#antidepressants — Public Fediverse posts
Live and recent posts from across the Fediverse tagged #antidepressants, aggregated by home.social.
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Psilocybin and standard antidepressants both shift the brain away from negative biases
#psilocybin #antidepressants #depressionresearch #mentalhealth #psychiatry #neuroscience #affectivebias #psychology #health
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Psilocybin and standard antidepressants both shift the brain away from negative biases
#psilocybin #antidepressants #depressionresearch #mentalhealth #psychiatry #neuroscience #affectivebias #psychology #health
-
Psilocybin and standard antidepressants both shift the brain away from negative biases
#psilocybin #antidepressants #depressionresearch #mentalhealth #psychiatry #neuroscience #affectivebias #psychology #health
-
Psilocybin and standard antidepressants both shift the brain away from negative biases
#psilocybin #antidepressants #depressionresearch #mentalhealth #psychiatry #neuroscience #affectivebias #psychology #health
-
Psilocybin and standard antidepressants both shift the brain away from negative biases
#psilocybin #antidepressants #depressionresearch #mentalhealth #psychiatry #neuroscience #affectivebias #psychology #health
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DATE: September 18, 2026 at 02:00PM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Do antidepressants actually alter brain structure? A massive neuroscience study weighs in
A massive brain imaging study has found that subtle differences in the brain structure of people taking antidepressants are largely explained by the severity of their depression, rather than the medications themselves. The research also suggests that the relationship between depression, medication use, and brain anatomy changes across a person’s lifespan, with younger patients showing distinct structural patterns. The findings were published in Molecular Psychiatry.
Major depressive disorder is a severe and persistent form of depression that ranks among the leading causes of disability worldwide. To treat it, doctors frequently prescribe antidepressant medications, yet the exact biological mechanisms by which these drugs alter the brain remain somewhat elusive.
A 2006 theoretical framework proposed that chronic stress and depression might damage brain cells, and that antidepressants could stimulate the growth of new cells in deep brain regions. Supporting this idea, a study covered by PsyPost in 2026 indicated that treatments like duloxetine could help normalize the microscopic structure of brain tissue in depressed patients, whereas those given a placebo saw their brain tissue drift further from healthy levels.
To investigate these effects on a larger scale, researchers needed massive datasets. In prior work, the ENIGMA consortium, an international network of brain researchers, mapped how depression physically alters the brain. For instance, a 2015 study from the group found that people with major depression tend to have a smaller hippocampus, which is a seahorse-shaped structure deep in the brain that plays a primary role in memory and emotion.
Building on this lineage, researchers analyzed data from this same international network to see if antidepressant use actually counteracts these structural brain changes, and whether those effects differ depending on a patient’s age and sex.
“In several of our previous large international ENIGMA studies of depression, we kept seeing an intriguing pattern: the most widespread brain differences were often found in people with depression who were taking antidepressants at the time of their brain scan,” Lianne Schmaal, head of Mood & Anxiety Disorders Research and chair of the ENIGMA MDD consortium at Orygen and the Centre for Youth Mental Health at The University of Melbourne, told PsyPost.
“We wanted to understand that pattern better,” Schmaal explained. “Our earlier studies did not have sufficiently detailed information about how long people had been taking antidepressants or which type they were taking, and they could not tell us whether the differences we observed were related to the medication itself or to the reasons people were taking medication in the first place.”
To answer these questions, Schmaal, lead author Chaira Serrarens, and their colleagues pooled data from 32 different international cohorts, yielding a total sample of 8,696 individuals. This massive group was divided into three categories: 2,076 people with major depressive disorder who were currently taking antidepressants, 1,495 people with the disorder who were not taking antidepressants, and 5,125 healthy controls with no history of the condition.
“One of the strengths of this study is its scale,” Schmaal said. “By bringing together almost 8,700 people from 32 research cohorts around the world and analyzing their brain scans using harmonized methods, we could identify subtle patterns that smaller studies would struggle to detect reliably.”
All participants underwent structural magnetic resonance imaging (MRI), a technique that uses strong magnetic fields and radio waves to create highly detailed, three-dimensional pictures of brain anatomy. The researchers processed these brain scans using automated software to measure three main things. First, they measured the thickness of the cerebral cortex, which is the wrinkled outer layer of the brain responsible for higher-level thinking and processing. Second, they measured the total surface area of this outer layer. Third, they measured the volume of subcortical structures, which are the specialized hubs located deep beneath the outer cortex.
To ensure a fair comparison, the statistical models accounted for the participants’ age, sex, and total head size. The researchers also gathered clinical data from the depressed patients, including the severity of their current symptoms based on standard psychological questionnaires, their number of past depressive episodes, and, for a smaller subset, the specific type of antidepressant they were taking.
The brain scans revealed a complex relationship between age, medication status, and brain structure. For example, younger individuals in the medicated group (those under 50 years old) showed a thinner middle temporal gyrus compared to both the unmedicated patients and the healthy controls. The middle temporal gyrus is a ridge on the side of the brain involved in processing sensory information and emotional cues. In older individuals, this difference between the groups disappeared, with the lines crossing over around age 50.
“One of the most interesting findings was that age seemed to matter,” Schmaal noted. “Some of the differences associated with antidepressant use were most apparent in younger people and were not seen in the same way in older adults. That suggests we should not necessarily assume that the relationship between antidepressant treatment and the brain is the same across the lifespan.”
When looking at the overall effects of medication regardless of age, the researchers found that patients currently taking antidepressants had a smaller hippocampus and a thinner inferior temporal gyrus compared to patients who were not taking the drugs. The researchers ran extra tests to see if these differences were simply due to the medicated patients having a longer or more stubborn history of depression. The structural differences held true even when adjusting for the number of past depressive episodes or whether the patient was currently in remission.
However, the researchers caution that these alterations are not glaringly obvious on an individual level. “The differences were small,” Schmaal told PsyPost. “They are detectable because we were able to combine data from thousands of people, but they are nowhere near large enough to look at an individual person’s brain scan and determine whether they have taken antidepressants, or to use these measures in clinical decision-making.”
The differences between the medicated and unmedicated groups also vanished when the researchers accounted for the severity of current depressive symptoms. The people in the medicated group generally reported feeling worse at the time of the scan than the unmedicated group. This indicates that the structural differences in the temporal lobe and hippocampus might be tied more to how severely depressed a person is currently feeling, rather than being a direct physical result of the medication itself.
“We tried to account for factors such as current symptoms, number of previous depressive episodes and whether someone had recurrent depression, but it is impossible to completely separate medication use from illness severity in this kind of study,” Schmaal explained.
“Despite exploring every possible difference between those taking and those not taking antidepressants, there were only very small differences in very few brain areas which disappeared when taking into account other important differences between these groups,” Roland Zahn, a professor of Mood Disorders and Cognitive Neuroscience at King’s College London’s Centre for Affective Disorders who was not involved in the research, told PsyPost.
Zahn, who also serves as co-programme lead for the MSc Affective Disorders and shares research updates via his lab blog, added: “One important difference between the groups was that people taking antidepressants had much higher levels of depressive symptoms as measured on a gold standard observer-rated scale known to correlate with subtle changes in brain structure from other studies. When accounting for this crucial difference between the groups, the subtle differences in thickness of some of the brain areas in those taking antidepressants disappeared.”
The study also highlighted brain changes that seem driven by the depression diagnosis itself rather than the medication. Younger patients with depression, regardless of whether they took medication, had a smaller thalamus compared to healthy controls. The thalamus acts as a central relay station for sensory and motor signals in the brain. These younger patients also exhibited a thinner cortex in several regions across the frontal, occipital, and parietal lobes when compared to healthy individuals, a gap that was not present in the older participants.
In a smaller exploratory analysis, the researchers looked at specific types of antidepressants, comparing selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), and mirtazapine. They found an age-specific pattern here as well. Older adults (over the age of 40) taking mirtazapine had a thicker rostral anterior cingulate cortex compared to older adults taking SSRIs or SNRIs.
This brain region sits in the frontal lobe and is heavily involved in emotional regulation and reward processing. The authors suggest that mirtazapine might trigger a distinct neuroplastic response in this area, though they also note that mirtazapine is often prescribed for specific symptoms like insomnia or after other drugs have failed, which might influence the results.
“The authors acknowledge that they cannot establish causal relationships and particularly their comparison of different antidepressants is exploratory and based on a much smaller group, based on a single time point,” Zahn noted. “The problem is that there are several factors influencing the reason why someone is taking one antidepressant rather than another and the authors acknowledge, they were not able to account for that as this is a large study with limited clinical background information.”
The researchers also investigated how long patients had been on their current medication, finding no clear association between duration of use and structural changes. “We also did not find evidence that a longer duration of current antidepressant use was associated with greater brain differences,” Schmaal said. “That is reassuring in one sense, but it needs to be interpreted cautiously because detailed information on duration was available for only a subset of participants, and importantly we did not have people’s complete lifetime history of antidepressant exposure.”
The findings are in tension with research covered by PsyPost earlier this year, which found that patients taking the antidepressant escitalopram experienced increases in right hippocampal volume during their treatment. Both studies measure hippocampal volume via MRI in depressed patients taking antidepressants, but that earlier study tracked longitudinal within-person volume changes over weeks of treatment, whereas the new study assessed cross-sectional volume differences between different groups of medicated and unmedicated patients at a single point in time.
However, the ENIGMA study’s immense size adds significant weight to its findings. “This is a very important study in that it was able to merge data from thousands of people and therefore had the ability to detect very small differences,” Zahn said. “It thereby challenged findings from non-human animals as well as findings in smaller studies.”
As with all research, there are a few things to keep in mind. The study relies on a cross-sectional design, meaning the participants were only scanned once. Because the researchers did not track the same individuals over time, they cannot definitively say whether the antidepressants caused the observed brain differences, or if people with certain brain shapes and symptom severities are simply more likely to be prescribed antidepressants.
“The main misinterpretation I would want to avoid is that this study shows antidepressants cause the brain to shrink or cause brain damage. It does not,” Schmaal said. “Imagine taking a photograph of two groups of people today: one group taking antidepressants and another group not taking them. Even if their brains differ on average, that photograph cannot tell you what caused the difference or what their brains looked like before treatment.”
Zahn echoed this caution, emphasizing that brain anatomy is highly variable. “It is also important to note that the structure of our brains constantly changes and the biggest driver of such change is age,” he said. “It is also important to note that large individual differences in brain structure exist with little impact on functioning.”
Because of this limitation, the findings should not alter how patients currently manage their condition. “That is why these results should not be used to make decisions about starting or stopping antidepressants,” Schmaal added. “Those decisions need to be based on the balance of benefits and risks for an individual person and discussed with their treating clinician.”
The researchers also lacked data on the participants’ lifetime history of medication use, meaning some people in the “unmedicated” group might have taken antidepressants in the past. Other factors that shape brain anatomy over a lifespan, such as education, lifestyle habits, or early signs of neurodegenerative diseases in older adults, could not be fully accounted for across all 32 international sites.
“The next critical step is longitudinal research,” Schmaal told PsyPost. “Ideally, we need to follow people from before, or very soon after, they first start an antidepressant and repeatedly assess both their mental health and their brain over several years.”
“The next step as the authors acknowledge is to investigate multiple time points in datasets which contain more detail about other relevant factors, such as other conditions, and response to previous treatments,” Zahn added.
