Cancer And Glucose (sugar)

[Westside PUFAs]

Also, does Amanda Mary not know that the brain and red blood cells burn a metric f**kton of glucose everyday? She's so anti-glucose but it seems she missed what glucose actually is:

"Brain. Glucose is virtually the sole fuel for the human brain, except during prolonged starvation. The brain lacks fuel stores and hence requires a continuous supply of glucose. It consumes about 120 g daily, which corresponds to an energy input of about 420 kcal (1760 kJ), accounting for some 60% of the utilization of glucose by the whole body in the resting state. Much of the energy, estimates suggest from 60% to 70%, is used to power transport mechanisms that maintain the Na+-K+ membrane potential required for the transmission of the nerve impulses. The brain must also synthesize neurotransmitters and their receptors to propagate nerve impulses. Overall, glucose metabolism remains unchanged during mental activity, although local increases are detected when a subject performs certain tasks.

Glucose is transported into brain cells by the glucose transporter GLUT3. This transporter has a low value of KMfor glucose (1.6 mM), which means that it is saturated under most conditions. Thus, the brain is usually provided with a constant supply of glucose. Noninvasive 13C nuclear magnetic resonance measurements have shown that the concentration of glucose in the brain is about 1 mM when the plasma level is 4.7 mM (84.7 mg/dl), a normal value. Glycolysis slows down when the glucose level approaches the KM value of hexokinase (~50 μM), the enzyme that traps glucose in the cell (Section 16.1.1). This danger point is reached when the plasma-glucose level drops below about 2.2 mM (39.6 mg/dl) and thus approaches the KM value of GLUT3.

Fatty acids do not serve as fuel for the brain, because they are bound to albumin in plasma and so do not traverse the blood-brain barrier. In starvation, ketone bodies generated by the liver partly replace glucose as fuel for the brain."

Each Organ Has a Unique Metabolic Profile - Biochemistry - NCBI Bookshelf

 

[Amazoniac]

Much of the energy, estimates suggest from 60% to 70%, is used to power transport mechanisms that maintain the Na+-K+ membrane potential required for the transmission of the nerve impulses.

"The main function of the central nervous system is the generation, processing and transmission of impulses. These activities can only be accomplished if the key ions, Na +, K + and Ca 2+ are maintained in electrochemical disequilibrium across the neuronal plasma membrane which requires a constant input of energy. For this reason 50-60% of total ATP produced in brain is used to support ion movements."
Ions and energy in mammalian brain

Glad that you returned posting!

 

[Such_Saturation]

Except ion gradients are maintained hours after death.

 

[burtlancast]

Besides a few useful tips, I have yet to read a comprehensive cancer treatment by Ray.

He's more concerned on prevention than cure.

I suspect he acknowledges and fears the heat associated with it.

 

[Such_Saturation]

Yea but he still doesn't think you should cut sugars when you have cancer.

 

[jyb]

He's more concerned on prevention than cure.

I tend to think the exact opposite about most of his work, for health in general not just cancer.

 

[burtlancast]

Yea but he still doesn't think you should cut sugars when you have cancer.

Salt and flaxseed aside, he endorses Gerson's original work, which consisted in a low fat, low protein, high carbohydrate, low sugar (maple syrup (grade B) or honey or unrefined blackstrap molasses may be used at 1-2 teaspoons a day maximum) diet.

 

[Such_Saturation]

xxxxxx was diagnosed with Hodgkins lymphoma almost 3 years ago at age 28. She chose to go to Cologne, to the Centre for Maligne Lymphoma. .......the most powerful chemo therapy BEACOPP was developed there by a doctor called Volker Diehl. Xxxxxxx was treated by his number one student and the chief of the clinic, Prof. Dr. Engert and his collegs Prof. Dr. Borchmann and Dr. Elter. During the first chemotherapies (with ABVD) she studied Ray Peat and was in constant contact with him.

Xxxx started to use progesterone (progest-e-complex) even before the chemo therapy to make up for the estrogen dominance which lead to the cancer in the first place. She used one bottle per week during the chemo and never lost her hair or her white blood cells.

