Sinusitis FAQ » Pathophysiology

a neuroscientific basis for using benzos in panic disorder

admin — Thu, 02 Mar 2006 00:00:00 +0000

Question:

J Psychiatry Neurosci. 2005 May;30(3):167-75. Selective GABAergic treatment for panic? Investigations in experimental panic induction and panic disorder. Zwanzger P, Rupprecht R. Anxiety Research Unit and Anxiety Outpatient Clinic, Department of Psychiatry, Ludwig-Maximilians-Universitat, Munich, Germany. Gamma-Aminobutyric acid (GABA) is the *most important inhibitory neurotransmitter* in the central nervous system (CNS). It exerts its rapid inhibitory action mostly through *GABA(A) receptors*, which are targets for *benzodiazepines*, barbiturates, neuroactive steroids and distinct *anticonvulsive agents*. **There is considerable evidence that dysfunction of GABA(A) receptors or dysregulation of GABA concentrations in the CNS (or both) plays an important role in the pathophysiology of panic disorder**. Currently, benzodiazepines are the only drugs directly targeting the GABA(A) receptors that are approved for the treatment of anxiety disorders. Because of their well-known anxiolytic effects, they are widely used in this setting, but *side effects limit their use in long-term treatment* (note: that’s controversial. I’ve been on Klonopin for 19 years). The question of whether drugs that selectively *increase GABA concentrations* in the CNS could improve symptoms of anxiety has been discussed. Recent investigations by our group have demonstrated that enhancement of endogenous GABA (through blockade of *GABA transaminase* by vigabatrin, or through *inhibition of GABA transporters* by tiagabine) exerts anxiolytic effects on experimentally induced panic. (Note: the above vigabatrin inhibits the breakdown of GABA by GABA transaminase, and thus increases GABA concentration. It will not be approved in the USA because a side effect is impairment of vision. The above tiagabine, trade name *Gabitril*, is now available in the USA as an anticonvulsant. It inhibits the reuptake of GABA, and thus increases GABA concentration.) Our studies in *healthy volunteers* have shown that both compounds lead to a significant reduction in panic symptoms elicited by cholecystokinin-tetrapeptide (CCK-4). Moreover, benzodiazepine-like effects on the activity of the hypothalamic-pituitary-adrenal axis have been observed in association with vigabatrin treatment. Small open studies in patients with panic disorder also showed an improvement in panic and anxiety with both compounds. This review summarizes our recent research on the effects of selective GABAergic treatment in experimentally induced panic and outlines the possible role of compounds targeting the GABA binding site of the GABA(A)-benzodiazepine receptor for the treatment of panic and anxiety. PMID: 15944741 [PubMed - indexed for MEDLINE] — The charter is available at: http://readystump.algebra.com/~asapm

Response:

— The charter is available at: http://readystump.algebra.com/~asapm

Response:

J Psychiatry Neurosci. 2005 May;30(3):167-75. Selective GABAergic treatment for panic? Investigations in experimental panic induction and panic disorder. Zwanzger P, Rupprecht R. … Currently, benzodiazepines are the only drugs directly targeting the GABA(A) receptors that are approved for the treatment of anxiety disorders. Because of their well-known anxiolytic effects, they are widely used in this setting, but *side effects limit their use in long-term treatment* (note: that’s controversial. I’ve been on Klonopin for 19 years).

I’ll second that! I’ve been using alprazolam (Xanax) for about a decade now and have yet to experience adverse side effects nor increased dependence (works as well now as it did when I started). My dosage is purely PRN (some days I use none at all, up to 3 or rarely 4-mg during very bad days, on average about 1.5-mg per day). Best Wishes, Arthur — The charter is available at: http://readystump.algebra.com/~asapm

Response:

I’ve been taking .75 mgs per day of Xanax for about 3 weeks now, after a SEVERE panic attack (combined w/ hyperventilation) which sent me to the ER (it was my first attack I thought I was having a heart attack, despite the fact that I’m only 35 yrs old.) I love it – I can’t believe how much it has helped me! I only hope that my doctor keeps prescribing it for me, as I think it is working very well and don’t need see any need to switch. — The charter is available at: http://readystump.algebra.com/~asapm

Response:

It likely has to do with profit margins, but that’s just a guess on my part. I would be interested to know what kind of profit percentage drug companies make on, for instance, generic clonazepam, and compare it to that of name-brand Wellbutrin or Prozac. I wonder if that information is available to the general public. Deirdre

The profit margins are huge for non-generic medications sold in the USA. There are a few factors for this. 1. There is a very large initial outlay of money to bring a new medication to market. The research has to be done. Then all the trial studies to prove the medication is safe and effective so it can get FDA approval. Once on the market, the non-generic medication has a limited time that it is patent protected. This time period is where the pharmaceutical company can charge crazy prices so it can get back the initial costs and make a profit before the generics are allowed. 2. Here in the USA we pay more for the same medication than most other places in the world. We (USA) are subsidizing medications for most of the world. The pharmaceutical companies say they "donate" medications to needy nations/people around the world. The pharmaceutical companies are not really doing that. They are selling medications in those places as cost or a small loss, while they recoup it all here in the USA. Our close neighbors in Canada can get the same medication for a lot less than we have to pay here in the USA. I only see two solutions. 1. Make *all* medical research sponsored by tax dollars only. This way all the fruits of this research will be in the *public domain*. Any private company can then use that research. Since anyone can use this research the only thing companies can do is *compete*. They will have to compete on prices/services. 2. Go to a full socialized health system similar to Denmark. A friend of mine is from Denmark and according to her the health system there is much, much better. Everyone is covered. No one has to worry about whether they will eat or get their medication. Jim — The charter is available at: http://readystump.algebra.com/~asapm

Response:

- Hide quoted text — Show quoted text – why is the general opinion of most psychiatrists in favor of ssri’s over benzo’s for anxiety and panic? what is their problem with benzo’s? They usually site 3 reasons: 1) benzos can cause dependence (but so can antidepressants) 2) benzos can cause a withdrawal syndrome when stopped (so can antidepressants) 3) benzos are "addictive" (studies have shown that benzo abuse is rare in people with anxiety disorders) And another factor is that psychiatry professors who teach residents and write the psychiatric textbooks are very often paid consultants by the manufacturers of antidepressants. I am uncertain to what extent this biases them against benzos and for antidepressants. Chip

Response:

chip,

I’ve been on an SSRI, Zoloft, to prevent depression for several years, and it works. But I think the benzos are better for anxiety. thats why i keep wrestling with the thought that i would be better off on a benzo instead. i hate not knowing who to trust, we put our lives in these pdocs hands…and to think that their hands may be controlled by the strings of corporations makes me very uneasy.

You make some good points, Russ. Chip — The charter is available at: http://readystump.algebra.com/~asapm

Response:

why is the general opinion of most psychiatrists in favor of ssri’s over benzo’s for anxiety and panic? what is their problem with benzo’s?

SSRI’s are hyped up big time while benzos are (wrongly) felt to be *addictive*. They should do their homework. Philip — The charter is available at: http://readystump.algebra.com/~asapm

Response:

chip,

Response:

why is the general opinion of most psychiatrists in favor of ssri’s over benzo’s for anxiety and panic? what is their problem with benzo’s? — The charter is available at: http://readystump.algebra.com/~asapm

Response:

why is the general opinion of most psychiatrists in favor of ssri’s over benzo’s for anxiety and panic? what is their problem with benzo’s?

They usually site 3 reasons: 1) benzos can cause dependence (but so can antidepressants) 2) benzos can cause a withdrawal syndrome when stopped (so can antidepressants) 3) benzos are "addictive" (studies have shown that benzo abuse is rare in people with anxiety disorders) And another factor is that psychiatry professors who teach residents and write the psychiatric textbooks are very often paid consultants by the manufacturers of antidepressants. I am uncertain to what extent this biases them against benzos and for antidepressants. Chip — The charter is available at: http://readystump.algebra.com/~asapm

Response:

J Psychiatry Neurosci. 2005 May;30(3):167-75. Selective GABAergic treatment for panic? Investigations in experimental panic induction and panic disorder.

