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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 13 of 13. This is the beginning of the thread.
Posted by bulldog2 on January 18, 2007, at 13:04:47
Is this combination allowed or forbidden? I'm Due to start emsam but I am currently on vicodin from an oral surgery procedure.
Posted by Phillipa on January 18, 2007, at 14:49:23
In reply to Emsam Interaction With Vicodin?, posted by bulldog2 on January 18, 2007, at 13:04:47
If all else fails google their website. Not sure. Love Phillipa
Posted by laima on January 18, 2007, at 19:10:09
In reply to Emsam Interaction With Vicodin?, posted by bulldog2 on January 18, 2007, at 13:04:47
Possibly dicey- maybe ask your pharmacist and doctor to avoid a problem. Is codeine an opiate? I think opiates can cause seratonin syndrome.> Is this combination allowed or forbidden? I'm Due to start emsam but I am currently on vicodin from an oral surgery procedure.
Posted by Quintal on January 18, 2007, at 19:43:43
In reply to Re: Emsam Interaction With Vicodin?, posted by laima on January 18, 2007, at 19:10:09
Yes, codeine is an opiate but it's the synthetic opiates like tramadol and pethidine that can cause serotonin syndrome. I ran the combo through an interaction checker and it revealed no problems but not all interactions are documented and this may be an oversight. Some people have combined opiates with MAOIs without serious adverse effects. The most common side effect from the MAOI/opiate combo is hypotension.
Q
Posted by laima on January 18, 2007, at 20:52:38
In reply to Re: Emsam Interaction With Vicodin?, posted by Quintal on January 18, 2007, at 19:43:43
Oh- good to know. So there is a distinction-I guess that's why I was able to have morphine while on Emsam. I think some drug guides perhaps are brief and seem to generalize, like saying "no opiates". ps- That morphine sure seemed to be anti-depressing.> Yes, codeine is an opiate but it's the synthetic opiates like tramadol and pethidine that can cause serotonin syndrome. I ran the combo through an interaction checker and it revealed no problems but not all interactions are documented and this may be an oversight. Some people have combined opiates with MAOIs without serious adverse effects. The most common side effect from the MAOI/opiate combo is hypotension.
>
> Q
Posted by Honore on January 18, 2007, at 21:53:50
In reply to Re: Emsam Interaction With Vicodin?, posted by laima on January 18, 2007, at 20:52:38
I've used it-- with no problem, if that helps.
I'm not sure I asked my pdoc about Vicodin per se, but had asked about Tylenol 3 (tylenol and codeine), which I've also taken quite a bit.
It';s always a good idea to ask, though, when in doubt.
Honore
Posted by Quintal on January 18, 2007, at 22:27:10
In reply to Re: Emsam Interaction With Vicodin?, posted by laima on January 18, 2007, at 20:52:38
>Oh- good to know. So there is a distinction-I guess that's why I was able to have morphine while on Emsam. I think some drug guides perhaps are brief and seem to generalize, like saying "no opiates". ps- That morphine sure seemed to be anti-depressing.
That's true. Codeine is metabolized to morphine by the liver and it has little or no analgesic action if taken with drugs that block the cytochrome P450 enzyme CYP2D6 such as Prozac and Celexa. One of natures most effective antidepressants IMHO.
Q
Posted by laima on January 19, 2007, at 12:54:02
In reply to Re: Emsam Interaction With Vicodin? » laima, posted by Quintal on January 18, 2007, at 22:27:10
Whoa- are you serious? Codeine, as vicodine, had very, very little effect for my post-gum surgery pain-even when I doubled up on it- and I was using zoloft (monotherapy) at the time! I wonder if that's why? Quintal, you might have just solved a mystery or two which have bugged me for several years. Do you know if it goes the other way, too- ie, could codeine render an ssri ineffective, or at least mess around with its actions? I sunk into a really horrific depression immediately after that surgery, and ssris conked out for me for good around that time, too.> That's true. Codeine is metabolized to morphine by the liver and it has little or no analgesic action if taken with drugs that block the cytochrome P450 enzyme CYP2D6 such as Prozac and Celexa. One of natures most effective antidepressants IMHO.
