Pyruvate dehydrogenase function depends on thiamine (B1)

[JES]

I simply say that it lacks positive studies behind it. Good to hear, but we still need real medicine, e.g. ritux - which btw needs to prove efficacy in a phase 3 study.

I read from your profile that you've been getting ritux infusions. Just curious about what has been your response to it?

 

[Chocolove]

Me thinks a personal trial of allithiamine, along with magnesium L-threonate, since it crosses the blood brain barrier, is a worthwhile adventure.

 

[Marky90]

I read from your profile that you've been getting ritux infusions. Just curious about what has been your response to it?

No response, unfortunately.

 

[Sidereal]

@Sidereal According to Dr. Jessica Weiser:

"Both biotin and pantothenic acid–vitamin B5—are absorbed from the intestines via the same receptors..

When taking biotin supplements, the amount of biotin in the gut far outweighs the quantity of vitamin B5,... thereby leading to a relative vitamin B5 deficiency.

Pantothenic acid is thought to regulate the barrier function of the surface layer on skin and can reduce acne lesions. Therefore, a deficiency of pantothenic acid—or excess of biotin—could lead to acne flares.”

In simpler terms, you could be giving yourself a deficiency of B5 by taking an excess of biotin.

Bad reaction to B5 too unfortunately.

Do you have ME/CFS? Bad reactions to vitamins we are deficient in are commonplace around here.

 

[Chocolove]

@Sidereal

Do you have ME/CFS? Bad reactions to vitamins we are deficient in are commonplace around here.

I don't know if I have ME/CFS. I do know have extreme adrenal problems - probably some adrenal atrophy from 8 years of corticosteroids, and a possible adrenal hemorrhage... extreme fatigue, PEM, managed to get out of POTS, have had a lot of infectious issues...

I had an extremely bad reaction when I took a 1000 mcg pill of L-5 - Methylfolate - as in on the floor, hoping I would survive, (even though I had been taking MeB12.).

A half a year later, I now take a half tab of a Jarrow Me12 (1000 mcg) + 5-MTHF (Quatrefolic 400 mcg) + B6 (P5P 1.5 mg) on a daily or every other day basis. This helps a lot - better mental clarity and energy, but I'm still extremely weak. I have some methylation issues and perhaps starting the rusty engine at full speed made me crash. Doing the start low, go slow now.

When one has severe adrenal problems, according to Dr. Lam, B vitamins can be way too stimulating if not chosen and used properly in judicious amounts. Many things can cause paradoxical reactions when the adrenals are near failure.

Recommendations are generally to take a B complex, since one doesn't want to cause depletion of another B vitamin through imbalance. I do take other Bs in small amounts to keep things steady. And I do take some Pantethine. Sometimes things seem to get out of balance and I often feel a strong hunger for something. Backing off a bit, or adding in something that might be needed can help....if one can figure out what that is....very tricky. So I've been studying up on it.

It's been a long slow battle. I figured out that my body had long been missing some essential nutrients. These included magnesium and iodine which are commonly deficient in many people, and true vitamin A - after finding out that conversion of carotene to vitamin A is very poor. I am now on the path to living after adding in these missing nutrients and have fewer infectious issues.

I'm finding strengthened immunity and better mental clarity, little by little. Adrenals take a long time to rebuild/recover. Even minor things can cause a huge setback.

 

[eljefe19]

@Sidereal


I don't know if I have ME/CFS. I do know have extreme adrenal problems - probably some adrenal atrophy from 8 years of corticosteroids, and a possible adrenal hemorrhage... extreme fatigue, PEM, managed to get out of POTS, have had a lot of infectious issues...

I had an extremely bad reaction when I took a 1000 mcg pill of L-5 - Methylfolate - as in on the floor, hoping I would survive, (even though I had been taking MeB12.).

A half a year later, I now take a half tab of a Jarrow Me12 (1000 mcg) + 5-MTHF (Quatrefolic 400 mcg) + B6 (P5P 1.5 mg) on a daily or every other day basis. This helps a lot - better mental clarity and energy, but I'm still extremely weak. I have some methylation issues and perhaps starting the rusty engine at full speed made me crash. Doing the start low, go slow now.

When one has severe adrenal problems, according to Dr. Lam, B vitamins can be way too stimulating if not chosen and used properly in judicious amounts. Many things can cause paradoxical reactions when the adrenals are near failure.