“Ultimately, the goal is not simply to ask whether antidepressants affect the brain,” Schmaal concluded. “We want to understand how they affect the developing and adult brain, whether those effects differ between individuals and across different ages, and whether any brain changes relate to treatment benefit, side effects or longer-term outcomes.”
The study, “Regional brain morphology and current antidepressant use: findings from 32 international cohorts from the ENIGMA major depressive disorder working group,” was authored by Chaira Serrarens, Yara J. Toenders, Elena Pozzi, André Aleman, Nina Alexander, Zeynep Başgöze, Vladimir Belov, Klaus Berger, Katharina Brosch, Robin Bülow, Geraldo Filho Busatto, Liliana P. Capitão, Colm G. Connolly, Baptiste Couvy-Duchesne, Kathryn R. Cullen, Udo Dannlowski, Christopher G. Davey, Greig I. de Zubicaray, Danai Dima, Katharina Dohm, Verena Enneking, Tracy Erwin-Grabner, Ulrika Evermann, Cynthia H. Y. Fu, Paola Fuentes-Claramonte, Beata R. Godlewska, Ali Saffet Gonul, Ian H. Gotlib, Roberto Goya-Maldonado, Hans J. Grabe, Nynke A. Groenewold, Dominik Grotegerd, Oliver Gruber, Tim Hahn, Geoffrey Hall, Ben J. Harrison, Walter Heindel, Marco Hermesdorf, Tiffany C. Ho, Naho Ichikawa, Eri Itai, Neda Jahanshad, Hamidreza Jamalabadi, Alec J. Jamieson, Andreas Jansen, Tilo Kircher, Bonnie Klimes-Dougan, Bernd Krämer, Axel Krug, Thomas M. Lancaster, Elisabeth J. Leehr, Meng Li, David E. J. Linden, Frank MacMaster, Katie L. McMahon, Sarah E. Medland, David M. A. Mehler, Susanne Meinert, Benson Mwangi, Igor Nenadić, Go Okada, Yasumasa Okamoto, Nils Opel, Julia-Katharina Pfarr, Edith Pomarol-Clotet, Maria J. Portella, Ronny Redlich, Liesbeth Reneman, Jonathan Repple, Kai Ringwald, Elena Rodriguez-Cano, Pedro G. P. Rosa, Matthew D. Sacchet, Philipp G. Sämann, Raymond Salvador, Anouk Schrantee, Hotaka Shinzato, Kang Sim, Egle Simulionyte, Jair C. Soares, Dan J. Stein, Frederike Stein, Benjamin Straube, Lachlan T. Strike, Florian Thomas-Odenthal, Sophia I. Thomopoulos, Paul M. Thompson, Marie-Jose van Tol, Paula Usemann, Aslihan Uyar, Nic van der Wee, Steven van der Werff, Yolanda Vives-Gilabert, Henry Völzke, Martin Walter, Sarah Whittle, Katharina Wittfeld, Adrian Wroblewski, Mon-Ju Wu, Tony T. Yang, Giovana B. Zunta-Soares, Dick J. Veltman, Lianne Schmaal, and Laura S. van Velzen.
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #antidepressants #brainstructure #ENIGMA #MDD #hippocampus #neuroimaging #MolecularPsychiatry #depressionresearch #lifespan #neuroplasticity
-
DATE: September 18, 2026 at 02:00PM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Do antidepressants actually alter brain structure? A massive neuroscience study weighs in
A massive brain imaging study has found that subtle differences in the brain structure of people taking antidepressants are largely explained by the severity of their depression, rather than the medications themselves. The research also suggests that the relationship between depression, medication use, and brain anatomy changes across a person’s lifespan, with younger patients showing distinct structural patterns. The findings were published in Molecular Psychiatry.
Major depressive disorder is a severe and persistent form of depression that ranks among the leading causes of disability worldwide. To treat it, doctors frequently prescribe antidepressant medications, yet the exact biological mechanisms by which these drugs alter the brain remain somewhat elusive.
A 2006 theoretical framework proposed that chronic stress and depression might damage brain cells, and that antidepressants could stimulate the growth of new cells in deep brain regions. Supporting this idea, a study covered by PsyPost in 2026 indicated that treatments like duloxetine could help normalize the microscopic structure of brain tissue in depressed patients, whereas those given a placebo saw their brain tissue drift further from healthy levels.
To investigate these effects on a larger scale, researchers needed massive datasets. In prior work, the ENIGMA consortium, an international network of brain researchers, mapped how depression physically alters the brain. For instance, a 2015 study from the group found that people with major depression tend to have a smaller hippocampus, which is a seahorse-shaped structure deep in the brain that plays a primary role in memory and emotion.
Building on this lineage, researchers analyzed data from this same international network to see if antidepressant use actually counteracts these structural brain changes, and whether those effects differ depending on a patient’s age and sex.
“In several of our previous large international ENIGMA studies of depression, we kept seeing an intriguing pattern: the most widespread brain differences were often found in people with depression who were taking antidepressants at the time of their brain scan,” Lianne Schmaal, head of Mood & Anxiety Disorders Research and chair of the ENIGMA MDD consortium at Orygen and the Centre for Youth Mental Health at The University of Melbourne, told PsyPost.
“We wanted to understand that pattern better,” Schmaal explained. “Our earlier studies did not have sufficiently detailed information about how long people had been taking antidepressants or which type they were taking, and they could not tell us whether the differences we observed were related to the medication itself or to the reasons people were taking medication in the first place.”
To answer these questions, Schmaal, lead author Chaira Serrarens, and their colleagues pooled data from 32 different international cohorts, yielding a total sample of 8,696 individuals. This massive group was divided into three categories: 2,076 people with major depressive disorder who were currently taking antidepressants, 1,495 people with the disorder who were not taking antidepressants, and 5,125 healthy controls with no history of the condition.
“One of the strengths of this study is its scale,” Schmaal said. “By bringing together almost 8,700 people from 32 research cohorts around the world and analyzing their brain scans using harmonized methods, we could identify subtle patterns that smaller studies would struggle to detect reliably.”
All participants underwent structural magnetic resonance imaging (MRI), a technique that uses strong magnetic fields and radio waves to create highly detailed, three-dimensional pictures of brain anatomy. The researchers processed these brain scans using automated software to measure three main things. First, they measured the thickness of the cerebral cortex, which is the wrinkled outer layer of the brain responsible for higher-level thinking and processing. Second, they measured the total surface area of this outer layer. Third, they measured the volume of subcortical structures, which are the specialized hubs located deep beneath the outer cortex.
To ensure a fair comparison, the statistical models accounted for the participants’ age, sex, and total head size. The researchers also gathered clinical data from the depressed patients, including the severity of their current symptoms based on standard psychological questionnaires, their number of past depressive episodes, and, for a smaller subset, the specific type of antidepressant they were taking.
The brain scans revealed a complex relationship between age, medication status, and brain structure. For example, younger individuals in the medicated group (those under 50 years old) showed a thinner middle temporal gyrus compared to both the unmedicated patients and the healthy controls. The middle temporal gyrus is a ridge on the side of the brain involved in processing sensory information and emotional cues. In older individuals, this difference between the groups disappeared, with the lines crossing over around age 50.
“One of the most interesting findings was that age seemed to matter,” Schmaal noted. “Some of the differences associated with antidepressant use were most apparent in younger people and were not seen in the same way in older adults. That suggests we should not necessarily assume that the relationship between antidepressant treatment and the brain is the same across the lifespan.”
When looking at the overall effects of medication regardless of age, the researchers found that patients currently taking antidepressants had a smaller hippocampus and a thinner inferior temporal gyrus compared to patients who were not taking the drugs. The researchers ran extra tests to see if these differences were simply due to the medicated patients having a longer or more stubborn history of depression. The structural differences held true even when adjusting for the number of past depressive episodes or whether the patient was currently in remission.
However, the researchers caution that these alterations are not glaringly obvious on an individual level. “The differences were small,” Schmaal told PsyPost. “They are detectable because we were able to combine data from thousands of people, but they are nowhere near large enough to look at an individual person’s brain scan and determine whether they have taken antidepressants, or to use these measures in clinical decision-making.”
The differences between the medicated and unmedicated groups also vanished when the researchers accounted for the severity of current depressive symptoms. The people in the medicated group generally reported feeling worse at the time of the scan than the unmedicated group. This indicates that the structural differences in the temporal lobe and hippocampus might be tied more to how severely depressed a person is currently feeling, rather than being a direct physical result of the medication itself.
“We tried to account for factors such as current symptoms, number of previous depressive episodes and whether someone had recurrent depression, but it is impossible to completely separate medication use from illness severity in this kind of study,” Schmaal explained.
“Despite exploring every possible difference between those taking and those not taking antidepressants, there were only very small differences in very few brain areas which disappeared when taking into account other important differences between these groups,” Roland Zahn, a professor of Mood Disorders and Cognitive Neuroscience at King’s College London’s Centre for Affective Disorders who was not involved in the research, told PsyPost.
Zahn, who also serves as co-programme lead for the MSc Affective Disorders and shares research updates via his lab blog, added: “One important difference between the groups was that people taking antidepressants had much higher levels of depressive symptoms as measured on a gold standard observer-rated scale known to correlate with subtle changes in brain structure from other studies. When accounting for this crucial difference between the groups, the subtle differences in thickness of some of the brain areas in those taking antidepressants disappeared.”
The study also highlighted brain changes that seem driven by the depression diagnosis itself rather than the medication. Younger patients with depression, regardless of whether they took medication, had a smaller thalamus compared to healthy controls. The thalamus acts as a central relay station for sensory and motor signals in the brain. These younger patients also exhibited a thinner cortex in several regions across the frontal, occipital, and parietal lobes when compared to healthy individuals, a gap that was not present in the older participants.
In a smaller exploratory analysis, the researchers looked at specific types of antidepressants, comparing selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), and mirtazapine. They found an age-specific pattern here as well. Older adults (over the age of 40) taking mirtazapine had a thicker rostral anterior cingulate cortex compared to older adults taking SSRIs or SNRIs.
This brain region sits in the frontal lobe and is heavily involved in emotional regulation and reward processing. The authors suggest that mirtazapine might trigger a distinct neuroplastic response in this area, though they also note that mirtazapine is often prescribed for specific symptoms like insomnia or after other drugs have failed, which might influence the results.
“The authors acknowledge that they cannot establish causal relationships and particularly their comparison of different antidepressants is exploratory and based on a much smaller group, based on a single time point,” Zahn noted. “The problem is that there are several factors influencing the reason why someone is taking one antidepressant rather than another and the authors acknowledge, they were not able to account for that as this is a large study with limited clinical background information.”
The researchers also investigated how long patients had been on their current medication, finding no clear association between duration of use and structural changes. “We also did not find evidence that a longer duration of current antidepressant use was associated with greater brain differences,” Schmaal said. “That is reassuring in one sense, but it needs to be interpreted cautiously because detailed information on duration was available for only a subset of participants, and importantly we did not have people’s complete lifetime history of antidepressant exposure.”
The findings are in tension with research covered by PsyPost earlier this year, which found that patients taking the antidepressant escitalopram experienced increases in right hippocampal volume during their treatment. Both studies measure hippocampal volume via MRI in depressed patients taking antidepressants, but that earlier study tracked longitudinal within-person volume changes over weeks of treatment, whereas the new study assessed cross-sectional volume differences between different groups of medicated and unmedicated patients at a single point in time.
However, the ENIGMA study’s immense size adds significant weight to its findings. “This is a very important study in that it was able to merge data from thousands of people and therefore had the ability to detect very small differences,” Zahn said. “It thereby challenged findings from non-human animals as well as findings in smaller studies.”
