And found it interesting so I emailed Professor Thomas Seyfried suggesting he looked at the relevance of nucleosolic acetyl-CoA levels from the perspective of splicing issues. He then sent me two of his papers which I upload below.
It does appear, however, that this (Mitochondrial Metabolic Theory) analysis of cancer is more likely to be true than the Somatic Mutation Theory.
Very interesting. Glutamine noted… also interesting re: acute hyperthermia (mimetic for a high fever), which I had just recently seen pop up in unrelated discussions about dementia treatments.
A ketogenic diet is useful in treating many diseases and conditions, such as hypoglycemia, obesity, sarcopenia, epilepsy, and possibly certain cancers.
Apparently neurodegenerative ones too. I was disappointed in Peter Attia’s responses on this in an interview I recently watched. He seemed to be far less knowledgeable than I had assumed, truly a jack of all trades and master of none once the discussion gets down in the weeds.
I’ve seen interview after interview with neurologists singing the praises of ketosis for stalling all sorts of dementias.
Combining Professor Seyfried’s hypothesis that cancer is primarily a mitochondrial disease with another thread on this forum about mitochondria in cells at remote parts of the body communicating through chemical signals somehow raises some possibilities. Is mitochondrial signaling related to cancer metastasis? Dr. Seyfried observes that cancer mutations are rarely in the nucleus of the cell. Are we on verge of finally understanding how cancer occurs and spreads at the cellular level?
When I search in the literature I see references to cancer cells using other amino acids besides glutamine as a source of energy. What’s his take on that?
Could you ask? Or give me his contact info so I can take it up?
I mean a prolonged water fast would starve the cancer of all these sources but I don’t know how long it would need to be and if it would be feasible.
I’m sorry I meant the original, Seyfried. He makes it sound as though without glucose and glutamine cancer cells have no energy source. Other research I linked to shows that cancer can thrive off of other amino acids as well. You might remember the source as it was posted on the thread re: glycine, and specifically mentions how serine can feed cancer.
I’m not sure, actually. The liver can turn protein into sugar. Not sure if it can do the same to fat. But my point here is just to make sure what Seyfried is saying pans out in the face of other research claiming other amino acids can be metabolized by cancer.
Short answer courtesy of Dr. Oracle:
What is Gluconeogenesis
Gluconeogenesis is the metabolic pathway through which glucose is synthesized from non-carbohydrate sources.
Mainly occurs in the liver, but also in the kidneys and small intestine.
Where Gluconeogenesis Occurs:
Primarily in the liver
Also occurs in the kidneys and small intestine, but to a lesser degree
Substrates Used for Gluconeogenesis
Lactate
Glycerol Amino acids (alanine, glutamine, serine, threonine, methionine, valine, arginine, histidine, proline, aspartate, asparagine, glutamate, and tryptophan)
I’m a big fan of Inigo. He’s been discussing/researching cancer as it relates to metabolism for quite some time. If interested, check out his research.
Not cheap but not ridiculous either and you’ve invested a lot of time and effort and supplements into your routine so I’d be curious how your mitochondria score.
I totally agree with all the above. Concerning Attia, his guests are, most of the time, very knowledgeable and interesting but he himself often looks like he only has a shallow understanding of the subjects.
In fact it depends which cancer. Some are sensitive to glucose depletion but others can use other energy sources like fatty acids, proteins, etc.
Worse in some cases the glucose depletion can make the cancer more aggressive like in this 2023 paper for instance:
Rewiring of energy metabolism is a hallmark of cancer, and the increased dependency on glucose is a common characteristic of cancer cells […]
However, the clinical results with metabolic therapies targeting glucose have been disappointing, likely due to cancer cell plasticity and adaptation mechanisms (Cargill et al, 2021). The complex adaptations induced in cancer cells by glucose restriction are not known. Here, we report the discovery that glucose restriction induces de-differentiation and promotes aggression of lung adenocarcinoma (LUAD) cells.[…] leading to a highly aggressive and metastatic phenotype.
In fact they were looking at using SGLT2 inhibitors for that but found out that it might end up worse:
We previously showed that pharmacological inhibition of SGLT2 in murine LUAD results in reduction of the tumor burden and improvement of survival (Scafoglio et al., 2018). However, mice eventually develop aggressive tumors and die even during the treatment.
Yes, so it runs directly against the claims made by Seyfried in the original video in this thread. He says doesn’t matter the type of cancer or its mutations, the cells run either on glucose or the fermentation of glutamine — nothing else. So it seems like a blanket categorical statement in light of other sources. And trust me, I’d love for it to be that simple.
But surely he’s a serious researcher and must be aware of all these papers. So maybe I’m missing something.
