Setting Boundaries in Relationships

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

What are boundaries?

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Good fences make good neighbors

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

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

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

How to set up healthy boundaries

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

Parenting and boundaries

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

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

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

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

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

Keep your boundaries, and express empathy.

Boundaries in romantic relationships

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

Be honest and open right from the start.

Physical boundaries

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

Spiritual boundaries

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

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

Conversational boundaries

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

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

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

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

Dealing with relationships and change

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

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

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

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

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

 

The History and Nuances of Bipolar Illness

Below is a detailed review of the podcast episode, with most of the content that Dr. Michael Cummings and I (Dr. Puder) discussed.  Special thanks to Arvy Wuysang (MS4) for his work in the initial transcription and organization.

The history & nuances of bipolar illness

Bipolar Illness was first discovered by Emil Kraepelin, who was also the first to describe schizophrenia in the 19th century.

Kraepelin noticed another major mental illness in which people had episodic disturbances of mood. He saw either elevation of mood and increased energy, along with a decreased need for sleep, and often impulsive or psychotically related behaviors.

Then, the same patient would experience the opposite, sleeping through the day, demonstrating lowered energy and depression.  These patients were noted to have normal function in-between these episodes. 

Nuances of the bipolar illness diagnosis

The Diagnostic Statistical Manual of Mental Disorders (DSM) identifies bipolar illness primarily by the presence of at least one episode of mood elevation to help distinguish it from unipolar or major depressive disorder.

Here are some defining symptoms:

  • Patients are fairly normal between episodes.
  • When they’re manic, their mood elevates their lack of sleep. They will sleep four to five hours at first, later progresses to no sleep at all on a nightly basis.

  • Every true manic episode will end in three places: hospitalization of some type, jail, or death.

  • Initial peak is in the 20s and 30s. Although, people suspect that many individuals who become bipolar don’t initially declare themselves.

  • They often present with a series of recurrent depressive episodes and then, at some point, they exhibit a period of mood elevation meeting the criteria for either hypomania or mania, which earns them the diagnostic label of bipolar mood disorder.  

  • There are two types. Type I, in which the person has fully evolved to mania or mood elevation and fully evolved episodes of depression. Type II, in which the person may have a milder form of mood elevation but still has fully evolved periods of depression.

  • Grandiosity is a major part of mania. Although historically some people with bipolar illness have often been incredibly productive during episodes of mood elevation, before they become disorganized or psychotic.

  • There is often impaired judgment during manic episodes. For example, someone who is manic will propose to 5 different girls, max out multiple credit cards, buy extra houses/cars/boats, etc.

Bipolar and the limbic system

Underlying pathophysiology is centered around the limbic system. Involves the temporal lobes and and structures which swings upward into the mamillary bodies into the anterior cingulate gyrus, which then projects forward into the frontal lobe. That circuit goes through periods of hypo-activity or depression in people who are bipolar. They have depressed metabolic rates of the system upto 30 to 40 % below normal. During periods of mood elevation, there is an increase in metabolic activity and instability in that limbic circuit. The mood is an element of that, but the person’s overall activity, sleep-wake cycle, circadian rhythms, along with all the things related to the functioning of the limbic system are disturbed in bipolar illness.

 Bipolar illness and sleep patterns

There are some models of the illness that suggest that perhaps the core of the pathophysiology of bipolar illness is an abnormally regulated biological clock.

In most of us, the nerve cells, the neurons that make up the biological clock, are very tightly linked to each other in terms of their operation. They literally form two pacemakers or oscillators in a very small structure that sits right on top of the optic chiasm called the supraoptic nucleus.

Normally all of our circadian rhythms are regulated by this master clock. In healthy people, it’s very difficult to get the two oscillators to separate from each other. In bipolar people, those oscillators drift apart relatively easily. Something as simple as loss of sleep during the latter half of the night will cause them to diverge from each other.

When that begins to happen, the overall functioning of the limbic system begins to oscillate in an unstable manner.

People have looked at things like disturbed sleep as being a very common precipitous of a mood episode. If somebody has a difficult day or disturbing event, and they’re genetically vulnerable to being bipolar, they may not sleep well at night, and the next night they may not need to sleep as much. The night after that, they really don’t sleep, and then their mood begins to elevate and another episode is initiated.

