![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 16 of 16. This is the beginning of the thread.
Posted by bluedog on November 23, 2002, at 21:53:45
Here's a link to an interesting article on KLONOPIN in the treatment of Chronic Fatigue Syndrome (CFS)
see http://www.immunesupport.com/library/showarticle.cfm/id/3154
I wonder how many of us are suffering from depression and other mental conditions due to undiagnosed CFS symptoms?
Posted by JaneB on November 23, 2002, at 22:42:19
In reply to KLONOPIN and chronic fatigue, posted by bluedog on November 23, 2002, at 21:53:45
Posted by Guy on November 25, 2002, at 12:42:06
In reply to KLONOPIN and chronic fatigue, posted by bluedog on November 23, 2002, at 21:53:45
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?
Posted by bluedog on November 25, 2002, at 21:39:52
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?
Here is an example of a study that could support the hypothesis that untreated anxiety could cause cell death (see http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1361523&form=6&db=m&Dopt=b )1: J Neurobiol 1992 Nov;23(9):1261-76 Related Articles, Cited in PMC, Books, LinkOut
Excitotoxic cell death.Choi DW.
Department of Neurology, Washington University School of Medicine, St. Louis, Missouri 63110.
Excitotoxicity refers to the ability of glutamate or related excitatory amino acids to mediate the death of central neurons under certain conditions, for example, after intense exposure. Such excitotoxic neuronal death may contribute to the pathogenesis of brain or spinal cord injury associated with several human disease states. Excitotoxicity has substantial cellular specificity and, in most cases, is mediated by glutamate receptors. On average, NMDA receptors activation may be able to trigger lethal injury more rapidly than AMPA or kainate receptor activation, perhaps reflecting a greater ability to induce calcium influx and subsequent cellular calcium overload. It is possible that excitotoxic death may share some mechanisms with other forms of neuronal death.
Publication Types:
Review
Review, AcademicPMID: 1361523 [PubMed - indexed for MEDLINE]
Here is another statement I found relating to this phenomenom (at the following link see http://kuhttp.cc.ku.edu/cwis/units/biol/bhawk00/neuro.html )"Despite its impressive design and function, the brain shows vulnerability to its own processes. In fact, excitatory circuits in the brain can, in essence, burn themselves out through overstimulation. These neurons die from what is called excitatory neurotoxicity, which is of great interest to Dr. Jang-Yen Wu, faculty member in the department of Molecular Biosciences." (At University of Kansas)
I am not that great at pure scientific research but I would recommend that you do searches under the following headings:-1. excitatory neurotoxicity
2. excitotoxicity
3. excitotoxic cell death
I think Larry Hoover may be able to help out in providing any reasearch that would either support or refute the above theory.bluedog
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 )
Posted by Larry Hoover on November 26, 2002, at 11:36:31
In reply to Re: Anxiety Causes Brain Damage???? » Guy, posted by bluedog on November 25, 2002, at 22:24:06
> > 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;
>
> Selenium deficiency increases susceptibility to glutamate-induced excitotoxicity.> 1: J Neurosci Res 2001 Nov 15;66(4):612-9
>
> Role of taurine in regulation of intracellular calcium level and neuroprotective function in cultured neurons.> 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.I was asked to comment on this issue. It's exceedingly complicated. I'm going to try and give a balanced reply.
Many long-held beliefs about the brain are falling by the wayside, as investigative tools (and investigators) become more sophisticated. It was once thought that you were born with a huge number of brain cells, and it was downhill all the way to old age; you kept losing brain cells until your brain just lost functions altogether. That's not true. New brain cells, and new connectivity, arise because of brain stimulation. There is an aspect of "use it or lose it" about the brain, but also "use it and gain".
Some of the newer ideas about brain function have come together under the concept of 'plasticity', the ability of the brain to adapt to the demands placed upon it. A concert violinist will have a physically larger, and more complex, segment of the motor cortex which controls the left hand (in the usual left-fingering and right-bowing model) than your typical person. It gets bigger because of the demand (though it might have been a little bigger to start with).
What happens under stress is also an adaptive process. Having a brain that is alert and responsive to the environment tends to preserve the reproductive potential of the gonads.
