Posted by KaraS on April 7, 2005, at 3:12:47
In reply to Re: Read this before answering my previous post » KaraS, posted by franco neuro on April 5, 2005, at 22:16:14
> Hi Franco,
> I was beginning to worry that everyone abandoned this thread. :-) The fatigue seemed to lesson yesterday but reappeared with a vengeance today. I had been taking 1/4 grain of Dr. Braverman's thyroid formula, but I stopped a couple of days ago. I decided to take it this morning and am wondering if that contributed to the fatigue, because I called his office today and they told me my thyroid antibodies came back high. So maybe the thyroid hormone is causing an immune reaction. I doubt it. I think it's the dopamine paradox and/or the double edged sword that is norepinephrine. I'll keep taking it for a while and see what happens.
I have the antibodies also. I read that they are in response to a protein in the thyroid gland and not to the thyroxin itself. (I wouldn't put money on it though.)
> I know the feeling. I'm always afraid that I'll do more harm to my already messed up brain/body. But what I'm more afraid of is never feeling healthy again and having the rest of my life pass me by like the last few years have. Having said that, the AP's will probably be my medications of last resort.
Same here but particularly with the APs. I don't think there's any long-term data on low dosage usage of them for depression. Have you considered MAOIs at all?
> Here's what it says in Stephen M. Stahl's "Essential Psychopharmacology: The Prescriber's Guide", amisulpride:
> -Is possibly a dopamine stabilizer and dopamine agonist.
> -Theoretically blocks presynaptic DA 2 receptors at low doses.
> -Theoretically blocks postsynaptic DA 2 receptors at high doses.
> -May be a partial agonist at DA 2 receptors, which would theoretically reduce DA output when DA concentrations are high and increase output when DA concentrations are low.
> -Blocks DA 3 receptor, which may contribute to it's clinical action.
> -Unlike other atypical AP's, amisulpride does not have potent actions at serotonin receptors.
I did know that it behaves differently at lower dosages so I guess that would mean it's a dopamine stabilizer. That's good info. Thanks.
> > I've also heard that it can have some less than desirable side effects.
> Amen. Any drug that blocks DA can have some scary side effects.
I've also heard it affects prolactin levels.
> > I also didn't know that about hydergine. I have always thought of it in terms of Ach only. Have you tried it?
> You might be thinking of Galantamine, which is a cholinesterase inhibitor.
No, I was thinking about hydergine. I just didn't know enough about it.
> The million dollar question?
> > Dr. Goldstein doesn't address that, does he?
> As a matter of fact, I started flipping through the nearly 500 pages of "Tuning the Brain" and managed to find this tasty tidbit... are my additions...
> "I am being drawn to the conclusion that fatigue is, at least in part, related to NAc [nucleus accumbens] DA release, or the insufficiency thereof. PFC [prefrontal cortex], even mPFC [medial prefrontal cortex] , hypoactivity is common in neurosomatic disorders."
> He continues...
> "If the mPFC DA is insufficient, there will be hyperglutamatergic input to presynaptic D2 autoreceptors [BINGO!] on mesoaccumbens DA neurons, which is the apparent situation in neurosomatic disorders."
> I new it had to do with the EAA's glutamate and/or NMDA. As a matter of fact this is pretty much the thrust of his whole theory. Earlier in the book he says...
> "The ultimate goal increasingly appears to be (for most patients) to reduce the sensitivity of the NMDA receptor, one of the primary receptors for the excititory amino acid (EAA) glutamate."
> "...it would make sense to decrease glutamate neurotransmission in a patient who has a disorder of synaptic gating, those who do poorly in high-stimulus environments, such as malls, and those who are overly sensitive to many sensory inputs as is frequently seen in CFS, FMS, IBS, multiple chemical sensitivities (MCS), PMS, and too many other 'esses' than I care to mention."
> Oh man do car exhaust and chemical smells kill me. I can smell someone spraying perfume on half a block away! Everyone's always telling me "what are you talking about I don't smell anything." And sure enough someone will come around the corner with a perfume bottle in their hand.
> This is turning into the mother of all posts. But that guy in Florida did get back to me and seems pretty real. I believe he may have consulted Dr. Goldstein on the phone but never saw him in person. He said he was lucky to have an alternative type doctor who, although she wasn't too keen on meds., was willing to help him out. As far as Dr. Braverman goes, he did give me the Wellbutrin but I'm not sure he's the guy to try out Goldstein's protocol with. You have to understand it's hard to see the guy in person. You're lucky to get a minute with him. My freind gave him "Tuning the Brain" a few months ago and now he acts like he doesn't remember it. And on his radio show a few weeks back he was virtually quoting from it. It's the ego thing again. But we'll see. If you read my post on the other thread below you'll see my argument as to why a paradoxical response to a stimulant almost has to be due to the autoreceptor. (I'm still waiting patiently for someone to respond to it. Any input will help.) Of course I'm no scientist and Dr. Goldstein does mention a possible problem with the DA transporter (but only in passing). But I doubt I'll ever boost my DA without first using a glutamate/NMDA antagonist. I should pummel my postsynaptic receptors with a stimulant just to make sure they're not just really downregulated. But I doubt this is the case. Ok I'll end this post now before I pass out...
You're too funny. What NMDA antagonist do you have in mind? Have you tried memantine? Emme is currently using it in low dose (alone I believe) and has had some success as an antidepressant.