Genetic markers of bipolar illness.

Bipolar is typically passed on genetically, and can be linked with other similar markers of illness. Around 100 genetic markers have been linked to bipolar illness.

They overlap with schizophrenia in part, but not entirely. People with bipolar illness have a much more normal brain in terms of development then do people with schizophrenia. But, there appears to be an inherent defect in the operation of the limbic system elements with these periodic repeating of overactivity and underactivity, plausibly related to the core biological clock.

Mood stabilizers have an effect in terms of decreasing and stabilizing the activity of the limbic system. They tend to push that clock back toward being phase-linked or operating together as a single oscillator, rather than as divergent oscillators.  

Mood Stabilizers

History of Lithium

The very first mood stabilizer discovered was lithium. It was very popular in the 19th century for the treatment of gout because it decreases uric acid crystals.

In the 1940s, a psychiatrist named John Cade (1912-1980) served in World War II and was a prisoner of war for three years. After the war, he worked in a repatriation hospital in Australia and became fascinated with bipolar illness. At the time, he looked at the earlier history and thought that uric acid somehow caused bipolar illness. That turned out to be a wrong hypothesis. But, it led him to use lithium urate, a soluble form of uric acid, in hamsters, to see what would happen. The hamsters got lethargic and sleepy upon administration.

He decided to give his lithium compound to ten patients—six of them were bipolar, four of them were schizophrenic. They all became less agitated, though the schizophrenics didn’t change all that much. However, all of the bipolar patients’ moods stabilized.  

It’s amazing how he didn’t kill any of these patients in spite of giving them gigantic doses of lithium. His initial dose was 1300 mg, three times a day. Most of the patients got ill with that. If you give somebody too much lithium, they develop nausea, tremor, and diarrhea. You can make them very seriously ill with lithium because it has a very narrow therapeutic index. The distance between therapeutic and toxic is not very far. Optimal dose for most patients 0.6 - 1.0 mmol/L. Toxicity usually begins at about 1.5 mmol/L, serious toxicity begins at about 2.0 mmol/L.

At Loma Linda and at patton State Hospital, most patients start at 900 mg at night, obtain a plasma concentration five to seven days later, and then adjust the dose.

Dosing lithium

Lithium should never be given in divided doses.

The kidneys is spared by having a long trough period between lithium doses, so it is best to give it at bedtime.

Lithium tends to decrease urine concentrating capacity. Almost everyone who takes lithium, their urine output will increase by about 20%, and their water intake will correspondingly increase by about 20% to compensate. There are a few people who get much more severe diabetes insipidus, an insensitivity to anti-diuretic hormone in the kidney.

Over the course of many years, about 5% of people who take lithium will develop mild to moderate degrees of renal failure or insufficiency. That risk is minimized by keeping the lithium level < 1.0 meq/L and also by giving Lithium only once a day.  

Lithium and suicidality

It’s clear that lithium reduces suicidality, which may be a product of its ability to inhibit impulsivity. Suicide rates are substantially lower when people take lithium.

In the healthy population, when they’ve done studies in areas with very low concentrations of lithium in the groundwater, rates of suicide and rates of homicide are lower in areas with lithium in the groundwater compared to areas that don’t have lithium in the groundwater.

The amount of lithium that people are getting from the groundwater would be roughly the equivalent of taking 3 milligrams of lithium a day. This means that in the healthy non-bipolar non-mood disordered brain, it doesn’t take very much lithium to make people somewhat less violent.

When would you take someone off Lithium?

    • The best measure for lithium is to measure the eGFR (estimated glomerular filtration rate). If the eGFR declines to 50 or less, the person should not take lithium.

    • The other common adverse effect that lithium has is to make the person hypothyroid.

      • Lithium tends to decrease the synthesis and secretion of thyroid hormone. The good news is that if it makes somebody hypothyroid, we can easily replace the thyroid hormone with Levothyroxine, a synthetic analogue of the hormone. Frankly, your body doesn’t care whether you get your thyroid hormone from your thyroid gland or from a tablet.