The alerting process, though, places demands on other aspects of brain function. There are resources in place whose sole purpose is to protect the brain from it's own alerting processes. These protective resources are finite; they can become depleted. Huge, but temporary stress, or chronic, low-level stress do the same thing, in the end. They both overwhelm defensive mechanisms, those dedicated to shutting down the excitatory alerting processes. In the absence of chemical defenses, the brain will allow cells to die, to protect other cells from injury arising from unbalanced excitation. Unfortunately, the cells in the brain linked to affect are particularly vulnerable to this kind of excitotoxic injury.
There is growing evidence that these losses are not permanent. Given the right kinds of supports, these lost neurons can be fully replaced. It seems that it doesn't matter if the remission is caused by drugs, or talk therapy, or spontaneous factors, the restoration of brain function is visible in brain imaging like functional-MRI and SPECT.
I left the references to nutritional aspects of stress-resistance in place because these are aspects under individual control. You may not be able to control your stress level as much as you can control your diet.
You may recall that I have discussed the methionine/homocysteine cycle, and its relationship to SAMe and depression. Well, there's more to it than that. Sometimes I stop talking about something for no other reason than to reduce the complexity, not because it isn't important.
Glutathione is a major neuro-protective chemical in the brain. It derives from methionine metabolism. Taurine is a major neuro-protective chemical in the brain. It derives from methionine metabolism. What glutathione, taurine and methionine have in common is that they are, or contain, sulphur-containing amino acids. Sulphur metabolism is heavily disrupted by stress. This article does an excellent job of explaining much of the intricacies of methionine metabolism.
http://www.thorne.com/altmedrev/fulltext/homo2-4.html
I strongly recommend that you explore the Thorne site. Just shorten the URL to end at altmedrev/ for example, and look around. Lots of free info.
This one is more specific to glutathione:
http://www.redwings.org/HTMLarts/gshhealtha.htm
One of the best predictors of glutathione in brain tissues is alpha-lipoic acid status. There is a strong, positive correlation. And, surprise surprise, alpha-lipoic acid is a sulphur compound. So is glucosamine.
Then, you have selenium, which is an antioxidant powerhouse all by itself, but which also acts in concert with some of the sulphur compounds, as e.g. seleno-methionine or seleno-glutathione. It is also a key component of enzymes which act synergistically with other antioxidants, like superoxide dismutase (SOD), or glutathione reductase.
I'm just trying to put things in context. Your brain prunes overactive cells. It has to, to control input. You temporarily reduce some functions. But, those functions can be restored by changing the circumstances the brain is functioning under.
There are genetic influences to all of this (can't do much about that), experiential factors (early childhood experience can permanently affect some aspects of susceptibility to stress-overload) which are amenable to cognitive therapy, nutritional factors, and so on.
Everything's got yin and yang. I prefer not to focus on the negative aspects of stress-reactivity. I prefer to focus on those things I can change. Diet certainly falls in the latter category. You are what you eat.
Lar
Posted by Larry Hoover on November 26, 2002, at 12:21:26
In reply to Re: Anxiety Causes Brain Damage???? - Larry Hoover » Guy, posted by bluedog on November 25, 2002, at 21:39:52
J Neurochem 1994 Aug;63(2):596-602
Physiological elevations of glucocorticoids potentiate glutamate accumulation in the hippocampus.
Stein-Behrens BA, Lin WJ, Sapolsky RM.
Department of Biological Sciences, Stanford University, California 94305.
Glucocorticoids (GCs) are secreted during stress and can damage the hippocampus over the course of aging and impair the capacity of hippocampal neurons to survive excitotoxic insults. Using microdialysis, we have previously observed that GCs augment the extracellular accumulation of glutamate and aspartate in the hippocampus following kainic acid-induced seizures. In that study, adrenalectomized rats maintained on minimal GC concentrations were compared with those exposed to GCs elevated to near-pharmacological levels. We wished to gain insight into the physiological relevance of these observations. Thus, we have examined the effects of GCs over the normal physiological range on glutamate and aspartate profiles; this was done by implanting adrenalectomized rats with GC-secreting pellets, which produce stable and controllable circulating GC concentrations. We observe that incremental increases in GC concentrations cause incremental increases in glutamate accumulation before the kainic acid insult, as well as in the magnitude of the glutamate response to kainic acid. Elevating GC concentrations from the circadian trough to peak doubled cumulative glutamate accumulation, whereas a rise into the stress range caused a fourfold increase in accumulation. Similar, although smaller, effects also occurred with aspartate accumulation (as well as with taurine but not glutamine accumulation). These data show that the highly elevated GC concentrations that accompany neurological insults such as seizure or hypoxia-ischemia will greatly exacerbate the glutamate accumulation at that time. Furthermore, stress levels of GCs augmented glutamate accumulation even in the absence of an excitotoxic insult, perhaps explaining how sustained stress itself damages the hippocampus.
