Health Matters

Painful small-fiber neuropathy in Sjogren syndrome
Chai J, Herrmann DN, Stanton M, Barbano RL, Logigian EL.
Department of Neurology, University of Rochester, Rochester, NY, USA.
Neurology. 2005 Sep 27;65(6):925-7

Of 20 consecutive patients with Sjogren neuropathy, 16 (80%) presented with burning feet and 12 (60%) with non-length-dependent sensory symptoms. Leg and thigh skin biopsies, performed in 13 patients, including 7 with normal electrophysiology, showed either reduced epidermal nerve fiber (ENF) density or abnormal morphology. ENF loss was frequently non length dependent, suggesting that patients with this disorder commonly have a small-fiber sensory neuronopathy rather than a "dying-back" axonopathy.

PMID: 16186536 [PubMed - indexed for MEDLINE]

A no of docs (about 5 or more) have suggested I had Sjogren's from my symptoms, and left it at that. I have never had specific tests for it though?

I still have some feet burning and neuropathy (numbness/pain etc), , and a little in lips and hands but not really that noticeable..bottom of legs still scaly and dry.
Eyes now moist as I need, and stinging stopped almost..still red though, more so at some times than others.. never clear
Moist in mouth and skin still dry but much better..
Hoping this continues, and looking out for anything relating thiamin to Sjrogen's now too..--------------------------------------

Neurologic manifestations in primary Sjogren syndrome: a study of 82 patients.Delalande S, de Seze J, Fauchais AL, Hachulla E, Stojkovic T, Ferriby D, Dubucquoi S, Pruvo JP, Vermersch P, Hatron PY.
Department of Neurology, CHRU Lille, France.

Neurologic involvement occurs in approximately 20% of patients with primary Sjogren syndrome (SS). However, the diagnosis of SS with neurologic involvement is sometimes difficult, and central nervous system (CNS) manifestations have been described rarely. We conducted the current study to describe the clinical and laboratory features of SS patients with neurologic manifestations and to report their clinical outcome. We retrospectively studied 82 patients (65 women and 17 men) with neurologic manifestations associated with primary SS, as defined by the 2002 American-European criteria. The mean age at neurologic onset was 53 years. Neurologic involvement frequently preceded the diagnosis of SS (81% of patients). Fifty-six patients had CNS disorders, which were mostly focal or multifocal. Twenty-nine patients had spinal cord involvement (acute myelopathy [n = 12], chronic myelopathy [n = 16], or motor neuron disease [n = 1]). Thirty-three patients had brain involvement and 13 patients had optic neuropathy.
The disease mimicked relapsing-remitting multiple sclerosis (MS) in 10 patients and primary progressive MS in 13 patients.
We also recorded diffuse CNS symptoms: some of the patients presented seizures (n = 7), cognitive dysfunction (n = 9), and encephalopathy (n = 2). Fifty-one patients had peripheral nervous system involvement (PNS). Symmetric axonal sensorimotor polyneuropathy with a predominance of sensory symptoms or pure sensory neuropathy occurred most frequently (n = 28), followed by cranial nerve involvement affecting trigeminal, facial, or cochlear nerves (n = 16). Multiple mononeuropathy (n = 7), myositis (n = 2), and polyradiculoneuropathy (n = 1) were also observed. Thirty percent of patients (all with CNS involvement) had oligoclonal bands. Visual evoked potentials were abnormal in 61% of the patients tested. Fifty-eight patients had magnetic resonance imaging (MRI) of the brain. Of these, 70% presented white matter lesions and 40% met the radiologic criteria for MS. Thirty-nine patients had a spinal cord MRI. Abnormalities were observed only in patients with spinal cord involvement. Among the 29 patients with myelopathy, 75% had T2-weighted hyperintensities. Patients with PNS manifestations had frequent extraglandular complications of SS. Anti-Ro/SSA or anti-La/SSB antibodies were detected in 21% of patients at the diagnosis of SS and in 43% of patients during the follow-up (mean follow-up, 10 yr). Biologic abnormalities were more frequently observed in patients with PNS involvement than in those with CNS involvement. Fifty-two percent of patients had severe disability, and were more likely to have CNS involvement than PNS involvement. Treatment by cyclophosphamide allowed a partial recovery or stabilization in patients with myelopathy (92%) or multiple mononeuropathy (100%). The current study underlines the diversity of neurologic complications of SS. The frequency of neurologic manifestations revealing SS and of negative biologic features, especially in the event of CNS involvement, could explain why SS is frequently misdiagnosed. Screening for SS should be systematically performed in cases of acute or chronic myelopathy, axonal sensorimotor neuropathy, or cranial nerve involvement. The outcome is frequently severe, especially in patients with CNS involvement. Our study also underlines the efficacy of cyclophosphamide in myelopathy and multiple neuropathy occurring during SS. Copyright 2004 Lippincott Williams & Wilkins

PMID: 15342972 [PubMed - indexed for MEDLINE]

maybe that's what I had with the remitting-relapsing MS symptoms since about 30ish ?..when my health problems really started?

I still have this hypothesis that diabetic neuropathy may be helped by Low B1.. caused maybe by high glucose levels in blood that may be reducable by B1 supplementation?

Small fiber neuropathy and neurovascular disturbances in diabetes mellitus.Vinik AI, Erbas T, Stansberry KB, Pittenger GL.
Strelitz Diabetes Research Institutes, Department of Medicine and Pathology/Anatomy/Neurobiology, Eastern Virginia Medical School, Norfolk, Virginia, USA.

Functional and organic abnormalities in small unmyelinated C fibers are the hallmark of type 2 diabetes. These may be silent clinically or present with burning feet, neurovascular abnormalities, wherein warm, cold, and heat pain thresholds are disturbed in association with impairment in skin blood flow and loss of PGP 9.5 immunostaining nerves in the skin. There is a dysfunctional phase preceding organic structural damage to the neurovascular unit. It coexists with elements of the metabolic syndrome, particularly insulin resistance (IR), elevated systolic blood pressure, and diabetic dyslipidemia i.e. dysfunction of the neurovascular unit may contribute to IR due to compromised blood flow with decreased delivery of fuels to their target tissues. If this proves to be the case, it will become important to re-focus energies on the defective neuropeptidergic regulation of blood flow as an approach to ameliorating diabetes. Because there is a functional phase that precedes structural damage, reversibility of the defect is achievable.

PMID: 11460591 [PubMed - indexed for MEDLINE]

My PN-feet burning is gradually reducing but is still there all the time, intensity varies; and so far I havn't been able to pick why?.. it could be getting better slowly with this B1 therapy?.. hopefully. I guess if nerves have been damaged it may take a while to regrow etc.. well sure hope they do!
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Postgrad Med. 1989 Jun;85(8):301-6.
Thiamine deficiency neuropathy. It's still common today.Skelton WP 3rd, Skelton NK.
James A. Haley Veterans Hospital, Tampa, FL 33612.

Despite the fact that thiamine deficiency neuropathy is increasing in incidence in our society, it remains an underdiagnosed disorder. The typical complaints of weakness and burning feet are often regarded as trivial by the attending physician. Electrophysiologic studies are sensitive and often provide supportive evidence to aid in the diagnosis. Since chronic pain therapy is often ineffective, a high index of suspicion should be maintained to help ensure early diagnosis and successful intervention.

PMID: 2542916 [PubMed - indexed for MEDLINE]
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2: PAGANONI C. Related Articles, Links
[Cocarboxylase in the treatment of the Gougerot-Howers-Sjogren syndrome.]
Ann Ottalmol Clin Ocul. 1961 Nov;87:663-6. Italian. No abstract available.
PMID: 14483145 [PubMed - OLDMEDLINE for Pre1966]

I haven't as yet tried to get this paper.. plus I don't read Italian

but it MAY say there is a link..known back in 1960's but since forgotten?
maybe they use B1 therapy for Sjrogen's??
note cocarboxylase is an enzyme that needs B1.
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If its just a remission its the best I've been in for a while :-), and it keeps improving!

Rheumatology 2001; 40: 1085-1088

Outcome measures in Sjögren's syndrome

Iron
http://www.acu-cell.com/femn.html

says adrenal disturbances will affect the balance between iron and thiamine 

Just wondering if low thiamin prevented me from getting my ferritin up without iron going over high(above normal range) and me developing symptoms of "ROS" (reactive oxygen species and oxidative damage).
I haven't found anything as yet, but above was interesting. I wish there was more detail though.(ahh for some refs, sources or even the detail  in reaching this

"Manganese is a much neglected, but extremely important mineral when trying to stabilize blood sugar, particularly with hypoglycemic individuals, and for lowering total cholesterol (cholesterol-lowering drugs actually raise manganese). It has strong estrogenic properties, and as a result is the most important element when nutritionally treating menopausal symptoms, osteoporosis, and postpartum depression, for which manganese, along with Vitamin B1, is most effective."
There's a lot of Manganese in tea, .. perhaps that's why I find it difficult to limit drinking tea... I need the oestrogen; the stabilizing of blood sugar; and lowering cholesterol , Wow, all rolled in one!!
Did you note that too.. Vitamin B1 for post partum depression... similar to thryoid hormones there.
and all the only things in the next para too..
"Just like iron, manganese can be helpful with some types of asthma, where lung capacity measurably increases proportional to manganese intake. Extra supplementation of manganese may be helpful in some cases of carpal tunnel syndrome, deafness, epilepsy, infertility, and lack of libido in both sexes.
In addition, individuals who regularly dislocate joints (particularly knee joints), frequently present with insufficient cellular manganese levels, so normalizing manganese in those cases will permanently solve that problem.

