New research has found a significant association between participating in low to moderate intensity exercise and reduced rates of depression. Researchers carried out an umbrella review of studies carried out across the world to examine the potential of physical activity as a mental health intervention.
The analysis, published in the journal Neuroscience and Biobehavioural Reviews, found that physical activity reduced the risk of depression by 23% and anxiety by 26%. A particularly strong association was found between low and moderate physical activity, which included activities such as gardening, golf and walking, and reduced risk of depression. But this was not strongly observed for high intensity exercise.
Physical activity was also significantly associated with reduced risk of severe mental health conditions, including a reduction in psychosis/schizophrenia by 27%. The results were consistent in both men and women, and across different age groups and across the world.
Lead author Lee Smith, Professor of Public Health at Anglia Ruskin University (ARU), said: “Preventing mental health complications effectively has emerged as a major challenge, and an area of paramount importance in the realm of public health. These conditions can be complex and necessitate a multi-pronged approach to treatment, which may encompass pharmacological interventions, psychotherapy, and lifestyle changes.
“These effects of physical activity intensity on depression highlight the need for precise exercise guidelines. Moderate exercise can improve mental health through biochemical reactions, whereas high-intensity exercise may worsen stress-related responses in some individuals.
“Acknowledging differences in people’s response to exercise is vital for effective mental health strategies, suggesting any activity recommendations should be tailored for the individual.
“The fact that even low to moderate levels of physical activity can be beneficial for mental health is particularly important, given that these levels of activity may be more achievable for people who can make smaller lifestyle changes without feeling they need to commit to a high-intensity exercise programme.”
Coronary artery disease and major depression may be genetically linked via inflammatory pathways to an increased risk for cardiomyopathy, a degenerative heart muscle disease, researchers at Vanderbilt University Medical Center and Massachusetts General Hospital have found.
Their report, published in Nature Mental Health, suggests that drugs prescribed for coronary artery disease and depression, when used in combination, potentially may reduce inflammation and prevent the development of cardiomyopathy.
“This work suggests that chronic low-level inflammation may be a significant contributor to both depression and cardiovascular disease,” said the paper’s corresponding author, Lea Davis, PhD, associate professor of Medicine in the Division of Genetic Medicine and Vanderbilt Genetics Institute.
The connection between depression and other serious health conditions is well known. As many as 44% of patients with coronary artery disease (CAD), the most common form of cardiovascular disease, also have a diagnosis of major depression. Yet the biological relationship between the two conditions remains poorly understood.
A possible connection is inflammation. Changes in the levels of inflammatory markers have been observed in both conditions, suggesting that there may be a common biological pathway linking neuroinflammation in depression with atherosclerotic inflammation in CAD.
In the current study, the researchers used a technique called transcriptome-wide association scans to map single nucleotide polymorphisms (genetic variations) involved in regulating the expression of genes associated with both CAD and depression.
The technique identified 185 genes that were significantly associated with both depression and CAD, and which were “enriched” for biological roles in inflammation and cardiomyopathy.
This suggests that predisposition to both depression and CAD, which the researchers called (major) depressive CAD, or (m)dCAD, may further predispose individuals to cardiomyopathy.
However, when the researchers scanned large electronic health record databases at VUMC, Mass General, and the National Institutes of Health’s All of Us Research Program, they found the actual incidence of cardiomyopathy in patients with the enriched genes for (m)dCAD was lower than in patients with CAD alone.
One possible explanation is that medications prescribed for CAD and depression, such as statins and antidepressants, may prevent development of cardiomyopathy by reducing inflammation, the researchers concluded.
“More research is needed to investigate optimal treatment mechanisms,” Davis added, “but at a minimum this work suggests that patient heart and brain health should be considered together when developing management plans to treat depression or cardiovascular disease.”
A global collaborative research group has identified brain energy metabolism dysfunction leading to altered pH and lactate levels as common hallmarks in numerous animal models of neuropsychiatric and neurodegenerative disorders. These include models of intellectual disability, autism spectrum disorders, schizophrenia, bipolar disorder, depressive disorders, and Alzheimer’s disease. The findings were published in eLife.