Glia 1998 Feb;22(2):149-60
4-hydroxynonenal, a lipid peroxidation product, impairs glutamate transport in cortical astrocytes.Blanc EM, Keller JN, Fernandez S, Mattson MP.
Sanders-Brown Research Center on Aging, University of Kentucky, Lexington 40536-0230, USA.
Astrocytes possess plasma membrane glutamate transporters that rapidly remove glutamate from the extracellular milieu and thereby prevent excitotoxic injury to neurons. Cellular oxidative stress is increased in neural tissues in a variety of acute and chronic neurodegenerative conditions. Recent findings suggest that oxidative stress increases neuronal vulnerability to excitotoxicity and that membrane lipid peroxidation plays a key role in this process. We now report that 4-hydroxynonenal (HNE), an aldehydic product of membrane lipid peroxidation, impairs glutamate transport in cultured cortical astrocytes. Impairment of glutamate transport occurred within 1-3 h of exposure to HNE; FeSO4, an inducer of membrane lipid peroxidation, also impaired glutamate transport. Vitamin E prevented impairment of glutamate transport induced by FeSO4, but not that induced by HNE, consistent with HNE acting as an effector of lipid peroxidation-induced impairment of glutamate transport. Glutathione, which binds and thereby detoxifies HNE, prevented HNE from impairing glutamate transport. Western blot, immunoprecipitation, and immunocytochemical analyses using an antibody against HNE-protein conjugates provided evidence that HNE covalently binds to many different astrocytic proteins including the glutamate transporter GLT-1. Data further suggest that HNE promotes intermolecular cross-linking of GLT-1 monomers to form dimers. HNE also induced mitochondrial dysfunction and accumulation of peroxides in astrocytes. Impairment of glutamate transport and mitochondrial function occurred with sublethal concentrations of HNE, concentrations known to be generated in cells exposed to various oxidative insults. Collectively, our data suggest that HNE may be an important mediator of oxidative stress-induced impairment of astrocytic glutamate transport and may thereby play a role in promoting neuronal excitotoxicity.
Annu Rev Neurosci 1999;22:105-22
Stress and hippocampal plasticity.McEwen BS.
Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology, Rockefeller University, New York, New York 10021, USA. mcewen@rockvax.rockefeller.edu
The hippocampus is a target of stress hormones, and it is an especially plastic and vulnerable region of the brain. It also responds to gonadal, thyroid, and adrenal hormones, which modulate changes in synapse formation and dendritic structure and regulate dentate gyrus volume during development and in adult life. Two forms of structural plasticity are affected by stress: Repeated stress causes atrophy of dendrites in the CA3 region, and both acute and chronic stress suppresses neurogenesis of dentate gyrus granule neurons. Besides glucocorticoids, excitatory amino acids and N-methyl-D-aspartate (NMDA) receptors are involved in these two forms of plasticity as well as in neuronal death that is caused in pyramidal neurons by seizures and by ischemia. The two forms of hippocampal structural plasticity are relevant to the human hippocampus, which undergoes a selective atrophy in a number of disorders, accompanied by deficits in declarative episodic, spatial, and contextual memory performance. It is important, from a therapeutic standpoint, to distinguish between a permanent loss of cells and a reversible atrophy.
Exp Gerontol 1998 Nov-Dec;33(7-8):713-27
Neurosteroids, brain damage, and mental illness.
Herbert J.
Department of Anatomy and MRC Cambridge Centre for Brain Repair, University of Cambridge, UK.