Recommendations are generally to take a B complex, since one doesn't want to cause depletion of another B vitamin through imbalance. I do take other Bs in small amounts to keep things steady. And I do take some Pantethine. Sometimes things seem to get out of balance and I often feel a strong hunger for something. Backing off a bit, or adding in something that might be needed can help....if one can figure out what that is....very tricky. So I've been studying up on it.

It's been a long slow battle. I figured out that my body had long been missing some essential nutrients. These included magnesium and iodine which are commonly deficient in many people, and true vitamin A - after finding out that conversion of carotene to vitamin A is very poor. I am now on the path to living after adding in these missing nutrients and have fewer infectious issues.

I'm finding strengthened immunity and better mental clarity, little by little. Adrenals take a long time to rebuild/recover. Even minor things can cause a huge setback.

Have you ever had viral titer testing or bacterial? I found that Oxymatrine and other immune modulators have helped tremendously with that ill feeling, like a flu, perhaps that interests you? Feel free to PM me.

 

[Chocolove]

@eljefe19 Thanks. I appreciate that.

Back in 2003 I got something like norovirus - extremely violent. Afterwards my ANA was very high. My immune system was stuck full on, overreacting to walk of a few steps by going into hives, when speaking for 30 seconds by my throat swelling, losing voice, needing frozen yogurt to keep my throat swelling under control, an emergency state that continued for 6 months. I was sent from doctor to doctor finally ending up a rheumatologist, who pronounced without conducting the 5 panels of testing needed, that I had some sort of lupus like syndrome and would have to be on corticosteroids for life.

Corticosteroids can knock down the immune system to stop an autoimmune reaction...but they knock down the immune system so you end up getting every possible disease and the worst case of it. 8 years later I saw a different rheumatologist who spotted the negligence of the first, and we did the testing finding no sign of any lupus like syndrome. I should have been put on corticosteroids for perhaps a week or two at most to stabilize.

8 years into this, we didn't know if I would be able to come off the corticosteroids - 3 weeks is considered by the medical establishment a long time to be on them. The HPA axis works on a negative feedback mechanism and the man made corticosteroids have too long a half life (last in your system too long) preventing any negative feed back.

As a result, the adrenals atrophy, and may or may not "wake up" when the steroid supply diminishes. It takes a trial of extremely slow tapering - without any infections which cause a much greater need for corticosteroids, in order to come off the steroids. Sadly many end up on corticosteroids for life like those with Addison's Disease, a very horrible state.

I finally succeeded in getting off the steroids, a major achievement. I slowly and gently began to build myself back up. After a couple of years I thought my adrenals were pretty much back to normal, started with some caffeine and got into trouble when a bad respiratory infection hit that I couldn't kick for 4 months.

I had managed at this point to run my genetics and discovered that, not uncommonly, I had several genes that do not allow for conversion of any carotene to vitamin A. Vitamin A is known as the anti-infection vitamin. Real vitamin A is found in a few foods in small amounts, and in liver with the best amount, none of which I was consuming.

When I read up on vitamin A deficiency I discovered that perhaps this was a foundational reason why I was getting sick so much in the first place before the corticosteroids....and further it is potentially possible that my immune system went into overdrive due to the lack of vitamin A. I was exhibiting many signs of vitamin A deficiency, that no one but myself discovered.

What MD would notice? They are not trained in nutrition, rarely examine their patients, conduct 5-15 minute appointments,... They will just throw a pill at you and see what happens. Then they put you on a bicycle, specialist after specialist...They have no time to put in the hours to investigate a single person's ailments. Many people feel safe taking those "tested medicines," but they don't realize that prescription drugs are available only by prescription because they are very dangerous - they do harm - often permanent damage.

About four years ago, I came down with chicken pox, diagnosed myself through google and managed to get to the doctor in time to obtain the drug of choice which thwarted billions of pox just starting to show. Of course like many viruses, it changes form and stays within your system, evolved waiting for a weakness in your immune system to proliferate, showing up next time as shingles. We cannot rid ourselves of many organisms. But we can strengthen ourselves with nutrients to put them in a recessed state.

I have used herbs that are adaptogens to good effect, but I am wary of immune modulator drugs. All along it is likely that I most needed a better foundation in nutrients to develop a strong and healthy immune system. Throwing immune drugs into an imperfect system only made things much worse and nearly killed me.

