Episodes

  • 00:50:04

    What is psychodynamic theory?

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    On this week’s episode of the podcast, I interviewed Allison Maxwell-Johnson, a social worker and PhD student of clinical social work. I refer patients to her regularly for psychoanalysis, and she has had a wonderful impact on their mental health journey.

    

    Psychodynamic therapy is a form of talk therapy where the practitioner work focuses on the patient’s emotion, fantasies, dreams, unconscious drives and wishes, early and current life relationships, and the relationship that is forming between the patient and therapist.

    The history of psychodynamic therapy

    Sigmund Freud is known as the father of psychodynamic therapy. He practiced in the late 1800’s and early 1900’s. Some psychiatrists and therapists think that Freud has been debunked because he is a controversial figure. But my colleague, Allison Maxwell, and I, think his impact on furthering the mental health field has been positive.

    Historically, people with borderline personality disorder, somatic disorder and post traumatic stress disorder (PTSD) were all grouped under the title of “hysteria.” A few hundred years ago, these people would have been killed as witches, put in asylums, and there wasn’t much ability to, or interest in, digging into their psyche. There was certainly no warmth or empathy given to them.

    Freud began to grapple with those deeper, tougher issues, claiming it wasn’t just a medical disorder. He gave empathy, and a level of connectedness to his patients that hadn’t been done before. As the first psychoanalyst, he was a pioneer in his field, and he figured out that having an emotionally connected relationship with his patients (he would even have is patients over for dinner and go for walks with them) could actually heal the patient.

    Affect

    Affect is something therapists need to pay attention to when it comes to each individual patient. It’s about noting the facial and emotional state of the person. Is the patient emotionally flat or expressive? Are they depressed or happy? Are they peaceful or agitated?

    We focus on their emotional state and try to lean in to understand what a patient is feeling during a session. As the doctor or therapist, what is the emotional reaction you're having to the patient, in the moment? Analyze the situation—both your feelings and theirs. Ask them for clarification on their feelings, then ask yourself how you can use that information to understand and connect with the patient emotionally.

    There are multiple emotions going on which can be conflicting. We need to ask ourselves if we can empathize with the distress that is in the room.

    It’s not only about intellectually understanding what’s happening with a patient, or diagnosis. It’s about understanding how to create an emotional connection and help someone.

    Transference

    A therapist applies the principle of transference when we pay attention to the emotional state the patient has towards them. If the therapist reminds them of their abusive father, and they react emotionally, it’s a classic transference situation.

    Understanding transference can help a therapist remain empathic and curious, even when a patient is angry at them. Transference can be seen in their complete reaction towards you, both from their past, and how you are interacting with them.

    Countertransference

    As therapists, we are also humans. We will have reactions to the patients we work with. Countertransference is the complete reaction we have towards our patients, both coming from how the patient reminds us of people from our past, and our reaction towards the things that the patient is uniquely doing.

    The unconscious exists both in our patients and in us. If we can keep countertransference in our awareness as therapists, we can try to understand what is happening interpersonally—why we do or don’t like our patient, and why we feel angry or upset with our patients.

    As therapists, we should not react to our patients out of direct emotion, but understand that countertransference is happening, and be curious about the meanings behind our feelings, and their feelings towards us.

    Studies that show psychodynamic theory works:

    For the curious, read this article by Jonathan Shedler, “The Efficacy of Psychodynamic Psychotherapy” PDF

    Mentalization-based therapy

    Mentalization therapy is an emotion-focused therapy for people with borderline personality disorder. It helps them question whether they are accurately mentalizing, or understanding, their own experiences and their therapists emotional experiences. The positive effect of mentalization-based therapy is measurable. It has a mean effect size of 1-2, meaning it is 1-2 standard deviations from the control group—it works.

    People who were in and out of psychiatric hospitals with suicide attempts, after mentalization therapy, can have great success in achieving a normal life.

    Study on Mentalization based therapy with 8 year follow up: PDF

    Transference Based Therapy:

    Article on transference focus therapy increasing a patient’s narrative coherence and reflective function: PDF

    In conclusion

    As therapists, including psychodynamic principles can help us connect with our patients. It will protect us from burnout, and give our patients the chance to feel emotionally connected with someone, in a corrective and healing way. It can be incredibly rewarding, rather than draining, when we feel connected, and our patients usually express gratitude as they heal.



  • 00:11:28

    Advice for medical students applying to psychiatric residency

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    Timothy Lee has talked to thousands of medical students about how to applying for residency programs, and here, he gives us a few tips on how to make it through the gauntlet, and how to have your best chance at landing the program you want.


    Here is what Timothy Lee says:

    Stay calm

    Many students have been fine tuning their personal statements, and trying to get their resume just right, or hurrying to press the faculty to write letters of recommendation. It can be very stressful.


    It’s okay to turn in information a little bit later, in order to have all of the paperwork you need. It’s even okay to review your statement after you’ve already turned it in. No one will lower their opinion based on that. You will need to have applied for the majority of the programs you are interested in by early or mid-October, otherwise the program director might wonder if you’re applying to them later as a backup plan.

    What matters in a personal statement?

    Every program director will have different opinions on what you write, and every program director will be looking for different things from your personal statement. For some people, it’s a chance to get to know the applicant a little bit. For others, it doesn’t really matter that much.


    As long as your grammar and syntax are competent, you should be fine. Some people don’t worry about the format, and others are more particular. To be on the safe side, if you have access to a good mentor, run it by them. Also, don’t be too wordy—stick to a page and a half.

    Do step scores matter?

    Step scores are a very convenient screening tool for what matters, but there are studies that show that step scores are not directly correlated to success in residency performance. They are helpful, but are not the end-all-be-all. It’s only one part of the picture of an applicant. However, if you are going for a highly-competitive school, you might need to worry about step scores a bit more.

    Apply to the right number of programs

    The number of programs is not the only way to increase your chance of success of getting in. Pay attention to the types of programs you are applying to as well. If you are applying for a good number of programs, make sure at least half of them are are ones you are a solid and potentially attractive candidate for.

    Keep a good perspective

    Ultimately, you are more than your CV, step score, or personal statement. If patients like you, that’s going to go a long ways. Your patients won’t know your scores, or where you graduated from medical school. They will know if you were competent, caring and connected. That is ultimately what matters.


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  • 00:45:50

    Therapeutic Alliance Part 1

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    What is a therapeutic alliance?

    The therapeutic alliance is a collaborative relationship between the physician and the patient. Together, you jointly establish goals, desires, and expectations of your working partnership.

    Every interview with a patient, whether it’s for diagnostic, intake, evaluative, or psychopharmacology purposes, has therapeutic potential. The treatment starts from your first greeting—how you listen, empathize, and even how you say goodbye.  

    It’s built from a partnership and dialogue, like any other relationship. It’s not built from medical interrogation. It’s not about pulling medical information to be able to make a diagnosis. We have to make it a positive experience for patient, so they can begin to talk about what's negative in their lives.

    The therapeutic alliance is full of meaning, and it uses every emotional transaction therapeutically. If they get angry, sad, or have fear you will abandon them, as a therapist, it’s our job to figure out how to help them through that feeling within the relationship. The doctor can express desire for the patient to share, in real time, how the patient is feeling, even about his or her relationship with the doctor.

    Why do we care?

    We all know that some talk therapists have better outcomes than other talk therapists. What’s interesting though, is that some some psychiatrists’ placebos worked better than other psychiatrists’ active drugs. One study of NIMH data of 112 depressed patients treated by 9 psychiatrists with placebo or imipramine, found that variance in BDI score (a score that measures depression) due to medication, was 3.4% and variance due to psychiatrist was 9.1%. One-third of psychiatrists had better outcomes with the placebo than one-third had with imipramine.  

    Another book argues that the therapist is more important to outcome than theory or technique. Many other studies have shown that therapeutic alliance directly correlates to success rates.

    What builds a therapeutic alliance?

    Research shows there are a few things that grow therapeutic alliance:

    Expertness

    Facilitating a greater level of understanding

    When residents are worried they are an imposter, I tell them that humility is good, but realize that you have experience that most will never have, medical school, being highly educated, being around vast different ways of thinking and reflecting on the world...

    Consistency

    Structuring your office to run on time.

    Being consistent to respond to refill request, lab results, or patient’s questions.

    Non-verbal gestures

    Eye contact

    Leaning forward

    Mirroring of emotion occurs naturally when people pay attention to emotion

    Maintenance of the therapeutic frame

    A dual relationship (eg, dating) breaks down therapeutic alliance. Patients will test the frame. It can be helpful to say, "There will be positive and negative feelings between us and what will be safe is to talk about them."

    Empathy, attunement, positive regard

    Patient: “Therapist is both understanding and affirming."

    Patient: “Therapist adopts supportive stance.”

    Patient: “Therapist is sensitive to patient’s feelings, attuned to patient, empathic.”

    Research has found that for beginning therapists, setting and maintaining treatment goals is harder

    Research has shown that strength of therapeutic bond is not associated with level of training

    Therapist should appear alert, relaxed and confident rather than bored, distracted and tired

    Foundational concepts of the therapeutic alliance

    Our profession gives us a privileged glimpse into the human heart and mind. Each patient is idiosyncratic, unique, precious. Each patient has unique strengths which we should place focus on.  Some therapists can be in a hurry to find out what's wrong, but we should also want to find out what's right with our patients.

    Our own feelings, as therapists, about the session are not intrusions but clues. If you are experiencing boredom, perhaps you are not understanding the main point the patient is trying to explain. Be curious for what you are missing. If you start feeling something different than you did at the beginning of the encounter, notice it. Try to empathize for the patient with what changed.

    Our goal is for the patient to feel understood, heard, accepted, felt. To be understood is to be accepted.

    A strong alliance will provide a "Corrective Emotional Experience"  (Franz Alexander), which means past relational pain and difficulties are worked out in a new relationship. When your subjectivity (your feelings, thoughts, goals) come into contact with the patient's subjectivity, a unique "intersubjective relationship" is formed from your mutual influencing of each other. A new dyad (2 coming together) is formed by looking at new meanings, understandings and connectedness. As a therapist, you are a “participant observer” as you observe the patient’s behavior and also become a “significant other” in their life through your interactions (Harry Stack Sullivan).

    Here are some things to consider on a first encounter with a patient:

    The patient will feel: examined, fear being seen as crazy, fear of not being liked, discouraged, hopeless, helplessness, needy, fear you are a mind reader, or even fear that you sleep with your patients.

    In developing this relationship, it’s important to understand they can formulate defenses that are adaptive. Try to empathize with that underlying emotion. Starting with what's an adaptive response and solves something, looking for what’s maladaptive does not.

    The patient may question your competence. They might say you look very young to be a doctor. The appropriate response would be to dig down and see why they are feeling what they are feeling. Say something like,"Perhaps you were looking for someone who looks older; of course you’re entitled to worry about how competent I am and how much I may be able to help you."

    Therapists are always worried about being ineffectual. It's very natural to feel like an impostor in our position. It’s also normal to feel—when someone's angry at us, our mirror neurons lead us to be angry back.

    Always face the patient, without desks between you, lean slightly forward, give appropriate eye contact, and do not do excessive note taking (you should be observing at least 90% of the time). Ideally, a clock is positioned behind the patient which can easily be seen by you without making obvious movements.

    On Listening: An Active Process

    Connection is non-verbal, and is equally as important as verbal communication, sometimes more so.

    Omissions (what is not said) in the patient's stories and memories are important.

    Point out common patterns you hear.

    If every time you say something to the patient he says "no, that's not it" then point out that to the patient.  

    Be aware when asking "why" questions, you are likely going to arouse the same defensive emotional reactions that occurred when the patient as a child was asked "why did you do that?" by the parent.  At times, "why" can communicate disapproval. For example you ask, "Why do you feel that?" And they say, "I DON'T KNOW! Are not you the doctor!"

    Dr. Tarr has some good advice on nonverbal communication: "I participate. I respond. I react to my patient and to his verbal and nonverbal communications.  At the same time I observe what's going on, what the patient is saying and what he is not saying. I am particularly attuned to evidences of anxiety, to what I am feeling and thinking, and where, if anywhere, the interchanges are going. I am wondering how best to formulate for this particular patient what I observe that may help him feel understood and responded to."

    Observe that defenses (sublimation, reaction formation, intellectualization), although they reduce anxiety, may misrepresent reality.  

    Assume an attitude of "reverie," like a good maternal object, receiving toxic stuff from patients and then giving it back to them in a detoxified form (Wilfred Bion).

    Create a "holding" place for patients in which patients have a transitional or play space (Donald Winnicott).

    Listen in a way that notes what the patient is trying to say about your relationship.

    Patient: "I feel lonely even when I am with people."  Doctor: "Do you feel lonely here with me now?" Patient: "No, I feel you understand me somewhat."  Doctor: "I want to know if there are any times where you feel more lonely in our sessions, it will help me to understand what is going on between us."

    Listen to their moment to moment change in emotions.

    Try to enter a bit into their feeling, be present with them, mirror the emotion/feeling, use their own words, ask them to find their own words.

    If you don’t get why they are sad, then stay with it, ask them more questions, have them deepen your understanding of it.

    Once they feel you truly understand the effect will change. When people feel heard, deeply understood, it is pleasurable.  

    Shame- patient looks down

    “I can understand why talking about this must be difficult.”

    “Perhaps as you talk about this you feel…”

    Try to find the adaptive function: “I hear switching to a new doctor is hard, I think that is a common experience, I think it is adaptive to be hesitant at first in what you share, we are just meeting."

    Anger/Frustration:

    “Would you say that as you mentioned this you feel frustrated.”

    Find the adaptive function: “your anger here seemed to have the goal to protect you and your family”  “your anger likely kept you alive!"

    Sadness

    “Perhaps you are feeling sad as you say this?”

    Find the adaptive function: “it makes sense that you feel sad here, I think crying and feeling sad shows how much you valued your dad and therefore the loss hurts that much more."

    Disgust

    “I am wondering if you feel disgusted by this?”

    “I hear you feel disgusted…” (ask with a questioning tone).

    Find the adaptive function: “Feeling disgusted by how your sisters turned on you and cast you out of the family makes sense, it sickens you to see the level of their resentment and bitterness."

    Fear

    “I hear a deep concern or perhaps fear regarding this.”

    “Might there be a deep concern or perhaps fear regarding this?”

    Find the adaptive function: “After your traumatic event, it makes sense that you would no longer want to put yourself in that situation, it sounds like you are trying to protect yourself."

    Listen to the patient’s goals, purposes, aspirations, fears, hopes, values, meanings.

    How do you create and maintain a working alliance:

    Be sensitive to empathic strains and prevent them from developing into empathic ruptures.  

    Ask for feedback. Reflect on the "we" aspect of the encounter. If the intervention/participation failed to have the desired result then look at what went wrong with the communication.  

    “As we were talking together when did you really feel we were on the same page?”  

    “When did you feel we were understanding each other?”

    “When did you feel we were communicating meaningfully?”  

    “When were you feeling disappointed?”

    “When did you fell I was not responding enough?”  

    “When did you feel frustrated, misunderstood, or impatient?”

    Be able to define and predict interpersonal conflicts that may cause a disruption of the shared empathic relationship. Set the groundwork for openness.

    For example:  

    Doctor: "Tell me about your past psychiatrist?  “What worked and what were your disappointments with your past psychiatrist?"

    Patient: "He was kind of a jerk."  

    Doctor: "Can you tell me more about that?"  

    Patient: "He always would just stare at this computer, and often answered his pager during sessions."  

    Doctor: "Thank you for sharing that, I will stop typing and finish this later, I hope that if you ever have any feedback for me you will know that I will want to hear it, even if it is negative, and will appreciate knowing your experience of things."

    Patient: “Ooo I was not talking about you.”

    Doctor: “Ok, nevertheless it is a good reminder to not be focused on the computer, but if you are bothered by things or frustrated it will be helpful to know.”

    The therapeutic alliance is an incredibly powerful relationship, and if it is managed with care, it can affect positive change in a patient’s life.

    In future episodes on therapeutic alliance I will dig deeper into specifics of it, and pull upon the depth of my mentorship from Dr. John Tarr.

  • 01:10:20

    How to Treat Emotional Trauma

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    This week on the podcast I spoke with fellow therapist, Randy Stinnett Psy. D, about how trauma works, and how we can help our patients overcome it.  

    What is trauma?

    Emotional trauma comes from stress that is overwhelms a person’s neurological system. Some stress can be good and formative, or it can be bad and get stuck in the brain, causing someone deep emotional pain.

    Think of climbing Mount Everest. Some people choose to do that, and it’s easily one of the most stressful situations you can put yourself in on purpose. That’s good stress if you have trained for years and are ready for it. If someone forced you to climb Mount Everest, it would register in the brain as a trauma.

    Trauma is too big for the mind, brain, and nervous system to assimilate. It’s a memory, or experience, that gets stuck because the person believed it would result in their death, or at least serious injury.

    The brain has several mechanisms to keep something stuck so that the person will remember it, and try to avoid getting hurt in the same way in the future. It is a survival instinct.

    People commonly demonstrate symptoms of trauma when they’ve:

    Experienced a sexual violation

    Seen violence

    Experienced violence or abuse

    Been neglected—experienced the absence of something that they should have had.

    Been in near death experiences like car accidents or war

    People who have PTSD, or post traumatic stress disorder, have experienced a soul-level of brokenness, and even talking about the event, or having a memory of it, can bring it back with the same force that occured in the actual accident. They often have recurring nightmares, or repetitive symptoms that continue long after the event.

    Typical PTSD symptoms alternate between chronic shut down and fight and flight

    Fight and flight symptoms are:

    Sweating, nightmares, flashbacks, anger, rage, panic, hypervigilance, tense muscles, painful knotted gut

    Shut down symptoms are:

    Dissociation, freezing, emotional detachment, voice trembling, difficulty getting words out, numbness, apathy, fear, helplessness, dizzy, empty, nausea

    Moments in connection mode look like:

    curiosity, exploration, relaxed and full breathing, feeling grounded, true smiles

    Body movement and trauma

    We’ve all heard the reference to Pavlov’s dogs—the bell rings and the dogs salivate because they know it is dinnertime. Pavlov discovered many more things than that dogs drool. Once, his lab was flooded with freezing water that nearly filled the cages of the dogs. When they were finally able to get the dogs free, the dogs interacted differently with the world around them. They seemed hopeless.

    Humans work the same way.

    PTSD rates were 16% for survivors of 911, and 33% for survivors of Hurricane Katrina. Why? Traumatologists speculate it was because during 911, survivors were running away from the catastrophe to save their lives. In Katrina, the victims were airlifted out and placed in gyms, for sometimes months at a time. Those in lower socioeconomic levels had no money, no home, and nowhere to go—they were trapped.

