Posts belonging to Category 'Addiction Severity Index'

Did you hear the one about angiotensin blockers?

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That makes it a prophylaxis with some effect, but not a huge amount. What may be hidden is why the amount of people that actually reacted to this treatment did so. – Hide quoted text — Show quoted text – Tronvik E, Stovner LJ, Helde G, Sand T, Bovim G.  Prophylactic treatment of migraine with an angiotensin II receptor blocker: a randomized controlled trial.  JAMA 2003 Jan 1;289(1):65-9. Abstract:  CONTEXT: There is a paucity of effective, well-tolerated drugs available for migraine prophylaxis. OBJECTIVE: To determine whether treatment with the angiotensin II receptor blocker candesartan is effective as a migraine-prophylactic drug. DESIGN AND SETTING: Randomized, double-blind, placebo-controlled crossover study performed in a Norwegian neurological outpatient clinic from January 2001 to February 2002. PATIENTS: Sixty patients aged 18 to 65 years with 2 to 6 migraine attacks per month were recruited mainly from newspaper advertisements. INTERVENTIONS: A placebo run-in period of 4 weeks was followed by two 12-week treatment periods separated by 4 weeks of placebo washout. Thirty patients were randomly assigned to receive one 16-mg candesartan cilexetil tablet daily in the first treatment period followed by 1 placebo tablet daily in the second period. The remaining 30 received placebo followed by candesartan. MAIN OUTCOME MEASURES: The primary end point was number of days with headache; secondary end points included hours with headache, days with migraine, hours with migraine, headache severity index, level of disability, doses of triptans, doses of analgesics, acceptability of treatment, days of sick leave, and quality-of-life variables on the Short Form 36 questionnaire. RESULTS: In a period of 12 weeks, the mean number of days with headache was 18.5 with placebo vs 13.6 with candesartan (P =.001) in the intention-to-treat analysis (n = 57). Some secondary end points also favored candesartan, including hours with headache (139 vs 95; P<.001), days with migraine (12.6 vs 9.0; P<.001), hours with migraine (92.2 vs 59.4; P<.001), headache severity index (293 vs 191; P<.001), level of disability (20.6 vs 14.1; P<.001) and days of sick leave (3.9 vs 1.4; P =.01), although there were no significant differences in health-related quality of life. The number of candesartan responders (reduction of or =50% compared with placebo) was 18 (31.6%) of 57 for days with headache and 23 (40.4%) of 57 for days with migraine. Adverse events were similar in the 2 periods. CONCLUSION: In this study, the angiotensin II receptor blocker candesartan provided effective migraine prophylaxis, with a tolerability profile comparable with that of placebo. I haven’t a clue how that fits into the overall picture.  I suspect it applies to some special subset of migraineurs, and someday we will know which set and why.  The efect seems less robust that that for Coenzyme Q10, for example, but still seems significant.

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Tronvik E, Stovner LJ, Helde G, Sand T, Bovim G.  Prophylactic treatment of migraine with an angiotensin II receptor blocker: a randomized controlled trial.  JAMA 2003 Jan 1;289(1):65-9. Abstract:  CONTEXT: There is a paucity of effective, well-tolerated drugs available for migraine prophylaxis. OBJECTIVE: To determine whether treatment with the angiotensin II receptor blocker candesartan is effective as a migraine-prophylactic drug. DESIGN AND SETTING: Randomized, double-blind, placebo-controlled crossover study performed in a Norwegian neurological outpatient clinic from January 2001 to February 2002. PATIENTS: Sixty patients aged 18 to 65 years with 2 to 6 migraine attacks per month were recruited mainly from newspaper advertisements. INTERVENTIONS: A placebo run-in period of 4 weeks was followed by two 12-week treatment periods separated by 4 weeks of placebo washout. Thirty patients were randomly assigned to receive one 16-mg candesartan cilexetil tablet daily in the first treatment period followed by 1 placebo tablet daily in the second period. The remaining 30 received placebo followed by candesartan. MAIN OUTCOME MEASURES: The primary end point was number of days with headache; secondary end points included hours with headache, days with migraine, hours with migraine, headache severity index, level of disability, doses of triptans, doses of analgesics, acceptability of treatment, days of sick leave, and quality-of-life variables on the Short Form 36 questionnaire. RESULTS: In a period of 12 weeks, the mean number of days with headache was 18.5 with placebo vs 13.6 with candesartan (P =.001) in the intention-to-treat analysis (n = 57). Some secondary end points also favored candesartan, including hours with headache (139 vs 95; P<.001), days with migraine (12.6 vs 9.0; P<.001), hours with migraine (92.2 vs 59.4; P<.001), headache severity index (293 vs 191; P<.001), level of disability (20.6 vs 14.1; P<.001) and days of sick leave (3.9 vs 1.4; P =.01), although there were no significant differences in health-related quality of life. The number of candesartan responders (reduction of or =50% compared with placebo) was 18 (31.6%) of 57 for days with headache and 23 (40.4%) of 57 for days with migraine. Adverse events were similar in the 2 periods. CONCLUSION: In this study, the angiotensin II receptor blocker candesartan provided effective migraine prophylaxis, with a tolerability profile comparable with that of placebo. I haven’t a clue how that fits into the overall picture.  I suspect it applies to some special subset of migraineurs, and someday we will know which set and why.  The efect seems less robust that that for Coenzyme Q10, for example, but still seems significant.

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psoraxine, new promising drug?

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Exerpt from an article for a new drug which may be safer than the Remicades, Xanelim (monoclonal anti-body) and the new other treatments but along way off from being ready for use in the US. http://biz.yahoo.com/prnews/020204/nym040_1.html Astralis has completed clinical studies in Venezuela using PSORAXINE to treat nearly 3,000 Psoriasis patients, the majority of whom responded positively with few side effects. Of the nearly 3,000 treated patients, 638 achieved complete remission, while nearly half of all patients experienced a reduction in disease of between 70% and 90%, as measured by the Psoriasis Area and Severity Index (PASI), a validated outcomes measure. Overall, 96% of the patients had a positive response to PSORAXINE, although these results have not yet been independently verified. http://www.otcjournal.com/profiles/astr/20011009-1.html The three leading drugs; Amevive, Xanelim, and MEDI-507 are all monoclonal antibodies. None of these drugs could be considered a true vaccine, as the introduction of anitbodies into the bloodstream will eventually cause the body to build up an immunity to the treatments. Psoraxine, Astralis’s drug, is truly a vaccine. Psoraxine is a peptide developed because Astralis has identified a gene. Therefore, there will be no build up of immunity in the body. MEDI-507 is the leading candidate and most effective of the three drugs nearing the completion of the FDA Approval process. However, in clinical trials MEDI-507 was able to reduce the PASI value by 75% in 39% of cases. In clinical trials in Venezuela, Psoraxine was able to reduce PASI values by 75% in 74% of cases, making the drug twice as effective as the leading competitor. My take on this. Since the drug was not tested in the U.S. who knows exactly how well it really works, but let’s keep our fingers crossed. Son

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Exerpt from an article for a new drug which may be safer than the Remicades, Xanelim (monoclonal anti-body) and the new other treatments but along way off from being ready for use in the US. http://biz.yahoo.com/prnews/020204/nym040_1.html Astralis has completed clinical studies in Venezuela using PSORAXINE to treat nearly 3,000 Psoriasis patients, the majority of whom responded positively with few side effects. Of the nearly 3,000 treated patients, 638 achieved complete remission, while nearly half of all patients experienced a reduction in disease of between 70% and 90%, as measured by the Psoriasis Area and Severity Index (PASI), a validated outcomes measure. Overall, 96% of the patients had a positive response to PSORAXINE, although these results have not yet been independently verified.

The numbers are suspiciously close to the criteria the FDA uses. I’d love to believe in it, but the article was more about finance, and had only one other line about technology, and that struck me as a bit odd. Here’s hoping. J.

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What's new with Amevive?

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That was it! Thanks Kim. – Hide quoted text — Show quoted text – I wonder if that’s what I was getting in the last clinical trial I was in. It was mid 2000 to early 2001. I know it was a Biogen product but IIRC it was referred to as LFTP11 Yes, that was likely Amevive, which is just Biogen’s brand name (FWIW, the actual ‘drug name’ is Alefacept). Actual study name was LFA3TIP, referencing the part of the autoimmune system targetted. Kim The Psoriasis Newsgroup Resource FAQ can be found at               http://pfaq.cjb.net but will also be coming soon (twice a month) to a            newsgroup near you…

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I wonder if that’s what I was getting in the last clinical trial I was in. It was mid 2000 to early 2001. I know it was a Biogen product but IIRC it was referred to as LFTP11 or something along those lines. It was a weekly injection (yippee) but seemed to be working well. I could tell I was getting the real stuff as I was starting to clear. I ended up missing two injections near the end of the first part of the trial because I’d been sick so I never got completely cleared up. The second part of the trial there was no effect so I had to be getting placebo. I’d really hoped I’d get the real thing because it was working so well. Anyway, if it is the same thing I recommend biting the bullet and getting the injections when it’s available. You’ll feel like a pincushion but I find that preferable to people looking at you like you’re a leper or worse.

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I wonder if that’s what I was getting in the last clinical trial I was in. It was mid 2000 to early 2001. I know it was a Biogen product but IIRC it was referred to as LFTP11 or something along those lines. It was a weekly injection (yippee) but seemed to be working well. I could tell I was getting the real stuff as I was starting to clear. I ended up missing two injections near the end of the first part of the trial because I’d been sick so I never got completely cleared up. The second part of the trial there was no effect so I had to be getting placebo. I’d really hoped I’d get the real thing because it was working so well. Anyway, if it is the same thing I recommend biting the bullet and getting the injections when it’s available. You’ll feel like a pincushion but I find that preferable to people looking at you like you’re a leper or worse.

When you had the clearing did it return?

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Sorry I was just havning a bad day. I do like the sound of the no rebound effect. That in of itself might make it worth it. If it "cured" half and it never came back.. then the other half could be treated another way. I’d find it a God send..

It does return, but it’s supposed to take several months, on average. I gather this is better than with Enbrel, and it’s better than the other biotech drug in trials, Xanelim from Xoma, which they said worked faster but the psoriasis returned sooner. That’s why the most recent studies are for people getting it a second time, to see if it works again at all, or better, or what.   J.

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Yeah but only because I didn’t fully clear. It did seem to be slower coming back though. If I’d gotten the last two injections and gotten the real stuff instead of placebo the second half I believe I would’ve cleared completely. – Hide quoted text — Show quoted text – When you had the clearing did it return?

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I wonder if that’s what I was getting in the last clinical trial I was in. It was mid 2000 to early 2001. I know it was a Biogen product but IIRC it was referred to as LFTP11

Yes, that was likely Amevive, which is just Biogen’s brand name (FWIW, the actual ‘drug name’ is Alefacept). Actual study name was LFA3TIP, referencing the part of the autoimmune system targetted. Kim The Psoriasis Newsgroup Resource FAQ can be found at               http://pfaq.cjb.net but will also be coming soon (twice a month) to a            newsgroup near you…

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– Hide quoted text — Show quoted text – I find ~12% success in total clearing or almost clear kinda low…  Of the 53% that improved.. what exactlly is improve? Just a small patch 1 inch by 1 inch or something else?  What’s a "small number"? Ranter, Usually, I’m second to nobody in my cynicism about drug company reports.  However, there are a handfull of things about Amevive that make me more optimistic. The technology involved is supposed to be more focused than any previous treatment, and I like their story.  The anecdotal reports on this group have been quite positive, and there seem few reports of serious side-effects.  The latest report makes a point of saying no rebound has been observed, which is very interesting (if true, …), as it weighs on all of the crackpot theories we exchange around here. Yes, the most interesting issue is what "improvement" means, for those who don’t clear.  Heck, I’m suspicious about what "clear" means! Y’know, even mtx and Neoral don’t clear many people 100%, so what are we talking about?  Inquiring minds want to know. I still want to know what happens if someone takes Amevive and Enbrel at the same time.  I mean, besides having a lot of holes punched in them to take all the stuff.  Of course, it may be years before they do any trials on that, if it works, approve the combined treatment. I was really itching for Amevive (so to speak) a year ago.  The lower numbers reported do make it seem less promising, but I’m still hopeful.  Only, the FDA has some threshhold, 75% have to improve 50%, or something like that.  If Amevive doesn’t make those numbers, well, for its lower side-effects and to gain experience combining it with other treatments, I hope it might still be approved. Even if it is, sounds like it’s going to be expensive and (ouch!) painful.  Wish it could come in chewable, fruit-flavored tablets, or at least a once-a-year poke.  But, to me it seems promising as-is.

Sorry I was just havning a bad day. I do like the sound of the no rebound effect. That in of itself might make it worth it. If it "cured" half and it never came back.. then the other half could be treated another way. I’d find it a God send..

