Ketogenic diet causes cancer?


(John) #1

Recently, I was in a conversation with another about ketogenic diets when some guy butted in and said ketogenic diets made some cancers worse. He was eating a … My brain shut off. he couldn’t cite any studies or any evidence but was convinced this is what doctors have said.

Does anyone know what media article, or youtube video he thinks he watched.


(TJ Borden) #2

I think you have your answer.


(Amy Ramadan) #3

Wow… Just WOW!!!


(Mike Glasbrener) #4

Nope! But I’ve seen studies showing fasting and low insulin helps!


(Todd Allen) #5

I think it is possible to do a poorly formulated unhealthy keto diet that could raise the risk of cancer with low quality highly processed foods such as corn, canola and soy oils, cheap processed meat and cheese “food products”, perhaps made worse by frying things to a crisp and zero attention to electrolytes and micronutrients. But I suspect it would still be healthier than a SAD diet with similar mistakes.


(Chris) #6

This guy is cancer.


(Crow T. Robot) #7

I’m sure some doctors have said this – there are a number of famous doctors who are animal rights’ activists, and they will say just about anything to promote veganism. So help me, PCRM.

There is a fact that is probably used to support this idea, which is true: certain cancers also can use fat for fuel and not just glucose. Thereby making the keto diet not especially helpful to cope with those specific cancers (though in no way “causing cancer”).

HOWEVER, the keto diet can help prevent the development of those cancers, even if it’s not helpful for reducing their existence if already developed. So…


(Bunny) #8

What he is eating is what causes it! A real ignoramous that want’s to enjoy that junk food without consequence!

“Use fat for fuel?” hmmmmmmmm?

image image

I am looking to see where cancer is “using fat for fuel?”

  1. “…Dr Gary Fettke also believes that the problem with modern cancer treatment is that it ignores the glucose metabolism. …” “…Dr Gary Fettke has a vested interest in this research as he had brain cancer 15 years ago. He switched to a ketogenic diet and essentially starved the cancer. …” …More
  1. Do Ketones Fuel Cancer? The Low-Carb Experts Respond: “…I know about this study. The study has serious problems. I wrote a letter to the editor of the journal regarding the flaws in the study. I discussed these flaws with Dr. Richard Veech at the NIH, who concurred with my concerns. Unfortunately, these types of studies will occasionally appear in the literature mainly because the reviews, who know about molecular biology, are unfamiliar with the old literature on energy metabolism. …” - DR. THOMAS SEYFRIED, Boston College cancer researcher

Here’s Dr. Seyfried’s letter that never got published in the journal:

October 20, 2010
Dr. M.V. Blagosklonny
Editor-in-Chief, Cell Cycle
Roswell Park Cancer Institute
Buffalo, NY

Dear Dr. Blagosklonny,

I am writing in reference to an article that appeared in the September 1 issue of Cell Cycle by Bonuccelli, et al., entitled: “Ketones and lactate “fuel” tumor growth and metastasis: Evidence that epithelial cancer cells use oxidative mitochondrial metabolism”.

The authors have made serious errors in their data interpretation and the conclusions of their article. There is no evidence in the biochemical literature that ketone bodies can be made from pyruvate in fibroblasts. It is common knowledge in biochemistry that ketone bodies are derived from fatty acid beta-oxidation in liver mitochondria. This information is also presented in the cited articles from Veech and co-workers.

The authors present evidence showing that the ketone body 3-hydroxy-butyrate does not enhance lung metastasis (Fig. 4A), yet the paper title indicates that ketones fuel tumor growth and metastasis. The paper title and abstract are therefore misleading.

Furthermore, no evidence was presented in the paper showing that the MDA-MB-231 cells can survive using only L-lactate or ketone bodies as metabolic fuels. While the authors recommend that it may be unwise to use lactate-containing i.v. solutions in cancer patients, the authors should also recognize that lactate is metabolized to glucose in the liver through the Cori cycle. It is well documented that glucose can stimulate tumor growth. No information was provided on food intake or body weights of the treated and control mice. No information was presented on blood glucose or ketone levels in the tumor bearing mice used in the study. It is difficult to assess the effects of drug injections without this information. Finally, no evidence was presented showing that OxPhos is operational in the MDA-MB-231 tumor cells. Gene expression profiles do not provide the required biochemical and physiological evidence for establishing operational OxPhos in tumor cells.

