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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 Michael Bell on May 15, 2003, at 22:06:33
HOW DO WE REDUCE ANXIETY AND EXPERIENCE A PROSOCIAL EFFECT AT THE SAME TIME?
This seems to be the question on a lot of people's minds. If you don't mind taking the time, please read the following submission. It deals with a different approach to anxiety relief, and it tries to answer the above question.
A little while back I had posted a theory about which neurotransmitters were implicated in anxiety disorders (especially social anxiety). The crux of that theory was that the number 1 culprit behind anxiety was dysfunction of the GABA system. I'm sure this comes as no shock to anyone, since the four most effective drugs for anxiety have profound effects on the GABA system - namely, Klonopin, Nardil, alcohol and GHB. I also mentioned that, contrary to what many were saying, I believed social phobics and anxious people in general had perpetually high levels of dopamine, in turn leading to downregulation and poor dopamine transmission.
I still adhere to that theory, but something has been bothering me. In my neverending quest to defeat social phobia, I have tried a lot of drugs & supplements, and surprise surprise, the GABA agonists were by far the most effective. HOWEVER, what I noticed was that the more the drug potentiated GABA, the more anhedonia/dysthymia I experienced. On the flip side, when I was taking dopamine agonists, I became more anxious, but also more sensitive to reward (though the anxiety was more prevalent). Also, there would be poop-out w/ dopamine agonists after a short period of time.
It was so enraging... take gaba drugs, and the anxiety lessens, but so does pleasure. Take dopamine drugs, and the anxiety increases, but so does pleasure. Take both, and you have something in between, but nowhere near what the real thing should be like.
So this got me thinking about the stress cycle, a subject that has been studied over and over again. And I think the answer to that question might be found here.
The stress cycle goes like this (imagine it as a four-step process): [STEP 1]: Any kind of stress (environmental, psychological, physical, etc.) causes the body's OPIOID levels to decrease. This causes us to experience a sense of urgency, and can lead to irritability and anger. [STEP 2]: Low OPIOID levels in turn causes two main reactions to happen at the same time: DOPAMINE levels increase (feelings of alertness and anxiety) and GABA levels to decrease (insecurity, anxiety, unexplainable panic). Continuous dopamine release eventually leads to mental fatigue. [STEP 3]: Meanwhile, low GABA levels also leads to two simultaneous occurrences - a decrease in SEROTONIN (insomnia) and increase in NOR/EPINEPHRINE(physiological signs of anxiety - racing heartbeat, quick emotional response, ETC.) [STEP 4]: The low SEROTONIN levels force OPIOID levels lower, and the cycle continues.
For a great and simple diagram of this cycle, check the following link: http://www.metromkt.net/calm/20brain3.html
Now here's where it gets interesting. Anxiety and stress have been proven to be inextricably linked, and may be twins born from the same process. This may explain why GABA and DOPAMINE drugs effect us the way they do. Hypothetically, let's say we take Klonopin and a dopamine agonist to try and "fix" the anxiety/anhedonia problem. This in theory would rectify STEP 2 in the stress cycle - aka the GABA and DOPAMINE. Even if this caused all the following steps (3 & 4) to be fixed, we've still neglected step (1), which is the lowering of OPIOID levels. Just because serotonin levels may no longer drop, someone with dysfunctional OPIOID levels will still not be "whole" if we don't address the opioid dysfunction directly. Remember, step one is the catalyst behind this entire process, so in effect we're treating the symptoms of stress, and not the cause.
Okay, so now we've fixed dopamine and gaba. BUT EVEN THOUGH WE'VE FIXED THE DOPAMINE & GABA PROBLEMS, WE STILL DON'T GET A NICE BALANCE OF ANXIETY RELIEF AND ANHEDONIA RELIEF. WHY?? Because step (1), which is the lowering of OPIOID levels, is still broken.