I had taken a multi-vitamin/mineral supplement for most of my life and naïvely thought this insured me. In some areas it probably did. But unfortunately, the general supplements contain carotene not vitamin A (to avoid any chance of overdose on this fat soluble vitamin). It was only my genetic investigation that woke me up to the need for real vitamin A.

Now I eat liver. So much horror and expense might have been avoided had I just gotten good nutrition.

 

[eljefe19]

Congratulations for getting off the steroids!!! My story was similar except my disease was (I thought) general anxiety disorder and I had a doctor who cowtowed to my addictive personality and I spent months on mad Xanax. Getting off of it was like having to learn to live again.

As far as your disease, do you have a CFS or ME diagnosis? I am interested in adding Vitamin A to my regimen. How do you dose to avoid overdose?

 

[Asklipia]

@Chocolove , I have been taking allithiamine for about a year I think, in the form of Alinamin Ex Plus. It has been very beneficial in the sense that I felt quite well a year ago, and know feel even better.
In retrospect I understand how I might have crashed a few times, most probably because I was borderline Thiamin-deficient.
- I used to eat quite a lot of raw oysters and raw fish AT A TIME
- I love brussel sprouts and have overdosed on them then crashed and did not understand why
- I have spent a lot of time in the sun in places where the sun is not normal (ozone layer missing) and this made me crash severely several times.
There is this Swedish study that just came out showing an increase in wildlife thiamin deficiency.
One of the causes of thiamin deficiency is UV exposure and it might be one reason that I responded well to allithiamine and not at all to normal B1. Maybe lipophilic thiamine is needed because thiamine in the blood might be destroyed by UV more easily?
Another line of thought for me is that B vitamins are extremely sensitive to light. Blue light I learnt at school (maybe wrong? That was 50 years ago... ) destroys thiamin. A lot of lights inside the house and computer screens etc emit blue light. Outside UV and inside blue light, maybe it does take thiamin supplementation several times a day in small doses to feel normal.

 

[Sidereal]

@Chocolove

Sorry to hear you've been through the wringer. Well done on surviving rheumatology and getting off the steroids. 8 years, wow. I've had similar experiences with rheumatologists. Very high ANA titre, antiphospholipid antibodies (both perfectly consistent with a diagnosis of ME/CFS which of course they know nothing about so they try to shoehorn you into a lupus diagnosis). I've seen a lot of crazy doctors over the years but that specialty surely takes the cake. I was only on prednisone for a month but it damned near killed me in the aftermath when I was passing out with hypoglycaemia and other complications of adrenal insufficiency.

My immune system was stuck full on, overreacting to walk of a few steps by going into hives, when speaking for 30 seconds by my throat swelling, losing voice, needing frozen yogurt to keep my throat swelling under control, an emergency state that continued for 6 months.

I've been in a very similar state. When this problem was at its worst I was getting throat swelling from any autonomic "challenge" like standing up or drinking a glass of water. I was also down to literally two foods that I could eat without anaphylaxis.

Have you looked into mast cell activation syndrome (MCAS)? We have a whole subforum here about it. It's a not uncommon comorbidity in POTS and ME/CFS.

I had an extremely bad reaction when I took a 1000 mcg pill of L-5 - Methylfolate - as in on the floor, hoping I would survive, (even though I had been taking MeB12.).

Same here, years ago. Took 1/4 of an 800 mcg tablet of 5-MTHF and collapsed on the floor, unable to breathe, losing consciousness. Now of course I can take it with no problems but I don't because I think pushing methylation is a mistake.

When I read up on vitamin A deficiency I discovered that perhaps this was a foundational reason why I was getting sick so much in the first place before the corticosteroids....

I would caution against any potentially simplistic explanations like vitamin A deficiency or any other vitamin deficiency. ME/CFS is not caused by vitamin deficiencies; the illness itself seems to cause us to become deficient in many things. That isn't to say that vitamins can't help (or hurt).

I was sick with something every 3-4 weeks in the 10+ years leading up to my first official ME/CFS crash. In my case supplementing retinol did nothing except make D3 less toxic.

