One of the more controversial components of the Neuralink presentation was Musk’s inclusion of his beliefs about the future of humanity and artificial intelligence. During the press release he stated one of his goals was to create the ability to achieve a “full symbiosis with artificial intelligence,” essentially removing the “existential threat of AI” which he believes will one day “leave us behind” (Neuralink, 2019). This goal has been met with a bit more skepticism, especially by the national media, than the medical applications of Neuralink’s BMI. Forbes describes it as “a bit more fantastical” than the company’s primary goal of treating brain disorders (Knapp, 2019). Other publications have been far less kind, such as The Atlantic, which published its coverage of the Neuralink press release with the title: “Elon Musk’s Next Wild Promise: If someone is going to revolutionize what it means to be human, do we want it to be a tech titan?” (Mull, 2019). Although the New York Times surmised that “one of the biggest challenges may be for his scientists to match his grand vision,” (Markoff, 2019), it serves as a good example of what most major media outlets have chosen to do: stick to the facts.
Below is a detailed review of the podcast episode, with most of the content that Dr. Michael Cummings and I (Dr. Puder) discussed. Special thanks to Arvy Wuysang (MS4) for his work in the initial transcription and organization.
The history & nuances of bipolar illness
Bipolar Illness was first discovered by Emil Kraepelin, who was also the first to describe schizophrenia in the 19th century.
Kraepelin noticed another major mental illness in which people had episodic disturbances of mood. He saw either elevation of mood and increased energy, along with a decreased need for sleep, and often impulsive or psychotically related behaviors.
Then, the same patient would experience the opposite, sleeping through the day, demonstrating lowered energy and depression. These patients were noted to have normal function in-between these episodes.
Nuances of the bipolar illness diagnosis
The Diagnostic Statistical Manual of Mental Disorders (DSM) identifies bipolar illness primarily by the presence of at least one episode of mood elevation to help distinguish it from unipolar or major depressive disorder.
Here are some defining symptoms:
Patients are fairly normal between episodes.
When they’re manic, their mood elevates their lack of sleep. They will sleep four to five hours at first, later progresses to no sleep at all on a nightly basis.
Every true manic episode will end in three places: hospitalization of some type, jail, or death.
Initial peak is in the 20s and 30s. Although, people suspect that many individuals who become bipolar don’t initially declare themselves.
They often present with a series of recurrent depressive episodes and then, at some point, they exhibit a period of mood elevation meeting the criteria for either hypomania or mania, which earns them the diagnostic label of bipolar mood disorder.
There are two types. Type I, in which the person has fully evolved to mania or mood elevation and fully evolved episodes of depression. Type II, in which the person may have a milder form of mood elevation but still has fully evolved periods of depression.
Grandiosity is a major part of mania. Although historically some people with bipolar illness have often been incredibly productive during episodes of mood elevation, before they become disorganized or psychotic.
There is often impaired judgment during manic episodes. For example, someone who is manic will propose to 5 different girls, max out multiple credit cards, buy extra houses/cars/boats, etc.
Bipolar and the limbic system
Underlying pathophysiology is centered around the limbic system. Involves the temporal lobes and and structures which swings upward into the mamillary bodies into the anterior cingulate gyrus, which then projects forward into the frontal lobe. That circuit goes through periods of hypo-activity or depression in people who are bipolar. They have depressed metabolic rates of the system upto 30 to 40 % below normal. During periods of mood elevation, there is an increase in metabolic activity and instability in that limbic circuit. The mood is an element of that, but the person’s overall activity, sleep-wake cycle, circadian rhythms, along with all the things related to the functioning of the limbic system are disturbed in bipolar illness.
Bipolar illness and sleep patterns
There are some models of the illness that suggest that perhaps the core of the pathophysiology of bipolar illness is an abnormally regulated biological clock.
In most of us, the nerve cells, the neurons that make up the biological clock, are very tightly linked to each other in terms of their operation. They literally form two pacemakers or oscillators in a very small structure that sits right on top of the optic chiasm called the supraoptic nucleus.
Normally all of our circadian rhythms are regulated by this master clock. In healthy people, it’s very difficult to get the two oscillators to separate from each other. In bipolar people, those oscillators drift apart relatively easily. Something as simple as loss of sleep during the latter half of the night will cause them to diverge from each other.
When that begins to happen, the overall functioning of the limbic system begins to oscillate in an unstable manner.
People have looked at things like disturbed sleep as being a very common precipitous of a mood episode. If somebody has a difficult day or disturbing event, and they’re genetically vulnerable to being bipolar, they may not sleep well at night, and the next night they may not need to sleep as much. The night after that, they really don’t sleep, and then their mood begins to elevate and another episode is initiated.
Genetic markers of bipolar illness.
Bipolar is typically passed on genetically, and can be linked with other similar markers of illness. Around 100 genetic markers have been linked to bipolar illness.
They overlap with schizophrenia in part, but not entirely. People with bipolar illness have a much more normal brain in terms of development then do people with schizophrenia. But, there appears to be an inherent defect in the operation of the limbic system elements with these periodic repeating of overactivity and underactivity, plausibly related to the core biological clock.
Mood stabilizers have an effect in terms of decreasing and stabilizing the activity of the limbic system. They tend to push that clock back toward being phase-linked or operating together as a single oscillator, rather than as divergent oscillators.
History of Lithium
The very first mood stabilizer discovered was lithium. It was very popular in the 19th century for the treatment of gout because it decreases uric acid crystals.
In the 1940s, a psychiatrist named John Cade (1912-1980) served in World War II and was a prisoner of war for three years. After the war, he worked in a repatriation hospital in Australia and became fascinated with bipolar illness. At the time, he looked at the earlier history and thought that uric acid somehow caused bipolar illness. That turned out to be a wrong hypothesis. But, it led him to use lithium urate, a soluble form of uric acid, in hamsters, to see what would happen. The hamsters got lethargic and sleepy upon administration.
He decided to give his lithium compound to ten patients—six of them were bipolar, four of them were schizophrenic. They all became less agitated, though the schizophrenics didn’t change all that much. However, all of the bipolar patients’ moods stabilized.
It’s amazing how he didn’t kill any of these patients in spite of giving them gigantic doses of lithium. His initial dose was 1300 mg, three times a day. Most of the patients got ill with that. If you give somebody too much lithium, they develop nausea, tremor, and diarrhea. You can make them very seriously ill with lithium because it has a very narrow therapeutic index. The distance between therapeutic and toxic is not very far. Optimal dose for most patients 0.6 - 1.0 mmol/L. Toxicity usually begins at about 1.5 mmol/L, serious toxicity begins at about 2.0 mmol/L.
