Guest guest Posted June 8, 2007 Report Share Posted June 8, 2007 ' I catch plenty of news, sound bites. the problem in my opinion is that you have 1 trillion bacteria that produce toxins that are embedded into your fat cells..And this is not important? or the missing link? in the genetics of things. > > > This is some enormous new disease loci study covering seven common > diseases... 2-3,000 individuals in each group. I don't know if that > makes it the biggest study of it's kind for some of these diseases - > but I'm guessing so, since 50 labs worked on this cooperative. > > I'm posting it for Tony... > > " [...] Case-control comparisons identified 24 independent association > signals at P < 5e-7: 1 in bipolar disorder, 1 in coronary artery > disease, 9 in Crohn's disease, 3 in rheumatoid arthritis, 7 in type 1 > diabetes and 3 in type 2 diabetes. [...] We observed association at > many previously identified loci, and found compelling evidence that > some loci confer risk for more than one of the diseases studied. [...] > The importance of appropriately large samples was confirmed by the > modest effect sizes observed at most loci identified. " > > http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html > > Haha, you'll like that last sentence, Tony. Modest effect sizes. > Sounds like no one gene makes a real big difference in any of these > diseases. > > I don't think that rules out the possibility that some of them could > be autoimmune diseases (in some stronger or weaker sense), as there > are sooo many genes that can influence thresholds for loss of > self-tolerance. But it does tend to make it seem more likely that > something big is missing in the ideas most people have of these diseases. > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 9, 2007 Report Share Posted June 9, 2007 Bob I hear what your saying BUT. The first thing I noticed when looking for the simple explanation of why am I told everything's normal in my tests, when I feel like this. I took my query under my arm and headed to my cousins whose blood work was being monitored for something he was taking, but otherwise extremely healthy.THE FIRST THING THAT WAS OBVIOUS IS THAT PEOPLE WITH THESE DISORDERS 'WHILE SUFFERING' NOT THE BLOOD TEST TAKEN WHEN YOU WERE OK TO GO AND HAVE IT DRAWN, HAVE LOTS OF HAEMOLYSIS- DESTRUCTION OF RED CELLS BY IMO 'TOXINS'. These are the same guys that hurt and damage your internals making it look like someone's passed a blow torch thru your inards.Also the platelet clumping (intravascular coagulation) that see's there numbers drop.Often when so called herxing.. So to sit here and have an intelligent arguement about an immune system that's gone awry is silly, when an abvious shift from an external source, a TOXIN, can be easily observed..I also recall early in the piece describing to a doctor my fibromyalgia feels like acid running thru your veins. > > > > > > > > > This is some enormous new disease loci study covering seven common > > > diseases... 2-3,000 individuals in each group. I don't know if that > > > makes it the biggest study of it's kind for some of these diseases - > > > but I'm guessing so, since 50 labs worked on this cooperative. > > > > > > I'm posting it for Tony... > > > > > > " [...] Case-control comparisons identified 24 independent > > association > > > signals at P < 5e-7: 1 in bipolar disorder, 1 in coronary artery > > > disease, 9 in Crohn's disease, 3 in rheumatoid arthritis, 7 in type > > 1 > > > diabetes and 3 in type 2 diabetes. [...] We observed association at > > > many previously identified loci, and found compelling evidence that > > > some loci confer risk for more than one of the diseases studied. > > [...] > > > The importance of appropriately large samples was confirmed by the > > > modest effect sizes observed at most loci identified. " > > > > > > > > http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html> > > > > > > Haha, you'll like that last sentence, Tony. Modest effect sizes. > > > Sounds like no one gene makes a real big difference in any of these > > > diseases. > > > > > > I don't think that rules out the possibility that some of them could > > > be autoimmune diseases (in some stronger or weaker sense), as there > > > are sooo many genes that can influence thresholds for loss of > > > self-tolerance. But it does tend to make it seem more likely that > > > something big is missing in the ideas most people have of these > > diseases. > > > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 9, 2007 Report Share Posted June 9, 2007 Bob That is rediculous.. When you attempt therapy you have to know what your going after, been there, done that, failed, is alway's the case for people with a simple urinry tract infection. Some have been thru these episodes on upto 18 occasions(thru there medical history) and still haven't cleared them. You've also got to have a look at what is going on in your own case- YOUR DESCRIBING YOUR WIFE AS SOMEONE THAT'S BEING CONSTANTLY THRASHED TO WITHIN AN INCH OF HER LIFE AND YOUR SITTING HERE COMFORTABLE THAT IT MAY BE MULTIFACTORAL- AND POSSABLY HER IMMUNE SYSTEM ATTACKING HER? DO YOU REALISE THAT MOST PEOPLE HAVE ONE THING OCCUR THAT TIPS THEM OVER-MONO-SURGERY -INJURY-WHIPLASH-COURSE OF ANTIBIOTICS-TICK BITE (ONE FOR PAULA) and you feel comfortable that her epsiodes of what should be best described as TOXEMIA aren't real... it's all due to an immune system that's gone whacky. Why don't you ask your wife while she's suffering if she would accept TOXEMIA as the best explanation for her ilness- we don't need you to tell us ask her...She may be the one that opens your eyes or maybe you should look at what comes out after a historectomy-it's pretty obvious that something needs better explaining when things come out that have been giving long term pain and look like someone's attacked part of the anatomy with a blowtorch. tony > >> > > >> > > >> > This is some enormous new disease loci study covering seven > >> common > >> > diseases... 2-3,000 individuals in each group. I don't know > >> if that > >> > makes it the biggest study of it's kind for some of these > >> diseases - > >> > but I'm guessing so, since 50 labs worked on this cooperative. > >> > > >> > I'm posting it for Tony... > >> > > >> > " [...] Case-control comparisons identified 24 independent > >> association > >> > signals at P < 5e-7: 1 in bipolar disorder, 1 in coronary > >> artery > >> > disease, 9 in Crohn's disease, 3 in rheumatoid arthritis, 7 > >> in type > >> 1 > >> > diabetes and 3 in type 2 diabetes. [...] We observed > >> association at > >> > many previously identified loci, and found compelling > >> evidence that > >> > some loci confer risk for more than one of the diseases > >> studied. > >> [...] > >> > The importance of appropriately large samples was confirmed > >> by the > >> > modest effect sizes observed at most loci identified. " > >> > > >> > > >> http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html > >> <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html> > >> > > >> > Haha, you'll like that last sentence, Tony. Modest effect > >> sizes. > >> > Sounds like no one gene makes a real big difference in any > >> of these > >> > diseases. > >> > > >> > I don't think that rules out the possibility that some of > >> them could > >> > be autoimmune diseases (in some stronger or weaker sense), > >> as there > >> > are sooo many genes that can influence thresholds for loss of > >> > self-tolerance. But it does tend to make it seem more > >> likely that > >> > something big is missing in the ideas most people have of > >> these > >> diseases. > >> > > >> > >> > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 9, 2007 Report Share Posted June 9, 2007 Bob Again, you describe thinking you've nearly lost your wife on several occasions... THIS IS TOXEMIA that is thrashing her to death, not autoimmune bullshit.. tony > >> > > >> > > >> > This is some enormous new disease loci study covering seven > >> common > >> > diseases... 