    • Dermatologic side effects

      • Psoriasis is a contraindication to lithium use. It will greatly worsen psoriasis.

      • If the person is prone to cystic acne, lithium will typically cause a worsening of cystic acne.

      • One of the effects of lithium is to increase oil secretion in the skin. That can lead to both increased psoriatic plaques and cystic acne.

History of other mood stabilizers

The reason we have other treatments for bipolar illness, is largely the result of the work of Robert Post.

Post was a psychiatrist who worked at NIMH and was doing an unrelated experiment. He was looking at kindling, or increased sensitivity of the limbic system, by putting electrodes into mouse temporal lobes and giving them a one second electrical stimulus once a day.

Initially, when you do that, nothing happens.

But about day two or three, the mouse will have a complex partial seizure, a temporal lobe seizure. If you keep doing it pretty soon the mouse will start having spontaneous seizures. Robert Post looked at that and thought that the nerve cells of the limbic system can become more and more sensitive, more and more hyperactive, less and less well-controlled. He thought that he could block that effect, in terms of seizures, with anticonvulsants. He then, made a leap in logic, thought that perhaps mood episodes are acting like electrical stimulus causing kindling in the limbic system for people with recurrent mood episodes, like in bipolar patients.

He decided to treat some bipolar patients with an anti-epileptic.

The first medicine he used was Carbamazepine (Tegretol). Tegretol is a very difficult drug to use because it induces its own metabolism, so the level keeps falling. It also is fairly toxic with respect to the bone marrow. So, you have to watch out for loss of white cells, red cells, platelets.

He fairly soon turned to another anti-epileptic, valproic acid, which is a branched-chain fatty acid. He found that it was also effective in treating bipolar illness. Turned out that compared to lithium, valproic acid was more effective if the person was a rapid-cycling bipolar patient having more than four episodes a year. (Although lithium remain superior if the person is a classic type I bipolar patient.)

In young women in general, valproic acid it can be problematic because it can cause Polycystic Ovary Disease.

  • In pregnancy, it causes not only a risk of neural tube defects such as spina bifida, it also decreases the intellectual capacity of the offspring by about 10 IQ points, and roughly doubles the risk of autism in the offspring. It also causes hirsutism and weight gain.

Psychiatry has pretty much examined every anti-epileptic introduced since to see if it had mood stabilizing properties.

Lamotrigine (Lamictal) for example, does treat bipolar depression and does stabilize mood cycling, but has almost no benefit with respect to mood elevation. In fact, Lamotrigine as a monotherapy may actually cause switches into mania in some patients.

People have looked at Topiramate and found that it may have some prophylactic capability but doesn’t seem very effective at all if the person is already manic or depressed. If their mood is already stable, and you’re just trying to decrease the cycling, it may have some benefit.

Lamictal, used as a mood stabilizer, may have gotten more use than it should because although it does have antidepressant properties in bipolar illness, it is certainly not a benign drug.

People were initially attracted to it because there’s not a lot of laboratory monitoring involved. The plasma concentrations of lamotrigine don’t correlate very well with its efficacy because it is very rapidly cleared from the blood compartment and taken into tissue. It’s easy to administer and when you’re not using it for seizures, usually can be dosed all at bedtime.

It does carry a risk of Stevens-Johnson Syndrome, which is severe malignant rash, and which the person winds up looking like a burn victim because their skin literally dies and falls off.

It also can cause lymphohistiocytosis, which is a similar autoimmune process, but involving the blood vessels and internal organs. Luckily, that is rare, but it's also typically a life threatening response to the drug

The risk of the side effects above are increased by titrating the drug to rapidly. They discovered the side effects when they were using the drug initially for seizures. They were often increasing the dose by a hundred milligrams a day starting at 100 mg, and by day four, the person was on 400 milligrams. They found a 9% increased rate of malignant rash. If you slow down and don’t go faster than around 25 to 50 milligrams a week in the titration, the risk is reduced, but it’s still not zero. It’s probably less than one half of 1%, but it is a caution.

