This Is MS Multiple Sclerosis Knowledge & Support Community

Hello..this is to Jimmylegs, the ultimate vitamin expert or to anyone else with a similar experience.

I will try to be as short and concise as possible.

I was diagnosed with MS in May. My fatigue and stomach issues continue to be an issue. I had an endoscopy in August with a preliminary diagnosis of autoimmune gastritis. Was then referred to the Univ. here locally to have another endoscopy with an ultrasound to get out one of the tumors that was in deeper and required equipment my local hospital do not have available. My gastro told me that the dr. at the U would do a full work up and see how my B12 is affected in all this....that this could be tied in with my MS and Hashi thyroid.

Thus, the endoscopy at the U was last week and basically I didn't even talk with the doctor, only the Fellow, who told me that I had gastritis and I will be fine and probably have need a follow up in about six months. So, I called my gastro to set a follow up with him and can't get in for several months, so I called his assistant. I talked with her today. She was surprised that my primary gastro hadn't received anything from the U and asked if the U Gastro talked with me about pernicious anemia, because that is what my gastro suspected and put that in the report. I told her that he didn't mention that or really anything other than what the removal of the tumors would entail. She asked if they pulled blood, but I don't think I have had a full blood panel since March. She sounded frustrated and she got me into see my primary gastro in a couple of weeks.

The side note is that I have been taking 500 mg sublingual B12 for several years. (Recommendation from my psychiatrist.) When I saw an MS neuro specialist in July following my MS diagnosis in May, he thought my B12 was low and that I should increase my dose. Thus, since July I have been taking 1000 sublingual.

The Vitamin B12 test in March 2009 was 353 pg/ml with a range of 211-911. My Ferritin, Serum was 83 ng/ml with a range of 10-291.

I feel so frustrated and so tired of being tired and exhausted. I have been battling fatigue since at least the beginning of this year and it seems like it will never stop. In January I started working part time and I am a mom to two elementary school girls. I have always had a lot of energy, but now I am afraid to plan anything, have people over for dinner or go anywhere, because I am not sure that I can handle it. I guess when I got diagnosed in an exacerbation in May that probably started in late 2008 or early 2009, I thought that I would start feeling better by the fall. Yes, I am better, but no where close to the person I was one year ago.

So my plan: 1) call the U and find out if they did a blood draw and B12 panel, if so, get it sent to my primary gastro; 2) call my primary doctor to confirm if she has any other blood draws since March; 3) call my gastro as see if I can have a blood draw prior to our meeting in Oct. so he will have most recent results.

Is there anything else that I am missing? Does this sound logical? Any insight is greatly appreciated!!

hey there pager, i will have a dig into all this and get back to you. off the top, it sounds good that you are getting a handle on the situation via bloodwork. this i like. keep an eye out for more info and probably a bunch of questions

hi again, okay to start off it looks like autoimmune gastritis can be linked to h. pylori. that is a bacterial infection which uses 'urease' to neutralize stomach acid. so for starters you can consider a supplement of betaine hydrochloric acid to increase stomach acidity, and you can also look into the antibacterial properties of oil of oregano (such as p73 oreganol) and cranberry - here's an abstract:

Ulcer-associated dyspepsia is caused by infection with Helicobacter pylori. H. pylori is linked to a majority of peptic ulcers. Antibiotic treatment does not always inhibit or kill H. pylori with potential for antibiotic resistance. The objective of this study was to determine the potential for using phenolic phytochemical extracts to inhibit H. pylori in a laboratory medium. Our approach involved the development of a specific phenolic profile with optimization of different ratios of extract mixtures from oregano and cranberry. Subsequently, antimicrobial activity and antimicrobial-linked urease inhibition ability were evaluated. The results indicated that the antimicrobial activity was greater in extract mixtures than in individual extracts of each species. The results also indicate that the synergistic contribution of oregano and cranberry phenolics may be more important for inhibition than any species-specific phenolic concentration. Further, based on plate assay, the likely mode of action may be through urease inhibition and disruption of energy production by inhibition of proline dehydrogenase at the plasma membrane.

you have a lot of different things going on so this is just introductory info and we'll need to see if everything that comes out of this will work together.

more to come,
JL

you say autoimmune, i say vitamin d3 (you know i had to go there)...:

regulatory T cells and gastritis:

