Cancer And Glucose (sugar)

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jb116

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The logic isn't sound when you think of the whole picture. Gas is flammable, should we not use it for fuel in our cars?
For every negative effect taken out of context, the proper use of any fuel in biology or automobiles could of course come across as looking evil. But the whole picture dictates what the best approach is. What's more reasonable is probably using sugar to spare protein, lots of B Vitamins regimented, especially b1 and b3, essentially low or no fat, and aspirin. Some sugar will be used but the more and more oxidative metabolism is restored; the more pyruvate dehydrogenase is replenished and the more free fatty acids can be inhibited, the better the tides can turn for sugar towards being anti-cancerous.
 

Ella

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I would look at the studies below before jumping on the ketogenic diet for cancer. Some of the most promising drugs lately are FAS inhibitors, FAO inhibitors, or lipolysis inhibitors. A high fat diet will negate most of the effects of these drugs.
Cancer Addiction To Fat Confirmed; Niacinamide As Possible Treatment
Dietary Fat And Its Oxidation Drives Cancer Metastasis
Achilles Heel Of Cancer Found - Its Addiction To Fat

Cancer cells use amino acids to convert them to sugar and then use the sugar to synthesize fat and then oxidize that fat. Given how inefficient that process is energetically, it explains some of the reasons (besides inflammation) for cachexia - a person restricting sugar will quickly lose muscle mass and fat in order to drive that inefficient process of fat synthesis.


Thanks for reminding me Haidut. This is why it scared me about my weight loss. There is no fear I'll adopt a ketogenic diet as I am still carrying a shitload in adipose tissue which concerns me when I release FFAs into circulation. My current state is that akin to a high- fat diet. I think that even if I have avoided PUFAs for decades, any type of fatty acids is going to fuel carcinognesis. Peat states a fat % somewhere between 20 - 30 is OK. That is a huge range and I am assuming somewhere around 30% is OK for females to aim for. I know plenty of skinny females that have died from cancer at a young age. In fact no fat ones???? So being in a constant fat burning state was their achilles heel. And this is the dilemma for me. Should I just submit my body to a couple of days of fasting a week to speed up the process or continue to slowly infuse my system with free fatty acids. I don't think I can tolerate more fruit. It is Autumn now and root veggies and leafy greens will be on the menu and see how I fair. My body is over sweet; maybe it knows summer harvest is over??? I think I need to do more muscle work with more sunshine to speed the process without crashing my adrenals.

My fear with this whole ketosis epidemic is that more young people will be lost to cancer. I witnessed many young people die from cancer doing paleo and gym workouts in the past 5 years. Many of them young males which is revealing. Meat jerkies, chicken and protein powder is a recipe for an early grave. There are young wives with tiny children without husbands and fathers. Young men that didn't make to the altar with their sweetheart; left grieving. I find it too distressing that in 2017, we are still debating on how to feed ourselves.
When I originally tried niacinamide I got terrible headaches, I can take the same dose now and don't get headaches and take it before bed which means I must be storing glycogen.
 

raypeatclips

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All I am saying is that low stomach acid is present in virtually all cases of hypothyroidism (hence the explosion of SIBO epidemic recently), and so is low CO2. When you don't produce enough gastric acid you won't digest the food properly and it won't absorb well. This applies even to carbohydrates like sucrose or starch, which are the main sources of CO2 production. Without enough stomach acid the hydrolysis of these macronutrients is incomplete at best and not only you end up with less absorbed food but the indigested food contributes to development of SIBO and feeds the colonic bacteria to produce endotoxin.
So, yes, if you produce less stomach acid than the food eaten requires for proper digestion then you'll produce less CO2.
The Digestion & Absorption of Sucrose
Absorption of Monosaccharides

What makes it a vicious circle is that CO2 ie required for stomach acid production.
The source of carbon dioxide for gastric acid production. - PubMed - NCBI
So, once a person is stuck in this loop I guess somehow raising either CO2 or stomach acid pharmacologically would be the only way out. Thiamine, betaine, pepsin, etc can help in such cases. Thiamine is probably crucial as it can help both stomach acid production and CO2 generation.