The other caution with the drug of course in bipolar patients is it sometimes is not a very good monotherapy because it doesn’t provide any protection against mood elevation. It seems to be effective in treating the depressed phase of the illness, but not the manic or hypomanic phase.

Oxcarbazepine has flunked multiple trials as a mood stabilizer. Oxcarbazepine differs from Carbamazepine in only one bond. In carbamazepine the bond between carbons 10 and 11 is an epoxide bond, while in oxcarbazepine that same bond is an ester bond.

It appears, however, that the mood stabilizing properties of carbamazepine result from the epoxide metabolite, and of course oxcarbamazepine does not produce that metabolite.

Oxcarbazepine can, in some individuals, reduce impulsivity, which seems to be a truism across the anti-epileptic drugs, but it’s not an effective bipolar treatment.

There was only one study looking at it in forensic settings for impulsive or violent patients. It was a self-funded single investigator study and it’s been the only study that was ever produced, never replicated. It was suspicious in that the patients were all outpatients, self-recruited via newspaper ad. It’s database even for impulsivity and so forth is pretty limited. It does have some application in that regard, but it is not as good as people hoped.

People became enamored with it simply because it was easier to use than carbamazepine, which isn’t to say that it’s benign. It induces hepatic enzymes, it causes dangerous hyponatremia in about 2.5% of the people who take it.

There haven’t been any really good studies identifying it as an anxiolytic. Like most anti-epileptics, it can be sedating and somewhat calming, but you could get the same effect from literally any of the anti-epileptic drugs, probably safer would be gabapentin.  

Antipsychotic use as mood stabilizer

Some of the second generation antipsychotics have also shown mood stabilizing properties, albeit as an addon to a primary or classic mood stabilizer. This include drugs like Aripiprazole, Brexpiprazole, Cariprazine, Olanzapine, and Quetiapine. Quetiapine in particular is effective in treating bipolar depression, as is Lurasidone.

Antidepressants as mood stabilizers

Do not give an antidepressant to a bipolar depressed patient!

There are now a host of studies suggesting that antidepressants offer little or no benefit with respect to depression in bipolar illness. It serves only to increase the rate of mood cycling and to risk a switch into mania.

Cognitive side effects of mood stabilizers

Lithium typically causes cognitive impairment only if the plasma concentration is too high, in which case it can cause decreased brain function all the way up to coma if the concentration is high enough. However, lithium used at therapeutic concentrations actually is neurotrophic.

It’s been used now in some demented patients with modest results. MRI scans will show a thickening of the cortex if you put somebody on lithium.

In contrast to lithium, antiepileptic drugs almost universally tend to dull cognitive performance. For example, one of the tip-offs that you’re giving the person too much topiramate is they start to lose the ability to find nouns, they become anomic.

Barbiturate and Benzodiazepine use in bipolar illness

Barbiturates were introduced in 1903. At that time, they were essentially the only psychiatric medication available. They treated literally everything that involved mood elevation or agitation with a barbiturate.

In the middle ages, individuals that seemed to have manic episodes as we understand it today, were considered witches. They were given doses of sedation that would bring a normal person down. These manic individuals, however, would not be sedated with those doses.

This is described in the book The Witches’ Hammer. Most of these tests were designed so that if you were the accused, you most likely won’t pass them. For example, one of the tests was being tied up and thrown into a mill pond. If you drowned, you were concluded not to be a witch, but of course you were dead. If you manage to float and you survived, you were concluded to have done so via witchcraft, in which case they retrieved you from the water and subsequently burned you.

Frankly, psychiatry has come a long way!

Importance of sleep hygiene in bipolar illness

One of the most important things to teach bipolar patients is to emphasize the importance of sleep hygiene.  They should go to bed at the same time every night. It’s dangerous for them to casually stay up to watch tv or a movie etc. That may be a setup for them to have the next episode of mood disturbance.

If they’re having difficulty sleeping, this is a group in which long term use of one of the Z drugs may be appropriate.

Dr. Cummings’ personal favorite in that group is Eszopiclone (Lunesta), because it has a longer half-life. It’s half-life is around 4-6 hours, so it’s long enough that the person will actually stay asleep. It also has a broad dose range, 1 mg - 8 mg at night.