As with all research, there are a few things to keep in mind. The study relies on a cross-sectional design, meaning the participants were only scanned once. Because the researchers did not track the same individuals over time, they cannot definitively say whether the antidepressants caused the observed brain differences, or if people with certain brain shapes and symptom severities are simply more likely to be prescribed antidepressants.
“The main misinterpretation I would want to avoid is that this study shows antidepressants cause the brain to shrink or cause brain damage. It does not,” Schmaal said. “Imagine taking a photograph of two groups of people today: one group taking antidepressants and another group not taking them. Even if their brains differ on average, that photograph cannot tell you what caused the difference or what their brains looked like before treatment.”
Zahn echoed this caution, emphasizing that brain anatomy is highly variable. “It is also important to note that the structure of our brains constantly changes and the biggest driver of such change is age,” he said. “It is also important to note that large individual differences in brain structure exist with little impact on functioning.”
Because of this limitation, the findings should not alter how patients currently manage their condition. “That is why these results should not be used to make decisions about starting or stopping antidepressants,” Schmaal added. “Those decisions need to be based on the balance of benefits and risks for an individual person and discussed with their treating clinician.”
The researchers also lacked data on the participants’ lifetime history of medication use, meaning some people in the “unmedicated” group might have taken antidepressants in the past. Other factors that shape brain anatomy over a lifespan, such as education, lifestyle habits, or early signs of neurodegenerative diseases in older adults, could not be fully accounted for across all 32 international sites.
“The next critical step is longitudinal research,” Schmaal told PsyPost. “Ideally, we need to follow people from before, or very soon after, they first start an antidepressant and repeatedly assess both their mental health and their brain over several years.”
“The next step as the authors acknowledge is to investigate multiple time points in datasets which contain more detail about other relevant factors, such as other conditions, and response to previous treatments,” Zahn added.
“Ultimately, the goal is not simply to ask whether antidepressants affect the brain,” Schmaal concluded. “We want to understand how they affect the developing and adult brain, whether those effects differ between individuals and across different ages, and whether any brain changes relate to treatment benefit, side effects or longer-term outcomes.”
The study, “Regional brain morphology and current antidepressant use: findings from 32 international cohorts from the ENIGMA major depressive disorder working group,” was authored by Chaira Serrarens, Yara J. Toenders, Elena Pozzi, André Aleman, Nina Alexander, Zeynep Başgöze, Vladimir Belov, Klaus Berger, Katharina Brosch, Robin Bülow, Geraldo Filho Busatto, Liliana P. Capitão, Colm G. Connolly, Baptiste Couvy-Duchesne, Kathryn R. Cullen, Udo Dannlowski, Christopher G. Davey, Greig I. de Zubicaray, Danai Dima, Katharina Dohm, Verena Enneking, Tracy Erwin-Grabner, Ulrika Evermann, Cynthia H. Y. Fu, Paola Fuentes-Claramonte, Beata R. Godlewska, Ali Saffet Gonul, Ian H. Gotlib, Roberto Goya-Maldonado, Hans J. Grabe, Nynke A. Groenewold, Dominik Grotegerd, Oliver Gruber, Tim Hahn, Geoffrey Hall, Ben J. Harrison, Walter Heindel, Marco Hermesdorf, Tiffany C. Ho, Naho Ichikawa, Eri Itai, Neda Jahanshad, Hamidreza Jamalabadi, Alec J. Jamieson, Andreas Jansen, Tilo Kircher, Bonnie Klimes-Dougan, Bernd Krämer, Axel Krug, Thomas M. Lancaster, Elisabeth J. Leehr, Meng Li, David E. J. Linden, Frank MacMaster, Katie L. McMahon, Sarah E. Medland, David M. A. Mehler, Susanne Meinert, Benson Mwangi, Igor Nenadić, Go Okada, Yasumasa Okamoto, Nils Opel, Julia-Katharina Pfarr, Edith Pomarol-Clotet, Maria J. Portella, Ronny Redlich, Liesbeth Reneman, Jonathan Repple, Kai Ringwald, Elena Rodriguez-Cano, Pedro G. P. Rosa, Matthew D. Sacchet, Philipp G. Sämann, Raymond Salvador, Anouk Schrantee, Hotaka Shinzato, Kang Sim, Egle Simulionyte, Jair C. Soares, Dan J. Stein, Frederike Stein, Benjamin Straube, Lachlan T. Strike, Florian Thomas-Odenthal, Sophia I. Thomopoulos, Paul M. Thompson, Marie-Jose van Tol, Paula Usemann, Aslihan Uyar, Nic van der Wee, Steven van der Werff, Yolanda Vives-Gilabert, Henry Völzke, Martin Walter, Sarah Whittle, Katharina Wittfeld, Adrian Wroblewski, Mon-Ju Wu, Tony T. Yang, Giovana B. Zunta-Soares, Dick J. Veltman, Lianne Schmaal, and Laura S. van Velzen.
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #antidepressants #brainstructure #ENIGMA #MDD #hippocampus #neuroimaging #MolecularPsychiatry #depressionresearch #lifespan #neuroplasticity
-
DATE: September 18, 2026 at 02:00PM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Do antidepressants actually alter brain structure? A massive neuroscience study weighs in
A massive brain imaging study has found that subtle differences in the brain structure of people taking antidepressants are largely explained by the severity of their depression, rather than the medications themselves. The research also suggests that the relationship between depression, medication use, and brain anatomy changes across a person’s lifespan, with younger patients showing distinct structural patterns. The findings were published in Molecular Psychiatry.
Major depressive disorder is a severe and persistent form of depression that ranks among the leading causes of disability worldwide. To treat it, doctors frequently prescribe antidepressant medications, yet the exact biological mechanisms by which these drugs alter the brain remain somewhat elusive.
A 2006 theoretical framework proposed that chronic stress and depression might damage brain cells, and that antidepressants could stimulate the growth of new cells in deep brain regions. Supporting this idea, a study covered by PsyPost in 2026 indicated that treatments like duloxetine could help normalize the microscopic structure of brain tissue in depressed patients, whereas those given a placebo saw their brain tissue drift further from healthy levels.
To investigate these effects on a larger scale, researchers needed massive datasets. In prior work, the ENIGMA consortium, an international network of brain researchers, mapped how depression physically alters the brain. For instance, a 2015 study from the group found that people with major depression tend to have a smaller hippocampus, which is a seahorse-shaped structure deep in the brain that plays a primary role in memory and emotion.
Building on this lineage, researchers analyzed data from this same international network to see if antidepressant use actually counteracts these structural brain changes, and whether those effects differ depending on a patient’s age and sex.
“In several of our previous large international ENIGMA studies of depression, we kept seeing an intriguing pattern: the most widespread brain differences were often found in people with depression who were taking antidepressants at the time of their brain scan,” Lianne Schmaal, head of Mood & Anxiety Disorders Research and chair of the ENIGMA MDD consortium at Orygen and the Centre for Youth Mental Health at The University of Melbourne, told PsyPost.
“We wanted to understand that pattern better,” Schmaal explained. “Our earlier studies did not have sufficiently detailed information about how long people had been taking antidepressants or which type they were taking, and they could not tell us whether the differences we observed were related to the medication itself or to the reasons people were taking medication in the first place.”
To answer these questions, Schmaal, lead author Chaira Serrarens, and their colleagues pooled data from 32 different international cohorts, yielding a total sample of 8,696 individuals. This massive group was divided into three categories: 2,076 people with major depressive disorder who were currently taking antidepressants, 1,495 people with the disorder who were not taking antidepressants, and 5,125 healthy controls with no history of the condition.
“One of the strengths of this study is its scale,” Schmaal said. “By bringing together almost 8,700 people from 32 research cohorts around the world and analyzing their brain scans using harmonized methods, we could identify subtle patterns that smaller studies would struggle to detect reliably.”
All participants underwent structural magnetic resonance imaging (MRI), a technique that uses strong magnetic fields and radio waves to create highly detailed, three-dimensional pictures of brain anatomy. The researchers processed these brain scans using automated software to measure three main things. First, they measured the thickness of the cerebral cortex, which is the wrinkled outer layer of the brain responsible for higher-level thinking and processing. Second, they measured the total surface area of this outer layer. Third, they measured the volume of subcortical structures, which are the specialized hubs located deep beneath the outer cortex.
To ensure a fair comparison, the statistical models accounted for the participants’ age, sex, and total head size. The researchers also gathered clinical data from the depressed patients, including the severity of their current symptoms based on standard psychological questionnaires, their number of past depressive episodes, and, for a smaller subset, the specific type of antidepressant they were taking.
The brain scans revealed a complex relationship between age, medication status, and brain structure. For example, younger individuals in the medicated group (those under 50 years old) showed a thinner middle temporal gyrus compared to both the unmedicated patients and the healthy controls. The middle temporal gyrus is a ridge on the side of the brain involved in processing sensory information and emotional cues. In older individuals, this difference between the groups disappeared, with the lines crossing over around age 50.
“One of the most interesting findings was that age seemed to matter,” Schmaal noted. “Some of the differences associated with antidepressant use were most apparent in younger people and were not seen in the same way in older adults. That suggests we should not necessarily assume that the relationship between antidepressant treatment and the brain is the same across the lifespan.”
When looking at the overall effects of medication regardless of age, the researchers found that patients currently taking antidepressants had a smaller hippocampus and a thinner inferior temporal gyrus compared to patients who were not taking the drugs. The researchers ran extra tests to see if these differences were simply due to the medicated patients having a longer or more stubborn history of depression. The structural differences held true even when adjusting for the number of past depressive episodes or whether the patient was currently in remission.
However, the researchers caution that these alterations are not glaringly obvious on an individual level. “The differences were small,” Schmaal told PsyPost. “They are detectable because we were able to combine data from thousands of people, but they are nowhere near large enough to look at an individual person’s brain scan and determine whether they have taken antidepressants, or to use these measures in clinical decision-making.”
The differences between the medicated and unmedicated groups also vanished when the researchers accounted for the severity of current depressive symptoms. The people in the medicated group generally reported feeling worse at the time of the scan than the unmedicated group. This indicates that the structural differences in the temporal lobe and hippocampus might be tied more to how severely depressed a person is currently feeling, rather than being a direct physical result of the medication itself.
“We tried to account for factors such as current symptoms, number of previous depressive episodes and whether someone had recurrent depression, but it is impossible to completely separate medication use from illness severity in this kind of study,” Schmaal explained.
“Despite exploring every possible difference between those taking and those not taking antidepressants, there were only very small differences in very few brain areas which disappeared when taking into account other important differences between these groups,” Roland Zahn, a professor of Mood Disorders and Cognitive Neuroscience at King’s College London’s Centre for Affective Disorders who was not involved in the research, told PsyPost.
Zahn, who also serves as co-programme lead for the MSc Affective Disorders and shares research updates via his lab blog, added: “One important difference between the groups was that people taking antidepressants had much higher levels of depressive symptoms as measured on a gold standard observer-rated scale known to correlate with subtle changes in brain structure from other studies. When accounting for this crucial difference between the groups, the subtle differences in thickness of some of the brain areas in those taking antidepressants disappeared.”
The study also highlighted brain changes that seem driven by the depression diagnosis itself rather than the medication. Younger patients with depression, regardless of whether they took medication, had a smaller thalamus compared to healthy controls. The thalamus acts as a central relay station for sensory and motor signals in the brain. These younger patients also exhibited a thinner cortex in several regions across the frontal, occipital, and parietal lobes when compared to healthy individuals, a gap that was not present in the older participants.
