The Ketogenic diet and cancer – part 2 of 8
(NaturalHealth365) In my previous article, I discussed some of the more notable “cancer miracles” promoted by the media and scientific community that ultimately proved to be disappointments. The most recent theoretical breakthrough, one which seems to have gripped the alternative world first before filtering into mainstream academic thinking, is the “ketogenic diet.”
Editor’s Note: To access the entire series of articles, anytime, simply visit the Ketogenic Diet and Cancer section of our website, NaturalHealth365.com
In 2012, Dr. Thomas Seyfried, a PhD basic science researcher, published the book, Cancer as a Metabolic Disease, announcing to the world that a high-fat, no carbohydrate ketogenic diet represents the solution to cancer prevention as well as to cancer treatment. His monograph has been greeted with much acclaim, though not yet at the level reached at the height of the interleukin-2 hysteria in 1985.
Dr. Seyfried, whom I do not personally know, is hardly an “alternative” medical scientist, since judging by his credentials listed on the back cover of the book his pedigree seems conventionally academic:
THOMAS N. SEYFRIED, PHD, has taught and conducted research in the fields of neurogenetics, neurochemistry, and cancer for more than twenty-five years at Yale University and Boston College. He has published more than 150 scientific articles and book chapters …
A closer look at Dr. Thomas Seyfried and his work
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Certainly Dr. Seyfried has put together a most impressive achievement, chronicling in great detail his belief that cancer does not develop from genetic alterations – as is generally believed – but as a result of changes in fundamental cell physiology, specifically changes in energy production, that in turn lead to the cancer phenotype. In essence, the genes remain intact, but metabolism goes awry.
The book summarizes, then enlarges upon, the concepts of Otto Warburg, MD, the great German scientist who won the Nobel Prize in Medicine and Physiology in 1931 for his work on cellular oxidation and energy production. No scientist has ever been nominated more frequently for the cherished Prize than Dr. Warburg, but he lost his chance for a second win, according to some sources, in 1944 after Hitler ordered that no German scientist could accept the award.
Who is Dr. Otto Warburg?
To sum up decades of Warburg briefly, mammalian cells create and store usable energy in the form of the adenosine triphosphate (ATP) molecule. Production of ATP is a complex affair involving three distinct and sequential series of cellular reactions that begin with the breakdown of the six-carbon sugar glucose. The first of these processes, glycolysis, does not require oxygen and occurs in the cytoplasm; the second, the citric acid cycle, occurs within the mitochondria, the oval shaped organelles dispersed within the cytoplasm, and requires oxygen; and the third, and most productive in terms of ATP generation, electron transport, proceeds in the membranes of mitochondria and also needs oxygen.
In normal mammalian cells, glycolysis represents the starting point of energy synthesis. Its end product, pyruvic acid, is in turn shunted first into the citric acid cycle, then ultimately into the electron transport chain. Along the way, a complex series of step-wise reactions releases multiple energy-rich ATP molecules.
Based on his years studying cellular metabolism, Dr. Warburg proposed that cancer cells, unlike normal cells, rely exclusively on anaerobic glycolysis for energy. Such cells do fine in the absence of oxygen, since the metabolic machinery of glycolysis doesn’t require it.
Warburg claimed that in these abnormal cells glycolysis actually uncouples from the citric acid cycle and electron transport, leaving the cells dependent solely on this rather inefficient mechanism for survival. Bacteria also synthesize their ATP energy exclusively from glycolysis, in the process we know as fermentation.
This uncoupling of glycolysis from the citric acid cycle and electron transport, and the supposed fundamental dependency of cancer cells on anaerobic metabolism, has been studied extensively since Warburg’s day, with many scientists around the world claiming to confirm, then adding to, Warburg’s hypothesis. As Dr. Seyfried correctly points out, in more recent times, cancer researchers have begun drifting away from the study of disordered cellular physiology, enamored as they are of genetic abnormality as the primary and only driving force in cancer formation and growth.
Warburg’s ideas about faulty metabolism seem to have been overshadowed by the elegance of, and fascination for, the “genetic cause of cancer.”
