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.
Thursday, September 24, 2009
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.
References
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Bond, C., LaForge, S., Tian, M., Melia, D., Zhang, S., Borg, L., et al. (1998). Single-nucleotide polymorphism in the human mu opiod receptor gene alters beta-endorphin binding and activity: Possible implications for opiate addiction. Proc Natl Acad Sc, 95, 9608-9613.
Collier, G. & Levitsky, D. (1968). Operant running as a function of deprivation and effort. J Comp Physiol Psychol, 66, 522-523.
Davis, C & Claridge, G. (1998). The eating disorders as addiction: psychobiological perspective. Addictive Behaviors, 23, 463-475.
Dai, X., Thavundayil, J., & Glanoulakis, C. (2005). Difference in the peripheral levels of beta-endorphin in response to alcohol and stress as a function of alcohol dependence and family history of alcoholism. Alcoholism: Clinical and Experimental Research, 29, 1965-1975.
del Arbol, J. L., Raya, M., Munoz, J., Ojeda, L., Lopez-Cascales, A., Irles, J., Miranda, M., et al. (2007). Plasma concentrations of beta-endorphin in smokers who consume different numbers of cigarettes per day. Pharmacol Biochem Behav, 67, 25-28.
Dimidjian, S., Hollon, S., Dobson, K., Schmaling, K., & Kohlenberg, R., et al. (2006). Randomized control trial of behavioral activation, cognitive therapy, and antidepressant medication in the acute treatment of adults with major depression. Journal of Consulting and Clinical Psychology, 74, 658-670.
Favazza, A. & Conteiro, K. (1988). The plight of chronic self-mutilators. Community and Mental Health Journals. 24(1), 22-30.
George, S. R., & Van Loon, G. R. (1982). Beta-Endorphin alters dopamine uptake by the dopamine neurons of the hypothalamus and striatum. Brain Res, 248, 293-303.
Ghadirian, A., Gianoulakis, C., & Nair, A. (1988). The effect of electroconvulsive therapy on endorphins in depression. Biol Psychiatry, 23, 459-464.
Hayes, S., Follette, V. & Linehan, M. (2004). Mindfulness and Acceptance: Expanding the cognitive-behavioral tradition. New York: Guilford Press, 160.
Knubben, K., Reischies, F., Adli, M., Schlattmann, P., Bauer, M., & Dimeo, F. (2007). A randomized, controlled study on the effects of a short-term endurance training programme in patients with major depression. Br J Sports Med, 41, 29-33.
Lee, Y., Joe, K., Sohn, I., Na., C., Kee, B., & Chae, S. C. (2005). hanges of smoking behavior and serum adrenocorticotropic hormone, cortisol, prolactin, and andogenous opiod levels in nicotine dependence after naltrexone treatment. Prog Neuropsychopharmacol Biol Psychiatry, 29, 639-647.
Maes, M., Meltzer, H., Cosyns, P., Calabrese, J., D’hondt, P., & Blockx, P. (1994). Adrenocorticotropic hormone, beta-endorphin and cortisol responses to CRH in unipolar depressed patients pretreated with dexamethasone. Prog Neuro-psychopharmacol & boil psychiat, 18, 1273-1292.
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.
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
Avena, N.M., Rada, P., & Hoebel, B.G. (2008). Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake. Nueroscience & Biobehavioral Reviews, 32(1), 20-39.
Bender, T., Nagy, G., Barna, I., Tefner, I., Kadas, E. & Geher, P. (2007). The effect of physical therapy on beta-endorphin levels. Eur J Appl Physiol, 100, 371-382.
Bond, C., LaForge, S., Tian, M., Melia, D., Zhang, S., Borg, L., et al. (1998). Single-nucleotide polymorphism in the human mu opiod receptor gene alters beta-endorphin binding and activity: Possible implications for opiate addiction. Proc Natl Acad Sc, 95, 9608-9613.
