The significance of glucose, insulin and potassium for immunology and oncology: a new model of immunity

[LLight]

The significance of glucose, insulin and potassium for immunology and oncology: a new model of immunity

A recent development in critical care medicine makes it urgent that research into the effect of hormones on immunity be pursued aggressively. Studies have demonstrated a large reduction in mortality as a result of infusion with glucose, insulin and potassium. ...

www.ncbi.nlm.nih.gov

Conclusion
We conclude that TGIK has anti-tumor activity when administered intratumorally, probably by stimulating lymphocytes to attack tumors. This is similar to the effect of GIK on reducing sepsis in critical care patients. We suggest that when GIK is administered exogenously, it restores immune competence to the critically ill or cancer patient and causes destruction of pathogens or tumors, while endogenous resources are devoted to repair. This implies that hormonal therapy may be useful in treating various other pathologies involving immune suppression, as well as malignancies. We also propose research that could bring resolution of the controversy over mechanism and point the way to new therapeutic strategies for numerous diseases including chronic infections and auto-immune diseases.

 

[yerrag]

Interesting and thank you! @LLight

It appears to me to be a rather basic procedure that needs to be stated as it has been overlooked with having so many choices available. In a metabolically healthy and balanced person, with no deficiencies, having enough TGIK is a natural consequence. But with patients that do not fit this profile, which is more common, having to resort to TGIK therapy would have good effects.

Prior to reading this, I am guided by the idea that if the wbc has plenty of neutrophils, the infection would be bacterial, and if the wbc has plenty of lymphocytes, the infection would be viral. But now I see that as a rule of thumb - a guide that is fast and loose with its categorization. The review would differ on this. As it turns out, if the immune response is heavily dependent on the innate immune response, it would be producing plenty of inflammatory cytokines. Whereas if there is a significant involvement of lymphocytes of the T variety, there would also be plenty of anti-inflammatory cytokines involved in fighting pathogens. This would lessen the debilitating symptoms characterized by an autoimmune response.

Over the past year, I've lost plenty of potassium because I wasn't aware till recently that I've been urinating too much and that I've lost plenty of potassium. Last week, I tested myself on my sugar regulation with the 5hr OGTT (oral glucose tolerance test) and I failed the test. I attribute this to my potassium stores having gone low. Because of this, the consistency of conversion of T4 to T3 by the liver would be impacted as well, as for this conversion to be consistent, the supply of energy must be consistent to the liver. With poor blood sugar regulation, this supply becomes unreliable and a momentary loss of T3 supply would have snowball effects that would last. So I've been taking a drop of T3- 8mcg - after each meal in the hope that it could cover the slack and eventually get the energy flow back to normal. For the potassium, I'm drinking juice from a local citrus fruit in season (dalandan), and since it isn't as naturally sweet as an orange, I'd have to add white sugar. This would be my equivalent TGIK therapy.

Without the good sugar metabolism, my acid-base balance is also off. I've been having testing really acidic at the start, but slowly it's coming around and my acid-base balance has improved. I'm using urine pH as a surrogate marker for serum/ecf pH.

I'm grappling with high urination rates and with heavy foaming. I have a sense that the high acidity and the high urination rates has a lot to do with an existing low-level infection. All the more important for me to beef up my sugar metabolism, and TGIK will help as I figure out how to lower my urination rate and its foaming. Somehow, it all will come together as part of solving my hypertension, which is tied in chiefly with infection and inflammation. They are all connected and glued together.

Thanks for sharing!

 

[LLight]

Over the past year, I've lost plenty of potassium because I wasn't aware till recently that I've been urinating too much and that I've lost plenty of potassium. Last week, I tested myself on my sugar regulation with the 5hr OGTT (oral glucose tolerance test) and I failed the test. I attribute this to my potassium stores having gone low. Because of this, the consistency of conversion of T4 to T3 by the liver would be impacted as well, as for this conversion to be consistent, the supply of energy must be consistent to the liver. With poor blood sugar regulation, this supply becomes unreliable and a momentary loss of T3 supply would have snowball effects that would last. So I've been taking a drop of T3- 8mcg - after each meal in the hope that it could cover the slack and eventually get the energy flow back to normal. For the potassium, I'm drinking juice from a local citrus fruit in season (dalandan), and since it isn't as naturally sweet as an orange, I'd have to add white sugar. This would be my equivalent TGIK therapy.