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FDA meeting on it in May. They’ve been all over the local news ralking about imminent approval since it ties in with their most recent earnings release http://www.biogen.com/site/content/releasespressrelease_subpage_156.asp

Thanks, Kim. I’ve been watching Biogen stock go down recently, some other drug of theirs (Avonex?) is having competitive pressures, nothing much else new for them but Amevive, … J.

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I find ~12% success in total clearing or almost clear kinda low…  Of the 53% that improved.. what exactlly is improve? Just a small patch 1 inch by 1 inch or something else?  What’s a "small number"?

Ranter, Usually, I’m second to nobody in my cynicism about drug company reports.  However, there are a handfull of things about Amevive that make me more optimistic. The technology involved is supposed to be more focused than any previous treatment, and I like their story.  The anecdotal reports on this group have been quite positive, and there seem few reports of serious side-effects.  The latest report makes a point of saying no rebound has been observed, which is very interesting (if true, …), as it weighs on all of the crackpot theories we exchange around here. Yes, the most interesting issue is what "improvement" means, for those who don’t clear.  Heck, I’m suspicious about what "clear" means! Y’know, even mtx and Neoral don’t clear many people 100%, so what are we talking about?  Inquiring minds want to know. I still want to know what happens if someone takes Amevive and Enbrel at the same time.  I mean, besides having a lot of holes punched in them to take all the stuff.  Of course, it may be years before they do any trials on that, if it works, approve the combined treatment. I was really itching for Amevive (so to speak) a year ago.  The lower numbers reported do make it seem less promising, but I’m still hopeful.  Only, the FDA has some threshhold, 75% have to improve 50%, or something like that.  If Amevive doesn’t make those numbers, well, for its lower side-effects and to gain experience combining it with other treatments, I hope it might still be approved. Even if it is, sounds like it’s going to be expensive and (ouch!) painful.  Wish it could come in chewable, fruit-flavored tablets, or at least a once-a-year poke.  But, to me it seems promising as-is. J.

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It’s waiting for FDA approval, … any news?  Anyone on one of the continuing trials, heard anything interesting? I found this, but it’s a month old already: … The clinical response to Amevive (alefacept) was consistent over repeated courses of treatment, suggesting that subsequent courses have a similar profile as the initial course of treatment. Patients received two courses of study therapy, and clinical response was evaluated at two weeks post dosing using the Psoriasis Area and Severity Index (PASI). Responses were observed within the first four weeks and tended to be more rapid with the second course of treatment. (more rapid, good!) There were no reports of disease rebound, a condition where a patient’s psoriasis becomes substantially more severe than at baseline once treatment is withdrawn. (no rebound!) Burt A. Adelman, M.D., Biogen’s Vice President of Medical Research, said, "The potential of Amevive to provide the needed long-term and sustained solution for patients with moderate to severe chronic psoriasis is an exciting discovery for us. These data move us closer to our final goal of improving both the duration of response and safety for patients with moderate to severe chronic plaque psoriasis. We are looking forward to the results of the Phase III clinical trials which will be available mid-year." (mid-year? come on Burt, hurry it up!) Amevive is a disease-modifying agent with a highly selective mode of action targeting a subset of T-cells – the memory effector T-cells – that play a critical role in the pathogenesis of psoriasis. Earlier Phase II trials yielded promising results including remission in some patients without rebound. To date more than 1,500 people have been treated with Amevive. (some, …) Psoriasis is a T-cell mediated inflammatory disorder of the skin that can cause considerable discomfort. It is a disease for which there is no cure and affects people of all ages. Psoriasis affects approximately two percent of the populations of European and North America. The rash of psoriasis consists of red, scaly areas that commonly occur on the scalp, elbows and knees. In moderate and severe cases, the involved areas can be extensive and cover a substantial percentage of a patient’s body. In addition, limited disease can be considered severe if occurring on critical areas such as the palms or soles. Although individuals with mild psoriasis can often control their disease with topical agents, more than one million patients worldwide require ultraviolet or systemic immunosuppressive therapy. (so, target market worldwide is on the order of 1,000,000) J.

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It’s waiting for FDA approval, … any news?  Anyone on one of the continuing trials, heard anything interesting? http://www.psoriasis.org/amevive.aug01.htm New psoriasis drug filed for FDA approval Review process for Amevive could take 12 months or more Biogen announced on Aug. 6, 2001, that it has submitted data to the U.S Food and Drug Administration (FDA) to evaluate the use of alefacept (pronounced uh-LEF-uh-sept, and also known by the brand name Amevive) for the treatment of moderate to severe plaque psoriasis. …

I always like their way with words  Reportedly, 28 patients (out of 229 in the phase II study) who received Amevive alone were clear or almost clear of psoriasis after 12 weeks of treatment. Overall, 53 percent of patients improved. The most frequently reported side effects included headache, itching and flu-like symptoms, but were in small numbers of patients. I find ~12% success in total clearing or almost clear kinda low…  Of the 53% that improved.. what exactlly is improve? Just a small patch 1 inch by 1 inch or something else?  What’s a "small number"?

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It’s waiting for FDA approval, … any news?  Anyone on one of the continuing trials, heard anything interesting?

http://www.psoriasis.org/amevive.aug01.htm New psoriasis drug filed for FDA approval Review process for Amevive could take 12 months or more Biogen announced on Aug. 6, 2001, that it has submitted data to the U.S Food and Drug Administration (FDA) to evaluate the use of alefacept (pronounced uh-LEF-uh-sept, and also known by the brand name Amevive) for the treatment of moderate to severe plaque psoriasis. … — Let’s see, it’s, um, still April now, May, June, July, August, … geez.  I thought two years ago it would be out in 2001.  Well, at least there’s more sunshine from now thru August, … J.

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It’s waiting for FDA approval, … any news?  Anyone on one of the continuing trials, heard anything interesting?

FDA meeting on it in May. They’ve been all over the local news ralking about imminent approval since it ties in with their most recent earnings release http://www.biogen.com/site/content/releasespressrelease_subpage_156.asp The Psoriasis Newsgroup Resource FAQ can be found at               http://pfaq.cjb.net but will also be coming soon (twice a month) to a            newsgroup near you…

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PA…Enbrel approval

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Hoping to get Enbrel very soon, I was on the list and recieved my Enbrel card over 6 months ago. I was just waiting for the approval. I am so happy I could scream. Imagine a life without dependency on narcotics. I wish everyone who is going to try this the very best. Peace and Love Lorraine

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Thank you too, Gloria, for making my day!                                             Be well,  Patty *~A friend is someone who reaches out for your hand, and touches your heart.~*

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ENBREL(R) (etanercept) Is First Therapy Approved for Treatment of Psoriatic Arthritis SEATTLE, Jan. 16 /PRNewswire-FirstCall/ — Immunex Corporation (Nasdaq: IMNX – news) and Wyeth-Ayerst Laboratories, a division of American Home Products (NYSE: AHP – news) announced today that the U.S. Food and Drug Administration (FDA) has approved ENBREL

Has Enbrel been officially approved for PA yet ?

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I have PA and know that it was not offically approved for PA a while back. Has it been at this point? Thanks, Scott

This is the latest that I am aware of. JDShine For Immediate Release, July 16, 2001 CONTACT: Robin Shapiro (media) Immunex 206.389.4040 Mark Leahy (investors) Immunex 206.389.4363 ENBREL

New treatment tests underway at UM – Alefacept

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– Hide quoted text — Show quoted text -Psoriasis treatment shown to clear or reduce painful skin symptoms Treatment gives lasting relief by targeting specific immune system reaction Unique therapy originated at University of Michigan; may go before FDA this year … Because alefacept uses the part of LFA-3 that attaches to CD2 on the surface of T cells, it completes that half of the handshake – and because it has two LFA-3 fragments close to one another, it only binds with memory effector T cells that have a high concentration of CD2. But, with the other half of LFA missing, the handshake with a dendritic cell is impossible. It’s almost as if the T cell is shaking hands with a fake hand-on-a-stick out of a circus clown’s routine. In the meantime, the immunoglobulin tail of the alefacept molecule sticks out, and signals natural killer cells and macrophages to come attack. When these cells spot the T cell on the other end of the alefacept molecule, they start a process that causes the T cell to self-destruct – a kind of cell death called apoptosis.

… Very nice, thanks! Go Wolverines! J.

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Psoriasis treatment shown to clear or reduce painful skin symptoms Treatment gives lasting relief by targeting specific immune system reaction Unique therapy originated at University of Michigan; may go before FDA this year  ANN ARBOR, MI – A specially designed molecule that blocks a specific immune-system reaction can significantly ease or clear the painful symptoms of psoriasis – relief that continues even after treatment stops, a newly published study finds. In this week’s New England Journal of Medicine, a multi-center team led by researchers from the University of Michigan Health System and the University of Utah Health Sciences Center report the promising results of a clinical trial of a unique targeted therapy called alefacept. The double-blind randomized trial evaluated three different doses of injected alefacept against placebo in 229 patients with chronic psoriasis. Patients who received alefacept experienced a sizable reduction in the severity of their psoriasis, and a corresponding reduction in specific cells of their immune systems. Psoriasis severity declined by about one-half, and a quarter of patients saw their skin clear completely or nearly so. Their relief usually lasted months after the 12-week treatment was over. The results help confirm that certain immune-system molecules play a key role in psoriasis, which stems from a runaway immune response in the skin and causes skin itching, redness, flaking, pain, and cracking in about 2 percent of the population, or 5.5 million people, each year. The new basic knowledge may help further improve treatment of the disease, which currently relies on broad-based anti-inflammation techniques with limited effectiveness or side effects. "It appears we now have what we’ve been looking for – a therapy that selectively works on the specific immune system components involved in psoriasis and is very safe," says Charles N. Ellis, M.D., who was selected to help design and lead the phase II study because of his long experience studying and treating the immune response in psoriasis. Ellis is associate chair of dermatology at UMHS and chief of dermatology at the VA Ann Arbor Healthcare System. Alefacept traces its roots to research done at the U-M in the mid-1990s by a team led by former dermatology faculty member Kevin D. Cooper, M.D. It is now being developed by Biogen, Inc. of Cambridge, MA under the product name Amevive, and has shown further promise in phase III trial results released by the company in June. It may be submitted to the Food and Drug Administration for review this year. Currently, it is not available to patients outside clinical trials. The U-M and Biogen share the patent on the engineered molecule with Cooper, who is now chair of dermatology at Case Western Reserve University. Ellis has no financial connection to the patent, and no patients in the study were treated at UMHS. Ellis shared leadership of the study with Gerald G. Krueger, M.D., a professor of dermatology at the University of Utah School of Medicine. Biogen, which funded the study, compensates Ellis and Krueger for consulting on the development and testing of the alefacept product. The study’s design included evaluation of symptoms using the physician-scored Psoriasis Area-and-Severity Index, or PASI, and blood tests showing the levels of certain immune system components before, during and after the 12 weeks of weekly injections. "We wanted to evaluate not only the clinical efficacy of alefacept, but also the response it provoked in the body’s immune response system at the cellular level," says Krueger. "Only in this way could we confirm that the molecule was producing the desired targeted effect. And indeed, we found it was." The results seen using this two-pronged approach help confirm that alefacept directly affects psoriasis-related inflammation through its specific immune-blocking action – without undercutting the rest of the immune system and its ability to fight off infection. Blood levels of certain immune-system cells were shown to drop at the same time that symptoms eased. The promise of a new tool against psoriasis, especially one that zeroes in on the immune response involved in the disease, is exciting, says Ellis. "This is a unique approach that targets a specific cell that drives the over-responsive immune system in psoriasis," he comments. Only in recent years have Cooper and others pieced together enough information about the intricate dance of molecular immunology to give the insight needed to design tailored treatments. The process started more than a decade ago when Ellis and colleagues performed research that led to a paradigm shift: instead of seeing psoriasis as the product of abnormal skin cells, they found that the disease was instead driven by immune system processes gone wild. This realization came from Ellis’ and others’ treatment of psoriasis with cyclosporine, a broad anti-immune response drug often given to organ transplant recipients. It also helped explain why standard treatments like topical creams, ultraviolet light therapy and methotrexate, a cancer drug, worked – they helped diminish the immune system’s runaway action and thereby decreased symptoms. Researchers have since found out that psoriasis depends on the successful completion of a particular "handshake" between immune system agents known as T cells and antigen-presenting, or dendritic, cells. The process starts when dendritic cells, which are a kind of master cell for immune response, show a protein called LFA-3 on their surface. The LFA-3 protein latches on to a receptor on the T cells called CD2, completing the handshake and prompting the T cells to set off on a path that leads to inflammation. As the process repeats, individual T cells can build up their level of surface CD2 and other proteins, earning them the name "memory effector cells" and making them more able to prompt inflammation. As a result, CD2-rich memory effector T cells are a good target in psoriasis treatment. Cooper’s research at UMHS, performed in conjunction with Biogen, helped piece together this specific knowledge and led to the realization that a new molecule could be designed to interfere with this crucial handshake. After several years of research, alefacept was developed. Alefacept’s targeted immunological action comes from its unique molecular design, a Y shape that combines the heads of two LFA-3 molecules with the tail of an immunoglobulin molecule that usually signals the immune system’s "attack dogs", called natural killer cells and macrophages, to come fight off invaders. Because alefacept uses the part of LFA-3 that attaches to CD2 on the surface of T cells, it completes that half of the handshake – and because it has two LFA-3 fragments close to one another, it only binds with memory effector T cells that have a high concentration of CD2. But, with the other half of LFA missing, the handshake with a dendritic cell is impossible. It’s almost as if the T cell is shaking hands with a fake hand-on-a-stick out of a circus clown’s routine. In the meantime, the immunoglobulin tail of the alefacept molecule sticks out, and signals natural killer cells and macrophages to come attack. When these cells spot the T cell on the other end of the alefacept molecule, they start a process that causes the T cell to self-destruct – a kind of cell death called apoptosis. "So, not only does alefacept block the handshake that makes inflammation possible – it also leads to the death of the very cells that are crucial to prompting that inflammation in the future," Ellis says. "Counts of memory-effector T cells in patients’ blood declined by about 50 percent. This reduction indicates that alefacept therapy may be called a disease-remitting treatment." This highly specific action is what might give alefacept an edge over other more standard treatments, Ellis suspects. No patients in the newly reported study experienced serious side effects, and the side effects that were noted occurred in only a slightly higher percentage of the patients who received alefacept than in patients who received a placebo. The same has been found in the recently released Phase III results. By comparison, cyclosporine can be toxic to kidneys, methotrexate can harm the liver, and UV therapy can increase the risk of skin cancer. The killing of memory effector T cells also appears to be important to alefacept’s lasting response. Some patients went more than a year without recurrence of their disease after completing treatment, while others experienced relief for months. Although no direct comparison was made, the maintenance of symptom reduction lasted longer than most psoriasis treatments typically provide, Ellis says. Other data not included in the new paper but presented recently by Ellis show that later retreatment with alefacept produced a similar effect as the first treatment, suggesting that the drug won’t diminish in effectiveness over time like some psoriasis treatments do. The reduction in symptoms without significant side effects that alefacept therapy provided also meant a boost to patients’ quality of life, Ellis adds. Research he presented at a recent scientific meeting showed alefacept recipients reported being less self-conscious about their skin’s appearance and less hampered by the physical symptoms. The new and promising alefacept treatment uses the latest basic knowledge about psoriasis to fight back at the disease process. But, says Ellis, there is more to learn – including the trigger that sets off the skin-inflaming condition in the first place. The genetic component, suspected because of the tendency of psoriasis to run in families, must still be found, as must the conditions that cause the initial and chronic flare-ups in specific patients. Alefacept is not currently being tested at UMHS, but patients interested in other psoriasis clinical trials at UMHS may call 734-764-DERM (3376). Written by … read more »

