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The Dark Triad (Psychopathy, Narcissism, Machiavellianism), sexually violent predators, Ted Bundy, and porn.

On this week’s episode of the podcast, I interview...quite a few people! We are covering Ted Bundy, America’s most infamous serial killer, and since the world has been fascinated by him lately, I figured I’d get a group of mental health professionals in a room to talk about him. His horrific acts made the news and have scared people for decades now, and rightfully so. Did media and pornography cause this? What was his diagnosis and was it correct? We have so many questions...


As my special guests and panel of experts, I invited Dr. Tony Angelo, who is head of services for a local prison and in charge of prisoners transitioning into normal life. I also invited Dr. Randy Stinnett, a clinical psychologist who co-manages an outpatient behavioral health department in a local community health clinic. Also with me is Nathan Hoyt and Adam Borecky, 4th year medical students who will be going into psychiatry.


Traits of psychopathic antisocial behavior


Criminals like Ted Bundy are skilled manipulators. They often scope their environment to see who will be the easiest to manipulate. They will treat you like you are their long, lost friend, but everything they do is an attempt to pull you in. They “hook” you so that they can get you to do something for them.

Ted Bundy came off as friendly and charming, described as “one of us.”  A friend of his from Washington State even said, “He’s the kind of person you’d want your sister to marry.” As disturbing as this is, it is a common trait of psychopathic antisocial behavior.

Ted Bundy displayed many traits of psychopathic antisocial behavior. Some of the most recognizable traits were:

  • Viewing others as a pawn in his chess game

  • Master manipulator

  • Desire control/power

  • Sexual gratification in his choices

  • Enjoyed having an audience

  • Calculated predatory aggression

  • Strategic planning

  • Feeling that some other entity is operating inside of him

Empathy qualities:

  • Normal cognitive empathy

  • Very low affective empathy


Someone with low affective empathy will not feel your emotions or know your emotions from a mirror neuron experience. Rather he can only read facial expressions and body language without allowing cognitive but not affective empathy.  


In episode 2 of the Ted Bundy documentary on Netflix, Confessions with a Serial Killer, in his first arrest Ted Bundy said, “A funny thing happened to me on the way to labor law class. I got two weeks on the spa on the labor floor here. And, a yes, I intend to complete my legal education to become a lawyer, and be a damn good lawyer. Uh, I think things are going to work out, thats about all I can say.”


When he said this, he had a right sided smile and outwardly looked fairly happy and calm. According to studies done about microexpressions, the right sided smile is usually demonstrating contempt, but for him does not look as negative, and because in so many of his videos he has it on his face, he likely thought highly of himself and looked down on others.

I have noted that very good liars look positive, but often still leak microexpressions of very subtle negative emotion. Bundy seems to have expressed anger when he felt thwarted. In his statement, he makes a joke, yet showed a flash of fear or sadness while doing so. Bundy’s emotions of fear, anger, sadness, and pain leaked out through the microexpressions on his face, which are always a truth-telling mechanism.

Below is the quote with my inserted microexpressions in it:

“[contempt] A funny [anger] thing happened to me on the way to labor law class. I got two weeks on the spa on the labor floor here [fear or sadness]. And, a yes [contempt, sadness or fear], I intend to complete my legal education to become a lawyer, and [contempt] be a damn good lawyer [anger]. Uh [pain], I think things are going to work out [fear], thats about all I can say.”

*Note it is hard to determine exact expressions from the poor quality of this video- but my microexpression research team discussed the above and this was our consensus.  The fear or sadness comment comes from the eyebrows going up in the middle, but it is hard to determine if there is fear or sadness due to the poor quality of film.


It is believed psychopaths feel little or no fear. Did Ted Bundy feel afraid?

Most of the video of Ted Bundy did not show a physiological reaction to stress. But it is likely to some degree (although much less than others) that he experienced fear.  It is thought that those with primary psychopathy have dysfunctional emotional processing due to issues in their amygdala. Studies show they have less fear then control groups and secondary psychopaths (more the sociopath or baked ones) which have more trait anxiety or fear (Skeem, 2007).    

What was Ted Bundy’s possible diagnosis?

Primary psychopathy: These typically have low affective empathy and low fear, however not all that are primary psychopaths become criminals. They are sometimes able to still follow the rules while not having any fear or empathy and can even be prosocial.

Sociopath (or secondary psychopathy): These are typically “baked” into being anti-social. Sociopaths are typically “made” to be the way they are, often resulting from a traumatic childhood. Abuse and trauma may influence their later life ability to attach to others.  They have higher trait fear, more borderline traits and more mental disorders.

