie some types of treatment-resistant depression.

John Krystal, MD, Editor of Biological Psychiatry, said of the work, “We have limited understanding of the neurobiology of treatment-resistant forms of depression. This study identifies a depression risk mechanism for stress-related behaviours that fail to respond to a standard antidepressant but respond well to ketamine. This may suggest that the risk mechanisms associated with the LHPP gene shed light on the poorly understood biology of treatment-resistant forms of depression.”

Dr Zhang added, “Together, our findings identify LHPP as an essential player driving stress-induced depression, implying targeting LHPP as an effective strategy in MDD therapeutics in the future.”

Source: Elsevier

Fear is in the Eye of the Beholder, Researchers Find

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Looking away from something frightening may be due to a specific cluster of neurons in a visual region of the brain, according to new research at the University of Tokyo. Researchers found that, in fruit fly brains, these neurons release a chemical called tachykinin which appears to control the fly’s movement to avoid facing a potential threat. Fruit fly brains can offer a useful analogy for larger mammals, so this study, published in Nature Communications, may help studies of human reactions to fearful situations and phobias.

“We discovered a neuronal mechanism by which fear regulates visual aversion in the brains of Drosophila (fruit flies). It appears that a single cluster of 20-30 neurons regulates vision when in a state of fear. Since fear affects vision across animal species, including humans, the mechanism we found may be active in humans as well,” explained Assistant Professor Masato Tsuji from the Department of Biological Sciences at the University of Tokyo.

The team used puffs of air to simulate a physical threat and found that the flies’ walking speed increased after being puffed at. The flies also would choose a puff-free route if offered, showing that they perceived the puffs as a threat (or at least preferred to avoid them). Next the researchers placed a small black object, roughly the size of a spider, 60 degrees to the right or left of the fly. On its own the object didn’t cause a change in behavior, but when placed following puffs of air, the flies avoided looking at the object and moved so that it was positioned behind them.

To understand the molecular mechanism underlying this aversion behavior, the team then used mutated flies in which they altered the activity of certain neurons. While the mutated flies kept their visual and motor functions, and would still avoid the air puffs, they did not respond in the same fearful manner to visually avoid the object.

“This suggested that the cluster of neurons which releases the chemical tachykinin was necessary for activating visual aversion,” said Tsuji. “When monitoring the flies’ neuronal activity, we were surprised to find that it occurred through an oscillatory pattern, ie, the activity went up and down similar to a wave. Neurons typically function by just increasing their activity levels, and reports of oscillating activity are particularly rare in fruit flies because up until recently the technology to detect this at such a small and fast scale didn’t exist.”

By giving the flies genetically encoded calcium indicators, the researchers could make the flies’ neurons shine brightly when activated. Thanks to the latest imaging techniques, they then saw the changing, wavelike pattern of light being emitted, which was previously averaged out and missed.

Next, the team wants to figure out how these neurons fit into the broader circuitry of the brain. Although the neurons exist in a known visual region of the brain, the researchers do not yet know from where the neurons are receiving inputs and to where they are transmitting them, to regulate visual escape from objects perceived as dangerous.

“Our next goal is to uncover how visual information is transmitted within the brain, so that we can ultimately draw a complete circuit diagram of how fear regulates vision,” said Tsuji. “One day, our discovery might perhaps provide a clue to help with the treatment of psychiatric disorders stemming from exaggerated fear, such as anxiety disorders and phobias.”

Source: University of Tokyo

The Eyes may Hold the Secret to the Greatest Benefits from TMS Therapy

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A pair of recently published studies from researchers at UCLA Health suggest that measuring changes in how pupils react to light could help predict recovery from depression and personalise transcranial magnetic stimulation (TMS) treatment of major depressive disorder.

TMS is a safe, non-invasive therapy that uses magnetic fields to stimulate parts of the brain involved in mood regulation. While TMS is proven effective, not all patients respond equally well to the therapy. The ability to predict who will benefit most could allow doctors to better customise and target treatments.

In two recent studies, UCLA scientists found that the pupil’s response to light before treatment correlated with improvements in depression symptoms over the course of therapy. Pupil size reflects activation of the autonomic nervous system, which controls involuntary functions and is negatively impacted in people with depression.

The first study, appearing in the Journal of Affective Disorders, reports on outcomes for 51 patients who underwent daily TMS sessions. Before receiving treatment, researchers measured the patients’ baseline pupillary constriction amplitude, or CA: how much the pupil shrinks when exposed to light. The pupil’s constriction is an indicator of parasympathetic nervous system function. The researchers found a significant association between baseline pupil constriction amplitude and symptom improvement, indicating that a greater constriction amplitude at baseline was associated with a better outcome. In other words, those with larger pupil constriction in response to light at baseline showed greater symptom improvement over their full treatment.

