Cancer And Glucose (sugar)

[haidut]

Indirect Effects of Glucose Availability

Besides delivering more glucose to the tumor tissue, hyperglycemia has two other important negative effects for the host: First, as pointed out by Ely and Krone, even modest blood glucose elevations as they typically occur after a Western diet meal competitively impair the transport of ascorbic acid into immune cells.[88,91] Ascorbic acid is needed for effective phagocytosis and mitosis, so that the immune response to malignant cells is diminished. Second, it has been shown in vitro and in vivo that hyperglycemia activates monocytes and macrophages to produce inflammatory cytokines that play an important role also for the progression of cancer[92–94] (see below). Third, high plasma glucose concentrations elevate the levels of circulating insulin and free IGF1, two potent anti-apoptotic and growth factors for most cancer cells.[60] Free IGF1 is elevated due to a decreased transcription of IGF binding protein (IGFBP)- 1 in the liver mediated by insulin.[95] Due to expression of GLUT2, the β-cells of the pancreas are very sensitive to blood glucose concentration and steeply increase their insulin secretion when the latter exceeds the normal level of ~5 mM. In the typical Western diet consisting of three meals a day (plus the occasional CHO-rich snacks and drinks), this implies that insulin levels are elevated above the fasting baseline over most of the day. Both insulin and IGF1 activate the PI3K/Akt/mTOR/HIF-1α pathway by binding to the IGF1 receptor (IGF1R) and insulin receptor (IR), respectively (Figure 2). In addition, insulin stimulates the release of the pro-inflammatory cytokine interleukin (IL)-6 from human adipocytes.[96] Thus, it could be hypothesized that a diet which repeatedly elevates blood glucose levels due to a high GL provides additional growth stimuli for neoplastic cells. In this respect, Venkateswaran et al. have shown in a xenograft model of human prostate cancer that a diet high in CHO stimulated the expression of IRs and phosphorylation of Akt in tumor tissue compared to a low CHO diet.[97] In colorectal,[27] prostate[24] and early stage breast cancer patients[23,98] high insulin and low IGFBP-1 levels have been associated with poor prognosis. These findings again underline the importance of controlling blood sugar and hence insulin levels in cancer patients. Dietary restriction and/or a reduced CHO intake are straightforward strategies to achieve this goal.



Altered Nutritional Needs of Cancer Patients

Cancer patients and those with metabolic syndrome share common pathological abnormalities. Since 1885, when Ernst Freund described signs of hyperglycemia in 70 out of 70 cancer patients,[99] it has been repeatedly reported that glucose tolerance and insulin sensitivity are diminished in cancer patients even before signs of cachexia (weight loss) become evident.[100–102] Both diabetes and cancer are characterized by a common pathophysiological state of chronic inflammatory signalling and associated insulin resistance. In cancer patients, insulin resistance is thought to be mediated by an acute phase response that is triggered by pro-inflammatory cytokines such as tumor necrosis factor (TNF)-?.[101] and IL-6[103] In animal and human studies, removal of the tumor resulted in improved glucose clearance, suggesting that these cytokines are secreted, at least in part, from the tumor tissue itself.[104,105] The impact on the metabolism of the host is illustrated in Figure 3. In the liver, the inflammatory process leads to increased gluconeogenesis that is fuelled by lactate secreted from the tumor as well as glycerol from fatty acid breakdown and the amino acid alanine[106] from muscle proteolysis. Gluconeogenesis is an energy-consuming process and might contribute to cancer cachexia by increasing total energy expenditure. Despite increased lipolysis, hepatic production of ketone bodies is usually not enhanced in cancer patients.[107,108] This is in contrast to starvation, where the ketone bodies acetoacetate and β-hydroxybutyrate counteract proteolysis by providing energy for the brain and muscles.[109] In muscle, glucose uptake and glycogen synthesis are inhibited already at early stages of tumor progression, while fatty acid oxidation remains at normal levels or is increased.[110,111] In the latter case, more fat has to be provided from lipolysis in the adipose tissue. In addition, muscles progressively lose protein to provide amino acids for hepatic synthesis of acute-phase proteins and as precursors for gluconeogenesis. Thus, insulin resistance contributes to fat loss and muscle wasting, the two hallmarks of cancer cachexia. At the same time, it makes more glucose in the blood available for tumor cells.

That insulin resistance is probably produces by the elevated FFA caused by the tumor thriving on fat. Instead of removing the tumor, inhibiting lipolysis and/or fat oxidation would have had the same effect as the study on leukemia found with the (toxic) drug etomoxir.

 

[burtlancast]

You realize that's exactly like wanting to restrict sugar in diabetes, right?

Diabetes can be reversed by lowering circulating PUFAS and increasing glucose concentrations in the blood.

Trying this approach in cancer will only make the cancer cells grow faster because of the increased availability of glucose.

You can't make a cancer go away by (over)feeding him.

It's been shown that the efficiency of some orthodox cancer drugs is increased by lowering the blood glucose.

Cancer cells don't like low blood glucose.

A cancer diet like Gerson devised will keep the cancer's growth rate in check while the other nutrients help the body fight the cancer.
He was among the first to use niacin, aspirin and Vit C, as well as thyroid.

If any cancer patient wants to eat sugary drinks, chocolate bars, sweets, or pure saccharose by fear of having the cancer dissolve the body's proteins in the absence of glucose (which is really impossible) , he better have a sure way of quickly
killing the fast growing cancer cells.

Or else.

By no means do i say the substances Haidut posted aren't helpful, and by no means do i say the Gerson therapy heals every cancer.

But if i do have cancer, i will go by what's been proven clinically at the patient's bed, instead of what hasn't been yet.

 

[burtlancast]

High Glucose Promotes Tumor Invasion and Increases Metastasis-Associated Protein Expression in Human Lung Epithelial Cells

https://www.karger.com/Article/FullText/373928


Study Indicates Cancer Cells Alter Glucose Metabolism to Enhance Energy Production and Cell Growth


"The effects of energy production inhibitors on mitochondrial function in normal and cancer cells were also compared. Cancer cell mitochondrial inhibition with specific agents decreased energy levels by 30-40%; while in normal cells energy production was reduced by 60%. Cancer cells appear to better withstand interference with energy synthesis in mitochondria since they rely mainly on glycolysis as an energy producing mechanism."

Study Indicates Cancer Cells Alter Glucose Metabolism to Enhance Energy Production and Cell Growth

 

[ecstatichamster]

Ketones do supply food to the brain though. In great abundance.