    The body is designed to move away from danger, but if the body can’t move, trauma can set in.

    Attachment based trauma

    Having a negative attachment with parents often sets people up for later traumas in life to be a bigger assault on the nervous system and psychological functioning, than it would have been as a standalone event.

    Patients who experience unhealthy attachments often struggle with emotional regulation and boundaries.  

    Many people, as children, were not heard and mirrored in their emotions and experiences. When they discussed their problems with their parent, and it was met with disdain or shut down, the patient has most likely developed the idea that they have no voice. The stress was not contained and thus all the raw emotion is still there and unprocessed. This leads something to continue to be traumatic in the brain.  

    This follows the same pattern as polyvagal theory. When we are in connection mode, we are open hearted and happy. When we feel stress, or lack of connection, our sympathetic nervous system kicks in and we switch into fight or flight mode. If that disconnection continues, our parathetic nervous system takes over and we go into full-on shutdown. When children are repeatedly ignored or abused, they switch in and out of shutdown mode, causing trauma.

    Polyvagal theory and attachment theory, and how they affect children (and adults too), are demonstrated best in the Still Face Experiment video (link to prior article I wrote on that experiment).

    Attachment trauma is repeated trauma. It can occur in childhood, or any other time throughout our lives within relationships.

    Notes to therapists on dealing with PTSD

    Studies show that having an emotionally connected therapist, while someone is reprocessing their traumatic memories, can help heal the emotional damage of those memories.

    Displaying emotional stability

    Patients often superimpose all of their abusers onto their therapists. As therapists, we need to realize this, and stay steady during the entire course of therapy. Remaining calm, safe and empathic is one of the most healing things we can do for them.

    It is a way of being, not just an action, or a reaction, towards our patients.

    Receiving feedback

    As therapists, it’s important to be able to receive feedback from our patients about what is working for them without it being an adversarial situation.

    We must respond in a way that allows the patient to have their own voice. First, validate their emotional experience of the patient. Next, thank them for being honest with you. Ask for the whole story behind their feedback.

    I am not saying this as some sort of technique, but rather this should come out of the belief that 1) their emotional experience is valid and needs a voice 2) it takes courage to voice any feedback and this is important for their growth and success.

    When these things are truly believed, we are empathizing and thanking them, out of the core of our being, and not just as a technique.  

    Where they were expecting rejection, you end up validating their experience. Finally, ask them how it feels, in the moment, to be heard and to be able to safely express their opinion. Allow them to experience a felt difference between you and their abusers. This provides a corrective emotional experience!

    Know when to limit the stress

    Understanding the different nervous system’s functions will help you know when enough is enough for your patient.

    Study the symptoms of the activation of the somatic, autonomic, sympathetic, and parasympathetic nervous systems. This is imperative, and if you cannot slowly uncover the stressful situations in a way that the patient can manage it without engaging shutdown mode, you will end up doing more damage than good.

    Emotional connection

    One psychiatry resident asked my mentor, Dr. John D Tarr, if it was better to keep inpatient people at an emotional distance, so the patient would not get attached and want to continue to stay in the hospital. My mentor responded that we always want to be connected to our patients, to be empathic. When we feel they are getting attached and don’t want to leave, we need to open up that dialogue to how we can help them experience connection outside of the hospital.

    Studies show that patients who feel connected to their doctor are more engaged in treatment—they go to therapy, take their medications, and continue their mental health journey.

    Trauma-based memories are different from normal memories, like knowing what you ate for breakfast this morning. Trauma-based memory has a sensory aspect to it. They are stored in a different part of the brain than where we function for our daily, normal connection mode.

    As therapists, when we access those memories with patients, the patient begins to switch to a different part of their mind, and demonstrate symptoms of trauma physically. They may tremble, sweat, and sometimes even their voice changes—it can be hard to get the words out, they whisper, they sound child-like.

    To understand how people respond to trauma, we have to know that emotions have primacy, or first dibs, on our reactions. Our brain deems them more important than our executive functioning—our ability to reason and plan our lives’ daily tasks.  

    If the patient is open to it and we have established a good, trusted attachment and connection, we will talk about their traumatic memories. If we do not have a connection in that way, I will not explore deep traumatic memories with them. It is more important to build a safe, secure relationship first.

    Trauma gets stuck in the non-analytical parts of the brain—our emotions, creativity, experiences, art. It’s image-based, somatic (physical body), it’s non-verbal. Parts of the left hemisphere of the brain deals with logic, reasoning and language. To integrate this part of the brain, the patient will have to access the emotional parts and then put words to their experiences.   

    In that conversation, these are some of the questions I will ask:

    What did you see?

    What did you feel emotionally?

    What did your body experience?

    What do you believe about yourself as a result?

    Allow for freedom

    Also, when we require our patients to do anything, even to stay for the whole hour of therapy if they do not want to, we are reinforcing the trapped feeling. Keep an open dialogue about what your patient is feeling throughout the therapy session.

    If the patient is suicidal with a plan and intent, they likely need a safe place to get through the intense time. I will tell them, “My goal is to not keep you here indefinitely. We will come up with a plan to get you out of here, and for you to be healthy.”

    In general, try to give your patients, especially the PTSD ones, choices. Create boundaries and give guidance, but allow them to have freedom in their choices.

    Summary  

    In this first discussion with Dr. Stinnett, I wanted to highlight some introductory understanding on trauma.  We discussed how trauma is stored differently in the brain and how the polyvagal theory is connected with this journey.  We highlighted the importance of emotion, connection and feedback. Please leave comments below on your thoughts regarding this blog and podcast!  

  • 00:51:32

    Setting Boundaries in Relationships

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    This episode can be found on iTunes podcast, Sitcher, Overcast and Google Play.  

    What are boundaries?

    When we refer to boundaries, we are talking about emotional walls that are healthy. Boundaries are meant to keep us in relationship with the people that we love.

    Think of them as your property lines around your house. You know where your lines are, where your property ends and your neighbors begins. Therefore you know what you are supposed to take care of and what your neighbor is supposed to take care of.

    A boundary defines our self. Within ourselves, our “property” consists of our physical body, our desires, our intellect, and our ability to make decisions. It gives us a sense of defining what is “me” and what is “not me.”

    We are not supposed to take on too much of other people’s emotional experiences. When I was a newly practicing psychiatrist, I didn’t know that, and I felt depressed after meeting with a depressed patient. It is possible to have an understanding of what is happening in someone’s emotional world, but not take it on yourself.

    There is a psychological principle that is common among people who struggle with having good boundaries with others. It’s called “siding with the aggressor.” For example, if someone grows up in a home where the father is constantly displaying angry behavior, a child might learn to develop a sense of humor if he or she learns that will diffuse the situation. Rather than running away from, or fighting back, these people joined with the aggressors, paying attention to them, calming them, helping them.

    Early on in childhood, people who side with the aggressor understand how to make others happy. This continues into adulthood and is formative in new relationships in how the person would choose to interact with others.

    I don’t think of it as a weakness, I think of it almost as a superpower—these people are incredibly skilled interpersonally when they get older. They know how to react to others, how to make others happy, and how to make angry people calm down. They are great peacemakers, therapists, and psychiatrists. It was an adaptive feature for them in childhood.

    But as they grow into adulthood, they need to learn to choose when to use this superpower, or when to have a boundary.

    My wife, Lindsay, first began learning about boundaries when she was experiencing burnout as a young, working woman. She never said no, always went above and beyond the requirements of her job. And at the end of the night, she was exhausted. After awhile, she started to become upset—upset at herself, and even a her situation.

    Within the Big 5 personality types test, Lindsay scores high in Trait Agreeableness. People who are high in that trait value relationships, are empathic and helpful. They will do things they don’t want to, merely to maintain their relationships. Women typically test higher in the trait than men.

    I see many women come into my practice who have high markers of agreeableness—they haven’t found (or been able to express) their boundaries. They have issues with chronic pain, problems with expressing anger, either within themselves, or towards others.  

    It’s also common that these people have no idea that their “helpfulness” is causing them huge amounts of physical pain. People who are caretakers, who feel looped in to being someone’s source for happiness, life, wellbeing, often get looped into these types of situations if they don’t have a strong sense of self. Obviously, many people are caretakers for their relatives. I’m not talking about being a nice person versus being selfish, or being a caretaker versus letting someone you love be alone.

    I’m talking about the emotional position of your heart during those situations. Are you able to say no when you need to? Are you asking for help when you need to? Are you taking time for yourself? Are you in pain? What is your emotional state when someone calls and asks for help? Do you check in with yourself before you say yes?

    How do you know when you need to start establishing boundaries?

    Typically, with people who have no boundaries, the resentment will build and build, and they will do something drastic to relieve their pain—cut off the relationship, quit caretaking altogether, stop being friends with the person, get a divorce. Or the resentment will build up in their body, causing either depression (as the anger is turned inward) or body pain (as the body carries the burden).

    The truth is though, that when someone with no boundaries says yes, it might be ingenuine. They are saying yes out of guilt and obligation, not out of a true desire to say yes.

    When we do things out of obligation or compulsion, we lose passion for that task, and begin to build resentment. If we aren’t making the choice to say yes, we are thus protecting our ability to say yes to our passions, joys and desires.

    Good fences make good neighbors

    As you’re setting up your “fence,” you want to keep the bad out, but it will also keep the good in.

    When we talk to people about boundaries, they are often scared of beginning to say no.

    When you learn to say no, and you begin to make new friendships with people, you will tend to set higher standards for how you want to be treated during those relationships.

    How to set up healthy boundariesLook at the people you have a hard time saying “no” to. Is it your boss? Someone in authority? Someone who is a family member?What do you fear losing from them if you say no? Is it love? Respect? Provision? For a boundary-less person, being a pacifier has some advantage. Maybe you were the peacekeeper in your house growing up. Maybe you weren’t allowed to say no. Maybe abuse was involved. Or maybe you were simply a sensitive, sweet child who heard repetitively that it was a good thing to be kind and helpful. Whatever the case, there is some sort of relational reward to say yes, and to keep the peace. Pay attention to what you’re getting out of saying yes to that person.Become aware of body sensations you're having when you think of setting boundaries, of saying no to someone. Do you feel tightness in your chest? Numbness in your hands? Is your heart racing? Do you have anxiety?Have a pre-programmed response for when someone asks you for something. Lindsay likes to say, “Can I get back to you later with an answer?” It allows her to take off the social pressure of saying yes immediately, and be able to respond with a truthful answer later on.Before you say yes to anything, think about your ultimate goals and boundaries. We all have a purpose, we are all unique. If we spend all of our time doing only what other people want us to do, we won’t accomplish our goals. When we start to focus on ourselves more, we can see where the opportunities to say yes, or no, will take us, and we can see if they line up with our ultimate goals.Have safe people in your life, so that when you don’t have the strength to say no or speak up, you can talk to them. You can ask for help. It could be a therapist or just someone you can feel safe with. Lindsay has a group of women she has talked to once a week for 12 years. On that phone call, they discuss what they are dealing with and how they are growing.Have conversations with your current friends where you set boundaries. I go on walks with people all of the time. I often ask if we can switch topics on the way back. Normally I would be the listener the whole walk, but with my new boundary, it lets me also talk about something that’s going on in my life. People are always responsive when I ask for this, and it’s always positive. People who are higher empathy have a harder time asking for what they need.Throughout our lives, we have new possibilities for relationships every day. We can take care with adding those who are good, positive, safe people, who will understand our “no” and will allow us to uphold our new boundaries. When you’re looking for new, good friends, look for people who are full of grace. They are also full of truth—they are kind and open, but also honest.Parenting and boundaries

    Children are difficult to have boundaries with. It can be because we love them and want to give them the world, because we know they aren’t fully emotionally developed, or because we want to ease some of our own exhaustion by giving in!

    One key to holding our boundaries when our kids throw temper tantrums is to respond to tears with empathy, not just say “yes” to ease our discomfort. If we resonate with them, it will help both us and them. For example, if your child is screaming and crying about leaving the park early, try saying, “I know it must feel hard for you to leave something that is so fun. We will come back again. Nevertheless right now, it’s time to go. At home, you have toys too and can play with them.” This offers empathy, hope and it keeps a boundary.

    If we give in and let them stay, we are teaching them a bad habit. We should never set a boundary that we aren’t willing to follow through on. It helped Lindsay and I to remember the statistic that even giving in to 1 out of every 8 tantrums taught the child that tantrums worked, and they would win. It reinforced their negative behavior.

    If we make them leave and don’t care that they are upset, we aren’t recognizing their emotions and are being unempathic.

    Letting children feel stress, and being empathic and reassuring when they’ve completed the task, is more helpful for them as they grow. If you step in every time and relieve the stress (such as not making them go to school when they don’t want to), you’re not preparing them for adulthood.

    Keep your boundaries, and express empathy.

    Boundaries in romantic relationships

    Dating is hard work. There are several boundaries to navigate during dating. When you have talks about boundaries in dating, if they don’t respond appropriately, you definitely need to evaluate whether you want to continue dating them or not.

    Be honest and open right from the start.

    Physical boundaries

    This is a hot topic in society today—consent, verbal consent, being able to talk and have conversations. Many of my patients do not want to follow through with physical relationships with people, but they have a hard time saying the actual word “no” when they are in the moment. Define what you want and don’t want, long before you get into another relationship. If someone does not respect your “no” that should be a deal breaker.

    Spiritual boundaries

    Define what you want and don’t want, what you believe spiritually. What are your worldview deal breakers? Defining your deal breakers and writing them down, and asking your friends to help keep you accountable, is important.

    If you are Muslim, Jewish, or Christian, make sure that you know what you want in a partner, and that you aren’t letting go of boundaries that will one day matter to you again, just so you can date someone.

    Conversational boundaries

    Part of dating now is “ghosting,” or shutting down communications when you don’t want to have real conversations about how you’re experiencing someone. I believe this has developed unhealthy communication patterns in society.

    When Lindsay and I were dating, she almost broke up with me because I demonstrated some anxious behaviors during our dinners together. I would shake my leg, or eat three loaves of bread in ten minutes! She nearly ended it without telling me why—she just thought I was odd.

    But when she talked to her friends, they urged her to communicate how she was experiencing me. When she told me what she was feeling, and I told her I was behaving that way becuase I was nervous—I was so into her! She was pleasantly surprised and we continued dating. Now, we have been married for 6 years and have two children together.

    When you’re dating, make it a point to not shut down just because you’re having a negative experience of someone (if that experience isn’t too bad, of course). Try communicating to the person what you’re feeling. This will go a long way in setting up the relationship (and changing your personal habits) to developing positive communication patterns.

    Dealing with relationships and change

    People view consistency as a positive. That means that as humans, we are wired to strive for create an equilibrium in our relationships. And agreeable, boundary-less people strive for consistency in behavior more than others.

    When someone that didn’t have boundaries starts saying “no,” the people in their lives start to sit up and notice what they would deem “inconsistency.” The first time you say you cannot help with that thing you’ve helped with every week, they may be nice about it. But the second and third time, they’ll start to say that sentence we all fear…”you’ve changed…”

    When you grow in your boundaries, there will be people who don’t like them. They will shame you, yell at you, push every button that they can to get you to comply in the way that you used to.

    Understand that by saying no, you may not be as helpful in relationships, volunteer organizations, or work situations as you used to be.

    But, by saying no, you will also free up your time to be able to accomplish what only you can accomplish in your life. Saying no to trivial things that are daily time-vampires will free you up to do the things you are passionate about. That passion will grow, your freedom will grow, and you’ll be able to really start to feel in control of your own life and schedule again. People will respect you.

  • 00:52:13

    The History and Nuances of Bipolar Illness

    Psychiatry & Psychotherapy Podcast starstarstarstarstar
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    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.  

    Mood StabilizersHistory 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.

    Dosing lithium

    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.  

  • 00:59:11

    The History, Mechanism and Use of Antidepressants

    Psychiatry & Psychotherapy Podcast starstarstarstarstar
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    In this week’s episode of the podcast, Dr. Michael Cummings and I talk about the history of antidepressants, and their use in overcoming depression and anxiety disorders.  Below is a short blog on the topic to complement the podcast and subsequently I you can find detailed notes on the topic further below.

    What is depression?

    The overarching term “depression” is characterized by feelings of sadness and hopelessness, anxiety, and loss of pleasure.  

    But there are many different types of depression and depressive disorders:

    Psychotic depression

    Bipolar disorder with depression

    Seasonal affective disorder

    Major depression

    Chronic depression (dysthymia)

    Postpartum depression

    Premenstrual dysphoric disorder

    Atypical depression

    Melancholic depression

    Depression due to a medical illness or medication

    Some symptoms of depression are:

    Weight gain or loss

    Sadness

    Anxiety

    Agitation

    Social isolation

    Sleep problems

    Guilt

    Loss of pleasure

    Loss of interest in activities

    Mood swings

    Major depression

    Major depression is characterized by a continuous feeling of sadness—it does not lift for long periods of time. The average length of an episode of major depression, if not treated, last around 11 months. People with major depressive disorder often had an average of four to eight episodes during their lifetime.

    Each episode of major depression usually makes the next episode more likely.

    The annual prevalence rate for major depression estimated in the US and in Europe ranges from 2-7%. But, if somebody has an episode of major depression, the odds that they have a second episode at some point in their life rises to almost 50%. Then, for each episode they have after that, the probability of the next one becomes more likely.

    For people who had recurrent episodes of major depression, by the time they were in their 50s, 60s, or 70s, they had often become chronically depressed or apathetic; their life had deteriorated significantly.

    Melancholic depression

    Melancholic depression is at the severe end of the depressive spectrum.

    These people have a severe loss of enjoyment, and they usually lack energy. They often develop mood congruent psychotic symptoms, such as delusions that they are guilty for everything in the world.

    This tends to be the most resistant form of depression. When severe. people who suffer with melancholic depression sometimes require electroconvulsive therapy to snap them out of a depressive state.

    Is depression a chemical imbalance?  

    People with recurring bouts of major depression can actually experience anatomical damage to the cortex and the spine, because depression is caused by, and can also cause further, chemical changes in the brain. How does this work?

    One main marker for major depressive occurence is a rise in the release of corticotropin from the pituitary, which eventually stimulates our adrenal glands to produce more cortisol.

    There is a 30-40% decline in the rate of metabolic activity among neurons. Lowered metabolic activity among neurons.

    There is a steep decline in the production of neurotrophic factors, proteins that promote neuron activity and cell growth in the brain. As a consequence, there is a thinning of the cortex, a loss of the dendritic spines on neurons.