The second study, published in Brain Stimulation, went further and compared patients who were treated for depression with one of two common TMS protocols: 10Hz stimulation and intermittent theta burst stimulation (iTBS). In 10Hz stimulation, magnetic pulses are delivered in a continuous and relatively high-frequency stimulation. iTBS is a faster form of stimulation with bursts of three pulses at 50Hz, repeated with short breaks between bursts. This pattern is thought to mimic the natural rhythm of certain brain activities.

The researchers found that people with slower pupillary constriction had significantly greater improvement in depression after 10 sessions if they received iTBS rather than 10Hz treatment.

“These results suggest we may be able to use a simple test of the pupil to identify who is most likely to respond to electromagnetic stimulation of the brain to treat their depression,” said researcher Cole Citrenbaum, lead author of both studies.

Tailored TMS treatments

The researchers propose that measuring pupillary reactivity before starting TMS could guide treatment selection. “Additionally, we may be able to tailor the frequency of stimulation to the individual patient to maximise their benefit from treatment,” Citrenbaum said.

“At the present time, about 65% of patients treated with TMS have a substantial improvement in their depression,” said Dr Andrew F. Leuchter, senior author of both studies. “Our goal is to have more than 85% of patients fully recover from depression. As we better understand the complex brain activity underlying depression, we move closer to matching patients with the treatments that ensure their full recovery. Pupil testing may be one useful tool in reaching this goal.”

The studies add to growing evidence on the benefits of biologically-based personalization in treating major depression. UCLA researchers plan further trials to confirm the value of pupillometry in optimizing transcranial magnetic stimulation.

Source: University of California – Los Angeles Health Sciences

Ketamine’s Effect on Depression is Essentially Placebo Effect

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Over the years, studies have demonstrated the psychoactive drug ketamine’s effect on depression, providing profound and fast relief to many people. But these studies have a critical flaw: participants usually can tell whether they have been given ketamine or a placebo. Even in blinded trials in which participants are not told which they received, ketamine’s oftentimes trippy effects are a dead giveaway.

In a new study published in Nature Mental Health, Stanford Medicine researchers devised a clever workaround to hide the psychedelic, or dissociative, properties of the anesthetic first developed in 1962. They recruited 40 participants with moderate to severe depression who were also scheduled for routine surgery, then administered a single infusion of ketamine (0.5 mg kg−1) or placebo (saline) during usual anaesthesia.

All researchers and clinicians involved in the trial also were blinded to which treatment patients received. The treatments were revealed two weeks later.

The researchers were amazed to find that both groups experienced the large improvement in depression symptoms usually seen with ketamine.

“I was very surprised to see this result, especially having talked to some of those patients who said ‘My life is changed, I’ve never felt this way before,’ but they were in the placebo group,” said Boris Heifets, MD, PhD, assistant professor of anaesthesiology, perioperative and pain medicine, and senior author.

Just one day after treatment, both the ketamine and placebo groups’ scores on the Montgomery-Åsberg depression rating scale (MADRS) dropped, on average, by half. Their scores stayed roughly the same throughout the two-week follow-up.

“To put that into perspective, that brings them down to a category of mild depression from what had been debilitating levels of depression,” said Theresa Lii, MD, a postdoctoral scholar in the Heifets lab and lead author of the study.

What does it all mean?

The researchers concede that their study, having taken an unexpected turn, raises more questions than it answers.

“Now all the interpretations happen,” said Alan Schatzberg, MD, a co-author of the study. “It’s like looking at a Picasso painting.”

The researchers determined that it was unlikely the surgeries and general anaesthesia account for the improvements because studies have found that depression generally does not change after surgery; sometimes, it worsens.

A more likely interpretation, the researchers said, is that participants’ positive expectations may play a key role in ketamine’s effectiveness.

At their last follow-up visit, participants were asked to guess which intervention they had received. About a quarter said they didn’t know. Of those who ventured a guess, more than 60% guessed ketamine.

Their guesses did not correlate with their treatment – confirmation of effective blinding – but rather with how much better they felt.

Source: Stanford Medicine

Study Reveals Great Variability in Pregnant Women’s Body Images

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A new study published in the journal BMC Pregnancy and Childbirth has found considerable variability in the ways pregnancy affects women’s perceptions of their own body, including experiences of negative body image.