Manganese is important to many enzyme systems such as protein metabolism, bone formation, and the synthesis of L-dopamine and cholesterol, as well as carbohydrate metabolism, where it is required for the synthesis of glucose from non-carbohydrate substances (gluconeogenesis). As a cofactor in glycolysis, manganese aids glucose metabolism.

It is also needed for normal brain and muscle function, blood clotting, and DNA and RNA synthesis, and it activates the enzyme responsible for the formation of urea. Manganese may help with some symptoms of Parkinson's disease such as muscle rigidity and twitching, although an excessive level of manganese can in itself produce Parkinsonian syndrome from a loss of dopamine in the brain cells.
L-dopa, which converts to dopamine in the brain, is used in the treatment of manganese toxicity to reduce the symptoms. High levels of manganese can produce violence and other mental changes,including a psychiatric disorder resembling schizophrenia."

then it says that Thiamin (vitB1)is an antagonist of manganese...so perhaps that's why I have been craving tea so much since starting thiamin injections
I think I'll take some Mn for a while to build up my levels. If I need it , it may reduce my cup of tea cravings!
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"An individual who is prone for gout might need more pantothenic acid (Vitamin B5) but less lecithin, while anyone with a tendency for iron overload would need less Vitamin B1, but much more Vitamin B2.

Some of those suffering from hypoadrenalism (Addison's disease) would benefit from extra Vitamin B1 and/or choline for their sodium-raising properties, while sodium-sensitive individuals or anyone with a tendency for hyperadrenalism (Cushing's disease) might benefit from extra Vitamin B2 and folic acid, which have a sodium-lowering effect.

Anyone suffering from low blood sugar episodes should avoid larger amounts of Vitamin B6 and C, which can cause blood sugar to drop even more, but they are generally helped with extra niacinamide and/or biotin. There are claims that diabetics may benefit from larger amounts of biotin, but patient feedback and blood sugar measurements have been to the contrary.

Those with a tendency for mild Hyperthyroidism (see also Acu-Cell "Bromine") may benefit from PABA, another member of the B-vitamin complex, but they should be careful taking extra Vitamin B6.

Higher amounts of Vitamin B6 will also increase magnesium retention, although this only takes place following long-term oral supplementation, while regular Vitamin B6 injections will quickly result in a high magnesium / low calcium ratio.

If not matched to a patient's requirements, which happens frequently when Vitamin B6 + B12 injections are given at Weight Loss Clinics, a severe calcium deficiency develops. This by itself - or when aggravated by an overstimulated thyroid from regular Vitamin B6 + B12 shots - can result in insomnia, heart palpitations, chest pains, anxieties, depression, mood swings, joint / muscle pains, and/or other symptoms.

In someone suffering from Hypothyroidism and low sodium, Vitamin B6 supplementation on a long-term basis has the potential to eventually lower thyroid functions even more, although a brief boost will still take place every time Vitamin B6 is injected or taken orally. In addition, Vitamin B6 will only affect T4 (thyroxine) levels, but no conversion to T3 (triiodothyronine) takes place - causing a T3 / T4 thyroid ratio conflict, so rather than trying to boost thyroid functions with Vitamin B6 injections for weight loss purposes, iodine, as well as selenium and tyrosine status should be checked and corrected instead.
Another consideration when supplementing larger doses of Vitamin B6 as pyridoxine is the inhibiting effect on Pyridoxal-5-Phosphate (P5P), which is the natural form of Vitamin B6, so if amounts larger than 50mg are taken per day, or if they are taken on an ongoing basis, the pills should also contain a small percentage as pyridoxal-5-phosphate to avoid the potential of causing neurological damage.

However, regardless of the type, excessive intake of both - P5P or pyridoxine - when not needed, may also lead to nerve and/or spinal degeneration, specifically affecting T1 (with right-sided symptoms in the upper back / shoulder area) and at L2, along with general osteo-arthritic changes in various joints.
As a result, Vitamin B6 therapy should only be used for someone with an otherwise difficult-to-manage low magnesium / high calcium ratio."

http://www.acu-cell.com/bx.html

this site looks good.. a lot more here on the interactions..  wish I knew where they sourced some of this info though...reading into this in more detail though, a lot is not really applicable..at least with MY experience with B1..and I'm not happy with no refs..but it is something to  consider.  
I like how they don't just recommend to take lots o a 'balanced' b complex for 'cover' too...not saying one doesn't need to "balance'.. just all the supps with 100(mg or mcg) of each or 50 or each..arent a '"balance" in the longer term for most . personally I think most should not take any more than 25 daily  of this type of ?balanced" B..and add in what is really needed..like more B1 or B6  or B2 depending on individual.
It IS difficulr to find this under a 50 though!!
I note KELP conatins a lot of stuff you can't get anywhere ..like tin, so that is a good "balance" food.
I'm also puzzled by this "left " and "right" receptor phrase.. receptors are proteins that move and change shape..not something static, they do have an binding site .. but the receptor could rotate/move??.. confused by this... doesn't sound "right"

#1 — Fatigue and thyroid disease
... 's why teitelbaum was looking at d-ribose (update 27 on page) " Research: Benefit of Ribose in a Patient With Fibromyalgia 01-31-2005 Journal: Pharmacotherapy Posted on MedScape 01/07/2005 Benjamin Gebhart, Pharm.D.; James A. Jorgenson, M.S., FASHP ... [ 3308.13]
Thyroid Disease: UK & Ireland | 9/17/05 | by tealady | View in discussion (50 Messages)
#2 — Fatigue and thyroid disease
... a teaspoon full? When you asked for opinions at the beginning of this thread and I said yeah, might well work as d-ribose was being looked at for fibromyalgia and CoQ10 and carnitine were also in there as contenders especially with mitochondrial ... [ 3308.12]
Thyroid Disease: UK & Ireland | 9/17/05 | by tealady | View in discussion (50 Messages)
#3 — Fatigue and thyroid disease
... here that's all. I think I emailed you in reply, but I'm gradually working thru this nacklog of emails:-) I had to stop the d-ribose as i found it built up in me (I think) after a couple of months. I was taking a half small cap a day of it ... [ 3308.49]
Thyroid Disease: UK & Ireland | 3/26/06 | by tealady | View in discussion (50 Messages)
#4 — Fatigue and thyroid disease
... Teitelbaum? I think from memory is doing a d-ribose trial now ? It came on an email asking for participants. Sounds interesting. I know I tried CoQ10 by itself and it was helpful for 3 months or so..gums improved and I felt better, but after that I ... [ 3308.3]
Thyroid Disease: UK & Ireland | 8/22/05 | by tealady | View in discussion (50 Messages)
#5 — Fatigue and thyroid disease
... and best wishes, and glad we are finally getting to discuss all of this!!(fingers crossed) Jan PS I was wondering if maybe d-ribose might be a form that sidesteps any insulin resistance buildup issues? I don't know enough about all of this. I've ... [ 3308.18]
Thyroid Disease: UK & Ireland | 9/17/05 | by tealady | View in discussion (50 Messages)
#6 — Animal Vegetable Mineral
... ya havent I'm no worse off here.. need to find a new chemist as others have gone the T3 only route.... sigh Could see about d-ribose I guess, but I'm not sure if I can get that one as yet..and that will prnbably make it a 4 times a day schedule.. ... [ 3330.29]
Thyroid Disease: UK & Ireland | 9/24/05 | by tealady | View in discussion (30 Messages)

http://www.arabidopsis.org:1555/ARA/NEW-IMAGE?type=PATHWAY&object=RIBOKIN-PWY

looks like you need transketolase (vitamin B1 is a needed cofactor) to use d-ribose.. in the pathway from d-ribose-5-phosphate to D-glyceraldehyde-3-phosphate ..

that's why initially I was better with d-ribose, then I got worse.. seemed to dam up.. and it probably was after it used up a lot of my B1!!!

This is a useful summary, best I've found so far, and not Toooo technical, ..it comes from a link on thiamine in cell culture, but describes in brief the mechanism/pathways of thiamine.
As you can see, thaimin is necessary to make one feel one can breathe and get oxygen.. at least that's one of the first effects I think I noticed after at most 3 months! I can breathe deeply and slowly .. haven't been able to do that for a while.
Note iron may destroy thiamin.. so I don't personally think one should take supplememtal iron if ferritin over around 27.(self learnt)
link

Thiamine is a required nutrient that is taken up by cells via a carrier-mediated system that may be regulated by calmodulin. The active vitamin form, thiamine pyrophosphate (TPP), is synthesized from ATP and thiamine by thiamine diphosphokinase (EC 2.7.6.2). TPP is an enzyme cofactor. TPP containing enzymes are involved in energy metabolism and amino acid synthesis. Pyruvate cannot be metabolized effectively if thiamine is not provided to cells in vitro. The metabolism of pyruvate to acetyl-CoA is a critical reaction in cells that is mediated by the pyruvate dehydrogenase complex. Thiamine is one of three vitamins required for this complex to function>.
5mg daily orally has no effect on this path, 25mg does ; __LINK PLS click on..

Energy Production: TPP is a cofactor of two enzymes involved with the citric acid cycle. These enzymes bind and decarboxylate alpha-keto acids and facilitate the transfer of the aldehydes to enzyme CoA.

Pyruvate dehydrogenase is part of the pyruvate dehydrogenase complex that converts pyruvate into acetyl-CoA. Acetyl-CoA provides 2-carbon units to the citric acid cycle.
Alpha-keto glutarate dehydrogenase is part of the alpha-keto glutarate dehydrogenase complex that converts alpha-keto glutarate into succinyl-CoA. Succinyl CoA is converted into succinate.
The glycolytic pathway is the primary route for sugar degradation. However, an alternative pathway called the pentose phosphate pathway (hexose monophosphate shunt) also exists in cells. Oxidation of sugars through this pathway leads to the reduction of NADP to NADPH and the formation of D-ribose. NADPH is an important reducing agent for a number of metabolic processes and D-ribose is needed for nucleic acid synthesis. The TPP containing enzyme transketolase converts sugars formed in the pentose phosphate pathway back into sugars that can be metabolized by the glycolytic pathway. Hence, transketolase acts to bridge the two pathways and increases the efficiency of energy utilization.

