Where do we get the idea to eat or have sex? Maybe we don't. As Pinker argues, we're not a blank slate. Perhaps the impulse to engage in self-injury when under extreme emotional distress is also inborn.
We are starting to understand the havoc stress wreaks on the body. We are also starting to understand the strong endogenous physiological calming effect self-injury prompts. In this context, I wonder if self-injury acts almost like an inoculation - when given a small amount of manageable physical adversity, the body's soothing and contentment system is able to overcompensate and fortify itself. Maybe the body intuitively knows to default to self-injury under periods of stress because there are dramatic and sudden decrease anxiety due to increases in endogenous calming agents, being that stress is particularly harmful to the body. [There's something about stress triggering autoimmune diseases here that should be looked at. Perhaps it isn't a coincidence that Benadryl can be used both as an antianxiety as well as an antihistamine.]
After all, humans are not the only animals that engage in self-injury (e.g. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2486411/). My first published study (cited in TIME here) mentions that a certain percentage of people report getting the idea to engage in self-injury from an outside source; however, the other side of that is that some people report never having learned the idea from anyone. Perhaps it is, in fact, an inborn impulse we have that is defaulted to in times of stress because it is protective to the body against stress. This is not to say, of course, that some people don't get the idea to cut from other people. Surely this must be the case. But what about the people who spontaneously start cutting without outside influence? How can that be explained?
I'm beginning to think that the impulse to hurt oneself is a hardwired fail-safe.
Tuesday, July 19, 2011
Sunday, April 17, 2011
Is Multiple Personality Disorder Real?
Although it is very rare, early in my career I met two (different) people with Dissociative Identity Disorder (DID; formerly known as Multiple Personality Disorder). The first person I met with DID was a patient at a clinic in Harvard Square, where I was conducting research. Over the course of my two years there, I watched her slowly unravel from displaying one personality to many. By the time I left, she had the voice and demeanor of a seven year old child. Frankly, witnessing this was quite unsettling.
The second person I met with DID was in the psychiatric emergency room at Massachusetts General Hospital, where I was working on another study. I remember the conversations amongst the staff about her case well - some thought she was faking it, while some thought a diagnosis of DID was legitimate.
In short, this is what I think:
People with Borderline Personality Disorder, which is characterized by self-injury, suicide attempts, extreme mood swings, and stormy relationships also has another very important feature that is often less discussed - identity disturbance. Basically, very different personae are displayed depending on the situation. As Kiera Van Gelder describes in The Buddha and The Borderline, a memoir about recovery from this disorder, she would be a hippie one day and a goth the next if it would get her the sexual attention she wanted. In other words, she would drastically change her personality from day to day (in this case, it was for social approval).
The problem is this: A therapist looking at someone who is a goth one day and a hippie the next might conclude that these are just various forms of the self that need to be expressed. (Yikes!)
While chameleoning can be viewed as adaptive in a sense, the person with BPD / identity disturbance seems to be paying little attention to whether or not they actually enjoy a given activity they are engaging in for social approval. Often, people use these different personae as a tool - and a tool only. The who acts as a hippie today has no real affinity for hippie culture in itself. Expression of one's "hippie side" is resoundingly not to be encouraged.
Introducing certain types of therapy that emphasize different parts of the self to people who already have identity disturbance, may cause further polarization. The patient may be reinforced for behaving in certain ways and expressing themselves from various personalities. Hence, the development of DID. Without a question in my mind, this is what happened with the first patient with DID I watched unravel - she initially had a diagnosis of Borderline Personality Disorder (w/ the identity disturbance feature) - and in two years time (after "parts therapy") she had multiple personalities.
People with identity disturbances crave belonging and unity of their behaviors by definition. Slapping a label of DID on someone who is desperately trying to figure out who they are is dangerous. The person knows that a lot effort needs to be put in to establish a sense of self. These uncharted territories of not living for social approval are scary. This unifying label is an excuse to avoid all the anxiety that will come with establishing a sense of self. It is easier to exaggerate the different forms of self that already exist and diverge further.
In the effort to display many personalities, a unifying role of being an interesting patient is maintained.
While the presentation of someone having several personality disorders is certainly real, I highly doubt this is organic. It seems to me that this disorder is related to the same underlying identity disturbance seen in Borderline Personality Disorder. In fact, I'd be willing to bet that a very large number of DID cases are really Borderline cases gone horribly astray due to treatment with talk therapies that have not been supported by research.
I'd also like to add that after having worked with people who have schizophrenia, there is a definite psychotic flavor to DID as well. My gut feeling is that the core underlying feature is the identity disturbance seen in BPD on top of a psychotic tendency to believe what the mind is constructing. It is these two underlying features that combine to the expression of different personalities. In no way do I think there are actually two different personalities encased in one person. In short, I'd reason that DID is simply a specific form psychosis with the core BPD component of identity disturbance.
In treatment, instead of focusing on expression of various external presentations, focus should be on developing a sense of self. Figuring out what the person likes independent from the approval or opinions of others seems vital.
Lastly, unlike depression or anxiety, there is an ego-syntonic feel to multiple personality disorder. In other words, people like having the disorder to some degree and want to continue any associated dysfunctional behavior. Another example of ego-syntonic disorders would be anorexia, where people typically want to continue restricting food intake. In the case of DID, people want to keep their multiple personalities, as they are potentially useful in different circumstances. As such, the expression of different personalities should be particularly discouraged by all staff members at a facility once rapport has been developed and treatment is underway.
The second person I met with DID was in the psychiatric emergency room at Massachusetts General Hospital, where I was working on another study. I remember the conversations amongst the staff about her case well - some thought she was faking it, while some thought a diagnosis of DID was legitimate.
In short, this is what I think:
People with Borderline Personality Disorder, which is characterized by self-injury, suicide attempts, extreme mood swings, and stormy relationships also has another very important feature that is often less discussed - identity disturbance. Basically, very different personae are displayed depending on the situation. As Kiera Van Gelder describes in The Buddha and The Borderline, a memoir about recovery from this disorder, she would be a hippie one day and a goth the next if it would get her the sexual attention she wanted. In other words, she would drastically change her personality from day to day (in this case, it was for social approval).
The problem is this: A therapist looking at someone who is a goth one day and a hippie the next might conclude that these are just various forms of the self that need to be expressed. (Yikes!)
While chameleoning can be viewed as adaptive in a sense, the person with BPD / identity disturbance seems to be paying little attention to whether or not they actually enjoy a given activity they are engaging in for social approval. Often, people use these different personae as a tool - and a tool only. The who acts as a hippie today has no real affinity for hippie culture in itself. Expression of one's "hippie side" is resoundingly not to be encouraged.
Introducing certain types of therapy that emphasize different parts of the self to people who already have identity disturbance, may cause further polarization. The patient may be reinforced for behaving in certain ways and expressing themselves from various personalities. Hence, the development of DID. Without a question in my mind, this is what happened with the first patient with DID I watched unravel - she initially had a diagnosis of Borderline Personality Disorder (w/ the identity disturbance feature) - and in two years time (after "parts therapy") she had multiple personalities.
People with identity disturbances crave belonging and unity of their behaviors by definition. Slapping a label of DID on someone who is desperately trying to figure out who they are is dangerous. The person knows that a lot effort needs to be put in to establish a sense of self. These uncharted territories of not living for social approval are scary. This unifying label is an excuse to avoid all the anxiety that will come with establishing a sense of self. It is easier to exaggerate the different forms of self that already exist and diverge further.
In the effort to display many personalities, a unifying role of being an interesting patient is maintained.
While the presentation of someone having several personality disorders is certainly real, I highly doubt this is organic. It seems to me that this disorder is related to the same underlying identity disturbance seen in Borderline Personality Disorder. In fact, I'd be willing to bet that a very large number of DID cases are really Borderline cases gone horribly astray due to treatment with talk therapies that have not been supported by research.
I'd also like to add that after having worked with people who have schizophrenia, there is a definite psychotic flavor to DID as well. My gut feeling is that the core underlying feature is the identity disturbance seen in BPD on top of a psychotic tendency to believe what the mind is constructing. It is these two underlying features that combine to the expression of different personalities. In no way do I think there are actually two different personalities encased in one person. In short, I'd reason that DID is simply a specific form psychosis with the core BPD component of identity disturbance.
In treatment, instead of focusing on expression of various external presentations, focus should be on developing a sense of self. Figuring out what the person likes independent from the approval or opinions of others seems vital.
Lastly, unlike depression or anxiety, there is an ego-syntonic feel to multiple personality disorder. In other words, people like having the disorder to some degree and want to continue any associated dysfunctional behavior. Another example of ego-syntonic disorders would be anorexia, where people typically want to continue restricting food intake. In the case of DID, people want to keep their multiple personalities, as they are potentially useful in different circumstances. As such, the expression of different personalities should be particularly discouraged by all staff members at a facility once rapport has been developed and treatment is underway.
Sunday, March 13, 2011
Sex - Benefits of Talk Therapy Over Medication
Unlike stereotypical versions of talk therapy where a doctor claims you want to have sex with your mother, a newer treatment called Cognitive Behavioral Therapy (CBT), has been shown by plenty of studies to actually work.
Not only that, it changes your biology. Unlike other talk therapies, this type of treatment involves active learning and homework. As such, it can cause beneficial increases in the size of your brain that controls complex thinking - the cerebral cortex. In fact, CBT has also been shown to be just as effective as medication, just with longer lasting effects.
I would imagine that CBT continues to be beneficial after ending treatment because the time was taken over numerous sessions to rewire the brain. On the other hand, medication may act more by forcing it to function differently for a short period of time. Many drugs also come with a lot of negative side effects.
Unlike a lot of depression medications, CBT just doesn't numb your sexual experience. As Kiera Van Gelder so eloquently describes in her fantastic recovery memoir, The Buddha and The Borderline: "Sometimes when I see his body or smell his scent, I want to consume him with all of my senses. Then, when we meet skin on skin, it's like hitting a thick glass wall. 'It's the medication.' I tell him."
Although it may be advisable for some people to be on medication while in CBT, if you are choosing between talk therapy and drugs, make sure to do your homework. Trying a CBT therapist before medication might be a favorable option for you.
For more posts, check out The Psychology Easel and follow me on Twitter at @TaraDeliberto.
Not only that, it changes your biology. Unlike other talk therapies, this type of treatment involves active learning and homework. As such, it can cause beneficial increases in the size of your brain that controls complex thinking - the cerebral cortex. In fact, CBT has also been shown to be just as effective as medication, just with longer lasting effects.
I would imagine that CBT continues to be beneficial after ending treatment because the time was taken over numerous sessions to rewire the brain. On the other hand, medication may act more by forcing it to function differently for a short period of time. Many drugs also come with a lot of negative side effects.
Unlike a lot of depression medications, CBT just doesn't numb your sexual experience. As Kiera Van Gelder so eloquently describes in her fantastic recovery memoir, The Buddha and The Borderline: "Sometimes when I see his body or smell his scent, I want to consume him with all of my senses. Then, when we meet skin on skin, it's like hitting a thick glass wall. 'It's the medication.' I tell him."
Although it may be advisable for some people to be on medication while in CBT, if you are choosing between talk therapy and drugs, make sure to do your homework. Trying a CBT therapist before medication might be a favorable option for you.
For more posts, check out The Psychology Easel and follow me on Twitter at @TaraDeliberto.
Saturday, March 12, 2011
Thoughts on Secret Fears of the Super Rich
by Tara Deliberto
I came across this article "Secret Fears of the Super Rich," and thought it was pretty interesting. I posted a link to it in an online forum, and one of the readers responded with this Ayn Rand quote: "Only the man who does not need it, is fit to inherit wealth, the man who would make his fortune no matter where he started."
Here are my brief thoughts on this marvelous quote from a psychological perspective:
Being in my line of work, I'm acutely aware of the fact that people need to build their own sense of mastery. Without mastery, feelings of helpless set in and a general lack of motivation is fostered. Translated into clinical terms, people become depressed and anxious. So perhaps if an individual is given everything, their sense of mastery can be diminished because they have not had to take opportunities to succeed on their own.
There are several possible reasons why these opportunities are not taken. For one, when the bar is set so high by a family member who built a fortune, it may be too frightening to even approach success. It is seems safer not to attempt anything at all and live a comfortable life. But is it better for one's own well being to never have tried?
While fear of failure might drive this behavior, the possibility also exists that it is that once wealth is attained or inherited, there may simply be no perceived need to achieve. Perhaps if the same person who inherits wealth and chooses not to engage in tasks to build mastery is put under real pressure, he or she might very successfully build resources. But without ever needing to, attempts are not made to earn one's own living.
In short, I'm conceptualizing two paths, the first would be an anxiety-avoidance path while the second is a contentment/maintenance path.
Whether or not they want to, people who inherit money may benefit from continually engaging in mercenary tasks where failure is possible along with adopting an accepting attitude that they may never achieve at the level of their family members. The idea is that when any amount of success is achieved, their own sense of mastery may increases, motivation can ignite, and life many feel more purposeful.
I think this idea fits nicely w/ Ayn Rand's - one needs to be motivated to achieve for their own sense of self-worth. Sometimes having an inheritance can take away one's own sense of importance while increasing entitlement. While importance and entitlement are often linked, perhaps they are very different constructs. While a person may not view themselves as being meaningfully able to contribute to the world (importance), they may think they deserve everything (entitlement).
I came across this article "Secret Fears of the Super Rich," and thought it was pretty interesting. I posted a link to it in an online forum, and one of the readers responded with this Ayn Rand quote: "Only the man who does not need it, is fit to inherit wealth, the man who would make his fortune no matter where he started."
Here are my brief thoughts on this marvelous quote from a psychological perspective:
Being in my line of work, I'm acutely aware of the fact that people need to build their own sense of mastery. Without mastery, feelings of helpless set in and a general lack of motivation is fostered. Translated into clinical terms, people become depressed and anxious. So perhaps if an individual is given everything, their sense of mastery can be diminished because they have not had to take opportunities to succeed on their own.
There are several possible reasons why these opportunities are not taken. For one, when the bar is set so high by a family member who built a fortune, it may be too frightening to even approach success. It is seems safer not to attempt anything at all and live a comfortable life. But is it better for one's own well being to never have tried?
While fear of failure might drive this behavior, the possibility also exists that it is that once wealth is attained or inherited, there may simply be no perceived need to achieve. Perhaps if the same person who inherits wealth and chooses not to engage in tasks to build mastery is put under real pressure, he or she might very successfully build resources. But without ever needing to, attempts are not made to earn one's own living.
In short, I'm conceptualizing two paths, the first would be an anxiety-avoidance path while the second is a contentment/maintenance path.
Whether or not they want to, people who inherit money may benefit from continually engaging in mercenary tasks where failure is possible along with adopting an accepting attitude that they may never achieve at the level of their family members. The idea is that when any amount of success is achieved, their own sense of mastery may increases, motivation can ignite, and life many feel more purposeful.
I think this idea fits nicely w/ Ayn Rand's - one needs to be motivated to achieve for their own sense of self-worth. Sometimes having an inheritance can take away one's own sense of importance while increasing entitlement. While importance and entitlement are often linked, perhaps they are very different constructs. While a person may not view themselves as being meaningfully able to contribute to the world (importance), they may think they deserve everything (entitlement).
Friday, March 4, 2011
Does A Therapist Judges You?
Today I received a question from a man in Mumbai asking if I went into being a psychologist so I could be in a position to judge people. He expressed the sentiment that everyone must understand that we are in no place to judge others and that he prefers a live at let live philosophy.
Here's my response:
Thanks for the post. Since many people share your opinion, I think this question is particularly important to address.
I can understand that without an introduction to the type of treatment I practice, one may assume therapists just want to judge people. In fact, it is just the opposite! People come into my office with a series of judgments about themselves that we work together to debunk. I've seen people who have made wonderful contributions to society but seem to think that they are completely worthless. My job is simply to neutralize judgments. We help people to stop harshly judging themselves so that they can function better and suffer less.
While many people are not in need of treatment, I'm afraid that many people are seriously troubled and on the fence abut whether or not they should end their own lives. With suicidal people, a live and let live philosophy wouldn't exactly work out. And just because someone is contemplating suicide, does not make them worthless and deserving to die, it just means they are suffering from what can feel like a tortured internal experience. They come to treatment of their own volition because there is a piece of them that wants to get better. Therapists don't force clients into treatment.
There have been many research studies on the type of therapy I do showing that the techniques are in fact useful in helping people build a life worth living. Therapy, when practiced well, is much more than a series of judgments - it is an effective way to retrain people's thoughts and behaviors.
Here's my response:
Thanks for the post. Since many people share your opinion, I think this question is particularly important to address.
I can understand that without an introduction to the type of treatment I practice, one may assume therapists just want to judge people. In fact, it is just the opposite! People come into my office with a series of judgments about themselves that we work together to debunk. I've seen people who have made wonderful contributions to society but seem to think that they are completely worthless. My job is simply to neutralize judgments. We help people to stop harshly judging themselves so that they can function better and suffer less.
While many people are not in need of treatment, I'm afraid that many people are seriously troubled and on the fence abut whether or not they should end their own lives. With suicidal people, a live and let live philosophy wouldn't exactly work out. And just because someone is contemplating suicide, does not make them worthless and deserving to die, it just means they are suffering from what can feel like a tortured internal experience. They come to treatment of their own volition because there is a piece of them that wants to get better. Therapists don't force clients into treatment.
There have been many research studies on the type of therapy I do showing that the techniques are in fact useful in helping people build a life worth living. Therapy, when practiced well, is much more than a series of judgments - it is an effective way to retrain people's thoughts and behaviors.
Acceptance and Commitment Therapy is Officially Listed as Effective!
Great news! The United States Substance Abuse and Mental Health Services Administration (SAMHSA) has now listed Acceptance and Commitment Therapy (ACT), a therapy I practice that is based on Eastern Mindfulness techniques, as an official treatment that has been shown by research to work!!
This is part of SAMHSA'sNational Registry of Evidence-based Programs and Practices (NREPP). What a wonderful initiative. Bravo.
http://174.140.153.167/ViewIntervention.aspx?id=191&
This is part of SAMHSA'sNational Registry of Evidence-based Programs and Practices (NREPP). What a wonderful initiative. Bravo.
http://174.140.153.167/ViewIntervention.aspx?id=191&
The Relationship between Negative Thoughts & Serotonin
I'm happy to be a member of an online community where some intellectual forum discussions are generated. In this setting, a question was posed to me pertaining to the relationship between negative thinking and serotonin from Scott in Auckland. Since other people may be curious about the same topic, I thought I'd post my response here.
Reply:
I absolutely love this question! The interplay between what we do as psychologists and biology is one of my favorite topics. How we are trained through all of our collective learning experiences to think - and more specifically, appraise, evaluate, and interpret - has a direct effect on our physiology and biology.
For those of you not familiar with Cognitive Behavioral Therapy (CBT) it involves very active Socratic questioning on the therapists part about thoughts the patient currently has. This type of therapy is in stark contrast to old-fashioned Freudian type therapies that mainly just involve combing over events of your past. If a patient comes into my office and says "I'm a loser," my response would be "Oh, yeah? It must stink to think that. But what is the evidence that you're a loser?... Have you ever won anything?... Even if you are a loser now - whatever that means - will you always be a loser?" etc.
After all this questioning, we usually end up laughing together about what I ridiculous statement "I'm a loser" really is and how true it can feel. Through this process, the rift between what our mind thinks and what is actually true is created. After the initial separation between thought and belief is fostered, we go come up with rational responses to these types of negative automatic thoughts like "I'm a loser" and practicing mentally rehearsing the rational responses as homework.
So, that is a brief description of the cognitive piece of cognitive-behavioral therapy. Interestingly, the behavioral piece has been shown to be more effective than the cognitive piece at changing the interpretation of thoughts. Let's take, for example, someone who has social phobia. You can tell them that their phobia of talking to other people is silly all you want, but they still may not believe you. The best thing to do is act.
We start small. I might grab the secretary into the therapy room and ask her to have a 5 minute conversation about something like traveling with the patient. After five minutes, the secretary says it was lovely chatting and leaves. Now, that wasn't so bad was it?
Then as homework assignments, the patient is to engage in social activities, starting with a small anxiety producing task, and working their way up to doing something very scary like public speaking, over the course of weeks. In this way, their own thoughts are directly challenged by the outcome of their behavior. They always think it will be worse than it ends up being. In this way, they engage in little "behavioral experiments" that directly test their maladaptive beliefs.
It is worth noting here that while the behavioral piece has been shown to be more effective, people may not be willing to engage in the behavioral piece without both a strong rationale for it. It is my opinion that going through the cognitive part of the therapy and disputing thoughts that automatically pop up is an extremely useful first step that must be taken with a vast majority of people before jumping into the behavioral piece. In fact, a client of mine expressed this sentiment completely of her own accord to me today.
