A collection of postings on a range of issues is available on our website (www.mjacksongroup.ca). This month’s post is again from Ken Pope’s listserv, where he kindly provides daily summaries of current articles in the field.
Medscape includes an article: “Coffee’s Brain-Boosting Effect Goes Beyond Caffeine.”
Here are some excerpts:
Coffee’s ability to boost alertness is commonly attributed to caffeine, but new research suggests there may be other underlying mechanisms that explain this effect.
“There is a widespread anticipation that coffee boosts alertness and psychomotor performance. By gaining a deeper understanding of the mechanisms underlying this biological phenomenon, we pave the way for investigating the factors that can influence it and even exploring the potential advantages of those mechanisms,” study investigator Nuno Sousa, MD, PhD, with the University of Minho, Braga, Portugal, said in a statement.
The study was published in Frontiers in Behavioral Neuroscience.
Caffeine Can’t Take All the Credit
<snip>
The researchers investigated the neurobiological impact of coffee drinking on brain connectivity using resting-state functional magnetic resonance imaging (fMRI).
They recruited 47 generally healthy adults (mean age, 30; 31 women) who regularly drank a minimum of one cup of coffee per day. Participants refrained from eating or drinking caffeinated beverages for at least 3 hours prior to undergoing fMRI.
To tease out the specific impact of caffeinated coffee intake, 30 habitual coffee drinkers (mean age, 32; 27 women) were given hot water containing the same amount of caffeine, but they were not given coffee.
The investigators conducted two fMRI scans ― one before, and one 30 minutes after drinking coffee or caffeine-infused water.
Both drinking coffee and drinking plain caffeine in water led to a decrease in functional connectivity of the brain’s default mode network, which is typically active during self-reflection in resting states.
This finding suggests that consuming either coffee or caffeine heightened individuals’ readiness to transition from a state of rest to engaging in task-related activities, the researchers note.
However, drinking a cup of coffee also boosted connectivity in the higher visual network and the right executive control network, which are linked to working memory, cognitive control, and goal-directed behavior ― something that did not occur from drinking caffeinated water.
“Put simply, individuals exhibited a heightened state of preparedness, being more responsive and attentive to external stimuli after drinking coffee,” said first author Maria Picó-Pérez, PhD, with the University of Minho.
<snip>
Certain effects were specific to coffee drinking, “likely influenced by factors such as the distinct aroma and taste of coffee or the psychological expectations associated with consuming this particular beverage,” the researcher write.
The investigators report that the observations could provide a scientific foundation for the common belief that coffee increases alertness and cognitive functioning.
Ken Pope
Ken Pope, Nayeli Y. Chavez-Dueñas, Hector Y. Adames, Janet L. Sonne, and Beverly A. Greene
A collection of postings on a range of issues is available on our website (www.mjacksongroup.ca). This month’s post is again from Ken Pope’s listserv, where he kindly provides daily summaries of current articles in the field.
After such an intense week—especially with the Supreme Court decisions that will have such extraordinary effects on so many lives—it seemed like Jancee Dunn’s interview with David Saderis on walking might be a good way to wind down:
David Sedaris is an avid walker, humorist, and author of 13 books, including “Me Talk Pretty One Day” and “Happy-Go-Lucky.” Sedaris, who splits his time between New York City and Sussex, England, has been walking every day since 2014, when he started tracking his steps with a Fitbit. He has walked in cities all over the world, including Tokyo and Reykjavik. He even had a garbage truck named after him in England, where he combines walking and picking up trash.
We chatted about his walking schedule and the lengths he’ll go to in order to maintain his daily goal of 21,000 steps (at least).
What are your walking plans for today?
I will walk from, I don’t know, 3 o’clock until 7 o’clock. I mean, I need to walk a minimum of 10 miles.
Every single day?
Yeah. I have calves like upside down bowling pins, and a lot of people think they’re implants.
What happens if you don’t walk? Do you not feel like yourself?
I have an Apple Watch, and you have to fill in three circles on it. But it’ll write me and say, “You’ve filled in all your circles for 1,800 days.” So I can’t break that.
It would be much more, but years ago, I flew from Los Angeles to Sydney, and I crossed the international date line, and I lost the day. It wasn’t my fault, but I lost my perfect record on my Apple Watch. So I had to start over.
I was on a plane in Australia in January, and I thought I was going to have five hours at my hotel, but it was just a fiasco with the flight. So I wound up running in place in my airplane seat for an hour and a half, maybe.
Like, soft footfalls? I’m not picturing it clearly.
My feet were on the ground, but I moved my arms like I was running.
You didn’t know your seatmate?
No. I mean, I would have hated to sit next to me. But you get the steps that way if you have to. I figure you deserve the points for humiliating yourself.
And I think you get points for ingenuity. Like one night, my flight was canceled. I get into a car for nine hours, I got to the town for my show, and I had to go straight to the theater and straight to the stage. And I wasn’t close to my watch goal.
So this young woman came to get a book signed and I said, “What are you going to do now?” So she said, “Now? I’m not doing anything.” And I took my watch off. I put it on her wrist. I gave her $20 and I said, “I’m going to need you to walk for two miles.”
Why did you transition from a Fitbit to an Apple Watch?
I had a friend who wanted to be Fitbit friends. Fitbit friends, I always just destroy them. But she destroyed me. If I walked 24 miles in a day, she would walk 24 and a quarter, because she lived in an earlier time zone. It just drove me out of my mind.
And Hugh, my boyfriend, said, “Just unfriend her.” And I said, “I can’t. That just doesn’t look right.” So instead, I just threw my Fitbit away.
What’s the longest walk you’ve taken? I read that it was 22 miles.
No, it was 91,000 steps. Forty-one miles. I can do 22 in my sleep.
Does Hugh often walk with you?
No, he never goes with me. It’s like, anything I do, I have to overdo, and ruin, you know? So he just doesn’t want to be a part of that.
For anybody who’s got an obsessive-compulsive nature, a Fitbit or an Apple Watch will do the job. Like, the idea that I have 1,680 days of a perfect record, I’m never going to break that for anything.
What could make you break that?
If I were to be crossing the street and I looked up and I saw a car speeding toward me, my first thought would be “my watch.”
Ken Pope
Ken Pope, Nayeli Y. Chavez-Dueñas, Hector Y. Adames, Janet L. Sonne, and Beverly A. Greene
A collection of postings on a range of issues is available on our website (www.mjacksongroup.ca). This month’s post is again from Ken Pope’s listserv, where he kindly provides daily summaries of current articles in the field.
Good Rx released a report:
8 Medications That Can Cause Depression as a Side Effect
Have you ever felt depressed or know someone who has depression? It’s likely. Depression is a common mental health condition that’s estimated to affect at least 5% of adults worldwide. And since many cases of depression go under the radar, this number is likely much higher.
There are often underlying themes among people who experience symptoms of depression. Certain factors can increase your risk for it, including brain function, genetics, and your life circumstances. It doesn’t help when medications add to this list and cause or exacerbate your symptoms.
Here, we’ll discuss eight common medications that have been linked to new or worsening depression.
Corticosteroids can cause imbalances in neurotransmitters, or chemical messengers, in your brain. These changes have the potential to affect your mental health. Corticosteroids have been shown to increase the risk of depression, anxiety, and insomnia in some cases. Irritability is also possible.
Thankfully, this doesn’t happen to everyone. Mood symptoms caused by corticosteroids depend on your medication dose and usually occur during the first few weeks of treatment. Developing depression is also less likely among people taking a short-term steroid burst or applying a steroid medication topically to your eyes, skin, or joints.
2. Parkinson’s medications like Sinemet
Depression is common in people living with Parkinson’s disease. The condition itself can cause changes in brain chemistry that contribute to depression and anxiety.
Medications used to treat Parkinson’s disease can also cause depression. According to one study, levodopa can worsen depression — especially when used at high doses. Levodopa is a key ingredient in Sinemet (carbidopa/levodopa), a common Parkinson’s medication.
On the other hand, the same study found no link between dopamine agonist use and depression. Dopamine agonists are another option for treating Parkinson’s disease and work by raising dopamine levels in the brain. Examples of these Parkinson’s medications include ropinirole, pramipexole, and rotigotine.
3. Hormonal contraceptives
Hormonal contraceptives are a type of birth control that use specific versions of estrogen and/or progestin (sex hormones) to prevent pregnancy. Some common examples include birth control pills or patches, intrauterine devices (IUDs), and vaginal rings.
Research studying the link between hormonal contraceptives and depression has gone back and forth. The true answer likely lies somewhere in the middle. For instance, one large study found that hormonal contraceptives could increase your depression risk by a small amount.