High Glucose Promotes Tumor Invasion and Increases Metastasis-Associated Protein Expression in Human Lung Epithelial Cells

https://www.karger.com/Article/FullText/373928

do you really trust an in vitro study much? Why can't someone give rats cancer and feed them sugar vs control rats? So many studies are so flawed in this area.

 

[burtlancast]

do you really trust an in vitro study much? Why can't someone give rats cancer and feed them sugar vs control rats? So many studies are so flawed in this area.

Inducing tumors in rats isn't as easy or straightforward as it seems. This has plagued cancer research for tens of years.

Ray wrote about Leonell Strong's mouse strain that he bred at great pains and efforts to naturally develop cancer.

"

In the 1960s I read some articles in a small town newspaper about Leonell Strong’s cancer research, and his treatment by the American Cancer Society and the Salk Institute. Leonell Strong had developed strains of mice for use in cancer research. In some of the strains, 100% of the females developed mammary cancer. Strong had demonstrated that these strains had very high levels of estrogen. He showed me mice that he had treated with simple extracts of liver, that were free of cancer, and whose descendants remained free of cancer for several generations.

Strong had received his PhD in genetics under T. H. Morgan. For a person trained in classical genetics, and who had spent his career developing the supposedly genetically determined cancer trait, the elimination of the trait by a few injections must have been hard to understand, but at least he tried to understand it.

When he had earlier demonstrated the presence of a virus in the milk of cancer-prone mice, and when he showed the role of heredity in cancer, he was popular with the cancer business, but when he showed that “genetic” cancer could be eradicated with a simple treatment, he became the object of official abuse. He said that the Salk institute had offered him a position to induce him to move with his large colony of mice from New York to San Diego, but when he arrived he found that he had no job, and his records of decades of research had been lost. He said that a memo which was discovered in a lawsuit revealed that the institute had just wanted his mice, and never intended to give him the promised job. For the cancer establishment, his discovery of a way to prevent cancer was not welcome."

 

[Such_Saturation]

Diabetes can be reversed by lowering circulating PUFAS and increasing glucose concentrations in the blood.

Trying this approach in cancer will only make the cancer cells grow faster because of the increased availability of glucose.

You can't make a cancer go away by (over)feeding him.

It's been shown that the efficiency of some orthodox cancer drugs is increased by lowering the blood glucose.

Cancer cells don't like low blood glucose.

A cancer diet like Gerson devised will keep the cancer's growth rate in check while the other nutrients help the body fight the cancer.
He was among the first to use niacin, aspirin and Vit C, as well as thyroid.

If any cancer patient wants to eat sugary drinks, chocolate bars, sweets, or pure saccharose by fear of having the cancer dissolve the body's proteins in the absence of glucose (which is really impossible) , he better have a sure way of quickly
killing the fast growing cancer cells.

Or else.

By no means do i say the substances Haidut posted aren't helpful, and by no means do i say the Gerson therapy heals every cancer.

But if i do have cancer, i will go by what's been proven clinically at the patient's bed, instead of what hasn't been yet.

There's no difference in the context of diabetes and cancer, so why would you behave differently? And what makes you accept Ray Peat's (what allegedly are) opinions in a selective manner instead of all of them?

 

[tara]

by fear of having the cancer dissolve the body's proteins in the absence of glucose (which is really impossible)

IIUC, cachexia is an expected effect of cancer - I didn't think this was controversial, either in the mainstream or with Peat? This arises because the body proteins are used for gluconeogenesis, right?

 

[burtlancast]

There's no difference in the context of diabetes and cancer, so why would you behave differently?

I would like to remind you the cure and cause of both of these diseases is still unknown (altough Ray has written excellent insights about diabetes).

When all cases of diabetes and cancer in the world will be cured, i'll be glad to answer you.

 

[haidut]

IIUC, cachexia is an expected effect of cancer - I didn't think this was controversial, either in the mainstream or with Peat? This arises because the body proteins are used for gluconeogenesis, right?

This. Also inflammation (probably driven by PUFA metabolites). See below.
Nsaid (aspirin) May Prevent Cancer Cachexia (wasting) | Ray Peat Forum

 

[Such_Saturation]

I would like to remind you the cure and cause of both of these diseases is still unknown (altough Ray has written excellent insights about diabetes).

When all cases of diabetes and cancer in the world will be cured, i'll be glad to answer you.

Cured by whose measure? We seem to be mixing mainstream views and alternative views at our discretion, using one or the other to discredit the other when we see fit. Max Gerson was a fraudster if we ask the National Cancer Institute. That kind of only leaves the in vitro stuff...

 

[burtlancast]

Max Gerson was a fraudster if we ask the National Cancer Institute.

"Gerson was definitely on to something, and was curing migraine and cancer. But he very typically would give his patients a couple of grains of Armour thyroid, and very often, coffee enemas. And they were always having a very high ratio of carbohydrates to protein. So they were low on methionine, tryptophane, and the potentially toxic amino acids. And generally, lots of things in his program were very well founded. But there just wasn’t enough information at that time about how the balance of the alkaline minerals works."

Transcript of "Biochemical Health: Reduction and Oxidation" by Ray Peat

So, according to Ray, Gerson is legit.

I'm still waiting for him to explain why placing a cancer or tuberculosis patient on a saltless diet causes him to excrete more sodium than on a normal diet for up to 14 days after the beginning of the diet.

"All poisons and other substances difficult to eliminate are stimulants for the sick tissues, especially liver and kidneys. :that condition seems to be the reason why sodium chloride excretion increases in tuberculosis, cancer and other chronic diseases after two to three days on a saltless diet, and this condition stays at that higher level for about eight to ten or fourteen days, corresponding to a favorable development in the course of the disease. After that is accomplished, it stays near the normal level with the saltless diet, but shows a higher Na-Cl excretion, together with more fluid from time to time for two to three days, and, later for one day."

A cancer therapy (original Gerson book; pg 165-166).


Ray has been absolutely unable to come with a credible explanation for this phenomenon; he has avoided answering it when specifically asked (see interview transcript).

 

[haidut]

"Gerson was definitely on to something, and was curing migraine and cancer. But he very typically would give his patients a couple of grains of Armour thyroid, and very often, coffee enemas. And they were always having a very high ratio of carbohydrates to protein. So they were low on methionine, tryptophane, and the potentially toxic amino acids. And generally, lots of things in his program were very well founded. But there just wasn’t enough information at that time about how the balance of the alkaline minerals works."