While we have discussed both the cognitive and the behavioral piece at this point, there is a third very important piece that changes our relationship to our thoughts - Eastern mindfulness practice. Learning to be aware of our thoughts and release the less useful ones is extraordinarily helpful as well. As a side note, I practice letting go of thoughts every day during yoga, which I use as a moving meditation more than exercise. '
I'll talk more later about integrating these components of treatment, but for now, back to your question! There have been many studies showing that CBT is as useful as treating depression as antidepressants; however, CBT has the added effect of continuing to work even after treatment ends. In terms of whether or not it increases serotonin in the synapse, there are huge ongoing clinical trials in the U.S. examining this right now. So far the evidence points that learning to regulate your emotions through these types of treatments does effect serotonin.
Here's a link to clinical trial information.
Reply:
I absolutely love this question! The interplay between what we do as psychologists and biology is one of my favorite topics. How we are trained through all of our collective learning experiences to think - and more specifically, appraise, evaluate, and interpret - has a direct effect on our physiology and biology.
For those of you not familiar with Cognitive Behavioral Therapy (CBT) it involves very active Socratic questioning on the therapists part about thoughts the patient currently has. This type of therapy is in stark contrast to old-fashioned Freudian type therapies that mainly just involve combing over events of your past. If a patient comes into my office and says "I'm a loser," my response would be "Oh, yeah? It must stink to think that. But what is the evidence that you're a loser?... Have you ever won anything?... Even if you are a loser now - whatever that means - will you always be a loser?" etc.
After all this questioning, we usually end up laughing together about what I ridiculous statement "I'm a loser" really is and how true it can feel. Through this process, the rift between what our mind thinks and what is actually true is created. After the initial separation between thought and belief is fostered, we go come up with rational responses to these types of negative automatic thoughts like "I'm a loser" and practicing mentally rehearsing the rational responses as homework.
So, that is a brief description of the cognitive piece of cognitive-behavioral therapy. Interestingly, the behavioral piece has been shown to be more effective than the cognitive piece at changing the interpretation of thoughts. Let's take, for example, someone who has social phobia. You can tell them that their phobia of talking to other people is silly all you want, but they still may not believe you. The best thing to do is act.
We start small. I might grab the secretary into the therapy room and ask her to have a 5 minute conversation about something like traveling with the patient. After five minutes, the secretary says it was lovely chatting and leaves. Now, that wasn't so bad was it?
Then as homework assignments, the patient is to engage in social activities, starting with a small anxiety producing task, and working their way up to doing something very scary like public speaking, over the course of weeks. In this way, their own thoughts are directly challenged by the outcome of their behavior. They always think it will be worse than it ends up being. In this way, they engage in little "behavioral experiments" that directly test their maladaptive beliefs.
It is worth noting here that while the behavioral piece has been shown to be more effective, people may not be willing to engage in the behavioral piece without both a strong rationale for it. It is my opinion that going through the cognitive part of the therapy and disputing thoughts that automatically pop up is an extremely useful first step that must be taken with a vast majority of people before jumping into the behavioral piece. In fact, a client of mine expressed this sentiment completely of her own accord to me today.
While we have discussed both the cognitive and the behavioral piece at this point, there is a third very important piece that changes our relationship to our thoughts - Eastern mindfulness practice. Learning to be aware of our thoughts and release the less useful ones is extraordinarily helpful as well. As a side note, I practice letting go of thoughts every day during yoga, which I use as a moving meditation more than exercise. '
I'll talk more later about integrating these components of treatment, but for now, back to your question! There have been many studies showing that CBT is as useful as treating depression as antidepressants; however, CBT has the added effect of continuing to work even after treatment ends. In terms of whether or not it increases serotonin in the synapse, there are huge ongoing clinical trials in the U.S. examining this right now. So far the evidence points that learning to regulate your emotions through these types of treatments does effect serotonin.
Here's a link to clinical trial information.
Thursday, March 3, 2011
Do We Have The Ability to Change?
Similar to the last entry, here I repost my responses to questions posed to me in a forum thread from Eline, whose blog you can find at (http://businessbabyandblog.blogspot.com/).
Eline's Question:
My knowledge of phychology is at best very basic, but I do find it a fascinating subject, and I'm also interested in coaching, and I'd love to know what you think about a question that I have asked myself lately... On the one hand, the hypothesis is that there is high hereditability for almost everything (including personality), and that anything non genetic comes from non shared environment, and thus that personality traits are stable over time. On the other hand, I believe in free will, and that it's possible to change your values, beliefs, thoughts and actions. Taking it further, if you believe in free will, to what extent could we use the plasticity of the brain to shape and transform our personality ourselves? I'm thinking, with so many self-help books on the market, what proportion of identity is really up to us?
My Reply:
You ask a very interesting question! Speaking very broadly - from a combination of fancy statistics and studying identical twins who were adopted into different families, we have estimates that genetics and environment contribute about equally to various personality traits, behaviors, and disorders. Let's first discuss these factors before getting into free will.
From an evolutionary perspective, this makes sense. It is favorable to survival to have some traits passed on from one generation to the next. On the other hand, there needs to be some room for adaptability.
In some people personality traits are really stable across time; however, stability cannot be confused with heritability. In other words, just because something is stable, doesn't mean that it is inherited or genetic. For example, someone could have experienced something extremely traumatic early on in their childhood and would remain fearful and avoidant their entire lives. In this case, the environment would be the main contributor to a fearful and avoidant personality. While this is true, a complex interplay of genetic and environmental factors after the trauma may also maintain a fearful personality.
As someone who studies the treatment of "personality disorders," which are considered to be such stable disorders that they are part of one's personality, I can tell you that personality disorders are not stable over time. A very difficult disorder to treat called Borderline Personality Disorder - which involves suicidal tendencies, behaviors like cutting, chronic feelings of emptiness etc - has been shown to be effectively treated with a talk-therapy called Dialectical Behavior Therapy (DBT). This suggests, that even very difficult and stable traits can be changed with a psychological treatment. Because it is obviously not gene therapy, therapeutic change can be viewed as the environment (along with the individual) shaping behavior.
As I mentioned on this thread where this blog post originated, the mind and body are shaped by the environment. Talk-therapies and experiences can actually re-wire the brain. So even if we're born with a genetic predisposition to something, we can mold it, within certain limitations that are hard to estimate, with experience. There is, however, very likely an element of choice in whether to proceed with and effective treatment.
Although this is likely the case, free will is a really difficult topic to discuss with confidence. We are often very influenced by factors completely outside of our awareness. We also make up reasons for why we do things, when we really have no idea why on earth we do. Many cleverly designed studies have shown this.
With that being said, my own ideas on free will are this: when we become aware of our thoughts and actions, perhaps through the practice of meditation, we have an increased ability to choose. As we hone this ability, over time, we become less like a pinball careening towards different springs that just send us hurling in random directions. We can shape the way in which are brains are rewired by choosing to practice a craft, studying a topic, or participating in an effective treatment like CBT or DBT where psychological management skills are learned.
Eline's Repsonse:
How interesting! Thanks for such a complete answer! I just completed an introductory course in psychology and am having a hard time putting the pices together. What you say really makes sense..
Now I'm thinking about meditating again, I did it for a while, but never really made it a routine or a priority.. :)
My Response:
Eline, my pleasure! If you have any more questions, this thread is here :)
I absolutely love meditation - I research, practice, and teach it. I just wrote an article about meditation here:
http://www.tidytemple.com.au/AnnouncementRetrieve.aspx?ID=45454
If you have the time to check it out, let me know what you think!
Eline's Response:
Great article! I used to share the same misconceptions you address, and I'm sure there are many like me.. I also like the idea of starting with 2 minutes, I started directly at 15 and found it really long, maybe that's why I stopped
My Response:
Thanks for the positive feedback, Eline! It is much appreciated.
Eline's Question:
My knowledge of phychology is at best very basic, but I do find it a fascinating subject, and I'm also interested in coaching, and I'd love to know what you think about a question that I have asked myself lately... On the one hand, the hypothesis is that there is high hereditability for almost everything (including personality), and that anything non genetic comes from non shared environment, and thus that personality traits are stable over time. On the other hand, I believe in free will, and that it's possible to change your values, beliefs, thoughts and actions. Taking it further, if you believe in free will, to what extent could we use the plasticity of the brain to shape and transform our personality ourselves? I'm thinking, with so many self-help books on the market, what proportion of identity is really up to us?
My Reply:
You ask a very interesting question! Speaking very broadly - from a combination of fancy statistics and studying identical twins who were adopted into different families, we have estimates that genetics and environment contribute about equally to various personality traits, behaviors, and disorders. Let's first discuss these factors before getting into free will.
From an evolutionary perspective, this makes sense. It is favorable to survival to have some traits passed on from one generation to the next. On the other hand, there needs to be some room for adaptability.
In some people personality traits are really stable across time; however, stability cannot be confused with heritability. In other words, just because something is stable, doesn't mean that it is inherited or genetic. For example, someone could have experienced something extremely traumatic early on in their childhood and would remain fearful and avoidant their entire lives. In this case, the environment would be the main contributor to a fearful and avoidant personality. While this is true, a complex interplay of genetic and environmental factors after the trauma may also maintain a fearful personality.
As someone who studies the treatment of "personality disorders," which are considered to be such stable disorders that they are part of one's personality, I can tell you that personality disorders are not stable over time. A very difficult disorder to treat called Borderline Personality Disorder - which involves suicidal tendencies, behaviors like cutting, chronic feelings of emptiness etc - has been shown to be effectively treated with a talk-therapy called Dialectical Behavior Therapy (DBT). This suggests, that even very difficult and stable traits can be changed with a psychological treatment. Because it is obviously not gene therapy, therapeutic change can be viewed as the environment (along with the individual) shaping behavior.
As I mentioned on this thread where this blog post originated, the mind and body are shaped by the environment. Talk-therapies and experiences can actually re-wire the brain. So even if we're born with a genetic predisposition to something, we can mold it, within certain limitations that are hard to estimate, with experience. There is, however, very likely an element of choice in whether to proceed with and effective treatment.
Although this is likely the case, free will is a really difficult topic to discuss with confidence. We are often very influenced by factors completely outside of our awareness. We also make up reasons for why we do things, when we really have no idea why on earth we do. Many cleverly designed studies have shown this.
With that being said, my own ideas on free will are this: when we become aware of our thoughts and actions, perhaps through the practice of meditation, we have an increased ability to choose. As we hone this ability, over time, we become less like a pinball careening towards different springs that just send us hurling in random directions. We can shape the way in which are brains are rewired by choosing to practice a craft, studying a topic, or participating in an effective treatment like CBT or DBT where psychological management skills are learned.
Eline's Repsonse:
How interesting! Thanks for such a complete answer! I just completed an introductory course in psychology and am having a hard time putting the pices together. What you say really makes sense..
Now I'm thinking about meditating again, I did it for a while, but never really made it a routine or a priority.. :)
My Response:
Eline, my pleasure! If you have any more questions, this thread is here :)
I absolutely love meditation - I research, practice, and teach it. I just wrote an article about meditation here:
http://www.tidytemple.com.au/AnnouncementRetrieve.aspx?ID=45454
If you have the time to check it out, let me know what you think!
Eline's Response:
Great article! I used to share the same misconceptions you address, and I'm sure there are many like me.. I also like the idea of starting with 2 minutes, I started directly at 15 and found it really long, maybe that's why I stopped
My Response:
Thanks for the positive feedback, Eline! It is much appreciated.
The First and Ultimate Primary Emotion - Fear
A member of an online community to which I belong posed this very interesting question to me on a psychology thread: Could fear be the origin of the entire spectrum of human emotion?
My answer:
Very thought provoking question. Fear is certainly what we consider a primary human emotion (among other emotions, e.g. happiness, anger, and sadness). Thinking about fear as the first emotion to appear in living things evolutionarily though is interesting.
[When we talk about origins, there are two types: a single person's individual origins and evolutionary origins. Being that each person comes into the world with a complex nervous system, it doesn't make sense to think of fear as being each individual's ultimate primary emotion. Considering this question in an evolutionary sense is far more interesting.]
In an evolutionary sense, fear is - of course - vital. Fear as a threat detection and deflection system certainly seems to rank #1 in terms of importance.
In fact, earlier in the thread in which this blog post originated, I discussed Kandel's Nobel Peace Prize winning work on the "memory" of slugs. The response that sea slugs can "remember" to recoil after being pinched in the gill is certainly very interesting. While this borders on what may seem like a classical conditioning response, there could be the beginnings of fear like responses here. [In terms of fear and how it relates to memory, it may be interesting to note here that fear evokes a release of calcium in the brain that leads to highly ingrained encoding of information.]
Although Freud might have said that sex drive is more primary, I'm not so sure. Perhaps fear responses were actually first to develop evolutionarily and reproduction urges (which aren't really emotions anyhow) came about later. But sex, and it's relation to love, seem way more advanced than fear. As far as a sea slugs is concerned - it is a hermaphrodite so a drive to (at least) seek out sex probably isn't that developed.
Along with sex, maybe other positive emotions simply aren't as necessary from an evolutionary standpoint. In fact, maybe emotions from being comforted and soothed developed after fear as a way to reduce and control it. Paul Gilbert Ph.D. talks about the importance of the physiological Soothing and Contentment System - but soothing from what? My guess is anxiety / fear - which was on the scene first.
Along with positive feelings of being soothed, exhilaration or happiness might also be linked to fear. Just think about the last time you were on a rollercoaster. Since the feeling of fear seems more important than exhilaration, it may be the case that feeling exhilaration developed out of the fear system.
[Hm - just had a thought about bipolar disorder and the sadness and happiness responses being a result of a dysregulation of anxiety systems, one that leads to prolonged depression and the other that leads to constant exhilaration. Anyhow - back to the original question.]
After talking about some positive feelings and the link to anxiety, let's consider anger. We know that someone's "threat detection system" is activated when they're angry. In other words, they may feel anxiety, and anger is the motivator to act. Therefore, the argument could be made that anxiety is first and anger has developed secondarily in the more advanced fight or flight system. We now have two options in response to anxiety: fight (anger) or flee.
Ok, now let's shift from talking about fear arising first on the evolution scene, to fear underlying our everyday experiences now.
For fun, let's consider the link between fear and depression as a psychiatric disorder. When first reading this question, my mind immediately jumped to the link between these two things. Prolonged fear / stress releases enormous amounts of cortisol, which impairs the functioning of the brain (for the scientifically curious - along the Hypothalamic Pituitary Adrenal axis) and leads to depression. Therefore, prolonged fear / stress is experienced first, and we think this is one route to depression.
Now, I realize depression is a psychiatric disorder linked to sadness, but it is not sadness itself. Therefore, saying fear always prompts sadness would not be a logical inference per se. On the other hand, these symptoms may be intimately linked whereas fear sometimes comes first. For instance, one may experiencing horror at the loss of a loved one first, and then deep sorrow. Typically people don't go straight to sad. There is usually shock (perhaps an anxiety response) and then sadness kind of sinks in either seconds, minutes, hours, or days later.
Flipping back into evolutionary terms, it seems that sadness is quite an advanced emotion compared to fear. While I can imagine an insect having a developed reactionary response with the rudimentary beginnings of a fear system, I can't necessarily picture a sorrow system.
In short, I think the case can be made that fear (as it stems from stimulus / threat detection) may be the ultimate primary emotion.
My answer:
Very thought provoking question. Fear is certainly what we consider a primary human emotion (among other emotions, e.g. happiness, anger, and sadness). Thinking about fear as the first emotion to appear in living things evolutionarily though is interesting.
[When we talk about origins, there are two types: a single person's individual origins and evolutionary origins. Being that each person comes into the world with a complex nervous system, it doesn't make sense to think of fear as being each individual's ultimate primary emotion. Considering this question in an evolutionary sense is far more interesting.]
In an evolutionary sense, fear is - of course - vital. Fear as a threat detection and deflection system certainly seems to rank #1 in terms of importance.
In fact, earlier in the thread in which this blog post originated, I discussed Kandel's Nobel Peace Prize winning work on the "memory" of slugs. The response that sea slugs can "remember" to recoil after being pinched in the gill is certainly very interesting. While this borders on what may seem like a classical conditioning response, there could be the beginnings of fear like responses here. [In terms of fear and how it relates to memory, it may be interesting to note here that fear evokes a release of calcium in the brain that leads to highly ingrained encoding of information.]
Although Freud might have said that sex drive is more primary, I'm not so sure. Perhaps fear responses were actually first to develop evolutionarily and reproduction urges (which aren't really emotions anyhow) came about later. But sex, and it's relation to love, seem way more advanced than fear. As far as a sea slugs is concerned - it is a hermaphrodite so a drive to (at least) seek out sex probably isn't that developed.
Along with sex, maybe other positive emotions simply aren't as necessary from an evolutionary standpoint. In fact, maybe emotions from being comforted and soothed developed after fear as a way to reduce and control it. Paul Gilbert Ph.D. talks about the importance of the physiological Soothing and Contentment System - but soothing from what? My guess is anxiety / fear - which was on the scene first.
Along with positive feelings of being soothed, exhilaration or happiness might also be linked to fear. Just think about the last time you were on a rollercoaster. Since the feeling of fear seems more important than exhilaration, it may be the case that feeling exhilaration developed out of the fear system.
[Hm - just had a thought about bipolar disorder and the sadness and happiness responses being a result of a dysregulation of anxiety systems, one that leads to prolonged depression and the other that leads to constant exhilaration. Anyhow - back to the original question.]
After talking about some positive feelings and the link to anxiety, let's consider anger. We know that someone's "threat detection system" is activated when they're angry. In other words, they may feel anxiety, and anger is the motivator to act. Therefore, the argument could be made that anxiety is first and anger has developed secondarily in the more advanced fight or flight system. We now have two options in response to anxiety: fight (anger) or flee.
Ok, now let's shift from talking about fear arising first on the evolution scene, to fear underlying our everyday experiences now.
For fun, let's consider the link between fear and depression as a psychiatric disorder. When first reading this question, my mind immediately jumped to the link between these two things. Prolonged fear / stress releases enormous amounts of cortisol, which impairs the functioning of the brain (for the scientifically curious - along the Hypothalamic Pituitary Adrenal axis) and leads to depression. Therefore, prolonged fear / stress is experienced first, and we think this is one route to depression.
Now, I realize depression is a psychiatric disorder linked to sadness, but it is not sadness itself. Therefore, saying fear always prompts sadness would not be a logical inference per se. On the other hand, these symptoms may be intimately linked whereas fear sometimes comes first. For instance, one may experiencing horror at the loss of a loved one first, and then deep sorrow. Typically people don't go straight to sad. There is usually shock (perhaps an anxiety response) and then sadness kind of sinks in either seconds, minutes, hours, or days later.
Flipping back into evolutionary terms, it seems that sadness is quite an advanced emotion compared to fear. While I can imagine an insect having a developed reactionary response with the rudimentary beginnings of a fear system, I can't necessarily picture a sorrow system.
In short, I think the case can be made that fear (as it stems from stimulus / threat detection) may be the ultimate primary emotion.
Monday, February 21, 2011
Amelia's Website
Here is a link to my very talented colleague's website. She has some really great studies on emotion regulation available on it. A link to her website can also be found in the a section on right-hand column of this blog entitled "Other Psychology Blogs & Websites."
Saturday, February 5, 2011
Why Do People Cut Themselves?
by Tara Deliberto
Celebrities like Megan Fox, Angelina Jolie, and Demi Lavato have all purposely cut themselves. But why?
Well, it isn't all that clear. And the answer "they do it just for attention" doesn't make too much sense.
Sure, getting attention could be part of the answer, but it's not that simple. If you've never cut yourself, consider this: of all the things you could possibly do for attention, is carving your skin with a razor really at the top of the list? Probably not.
After researching self-injury for several years, one thing seems certain - cutting immediately halts emotional pain. It might seem backwards that physical pain stops psychological pain. But we need to take a closer look.
Starting Generally
I would actually say a major contributing factor to self-injury is actually our tendency to make things too simple. Allow me to explain. Although judging what is right and wrong is super complicated - hence the whole legal system - we are quick to slap labels on people like "good" or "bad." But life is more nuanced than that! Of course labeling helps us communicate, but a lot of very important information gets lost when we stamp something as "good" or "bad."
More Specifically
Now getting more directly to the point of this post, the very same language we use to describe our world and communicate ideas to others, is used to communicate to ourselves. We think in words. We label ourselves as good or bad. We tell ourselves we are good or bad.
And what people are telling themselves right before they cut is nearly unbearable to hear. I'd imagine their mind is shouting things at them like "You're a worthless bitch. How could anyone love you? You disgust me."
The thing is, I don't think I've ever met a totally worthless, unlovable, and disgusting human being, whatever that is. It is usually very clear from a third party perspective that the self-talk of a person who cuts, is incredibly harsh and one-sided. Despite this, people go on labeling themselves anyhow.