It is the OPIOID DYSFUNCTION problem where I beleive the missing link lies. OPIOIDS & their receptors are extremely important in the reward cascade cycle. Dysfunction has been tied to reward-deficiency syndrome, anhedonia & physical pain. Opioid ANTagonists have been shown to curtail social activity in rhesus monkeys (scientists speculate that the monkeys may have reduced pleasure in socializing with others) Opioid function plays a huge role in pleasure, pain, euphoria, satisfaction and, as we know, stress. In fact, the dopamine reward pathway is very intermingled with opioid function, and some studies have found that there is a completely separate reward/pleasure pathway that is distinct from the dopamine pathway. It is my belief that trying to adjust dopamine and GABA levels like some sort of chemical equalizer may help somewhat, but that OPIOID function plays a vital role in getting the balance right between anxiety relief and reward/pleasure. And ALCOHOL, which is known to cause anxiety relief and increased pleasure, has been proven to stimulate the opioid receptors.
It may be that opioid dysfunction is the cornerstone of the anxiety/stress process, but that use of Klonopin and other GABA drugs allow us to "catch" the cycle before the anxious feelings set in. Or it may be that the opioid system needs to be tweaked to fill in the gap left over from gaba and dopamine treatment, so that our pleasure/reward system can be jumpstarted again. But either way we're still not addressing the opioid issue.
If you have any input, please feel free to respond, bash, expand, whatever. We're all looking for the same thing on this board, and with open communication we may eventually find the answer.
Posted by Ritch on May 15, 2003, at 22:24:28
In reply to STRESS CYCLE - theory about anxiety treatment, posted by Michael Bell on May 15, 2003, at 22:06:33
Perhaps this is why heavy intense aerobic exercise can help a lot because of alteration of endorphins. In the past most folks had to tote a lot of stuff all day long and were mightily worn out when the day was done (usually at sunset). Going way back you might have to walk miles and miles every day foraging for food. Maybe the "runner's high" is partly anxiety relief?
Posted by Caleb462 on May 15, 2003, at 22:34:09
In reply to STRESS CYCLE - theory about anxiety treatment, posted by Michael Bell on May 15, 2003, at 22:06:33
> The stress cycle goes like this (imagine it as a four-step process): [STEP 1]: Any kind of stress (environmental, psychological, physical, etc.) causes the body's OPIOID levels to decrease. This causes us to experience a sense of urgency, and can lead to irritability and anger. [STEP 2]: Low OPIOID levels in turn causes two main reactions to happen at the same time: DOPAMINE levels increase (feelings of alertness and anxiety) and GABA levels to decrease (insecurity, anxiety, unexplainable panic). Continuous dopamine release eventually leads to mental fatigue. [STEP 3]: Meanwhile, low GABA levels also leads to two simultaneous occurrences - a decrease in SEROTONIN (insomnia) and increase in NOR/EPINEPHRINE(physiological signs of anxiety - racing heartbeat, quick emotional response, ETC.) [STEP 4]: The low SEROTONIN levels force OPIOID levels lower, and the cycle continues.
Sorry, but this is just plain wrong. Low opiod activity does not cause high dopamine/low GABA. In fact, it's the exact opposite - high opiod activity causes this reaction. Agonism of mu-opiod receptors INHIBITS the release of GABA onto dopamine-containing neurons, causing a jump in dopamine activity. So HIGH (not low) opiod activity = high dopamine/low GABA. You've got it backwards.> For a great and simple diagram of this cycle, check the following link: http://www.metromkt.net/calm/20brain3.html
Are you trying to sell Becalm'd? I apoligize if you aren't, I just found it strange that you're taking information from a site trying to sell a product - this is not a reliable source.
I agree that the brain's opiod system is crucial to mental/emotional/social well-being, and is neglected in psychiatry. But your neuropharmacology is all wrong. Also, I don't believe problems can be simplifed down to mere neurotransmitter "lows" and "highs". The brain is much more complex than this. The fact is no one completely knows how the brain truly works, and therefore no one completely knows the facts of psychiatric disorders.
Posted by Michael Bell on May 15, 2003, at 23:40:19
In reply to Re: STRESS CYCLE - theory about anxiety treatment, posted by Caleb462 on May 15, 2003, at 22:34:09
Caleb462 - no offense, but you're mistaken. Stress does cause opioid levels to diminish. Opioids are released to combat the stress. Once released, the overall levels of opioids diminish. Eventually a point is reached reaches where there are not enough of these "feel good" chemicals to adequately fight all the stress, and so the physiological responses are in evidence. Interestingly, you say that high opioid "activity" causes low GABA/high dopamine, and I think you're making my point without realizing it. High opioid "activity" is taking place BECAUSE the opioids are being released to combat the stress. In other words, opioids are released during stress (hence the high activity), which causes the "stock" levels to decrease. It's the same type of idea with dopamine. When dopamine is released, the overall brain levels of the neurotransmitter decrease, and the supply is restocked through either more dopamine production, reuptake, etc.