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Critique of "Clinical Outcomes of a Diagnostic and Treatment Protocol in Allergy/Sensitivity Patients"

Question:

Do you agree with all of the "points" made in John Bain’s <choke!! "rebuttal" of my critique of the Kail study? Please tell me this is all just one big joke, John!  You can’t be serious!

Completely serious Bubba.   You misunderstood the type of study.   Your objections were invalid. This was a perfectly acceptable Level II consecutive case series, not an RCT. Feel free to go over it point by point. I made the same rebuttal when TDN made her points. Best wishes — John Bain UK TV Sound Director, magnotherapy user & distributor http://members.aol.com/JBainSI/Magnotherapy.html Surround Sound for Television

Response:

– Hide quoted text — Show quoted text – Nice job, jbain. Let’s see if bubba can counter your points. Or will he just keep posting his belief that the study is junk science after you have refuted it? ..diane, Do you agree with all of the "points" made in John Bain’s <choke!! "rebuttal" of my critique of the Kail study? I said I thought jbain did a good job. That’s not what I asked!  Avoiding the tough questions again, ..diane?

No, Bubba, you do that…..just like you did below, instead of countering jbain’s refutation of your "argument". You don’t need to know whether I agree with jbain’s comments or not in order to address them. I thought he made some good points……further supported by the fact that no one has been able to counter them yet. Can you counter any of his points? I think John was just having fun with everyone here at MHA.  At least, I hope he was!

Sorry, Bubba, that is not countering his refutation of your "argument". So apparently you can’t. – Hide quoted text — Show quoted text – Bubba is a true (dis)believer. ..diane <BIG SNIP Please tell me this is all just one big joke, John!  You can’t be serious! Sorry, bubba, that doesn’t counter his points. Avoidance never does. Care to try again? Or shall we just take this as evidence that you can’t counter his points….. Just because I choose not to counter John Bain’s moronic "points" does not mean that I cannot do so.  It would be a complete waste of my time.

Your inability to counter his refutation of your argument is noted. which demonstrates that your belief that the study is junk science is baseless. Only in your mind, ..diane.

Not at all. You can’t counter his refutation of your "argument", so your argument is worthless. Therefore your belief is baseless. Any scientifically literate person would conclude that Kail’s study is junk science.

A scientifically literate person could support that conclusion if they presented it. But no scientifically literate person has either presented it or supported it. Moreover, I have a policy of not responding to the messages of those people who are in my kill-file.

Excuses, excuses. They don’t hide that you can’t counter his refutation of your "argument". Current kill-file occupants:

Bubba, I doubt anyone cares who is in your killfile. ..diane

Response:

- Hide quoted text — Show quoted text – Moreover, I have a policy of not responding to the messages of those people who are in my kill-file. Current kill-file occupants: John Bain Kaalga TheOtherOne On probation: Jan Drew gee, all bubba needs to do now is throw diane and BL into his filter too and he won’t have a soul to troll…er, talk to!!!! ((bubba filtered me during a discussion/debate about scientific proof of acupuncture’s efficiacy)) bubba, **for all of his love of percentages and how much proof a modality needs to be scientifically accepted**,  (ie replicated gold standard studies) apparently has a bit of a soft spot for acupuncture. so he doesn’t wish to be put in the MHA spotlight where his own beliefs in an unproven modality are concerned. i’m still wondering if he’s ever tried acupuncture for his allergies and what happened if he did…… anyway, bubba prefers to force the attention on NAET and ‘debate’ that issue with diane and BL. over and over and over and over again. ((i’m not sure why he keeps jan unfiltered. batting practice?)) i have **alot** of respect for the posters who will actually take the time to civilly and as honestly as possible discuss acupunture here at mha. (ian goddard, anthony campbell, greg dember, even ole henry) sadly, they don’t stick around very long….and these other boys are too chicken…… bawk…bawk bawk bawk…… <G — Red meat is NOT bad for you. Now blue-green meat, THAT’S bad for you! Tommy Smothers considering acupuncture? read this:  http://skepdic.com/acupunc.html

Bubba is as obsessed as Rich. Time to let it go. Jan

Response:

Moreover, I have a policy of not responding to the messages of those people who are in my kill-file. Current kill-file occupants: John Bain Kaalga TheOtherOne On probation: Jan Drew

gee, all bubba needs to do now is throw diane and BL into his filter too and he won’t have a soul to troll…er, talk to!!!! ((bubba filtered me during a discussion/debate about scientific proof of acupuncture’s efficiacy)) bubba, **for all of his love of percentages and how much proof a modality needs to be scientifically accepted**,  (ie replicated gold standard studies) apparently has a bit of a soft spot for acupuncture. so he doesn’t wish to be put in the MHA spotlight where his own beliefs in an unproven modality are concerned. i’m still wondering if he’s ever tried acupuncture for his allergies and what happened if he did…… anyway, bubba prefers to force the attention on NAET and ‘debate’ that issue with diane and BL. over and over and over and over again. ((i’m not sure why he keeps jan unfiltered. batting practice?)) i have **alot** of respect for the posters who will actually take the time to civilly and as honestly as possible discuss acupunture here at mha. (ian goddard, anthony campbell, greg dember, even ole henry) sadly, they don’t stick around very long….and these other boys are too chicken…… bawk…bawk bawk bawk…… <G — Red meat is NOT bad for you. Now blue-green meat, THAT’S bad for you! Tommy Smothers considering acupuncture? read this:  http://skepdic.com/acupunc.html

Response:

Nice job, jbain. Let’s see if bubba can counter your points. Or will he just keep posting his belief that the study is junk science after you have refuted it? ..diane, Do you agree with all of the "points" made in John Bain’s <choke!! "rebuttal" of my critique of the Kail study?

I said I thought jbain did a good job. Can you counter any of his points? Bubba is a true (dis)believer. ..diane <BIG SNIP Please tell me this is all just one big joke, John!  You can’t be serious!

Sorry, bubba, that doesn’t counter his points. Avoidance never does. Care to try again? Or shall we just take this as evidence that you can’t counter his points…..which demonstrates that your belief that the study is junk science is baseless. ..diane

Response:

– Hide quoted text — Show quoted text – Nice job, jbain. Let’s see if bubba can counter your points. Or will he just keep posting his belief that the study is junk science after you have refuted it? ..diane, Do you agree with all of the "points" made in John Bain’s <choke!! "rebuttal" of my critique of the Kail study? I said I thought jbain did a good job.

That’s not what I asked!  Avoiding the tough questions again, ..diane? Can you counter any of his points?

I think John was just having fun with everyone here at MHA.  At least, I hope he was! – Hide quoted text — Show quoted text – Bubba is a true (dis)believer. ..diane <BIG SNIP Please tell me this is all just one big joke, John!  You can’t be serious! Sorry, bubba, that doesn’t counter his points. Avoidance never does. Care to try again? Or shall we just take this as evidence that you can’t counter his points…..

Just because I choose not to counter John Bain’s moronic "points" does not mean that I cannot do so.  It would be a complete waste of my time. which demonstrates that your belief that the study is junk science is baseless.

Only in your mind, ..diane.  Any scientifically literate person would conclude that Kail’s study is junk science. Moreover, I have a policy of not responding to the messages of those people who are in my kill-file. Current kill-file occupants: John Bain Kaalga TheOtherOne On probation: Jan Drew ..diane

– Bubba "Friends don’t let friends use NAET (Nambudripad’s Allergy Elimination Techniques)."

Response:

Nice job, jbain. Let’s see if bubba can counter your points. Or will he just keep posting his belief that the study is junk science after you have refuted it?

..diane, Do you agree with all of the "points" made in John Bain’s <choke!! "rebuttal" of my critique of the Kail study? Bubba is a true (dis)believer. ..diane

<BIG SNIP Please tell me this is all just one big joke, John!  You can’t be serious! — Bubba For email, take out the dog.

Response:

Nice job, jbain. Let’s see if bubba can counter your points. Or will he just keep posting his belief that the study is junk science after you have refuted it? Bubba is a true (dis)believer. ..diane

– Hide quoted text — Show quoted text – Altern Med Rev 2001 Apr;6(2):188-202 Clinical outcomes of a diagnostic and treatment protocol in allergy/sensitivity patients. Kail K. <snip I have listed several of the problems with this study that I have been able to identify.  (NOTE: This list is not exhaustive.) (1) There were no controls used in this study. It is a Level II case series.   They do not have controls by definition. Look it up in the Levels of Evidence. (2) The study was not blinded (single or double). Ditto, case series do not have controls.   They are patients as they walk through the door. (3) The subjects paid for the treatment. "Average cost of the desensitization protocol (all costs included) was $822.16."  It is reasonable to assume that study subjects who must pay for a treatment are more likely to believe that the treatment was effective than if the same subjects had participated in a study in which there was no charge for the treatment. Ditto again.   This is a case series, an unbroken stream of patinets as they walked through the doors of the clinic. (4) An instrument (the Allergy Symptom Severity Index) was developed by the author of this study to measure the symptomatic improvement in the subjects of this study.  This instrument has never been validated. Irrelevant, it is the change in ASSI that proves the point.  If the instrument were invalid, there would be no difference in scores.   89% of patients rated the results of the treatment good to excellent. (5) Treatment in addition to the desensitization protocol was provided that could have been responsible for some percentage or possibly all of the subjects’ reported symptomatic improvement: Irrelevant, the total treatment was provided by the practitioner.   It was all part of the treatment he applies. (6) During the course of the study, there were changes in the medications that the patients were taking.  These medication changes have the potential to confound the results of the study, because these medications likely also produce "symptoms of allergy/sensitivity disease." All part of the treatment.   The total treatment was effective. This was a case series, not a controlled study aimed at finding what parts of the treatment were necessary. (7) There is no credible evidence that the subjects in this study actually had allergies or sensitivities.  According to Kail, the subjects were "suffering from symptoms of allergy/sensitivity disease."  Symptoms of allergies and sensitivities are nonspecific.  One can have symptoms of allergies or sensitivities and have neither allergies nor sensitivities. They presented with what they called allergies or sensitivities, which were identifiable by the practitioner. They left satisfied that the condition was ‘cured’. The treatment was successful. The best possible outcome in a case series. Therefore, the title of Kail’s study – "Clinical outcomes of a diagnostic and treatment protocol in allergy/sensitivity patients" – misrepresents the facts that are presented in the text of the study. Nope, the patients presented with allergies or sensitivities. That’s why they went to the practitioner. The outcomes of the treatment were reported. Perfectly straightforward case series. Bubba doesn’t seem to understand the difference between a case series and an RCT. Case series of this type are included in ‘evidence based medicine’. It is the only form of evidence an AM practitioner can supply. The conclusions stand. "This protocol demonstrated efficacy without serious toxicity and no long-term adverse effects. It is natural, non-invasive, and does not require long periods of avoidance of offending foods or environmental stimuli. The desensitization protocol is a low-cost, effective therapy for the treatment of patients suffering from symptoms of allergy/sensitivity disease. " Just needs independent verification now. Any bets on how long it will take? Best wishes — John Bain UK TV Sound Director, magnotherapy user & distributor http://members.aol.com/JBainSI/Magnotherapy.html Surround Sound for Television

Response:

There are a number of problems with a recent study that attempted to evaluate a treatment called NEAT.  This treatment is very similar to a treatment called NAET (Nambudripad’s Allergy Elimination Techniques). Altern Med Rev 2001 Apr;6(2):188-202 Clinical outcomes of a diagnostic and treatment protocol in allergy/sensitivity patients. Kail K.

