Someone has asked me about …..

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    The link between Candida, Adrenal Fatigue, Thyroid, and Mercury.

    Of course, there is a link where Mercury plays a big role.

    Mercury loves to attack the thyroid gland, depress the immune system, specially Cell-mediated immunity allowing candida to growth. When the thyroid is malfunctioning, there is influence on the Adrenal glands.

    Mercury must be out !!!

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    Environment International 40 (2012) 39–4

    Mercury and thyroid autoantibodies in U.S. women, NHANES 2007–2008

    Carolyn M. Gallagher, Jaymie R. Meliker


    Associations between positive thyroid autoantibodies and total blood mercury in women were evaluated using the National Health and Nutrition Examination Survey (NHANES), 2007–2008. Women are at increased risk for autoimmune disorders, mercury exposure has been associated with cellular autoimmunity and mercury accumulates in the thyroid gland. We used multiple logistic regression to evaluate the associations between total blood mercury and thyroglobulin autoantibody antibody positivity and thyroid peroxidase autoantibody positivity in non-pregnant, non-lactating women aged 20 and older not currently using birth control pills or other hormone therapies, adjusted for demographic factors, menopausal status, nutrient intake and urine iodine (n =2047). Relative to women with the lowest mercury levels (≤0.40 μg/L), women with mercury >1.81 μg/L (upper quintile) showed 2.24 (95% CI =1.22, 4.12) greater odds for thyroglobulin autoantibody positivity (ptrend=0.032); this relationship was not evident for thyroid peroxidase autoantibody positivity. Results suggest an association between mercury and thyroglobulin autoantibody positivity


    The heavy metal mercury accumulates in the human thyroid gland, as shown in studies of occupationally exposed workers (Falnoga et al., 2000; Nylander and Weiner, 1991) and industrially exposed residents (Falnoga et al., 2000).

    Higher levels of hair mercury, an indicator of organic mercury exposure (ATSDR, 1999), have been associated with detectable antinucleolar autoantibodies, biomarkers of cellular autoimmunity, in a non-occupationally-exposed, fisheating riverine population (Silva et al., 2004). In addition, removal of inorganic mercury-containing dental amalgams resulted in significantly decreased levels of the thyroid autoantibodies thyroglobulin antibody (TgAb) and thyroid peroxidase antibody (TPOAb) (Sterzl et al., 2006) suggesting a positive association between mercury and these antibodies.

    Thyroglobulin antibody is an antibody against the thyroid protein thyroglobulin, and thyroid peroxidase antibody is directed against thyroid peroxidase, a thyroid enzyme. Elevated levels of thyroid autoantibodies have been observed in patients with autoimmune disorders: TgAb in patients with systemic lupus erythematosus (Lu et al., 2006; Parente et al., 2009; Porkodi et al., 2004) and both TgAb and TPOAb in patients with autoimmune thyroiditis (Baskin, 2006), rheumatoid arthritis (Atzeni et al., 2008; Porkodi et al., 2004), pernicious anemia (Chan et al., 2009), fibromyalgia (Bazzichi et al., 2007; Pamuk and Cakir, 2007) and diabetes (Prazny et al., 2005).

    Women are at increased risk for autoimmune disease (Dunaif, 2010) and mortality (Walsh and Rau, 2000). The association between total blood mercury and thyroid autoantibodies, however, has not been evaluated in a U.S. population representative sample of adult women. Therefore, the primary objective of the current study is to examine this relationship in US women.

    Studies have also shown that thyroid autoantibodies TgAb and TPOAb are prognostic indicators for long-term risk of hypothyroidism (Li et al., 2008; Vanderpump et al., 1995; Walsh et al., 2010), a disorder of thyroid hormone deficiency more prevalent in women and most commonly caused by autoimmune thyroiditis (NIH, 2011). Most recently, Hutfless et al. (2011) found increased odds for autoimmune thyroid disease associated with TgAb or TPOAb positivity during the 2–7 years preceding diagnosis. The measurement of thyroid stimulating hormone, or thyrotropin, is the most valuable test to diagnose hypothyroidism and subclinical hypothyroidism, or mildly elevated thyrotropin (Baskin, 2006). Walsh et al. (2010) showed that, among women with baseline thyrotropin levels above 4.0 μIU/ml coincident with TgAb or TPO positivity, the prevalence of hypothyroidism after 13 years was 85.7%. The relationship between mercury exposure and this indicator of autoimmune hypothyroidism risk, however, has not been evaluated in a large, population-representative sample. Therefore, a secondary aim of the current study is to evaluate the association between total blood mercury and elevated thyrotropin coincident with thyroid antibody positivity. A third aim was to evaluate the association between total blood mercury and thyrotropin in US women.