And no, I'm not selling BCalmed. Though I probably should, if it would let me keep my cable on for more than a month at a time, heh heh. I laughed when I read that b/c I had just been thinking today that with all the money I've spent on medication & supplements, I should've probably just taken that money and invested in one of these companies!
And finally... of course the brain is much more complex than just adjusting the "highs and lows" of neurotransmitter levels. Trust me, I have no doubt that we've barely even tapped the surface of the brain's potential and physiology. But the fact that no one truly knows how the brain really works should not stop people from theorizing and discussing these things. We don't know how a lot of things in this world work, but we'd still be in the dark ages if we never challenged ourselves to find out how they do. My point was just that maybe there's another system that we've been forgetting about.
Later.
> > The stress cycle goes like this (imagine it as a four-step process): [STEP 1]: Any kind of stress (environmental, psychological, physical, etc.) causes the body's OPIOID levels to decrease. This causes us to experience a sense of urgency, and can lead to irritability and anger. [STEP 2]: Low OPIOID levels in turn causes two main reactions to happen at the same time: DOPAMINE levels increase (feelings of alertness and anxiety) and GABA levels to decrease (insecurity, anxiety, unexplainable panic). Continuous dopamine release eventually leads to mental fatigue. [STEP 3]: Meanwhile, low GABA levels also leads to two simultaneous occurrences - a decrease in SEROTONIN (insomnia) and increase in NOR/EPINEPHRINE(physiological signs of anxiety - racing heartbeat, quick emotional response, ETC.) [STEP 4]: The low SEROTONIN levels force OPIOID levels lower, and the cycle continues.
>
>
> Sorry, but this is just plain wrong. Low opiod activity does not cause high dopamine/low GABA. In fact, it's the exact opposite - high opiod activity causes this reaction. Agonism of mu-opiod receptors INHIBITS the release of GABA onto dopamine-containing neurons, causing a jump in dopamine activity. So HIGH (not low) opiod activity = high dopamine/low GABA. You've got it backwards.
>
> > For a great and simple diagram of this cycle, check the following link: http://www.metromkt.net/calm/20brain3.html
>
> Are you trying to sell Becalm'd? I apoligize if you aren't, I just found it strange that you're taking information from a site trying to sell a product - this is not a reliable source.
>
> I agree that the brain's opiod system is crucial to mental/emotional/social well-being, and is neglected in psychiatry. But your neuropharmacology is all wrong. Also, I don't believe problems can be simplifed down to mere neurotransmitter "lows" and "highs". The brain is much more complex than this. The fact is no one completely knows how the brain truly works, and therefore no one completely knows the facts of psychiatric disorders.
Posted by Caleb462 on May 16, 2003, at 0:52:47
In reply to Re: STRESS CYCLE - theory about anxiety treatment » Caleb462, posted by Michael Bell on May 15, 2003, at 23:40:19
> Caleb462 - no offense, but you're mistaken. Stress does cause opioid levels to diminish. Opioids are released to combat the stress. Once released, the overall levels of opioids diminish. Eventually a point is reached reaches where there are not enough of these "feel good" chemicals to adequately fight all the stress, and so the physiological responses are in evidence. Interestingly, you say that high opioid "activity" causes low GABA/high dopamine, and I think you're making my point without realizing it. High opioid "activity" is taking place BECAUSE the opioids are being released to combat the stress. In other words, opioids are released during stress (hence the high activity), which causes the "stock" levels to decrease. It's the same type of idea with dopamine. When dopamine is released, the overall brain levels of the neurotransmitter decrease, and the supply is restocked through either more dopamine production, reuptake, etc.
>
I never stated that stress did not cause opiod levels to diminish. Temporarily, it quite possibly does. And over a long period of time (as is seen with anxiety disorders, etc.), there probably is a desperate lack of endegenous mu/delta opiod activity. Whether this is directly related to a physical deficit in the opiods cannot be said with any certainty however.Anyway... I was simply arguing the neurochemistry. HIGH opiod activity will cause high dopamine activity/low GABA activity - that's just how the brain works. Part of the reason opiods are rewarding is that they prevent GABA from inhibiting dopamine release.