I’ve *never* heard of anybody having any success with Gabitril. Of course I haven’t read the study itself but I’m far from convinced. Philip (gimme a benzo any time) – Hide quoted text — Show quoted text – Zwanzger P, Rupprecht R. Anxiety Research Unit and Anxiety Outpatient Clinic, Department of Psychiatry, Ludwig-Maximilians-Universitat, Munich, Germany. Gamma-Aminobutyric acid (GABA) is the *most important inhibitory neurotransmitter* in the central nervous system (CNS). It exerts its rapid inhibitory action mostly through *GABA(A) receptors*, which are targets for *benzodiazepines*, barbiturates, neuroactive steroids and distinct *anticonvulsive agents*. **There is considerable evidence that dysfunction of GABA(A) receptors or dysregulation of GABA concentrations in the CNS (or both) plays an important role in the pathophysiology of panic disorder**. Currently, benzodiazepines are the only drugs directly targeting the GABA(A) receptors that are approved for the treatment of anxiety disorders. Because of their well-known anxiolytic effects, they are widely used in this setting, but *side effects limit their use in long-term treatment* (note: that’s controversial. I’ve been on Klonopin for 19 years). The question of whether drugs that selectively *increase GABA concentrations* in the CNS could improve symptoms of anxiety has been discussed. Recent investigations by our group have demonstrated that enhancement of endogenous GABA (through blockade of *GABA transaminase* by vigabatrin, or through *inhibition of GABA transporters* by tiagabine) exerts anxiolytic effects on experimentally induced panic. (Note: the above vigabatrin inhibits the breakdown of GABA by GABA transaminase, and thus increases GABA concentration. It will not be approved in the USA because a side effect is impairment of vision. The above tiagabine, trade name *Gabitril*, is now available in the USA as an anticonvulsant. It inhibits the reuptake of GABA, and thus increases GABA concentration.) Our studies in *healthy volunteers* have shown that both compounds lead to a significant reduction in panic symptoms elicited by cholecystokinin-tetrapeptide (CCK-4). Moreover, benzodiazepine-like effects on the activity of the hypothalamic-pituitary-adrenal axis have been observed in association with vigabatrin treatment. Small open studies in patients with panic disorder also showed an improvement in panic and anxiety with both compounds. This review summarizes our recent research on the effects of selective GABAergic treatment in experimentally induced panic and outlines the possible role of compounds targeting the GABA binding site of the GABA(A)-benzodiazepine receptor for the treatment of panic and anxiety. PMID: 15944741 [PubMed - indexed for MEDLINE]

– The charter is available at: http://readystump.algebra.com/~asapm

Response:

Oxidative stress and diabetic neuropathy

admin — Sat, 18 Oct 2003 00:00:00 +0000

Question:

I take him seriously too!

See my reply to BL; I meant Tom (ironjustice), not Ted. Who did you mean? Cheers Alan, T2, Oz — Everything in Moderation – Except Laughter.

Response:

I take him seriously too! See my reply to BL; I meant Tom (ironjustice), not Ted. Who did you mean?

Ack! What a mistake! I thought you meant Ted. *hanging my head in shame* — Type 2 http://users.bestweb.net/~jbove/

Response:

– Hide quoted text — Show quoted text – Ted, you seem educated. Look up the words "monomania" and "fanatic" in your dictionary. You detract from some of the occasional good links you provide because you are no longer taken seriously. Cheers Alan, T2, Oz He is taken seriously by many here. Myself included. Sleepy Save the whales. Collect the whole set. Fair enough Sleepy. I do read the good links. I know he won’t agree, but it was actually meant as advice, albeit I was a bit strong I suppose.. Cheers Alan, T2, Oz

If you meant crackpot tom aka doe aka iron justice aka jesus was a vegetarian, I take it all back. The white coats just haven’t caught up to him yet! Sleepy Save the whales. Collect the whole set.

Response:

"What are the mechanisms that underlie the development of microvascular complications? (snipped) http://www.jci.org/cgi/content/full/111/4/431

There are a number of graphics that show the various pathways towared diabetic complications in the following article. Page 5 shows a great deal of similarity with the pathways in the above article. The same could be said for the discussion by Dr. John Buse in pages 36-47. He gives current therapies for microvascular complications on page 36. There are a more detailed accounts of these complications and some of the drugs undergoing trials for their treatment to let you know what may be down the pipeline. Earlier discussions mention the commonality amongst the diabetic complications. "There is a common pathologic change no matter whether you look at the retina, the kidney, or the nerve. The changes that one sees are related to base membrane, endothelium, and pericytes. This (graphic) shows the retina, the glomerulus, and the nerve. The changes are those of thickening of base membrane, endothelial cell changes, and pericyte cell death. These are common to all the so-called microvascular complications of diabetes." Furthermore, the complications can begin even at the stage of impair glucose tolerance. Changes are occuring in the eye before there are obvious signs of retinopathy. This is true in the kidneys and nerves. These changes may not be transparent to the patient. Hyperglycemia is still the main culprit but not the only one. Pathways Leading to Diabetic Microvascular Complications and the Latest Clinical Therapies http://www.medscape.com/viewprogram/2636 Frank

Response:

Yep. Thanks for pointing that out. My apologies Ted; we argue at times, but I did mean Tom in this case. Once again finger trouble, I think I’d better get a proof-reader. Mea culpa. Cheers Alan, T2, Oz — Everything in Moderation – Except Laughter.

Response:

Ted, you seem educated. Look up the words "monomania" and "fanatic" in your dictionary. You detract from some of the occasional good links you provide because you are no longer taken seriously. Cheers Alan, T2, Oz He is taken seriously by many here. Myself included.

I take him seriously too! — Type 2 http://users.bestweb.net/~jbove/

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Doe is an anti-iron nut. He keeps stretching various pro-vegatarian tests and studies to claim that all diabetes is caused by iron, much as Betty Martini claims that all brain tumors and cellulite are actually lumps of Sweet&Low embedded in your body. Ignore him and get on with your life….

Response:

OK people. I think Alan meant Tom, not Ted, due to the thread. Ted hasn’t posted to this thread. Furthermore Ted rarely provides "links." Tom does. Tom– you know, he’s our iron man, and we can’t figure out his connection to diabetes, but he quotes MEDL:INE studies all the time about iron, vegetarianism, etc.. Once in a while it will be about something else but usually it is an iron chelator. Ted–everyone knows him, but we haven’t seen much of him lately. Alan wasn’t your post about Tom? Alan, IMHO Tom is incapable of following your advice. Nice try. – Hide quoted text — Show quoted text -He is taken seriously by many here. Myself included. Sleepy Save the whales. Collect the whole set. Fair enough Sleepy. I do read the good links. I know he won’t agree, but it was actually meant as advice, albeit I was a bit strong I suppose.. Cheers Alan, T2, Oz — Everything in Moderation – Except Laughter.

BL "As the waves pass the rock, their shape is changed. There is a hologram of the rock within the wave that comes forward and crashes on the beach, then there’s a reflected wave back." Ralph Abraham "I’d like to learn to windsurf." BL

Response:

He is taken seriously by many here. Myself included. Sleepy Save the whales. Collect the whole set.

Response:

- Hide quoted text — Show quoted text – Ted, you seem educated. Look up the words "monomania" and "fanatic" in your dictionary. You detract from some of the occasional good links you provide because you are no longer taken seriously. Cheers Alan, T2, Oz He is taken seriously by many here. Myself included. Sleepy Save the whales. Collect the whole set.

Fair enough Sleepy. I do read the good links. I know he won’t agree, but it was actually meant as advice, albeit I was a bit strong I suppose.. Cheers Alan, T2, Oz — Everything in Moderation – Except Laughter.

Response:

- Hide quoted text — Show quoted text – Frank, thanks – so what do we do about it? Likely control BG to prevent oxidative stress – what about anti-oxidant foods like green tea, dark choc, blueberries, etc? This article speaks to the finding of lowering of iron stores down to the levels found commonly in vegetarians. Iron reduction therapy has been coined to be the FUTURE in effective antioxidant therapy due to its effectiveness and price. Doe is an anti-iron nut. He keeps stretching various pro-vegatarian tests and studies to claim that all diabetes is caused by iron, much as Betty Martini claims that all brain tumors and cellulite are actually lumps of Sweet&Low embedded in your body. Ignore him and get on with your life….