Negative body image during pregnancy is known to have serious adverse effects on both the mother and baby. Overall, average levels of body image dissatisfaction were found to be similar for pregnant women compared to the general female population, but on an individual basis, the research discovered large differences, both positive and negative.

The study is thought to be the first meta-analysis comparing pregnant and non-pregnant women, and was led by academics from Anglia Ruskin University (ARU) and the University of York.

The researchers initially screened 2017 separate academic studies, before focusing on 17 studies that provided comparable data. In total, the research included 5200 responses from women who were pregnant and 4172 responses from women who were not pregnant.

By synthesising results from multiple studies, the new research found women’s body image dissatisfaction overall was not statistically different during pregnancy compared with when not pregnant. However, when looking at the separate studies that formed part of the meta-analysis, there are significant variations on an individual level.

Body image dissatisfaction in pregnancy is made up of a combination of complex factors related to the positive and negative experiences of each woman, the researchers believe. For some, body image satisfaction will worsen during pregnancy because of ‘feeling fat’, while others describe feeling that their body is out of their control because they are aware their body will change but cannot stop it. Unrealistic portrayals of pregnant women in the media, often edited to remove uneven skin tone and stretch marks, are also believed to contribute to body image dissatisfaction.

Other pregnant women report having improved body positivity compared to when not pregnant, as they no longer compare their body to the ‘thin ideal’. Some say the improvement is because they place less attention on how their body looks and more on its functionality, focusing on the foetus’s health and their maternal role.

Understanding the causes of body image dissatisfaction in pregnant women is important since it can have physical and mental consequences for mother and baby. Many women who display body image dissatisfaction during pregnancy also exhibit depression and anxiety, both postnatally and longer term. This can lead to negative emotional, cognitive, and behavioural outcomes for the child, as well as poor quality mother-infant interactions.

In addition, body image dissatisfaction has been linked with physical illness as the expectant mother may engage in practices such as unhealthy eating, dieting, purging, and fasting. This can have unwanted negative effects on the foetus, such as low birth weight and premature birth.

Lead author Anna Crossland, University of York, said: “Due to the impact that body dissatisfaction can have on the expectant mother and foetus, it is vital to understand how body image dissatisfaction may change on an individual basis when women are pregnant. What our study has found is there is no universal experience during pregnancy, and so we shouldn’t assume how people feel. Pressures about how we look are still felt by some people during pregnancy and it is much more helpful to ask how someone is, rather than commenting on their appearance.”

Co-author Dr Elizabeth Kirk, Senior Lecturer in Psychology at Anglia Ruskin University, said: “Our earlier work found that women who didn’t feel good about their changing bodies in pregnancy reported lower feelings of bonding with their unborn baby. Therefore, it is crucial that we better understand and support women’s body image during pregnancy, to help women on an individual basis.”

Source: Anglia Ruskin University

We may now Know the Reason why SSRIs Take so Long to Kick in

Source: CC0

Selective serotonin reuptake inhibitors (SSRIs) normally take a few weeks before any improvements manifest, but the reasons why it takes so long have remained unclear since their first introduction 50 years ago. Now, new research provides the first human evidence that this is due to physical changes in the brain, which leads to greater brain plasticity developing over the first few weeks of SSRI intake. This may also begin to explain one of the mechanisms of how antidepressants work.

This work is presented at the ECNP conference in Barcelona, and also has been accepted in a peer-reviewed journal.

Clinician have long been puzzled as to why SSRIs take a relatively long time before having an effect. Researchers in Copenhagen, Innsbruck, and University of Cambridge have undertaken a randomised, double-blind placebo-controlled study in a group of healthy volunteers which shows a gradual difference in how many nerve cell connections (synapses) the brain cells have between those taking the antidepressants and a control group, depending on how long the treatment lasts.

In the study, 17 volunteers were given a 20mg daily dose of the SSRI escitalopram, with 15 volunteers given a placebo. Between three and five weeks after starting the trial, their brains were scanned with a PET (Positron Emission Tomography) scanner, which showed the amount of synaptic vesicle glycoprotein 2A in the brain: this is an indicator of the presence of synapses, so the more of the protein is found in an area, the more synapses are present in that area (ie, greater synaptic density). These scans showed significant between-group differences in how the synapse density evolved over time.

Researcher Professor Gitte Knudsen (of Copenhagen University Hospital) said:

“We found that with those taking the SSRI, over time there was a gradual increase in synapses in the neocortex and the hippocampus of the brain, compared to those taking placebo. We did not see any effect in those taking placebo.”

The neocortex, which takes up around half of the brain’s volume, deals with higher functions, such as sensory perception, emotion, and cognition. The hippocampus, which is found deep in the brain, handles functions of memory and learning.

