To put it in context, this is a message I've written in a group about LDI, a therapy I am following. So, I take as granted that in that group, people knows the "argot" or the abbreviations typically related to the therapy. I am posting it in my wall as well, in case it might be of interest to any of my friends who are not familiarized with the therapy.
"TESTS TO FOLLOW LDI EFFECTIVENESS:
Hi guys. As I have been telling since I started to study LDI and decided to follow it, it is my believe from the data I extrapolated from peer-review papers on EPD and also on some other types of Specific-Antigen-Based-Immunotherapie approaches or AIT (trialed successfully for chronic infections and for autoimmune diseases), that chronic Lyme disease and ME/CFS share a common immune profile, and that because both condition meet two crucial characteristics (1. Symptoms are the result of an improperly set immune system and to the subsequent inflammation and autoimmune processes; 2. The immune response observed is that expected from a chronic intracellular infection), they could benefit from LDI given that all the conditions I analyzed that benefited from other types of AIT, also shared these common points.
You can read the details of my hypothesis in the document I wrote:
http://www.sfc-em-investigacion.com/dow ... php?id=359" onclick="window.open(this.href);return false;
In order to prove whether or not LDI actually works under the premises I proposed, I tested myself for some immune parameters that I think, if I get better from the therapy, will be able to confirm that unless in my case LDI not only promotes tolerance but also causes a immune deviation towards a “healthy” response that will: 1. Eliminate the symptoms and 2. Restore a proper immune profile.
Basically, the improper immune response that would be causing our symptoms is defined by a depressed intracellular or Th1 acquired response, which can be chronically inhibited by a “non-inflammatory” Th2 (extracellular response) and a “non-inflammatory” Th17. Also the innate response should be affected (it can be measured by the number or activity of certain subsets of NKs, for example. Moreover, inflammation can be inferred directly from pro-inflammatory cytokines, and also through PGE2 levels (I think this molecule plays a key role in this pathological cycle, even though it is known to be an antiinflamatory substance—well, it is, but participates in keeping the inflammation going).
I wish I could have afforded more tests, but I think the following ones came back just as I expected, and might shed light on how LDI works and on whether they could be used to monitor the progress while on the therapy (I plan to re-test when I start, hopefully, feeling better by following LDI):
IL2/IL4: 7 (2-100)
INF-gamma/IL4: 6 (10-350)
*** IL2 and INF-gamma are Th1 mediators while IL-4 is a Th2 cytokine, so clearly my profile at this moment was low Th1 and high Th2
NK CD56+CD16+: 1 (3-95)
NK CD57+CD3-: 60 (60-360)
*** These indicate low innate cellular response (the CD57 is more specific of Lyme—although this is controversial in the literature--, and during the last 6 years it has been always either low or in the lowest limit of the normal range. The CD56 belong to a larger subset of NKs, so even though it is not always found low in ME/CFS or in chronic Lyme, I think it is a wise to measure them, as they show a bigger picture of the status of the whole NKs.
Prostaglandine E2: 18.92 (0.17-6.45)
IL-8: 706 (0-15)
MCP-1: 192 (0-165)
*** I have been measuring PGE2 during the last 6 years, and it has always come up high. I think it is a fantastic test to show chronic systemic inflammation, especially of the CNS. As for the other pro-inflammatory cytokines, also showing inflammation, they vary quite a lot from one test to the next, but the trend is clear: chronic systemic inflammation (note that MCP-1 is quite specific for Borrelia B. as well).
IL-10: 3 (0-5)
TGF-beta-1: 3048 (1674-12400)
These are the only markers related with tolerance. In theory both cytokines should raise in their total value when tolerance is induced by LDI. Well, these are cytokines measured in serum, and their results are not much reliable on their own (as isn’t any cytokine in blood). For properly assessing the meaning of cytokines they need to be interpreted together with other markers, and also see how they change over time (the trend). Ideally I should have measured the T regs, but the laboratory didn’t measure them, plus it is very difficult to know which markers to test in order to get accurate results of the ones we really want to observe, since they are not regularly measurde in the clinical practice.
In short, my immune profile seems to be as the literature has clearly demonstrated on ME/CFS and on LONG-TERM-chronic Lyme disease (not so much evidence on the later): Th1 depressed, Th2 elevated, chronic and systemic inflammation. Also, I know I suffer from autoimmune processes as I suffer from vitiligo, so here’s another piece of the puzzle. I’d only have to prove that my “tolerance” is not appropriate towards some antigens. This is fairly difficult to analyze. I have reviewed the cytokines I’ve measured during the last 6 years and the 2 cytokines that are considered to be key molecules in promoting tolerance (i.e., IL-10 and TGF-beta), have been always low or low-normal. Given that the normal reference ranges might actually not be very well established, I am cautious with these results. If they do increase in further tests, then I'll be in a position to draw more solid conclusions.
Alright, so this is the first step. The next one is to finally find the core doses of the antigens I might need, and IF I improve with LDI I will re-test and will let you know if any of these tests seems accurate in my case to measure LDI ability to restore a proper immune profile, as it is my believe it does.
Hope it helps!
Best,
Sergio"
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