Nico .. is stupid .. Listen to him and you will be stupid .. too .. Oh yeah .. AND will continue to have diabetes .. Who loves ya. Tom Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com Man Is A Herbivore! http://pages.ivillage.com/ironjustice/manisaherbivore DEAD PEOPLE WALKING http://pages.ivillage.com/ironjustice/deadpeoplewalking

Response:

Thanks Frank – think I keep eating my blueberries. – Hide quoted text — Show quoted text – Brad: thanks – so what do we do about it? Likely control BG to prevent oxidative stress – what about anti-oxidant foods like green tea, dark choc, blueberries, etc? 2) nonenzymatic glycation of proteins yielding advanced glycation end-products (AGEs); (Note: metformin falls under this category as an inhibitor of AGE. Not all drugs are bad.) I saw this article on another ng and reposted it here. Diabetes Metab. 2003 Sep;29(4 Pt 2):88-94. Mitochondrial metabolism and type-2 diabetes: a specific target of metformin. Leverve X, Guigas B, Detaille D, Batandier C, Koceir E, Chauvin C, Fontaine E, Wiernsperger N. INSERM E-0221 Bioenergetique Fondamentale et Appliquee, Universite Joseph-Fourier, Grenoble, France. Several links relate mitochondrial metabolism and type 2 diabetes or chronic hyperglycaemia. Among them, ATP synthesis by oxidative phosphorylation and cellular energy metabolism (ATP/ADP ratio), redox status and reactive oxygen species (ROS) production, membrane potential and substrate transport across the mitochondrial membrane are involved at various steps of the very complex network of glucose metabolism. Recently, the following findings (1) mitochondrial ROS production is central in the signalling pathway of harmful effects of hyperglycaemia, (2) AMPK activation is a major regulator of both glucose and lipid metabolism connected with cellular energy status, (3) hyperglycaemia by inhibiting glucose-6-phosphate dehydrogenase (G6PDH) by a cAMP mechanism plays a crucial role in NADPH/NADP ratio and thus in the pro-oxidant/anti-oxidant cellular status, have deeply changed our view of diabetes and related complications. It has been reported that metformin has many different cellular effects according to the experimental models and/or conditions. However, recent important findings may explain its unique efficacy in the treatment of hyperglycaemia- or insulin-resistance related complications. Metformin is a mild inhibitor of respiratory chain complex 1; it activates AMPK in several models, apparently independently of changes in the AMP-to-ATP ratio; it activates G6PDH in a model of high-fat related insulin resistance; and it has antioxidant properties by a mechanism(s), which is (are) not completely elucidated as yet. Although it is clear that metformin has non-mitochondrial effects, since it affects erythrocyte metabolism, the mitochondrial effects of metformin are probably crucial in explaining the various properties of this drug. PMID: 14502105 [PubMed - in process] Frank

Response:

Brad: thanks – so what do we do about it? Likely control BG to prevent oxidative stress – what about anti-oxidant foods like green tea, dark choc, blueberries, etc? 2) nonenzymatic glycation of proteins yielding advanced glycation end-products (AGEs); (Note: metformin falls under this category as an inhibitor of AGE. Not all drugs are bad.)

I saw this article on another ng and reposted it here. Diabetes Metab. 2003 Sep;29(4 Pt 2):88-94. Mitochondrial metabolism and type-2 diabetes: a specific target of metformin. Leverve X, Guigas B, Detaille D, Batandier C, Koceir E, Chauvin C, Fontaine E, Wiernsperger N. INSERM E-0221 Bioenergetique Fondamentale et Appliquee, Universite Joseph-Fourier, Grenoble, France. Several links relate mitochondrial metabolism and type 2 diabetes or chronic hyperglycaemia. Among them, ATP synthesis by oxidative phosphorylation and cellular energy metabolism (ATP/ADP ratio), redox status and reactive oxygen species (ROS) production, membrane potential and substrate transport across the mitochondrial membrane are involved at various steps of the very complex network of glucose metabolism. Recently, the following findings (1) mitochondrial ROS production is central in the signalling pathway of harmful effects of hyperglycaemia, (2) AMPK activation is a major regulator of both glucose and lipid metabolism connected with cellular energy status, (3) hyperglycaemia by inhibiting glucose-6-phosphate dehydrogenase (G6PDH) by a cAMP mechanism plays a crucial role in NADPH/NADP ratio and thus in the pro-oxidant/anti-oxidant cellular status, have deeply changed our view of diabetes and related complications. It has been reported that metformin has many different cellular effects according to the experimental models and/or conditions. However, recent important findings may explain its unique efficacy in the treatment of hyperglycaemia- or insulin-resistance related complications. Metformin is a mild inhibitor of respiratory chain complex 1; it activates AMPK in several models, apparently independently of changes in the AMP-to-ATP ratio; it activates G6PDH in a model of high-fat related insulin resistance; and it has antioxidant properties by a mechanism(s), which is (are) not completely elucidated as yet. Although it is clear that metformin has non-mitochondrial effects, since it affects erythrocyte metabolism, the mitochondrial effects of metformin are probably crucial in explaining the various properties of this drug. PMID: 14502105 [PubMed - in process] Frank

Response:

Brad: thanks – so what do we do about it? Likely control BG to prevent oxidative stress – what about anti-oxidant foods like green tea, dark choc, blueberries, etc?

You are on the right track for some of the oxidative stress mechanisms when you discuss diet/foods. There have been post to this ng on most of these mechanism to some degree or another. You can do Google searches on your own or search the Google groups archives at http://www.google.com/grphp. Address each of the four mechanisms individually. Search links for some journals where you might find something on these mechanisms: 1) http://diabetes.diabetesjournals.org/search.dtl 2) http://www.jbc.org/search.dtl 3) http://intl-jcem.endojournals.org/search.dtl 4) http://edrv.endojournals.org/search.dtl Quentin has written quite a few post that relate to the anti-oxidant aspects of foods, i.e, polyphenols. The following link includes more than his. http://groups.google.com/groups?q=polyphenols&ie=ISO-8859-1&hl=en&btn… I posted the following link: http://groups.google.com/groups?q=polyphenols&start=20&hl=en&lr=&ie=U… "What are the mechanisms that underlie the development of microvascular complications? … microvascular complications share a common pathophysiology. … four major pathways of glucose metabolism in the development of microvascular complications. … direct or indirect consequence of hyperglycemia-mediated superoxide overproduction by the mitochondrial electron transport chain. Either inhibition of superoxide accumulation or euglycemia restores the metabolic and vascular imbalance and blocks both the initiation and progression of complications." Source: Oxidative stress and diabetic neuropathy: a new understanding of an old problem – http://www.jci.org/cgi/content/full/111/4/431 These include: 1) increased polyol pathway activity leading to sorbitol and fructose accumulation, NAD(P)H-redox imbalances, and changes in signal transduction; http://groups.google.com/groups?q=polyol+pathway&hl=en&lr=&ie=UTF-8&s… 2) nonenzymatic glycation of proteins yielding advanced glycation end-products (AGEs); (Note: metformin falls under this category as an inhibitor of AGE. Not all drugs are bad.) http://groups.google.com/groups?hl=en&lr=&ie=ISO-8859-1&q=nonenzymati… 3) activation of PKC thereby initiating a cascade of stress responses, http://groups.google.com/groups?hl=en&lr=&ie=ISO-8859-1&q=activation+… and 4) increased hexosamine pathway flux. http://groups.google.com/groups?hl=en&lr=&ie=ISO-8859-1&q=hexosamine+… This kind of research can take a lot of time and energy. Enjoy! Frank

Response:

Frank, thanks – so what do we do about it? Likely control BG to prevent oxidative stress – what about anti-oxidant foods like green tea, dark choc, blueberries, etc?

This article speaks to the finding of lowering of iron stores down to the levels found commonly in vegetarians. Iron reduction therapy has been coined to be the FUTURE in effective antioxidant therapy due to its effectiveness and price. <

Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com Man Is A Herbivore! http://pages.ivillage.com/ironjustice/manisaherbivore DEAD PEOPLE WALKING http://pages.ivillage.com/ironjustice/deadpeoplewalking

Response:

Frank, thanks – so what do we do about it? Likely control BG to prevent oxidative stress – what about anti-oxidant foods like green tea, dark choc, blueberries, etc? – Hide quoted text — Show quoted text – "What are the mechanisms that underlie the development of microvascular complications? … microvascular complications share a common pathophysiology. … four major pathways of glucose metabolism in the development of microvascular complications. These include: 1) increased polyol pathway activity leading to sorbitol and fructose accumulation, NAD(P)H-redox imbalances, and changes in signal transduction; 2) nonenzymatic glycation of proteins yielding advanced glycation end-products (AGEs); 3) activation of PKC thereby initiating a cascade of stress responses, and 4) increased hexosamine pathway flux. While specific inhibitors of each pathway block one or more diabetic microvascular complications, only recently has a link been established that provides a unified mechanism of tissue damage. Each pathway becomes perturbed as a direct or indirect consequence of hyperglycemia-mediated superoxide overproduction by the mitochondrial electron transport chain. Either inhibition of superoxide accumulation or euglycemia restores the metabolic and vascular imbalance and blocks both the initiation and progression of complications." Source: Oxidative stress and diabetic neuropathy: a new understanding of an old problem http://www.jci.org/cgi/content/full/111/4/431 A graphic flow chart of the above mentioned mechanisms: Mechanisms leading to neuronal degeneration in hyperglycemia involve reactive oxygen species (ROS) formation. http://www.jci.org/content/vol111/issue4/images/large/JCI0317863.f1.jpeg Frank

Response:

