psychotherapy podcast

The science behind forgiveness and how it affects our mental health

What is forgiveness?

On this week’s episode of the podcast, I talk about the power of forgiveness. It’s scientifically proven that forgiveness can affect our health. As mental health professionals, this has important impacts both personally and professionally. I have also included a downloadable PDF for you to give your patients to help you walk them through the act of forgiving.

As a therapist, when I say the word “forgiveness,” my patients can shut down if I don’t explain it properly. Why? Because just the need for forgiveness is proof that they have been wronged. When we are wronged, it can be hard to let go of that hurt. That’s why I wanted to start out by saying what forgiveness (and this episode) is not about.

Forgiveness is not:

  • It is not approving.

  • It is not excusing the action, denying it, or overlooking it.

  • It is not just moving on (particularly not with cold indifference).

  • It is not forgetting or pretending it did not occur.

  • It is not justifying or letting go of possibly needed justice.

  • It is not calming down.

  • It is not a bargain or negotiation.

  • It is more than ceasing to be angry.

  • It is more than being neutral towards the other.

  • It is more than making oneself feel good.

  • It is one step towards reconciliation, but it is different from reconciliation, which requires a sincere apology from all parties.  

  • It is not dependent on the one you forgive—that would give the other power to control you by keeping you in your bitterness. Consider Corrie Ten Boom, who forgave the Nazis after losing her family in the Holocaust, or Marietta Jaeger who, after her daughter was kidnapped and brutally murdered, was able to forgive. People can forgive, even when the person who wronged them is unknown or dead.

  • It is not a one time event, but may need to be repeated (sometimes the hurt comes back, sometimes you need to start every morning with forgiveness).

  • It is not a restoration of full trust (trust takes time to develop or to be reinstated).

So what is forgiveness?

The Definition of Forgiveness:

Forgiveness is a process. It involves allowing yourself to feel the negative emotions you justly have towards an offense, and really putting the wrong into words in a congruent and authentic truthful way. Then choosing to release it, either giving it to a higher power, or letting it go to a cosmic sense of justice, or earthly legal justice system, and then continuing the process until negative affect is replaced with peace, empathy and compassion. When someone forgives they no longer have a portion of their daily life consumed in negative feelings towards the person or situation.  

“People, on rationally determining that they have been unfairly treated, forgive when they willfully abandon resentment and related responses (to which they have a right) and endeavor to respond to the wrongdoer based on the moral principle of beneficence, which may include compassion, unconditional worth, generosity, and moral love (to which the wrongdoer, by nature of the harmful act or acts, has no right)”  (Enright, 2015).

Elliot (2010) cited Enright and Fitzgibbons (2000) and came up with two types of forgiveness:

Decisional forgiveness: the experience of granting forgiveness without eliminating the emotion, but in this, resentment may continue. It involves a cognitive model where therapist works with the client one time to make decision to forgive.

Emotional forgiveness: the patient must demonstrate changes in emotion and motivation toward their offender.

Studies show that:

Decisional forgiveness can reduce hostility, but it is only marginally effective in improving stress levels or emotional health (Elliot 2010 citing Baskin and Enright 2004, Worthington 2007). This means that emotional forgiveness is the goal of all forgiveness therapy.

What’s the most effective way to help our patients forgive?

Individual therapy that accomplishes Enright’s 4 phases over 20 encounters is “clearly most effective” way to actually accomplish forgiveness. (Elliot 2010 citing Lundahl 2008)

Why should we care about forgiveness?

Forgiveness isn’t a “nice thing to do,” it has real health ramifications that have been thoroughly studied, and it’s a fact that the act of forgiving can be a real change agent in therapy and long term health.

Here are the studies:

  • People who live with depression and a history of maltreatment have an upregulation of their inflammatory response compared to those with no history of maltreatment (Danese et al. 2007 as cited by Elliot 2010)

  • Unforgiveness is reflected in specific cortisol levels, adrenaline production, and cytokine balance (Elliot 2010 citing Worthington 2005)

  • Cause-effect relationship between pain and anger is similar to the anger-depression relationship. some studies show that just the anticipation of pain is associated with anger. (Okifuji 1999)

  • Chronic pain often arises from injury, or accident, thus anger is directed usually at the one responsible, or oneself. (Greenwood 2003)