The steroidal environment of the brain has marked consequences for both its structure and function. Social or physical stress has deleterious results on hippocampal function. This can be replicated by raising corticoids, which are also highly responsive to stress. Corticosterone, the major glucocorticoid in the rat, induces neuronal death in primary hippocampal cultures. Elevated corticoids also induce mood changes, and these are well known to be associated with stress, particularly chronic stress such as social adversity accentuated by intercurrent aversive life events. DHEA, a second adrenal steroid, has a very different developmental history, increasing rapidly during childhood, reaching a peak in youth, and declining thereafter in both blood and CSF. DHEA, in contrast to corticoids, has brain protective actions. It reduces the neurotoxic actions of glutamate analogues (such as NMDA) as well as those of corticoids. Evidence from several sources suggests that DHEA can act as an antiglucocorticoid. DHEA levels are reduced in major depressive disorders in both adolescents and adults, and a raised cortisol/DHEA ratio (together with intercurrent life events) predicts delayed recovery. DHEA may have a role in the treatment of depression. Together, these findings suggest that altered steroidal environment, whether induced by stress or aging, can have appreciable results on the cellular structure of the brain as well as on its function, although links between the two sets of findings are still tentative.
Hum Psychopharmacol 2001 Jan;16(S1):S7-S19
Stress and hippocampal plasticity: implications for the pathophysiology of affective disorders.
McEwen BS, Magarinos AM.
Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology, The Rockefeller University, New York, NY, USA.
The hippocampal formation, a structure involved in declarative, spatial and contextual memory, is a particularly sensitive and vulnerable brain region to stress and stress hormones. The hippocampus shows a considerable degree of structural plasticity in the adult brain. Stress suppresses neurogenesis of dentate gyrus granule neurons, and repeated stress causes atrophy of dendrites in the CA3 region. In addition, ovarian steroids regulate synapse formation during the estrous cycle of female rats. All three forms of structural remodeling of the hippocampus are mediated by hormones working in concert with excitatory amino acids (EAA) and N-methyl-D-aspartate (NMDA) receptors. EAA and NMDA receptors are also involved in neuronal death that is caused in pyramidal neurons by seizures and by ischemia and prolonged psychosocial stress. In the human hippocampus, magnetic resonance imaging studies have shown that there is a selective atrophy in recurrent depressive illness, accompanied by deficits in memory performance. Hippocampal atrophy may be a feature of affective disorders that is not treated by all medications. From a therapeutic standpoint, it is essential to distinguish between permanent damage and reversible atrophy in order to develop treatment strategies to either prevent or reverse deficits. In addition, remodeling of brain cells may occur in other brain regions. Possible treatments are discussed.
Neuroscience 1996 Nov;75(1):231-43
Immunocytochemical localization of seleno-glutathione peroxidase in the adult mouse brain.Trepanier G, Furling D, Puymirat J, Mirault ME.
Department of Genetic and Molecular Medicine, CHUL Research Center, Sainte-Foy, Quebec, Canada.
Cytoplasmic seleno-glutathione peroxidase, by reducing hydrogen peroxide and fatty acid hydroperoxides, may be a major protective enzyme against oxidative damage in the brain. Oxidative damage is strongly suspected to contribute to normal aging and neurodegenerative process of Alzheimer's and Parkinson's diseases. We report here an immunocytochemical analysis of the localization of glutathione peroxidase in the adult mouse brain, carried out with an affinity-purified polyclonal antibody. Most of the brain areas analysed showed weak to strong glutathione peroxidase immunoreactivity, expressed in both neurons and glial cells. The strongest immunoreactivity was found in the reticular thalamic and red nuclei. Highly immunoreactive neurons were observed in the cerebral cortex (layer II), the CA1, dentate gyrus and pontine nucleus. Other regions, such as the caudate-putamen, septum nuclei, diagonal band of Broca, hippocampus, thalamus and hypothalamus, showed moderate staining. This study provides original information about the wide distribution of glutathione peroxidase in the mouse brain. Double-staining experiments indicated that specific subsets of cholinergic neurons in septal and diagonal band nuclei were negative for this antigen. Similarly, many dopaminergic neurons of the substantia nigra pars compacta expressed low levels of glutathione peroxidase antigen, in contrast to the ventral tegmental area, wherein most catecholaminergic cells were strongly positive. A lack of glutathione peroxidase in subsets of dopaminergic or cholinergic neurons may thus confer a relative sensitivity of these cells to oxidative injury of various origins, including catecholamine oxidation, neurotoxins and excitotoxicity.