Transcript of "Biochemical Health: Reduction and Oxidation" by Ray Peat

So, according to Ray, Gerson is legit.

I'm still waiting for him to explain why placing a cancer or tuberculosis patient on a saltless diet causes him to excrete more sodium than on a normal diet for up to 14 days after the beginning of the diet.

"All poisons and other substances difficult to eliminate are stimulants for the sick tissues, especially liver and kidneys. :that condition seems to be the reason why sodium chloride excretion increases in tuberculosis, cancer and other chronic diseases after two to three days on a saltless diet, and this condition stays at that higher level for about eight to ten or fourteen days, corresponding to a favorable development in the course of the disease. After that is accomplished, it stays near the normal level with the saltless diet, but shows a higher Na-Cl excretion, together with more fluid from time to time for two to three days, and, later for one day."

A cancer therapy (original Gerson book; pg 165-166).


Ray has been absolutely unable to come with a credible explanation for this phenomenon; he has avoided answering it when specifically asked (see interview transcript).

The reason for the sodium loss in cancer and other chronic diseases has to do (partially) with the release of vasopressin. Why chronic dieases tend to result in high vasopressin/ADH release I don't know.
Syndrome of inappropriate antidiuretic hormone secretion - Wikipedia, the free encyclopedia

Also, the increase of estrogen in any stressful condition will make the cells hypotonic by increasing sodium excretion, and that extra sodium finds its way in urine and sweat.

 

[burtlancast]

The reason for the sodium loss in cancer and other chronic diseases has to do (partially) with the release of vasopressin. Why chronic dieases tend to result in high vasopressin/ADH release I don't know.
Syndrome of inappropriate antidiuretic hormone secretion - Wikipedia, the free encyclopedia
.

The syndrome you're describing includes an
" increase in blood volume (hypervolemia) often resulting in dilutional hyponatremia in which the plasma sodium levels are lowered and total body fluid is increased." (wikipedia)

This is in direct opposition to what Gerson observed and wrote:

"The main task of the saltless diet is to eliminate the retained Na, Cl, H20, together with toxins and poisons from the tissues all over the body."

Gerson observed an increased release of Na Cl toegether with excess water, bringing a decrease in local edema, which progressively disappear.

So, vasopressin has nothing to do with it.

Also, the increase of estrogen in any stressful condition will make the cells hypotonic by increasing sodium excretion, and that extra sodium finds its way in urine and sweat

You're describing the opposite of what Gerson observed: according to you, the estrogen dominant patient rapidly loses sodium in the urine and sweat. Reversing this estrogen dominance through the Gerson therapy would see the body retain more sodium than before the estrogen dominance; that's exactly the inverse of what Gerson observed and wrote about.

 

[haidut]

The syndrome you're describing includes an
" increase in blood volume (hypervolemia) often resulting in dilutional hyponatremia in which the plasma sodium levels are lowered and total body fluid is increased." (wikipedia)

This is in direct opposition to what Gerson observed and wrote:

"The main task of the saltless diet is to eliminate the retained Na, Cl, H20, together with toxins and poisons from the tissues all over the body."

Gerson observed an increased release of Na Cl toegether with excess water, bringing a decrease in local edema, which progressively disappear.

So, vasopressin has nothing to do with it.




You're describing the opposite of what Gerson observed: according to you, the estrogen dominant patient rapidly loses sodium in the urine and sweat. Reversing this estrogen dominance through the Gerson therapy would see the body retain more sodium than before the estrogen dominance; that's exactly the inverse of what Gerson observed and wrote about.

In the quote from Gerson you provided he says the purposes of sodium restriction would be to "decrease local edema". The SIADH condition results in increase in total body fluid as the quote from Wikipedia shows. So, cancer patients do seem to have edema. Gerson thinks that the edema will be eliminated through sodium restriction. I humbly disagree, and not to mention that restricting sodium will raise aldosterone, so the person will end up losing sodium, magnesium and potassium. Loss of the alkaline minerals can trigger muscle loss even in healthy people. I am not saying Gerson wasn't on to something. But maybe there were other factors at play that he did not care to record or did not notice b/c they were not considered relevant at the time.

 

[Wilfrid]

And what about the following, plausible, explanations of the high sodium excretion thing (if we may consider that cancer could make cell hypertonic, and not hypotonic, by augmentation of intracellular sodium concentration in lieu of K) while on a salt-less diet ( especially with degenerative diseases):

http://doctordonato.com/wp-content/uploads/pdfs/A-Paradigm-in-Cellular-Biology.pdf

Pathology of structured water and associated cations in cells (ther tissue damage syndrome) and its medical treatment. - PubMed - NCBI

The above links have the advantage of reconciling the work of Ling and some few other scientists with Gerson's clinical observations. It makes, at least, the phenomenum understandable on the cellular level as well as why such a high excretion of sodium while on the return to the homeostasis, no?
Maybe the work of Louis E. Kervran, while contested by mainstream scientific media ( but the research made by Kervran is still going on in Russia ), on biological transmutation are worth considering too.

 

[burtlancast]

and not to mention that restricting sodium will raise aldosterone, so the person will end up losing sodium, magnesium and potassium. Loss of the alkaline minerals can trigger muscle loss even in healthy people.

Excess aldosterone, and loss of alkaline minerals, as you wrote, is entirely out of the question. The diet expressly increases those in the body; this phenomena is actually often cited as one of the central mechanism the diet manages to cure people.

If you read the transcript in it's entirety, Ray himself explains Gerson's diet did contain a normal amount of sodium from the vegetable juices, together with an overabundance of other alkaline minerals like calcium, magnesium and especially potassium, which Gerson considered most important, to the point of adding potassium salts to the hourly juices.

In the quote from Gerson you provided he says the purposes of sodium restriction would be to "decrease local edema". The SIADH condition results in increase in total body fluid as the quote from Wikipedia shows. So, cancer patients do seem to have edema. Gerson thinks that the edema will be eliminated through sodium restriction. I humbly disagree

Gerson observed the loss of sodium and the resolution of local edema in nearly every degenerative disease he treated; it's not just cancer patients.

And he wasn't the only one making these observations: 446 out of 450 skin tuberculosis patients were cured with his saltless diet in the University of Munich’s 1928 tuberculosis trial, under the supervision of Ferdinand Sauerbrush and his assistant Herrmansdorfer .