  • General intensity of anger is important, but also specific targets of anger seem to be essential factors in understanding adaptation to chronic pain. Some research has shown that inward anger is more common in those with chronic pain vs. those individuals with different targets of anger. A study using the MPI (multidimensional pain inventory- a 60 item self reported inventory to assess different aspects of chronic pain) showed that 88 people endorsed anger at themselves and scored 0.38 on the anger inventory. Those that endorsed anger at other targets all scored below 0.30. Anger should be viewed as a multifactorial construct in chronic pain. (Okifuji 1999)

Specifically, in chronic low back pain, a preliminary study of 61 adult patients with chronic low back pain (31 recruited from pain and palliative clinic, and 30 recruited from community) showed patients with higher scores on forgiveness-related variables (‘current level of forgiveness’ as measured by Enright Forgiveness Inventory and ‘forgiveness self efficacy’ as measured by the Forgiveness Self-Efficacy Scale) reported lower levels of pain, anger, and psychological distress.

Patients who scored  (Carson 2005) analysis revealed that “state anger largely mediated associations between forgiveness variables and sensory pain, whereas the association between current forgiveness and affective pain was mostly independent of state anger.”

What is bitterness?

When someone continues to hold on to unforgiveness, they can become what we would call “bitter.” Bitter people are exactly like that word describes—so steeped in resentment that they become unpalatable.

Clues that someone may be bitter:

  • Do they continually replay past hurts over and over?

  • Do they hold onto the pain?

  • Do they try to avoid someone?  

  • Do they quickly get angry with someone?

  • Do they speak trashfully or verbally malign someone?

  • Do they find that their bitterness is more associated with the proximity of the person who wronged them than the magnitude of the event?

  • What percent of their emotional energy is spent on this topic?  

* Recurrent resentment affects all relationships and takes up room in one’s emotional life.

What does research say about bitterness?

  • Ten years or more after a divorce, ½ of women and ⅓ of men are still intensely angry at their former spouses, and anger becomes an ongoing, dominant presence in their children as well (Wallerstein).  

  • Forgiving people have been found to have a lower blood pressure at baseline. (Larsen 2012)

  • “Recalled experiences of betrayal that were less forgiven were associated with greater cardiovascular reactivity as indexed by greater diastolic blood pressure, mean arterial pressure, and rate-pressure product…higher trait forgiveness was negatively associated with lower resting blood pressure and better post-stress recovery.” (Lawler 2005 citing Lawler 2003)

  • Those who measured high in hostility, 20-25 years later, had higher rates of heart disease (Shekelle 1983, Barefoot 1983).

  • When discussing the narrative of injustice, those with an understanding of forgiveness showed less anger expressions (Tina Huang, “Cross Cultural and Real-Life Validation”).

How can someone forgive?

If the previous studies about the negative effects of not forgiving aren’t enough, let’s look at some of the positive effects of forgiving.

Personal health results of forgiving:

  • Changes anxiety into inner peace, reduces symptoms of depression, anger, and paranoia (Dr. R. C. Hunter, 1978).

  • Genuine acts of forgiveness lead to overall improvement in the person’s emotional maturity and increases the capacities for courage, nurturance of others, and love (Dr. Morton Kaufman “The courage to forgive” 1984).

  • Reduces fear. Impulses of anger and revenge subside and are replaced by more appropriate expressions of anger (Dr. Richard Fitzgibbons).

  • Hypertension may be reduced (Huang 1990).

  • Patients with fibromyalgia who were taught forgiveness education had a significant decrease in symptoms (Lee, 2014).

  • Incest survivors showed significant improvement after a 1 year forgiveness education process (Robert Enright, 1994, 1995).

  • A study that looked at 20 psychologically abused and divorced women, some who had remarried and some who had not. All participants scored above 41 on the Psychological Abuse Survey was considered indicative of a present and serious pattern of emotional abuse. Randomized between forgiveness therapy (FT: based on the Enright model) with an alternative treatment (AT: anger validation, assertiveness, interpersonal skill building). The study found that the FT group showed a greater improvement in forgiveness, self-esteem, state anxiety, trait anxiety, depression, environmental mastery, finding meaning, post-traumatic stress symptoms all determined by pre-and post surveys and questionnaires. The FT group had an effect size of 1.79 and represents a shift from below normal levels to normative levels. (Reed 2006)

Spiritual Connection

Some patients highly value their higher power. You can ask them to turn to their spiritual power and ask for the grace to have the willingness to forgive. They can give the spiritual power the opportunity to work in their lives in that way. Some have had powerful forgiveness experiences with their higher power.