"What are the mechanisms that underlie the development of microvascular complications? … microvascular complications share a common pathophysiology. … four major pathways of glucose metabolism in the development of microvascular complications. These include: 1) increased polyol pathway activity leading to sorbitol and fructose accumulation, NAD(P)H-redox imbalances, and changes in signal transduction; 2) nonenzymatic glycation of proteins yielding advanced glycation end-products (AGEs); 3) activation of PKC thereby initiating a cascade of stress responses, and 4) increased hexosamine pathway flux. While specific inhibitors of each pathway block one or more diabetic microvascular complications, only recently has a link been established that provides a unified mechanism of tissue damage. Each pathway becomes perturbed as a direct or indirect consequence of hyperglycemia-mediated superoxide overproduction by the mitochondrial electron transport chain. Either inhibition of superoxide accumulation or euglycemia restores the metabolic and vascular imbalance and blocks both the initiation and progression of complications." Source: Oxidative stress and diabetic neuropathy: a new understanding of an old problem http://www.jci.org/cgi/content/full/111/4/431 A graphic flow chart of the above mentioned mechanisms: Mechanisms leading to neuronal degeneration in hyperglycemia involve reactive oxygen species (ROS) formation. http://www.jci.org/content/vol111/issue4/images/large/JCI0317863.f1.jpeg Frank

Response:

Hulda's zapper and root canals

admin — Sun, 01 Jun 2003 00:00:00 +0000

Question:

Oh!, Then under those conditions, root canals should last indefinitely then. Is that a false assumption ? Rod.

– Hide quoted text — Show quoted text – Now you have noticed the flaw in the theory that teeth that have been treated with Root Canal Therapy are a safe harbor for bacteria. It is a false assumption. Teeth that have been endodontically treated are obturated (hermetically sealed) from within; most commonly with gutta percha and a sealer. There is nothing for the bacteria to metabolize (eat) and most sealers contain CaOH which is deadly to bacteria but quite innocuous to living human tissue, in fact it is beneficial to bone. So you have these conditions, no food source, and no space to expand or multiply in. Result ? dead bacteria, no colony, no infection, no reason to extract adequately endodontically treated teeth. No zapper required. If these bacteria survive in the holes and the holes are not porous- what do they eat? Anth And as all should know it’s the toxin that is more dangerous yeah but ya gotta have the organism to get the toxin?? right..more research…you do it,,and let me know!!! rb

Response:

Oh!, Then under those conditions, root canals should last indefinitely then. Is that a false assumption ? Rod.

REPLY: Yeah if the tooth doesn’t crack first! Joel

Response:

Once the teeth and colon have been colonized by *Clostridium*, they can not be easily eradicated. No immune power can reach the colony in the teeth; there is no circulation to the fillings. So all immune support fails.

`WHAT???? now is the great hulda clark talking about clostridium botulinum (ya know botulism??) or clostridium tetani (ya know..causes tetanus??) in neither case can this organism "colonize" a tooth.. in fact…the quote states there is NO circulation to the fillings…how then does she suppose such organisms got there in the FIRST place??? If it is tetani..aka lockjaw…one is in deep doodo…if botulism..well..we all know what happens if you get that.. yikes…I cannot believe you BELIEVE this crackpot enuf to actually quote such garbage..you both need a heavy duty course in pathophysiology.. seeping carinogens, y

what pray tell is a "seeping carinogens"…and if there IS no circulation…how could anything seep? They once were infected–before you had them *repaired*, Now they are infected again and must be removed.

again…but Jan…she says there IS NO circulation…so how did the evil pathogens gain entry?? probably a defective zapper.. On pages 463 and 467 she shows CT scans of two patients and explanation of what was found.

were said CT scans verified by a REAL honest to goodness doctor??? yikes… rb

Response:

A couple of days ago, Jan posted something which said that teeth were porous and that root canal therapy did something bad to the circulation of fluids into and out of teeth. I will dig out the message and post the relevant parts here. It will be interesting to see whether that post contradicts St Hulda’s claim about circulation. — The Millenium Project http://www.ratbags.com/rsoles The Green Light http://www.ratbags.com/greenlight

Response:

If these bacteria survive in the holes and the holes are not porous- what do they eat? Anth

– Hide quoted text — Show quoted text – And as all should know it’s the toxin that is more dangerous yeah but ya gotta have the organism to get the toxin?? right..more research…you do it,,and let me know!!! rb

Response:

If these bacteria survive in the holes and the holes are not porous- what do they eat? Anth

good one..maybe each other??? rb

Response:

Hulda Clark is a charlatan. The ‘zapper’ is a worthless device

I concur. See: http://www.uoguelph.ca/~kkolas/

Response:

So you have these conditions, no food source, and no space to expand or multiply in. Result ? dead bacteria, no colony, no infection, no reason to extract adequately endodontically treated teeth.

None of this matters to Hulda. If her Syncrometer detects Clostridium, that means it is present. Remember: "the Syncrometer

paging Teri Roberts

admin — Thu, 10 Apr 2003 00:00:00 +0000

Question:

- Hide quoted text — Show quoted text – MM has been THE leading migraine researcher for about the last 25 years. After I answered "boxingnut", I went to the link he provided only to "boxingnut" asked for. Apparently, he doesn’t read what he posts. Also, one needs to have a background in medicine in order to understand MM’s writings. MM, with the help of others, provided the theoretical basis for sumatriptan, btw. That’s his contribution. Only took a couple of decades. Hi, Richard. As Jack said, Dr. Moskowitz is a pioneer researcher and theorist. Looking at the URL you posted, it looks as if some of his current work could also lead to more effective preventives. There are links on that page to abstracts of his publications. You might find them interesting reading. I know I’ll be marking that page so I can go back and read them. Teri This is for Teri or anyone else who might know more about this Doctors’ research. His name is Moskowitz and here is a website I’ve had for some time on him. I can’t find anything else and I’d like to know if anyone else does. He seems to be working on a more precise targeting of the origin point of the migraine process and looking to develop more specific classes of drugs to abort the process. http://research.neurosurgery.mgh.harvard.edu/moskowitz.htm Thanks Richard the Hubby

Thanks Jack. I tried going through the articles attributed with MM but I couldn’t really decipher them to my satisfaction. I was hoping someone might have more info in layman’s terms I could access. Sounds like he’s on the right track. My wife can’t tolerate the triptans. She gets very unbearable chest pain and has even broken into hives. I’m hoping a new class of medication, which is more specific, will soon be available. Richard The Hubby

Response:

MM has been THE leading migraine researcher for about the last 25 years. After I answered "boxingnut", I went to the link he provided only to "boxingnut" asked for. Apparently, he doesn’t read what he posts. Also, one needs to have a background in medicine in order to understand MM’s writings. MM, with the help of others, provided the theoretical basis for sumatriptan, btw. That’s his contribution. Only took a couple of decades. – Hide quoted text — Show quoted text – Hi, Richard. As Jack said, Dr. Moskowitz is a pioneer researcher and theorist. Looking at the URL you posted, it looks as if some of his current work could also lead to more effective preventives. There are links on that page to abstracts of his publications. You might find them interesting reading. I know I’ll be marking that page so I can go back and read them. Teri This is for Teri or anyone else who might know more about this Doctors’ research. His name is Moskowitz and here is a website I’ve had for some time on him. I can’t find anything else and I’d like to know if anyone else does. He seems to be working on a more precise targeting of the origin point of the migraine process and looking to develop more specific classes of drugs to abort the process. http://research.neurosurgery.mgh.harvard.edu/moskowitz.htm Thanks Richard the Hubby

Response:

Hi, Richard. As Jack said, Dr. Moskowitz is a pioneer researcher and theorist. Looking at the URL you posted, it looks as if some of his current work could also lead to more effective preventives. There are links on that page to abstracts of his publications. You might find them interesting reading. I know I’ll be marking that page so I can go back and read them. Teri

– Hide quoted text — Show quoted text – This is for Teri or anyone else who might know more about this Doctors’ research. His name is Moskowitz and here is a website I’ve had for some time on him. I can’t find anything else and I’d like to know if anyone else does. He seems to be working on a more precise targeting of the origin point of the migraine process and looking to develop more specific classes of drugs to abort the process. http://research.neurosurgery.mgh.harvard.edu/moskowitz.htm Thanks Richard the Hubby

Response:

If you’re talking about Michael Moskowitz at Harvard neurolgy, he’s one of the leading theorist in migraine research, and the trigemino-vascular theory (current theory) is attributable to him. Jack – Hide quoted text — Show quoted text – This is for Teri or anyone else who might know more about this Doctors’ research. His name is Moskowitz and here is a website I’ve had for some time on him. I can’t find anything else and I’d like to know if anyone else does. He seems to be working on a more precise targeting of the origin point of the migraine process and looking to develop more specific classes of drugs to abort the process. http://research.neurosurgery.mgh.harvard.edu/moskowitz.htm Thanks Richard the Hubby

