Non-technical Summation:  (For definitions go to http://healthfully.org/rh/id6.html ).  Nearly all aggressive malignant cancers[1] have disabled their mitochondria, the capsules with cells that are the source for the body’s energy molecule ATP.  This damage to the mitochondrial shuts down the principle metabolic pathways within cancer cells:  fat metabolism and aerobic (with oxygen) glucose metabolism; they occur only in the mitochondria.  A third way of producing the major energy molecule ATP occurs in the cytoplasm (an area outside the mitochondria) through anaerobic (without oxygen) glucose metabolism—a very inefficient way for producing ATP.  It takes 17 times more glucose to produce the same amount of ATP in a cancer cell and much more if the cancer is rapidly growing.  This extremely high demand by cancer for glucose makes the cancer very vulnerable to an extremely low carbohydrate diet (low glucose). Thus is called a ketogenic diet, or KD.  It will starve the cancer cells and thereby stop its growth and possible shrink or in some cases through programmed cell death (apoptosis) destroy the cancer.  What happens to the cancer depends upon the functionality of its mitochondria.  This ketogenic diet has at most mild side effects—mainly lethargy-- as the body switches from glucose metabolism during the first 2 weeks.  Since normal cells have functional mitochondria, while on ketogenic diet, they will continue to metabolize fat to produce ATP.  This type of diet has been used for at least century to treat type-1 diabetes (insulin dependent), epilepsy, obesity, and cancer.  There are hundreds of medical journal articles on this type of treatment.  The damaged to the mitochondria became general knowledge among oncologist when in 1924 the future Nobel Laurite Otto Warburg published his seminal paper on the abnormal metabolism of cancer cells, commonly known as the Warburg effect.  In it he proposed starving the cancer. 

Ketogenic diet and starving cancer

Ketogenic diet (KD) results in insufficient serum glucose for glycolysis, thus forces the cells to produce ATP from other sources mainly fatty acid, and during starvation amino acids.  The KD diet has been shown to cure obesity, insulin resistance, and type-2 diabetes, and has been used with very positive results in the treatment of cancer, epilepsy, and type 1-diabetse.  For cancer it first made the modern medical literature in 1883.  Galen (the Greek physician in the Roman Empire whose Latin works formed the foundation for Western medical science) wrote cancer and KD, “’might afford a cure in mild cases and be helpful in others’….  The first modern study of fasting as treatment for epilepsy was in France in 1911… The ketogenic diet reduces seizure frequency by more than 50% in half of the patients who try it and by more than 90% in a third of patients” Wiki.  However pharma being pharma recommends drugs as the first line of treatment, exaggerates the side effects of KD, and considers KD the last resort, and of course used in addition to their tranquilizers mislabeled anti-seizure drugs.  Given the side effects of recommended doses of Valproate  and other “anti-seizure” drugs the order in  treatment guidelines is backwards.  Of course one has less seizures with sleeping longer, since seizures don’t normally occur when sleeping.  I have observed in others the cloud in which those tranquilizers put the patients.[1]   Even for those who seem to tolerate the tranquilizer, this type of drug nearly always significantly lowers the quality of life, and they are very addicting.  KD’s mechanism for epilepsy I have not researched. 

The mechanism for cancer starvation turns upon the fact that most real cancers[2] are dependent upon only glucose for the production of ATP, and not fatty acids.   KD starves the cancer.  Unfortunately medical textbooks and Wikipedia barely broach this form of treatment, though there is an extensive body of journal literature.  My two oncology textbooks have no entries.  Otto Warburg, a giant of medical science, described the metabolic process of cancer growth, called the Warburg hypothesis  Though he considered “the prime cause of cancer is the replacement of the respiration of oxygen in normal body cells by a fermentation of sugar” [it turns out that] the metabolic changes are considered to be a result of these mutations rather than a cause” Wiki. This is more pharma twaddle, for Warburg, at least by 1956 Otto did not propose this rather he stated that [nearly] all cancers have defective metabolism, and both treatment and prevent can be achieved through extreme low carb diet and a group of “selective respiratory enzymes including cytohemin and d-amino-Levulinic.  It is in the financial interest of pharma to stonewall the topic of treating cancer by a ketogenic diet. Thus there are but two sentences in the Wikipedia  KD article  on treating cancer, e.g.,  “establishing [KD] clinical trials is probably warranted.”  Pharma KOLs (Key Opinion Leaders provide most of the medical material in Wikipedia.   KD for starving cancer has over 100 related journal articles.  It is one of the two best general cancer treatments.[3] 

