Antidepressants: always believed to be a go-to for treating anxiety disorders. New research says mindfulness-based stress reduction works just as well. I think we ought to talk about it, don’t you?
’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.’
First a TCA, then a variety of SSRIs. I’ve been using antidepressants for anxiety disorders for 33 years.
But if that was my sole intervention, I’d have anxiety’d myself into insanity by now.
The results of a recent randomized clinical trial led by researchers at Georgetown University Medical Center caught my attention.
Here’s why…
Mindfulness-based stress reduction is as effective as an antidepressant for treating anxiety disorders
To the bottom-line, the Georgetown team found that a guided mindfulness-based stress reduction program was as effective as using the SSRI antidepressant escitalopram (Lexapro) for the treatment of anxiety disorders – generalized, social, panic, specific phobias.
The work appeared in JAMA Psychiatry on November the 9th of this year.
Study first author, Dr. Elizabeth Hoge…
Our study provides evidence for clinicians, insurers and health care 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.
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 center.
Let’s learn about it…
What is mindfulness-based stress reduction?
Mindfulness-based stress reduction (MBSR) is a therapeutic technique in which an instructor guides participants in weekly – typically one hour for eight weeks – practices like meditation and yoga in order to reduce stress levels.
It was founded in the 1970s by Dr. Jon Kabat-Zinn at the University of Massachusetts Medical School.
Kabat-Zinn developed it as an eight-week course to treat patients’ emotional and mental health, as well as chronic pain, when they hadn’t responded to traditional therapy.
The goal
The goal of MBSR is to bring people into the present moment so they can experience their thoughts and feelings non-judgmentally and avoid worrying about the past or future.
By the way, if you’d like to give it a go, make sure you connect with a qualified instructor. And if you’re using it to treat a physical ailment check in with your doc.
Back to the study…
Mindfulness-based stress reduction, antidepressants, and anxiety disorders: The study
“They say it’s just as good as an antidepressant. And it may even be fun.”
Between June 2018 and February 2020, the Georgetown team recruited 276 participants from three hospitals in Boston, New York City, and Washington, D.C.
They were randomly assigned to either the MBSR group or escitalopram.
The participants’ anxiety symptoms were assessed upon enrollment, completion of the intervention at eight weeks, and post-treatment at 12 and 24 weeks.
How it worked
MBSR was offered weekly for eight weeks. The protocol: two-and-a-half hour in-person classes, a daylong retreat weekend class during the 5th or 6th week, and 45 minute daily home practice exercises.
Escitalopram was flexibly dosed between 10 and 20 mg.
Mindfulness-based stress reduction, antidepressants, and anxiety disorders: The results
When it was all said and done, 102 patients had completed MBSR and 106 had completed their medication course. Not all of the participants got through their program, largely due to the pandemic.
The team used a validated assessment measure to rate the severity of symptoms across all disorders using a scale of 1-7 (7 being most severe).
Both groups saw a reduction in their anxiety symptoms: 1.35 points for MBSR and 1.43 for the antidepressant group. That’s statistically equivalent.
The mean for both groups at enrollment was 4.5. So we’re looking at a drop in anxiety symptoms right at 30%.
A valuable perspective
A 52-year-old female participant shared that she began practicing MBSR techniques 10 years ago and it’s transformed her life.
Interesting – she was selected for an MBSR study after responding to an advertisement asking, “Do you worry?”
Maybe you’ll connect with what she had to say…
I didn’t think of myself as anxious — I just thought my life was stressful because I had taken on too much. But I thought, ‘Yeah, I do worry.’ There was something excessive about the way I responded to my environment.
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 lifelong kind of training. Instead of my anxiety progressing, it went in the other direction, and I’m very grateful for that.
But you know what? Dr. Hoge emphasizes that in spite of the fact that MBSR works, not everyone is willing to devote the time and effort to make it happen.
Hey, I get it. Popping a pill is a whole lot easier. But it doesn’t provide much in the way of self-insight or life-coping techniques.
