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Re: Effexor an opiate? Probably not. JANNBEAU

Posted by Elizabeth on December 13, 2001, at 20:06:59

In reply to Re: Effexor an opiate? Probably not. Elizabeth, posted by JANNBEAU on December 13, 2001, at 11:41:32

> Hello, Elizabeth. Sorry I overreacted to your initial message. I'm rather new at this.

Don't worry about it. I think it's easy to misinterpret stuff over the net because there's no body language, facial expressions, etc. Just about everybody does it sometimes. It's still surprising to be at the other end of it, though! :-)

> I actually enjoyed your second posting. I've written some responses below. Please take them in the same spirit that you offered your comments.

Of course.

> Read your posting to dhldn. Didn't say much. Perhaps you could go into the detail with dhldn that you went into with me. I'd like to see HIS response.

My response to you also responded to his comments in greater depth. But he didn't post a response to my post. I'm not sure if he's a regular here, though.

Anyway, credentials don't mean much to me (especially since they're generally unproven on this forum). This is in part due to some of my experiences with psychiatrists who didn't know what they were talking about, but also to my general skepticism: I don't take what I hear as fact just because someone says it, regardless what letters that someone has after his or her name. :-) I expect everyone (not just laypeople) to show an understanding of what they're writing about.

> I do know that we don't have a clue about the myriad effects of today's meds. Not much different from the Middle Ages, huh, except there are so many more of them with which to contend.

I think our approach differs greatly from that of the Middle Ages, although some attitudes expressed by a lot of people (including medical and even scientific professionals) bear a disturbing resemblance to aspects of the Medieval world-view.

> I am bothered most by the fact that doctors prescribing them don't seem to think of this and do not discuss potential interactions, side effects.

Sometimes psychiatrists don't keep up with research on the drugs they prescribe, or on new off-label treatments. This is a serious problem. I think that part of it is that they assume that if another doctor is going to prescribe a drug that might interact, the other doctor will point out the interaction. Of course, this precludes the possibility that the patient have any control over his/her treatment.

> I always ask for the PI so that I will at least recognize an effect as being -perhaps- due to the new medication.

The trouble with the PI is the reverse: it includes every reported "side effect," even some which probably don't have anything to do with the drug. This can scare patients, to say the least, even making them unwilling to try the drug. It's misleading because most of these "side effects" are rare (especially the most serious ones), and *nobody* gets all or even most of them. I think that showing these lengthy lists to patients can do more harm than good. Unfortunately, the "patient information sheets" that pharmacies often keep are condescendingly lacking in real information.

> Not everyone has access to the information that we do nor do they have the sophistication to interpret it.

And that's the trouble with using the PI to educate patients about a drug.

> I take many Rx drugs for various things (HTN, hypercholesterolemia, etc) along with those I take for pain and, believe me, even if I knew nothing about the state of the "art" of developing, or more precisely, marketing new drugs (I worked in clinical pharmaceutical development for several years), I would be skeptical and watchful whenever I'm prescribed a "new" medication.

I recently moved from Boston, and now I'm in, well, a place where there's not so much psychiatry research (to euphemize). And I've been finding that medications that are considered "new" or "cutting edge" here are ones that were in use in Boston several years ago. As a result I've grown very pessimistic about finding a doctor here who'll be willing (or even knowledgeable enough) to prescribe the things that have worked best for me (opioids, which are still stigmatized in most places) or to try new things which may help me and which I haven't tried already (because they don't know anything about any drugs that I would consider "new").

> > Actually, I went ahead and looked this one up, and according to the PI, the affinity of O-desmethyltramadol (let's call it ODT for short) for mu receptors is about *200* times that of the parent compound; interestingly, the PI adds that ODT is about six times as potent an *analgesic* as tramadol. (Hard to know what to make of this.)
> OK, I'll give you that one! As I said, I was working from memory and have only scanned the literature on Effexor.

But I'm still wondering -- how is it that ODT is 200 times as potent a mu agonist as tramadol, but only 6 times as potent an analgesic? That's the mystery to me.

> I stand by the dictionary's definition of narcotic analgesic.

I'm not saying it doesn't have a meaning, or even a medical meaning -- but it's outdated, and there are words

> The term is used routinely in both clinical practice and in research, along with others.

Clinical practice, sure. I recently came across a doctor who referred to buprenorphine as a "narcotic." (He was also very ignorant of its effects.) Recent research that I'm familiar with uses "opioid" or "opioid agonist."

> It doesn't matter as long as each party understands the concept.

I don't agree entirely. While I understood that you meant "opioid agonists" by "narcotics," your use of the word "narcotics" suggested a political bias which I've heard called "opiophobia." I don't believe you have this bias, though, so I suggest that you use the more modern and less politically loaded term.

> For instance, OxyContin (extended-release hydrocodone) is not very different from MSContin (long-acting morphine sulfate) in pain relieving activity, yet one has become a popular street drug (OxyContin) while the other (MS Contin) never became a popular street drug, despite the fact that MS Contin is formulated similarly and should give the same "high" from snorting or injection of the crushed tablets.

OxyContin is sustained-release oxycodone, not hydrocodone. The media have portrayed it as some new drug, when in fact it's just Percocet without the Tylenol and in a slow-release formulation. Its potential for abuse is greater than that of MS Contin because oxycodone has greater bioavailability than morphine when taken orally. Injecting the sustained-release drugs is pretty difficult and dangerous, BTW, because they contain so many binders. Hard-core addicts have been known to do it, but it's not trivial and the risk is significant.

> With respect to your final comment re mixed opioid agonists, check the history of Talwin (pentazocine). You might find, as I have read, that when pentazocine was first marketed, it rapidly became a "drug of abuse" or "street drug."