The saltless diet became an instant sensation during the 1930's , and was reproduced by clinicians all over the world.


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Bacmeister A, Rehfeldt P. [Phosphorlebertran und die Gerson-Hermannsdordersche Diat zur Heilung der Tuberkulose.] Dtsch Med Wochenschr 1930-03-21;56(12):480-481

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Baer G, Hermannsdorfer A, Kausc. Salt Free Diet in Tuberculosis. Munch Med Wochenschr 1929-01;

Banyai AL. The Dietary Treatment of Tuberclosis. Am. Rev. Tuberc. 1931-05;23:546-575

Barat I. Gerson's diet in treatment of pulmonary tuberculosis. Orv Hetil 1930-08-30;74:877-879

Barat I. [Uber den Wert der Gersondiat in der Behandlung der Lungentuberkulose.] Beitr. z. Klin. d. Tuberk. 1931;76:588-591

Beck O. Herrmannsdorfer Dietary Treatment of Tuberculosis: Theoretical Basis. Monatsschr Kinderheilkd 1930-10;48:276

Alexander H. Treatment of pulmonary tuberculosis with Salt-free diet. Munch Med Wochenschr 1930-06-06;77(23):971

Apitz G. Treatment of Tuberculosis of Lungs and of Other Organs with Salt-free Diet. Dtsch Med Wochenschr 1929-11-15;55:1918

Bentivoglio GC. [Levariazione del riflesso oculocardiaco nei bambini in sequito al trattamento dietetico di Gerson.] Pediatria (Napoli) 1933-12;41:1457-1483

Bertaccini G. [Hermannsdorfer-Sauerbruch nella tuberculosi: richerche sulla influenza del cloruro di sodio nella infezione tubercolare sperimentale del coniglio.] Gior. ital. di. dermat. e. sif. 1932-12;73:1775-1778

Bertaccini G. [A proposito della dieta Gerson-Herrmannsdorfer-Sauerbruch nella tuberculosi; richerche sulla influenza del cloruro di sodio nella infezione tubercolare sperimentale del coniglio; infezione cutanea.] Gior. ital. di. dermat. e. sif. 1933-12;74:1469-1486

Blumenthal F. Treatment of Tuberculosis of Skin with Special Consideration of Dietary Therapy. Med. Klin., Berlin. 1930-09-26;26:1432.

Bogen E, Rachmel W. Pulmonary Tuberculosis-- its dietary Treatment. Cal. & West. Med. 1932-11;37(5):292-296

Bommer S. Dietetic Treatment of Tuberculosis of Skin. Munch Med Wochenschr 1929-04-26;76:707

Bommer S, Bernhardt L. Dietary Treatment of Lupus Vulgaris. Dtsch Med Wochenschr 1929-08-02;55:1298.

Bommer S. [Neue Erfahrungen auf dem Gebeite der Hauttuberkulose mit besonderer Berucksichtigung der Gerson diat.] Strahlentherapie 1930;35:139-148.

Bommer S. [Beitrag zur Diatbehandlung von Lupus vulgaris.] Med Klin 1933;28:

Bommer S. Dietary treatment of skin tuberculosis. Am. Rev. Tuberc. 1933-02;27:209-215

Bommer S. Capillaroscopic study of skin following administration of Gerson-Herrmannsdorfer-Sauerbruch diet in treatment of injuries to skin. Dermatol Wochenschr 1933-09-23;97(38):1367-1372

Bommer S. [Zur frage der Wirkung von Sauerbruch-Herrmannsdorfer-Gerson Diat.] Dtsch Med Wochenschr 1934-05-18;60(20):735-739

Bommer S. [Salzarme Kost in Gefassystem (G.H.S.-Diat).] Klin Wochenschr 1934-10-27;43:148-158

Brezovsky. Sauerbruch-Gerson diet in treatment of tuberculosis of skin. Budapesti orvosi ujsag. 1930-07-17;28:769-773.


Bruusgaard E, Hval E. Gerson-Sauerbruch-Herrmannsdorfer diet treatment in skin tuberculosis and its results. Norskk. mag. f. laegevidensk. 1931-11;92(11):1157-1175

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Canal Feijoo EJ. [Regimen acido como tratamiento de la tuberculosis pulmonar.] Rev. med. latino-am 1931-04;16:981-992

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Cattell HW editor. Diet in Treatment of Tuberculosis. Internat. Clin. 1931;41(1):200

Clairmont P, Dimtza A. Dietary Treatment in Tuberculosis. Klin Wochenschr 1930-01;9:5.

Conrad AH. Lupus Vulgaris. Archiv. Dermat. Syph. 1931;24:688

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Crosti A, Solari E. [Ladieta di Gerson-Herrmannsdorfer-Sauerbruch nella tuberculosi cutanea. Osservazioni cliniche e richerche biologiche.] Gior. ital. di. dermat. e. sif. 1931-08;72:897-945

Csapo J, Peterfy M, Palfy E. Urinalysis in tubercular children kept on Sauerbruch-Herrmannsdorfer-Gerson diet. Orv Hetil 1931-11-07;75:1090

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Curschmann W. [Beobachtungen bei Gersonsche Diat.] Beitr. a. Klin. d. Tuberk. 1932-01-17;80:120-131
Danholt N. Culture of Tubercle Bacilli from Lupus Lesions of Patients Under the Gerson Herrmannsdorfer-Sauerbruch Diet. Acta Derm Venereol 1932-11;13:617

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This is just the published results up to the letter D; one gets the picture.

Ray has no real answer to this, and prefers to avoid the subject altogether, as the transcript shows.

 

[Wilfrid]

A medical application of the Ling Association-Induction Hypothesis: the high potassium, low sodium diet of the Gerson cancer therapy
By Freeman W. Cope, M.D.


" The high potassium, low sodium diet of the Gerson therapy has been observed experimentally to cure many cases of advanced cancer in man, but the reason was not clear. Recent studies from the laboratory of Ling indicate that high potassium, low sodium environments can partially return damaged cell proteins to their normal undamaged configuration. Therefore, the damage in other tissues, induced by toxins and breakdown products from the cancer, is probably partly repaired by the Gerson therapy through this mechanism.

The Gerson cancer therapy is an integrated set of medical treatments which has cured many cases of advanced cancer in man.It was developed empirically by Gerson in the course of 30 years of clinical experimentation. Essentially, he tried many variations and combinations of treatments on cancer patients, always retaining that which was successful and discarding that which was not. Gradually he evolved an integrated pattern of treatment which cured many cases of advanced cancer, 50 of which are described in clinical detail in his book.

