Approximately one in seven patients who discontinued their use of antidepressants experienced discontinuation symptoms, according to a wide-ranging analysis published in The Lancet Psychiatry. In arriving at this figure, the researchers accounted for a high frequency of anticipated discontinuation symptoms.
The emergence of adverse symptoms after antidepressant cessation has been described as far back as 1959, but was mostly neglected until the late 1990s. Today, the existence of antidepressant discontinuation symptoms is widely accepted, with transnational guidelines suggesting safe tapering. They can be highly variable and non-specific, with the most frequently reported symptoms being dizziness, headache, nausea, insomnia, and irritability. It has been reported that symptoms typically occur within a few days and are usually transient, but can last up to several weeks or months.
The incidence and severity of symptoms remained controversial however, with estimates ranging up to a majority (56%) of patients experiencing them, half of them severe. Previous reviews have been criticised for bias, and medical opinions are polarised on the subject.
The researchers reviewed 79 studies involving more than 21 000 participants, and found that about one-third of patients experienced symptoms such as headaches, nausea, insomnia, and irritability after accounting for patient expectations. Even in patients taking placebo, 17% experienced symptoms – suggesting that this is attributable to patient expectations about the adverse effects of stopping the drug.
After taking this into account, roughly one in seven individuals had antidepressant discontinuation symptoms. Neither tapering nor abrupt cessation of the drugs made no difference in the proportion of people who experienced discontinuation symptoms.
In addition, about 1 in 35 people experienced severe discontinuation symptoms. Desvenlafaxine, venlafaxine, imipramine, and escitalopram were associated with higher frequencies of discontinuation symptoms, and imipramine, paroxetine, and either desvenlafaxine or venlafaxine were associated with higher symptom severity. The authors cautioned that there was substantial heterogeneity of results.
Evidence suggests serotonin-boosting actions relieve depression by restoring normal communication and connections in the brain
Photo by Sydney Sims on Unsplash
Researchers at the University of Colorado Anschutz Medical Campus have established a new framework for understanding how classic antidepressants work in treating major depressive disorder (MDD), reemphasising their importance and aiming to reframe clinical conversation around their role in treatment.
The nature of the dysfunction at the root of MDD has been under investigation for decades. Classic antidepressants, such as SSRIs (selective serotonin reuptake inhibitors, such as fluoxetine) cause an elevation in serotonin levels, a key neurotransmitter. This observation led to the idea that antidepressants work because they restore a chemical imbalance, such as a lack of serotonin.
But subsequent years of research showed no significant decrease in serotonin in people with depression. While experts have moved away from this hypothesis due to lack of concrete evidence, this has led to a shift in public opinion on the effectiveness of these medications.
Antidepressants, such as SSRIs and serotonin and norepinephrine reuptake inhibitors (SNRIs), are still effective in alleviating depressive episodes in many patients, however. In a paper published in Molecular Psychiatry, researchers outline a new framework for understanding how antidepressants are efficacious in treating MDD. This framework helps clarify how antidepressants like SSRIs can still be helpful, even if MDD isn’t caused by a lack of serotonin.
Evidence points to a communication problem
“The best evidence of changes in the brain in people suffering from MDD is that some brain regions are not communicating with each other normally,” said Scott Thompson, PhD, professor in the Department of Psychiatry and senior author. “When the parts of the brain responsible for reward, happiness, mood, self-esteem, even problem-solving in some cases, are not communicating with each other properly, then they can’t do their jobs properly,” Thompson said.
“There is good evidence that antidepressants that increase serotonin, like SSRIs, all work by restoring the strength of the connections between these regions of the brain. So do novel therapeutics such as esketamine and psychedelics. This form of neuroplasticity helps release brain circuits from being ‘stuck’ in a pathological state, ultimately leading to a restoration of healthy brain function,” Thompson said.
Thompson and colleagues liken this theory to a car running off the road and getting stuck in a ditch, requiring the help of a tow truck to pull the car out of its stuck state, allowing it to move freely down the road again. Researchers are hoping healthcare providers will use their examples to bolster conversations with apprehensive patients about these treatments, helping them better understand their condition and how to treat it.
Study aims to reshape the conversation
“We are hoping this framework provides clinicians new ways to communicate the way these treatments work in combating MDD,” said C. Neill Epperson, MD, co-author of the paper and professor of the Department of Psychiatry at the CU School of Medicine.