To read the full text of this study, use the following URL: http://www.thorne.com/altmedrev/.fulltext/6/2/188.html — Bubba For email, take out the dog.

Response:

Altern Med Rev 2001 Apr;6(2):188-202 Clinical outcomes of a diagnostic and treatment protocol in allergy/sensitivity patients. Kail K. <snip I have listed several of the problems with this study that I have been able to identify.  (NOTE: This list is not exhaustive.) (1) There were no controls used in this study.

It is a Level II case series.   They do not have controls by definition.   Look it up in the Levels of Evidence. (2) The study was not blinded (single or double).

Ditto, case series do not have controls.   They are patients as they walk through the door. (3) The subjects paid for the treatment. "Average cost of the desensitization protocol (all costs included) was $822.16."  It is reasonable to assume that study subjects who must pay for a treatment are more likely to believe that the treatment was effective than if the same subjects had participated in a study in which there was no charge for the treatment.

Ditto again.   This is a case series, an unbroken stream of patinets as they walked through the doors of the clinic. (4) An instrument (the Allergy Symptom Severity Index) was developed by the author of this study to measure the symptomatic improvement in the subjects of this study.  This instrument has never been validated.

Irrelevant, it is the change in ASSI that proves the point.  If the instrument were invalid, there would be no difference in scores.   89% of patients rated the results of the treatment good to excellent. (5) Treatment in addition to the desensitization protocol was provided that could have been responsible for some percentage or possibly all of the subjects’ reported symptomatic improvement:

Irrelevant, the total treatment was provided by the practitioner.   It was all part of the treatment he applies. (6) During the course of the study, there were changes in the medications that the patients were taking.  These medication changes have the potential to confound the results of the study, because these medications likely also produce "symptoms of allergy/sensitivity disease."

All part of the treatment.   The total treatment was effective. This was a case series, not a controlled study aimed at finding what parts of the treatment were necessary. (7) There is no credible evidence that the subjects in this study actually had allergies or sensitivities.  According to Kail, the subjects were "suffering from symptoms of allergy/sensitivity disease."  Symptoms of allergies and sensitivities are nonspecific.  One can have symptoms of allergies or sensitivities and have neither allergies nor sensitivities.  

They presented with what they called allergies or sensitivities, which were identifiable by the practitioner. They left satisfied that the condition was ‘cured’. The treatment was successful. The best possible outcome in a case series. Therefore, the title of Kail’s study – "Clinical outcomes of a diagnostic and treatment protocol in allergy/sensitivity patients" – misrepresents the facts that are presented in the text of the study.

Nope, the patients presented with allergies or sensitivities.   That’s why they went to the practitioner. The outcomes of the treatment were reported. Perfectly straightforward case series. Bubba doesn’t seem to understand the difference between a case series and an RCT. Case series of this type are included in ‘evidence based medicine’. It is the only form of evidence an AM practitioner can supply. The conclusions stand. "This protocol demonstrated efficacy without serious toxicity and no long-term adverse effects. It is natural, non-invasive, and does not require long periods of avoidance of offending foods or environmental stimuli. The desensitization protocol is a low-cost, effective therapy for the treatment of patients suffering from symptoms of allergy/sensitivity disease. " Just needs independent verification now. Any bets on how long it will take? Best wishes — John Bain UK TV Sound Director, magnotherapy user & distributor http://members.aol.com/JBainSI/Magnotherapy.html Surround Sound for Television

Response:

There are a number of problems with a recent study that attempted to evaluate a treatment called NEAT.  This treatment is very similar to a treatment called NAET (Nambudripad’s Allergy Elimination Techniques). Altern Med Rev 2001 Apr;6(2):188-202 Clinical outcomes of a diagnostic and treatment protocol in allergy/sensitivity patients. Kail K. OBJECTIVES: This level II outcome study was conducted to examine the efficacy and toxicity of a diagnostic and treatment protocol using electrodermal screening (EDS) in allergy/sensitivity patients. METHODS: Ninety-six patients with a diagnosis of allergy or sensitivity entered the study between 1994 and 1998; 90 participants completed the study. All participants followed the same protocol, and all interactions were with a single clinician at a single site. The Allergy Symptom Severity Index (ASSI) was developed to record symptomatic information. EDS – conductance measurement 1/( – of specific acupuncture points was used as an objective endpoint (indicator of outcome) and for identification of antigens, according to Voll criteria. All measurements were taken before and after treatment, and EDS was carried out at all treatment sessions. Outcome criteria suggesting efficacy were reduction in ASSI score, reduction in number of items testing positive, and normalization of conductance measurements. A statistical analysis of the outcomes was performed using the student’s paired t-test. RESULTS: There was a statistically significant change in pre- and post-treatment measurements of the ASSI.  The conductance measurements normalized and the number of items testing positive decreased compared to pre-treatment testing. In addition to these parameters, 87.2 percent of subjects rated efficacy as good to excellent, and less than one-percent rated the outcome as poor. The outcome demonstrated longevity, meaning that people who had their post-treatment evaluation up to three years after primary treatment were still showing minimal ASSI scores, with no additional treatment. The treatment appeared to work equally well across age groups and gender. Forty-eight percent of participants had an aggravation of symptoms after treatment, lasting an average of 10 hours, with reactions described as mild to moderate. Average cost of the desensitization protocol (all costs included) was $822.16. CONCLUSIONS: This protocol demonstrated efficacy without serious toxicity and no long-term adverse effects. It is natural, non-invasive, and does not require long periods of avoidance of offending foods or environmental stimuli. The desensitization protocol is a low-cost, effective therapy for the treatment of patients suffering from symptoms of allergy/sensitivity disease. Publication Types: Clinical trial PMID: 11302781 I have listed several of the problems with this study that I have been able to identify.  (NOTE: This list is not exhaustive.) (1) There were no controls used in this study. (2) The study was not blinded (single or double). (3) The subjects paid for the treatment. "Average cost of the desensitization protocol (all costs included) was $822.16."  It is reasonable to assume that study subjects who must pay for a treatment are more likely to believe that the treatment was effective than if the same subjects had participated in a study in which there was no charge for the treatment. (4) An instrument (the Allergy Symptom Severity Index) was developed by the author of this study to measure the symptomatic improvement in the subjects of this study.  This instrument has never been validated. (5) Treatment in addition to the desensitization protocol was provided that could have been responsible for some percentage or possibly all of the subjects’ reported symptomatic improvement: "Therapy for support and repair of barrier (gut, mucus membranes, and skin) and associated organ dysfunctions was given." "Perhaps the most interesting finding is that these changes were accomplished with the application of acupressure, and use of homeopathic remedies which were never ingested by the participants. All changes occurred purely from an energy therapy. The only medications given were to support gut barrier integrity, digestive function, mucus membrane integrity, skin health, and organ balancing, in order to prevent re- sensitization. The desensitization protocol is a low cost, effective therapy for the treatment of patients suffering allergies and sensitivities." But earlier in the paper (in the "Hypothesis" section), Kail wrote the following: "People become sensitized to substances due to a breakdown in barrier functions (skin, mucus membranes, and digestion), which allows larger molecules into the bloodstream than would normally appear there, thus triggering a sensitivity response which causes inflammatory chemical release and resulting allergic symptoms." If Kail believes that the allergic symptoms were most likely the result of "a breakdown in barrier functions (skin, mucus membranes, and digestion)," then how can he claim that "(a)ll changes occurred purely from an energy therapy"?  According to Kail’s own hypothesis, the most likely explanation for the symptomatic improvement would be the (unnamed) medications given to the subjects "to support gut barrier integrity, digestive function, mucus membrane integrity, skin health, and organ balancing." (6) During the course of the study, there were changes in the medications that the patients were taking.  These medication changes have the potential to confound the results of the study, because these medications likely also produce "symptoms of allergy/sensitivity disease." "Patients reported discontinuing or decreasing pharmaceutical medication 52.2 percent of the time, and 69.3 percent were able to suspend office visits after treatment." (7) There is no credible evidence that the subjects in this study actually had allergies or sensitivities.  According to Kail, the subjects were "suffering from symptoms of allergy/sensitivity disease."  Symptoms of allergies and sensitivities are nonspecific.  One can have symptoms of allergies or sensitivities and have neither allergies nor sensitivities.   Although Kail states that the patients had "an established diagnosis of allergy/sensitivity disease," it appears that these diagnoses were made solely on the basis of the results from the use of the electrodermal screening device.  A recent study concluded that "(e)lectrodermal testing cannot be used to diagnose environmental allergies" (Is electrodermal testing as effective as skin prick tests for diagnosing allergies? A double blind, randomised block design study. Lewith GT, Kenyon JN, Broomfield J, Prescott P, Goddard J, Holgate ST. BMJ 2001 Jan 20;322(7279):131-4). Therefore, the title of Kail’s study – "Clinical outcomes of a diagnostic and treatment protocol in allergy/sensitivity patients" – misrepresents the facts that are presented in the text of the study. — Bubba For email, take out the dog.

Response:

TO ALL ALT.SUPPORT TINNITUS READERS: FROM MIKE COHEN

Question:

This one DID come from Mindspring Enterprises (Nagler’s daughter’s ISP) *************************************************************************** * Open Letter to Lix and Blue – You have turned this support and discussion forum into a cesspool. Grossan is gone. Gutnick is gone. And now I am gone. There is nobody left here who actually treats tinnitus patients. It’s the way you want it.  It’s the way you now have it. My congratulations. stephen nagler

Response:

TO ALL ALT.SUPPORT TINNITUS READERS: Here is a recently exchange between Mike Cohen of Israel and a gentleman from South America.  Mike came to Israel from Chicago 4 1/2 years ago to be treated by Dr. Shemesh at Hadassah Hospital. Recently married and recovered from tinnitus, he now edits an independent tinnitus-related newsletter, TINNITUS NEWSLETTER FROM ISRAEL.  Here lay people and professionals from around the world share tinnitus and related disorders ideas in an atmosphere of mutual respect. Lately in the newsletter and in private emails, the feasibility of Israeli distance treatment for tinnitus is being discussed as well as how people from around the world cope with tinnitus.  The newsletter also offers a valuable counterpoint to the "media-driven mania" of certain pricey treatments — popular but of dubious value. TINNITUS NEWSLETTER FROM ISRAEL is based on the ethical "We are all responsible for each other."  No names or email addresses are published without permission. For a free subscription, email Mike at: n…@netvision.net.il You may also visit his website at: http://tinnitus.itgo.com/Mike/mikecohen.htm ————————————– EMAIL RECEIVED ON MAY 16th:

Please send me more details on the treatment by distance. It’s very difficult for me to make the trip and stay en Israel so much time. I live in Venezuela, and suffer tinnitus for so many years.  It got worse, I’m afraid I cant stand it for much more time. I went to Atlanta, TRT didn’t work. I really need some help. Thank You.  [name withheld]

EMAIL RESPONSE ON MAY 16th: Thank you for your email.  I am sorry you are suffering so. Dr. Shemesh would like you to fax him directly at Hadassah Hospital and he will send you the details on the tinnitus distance treatment. Please fax him at: 011-972-2-677-6600 and include a fax number where he can fax back to you (or if you don’t have a fax, use a friend’s or somewhere where they will notify you when you receive a fax back, — plus include your name and your street address on the fax and maybe also include the information below). Kind wishes, Mike Cohen n…@netvision.net.il — Michael Cohen E-mail-  n…@netvision.net.il 45 Beersheva St.      Website- http://tinnitus.itgo.com/Mike/mikecohen.htm Jerusalem, 94507 Home phone-  011-972-2-625-9113 ISRAEL Cellular phone-  011-972-50-605-398

Response:

"Ray Ennis" <stela…@maui.net

wrote: TO ALL ALT.SUPPORT TINNITUS READERS: Here is a recently exchange between Mike Cohen of Israel and a gentleman from South America.  Mike came to Israel from Chicago 4 1/2 years ago to be treated by Dr. Shemesh at Hadassah Hospital. Recently married and recovered from tinnitus, he now edits an independent tinnitus-related newsletter, TINNITUS NEWSLETTER FROM ISRAEL.  Here lay people and professionals from around the world share tinnitus and related disorders ideas in an atmosphere of mutual respect.