Collier, G. & Levitsky, D. (1968). Operant running as a function of deprivation and effort. J Comp Physiol Psychol, 66, 522-523.
Davis, C & Claridge, G. (1998). The eating disorders as addiction: psychobiological perspective. Addictive Behaviors, 23, 463-475.
Dai, X., Thavundayil, J., & Glanoulakis, C. (2005). Difference in the peripheral levels of beta-endorphin in response to alcohol and stress as a function of alcohol dependence and family history of alcoholism. Alcoholism: Clinical and Experimental Research, 29, 1965-1975.
del Arbol, J. L., Raya, M., Munoz, J., Ojeda, L., Lopez-Cascales, A., Irles, J., Miranda, M., et al. (2007). Plasma concentrations of beta-endorphin in smokers who consume different numbers of cigarettes per day. Pharmacol Biochem Behav, 67, 25-28.
Dimidjian, S., Hollon, S., Dobson, K., Schmaling, K., & Kohlenberg, R., et al. (2006). Randomized control trial of behavioral activation, cognitive therapy, and antidepressant medication in the acute treatment of adults with major depression. Journal of Consulting and Clinical Psychology, 74, 658-670.
Favazza, A. & Conteiro, K. (1988). The plight of chronic self-mutilators. Community and Mental Health Journals. 24(1), 22-30.
George, S. R., & Van Loon, G. R. (1982). Beta-Endorphin alters dopamine uptake by the dopamine neurons of the hypothalamus and striatum. Brain Res, 248, 293-303.
Ghadirian, A., Gianoulakis, C., & Nair, A. (1988). The effect of electroconvulsive therapy on endorphins in depression. Biol Psychiatry, 23, 459-464.
Hayes, S., Follette, V. & Linehan, M. (2004). Mindfulness and Acceptance: Expanding the cognitive-behavioral tradition. New York: Guilford Press, 160.
Knubben, K., Reischies, F., Adli, M., Schlattmann, P., Bauer, M., & Dimeo, F. (2007). A randomized, controlled study on the effects of a short-term endurance training programme in patients with major depression. Br J Sports Med, 41, 29-33.
Lee, Y., Joe, K., Sohn, I., Na., C., Kee, B., & Chae, S. C. (2005). hanges of smoking behavior and serum adrenocorticotropic hormone, cortisol, prolactin, and andogenous opiod levels in nicotine dependence after naltrexone treatment. Prog Neuropsychopharmacol Biol Psychiatry, 29, 639-647.
Maes, M., Meltzer, H., Cosyns, P., Calabrese, J., D’hondt, P., & Blockx, P. (1994). Adrenocorticotropic hormone, beta-endorphin and cortisol responses to CRH in unipolar depressed patients pretreated with dexamethasone. Prog Neuro-psychopharmacol & boil psychiat, 18, 1273-1292.
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.
Wednesday, October 15, 2008
Resume` / Cirriculum Vitae
TARA L. DELIBERTO
Doctoral Candidate
tara.deliberto@gmail.com
________________________________________________________________________________________________
EDUCATION:
Boston University, Sargent College
Boston, Massachusetts
Received Bachelor of Science: Vocational Counseling
Harvard University
Cambridge, Massachusetts
Psychology Courses
Hofstra University
Hempstead, NY
Doctoral Candidate
Received Master's Degree
CLINICAL RESEARCH EXPERIENCE:
June 2005 to Present
Laboratory for Clinical and Developmental Research headed by Matthew Nock, Ph.D.