At Loma Linda and at patton State Hospital, most patients start at 900 mg at night, obtain a plasma concentration five to seven days later, and then adjust the dose.
Lithium should never be given in divided doses.
The kidneys is spared by having a long trough period between lithium doses, so it is best to give it at bedtime.
Lithium tends to decrease urine concentrating capacity. Almost everyone who takes lithium, their urine output will increase by about 20%, and their water intake will correspondingly increase by about 20% to compensate. There are a few people who get much more severe diabetes insipidus, an insensitivity to anti-diuretic hormone in the kidney.
Over the course of many years, about 5% of people who take lithium will develop mild to moderate degrees of renal failure or insufficiency. That risk is minimized by keeping the lithium level < 1.0 meq/L and also by giving Lithium only once a day.
Lithium and suicidality
It’s clear that lithium reduces suicidality, which may be a product of its ability to inhibit impulsivity. Suicide rates are substantially lower when people take lithium.
In the healthy population, when they’ve done studies in areas with very low concentrations of lithium in the groundwater, rates of suicide and rates of homicide are lower in areas with lithium in the groundwater compared to areas that don’t have lithium in the groundwater.
The amount of lithium that people are getting from the groundwater would be roughly the equivalent of taking 3 milligrams of lithium a day. This means that in the healthy non-bipolar non-mood disordered brain, it doesn’t take very much lithium to make people somewhat less violent.
When would you take someone off Lithium?
The best measure for lithium is to measure the eGFR (estimated glomerular filtration rate). If the eGFR declines to 50 or less, the person should not take lithium.
The other common adverse effect that lithium has is to make the person hypothyroid.
Lithium tends to decrease the synthesis and secretion of thyroid hormone. The good news is that if it makes somebody hypothyroid, we can easily replace the thyroid hormone with Levothyroxine, a synthetic analogue of the hormone. Frankly, your body doesn’t care whether you get your thyroid hormone from your thyroid gland or from a tablet.
Dermatologic side effects
Psoriasis is a contraindication to lithium use. It will greatly worsen psoriasis.
If the person is prone to cystic acne, lithium will typically cause a worsening of cystic acne.
One of the effects of lithium is to increase oil secretion in the skin. That can lead to both increased psoriatic plaques and cystic acne.
History of other mood stabilizers
The reason we have other treatments for bipolar illness, is largely the result of the work of Robert Post.
Post was a psychiatrist who worked at NIMH and was doing an unrelated experiment. He was looking at kindling, or increased sensitivity of the limbic system, by putting electrodes into mouse temporal lobes and giving them a one second electrical stimulus once a day.
Initially, when you do that, nothing happens.
But about day two or three, the mouse will have a complex partial seizure, a temporal lobe seizure. If you keep doing it pretty soon the mouse will start having spontaneous seizures. Robert Post looked at that and thought that the nerve cells of the limbic system can become more and more sensitive, more and more hyperactive, less and less well-controlled. He thought that he could block that effect, in terms of seizures, with anticonvulsants. He then, made a leap in logic, thought that perhaps mood episodes are acting like electrical stimulus causing kindling in the limbic system for people with recurrent mood episodes, like in bipolar patients.
He decided to treat some bipolar patients with an anti-epileptic.
The first medicine he used was Carbamazepine (Tegretol). Tegretol is a very difficult drug to use because it induces its own metabolism, so the level keeps falling. It also is fairly toxic with respect to the bone marrow. So, you have to watch out for loss of white cells, red cells, platelets.
He fairly soon turned to another anti-epileptic, valproic acid, which is a branched-chain fatty acid. He found that it was also effective in treating bipolar illness. Turned out that compared to lithium, valproic acid was more effective if the person was a rapid-cycling bipolar patient having more than four episodes a year. (Although lithium remain superior if the person is a classic type I bipolar patient.)
In young women in general, valproic acid it can be problematic because it can cause Polycystic Ovary Disease.
In pregnancy, it causes not only a risk of neural tube defects such as spina bifida, it also decreases the intellectual capacity of the offspring by about 10 IQ points, and roughly doubles the risk of autism in the offspring. It also causes hirsutism and weight gain.
Psychiatry has pretty much examined every anti-epileptic introduced since to see if it had mood stabilizing properties.
Lamotrigine (Lamictal) for example, does treat bipolar depression and does stabilize mood cycling, but has almost no benefit with respect to mood elevation. In fact, Lamotrigine as a monotherapy may actually cause switches into mania in some patients.
People have looked at Topiramate and found that it may have some prophylactic capability but doesn’t seem very effective at all if the person is already manic or depressed. If their mood is already stable, and you’re just trying to decrease the cycling, it may have some benefit.
Lamictal, used as a mood stabilizer, may have gotten more use than it should because although it does have antidepressant properties in bipolar illness, it is certainly not a benign drug.
People were initially attracted to it because there’s not a lot of laboratory monitoring involved. The plasma concentrations of lamotrigine don’t correlate very well with its efficacy because it is very rapidly cleared from the blood compartment and taken into tissue. It’s easy to administer and when you’re not using it for seizures, usually can be dosed all at bedtime.
It does carry a risk of Stevens-Johnson Syndrome, which is severe malignant rash, and which the person winds up looking like a burn victim because their skin literally dies and falls off.
It also can cause lymphohistiocytosis, which is a similar autoimmune process, but involving the blood vessels and internal organs. Luckily, that is rare, but it's also typically a life threatening response to the drug
The risk of the side effects above are increased by titrating the drug to rapidly. They discovered the side effects when they were using the drug initially for seizures. They were often increasing the dose by a hundred milligrams a day starting at 100 mg, and by day four, the person was on 400 milligrams. They found a 9% increased rate of malignant rash. If you slow down and don’t go faster than around 25 to 50 milligrams a week in the titration, the risk is reduced, but it’s still not zero. It’s probably less than one half of 1%, but it is a caution.
The other caution with the drug of course in bipolar patients is it sometimes is not a very good monotherapy because it doesn’t provide any protection against mood elevation. It seems to be effective in treating the depressed phase of the illness, but not the manic or hypomanic phase.
Oxcarbazepine has flunked multiple trials as a mood stabilizer. Oxcarbazepine differs from Carbamazepine in only one bond. In carbamazepine the bond between carbons 10 and 11 is an epoxide bond, while in oxcarbazepine that same bond is an ester bond.
