Discussion in 'Institute of Medicine (IOM) Government Contract' started by justy, Feb 12, 2015.
After careful examination of all the evidence I have come across so far, I have concluded that Horowitz is MOST LIKELY a quack, and chronic Lyme Disease-MSIDS is mostly nonsense. He's actually very smart, but I think he's way overly biased in favor of his Lyme crusade. There is a SMALL chance that LLMDs may be right, though it's very tiny. Or they could be right about certain parts. Just my opinion so far, but time will tell.
In relation to CFS/FM, he thinks many of the cases are caused by Lyme, which is nonsense, actually the opposite.
Lyme doesn't fall under the umbrella of me/cfs. While it can be a triggering factor, not all people who have Lyme develop me/cfs. They are separate medical conditions.
He's confusing PEM with "fatigue". Hence he obviously has no idea what ME patients are experiencing.
I am amazed at your ability to identify Horowitz as a quack when such people as P. D. White are loose in the field, and apparently considered respectable. I am also astounded by your unerring grasp of diseases of unknown etiology. (I know nothing about Horowitz or you. I'm simply wondering how anyone discriminates.) I also wonder if you are aware of a pathologist named Alan MacDonald, and his work on borreliosis, or the opinions of late Willy Burghdorfer, who might know something about borrelia burghdorferi. (You might also consider the effectiveness of blood tests which can fail when samples of synovial fluid contain visible spirochetes.) These claims have now spurred other pathologists to discover a species, borrelia miyamotoi, in U.S. patients which had not previously even been considered. This has now been published in that most respectable of U.S. journals, NEJM.
What basis do you have to dismiss chronic Lyme?
What basis do you have to claim that "Lyme doesn't cause CFS, but actually the opposite"?
And other tick-born infections as well. Midichloria Mitochondrii is a rather fascinating new bacteria discovered in just 2006. It infects the mitochondria in the ovaries of 100% of the females of at least some tick species, and is present in about half of the males as well.
Some ME patients have begun being tested for it at a Belgian university, and at least one PR forum member has tested positive for its DNA, though at least one other patient has tested negative. It's still unknown what effect this has on humans, if any, but it opens up some fascinating possibilities regarding a bacteria which seems to consume mitochondria and has a significantly greater prevalence in the females of its transmission vector.
Hence I think it's very possible that both chronic-Lyme deniers and chronic-Lyme supporters are correct. Perhaps it's not the one strain of Lyme which is causing ongoing problems, but rather it's other strains of Lyme, or other co-infections, including ones which aren't yet understood or even detected.
I was recently reading they have discovered up to 100 different strains of borrellia.
I wanted to add to your comment on denial/support of chronic Lyme with the work of Dr. Brigitte Huber. Apparently, about 20% of people who get Lyme and get treated never bounce back, and become chronic. Dr. Huber has looked for genetic differences between those two groups and found an interesting correlation. People that got antibiotic treatment but didn't get better (what's referred to as chronic Lyme) had in common the HLA-DR4 transgene. People with this transgene that are infected by Lyme, their T cells produce interferon gamma, an inflammatory response, instead of antibodies. The rest of the subjects (HLA-DR11) produced antibodies that fought the pathogen, instead of interferon gamma. Radical responses with radical results.
Here's a simple explanation of this process, but there are more detailed scientific papers on this subject online: http://www.whatayear.org/02_10.html
Personally, I would appreciate if Vic would expand on his observation concerning Horowitz,"In relation to CSF/FM, he thinks many cases are caused by Lyme, which is nonsense, actually the opposite."
I am curious as to how CSF/FM can cause Lyme.
I don't think Horowitz is saying M.E doesn't exist but that there is such a huge overlap in symtpoms that many people are wrongly diagnosed with M.E/CFS when they may in fact have MSIDS - which includes Lyme, co infections, heavy metals issues, biotoxin illness etc.
My own Dr - KDM is in contact with Horowitz and recently asked me to take the visual contrast test for biotixin illness as he is also seeing the many different infections and illnesses that go to make up this disease - there is a huge overlap! most people I have spoken to with chronic Lyme where told they had CFS/M.E to begin with and some start to get better when they treat the underlying issues - after all KDM now finds bacterial infections in about 90% of his patients!
