U of U Researchers May Have Discovered a Breakthrough for Treating Lyme Disease (KUTV) A scientific breakthrough that could change the lives of those suffering from Lyme disease and rheumatoid arthritis as researchers at the University of Utah's Department of Pathology identifies a gene deficiency that makes individuals susceptible to developing severe inflammatory arthritis.
Their findings were published Thursday in the Journal of Clinical Investigation. Their work - 20 years in the making - gives new insight into how the condition develops and into possible treats or even find a cure.
Dr. Janis Weis, Professor of Pathology at the U, started the study with former BYU professor Corey Tuscher, now with the University of Vermont, the goal is to identify the cellular processes that influence the severity of Lyme arthritis, "Why do some people get sick and other people do not."
Their findings became so much more than that, possibly improving the lives of those who suffer from Lyme disease but also rheumatoid arthritis, where symptoms can be similar.
Four years ago, Dr. Kenneth KC Bramwell came on board. "When I started, they had essentially a big haystack and I needed to find the needle in that haystack," Dr. Bramwell told 2News. He said through a process of refinement, they found it, "We've identified a gene, a pathway, and potentially a therapeutic strategy."
The lead author of the study, Dr. Bramwell explains they were able to correct that partial deficiency in test animals, and feel the results will be similar in patients. "We think that if we can achieve that, potentially through a drug target, we could essentially reduce the severity of disease in the human population."
They say the findings are exciting and they can't wait to take the next step working with the Centers for Disease Control and hospitals. A grant is currently under consideration to fund their work moving forward. Thus far, funding is thanks to the National Institutes of Health and The Arthritis Foundation.
By Amy Nay
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Keebler
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- "a gene deficiency" "cellular processes"
well, lyme can CAUSE genetic changes, actually alter and damage DNA.
I think they are looking at damage from lyme and not the cause of lyme. It's an infection. Why they don't want to accept that seems to be a problem with the direction of research.
"Why do some people get sick and other people do not."
Pamela Weintraub has discussed that in her book "Cure Unknown" some of the points (not all) she considers include:
Well, it can depend upon the STRAIN, the different forms of lyme (and how it can appear that someone is not ill but the cyst form is just letting it hide out for now), and the number and kind of COINFECTIONS, etc.
And that some with serious lyme don't have trouble with joints but with their heart, their brain, etc.
They fail to take any of that into account.
Oh, and that most doctors are just so ignorant and let patients just get sicker and sicker.
I'd feel better about their research if they actually had any ILADS educated researchers on their team, so someone there would actually know the science of how lyme works and all the tagged-on considerations involved to begin with.
They need to understand how lyme damages genes in the first place. Some ILADS researchers are far ahead of them on that aspect already.
Still, they say they have "identified a gene, a pathway, and potentially a therapeutic strategy."
I would like to have some ILADS researchers take a look at that before I get too excited. -
[ 01-10-2014, 04:30 AM: Message edited by: Keebler ]
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CherylSue
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Keebler, you raise a good point. My lyme was definitely more neuro than arthritic. Why is that?? Genes?
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phyl6648
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Mine is more Neuro that arthritic too.. The vertigo, ears ringing, weird head feelings, vision depression/ anxiety and extreme fatigue etc....
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Keebler
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- CherylSue,
Everyone has some kind of weak gene thing going on. From what I've read, why some have more neuro involvement is not that they all have the same gene weakness but, likely, more so that certain STRAINS or MUTATIONS of lyme just seem to attack different body systems.
And the stages of even the "same" lyme are going to be different in different people . . . and the treatment or (more often) inadequate treatment that encourages chronic lyme . . .or even complete lack of treatments . . . liver condition, etc. are also huge variables.
Even separating out lyme from all the tick-borne infection soup, lyme, itself, is never the SAME lyme. But most doctors don't know that.
Lyme can attack a healthy system as well as a weak one. So, while if you have a particular gene issue going on, that might be of help to know, IMO, since lyme can attack even the strongest of the strong, it's not always that the person had a certain weakness to begin with.