“Much of the public conversation around the effectiveness of antidepressants, and the role serotonin plays in diagnosis and treatment, has been negative and largely dangerous,” Epperson said. “While MDD is a heterogenous disorder with no one-fits-all solution, it is important to emphasise that if treatments or medications are working for you, then they are lifesaving. Understanding how these medications promote neuroplasticity can help strengthen that message.”
Rapid-acting antidepressants, including ketamine, scopolamine and psilocybin, have been found to have immediate and lasting positive effects on mood in patients with major depressive disorder but how these effects arise is unknown. New research led by the University of Bristol and published in Science Translational Medicine explored their neuropsychological effects and found that all three of these drugs can modulate affective biases associated with learning and memory.
Negative affective biases are a core feature of major depressive disorder. Affective biases occur when emotions alter how the brain processes information and negative affective biases are thought to contribute to the development and continuation of depressed mood.
The research team used an affective bias test, based on an associative learning task, to investigate the effects of rapid-acting antidepressants (RAADs) in rats.
They found that all the treatments were able to reduce negative affective biases associated with past experiences but there were additional characteristics of the dissociative anaesthetic, ketamine, and the serotonergic psychedelic, investigational COMP360 psilocybin (Compass Pathways’ proprietary formulation of synthetic psilocybin), which could explain why the effects of a single treatment can be long-lasting.
The findings suggest that these sustained effects are due to adaptive changes in the brain circuits which control affective biases, and these can influence how past experiences are remembered.
The effects at low doses were very specific to affective bias modulation and were localised to the prefrontal cortex of the brain, a region known to play an important role in mood.
Emma Robinson, Professor of Psychopharmacology in the School of Physiology, Pharmacology & Neuroscience at Bristol, and lead author, said: “Using a behavioural task we showed that drugs that are believed to have rapid and sustained benefits in depressed patients, specifically modulate affective biases associated with past experiences, something which we think is really important for understanding why they can improve a patient’s mood so quickly.
“We also found differences in how ketamine, scopolamine and COMP360 psilocybin interact with these neuropsychological mechanisms which may explain why the effects of a single treatment in human patients can be long-lasting, days (ketamine) to months (psilocybin).
“By using an animal model, we have been able to investigate these important interactions with learning and memory processes and neural plasticity and propose a two-stage model that may explain the effects we observe.”
In the task, each animal learnt to associate a specific digging material with a food reward under either treatment or control conditions.
The treatment condition is designed to generate a change in the animal’s affective state and a choice test is used to quantify the affective bias this generates.
Acute treatment with the RAADs ketamine, scopolamine, or psilocybin prevented the retrieval of the negative affective bias induced in this model.
However, the most exciting finding was at 24 hours after treatment when low, but not high, doses of ketamine and psilocybin led to a re-learning effect where the negatively biased memory was retrieved with a more positive affective valence.
Only psilocybin, but not ketamine or scopolamine treatment also positively biased new experiences.
Exploring in more detail the re-learning effects of ketamine in the studies, the researchers found they were protein synthesis-dependent, localised to the medial prefrontal cortex and could be modulated by cue-reactivation, consistent with their predictions of experience-dependent neural plasticity.
The study’s findings propose a neuropsychological mechanism that may explain both the immediate and sustained effects of RAADs, potentially linking their effects on neural plasticity with mood.
A cheap and widely available prescription drug can improve symptoms of irritable bowel syndrome in patients seen in GP surgeries, according to research findings published in The Lancet and presented today at UEG Week 2023.
Amitriptyline, a tricyclic which is commonly used at low doses for a range of health concerns, has been found to improve irritable bowel syndrome (IBS) symptoms too, according to the results of the ATLANTIS trial.
The study was conducted in primary care, with GPs prescribing the drug and patients managing their own dose based on the severity of their symptoms, using an adjustment document designed for the trial. Most people with IBS are seen and managed in primary care by their GP, which means that the results of this trial are likely to be applicable to many people with the condition.
Led by researchers at the Universities of Leeds, Southampton, and Bristol and funded by the National Institute for Health and Care Research (NIHR), the study showed that patients taking amitriptyline were almost twice as likely to report an overall improvement in symptoms as those taking a placebo.
