the link between mercury and immunosuppression?

Home The Candida Forum Candida Research the link between mercury and immunosuppression?

This topic contains 4 replies, has 4 voices, and was last updated by  dvjorge 5 years, 3 months ago.

Viewing 5 posts - 1 through 5 (of 5 total)
  • Author
    Posts
  • #113591

    klips32
    Participant
    Topics: 65
    Replies: 183

    http://pac.iupac.org/publications/pac/pdf/2009/pdf/8101×0153.pdf

    I’m still searching for the precise link between high mercury levels in body and immunosuppression/alteration(autoimmune etc.) toward getting more susceptible to fungi/yeast infections/allergic reaction vs. same.

    From the above article: ” The changes in cytokine production reflect changes in T-cell populations, and mercury(II) chloride has been proposed to cause immune dysfunction by favoring activation of TH2 cells over TH1 lymphocytes [36]. Some of these immunostimulatory effects are related to autoimmune effects.”

    Test on mice with TH2 dominant response and a TH1 dominant response vs. c. albicans has shown that the TH1 dominant had no problems getting rid of the yeast compared to TH2 dominant. This is nothing new in our world, just wanted to clarify. Will see if I can find the exact study again.

    Can anyone say anything more on this topic? More studies? What I have here is not conclusive.

    #113600

    ThomasJoel2
    Participant
    Topics: 9
    Replies: 375

    klips32;52112 wrote: http://pac.iupac.org/publications/pac/pdf/2009/pdf/8101×0153.pdf

    I’m still searching for the precise link between high mercury levels in body and immunosuppression/alteration(autoimmune etc.) toward getting more susceptible to fungi/yeast infections/allergic reaction vs. same.

    From the above article: ” The changes in cytokine production reflect changes in T-cell populations, and mercury(II) chloride has been proposed to cause immune dysfunction by favoring activation of TH2 cells over TH1 lymphocytes [36]. Some of these immunostimulatory effects are related to autoimmune effects.”

    Test on mice with TH2 dominant response and a TH1 dominant response vs. c. albicans has shown that the TH1 dominant had no problems getting rid of the yeast compared to TH2 dominant. This is nothing new in our world, just wanted to clarify. Will see if I can find the exact study again.

    Can anyone say anything more on this topic? More studies? What I have here is not conclusive.

    I won’t give you a link to a scientific study, but some information that may help guide you in order to find what you’re looking for.

    From what I understand, mercury is one of the big factors that can disrupt the methylation cycle. Once the methylation cycle is not functioning properly a whole host of things go wrong. Amy Yasko writes the following in her Pathways book:

    Methylation also plays a key role in the ability of our immune system to recognize foreign bodies or antigens to which it needs to respond. Whenever there is an assault on the immune system, the body must synthesize new T cells, which belong to your white blood cells. These cells help fight viral and parasitic infections, and are also needed to help to control B cells, which produce antibodies. Due to mutations in the methylation pathway, you may lack the ability to produce the methyl groups necessary for making new cells. When that occurs, there is an increased tendency to produce B cells, which may therefore result in an autoimmune disorder. When I and my practitioner colleagues look at the blood work of many of the children, we often find these kinds of imbalances–they have too many auto-antibodies, not enough of a T-cell response, and too much of a B-cell response. I have seen several cases in which the level of auto-antibodies has declined after proper methylation cycle supplementation.

    Methylation of DNA also regulates immune cells. Immune receptor DNA is initially in the “off” state and remains that way until the immune cells need to differentiate in order to respond to an intruder. As you will learn in greater detail below, at that time the DNA loses its methyl groups in a regulated fashion and the DNA is turned “on.”

    As we have just seen, methylation is generally correlated with the silencing of genes. But research has also shown that when genes are not methylated at specific points, the immune system can be tricked into reacting against itself.

    So, to sum up, methyl groups help turn your genes on and off. They also help determine the ways your immune system reacts. Unless methylation is operative, the immune system may react when it’s not needed, creating autoimmune disorders, or fail to respond to actual threats when it is needed.

    #113638

    impossible
    Member
    Topics: 16
    Replies: 606

    Good one TJ!

    Relationship of mercury and glutathione-
    http://www.ncbi.nlm.nih.gov/pubmed/15527868

    Relationship of glutathione and Th1/Th2 response
    http://www.pnas.org/content/95/6/3071.short
    There is a gold mine of links with this one too.

    #113639

    dvjorge
    Participant
    Topics: 283
    Replies: 1368

    Altern Med Rev. 2003 Aug;8(3):223-46.
    Th1/Th2 balance: the hypothesis, its limitations, and implications for health and disease.
    Kidd P.
    Abstract
    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.

    #113640

    dvjorge
    Participant
    Topics: 283
    Replies: 1368

    Self-test monitoring of the Th1/Th2 balance in health
    and disease with special emphasis on chronic fatigue
    syndrome/myalgic encephalomyelitis

    Chris Roelant1
    * and Kenny De Meirleir2

    1Protea Biopharma N.V., De Tyraslaan 111, 1120 Neder-Over-Heembeek, Belgium.
    2Department of Human Physiology, Free University of Brussels (VUB), Brussels, Belgium.

    Accepted 18 October, 2011

    A simple “self-test” principle is described which allows patients to evaluate their Th1/Th2 balance
    repeatedly over short periods of time to follow-up the effects of taking pre- and probiotics,
    neutraceuticals, drugs or any other therapeutic strategy to balance Th1/Th2 status. By analysing a large
    number of first morning urine samples obtained from individuals with medical conditions associated
    with an overactive Th2 arm (ulcerative colitis, autism, blastocystis, mercury poisoning and viral
    infection), a reaction principle was discovered that uses a redox-active colorimetric substrate changing
    color upon reaction with metabolites present at high concentration in the urine samples of Th2-shifted
    individuals. The development of color is time-dependent and quantitative. Moreover, 75% of urine
    samples obtained from chronic fatigue/myalgic encephalomyelitis patients produced a time-dependent
    and quantitative change of color compared to only 4% of the controls (perfectly healthy population),
    providing evidence that chronic fatigue syndrome/myalgic encephalomyelitis is a condition associated
    with an overactive Th2 arm.

    See this fragment :

    Solidification of the vicious circle: After the vicious circle has developed involving the methylation cycle block and the depletion of glutathione, another factor must come into play to lock in this situation chronically. It seems likely that buildup of toxins is the factor responsible for this, by blocking the formation of methylcobalamin and thus the activity of methionine synthase. It has been shown that one of the important roles of glutathione normally is to protect the very much smaller (by six orders of magnitude) concentrations of cobalamins from reaction with toxins by forming glutathionylcobalamin (134). Without this protection, cobalamins are vulnerable to reaction with a variety of toxins. An example is mercury. It has been found that very small concentrations of mercury are required to block the methionine synthase reaction (135). Because of this additional factor, attempts simply to correct the glutathione depletion and the oxidative stress after the cobalamins have reacted with toxins in most cases will not restore normal function of the methylation cycle (1).

Viewing 5 posts - 1 through 5 (of 5 total)

The topic ‘the link between mercury and immunosuppression?’ is closed to new replies.