Thiamine (Vitamin B1) - A common deficiency in disorders of energy metabolism, cardiovascular and nervous system dysfunction

Keyhole

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Thiamine for kidney stones or bladder stones

Thiamine TTFD shown to significantly increase stone ejection when compared with controls. The mechanism of action is likely related to TTFD's excitatory action on the nerve cells lining the urinary tract. It has been used to treat bladder problems, such as urinary retention, incontinence, and neurogenic bladder.

In activated the nervous system "down there", it helps to propel stones out of the body through increasing peristalsis.

1) On 659 cases of lithureteria seen in urology departments of 52 main hospitals in all Japan, statistical observation was made on the effect of TTFD promoting discharge of the calculi.

2) Upon such 4 major factors as drug administration, sex, location of the calculi and size of calculi, variance analysis was performed concerning number of days required for drainage of calculus and transition of calculus. All of 4 factors were highly significant.

3) The results of x2-test on the number of days from the initial colic pain to discharge of calculus showed that the dranage is promoted in TTFD injected gronp compared to controls with, significant difference in the cases with the calculi located in the lower part of the ureter.

4) The results of X2-test on the number of days from clinical confirmation of presence of calculus to drainage of calculus showed that the discharge is promoted in TTFD injected group with significant difference in the cases of calculi located in the middle part of the ureter among those dranged them within a month and in upper and middle parts of the ureter among those discharged them within two months, respectively.

5) The results of x2-test on the number of days from the initial colic pain to discharge of calculus showed that the discharge is promoted in TTFD injected group compared to the controls with significant difference in cases with the size of calculi 5~10mm×0.5mm among those discharged them within 2 months.

6) The results of same x2-test on the number of days from the confirmation of presence to discharge of calculus showed that the discharge is promoted not only in TTFD injected group but ALSO IN TTFD ORALLY administered group than controls with significance.

7) The results of the cumulative discharge rate pursueing the days required for discharge indicated that the drainage is especially accelerated in TTFD injected group. The rate was higher in the male group than in the female when it was calculated from the time of initial colic pain. The cumulative discharge rates by location and size of the calculus showed better effectiveness of the drug in the groups of middle part of the ureter and small calculi, respectively.

8) Based on the results of analysis, it was concluded that the use of TTFD, especially injection of it, is capable of promoting the discharge of ureteral calculi in comparison with non-administered controls.
https://repository.kulib.kyoto-u.ac.jp/dspa…/handle/…/113235

Thiamine TTFD was also shown to increase urinary oxalic acid levels:

Effect of Administration of Thiamine Tetrahydrofurfuryl Disulfide and Citric Acid on the Urinary Vitamin C and Oxalic Acid Excretion

"The present investigation was undertaken to study the effects of TTFD and citric acid on the urinary vitamin C and oxalic acid excretion in adult humans.In the first experiment, 4 adults ingested 50mg of TTFD daily for 4 days. In the second experiment, 4 adults ingested 5 g of citric acid for 4 days. By the administration of TTFD, rate of utilization of vitamin C was steadily increased, and the amount of urinary oxalic acid also increased.

By the administration of citric acid, the rate of vitamin C utilization was lowered, especially in the patients of anemia and it caused the deficiency of vitamin C which suggests some disturbances of its utilization. The influence of citric acid was considerably strong."
https://www.jstage.jst.go.jp/…/38_KJ0000…/_article/-char/ja/
 

Keyhole

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Here is a little post I wrote on the relationship between intracellular electrolytes (potassium) and thiamine. It seems that people can become deficient on the intracellular level, whilst maintaining "normal" blood measurements.

Whilst I always suspected a direct link between potassium & thiamine deficiency (outside of the context of refeeding syndrome), I had not come across any direct research elucidating the mechanisms – until NOW. In short, thiamine deficiency causes intracellular potassium wasting:

Thiamine TTFD, Intracellular Potassium Deficiency, and the Heart ♥️

Animal research in rats showed that chronic thiamine deficiency increases sodium tissue content in heart, liver and skeletal muscle by 18-35%, while also decreasing potassium content by 18-25%[1]. Interestingly, although tissue levels were altered, plasma levels of these electrolytes remained unaffected and stayed within the normal-high range (sodium at 141.6 & potassium at 4.8). This means that blood measurements did NOT reflect tissue content.

The thiamine deficient group also displayed remarkably lower levels of stored liver glycogen (0.3gm/100 vs 2.7gm/100 in controls). This inability to store glycogen is one factor which helps to explain the strong tendency towards hypoglycemia seen in many people with a thiamine deficit.

Interestingly, the researchers showed a shift towards an increased level of extracellular water and reduced intracellular water. This finding, along with the shift in intracellular electrolyte concentrations, is 100% consistent with Ling’s Association-Induction hypothesis.

In short, the bioenergetic state of the cell governs its ability to retain potassium ions and structure water into a gel-like phase. A cell with plentiful ATP can maintain this ability, independent of the “sodium potassium pump”. On the other hand, cells lacking energy lose their capacity to retain potassium, intracellular water becomes “unstructured”, intracellular concentration of sodium ions increases and the electronic state of the cell is changed. This causes water to “leak” out of the cells into the extracellular space to produce a localised edema of sorts. Thiamine, playing a CENTRAL role in energy metabolism, is partially responsible for maintaining healthy redox balance & a continual supply of ATP. Hence, it is no wonder why a deficiency of this essential nutrient produces such drastic changes in the cellular electrolyte balance.

The cells of the heart are particularly susceptible to a disturbance in electrolytes. One Japanese study on coronary insufficiency in dogs showed elevated sodium and reduced potassium content in the insufficient left ventricle [2]. Intravenous administration of 50mg thiamine TTFD restored electrolyte balance, likely through improving tissue energy metabolism, to increase potassium and reduce sodium content.

Likewise, the same effect was also demonstrated in isolated Guinea pig atria kept in potassium-free medium [3]. TTFD added to cells or administered as a pre-treatment prevented to loss of potassium and increase in sodium which was shown to occur in controls. Importantly, this effect was NOT achieved by thiamine HCL or another derivative studied. TTFD also entered the atrial cells much more readily than other forms.

Low potassium is a known driver of cardiac arrhythmias, and TTFD possesses anti-arrhythmic properties [4] and has historically been used to treat various types of arrhythmia in Japan.

Furthermore, thiamine TTFD was also been shown to be protective against the cardiac toxin Strophanthin-G, preventing the loss of potassium once again to preserve cardiac function [5]. Likewise, atrial cell damage through exposure to the mitochondrial toxin N-ethylmaleimide was also prevented by high concentrations of TTFD in-vitro [6]. This protective action was attributed to the prosthetic group specific to TTFD, and NOT the thiamine molecule itself.