Amino Acid Synthesis: TPP containing enzymes are required for the synthesis of the three amino acids; valine, isoleucine and leucine. All three of these amino acids are synthesized from pyruvate. TPP-enzyme bound acetyl groups are transferred directly into the synthetic pathways for valine and isoleucine. The acetyl group used to synthesize leucine is first transferred from a TPP-enzyme to acetyl-CoA and then into the leucine synthetic pathway.
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Thiamine is a substituted pyrimidine linked to a substituted thiazole by a methylene group. It is generally added to cell culture as thiamine-2HCl.

. Formula C12H18Cl2N4OS
. Molecular Weight = 337.28
. Very water soluble
. Unstable in aqueous solutions above pH 5.5
. May react with other media components-pyridoxal, iron, pyruvate (other alpha keto acids), and free radicals
. Oxidizes to thiochrome

The metabolically active form of thiamine is the diphosphate. It is formed by the enzymatic replacement of the hydroxyl group of the thiazole 5-hydroxyethyl side chain with pyrophosphate. Its biochemical activity is mediated by the thiazole moiety. The reactive chemistry of thiamine and thiamine pyrophosphate should be similar in solution.

Possible Chemical Instability in Cell Culture:
Thiamine is not a very stable molecule. It can participate in a wide range of reactions that result in its destruction.

The metabolically relevant reaction site of thiamine and TPP is carbon 2 of the thiazole ring. It is situated between nitrogen and sulfur atoms. The proton on this carbon is acidic and at pH above 5.5 it dissociates to form a carbanion which undergoes nucleophilic addition to carbonyl groups.
In the presence of alpha keto acids, such as pyruvate or alpha keto glutarate, thiamine may form thiamine:keto-acid adducts. The redox and pH conditions in the media will affect the degradation of these keto acids into aldehydes (reducing conditions) or acids (oxidizing conditions) and carbon dioxide.

Thiamine and TPP contain a primary amine on the pyrimidine moiety. This primary amine may form a Schiff base with pyridoxal or other aldehydes. In the presence of transition metals, such as iron, Schiff bases may cause the destruction of thiamine.

Oxidizing and reducing agents can destroy thiamine. One oxidation product is thiochrome. This molecule that may be detected by its fluorescence under uv light. Hypochlorite, sulfites and SO2 degrade thiamine. Sulfur dioxide reacts irreversibly with thiamine to yield pyrimidine sulfonic acid and 4-methylhydroxyethyl thiazole. These molecules can form in oxidatively stressed media.

Mechanism of Action:
TPP is a coenzyme for two types of enzymes, alpha-keto acid dehydrogenases and transketolases, both of which cleave a C-C bond adjacent to a carbonyl group releasing either carbon dioxide or an aldehyde. The resulting product is then transferred to an acceptor molecule.

Alpha-keto acid dehydrogenases decarboxylate alpha-keto acids. The decarboxylation product is then transferred to coenzyme A (CoA).

Transketolase cleaves the C-C bond adjacent to the carbonyl group of an alpha-keto sugar to give an activated glycoaldehyde. The glycoaldehyde is then combined with an aldose to give a new ketose.

The pentose reaction requires transketolase and thiamine pyrophosphate as cofactors,’ and apparently this step is dependent upon adequate concentration of the thiamine enzyme cofacton for completion. Otherwise there is an accuniulation of pentose.” In this investigation, alterations in pentose levels were used for rapid study of changes produced inrelation to thiamine.

note:5mg per day had no effect.. 25mg was the next level they used.. is as effective as a higher dose in normal people.
I find 5mg per day to be ineffective and 25mg per day intrmuscularly to make a difference. no more is needed.. my legs get heavy..and I just feel its too much.
I suggest a level somewhere between 10mg and 25mg per day. I take it divided into 2 doses usually.. although I have one day off in 3 now , and hope to reduce.

Effects of thiamine medication on Pentose levels in the red cell were studied by following the enythrocyte levels in normal control subjects, patients with infectious hepatitis and four patients with early bronchogenic carcinoma. Thiamine was administered by three different routes : intramuscularly, 50 mg. twice a day ; intravenously, 50 mg. and orally

Pentose levels (Table I) determined on red cell samples obtained from normal patients were found to range from 1 18.4 to 145.2 mmg. with an average level of 130 mmg. (standard deviation of 5. 1 mmg.) which is comparable to the figures of 133 ± 13 mmg. found by Wolfe.’ Addition of TPN increased the control level of 130 mmg. to 152 mmg. (Table ii). Thiaminase, by inactivating thiamine, raised the control level of 130.2 mmg. to 192 mmg. Direct addition of thiamine demonstrated little change in pentose levels. Patients receiving xylose orally demonstrated maximum absorption at two hours, raising an average control level of 139.0 mmg. to 161.0 mmg. with an associated positive urine pentose test.

The control levels (Table Iv) in the normal patients receiving thiamine averaged 138.5 ± 4.5 mmg. (Table iv) . After thiamine was given for seven to ten days, the level was depressed to an average of 112.8 mmg., with minimal changes at later intervals. Coinpanison of the effect of various dosages did not demonstrate correlation with the amount given, and the depression of pentose levels reached the same range by ten days. The use of 5 mg. of thiamine orally did not seem to affect the pentose level.

COMMENTS

Red cells of normal subjects were studied to determine the presence of pentose as formed in the glucose oxidative pathway and the relation of this level to thiamine activity. The source of this pathway is glucose-fl-phosphate, and entry from this step into the other reaction of the shunt can be augmented by the addition of TPN as demonstrated by Touster and Siperstein9 and the findings here, and by activating the pathway with methylene blue as in the method of Bnin and Wolfe.24 In part of the pathway, the pentose reaction (which requires transketolase and thiamine pyrophosphate as cofactors) has been found to be hindered by lack of thiamine in the body. This can be produced by thiamine deficiency,” or by the action of thiamine analogues on thiamin,4 or by using thiaminase as in this study. All of these result in an elevation of the red cell pentose level.

Thiamine, as administered to patients in this study, in dosages greater than 25 mg. orally

given daily, lowered the ned cell pentose level to an average of 112.8 mmg. Thiamine, in vitro, did not alter the level. The depression occurred most rapidly with intravenous thenapy, somewhat slower by the intramuscular route, and slowest by the oral route. All subjects eventually attained the sanie degree of depression regardless of the route or dosage.

The difference in effect of thiamine, in vivo and in vitro, probably represents the metabolic requirement for the active enzyme form. , thiamine pynophosphate. The depression in the pentose level after thiamine therapy reflected the increased intracellular level. Measurement of thiamine can be accomplished directly by chemical study or bioassay, on indirectly by measuring some product of metabolism which is altered by thiamine. Since the pentose reactions in the glucose oxidative pathway were altered inversely by thiamine, determination of human red cell pentose levels would seem to represent an indirect method of measuring thiamine activity.

SUMMARY

In the metabolism of glucose, the hexomonophosphate on direct glucose oxidative pathway involves the formation of pentoses which nequire the presence of thiamine pynophosphate for further reaction. The pentose level was studied in human red cells. Normal patients had values of l3ı.() ± 5. 1 j.ig. This level could be increased by in vitro addition of TPN, which apparently facilitated the pentose shunt, and thiaminase which inactivated thiamine.

Thiamine therapy depressed the pentose level to an average of 112.8 ± 5.5 regardless of the route on dosage over 25 mg. Similar levels were found in patients with infectious hepatitis and lung carcinoma. These studies demonstrated that human red cell pentose determinations varied inversely with alterations of thiamine activity.

