Thiamine Deficiency Causes Intracellular Potassium Wasting

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The role of thiamine in potassium deficiency
Whilst I always suspected a direct link between potassium and 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.

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%. Interestingly, although tissue levels were altered, plasma levels of these electrolytes remained unaffected and stayed within the normal-high range (sodium at 141.6 and 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 deficiency.

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” and 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 and a continuous supply of ATP. Hence, it is no wonder why a deficiency of this essential nutrient produces such drastic changes in the cellular electrolyte balance.

Thiamine, TTFD, Potassium, and Heart Function

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. Intravenous administration 50mg thiamine, in the form of thiamine tetrahydrofurfuryl disulfide (TTFD), a derivative of thiamine with higher bioavailability and solubility than other formulations, restored electrolyte balance, likely through improving tissue energy metabolism.

Likewise, the same effect was also demonstrated in isolated Guinea pig atria kept in potassium-free medium. TTFD added to cells or administered as a pre-treatment prevented the 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, demonstrating its superior absorbability and perhaps suggesting that this form would be useful for addressing cardiac thiamine insufficiency.

Low potassium is a known driver of cardiac arrhythmias, and TTFD possesses anti-arrhythmic properties 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. Likewise, atrial cell damage through exposure to the mitochondrial toxin N-ethylmaleimide was also prevented by high concentrations of TTFD in-vitro. 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. In cases where potassium deficiency is suggested, thiamine deficiency may be indicated, and TTFD might used to more safely correct the electrolyte balance.

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7 Comments

  1. I enjoyed reading your post, Ellliot. I think that hypokalemia in thiamine deficiency is due to lack of ATP for the sodium/potassium membrane pumps. In fact. I believe that energy deficiency may be at the root of disease, period! Many years ago, I visited Hans Selye in Montreal. He described the General Adaptation Syndrome (GAS) as the energy requiring response to trauma and/or infection in animal systems. He believed that human diseases were “diseases of adaptation”, or failed GAS from lack of energy. Skelton, one of his students produced the GAS in an animal by inducing thiamine deficiency. Selye was convinced that we would be adapting his research to the practice of 21st century medicine. I believe that he was right but instead, he has been forgotten. I keep trying to revive him. Thiamine is a unique nutrient because of its many different functions in energy metabolism. Used as a “drug” in megadoses, or better still, as TTFD, it is capable of stimulating a return of mitochondrial function.

  2. Brilliant article. I did not know about Ling’s hypothesis and would like to look into it. But what you say matches with Emanuel Revici’s potassium utilization schema: anabolic-anaerobic-alkaline imbalances are associated with high cellular potassium, low serum potassium, low cellular hydration and high tissue water (edema), and catabolic-aerobic-acidic imbalances being opposite in shifts. Revici studied this extensively, but did not connect it to thiamine. But he did develop a highly accurate potassium-utilization test involving comparison of serum potassium to total-blood potassium, the latter as measured by the same serum-testing equipment, but using a 9:1 dilution of whole blood in distilled or deionized water. This brings the whole-blood potassium concentration (average 38 mEq/L) down into the serum-testing range, which needs only a shift in the decimal point to correct the units. Appreciate the article!

  3. This is interesting. It’s something that I suspected (based only on empirical evidence), but wasn’t able to figure out. Could this explain in part, I wonder, why Covid-19 patients become very potassium-deficient, especially if they don’t supplement thiamine?

    1. I think thiamine deficiency is at the root of many of the symptoms attributed to COVID, particularly with the hospitalized and more severe cases. Everything points to mitochondrial failure in the covid related deaths.

      1. I wonder why it isn’t addressed more often? From what I have seen, the only Dr to mention it is Professor Marik…

        1. And it appears he has removed it from the latest iteration of his protocol, at least a copy that I saw recently.
          I am not sure why it isn’t addressed more frequently. I think most assume we solved it with food fortification, failing to realize that those types of foods tend to be more of a drain on thiamine than any fortification can overcome.

    2. Additional evidence: patients with Covid-19 disease often have a low oxygen saturation and a chest x-ray that reportedly “looks more like edema” both of which are found in thiamine deficiency. Furthermore, TD is found in patients with critical disease and following GI surgery. Unfortunately TTFD is “not approved” by the FDA and is not available I/V but IS available as Lipothiamine in tablets and as Allithiamine in powder form. O how I wish that this could be better known as a potential life saver in Covid-19!!!!

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