Steps in the process of forgiveness:

How can we help our patients forgive those who have wronged them? Sometimes our patients have experienced things that can hurt to even hear about. Helping them move from trauma and anger into a place of forgiveness so they can live a healthy emotional life can be difficult to navigate. But, it is a worthy journey to pursue.

Here are the steps I walk through with my patients using a workbook sheets I have created. I have included a FREE DOWNLOADABLE PDF below that you can give to your patients to fill out. It walks them through the steps in detail, giving them a drawing to fill out and journaling exercises with specific questions to answer that will help them process their trauma and grief.


Further Reading on Forgiveness:

“Forgiveness is a Choice” Enright

Bradley, L. A., McKendree-Smith, N. L., Alberts, K. R., Alarcón, G. S., Mountz, J. M., & Deutsch, G. (2000). Use of neuroimaging to understand abnormal pain sensitivity in fibromyalgia. Current Rheumatology Reports, 2, 141–148.  

Brand BL, Alexander PC. “Coping with incest: the relationship between recollections of childhood coping and adult functioning in female survivors of incest.” J Trauma Stress. (2003):185–93.

Enright, R. D. Forgiveness is a choice. (2001) Washington, DC: American Psychological Association.

Fernandez, Ephrem, and Dennis C. Turk. "The Scope and Significance of Anger in the Experience of Chronic Pain." Pain (1995) 61(2):165-75.

Greenwood K, Thurston R, Rumble R, Waters S, Keefe F. Anger and persistent pain: Current status and future directions. Pain. (2003);103:1–5.

Knight JR, Hugenberger GP. On Forgiveness. Southern Medical Journal. (2007). 100(4):420-421.

Larsen BA, Darby RS, Harris CR, Nelkin DK, Milam PE, Christenfeld NJ. The immediate and delayed cardiovascular benefits of forgiving. Psychosom Med. (2012) Sep;74(7):745-50.

Lawler, K. A., Jarred W. Y., Rachel L. Piferi, Rebecca L. Jobe, Kimberley A. E, and Warren H. J. The Unique Effects of Forgiveness on Health: An Exploration of Pathways. J Behav Med Journal of Behavioral Medicine (2005). 28(2): 157-67. Web.

Lee YR, Enright RD. “A Forgiveness Intervention for Women With Fibromyalgia Who Were Abused in Childhood: A Pilot Study.” Sprituality in Clinical Practice. (2014). 1(3):203–217

Lichtenfeld S, Buechner VL, Maier MA, Fernandez-Capo M. Forgive and Forget: Differences between Decisional and Emotional Forgiveness.PLoS One. (2015) May 6;10(5):e0125561.

Moons, Wesley G., Naomi I. Eisenberger, and Shelley E. Taylor. "Anger and Fear Responses to Stress Have Different Biological Profiles." Brain, Behavior, and Immunity (2010) 24(2):215-19.

Muscatello MR, Bruno A, Scimeca G, Pandolfo G, Zoccali RA. “Role of negative affects in pathophysiology and clinical expression of irritable bowel syndrome.” World J Gastroenterol.2014;20:7570–7586.

Okifuji A, Turk DC, Curran SL. Anger in chronic pain: investigations of anger targets and intensity. J Psychosom Res. 1999;47(1):1–12.

Reed GL, Enright RD. The Effects of Forgiveness Therapy on Depression, Anxiety, and Posttraumatic Stress for Women After Spousal Emotional Abuse. Journal of Consulting and Clinical Psychology. (2006). 74(5):920 –929.

Schmidt S, Grossman P, Schwarzer B, Jena S, Naumann J, Walach H. “Treating fibromyalgia with mindfulness-based stress reduction: results from a 3-armed randomized controlled trial.” Pain. (2011).152(2):361–9.

Strang S., Utikal V., Fischbacher U., Weber B., Falk A. “Neural correlates of receiving an apology and active forgiveness: an fMRI study.” PLoS ONE. 9:e87654 (2014). 10.137.

White, JM. “Pleasure Into Pain: The consequences of long-term opioid use.” Addictive Behaviors. (2004). 29:(1311-1324).

Winfield JB. Psychological determinants of fibromyalgia and related syndromes. Curr Rev Pain. 2000. 4(4):276-86.