Response:

This is for Teri or anyone else who might know more about this Doctors’ research. His name is Moskowitz and here is a website I’ve had for some time on him. I can’t find anything else and I’d like to know if anyone else does. He seems to be working on a more precise targeting of the origin point of the migraine process and looking to develop more specific classes of drugs to abort the process. http://research.neurosurgery.mgh.harvard.edu/moskowitz.htm Thanks Richard the Hubby

Response:

Have you tried any of the ergotamines such as DHE 45 or the Migranal for your wife? Michelle

– Hide quoted text — Show quoted text – MM has been THE leading migraine researcher for about the last 25 years. After I answered "boxingnut", I went to the link he provided only to "boxingnut" asked for. Apparently, he doesn’t read what he posts. Also, one needs to have a background in medicine in order to understand MM’s writings. MM, with the help of others, provided the theoretical basis for sumatriptan, btw. That’s his contribution. Only took a couple of decades. Hi, Richard. As Jack said, Dr. Moskowitz is a pioneer researcher and theorist. Looking at the URL you posted, it looks as if some of his current work could also lead to more effective preventives. There are links on that page to abstracts of his publications. You might find them interesting reading. I know I’ll be marking that page so I can go back and read them. Teri This is for Teri or anyone else who might know more about this Doctors’ research. His name is Moskowitz and here is a website I’ve had for some time on him. I can’t find anything else and I’d like to know if anyone else does. He seems to be working on a more precise targeting of the origin point of the migraine process and looking to develop more specific classes of drugs to abort the process. http://research.neurosurgery.mgh.harvard.edu/moskowitz.htm Thanks Richard the Hubby Thanks Jack. I tried going through the articles attributed with MM but I couldn’t really decipher them to my satisfaction. I was hoping someone might have more info in layman’s terms I could access. Sounds like he’s on the right track. My wife can’t tolerate the triptans. She gets very unbearable chest pain and has even broken into hives. I’m hoping a new class of medication, which is more specific, will soon be available. Richard The Hubby

Response:

1) Delayed inflammation in rat meninges: implications for migraine pathophysiology – Nitric oxide in humans (in the blood stream) has been found to cause migraines 4 to 6 hours after being administered. By introducing an enzyme to stop the formation of nitric oxide from that drug, two thirds of migraineurs had less painful headaches as a result. In a rat treated as though it were a human (which is pretty standard for drug development and pretty good as an indicator) levels of nitric oxide were induced in the brain. Then they watched what chemicals, etc. were secreted in the rat and where they occurred in order to find out what was doing the reaction. The conclusion was that it was the "dura mater", a layer of cells surrounding the brain, and not the brain itself, that was reacting to the presence of nitric oxide. They noticed this between 2 and 6 hours after administering the drug. The hypothesis is that the same effect happens in humans. This gives them 2 targets – to stop nitric oxide formation and to alleviate the reaction within the dura mater; also if the time delay allows treatment or not (once it’s started you may have to treat the symptoms and not the cause). – Hide quoted text — Show quoted text – This is for Teri or anyone else who might know more about this Doctors’ research. His name is Moskowitz and here is a website I’ve had for some time on him. I can’t find anything else and I’d like to know if anyone else does. He seems to be working on a more precise targeting of the origin point of the migraine process and looking to develop more specific classes of drugs to abort the process. http://research.neurosurgery.mgh.harvard.edu/moskowitz.htm Thanks Richard the Hubby

Response:

I believe much such information is in the Google archives. It’s very complicated, and requires a background for this material. Anyone REALLY interested could search Medline and Google. From Medline, one can order the original articles. They are also linked to by his site below. I don’t think I could write a laymans’s version of curent migraine theory. I’ve thought about it many times, but it requires I assume too much on the part of the reader to not compromise science without writing a basic science text——,no thank you. Those who are motivated can find it. After all, I’m not suggesting anyone drive to the library, park, walk, and hunt throught the stacks, before heading for the change machine to use the copier. Nothing that radical. Jack – Hide quoted text — Show quoted text – Maybe so. I have only just started looking into this and settled for a quickie translation of the published piece. What would be good is if you could contribute to the other thread on "Research into migraine" with a summary of his theories and the papers that have been published to follow it up. How about it? Then we can all benefit – I am only an "informed layman", after all, and not a doctor or pharmacologist. Moskowitz’s work came long before the nitric oxide ideas. Moskowitz’s theory, IMHO, is nowhere to be found in the text below: Jack 1) Delayed inflammation in rat meninges: implications for migraine pathophysiology – Nitric oxide in humans (in the blood stream) has been found to cause migraines 4 to 6 hours after being administered. By introducing an enzyme to stop the formation of nitric oxide from that drug, two thirds of migraineurs had less painful headaches as a result. In a rat treated as though it were a human (which is pretty standard for drug development and pretty good as an indicator) levels of nitric oxide were induced in the brain. Then they watched what chemicals, etc. were secreted in the rat and where they occurred in order to find out what was doing the reaction. The conclusion was that it was the "dura mater", a layer of cells surrounding the brain, and not the brain itself, that was reacting to the presence of nitric oxide. They noticed this between 2 and 6 hours after administering the drug. The hypothesis is that the same effect happens in humans. This gives them 2 targets – to stop nitric oxide formation and to alleviate the reaction within the dura mater; also if the time delay allows treatment or not (once it’s started you may have to treat the symptoms and not the cause). This is for Teri or anyone else who might know more about this Doctors’ research. His name is Moskowitz and here is a website I’ve had for some time on him. I can’t find anything else and I’d like to know if anyone else does. He seems to be working on a more precise targeting of the origin point of the migraine process and looking to develop more specific classes of drugs to abort the process. http://research.neurosurgery.mgh.harvard.edu/moskowitz.htm Thanks Richard the Hubby

Response:

Moskowitz’s work came long before the nitric oxide ideas. Moskowitz’s theory, IMHO, is nowhere to be found in the text below: Jack – Hide quoted text — Show quoted text – 1) Delayed inflammation in rat meninges: implications for migraine pathophysiology – Nitric oxide in humans (in the blood stream) has been found to cause migraines 4 to 6 hours after being administered. By introducing an enzyme to stop the formation of nitric oxide from that drug, two thirds of migraineurs had less painful headaches as a result. In a rat treated as though it were a human (which is pretty standard for drug development and pretty good as an indicator) levels of nitric oxide were induced in the brain. Then they watched what chemicals, etc. were secreted in the rat and where they occurred in order to find out what was doing the reaction. The conclusion was that it was the "dura mater", a layer of cells surrounding the brain, and not the brain itself, that was reacting to the presence of nitric oxide. They noticed this between 2 and 6 hours after administering the drug. The hypothesis is that the same effect happens in humans. This gives them 2 targets – to stop nitric oxide formation and to alleviate the reaction within the dura mater; also if the time delay allows treatment or not (once it’s started you may have to treat the symptoms and not the cause). This is for Teri or anyone else who might know more about this Doctors’ research. His name is Moskowitz and here is a website I’ve had for some time on him. I can’t find anything else and I’d like to know if anyone else does. He seems to be working on a more precise targeting of the origin point of the migraine process and looking to develop more specific classes of drugs to abort the process. http://research.neurosurgery.mgh.harvard.edu/moskowitz.htm Thanks Richard the Hubby

Response:

Maybe so. I have only just started looking into this and settled for a quickie translation of the published piece. What would be good is if you could contribute to the other thread on "Research into migraine" with a summary of his theories and the papers that have been published to follow it up. How about it? Then we can all benefit – I am only an "informed layman", after all, and not a doctor or pharmacologist. – Hide quoted text — Show quoted text – Moskowitz’s work came long before the nitric oxide ideas. Moskowitz’s theory, IMHO, is nowhere to be found in the text below: Jack 1) Delayed inflammation in rat meninges: implications for migraine pathophysiology – Nitric oxide in humans (in the blood stream) has been found to cause migraines 4 to 6 hours after being administered. By introducing an enzyme to stop the formation of nitric oxide from that drug, two thirds of migraineurs had less painful headaches as a result. In a rat treated as though it were a human (which is pretty standard for drug development and pretty good as an indicator) levels of nitric oxide were induced in the brain. Then they watched what chemicals, etc. were secreted in the rat and where they occurred in order to find out what was doing the reaction. The conclusion was that it was the "dura mater", a layer of cells surrounding the brain, and not the brain itself, that was reacting to the presence of nitric oxide. They noticed this between 2 and 6 hours after administering the drug. The hypothesis is that the same effect happens in humans. This gives them 2 targets – to stop nitric oxide formation and to alleviate the reaction within the dura mater; also if the time delay allows treatment or not (once it’s started you may have to treat the symptoms and not the cause). This is for Teri or anyone else who might know more about this Doctors’ research. His name is Moskowitz and here is a website I’ve had for some time on him. I can’t find anything else and I’d like to know if anyone else does. He seems to be working on a more precise targeting of the origin point of the migraine process and looking to develop more specific classes of drugs to abort the process. http://research.neurosurgery.mgh.harvard.edu/moskowitz.htm Thanks Richard the Hubby

Response:

~ Food Induced Cushings ~

admin — Wed, 05 Feb 2003 00:00:00 +0000

Question:

Are you getting enough Chromium Picolinate 200 mcg? This is supposed to relieve glucose intolerance. A deficiency of Chromium Picolinate can result in Adult Onset Diabetes. One other note, don’t eat Froot Loops Cereal in front of the TV set! Check out The Vitamin Shoppe online at www.vitaminshoppe.com or call 1-800-223-1216 and have them send you a catalog of all the fine products they have on sale for mail-order. I’d tell you to get other pills that they sell which would be beyond the scope of all medical practice but why don’t you get back to me here after you spend a few weeks taking Chromium Picolinate.