So you don't think the typical SIBO treatment of various antibiotics is good? Surely in the state of low CO2 etc, the problem might return after antibiotics have stopped? So thiamine, caffeine and all the other things you have mentioned for increasing gastric acid, is what you would recommend for SIBO?
 

haidut

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So you don't think the typical SIBO treatment of various antibiotics is good? Surely in the state of low CO2 etc, the problem might return after antibiotics have stopped? So thiamine, caffeine and all the other things you have mentioned for increasing gastric acid, is what you would recommend for SIBO?

Antibiotics will provide at most temporary relief. Ultimately, CO2 and proper metabolism is needed for acid production. Some people on the forum have suggested betaine Hcl combined with Pepsin as another option.
 

raypeatclips

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Antibiotics will provide at most temporary relief. Ultimately, CO2 and proper metabolism is needed for acid production. Some people on the forum have suggested betaine Hcl combined with Pepsin as another option.

I recall you were negative about betaine hcl supplements, have I got that right? Have you changed your mind on them at all?
 

haidut

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I recall you were negative about betaine hcl supplements, have I got that right? Have you changed your mind on them at all?

Yes, I think betaine is a strong methyl donor and as such can cause issues with thyroid and even cancer. Thiamine, caffeine, and glycine/gelatin seem to be able to achieve the same (at least according to me) without the risks of betaine.
 

nikolabeacon

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So you don't think the typical SIBO treatment of various antibiotics is good? Surely in the state of low CO2 etc, the problem might return after antibiotics have stopped? So thiamine, caffeine and all the other things you have mentioned for increasing gastric acid, is what you would recommend for SIBO?

Probably this can explain why Fats of any kind are rumoured to increase endotoxin load and worsen SIBO. For someone that have very strong stomach its not a problem but over time high fat can promote poor digestion and decreased acid.


"On the other hand, fats tend to inhibit gastric secretion so that an excessive proportion of fat in the diet might weaken digestion in the stomach."

"Any diet therefore that has the effect of diminishing or neutralizing the stomach acid which othervise would reach the small intestine is unfavorable for pancreatic digestion."

"Broths, milk, dextrin, dextrose exert a pronounced influence which makes the rational the taking of soups or bouillon as the first dinner course or the eating of toasted bread or zweiback by persons with weak digestion."

--- Principles of Human Nutrition

Apart from eating carbohydrates and proteins ...Also small meals are mentioned as another good measure for people with weak digestion and for increase in stomach acid.
 

yerrag

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This is an interesting thread, and the question of whether sugar feeds cancer or not seems to not have been resolved.

My orientation is towards avoiding fat and using sugar. It's based on my view that whether there is cancer or not in the person, the body's needs are for efficient metabolism to provide it with energy to sustain, repair, and to protect itself. The most efficient metabolic pathway is oxidative metabolism, which also for an environment that is supportive of the body's balance with carbon dioxide. When there is no cancer, the body will be able to go on in a balanced state of health. When there is a cancer forming, the body will be able to nip a developing cancer in the bud.

A body with a more advanced stage of cancer has been suffering chronic stress, and this environment has brought about the growth of cancer. Given my understanding that cancer is not a genetic condition, and an environmental condition, I am more disposed to treat cancer by restoring an environment that is free, or has a practical minimum, of these stressors - lactic acid, endotoxin, serotonin, nitric oxide, cortisol, adrenaline, estrogen, and would have a supply of protective substances from within - carbon dioxide, thyroid, pregnenolone, progesterone, and sugar. To develop this environment, one has to have the energy to sustain it, and that would mean restoring and ensuring that energy is produced with oxidative metabolism, and not with other metabolic pathways such as aerobic and anaerobic glycolysis, which often would involve the breakdown of fat and protein, as opposed to simply using glucose. Oxidative metabolism provides the most efficient production of energy, and the by-product carbon dioxide further sustains this efficient metabolism. Other metabolic pathways are not only inefficient, but produce stress conditions, as brought about by the production of lactic acid.

A body that has come to rely less on oxidative metabolism and more on the altenate pathways will put itself in a state of chronic stress. Aside from energy being wasted by the wrong choice of pathway , the body will also waste energy on carrying out its work of sustaining, repairing, and protecting itself. The lack of carbon dioxide, for example, will require more effort to deliver oxygen to its tissues. This may require a higher heart rate, and/or a higher breathing rate.