This empirically derived cancer therapy contained a number of unconventional features, which were justified by the fact that they did indeed cure advanced cancer. From the nature of the measures that gave good results, and from the laboratory medical science available at that time, Gerson attempted to deduce the reasons why his therapy was effective in curing cancer. His deductions led to some unconventional ideas regarding the nature of human cancer and the mechanisms of therapy. Some of his hypotheses were vaguely stated and incompletely validated, but they are of great importance because they imply that those approaches to cancer therapy that will be effective are mostly different from those now used.

This paper shows how modern work on cation association and water structuring in cells supports and makes more precise some of the deductions Gerson made from his medical experimentation with cancer patients.

An essential component of Gerson’s cancer therapy was the use of a low Na, high K diet. Indeed, he found experimentally that cancers regressed faster if large quantities of inorganic solutions of K were given in addition to a diet which was already high in K.

Gerson attempted to understand the biochemical and biophysical reasons for the observed success of low Na and high K diets in the cure of cancer. He recognized the importance of this question and devoted much space in his book to correlations with known experimental facts. He observed that cancer patients always had marked degeneration of other tissues, especially of the liver presumably due to toxic factors, of unknown type, produced by the cancer. Gerson observed that this situation became worse when medical treatments destroyed the cancer, which released toxic tissue breakdown products, which poisoned other tissues, which led to coma and death unless vigorous measures were taken to prevent this. Gerson (ref. 2, pg. 98) noted that earlier investigators had shown that tissue damage due to administration of various poisons causes liver tissue to lose K and gain Na. Gerson also noted (ref 2, pg. 97 and 165) that when cancer patients were under treatment, they lost extra Na from the body in the urine, which implied that part of the process of recovery of the human body from cancer disease was replacement of excess Na by K in damaged tissues.

Gerson made the general deduction that a major part of the reason for the observed success of low Na, high K diets in treatment of cancer was that they forced a correction of the generalized tissue damage, of which low tissue K and high tissue Na were a part.

It will now be shown that modern experimental evidence and concepts support and make more precise this conclusion.

Modern experimental evidence indicates that the cell should be regarded as analogous to an ion exchanger resin granule with structured water in the interstices and with potassium and sodium ions associated with fixed negative charges on the protein matrix. This line of investigation was initiated by Ling, who called it the "association-induction hypothesis," and was extended by others, including Damadian, who used the terms "ion exchanger resin" and "cytotonus model" of the cell.

Tissue damage, from any cause and in any tissues, produces a similar set of changes in tissue salt and water, which Cope has called the "tissue damage syndrome." This pattern is clearly shown in experiments by Ling and Ochsenfeld with muscle poisoned by iodoacetamide and has been discussed from the above point of view by Cope. The most easily observed components of the tissue damage syndrome, as seen in the experiments of Ling and Ochsenfeld (ref. 9, Fig. 1), are decreased cell K, increased cell Na, and increased cell water (cell swelling or tissue edema). The conceptual pattern responsible for these observed changes, conceived first by Ling as part of his association-induction hypothesis, is as follows:

The proteins of the cell are able to exist in either of two different configurational states: a normal configuration, and a damaged configuration. The two different protein configurational states induce two different sets of water structuring and cation association states. In the healthy cell, the cell proteins have their normal configurational state in which negatively charged sites on the protein matrix have a large preference for associaton with K rather than Na, and cell water is highly structured so that its solubility for both K and Na is low. The result is high cell K and low cell Na concentrations. The ability of the cell proteins to stay in the normal configurational state is dependent on the integrity of the cell (freedom from chemical or physical damage).

In the damaged cell, the cell proteins change to the damaged configurational state. In that state the cell proteins lose their preference for associaton with K rather than Na, lose much of their ability to structure water, and probably lower their contractility, with the result that K leaves the cell, is replaced by Na, and the water content of the cell increases (the cell swells).

The high K, low Na diet of the Gerson cancer therapy is a logical strategy for improving the health of the body tissues, of which probably all and certainly the liver are suffering from the tissue damage syndrome, some components of which were observed and recognized by Gerson earlier in this paper.

In the damaged or partly damaged cell, the cell proteins lose all or part of the preference of their sites for associating with K rather than Na. Nevertheless, a competition between K and Na for these sites still exists. Therefore if in the environment around the cell the concentration of K is increased compared to Na, the association sites are forced to accept more K and less Na because of the cooperative interactions between association sites, as shown by Ling and Bohr. This tends to restore the normal configuration of the proteins. Therefore, treatment with the Gerson diet to increase tissue K+ concentration and to decrease tissue Na+ concentration is a logical therapy for the tissue damage syndrome in the cancer patient. "

By increasing tissue potassium concentration ( with diet and / or supplements to the point of overabundance ) along with the help of a low sodium diet/intake, the body is forced to excrete more sodium, as a part of an endogenous regulation process described by Ling, up to the point where injured tissue is restored to its fully functional state. And the more effectively the body excrete the sodium the more favorable the disease outcome is ( doing this probably require enough left vital energy for the sick patient, the same vital energy that would be, probably, lacking for people who were treated by previous exogenous/endogenous treatment like surgery/chemo/radiation ect.... ).
Hence, the fondamental importance for a return to a healthy Na/K intracellular ratio and cell proteins' homeostasis for an effective " cure " of the injured tissue.
I think that was what Gerson saw in his day-to-day observations, but wasn't able to explain at his time of clinical practice, without the rescue of Gilbert Ling's association-induction hypothesis.
Sounds good for a credible explanation,no?

Just an add to my post above. :)

 

[haidut]

Excess aldosterone, and loss of alkaline minerals, as you wrote, is entirely out of the question. The diet expressly increases those in the body; this phenomena is actually often cited as one of the central mechanism the diet manages to cure people.

If you read the transcript in it's entirety, Ray himself explains Gerson's diet did contain a normal amount of sodium from the vegetable juices, together with an overabundance of other alkaline minerals like calcium, magnesium and especially potassium, which Gerson considered most important, to the point of adding potassium salts to the hourly juices.



Gerson observed the loss of sodium and the resolution of local edema in nearly every degenerative disease he treated; it's not just cancer patients.

