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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 25 of 29. This is the beginning of the thread.
Posted by tallclaire1982 on November 17, 2006, at 16:05:30
I AM WONDERING WHAT EACH OF THEM DO, AS I HAVE SOME SYMPTOMS WHICH I AM HOPING TO GET RID OF WITH AMINO ACID SUPPLEMENTS RATHER THAN DRUGS.
I HAVE READ THAT WHEN U BOOST SEROTONIN DOMPAMINE CAN BE LOWERED THATS Y U GET ANXIOUS.. I DONT REALLY UNDERSTAND IT ALL! I WAS HOPING THAT WITH MY LIST OF SYMPTOMS SOMEONE CAN MABIE SUGGEST WHATS GOING ON IN MY BRAIN! HOPE IT ALL MAKES SENSE.
LOW MOODS ON SOME DAYS
ANXIETY FEELING ON EDGE EVERYDAY..OUT OF THE BLUE
NO SOCIAL ANXIETY
OCD SYMPTOMS.. OBBSESSIVE THOUGHTS MOST DAYS CAUSING ANXIETY TO WORSEN
FATIGUE MORE PROFOUND ON DAYS WHERE I FEEL SAD
CONCENTRATION IS FINEHOPE SOMEONE CAN OFFER ME ANY INFO OR WEBSITES WITH INFO ON THEM
THANKS
Posted by linkadge on November 17, 2006, at 18:30:31
In reply to CLEVER ONES!..NEED INFO ON BRAIN NEUROTRANSMITTERS, posted by tallclaire1982 on November 17, 2006, at 16:05:30
A start might be a good chart I found at:
http://www.hbcprotocols.com/chart.html
Linkadge
Posted by ronaldo on November 18, 2006, at 3:02:48
In reply to Re: CLEVER ONES!..NEED INFO ON BRAIN NEUROTRANSMITTERS, posted by linkadge on November 17, 2006, at 18:30:31
Thanks for that Linkadge.
There was also a chart which SLS (Scott) had which I stumbled across. I can't remember what it was about now but I can remember thinking it was very uselful. At the time however it was a bit too advanced for me and so I failed to bookmark it. Do you know what I am talking about? If so can you help me to find it? I really ought to be asking Scott about this. Please forgive me for jumping onto your thread, tallclaire, but it may also be of interest to you....
...ronaldo
Posted by linkadge on November 18, 2006, at 8:53:42
In reply to Re: CLEVER ONES!..NEED INFO ON BRAIN NEUROTRANSMITTERS » linkadge, posted by ronaldo on November 18, 2006, at 3:02:48
This one ?
http://sl.schofield3.home.att.net/medicine/psychiatric_drugs_chart.html
Posted by ronaldo on November 18, 2006, at 9:28:57
In reply to Re: CLEVER ONES!..NEED INFO ON BRAIN NEUROTRANSMITTERS, posted by linkadge on November 18, 2006, at 8:53:42
Posted by tallclaire1982 on November 18, 2006, at 12:09:28
In reply to Re: CLEVER ONES!..NEED INFO ON BRAIN NEUROTRANSMITTERS, posted by linkadge on November 17, 2006, at 18:30:31
> A start might be a good chart I found at:
>
> http://www.hbcprotocols.com/chart.html
>
> LinkadgeTHANKS ALOT I WAS HOPING U WOULD JUMP IN LINKAGE. I WAS THINKING I NEEDED SEROTONIN, DOES IT SOUND LIKE IT FROM MY SYMPTOMS? ALSO IF IT MAKES ME MORE ANXIOUS DOES THAT MEAN I DONT NEED SEROTONIN OR THAT I NEED SOMETHING ADDED LIKE SOMETHING TO MAKE UP ANOTHER TRANSMITTER, MAKING SENSE?
Posted by Racer on November 18, 2006, at 13:51:00
In reply to Re: CLEVER ONES!..NEED INFO ON BRAIN NEUROTRANSMITTERS » linkadge, posted by tallclaire1982 on November 18, 2006, at 12:09:28
> >
> THANKS ALOT I WAS HOPING U WOULD JUMP IN LINKAGE. I WAS THINKING I NEEDED SEROTONIN, DOES IT SOUND LIKE IT FROM MY SYMPTOMS? ALSO IF IT MAKES ME MORE ANXIOUS DOES THAT MEAN I DONT NEED SEROTONIN OR THAT I NEED SOMETHING ADDED LIKE SOMETHING TO MAKE UP ANOTHER TRANSMITTER, MAKING SENSE?First, it's a lot easier to read if you take capslock off... ;-)
The thing about the neurotransmitter theories is that they're general guidelines. While the theories are there, and there is support for them, they're not necessarily as black and white as "if you have anxiety, that's serotonin; if concentration is an issue, that's dopamine." It's much more of a "well, anxiety often responds best to serotonergic medications, so it's probably related to the serotonin system..." Also, while the drugs can be broadly classed -- serotinergic drugs, etc -- they're all much less selective than that might sound. While a drug might be basically dopaminergic, for example, it may also effect, say, liver enzymes that will effect something totally unrelated to the dopamine system. The selectivity of these drugs is not absolute. And finally, every time you manipulate one neurotransmitter, you're going to change the balance between them all. Even if you had a drug which ONLY affected one neurotransmitter, it would still create a different ratio between them all. These are the reasons it's not really possible to say, "If you have this symptom, this neurotransmitter has to be changed."
