Context truly is everything. We could call throwing 300 pounds on your back and making you go from a sit to stand position repeatedly a quite stressful event couldn't we? So obviously the hormone cascade necessary to burn glucose under these circumstances are stress hormones right? Thats the logic you article seems to be working with. I don't agree.
"Fatty acid oxidation is by and large inefficient and increasingly activates pathways that cause oxidative stress, inflammation and apoptosis" This is a statement and not backed up by fact. We could argue this point for carbs also ....
From Lucas Tufar (same fella that made the mathematical point that ketosis is not stressful):
"You are correct, the generation of ROS is in the ETC. But it differs from electrons derived from glucose or fatty acids. Glucose generates more NADH+, which then transfer electrons to complex I (NADH dehydrogenase). Fatty acids produce almost an equal amount of NADH+ and FADH2, which utilizes preferentially complex II (succinate dehydrogenase).
1 molecule of glucose:
Ratio NADH+:FADH2 = 5:1
1 molecule of palmitate:
Ratio NADH+:FADH2 = 2:1
Complex I is the main producer of ROS in the ETC, along with complex III. See:
Mitochondria and reactive oxygen species. [Hypertension. 2009] - PubMed - NCBI
Localization of the site of oxygen radic... [J Bioenerg Biomembr. 2000] - PubMed - NCBI
Another complex which is utilized by catabolism of fatty acids is the electron-transferring flavoprotein.
A good, comprehensive review can be found Glucose Hysteresis as a Mechanism in Dietary Restriction, Aging and Disease
And, the basics http://themedicalbiochemistrypage.or...html#complexes "
Since you just quoted some Ray I'll just qoute Lucas. But there are studies to back it up. Also appears to be a bit more recent. Not really trying to prolong the agony of this discussion again. Just posting this to show that there are more ways than you can shake a stick at to analyze stress and function in a system as complex as we are.