So it would seem that thiamine, probably through its effects on energy metabolism inside cells, and perhaps due to an unknown “kosmotropic” property of TTFD [?], is extremely important for regulating cell ion concentrations. In thiamine deficiency, an underlying intracellular potassium deficiency may be going unnoticed due to unremarkable blood levels.

References

1. Pecora, L. J. (1952). Electrolyte Changes in Tissues of Chronic Thiamine Deficient Rats and Influence of Certain Steroids. American Journal of Physiology-Legacy Content, 169(3), 554–560. doi:10.1152/ajplegacy.1952.169.3.554

2. Ichihara, I. (1964) EFFECTS OF VITAMINS ON ELECTROLYTES METABOLISM IN CARDIAC MUSCLE OF EXPERIMENTAL CORONARY INSUFFICIENCY DOG. doi: https://doi.org/10.20632/vso.30.2_168

3. SHINOZAKI, H. MORITA, M. SUGIMOTO, J. NAGATA, M. (1971) Thiamine Tetrahydrofurfuryl Disulfide and Potassium Ions in Atria. doi: https://doi.org/10.20632/vso.44.1_37

4. Tsunoda, Y. PHARMACOLOGICAL AND CLINICAL STUDIES ON THE ANTIARRHYTHMIC PROPERTY OF THIAMINE AND ITS DERIVATIVES, COCARBOXYLASE AND THIAMINE TETRAHYDROFURFULYLDISULFIDE. doi: https://doi.org/10.20632/vso.36.6_567

5. SUGIMOTO, J., NAGATA, M., & NISHIKUBO, Y. (1973). THE INFLUENCE OF THIAMINE TETRAHYDROFURFURYLDISULFIDE AGAINST STROPHANTHIN-G TOXICITY IN GUINEA-PIG ATRIA. Japanese Circulation Journal, 37(5), 491–496. https://doi.org/10.1253/jcj.37.491

6. Nishikubo, Y. (1979). Protective Effect of an Alkyl Disulfide Compound against the Toxic Action of N-Ethylmaleimide (NEM) in Isolated Rat Atria. The Journal of Kansai Medical University, 31(1), 90–101.
https://doi.org/10.5361/jkmu1956.31.1_90
 

Keyhole

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In Japan, TTFD is well known to address upper-GI constipation. A common phenotype I see, usually in prime-age males, is severe constipation with bloating, GERD, gastroparesis, and maldigestion. These symptoms are usually accompanied by fatigue, some cardiovascular and neurological abnormalities also. Many times, high dose TTFD can address the issue within a few days. I actually had one fella who was only able to pass a bowel movement usually once every 2-3 weeks! Within a few days of TTFD, he has been regular ever since. I actually see this happening very often.

When Gut Issues, SIBO & IBS-Constipation are just unrecognized thiamine deficiency:

In many people, chronic upper constipation and GERD are misdiagnosed as bacterial overgrowth. Unfortunately, they are often non-responsive to antimicrobial treatments. Yet, sometimes the issues are literally fixed within a few days of vitamin B1 repletion. This has shown me that often times, the "SIBO" or "IBS" is simply a symptom of an underlying systemic problem.

The gastrointestinal tract is one of the main systems that can be affected by a deficiency of thiamine (vitamin B1). Clinically, a severe deficiency in this nutrient can produce a condition called “Gastrointestinal Beriberi”, which in my experience is massively underdiagnosed and often mistaken for SIBO or IBS-C. The symptoms may include GERD, gastroparesis, slow or paralysed GI motility, inability to digest foods, extreme abdominal pain, bloating and gas. People with this condition often experience negligible benefits from gut-focused protocols, probiotics or anti-microbial treatments. They also have a reliance on betaine HCL, digestive enzymes, and prokinetics or laxatives.

So let’s examine why thiamine is essential for maintaining a healthy gut, and what happens in a deficiency.

The GI tract possesses its own individual enteric nervous system (ENS), often referred to as the "second brain". Although the ENS can perform its job somewhat autonomously, inputs from both the sympathetic and parasympathetic branches of the autonomic nervous system serve to modulate gastrointestinal functions. The upper digestive organs are mainly innervated by the vagus nerve, which exerts a stimulatory effect on digestive secretions, motility, and other functions. Vagal innervation is necessary for dampening inflammatory responses in the gut and maintaining gut barrier integrity [1]

The lower regions of the brain responsible for coordinating the autonomic nervous system are particularly vulnerable to a deficiency of thiamine. Consequently, the metabolic derangement in these brain regions caused by deficiency produces dysfunctional autonomic outputs and “misfiring”, which goes on to exert detrimental effects on every bodily system - including the gastrointestinal organs.

However, the severe gut dysfunction in this context is not only caused by faulty central mechanisms in the brain, but also by tissue specific changes which occur when cells lack thiamine. The primary neurotransmitter utilized by the vagus nerve is acetylcholine. Enteric neurons also use acetylcholine to initiate peristaltic contractions necessary for proper gut motility. Thiamine is necessary for the synthesis of acetylcholine and low levels produce an acetylcholine deficit [2], which leads to reduced vagal tone and impaired motility in the stomach and small intestine.

In the stomach, thiamine deficiency inhibits the release of hydrochloric acid from gastric cells [3] and leads to hypochlorydria (low stomach acid). The rate of gastric motility and emptying also grinds down to a halt, producing delayed emptying, upper GI bloating, GERD/reflux and nausea [4]. This also reduces one’s ability to digest proteins. Due to its low pH, gastric acid is also a potent antimicrobial agent against acid-sensitive microorganisms. Hypochlorydria is considered a key risk factor for the development of bacterial overgrowth.

The pancreas is one of the richest stores of thiamine in the human body, and the metabolic derangement induced by thiamine deficiency causes a major decrease in digestive enzyme secretion [5] . This is one of the reasons why those affected often see undigested food in stools. Another reason likely due to a lack of brush border enzymes located on the intestinal wall, which are responsible for further breaking down food pre-absorption. These enzymes include sucrase, lactase, maltase, leucine aminopeptidase and alkaline phosphatase. Thiamine deficiency was shown to reduce the activity of each of these enzymes by 42-66%. [6].