Not only do people who cut tell themselves abusive things, they believe them too. This is a very important distinction. Once people learn to determine the difference between having a thought and believing it in therapy, we usually see symptoms improving a lot. It is one thing to think "Wow, I am a bad person," acknowledging it as just a thought, and moving on. It is another thing to think "Wow, I am a bad person" and believe it.
With a new understanding of abusive self-talk in the mind, let's shift to discussing the body.
The Body
Let's just say you're strolling along, thinking about how beautiful the sky is, when you walk into a telephone pole. The second after your toe smashes into the pole, are you still thinking about that beautiful sky? Probably not. You're just thinking about how much your damn toe hurts.
Now, what if you were thinking about how you're such a selfish slut? What if you believed it? Would you rather be in the emotional anguish that comes along with berating yourself or would it be easier to have your toe hurt?
Yeah, that's what I thought. You'd rather stub your toe, wouldn't you?
Right after the body sustains an injury, it is kind of hard to be caught up in your thoughts. The physical pain provides a mental break from really horrible self-talk. The pain becomes a vacation.
[It is worth mentioning that even if the emotional pain isn't necessarily tied to what some people might call irrational thought (but is from an actual loss or event), it still be halted by self-injury. Usually though, I'd bet there is some degree of extreme thought causing the pain to be increasingly intense.]
Now back to talking about cutting for attention. Sure, people could also be cutting for attention, but the picture is clearly a lot more complicated. On either side of the spectrum, you may have people who solely for attention, and on the other, people who cut and have never told anyone. Most likely, people cut for several reasons. Now, let's take this discussion a bit further from here.
While it seems that verbal thoughts like "You're a worthless cow" repeating over and over might be an important factor, there are many more pieces of the puzzle.
The Physiology of Self-Injury
There are some non-human primates, especially neglected ones, who tear out bits of fur when they're distressed. They actually harm themselves.
[Side note: The thought of a neglected monkey pulling out tufts of fur can be pretty upsetting, cant it? Unfortunately, while it is easy for some of us to have sympathy for monkeys who hurt themselves, it is more difficult to take a non-judgmental stance towards humans who cut.]
While these neglected monkeys harm themselves like humans, they don't have language capacities like us. Therefore, it's not very likely that abusive self-talk leads to self-harm in non-human primates. Percentage wise, the non-human primate self-injury may be maintained much more by the emotional, rather than a linguistic or symbolic system.
While language is a new development on the evolutionary scene, emotions are not. Emotions have been around for a while, without the complication of human language. As any loving pet owner like myself could tell you, animals have emotions.
What happens on a physiological level after someone cuts is not currently understood; however, my guess is that there is a release of endorphins, which make you feel good. We also know that heart-rate dramatically drops after cutting in people who often self-injure.
In short, on a mental/language level as well as an emotional level, there is likely some serious relief occurring right after cutting.
Wrapping Up
The way I see it at this particular point in time, is that very upsetting abusive self-talk is immediately halted, there a shift of attention to the cut, and endorphins are released, which serves to calm the body further.
Of course, the reasons people cut are diverse and they change over time. This may not be true for everyone. For instance, people may also cut to feel something if they're feeling nothing or numb. An additional reason people report cutting is to punish themselves. Perhaps sometime soon I'll write about these functions as well; however, it seems to me that the main function of cutting is to help reduce negative feelings in the moment.
Thankfully though, wonderful treatments like Dialectical Behavior Therapy (DBT) have been invented to help with cutting. If you or someone you love engages in self-injury, there are wonderful resources available. Go online and find a DBT therapist near you or join a DBT Skills Group near you.
Blog Info
For more posts on self-injury, check out The Psychology Easel's Self-Injury Section.
Feel free to follow me on Twitter at @TaraDeliberto and subscribe to this blog in the right sidebar.
Do You Self Harm?
If you engage in self-injury, an excellent resource is S.A.F.E. Alternatives, an absolutely wonderful organization devoted to the treatment of self-injury (you can visit their website at http://www.selfinjury.com/).
Also, a very helpful book on directly treating self-injury is Bodily Harm. Select this book in the icon above to purchase.
The best treatment for cutting is Dialectical Behavior Therapy (DBT). Find a DBT therapist near you.
Celebrities like Megan Fox, Angelina Jolie, and Demi Lavato have all purposely cut themselves. But why?
Well, it isn't all that clear. And the answer "they do it just for attention" doesn't make too much sense.
Sure, getting attention could be part of the answer, but it's not that simple. If you've never cut yourself, consider this: of all the things you could possibly do for attention, is carving your skin with a razor really at the top of the list? Probably not.
After researching self-injury for several years, one thing seems certain - cutting immediately halts emotional pain. It might seem backwards that physical pain stops psychological pain. But we need to take a closer look.
Starting Generally
I would actually say a major contributing factor to self-injury is actually our tendency to make things too simple. Allow me to explain. Although judging what is right and wrong is super complicated - hence the whole legal system - we are quick to slap labels on people like "good" or "bad." But life is more nuanced than that! Of course labeling helps us communicate, but a lot of very important information gets lost when we stamp something as "good" or "bad."
More Specifically
Now getting more directly to the point of this post, the very same language we use to describe our world and communicate ideas to others, is used to communicate to ourselves. We think in words. We label ourselves as good or bad. We tell ourselves we are good or bad.
And what people are telling themselves right before they cut is nearly unbearable to hear. I'd imagine their mind is shouting things at them like "You're a worthless bitch. How could anyone love you? You disgust me."
The thing is, I don't think I've ever met a totally worthless, unlovable, and disgusting human being, whatever that is. It is usually very clear from a third party perspective that the self-talk of a person who cuts, is incredibly harsh and one-sided. Despite this, people go on labeling themselves anyhow.
Not only do people who cut tell themselves abusive things, they believe them too. This is a very important distinction. Once people learn to determine the difference between having a thought and believing it in therapy, we usually see symptoms improving a lot. It is one thing to think "Wow, I am a bad person," acknowledging it as just a thought, and moving on. It is another thing to think "Wow, I am a bad person" and believe it.
With a new understanding of abusive self-talk in the mind, let's shift to discussing the body.
The Body
Let's just say you're strolling along, thinking about how beautiful the sky is, when you walk into a telephone pole. The second after your toe smashes into the pole, are you still thinking about that beautiful sky? Probably not. You're just thinking about how much your damn toe hurts.
Now, what if you were thinking about how you're such a selfish slut? What if you believed it? Would you rather be in the emotional anguish that comes along with berating yourself or would it be easier to have your toe hurt?
Yeah, that's what I thought. You'd rather stub your toe, wouldn't you?
Right after the body sustains an injury, it is kind of hard to be caught up in your thoughts. The physical pain provides a mental break from really horrible self-talk. The pain becomes a vacation.
[It is worth mentioning that even if the emotional pain isn't necessarily tied to what some people might call irrational thought (but is from an actual loss or event), it still be halted by self-injury. Usually though, I'd bet there is some degree of extreme thought causing the pain to be increasingly intense.]
Now back to talking about cutting for attention. Sure, people could also be cutting for attention, but the picture is clearly a lot more complicated. On either side of the spectrum, you may have people who solely for attention, and on the other, people who cut and have never told anyone. Most likely, people cut for several reasons. Now, let's take this discussion a bit further from here.
While it seems that verbal thoughts like "You're a worthless cow" repeating over and over might be an important factor, there are many more pieces of the puzzle.
The Physiology of Self-Injury
There are some non-human primates, especially neglected ones, who tear out bits of fur when they're distressed. They actually harm themselves.
[Side note: The thought of a neglected monkey pulling out tufts of fur can be pretty upsetting, cant it? Unfortunately, while it is easy for some of us to have sympathy for monkeys who hurt themselves, it is more difficult to take a non-judgmental stance towards humans who cut.]
While these neglected monkeys harm themselves like humans, they don't have language capacities like us. Therefore, it's not very likely that abusive self-talk leads to self-harm in non-human primates. Percentage wise, the non-human primate self-injury may be maintained much more by the emotional, rather than a linguistic or symbolic system.
While language is a new development on the evolutionary scene, emotions are not. Emotions have been around for a while, without the complication of human language. As any loving pet owner like myself could tell you, animals have emotions.
What happens on a physiological level after someone cuts is not currently understood; however, my guess is that there is a release of endorphins, which make you feel good. We also know that heart-rate dramatically drops after cutting in people who often self-injure.
In short, on a mental/language level as well as an emotional level, there is likely some serious relief occurring right after cutting.
Wrapping Up
The way I see it at this particular point in time, is that very upsetting abusive self-talk is immediately halted, there a shift of attention to the cut, and endorphins are released, which serves to calm the body further.
Of course, the reasons people cut are diverse and they change over time. This may not be true for everyone. For instance, people may also cut to feel something if they're feeling nothing or numb. An additional reason people report cutting is to punish themselves. Perhaps sometime soon I'll write about these functions as well; however, it seems to me that the main function of cutting is to help reduce negative feelings in the moment.
Thankfully though, wonderful treatments like Dialectical Behavior Therapy (DBT) have been invented to help with cutting. If you or someone you love engages in self-injury, there are wonderful resources available. Go online and find a DBT therapist near you or join a DBT Skills Group near you.
Blog Info
For more posts on self-injury, check out The Psychology Easel's Self-Injury Section.
Feel free to follow me on Twitter at @TaraDeliberto and subscribe to this blog in the right sidebar.
Do You Self Harm?
If you engage in self-injury, an excellent resource is S.A.F.E. Alternatives, an absolutely wonderful organization devoted to the treatment of self-injury (you can visit their website at http://www.selfinjury.com/).
Also, a very helpful book on directly treating self-injury is Bodily Harm. Select this book in the icon above to purchase.
The best treatment for cutting is Dialectical Behavior Therapy (DBT). Find a DBT therapist near you.
Tuesday, February 1, 2011
The Next Evolutionary Step for Humans
by Tara Deliberto
Recently a friend asked me what I thought the next evolutionary step for humans would be. My answer: the ability to be mindful. Most of us go through life without being present in the moment. The ability to have awareness of our own thoughts opens the door for greater control. Afterall, medititation increases the very part of the brain that is newest on the evolutionary scene - the neo cortex.
Recently a friend asked me what I thought the next evolutionary step for humans would be. My answer: the ability to be mindful. Most of us go through life without being present in the moment. The ability to have awareness of our own thoughts opens the door for greater control. Afterall, medititation increases the very part of the brain that is newest on the evolutionary scene - the neo cortex.
Friday, January 7, 2011
A Remaining Thought on Control
by Tara Deliberto
Today my meditation and yoga teacher described that the point of the practice this: to use the mind to release the mind. I think that pretty much sums it up.
Yoga (and life) is learning to find the balance between effort and ease.
Today my meditation and yoga teacher described that the point of the practice this: to use the mind to release the mind. I think that pretty much sums it up.
Yoga (and life) is learning to find the balance between effort and ease.
Tuesday, December 28, 2010
Control
by Tara Deliberto
While new Western treatments incorporating the use of mindfulness techniques have an emphasis on decreasing control, many practitioners and patients alike are confused by the apparent increase in control over thoughts and emotions it fosters.
By increasing one's awareness of the thoughts, bodily sensations, and interaction between the two, one creates distance between the mind and what is produced by the body. This naturally produces an increasing sense of mastery over the self, which in essence is control. If you are able to focus your attention on your left pinkie toe during a meditation, for example, you are absolutely controlling your thoughts.
Now, if meditation fosters control of the mind and has been shown by numerous studies to be extremely effective in treating psychological disorders, why is control generally considered to be a bad thing? Why do third wave treatments proudly claim to decrease control? Well, when people attempt control techniques such as forcefully suppressing thoughts or changing their environment in a service to avoid their emotions, it generally leads to more suffering. This type of control, which is likely mediated by absolutes or black and white thinking, is what I like to think of as ineffective control. It doesn't allow for the experience of emotions. This is what mindfulness-based treatments decrease. While people may actively try and control their experience by using alcohol to avoid emotions, for example, those who overuse this strategy and are labeled alcoholics are typically said to be "out of control." Used in this way, the phrase "out of control" implies a lack of mindful control over the attempts to ineffectively control one's emotions.
Conversely, learning to mindfully control one's attention has been shown to be a favorable strategy in coping with a very wide range of problematic behaviors. It also does not involve black and white thinking. There is an emphasis on being aware of one's thoughts, bodily sensations, and experiences, without actively trying to change what cannot be changed. The difference between trying to control one's experience through the suppression of emotions versus through active focus on present are extreme; however, (if you ask me) both are technically control strategies. The latter type of strategy though, leaves room for the experience of negative emotions and thoughts when avoiding them would lead to more struggling. This is effective and adaptive.
It should be noted, however, that avoiding negative emotions may be a very favorable strategy on some occasions - for example, a woman may avoid continuing to feel negative emotions brought on by an abusive husband by leaving. In my experience some mindfulness practitioners actually misapply the idea that one should experience negative emotion by encouraging clients to endure painful situations when in reality, their patients are actually avoiding another set of negative emotions such as loneliness or fear of the unknown. It is tolerance to this latter set of emotions that needs to be fostered. Eagerness in encouraging clients to experience any negative emotions must be curbed with reason and a careful examination of what types of emotions are functional to avoid. Strict adherence to any set of rules without individual reasoning is certainly not favorable.
In the literature and when discussing attempts to change one's experience from what it has been, I think techniques should be labeled as ineffective control strategies or mindfully aware control strategies on an individual and situational basis.
While new Western treatments incorporating the use of mindfulness techniques have an emphasis on decreasing control, many practitioners and patients alike are confused by the apparent increase in control over thoughts and emotions it fosters.
By increasing one's awareness of the thoughts, bodily sensations, and interaction between the two, one creates distance between the mind and what is produced by the body. This naturally produces an increasing sense of mastery over the self, which in essence is control. If you are able to focus your attention on your left pinkie toe during a meditation, for example, you are absolutely controlling your thoughts.
Now, if meditation fosters control of the mind and has been shown by numerous studies to be extremely effective in treating psychological disorders, why is control generally considered to be a bad thing? Why do third wave treatments proudly claim to decrease control? Well, when people attempt control techniques such as forcefully suppressing thoughts or changing their environment in a service to avoid their emotions, it generally leads to more suffering. This type of control, which is likely mediated by absolutes or black and white thinking, is what I like to think of as ineffective control. It doesn't allow for the experience of emotions. This is what mindfulness-based treatments decrease. While people may actively try and control their experience by using alcohol to avoid emotions, for example, those who overuse this strategy and are labeled alcoholics are typically said to be "out of control." Used in this way, the phrase "out of control" implies a lack of mindful control over the attempts to ineffectively control one's emotions.
Conversely, learning to mindfully control one's attention has been shown to be a favorable strategy in coping with a very wide range of problematic behaviors. It also does not involve black and white thinking. There is an emphasis on being aware of one's thoughts, bodily sensations, and experiences, without actively trying to change what cannot be changed. The difference between trying to control one's experience through the suppression of emotions versus through active focus on present are extreme; however, (if you ask me) both are technically control strategies. The latter type of strategy though, leaves room for the experience of negative emotions and thoughts when avoiding them would lead to more struggling. This is effective and adaptive.
It should be noted, however, that avoiding negative emotions may be a very favorable strategy on some occasions - for example, a woman may avoid continuing to feel negative emotions brought on by an abusive husband by leaving. In my experience some mindfulness practitioners actually misapply the idea that one should experience negative emotion by encouraging clients to endure painful situations when in reality, their patients are actually avoiding another set of negative emotions such as loneliness or fear of the unknown. It is tolerance to this latter set of emotions that needs to be fostered. Eagerness in encouraging clients to experience any negative emotions must be curbed with reason and a careful examination of what types of emotions are functional to avoid. Strict adherence to any set of rules without individual reasoning is certainly not favorable.
In the literature and when discussing attempts to change one's experience from what it has been, I think techniques should be labeled as ineffective control strategies or mindfully aware control strategies on an individual and situational basis.
Sunday, December 5, 2010
Combining Cognitive Therapy and Mindfulness
by Tara Deliberto
I was lucky enough to have the opportunity yesterday to get together with a neuroscientist friend and colleague with whom I used to work in Cambridge, MA. Eventually we got on the topic of merging ACT & CBT and he asked some thought provoking questions I thought I would share.
The first question - and the topic of this blog post - that got me really thinking was something like: "how long does it take before an alternative rational response replaces the (long-ingrained and continually environmentally reinforced) negative & irrational automatic thoughts?" In the moment I threw out some arbitrary response based on my extensive 2.5 years of clinical experience (lol), and immediately realized I had no clue what the answer was. Being as sharp as he is, he also immediately realized (but politely pointed out) that my response was b.s. Of course it will vary for every person, but we came to the conclusion that duration of irrational thought replacement it is probably a lot longer than the literature on how quickly people respond to CBT would suggest.
While CBT can reduce symptoms in a handful of sessions - maybe around 10-15 - and CBT w/ d-cycloserine for fear reconditioning can reduce symptoms in even fewer sessions, the time it takes before negative automatic thoughts are completely replaced could widely vary. In fact, they may never disappear. Members of the ACT community actually set expectations that negative automatic thoughts never decrease in frequency (for decent reasons I won't expound upon here). Furthermore, the difference between completely disappearing and having thoughts that one relates to effectively enough to show up as a statistically v.s. clinically significant decreases in symptoms are all very different things. While clinical improvement may be apparent from research, it is likely that people continue to have intrusive thoughts (that are experienced as at least unpleasant) well after their 10-15 sessions of CBT have ended.
There are also likely varying stages of having negative automatic thoughts disappear, ranging from:
- the thought pops up, it is suppressed, and reoccurs w/ a vengeance
- the thought pops up and one struggles to restructure it w/ a rational response
- the thought pops up and one is able to quickly ward it off w/ a rational response
- the thought pops up and one immediately labels it as irrational & mindfully releases it
- the thoughts generally tend to decrease in intensity/frequency over time
- the thought is completely irradiated
Now, the question my friend asked is important because it lead us to this idea: if there is some truth to these stages, mindfully dismissing something in the moment might interfere with the practicing of retraining the mind to have different and rational responses to the thoughts.
Perhaps if one truly retrains the mind away from irrational thoughts, they will decrease in frequency, which is arguably more favorable than continually having negative intrusive thoughts pop up that one learns to relate to differently with the use of mindfulness. It should be noted, however, that mindful awareness and release of thoughts may also, as a practice, decrease the frequency of thoughts over time. At this point, everything is speculative and is simply (what I would consider to be) interesting food for thought.
While the constant use of mindfulness early in treatment may hypothetically interfere in some way w/ long-term retraining, it is certainly a very useful practice in many situations like when refocus in the moment is paramount. Being mindfully aware of thoughts also has the major benefit of preventing people from slipping back into responding to certain irrational thoughts as if they were real and/or of utility.
I know a lot of people may have an issue with framing mindfully releasing a thought in this way; however, I am not suggesting it is a form of suppression. With mindfulness of thoughts, there is an active acknowledgement and awareness of the thoughts, which separates it from suppression. However, when it is feasible, encouraging the patient to extensively retrain themselves with engaging in active grappling with irrational thoughts might be favorable before moving into a mindfulness-based approach.
It should be noted. however, that thought disputation may not be a particularly useful type of practice for people with Borderline Personality Disorder. In fact, for this population, it might be favorable to start with mindfulness of thoughts and thought defusion exercises. In fact, research I presented in 2006 at a conference in Chicago suggests that appraising thoughts might actually be a mechanism of change in Dialectical Behavior Therapy - a treatment for BPD that does not (really) use cognitive disputation. So that mindfulness of thoughts may foster their reappraisal naturally.
I was lucky enough to have the opportunity yesterday to get together with a neuroscientist friend and colleague with whom I used to work in Cambridge, MA. Eventually we got on the topic of merging ACT & CBT and he asked some thought provoking questions I thought I would share.
The first question - and the topic of this blog post - that got me really thinking was something like: "how long does it take before an alternative rational response replaces the (long-ingrained and continually environmentally reinforced) negative & irrational automatic thoughts?" In the moment I threw out some arbitrary response based on my extensive 2.5 years of clinical experience (lol), and immediately realized I had no clue what the answer was. Being as sharp as he is, he also immediately realized (but politely pointed out) that my response was b.s. Of course it will vary for every person, but we came to the conclusion that duration of irrational thought replacement it is probably a lot longer than the literature on how quickly people respond to CBT would suggest.