2-3,000 individuals in each group. I don't know > >> if that > >> > makes it the biggest study of it's kind for some of these > >> diseases - > >> > but I'm guessing so, since 50 labs worked on this cooperative. > >> > > >> > I'm posting it for Tony... > >> > > >> > " [...] Case-control comparisons identified 24 independent > >> association > >> > signals at P < 5e-7: 1 in bipolar disorder, 1 in coronary > >> artery > >> > disease, 9 in Crohn's disease, 3 in rheumatoid arthritis, 7 > >> in type > >> 1 > >> > diabetes and 3 in type 2 diabetes. [...] We observed > >> association at > >> > many previously identified loci, and found compelling > >> evidence that > >> > some loci confer risk for more than one of the diseases > >> studied. > >> [...] > >> > The importance of appropriately large samples was confirmed > >> by the > >> > modest effect sizes observed at most loci identified. " > >> > > >> > > >> http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html > >> <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html> > >> > > >> > Haha, you'll like that last sentence, Tony. Modest effect > >> sizes. > >> > Sounds like no one gene makes a real big difference in any > >> of these > >> > diseases. > >> > > >> > I don't think that rules out the possibility that some of > >> them could > >> > be autoimmune diseases (in some stronger or weaker sense), > >> as there > >> > are sooo many genes that can influence thresholds for loss of > >> > self-tolerance. But it does tend to make it seem more > >> likely that > >> > something big is missing in the ideas most people have of > >> these > >> diseases. > >> > > >> > >> > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 9, 2007 Report Share Posted June 9, 2007 Bob I threw my last post at you because it just bounced around my head that all I knew was your wife was being thrashed to within an inch of her life.I call this TOXEMIA, you somewhat agree..And now for some fuked up reason you still think there's more to the puzzle. Try dehydration from long term inflammation due to toxemia. Try low blood volume from the same set of circumstances..What do you think long term inflmammtion/low blood volume/dehydration/followed by mineral inbalances provides? Perfectly functioning organs?A nice glowing head of hair?It provides a managery that if you try an interpret will take a life timewith no answers.. BOB GO BACK AND DISCOVER WHAT IS CAUSING THE TOXEMIA IN YOUR WIFES CASE......and stop feeding us it's a lot of things causing this ONE problem.. tony > > > >> > > > > >> > > > > >> > This is some enormous new disease loci study covering > > seven > > > >> common > > > >> > diseases... 2-3,000 individuals in each group. I don't > > know > > > >> if that > > > >> > makes it the biggest study of it's kind for some of > > these > > > >> diseases - > > > >> > but I'm guessing so, since 50 labs worked on this > > cooperative. > > > >> > > > > >> > I'm posting it for Tony... > > > >> > > > > >> > " [...] Case-control comparisons identified 24 > > independent > > > >> association > > > >> > signals at P < 5e-7: 1 in bipolar disorder, 1 in > > coronary > > > >> artery > > > >> > disease, 9 in Crohn's disease, 3 in rheumatoid > > arthritis, 7 > > > >> in type > > > >> 1 > > > >> > diabetes and 3 in type 2 diabetes. [...] We observed > > > >> association at > > > >> > many previously identified loci, and found compelling > > > >> evidence that > > > >> > some loci confer risk for more than one of the diseases > > > >> studied. > > > >> [...] > > > >> > The importance of appropriately large samples was > > confirmed > > > >> by the > > > >> > modest effect sizes observed at most loci identified. " > > > >> > > > > >> > > > > >> > > http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html> > > > >> > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html> > > > > >> > > > > >> > Haha, you'll like that last sentence, Tony. Modest > > effect > > > >> sizes. > > > >> > Sounds like no one gene makes a real big difference in > > any > > > >> of these > > > >> > diseases. > > > >> > > > > >> > I don't think that rules out the possibility that some > > of > > > >> them could > > > >> > be autoimmune diseases (in some stronger or weaker > > sense), > > > >> as there > > > >> > are sooo many genes that can influence thresholds for > > loss of > > > >> > self-tolerance. But it does tend to make it seem more > > > >> likely that > > > >> > something big is missing in the ideas most people have > > of > > > >> these > > > >> diseases. > > > >> > > > > >> > > > >> > > > > > > > > > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 9, 2007 Report Share Posted June 9, 2007 Bob The other thing that I can try and teach you to learn about which we have been touching on is how this toxemia cycle starts. The quorum sensing bacterial communication stuff that occurs to give you the whole quagmire of your wife in distress and thrashed to within an inch of her life by the oncoming toxemia.We as a community have discovered that what we eat, the climate, and light around us can also determine how this toxemia will impact us.. you seem to avoid this-your basically listening to people like HARRY HIGH PANTS(rich) whom have strategies for managing these diseases,which deep down we already follow to some degree from our own trial and error stuff.. tony > > > >> > > > > >> > > > > >> > This is some enormous new disease loci study covering > > seven > > > >> common > > > >> > diseases... 