 

[Chocolove]

- I used to eat quite a lot of raw oysters and raw fish AT A TIME

Thiamine - Wikipedia
https://en.wikipedia.org/wiki/Thiamine
Thiamine, also known as thiamin or vitamin B 1, ... Thiamine is degraded by thermolabile thiaminases (present in raw fish and shellfish). No problem with cooked.

Thiamine Antagonists
Thiamine in foods can be degraded in a variety of ways. Sulfites, which are added to foods usually as a preservative,[20] will attack thiamine at the methylene bridge in the structure, cleaving the pyrimidine ring from the thiazole ring.[8] The rate of this reaction is increased under acidic conditions. Thiamine is degraded by thermolabile thiaminases (present in raw fish and shellfish[7]). Some thiaminases are produced by bacteria. Bacterial thiaminases
are cell surface enzymes that must dissociate from the membrane before being activated; the dissociation can occur in ruminants under acidotic conditions. Rumen bacteria also reduce sulfate to sulfite, therefore high dietary intakes of sulfate can have thiamine-antagonistic activities.

Thiamine deficiency due to sulphur dioxide preservative in ‘pet meat’ – a case of déjà vu
http://www.catvet.com.au/articles/thiamine_deficiency_pdf.pdf

Plant thiamine antagonists are heat-stable and occur as both the ortho- and para-hydroxyphenols. Some examples of these antagonists are caffeic acid, chlorogenic acid, and tannic acid. These compounds interact with the thiamine to oxidize the thiazole ring, thus rendering it unable to be absorbed.

Tannins, found in coffee and tea can react with thiamine by turning it into a form that is difficult for the body to absorb, potentially leading to digestive problems and a thiamine deficiency.

Two flavonoids, quercetin and rutin, have also been implicated as thiamine antagonists.[8]

Wernicke encephalopathy caused by Thiamine (B1) deficiency is often undiagnosed. "Particularly in those who suffer from alcoholism or AIDS, the diagnosis is missed on clinical examination in 75 to 80 percent of cases," wrote the researchers. Yet sadly, those disorders are well known to cause B1 deficiency. This serious neurologic disorder is associated with eye problems like double vision and involuntary eye movement, and can even lead to irreversible brain damage and death, according to researchers at Loyola University Medical Center.

There is this Swedish study that just came out showing an increase in wildlife thiamin deficiency

Hansson and colleagues, whose findings are published in the journal Scientific Reports, aren’t the first scientists to find thiamine deficiencies in wildlife. Initial reports came in the mid-1990s, when deficiencies were linked to widespread die-offs in young salmon. But the new study, they write, shows the phenomenon to be “considerably more widespread and severe than previously reported.”

“Many health effects, including abnormal behaviour, observed in biota today may well be due to thiamine deficiency,” write Hansson’s team. To be sure, this hasn’t been conclusively demonstrated, but the researchers think attention is urgently required. “Many wildlife populations are declining at rates higher than can be explained by known threats to biodiversity,” they write, and “thiamine deficiency has emerged as a possible contributing cause.”

The biggest question of all is why this is happening in the first place. Among the hypotheses are a shift in thiamine-producing algae populations or exposure to environmental pollutants that interfere with thiamine uptake. “The biogeochemical environment is highly impacted by human activities,” says Hansson.
http://www.anthropocenemagazine.org/2017/01/thiamine-deficiency-wildlife/

"Like most vitamins, thiamine is taken up into the body and then immediately modified into a number of derivatives. The most famous is thiamine diphosphate (also known as TPP)—this thiamine is the one that plays a part in a bunch of energetic reactions in glucose metabolism. If you want your citric acid cycle (link is external) to run (and believe me, you do), you need thiamine diphosphate. Bodybuilders and BCAA chuggers take note: you also need TPP to decarboxylate the keto acids derived from the branched chain amino acids. You also need TPP in the pentose shunt, which is an important extra-energy and detox pathway. Deficiency of TPP is what eventually shows up as Wernike's encephalopathy and Korsakoff's psychosis among the present day severe alcoholic set.