    The history of antidepressants

    Doctors used to believe depression was norepinephrine or serotonin deficiency. We now view depression as the inability of the limbic system to be modulated by the neurotransmitters.

    Antidepressant medications target this problem by increasing the ability of these molecules that deal with our emotions, motivations and memory to do what they need to do.

    Before antidepressants

    Prior to the discovery of antipsychotics and and antidepressants, depressed and anxious patients were sent to restful places, or asylums. In the late 19th century, the number of asylums surged.

    They used psychoanalysis and psychotherapy to treat patients, but there was no medicinal treatment for psychiatric issues. They sometimes used chemically induced convulsive therapy to induce a grand mal seizure two to three times a week, and it was quite a brutal treatment.  

    Electrical induction of convulsive therapy came about in the 1940s. It was widely used in both mood disorders and psychosis.

    As a result of these two treatments, people had broken bones and muscle damage. Because of that, electroconvulsive therapy developed a horrible reputation.

    The treatment was later reformed in terms of paralyzing people and using anesthesia prior to treatment. These steps made electroconvulsive therapy much more humane than it originally was. Now people don’t experience the side effects they would have back then. It still remains the most effective treatment there is for severe melancholic or catatonic depression.

    As I discussed in a previous blog on psychopharmacology, in 1940 the original antipsychotic was originally an antihistamine. When doctors noticed the sedative effect it had, they started prescribing it for pre-surgery anxiety. It was the first time doctors prescribed a medication to treat mood.

    In 1951, Dr. Roland Kuhn discovered that imipramine, a drug originally tried for psychosis, was not in fact effective in treating psychosis. He did found that imipramine was effective in improving mood and anxiety symptoms.

    This led to to the discovery of other tricyclic antidepressants, such as amitriptyline, nortriptyline, and desipramine.

    First generation antidepressants

    After World War II, there was a surplus of hydrazine missile fuel leftover. People began experimenting with hydrazine as a base compound for development of drugs.

    One of the first drugs that came out of that endeavor was Isocarboxazid, which was initially used to treat tuberculosis.

    It turned out that a few people who were being treated for tuberculosis happened to be bipolar and became manic while taking isocarboxazid, which led to the discovery of monoamine oxidase inhibitors (MAOIs).

    MAOIs stop the breakdown of serotonin, dopamine and norepinephrine in the brain. MAOIs stop that enzyme from removing those chemicals from the brain. The result is more balanced neurotransmitters—and a lack of depression.

    Still, the possible side effects including incredibly high blood pressure when eating certain foods made scientists keep searching for better alternatives.

    SSRI antidepressants

    Selective serotonin reuptake inhibitors were introduced to the market in 1987, with the introduction of Fluoxetine. The SSRIs were almost instantly popular because they were much safer.

    These drugs increase the amount of serotonin available in the brain.

    The SSRI became very widely used very quickly for treatment of depression.

    They have even been found useful because the increased serotonin input to the limbic system they create (the part of our brain that deals with motivation, learning, emotions and memory) decreases the amount of anxiety and vigilance that the person has.

    SSRI was also found to be effective for:

    Post traumatic stress disorder (PTSD)

    Obsessive compulsive disorder (OCD)

    Generalized anxiety disorder (GAD)

    Social phobias

    Impulse based disorders (like binge eating)

    If someone was still resistant to SSRI medication and is still depressed, electroconvulsive therapy is still the best option available.

    When do you prescribe antidepressants?

    If the initial episode of depression is not severe to the point that it’s inducing suicidal ideation or impairing their ability to engage in activities of daily living, then psychotherapy and exercise should be the first treatment.

    If the following statements are true, antidepressants could be prescribed:

    The person doesn’t respond to exercise positively with fewer depressive symptoms

    Psychotherapy does not seem to be helping

    The depression is becoming severe

    Their family is genetically tended towards depression

    Overall, about 40% of the probability of becoming depressed is genetically determined, the other 60% arising from the environment.

    There are also important gender differences, women during their reproductive years have about twice the rate of major depression compared to men.

    If somebody has recurrent episodes of depression, an antidepressant should be considered, and possibly continued indefinitely.  However I often recommend for these patients a combination of treatments including exercise, diet, effective therapy, and over time can get them on lower doses or less medications.

    Below is a detailed review of the episode, with most of the content.  Thanks Arvy Wuysang (MS4) for your help with this!

    History of Antidepressants

    The investigation of antihistamines leading to the discovery of promethazine, chlorpromazine brought on a decade of intensive discovery and investigation of different antipsychotic compounds.

    Swiss Psychiatrist, Dr. Roland Kuhn (1912 - 2005) discovered the Tricyclic Antidepressant, Imipramine.

    His experiments with Imipramine led him to the discovery that it was not effective in treating psychosis. However, he found that Imipramine was effective in improving mood and anxiety symptoms.

    This led to to the discovery of other Tricyclic Antidepressants, both tertiary and secondary amines, such as amitriptyline, nortriptyline, and desipramine.

    As an after effect of World War II, there was a great amount of hydrazine missile fuel leftover. People began experimenting with hydrazine as a base compound for development of drugs.

    One of the first drugs that came out of that endeavor was Isocarboxazid, which was initially used to treat Tuberculosis.

    It turned out that a few people who were being treated for TB happened to be Bipolar and became manic while taking Isocarboxazid, which led to the discovery of Monoamine Oxidase Inhibitors (MAOIs).

    How were people treated for depression before the discovery of MAOIs?

    Sent to restful places in the country, the asylum movement of the late 19th century.

    Psychotherapy, psychoanalysis

    Convulsive therapy, discovered by the psychiatrist Von Meduna in Hungary.

    Was not originally electrically induced, was chemically induced convulsive therapy instead, quite a brutal treatment.

    Electrical induction of convulsive therapy came about in the 1940s. It became widely used in both mood disorders and psychosis.

    The treatment was later reformed in terms of paralyzing people and using anesthesia prior to treatment. These steps made Electroconvulsive therapy a much more humane treatment. It still remains the most effective treatment there is for severe melancholic depression.

    There were no effective pharmacological treatments for depression before the MAOIs.

    Winston Churchill, was thought to have depression and was treated with Amphetamines, which was later known to be ineffective as an antidepressant.

    Amphetamines or Methylphenidate are still occasionally used in anergic depressions, such as in HIV, or in the elderly depressed person who has a severe lack of energy as part of their depressive illness, but in combination with antidepressants.

    If someone with melancholic depression does not get treatment, how does the progression of their disease look like?

    A fairly negative development. The average length of an episode of major depression, if not treated, last around 11 months. People often had an average of four to eight episodes during their lifetime.

    Each episode of major depression makes the next episode more likely. The annual prevalence rate for major depression estimated in the US and in Europe ranges from 2-7%. But, if somebody has an episode of major depression, the odds that they have a second episode at some point in their life rises to almost 50%. Then, for each episode they have after that, the probability of the next one becomes more likely. For people who had recurrent episodes of major depression, by the time they were in their 50s, 60s, or 70s, they had often become chronically depressed, apathetic; their life had deteriorated significantly.

    What physiological effects within the brain contributes to the greater likelihood of a subsequent episode of depression?

    Major depression, aside from changing neurotransmitter signaling, reduces the metabolic rate of neurons in the brain. There is a 30-40% decline in the rate of metabolic activity among neurons. There is a steep decline in the production of neurotrophic factors, proteins that promote neuron activity and cell growth in the brain. As a consequence, there is a thinning of the cortex, a loss of the dendritic spines on neurons. There was evidence that although recovery after major depression is nearly back to original baseline, particularly in recurrent depression, or in people who alternate between major depression and a more minor form of depression called dysthymia, their brain may undergo gradually increasing anatomical damage (cortex and dendritic spines). The accumulating pathology appears to set them up for the next episode, to be more vulnerable to stress diathesis and the occurrence of the next episode of depression.

    One of the key chief characteristics of major depression is a rise in the release of Corticotropin Releasing Hormones (CRH), which in turn produces an increase in the release of Adrenocorticotropic hormone from the pituitary that stimulates the adrenal glands to produce more cortisol.

    Cortisol functions as a stress hormone. The intent is to help counterbalance stress and return us to a baseline state. However, in major depression that positive benefit fails, and essentially the person’s brain winds up being exposed to chronically elevated levels of cortisol, which has an involutional effect on DNA transcription in cells in the brain, particularly in the limbic system. This have been suggested as the source of treatment resistance as people develop more episodes of depression.

    How does melancholic depression differ from other types of depression?

    Melancholic depression is at the severe end of the depressive spectrum. These people have a severe loss of enjoyment, they’re anhedonic, they lack energy. They often develop mood congruent psychotic symptoms, such as delusions that they are guilty for everything in the world. They have very pronounced negative rumination. They lose interest in food. In fact, if they’re not treated, they just sort of curl up and die.

    Tends to be the most resistant form of depression. These people often wind up requiring electroconvulsive therapy to them out of that depressive state.

    Depression comes in a range of severity. Dysthymic disorder, is the chronic milder form of depression. Major depression, starts just above dysthymia, and progresses to Melancholic depression.

    How severe of a depression warrants a treatment with antidepressants?

    If the initial episode of depression is not severe to the point that it’s inducing suicidal ideation or impairing their ability to engage in activities of daily living, then psychotherapy should be the first treatment. Psychotherapies such as cognitive behavioral therapy, interpersonal therapy, and brief analytic psychotherapy have been demonstrated to be effective in treating depression. Exercise also can be a benefit in mild to moderate depressions.

    If, however, the person doesn’t respond to those treatments, or the depression is becoming severe, or in particular, if this is somebody whose family is somewhat genetically loaded for depression, then treatment with antidepressants becomes a larger consideration. Overall, it’s thought that about 40% of the probability of becoming depressed is genetically determined, the other 60% arising from the environment. There are also important gender differences, women during their reproductive years have about twice the rate of major depression compared to men. Premenarche and postmenopausal women have the same rate of depression as men, suggesting that hormonal cycling during the reproductive years may add an additional burden in terms of vulnerability to depression in women.

    If somebody has recurrent episodes of depression, the thinking is very much along the lines of they should be on an antidepressant and it should be continued indefinitely. It used to be that if somebody recovered from depression, then after a year, everyone would be tapered off and discontinued. That changed when people began to recognize the progressive nature of major depression. Each episode makes the next one more likely, and the more episodes people have, the more resistant it is to treatment. We should be working to avoid the circumstance in which we now have an elderly depressed person who has lost the capacity to respond to most of the tools we have to work with. That’s a very difficult position to be. These are cases where we find ECT to be the only treatment that works.

    The advent of SSRIs

    The first antidepressants, the TCAs, were never a comfortable medication class in usage. This is largely because these drugs are cardiotoxic at relatively low concentrations. Six to eight times the therapeutic concentration is a potentially lethal concentration. So, taking a week’s worth at one time stood a pretty good chance of killing somebody. In a population prone to suicidal thoughts, that’s not a very comfortable position to be in. In the case of MAOIs, if the person is exposed to tyramine from food, or to sympathomimetic agents, cold medications in many cases, can produce hypertensive crisis with blood pressures that can cause vascular damage or death.

    The SSRIs were almost instantly popular after the introduction of Fluoxetine, in large part not because they were more effective than the older antidepressants, but because they were much safer. These drugs selectively inhibit the reuptake transporter for serotonin, thereby increasing the amount of serotonin available in the brain. But by and large, they don’t do a great deal else that is toxic or likely to produce problems. So that if somebody overdoses on an SSRI antidepressant alone, it’s almost impossible to kill the person. If you mix it with an agent that has other means for increasing serotonin, it can produce serotonin syndrome, which can cause death, but that’s a relatively rare negative outcome.

    The SSRI became very widely used very quickly for treatment of both major depression and dysthymia. For a host of anxiety disorders they have been found useful because increased serotonin input to the limbic system, particularly the anterior temporal lobe and the amygdala, decreases the amount of anxiety and vigilance that the person has. SSRI was also found to be effective for PTSD, OCD, GAD, social phobias, and even in impulse based disorders like binge eating.

    The SSRI antidepressants account for about 70% of the antidepressant prescriptions in the United States each year. They are as effective as the mix serotonin norepinephrine antidepressants, in mild to moderate levels of depression. They tend to become less effective than mixed mechanism agents in severe and melancholic depressions.

    The current model for depression have moved away from the basic idea of norepinephrine or serotonin deficiency. We now view depression as the inability of the limbic system to be modulated by the neurotransmitters. Antidepressants target this dysfunction by increasing the modulatory range of these molecules. It may be that in more severe depression, using a single lever to try to push the limbic system back into operating normally just isn’t as effective as using more than one lever.

    What are our treatment options for patients with melancholic depression that are resistant to antidepressants?

    ECT would be the best option in severe melancholic depression. There are other adjuncts available that have been looked at that show promise. Transcranial magnetic stimulation has shown positive benefit in terms of augmenting antidepressants, as has vagus nerve stimulation in some chronic recurrent depressions. Combining the antidepressant with an effective psychotherapy has been shown to have additive benefits. In many cases of depression, it calls for a multimodal intervention.

    One of the caveats with the antidepressants is that their efficacy is more limited than we would like it to be. If you look at most antidepressant studies, they report effectiveness in around 60 to 65 percent of samples based on the definition of response as a 50 percent reduction in depressive symptoms. If you’re severely depressed, it’s great to have a 50% reduction, but that doesn’t mean that you’re well. If you look at how many people go into remission in those studies, you’re now talking about numbers down in the range of about a third. That’s not a very satisfactory outcome if you’re the depressed patient. So, our antidepressant treatments indeed do have limits.

    We’ve looked at ways of augmenting antidepressants. Combining antidepressants with different mechanisms. Augmentation with mood stabilizers like lithium. In women in particular, supplementation with thyroid hormone is effective in some patients. One of the caveats in this as well, is that many people who are depressed and receive treatment don’t really receive adequate treatment. A number of years ago, the American Psychiatric Association (APA) did a survey in both primary care and psychiatric offices looking at dose and duration of treatment for major depression. They found that depressed people in primary care offices got what they judged to be adequate treatment about 41% of the time, and in psychiatric offices about 61% of the time. As psychiatrists, one of the things we can do is to be sure that our patients receive an adequate dose of antidepressants for an adequate duration. Duration in this case means at least six to eight weeks to see if the person will respond, while pushing the dose to the upper therapeutic range.

    The black box warning of SSRIs in increasing suicidality for younger patients.

    When you start treating somebody with an antidepressant, their energy level and their neurovegetative signs often respond before their mood does. This means that you have a more energetic depressed person. Studies going back decades suggests that that exposes the person to a period of vulnerability to suicidal ideation and impulse. The warning that the FDA issued was correct, that in giving somebody an SSRI will increase their risk of suicidal ideation early in the course of treatment. Their intent in issuing the warning was to try to clinicians to follow the patients closely during the first few weeks of starting the SSRI. Unfortunately, what happened because of the warning was that many prescribers stopped prescribing SSRIs for children, adolescents, and young adults. As a result, the actual rates of suicide went up, because young people were suffering from depression and were not receiving appropriate treatment. It was a great example of unintended consequences.

    Studies that looked at this concluded that the group receiving SSRIs had more suicidal thoughts, but their rate of completed suicide did not differ from the placebo group. And overtime, as their depression improved, their risk of suicide declined.

    Increased anxiety in the early stages of SSRI usage.

    Serotonin decreases dopamine release and that may cause akathisia in some patients, particularly elderly patients who may not have a lot of dopamine reserve to begin with. Increased anxiety initially is possible. When these drugs are used to treat anxiety disorders, it’s very important to educate the patient that initially their intensity of anxiety is likely to increase before it decreases because these drugs increase the amount of serotonin available within a few hours. In contrast, the improvement of symptoms is dependent on more downstream processes, such as downregulation of postsynaptic receptors and changes in second messenger populations inside the neurons, those processes take weeks. In many cases, you may need to use an anxiolytic to transiently dampen the effect of the antidepressant.

    Panic Disorders

    Initial panic attacks can be severe. Individuals with these conditions literally feel as if they are dying. This is a result of a false triggering of our fight or flight response. Essentially, having a panic attack would be a normal response to a life-threatening event of some kind. That system is largely located in the non-dominant temporal lobe, and involves the amygdala, the anterior temporal lobe, and the parahippocampal complex. That part of the brain is there to chronically monitor the environment for threats and allow you to either fight or run away before something bad happens to you. In some people, though, it appears that that system is triggered way too easily, it goes off when there is no threat. This becomes a horrible experience. People develop all sorts of anticipatory anxieties depending on what their environment is at the time the panic happens.

    These people often need help with behavioral exposure therapies to make them less sensitive to those environments. In fact, that’s thought to be how people with panic disorder, if it goes untreated, eventually become agoraphobic. They can’t go out of their own house, or in some cases their own room, because they’ve become phobic to the entire world.

    Use of Chlomipramine in OCD

    A number of studies have demonstrated that Chlomipramine are more effective for OCD than SSRI. SSRI can be highly effective for OCD if dosing is increased beyond what is required for depression, in the range of 300 mg a day or more. And instead of taking four to six weeks to get a response, it may take eight to twelve weeks. Chlomipramine, on the other hand is more effective because the effect is felt sooner. It is a very robust increaser of serotonin and may have some affinity for norepinephrine as well. It’s antihistaminic, tends to be anxiolytic. The combination of these effects may be why it is overall more effective. It’s a somewhat difficult drug to tolerate because it’s also a good alpha-adrenergic blocker, so it lowers blood pressure. People can get dizzy or can faint if they are taking too much. It’s very anticholinergic, which gives people blurry vision, dry mouth, constipation, and urinary retention.

    Decreased libido and difficulty of ejaculation as a side effect of SSRI use.

    Increasing serotonin tends to dramatically impair sexual function. In males it can result in erectile dysfunction, delayed orgasm, or anorgasmia. In females, it can result in vaginal dryness or anorgasmia as well.

    Arousal is based on activity by the parasympathetic nervous system using acetylcholine. Orgasm is based on the triggering by the sympathetic system using norepinephrine, increasing serotonin. The spinal cord can interfere with both of those processes.

    In most of the original package inserts for SSRI, they quoted dysfunction figures of 5-7%. Those were falsely low because they only reported those cases where people stated this spontaneously. When you actually ask people, how many were having difficulties, it’s more like 50-70% have some degree of sexual dysfunction. The dysfunction can be mild or it can be severe, with loss of functioning all together.

    Moving to a mixed mechanism agent will help fix that. Use of Buproprion, which is mostly noradrenergic, can sometimes reverse that effect of the SSRI. More recently, there are now SSRIs that also directly stimulate 5HT-1a receptors. Their rate of sexual side effects is much lower. But because they are proprietary drugs, they are much more expensive than generic SSRI antidepressants.