>
> Q
Posted by bulldog2 on January 19, 2007, at 14:59:25
In reply to Re: Emsam Interaction With Vicodin? » Quintal, posted by laima on January 19, 2007, at 12:54:02
I know they specifically say no demerol or propoxypene with an maoi as they elevate serotonin and you might get a serotonin crisis. I called the emsam hot line and they were very vague about the rest of the opiates. Basically saying they didn't know. I guess morphine has no serotonin properties so it's safe.
Posted by Larry Hoover on January 21, 2007, at 9:05:45
In reply to Re: Emsam Interaction With Vicodin? » Quintal, posted by laima on January 19, 2007, at 12:54:02
>
> Whoa- are you serious? Codeine, as vicodine, had very, very little effect for my post-gum surgery pain-even when I doubled up on it- and I was using zoloft (monotherapy) at the time!For clarification.....
Vicodin is dihydrocodeinone, not codeine. However, it undergoes a similar desmethylation reaction via 2D6, producing dihydromorphinone (hydromorphone, a.k.a. Dilaudid), which is certainly a dominant reason for its narcotic effects.
The 2D6 enzyme has over 100 known genetic variants. In a functional sense, variation in reaction rates exhibited by those genotypes can be over 100-fold. Not 100% difference, 100 times.
People with low 2D6 activity are called slow metabolizers. In Caucasians, that's roughly 10% of the population. For those people, codeine does sweet f all, except for its side effects. I would expect Vicodin to be similarly ineffective.
At the other end of the spectrum are the rapid metabolizers. An oral dose of codeine almost instantaneously converts to morphine, and narcotic intoxication results. Again, perhaps 10% of the population get this reaction.
In between are all the rest, showing still substantial inter-individual variability in reaction rates. As codeine (and dihydrocodeinone) are really pro-drugs (i.e. they are metabolized into more active forms), they serve as something like slow-release versions of morphine and hydromorphone, respectively.
What messes up this already messed up system are all those other drugs which inhibit enzyme 2D6, including virtually all of the SSRIs (speaking from memory). They will turn normal or rapid metabolizers into poor metabolizers.
Myself, I'm a poor metabolizer to begin with. IMHO, it is 2D6 poor metabolizers who are most vulnerable to liver toxicity from nefazodone (Serzone), an effect which led to its withdrawal from most markets.
> I wonder if that's why?
It's pretty good circumstantial evidence.
> Quintal, you might have just solved a mystery or two which have bugged me for several years. Do you know if it goes the other way, too- ie, could codeine render an ssri ineffective, or at least mess around with its actions?
The interaction could be significant, but the results are complex. It depends on the genetic activity of other P450 enzyme systems, and the relative potencies of metabolites. But, the answer is yes.
> I sunk into a really horrific depression immediately after that surgery, and ssris conked out for me for good around that time, too.
Opiates can induce very black depression, particularly immediately following cessation. Antidepressants can indeed be overwhelmed by the opioid-receptor mediated depression.
Lar
Posted by laima on January 21, 2007, at 9:25:37
In reply to Re: Emsam Interaction With Vicodin? » laima, posted by Larry Hoover on January 21, 2007, at 9:05:45
Posted by fuchsia on January 22, 2007, at 3:56:07
In reply to Re: Emsam Interaction With Vicodin? » laima, posted by Larry Hoover on January 21, 2007, at 9:05:45
Larry, I was tested recently and I am a poor metabolizer also. I was wondering if you (or anyone else who is a poor metabolizer) are having more troubles with your health than others.
I have tried so many medicines over the years and I always ended up having to take very small doses. Before it became obvious that I needed a small dose of most things I endured very severe side effects.
My nerves are so bad these days (to avoid going into all my symptoms) that I can't help thinking I've been damaged by the meds and possibly the odd blast of pesticide or other environmental chemical besides. I really fear I'll be one of these ones who get parkinson's as a result of dopaminergic neuron death due to chemical exposure, presuming a poor metabolizer ends up with more chemical exposure than a rapid metabolizer.