Now the trial team is recommending that GPs support their patients with IBS to use amitriptyline to manage their symptoms – and has made the dose adjustment document available for clinicians and patients.
Co-chief Investigator Alexander Ford, Professor of Gastroenterology in the University of Leeds’s School of Medicine, said: “Amitriptyline is an effective treatment for IBS and is safe and well tolerated. This new rigorously conducted research indicates that general practitioners should support patients in primary care to try low-dose amitriptyline if their IBS symptoms haven’t improved with recommended first-line treatments.”
Most treatments for IBS, which affects around 1 in 20 people, only have a modest effect and people often have ongoing troublesome symptoms.
Amitriptyline was originally used at high doses to treat depression, but is now superseded by newer and better antidepressants.
Previous small trials of low-dose tricyclic antidepressants for IBS suggested a possible benefit in patients seen in hospital clinics, who often have more difficult to treat symptoms, but this new study is the first randomised controlled trial of low-dose amitriptyline versus a placebo tablet for IBS in primary care. It is also the largest trial of amitriptyline for IBS undertaken worldwide.
GPs already prescribe low-dose amitriptyline to treat chronic nerve and back pain, and to help prevent migraine attacks. NICE guidelines currently state that GPs could consider using a low dose tricyclic, like amitriptyline, for IBS but, until now, the evidence for a benefit has been uncertain.
Based on the results of the trial, which showed a clear benefit of amitriptyline, GPs can offer low-dose amitriptyline to people with IBS as part of shared decision making if symptoms don’t improve with first-line treatments.
Co-chief Investigator Hazel Everitt, Professor of Primary Care Research at the Primary Care Research Centre, University of Southampton, said: “Prior to ATLANTIS, GPs haven’t often prescribed amitriptyline for IBS as the research evidence was uncertain, but our new research provides good evidence of benefit.
“GPs already prescribe low-dose amitriptyline for other conditions, such as chronic pain and poor sleep, and when we interviewed GPs as part of this research, they were willing to prescribe it for IBS if the research evidence supported this. Participants were also keen to have another option to try to help their IBS symptoms and most were happy to self-adjust their dose depending on symptoms and side effects.’’
Some 463 people with IBS took part, recruited from 55 general practices across the UK.
Participants were put at random into two groups – those receiving amitriptyline and those receiving a placebo. Participants controlled how many tablets of the trial medication they took, receiving support via the patient dose adjustment document that was developed with patient representatives especially for this trial. This enabled participants to increase or decrease the number of tablets based on their IBS symptoms and any side effects experienced.
IBS scores were measured using the IBS-SSS scale. Amitriptyline participants scored a 99-point improvement compared with a 69-point improvement among placebo participants.
Participants taking amitriptyline reported a bigger improvement in their symptom scores after six months compared with those taking a placebo. Those taking amitriptyline were almost twice as likely as those taking a placebo to report an overall improvement in IBS symptoms, with amitriptyline performing better across a wide range of IBS symptom measures.
Researchers monitored participants’ anxiety or depression scores and found that they were not altered – suggesting that the beneficial effects of the medication were via the gut, not because of any effect as an antidepressant.
No safety concerns were identified and side effects in people on amitriptyline were mostly mild, such as a dry mouth in the morning.
Matthew Ridd, GP and Professor of Primary Health Care at the Centre for Academic Primary Care, University of Bristol, said: “Pragmatic trials like this are always challenging to do in primary care and the team worked hard to overcome the additional challenges of the Covid-19 pandemic. It’s fantastic that we’ve found that amitriptyline is an effective and safe option for patients with IBS to try.”
Amanda Farrin, Professor of Clinical Trials and Evaluation of Complex Interventions, who leads the Complex Intervention Division of the Leeds Clinical Trials Research Unit, said: “The participants in the ATLANTIS trial had moderate to severe symptoms and an average duration of IBS of 10 years. The fact that amitriptyline had such a big effect over a placebo is significant because it can help improve the quality of life of patients with this condition.”
Professor Andrew Farmer, Director NIHR’s Health Technology Assessment (HTA) Programme, said: “The results of this study are hugely encouraging. It shows that a drug already widely available to treat a number of other conditions appears to be safe and effective for people with IBS. The findings the research team have shared around the adjustment of dosages can be tremendously helpful to GPs in guiding them when treating patients.