The continual wrong metabolic pathway being used imposes on the body chronic stress conditions, and provides the environment for cancer. Seen this way, one can view cancer as a deadly disease of metabolism. If we are to get rid of cancer, and to recover fully, we have to change the environment. To change the environment, we need to give the body to the nurturing effects of oxidative metabolism. With the right environment, cancer cells will not thrive. Cells will regain the ability to differentiate and regenerate, and phagocytes will be made available to destroy cancer cells. But the energy needed can only be provided by oxidative metabolism, and the key ingredients needed are oxygen and sugar.

I cannot see why not feeding sugar will help the body fight cancer. Even if we suppose that sugar is feeding cancer, do we keep sugar out just because it aids the enemy? Are we not strengthening the body more than we are aiding the enemy? Sugar will make the body stronger more than it helps the cancer. But with fat, I'm afraid it will be the other way around.
 
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this study shows low glucose and low pH/hypoxia lead to cancer, which makes a lot of sense

btw, CHO are hamster ovarian cells, a common model

Glucose starvation and acidosis: effect on experimental metastatic potential, DNA content and MTX resistance of murine tumour cells. - PubMed - NCBI
Exposure to oxygen deprivation in vitro has been reported to cause drug resistance in CHO cells (Rice et al., 1986; PNAS 83, 5978) and enhancement of experimental metastatic (colonisation) ability of murine tumour cells (Young et al., 1988; PNAS 85, 9533). Both these studies also demonstrated the induction of a subpopulation of cells with excess DNA content. Since the micromilieu in tumours results in exposure of the tumour cells to conditions of acid pH and nutrient deprivation, as well as hypoxia, we have examined the effect of exposure to acidosis (pH 6.5) and glucose starvation on drug resistance, cellular DNA content and the experimental metastatic ability of KHT sarcoma and B16F1 melanoma cells. Cells were exposed to these conditions for 24 and 48 h and tested for resistance to methotrexate (MTX) or experimental metastatic ability either immediately following these exposures or after 24 or 48 h of recovery in normal growth medium. Both cell lines demonstrated an enhancement of colonisation potential, which was most marked when cells were injected after 48 h of exposure followed by a 24 or 48 h recovery period. Flow cytometric analysis demonstrated an increase in the fraction of KHT cells with excess DNA following both glucose starvation and acidosis we observed only a small increase in MTX resistance following acidic exposure of cells and no change following glucose starvation. Since both acidosis and glucose starvation are known to induce glucose regulated proteins (grp), a subset of the stress protein family, we studied the effect of treatment with another known inducer, 2-deoxyglucose. We found that this agent affected the metastatic efficiency of KHT cells in a manner similar to that observed following exposure to glucose starvation and acidosis. However, further studies are required to establish what role, if any, grp play in this effect. In conclusion this study shows that transient exposure of murine tumour cells to an acidic or glucose deprived environment can cause progression in terms of metastatic potential.
 

yerrag

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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.

This study talks about hyperglycemia and its dire effects. In trying to read into this, I see this as not necessarily saying that sugar in itself is harmful, but says that too much sugar in the blood is harmful, as in "hyperglycemia." Because taking sugar (glucose, to be more specific) has a hyperglycemic (as well as hypoglycemic, when the insulin kicks in strongly) effect on people with problems with sugar metabolism, the problem can be said to arise with people with impaired sugar metabolism, and not for people with healthy sugar metabolism. That said, it may be assumed that cancer patients have problem with sugar metabolism, and as such, sugar intake can be harmful as this study suggests.

But isn't the approach to keep the cancer patients blood sugar levels normal while allowing the patients to take in sugar? If the sugar is high-fructose rather than high in glucose, wouldn't the patients be able to take in sugar and metabolize it better, and avoid hyperglycemia? And wouldn't the use of aspirin and niacinamide be able to prevent lipid peroxidation and the release of free fatty acids into the bloodstream, such that sugar metabolism wouldn't be blocked, and the blood sugar would not rise to hyperglycemic levels because it is being used up by the tissues?

