Posted on 05/07/2002 8:48:34 AM PDT by liberallarry
Edited on 09/03/2002 4:50:26 AM PDT by Jim Robinson. [history]
After thousands of studies, hundreds of millions of prescriptions and tens of billions of dollars in sales, two things are certain about pills that treat depression: Antidepressants like Prozac, Paxil and Zoloft work. And so do sugar pills.
(Excerpt) Read more at washingtonpost.com ...
The mood elevating effect of the dextrose (sugar pills, remember?) in the packets of NutraSweet is balancing out the mood depressing effect of the aspartame!!! Those clever, clever people at NutraSweet!!! What will they think of next!!!
Might be closer than you think. I wonder if the people helped by the sugar pills are the same ones whose depression is caused/worsened by aspartame? Their bodies are screaming for sugar, and being tricked by a sweet taste, gearup to handle it, crashing their blood glucose levels, and kicking them into worsened depression. So they join a deperssion study and are given real sugar...
Is that in comparison with antipsychotics, antidepressants and/or other candidate CNS drugs, or across the spectrum of all indications? Also, are there any studies on this matter? Thanks.
For me, after I figured out Aspartame was giving me problems, and excluded it from my diet my symptoms greatly improved.
Unfortunately I never fully went back to my starting point. I have used Prozac For me it was a miracle drug. Relief started within a week of starting. My chronic migraines vanished, (something which BTW survived years of and $10's of thousands of Scientology counseling), my creativity went WAY up, as evidenced by my lab notebooks, I have since gotten 4 US Patents. I have since been able to taper off of Prozac and have had lasting benefit.
Granted, this is anecdotal, and you will discout it as meaningless, since it doesn't fit your fixed idea, but it is what's true for me...
Is that in comparison with antipsychotics, antidepressants and/or other candidate CNS drugs, or across the spectrum of all indications? Also, are there any studies on this matter? Thanks.
I'm guessing that it tracks the increase of Aspartame in the general diet. But that's just a guess...
If you knew me, you would know that I don't dismiss anyone's personal experiences as meaningless.
Good luck to you. I'm sure your pocketbook is better off since getting away from the cultists.
Nahh, I up and got married. Last spousal support check was on the first....
Out of a bad cult, and into a worse one, huh?
LOL!
I'm sure of that, although I live in the same state (Florida), and the town that John Travolta has just moved to (part-time, I'm sure), Ocala.
Well, you already knew I'm vicious, right?
Should I tell him that you married a liberal?
And he didn't convert her -- some politician,
but heck, Kumbaya, "Can't we all just, get along".
Sorry, I can't say. I can't access anything beyond the abstract.
Placebo, Antidepressant May Lift Depression Via Common MechanismEmphases mine.
BETHESDA, MD (NIH) -- Whether it's a widely prescribed medication or a placebo, a successful treatment for depression must trigger a common pattern of brain activity changes, suggests a team of researchers funded by the National Institute of Mental Health.
Using functional brain imaging, Helen Mayberg, M.D., and colleagues at the University of Texas Health Science Center, San Antonio, have found increased activity in the cortex accompanied by decreases in limbic regions in patients who responded to either the popular antidepressant fluoxetine or to a placebo. They propose that this pattern of changes may be necessary for therapeutic response. However, patients who responded to fluoxetine also experienced unique changes in lower areas -- brainstem, striatum and hippocampus -- thought to confer additional advantage in sustaining the response long term and preventing relapse. The researchers report on their Positron Emission Tomography (PET scan) study in the May 2002 American Journal of Psychiatry. "Our findings do not support the notion that antidepressants work merely via a placebo effect," cautioned Mayberg, who has since moved to the Rotman Research Institute at the University of Toronto. "Patients on active medication who failed to improve did not sustain the brainstem, striatal and hippocampus changes unique to antidepressant responders."
In the randomized, double blind trial, 17 middle-aged men, hospitalized for unipolar depression, received either fluoxetine or placebo for 6 weeks. Rating scales revealed that 4 of the men responded to placebo and another 4 showed comparable improvement with the active medication. Nine patients failed to get better.
"Treatment with placebo is not absence of treatment, just absence of active medication," note the researchers, citing possible therapeutic benefits of a change in environment and the supportive, therapeutic milieu of an inpatient psychiatric ward.
PET scans traced the destination of a radioactive form of glucose - the brain's fuel - to detect brain activity patterns. After 6 weeks, brains of men who responded to either treatment showed "remarkable concordance:" Activity increased in prefrontal cortex, posterior cingulate, premotor, parietal cortex, and posterior insula. Activity decreased in subgenual cingulate, parahippocampus, thalamus and hypothalamus.
Men who responded to fluoxetine, in addition, showed changes in certain lower brain areas -- brainstem, hippocampus, striatum and anterior insula. Brain areas activated in the fluoxetine responders were also somewhat larger. The brain stem and hippocampus appear to have important input in sustaining the cortical/limbic changes, suggest the researchers, who note that absence of changes in these lower brain areas in placebo responders may render them at higher risk for relapse, which several previous clinical studies have shown.
Although both placebo and antidepressant responders showed increased activity in the posterior cingulate (see graphic) at 6 weeks, this change had already occurred in placebo responders at 1 week. Together with other evidence, this suggests that the ability to increase activity in the posterior cingulate may be an early indicator of a brain's capacity to change and respond to treatment, says Mayberg. Medications that take a "bottom up" approach or non-drug, cognitive "top-down" interventions should work equally well. However, a need for progressively more aggressive treatments could signal "poor adaptive capacity" in the cortex/limbic network found to change in responders, say the researchers.
BTW, the study that started this entire thread only had seventeen people in it.
My main problem is with the unscientific effort by shrinks to describe these drugs as medicines by shrinks who want to be regarded as equivalent (largely for reimbursement purposes) to real medical doctors treating real diseases. The ideology which forms the basis of this effort had dramatically fueled the victimology which has plagued our society from top to bottom.
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