She started using thyroid hormones to balance the hypothyroidism that had been a part of her life since puberty but not noticed by other doctors.

She ate a very strict diet without any PUFA since there are no cancers without PUFA. She ate carrots and coconut oil and fruit and cheese and sugar and salt and drank milk and orange juice and gelatine.

She supplemented vitamins E, A, D3, niacinamid.

She used 3g of aspirin a day for 2 years and uses 1g a day now because aspirin alone fights cancer and prevents every kind of cancer known except lung cancer.

She used heat bulbs for many hours a day during winter and had baths with epsom salt and baking soda and used baking soda a few times a day.

She read every article by Ray Peat and still reads them and his newsletter and listens to his interviews.

After three months of studying sheasked Ray Peat for information about radiation "therapy". He sent studies about the abscopal and the bystander effect she read. After that she quit the chemotherapy (after 3 cycles) and never went back for radiation or any other reason, nor to this hospital nor to any other doctor.
During the last 3 years (as soon as the chemo problems had worn off, about 3 months it took) she has been healthier than ever before in her life. She will never get cancer or any other diseases again.

 

[burtlancast]

That's a great account.

But how do i know Ray specifically advised her, besides all his various recommendations, to eat sugar ?

She obviously did a lot of things that she read ( thyroid , by the way, is part of the Gerson therapy) besides the chemo, and these things could have made her better DESPITE the sugar.

I would be shocked to hear Ray specifically advising cancer patients to eat pure sugar.

And i would also be curious about all the cancer people who followed Ray's writings yet didn't make it.

 

[Such_Saturation]

He even says that cancer eats fat...

 

[burtlancast]

He even says that cancer eats fat...

In medicine, clinical results generally supersede scientific data, because the later is always perfectible and changing.

Ray's adamant on milk being good, but stubbornly refuses to look at the more recent scientific evidence on A1 milk causing widespread chronic inflammation.

This was started by collecting epidemiological data about type 1 diabetes and heart disease incidence according to the type of casein consumed.

The scientific evidence Ray originally relied on has been perfected with possible dramatic implications. It was all made possible by acknowledgment of clinical evidence.

 

[Such_Saturation]

He's also adamant on "follow the money" and there's plenty of it in the A2 milk industry.

 

[Forsythia]

If you don't eat cholesterol, your body will make it. If you don't eat sugar, your body will make it. Keeping your metabolism running at its peak is the best defense against abhorent (cancer) cells.

 

[haidut]

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".

 

[Such_Saturation]

I love these alternative media websites that preach love and affection all day long, and then don't hesitate to advise people on how to ruthlessly "starve cancer".

 

[burtlancast]

Glucose Availability as a Promoter of Cancer Growth

Taken together, increased glucose flux and metabolism promotes several hallmarks of cancer such as excessive proliferation, anti-apoptotic signalling, cell cycle progression and angiogenesis. It does so, however, at the expense of substrate inflexibility compared to normal cells. It is clear that the high proliferative phenotype can only be sustained as long as a steady supply of substrates for ATP production is available. Thus, with progressive tumorigenesis, cancer cells become more and more 'addicted' to aerobic glycolysis[53] and vulnerable to glucose deprivation. Indeed, several studies have shown that malignant cells in vitro quickly lose ATP and commit apoptosis when starved of glucose.[78–80] Masur et al. showed that diabetogenic glucose concentrations (11 mM) compared to physiological ones (5.5 mM) lead to altered expression of genes that promote cell proliferation, migration and adhesion in tumor cell lines from several organs including breast, colon, prostate and bladder.[81] Adding insulin to the high-glucose medium further enhanced proliferation rates by 20–40% and promoted activation of the PI3K pathway. The question is whether altered blood glucose levels have similar effects on tumor growth in vivo. Theoretically, low blood glucose might cut some of the most hypoxic tumor cells from their diffusion-limited fuel supply. Gatenby and Gillies originally proposed this mechanism as an explanation for necrotic areas often found within tumor tissue,[82] but they later revised this hypothesis based on a mathematical model that predicted only a modest decline of glucose concentrations with distance from the closest blood vessel.[69] There are, however, several lines of evidence pointing towards a strong correlation between blood glucose levels and tumor growth in vivo that might indicate other important effects mediated by glucose. For example, the reduction of plasma glucose levels in tumor-bearing animals induced through calorie restriction may be responsible, directly or indirectly, for the significantly prolonged survival compared to normal-fed controls.[83,84] In 1962, Koroljow reported the successful treatment of two patients with metastatic tumors by an insulin-induced hypoglycemic coma.[85] Hyperglycemia, on the other hand, is a predictor of poor survival in patients with various cancers[22,26,86–88] and has been positively correlated to an increased risk for developing cancer at several sites including the pancreas, esophagus, liver, colon, rectum, stomach and prostate in large cohort studies.[25,89,90]