Witvliet CVO, Phipps KA, Feldman ME. Beckham JC. “Posttraumatic mental and physical health correlates of forgiveness and religious coping in military veterans.” J. Trauma Stress. (2004) 17:269–273.





Psychiatric Approach to Delirium with Dr. Timothy Lee

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This week on the podcast, I am joined by Dr. Timothy Lee, the Loma Linda residency program director and the head of medical consult and liaison services. One of his specialities is delirium, so this week we will be discussing both hypoactive and hyperactive delirium.  

What is delirium?

Delirium is an acute change in a person’s sensorium (the perception of one’s environment or understanding of one’s situation). It can include confusion about their orientation, cognition or mental thinking.

With hyperactive delirium, a patient can become aggressive, violent and agitated with those around them. A patient experiencing delirium can have hallucinations and hear things, they can become paranoid, and they are overall confused. A family, or non-psychiatric medical staff, might be concerned that the patient is experiencing something like schizophrenia.

Hyperactive delirium symptoms in patients:

  • Waxing and waning—it comes and goes

  • Issues with concentration

  • Pulling out medical lines

  • Yelling profanities

  • Throwing things

  • Agitated

  • Responding to things in the room that aren’t there

  • Not acting like themselves

Hypoactive delirium is much more common than hyperactive delirium (based on research studies), but it is often missed because the presentation is much less dramatic. People with hypoactive delirium are confused and disoriented, but they do not express their confusion verbally or physically.

Hypoactive delirium symptoms:

  • Slower movement

  • Softer speech

  • Slower responses

  • Withdrawn

  • Not eating as much

Often, nurses and physicians can miss the fact that the patient has the typical confusion that denotes delirium because the patient is quieter, so it doesn’t come to the attention of the medical team or psychiatrist consult service.

Delirium can even be confused for depression. One Mayo Clinic study showed that when consulting a doctor about their depression, 67% of the time, the patient ended up having delirium.

Why does delirium happen?

Often we see it happen, even to relatively healthy people, in physically stressful situations—post surgery, during an acute illness, or even just being stuck in the hospital for a few days. This does not mean it is indicative of a sudden onset of a long term mental illness, such as schizophrenia.

To consider what can cause delirium, I like to think systematically from the top of the body and work my way down. This is by no means exhaustive, but it can be helpful.

Many things can cause delirium. I like to think about starting at the top of the body and going down, as a way to not miss the cause. Here are a few we would consider as we go down the body:

  • Stroke—check strength in both arms and legs, have the patient smile

  • Hypertensive emergency

  • Infection or meningitis

  • Physical trauma—concussion, head injury with initial loss of consciousness, then after regaining consciousness they can have delirium

  • Brain bleeding

  • Medications that affect the brain, such as ones that produce anticholinergic side effects. (They suppress acetylcholine, causing brain imbalances and confusion. Anti-allergy medicines, pain medications, and some psychiatric medications are anticholinergic.)

  • Circulatory issues

  • Thyroid imbalances or parathyroid hormones

  • Cancer

  • Heart attack

  • Traumatic injury to the heart

  • Aspiration pneumonia

  • Lung infection

  • Lung cancer

  • Viral pneumonia

  • Pancreatic inflammation

  • Urinary tract infections in women

  • Liver cirrhosis

  • Hepatitis

  • Gallbladder inflammation

  • Low bilirubin

  • Hepatic encephalopathy

How do we identify delirium in a patient?

Asking certain questions to the patient and/or medical team and family can help us understand if the patient is experiencing delirium. Often, a patient experiencing delirium will still know where they are, what they are doing, and who they are. The main test to really determine if it’s delirium is the “clock drawing” where we ask the patient to draw a clock with the hands showing 11:10.

Here are some questions and tasks we ask the patient to answer and perform to test for delirium:

  • Does the person know who they are?

  • Does the person know where they are?

  • In what detail does the person understand where they are?

  • Does the person know the date?

  • Can they orient to the situation? Do they know why they are there and the circumstances that led to them being in the hospital?

  • We might ask the patient to repeat back a few words for us.

  • We will ask them later if they remember the three words we asked previously.

  • We test for concentration, like asking the days of the week in reverse order.

  • We try to assess their visual and spatial ability.

  • We might ask them to draw a clock to look for spacing, impairments, or difficulties.  