    Buproprion and Mirtazapine use for males with previous sexual dysfunction due to SSRI

    Buproprion is almost purely noradrenergic, consequently does not interfere with sexual functioning. In fact, it may actually improve the libido much more than the SSRIs.

    Mirtazapine is a unique drug that in that at higher doses it increases norepinephrine release by inhibiting auto-receptors for norepinephrine, alpha-2 receptors in the locus ceruleus. So you get more norepinephrine output. It also blocks 5-HT2a receptors, so it acts as a serotonin antagonist which may also provide some benefit with respect to sexual functioning.

    Benefits of optimizing testosterone levels in relation to depression.

    Unlike women, men don’t go through a tightly defined menopause with a sharp drop off in testosterone production. The peak of testosterone production in most men, however, is around 18 or 19 years of age. And then there’s a gradual steady decline thereafter. So that by the time somebody is in their fifth or sixth decade, erectile dysfunction becomes fairly common. It’s estimated that about 40% of males over 50 have some degree of erectile dysfunction. Checking their testosterone is worthwhile, because you may find out that they’re in a subpopulation that have had a more rapid decline than other people.

    Sildenafil, the PDE5 inhibitor can be highly effective in treating erectile dysfunction as a side effect of antidepressants. Cialis daily can be more effective if taken daily due to the long half life and build up.  

    Trazodone is less often effective than the PDE5 inhibitors. Because it’s an alpha antagonist it can work. The adverse effect, commonly known, is to cause priapism, a prolonged and painful erection. The other caveat is that it is a very potent antihistaminic drug. So you can wind up with the unfortunate situation of somebody who now is sexually functional but is too sleepy to be interested.

    We further talked about psychosocial details in the podcast.

    Concluding thoughts

    If we learn how to better modulate cortisol, that may help us a lot with treating refractory depression. There also are continuing developments going on in terms of learning more about direct electrical stimulation of the brain, which may be helpful in treating depressive and anxiety disorders. Once we evolve to the point where we have medications that can directly help increase some of the neurotrophic factors in the brain, that also may go a long way toward altering the long term course of depressive illness. With the medications we have now, we currently have to work with ⅔ response rate and ⅓ remission rate, which is just not adequate by anyone’s standards.

  • 01:38:11

    Emotional Shutdown—Understanding Polyvagal Theory

    Psychiatry & Psychotherapy Podcast starstarstarstarstar
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    “Polyvagal Theory Simplified”

    By David Puder, M.D.

    Polyvagal theory explains three different parts of our nervous system and their responses to stressful situations. Once we understand those three parts, we can see why and how we react to high amounts of stress.

    If polyvagal theory sounds as exciting as watching paint dry, stick around, trust me. It’s a fascinating explanation of how our body handles emotional stress, and how we can use different therapies it to rewrite the effect of trauma. 

    Why is polyvagal theory important?

    For therapists, and pop-psychology enthusiast alike, understanding polyvagal theory can help with:

    Understanding trauma and PTSD

    Understanding the dance of attack and withdrawal in relationships

    Understanding how extreme stress leads to dissociation or shutting down

    Understanding how to read body language

    We like to think of our emotions as ethereal, complex, and difficult to categorize and identify.

    The truth is that emotions are responses to a stimulus (internal or external). Often they happen out of our awareness, especially if we are out of touch, or incongruent, with our inner emotional life.

    Our primal desire to stay alive is more important to our body than even our ability to think about staying alive. That’s where polyvagal theory comes in to play.

    The nervous system is always running in the background, controlling our body functions so we can think about other things—like what kind of ice cream we’d like to order, or how to get that A in med school. The entire nervous system works in tandem with the brain, and can take over our emotional experience, even if we don’t want it to.

    A story about a gazelle...

    Animals are a great example of how we handle stress, because they react primally, without awareness. They do what we would, if we weren't so well tamed.

    If you have ever watched a National Geographic Africa special, you’ve seen a lioness chase a gazelle. A group of gazelles is grazing, and suddenly one looks up, hyper aware of what is happening around him. The whole group notices and pays attention.

    After a moment, the lioness starts her chase. The gazelle she’s singled out runs as fast as he can (sympathetic nervous system), until he is caught. When he is caught, he instantly goes limp (parasympathetic nervous system).

    The lioness drags the gazelle back to her cubs, where they begin to play with it before they go in for the kill. If the lioness gets distracted, and the gazelle sees a moment of opportunity, he’s up and sprinting off again, looking like he suddenly came back to life (back into sympathetic nervous system response).

    When the gazelle was caught, with fangs around his neck, his shutdown response kicked in—he froze. When he saw the opportunity to run, his fight or flight kicked in, and he ran.

    Poyvagal theory covers those three states—connection, fight or flight, or shutdown. 

    Here's how they work...

    Connection Mode

    or...rest and relaxation...or myelinated vagus nerve of the parasympathetic nervous system coming from the nucleus ambiguus response

    During non-stressful situations, if we are emotionally healthy, our bodies stay in a social engagement state, or a happy, normal, non-freak-out state.

    I like to call it “connection.” By connection, I mean that we are capable of a “connected” interaction with another human being. We are walking around, unafraid, enjoying our day, eating with friends and family and our body and emotions feel normal.  

    It’s also called ventral vagal response, because that’s the part of the brain that is activated during connection mode. It’s like a green light for normal life.

    How does this look and feel?

    Our immune system is healthy.

    We feel normal happiness, openness, peace, and curiosity about life.

    We are sleeping well and eating normally.

    Our face is expressive.

    We emotionally relate to others.

    We more easily understand and listen to others.

    Our body feels calm and grounded.

     

    Freeze, Flight, Fight, or Puff Up

    ...or the sympathetic nervous system response

    The sympathetic nervous system is our immediate reaction to stress that affects nearly every organ in the body.

    The sympathetic nervous system causes that “fight or flight” state we have all heard of. It gives us those cues so that it can keep us alive.

    How does this happen? How does this look and feel?

    We sense a threat and freeze to scan the surroundings for real danger.

    We release cortisol, epinephrine and norepinephrine to help us accomplish what we need to—get away, or fight our enemy.

    Our heartbeat spikes, we sweat, and we feel more mobilized.

    We feel anxious, afraid, or angry.

    There may be flashes of facial expressions of fear and anger, with the background of more of a still face.  If positive emotions are present, they usually look forced.

    Our digestion slows down as blood rushes to the muscles.

    Our blood vessels constrict to the intestines and dilate to the muscles needed to run or fight.

    We may want to run away, or punch someone, or react physically in some way, or just puff-up and look scary.

    Our muscles may feel tense, electric, tight, vibrating, aching, trembling, and hard.

    Our hands may be clammy.  

    Our stomach may be painfully knotted.

    All our senses focus.   

    Our gestures may show guarding of our vital organs, fists clenched, or puffing ourselves up to look bigger or stronger.

    In fight or flight, at some level we believe we can still survive whatever threat we think is dangerous.

    Shut Down

    ...or the Unmyelinated Vagus of the Parasympathetic Nervous System coming from the Dorsal Motor Nucleus

    What’s interesting about this part of the parasympathetic nervous system? Its function is to keep us frozen as an adaptive mechanism to help us survive to either fight or flight again.

    When David Livingston was attacked by a lion, he later reported, “it caused a sort of dreaminess in which there was no sense of pain nor feeling of terror, though quite conscious of all that was happening.”

    When our sympathetic nervous system has kicked into overdrive, and we still can’t escape and feel impending death the dorsal vagal parasympathetic nervous system takes control.

    It causes freezing or shutdown, as a form self preservation. (Think of someone who passes out under extreme stress.)

    How does this look and feel?

    Emotionally, it feels like dissociation, numbness, dizzy, hopelessness, shame, a sense of feeling trapped, out of body, disconnected from the world

    Our eyes may look fixed and spaced out

    The dorsal motor nucleus through the unmyelinated vagus nerve decreases our heart rate, blood pressure, facial expressions, sexual and immune response systems

    We may be triggered to feel nauseated, throw up, defecate, spontaneously urinate

    We may feel low or no pain

    Our lungs (bronchi) constrict and we breathe slower

    We may have difficulty getting words out or feel constriction around our throat

    Our brain has decreased metabolism and this causes a loss of body awareness, limp limbs, decreased ability to think clearly, and decreased ability to lay down narrative memories

    Our body posture may collapse or curl up in a ball

    In shutdown mode, at some level our nervous system believes we are in a life-threatening situation, and it tries to keep us alive through keeping our body still.

    Some people who have had both attachment trauma and subsequent trauma can have chronic suicidality, and dissociation episodes that last days to months. Research shows that long term solutions include:

    Dialectical behavioral therapy

    Mentalization based therapy

    Transference focused therapy

    How trauma affects the nervous system

    As humans, we do the same thing as that gazelle when we perceive emotional or physical danger. We alternate between peaceful grazing (parasympathetic - connection mode), fight or flight (sympathetic system- fight and flight) or shutdown (parasympathetic- shut down mode).

    Our response is all in our perception of the event. Maybe someone was just playing a game when they jumped out to scare us, but we fainted. Whatever the reason, whether the incident was intentional or not, our body shifted into shutdown mode, we registered it as a trauma. our body shifted into shutdown mode.

    Or maybe the trauma event was really, life threatening, and our nervous system responded appropriately to the stimuli.

    No matter what the cause was, our brain believed what was happening was life threatening enough that it caused our body to go into flight, flight, or shutdown mode.

    If someone has been through such a traumatic event that their body tips into shutdown response, any event that reminds the person of that life-threatening occurrence can trigger them into disconnection or dissociation again.

    People can even live in a state of disconnection or shutdown for days or months at a time.

    Veterans often experience this during loud, sudden noises such as fireworks or thunderstorms. A woman who was raped might quickly switch into hypervigilant or dissociated response if she feels someone is following her. Someone who was abused might be triggered when even another person starts yelling.

    The problem occurs when we haven’t processed the original trauma in such a way that the original trauma is resolved.

    That’s what PTSD (post-traumatic stress disorder) is—our body’s overreaction to a small response, and either stuck in fight and flight or shut down. 

    People who experience trauma and the shutdown response usually feel shame around their inability to act, when their body did not move. They often wish they would have fought more during those moments.  

    A Vietnam vet may feel they failed their companions who died around them while they stood, frozen in fear. A rape victim may feel he or she didn’t fight off their rapist because they froze. A victim of abuse may feel they quit trying to escape their abuser, and that they are weak or failed.

    Much of “stress” training, which trains people to continue to remain in fight and flight mode, aims to keep people out of dissociation during real life or death situations. Unfortunately, these practices aren’t common beyond elite sports teams or special forces.  The right amount of stress, with good recovery, can lead our nervous systems into higher levels of adaptation.  

    Coming out of shutdown mode

    So how do we climb back out of shutdown mode?

    The opposite of the dorsal vagal system is the social engagement system.

    So, in short, what fixes shutdown mode is bringing someone into healthy social engagement, or proper attachment.

    Getting down into the nuts and bolts of how this works in our body can help us understand why we feel the way we do physically when your body is in fight, flight, or shut down mode.

    When we understand why our body reacts the way it does, like a string of clues and some basic science about the brain, we can understand how to switch states. We can begin to move out of the fight or flight state, out of the shutdown mode, and back into the social engagement state.

    As therapists, whether we are just establishing a connection with a new, anxious patient, or helping them deal with their deepest traumatic memories, knowing how to navigate the polyvagal states is important.

    It can also be helpful if you have just identified yourself in some of these symptoms. Such as, “When I’m with my parents, even as an adult, and they start fighting, I feel lightheaded and disconnected.”

    If you’ve seen some of these things in yourself, hopefully through therapy, and even understanding how this works, you can pull yourself out of a disconnected state.

    Studies show that some parts of the brain shut down during the recall of traumatic events, including the verbal centers and the reasoning centers of the brain (Van Der Kolk, 2006).

    This is why it’s important to conduct therapy, or coming out of shutdown mode, in a safe, healthy way, in a safe, healthy environment. This is why positive attachment is imperative. Otherwise, you run the risk of retraumatizing the patient.

    Because I am a psychiatrist, I am going to write this to demonstrate how to help a patient switch out of shutdown mode.

    However, these tips still apply to those who are just understanding how shutdown mode works. And it can even help those who feel shut down to begin to know how to try and attain a healthy social engagement mode again.

    Have a trust-based relationship. Because of the potential to re-traumatize, don’t even address intensely traumatic events—especially ones where you think shutdown mode kicked in, until the therapeutic relationship feels deeply connected.

    It’s important as the therapist to allow the patient to express things they couldn’t express to other people—shameful feelings, anger, sexual response, anything that feels frightening to share with others.

    Find your own calm center. If you can empathize with their distress, stay in the moment with them, and help them feel connected during their shutdown, you are throwing them a lifeline. You’re helping them come out of shutdown, into social engagement.

    It’s important to fight against the urge to dissociate, no matter how gruesome the subject matter is. As therapists, we could dissociate because of the mirror neuron response—to mirror our patient’s brain, and because when hearing horrific trauma, it’s easy to imagine it happening to us.

    The human experience is so powerful that when we re-engage the trauma, with someone else to support us, it rewrites that event in our brain, adding in the feeling of being supported within the trauma memory. We create new neural pathways around the trauma, and we can change our body’s response to it.
     

    Let the patient lead. Don’t go on a witch hunt. If the patient brings it up, lean into the subject. But it is harmful to prompt the patient into something that isn’t there by asking leading questions and trying to get them to confess. Don’t let your own experience lead you to imagine they have also experienced something.  

    Normalize their response. The entire polyvagal theory should make us say “thank you!” to our bodies. Even if that systems is overactive at times—unwarranted panic or anxiety—that our body is watching out for us, trying to keep us alive.

    Our body reacting in that way is the same thing as the gazelle either running away or going limp. And gazelles have no idea what emotions are in the first place.

    Now that the patient understands that their emotional response was adaptive, primal, and appropriate, we can get rid of the shame that their non-reaction caused.

    Help them find their anger. Anger is an incredibly adaptive emotion, and it’s one we don’t allow ourselves to have. We think anger is bad. But really, anger shows us where our healthy boundaries were crossed.

    Anger gives us energy to overcome the obstacle. We can help the patient see they had the emotional energy to overcome, but the energy wasn’t able to be manifested at the time they wanted it.

    If, in a session, we can get a patient to identify their anger, they will see that they were not completely unresponsive to the traumatic event. If we can help them feel even the tiniest movement of a microexpression of anger on their face—the slight downturn of the inner eyebrows—we can show them their body didn’t totally betray them in that moment.

    We can reconnect their body and their feelings to their emotions. This helps develop a state of congruence—where their inside feelings match their outer demonstrations of those feelings.

    Further, as a dissociative memory is explored, finding anger and reducing shame allows for the memory to fundamentally change. Anger brings them out of dissociation, even if it is anger at you, the therapist!
     

    Introduce body movement. Because shutdown causes us to freeze, reactivating body movements while talking about the trauma is a great way to reconnect the body and mind, to bring them out of shutdown.

    For example, one of my patients was in an accident. When the EMS showed up, they strapped her to a gurney to load her into the back of an ambulance. More than the actual accident, being trapped on that gurney was traumatic for her. For the entire ride to the hospital, she was terrified that she’d hurt her neck, and all of the anxiety that surrounds a neck injury caused her to be frozen in fear.

    Even in talking about the trauma in the therapy session, her body was stiff, frozen, and she was dissociating.

    I asked her, “In what way would you have wanted to move during that moment?” She said she would have wanted her arms to be able to move. I asked her to slowly, mindfully, move her arms in the way she would have wanted to.

    It’s important to do the movement mindfully and slowly, focusing on the sensation of the movement. That patient felt a huge release of energy. In the following sessions, she was able to tell the memory as a narrative, instead of dissociating.

    Having the patient move—slow punching, kicking, twisting, running slowly in place—flips the person from shutdown into the fight or flight mode, with the goal being to move into connection, or social engagement, mode.

    Body movement exercises, in conjunction with talking to a therapist, can fundamentally change the memory.
     

    Practicing assertiveness. Emotional shutdown can occur within relationships where one person feels they cannot communicate with the other person well.

    One therapist, John Gottman, describes this practice as stonewalling. Practicing assertiveness can help the patient feel more in control of their emotional state, and feel safe to move into healthy relationship patterns.

    Breath work, mindfulness, and yoga all have a role in becoming more connected to your here and now body. I will discuss this subject at length in a future podcast.  
     

    Become a Judo Master and practice strength training. Teaching yourself how to better protect yourself in the future can be powerful and also resets the stress system over time. I talked about strength training in a prior episode, and in the future will talk about learning to fight as an active way to not remain passive or a victim both in mindset and capability.  Further doing something hard, on an ongoing basis, allows for building inner strength which can keep you in fight and flight longer before going into shut down.

    Van der Kolk, B. A. (2006). Clinical implications of neuroscience research in PTSD. Annals of the New York Academy of Sciences, 1071(1), 277-293.

     

  • The Psychology of Procrastination

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    My podcast guest this week, Dr. Jackson Brammer, says he used to be an expert procrastinator.

    But after some research into why people procrastinate, he found a few tricks and tips to help him on his journey to live a more balanced life.

    Dr. Brammer started this path by investigating Impostor Syndrome. Impostor Syndrome involves feeling like you're not the person people think you are—as if you’re deceiving everyone. People with Imposter Syndrome believe if someone knew the real them, they would never receive the same level of trust or responsibility.

    People who deal with Impostor Syndrome take negative statements and magnify them, adding them to the pile of proof that they aren’t as capable as people believe them to be.

    For Dr. Brammer, Imposter Syndrome came from his ability to excel in school, despite consistently cramming for assignments and tests. He felt that someday he would be “caught” and everyone would know that he had “faked” competence.

    Recognizing this link led to the revelation that fighting procrastination might help him stop feeling like he didn’t deserve to be in his position.

    The Psychology of Procrastination

    Jackson Brammer, M.D., David Puder, M.D.

    What is procrastination?

    Procrastination is the act of avoiding something through delay or postponement.

    You might be procrastinating when:

    There is a gap between your intention and action

    You feel like avoiding something

    You find yourself  easily distracted

    You feel overwhelmed by tasks at the last minute

    You always feel rushed to complete a project

    You’re hesitant to truthfully update someone on your progress

    It usually brings about feelings of:

    Shame

    Guilt

    Anxiety

    Regret

    Anger

    Inauthenticity

    Why do we procrastinate?