> And no, I'm not selling BCalmed. Though I probably should, if it would let me keep my cable on for more than a month at a time, heh heh. I laughed when I read that b/c I had just been thinking today that with all the money I've spent on medication & supplements, I should've probably just taken that money and invested in one of these companies!
>
> And finally... of course the brain is much more complex than just adjusting the "highs and lows" of neurotransmitter levels. Trust me, I have no doubt that we've barely even tapped the surface of the brain's potential and physiology. But the fact that no one truly knows how the brain really works should not stop people from theorizing and discussing these things. We don't know how a lot of things in this world work, but we'd still be in the dark ages if we never challenged ourselves to find out how they do. My point was just that maybe there's another system that we've been forgetting about.
>
> Later.No argument here. However, dealing with the opiod system directly is tricky. Mu-agonists will never be effective anti-depressants for the majority of people, oh sure, they are THE best anti-depressants available. Of course, they inevitably lead to tolerance, depedance, addiction, withdrawl, etc. For a small minority of depressed people, mu-agonists should be an available option - but it's never going to be widespread.
What needs to be explored are things like Delta-agonists and kappa-antagonists, though who knows when this will happen.Interestingly, however, current anti-depressants DO indirectly effect the opiod system. Those on SSRIs long term, for instance, generally show a higher level of beta-endorphins.
Sorry if my previous post (or this one!) came off as rude or anything, I tend to do that on occasion without realizing it.
Posted by daizy on May 16, 2003, at 8:46:42
In reply to STRESS CYCLE - theory about anxiety treatment, posted by Michael Bell on May 15, 2003, at 22:06:33
Useful info Michael, thanx! It explains why when I was taking Effexor, it made me more agitated and anxious, and now that Im taking a TCA its reducing my anxiety, and my ability to feel other emotions, such as pleasure and sadness. What do you suppose is the solution to this problem?
HOW DO WE REDUCE ANXIETY AND EXPERIENCE A PROSOCIAL EFFECT AT THE SAME TIME?
>
> This seems to be the question on a lot of people's minds. If you don't mind taking the time, please read the following submission. It deals with a different approach to anxiety relief, and it tries to answer the above question.
>
> A little while back I had posted a theory about which neurotransmitters were implicated in anxiety disorders (especially social anxiety). The crux of that theory was that the number 1 culprit behind anxiety was dysfunction of the GABA system. I'm sure this comes as no shock to anyone, since the four most effective drugs for anxiety have profound effects on the GABA system - namely, Klonopin, Nardil, alcohol and GHB. I also mentioned that, contrary to what many were saying, I believed social phobics and anxious people in general had perpetually high levels of dopamine, in turn leading to downregulation and poor dopamine transmission.
>
> I still adhere to that theory, but something has been bothering me. In my neverending quest to defeat social phobia, I have tried a lot of drugs & supplements, and surprise surprise, the GABA agonists were by far the most effective. HOWEVER, what I noticed was that the more the drug potentiated GABA, the more anhedonia/dysthymia I experienced. On the flip side, when I was taking dopamine agonists, I became more anxious, but also more sensitive to reward (though the anxiety was more prevalent). Also, there would be poop-out w/ dopamine agonists after a short period of time.
>
> It was so enraging... take gaba drugs, and the anxiety lessens, but so does pleasure. Take dopamine drugs, and the anxiety increases, but so does pleasure. Take both, and you have something in between, but nowhere near what the real thing should be like.
>
> So this got me thinking about the stress cycle, a subject that has been studied over and over again. And I think the answer to that question might be found here.
>
> The stress cycle goes like this (imagine it as a four-step process): [STEP 1]: Any kind of stress (environmental, psychological, physical, etc.) causes the body's OPIOID levels to decrease. This causes us to experience a sense of urgency, and can lead to irritability and anger. [STEP 2]: Low OPIOID levels in turn causes two main reactions to happen at the same time: DOPAMINE levels increase (feelings of alertness and anxiety) and GABA levels to decrease (insecurity, anxiety, unexplainable panic). Continuous dopamine release eventually leads to mental fatigue. [STEP 3]: Meanwhile, low GABA levels also leads to two simultaneous occurrences - a decrease in SEROTONIN (insomnia) and increase in NOR/EPINEPHRINE(physiological signs of anxiety - racing heartbeat, quick emotional response, ETC.) [STEP 4]: The low SEROTONIN levels force OPIOID levels lower, and the cycle continues.