It appears, however, that the mood stabilizing properties of carbamazepine result from the epoxide metabolite, and of course oxcarbamazepine does not produce that metabolite.
Oxcarbazepine can, in some individuals, reduce impulsivity, which seems to be a truism across the anti-epileptic drugs, but it’s not an effective bipolar treatment.
There was only one study looking at it in forensic settings for impulsive or violent patients. It was a self-funded single investigator study and it’s been the only study that was ever produced, never replicated. It was suspicious in that the patients were all outpatients, self-recruited via newspaper ad. It’s database even for impulsivity and so forth is pretty limited. It does have some application in that regard, but it is not as good as people hoped.
People became enamored with it simply because it was easier to use than carbamazepine, which isn’t to say that it’s benign. It induces hepatic enzymes, it causes dangerous hyponatremia in about 2.5% of the people who take it.
There haven’t been any really good studies identifying it as an anxiolytic. Like most anti-epileptics, it can be sedating and somewhat calming, but you could get the same effect from literally any of the anti-epileptic drugs, probably safer would be gabapentin.
Antipsychotic use as mood stabilizer
Some of the second generation antipsychotics have also shown mood stabilizing properties, albeit as an addon to a primary or classic mood stabilizer. This include drugs like Aripiprazole, Brexpiprazole, Cariprazine, Olanzapine, and Quetiapine. Quetiapine in particular is effective in treating bipolar depression, as is Lurasidone.
Antidepressants as mood stabilizers
Do not give an antidepressant to a bipolar depressed patient!
There are now a host of studies suggesting that antidepressants offer little or no benefit with respect to depression in bipolar illness. It serves only to increase the rate of mood cycling and to risk a switch into mania.
Cognitive side effects of mood stabilizers
Lithium typically causes cognitive impairment only if the plasma concentration is too high, in which case it can cause decreased brain function all the way up to coma if the concentration is high enough. However, lithium used at therapeutic concentrations actually is neurotrophic.
It’s been used now in some demented patients with modest results. MRI scans will show a thickening of the cortex if you put somebody on lithium.
In contrast to lithium, antiepileptic drugs almost universally tend to dull cognitive performance. For example, one of the tip-offs that you’re giving the person too much topiramate is they start to lose the ability to find nouns, they become anomic.
Barbiturate and Benzodiazepine use in bipolar illness
Barbiturates were introduced in 1903. At that time, they were essentially the only psychiatric medication available. They treated literally everything that involved mood elevation or agitation with a barbiturate.
In the middle ages, individuals that seemed to have manic episodes as we understand it today, were considered witches. They were given doses of sedation that would bring a normal person down. These manic individuals, however, would not be sedated with those doses.
This is described in the book The Witches’ Hammer. Most of these tests were designed so that if you were the accused, you most likely won’t pass them. For example, one of the tests was being tied up and thrown into a mill pond. If you drowned, you were concluded not to be a witch, but of course you were dead. If you manage to float and you survived, you were concluded to have done so via witchcraft, in which case they retrieved you from the water and subsequently burned you.
Frankly, psychiatry has come a long way!
Importance of sleep hygiene in bipolar illness
One of the most important things to teach bipolar patients is to emphasize the importance of sleep hygiene. They should go to bed at the same time every night. It’s dangerous for them to casually stay up to watch tv or a movie etc. That may be a setup for them to have the next episode of mood disturbance.
If they’re having difficulty sleeping, this is a group in which long term use of one of the Z drugs may be appropriate.
Dr. Cummings’ personal favorite in that group is Eszopiclone (Lunesta), because it has a longer half-life. It’s half-life is around 4-6 hours, so it’s long enough that the person will actually stay asleep. It also has a broad dose range, 1 mg - 8 mg at night.
It’s been used to treat primary insomnia in some individuals for up to decades without development of complete tolerance, or resulting in any withdrawal syndrome if the medication is stopped.
Education for bipolar patients
Patients and families need to realize that the more episodes of illness they have, the more resistant to treatment the illness will become, and the less responsive the illness will become to medications. This idea goes back to Robert Post’s study on kindling.
Additionally, when people have more episodes, the cycle tends to become progressively shorter. If they were initially having an episode every two or three years, it may suddenly occur every year, to having multiple episodes for a year.
One of the major costs for both families and individuals who are bipolar is that severe depression or severe mania is incredibly disruptive to the individual’s life. It can destroy their marriage, their job, and cause large setbacks.
I (Dr. Puder) will bring patient's families in, get them on board with a plan to identify early symptoms such as decreased sleep, increased energy, and change in physical activity. I want the family to keep in close contact with me if these things are developing, and I will alway get them in within the week.
Role of psychotherapy in bipolar illness
For many bipolar patients, the common pathway into a mood episode is an environmental stressor that causes sleep disturbance, which then sets off the instability that they have innately in their internal clock, and then they’re off into a mood episode. Teaching the person good sleep hygiene, teaching them to be better able to cope with stressors is crucial.
Psychotherapy can also train them to become more self aware, so that they may be able to spot earlier changes in their mood and recognize an impending episode sooner. This allows them to seek for intervention before things get out of hand.
Focus on developing healthy habits like exercise and healthy diet.
This week on the podcast, Ginger Simonton, PhD candidate, and I (Dr. David Puder) talk about about how to deal with emotional detachment. In the psychiatry world, we call the state of emotional detachment, congruence.
What is congruence?
Psychological congruence is someone’s ability to feel and express their inner emotions in a consistent manner with their outer world—their speech and body language.
As an example, have you ever smiled when you’re talking about something sad? Or felt very emotional, yet had a flat face and still posture? Have you ever felt angry, but pushed it down and developed a headache? These are incongruent speech and behavior patterns.
Incongruence happens when we’ve lost touch with our inner world, our emotions that are represented with bodily sensations. Many of my patients experience emotions, but have a hard time expressing them with words, so they shove them out of their experience.
Emotions are unavoidable.
We experience them all the time, whether we know it or not. Common terms for pushing them out of our awareness are suppression, denial, repression, and other defense mechanisms. We may think we can suppress our emotions, but they will come out in one way or another—sometimes through physical pain and illness.
There is extensive research on how the body processes emotion, and how that affects us physically. One of my favorite books on this subject is The Body Keeps the Score, by Bessel van der Kolk and The Feeling of What Happens by Antonio Damasio. I have spoken about the science of emotion in part 1, part 2, part 3 on microexpression and a popular episode on the polyvagal theory which give the science and application of understanding emotion.