Understand that intestinal alkaline phosphatase enzymes are responsible for cleaving phosphate from the active forms of vitamins found in foods, which is a necessary step in absorption. Without these enzymes, certain (forms of) vitamins including B6 (PLP), B2 (R5P), and B1 (TPP) CANNOT be absorbed and will remain in the gut. Another component of the intestinal brush border are microvilli proteins, also necessary for nutrient absorption, were reduced by 20% in the same study. Gallbladder dyskinesia, a motility disorder of the gallbladder which reduces the rate of bile flow, has also been found in thiamine deficiency [7].

Together, these factors no doubt contribute to the phenomena of “malnutrition induced malnutrition”, a term coined by researchers to describe how thiamine deficiency can lead to all other nutrient deficiencies across the board. In other words, a chronic thiamine deficiency can indirectly produce an inability to digest and absorb foods, and therefore produce a deficiency in most of the other vitamins and minerals. In fact, this is indeed something I see frequently. And sadly, as thiamine is notoriously difficult to identify through ordinary testing methods, it is mostly missed by doctors and nutritionists.

To summarize, B1 is necessary in the gut for:

- Stomach acid secretion and gastric emptying
- Pancreatic digestive enzyme secretion
- Intestinal brush border enzymes
- Intestinal contractions and motility
- Vagal nerve function


Based on the above, is it any wonder why thiamine repletion can radically transform digestion? I have seen miracles with B1 repletion. Many individuals with “SIBO & “IBS”, who were unable to pass a bowel movement for weeks at a time, began going regularly and no longer required digestive aids after addressing their thiamine deficiency.

In fact, the ability of thiamine to address these issues has been known for a long time in Japan. Specifically, the form of thiamine shown to be superior in several studies is thiamine TTFD.

One study investigated the effect of TTFD on the jejunal loop of non-anesthetized & anesthetized dogs. They showed that intravenous administration induced a slight increase in tone and a “remarkable increase” in the amplitude of rhythmic contractions for twenty minutes. Furthermore, TTFD applied topically inside lumen of the intestine also elicited excitation [8].

Another study performed on isolated guinea pig intestines showed provided similar results [9], where the authors concluded that the action of TTFD was specifically through acting on the enteric neurons rather than smooth muscle cells.
Along with TTFD, other derivatives have also been shown to influence gut motility. One study in rats showed an increase in intestinal contractions for all forms of thiamine including HCL, BTDS, TTFD, and TPD [10]. Another in white rats also found most thiamine derivatives to be effective within minutes [11].

Most interestingly, thiamine derivatives were studied in mice with artificially induced constipation by atropine and papaverine. The researchers tested whether several thiamine derivatives could counteract the constipation – TPP, Thiamine HCL, TTFD, BTDS (S-Benzoyl thiamine disulphide - somewhat similar to benfotiamine). Of all the forms of thiamine tested, TTFD was the ONLY one which could increase gut motility. Furthermore, they ALSO showed that TTFD did not increase motility in the non-treatment group (non-poisoned with atropine). This indicated that TTFD did not increase motility indiscriminately, but only when motility was dysfunctional [12]

Severe constipation and gastroparesis have been identified in patients with post-gastrectomy thiamine deficiency, and three days of I.V TTFD at 100mg followed by 75mg orally produced improvement in gastroparesis within a few weeks [13].

REFERENCES
1. Bonaz, B., Bazin, T., & Pellissier, S. (2018). The Vagus Nerve at the Interface of the Microbiota-Gut-Brain Axis. Frontiers in Neuroscience, 12. https://doi.org/10.3389/fnins.2018.00049
2. Nakagawasai O, Tadano T, Hozumi S, Tan-No K, Niijima F, Kisara K, (2000) Brain Res Bull. Jun; 52(3):189-96.
3. Levin LG; Mal’tsev GIu; Gapparov MM. (1978). [Effect of Thiamine Deficiency in Hydrochloric Acid Secretion in the Stomach].
4. Tjong, E., & Peng, Y.-Y. (2019). Gastrointestinal Beriberi and Wernicke’s Encephalopathy Triggered by One Session of Heavy Drinking. Case Reports in Neurology, 11(1), 124–131. https://doi.org/10.1159/000499601
5. Singh, M. (1982). Effect of thiamin deficiency on pancreatic acinar cell function. The American Journal of Clinical Nutrition, 36(3), 500–504. https://doi.org/10.1093/ajcn/36.3.500
6. Mahmood, S., Dani, H. M., & Mahmood, A. (1984). Effect of dietary thiamin deficiency on intestinal functions in rats. The American Journal of Clinical Nutrition, 40(2), 226–234. https://doi.org/10.1093/ajcn/40.2.226
7. Tjong, E., & Peng, Y.-Y. (2019). Gastrointestinal Beriberi and Wernicke’s Encephalopathy Triggered by One Session of Heavy Drinking. Case Reports in Neurology, 11(1), 124–131. https://doi.org/10.1159/000499601
8. Hukuhara, T. Nanba, R. Siina, H. Effect of Thiamine Tetrahydrofurfuryl Disulfide upon the Intestinal Motility (1965). doi: https://doi.org/10.20632/vso.31.5_398
9. HUKUHARA, T., & FUKUDA, H. (1965). The effects of thiamine tetrahydrofurfuryl disulfide upon the movement of the isolated small intestine. The Journal of Vitaminology, 11(4), 253–260. https://doi.org/10.5925/jnsv1954.11.253
10. Fujioka, F. Ichitsuki. S. Suzuki, T. Sahashi, K. (1966). Effects of vitamin B1 and its derivatives on the intestinal motility of the isolated rat. doi: https://doi.org/10.20632/vso.34.4_390
11. Sahashi, K. Fujioka, F. Maekawa, A. Hitotsuki, S. Suzuki, T. (1965) Effects of vitamin B_1 and inosine on the intestinal motility of the white rat (Abstracts of the Papers Presented at the 155th Conference). doi: https://doi.org/10.20632/vso.31.1_95_4
12. Nagata, M. & Sugimoto, J. (1973) Experimental constipation in mice by combined use of Atropine and Papaverine and examination of sub-lagging action of Bisacodyl, Casanthranol, magnesium sulfate, rhubarb and Thiamine derivatives. doi: https://doi.org/10.5361/jkmu1956.25.3_300
13. Koike, H. (2001). Postgastrectomy polyneuropathy with thiamine deficiency. Journal of Neurology, Neurosurgery & Psychiatry, 71(3), 357–362.
https://doi.org/10.1136/jnnp.71.3.357
 

mrtn

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Thanks, you're right, I have a bottle and looked it up. I wondered because the first paragraph here says that it "is similar in structure to allithiamine".
 

