Here is an update about omega-3 supplementation:
For a bit of background on omega-3 supplementation, see my other posts about this:
http://garthkroeker.blogspot.ca/2009/02/omega-3-supplementation.html
http://garthkroeker.blogspot.ca/2011/01/omega-3-deficiency-and-low-dietary.html
A meta-analysis from 2012 and some ensuing discussion has led to a few more recommendations (see http://www.ncbi.nlm.nih.gov/pubmed/22488258):
1) acute beneficial effects for mood may be present only for more severe symptoms. However, I am curious about the preventative effects from continuous supplementation over a period of years; the data does not give us a clear answer about this yet.
2) the EPA dose may need to be as high as 4 grams per day, certainly much higher than the 1 gram per day range frequently used in some of the studies.
Monday, June 3, 2013
Risk factors for psychotic relapse
Alvarez-Jimenez et al. have done a good meta-analysis looking at risk factors for relapse of psychotic symptoms, published in Schizophrenia Research (2012;139-116-128).
The authors conclude that there are four major factors associated with increased risk of relapse in schizophrenia and other psychotic disorders:
1) non-compliance with meds (increases risk x4)
2) substance use (increases risk x3)
3) criticism from caregivers (increases risk x2.3) -- conversely better social support is associated with reduced risk of relapse
4) poorer premorbid adjustment (increased risk x2.2)
Interestingly, the authors conclude that factors such as diagnosis, length of illness, length of untreated symptoms, demographic variables, and cognitive function, are not associated with relapse risk.
Clearly, these findings add to the recommendations for helping patients who have had psychotic symptoms, and their families:
1) medication compliance is extremely important!
2) substance use must be avoided!
3) caregivers must work hard to avoid hostile or critical comments towards the patient
One question I have about these findings, however, is how causative some of these factors are. It could be argued that an individual who is already more likely to relapse may be more likely to be non-compliant with medication, be more likely to engage in substance use, and may be more likely to behave in a way which elicits more criticism from other people. The existence of these "risk factors" may indicate that the underlying disorder was more severe. So, some or all of these risk factors may simply be non-causal associations.
In order to more definitively show that risk factors #1-#3 are causative (and therefore controllable or reversable), we would have to show evidence that externally improving medication compliance in a previously non-compliant person would clearly reduce relapse rate. And we would need to show that a change in caregiver environment would produce a change in subsequent relapse rate.
There is some such evidence, but I think it would be good to see a careful meta-analysis looking at risk-factor management in reducing relapse rate.
Another thought I have about these findings is that the recommendations are appropriate not just for people who have had psychotic symptoms, but for all psychiatric conditions, and even for all members of the whole population! That is, avoidance of substance abuse and having good social support with minimal hostility and criticism is probably good and protective for everybody's mental and physical health! But we would have to look further at the research to see if this thought of mine has been proven.
The authors conclude that there are four major factors associated with increased risk of relapse in schizophrenia and other psychotic disorders:
1) non-compliance with meds (increases risk x4)
2) substance use (increases risk x3)
3) criticism from caregivers (increases risk x2.3) -- conversely better social support is associated with reduced risk of relapse
4) poorer premorbid adjustment (increased risk x2.2)
Interestingly, the authors conclude that factors such as diagnosis, length of illness, length of untreated symptoms, demographic variables, and cognitive function, are not associated with relapse risk.
Clearly, these findings add to the recommendations for helping patients who have had psychotic symptoms, and their families:
1) medication compliance is extremely important!
2) substance use must be avoided!
3) caregivers must work hard to avoid hostile or critical comments towards the patient
One question I have about these findings, however, is how causative some of these factors are. It could be argued that an individual who is already more likely to relapse may be more likely to be non-compliant with medication, be more likely to engage in substance use, and may be more likely to behave in a way which elicits more criticism from other people. The existence of these "risk factors" may indicate that the underlying disorder was more severe. So, some or all of these risk factors may simply be non-causal associations.
In order to more definitively show that risk factors #1-#3 are causative (and therefore controllable or reversable), we would have to show evidence that externally improving medication compliance in a previously non-compliant person would clearly reduce relapse rate. And we would need to show that a change in caregiver environment would produce a change in subsequent relapse rate.
There is some such evidence, but I think it would be good to see a careful meta-analysis looking at risk-factor management in reducing relapse rate.