As psychotherapists, our job is to help people reconnect to those emotions, and be able to experience them in healthy ways. People bury so many of our psychological problems in our bodies that we don’t even feel comfortable in our bodies anymore, and we prefer to be numb.
People further push unwanted emotions out of their experience through use of drugs, alcohol, and other addictions like porn, gambling, movie binging, or mindlessly scrolling forever on social media.
How do we develop incongruence?
But we don’t start out as emotionally disconnected, or incongruent. As children, we express our emotions as we feel them. If we are happy, we giggle, smile, or stick out our tongue as we work on a project. If we are sad, we cry. If we are angry, we bite, yell, spit or claw. If we have disgust we spit things out, push things away and protest against putting things in our mouth!
If our emotions are mirrored back, and our caretaker acknowledges them verbally, them we optimally will be connected to our bodily responses from a young age. This is why I always recommend starting any discipline or high emotional moment with kids by empathically mirroring their emotions in words, and adding meaning to why they might feel such a way.
To get along with others, most kids, over time, develop a normal adaptive way to conceal emotions, which helps function in family and friendships. We learn that there is a context for truly sharing what is going on, and this is a good thing. Sometimes suppressing strong emotion until later is helpful!
Stronger issues develop when repeated messages invalidate or shame our experience, or trauma moves us away from being congruent with our inner experience. It is also possible that there is no one who an individual connects with enough to be congruent around.
For example, if everyone you know would shame or attack you, it might not be a good idea to bring out your deepest thoughts and emotions. These kinds of households often have heavy drugs or alcohol, severe mental illness, or predators.
We are meaning-making creatures. We assign meaning to events in our lives, and that meaning becomes our guiding belief and principle, especially in key developmental periods in childhood.
These meanings shape how we are going to interact with the world. Although unconscious and out of our awareness most of the time, when we live out of congruence without ourselves, it leads us to form these earlier, shaping meanings. (click here for more on the science of meaning)
How incongruence develops:
A trauma occurs. A child hears his parents fighting. The child, when in the midst of it, seems to be physically sick, and this distracts the parents from their fighting and thus decreases the fighting.
We assign meaning to it. The child, as always, relates everything back to him or herself. They think, “If there is yelling, if I become ill, the yelling will stop.”
We structure habits and actions around that belief. The person continues to use being ill as an adaptive response to calm the parent’s hostility. Any emotional pain and discomfort is thus learned to be responded to when in the midst of only physical pain.
We see patterns in our lives that reflect that belief. We react repeatedly in a way that demonstrates our belief. We notice it affects our relationships, and that further cements the belief in our lives. New connections are found with caring physicians, maybe specialists who have concern for the medical issues, which further reinforces illness being a way to both calm disagreements and get connection needs met.
We have to either live with it, or deal with it. Until we revisit that moment and that decision, we cannot sift through that core belief. There is incredible hope for people with incongruence.
The response to a healthy therapeutic relationship and subsequent changes in behavior can be astounding. To deal with it, it is necessary to both find new ways of connecting with others but also not be able to use the incongruent way of being for an adaptive means.
How do we fix incongruence?
Our goal as we progress in life is to connect our physical body, emotional experience and verbal communication. The best public speakers seem to speak from the core of their being. The most powerful messages come from getting in touch with ourselves and integrating it.
We can introduce the concept of reconnecting with the self in several ways:
Art helps people bypass the logical areas of the brain and produce something raw and congruent to their inner experience. Painting, drawing, working with clay, or other forms of art help us connect with things deep down in our inner experience. Sometimes we ask people to make a self portrait or a picture of their home to discover new things and access something true.
Then we ask for people to describe their pictures and link the congruent space of the art with what they share.
Ginger often uses the phrase “inner child” but I like to describe it as the “true self,” or the core of our being. Living congruently out of the “true self” is when how you imagine yourself lines up with what you do and how you articulate yourself. This is not a new idea, Karen Horney’s Neurosis and Human Growth is my favorite author on this topic.
Learning that we sometimes have hidden this part of ourselves, and then gaining access to it and learning to live by it can be powerful. When we are around people who can give us grace and truth as we progress, we can find this more and more.
Bodyscan (or interception)
Patients who have dealt with trauma often dissociate from their bodies. Even in this era of technology, it’s easy to forget we have bodies. People spend most of their time disconnected, scrolling the internet.
When we experience our body and work through emotions at the same time, it brings us into ourselves and develops congruence.
Ginger likes to ask the following questions when her patient is experiencing a triggering event, to be able to dig down to the root cause of incongruence:
What is your body feeling as you talk about that?
What emotion would you name that feeling you’re having?
When is the last time that you remember your body feeling that way? The patient’s answer to this must be close to the original time of trauma, something usually in their childhood.
I like to ask as well:
As you say that what are you feeling in your body?
If your body could say something what would it say?
I want to access their bodily memories and the source of their pain.
Taper off of harmful and unhelpful drugs.
It’s easier to medicate incongruence, rather than actually deal with the root of it. It’s quicker. Substances like alcohol and drugs deeply affect people’s emotions. When patients are self medicating, they are usually trying to rid themselves of a symptom of emotional pain.
I like to ask them, “What are you getting out of the substances? Sleep? Peace?” Once we can answer that question, we can get to the bottom of where the anxiety and fear or anger comes from. We can begin to develop congruence, which will in turn, bring peace.
People medicate with illegal, and prescribed, legal drugs, as a way of dealing with emotional pain.
Some doctors and therapists can be symptom based, rather than focused on what is underneath the symptoms. When they see a patient, they can be on a hunt, trying to identify what’s wrong, the bottom line, and then find a medication that will relieve symptoms.
When we do that as therapists, we connect with the patient’s illness narrative, rather than who their core is, before they developed these problems.
Some patients who come to see us are taking 20-33 pills a day for all their different illnesses. If there is so much medication involved, it can become difficult to do psychotherapy as likely the sensorium or total brain function is impaired.
We have found when we establish a secure emotional connection with them, we can get some of these medications off the table, and then our patients can start to develop a range of emotions.
Through an attachment with a a therapist, that is trusting and meaningful, people can start to feel what before they either consciously or unconsciously suppressed. I have spoken about the worst medications here.
How to stay congruent during tough circumstances.
It is tough to apply all that patients have learned through therapy in their everyday lives. Our families and friends love homeostasis—usually, the people around us want us to stay the same. They say, “you’ve changed,” as if that’s a bad thing.
When we’ve been healed, when we are congruent with ourselves, it can be difficult for our friends and family to accept the “new us.” They connect more easily with the old us.
