![[dr. bob]](/dr-bob-sm.gif)
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 HKristina on January 9, 2006, at 12:57:06
Hello.
I was diagnosed as ADD when I was 19... and have been on ritalin since. I was the type of student that either made an A or an F. I have always procrastinated and I seem to quit just about everything.
I started having panic attacks when I was 20. They were constant. I believed I had a brain tumor, or other ailment that would cause instant death. My Primary Care Doc told me I was a Hypochondriac. I did some research and learned that a high dose of SSRI could help. 200mg of Zoloft took it away, and it has never returned.However, I did become a fat zombie within a year. I had been skinny all my life before that. My family insisted I was depressed. I would say it was more pure apathy. I watched TV. I was still very hopeful about coming out of the smog. About 3 years later, I went off the Zoloft. I felt better. Lost all the weight. Started exercizing.
Within a year, I was so completely hyperfocused in some weird love triangle, and too anxious to get out. I started drinking, and was pretty much a crazy (I mean that pretty much literally) drunk for a good year after.
Something is wrong with me. I have had typical panic disorder. Then I have a substance abuse problem. Now I am very depressed. I am apathetic, not able to experience pleasure, unmotivated, lethargic, I feel defective, I have sleep disturbances, (my weight is oddly increasing again though I don't eat that much)... My affect in the past is gregarious, though I had horrible social anxiety as a child. I was a model in NYC. I could paste on a smile despite what was going on inside. I have always lived in my head very much.... but it always wasn't a bad place to be. Now it's driving me nuts. I'm 33 years old now, barely functioning, and desperately wanting relief.
Another thing, I've always been extremely disorganized.
I went on Cymbalta 3 weeks ago, and found some relief. I am taking 60 mgs. My primary care doctor just added Lamitcal, but I am still taking only 25 mg. I've only been on it three days, but it seems to be making me anxious.
I guess I am looking for a diangosis. In the past, I can be very playful, full of energy, but I've never slept with strangers (unless drunk), or did other manic-type of behavior.
I have a good IQ, I am physically healthy, yet I can't seem to function or accomplish anything.
Does anybody have a clue as to what could be wrong with me?
Thank you.
Heather
Posted by HKristina on January 9, 2006, at 13:20:32
In reply to Looking for a Diagnosis, Medicine Input, posted by HKristina on January 9, 2006, at 12:57:06
Sorry. I got the chronology wrong. I actually had the panic disorder, which turned into near agoraphobia before I was diagnosed with ADD. The Ritalin did not set it off. Also, I would say that I have always felt "not normal" even as a child; though I was able to be social without masking or guarding. When I read about the accounts of mixed states of BPII, it does seem to resonate. And I also used to feel that life was cyclic, but that was when I was in my late-teens early twenties.
Posted by Spiro Ghetti on January 9, 2006, at 13:53:45
In reply to Looking for a Diagnosis, Medicine Input, posted by HKristina on January 9, 2006, at 12:57:06
I'm no expert, but maybe I can have some input; Obessive Compulsive Disorder, anxiety, and depression usually happen hand in hand in the susceptible population. It seems you have the OCD/Depression/Anxiety bundle happening during various time of your life.
Given some of your symptoms, some might say you should get tested for Hypothyroidism, but I doubt that's the problem. As someone who's been through this type of pain and confusion, I can say with tremendous confidence this type of thing is psychological.
You do not have a physical illness.
You might want to look into medical/psychological treatments avaliable for OCD/Depression/anxity. The same medications usually address all three (e.g. LUVOX)
Posted by Emily Elizabeth on January 9, 2006, at 16:40:53
In reply to Looking for a Diagnosis, Medicine Input, posted by HKristina on January 9, 2006, at 12:57:06
Welcome to Babble! I'm not sure that I have a ton of input on your actual questions, but I would like to be as helpful as possible. I guess I have a few questions:
1. How much do the attn symptoms effect your day to day life now? Have you been able to hold a job? Have you been able to do well at a job? If this is a big concern, it might be worth it to look into neuropsychological testing w/ a psychologist--it might help separate out if you have attn probs, a learning disability, emotional probs, etc. It also could help illuminate what direction to take w/ meds and other possible interventions.