    We procrastinate because our brains receive a reward for avoidance. Avoidance brings immediate relief from the distress associated with the task. Although we may experience discomfort in the final moments before a task is due, we rarely think about the past or future when procrastinating.

    This creates a problematic cycle, one that erodes at our self-confidence. It also causes us to keep up a steady stream of “I should be…” in our subconscious minds.

    The ingredients for procrastination
    Personal Factors of Procrastination

    There are fixed factors related to procrastination, things that are innate to each of our different psychological experiences. For example, someone with ADHD is more likely to procrastinate.

    The fixed personal factors are:

    Higher Impulsivity

    Lower conscientiousness—lower drive to be organized and accomplish.

    Limited attention-span

    Boredom / Low Interest - Interest can be considered an emotion with motivational properties related to approach

    There are also variable factors—things like our environment, our health that day, and other things that might affect our tendency to procrastinate.

    The variable personal factors are:

    Willpower

    Willpower is like a muscle. It can become tired, temporarily, after extensive use. However, we can strengthen our willpower through routine exercise. Try to place your willpower-hungry tasks at the beginning of the day. Also, take up some form of regular willpower exercise.

    Distress tolerance

    Willingness to ask for help

    Being unwilling to ask for help can relate to Impostor Syndrome, and can fuel procrastination. It is often based in the lie that we “should” be able to complete something without assistance.

    Task-focused vs value-focused

    Self-consciousness & anxiety

    A common but counter-intuitive driver of procrastination is fear of failure. We protect the self temporarily by avoiding the task that threatens it.

    The variable task or system-based factors are:

    Unclear goals & expectations

    This can become paralyzing, especially when we are unwilling to ask for help. Procrastinators may find themselves unable to start something because they don’t know how to start, but they don’t want to show “weakness” by needing to ask for clarification.

    Unrealistic goals & expectations

    Can lead to thoughts such as "I might as well not even try."

    Distractions

    Distractions from electronic notifications and office visitors can contribute significantly to our tendency to avoid.

    Lack of accountability or mentors

    Procrastination thrives in secrecy and isolation.

    How do we procrastinate?

    As we build a habit of procrastinating, we develop false beliefs that worsen the habit.

    “I work better under pressure.”

    This is simply not true. It would be more accurate to say, "I work under pressure." The adrenaline spike and stress of the situation make us think we are better off waiting, but in reality it’s unlikely that our delay will make the final product any better.

    “I’ll feel more like it later.”
    We deceive ourselves into thinking that we'll feel like completing the task later. We think we’ll drink caffeine, get a mental boost, or find the “perfect time” to do the task, but it never comes.

    “I did pretty well, considering I waited until the last minute.”
    This is a self-protective belief. If we don’t try and we fail, there is less reflection on the self than if we try our hardest and fail. We won’t discover our true potential if we don’t give ourselves ample time.

    “I have plenty of time, I'll do it later.”
    We are undervaluing the future self when we think this way. Humans are terrible at predicting the future. We often don’t start the project early enough to know how much time we’ll actually need.

    “I’ve planned and organized how I will complete the task, it’s time for a break!”

    Planning more than only the first step can be its own form of procrastination. Sometimes doing “good” for awhile gives us permission to do “bad.”

    “This is stupid, I don't even care about it.”
    Our fear and insecurities can lead to us devalue the entire project altogether. If you talk yourself into believing you don’t care about it, it won’t hurt as much if you fail. This is another self-protective belief.

    “There must be some way I can just not do this.”
    There isn't an easy fix for procrastination—we usually still have to complete the task.

    How do we stop procrastinating?Admit it

    To even begin to change, we have to become aware of the problem, then accept it. Once we accept it, we can often find the courage to change our patterns.

    Catch the cognitive distortions

    If you want to pursue therapy for your procrastination, cognitive behavioral therapy can help. More specifically, cognitive behavioral therapy will help you identify your cognitive distortions. The second episode of the Psychiatry and Psychotherapy podcast deals with cognitive distortions.

    Go through the list of false beliefs we listed and journal your common cognitive distortions.

    Here’s the quick breakdown of how you can look at your thinking patterns when you decide to procrastinate:

    Recognize when you have the emotion about the task you want to delay. Sometimes the emotion will disguise itself as a physical sensation, such as anxiousness, nausea, or a rapid heartbeat.

    Look at the thoughts that come with that emotion. Such as, “This is stupid, I don’t even care about it.”

    Look at the cognitive distortions that came with the thought. Is the task actually “stupid,” or is it something you should do, you’re just afraid to do it, so you’re demeaning it in case you fail? Be honest with yourself in your answer.

    Repeat. This can help you rebuild a habit of identifying the things we tell ourselves and have always accepted as truth.  

    Build your willpower

    Tackle the high-willpower tasks earlier in the day. Earlier in the morning, when your cortisol is high, when your brain is fresh, you’ll be able to take on the tasks you’ll need to be highly motivated for.

    Start strength training, or another disciplined physical task. I’ve found that with strength training, even if I don’t want to begin, and even if the whole workout is miserable, it teaches me that I can will my body to do what the program requires.  This is good for willpower training.  Another will power builder is to choose a difficult book, decide to read it in let us say 60 days, and then divide the book up into 60 parts to read every day.  I often recommend this to psychiatry residents and NPs I train, challenging them to read 3 books in 60 days using this method.

    Forgive yourself

    Practice self-forgiveness when you identify the pattern. We are both aware that we feel frustrated with ourselves when we know we’ve been procrastinating. That frustration is a sign we are trying to change, but it isn’t helpful in the actual change. It can lead to sadness and a lack of self confidence, which can worsen the pattern of procrastination because negative emotions lead to avoidance.

    Self-forgiveness reduces the negative emotions we associate with a task, thus reducing future avoidance and offering ourselves an encouraging approach instead.

    How can you practice self-forgiveness?

    Identify the emotions you feel that are associated with past tasks you haven’t completed.

    Identify the emotions behind tasks you felt you didn’t excel in, or that didn’t turn out the way you wanted them to when you did complete them.  

    Accept the emotion that is there, have self compassion and forgiveness for the emotional experience you had.

    Practice Mindfulness

    Mindfulness is another way to help fix procrastination. Mindfulness will help you be able to identify mental patterns, such as cognitive distortions. When we pay attention to ourselves through the gentle observation of mindfulness, we aren’t striving to “fix” or self-judge. Since becoming aware of the problem is one of the first ways we are able to change, mindfulness helps us be more aware of our actions in general. It can also serve as a form of willpower training.

    Download a good meditation, or use the app Headspace, and practice it daily to develop a habit of mindfulness.

    Define and focus on your values

    One of the most important things you can do is align your tasks and goals to your values. This automatically undercuts any excuses you’ll have because ultimately, the task, if you’ve signed up for it, aligns with your values.

    For example, if there’s a task associated with your job that you don’t want to do, you can still link it with something you believe in. Bottom line is that we value patient care, so even we don’t necessarily feel like doing small tasks throughout the day, we still do them because we link them to our deeper values.

    Define your goals

    It will also help to be able to clarify your goals—daily, weekly, monthly. Make those goals realistic so you don’t talk yourself out of them. Then, merely focus on starting the tasks, not completing them.

    Make the goals small and manageable, and focus only on what the very next step should be. In this way, you’re setting yourself up for positive reinforcement, instead of the negative thoughts that usually accompany procrastination. Avoid over-planning as a form of procrastination.

    Psych yourself up for the task

    Sometimes we need more encouragement to complete a task we are dreading. It’s why people have workout playlists. You can use the same psychology behind that to prepare for even daily tasks. Get a pour-over, trendy coffee, plan a reward for when you complete the task, figure out what makes you want to follow through, and do it.

    Since using all of these tools to beat his habit of procrastination, Dr. Brammer has been able to add more things to his life, and is still able to accomplish it all and feel confident. He’s happily married, a father of two, involved in his church, in a band, and is a practicing psychiatrist.

    Have you ever dealt with procrastination? What do you find your cognitive distortions are—what are the things you tell yourself to make yourself feel better about putting things off?

    For further reading on procrastination, check out some of Timothy Pychyl’s research.

  • 01:01:56

    How to Fix Emotional Detachment

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    This week on the podcast, Ginger Simonton, PhD candidate, and I 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.

    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.  

    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

    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.  

     True Self 

    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.  

     

    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.

    Special thanks to the MEND team for allowing me to collaborate with them!  Here is a link to the long version of how the MEND program works.  Here is a link to the program.    

  • 00:45:29

    The History and Use of Antipsychotics

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    In my last post, Dr. Cummings and I talked about what psychopharmacology is, how medicine works in our body, and what factors affect medicine absorption rates.

    In the latest podcast, Dr. Cummings and I talked about antipsychotics, the particular branch of psychopharmacology that deals with medicines that treat psychotic experiences and other mental disorders, such as:

    Schizophrenia

    Severe depression

    Severe anxiety

    Bipolar disorder

    Psychosis exhibiting hallucinations and delusions

    The history of first generation antipsychotics

    The use of antipsychotics as medication began in 1933 in France. The research around developing antihistamines evolved into the introduction of promethazine. This drug produced sedative side effects, so doctors started prescribing it before surgeries as a calming agent.

    Eventually, a doctor studied the derivatives of promethazine, altered it, and developed chlorpromazine. It was mostly used as a pre-surgery anti-anxiety pill, until psychiatrists took note of the calming effect of the drug and began prescribing it to their patients.

    Prior to chlorpromazine, the options for treating psychotic patients were electroconvulsive therapy, hydrotherapy, and putting patients in an insulin coma. None of those are antipsychotic in nature.

    When two psychiatrists, Dr. Delay and Dr. Deniker, gave 38 psychotic patients a test round of chlorpromazine, they noticed the patients were calmer, and also less psychotic—they had less delusional thinking, fewer hallucinations, and fewer psychomotor-agitation symptoms. Deniker and Delay began giving talks on the benefits of the drug, and in 1955, chlorpromazine became available in the United States. Chlorpromazine is still used today as a treatment for different mental illnesses and mood disorders.

    Once the government saw the positive effects of chlorpromazine, it began to shut down mental health facilities. There was no longer as large of a need to house psychotic patients, and they saw an opportunity to cut costs. However, they did not create adequate sources in the community for ongoing care. California alone is estimated to have 40-60% of homeless people that have a mental disorder.

    Once chlorpromazine became a success, pharmaceutical companies rushed to create their own version of an antipsychotic drug. Because chlorpromazine was the grandfather of the first generation of antipsychotic drugs, the rest of that generation can be categorized by their ability to merely block dopamine D2 receptors in the brain.

    In repeated studies, dopamine antagonism is responsible for 92% of their effectiveness. It also led to the thought that people were psychotic because they had too much dopamine. Since then we have found that their are much more complex psychopharmacological dynamics going on in psychosis.   

    Second generation antipsychotics

    The next set of antipsychotics that came on the market were clozapineolanzapine, risperidone, and other related drugs. Those medications had less effects on motor movement than the first generation drugs.

    Clozapine is a poor antagonist of dopamine- blocking 30-40% of dopamine receptors but also promotes the activation of glutamate through activation of NMDA receptor, which increases activity in the frontal lobe (which helps with schizophrenia’s negative symptoms).  

    Clozapine had more system-wide changes than just dopamine suppression, and it had more positive response from patients. It was more effective—40-60% of people who won’t respond to a first generation antipsychotic, do respond to clozapine.

    However, in Finland in 1975, 6 people taking clozapine died due to agranulocytosis (lowered white blood cell count, leading to a severe lack of immunity). A lowered neutrophil count (called agranulocytosis) can show potential problems with fighting off normal bacteria we live with all the time.  When patients are on clozapine, initially they need weekly blood checks for this reason.

    Despite the risks, clozapine can be an incredible drug—I have one patient who was schizophrenic and homeless, and she is now back in school and recently graduated with a perfect GPA! People who had been dysfunctional for decades, who are given clozapine, can become extremely high functioning.  Key to success here was her willingness to work with me, despite having to try different things before something worked. 

    A trial run on a antipsychotic should be done at a minimum of 6 weeks, and blood tests must be conducted to make sure that the concentration of the medicine is at good therapeutic-dose levels. Dosage alone is sometimes not enough because we all metabolise drugs so differently.  I have uploaded recommended levels in my resource page.

    Third generation antipsychotics

    What is deemed the third generation of antipsychotics, aripiprazole and brexpiprazole are partial dopamine receptor agonists.  They keep dopamine at a max of 25% in the brain which due to the high affinity to the receptor it does not vary much based on dose.  

    The good thing about this generation of drugs is that they don’t lower blood pressure, cause insulin resistance, and are not sedating in nature.

    It works for some people, it doesn’t for others. But when it does work, it works really well.

    Side effects of psychiatric medicines

    Akathisia is the inability to stay still, characterized by a feeling of inner busyness. It is a miserable side effect, exhausting to the patient.

    If someone is experiencing this, they should immediately call their psychiatrist or go to an emergency room.

    One of Dr. Cumming’s patients described it as “ants running up and down the bones of his legs.” It usually involves an anxious feeling, and a desire to move the lower extremities of the legs. Akathisia can be caused by any drug that lowers dopamine (including SSRIs).

    This syndrome is so complex because it involves several compounds, including dopamine, norepinephrine, acetylcholine, and serotonin inputs. Options for treatment include: choosing a lower dosage, picking another dopamine antagonist that is less strong (quetiapine or clozaril), or prescribing a drug like amantadine, propranolol, mirtazapine or clonazepam (more nuance in the podcast on this).

    It is a harmful disorder, and one to watch out for in patients. If a patient is sent home from the hospital experiencing these symptoms, but is not properly vetted for akathisia, a doctor could be subject to serious legal repercussions.

    The questions to test a patient for akathisia are:

    Is the person moving? Can they not sit still?

    What is their internal sense of restlessness and anxiety?

    How much are they distressed by these feelings?

    Acute dystonia involves muscle spasms and it affects movement, causing the posture to twist abnormally. It can be painful for patients to experience. This occurs because of too little dopamine in the basal ganglia part of the brain.

    Parkinsonism involves muscle stiffness and slower movements. It’s usually uncomfortable, but not a miserable side effect. This also occurs because of too little dopamine in the basal ganglia part of the brain.

    The future of antipsychotics

    With each generation of new medicines, we’ve gotten closer to being able to help people stabilize their psychosis. We haven’t been able to achieve complete wellness.

    Dr. Cummings says he has hope that with further advances in the medical field, we will be able to identify who is at risk. There is hopeful data that we may be able to one day prevent the development of schizophrenia.

    History of Antipsychotics (notes by Arvy Tj Wuysang).

    1933, France

    Initiative to develop antihistamine as treatment began

    1947

    Promethazine

    Produced sedation and calmness in animal models

    Not highly effective in humans, but found to provide calmness in preoperative settings

    1950

    Discovery of Promethazine Derivatives, especially Chlorpromazine

    Initially tried in a surgical military hospital in France by Dr. Henri Laborit (1914-1995)

    Successful in making people calm and indifferent to impending surgery

    The medication was tried it in a volunteer

    The individual reported favorable effects, until he stood up and promptly fainted

    Determined as not safe in pre-operative setting because it was too effective as alpha-adrenergic antagonist in lowering blood pressure

    1952

    Dr. Pierre Deniker (1917-1998), psychiatrist, with Dr. Jean Delay (1907-1987), his superintendent in Sainte-Anne’s Hospital in Paris, led the Chlorpromazine introduction as a psychopharmacologic agent

    They were interested in the calming effect of the drug

    Tried the drug in psychotic agitated patients

    Treatment options in those days were limited to:

    Electroconvulsive Therapy

    Hydrotherapy

    Insulin coma

    None of which were antipsychotic in nature

    Tried it in 38 patients, made patients calmer, and less psychotic!

    Especially effective for positive psychotic symptoms like hallucinations, delusional thinking, psychomotor agitation

    Findings were impressive enough that Deniker began giving talks about the drug, including a conference in Montreal, that led to its introduction in North America

    1955

    Chlorpromazine was approved for usage as antipsychotic in the US

    Subsequently used worldwide

    Led to the deinstitutionalization of a lot of psychotic patients

    Created a problem of lack of follow up of psychotic patients

    I.e. California has around 357,000 homeless individuals, estimated 40-60% suffer from mental disorder with schizophrenia spectrum highly represented in that percentage

    State spends about $200,000 per year per person to care for people committed to state hospitals. Funds committed to patients that are discharged from state hospitals are very minimal.

    Led to development of a whole host of antipsychotic agents

    1960s

    There was an explosion in the invention of antipsychotic drugs

    US FDA took a stance, did not allow approval of antipsychotic drugs that are not clearly better than chlorpromazine or haloperidol

    1st generation antipsychotics all work by blocking Dopamine D2 receptors in the brain, counts for 92-23% of variance in mechanism

    Led to the simplistic dopamine hypothesis of psychosis

    1958

    2nd generation antipsychotic discovered by Eichenberger and Schmutz from the Swiss pharmaceutical company Wander AG, Clozapine

    Created because 2 other -antadine antipsychotics have been successful, Loxitane (Loxapine) and Perlapine

    Clozapine was initially thought of as a failure because it did not produce dystonia in white lab mice, as expected in 1st generation antipsychotics where it blocks dopamine effects in the brain

    Clozapine found to be a poor antagonist to dopamine, only blocks 30-40% of dopamine receptors. Although, it promotes release of glutamate, by binding to an allosteric site for glycine in the NMDA receptor, which in turn increases activity in the frontal lobe and suppresses dopamine release in the mesolimbic system.

    A number of small studies in the 1960s found that patients that don’t respond to 1st generation antipsychotics responded well to Clozapine treatment by showing better response of both positive and negative symptoms of schizophrenia.

    1970s

    1972, Clozapine usage was introduced in Austria

    1974, Clozapine usage was introduced in Germany

    40-60% of people that did not respond well to 1st generation antipsychotics, responded well to Clozapine

    1975, 5 people in Finland died after Clozapine treatment due to agranulocytosis

    Clozapine found to trigger formation of antibodies targeting bone marrow cells that make neutrophils and essentially shut down a person’s immune system

    Must monitor Absolute Neutrophil Count closely when prescribing Clozapine

    Monitor weekly for 6 months, then every 2 weeks for another 6 months, and monthly for another year (in the USA)

    Risk for agranulocytosis decreases with time: peaks at 4 months of exposure at about 1.3%, .38% after 1 year of exposure, .06% after 2 years of exposure

    Clozapine usage in the US today

    Siskind, D., McCartney, L., Goldschlager, R., & Kisely, S. (2016). Clozapine v. first-and second-generation antipsychotics in treatment-refractory schizophrenia: systematic review and meta-analysis. The British Journal of Psychiatry, 209(5), 385-392.