>
> For a great and simple diagram of this cycle, check the following link: http://www.metromkt.net/calm/20brain3.html
>
> Now here's where it gets interesting. Anxiety and stress have been proven to be inextricably linked, and may be twins born from the same process. This may explain why GABA and DOPAMINE drugs effect us the way they do. Hypothetically, let's say we take Klonopin and a dopamine agonist to try and "fix" the anxiety/anhedonia problem. This in theory would rectify STEP 2 in the stress cycle - aka the GABA and DOPAMINE. Even if this caused all the following steps (3 & 4) to be fixed, we've still neglected step (1), which is the lowering of OPIOID levels. Just because serotonin levels may no longer drop, someone with dysfunctional OPIOID levels will still not be "whole" if we don't address the opioid dysfunction directly. Remember, step one is the catalyst behind this entire process, so in effect we're treating the symptoms of stress, and not the cause.
>
> Okay, so now we've fixed dopamine and gaba. BUT EVEN THOUGH WE'VE FIXED THE DOPAMINE & GABA PROBLEMS, WE STILL DON'T GET A NICE BALANCE OF ANXIETY RELIEF AND ANHEDONIA RELIEF. WHY?? Because step (1), which is the lowering of OPIOID levels, is still broken.
>
> It is the OPIOID DYSFUNCTION problem where I beleive the missing link lies. OPIOIDS & their receptors are extremely important in the reward cascade cycle. Dysfunction has been tied to reward-deficiency syndrome, anhedonia & physical pain. Opioid ANTagonists have been shown to curtail social activity in rhesus monkeys (scientists speculate that the monkeys may have reduced pleasure in socializing with others) Opioid function plays a huge role in pleasure, pain, euphoria, satisfaction and, as we know, stress. In fact, the dopamine reward pathway is very intermingled with opioid function, and some studies have found that there is a completely separate reward/pleasure pathway that is distinct from the dopamine pathway. It is my belief that trying to adjust dopamine and GABA levels like some sort of chemical equalizer may help somewhat, but that OPIOID function plays a vital role in getting the balance right between anxiety relief and reward/pleasure. And ALCOHOL, which is known to cause anxiety relief and increased pleasure, has been proven to stimulate the opioid receptors.
>
> It may be that opioid dysfunction is the cornerstone of the anxiety/stress process, but that use of Klonopin and other GABA drugs allow us to "catch" the cycle before the anxious feelings set in. Or it may be that the opioid system needs to be tweaked to fill in the gap left over from gaba and dopamine treatment, so that our pleasure/reward system can be jumpstarted again. But either way we're still not addressing the opioid issue.
>
> If you have any input, please feel free to respond, bash, expand, whatever. We're all looking for the same thing on this board, and with open communication we may eventually find the answer.
Posted by daizy on May 16, 2003, at 12:35:15
In reply to Re: STRESS CYCLE - theory about anxiety treatment, posted by daizy on May 16, 2003, at 8:46:42
Can you take two different AD's at once? For example an SSRI and a TCA? or doesnt that work?
Posted by Ritch on May 16, 2003, at 13:03:54
In reply to Re: STRESS CYCLE - theory about anxiety treatment, posted by daizy on May 16, 2003, at 12:35:15
> Can you take two different AD's at once? For example an SSRI and a TCA? or doesnt that work?
Absolutely. That's the only way I can get a reasonable response to the things. If you combine a TCA with an SSRI, you might want to use nortriptyline or desipramine instead of the others (they are a little easier to tolerate).
Posted by Barbara Cat on May 19, 2003, at 12:54:50
In reply to STRESS CYCLE - theory about anxiety treatment, posted by Michael Bell on May 15, 2003, at 22:06:33
Yes, yes, yes to opiods being a missing link. I totally agree and have had the same theory for years. I have first hand experience with this. Having BPII mixed states with severe depression and anxiety at times, I've been on the whole gamut of typical meds which have had the same frustrating see-saw pleasure/anhedonia effect as you describe. However, I also have fibromyalgia and have ongoing monthly scripts for vicodin and oxycodone. I don't abuse them or take them regularly, however I do take them for psychic rather than physical pain. I've learned that when I'm going through a very rough time, taking an opiod will lift me up, help me to think more clearly, and even give me a good even supply of energy. I take a small amount and have had no addiction urges at all. About the only thing negative is the constipation effects for which I take a fiber and greens supplement.