2. Have you worked w/ a therapist? Was it helpful?
3. Have you ever seen an actual psychiatrist? I think that a gp is probably in over his head here--no offense to you or your doc. GP's don't recieve enough specialized training in psychopharmacology to be combining meds like the ones you are on. It is not to say that all pdocs out there are great, but they are more likely to have the right training to treat your probs. Also, a pdoc would better be able to rule out other mental health issues.
Please write back and I (and probably others) will do our best to be helpful!
Best,
EE
Posted by HKristina on January 9, 2006, at 16:59:54
In reply to Re: Looking for a Diagnosis, Medicine Input » HKristina, posted by Emily Elizabeth on January 9, 2006, at 16:40:53
Thank you for responding!
Emily,
Earlier in my life, I felt that my attention problems were the primary problem, but I would almost definately say that emotional problems are the ruling problem here. Can emotional problems even be treated with psychotropic medications?
As far as work.... No, it doesn't seem like I can maintain at anything without crashing. Whether or not my behavior creates failure, and then the depression, or if the depression/anxiety causes the behavior... I have no idea.
I have been seen by 3 psychiatrists. 1. I was 18. She spent 15 minutes with me and diagnosed me as bipolar. She said she was positive. I did some research, and it seemed implausible, so I did not see her again or take the prescribed Lithium. 2. I was 19 and went to a Pdoc for my concerns about ADD after reading an article in a magazine. I was prescribed Ritalin then. 3. I went when I was 26 and was diagnosed with OCD/anxiety and was put on Zoloft.
I have never seen a therapist. And my father presented with similar problems that I exhibit, but he was a very functional physician (though he had a wife, secretaries, etc).
I am very indecisive and took many various routes of study in college, not really finishing any of them. I am extremely disorganized and it is a very disruptive problem. I get organized once in a blue moon, but lack the ability to maintain it.
Earlier in my life, I have been able to be somewhat resiliant... blaming each failure on this or that... and that I could overcome my deficiencies and be productive... but I am at the point now where I feel like I must truly be defective... unable to accomplish anything. I seem to have alot of maladaptive behaviors.
And my mind does race... and always has in an anxious way... few times have there been positive racings. I feel miserable and despaired on minute, and literally the next minute, I feel somewhat ok... but not enough to be able to even really move much. I spend most of my time on the couch, zoning out on TV, with my mind and emotions just all over the place.
I hope I answered everything in the way you were looking for... And thank you so much.
Heather
Posted by Phillipa on January 9, 2006, at 19:47:32
In reply to Re: Looking for a Diagnosis, Medicine Input, posted by HKristina on January 9, 2006, at 16:59:54
Hi Heather did you say your mind races no concentration and that you have OCD? Did you ever try luvox? Fondly, Phillipa
Posted by HKristina on January 10, 2006, at 15:18:39
In reply to Re: Looking for a Diagnosis, Medicine Input » HKristina, posted by Phillipa on January 9, 2006, at 19:47:32
My Doctor added Depakote today. I feel like a shiny new penny. I don't know if this is indicative of a probable dx of Bipolar II. It's the best I have felt in years. I wonder if I was experiencing many cycles of mixed states. Does anyone know if that's even plausible?
Thank you so much to everyone that has written.
Heather
Posted by Emily Elizabeth on January 11, 2006, at 0:54:33
In reply to Re: Looking for a Diagnosis, Medicine Input, posted by HKristina on January 10, 2006, at 15:18:39
We'll keep our fingers crossed that it keeps working!
My best advice is to find a good psychologist and psychiatrist. Sounds like you have a complex history and someone sharp needs to sort it out.
Didn't you say that you are in NYC? If so, that is probably a good thing--lots of the country's top docs work there. Good luck to you. Please keep posting and let us know how we can help!
Best,
EE
Posted by Tomatheus on January 11, 2006, at 12:52:56
In reply to Looking for a Diagnosis, Medicine Input, posted by HKristina on January 9, 2006, at 12:57:06
Heather,
You might want to consider trying an MAOI -- if not now, possibly at some point in the future. Let me quickly summarize the extent to which MAOIs have demonstrated efficacy in the treatment of your various diagnoses and primary symptoms.
1) Panic disorder:
Several controlled studies have found MAOIs to be effective in the treatment of panic disorder. According to Liebowitz et al. (1990), several older studies comparing MAOIs with the tricyclic antidepressants in terms of their efficacy in treating panic disorder have found the MAOIs to be superior. The MAOIs Nardil and Parnate have not been approved by the FDA for use in panic disorder, but they are sometimes used (successfully) in treatment-refractory patients.