Posted by Guy on November 26, 2002, at 19:08:32
In reply to KLONOPIN and chronic fatigue, posted by bluedog on November 23, 2002, at 21:53:45
Wow, this is really detailed stuff and it will take some time to digest. Larry, are you some kind of scientist or researcher?? It sure sounds like it. Thanks for all the info...I'll do my best.
Posted by Larry Hoover on November 26, 2002, at 20:10:18
In reply to Information Overload, posted by Guy on November 26, 2002, at 19:08:32
> Wow, this is really detailed stuff and it will take some time to digest. Larry, are you some kind of scientist or researcher??
Both.
>It sure sounds like it. Thanks for all the info...I'll do my best.
If there's anything I can "translate" or explain, I'd be happy to do that. I can't speak to everybody's understanding level at the same time....some understand the terminology and such better than others to begin with.
Posted by bluedog on November 26, 2002, at 20:53:59
In reply to Re: Information Overload, posted by Larry Hoover on November 26, 2002, at 20:10:18
> > Wow, this is really detailed stuff and it will take some time to digest. Larry, are you some kind of scientist or researcher??
>
> Both.
>
> >It sure sounds like it. Thanks for all the info...I'll do my best.
>
> If there's anything I can "translate" or explain, I'd be happy to do that. I can't speak to everybody's understanding level at the same time....some understand the terminology and such better than others to begin with.
>Larry
Thanks again for pitching in with your knowledge and thanks for your very understandable explanation of the scientific research.
I know that you are worried that you are gettig too complex with some of your explanations but I would like to say that I personally find your summaries easy to understand and extremely helpful. Often when I am struggling with the primary sources of scientific research your synopses make sense of and bring together a vast amount of information from disparate sources into one place. I also find the links you provide to articles that do the same (ie bring together and summarise the disparate research in a particular area and present it in an understandable format) very valuable to my understanding.
Please keep it coming!!!
Thanks
bluedog
Posted by Guy on November 26, 2002, at 21:49:54
In reply to KLONOPIN and chronic fatigue, posted by bluedog on November 23, 2002, at 21:53:45
I've just reread the material and links provided by bluedog and Larry and I think I'm beginning to understand most of it. I'm truly amazed at how much information is available regarding the effects of stress on the body...it's really quite fascinating. (I wonder how many of the doctors out there are keeping abreast of all this research.) I'm going to print everything off and discuss it with my shrink when I see him next week. Thanks again for all the info. Larry, I may take you up on your offer to explain further once I've read everything a few more times.
Posted by bubblegumchewer on November 27, 2002, at 8:27:56
In reply to Very interesting!, posted by Guy on November 26, 2002, at 21:49:54
In my experience health professionals don't enjoy such discussions and in fact don't even enjoy any questions; they look at me as if I'm the uptight patient who worries too much about what she reads. In other words, they are patronizing, impatient, and uninterested in expanding their own horizons. Wait, I did have a doctor once who was happy to think... I owe her thousands now and our relationship now is vicious collector - harrassed collectee. I am glad for you, Guy, if you have a doctor who is happy to discuss subjects of interest to you. Let us know how it goes.
Geez, I'm in a mood today - no coffee yet - that's it!
Posted by johnj on November 27, 2002, at 9:41:49
In reply to Re: Information Overload, posted by Larry Hoover on November 26, 2002, at 20:10:18
Larry,
I have been gone for a bit, but I wanted to thank you for your response to my post. It is hard to know which vitamins to try. I am thinking about DHEA, co enzyme Q10, and maybe taurine to see if I have any positive responses. I read that co Q10 should be taken if a person is on a TCA. Don't know much about the others though. Thanks again. take care
johnj
Posted by Larry Hoover on November 27, 2002, at 11:17:56
In reply to Thanks for the posts » Larry Hoover, posted by johnj on November 27, 2002, at 9:41:49
> Larry,
> I have been gone for a bit, but I wanted to thank you for your response to my post.You're welcome.
>It is hard to know which vitamins to try.
I strongly urge you to try them one at a time, so you have a clear idea of the effects.