More work to be done
Hit your app store and you’ll find all sorts of guided meditation apps. As convenient as they are, Hoge points out that the team doesn’t know how apps compare with the full in-person, weekly group class experience. That calls for some work.
Additionally, the team conducted a second phase of the study during the pandemic that involved moving the treatments to an online videoconference. They want to analyze its efficacy.
Finally, the team hopes to explore the effects of MBSR on sleep and depression.
What do you think?
There you have it. Mindfulness-based stress reduction is as effective as an SSRI antidepressant.
I’m not the least bit surprised. You?
So the question is will we give it a go? And keep in mind, it can be used as a primary or complementary treatment.
Treating depression with psilocybin. A hot topic for years; however, the medical establishment and government officials haven’t been receptive to the medicinal use of psychedelics. Let’s see if minds are opening…
…psilocybin works faster and better on most measures, and has a different and slightly better side effect profile than current antidepressants.
Those “shrooms” in the image contain psilocybin, a hallucinogenic chemical compound.
Psilocybin has fueled many a spiritual and recreational trip. And now it’s getting renewed attention as a potential treatment for emotional and mental disorders.
Update 12.16.22 From a reader’s comment (This is an FYI, not a recommendation. Furthermore, with very few exceptions, it’s illegal.): “After 3 1/2 yrs the ket(amine) didn’t keep working. I had been reading and studying the effects of micro dosing Psilocybin. I found a mycologist who is making mushroom chocolate bars. After adjusting the dose to 100mg 4 days on, then 3 days off I find myself free of my psych meds. Three months now, micro dosing I have little to no side effects and my depression, Anx, and PTSD are in check.”
Okay, happened upon a fascinating article in the journal, Nature. In his piece, “Will psychedelics be a ‘revolution in psychiatry’?”, science journalist Asher Mullard interviews neuropsychopharmacologist Dr. David Nutt.
Dr. Nutt is a professor at Imperial College London and the chairman of Drug Science, a non-profit he founded to provide independent, evidence-based information on drugs.
Nutt has been a controversial figure over the years, his views at times ruffling professional and political feathers. Is that a bad thing?
Barriers for psychedelic-assisted therapies
Mr. Mullard opens his article by pointing out that trial design considerations, regulatory hurdles, and economics continue to present barriers for psychedelic-assisted therapies.
He goes on to say that in the 1970s, early in Dr. Nutt’s career, there was evidence that psychedelics could work wonders in mental health. However, the medical establishment was overly concerned about the perceived dangers of mind-altering agents. As a result, government officials made the compounds illegal, and research into potential therapeutic uses came to a halt.
Continued advocacy
According to Mullard, Nutt and others have continued to advocate for open-mindedness, as a growing body of evidence supports the view that psychedelics could provide a much needed boost for psychiatric medicine.
For instance, phase III trial results for MDMA (Ecstasy) in the treatment of PTSD show the drug, in conjunction with psychotherapy, improved outcomes. And though Dr. Nutts’ phase II trial of psilocybin for the treatment of depression missed its primary end point, progress was made on several fronts and research work continues.
In fact, if you go to ClinicalTrials.gov and enter psilocybin in “Other terms,” you’ll get details on scores of studies, featuring a variety of emotional and mental situations.
Participate
By the way, if you’re interested in participating in a psilocybin – any – clinical trail, why not head over to the ClinicalTrials site, pick out a study that fits, and reach out to the contact person?
Okay, what you’re about to read comes from Dr. Nutt in response to Mullard’s questions. No way could I include content from the entire interview. I just want to bring you a quality psilocybin for depression introduction. And you can do some digging if you’d like to learn more.
Medicinal use of psychedelics: Psilocybin and depression
As Dr. Nutt was discussing his dosing of patients with psilocybin in the 2000s, he stated his work with psychedelics was an effort to understand the psychedelic state.
Nutt observed that the brain’s cerebral cortex is full of 5-HT (serotonin) receptors, so it’s important to understand what they’re doing. Why are they there? How will psilocybin effect them?
Through the work, Nutt and his team learned that parts of the brain related to depression can actually be turned off. And it was then that they seriously began to think about the therapeutic uses of psilocybin.
