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Dr. Pridgen's 9 different cocktail mix patents & research under Dr. Carol Duffy name

Jon_Tradicionali

Alone & Wandering
Messages
291
Location
Zogor-Ndreaj, Shkodër, Albania
@boohealth

Latent herpesvirus infection in human trigeminal ganglia causes chronic immune response.

http://www.ncbi.nlm.nih.gov/m/pubmed/14633592/?i=2&from=/17021407/related


It's entirely credible to say that it's not the HSV-1 itself that's to blame, but the immune response to it, which in our case is abnormal. T cells/Inflammatory cytokines are summoned to clear the virus but they can never achieve it hence it becoming chronic.

Let's see what Pridgen has got to say on Monday anyway.
 

boohealth

Senior Member
Messages
243
Location
south
@JonTraditionali You're suggesting that everybody with CFS simply had the same aberrant immune response to whatever pathogen of whatever variety, or perhaps toxic exposure--etc. I don't know why you speculate that it's that simple. It would be like saying all cancer is the same--uncontrolled cell growth. And though that's true--it's meaningless in terms of treatment. Tumors of one type have common mutations--and are treated by certain drugs--others have other mutations, and are treated with other drugs. IE you wouldn't treat prostate cancer with Gleevac.

You wouldn't treat a strep infection with doxcycyline.

You wouldn't treat a rickettsial infection with amoxicillin.

Etc. So it's kind of meaningless to say that somebody's immune system couldn't handle an infection. There could be many reasons for that, anyway. One reason could be genetic variation. Molecular mimicry. The "wrong" receptor (the CCR5 receptor protects against HIV but causes you to get a much more virulent case of west nile, for instance). A strong inflammatory response that derails the immune system. And on and on. Or there could be helper viruses or infections that trigger a latent one. Immune system might be overwhelmed by the "swarm" of microbes Stephen Buhner talks about in "lyme"--where ticks host many species of bugs, and they synergistically enhance each other.

Too simple...life ain't that simple.
 

JT1024

Senior Member
Messages
582
Location
Massachusetts
The American College of Rheumatology is meeting in Boston over the next several days.

Dr. Pridgen is presenting his finding at 4:30 pm in room 104B at the Boston Convention Center.

Boston Convention & Exhibition Center
415 Summer Street
Boston, MA 02116

Fibromyalgia, Soft Tissue Disorders, Regional and Specific Clinical Pain Syndromes II: Clinical Perspectives
Moderators: Muhammad Yunus, MD and Lisa Suter, MD

1878. A Combination of Celecoxib and Famciclovir Is Efficacious in the Treatment of Fibromyalgia: Results of a Phase IIa Randomized, Double-Blind, Placebo-Controlled Study
William Pridgen1, Carol Duffy2, Judith Gendreau3 and R Michael Gendreau3, 1 Innovative Med Concepts, Tuscaloosa, AL, 2University of Alabama, Tuscaloosa, AL, 3Gendreau Consulting, LLC, Poway, CA
 

Jon_Tradicionali

Alone & Wandering
Messages
291
Location
Zogor-Ndreaj, Shkodër, Albania
@boohealth

I gave a suggestion, backed up with a study from PubMed.
I'm unsure why you find that so outrageous.

ElZakker theorised any pathogen, be it virus/bacteria, can infect the vagus nerve which T cells cannot deal with as its immunoproviliged. Hence they patrol chronically.

Pridgens study found vagus nerve wasn't immunoprivilidged as previously thought.

How can it be meaningless to say that the faulty T cells should be adressed rather than trying to treat herpes which there is no effective treatment as of yet?

I've never said this to be simple, just exploring different theories.
 
Messages
15,786
It would be like saying all cancer is the same--uncontrolled cell growth. And though that's true--it's meaningless in terms of treatment.
I don't think he suggested that having a similar underlying pathology would result in everyone getting the same treatment, unless I missed something?

But maybe it makes more sense to think of the various infections as symptoms in ME patients, rather than as discrete diseases. Hence the different symptoms (infections) in each patient can be specifically treated and managed. But also a cure/treatment for the underlying immune pathology could be applied, which could result in the symptoms (infections) no longer arising chronically and therefore no longer requiring treatment.
 
Last edited:

Iquitos

Senior Member
Messages
513
Location
Colorado
The American College of Rheumatology is meeting in Boston over the next several days.

Dr. Pridgen is presenting his finding at 4:30 pm in room 104B at the Boston Convention Center.