However, the study did find that depression was more likely to happen among certain hormonal contraceptive users:
Teens ages 15 to 19 years old
Women taking progestin-only contraceptives (such as the “mini-pill”)
Women using non-oral forms of hormonal contraception, such as a patch or vaginal ring
4. Stimulants like Adderall
Stimulantslike Adderall (amphetamine salts)are popular drugs for conditions like ADHD (attention-deficit hyperactivity disorder) and narcolepsy. In many cases, these medications work to improve your attention and mood.
However, stimulants are controlled substances. They come alongside a risk for misuse and dependency. What’s more, depression can occur in people who are experiencing withdrawal from stimulants like Adderall. Be sure to follow your healthcare provider’s instructions carefully when taking and stopping a stimulant.
5. Anticonvulsants like lamotrigine
Anticonvulsants, or antiepileptics, are medications that treat seizure disorders. While some of these medications can improve your mood, others can worsen it. Lamotrigine (Lamictal, Lamictal XR), gabapentin (Neurontin, Horizant), and phenytoin (Dilantin, Phenytek) are common examples.
All anticonvulsant medications have an FDA-required warning on their label that says they have a risk for causing suicidal thoughts and behavior. However, some health experts have mixed opinions on this. For instance, epilepsy alone can increase the risk of developing depression. Untreated epilepsy also poses a larger risk than the relatively small risk of mental health changes with these medications.
All the same, it’s important to remember that anticonvulsants have the potential to affect your mood. You should contact your healthcare provider if you experience any changes in your mental health status after starting a new anticonvulsant medication.
In a recent study analyzing the mood of more than 16,000 adults in the U.S., PPIs were found to potentially increase the risk of depression. They could also increase the risk of suicidal thoughts or behavior. Another study found that 14% of depression cases could be avoided by stopping PPIs.
Health experts are still learning about the effects of PPIs on mental health. If you’re concerned about the risk of depression with PPIs, make sure to have a discussion with your healthcare provider.
7. Opioids
Opioids are strong pain-relieving medications. They’re effective for this purpose, but they also have a number of risks attached to them. One of these is an increased risk of depression. Examples of opioids are tramadol, oxycodone, and methadone.
One study found that around 10% of people prescribed opioids may develop depression at some point. People who took opioids for 30 days (1 month) or longer were more likely to develop depression.
8. Antidepressants
Although it may sound strange, starting an antidepressant can initially make your depression symptoms feel worse. Antidepressants don’t actually make your depression worse, but their initial side effects can be similar to the symptoms of depression (being tired, changes in sleep and appetite, etc.).
These side effects can make you second guess starting an antidepressant in the first place. But rest assured that this is normal. For most people, these side effects are temporary. You should start to notice a positive difference within a few weeks, and you should feel the medication’s full benefits within 4 to 8 weeks.
You shouldn’t stop taking an antidepressant without talking to your healthcare provider first.
When should I contact my healthcare provider about medications that cause depression as a side effect?
It’s important to talk with your healthcare provider if you’re feeling depressed at any point. When discussing your symptoms, include details about any medications you’re currently taking and those you’ve taken in the recent past. Being thorough with your medication list is important — many different types of medications can cause depression, not just the ones discussed above.
With this information, your healthcare provider can determine if any of your medications could be contributing to your symptoms. If so, they can help you decide if your medications need to be changed or if you should seek additional help from another healthcare professional.
The bottom line
Depression is a possible side effect of many medications, such as corticosteroids, anticonvulsants, and opioids. However, many of the health conditions these medications treat can also cause depression. If you’re experiencing depressive symptoms or worsening mental health changes, talk with your healthcare provider to determine the best path forward.
If you or someone you know is struggling with depression or has had thoughts of harming themselves or taking their own life, get help.
The National Suicide Prevention Lifeline (988) provides 24/7, free, confidential support for people in distress, as well as best practices for professionals and resources to aid in prevention and crisis situations.
Ken Pope
Ken Pope, Nayeli Y. Chavez-Dueñas, Hector Y. Adames, Janet L. Sonne, and Beverly A. Greene
“…the Law of Unintended Consequences, stronger than any written Law. ‘Whether or not what you do has the effect you want, it will have three at least you never expected, and one of those usually unpleasant.'”
—James Oliver Rigney, Jr. (1948-2007) writing under the pen name Robert Jordan, The Wheel of Time
A collection of postings on a range of issues is available on our website (www.mjacksongroup.ca). This month’s post is again from Ken Pope’s listserv, where he kindly provides daily summaries of current articles in the field.
Yahoo News includes an article: “‘There’s a temptation to lump octogenarians together’: What you should know about work and aging-brain health.”
Here are some excerpts:
In the upper echelons of politics, there’s no shortage of men and women working well past the conventional retirement age.
Sen. Dianne Feinstein, D-Calif., who turns 90 next month, has said she won’t seek reelection in 2024, but she continues to serve as the oldest member of the U.S. Senate,despite a recent extended medical absence and questions about her mental acuity. In the 2024 presidential election, voters are likely to face a standoff between President Biden, who will be 82 next November, and former President Trump, who will be 78.
Experts have said that working into old age can be beneficial and improve longevity — but only if it’s by choice; being forced to do so for financial reasons has the opposite effect.
<snip>
So what are the cognitive challenges of working as an older adult — and what can aging professionals bring to the table?
What happens to the brain as we age?
A doctor looks at a magnetic resonance imaging (MRI) film that shows a neurodegenerative illness in an aging patient.
The National Institute on Aging says that as we get older, it’s not just our bodies that begin to look different — physical changes occur in the brain as well. Certain areas of the brain begin to shrink, “especially those important to learning and other complex mental activities”; communication between nerve cells in certain regions may not be as effective; there’s more inflammation; and “blood flow in the brain may decrease.”
These physical changes can correlate with changes in mental function too, but experts say there’s no fixed, universal mold when it comes to aging.
“I just saw someone in my clinic yesterday who was 86, and she really looks like she’s in her late 60s or early 70s,” Dr. Sharon Sha, a clinical professor of neurology and chief of the Memory Disorders Division at Stanford University, told Yahoo News. “I’ve met 90-year-olds who run ultramarathons, so their joints and their cardiovascular function and their brain is not reflective of a typical 90-year-old. So yes, brains can be acting very differently.”
Sha also notes that while some changes in mental function are to be expected, we’re not all predestined to encounter dementia when we get older.
According to a recent study by Columbia University, almost 10% of U.S. adults ages 65 and older have dementia, and an additional 22% have mild cognitive impairment. Instances of cognitive impairment do increase with age, though they’re still in the minority; while 3% of people between 65 and 69 have dementia, that number rises to 35% of people ages 90 and over.
<snip>
What are some challenges to working as an octogenarian?
Even for an otherwise healthy individual, some cognitive changes are to be expected. Sha said that for many people that means changes in the following:
Processing speed: “As we get older, there’s some decline in how quickly we’re thinking.”
Working memory: “The amount of total information that we can hold can diminish slightly, but not to a significant amount.”
“Our bodies are not what they once were,” David Myers, an 80-year-old professor at Hope College in Holland, Mich., said in an email to Yahoo News.
“The stairs have gotten steeper, the newsprint smaller, others’ voices fainter, our sleep more interrupted. Our memories and reasoning are less speedy. We more often experience brain freezes as we try to retrieve someone’s name or the next point we were about to make.”
What benefits can older workers bring to the table?
Boat-building craftsman.
Yet Myers said there are plenty of gifts as well as challenges to being a working octogenarian. As a social psychologist, Myers defies many of the conventional stereotypes affiliated with aging in the U.S.; he recently published a book of essays on “curiosities and marvels of the human mind” — the latest of 18 books he has written.
“There’s a temptation to lump octogenarians together, when actually their stamina and abilities vary much more than, say, 8-year-olds,” Myers said. “At 80, some are approaching death while others remain energized, purpose-filled and quick-witted.”
He said there are several advantages to being an older working professional:
Crystallized intelligence: “Although we octogenarians don’t think as quickly (our ‘fluid intelligence’ is subsiding), our ‘crystallized intelligence’ — our lifetime of knowledge and the ability to apply it — remains strong.”
Wisdom: “Older adults often benefit from a greater ability to keep things in perspective, to navigate conflicts and to appreciate the limits of their own knowledge. It takes experience to know what you don’t know.”
Emotional stability: “As teens and young adults, we rode an emotional roller coaster. In later life, our feelings mellow. We’re better able to look beyond the moment. Compliments produce less elation, criticisms less despair or irritation. Thus when facing the day’s slings and arrows, we can better take a big-picture perspective.”