I agree Dr. Seyfried has done us all a great service by redefining, re-emphasizing and refining Dr. Warburg’s remarkable research from 80 years ago. He makes the case, using the contemporary basic science data, to support Warburg’s belief that cancer cells depend solely on glycolysis for survival, with his claim regarding the uncoupling of this sugar-fueled, oxygen-independent process from the citric acid cycle and the electron transport chain. But he goes a major step further, stating as fact that since cancer cells depend on anaerobic glucose metabolism for energy, they can be stopped in their tracks by depriving them of blood glucose.
Our normal healthy cells, be they situated in the brain or the skin of our feet, do prefer glucose as their primary energy source, obtained from the sugar circulating in the blood. That “blood sugar” comes from a variety of sources, including dietary carbohydrates occurring in fruits, starchy vegetables like potatoes, and grains. The complex carbohydrates in such foods are broken down into glucose during the digestive process, catalyzed by a variety of carb-specific enzymes like amylase.
We also maintain a certain amount of stored sugar as glycogen, found in the liver and muscle and formed when glucose molecules link up to one another in complex chains. In times of need and if deprived of dietary carbohydrates, our liver and muscle cells can break down glycogen into glucose for release into the bloodstream. Our liver cells can also, when necessary, convert certain amino acids such as alanine into glucose.
However, our glycogen supplies in the liver and muscle are quite limited, providing only an 8-12 hour emergency supply. So during a fast, or starvation, or on a diet providing no carbohydrates in any form, we quickly run out of glycogen. In this situation, through a variety of neural and hormonal signaling, our fat cells, or adipocytes, begin releasing free fatty acids into the blood stream. These fatty acids can in turn be used by our cells in the alternate ATP producing process of beta oxidation.
The end result of this series of reactions, acetyl coenzyme A, can then be shunted into the citric acid cycle and the electron transport chain, to produce maximum amounts of energy-rich ATP.
Though most of our cells can utilize fatty acids of all stripes via beta oxidation to create ATP energy, our central nervous system is at somewhat of a disadvantage. In fact, long chain fatty acids with 14 or more carbons, which can yield the most ATP from beta oxidation, do not cross the blood-brain barrier. However, in a state of prolonged dietary carbohydrate depletion, the liver begins converting acetyl coenzyme A into various ketone bodies, such as acetoacetate and beta hydroxy butyric acid, which easily penetrate into the brain and which can, like acetyl coenzyme A, be shunted into the citric acid cycle and then the electron transport chain, providing the brain with ATP.
On a low carb or no carb diet, our billions of cells in all our tissues and organs switch their energy mechanics from a process driven by glucose to one propelled by fatty acids and ketone bodies. The term “ketosis” simply means the state in which, in the absence of sufficient glucose, our liver synthesizes ketones from acetyl coenzyme A.
However, even on a no carb, all meat, high-fat diet, we will still be consuming some glucose in the form of glycogen stored in muscle and organ meats, and our livers will continue to convert some dietary amino acids into glucose, so blood sugar levels never hit zero on such a diet. But in such cases, the amounts produced will be minimal.
Though our normal cells do just fine in the absence of carbohydrates, cancer cells, Dr. Seyfried claims, do not. These cells, he says, can never use fatty acids or ketone bodies for any significant energy production, since the citric acid cycle and electron transport in them remain basically inactive. So, he proposes, as the culmination of his exegesis, that on a high fat, moderate protein, no carb diet, a cancer patient will deprive his or her deadly abnormal cells of their only useful source of energy, blood glucose, leading to apoptosis, or cell death.
It’s that simple. No dietary sugar, no cancer.
The science is impressive, the conclusion, to many it seems, extraordinarily promising. But, is this ketogenic diet really a “new” idea or simply an old one, repackaged for the 21st century? And, can history teach us anything about its efficacy against cancer, or any other disease?
In the next article in the series, I will explore these very questions.
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About the author: Dr. Nicholas Gonzalez graduated from Brown University (Phi Beta Kappa, magna cum laude), and worked as a journalist before receiving his medical degree from Cornell University Medical College. During a fellowship under Dr. Robert Good, former President of Sloan-Kettering, Dr. Gonzalez evaluated an enzyme-based nutritional therapy for use against advanced cancer, as documented in his book One Man Alone. Since 1987, Dr. Gonzalez has been in practice in New York. His other books include, “The Trophoblast and the Origins of Cancer”, and “What Went Wrong” – which portrays Dr. Gonzalez’s battle to have his therapy tested in an NCI clinical study. For more information about Dr. Gonzalez – visit: Dr-Gonzalez.com
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