Boston Convention & Exhibition Center
415 Summer Street
Boston, MA 02116

Fibromyalgia, Soft Tissue Disorders, Regional and Specific Clinical Pain Syndromes II: Clinical Perspectives
Moderators: Muhammad Yunus, MD and Lisa Suter, MD

1878. A Combination of Celecoxib and Famciclovir Is Efficacious in the Treatment of Fibromyalgia: Results of a Phase IIa Randomized, Double-Blind, Placebo-Controlled Study
William Pridgen1, Carol Duffy2, Judith Gendreau3 and R Michael Gendreau3, 1 Innovative Med Concepts, Tuscaloosa, AL, 2University of Alabama, Tuscaloosa, AL, 3Gendreau Consulting, LLC, Poway, CA
What day?
 

boohealth

Senior Member
Messages
243
Location
south
You and me both.

You are both assuming a common pathology to all ME, and that's not the case, unless you are speaking very generically--per my cancer example where cancer is uncontrolled growth. Which really doesn't help anybody define anything very useful in terms of understanding individual cancers, and potential treatments. You might like that idea because it gives a smooth coherence to "ME" and shows a fundamental underlying flaw or abnormality (or several) that everybody has which is why they can't keep this or that pathogen under control. But it's not the case. It's extreme oversimplification and not how complex biology works.
 

boohealth

Senior Member
Messages
243
Location
south
It is always the case that genetics plus environment creates an individual's fate. Environment can be both purely physical (a toxin, a pathogen, or numerous such...or signals in the mother's womb, chemicals she transfers, and also signals in her milk etc)...psychological translated into physical (extreme trauma/stress)...and then genetics (some people handle stress well and others are very vulnerable, for instance). Identical twin studies that looked at elderly twins did not find concordance that would reflect your assumptions. One could be perfectly healthy and the other a rheumatic cardiac mess. It depends on how your genes interact with your luck/fate. Thus if you have the ccr5 receptor you will be immune to HIV. But if you are unlucky enough to get West Nile with that receptor, you are going to be in trouble.
 

boohealth

Senior Member
Messages
243
Location
south
Take the case of autoimmune narcolepsy from the H1N1 vaccine. Turns out there is a peptide sequence in that flu (and also in the vaccine) that is too similar to a small percentage of people's own tissue. So their body goes autoimmune, manifesting as narcolepsy--to my recollection because of where that tissue is in the CNS, but I read this some months ago. Far more people were vaccinated than would have actually been exposed to the flu, so enough people got autoimmune narcolepsy that they investigated it. Luck of the draw. Encounter the wrong pathogen for *you*, because of for instance molecular mimicry, and you may get sick. But there is no widespread coherent platonic underlying abnomality in ME.
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
It's extreme oversimplification and not how complex biology works.
This statement is itself extreme oversimplification.

We do not know if ME is one disease, with one core mechanism, or two (which I think likely and can elaborate on), or a mishmash of different diseases. ME might even not be ME, but a form of MS on the other end of a spectrum, though I think this unlikely. (What if the prototypical lesions in MS are in fact a biomarker for a subgroup?)

Now CFS is definitely a syndrome with many diseases. One core mechanism for CFS is very very unlikely.

There is the issue that the intracellular pathogens that trigger ME typically have the capacity to infect both the gut and B cells. This might be important.

Let me point out thought that most of us have mycotoxins, and most of us seem to have worm parasites though this last is far from being substantiated (see the work of Larry Klapow).

Currently if I were to name a mechanism based on the presumption that ME is one disease, then it would be enteroviruses. There are other candidates though. Most criticisms of this idea can be shown to be invalid except one - it remains to be proven.

The idea that different pathogens can trigger a single kind of neuroimmune response that we call ME is growing momentum. There is a lot of data suggesting this might be the case. Suggesting. It remains to be proven.