In a smaller exploratory analysis, the researchers looked at specific types of antidepressants, comparing selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), and mirtazapine. They found an age-specific pattern here as well. Older adults (over the age of 40) taking mirtazapine had a thicker rostral anterior cingulate cortex compared to older adults taking SSRIs or SNRIs.
This brain region sits in the frontal lobe and is heavily involved in emotional regulation and reward processing. The authors suggest that mirtazapine might trigger a distinct neuroplastic response in this area, though they also note that mirtazapine is often prescribed for specific symptoms like insomnia or after other drugs have failed, which might influence the results.
“The authors acknowledge that they cannot establish causal relationships and particularly their comparison of different antidepressants is exploratory and based on a much smaller group, based on a single time point,” Zahn noted. “The problem is that there are several factors influencing the reason why someone is taking one antidepressant rather than another and the authors acknowledge, they were not able to account for that as this is a large study with limited clinical background information.”
The researchers also investigated how long patients had been on their current medication, finding no clear association between duration of use and structural changes. “We also did not find evidence that a longer duration of current antidepressant use was associated with greater brain differences,” Schmaal said. “That is reassuring in one sense, but it needs to be interpreted cautiously because detailed information on duration was available for only a subset of participants, and importantly we did not have people’s complete lifetime history of antidepressant exposure.”
The findings are in tension with research covered by PsyPost earlier this year, which found that patients taking the antidepressant escitalopram experienced increases in right hippocampal volume during their treatment. Both studies measure hippocampal volume via MRI in depressed patients taking antidepressants, but that earlier study tracked longitudinal within-person volume changes over weeks of treatment, whereas the new study assessed cross-sectional volume differences between different groups of medicated and unmedicated patients at a single point in time.
However, the ENIGMA study’s immense size adds significant weight to its findings. “This is a very important study in that it was able to merge data from thousands of people and therefore had the ability to detect very small differences,” Zahn said. “It thereby challenged findings from non-human animals as well as findings in smaller studies.”
As with all research, there are a few things to keep in mind. The study relies on a cross-sectional design, meaning the participants were only scanned once. Because the researchers did not track the same individuals over time, they cannot definitively say whether the antidepressants caused the observed brain differences, or if people with certain brain shapes and symptom severities are simply more likely to be prescribed antidepressants.
“The main misinterpretation I would want to avoid is that this study shows antidepressants cause the brain to shrink or cause brain damage. It does not,” Schmaal said. “Imagine taking a photograph of two groups of people today: one group taking antidepressants and another group not taking them. Even if their brains differ on average, that photograph cannot tell you what caused the difference or what their brains looked like before treatment.”
Zahn echoed this caution, emphasizing that brain anatomy is highly variable. “It is also important to note that the structure of our brains constantly changes and the biggest driver of such change is age,” he said. “It is also important to note that large individual differences in brain structure exist with little impact on functioning.”
Because of this limitation, the findings should not alter how patients currently manage their condition. “That is why these results should not be used to make decisions about starting or stopping antidepressants,” Schmaal added. “Those decisions need to be based on the balance of benefits and risks for an individual person and discussed with their treating clinician.”
The researchers also lacked data on the participants’ lifetime history of medication use, meaning some people in the “unmedicated” group might have taken antidepressants in the past. Other factors that shape brain anatomy over a lifespan, such as education, lifestyle habits, or early signs of neurodegenerative diseases in older adults, could not be fully accounted for across all 32 international sites.
“The next critical step is longitudinal research,” Schmaal told PsyPost. “Ideally, we need to follow people from before, or very soon after, they first start an antidepressant and repeatedly assess both their mental health and their brain over several years.”
“The next step as the authors acknowledge is to investigate multiple time points in datasets which contain more detail about other relevant factors, such as other conditions, and response to previous treatments,” Zahn added.
“Ultimately, the goal is not simply to ask whether antidepressants affect the brain,” Schmaal concluded. “We want to understand how they affect the developing and adult brain, whether those effects differ between individuals and across different ages, and whether any brain changes relate to treatment benefit, side effects or longer-term outcomes.”
The study, “Regional brain morphology and current antidepressant use: findings from 32 international cohorts from the ENIGMA major depressive disorder working group,” was authored by Chaira Serrarens, Yara J. Toenders, Elena Pozzi, André Aleman, Nina Alexander, Zeynep Başgöze, Vladimir Belov, Klaus Berger, Katharina Brosch, Robin Bülow, Geraldo Filho Busatto, Liliana P. Capitão, Colm G. Connolly, Baptiste Couvy-Duchesne, Kathryn R. Cullen, Udo Dannlowski, Christopher G. Davey, Greig I. de Zubicaray, Danai Dima, Katharina Dohm, Verena Enneking, Tracy Erwin-Grabner, Ulrika Evermann, Cynthia H. Y. Fu, Paola Fuentes-Claramonte, Beata R. Godlewska, Ali Saffet Gonul, Ian H. Gotlib, Roberto Goya-Maldonado, Hans J. Grabe, Nynke A. Groenewold, Dominik Grotegerd, Oliver Gruber, Tim Hahn, Geoffrey Hall, Ben J. Harrison, Walter Heindel, Marco Hermesdorf, Tiffany C. Ho, Naho Ichikawa, Eri Itai, Neda Jahanshad, Hamidreza Jamalabadi, Alec J. Jamieson, Andreas Jansen, Tilo Kircher, Bonnie Klimes-Dougan, Bernd Krämer, Axel Krug, Thomas M. Lancaster, Elisabeth J. Leehr, Meng Li, David E. J. Linden, Frank MacMaster, Katie L. McMahon, Sarah E. Medland, David M. A. Mehler, Susanne Meinert, Benson Mwangi, Igor Nenadić, Go Okada, Yasumasa Okamoto, Nils Opel, Julia-Katharina Pfarr, Edith Pomarol-Clotet, Maria J. Portella, Ronny Redlich, Liesbeth Reneman, Jonathan Repple, Kai Ringwald, Elena Rodriguez-Cano, Pedro G. P. Rosa, Matthew D. Sacchet, Philipp G. Sämann, Raymond Salvador, Anouk Schrantee, Hotaka Shinzato, Kang Sim, Egle Simulionyte, Jair C. Soares, Dan J. Stein, Frederike Stein, Benjamin Straube, Lachlan T. Strike, Florian Thomas-Odenthal, Sophia I. Thomopoulos, Paul M. Thompson, Marie-Jose van Tol, Paula Usemann, Aslihan Uyar, Nic van der Wee, Steven van der Werff, Yolanda Vives-Gilabert, Henry Völzke, Martin Walter, Sarah Whittle, Katharina Wittfeld, Adrian Wroblewski, Mon-Ju Wu, Tony T. Yang, Giovana B. Zunta-Soares, Dick J. Veltman, Lianne Schmaal, and Laura S. van Velzen.
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #antidepressants #brainstructure #ENIGMA #MDD #hippocampus #neuroimaging #MolecularPsychiatry #depressionresearch #lifespan #neuroplasticity
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DATE: September 16, 2026 at 05:04AM
SOURCE:
NEW YORK TIMES PSYCHOLOGY AND PSYCHOLOGISTS FEEDTITLE: What R.F.K. Jr. Gets Wrong — and Right — About Antidepressants
URL: https://www.nytimes.com/2026/09/16/opinion/ssris-mental-health-depression.html
What’s missing in the national conversation on mental health medication.
URL: https://www.nytimes.com/2026/09/16/opinion/ssris-mental-health-depression.html
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DATE: September 16, 2026 at 05:04AM
SOURCE:
NEW YORK TIMES PSYCHOLOGY AND PSYCHOLOGISTS FEEDTITLE: What R.F.K. Jr. Gets Wrong — and Right — About Antidepressants
URL: https://www.nytimes.com/2026/09/16/opinion/ssris-mental-health-depression.html
What’s missing in the national conversation on mental health medication.
URL: https://www.nytimes.com/2026/09/16/opinion/ssris-mental-health-depression.html
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-
DATE: September 16, 2026 at 05:04AM
SOURCE:
NEW YORK TIMES PSYCHOLOGY AND PSYCHOLOGISTS FEEDTITLE: What R.F.K. Jr. Gets Wrong — and Right — About Antidepressants
URL: https://www.nytimes.com/2026/09/16/opinion/ssris-mental-health-depression.html
What’s missing in the national conversation on mental health medication.
URL: https://www.nytimes.com/2026/09/16/opinion/ssris-mental-health-depression.html
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DATE: September 15, 2026 at 08:00AM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Common antidepressants might help liver cells clear a dangerous type of cholesterol
Common antidepressants might help lower a stubborn, disease-causing type of cholesterol by helping liver cells absorb it from the bloodstream. This unintended side effect could eventually provide a dual-purpose treatment for patients facing both depression and an elevated risk of heart disease. The findings were published in the Journal of Lipid Research.
Lipoprotein(a) is a complex particle in the blood that carries fats and cholesterol throughout the body. It is structurally similar to low-density lipoprotein, commonly known as bad cholesterol. However, it contains an extra protein called apolipoprotein(a) that makes it particularly prone to causing blockages in arteries. High levels of this molecule are genetic and affect at least a fifth of the population of European descent.
Traditional cholesterol-lowering medications, such as statins, fail to reduce these specific particles in the blood. The lack of targeted clinical treatments leaves a major gap in preventing cardiovascular disease for many patients. Researchers are actively trying to understand exactly how the human body clears this molecule from circulation.
Cells absorb molecules from their environment through a process called endocytosis, which involves the cell membrane folding inward to swallow outside material. A specific type of endocytosis called macropinocytosis, or cellular drinking, handles the uptake of this particular cholesterol particle. During cellular drinking, the cell membrane extends outward to gulp large amounts of surrounding fluid and particles.
Researchers from the University of Otago and the University of New South Wales, led by Nikita Deo, Sally P. A. McCormick, and Gregory M. I. Redpath, wanted to map the mechanics of this cellular drinking. They sought to identify exactly what stimulates liver cells to absorb the particles.
The research team initially tested a drug called imipramine on human liver cells grown in a laboratory. Imipramine is an older tricyclic antidepressant that previous laboratory studies identified as a blocker of cellular drinking. The researchers treated the liver cells with the drug overnight and then introduced the cholesterol particles into the fluid bathing the cells.
After a short incubation period, the team measured how much of the substance the cells had absorbed. Instead of blocking the process, the drug caused the cells to absorb nearly three times as much of the cholesterol. The researchers confirmed this was an isolated effect by testing regular bad cholesterol, which the drug did not affect.
This unexpected outcome prompted the team to test newer, more frequently prescribed antidepressants known as selective serotonin reuptake inhibitors. These drugs treat depression by blocking a specific transport protein from pulling serotonin back into cells. This mechanism leaves more of the mood-regulating chemical active in the space outside the cells.
The researchers repeated the cell culture experiment using the common drugs citalopram, sertraline, and fluoxetine. Citalopram increased the cholesterol uptake in the liver cells to a degree similar to imipramine. Sertraline and fluoxetine did not alter the uptake levels. A later test with paroxetine showed it also boosted cellular absorption of the particles.
To figure out how imipramine and citalopram caused this effect, the researchers looked at the outer boundary of the liver cells. The cholesterol molecules must anchor to the cell surface before the cell can swallow them. The team cooled the cells to temporarily halt the swallowing process, added the cholesterol, and used fluorescent tags to measure how much stuck to the outside of the cells.