Medscape: Medscape Access

 

[Such_Saturation]

correlation

Ah I see.

significantly prolonged survival compared to

Sounds enticing!

 

[haidut]

Glucose Availability as a Promoter of Cancer Growth

Taken together, increased glucose flux and metabolism promotes several hallmarks of cancer such as excessive proliferation, anti-apoptotic signalling, cell cycle progression and angiogenesis. It does so, however, at the expense of substrate inflexibility compared to normal cells. It is clear that the high proliferative phenotype can only be sustained as long as a steady supply of substrates for ATP production is available. Thus, with progressive tumorigenesis, cancer cells become more and more 'addicted' to aerobic glycolysis[53] and vulnerable to glucose deprivation. Indeed, several studies have shown that malignant cells in vitro quickly lose ATP and commit apoptosis when starved of glucose.[78–80] Masur et al. showed that diabetogenic glucose concentrations (11 mM) compared to physiological ones (5.5 mM) lead to altered expression of genes that promote cell proliferation, migration and adhesion in tumor cell lines from several organs including breast, colon, prostate and bladder.[81] Adding insulin to the high-glucose medium further enhanced proliferation rates by 20–40% and promoted activation of the PI3K pathway. The question is whether altered blood glucose levels have similar effects on tumor growth in vivo. Theoretically, low blood glucose might cut some of the most hypoxic tumor cells from their diffusion-limited fuel supply. Gatenby and Gillies originally proposed this mechanism as an explanation for necrotic areas often found within tumor tissue,[82] but they later revised this hypothesis based on a mathematical model that predicted only a modest decline of glucose concentrations with distance from the closest blood vessel.[69] There are, however, several lines of evidence pointing towards a strong correlation between blood glucose levels and tumor growth in vivo that might indicate other important effects mediated by glucose. For example, the reduction of plasma glucose levels in tumor-bearing animals induced through calorie restriction may be responsible, directly or indirectly, for the significantly prolonged survival compared to normal-fed controls.[83,84] In 1962, Koroljow reported the successful treatment of two patients with metastatic tumors by an insulin-induced hypoglycemic coma.[85] Hyperglycemia, on the other hand, is a predictor of poor survival in patients with various cancers[22,26,86–88] and has been positively correlated to an increased risk for developing cancer at several sites including the pancreas, esophagus, liver, colon, rectum, stomach and prostate in large cohort studies.[25,89,90]

Medscape: Medscape Access

Even if one kills the cancer cells, the ones that replace them will be just as "cancerous". It is a systemic problem, otherwise things like surgery and radiation would have wiped out this disease by now. The virtual guarantee of recurrence of any cancer in any tissue if it has progressed beyond the so-called "carcinoma in situ" shows that it is the organism as a whole that supports the cancer growth and not the local tissue malignancy. Killing, starving, poisoning, burning or causing suicide of cancer is flawed thinking and has to stop. Cancer cells have high rate of death on their own, even without the toxic treatments, and that is (part of) the reason for elevated LDH in cancer patients - i.e. high rate of cell death and renewal in tumor. So, killing the cancer cells is really doing nothing do reverse the environmental carcinogenicity, and actually actively promotes it (with a few exceptions like anthracycline treatment).

 

[burtlancast]

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.

 

[Such_Saturation]

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