We simply do not know. I suspect ME is two diseases, one of which is enterovirus related, and the other isn't. I cannot rule out combinations of pathogens, latent viral reactivation from a current infection, toxin or injury, immunological alteration of internal setpoints (especially in the mid and lower brain), and so on. We need to follow the science, fund good science, and criticize all related science, good or bad, but especially bad.
 

voner

Senior Member
Messages
592
here is the abstract, etc. of Dr. Pridgens ACR 2014 paper:

1878 - A Combination of Celecoxib and Famciclovir Is Efficacious in the Treatment of Fibromyalgia: Results of a Phase IIa Randomized, Double-Blind, Placebo-Controlled Study
Monday, November 17, 2014: 4:30 PM
104 B (Boston Convention and Exhibition Center)
Presentation Number: 1878

William Pridgen1, Carol Duffy2, Judith Gendreau3 and R Michael Gendreau3, 1Innovative Med Concepts, Tuscaloosa, AL, 2University of Alabama, Tuscaloosa, AL, 3Gendreau Consulting, LLC, Poway, CA

Background/Purpose:
Fibromyalgia (FM) is a common chronic pain syndrome with symptoms that include widespread pain, fatigue, sleep disruption and cognitive impairment. It is known that infections and other types of stressors are capable of triggering the development of FM. We hypothesize that these stressors could be responsible for triggering a reactivation of latent herpesviruses, and that this reactivation could in turn lead to the central nervous system dysregulation seen in this condition. The present study was designed to evaluate an anti-viral drug combination selected for activity against herpes class viruses.

Methods:

A total of 143 patients selected using the ACR 2010 FM criteria were enrolled at 12 sites in a 16-week, double-blind, placebo-controlled trial. Patients were randomized (1:1) to receive a proprietary combination of celecoxib + famciclovir or placebo. Outcome measures included a 24-hour recall pain numeric rating scale (NRS), Fibromyalgia Impact Questionnaire (FIQ-R), Patient Global Impression of Change (PGIC), and the PROMIS fatigue short form at baseline, and after 6, 12 and 16 weeks of study participation.

Results:

The primary efficacy endpoint was change in pain from baseline. Pain reduction was evaluated using the pain NRS and the 7-day recall pain item from the FIQ-R. Change from baseline was determined using an MMRM approach with LOCF/ BOCF imputation for missing data. A significant decrease in pain was observed for patients on treatment vs. placebo at 16 weeks by both measures. The absolute change on the NRS was -1.9 units vs -1.1, comparing active to placebo (p=0.031). On the FIQ-R item, the change was -2.2 vs -0.92 (p=0.001). Key secondary endpoints included analysis of the PGIC, where a value of “1” or “2” was considered a clinical responder. Significantly improved PGIC response rates were noted at endpoint: 33.3% for active vs 19.2% in placebo patients (p=0.031). Total FIQR score change at the endpoint visit was -17.54 vs -7.87 (p=0.002), while changes in the 3 domains were 14.29 vs -5.44 (p=0.004) for Function, -4.29 vs -1.89 (p=0.003) for Overall Impact, and -16.77 vs -7.90 (p=0.004) for Symptoms. In addition, improvements in fatigue were seen at endpoint on the PROMIS fatigue (-7.62 units vs -4.15; p=0.020).

The safety profile was especially encouraging. Despite the celecoxib component, gastrointestinal and nervous system treatment emergent adverse events were reported significantly more often in the placebo treatment group (GI: 29.0% vs 42.5%; nervous system: 17.4% vs 23.3%; active to placebo), and study completion rates favored active treatment over placebo (82.6% vs. 60.8%) (largely driven by higher placebo discontinuation rates due to adverse events and lack of efficacy).

Conclusion:

A proprietary combination of famciclovir, which we postulate is inhibiting herpesvirus replication, and celecoxib, known to inhibit both herpesvirus replication and reactivation, was efficacious in treating multiple symptoms of FM. Given the simultaneous improvement in many domains and the surprising tolerability of this combination of drugs, we believe this combination warrants further study as a potential new therapy for fibromyalgia patients.


Keywords: fibromyalgia and viruses

Disclosure: W. Pridgen, Innovative Med Concepts, Innovative Med Concepts ; C. Duffy, Innovative Med Concepts, Innovative Med Concepts ;J. Gendreau, Innovative Med Concepts ; R. M. Gendreau, Innovative Med Concepts, Innovative Med Concepts
 

Jon_Tradicionali

Alone & Wandering
Messages
291
Location
Zogor-Ndreaj, Shkodër, Albania
New oral medication shows promise in treating fibromyalgia
Posted in: Drug Trial News | Medical Condition News

Published on November 18, 2014 at 10:59 AM

A new oral medication known as IMC-1, developed by Innovative Med Concepts, proved highly effective at reducing pain and other symptoms of fibromyalgia (FM) in patients in a recent clinical trial.

Detailed results of the randomized, double-blinded, placebo-controlled Phase II study, known as PRID-201, were presented today at the 2014 American College of Rheumatology annual meeting in Boston by William L. Pridgen, M.D., FACS, founder and CEO of Innovative Med Concepts.