Some tests that are common to determine delirium are:

  • The Mini Mental Status Exam (MMSE)

  • The Montreal Cognitive Assessment

How to help

It is important, if the patient has loved ones with them, to educate the family about delirium, because both hypoactive and hyperactive delirium can be terrifying to watch.

When it comes to giving medications, it’s important to follow a few rules, Dr. Lee says. Giving medications with anticholinergic side effects can make the patient more agitated. When prescribing meds, be careful not to switch from a hyperactive delirium presentation to a hypoactive delirium presentation by just sedating the patient but maintaining confusion. Medications like benzodiazepine, barbiturates, sedatives and pain medications (beyond what is needed for pain) can all cause worsening of delirium.

If the confusion is from an infection, an antibiotic should eventually help the cause of the delirium, however it may take a few days for the confusion to improve after the cause is eliminated.  At times antipsychotic medications are used to help the delirium and reduce the time needed to stay in the hospital.

Even after the cause of the delirium is gone, and the delirium seems to have improved very quickly, a person may still have lingering cognitive issues. It’s important to be conservative in terms of how quickly you taper them off of the antipsychotic medication used to treat the delirium.





Therapeutic Alliance Part 1

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What is a therapeutic alliance?

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

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

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

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

Why do we care?

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

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

What builds a therapeutic alliance?

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

Expertness

  • Facilitating a greater level of understanding

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

Consistency

  • Structuring your office to run on time.

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

Non-verbal gestures

  • Eye contact

  • Leaning forward

  • Mirroring of emotion occurs naturally when people pay attention to emotion

Maintenance of the therapeutic frame

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

Empathy, attunement, positive regard

  • Patient: “Therapist is both understanding and affirming."

  • Patient: “Therapist adopts supportive stance.

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

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

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

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

Foundational concepts of the therapeutic alliance

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

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

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

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

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

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

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

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

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

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

On Listening: An Active Process

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

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

  • Point out common patterns you hear.

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

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

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

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

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

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

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

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

  • Listen to their moment to moment change in emotions.

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

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

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

    • Shame- patient looks down

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

      • Perhaps as you talk about this you feel…”

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

    • Anger/Frustration:

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

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

    • Sadness

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

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

    • Disgust

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

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

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

    • Fear

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

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

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

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

How do you create and maintain a working alliance:

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

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

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

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

  • “When did you feel we were communicating meaningfully?”  

  • “When were you feeling disappointed?”

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

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

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

For example:  

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

Patient: "He was kind of a jerk."  

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

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

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

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

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

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

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

How to Treat Emotional Trauma

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

What is trauma?

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

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

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

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

People commonly demonstrate symptoms of trauma when they’ve:

 

  • Experienced a sexual violation

  • Seen violence

  • Experienced violence or abuse

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

  • Been in near death experiences like car accidents or war

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

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

  • Fight and flight symptoms are:

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

  • Shut down symptoms are:

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

  • Moments in connection mode look like:

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

 

Body movement and trauma

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

Humans work the same way.

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

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

 

Attachment based trauma

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

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

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

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

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

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

 

Notes to therapists on dealing with PTSD

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

Displaying emotional stability

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

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

Receiving feedback

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

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

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

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

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

Know when to limit the stress

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

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

Emotional connection

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

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

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

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

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

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

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

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

  • What did you see?

  • What did you feel emotionally?

  • What did your body experience?

  • What do you believe about yourself as a result?

Allow for freedom

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

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

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

Summary  

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

 

The History and Nuances of Bipolar Illness

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

The history & nuances of bipolar illness

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

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

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

Nuances of the bipolar illness diagnosis

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

Here are some defining symptoms:

  • Patients are fairly normal between episodes.

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

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

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

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

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

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

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

Bipolar and the limbic system

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

 Bipolar illness and sleep patterns

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

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

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

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

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

Genetic markers of bipolar illness.

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

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

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

Mood 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.

    1. 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.

    2. 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.

    1. 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.

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

The History, Mechanism and Use of Antidepressants

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

 

What is depression?

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

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

  • Psychotic depression

  • Bipolar disorder with depression

  • Seasonal affective disorder

  • Major depression

  • Chronic depression (dysthymia)

  • Postpartum depression

  • Premenstrual dysphoric disorder

  • Atypical depression

  • Melancholic depression

  • Depression due to a medical illness or medication

Some symptoms of depression are:

  • Weight gain or loss

  • Sadness

  • Anxiety

  • Agitation

  • Social isolation

  • Sleep problems

  • Guilt

  • Loss of pleasure

  • Loss of interest in activities

  • Mood swings

Major depression

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

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

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

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

Melancholic depression

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

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

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

Is depression a chemical imbalance?  