While CBT can reduce symptoms in a handful of sessions - maybe around 10-15 - and CBT w/ d-cycloserine for fear reconditioning can reduce symptoms in even fewer sessions, the time it takes before negative automatic thoughts are completely replaced could widely vary. In fact, they may never disappear. Members of the ACT community actually set expectations that negative automatic thoughts never decrease in frequency (for decent reasons I won't expound upon here). Furthermore, the difference between completely disappearing and having thoughts that one relates to effectively enough to show up as a statistically v.s. clinically significant decreases in symptoms are all very different things. While clinical improvement may be apparent from research, it is likely that people continue to have intrusive thoughts (that are experienced as at least unpleasant) well after their 10-15 sessions of CBT have ended.
There are also likely varying stages of having negative automatic thoughts disappear, ranging from:
- the thought pops up, it is suppressed, and reoccurs w/ a vengeance
- the thought pops up and one struggles to restructure it w/ a rational response
- the thought pops up and one is able to quickly ward it off w/ a rational response
- the thought pops up and one immediately labels it as irrational & mindfully releases it
- the thoughts generally tend to decrease in intensity/frequency over time
- the thought is completely irradiated
Now, the question my friend asked is important because it lead us to this idea: if there is some truth to these stages, mindfully dismissing something in the moment might interfere with the practicing of retraining the mind to have different and rational responses to the thoughts.
Perhaps if one truly retrains the mind away from irrational thoughts, they will decrease in frequency, which is arguably more favorable than continually having negative intrusive thoughts pop up that one learns to relate to differently with the use of mindfulness. It should be noted, however, that mindful awareness and release of thoughts may also, as a practice, decrease the frequency of thoughts over time. At this point, everything is speculative and is simply (what I would consider to be) interesting food for thought.
While the constant use of mindfulness early in treatment may hypothetically interfere in some way w/ long-term retraining, it is certainly a very useful practice in many situations like when refocus in the moment is paramount. Being mindfully aware of thoughts also has the major benefit of preventing people from slipping back into responding to certain irrational thoughts as if they were real and/or of utility.
I know a lot of people may have an issue with framing mindfully releasing a thought in this way; however, I am not suggesting it is a form of suppression. With mindfulness of thoughts, there is an active acknowledgement and awareness of the thoughts, which separates it from suppression. However, when it is feasible, encouraging the patient to extensively retrain themselves with engaging in active grappling with irrational thoughts might be favorable before moving into a mindfulness-based approach.
It should be noted. however, that thought disputation may not be a particularly useful type of practice for people with Borderline Personality Disorder. In fact, for this population, it might be favorable to start with mindfulness of thoughts and thought defusion exercises. In fact, research I presented in 2006 at a conference in Chicago suggests that appraising thoughts might actually be a mechanism of change in Dialectical Behavior Therapy - a treatment for BPD that does not (really) use cognitive disputation. So that mindfulness of thoughts may foster their reappraisal naturally.
Monday, November 22, 2010
Can Two Useful But Contradictory Treatments be Combined?
by Tara Deliberto
In no way do I think that Acceptance and Commitment Therapy (ACT) and Cognitive Therapy (CT) are incompatible. In fact, combining techniques from both treatment modalities in a preplanned sequence has great potential.
For argument's sake, let's assume that the two treatments can be merged in a meaningful way. If they can be merged, how would we go about integrating the different techniques (we'll save integrating the philosophies for a different day)? Well, some may argue that placing an emphasis on honing the ability to catch thoughts with the use of mindfulness techniques must precede the teaching of disputing irrational thoughts. At first glance this seems logical perhaps because it is assumed that one must be mindfully aware of a thought before being able to dispute it. I'm not so sure.
Through cognitive restructuring, if patients are first made aware of the fact that their thoughts are irrational, they may have a better framework in which to do ACT work. After cognitive restructuring, they have not only identified which thoughts are dysfunctional or irrational, but have been lead through a reasoning process of why these thoughts are inaccurate. Now with a deeper understanding of why their thoughts are irrational and a clinically significant lesser degree of belief in the verity of the content of these thoughts, they could be in a better position to recognize from which cognitions are best to defuse. Speaking practically from an ACT perspective, using the chessboard metaphor as an example, patients may better be able to identify the "black" pieces from which to defuse, while still being able to maintain self-as-context (i.e. understanding that they are the chessboard that houses the battling white and black pieces). After cognitive restructuring and focusing on self-as-context, it seems to me that people have a greater fighting chance of being able to accomplish the very cerebrally taxing feat of letting thoughts float by. In short, by first providing cognitive restructuring and framing the self as a container of both rational and irrational thoughts, increased understanding, use, and efficacy of mindfulness techniques may follow.
Of course I recognize that "irrational" thoughts are not the only type of cognitions associated with negative or dysregulated affect. There are a range of painful memories, facts, images, and maybe even manic tendencies with which disputation may not be particularly effective, and whereby defusion and mindfulness may be more appropriate; however, systematically disputing the cognitions associated with negative affect that are irrational before getting into ACT work may still generally be helpful.
Thoughts?
In no way do I think that Acceptance and Commitment Therapy (ACT) and Cognitive Therapy (CT) are incompatible. In fact, combining techniques from both treatment modalities in a preplanned sequence has great potential.
For argument's sake, let's assume that the two treatments can be merged in a meaningful way. If they can be merged, how would we go about integrating the different techniques (we'll save integrating the philosophies for a different day)? Well, some may argue that placing an emphasis on honing the ability to catch thoughts with the use of mindfulness techniques must precede the teaching of disputing irrational thoughts. At first glance this seems logical perhaps because it is assumed that one must be mindfully aware of a thought before being able to dispute it. I'm not so sure.
Through cognitive restructuring, if patients are first made aware of the fact that their thoughts are irrational, they may have a better framework in which to do ACT work. After cognitive restructuring, they have not only identified which thoughts are dysfunctional or irrational, but have been lead through a reasoning process of why these thoughts are inaccurate. Now with a deeper understanding of why their thoughts are irrational and a clinically significant lesser degree of belief in the verity of the content of these thoughts, they could be in a better position to recognize from which cognitions are best to defuse. Speaking practically from an ACT perspective, using the chessboard metaphor as an example, patients may better be able to identify the "black" pieces from which to defuse, while still being able to maintain self-as-context (i.e. understanding that they are the chessboard that houses the battling white and black pieces). After cognitive restructuring and focusing on self-as-context, it seems to me that people have a greater fighting chance of being able to accomplish the very cerebrally taxing feat of letting thoughts float by. In short, by first providing cognitive restructuring and framing the self as a container of both rational and irrational thoughts, increased understanding, use, and efficacy of mindfulness techniques may follow.
Of course I recognize that "irrational" thoughts are not the only type of cognitions associated with negative or dysregulated affect. There are a range of painful memories, facts, images, and maybe even manic tendencies with which disputation may not be particularly effective, and whereby defusion and mindfulness may be more appropriate; however, systematically disputing the cognitions associated with negative affect that are irrational before getting into ACT work may still generally be helpful.
Thoughts?
Thursday, September 9, 2010
How We Value Money - Response to the Previous Post
A friend of mine recently had a very interesting comment on the last post:
You say that people assign a higher value to items once they own them. Could it be the opposite for status/striving items?
My response:
It makes complete sense that results could vary between studies where objects are earned versus given. My inclination is that some items without social status that are earned may actually garner more emotional attachment. For example, if a high school kid earned money to buy his own cheap car, he/she may be more emotionally attached to the car than a kid who was given the cheap car. On the other hand, it makes sense to me that if a person earns a particular object with the idea in mind that it will generate social status, they might value it less once it is attained. My quick thoughts on the reasons for this (that are actually clinical in nature) are that one may be jealous when seeing others with certain items and incorrectly assume that once they have these items, their jealousy will subside. In other words, there is an assumption that having certain items will create happiness (for example) because a lack of the items creates jealousy. Therefore, when the item is attained and does not provide the anticipated positive feelings, it may be emotionally devalued. At the core of the issue would be emotionality or perceived importance surrounding wealth. But I do realize that one can be goal oriented without jealousy. So if a person with a high desire for achievement were to attain a goal to buy a high social status item, they might be left feeling unfilled simply due to an insatiable drive for achievement. My guess is that people will have varying degrees of both jealousy and drive for achievement that will lead to different emotional valuations of both high and neutral status items.
In short, I would say that while emotional attachment might generally increase for items that were earned, perhaps it is a different story with earned items that an individual perceives to have social status when jealousy and drive for achievement are considered.
You say that people assign a higher value to items once they own them. Could it be the opposite for status/striving items?
My response:
It makes complete sense that results could vary between studies where objects are earned versus given. My inclination is that some items without social status that are earned may actually garner more emotional attachment. For example, if a high school kid earned money to buy his own cheap car, he/she may be more emotionally attached to the car than a kid who was given the cheap car. On the other hand, it makes sense to me that if a person earns a particular object with the idea in mind that it will generate social status, they might value it less once it is attained. My quick thoughts on the reasons for this (that are actually clinical in nature) are that one may be jealous when seeing others with certain items and incorrectly assume that once they have these items, their jealousy will subside. In other words, there is an assumption that having certain items will create happiness (for example) because a lack of the items creates jealousy. Therefore, when the item is attained and does not provide the anticipated positive feelings, it may be emotionally devalued. At the core of the issue would be emotionality or perceived importance surrounding wealth. But I do realize that one can be goal oriented without jealousy. So if a person with a high desire for achievement were to attain a goal to buy a high social status item, they might be left feeling unfilled simply due to an insatiable drive for achievement. My guess is that people will have varying degrees of both jealousy and drive for achievement that will lead to different emotional valuations of both high and neutral status items.
In short, I would say that while emotional attachment might generally increase for items that were earned, perhaps it is a different story with earned items that an individual perceives to have social status when jealousy and drive for achievement are considered.
Tuesday, May 11, 2010
Monks & Money
by Tara Deliberto
The study of individual decision making is certainly incomplete without taking into account several elements of human psychology. Rather than thinking rationally about decisions to ensure a favorable outcome, people tend to make decisions without a rational foundation, often defaulting to a set of heuristics (Amir & Ariely, 2007). Without knowledge of these psychological components at work, risky or detrimental choices cannot be understood.
One of the most established phenomena in the psychology of human decision making is that people are generally loss averse. Not only do people feel negatively about loss, but losses tend to loom larger than gains (Ariely, Huber, & Wertenbroch, 2005). In other words, people view something as more valuable when they give it up than when they acquire it. Greater value is given to an item after it comes into one’s possession than beforehand. In a study conducted by Knestch (1989), the results showed that people were unwilling to trade the item they received, whether it be a mug or a candy bar, despite random assignment. While loss aversion has been found to exist with the exchange of goods in other studies as well (Kahneman, Knestch, and Thaler (1990), it has not been found to exist for the exchange of money or other goods that are used as currency (Heath & Soll, 1996, Thaler, 1985).
While a loss is inherently averse, it is subjective in that current endowment of both goods and money must be taken into consideration. For instance, the loss of a sandwich to a wealthy person is not felt as strongly as the loss of a sandwich to someone who is destitute. By the same token, the loss of $50 to a millionaire would be felt as less dramatically than a loss of $50 to a typical college student. This is known as the endowment effect.
Ariely et al. press the field forward by proposing potential mediators to both loss aversion and the endowment effect. First, emotional attachment goods may increase reluctance to part with them. In support of this theory, a study by Strahilevitz and Loewenstein (1998) showed that consumers adopt more ownership of items over time, providing support for moderation of loss aversion. Along with emotional attachment, Ariely et al. offer perspective change as a second mediator. While buyers are trying to minimize costs, sellers are trying to maximize gains. As a result, a price gap emerges. This gap is a product of the fact that people value items from different perspectives. In support of this notion, Carmon and Ariely (2000) have found that ticket sales to major sporting events depended on the manipulation of various benefits and opportunity costs, causing a shift in perspective about the purchase. In short, personal valuations of the monetary worth of products vary. Loss aversion could be mediated by one’s perspective of the good.
Furthermore, Dhar and Wertenbroch (2000) suggest that perhaps emotional attachment and cognitive perspective change could actually mediate the loss aversion for money. Although loss aversion has been seen to occur on a lesser scale than for money than goods, it is thought that cognitive allocation of money for certain goods could enhance loss aversion for currency. If the person’s perspective is that the money is to be spent on certain goods, feelings of loss over potential or intended goods may be felt.
While emotional attachment and perspective changes may very well mediate loss aversion and the endowment effect, another element of human perception of money particularly piques the author’s interest. Perhaps a mediator of the endowment effect for money could be the qualitative valuation differences of money. In other words, people place different levels on importance on money despite their current endowment. For example, the loss of $5,000 to a typical millionaire might be felt more dramatically than the loss of $5,000 to a hippy choosing to live on a commune who also happens to be a millionaire. The hippy may simply care less about money. Although their endowments are matched, they still may view the loss differently.
Perhaps this may partially be explained by a cultural overgeneralization of the value of the dollar. In other words, perhaps Americans tend to assume that other cultures may also highly value money. To demonstrate the point, an extreme example will be used: while many people in America strive to acquire wealth, Buddhist monks and people from communist countries, for example, place a very different personal value on currency. Although this concept is slightly similar to perspective change, Ariely et al discuss this potential mediator as short-term shifts rather than long-term persisting value differences. While they may be different constructs, perhaps perspective change and valuation are at opposing extremes of a larger unified construct of attitudes towards money. Furthermore, the construct of qualitative valuation differences of money is different than the idea of emotional attachment because it is not describing affection with a certain object, but a personalized concept of the importance of money. As previously mentioned, emotional attachment was only found with objects, not money. People who value money are not emotional attached to the money itself. An example of a group with a true emotional attachment to money might be coin collectors, while a group of people who think of money as important might be MBA students.
While it may be useful to utilize the example of Buddhist monks valuing money less than a typical American, it seems rational that varying degrees of qualitative valuations of money exist amongst Western people as well. The author thinks that differences in valuations are relevant because they have the capacity to highly impact decision making. Related to how one valuates money, may be irrational decision making. As a simple example, holding endowment constant, if one places importance on money itself, more of it may be saved rather than spent.
Other variables of interest might include the distinction between viewing money as a means to acquire goods versus a reward for work. It is the author's hypothesis that viewing money more as a reward than as a mean to acquire good would result in more conservative decision making.
An interesting study might assess differences in valuation of money amongst poker players and correlations to how they play the game. This particular subgroup was conceived as a sample for a hypothetical study because polarizations between placing high and low importance on money might be able to be studied in this population. Some may think of poker chips as directly relating to how many goods they are able to acquire, while other player may have more distance, and simply view the chips worth hefty amounts of money more as just small round discs of plastic. My guess is the players viewing money as chips may make more rational decisions in the game over time. While this doesn't exactly examine valuation of money, it may clearly depict how people make decisions based on how they perceive money.
Additionally, after this type of distinction is measured, a study might be able to code and quantify specific moves within a given set of games. Actual decision making regarding money could be observed this way. Perhaps there is a better way to execute the evaluation of the presence and socially relevant impact of varying valuations of money, but it is the author’s rough idea that poker players might be an interesting subgroup to study.
While the idea of individual valuation of money effecting decision making may seem reasonable, the author has not found literature on this topic. It was particularly surprising to find personal valuation of money was not mentioned anywhere as a potential mediator of the endowment effect. In short, research should be done in the area. First it must be determined if the phenomena exists. If it is found to exist, exploring it's role in decision making may provide useful insight into irrational and rational behavior regarding money.
The study of individual decision making is certainly incomplete without taking into account several elements of human psychology. Rather than thinking rationally about decisions to ensure a favorable outcome, people tend to make decisions without a rational foundation, often defaulting to a set of heuristics (Amir & Ariely, 2007). Without knowledge of these psychological components at work, risky or detrimental choices cannot be understood.
One of the most established phenomena in the psychology of human decision making is that people are generally loss averse. Not only do people feel negatively about loss, but losses tend to loom larger than gains (Ariely, Huber, & Wertenbroch, 2005). In other words, people view something as more valuable when they give it up than when they acquire it. Greater value is given to an item after it comes into one’s possession than beforehand. In a study conducted by Knestch (1989), the results showed that people were unwilling to trade the item they received, whether it be a mug or a candy bar, despite random assignment. While loss aversion has been found to exist with the exchange of goods in other studies as well (Kahneman, Knestch, and Thaler (1990), it has not been found to exist for the exchange of money or other goods that are used as currency (Heath & Soll, 1996, Thaler, 1985).
While a loss is inherently averse, it is subjective in that current endowment of both goods and money must be taken into consideration. For instance, the loss of a sandwich to a wealthy person is not felt as strongly as the loss of a sandwich to someone who is destitute. By the same token, the loss of $50 to a millionaire would be felt as less dramatically than a loss of $50 to a typical college student. This is known as the endowment effect.
Ariely et al. press the field forward by proposing potential mediators to both loss aversion and the endowment effect. First, emotional attachment goods may increase reluctance to part with them. In support of this theory, a study by Strahilevitz and Loewenstein (1998) showed that consumers adopt more ownership of items over time, providing support for moderation of loss aversion. Along with emotional attachment, Ariely et al. offer perspective change as a second mediator. While buyers are trying to minimize costs, sellers are trying to maximize gains. As a result, a price gap emerges. This gap is a product of the fact that people value items from different perspectives. In support of this notion, Carmon and Ariely (2000) have found that ticket sales to major sporting events depended on the manipulation of various benefits and opportunity costs, causing a shift in perspective about the purchase. In short, personal valuations of the monetary worth of products vary. Loss aversion could be mediated by one’s perspective of the good.
Furthermore, Dhar and Wertenbroch (2000) suggest that perhaps emotional attachment and cognitive perspective change could actually mediate the loss aversion for money. Although loss aversion has been seen to occur on a lesser scale than for money than goods, it is thought that cognitive allocation of money for certain goods could enhance loss aversion for currency. If the person’s perspective is that the money is to be spent on certain goods, feelings of loss over potential or intended goods may be felt.
While emotional attachment and perspective changes may very well mediate loss aversion and the endowment effect, another element of human perception of money particularly piques the author’s interest. Perhaps a mediator of the endowment effect for money could be the qualitative valuation differences of money. In other words, people place different levels on importance on money despite their current endowment. For example, the loss of $5,000 to a typical millionaire might be felt more dramatically than the loss of $5,000 to a hippy choosing to live on a commune who also happens to be a millionaire. The hippy may simply care less about money. Although their endowments are matched, they still may view the loss differently.
Perhaps this may partially be explained by a cultural overgeneralization of the value of the dollar. In other words, perhaps Americans tend to assume that other cultures may also highly value money. To demonstrate the point, an extreme example will be used: while many people in America strive to acquire wealth, Buddhist monks and people from communist countries, for example, place a very different personal value on currency. Although this concept is slightly similar to perspective change, Ariely et al discuss this potential mediator as short-term shifts rather than long-term persisting value differences. While they may be different constructs, perhaps perspective change and valuation are at opposing extremes of a larger unified construct of attitudes towards money. Furthermore, the construct of qualitative valuation differences of money is different than the idea of emotional attachment because it is not describing affection with a certain object, but a personalized concept of the importance of money. As previously mentioned, emotional attachment was only found with objects, not money. People who value money are not emotional attached to the money itself. An example of a group with a true emotional attachment to money might be coin collectors, while a group of people who think of money as important might be MBA students.
While it may be useful to utilize the example of Buddhist monks valuing money less than a typical American, it seems rational that varying degrees of qualitative valuations of money exist amongst Western people as well. The author thinks that differences in valuations are relevant because they have the capacity to highly impact decision making. Related to how one valuates money, may be irrational decision making. As a simple example, holding endowment constant, if one places importance on money itself, more of it may be saved rather than spent.
Other variables of interest might include the distinction between viewing money as a means to acquire goods versus a reward for work. It is the author's hypothesis that viewing money more as a reward than as a mean to acquire good would result in more conservative decision making.
An interesting study might assess differences in valuation of money amongst poker players and correlations to how they play the game. This particular subgroup was conceived as a sample for a hypothetical study because polarizations between placing high and low importance on money might be able to be studied in this population. Some may think of poker chips as directly relating to how many goods they are able to acquire, while other player may have more distance, and simply view the chips worth hefty amounts of money more as just small round discs of plastic. My guess is the players viewing money as chips may make more rational decisions in the game over time. While this doesn't exactly examine valuation of money, it may clearly depict how people make decisions based on how they perceive money.
Additionally, after this type of distinction is measured, a study might be able to code and quantify specific moves within a given set of games. Actual decision making regarding money could be observed this way. Perhaps there is a better way to execute the evaluation of the presence and socially relevant impact of varying valuations of money, but it is the author’s rough idea that poker players might be an interesting subgroup to study.
While the idea of individual valuation of money effecting decision making may seem reasonable, the author has not found literature on this topic. It was particularly surprising to find personal valuation of money was not mentioned anywhere as a potential mediator of the endowment effect. In short, research should be done in the area. First it must be determined if the phenomena exists. If it is found to exist, exploring it's role in decision making may provide useful insight into irrational and rational behavior regarding money.