It seems to me that saying sugar is bad for the cancer patient is like saying water is bad for a land robbed of trees. Because water causes flooding. Where it is the land that is in need of remedial action. The land has no trees to take in the water, and all that water from rain is turning into a flash flood and killing hiking bystanders on its way to the sea. The solution is not to stop the rain (if that is at all possible), but to put in stop gap measures such as better drainage, while replanting trees and giving it time for the land to be nursed back to health.
 

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

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

The high glucose value of 25 mM is greek to me. Can anyone convert to mg/dL?

If the study's conclusions is based on high blood glucose levels, it still doesn't say anything about normal blood glucose levels being bad. If the cancer patient is given sugar and can maintain normal blood glucose levels, this study's conclusions cannot apply.
 

yerrag

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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

I want to put the study in context of common medical practices of treating patients. Patients are given oxygen with atmospheric air. They are not given any carbon dioxide support at all. No carbogen. No baking soda solutions. It would be reasonable to assume that cancer patients have impaired energy metabolism, and because of this condition, they would already lack carbon dioxide in their blood. In such a condition, their blood is not releasing enough oxygen to the body's tissues. This would limit their energy production such that the body would continue to run on aerobic glycolysis or anaerobic glycolysis, instead of oxidative metabolism. The sugar would certainly not be used efficiently, and the by-product production of lactic acid would continue to make the body worse.

Make another study, put in carbogen for breathing, and let's see what happens. Then maybe, the conclusions would be different.

Also, given that a typical hospital setting very easily gives a false negative to hypothyroidism, with its flawed use of endocrine markers TSH, Free T3, and Free T4, they would usually not address an underlying hypothyroid condition. Not addressing this puts them on a wild good chase, and to making conclusions without qualifying enough the parameters of their study.
 
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yerrag

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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.

Call me crazy, but if salt is being released, it's the body's attempt to increase uric acid. The need for uric acid production necessitates hypoxic conditions thru constriction of blood vessels. To constrict the blood vessels, blood volume has to decrease to be able to be in balance with the lower cross sectional area of the blood vessels. There could be a higher blood pressure as a result as well.
 

haidut

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The high glucose value of 25 mM is greek to me. Can anyone convert to mg/dL?

If the study's conclusions is based on high blood glucose levels, it still doesn't say anything about normal blood glucose levels being bad. If the cancer patient is given sugar and can maintain normal blood glucose levels, this study's conclusions cannot apply.

It usually means 25mM/L. To get that you'd need a bolus dose of about 130g - 150g glucose, which is doable but it will not be sustained as insulin will kick in and blood glucose will drop. To be diagnosed as diabetic you need to register blood glucose levels above 7mM/L, and only people in danger of slipping in diabetic coma from hyperglycemia come close to 20mM/L. So, not a study relevant for most people, even ones with diabetes.
 

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Peat Used To Be A Fan Of Low Carb, No Sugar Diets

J Clin Invest. 2008 Dec;118(12):3930-42. doi: 10.1172/JCI36843. Epub 2008 Nov 20.
Targeting lactate-fueled respiration selectively kills hypoxic tumor cells in mice.
Sonveaux P1, Végran F, Schroeder T, Wergin MC, Verrax J, Rabbani ZN, De Saedeleer CJ, Kennedy KM, Diepart C, Jordan BF, Kelley MJ, Gallez B, Wahl ML, Feron O, Dewhirst MW.
Author information

Abstract
Tumors contain oxygenated and hypoxic regions, so the tumor cell population is heterogeneous. Hypoxic tumor cells primarily use glucose for glycolytic energy production and release lactic acid, creating a lactate gradient that mirrors the oxygen gradient in the tumor. By contrast, oxygenated tumor cells have been thought to primarily use glucose for oxidative energy production. Although lactate is generally considered a waste product, we now show that it is a prominent substrate that fuels the oxidative metabolism of oxygenated tumor cells. There is therefore a symbiosis in which glycolytic and oxidative tumor cells mutually regulate their access to energy metabolites. We identified monocarboxylate transporter 1 (MCT1) as the prominent path for lactate uptake by a human cervix squamous carcinoma cell line that preferentially utilized lactate for oxidative metabolism. Inhibiting MCT1 with alpha-cyano-4-hydroxycinnamate (CHC) or siRNA in these cells induced a switch from lactate-fueled respiration to glycolysis. A similar switch from lactate-fueled respiration to glycolysis by oxygenated tumor cells in both a mouse model of lung carcinoma and xenotransplanted human colorectal adenocarcinoma cells was observed after administration of CHC. This retarded tumor growth, as the hypoxic/glycolytic tumor cells died from glucose starvation, and rendered the remaining cells sensitive to irradiation. As MCT1 was found to be expressed by an array of primary human tumors, we suggest that MCT1 inhibition has clinical antitumor potential.