The research group, comprising 131 researchers from 105 laboratories across seven countries, sheds light on altered energy metabolism as a key factor in various neuropsychiatric and neurodegenerative disorders. While considered controversial, an elevated lactate level and the resulting decrease in pH is now also proposed as a potential primary component of these diseases. Unlike previous assumptions associating these changes with external factors like medicationa, the research group’s previous findings suggest that they may be intrinsic to the disorders. This conclusion was drawn from five animal models of schizophrenia/developmental disorders, bipolar disorder, and autism, which are exempt from such confounding factorsb. However, research on brain pH and lactate levels in animal models of other neuropsychiatric and neurological disorders has been limited. Until now, it was unclear whether such changes in the brain were a common phenomenon. Additionally, the relationship between alterations in brain pH and lactate levels and specific behavioural abnormalities had not been clearly established.
This study, encompassing 109 strains/conditions of mice, rats, and chicks, including animal models related to neuropsychiatric conditions, reveals that changes in brain pH and lactate levels are a common feature in a diverse range of animal models of conditions, including schizophrenia/developmental disorders, bipolar disorder, autism, as well as models of depression, epilepsy, and Alzheimer’s disease. This study’s significant insights include:
I. Common Phenomenon Across Disorders: About 30% of the 109 types of animal models exhibited significant changes in brain pH and lactate levels, emphasising the widespread occurrence of energy metabolism changes in the brain across various neuropsychiatric conditions.
II. Environmental Factors as a Cause: Models simulating depression through psychological stress, and those induced to develop diabetes or colitis, which have a high comorbidity risk for depression, showed decreased brain pH and increased lactate levels. Various acquired environmental factors could contribute to these changes.
III. Cognitive Impairment Link: A comprehensive analysis integrating behavioural test data revealed a predominant association between increased brain lactate levels and impaired working memory, illuminating an aspect of cognitive dysfunction.
IV. Confirmation in Independent Cohort: These associations, particularly between higher brain lactate levels and poor working memory performance, were validated in an independent cohort of animal models, reinforcing the initial findings.
V. Autism Spectrum Complexity: Variable responses were noted in autism models, with some showing increased pH and decreased lactate levels, suggesting subpopulations within the autism spectrum with diverse metabolic patterns.
“This is the first and largest systematic study evaluating brain pH and lactate levels across a range of animal models for neuropsychiatric and neurodegenerative disorders. Our findings may lay the groundwork for new approaches to develop the transdiagnostic characterisation of different disorders involving cognitive impairment,” states Dr Hideo Hagihara, the study’s lead author.
Professor Tsuyoshi Miyakawa, the corresponding author, explains, “This research could be a stepping stone towards identifying shared therapeutic targets in various neuropsychiatric disorders. Future studies will centre on uncovering treatment strategies that are effective across diverse animal models with brain pH changes. This could significantly contribute to developing tailored treatments for patient subgroups characterized by specific alterations in brain energy metabolism.”
The exact mechanism behind the reduction in pH and the increase in lactate levels remains elusive. But the authors suggest that, since lactate production increases in response to neural hyperactivity to meet the energy demand, this might be the underlying reason.
Using the old anaesthesia drug ketamine to pull people out of the depths of severe depression has gone from fringe idea to widespread use in just a few years. Sparked by promising studies and stories of lives transformed, clinics offering intravenous infusions of ketamine have popped up in the US. Some also offer a newer, more expensive, nasal spray version.
But major questions remain about who ketamine can help, why some people get tremendous relief within days or weeks while others don’t, and the costs and benefits of different ways of delivering the drug.
New findings just came out from a study that seeks to answer some of those questions. They add more evidence about the power of IV ketamine to help some of the most severely ill people with depression or bipolar disorder who haven’t gotten relief from other treatments, including many who have frequent suicidal thoughts.
Called Bio-K, the study involved 74 people treated at four clinics in Michigan, Maryland and Minnesota. After just three infusions of ketamine over 11 days, 52% of participants saw their severe depression ease so much they achieved remission. Another 15% responded somewhat.
Half of those who had thought often of suicide before receiving ketamine experienced a dramatic drop in those impulses. The results are published in the Journal of Affective Disorders.
“These participants are very representative of the sickest patients we see, with more than 80% reporting suicidality that would have excluded them from other depression treatment studies,” said University of Michigan Health psychiatrist and study leader Sagar Parikh, MD.
“As in other studies of ketamine, the initial response to treatment was a strong predictor of who would do well,” he added. “Two-thirds of those who responded after one infusion went on to achieve remission, while those who hadn’t responded measurably after two infusions were unlikely to start to respond after an additional one.”
Who responds and why?
What’s the difference between them and those who responded? That’s a key focus of Bio-K, which is funded by donors to the U-M Eisenberg Family Depression Center.