Thursday, September 24, 2009
Meditation Increases the Size of Your Brain!
by Tara Deliberto
Meditation can actually increase the size of your cortex!
Here is a link to the article I read in the Gazette a couple of years ago.
There are many speculations as to what this increase in structure size has to do with increases in function; however, maybe we can piece some of the easy answers together by thinking about:
1) what functions of the cortex have been already been established
2) with what people self-report meditation helps them
First, the cortex is thought to control "higher-order" functioning, mainly rational thinking and mental control. Although I am not a Freud fan, it might be useful to illustrate the functions of the cortex by commenting that this is the structure where Freud's superego would reside in the brain. Because the cortex can be likened to a muscle in that size is positively correlated with strength/function (unless the increase in size is due to disease etc), we can assume that a bigger cortex means a higher capacity to carry out higher-order functions.
Second, it is very important to note that although SOME people use meditation to reduce stress in the moment, the focus of most serious meditation is NOT to be calm. One of the main focuses of meditation is to heighten awareness and become more in tune with what we are experiencing in the present moment. In this article, they did not use a stress-reduction exercise but one aimed at deep focus. Because thoughts intrusively pop in our minds about anything at all, it is an enormous task of self-control to focus on the immediate surroundings. Perhaps not surprisingly, most people report an increase in self-control as a result of meditation.
With that being said, I'm going to guess that this (very broadly) means meditation can really help increase self-control. If you practice self-control exercises through meditation, the part of your brain devoted to self-control (the cortex) gets bigger.
Meditation can actually increase the size of your cortex!
Here is a link to the article I read in the Gazette a couple of years ago.
There are many speculations as to what this increase in structure size has to do with increases in function; however, maybe we can piece some of the easy answers together by thinking about:
1) what functions of the cortex have been already been established
2) with what people self-report meditation helps them
First, the cortex is thought to control "higher-order" functioning, mainly rational thinking and mental control. Although I am not a Freud fan, it might be useful to illustrate the functions of the cortex by commenting that this is the structure where Freud's superego would reside in the brain. Because the cortex can be likened to a muscle in that size is positively correlated with strength/function (unless the increase in size is due to disease etc), we can assume that a bigger cortex means a higher capacity to carry out higher-order functions.
Second, it is very important to note that although SOME people use meditation to reduce stress in the moment, the focus of most serious meditation is NOT to be calm. One of the main focuses of meditation is to heighten awareness and become more in tune with what we are experiencing in the present moment. In this article, they did not use a stress-reduction exercise but one aimed at deep focus. Because thoughts intrusively pop in our minds about anything at all, it is an enormous task of self-control to focus on the immediate surroundings. Perhaps not surprisingly, most people report an increase in self-control as a result of meditation.
With that being said, I'm going to guess that this (very broadly) means meditation can really help increase self-control. If you practice self-control exercises through meditation, the part of your brain devoted to self-control (the cortex) gets bigger.
Thursday, March 12, 2009
The Common Bond Between Self-Control & Addiction: Glucose?
by Tara Deliberto
Believe it or not, glucose levels can have direct effects on your ability to control yourself. Studies done by Gailliot et al. show that slightly depleted glucose levels lead to more errors on tasks and less persistence, indicating decreased self-control. Because our natural instincts are so strong, the act of self-control over these impulses are thought to be the most mentally expensive cognitive ability.
Although we are less able to process glucose at night, some people have trouble controlling their glucose regardless of the time of day. Considering depleted glucose leads to a lack of self-control, perhaps it isn't surprising to learn that evidence suggests people who engage in criminal behavior have problems processing glucose. Along with criminal behavior, it makes sense to me that people with addictions may have similar physiological deficits.
Interestingly, there is evidence to suggest that people can actually be physiologically addicted to sugar. While one can develop a psychological addiction to almost anything, physiological addiction is indicated by the presence of a withdrawal process after the substance ceases to be used. Because the drug naloxone will induce withdrawal only if a person has a physiological addition, administering this drug tells us whether or not an addiction is present. Fascinatingly, it has been shown that giving this drug to rats consuming large quantities of glucose in fact causes withdrawal, indicating that physiological addition to sugar is possible(Colantioini et al., 2002).
Are you thinking what I'm thinking?
While it may be a stretch... perhaps over time people are negatively reinforced (this is when an aversive stimulus is taken away, not when a punishment is introduced)after eating sugar and not engaging in a problematic behaviors. They could even be positively reinforced by being able to complete a task successfully (etc) after consuming glucose. If addiction could be mediated by the inefficient processing of glucose, could increasing sugar intake work as a self-medicating impulse control process?
Although sugar consumption may act directly on the problematic system, other behaviors are most likely a result of the lack of regulation without the direct self-medicating component. For example, while drinking excessively could be used to self-medicate emotional problems, the immediate effect of drinking 15 beers is depleted glucose, not increased glucose. Although the impulsive act of drinking to excess in the first place could be partially due to a lack of glucose (with alcohol exacerbating lack of control), alcohol consumption doesn't act to solve the potential underlying problem of glucose being processed ineffciently in the way the sugar consumption may.
Any thoughts?
P.S. This is an edit from 2/15/12 - I just read a review paper by David Benton in Clinical Nutrition, 29, that suggests sucrose is not physiologically addicting in the same way substances are. Interesting.
Believe it or not, glucose levels can have direct effects on your ability to control yourself. Studies done by Gailliot et al. show that slightly depleted glucose levels lead to more errors on tasks and less persistence, indicating decreased self-control. Because our natural instincts are so strong, the act of self-control over these impulses are thought to be the most mentally expensive cognitive ability.
Although we are less able to process glucose at night, some people have trouble controlling their glucose regardless of the time of day. Considering depleted glucose leads to a lack of self-control, perhaps it isn't surprising to learn that evidence suggests people who engage in criminal behavior have problems processing glucose. Along with criminal behavior, it makes sense to me that people with addictions may have similar physiological deficits.
Interestingly, there is evidence to suggest that people can actually be physiologically addicted to sugar. While one can develop a psychological addiction to almost anything, physiological addiction is indicated by the presence of a withdrawal process after the substance ceases to be used. Because the drug naloxone will induce withdrawal only if a person has a physiological addition, administering this drug tells us whether or not an addiction is present. Fascinatingly, it has been shown that giving this drug to rats consuming large quantities of glucose in fact causes withdrawal, indicating that physiological addition to sugar is possible(Colantioini et al., 2002).
Are you thinking what I'm thinking?
While it may be a stretch... perhaps over time people are negatively reinforced (this is when an aversive stimulus is taken away, not when a punishment is introduced)after eating sugar and not engaging in a problematic behaviors. They could even be positively reinforced by being able to complete a task successfully (etc) after consuming glucose. If addiction could be mediated by the inefficient processing of glucose, could increasing sugar intake work as a self-medicating impulse control process?
Although sugar consumption may act directly on the problematic system, other behaviors are most likely a result of the lack of regulation without the direct self-medicating component. For example, while drinking excessively could be used to self-medicate emotional problems, the immediate effect of drinking 15 beers is depleted glucose, not increased glucose. Although the impulsive act of drinking to excess in the first place could be partially due to a lack of glucose (with alcohol exacerbating lack of control), alcohol consumption doesn't act to solve the potential underlying problem of glucose being processed ineffciently in the way the sugar consumption may.
Any thoughts?
P.S. This is an edit from 2/15/12 - I just read a review paper by David Benton in Clinical Nutrition, 29, that suggests sucrose is not physiologically addicting in the same way substances are. Interesting.
Thursday, February 12, 2009
TIME Magazine Article that Refers to My Paper!!
by Tara Deliberto
And now for some shameful self-promotion:
Here is a link to a TIME Magazine article on self-embedding that refers to a paper I wrote with Dr. Matt Nock!
The statistic that 38% of people get the idea to self-injure from the peers and 13% from the media is from Deliberto & Nock 2008. Personally, I think the other 49% is more interesting (right?! if there is no external source of the idea, how does it come about?!?), but I'm extremely grateful that the information is getting out there.
And now for some shameful self-promotion:
Here is a link to a TIME Magazine article on self-embedding that refers to a paper I wrote with Dr. Matt Nock!
The statistic that 38% of people get the idea to self-injure from the peers and 13% from the media is from Deliberto & Nock 2008. Personally, I think the other 49% is more interesting (right?! if there is no external source of the idea, how does it come about?!?), but I'm extremely grateful that the information is getting out there.
Friday, January 30, 2009
One Argument for Measuring Decreases in Anxiety: Depression
by Tara Deliberto
This post is an augmentation of a previous post entitled "Two Thoughts on Depression: Dexamethasone Suppression Tests and Cortisol."
As stated in previous entries, Acceptance and Commitment Therapy (ACT) does not advocate conscious attempts at anxiety reduction in favor of having the client experience and work through anxiety. Although I really do think this is a useful skill for many reasons (honest! see previous posts), I would argue it is very important not to lose sight of how important long term anxiety reduction can be for the health of the patient.
We know several facts:
1. Prolonged anxiety leads to prolonged cortisol exposure
2. Prolonged cortisol exposure leads to dysfunctions of the Hypothalamic-Pituitary-Adrenal axis (HPA-axis; which is involved w/ regulating emotions)
3. HPA dysfunction can lead to depression
Along with many other reasons previously stated, because constantly experiencing anxiety rather than decreasing anxiety may lead to depression (and I'd bet other physiological problems), I would argue that treatment should include as ONE metric, measurable decreases in the experience of anxiety over time.
If that is too subjective for you, I would advocate going straight to the source and measuring early morning levels of cortisol over time. Afterall, studies such as the one published in 2005 by Portella et al. suggest that elevated morning levels of cortisol can be a *risk factor* for depression, not just an indicator of current depression. I realize this is usually only done in research and not clinical practice; however, psychology should move in the direction of making clinical decisions from hard physiological data. I don't think it is beyond reason to suggest that in the future, people should be able to go to the doctor, expectorate (aka drool) into a tube, and have their cortisol levels tested a few times a year to see if they're at risk for developing depression, one of the most costly diseases in the country that puts people at risk for death by suicide.
This post is an augmentation of a previous post entitled "Two Thoughts on Depression: Dexamethasone Suppression Tests and Cortisol."
As stated in previous entries, Acceptance and Commitment Therapy (ACT) does not advocate conscious attempts at anxiety reduction in favor of having the client experience and work through anxiety. Although I really do think this is a useful skill for many reasons (honest! see previous posts), I would argue it is very important not to lose sight of how important long term anxiety reduction can be for the health of the patient.
We know several facts:
1. Prolonged anxiety leads to prolonged cortisol exposure
2. Prolonged cortisol exposure leads to dysfunctions of the Hypothalamic-Pituitary-Adrenal axis (HPA-axis; which is involved w/ regulating emotions)
3. HPA dysfunction can lead to depression
Along with many other reasons previously stated, because constantly experiencing anxiety rather than decreasing anxiety may lead to depression (and I'd bet other physiological problems), I would argue that treatment should include as ONE metric, measurable decreases in the experience of anxiety over time.
If that is too subjective for you, I would advocate going straight to the source and measuring early morning levels of cortisol over time. Afterall, studies such as the one published in 2005 by Portella et al. suggest that elevated morning levels of cortisol can be a *risk factor* for depression, not just an indicator of current depression. I realize this is usually only done in research and not clinical practice; however, psychology should move in the direction of making clinical decisions from hard physiological data. I don't think it is beyond reason to suggest that in the future, people should be able to go to the doctor, expectorate (aka drool) into a tube, and have their cortisol levels tested a few times a year to see if they're at risk for developing depression, one of the most costly diseases in the country that puts people at risk for death by suicide.
Wednesday, January 28, 2009
D-Cycloserine and Evaluative Conditioning
by Tara Deliberto
I'd like to preface this blog post by saying that I've chosen this particular medium through which to share my thoughts with you because I am able to take leaps & bounds beyond the current state of research without having it irreversibly published for eternity and marring my name. In this post, I take two budding areas of research, combine them, and proceed to *attempt* (cut me some slack!) following the combination of facts to their logical conclusion.
So here are the two budding areas of psychological research:
1) The drug D-Cycloserine (DCS) is known to help enhance behavioral unlearning during psychological treatment. For example, while a person may have learned to fear spiders and subsequently developed a spider phobia, DCS will accelerate the speed at which the person unlearns the fear of spiders during behavior therapy. In this case, behavior therapy would involve repeated exposure to spiders until the fear subsides. In addition, DCS prolongs the effects of this type of behavioral therapy. This process is theorized to work by changing cognitive associations, not necessarily conscious thoughts, over time.
2) Along w/ DCS being a very exciting new avenue of research, psychologists have developed a new type of technique called Evaluative Conditioning that implements a computer task that helps retrain the mind's associations. For example, while a person with depression associates sadness w/ themselves, repeatedly asking the person to pair a smiley face with the word "me" during a computer task will help retrain the previous association so that the person now associates happiness w/ themselves.
With these facts in mind, I would argue it is worth studying the combined effects of DCS and Evaluative Conditioning. It seems to me that DCS will probably enhance the effects of Evaluative Conditioning. Right? The idea here being: since Evaluative Conditioning is used to retrain cognitive associations and DCS has been used to facilitate exposure therapy (i.e. unlearning behavior), which is hypothesized to work via changing associations, the use of DSC w/ Evaluative Conditioning could enhance the retraining of maladaptive associations. Of note, it would most likely only work if the evaluative conditioning stimuli were potent enough to instill fear in participants as DCS only facilitates fear learning. Perhaps the fear doesn't even have to be specific to what the person's pathology is - maybe watching a scary movie beforehand would suffice.
Initially I was thinking that lessening the role of the therapist could lead to the benefit (eventually & if it worked) to decreased cost of treatment; however, paying to use the computer program along w/ the cost of the medication could be prove to be steep. In any event, if the combined effects of DCS and Evaluative Conditioning statistically outperform other methods of treatment, that fact would be useful in and of itself.
On the other hand, if the combined effects prove to be on par with similar psychological treatments, the use of either combined DCS+EC or DCS+regular therapy should be evaluated for specific use in different populations. For example, people w/ autism may respond better to DCS+EC than DCS+regular therapy because of the removed social component. I do realize, though, that one could argue that removing the social component of treatment for people w/ autism could be detrimental because social interaction could facilitate increased social skill. However, to get rid of a troublesome fears quickly, a combined DCS+EC treatment could theoretically be useful. Furthermore, in addition to DCS+EC, a separate targeted social intervention treatment would probably be called for.
I'd like to preface this blog post by saying that I've chosen this particular medium through which to share my thoughts with you because I am able to take leaps & bounds beyond the current state of research without having it irreversibly published for eternity and marring my name. In this post, I take two budding areas of research, combine them, and proceed to *attempt* (cut me some slack!) following the combination of facts to their logical conclusion.
So here are the two budding areas of psychological research:
1) The drug D-Cycloserine (DCS) is known to help enhance behavioral unlearning during psychological treatment. For example, while a person may have learned to fear spiders and subsequently developed a spider phobia, DCS will accelerate the speed at which the person unlearns the fear of spiders during behavior therapy. In this case, behavior therapy would involve repeated exposure to spiders until the fear subsides. In addition, DCS prolongs the effects of this type of behavioral therapy. This process is theorized to work by changing cognitive associations, not necessarily conscious thoughts, over time.
2) Along w/ DCS being a very exciting new avenue of research, psychologists have developed a new type of technique called Evaluative Conditioning that implements a computer task that helps retrain the mind's associations. For example, while a person with depression associates sadness w/ themselves, repeatedly asking the person to pair a smiley face with the word "me" during a computer task will help retrain the previous association so that the person now associates happiness w/ themselves.
With these facts in mind, I would argue it is worth studying the combined effects of DCS and Evaluative Conditioning. It seems to me that DCS will probably enhance the effects of Evaluative Conditioning. Right? The idea here being: since Evaluative Conditioning is used to retrain cognitive associations and DCS has been used to facilitate exposure therapy (i.e. unlearning behavior), which is hypothesized to work via changing associations, the use of DSC w/ Evaluative Conditioning could enhance the retraining of maladaptive associations. Of note, it would most likely only work if the evaluative conditioning stimuli were potent enough to instill fear in participants as DCS only facilitates fear learning. Perhaps the fear doesn't even have to be specific to what the person's pathology is - maybe watching a scary movie beforehand would suffice.
Initially I was thinking that lessening the role of the therapist could lead to the benefit (eventually & if it worked) to decreased cost of treatment; however, paying to use the computer program along w/ the cost of the medication could be prove to be steep. In any event, if the combined effects of DCS and Evaluative Conditioning statistically outperform other methods of treatment, that fact would be useful in and of itself.
On the other hand, if the combined effects prove to be on par with similar psychological treatments, the use of either combined DCS+EC or DCS+regular therapy should be evaluated for specific use in different populations. For example, people w/ autism may respond better to DCS+EC than DCS+regular therapy because of the removed social component. I do realize, though, that one could argue that removing the social component of treatment for people w/ autism could be detrimental because social interaction could facilitate increased social skill. However, to get rid of a troublesome fears quickly, a combined DCS+EC treatment could theoretically be useful. Furthermore, in addition to DCS+EC, a separate targeted social intervention treatment would probably be called for.
Wednesday, January 21, 2009
More Cognitive Defusion vs Cognitive Reappraisal Thoughts
by Tara Deliberto
Note: It may be best to read the post immediately prior to this one first, "Quibbles with Acceptance and Commitment Therapy."
Topic: Currently, Acceptance and Commitment Therapy completely rejects the use of thought manipulation techniques used in Cognitive Therapy in favor of meditative mindfulness techniques.
Thoughts: It seems like the next line of research in psychological treatment should focus on the implementation of specific techniques for specific problems (a`la Barlow's unified treatment protocol). Being that cognitive reappraisal (CR) and cognitive defusion (CD) are, in fact, two different techniques, I've simply been wondering (and I'm sure I'm not alone) whether or not one technique can be more useful than the other in certain situations.
[definitions: CR = a technique used in Cognitive Therapy that involves monitoring and evaluating negative thoughts and replacing them with positive thoughts/images; CD = a technique used in Acceptance and Commitment Therapy that involves deliteralizing the meaning of thoughts by actively "observing thoughts as thoughts" and recognizing that all thoughts may not be true ]
For the sake of providing an example, while CR may be more effective during moments of anhedonia (inability to experience pleasure) in that it could get the client actively engaged in positive thinking [which may or may not enable the person to engage in active behavior but I would argue, decreases suffering in the present moment], CD may be more suitable for moments of anxiety in that it has the quiet quality of observing and focus on being present while anxiety arouses people and can cause a lack of presence. I use the term "moments" here in order to highlight that comorbidity of anxiety and depression is common and implementing the different tools at different times for the same person may be beneficial. Simply, I think that abandoning cognitive therapy (CT) techniques such as CR completely without conclusive research indicating one method is superior in all cases to the other is premature.
Referring back to the comment about decreasing suffering by using CR as a technique for people w/ anhedonia: On a slightly more theoretical note, I have been struggling with the idea of whether or not the primary/ultimate goal of therapy should be on helping the person to live life in accordance with ones values as in Acceptance and Commitment Therapy (ACT) or to decrease the net amount of life suffering. Perhaps decreasing the total amount of life suffering should be done through helping the person live life in accordance with ones values. As per my previous post, I think that perhaps behaviorally activating by living life in accordance with one's values should decrease long-term suffering and shouldn't be an end in itself. Perhaps, somewhat ironically, if the client concentrates on symptom reduction as the end goal of behavioral activation (BA), less symptom reduction could possibly occur. With the mindset that engaging in BA will lead to symptom reduction, if the effects are not immediate, the person may abandon the strategy. Because ACT encourages people to engage in BA regardless of outcome, the person may be more likely to continue engaging in BA as a result of a lack of discouragement about immediate results; however, I would argue that it is important not to lose sight of the fact that decreasing suffering should be the ultimate goal, even if it is not presented to the client in this light. I fear the mindset that decreasing suffering or increasing positive emotion isn't important may lead to the rejection useful techniques such as CR that may help the person lead life in accordance with their values.
[definition: BA = getting the client to engage in meaningful behavior; this technique is now thought to be the most potent component across various forms of psychological treatments]
From a funcitonal perspective (and in keeping with the thoughts expressed in me previous blog post about the endogenous reward system) it seems that both thinking positively through CR and BA can activate the reward system in the brain. My guess is that BA would be more potent than changing a negative thought to a positive one, but both could produce similar effects- reward via positive reinforcement in the form of opioids. While BA and CR may work through positive reinforcement, CD may work through negative reinforcement- taking an aversive stimulus away (NOT to be confused with introducing a punishment). By distancing oneself from a negative thought, the aversiveness is decreased. If viewed in the light that both CR/BA and CD work on reinforcement schedules by decreasing suffering, the notion that it isn't important to decrease suffering in therapy no longer makes much sense to me.