full PDF

Some studies which indicate that with Hashi's, iodine restriction (not supplementation) is the best way to go. Iodine supplementation can cause problems for Hashi's folks
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Clark CD, Bassett B, Burge MR. Effects of kelp supplementation on thyroid function in euthyroid subjects. Endocr Pract 2003; 9(5):363-369
CONCLUSION: Short-term dietary supplementation with kelp significantly increases both basal and poststimulation TSH.
maybe good or bad, maybe why my TSH didn't rise as high as it may have from my symptoms?, if TSH could rise as needed I would have made more thyroid hormones myself, ie. may not have functioned as subclinical hypo?.. and my thyroid hormones may NOt have needed boosting with thyroid meds? OTOH.. higher TSH may cause a rise in hashimoto antibodies
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Kahaly GJ, Dienes HP, Beyer J, Hommel G. Iodide induces thyroid autoimmunity in patients with endemic goitre: a randomised, double-blind, placebo-controlled trial. Eur J Endocrinol 1998; 139(3):290-297
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Randomized, double blind, placebo-controlled trial of low dose iodide in endemic goiter
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Kasagi K, Iwata M, Misaki T, Konishi J. Effect of iodine restriction on thyroid function in patients with primary hypothyroidism. Thyroid 2003; 13(6):561-567
”In conclusion, (1) primary hypothyroidism was recovered following iodine restriction in more than half of the patients, and (2) the reversibility of hypothyroidism was not significantly associated with Hashimoto's thyroiditis but with increased (99m)Tc uptake and elevated non-hormonal iodine levels.”
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Konno N, Makita H, Yuri K, Iizuka N, Kawasaki K. Association between dietary iodine intake and prevalence of subclinical hypothyroidism in the coastal regions of Japan. J Clin Endocrinol Metab 1994; 78(2):393-397
”These results indicate that 1) the prevalence of hypothyroidism in iodine sufficient areas may be associated with the amount of iodine ingested; 2) hypothyroidism is more prevalent and marked in subjects consuming further excessive amounts of iodine; and 3) excessive intake of iodine should be considered an etiology of hypothyroidism in addition to chronic thyroiditis in these areas.”
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Papanastasiou L, Alevizaki M, Piperingos G, Mantzos E, Tseleni-Balafouta S, Koutras DA. The effect of iodine administration on the development of thyroid autoimmunity in patients with nontoxic goiter. Thyroid 2000; 10(6):493-497
”The administration of iodized oil to patients with small nontoxic goiter in an iodine-replete area was accompanied by the development of abnormal levels of ThAbs in some cases and by an increase in thyroid lymphocytic infiltration.”
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Rose NR, Bonita R, Burek CL. Iodine: an environmental trigger of thyroiditis. Autoimmun Rev 2002; 1(1-2):97-103
”… A body of clinical and epidemiologic evidence points to excessive ingestion of iodine as an environmental agent. In genetically determined thyroiditis in animals, iodine enrichment has been shown to increase the incidence and severity of disease.”
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Yoon SJ, Choi SR, Kim DM, Kim JU, Kim KW, Ahn CW et al. The effect of iodine restriction on thyroid function in patients with hypothyroidism due to Hashimoto's thyroiditis. Yonsei Med J 2003; 44(2):227-235
” In conclusion, 78.3% of patients with hypothyroidism due to Hashimoto's thyroiditis regained an euthyroid state iodine restriction alone. Both a low initial serum TSH and a high initial urinary iodine concentration can be predictable factors for a recovery from hypothyroidism due to Hashimoto's thyroiditis after restricting their iodine intake.”
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Although lutein has been extensively investigated for its potential role in guarding against age-related macular degeneration, some earlier studies also have shown that a daily lutein supplement may increase the skin's natural antioxidant system and protect against damage from the sun’s ultraviolet rays. But this is the first study to investigate lutein for more specific effects on the skin.

The study included female Italian subjects ages 25 to 50. Researchers divided the subjects into different test groups and administered 10 mg of oral lutein and/or 50 ppm of lutein in a topical formulation each day for 12 weeks.

Results indicated that oral lutein supplementation increased skin hydration by 38 percent, skin elasticity by 8 percent, and the level of superficial lipids by 33 percent compared to the placebo. In keeping with its antioxidant reputation, lutein also decreased oxidation of lipids by 55 percent, indicating it could help the lipids in skin from deteriorating due to free radical damage.

Subjects who received both oral and topical lutein experienced a 60 percent increase in hydration, a 20 percent increase in elasticity and a 50 percent increase in skin lipids.

According to the researchers, a major international peer-reviewed journal has accepted an article about the study, which is expected to appear in the coming months.

Reference:
Morganti P, et. al. Clinical evidence for lutein and zeaxanthin in skin health, part 1: comparison of placebo, oral, topical and combined oral/topical xanthophylls treatments. Presented at the Beyond Beauty Conference, Paris, France, September 12, 2006.
[link]

This IS about Crocodile feeding.. but I was surprised to see it mentions oily fish as containing thiamiase? .. I guess it has to be raw or the enzyme thiaminase is destroyed, BUT I hadn't heard of thiaminase in oily fish before
I was wondering.. what about fish oil?
The freezing and defrosting would lower B1 in any food..as does cooking.
maybe that's why fish oil doesn't agree with me.. but still doesn't explain the pimples I get from fish oil!! I don't get pimples from B1 deficiency, and thiaminase is an enzyme and therefore a protein... so fish oil should be OK.
However, they do mention Thiaminase being greater in "oily" fish..and I know someone who took fish oil (just 3 caps of 1g each a day) and noted a drop in his exercise performance; couldn't put in the "burst" at the end of a race, and took longer to recover. On stopping fish oil supps his performance recovered.
So maybe there is something about fish oil reducing B1 slightly??

"As mentioned earlier in the diet section, vitamin B1 deficiency is common in diets comprised primarily of fish. Many fish, especially oily marine species, contain high levels or thiaminase which breaks down vitamin B1 (thiamine) and renders it unavailable to the crocodile. The freezing / thawing process exacerbates this problem. Symptoms of B1 deficiency include muscle tremors and twitching, and the problem can be corrected with B1 supplements, heating fish briefly to denature the enzyme, and an improvement in the diet. Another common problem with fish diets is steatitis: necrosis of fatty tissue caused by excess polyunsaturated fatty acids which begin to oxidise when the fish are not totally fresh. Vitamin E supplement (which acts as an anti-oxidant) or an improvement in the diet to include mammals and birds can address the problem." [link]

dopamine
Vesicular dysfunction during experimental thiamine deficiency is indicated by alterations in dopamine metabolism
-------------------------------------

The below seems to be suggesting a cause of CFS and fibromyalgia could possibly be lowered dopamine, which may possibly be due to suboptimal thiamin (B1)...
.. of course, it may not be either!

"Studies have shown that chronic stress, however, can contribute to a disruption of normal hippocampus function. The hippocampus plays a major role in pain perception and memory formation, and it is involved in controlling the production of that crucial brain neurotransmitter, dopamine. Dopamine abnormalities have been linked to "restless leg syndrome," increased pain, and feelings of self doubt, anxiety, and problems with memory formation.

If the "Dopamine Hypothesis" is correct, then it is reasonable to assume that drugs that restore normal dopamine levels and activity in the brain should have a therapeutic effect when administered to Fibromyalgia patients.

And this is where the "Dopamine Hypothesis" picks up steam. Andrew Holman, MD, recently conducted a controlled, double blind study of the drug pramipexole with several Fibromyalgia patients. Pramipexole, sold under the brand name Mirapex™, is approved for treatment for Parkinson's disease - a primary dopamine disorder. Patients experienced significant improvement in their symptoms. Another drug that affects dopamine and has been approved by the FDA as a treatment for restless legs syndrome - ropinirole - also met with remarkable success in another recent Fibromyalgia study conducted by Dr. Holman.

All told, the Dopamine Hypothesis looks promising for several reasons. It ties in nicely to the pathogenesis of the disease - that the onset of Fibromyalgia frequently occurs during times of prolonged or intense emotional or physical stress, when the hippocampus may become overworked and become dysfunctional as a result. And it ties into the fact that dopamine, which is largely regulated by the hippocampus, may cause many of the symptoms of Fibromyalgia" are lowered ? I guess the Parkinson drugs are designed to "up" dopamine? .. I need to check on these specific drugs
[link]

-------------------------------------

US: Spinach Sickens 109 in 19 States 17th Sept 06
The outbreak of E. coli O157:H7 associated with bagged spinach now numbers 109 cases, including 16 cases of hemolytic uremic syndrome and one death, the FDA announced last night.

The agency advised against eating fresh spinach "until further notice."

FDA statement

Lettuce also has been known to cause this in US.
I wonder ..is it the fertiliser used?

On the ten news tonight they mentioned a study showed glucosamine producing a diabetic state 'within' cells, and also mentioned this may led to diabetes, and also infertility on some animals in the study. At least this was the gist I thought I heard?
I looked up the channel 10 news site.. but nix. BBC where are u!!

just posting this as a reminder to myself to find out more about this as I take a glucosamine chrondritin MSM powder mix to help with my knee joints, although I'm unsure if it has any effect, BUT I have been getting this 'intense burning'(more at some times than others, but always something PN-like, which seems to match the description of diabetic neuropathy in my feet.. so I'm wondering if glucosamine is causing or worsening this?

Searching on pubmed I found these below: but there is more. I did a pubmed search on "glucosamine diabetic within cells".

Glucosamine-induced insulin resistance in L6 muscle cells

Glucosamine induces lipid accumulation and adipogenic change in C2C12 myoblasts.
Biochem Biophys Res Commun. 2005 Mar 11;328(2):369-74.
PMID: 15694357 [PubMed - indexed for MEDLINE]

Hyaluronic acid production and CD44 expression in cultured dermal fibroblasts of patients with non-insulin-dependent diabetes mellitus with and without chronic ulcers on the lower extremity."We observed that diabetic fibroblasts of both groups produced more L-lactate ( approximately 30%) and incorporated more (3)H-glucosamine into the medium hyaluronic acid ( approximately 28%) than controls"
I got lost with this study, but it shows something is going on with hyaluronic acid and lactate
"Hyaluronic acid metabolism and CD44 expression are regulated by lactate, where their increased production is considered to affect the properties of fibroblasts in non-insulin-dependent diabetes mellitus"

Will look at more later...

J Clin Invest. 1968 October; 47(10): 2268–2280. (probably a lot more kown now!)Encephalopathy of thiamine deficiency: studies of intracerebral mechanismsDavid W. McCandless and Steven Schenker
The Liver-Gastroenterology Unit, The Department of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Texas 75235

Abstract
Thiamine-deficient encephalopathy is characterized by morphologic lesions in the brainstem and less extensively in the cerebellum, but the early neurologic signs reverse rapidly and fully with thiamine, indicating a metabolic disorder. The suggested causal mechanisms of the encephalopathy involve two thiamine-dependent enzymes: (a) impairment of pyruvate decarboxylase activity with decreased cerebral energy (ATP) synthesis, and (b) reduction of transketolase activity with possible impairment of the hexose monophosphate shunt and subsequent decrease in NADPH formation. The latter may be important in maintaining glutathione in a reduced form (GSH), which apparently functions by keeping enzymes in a reduced (active) conformation.