Keyhole

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Thanks, you're right, I have a bottle and looked it up. I wondered because the first paragraph here says that it "is similar in structure to allithiamine".
"Allithiamine" the supplement is the same thing as fursultiamine, or TTFD. It is a molecule of thiamine with a prosthetic mercaptan group attached to the sulfur atom of the thiamine to form a disulfide bridge. This is made by reacting thiamine with a form of allicin, the chemical found in garlic.

TTFD is very similar in structure to the GENUINE form of allithiamine, which is only found in garlic. The problem with genuine allithiamine was that anyone who took it stunk like garlic for days afterwards. That is why TTFD was originally produced, to provide the same chemical benefits of allithiamine, but without the gross smell that accompanied it.
 

Beau

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Awesome work Keyhole. Looking forward to trying this out to see if it helps with some bladder discomfort I've been experiencing off and on for the last 2-3 months.
 

jhonny

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I agree wholeheartedly. I've just watched your last few videos on you tube( one a repeat watch ) and to a non medical person your presentation is clear, detailed and most important for the lay person, understandable. Thank you
I absolutely agree! In fact, Elliot's presentations makes it less difficult (given the complexity of the subject) even for people like me, whose mother tongue is not English.
Thank you @Keyhole
 

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Keyhole

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Thiamine TTFD – Nerve Damage, Trigeminal Neuralgia, and Hearing Loss

Neuropathy is a well established consequence of chronic thiamine deficiency. It is known that thiamine supports nerve conduction, and plays several roles in maintaining healthy neurological function in both the central and peripheral nervous systems.
Damage to nerves in the periphery might produce paraesthesia (tingling), burning, numbness, or even chronic pain. A few symptoms of central injury can include hearing loss/deafness, visual disturbances or blindness.

One reason for nerve damage in thiamine deficiency relates to a downregulation of transketolase, which is an enzyme involved in the pentose phosphate pathway. One function of this pathway is to provide reducing power for the regeneration of glutathione, the primary intracellular antioxidant. In thiamine deficiency, a lack of reduced glutathione renders nerve tissue susceptible to injury from oxidative onslaught.

The downregulation of transketolase is also especially dangerous when paired with hyperglycaemia. Elevated flux of glucose through the glycolytic pathway produces a build-up of specific intermediates which, in the context of low transketolase activity, are shunted towards alternate pathways (polyol, protein kinase C, hexosamine, and AGE) [1].

The consequences of this include increased protein glycation, inflammation, glutathione depletion, and oxidative stress. Together, these effects contribute to the destruction of nervous tissue and eventual neuropathies.

Various forms of thiamine have been shown to address peripheral nerve damage through increasing transketolase activity, restoring normal function of the pentose phosphate pathway and improving cellular energy metabolism.

In the central nervous system, thiamine plays central roles in maintaining healthy myelin sheath and brain function. In fact, thiamine is so important for a healthy brain that a severe deficiency can produce substantial neurological damage which, in some cases, is thought to be irreversible.

In addressing chronic thiamine deficiency, it is important to use a form which has been shown to penetrate the brain via the blood brain barrier, so that it is capable of saturating both central and peripheral cells. Here is where disulfide forms of thiamine such as TTFD can come in handy.

The actions of thiamine disulfides (TPD & TTFD) on nerve damage and regeneration were studied extensively throughout the 1950s and 60s in Japan. It was recognised that these forms were superior to thiamine HCL and TPP.

Thiamine TPD was shown to increase axonal growth in chick embryos by 1.5 times, whilst very large doses could regenerate the sciative nerve in rabbits. The same researchers demonstrated remarkable protection of neurons against damage (polyneuritis) from acrylamide poisoning with ultra high concentrations of TPD [2].

In another study, three B vitamins (B1 as TTFD, B6 as P5P & B12 as OH-B12) were administered to diabetic white rats with sciatic nerve damage and Schwann cell atrophy [3]. The nutrients were each given separately or as a combination, and the only individual nutrient capable of reducing nerve damage and atrophy was TTFD.

However, the interesting finding was that when ALL THREE vitamins were administered together in combination, this provided the best results. This finding is in support of Lonsdale’s findings that thiamine was best administered in conjunction with the other B vitamins for maximal effect.

TTFD was also found to reduce vibratory perception in patients diabetic neuropathy [4]. A combination of riboflavin (7.5mg) and TTFD (75mg) proved effective for reducing neuropathic sensations after 1-3 months. This was also accompanied by improved tolerance of fructose and reduced levels of pyruvate and a-ketoglutarate.

Stabbing pain, burning or tingling sensations of the face can be caused by neurological damage as part of a condition called trigeminal neuralgia. In one study, researchers investigated whether two different forms of thiamine could improve TGN symptoms [5]. They used 100mg of thiamine HCL and 15-90mg of thiamine TPD.

Although both therapies provided benefits, TPD was shown to be far more effective (78%) for reducing, or in some cases, completely eliminating trigeminal neuralgia pain.

The thiamine disulfides have also shown promise in addressing hearing difficulties and improving sensory perception. A series of experiments were performed on the effects of intravenous TTFD (50mg) on acoustic hearing mechanisms[6].

Hearing acuity increased for 6 hours post-administration, whilst temporary hearing loss after high level sound exposures (temporary threshold shift) was also improved. The researchers theorised that TTFD exerted a positive influence on the acoustic neural mechanism at the synaptic level.

A separate study on neural deafness investigated the effects of oral and intravenous administration of TTFD [7]. One method involved 50mg TTFD and 50mg riboflavin orally, and the other involved 50mg TTFD injected intravenously. Both I.V and oral routes were similarly effective in providing satisfactory improvement in hearing, and this also included a case of long-term deafness from streptomycin poisoning of three years.

Another much larger study used an oral dose of 150mg TTFD daily in 267 patients with perceptive deafness [8]. Importantly, they showed that in those who commenced treatment within one week of symptom onset, TTFD proved to be 79.2% effective.

Furthermore, treatment was 74.3% effective in those who started treatment within one month of symptom onset
. In contrast, long-term disease was much less responsive to therapy, and so this reduced the overall effectiveness to a total of 34.5%. Based on these results, the authors emphasised that TTFD should be started immediately to increase chances of recovery in this condition.