……. Mike Cohen still has tinnitus … and so do you, Ray. Now Shemesh boasts a 90% CURE rate.  You and Mike are the greatest advocates of this treatments … so if you two are not "cured," something does not make sense. Please define for us what "recovered" means. stephen nagler

Response:

Don’t bother Mike or Ray…it only opens up the discussion for disproof by whatever method it takes and if they can’t do that he will discredit you as an asshole or whatever it takes. Listen to the sound again of a mind slamming shut? Why bother. It was slammed and locked when he went insane with his tinnitus. We all hear you and don’t need Nagler’s personal attacks on yourselves or your "cure". "Stephen Nagler" <nag…@tinn.com

wrote in message

news:6vctgt8mpv9a06fl8gs2dnr9bc8pohg9va@4ax.com… – Hide quoted text — Show quoted text -

"Ray Ennis" <stela…@maui.net wrote: TO ALL ALT.SUPPORT TINNITUS READERS: Here is a recently exchange between Mike Cohen of Israel and a gentleman from South America.  Mike came to Israel from Chicago 4 1/2 years ago to be treated by Dr. Shemesh at Hadassah Hospital. Recently married and recovered from tinnitus, he now edits an independent tinnitus-related newsletter, TINNITUS NEWSLETTER FROM ISRAEL.  Here lay people and professionals from around the world share tinnitus and related disorders ideas in an atmosphere of mutual respect. ……. Mike Cohen still has tinnitus … and so do you, Ray. Now Shemesh boasts a 90% CURE rate.  You and Mike are the greatest advocates of this treatments … so if you two are not "cured," something does not make sense. Please define for us what "recovered" means. stephen nagler

Response:

"L

Psoriasis, dermatitis, and candida

Question:

Yeah, I’ve since revised my view after reading DaveW’s references. I don’t think Psoriasis is necessarily caused by systemic candida infection at all. *Localized*, perhaps, but its hard to know if its actually the cause–that old "which came first, the chicken or the egg?" thing. I could see candida (and other surface micros) perpetuating Psoriasis on the skin–perhaps acting as a trigger also for an immune system that is already made faulty.

Anybody know how much testing for skin fungal infections costs?  I don’t, but if it’s cheap enough, and you’ve got long-lasting, treatment-resistant psoriasis, it might be worth the expense to get the possibility checked out. Again, insurance companies are starting to balk at paying for antifungals without test results showing they’re needed, so "trying" an antifungal may be less cost-effective than getting tested, depending on the prices involved.  In my opinion, it’d be better to *know*, anyway, instead of guessing that because an antifungal led to a decrease in psoriasis, there must have been fungi in there (not always true, and the antifungal might not work the next time). – Dave W. http://members.aol.com/psorsite/

Response:

Dear William, and most of what DaveW posted i concur with

<snip Yeah, I’ve since revised my view after reading DaveW’s references. I don’t think Psoriasis is necessarily caused by systemic candida infection at all. *Localized*, perhaps, but its hard to know if its actually the cause–that old "which came first, the chicken or the egg?" thing. I could see candida (and other surface micros) perpetuating Psoriasis on the skin–perhaps acting as a trigger also for an immune system that is already made faulty.  William said; Personally, though I "only" have medically-induced seborrheic dermatitis (on my face, brought on by Retin-A, and perhaps exacerbated by various antibiotics precribed to me by different derms over the years), in addition to my topical anti-fungal treatments, Why did you use retin a in the first place? and why did you need the antibiotics…: ? for what?

My doctor at the time, a GP, prescribed it for *acne*–Retin-A combined with Panoxyl (benzoyl peroxide) cream. It totally messed up my face–turned it beet-red, made it flake and scale, took away elasticity, etc. The antibiotics came later with other doctors while I was in college, for acne, but also for whatever was wrong with my skin, which they couldn’t figure out even though I *told* them over and over how it got to be a red, flaky mess. (Some of the redness went away after I stopped the Retin-A, as did much of the flaking, but I had a major problem Sophomore year that started to look like eczema). If I’d known as a stupid high school kid what I do now about how to treat acne by adjusting diet, sleep, etc (naturally), I could have saved myself 12 years of a living Hell. – Hide quoted text — Show quoted text – You then said: I will be adding a probiotic acidophilus supplement (in my case, I’m going to try Udo’s Gold) to balance out any imbalance of flora in my stomach and body (I’m also going to ad I use which ever is the cheapest of the flax oils myself…they all taste the same to me and i sorta like em now..after a few years of one tbls a day…i did try two for a while and didn’t see much diff….and i stop when i run out for a few weeks…and run back to the store for more…either barleans, spectrum or natures sunshine…i usually get the 12oz..as long as it is refrigerated it seems okay…i do try to consume within the 45 day-60 day time period

<snip I’m just going to use the Udo’s microflora for about a month. I don’t think I have a major imabalance in my gut or anything, but just to be on the safe side. I’m using Udo’s oil blend also to be on the safe side. I don’t think I’m getting the optimal amount of monunsaturated fats in my diet otherwise. Randall

My treatment so far using topical anti-fungals appears to be having an effect. My skin is getting smoother (incrementally, I’ll admit), some of the redness/irritation has faded, and it seems more pliable–stronger. I know it’s not just the moisturizing effect of the cream I use during the day because mositurizers in the past has had the opposite effect–my skin would scale more without it, which I would notice when washing–my skin doesn’t scale now when I wash. I know this is going to take months. My skin needs to regenerate properly–evenly, instead of at different rates in response to the candida, so I need to keep killing the candida with the topicals until my skin’s protective barrier is in place again (for the first time in 12 years) and able to do its job normally. My skin is also very oily, because it can’t keep the moisture in because of the missing barrier, so it pumps out more sebum (which leads to much of the acne); when my skin is repaired, my face should get much less oily. At any rate, I’ve gota plan, that, for *my* condition, looks sound. I kept trying to apply it for Psoriatics, because many of our symptoms look similar, but in the end they’re not the same thing. I don’t have the problems I have on my face anywhere else on my body. My immune system isn’t to blame–it’s the candida (as per my last derm’s diagnosis of seborrheic dermatitis). -Will

Response:

Dear William, you said: ‘Net about the role of a candida albicans infection asbeing causative in various diseases. The infection, if systemic, can cause a whole host of diseases that are actually symptoms of the infection itself.

and most of what DaveW posted i concur with….i did get my fecal matter examined and was miffed that i only had moderate levels of candida…(12 yrs ago) when the issue was going good…Dr Crooks (funny huh- crook) Book "The Yeast Connection" was published in 1983..so i suppose a fair amount of peer review had already began…after reading the book…i was so sure that my Natural groovy "i can heal anything" type doctor would find all this yeast and wipe it all out with a little antibiotics…that i was sure that a cure was around the corner..the heck with my derm…this natural guy (alt) was the ticket…….oh well….the rest is history…on that one….good posts DaveW…what a asset you are…..i love it…now if we could spread some fairy dust around and magically change some of them thru the pleomorhic route to less obnoxious contributers…er…a maggot becomes a fly..? hmmm’…worm becomes a butterfly….(better)..oh well the ploymorhics in this ng will be more help then they know…..as devils advocate or angels appologist…. William said; If you do a search of the ‘Net for candida albicans infections (I tried "candida" and "fibromyalgia" together and got a slew of info and lists of interconnected symptoms), you’ll understand what I mean whe I say tha

why not go and do a search on Chlamydia as we all pop out of the womb and have a good chance of getting that…who knows maybe there is a link there…as there is a link with heart disease to Chlamydia pneumoniae from the mouth (focal point?) and then systemic? So, maybe the little critters do change from a loving little bacteria into the crawling eye….for p people….but not likely….i guess as there are loads of bugs…more then howard hughes suspected i am sure….oh those filthy little germs…..But, as in the latest rage, as mentioned previous….there is a entrance point for CJDnv thru tonsilitis..the scientist are now hypothesizing..and with the Doc down in Oz who consummed the Helio Bacterpylori and then used antibiotics to cure his ulcers….and thus proved the agent of disease and cure….we are left with…a lot of us got strep…and whammo developed p….now as to why everyone doesn’t get p that has strep is the 64K question….you can follow all the nostrums in the alt/natural world and still not beat it… you said: Personally, though I "only" have medically-induced seborrheic dermatitis (on my face, brought on by Retin-A, and perhaps exacerbated by various antibiotics precribed to me by different derms over the years), in addition to my topical anti-fungal treatments,

Why did you use retin a in the first place? and why did you need the antibiotics…: ? for what? You then said: I will be adding a probiotic acidophilus supplement (in my case, I’m going to try Udo’s Gold) to balance out any imbalance of flora in my stomach and body (I’m also going to ad

I use which ever is the cheapest of the flax oils myself…they all taste the same to me and i sorta like em now..after a few years of one tbls a day…i did try two for a while and didn’t see much diff….and i stop when i run out for a few weeks…and run back to the store for more…either barleans, spectrum or natures sunshine…i usually get the 12oz..as long as it is refrigerated it seems okay…i do try to consume within the 45 day-60 day time period..i suppose that some BHT could be added to it…Durk Pearson trick from the book Life Extension….( and he ate a gram or two of BHT for herpes virus as the BHT removes the coat from the virus…try that one…i dare ya…) as to probiotics, you can take a proflora whey powder (carbo not protein) to grow the good flora in your large intestine…or Jerusalem Artichoke works to…. avoid all meat and alcohol for at least a month or two…to regrow or repopulate good flora..and once you do the good flora will pick up the slack and you won’t need to take a B vit supplement….as they will provide them….if you want more info on this route i will be glad to help….contact me off list Will…. And good luck… Randall

Response:

Well $hit, I’m all out of ideas! I think maybe I was trying too hard to link candida to psorasis because it seems to be the ongoing problem for me (with the s.dermatitis). I’d like to point out just one question I have about your argument, however–not that it makes a real difference to the conclusion for psoriatics. You say:  " The above is almost definitely untrue.  The body fights infection by throwing more *immune* cells at it, not by growing more skin.  The reason the skin is growing so much is that the "wound healing" routine in psoriatic skin is "turned on," for a basic explanation.  If your hypothesis, above, were true, than the scaling we experience would be common for *any* skin infection, and it’s simply not.  We’d probably also see psoriasis in other animals.  It doesn’t exist, naturally, for anyone but us humans."