Response:

Hi Gang – PLEASE REPOST I’m posting this information to help with other peoples quest to try and pin down their symptoms. Please repost this to as many news groups and Cushings websites you may know of as it valuable information about a rare form of Cushings. Many of the symptoms of Cushings relate to many problems both physically and mentally. http://www.cushingssyndrome.org/search.asp Don’t let some of the medical terms be a detour to researching the symptoms online. Many many people go undiagnosed for years. GOOD NEWS I accidentally came across a mention of "Food Induced Cushings" researching articles about the "Salivary Cortisol Test". Meanwhile it can be found at: http://pituitarysociety.med.nyu.edu/raff.htm Cushings causes Cortisol (the flight or fight hormone) to be over produced. And when constantly released into the body can be very damaging and can cause different reactions depending on the person. I contacted Dr. Raff and explaining how I have been diagnosed with Cushings Disease with my high ACTH, Cortisol, and an MRI showing the benign tumor on my pituitary gland (in the brain). But the normal Cushings symptoms weren’t always consistent with the typical Cushings Disease because it occured whenever I ate food. The symptoms I experienced was immediately upon eating food. They are "brain fog", mood swing, lost, disorientation, confusion, body aches, skin sensitivity, depression, and sudden exhaution. The feeling is as if you have pulled two all nighters studying. This can last for 15 minutes to all day. I react very violently to high-glycemic foods and caffeine which I avoid. It has gradually gotten worse over the past year and I react now to all foods. It’s inconsistent though as to what foods will trigger the level of reaction. I thought I was allergic to sugar (glucose intolerant) or have hyperthyroidism (Graves disease) as it runs in my family. I was tested for these and many other things with none of them being positive. It turns out that my symptoms to not correlate to Food Induced Cushings because of having elevated ACTH levels. But this is such rare information that I wanted to post it to have record of it. (Incidentally he suggested that I may have developed early Type 2 Diabetes Mellitus but I have monitored my blood sugar levels – and still do – long before the Cushings diagnosis and they are very normal. So…the quest continues. I’ll be having an IPSS (inferior petrosal sinus sampling) test perfomed soon. Nevertheless – here is the responses the Dr. Hershal Raff and Dr. Andre Lacroix, some of the leading experts in the field of Food-induced Cushings: RESPONSE FROM DR. Hershal Raff BLNDHRSE – "Food-induced Cushing’s" is commonly thought of as the expression of aberrant (usually not expressed) receptors on the adrenal gland. The most common form is the expression of receptors for GIP (glucose-dependent insulinotropic peptide). GIP is released in response to food and is involved in the stimulation of insulin during a meal. Food-induced Cushing’s is NOT consistent with elevations in ACTH since this is a form of "ACTH-independent Cushing’s syndrome." It is called ACTH-independent because the adrenal is the primary cause of the disease – autonomous or GIP-stimulated cortisol inhibits ACTH release via negative feedback. The post-prandial symptoms you describe are probably not caused by cortisol. However, it is possible that you have developed secondary diabetes due to cortisol-induced inhibition of insulin-stimulated glucose uptake. Have you ever had a post-meal blood glucose and insulin level done? That would definitely be worth doing – you may have early Type 2 Diabetes Mellitus secondary to cortisol excess. Food-induced Cushing’s is definitely not caused by a pituitary tumor and usually does not cause the acute symptoms that you describe. [Getting inferior petrosal sinus sampling (IPSS)] is EXACTLY what we would do (assuming that your urine free cortisol and bedtime salivary cortisols are elevated and that your plasma ACTH is not suppressed). Dr. Raff. Dr. Hershel Raff. Professor of Medicine and Physiology, Medical College of Wisconsin Director, Endocrine Research Laboratory St. Luke’s Medical Center Milwaukee, Wisconsin RESPONSE FROM DR. ANDRE LACROIX BLNDHRSE – Dr Raff is right. GIP-dependent Cushing’s is an adrenal cause with suppressed ACTH. High cortisol levels often change appetite. In some patients with Cushing’s disease the normal stimulation of ACTH and cortisol which occurs after protein meals can be present in the pituitary ACTH-secreting tumor with elevations of cortisol and ACTH after meals. Dr. Lacroix Dr, Andre Lacroix, m.d. Chairman, Department of Medicine of CHUM Professor of Medicine Head, Laboratory of Endocrine Pathophysiology Research Center, H

~ Food Induced Cushings ~

admin — Wed, 05 Feb 2003 00:00:00 +0000

Question:

Response:

Hi Gang – ——————————– PLEASE REPOST ——————————– I’m posting this information to help with other peoples quest to try and pin down their symptoms. Please repost this to as many news groups and Cushings websites you may know of as it valuable information about a rare form of Cushings. Many of the symptoms of Cushings relate to many problems both physically and mentally. http://www.cushingssyndrome.org/search.asp Don’t let some of the medical terms be a detour to researching the symptoms online. Many many people go undiagnosed for years. ——————————– GOOD NEWS ——————————– I accidentally came across a mention of "Food Induced Cushings" researching articles about the "Salivary Cortisol Test". Meanwhile it can be found at: http://pituitarysociety.med.nyu.edu/raff.htm Cushings causes Cortisol (the flight or fight hormone) to be over produced. And when constantly released into the body can be very damaging and can cause different reactions depending on the person. I contacted Dr. Raff and explaining how I have been diagnosed with Cushings Disease with my high ACTH, Cortisol, and an MRI showing the benign tumor on my pituitary gland (in the brain). But the normal Cushings symptoms weren’t always consistent with the typical Cushings Disease because it occured whenever I ate food. The symptoms I experienced was immediately upon eating food. They are "brain fog", mood swing, lost, disorientation, confusion, body aches, skin sensitivity, depression, and sudden exhaution. The feeling is as if you have pulled two all nighters studying. This can last for 15 minutes to all day. I react very violently to high-glycemic foods and caffeine which I avoid. It has gradually gotten worse over the past year and I react now to all foods. It’s inconsistent though as to what foods will trigger the level of reaction. I thought I was allergic to sugar (glucose intolerant) or have hyperthyroidism (Graves disease) as it runs in my family. I was tested for these and many other things with none of them being positive. It turns out that my symptoms to not correlate to Food Induced Cushings because of having elevated ACTH levels. But this is such rare information that I wanted to post it to have record of it. (Incidentally he suggested that I may have developed early Type 2 Diabetes Mellitus but I have monitored my blood sugar levels – and still do – long before the Cushings diagnosis and they are very normal. So…the quest continues. I’ll be having an IPSS (inferior petrosal sinus sampling) test perfomed soon. Nevertheless – here is the responses the Dr. Hershal Raff and Dr. Andre Lacroix, some of the leading experts in the field of Food-induced Cushings: ——————————– RESPONSE FROM DR. Hershal Raff ——————————– BLNDHRSE – "Food-induced Cushing’s" is commonly thought of as the expression of aberrant (usually not expressed) receptors on the adrenal gland. The most common form is the expression of receptors for GIP (glucose-dependent insulinotropic peptide). GIP is released in response to food and is involved in the stimulation of insulin during a meal. Food-induced Cushing’s is NOT consistent with elevations in ACTH since this is a form of "ACTH-independent Cushing’s syndrome." It is called ACTH-independent because the adrenal is the primary cause of the disease – autonomous or GIP-stimulated cortisol inhibits ACTH release via negative feedback. The post-prandial symptoms you describe are probably not caused by cortisol. However, it is possible that you have developed secondary diabetes due to cortisol-induced inhibition of insulin-stimulated glucose uptake. Have you ever had a post-meal blood glucose and insulin level done? That would definitely be worth doing – you may have early Type 2 Diabetes Mellitus secondary to cortisol excess. Food-induced Cushing’s is definitely not caused by a pituitary tumor and usually does not cause the acute symptoms that you describe. [Getting inferior petrosal sinus sampling (IPSS)] is EXACTLY what we would do (assuming that your urine free cortisol and bedtime salivary cortisols are elevated and that your plasma ACTH is not suppressed). Dr. Raff. Dr. Hershel Raff. Professor of Medicine and Physiology, Medical College of Wisconsin Director, Endocrine Research Laboratory St. Luke’s Medical Center Milwaukee, Wisconsin ——————————– RESPONSE FROM DR. ANDRE LACROIX ——————————– BLNDHRSE – Dr Raff is right. GIP-dependent Cushing’s is an adrenal cause with suppressed ACTH. High cortisol levels often change appetite. In some patients with Cushing’s disease the normal stimulation of ACTH and cortisol which occurs after protein meals can be present in the pituitary ACTH-secreting tumor with elevations of cortisol and ACTH after meals. Dr. Lacroix Dr, Andre Lacroix, m.d. Chairman, Department of Medicine of CHUM Professor of Medicine Head, Laboratory of Endocrine Pathophysiology Research Center, H