>I am thinking about DHEA, co enzyme Q10, and maybe taurine to see if I have any positive responses. I read that co Q10 should be taken if a person is on a TCA. Don't know much about the others though. Thanks again. take care
> johnjIf you're thinking about DHEA, why don't you try some licorice root first? Make sure it's not the de-glycorrhizinated form (DGL). You want the whole root. Walmart has it. Use it for about a week, and if it makes you feel more balanced, you probably have an adrenal problem, which might be helped by DHEA.
One of the symptoms that is strongly suggestive of CoQ-10 deficiency is gum disease.
Taurine is broadly called an amino acid, but the acid part is sulphonic acid. It is not a constituent of any protein, but is always found as a free molecule. Taurine synthesis in humans may not keep up to demand, but meat is a good source. I cannot see how you could hurt yourself with taurine supplements. Some people advocate whey protein powder for taurine and glutathione precursors (relatively high cystine content).
More than you ever wanted to know about taurine:
http://www.thorne.com/altmedrev/fulltext/taurine3-2.html
Posted by johnj on November 27, 2002, at 14:37:36
In reply to Re: Thanks for the posts, posted by Larry Hoover on November 27, 2002, at 11:17:56
Larry,
thanks for the link! Since alcholism and macular degeneration run in my family I can't see how a trial of taurine would hurt at all. I appreciate the link.
Posted by bluedog on November 28, 2002, at 3:03:38
In reply to Re: Anxiety Causes Brain Damage????, posted by Larry Hoover on November 26, 2002, at 11:36:31
I have taken the liberty of linking to a post by ItsHowdyDudyTime in the thread down below called "is depression damaging my brain?" which reads as follows:-
http://www.dr-bob.org/babble/20021127/msgs/129658.html
"Posted by ItsHowdyDudyTime on November 27, 2002, at 21:11:02
In reply to Is depression damaging my brain?, posted by catmint on November 26, 2002, at 0:54:02
OK I found out I was posting those in Spanish and coming out weird. This should come out normally.
To answer your question, yes depression does damage the brain. Particularly when the depression is severe, left untreated or partially treated for long time periods. What is a long time period? Several years is what I was told by a famous TRD researcher at a elite teaching hospital. Severe depression causes literal atrophy of brain tissue, the frontal lobes shrink in size, the hippocampus atropies. There are many physical brain changes that occur in severe depression.
This is all the reason to catch it early, get a correct diagnosis early on and get on the correct class of psychiatric medication early on. Stringing things along only prolongs recovery. Those who have had severe, untreated or partially treated depression for years on end oftentimes find it nearly impossible to fully recover no matter what they do. This is the hard, sad reality of severe mental illness.
ECT is probably your best bet if you are one of these folks who has ignored your mood disorder for years. MAOIs are also good for longstanding, severe and unsuccessfully treated depression. MAOIs can be combined with mood stabilizers like lithium or depakote in bipolar individuals.
Severe mood disorders are nothing to play around with. They tend to sneak up on you, snowball, get worse and worse and one day you realize you are chronically disabled...or worse almost dead. All because you didnt handle it properly in the beginning. Do not underestimate the severity and lethality of a severe mood disorder and Im not even talking about suicide here. Im talking about things like you will never have another good night of sleep for the rest of your life, severe cognition problems, lack of sex drive for the rest of your life which results in inability to maintain meaningful relationships with the opposite sex. Its just bad news and its too bad more people dont understand the true nature of severe depression or manic depression left untreated or undertreated."
Larry has already mentioned it but these two threads are dealing with the same topic!!
I couldn't agree more with what howdydudy writes!! I had an appointment with my psychiatrist today and (surprise, surprise) he was in complete agreement with the sorts of views that have been bandied about in these threads. He says that he has observed severe cognitive dysfunction including concentration and memory problems in patients who have suffered long term anxiety and depression which he attributes to brain damage (either the death or atrophy of brain neurons) caused by phenomena such as excitotoxicity.
He also agrees with my view that in the future there will be a new medical specialty in nutrition and that these nutritional specialists will be held in as high regard by their medical peers as cardiologists, neurologists and psychiatrists and they will take away a lot of the patients who are currently being seen by the other specialty fields.
bluedog
This is the end of the thread.
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