I've stumbled upon this one after reading your (recent?, I don't remember) emphasis on potassium and re-reading a post of @Amazoniac about how intracellular potassium is needed for water structure and how high potassium nutrition could be (at least in part) the basis of the Gerson therapy.

Showerthought : this paper made me think that diabetes patients generally have high insulin and high blood glucose. May they "just" lack the potassium? If they were not deficient, they would basically in the situation of this protocol (T3 excluded). Diabetes is often correlated with infections too. Maybe the body is waiting for the potassum to be sufficient before lauching the "assault".

I happen to drink lemon juice too at this time. Are they all high in potassium or is this just this type (the dalandan)?

 

[yerrag]

Showerthought : this paper made me think that diabetes patients generally have high insulin and high blood glucose. May they "just" lack the potassium? If they were not deficient, they would basically in the situation of this protocol (T3 excluded). Diabetes is often correlated with infections too. Maybe the body is waiting for the potassum to be sufficient before lauching the "assault".

I had to go back to reading the article. After 3 passes, I'm still at a loss on putting my thoughts together, to answer your question.

Since type 2 diabetics are insulin resistant, having high insulin and yet having high blood sugar, it could very well be that the reason that condition exists is that, as you say, is low potassium. Low potassium has more effect on sugar absorption by tissues than insulin (contrary to the general notion), and if potassium is deficient, and sugar is not being absorbed, then blood sugar will rise. This triggers insulin to be secreted by the pancreas, with little or no effect on lowering blood sugar, because no matter how much insulin accumulates, blood sugar won't go down simply because potassium is lacking.

A state of high insulin makes the lymphocyte unresponsive to being activated, even when challenged by an antigen:

"...it has been shown that "...CS lymphocytes after 4 hours of hyperinsulinemia in the normal subjects... had a sharp reduction in insulin-supported lymphocyte mediated cytotoxicity [74]. A lymphocyte cannot respond if levels of insulin are high before it is challenged by an antigen." p. 9

Because of this condition, the immune system would be restricted to using its innate portion, and without the adaptive leg to do its part, the response would be characterized by production of inflammatory cytokines by neutrophils and macrophages. So, not only is there an insufficient response to infection by the inability to activate the lymphocytes of the adaptive immune system, there would also be a chronic inflammatory response in dealing with the infection.

I think you're spot on with the potassium needing to be supplemented by diabetics to such extent that their potassium stores are made sufficient. Potassium isn't only needed for sugar absorption though, it's also needed for membrane integrity of cells, and this integrity is needed to help maintain calcium balance. By balance it's maintaining a calcium extra/intracellular ratio of 15000:1, and this ratio provides the ionic gradient needed for optimal expansion and contraction of heart muscles. This makes for efficient pumping of blood, and this certainly impacts energy production which is needed also by the immune system to deal with infections effectively.

 

[yerrag]

I just don't know how I can apply this information to my case of having high inflammation causing my high blood pressure. There is a link somewhere. While I'm not diabetic, which makes me discount the possibility of high insulin and high blood sugar affecting my immune system response, I'm wondering at whether my T-lymphocyte response is compromised. It bothers me that it may be that my adaptive immune response may have been tampered with by vaccination, leading it to prefer to produce B-cell antibodies instead of cytotoxic T lymphocytes (CTL) to deal with infection. The CTL would just kill cleanly pathogens, whereas B-cell antibodies would form immune complexes (IC) which would accumulate in organs (such as kidneys, liver, and heart) and which would provoke the immune system to treat it as a foreign substance, which would elicit macrophages to attack it and produce inflammatory cytokines in the process.

 

[gaze]

andrewkimblog.us

andrewkimblog.us

I like andrew kim's articles on it. he tends to disagree with peat, and I lean toward his ideas as well

 

[LLight]

While I'm not diabetic, which makes me discount the possibility of high insulin and high blood sugar affecting my immune system response, I'm wondering at whether my T-lymphocyte response is compromised.

I did not check extensively but I heard that leptin could also be an hormone powerfully influencing the immune system (toward inflammation probably, it's a cytokine).

I'm not sure it is easy to measure but a sign of high leptin should be disorganized hunger patterns if I'm not mistaken.

I don't know the potential causes of such issue though.