My question is that, the body’s immune system fights infections and heals wounds through different mechanisms, but is it possible for the body to switch to a different mechanism if the first it tries isn’t working? What I mean is, if your body sensed something like candida or whatever in your skin, and threw some antibodies, etc, at it, and that didn”t stop it, might it then turn on the "wound healing" component as a last resort? I mean, the body knows what the body knows; wound healing involves an increased rate of skin cell turnover, among other things–if it didn’t, then wounds would be limited to healing after at least about 28 days, which is considered the "normal" skin turnover rate. You get a wound, it heals, the scab falls off. The body senses a problem with the skin in whatever area and speeds up its renewal/replacement process. Now, for me, it would seem to make sense, because my problem has always been in the same locale, and my derm diagnosed my condition as being caused/related to candida. My body has thus treated the skin in the affected area as an ongoing wound because the skin’s protective layer was originally stripped away by the topical meds, which in turn allowed the candida to penetrate deeper into the skin than it’s supposed to. Just how far into the skin can antibodies actually reach? As far as the blood will carry it, right? Except there are no blood vessels in the outer (dead) layers of skin. Which of course would beg the question of how the body knows there’s an infectious organisms there, but the organism must consistently penetrate deep enough for the body to sense it. Therefore, antibodies would only clear an infection as far as the skin’s natural protective layer–that layer, supposedly, being a barrier to bacteria and fungi. My barrier is effectively gone, so my body is sensing the candida, and not being able to stop it with antibodies alone, turns on the "wound healing" process as another line of defense. Except that because this wound healing is going on at different rates throughout the affected skin, the protective layer never gets re-built because the layers are all askew instead of nice and even (the layer cake pounded by a hammer analogy). So, by killing the candida myself (with topicals)so that my body won’t sense the infection, it *should* turn off this wound-healing process of sped-up skin renewal, which would allow for the next layers of skin to develop evenly (and the older ones to eventually shed), thus restoring the protective barrier. Lotta "ifs", I know. I can’t think of anything else but the diagnosed candida that would be causing this "wound healing" mechanism in my own skin. For psoriatics, I have a guess about why some of the scaling shows up symetrically. Are the symetrical areas parts of your body that might be dry anyway? I mean, lots of people’s elbows get dry. If that lack of moisture were affecting the integrity of the skin–the elasticity, protective barrier, etc, and enough irritation were sensed, might the body then not try to "heal" it? Maybe with psoriatics the body is over-reacting to this dry skin? Just a theory. Might explain why it can be symetrical. –Will

– Hide quoted text — Show quoted text – …Again, from what I’ve learned so far, psoriasis appears to be the body’s immune system reacting to something in the skin. That’s too simplified a view, though.  Strep *throat* often triggers psoriasis, in those people with the correct genetic makeup (don’t forget that part). The skin tries to rid itself of over-colonizing microorganisms by speeding up its renewal rate, thus the flaking and scaling, and the pink/red lesions or scales that are skin cells that are still alive (and tender). The skin needs to do this because the invading microorganisms *could* eventually reach the bloodstream the farther into the skin they’re able to penetrate. The body is making the skin "push back" the wave of microorganisms to keep that from happening. The above is almost definitely untrue.  The body fights infection by throwing more *immune* cells at it, not by growing more skin.  The reason the skin is growing so much is that the "wound healing" routine in psoriatic skin is "turned on," for a basic explanation.  If your hypothesis, above, were true, than the scaling we experience would be common for *any* skin infection, and it’s simply not.  We’d probably also see psoriasis in other animals.  It doesn’t exist, naturally, for anyone but us humans. My guess (educated, yes, but still just my guess) is that the psoriatic scaling appears in different parts of the body as the body reacts to any shift in micro-flora population. Now, this could be because the microorganisms really are over-colonizing (like with me), or because the body’s immune system is out of whack and over-reacting to everything. If either, it’d have to be more of the latter, since, as Graham has pointed out, psoriasis is often symmetrical.  I don’t see how Candida, for example, could possibly have "guessed" to infect both my elbows, preferentially, first, before moving onto my scalp, and then my lower shins – and affected *nothing* in between. … There are so many diseases and conditions that have been linked to candida infections that, unless one does some major testing and statistical analysis, there’s no way to know (or correllate) for sure… That’s actually one of the problems of the Candida hypothesis: too much going on.  Turn the claims around, and the implication is that by getting rid of Candida, a person can successfully rid themselves of all these horrible diseases.  There’s no such thing as a panacea, yet, which brings into question the entire theory, since the Candida advocates suggest strongly that anti-Candida therapies *are* panaceas. … What I’m wondering is if an imbalance of candida in the gut could lead to an over-reactive generalized immune response that would affect the skin like psoriatics experience, or if the candida would have to be in one’s blood and/or in the muscles?… Again, see "strep throat and psoriasis."  The hypothesis reads, basically: *If* a microorganism, due to its particular antigens, can induce psoriasis, there’s only a need for the immune system to be *presented* with that antigen for the skin symptoms to develop.  Doesn’t matter *where* the antigen shows up, since the theory is that the skin is presenting *similar* proteins that the immune system "reads" as the *same* antigens, and so mounts a response wherever those proteins are found.  Don’t assume that the immune cells never go anywhere.  As a matter of routine, they move about everwhere in the body, "patrolling" if you will (except for a very few special locations).  An immune cell which "meets" strep in the tonsils could easily be among those which being a psoriatic plaque on a knee. … What mainstream medical science seems only half-aware of right now is that the body is a "system". Everything interconnects. Every drug we put on or into our bodies has the potential to throw this system out of whack. Mainstream medicine actually knows this quite well.  This is one of the reasons for clinical trials of drugs – attempting to ensure the drugs don’t often do things that are unexpected or fatal.  But, since everybody is different, unexpected things happen all the time, so minimization, not elimination, of the risks is the only option. We, as humans, are not the only organism walking around in our shoes. We are actually symbiotic with a number of bacteria (and yes, even fungi). Killing off all the bacteria and fungi would result in us getting quite sick.  They’re necessary for proper digestion, as well as defense against more harmful bacteria and fungi… I don’t believe this very much, especially considering those patients who receive massive doses of broad-spectrum antibiotics in response to sepsis or other drastic infections.  Yes, there exist bacteria which manufacter some B-vitamins for us in our guts (and which infants lack at birth), but the theory you propose above would have the "Boy in the Bubble" dying *because* he was in the Bubble. From another post: I’ll freely admit I couldn’t find anything on the NIH or CDC or Health Canada sites, but then it doesn’t suprise me because they seem to be more drug-oriented and "mainstream" rather than addressing the body’s systemic issues. I found the following on the CDC Web site in about 30 seconds, going to the "Health Topics A to Z" section:    http://www.cdc.gov/ncidod/dbmd/diseaseinfo/candidiasis_t.htm Appears to claim that infections of Candida serious enough to present symptoms (as listed) have an incidence of 8 in 100,000 of the general population.  That’s 0.008%.  Compared to psoriasis’ 2%. Here’s some more light reading for you:    "…There

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Response:

Hi Everyone, In the past  I have asked my Dr. and my rheumatologist if it were possible that I had a systemic yeast infection, they both said that if I did that I would be so sick I’d be in a hospital, neither took me seriously.  I do have Candida,compromised by being on anti-biotics for years and being diabetic.  I’m seeing my Derm tomorrow after being fairly clear for quite awhile.  I"m now covered with guttate P.  I"m wondering if an overgrowth of yeast could be followed by P?  That’s one of the ? I’ll be asking tom. Has anyone else had any experience with this? I also have PA and Fibromyaglia/CFIDS Gentle Hugs to all, Shirley – Hide quoted text — Show quoted text – I’ve been doing a lot of reading on the ‘Net about the role of a candida albicans infection asbeing causative in various diseases. The infection, if systemic, can cause a whole host of diseases that are actually symptoms of the infection itself. I bring this up because a lot of you with psoriasis seem to have other ailments as well, like arthritis, fibromyalgia, chronic fatigue, sleeplessness, and the like. Apparently, these, as well as psoriasis, eczema, etc, are also symptoms of candida infections. If you do a search of the ‘Net for candida albicans infections (I tried "candida" and "fibromyalgia" together and got a slew of info and lists of interconnected symptoms), you’ll understand what I mean whe I say that many of you may in fact be suffering from systemic candida infections. Do a search for "antifungal" as well–it turned up some pretty interesting stuff, including causes of fungal infections, symptoms, and treatments. FYI, I found Google.com to be the best for this kind of search, but use whatever you like… Personally, though I "only" have medically-induced seborrheic dermatitis (on my face, brought on by Retin-A, and perhaps exacerbated by various antibiotics precribed to me by different derms over the years), in addition to my topical anti-fungal treatments, I will be adding a probiotic acidophilus supplement (in my case, I’m going to try Udo’s Gold) to balance out any imbalance of flora in my stomach and body (I’m also going to add Udo’s Gold Blend of monounsaturated oils, but that’s for my overall health, as is the multivitamin and b-complex I’ll also be adding). For anyone who wants to try the same kind of regimine, use whatever brands you’re most comfortable with. I really believe though that the systemic approach (internal and external), kept up for a number of months, is going to work for me, and I truly hope for anyone else who tries it too. –Will

Response:

…Again, from what I’ve learned so far, psoriasis appears to be the body’s immune system reacting to something in the skin.

That’s too simplified a view, though.  Strep *throat* often triggers psoriasis, in those people with the correct genetic makeup (don’t forget that part). The skin tries to rid itself of over-colonizing microorganisms by speeding up its renewal rate, thus the flaking and scaling, and the pink/red lesions or scales that are skin cells that are still alive (and tender). The skin needs to do this because the invading microorganisms *could* eventually reach the bloodstream the farther into the skin they’re able to penetrate. The body is making the skin "push back" the wave of microorganisms to keep that from happening.

The above is almost definitely untrue.  The body fights infection by throwing more *immune* cells at it, not by growing more skin.  The reason the skin is growing so much is that the "wound healing" routine in psoriatic skin is "turned on," for a basic explanation.  If your hypothesis, above, were true, than the scaling we experience would be common for *any* skin infection, and it’s simply not.  We’d probably also see psoriasis in other animals.  It doesn’t exist, naturally, for anyone but us humans. My guess (educated, yes, but still just my guess) is that the psoriatic scaling appears in different parts of the body as the body reacts to any shift in micro-flora population. Now, this could be because the microorganisms really are over-colonizing (like with me), or because the body’s immune system is out of whack and over-reacting to everything.

If either, it’d have to be more of the latter, since, as Graham has pointed out, psoriasis is often symmetrical.  I don’t see how Candida, for example, could possibly have "guessed" to infect both my elbows, preferentially, first, before moving onto my scalp, and then my lower shins – and affected *nothing* in between. … There are so many diseases and conditions that have been linked to candida infections that, unless one does some major testing and statistical analysis, there’s no way to know (or correllate) for sure…

That’s actually one of the problems of the Candida hypothesis: too much going on.  Turn the claims around, and the implication is that by getting rid of Candida, a person can successfully rid themselves of all these horrible diseases.  There’s no such thing as a panacea, yet, which brings into question the entire theory, since the Candida advocates suggest strongly that anti-Candida therapies *are* panaceas. … What I’m wondering is if an imbalance of candida in the gut could lead to an over-reactive generalized immune response that would affect the skin like psoriatics experience, or if the candida would have to be in one’s blood and/or in the muscles?…

Again, see "strep throat and psoriasis."  The hypothesis reads, basically: *If* a microorganism, due to its particular antigens, can induce psoriasis, there’s only a need for the immune system to be *presented* with that antigen for the skin symptoms to develop.  Doesn’t matter *where* the antigen shows up, since the theory is that the skin is presenting *similar* proteins that the immune system "reads" as the *same* antigens, and so mounts a response wherever those proteins are found.  Don’t assume that the immune cells never go anywhere.  As a matter of routine, they move about everwhere in the body, "patrolling" if you will (except for a very few special locations).  An immune cell which "meets" strep in the tonsils could easily be among those which being a psoriatic plaque on a knee. … What mainstream medical science seems only half-aware of right now is that the body is a "system". Everything interconnects. Every drug we put on or into our bodies has the potential to throw this system out of whack.

Mainstream medicine actually knows this quite well.  This is one of the reasons for clinical trials of drugs – attempting to ensure the drugs don’t often do things that are unexpected or fatal.  But, since everybody is different, unexpected things happen all the time, so minimization, not elimination, of the risks is the only option. We, as humans, are not the only organism walking around in our shoes. We are actually symbiotic with a number of bacteria (and yes, even fungi). Killing off all the bacteria and fungi would result in us getting quite sick.  They’re necessary for proper digestion, as well as defense against more harmful bacteria and fungi…

I don’t believe this very much, especially considering those patients who receive massive doses of broad-spectrum antibiotics in response to sepsis or other drastic infections.  Yes, there exist bacteria which manufacter some B-vitamins for us in our guts (and which infants lack at birth), but the theory you propose above would have the "Boy in the Bubble" dying *because* he was in the Bubble. From another post: I’ll freely admit I couldn’t find anything on the NIH or CDC or Health Canada sites, but then it doesn’t suprise me because they seem to be more drug-oriented and "mainstream" rather than addressing the body’s systemic issues.