    15-20% of patients in California State Hospitals are on Clozapine, 53% in New York State

    Response rates to drugs other than Clozapine is pretty miserable in State Hospitals

    Olanzapine response rate even at high plasma concentrations is only 9%, compared to 40-60% for Clozapine. Every other antipsychotics’ response rate is between 0-5% for the severely psychotic, mentally ill patients.

    If patients meet Kane criteria (after John M. Kane)---treatment failure after two clearly adequate trials of antipsychotic treatment with minimum of 6 weeks duration with therapeutic plasma concentration---odds that they will respond to anything other than Clozapine is fairly low.

    Common mistake that clinicians make is to go by dosage as a measure of whether a person is receiving adequate medication

    Dosages only weakly correlates with plasma concentration since the metabolism of antipsychotic drugs is so variable

    Measuring plasma concentration to reach therapeutic levels is crucial in antipsychotic drugs administration, especially in patients who are seemingly refractory to treatment, to ensure adequate treatment

    Akathisia as side effect of antipsychotics

    Very rarely happens with Clozapine use

    Akathisia is a very miserable side effect of antipsychotics, described as “ants crawling up and down the bone of your legs” by a particular patient

    Characterized both by internal sense of anxiety and a near irresistible urge to move

    Barnes Akathisia Rating Scale, most commonly used to measure akathisia symptoms. Based on three main factors:

    Objective movement

    Internal sense of restlessness and anxiety

    How much are they distressed by these feelings

    Akathisia is a concerning and common reason for malpractice

    Underlying pathophysiology of akathisia is distinct compared to other extrapyramidal symptoms, involves not only dopamine and acetylcholine. It also involves norepinephrine and serotonin inputs to basal ganglia, makes it a difficult syndrome to treat successfully.

    Treatment options for akathisia:

    Use a less robust dopamine antagonist, such as Quetiapine or Clozapine

    Use lower dose of the antipsychotic

    Use Amantadine, increases dopamine release in the basal ganglia

    Was originally devised to treat influenza A

    Discovered to be effective in treating extrapyramidal symptoms, also effective for tardive dyskinesias (15% respond to amantadine)

    However, it is not as effective as B-blockers or Mirtazapine

    Amantadine is not anticholinergic (no memory problems, no GI side effects, no blurred vision, no urinary retention)

    Head-to-head trial between Propranolol versus Mirtazapine versus placebo, shows mirtazapine as more effective in treating akathisia

    Poyurovsky, M., Pashinian, A., Weizman, R., Fuchs, C., & Weizman, A. (2006). Low-dose mirtazapine: a new option in the treatment of antipsychotic-induced akathisia. A randomized, double-blind, placebo-and propranolol-controlled trial. Biological psychiatry, 59(11), 1071-1077.

    Mirtazapine at 15 mg at bedtime was effective in 43% of patients

    Placebo was effective in 7% of patients

    Akathisia may present as side effect in SSRIs and antiemetics (compazine)

    Expected or Therapeutic plasma concentration ranges for antipsychotics and mood stabilizers

    DSH Psychotropic Medication Policy (see resource page)

    Aripiprazole (Abilify)

    3rd generation antipsychotics, partial dopamine agonist

    Has high affinity for dopamine receptors, higher than 1st and 2nd generation antipsychotics. If Aripiprazole is present at therapeutic concentrations, 1st and 2nd generation will have very little interaction with dopamine receptors.

    Keeps dopamine signaling at about 25% of dopamine’s maximum signal transduction, tends to produce all or nothing response in terms of treating psychotics. Not much ability to vary where dopamine is blocked because of it’s high affinity.

    Side effect profile is very favorable. Largely metabolically neutral, tend not to cause weight gain, glucose intolerance, and lipid abnormalities. Low affinity for alpha receptors or histamine receptors, is not very sedating and does not lower blood pressure.

    Use outside of schizophrenia

    I.e. risperidone and olanzapine also exhibit utility as mood stabilizer and antidepressant.

    3rd generation antipsychotics also tend to improve mood, driven by quality of the molecules and in part by the desire of pharmaceutical companies to broaden their market

    Use in dissociative state, such as Borderline Personality Disorder

    Antipsychotics can help bring patients out of dissociative state in short period of time

    Borderline patients was found to have a significant limbic dysfunction, hence antipsychotics may be helpful

    Future of Schizophrenia Spectrum Treatment

    There is great need to identify individuals at risk for the disease and treat them with lower dose of antipsychotics. Hopeful data is currently present in support of this approach to lower the incidence and prevalence of schizophrenia.

  • 00:50:33

    How Psychiatric Medications Work with Dr. Cummings

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    This week I interviewed Dr. Cummings, a psychopharmacologist, on the Psychiatry and Psychotherapy Podcast. Below is a brief introduction to the episode. For more detailed notes by Dr. Cummings, go to my resource page.  

    What is psychopharmacology?

    Psychopharmacology is a branch of psychiatry that deals with medications that affect the way the brain works. The medicines used in psychopharmacology treat illnesses whose primary concerns and issues are mood, cognitive processes, behavioral control, and major mental disorders.

    It is a unique branch of pharmacology because the illnesses are usually addressed by both medication and psychotherapy.

    What makes a drug psychiatric in nature?

    What makes a drug labeled as psychotherapeutic, is the intent behind the prescription. Some drugs will serve more than one purpose, so understanding why it was prescribed is important. For example, valproic acid is helpful in treating seizure disorders, and also bipolar disorder. For the seizure disorder, it would not be considered a psychotherapeutic drug. For the bipolar disorder, it would be considered a psychotherapeutic drug.

    How do medications work?

    All medicines go through the same steps of digestion in our bodies. They are liquified in the stomach, and then absorbed. The drug travels through the liver, and then into the blood supply, which brings it to the organ it was designed to target.

    Our bodies have receptor sites, made of protein, that sit on the surface of a neuron, or a nerve cell in the brain. The drug, when it reaches that receptor, either binds to it and blocks it, or it can help the neurotransmitter work to further what it does naturally.

    For example, caffeine is an adenosine blocker. Adenosine is a naturally occurring molecule in our bodies that calms us down as the day wears on, preparing us for sleep. Caffeine, as a drug, blocks our natural adenosine from reaching its receptor; it keeps us awake.

    Medicines work in the same way—inhibiting or helping certain molecules reach their targeted organs.

    How absorption and dosage rates affect medicine

    Many things can affect absorption rate, and medications absorb at different rates, and at different potencies.

    Things like gastric bypass, (when they take out a part of the stomach and intestines) can affect absorption rate of drugs. One of my patients had a stomach surgery, and afterwards, their depression came back. I told them to start grinding their pills to help with absorption rate of their antidepressant, and their medication started working again.

    Our livers play the main part in absorption. Sometimes they are gatekeepers, and they can hinder absorption rates dramatically. Animals and plants have been at war for thousands of years. Plants create toxins to try to discourage animals from eating them. Our livers develop different enzymes to break down those toxins in order to make the plants safe for our bodies. Those same enzymes break down medications. Our bodies are constantly adapting and changing, adjusting to what we consume.

    As a psychiatrist, it’s important to pay attention to absorption rates to make sure our patients are getting maximum benefit. Maybe a patient has defected genes that limit absorption rate, or deficient enzymes to break down the medication. Or maybe other medications are interacting and changing absorption rates.

    A few times in my practice I have seen patients come in on multiple medications which are interacting poorly. For example, they are on a medication called amitriptyline and also on something that blocks its breakdown like fluoxetine. In our session they complain that they are confused and disoriented. I figure out that the drugs they’ve been prescribed is either inhibiting, interacting with, or increasing the effect of another medication. Once we learn that, we can make changes to their prescriptions, and they return to feeling normal.

    When you change the concentration of a medication, you can destroy the entire point of the prescription in the first place. There are numerous computer programs that can help us determine problems with drug interactions. Those programs can sometimes point out what could become a clinical problem, but often point out minor, irrelevant interactions.

    Just prescribing medicines, without taking into account the individual ecosystems we each have, is often a practice of trial and error. With properly administered tests and observation, we can move towards an effective dose and effective treatment plan.

    Because there are so many things that can change a drug level in the body, taking a plasma concentration may be the best way to assess if the dose is appropriate (check out my resource page for a list of appropriate levels). A high or low blood level might hint that the person is a rapid metabolizer, poor metabolizer, has GI issues with absorption, or has other medications or supplements that are increasing or decreasing the dose.  

    How to reduce negative side effects

    One of the reasons that people develop problems with psychiatric side effects to medications is because they are increased too fast. There is a balance between wanting to get someone to an appropriate dose, and minimizing side effects.  

    Too often, patients are prescribed a medication at full force and, due to sudden side effects patients will quit taking the medication.

    If the medicines were administered in a slower onramp, giving time and attention to their perceived absorption rates and side effects, many problems with those medications would stop.

    Is therapy or medication more helpful?

    There are many trains of thought on psychotherapy and medication. Some people want a pill to fix everything. However, not everything is a chemical imbalance in the body and can be fixed with a pill.

    If someone comes to me with a psychiatric problem, I almost always recommend psychotherapy, and often prescribe medication. Medications help, especially if someone has severe mental illness. If levels are mild to moderate, I find psychotherapy and lifestyle changes (like strength training and diet) are more effective for long term success.

    Rates of prescribing medication has increased and use of psychotherapy has decreased. Too many patients are taking medication without psychotherapy or lifestyle changes. One study shows that 73% of antidepressants are prescribed by primary care physicians (Mojtabai, 2008).  Antidepressant use has increased from 1996 to 2005 from 6% to 10% while rates of therapy have gone down from 31% to 20% for those on antidepressants (Olfson, 2009).

    Because of that, people are not being treated in the most effective way possible. This is especially the case when considering the treatment of psychological trauma, for which talk therapy can cure in ways medications can not.

    Through both medications and psychotherapy, we can rewire the brain. In one study on obsessive compulsive disorder (OCD), two groups of people were studied—those who underwent cognitive behavioral therapy, and those that took medication. The therapy was found to be as helpful in eliminating OCD symptoms. However, the OCD symptoms returned when the medication was stopped. The symptoms did not return when the person had received cognitive behavioral therapy.

    Dr. Cummings uses a simple guideline to see if someone would benefit from medicine or talk therapy. If what the person is depressed about is something in their lifestyle—their weight, their job, their relationship, lifestyle changes and talk therapy will probably be most effective.

    If someone is experiencing neurovegetative symptoms of depression, such as: loss of appetite or increased appetite, severe energy loss, severe sleep disturbance with early morning awakening, physically slowed down, they are suffering from brain disturbances that are helped by medication.

    For more notes by Dr. Cummings, go to my resource page.  

    Mojtabai, R., & Olfson, M. (2008). National patterns in antidepressant treatment by psychiatrists and general medical providers: results from the national comorbidity survey replication. The Journal of clinical psychiatry.


    Olfson, M., & Marcus, S. C. (2009). National patterns in antidepressant medication treatment. Archives of general psychiatry, 66(8), 848-856.

    See below for notes on the episode writen by Arvy Tj Wuysang.  

    Defining Psychopharmacology and Psychopharmacologic Agents

    Psychopharmacology: Study of medications and substances that affect how the brain works, both positively and negatively

    “Intent” in using versatile drug classes as psychotherapeutic agents

    Valproic Acid usage as an anti-epileptic drug vs mood disorder drug

    Caffeine usage as stimulant

    Metabolism and Physiologic Distribution of Psychopharmacologic Agents

    Gastrointestinal surgeries and their effect on psychiatric drugs’ absorption

    Olanzapine will not be absorbed as effectively in individuals who had Gastric Bypass Surgery because of its slow absorption. Lorazepam, on the other hand, has a characteristically rapid absorption and will not have much disturbance in its absorption even in the context of post Gastric Bypass Surgery.

    Properties of drug absorption within the liver

    Cytochrome P450 enzymes

    Evolutionary developed to metabolize plant toxins

    Common classes that plays significant role in psychiatric drug metabolism

    2D6, 2A4, 1A2

    Interaction with other drugs

    2D6 blockers (Fluoxetine, Paroxetine, Bupropion) will elevate plasma Amitriptyline levels.

    Inducers will decrease plasma levels

    Benefits of using drug-drug interaction applications/softwares

    Importance of monitoring plasma levels versus genetic testing in determining effective/safe dosage

    UCLA Imipramine Titration Study

    If receptors are given time to adapt to the medications, oftentimes side effects may be minimal

    Imipramine titration goal of 150 mg

    1st group: increase of 25 mg increments per week

    experienced significant side effects (sleepy, dry mouth, low BP)

    2nd group: increase of 10 mg increments per week

    achieved the same blood levels as the first group but experienced minimal side effects

    How do psychiatric drugs work?

    Most bind to receptor sites that typically sit on the surface of a neuron and initiate a variety of action related to a particular neurotransmitter

    Agonists

    Antagonists  

    Partial agonists

    Reuptake inhibitors

    Immediate vs Delayed Effect of different classes of psychiatric drugs are determined to their specific kinetic mechanisms

    Benzodiazepine, ETOH has immediate effect

    SSRI works through initiation and adaptation, produce downstream 2nd messenger effects, needs time and repetition to take effect, analogous to how psychotherapy works.

    Baxter, L. R., Schwartz, J. M., Bergman, K. S., Szuba, M. P., Guze, B. H., Mazziotta, J. C., ... & Phelps, M. E. (1992). Caudate glucose metabolic rate changes with both drug and behavior therapy for obsessive-compulsive disorder. Archives of general psychiatry, 49(9), 681-689.

    Studied people with OCD, especially contamination obsession, for 6 weeks.

    1st group: behavior response prevention

    2nd group: fluoxetine

    Both have similar biological effect in terms of their neurologic circuits as portrayed on PET scan imaging

    At 6 months follow up, group with behavior response prevention has more permanent behavior change.

    Follow up study of using combination of SSRI and behavior response prevention showed greater benefit than either treatment alone.

    How long should one stay on antidepressants?

    Dependent on frequency and severity of depressive episodes

    Single depressive episode

    Treat to remission, keep in remission for 1 year, gradually taper the antidepressant

    2-3 episodes of depression

    Essentially, needs to stay on antidepressants permanently

    Remains vulnerable to depression

    Antidepressants ameliorates symptoms, but does not cure underlying pathophysiology

    Each episode makes the next episode more likely!

    Analogous to Diabetes Mellitus treatment

    I.e., Blood sugar needs to be controlled for the rest of the patient’s life

    How do we determine between using medications versus lifestyle therapy in treating psychiatric conditions?

    Depends on presentation

    If merely dysphoric, can start by introducing lifestyle changes

    If greater severity, showing neurovegetative signs, may start with medications right away

    Neurovegetative signs: Loss/increase of appetite, significant weight changes, severe loss of energy, severe sleep disturbance, psychomotor agitation/reduction

    Pathophysiology of Depression

    Multifactorial, not merely a single neurotransmitter deficiency

    Core dysfunction of limbic system, influenced by disruption of multiple neurotransmitters

    Inflammation may play a role through cytokine dysregulation

    Kirsch, I., & Sapirstein, G. (1998). Listening to Prozac but hearing placebo: A meta-analysis of antidepressant medication. Prevention & Treatment, 1(2), 2a.

    Only ⅓ of patients studied had full remission of depression symptoms with antidepressants.

    Variety of placebo effects in depression studies

    Dr. Cummings has recommended these articles to read along with this session (thank you Mona Mojtahedzadeh M.D. for organizing them and adding some notes):

    1. Duman, R. S., & Aghajanian, G. K. (2012). Synaptic dysfunction in depression: potential therapeutic targets. science, 338(6103), 68-72.

    Depression is associated with reduced brain size and decreased neuronal synapses in regions that regulate mood and cognition (the prefrontal cortex and the hippocampus).

    Antidepressants can block or reverse these deficits.

    Typical antidepressants have limited efficacy and delayed response times (weeks to months).

    Ketamine is a N-methyl-D-aspartate receptor antagonist that has been proven to produces antidepressant responses in patients who are resistant to typical antidepressants within hours.

    Ketamine has been shown to rapidly induce synaptogenesis.

    Ketamine can also reverse the synaptic deficits caused by chronic stress.

    Findings highlight the importance of a synaptogenic hypothesis of depression and treatment response.

    2. Thompson, J., Thomas, N., Singleton, A., Piggott, M., Lloyd, S., Perry, E. K., ... & Ferrier, I. N. (1997). D2 dopamine receptor gene (DRD2) Taq1 A polymorphism: reduced dopamine D2 receptor binding in the human striatum associated with the A1 allele. Pharmacogenetics, 7(6), 479-484.

    3. Hyman, S. E., & Nestler, E. J. (1996). Initiation and adaptation: a paradigm for understanding psychotropic drug action. The American journal of psychiatry, 153(2), 151.

    4. Tracy, T. S., Chaudhry, A. S., Prasad, B., Thummel, K. E., Schuetz, E. G., Zhong, X. B., ... & Tay-Sontheimer, J. (2016). Interindividual Variability in Cytochrome P450–Mediated Drug Metabolism. Drug Metabolism and Disposition, 44(3), 343-351.

    5. Hunsberger, J., Austin, D. R., Henter, I. D., & Chen, G. (2009). The neurotrophic and neuroprotective effects of psychotropic agents. Dialogues in clinical neuroscience, 11(3), 333.

    6. psychotropic medications: overview seminar core handout

    7. McCutcheon, R., Beck, K., Bloomfield, M. A., Marques, T. R., Rogdaki, M., & Howes, O. D. (2015). Treatment resistant or resistant to treatment? Antipsychotic plasma levels in patients with poorly controlled psychotic symptoms. Journal of Psychopharmacology, 29(8), 892-897.

    Big number of patients with schizophrenia have poor response to antipsychotics medications.

    Possible causes are subtherapeutic plasma levels of the medication or medication ineffectiveness.

    This study examines 36 patients with treatment resistant schizophrenia and assesses the extent of subtherapeutic antipsychotic plasma levels and the frequency of antipsychotic plasma level monitoring in standard clinical practice.

    Antipsychotic plasma levels were found to have been measured in only one patient in the year prior to our study.

    Over one-third of patients had subtherapeutic antipsychotic levels.

    In detail: sixteen (44%) patients showed either undetectable (19%) or subtherapeutic levels (25%), and 20 (56%) patients had levels in the therapeutic range.

    Black ethnicity, shorter duration of current treatment, and antipsychotics other than olanzapine and amisulpride were factors significantly associated with subtherapeutic plasma levels.

    This study indicates higher chances for under-treatment rather than treatment-resistance for those patients with poor response to antipsychotic medications.