So why would denying cancer glucose for metabolism starve cancer?  Most cancer have severely damaged mitochondria[4] thus are not able to obtain ATP (the energy molecule) from metabolic processes which occur only in the mitochondria.  This defect in cancer cells makes them dependent upon just one metabolic source for ATP, that of glucose. Through anaerobic oxidation, [5]  The mitochondrial processes for ATP include metabolism of fatty acids (fats), and of ketone bodies[6] which are derived from fatty acids (fat).   Instead of relying upon the mitochondria, metabolism of glucose occurs through anaerobic process in the cytoplasm[7] of the cancer cells.  However, the cytoplasm cannot metabolize free fatty acids (fats) or ketone bodies.[8]  Thus extremely low serum glucose starves the cancer cells.  Normal cells simply use metabolize fat in the mitochondria to produce the essential ATP molecules.[9]  It is thought that the shutting down of the mitochondria is a necessary adaption by cancer to avoid programmed cell death (apoptosis).[10]  Cancer requires lots of ATP for to power the chemical reactions that produce a new cancer cell during mitosis (cell division), from 8 to 200 times the amount of mitochondrial aerobic  glucose—depending on how rapidly the cancer is growing.  For the above reasons starving cancer is a safe and effective way to prolong life without major side effects, and in some cases to cure metastatic cancer. 

Adaption to low carb diet:  As prior stated other tissues switch to the utilization of FFAs (free fatty acids, the transport form of triglycerides).  Once adaption to KD occurs, after about 3 days (see table below) bodily function mental and physical are at or above their levels of a carb-rich diet.  Three super-stars of basketball (Kobe Bryant, James Le Barron, and Carmel Anthony) are on a low carb diet.  However, the nervous system is normally dependent on aerobic glucose metabolism, and it switches to ketone metabolism while the other tissues increase the metabolism of FFAs , at p 6.  The body is adapted to this diet.  This is not surprising, for example those in the extreme northern climates lack for nearly the entire year sources of carbs, except for a small amount of glycogen found in meats. 

 Table 1.  The five stages of starvation from the time of last ingestion (reprinted from Cahill, 1983, page 2).   

So what have been the clinical results?   “Niakan (2010) concluded that over 1,000 similar spontaneous remissions are most likely due to hypoglycemia and hypoxia [lack of oxygen] (arguably a direct consequence of the hypoglycemia).  Preclinical animal studies demonstrate promising results by cutting cancer's nutrient supply (Mukherjee et al., 2002, 2004; Zhou et al., 2007; Otto et al., 2008; Mavropoulos et al., 2009; Shelton et al., 2010; Stafford et al., 2010; De Lorenzo et al., 2011; Sivananthan, 2013; Jiang and Wang, 2013)” Cornell U. 2014” Kapelner 2014.  Clinical trials on cancer patients have two hurdles that of ethics review boards which must approve the trial, and that of funding.  Both are significant because of the university profitable alliance with pharma, and pharma is unwilling to put cancer patients before profits.  The only clinical trial was too small, the patient too near death, and the funding too limited to be considered as resolving the question of benefits.  Out of 16 terminal patients, only 2 were able to follow the dietary protocols for the 12 weeks of trial, and 7 had moderate dietary compliance. Of the 7 who failed to comply, 2 had impaired food intake, 2 died, and the rest were too ill to follow the diet.  This contrast very significantly with intractable epileptic patience, they have very good compliance in clinical trials.[11]  More positive is the treating of 2 pre-teens in 1993 with advanced brain cancer. Compliance and response were excellent.  One is still alive 10 years later.    