REFERENCES
1. Page GLJ, Laight D, Cummings MH. Thiamine deficiency in diabetes mellitus and the impact of thiamine replacement on glucose metabolism and vascular disease. International Journal of Clinical Practice. 2011;65(6):684-690. doi:10.1111/j.1742-1241.2011.02680.x
2. Nakazawa, T, Kuroshima A, Komiya H, Inokari Y, Hozumi N. Basic study on recovery of nerve function: Significance of biological administration of Thiamine propyldisulfide in large dose. J-Stage. 1965;32(5):434-447. doi:10.20632/vso.32.5_434
3. Ikeda, Fukuda N, Shino C, Iwatsuka K, Yuji N. Effects of Vitamin B1 on Sciatic Nerve Damage in Alloxan Diabetic White Rats: Especially Effects of B6 and B12 on B1 Effects. J-Stage. 1979;53(12):523-529. doi:10.20632/vso.53.12_523
4. Zhengjiu H, Yukio F, Yukiji N, Yuanliang Q. The effect of the treatment of the vibration of the limbs in patients with diabetes. J-Stage. 1964;29(4):249-254. doi:10.20632/vso.29.4_249
5. Hachiro T, Akio S. High-unit Vitamin B1 and Alinamin (Vitamin B1 derivative) Therapy for Trigeminal Neuralgia. Journal of Oral Surgery Society of Japan. 1955;1(1):24-26. doi:10.5794/jjoms1955.1.24
6. Yoshihara Yu, Hiramatsu Yoshiro, Fujimori Keman, Tsujiu Hisao, Hashimoto Hilight. Efficacy of alinamin (TTFD) for hearing fatigue, with special reference to its mechanism of action. J-Stage. 1965;29(4):249-254. doi:10.20632/vso.29.4_249
7. YAMANAKA Y, MATSUMORI S, OHTA Y, KONISHI Y. Effect of Alinamin F on Deafness. Practica Oto-Rhino-Laryngologica. 1963;56(10):568-573. doi:10.5631/jibirin.56.568
8. HIROTO I, HIRANO M, HAGIO R, SUEYOSHI K, OHNO T. Massive Dosage Alinamin F Therapy of Perceptive Deafness. Practica Oto-Rhino-Laryngologica. 1964;57(2):98-103. doi:10.5631/jibirin.57.98
 

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OK, so this article has taken me the best part of a week to research, write, and reference.


Why does high-dose thiamine help people with EMF-hypersensitivity? Can thiamine in high doses help to protect the brain against EMFs?

This is a long and detailed post. I have written this to highlight some of the possible reasons why people with EMF-sensitivity appear to benefit greatly from thiamine TTFD supplementation in high doses. To be clear, we are not simply looking at "nutritional supplementation". Instead, thiamine can be used in a pharmacological way to "kickstart" enzymes which are downregulated by oxidative stress. In other words, thiamine can be used as a tool even when thiamine status is "normal" to boost innate defenses.

SUMMARY:

- EHS/EMF-Sensitivity is a genuine physiological condition characterised by altered biomarkers associated with oxidative stress

- EMF exposure alters levels of neurotransmitters including acetylcholine, dopamine, norepinephrine, and glutamate. Excess glutamate may produce excitotoxicity, which can lead to cell death.

- EMF exposure produces damage to neurons and brain tissue via increased generation of ROS

- EMF exposures can damage mitochondria in several ways to cause mitochondrial dysfunction, which further enhances ROS production and reduces ATP

- The oxidative burden associated with chronic EMF is associated with reduced levels of antioxidants including melatonin, glutathione, and other antioxidant enzymes.


THIAMINE FOR CELL PROTECTION

- Thiamine’s key role as a cofactor in mitochondrial energy metabolism to support ATP synthesis, with high doses bypassing mitochondrial dysfunction produced by brain injury

- Thiamine’s role in supporting the antioxidant system through the pentose phosphate pathway, boosting endogenous antioxidant enzymes shown to protect the brain against oxidative stress and toxicity

- As a site-directed antioxidant to combat ROS

- Thiamine’s ability to protect cells against neurotransmitter imbalances including glutamate excitotoxicity, and in supporting myelin synthesis.

- Thiamine TTFD’s ability to cross the blood brain barrier, saturate brain cells, and provide a secondary antioxidant molecule in the form of a prosthetic mercapatan group.


Is EMF-Sensitivity/EHS a real condition?

I have many clients who are sensitive to (electromagnetic frequencies/ radiation), and several respond very well to specific nutrients. One of those nutrients is thiamine tetrahydrofurfuryl disulfide.

For those who are not aware, electromagnetic hypersensitivity syndrome is characterised by collection of symptoms which manifest when someone comes in close contact with non-native electromagnetic frequencies. Non-native refers to the unnatural, man-made EMF emitted from electronic devices, mobile phones, Wifi, dirty mains electricity, and overhead power lines etc.

The symptoms of EHS are wide and varied in number, but they typically include brain fogginess, insomnia, skin rashes, palpitations, anxiety, depression, physical sensations of pain, headaches and migraines, neuropathies and parasthesias, and burning sensations in the limbs.

Unfortunately, many patients with this condition are dismissed by their physicians, who consider the origin of these symptoms to be purely “psycho-somatic”.

Despite conventional medical claims that EHS is primarily “psychosomatic”, there have been several researchers who have demonstrated real, physiological changes occurring in EHS. These changes are indicative of increased levels of oxidative stress like those found in multiple chemical sensitivity syndrome. Patients with EHS were found to have increased blood concentrations of malondialdehyde (a lipid peroxide), oxidized glutathione, and nitrotyrosine. Beneficial glutathione-associated biomarkers were lower in 20-40%, and RBC superoxide dismutase and glutathione peroxidase activity were increased in 60% & 19%, respectively. Overall, this trial showed that 80% of EHS sufferers presented with one, two or three elevated biomarkers of oxidative stress [1].

In another study, EHS patients were shown to have higher levels of oxidized antioxidants vitamin E and coenzyme Q10 [2]. RBC glutathione-S-transferase was decreased, along with reduced glutathione. Furthermore, genetic analysis identified two genotypes related to glutathione status [GSTM1 (*0/*0) + GSTT1 (*0/*0)] which were more common in EHS sufferers compared with controls. This specific combination conferred a 9.7 times higher risk of developing EHS, which suggests that some people may be more genetically susceptible to developing this condition than others.

EHS patients were matched with controls in a study measuring cortical excitability parameters using transcranial magnetic stimulation [3]. Those with EHS were found to display significant differences in cognitive and neurobiological activity, demonstrating genuine functional changes in brain function which occur in this condition. One individual with self-diagnosed EHS was shown to have abnormalities on functional MRI scanning which looked similar to traumatic head injury [4]. Whilst another double-blinded case study demonstrated clear somatic responses to EMF exposure which included muscle twitching, arrhythmia, headache and temporal pain [5].