And beyond all that, your mileage will vary... We all react differently to medications, because of differences in our personal chemistry. If you're female, you'll also react slightly differently throughout your menstrual cycle; and everyone will react differently at different stages of life.
So, after all that, what do I think in your case? I think your best bet is to look back at the drugs you've tried, at which of them seemed to help, which made things worse, which symptoms each affected, etc. That's usually a pretty good starting place when you're looking for a new medication. Also, you listed a few pretty vague symptoms, but you didn't mention some other things: is there a pattern to your symptoms? Have you received any diagnosis from a doctor? Is it major depressive disorder? Bipolar? Froot Loops? (I dunno, just ran out of what dx's there are out there...) Those things can make a difference, too.
In terms of your specific symptoms: low moods on some days could be anything -- including normal variation. Could be you're just sad some days, for normal reasons. Concentration troubles can be from anxiety, and OCD-like symptoms are anxiety related. Serotonin is associated with anxiety, so an SSRI is likely a good starting place. (Dopamine isn't particularly associated with anxiety, as far as I know.)
Good luck.
Posted by tallclaire1982 on November 18, 2006, at 13:57:20
In reply to Re: CLEVER ONES!..NEED INFO ON BRAIN NEUROTRANSMIT » tallclaire1982, posted by Racer on November 18, 2006, at 13:51:00
thanks i havent tried drugs they r a last resort for me.
im gonna try tryptophan i think c how it goes, might add some tyrosone to the mix later on depends how i go
Posted by linkadge on November 19, 2006, at 9:00:40
In reply to Re: CLEVER ONES!..NEED INFO ON BRAIN NEUROTRANSMITTERS » linkadge, posted by tallclaire1982 on November 18, 2006, at 12:09:28
I can't really say anything. The first thing you need to know is that the monoamine hypothesis is just a hypothesis. Contrary to popular belief, there have been no consistent findings of disturbed serotonergic etc functioning in mood disorders. There are many possable reasons for anxiety, one of which may or may not be imbalences in serotonin.
As a crude guideline I suppose you could start with an SSRI.
Linkadge
Posted by Racer on November 19, 2006, at 14:32:35
In reply to Re: CLEVER ONES!..NEED INFO ON BRAIN NEUROTRANSMITTERS, posted by linkadge on November 19, 2006, at 9:00:40
> I can't really say anything. The first thing you need to know is that the monoamine hypothesis is just a hypothesis. Contrary to popular belief, there have been no consistent findings of disturbed serotonergic etc functioning in mood disorders.
Latest I've seen were studies showing impaired *turnover* of serotonin in some areas of the brain. In other words, there's a "normal" amount of serotonin available, but there's a much lower amount of serotonin being produced, which implies a lower amount of serotonin being used.
But, despite that, you're right -- the whole monoamine theory is pretty recursive: "since these drugs make more of the monoaminic neurotransmitters available, then too little of them must cause the problem the drugs treat."
Posted by linkadge on November 19, 2006, at 15:04:14
In reply to Re: CLEVER ONES!..NEED INFO ON BRAIN NEUROTRANSMIT » linkadge, posted by Racer on November 19, 2006, at 14:32:35
There are all sorts of findinigs but they do not paint any consistant picture.
For instance, some studies show high activity of the serotonin transporter, ie excessive serotonin uptake, but other (probably an equal number of) studies have found diminished serotonon uptake. Some studies have found altered levels of serotonin binding, while others have not.
Some studies have found exaggerated responces to tryptophan depletion while others have not. Some have found altered monoamine oxidase function while others have not. Some have found reduced metabolites of serotonin 5-HIAA while other have not. (Keep in mind that even if 5-HIAA levels are low, serotonin uptake inhibitors and MAOI's actually decrease this further)
Linkadge
Posted by notfred on November 19, 2006, at 15:12:09
In reply to Re: CLEVER ONES!..NEED INFO ON BRAIN NEUROTRANSMIT » linkadge, posted by Racer on November 19, 2006, at 14:32:35
> Latest I've seen were studies showing impaired *turnover* of serotonin in some areas of the brain. In other words, there's a "normal" amount of serotonin available, but there's a much lower amount of serotonin being produced, which implies a lower amount of serotonin being used.