Unfortunately, the author’s provide misinformation. Such information will cause confusion in the field. I am surprised that the reviewers of this paper did not mention these issues in their critique, as some of the evidence and statements presented contradict basic principles of biochemistry as specified in any general textbook on the subject. If further evidence is needed to support my concerns, I would suggest contacting Drs. Richard Veech, Theodore B. VanItallie and Jong Rho.

Sincerely,
Thomas N. Seyfried, Ph.D.


(Charlie Kathopoulis) #9

Just to play devils advocate here - if one has a BRAF V600E mutation, fat will fuel tumour growth. This mutation is seen in melanomas (50%), hairy-call leukemias (100% and more so if one is a Wookiee), colorectal cancer (10%), prostate cancer (10%) and multiple myeloma (5%). It is suggested that this mutation is tested for by anyone who is battling cancer and their diet modified accordingly.

However, and assuming one does not have the aforementioned mutation, ketogenic diets have shown positive results during radiation therapy, glioblastomas, advanced PET positive cancers, cancer cachexia (weakness and wasting of the person), and even possibly assists in chemotherapy (possibly).

One means of how this happens is the ‘Warburg Effect’ - where cancer cells net a total of 2 ATP from a single glucose molecule, whilst normal cells net 38 ATP form the same glucose molecule. Fundamentally cancer cells are hungry inefficient little buggers who need massive amounts of glucose to keep up with their energy demands.

[Low Carb Caufield 5th Oct, 2017 Melbourne Aust. Talk by Dawn Lemanne MD PMH Oregon Integrative Oncology] - I’ll post the link to her Gold Coast talk.


(Bunny) #10

Now my brain is ticking on this acetate and glucose cancer cell metabolism thing, going to look at this more in the future, have my eye on this booger==>pkcz (this guy MIGHT be responsible for whether or not the cancer cell metabolizes acetate or glucose):

“Limiting dietary fat intake and monitoring circulating acetoacetate levels might be beneficial in patients with BRAF V600E melanoma or other related cancers,” Chen says. “At this point, we can’t be specific about diet suggestions, because we need to know more about**.” …More

Eating too much sugar causes it (melanoma) to begin with or Advanced Glycation End Products in Foods but how would you trick the cancer into cellular death after the fact? FASTING maybe?

“…We show that glutamine supplementation is not sufficient to prevent loss of cell viability in a subset of glucose-deprived melanoma cells, but synergizes with acetate to support cell survival. Glucose-deprived melanoma cells depend on both oxidative phosphorylation and acetate metabolism for cell survival. …” …More

Glucose deprived cells synergize with phosphorylation and acetate hmmm?

What is causing that?

“…Classically, ceramide is thought to induce death, growth inhibition, and senescence in cancer cells. However, it is now clear that this simple picture of ceramide no longer holds true. Recent studies suggest that there are diverse functions of endogenously generated ceramides, which seem to be context dependent, regulated by subcellular/membrane localization and presence/absence of direct targets of these lipid molecules. For example, different fatty-acid chain lengths …” …More

”…Together, this argues that glucose and acetate metabolites are the dominant TCA cycle fuels in these cancers. …”

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“…Initially, using orthotopic models with patient-derived material, they illustrate that acetate contributes a significant fraction of carbon to TCA cycle intermediates. Moreover, they show, using the identical technique in human patients, that brain tumors growing in human beings metabolize acetate in a manner nearly identical to tumors grown orthotopically in the mouse brain. Collectively, these results have several important therapeutic implications. First, they provide a clear demonstration that acetate is a metabolic fuel in vivo that is preferentially utilized by a subset of cancers. They also illustrate that this is mediated by ACSS2, whose expression correlates with tumor aggressiveness in the six different organ diseases analyzed. This suggests that acetate avidity and metabolism may be a general feature of many cancers. In contrast, normal cells appear unaffected by loss of ACSS2-mediated acetate metabolism, as ACSS2 null mice do not exhibit any overt phenotypic defects. Taken together, it is reasonable to conclude that acetate metabolism may represent an addiction of certain cancer cells. Furthermore, the results presented in these studies illustrate the clinical applicability of two different acetate-measuring technologies—i.e., [11C]acetate-PET and [13C]acetate-NMR. Such strategies could be used to identify patients likely to respond to an antimetabolism therapy and could also be used as markers of therapeutic response. …” “…Exogenous acetate, in this case, is treated equivalently to that generated by deacetylation. Regardless of the mechanism(s) by which cancer cells utilize acetate, the insights provided by these studies position acetate metabolism as a potentially exploitable vulnerability in cancer metabolism. …”…More