2-3,000 individuals in each group. I don't > > know > > > >> if that > > > >> > makes it the biggest study of it's kind for some of > > these > > > >> diseases - > > > >> > but I'm guessing so, since 50 labs worked on this > > cooperative. > > > >> > > > > >> > I'm posting it for Tony... > > > >> > > > > >> > " [...] Case-control comparisons identified 24 > > independent > > > >> association > > > >> > signals at P < 5e-7: 1 in bipolar disorder, 1 in > > coronary > > > >> artery > > > >> > disease, 9 in Crohn's disease, 3 in rheumatoid > > arthritis, 7 > > > >> in type > > > >> 1 > > > >> > diabetes and 3 in type 2 diabetes. [...] We observed > > > >> association at > > > >> > many previously identified loci, and found compelling > > > >> evidence that > > > >> > some loci confer risk for more than one of the diseases > > > >> studied. > > > >> [...] > > > >> > The importance of appropriately large samples was > > confirmed > > > >> by the > > > >> > modest effect sizes observed at most loci identified. " > > > >> > > > > >> > > > > >> > > http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html> > > > >> > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html> > > > > >> > > > > >> > Haha, you'll like that last sentence, Tony. Modest > > effect > > > >> sizes. > > > >> > Sounds like no one gene makes a real big difference in > > any > > > >> of these > > > >> > diseases. > > > >> > > > > >> > I don't think that rules out the possibility that some > > of > > > >> them could > > > >> > be autoimmune diseases (in some stronger or weaker > > sense), > > > >> as there > > > >> > are sooo many genes that can influence thresholds for > > loss of > > > >> > self-tolerance. But it does tend to make it seem more > > > >> likely that > > > >> > something big is missing in the ideas most people have > > of > > > >> these > > > >> diseases. > > > >> > > > > >> > > > >> > > > > > > > > > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 9, 2007 Report Share Posted June 9, 2007 Bob you don't understand nor are trying to understand infections.My best friends father has been dealing with a UTI for 20 years he originally had his bladder removed years earlier for cancerous reasons.Your here trying to teach us that it's not the infection part, that's been taken care of, its the other bits?just take a step back and get your head around biaxin is only managing a few symptoms of the infection- it's just denting the surface of the real underlying infectious problem ..Bob you need 100 times the amount of penicillin or other drug offered up to take care of an infectious arthritis.....tony > > > > > >> > > > > > > >> > > > > > > >> > This is some enormous new disease loci study covering > > > > seven > > > > > >> common > > > > > >> > diseases... 2-3,000 individuals in each group. I don't > > > > know > > > > > >> if that > > > > > >> > makes it the biggest study of it's kind for some of > > > > these > > > > > >> diseases - > > > > > >> > but I'm guessing so, since 50 labs worked on this > > > > cooperative. > > > > > >> > > > > > > >> > I'm posting it for Tony... > > > > > >> > > > > > > >> > " [...] Case-control comparisons identified 24 > > > > independent > > > > > >> association > > > > > >> > signals at P < 5e-7: 1 in bipolar disorder, 1 in > > > > coronary > > > > > >> artery > > > > > >> > disease, 9 in Crohn's disease, 3 in rheumatoid > > > > arthritis, 7 > > > > > >> in type > > > > > >> 1 > > > > > >> > diabetes and 3 in type 2 diabetes. [...] We observed > > > > > >> association at > > > > > >> > many previously identified loci, and found compelling > > > > > >> evidence that > > > > > >> > some loci confer risk for more than one of the diseases > > > > > >> studied. > > > > > >> [...] > > > > > >> > The importance of appropriately large samples was > > > > confirmed > > > > > >> by the > > > > > >> > modest effect sizes observed at most loci identified. " > > > > > >> > > > > > > >> > > > > > > >> > > > > > > http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html> > > > > > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html> > > > > > > >> > > > > > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html> > > > > > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html> > > > > > > > > > >> > > > > > > >> > Haha, you'll like that last sentence, Tony. Modest > > > > effect > > > > > >> sizes. > > > > > >> > Sounds like no one gene makes a real big difference in > > > > any > > > > > >> of these > > > > > >> > diseases. > > > > > >> > > > > > > >> > I don't think that rules out the possibility that some > > > > of > > > > > >> them could > > > > > >> > be autoimmune diseases (in some stronger or weaker > > > > sense), > > > > > >> as there > > > > > >> > are sooo many genes that can influence thresholds for > > > > loss of > > > > > >> > self-tolerance. But it does tend to make it seem more > > > > > >> likely that > > > > > >> > something big is missing in the ideas most people have > > > > of > > > > > >> these > > > > > >> diseases. > > > > > >> > > > > > > >> > > > > > >> > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 10, 2007 Report Share Posted June 10, 2007 Bob I come into the forum have a quick read and ramble off a few things. You said this provides no purpose. I think our communication proved beyond doubt that when your being thrashed to within an inch of your life, it needs an explanation, and the fact that the word 'TOXEMIA' is possably the best description of these catasrtrophic events as opposed to some wishy, washy, Yasko style Rich explanation, we've achieved heaps. What you fail to understand, regardless of how it's described, is that YOUR WIFE NEEDS TO IDENTIFY WHAT IS CAUSING HER TOXEMIA.This is generally non invasive and inexpensive, in the scheme of things.But again we'll get the multifactoral crap, crap, and more crap approach- to keep things extremely complicated because these conditions need to be extremely complicated.Mate in 100 plus years of disease the healthy immune system isn't going to help anything. So pursuing this angle which seems popular, goes against the trend of everything that is scientific commonsense..We basically need vaccinating against 20 or 30 viruses, bacteria and more importantly there toxins..this is what science has offered up for the past 100 years- the boost the immune system stuff is the big buck hype that doesn't cure disease I'm afraid. So Bob being content sitting at every doctors appointment time and time again, and possably making no progress, but offering up confusing crap, is detremental to your wifes health I'm afraid.. > > > > > > > >> > > > > > > > > >> > > > > > > > > >> > This is some enormous new disease loci study covering > > > > > > seven > > > > > > > >> common > > > > > > > >> > diseases... 2-3,000 individuals in each group. I don't > > > > > > know > > > > > > > >> if that > > > > > > > >> > makes it the biggest study of it's kind for some of > > > > > > these > > > > > > > >> diseases - > > > > > > > >> > but I'm guessing so, since 50 labs worked on this > > > > > > cooperative. > > > > > > > >> > > > > > > > > >> > I'm posting it for Tony... > > > > > > > >> > > > > > > > > >> > " [...] Case-control comparisons identified 24 > > > > > > independent > > > > > > > >> association > > > > > > > >> > signals at P < 5e-7: 1 in bipolar disorder, 1 in > > > > > > coronary > > > > > > > >> artery > > > > > > > >> > disease, 9 in Crohn's disease, 3 in rheumatoid > > > > > > arthritis, 7 > > > > > > > >> in type > > > > > > > >> 1 > > > > > > > >> > diabetes and 3 in type 2 diabetes. [...] We observed > > > > > > > >> association at > > > > > > > >> > many previously identified loci, and found compelling > > > > > > > >> evidence that > > > > > > > >> > some loci confer risk for more than one of the diseases > > > > > > > >> studied. > > > > > > > >> [...] > > > > > > > >> > The importance of appropriately large samples was > > > > > > confirmed > > > > > > > >> by the > > > > > > > >> > modest effect