It is worth noting that while BA releases opioids, it may not necessarily equate a feeling of happiness, and therefore a direct reward in the form of positive reinforcement. From a more biological perspective, during BA, the release of opioids may not result in an overall emotion of happiness, but perhaps their release has effects on a subconscious level (for lack of a better term). I'm trying to get at the essence of what maintains a behavior biologically. I implicate opioids, but it may be any known or unknown substance in the brain that is released during BA that helps form associations between action and reward (see the part Endogenous Reward System post pertaining to feedback loops).
From a psychological perspective, I would argue that although BA may not lead directly to a feeling of happiness (i.e. when a person with depression first gets off the couch, it is dreadful), it may still be maintained via positive reinforcement because by behaviorally activating, one is living life in accordance w/ ones values, which may lead to a more abstract reward than feeling intense bodily pleasure in the moment. I'm sure physiologists and hard scientists may have a problem with this view; however, my stance is one of actually erring on the side of pure biology. I think that all thoughts are biological - even the more abstract ones that science has yet to understand. I would argue that a biological reward must exist even for the experience and consequent emotions of abstract thought. After all, when biological brain tissue dies, so does abstract thought.
Note: It may be best to read the post immediately prior to this one first, "Quibbles with Acceptance and Commitment Therapy."
Topic: Currently, Acceptance and Commitment Therapy completely rejects the use of thought manipulation techniques used in Cognitive Therapy in favor of meditative mindfulness techniques.
Thoughts: It seems like the next line of research in psychological treatment should focus on the implementation of specific techniques for specific problems (a`la Barlow's unified treatment protocol). Being that cognitive reappraisal (CR) and cognitive defusion (CD) are, in fact, two different techniques, I've simply been wondering (and I'm sure I'm not alone) whether or not one technique can be more useful than the other in certain situations.
[definitions: CR = a technique used in Cognitive Therapy that involves monitoring and evaluating negative thoughts and replacing them with positive thoughts/images; CD = a technique used in Acceptance and Commitment Therapy that involves deliteralizing the meaning of thoughts by actively "observing thoughts as thoughts" and recognizing that all thoughts may not be true ]
For the sake of providing an example, while CR may be more effective during moments of anhedonia (inability to experience pleasure) in that it could get the client actively engaged in positive thinking [which may or may not enable the person to engage in active behavior but I would argue, decreases suffering in the present moment], CD may be more suitable for moments of anxiety in that it has the quiet quality of observing and focus on being present while anxiety arouses people and can cause a lack of presence. I use the term "moments" here in order to highlight that comorbidity of anxiety and depression is common and implementing the different tools at different times for the same person may be beneficial. Simply, I think that abandoning cognitive therapy (CT) techniques such as CR completely without conclusive research indicating one method is superior in all cases to the other is premature.
Referring back to the comment about decreasing suffering by using CR as a technique for people w/ anhedonia: On a slightly more theoretical note, I have been struggling with the idea of whether or not the primary/ultimate goal of therapy should be on helping the person to live life in accordance with ones values as in Acceptance and Commitment Therapy (ACT) or to decrease the net amount of life suffering. Perhaps decreasing the total amount of life suffering should be done through helping the person live life in accordance with ones values. As per my previous post, I think that perhaps behaviorally activating by living life in accordance with one's values should decrease long-term suffering and shouldn't be an end in itself. Perhaps, somewhat ironically, if the client concentrates on symptom reduction as the end goal of behavioral activation (BA), less symptom reduction could possibly occur. With the mindset that engaging in BA will lead to symptom reduction, if the effects are not immediate, the person may abandon the strategy. Because ACT encourages people to engage in BA regardless of outcome, the person may be more likely to continue engaging in BA as a result of a lack of discouragement about immediate results; however, I would argue that it is important not to lose sight of the fact that decreasing suffering should be the ultimate goal, even if it is not presented to the client in this light. I fear the mindset that decreasing suffering or increasing positive emotion isn't important may lead to the rejection useful techniques such as CR that may help the person lead life in accordance with their values.
[definition: BA = getting the client to engage in meaningful behavior; this technique is now thought to be the most potent component across various forms of psychological treatments]
From a funcitonal perspective (and in keeping with the thoughts expressed in me previous blog post about the endogenous reward system) it seems that both thinking positively through CR and BA can activate the reward system in the brain. My guess is that BA would be more potent than changing a negative thought to a positive one, but both could produce similar effects- reward via positive reinforcement in the form of opioids. While BA and CR may work through positive reinforcement, CD may work through negative reinforcement- taking an aversive stimulus away (NOT to be confused with introducing a punishment). By distancing oneself from a negative thought, the aversiveness is decreased. If viewed in the light that both CR/BA and CD work on reinforcement schedules by decreasing suffering, the notion that it isn't important to decrease suffering in therapy no longer makes much sense to me.
It is worth noting that while BA releases opioids, it may not necessarily equate a feeling of happiness, and therefore a direct reward in the form of positive reinforcement. From a more biological perspective, during BA, the release of opioids may not result in an overall emotion of happiness, but perhaps their release has effects on a subconscious level (for lack of a better term). I'm trying to get at the essence of what maintains a behavior biologically. I implicate opioids, but it may be any known or unknown substance in the brain that is released during BA that helps form associations between action and reward (see the part Endogenous Reward System post pertaining to feedback loops).
From a psychological perspective, I would argue that although BA may not lead directly to a feeling of happiness (i.e. when a person with depression first gets off the couch, it is dreadful), it may still be maintained via positive reinforcement because by behaviorally activating, one is living life in accordance w/ ones values, which may lead to a more abstract reward than feeling intense bodily pleasure in the moment. I'm sure physiologists and hard scientists may have a problem with this view; however, my stance is one of actually erring on the side of pure biology. I think that all thoughts are biological - even the more abstract ones that science has yet to understand. I would argue that a biological reward must exist even for the experience and consequent emotions of abstract thought. After all, when biological brain tissue dies, so does abstract thought.
A Few Quibbles with Acceptance and Commitment Therapy
by Tara Deliberto
In a recent lab meeting, I was engaged in a discussion of the paradigm shift between the focus of therapy being symptom reduction, as seen in other therapies (i.e. cognitive-behavioral therapy), towards helping the client to live a life in accordance with their values, as in ACT. The irresolution of an argument centering on this point prompted me to write this entry.
In ACT there is not only an emphasis on living life in accordance with one’s values, but it seems a fairly outright denunciation of attempting to control or manipulate thoughts as a form of emotion regulation. Although I am aware of the research indicating thought/expressive suppression is an unsuccessful method of controlling thoughts/emotions, often resulting in increases in the targeted thoughts/emotions, there is evidence to suggest that cognitive reappraisal, the revaluation of negative thoughts, is effective (in fact, I presented research at the Associations for Behavioral and Cognitive Therapies conference in 2006 on cognitive reappraisal being a potential mechanism of change in intensive DBT). I understand that because attempts at suppressing thoughts are futile, as a therapist one should not encourage this; however, I do not understand what appears to possibly be an overgeneralization to advise against ever attempting forms of thought manipulation, especially when reappraising cognitions appears to be beneficial [If this blog entry were actual dialogue, this would be the point where I may get into a semantics discussion with ACT practitioners about the word “beneficial.” Although this word was previously used in reference to symptom reduction, I would argue that it is safe to say that using cognitive reappraisal as a tool can also help one to lead a life in accordance with one’s values.].
That is not to say, of course, that cognitive reappraisal should be a focus of the treatment or that mindfulness should be abandoned. Quite the opposite. I am merely suggesting that perhaps all attempts at thought/emotion manipulation should not be abandoned. Perhaps mindfulness can be used as a tool the majority of the time for some problems whereas cognitive reappraisal can be used as a tool occasionally for other types.
Of note, I have come to conceptualize two types of mindfulness, which may be incorrect, but here they are:
1) allowing oneself to fully experience a thought/emotion without attempt at suppression
2) allowing oneself to view thoughts/emotions objectively as thoughts/emotion
I realize the following thought is not original; however, it may be worth noting here that the first conceptualization of mindfulness may be effective through means similar to that of exposure. Basically, if one stops avoiding or attempting to avoid the emotion, it is learned that the emotion can be experienced and survived.
I have not previously heard interpretations of why I think the second type of mindfulness may be effective. I realize that while mindfulness and defusion are separate concepts, perhaps mindfulness facilitates defusion, the process of observing thoughts as thoughts. Through mindfulness practices such as watching our thoughts float by, maybe we are essentially creating distance with our thoughts. This distance may help facilitate a non-judgmental stance of one’s thoughts. I was attempting to make the point that maybe the non-judgmental quality of viewing thoughts in essence may be a “reappraisal” of the thoughts in that they no longer hold a negative valence (not that they are being judged as positive, per se). At the end of the process of cognitive reappraisal, thoughts also no longer hold negative valences. Perhaps the reasons why mindfulness & cognitive defusion along with cognitive reappraisal seem to be effective could be similar, not that they are necessarily the same process. In short, these processes may achieve similar ends through different means. I do, however, suspect that mindfulness probably achieves these means in a more effective manner. Because people with emotional disorders are in the habit of attempting to suppress thoughts while healthy controls are more able to accept their negative emotions and function in society, an approach geared away from thought manipulation in general may be appropriate.
In addition, I am aware that in light of the recent literature suggesting that behavioral activation- simply put, carrying out daily activities despite symptoms- is a main mechanism of change in many psychological treatments, all the talk of cognitions seems futile; however, I think it is necessary. It is interesting that behavioral activation is so closely in line with the goal of ACT: living life towards ones values in the context of one’s symptoms. With this as a treatment goal, one is essentially turning the client’s attention away from thought/emotional suppression and gearing them to behaviorally activate. The “gearing” or framework in which the behavioral activation is nestled may be the determining factor in whether or not one actually begins to behaviorally activate or start living life in accordance with one’s values. Therefore packaging behavioral activation in ACT with mindfulness may be more useful than packaging it with the cognitive (and other) pieces of cognitive behavioral therapy. It is also of note that while in cognitive-behavioral/behavioral therapy, behavioral activation is the means through which symptoms are reduced, in ACT, the goal is to behaviorally activate without necessary symptom reduction. It is possible that gearing the therapy without the expectation of symptom reduction, as in ACT, may actually result in greater symptom reduction than CBT for some people. Again, this could possibly be because people with emotional disorders are constantly struggling with control and suppression of thoughts/emotions so that when they are in a context encouraging them to largely give up control, behavioral activation could be facilitated more so than in a treatment focused on symptom reduction.
In a recent lab meeting, I was engaged in a discussion of the paradigm shift between the focus of therapy being symptom reduction, as seen in other therapies (i.e. cognitive-behavioral therapy), towards helping the client to live a life in accordance with their values, as in ACT. The irresolution of an argument centering on this point prompted me to write this entry.
In ACT there is not only an emphasis on living life in accordance with one’s values, but it seems a fairly outright denunciation of attempting to control or manipulate thoughts as a form of emotion regulation. Although I am aware of the research indicating thought/expressive suppression is an unsuccessful method of controlling thoughts/emotions, often resulting in increases in the targeted thoughts/emotions, there is evidence to suggest that cognitive reappraisal, the revaluation of negative thoughts, is effective (in fact, I presented research at the Associations for Behavioral and Cognitive Therapies conference in 2006 on cognitive reappraisal being a potential mechanism of change in intensive DBT). I understand that because attempts at suppressing thoughts are futile, as a therapist one should not encourage this; however, I do not understand what appears to possibly be an overgeneralization to advise against ever attempting forms of thought manipulation, especially when reappraising cognitions appears to be beneficial [If this blog entry were actual dialogue, this would be the point where I may get into a semantics discussion with ACT practitioners about the word “beneficial.” Although this word was previously used in reference to symptom reduction, I would argue that it is safe to say that using cognitive reappraisal as a tool can also help one to lead a life in accordance with one’s values.].
That is not to say, of course, that cognitive reappraisal should be a focus of the treatment or that mindfulness should be abandoned. Quite the opposite. I am merely suggesting that perhaps all attempts at thought/emotion manipulation should not be abandoned. Perhaps mindfulness can be used as a tool the majority of the time for some problems whereas cognitive reappraisal can be used as a tool occasionally for other types.
Of note, I have come to conceptualize two types of mindfulness, which may be incorrect, but here they are:
1) allowing oneself to fully experience a thought/emotion without attempt at suppression
2) allowing oneself to view thoughts/emotions objectively as thoughts/emotion
I realize the following thought is not original; however, it may be worth noting here that the first conceptualization of mindfulness may be effective through means similar to that of exposure. Basically, if one stops avoiding or attempting to avoid the emotion, it is learned that the emotion can be experienced and survived.
I have not previously heard interpretations of why I think the second type of mindfulness may be effective. I realize that while mindfulness and defusion are separate concepts, perhaps mindfulness facilitates defusion, the process of observing thoughts as thoughts. Through mindfulness practices such as watching our thoughts float by, maybe we are essentially creating distance with our thoughts. This distance may help facilitate a non-judgmental stance of one’s thoughts. I was attempting to make the point that maybe the non-judgmental quality of viewing thoughts in essence may be a “reappraisal” of the thoughts in that they no longer hold a negative valence (not that they are being judged as positive, per se). At the end of the process of cognitive reappraisal, thoughts also no longer hold negative valences. Perhaps the reasons why mindfulness & cognitive defusion along with cognitive reappraisal seem to be effective could be similar, not that they are necessarily the same process. In short, these processes may achieve similar ends through different means. I do, however, suspect that mindfulness probably achieves these means in a more effective manner. Because people with emotional disorders are in the habit of attempting to suppress thoughts while healthy controls are more able to accept their negative emotions and function in society, an approach geared away from thought manipulation in general may be appropriate.
In addition, I am aware that in light of the recent literature suggesting that behavioral activation- simply put, carrying out daily activities despite symptoms- is a main mechanism of change in many psychological treatments, all the talk of cognitions seems futile; however, I think it is necessary. It is interesting that behavioral activation is so closely in line with the goal of ACT: living life towards ones values in the context of one’s symptoms. With this as a treatment goal, one is essentially turning the client’s attention away from thought/emotional suppression and gearing them to behaviorally activate. The “gearing” or framework in which the behavioral activation is nestled may be the determining factor in whether or not one actually begins to behaviorally activate or start living life in accordance with one’s values. Therefore packaging behavioral activation in ACT with mindfulness may be more useful than packaging it with the cognitive (and other) pieces of cognitive behavioral therapy. It is also of note that while in cognitive-behavioral/behavioral therapy, behavioral activation is the means through which symptoms are reduced, in ACT, the goal is to behaviorally activate without necessary symptom reduction. It is possible that gearing the therapy without the expectation of symptom reduction, as in ACT, may actually result in greater symptom reduction than CBT for some people. Again, this could possibly be because people with emotional disorders are constantly struggling with control and suppression of thoughts/emotions so that when they are in a context encouraging them to largely give up control, behavioral activation could be facilitated more so than in a treatment focused on symptom reduction.
Friday, January 16, 2009
Thoughts on the Course of Self-Injury
by Tara Deliberto
Non-Suicidal Self-Injury (NSSI) refers to the direct and delibertate destruction of one's own body tissue without intent to die. Most people who engage in NSSI use razor blades or knifes to break the skin in an attempt to regulate their emotions. I usually describe NSSI in this way to my friends: Did you ever see a movie where someone was losing control, a friend slapped them in the face, and then the person suddenly regained control? Well, NSSI is like that only it is the person who hurts themselves. To the shock of most of my friends, less often, people report engaging in NSSI for social gain- i.e. getting attention or eliciting sympathy.
Nock & Prinstien outline the four reasons/functions people report for engaging in NSSI; however, not only can one person be engaging in NSSI for two or more reasons in one instance, I think there is a more dynamic process of development and maintenance of NSSI through various functions at different times.
At first I thought social reinforcement ("doing it for attention") could certainly be a secondary gain of engaging in NSSI (exactly like social support being a "secondary gain" in treatment of medical illnesses) and therefore, help maintain the behavior after the first episode. Then I started thinking... well, for that matter, one could also initially engage in NSSI primarily for social approval and also feel a decrease in physiological arousal, right?. That lead me down the path of wondering what functions maintain the behavior over time.
Surely, one can start engaging in NSSI solely for social reinforcement, which then elicits a positive emotion. But then, after a while, perhaps engaging in NSSI in the absence of reinforcement from other people can decreases negative emotions without necessitating actually receiving support (Pavlov's dog style!!!). Again... for that matter... the reverse is probably true too! For example, some people could engage in NSSI for the first time in the total absence of social support and receive an automatic decrease in physiological arousal. Over time, after eventually sharing this information and gaining social support, the behavior that was once used as a tool for automatic physiological arousal decreases can be used to solicit social support.
I would certainly expect an even more complex and dynamic system of functions maintaining the behavior to develop over time, with each relevant function contributing a varying amount. Additionally, I would expect the range of situations prompting the usage of NSSI to range anywhere from narrow to broad/generalized over time (meaning that it can go from broad to narrow to broad... or narrow to broad to stopping completely... or any combination over time, NOT just narrow to broad!).
In short: NSSI is a multipurpose tool that is automatically picked out of the toolbox in response to a wide array of situations and can fix the problems in different ways over time.
Non-Suicidal Self-Injury (NSSI) refers to the direct and delibertate destruction of one's own body tissue without intent to die. Most people who engage in NSSI use razor blades or knifes to break the skin in an attempt to regulate their emotions. I usually describe NSSI in this way to my friends: Did you ever see a movie where someone was losing control, a friend slapped them in the face, and then the person suddenly regained control? Well, NSSI is like that only it is the person who hurts themselves. To the shock of most of my friends, less often, people report engaging in NSSI for social gain- i.e. getting attention or eliciting sympathy.
Nock & Prinstien outline the four reasons/functions people report for engaging in NSSI; however, not only can one person be engaging in NSSI for two or more reasons in one instance, I think there is a more dynamic process of development and maintenance of NSSI through various functions at different times.
At first I thought social reinforcement ("doing it for attention") could certainly be a secondary gain of engaging in NSSI (exactly like social support being a "secondary gain" in treatment of medical illnesses) and therefore, help maintain the behavior after the first episode. Then I started thinking... well, for that matter, one could also initially engage in NSSI primarily for social approval and also feel a decrease in physiological arousal, right?. That lead me down the path of wondering what functions maintain the behavior over time.
Surely, one can start engaging in NSSI solely for social reinforcement, which then elicits a positive emotion. But then, after a while, perhaps engaging in NSSI in the absence of reinforcement from other people can decreases negative emotions without necessitating actually receiving support (Pavlov's dog style!!!). Again... for that matter... the reverse is probably true too! For example, some people could engage in NSSI for the first time in the total absence of social support and receive an automatic decrease in physiological arousal. Over time, after eventually sharing this information and gaining social support, the behavior that was once used as a tool for automatic physiological arousal decreases can be used to solicit social support.
I would certainly expect an even more complex and dynamic system of functions maintaining the behavior to develop over time, with each relevant function contributing a varying amount. Additionally, I would expect the range of situations prompting the usage of NSSI to range anywhere from narrow to broad/generalized over time (meaning that it can go from broad to narrow to broad... or narrow to broad to stopping completely... or any combination over time, NOT just narrow to broad!).
In short: NSSI is a multipurpose tool that is automatically picked out of the toolbox in response to a wide array of situations and can fix the problems in different ways over time.
Two Thoughts on Depression: Dexamethasone Suppression Tests and Cortisol
by Tara Deliberto
Cortisol and Depression:
1) The research on depression shows us that when dexamethasone is administered to people w/ depression and controls, people with depression do not show a decrease in their cortisol levels unlike their non-depressed counter-parts. In addition, we know that increased glucocorticoids such as cortisol increases the susceptibility of the brain (Gubba et al 2000; Sapolsky, 1985). Judging from these facts, it seems to me that people with a predisposition to non-suppression of cortisol who are on long term steroid treatment (i.e. people w/rheumatoid arthritis taking prednisone), could end up with depression because of prolonged exposure to cortisol as a side effect from the drug.
2) We also know that people with depression have higher levels of early morning cortisol. Although people w/ depression may have trouble suppressing cortisol in general, perhaps the early morning elevations of cortisol could, in part, simply have to do with having bad dreams. Chronically high level of cortisol produced during sleep could possibly lead to a dysfunctional HPA axis (hypothalamic-pituitary-adrenal axis - part of the neuroendocrine system that helps regulate stress). If this could be the case, perhaps treating people with prodromal depression/ depression with both drugs that have been shown to decrease production of nocturnal cortisol (probably through the decreased occurrence of nightmares) and perhaps even training in lucid dreaming or relaxation may be useful. Because high levels of anxiety can lead to prolonged problems, unlike many of my Acceptance and Commitment Therapy counterparts, I would argue that stress reduction training can be a very useful long term benefit.