I found the following on the CDC Web site in about 30 seconds, going to the "Health Topics A to Z" section:    http://www.cdc.gov/ncidod/dbmd/diseaseinfo/candidiasis_t.htm Appears to claim that infections of Candida serious enough to present symptoms (as listed) have an incidence of 8 in 100,000 of the general population.  That’s 0.008%.  Compared to psoriasis’ 2%. Here’s some more light reading for you:    "…There were no differences in the colonization with Candida     albicans and in the level of Candida antibody titres between     [psoriasis] patients and a healthy control group…"    - http://www.pinch.com/skinny?medline=20060304    Immune cells of psoriatics respond significantly more to group    A strep than to C. albicans.  The Candida response, apparently,    was no different between psoriatics and controls.    - http://www.pinch.com/skinny?medline=98114977    "…Candida infections of the skin were seen more often in     psoriasis patients compared to controls. Differentiating between     Type I (early onset) and Type II (late onset) psoriasis only Type     I psoriasis patients presented with decreased dermatophyte     infections and increased Candida colonization of the intestinum.     However, patients with Type II psoriasis demonstrated an increased     rate of candidosis cutis and candidosis oris as compared to     controls. . . Our results show that the influence of fungal     infections on the two skin diseases investigated is not as strong     as often considered."    - http://www.pinch.com/skinny?medline=98037225    "…None of the skin [T-cell lines] responded to … Candida     albicans…"    - http://www.pinch.com/skinny?medline=97247320    One of the two studies I mentioned says: "…In addition, patients    with erysipelas, acne, psoriasis, and atopic dermatitis showed a    [mucocutaneous] candidosis significantly more often ([relative risk]    between 1.3 and 1.6)…"    - http://www.pinch.com/skinny?medline=95356786    "The microflora of 297 psoriasis patients was extensively examined…     Associated organisms thought to provoke a psoriatic attack were as     follows: streptococcal groups A, B, C, D, F, G, S viridans, S     pneumoniae; Klebsiella pneumoniae, oxytoca; Escherichia coli;     Enterobacter cloacae, E aerogenes, E agglomerans; Proteus mirabilis,     P vulgaris; Citrobacter freundii, C diversus; Morganella morganii;     Pseudomonas aeruginosa, P maltiphilia, P putida; Serratia marcescens;     Acinetobacter calbio aceticus, A luoffi; Flavobacterium specie; CDC     groups Ve-1, Ve-2, E-o2; Bacillus subtilis, cereus; Staphylococcus     aureus; Candida albicans, C parapsilosis; Torulopsis, glabrata;     Rhodotorula and dermatophytes. One or more antistreptococal enzyme     tests was positive in 50% of patients…"    - http://www.pinch.com/skinny?medline=91137055    "Recent reports have suggested a role of Candida colonization of gut     in psoriatic patients. In this study, intestinal yeasts and anti-     candida immune response were investigated in 39 patients with     psoriasis vulgaris. Anti-candida antibodies were determined by     indirect haemagglutination (IHAT) and indirect immunofluorescence     (IFAT) tests. Stool specimens showed 93pc C. albicans colonization     but none of the patients showed clinical candidiasis. Four patients     showed an increased IHAT titer and six patients showed an increased     IFAT titer, the others were all in normal limits. Anti-Candida     antibody titers did not correlate with PASI (Psoriasis area and     severity index) scores."    - http://www.pinch.com/skinny?medline=91129925    "…Yeasts were detected in 68% of the [343] psoriatics … but in     only 54% of the controls (n = 50). Qualitative analysis revealed a     predominance of Candida albicans… Germ cell concentration of     10(4) cells per ml and above were measured in 38% of the psoriatics     … but in only 22% of the test subjects with healthy skin. There     was no correlation between the concentration levels of yeasts in the     faeces and the extent of psoriasis or atopic dermatitis."    - http://www.pinch.com/skinny?medline=90279712 Allow me to clarify more my ‘take’ on Candida and psoriasis: Yes, Candida *can* trigger psoriasis, much like strep can.  Is it responsible for a majority of psoriasis cases?  I doubt it.  Candida can also be a "secondary" infection of psoriasis plaques, making them more difficult to treat, simply because the infection will keep the immune system more ‘vigilant’ in those areas.  There are tests which can be done, Candida doesn’t "hide" well.  Is there much reason to believe that an anti-Candida therapy will result in the elimination of psoriasis?  As far as the evidence I’ve

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Response:

Dear William, Sorry for typos and misspells.. As to strep and p…..and CJD- new variant…it is the new plague, at least if you believe the hysterical press…. it is not strep…..i am wrong again…it is tonsilitis….that is now being looked at for nvCJD as a common factor, among the infected and deceased….demo. check- how many here had tonsilitis or strep right before they first developed p? I once had strep 15 yrears into my p and can’t remember if it flared me….i was pretty bad at the time as i recall….late 20’s at the time….went water skiing and bingo three days of sore throats…. I said: ds me of the problems coming on line with nvCJD…and only the people with streph throat are the ones getting it…..a

change strep to tonsilitis….above…… If anyone wants a copy of this post…let me know….its from a microbiologist and is very interresting….or i can post if here…. As to the relevance ….just think…as if all the other crap O theorys don’t explain P now we have prions to deal with….what if….we are infected with prions and it manifests as p? now that should scramble your noggins….it does mine….time to go outside for some vit. D (sunshine) …todays  info….a normal caucasian needs only 3-4 minutes a day 3-4 times a week…three quarters of the year…to get all the vit.D he needs to avoid dairy enriched milk (D)….I wonder how much p sufferers need? And this is for a guy with short sleeves and pants on…..bare arms and face only….vit D also in cod liver oil…anyone try that one….? Randall

Response:

Dear Wialliam, you said……and Dave (congrats for coming surprise….i loved that moment when they plooped out….all gooeey and all…i cut the cord..and washed em….and have it all on tape…that was over 20 and 18 yrs ago…) I’ve been doing a lot of reading on the ‘Net about the role of a candida albicans infection asbeing causative in various diseases. The infection, if systemic, can cause a whole host o

its more or less a Rube Goldberg machine on steroids…..one candida has 70+ endotoxins…thats some excretions…..poop….now go find out which one causes the tnf (tumour necrosis factor- to go off ratio….and why is there no angiogenisis as in cancer?)….this reminds me of the problems coming on line with nvCJD…and only the people with streph throat are the ones getting it…..as there needs to be an entrance point for the prions? and if its so prevalent why aren’t there more cases…..which brings me back to p as streph is a focal point ……for many as a precursor…..more curious sh*t and P…..good luck…with your googling…gotta go…..maybe i’ll do some searches and repost em tomorrow….. Randall

Response:

Here are some pertinent links. I’ll freely admit I couldn’t find anything on the NIH or CDC or Health Canada sites, but then it doesn’t suprise me because they seem to be more drug-oriented and "mainstream" rather than addressing the body’s systemic issues. Anyway, take the following information as you will. Some of these sites were product-oriented, some weren’t. I tried to weed out the obvious product-pushers. http://neuro-www.mgh.harvard.edu/forum/GeneralNeurologyF/3.7.982.11PM… POSSIBILITY (excerpt from "The Yeast Connection") http://cassia.org/candida.htm http://cassia.org/CanDiscussion.htm (talks about candida infection arising after antibiotic treatment for Lyme, but the discussion is relevant) http://www.healthwell.com/delicious-online/D_backs/Nov_97/natheal.cfm http://www.chetday.com/candida.html  (he does sell books) http://www.infosky.net/~alexmi/candida.htm#10 (a candida FAQ…) http://www.sheilas.com/newsletters/candida.html And here’s that article from Quackwatch, which I read through: http://www.familyinternet.com/quackwatch/01QuackeryRelatedTopics/cand… l It certainly seems possible that candida overgrowth was being attributed far too often to various disorders without direct evidence. I’d like to point out, however, that one has only to order the specific laboratory tests to see for sure whether they have a candida problem. I would rather have the tests done than answer the questionaire in Dr. Crook’s book if I wanted to know for sure. Dr. Crook seems to have been onto the right idea, but he ran with the idea a little bit too far. Let’s not throw out the baby with the bathwater, however, as the Quackwatch article wants to. Candida can definitely be a problem, even in people who are not on immunosuppressants. I would also like to point out that just because the mainstream medical community has doubts about the role of candida in various diseases and disorders, we’re talking about the same medical community that approved the drugs I used on my face for acne that ended up inflicting my condition on me. I would like to emphasize to everyone here that *you should go by your own observations* of what’s wrong and what works for you. I had a dermatologist who diagnosed me with seborrheic dermatitis–something that 5 preceeding doctors had totally missed and misdiagnosed! My condition, as it was explained to me, arises out of an overgrowth of yeast (my derm thought this was in part related to testosterone levels, as he was discounting the effect of the original topical drugs on my face–my face being the ONLY place I have this condition). He prescribed oral Diflucan which didn’t fix the problem (he was going to prescribe a topical at first, but at the time I’d had trouble with topicals in the past and didn’t want to chance it; now that I know what I know, I can use the topicals with no problem). I have observed my diet for 12 years, and I know exactly which foods affect my skin. Sugar, as is known, feeds the yeast, and whenever I eat it I get a break-out because of the yeast proliferating (and clogging my pores) from the influx of glucose. These are things I have observed myself, backed up by known scientific fact (i.e., what yeast is, what it feeds on, etc). Dairy also feeds yeast because of the milk sugar. Fruit can feed it, though the fruit sugar doesn’t convert to glucose completely, as some of it remains as fructose (it’s about 50-50) upon entering the bloodstream, so the effect isn’t quite as dramatic as cane sugar. What it all comes down to is this: yeast overgrowth in the gut can be fixed without the use of drugs. There are plenty of over-the-counter supplements–and foods–that can stabilize microflora safely and effectively (given enough time, which is usually a few months). The cost is minimal. The potential reward–your health–is invaluable. I can’t say for sure that candida overgrowth causes psoriasis, though it at least seems to be true in reverse with the high number of psoriasis patients showing increased candida levels. I happen to know for a fact that it’s the problem in my case. And my symptoms happen to mirror very closely the symptoms of psoriatics. As I’ve said before, I’ll be continuing my own course of self-treatment over the next several months and will post here whatever results I attain. –Will – Hide quoted text — Show quoted text – I’ve been doing a lot of reading on the ‘Net about the role of a candida albicans infection asbeing causative in various diseases. The infection, if systemic, can cause a whole host of diseases that are actually symptoms of the infection itself. Unfortunately, a lot of the stuff on the ‘Net about Candida ‘overgrowths’ appears to be quackery.  There exist doctors who make a living by diagnosing Candida infections where none exist, based on nothing but symptoms, and claiming that no "test" can make a proper daignosis. Which is quite strange since such tests exist. I definitely saw Web sites that appeared to be geared toward only selling some product or other to remedy Candida infections. I also saw what appeared to be genuine "news" sites, as in medical databases, where no product line was advocated or linked to, which also had much information on the Candida problem. I would definitely advise anyone else looking into this to consider that, with many other diseases out there, there are definitely quacks who latch onto a few bits of information about a particular disease and then use that info as evidence of why their product should help you. There definitely *are* blood tests available for Candida, but those would only be of use where the infection has actually gotten into the bloodstream. Stool tests might be helpful to show if the flora in the gut is imbalanced toward Candida overgrowth, but that won’t diagnose a problem that is limited to a person’s skin… It’s gotten to the point where more and more insurance companies *refuse* to pay for antifungal medications without also seeing Candida-test data which supports the claim of fungal infection. As with the tests I pointed out above, one would definitely want a whole battery of tests done to be sure their bases are covered. One test won’t necessarily indicate an infection. Quackwatch calls Candidiasis a "Fad Diagnosis":    http://www.quackwatch.com/01QuackeryRelatedTopics/candida.html One of the most interesting points in the Quackwatch article is that a report from Loyola concluded that "the advice of yeast connection [the book by Dr. Crook] advocates may be inappropriate even for illnesses in which Candida is implicated." Again, one of those examples where a particular doctor or writer got hold of some pertinent information about a disease and then made a bunch of "logical" conclusions as to what would help. Not much different from the quacky Websites except that this person managed to get published. Hell, Atkins managed to get HIS diet book published, but I wouldn’t recommend it as a way of eating to anyone from this planet. It doesn’t mean that the underlying problem doesn’t exist, however. Don’t let the quacks alone decide for you whether a candida infection truly could exist or not where none is necessarily originally suspected. How does Candida relate to psoriasis?  I’ve seen exactly two studies which give fair evidence of some sort of connection.  These reports said, basically, that psoriatics are 30-60% more likely than the general public to suffer from yeast "overgrowths" (at levels defined by the researchers, in terms of *stool* populations).  In other words, if 10% of the population have active Candida infections, then 13-16% of psoriatics probably will, too. I think a skin test, perhaps a biposy, would be more revealing than a stool sample. Although I will admit that psoriatics perhaps have more of a systemic problem than someone like myself with localized seborrheic dermatitis. It appears that candida can infect a person in three ways, singly and in any combination of: overgrowth in the skin, overgrowth in the gut, and infection in the blood. From what I’ve read, the first two are much more likely than the third, and the third can be extremely life-threatening (more common in patients taking immunosuppressants, suffering from HIV, etc) in some cases, and can also lead to a host of different symptoms, like fibromyalgia, arthritis, chronic fatigue, and so on. Does this mean that the psoriasis in that 13-16% is caused by Candida? Nope.  Nobody knows.  Does it mean that the psoriasis simply "allows" more Candida infections?  Again, nobody knows.  A clue, though, exists in the opening paragraphs of the Quackwatch article.  Seems that people on immunosuppressants get more infections than others.  Does the "extra" percentage of psoriatics with Candida infections equate to the percentage of psoriatics on immunosuppressive therapy?  I don’t know. Again, from what I’ve learned so far, psoriasis appears to be the body’s immune system reacting to something in the skin. The skin tries to rid itself of over-colonizing microorganisms by speeding up its renewal rate, thus the flaking and scaling, and the pink/red lesions or scales that are skin cells that are still alive (and tender). The skin needs to do this because the invading microorganisms *could* eventually reach the bloodstream the farther into the skin they’re able to penetrate. The body is making the skin "push back" the wave of microorganisms to keep that from happening. My guess (educated, yes, but still just my guess) is

… read more »

Response:

I’ve been doing a lot of reading on the ‘Net about the role of a candida albicans infection asbeing causative in various diseases. The infection, if systemic, can cause a whole host of diseases that are actually symptoms of the infection itself. Unfortunately, a lot of the stuff on the ‘Net about Candida ‘overgrowths’ appears to be quackery.  There exist doctors who make a living by diagnosing Candida infections where none exist, based on nothing but symptoms, and claiming that no "test" can make a proper daignosis. Which is quite strange since such tests exist.