sizes observed at most loci identified. " > > > > > > > >> > > > > > > > > >> > > > > > > > > >> > > > > > > > > > > > > http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html> > > > > > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html> > > > > > > > > > > > > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html> > > > > > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html> > > > > > > > > > > > >> > > > > > > > > > > > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html> > > > > > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html> > > > > > > > > > > > > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html> > > > > > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html> > > > > > > > > > > > > > > > > >> > > > > > > > > >> > Haha, you'll like that last sentence, Tony. Modest > > > > > > effect > > > > > > > >> sizes. > > > > > > > >> > Sounds like no one gene makes a real big difference in > > > > > > any > > > > > > > >> of these > > > > > > > >> > diseases. > > > > > > > >> > > > > > > > > >> > I don't think that rules out the possibility that some > > > > > > of > > > > > > > >> them could > > > > > > > >> > be autoimmune diseases (in some stronger or weaker > > > > > > sense), > > > > > > > >> as there > > > > > > > >> > are sooo many genes that can influence thresholds for > > > > > > loss of > > > > > > > >> > self-tolerance. But it does tend to make it seem more > > > > > > > >> likely that > > > > > > > >> > something big is missing in the ideas most people have > > > > > > of > > > > > > > >> these > > > > > > > >> diseases. > > > > > > > >> > > > > > > > > >> > > > > > > > >> > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 10, 2007 Report Share Posted June 10, 2007 Bob, I don't know the answers but have a couple of thoughts. One is that a lot of us seem to respond to Zithromax and not Biaxin. I don't know why. It is just true. The other is an odd experience I had a couple of weeks ago. You know I have the strange 1 year headache which is probably caused by MRSA which has gotten into my sinuses and head. Well, I used Bactroban swabs and Xylotol spray 2 weeks ago. In two days I had swollen glands, sore throat and a low grade fever. Oops. My wonderful doctor who tries to help me sort things out suggested I just use the Xylotol and see what happens. So I am starting back on that today. All of that to say I hear you when you say your wife can't tolerate massive combos and doses of various antibiotics. We've all got to hang together and keep searching for solutions. I still believe they are out there. a Carnes - back from Zion > > HI TONY. I HEAR YOU. I think you misunderstand though. We believe > toxemia is her main problem, actually. I don't believe her immune > system is attacking her and never said I did. I was just having a > conversation about auto immune disease. My wife would however agree > that her immune system is malfunctioning. It is severely up- regulated > much of the time and over-reacts to most everything. It doesn't know > when / how to shut off. Seasonally, in the fall, it tends to > down-regulate so that she catches every sniffle in the air. That is > clearly abnormal. It's merely an observation about how one of her body > systems (doesn't) work, though; it's not a judgment about her, or the > reality of her symptoms or suffering. > > I would take personal offense to the suggestion that I think her > symptoms " aren't real " , except that I have no idea how you could > rationally draw such a conclusion from anything I've ever written about > her. Her symptoms are all too real. I think your problem is that you > don't see anything as real unless it's bacterially caused, and you > therefore assume that I don't think her symptoms are real because I > don't believe they are 100% the result of infection. For what it's > worth, though, we are working primarily on the infectious angle and I > would credit pathogens for 90% of her symptoms even if I think the > organisms are opportunistic because of some completely different cause > -- probably in my opinion environmental poisoning combined with genetic > vulnerability. The latter is water over the dam, of course, and the > pathogens are something we can actually do something about. My greatest > fear is that we will not be able to permanently banish them if we can > never find and fix the underlying cause, however. > > The main problem with aggressive antibiotic therapy is that her burden > of pathogens is so high that any significant progress in killing them > creates a toxic storm. Or what you would call toxemia. We have > actually worked out a protocol with Biaxin that sort of works for her > and are currently pursuing it, but it's a white-knuckle balancing act. > Doing it wrong without consideration of all the factors involved, only > makes her more miserable and could well kill her. Doing it right brings > relief and something vaguely resembling quality of life. We are slowly > figuring out what's right for her. > > --Bob > > dumbaussie2000 wrote: > > > > > > Bob > > That is rediculous.. When you attempt therapy you have to know what > > your going after, been there, done that, failed, is alway's the case > > for people with a simple urinry tract infection. Some have been thru > > these episodes on upto 18 occasions(thru there medical history) and > > still haven't cleared them. > > You've also got to have a look at what is going on in your own case- > > YOUR DESCRIBING YOUR WIFE AS SOMEONE THAT'S BEING CONSTANTLY THRASHED > > TO WITHIN AN INCH OF HER LIFE AND YOUR SITTING HERE COMFORTABLE THAT > > IT MAY BE MULTIFACTORAL- AND POSSABLY HER IMMUNE SYSTEM ATTACKING HER? > > DO YOU REALISE THAT MOST PEOPLE HAVE ONE THING OCCUR THAT TIPS THEM > > OVER-MONO-SURGERY -INJURY-WHIPLASH-COURSE OF ANTIBIOTICS-TICK BITE > > (ONE FOR PAULA) and you feel comfortable that her epsiodes of what > > should be best described as TOXEMIA aren't real... it's all due to an > > immune system that's gone whacky. > > Why don't you ask your wife while she's suffering if she would accept > > TOXEMIA as the best explanation for her ilness- we don't need you to > > tell us ask her...She may be the one that opens your eyes or maybe > > you should look at what comes out after a historectomy-it's pretty > > obvious that something needs better explaining when things come out > > that have been giving long term pain and look like someone's attacked > > part of the anatomy with a blowtorch. > > tony > > > > > > > >> > > > > >> > > > > >> > This is some enormous new disease loci study covering > > seven > > > >> common > > > >> > diseases... 