hey there pager, well i guess it's just that i have been obsessed with all this kind of thing since dx in 2006. i literally did nothing but read 12 hours a day for something like 8 months straight, maybe it was 8 hours a day for 6 months, something like that (i *don't* have kids!). i managed to squeeze a bit of school in there somehow, but seriously, i think it's a control thing.. i HAD to understand what was going on and why it could be happening to me.
i can't claim to understand everything i have posted above, for example the links posted by the vitamin d council, some of those are over my head.
as for the rest of it, i have just gotten adept at googling for academic research on nutrition and health/disease. mostly what i do is research other ppl's smarts and just relay!
hope you get some down time this weekend. the salient points of what i have posted so far are:
1) an infection of some kind might be a factor in your case (AG doesn't have to be autoimmune OR bacteria; could be both - case in point, while MS is theoretically autoimmune, we also have an entire gang of antibiotics protocol followers here at TIMS, based on the idea that MS is related to C. pneumoniae infection)
2) you may be able to get tested for h. pylori infection
3) if you do have an infection, you don't necessarily have to depend on pharma antibiotics
4) if your autoimmune condition is linked to h. pylori infection, then you probably have a low stomach acid condition due to the urease. again, there are tools such as betaine HCL to help combat that too.
5) in autoimmune conditions, the immune system has 'attack' signals, but is low on the 'stop attacking' signals, or 'brakes'.
6) regulatory T-cells (brakes) are low in both autoimmune gastritis and MS.
7) vitamin d3 is one nutrient which 'boosts' your immune system by increasing regulatory T-cells, or 'brakes'.
optimal d3 status, per latest research, is in the 100 - 250 nmol/L range. personally i go for 150.
9) your vitamin d3 status could also be linked to your hashimoto's thyroiditis (hypothyroidism)
10) there are links between hypothyroidism and low selenium status (i have posted optimal selenium numbers - taken from studies which compared selenium in various kinds of patients, vs in healthy controls - on my 'orthomolecular biochemistry' regimen thread)
11) low selenium status can increase your susceptibility to infection.. and here we are full circle!
anyway, let me know when you've had a chance to absorb/digest, and then we can get into things a bit further.
have a great weekend, and you're more than welcome.
one final abstract, just to show the overlaps between h.pylori and autoimmune gastritis:
Haematologica. 2005 May;90(5):585-95.
Role of autoimmune gastritis, Helicobacter pylori and celiac disease in refractory or unexplained iron deficiency anemia.
BACKGROUND AND OBJECTIVES: Conventional endoscopic and radiographic methods fail to identify a probable source of gastrointestinal blood loss in about one third of males and post-menopausal females and in most women of reproductive age with iron deficiency anemia (IDA). Such patients, as well as subjects refractory to oral iron treatment, are often referred for hematologic evaluation. DESIGN AND METHODS: Patient clinic, screened for non-bleeding gastrointestinal conditions including celiac disease (antiendomysial antibodies), autoimmune atrophic gastritis (hypergastrinemia with strongly positive antiparietal cell antibodies) and H. pylori infection (IgG antibodies confirmed by urease breath test). RESULTS: The mean age of all subjects was 39+/-18 years, and 119 of 150 were females. We identified 8 new cases of adult celiac disease (5%). Forty IDA patients (27%) had autoimmune atrophic gastritis of whom 22 had low serum vitamin B12 levels. H. pylori infection was the only finding in 29 patients (19%), but was a common co-existing finding in 77 (51%) of the entire group. Refractoriness to oral iron treatment was found in 100% of patients with celiac disease, 71% with autoimmune atrophic gastritis, 68% with H. pylori infection, but only 11% of subjects with no detected underlying abnormality. H. pylori eradication in previously refractory IDA patients in combination with continued oral iron therapy resulted in a significant increase in hemoglobin from 9.4+/-1.5 (mean +/- 1SD) before, to 13.5+/-1.2 g/ dL (p<0.001 by paired t test) within 3 to 6 months. INTERPRETATION AND CONCLUSIONS: The recognition that autoimmune atrophic gastritis and H. pylori infection may have a significant role in the development of unexplained or refractory IDA in a high proportion of patients should have a strong impact on our daily practice of diagnosing and managing IDA.