I found this to be really interesting and am curious to hear others' thoughts. I have not read the whole study yet. It seems this conflicts with the idea that a ketogenic diet could be beneficial, unless I'm not understanding something. Does anyone know of similar studies?
https://medicalxpress.com/news/2018-10-fat-fuels-aggressive-brain-cancers.html
Here's a sci-hub link to the actual study.
ReplyDeletehttp://sci-hub.tw/http://emboj.embopress.org/content/early/2018/10/15/embj.201798772.long
I'll give it a read and see what I get from it.
In the study they identified two populations of glioma cells, slow cycling cells (SCC) and fast cycling cells (FCC) which had very different metabolic strategies. SCC were more invasive and chemoresistant and more dependent on mitochondrial metabolism and fatty acid oxidation, while FCC were more proliferative, chemosensitive, and more dependent on glucose, but less dependent on mitochondrial metabolism.
ReplyDeleteVery interestingly, FCC-enriched gliomas implanted into mice were sensitive to a high fat, low carb diet, while SCC-enriched gliomas were insensitive. Furthermore, recurrent/treatment resistant tumors showed gene expression profiles more characteristic of SCC than FCC.
SCC were also more dependent on autophagy than FCC:
"Together, our
observations suggest that SCCs may engage in autophagy mechanisms
to metabolize stored lipid, particularly in response to metabolic
stress."
Several inferences can be made based on this paper:
one is that a ketogenic diet will be effective only on one population of cells (FCC) but not on another population (SCC), and that a truly effective metabolic approach would need to target both of these populations.
secondly, a ketogenic diet may be more effective in a newly diagnosed brain tumor with a higher proportion of FCC, and less effective in a recurrent tumor with a higher proportion of SCC.
Ideally a ketogenic diet targeting the FCC population would be combined with therapies targeting mitochondria and fatty acid metabolism/transport to address the SCC population.
In general this paper is another great example of why it is called glioblastoma MULTIFORME.
Hi Stephen,
DeleteThis was my understanding as well.
I have been on a ketogenic diet for over 1.5 years now, but my tumor is "only" a grade 2, so I have not idea whether this would apply.
So beyond just glioblastoma being "Multiforme", it does highlight how each tumor in each patient can be different...
This is the whole basis for "the cocktail approach" - it's necessary to target different subpopulations within the same tumor, and a single agent is not likely to do that effectively.
Delete