“On each occasion, participants ingested a hot, chocolate-flavoured drink consisting of either one of three fat emulsions (oil tests) or of water (control) every hour for the first 12 h followed by every 2 h for the remainder of the study, ..." I feel sick just thinking about that.
Surely the correct way to get a correct result is to have people eating normally with controlled diets and then do a standard insulin response test. Also, long term is what we want to know about not some short trial where there could be short term metabolic responses to a very unnatural eating pattern.
It appears as if a lot of effort has gone into making what we know unknowable based on the way they design these studies? Lots of money spent - how is it that we don't have enough proper science to clearly answer these questions?
I would note that people with T2D probably have accumulated damage to their livers (and possibly pancreas). So there are two questions - Do PUFAs cause inappropriate insulin sensitivity in healthy people? and do PUFAs cause inappropriate insulin sensitivity in people with the damage that causes T2D. (Sadly, I think the damage is permanent). People with T2D end up with chronically elevated insulin levels.
So Tucker seems to be asking if the change in insulin sensitivity is immediate or generated over the course of long term exposure to PUFAs that damage tissues?
All these questions could be answered using synthetic diets ( as in Vivonex 100, Winitiz, Greenstien etc). Real experimental science varies only one variable at a time. Using diets that are not chemically defined does not help us much - we are left guessing if the results are due to one component while several are changed at once.
The other issue is that different tissues have different insulin sensitivity - but that is not the case. The tissues in the liver/adipose/muscles do not respond the same. And - the assumption that insulin is only involved with glucose is just wrong - but leads to the assumption that insulin sensitivity for glucose is the same as for triggering fat storage.
It turns out that BOTH high levels of LA and fructose can damage the liver - but what is particularly interesting is that the damages don't just add. This begs the question if the ongoing T2D pandemic might be caused by the combination of high PUFA + high fructose found in the average Western diet.
“On each occasion, participants ingested a hot, chocolate-flavoured drink consisting of either one of three fat emulsions (oil tests) or of water (control) every hour for the first 12 h followed by every 2 h for the remainder of the study, ..." I feel sick just thinking about that.
Surely the correct way to get a correct result is to have people eating normally with controlled diets and then do a standard insulin response test. Also, long term is what we want to know about not some short trial where there could be short term metabolic responses to a very unnatural eating pattern.
It appears as if a lot of effort has gone into making what we know unknowable based on the way they design these studies? Lots of money spent - how is it that we don't have enough proper science to clearly answer these questions?
I would note that people with T2D probably have accumulated damage to their livers (and possibly pancreas). So there are two questions - Do PUFAs cause inappropriate insulin sensitivity in healthy people? and do PUFAs cause inappropriate insulin sensitivity in people with the damage that causes T2D. (Sadly, I think the damage is permanent). People with T2D end up with chronically elevated insulin levels.
So Tucker seems to be asking if the change in insulin sensitivity is immediate or generated over the course of long term exposure to PUFAs that damage tissues?
All these questions could be answered using synthetic diets ( as in Vivonex 100, Winitiz, Greenstien etc). Real experimental science varies only one variable at a time. Using diets that are not chemically defined does not help us much - we are left guessing if the results are due to one component while several are changed at once.
The other issue is that different tissues have different insulin sensitivity - but that is not the case. The tissues in the liver/adipose/muscles do not respond the same. And - the assumption that insulin is only involved with glucose is just wrong - but leads to the assumption that insulin sensitivity for glucose is the same as for triggering fat storage.
It turns out that BOTH high levels of LA and fructose can damage the liver - but what is particularly interesting is that the damages don't just add. This begs the question if the ongoing T2D pandemic might be caused by the combination of high PUFA + high fructose found in the average Western diet.