psychiatry podcasts

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.





What is psychodynamic theory?

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

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

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

The history of psychodynamic therapy

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

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

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

Affect

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

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

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

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

Transference

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

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

Countertransference

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

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

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

Studies that show psychodynamic theory works:

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

Mentalization-based therapy

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

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

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

Transference Based Therapy:

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

In conclusion

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



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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