Some researchers have proposed that EMF-sensitivity may be related to heavy-metal toxicity and exposure. Although one study showed no differences in blood metal concentrations in EHS [6], it is well established that blood levels are not always reflective of tissue metal concentrations. Case studies in Japan correlated dental titanium implants with EHS-related symptoms such as vertigo and dizziness. Interestingly, these symptoms disappeared after the metal implants were removed, leading the researchers to theorize that the titanium was acting as some form of “antennae” for EMF radiation [7].

In addition, the EMF emitted from mobile devices has the capacity to increase the release of mercury vapor from amalgam fillings into saliva [8]. The same effect can also occur through exposure to magnetic resonance imaging (MRI) scanning [9]. Since mercury is a highly neurotoxic substance, it is believed that heavy metal poisoning may be responsible for producing or exacerbating the symptoms associated with EHS.

Based on the above data, coupled with innumerable anecdotes, it would indeed appear that EHS is a genuine physiological condition. This condition appears to feature alterations in brain function, clear differences in biomarkers associated with increased oxidative stress, and somatic responses upon exposure to EMF devices.

However, this does not mean that EHS sufferers are the only ones who are negatively impacted by exposure to nn-EMF. In fact, there is a vast body of literature demonstrating substantial damage done to cellular systems upon exposure to this radiation. To go through all of the evidence would be frankly impossible, and even a comprehensive overview is way beyond the scope of this article.

However, to understand why the addition of specific nutrients may be beneficial in protecting the brain from the negative consequences of EMF exposure, we need to examine some of the processes that occur at the molecular level with irradiation.

EMF EFFECTS ON THE BRAIN

The exact mechanisms by which different frequencies of EMF interact with different cell types have not yet been fully characterised. It is thought to involve voltage-gated calcium channel activation and calcium efflux, resulting in elevated nitric oxide synthesis, peroxynitrite free radicals, neuro-inflammatory cascades and glutamate-neuro excitotoxicity. What is clear, however, is that mitochondrial dysfunction and oxidative stress are the main drivers behind EMF-induced brain injury.

The high rate of oxygen consumption and metabolism of the brain, coupled with its high neuronal membrane content of unsaturated fatty acids, make it uniquely susceptible to oxidative damage. This, paired with the fact that mobile devices are generally positioned in close proximity to the face and head, render the brain a prime target for electromagnetic radiation.

Neuro-excitotoxicity is a phenomenon characterised by excessive release of the excitatory neurotransmitter glutamate and subsequent activation of NMDA receptor and AMPA receptors. The persistent and extreme stimulation of neuronal activity yields high levels of reactive oxygen species (ROS), and eventually leads to cell degeneration and death. Excitotoxicity is considered to be one of the main underlying drivers behind neurodegeneration, brain injury and age-related cognitive decline.

EMF in the ELF range can indeed influence glutamate concentrations at the neuronal synapse, producing 40% higher or 35% lower concentrations depending on the frequency, intensity, and duration of exposure [10].

A variety of proteins involved in the glutamate receptor signalling pathway in the hippocampus were also significantly elevated after prolonged exposure to radio-frequency EMFs (900-1200MHz) [11].

RF-EMF exposure also enhanced glutamate-induced cytotoxicity and cell death in mouse hippocampal HT22 cells, and the introduction of an antioxidant (NAC) provided complete protection against this [12]. Together, these results suggest that excess glutamate may indeed play a key role in EMF-induced brain damage, and this is an important point to remember. However, there are also other neurotransmitters which are affected through EMF exposure, albeit in different ways.

Hippocampal acetylcholine release was decreased by 40% after exposure to 2.45 GHz radiation a 4mW/cm2, whereas it was unaffected at lower intensity [13]. Additionally, one hour of 800 MHz also produced no changes in acetylcholine, but 14 hours induced a 43% decrease. This suggests that changes in the cholinergic system of this brain region can be altered in different ways depending on the power output and frequency of radiation.

Another study showed significant disturbances in norepinephrine (noradrenaline), dopamine, and 5-hydroxytrypophan, with the authors concluding that these changes “may underlie many of the adverse effects reported after EMR including memory, learning, and stress.” [14]
Alterations in N-methyl-d-aspartate (NMDA) and GABAA receptors, along with dopamine transporters, were also found in rat brains exposed to 15 minutes of 900-MHz radiation emitted from a GSM device. That same study identified a strong glial reaction in the striatium region of the brain, potentially suggestive of neuronal damage [15].

A separate experiment showed that other areas of the brain including the cortex, hippocampus, and basal ganglia exhibited significant neuronal damage after rats were exposed to a GSM device for just 2 hours [16]. Numerous other studies have demonstrated neurobehavioral impairments [17], increase blood-brain barrier permeability [18], brain structure alterations [19] and cognitive deficits [20].

To make matters worse, 5 hours per day of 835 MHz RF-EMF caused great damage to the myelin sheath which resulted in demyelination. Just for your reference, myelin is the protective fatty coating which lines neurons, and is essentially responsible for facilitating the passage of signals from one neuron to the next. Without myelin, nerve signals cease and the nervous system as a whole is unable to effectively coordinate activity. Progressive demyelination has been identified in several neurodegenerative conditions, one of which is Multiple Sclerosis [21].

As I highlighted previously, the common offender in EMF-related tissue and cellular damage is disturbed redox balance and oxidative stress. The body’s main defence against this is the endogenous antioxidant system, which is tasked with protecting cells from the destructive effects of reactive oxygen species. When this innate system is unable to effectively manage oxidative injury, this is referred to as “oxidative stress”. Reduced antioxidant capacity in the context of elevated ROS can quite easily lead to nerce cell death and tissue destruction, so it is crucially important to maintain a healthy balance between oxidants and reducing agents.

Mitochondria, as the main metabolic hub responsible for energy synthesis in the cells, are known to be the main source of intracellular ROS. ROS generation occurs as a normal byproduct of energy metabolism and plays a variety of important signalling roles, but can increase to pathological levels when mitochondria are stressed, damaged and dysfunctional. And like I said before, perhaps one of the primary mechanisms behind EMF-induced damage is mitochondrial dysfunction.

Mitochondria appear to be quite susceptible to injury from EMFs. Long-term, low dose cumulative MW-EMF exposure leads to structural damage which includes swelling, cavitation, and broken cristae of mitochondria in the hippocampus and cortex [22].