Antisocial Personality Disorder:  This is how the DSM classifies people who have a history of illegal behaviors, deceit, impulsivity, failure to plan ahead, aggressiveness, reckless disregard for safety, irresponsibility and lack of remorse.  This is usually a criminal psychopath or sociopath with repetitive crimes. They display low empathy and low connection with others. Their behavior usually results in crimes against others.  

Ted Bundy’s bipolar diagnosis:

When Ted Bundy was assessed while awaiting his death sentence, he was given a diagnosis of bipolar disorder. However, most depressed people become less violent and don’t have much of a desire to have sex. It is also interesting to note that out of all of the violent events that happen in the US, only 5% of them are due to mental illness (Stuart, 2003). Therefore, we can conclude that most violent acts are not done by people with mental illness.

Could he have been in a manic state?

Most manic states end in death, jail or psychiatric hospitalization. Ted Bundy had no record of being hospitalized in a psychiatric hospital and was only put in jail after he was caught. Bundy was also capable of living a “normal” life. He was an active citizen, joined a church, was married and involved in politics. He played these roles for years.


With mania, this would not have been possible. Those who are manic cannot stop their mania. Also, Ted Bundy displayed reason in the midst of his crimes. He covered his tracks and could pretend to be something he wasn’t. Those who are manic do not have the ability to pretend to be something they are not, nor have the ability to plan and cover up.

DSM 5 antisocial disorder:

Ted Bundy would fall more in line with a DSM 5 antisocial disorder leaning more towards primary psychopathy. With this disorder, you must be 18 years or older and have commited conduct disorder before age 15. Also prevalent is a pervasive pattern of disregard for the rights of others since the age of 15 and psychopathic manifestations. Additionally, they must meet 3 or more of the following behaviors:

  • Fail to conform to lawful behaviors

  • Deceitfulness

  • Impulsivity

  • Irritability

  • Aggressiveness

  • Reckless disregard for the safety of others

  • Irresponsibility

  • Lack of remorse

Nearly all of these traits were displayed in Ted Bundy’s pattern of behavior. Even when he was young he showed predatory aggression (which I discuss in a prior episode) when he set up tiger traps at camp and injured a young girl. Although he prayed with people before his death, Ted Bundy’s memorable quote, “I am in the enviable position of not having to feel any guilt,” showed he was wired with some primary psychopathy.

Low IQ

Although Ted Bundy has been referred to as a criminal “mastermind,” he may have had a average or only slightly above average IQ. The article by Ceci, 1996, found that cognitive ability tends to be a good predictor of academic performance; measures of academic achievement (LSAT, GRE, SAT) correlate very highly with measures of cognitive ability.

Although we do not know Bundy’s actual LSAT score, only that he believed it was “mediocre,” there is certainly no evidence that states he was a genius.  Rather than a genius, I would say he was not impulsive, very calculated, and often planned and put a lot of energy into his criminal actions.

Hearing voices

Ted Bundy often referenced hearing voices that told him to do bad things. However, it is not believed he had schizophrenia. Occasionally antisocials will use this as a way to avoid responsibility for their behaviors.

We call it MBD: minimize, blame and deny

Was pornography to blame?

Ted Bundy blamed his behaviors on pornography. However, pornography is not viewed as a cause of sexual violence. In persons who have preexisting conditions for sexual violence, it is a viewed as a contributing factor.

In Episode 4 of the documentary, he is quoted as saying, “I never said (pornography) made me do it. I said that to get them to help me. I did (murder) because I wanted to do it.”

The research confluence theory states men with hyper masculinity that also involves psychopathic tendencies have low agreeableness, abuse, hostility towards women, impersonal sexuality combined with sexual permissiveness. When you have a confluence of those two things and violent pornography it may be a contributing factor to Ted Bundy’s violent, abhorrent behavior.

It is important to note that pornography has not been present in our society for very long. Yet, crimes against women have been happening since the beginning of time. It is because of this fact that many doubt that pornography is to blame for crimes of this nature.

Hald, 2010,  found that the correlation between violent pornography and attitudes supporting violence against women (r=0.24) was significantly higher (P< 0.001) than the correlation between nonviolent pornography and attitudes supporting violence against women (r=0.13): however these are still low correlations.  