“IBS affects a significant number of people in the UK and can have a debilitating effect on their day-to-day lives. This is another excellent example of how high-quality research can lead to positive changes in health and social care practice and treatments for the benefit of patients and healthcare professionals.”
The first study to compare effects of antidepressants with running exercises for anxiety, depression and overall health shows that they have about the same benefits for mental health, with health benefits for those assigned to running.
Professor Brenda Penninx from Vrije University, Amsterdam, presented the work at the ECNP conference in Barcelona (after recent publication in the Journal of Affective Disorders). Prof Penninx said, “We wanted to compare how exercise or antidepressants affect your general health, not just your mental health.”
The 16-week course of running over the same period scores higher in terms of physical health improvement, whereas antidepressants lead to a slightly worse physical condition, as has been suggested by previous studies. However, the drop-out rate was much higher in the group which initially chose exercise.
The researchers studied 141 patients with depression and/or anxiety. They were offered a choice of treatment; SSRI antidepressants for 16 weeks, or group-based running therapy for 16 weeks. 45 chose antidepressants, with 96 participating in running. The members of the group which chose antidepressants were slightly more depressed than the members of the group which chose to take running.
Professor Penninx said, “This study gave anxious and depressed people a real-life choice, medication or exercise. Interestingly, the majority opted for exercise, which led to the numbers in the running group being larger than in the medication group.”
Treatment with antidepressants required patients to adhere to their prescribed medication intake but this generally does not directly impact on daily behaviours. In contrast, exercise directly addresses the sedentary lifestyle often found in patients with depressive and anxiety disorders by encouraging persons to go outside, set personal goals, improve their fitness and participate in a group activity.
The antidepressant group took the SSRI Escitalopram for 16 weeks. The running group aimed for two to three closely supervised 45-minute group sessions per week (over 16 weeks). The adherence to the protocol was lower in the running group (52%) than in the antidepressant group (82%), despite the initial preference for running over antidepressants.
At the end of the trial, around 44% % in both groups showed an improvement in depression and anxiety, however the running group also showed improvements in weight, waist circumference, blood pressure, and heart function, whereas the antidepressant group showed a tendency towards a slight deterioration in these metabolic markers.
“Both interventions helped with the depression to around the same extent. Antidepressants generally had worse impact on body weight, heart rate variability and blood pressure, whereas running therapy led to improved effect on general fitness and heart rate for instance. We are currently looking in more detail for effects on biological aging and processes of inflammation’,” Prox Benninix said.
Physical activity is a good option, but antidepressants still have a role
Prof Benninx noted that it is not a case of one or the other when it comes to treating depression. “It is important to say that there is room for both therapies in care for depression. The study shows that lots of people like the idea of exercising, but it can be difficult to carry this through, even though the benefits are significant. We found that most people are compliant in taking antidepressants, whereas around half of the running group adhered to the two-times-a-week exercise therapy. Telling patients to go run is not enough. Changing physical activity behaviour will require adequate supervision and encouragement as we did by implementing exercise therapy in a mental health care institution.”
She added: “Antidepressants are generally safe and effective. They work for most people. We know that not treating depression at all leads to worse outcomes; so antidepressants are generally a good choice. Nevertheless, we need to extend our treatment arsenal as not all patients respond to antidepressants or are willing to take them. Our results suggest that implementing exercise therapy is something we should take much more seriously, as it could be a good – and maybe even better – choice for some of our patients.
“In addition, let’s also face potential side effects our treatments can have. Doctors should be aware of the dysregulation in nervous system activity that certain antidepressants can cause, especially in patients who already have heart problems. This also provides an argument to seriously consider tapering and discontinuing antidepressants when depressed or anxious episodes have remitted. In the end, patients are only truly helped when we are improving their mental health without unnecessarily worsening their physical health.”
Mania is a possible but rare side effect of treatment with antidepressant medication in adults, but there is little known about its occurrence in children and adolescents. A newly published paper in JAMA Psychiatry investigated this, finding no evidence of mania/hypomania induced by antidepressants by 12 weeks after treatment initiation. However, caution is necessary in treatment for children with more severe depression or where a parent has bipolar disorder.
“In children and adolescents with unipolar depression, we did not find evidence of antidepressant-induced mania/hypomania by 12 weeks after treatment initiation”, says first author Suvi Virtanen, postdoctoral researcher at Karolinska Insitutet. “This corresponds to the timeframe for antidepressants to exert their psychotropic effect and when treatment-induced mania is expected to emerge. Hospitalisations, parental bipolar disorder, and the use of antipsychotics and antiepileptics were the most important predictors of mania/hypomania.”