2-3,000 individuals in each group. I don't > > know > > > >> if that > > > >> > makes it the biggest study of it's kind for some of > > these > > > >> diseases - > > > >> > but I'm guessing so, since 50 labs worked on this > > cooperative. > > > >> > > > > >> > I'm posting it for Tony... > > > >> > > > > >> > " [...] Case-control comparisons identified 24 > > independent > > > >> association > > > >> > signals at P < 5e-7: 1 in bipolar disorder, 1 in > > coronary > > > >> artery > > > >> > disease, 9 in Crohn's disease, 3 in rheumatoid > > arthritis, 7 > > > >> in type > > > >> 1 > > > >> > diabetes and 3 in type 2 diabetes. [...] We observed > > > >> association at > > > >> > many previously identified loci, and found compelling > > > >> evidence that > > > >> > some loci confer risk for more than one of the diseases > > > >> studied. > > > >> [...] > > > >> > The importance of appropriately large samples was > > confirmed > > > >> by the > > > >> > modest effect sizes observed at most loci identified. " > > > >> > > > > >> > > > > >> > > http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html> > > > >> > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html> > > > > >> > > > > >> > Haha, you'll like that last sentence, Tony. Modest > > effect > > > >> sizes. > > > >> > Sounds like no one gene makes a real big difference in > > any > > > >> of these > > > >> > diseases. > > > >> > > > > >> > I don't think that rules out the possibility that some > > of > > > >> them could > > > >> > be autoimmune diseases (in some stronger or weaker > > sense), > > > >> as there > > > >> > are sooo many genes that can influence thresholds for > > loss of > > > >> > self-tolerance. But it does tend to make it seem more > > > >> likely that > > > >> > something big is missing in the ideas most people have > > of > > > >> these > > > >> diseases. > > > >> > > > > >> > > > >> > > > > > > > > > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 11, 2007 Report Share Posted June 11, 2007 Bob, you are a good man. I think you told me this before about the Zithromax. I wish you both the BEST. a > > She can't tolerate Zithro at all. Strangely, aside from a massive > cytokine storm, the symptoms are what we associate with mobilization of > mercury: dark depression and emotional lability, which in her case are > particularly striking because that is so contrary to her fundamental nature. > > Tried mino once, tore her stomach up right away and took months to > recover. These kinds of atypical responses make abx really challenging. > > Biaxin brings about promising clinical results but is hard on the > stomach; even so she managed a three week course which for her is a huge > accomplishment. And then the doctor tried adding Ceftin. > > Ceftin has been tolerated fine in the past by itself, though it didn't > produce clinical results one way or the other. But combined with > Biaxin, Ceftin produced an immediate heavy die off of something. The > toxins overwhelmed her liver, liver enzymes went through the roof, and > coincidentally or not, she threw a gall stone (completely new problem -- > whoopee). > > At this point one of her doctors is convinced the gall bladder needs to > go, that it's a locus of infection and in any case should be removed > while it's elective, not wait until it's a crisis. He wants to > stabilize her for a couple of months and then do the laproscopic > procedure to take it out. The other doctor is more conservative and > doesn't recommend attempting surgery unless she has another attack. He > puts the odds of such an attack at 20%. > > Unless she has another attack, we are going to move heaven and earth to > avoid the knife because with the severe MCS, the combination of a > hospital stay and anesthesia could well run her into the ground, if not > do her in altogether. For now, she is just starting the Biaxin again by > itself. > > --Bob > > pjeanneus wrote: > > > > Bob, > > I don't know the answers but have a couple of thoughts. One is that a > > lot of us seem to respond to Zithromax and not Biaxin. I don't know > > why. It is just true. > > > > The other is an odd experience I had a couple of weeks ago. You know > > I have the strange 1 year headache which is probably caused by MRSA > > which has gotten into my sinuses and head. Well, I used Bactroban > > swabs and Xylotol spray 2 weeks ago. In two days I had swollen > > glands, sore throat and a low grade fever. Oops. > > > > My wonderful doctor who tries to help me sort things out suggested I > > just use the Xylotol and see what happens. So I am starting back on > > that today. > > > > All of that to say I hear you when you say your wife can't tolerate > > massive combos and doses of various antibiotics. > > > > We've all got to hang together and keep searching for solutions. I > > still believe they are out there. > > > > a Carnes - back from Zion > > > > > > > > HI TONY. I HEAR YOU. I think you misunderstand though. We > > believe > > > toxemia is her main problem, actually. I don't believe her immune > > > system is attacking her and never said I did. I was just having a > > > conversation about auto immune disease. My wife would however > > agree > > > that her immune system is malfunctioning. It is severely up- > > regulated > > > much of the time and over-reacts to most everything. It doesn't > > know > > > when / how to shut off. Seasonally, in the fall, it tends to > > > down-regulate so that she catches every sniffle in the air. That > > is > > > clearly abnormal. It's merely an observation about how one of her > > body > > > systems (doesn't) work, though; it's not a judgment about her, or > > the > > > reality of her symptoms or suffering. > > > > > > I would take personal offense to the suggestion that I think her > > > symptoms " aren't real " , except that I have no idea how you could > > > rationally draw such a conclusion from anything I've ever written > > about > > > her. Her symptoms are all too real. I think your problem is that > > you > > > don't see anything as real unless it's bacterially caused, and you > > > therefore assume that I don't think her symptoms are real because I > > > don't believe they are 100% the result of infection. For what it's > > > worth, though, we are working primarily on the infectious angle and > > I > > > would credit pathogens for 90% of her symptoms even if I think the > > > organisms are opportunistic because of some completely different > > cause > > > -- probably in my opinion environmental poisoning combined with > > genetic > > > vulnerability. The latter is water over the dam, of course, and > > the > > > pathogens are something we can actually do something about. My > > greatest > > > fear is that we will not be able to permanently banish them if we > > can > > > never find and fix the underlying cause, however. > > > > > > The main problem with aggressive antibiotic therapy is that her > > burden > > > of pathogens is so high that any significant progress in killing > > them > > > creates a toxic storm. Or what you would call toxemia. We have > > > actually worked out a protocol with Biaxin that sort of works for > > her > > > and are currently pursuing it, but it's a white-knuckle balancing > > act. > > > Doing it wrong without consideration of all the factors involved, > > only > > > makes her more miserable and could well kill her. Doing it right > > brings > > > relief and something vaguely resembling quality of life. We are > > slowly > > > figuring out what's right for her. > > > > > > --Bob > > > > > > dumbaussie2000 wrote: > > > > > > > > > > > > Bob > > > > That is rediculous.. When you attempt therapy you have to know > > what > > > > your going after, been