The National Institute on Aging says there may be some positive cognitive changes too, with many studies showing that older adults “have more extensive vocabularies and greater knowledge of the depth of meaning of words than younger adults.”
How to keep your brain healthy and spry as you get older
Women doing yoga exercises at a park.
While genes and family history can play some role in how well you age, the Centers for Disease Control and Prevention says that “up to 40% of dementia cases may be prevented or delayed.”
A lot of brain health comes down to lifestyle choices, and Sha shared a few pieces of advice that she usually gives to her patients for better brain aging — with one tip ranking the highest.
“Exercise, exercise, exercise. Research studies are really confirming how much aerobic exercise is important for brain health,” Sha said. “I think getting your heart rate up is important 30 minutes a day, if you can do that at the minimum.”
A heart-healthy Mediterranean diet — rich in plant-based foods like seeds, vegetables and whole grains as well as fish — can do wonders for the brain as well.
While there are no specific “brain games” that offer a surefire way to better brain health, cognitive stimulation plays a significant role too.
In addition to daily exercise, Myers says it is this “active engagement” that has helped him stay sharp into his 80s — “through reading and writing and interactions that keep my brain alive and growing, and my life still purpose-filled.”
Ken Pope
Ken Pope, Nayeli Y. Chavez-Dueñas, Hector Y. Adames, Janet L. Sonne, and Beverly A. Greene
A collection of postings on a range of issues is available on our website (www.mjacksongroup.ca). This month’s post is again from Ken Pope’s listserv, where he kindly provides daily summaries of current articles in the field.
JAMA includes an article: “Borderline Personality Disorder: A Review.”
The authors are Falk Leichsenring, DSc1,2; Nikolas Heim, MA, MSc3; Frank Leweke, MD1; Carsten Spitzer, MD2; Christiane Steinert, PhD1,3; Otto F. Kernberg, MD4.Here’s how it opens:
Borderline personality disorder (BPD) is characterized by alterations in self-image and interpersonal relationships marked by sudden shifts between extremes of idealization (extremely positive views about the self or others) and devaluation (extremely negative views about the self or others).1,2 People with BPD typically experience intense anxiety, irritability, or dysphoria as well as impulsive behavior with regard to spending, sexual activity, substance misuse, or binge eating.1 Borderline personality disorder affects approximately 0.7% to 2.7% of adults.3,4
This Review summarizes current evidence regarding the epidemiology, pathophysiology, diagnosis, and treatment of BPD in adults.
Here’s another excerpt: Although BPD affects approximately 0.7% to 2.7% of adults in the general population,3,4 higher prevalence rates were reported in primary care (6%), patients using outpatient psychiatric services (11%-12%), and patients treated in psychiatric hospitals (22%).4,5 In a US community sample of 34 481 adults, 2.7% had been diagnosed with BPD in their lifetime. In this study, only slightly higher rates were observed in women compared with men (3% vs 2.4%),6 while among 3800 patients treated in a psychiatric outpatient setting, considerably higher rates of BPD were found in women compared with men (72% vs 28%).5 The age of onset varies, but symptoms are usually manifest in early adulthood.1 Borderline personality disorder is associated with severe social and vocational impairments, such as inability to hold a job, high rates of comorbid mental disorders and somatic diseases, more frequent use of outpatient and inpatient medical services, high rates of suicide, and high direct medical and indirect costs (eg, sick-leave days). These factors are more common in patients with BPD compared with patients with anxiety and depressive disorders, diabetes, epilepsy, or Parkinson disease.7–12 Only approximately 16% of people with BPD were reported to be married or living with a partner and only about 35% had good work or school performance.13 People with BPD had worse global social functioning than people with other personality disorders (avoidant and obsessive-compulsive personality disorders) and higher rates of comorbid major depressive disorder.14
More patients with BPD than patients with other personality disorders die by suicide. A 24-year prospective follow-up study including 290 patients with BPD and 72 patients with other personality disorders reported that 5.9% of patients with BPD died by suicide compared with 1.4% of patients with other personality disorders.12
Another excerpt: Borderline personality disorder is associated with significantly higher prevalences of other mental disorders.16 In the US study of 34 481 community-dwelling adults, people with BPD had higher rates of the following mental disorders in their lifetime: mood disorders such as major depression or bipolar disorder (83%), anxiety disorders (85%), substance use disorders (78%), posttraumatic stress disorder (PTSD) (30%), and other personality disorders (53%).6
In the general population, including approximately 12% of individuals with personality disorders including BPD,19 lifetime prevalence rates of mood disorders, anxiety disorders, PTSD, substance use disorders, and personality disorders were 21%, 34%, 8%, 3%, and 12%, respectively.19-21
Of patients with BPD, approximately 10% had bipolar I disorder (depressive and manic episodes) and an additional 10% had bipolar II disorder (depressive and hypomanic episodes).22,23 Among people with attention-deficit/hyperactivity disorder, the lifetime rate of BPD was 37.7%.24
In older compared with younger patients with BPD, a shift in symptoms toward more depression, feelings of emptiness, and somatic problems has been described.25-27
As people with BPD become older, emotional dysregulation, unstable interpersonal relationships, anger, and attachment insecurity typically persist, whereas impulsivity and identity disturbances tend to decrease.25,26 In older people with BPD, self-harm may manifest as nonadherence to medications or misuse of medication.26
Another excerpt: Genetic factors and adverse childhood experiences may interact to influence brain development through altered hormones and neuropeptides, increasing the risk of BPD.7,37-40 Adverse childhood experiences may modulate gene expression and lead to stable personality traits.7,38,41 Borderline personality disorder is more common in people with a family history of BPD.7,42 For example, a population-based Swedish study including 1 851 755 participants, of whom 11 665 (0.6%) had a diagnosis of BPD according to the ICD-10, estimated heritability of BPD at 46%; the remaining 54% of variance was explained by nonshared environmental factors.43 The hazard ratio was highest in identical twins (11.5; 95% CI, 1.6-83.3). The risk of receiving a BPD diagnosis was increased 4.7-fold for full siblings.43 However, no single-nucleotide variants have been identified for BPD.44 Adverse childhood experiences including physical, sexual, or emotional abuse and neglect are more common in people with BPD.16,45,46 However, not all people diagnosed with BPD have a history of adverse childhood experiences.45 An empirically supported model of the neurobiology of BPD does not exist, as meta-analyses on neuroendocrinological processes47-49 and brain functioning50,51 found only a few differences in these variables among people with BPD compared with healthy controls. The most consistent finding was hyperactivity of the amygdala,50,51 but its role remains unclear.52
Another excerpt: Patients with BPD should be informed of their diagnosis, the expected course of the disorder, etiology, and treatment options.54 Clinicians should set clear boundaries, avoid responding to provocative behavior, avoid polypharmacotherapy, and facilitate open communication and agreement on a consistent approach with all treating clinicians to prevent a situation in which some clinicians are regarded as “good” and others as “bad” (Table 1).54,55,67 The patient should be informed that effective methods of psychotherapy exist and that medications are appropriate only for treating discrete comorbid mental disorders or in situations of crisis, such as suicidal behavior, extreme anxiety, or psychotic episodes. This education of patients facilitates an alliance between patients and clinicians and may encourage patients to take part in psychotherapy.7 Typical crises in BPD consist of suicidal behavior or ideation, extreme anxiety, psychotic episodes, or other extreme behavior likely to endanger the patient or others, usually caused by interpersonal problems such as real or imagined abandonment or by shifts from idealization to devaluation. Life-threatening behaviors (eg, suicidal, self-mutilating, or high-risk behaviors, as well as attacks against others) should be identified and promptly treated (see Pharmacotherapy section and Table 1). With regard to comorbid mental disorders, experts suggest that comorbid bipolar I disorder, early-onset complex PTSD, severe substance misuse, and anorexia should be treated before BPD, since these disorders need to be well controlled before BPD can be treated successfully.7 In contrast, for patients who have comorbid depressive disorder, panic disorder, adult-onset PTSD, intermittent substance use disorder, or bulimia, treating BPD should take priority since these disorders will likely improve once BPD is controlled. In a randomized trial of 68 family members of patients with BPD, group psychoeducation about the disorder along with self-care and peer support skills reduced the emotional stress associated with BPD in family members compared with a wait-list control condition.68 If specialized methods of psychotherapy are not available, experienced mental health professionals may apply psychoeducation (informing a patient about the disorder and its treatments) or manage acute crises using pharmacotherapy and clinical management as described in the Pharmacotherapy section.69 Benefit for this generalist model of treating patients with BPD has emerged from several randomized clinical trials.70-72 This type of care can be carried out by experienced clinicians without training in the specialized methods of psychotherapy discussed below.69
