Ott J, Promberger R, Kober F, Neuhold N, Tea M, Huber JC, Hermann M
Hashimoto's disease is characterized by chronic inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. of the thyroid gland, often leading to a less than sufficient production of the hormones T3 and T4. In some cases hormone replacement therapy may alleviate the majority of symptoms, at least for a while, while in other cases euthyroid patients suffer from a variety of symptoms; lethargy and fatigue being prominent symptoms.1)
Women with Hashimotos thyroiditis suffer from a high symptom load. Hypothyroidism is only a contributing factor to the development of associated conditions.2)
An infectious etiology has long been suspected in different thyroid diseases, including Hashimoto's thyroiditis. As with many other inflammatory diseases most reasearchers appear to be searching for one specific culprit, something which seems ulikely in light of the many findings of links to many different viruses and bacteria in thyroid disease. Further, in the light of last few years' progress in metagenomics, a multimicrobial, successive type infection appears more likely to drive the disease process.3)
Also, inflammatory thyroid disease has also been shown to occur as part of the immmunopathology resulting from treatment of HIV infection.10) In line with the Marshall PathogenesisA description for how chronic inflammatory diseases originate and develop. of inflammatory disease, this is most readily explained by an enhanced function of the immune system upon initiating antiviral therapy, revealing subclinical thyroid disease and multimicrobial infection of the thyroid gland.
Patients suffering from Hashimoto's disease have lower levels of vitamin 25-DThe vitamin D metabolite widely (and erroneously) considered best indicator of vitamin D "deficiency." Inactivates the Vitamin D Nuclear Receptor. Produced by hydroxylation of vitamin D3 in the liver., and disease severity correlates with vitamin D levels.11) In line with the Marshall Pathogenesis of inflammatory disease, this points to microbes having subverted the function of the vitamin D receptorA nuclear receptor located throughout the body that plays a key role in the innate immune response..
However please note that S354 thru S357 (Impact of MP on hormones, pages 1 thru 4) are missing; refused me access for some unknown reason, so that content is still needed.--dody 2/22/09
Thyroid function affects bone health
Close to our science is this paper showing that the Alpha Thyroid receptor is key to bone structure. http://tinyurl.com/mlaea
A simpler summary of what is known is found here http://tinyurl.com/nwpaj
My molecular genomics shows that 1,25-DPrimary biologically active vitamin D hormone. Activates the vitamin D nuclear receptor. Produced by hydroxylation of 25-D. Also known as 1,25-dihydroxycholecalciferol, 1,25-hydroxyvitamin D and calcitirol. directly acts on the alpha-1-Thyroid receptor, with higher affinity even than it has for the VDRThe Vitamin D Receptor. A nuclear receptor located throughout the body that plays a key role in the innate immune response.. This is clearly an important pathway towards the osteopenia we often see in Th1 diseaseAny of the chronic inflammatory diseases caused by bacterial pathogens., especially when folks exhibit hypothyroid symptoms.
Symptoms of Hyperthyroidism (overactive thyroid)
Anemia Anorexia Anxiety Breathing Difficulties (shortness of breath) Constipation Depression Diarrhea Dyslexia (difficulty with reading, calculating, thinking) Erratic behavior, Excessive mood swings Eye problems (blurring; double vision; gritty, achy, dry, irritated red eyes; bulging eyes; light sensitivity; jumpy eyes; watery eyes) Fatigue (all the time, despite sleep sufficiency) Fertility problems Goiter (enlarged thyroid gland) Hair problems ( thinning and loss, textural changes) Hearing disabilities (tinnitus, ear ringing among them) High blood pressure High cholesterol Hypersensitivity to heat (heat intolerance) Increased appetite Increased frequency of stools (without diarrhea) Increased sweating Insomnia or restless sleep Low resistance to infections Menstrual changes (flow, duration) Mental challenges (forgetfulness, brain fogThe loss of intellectual functions such as reasoning; memory loss; and other neurological abilities that is severe enough to interfere with daily functioning., uncontrollable rages) Muscle weakness (arm triceps, leg quadriceps) Nail problems Osteoporosis (demineralization and weakening of the bones) Palpitations (rapid, forceful or irregular heart beats) PMS (premenstrual syndrome) Restlessness Sexual dysfunction (low drive in both sexes, impotence in men) Skin Changes (rashes, dry, itchy, patchy) Swelling (facial, eye or leg) Tachycardia (rapid heart beat) Throat problems (difficulty swallowing, sore throat) Tremors (shaking hands) Voice changes (hoarse, husky) Weakness (overall, all the time) Weight fluctuation (gain or more commonly loss, 6-10 lbs.)
Conceptually the 'hyper' condition (without supplementation) would occur with a hormone when a different part of the concentration control-system becomes dysfunctional. The hormonal systems typically keep their hormones under tight control. Pathogen-induced-mutations pervert that control.
Basic information on thyroid disease
Thyroid Disorders [INTERNAL LINK–I don't know how to create the link here–dody 2/22/09]
Wilson's syndrome (filelink)
Wilson's syndrome is controversial.
This article explains why The American Thyroid Association states there is
…no scientific evidence supporting the existence of “Wilson's syndrome.”
and the rebuttal:
Please research carefully and discuss this issue which your doctor.