there, done that, failed, is alway's the > > case > > > > for people with a simple urinry tract infection. Some have been > > thru > > > > these episodes on upto 18 occasions(thru there medical history) > > and > > > > still haven't cleared them. > > > > You've also got to have a look at what is going on in your own > > case- > > > > YOUR DESCRIBING YOUR WIFE AS SOMEONE THAT'S BEING CONSTANTLY > > THRASHED > > > > TO WITHIN AN INCH OF HER LIFE AND YOUR SITTING HERE COMFORTABLE > > THAT > > > > IT MAY BE MULTIFACTORAL- AND POSSABLY HER IMMUNE SYSTEM ATTACKING > > HER? > > > > DO YOU REALISE THAT MOST PEOPLE HAVE ONE THING OCCUR THAT TIPS > > THEM > > > > OVER-MONO-SURGERY -INJURY-WHIPLASH-COURSE OF ANTIBIOTICS-TICK BITE > > > > (ONE FOR PAULA) and you feel comfortable that her epsiodes of what > > > > should be best described as TOXEMIA aren't real... it's all due > > to an > > > > immune system that's gone whacky. > > > > Why don't you ask your wife while she's suffering if she would > > accept > > > > TOXEMIA as the best explanation for her ilness- we don't need you > > to > > > > tell us ask her...She may be the one that opens your eyes or maybe > > > > you should look at what comes out after a historectomy-it's pretty > > > > obvious that something needs better explaining when things come > > out > > > > that have been giving long term pain and look like someone's > > attacked > > > > part of the anatomy with a blowtorch. > > > > tony > > > > > > > > > > > > > >> > > > > > > >> > > > > > > >> > This is some enormous new disease loci study covering > > > > seven > > > > > >> common > > > > > >> > diseases... 2-3,000 individuals in each group. I don't > > > > know > > > > > >> if that > > > > > >> > makes it the biggest study of it's kind for some of > > > > these > > > > > >> diseases - > > > > > >> > but I'm guessing so, since 50 labs worked on this > > > > cooperative. > > > > > >> > > > > > > >> > I'm posting it for Tony... > > > > > >> > > > > > > >> > " [...] Case-control comparisons identified 24 > > > > independent > > > > > >> association > > > > > >> > signals at P < 5e-7: 1 in bipolar disorder, 1 in > > > > coronary > > > > > >> artery > > > > > >> > disease, 9 in Crohn's disease, 3 in rheumatoid > > > > arthritis, 7 > > > > > >> in type > > > > > >> 1 > > > > > >> > diabetes and 3 in type 2 diabetes. [...] We observed > > > > > >> association at > > > > > >> > many previously identified loci, and found compelling > > > > > >> evidence that > > > > > >> > some loci confer risk for more than one of the diseases > > > > > >> studied. > > > > > >> [...] > > > > > >> > The importance of appropriately large samples was > > > > confirmed > > > > > >> by the > > > > > >> > modest effect sizes observed at most loci identified. " > > > > > >> > > > > > > >> > > > > > > >> > > > > > > http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html> > > > > > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html> > > > > > > >> > > > > > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html> > > > > > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html > > <http://www.nature.com/nature/journal/v447/n7145/abs/nature05911.html> > > > > > > > > > >> > > > > > > >> > Haha, you'll like that last sentence, Tony. Modest > > > > effect > > > > > >> sizes. > > > > > >> > Sounds like no one gene makes a real big difference in > > > > any > > > > > >> of these > > > > > >> > diseases. > > > > > >> > > > > > > >> > I don't think that rules out the possibility that some > > > > of > > > > > >> them could > > > > > >> > be autoimmune diseases (in some stronger or weaker > > > > sense), > > > > > >> as there > > > > > >> > are sooo many genes that can influence thresholds for > > > > loss of > > > > > >> > self-tolerance. But it does tend to make it seem more > > > > > >> likely that > > > > > >> > something big is missing in the ideas most people have > > > > of > > > > > >> these > > > > > >> diseases. > > > > > >> > > > > > > >> > > > > > >> > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 11, 2007 Report Share Posted June 11, 2007 Well, despite my investigation of odds ratios and relative risks, I still find ORs hard to digest. Fortunately, it seems that whenever the outcome (in this case, the disease state) has a low probability, the OR and RR are very similar. All these diseases have a prevalence lower than 1-2%, except maybe type 2 diabetes, so the OR ~= the RR. I calculated the ORs and RRs for an allele whose presence adjusts a risk from 1% to 2%: OR: 2.02 RR: 2.00 and one that adjusts a risk from 2% to 8%: OR: 4.26 RR: 4.00 ....basically the same deal. So there's plenty of room here to just read the OR as an RR. Table 2, where they give already-strongly-supported associations which their cohorts confirm, gives no measure of strength of association that I am familiar with. Pretty short table anyways, outside the diabeteses. Table 3 gives novel associations, with both heterozygote and homozygote ORs. On to what's dealt with in the texts. In coronary artery disease there was some stuff related to methylation that Rich might be interested in... they mention homocysteine in this connection. CROHNS: interesting stuff here. They confirmed the old news of the CARD15/NOD2 null mutation conferring risk. Also the more recent IL-23r finding. Then there's 4 strong new ones which they say have been replicated with the studies reported elsewhere. One related to autophagy, though I think I heard about this previously. One involved in the development of the gut. One in a T cell signaling molecule also involved in RA and diabetes1. And finally one marker within a brain gene which they suggest is linked to a nearby gene affecting activity of resident peritoneal macrophages. Then there's some weaker stuff, pretty much all immune-related. Maybe I'll read more of this paper later... I need some food... but I'll say this: These new Crohn's associations all have homozygote odds ratios of 2.3 or less. The authors don't discuss the comparative functionality of the alleles in question. That's too bad, because the strength of association for a given allele should be proportional to the product of the centrality of its gene to the disease process, *multiplied by* the disease allele's functional differences from the other alleles of that gene. These alleles, looking at their ORs, obviously don't make a huge difference in whether you get Crohn's. But, if the functionality of the alleles being compared is very similar, then even a small disease association for one allele could mean that that allele's *gene product* is very important in the disease process - even though the allele is of low import in disease predisposition. On the other hand, if the allele in question is totally nonfunctional like the truncated CARD15/NOD2 allele related to Crohn's, then it had better have a serious odd ratio (it sure does) - otherwise that gene probably isn't very highly related to the disease process, but instead is only remotely related. It's kind of like this made-up example. Say you are exploring the causes of car crashes and say they probably almost all have a common final process, but you don't know what it is. All cars in the population, regardless of make and model, have steering wheel ABC or steering wheel XYZ installed more or less randomly. You find that steering wheel ABC is 2% more slippery than XYZ and confers a 1.10x greater risk of car crash compared to XYZ, with p < 0.02. Then you would conclude that while XYZ is slightly preferable, steering wheel slippage seems to be really important and central in car crashes. Whereas, if ABC was 100 times more slippery than XYZ (ie, ABC is a virtually nonfunctional allele), yet it still conferred only a 1.10x greater risk of crashing, you would still mildly prefer XYZ (that doesn't change at all), but you would conclude that really steering wheel slippage is not very important in car crashes. I don't think(?) near-nonfunctional alleles are that common in the mammalian genome, but I know of several examples of alleles with ~2x differences in function. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 12, 2007 Report Share Posted June 12, 2007 I've only skimmed the paper and the editorial, but the editorial says that the autophagy gene is the *second* one identified for Crohn's: " For Crohn's disease, one of the newly identified6 susceptibility genes is of particular interest because it is proposed to control the spread of intracellular pathogens by autophagy — the process of cellular self-digestion. This is the second gene to be implicated in Crohn's disease through involvement in autophagy; the first was identified earlier this year,.... " http://www.lhl.uab.edu:15087/nature/journal/v447/n7145/full/447645a.h tml IL-23 signaling promotes Th17 development, and the current rap on Th17s is that they probably kill extracellular bacteria and extracellular fungi. So it's sort of odd that Crohn's is associated with two genes that may target intracellular pathogens and one that may target extracellular bacteria/fungi. I wonder if the autophagy alleles and the IL23r allele enhance Crohn's risk even more when combined, or if this suggests instead that there exist unrelated subsets of Crohn's wherein each subset is dealing with different microbes. In a vague sense, I'm inclined to think that some Crohn's involves intracellular microbes and that in these cases Th1 cells and macrophages partner up to promote granulomas and the hypervitaminosis D that Abreu et al reported, whereas other patients are responding to extracellular bacteria and don't develop granulomas. I've read a statement or two about Crohn's being associated with granuloma formation, but I haven't seen anything consistent on this--as if granulomas are optional for the diagnosis. > > CROHNS: interesting stuff here. They confirmed the old news of the > CARD15/NOD2 null mutation conferring risk. Also the more recent IL- 23r > finding. Then there's 4 strong new ones which they say have been > replicated with the studies reported elsewhere. One related to > autophagy, though I think I heard about this previously. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 12, 2007 Report Share Posted June 12, 2007 > This is the second gene to be implicated in > Crohn's disease through involvement in autophagy; the first was > identified earlier this year,.... " Oops I need to eat my wheaties. Thanks for pointing that out; it's extremely interesting news. > So it's sort of odd that Crohn's is associated with two genes that > may target intracellular pathogens and one that may target > extracellular bacteria/fungi. That is weird. As you know I usually emphasize the thought that some factors involved in a disease's genesis may not be involved in its perpetuation, so that would be one way of ending up with an odd-looking melange of genes. On that note one might think about, say, a bacterium becoming established in the lumen for some weeks before ultimately invading enteric cell plasm. (It has to be at least 2 weeks, I guess, so that lumenal Th immunity can kick in, since we are trying to get involvement of extracellular Th immunity genes accounted for.) > I've read a statement or two about Crohn's being > associated with granuloma formation, but I haven't seen anything > consistent on this--as if granulomas are optional for the diagnosis. I had the sense, but a soft and vague sense, that it was " usually " granulomatous. However, I do recall pretty clearly reading that something like 10-15% of IBD patients were ambiguous between Crohn's and UC. Considering the quite poor concordance in dx of schizophrenia, eventual reassignment of many former MS diagnosees (something like 10+% IIRC), existence of mixed connective tissue disorders (not sure how common these are), etc, it seems a lot of the dxs we are interested in are not all that sharp. I bet there are more examples too that I'm not aware of. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 12, 2007 Report Share Posted June 12, 2007 It's worth noting that confirmation in a separate group of subjects - apparantly already completed for most of the new polymorphisms identified in this project - is the gold standard. So that's good. Apparently it's the only really good way to do the confirmation, because of the Bonferoni (multiple comparison) issues of making an immense number of comparisons while wanting to keep the chances of type 1 error (false rejection of the null hypothesis) under 0.05. I have no real desire to understand why, but some statisticians think the full Bonferoni correction is too conservative, and they seem to agree that in any event it reduces the precision of confidence. Whereas independent cohort confirmation yields a true p value with no complication. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 14, 2007 Report Share Posted June 14, 2007 The paper was sent to me by a friend- and I've read it twice. Basically what it's saying is not new- that Sarc (and some other diseases or syndromes) are the result of un sucessfull clearance of an infectious agent (either viral or bacterial)with the result being a hyopersensitivity, dysregulation and a suppression of the immune system (all at the same time), presenting as a certain set of symptoms depending on the genetic make-up of the host. That's the overview. But when you look at the details in the paper, you see: " observed to correlate with the presence of M. Tuberculosis DNA fragments " and " Biopsy material from 30 Swedish patients with Sarc confirmed immunohistochemical evidence of Rickettsia-like organisms " . Note the word CONFIRMED. We know looking at antibody's for proof of an infectious agent doesn't yield truthfull results as to whether the bug's there (or it's DNA fragments) are there or not. Chronic Sarc probably isn't any different from chronic Lyme - and foreign DNA products ( of latent living ) bacteria could very well be the cause. It's how to get 'em I wanna know. Barb PS SO I wonder if Trevor Marshall was consulted? I skimmed the 89 references in this paper and didn't see a single reference to him. > > I've only skimmed the paper and the editorial, but the editorial > says that the autophagy gene is the *second* one identified for > Crohn's: > > " For Crohn's disease, one of the newly identified6 susceptibility > genes is of