I definitely saw Web sites that appeared to be geared toward only selling some product or other to remedy Candida infections. I also saw what appeared to be genuine "news" sites, as in medical databases, where no product line was advocated or linked to, which also had much information on the Candida problem. I would definitely advise anyone else looking into this to consider that, with many other diseases out there, there are definitely quacks who latch onto a few bits of information about a particular disease and then use that info as evidence of why their product should help you. There definitely *are* blood tests available for Candida, but those would only be of use where the infection has actually gotten into the bloodstream. Stool tests might be helpful to show if the flora in the gut is imbalanced toward Candida overgrowth, but that won’t diagnose a problem that is limited to a person’s skin… It’s gotten to the point where more and more insurance companies *refuse* to pay for antifungal medications without also seeing Candida-test data which supports the claim of fungal infection.

As with the tests I pointed out above, one would definitely want a whole battery of tests done to be sure their bases are covered. One test won’t necessarily indicate an infection. Quackwatch calls Candidiasis a "Fad Diagnosis":    http://www.quackwatch.com/01QuackeryRelatedTopics/candida.html One of the most interesting points in the Quackwatch article is that a report from Loyola concluded that "the advice of yeast connection [the book by Dr. Crook] advocates may be inappropriate even for illnesses in which Candida is implicated."

Again, one of those examples where a particular doctor or writer got hold of some pertinent information about a disease and then made a bunch of "logical" conclusions as to what would help. Not much different from the quacky Websites except that this person managed to get published. Hell, Atkins managed to get HIS diet book published, but I wouldn’t recommend it as a way of eating to anyone from this planet. It doesn’t mean that the underlying problem doesn’t exist, however. Don’t let the quacks alone decide for you whether a candida infection truly could exist or not where none is necessarily originally suspected. How does Candida relate to psoriasis?  I’ve seen exactly two studies which give fair evidence of some sort of connection.  These reports said, basically, that psoriatics are 30-60% more likely than the general public to suffer from yeast "overgrowths" (at levels defined by the researchers, in terms of *stool* populations).  In other words, if 10% of the population have active Candida infections, then 13-16% of psoriatics probably will, too.

I think a skin test, perhaps a biposy, would be more revealing than a stool sample. Although I will admit that psoriatics perhaps have more of a systemic problem than someone like myself with localized seborrheic dermatitis. It appears that candida can infect a person in three ways, singly and in any combination of: overgrowth in the skin, overgrowth in the gut, and infection in the blood. From what I’ve read, the first two are much more likely than the third, and the third can be extremely life-threatening (more common in patients taking immunosuppressants, suffering from HIV, etc) in some cases, and can also lead to a host of different symptoms, like fibromyalgia, arthritis, chronic fatigue, and so on. Does this mean that the psoriasis in that 13-16% is caused by Candida? Nope.  Nobody knows.  Does it mean that the psoriasis simply "allows" more Candida infections?  Again, nobody knows.  A clue, though, exists in the opening paragraphs of the Quackwatch article.  Seems that people on immunosuppressants get more infections than others.  Does the "extra" percentage of psoriatics with Candida infections equate to the percentage of psoriatics on immunosuppressive therapy?  I don’t know.

Again, from what I’ve learned so far, psoriasis appears to be the body’s immune system reacting to something in the skin. The skin tries to rid itself of over-colonizing microorganisms by speeding up its renewal rate, thus the flaking and scaling, and the pink/red lesions or scales that are skin cells that are still alive (and tender). The skin needs to do this because the invading microorganisms *could* eventually reach the bloodstream the farther into the skin they’re able to penetrate. The body is making the skin "push back" the wave of microorganisms to keep that from happening. My guess (educated, yes, but still just my guess) is that the psoriatic scaling appears in different parts of the body as the body reacts to any shift in micro-flora population. Now, this could be because the microorganisms really are over-colonizing (like with me), or because the body’s immune system is out of whack and over-reacting to everything. And the main reason I don’t know is that I don’t know what percentage of the general population have Candida troubles.  The abstracts I’ve read do not have that data.  No information I’ve ever seen has that data. That, Will, might be a good starting place for you and others interested in this idea: find a *reliable* source for Candida-infection data (but keep in mind that nearly 100% of the population has *some* Candida, it’s only when it gets out of hand that it supposedly becomes a problem).  Anyone who claims 1/3rd or more is probably yanking your chain.

Anyone who claims any set percentage at this point is only guessing. There are so many diseases and conditions that have been linked to candida infections that, unless one does some major testing and statistical analysis, there’s no way to know (or correllate) for sure. I’m thinking that the problem is more common than is suspected. Symptoms vary because the immune system can respond in any number of ways to a systemic infection. When it’s just in the skin, it’s more obvious–the symptoms are consistent and observable. Changes in diet that shouldn’t affect healthy skin create major changes in candida-infected skin (this I know from personal observation, as I’m sure others do). What I’m wondering is if an imbalance of candida in the gut could lead to an over-reactive generalized immune response that would affect the skin like psoriatics experience, or if the candida would have to be in one’s blood and/or in the muscles? For example, with my face, I know its localized and apparently not in the blood, simply because I’m affected in the exact areas and patterns in which I used the original (12 years ago) Retin-A/Panoxyl combo that thinned out my skin, turned it red, made it scale, and allowed the candida to overgrow. I get hives–only on my face, nowhere else, and for no apparent reason. ANY allergen will set them off. I take Claritin to block the histimine reaction, and that works. This, to me, is obvious evidence that my immune system is already over-reacting to localized activity on my face. There is such an over-whelming immune response already present that it reacts immediately to anything. Hell, cuts and scratches on my face heal much faster than anywhere else on my body! Anyway, though it seems obvious to me, with a disease like psoriasis, it’s definitely harder to pin down. As you suggest I will look for a totally reliable source on candida-related illness. On the other hand, Will, your particular disease has quite a bit of evidence pointing towards M. furfur and other fungi as causative factors. Candida may well have a much greater role in seborrheic dermatitis than in psoriasis.

One thing with my disease is that nobody, and I mean *absolutely nobody* else in my family, direct or removed, has had anything like this. They all have great skin. I happen to know that my condition was medically-induced. Before I used that topical $hit (prescribed for acne, by the way) that ruined my life for the past 12 years, I had never had symptoms like I’ve had since. After I stopped using the topicals but continued to have problems, I was prescribed a variety of antibiotics by successive doctors, which I believe only contributed to the candida overgrowth by killing off competing flora. Oh, I’ve also read abstracts which show fairly well that using antifungal therapy for, say, chronic fatigue syndrome is just about worthless as compared to placebo.  Bits and pieces of Candida ‘overgrowth’ theory are being shown to just be wrong.

This conclusion would actually make sense, depending on the length and type of therapy involved if candida were actuallly at fault. If the problem is in the gut only, then the gut flora needs to be balanced out–candida needs to be reduced, while other bacteria (like acidophilus) needs a chance to colonize. This can take months. If it’s (also) in the blood, antibiotics taken for more than a few months would be necessary, with the downside being that those antibiotics could kill off candida’s naturally competing flora in the gut and elsewhere, so steps would have to be taken to try to keep the flora as balanced as possible during such antifungal therapy. It’s like a see-saw–one side goes down, the other goes up. I don’t know what it is about candida–because its a … read more »

Response:

I’ve been doing a lot of reading on the ‘Net about the role of a candida albicans infection asbeing causative in various diseases. The infection, if systemic, can cause a whole host of diseases that are actually symptoms of the infection itself.

Unfortunately, a lot of the stuff on the ‘Net about Candida ‘overgrowths’ appears to be quackery.  There exist doctors who make a living by diagnosing Candida infections where none exist, based on nothing but symptoms, and claiming that no "test" can make a proper daignosis. Which is quite strange since such tests exist. It’s gotten to the point where more and more insurance companies *refuse* to pay for antifungal medications without also seeing Candida-test data which supports the claim of fungal infection. Quackwatch calls Candidiasis a "Fad Diagnosis":    http://www.quackwatch.com/01QuackeryRelatedTopics/candida.html One of the most interesting points in the Quackwatch article is that a report from Loyola concluded that "the advice of yeast connection [the book by Dr. Crook] advocates may be inappropriate even for illnesses in which Candida is implicated." How does Candida relate to psoriasis?  I’ve seen exactly two studies which give fair evidence of some sort of connection.  These reports said, basically, that psoriatics are 30-60% more likely than the general public to suffer from yeast "overgrowths" (at levels defined by the researchers, in terms of *stool* populations).  In other words, if 10% of the population have active Candida infections, then 13-16% of psoriatics probably will, too. Does this mean that the psoriasis in that 13-16% is caused by Candida? Nope.  Nobody knows.  Does it mean that the psoriasis simply "allows" more Candida infections?  Again, nobody knows.  A clue, though, exists in the opening paragraphs of the Quackwatch article.  Seems that people on immunosuppressants get more infections than others.  Does the "extra" percentage of psoriatics with Candida infections equate to the percentage of psoriatics on immunosuppressive therapy?  I don’t know. And the main reason I don’t know is that I don’t know what percentage of the general population have Candida troubles.  The abstracts I’ve read do not have that data.  No information I’ve ever seen has that data.  That, Will, might be a good starting place for you and others interested in this idea: find a *reliable* source for Candida-infection data (but keep in mind that nearly 100% of the population has *some* Candida, it’s only when it gets out of hand that it supposedly becomes a problem).  Anyone who claims 1/3rd or more is probably yanking your chain. On the other hand, Will, your particular disease has quite a bit of evidence pointing towards M. furfur and other fungi as causative factors. Candida may well have a much greater role in seborrheic dermatitis than in psoriasis. Oh, I’ve also read abstracts which show fairly well that using antifungal therapy for, say, chronic fatigue syndrome is just about worthless as compared to placebo.  Bits and pieces of Candida ‘overgrowth’ theory are being shown to just be wrong. All this isn’t to say, of course, that if you’ve got a genuine problem with this or any other fungus, it shouldn’t be treated.  But it might be better treated by professionals other than the so-called "Yeast Connection advocates." – Dave W. http://members.aol.com/psorsite/

Response:

I’ve been doing a lot of reading on the ‘Net about the role of a candida albicans infection asbeing causative in various diseases. The infection, if systemic, can cause a whole host of diseases that are actually symptoms of the infection itself. I bring this up because a lot of you with psoriasis seem to have other ailments as well, like arthritis, fibromyalgia, chronic fatigue, sleeplessness, and the like. Apparently, these, as well as psoriasis, eczema, etc, are also symptoms of candida infections. If you do a search of the ‘Net for candida albicans infections (I tried "candida" and "fibromyalgia" together and got a slew of info and lists of interconnected symptoms), you’ll understand what I mean whe I say that many of you may in fact be suffering from systemic candida infections. Do a search for "antifungal" as well–it turned up some pretty interesting stuff, including causes of fungal infections, symptoms, and treatments. FYI, I found Google.com to be the best for this kind of search, but use whatever you like… Personally, though I "only" have medically-induced seborrheic dermatitis (on my face, brought on by Retin-A, and perhaps exacerbated by various antibiotics precribed to me by different derms over the years), in addition to my topical anti-fungal treatments, I will be adding a probiotic acidophilus supplement (in my case, I’m going to try Udo’s Gold) to balance out any imbalance of flora in my stomach and body (I’m also going to add Udo’s Gold Blend of monounsaturated oils, but that’s for my overall health, as is the multivitamin and b-complex I’ll also be adding). For anyone who wants to try the same kind of regimine, use whatever brands you’re most comfortable with. I really believe though that the systemic approach (internal and external), kept up for a number of months, is going to work for me, and I truly hope for anyone else who tries it too. –Will

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What is PASI score?

Question:

What is PASI(Psoriasis area and severity index) score? How to extimate psoriasis with PASI score? I am a medical student in Japan. I really appreciate any help. — Masaya Ishibashi

Response:

What is PASI(Psoriasis area and severity index) score? How to extimate psoriasis with PASI score? I am a medical student in Japan. I really appreciate any help.

Here are two old posts from a helpful person named "Alberto" which answer these questions: I do not know, exactly, how to determine the percentage of coverage of just one body part (the legs, for example).  I do know that for the *whole* body, the size of the palm of one hand is about equal to 1% of total skin surface, but that does not hold true for the head (which is only 10%), or the other three body areas used in calculating the full PASI score. There may be psoriasis researchers at your school who will be able to tell you, as there has been a good amount of psoriasis research published from Japan:    http://www.pinch.com/skinny?medline=psoria*+japan [Posted and emailed] – Dave W. http://members.aol.com/psorsite/

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