The synthesis of TPP from free thiamin requires magnesium,...but current magnesium intakes in the US population are below recommended levels.
http://lpi.oregonstate.edu/mic/vitamins/thiamin
http://lpi.oregonstate.edu/mic/minerals/magnesium

Thiamine, with its key role in central nervous system energy production, can give us clues as to the pathology of syndromes such as Alzheimer's Dementia. Folks with AD have normal thiamine levels, but low levels of the metabolically active TPP, suggesting problems with energy regulation. Giving people with AD extra thiamine can sometimes help the symptoms."
https://www.psychologytoday.com/blo...04/nutritional-brain-bomb-thiamine-deficiency

There is speculation that the primary etiology for thiamin deficiency in people with obesity is a diet high in simple sugars and low in whole grains, legumes, and other whole foods that naturally contain thiamin. Not only do simple sugars lack thiamin, but the metabolism of foods high in sugar requires relatively high amounts of thiamin and may therefore accelerate its depletion (11, 16, 26). Indeed, this concept is supported by a small study in 12 healthy volunteers that found that an increase in dietary carbohydrate (from 55% to 65% to 75% of total energy intake for 8 d) although thiamin intake, total energy intake, and physical activity levels remained constant caused a decrease of plasma and urine thiamin amounts (27).
http://advances.nutrition.org/content/6/2/147.full

 

[Chocolove]

Further, according to Dr. Jeffrey Dach MD:
"Conclusion – Overwhelming Evidence

I was taught in medical school that diabetes was caused by either inadequate insulin production (Type I) or insensitivity to insulin (type II Diabetes). This is not the complete story, and a paradigm shift has occurred in thinking about the underlying mechanism of diabetes.

Current research reveals that diabetes is a thiamine deficiency state, which is the primary cause of diabetic complications. The evidence is now overwhelming that treatment of the diabetic patient should include thiamine supplementation."

Underlying all diabetic conditions is poor sugar control or hyperglycemia. Hyperglycemia can be due to a lack of insulin as in Type 1 diabetes or insulin resistance as in Type 2 diabetes. In either case, the corresponding diabetic complications that evolve over time in many diabetics, the cardiovascular disease, retinopathy, peripheral nerve and vascular damage, represent the effects of sustained hyperglycemia.

Until recently, the mechanisms by which diabetic vascular damage developed eluded researchers. Although multiple, seemingly discrete biomarkers had been identified, no single, unifying mechanism was understood. It turns out that diabetics, both Type 1 and Type 2, are severely deficient in thiamine or vitamin B1 and that thiamine is required for glucose control at the cell level. Why is thiamine deficient in diabetics and how does thiamine manage glucose control? The answers to those questions highlight the importance of micronutrients in basic cellular functioning, particularly mitochondrial functioning, and the role of excessive sugar in disease.
http://www.hormonesmatter.com/diabetes-thiamine-treatment-opportunity/

Clin Med Insights Endocrinol Diabetes. 2014 Jan 23;7:1-6. doi: 10.4137/CMED.S13573. eCollection 2014.
Metabolic Benefits of Six-month Thiamine Supplementation in Patients With and Without Diabetes Mellitus Type 2.
Al-Attas O1, Al-Daghri N1, Alokail M1, Abd-Alrahman S2, Vinodson B2, Sabico S2.
Author information

• 1Center of Excellence in Biotechnology Research, King Saud University, Riyadh, Saudi Arabia. ; Biomarkers Research Program, Biochemistry Department, College of Science, King Saud University, Riyadh, Saudi Arabia. ; Prince Mutaib Chair for Biomarkers of Osteoporosis, Biochemistry Department, College of Science, King Saud University, Riyadh, Saudi Arabia.
• 2Biomarkers Research Program, Biochemistry Department, College of Science, King Saud University, Riyadh, Saudi Arabia.

Abstract
Thiamine deficiency has been documented to be prevalent in patients with diabetes mellitus, and correction of thiamine deficiency in this population may provide beneficial effects in several cardiometabolic parameters, including prevention of impending complications secondary to chronic hyperglycemia. In this interventional study, we aim to determine whether thiamine supplementation is associated with cardiometabolic improvements in patients with diabetes mellitus type 2 (DMT2).

A total of 86 subjects (60 DMT2 and 26 age- and BMI-matched controls) were included and were given thiamine supplements (100 mg/day) for six months. Anthropometrics and metabolic profiles were measured routinely. Serum thiamine and its derivatives were measured using high performance liquid chromatography. In all groups, there was a significant decrease in total cholesterol after three months (p = 0.03) as well as in HDL cholesterol after six months of thiamine supplementation (p = 0.009).