Dr. Nutt continues to believe psychedelics are going to be a revolution in psychiatry. But hear me, psychotherapy has to be a key component of any psychedelic regimen.
Psilocybin versus antidepressants
SSRI antidepressants work on 5-HT1A receptors in the limbic system
It’s Dr. Nutt’s opinion that psilocybin works faster and better on most measures, and has a different and slightly better side effect profile than current antidepressants. And that’s because there are fundamental differences in the way the drugs work.
SSRIs
Nutt used selective serotonin reuptake inhibitor (SSRI) antidepressants for purposes of comparison.
He explained that SSRIs work on 5-HT1A receptors in the limbic system (located beneath the cerebral cortex – the outer layer of the brain). The action allows the brain to heal from the effects of chronic stress. He described it as putting a plaster cast on a broken leg to support the bone until it heals.
Psilocybin
He went on to say the psychedelics, including psilocybin, work in the cerebral cortex via 5-HT2A receptors. The action disrupts the repetitive negative thinking that’s so troubling in depression. Nutt referred to it as resetting the brain’s thinking process.
He also mentioned that impacting the 5-HT2A receptor seems to be very powerful in terms of driving neuroplasticity, a miraculous natural healing dynamic.
In summary, Dr. Nutt stated that psilocybin’s mechanism of action is at the network level. The mechanism of action for the SSRIs occurs at the synapse level.
Let’s wrap it up
We can’t rely solely upon the meds development pipeline when it comes to relief for the emotional and mental disorders. That’s why research work has to continue with the psychedelics. There’s way too much at stake.
But as much promising evidence as there’s been over the years pertaining to the psychedelics, questions remain. Dr. Nutt from the article…
How do you sustain wellness after a psychedelic? Okay, so people get better. But do they stay well? And how do you maximize staying well? Do you keep giving psychedelics or do you put people on an SSRI, or in psychotherapy?
Limbic system image: Author: Bruce Blaus Blausen.com staff (2014). “Medical gallery of Blausen Medical 2014,” no changes made. Creative Commons Attribution 3.0 Unported
All those Chipur mood and anxiety info and inspiration articles. Gotta’ hit the titles.
The brain generates mood and anxiety symptoms. And there are no coincidences. I’ve always loved learning about the bio goings on. You too? Let’s delve into Brodmann areas…
Can you see the role Brodmann areas play in depression interventions? Deep brain stimulation and transcranial magnetic stimulation have become effective treatments.
When it comes to relief for our mood and anxiety woes, many of us look exclusively to the meds development pipeline.
That’s understandable, but the contribution of things like what you’re about to read is just as important and hopeful – if not more.
“How the brain balances emotion and reason”
Bumped into an article on ScienceDaily entitled “How the brain balances emotion and reason.” It detailed recent work by Mary Kate P. Joyce and associates, which was published in The Journal of Neuroscience.
I read about how emotional balance goes haywire in mood disorders such as depression, leading to unchecked negative emotions and the inability to snap out of rumination.
Area 32 and 25?
Then I read that all this emotional balance biz is handled by brain region area 32. And if that wasn’t enough, the article said people with depression often have an overactive area 25, which is involved in emotional expression.
Now, I’m familiar with Area 51, the classified Air Force facility in Nevada. But area 32, area 25? I needed to know more.
What are Brodmann areas?
In 1909, German anatomist Korbinian Brodmann defined and numbered regions of the cerebral cortex based upon cytoarchitecture – the study of the cellular composition of the tissues of the central nervous system under a microscope.
So why did Brodmann bother? It was about organization, because different parts of the cortex are involved in different cognitive and behavioral functions. And they all work together to make us who we are.
Because of his hard work, we know that humans have 52 Brodmann areas.
Cerebral cortex
Let’s take a moment for the cerebral cortex. It’s the 2-4 millimeter thick outer covering of the surface of the brain hemispheres. It’s all gray matter and comprises 40% of our brain mass.
Without the cerebral cortex we have no attention, perception, awareness, thought, memory, language, consciousness, or sensory and motor functioning.