Both imipramine and citalopram roughly doubled the amount of cholesterol anchored to the cell surface. The drugs did not change the cells’ ability to bind to standard sugar molecules used as a control. This confirmed that the medications specifically enhanced the cell’s grip on this exact type of cholesterol.
Because these drugs increase the availability of serotonin outside the cells, the researchers hypothesized that serotonin itself might be driving the surface binding. They added pure serotonin to the liver cell cultures overnight and tracked the cholesterol particles. The serotonin treatment produced the same outcome as the medications.
The serotonin drastically increased both the amount of cholesterol sticking to the cell surface and the amount the cells eventually absorbed. This suggests the antidepressants enhance cholesterol absorption by increasing local serotonin levels. The serotonin then somehow alters the cell surface to make it more receptive to the passing cholesterol particles.
The team also explored why sertraline failed to enhance the absorption process despite being in the same class of drugs. Some forms of cellular drinking rely on a specific structural protein called dynamin. Dynamin acts like a lasso, pinching off the newly formed internal pouches so they can detach and drop into the cell interior.
Previous research shows sertraline can interfere with dynamin, preventing it from pinching off the pouches. The researchers tested this by tracking a different molecule known to require dynamin for absorption. Sertraline blocked this control molecule from entering the cells. Its interference with dynamin likely prevents it from enhancing cholesterol uptake.
To understand the mechanics of the surface binding, the researchers examined specific anchor proteins on the liver cells. They used fluorescent tags to measure the presence of a receptor known to grab the cholesterol particles. Treating the cells with imipramine or serotonin increased the amount of this receptor on the cell surface.
Citalopram did not increase this specific receptor. However, it did boost the presence of an accessory protein that helps orchestrate the swallowing process. The precise mechanism linking citalopram, serotonin, and this accessory protein requires further mapping.
Finally, the team tracked where the cholesterol went after the cells swallowed it. They used chemical markers to see if the cells sent the particles to internal compartments meant for degradation or compartments meant for recycling material back outside the cell. The cells treated with imipramine and citalopram routed the extra cholesterol into the recycling compartments.
The researchers suspect this recycling process strips the harmful lipid component from the particle before sending the harmless protein portion back into the bloodstream. If true, the overall impact would still be a reduction in cardiovascular risk.
This study relied exclusively on isolated cells in a laboratory. The behavior of these drugs and the cholesterol particles might differ inside a living human body. The liver interacts with many different tissues and chemical signals that a petri dish cannot replicate.
Additionally, the concentration of citalopram used in the main experiments was roughly twice the maximum dose prescribed to human patients. The serotonin levels tested were also much higher than typical biological conditions. While the paroxetine tests matched clinical doses, animal studies or human trials are needed to verify if these medications can safely lower this dangerous cholesterol in patients.
People suffering from depression often exhibit higher levels of this specific cholesterol, elevating their risk of heart attacks and strokes. Identifying an existing, affordable medication that manages both mood and cardiovascular risk could simplify treatment regimens for vulnerable patients.
The study, “Antidepressants stimulate lipoprotein(a) macropinocytosis via serotonin-enhanced cell surface binding,” was authored by Nikita Deo, Halima Siddiqui, Katie Peppercorn, Golnoush Madani, Alexandria Rutherford-Blyth, Malcolm Rutledge, Michael J. A. Williams, Sally P. A. McCormick, and Gregory M. I. Redpath.
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #Lipoprotein(a) #antidepressants #serotonin #macropinocytosis #liverhealth #cardiovascularrisk #cholesterollowering #statinsfail #dualtherapy #lipidresearch
-
DATE: September 15, 2026 at 08:00AM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Common antidepressants might help liver cells clear a dangerous type of cholesterol
Common antidepressants might help lower a stubborn, disease-causing type of cholesterol by helping liver cells absorb it from the bloodstream. This unintended side effect could eventually provide a dual-purpose treatment for patients facing both depression and an elevated risk of heart disease. The findings were published in the Journal of Lipid Research.
Lipoprotein(a) is a complex particle in the blood that carries fats and cholesterol throughout the body. It is structurally similar to low-density lipoprotein, commonly known as bad cholesterol. However, it contains an extra protein called apolipoprotein(a) that makes it particularly prone to causing blockages in arteries. High levels of this molecule are genetic and affect at least a fifth of the population of European descent.
Traditional cholesterol-lowering medications, such as statins, fail to reduce these specific particles in the blood. The lack of targeted clinical treatments leaves a major gap in preventing cardiovascular disease for many patients. Researchers are actively trying to understand exactly how the human body clears this molecule from circulation.
Cells absorb molecules from their environment through a process called endocytosis, which involves the cell membrane folding inward to swallow outside material. A specific type of endocytosis called macropinocytosis, or cellular drinking, handles the uptake of this particular cholesterol particle. During cellular drinking, the cell membrane extends outward to gulp large amounts of surrounding fluid and particles.
Researchers from the University of Otago and the University of New South Wales, led by Nikita Deo, Sally P. A. McCormick, and Gregory M. I. Redpath, wanted to map the mechanics of this cellular drinking. They sought to identify exactly what stimulates liver cells to absorb the particles.
The research team initially tested a drug called imipramine on human liver cells grown in a laboratory. Imipramine is an older tricyclic antidepressant that previous laboratory studies identified as a blocker of cellular drinking. The researchers treated the liver cells with the drug overnight and then introduced the cholesterol particles into the fluid bathing the cells.
After a short incubation period, the team measured how much of the substance the cells had absorbed. Instead of blocking the process, the drug caused the cells to absorb nearly three times as much of the cholesterol. The researchers confirmed this was an isolated effect by testing regular bad cholesterol, which the drug did not affect.
This unexpected outcome prompted the team to test newer, more frequently prescribed antidepressants known as selective serotonin reuptake inhibitors. These drugs treat depression by blocking a specific transport protein from pulling serotonin back into cells. This mechanism leaves more of the mood-regulating chemical active in the space outside the cells.
The researchers repeated the cell culture experiment using the common drugs citalopram, sertraline, and fluoxetine. Citalopram increased the cholesterol uptake in the liver cells to a degree similar to imipramine. Sertraline and fluoxetine did not alter the uptake levels. A later test with paroxetine showed it also boosted cellular absorption of the particles.
To figure out how imipramine and citalopram caused this effect, the researchers looked at the outer boundary of the liver cells. The cholesterol molecules must anchor to the cell surface before the cell can swallow them. The team cooled the cells to temporarily halt the swallowing process, added the cholesterol, and used fluorescent tags to measure how much stuck to the outside of the cells.
Both imipramine and citalopram roughly doubled the amount of cholesterol anchored to the cell surface. The drugs did not change the cells’ ability to bind to standard sugar molecules used as a control. This confirmed that the medications specifically enhanced the cell’s grip on this exact type of cholesterol.
Because these drugs increase the availability of serotonin outside the cells, the researchers hypothesized that serotonin itself might be driving the surface binding. They added pure serotonin to the liver cell cultures overnight and tracked the cholesterol particles. The serotonin treatment produced the same outcome as the medications.
The serotonin drastically increased both the amount of cholesterol sticking to the cell surface and the amount the cells eventually absorbed. This suggests the antidepressants enhance cholesterol absorption by increasing local serotonin levels. The serotonin then somehow alters the cell surface to make it more receptive to the passing cholesterol particles.
The team also explored why sertraline failed to enhance the absorption process despite being in the same class of drugs. Some forms of cellular drinking rely on a specific structural protein called dynamin. Dynamin acts like a lasso, pinching off the newly formed internal pouches so they can detach and drop into the cell interior.
Previous research shows sertraline can interfere with dynamin, preventing it from pinching off the pouches. The researchers tested this by tracking a different molecule known to require dynamin for absorption. Sertraline blocked this control molecule from entering the cells. Its interference with dynamin likely prevents it from enhancing cholesterol uptake.
To understand the mechanics of the surface binding, the researchers examined specific anchor proteins on the liver cells. They used fluorescent tags to measure the presence of a receptor known to grab the cholesterol particles. Treating the cells with imipramine or serotonin increased the amount of this receptor on the cell surface.
Citalopram did not increase this specific receptor. However, it did boost the presence of an accessory protein that helps orchestrate the swallowing process. The precise mechanism linking citalopram, serotonin, and this accessory protein requires further mapping.
Finally, the team tracked where the cholesterol went after the cells swallowed it. They used chemical markers to see if the cells sent the particles to internal compartments meant for degradation or compartments meant for recycling material back outside the cell. The cells treated with imipramine and citalopram routed the extra cholesterol into the recycling compartments.
The researchers suspect this recycling process strips the harmful lipid component from the particle before sending the harmless protein portion back into the bloodstream. If true, the overall impact would still be a reduction in cardiovascular risk.
This study relied exclusively on isolated cells in a laboratory. The behavior of these drugs and the cholesterol particles might differ inside a living human body. The liver interacts with many different tissues and chemical signals that a petri dish cannot replicate.
Additionally, the concentration of citalopram used in the main experiments was roughly twice the maximum dose prescribed to human patients. The serotonin levels tested were also much higher than typical biological conditions. While the paroxetine tests matched clinical doses, animal studies or human trials are needed to verify if these medications can safely lower this dangerous cholesterol in patients.
People suffering from depression often exhibit higher levels of this specific cholesterol, elevating their risk of heart attacks and strokes. Identifying an existing, affordable medication that manages both mood and cardiovascular risk could simplify treatment regimens for vulnerable patients.
The study, “Antidepressants stimulate lipoprotein(a) macropinocytosis via serotonin-enhanced cell surface binding,” was authored by Nikita Deo, Halima Siddiqui, Katie Peppercorn, Golnoush Madani, Alexandria Rutherford-Blyth, Malcolm Rutledge, Michael J. A. Williams, Sally P. A. McCormick, and Gregory M. I. Redpath.
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #Lipoprotein(a) #antidepressants #serotonin #macropinocytosis #liverhealth #cardiovascularrisk #cholesterollowering #statinsfail #dualtherapy #lipidresearch
-
DATE: September 15, 2026 at 08:00AM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Common antidepressants might help liver cells clear a dangerous type of cholesterol
Common antidepressants might help lower a stubborn, disease-causing type of cholesterol by helping liver cells absorb it from the bloodstream. This unintended side effect could eventually provide a dual-purpose treatment for patients facing both depression and an elevated risk of heart disease. The findings were published in the Journal of Lipid Research.
Lipoprotein(a) is a complex particle in the blood that carries fats and cholesterol throughout the body. It is structurally similar to low-density lipoprotein, commonly known as bad cholesterol. However, it contains an extra protein called apolipoprotein(a) that makes it particularly prone to causing blockages in arteries. High levels of this molecule are genetic and affect at least a fifth of the population of European descent.
Traditional cholesterol-lowering medications, such as statins, fail to reduce these specific particles in the blood. The lack of targeted clinical treatments leaves a major gap in preventing cardiovascular disease for many patients. Researchers are actively trying to understand exactly how the human body clears this molecule from circulation.
Cells absorb molecules from their environment through a process called endocytosis, which involves the cell membrane folding inward to swallow outside material. A specific type of endocytosis called macropinocytosis, or cellular drinking, handles the uptake of this particular cholesterol particle. During cellular drinking, the cell membrane extends outward to gulp large amounts of surrounding fluid and particles.
Researchers from the University of Otago and the University of New South Wales, led by Nikita Deo, Sally P. A. McCormick, and Gregory M. I. Redpath, wanted to map the mechanics of this cellular drinking. They sought to identify exactly what stimulates liver cells to absorb the particles.