Another thought I have about these findings is that the recommendations are appropriate not just for people who have had psychotic symptoms, but for all psychiatric conditions, and even for all members of the whole population! That is, avoidance of substance abuse and having good social support with minimal hostility and criticism is probably good and protective for everybody's mental and physical health! But we would have to look further at the research to see if this thought of mine has been proven.
Friday, January 11, 2013
Lamotrigine review: bipolar depression, unipolar depression, borderline personality, OCD
Lamotrigine is a novel anticonvulsant. Clearly it is useful for treating epilepsy, in terms of reducing seizure frequency in difficult cases, with a better side-effect profile than many other anti-seizure medications.
It has been used in psychiatry for over 10 years, mainly to treat bipolar depression. Initial studies were quite encouraging. More recent studies have been a bit more mixed.
Here are a few recent references:
http://www.ncbi.nlm.nih.gov/pubmed/21367355
this was a large study of using lamotrigine as an augmentation to treat unipolar depression. It did not show that lamotrigine was useful overall. But it appeared much more effective in a subgroup of patients with much more severe depression. Average doses were about 200 mg/d, maximum 400 mg.
http://www.ncbi.nlm.nih.gov/pubmed/19636254
this study showed improvements in affective lability with lamotrigine vs. placebo, in patients with borderline personality, using a flexible dose (average about 100 mg/day).
http://www.ncbi.nlm.nih.gov/pubmed/19200421 200 mg/d lamotrigine helpful for bipolar depression as add-on with lithium x 8 wks
http://www.ncbi.nlm.nih.gov/pubmed/23107222
no difference in depression scores with lamotrigine vs placebo as add on for bipolar patients
http://www.ncbi.nlm.nih.gov/pubmed/22351381 adding lamotrigine 100 mg to an SSRI improved symptoms (about 30% reduction in YBOCS score) in OCD patients, compared to placebo, after 16 weeks.
In conclusion, I think lamotrigine is in the "why not give it a try" category for a variety of problems. It might possibly help for treating depression in bipolar patients, or even as an augmentation in unipolar depression. It might be useful in OCD patients, and in borderline personality. It may be one of those agents which helps some individuals very well, even though the average effect for a group of similarly afflicted individuals may be unremarkable. Another possibility is that it could help with certain symptom domains, such as obsessionality, ruminativeness, etc. which could occur more prominently in some but not all patients with mood or personality disorders.
I think the big advantage of lamotrigine is that it is quite well-tolerated, with a benign side-effect profile, except for a small risk of a dangerous rash and a few other rare serious problems, which just need to be watched for carefully.
It has been used in psychiatry for over 10 years, mainly to treat bipolar depression. Initial studies were quite encouraging. More recent studies have been a bit more mixed.
Here are a few recent references:
http://www.ncbi.nlm.nih.gov/pubmed/21367355
this was a large study of using lamotrigine as an augmentation to treat unipolar depression. It did not show that lamotrigine was useful overall. But it appeared much more effective in a subgroup of patients with much more severe depression. Average doses were about 200 mg/d, maximum 400 mg.
http://www.ncbi.nlm.nih.gov/pubmed/19636254
this study showed improvements in affective lability with lamotrigine vs. placebo, in patients with borderline personality, using a flexible dose (average about 100 mg/day).
http://www.ncbi.nlm.nih.gov/pubmed/19200421 200 mg/d lamotrigine helpful for bipolar depression as add-on with lithium x 8 wks
http://www.ncbi.nlm.nih.gov/pubmed/23107222
no difference in depression scores with lamotrigine vs placebo as add on for bipolar patients
http://www.ncbi.nlm.nih.gov/pubmed/22351381 adding lamotrigine 100 mg to an SSRI improved symptoms (about 30% reduction in YBOCS score) in OCD patients, compared to placebo, after 16 weeks.
In conclusion, I think lamotrigine is in the "why not give it a try" category for a variety of problems. It might possibly help for treating depression in bipolar patients, or even as an augmentation in unipolar depression. It might be useful in OCD patients, and in borderline personality. It may be one of those agents which helps some individuals very well, even though the average effect for a group of similarly afflicted individuals may be unremarkable. Another possibility is that it could help with certain symptom domains, such as obsessionality, ruminativeness, etc. which could occur more prominently in some but not all patients with mood or personality disorders.
I think the big advantage of lamotrigine is that it is quite well-tolerated, with a benign side-effect profile, except for a small risk of a dangerous rash and a few other rare serious problems, which just need to be watched for carefully.