Brodmann areas and depression
Brodmann area 32 (BA32) is the dorsal anterior cingulate. According to Dr. Joyce’s work, the area maintains emotional equilibrium by relaying information between cognitive and emotional brain regions.
That action puts the kibosh on negative emotions and rumination.
Cingulate Region
But then there’s area 25, located in the subgenual area of the cingulate region. It’s just below and connected to BA32.
Dorsolateral prefrontal cortex connections
We already know that people with depression often have an overactive BA25, a region involved in emotional expression. But what’s really interesting are the connections between the dorsolateral prefrontal cortex (DLPFC, a cognitive region), BA25, and BA32.
In rhesus monkeys, the DLPFC connects to the deepest layers of BA32, where the strongest inhibitory neurons reside. BA32 connects to every layer of BA25, allowing it to be a powerful regulator of BA25 activity.
In the brains of the non-depressed, the DLPFC signals to BA32 to balance BA25 activity, allowing emotional equilibrium. But in depression, silence from the DLPFC results in too much BA25 activity and out of control emotional processing.
Deep brain and transcranial magnetic stimulation
A portion of the cingulate gyrus (part of the cingulate cortex), which consists of BA25, as well as parts of BA32, is believed to play an important role in the generation of major depressive disorder. That being the case, it’s been a target of deep brain stimulation.
Indeed, in 2005, renowned neurologist Helen S. Mayberg and collaborators described how they successfully treated a number of depressed individuals – people virtually catatonic with depression despite years of talk therapy, drugs, and electroconvulsive therapy (ECT) – with deep brain stimulation in BA25.
Think about how incredible that is.
But there’s more. A recent study found that transcranial magnetic stimulation is more clinically effective in treating depression when targeted specifically at BA46 (a portion of the frontal cortex), because the area has functional connectivity with BA25.
Hope beyond meds development
Can you see the role Brodmann areas play in depression interventions? Deep brain stimulation and transcranial magnetic stimulation have become effective treatments.
And the best part is, the science is young. I’m sure there’s much more to come.
Now you know why I believe relief – hope – extends well beyond the meds development pipeline. And that’s great news because, frankly, there isn’t a whole lot to write home about.
In fact, I’ll go so far as to say I’m more excited about targeting Brodmann areas for direct depression intervention than I was about the approval of esketamine (Spravato).
Thought you ought to know
In the brain there are no coincidences. And the more we can learn about why we’re depressed or anxious, the more comfortable we can become with our circumstances.
For more than 100 years, Brodmann areas have provided direction and insight for research work and treatment. I believe they’ll continue to make a significant contribution.
Thought you ought to know.
So many more Chipur mood and anxiety info and inspiration articles. Head to the titles.
Slick detective work is essential when it comes to understanding the neurobiology of OCD. But the hopeful part comes with how that work translates into relief. I mean, scientists can talk a good game, but who can’t? What say we get down to cases…
The docs then introduce the question: Can imaging be used to direct or predict treatment response? Well, just like using a brain scan to diagnose an individual case of OCD, which we discussed in Part 1…
We started this two-part series with a same-titled piece last week, featuring the work of Dr. Jon Grant and Dr. Samuel Chamberlain. Their Psychiatric Times article, Exploring the Neurobiology of OCD: Clinical Implications, is full of recent research information, as well as news on treatment developments.
Part 1 of our series handled the former. Now it’s time to address the latter.
Advances in Understanding the Neurobiology of OCD: Treatment Impact
As they did when discussing advances in understanding the neurobiology of obsessive-compulsive disorder (OCD), Grant and Chamberlain cleverly open their discussion of the impact on treatments with a vignette…
Joseph is 28 and has a 10-year history of severe OCD. Of particular significance are contamination obsessions and washing compulsions, extensive procrastination, and repetitive list-making/doodling. Joseph is incapacitated by his illness and has difficulty leaving the house to work or socialize. Joseph has been treated with assorted selective serotonin reuptake inhibitors (SSRIs), on occasion augmented by a low-dose antipsychotic and n-acetylcysteine. He’s also participated in extensive cognitive behavioral therapy (CBT) using exposure and response prevention.