To examine some of these postulated mechanisms, in this study we measured pyruvate decarboxylase and transketolase activity, lactate, ATP and GSH levels in the cerebral cortex, cerebellum, and brainstem, and thiamine concentration in whole brain of rats with diet-induced low thiamine encephalopathy. Pair-fed and normally fed asymptomatic control animals were similarly investigated. To assess the functional importance of some of our results, we repeated the studies in rats, immediately (16-36 hr) after reversal of the neurological signs with thiamine administration.

The data obtained led to the following conclusions: (a) Brain contains a substantial reserve of thiamine in that thiamine level has to fall to below 20% of normal before the onset of overt encephalopathy and an increase in brain thiamine to only 26% of normal results in rapid reversal of neurologic signs. (b) Both cerebral transketolase and pyruvate decarboxylase activities are impaired in low thiamine encephalopathy and the abnormality in the pyruvate decarboxylase is reflected in a rise in brain lactate. These biochemical abnormalities occur primarily in the brainstem and cerebellum, the sites of the morphologic changes. (c) Although the fall in cerebral transketolase is about twofold greater than that of pyruvate decarboxylase activity during encephalopathy, both enzymes rise on reversal of neurologic signs and the degree of the transketolase rise is slight. Accordingly, this study cannot ascertain the relative functional importance of these two pathways in the induction of the encephalopathy. The data suggest, however, that the depression of transketolase is not functionally important per se, but may only be an index of some other critical aspect of the hexose monophosphate shunt. (d) The normal cerebral ATP concentration and small GSH fall during encephalopathy, with little GSH rise on reversal of neurologic signs, suggest that a depletion of neither substance is instrumental in inducing thiamine-deficient encephalopathy.
Full text available on link (free)

This is why pork has a lot of thiamin in it.. it has to make for the inefficient thaimine triphosphatase .. so I'm still unsure if that means that pork thiamin isnt as efficient when eaten by humans or not!!!

Pork is said to contain very high thiamin levels ..and I confirm it after eating Xmas osk and observing my son's preference for sweet and sour pork in Chinese cooking and how I feel better if I eat at least some of the pork too with the white rice.
I used to wonder why I'd feel wiped otherwise..now I know what to do to avoid being wiped after Chinese.. it wasnt the MSG after all.. the restauarnt owner/cook always claimed he used none..and he was a friend of my daughters who worked there too for a while.

Edited -added end Jan2007
Over Xmas and for a few weeks after I ate a LOT of ham (having bought half a leg of ham and frozen some of it in pieces).
I found I started too easily gaining weight and needed steadily reducing amounts of B1 .. just packing on the tummy ..like premenopausal weight gain(only it didnt stop, I used to go from a non US 9 to a 13 premenopausally and lose it with periods..)..and had to stop the injections altogether. I found after a while I started gradually (very slowly) losing the weight and becoming ,more fatigued and constipated as the ham in my body decreased (after i stopped eating it for a few days).

just jotting down some thoughts here----------------------------

: Biochim Biophys Acta. 2005 Aug 30;1725(1):93-102. Links
Pig tissues express a catalytically inefficient 25-kDa thiamine triphosphatase: insight in the catalytic mechanisms of this enzyme.Szyniarowski P, Lakaye B, Czerniecki J, Makarchikov AF, Wins P, Margineanu I, Coumans B, Grisar T, Bettendorff L.
Center for Cellular and Molecular Neurobiology, University of Liege, B-4000 Liege, Belgium.

Thiamine triphosphate (ThTP) is found in most organisms and may be an intracellular signal molecule produced in response to stress. We have recently cloned the cDNA coding for a highly specific mammalian 25-kDa thiamine triphosphatase. The enzyme was active in all mammalian species studied except pig, although the corresponding mRNA was present. In order to determine whether the very low ThTPase activity in pig tissues is due to the absence of the protein or to a lack of catalytic efficiency, we expressed human and pig ThTPase in E. coli as GST fusion proteins. The purified recombinant pig GST-ThTPase was found to be 2-3 orders of magnitude less active than human GST-ThTPase. Using site-directed mutagenesis, we show that, in particular, the change of Glu85 to lysine is responsible for decreased solubility and catalytic activity of the pig enzyme. Immunohistochemical studies revealed a distribution of the protein in pig brain very similar to the one reported in rodent brain. Thus, our results suggest that a 25-kDa protein homologous to hThTPase but practically devoid of enzyme activity is expressed in pig tissues. This raises the possibility that this protein may play a physiological role other than ThTP hydrolysis.

PMID: 16000236 [PubMed - indexed for MEDLINE]

Biotin
Biotin is another with me. I think I feel a bit better after sucking a 1000mcg biotin sublingual, but my multi had 1.5 mg of biotin in it. So I thought I should have been covered there!!.. although only took about 1/3 of multi daily. Still, 500mcg should have been more than enough.

I do have the low biotin symptoms, which is why I was supplementing in it
Thing is, all my kids had cradle cap as babies, but my eldest son was the worst I've ever seen in extent and lasted to over a year.. so it could be biotin?

I do seem to need biotin now I've increased my B1..and at least 1000mcg a day.. perhaps more.

I've been taking 1000mcg of biotin a day (as a sublingual lozenge)..Natures way..
Maybe that is helping with the PN instead of/ as well as, the B1

Also long-term antibiotic use can interfere with biotin production in the intestine ..
rrrring!!
When in UK. mid 2004, I was on doxycycline for 5 weeks( attempt at treating for possible Lyme). I stopped as teeth were turning brown and
I noticed after this that my nails had gone thick and were splitting ..and ridges..never had b4..(and for a few weeks after returned home until they regrew)lack of biotin??(I was thinking it was calcium in the water!)
" long-term antibiotic use can interfere with biotin production in the intestine "
"Biotin can be used to treat frail, splitting or thin fingernails "

Biotin

Biotin is a member of the B complex family, but is not actually a vitamin. It is a coenzyme that works with them. Also known as vitamin H and coenzyme R, it was first isolated and described in 1936. It is water soluble and very unstable; it can be destroyed by heat, cooking, exposure to light, soaking, and prolonged contact with water, baking soda, or any other alkaline element. It can be absorbed from food, but a “large portion” is made by “good” intestinal bacteria; the use of oral antibiotics or an intestinal yeast/bacterial infection can cause a biotin deficiency.

Like the other B vitamins, biotin is involved in the digestion of glucose, fatty acids, and amino acids, and it aids cell growth and replication.

Biotin works in synergy with insulin in the body, and independently increases the activity of the enzyme glucokinase. Glucokinase is responsible for the first step of glucose utilisation, and is therefore an essential component of normal bodily functioning. Glucokinase occurs only in the liver, and in sufferers from diabetes its concentration may be extremely low. Supplements of biotin may have a significant effect on glucose levels for both type 1 and type 2 diabetics.

A severe deficiency in infants (who do not yet have good intestinal bacteria) causes “cradle cap” (seborrheic dermatitis), which is excessive oil deposits and dandruff on the head; biotin supplements in infants can cure this condition, but in adults a full range of B vitamins is needed to properly metabolize fatty acids.

Benefits:
1) Aids cell growth
2) Helps use other B vitamins
3) Prevents yeast from changing from single-cell form to the much more dangerous colony form
4) Helps nails and hair grow; a deficiency can cause hair loss and brittle nails.
5) Helps nerve tissue.

Forms:
Biotin exists as both biotin and as biocytin, a complex from brewer’s yeast composed of 65.5 % biotin.

---------------------
http://www.umm.edu/altmed/ConsSupplements/VitaminHBiotincs.html
Deficiency, uncommon in humans, may result in hair loss, dry scaly skin, cracking in the corners of the mouth (called cheilitis), swollen and painful tongue that is magenta in color (glossitis), dry eyes, loss of appetite, fatigue, insomnia, and depression. Animals deficient in biotin during pregnancy are more likely to deliver newborns with birth defects such as a cleft palate. Research in this area for pregnant women is underway. One situation in which biotin deficiency does often develop is in people who have been on parenteral nutrition (nutrition administered intravenously rather than through the mouth or stomach) for a long period of time. It may also been seen in people who have been on long-term therapy with anticonvulsants, antibiotics, and sulfa drugs.

Interestingly, vegetarians are able to absorb more biotin from the gastrointestinal tract than meat eaters. Biotin is often recommended for strengthening hair and nails and is found in many cosmetic products for hair and skin.

------
Below is a partial list of the health problems biotin may help treat:

Hair and Nail Problems
Biotin supplements may improve thin, splitting, or brittle toe and fingernails as well as hair health. Biotin has also been used to combat alopecia (partial or complete loss of hair) in both children and adults.

Cradle Cap (Seborrheic Dermatitis)
Infants deficient in biotin often develop this scaly scalp condition. Some infants may respond to biotin supplementation either through formulas or breast milk. While studies have not confirmed the value of biotin for treating cradle cap, there are individual reports of some infants doing better with this treatment.

Similarly, children with a rare inherited metabolic disorder called phenyulketonuria (PKU; in which one is unable to break down the amino acid phenylalanine) often develop skin conditions such as eczema and seborrheic dermatitis in areas of the body other than the scalp. The scaly skin changes that occur in people with PKU may be related to poor ability to use biotin. Increasing dietary biotin in the diet seems to improve seborrheic dermatitis.

Biotinidase Deficiency
Biotin supplementation is usually given to babies and children with this unusual inherited condition. Biotinidase deficiency is often associated with seizures, skin disorders, bald spots, hearing loss, visual disturbances, and developmental delay. The inherited form of biotinidase deficiency is seen most commonly in people from Saudi Arabia.

Use of valproic acid, a medication for seizure disorders, can cause a biotinidase deficiency leading to skin rashes and hair loss. Biotin supplements may prevent or treat some of the side effects from this prescription drug.