I also agree with Rich about exercise raising endorphins, but severe anhedonia makes exercise very unpalatable. There needs to be more research into finding a way to kick start those endorphins without addiction potential. - BarbaraCat
Posted by Barbara Cat on May 19, 2003, at 13:03:29
In reply to Re: STRESS CYCLE - theory about anxiety treatment, posted by daizy on May 16, 2003, at 8:46:42
> now that Im taking a TCA its reducing my anxiety, and my ability to feel other emotions, such as pleasure and sadness.
I've been on 'em all and taking a TCA (nortriptyline) and lithium has been the most effective AD combo for me. SSRI's were disasters in many ways, especially for a mixed-state bipolar-II like myself.
Posted by McPac on May 19, 2003, at 21:06:00
In reply to Re: STRESS CYCLE - theory about anxiety treatment, posted by Barbara Cat on May 19, 2003, at 13:03:29
"I've been on 'em all and taking a TCA (nortriptyline) and lithium has been the most effective AD combo for me. SSRI's were disasters in many ways, especially for a mixed-state bipolar-II like myself".
Barb, I don't know if you would recall this but I mentioned lithium to you and some others here a LONG time ago as possibly being a "missing link" for many folks...I've used it myself for ages....I've got to ask you though, regarding this statement that you made, "SSRI's were disasters in many ways, especially for a mixed-state bipolar-II like myself"......exactly WHAT did the ssri's DO to you that was a disaster? (I ask this because I have always noticed that so many of your posts sound like me to a "T" (symptoms, med reactions), lol,.....also....were the ssri's a disaster to you while you were ON a mood stabilizer (like lithium) OR were the ssri's a disaster when you were NOT on a mood stabilizer at the same time? (For me, for example, I can handle Zoloft quite well when I'm also ON lithium....BUT taking Zoloft WITHOUT lithium is a DISASTER for me! Wondering if it might be the same for you? Take care Barb!
Posted by Questionmark on May 19, 2003, at 21:33:22
In reply to Re: STRESS CYCLE - theory about anxiety treatment, posted by Caleb462 on May 16, 2003, at 0:52:47
i was also under the definite impression that increased opioid activity results in increased DA activity and decreased GABA activity. But the brain is so freaking complex-- do you think enhanced opioid transmission might increase DA activity in some parts of the brain and inhibit DA activity in others?
Posted by Barbara Cat on May 20, 2003, at 0:51:11
In reply to Barb, CYCLE - theory about anxiety treatment, posted by McPac on May 19, 2003, at 21:06:00
Hi Mike, good hearing from you. Let's see. It's difficult to say definitely but I have to think that if I was on lithium at the time of my SSRI trials I wouldn't have the bad reactions. The red flag that should have warned someone was that I'd immediately feel wired within 3 days of starting an SSRI, speedy, panic attacks, etc. Then things would subside and I wouldn't get panic attacks anymore but would slide into a deep dark lonely place. Then sure enough, my pdoc would say, well, you probably need more of that drug. So same thing, immediate frantic reaction then sliding into the darkness. Which made me feel desperate, I mean, if our present day miracle drugs couldn't help me then I was lost. I started lithium while I was on Remeron which after a great start, went South like all the others. Lithium pulled me out of the descent like a true miracle. I went off Remeron eventually and lithium was not enough on its own to prevent depression so I added lamictal. It too pooped out.
Now I'm on nortriptyline, a little lamictal and 600 mg lithium. I recently lost my bottle of lithium and was without for over a week, and sure enough, that very scary disordered dark place started showing up. I truly believe that no matter what other med combo I try, lithium is my mainstay, the one thing that holds all the others together. I can now get depressed, anxious, and all the other 'normal' expressions of life, but on lithium I have no fear of falling into the pit of Doom. Bipolar mixed states is truly one of the inner circles of Hell.
I'd like to hear your thoughts and experiences as well. - Barbara
This is the end of the thread.
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