It’s been used to treat primary insomnia in some individuals for up to decades without development of complete tolerance, or resulting in any withdrawal syndrome if the medication is stopped.

Education for bipolar patients

Patients and families need to realize that the more episodes of illness they have, the more resistant to treatment the illness will become, and the less responsive the illness will become to medications. This idea goes back to Robert Post’s study on kindling.

Additionally, when people have more episodes, the cycle tends to become progressively shorter. If they were initially having an episode every two or three years, it may suddenly occur every year, to having multiple episodes for a year.

One of the major costs for both families and individuals who are bipolar is that severe depression or severe mania is incredibly disruptive to the individual’s life. It can destroy their marriage, their job, and cause large setbacks.

I (Dr. Puder) will bring patient's families in, get them on board with a plan to identify early symptoms such as decreased sleep, increased energy, and change in physical activity.  I want the family to keep in close contact with me if these things are developing, and I will alway get them in within the week.  

Role of psychotherapy in bipolar illness

    • For many bipolar patients, the common pathway into a mood episode is an environmental stressor that causes sleep disturbance, which then sets off the instability that they have innately in their internal clock, and then they’re off into a mood episode. Teaching the person good sleep hygiene, teaching them to be better able to cope with stressors is crucial.

    • Psychotherapy can also train them to become more self aware, so that they may be able to spot earlier changes in their mood and recognize an impending episode sooner. This allows them to seek for intervention before things get out of hand.

    • Focus on developing healthy habits like exercise and healthy diet.  

The History, Mechanism and Use of Antidepressants

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

 

What is depression?

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

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

  • Psychotic depression

  • Bipolar disorder with depression

  • Seasonal affective disorder

  • Major depression

  • Chronic depression (dysthymia)

  • Postpartum depression

  • Premenstrual dysphoric disorder

  • Atypical depression

  • Melancholic depression

  • Depression due to a medical illness or medication

Some symptoms of depression are:

  • Weight gain or loss

  • Sadness

  • Anxiety

  • Agitation

  • Social isolation

  • Sleep problems

  • Guilt

  • Loss of pleasure

  • Loss of interest in activities

  • Mood swings

Major depression

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

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

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

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

Melancholic depression

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

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

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

Is depression a chemical imbalance?  

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

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

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

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

The history of antidepressants

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

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

Before antidepressants

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

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

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

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

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

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

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

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

First generation antidepressants

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

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

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

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

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

SSRI antidepressants

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

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

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

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

SSRI was also found to be effective for:

  • Post traumatic stress disorder (PTSD)

  • Obsessive compulsive disorder (OCD)

  • Generalized anxiety disorder (GAD)

  • Social phobias

  • Impulse based disorders (like binge eating)

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

When do you prescribe antidepressants?

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

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

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

  • Psychotherapy does not seem to be helping

  • The depression is becoming severe

  • Their family is genetically tended towards depression

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

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

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


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

  • History of Antidepressants

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

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

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

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

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

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

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

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

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

      • Psychotherapy, psychoanalysis

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

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

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

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

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

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

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

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

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

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

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

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

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

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

  • How does melancholic depression differ from other types of depression?

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

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

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

  • How severe of a depression warrants a treatment with antidepressants?

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

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

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

  • The advent of SSRIs

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

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

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

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

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

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

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

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

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

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

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

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

    • Increased anxiety in the early stages of SSRI usage.

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

    • Panic Disorders

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

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

    • Use of Chlomipramine in OCD

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

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

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

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

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

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

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

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

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

    • Benefits of optimizing testosterone levels in relation to depression.

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

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

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

      • We further talked about psychosocial details in the podcast.

    • Concluding thoughts

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

Emotional Shutdown—Understanding Polyvagal Theory

What is polyvagal theory?

By David Puder, M.D.

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

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

Why is polyvagal theory important?

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

  • Understanding trauma and PTSD

  • Understanding the dance of attack and withdrawal in relationships

  • Understanding how extreme stress leads to dissociation or shutting down

  • Understanding how to read body language

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

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

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

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

A story about a gazelle...

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

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

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

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

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

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

Here's how they work...