Another rare inherited metabolic disorder (which looks very much like biotinidase deficiency) is called holocaroxylase synthetase deficiency. This type of deficiency also alters biotin metabolism and infants with this condition tend to improve from biotin supplements.

Diabetes
People with type 2 diabetes often have low levels of biotin. Biotin may be involved in the synthesis and release of insulin. Preliminary studies in both animals and people suggest that biotin may help improve blood sugar control in those with diabetes, particularly type 2 diabetes. More research in this area would be helpful.

Peripheral Neuropathy
There have been reports of biotin supplements improving the symptoms of peripheral neuropathy for some people who developed this condition from either long-standing diabetes or on-going hemodialysis for kidney failure. Peripheral neuropathy refers to damage to the nerves of the extremities, most commonly the feet and calves. It is felt as numbness, tingling, burning or strange sensations, and may be accompanied by pain, muscle weakness, and difficulty walking. People who have taken biotin for these purposes tend to notice improvement as early as 1 to 3 months after starting the supplement.

Candida Infections
Candida infections affect the skin, mouth, and vagina and are caused by a yeast-like fungus. Possible symptoms include white patches in the mouth or on the throat, painful cracks at the corners of the mouth, skin rashes found commonly in the groin, between fingers and toes, and under the breasts, and vaginal itching and irritation with a curd-like discharge. Some believe that people with a biotin deficiency may be more likely to become infected with candida. It is not clear, however, whether increasing biotin in the diet or taking biotin supplements will prevent or treat this condition. There has been one case report of a woman with frequent, recurrent vaginal candida infections who did improve after taking biotin supplements for three months.

High Cholesterol
Animal studies and a few human studies suggest that low levels of biotin are associated with high total and LDL ("bad") cholesterol. It is not known, however, if biotin supplementation or increased biotin in the diet improves cholesterol.
----------------
Biotin contributes to the health of skin, hair, nerves, bone marrow, sex glands, and sebaceous glands. Apart from being a vital cofactor to several enzymes, biotin is essential in carbohydrate metabolism and the synthesis of fatty acids. It is also involved in the transformation of amino acids into protein.
Biotin plays a role in cell growth and division through its role in the manufacture of DNA and RNA, the genetic components of cells.

Adequate biotin is required for healthy nails and hair, and biotin deficiency is known to be a factor in balding and the premature greying of hair. It has been claimed that, as part of an orthomolecular regime, it can reverse the greying of hair. When PABA and biotin are taken together in adequate amounts they can restore hair colour. Biotin supplements will also effectively treat weak, splitting nails.

Biotin can be a valuable tool to combat yeast infections, which are notoriously difficult to eradicate. In their book The Yeast Syndrome, John Parks Trowbridge and Morton Walker describe how adequate levels of biotin can prevent Candida albicans from developing from its yeast-like state into fungal form, in which it sends out mycelium that further invade body organs.

Seborrheic dermatitis, or Leiner's disease, which is a non-itchy, red scaling rash affecting infants during the first three months of life, is also treated with biotin and other B complex vitamins.

Biotin has been used in conjunction with other nutrients as part of weight loss programs, as it aids in the digestion and breakdown of fats.

High doses of biotin are sometimes used to treat diabetes since it enhances sensitivity to insulin and effectively increases levels of enzymes involved in glucose metabolism. Biotin is also used to treat peripheral neuropathy, a complication of diabetes, and those with Duchenne muscular dystrophy, who suffer from metabolic deficiencies.

Long-term antibiotic use can interfere with biotin production in the intestine and increase the risk of deficiency symptoms, such as dermatitis, depression, hair loss,2anemia, and nausea. Long-term use of anti-seizure medications may also lead to biotin deficiency.3Alcoholics, people with inflammatory bowel disease, and those with diseases of the stomach have been reported to show evidence of poor biotin status. However, the usefulness of biotin supplementation for these people remains unclear.4 In animals, and possibly in humans, biotin deficiency can cause birth defects.5 As biotin deficiency may occur in as many as 50% of pregnant women,6 it seems reasonable to use a prenatal multiple vitamin and mineral formula that contains biotin.
from here

-----------------------
Dietary Sources

brewer's yeast. Bacteria in the intestine also produce significant amounts of biotin.
which I bet it's absorbable by body.
other animals have bacteria in gut that makes thiamin(B1) too.. and its used by the body:-), and some from food in diet too.

also deficiency of biotin can be caused by antibiotics etc ..things that destroy the gut healthy flora..

Brewer's yeast
Organ meats (liver, kidney)
egg yolk
Nuts (almonds, peanuts, pecans, walnuts) and nut butters
Soybeans, soy
Other legumes (beans, blackeye peas, peanuts)
peanut butter, peanuts
Oatbran, oatmeal
mushrooms
bananas
nuts
cauliflower,beans, ,chocolate, molasses, dairy products,
wheat germ, and whole grains,breads
fish?? kidney, legumes, organ meats,liver, meat,oysters,poultry

Raw egg whites contain a protein called Avidin that interferes with the absorption of biotin. It is always recommended that people avoid eating raw eggs because of food poisoning caused by Salmonella. Food-processing techniques can destroy biotin.
Less-processed versions of the foods listed above will contain more biotin.
------------------------------------
Biotin for diabetic peripheral neuropathy

A Multidisciplinary Approach to Diabetic Neuropathy TreatmentResearch has indicated that biotin in high doses could be suggested for diabetic patients for the prevention and management of peripheral neuropathy. ...
www.geocities.com/bsy53/dn/neuropat.html
------------------------
http://ezinearticles.com/?Hair-Loss:-Biotin-is-Food-for-Your-Hair&id=126771
A deficiency of biotin may cause hair to become frail and unhealthy, and hair breakage, which may result in hair loss. Biotin also keeps your skin and nails healthy as well as being an important element of new hair growth. Supplements are sometimes needed to return biotin levels to normal, but it is recommended to include biotin regularly in your diet. Two foods containing good quantities of biotin are liver and egg yolks. You would have to eat thousands of calories worth daily to get enough for your hair needs, which is why I would also suggest biotin supplements.

Foods full of biotin include brewer's yeast, green peas, oats, soybeans, walnuts, sunflower seeds, green peas, bulgur and brown rice. In terms of the egg yolks, your body's ability to digest and assimilate biotin decreases with high intake levels of protein. Biotin binds easily to proteins, making it unavailable to your body, which in turn causes biotin deficiency and hair loss. Try to steer clear of raw eggs in your diet, and cut down on protein powders and bars. Use one of the many shampoos that contain biotin and silica.

Additionally, those with type A blood(me) don't have the ability to fully absorb B vitamins. Biotin is classified as a Vitamin B, so if you have Type A blood, adding higher doses of 5-8 grams twice daily will be needed to help prevent hair loss. At this time, there are no known side effects at this dosage level.

People suffering from heartburn, acid reflux, or GERD and who are taking antacids may absorb biotin less and hair loss may occur as a result. Therefore watch your use of over-the-counter antacids if you are worried about hair loss.

------------------------
http://www.healthyeatingclub.com/APJCN/ProcNutSoc/1980-1989/1983/1983%20p206.pdf
Rapid Tissue depletion in liver and kidney occur BEFORE any signs of biotin deficiency like growth rate slowed in birds!
Tissue depletion of biotin and the development of deficiency symptoms and the fatty liver and kidney syndrome.
Proc Nutr Soc Aust 1983; 8:206
-------------------------

http://www.ncbi.nlm.nih.gov/entrez/utils/fref.fcgi?itool=Abstract-def&PrId=3016&uid=15871139&db=pubmed&url=http://www.journals.uchicago.edu/cgi-bin/resolve?AJHG42232

Biotin-responsive basal ganglia disease maps to 2q36.3 and is due to mutations in SLC19A3.

Biotin-responsive basal ganglia disease (BBGD) is a recessive disorder with childhood onset that presents as a subacute encephalopathy, with confusion, dysarthria, and dysphagia, and that progresses to severe cogwheel rigidity, dystonia, quadriparesis, and eventual death, if left untreated. BBGD symptoms disappear within a few days with the administration of high doses of biotin (5-10 mg/kg/d). On brain magnetic resonance imaging examination, patients display central bilateral necrosis in the head of the caudate, with complete or partial involvement of the putamen. All patients diagnosed to date are of Saudi, Syrian, or Yemeni ancestry, and all have consanguineous parents. Using linkage analysis in four families, we mapped the genetic defect near marker D2S2158 in 2q36.3 (LOD=5.9; theta=0.0) to a minimum candidate region (approximately 2 Mb) between D2S2354 and D2S1256, on the basis of complete homozygosity. In this segment, each family displayed one of two different missense mutations that altered the coding sequence of SLC19A3, the gene for a transporter related to the reduced-folate (encoded by SLC19A1) and thiamin (encoded by SLC19A2) transporters.

PMID: 15871139 [PubMed - indexed for MEDLINE]

Bob
http://www.journals.uchicago.edu/AJHG/journal/issues/v77n1/42232/42232.html

Thiamine Intestinal Transport and Related Issues: Recent Aspects

Gianguido Rindi1 and Umberto Laforenza
P.S.E.B.M. 2000, Vol 224:246–255]

Abstract. In the intestinal lumen thiamine is in free form and very low concentrations. Absorption takes place primarily in the proximal part of the small intestine by means of a dual mechanism, which is saturable at low (physiological) concentrations and diffusive at higher. Thiamine undergoes intracellular phosphorylation mainly to thiamine pyrophosphate, while at the serosal side only free thiamine is present. Thiamine uptake is enhanced by thiamine deficiency, and reduced by thyroid hormone and diabetes.
The entry of thiamine into the enterocyte, as evaluated in brush border membrane vesicles of rat small intestine in the absence of H+ gradient, is Na+- and biotransformation-independent, completely inhibited by thiamine analogs and reduced by ethanol administration and aging.