    To the best of our knowledge, this is the first epidemiologic study to investigate the relationship between mercury and thyroid autoantibodies. We report an association between blood mercury and thyroglobulin antibody positivity in US women.

    Statistical adjustment for covariates did not substantially alter these relationships. Although we do not know the association between mercury and overt autoimmune disease among the women in this study, earlier research identified thyroglobulin antibody positivity as characteristic of other autoimmune diseases.

    Given widespread exposure to low-levels of mercury in the general population, longitudinal research is merited to evaluate associations between biomarkers of mercury exposure and conditions associated with elevated thyroglobulin autoantibodies, such as systemic lupus erythematosus, fibromyalgia, pernicious anemia, diabetes, rheumatoid arthritis, autoimmune thyroiditis, and thyroid cancer.

    Environment International
    A Journal of Environmental Science, Risk & Health
    Incorporating Progress in Environmental Science

    Environment International covers all disciplines engaged in the field of environmental research. It seeks to quantify the impact of contaminants in the human environment, and to address human impacts on the natural environment itself. We recognize that scientific issues related to environmental health and human welfare are inherently interdisciplinary and, therefore, we welcome articles that cover the entire spectrum of sources, pathways, sinks and interactions between environmental pollutants, whether chemical, biological or physical. The primary criteria for publication are scientific quality and environmental significance.

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    For years I’ve read news stories about dental mercury amalgam fillings that failed to ask vital follow up questions for one to form a better understanding of the true risks involved with exposure to mercury fillings. Rarely was a toxicologist, neurologist or bio-chemist interviewed. Instead, the stories would always give dentists such prominence when promoting the safety of a substance of which they knew nothing about, all while never acknowleding the much lower levels of mercury at which our government has removed other products from the market. So now I’m doing what I can to help raise awareness of the many dangerous aspects of dental mercury fillings.

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    Thanks for bringing this up Jorge.

    I did a trial of T3 (called cytomel in the US) in the summer because nothing else was budging my symptoms.
    My constipation disappeared, my bloating was down 70%, my burping was down 90%, my energy was 50% improved. That tells me something.

    I don’t have thyroid autoantibodies though. I’ve tested for it several times.
    I’ve been wondering if my thyroid receptors aren’t accepting the T3 well so taking extra helps.

    I don’t know how for my case but this seems to be a huge factor.

    I have also learned that antibiotics kill by inducing oxidative stress. My digestive problems started after a round of IV antibiotics. I’ve been thinking my problems may be more related to that than the candida.

    My hypothesis now is that the antibiotics caused a lot of oxdiative stress including stress to the thyroid. This allowed an overgrowth in the upper gut which itself produces oxidative stress, thus perpetuating the problem.

    I continue with the enemas as well.

    For adrenal/thyroid ifnormation I really like ‘stop the thyroid madness’ and Paul Robinson


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    Personally, this is one of the most critical elements to grasp when dealing with candida. After months of concentrating on learning about candida, I have only just begun to try to grasp the complexity of the endocrine systems and how candida is only a symptom of malfunction within these systems.

    Highly recommend everyone within this forum start researching endocrine systems to learn all they can. It could very well be the missing component towards improved health.

    Blessings and thank you Jorge for the informative post.

    Hope others with even more knowledge to share will continue to post on this critical subject to help us all understand as much as possible.

    God bless.


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    Chronic Mucocutaneous Candidiasis (CMC)

    CMC is characterized by persistent Candida (fungus) infections of the mucous membranes, scalp, skin and nails, but not of the blood stream or internal organs (i.e. not systemic candidiasis). CMC is usually congenital and often hereditary, with onset in infancy manifested by persistent oral Candida infections (thrush). Later, the nails and skin become chronically infected. These infections respond to anti-Candida treatment but recur when the treatment stops.

    CMC is associated with a selective T-cell deficiency to Candida and a few related fungi, but otherwise their immune system is fine. The most common abnormal laboratory test is a negative delayed hypersensitivity skin test to Candida antigen despite widespread Candida infection.

    One hereditary form of CMC is the APECED Syndrome (autosomal recessive polyendocrinopathy-candidiasis-ectodermal dysplasia) associated with multiple endocrine problems (eg hypothyroidism or Addison disease) due to an AIRE gene defect on chromosome 21. A few CMC patients develop severe hepatitis or bronchiectasis. Treatment requires life-long antifungal medicines.

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