Another excerpt:
Although the 2001 American Psychiatric Association practice guidelines for BPD recommended antidepressants such as fluoxetine, sertraline, or venlafaxine; mood stabilizers such as lithium carbonate, carbamazepine, or valproate; antipsychotics such as haloperidol; monoamine oxidase inhibitors such as phenelzine or tranylcypromine; or benzodiazepines such as alprazolam or clonazepam for affective dysregulation and impulsive behavior dyscontrol, new evidence has accumulated since these guidelines were published.73
No class of psychoactive medication has been consistently effective in treating BPD in randomized clinical trials, and therefore no medications have been approved by the US Food and Drug Administration or licensed for use in BPD in the UK.7,74–76For these reasons, the UK National Institute for Health and Care Excellence (NICE) guideline does not recommend pharmacotherapy to treat any core symptom of BPD (eg, marked emotional instability, transient stress-related paranoid ideation).61,62 This is consistent with reviews of functional magnetic resonance imaging studies showing that pharmacotherapy does not induce changes in brain activity or brain connectivity,77 whereas psychotherapy appears to alter neural activities and connectivity of regions subserving executive control and emotion regulation.78 The NICE guideline recommends pharmacotherapy in BPD only for discrete and severe comorbid disorders such as severe depressive disorders, including suicidal ideation or severe anxiety disorders. For these types of comorbid disorders in BPD, selective serotonin reuptake inhibitors such as escitalopram, sertraline, or fluoxetine may be used. Antipsychotic drugs are not recommended by the NICE guideline for medium- or long-term treatment of BPD. For specific recommendations regarding the treatment of comorbid conditions in BPD, NICE recommends consulting the NICE clinical guidelines for the respective disorders. Few randomized clinical trials have focused on BPD with distinct comorbidities.76 Most randomized clinical trials of pharmacotherapy excluded patients with comorbid major depressive disorder, bipolar disorder, psychotic disorders, or substance-related disorders, limiting available evidence for patients with BPD and these comorbidities.76For the management of crises in BPD as defined above, NICE recommends verbal intervention (eg, trying to understand a crisis from a patient’s view) (Table 1) and short-term pharmacotherapy using a single drug, with the minimum effective dose or prescribing fewer tablets more frequently if there is a risk of overdose.61For treatment of acute crises in BPD, sedative antihistamines (eg, promethazine) or low-potency antipsychotics (eg, quetiapine), but not benzodiazepines (eg, diazepam, lorazepam), may be used as part of an overall treatment plan agreed on by all participating clinical practitioners (Table 2).62 The duration of pharmacological treatment should be agreed on with the patient and is not recommended for longer than 1 week.61,62Sedative antihistamines such as promethazine, however, are not licensed in either the US or in the UK for BPD; therefore, informed consent should be obtained and documented.61 This includes informing patients that promethazine is associated with abuse80 and should be used with caution in a disorder in which patients have higher rates of substance abuse. For insomnia in BPD, general advice about sleep hygiene without medication prescription is recommended. For short-term management of insomnia, “Z-drugs” (eg, zolpidem or eszopiclone) may be prescribed.61 Due to concerns about dependency, use of Z-drugs is recommended only for severe insomnia, with the lowest dose possible and for no longer than 4 weeks.81
Short-term symptoms of depression or anxiety that are part of BPD emotional instability and that can be related to specific triggering situations such as interpersonal problems should not be misinterpreted as comorbid disorders and should be treated solely with psychotherapy.
Another excerpt: Psychotherapy is first-line treatment for BPD and should be recommended to all patients with BPD.7,61,82Several meta-analyses of randomized clinical trials have shown that psychotherapy is associated with benefit for patients with BPD (Table 3). A Cochrane series of meta-analyses that included a total of 75 randomized clinical trials with 4507 patients provided evidence regarding efficacious therapies for BPD.60 For example, in a meta-analysis of 22 randomized clinical trials with 1244 patients comparing psychotherapy with usual care, psychotherapy was associated with significant improvement in symptom severity compared with usual care, with a medium effect size (standardized mean difference [SMD], −0.52) (Table 3).60 This effect size exceeded the minimum clinically relevant difference for BPD symptom severity (SMD, 0.43) and represented a clinically relevant reduction.60 Psychotherapy was not associated with higher rates of adverse effects compared with usual care (risk ratio, 0.86; 95% CI, 0.14-5.09; P = .86 [4 trials; n = 571]).60 Several types of psychotherapy for BPD exist (eTable in the Supplement). A subgroup analysis from the Cochrane meta-analysis60 compared dialectical behavior therapy, psychodynamic therapy, cognitive behavior therapy, and eclectic therapy in data from 17 randomized clinical trials and 1045 patients. There were no significant differences between these treatments for the outcome of symptom severity or psychosocial functioning (P = .88). Dialectical behavior therapy, a form of cognitive behavior therapy specifically developed for treatment of BPD, focuses on increasing a patient’s motivation to engage in treatment and problem-solving strategies, and uses group skills training to help regulate emotions and interpersonal relationships and telephone coaching in times of crises between regular sessions (eTable in the Supplement). Compared with usual care, dialectical behavior therapy was associated with a medium between-group effect size (SMD) of −0.60 for improving BPD severity (Table 3) and small between-group effect sizes for self-harm (SMD, −0.28) and psychosocial functioning (SMD, −0.36), with low to moderate heterogeneity (I2 = 42%, 0%, and 31%, respectively).60Psychodynamic therapy proved to be efficacious in treatment of BPD as well.83 Psychodynamic therapy includes a family of psychotherapeutic approaches that focus on identification of recurring patterns of behavior related to the self and others, including the therapeutic relationship, expression of emotion, exploration of defensive (avoidance) patterns, and discussion of past experiences that have an effect on a patient’s present experiences.85Specific forms of psychodynamic therapy have been developed that tailor treatment specifically to BPD, such as transference-focused psychotherapy and mentalization-based therapy (eTable in the Supplement). In a meta-analysis that included 16 randomized clinical trials and 1081 participants, psychodynamic therapy was associated with medium between-group effect sizes compared with usual care (Table 3) for the outcomes of core BPD symptoms (SMD, −0.65), suicide-related outcomes (SMD, −0.67), and psychosocial functioning (SMD, −0.57), with low or moderate heterogeneity (I2 = 15%, 40%, and 60%, respectively) (John R. Keefe, written communication of data for comparison of psychodynamic therapy with usual care for the meta-analysis by Barber et al,83 November 3, 2021).
Another excerpt: An observational study of 290 patients with BPD reported that over a 10-year period, 50% recovered, defined as symptomatic remission and good social and vocational functioning over a 2-year period.89 Among the patients who recovered, 34% lost their recovery and 30% had a recurrence of BPD symptoms and diagnosis after a 2-year long remission.89 (In these studies, recovery was defined as symptomatic recovery in combination with excellent social and vocational functioning over 2 years. Recurrence was defined as recurrence of classic BPD symptoms.) In contrast, 93% of BPD patients attained remission from BPD lasting 2 years and 86% attained remission lasting 4 years.89 Excellent recovery, defined as remission of BPD or other personality disorders and good social and full-time vocational functioning, occurred in 39% of patients with BPD compared with 73% of patients with other personality disorders.90 However, most individuals with BPD in these longitudinal studies received pharmacotherapy or psychotherapy. Therefore, these remission rates may be better than the natural history of untreated BPD over time and might be related to these therapies.91
Here’s how the article concludes:
Borderline personality disorder affects approximately 0.7% to 2.7% of adults and is associated with functional impairment and greater use of medical services. Psychotherapy with dialectical behavior therapy and psychodynamic therapy are first-line therapies for BPD, while psychoactive medications do not improve the primary symptoms of BPD.
REPRINTS & OTHER CORRESPONDENCE:
Falk Leichsenring, DSc, Department of Psychosomatics and Psychotherapy, University of Giessen, Ludwigstrasse 76, 35392 Giessen, Germany (falk.leichsenring@psycho.med.uni-giessen.de).
Ken Pope
Ken Pope, Nayeli Y. Chavez-Dueñas, Hector Y. Adames, Janet L. Sonne, and Beverly A. Greene
“Yes, the newspapers were right: snow was general all over Ireland. It was falling softly upon the Bog of Allen and, further westwards, softly falling into the dark mutinous Shannon waves. It was falling too upon every part of the lonely churchyard where Michael Furey lay buried. It lay thickly drifted on the crooked crosses and headstones, on the spears of the little gate, on the barren thorns. His soul swooned slowly as he heard the snow falling faintly through the universe and faintly falling, like the descent of their last end, upon all the living and the dead.”