I've heard that story. I think that it's unlikely that a heroin addict would be interested in Talwin; it's likely that a heroin user would feel *worse* on Talwin. So I think that it's most likely that the people "abusing" these drugs were not hard-core addicts, but young people who were going through a phase of "experimenting" with drugs, and that the attraction of the drugs to these people lay in their "forbidden" status (since they had been identified as opioids or "narcotics").

Anyway, kappa opioids don't have much attraction for people who prefer mu agonists. The other partial/mixed agonists are the partial mu agonists, such as buprenorphine and dezocine. There have been some reports of buprenorphine "abuse," but (having plenty of personal experience with this drug) I'm skeptical. Buprenorphine is a poor substitute for heroin, but an addict in withdrawal is liable to be willing to take whatever s/he can get, and buprenorphine does block withdrawal symptoms. It can also be used to detox oneself and causes hardly any withdrawal symptoms of its own. For recreational or experimental users, buprenorphine could indeed have appeal due to its ability to produce feelings of contentment. Any or all of these uses may have been considered "abuse" by the authors of the reports. One thing that a lot of professionals do not seem to realize (although it should have been covered in their educations) is that using a drug to feel better does not necessarily constitute abuse, even if the drug use is illegal. This is but one of many ways that the government has invaded the doctor's office: by leading doctors to believe that the legal status of a drug defines whether its use is pathological or not.

> Such abuse did not stop until the manufacturer reformulated the drug to add an opioid antagonist to prevent the "high" accompanying illegal use.

The addition of naloxone prevents injection, actually (naloxone isn't orally active, and pentazocine taken orally is really unimpressive, even moreso than it is when injected).

> I read the PI and did not expect that I would hurt for six hours after taking the med.

I'm still surprised that it took *that* long for it to work for you. It might be that you are slower at metabolizing drugs through this pathway (cytochrome P450 2D6); there might have been other factors at work as well (too low a dose of Ultram, for example).

> I used it for about a week with Effexor before developing what I assume was serotonin syndrome; at no time did I get any significant pain relief.

What symptoms did you have? Like I said, I never found Ultram to be worth using for pain -- or for depression, for that matter -- and the evidence (high measured TCA levels, odd reactions to dextromethorphan) suggests that I'm deficient in CYP 2D6. This lends credence to your hypothesis that most of the analgesic activity of Ultram is due to ODT.

> In fact, I was probably overdosing myself because I continued to hurt, despite Effexor's analgesic potential.

I'll let you know if I get any pain relief from Effexor; my back pain continues so far (mainly in the morning, when I haven't recently taken buprenorphine), but I'm only taking 75 mg/day of Effexor.

> Ultram has this effect on me as does codeine.

Well, then you're probably metabolizing them normally, or close enough to normally.

> Nightmares or "vivid" dreams have been associated with oxycontin. Why would one not expect the same from other drugs of like action?

I wasn't aware that vivid dreaming was associated with any opioid. They tend to suppress REM sleep, if anything, and they don't have the peculiar effects on REM sleep that are seen with SSRIs and Effexor (where REM density is increased -- this is thought to lead to the vivid dreaming often seen as a side effect of SRI antidepressants).

> I have to accept the above comment, qualified by your following statement. Perhaps I've been led astray by the good doctor's posting?

I'm not going to question somebody's claim of credentials, although in this case I'm not sure what the credential means. But as I said above, I've seen too many cases where people didn't live up to their credentials -- and many cases of lay-people having surprising knowledge that they attained by themselves -- to pay much attention to a person's credentials or lack thereof.

> I understand this concept. I do not argue that Effexor is not an SRI (not an SSRI), just that it may have more than ONE mechanism of action and that the results of this "mixed" mechanism may be different from what one would expect with a "pure" SRI.

Generally what we've seen with Effexor has suggested that its original marketing as "Prozac with a punch" was pretty accurate: it can have nastier side effects than SSRIs (but the same general *type* of side effects), and it also can work in situations where SSRIs aren't so effective (e.g., severe or melancholic depression). The NE reuptake inhibition is likely responsible for the hypertension sometimes caused by Effexor (most TCAs block alpha1-adrenergic receptors, which may tend to lower blood pressure, canceling out this effect; Effexor, like the SSRIs, doesn't have the antagonist effects at histaminergic, cholinergic, and noradrenergic receptors that are seen with most of the TCAs).

> > The list from the Effexor PI is pretty exhaustive. That's not surprising since the PIs typically list every reported side effect and could be expected to do the same with withdrawal symptoms.
> I am aware of the FDA's requirements for listing side effects and withdrawal effects.

Then you're aware that this list of withdrawal symptoms should not be taken as a list of symptoms all of which anyone discontinuing Effexor is liable to experience! Only a few of them are all that common.

> I'm not worried! This was supposed to be an intellectual discussion.

Good! My favorite kind.

> I take hydrocodone a couple of times a day and propoxyphene at night. Why would I be "worried" about the proposed "opioid" effects of Effexor?

I wasn't just addressing you there, but anyone who's reading this conversation. I would hate for people to avoid Effexor (a pretty good AD, though it often has nastier side effects and w/d symptoms than the SSRIs) for fear that they might become opioid-dependent!

> I also have NEVER had difficulty stopping any drug I took, so don't expect to die from discontinuing Effexor.

Some drugs -- such as alcohol, barbiturates, and (to a *much* lesser degree) benzodiazepines -- have the potential to cause serious, even fatal withdrawal symptoms (generalized seizures, for example). Opioid withdrawal is exceedingly unpleasant (even for people who are just watching it, not experiencing it!), but it's *not* fatal.

> Again, I've just enjoyed the intellectual stimulation of this conversation.

Thanks. Me too. :-)





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