    On another note, the measurement of antipsychotic levels may be under-utilised.

  • 00:42:50

    Using Microexpressions in Psychotherapy

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    The last two weeks, we’ve covered using Microexpressions to Make Microconnections and the  Microexpressions of Fear, Surprise, Disgust and Creating Connection. We discussed what microexpressions are, what each of the different emotions are, and how they look on the face.

    Learning about microexpressions develops a deeper connection with others—whether in therapy, or just in everyday relationships.

    Microexpressions are tiny facial movements that give us cues to what someone is feeling. Their eyebrows might twitch down for a moment to display anger. Or the sides of their mouth might stretch horizontally to show they are afraid.

    Our goal as therapists is to understand what emotion our patients are feeling, and to develop our empathy towards them through understanding the reason behind that emotion. Understanding microexpressions can lead to micromoments of connection by developing a greater closeness between you and your patient.

    Microexpressions happen out of our awareness, and can be great cues to what someone is unconsciously feeling.

    Using microexpressions to understand the unconsciousMicroexpressions develop our identity

    We are always picking up on some level of people’s microexpressions, whether we are trained in it or not. Many people intrinsically understand what others feel. This understanding can become our social mirror as we are growing up.

    If we have an ability to make people smile when we are children, we may try to reinforce that reaction from others by building our interactions around humor. Then we are known as the “funny” one. These cues people give us can become a part of our identity.

    One of my patients had a facial deformity. She noticed, and internalized, the messaging that she was “disgusting” to look at, based on other people’s facial expressions when they saw her. That led to deep feelings of disgust about herself. She often showed a microexpression of disgust on her face when she was talking about herself. Over time spent in therapy, she was able to create her values, her beliefs, and determine that as a human, she was more than her deformity.

    Internalizing people’s microexpressions as feedback about ourselves can be helpful or harmful. When we learn more about microexpressions, we are able to develop techniques to delve deeper into people’s reactions and understand that those reactions are often not about us, but about the other person’s experience.

    Through understanding microexpressions, we learn that we do not need to take every reaction and internalize it as part of our identity, either positive or negative. With our patients, seeing microexpressions as they talk about themselves can help us uncover deep seated beliefs—whether it’s disgust, arrogance, or any number of other emotions.

    Microexpressions reveal object relations

    Object relations is a theory about how we internalize early attachment figures and then subsequently understand future in relationships. For example, if we have a tense relationship with our father, and then we might expect or recreate tense relationships with our male teachers, male boss, and male therapist, as a way to make sense of the world and hope to have a different outcome.

    We most often create these emotions towards early developmental relationships, then paint our beliefs about them on others throughout our lives, unless we deal with our feelings towards those people, and begin to be able to distinguish and differentiate, i.e., “not all authority figures are evil.”

    In therapy, microexpressions can be helpful to unearth some of these emotions. The relationship between a therapist and a patient can represent, to the patient, many different relationships. Being a safe person for them to discuss their feelings with is the most important part of therapy.

    Reading microexpressions can help us understand the emotions still present that the patient feels towards early attachment figures. These may come out as they discuss a current issue, and then express a strong emotion. If you focus in on the part of the story where the emotion was present, then they might start eventually talking about early attachment figures like their emotionally distant dad or angry mother.  

    The microexpression allows us to know where to focus in, and listen closely in their story. They are not only important to pay attention to when it comes to how a patient feels about others, but also how they feel about us. Knowing how they feel about us, as their doctors, helps to be able to identify what are overarching, negative early life experiences and how we can help them work through those feelings so that they can live more present and thriving in the present.  

    Talking about Dreams reveals microexpressions

    As therapists, listening to dreams can give you a great glimpse into your patient’s inner emotional life. Studies show that memories more easily develop around negative emotions, and those negative moments can form points of organization for our memory. They found that PET scans showed that the parts of the brain that store our memories are also the ones activated during REM sleep.

    Dreams usually demonstrate what’s most emotionally relevant to work on during psychotherapy. As patients are telling me their dreams, they will show microexpressions while reporting the narrative of the dream. Through discussing the dream, they can talk about emotions and desires they might not have consciously allowed themselves to have.

    For example, if a patient is feeling trapped in a job or relationship, she may have a dream she is trapped in a box, or stuck underwater. She will be able to express her emotions during the description of the dream—her fear, anger, surprise, disgust. She may not be ready to talk about her relationship or job, but she can unearth the unconscious emotions of the dream and feel comfortable talking about that. In the end, her thoughts will go to areas of her life where she feels stuck, and then suddenly realize what the dream might mean.

    As psychotherapy progresses and the person unpacks their emotions, the dreams change to be more positive. When a patient feels supported, heard and psychologically safe, they begin to unpack deeper, unconscious emotions they once only felt in dreams.

    Psychological Defense and microexpressions

    People experience psychological defense as a way of creating an alternative, safe reality for themselves. It’s an adaptive way to defend against their feelings, their reality, and the state of their mental health. Psychological defense is largely an unconscious, adaptive process.

    Sometimes a patient will have a thought that is too distressing to pay attention to. Their brain will then send what we call “signal anxiety,” or a message that this thought, emotion, or desire must be suppressed from consciousness. As a result, they might have a psychological defense act as a way to adaptively defend against these thoughts. For example, they might suppress a thought to later deal with, deny that it happened, or go wash the car to get their aggression .

    Another example where microexpressions will help is if a patient says they aren’t angry at a person. They may believe that, or may try to believe that. Maybe that person harmed them in a huge way. Prior to saying, “I’m not angry,” their face may have flashed a microexpression of anger, letting you know that perhaps they are denying what is truly going on.

    The best thing to know here, is that psychological defenses are there for adaptive reasons, and the patient needs to feel safe enough to have them soften. If you empathize with the distress that comes with the defense you will be helping them get to what is under it.

    Warnings about using microexpressions in therapyMiscategorization

    When I first started learning about microexpressions, I would tell people, “When you told that story, you flashed an expression of anger.” Then the patient would be angry at me for assuming they were angry. Maybe the patient hadn’t even had the chance to process on their own that they were, in fact, angry. Or maybe I was just wrong about what I was assuming! Either way, I didn’t give them the space to find their own emotions.

    It’s important to allow people to mine their own feelings, and even discover the meaning behind the feeling. If they are telling a story and show a microexpression of anger, be curious about their feelings in that moment. Ask them to draw out the emotion and describe it. Be gentle with your word choices.

    The danger is when we are wrong about what we think someone is feeling, but we aren’t accurate, and we assume we are still correct.  

    Emotional contagion

    As we learn about microexpressions, we see that there are hundreds of them being expressed in any one-hour therapy session. It can be overwhelming if we take responsibility for another person’s emotional life. It’s important to know the difference between their feelings and our own feelings, so we don’t own their emotions.

    When I first started in my psychiatry rounds in medical school, I didn’t understand emotional contagion. I began to feel depressed after different conversations with suicidal patients. After talking to several mentors about it, I realized I was internalizing my patients’ emotions, and having issues with self/other distinction. Their emotions were contagiously experienced in my head, and I had little defenses against feeling overwhelmed.  

    Now, before I go into any therapy session with a patient, I take an emotional gauge of myself. I see how I’m feeling, what my natural, resting emotional state is. When I enter the therapy session, I am able to categorize what is additional to my experience—sadness, anxiety, joy, fear, as the other person's, not mine. I am also able to deeper empathize with their feelings because I am not in a confused emotional state.

    When we delve too deeply and become emotionally distressed with our patients, it inhibits our ability to offer insight, reflect, or therapeutically help the other person. Feeling deeply can be a tool in therapy for developing connection, but make sure you have healthy boundaries, too.

    Being able to understand the patient and their reality can also help us own our own reaction to them. Maybe the patient reminds us of someone we know, and we are putting negative feelings on them.

    Rushing the process

    Maybe you repeatedly notice anger on your patient’s face during conversations about their father. Here’s the catch—maybe they don’t know they are angry at their father yet. If you rush that revelation, you are taking away their emotional experience of uncovering their feelings.

    Letting someone use their words, and not forcing word choice, is important. If they say “frustration” and not anger, you should also say “frustration” and not the word anger. Allow them to have their own process.

    Allow feedback

    People are the experts of their own inner world. Microexpressions, though incredibly helpful, only give us hints. They do not give us a perfect map of someone’s entire emotional experience.

    When you express curiosity about what someone is feeling, allow them to correct you if you offer specific word choices or suggestions. Ask them to clarify, and accept their explanations about what they were feeling.

    Learn about microexpressions

    It is helpful, when implemented correctly, to learn about microexpressions and use that knowledge to develop micromoments of connection.

    To learn more about microexpressions, download the Emotion Connection IOS app.

    For full PDF of the episode with citations and further notes go here

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  • 00:47:34

    Microexpressions: Fear, Surprise, Disgust, Empathy, and Creating Connection Part 2

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    On the last Psychiatry and Psychotherapy podcast and blog, we talked about how Microexpressions make Microconnections, their role in therapy and how learning about them can increase our emotional connection to others.

    This week, we will continue uncovering how different microexpressions look on the face and feel in our body, and their corresponding emotions.

    Fear

    Fear is an adaptive emotion—its original goal is to keep us safe and alive. When someone pulls into our lane on the interstate, it’s fear and our ability to quickly jerk the steering wheel straight that saves our lives. When we encounter heights, snakes, or frightening people in a dark alley at night, fear is the emotion we feel.

    As children, we have fears of abandonment from our mothers, and at around two years old, we begin to experience stranger anxiety. As we grow, we read our parents and see what they are afraid of, so we can form protective fear patterns. Even different genders receive different messaging about fear. Parents teach male children to be more fearless, empowering and enabling, more courageous. They teach females to be more cautious, careful and more fearful.  

    Fear, demonstrated on the face in a microexpression, looks like:

    Eyebrows drawing up and together with tension in the forehead

    Lower eyelids tensing

    Mouth opening horizontally in an interaction

    Fear can bond people together but also separate us from having an emotional connection. In any emotional interaction, we are experiencing a state of calmness, fight/flight, or disconnection.

    Fear and anger come into play in both fight and flight. When we notice someone exhibiting fear when we are interacting with them, it’s important to be curious as to why. Are they fearful because of the interaction with us? Or are they fearful because they are accounting a story about something that scared them?

    When someone experiences fear, it’s important to strive for a healthy connection again. That person may experience fear because of vulnerability or shame. Because fear’s goal is to stay safe, it can cause disconnection. Establish a psychologically safe place for them to feel connected, rather than fight or flight.

    Dealing with fear

    Listen to your voice of courage that’s inside of you. Anytime there is fear, there is also a courageous part of us that is sending different messages too, we just need to focus on it and therefore turn up the volume of the courage signals. When we get stuck, frozen, in a state of fight or flight, we can choose to engage the object of fear anyway. We can choose courage.

    Experiencing fear during sporting events or performances is a great way to think about this. Fear can be decreased over time. When we train often enough, or compete often enough, that fear response slowly decreases. After plenty of performances, after plenty of sport competition events, we start to normalize that fear and courage takes over—training gives us confidence in the face of fear.

    We can learn how to handle fear without being totally overwhelmed by facing the cause of our fear in slow, small increments. It can create an adaptation, rather than stress. Even cardiovascular health is tied to your emotional ability to handle fight or flight. By training physically, you are actually training for interpersonal stressors as well by spiking your adrenaline, breathing and heart rate.

    Beyond behavioral therapy help, you can do mental exercises to regain control of your body during fear. Even simply saying out loud, “I am experiencing fear” can feel normalizing. Also, through meditation and breathing, you can reset your heart rate and breathing, and calm your body’s fear responses.

    Surprise

    On the face, the microexpression of surprise looks similar to fear, but where fear affects the face on a more horizontal axis, surprise affects the face on a more vertical axis. Surprise looks like:

    Rising and rounding eyebrows

    Rising upper eyelid

    Sometimes mouth falling open with lips relaxing

    Note: rising eyebrows can also be a conversational signal emphasizing something.

    Surprise can be awe, curiosity, a revelation. It can be a more transitory emotion—quickly moving on to fear, anger or joy. When someone is exhibiting surprise on their face, be curious about why, ask them if the answer isn’t obvious—such as them arriving at their own surprise party—and you may learn something new about them.

    Disgust

    People rarely use the word “disgust.” They’ll talk about happiness, anger or fear or other emotions. But disgust is something that we don’t understand as easily without dipping back into the primal reasons for the emotion, and how it is helpful in modern day interactions.

    Originally, disgust was an important emotion for survival. It standardized hygiene and behavioral norms. If a caveman or woman ate something gross, or fell out of line with the accepted hygiene of the day, they were shunned from the group. If they slept with a relative or animal, ate another human, or did not clean food properly, they aroused disgust in their tribe, and were exiled or even killed.

    Without disgust, there would be less social norms, less “rules” for relating to each other and maintaining health codes. It’s a powerful emotion that drives behavior.

    Disgust as a microexpression looks like:

    Wrinkling around the nose

    Upper lip rising

    Eyebrows move down without tension (contrast this with anger where the eyebrows are pulled together and the eyelids are raised and tense).

    I feel that people need to be more aware of disgust as a microexpression, and learn what it is trying to communicate to them. It’s not just about a survival mechanism, such as smelling rancid milk and being able to avoid getting sick. It’s also about how our spouse treats us, how we feel when we watch interactions between other people.

    The negative effects of disgust, when it is taken too far, can be damaging and horrific. Racism and sexism are examples of disgust gone wrong. It can be dehumanizing. Even listening to Hitler’s conversation at his dinners, experts have analyzed disgust-oriented language. Much of his propaganda was even disgust-provoking propaganda.

    People who are an object of someone’s disgust experience deep shame. Sometimes, that is warranted—such as when that person has broken a societal rule like pedophelia. But as a therapist, I have to have a lower threshold of disgust when it comes to hearing people’s secrets.

    After awhile, I think that disgust, like fear, can be adaptable. I have heard all manners of secrets, and I rarely feel disgust anymore. Instead, I feel I need to exhibit psychological safety, so the patient feels open to talking about the things they cannot tell anyone. Through talk therapy, hopefully I can help them feel less shame and understand their unique journey and struggles more fully.

    Using microexpressions in interactions

    The first key to using microexpressions is to pay attention. Look at the person’s face, be interested and curious about what emotional state they are in. Notice the facial movements, and listen to what they are saying. Is what they are expressing maybe outside of their awareness as they talk? Does the emotion they are showing match what they are talking about?

    As a therapeutic tool, understanding microexpressions is a way of gathering information about someone else. Use that information to respond in a way that shows the person you are desiring to connect.

    Paying attention to microexpressions actually creates empathy. We have mirror neurons—neurons in our brain that are devoted to telling us what someone else is feeling. Those neurons light up when we watch someone else doing something, or feeling something. When we see someone bite into hamburger on a commercial, it might make us hungry, even causing our stomach to rumble or our mouths to make extra saliva. When we see someone cry, it might make us cry. Your brain will light up, to some degree, as if you are experiencing someone else's emotions. We can train ourselves to pay attention to those neurons to better be able to connect with people.

    Some people experience either less or more empathy than what is considered normal. This can be because of a disorder, or because of emotional burnout. Even experiencing emotional overload causes a decrease in empathy.

    Being able to determine the difference between yourself and the other person is another important part of empathy. Learning about microexpressions can help you do that—you can see their emotions, and recognize they are the one experiencing it, and you can respond to the emotion, but you do not have to own it as your own.

    Tune in next week to hear part three of Microexpressions. If you'd like to try out the app that trains people how to read microexpression, go here: IOS Emotion Connection App

    For full PDF of the episode with citations and further notes go to: https://psychiatrypodcast.com/resource-page/

  • Microexpressions to Make Microconnections Part 1

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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.

    Happiness

    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.

    Sadness

    Emotion: Sadness

    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.

    Fear

    Emotion: Fear

    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). 

    Disgust

    Emotion: Disgust

    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.

    Pride/contempt

    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.

    Surprise

    Emotion: Surprise

    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.

    Anger

    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

  • 00:37:11

    Hormonal Contraceptives & Mental Health

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    Do Hormonal Contraceptives Cause Depression? How Do Estrogen and Progesterone Influence Behavior and The Brain?

    Many women take hormonal contraceptives as a way of preventing pregnancy, or for other health reasons. These contraceptives basically use hormones to stop your body from ovulating.

    But do you ever wonder if changing your hormones can affect more than just your chances of getting pregnant?  

    Birth control has many positive effects too, other than just preventing unwanted pregnancy. It can help with:

    Acne

    Depression in elderly

    Hirsutism

    Heavy periods

    Maintaining bone density

    Decreased risk of certain cancers

    Premenstrual dysphoric disorder

    How hormones work without the pill

    In a woman that’s not on the pill, early in their cycle, they’ll have the least amounts of estrogen and progesterone in their body. Around ovulation, estrogen will rise, which changes their mood, causing them to experience more of the reward hormone, dopamine, and even the happy hormone, serotonin. Later in the cycle, progesterone rises too, changing the emotional state again. The drop in hormones and Progesterone is the depressant hormone, so this is typically what causes the pre-period moodiness that some women feel.

    This hormonal shift does not happen, or happens very subtly in women who are on birth control.

    Using a hormonal contraceptive changes your body’s chemistry, and alters your hormones. When you change your body chemistry, you may have influences on your mood, desire, all sorts of things we wouldn’t normally consider when we are only looking for the benefits.

    Here are some of the things hormone contraceptives can effect:

    What women find attractive

    Scientists noticed that women who were ovulating, and not on the pill, had an increased attraction to more masculine faces, dominant male behavior, taller men, deeper voices, versus when they were not ovulating. Ovulating women also wanted to go to public events more, and had more sexual fantasies. When they weren’t ovulating, women looked for a man who is more empathic, more fatherly, more compassionate.

    Depression

    One study followed a group of women for a number of years to see if their mood changed. They found that the younger (15-19) contraceptive group was 1.7-1.8 times more at risk of depression and being prescribed antidepressants. Specifically, younger women (15-19), and those who were prescribed progesterone-based pills, were at highest risk of depression. Also, most of these women experienced the depression onset at around 2 months - 1 year.

    If you’re older, taking a more estrogen-based hormone, have been on it for awhile, and are not depressed and have been taking hormonal contraceptives for more than one year, I would say you are probably not at risk of developing depression because of contraceptives. Now, that said, there are tons of reasons that people get depressed—life situations, genetics, health—it’s not just related to hormones. If you are concerned about depression, talk to your doctor about it.