A collection of postings on a range of issues is available on our website (www.mjacksongroup.ca). This month’s post is again from Ken Pope’s listserv, where he kindly provides daily summaries of current articles in the field.Cell includes a study: “Brief structured respiration practices enhance mood and reduce physiological arousal.”
The authors Melis Yilmaz Balban, Department of Neurobiology, School of Medicine, Stanford University, et al. Here’s how it opens:
Breathing is a life-sustaining bodily function, facilitating oxygenation and carbon dioxide disposal, but scientific studies on its significance for the mind-body connection have been limited. Embedded in ancient practices for centuries, breathwork has emerged as an intervention due to its reported health benefits. The COVID-19 pandemic highlighted the importance of simple, fast-acting, and cost-effective techniques to address widespread physical and mental health challenges and limited access to health care. While the neurobiology of breath has been studied both in animals and humans,1 little comparative data exist on the effects of different breathing techniques or the amount of breathing exercise that must be performed to produce those effects.
The pattern and depth of breathing have direct physiological impact on oxygenation level, heart rate, ventilation, and blood pressure.2 Slow breathing at a rate of six breaths per minute reduces chemoreceptor reflex response to hypercapnia and hypoxia compared with spontaneous respiration at 15 breaths per minute.3 Impairment of baroreceptor reflex sensitivity plays a role in the etiology of hypertension, and how we breathe has numerous other major health implications. Heart rate and blood pressure decrease with slow breath in patients with essential hypertension compared with higher-frequency breathing.4 Breathing training has also been shown to improve quality of life for asthmatics and to decrease use of bronchodilators.5 Furthermore, there is evidence that nasal breathing affects the CNS differently than mouth breathing. While nasal breathing synchronizes electrical activity in the olfactory cortex as well as amygdala and hippocampus, mouth breathing does not,6 which has implications for stress management and treatment of anxiety. Moreover, the mere act of inhaling has been shown to increase alertness levels and learning in humans.7
It is also clear that different emotional and cognitive states alter the depth and frequency of breathing,8,9,10,11,12 which likewise impacts emotional state, in part by regulation of carbon dioxide levels.13,14,15,16,17 There is growing evidence that brain-body states, ranging from sleep to stress to physical activity to meditation, can help people buffer and better manage stressors. A review of Yogic breathing practices reported increased feelings of peacefulness, improved reaction time and problem solving, decreased anxiety, and reduction of mind wandering and intrusive thoughts.18,19
Here’s the abstract: Controlled breathwork practices have emerged as potential tools for stress management and well-being. Here, we report a remote, randomized, controlled study (NCT05304000) of three different daily 5-min breathwork exercises compared with an equivalent period of mindfulness meditation over 1 month. The breathing conditions are (1) cyclic sighing, which emphasizes prolonged exhalations; (2) box breathing, which is equal duration of inhalations, breath retentions, and exhalations; and (3) cyclic hyperventilation with retention, with longer inhalations and shorter exhalations. The primary endpoints are improvement in mood and anxiety as well as reduced physiological arousal (respiratory rate, heart rate, and heart rate variability). Using a mixed-effects model, we show that breathwork, especially the exhale-focused cyclic sighing, produces greater improvement in mood (p < 0.05) and reduction in respiratory rate (p < 0.05) compared with mindfulness meditation. Daily 5-min cyclic sighing has promise as an effective stress management exercise.
Here’s a graphical abstract:
Here’s how the Discussion opens: We conducted a randomized controlled study to compare the psychophysiological effects of 5-min daily practice of three different breathing exercises and mindfulness meditation over 1 month. We assessed group differences in acute effects by using a linear mixed-effects modeling approach that took into account multiple measurements from each participant and the effect of adherence. We also looked at baseline and post-study measurements of sleep-related daytime disturbances, trait anxiety, and slopes of physiological measures throughout the study. We found differential effects of these exercises on both daily acute measures and physiological measures over the course of the study.
While all four groups showed significant daily improvement in positive affect and reduction in state anxiety and negative affect, there were significant differences between mindfulness meditation and breathwork in positive affect (Figures 2 and 3). Our daily monitoring and mixed-effects modeling approach allowed us to measure impacts throughout the study and revealed that the positive affect benefits of the breathwork exercises increased with more practice over time (Figure 2). Specifically, the cyclic sighing group showed more increase in positive affect toward the end of the study in a way that was significantly different than that for those randomized to mindfulness meditation, who had the least increase in positive affect (Figure 3). Overall, breathwork practices, particularly cyclic sighing, were more effective than mindful meditation in increasing positive affect, supporting our hypothesis that intentional control over breath with specific breathing patterns produces more benefit to mood than passive attention to one’s breath, as in mindfulness meditation practice.
Another excerpt: Our study monitored subjects daily and collected daily physiological data remotely, a capability that was forced by the COVID restrictions but was enabled by the wearable technology that the WHOOP strap offered. The use of wearables enabled us to assess the changes longitudinally as opposed to just in two time points before and after the study and revealed differences in groups over time that would not be otherwise possible.58 It also allowed us to include a geographically diverse participant pool. A limitation of this remote study was having less control over some variables that may influence the results such as knowing how exactly the subjects practiced the exercises or controlling exactly how long they practiced. We advise future remote studies to take such variables into consideration. Overall, the study showed that remote administration of interventions is effective and that physiological monitoring is possible. Our results also support the importance of the discipline of daily practice to see substantial effects. Altogether, our study paves the way for deeper in-lab and remote mechanistic explorations to understand the differential impacts that distinct breathing techniques can have on mood and respiratory function.
REPRINTS & OTHER CORRESPONDENCE:
David Spiegel, Department of Psychiatry & Behavioral Sciences, School of Medicine, Stanford University, Stanford, CA 94305; & USA Center for Stress and Health, School of Medicine, Stanford University, Stanford, CA 94305, USA dspiegel@stanford.edu
Ken Pope
Ken Pope, Nayeli Y. Chavez-Dueñas, Hector Y. Adames, Janet L. Sonne, and Beverly A. Greene
A collection of postings on a range of issues is available on our website (www.mjacksongroup.ca). This month’s post is again from Ken Pope’s listserv, where he kindly provides daily summaries of current articles in the field.
The article is as follows:Sleep Medicine Reviews has scheduled a study for publication in a future issue: “The effect of caffeine on subsequent sleep: A systematic review and meta-analysis.” The authors are Carissa Gardiner a b, Jonathon Weakley a b c, Louise M. Burke d, Gregory D. Roach e, Charli Sargent e, Nirav Maniar b f, Andrew Townshend a b, & Shona L. Halson a b.
Here’s how it opens: Sleep is an essential component of physical and emotional wellbeing [1]. Current recommendations outline the need for healthy adults to achieve seven to 9 h of sleep per night [2]. Despite the innate requirement to attain healthy sleep, insufficient sleep is a growing public health challenge. It is estimated that 20–45% of the population around the world are sleep deprived [[3], [4], [5], [6]]. Short and fragmented sleep bouts may result in impaired cognitive functioning, diminished mood, and increased risk of accident or injury [1]. When sustained chronically, insufficient sleep contributes to the risk of health epidemics with a heightened probability of cardiometabolic disease and mental health disorders [7,8]. Negative outcomes of this nature carry a significant cost to the individual and society, through compromised health and reduced productivity [9]. As such, recommendations for positive sleep behaviours have been developed to provide individuals with strategies to optimise their sleep quantity and quality [10].
A common behavioural recommendation to optimise sleep is to avoid caffeine in close proximity to bedtime [10]. Caffeine is a widely accessible psychostimulant found in foods, supplements, and medications [11]. With its status as a socially acceptable drug, caffeine is consumed by approximately 80% of the world’s population [12]. Caffeine is an adenosine antagonist suggested to acutely reduce sleep pressure through action on the homeostatic component of sleep-wake regulation [13]. This action stimulates the central nervous system with a resulting decrease in the perception of fatigue and sleepiness [14]. For this reason, caffeine is commonly consumed throughout the day in response to insufficient sleep to promote a state of wakefulness [15]. However, the use of caffeine to stimulate wakefulness may result in impaired onset and maintenance of subsequent sleep [16], potentially creating a cycle of diminished sleep and subsequent caffeine reliance [17].