2) ADD:
MAOIs are not approved by the FDA for the treatment of ADD/ADHD, and they are rarely - if ever - prescribed for this condition. However, in a study that aimed to determine the effectiveness of both dextroamphetamine sulfate (generic for Dexedrine) and MAOIs in the treatment of childhood "ADD with hyperactivity," Zametkin et al. (1985) found that the MAOIs had "immediate, clinically significant benefit and were clinically indistinguishable from dextroamphetamine." All of the participants (14 boys with a mean age of 9.2 years) went through two trials: one with dextroamphetamine, and the other with an MAOI (either Parnate or clorgyline, an irreversible MAO-A inhibitor that has only been used in research studies). Zametkin et al. (1985) concluded that MAOIs may be "useful alternative treatments in selected cases of ADD."
3) Hypochondriasis:
The efficacy of MAOIs in the treatment of hypochondriasis is unclear, largely because no published study that I am aware of has specifically attempted to examine the nature of the relationship between hypochondriasis and MAOI responsiveness. I was able to locate a research article on a controlled study that measured the effectiveness of the MAOI Nardil on several measures of depression and anxiety. One of these measures was "hypochondriasis-agitation." The study, conducted by Ravaris et al. (1976), found that participants who were given 60 mg/day of Nardil showed greater improvement in their hypochondriasis-agitation scores than those who were given either 30 mg/day of Nardil or a placebo. Although data on the relationship between hypochondriasis and MAOI responsiveness are largely lacking, the possibility that MAOIs may be effective at treating the symptoms of hypochondriasis seems to be at least somewhat likely.
4) Depression:
The MAOIs Nardil and Parnate are FDA-approved for the treatment of depression and are believed to be of particular value in the treatment of patients with "atypical" features, bipolar depression, and treatment-refractory depression (Fiedorowicz & Swartz, 2004). In a meta-analysis (a research article that summarizes and analyzes the findings of multiple clinical trials) on the efficacy of MAOIs in depression, Thase et al. (1995) found that MAOIs tend to be less effective than tricyclic antidepressants in inpatients, but tend to be more effective than the tricyclics in patients with atypical depression. Patients with atypical depression must report having a reactive mood and at least one of the four following symptoms: overeating, oversleeping, a "leaden paralysis" feeling, and personal rejection sensitivity (Quitkin et al., 1988). Other researchers have concluded that MAOI responders often experience comorbid symptoms of depression and anxiety and do not show "significant melancholic depressive features" (Liebowitz et al., 1990). So, in a nutshell, MAOIs tend to be relatively comparable to most other antidepressants in terms of their overall effectiveness in the treatment of depression, but they are usually only used as third- or fourth-line treatments (if that) because of their side effects, especially the need to maintain a special diet to avoid experiencing a potentially (but rarely) fatal hypertensive crisis. But for certain depressed patients (e.g., atypical depressives, treatment-resistant depressives, depressives with comorbid anxiety symptoms, and some bipolar depressives), MAOIs are believed to be particularly useful.
5) Excessive alcohol consumption:
MAOIs obviously aren't used to treat substance/alcohol use disorders per se, but I think it's important to note that there is a significant positive relationship between major depression and alcohol use disorders. As Grant & Harford (1995) reported, "comorbidity of alcohol use disorders and major depression is pervasive in the general population." So, even though one cannot say conclusively that depression *causes* alcohol use disorders, or vice versa, it is clear that the two variables are related. It also remains possible (and somewhat likely, in my opinion) that your excessive alcohol consumption during that year or so of your life may have been a manifestation of your depressive and other psychiatric symptoms.
6) Social anxiety:
Even though SSRIs are almost always used in the first-line of treatment of social anxiety disorder because of their favorable safety profile in comparison to the MAOIs, comparative research trials have consistently shown the MAOI Nardil to be the most effective medication for treating social anxiety disorder. According to Aarre (2003), patients with social anxiety disorder should not be considered treatment resistant unless they have been offered a Nardil trial.