The research team initially tested a drug called imipramine on human liver cells grown in a laboratory. Imipramine is an older tricyclic antidepressant that previous laboratory studies identified as a blocker of cellular drinking. The researchers treated the liver cells with the drug overnight and then introduced the cholesterol particles into the fluid bathing the cells.
After a short incubation period, the team measured how much of the substance the cells had absorbed. Instead of blocking the process, the drug caused the cells to absorb nearly three times as much of the cholesterol. The researchers confirmed this was an isolated effect by testing regular bad cholesterol, which the drug did not affect.
This unexpected outcome prompted the team to test newer, more frequently prescribed antidepressants known as selective serotonin reuptake inhibitors. These drugs treat depression by blocking a specific transport protein from pulling serotonin back into cells. This mechanism leaves more of the mood-regulating chemical active in the space outside the cells.
The researchers repeated the cell culture experiment using the common drugs citalopram, sertraline, and fluoxetine. Citalopram increased the cholesterol uptake in the liver cells to a degree similar to imipramine. Sertraline and fluoxetine did not alter the uptake levels. A later test with paroxetine showed it also boosted cellular absorption of the particles.
To figure out how imipramine and citalopram caused this effect, the researchers looked at the outer boundary of the liver cells. The cholesterol molecules must anchor to the cell surface before the cell can swallow them. The team cooled the cells to temporarily halt the swallowing process, added the cholesterol, and used fluorescent tags to measure how much stuck to the outside of the cells.
Both imipramine and citalopram roughly doubled the amount of cholesterol anchored to the cell surface. The drugs did not change the cells’ ability to bind to standard sugar molecules used as a control. This confirmed that the medications specifically enhanced the cell’s grip on this exact type of cholesterol.
Because these drugs increase the availability of serotonin outside the cells, the researchers hypothesized that serotonin itself might be driving the surface binding. They added pure serotonin to the liver cell cultures overnight and tracked the cholesterol particles. The serotonin treatment produced the same outcome as the medications.
The serotonin drastically increased both the amount of cholesterol sticking to the cell surface and the amount the cells eventually absorbed. This suggests the antidepressants enhance cholesterol absorption by increasing local serotonin levels. The serotonin then somehow alters the cell surface to make it more receptive to the passing cholesterol particles.
The team also explored why sertraline failed to enhance the absorption process despite being in the same class of drugs. Some forms of cellular drinking rely on a specific structural protein called dynamin. Dynamin acts like a lasso, pinching off the newly formed internal pouches so they can detach and drop into the cell interior.
Previous research shows sertraline can interfere with dynamin, preventing it from pinching off the pouches. The researchers tested this by tracking a different molecule known to require dynamin for absorption. Sertraline blocked this control molecule from entering the cells. Its interference with dynamin likely prevents it from enhancing cholesterol uptake.
To understand the mechanics of the surface binding, the researchers examined specific anchor proteins on the liver cells. They used fluorescent tags to measure the presence of a receptor known to grab the cholesterol particles. Treating the cells with imipramine or serotonin increased the amount of this receptor on the cell surface.
Citalopram did not increase this specific receptor. However, it did boost the presence of an accessory protein that helps orchestrate the swallowing process. The precise mechanism linking citalopram, serotonin, and this accessory protein requires further mapping.
Finally, the team tracked where the cholesterol went after the cells swallowed it. They used chemical markers to see if the cells sent the particles to internal compartments meant for degradation or compartments meant for recycling material back outside the cell. The cells treated with imipramine and citalopram routed the extra cholesterol into the recycling compartments.
The researchers suspect this recycling process strips the harmful lipid component from the particle before sending the harmless protein portion back into the bloodstream. If true, the overall impact would still be a reduction in cardiovascular risk.
This study relied exclusively on isolated cells in a laboratory. The behavior of these drugs and the cholesterol particles might differ inside a living human body. The liver interacts with many different tissues and chemical signals that a petri dish cannot replicate.
Additionally, the concentration of citalopram used in the main experiments was roughly twice the maximum dose prescribed to human patients. The serotonin levels tested were also much higher than typical biological conditions. While the paroxetine tests matched clinical doses, animal studies or human trials are needed to verify if these medications can safely lower this dangerous cholesterol in patients.
People suffering from depression often exhibit higher levels of this specific cholesterol, elevating their risk of heart attacks and strokes. Identifying an existing, affordable medication that manages both mood and cardiovascular risk could simplify treatment regimens for vulnerable patients.
The study, “Antidepressants stimulate lipoprotein(a) macropinocytosis via serotonin-enhanced cell surface binding,” was authored by Nikita Deo, Halima Siddiqui, Katie Peppercorn, Golnoush Madani, Alexandria Rutherford-Blyth, Malcolm Rutledge, Michael J. A. Williams, Sally P. A. McCormick, and Gregory M. I. Redpath.
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #Lipoprotein(a) #antidepressants #serotonin #macropinocytosis #liverhealth #cardiovascularrisk #cholesterollowering #statinsfail #dualtherapy #lipidresearch
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There’s a surprisingly simple reason for England’s high antidepressant use: lots of people need them https://www.theguardian.com/commentisfree/2026/sep/14/england-record-antidepressant-use-gp-guidelines-overprescribing?CMP=share_btn_url
My latest article, for the... [checks notes] Guardian? Doesn't ring a bell, must be some new publication.
-
There’s a surprisingly simple reason for England’s high antidepressant use: lots of people need them https://www.theguardian.com/commentisfree/2026/sep/14/england-record-antidepressant-use-gp-guidelines-overprescribing?CMP=share_btn_url
My latest article, for the... [checks notes] Guardian? Doesn't ring a bell, must be some new publication.
-
There’s a surprisingly simple reason for England’s high antidepressant use: lots of people need them https://www.theguardian.com/commentisfree/2026/sep/14/england-record-antidepressant-use-gp-guidelines-overprescribing?CMP=share_btn_url
My latest article, for the... [checks notes] Guardian? Doesn't ring a bell, must be some new publication.
-
There’s a surprisingly simple reason for England’s high antidepressant use: lots of people need them https://www.theguardian.com/commentisfree/2026/sep/14/england-record-antidepressant-use-gp-guidelines-overprescribing?CMP=share_btn_url
My latest article, for the... [checks notes] Guardian? Doesn't ring a bell, must be some new publication.
-
There’s a surprisingly simple reason for England’s high antidepressant use: lots of people need them https://www.theguardian.com/commentisfree/2026/sep/14/england-record-antidepressant-use-gp-guidelines-overprescribing?CMP=share_btn_url
My latest article, for the... [checks notes] Guardian? Doesn't ring a bell, must be some new publication.
-
DATE: September 14, 2026 at 12:40PM
SOURCE: PSYCHIATRIC TIMESDirect article link at end of text block below.
The September issue of Psychiatric Times is now live! This month, we're debunking the top misleading claims about antidepressants.
Check out our exclusive digital issue now and follow along as articles are shared throughout the month. https://t.co/bZNsDZ960A https://t.co/ANmRCMCcu2
Here are any URLs found in the article text:
Articles can be found by scrolling down the page at Articles can be found at https://www.psychiatrictimes.com/news".
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-
DATE: September 14, 2026 at 12:40PM
SOURCE: PSYCHIATRIC TIMESDirect article link at end of text block below.
The September issue of Psychiatric Times is now live! This month, we're debunking the top misleading claims about antidepressants.
Check out our exclusive digital issue now and follow along as articles are shared throughout the month. https://t.co/bZNsDZ960A https://t.co/ANmRCMCcu2
Here are any URLs found in the article text:
Articles can be found by scrolling down the page at Articles can be found at https://www.psychiatrictimes.com/news".
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #psychotherapist #PsychiatricTimes #Antidepressants #MentalHealthAwareness #DigitalIssue #PsychiatryNews
-
DATE: September 14, 2026 at 12:40PM
SOURCE: PSYCHIATRIC TIMESDirect article link at end of text block below.
The September issue of Psychiatric Times is now live! This month, we're debunking the top misleading claims about antidepressants.
Check out our exclusive digital issue now and follow along as articles are shared throughout the month. https://t.co/bZNsDZ960A https://t.co/ANmRCMCcu2
Here are any URLs found in the article text:
Articles can be found by scrolling down the page at Articles can be found at https://www.psychiatrictimes.com/news".
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #psychotherapist #PsychiatricTimes #Antidepressants #MentalHealthAwareness #DigitalIssue #PsychiatryNews
-
DATE: September 14, 2026 at 12:40PM
SOURCE: PSYCHIATRIC TIMESDirect article link at end of text block below.
The September issue of Psychiatric Times is now live! This month, we're debunking the top misleading claims about antidepressants.
Check out our exclusive digital issue now and follow along as articles are shared throughout the month. https://t.co/bZNsDZ960A https://t.co/ANmRCMCcu2
Here are any URLs found in the article text:
Articles can be found by scrolling down the page at Articles can be found at https://www.psychiatrictimes.com/news".
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #psychotherapist #PsychiatricTimes #Antidepressants #MentalHealthAwareness #DigitalIssue #PsychiatryNews
-
Antidepressants Are Major Drivers of Suicides
The history of the newer antidepressant drugs is a remarkable demonstration of how fraud in the randomised trials…
#NewsBeep #News #Mentalhealth #Antidepressants #antidepressantsandsuicide #AU #Australia #Health #MentalHealth #SSRIs #SSRIsandsuicide
https://www.newsbeep.com/au/890595/ -
Antidepressants Are Major Drivers of Suicides
The history of the newer antidepressant drugs is a remarkable demonstration of how fraud in the randomised trials…
#NewsBeep #News #Mentalhealth #Antidepressants #antidepressantsandsuicide #AU #Australia #Health #MentalHealth #SSRIs #SSRIsandsuicide
https://www.newsbeep.com/au/890595/ -
Antidepressants Are Major Drivers of Suicides
The history of the newer antidepressant drugs is a remarkable demonstration of how fraud in the randomised trials…
#NewsBeep #News #US #USA #UnitedStates #UnitedStatesOfAmerica #Mentalhealth #Antidepressants #antidepressantsandsuicide #Health #MentalHealth #SSRIs #SSRIsandsuicide
https://www.newsbeep.com/us/846429/ -
Antidepressants Are Major Drivers of Suicides
The history of the newer antidepressant drugs is a remarkable demonstration of how fraud in the randomised trials…
#NewsBeep #News #US #USA #UnitedStates #UnitedStatesOfAmerica #Mentalhealth #Antidepressants #antidepressantsandsuicide #Health #MentalHealth #SSRIs #SSRIsandsuicide
https://www.newsbeep.com/us/846429/ -
https://www.europesays.com/ie/686647/ Antidepressants Are Major Drivers of Suicides #antidepressants #AntidepressantsAndSuicide #Éire #Health #IE #Ireland #MentalHealth #MentalHealth #SSRIs #SSRIsAndSuicide
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#MentalWealth #MentalHealth #GutHealth #Serotonin #Depression #Antidepressants #Wellbeing #MentalWellness #HealthAdvice #biohack #biohacking #biohacker #biohackingsecrets #GutHealthMatters #GutHealthy #GutHealthIsEverything #GutHealthDiet #GutHealthTips #GutHealthCoach #GaryBrecka #Tenex https://mastodon.social/@biohackingpathway/117261319742097317
-
DATE: September 8, 2026 at 11:00AM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Antidepressants show wide variation in physical side effects
URL: https://www.psypost.org/antidepressants-show-wide-variation-in-physical-side-effects/
Different antidepressants can have drastically different effects on a patient’s physical health, according to a recent review of medical research. Some medications cause substantial weight gain and increased blood pressure, while others lead to weight loss and lowered heart rates. The findings were published in The Lancet.