Significant reductions in ATP synthesis by hippocampal mitochondria were found in rats exposed to pulsed MW [23], whilst succinate dehydrogenase, a key enzyme in energy metabolism, also demonstrated much lower activity. Another mitochondrial enzyme called Cytochrome C oxidase (COX) is also affected. COX sits at the last step of ATP synthesis, where it is tasked with transferring electrons to oxygen to produce H2O and ATP. After irradiation with MW-EMF, COX enzyme activity, COX mRNA, and COX I protein were significantly reduced [23].

The exact ways by which EMFs destroy mitochondrial integrity are not yet fully not understood, although it seems to include the following:

- EMF can lead to abnormal expression of genes encoding proteins in the respiratory chain, producing errors in energy metabolism [24]

- EMF can damage the mitochondrial membrane though altering molecular rotation, vibration and collision frequency to produce changes in membrane structure [25]

- The activation of NADH oxidase by EMF mediates an increase in ROS, which likely targets the mitochondrial membrane, disrupts mitochondrial efficiency, and overwhelms the cell. Dysfunctional mitochondria then go on to produce more ROS in a vicious cycle. ROS may also damage mitochondrial and nuclear DNA, create DNA strand breakages and mutations, and reduce energy synthesis capacity [26].

- Calcium efflux or “overload” can occur, where high concentrations of calcium ions flood into the cell through voltage gated calcium channels. This can activate the mitochondrial permeability transition pore, resulting in swelling, fragmentation, and even cell death [27].

The resulting consequence is that cells lose the ability to make energy in an efficient, or “clean” way. Mitochondria begin to spew out excessive ROS. Likewise, the ROS generated via other sources can quite easily overwhelm our endogenous protective systems to produce a catastrophic state of oxidative stress.

Pineal release of melatonin, the brain’s primary antioxidant and radical scavenger, is substantially reduced under exposure to specific frequencies of radiation
. Unfortunately, low melatonin is a key risk factor for the development of neurological dysfunction, neurodegeneration, and other pathologies including cancer of various kinds. Furthermore, key intracellular antioxidants including glutathione, catalase, and superoxide dismutase are also deteriorated through ELF-EMF exposure at 60Hz [28].

EMF emitted by mobile devices was found to deplete key glutathione biomarkers including GSH (reduce glutathione), glutathione peroxidase, glutathione reductase and glutathione s-transferase in rat brains. Malondialdehyde, a marker of lipid peroxidation, was also greatly elevated [29].

A different study on guinea pig brain tissue also showed a reduction in GSH, catalase, and elevations in malondialdehyde [30]. Together, these biochemical parameters are consistent with a state of excessive oxidative stress in the brain cells.

It is important that you know there are many other studies demonstrating effects consistent with this. Namely, that chronic EMF exposure takes a massive toll on the endogenous antioxidants.

To summarize so far:

- EHS/EMF-Sensitivity is a genuine physiological condition characterised by altered biomarkers associated with oxidative stress

- EMF exposure alters levels of neurotransmitters including acetylcholine, dopamine, norepinephrine, and glutamate. Excess glutamate may produce excitotoxicity, which can lead to cell death.

- EMF exposure produces damage to neurons and brain tissue via increased generation of ROS

- EMF exposures can damage mitochondria in several ways to cause mitochondrial dysfunction, which further enhances ROS production and reduces ATP

- The oxidative burden associated with chronic EMF is associated with reduced levels of antioxidants including melatonin, glutathione, and other antioxidant enzymes.


With the above in mind, I hope that you can appreciate the genuine dangers posed by exposures to these electronic devices and other sources of electromagnetic radiation. Whilst I believe that the best protection against this is strict avoidance, it is frankly not possible in our modern world. Sleep and circadian hygiene, intelligent movement, stress-management and a nutrient-dense diet are "no-brainers".

However, these changes are not always successful. The next best solution is to devise strategies to aid our cell’s ability to mitigate some of the damage through supporting mitochondria and reducing the oxidative burden. As we will examine next, thiamine possesses many of the characteristics which make it a useful candidate for supporting neurological health and protecting cells against some of the detrimental effects exerted by EMFs.

EMF & THIAMINE CONNECTION

First, I should make clear that no studies (to my knowledge) that have been done on the direct actions of thiamine in relation to EMF. However, my clinical experience with people who have EHS coupled with the mechanistic data justifies the use of this nutrient in my opinion. Thiamine’s benefits for the brain and neurological system are well-established, and a thiamine deficiency is known to primarily manifest as neurological dysfunction in many cases.

The mitochondrial dysfunction and oxidative stress induced by EMF no doubt increase thiamine requirements. On the other hand, an oxidative environment is also thoroughly detrimental to thiamine homeostasis. Not only does oxidation increase the need for thiamine in the brain, but oxidative stress also disturbs thiamine homeostasis and negatively influences the enzymes which use thiamine as a cofactor.

Protecting cells from the destructive consequences of excessive oxidation requires a continual supply of energy. The active form of thiamine (TPP) plays a coenzyme role for multiple enzymes required for the generation of this energy in the form of ATP. The pyruvate dehydrogenase complex (PDHC), sitting at the entry point to oxidative metabolism of glucose, requires thiamine as a cofactor. The rate of glucose metabolism has been shown to rapidly increase in response to EMF in brain regions closest the antennae [31]. Alone, this naturally increases thiamine turnover.

Alpha-ketoglutarate dehydrogenase (KGDH) is another thiamine-dependent mitochondrial enzyme complex involved in the TCA cycle. Of all of the enzymes involved in energy metabolism, KGDH is one of the most sensitive to oxidative stress [32].

Several biological effects associated with EMFs have been shown to inactivate this enzyme, including elevations of nitric oxide and peroxynitrate [33], along with high intracellular calcium concentrations [34]. Since KGDH is one of the rate-limiting steps in mitochondrial oxidative metabolism, an inhibition of this enzyme can have severe downstream consequences, slowing down the rate of energy metabolism and producing an ATP deficit. For this reason, the downregulation/inactivation of KGDH is thought to play an integral part in the development of neurodegenerative processes.

However, this enzyme complex is not only necessary for energy turnover, but also plays a dual role in protecting neurons from the damaging effects of excess glutamate. Through anaplerosis, glutamate is fed into the TCA cycle as the energy intermediate alpha-ketoglutarate. In the context of low KGDH activity, a “backlog” of alpha-ketoglutarate results in the accumulation of glutamate. In line with this, evidence shows that thiamine deficiency increases extracellular glutamate concentrations [35] to induce neurotoxic lesions in the brain [36]. A deficiency also reduces glutamate uptake in neurons [37], which ordinarily helps to reduce extracellular glutamate concentrations, and this occurs likely through downregulation of GLT-1 and GLAST glutamate transporters [38].