Harvard University, Cambridge, Massachusetts
Former Position: Senior Laboratory Manager
Present Position: Research Collaborator
Responsibilities:
• Contribute to all aspects of the research process including: including literature reviews, creating measures, grant preparation, institutional review board application preparation, data collection, data entry, data management, data analysis, manuscript preparation, and manuscript editing
• Contribute to tracking participants in a randomized controlled trial of Dialectical Behavioral Therapy, two studies of implicit associations of suicide at Massachusetts General Hospital and Children’s Hospital Boston, a study of the psychophysiology of self-injury and coping strategies, and an online study pertaining to the course of non-suicidal self-injury
• Supervise undergraduate administrative assistants and research assistants
CLINICAL EXPERIENCE:
Spring 2005
Sydney Children’s Hospital
Sydney, Australia
Boston University Rehabilitation Counseling Intern
Responsibilities:
• Talk to children with terminal or psychiatric illness and their families
• Conduct daily one hour staff meetings to talk about any emotionally troubling occurring at work
Fall 2005 to Fall 2007
Two Brattle Center
Cambridge, Massachusetts
Outpatient Mental Health Facility Intern and Rehabilitation Counseling Assistant
Responsibilities:
• Attend and contributing to weekly therapist consultation meetings
• Attend a two semester Dialectical Behavioral Therapy didactic
• Review effective vocational assessments for the rehabilitation counseling
services offered at Two Brattle Center
• Collect information on client progress for clinical purposes
Fall 2008 to Spring 2010
Psychological Evaluation, Research, Counseling Clinic
Hempstead, NY
Acceptance and Commitment Therapist & Research Coordinator
Responsibilities:
• Attends weekly didactic and research meetings
• Conducts Telephone intakes
• Treats patients
• Revises clinic protocols
• Designs, implements, and prepares the results of studies on cognitive versus mindfulness-based techniques
Summer 2010 to Present
American Institute of Cognitive Therapy
Manhattan, NY
ACT & CBT Therapist
Responsibilities:
• Treats patients
• Attends weekly supervision and clinical meetings
PUBLICATIONS:
Glassman, L. H., Weierich, M. R., Hooley, J. M., Deliberto, T. L., & Nock, M. K. (2007). Child maltreatment, non-suicidal self-injury, and the mediating role of self-criticism. Behaviour Research and Therapy, 45, 2483-2490.
Nock, M. K., Wedig, M. M., Janis, I. B., & Deliberto, T. L. (2008). Self-injurious thoughts and behaviors. In J. Hunsley & E. Mash, A guide to assessments that work. New York : Oxford University Press.
Deliberto, T. L., & Nock, M. (2008). An exploratory study of correlates, onset, and offset, of non-suicidal self-injury. Archives of Suicide Research, 12, 219-231.
Nock, M. K., & Deliberto, T. L. (2009). Non-suicidal self-injury. In, P.S. Jensen & C.A. Galanter (Eds.), DSM-IV-TR Casebook and Treatment Guide for Child Mental Health.
Nock, M. K., Deliberto, T. L., & Hollander, M. (in press). Resolving treatment complications associated with the presence of comorbid personality disorders. In, M. W. Otto & S. G. Hofmann (Eds.), Resolving treatment complications in anxiety disorders. New York: Springer.
Nock, M.K., Park, J. L., Finn, C.T., Deliberto, T. L., Dour, H., & Banaji, M. R. (in press). Measuring the Suicidal Mind: Implicit Cognition Predicts Suicidal Behavior. Psychological Science.
PUBLICATIONS SUBMITTED/
IN PREPARATION:
Nock, M.,, Berry Mendes, W., Deliberto, T. L., & Dour, H. (submitted). Psychophysiology of non-suicidal self-injury.
Deliberto, T. L., & Nock, M. (in preparation). Diagnostic correlates of non-suicidal self injury among adolescents.
Nock, M. K., Deliberto, T. L., Teper, R., Photos, V. I., Prichett, M., Cha, C. B., Hollander, M. & Wheelis, J. (in preparation). Intensive Dialectical Behavior Therapy for adolescents: Initial evidence for effectiveness, moderators, and mechanisms of change.
Nock, M. K., Deliberto, T. L., Teper, R., Gero, Z., Jeram, M., Photos, V., Wedig, M., Cha, C. B., & Wheelis, J. (in preparation). Intensive Dialectical Behavior Therapy for adults: Initial evidence for effectiveness, moderators, and mechanisms of change.