The half-life of caffeine displays large variation across healthy adults (two to 10 h) [18], making it difficult to identify the appropriate time of day to discontinue caffeine intake to minimise disruptions to sleep. Currently, recommendations for positive sleep behaviours display a lack of precision in terminology. For example, the American Academy of Sleep Medicine warns that caffeine may cause sleep disruption if taken “too close to bedtime” [19], while the Sleep Health Foundation suggests consumers should “avoid caffeine close to bedtime” [20]. The lack of precision in these recommendations may limit the ability of consumers to make evidence-based decisions regarding the timing of their caffeine intake. A previous systematic review by Clark and Landolt [21] confirmed the negative association between caffeine and subsequent sleep. However, this review did not include a quantitative synthesis of the findings. In particular, the impact of the dose and timing of caffeine intake on subsequent sleep has yet to be quantified systematically. The aims of this systematic review and meta-analysis are to: 1) establish the level of evidence for the effect of caffeine intake on the characteristics of subsequent sleep (i.e., total sleep time, sleep onset latency, rapid eye movement (REM) onset latency, wake after sleep onset, sleep efficiency, sleep architecture, and subjective sleep quality; 2) quantify the effect of caffeine intake on the characteristics of subsequent sleep; and 3) quantify the influence of the dose and timing of caffeine intake on the characteristics of subsequent sleep. The review will provide evidence-based guidance to support recommendations regarding caffeine consumption to minimise decrements in subsequent sleep.
Here’s the abstract: The consumption of caffeine in response to insufficient sleep may impair the onset and maintenance of subsequent sleep. This systematic review and meta-analysis investigated the effect of caffeine on the characteristics of night-time sleep, with the intent to identify the time after which caffeine should not be consumed prior to bedtime. A systematic search of the literature was undertaken with 24 studies included in the analysis. Caffeine consumption reduced total sleep time by 45 min and sleep efficiency by 7%, with an increase in sleep onset latency of 9 min and wake after sleep onset of 12 min. Duration (+6.1 min) and proportion (+1.7%) of light sleep (N1) increased with caffeine intake and the duration (−11.4 min) and proportion (−1.4%) of deep sleep (N3 and N4) decreased with caffeine intake. To avoid reductions in total sleep time, coffee (107 mg per 250 mL) should be consumed at least 8.8 h prior to bedtime and a standard serve of pre-workout supplement (217.5 mg) should be consumed at least 13.2 h prior to bedtime. The results of the present study provide evidence-based guidance for the appropriate consumption of caffeine to mitigate the deleterious effects on sleep.
Here are the practice points: 1. Consuming caffeine prior to sleep reduces total sleep time and sleep efficiency, and increases sleep onset latency and wake after sleep onset. 2. Caffeine consumption alters subsequent sleep architecture with an increase in the occurrence of light sleep (N1) and a reduction in the occurrence of deep sleep (N3 and N4). 3. Reductions in total sleep time are dependent on the final dose of caffeine and the time of day that it is consumed relative to bedtime, with greater reductions occurring when larger doses are consumed closer to bedtime. 4. To avoid reductions in total sleep time, coffee (107.5 mg per 250 mL) should be consumed at least 8.8 h prior to bedtime and a standard serve of pre-workout supplement (217 mg) should be consumed at least 13.2 h prior to bedtime.
REPRINTS & OTHER CORRESPONDENCE:
Jonathon Weakley, School of Behavioural and Health Sciences, Australian Catholic University, Brisbane, Australia — Jonathon.Weakley@acu.edu.au
Ken Pope
Ken Pope, Nayeli Y. Chavez-Dueñas, Hector Y. Adames, Janet L. Sonne, and Beverly A. Greene
On a dark desert highway Cool wind in my hair Warm smell of colitas Rising up through the air Up ahead in the distance I saw a shimmering light My head grew heavy and my sight grew dim I had to stop for the night
There she stood in the doorway I heard the mission bell And I was thinking to myself “This could be Heaven or this could be Hell” Then she lit up a candle And she showed me the way There were voices down the corridor I thought I heard them say
Welcome to the Hotel California Such a lovely place (such a lovely place) Such a lovely face Plenty of room at the Hotel California Any time of year (any time of year) You can find it here
Her mind is Tiffany-twisted She got the Mercedes Benz She got a lot of pretty, pretty boys That she calls friends How they dance in the courtyard Sweet summer sweat Some dance to remember Some dance to forget
So I called up the Captain “Please bring me my wine” He said, ‘We haven’t had that spirit here Since 1969″ And still those voices are calling from far away Wake you up in the middle of the night Just to hear them say
Welcome to the Hotel California Such a lovely place (such a lovely place) Such a lovely face They livin’ it up at the Hotel California What a nice surprise (what a nice surprise) Bring your alibis
Mirrors on the ceiling The pink champagne on ice And she said, ‘We are all just prisoners here Of our own device” And in the master’s chambers They gathered for the feast They stab it with their steely knives But they just can’t kill the beast
Last thing I remember, I was Running for the door I had to find the passage back To the place I was before “Relax, ” said the night man “We are programmed to receive You can check out any time you like But you can never leave”
A collection of postings on a range of issues is available on our website (www.mjacksongroup.ca). This month’s post is again from Ken Pope’s listserv, where he kindly provides daily summaries of current articles in the field.
The article is as follows:The Washington Post includes an article: “What causes your brain to procrastinate and how to face it.”
Here are some excerpts: A 2022 study in the journal Nature Communications suggests that a root of procrastination may lie in a cognitive bias — we believe that doing tasks will somehow be easier in the future.
“You know it’s going to stink in the future just as much as it’s going to stink doing it now, but internally you just can’t help yourself,” said Samuel McClure, professor of psychology and cognitive neuroscientist at Arizona State University.
“It’s a fascinating phenomenon — that myopia you can’t escape — even though if you just stop and think about it, it’s ludicrous.”
There is individual variation, but “procrastination is a tendency that we all encounter in our life in different domains, or at different time points in our lives,” said Raphaël Le Bouc, a neurologist at the Paris Brain Institute and author of the study. “But the true cognitive mechanisms behind it are not really known. And this might be a reason why it’s difficult to overcome this tendency.”
Procrastinating brains believe that tasks will be easier in the future Researchers asked 43 adults to rate their preferences for receiving smaller rewards quicker or larger rewards later, as well as for performing easier tasks sooner or moreeffortful tasks later. For rewards, earlier research has shown that humans tend to be more impulsive and prefer a smaller reward sooner over a larger reward later, a finding that was replicated in Le Bouc’s study. A bird in hand now is worth two in some future bush.
His study also shows people similarly discount and downplay future effort, preferring an easiertask now vs. a more difficult one in the future, such as memorizing 10 digits of pi in one day or 20 digits by next week.
When the researchers had 27 of the 43 subjects perform the same experiment in an fMRI neuroimaging machine, one brain area stood out as central to making this cost-benefit calculation — the dorsal medial prefrontal cortex.
Brain activity in this region seemed to combine information about rewards and efforts for a task; more effortful tasks increased its neural activity, while more rewards decreased it.
When you are struggling to decide because the choices are almost equal, that is when this brain area is most active, said McClure, who was not involved in the study. This fits with the subjective feeling of procrastination, he said: “You’re struggling with it and doing it anyway.”
Procrastination-prone brains were especially sensitive to the idea that doing tasks in the future was much easier.
“When they imagine doing an effort in one month, for them, the cost decreases a lot,” Le Bouc said. But for non-procrastinators, the cost decreases much slower. <snip>
Procrastinating is more likely when the task is harder
To measure procrastination more directly in the lab, the researchers asked the participants to choose whether to perform tasks for a reward now, or the same task tomorrow for the same reward. The participants were informed that they would need to perform one of the tasks on their chosen day. <snip>
As expected, the more effort something takes, or the less rewarding the task, the more likely the participants were to want to procrastinate.
Crucially, the more someone downplayed how difficult future tasks would be, the more likely they would be to delay the task. <snip>
Procrastination is also not a one-time decision, but one we get to make repeatedly to put off the task until the proverbial tomorrow.
<snip> To assess procrastination behavior in more real-life settings, the researchers turned to bureaucratic busywork.
Participants were informed that to receive their payment, they had to fill out at home and return 10 pieces of arduous administrative paperwork such as documents for passport and driver’s license renewals, within 30 days. “The forms actually were quite boring,” Le Bouc said.
Using their behavioral and brain imaging data, the researchers were able to build a computational model to predict how long each person would delay completing the paperwork. Almost everyone procrastinated to some extent.
<snip> For both the in-lab and at-home experiments, the hallmark of procrastination severity was how much each individual believed the tasks would be less effortful in the future by making certain choices. Differences in the neural activity of the dorsomedial prefrontal cortex also predicted participant procrastination predilection.
In other words, the more your brain discounts how much effort is required to do something in the future, the more likely you are to procrastinate.
