richvank Methylation defect, Rnase L, Elastase and cancer? | ProHealth Fibromyalgia, ME/CFS and Lyme Disease Forums

richvank Methylation defect, Rnase L, Elastase and cancer?

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frango2

New Member
Hello again-

Sorry for all the questions this week, but this one is general and perhaps of interest to others here.

Online there are quite a few studies showing a link between both Methylation defects and elevated Elastase/Rnase-L levels and cancer, particularly of the digestive tract.

What are your thoughts on this?

Is extra or early screening prudent for those of us with one or both of these issues?

Thanks so much.
 

richvank

New Member
Hi, frango2.

Online there are quite a few studies showing a link between both Methylation defects and elevated Elastase/Rnase-L levels and cancer, particularly of the digestive tract.

What are your thoughts on this?

***I'm not familiar with this work. Was it done by Dr. Kenny de Meirleir's group?

Is extra or early screening prudent for those of us with one or both of these issues?

***I can't give an opinion about this, because I'm not familiar with the work. Generally speaking, I think it's wise for everyone to have a colonoscopy periodically, with stool testing for occult blood in between.

***Dr. de Meirleir and I have different hypotheses about how methylation cycle block and elevated RNase-L are related. In my hypothesis, because of glutathione depletion and the partial methylation cycle/folate cycle block, the body cannot mount a proper cell-mediated immune response to infection. I believe that this is the reason RNase-L stays elevated in many PWCs. Normally, it would rise early in the infection, and would fight a relatively brief holding action until the T cells were able to proliferate and take over. But since they are not able to proliferate, RNase-L stays elevated.

***Dr. de Meirleir's group believes that elastase is responsible for cleaving RNase-L to make the low-molecular weight form which is unregulated. I believe that calpain is actually what cleaves it, when glutathione drops sufficiently to activate calpain. I don't believe that elastase can cleave RNase-L inside living cells, because it is compartmentalized in vesicles, while the RNase-L is in the cytosol. They should thus not be in contact inside living cells. Dr. de Meirleirs' group is continuing to study this in the laboratory.

Thanks so much.

***You're welcome. Sorry I can't be of more help on this question.

***Rich
 

tooks

Member
Hi Rich,

The following was written in 2002 by someone with an almost-awarded Ph.D. in biochemisty. Compelling interests took him in other directions where he has made significant contributions--much of this done from bed--as he was one of those "hit" at Incline Village in 1985.

Rnase enzyme deficiency disease is his diagnosis. After skimming his analysis, I wonder if you could comment on whether this is basically the same as the Rnase-L excess you commented on to Frango 2, and how it might respond to the simplified protocol? He is a friend of a friend and may or may not be aware of the work you are doing. If it might be of benefit, I'd like to pass on the information. Thanks.

"RNase is an enzyme produced by the human body when it is attacked by viruses or bacteria. As the name implies, RNase denatures messenger RNA wherever it finds it. As it comes in contact with the invading virus or bacteria, it destroys its RNA and thus kills the invader. This is a very quick-acting defense mechanism, unlike the slower production of T cells, B cells, etc., which can take days or even weeks, and thus is one of the body's first lines of defense.

In REDD, the mechanism that produces RNase is damaged by any number of causes, the most notable being environmental toxins....[In my case] a widely circulated hypothesis is that this outbreak was triggered by a local toluene spill....

Once the damage is done, the body begins producing a shortened but highly active form of RNase (37 kD instead of 80 kD). This 37 kD RNase has no turn-off mechanism, because the body only recognizes the 80 kD forms. Therefore, the body keeps producing this 37kD RNase, which then proceeds to attack the RNA in literally every cell in the body....

One of the first things damaged by this defective RNase is the glutathione system, which is one of the body's major anti-oxidant systems. This leaves the body open to serious damage by its own free radical cascades. The areas most damaged are those that produce the most energy and free radicals, namely, the mitochrondria, or the small organelles in cells that produce all of the body's energy.

As the condition progresses, more and more mitochrondria are damaged and destroyed. In severe cases, the person is bedridden for the rest of their lives.... Another system quickly damaged is the body's Th1 immune system, which is responsible for intracellular protection (i.e., protection against pathogens that attack inside the cell, like viruses and primitive bacteria such as mycoplasma).

An opportunistic bug is defined as one that is already present pretty much everywhere (and is already crawling all over you), but only attacks when a portion of the immune system fails. In the case of REDD, the opportunistic viruses are hhv6, epstein barr, and CMV; and on the bacterial side, mycoplasma. Over 70% of REDD patients have active hhv6, and over 60% have active mycoplasma infections....

The first phase of the illness lasts about 5 yrs, and comes to an end, ironically, when the body's capacity to synthesize protein is so badly damaged that it can no longer make any RNase, either. The person then enters a second phase, which lasts about ten years, where things are relatively quiet in terms of the illness itself, it's just that their physical activity is severely compromised and they live in what has been called a "functional bubble," often having only a few hours a day of walking-around time....

The third phase begins when the cumulative damage to various tissue systems starts to take a toll. Basically, it just opens the body up to new attacks by the 37 kD RNase. Every time you get an infection, cold, flu, or fever, your body produces interferon, which tells cells to start producing RNase—which in this case is, of course, defective. So more mitochrondrial damage, etc.

The basic symptom is "hypoxia," or lack of oxygen in the cells (due to damaged mitochrondria), so you feel like you are suffocating most of the time, and you're often bedridden around the clock (literally)....

The central problem is when I get one (or two or three) of the opportunistic infections on top of the REDD. Think of the worst case of flu you've ever had, subtract 80% of your energy, and that's sorta what it's like—but fortunately it only lasts for 6 or 8 months….."

Last December he nearly died, but has rallied and is fully at work again. It would be great if there were some aspect he had not considered, that could help him. He is brilliant and it would be a loss to the world if he were to die prematurely.

Susan
 

richvank

New Member
Hi, Susan.

I think this guy has put together an interesting hypothesis. It differs from mine in the cause and effect sequence, but he deals with many of the same issues.

He suggests that the low molecular weight RNase-L causes the glutathione depletion, while I'm suggesting that glutathione depletion causes the formation of the low molecular weight RNase-L, via activation of calpain.

It would be fine with me if you pass on my hypothesis to him. Maybe treatment to lift the methylation cycle block would help him.

Rich
 

tooks

Member
Rich,

And thanks also for making available that great power point presentation--what a clear teaching tool. Guess who is sending it to her doctor!

I think you might be interested in the person's account of his recent brush with death and his interpretation of it. I had the date wrong--it was December 06.

I don't want to flash his name around the web without his permission, so I'll email it to you, if you don't mind. It is not a secret--he published it on his website.

I think he feels he is in a race with his body to get his work done before his body gets done in. Very sad.

Susan
 
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