Millions of people rely on prescription medications to manage mental health conditions. Up to 17 percent of adults in Europe and North America currently take antidepressants. While these drugs are effective at treating mood disorders, they can also cause unintended bodily changes. These physical side effects are a common reason why people stop taking their prescribed treatments.
Medical guidelines recommend that doctors discuss potential physical changes with patients before starting a prescription. However, it can be difficult for physicians to provide precise comparisons between specific drugs.
Toby Pillinger and Atheeshaan Arumuham of King’s College London led the research team to address this knowledge gap. They worked alongside other international experts, including Orestis Efthimiou of the University of Bern, Oliver D. Howes of King’s College London, and Andrea Cipriani of the University of Oxford. The team wanted to determine exactly how different medications compare in terms of physical side effects. They also wanted to see if factors like age or starting weight influenced these bodily reactions.
To answer these questions, the researchers conducted a network meta-analysis. This type of statistical study pools data from multiple independent trials. It allows researchers to compare treatments that might never have been tested directly against each other in the same room. By linking trials through a common comparator, researchers can estimate how two different drugs would perform head-to-head.
The team gathered data from 151 randomized controlled trials and 17 government regulatory reports. The resulting large study included 58,534 participants. The researchers evaluated 30 different antidepressants prescribed for acute psychiatric treatment, which typically lasted about eight weeks.
The analysis revealed major differences in how these drugs affect body weight. People taking agomelatine experienced the most weight loss, losing an average of about 2.4 kilograms compared to those taking a placebo, an inactive control pill. On the other end of the spectrum, maprotiline and amitriptyline caused the most weight gain, adding up to 1.8 kilograms on average. This created a roughly four-kilogram gap between the highest and lowest weight-altering medications.
The researchers estimated that almost half of the people taking maprotiline or amitriptyline would gain a noticeable amount of weight. Medications that caused the most weight gain were generally those known to block specific histamine and serotonin receptors, which act as chemical docking stations in the brain. Over time, extra weight can elevate a person’s risk for metabolic issues and joint stress.
Cardiovascular changes also varied widely depending on the specific medication. Nortriptyline increased patients’ heart rates by an average of nearly 14 beats per minute. By contrast, fluvoxamine lowered heart rates by about eight beats per minute. This difference amounts to a 21-beat-per-minute gap between the two drugs.
Blood pressure effects showed a similar split among the evaluated medications. Amitriptyline raised systolic blood pressure, which measures the pressure in your arteries when your heart beats, by almost five millimeters of mercury. Nortriptyline lowered the same metric by over six millimeters of mercury. The researchers noted that these cardiovascular shifts could influence a patient’s long-term risk for heart disease, especially if the changes persist over several years.
The medications that increased blood pressure were largely serotonin-noradrenaline reuptake inhibitors, or tricyclic antidepressants. These drug classes share a mechanism that affects the neurotransmitter noradrenaline. This chemical messenger plays a well-documented role in blood pressure regulation.
The researchers also tracked metabolic markers like cholesterol and blood sugar. Paroxetine, duloxetine, desvenlafaxine, and venlafaxine were associated with measurable increases in total cholesterol. Duloxetine was also linked to increased blood glucose levels. These metabolic increases occurred even though the medications themselves generally caused patients to lose body weight.
Some medications also affected liver function tests. Duloxetine, desvenlafaxine, and levomilnacipran caused increases in the concentration of certain liver enzymes. These enzymes are proteins that help the organ filter blood and break down medications. While these enzyme elevations were substantial enough to measure, the researchers noted that the amounts were not high enough to pose an immediate medical threat to most patients.
The team did not find that any of the evaluated antidepressants altered heart rhythm intervals to a problematic degree. The medications also did not have a strong effect on sodium levels, potassium levels, or kidney function markers during the trial periods.
In a separate analysis, the researchers examined how patient characteristics influenced these side effects. They used a statistical technique called meta-regression to look for trends across the different study populations. They found that groups of patients with higher starting body weights experienced larger medication-induced increases in blood pressure and liver enzymes. Populations with a higher average age saw larger medication-induced increases in blood sugar.
Finally, the team wanted to know if experiencing physical side effects was linked to mental health improvements. In patients with severe psychiatric conditions like schizophrenia, past research has shown a correlation between metabolic disturbances and improved symptoms. To test this concept in depression, the researchers looked specifically at trials involving patients with major depressive disorder.
The researchers compared the change in depressive symptoms against changes in weight, cholesterol, and blood sugar across the studies. They did not find a correlation between improved mental health and metabolic side effects. This suggests that patients do not need to experience physical changes to get the mental health benefits of the medication.
A primary limitation of this research is the short duration of the included trials. Most studies lasted only eight weeks, meaning the long-term physical effects of these medications remain unconfirmed by this specific analysis. Some cardiovascular shifts might fade over time, while other metabolic changes could worsen over a period of years.
The trials also mostly included younger, relatively healthy individuals taking only one medication. This focus might obscure side effects that occur more frequently in older adults or people taking multiple drugs at once. Real-world observational data suggests that certain antidepressants might increase the risk of low sodium or heart rhythm problems in older populations. The researchers suggest that doctors should consider both clinical trial data and real-world observations when prescribing medications to older or medically vulnerable patients.
The study, “The effects of antidepressants on cardiometabolic and other physiological parameters: a systematic review and network meta-analysis,” was authored by Toby Pillinger, Atheeshaan Arumuham, Robert A McCutcheon, Enrico D’Ambrosio, Georgios Basdanis, Marco Branco, Richard Carr, Valeria Finelli, Toshi A Furukawa, Siobhan Gee, Adrian Heald, Sameer Jauhar, Zihan Ma, Valentina Mancini, Calum Moulton, Georgia Salanti, David M Taylor, Anneka Tomlinson, Allan H Young, Orestis Efthimiou, Oliver D Howes, and Andrea Cipriani.
URL: https://www.psypost.org/antidepressants-show-wide-variation-in-physical-side-effects/
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #Antidepressants #SideEffects #Cardiometabolic #DepressionTreatment #WeightChange #BloodPressure #Cholesterol #MetabolicHealth #NetworkMetaAnalysis #TheLancet
-
DATE: September 8, 2026 at 11:00AM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Antidepressants show wide variation in physical side effects
URL: https://www.psypost.org/antidepressants-show-wide-variation-in-physical-side-effects/
Different antidepressants can have drastically different effects on a patient’s physical health, according to a recent review of medical research. Some medications cause substantial weight gain and increased blood pressure, while others lead to weight loss and lowered heart rates. The findings were published in The Lancet.
Millions of people rely on prescription medications to manage mental health conditions. Up to 17 percent of adults in Europe and North America currently take antidepressants. While these drugs are effective at treating mood disorders, they can also cause unintended bodily changes. These physical side effects are a common reason why people stop taking their prescribed treatments.
Medical guidelines recommend that doctors discuss potential physical changes with patients before starting a prescription. However, it can be difficult for physicians to provide precise comparisons between specific drugs.
Toby Pillinger and Atheeshaan Arumuham of King’s College London led the research team to address this knowledge gap. They worked alongside other international experts, including Orestis Efthimiou of the University of Bern, Oliver D. Howes of King’s College London, and Andrea Cipriani of the University of Oxford. The team wanted to determine exactly how different medications compare in terms of physical side effects. They also wanted to see if factors like age or starting weight influenced these bodily reactions.
To answer these questions, the researchers conducted a network meta-analysis. This type of statistical study pools data from multiple independent trials. It allows researchers to compare treatments that might never have been tested directly against each other in the same room. By linking trials through a common comparator, researchers can estimate how two different drugs would perform head-to-head.
The team gathered data from 151 randomized controlled trials and 17 government regulatory reports. The resulting large study included 58,534 participants. The researchers evaluated 30 different antidepressants prescribed for acute psychiatric treatment, which typically lasted about eight weeks.
The analysis revealed major differences in how these drugs affect body weight. People taking agomelatine experienced the most weight loss, losing an average of about 2.4 kilograms compared to those taking a placebo, an inactive control pill. On the other end of the spectrum, maprotiline and amitriptyline caused the most weight gain, adding up to 1.8 kilograms on average. This created a roughly four-kilogram gap between the highest and lowest weight-altering medications.
The researchers estimated that almost half of the people taking maprotiline or amitriptyline would gain a noticeable amount of weight. Medications that caused the most weight gain were generally those known to block specific histamine and serotonin receptors, which act as chemical docking stations in the brain. Over time, extra weight can elevate a person’s risk for metabolic issues and joint stress.
Cardiovascular changes also varied widely depending on the specific medication. Nortriptyline increased patients’ heart rates by an average of nearly 14 beats per minute. By contrast, fluvoxamine lowered heart rates by about eight beats per minute. This difference amounts to a 21-beat-per-minute gap between the two drugs.
Blood pressure effects showed a similar split among the evaluated medications. Amitriptyline raised systolic blood pressure, which measures the pressure in your arteries when your heart beats, by almost five millimeters of mercury. Nortriptyline lowered the same metric by over six millimeters of mercury. The researchers noted that these cardiovascular shifts could influence a patient’s long-term risk for heart disease, especially if the changes persist over several years.
The medications that increased blood pressure were largely serotonin-noradrenaline reuptake inhibitors, or tricyclic antidepressants. These drug classes share a mechanism that affects the neurotransmitter noradrenaline. This chemical messenger plays a well-documented role in blood pressure regulation.
The researchers also tracked metabolic markers like cholesterol and blood sugar. Paroxetine, duloxetine, desvenlafaxine, and venlafaxine were associated with measurable increases in total cholesterol. Duloxetine was also linked to increased blood glucose levels. These metabolic increases occurred even though the medications themselves generally caused patients to lose body weight.
Some medications also affected liver function tests. Duloxetine, desvenlafaxine, and levomilnacipran caused increases in the concentration of certain liver enzymes. These enzymes are proteins that help the organ filter blood and break down medications. While these enzyme elevations were substantial enough to measure, the researchers noted that the amounts were not high enough to pose an immediate medical threat to most patients.
The team did not find that any of the evaluated antidepressants altered heart rhythm intervals to a problematic degree. The medications also did not have a strong effect on sodium levels, potassium levels, or kidney function markers during the trial periods.
In a separate analysis, the researchers examined how patient characteristics influenced these side effects. They used a statistical technique called meta-regression to look for trends across the different study populations. They found that groups of patients with higher starting body weights experienced larger medication-induced increases in blood pressure and liver enzymes. Populations with a higher average age saw larger medication-induced increases in blood sugar.
Finally, the team wanted to know if experiencing physical side effects was linked to mental health improvements. In patients with severe psychiatric conditions like schizophrenia, past research has shown a correlation between metabolic disturbances and improved symptoms. To test this concept in depression, the researchers looked specifically at trials involving patients with major depressive disorder.
The researchers compared the change in depressive symptoms against changes in weight, cholesterol, and blood sugar across the studies. They did not find a correlation between improved mental health and metabolic side effects. This suggests that patients do not need to experience physical changes to get the mental health benefits of the medication.
A primary limitation of this research is the short duration of the included trials. Most studies lasted only eight weeks, meaning the long-term physical effects of these medications remain unconfirmed by this specific analysis. Some cardiovascular shifts might fade over time, while other metabolic changes could worsen over a period of years.