All road point to the origin and progression of cancer pass through the mitochondria, and the hallmark of cancer is malfunction in oxidative phosphorylation to varying degrees (Seyfied et al. 2014).  This implies that cancer cells do not have access to non-glycolytic fuels that demand full oxidative combustion in the Krebs cycle, namely fatty acids and the ketone bodies beta-hydroxybutyrate.  So what has the results of starving cancer?   

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Ketosis /kɨˈtoʊsɨs/ is a metabolic state where most of the body's energy supply comes from ketone bodies in the blood, in contrast to a state of glycolysis where blood glucose provides most of the energy.  It is characterised by serum concentrations of ketone bodies over 0.5 millimolar, with low and stable levels of insulin and blood glucose.[1][2]  In glycolysis, higher levels of insulin promote storage of body fat and block release of fat from adipose tissues, while in ketosis, fat reserves are readily released and consumed..^[5][7]  For this reason, ketosis is sometimes referred to as the body's "fat burning" mode.^[8] …  If the diet is changed from one that is high in carbohydrates to one that does not provide sufficient carbohydrate to replenish glycogen stores, the body goes through a set of stages to enter ketosis. During the initial stages of this process, blood glucose levels are maintained through  gluconeogenesis,  and the adult brain does not [normally] burn ketones [the blood level is 0.01 mmol/L, but during ketoses it is 2.5 to 9.7mmol/L].  However, the brain makes immediate use of ketones for lipid synthesis in the brain.  After about 48 hours of this process, the brain starts burning ketones in order to more directly use the energy from the fat stores that are being depended upon, and to reserve the glucose only for its absolute needs, thus avoiding the depletion of the body's protein store in the muscles.^[14]

Ketosis is deliberately induced by use of a ketogenic diet as a medical intervention in cases of intractable epilepsy. .^[12]   Other uses of low-carbohydrate diets remain controversial.^[15][16] Induced ketosis or low-carbohydrate diet terms have very wide interpretation. Therefore, Stephen S. Phinney and Jeff S. Volek coined the term "nutritional ketosis" to avoid the confusion.^[17]  Carbohydrate deprivation to the point of ketosis has been argued both to have negative^[18] and positive effects on health.^[19][20] 

https://en.wikipedia.org/wiki/Ketosis

Less than 30 grams of carbs per day, insulin upregulates the insulin like growth fact IGF1 … enzymes which stimulate cancer growth, protein storage, cellular absorption of glucose, and a potent inhibitor of programmed cell death

Warburg effect --wiki  

Review article | Published 9 September 2011, doi:10.4414/smw.2011.13250
Cite this as: Swiss Med Wkly. 2011;141:w13250

Wiki: 

Basis

In oncology, the Warburg effect is the observation that most cancer cells predominantly produce energy by a high rate of glycolysis followed by lactic acid fermentation in the cytosol,^[4] rather than by a comparatively low rate of glycolysis followed by oxidation of pyruvate in mitochondria as in most normal cells.^[5][6][7] The latter process is aerobic (uses oxygen). Malignant, rapidly growing tumor cells typically have glycolytic rates up to 200 times higher than those of their normal tissues of origin; this occurs even if oxygen is plentiful.  The Warburg effect may simply be a consequence of damage to the mitochondria in cancer or an adaptation to low-oxygen environments within tumors [because of the ATP needed for the high rate of mitosis], or a result of cancer genes shutting down the mitochondria because they are involved in the cell's apoptosis program which would otherwise kill cancerous cells. It may also be an effect associated with cell proliferation [yes]. Since glycolysis provides most of the building blocks required for cell proliferation, cancer cells (and normal proliferating cells) have been proposed to need to activate glycolysis, despite the presence of oxygen, to proliferate .^[11]   [This process would also help explain in part the high rate of mutation in cancer cells, since the reactive products of metabolism are now produced outside the mitochondria, and secondly because by reducing the contribution of the mitochondria, the uptake of glucose is reduced, thus leading to a higher rate of intracellular glycation.] 