Antisocial personality disorder and psychopathy as a mental illness:  

Just because antisocial personality disorder is in the DSM, it doesn’t mean it should be viewed the same way we view schizophrenia, bipolar, major depressive disorder, etc. Largely, antisocial personality disorder is not something that is treated by psychiatrists. There is no medication for it and most with this disorder are not interested in help. If they come to see a psychiatrist, it is typically because they want something from you.

Narcissism diagnosis:

Ted Bundy had traits of narcissism as displayed in the DSM 5 criteria: a pervasive pattern of grandiosity, lack of empathy and a need for admiration which begins by early adulthood. To meet the criteria, 5 or more of the following behavioral features must be met:

  • grandiose sense of self-importance

  • preoccupied with fantasies of unlimited success and power

  • special or unique and can only associate with high status entities

  • requiring excessive admiration

  • sense of entitlement

  • exploitative

  • lack of empathy

  • often envious of others and believes others envy him or her

  • arrogance and haughtiness

I would add that some narcissists are low-self esteem, but I believe he was a high self-esteem psychopathic narcissist.  

Machiavellianism

Machiavellianism overlaps with narcissism and antisocial disorders. They are more likely to deceive and manipulate others for their own personal gain. They see people as objects for use and manipulation. They will have normal amounts of empathy unless they have traits of psychopathy.

The opposite of machiavellianism are people who display honesty and altruism.

In viewing Ted Bundy, it is highly probable that he displayed high Machiavellianism with traits of psychopathy and narcissism—thus having all the dark triad.

How did Ted Bundy come to be this way?

Home-grown sociopaths don’t necessarily have a need to be seen and appreciated by others. They often have been made the way they are due to horrific abuse, and usually prefer to be left alone. But, psychopaths who are born with low physiological arousal, have more of the predatory aggression which we see in Ted Bundy.

A person with primary psychopathy can either choose to live in society and do things to help, although without empathy and with difficulty attaching to others. Or they can choose to do illegal things to get their drives met. Whichever one they choose will write their brain and pattern of behavior that they will follow. These people can be incredibly helpful to society or incredibly harmful.

Determinism versus free will

It often comes down to determinism versus free will. In other words, did he make the choices or did his mental illness cause them? Ted Bundy went to prison for the choices he made, not the psychological predisposition that he had. However, when one goes into determinism, they will blame others for the choices that they made.

It is important to remember these people do have a choice. Because, ultimately, there is another dimension here, which is the moral dimension. We all have the responsibility to others and to society.

However, there are people who have less choice than others. For example, a person with a frontal lobe injury will have less “choice” than someone who does not. Ultimately, choice must be in line with responsibility. But I have known people to “check themselves in” for desires to do bad things, and get help. Sometimes we only have a small choice to change our environment.

Treatment

With the Ted Bundy type of psychopath, therapy will most likely not benefit them. This type of person should be put in prison for life.

Therapists must be especially on guard with someone like this, which can be uncomfortable for therapists and clinicians. You must view your interactions with them like a chess match. Because, everything about your interactions is a game to them.

Towards their therapists, they may exhibit these types of behaviors:

  • Play into your desire to “make a difference,” which is fertile ground for them to manipulate you.

  • Express prosocial behaviors.

  • Trap you by making you believe you have reached them in a way no one else has.


However, the “baked” sociopaths, or those with features of antisocial behaviors, can benefit from therapy. Clients will very rarely be as healthy and whole as you want them to when they leave therapy.


However, the goal is for them to leave with better connection to people, not use sex as a coping strategy, be more intimate (non-sexually) with humans, and relate better to authority. This will lower their risk of sexual violence, and help them on a track to be able to fit into society.

Approaching therapy

You can give all the tests you want, but one of the most valid tests of psychopathy is the “hair on the back of your neck” test. You just know it when you’re in the presence of psychopathy. It will alarm your body’s natural detection mechanisms. You can just “feel” it. I know that isn’t technical jargon, but it’s so true.

The goal in therapy should be to change their mindset away from objectifying people. It is suggested that you get access to their large criminal history in order to learn what they have done and use that strategically in their treatment. This will arm you with the knowledge of what they have done and what they are capable of.

Approaching them with the idea that they are likely to continue their cycle of behavior unless they do something to change it is an ideal approach. Discussing the importance of change itself and how change occurs can be helpful.

Focus primarily on the dynamic risk factors or “stable factors”:

  • Issues with authority

  • Intimacy

  • Hostility and attitudes towards women

Targeting those aspects one by one and digging into each one is a strategic approach. Improvement in each of these areas will lessen their risk of continuing their behaviors significantly.