Antidepressants are increasingly prescribed to paediatric patients with unipolar depression (as opposed to bipolar depression which is seldom diagnosed in childhood), but little is known about the risk of treatment-emergent mania (ie, the transition from depression into mania shortly after the initiation of antidepressant treatment). Previous research suggests paediatric patients may be particularly vulnerable to this adverse outcome. The results provide complementary information to randomised clinical trials (RCTs) from a large cohort of patients treated in a real-world setting.
The researchers conducted a register-based study on children and adolescents, aged 4–17, diagnosed with unipolar depression between 2006 and 2019. They applied the emulation of target trial framework to guide the study design and analysis, reducing the bias of observational studies and mimicking a RCT.
Antidepressant treatment was unrelated to the risk of mania/hypomania, suggesting other characteristics are more relevant when evaluating which patients may have an increased risk of switching from unipolar depression into mania. “Our model using administrative information from several national registers had a moderate predictive ability, suggesting it is possible to identify patients at high risk for mania/hypomania with a prognostic clinical prediction model. The model has potential to be improved in later work”, says senior author Zheng Chang, Principal Researcher at the Department of Medical Epidemiology and Biostatistics.
New research from Rice University finds that antidepressants may actually reduce negative memories in individuals suffering from depression while improving overall memory function. The study, appearing in Frontiers in Human Neuroscience, examines how antidepressant use in depressed individuals affects memories, both good and bad.
Stephanie Leal, an assistant professor of psychological sciences, is the study’s lead author. She said the study’s main finding about the link between antidepressants and memories was an important one, because there is still much to be learned about how these drugs work.
“While antidepressants have been around since the 1950s, we still don’t really know how they work,” Leal said. “They only work about 50% of the time, and users often have to go through multiple types of antidepressants to get to a place where they actually feel like the drugs are beneficial. We don’t fully understand how these drugs reduce depressive symptoms and why they are so often ineffective. That’s a big problem.”
The study’s results suggest that antidepressants, when effective, can shift memory dynamics toward healthy function, Leal said.
“How antidepressants affect cognition is a hugely understudied area of research,” she said. “By measuring how antidepressants impact memory, we can use this information to better select treatments depending on people’s symptoms of depression.”
The study included 48 participants ages 18–35. All individuals were surveyed and had been actively taking antidepressants (regardless of the type of antidepressant and diagnosis) for at least one month prior to participation in the study. Researchers are conducting a follow-up study is to examine how the brain responds to antidepressants.
Treatment with modern antidepressants may help prevent patients with bipolar disorder from relapsing into a depressive episode, according to an international clinical trial published in the New England Journal of Medicine. The findings challenge current clinical practice guidelines and could change how bipolar depression is managed around the world.
“Treating depression in bipolar disorder is challenging and the depressive episodes can be quite devastating for patients and their families,” said Dr Lakshmi Yatham, professor and head of the department of psychiatry at UBC, and the study’s lead author. “Reducing the risk of relapse is important because it can provide patients with a great deal of stability that ultimately lets them get back to the activities they enjoy and can greatly improve their quality of life.”
Patients with bipolar disorder experience extreme changes in their emotional state that cycle through periods of intense highs (mania or hypomania) and lows (depression). During depressive episodes, patients can experience feelings of sadness, hopelessness and loss of interest or pleasure in activities, in addition to trouble sleeping, changes in appetite and suicidal thoughts.
Antidepressant adjunctive therapy, in which antidepressants are prescribed alongside mood stabilisers and/or second-generation antipsychotic medications, is a commonly used strategy by clinicians to treat depressive episodes. However, the duration of this therapy is hotly debated due to a lack of evidence and concerns that antidepressants may induce mania, mixed states or rapid cycling between mania and depression.
Practice guidelines for the management of bipolar disorder published by the Canadian Network for Mood and Anxiety Treatments (CANMAT) and International Society for Bipolar Disorders (ISBD) currently recommend discontinuing antidepressant treatment eight weeks after remission of depression.
“It’s an area that hasn’t been widely studied and there is not a lot of consensus among experts,” said Dr Yatham. “Some studies have shown that up to 80 percent of patients continue receiving antidepressants for six months or longer.”