[Check #s 11  -abstract of modest interest, point out cancer & some tumors cells switch oxidative phosphorylation to glycolysis  in the presences of oxygen, article on why and how of process NEED TO SEE FULL ARTICLE, 2008 The Warburg effect: why and how do cancer cells activate glycolysis in the presence of oxygen?]

Possible explanations of the effect

The Warburg effect may simply be a consequence of damage to the mitochondria in cancer, or an adaptation to low-oxygen environments within tumors, or a result of cancer genes shutting down the mitochondria because they are involved in the cell's apoptosis program which would otherwise kill cancerous cells. It may also be an effect associated with cell proliferation. Since glycolysis provides most of the building blocks required for cell proliferation, cancer cells (and normal proliferating cells) have been proposed to need to activate glycolysis, despite the presence of oxygen, to proliferate .^[11] Evidence attributes some of the high aerobic glycolytic rates to an overexpressed form of mitochondrially-bound hexokinase^[12] responsible for driving the high glycolytic activity. In kidney cancer, this effect could be due to the presence of mutations in the Von Hippel–Lindau tumor suppressor gene upregulating glycolytic enzymes, including the M2 splice isoform of pyruvate kinase ^[13]0

****In March 2008, Lewis C. Cantley and colleagues at the Harvard Medical School announced they had identified theenzyme that gave rise to the Warburg effect.^[14][15] The researchers stated tumor M2-PK, a form of the pyruvate kinase enzyme, is produced in all rapidly dividing cells, and is responsible for enabling cancer cells to consume glucose at an accelerated rate; on forcing the cells to switch to pyruvate kinase's alternative form by inhibiting the production of tumor M2-PK, their growth was curbed. The researchers acknowledged the fact that the exact chemistry of glucose metabolism was likely to vary across different forms of cancer; but PKM2 was identified in all of the cancer cells they had tested. This enzyme form is not usually found in healthy tissue, though it is apparently necessary when cells need to multiply quickly, e.g. in healing wounds or hematopoiesis.

Studies from various international working groups have revealed a significantly increased amount of Tumor M2-PK in EDTA-plasma samples of patients with renal, lung, breast, cervical and gastrointestinal tumors (oesophagus, stomach, pancreas, colon, rectum), as well as melanoma, which correlated with the tumor stage.  https://en.wikipedia.org/wiki/Tumor_M2-PK

In oncology, the Warburg effect is the observation that most cancer cells predominantly produce energy by a high rate of glycolysis followed by lactic acid fermentation in the cytosol,^[4] rather than by a comparatively low rate of glycolysis followed by oxidation of pyruvate in mitochondria as in most normal cells.^[5][6][7] The latter process is aerobic (uses oxygen). Malignant, rapidly growing tumor cells typically have glycolytic rates up to 200 times higher than those of their normal tissues of origin; this occurs even if oxygen is plentiful.  The Warburg effect may simply be a consequence of damage to the mitochondria in cancer or an adaptation to low-oxygen environments within tumors [because of the ATP needed for the high rate of mitosis], or a result of cancer genes shutting down the mitochondria because they are involved in the cell's apoptosis program which would otherwise kill cancerous cells. It may also be an effect associated with cell proliferation [yes]. Since glycolysis provides most of the building blocks required for cell proliferation, cancer cells (and normal proliferating cells) have been proposed to need to activate glycolysis, despite the presence of oxygen, to proliferate .^[11]   [This process would also help explain in part the high rate of mutation in cancer cells, since the reactive products of metabolism are now produced outside the mitochondria, and secondly because by reducing the contribution of the mitochondria, the uptake of glucose is reduced, thus leading to a higher rate of intracellular glycation.] 