7) Cycling:
Ok, I kind of cheated and found what you wrote in another thread, but I noticed that you wrote that you experienced some "cycling" between depression and euthymia on no meds and then experienced more significant cycling on SSRIs. What I'm about to say comes both from my own experience and from research studies, but basically I do think that there is some evidence that MAOIs tend to be the best antidepressants for patients who rapid cycle in response to SSRIs and/or SSNRIs (and also possibly tricyclics). I can say from my own personal experience that I experienced SSRI-induced cycling, but never experienced any hypomanic symptoms of any sort on Nardil, Parnate, or moclobemide monotherapy. All rapid cyclers may not be able to tolerate MAOIs as well as I have (from the perspective of their tendency to induce hypomania), but there is some evidence that they're less likely to induce cycling than other antidepressants. Furthermore, clorgyline (an irreversible MAO-A inhibitor that has been used exclusively in research) has demonstrated some capacity to prolong the duration and lessen the severity of mood cycles in patients with endogenous rapid-cycling bipolar disorder (Potter et al., 1982).
Well, to sum things up really quickly, there is little doubt in my mind that you fit the profile of a potential MAOI responder. Of course, patients taking MAOIs are required to follow a special diet that restricts foods such as aged cheeses, salami, pepperoni, dried sausages, spoiled meats, fermented soy products, tap beer, sauerkraut, and broad beans. So, you'd have to be willing to make some sacrifices. But in my opinion, refraining from eating the foods on the MAOI diet list is a small price to pay for patients who get clinically significant relief from MAOIs. Of all the MAOIs (Nardil, Parnate, Marplan, selegiline, moclobemide, and a few others -- depending on where you live), I would recommend the "old" Nardil. The problem with this, unfortunately, is that the "old" Nardil was replaced with the new Nardil about two years, so there won't ever be a way to get the "old" Nardil unless those who are in the process of taking action against Pfizer succeed at making the "old" Nardil available once again. But as far as my suggestion, I'm not going to lie; I do think that the "old" Nardil would probably be your best bet. Since you can't take that, though, I guess I'm going to have to suggest that the "new" Nardil is probably your best choice since it generally tends to be the MAOI of choice for patients with symptoms of both depression and anxiety.
Hope this helps. I've technically started a little "Babble break," but I felt that I had to reply to your message first. So, I probably won't be reading the boards much for the next few weeks, but I'll check up on things every now and then, and I'll have my Babblemail on.
Tomatheus
==
REFERENCES
Aarre, T. F. (2003). Phenelzine efficacy in refractory social anxiety disorer: A case series. Nordic Journal of Psychiatry, 57, 313-15.
Grant, B. F., & Harford, T. C. (1995). Comorbidity between DSM-IV alcohol use disorders and major depression: Results of a national survey. Drug and Alcohol Dependence, 39, 197-206.
Fiedorowicz, J. G., & Swartz, K. L. (2004). The role of monoamine oxidase inhibitors in current psychiatric practice. Journal of Psychiatric Practice, 10, 239-48.
Liebowitz, M. R., Hollander, E., Schneier, F., Campeas, R., Welkowitz, L., Hatterer, J., et al. (1990). Reversible and irreversible monoamine oxidase inhibitors in other psychiatric disorders. Acta Psychiatrica Scandinavica, Suppl 360, 29-34.
Potter, W. Z., Murphy, D. L., Wehr, T. A., Linnoila, M., & Goodwin, F. K. (1982). Clorgyline: A new treatment for patients with refractory rapid-cycling disorder. Archives of General Psychiatry, 39, 505-10.
Quitkin, F. M., Stewart, J. W., McGrath, P. J., Liebowitz, M. R., Harrison, W. M., Tricamo, E., et al. (1988). Phenelzine versus imipramine in the treatment of probably atypical depression: Defining syndrome boundaries of selective MAOI responders. American Journal of Psychiatry, 143, 306-11.
Ravaris, C. L., Nies, A., Robinson, D. S., Ives, J. O., Lamborn, K. R., & Korson, L. (1976). A multiple-dose, controlled study of phenelzine in depression-anxiety states, Archives of General Psychiatry, 33, 347-50.
Thase, M. E., Trivedi, M. H., & Rush, A. J. (1995). MAOIs in the contemporary treatment of depression. Neuropsychopharmacology, 12, 185-219.
Zametkin, A., Rapoport, J. L., Murphy, D. L., Linnoila, M., & Ismond, D. (1985). Treatment of hyperactive children with monoamine oxidase inhibitors. Archives of General Psychiatry, 42, 969-73.
Posted by HKristina on January 12, 2006, at 13:08:58
In reply to Re: Looking for a Diagnosis, Medicine Input » HKristina, posted by Tomatheus on January 11, 2006, at 12:52:56
Thomatheus,
You are so kind. Thank you so much!