A third of all Bio-K participants didn’t respond to ketamine by the end of the three infusions provided under the study, leaving them to cope with one more failure in a series of attempted treatments.
The team’s in-depth interviews with some of these non-responders show how difficult that can be, as the team reported in a paper last year.
By studying molecules in blood samples from the study’s participants, the Bio-K team hopes to find biomarkers that could predict who is most likely to get relief from ketamine, and who should try other options.
The study is evaluating cell signaling proteins, inflammatory markers and molecules that can indicate rates of cell metabolism in mitochondria. Early results from those analyses should be available in the next year.
From research to clinical use
In the meantime, the strength of the response in Bio-K participants helped fuel the founding of an IV ketamine clinic at University of Michigan Health, says Parikh, who oversees the clinic.
U-M now accepts referrals from providers across the region who have patients with treatment-resistant depression and need another option after trying at least four medications.
Patients come to the main U-M medical campus around eight times during the span of a month for infusions under the care of psychiatrists, anaesthesiologists and other clinicians.
Parikh and his colleagues even wrote a guide for other hospitals on how best to set up and run such a clinic.
A newer version
Meanwhile, the nasal spray form of ketamine, called esketamine and sold under the name Spravato, has captured attention in recent years for its potential to ease disabling and life threatening symptoms without requiring an IV.
The spray involves a form of the drug manufactured by a pharmaceutical company in a way that isolates just one variety of the ketamine molecule, which allowed the company to seek a specific FDA approval.
Parikh notes that U-M was one of the sites for the original small study that led to Spravato’s approval by the FDA, and another larger study sponsored by Janssen, the drug’s manufacturer, that recently concluded. In addition to serving as the local principal investigator for these studies, Parikh also briefly served as a consultant to the company.
Based on the experience in these studies, U-M hopes to start offering Spravato alongside IV ketamine on a clinical basis. Even though it’s not given through an intravenous drip, the nasal spray still requires careful observation of patients under the FDA’s approval conditions.
IV vs nasal spray
Even as researchers search for biomarkers to predict ketamine response, clinicians find themselves with a conundrum: Which patients should start with IV ketamine, and which with Spravato? And how do the two compare head to head in actual response to treatment?
That’s what researchers at Yale University, U-M and their colleagues will soon try to find out, through a new study just funded by the federal Patient-Centered Outcomes Research Institute.
The study, which will begin enrolling up to 400 people at six sites nationwide later this year, will randomly assign people with treatment resistant depression to either the IV or nasal spray form of the drug. They’ll then receive that treatment for about four weeks, and have their symptoms monitored during treatment and for months afterward.
Such a head-to-head study might help inform insurers that haven’t yet started covering one or both forms of ketamine, Parikh noted.
More about the Bio-K results
In the meantime, the treatment response results from the Bio-K study and other studies can help more patients and clinicians understand the impact of IV ketamine.
Although Bio-K accepted people who were suicidal, which many antidepressant medication studies do not, it did not include people who use cannabis or those who have an active substance use disorder, schizophrenia or psychosis. But participants had to have failed to respond to at least two antidepressant or mood stabilising medications after at least eight weeks, or failed to respond to six sessions of ECT, the treatment based on electric stimulation of the brain that has been seen as the last resort for many patients.
The study found that it did not matter if they got their infusions slowly over 100 minutes or in a standard session of 40 minutes.
At the start of the study, the average score of participants on a standard depression scale called MADRS was 28; that average dropped to 11 at 24 hours after the third infusion. A score of 10 or below is considered depression free, or remission, and a drop in score of at least 50% of the total score is considered response. In all, 67% achieved what is considered response, and 52% reached remission.
People with depression have higher body temperatures, suggesting there could be a mental health benefit to lowering the temperatures of those with the disorder, a new UC San Francisco-led study found. The study, published in Scientific Reports, only indicated an association, not a causative effect in either direction.
It’s also unknown whether the higher body temperature observed in people with depression reflects decreased ability to self-cool, increased generation of heat from metabolic processes or a combination of both.
Researchers analysed data from more than 20 000 international participants who wore a device that measures body temperature, and also self-reported their body temperatures and depression symptoms daily.
The seven-month study began in early 2020 and included data from 106 countries. The results showed that with each increasing level of depression symptom severity, participants had higher body temperatures.
The body temperature data also showed a trend toward higher depression scores in people whose temperatures had less fluctuation throughout a 24-hour period, but this finding didn’t reach significance.