Nothing contained in this site is or should be considered, or used as a substitute for, medical advice, diagnosis or treatment by your physician. Meg Mangin R.N. Former Team Member
Joined: Sat Jul 10th, 2004 Location: Menomonie, Wisconsin USA Posts: 17283 Status: Offline
Posted: Thu Jan 11th, 2007 20:17
(filelink) Members' experiences
I am watching my (thyroid) antibody count drop as I progress on the MP. I've been on the MP for almost a year now. My Thyroid itself has been herxing, as the nasty bugs die and irritate the tissue,so the thyroid can't work as well, as I have noted at the start of each phase: my TSH (thyroid stimulating hormone = demand for thyroid to “produce more juice” ) jumped when I started phase I and again on phase II & III. That went along with pain and swelling in my throat and hair-loss, which was a hypo-thyroid symptom. Then it levelled out as my body progressed through the phases.
So a chart of my TSH would show a spike each time, as herxing commenced, then return to normal. However, my thyroid antibodies count, which started “off the chart” has steadily declined throughout. From >1000 to something in the 200s. I look forward to seeing a big fat 'zero' one day I know we officially “don't believe in autoimmunity” according to the MP theory, however the mainstream medical community does, and anything that can illustrate “recovery from autoimmunity” is useful as well as heartening.
The hair-loss is something I've come to expect and it grows back each time - giving an interesting natural “layered” effect! HaHaHa~Claudia
-When I became jittery, anxious, restless, or teary-eyed, I soon came to realize that my physician needed to adjust my thyroid medication. Thus, please understand that your body is experiencing great hormonal changes as you progress on the protocol, so the new or repeated symptoms are to be expected. ~Carole
-My thyroid medication was reduced and then ceased when I noticed more chest symptoms. ~Aussie Barb
-I got an email from my doctor today, My Vit D level is down to 11 and my TSH is WAY low. He told me to stop my cytomel immediately. I am having minimal symptoms and my hot flashes have completely vanished within the last week or so. ~ctaegar (member in phase 2 with Hashimoto's thyroiditis)
Patients experiences with thyroid supplementation
Is hair change common in Th1 diseasesThe chronic inflammatory diseases caused by bacterial pathogens.? [internal link]
s354, s355, s356, s357 = Impact of MP on hormones, pages 1 thru 4: For some odd reason, although logged into the site (and it said so on the page), I got the you-do-not-have-permission message when I tried to access these pages. I tried to re-log in but of course I was already logged in… So these 4 are missing here.–Dody 2/22/09
The effect of Th1 inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. on the thyroid hormones
Dr. Marshall has created a diagram summarizing some of the key relationships between the body's hormones and 1,25-D. You can access it at http://autoimmunityresearch.org/hormones.pdf
Hypervitaminosis-D Symptoms (High 1,25-D)
Control of body temperature
Control of body temperature is at least partly regulated by the Thyroid Nuclear ReceptorsIntracellular receptor proteins that bind to hydrophobic signal molecules (such as steroid and thyroid hormones) or intracellular metabolites and are thus activated to bind to specific DNA sequences which affect transcription., which are profoundly affected by the runaway production of 1,25-D in the Th1 diseases. The thyroid interaction of 1,25-D is covered in my new paper, which should be available in a month or two. See Vitamin D Discovery outpaces FDA decision making
s203: Parathyroid Hormone and Th1 inflammation
“1,25-D spreads from the site of the inflammation (where it is acting as a cytokineAny of various protein molecules secreted by cells of the immune system that serve to regulate the immune system.) through the bloodstream (acting as a hormone)… 1,25-D directly controls the Parathyroid Hormone (PTH) and thence the Thyroid hormones as well as a number of other metabolic pathways, so it is pretty powerful feedback to the body systems, and when the bacteria interrupt that feedback path everything goes unstable (that's how a control-systems engineer might describe it).”
Prevalence of Yersinia plasmid-encoded outer protein (Yop) class-specific antibodies in patients with Hashimoto's thyroiditis13)
Clin Microbiol Infect. 2001 Mar;7(3):138-43. Prevalence of Yersinia plasmid-encoded outer protein (Yop) class-specific antibodies in patients with Hashimoto's thyroiditis. Chatzipanagiotou S, Legakis JN, Boufidou F, Petroyianni V, Nicolaou C. Department of Clinical Microbiology, Aeginition Hospital, Medical School, National University of Athens, Athens, Greece. email@example.com Abstract OBJECTIVE: To investigate the prevalence of class-specific antibodies (IgG, IgA) to Yersinia enterocolitica plasmid-encoded outer proteins (Yops) in patients with diagnosed Hashimoto's thyroiditis. METHODS: Seventy-one patients with Hashimoto's disease, 464 healthy blood donors and 250 patients with non-postinfectious rheumatic disorders (matched controls) were tested for class-specific antibodies to Yops. Anti-Yop antibodies were determined by ELISA and Western blot. RESULTS: The prevalence of class-specific antibodies to Yops as determined by ELISA was 14-fold higher (20 of 71; 28.2%) in people with Hashimoto's thyroiditis than in the two control groups. These results were confirmed by the Western blot, with 16 positive sera, three equivocal and one negative. CONCLUSIONS: There is strong clinical and seroepidemiologic evidence for an immunopathologic causative relationship between Yersinia enterocolitica infection and Hashimoto's thyroiditis. Further investigation concerning the mechanisms involved and the possible effects of antibacterial chemotherapy on the outcome of Hashimoto's disease is warranted. PMID: 11318812