Regulatory T cells curb unwanted immune responses and regulate responses to microflora and it is now clear that regulatory T cells play an important role in a number of chronic inflammatory diseases of the gut. First, regulatory T cells are crucial in controlling immune responses to gastric autoantigens and thus preventing autoimmune gastritis and pernicious anemia. Second, regulatory T cells may modulate the response to Helicobacter pylori, thus affecting the ability of the immune system to clear the pathogen and mediate damage to the gastric mucosa. Finally, regulatory T cells play an important role in preventing damaging inflammatory responses to commensal organisms in the lower gut, thus guarding against inflammatory bowel diseases. In the present review, we examine the actions of regulatory T cells in the gut and conclude that further understanding of regulatory T cell biology may lead to new therapeutic approaches to chronic gastrointestinal disease.

regulatory tcells, ms, and vitamin d3

In several autoimmune diseases, including multiple sclerosis (MS), a compromised regulatory T cell (Treg) function is believed to be critically involved in the disease process. In vitro, the biologically active metabolite of vitamin D has been shown to promote Treg development. A poor vitamin D status has been linked with MS incidence and MS disease activity

more to come...

a totally unbiased set of links on HT and vit d3

http://www.vitamindcouncil.org/science/ ... itis.shtml

Hashimoto's Thyroiditis

Association of vitamin D receptor gene 3'-variants with Hashimoto's thyroiditis in the Croatian population.
Int J Immunogenet. 2008 Apr;35(2):125–31.

Seasonality of month of birth of patients with Graves' and Hashimoto's diseases differ from that in the general population.
Eur J Endocrinol. 2007 Jun;156(6):631–6.

Biological and clinical aspects of the vitamin D binding protein (Gc-globulin) and its polymorphism.
Clin Chim Acta. 2006 Oct;372(1–2):33–42. Review.

Vitamin D receptor gene polymorphisms are associated with risk of Hashimoto's thyroiditis in Chinese patients in Taiwan.
J Clin Lab Anal. 2006;20(3):109–12.

Hashimoto's thyroiditis in a patient with non-Hodgkin's thyroid lymphoma of B cell type and originated from mucosa-associated lymphoid tissue (MALT): A case report.
J Med Assoc Thai. 2005 Jun;88 Suppl 1:S73–8.

A promoter polymorphism of the CYP27B1 gene is associated with Addison's disease, Hashimoto's thyroiditis, Graves' disease and type 1 diabetes mellitus in Germans.
Eur J Endocrinol. 2004 Aug;151(2):193–7.

Genetic markers in thyroid autoimmune diseases.
Z Arztl Fortbild Qualitatssich. 2004 May;98 Suppl 5:13–5. Review.

Vitamin D 1alpha-hydroxylase (CYP1alpha) polymorphism in Graves' disease, Hashimoto's thyroiditis and type 1 diabetes mellitus.
Eur J Endocrinol. 2002 Jun;146(6):777–81.

A polymorphism within the vitamin D-binding protein gene is associated with Graves' disease but not with Hashimoto's thyroiditis.
J Clin Endocrinol Metab. 2002 Jun;87(6):2564–7.

Vitamin D receptor gene polymorphisms in Hashimoto's thyroiditis.
Thyroid. 2001 Jun;11(6):607–8.

Hypoparathyroidism, moniliasis, Addison's and Hashimoto's diseases. Hypercalcemia treated with intravenously administered sodium sulfate.
N Engl J Med. 1964 Oct 1;271:708–13.

selenium and the thyroid:

Selenium and the thyroid: how the relationship was established
B Corvilain, B Contempre, AO Longombe, P Goyens, C Gervy-Decoster, F Lamy, JB Vanderpas and JE Dumont
Department of Pediatrics, School of Public Health, University of Brussels, Belgium.

Several hypotheses concerning consequences of selenium deficiency on iodine metabolism can be proposed on the basis of experimental studies in rats and from epidemiological and experimental studies in humans. By decreasing intracellular GSH peroxidase activity, selenium deficiency may increase hydrogen peroxide (H2O2) supply and lead over several weeks to the thyroid atrophy observed in myxoedematous cretins. By improving thyroid hormone synthesis and by decreasing peripheral thyroxin (T4) deiodination, selenium deficiency could protect fetal brain T4 supply and thus prevent neurologic cretinism. Selenium deficiency may protect against iodine deficiency by decreasing T4 metabolism--and thus iodide leakage and--perhaps also by increasing H2O2 supply and thyroid hormone synthesis and thus thyroid efficiency.

