I think there's a school of thought that says a shift to Th2 is involved in things as bothersome as seasonal allergies on down to things as awful as chronic fatigue, etc. I don't know if there's anything to actually back that hypothesis up, though.
From the little that I read it seems some bacteria/viruses associated with CFS produce proteins that mimic the activities of certain cytokines (i.e. IL-10) and this lowers the activity of Th1 and increases that of Th2. Th1 immune activity is needed to fight off things like bacteria/viruses/fungi. Being Th2 dominant makes you more responsive towards certain antigens and allergies and they say this is what causes food allergies/IBS, etc. So you see how these clever buggers manipulate our immune systems to increase their survival? The biggest problem with this is you will never get rid of a viral/bacterial/fungal infection becuase your immune system doesn't back you up. This is what leads the way to chronic infections and thus, chronic fatigue.
This is a Doctor talking about CFS
http://www.nbc6.net/...382/detail.html She says the term "chronic fatigue syndrome" is a misnomer. It Should have been called Chronic neuroInflammatory disease and that an Immune disorder is at the base of all this (Th1/Th2 balance?). For the neuroinflammation idea, I started using Luteolin some months back. I mix it with colostrum and 98% Resveratrol and drink it every morning fasted. Don't know if it's helping or not.
You can actually have your Natural Killer cell function tested to determine if you're Th1 weak. I think it runs at $300 or so..
This is an article Krillin posted here before, it's pretty good reading.
http://www.ei-resour.....m-(th1th2)-/There are some other things that can disrupt the Th1/Th2 in favor of Th2 like Mercury tox.
1: Altern Med Rev. 2003 Aug;8(3):223-46. Links
Th1/Th2 balance: the hypothesis, its limitations, and implications for health and disease.
One theory of immune regulation involves homeostasis between T-helper 1 (Th1) and T-helper 2 (Th2) activity. The Th1/Th2 hypothesis arose from 1986 research suggesting mouse T-helper cells expressed differing cytokine patterns. This hypothesis was adapted to human immunity, with Th1- and Th2-helper cells directing different immune response pathways. Th1 cells drive the type-1 pathway ("cellular immunity") to fight viruses and other intracellular pathogens, eliminate cancerous cells, and stimulate delayed-type hypersensitivity (DTH) skin reactions. Th2 cells drive the type-2 pathway ("humoral immunity") and up-regulate antibody production to fight extracellular organisms; type 2 dominance is credited with tolerance of xenografts and of the fetus during pregnancy. Overactivation of either pattern can cause disease, and either pathway can down-regulate the other. But the hypothesis has major inconsistencies; human cytokine activities rarely fall into exclusive pro-Th1 or -Th2 patterns. The non-helper regulatory T cells, or the antigen-presenting cells (APC), likely influence immunity in a manner comparable to Th1 and Th2 cells. Many diseases previously classified as Th1 or Th2 dominant fail to meet the set criteria. Experimentally, Th1 polarization is readily transformed to Th2 dominance through depletion of intracellular glutathione, and vice versa. Mercury depletes glutathione and polarizes toward Th2 dominance. Several nutrients and hormones measurably influence Th1/Th2 balance, including plant sterols/sterolins, melatonin, probiotics, progesterone, and the minerals selenium and zinc. The long-chain omega-3 fatty acids EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid) significantly benefit diverse inflammatory and autoimmune conditions without any specific Th1/Th2 effect. Th1/Th2-based immunotherapies, e.g., T-cell receptor (TCR) peptides and interleukin-4 (IL-4) injections, have produced mixed results to date.
PMID: 12946237 [PubMed - indexed for MEDLINE
Edited by Lufega, 09 December 2008 - 06:47 AM.