But the benefits of thiamine in protecting against glutamate excitotoxicity and mitochondrial dysfunction are NOT simply limited to those who are thiamine deficient. This point was wonderfully illustrated in a study on traumatic brain injury in rats [39]. Researchers found that pre-treatment with high dose thiamine (400mg/KG) completely prevented oxidative stress-induced inactivation of alpha-ketoglutarate dehydrogenase, reduced glutamate concentrations, and increased the rate at which it was fed into the TCA cycle, thereby maintaining good mitochondrial function.

In other words, despite having normal thiamine status, HIGH DOSES were necessary to protect mitochondrial function from the damage caused by traumatic brain injury.
Recall the fMRI study above, where researchers likened the results of an EHS patient to that of traumatic brain injury? The neurochemical changes associated with TBI are similar in many ways to chronic EMF exposure – glutamate excitotoxicity, chronic oxidative stress, mitochondrial dysfunction and neuroinflammation.

This suggests that thiamine can be used in a pharmacological way to protect the brain in a way that is independent of nutritional status. By kick-starting the activity of specific enzymes, it can help to “bypass” the stressor and restore normal function. And this is basically what I witness clinically with people who suffer from EHS.

Thiamine’s potential role in protecting brain cells against damage by EMF also relates to another thiamine-dependent enzyme called transketolase, which acts as a “bridge” in the pentose phosphate pathway (PPP). Transketolase is thought to be a “redox-sensitive regulatory mechanism to increase flux through the PPP in times of oxidative stress” [40]. When excessive oxidation occurs in cells, this inevitably raises the requirement for glutathione to counteract the damage.

Cells regenerate glutathione by using the NADPH generated in the PPP. Hence, increased oxidation means increased transketolase activity, which, by definition, also translates to an increased thiamine requirement. And not only does pathway this supply reducing power to regenerate glutathione, but also diverts resources towards fatty acid synthesis required for maintaining the myelin sheath. This is especially important in the context of EMF-induced myelin sheath degeneration and demyelination.

As we examined earlier, low glutathione and other intracellular antioxidants are characteristic biomarkers of EHS/EMF-sensitivity. In fact, EMF exposure alone is enough to deplete brain levels of these antioxidants and render cells susceptible to oxidative damage.

Again, thiamine can be used in a pharmacological way to prevent this antioxidant deficit and protect cells from toxicity. Although there are no studies looking at thiamine in the context of EMF specifically, active thiamine (TPP) has been used successfully for toxic exposures which produce similar neurochemical changes. High dose thiamine prevents oxidative damage caused by cisplatin in both liver [41]and brain [42], reducing markers of lipid peroxidation, DNA damage, and increasing levels of key antioxidants - reduced glutathione and superoxide dismutase.

In brain methotrexate toxicity, TPP prevented the increase in lipid peroxidation and maintained levels of reduced glutathione, glutathione peroxidase, and superoxide dismutase [43]. A lipid-soluble disulphide derivative of thiamine called sulbutiamine was shown to have a similar protective effect on glutathione and significantly reduced reactive oxygen species in retinol ganglion cells [44].

THIAMINE AS AN ANTIOXIDANT


However, these anti-oxidative effects are likely not solely due to thiamine’s role as a cofactor for transketolase. Rather, one possible function of the thiamine molecule is a site-directed antioxidant. Thiamine can exert antioxidant effects on ascorbic acid [45], aldehydes and polyphenols [46], and scavenge superoxide [47].

When complexed with ascorbic acid, it was also shown to inhibit the oxidation of dopamine [48]. The suggested mechanism by which it directly quenches free radicals and hydroperoxides is by the transfer of two electrons from the NH2 group of the pyrimidine ring of the thiamine molecule [46].

Interestingly, thiamine can reverse forms of oxidative stress which are not directly related to its coenzyme function. Lipid peroxidation and glutathione reductase activity in cardiac hypertrophy were normalized with thiamine supplementation [49], along with free radical oxidation of oleic acid in rat liver microsomes [46].

So it would seem that thiamine might be useful in counteracting many of the specific problems caused by EMF exposure. When considering the different types of thiamine which might come in handy in this context, it is important to use a form which can saturate the brain. Thiamine TTFD has long been studied and utilised for this purpose.

I have written about this several times before and have also published multiple videos on the clinical benefits of TTFD. Not only does TTFD possess ultra bioavailability, but it also contains a unique sulfur-containing prosthetic mercaptan group which can be used independently to support oxidative stress.

In short, TTFD plays dual roles in supporting thiamine status and also providing antioxidant power to protect cells from the damaging effects of free radicals. TTFD is the form which many have used to address EMF-hypersensitivity symptoms with great success.

To conclude, the following characteristics make thiamine a prime candidate for pharmacological use in providing protection against EMF-induced injury:

- Thiamine’s key role as a cofactor in mitochondrial energy metabolism to support ATP synthesis, with high doses bypassing mitochondrial dysfunction produced by brain injury

- Thiamine’s role in supporting the antioxidant system through the pentose phosphate pathway, boosting endogenous antioxidant enzymes shown to protect the brain against oxidative stress and toxicity

- As a site-directed antioxidant to combat ROS

- Thiamine’s ability to protect cells against neurotransmitter imbalances including glutamate excitotoxicity, and in supporting myelin synthesis.

- Thiamine TTFD’s ability to cross the blood brain barrier, saturate brain cells, and provide a secondary antioxidant molecule in the form of a prosthetic mercapatan group.


As an aside, there are several other nutrients which I recommend in conjunction with thiamine to support EHS.

These include selenium, melatonin, and vitamin E. However, there are multiple nutrients which have received attention in the research community and show excellent promise for protecting cell metabolism. Many studies have demonstrated protective effects on melatonin specifically in relation to EMF damage. Melatonin was shown to reduce lipid peroxidation and boost glutathione peroxidase and reduced glutathione after wifi exposure [50].

According to another study, melatonin protected hippocampal cells through reducing malondialdehyde and reversing the loss of glutathione peroxidase, SOD, and catalase [51]. Finally, both melatonin and omega 3 fatty acids protected against damage and cell death in the hippocampus [52]. Other research has also highlighted significant benefits from vitamin C [53], N-acetylcysteine, Vitamin E [54, 55], Selenium [56], zinc [57], and folate [58].
 

mrtn

Jedi Council Member
Thanks keyhole, awesome article!
I found a couple of typos:
Code:
hydroxytrypophan (trypto)
nerce cell (nerve?)
though altering molecular rotation (through?)
reduce glutathione (reduced?)
does pathway this (?)
 
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