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#3698 - 06/23/08 04:10 PM
Re: The Lyme Disease End Game
[Re: Rich_Van_K]
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Connie
Spirochete Hunter
Registered: 03/06/08
Posts: 58
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Hi Rich,
Thanks for your comprehensive response!
It is late and I have to get on a plane early tomorrow AM, so will respond more at length when I get a chance (I'm going to a Lyme-autim conference so might be a week or so), but I wanted to at least let you know that I appreciate your efforts to share what you have learned. I will definitely look into the reports you mention. I would be curious to see what degree of healing people are having with the methylation protocol.
Take care, and best wishes to you, too! 
Connie
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#3701 - 06/24/08 12:05 PM
Re: The Lyme Disease End Game
[Re: Rich_Van_K]
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Connie
Spirochete Hunter
Registered: 03/06/08
Posts: 58
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Hi Pawel and Rich,
Well here I am again...I ended up having more time today than I thought (due to missing an airplane...)
Thank you both for your great insights! :-)
Pawel, you make some excellent points about the healing process. I agree with your thoughts on this.
And holy cow, Rich, you sure can write!...thanks for the in-depth explanation of your CFS theory. Obviously, if there are physicians practicing this approach with success, then you have really done your homework. I will have a look at the groups and studies.
I may be interested in posting a blog post on this theory, at some point, if you don't mind!
Also, if you have the time, I'd like to just ask you a couple of more questions.
First, do you have the details documented somewhere about how glutathione works with the other nutritional agents in the treatment plan to fix the methylation block?
Second, you mention in one of your messages above that, "The adrenals are not at fault (re. HPA dysfunction), as shown by results on the cortrosyn test." What is the cortrosyn test?
Does this somehow measure the source of adrenal insufficiency (ie, whether it is a result of a pituitary problem or directly attributable to the adrenals?)
While many of your points convince me, I'm not sure I yet agree that HPA dysfunction is mainly a result of glutathione depletion. (Personally, I had adrenal fatigue prior to Lyme, so if your theory is correct, then is it possible that my glutathione was being depleted due to factors other than borrelia? Would emotional stress do it, too?
I happen to think that living in fight-or-flight mode for too many years (again, due to emotional stress), caused my cortisol levels to skyrocket, which, over the long term, caused adrenal insufficiency and immune suppression, as sustained high levels of cortisol lower T and NK-cell production. I have improved only as I have treated my stress levels.
I also thought HPA-dysfunction could be a direct result of borrelia neurotoxins stuck to receptor sites on the HPA-axis.
Anyway, just more thoughts! Feel free to respond or leave 'em be.
Thanks again,
Connie
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#3703 - 06/25/08 10:32 AM
Re: The Lyme Disease End Game
[Re: Connie]
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Rich_Van_K
New Researcher
Registered: 06/21/08
Posts: 8
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Hi, Connie.
Thanks for your comments. My responses are at the asterisks below:
I may be interested in posting a blog post on this theory, at some point, if you don't mind!
***That would be fine with me, and if you need more information, let me know.
Also, if you have the time, I'd like to just ask you a couple of more questions.
***O.K., I'll give them a shot!
First, do you have the details documented somewhere about how glutathione works with the other nutritional agents in the treatment plan to fix the methylation block?
***Glutathione itself is not included in the five supplements in the so-called "simplified treatment approach" that are listed earlier in this series of posts. Some people have found that adding it helps. The reason it helps (provided the extra sulfur metabolites do not overload the sulfite oxidase enzyme and cause symptoms due to elevated sulfite, which occurs in some people) is that glutathione, as the basis of the antioxidant enzyme system in the body, counters oxidative stress. Oxidative stress is what initially triggers a shutdown of methionine synthase and the methylation cycle. It does this by oxidizing the cobalt ion in cobalamin (vitamin B12) from the +1 to the +2 oxidation state. B12 acts as a coenzyme for methionine synthase. This is a normal control mechanism that is used by the cell to divert more flow from homocysteine down the transsulfuration pathway, so that more glutathione can be synthesized to counter the oxidative stress. This normally switches back when the oxidative stress has been taken care of. However, in CFS and autism, it doesn't switch back, and I have suggested that the reason is that toxins react with B12 and waylay it, so that it cannot be converted to methylcobalamin to replace the cobalamin that has the oxidized cobalt ion, and get methionine synthase turned on again.
***So the short answer is that glutathione can help to keep the cobalt ion from being oxidized and shutting down methionine synthase.
Second, you mention in one of your messages above that, "The adrenals are not at fault (re. HPA dysfunction), as shown by results on the cortrosyn test." What is the cortrosyn test?
Does this somehow measure the source of adrenal insufficiency (ie, whether it is a result of a pituitary problem or directly attributable to the adrenals?)
***Yes. In the cortrosyn test, a synthetic form of ACTH is given, and the cortisol level is monitored. If the adrenals are O.K., they will put out cortisol when this is done. If they do, the problem is not primary adrenal insufficiency, but it is secondary, i.e. in the pituitary, or tertiary, i.e. in the hypothalamus. The HPA axis blunting in most cases of CFS does not appear to be due to primary adrenal insufficiency.
While many of your points convince me, I'm not sure I yet agree that HPA dysfunction is mainly a result of glutathione depletion. (Personally, I had adrenal fatigue prior to Lyme, so if your theory is correct, then is it possible that my glutathione was being depleted due to factors other than borrelia? Would emotional stress do it, too?
***Yes, and yes. If you read my 2004 poster paper at the IACFS conference, you can see a discussion of various factors that can contribute to the depletion of glutathione. I'll post it to the files section of the Lyme-and-rife group's website.
I happen to think that living in fight-or-flight mode for too many years (again, due to emotional stress), caused my cortisol levels to skyrocket, which, over the long term, caused adrenal insufficiency and immune suppression, as sustained high levels of cortisol lower T and NK-cell production. I have improved only as I have treated my stress levels.
***Right on! Connie, you could have been a "poster girl" for my 2004 poster paper!(:-) Emotional stress is a biggie, and seems to be especially so in the females with CFS. This is not intended to be a sexist remark, but is an observation I've made from studying questionnaires I've given to a large number of people with CFS over several years. Emotional stress plays an important role in the onset of many cases of CFS. It also seems to be true that it is not involved in all cases. There are some "rough and tough, macho-type" guys who don't seem to have a history of emotional stress (and I think they are being honest about it), but still have developed CFS. There are many ways to raise cortisol and epinephrine, which leads to glutathione depletion, and also ways to deplete glutathione separately, and the combinations differ for different cases. What these cases have in common, in my hypothesis, is that glutathione becomes depleted and a chronic block develops at methionine synthase. A genomic predisposition is necessary, at least in the sporadic cases of CFS, to facilitate this mechanism. In the epidemic or cluster cases of CFS, the genomic factor does not seem to be as important, perhaps because a very virulent virus is involved.
I also thought HPA-dysfunction could be a direct result of borrelia neurotoxins stuck to receptor sites on the HPA-axis.
***Dr. Ritchie Shoemaker has advocated a mechanism like this, and it may be valid as well. There could very well be more than one mechanism interfering with proper operation of the HPA axis. In people who have inherited certain isotypes of the HLA (human leukocyte antigen) system, Dr. Shoemaker argues that the biotoxins are not recognized and taken out by the immune system, so they build up and remain in the body, producing lots of mischief. It may well be that the complete treatment of Lyme disease in people with these HLA isotypes must include something like his cholestyramine treatment. I think that treatment of this subgroup as well as others might also need to include treatment to lift the methylation cycle block.
Best regards,
Rich
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