Source: Targeting lactate-fueled respiration selectively kills hypoxic tumor cells in mice. - PubMed - NCBI

See following article:

Do Ketones Fuel Cancer? The Low-Carb Experts Respond « Jimmy Moore's Livin' La Vida Low-Carb Blog
 

Philomath

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Wow, so much disinformation from actual doctors!

OK, first and foremost, the statement about cancer cells being somehow hooked on sugar is wrong. Cancer cells actually love fat more than anything else:
Cancer cells use fat oxidation for survival | Ray Peat Forum

All you need to read is the first paragraph. Niacinamide/Aspirin to the rescue of every cancer patient! Well, it is probably not enough but you get the point.

Couple of other points. Despite what "cancer gurus" like Amanda Mary say you cannot simply deprive cancer cells of glucose. The cancer will get its glucose either from diet or by eating your muscles at an amazing speed. And if it breaks down muscle tissue it will not only kill the person much faster through cachexia but the breakdown of muscle tissue will also generate glutamine, which cancer cells also love and thrive on; arginine, which will increase NO production; and cysetine, which will help the cancer increase its reductive potential, provide even more sulfhydryl groups for cancer growth, and serve as a powerful anti-oxidant for the tumor to resist destruction from chemotherapy, radiation, and even internal ROS.
There is a reliable way to starve cancer cells of glucose and that is by feeding the organism the so-called 2-deoxy-d-glucose (2-DG).
2-Deoxy-D-glucose - Wikipedia, the free encyclopedia

Given the pervasiveness of this flawed thinking, 2-DG is of course being tried to starve tumors of sugar. It failed, even though initially it seems to restrain tumor growth. Dietary restriction of sugar seems to have the same effects and then the tumor rebounds because it starts to break down muscle tissue for sugar. And of course, like anything that inhibits glucose oxidation, 2-DG has serious cardiac side effects.
"...2-DG is uptaken by the glucose transporters of the cell. Therefore, cells with higher glucose uptake, for example tumor cells, have also a higher uptake of 2-DG. Since 2-DG hampers cell growth, its use as a tumor therapeutic has been suggested, and in fact, 2-DG is in clinical trials [3] A recent clinical trial showed 2-DG can be tolerated at a dose of 63 mg/kg/day, however the observed cardiac side-effects (prolongation of the Q-T interval) at this dose and the fact that a majority of patients' (66%) cancer progressed casts doubt on the feasibility of this reagent for further clinical use.[4] However, it is not completely clear how 2-DG inhibits cell growth. The fact that glycolysis is inhibited by 2-DG, seems not to be sufficient to explain why 2-DG treated cells stop growing."

Now, a much saner approach would be not to somehow deprive the tumor of sugar but consider cancer cells as cells that cannot fully metabolize sugar. It is well-known and undisputed that cancer cells have dramatically downregulated activity and levels of PDH. That is the main reason they overproduce lactate. When glucose is metabolized it produces pyruvate and NADH. If PDH is working, pyruvate is converted into Acyl-Co-A and feeds into the Krebs cycle. If PDH is not working, both pyruvate and NADH build up. The cell depends on NAD for survival and will do anything to get it back. Typically, if metabolilsm is working well, NADH will be oxidized back into NAD in the electron transport chain. However, in hypoxic conditions or malfunctioning metabolism there is no way to oxidize NADH back to NAD. So, the cell used the only material available to it for oxidation and that is the excess pyruvate that builds up during glycolysis. The enzyme lactate dehydrogenase (LDH) is what takes pyruvate and NADH and used pyruvate to oxidize NADH back to NAD and that process converts pyruvate to lactate. However, even that process is not sufficient to meet the NAD needs to of the cells quickly enough so they die. That is why people with cancer have abnormally high LDH levels - first because it is elevated to convert pyruvate to lactate and NADH to NAD, and second because when even that process is not fast enough the cell dies spilling its LDH into the bloodstream.
So, what does one do in situations like that?