And he wasn't the only one making these observations: 446 out of 450 skin tuberculosis patients were cured with his saltless diet in the University of Munich’s 1928 tuberculosis trial, under the supervision of Ferdinand Sauerbrush and his assistant Herrmansdorfer .

The saltless diet became an instant sensation during the 1930's , and was reproduced by clinicians all over the world.


Ahringsmann H. [Historische Bemerkung zu der neuen Diatehandlung der Tuberkulose nach Gerson-Suerbruch-Herrmansdorfer.] Munch Med Wochenschr 1929-09;76:1565.

Axmann. Dietary Treatment in tuberculosis of the Skin. Munch Med Wochenschr 1930-09-25;77:707.

Bacmeister A, Rehfeldt P. [Phosphorlebertran und die Gerson-Hermannsdordersche Diat zur Heilung der Tuberkulose.] Dtsch Med Wochenschr 1930-03-21;56(12):480-481

Bacmeister A. [Interne Behandlung der Lungentuberkulose.] Med Welt 1930-04-05;4(14):474-476

Baer G, Hermannsdorfer A, Kausc. Salt Free Diet in Tuberculosis. Munch Med Wochenschr 1929-01;

Banyai AL. The Dietary Treatment of Tuberclosis. Am. Rev. Tuberc. 1931-05;23:546-575

Barat I. Gerson's diet in treatment of pulmonary tuberculosis. Orv Hetil 1930-08-30;74:877-879

Barat I. [Uber den Wert der Gersondiat in der Behandlung der Lungentuberkulose.] Beitr. z. Klin. d. Tuberk. 1931;76:588-591

Beck O. Herrmannsdorfer Dietary Treatment of Tuberculosis: Theoretical Basis. Monatsschr Kinderheilkd 1930-10;48:276

Alexander H. Treatment of pulmonary tuberculosis with Salt-free diet. Munch Med Wochenschr 1930-06-06;77(23):971

Apitz G. Treatment of Tuberculosis of Lungs and of Other Organs with Salt-free Diet. Dtsch Med Wochenschr 1929-11-15;55:1918

Bentivoglio GC. [Levariazione del riflesso oculocardiaco nei bambini in sequito al trattamento dietetico di Gerson.] Pediatria (Napoli) 1933-12;41:1457-1483

Bertaccini G. [Hermannsdorfer-Sauerbruch nella tuberculosi: richerche sulla influenza del cloruro di sodio nella infezione tubercolare sperimentale del coniglio.] Gior. ital. di. dermat. e. sif. 1932-12;73:1775-1778

Bertaccini G. [A proposito della dieta Gerson-Herrmannsdorfer-Sauerbruch nella tuberculosi; richerche sulla influenza del cloruro di sodio nella infezione tubercolare sperimentale del coniglio; infezione cutanea.] Gior. ital. di. dermat. e. sif. 1933-12;74:1469-1486

Blumenthal F. Treatment of Tuberculosis of Skin with Special Consideration of Dietary Therapy. Med. Klin., Berlin. 1930-09-26;26:1432.

Bogen E, Rachmel W. Pulmonary Tuberculosis-- its dietary Treatment. Cal. & West. Med. 1932-11;37(5):292-296

Bommer S. Dietetic Treatment of Tuberculosis of Skin. Munch Med Wochenschr 1929-04-26;76:707

Bommer S, Bernhardt L. Dietary Treatment of Lupus Vulgaris. Dtsch Med Wochenschr 1929-08-02;55:1298.

Bommer S. [Neue Erfahrungen auf dem Gebeite der Hauttuberkulose mit besonderer Berucksichtigung der Gerson diat.] Strahlentherapie 1930;35:139-148.

Bommer S. [Beitrag zur Diatbehandlung von Lupus vulgaris.] Med Klin 1933;28:

Bommer S. Dietary treatment of skin tuberculosis. Am. Rev. Tuberc. 1933-02;27:209-215

Bommer S. Capillaroscopic study of skin following administration of Gerson-Herrmannsdorfer-Sauerbruch diet in treatment of injuries to skin. Dermatol Wochenschr 1933-09-23;97(38):1367-1372

Bommer S. [Zur frage der Wirkung von Sauerbruch-Herrmannsdorfer-Gerson Diat.] Dtsch Med Wochenschr 1934-05-18;60(20):735-739

Bommer S. [Salzarme Kost in Gefassystem (G.H.S.-Diat).] Klin Wochenschr 1934-10-27;43:148-158

Brezovsky. Sauerbruch-Gerson diet in treatment of tuberculosis of skin. Budapesti orvosi ujsag. 1930-07-17;28:769-773.


Bruusgaard E, Hval E. Gerson-Sauerbruch-Herrmannsdorfer diet treatment in skin tuberculosis and its results. Norskk. mag. f. laegevidensk. 1931-11;92(11):1157-1175

Bruusgaard E. [Uber die Herrmannsdorfersche Diatbehandlung von Hauttuberkulose.] Acta Derm Venereol 1932-11;13:628-642

Bussalai. [Ladieta di Gerson-Herrmannsdorfer nel Lupus. (Nota preventi). Con presentazioni di ammalati, di preparti microscopi e di fotografie.] Gior. ital. di. dermat. e. sif. (supp.fasc.1) 1931;1:10-13

Canal Feijoo EJ. [Regimen acido como tratamiento de la tuberculosis pulmonar.] Rev. med. latino-am 1931-04;16:981-992

Canal Feijoo EJ. [Regimen acido como tratamiento de la tuberculosis pulmonar.] Rev. espan. de . med. y cir 1933-03;16:124-128

Cattell HW editor. Diet in Treatment of Tuberculosis. Internat. Clin. 1931;41(1):200

Clairmont P, Dimtza A. Dietary Treatment in Tuberculosis. Klin Wochenschr 1930-01;9:5.

Conrad AH. Lupus Vulgaris. Archiv. Dermat. Syph. 1931;24:688

Crosti A, Solari E. [Ladieta Sauerbruch-Herrmannsdorfer-Gerson nella tuberculosi cutanea; reperti clinice, biochimici, istopatologici (con dimostrazioni di fotografie).] Gior. ital. di. dermat. e. sif. (supp.fasc.1) 1931;1:13-16

Crosti A, Solari E. [Ladieta di Gerson-Herrmannsdorfer-Sauerbruch nella tuberculosi cutanea. Osservazioni cliniche e richerche biologiche.] Gior. ital. di. dermat. e. sif. 1931-08;72:897-945

Csapo J, Peterfy M, Palfy E. Urinalysis in tubercular children kept on Sauerbruch-Herrmannsdorfer-Gerson diet. Orv Hetil 1931-11-07;75:1090

Csapo J, Peterfy M, Palfy E. [Harnutersuchungen bei der Diat nach Sauerbruch-Herrmannsdorfer-Gerson.] Arch. f. Kinderfh. 1932;96:231-235

Curschmann W. [Einklarendes Wort zur ablehnenden Kritik der Ernahrungsbehandlung der Tuberkulose. Erwiderungen auf die Aufsatze von Sauerbruch und Herrmannsdorfer.] Munch Med Wochenschr 1930-12-19;77:2196.