>
Extending on what Racer said, another question is "is this cause or effect ?". When looking at neurotransmitters and depression are we seeing changes which are **caused by** depression or do these changes **cause** depression ?If it is the latter case then the meds should work much better than they do. They should be highly effective, as they treat the root cause of depression. "highly effective" is not a word that comes to mind to describe most psyco meds.
Posted by Caedmon on November 19, 2006, at 16:07:15
In reply to Re: CLEVER ONES!..NEED INFO ON BRAIN NEUROTRANSMITTERS, posted by linkadge on November 19, 2006, at 9:00:40
> I can't really say anything. The first thing you need to know is that the monoamine hypothesis is just a hypothesis. Contrary to popular belief, there have been no consistent findings of disturbed serotonergic etc functioning in mood disorders. There are many possable reasons for anxiety, one of which may or may not be imbalences in serotonin.>
Yes I agree that findings are inconsistent.
However linkadge, what do you make of those studies in which monoamine depletion caused low mood states in normal subjects? (I forget how this is done, and the exact methods used in such studies but I think you know what I'm onto.) This sounds like a good experimental design, not a descriptive one, which would allow you to draw a conclusion of cause and effect. I.e. if monoamines are low, mood is lowered.
(Doesn't mean the reverse would be true [if mood is lowered, monoamines are low]. But just curious what you knew or thought about this. I've only really skimmed over anything written on it.)
- Chris
Posted by tallclaire1982 on November 19, 2006, at 16:23:49
In reply to Re: CLEVER ONES!..NEED INFO ON BRAIN NEUROTRANSMIT » linkadge, posted by Caedmon on November 19, 2006, at 16:07:15
wow i dont have a clue what u r all on about LOL!!! i will have to do a trial and error i suppose :)
Posted by Racer on November 19, 2006, at 16:39:06
In reply to Re: CLEVER ONES!..NEED INFO ON BRAIN NEUROTRANSMIT » linkadge, posted by Caedmon on November 19, 2006, at 16:07:15
> >
>
> However linkadge, what do you make of those studies in which monoamine depletion caused low mood states in normal subjects? (I forget how this is done, and the exact methods used in such studies but I think you know what I'm onto.)I think I've read those studies, too. I can't comment on the results, but as I recall, the method was to have volunteers drink an amino acid solution which did not contain tyrosine nor tryptophan, the dietary precursors to dopamine/norepinephrine and serotonin. Since all the other amino acids were present, it altered the ratios of amino acids crossing the blood brain barrier, and thus the balance of neurotransmitters in the brain.
From what I've read, they used Hershey's syrup to make the amino acid solution palatable. I certainly hope this does not mean that Hershey's syrup leads to lowered mood...
Posted by tallclaire1982 on November 19, 2006, at 16:41:46
In reply to Re: CLEVER ONES!..NEED INFO ON BRAIN NEUROTRANSMIT, posted by Racer on November 19, 2006, at 16:39:06
i read something about them giving something to deplete them of serotonin in OCD paitents and then added tryptophan to see if they got better and they did
Posted by linkadge on November 19, 2006, at 17:41:56
In reply to Re: CLEVER ONES!..NEED INFO ON BRAIN NEUROTRANSMIT, posted by notfred on November 19, 2006, at 15:12:09
This is true. Cause or effect? Depression may cause you to frown, but frowning does not make one clinically depression.
Linkadge
Posted by linkadge on November 19, 2006, at 17:48:09
In reply to Re: CLEVER ONES!..NEED INFO ON BRAIN NEUROTRANSMIT » linkadge, posted by Caedmon on November 19, 2006, at 16:07:15
Thats what I was talking about with the tryptophan depletion. It you look at the results of those studies too, they do not paint any clear pictures.
You can experiementally cause tryptophan depletion for instance, by giving people a drink high in other amino acids. This doesn't consistently cause depression in normal controlls. Sometimes it does, sometimes it doesn't.
The only semi-consistent results are that tryphophan depletion precipitates depression in those treated with SSRI's, but not in unmedicated depressed people, depressed people treated with NRI's, or normal controlls.
Linkadge
Posted by linkadge on November 19, 2006, at 17:50:51
In reply to Re: CLEVER ONES!..NEED INFO ON BRAIN NEUROTRANSMIT » Caedmon, posted by linkadge on November 19, 2006, at 17:48:09
There is the "receptor site" downregulation hypothesis, which states that mood improvement only occurs after downregulation of postsynaptic serotonin and norepinephrine receptors.
If this is true, then acute changes in monoamine levels will have very little if any effect on mood.