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

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

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

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

The history of antidepressants

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

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

Before antidepressants

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

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

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

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

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

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

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

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

First generation antidepressants

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

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

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

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

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

SSRI antidepressants

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

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

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

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

SSRI was also found to be effective for:

  • Post traumatic stress disorder (PTSD)

  • Obsessive compulsive disorder (OCD)

  • Generalized anxiety disorder (GAD)

  • Social phobias

  • Impulse based disorders (like binge eating)

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

When do you prescribe antidepressants?

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

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

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

  • Psychotherapy does not seem to be helping

  • The depression is becoming severe

  • Their family is genetically tended towards depression

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

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

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


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

  • History of Antidepressants

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

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

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

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

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

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

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

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

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

      • Psychotherapy, psychoanalysis

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

  • The advent of SSRIs

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

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

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

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

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

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

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

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

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

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

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

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

    • Increased anxiety in the early stages of SSRI usage.

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

    • Panic Disorders

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

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

    • Use of Chlomipramine in OCD

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

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

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

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

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

      • Moving to a mixed mechanism agent will help fix that. Use of Buproprion, which is mostly noradrenergic, can sometimes reverse that effect of the SSRI. More recently, there is now a SSRI (vilazodone) that also is a partial agonists for the 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

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“Polyvagal Theory Simplified”

By David Puder, M.D.

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

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

Why is polyvagal theory important?

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

  • Understanding trauma and PTSD

  • Understanding the dance of attack and withdrawal in relationships

  • Understanding how extreme stress leads to dissociation or shutting down

  • Understanding how to read body language

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

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

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

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

A story about a gazelle...

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

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

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

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

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

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

Here's how they work...

Connection Mode

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

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

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

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

How does this look and feel?

  • Our immune system is healthy.

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

  • We are sleeping well and eating normally.

  • Our face is expressive.

  • We emotionally relate to others.

  • We more easily understand and listen to others.

  • Our body feels calm and grounded.

 

Freeze, Flight, Fight, or Puff Up

...or the sympathetic nervous system response

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

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

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

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

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

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

  • We feel anxious, afraid, or angry.

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

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

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

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

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

  • Our hands may be clammy.  

  • Our stomach may be painfully knotted.

  • All our senses focus.   

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

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

Shut Down

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

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

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

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

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

How does this look and feel?

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

  • Our eyes may look fixed and spaced out

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

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

  • We may feel low or no pain

  • Our lungs (bronchi) constrict and we breathe slower

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

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

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

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

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

  • Dialectical behavioral therapy

  • Mentalization based therapy

  • Transference focused therapy

How trauma affects the nervous system

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

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

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

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

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

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

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

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

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

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

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

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

Coming out of shutdown mode

So how do we climb back out of shutdown mode?

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

 

The Psychology of Procrastination

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

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

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

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

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

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

The Psychology of Procrastination

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

What is procrastination?

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

You might be procrastinating when:

  • There is a gap between your intention and action

  • You feel like avoiding something

  • You find yourself  easily distracted

  • You feel overwhelmed by tasks at the last minute

  • You always feel rushed to complete a project

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

It usually brings about feelings of:

  • Shame

  • Guilt

  • Anxiety

  • Regret

  • Anger

  • Inauthenticity

Why do we procrastinate?

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

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

The ingredients for procrastination


Personal Factors of Procrastination

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

The fixed personal factors are:

  • Higher Impulsivity

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

  • Limited attention-span

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

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

The variable personal factors are:

  • Willpower

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

  • Distress tolerance

  • Willingness to ask for help

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

  • Task-focused vs value-focused

  • Self-consciousness & anxiety

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

The variable task or system-based factors are:

  • Unclear goals & expectations

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

  • Unrealistic goals & expectations

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

  • Distractions

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

  • Lack of accountability or mentors

Procrastination thrives in secrecy and isolation.

How do we procrastinate?

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

“I work better under pressure.”

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

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

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

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

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

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

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

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

How do we stop procrastinating?

Admit it

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

Catch the cognitive distortions

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

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

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

  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.

 

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