In other words, since we know that prolonged anxiety leads to prolonged cortisol exposure, which could lead to dysfunction of the HPA axis, which leads to depression... maybe we shouldn't discount trying to decrease anxiety!
Cortisol and Depression:
1) The research on depression shows us that when dexamethasone is administered to people w/ depression and controls, people with depression do not show a decrease in their cortisol levels unlike their non-depressed counter-parts. In addition, we know that increased glucocorticoids such as cortisol increases the susceptibility of the brain (Gubba et al 2000; Sapolsky, 1985). Judging from these facts, it seems to me that people with a predisposition to non-suppression of cortisol who are on long term steroid treatment (i.e. people w/rheumatoid arthritis taking prednisone), could end up with depression because of prolonged exposure to cortisol as a side effect from the drug.
2) We also know that people with depression have higher levels of early morning cortisol. Although people w/ depression may have trouble suppressing cortisol in general, perhaps the early morning elevations of cortisol could, in part, simply have to do with having bad dreams. Chronically high level of cortisol produced during sleep could possibly lead to a dysfunctional HPA axis (hypothalamic-pituitary-adrenal axis - part of the neuroendocrine system that helps regulate stress). If this could be the case, perhaps treating people with prodromal depression/ depression with both drugs that have been shown to decrease production of nocturnal cortisol (probably through the decreased occurrence of nightmares) and perhaps even training in lucid dreaming or relaxation may be useful. Because high levels of anxiety can lead to prolonged problems, unlike many of my Acceptance and Commitment Therapy counterparts, I would argue that stress reduction training can be a very useful long term benefit.
In other words, since we know that prolonged anxiety leads to prolonged cortisol exposure, which could lead to dysfunction of the HPA axis, which leads to depression... maybe we shouldn't discount trying to decrease anxiety!
Thursday, October 16, 2008
Endogenous Reward System: the Etiology and Treatment of Depression
by Tara Deliberto
Summary
The possibility exists that dysfunction at various levels of a biological reward system, such as the dopaminergic mesolimbic pathway, could be involved in etiology and maintenance of depression. Current descriptions of the role that specific factors, such as dopamine, play in the endogenous reward system have been incomplete; therefore, other factors are likely involved as well.
Keywords: Depression, endorphin, beta-endorphin, etiology, treatment
Introduction
It is well known that environmental reinforcement has an effect on one’s behavior; therefore, a biological system through which the organism is able to process and experience reinforcement must exist, yet is not extremely well understood. It is possible that through dysfunction at various levels of a biological reward system, psychological disorders such as depression can result or be maintained. Furthermore, if acquired or genetic dysfunctions in the biological reward system result in psychopathology, it can be argued that ameliorating these problems can result in further success in treating depression.
Several possible brain structures have emerged as being involved in the biological reward system. In recent years, the nucleus accumbens (NAS) has been supported as the key structure in the reward center of the brain. The involvement of the NAS in reinforcement has been demonstrated for both natural (logically related to the task) and artificial rewards (not logically related to the task; Rada, Colasante, Skirzewski, Hernandez & Hoebel, 2006). Reinforcement is hypothesized to be mediated through regulation of dopamine in the NAS; however, several pieces of evidence point to additional contributing factors. For example, while depletion of dopamine in the NAS has been shown to affect operant responding, it does not necessarily affect unconditioned reinforcement (Salmone & Correa, 2002). This means that DA does not affect conditioning to reinforcers that are naturally reinforcing. Because natural reinforcers such as food can be quite strong, DA’s role in conditioning may not be as important as previously thought. Therefore, other biological factors are likely involved in learning through reinforcement.
Also present in the NAS is beta-endorphin, an endogenous opioid peptide that has been implicated in the reward process. For example, it has been shown that beta-endorphin levels have increased in the NAS in rats during extinction learning. The results from this study indicate that beta-endorphin can be involved in both learning and adaptive responding to distress (Rada et al., 2006). Because beta-endorphin may be involved with operant conditioning and responses to stress, it could be involved with the onset or maintenance of depression (and impulsive behavior as well).
Role of beta-Endorphin in Onset
Due to a possible dysfunction in the reward system from environmental or biological etiology, the organism may not experience the environment as rewarding. It has been well-observed that people may actively seek out maladaptive ways to be rewarded. Various addictive disorders such as alcoholism, opiate addiction, cigarette smoking, excessive exercise, and starvation have all been linked to beta-endorphin dysfunction, and therefore, can possible be viewed as reward seeking behaviors. For example, people with a high genetic risk for developing alcoholism have lower levels of beta-endorphin. Perhaps not surprisingly, drinking alcohol increases levels of beta-endorphin (Dai, Thavundayil & Glanoulakis, 2005; Zalewska-Kaszubska & Czarnecka , 2005). In addition, it has been indicated that single-nucleotide polymorphism in the mu opiod receptor gene alters beta-endorphin binding and activity exists and could be related to opiate addiction (Bond, LaForge, Tian, Melia, Zhang, Borg, et al., 1998). Furthermore, people who smoke cigarettes have lower levels of basal beta-endorphin than those who do not smoke (Lee, Joe, Sohn, Na, Kee & Chae, 2005). Those who smoke more than 20 cigarettes per day have lower levels of beta-endorphin than those who smoke less than 10 cigarettes per day. In addition, those who smoke less than 10 cigarettes per day have lower beta-endorphin levels than controls (de Arbol, Munoz, Ojeda, Cascales, Irles, Miranda, et al., 2000). In addition, people with autism who engage in non-suicidal self-injury, the direct and deliberate destruction of one’s own body tissue without intent to die, have been shown to have lower baseline levels of beta-endorphin compared to controls (Sandman, Barron, Chicz-DeMet, & DeMet, 1990). It is also possible that engaging in self-injury increases beta-endorphin (Favazza & Conteiro, 1988). Increasingly, high frequency of engaging in this behavior is coming to be viewed as addiction. Along with self-injury beginning to be viewed as an addiction, food/sugar addiction is also being considered. It has recently been shown that endogenous opiods play a role in what is viewed as sugar addiction (Avena, Rada, Hoebel, 2008). Excessive exercise as well as starvation have also been shown to increase beta-endorphin (Davis & Claridge, 1998). In rats, activity anorexia- the phenomenon in which after rats are exposed to an intermittent schedule of food reinforcement for lever pressing, they run in the wheel in their cage for the period between reinforcers- has been observed. In activity anorexia, within a week of being reinforced on a variable ratio schedule, rats will run up to 12 miles in one day and voluntarily deny food when it is presented (Collier, G. & Levitsky, 1968). If allowed to continue, rats will starve themselves to death. It seems that a positive feedback loop (simply stated, which continues in the same direction as the problem) develops in which increased running and decreased eating are somehow reinforced. This phenomenon suggests that a strong, endogenous, biological reward system maintains these behaviors, which may have developed for evolutionary purposes but become maladaptive under certain conditions, such as when food is presented and denied. It is probable that due to an environmental or a directly biological (such as a genetic predisposition) factor causing dysfunction in the reward system, people actively seek out stimuli that raise their beta-endorphin levels such as smoking, drinking, exercising, and restricting food intake. People with reward system dysfunctions could seek out stimuli that are both maladaptive and potent in an effort to change their experiences.
As with disorders like substance abuse and anorexia nervosa, it is possible that people with major depression have dysregulated reward or pleasure systems. Indeed, a major symptom of depression, anhedonia, is described as the lack of ability to feel pleasure. It has been shown that people with major depression release a smaller amount of beta-endorphin compared to controls when presented with a social stressor (Young, Lopez, Murphy-Weinberg, Watson & Akil, 2000). Similar to learned helplessness, it is possible that depression results from learning that physiological rewards cannot be experienced either because of a direct inability to experience pleasure from the reward, the inability to make the association between the award and the experience of pleasure, an actual lack of rewards in the environment (or excess of punishments), or any combination of biological and environmental factors within a given person. The possibility also exists that due to dysfunction involved with beta-endorphin, specific learned helplessness towards gaining weak adaptive rewards and specific addictions to potent maladaptive reinforcers can co-occur in one organism, for example, comorbidity between major depression and alcohol dependence.
Although the studies mentioned above may indicate that beta-endorphin may be involved in the experience of pleasure and aid in the formation of associations between stimuli and responses, the results of several studies appear to be contrary to this notion. For example, lateral hypothalamus self-stimulation (LHSS) has been shown to be an effective reinforcer in rats; however, increases in extracellular levels of beta-endorphin in rats were not observed in the NAS as a result of LHSS in one study (Zangen & Shalev, 2003). These results indicate that stimulation of the lateral hypothalamus may not related to beta-endorphin in the reward system; however, the results of the study indicate that beta-endorphin may play a role adaptively responding to stress because extracellular levels increased in the NAS during extinction and presentation to aversive stimuli. In addition, Maes, et al (1994) found that administering corticotrophin-releasing hormone (CRH) 9.5 hours after dexamethasone resulted in enhancement of beta-endorphin. If a lack of beta-endorphin is involved in depression, one might expect that beta-endorphin would be decreased rather than increased in people with depression compared to controls; however, since no control group was used and all participants had depression, it remains unclear if people with depression have less beta-endorphin secretion compared to controls. Also in this study, levels of beta-endorphin were not different between people with major or minor depression. This indicates that the level of beta-endorphin may not be related to clinical severity of depression. It is important to remember that the role of beta-endorphin in the onset, maintenance, and treatment of depression remains speculative.
Despite this contradictory evidence, several different pieces of information regarding dopamine and serotonin may provide a link for beta-endorphin with depression. For example, beta-endorphin has been shown to decrease dopamine turnover in the hypothalamus and striatum (George & Van Loon, 1982). Antidepressant drugs such as bupropion (Wellbutrin) that act by selectively inhibiting the uptake of dopamine may indirectly work by acting on endorphins as well. Serotonin, a neurotransmitter known to be involved with major depression, when given to rats either exogenously or endogenously, facilitates the release of beta-endorphin in the arcuate nucleus in the hypothalamus and the NAS (Zangen, Nakash, & Yadid, 1999). Therefore, it is possible the interaction between serotonin and beta-endorphin is responsible for part of the effectiveness of selective serotonin reuptake inhibitors (SSRIs) used to treat depression.
Role of beta-Endorphin in Treatment
Not only may beta-endorphin be involved in the onset of depression, it may be involved in various forms of treatments as well. Recently, a N-methyl-D-aspartate (NDMA) receptor antagonist, also known as ketamine hydrochloride, was administered in a randomized, placebo controlled, double-blind study to a group of people with depression. After only two hours after administration, the low dose of ketamine had an antidepressant effect that lasted about a week (Zarante, Singh, Carlson, Butsche, Ameli, Luckenbaugh, et al., 2006). Of those who received ketamine, 71% met criteria for response and 29% met criteria for remission the day after administration. Therefore, 100% of patients at least had an immediate response to ketamine. Furthermore, 35% of those treated with ketamine maintained a response for at least 1 week. Perhaps not surprisingly, ketamine has been shown to directly act on the reward system by stimulating both immediate and delayed secretion of beta-endorphin in mice. In this study, ketamine increased secretion of beta-endorphin in some participants that was up to three times greater than their level at baseline (YaDaeu, Morelli & Billingsley, 2003). Although it may be unanticipated to see ketamine, also a street drug, be administered as a prescription, perhaps it would be effective to have controlled low dosages at a hospital where a doctor or nurse would administer the drug to a patient starting SSRI treatment during the first few weeks SSRIs are not effective. Theoretically, this could reduce the suicide risk for people with depression, providing that ketamine interacts with SSRIs in a safe manner. As suicide rates are highest in the immediate post-hospitalization period (Qin & Nordentoft, 2005), a fast acting drug, that is perhaps directly acting on the biological dysfunction seen in major depression, could have a large impact on suicide and depression.
For example, electro-convulsive shock therapy (ECT) has been shown to increase the level of beta-endorphin. In particular, ECT has been shown to activate the hypothalamic-pituitary-adrenal (HPA) axis, known to be involved in depression, resulting in a release of beta-endorphin (Young, Gruhnhaus, Haskett, Pande, Murphy-Weinberg, Akil, et al, 1991). The results from this study indicate that the effect of ECT on length of seizure has a relationship to the amount of beta-endorphin released during treatment, with decreasing duration of seizures leading to decreases in beta-endorphin. Perhaps with the advancement of research on opioids, ECT will no longer be needed to treat people with depression because the mechanisms through which ECT are effective may be uncovered and able to be administered in a more favorable manner: pharmaceutically. If ketamine and ECT do work through similar mechanisms, it would be interesting to conduct an experiment comparing the effects of ECT and ketamine as treatments for depression. Although evidence exists for the release of beta-endorphin during ECT, one study found that levels of endorphins were returned to baseline after administration of ECT [19]. In addition, there was an increase in endorphin level in all ten participants, one of whom was a control. This study provides evidence that endorphin level increases in response to stress, perhaps similarly to cortisol, rather than acting as a mechanism through which ECT is effective; however it is conceivable that perhaps even a brief period of experiencing pleasure as a result of beta-endorphin release after a serious episode of depression is enough for the person to learn that they can experience happiness. Perhaps a brief period of happiness is enough to instill a feeling of hope that perhaps the person will be able to experience happiness again in the future. Perhaps ECT could act as a jump start into a negative feedback loop (which reverses in direction away from depression and toward equilibrium).
Aside from pharmaceutical treatments and ECT, it is possible that increased beta-endorphin is also a mechanism behind psychological treatments. Although studies have shown that cognitive-behavioral therapy (CBT) is effective, studies aimed at determining mechanisms of change have pointed to behavioral activation (BA) as the component of treatment that accounts for the vast majority of symptom decreases (YaDaeu, Morelli, & Billingsley, 2003). An intervention strategy used in BA is increasing the client’s engagement in pleasurable activity and increasing mastery over situations. The activities are presented to clients in gradations, so that clients are gradually and reliably reinforced. In BA, clinicians often remark that “activity breeds activity” (Hayes, S., Follette, V. & Linehan, 2004), possibly indicating some evidence for a negative feedback loop. While no studies have measured beta-endorphin levels throughout the course of BA treatment, as activity increases, it is possible that beta-endorphin is involved in active engagement in behavior and learning positive associations with being active. If it is shown that beta-endorphin levels are increased through BA (either in frequency or strength of release), evidence would be provided for a potential biological mechanisms through which activity would breed more activity. BA may act through showing people from their own experience that they can engage in pleasurable activity. Perhaps similarly to ECT, engaging in behavioral activity after a depressive episode could have the propensity to instill a feeling of hope at the initiation of treatment from beta-endorphin release. In short, while BA is a psychological mechanism of change, perhaps a negative feedback loop can be a biological mechanism of change underlying the psychological experience of symptom improvement. Because BA has been a successful treatment in major depression, researchers are beginning to contemplate the role of behavioral inactivation as a cause of depression. Future studies examining how behavioral inactivity could result in major depression are needed. Like the positive feedback loop previously mentioned in regards to activity anorexia in rats, a positive feedback loop could be the cause for onset of major depression in humans while BA could result in a negative feedback loop that reverses the effects of depression.
Similar to BA, an evolving therapy called Positive Psychotherapy (PPT) has been developed by positive psychologists for people with depression (Seligmnan, Steen, Park, & Peterson, 2005). Amongst other techniques, PPT therapists employ discussion about self-identified positive qualities, having clients document why they are grateful, and having clients engage in pleasurable activities. While PPT is a new therapy, evidence exists that people treated with PPT have decreased depressive symptoms compared to a control condition receiving treatment as usual; however, PPT has not yet been compared to CBT or BA. Like BA, it can be argued that release of beta-endorphin can be involved in the formation and maintenance of associations between engaging in pleasurable activity and being rewarded, and therefore, be one potential mechanism through with the therapy is effective.
While BA and PPT include activity for treating depression, many studies have been conducted that directly examine the role of exercise on depression. Through various studies, perhaps the most supported link between psychological interventions and beta-endorphin release has been in the use of exercise to treat psychological disorders. For example, one recent study examined 38 inpatients with major depression who were randomly assigned to an exercise or non-exercise group. After 10 days, the reduction of depressive symptoms and the number of patients who experienced clinical response during inpatient treatment were significantly larger than the non-exercise group (Knubben, Reischies, Adli, Schlattmann, Bauer, & Dimeo, 2007) and the increase in beta-endorphin as a result of exercise is a well-documented phenomenon (Bender, Nagy, Barna, Tefner, Kadas & Geher, 2007). Like BA and PPT, the mechanism through which exercise is effective could possibly be beta-endorphin release or reward system activation. Because exercise most likely increases more beta-endorphin than BA or PPT, it would be interesting to see if exercise is a more potent form of treatment than BA or PPT.
While many studies were conducted to measure beta-endorphin and other endogenous opioids in people with depression during the 1980’s and 1990’s, research has waned in recent years. Perhaps studying neurotransmitters such as serotonin, norepinephrine, and dopamine was seen as having more promising clinical utility because administering opiates directly was not viewed as a viable option. Although opiates are dangerous because of the potential for abuse, recent findings on the strong and immediate effects of administering ketamine to people with depression may spark a renewed interest in the study of beta-endorphin and may prompt researchers to find a way to safely administer agents that act on beta-endorphin amongst other neurotransmitters. Although this paper attempts to link beta-endorphin to a wide variety of biological functions (the experience of pleasure and the formation of associations through conditioning), possible onset and maintenance of psychological disorders and unhealthy behaviors (alcoholism, opiate addition, smoking, anorexia nervosa, bulimia nervosa, and major depression), and treatments for major depression (SSRIs, ECT, BA, PPT, and exercise), many other biological mechanisms also contribute. Although examining only beta-endorphin as the sole mechanism in psychological disorders and treatment is vastly overly simplistic, the intention of this paper is to point to beta-endorphin as one possible contributing factor that is perhaps underutilized as tool in the treatment of major depression and understudied in relation to the onset of psychological disorders. Although, as evidence suggests that beta-endorphin may be involved in forming associations between behaviors and the feeling of pleasure as well as the experience of pleasure itself, future studies should focus on determining if beta-endorphin is directly related to the onset, maintenance, and treatment of major depression and other psychologically maladaptive behaviors.
Overall, it is interesting to consider that a deficiency of a substance like beta-endorphin could naturally lead to people engaging in behaviors that increase beta-endorphin such as drug use or result in the experience of depression. It is also worth noting that various forms of treatments for depression such as ECT, medication, psychological therapy, and exercise therapy all may increase beta-endorphin as well, implicating the treatment work through correcting a deficiency.
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Rada, P., Colasante, C., Skirzewski, M., Hernandez, L., & Hoebel, B. (2006). Behavioral depression in the swim test causes biphasic, long-lasting change in accumbens acetylcholine release, with partial compensation by acetylcholinesterase and muscarinic-1 receptors. Neuroscience, 141, 67-76.
Salmone, J. & Correa, M. (2002). Motivational views of reinforcement: implications for understanding the behavioral functions of nucleus accumbens dopamine. Behavioral Brain Research, 137, 3-25.
Sandman, C.A. Barron, J.K., Chicz-DeMat, A. & DeMat, E.M. (1990). Plasma-B-endorphin levels in patients with self-injurious behavior and stereotypy. American Journal of Mental Retardation, 95(1), 84-92.
Seligmnan, M., Steen, T., Park, N., & Peterson, C. (2005). Positive Psychology Progress: empirical validation of interventions. American Psychologist, 60, 410-421.
Taylor, A.H., Ussher, M.H., Faulkner, G. (2007). The acute effects of exercise on cigarette cravings, withdrawal symptoms, affect, and smoking behaviour: a systematic review. Addiction, 102(4), 534-43.
Rothman, R.B. Blough, B.E., & Baumann, M.H. (2008). Dopamine/serotonin releasers as medications for stimulant addictions. Progress in Brain Research, 172, 385;406.
Wallenstein, M.B. & Nock, M.K. (2007). Physical exercise as a treatment for non-suicidal self-injury: evidence from a single-case study. American Journal of Psychiatry, 164(2),350-351.
YaDaeu, J., Morelli, C., & Billingsley, J. (2003). Ketamine stimulates secretion of beta-endorphin from a mouse pituitary cell line. Regional Anesthesia and Pain Medicine, 28, 12-16.
Young, E., Lopez, J., Murphy-Weinberg, V., Watson, S., & Akil, H. (2000). Hormonal evidence for altered responsiveness to social stress in major depression. Neuropsychopharmacology, 23, 411-418.
Young, E.A., Grunhaus, L., Haskett, R.F., Pande, A., Murphy-Weinberg, V., Akil, H., et al. (1991). Heterogeneity in the beta-endorphin immunoreactivity response to electroconvulsive therapy. Arch Gen Psychiatry, 48, 534-539.
