Posted by bluedog on November 25, 2002, at 22:24:06
In reply to Anxiety Causes Brain Damage????, posted by Guy on November 25, 2002, at 12:42:06
> This article seems to say that constant untreated anxiety causes cell death in the brain (i.e brain damage). If so, I musn't have very much brain left! This is the first I've heard of this nasty business. Does anyone have any more info?
There appears to be evidence that diet and supplements can play a large role in protecting your brain from problems relating to anxiety.eg.
1: FASEB J 2002 Nov 1; [epub ahead of print] Links
Selenium deficiency increases susceptibility to glutamate-induced excitotoxicity.Savaskan NE, Brauer AU, Kuhbacher M, Eyupoglu IY, Kyriakopoulos A, Ninnemann O, Behne D, Nitsch R.
Excitotoxic brain lesions, such as stroke and epilepsy, lead to increasing destruction of neurons hours after the insult. The deadly cascade of events involves detrimental actions by free radicals and the activation of proapoptotic transcription factors, which finally result in neuronal destruction. Here, we provide direct evidence that the nutritionally essential trace element selenium has a pivotal role in neuronal susceptibility to excitotoxic lesions. First, we observed in neuronal cell cultures that addition of selenium in the form of selenite within the physiological range protects against excitotoxic insults and even attenuates primary damage. The neuroprotective effect of selenium is not directly mediated via antioxidative effects of selenite but requires de novo protein synthesis. Gel shift analysis demonstrates that this effect is connected to the inhibition of glutamate-induced NF-kB and AP-1 activation. Furthermore, we provide evidence that selenium deficiency in vivo results in a massive increase in susceptibility to kainate-induced seizures and cell loss. These findings indicate the importance of selenium for prevention and therapy of excitotoxic brain damage.
PMID: 12424220 [PubMed - as supplied by publisher]
1: J Neurosci Res 2001 Nov 15;66(4):612-9 Related Articles, Links
Role of taurine in regulation of intracellular calcium level and neuroprotective function in cultured neurons.Chen WQ, Jin H, Nguyen M, Carr J, Lee YJ, Hsu CC, Faiman MD, Schloss JV, Wu JY.
Department of Molecular Biosciences, University of Kansas, Lawrence, Kansas 66045, USA.
Glutamate-induced excitotoxicity has been implicated as an important mechanism underlying a variety of brain injuries and neurodegenerative diseases. Previously we have shown that taurine has protective effects against glutamate-induced neuronal injury in cultured neurons. Here we propose that the primary underlying mechanism of the neuroprotective function of taurine is due to its action in preventing or reducing glutamate-induced elevation of intracellular free calcium, [Ca(2+)](i). This hypothesis is supported by the following findings. First, taurine transport inhibitors, e.g., guanidinoethyl sulfonate and beta-alanine, have no effect on taurine's neuroprotective function, suggesting that taurine protects against glutamate-induced neuronal damage through its action on the extracellular membranes. Second, glutamate-induced elevation of [Ca(2+)](i) is reduced to the basal level upon addition of taurine. Third, pretreatment of cultured neurons with taurine prevents or greatly suppresses the elevation of [Ca(2+)](i) induced by glutamate. Furthermore, taurine was found to inhibit the influx but not the efflux of (45)Ca(2+) in cultured neurons. Taurine has little effect on the binding of [(3)H]glutamate to the agonist binding site and of [(3)H]MDL 105,519 to the glycine binding site of the N-methyl-D-aspartic acid receptors, suggesting that taurine inhibits (45)Ca(2+) influx through other mechanisms, including its inhibitory effect on the reverse mode of the Na(+)/Ca(2+) exchangers (Wu et al. [2000] In: Taurine 4: taurine and excitable tissues. New York: Kluwer Academic/Plenum Publishers. p 35-44) rather than serving as an antagonist to the N-methyl-D-aspartic acid receptors. Copyright 2001 Wiley-Liss, Inc.
PMID: 11746381 [PubMed - indexed for MEDLINE]
I'm sure you'd be able to find may other examples to support this view.
I would say that the article I linked to on Klonopin suggests that Klonopin can also be used to assist in protecting the brain by affecting the functions of the GABA and NMDA receptors in the brain. Diet can also help. In fact Dr Paul Cheney doesn't only suggest Klonopin as an effective treatment but that Klonopin can be used in an overall treatment plan to get your overall health back.(see http://www.immunesupport.com/library/showarticle.cfm/ID/3157/searchtext/sieverling/T/CFIDS_FM )
poster:bluedog
thread:128992
URL: http://www.dr-bob.org/babble/20021122/msgs/129331.html