selenium and infection (what i get from the following is that it's important to know your selenium status, and i do have info on optimal selenium kicking around somewhere... the idea being that selenium goes where it's needed... and it seems to me that if you didn't quite have enough, that might not happen in the way it's meant to):

Plasma and gastric tissue selenium levels in patients with Helicobacter pylori infection
Résumé / Abstract
Goals: We investigated plasma and gastric mucosal selenium levels in patients with Helicobacter pylori (HP)-associated histopathologic findings in their gastric antral mucosa. Study: Before and after a successful HP eradication therapy, we quantitated the plasma and antral selenium levels in patients with HP-associated chronic antral gastritis using atomic absorption flame emission spectrometry. The same measurements were done in patients with dyspeptic complaints who had normal antral histology and negative urease test. Results: Thirty-four patients were studied, of whom 24 had HP-associated chronic antral gastritis confirmed by histology and positive urease test; the control group included 10 healthy patients. There was no difference between the groups with regard to age, gender, and number of smokers. All patients with HP infection were diagnosed with diffuse antral gastritis. Histopathology showed that 11 (49%) had some degree of atrophy. Of the 11 patients, 7 were classified as having chronic atrophic gastritis (CAG) without intestinal metaplasia (IM), 4 had IM, and none had dysplasia. The plasma concentrations of selenium were found to be very similar in controls and HP-infected subjects (68.0 ± 25.97 μg/L and 71 ± 32.9 μg/L, respectively; p > 0.05). The antral biopsy samples of the patients with HP-associated gastritis contained significantly higher levels of tissue selenium than the controls (20.17 ± 19.74 μg/g and 2.83 ± 1.42 μg/g, respectively; p < 0.05). Also, it was shown that antral tissue selenium levels decrease after successful HP eradication therapy (20.17 ± 19.4 μg/g and 7.4 ± 4.56 μg/g, respectively; t < 0.05). The patients with HP gastritis were assigned to mild, moderate, and severe gastritis groups, according to the histopathologic degree of inflammation present. The antral gastric selenium levels were significantly higher in patients with moderate and severe HP gastritis (21.13 ± 22.5 μg/g and 22.81 ± 17.35 μg/g, respectively) than in patients with mild gastric inflammation (9.53 ± 10.3 μg/g; p < 0.05). The selenium concentrations in the biopsies of patients with CAG were significantly lower than in those with HP gastritis who did not have CAG (9.45 ± 6.44 μg/g vs. 19.13 ± 22.48 μg/g, respectively; p < 0.05). Conclusions: Selenium accumulates in gastric tissue when it is needed, as is the case in HP-related antral inflammation. This reactive increase in gastric mucosal selenium seems to disappear in the presence of precancerous gastric lesions in the setting of HP-associated gastritis.

selenium and fungal infection:

The effects of selenium deficiency on the responses to Candida albicans infection were examined in mice. When selenium-deficient and selenium-supplemented mice were given i.v. injections of 0.1 ml suspensions of 1 x 105 or 5 x 104 C. albicans in 0.9% sterile saline, deaths in the selenium-deficient animals started after 2.5–3.5 d compared with 7–8.5 d in the selenium-supplemented animals. Further studies demonstrated that 3 d after an i.v. injection of 1 x 105 C. albicans, significantly more of the microorganisms were found in the kidneys (P < 0.001), livers (P < 0.025) and spleens (P < 0.01) of the selenium-deficient mice compared with the same organs of selenium-supplemented animals. Selenium deficiency was also demonstrated to impair the ability of mouse neutrophils to kill C. albicans in in vitro tests. The possible relationships of this defect in function to decreased resistance to C. albicans infection is discussed.

Serum selenium in acute infections

Summary We measured the serum selenium concentration in 64 patients with uncomplicated viral (n=33) or bacterial (n=31) infections during the acute stage of infection, during the early convalescent phase and after a minimum recovery period of three weeks and compared it to serum iron values. Both selenium (mean ± SEM: 70.3±2.3 µg/l vs 79.4±2.2 µg/l, p<0.0001) and iron (8.4±0.8 µg/l vs 16.7±0.9 µg/l, p<0.0001) concentrations showed significant depressions in the acute stage of infection compared with the values after the recovery. The reduction of serum selenium did not correlate with the severity of infection measured by fever. We conclude that acute infections decrease serum selenium levels regardless of the infective agent. The changes are of interest because of the possible connection between selenium and the immune system.