Medication news 3.

admin — Wed, 23 Oct 2002 00:00:00 +0000

Question:

Interesting Stan "Sylvain Van der Walde" skrev i meddelandet news:LFEt9.2425$yK6.129620@newsfep1-win.server.ntli.net… – Hide quoted text — Show quoted text -> Depression Expert Column Series > Are Two Monoamines Better Than One for Depression? > William J. Burke, MD > Medscape Psychiatry & Mental Health 7(2), 2002.

Raynaud's Phenomenon

admin — Sat, 23 Mar 2002 00:00:00 +0000

Question:

Interesting! I have been diagnosed with Reynaud’s for about 5 years now. Had no idea it was related to also being diabetic!

Response:

Interesting! I have been diagnosed with Reynaud’s for about 5 years now. Had no idea it was related to also being diabetic!

I have been studying the effects of hemodilution due to the fact it seems to be ‘glorified’ .. bloodletting. I ran across this study for Raynaud’s .. It seems the ‘word’ hemodilution is used in various .. contexts. One context is .. extreme blood loss = hemodilution .. which to me would mean .. bloodletting .. ? Major blood loss, however,results in extreme hemodilution, and the transfusion of red blood cells may finally become necessary to maintain arterial oxygen content and to preserve tissue oxygenation. It seems it greatly improves circulation .. due to the ‘thinning’ of the blood. V.A. Mamurov Therapeutic effect of prolonged normovolemic hemodilution in patients with Raynaud’s disease 51 patients with Raynaud’s disease hase undergone prolonged normovolemic hemodilution (PNH) with a good effect. Disappearance of painful syndrome in 78,43% of cases, and a significant decrease of pains in 21,37% of cases was demonstrated. Complete healing of ulcero-necrotic defects of end phalanges of the hands was observed in 7 patients of 10 and partial – in 3. A significant remission of the disease in follow-up period was obtained. Thus, prolonged normovolemic hemodilution has resulted in significant improvement of short- and long-term results of treatment in patients with Raynaud’s disease. These aricles speak to the effects of hemodilution. It seems even ‘extreme’ anemia does not affect the oxygen in the blood at all.. ? Vestn Khir Im I I Grek 1991 Jun;146(6):33-6 [Blood rheological disorders in patients with postthrombotic disease and the means for their correction]. [Article in Russian] Kargin VD, Khlebnikov VA, Fregatova LM An analysis of results of rheological properties of blood in 45 patients with different forms of postthrombotic disease of lower extremities has shown that 78% of the patients have erythrocytosis and all the patients have hyperviscosity shifts. Correction of the hemorheological changes by the methods of transfusion therapy (plasmapheresis, exfusion of blood, hemodilution) allowed to reduce the microcirculatory disorders in the diseased extremity in this group of patients. PMID: 1668489, UI: 92377110 Save the above report in [Macintosh] [Text] format Order documents on this page through Loansome Doc Int Angiol 1986 Jul-Sep;5(3):151-4 Isovolemic hemodilution: a therapeutical intervention for improving microcirculation. Rudofsky G A controlled reduction of hematocrit levels can be of value in the conservative treatment of inoperable arterial occlusive disease in advanced clinical stages. Long term success can be achieved in up to nearly 50%. The more and the longer the occlusions, the poorer the results. PMID: 3559316, UI: 87167905 Save the above report in [Macintosh] [Text] format Order documents on this page through Loansome Doc Angiology 1986 Feb;37(2):124-7 Peripheral vascular disease: flow studies and clinical results after isovolemic hemodilution–case reports. Caputi CA, De Carolis G The authors, after a brief introduction concerning hemorheology pathophysiology, report the results of a study on 18 patients suffering from vascular disease at the second, third and fourth stage (Fontaine) who underwent isovolemic hemodilution therapy. The Travis Winsor index (evaluated by Doppler ultrasound) and the perfusion volume (evaluated by impedance rheography) were both significantly increased after treatment. In some patients such increase were also associated with a reduction of subjective symptoms. PMID: 3954151, UI: 86156986 Save the above report in [Macintosh] [Text] format Order documents on this page through Loansome Doc Acta Med Austriaca 1991;18 Suppl 1:23-7 [Hyper- or isovolemic hemodilution in patients with stage II peripheral arterial occlusive disease]. [Article in German] Kiesewetter H, Jung F, Blume J, Spitzer S, Birk A Abteilung fur Klinische Hamostaseologie und Transfusionsmedizin, Universitat des Saarlandes, Homburg Saar, BRD. The influence of hyper- and isovolaemic hemodilution using HES 200/0.5 6% (HES steril, Fresenius AG) on pain-free walking distance in patients with peripheral arterial occlusive disease stage II according to Fontaine was tested in a randomised investigation involving three groups. The increase in pain-free walking distance was significant both in the hypervolaemic and isovolaemic hemodilution group. The increase in both dilution groups did not differ but compared to a control group (infusion of Ringer lactate) it was significantly higher. Considerable changes concerning rheological parameters (decrease in haematocrit and plasma viscosity) were observed after isovolaemic hemodilution. Publication Types: * Clinical trial * Randomized controlled trial PMID: 1719729, UI: 92057498 Save the above report in [Macintosh] [Text] format Order documents on this page through Loansome Doc Vestn Khir Im I I Grek 1987 Sep;139(9):19-24 [Dynamics of regional blood circulation in normovolemic hemodilution in patients with arterial occlusive diseases]. [Article in Russian] Kuznetsov NA, Bogdanov AE Normovolemic hemodilution was used in 81 patients as preparation to reconstructive operation for the occlusion of main arteries of extremities. Regional hemodynamics was studied in 18 of them. It was established that acute hemodilution substantially increased the volume and tissue blood flow, regional systolic arterial pressure distal to the occlusion of the main vessel and reestablished the vessel tone. The oxygen transport became normal in the zones with preserved main blood flow and considerably increased in the places distal to the occlusion of the main artery. PMID: 3441964, UI: 88159982 Save the above report in [Macintosh] [Text] format Order documents on this page through Loansome Doc HYPEROXIA IN EXTREME HEMODILUTION O. Habler , K. Me

Rich Murray: Stoll: Omega-3 fatty acids from flaxseed oil for bipolar disorder May 1999 3.28.1 rmforall

admin — Wed, 28 Mar 2001 00:00:00 +0000

Question:

