LNN Posted January 21, 2012 Report Posted January 21, 2012 I've been noticing several posts that say their kids are being diagnosed with Hashimoto's Disease or it's being considered. I didn't pay much attention at first. But my DD7 is struggling with a recent/current epstein barr virus that's causing some seriously rough fatigue. You all know that methylation is my current "thing", so I went back to look at some research done by Rich Van Konyenburg, who's big in the Chronic Fatigue world. Attached is a link to his latest published research http://aboutmecfs.org.violet.arvixe.com/Trt/TrtMethylStudy09.pdf His theory: An individual inherits a genetic predisposition (polymorphisms in several of certain genes) toward developing CFS. (This genetic factor is more important for the sporadic cases than for the cluster cases of CFS.) • The person then experiences some combination of a variety of possible stressors (physical, chemical, biological, and/or psychological/emotional) that place demands on glutathione. • Glutathione levels drop, producing oxidative stress, removing protection from cobalamin (vitamin B12) and allowing toxins to accumulate. • Toxins react with cobalamin, lowering the rate of formation of methylcobalamin. • Lack of sufficient methylcobalamin inhibits the activity of methionine synthase, placing a partial block in the methylation and folate cycles. Sulfur metabolites drain excessively through the transsulfuration pathway to form cysteine. • Much of the cysteine is oxidized to cystine because of the state of oxidative stress, and is therefore not available for the synthesis of glutathione. An alternative pathway initiated with catalysis by cystathionine gamma lyase carries the cystine on to form hydrogen sulfide and thiosulfate, and the latter is excreted in the urine. • An interaction (vicious circle) is established between the partial block in the methylation cycle and glutathione depletion, and the disorder therefore becomes chronic. • A wide range of symptoms results from these chronic abnormalities in the basic biochemistry of the cells. • The dysfunction of the detoxication system and the immune system that results from this combination allows toxins and infections to accumulate over time, which increasingly produce effects of their own. • Treatment should be directed primarily at increasing the activity of methionine synthase. The resulting normalization of the methylation cycle, the folate metabolism and glutathione levels will restore function to the immune system and the detoxication system as well as to a wide range of other parts of the overall biochemistry. • It can be expected that die-off of pathogens and mobilization of stored toxins will initially produce some exacerbation of symptoms, but improvements will be experienced as the body burdens of toxins and active infections are decreased. Later in the paper, he describes the tests that were done on the participants. Among them: Thyroid panel (TSH, total T4, total T3) [13]: (performed initially and at 3 months). Thyroid peroxidase antibody was also measured initially and again at 6 months, if found to be positive. These tests were run to document hypo- or hyperthyroidism and to test for Hashimoto’s thyroiditis. Also, it was desired to determine whether the treatment would correct hypothyroidism, as had been reported anecdotally in a small number of cases treated prior to this study. Among his findings: The treatment was not found to completely correct hypothyroidism in this group of patients, though it had been reported to do so in a small number of patients prior to this study. However, the improvement in the values of total T3, the most active effector hormone in the hypothalamuspituitary- thyroid axis, suggests that the treatment did act in the direction of normalizing the operation of this axis.... ...Though there was (mostly mild) initial exacerbation of symptoms in over half the patients, the symptomatic improvement in at least two thirds of the patients was the dominant effect of the treatment. There was a significant decrease (by nearly half) in the average number of symptoms after 6 months of treatment, and significant improvements in all five of the self-rated symptomatic outcome measures. Four of the self-rated measures showed monotonic improvement with treatment time. The rating of overall feeling of wellbeing at 6 months was lower than the value to which it had risen at 3 months, but this decrease was not statistically significant. The fact that treatment of this type produced improvement in the whole range of symptoms experienced in CFS is evidence that the partial block at methionine synthase is fundamental to the pathophysiology of CFS, and this is consistent with the central feature of the GD-MCB hypothesis. And then I went to the Mayo Clinic web site to look into Hashimotos and saw Hashimoto's disease is an autoimmune disorder in which your immune system creates antibodies that damage your thyroid gland. Doctors don't know what causes your immune system to attack your thyroid gland. Some scientists think a virus or bacterium might trigger the response, while others believe a genetic flaw may be involved. A combination of factors, including heredity, sex and age, may determine your likelihood of developing the disorder. Hashimoto's disease is most common in middle-aged women and tends to run in families. So if a virus or infection can trigger hypothyroidism...yet Hashimoto's is supposed to be a middle-aged woman's disease and not a kid's disease, especially a boy's disease...Is it possible the Hashimoto's dx is sort of a "Don't know what it is but I'll stick this label on it" instead of a condition that's being caused by infection-triggered oxidative stress, glutathione depletion and/or something that could be fixed with a few supplements? As I said, I have no experience with thyroid issues. My DD is already on some but not all of what Van Konyenburg suggests and I'll be asking her Dr about doing the whole shebang when we see him. But it made me go "hmmm" and I wanted to put it out there for anyone who may want to look into it further.
Christianmom Posted January 21, 2012 Report Posted January 21, 2012 I don't know much about Hashimoto's, but I did read that it can cause the C4a to be elevated.
Dean1065 Posted January 22, 2012 Report Posted January 22, 2012 FWIW, I got Hashimotos Thyroiditis when I was 25. My daughter now has PANDAS. Her thyroid function tests are all normal.
AmySLP Posted January 22, 2012 Report Posted January 22, 2012 My daughter has fluctuating tsh, T3 & T4 have been normal and she is neg for antibodies (although she does not seem to mount antibodies to many things--- strep,vaccines.). We saw an endocrinologist who wants to watch the pattern and draw the labs every few months.
scossio Posted January 22, 2012 Report Posted January 22, 2012 My son was dx with Hashimoto's a year after all of his symptoms presented and he was not responding to any psych meds. A psych dr that we were seeing at the time sent him for blood work and found his levels to be more than 2x normal. An endo dx Hashimoto's b/c his ANA levels were extremely high also. His thyroid levels have been back to normal range for almost 2 yrs since he started treatment, but his pans symptoms are still there (waiting for 1st appt with Dr. B in 2 weeks!)
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