interesting aside: ran across a link between selenium status and fatty acids? remind me to get back to this later:

The content of polyunsaturated fatty acids, especially eicosapentaenoic acid, in serum cholesterol esters and phospholipids was positively correlated with selenium concentration.

stay tuned...

you may want to try to get your b12 up to 700 - if you take 2000 mcg per day you have to watch the timing or it can interfere with your night's sleep. if i recall correctly, it's when ppl take big doses in the morning that it messes with circadian rhythm - i'll double check on that for you.

also i am going to look into the narrower ranges within that iron range - my lab has ranges for "possibly deficient" "probably not deficient" and such, within the overall normal range. might be useful info for you to have too.

WOW! I am going to need to take some time this weekend away from the kids to digest all of this information. How do you know and understand all of this?

I don't think my gastro thinks it is infection (H.plyori) related, but autoimmune in nature. Please give me a couple of days to read through your posts when I don't have work or kids. (Which doesn't occur until the weekends and even then sometimes it is tough!)

Jimmylegs, thank you, thank you for all the research you have done! You amaze me! It is so greatly appreciated!!!!!!

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.

Hello JL, sorry it has been so long, but life seems to keep getting in the way.

I did see the gastro dr. and he says I have autoimmune metaplastic atrophic gastritis. He started me on B12 injections, my first last Monday. (Obviously, the sublingual B12 (1,000 daily) was not effective as my level was still in the 200's at 280.)

There is really no noticeable change in my energy level yet, but I have been having very, very vivid dreams. (Usually, I don't ever even remember my dreams, so I am finding this rather uncomfortable.) In your knowledge, is this normal or do you know anything about B12 injections?

hi pager, yes b12 has a lot to do with circadian rhythm and at high doses it can either help your sleep or mess with it depending on the time of day you get it.
it also enhances REM sleep which is when you dream.
so yes, there is a link between b12 deficiency and not having as many dreams.
i would think in time as you get used to it, you'd come to value having dreams and remembering them.

HTH,
JL

PS: have you asked the docs about the links in the research between h.pylori and autoimmune metaplastic atrophic gastritis? also, do you think you might look into getting d3 and selenium tested? these are important immune system nutrients...

JL, you are awesome. Thanks...now I don't think I am crazy. I have had more dreams this week that I remember having in YEARS! Last night I woke up at 3 am and the dreams just starting making me freak out a bit. My guess is that my body just got such a big jolt of it, it will take a bit of time to adjust. (He gave me just one dose, where my PCP said they would have done four doses over the course of a month and then go monthly....that might have been better for me.)

The gastro did test for h. pylori and it was negative. My D3 has been monitored and is good. I have been taking 2,000 IU daily, but just bumped it up to 3,000 daily since it is fall/winter here in the Rockies.

Based on your posts as well as others, I think my next blood test should also include folic acid (folate), selenium and zinc. I take 800 mg of folic acid daily (but missed a few days this week) and selenium and zinc are in my multi vitamin. So, I think I am okay.....

Thank you so much!! Really JL! We are fortunate to have you on this board!

hey there no probs
can i ask the number for the d3? will/did they tell you? (some docs still use the old version of "good" for d3)
good to know about the negative h.pylori!
sounds like your folic level will come back pretty good
selenium and zinc are good to know for sure, and it's not necessary but interesting to test uric acid too. that way you can watch the ua approach the same as healthy controls as you optimize your zinc levels. it's just fun (at least it is to me haha!)
glad to help!
JL

Okay, I guess the last D3 was in March. It was 56.6 in a range of 32-100. .The B12 then was 353 and then was 451 in May. My MS Specialist was concerned at that time that the B12 was low. (It was 280 in October)

The challenge, that I guess that you experience too, is that different doctors pull blood, but not for all the same things. The endo re: thyroid does one set, the neuros (general and MS) each do another, seperately and then gastro does something else. Then to get copies is hard, because they always seem to pull it after they meet with you and then if you don't have scheduled appointment, you have to drive back over and get a copy. I find it so difficult to manage.......

BTW, Uric acid and selenium were not listed on any of the tests, but Ferritin, Serum was in March and to me seems low: 83 ng/ml with a range of 10-291. Guess I should add all of this to my list for my neuro appointment in November. It is my follow up of six months following my MS diagnosis.

JL, again, thank you for all of your insight. This is a great board and I am so grateful for the support of everyone here!