Final Thoughts

There will always be that one in a million person who will use their predisposition to harm others and create a life of criminal behavior.

However, the glamorization of criminals like Ted Bundy from the media tend to breed a culture focused on the fear of these one in a million criminals.

It is important to remember that the media carries a bi-directional quality. Where the consumer drives what the media will pay attention to. Limiting the attention we give these types of criminals will lessen their need to be publicized and noticed.

For Nate Hoyt’s extensive notes on this episode - go here

Questions, comments, thoughts? Please comment on the picture that corresponds to this post on my instagram: @Dr.DavidPuder




How to Fix Emotional Detachment

Link to show on: iTunes, Google Play, Stitcher, Overcast, PlayerFM, PodBean, TuneIn, Podtail, Blubrry, Podfanatic


This week on the podcast, Ginger Simonton, PhD candidate, and I (Dr. David Puder) talk about about how to deal with emotional detachment. In the psychiatry world, we call the state of emotional detachment, congruence. 

What is congruence?

Psychological congruence is someone’s ability to feel and express their inner emotions in a consistent manner with their outer world—their speech and body language.

As an example, have you ever smiled when you’re talking about something sad? Or felt very emotional, yet had a flat face and still posture? Have you ever felt angry, but pushed it down and developed a headache? These are incongruent speech and behavior patterns.  

Incongruence happens when we’ve lost touch with our inner world, our emotions that are represented with bodily sensations. Many of my patients experience emotions, but have a hard time expressing them with words, so they shove them out of their experience.

Emotions are unavoidable.

We experience them all the time, whether we know it or not. Common terms for pushing them out of our awareness are suppression, denial, repression, and other defense mechanisms. We may think we can suppress our emotions, but they will come out in one way or another—sometimes through physical pain and illness.

There is extensive research on how the body processes emotion, and how that affects us physically. One of my favorite books on this subject is The Body Keeps the Score, by Bessel van der Kolk and The Feeling of What Happens by Antonio Damasio. I have spoken about the science of emotion in part 1, part 2, part 3 on microexpression and a popular episode on the polyvagal theory which give the science and application of understanding emotion.

As psychotherapists, our job is to help people reconnect to those emotions, and be able to experience them in healthy ways. People bury so many of our psychological problems in our bodies that we don’t even feel comfortable in our bodies anymore, and we prefer to be numb.

People further push unwanted emotions out of their experience through use of drugs, alcohol, and other addictions like porn, gambling, movie binging, or mindlessly scrolling forever on social media.

 

How do we develop incongruence?

But we don’t start out as emotionally disconnected, or incongruent. As children, we express our emotions as we feel them. If we are happy, we giggle, smile, or stick out our tongue as we work on a project. If we are sad, we cry. If we are angry, we bite, yell, spit or claw. If we have disgust we spit things out, push things away and protest against putting things in our mouth!  

If our emotions are mirrored back, and our caretaker acknowledges them verbally, them we optimally will be connected to our bodily responses from a young age. This is why I always recommend starting any discipline or high emotional moment with kids by empathically mirroring their emotions in words, and adding meaning to why they might feel such a way.

To get along with others, most kids, over time, develop a normal adaptive way to conceal emotions, which helps function in family and friendships. We learn that there is a context for truly sharing what is going on, and this is a good thing. Sometimes suppressing strong emotion until later is helpful!

Stronger issues develop when repeated messages invalidate or shame our experience, or trauma moves us away from being congruent with our inner experience. It is also possible that there is no one who an individual connects with enough to be congruent around.

For example, if everyone you know would shame or attack you, it might not be a good idea to bring out your deepest thoughts and emotions. These kinds of households often have heavy drugs or alcohol, severe mental illness, or predators.

We are meaning-making creatures. We assign meaning to events in our lives, and that meaning becomes our guiding belief and principle, especially in key developmental periods in childhood.

These meanings shape how we are going to interact with the world. Although unconscious and out of our awareness most of the time, when we live out of congruence without ourselves, it leads us to form these earlier, shaping meanings.  (click here for more on the science of meaning)

How incongruence develops:

  • A trauma occurs. A child hears his parents fighting. The child, when in the midst of it, seems to be physically sick, and this distracts the parents from their fighting and thus decreases the fighting.

  • We assign meaning to it. The child, as always, relates everything back to him or herself. They think, “If there is yelling, if I become ill, the yelling will stop.”