1. Boost PDH by any and all means possible. The chemical dicholoroacetate (DCA), that pretty much everybody has heard of as possible cancer treatment, boosts PDH activity. Unfortunately, it is also toxic to the glycolysis enzymes and eventually becomes a carcinogen itself. However, thiamine, which is a cofactor of PDH does not have these side effects and at least one study found it comparable to DCA for cancer treatment.
Thiamine acts similarly to DCA and may be helpful in cancer | Ray Peat Forum

Thiamine is also carbonic anhydrase inhibitor and will raise CO2 levels, which will also oppose lactate buildup.
Thiamine is a carbonic anhydrase inhibitor as effective as acetazolamide | Ray Peat Forum

And thiamine also lowers ammonia, which is likely to be high in people with cancer as they break down muscle tissue under the "wise" advice of their doctor to lower glucose intake.
Thiamine reduces both lactate and ammonia | Ray Peat Forum

In addition, to PDH, there is also PDC. That enzyme is a biotin-dependent enzyme and is an alternative "consumer" of pyruvate and converts it into oxaloacetate to also feed into the Krebs cycle. I don't know the exact dose for biotin but given the recent clinical trial with MS, starting with 300mg seems like a good bet since that dose raised ATP production and increased CO2.

2. Provide alternative oxidizing agents if oxygen is not available or unable (as in cancer) to oxidize NADH. Methylene blue is prime example of a substance that can completely replace oxygen in the metabolic pathways. It also stimulates the activities of electron transport chain comp[lexes II, III, and IV and also boosts levels of cytochrome C oxidase. Vitamin K can also serve as alternative electron carrier if CoQ10 is unavailable or very low (as in cancer).

3. Provide substances that oppose the Warburg phenotype systemically. Thyroid hormone, quinones, methylene blue, tetracyclines, dopamineric agents, anti-estrogens, anti-serotonin agents, anti-glucocorticoid agents, anti-aldosterone agents, etc can all contribute to that effect but thyroid hormone is the master regulator.

I can list at least 20 other steps that are key in inhibiting cancer growth and restoring normal cell function, but those are already posted on the forum. What gives me anxiety is that if these simple biochemical processes are not something that the doctor is likely to know and apply, then your doctor is much more likely to kill you than help you since these same biochemical principles apply to all therapies and all drugs for any condition. ANYTHING that inhibits respiration, be it in the step of glycolysis, Krebs cycle, or electron transport chain, WILL cause a disease of some kind and eventually cancer if the patient lives long enough and does not die from earlier complications.
I suppose creating a Wiki page that summarizes this well would greatly help in dispelling some of the myths being propagated by medical professionals that are so focused on their specific (and usually genetically-driven) field that none of them even tries to look at the big picture. You want to try for yourself? Next time you see your primary care doctor ask him/her what happens in the body when somebody restricts sugar intake. Jut ask for simple explanation of the processes that kick in and how the body adapts. I have tried it with 7 of my friends so far who are all M.D. and got either a blank stare or an insulted response "I don't work in metabolics/diabetes".
Provide alternative oxidizing agents if oxygen is not available or unable (as in cancer) to oxidize NADH. Methylene blue is prime example of a substance that can completely replace oxygen in the metabolic pathways. It also stimulates the activities of electron transport chain comp[lexes II, III, and IV and also boosts levels of cytochrome C oxidase. Vitamin K can also serve as alternative electron carrier if CoQ10 is unavailable or very low (as in cancer).
@haidut , how much methylene blue do you believe might be necessary for this?
 

haidut

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@haidut , how much methylene blue do you believe might be necessary for this?

Even 1mg-2mg should be able to lower lactate and if used in combination with another quinone like emodin or vitamin K then 1mg-2mg MB is probably enough. HUman studies with 15mg daily show potent effects on mental illness and since those issues are also due to elevated lactate and low CO2 then I guess up to 15mg daily could be used for cancer as well.
 

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