(Charlie Kathopoulis) #11

:slight_smile: Now you have me tjhinking and running back and forth to the attic to grab my old texts lol

Just briefly Dr Lemanne uses a mix of carbohydrate restriction, ketogenic diet and IF to treat patients. I recently listened to a pod cast with the Dudes with Thomas Seyfried and, if I recall correctly, Thomas mentioned a protocol of cyclical intervention when trating cancer due to the cyclical nature of insulin? I might be wrong (my wife says I probably am wrong - she loves me :slight_smile: ) but it might help explain how cancer cells can be attacked using dietrary intervention. It’s a little over my head but it is fascinating stuff. I’ll re-listen tonight and also check those links you posted :smiley:


#12

I’ve only skimmed the responses so might have missed this if someone already brought it up: most cancer cells feed on sugars, but some do (or can learn to) feed on ketones.
I think that if you’re using ketosis as a dietary intervention to help with cancer treatment, the first step is to confirm that your tumor is glycolytic.

That doesn’t mean that ketosis causes cancer, and in fact I think the lower glucose and inflammation is probably protective, but that might be what the chips-guy was referencing.
(though really the image of someone scarfing down a pastry and soda while talking health outcomes… oof).


(Bunny) #13

Not only glucose or acetate but insulin, cancer cells also have more insulin receptors than normal cells…

According to G. Edward Griffin this (video below) is the way Mother Nature kills cancer cells and prevents it from occurring and has to do with the pancreas or impaired pancreatic function (too much sugar) causing the cancer and production of trypsin and the nitrilosides/Vitamin B17/Laetrile that’s is more concentrated in grass fed animals besides plants and seeds… This may explain why the Inuit never get cancer!

“…If the pancreas is weak or if the rate of Trypsin can’t keep up, then nature has provided a second line of defense which poisons malignant cells while nourishing all the rest, which is the compound known as Amygdalin from foods containing Nitrilosides . This molecule contains two units of sugar, one of Benzaldehyde, and one of cyanide all tightly locked together within it. The only substance which can unlock this molecule and release the cyanide and benzaldehyde is an enzyme called ” Beta-glucosidanse .” This unlocking enzyme is not found to any dangerous degree anywhere in the body except in cancer cells where it is always present in great quantities. Therefore, unlocking takes place at the cancer cell, and only the cancer cell. Another important enzyme called Rhodanese is the ”protecting” enzyme because it neutralizes cyanide by converting it instantly to byproducts which actually are beneficial and essential for health. This enzyme is found in great quantities in every part of the body except the cancer cells which consequently are not protected. …” …More

The video below makes more sense to me than any theory or hypothesis I have ever read to date on the subject of cancer! This explains why it is a metabolic disease and not genetic or hereditary!

The Mechanism of the Nitriloside Theory of Cancer Elimination:

The Nitriloside molocule is made up of Benzaldehyde, Cyanide, and Sugar.

Over the past century, claims of a preventative and cure for cancer have existed based on a compound called Nitriloside which is found naturally occurring in many plants around the world.

This article examines aspects of scientific claims making up the theory that Nitrilosides are able to prevent cancerous tumors from forming and are also able to kill cancer cells that already exist. It presents a summary of the theory of how Nitrilosides eliminate cancer as well as presenting scientific studies which support and also counter the theory. …More

Jump to segments of this article…

A Summarized Description of the Theory of Nitriloside Cancer Elimination, From the Documentary Video ”A World Without Cancer, ” by G. Edward Griffin

Two Most Commonly Cited Studies which Purport to Refute the Mechanism of Nitriloside Cancer Elimination

The Presentation of Video Footage of Cancer Cells Dying When Exposed to Laetrile Under a Microscope Would Be Beneficial to Support the Theory (more endogenously complex?)

Scientific Reports of Ernst T. Krebs, Jr., John Beard, and Others Which Confirm the Mechanism of Nitriloside Cancer Elimination, from ”The Robert Cathey Research Source”

Excerpts From the Documentary and Book ”A World Without Cancer” by G. Edward Griffin

Conclusion


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