The findings shed light on how a novel depression treatment method might work, said Ashley Mason, PhD, the study’s lead author and associate professor of psychiatry at UCSF Weill Institute for Neurosciences.
A small body of existing, causal studies has found that using hot tubs or saunas can reduce depression, possibly by triggering the body to self-cool, for example, through sweating.
“Ironically, heating people up actually can lead to rebound body temperature lowering that lasts longer than simply cooling people down directly, as through an ice bath,” said Mason, who is also a clinical psychologist at the UCSF Osher Center for Integrative Health.
“What if we can track the body temperature of people with depression to time heat-based treatments well?”
“To our knowledge, this is the largest study to date to examine the association between body temperature – assessed using both self-report methods and wearable sensors – and depressive symptoms in a geographically broad sample,” added Mason. “Given the climbing rates of depression in the United States, we’re excited by the possibilities of a new avenue for treatment.”
Increases in symptoms of depression are associated with a subsequent increase in bodyweight when measured one month later, new research from the University of Cambridge has found.
The study, published in PLOS ONE, found that the increase was only seen among people with overweight or obesity, but found no link between generally having greater symptoms of depression and higher bodyweight.
Research has suggested a connection between weight and mental health – with each potentially influencing the other – but the relationship is complex and remains poorly understood, particularly in relation to how changes in an individual’s mental health influence their bodyweight over time.
To help answer this question, researchers at Cambridge’s Medical Research Council (MRC) Epidemiology Unit examined data from over 2,000 adults living in Cambridgeshire, UK, who had been recruited to the Fenland COVID-19 Study.
Participants completed digital questionnaires on mental wellbeing and bodyweight every month for up to nine months during the COVID-19 pandemic (August 2020 – April 2021) using a mobile app developed by Huma Therapeutics Limited.
Questions assessed an individual’s symptoms of depression, anxiety and perceived stress.
A higher score indicated greater severity, with the maximum possible scores being 24 for depression, 21 for anxiety and 40 for stress.
The team then used statistical modelling to explore whether having poorer mental wellbeing than usual was related to changes in bodyweight one month later.
The researchers found that for every increment increase in an individual’s usual score for depressive symptoms, their subsequent weight one month later increased by 45g.
This may seem small but would mean, for example, that in an individual whose depressive symptoms score rose from five to 10 (equal to an increase from ‘mild’ to ‘moderate’ depressive symptoms) it would relate to an average weight gain of 225g (0.225kg).
This effect was only observed in those individuals with overweight (defined as BMI 25-29.9kg/m2) or with obesity (BMI of over 30kg/m2). Individuals with overweight had on average an increase of 52g for each increment point increase from their usual depressive symptoms score and for those with obesity the comparable weight gain was 71g.
The effect was not seen in those individuals with a healthy weight.
First author Dr Julia Mueller from the MRC Epidemiology Unit said: “Overall, this suggests that individuals with overweight or obesity are more vulnerable to weight gain in response to feeling more depressed. Although the weight gain was relatively small, even small weight changes occurring over short periods of time can lead to larger weight changes in the long-term, particularly among those with overweight and obesity.
“People with a high BMI are already at greater risk from other health conditions, so this could potentially lead to a further deterioration in their health. Monitoring and addressing depressive symptoms in individuals with overweight or obesity could help prevent further weight gain and be beneficial to both their mental and physical health.”
The researchers found no evidence that perceived stress or anxiety were related to changes in weight.
Senior author Dr Kirsten Rennie from the MRC Epidemiology Unit said: “Apps on our phones make it possible for people to answer short questions at home more frequently and over extended periods of time, which provides much more information about their wellbeing. This technology could help us understand how changes in mental health influence behaviour among people with overweight or obesity and offer ways to develop timely interventions when needed.”
Although previous studies have suggested that poor mental health is both a cause and consequence of obesity, the research team found no evidence that weight predicted subsequent symptoms of depression.
The research was supported by the Medical Research Council.
Julia Mueller, Amy L. Ahern, Rebecca A. Jones, Stephen J. Sharp, Alan Davies, Arabella Zuckerman, Benjamin I. Perry, Golam M. Khandaker, Emanuella De Lucia Rolfe, Nick J. Wareham, Kirsten L. Rennie. The relationship of within-individual and between-individual variation in mental health with bodyweight: An exploratory longitudinal study. PLOS ONE, 2024; 19 (1): e0295117 DOI: 10.1371/journal.pone.0295117
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.”
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.”
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.
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.”