We have noticed that if the patient begins to grow, the whole family system needs to change as well.
To maintain newfound congruence and healthy mental states, patients work to find healthy relationships they can be congruent within. In the future I will talk about how to identify safe people and how to have healthy boundaries that keep us in relationships.
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What are microexpressions?
Microexpressions are brief, involuntary facial expressions that are cues to the true emotions that someone is feeling. We see microexpressions in tiny twitches of the brows, the lips and nose. They can last for as little as 1/15th of a second on the face.
Microexpressions are helpful because they send messages, both to ourselves, and to those we are trying to communicate with. Some are naturally better at sensing what someone else is feeling, but if you want a deeper clue into emotions and emotional connection, start to study microexpressions. We can even begin to understand ourselves a little better when we pay attention to them.
What are emotions?
Emotions are adaptive brain networks, expressed rapidly on the face and in the body. They carry messages about our environment or thoughts, and they have a specific goal or intention.
Although they appear ethereal in nature—fleeting feelings of happiness or sadness—emotions are actually grounded, measurable reactions. Each person, based on their experiences in life, will react differently to each stimuli. With each person, the reaction and meaning of the emotion lies within the lens we have.
Emotions have a purpose.
Emotions move us to action.
Emotions themselves are not good or bad.
We often do not decide to have emotions.
Emotion is a survival mechanism that we all have. For example, the purpose of anger is to protect and reconnect. Anger surfaces when we feel threatened—when a lion tries to attack our family—it gives us the physical response we need to attack what is attacking us. Fear is helpful to trigger our body to be able to outrun that lion when we need to—our heart starts pumping, adrenaline rushes in, survival mode turns on. In modern society, we’ve tried to suppress or deny those emotions, but they’re still there, and they’re still helpful. We just have to know what they are, and what to do with them.
What are the different emotions?
Scientists have lumped all of our complex feelings into seven, basic categories.
Emotion: Happy, Joy
Body Sensation: Positive warmth throughout the body, grounded feeling.
Microexpression: Mouth going up symmetrically, cheeks pulling up and change in contour, and eyes contracting (especially on the outside with classic “crows feet”).
Meaning and Goal of Emotion: Heartfully rejoicing, finding pleasure and wanting more of something, noting what brings you pleasure, feeling safe connection, having mutuality with someone, moving towards a goal.
Body Sensation: Heavy feeling in chest, decreased limb activity.
Microexpression: Inner eyebrows rising and outer eyelid dropping, pulling down of the lip corners, chin moving up, and lips showing a pout.
Goal of Emotion: Express loss over connection, an object, or attachment, invite solace and concern.
Body Sensation: Weight on chest, constriction around neck, butterflies in the stomach.
Microexpression: Upper eyelids rising high and longer than surprise, lower eyelids tensing, eyebrows drawing up and together with tension in the forehead, mouth opening horizontally.
Goal of Emotion: Preserve and maintain life, freeze to analyze danger, prepare to run or attack, puff up (to look dangerous).
Body Sensation: Queasy, feeling of wanting to vomit, gag feeling in the throat.
Microexpression: Wrinkling around the nose, upper lip rising, and eyebrows move down without tension (contrast this with anger where the eyebrows are pulled together and the eyelids are raised and tense).
Goal of Emotion: To move away from, avoid, reject, spit out, get away from.
Emotion: Pride, Smug, Contempt
Body Sensation: Increased sensation in the chest and head of euphoria, puffed up feeling in chest
Microexpression: One side of the lips rising faster than the other, or one side coming down slower than the other.
Goal of Emotion: To take pride in another’s success, proud when I succeed, feel superior, or diminish inferiority.
Body Sensation: Startle and jolt to the body
Microexpression: Rising and rounding eyebrows, co-occurring with rising upper eyelid, and sometimes mouth falling open with lips relaxing. Note: rising eyebrows can also be a conversational signal emphasizing something.
Goal of Emotion: Prepare for the next step, achieve familiarity with an object/situation so that you are better prepared when encountering a similar situation in the future.
Emotion: Anger, Frustration
Body Sensation: Tight chest, tension in neck and back, knots or burning in stomach.
Microexpression: A short tightening of the eyelids, eyebrows moving down and together, and sometimes lips pressing together. Rarely, showing of teeth. The tightening of eyelids and eyebrows for an extended period of time can also be seen when a person is concentrating or focusing, so context is important.
Meaning and Goal of Emotion: Overcome obstacle to move towards a particular goal (desire to reconnect with a loved one). Protect self or significant others—set up boundaries, have a voice, or be assertive. Attack when you feel no escape is possible either physically or psychologically.
Why should you learn about microexpressions?
Learning about microexpressions is helpful for emotional connection. Connection is largely based on empathy, and when we know what someone else is feeling, studies show we experience more empathy.
It can help raise the level of connection in personal life, in work, and even for people who have disorders that can cause emotional disconnection, such as schizophrenia.
Therapists and mental health workers, when tested, demonstrated they were no better at reading microexpressions than the average person. Another study also showed that therapists and mental health professionals overestimate how good they are at reading micrexpressions. We believe microexpression training would benefit therapists, and help them build a therapeutic alliance with their patients.
One study of 21,000 patients, showed that those who were under the care of doctors who demonstrated higher empathy, had 40% less life-threatening instances related with their diabetes. Higher empathy = better health outcomes. In another study about psychotherapists, the overall therapeutic connection impacted how well someone responded to both the placebo and the active medication.
Learning about microexpressions will help therapists be able to diagnose or identify depression, anxiety, and find underlying emotional responses to a story a patient is telling.
How do you learn about microexpressions?
Anyone can learn how to read microexpressions, and studies show that it really does help us feel more connected to people, and it helps us develop empathy.
Even when we lean in, and specifically pay attention to someone else’s emotions, we are better able to empathize with that person and connect. That’s a simple way to feel closer to someone, but to really go deeper into the science of emotional connection, you have to study microexpressions.
The most effective way to learn microexpressions is through a training program. I built a training app that can help. The app has over a hundred recorded videos of real facial expression responses. After the video plays, it will prompt you to guess the emotion the person expressed. Once you respond, the app gives you immediate feedback of the correct answer, along with what facial movements are involved in each emotion. Repetition is key in learning microexpressions.
The positive effects of microexpression training
There are incredible benefits to microexpression training, whether you are a healthcare professional or just someone who is interested in emotional connection.
It develops psychological safety.