Curschmann W. [Ergenbnisse salzloser Diatbehandlung nach Sauerbruch und Hermannsdorfer bei Lungentuberkulose und Knochentuberkulose.] Beitr. z. Klin. d. Tuberk. 1932;77:540-590

Curschmann W. [Beobachtungen bei Gersonsche Diat.] Beitr. a. Klin. d. Tuberk. 1932-01-17;80:120-131
Danholt N. Culture of Tubercle Bacilli from Lupus Lesions of Patients Under the Gerson Herrmannsdorfer-Sauerbruch Diet. Acta Derm Venereol 1932-11;13:617

Directives. [Richtlinien fur die Heilkostbehandlung der Tuberkulose nach Gerson-SauerbruchHerrman-nsdorfer.] Med Welt 1929-08-24;3:1229

Doerffel J. Clinical, Experimental and Chemical Studies on the Influence of Diet on Inflammatory changes in Healthy and Diseased Skin. Arch. f. Dermat .u. Syph. 1931-01-24;162:621

Doerffel J. Effect of a diet Low in Salt in Cases of Tuberculosis of the Skin. Arch. Dermat. Syph. 1932;26:762-764

Doerffel J, Goeckerman WH. Effect of a Diet Low in Salt in Cases of Tuberculosis of the Skin. Mayo Clin Proc 1932-02-10;7(6):73-78

Doerffel J, Passarge W. [Lokale Ektebinbehandlung der Hauttuberkulose bei gleichzeitigen Kochsalzarmer Diat (Gerson-Herrmannsdorfer-Sauerbruch).] Dermatol Wochenschr 1934-09-08;99(36):1173-1179

Drosdek-Praktische. [Erfahrungen mit der Gerson-Sauerbruch-Herrmannsdorfer-Diat.] Beitr. z. Klin. d. Tuberk. 1931;78:697-723

Duncan GG. Diet in the management of ascites. Med Clin North Am 1932;16(1):243-249

Eckhardt H. [DieStellung der Kruppelfursorge zur Gerson-Herrmannsdorfer-Sauerbruch-Diat bei der Knochengelentuberkulose.] Ztschr. f. Kruppelfursorge 1935-05/06;28:79

Egues J. [Regimen dietetico en los tuberculosos pulmonares.] Rev Asoc Med Argent 1932-12;46:1574-1581



This is just the published results up to the letter D; one gets the picture.

Ray has no real answer to this, and prefers to avoid the subject altogether, as the transcript shows.

Let's leave Gerson alone for a second. Based on the quotes about SIADH people with cancer and SIADH have increased total body fluids (edema) and are losing sodium (hyponatremia)? Doesn't that match what Peat is saying?

 

[burtlancast]

Let's leave Gerson alone for a second. Based on the quotes about SIADH people with cancer and SIADH have increased total body fluids (edema) and are losing sodium (hyponatremia)? Doesn't that match what Peat is saying?

Well, if you read further on Wiki about SIADH, it says :"Although the sodium level is low, SIADH is brought about by an excess of water rather than a deficit of sodium."

That's because Vasopressin causes an "Acute increase of sodium absorption across the ascending loop of henle. This adds to the countercurrent multiplication which aids in proper water reabsorption later in the distal tubule and collecting duct.[9]".

So i'm afraid we're just going in circles with this vasopressin thing.

By increasing tissue potassium concentration ( with diet and / or supplements to the point of overabundance ) along with the help of a low sodium diet/intake, the body is forced to excrete more sodium, as a part of an endogenous regulation process described by Ling, up to the point where injured tissue is restored to its fully functional state. And the more effectively the body excrete the sodium the more favorable the disease outcome is ( doing this probably require enough left vital energy for the sick patient, the same vital energy that would be, probably, lacking for people who were treated by previous exogenous/endogenous treatment like surgery/chemo/radiation ect.... ).
Hence, the fondamental importance for a return to a healthy Na/K intracellular ratio and cell proteins' homeostasis for an effective " cure " of the injured tissue.
I think that was what Gerson saw in his day-to-day observations, but wasn't able to explain at his time of clinical practice, without the rescue of Gilbert Ling's association-induction hypothesis.
Sounds good for a credible explanation,no?

Just an add to my post above. :)

Perfectly credible, indeed.

After Cope formulated his hypothesis of the tissue damage syndrome, based on the theories of Ling, he started looking in the medical literature to see if a high potassium/ low sodium diet had ever been shown to cure diseases (he had himself been trained as a medical doctor).

He was surprised to learn it had already been put successfully in practice by Gerson, as you wrote; he did find as well Demetrio Sodi-Pallares, a world famous Mexican cardiologist who used this diet to treat principally heart disease, and sometimes cancer.

Here's an extract about Pallares from the book " Bioelectromagnetic and Subtle Energy Medicine, Second Edition": we learn that not only Ling, Cope, Gerson, Pallares separately confirmed the deleterious effects of sodium, but so did Hans Selye !

" Pallares had initially become interested in the antagonistic roles of sodium and potassium in 1944 when his mother developed marked edema of the lower extremities, enlargement of the liver, and tremendous abdominal distention due to ascites. The diagnosis was heart failure due to coronary arteriosclerosis and her electrocardiogram showed a left bundle branch block. In those days, this usually meant a life expectancy of not more than 2 years but it would have been much less for his mother in view of her serious heart failure. She was receiving the standard treatment of mercurial diuretics ( used to deplete the body of sodium), digitalis, and a low cholesterol diet but she was allowed to have sodium rich foods that were low in fat. The aggressive diuretic therapy required to reduce her fluid retention caused severe cramps and left her feeling exhausted.