Thursday, January 10, 2013
N-acetylcysteine for OCD
I've written a post about N-acetylcysteine before (http://garthkroeker.blogspot.ca/2009/09/n-acetylcysteine-for-treatment-of.html), which suggested that it could be useful in treating compulsive behaviour disorders such as skin-picking.
A recent 2012 study by Afshar et al. has shown that NAC is useful for treating obsessive-compulsive disorder (OCD). Here's the reference: http://www.ncbi.nlm.nih.gov/pubmed/23131885
In this study, 48 patients with OCD who had not responded to an SSRI were given NAC up to 2400 mg/day or placebo, in addition to a continued dose of the same SSRI, for 12 weeks.
The NAC group had about a 40% reduction in YBOCS score (a quantitative measure of OCD symptoms) after 12 weeks, compared to a 20% reduction in the placebo group. This is a good, clinically relevant symptom change especially for a treatment-resistant group.
Mild gastrointestinal complaints were more common in the NAC group, but there was not a big difference in drop-out rates between placebo and NAC.
NAC works as as a glutamate-modulating agent, with possible anti-inflammatory effects. It is metabolized to the amino acid cystine after entering the brain.
So it appears that NAC could be a simple, low-risk, effective adjunct, or even a primary treatment modality, for obsessive-compulsive disorder.
I would be curious to see more research looking at NAC for other anxiety disorders, or for ruminative depression.
A recent 2012 study by Afshar et al. has shown that NAC is useful for treating obsessive-compulsive disorder (OCD). Here's the reference: http://www.ncbi.nlm.nih.gov/pubmed/23131885
In this study, 48 patients with OCD who had not responded to an SSRI were given NAC up to 2400 mg/day or placebo, in addition to a continued dose of the same SSRI, for 12 weeks.
The NAC group had about a 40% reduction in YBOCS score (a quantitative measure of OCD symptoms) after 12 weeks, compared to a 20% reduction in the placebo group. This is a good, clinically relevant symptom change especially for a treatment-resistant group.
Mild gastrointestinal complaints were more common in the NAC group, but there was not a big difference in drop-out rates between placebo and NAC.
NAC works as as a glutamate-modulating agent, with possible anti-inflammatory effects. It is metabolized to the amino acid cystine after entering the brain.
So it appears that NAC could be a simple, low-risk, effective adjunct, or even a primary treatment modality, for obsessive-compulsive disorder.
I would be curious to see more research looking at NAC for other anxiety disorders, or for ruminative depression.
Wednesday, January 9, 2013
Long-term clonazepam for panic disorder
The treatment of anxiety disorders, particularly panic disorder, should emphasize behavioural and cognitive therapy, exercise, lifestyle factors, etc.
But medication treatments can often be very helpful if these other therapies are not helping. The trend of thinking on this matter over the past few decades has been to preferentially use SSRI antidepressants, and to minimize the use of benzodiazepines such as clonazepam, due to concerns about side effects and dependence.
This study challenges that notion: http://www.ncbi.nlm.nih.gov/pubmed/22198456 It is a 3 year followup study (an excellent duration for a psychiatric study!) -- and compares paroxetine 40 mg/d with clonazepam 2 mg/d (all doses taken at bedtime) for treatment of panic disorder.
The clonazepam alone group did very similarly well to the paroxetine group, with even a slight edge of superiority over paroxetine. And there were fewer side effect complaints in the clonazepam group compared to paroxetine. There was no advantage to combined therapy (clonazepam + paroxetine).
While I still remain concerned about dependency and abuse problems with benzodiazepines, this type of study affirms that long-term benzodiazepine use may be helpful--and possibly superior to antidepressants--for some patients.
But medication treatments can often be very helpful if these other therapies are not helping. The trend of thinking on this matter over the past few decades has been to preferentially use SSRI antidepressants, and to minimize the use of benzodiazepines such as clonazepam, due to concerns about side effects and dependence.
This study challenges that notion: http://www.ncbi.nlm.nih.gov/pubmed/22198456 It is a 3 year followup study (an excellent duration for a psychiatric study!) -- and compares paroxetine 40 mg/d with clonazepam 2 mg/d (all doses taken at bedtime) for treatment of panic disorder.
The clonazepam alone group did very similarly well to the paroxetine group, with even a slight edge of superiority over paroxetine. And there were fewer side effect complaints in the clonazepam group compared to paroxetine. There was no advantage to combined therapy (clonazepam + paroxetine).
While I still remain concerned about dependency and abuse problems with benzodiazepines, this type of study affirms that long-term benzodiazepine use may be helpful--and possibly superior to antidepressants--for some patients.
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