How to face procrastinationThe findings from this study suggest there are two ways to tackle procrastination, though more research is needed.Remember the task. Because procrastination is a repeated decision, you need to remember you had something on your plate in the first place. “If you forget that at some point that you have this decision to make, then obviously you will never perform the task,” Le Bouc said.
Setting reminders for the task and prompting that decision more frequently may reduce your probability to procrastinate, he said.
Envision your future self. You could also try addressing the cognitive bias of believing a task is easier in the future head-on. Envisioning your future self — the one who will be saddled with unpaid bills, looming deadlines and unwashed dishes — could remind you that procrastinating is not making the task any easier.
This practice, known as episodic future thinking, has been used as a way of counteracting addiction or food cravings. “Trying to make these efforts in the future more vivid, more realistic, might increase the signal of the cost in your brain and might help you realize that, actually, the cost is going to be exactly the same as it would be now,” Le Bouc said.
Ken Pope
Hector Y. Adames, Nayeli Y. Chavez-Dueñas, Melba J.T. Vasquez, & Ken Pope:
A collection of postings on a range of issues is available on our website (www.mjacksongroup.ca). This month’s post is again from Ken Pope’s listserv, where he kindly provides daily summaries of current articles in the field.
The article is as follows: Pharmacological Research has scheduled a study for publication in a future issue: “Vitamin D protects against depression: Evidence from an umbrella meta-analysis on interventional and observational meta-analyses.” The authors are Vali Musazadeh et al.
Here’s how it opens: Depression is a mental disorder that causes disabling effects of mood and anxiety disorders. Depression has also become a leading global cause of disease burden [1], [2]. Based on the evidence from the World Health Organization, more than 264 million people are affected by depression worldwide [3]. In the wake of the COVID-19 outbreak, a number of studies have demonstrated a rise in depression psychopathology and suicide tendencies across a variety of countries [4]. Depressive symptoms were the most common mental health condition during the COVID-19 pandemic, ranging from 14.6 to 48.3% across all populations, according to a systematic review [5]. People who suffer from depression may feel sad, anxious, hopeless, helpless, irritable, worthless, guilty, or ashamed [6]. There might also be decreased appetite or overeating, and inability to exercise, or even suicide among them [7]. Antidepressants, which have been used for many years to treat depression, have raised concerns about their effectiveness and tolerance [8], [9], [10]. Furthermore, the failure of depression to respond to a wide range of pharmaceutical treatments [11] indicates that other mechanisms are involved in the pathogenesis of depression, such as those affecting neuroendocrine, immunological, neurotrophic, and metabolic systems [12]. In spite of these challenges, complementary treatments for depression appears to be helpful.
Vitamin D is a unique neurosteroid hormone that may play a role in depression [13]. Vitamin D has numerous functions in the brain such as neuroimmunomodulation, regulation of neurotrophic factors, neuroprotection, neuroplasticity, and brain development [14]. Also, vitamin D receptors can be found on the neurons and glia in many parts of the brain, including the cingulate cortex and the hippocampus [15]. Vitamin D deficiency may have played a significant role in stress-related depression during the COVID-19 pandemic, according to a growing body of literature [16]. Vitamin D is thought to influence the serotoninergic system and contribute to the maintenance of circadian rhythms, both of which are associated with depressive symptoms [16], [17]. As a result, it is biologically plausible that vitamin D might play an important role in the treatment of depressive disorders [13].
Another excerpt: In the current study, we included meta-analyses of randomized controlled trials (RCTs) and of observational studies (cohort and cross-sectional) that investigated the effect of vitamin D supplementation on depression symptoms considering the following criteria: reporting standardized mean difference (SMD), or odds ratio (OR) and their corresponding confidence intervals (CI) for vitamin D supplementation on depression symptoms. Other studies were excluded from this review, including original experimental studies, case reports, in vitro, ex-vivo, and in vivo investigations.
Here’s how the Discussion opens: The current umbrella meta-analysis summarized 15 meta-analyses, which inluded 65 RCTs, and 31 observational (cohort and cross-sectional) studies. According to the results, vitamin D supplementation was efficient in alleviating symptoms of depression and an inverse association was observed between higher serum levels of vitamin D intake and overall depression. Based on sub-group analyses, vitamin D supplementation in studies using dosage of > 5,000 IU/day, and intervention duration of ≤20-weeks exhibited stronger effects in lowering symptoms of depression. Morever, the inverse association between lower serum vitamin D levels and depression was stronger among participants aged ≤50 years.
Recent studies have shown a significant association between vitamin D insufficiency or deficiency and depressive disorders [32]. Receptors of vitamin D and 1-alphahydroxylase enzymes, involved in the hydroxylation of 25-hydroxy vitamin D (25OHD) to the active form 1,25-dihydroxy vitamin D, are present on neurons and glia in multiple regions of the brain, including prefrontal cortex, substantia nigra, cingulate cortex and hippocampus and hypothalamus which have an important role in the pathophysiology of depression [13], [30], [34], [39]. Vitamin D is involved in the synthesis of neurotrophic factors and neurotransmitters (serotonin, dopamine, adrenalin, and noradrenaline) through VDRs in the adrenal cortex and due to its steroidal structure, modulates the hypothalamic-pituitary-adrenal axis and GABA‐A receptors activity [30], [34].
During depression, inflammatory markers increase [34]. Meanwhile, vitamin D displays antioxidant effects in the central nervous system, enhances nerve growth factors and the gene expression of antioxidant agents, down-regulates cytokines and inflammatory mediators such as nuclear factor-kB, which is linked to psychosocial stress and depression [32]. In general, vitamin D prevents the onset of depression by taking role in sixmain pathways: 1) Controlling the expression of calcium homeostasis genes; 3) Controlling serotonin synthesis via alleviating tryptophan hydroxylase 2 (TPH2) expression and repressing tryptophan hydroxylase1 (TPH1); 4) Controlling inflammation by reducing the expression of inflammatory cytokines; 5) Controlling the expression of mitochondrial proteins that preserve normal mitochondrial respiration; and 6) Preventing the hypermethylation of gene promotors such as Jumonji domain-containing protein 1 A and 3 (JMJD1A, JMJD3) and lysine-specific demethylase 1 and 2 (LSD1, LSD2). These genes have a significant role in the activation of GABAergic neurons [29], [42]. Fig. 5 exhibits the mechanism of action of vitamin D in preventing and lowering symptoms of depression.
Another excerpt: Fig. 5. The mechanism of action of vitamin D in preventing and declining symptoms of depression.
Here’s how the article concludes: The present umbrella of meta-analyses confirms the potential benefits of vitamin D supplementation in reducing symptoms of depression and an inverse relationship between higher serum levels of vitamin D and overall depression. Vitamin D supplementation in studies using dosage of >5,000 IU/day and intervention duration of ≤20-weeks exhibited better effects in lower symptoms of depression. Moreover, a greater risk of depression was shown among participants aged ≤ 50 with lower serum vitamin D levels. REPRINTS & OTHER CORRESPONDENCE: Rania A. Mekary, School of Pharmacy, MCPHS University, 179 Longwood Avenue, Boston MA, 02115 rania.mekary@mcphs.edu Ken Pope Hector Y. Adames, Nayeli Y. Chavez-Dueñas, Melba J.T. Vasquez, & Ken Pope:Succeeding as a Therapist: How to Create a Thriving Practice in a Changing World(APA, September, 2022) Ken Pope, Melba J.T. Vasquez, Nayeli Y. Chavez-Dueñas, & Hector Y. Adames: Ethics in Psychotherapy & Counseling: A Practical Guide, 6th Edition (Wiley, 2021)
Parting with his poison – flash of diabolic tail in the dark room – he risked the rain again.
The peasants came like swarms of flies and buzzed the name of God a hundred times to paralyse the Evil One.
With candles and with lanterns throwing giant scorpion shadows on the mud-baked walls they searched for him: he was not found. They clicked their tongues. With every movement that the scorpion made his poison moved in Mother’s blood, they said.
May he sit still, they said May the sins of your previous birth be burned away tonight, they said. May your suffering decrease the misfortunes of your next birth, they said. May the sum of all evil balanced in this unreal world
against the sum of good become diminished by your pain. May the poison purify your flesh
of desire, and your spirit of ambition, they said, and they sat around on the floor with my mother in the centre, the peace of understanding on each face. More candles, more lanterns, more neighbours, more insects, and the endless rain. My mother twisted through and through, groaning on a mat. My father, sceptic, rationalist, trying every curse and blessing, powder, mixture, herb and hybrid. He even poured a little paraffin upon the bitten toe and put a match to it. I watched the flame feeding on my mother. I watched the holy man perform his rites to tame the poison with an incantation. After twenty hours it lost its sting.