Now, results from the world’s first randomised clinical trial assessing the duration of adjunctive antidepressant therapy suggest that extending the treatment period beyond current guidelines may help prevent depressive relapses.
The clinical trial, conducted at sites in Canada, South Korea and India, involved 178 patients with bipolar I disorder who were in remission from a depressive episode following treatment with modern antidepressant drugs (escitalopram or bupropion XL). The patients were randomly assigned to either continue antidepressant treatment for 52 weeks, or begin tapering off antidepressants at six weeks and switch to a placebo at eight weeks.
Over the year-long study, 46% of patients in the placebo group experienced a relapse of a mood event, compared to only 31% in the group that continued antidepressant treatment. While this primary outcome was not found to be statistically significant, the comparison included relapses that occurred during the first six weeks of the study when both groups were receiving the same treatment.
However, in an analysis from week six onward, when treatment between the two groups differed, patients that continued antidepressant treatment were 40% less likely to experience a relapse of any mood event, and 59% less likely to experience a depressive episode relative to the placebo group. There was no significant difference in the rate of manic episodes or the rate of adverse events between groups.
“From the point where the two groups began receiving different treatments, we see a significant benefit for patients who continued treatment with antidepressants,” said Dr Yatham.
Patients with bipolar I disorder experience depressive symptoms three times more frequently than manic symptoms. Previous studies have shown that suicide attempts and suicide deaths are at least 18 times more common during depressive episodes compared to during manic episodes.
“Stabilizing patients and keeping them stable by preventing relapse is critical and can quite literally be lifesaving,” said Dr Yatham. “Future revisions of bipolar guidelines will incorporate the evidence from this study and contribute to changes in clinical practice on how antidepressants will be used to manage patients with bipolar disorder.”
For patients with anxiety disorders, a guided mindfulness-based stress reduction program was as effective as use of the gold-standard drug escitalopram, according to results of a first-of-its-kind, randomised clinical trial published in JAMA Psychiatry.
“Our study provides evidence for clinicians, insurers, and healthcare systems to recommend, include and provide reimbursement for mindfulness-based stress reduction as an effective treatment for anxiety disorders because mindfulness meditation currently is reimbursed by very few providers,” says Elizabeth Hoge, MD, director of the Anxiety Disorders Research Program and associate professor of psychiatry at Georgetown and first author. “A big advantage of mindfulness meditation is that it doesn’t require a clinical degree to train someone to become a mindfulness facilitator. Additionally, sessions can be done outside of a medical setting, such as at a school or community centre.”
Anxiety disorders can be highly distressing; they include generalised anxiety, social anxiety, panic disorder and fear of certain places or situations, including crowds and public transportation, all of which can lead to an increased risk for suicide, disability and distress and therefore are commonly treated in psychiatric clinics. Drugs that are currently prescribed for the disorders can be very effective, but many patients either have difficulty getting them, do not respond to them, or find the side effects (e.g., nausea, sexual dysfunction and drowsiness) as a barrier to consistent treatment. Standardized mindfulness-based interventions, such as mindfulness-based stress reduction (MBSR), can decrease anxiety, but prior to this study, the interventions had not been studied in comparison to effective anti-anxiety drugs. Of note, approximately 15% of the U.S. population tried some form of meditation in 2017.
The clinicians recruited 276 patients between June 2018 and February 2020 from three hospitals in Boston, New York City and Washington, D.C., and randomly assigned people to either MBSR or escitalopram. MBSR was offered weekly for eight weeks via two and a half-hour in-person classes, a day-long retreat weekend class during the 5th or 6th week, and 45-minute daily home practice exercises. Patients’ anxiety symptoms were assessed upon enrolment and again at completion of the intervention at 8 weeks, along with post-treatment assessments at 12 and 24 weeks after enrolment. The assessments were conducted in a blinded manner — the trained clinical evaluators did not know whether the patients they were assessing received the drug or MBSR.
At the end of the trial, 102 patients had completed MBSR and 106 had completed their medication course. The patients were relatively young, with a mean age of 33 and included 156 women, which comprised 75% of the enrolees, mirroring the disease prevalence in the U.S.