Am I right to assume that you noticed that I no longer have the hypochondriasis or panic attacks and that you believe that I would benefit from Nardil due to the fact that a particular profile of people happen to have a neuropsyiological need that is congruent to the solution a MAOI provides?
I am very new to this on an investigational level, though I'm not new to feeling bad... :-).
I have a lot of questions. Do people ever acheive long term remission? These message boards are heart-breaking and discouraging. This seems to be really a life-long battle.... no magic bullet, which is hard for me to wrap my brain around... I much prefer instant gratification.I can't thank you enough.
Heather
Posted by Tomatheus on January 14, 2006, at 15:11:55
In reply to Re: Looking for a Diagnosis, Medicine Input » Tomatheus, posted by HKristina on January 12, 2006, at 13:08:58
Heather,
I'm sorry for taking so long to get back to your post. My responses are below...
> Am I right to assume that you noticed that I no longer have the hypochondriasis or panic attacks and that you believe that I would benefit from Nardil due to the fact that a particular profile of people happen to have a neuropsyiological need that is congruent to the solution a MAOI provides?Yes, I did notice that you described the occurrence of panic attacks and the symptoms of hypochondriasis (as well as the social anxiety and the excessive alcohol consumption) as psychiatric events that have since come to pass. Judging from your post, it seems pretty clear from my perspective that your psychiatric condition is manifesting itself primarily as depression. But I just thought that it would be helpful to examine the course of your illness as it has unfolded over time, especially so I could illustrate the fact that most of the primary symptoms associated with your various diagnoses are those that tend to respond reasonably well to MAOIs.
Now with respect to the second part of your question...
On occasion, I read posts here on Psycho-Babble and other discussion forums (mostly here, though) from patients whose symptomatic profiles, illness trajectories, and medication responses seem to be consistent with a certain genetically determined biochemical abnormality. But because there is so much uncertainty surrouding the causes of psychiatric illnesses in general -- and even more uncertainty on my part about any potential underlying pathologies because one can only understand another person's illness so well just from reading a discussion board posting -- I basically always refrain from suggesting that another person's illness might be caused, at least in part, by a specific abnormal variant in a given gene. But I've never had anyone ask me if I think that they might have a "neuropsyiological need that is congruent to the solution" that a suggested medication might provide (or anything along those lines). I'm assuming that you asked me this question because you wanted my honest response. So, considering that my honest response is what you're looking for, that's what I'm going to give you. But remember that I'm just a patient -- not a doctor or researcher -- and that my ideas are basically just hypothetical, even though there is some evidence in the scientific literature to support my ideas.
I've never said this before on this forum, and it would take me far too long to explain what I'm about to say in any amount of detail (plus, it would end up including more personal information about myself than I would prefer to provide here), but I have for some time suspected that the underlying cause of my psychiatric illness is the abnormally high production of monoamine oxidase A (MAO-A), the enzyme that metabolizes serotonin and norepinephrine in their respective neurons. Another structurally similar enzyme, monoamine oxidase B (MAO-B) is specific in its metabolism of benzylamine and phenylethylamine (Lotufo-Neto et al., 1999). Neuronal dopamine is believed to be metabolized primarily by MAO-A under normal conditions, but by both MAO-A and MAO-B when neuronal dopamine levels are abnormally high (Fornai et al., 1999).
Nardil and Parnate, the two MAOIs approved for the treatment of depression in the United States, are mixed inhibitors in that they inhibit both types of MAO at both high and low doses. Selegiline, which is used primarily in the treatment of Parkinson's disease, is preferential in its inhibition of MAO-B, but loses some of this preferentiality at higher doses. It is expected that a transdermal form of selegiline (Emsam) will be approved for the treatment of depression soon -- possibly as early as next month. There currently are not any MAOIs available for commercial consumption in the United States that are highly preferential in their inhibition of MAO-A. But moclobemide, a reversible inhibitor of MAO-A, is available in more than 50 countries worldwide (Lotufo-Neto et al., 1999). Unlike the aforementioned MAOIs, which are all irreversible in their inhibition of the MAO enzymes, moclobemide only binds to MAO-A temporarily before eventually losing its grip on the enzyme, so to speak. The irreversible inhibitors bind to MAO-A and MAO-B for the life of the enzymes, and the clinical effects of this irreversible inhibition (from just a single dose) can be felt for approximately two weeks. With moclobemide, the clinical effects of a sinle dose last approximately 16 hours in comparison. So, even though moclobemide might seem like the perfect medication for individuals with abnormally high levels of MAO-A, it is much less potent than the irreversible MAOIs. Furthermore, when Müller et al. (2002) investigated the relationship between moclobemide responsiveness and the genetic variants that encode for abnormally high MAO-A production, they did not find a statistically significant correlation between the two variables. If it is indeed true that the overproduction of MAO-A is at the root of my psychiatric illness (which is mostly depressive in nature), then my experience with moclobemide would be consistent with the findings of Müller et al. (2002). When I took moclobemide, I felt a slight antidepressant response during my first three to four days on the medication, but I felt next to nothing after that.