The trials also mostly included younger, relatively healthy individuals taking only one medication. This focus might obscure side effects that occur more frequently in older adults or people taking multiple drugs at once. Real-world observational data suggests that certain antidepressants might increase the risk of low sodium or heart rhythm problems in older populations. The researchers suggest that doctors should consider both clinical trial data and real-world observations when prescribing medications to older or medically vulnerable patients.
The study, “The effects of antidepressants on cardiometabolic and other physiological parameters: a systematic review and network meta-analysis,” was authored by Toby Pillinger, Atheeshaan Arumuham, Robert A McCutcheon, Enrico D’Ambrosio, Georgios Basdanis, Marco Branco, Richard Carr, Valeria Finelli, Toshi A Furukawa, Siobhan Gee, Adrian Heald, Sameer Jauhar, Zihan Ma, Valentina Mancini, Calum Moulton, Georgia Salanti, David M Taylor, Anneka Tomlinson, Allan H Young, Orestis Efthimiou, Oliver D Howes, and Andrea Cipriani.
URL: https://www.psypost.org/antidepressants-show-wide-variation-in-physical-side-effects/
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #Antidepressants #SideEffects #Cardiometabolic #DepressionTreatment #WeightChange #BloodPressure #Cholesterol #MetabolicHealth #NetworkMetaAnalysis #TheLancet
-
DATE: September 8, 2026 at 11:00AM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Antidepressants show wide variation in physical side effects
URL: https://www.psypost.org/antidepressants-show-wide-variation-in-physical-side-effects/
Different antidepressants can have drastically different effects on a patient’s physical health, according to a recent review of medical research. Some medications cause substantial weight gain and increased blood pressure, while others lead to weight loss and lowered heart rates. The findings were published in The Lancet.
Millions of people rely on prescription medications to manage mental health conditions. Up to 17 percent of adults in Europe and North America currently take antidepressants. While these drugs are effective at treating mood disorders, they can also cause unintended bodily changes. These physical side effects are a common reason why people stop taking their prescribed treatments.
Medical guidelines recommend that doctors discuss potential physical changes with patients before starting a prescription. However, it can be difficult for physicians to provide precise comparisons between specific drugs.
Toby Pillinger and Atheeshaan Arumuham of King’s College London led the research team to address this knowledge gap. They worked alongside other international experts, including Orestis Efthimiou of the University of Bern, Oliver D. Howes of King’s College London, and Andrea Cipriani of the University of Oxford. The team wanted to determine exactly how different medications compare in terms of physical side effects. They also wanted to see if factors like age or starting weight influenced these bodily reactions.
To answer these questions, the researchers conducted a network meta-analysis. This type of statistical study pools data from multiple independent trials. It allows researchers to compare treatments that might never have been tested directly against each other in the same room. By linking trials through a common comparator, researchers can estimate how two different drugs would perform head-to-head.
The team gathered data from 151 randomized controlled trials and 17 government regulatory reports. The resulting large study included 58,534 participants. The researchers evaluated 30 different antidepressants prescribed for acute psychiatric treatment, which typically lasted about eight weeks.
The analysis revealed major differences in how these drugs affect body weight. People taking agomelatine experienced the most weight loss, losing an average of about 2.4 kilograms compared to those taking a placebo, an inactive control pill. On the other end of the spectrum, maprotiline and amitriptyline caused the most weight gain, adding up to 1.8 kilograms on average. This created a roughly four-kilogram gap between the highest and lowest weight-altering medications.
The researchers estimated that almost half of the people taking maprotiline or amitriptyline would gain a noticeable amount of weight. Medications that caused the most weight gain were generally those known to block specific histamine and serotonin receptors, which act as chemical docking stations in the brain. Over time, extra weight can elevate a person’s risk for metabolic issues and joint stress.
Cardiovascular changes also varied widely depending on the specific medication. Nortriptyline increased patients’ heart rates by an average of nearly 14 beats per minute. By contrast, fluvoxamine lowered heart rates by about eight beats per minute. This difference amounts to a 21-beat-per-minute gap between the two drugs.
Blood pressure effects showed a similar split among the evaluated medications. Amitriptyline raised systolic blood pressure, which measures the pressure in your arteries when your heart beats, by almost five millimeters of mercury. Nortriptyline lowered the same metric by over six millimeters of mercury. The researchers noted that these cardiovascular shifts could influence a patient’s long-term risk for heart disease, especially if the changes persist over several years.
The medications that increased blood pressure were largely serotonin-noradrenaline reuptake inhibitors, or tricyclic antidepressants. These drug classes share a mechanism that affects the neurotransmitter noradrenaline. This chemical messenger plays a well-documented role in blood pressure regulation.
The researchers also tracked metabolic markers like cholesterol and blood sugar. Paroxetine, duloxetine, desvenlafaxine, and venlafaxine were associated with measurable increases in total cholesterol. Duloxetine was also linked to increased blood glucose levels. These metabolic increases occurred even though the medications themselves generally caused patients to lose body weight.
Some medications also affected liver function tests. Duloxetine, desvenlafaxine, and levomilnacipran caused increases in the concentration of certain liver enzymes. These enzymes are proteins that help the organ filter blood and break down medications. While these enzyme elevations were substantial enough to measure, the researchers noted that the amounts were not high enough to pose an immediate medical threat to most patients.
The team did not find that any of the evaluated antidepressants altered heart rhythm intervals to a problematic degree. The medications also did not have a strong effect on sodium levels, potassium levels, or kidney function markers during the trial periods.
In a separate analysis, the researchers examined how patient characteristics influenced these side effects. They used a statistical technique called meta-regression to look for trends across the different study populations. They found that groups of patients with higher starting body weights experienced larger medication-induced increases in blood pressure and liver enzymes. Populations with a higher average age saw larger medication-induced increases in blood sugar.
Finally, the team wanted to know if experiencing physical side effects was linked to mental health improvements. In patients with severe psychiatric conditions like schizophrenia, past research has shown a correlation between metabolic disturbances and improved symptoms. To test this concept in depression, the researchers looked specifically at trials involving patients with major depressive disorder.
The researchers compared the change in depressive symptoms against changes in weight, cholesterol, and blood sugar across the studies. They did not find a correlation between improved mental health and metabolic side effects. This suggests that patients do not need to experience physical changes to get the mental health benefits of the medication.
A primary limitation of this research is the short duration of the included trials. Most studies lasted only eight weeks, meaning the long-term physical effects of these medications remain unconfirmed by this specific analysis. Some cardiovascular shifts might fade over time, while other metabolic changes could worsen over a period of years.
The trials also mostly included younger, relatively healthy individuals taking only one medication. This focus might obscure side effects that occur more frequently in older adults or people taking multiple drugs at once. Real-world observational data suggests that certain antidepressants might increase the risk of low sodium or heart rhythm problems in older populations. The researchers suggest that doctors should consider both clinical trial data and real-world observations when prescribing medications to older or medically vulnerable patients.
The study, “The effects of antidepressants on cardiometabolic and other physiological parameters: a systematic review and network meta-analysis,” was authored by Toby Pillinger, Atheeshaan Arumuham, Robert A McCutcheon, Enrico D’Ambrosio, Georgios Basdanis, Marco Branco, Richard Carr, Valeria Finelli, Toshi A Furukawa, Siobhan Gee, Adrian Heald, Sameer Jauhar, Zihan Ma, Valentina Mancini, Calum Moulton, Georgia Salanti, David M Taylor, Anneka Tomlinson, Allan H Young, Orestis Efthimiou, Oliver D Howes, and Andrea Cipriani.
URL: https://www.psypost.org/antidepressants-show-wide-variation-in-physical-side-effects/
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #Antidepressants #SideEffects #Cardiometabolic #DepressionTreatment #WeightChange #BloodPressure #Cholesterol #MetabolicHealth #NetworkMetaAnalysis #TheLancet
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@hedders I was reminded to revisit #Suede on listening to their 2025 release #antidepressants. Very good stuff 😎👍
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@hedders I was reminded to revisit #Suede on listening to their 2025 release #antidepressants. Very good stuff 😎👍
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@hedders I was reminded to revisit #Suede on listening to their 2025 release #antidepressants. Very good stuff 😎👍
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@hedders I was reminded to revisit #Suede on listening to their 2025 release #antidepressants. Very good stuff 😎👍
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@hedders I was reminded to revisit #Suede on listening to their 2025 release #antidepressants. Very good stuff 😎👍
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When Medical Science Refuses to Correct Itself https://www.byteseu.com/2318171/ #antidepressants #Science #STAR*D
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Doctors are finally learning to manage antidepressant withdrawal
Comments: https://news.ycombinator.com/item?id=49472090
#HackerNews #antidepressants #mentalhealth #withdrawal #depression #treatment
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Doctors are finally learning to manage antidepressant withdrawal
Comments: https://news.ycombinator.com/item?id=49472090
#HackerNews #antidepressants #mentalhealth #withdrawal #depression #treatment
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Doctors are finally learning to manage antidepressant withdrawal
Comments: https://news.ycombinator.com/item?id=49472090
#HackerNews #antidepressants #mentalhealth #withdrawal #depression #treatment
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Doctors are finally learning to manage antidepressant withdrawal
Comments: https://news.ycombinator.com/item?id=49472090
#HackerNews #antidepressants #mentalhealth #withdrawal #depression #treatment
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Doctors are finally learning to manage antidepressant withdrawal
Comments: https://news.ycombinator.com/item?id=49472090
#HackerNews #antidepressants #mentalhealth #withdrawal #depression #treatment
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Antidepressants Can Change Peaceful Citizens into Killers
One of the best guarded secrets in psychiatry is that antidepressants increase the risk of violence, including suicide…
#NewsBeep #News #Medication #Akathisia #akathisiaandsuicide #Antidepressants #antidepressantsandhomicide #antidepressantsandsuicide #AU #Australia #Health
https://www.newsbeep.com/au/856699/ -
Antidepressants Can Change Peaceful Citizens into Killers
One of the best guarded secrets in psychiatry is that antidepressants increase the risk of violence, including suicide…
#NewsBeep #News #Medication #Akathisia #akathisiaandsuicide #Antidepressants #antidepressantsandhomicide #antidepressantsandsuicide #AU #Australia #Health
https://www.newsbeep.com/au/856699/ -
Antidepressants Can Change Peaceful Citizens into Killers
One of the best guarded secrets in psychiatry is that antidepressants increase the risk of violence, including suicide…
#NewsBeep #News #Medication #akathisia #akathisiaandsuicide #Antidepressants #antidepressantsandhomicide #antidepressantsandsuicide #Health #UK #UnitedKingdom
https://www.newsbeep.com/uk/739294/ -
https://www.europesays.com/ie/639228/ Antidepressants Can Change Peaceful Citizens into Killers #akathisia #AkathisiaAndSuicide #antidepressants #AntidepressantsAndHomicide #AntidepressantsAndSuicide #Éire #Health #IE #Ireland #Medication
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Do people realize the latest evidence still suggests #exercise is about as effective as #psychotherapy and #antidepressants for treating #depression (and may result in fewer adverse events)?
Recent review:: https://doi.org/10.1002/14651858.CD004366.pub7
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Do people realize the latest evidence still suggests #exercise is about as effective as #psychotherapy and #antidepressants for treating #depression (and may result in fewer adverse events)?
Recent review:: https://doi.org/10.1002/14651858.CD004366.pub7