particular interest because it is proposed to control > the spread of intracellular pathogens by autophagy — the process of > cellular self-digestion. This is the second gene to be implicated in > Crohn's disease through involvement in autophagy; the first was > identified earlier this year,.... " > > http://www.lhl.uab.edu:15087/nature/journal/v447/n7145/full/447645a.h > tml > > > IL-23 signaling promotes Th17 development, and the current rap on > Th17s is that they probably kill extracellular bacteria and > extracellular fungi. > > So it's sort of odd that Crohn's is associated with two genes that > may target intracellular pathogens and one that may target > extracellular bacteria/fungi. I wonder if the autophagy alleles and > the IL23r allele enhance Crohn's risk even more when combined, or if > this suggests instead that there exist unrelated subsets of Crohn's > wherein each subset is dealing with different microbes. > > In a vague sense, I'm inclined to think that some Crohn's involves > intracellular microbes and that in these cases Th1 cells and > macrophages partner up to promote granulomas and the > hypervitaminosis D that Abreu et al reported, whereas other patients > are responding to extracellular bacteria and don't develop > granulomas. I've read a statement or two about Crohn's being > associated with granuloma formation, but I haven't seen anything > consistent on this--as if granulomas are optional for the diagnosis. > > > > > > CROHNS: interesting stuff here. They confirmed the old news of the > > CARD15/NOD2 null mutation conferring risk. Also the more recent IL- > 23r > > finding. Then there's 4 strong new ones which they say have been > > replicated with the studies reported elsewhere. One related to > > autophagy, though I think I heard about this previously. > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 14, 2007 Report Share Posted June 14, 2007 Barb The paper I was referring to appears to have 143 references and it doesn't look like it mentions sarcoidosis. The link I gave to the commentary may not actually work for other people. Here's the PubMed citation to the paper started this topic with: http://tinyurl.com/2qyckl Here is the editorial I meant to cite: http://tinyurl.com/2vvyrm Can you give a PubMed citation to the sarcoidosis paper you're talking about? Matt > > > > I've only skimmed the paper and the editorial, but the editorial > > says that the autophagy gene is the *second* one identified for > > Crohn's: > > > > " For Crohn's disease, one of the newly identified6 susceptibility > > genes is of particular interest because it is proposed to control > > the spread of intracellular pathogens by autophagy — the process of > > cellular self-digestion. This is the second gene to be implicated > in > > Crohn's disease through involvement in autophagy; the first was > > identified earlier this year,.... " > > > > > http://www.lhl.uab.edu:15087/nature/journal/v447/n7145/full/447645a.h > > tml > > > > > > IL-23 signaling promotes Th17 development, and the current rap on > > Th17s is that they probably kill extracellular bacteria and > > extracellular fungi. > > > > So it's sort of odd that Crohn's is associated with two genes that > > may target intracellular pathogens and one that may target > > extracellular bacteria/fungi. I wonder if the autophagy alleles > and > > the IL23r allele enhance Crohn's risk even more when combined, or > if > > this suggests instead that there exist unrelated subsets of Crohn's > > wherein each subset is dealing with different microbes. > > > > In a vague sense, I'm inclined to think that some Crohn's involves > > intracellular microbes and that in these cases Th1 cells and > > macrophages partner up to promote granulomas and the > > hypervitaminosis D that Abreu et al reported, whereas other > patients > > are responding to extracellular bacteria and don't develop > > granulomas. I've read a statement or two about Crohn's being > > associated with granuloma formation, but I haven't seen anything > > consistent on this--as if granulomas are optional for the diagnosis. > > > > > > > > > > CROHNS: interesting stuff here. They confirmed the old news of the > > > CARD15/NOD2 null mutation conferring risk. Also the more recent > IL- > > 23r > > > finding. Then there's 4 strong new ones which they say have been > > > replicated with the studies reported elsewhere. One related to > > > autophagy, though I think I heard about this previously. > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 14, 2007 Report Share Posted June 14, 2007 Oh- sorry- read this one then - (sent to your account) it was the one I was referring to: " Considering an infectious etiology of Sarcoidosis " Clinics in Dermatology 2007 259-266 M>E> Ezzie, ELLiot Crouser MDs > > > > > > I've only skimmed the paper and the editorial, but the editorial > > > says that the autophagy gene is the *second* one identified for > > > Crohn's: > > > > > > " For Crohn's disease, one of the newly identified6 > susceptibility > > > genes is of particular interest because it is proposed to > control > > > the spread of intracellular pathogens by autophagy — the process > of > > > cellular self-digestion. This is the second gene to be > implicated > > in > > > Crohn's disease through involvement in autophagy; the first was > > > identified earlier this year,.... " > > > > > > > > > http://www.lhl.uab.edu:15087/nature/journal/v447/n7145/full/447645a.h > > > tml > > > > > > > > > IL-23 signaling promotes Th17 development, and the current rap > on > > > Th17s is that they probably kill extracellular bacteria and > > > extracellular fungi. > > > > > > So it's sort of odd that Crohn's is associated with two genes > that > > > may target intracellular pathogens and one that may target > > > extracellular bacteria/fungi. I wonder if the autophagy alleles > > and > > > the IL23r allele enhance Crohn's risk even more when combined, > or > > if > > > this suggests instead that there exist unrelated subsets of > Crohn's > > > wherein each subset is dealing with different microbes. > > > > > > In a vague sense, I'm inclined to think that some Crohn's > involves > > > intracellular microbes and that in these cases Th1 cells and > > > macrophages partner up to promote granulomas and the > > > hypervitaminosis D that Abreu et al reported, whereas other > > patients > > > are responding to extracellular bacteria and don't develop > > > granulomas. I've read a statement or two about Crohn's being > > > associated with granuloma formation, but I haven't seen anything > > > consistent on this--as if granulomas are optional for the > diagnosis. > > > > > > > > > > > > > > CROHNS: interesting stuff here. They confirmed the old news of > the > > > > CARD15/NOD2 null mutation conferring risk. Also the more > recent > > IL- > > > 23r > > > > finding. Then there's 4 strong new ones which they say have > been > > > > replicated with the studies reported elsewhere. One related to > > > > autophagy, though I think I heard about this previously. > > > > > > Quote Link to comment Share on other sites More sharing options...
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