According to Daniel J. Clauw, M.D., director of the Chronic Pain & Fatigue Research Center at the University of Michigan (Ann Arbor), commenting on the PRID-201 results, "IMC-1 shows promise as a potentially new treatment for the millions of people who suffer from this debilitating condition."

Fibromyalgia is a multi-symptom disorder involving widespread pain, fatigue, headaches, sleep problems, mood changes and inability to concentrate. Its causes are unknown. According to the National Fibromyalgia Association, an estimated 3-6 percent of people worldwide suffer from the condition—10 million people in the United States alone.

The 16-week study evaluated the efficacy and safety of IMC-1, a fixed-dose-combination of famciclovir and celecoxib. 143 FM patients were recruited at 12 U.S. clinics. Patients received either a combination treatment of IMC-1 or a matching placebo.

A new oral medication known as IMC-1, developed by Innovative Med Concepts, proved highly effective at reducing pain and other symptoms of fibromyalgia (FM) in patients in a recent clinical trial.

Detailed results of the randomized, double-blinded, placebo-controlled Phase II study, known as PRID-201, were presented today at the 2014 American College of Rheumatology annual meeting in Boston by William L. Pridgen, M.D., FACS, founder and CEO of Innovative Med Concepts.

According to Daniel J. Clauw, M.D., director of the Chronic Pain & Fatigue Research Center at the University of Michigan (Ann Arbor), commenting on the PRID-201 results, "IMC-1 shows promise as a potentially new treatment for the millions of people who suffer from this debilitating condition."

Fibromyalgia is a multi-symptom disorder involving widespread pain, fatigue, headaches, sleep problems, mood changes and inability to concentrate. Its causes are unknown. According to the National Fibromyalgia Association, an estimated 3-6 percent of people worldwide suffer from the condition—10 million people in the United States alone.

The 16-week study evaluated the efficacy and safety of IMC-1, a fixed-dose-combination of famciclovir and celecoxib. 143 FM patients were recruited at 12 U.S. clinics. Patients received either a combination treatment of IMC-1 or a matching placebo.

According to Dr. Pridgen, chronic tissue-resident herpes virus may be an underlying cause of fibromyalgia. IMC-1 represents a novel treatment by combining an anti-herpes virus nucleoside analog with the anti-herpes virus activity exhibited by a COX-2 inhibitor.

"Many herpes viruses are known to significantly upregulate COX enzymes in the body, which in turn are important for efficient viral replication," Pridgen said. "In theory, physical or emotional stress in patients can reactivate the virus and result in perpetuation of the symptoms of fibromyalgia. Effectively suppressing latent viruses may significantly improve the pain and related symptoms of FM."

The PRID-201 clinical study tested this hypothesis using the IMC-1 fixed-dose-combination. Patients in the trial rated their pain over the course of the study using a 0-10 numeric rating scale, with the study's primary endpoint being the reduction in average pain from baseline to week 16. Pain measured on both a 24-hour and seven-day recall basis met statistical significance, with the seven-day recall data achieving high statistical significance (p=0.001). Other therapeutic domains studied that showed statistical significance were Patient Global Impression (PGIC), all three Revised Fibromyalgia Impact Questionnaire (FIQ-R) domains, 30% and 50% Pain reduction responder analysis and the NIH PROMIS fatigue instrument.

Other noteworthy results from PRID-201: there was a lower discontinuation rate among patients in the IMC-1 arm compared to placebo, with 82.6 percent of patients randomized to IMC-1 completing the full 16 weeks of treatment versus 60.8 percent of patients on placebo. The discontinuation rate due to adverse events was almost three times lower for patients in the IMC-1 group 5.8% than for those on placebo 16.2% (p=0.012). While 41 percent of patients randomized to placebo used rescue medication, only 25 percent of those in the IMC-1 group required rescue medication (p=0.037).

"Compared to placebo, the relatively high completion rate, improved pain scores and the low rate of discontinuation because of adverse events are consistent with a well-tolerated and effective therapy," Dr. Clauw said.

SOURCE Innovative Med Concepts, LLC
.



http://www.news-medical.net/news/20...n-shows-promise-in-treating-fibromyalgia.aspx
 

Folk

Senior Member
Messages
217
I find that quite good...

Also... that's supposed to be the final dose? If I remember correclty Dr. Pridgens said that it would take more time to create the final solution.
 

voner

Senior Member
Messages
592