Professor Knudsen continued, “This points towards two main conclusions. Firstly, it indicates that SSRIs increase synaptic density in the brain areas critically involved in depression. This would go some way to indicating that the synaptic density in the brain may be involved in how these antidepressants function, which would give us a target for developing novel drugs against depression. The second point is that our data suggest that synapses build up over a period of weeks, which would explain why the effects of these drugs take time to kick in.

Commenting, Professor David Nutt (Imperial College, London) said “The delay in therapeutic action of antidepressants has been a puzzle to psychiatrists ever since they were first discerned over 50 years ago. So these new data in humans that uses cutting edge brain imaging to demonstrate an increase in brain connections developing over the period that the depression lifts are very exciting.  Also they provide more evidence enhancing serotonin function in the brain can have enduring health benefits.”

This is an independent comment, Professor Nutt was not involved in this work..

Source: EurekAlert!

Can Running Beat Antidepressants as a Treatment for Depression?

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The first study to compare effects of antidepressants with running exercises for anxiety, depression and overall health shows that they have about the same benefits for mental health, with health benefits for those assigned to running.

Professor Brenda Penninx from Vrije University, Amsterdam, presented the work at the ECNP conference in Barcelona (after recent publication in the Journal of Affective Disorders). Prof Penninx said, “We wanted to compare how exercise or antidepressants affect your general health, not just your mental health.”  

The 16-week course of running over the same period scores higher in terms of physical health improvement, whereas antidepressants lead to a slightly worse physical condition, as has been suggested by previous studies.  However, the drop-out rate was much higher in the group which initially chose exercise.

The researchers studied 141 patients with depression and/or anxiety. They were offered a choice of treatment; SSRI antidepressants for 16 weeks, or group-based running therapy for 16 weeks. 45 chose antidepressants, with 96 participating in running. The members of the group which chose antidepressants were slightly more depressed than the members of the group which chose to take running.

Professor Penninx said, “This study gave anxious and depressed people a real-life choice, medication or exercise. Interestingly, the majority opted for exercise, which led to the numbers in the running group being larger than in the medication group.”

Treatment with antidepressants required patients to adhere to their prescribed medication intake but this generally does not directly impact on daily behaviours. In contrast, exercise directly addresses the sedentary lifestyle often found in patients with depressive and anxiety disorders by encouraging persons to go outside, set personal goals, improve their fitness and participate in a group activity.  

The antidepressant group took the SSRI Escitalopram for 16 weeks. The running group aimed for two to three closely supervised 45-minute group sessions per week (over 16 weeks). The adherence to the protocol was lower in the running group (52%) than in the antidepressant group (82%), despite the initial preference for running over antidepressants.

At the end of the trial, around 44% % in both groups showed an improvement in depression and anxiety, however the running group also showed improvements in weight, waist circumference, blood pressure, and heart function, whereas the antidepressant group showed a tendency towards a slight deterioration in these metabolic markers.

“Both interventions helped with the depression to around the same extent. Antidepressants generally had worse impact on body weight, heart rate variability and blood pressure, whereas running therapy led to improved effect on general fitness and heart rate for instance. We are currently looking in more detail for effects on biological aging and processes of inflammation’,” Prox Benninix said.

Physical activity is a good option, but antidepressants still have a role

Prof Benninx noted that it is not a case of one or the other when it comes to treating depression. “It is important to say that there is room for both therapies in care for depression. The study shows that lots of people like the idea of exercising, but it can be difficult to carry this through, even though the benefits are significant. We found that most people are compliant in taking antidepressants, whereas around half of the running group adhered to the two-times-a-week exercise therapy. Telling patients to go run is not enough. Changing physical activity behaviour will require adequate supervision and encouragement as we did by implementing exercise therapy in a mental health care institution.”

She added: “Antidepressants are generally safe and effective. They work for most people. We know that not treating depression at all leads to worse outcomes; so antidepressants are generally a good choice. Nevertheless, we need to extend our treatment arsenal as not all patients respond to antidepressants or are willing to take them. Our results suggest that implementing exercise therapy is something we should take much more seriously, as it could be a good – and maybe even better – choice for some of our patients.  

“In addition, let’s also face potential side effects our treatments can have. Doctors should be aware of the dysregulation in nervous system activity that certain antidepressants can cause, especially in patients who already have heart problems. This also provides an argument to seriously consider tapering and discontinuing antidepressants when depressed or anxious episodes have remitted. In the end, patients are only truly helped when we are improving their mental health without unnecessarily worsening their physical health.”

Source: EurekAlert!