To briefly summarize a few of the studies that I have read concerning abnormally high MAO-A production, I am going to paste a paragraph that I wrote in a post that I made a few weeks ago (http://www.dr-bob.org/babble/20051221/msgs/592784.html):
[==beginning of pasted paragraph==]
I also think that there is a subgroup of individuals who stands to benefit from the selective inhibition of MAO-A. Studies that have measured MAO-A levels in cultured skin fibroblasts and placentas have found that levels of the enzyme vary "over 50-fold" among control individuals (Hotamisligil & Breakefield, 1991). Furthermore, variants of the MAO-A gene that encode for abnormally high levels of the enzyme have shown statistically significant associations with major depression and sleep disturbance in males (Du et al., 2004); depressed suicide in males (Du et al, 2002); major depression in females (Schulze et al., 2000); panic disorder in females (Deckert et al, 1999); anxiety disorders, agoraphobia, and specific phobias in females (Samochowiec et al., 2004), and ADHD in children (Domschke et al., 2005; Jiang et al., 2001). In my opinion, it seems possible that in some individuals, the genetic tendency to produce abnormally high levels of MAO-A could be just one of multiple genetic abnormalities that contributes to their illness. And the relationship between the abnormally high MAO-A levels and the ways in which the associated psychiatric illnesses manifest themselves does seem to be different in males than it is in females. This could be because the MAO-A gene is located on the X chromosome, because of estrogen's ability to influence MAO-A activity MAO-A activity (Chakravorty et al., 1997), or possibly both. But it seems clear that there are some individuals whose psychiatric symptoms are at least partially mediated by genetically determined high levels of MAO-A. Furthermore, MAO-A activity has been reported to rise significantly with aging (Hotamisligil et al., 1991), indicating that the selective inhibition of MAO-A may be beneficial in treating geriatric depression. So, between the genetic tendencies to produce abnormally high levels of MAO-A and the potential that hormonal differences could also influence MAO-A levels, there is little doubt in my mind that there are some individuals (note: I'm not saying *all* individuals) who would benefit from a potent selective inhibitor of MAO-A.
[==end of pasted paragraph==]
As you can see, the diagnoses and primary symptoms that you described in your posts match up pretty closely with the illnesses that have shown statistically significant associations with variants of the MAO-A gene that encode for abnormally high enzyme production in females. Can I say with 100 percent certainty that you have one of these high-activity variants of the MAO-A gene? Of course not; I have neither the know-how nor the technology to give you a genetic test. But the likelihood that your psychiatric condition might be mediated by abnormally high MAO-A levels seems likely enough from my perspective that I think it would probably be a good idea to try an MAOI.
Ideally (and hypothetically), the best way to counteract abnormally high MAO-A production would be to use a medication that just inhibits MAO-A. Actually, it would be even better in theory to use gene therapy, but that's another story. But unfortunately, even if you do produce abnormally high MAO-A levels and have the means to obtain moclobemide from outside the U.S., it would be my prediction that you would not be responsive to moclobemide -- remember that Müller et al. (2002) found no statistically significant relationship between patients who responded to moclobemide and those with the high-activity variants of the MAO-A gene. And even though clorgyline -- an irreversible MAOI known for being highly preferential to MAO-A over MAO-B -- is still used in animal research, it was never developed commercially and is no longer even produced for human consumption in research studies (SLS, 2000). So, if you're looking for an MAO-A inhibitor that actually produces the therapeutic effects associated with enzyme inhibition (i.e., not moclobemide), that basically leaves you with Nardil and Parnate. In other words, this means that you're basically going to have to settle for a medication that inhibits both MAO-A and MAO-B to a significant extent.
