In my last post commenter David asked the following question:
Ketosis has a pelnty (sic) of health benefits, for example what about the anti cancer effect? If you are carnivore but not in ketosis the cancer cell can use the excess glucose produced by the gluconeogenesis. The cancer cell can not run on ketones.[…]
The current mainstream opinion is that all cancer cells thrive on glucose and that we could, therefore, starve them out with a low- or zero-carb ketogenic diet.
This understanding is based on the research of Otto Warburg who was awarded the Nobel Prize in Physiology or Medicine in 1931 for his discovery in cancer research.
Warburg found out that there are two main differences between healthy cells and cancer cells.
- Healthy cells are rich in oxygen and have an alkaline pH-value.
- Cancer cells are low in oxygen and have an acidic pH-value.
This discovery is known as the Warburg Effect.
But is this information really up to date? Is it really so easy to starve off cancer cells?
Let’s not beat around the bush but jump right into the latest research studies.
But be warned. The following information is pretty demoralizing.
Current cancer research about the “Reverse Warburg Effect”
This breast cancer study  from 2011 shows that fatty acids fuel the growth of cancer cells both in vitro and in vivo.
Adipocyte-ovarian cancer cell coculture led to the direct transfer of lipids from adipocytes to ovarian cancer cells and promoted in vitro and in vivo tumor growth. Furthermore, coculture induced lipolysis in adipocytes and β-oxidation in cancer cells, suggesting adipocytes act as an energy source for the cancer cells. A protein array identified upregulation of fatty acid-binding protein 4 (FABP4, also known as aP2) in omental metastases as compared to primary ovarian tumors, and FABP4 expression was detected in ovarian cancer cells at the adipocyte-tumor cell interface. FABP4 deficiency substantially impaired metastatic tumor growth in mice, indicating that FABP4 has a key role in ovarian cancer metastasis. These data indicate adipocytes provide fatty acids for rapid tumor growth, identifying lipid metabolism and transport as new targets for the treatment of cancers where adipocytes are a major component of the microenvironment.
This study  from 2014 on glioblastoma (the most aggressive form of brain cancer) shows that activation of AMPK increases the uptake of fatty acids in cancer cells and fuels their growth.
Right now it seems that everyone is afraid of too much mTOR activation. But here we can clearly see that (at least in this particular case) AMPK activation speeds up cancer growth.
We show that the high levels of activated AMPK, observed in astrocytic tumours, increase extracellular lipid internalisation and reduce energy expenditure by inhibiting ‘de novo’ fatty acid (FA) synthesis, which allows tumour cells to obtain building blocks and energy to be able to create new organelles and new cells.
Our findings demonstrate that AMPK plays a crucial role in glioblastoma cell growth and suggest that blocking lipoprotein receptors could potentially be used as a plausible therapeutic approach for these and other type of tumours with high levels of AMPK.
This study  from 2013 states at the very beginning of the abstract that:
Cancer cell growth requires fatty acids to replicate cellular membranes.
Impairments in MAGL-dependent tumor growth are rescued by a high-fat diet, indicating that exogenous sources of fatty acids can contribute to malignancy in cancers lacking MAGL activity. Together, these findings reveal how cancer cells can co-opt a lipolytic enzyme to translate their lipogenic state into an array of protumorigenic signals.
This study  from 2012 on diffuse large beta cell lymphoma (cancer of the white blood cells) shows that this type of cancer not only thrives on fatty acids but also on our body’s strongest antioxidant glutathione. Moreover, this type of cancer can even use mitochondria for energy production.
We show that, compared with BCR-DLBCLs, OxPhos-DLBCLs display enhanced mitochondrial energy transduction, greater incorporation of nutrient-derived carbons into the tricarboxylic acid cycle, and increased glutathione levels. Moreover, perturbation of the fatty acid oxidation program and glutathione synthesis proved selectively toxic to this tumor subset.
But it gets even worse.
This study  from 2011 is titled “Pancreatic cancers require autophagy for tumor growth.”
This pancreatic cancer study  from 2014 shows how cancer cells don’t just ferment sugar but actually “breathe”(mitochondrial respiration) with the help of mitochondria.
And we’re still not done. It gets even worse than that.
This study  from 2012 shows that cancer cells can even use ketone bodies for their growth.
And even back in 1986 this study  already showed that fasting doesn’t decrease but actually increases the growth of cancer cells.
Fasting increased the rate of growth of the tumors 3 to 4 times over that measured in fed rats. This effect began during the first day of fasting and ended abruptly on refeeding. After refeeding tumor growth slowed to the rate in fed rats. Tumors from fed or fasted rats were not different in cellularity or dry weight/g wet weight. A positive growth response in the tumor required lipolysis and ketosis in the host.
I think this should be enough.
We already knew that cancer cells can utilize glucose for their growth. But now we have to admit that cancer cells are much more complex and that they can thrive on pretty much any substrate, including fatty acids and ketone bodies.
A few years ago a friend of mine has personally witnessed a case of a boy with brain cancer who was put on a ketogenic diet. The boy lost the fight. There was nothing that could help him.
On the other hand, I have witnessed a few cases of people who have successfully cured their cancer with a diet and lifestyle change.
With that said it’s important to understand that every type of cancer is different. Not all cancer cells are created equal. They are just as diverse as the tissues they reside in. Brain cancer, breast cancer, lung cancer, prostate cancer, skin cancer – they are all cancer but they all work differently.
This means that yes, some types of cancer which rely on glucose can be starved off with a ketogenic diet, whereas other types of cancer will thrive on this diet.
It’s really complicated and I can’t tell you what’s the right treatment for any specific type of cancer.
On the Dunning Kruger Effect curve, I’m at the bottom of the valley when it comes to cancer.
So I hope this answers your question, David. I still enjoy intermittent ketosis and my last post was not against ketosis per se but against long-term ketosis.
And since ketosis doesn’t work universally against cancer I can’t recommend it as a one-size-fits-all anti-cancer diet, either.
The perfect diet is highly individualized.