Connection Mode

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

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

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

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

How does this look and feel?

  • Our immune system is healthy.

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

  • We are sleeping well and eating normally.

  • Our face is expressive.

  • We emotionally relate to others.

  • We more easily understand and listen to others.

  • Our body feels calm and grounded.

 

Freeze, Flight, Fight, or Puff Up

...or the sympathetic nervous system response

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

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

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

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

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

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

  • We feel anxious, afraid, or angry.

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

  • Our digestion slows down as blood rushes to the muscles.

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

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

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

  • Our hands may be clammy.  

  • Our stomach may be painfully knotted.

  • All our senses focus.   

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

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

Shut Down

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

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

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

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

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

How does this look and feel?

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

  • Our eyes may look fixed and spaced out

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

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

  • We may feel low or no pain

  • Our lungs (bronchi) constrict and we breathe slower

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

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

  • Our body posture may collapse or curl up in a ball

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

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

  • Dialectical behavioral therapy

  • Mentalization based therapy

  • Transference focused therapy

How trauma affects the nervous system

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

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

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

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

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

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

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

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

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

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

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

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

Coming out of shutdown mode

So how do we climb back out of shutdown mode?

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

 

The Psychology of Procrastination

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

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

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

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

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

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

The Psychology of Procrastination

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

What is procrastination?

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

You might be procrastinating when:

  • There is a gap between your intention and action

  • You feel like avoiding something

  • You find yourself  easily distracted

  • You feel overwhelmed by tasks at the last minute

  • You always feel rushed to complete a project

  • You’re hesitant to truthfully update someone on your progress

It usually brings about feelings of:

  • Shame

  • Guilt

  • Anxiety

  • Regret

  • Anger

  • Inauthenticity

Why do we procrastinate?

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

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

The ingredients for procrastination


Personal Factors of Procrastination

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

The fixed personal factors are:

  • Higher Impulsivity

  • Lower conscientiousness—lower drive to be organized and accomplish.

  • Limited attention-span

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

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

The variable personal factors are:

  • Willpower

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

  • Distress tolerance

  • Willingness to ask for help

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

  • Task-focused vs value-focused

  • Self-consciousness & anxiety

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

The variable task or system-based factors are:

  • Unclear goals & expectations

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

  • Unrealistic goals & expectations

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

  • Distractions

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

  • Lack of accountability or mentors

Procrastination thrives in secrecy and isolation.

How do we procrastinate?

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

“I work better under pressure.”

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

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

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

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

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

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

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

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

How do we stop procrastinating?

Admit it

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

Catch the cognitive distortions

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

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

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

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

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

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

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

Build your willpower

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

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

Forgive yourself

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

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

How can you practice self-forgiveness?

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

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

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

Practice Mindfulness

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

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

Define and focus on your values

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

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

Define your goals

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

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

Psych yourself up for the task

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

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

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

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

 

Dealing with Emotional Detachment

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

What is congruence?

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

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

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

Emotions are unavoidable.

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

There is extensive research on how the body processes emotion, and how that affects us physically. One of my favorite books on this subject is The Body Keeps the Score, by Bessel van der Kolk and The Feeling of What Happens by Antonio Damasio.

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

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

 

How do we develop incongruence?

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

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

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

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

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

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

These meanings shape how we are going to interact with the world. Although unconscious and out of our awareness most of the time, when we live out of congruence without ourselves, it leads us to form these earlier, shaping meanings.  

How incongruence develops:

  • A trauma occurs. A child hears his parents fighting. The child, when in the midst of it, seems to be physically sick, and this distracts the parents from their fighting and thus decreases the fighting.  
     
  • We assign meaning to it. The child, as always, relates everything back to him or herself. They think, “If there is yelling, if I become ill, the yelling will stop.”
     
  • We structure habits and actions around that belief. The person continues to use being ill as an adaptive response to calm the parent’s hostility. Any emotional pain and discomfort is thus learned to be responded to when in the midst of only physical pain.
     
  • We see patterns in our lives that reflect that belief. We react repeatedly in a way that demonstrates our belief. We notice it affects our relationships, and that further cements the belief in our lives. New connections are found with caring physicians, maybe specialists who have concern for the medical issues, which further reinforces illness being a way to both calm disagreements and get connection needs met.
     