When we read a microexpression, it shows we are demonstrating an appreciation for the person you are listening to. You are giving time and attention to their feelings. Often, when we recognize a microexpression, we tend to mimic it on our own faces. When someone is sad, we are sad with them. When someone shows anger, we shake our head and demonstrate anger with them. When they feel heard and understood, they feel psychologically safe to give you accurate feedback.
It normalizes emotions.
When we cognitively understand that we are feeling anger or disgust, and not just living in the feeling, it allows us to begin to breakdown the why behind it. When we dig that deep, we can process responses that are out of context. Emotions should happen in the appropriate time, in an appropriate amount. Checking the why can help us untangle complex situations from our past, and help us deal with emotions in healthier ways in the future.
Also, rather than judging emotions, when we learn microexpressions, it brings our brains into the equation, so our responses are rarely trigger-happy. We are able to be curious about the why behind it, which is much more helpful in the long run.
If you’d like to keep learning about microexpressions, download a PDF with more detailed notes from this episode with all citations: https://psychiatrypodcast.com/resource-page/
If you'd like to try out the app that trains people how to read microexpression, go here: IOS Emotion Connection App
Our bodies are “wired” to perform. Learning how to consciously modulate your internal sympathetic state is the key to unlocking optimal performance. The autonomic nervous system (ANS) facilitates survival by generating the fight-or-flight response and promotes recovery following activation (the ability to relax). The ANS achieves this by balancing two complementary systems: the sympathetic nervous system (SNS) and the parasympathetic nervous system (PNS). For example, your ANS is currently adjusting your pupillary diameter, respiratory rate, blood pressure, heart rate, skin conductance, sweat production, sphincter tone and postural muscles (just to name a few) to allow you to focus your eyes to read this information without passing out, falling over, overheating or urinating on yourself.
The sympathetic nervous system (SNS) sends signals throughout the body to enhances its ability to respond to a perceived threat. For example, when a cave man encounters a bear, he must be able to rapidly harness enough energy to fight the bear or run away from it. The SNS achieves this by increasing oxygen mobilization, increasing heart rate and optimizing the utilization of stored energy to allow the cave man to quickly sprint away from the bear. If the threat becomes imminent (i.e. “I’m not fast enough”), “freeze” mode prompts the body to immediately enter an extreme state of energy conservation in a final attempt to maintain survival (decreased heart and respiratory rate, loss of muscle tone, etc). The parasympathetic nervous system (PNS) activates through myelinated nerve fibers from the nucleus ambiguus when the perceived threat has been removed and allows the body to rest and refuel. While instinct alone was sufficient to keep our cave man alive, this instinctual response system has not evolved with society’s modernization (not many of us are still being chased by angry bears). This disconnect allows the ANS to be hijacked by perceived threats on a continual basis and is an underlying cause of chronic stress, pathologic anxiety and poor performance.
The “freeze” mode can turn into a third system, with the activation of the unmyelinated dorsal vagal parasympathetic system. This system is “shut down mode” seen in animals that go limp when there is no escape possible. This is the place where public speakers lose their ability to get words out. This is also the place where athletes completely fall apart. This is the space our brain goes when traumatic things occur. We no longer feel our body and may feel light headed. Effective training prevents the performer to enter this place.
Breathing to relax
While the ANS has various “access points,” the most accessible conscious modulating benefit is often achieved through mastery of controlled breathing techniques. The goal of breathing exercises is to consciously create a desired state through stimulating the body’s chemoreceptors (located in the medulla oblongata) and subsequently causing the body to calm down.
The human body achieves maximized PNS activation during sleep. There are 3 major and distinct sleep stages, each with a correlating breath pattern. Relaxation through PNS activation is best achieved by controlled mastery of breathing patterns that replicate the unconscious breathing cycles seen in sleep onset and non-REM sleep. Sleep on-set is best replicated by utilizing “clearing” breaths. To use “clearing” breaths, exhale out fully and hold for as long as you can, which allows for an increase in pCO2. Repeat this 2-5 times before transitioning into 4-8 cycles of relaxed breathing in a 4 second, 7 second, then 8 second pattern.
Close your eyes
Breathe out through your nose regularly
Breathe out through your tightened lips until you feel a knot in your abdomen (about 8 sec)
Hold at full exhalation for 5-15 sec (the duration will increase with time and practice)
Repeat 2-5 times
4-7-8 BREATHING CYCLE:
Close your eyes
Breathe in through your nose for 4 sec
Hold at maximum inspiration for 7 sec
Exhale through your nose over 8 sec
Repeat 4-8 times (~2 min)
As your skill and comfort increases with these breathing techniques, you can achieve deeper relaxation when combined with visualization, positive self-talk and guided meditation.
Breathing for activation
Breathing for activation is best achieved by replicating the rapid breathing pattern seen during maximum sympathetic activation. A hallmark feature of panic attacks is rapid, shallow breathing (i.e. hyperventilation). Hyperventilation leads to decreased pCO2 which signals SNS activation, which jumpstarts physiologic shifts that can maximize your stored energy availability. Hyperventilation is followed by 1 or 2 clearing breaths to promote balanced activation of both the SNS and PNS. Without clearing breaths the SNS may become over-activated and lead to decreased performance.
RAPID CYCLING: diaphragmatic nasal breathing with use of accessory breathing muscles
Inhale rapidly over 1 sec
Exhale rapidly over 1 sec
Maintain pattern for 30-45 secs.
Exhale until you feel a knot in your abdomen
Hold at full expiration for 5-10 sec (the duration will increase with time and practice)
Repeat 1-2 times (~30 secs)
As your skill and comfort increases with these breathing techniques, you can achieve heightened activation by combining focused breathing with visualization, positive self-talk and internal coaching.
CAUTION: Breathing techniques, especially hyperventilation, may trigger lightheadedness, extremity tingling and even loss of consciousness. Due to these risks, these techniques should be practiced in a safe environment with supervision (not in water, while driving, etc.). Additionally, these skills require practice to achieve optimal effectiveness. Start slowly and increase the duration of breathing exercises with your comfort level.
Many athletes struggle with over-activation on performance day. Without proper training, it is easy for the pressure of performance to push even the most highly-trained and physically fit athletes into “freeze” mode. To maintain optimal performance, athletes must be able to monitor and modulate their internal state to maintain optimal activation (see the performance activation curve below). It is also important to note that the level of necessary activation varies from sport to sport.
For athletes who struggle with “freezing” or “choking” on game day, it is helpful to perform a retrospective behavior chain and begin to build a “game day routine” to build confidence and abort future over-activation. This requires focused attention on internal monitoring, effective usage of necessary breathing techniques, visualization, positive self-talk, internal coaching and relaxation techniques. The ultimate goal is to maintain performance within the “target zone” with the ability to implement learned techniques when the athlete catches their internal state trending towards under- or over-activation. The key to success is internal monitoring and prevention.