I've been taking Nardil for a little more than three months, and now that I'm at 75 mg/day, I actually feel like remisssion is within reach. I'm actually trying a rather unorthodox strategy right now to try to maximize Nardil's antidepressant effect (most likely the effects of MAO-A inhibition) without having to feel what I would I would describe as a sort of negative energy that I sometimes overpowers the antidepressant effect (possibly the effects of MAO-B inhibition). I can't say for sure that my strategy will work out, but I'm optimistic about it. I'll write more about this strategy after I give it enough time to evaluate my responsiveness to it. If my strategy doesn't work out, I could always try augmenting the Nardil with another medication (I'm thinking that Lamictal would be the best choice for this) to see if that might also help me get that antidepressant effect without getting that "negative energy." The point I'm trying to make in describing my current situation is that even though Nardil and Parnate might not provide the exact effect that you're looking for, you might be able to tweak your treatment strategy for either MAOI in such a way that it might make remission possible.
Tomatheus
==
REFERENCES
Chakravorty, S. G., & Halbreich, U. (1997). The influence of estrogen on monoamine oxidase activity. Psychopharmacology Bulletin, 33, 229-33.
Deckert, J., Catalano, M., Syagailo, Y. V., Bosi, M., Okladnova, O., Di Bella, D., et al. (1999). Excess of high activity monoamine oxidase A gene promoter alleles in female patients with panic disorder. Human Molecular Genetics, 8, 621-24
Domschke, K., Sheehan, K., Lowe, N., Kirley, A., Mullins, C., O'Sullivan, R., et al. (2005). Association analysis of the monoamine oxidse A and B genes with attention deficit hyperactivity disorder (ADHD) in an Irish sample: Preferential transmission of the MAO-A 941G allele to affected children. American Journal of Medical Genetics Part B (Neuropsychiatric Genetics), 134B, 110-14.
Du, L., Bakish, D. Ravindran, A., & Hrdina, P. D. (2004). MAO-A gene polymorphisms are associated with major depression and sleep disturbance in males. NeuroReport, 15, 2097-2101.
Du, L. Faludi, G., Palkovits, M. Sotonyi, P., Bakish, D., & Hrdina, P. D. (2002). High activity-related allele of MAO-A gene associated with depressed suicide in males. NeuroReport, 13, 1195-1198.
Fornai, F., Chen, K., Giorgi, F. S., Gesi, M., Alessandri, M. G., & Shih, J. C. (1999). Striatal dopamine metabolism in monoamine oxidase B-deficient mice: A brain dialysis study. Journal of Neurochemistry, 73, 2434-40.
Hotamisligil, G. S., & Breakefield, X. O. (1991). Human monoamine oxidase A gene determines levels of enzyme activity. American Journal of Human Genetics, 49, 383-92.
Jiang, S. Xin, R., Lin, S. Qian, Y., Tang, G., Wang, D., et al. (2001). Linkage studies between attention-deficit hyperactivity disorder and the monoamine oxidase genes. American Journal of Medical Genetics (Neuropsychiatric Genetics), 105, 783-88.
Lotufo-Neto, F., Trivedi, M., & Thase, M. E. (1999). Meta-analysis of the reversible inhibitors of monoamine oxidse type A moclobemide and brofaromine for the treatment of depression. Neuropsychopharmacology, 20, 226-47.
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SLS. (2000, October 2). Re: clorgyline - the agony and the ecstasy >> rogdog. Message posted to http://www.dr-bob.org/babble/20000926/msgs/45699.html
Posted by ed_uk on January 15, 2006, at 9:22:16
In reply to Re: Looking for a Diagnosis, Medicine Input » HKristina, posted by Tomatheus on January 14, 2006, at 15:11:55
Hi T
It would be interesting for you to try pirlindole.
Ed
Posted by Tomatheus on January 15, 2006, at 10:26:05
In reply to Re: Looking for a Diagnosis, Medicine Input » Tomatheus, posted by ed_uk on January 15, 2006, at 9:22:16
> It would be interesting for you to try pirlindole.
Yes, it would be.
I've been having some recent success with my strategy to taking Nardil, and I'll be sure to post a update here (probably in a few weeks) once I get a better idea as to how successful it will likely be in the long run.
But I'm always thinking about what my next step might be, just in case things don't work out, and pirlindole certainly would be an interesting medication to try if I can get my hands on it.
Tomatheus
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