  • We have to either live with it, or deal with it. Until we revisit that moment and that decision, we cannot sift through that core belief. There is incredible hope for people with incongruence.

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

 

How do we fix incongruence?

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

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

Art

Art helps people bypass the logical areas of the brain and produce something raw and congruent to their inner experience. Painting, drawing, working with clay, or other forms of art help us connect with things deep down in our inner experience. Sometimes we ask people to make a self portrait or a picture of their home to discover new things and access something true.

Then we ask for people to describe their pictures and link the congruent space of the art with what they share.  

 

True Self 

Ginger often uses the phrase “inner child” but I like to describe it as the “true self,” or the core of our being. Living congruently out of the “true self” is when how you imagine yourself lines up with what you do and how you articulate yourself. This is not a new idea, Karen Horney’s Neurosis and Human Growth is my favorite author on this topic.

Learning that we sometimes have hidden this part of ourselves, and then gaining access to it and learning to live by it can be powerful. When we are around people who can give us grace and truth as we progress, we can find this more and more.  

 

Bodyscan (or interception)

Patients who have dealt with trauma often dissociate from their bodies. Even in this era of technology, it’s easy to forget we have bodies. People spend most of their time disconnected, scrolling the internet.

When we experience our body and work through emotions at the same time, it brings us into ourselves and develops congruence.

Ginger likes to ask the following questions when her patient is experiencing a triggering event, to be able to dig down to the root cause of incongruence:

  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.  

 

How to stay congruent during tough circumstances.

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

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

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

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


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

The History and Use of Antipsychotics

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

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

  • Schizophrenia

  • Severe depression

  • Severe anxiety

  • Bipolar disorder

  • Psychosis exhibiting hallucinations and delusions

The history of first generation antipsychotics

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

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

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

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

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

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

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

Second generation antipsychotics

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

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

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

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

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

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

Third generation antipsychotics

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

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

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

Side effects of psychiatric medicines

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

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

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

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

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

The questions to test a patient for akathisia are:

  • Is the person moving? Can they not sit still?

  • What is their internal sense of restlessness and anxiety?

  • How much are they distressed by these feelings?

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

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

The future of antipsychotics

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

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


History of Antipsychotics (notes by Arvy Tj Wuysang).

    • 1933, France

      • Initiative to develop antihistamine as treatment began

    • 1947

      • Promethazine

        • Produced sedation and calmness in animal models

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

    • 1950

      • Discovery of Promethazine Derivatives, especially Chlorpromazine

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

        • Successful in making people calm and indifferent to impending surgery

        • The medication was tried it in a volunteer

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

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

    • 1952

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

        • They were interested in the calming effect of the drug

        • Tried the drug in psychotic agitated patients

          • Treatment options in those days were limited to:

            • Electroconvulsive Therapy

            • Hydrotherapy

            • Insulin coma

          • None of which were antipsychotic in nature

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

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

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

    • 1955

      • Chlorpromazine was approved for usage as antipsychotic in the US

      • Subsequently used worldwide

      • Led to the deinstitutionalization of a lot of psychotic patients

        • Created a problem of lack of follow up of psychotic patients

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

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

      • Led to development of a whole host of antipsychotic agents

    • 1960s

      • There was an explosion in the invention of antipsychotic drugs

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

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

      • Led to the simplistic dopamine hypothesis of psychosis

    • 1958

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

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

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

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

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

    • 1970s

      • 1972, Clozapine usage was introduced in Austria

      • 1974, Clozapine usage was introduced in Germany

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

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

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

        • Must monitor Absolute Neutrophil Count closely when prescribing Clozapine

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

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

    • Clozapine usage in the US today

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

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

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

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

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

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

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

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

      • Akathisia as side effect of antipsychotics

        • Very rarely happens with Clozapine use

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

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

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

          • Objective movement

          • Internal sense of restlessness and anxiety

          • How much are they distressed by these feelings

        • Akathisia is a concerning and common reason for malpractice

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

        • Treatment options for akathisia:

        • 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

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

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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