Many athletes struggle to consistently train at the level they perform. Often athletes report frustration that they can “turn it on” during a performance but feel unable to replicate that level of intensity in daily practice. For these athletes, it is important to understand the “performance activation curve” and learn to identify and replicate game-day performance on a routine basis. This requires focused attention on breathing techniques to achieve activation (rapid cycling and clearing breaths), visualization techniques, pre-performance routine, positive self-talk and internal coaching.
Join Dr. Eller on:
Optimize medical issues treatment:
Diabetes is a common disease that when treated properly has lower rates of depression and cognitive issues.
Diabetes has twice the rate of depression than that of nondiabetic comparison groups
When Type 2 Diabetes was brought under better control through medications, working memory significantly improved
Hypertensive patients without vascular complications had deficits with speed of cognition, episodic and working memory, and executive function.
Treat depression and mental health issues
Treat seizure disorders
Reduce polypharmacy (for example when baclofen and gabapentin were taken together they had cognitive effects but when taken alone did not in one study
Take off or minimize anticholinergic medications
Most commonly used: Hydroxyzine, Amitriptyline, Benztropine, Clozapine, Diphenhydramine, Doxepin, Imipramine, Methocarbamol, Nortriptyline, Olanzapine, Paroxetine, Quetiapine (see full list here)
Take off or minimize dose of antihistamine medications
Taper off benzodiazepines because of issues with psychomotor speed, memory, processing speed, attention, verbal memory, general intelligence, working memory, verbal reasoning (mean effect size -0.74) (xanax, klonopin, ativan, ect). Of note, after tapering off patients from chronic benzodiazepine use, there was significant improvement in sensorium. However compared to controls or normative data, there was an incomplete restoration of function at 6 months. Of note this could be because people who are on benzodiazepines often have multiple other stressors and things going on which could factor into this discrepancy. Of note, temazepam for sleep might be of less concern. Tapering off of these meds can be dangerous if done too fast; specifically there can be issues like having a seizure. Please work with a physician to slowly decrease these medications.
Zolpidem if taken 8 hours prior to driving or cognitive tests, it does not cause impairment, whereas if taken 4 hours prior does. At 2 hours after ingestion it causes cognitive issues and balance issues.
Minimize or take off opioids (vicodin, oxycodone)
In one animal study, opioids reduced neurogenesis by 42% in the hippocampal granule cell layer
Reduce or eliminate topiramate and valproate (of note, sometimes valproate has been helpful in hyperactive delirium with improvement in aggression)
Consider alternatives to carbamazepine or zonisomide
Medications with mild sensorium issues: gabapentin does not cause cognitive changes but does sometimes have occasional sedation issues at higher doses, oxcarbazepine (slight alpha wave slowing and some some issues with sedation), trazodone (mild issues with short-term memory, verbal learning, body sway, muscle endurance)
Medications without cognitive effects: Lamotrigine, Keppra (although 20% had complaints of somnolence), propranolol.
Poor sleep leads to decreased memory encoding, mood issues, worse concentration, driving accidents
Sleep counteracts the effects of chronic stress and allows the body’s immune system to “regenerate”
Set up patterns of rest (limiting caffeine and electronics at night before bed, consistent bed and wake times, and eliminating napping)
Diagnose and treat Obstructive Sleep Apnea and treat with CPAP and weight loss.
Uses in CPAP will improve short term memory, episodic memory, processing speed and mental flexibility
Another study showed that CPAP improved depression scores
Drug and Alcohol issues:
Get off THC
Persistent cannabis use showed greater IQ decline (6 points) and worse on neuropsychological tests with greater impairment of executive functioning and processing speed. There were also problems in attention, memory, learning, verbal IQ cited in other studies. Effects were worse when frequent cannabis use was used prior to age 18.
Use alcohol in moderation
1-6 drinks per week was shown to reduce risk of dementia whereas >14 drinks per week increased risk in a prospective cohort study
Recognize that acutely drinking 4 beverages of alcohol impairs planning, spatial recognition, memory, attention, and therefore sensorium.
Realize you have free will
In studies where they try to convince one group that they don’t have free will, it leads to them 1) being more likely to cheat 2) more likely to conform to social norms 3) reduced helping behavior and increased aggression and 4) not slow down after making an error to re-evaluate. I will go into the last finding, and in a future episode go over this in more detail.
In a study that looked at what would happen to people after they read something that argued that we don’t have free will. The group that read the paper arguing against free will compared to the control, did not slow down after making a mistake like normal people do, instead they proceeded in the game at the same speed. Post-error slowing was reduced in the no-free will group, this means that after making a mistake, they did not slow down, which is usually done by control processes. This is also seen in patients with schizophrenia and children with ADHD. Weakened belief in free will (intentional control) decreases the change they will monitor their performance. Lack of belief in free will -> reduced cognitive control processing involved in action monitoring -> more careless and impulsive behaviors -> display antisocial tendencies!
Questions? Look for the posts related to this content on one of my social media sites. I will try my best to answer the questions or plan to answer them in a future episode.
Dr. David Puder
For PDF with citations: https://psychiatrypodcast.com/resource-page
Special thanks to intellectual and research contributions from: Rebeka Sipma, Dr. Amul Shah, Ale-salvo Daniela, Adam Borechy, and Jaime Rudyk
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The most recent podcast on the Psychiatry & Psychotherapy Podcast is on the benefits of exercise for depression and cognitive function. I cover 17 studies on the benefits of different kinds of exercise, most specifically strength training.
Strength training may be underestimated in terms of improving cognitive function and depression. I wrote a blog about this in the past, and it is a passion of mine. Basically, strength makes people harder to kill.
Strength also keeps sensorium (total body health) up when faced with unplanned medical issues.
Post-ICU muscle weakness had overall worse survival outcomes.
Handgrip strength predicted functional outcome in hip-fractured women.
Low muscle mass (sarcopenia) increased risk of developing delirium in one large multisite study of 588 hospitalized elderly patients.
Once to twice weekly resistance training over 12 months improved executive function, selective attention, and even conflict resolution, whereas balance and tone training had deteriorated function
10 weeks of a supervised progressive resistance training program, performed three times a week, was shown to improve depression, as well as improve bodily pain, vitality, and social functioning. It was also shown to decrease limitations on routine activities from emotional problems.