Joseph’s Neurosurgery
After an ethics board review and approval, and making sure he understood risks and benefits, Joseph underwent a neurosurgical procedure to implant electrodes targeting his brain’s nucleus accumbens.
Some six months following this deep brain stimulation (DBS), and continuation of meds and CBT, Joseph reported a significant improvement in symptoms. He was even able to leave his home for work and social activities. With ongoing treatment, Joseph’s relief continued three years post-surgery.
Neuroimaging
According to Dr. Grant and Dr. Chamberlain, progression in neuroimaging has brought advances in the understanding of the neurobiology of OCD.
Still, how does that translate into the expansion of treatment approaches?
If you endure OCD, I’m thinking you know that current first-line, evidence-based treatments include SSRIs and/or CBT featuring exposure response prevention.
Grant and Chamberlain cite a recent systematic review and meta-analysis that indicates this approach shows superiority over placebo for the treatment of adult OCD. Fact is, these treatments have been used for over 30 years and haven’t been altered by advancing neurobiological research.
Neuroimaging has presented insights into brain mechanisms by which treatments may improve OCD. Study data show that structural and functional brain changes associated with OCD symptoms normalize to a degree with efficacious meds and psychotherapy treatment.
The docs then introduce the question: Can imaging be used to direct or predict treatment response?
Well, just like using a brain scan to diagnose an individual case of OCD, which we discussed in Part 1, there’s no existing evidence that treatment can be usefully predicted.
But the docs say that algorithms for treatment response can be built, including the ability to predict response to psychotherapy. Thing is, the approaches have yet to be generalized or show usefulness at the individual patient level in clinical practice. Sounds like there’s hope for the future, though.
More on Neurosurgical Techniques
As in Joseph’s deep brain stimulation or gamma ventral capsulotomy, neurosurgical techniques are at times used in the toughest treatment-resistant OCD cases. Well, results vary, to include no help at all.
That reality has led to researchers addressing the improvement of neurosurgical interventions based upon a more detailed understanding of the neurobiology of OCD.
For instance, a recent study used a clinical assessment and symptomatic provocation during functional MRI to enhance electrode placement for DBS in a sample of patients.
Let’s Wrap It Up
That three-pound mass of tissue and fluid encased in our skulls: I can’t think of anything more mysterious in the entire universe. And, of course, if you’re doing all you can to live with OCD – any emotional/mental disorder – mystery is the last thing you need.
Yes, I find work like Dr. Grant’s and Dr. Chamberlain’s slick and hopeful. And the cool thing is, they’re doing the investigative reporting on the creative and brilliant research work that marches onward.
There is no cure for depression. Heck, we don’t even have remedies that work for the majority of sufferers, the majority of the time. But we can’t throw up our arms in resignation. I mean, check-out these exciting high-tech treatment developments from UT Southwestern…
Yes, tools such as artificial intelligence, brain imaging, and blood tests hold the potential to revolutionize psychiatry in the coming years.
News flash! I buy into a bit of guilt when I write and post a science-based article. Here’s the dilemma. It’s important to bring you scientific information, especially research. After all, it’s knowledge pertaining to a huge piece of anyone enduring a mood or anxiety disorder. And it can bring hope.
The problem is, I can’t offer relief absolutes. I can’t say, “If you do ‘X,’ you’ll be misery-free.” That bothers me – a lot. But I guess that’s what has to happen right now as we try to understand the most mysterious three-pound mass on the planet.
Hmmm.
So okay, enough for lamentations. We have work to do. Let’s focus upon some very exciting research – and be glad for what we have…
The Groundbreaking Research Work
Researchers at UT Southwestern (University of Texas Southwestern Medical Center) initiated a national trial in 2011 to better understand the mood disorders. Actually, it was a multi-site trial that included Stanford, Harvard, and other institutions.
Lo and behold, the trial has recently produced what scientists are calling a “flagship finding”: a computer that can accurately predict whether an antidepressant (AD) will work based upon a patient’s brain activity. There’s the setup in our featured image.