The researchers used a validated assessment measure to rate the severity of symptoms of anxiety across all of the disorders using a scale of 1 to 7 (with 7 being severe anxiety). Both groups saw a reduction in their anxiety symptoms (a 1.35 point mean reduction for MBSR and 1.43 point mean reduction for the drug, which was a statistically equivalent outcome), dropping from a mean of about 4.5 for both, which translates to a significant 30% or so drop in the severity of peoples’ anxiety.
Olga Cannistraro, 52, says she uses her MBSR techniques as needed, but more than a decade ago, the practice transformed her life. She was selected for an MBSR study after responding to advertisement asking, “Do you worry?”
“I didn’t think of myself as anxious – I just thought my life was stressful because I had taken on too much,” she recalls. “But I thought ‘yeah, I do worry.’ There was something excessive about the way I responded to my environment.”
After participating in an earlier study led by Hoge, she learned two key MBSR techniques. “It gave me the tools to spy on myself. Once you have awareness of an anxious reaction, then you can make a choice for how to deal with it. It’s not like a magic cure, but it was a life-long kind of training. Instead of my anxiety progressing, it went in the other direction and I’m very grateful for that.”
“It is important to note that although mindfulness meditation works, not everyone is willing to invest the time and effort to successfully complete all of the necessary sessions and do regular home practice which enhances the effect,” Hoge said. “Also, virtual delivery via videoconference is likely to be effective, so long as the ‘live’ components are retained, such as question-and-answer periods and group discussion.”
Hoge points out that there are many phone apps that offer guided meditation, however researchers don’t know how apps compare with the full in-person, weekly group class experience.
Trial enrollment was wrapping up as the COVID pandemic started in early 2020 but most enrollees completed their eight-week course of treatment before the pandemic started. Additionally, the researchers conducted a second phase of the study during the pandemic that involved moving the treatments to an online, videoconference, and that will be the focus of future analyses. The researchers also hope to explore the effects of MBSR on sleep and depression.
A large Swedish study in the journal Neurologyfound that pregnant women taking selective serotonin reuptake inhibitors (SSRIs) or selective norepinephrine reuptake inhibitors (SNRIs) during the first trimester of was not linked to an increased risk for neonatal seizures and epilepsy in childhood.
Any increase in seizures or epilepsy is likely due to other factors, the researchers said.
“It’s not likely the medications themselves that are causing the seizures and epilepsy in children, but rather the reasons why these women are taking the medication,” according to Kelsey Kathleen Wiggs, a PhD candidate at Indiana University in Bloomington. There are also the other background factors that differ between women who do and do not use SSRI/SNRIs.
“When it rains, it pours,” Wiggs said. “Women who are taking antidepressants in pregnancy are doing that for lots of different reasons, and they might be at risk for different things than women who aren’t taking those medications in pregnancy.”
The study found an elevated risk for neonatal seizures (risk ratio [RR] 1.41) and epilepsy in early childhood (HR 1.21) among offspring of mothers who used antidepressants in pregnancy.
Adjustment for maternal indications for SSRI/SNRI use and background factors like smoking during pregnancy revealed that they were drivers for both associations: neonatal seizures (RR 1.10); epilepsy diagnosis at 5 years (HR 0.96). Parental history of epilepsy was not found to affect the association.
The findings provide a “conclusive answer” to these concerns with using SSRI/SNRIs during pregnancy, according to Anne Berg, PhD, and Torin Glass, BM, Bch, BAO.
“[SSRI/SNRIs] have been demonstrated to have serotonergic central nervous system effects and are associated with an observable withdrawal syndrome which may be seen in the neonate following in utero exposure,” noted Drs Berg and Glass, in an accompanying editorial.
“The authors understood that with a population-based data registry and huge sample size, they had more than sufficient statistical power to detect even a modest increase in risk,” the editorialists wrote. “They tested this hypothesis and were able to reject it, definitively!”
In order to determine whether antidepressants had a causal association with infant seizures and childhood epilepsy, the researchers analysed data from national Swedish healthcare registries on a total of 1 721 274 children in Sweden born between 1996 and 2011.
Participants were divided into two groups: one group of mothers who reported use of an SSRI (fluoxetine, citalopram, paroxetine, sertraline, fluvoxamine, escitalopram) or SNRI (venlafaxine, duloxetine) during the first trimester of pregnancy (n = 24 308), and another group with no reported antidepressant use (n = 1 696 966).
