Cancer basics and starving cancer--jk
Starving cancer by fasting and ketogenic diet, a review
Cancer as a metabolic disease, starving cancer--Seyfried, 2014
Highlites of Seyfried 2014 Plus 2 more articles
Ketogenic diet starves cancer, Seyfried Journal 2007
Role of Macrophages in metastatic cancer
Metabolic pathways and cancer growth--2008 review
Glutimate cancer treatments
Glutamine and cancer-2001 review
Blocking Glutimate metabolism by cancer
Ketogenic diet starves cancer, known as Warburg effect, 1924
Otto Warburg's article plus study of Warburg effect

Otto Warburg's article plus study of Warburg effect

The Prime Cause and Prevention of Cancer - Part 1
with two prefaces on prevention

Revised lecture at the meeting of the Nobel-Laureates on June 30, 1966
at Lindau, Lake Constance, Germany

Otto Warburg
Director, Max Planck-Institute for Cell Physiology, Berlin-Dahlem

A list of selected active groups of respiratory enzymes will soon be published, to which we recently added cytohemin and d-amino-Levulinic acid, the precursor of oxygen-transferring hemins. In the meantime commercial vitamin preparations may be used that contain, besides other substances, many active groups of the respiratory enzymes. Most of these may be added to the food. Cytohemin and vitamin B 12 may be given subcutaneously. (A synonym of "active group" is prosthetic" group of an enzyme.)…. On the other hand, because young metastases live in the body almost aerobically, inhibition by the active groups should be possible. Therefore we propose first to remove all compact tumors, which are the anaerobic foci of the metastasis. Then the active group should be added to the food, in the greatest possible amount, for many years, even for ever. This is a promising task. If it succeeds, then cancer will be a harmless disease.  Moreover, we discovered recently a) in experiments with growing cancer cells in vitro that very low concentrations of some selected active groups inhibit fermentation and the growth of cancer cells completely, in the course of a few days. From these experiments it may be concluded that de-differentiated cells die if one tries to normalize their metabolism. It is a result that is unexpected and that encourages the task of inhibiting the growth of metastases with active enzyme groups.

  1. In press in Hoppe-Seylers Zeitschrift für Physiologische Chemie 1967. 10 g riboflavin per ccm or 10 g d-Aminolevulinic acid inhibit in vitro growth and fermentation completely but inhibit respiration less. As expected, ascites cancer in vivo is not cured.

See Warburg on the origin of cancer cells, 1956 Science


J Bioenerg Biomembr.
 2007 Jun;39(3):211-22.

Warburg, me and Hexokinase 2: Multiple discoveries of key molecular events underlying one of cancers' most common phenotypes, the "Warburg Effect", i.e., elevated glycolysis in the presence of oxygen.


As a new faculty member at The Johns Hopkins University, School of Medicine, the author began research on cancer in 1969 because this frequently fatal disease touched many whom he knew. He was intrigued with its viscous nature, the failure of all who studied it to find a cure, and also fascinated by the pioneering work of Otto Warburg, a biochemical legend and Nobel laureate. Warburg who died 1 year later in 1970 had shown in the 1920s that the most striking biochemical phenotype of cancers is their aberrant energy metabolism. Unlike normal tissues that derive most of their energy (ATP) by metabolizing the sugar glucose to carbon dioxide and water, a process that involves oxygen-dependent organelles called "mitochondria", Warburg showed that cancers frequently rely less on mitochondria and obtain as much as 50% of their ATP by metabolizing glucose directly to lactic acid, even in the presence of oxygen. This frequent phenotype of cancers became known as the "Warburg effect", and the author of this review strongly believed its understanding would facilitate the discovery of a cure. Following in the final footsteps of Warburg and caught in the midst of an unpleasant anti-Warburg, anti-metabolic era, the author and his students/collaborators began quietly to identify the key molecular events involved in the "Warburg effect". Here, the author describes via a series of sequential discoveries touching five decades how despite some impairment in the respiratory capacity of malignant tumors, that hexokinase 2 (HK-2), its mitochondrial receptor (VDAC), and the gene that encodes HK-2 (HK-2 gene) play the most pivotal and direct roles in the "Warburg effect". They discovered also that like a "Trojan horse" the simple lactic acid analog 3-bromopyruvate selectively enters the cells of cancerous animal tumors that exhibit the "Warburg effect" and quickly dissipates their energy (ATP) production factories (i.e., glycolysis and mitochondria) resulting in tumor destruction without harm to the animals.


The “Warburg effect” likely provides the vast majority of cancerous tumors that exhibit this phenotype with a number of benefits.  One is biosynthesis.  A rapidly dividing cancer cell needs carbon precursors that are involved in the biosynthesis of cell building blocks.   The glycolytic pathway and its off-shoot the pentose phosphate pathway (hexose monophosphate shunt) are rich sources of precursors essential for the biosynthesis of nucleic acids, phospholipids, fatty acids, cholesterol, and porphyrins.    Thus maintain a high glycolytic rate within each tumor cell of a given tumor, even in the presence of oxygen (i.e., the “Warburg effect”) assures not only the tumor’s survival but its rapid growth.  A second advantage of the “Warburg effect” is likely involved in both tumor protection and invasion.   As tumor cells via glycolysis even in the presence of ozxygen produce latic acid and transport it out, this acid (i.e., its low pH) may both protect tumors (that are resistant to it) against attack by the immune system while inducing negative effects (chemical warfare) on normal surrounding cells, thus preparing them for invasion.  Finally, and not least important, the “Warburg effect also assures a longer tumor survival time if oxygen become limiting.

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As required by law, I am not recommending that the public do as I do.  I am only setting out why some scientist subscribe to a different theory of cancer and its treatment, and what I would do based on their theory.  See your physician for medical advice.