At the time, Sodi was involved in experimental electrocardiographic investigations at Mexico’s National Institute of Cardiology and when he inquired as to why she had to receive so many injections of the mercurial diuretic, his professors explained that it was to eliminate sodium chloride. He asked why they allowed her to eat foods rich in salt and was told that his mother had to be on a low cholesterol diet to delay the atherosclerotic process and that the injections would get rid of the salt.

He was not satisfied with this answer and, although he had little appropriate background, decided to develop a diet for her that would eliminate any food with a sodium content
higher than 100 mg/100 g. As it turned out, this was fortuitous, as he ended up with a diet that was not only low in sodium (around 360 mg) but also 10 times higher in potassium, and he did not realize how important this would prove to be. His mother followed the diet faithfully, was able to discontinue her medications, and went on to live a normal life for another 15 years. He began prescribing this dietary regimen for patients with other cardiovascular problems and found that most with congestive failure could be stabilized and usually only required digitalis and/or diuretics if they had acute pulmonary edema. The same was true for many others with essential hypertension, and it was not unusual for angina to disappear in weeks or even days after following the diet.

Exhilarated about his results, he tried to convince other physicians to try the diet in their patients to see if they got the same benefits.

Sodi went on to become a superb clinical cardiologist, authored some 20 cardiology texts, including over a dozen on the electrocardiogram alone, and his continued successes with the low salt diet only served to strengthen his belief in its benefits.

In spite of this opposition, he recommended it whenever he could and was encouraged by Hans Selye, who visited the Institute in 1959 during the International Symposium of Arteriosclerosis being held in Mexico City.

Selye presented his experiments demonstrating the damaging effects of sodium as well as the cardioprotective effects of potassium in animals subjected to stress. Compared to control animals, more extensive myocardial infarcts were seen in those who had been on a high sodium diet and given adrenal corticoids.

Potassium supplementation markedly reduced or prevented myocardial necrosis as seen in Figure 8.1.

FIGURE 8.1 Cadioprotective effect of potassium chloride, by Hans Syle. Left:
Massive necrosis visible as a white patch on the surface of the left
ventricle following ligature of the left coronary artery in a control
rat. Right: Complete prevention of the necrosis by pretreatment
with KCL in a litter made exposed to the same procedure.

As this could be demonstrated in animals with normal coronary arteries, it proved that myocardial infarction was not always due to obstruction of a coronary vessel that deprived
the myocardium of oxygen. At the time, heart attack, coronary occlusion, and myocardial infarction were often used interchangeably as if they were synonymous. However, it is
now clear that atherosclerotic occlusion of a coronary vessel, which occurs gradually, does not always result in a myocardial infarction and conversely, that myocardial infarction can result from excess catecholamine effects in the absence of coronary occlusion or even ischemia. This is not infrequent in pheochromocytoma and has also been reported as a complication of sympathomimetic drugs (isoproterenol, amphetamines), increased sensitivity to MAO inhibitors, and deaths related to sudden emotional stress, where characteristic “contraction bands” can be seen in the myocardium.1,2

Selye’s presentation also fell on deaf ears as it was contrary to current dogma and many felt that what happened to rats under laboratory conditions had little relevance for people.

In commenting on this several years later, Selye wrote:

"The very fact that scientists of so many countries have contributed to this monograph on metabolic cardiopathies bears witness to the great change in outlook that has been placed in the interpretation of pathogenesis of heart disease during the last decade. Barely eight years ago, in September 1959, at the International Symposium on Arteriosclerosis and Coronary Disease in Mexico City, I tried to prove that infarcts, like cardiac necroses, can be produced without vascular obstruction, that is, by combined treatment with electrolytes or corticoids and stress. At that time, with the notable exception of Dr. Sodi Pallares, few of the participants were prepared to believe that such metabolic factors could play a role in the genesis of true cardiac infarcts in man…..Although the functional effect of many electrolytes upon the heart has long been known, the finding that sodium increases and potassium and magnesium diminish the susceptibility to cardiac necroses was also received with the greatest reserve."

But what was the mechanism of action that explained the harmful effects of sodium and the benefits of potassium? Why did administering sodium cause fluid retention in patients while potassium did not, as both were monovalent cations?
In an acute myocardial infarction, three zones of injury can be distinguished. In the central portion of the damaged area, there is a core of necrotic tissue and dead cells due to the absence of oxygen. This is surrounded by an area of severe injury composed of cells that will die unless the metabolic derangement can be stopped or reversed. The damage lessens progressively in the periphery of this section that gradually merges into a larger third zone of cells that are less ischemic.
Here, structural damage is not as impressive, and although function is impaired compared to adjacent normal tissue, the abnormalities are reversible.

Sodi demonstrated that in experimental infarction produced by ligature of the left coronary artery in dogs, he could show a clear and consistent correlation between the degree of damage and intracellular concentrations of sodium and potassium as one progressed through these three zones from healthy muscle. The higher the concentration of sodium, the greater the degree of damage, but the reverse was true for potassium.

Compared to normal tissue, intracellular sodium in the ischemic area increased around 50%, compared to over 200% in the intermediate area of injury and more than 300% when the central necrotic core was reached. There was a corresponding decrease in potassium of 5% in ischemic tissue, 10% in the intermediate injury zone, and 18% in the
necrotic area. Although these figures varied with the location and size of the infarct, they showed the same consistent interrelationships.

Were these abnormalities in sodium and potassium merely a reflection of the degree of damage or could they possibly contribute to it? Was increased intracellular sodium the cause of cellular injury?

All atoms have shells orbiting around them filled with electrons to neutralize the positive charge of protons in the nucleus. The first shell contains two electrons and each successive shell contains eight electrons. The sodium atom has 11 electrons, two in the first shell, eight in the second, but only one in the third that it must get rid of to remain stable. The potassium atom has 19 electrons so it has three shells that are filled and a fourth that has only one electron.

In both situations, there is a need to remove the extra electron by finding an atom with a shell that needs more electrons to be filled. When this happens, one of the protons in the
nucleus is not balanced and these atoms now become monovalent positive ions or cations (Na+ and K+). A molecule of water (H2O) consists of two atoms of hydrogen, each having
a positive charge, and 1 atom of oxygen that has a negative charge. As the radius of the potassium ion, or the distance from the center of the nucleus to the external orbit, is greater than the radius for sodium it is easier for water molecules to cluster around the sodium ion. When the number of intracellular sodium ions increases, they attract more molecules of free water than potassium does and the resultant swelling of the cell interferes with normal function.

 

[Wilfrid]

Very insightful infos. Thanks, Burt.