Deliberto, T. L., & Nock, M. K. (in preparation). Stressful life events, but not family. environment or parental psychopathology, are related to adolescent self-injury.
Deliberto, T. L. & Nock, M. (in preparation). The mediating effect of social stress between emotion reactivity and number of suicide attempts in adolescents.
Deliberto, T. L., & Nock, M. (in preparation). Somatization mediates the relationship between emotional abuse and self-injury.
Deliberto, T. L., & Scardapane, J. (in preparation). Cognitive Therapy versus Acceptance and Commitment Therapy.
PRESENTATIONS:
Deliberto, T. L. (2006, Oct). Translation of a concept similar to psychodynamic transference into behavioral terminology: Behavior generalization. Presented at a Dialectical Behavior Therapy clinic. Cambridge, MA.
Deliberto, T. L. & Nock, M. (2006, Nov). How do adolescents learn about self-injury and how and why they try to stop? Presented at the 40th annual conference of the Association for Behavioral and Cognitive Therapies. Chicago, IL.
Deliberto, T. L., Photos, V., Wedig, M., Gero, Z., Wheelis, J. & Nock, M. (2006, Nov). Preliminary examination of potential mechanisms of change in intensive Dialectical Behavior Therapy. Presented at the 40th annual conference of the Association for Behavioral and Cognitive Therapies. Chicago, IL.
Deliberto, T. L. & Nock, M. (2006, Nov). Implicit associations about suicide of people receiving care in the psychiatric emergency department. Presented at a meeting for psychiatry residents at Massachusetts General Hospital. Boston, Massachusetts.
Deliberto, T. L., & Nock, M. K. (2007, May). Stressful life events, but not family environment or parental psychopathology, are related to adolescent self-injury. Presented at the 19th annual conference of the Association for Psychological Science. Washington, DC.
Nock, M. K., Banaji, M. R., Deliberto, T. L., Park, J. L., & Finn, C. T. (2007, May). Measuring implicit associations about suicide: Preliminary findings. In, Miranda, R. (Chair), Assessing cognitive biases in depression and suicidality using laboratory-based measures. Paper presented at the 19th annual conference of the Association for Psychological Science. Washington, DC.
Deliberto, T. L. & Nock, M. (2007, Nov). Diagnostic correlates of non-suicidal self-injury among adolescents. Presented at the 41st annual conference of the Association for Behavioral and Cognitive Therapies. Philadelphia, PA.
Deliberto, T. L. & Nock, M. (2008, Nov). The mediating effect of social stress between emotion reactivity and presence of self-injury in adolescents. Presented at the 42st annual conference of the Association for Behavioral and Cognitive Therapies. Orlando, FL.
Deliberto, T. L., & Nock, M. (in preparation for 2009, Nov). Somatization mediates the relationship between emotional abuse and self-injury. To be presented at the 43rd annual conference of the Association for Behavioral and Cognitive Therapies. New York, NY.
Deliberto, T. L., & Scardapane, J. (in preparation for 2009, Nov). Cognitive Therapy versus Acceptance and Commitment Therapy. To be presented at the 43rd annual conference of the Association for Behavioral and Cognitive Therapies. New York, NY.
ACKNOWLEDGEMENTS:
Barlow, D. H., Nock, M. K., & Hersen, M. (2008). Single-case experimental designs: Strategies for studying behavior change (third edition). Boston, MA: Allyn & Bacon.
Hollander, M. (2008). Helping Teens who Cut: Understanding and Ending Self-Injury. New York, NY: Guilford Press.
AWARDS:
The Julia Vane Memorial Scholarship in Graduate Studies
AFFILIATIONS:
Association for Behavioral and Cognitive Therapies
Association for Contextual and Behavioral Sciences
Association for Psychological Science
American Psychological Association
National Society of Collegiate Scholars
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