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Swiss article  http://www.smw.ch/content/smw-2011-13250/

 In 1924, Warburg found that cancer cells mainly rely on aerobic glycolysis: they produce a large proportion of the adenosine triphosphate (ATP) they need by metabolising glucose to lactate which they secrete, even in the presence of sufficient oxygen [5]. Compared to normal cells, the aerobic, oxidative breakdown of pyruvate (from glucose) and fatty acids in mitochondria is reduced. Warburg originally thought that defective mitochondria were the cause of both aerobic glycolysis and carcinogenesis. However, while mitochondrial defects have been observed in some tumours, most harbour fully functional mitochondria….  d that cancer cells mainly rely on aerobic glycolysis: they produce a large proportion of the adenosine triphosphate (ATP) they need by metabolising glucose to lactate which they secrete, even in the presence of sufficient oxygen [5]. Compared to normal cells, the aerobic, oxidative breakdown of pyruvate (from glucose) and fatty acids in mitochondria is reduced. Warburg originally thought that defective mitochondria were the cause of both aerobic glycolysis and carcinogenesis. However, while mitochondrial defects have been observed in some tumours, most harbour fully functional mitochondria.

High fasting blood glucose, insulin and insulin-like growth factor (IGF) concentrations stimulate the mTOR pathway and are also features of metabolic syndrome. The latter is known to positively correlate with cancer incidence, and we might expect that a diet preventing obesity and metabolic syndrome reduces the likelihood of developing cancer. But what appears to be straightforward in theory is often either hard to prove or not true. In the following, we will have a look at the evidence, after a discussion about the methodological difficulties of epidemiological studies on diet. 

Whether eating a high fat diet increases cancer incidence and mortality or not needs to be established by large, adequately powered, randomised and controlled interventional trials. No such study has yet been performed [12]. Nonetheless, case-control and cohort studies have shed some light on the question.[studies are flawed because of transfats, n-6 polyunsaturated fats, and rancidification of polyunsaturated fats all of which contribute to metabolic problems and thus probably the incidence of cancer.  Moreover most polyunsaturated oils are GMOs and contain pesticides.] 

Alcohol is the most frequent cause of hepatocellular carcinoma (HCC), accounting for about 40% of all cases. Regular consumption of more than 80 grams of alcohol per day for more than 10 years increases the risk for HCC approximately 5-fold, approaching an absolute risk of about 1% per year in alcoholic liver cirrhosis [56]. When adjusted for tobacco use and other potential confounding factors, alcohol consumption of more than 60 grams per day increases the relative risk for oral or hypopharyngeal squamous cell cancer 3.2 to 9.2 fold (reviewed by Goldstein et al. [57])

Intermittent fasting also reduces chemically induced hepatocarcinogenesis [91] and delays spontaneous tumorigenesis in p53-deficient mice [92].

Ketogenic diet

Fasting (including intermittent fasting) induces ketogenesis, the production of the ketone bodies β-hydroxy-butyrate and acetoacetate from fatty acids in the liver. Another way of achieving high blood concentrations of ketone bodies is by eating a ketogenic diet: Diets low in carbohydrates and high in fat (>50% of the energy intake) are called ketogenic. They share a number of biochemical and biological effects with calorie reduction schemes [95], and it has been suggested that, like calorie reduction, they might have anti-tumour activity.  Ketogenic diets have been employed as adjuvant therapy in a few cases of patients with brain tumours. The reports were positive, but anecdotal [96, 97]. Although, at this time, it is not known whether the method is applicable to other kinds of tumours [98], we think that physicians should be aware of the results obtained so far and keep track of future developments.

             Fructose is converted to fat only in the liver and insulin causes this fat to be stored in the liver.

Fatty liver >>>> IR in liver >>>> IR in muscle and fat tissues >>>> IR causes abnormal high insulin >>>> excess fat storage

           Carbs raises the insulin level in the body, and insulin causes body to burn glucose and store fat

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