The transport involves a saturable mechanism at low concentrations of vitamin and simple diffusion at higher.
Outwardly oriented H+ gradients enhance thiamine transport, whose saturable component is a Na+-independent electroneutral uphill process utilizing energy supplied by the H+ gradient, and involving a thiamine/ H+ 1:1 stoichiometric exchange.
(so does this mean the ATP pump?)

The exit of thiamine from the enterocyte, as evaluated in basolateral membrane vesicles, is Na+-dependent, directly coupled to ATP hydrolysis by Na+-K+-ATPase, and inhibited by thiamine analogs. Transport of thiamine by renal brush border membrane vesicles is similar to the intestinal as far as both H+ gradient influence and specificity are concerned. In the erythrocyte thiamine transport is a Na+-independent, electroneutral process yet with two components: saturable, prevailing at low thiamine concentrations, and diffusive at higher.

The saturable (specific) component is missing in patients of the rare disease known as thiamine-responsive megaloblastic anaemia (TRMA), producing a general disturbance of thiamine transport up to thiamine deficiency. The TRMA gene is located in chromosome 1q23.3.

Recently, the thiamine transporter has been cloned: it is a protein of 497 aminoacid residues with high homology with the reduced-folate transporter.

http://dx.doi.org/10.1046/j.1525-1373.2000.22428.x

---------------------------------------
Regulation of reduced-folate transporter-1 in retinal pigment epithelial cells by folate
www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15875363&dopt=Abstract

high folate levels in blood downregulated the folate transporter(and its asociated mRNA levels)..as expected
"Steady-state levels of Reduced-folate transporter-1 (RFT-1) mRNA and protein(ie the actual RTF transporter) decreased significantly in the presence of excess folate.
CONCLUSIONS: Excess folate levels downregulate RFT-1 in RPE."
----------------------------------------------
my RBC folate is over high?? without any supps(even with avoidance of added folate ) My Mum's RBC folate is over the top of normal too, not far but always over both of us. For some unknown to me reason we have never had our serum folate measured?..

http://jasn.asnjournals.org/cgi/content/full/14/5/1314

seems to be saying that serum folate is usually normal even if RBC folate is high..and its genetic..as I suspected ..and to do with glutamate something...???

and says no influence on serum folate, B12 or anything else.. so not relevant.. or as as far as known :-no effect of this genetic high red blood cell(RBC) folate
--------------------------------
also see following post(s) ~
http://tealady-health.blog.co.uk/2006/09/09/thiamin_transporters~1111873
edit [Bob]
http://www.journals.uchicago.edu/-AJHG/journal/issues/v77n1/42232/42232.html

Acta Paediatrica
Issue: Volume 95, Number 1 / January 2006
Pages: 99 - 104
Thiamine-responsive megaloblastic anaemia syndrome: Long-term follow-up and mutation analysis of seven families
Christopher J. Ricketts A1, Jayne A. Minton A1, Jacob Samuel A2, Indra Ariyawansa A3, Jerry K. Wales A4, Ivan F. Lo A5, Timothy G. Barrett A1
Abstract:
Aim: Thiamine-responsive megaloblastic anaemia syndrome (TRMA) is the association of diabetes mellitus, anaemia and deafness, due to mutations in SLC19A2, encoding a thiamine transporter protein. This is a unique monogenic form of vitamin-dependent diabetes for which there is limited long-term data. We aimed to study genotype–phenotype relationships and long-term follow-up in our cohort. Methods: We have studied 13 patients from seven families and have follow-up data for a median of 9 y (2–30 y).
Results: All patients originated from Kashmir or Punjab, and presented with non-immune, insulin-deficient diabetes mellitus, sensorineural deafness and a variable anaemia in the first 5 y of life, the anaemia progressing to megaloblastic and sideroblastic changes in the bone marrow. The anaemia and diabetes mellitus responded to oral thiamine hydrochloride 25 mg/d, but during puberty thiamine supplements became ineffective, and almost all patients require insulin therapy and regular blood transfusions in adulthood.
All patients are homozygous for mutations in the SLC19A2 gene. We have identified a novel missense mutation (T158R) that was excluded in 100 control alleles.
Conclusion: Diabetes in this syndrome is due to an insulin insufficiency that initially responds to thiamine supplements; however, most patients become fully insulin dependent after puberty.
 A mutation screening strategy is feasible and likely to identify mutations in almost all cases.
 My comment:  Puberty stopping the thiamin working is interesting; one thing is the oestrogen binding the thiamin, I presume testosterone may be also?...and maybe growth hormone had some effect as well?.. expect it to from some people's reaction to growth hormone, but couldnt find anything
--------------------------------------------
1: Pflugers Arch. 2004 Feb;447(5):641-6. Epub 2003 May 6. Links
SLC19: the folate/thiamine transporter family.
Ganapathy V, Smith SB, Prasad PD.
Department of Biochemistry and Molecular Biology, Medical College of Georgia, GA 30912-2100, Augusta, USA, vganapat@mail.mcg.edu

The SLC19 gene family of solute carriers is a family of three transporter proteins with significant structural similarity, transporting, however, substrates with different structure and ionic charge. The three members of this gene family are expressed ubiquitously and mediate the transport of two important water-soluble vitamins, folate and thiamine. The concentrative transport of substrates mediated by the members of this gene family is energized by transcellular H(+)/OH(-) gradient.
SLC19A1 is expressed at highest levels in absorptive cells where it is located in a polarized manner either in the apical or basal membrane, depending on the cell type. It mediates the transport of reduced folate and its analogs, such as methotrexate, which are anionic at physiological pH.
SLC19A2 is expressed ubiquitously and mediates the transport of thiamine, a cation at physiological pH. SLC19A3 is also widely expressed and is capable of transporting thiamine.
This review summarizes the current knowledge on the structural, functional, molecular and physiological aspects of the SLC19 gene family.

BOB_sent via email.. full text and pdf, titled 'the ABC of solute carriers'. or thiamin/folate transporters

some notes of interest in article:
"SLC19A1 expression... In addition, the activity and expression of the transporter are decreased by nitric oxide and hyperglycemia [18, 31]. "
as I suspected the high blood glucose-diabetes type2 link is maybe correlated wih thiamin levels, ie higher glucose levels reduce this transporter, so reduce thiamin levels..also higher NO reduce thiamin levels.

"Role of SLC19 gene family members in the homeostasis of folate and thiamine.
The SLC19 gene family plays an important role in the transport and homeostasis of folate and thiamine in the body. Since SLC19A1 has also been shown to transport mono- and pyro-phosphate derivatives of thiamine , all three members of the SLC19 gene family may play a role in the homeostasis of thiamine. (My comment:and note above (same paper)  SLC19A1 is  decreased by hyperglycemia and NO)
It is quite evident that the role of these transporters in non-polarized cells is to mediate the influx of folate and thiamine into the cells. However, in cells that mediate the transcellular transfer of these vitamins (e.g., the absorptive cells of the intestine and kidney, the syncytiotrophoblast in the placenta, and the retinal pigment epithelium), the exact role of these transporters is dependent on their polarized distribution in the apical membrane versus the basolateral/basal membrane. The distribution of SLC19A2 and SLC19A3 in these polarized cells has not yet been investigated and therefore it is difficult to predict their exact role in the transcellular movement of thiamine and consequently in thiamine homeostasis of the whole organism. On the other hand, recent advances in the area of subcellular localization of SLC19A1 in polarized cells have enhanced our understanding of the role of this transporter in the transcellular movement of folate"
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Related:
The gene mutated in thiamine-responsive anaemia with diabetes and deafness (TRMA) encodes a functional thiamine transporter.

Novel mutation in the SLC19A2 gene in an African-American female with thiamine-responsive megaloblastic anemia syndrome.   this one mentions thyroid
"At age 19, a thiamine-responsive normocytic anemia was discovered. She was diagnosed with autoimmune thyroiditis at 20 years and she experienced a psychotic episode associated with a mood disorder at age 21. With oral thiamine therapy, her insulin requirement decreased by 30% over a 20 month period"
Interestingly, 30% is approx the amount I have had to reduce my thyroid meds by since injecting myself with 20mg daily of thiamin( I think I've settled on). but its too early to say, and it could be a coincidence or another factor (EG. I added in kelp too).
Suggestion: we usually don't have the same gene mutation or knockout.. BUT if thiamin transporters are affected, then maybe we are seeing some effects of this that may be correctable by high thiamin intake
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Polarized expression of members of the solute carrier SLC19A gene family of water-soluble multivitamin transporters: implications for physiological function
Boulware MJ, Subramanian VS, Said HM, Marchant JS.
Biochem J. 2003 Nov 15;376(Pt 1):43-8
Humans lack biochemical pathways for the synthesis of the micro-nutrients thiamine and folate. Cellular requirements are met through membrane transport activity, which is mediated by proteins of the SLC19A gene family. By using live-cell confocal imaging methods to resolve the localization of all SLC19A family members, we show that the two human thiamine transporters are differentially targeted in polarized cells, establishing a vectorial transport system. Such polarization decreases functional redundancy between transporter isoforms and allows for independent regulation of thiamine import and export pathways in cells.
www.biochemj.org/bj/376/0043/bj3760043.htm
This is where I came across targeting to apical and basolateral membranes......
full text is available
Bob
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"high levels of folic acid may exacerbate the neurological consequences of a vitamin B12 deficiency"
Folate and brain function in the elderly

My Mum had a B12 level that was in normal range but still below the 400 where I think its worth a trial of B12 needles(349), and high (above range) red blood cell (RBC) folate. This is folic acid.
My levels in blood were similar: RBC folate above range, B12 345.