My mother only said Thank God the scorpion picked on me And spared my children.
A collection of postings on a range of issues is available on our website (www.mjacksongroup.ca). This month’s post is again from Ken Pope’s listserv, where he kindly provides daily summaries of current articles in the field.
The article is as follows:
The New York Times includes an article: “Antidepressants Don’t Work the Way Many People Think—The most commonly prescribed medications for depression are somewhat effective—but not because they correct a ‘chemical imbalance’” by Dana G. Smith.
Here are some excerpts:
Over the course of the Covid-19 pandemic, rates of depression and anxiety soared, and many Americans turned to antidepressant medication to help them cope. Even before the emergence of Covid, 1 in 8 American adults was taking an antidepressant drug. According to one estimate, that number rose by 18.6 percent during 2020. Zoloft is now the 12th most commonly prescribed medication in the United States.
Given this, you might assume that the question of how — and how well — these drugs work has been clearly answered. And yet recentpapers have challenged their efficacy and actions in the brain. Some researchers even say the medications are barely better than a placebo and ask whether they warrant such widespread use.
For psychiatrists, this debate is nothing new. Dr. David Hellerstein, a professor of clinical psychiatry at the Columbia University Irving Medical Center, said the question comes in many iterations but boils down to: Do antidepressants work?
“I think they do,” he said. “The best clinical trials and meta-analyses, most of them indicate that there’s some medication effect. I would say it’s less than we would like it to be.”
<snip>
If you take an antidepressant or are considering one, here’s what to know about how they work and how their effectiveness is measured.
What do we know about antidepressant effectiveness?
The most commonly prescribed type of antidepressants are selective serotonin reuptake inhibitors, or S.S.R.I.s. These include Prozac, Zoloft and Celexa.
The drugs prevent neurons from sucking up the neurotransmitter serotonin, allowing more of the chemical to float around in the brain. Other antidepressants increase circulating levels of different brain chemicals, such as norepinephrine and dopamine, in addition to serotonin. However, those drugs come with more side effects, so psychiatrists typically start people with depression on an S.S.R.I. first.
The largest study of antidepressants to date was the Sequenced Treatment Alternatives to Relieve Depression, or STAR*D, trial, which was conducted by the National Institute of Mental Health during the early 2000s. The clinical trial tested multiple antidepressants on nearly 3,000 people with depression, starting everyone on an S.S.R.I. If people didn’t respond to the S.S.R.I. after 12 weeks, they moved on to either another type of S.S.R.I. or a different class of antidepressants. Those include Effexor, a serotonin and norepinephrine reuptake inhibitor, or S.N.R.I., which boosts serotonin and norepinephrine levels; and Wellbutrin, which works similarly on norepinephrine and dopamine.
The trial continued in this way until people who weren’t responding to the medications had tried four different antidepressants.
By the end of the study, half of the participants had significantly improved after using either the first or second medication, and nearly 70 percent of people had become symptom-free by the fourth antidepressant.
“If you look at the STAR*D, better than 60 percent of those patients actually had a very good response after going through those various levels of treatment,” said Dr. Gerard Sanacora, a professor of psychiatry at the Yale School of Medicine.
“But it really did make people aware of the fact that these are not miracle treatments. There’s still a lot of people that are suffering despite having these treatments out there.”
One critique of the STAR*D trial is that it didn’t compare the medications against a placebo. Other research has shown that much of the benefit antidepressants provide comes not from their chemical effects in the brain but from a placebo effect. In one study, antidepressants helped people improve 9.6 points on a depression scale, while people taking a placebo improved 7.8 points, meaning that 80 percent of the benefit people experienced could be attributed to a placebo effect. Subsequent meta-analyses that combined multiple trials assessing the efficacy of several types of antidepressants have found that people are about 25 percent more likely to improve on a drug than on a placebo.
To Dr. Sanacora, what matters more than the source of the improvement — whether it’s the pharmacological action of the medication or the placebo effect, which he prefers to call the “nonspecific response” — is that patients got better after taking the drug. He points out that when you take an antidepressant, you benefit from both the drug’s chemical effects on the brain and the placebo (or nonspecific) effects, such as the daily reminder that you are doing something to help your mental health. But if you don’t take the medication, you don’t benefit at all.
“I worry that patients who are really struggling, especially now, when rates of depression are higher than ever, are going to hear this and get the idea that these drugs don’t work,” he said, referring to some of the skeptics’ claims. “That’s not true. They do work.”
Predicting who will improve on antidepressants and who won’t is virtually impossible. Attempts to use genetic screening to forecast a person’s potential treatment response haven’t panned out. Those tests provide information on how efficiently the body metabolizes the drug, but Dr. Sanacora said that is most useful for assessing adverse reactions, not effectiveness.
“I think it’s been oversold by some people that you could do a genetic test and it’s going to tell you which drug you’re going to respond to,” he said. “That has never been the case.”
How do these drugs work?
Experts initially thought that depression must be caused by low levels of neurotransmitters in the brain, in part because the first antidepressant drug — accidentally discovered in the 1950s — increased circulating amounts of the chemicals. Further research suggested that serotonin played an especially important role in mood.
This so-called “chemical imbalance” theory gained a foothold in the cultural psyche and was promoted by ads for the medications.
However, starting in the 1990s, researchers began to understand that depression was much more complicated and that serotonin played only a nominal role.
For one thing, S.S.R.I.s increase serotonin levels immediately, but it takes several weeks before people start to feel better. Studies also started to emerge showing that another brain system played a role: People with depression consistently have less volume in an area called the hippocampus that’s important for regulating mood.
The current prevailing theory, Dr. Hellerstein said, is that chronic stress can cause the loss of connections — called synapses — between cells in the hippocampus and other parts of the brain, potentially leading to depression. Antidepressants are now thought to work at least in part by helping the brain form new connections between cells.
Researchers aren’t exactly sure how increasing serotonin with an S.S.R.I. causes these synapses to regrow.
A paper published earlier this year made headlines for presenting several decades’ worth of evidence that people with depression don’t have less serotonin than people who are not depressed. To most psychiatrists, the paper didn’t reveal anything new, and it didn’t mean antidepressants aren’t effective (a widely held misinterpretation of the paper).
Instead it revealed a fundamental disconnect between how the public viewed depression and how the experts thought about it.
“To me, that is an old theory for depression,” said Dr. Daniel Iosifescu, a professor of psychiatry at N.Y.U. Langone Health.
“That was already invalidated 20 years ago, so we’re just essentially putting the nail in the coffin, so to speak.”
What alternatives to antidepressants are available?
Alternative treatments for depression have emerged that attempt to help the brain create new connections more efficiently — most notably ketamine and psychedelic therapy (which is not approved by the Food and Drug Administration).
These interventions appear to be about as effective as antidepressants, improving depression scores in roughly 60 percent of the people who try them. More significant is that they are able to treat some of the people who don’t respond to the traditional medications.
The drugs are seen as riskier and more invasive than antidepressants, though, so are meant to be used as a last resort, not a first-line treatment, Dr. Sanacora said.
Some psychiatrists have also started to recommend nonpharmaceutical treatments to help people with depression. Dr. Hellerstein said that when he evaluates a new patient, he now pays more attention to habits, such as sleep, diet and exercise, and would often recommend behavioral changes, therapy or meditation before medication.
“You’re making, I think, a more holistic assessment of that person’s way of living than maybe you did in the late 1980s,” Dr. Hellerstein said.
Finding the best solution for your depression, whether that’s an S.S.R.I., another antidepressant or a behavioral intervention, can take a lot of trial and error, but it’s important to remember that you do have options. And while psychiatrists acknowledge that S.S.R.I.s and other antidepressants are imperfect — and they hope a better drug will come along eventually — for the time being, they’re the best medications currently available.
“I wouldn’t write these older antidepressants completely off and say we should get rid of them,” Dr. Iosifescu said. “They do seem to work for a good number of patients.”
My swirling wants. Your frozen lips. The grammar turned and attacked me. Themes, written under duress. Emptiness of the nations. They gave me a drug that slowed the healing of wounds. I want you to see this before I leave: the experience of repetition as death the failure of criticism to locate the pain the poster in the bus that said: my bleeding is under control. A red plant in a cemetery of plastic wreaths. A last attempt: the language is a dialect called metaphor. These images go unglossed: hair, glacier, flashlight. when I think of a landscape I am thinking of a time. When I talk of taking a trip I mean forever. I could say: those mountains have a meaning but further than that I could not say. To do something very common, in my own way.
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.Molecular Psychiatry includes a study: “Antidepressants for the treatment of