Still, there are so many complexities within all this. And most who want to simplify lyme don't even know enough for a good foundation. They may stumble upon something that could be of help, of course, but I'll put my money on those who first have a better understanding of what lyme is, can be, and how it can work -- before they move on.
IMO, with funding grants and donations, the focus should be on training more doctors and getting people treatment.
It would be nice to be sure that anyone shooting off for such long range connections such as finding some genetic connection (or work that is intended to create a new market of genetic testing, correction) would first be required to know the basics about how lyme works.
The "genetic connection" they question may not really be there at all, were they to back up and look as the foundation & science of borrelia. I don't think lyme is just bad for those with certain tweaky genes. I think lyme, itself, does the tweaking.
But much depends upon the particular strain of lyme. They are not at all the same. -
[ 01-10-2014, 04:19 PM: Message edited by: Keebler ]
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Keebler
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- Dr. Alan MacDonald: Pathologist, Lyme Disease Expert
The Biology of Lyme Disease: An Expert's Perspective - July 2013
Because many of the symptoms of Lyme disease involve the nervous system, it was speculated that the spirochete produced a toxin that disrupted normal nerve function.
Through the use of DNA manipulations and a database of known protein toxin DNA sequences, a match was made with a selected Borrelia burgdorferi (Bb) gene and a specific toxin in the database.
Protein generated from this cloned Bb gene was examined biochemically and found to have characteristics similar to that of botulinum, the toxin of Clostridium botulinum, a zinc endoproteinase.1
The toxin from Bb belongs to a family of toxic proteins known as "zinc endoproteinases" or metalloproteases, and includes the toxin from the organism causing tetanus as well as those from many other well-known infectious diseases. . . . -------------------
For reference, then, as to the power of the borrelia toxin (which sure seems to attach any cells that would get in the way whether in a health person or one with genetic defects), it's "cousin" toxin (although not "cousin" "germ"):
Botulinum toxin is a protein produced by the bacterium Clostridium botulinum and is the most powerful neurotoxin yet discovered. . . . -
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Keebler
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How doxycycline can "turn off" some cellular activity that some see as cancer but it may really be lyme (or other chronic stealth infection) underlying it all
Another case of researchers not at all lyme literate, not at all even thinking of lyme . . . and they don't even know what they may have stumbled upon
Glad some folks are considering the possible lyme connections, though that lyme has CAUSED the genetic mutation / cancer problem and by treating the underlying cause, the gene settles down.
It's not treating the gene, it's treating the infection in the cells. But not everyone sees it that way. Maybe that's just the only way some will be able to get lyme treatment (or other chronic stealth infection), have it move on and develop into other conditions.
They love to research & treat cancer. Few besides the ILADS doctors want to ever consider serious repercussions from lyme - or from other chronic stealth infections (other TBD, mycoplasma, etc. or parasites). That's forbidden speech. -
[ 01-10-2014, 09:09 PM: Message edited by: Keebler ]
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Keebler
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- The nutrient deficiencies that lyme can cause can also cause "genetic deficiencies" - Magnesium is often very, very low with lyme.
Magnesium is responsive for over 300 different enzymatic processes in our bodies and when it's deficient, the cells, the genes are going to be affected.
just one example.
I'm not saying that the Utah group above may not be onto something but there is just something about the way that press release reads that signals caution to me.
It would be nice to have more detail beyond the "buzz words" of a PR release, of course.
Also, of note, more in neurological complications is the genetic issue of MTHFR genetic differences:
Topic: Methylation abnormalities connected with neurogenrative diseases
And, for many with liver issue of poor detoxification, the genetic issue of a porphyria (there are many different kinds).
Any of this can make lyme more miserable and more damaging. So, it will be of interest to see what the Utah group is really looking at, once they issue the full report. Let's just hope they are really lyme literate for a start. -
[ 01-11-2014, 03:04 AM: Message edited by: Keebler ]
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