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.
poster:Michael Bell
thread:226952
URL: http://www.dr-bob.org/babble/20030514/msgs/226952.html