Significant improvements were also observed in the mean serum levels of creatinine (p = 0.001), as well as thiamine and its derivatives in both serum and urinary levels across follow-up visits (p-values 0.002 and <0.001, respectively). In the DMT2 group, improvements were observed in lipid profile (mean serum LDL and total cholesterol with p-values 0.008 and 0.006, respectively), serum thiamine (p < 0.001), TMP (p < 0.001), TDP (p < 0.001), urinary thiamine (p < 0.001) and serum creatinine (p < 0.001). Thiamine supplementation is a promising adjuvant therapy for patients with DMT2. Longer clinical trials are needed to determine its protective effect in DMT2 complications.

KEYWORDS:
Saudi; diabetes mellitus type 2; supplements; thiamine

PMID: 24550684
PMCID: PMC3921172
DOI: 10.4137/CMED.S13573
[PubMed]
Free PMC Article

 

[Chocolove]

Have you looked into mast cell activation syndrome (MCAS)? We have a whole subforum here about it. It's a not uncommon comorbidity in POTS and ME/CFS.

This one may be of interest in re vitamin A and MCAS:

Available online 13 January 2017

In Press, Corrected Proof — Note to users

Review

Retinoic Acid and Immune Homeostasis: A Balancing Act

• Martje N. Erkelens1,
• Reina E. Mebius1, ,

In the immune system, the vitamin A metabolite, retinoic acid, is known for its role in inducing gut-homing molecules in T and B cells, inducing regulatory T cells (Tregs), and promoting tolerance.

However, it was suggested that retinoic acid (RA) can have a broad spectrum of effector functions depending on the local microenvironment. Under specific conditions, RA can also promote an inflammatory environment. We discuss the dual role of RA in immune responses and how this might be regulated.

Furthermore, we focus on the role of RA in autoimmune diseases and whether RA might be used as a therapeutic agent.

Retinoic Acid deficiency can result in the development of a broad spectrum of autoimmune diseases.

http://www.sciencedirect.com/science/article/pii/S147149061630223X


There is also substantial evidence to suggest that RA may help prevent the development of autoimmunity:

J Immunol. 2014 Apr 1;192(7):2953-8. doi: 10.4049/jimmunol.1303245.
Modulation of T cell and innate immune responses by retinoic Acid.
Raverdeau M1, Mills KH.
Author information

• 1Immune Regulation Research Group and Immunology Research Centre, School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin 2, Ireland.

Abstract
Retinoic acid (RA) is produced by a number of cell types, including macrophages and dendritic cells, which express retinal dehydrogenases that convert vitamin A to its main biologically active metabolite, all-trans RA. All-trans RA binds to its nuclear retinoic acid receptors that are expressed in lymphoid cells and act as transcription factors to regulate cell homing and differentiation. RA production by CD103(+) dendritic cells and alveolar macrophages functions with TGF-β to promote conversion of naive T cells into Foxp3(+) regulatory T cells and, thereby, maintain mucosal tolerance. Furthermore, RA inhibits the differentiation of naive T cells into Th17 cells.

However, Th1 and Th17 responses are constrained during vitamin A deficiency and in nuclear RA receptor α-defective mice. Furthermore, RA promotes effector T cell responses during infection or autoimmune diseases. Thus, RA plays a role in immune homeostasis in the steady-state but activates pathogenic T cells in conditions of inflammation.

PMID: 24659788
DOI: 10.4049/jimmunol.1303245
[PubMed - indexed for MEDLINE]
Free full text

 

[Asklipia]

I take enzymes in the form of Wobenzym. This has been very helpful but it contains Rutin! Another road to thiamine deficiency!

What brand of allithiamine are you trying?
@eljefe19 takes Cardiovascular Research Ecological Formulas Allithiamine which contains per serving (1 capsule): 50 mg TTFD (thiamin tetrahydrofurfuryl disulfide) + 75 mg Calcium (dicalcium phosphate) + 58 mg Phosphorus (dicalcium phosphate).
The allithiamine in this is TTFD, also known as Fursultiamine, developed by the Japanese Takeda, the company that produces Alinamin Ex Plus which I take.
All ingredients and benefits in this are listed here.

 

[Asklipia]

An interesting article about the different types of lipophilic thiamines and their effects:
Benfotiamine, a synthetic S-acyl thiamine derivative, has different mechanisms of action and a different pharmacological profile than lipid-soluble thiamine disulfide derivatives
As @alicec warned, benfotiamine does not cross the BBB.

