Fasting. Authentication. Inquire. Repeat
Cliff
Few “influencers” are as curiously analytical as Peter Dobromylskyj (Hyperlipid.blogspot.com) especially with his “Protons” theory. Despite its esoteric difficulty for the general audience one of the train of thought behind this is that of an alternate hypothesis on ROS / reactive oxygen playing a much underdiscussed role to insulin signalling and consequently ~ satiety signalling.Few “influencers” are as curiously analytical as Peter Dobromylskyj (Hyperlipid.blogspot.com) especially with his “Protons” theory. Despite its esoteric difficulty for the general audience one of the train of thought behind this is that of an alternate hypothesis on ROS / reactive oxygen playing a much underdiscussed role to insulin signalling and consequently ~ satiety signalling.
In this Podcast with Brian Sanders ~ this is what I consider a more approachable conversation to the above theory, however there are still nuances to be anticipated here particularly mid onwards.
Chiefly, the main discussion revolves around the controversial counter point on “insulin sensitivity” being favourable / proclaimed picture for metabolic health. Except that it is here counter-suggested to not be the case in some circumstances. In light of rodent studies, as well as the few human studies mentioned all appear to suggest that insulin sensitivity may not be perpetually ideal state as it permits both glycogen as well as fat storage.
Other topics to follow:
- General recite of our present failures of the present nutrition status quo.
- Low fat paradigm, before sinking to the fat metabolism particularly distinction between PUFAs vs SFA,
- Fructose, and how satiety signalling can be adversely impacted by these proxies.
- Brief thoughts on other alternative channel influencer circles ~ namely Dr. Raymond Peat.
Highlights
- Rodent studies are in some respect superior to human trials as they eliminate much of socio-cultural factors amongst the test subjects.
- PUFA N3, deriving from seafood, but not that of isolated fish oils ~ is metabolised very differently than PUFAs of N6 / vegetables / seed oils. It is suggested that PUFA N3 provide, if consumed away from PUFA N6 ~ the preferential signals for anti-oxidative recovery .
- Saturated Fats is suggested to be superior at satiety inducing than PUFA N6s ~ “at the cellular level”.
- ROS / reactive oxygen species is suggested to play a role to the above satiation signal; which sat fat / palmitic acids appears to induce stronger ROS signalling.
- The reason why vegetarian low fat diets appear to work well at mitigating / preventing free fatty acid release ~ is because of the very low intake of overall fat calories.
- A “Danish” study on women fed with high amount of 4-HNE derived oxidative products (one of many glycated lipids end products) appear to be less prone for fat storage when insulin resistance is prominent.
- Free fatty acid release amongst type 2 diabetics is said to be in the range of thousnd(s) of MMOL ranges ~ which is interestingly similar to highly athletic individuals.
- How the fate of excess fatty acid metabolism eventually arrives towards heat generation (or “uncoupling”). In other words ~ conversion of ATP into heat.
If you enjoy the above podcast upon which the above topic certainly remains very difficult to sift through in succinct / pragmatic explanation ~ I highly encourage visiting and following the channels below.
Visit Peter Dobromylskyj @ Hyperlipid
http://high-fat-nutrition.blogspot.com/
Visit Brian Sanders @ Peak Human podcast
Live-It-Forward,
AW.