Ah, but there’s more than just that. There have been several studies from the original trial that cumulatively show how high-tech strategies can help with objective diagnosis and the prescribing of depression treatments. Yes, tools such as artificial intelligence (AI), brain imaging, and blood tests hold the potential to revolutionize psychiatry in the coming years.
According to UT Southwestern psychiatrist and lead researcher Madhukar Trivedi, MD…
These studies have been a bigger success than anyone on our team could have imagined. We provided abundant data to show we can move past the guessing game of choosing depression treatments and alter the mindset of how the disease should be diagnosed and treated.
Now, you may be saying to yourself, “I thought that was what genetic testing was all about.” Keep in mind, what’s commonly known these days as “genetic testing” – choosing ADs based upon identifying specific biomarkers – isn’t at all what we’re talking about. Furthermore, “genetic testing” is very young science and its efficacy is questionable.
The Study Guts
Published in the journal Nature Biotechnology, the “flagship finding” results came from studying 300 participants with depression. They were randomly assigned to receive a placebo or a selective serotonin reuptake inhibitor (SSRI). I believe it was sertraline (Zoloft).
Researchers used electroencephalogram (EEG) to measure electrical activity in the brain’s cortex prior to treatment. The team then developed a machine-learning algorithm (the AI piece) to analyze and use the EEG data to predict which patients would benefit from meds within two months.
Wonderfully, AI accurately predicted outcomes. Even more, further research suggested that patients who were doubtful to respond to an AD were likely to improve with other interventions such as psychotherapy or brain stimulation.
Heck, the findings were validated in three additional patient groups.
Next steps include developing an AI interface that can be widely integrated with EEGs across the U.S. Seeking U.S. FDA approval is also on the to-do list.
Seems Dr. Trivedi is a busy guy. He initiated the 16-week EMBARC trial at four U.S. locations to establish biology-based, objective strategies to bring mood disorder relief.
EMBARC evaluated patients with major depressive disorder using brain imaging and assorted DNA, blood, and other tests. Why? Well, Trivedi was troubled by a finding from the infamous STAR*D study, which he led…
Two-thirds of patients don’t respond to their first antidepressant. Yikes!
So the good doctor reasoned it would be best to identify at the onset of treatment the most effective intervention for a particular patient.
Previous EMBARC studies had identified various predictive tests, including MRI, to examine brain activity at rest and during the processing of emotions.
From that, Trivedi came to the conclusion that EEG would likely be the tool of choice because it’s less expensive and in most cases equally as effective, if not more. Still, blood work and/or MRI may be indicated in some cases.
Trivedi states…
There are many signatures of depression in the body. Having all these tests available will improve the chances of choosing the right treatment the first time.
Continuing to work toward improving depression’s remission rate, Dr. Trivedi has initiated other biggee research projects. The D2K study will enroll 2,500 participants with depression and bipolar disorder, following them for 20 years. The RAD is a 10 year study of 2,500 10-24 year olds designed to uncover factors that reduce the risk of developing mood and anxiety disorders.
Utilizing some of these participants, Trivedi’s team will study results from several other tests to assess biological signatures in an effort to ascertain the most effective treatments.
That’ll Do It
I gotta’ tell ya’, I’m very excited about this work. And I’m thrilled that scientists like Dr. Trivedi are hot on the discovery and treatment trail of the mood and anxiety disorders.
Sure, I wish I was writing the post that announced a cure for depression, bipolarity, and anxiety. But we all know that article is down the road. After all, the brain. Right?
Nonetheless, let’s try to be glad – hopeful – that this fine work continues. I mean, it’s all we have – right now.
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According to Dr. Grant and Dr. Chamberlain, progression in neuroimaging has brought advances in the understanding of the neurobiology of OCD.
Published in the journal Nature Biotechnology, the “flagship finding” results came from studying 300 participants with depression. They were randomly assigned to receive a placebo or a selective serotonin reuptake inhibitor (SSRI). I believe it was sertraline (Zoloft).