When she was repeatedly telling me the same story and forgetful,
she responded well to a few ( about 4 to 6 over a few months) B12 injections. The injections were hydrocobalamin (in Australia).
After this I could hold a conversation with her again.

The following on folate transporters (FOLATE as well as Thiamin ):
http://tealady-health.blog.co.uk/2006/09/09/thiamin_transporters~1110229
http://tealady-health.blog.co.uk/2006/09/09/thiamin_transporters~1111873
technical ..
Mum and I both test as above normal range RBC folate.. but I couldn't see any implications of this from these studies.. other than that the serum folate may still be normal.

link2  This link uses megadoses that were perhaps more common a few decades ago. I'm cautious about megadoses myself ( That is high doses over 100 times the RDA and wouldn't personally take them and would NEVER recommend them) as the balance is lost in a more extreme way.
They used other B's together with B1and some minerals  for some balance, which I also find necessary.

I do this by taking a multiB, but I do take about 5 -25 times the RDA or so?. If one can do it with food .. like liver .. all the better!!  I think about 5 times the RDA is at least necessary when one is deficient to bring one out of deficiency. The RDA is really a minimal levels to prevent some diseases.. not a level for recovery where a deficiency exists I think?

I locate all the B1 posts by a tag search on B1.(just click on B1 under tags down RHS).
This is the "index" B1 post..and is still "under construction". , but  hopefully may be helpful.
Also the whole blog  can be searched by a google based search function in a search box way down RHS beneath the tags . 

I did Food Chemistry at uni last semester, and a few things clicked ; like the sulfites destroying B1 and the effect of Ergot(it also acts to increase thyroid hormones and adrenal hormones;Ergotamin was the ONLY drug that relieved my migraines for years), and effect of thyroid hormones on B1 (see below).
I am wondering if I was near borderline low B1 usually and sulfites etc. or thyroid hormones just kick me below the edge, producing deficiency symptoms. My endo says no, as its rare; but  I listen, then think about it.. ever hopeful

B1 ..history

B1 symptoms of deficiency.. from major to mild (sub optimal) and maybe too much  too much link2
The nervous and  digestive systems are commonly the first to be felt by a slight deficiency of thiamin[e] (B1). Early syptoms incluse irritability, anxiety, depression, poor muscle tone, and not absorbing nutrients well (thiamin helps with the production of HCl in stomach). Poor muscle tone also results in constipation.
The amount of thiamin rrequired bears a close relationship with the amount of carbs consumed. Sugars and alcohol don't provide any thiamin and yet use it up in their metabolism. Thiamin in tthe 1990's has been added to white flour in Australia, but is still not added in NZ.
The US/Canada also adds B1 to white rice. In Australia this is not done, so depletion of thiamin can occur if too much white rice is eaten. This does happes in Asia, with severe depletion causing beriberi and deaths.
The white rice does contian thiamin .. but more gets used in the metabolism of the white rice.
I suspect the amount of thiamin consumed in metabolism of a food  is closely correlated to its glycemic index.

b1 and sulfites  link1  link2 
B1 and apple cider
B1 and other foods with sulfites, SO2 etc ..and loses with sausages, and all foods incl sulfites,
also azo dyes in foods , tartrazine,
sulfa drugs
sulfates even?

B1 and alcohol link1, link2( to post 20 as a hypothesis only, refers posts 1 , 18  in thyroid forum thread)
B1 and caffeine, tea, coffee link1
Am J Clin Nutr. 1977 Oct;30(10):1680-5. says tannin is responsible for taking out vit B1 .. think milk binds tannins in tea? My symptoms seemed to worsen about when I started drinkng cranberry juice(which is high in tannnins), I already drank a lot of tea and some coffee occcasionally. Lately I got this taste on the back of my tongue and in my cheeks especially, but all over my mouth which I have now learnt to  recognise as tannin(I think?).  I guess it's like everything ..
The polyphenols /catechins/tannins or whatever you want to call them are great as antioxidants up to a certain point.... after which they become too high.. the lingering astringent taste in you mouth may let ya know (if its like me). Then too high tannins may reduce your B1?
 I had developed a wosening of the PN in my feet and the burning sensation had become quite intense and was spreading up to my kness..that and an ever present fatigue and a on-off short term memory -concentration-thought problems whch seemed to be declining.I'm hoping that stopping drinking the cranberry juice, and trying to sip some milk may help with the "too high tannins" and my symptoms may lessen? I'm also taking some B1 and a high B1 diet though as well.

B1 and nitrates? strong suspicion due to own experiences with high levels of nitrates and nitrites(not so high levels needed of nitrites as nitrates) that nitrates reduce thiamine too... so careful here
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B1 .. phosphorylation problem
subheading under phosphorylation problem .. B1 and VitD

B1 and carbs and glucose levels in blood and diabetes(1 and 2)diabetes link1 and insulin resistance..
including giving B1 before glucose to hypoglycemia in diabetics etc, also includes B1 and epileptics carb_link1

B1 and heart

B1 and PN (peripheral neuropathy)
So what is PN? link1
exercise helps with PN.. probably by better circulation?, maybe reduced glucose.. B1 may be involved??.. an idea did flicker thru mind somewhere and now lost again
.. but I think (for me and a few others I have chatted to on forums) that similar happens with lower doses of thyroid hormones in a few of us that may be B1 deficient ..even on good diets?
 Polyneuropathy from thiamin deficiency associated with thyrotoxicosis

B1 and MS    link1(includes Klenner protocol of B1 and liver extract)
link2
B1 and thyroid link1

B1 and CFS/M.E.
     www.geocities.com/bron.evans/cfs/cfs.html
     B1 and dopamine [link] : in relation to CFS

B1 and Sjrogens link
B1 and Metabolic acidosis link1 link2
B1 and low adrenals link1 

B1 and myofascial and tooth pulp pain 

Bob finds garlic fixes some of this.(the link being garlic contains allithiamin.. another form of B1).
I noticed a difference with higher B1 too I think.(in injections link at present)
possibly via  a  serotonin uptake incr; link1
(Thiamine deficiency: selective impairment of the cerebellar serotonergic system).
 I think that it's worth a trial of B1 or  chewing garlic(if you can do it.. Bob advises NOT to try this on an empty stomach  to see if it  alleviates nerve pain, tooth pain, myofascial pain.

B1 and Candida link1
B1 and mercury link1

B1 and Ca, Mg Ca Mg link1, piracetam mentioned too

B1 and Glutathione, NAD(P)H link1

B1 and Oestrogen link1
I know there is something going on with estrogen and B1.

Other possible B1 deficiency diseases.. some suggestions..
maybe marginal B1 deficiency is behind SIDS in part ?
maybe Kawasaki disease,
 others I've now forgotten again.. hey that's one.. memory, CFS etc.. may be involved to varying degrees migraines .. thru chloride permeability change? also may moderate low or high blood pressure also thru chloride channel permeability change..and perhaps a slight change in vasopressin??(hopeful here)

injections link1
injections link2
 
Kinetics of thiamin and thiamin phosphate esters in human blood, plasma and urine after 50 mg intravenously or orally. Half-life of different thiamine species.

 Other Recommended links
 Excellent reviews and articles reading that are too broad to put in only one category
http://tealady-health.blog.co.uk/2006/06/27/b1_earlier_links_sent_to_gmail~901507 
http://www.digitalnaturopath.com/treat/T157953.html 
http://www.carleton.ca/biology/2200/slides/lecture12_06.pdf basic vitamin slides 
http://www.nlm.nih.gov/medlineplus/druginfo/natural/patient-thiamin.html
http://www.pdrhealth.com/drug_info/nmdrugprofiles/nutsupdrugs/thi_0261.shtml

http://www.thyroidresearch.com/viewArticle.php?articleno=1529

work by:
H. T. R. Mount, M.B., M.S., F.R.C.S.[C], F.A.C.S.
PUBLICATION: C.M.A. JOURNAL/JUNE 2, 1973/VOL. 108

[[ My experience suggests that some factor or factors in liver extract, associated with vitamin BI, can induce remyelination in patients suffering from multiple sclerosis and probably in other cases of demyelinating diseases. It is suggested that this clinical finding should now be subjected to detailed laboratory studies in order to enlarge its use or to circumscribe its limitations. -

Therapy was begun with Lederle's liver extract, but production ceased in the spring of 1972. Connaught Laboratory liver, extract was used for a period of nine months.
Lilly's liver extract is now used..]]
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also Dr. F.R. Klenner's Protocol for MS
uses B1 and liver extract injectables for treating MS ...with some success over the years it appears
http://www.townsendletter.com/May2003/klennerprotocol0503.htm

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http://www.fedupwithfoodadditives.info/factsheets/Factsheet.htm

http://www.fedupwithfoodadditives.info/newsletters/contents.htm also comments on benzoate (may form benzene) in softdrinks as preservatives

http://www.fedupwithfoodadditives.info/

Food Additives E nos

Adverse Effects of Food additives

http://www.tncc.com.au/sites/tncc/index.php?pageId=55
http://www.tncc.com.au/sites/tncc/index.php
http://www.ohmbeverages.com.au/p_and_n_beverages.html scroll down to fuze in 600ml bottles..
I cant find the full ingredients .. so will have to type to ask your thoughts on
reconstituted apple juice 95.5%, passionfruit 3.5%, citric acid derived from lemon juice, natural flavour sourced from fruit, vitC, (doens't specify which form so assume ascorbic acid?), vit A (carotene),
dimethyl dicarbonate(242)[microbial control agent] .. that's the worry bit,
Carbon dioxide

says
* Dimethyl dicarbonate inactivates microbes and breaks down after packing within hours to components normally found in fruit, leaving Fuze preservative free