  • We structure habits and actions around that belief. The person continues to use being ill as an adaptive response to calm the parent’s hostility. Any emotional pain and discomfort is thus learned to be responded to when in the midst of only physical pain.

  • We see patterns in our lives that reflect that belief. We react repeatedly in a way that demonstrates our belief. We notice it affects our relationships, and that further cements the belief in our lives. New connections are found with caring physicians, maybe specialists who have concern for the medical issues, which further reinforces illness being a way to both calm disagreements and get connection needs met.

  • We have to either live with it, or deal with it. Until we revisit that moment and that decision, we cannot sift through that core belief. There is incredible hope for people with incongruence.

The response to a healthy therapeutic relationship and subsequent changes in behavior can be astounding. To deal with it, it is necessary to both find new ways of connecting with others but also not be able to use the incongruent way of being for an adaptive means.

 

How do we fix incongruence?

Our goal as we progress in life is to connect our physical body, emotional experience and verbal communication. The best public speakers seem to speak from the core of their being. The most powerful messages come from getting in touch with ourselves and integrating it.  

We can introduce the concept of reconnecting with the self in several ways:

Art

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:

  1. What is your body feeling as you talk about that?

  2. What emotion would you name that feeling you’re having?

  3. 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:

  1. As you say that what are you feeling in your body?

  2. If your body could say something what would it say?

I want to access their bodily memories and the source of their pain.  

 

Taper off of harmful and unhelpful drugs.

It’s easier to medicate incongruence, rather than actually deal with the root of it. It’s quicker. Substances like alcohol and drugs deeply affect people’s emotions. When patients are self medicating, they are usually trying to rid themselves of a symptom of emotional pain.

I like to ask them, “What are you getting out of the substances? Sleep? Peace?” Once we can answer that question, we can get to the bottom of where the anxiety and fear or anger comes from. We can begin to develop congruence, which will in turn, bring peace.

People medicate with illegal, and prescribed, legal drugs, as a way of dealing with emotional pain.

Some doctors and therapists can be symptom based, rather than focused on what is underneath the symptoms. When they see a patient, they can be on a hunt, trying to identify what’s wrong, the bottom line, and then find a medication that will relieve symptoms.

When we do that as therapists, we connect with the patient’s illness narrative, rather than who their core is, before they developed these problems.

Some patients who come to see us are taking 20-33 pills a day for all their different illnesses. If there is so much medication involved, it can become difficult to do psychotherapy as likely the sensorium or total brain function is impaired.

We have found when we establish a secure emotional connection with them, we can get some of these medications off the table, and then our patients can start to develop a range of emotions.

Through an attachment with a a therapist, that is trusting and meaningful, people can start to feel what before they either consciously or unconsciously suppressed.  I have spoken about the worst medications here.

 

How to stay congruent during tough circumstances.

It is tough to apply all that patients have learned through therapy in their everyday lives. Our families and friends love homeostasis—usually, the people around us want us to stay the same. They say, “you’ve changed,” as if that’s a bad thing.

When we’ve been healed, when we are congruent with ourselves, it can be difficult for our friends and family to accept the “new us.” They connect more easily with the old us.

We have noticed that if the patient begins to grow, the whole family system needs to change as well.

To maintain newfound congruence and healthy mental states, patients work to find healthy relationships they can be congruent within.  In the future I will talk about how to identify safe people and how to have healthy boundaries that keep us in relationships.

Questions, comments, thoughts? Please comment on the picture that corresponds to this post on my instagram: @Dr.DavidPuder

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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.    

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

    1. 1947

      • Promethazine

        • Produced sedation and calmness in animal models

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

    2. 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

    3. 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

    4. 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

    5. 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

    6. 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.

    7. 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

    8. 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:

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

  • Expected or Therapeutic plasma concentration ranges for antipsychotics and mood stabilizers

  • 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.

 

 

 

 

 

 

 

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?

  • 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


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.

Prescribing Strength Training for Depression

Recent studies show the power of strength training in treating depression. This blog and podcast episode discuss this important treatment of depression.

Using Microexpressions in Psychotherapy

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Link to show on: iTunes, Google Play, Stitcher, Overcast, PlayerFM, PodBean, TuneIn, Podtail, Blubrry, Podfanatic

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 unconscious

Microexpressions 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 therapy

Miscategorization

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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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

 

 

Hormonal Contraceptives & Mental Health

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

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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.

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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.

IMG_1630.PNG

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)

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  • 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.

 

Postpartum Depression with Dr. Pereau

Postpartum Depression with Dr. Pereau

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

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