Zalewska-Kaszubska, J. & Czarnecka, E. (2005). Deficit in beta-endorphin peptide and tendency to alcohol abuse. Peptides, 26, 701-705.
Zangen, A. & Shalev, U. (2003). Nuclues accumbens beta-endorphin levels are not elevated by brain stimulation reward but do increase with extinction. European Journal of Neuroscience, 17, 1067-1072.
Zangen, A., Nakash, R., & Yadid, G. (1999). Serotonin-mediated increases in the extracellular levels of beta-endorphin in the arcuate nucleus and the nucleus accumbens: a microdialysis study. J Neurochem, 73, 2569-2574.
Zarante, C., Singh, J., Carlson, P., Butsche, N., Ameli, R., Luckenbaugh, et al. (2006). A randomized trial of an N-Methyl-D-aspartate Antagonist in treatment-resistant major depression. Arch Gen Psychiatry, 6, 856- 864.
Summary
The possibility exists that dysfunction at various levels of a biological reward system, such as the dopaminergic mesolimbic pathway, could be involved in etiology and maintenance of depression. Current descriptions of the role that specific factors, such as dopamine, play in the endogenous reward system have been incomplete; therefore, other factors are likely involved as well.
Keywords: Depression, endorphin, beta-endorphin, etiology, treatment
Introduction
It is well known that environmental reinforcement has an effect on one’s behavior; therefore, a biological system through which the organism is able to process and experience reinforcement must exist, yet is not extremely well understood. It is possible that through dysfunction at various levels of a biological reward system, psychological disorders such as depression can result or be maintained. Furthermore, if acquired or genetic dysfunctions in the biological reward system result in psychopathology, it can be argued that ameliorating these problems can result in further success in treating depression.
Several possible brain structures have emerged as being involved in the biological reward system. In recent years, the nucleus accumbens (NAS) has been supported as the key structure in the reward center of the brain. The involvement of the NAS in reinforcement has been demonstrated for both natural (logically related to the task) and artificial rewards (not logically related to the task; Rada, Colasante, Skirzewski, Hernandez & Hoebel, 2006). Reinforcement is hypothesized to be mediated through regulation of dopamine in the NAS; however, several pieces of evidence point to additional contributing factors. For example, while depletion of dopamine in the NAS has been shown to affect operant responding, it does not necessarily affect unconditioned reinforcement (Salmone & Correa, 2002). This means that DA does not affect conditioning to reinforcers that are naturally reinforcing. Because natural reinforcers such as food can be quite strong, DA’s role in conditioning may not be as important as previously thought. Therefore, other biological factors are likely involved in learning through reinforcement.
Also present in the NAS is beta-endorphin, an endogenous opioid peptide that has been implicated in the reward process. For example, it has been shown that beta-endorphin levels have increased in the NAS in rats during extinction learning. The results from this study indicate that beta-endorphin can be involved in both learning and adaptive responding to distress (Rada et al., 2006). Because beta-endorphin may be involved with operant conditioning and responses to stress, it could be involved with the onset or maintenance of depression (and impulsive behavior as well).
Role of beta-Endorphin in Onset
Due to a possible dysfunction in the reward system from environmental or biological etiology, the organism may not experience the environment as rewarding. It has been well-observed that people may actively seek out maladaptive ways to be rewarded. Various addictive disorders such as alcoholism, opiate addiction, cigarette smoking, excessive exercise, and starvation have all been linked to beta-endorphin dysfunction, and therefore, can possible be viewed as reward seeking behaviors. For example, people with a high genetic risk for developing alcoholism have lower levels of beta-endorphin. Perhaps not surprisingly, drinking alcohol increases levels of beta-endorphin (Dai, Thavundayil & Glanoulakis, 2005; Zalewska-Kaszubska & Czarnecka , 2005). In addition, it has been indicated that single-nucleotide polymorphism in the mu opiod receptor gene alters beta-endorphin binding and activity exists and could be related to opiate addiction (Bond, LaForge, Tian, Melia, Zhang, Borg, et al., 1998). Furthermore, people who smoke cigarettes have lower levels of basal beta-endorphin than those who do not smoke (Lee, Joe, Sohn, Na, Kee & Chae, 2005). Those who smoke more than 20 cigarettes per day have lower levels of beta-endorphin than those who smoke less than 10 cigarettes per day. In addition, those who smoke less than 10 cigarettes per day have lower beta-endorphin levels than controls (de Arbol, Munoz, Ojeda, Cascales, Irles, Miranda, et al., 2000). In addition, people with autism who engage in non-suicidal self-injury, the direct and deliberate destruction of one’s own body tissue without intent to die, have been shown to have lower baseline levels of beta-endorphin compared to controls (Sandman, Barron, Chicz-DeMet, & DeMet, 1990). It is also possible that engaging in self-injury increases beta-endorphin (Favazza & Conteiro, 1988). Increasingly, high frequency of engaging in this behavior is coming to be viewed as addiction. Along with self-injury beginning to be viewed as an addiction, food/sugar addiction is also being considered. It has recently been shown that endogenous opiods play a role in what is viewed as sugar addiction (Avena, Rada, Hoebel, 2008). Excessive exercise as well as starvation have also been shown to increase beta-endorphin (Davis & Claridge, 1998). In rats, activity anorexia- the phenomenon in which after rats are exposed to an intermittent schedule of food reinforcement for lever pressing, they run in the wheel in their cage for the period between reinforcers- has been observed. In activity anorexia, within a week of being reinforced on a variable ratio schedule, rats will run up to 12 miles in one day and voluntarily deny food when it is presented (Collier, G. & Levitsky, 1968). If allowed to continue, rats will starve themselves to death. It seems that a positive feedback loop (simply stated, which continues in the same direction as the problem) develops in which increased running and decreased eating are somehow reinforced. This phenomenon suggests that a strong, endogenous, biological reward system maintains these behaviors, which may have developed for evolutionary purposes but become maladaptive under certain conditions, such as when food is presented and denied. It is probable that due to an environmental or a directly biological (such as a genetic predisposition) factor causing dysfunction in the reward system, people actively seek out stimuli that raise their beta-endorphin levels such as smoking, drinking, exercising, and restricting food intake. People with reward system dysfunctions could seek out stimuli that are both maladaptive and potent in an effort to change their experiences.
As with disorders like substance abuse and anorexia nervosa, it is possible that people with major depression have dysregulated reward or pleasure systems. Indeed, a major symptom of depression, anhedonia, is described as the lack of ability to feel pleasure. It has been shown that people with major depression release a smaller amount of beta-endorphin compared to controls when presented with a social stressor (Young, Lopez, Murphy-Weinberg, Watson & Akil, 2000). Similar to learned helplessness, it is possible that depression results from learning that physiological rewards cannot be experienced either because of a direct inability to experience pleasure from the reward, the inability to make the association between the award and the experience of pleasure, an actual lack of rewards in the environment (or excess of punishments), or any combination of biological and environmental factors within a given person. The possibility also exists that due to dysfunction involved with beta-endorphin, specific learned helplessness towards gaining weak adaptive rewards and specific addictions to potent maladaptive reinforcers can co-occur in one organism, for example, comorbidity between major depression and alcohol dependence.
Although the studies mentioned above may indicate that beta-endorphin may be involved in the experience of pleasure and aid in the formation of associations between stimuli and responses, the results of several studies appear to be contrary to this notion. For example, lateral hypothalamus self-stimulation (LHSS) has been shown to be an effective reinforcer in rats; however, increases in extracellular levels of beta-endorphin in rats were not observed in the NAS as a result of LHSS in one study (Zangen & Shalev, 2003). These results indicate that stimulation of the lateral hypothalamus may not related to beta-endorphin in the reward system; however, the results of the study indicate that beta-endorphin may play a role adaptively responding to stress because extracellular levels increased in the NAS during extinction and presentation to aversive stimuli. In addition, Maes, et al (1994) found that administering corticotrophin-releasing hormone (CRH) 9.5 hours after dexamethasone resulted in enhancement of beta-endorphin. If a lack of beta-endorphin is involved in depression, one might expect that beta-endorphin would be decreased rather than increased in people with depression compared to controls; however, since no control group was used and all participants had depression, it remains unclear if people with depression have less beta-endorphin secretion compared to controls. Also in this study, levels of beta-endorphin were not different between people with major or minor depression. This indicates that the level of beta-endorphin may not be related to clinical severity of depression. It is important to remember that the role of beta-endorphin in the onset, maintenance, and treatment of depression remains speculative.
Despite this contradictory evidence, several different pieces of information regarding dopamine and serotonin may provide a link for beta-endorphin with depression. For example, beta-endorphin has been shown to decrease dopamine turnover in the hypothalamus and striatum (George & Van Loon, 1982). Antidepressant drugs such as bupropion (Wellbutrin) that act by selectively inhibiting the uptake of dopamine may indirectly work by acting on endorphins as well. Serotonin, a neurotransmitter known to be involved with major depression, when given to rats either exogenously or endogenously, facilitates the release of beta-endorphin in the arcuate nucleus in the hypothalamus and the NAS (Zangen, Nakash, & Yadid, 1999). Therefore, it is possible the interaction between serotonin and beta-endorphin is responsible for part of the effectiveness of selective serotonin reuptake inhibitors (SSRIs) used to treat depression.
Role of beta-Endorphin in Treatment
Not only may beta-endorphin be involved in the onset of depression, it may be involved in various forms of treatments as well. Recently, a N-methyl-D-aspartate (NDMA) receptor antagonist, also known as ketamine hydrochloride, was administered in a randomized, placebo controlled, double-blind study to a group of people with depression. After only two hours after administration, the low dose of ketamine had an antidepressant effect that lasted about a week (Zarante, Singh, Carlson, Butsche, Ameli, Luckenbaugh, et al., 2006). Of those who received ketamine, 71% met criteria for response and 29% met criteria for remission the day after administration. Therefore, 100% of patients at least had an immediate response to ketamine. Furthermore, 35% of those treated with ketamine maintained a response for at least 1 week. Perhaps not surprisingly, ketamine has been shown to directly act on the reward system by stimulating both immediate and delayed secretion of beta-endorphin in mice. In this study, ketamine increased secretion of beta-endorphin in some participants that was up to three times greater than their level at baseline (YaDaeu, Morelli & Billingsley, 2003). Although it may be unanticipated to see ketamine, also a street drug, be administered as a prescription, perhaps it would be effective to have controlled low dosages at a hospital where a doctor or nurse would administer the drug to a patient starting SSRI treatment during the first few weeks SSRIs are not effective. Theoretically, this could reduce the suicide risk for people with depression, providing that ketamine interacts with SSRIs in a safe manner. As suicide rates are highest in the immediate post-hospitalization period (Qin & Nordentoft, 2005), a fast acting drug, that is perhaps directly acting on the biological dysfunction seen in major depression, could have a large impact on suicide and depression.
For example, electro-convulsive shock therapy (ECT) has been shown to increase the level of beta-endorphin. In particular, ECT has been shown to activate the hypothalamic-pituitary-adrenal (HPA) axis, known to be involved in depression, resulting in a release of beta-endorphin (Young, Gruhnhaus, Haskett, Pande, Murphy-Weinberg, Akil, et al, 1991). The results from this study indicate that the effect of ECT on length of seizure has a relationship to the amount of beta-endorphin released during treatment, with decreasing duration of seizures leading to decreases in beta-endorphin. Perhaps with the advancement of research on opioids, ECT will no longer be needed to treat people with depression because the mechanisms through which ECT are effective may be uncovered and able to be administered in a more favorable manner: pharmaceutically. If ketamine and ECT do work through similar mechanisms, it would be interesting to conduct an experiment comparing the effects of ECT and ketamine as treatments for depression. Although evidence exists for the release of beta-endorphin during ECT, one study found that levels of endorphins were returned to baseline after administration of ECT [19]. In addition, there was an increase in endorphin level in all ten participants, one of whom was a control. This study provides evidence that endorphin level increases in response to stress, perhaps similarly to cortisol, rather than acting as a mechanism through which ECT is effective; however it is conceivable that perhaps even a brief period of experiencing pleasure as a result of beta-endorphin release after a serious episode of depression is enough for the person to learn that they can experience happiness. Perhaps a brief period of happiness is enough to instill a feeling of hope that perhaps the person will be able to experience happiness again in the future. Perhaps ECT could act as a jump start into a negative feedback loop (which reverses in direction away from depression and toward equilibrium).
Aside from pharmaceutical treatments and ECT, it is possible that increased beta-endorphin is also a mechanism behind psychological treatments. Although studies have shown that cognitive-behavioral therapy (CBT) is effective, studies aimed at determining mechanisms of change have pointed to behavioral activation (BA) as the component of treatment that accounts for the vast majority of symptom decreases (YaDaeu, Morelli, & Billingsley, 2003). An intervention strategy used in BA is increasing the client’s engagement in pleasurable activity and increasing mastery over situations. The activities are presented to clients in gradations, so that clients are gradually and reliably reinforced. In BA, clinicians often remark that “activity breeds activity” (Hayes, S., Follette, V. & Linehan, 2004), possibly indicating some evidence for a negative feedback loop. While no studies have measured beta-endorphin levels throughout the course of BA treatment, as activity increases, it is possible that beta-endorphin is involved in active engagement in behavior and learning positive associations with being active. If it is shown that beta-endorphin levels are increased through BA (either in frequency or strength of release), evidence would be provided for a potential biological mechanisms through which activity would breed more activity. BA may act through showing people from their own experience that they can engage in pleasurable activity. Perhaps similarly to ECT, engaging in behavioral activity after a depressive episode could have the propensity to instill a feeling of hope at the initiation of treatment from beta-endorphin release. In short, while BA is a psychological mechanism of change, perhaps a negative feedback loop can be a biological mechanism of change underlying the psychological experience of symptom improvement. Because BA has been a successful treatment in major depression, researchers are beginning to contemplate the role of behavioral inactivation as a cause of depression. Future studies examining how behavioral inactivity could result in major depression are needed. Like the positive feedback loop previously mentioned in regards to activity anorexia in rats, a positive feedback loop could be the cause for onset of major depression in humans while BA could result in a negative feedback loop that reverses the effects of depression.
Similar to BA, an evolving therapy called Positive Psychotherapy (PPT) has been developed by positive psychologists for people with depression (Seligmnan, Steen, Park, & Peterson, 2005). Amongst other techniques, PPT therapists employ discussion about self-identified positive qualities, having clients document why they are grateful, and having clients engage in pleasurable activities. While PPT is a new therapy, evidence exists that people treated with PPT have decreased depressive symptoms compared to a control condition receiving treatment as usual; however, PPT has not yet been compared to CBT or BA. Like BA, it can be argued that release of beta-endorphin can be involved in the formation and maintenance of associations between engaging in pleasurable activity and being rewarded, and therefore, be one potential mechanism through with the therapy is effective.
While BA and PPT include activity for treating depression, many studies have been conducted that directly examine the role of exercise on depression. Through various studies, perhaps the most supported link between psychological interventions and beta-endorphin release has been in the use of exercise to treat psychological disorders. For example, one recent study examined 38 inpatients with major depression who were randomly assigned to an exercise or non-exercise group. After 10 days, the reduction of depressive symptoms and the number of patients who experienced clinical response during inpatient treatment were significantly larger than the non-exercise group (Knubben, Reischies, Adli, Schlattmann, Bauer, & Dimeo, 2007) and the increase in beta-endorphin as a result of exercise is a well-documented phenomenon (Bender, Nagy, Barna, Tefner, Kadas & Geher, 2007). Like BA and PPT, the mechanism through which exercise is effective could possibly be beta-endorphin release or reward system activation. Because exercise most likely increases more beta-endorphin than BA or PPT, it would be interesting to see if exercise is a more potent form of treatment than BA or PPT.
While many studies were conducted to measure beta-endorphin and other endogenous opioids in people with depression during the 1980’s and 1990’s, research has waned in recent years. Perhaps studying neurotransmitters such as serotonin, norepinephrine, and dopamine was seen as having more promising clinical utility because administering opiates directly was not viewed as a viable option. Although opiates are dangerous because of the potential for abuse, recent findings on the strong and immediate effects of administering ketamine to people with depression may spark a renewed interest in the study of beta-endorphin and may prompt researchers to find a way to safely administer agents that act on beta-endorphin amongst other neurotransmitters. Although this paper attempts to link beta-endorphin to a wide variety of biological functions (the experience of pleasure and the formation of associations through conditioning), possible onset and maintenance of psychological disorders and unhealthy behaviors (alcoholism, opiate addition, smoking, anorexia nervosa, bulimia nervosa, and major depression), and treatments for major depression (SSRIs, ECT, BA, PPT, and exercise), many other biological mechanisms also contribute. Although examining only beta-endorphin as the sole mechanism in psychological disorders and treatment is vastly overly simplistic, the intention of this paper is to point to beta-endorphin as one possible contributing factor that is perhaps underutilized as tool in the treatment of major depression and understudied in relation to the onset of psychological disorders. Although, as evidence suggests that beta-endorphin may be involved in forming associations between behaviors and the feeling of pleasure as well as the experience of pleasure itself, future studies should focus on determining if beta-endorphin is directly related to the onset, maintenance, and treatment of major depression and other psychologically maladaptive behaviors.
Overall, it is interesting to consider that a deficiency of a substance like beta-endorphin could naturally lead to people engaging in behaviors that increase beta-endorphin such as drug use or result in the experience of depression. It is also worth noting that various forms of treatments for depression such as ECT, medication, psychological therapy, and exercise therapy all may increase beta-endorphin as well, implicating the treatment work through correcting a deficiency.
References
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Qin, P & Nordentoft, M. Suicide risk in relation to psychiatric hospitalization: evidence based on longitudinal registers. Arch Gen Psychiatry, 62, 427-432.
Rada, P., Colasante, C., Skirzewski, M., Hernandez, L., & Hoebel, B. (2006). Behavioral depression in the swim test causes biphasic, long-lasting change in accumbens acetylcholine release, with partial compensation by acetylcholinesterase and muscarinic-1 receptors. Neuroscience, 141, 67-76.
Salmone, J. & Correa, M. (2002). Motivational views of reinforcement: implications for understanding the behavioral functions of nucleus accumbens dopamine. Behavioral Brain Research, 137, 3-25.
Sandman, C.A. Barron, J.K., Chicz-DeMat, A. & DeMat, E.M. (1990). Plasma-B-endorphin levels in patients with self-injurious behavior and stereotypy. American Journal of Mental Retardation, 95(1), 84-92.
Seligmnan, M., Steen, T., Park, N., & Peterson, C. (2005). Positive Psychology Progress: empirical validation of interventions. American Psychologist, 60, 410-421.
Taylor, A.H., Ussher, M.H., Faulkner, G. (2007). The acute effects of exercise on cigarette cravings, withdrawal symptoms, affect, and smoking behaviour: a systematic review. Addiction, 102(4), 534-43.
Rothman, R.B. Blough, B.E., & Baumann, M.H. (2008). Dopamine/serotonin releasers as medications for stimulant addictions. Progress in Brain Research, 172, 385;406.
Wallenstein, M.B. & Nock, M.K. (2007). Physical exercise as a treatment for non-suicidal self-injury: evidence from a single-case study. American Journal of Psychiatry, 164(2),350-351.
YaDaeu, J., Morelli, C., & Billingsley, J. (2003). Ketamine stimulates secretion of beta-endorphin from a mouse pituitary cell line. Regional Anesthesia and Pain Medicine, 28, 12-16.
Young, E., Lopez, J., Murphy-Weinberg, V., Watson, S., & Akil, H. (2000). Hormonal evidence for altered responsiveness to social stress in major depression. Neuropsychopharmacology, 23, 411-418.
Young, E.A., Grunhaus, L., Haskett, R.F., Pande, A., Murphy-Weinberg, V., Akil, H., et al. (1991). Heterogeneity in the beta-endorphin immunoreactivity response to electroconvulsive therapy. Arch Gen Psychiatry, 48, 534-539.
Zalewska-Kaszubska, J. & Czarnecka, E. (2005). Deficit in beta-endorphin peptide and tendency to alcohol abuse. Peptides, 26, 701-705.
Zangen, A. & Shalev, U. (2003). Nuclues accumbens beta-endorphin levels are not elevated by brain stimulation reward but do increase with extinction. European Journal of Neuroscience, 17, 1067-1072.
Zangen, A., Nakash, R., & Yadid, G. (1999). Serotonin-mediated increases in the extracellular levels of beta-endorphin in the arcuate nucleus and the nucleus accumbens: a microdialysis study. J Neurochem, 73, 2569-2574.
Zarante, C., Singh, J., Carlson, P., Butsche, N., Ameli, R., Luckenbaugh, et al. (2006). A randomized trial of an N-Methyl-D-aspartate Antagonist in treatment-resistant major depression. Arch Gen Psychiatry, 6, 856- 864.
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