Rich Murray: Stoll: Omega-3 fatty acids from flaxseed oil for bipolar disorder May 1999 3.28.1 rmforall March 28 2001 Hello Lloyd, Why not try 4 Tbs flaxseed oil daily? Be sure to drink only distilled or deionized water, to reduce arsenic, lead, mercury, fluoride, etc. 1943 Otowi Road Santa Fe NM 87505 505-986-9103 Prostaglandins Leukot Essent Fatty Acids 1999 May-Jun;60(5-6):329-37 Omega-3 fatty acids and bipolar disorder: a review. Stoll AL, Locke CA, Marangell LB, Severus WE Psychopharmacology Research Laboratory, McLean Hospital, Belmont, MA 02478, USA. The important role of the omega-3 fatty acids in the pathophysiology and treatment of bipolar disorder is now supported by a substantial body of indirect and direct evidence. This paper will describe the clinical and pharmacological features of bipolar disorder, review the available data regarding omega-3 fatty acids in bipolar disorder and provide recommendations for future research. Publication Types: Review Review, tutorial PMID: 10471117 Arch Gen Psychiatry 1999 May;56(5):407-12 Omega 3 fatty acids in bipolar disorder: a preliminary double-blind, placebo-controlled trial. Stoll AL, Severus WE, Freeman MP, Rueter S, Zboyan HA, Diamond E, Cress KK, Marangell LB Brigham and Women’s Hospital, Department of Psychiatry Harvard Medical School, Boston, BACKGROUND: Omega3 fatty acids may inhibit neuronal signal transduction pathways in a manner similar to that of lithium carbonate and valproate, 2 effective treatments for bipolar disorder. The present study was performed to examine whether omega3 fatty acids also exhibit mood-stabilizing properties in bipolar disorder. METHODS: A 4-month, double-blind, placebo-controlled study, comparing omega3 fatty acids (9.6 g/d) vs placebo (olive oil), in addition to usual treatment, in 30 patients with bipolar disorder. RESULTS: A Kaplan-Meier survival analysis of the cohort found that the omega3 fatty acid patient group had a significantly longer period of remission than the placebo group (P = .002; Mantel-Cox). In addition, for nearly every other outcome measure, the omega3 fatty acid group performed better than the placebo group. CONCLUSION: Omega3 fatty acids were well tolerated and improved the short-term course of illness in this preliminary study of patients with bipolar disorder. Publication Types: Clinical trial Randomized controlled trial Comment in: Arch Gen Psychiatry. 1999 May;56(5):413-6 Arch Gen Psychiatry. 2000 Jul;57(7):715 Arch Gen Psychiatry. 2000 Jul;57(7):716-7 PMID: 10232294 http://www.natmedpro.com/nmp/Bipolar.htm many nutrients http://www.windsofchange.com/ The Winds of Change Bipolar Disorder Support Group The Winds of Change, Inc., P.O. Box 251453 Plano, TX 75025-1453, Phone: 972-312-7772 http://bipolar.about.com/health/bipolar/index.htm?rnk=c1&terms=bipolar with Kimberly Bailey & Marcia Purse extensive links & http://www.drmcdougall.com/science/depression.html allergy to milk products and high-gluten foods (like wheat, barley, and rye) alt.support.depression.manic.moderated– 13 Sep 2000 by LyndaNP – View Thread http://www.medscape.com/medscape/cno/1999/APA/Story.cfm?story_id=704 1999 American Psychiatric Association Annual Meeting Day 4 – May 20, 1999 General Guidelines and Intricacies in the Treatment of Bipolar Disorder Frederick K. Goodwin, MD Writer: Tracey L. Irvin, MD Each psychiatrist should have a dietitian with whom they can consult on strategies for maintaining a diet low in simple carbohydrates in order to stabilize blood sugar. Patients with bipolar disorder tend to have unstable blood sugars, and many of the symptoms of hypoglycemia can be confused with those of the illness, or with side effects of the medication. In addition, patients should be encouraged to reduce their caffeine intake. Caffeine has the tendency to reduce the quality of sleep. This begins a vicious cycle in which decreased sleep quality leads to decreased daytime energy, leading to higher caffeine use. http://www.vegsource.com excellent diet info http://www.notmilk.com dairy toxicity http://www.litopia.com/jplant/ Jane Plant http://www.dorway.com aspartame toxicity http://www.truthinlabeling.org/ MSG toxicity http://www.soyonlineservice.co.nz soy toxicity http://www.thyroid-info.com Mary J. Shomon http://www.npwa.freeserve.co.uk/ fluoride toxicity http://www.electric-words.com/junk/junkindex.html junk science http://www.pbs.org/tradesecrets/transcript.html Moyers on chemicals

Response:

Rich Murray: Stoll: Omega-3 fatty acids from flaxseed oil for bipolar disorder May 1999 3.28.1 rmforall

Dr. Stoll used fish oil, not flaxseed oil, in his double-blind trial for bipolar disorder. See web page OMEGA-3 FATTY ACIDS & BIPOLAR DISORDER Highlights of a Lecture by Andrew L. Stoll, M.D., Director, Psychopharmacology Research Laboratory, McLean Hospital June 9, 1999 http://www.mddaboston.org/lect060999.html A citation: "In a double-blind study of 30 patients who were recently ill with bipolar disorder, Dr. Stoll found omega-3 fatty acids from concentrated fish oil to be an effective antidepressant and mood stabilizer. [...] Fish oil is currently the recommended source of omega-3. Flaxseed oil and perilla oil contain a different type of omega-3. Several cases of hypomania have occurred in people taking flaxseed oil, but the causes remain unclear." Other links: Omega-3 for Depression and Bipolar Suite101.com http://209.52.189.2/article.cfm/3694/48236 Omega-3 Fatty Acids Evaluated for Bipolar Disorder by Arline Kaplan Psychiatric Times December 1999 Vol. XVI Issue 12 http://www.mhsource.com/pt/p991211.html — Matti Narkia

Response:

I heard from someone who tried to use flax-seed oil as a mood stabiliser. He commented that it didn’t work for him.

– Hide quoted text — Show quoted text – Rich Rich Murray: Stoll: Omega-3 fatty acids from flaxseed oil for bipolar disorder May 1999 3.28.1 rmforall Dr. Stoll used fish oil, not flaxseed oil, in his double-blind trial for bipolar disorder. See web page OMEGA-3 FATTY ACIDS & BIPOLAR DISORDER Highlights of a Lecture by Andrew L. Stoll, M.D., Director, Psychopharmacology Research Laboratory, McLean Hospital June 9, 1999 http://www.mddaboston.org/lect060999.html A citation: "In a double-blind study of 30 patients who were recently ill with bipolar disorder, Dr. Stoll found omega-3 fatty acids from concentrated fish oil to be an effective antidepressant and mood stabilizer. [...] Fish oil is currently the recommended source of omega-3. Flaxseed oil and perilla oil contain a different type of omega-3. Several cases of hypomania have occurred in people taking flaxseed oil, but the causes remain unclear." Other links: Omega-3 for Depression and Bipolar Suite101.com http://209.52.189.2/article.cfm/3694/48236 Omega-3 Fatty Acids Evaluated for Bipolar Disorder by Arline Kaplan Psychiatric Times December 1999 Vol. XVI Issue 12 http://www.mhsource.com/pt/p991211.html — Matti Narkia

Response:

It really does take a Total System Chemistry Analysis (OVER TIME) to pull these stunts off. We are getting closer to understanding the variables. But that is all for the next decade or so. Sorry, rmg

I heard from someone who tried to use flax-seed oil as a mood stabiliser. He commented that it didn’t work for him.

Response:

Silicone allergy in ventriculoperitoneal shunts.

admin — Tue, 01 Aug 2000 00:00:00 +0000

Question:

Silicone allergy in ventriculoperitoneal shunts. Authors: Jimenez DF Keating R Goodrich JT Author Address: Department of Neurosurgery, Albert Einstein College of Medicine, Montefiore Medical Center, Bronx, NY 10467. Source: Childs Nerv Syst; VOL 10, ISS 1, 1994, P59-63 Abstract: Reported are the cases of three hydrocephalic patients who developed a clinically heterogenous entity with an allergic rejection of their silicone ventriculoperitoneal shunts. All of the patients had an original presentation indicative of a shunt infection, but laboratory analysis revealed sterile cerebrospinal fluid in all three cases. The typical course included recurrent skin breakdowns over the shunt tract, subsequent infections and development of fungating granulomas. Treatment, with successful resolution of the symptoms, included changing the shunt material from silicone to polyurethane, with immunosuppression in one patient and removal of the shunt altogether in the other two patients. The roles of the immune system and silicone in the pathophysiology of this condition are discussed.

Response:

Silicone allergy in ventriculoperitoneal shunts. Authors: JIMENEZ DF KEATING R GOODRICH JT Author Address: Div. Neurol. Surg., Dep. Surg., N 521 Health Sci. Cent., One Hospital Drive, Columbia, MO 65212, USA. Source: CHILD’S NERVOUS SYSTEM; 10 (1). 1994. 59-63. Abstract: BIOSIS COPYRIGHT: BIOL ABS. Reported are the cases of three hydrocephalic patients who developed a clinically heterogenous entity with an allergic rejection of their silicone ventriculoperitoneal shunts. All of the patients had an original presentation indicative of a shunt infection, but laboratory analysis revealed sterile cerebrospinal fluid in all three cases. The typical course included recurrent skin breakdowns over the shunt tract, subsequent infections and development of fungating granulomas. Treatment, with successful resolution of the symptoms, included changing the shunt material from silicone to polyurethane, with immunosuppression in one patient and removal of the shunt altogether in the other two patients. The roles of the immune system and silicone in the pathophysiology of this condition are discussed.