In a study looking at high and low intensities of progressive resistance training in adults >60 years old, a decrease in depression symptoms was more significant in the high intensity exercise group. The high intensity group was lifting 3x8 reps at 80% their one rep max, whereas the low intensity group was doing 20% of their one rep max. The depression scale assessed sleep, feelings of guilt, mood, anxiety and slowness of thought, speech, and action. Strength gain was directly associated with a reduction in depressive symptoms. Those in the high intensity group felt like they had more vitality than those in the other groups. Sleep quality improved significantly in all participants, with the greatest relative change in the high intensity group. Another important finding in this study was that there was an association between a change in depressive symptoms and gain in muscle strength.
Exercise In General
One study that looked at groups of people in a spread of 15 different studies found that a high level of physical activity had a 38% lower cognitive decline and those with low to moderate levels of physical activity had 35% lower cognitive decline than those that did not
One very recent article of a follow up of a group of 1,462 women over 44 years showed those with high fitness measured by a cycling machine had 88% lower risk of developing dementia compared to those with medium levels of fitness. Also those in the high fitness group that did develop dementia, had a delayed onset by 9.5 years compared to those with a low fitness level.
Exercise-induced epigenetic changes increased BDNF in mice allowing for increased brain plasticity
Exercise increases BDNF, uncoupling protein 2 (important for learning and memory), executive function of cognition (scheduling, planning, monitoring, task coordination), and therefore is neuro-generative, neuroadaptive, and neuroprotective. Further, it counteracts the effects of stress, both future stress (decreases learned helplessness when subjected to overwhelming stress), and past stress.
Exercise in the elderly was associated with improved executive function and processing speed
Exercise reduces the risk of cancer occurrence, progression, and mortality (Dhabhar 2014)
Exercise Duke Study: Exercise and Zoloft have a similar effect
Lifestyle changes upregulate and downregulate hundreds of genes.
Exercise and Diabetes:
One study on strength training of type 2 diabetes patients had those with diabetes only train one leg three times per week for 6 weeks. After clamping off the legs, they found the trained leg had better blood flow, increased leg glucose clearance, increased GLUT4, insulin receptor, protein kinase B-alph/B, glycogen synthase and GS total activity. Strength training enhances insulin action in skeletal muscles.
A study compared strength training with endurance training and found that the only a significant improvement was seen in the strength training group:
decline in HbA1c (8.3% to 7.1%),
decrease blood glucose (204mg/dL to 147mg/dL)
Total cholesterol (207mg/dL to 183mg/dL)
LDL (120mg/dL to 106mg/dL)
Trigliceride levels (229mg/dL to 150mg/dL)
My exercise recommendations:
I use a model called “Starting Strength” and recommend this book and watching these videos on technique:
Do 3 sets of 5 repetitions each to start out.
Consider getting a coach if you live by one, or an online coach if you want to be a garage warrior like I am!
This is a link to online coaching (use the discount code of “courage”)
For PDF with citations with links to articles go here.
How do we optimize our diet for total brain function?
What are the best diets for the brain and cognitive function?
How much does diet influence our sensorium?
What particular foods are important?
How do we change our genes to optimize our brain?
For PDF with citations, detailed notes, (which can be freely shared) go to:
In this episode, Dr. Puder addresses the fascinating realm of schizophrenia with Dr. Cummings, a previous guest in the show. Dr. Cummings is a psychiatrist with a wealth of experience from working at Patton State Hospital in California, one of the biggest forensic hospitals in the world.
Swedish survey about misperceptions of the environment found that roughly 50% of the population have had misperceptions that could be considered psychotic in nature.
The Loss of Brain in Schizophrenia
Schizophrenic patients lose 2% of brain mass per year for the first 5 year in the course of illness.
Living with Schizophrenia and Perception of Reality
Are Negative Symptoms in Schizophrenia Precipitated by Medications?
The Pathology, Biology, and Genetics of Schizophrenia
Cannabis Use and Risk For Schizophrenia
Counter-arguments Against Robert Whitaker’s “Anatomy of an Epidemic”
Emil Kraepelin, and the Early Studies on Schizophrenia
The majority of schizophrenic patients during Kraepelin’s observation became vegetative in their 40s.
After the advent of antipsychotic medications, schizophrenic patients are able to function until their 70s-80s
Gitlin 2001 Neuroleptic Discontinuation Study
Exacerbation or relapse was almost universal within 2 years in those who discontinued antipsychotics
Schizophrenia Prevention in High Risk Population
Australian study on children of schizophrenic parents (Yung, 2011)
Australian Study on Children of Schizophrenic Parents
Crime, Violence, Mass Shootings and Schizophrenia
Medical Management of Schizophrenia
1st Break Psychosis
Long-acting Injectable Antipsychotics in Early Illness
Exercise for schizophrenia increased hippocampal size by 12% vs. -1% for non exercising groups of patients (Pajonk, 2010)
Lifestyle, Diet Optimization
Gitlin, M., Nuechterlein, K., Subotnik, K. L., Ventura, J., Mintz, J., Fogelson, D. L., ... & Aravagiri, M. (2001). Clinical outcome following neuroleptic discontinuation in patients with remitted recent-onset schizophrenia. American Journal of Psychiatry, 158(11), 1835-1842.
Pajonk, F. G., Wobrock, T., Gruber, O., Scherk, H., Berner, D., Kaizl, I., ... & Backens, M. (2010). Hippocampal plasticity in response to exercise in schizophrenia. Archives of general psychiatry, 67(2), 133-143.
This week I had a discussion with Dr. Darcy Trenkle on the difficulty of providers to get psychiatric treatment, using ourselves as the examples. In a recent article nearly 40% of physicians surveyed said they would be reluctant to seek formal medical care for treatment of a mental health problem because of concern that this may put their medical license in jeopardy. Physicians have three times the national average for suicide and have unique stressors and often a culture not conducive to seeking help. We discussed difficulties we had in contemplating getting care for different issues we faced. Hopefully this will open a discussion regarding the conflicts providers have in engaging needed help. Dr. Trenkle is a psychiatrist in Southern California and is affiliated with Loma Linda University Health. She received her Medical Degree from Loma Linda University School of Medicine. She completed her residency training at Loma Linda University in 2015. She is the Medical Director for Electroconvulsive Therapy as well as Program Development for the Behavioral Medical Center at Loma Linda University. If you are a Medical Student, Resident or Attending listening to this and need help, please reach out to a local provider. We are open to receive emails if you are local, our names are searchable in the Loma Linda email system.