Cardiometabolic function isn't the same as metabolic syndrome. Cardiometabolic function would be like a spectrum or perhaps a map. Metabolic syndrome would be the section of spectrum(say red in the rainbow) or area on the map (like a swamp) that designates the "danger zone."

Here the term "optimal" is used and that's around 7 percent as having optimal cardiometabolic function. That doesn't instantly mean 93 percent are impaired. The other classes are **intermediate, which is half of people, ** and lastly poor which was ~44 percent.

https://www.nature.com/articles/s41568-021-00388-4

https://link.springer.com/article/10.1186/s40170-020-00237-2

Fat can be oxidized for ATP via β-oxidation (look up FAO or catabolism, or see above links.) Fat → fatty acids → β-oxidation → acetyl-CoA + electron carriers → electron transport chain → ATP.

Example: Palmitic acid, a 16-carbon fatty acid, undergoes 7 rounds of β-oxidation producing 8 acetyl-CoA total. After everything runs through the Krebs cycle and electron transport chain, you end up with roughly 106 ATP. Which is a huge amount compared with glucose(1 glucose is about 30 ATP.)

[–] jet@hackertalks.com 1 points 1 day ago* (last edited 1 day ago)

Cardiometabolic function isn’t the same as metabolic syndrome. Cardiometabolic function would be like a spectrum or perhaps a map. Metabolic syndrome would be the section of spectrum(say red in the rainbow) or area on the map (like a swamp) that designates the “danger zone.”

Here the term “optimal” is used and that’s around 7 percent as having optimal cardiometabolic function. That doesn’t instantly mean 93 percent are impaired. The other classes are **intermediate, which is half of people, ** and lastly poor which was ~44 percent.

I'm afraid your anchored on "metabolic syndrome" when I am referring to impaired metabolism, since that is driven by hyperinsulinemia - and thus demonstrates a epidemic of elevated insulin in the population at large which is driven by persistently elevated blood glucose... which is exactly the environment cancer needs to thrive.... And not optimal does mean a degree of impairment by definition.

Thanks for those links, they do demonstrate cancer has a very interesting metabolic plasticity, but they do not definitively show fatty acid ATP synthesis, your Shilpa review even indicates FAO is down regulated in a variety of known cancer types... However, I hope when you read my references you just missed the section in the above paper, which addresses your rebuttal:

https://doi.org/10.1007/s10863-025-10059-w - Questionable Assumption 5: Fatty acid oxidation can provide sufficient ATP production through OxPhos in cancer cells

Regardless if Fatty Acids have some role to play, can we agree that glucose is very much the favored fuel? So even if we disagree on metabolic mitochondrial dysfunction as the basis of cancer, can we agree there is no benefit to feeding EXTRA glucose into a cancer patient?

After everything runs through the Krebs cycle and electron transport chain, you end up with roughly 106 ATP. Which is a huge amount compared with glucose(1 glucose is about 30 ATP.)

Yes, this is addressed in the Seyfried paper above, the problem is in dysfunctional mitochondria glucose pathways while less efficient are massively upgraded... i.e. why the PET scan works.