 

[Asklipia]

Also an interesting aspect of allithiamine is that it is not affected by thiaminase. Since I don't intend to stop eating raw oysters.

 

[Chocolove]

Also an interesting aspect of allithiamine is that it is not affected by thiaminase. Since I don't intend to stop eating raw oysters.

The last time I had a raw oyster I was a child, sitting across the table from my father, a proudly vicious Marine Corps Drill Seargeant. Suddenly, the oyster I had just swallowed shot out of my mouth like a cannon squarely hitting my ferocious father in the chest. We were both so stunned I escaped certain death by Dad.

Diagnosis...Projectile vomiting most probably caused by Vibrio vulnificus is a rod-shaped bacterium that can tolerate salt, unlike most bacteria. It is a natural inhabitant of marine environments which concentrates in filter feeders such as oysters, especially found in areas with low salinity (0.5 to 2.0% sodium chloride) i.e., near shorelines and in estuaries where freshwater from rivers mixes with ocean saltwater, common to warmer waters such as along the coast of the Gulf of Mexico.

The overall mortality rate for V. vulnificus infection is 40%. No doubt this explains why my body was so quick and violent in expulsion of the oyster.
http://safeoysters.uga.edu/consumers/index.htm

Do you happen to have a source on the allithiamine not being affected by thiaminase?

 

[caledonia]

Yup, agreed.

Re: ALA, the dose makes all the difference in my experience. This is all anecdotal of course but standard dosing was massive amounts administered infrequently was clearly negative/harmful. Low dosing was shockingly beneficial but the sweet spot dose varied from day to day, week to week, month to month. It required a great deal of intuition and tinkering to get it right. I had to start with just 6 mg and slowly work up to 50 and eventually 100 mg q3h. Then that became too much and I had to go back down to 25 mg. Tricky substance. It seems to raise functional capacity and improve muscle power objectively (for instance, being able to squat and climb stairs for the first time in years) while at the same time increasing that subjective sensation of fatigue. Hard to explain.

You accidentally (almost) discovered the Cutler frequent dose chelation protocol.

Cutler uses frequent doses of ALA around the clock in rounds of a few days to chelate out mercury and other metals. Then take a break for several days to allow your body to recover.

The thing where you were able to increase the dose, but then had to drop back to a lower dose, could possibly be what Cutler calls the dump phase.

Or you overwhelmed your liver, adrenals, etc. by not chelating properly.

See my signature link for more info on the Cutler protocol.

ps. I am currently chelating using this protocol, and do get a bit of energy while I'm using the ALA.

 

[caledonia]

Yes, B1 is co-factor for the carbohydrate metabolism and citric acid cycle, also the active forms of B2 and B3 and lipoate (aka alpha lipoic acid). The toxic metals mercury and arsenic also inhibit this pathway.

https://www.ncbi.nlm.nih.gov/books/NBK22340/

I have testing which shows abnormalities in the carbohydrate metabolism and citric acid cycle. I've tried B1 and B2 and don't tolerate them. B3 above a certain amount slows the methylation cycle, which is also showing up inhibited in my tests.

I also have testing showing mercury and arsenic, and have many symptoms of those.

This is one reason I'm chelating them out using the Cutler frequent dose chelation protocol with ALA.

It's still early days, but I do get a bit of energy while taking the ALA.

Note, there is a right way and a wrong way to take ALA. It's easy to make yourself much worse.

See the Cutler frequent dose chelation link in my signature link for more info.

 

[Sidereal]

You accidentally (almost) discovered the Cutler frequent dose chelation protocol.

I didn't. I read his books years ago and followed his ALA dosing protocol because I was intrigued to read on chelation forums that some people were improving on the ALA which they attributed to an obviously completely incorrect explanation (mercury chelation). ALA was very helpful but after a number of months of doing this, ALA worsened my peripheral neuropathy and started to really wear me out. These problems were eliminated with allithiamine.

Lipoic acid and thiamine are cofactors in the pyruvate dehydrogenase complex. If you want to understand why ALA helps a bit in ME/CFS sometimes, it would be best to read the recent scientific studies about metabolomics in ME/CFS instead of regurgitating Cutler's writings from 15+ years ago when nothing was known about this condition.