    Natural fear response

    Women who are on hormone contraceptives are more likely to experience anxiety. Natural hormone levels help with fear extinction, or the ability to overcome fears. Birth control can inhibit our ability to regulate fear in stressful situations.

    Empathy

    In the part of the natural cycle, before ovulation, when estrogen is higher, women have an increased ability to recognize facial expressions of emotion. Hormonal contraceptives decrease brain responsiveness, making it more difficult to process emotion, and making recognition of negative emotions harder.

    Reward Pathway

    Ovulation also causes an increase in estrogen, which increases the brain reward pathways by increasing dopamine, our body’s pleasure response hormone.

    If you are on an oral contraceptive, the changes in hormones can cause a dampened reward processing, so there may be a decreased amount of pleasure you can experience through things like food, sex, or even social connectedness.

    My conclusion about the pill

    Overall, with the positive effects birth control has caused in society, namely, a decrease in teen pregnancy, it can be difficult how to integrate the new details emerging on the influence on mental health.

    I know my research into this has led me to be more aware of teens I treat who are taking hormonal contraception.  If you’re looking for the benefits of the pill, there are many types of contraceptives, and because every woman is different, there is not a one-size-fits-all option. Talk to your doctor about which one is best for you.

    --------------------------------------------------------------------------------------------------------------------

    Below are more detailed notes that Dr. Mona Mojtahedzadeh and Dr. David Puder worked on together to provide the scientific foundation to this episode.

    Intro:

    Our goal is to empower women to know more about the recent debate in the relationship between contraception and mental health.

    I first started thinking about this after hearing a talk by Kelly Brogan

    Worldwide, 100 million women use “the pill”.

    Approximately 82% of sexually active women in the USA use oral contraceptive pills (OCP) sometime during their reproductive years.

    17% of women aged 15-44 use “the pill”.

    The last decade in the USA, rates of teenage birth rate along with teenage pregnancy and abortion have decreased. Most researchers attribute this victory to improved access to contraception. (Carrol, 2017- New York Times)

    OCPs are prescribed for various reasons: prevention of unintended pregnancy; decreased risk of ovarian, endometrial, and colorectal cancers; preservation of bone mineral density; and at times prescribed for PMDD symptoms; acne and hirsutism; heavy menstrual bleeding. (Cheslak-Postava, 2014)

    Do Hormonal Contraceptives Increase Risk of Depression?

    One million women in the Denmark national registry, followed for 6.4 years (Skovlund, 2016),  ages 15 to 19 years old had higher risk of depression, even when they had no history of depression.

    The hormonal contraceptive group age 15-19 had an increased relative risk of 1.7 of first incidence of depression diagnosed in a psychiatric hospital

    The hormonal contraceptive group age 15-19 had an increases relative risk of 1.8 of first incidence of using an antidepressant

    Hard numbers are for the non-use, 10k prescriptions of antidepressants over 1.1 million person years vs use of oral combined 18.5k antidepressant prescriptions over 0.91 million person years (RR 1.8).

    The all progestin-only pill group age 15-19 had a 2.2 risk of first time antidepressant and 1.9 first diagnosis of depression in a psychiatric hospital

    Risk did not increase till 2 months after initiation of hormonal contraceptive use, peaked at 6 months and after one year decreased significantly

    Another study of 1236 women, ages 20-39 from the United States National Health and Nutrition Examination Survey (NHANES) found that “women who had used OC during adolescence showed an at least 1.7 times higher 1-year prevalence of depression in adulthood compared to both women who had never used OC, and to women who had only started using OC after adolescence.” (Anderl, 2017)

    Some critics:

    Large-cohort population, based studies (especially if the data is from an administrative database) have more chances to find a statistically significant result even if the results are not clinically significant.  However in the Denmark study all correlations showed similar things which would not occur if there was no link, and relative risks were high, especially for adolescent women.

    Are women who are accessing hormonal contraceptive methods accessing more health care system in general?  

    Previous studies looking at rates of depression did not find a correlation with OCPs or some even reported improvements in mood. Months earlier there was a systematic review study published in the European Journal of Contraception and Reproductive Health Care. Although they made it clear that we were lacking prospective studies, the data that did exist at the time showed no correlation between hormonal contraception and women’s moods, or actually had improvement in mood. Therefore, this new study has to be weighed along with the rest and can not replace all prior research.

    In the study it states that for every 100 women who did not used hormonal birth control, 1.7 were later prescribed antidepressant. For every 100 who did use, 2.2 were prescribed antidepressant. The difference is 0.5 percentage points meaning that if this was a randomized control trial, for every 200 women treated, one need to be treated with antidepressant. (Carrol, 2017- New York Times)

    The amount and types of progesterone hormone varies between different hormonal contraceptives. (Antiandrogenic progesterones are less possible to cause mood lability, lower chances of acne, and lower chances of increased appetite or weight gain.)

    We should not underestimate the role of molecular genetics in determining effects of hormonal contraceptives on women.

    “This study showed an association between birth control and depression. Specifically, both women who took oral contraceptives (which go through the bloodstream and to the whole body) and women who had progesterone IUDs (such as the Skyla or Mirena, which concentrate hormones in the uterus) seemed to have higher rates of depression. But like all epidemiologic studies, it can only prove that there is some correlation between hormones and depression (and only in this particular data set), not that one causes the other.” David Grimes, MD

    Pathophysiology: How do OCPs work in general compared to natural states of hormonal secretions?

    1.  Hormonal levels

    We want to weigh effects of amounts of hormones vs effects of pulsatility of hormones.  

    OCPs have much smaller levels of estrogen and progesterone (progesterone> estrogen) compared to a natural woman’s cycle.

    In general, progesterone is more causative for depressive episodes and estrogen is more to cause elevations in mood. Antiandrogenic progesterones are said to be causing less of mood lability and negative emotional effects.

    2.  Mode of secretion

    In the past it has been stated rapid declines in hormones have a negative impact on mood.

    In natural circumstances, the arcuate nucleus of the hypothalamus functions as pulse generator, resulting in hourly release of gonadotropin releasing hormone (GnRH) in to the hypothalamic-pituitary portal vasculature.

    This leads to a pulsatile plasma profile of luteinizing hormone (LH) and follicle-stimulating hormone (FSH)

    LH and FSH lead to a pulsatile increase in estrogen and progesterone.

    The pulsatile fashion of LH and FSH also regulates the growth and maturation of the graafian follicle in the ovary.

    Our neural clocks termed the hypothalamic GnRH pulse generator determines the pulse frequency but the amount of GnRH released in each pulse is determined by our estrogen and progestins.

    OCPs steady state inhibits GnRH therefore there is a lower level of estrogen and progesterone and no longer rapid shifts in estrogen and progesterone.

    In one study, triphasic OCPs (which correlate more to natural menstrual cycles) were more related to first episode depression than monophasic ones. (Cheslak-Postava, 2014)

    3.  Feedback mechanisms

    In a natural menstrual cycle, we have both negative AND positive feedback mechanisms involved. Approaching mid-cycle, we have a 36 hours increase in levels of estrogen which leads to  a surge in FSH, LH further to which we have a second surge in estrogen this time accompanied by progesterone prolonging through the second half of the cycle.

    OCPs solely act by negative feedback, decreasing hormonal states on all 3 levels therefore resulting in a much decreased states of estrogen and progesterone hormones. The low steady fashion of hormone exposure with OCPs, prevents FSH and LH surges and therefore subsequent ovulation.

    The pulsatile nature of hormonal secretions is essential for positive feedback mechanisms leading to maintenance of normal ovulatory menstrual cycles.

    Women are most euphoric around their ovulatory phases.

    OCPs prevent ovulation by providing a steady level of hormonal exposure therefore preventing the body to go through the plasma surges of the FSH/LH and subsequently the sex steroids. Because of this effect, women on OCP are deprived of the natural mood elevations experienced around and post time of ovulation.

    Point 2: OCP Have Unique Effects on the Brain

    Hormonal contraceptives cross the blood brain barrier

    Pulsatile nature of natural hormones

    In puberty the surges of sex hormones cause organizational changes in the brain (Peper, 2011)

    “Typical gray matter decreases in prefrontal, parietal, and temporal cortices taking place during puberty and adolescence were found to be related to increased levels of estradiol in girls and to increased levels of testosterone in boys.”

    OCP bind receptors in different brain regions

    Immediate changes (seconds to minutes)

    Decreased endogenous estrogen and progesterone

    Estrogen inhibits secretion of FSH

    Progesterone inhibits secretion of LH

    Absence of normal fluctuations

    Strongly reduced testosterone levels (to the level of follicular phase)

    Decreased effect of oxytocin on social-reward processing

    Epigenetic processes (takes months)

    28 women, ages 16 to 35, on hormonal contraception for 3 months were compared to controls and found to have these differences in the brain on MRI. (Lisofsky, 2016) The women on contraceptives had decreased gray matter volume in the left amygdala/anterior parahippocampal gyrus.

    Sex steroid hormones have effects on the cortical and subcortical regions involved in cognitive and emotional processing. Addition of progesterone to hormone therapy, has been shown to cause adverse mood effects in women. Mechanisms include: activation of (Y aminobutyric acid A) GABA-A receptor which is the major inhibitory system in the central nervous system (CNS) of humans. Also, external progestins more than natural progesterone, increase levels of monoamine oxidase which degrades serotonin concentrations. (Kleiber, 1996)

    Hormonal contraceptives decrease the ability to have fear extinction

    Women have 2x the rate of anxiety disorders, compared to men, specifically starting after puberty

    Estrogen can reduce fear, by enhancing fear extinction

    A single dose of estrogen can reduce fear extinction

    Low estrogen levels are associated with higher fear conditioning

    In one study, women with lower estrogen when showed a violent video, on subsequent days had elevated skin conductance and when going through a fear extinction task and also had stronger intrusive memories (Wegerer, 2014)

    High estrogen facilitates fear extinction and protects against the effects of stress by causing:

    increased activation of the ventromedial prefrontal cortex (vmPFC)- amygdala circuit during fear extinction

    Increased activation of anterior cingulate cortex (ACC) and dorsolateral PFC during emotional response inhibition important in fear regulation

    Downregulation of emotional and stress reactivity in the amygdala, hippocampus, hypothalamus, ACC, orbitofrontal cortex

    Women on OC during fear extinction:

    Displayed higher activation in the amygdala, thalamus, ACC, and vmPFC, and also had slower habituating skin conductance responses, which could suggest impaired fear extinction

    Women on OC had decreased reactivity of HPA axis (hypothalamic-pituitary-adrenal axis):

    When cortisol was given to women on OCs, they had increased hippocampal activation during a fear condition whereas in men or naturally cycling women had decreased activation.

    When in a non-stressful situation OC users had decreased amygdala activity towards negative pictures (Petersen, 2015)

    Empathy

    A single dose of estrogen in one study increased men’s empathy (increased physiological response to another’s pain, increased emotional (vicarious) reactivity) (Olsson, 2016)

    A recent systematic review concluded that facial emotional processing is enhanced during the follicular phase and oral contraceptives decreased brain responsiveness during different facial emotion processing tasks.  Postpartum and pregnant women may be in a hypervigilant state in regards to facial emotion processing. (Osorio, 2018)

    Reward Pathways

    Estrogen increases reward pathways by increasing dopamine whereas OC dampen reward processing changing social and sexual stimuli

    Partner Selection and Relationship:

    Women during ovulation had preference to more masculine faces, those on OCs did not have change in preference during the cycle. (Penton-Voak, 1999)

    Women have preference of more masculine bodies when their fertility is highest (Little, 2007)

    Other preferences include: vocal masculinity, video clips of dominant behavior, taller men

    Change in behavior seen: greater interest in public events where they could meet men, more sexual fantasies

    Women during ovulation are more attracted to more masculine male faces.  This was a study of 42 female volunteers at 2 different phases of their menstrual cycle. In general women favored a more masculine face but during ovulation there was an increased choice for the more masculine face. (Johnston, 2001)

    In women during the period before ovulation, testosterone normally predicts preference for masculine faces, but in women on OCs there was no link (Bobst, 2014)

    Preferences change in marriage when women get off of their OCs, if their partner is unattractive they may remain with higher dissatisfaction and if their partner is attractive they will have higher satisfaction (russell, 2014)

    Another study found that highest sexual satisfaction in women was found in those who either met their partner when not on OC and did not get on an OC or those who met their partner on an OC and continued on an OC (Roberts, 2014)

    Citations and Further reading:

    Further reading on IUD: article showing how uncommonly IUDs are used in the US

    Anderl, C., & Chen, F. S. (2017). Oral Contraceptive Use in Adolescence Predicts Vulnerability to Depression in Adulthood.

    Bobst, C., Sauter, S., Foppa, A., & Lobmaier, J. S. (2014). Early follicular testosterone level predicts preference for masculinity in male faces–But not for women taking hormonal contraception. Psychoneuroendocrinology, 41, 142-150.

    Brunton, L. L., Chabner, B., & Knollmann, B. C. (Eds.). (2011). Goodman & Gilman's the pharmacological basis of therapeutics.

    Cheslack-Postava, K., Keyes, K. M., Lowe, S. R., & Koenen, K. C. (2015). Oral contraceptive use and psychiatric disorders in a nationally representative sample of women. Archives of women's mental health, 18(1), 103-111.

    Grimes, D. A. (2015). Epidemiologic research with administrative databases: red herrings, false alarms and pseudo-epidemics. Human Reproduction, 30(8), 1749-1752.

    Johnston, V. S., Hagel, R., Franklin, M., Fink, B., & Grammer, K. (2001). Male facial attractiveness: Evidence for hormone-mediated adaptive design. Evolution and human behavior, 22(4), 251-267.

    Little, A. C., Jones, B. C., & Burriss, R. P. (2007). Preferences for masculinity in male bodies change across the menstrual cycle. Hormones and Behavior, 51(5), 633-639.

    Lisofsky, N., Riediger, M., Gallinat, J., Lindenberger, U., & Kühn, S. (2016). Hormonal contraceptive use is associated with neural and affective changes in healthy young women. Neuroimage, 134, 597-606.

    Montoya, E. R., & Bos, P. A. (2017). How oral contraceptives impact social-emotional behavior and brain function. Trends in cognitive sciences, 21(2), 125-136.

    Olsson, A., Kopsida, E., Sorjonen, K., & Savic, I. (2016). Testosterone and estrogen impact social evaluations and vicarious emotions: A double-blind placebo-controlled study. Emotion, 16(4), 515.

    Osório, F. L., de Paula Cassis, J. M., Machado de Sousa, J. P., Poli-Neto, O., & Martín-Santos, R. (2018). Sex Hormones and Processing of Facial Expressions of Emotion: A Systematic Literature Review. Frontiers in Psychology, 9, 529.

    Peper, J. S., Pol, H. H., Crone, E. A., & Van Honk, J. (2011). Sex steroids and brain structure in pubertal boys and girls: a mini-review of neuroimaging studies. Neuroscience, 191, 28-37.

    Penton-Voak, I. S., Perrett, D. I., Castles, D. L., Kobayashi, T., Burt, D. M., Murray, L. K., & Minamisawa, R. (1999). Menstrual cycle alters face preference. Nature, 399(6738), 741.

    Petersen, N., & Cahill, L. (2015). Amygdala reactivity to negative stimuli is influenced by oral contraceptive use. Social cognitive and affective neuroscience, 10(9), 1266-1272.

    Roberts, S. C., Little, A. C., Burriss, R. P., Cobey, K. D., Klapilová, K., Havlíček, J., ... & Petrie, M. (2014). Partner choice, relationship satisfaction, and oral contraception: The congruency hypothesis. Psychological Science, 25(7), 1497-1503.

    Russell, V. M., McNulty, J. K., Baker, L. R., & Meltzer, A. L. (2014). The association between discontinuing hormonal contraceptives and wives’ marital satisfaction depends on husbands’ facial attractiveness. Proceedings of the National Academy of Sciences, 111(48), 17081-17086.

    Skovlund, C. W., Mørch, L. S., Kessing, L. V., & Lidegaard, Ø. (2016). Association of hormonal contraception with depression. JAMA psychiatry, 73(11), 1154-1162.

    Wegerer, M., Kerschbaum, H., Blechert, J., & Wilhelm, F. H. (2014). Low levels of estradiol are associated with elevated conditioned responding during fear extinction and with intrusive memories in daily life. Neurobiology of learning and memory, 116, 145-154.

    https://www.nytimes.com/2017/04/03/upshot/birth-control-causes-depression-not-so-fast.html

    http://www.slate.com/articles/health_and_science/medical_examiner/2016/10/birth_control_is_linked_to_depression_in_one_flawed_study_that_doesn_t_mean.html

    World Health Organization, United Nations Population Fund, & Key Centre for Women's Health in Society. (2009). Mental health aspects of women's reproductive health: a global review of the literature. World Health Organization.

    Klaiber  EL, Broverman  DM, Vogel W, Peterson  LG, Snyder MB. Individual differences in changes in mood and platelet monoamine oxidase (MAO) activity during hormonal replacement therapy in menopausal women.  Psychoneuroendocrinology. 1996;21(7):575-592.

    Appendix:

    OCPs have more progesterone than estrogen. They only have small amounts of estrogen to stabilize endometrial lining and to reduce bleeding.

    OCPs in general cause improved quality of life by different means for example by reducing bleeding.

    Due to the molecular genetic phenomena, if one OCP not satisfactory, changing to a different one might be a solution.

    IUDs are not systemically absorbed; therefore, do not inhibit ovulation. They mainly act by inflammatory responses in uterus preventing implantation of the ovum. They also act by increasing cervical mucosal thickness.

    Copper IUDs act by the same inflammatory responses, also copper elements in the device are said to have paralyzing effects on sperms.

  • 00:49:46

    Postpartum Depression with Dr. Pereau

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    Dr. Pereau is incredibly honest and vulnerable in this emotional episode as
    she shares her story. Throughout it, she talks about the symptoms of her
    postpartum depression, including:

    * Intrusive thoughts

    * Emotional disconnection from her baby

    * Sleep deprivation

    * Poor focus

    * Hopelessness

    * Problems with concentration

    * Disconnection from passion and joy

    * Panic attacks and anxiety

    * Poor self care

  • 00:52:06

    Performance Enhancement with Dr. MaryEllen Eller

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    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 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.

     CLEARING BREATH:

    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.

    CLEARING BREATH:

    Inhale regularly

    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.

    Performance Day

    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.

    Training Day

    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:

    Facebook: @PhysicalTherapyRX

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  • Sensorium: Medications, Drugs (THC, Alcohol), Medical Issues, Sleep, and Free Will

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    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

    Treat OSA

    Medications:

    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.

    Sleep issues:

    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.  

    Best Regards,

    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