Agreed. Lots of overlap, but also many people are diagnosed with both (including yours truly). I have all the markers for ME/CFS, with severe autoimmunity issues, and also tested positive for Lyme via LTT Elispot. Sadly, no treatment has made a dent in my condition so far (antivirals for the off-the-charts EBV and HHV6 titers or ABX for Lyme)
My ME/CFS doctor is actually working together with a LLMD on my case, since nothing seems to make a difference in my titers, and my overall condition keeps getting slowly worse.
May I add that many, many people in the Phoneix Rising community (including moderators) have also battled with both Lyme and ME/CFS. While they are different conditions, the overlap is notable. As many people have suggested, ME/CFS (SEID) may have many different triggers, which could include borrellia. Again, since both conditions have been obscenely neglected by the medical authorities, we are pretty much in the dark here.
Great post @Antares in NYC
I agree. The Meirleir is the same story.
By the way i don't think they are quackers.
Incidentally, there are actually more than 100 strains of b. burghdorferi alone. (Added: this is subject to dispute, the very concept of bacterial species doesn't meet normal criteria for reproductive isolation of species. These little bugs exchange DNA in ways that would shock a sheep shagger.) We can then talk about b. afzelii and b. garinii, which also cause borreliosis classified as Lyme disease before we get into strains like b. miyamotoi said to cause relapsing fever, but not even suspected in patients without obvious symptoms of fever until recently. These are all strains known to cause disease in humans. Research typing strains is still being done, and the method being used to find them is similar to "DNA fingerprinting" in humans, based on tandem repeats in the genome. This introduces a serious problem for cheap detection: there are a many potential regions of genetic variability being used to "fingerprint" strains, and the numbers of repeats vary. This variability can cause variations in the number of times some proteins are expressed, and in the strength of immune response on which current testing depends. This problem is separate from the problem of detecting infection in immune-compromised patients, who may well be over-represented in ME/CFS. Evolutionary analysis of borrelia genomes indicate the genus produces new species at a rate which cannot be ignored.
We could also begin to talk about other borrelia strains found in wildlife near humans, but then the list grows rather long. Note that I am not going out of my way here to talk about spirochetes only found in Africa, which has the highest diversity of human genes, and of human pathogens. (But, then when was the last time we were bothered by an infectious disease out of Africa?)
Nothing about this is unique to genus borrelia. Genus treponema has been in humans for a long time, and while treponema denticola is usually considered more or less harmless, it has been found in brains of people who died with dementia. Treponema pallidum, in the same genus, has caused quite a bit of human disease termed syphilis.
We are still only talking about spirochetal diseases at this point. Want to argue that your local infectious disease specialists have a good understanding to just those I've named? Do we need to go on to other bacteria, like bartonella, or parasitic diseases like babesiosis or toxoplasmosis?
the longer one is ill with cfs/me the more infections one has and the harder it is to fight off other infections. So it wouldnt suprise me to see someone with long term cfs having viral reactivation and a host of other bacterial infections, l form bacteria, lyme etc.
we need a pill with a host of antivirals, antibiotics and immune stimulants all in one.
Or an immune modulator which brings the immune system back in shape.
What about having a diagnosis of CFS/ME SEID and later getting bit by a tick? I have ticks outside my patio every spring. When I can I love to walk near grass and woods with my dog. Precautions are taken and I'm aware of checking afterwards but who knows about the ticks you can't see.
That is the approach of Drs Like Horowitz and KDM - my treatment includes IVIG for the immune system, followed by antibiotics for killing the bacteria, followed by herbs to keep the bacteria under control. Then we move on to the next thing...molds? hormones? This is really just following Horowitz's idea of MSIDS 0 which I think is great because it presumes that people can be treated and at least have improvement in their health, even if they cant be cured.
Many people get worse by the aproach of dr. the Meirleir. He don't use a control group and his aproach have never been test blinded. Also the Meirleir use an unapproved test for Lyme at this moment. So you cannot say at this point you have lyme, why treat it then with heavy antibiotic. It is dangerous.
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