The changes in receptor sites might correlate to changes in NMDA receptor function.
Linkadge
Posted by Caedmon on November 19, 2006, at 18:22:04
In reply to Re: CLEVER ONES!..NEED INFO ON BRAIN NEUROTRANSMIT, posted by linkadge on November 19, 2006, at 17:50:51
Link! Interesting, I did not know all that!
>> There is the "receptor site" downregulation hypothesis, which states that mood improvement only occurs after downregulation of postsynaptic serotonin and norepinephrine receptors. >>
I'd heard this. Is this along the lines of the "brain-growin'" hypotheses I guess? (Neurotrophy is the big word for it?)
>> The changes in receptor sites might correlate to changes in NMDA receptor function.>>
How do they correlate? What is it that changes about NDMA receptors? This last part is totally new to me.- Chris
Posted by aeon on November 20, 2006, at 5:29:01
In reply to CLEVER ONES!..NEED INFO ON BRAIN NEUROTRANSMITTERS, posted by tallclaire1982 on November 17, 2006, at 16:05:30
I just can't see that neurotransmitters are the problem/cause. The unreliability of the studies where they try to induce depression (which turns out to be quite difficult as you have pointed out) through neurotransmitter depletion definitely point to something else.
However I can induce a depression in the guy who sits next to me atr work fairly reliably - just sneeze on him when I've got the flu. He'll feel like crap for at least seven days and he'll be off to the chemist to get drugs straight away "to feel better", even though he frowns on my weak will and mind for taking drugs for my states.
He he - inflammation is the most relaible way to induce depression (what I call sickness behaviour) and the depression comes from prostaglandins affecting just about every system in the body -
from neurotransmitters to cortisol and yes NMDA and BDNF, the HPA axis and all the other correlates.You can mask it but you can't cure it unless you get to the cause.
Cheers
aeon
Posted by linkadge on November 20, 2006, at 15:22:22
In reply to changes in NMDA receptor function » linkadge, posted by Caedmon on November 19, 2006, at 18:22:04
There is a slight difference. The neurotrophic theory of antidepressants is that hippocampal neurogenesis is critical for clinical improvement, ie the drug must grow new brain cells to work.
The NMDA receptor adaptation theory says that after repeated exposure to antidepressants there is a regional dampening of glutamatergic function. Ie the drug tames overactive limbic activity which may be present in neurotic types of depression.
Posted by linkadge on November 20, 2006, at 15:31:49
In reply to Re: CLEVER ONES!..NEED INFO ON BRAIN NEUROTRANSMIT, posted by aeon on November 20, 2006, at 5:29:01
Again, the inflamation theory of depression is just another theory.
There is *no consistent* data to suggest that alterations in immune status are the cause of depression. If this were true, anti-inflamitory agents would be as good as prozac, which they are not.
It is true that anti-inflamitory agents often augment antidepressant agents, ie studies with omega-3, turmeric, and I believe a depression study involving celebrex. But no, pure anti-inflamitory has remarkable antidepressant properties by iteself.
So, I don't think the root cause of *all* depression is inflamation.
Yes, interferon will induce depression, but one cannot conclude what depression is, buy the mechanisms of action of the drugs that may induce it.
In addition, not all depression is a result of stress. Some of my worst depressons occur in the summer, when I am under absolutely no stress at all.There are other theories too, such phospholipid imballence theories, where depression is a result of disturbed brain phospholipid content.
Some antidepressants have effect on phospholipid ballance.
Linkadge
Posted by zeugma on November 21, 2006, at 5:06:24
In reply to Re: changes in NMDA receptor function, posted by linkadge on November 20, 2006, at 15:22:22
> There is a slight difference. The neurotrophic theory of antidepressants is that hippocampal neurogenesis is critical for clinical improvement, ie the drug must grow new brain cells to work.
>
> The NMDA receptor adaptation theory says that after repeated exposure to antidepressants there is a regional dampening of glutamatergic function. Ie the drug tames overactive limbic activity which may be present in neurotic types of depression.>>Another facet of this theory is that there is a reciprocal enhancement of AMPA function: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=16442080
One difference between AMPA and NMDA receptors, which may be relevant for their AD and anti-AD actions, is their different effects on ion channels: NMDA stimulation stimulates Ca2+ phosphorylation while AMPA receptors stimulate K+ phosphorylation: this would result in a net decrease and increase in monoaminergic transmission respectively.
-z
Posted by Declan on November 21, 2006, at 16:06:40
In reply to Re: changes in NMDA receptor function, posted by zeugma on November 21, 2006, at 5:06:24
Maybe aniracetam, marketed as Ampamet, does something at AMPA receptors?
Not an AD, but it helps with verbal fluency perhaps.
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