Do you know if this correlation (I've seen it written about) between an increased risk of parkinson's and being a poor metabolizer is a strong one? I've also seen an article about the increased risk of another disease though I can't remember what that was. Maybe there will be others that are picked up on in due course.
fuchsia
Posted by Larry Hoover on January 22, 2007, at 7:54:12
In reply to talking about poor metabolizers » Larry Hoover, posted by fuchsia on January 22, 2007, at 3:56:07
> Larry, I was tested recently and I am a poor metabolizer also. I was wondering if you (or anyone else who is a poor metabolizer) are having more troubles with your health than others.
>
> I have tried so many medicines over the years and I always ended up having to take very small doses. Before it became obvious that I needed a small dose of most things I endured very severe side effects.I wouldn't say I have a greater number of health problems....I don't attribute my psych issues to 2D6 inefficiencies. I also am "Mr. Side Effect", and I also cannot tolerate typical doses of medication. Twice, side effects nearly killed me. I attribute my continued existence to my own vigilance and self-assessment skills. I am the gate-keeper of my mouth. I don't just swallow what the doctor says to swallow, any longer. I do things very carefully.
> My nerves are so bad these days (to avoid going into all my symptoms) that I can't help thinking I've been damaged by the meds and possibly the odd blast of pesticide or other environmental chemical besides.
The primary detoxicant for environmental chemicals is 3A4. I don't recall that there are any defective variants to this enzyme, and moreover, it is inducible. That means that if the toxicant load increases, so does the enzyme's activity. If you're concerned about maintaining 3A4 activity, stay away from grapefruit, as it inhibits this enzyme. St. John's wort enhances its function.
My nerves are bad (I have PTSD), but I attribute that to life history.
> I really fear I'll be one of these ones who get parkinson's as a result of dopaminergic neuron death due to chemical exposure, presuming a poor metabolizer ends up with more chemical exposure than a rapid metabolizer.
2D6 is typically a minor player in detox reactions. That said, the specific biotransformations mediated by this enzyme may play a critical role in very limited circumstances. I don't know of an environmental insult that increases the vulnerability of poor metabolizers at 2D6, off the top of my head.
> Do you know if this correlation (I've seen it written about) between an increased risk of parkinson's and being a poor metabolizer is a strong one? I've also seen an article about the increased risk of another disease though I can't remember what that was. Maybe there will be others that are picked up on in due course.
I hadn't heard of any correlations with 2D6 mutation and disease before you mentioned it, so I went to Pubmed, and took a serious look around. I find no evidence that 2D6 mutation is significantly responsible for the induction of any disease, except in very rare cases. And even then, the correlation found is not evidence of causation.
Whenever a mutation is found with some significant frequency in a population, you're going to get correlations with all sorts of other variables, simply by chance. If you examine a family cluster of Parkinson's disease, and find that all affected individuals have a poor metabolizer form of 2D6, you're likely to publish that finding. That will spur other researchers to look at their own cases, to see if the marker mutation has a similar incidence among them. When that was done, there was no evidence of any 2D6-induced vulnerability to Parkinson's. The most likely explanation, IMHO, is that Parkinson's disease only develops under the influence of multiple concurrent risk factors, one of which *might* be 2D6 low function. In a family group, it is far more likely that those other risk factors, also under genetic control, would tend to be found alongside the 2D6 mutation. In the general population, that same collection of risk factors is so uncommon, that it cannot be found in significant numbers, and no correlation is seen.
Other diseases, particularly liver disease and various cancers, have also been tentatively associated with 2D6 mutation, but once again, larger populations do not exhibit increased risk mediated by this specific defect. Breast cancer has the BRAC gene that clearly increases risk. The same does not appear to be true for 2D6.
Each of us, on average, has over 100 enzyme defects. Of course, those won't be the same ones, individually. And these are only the defects we've had the good luck to yet identify. The possible interactions of 100 or more variables approaches infinity. Which ones lead to disease? Beyond being careful which drugs and which dose I take, I'm not concerned.
> fuchsia
Nice flower. Nice name.
Lar
This is the end of the thread.
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