If the suggestion is that the brain may be responsible for some T2 then does this suggest stress as a precursor? I developed T2 at a highly stressful point in my life 2 years or so ago and have continued with significant stress since. With no familial background or predisposition and no obvious weight or health issues plus a background of heavy sport indulgence and decent diet, it has been a total surprise. A chronic back condition requiring 12 years of oxycontin use raises suspicions. Stress clearly affects cortisol and this affects glucose/insulin so has the brain compensated in sone form mistakenly and until stress can be diminished it could be a catch 22!??
Not sure, but it seems that if one was going to say high fat causes t2 because the mice ate high fat and they got fat and developed t2... One would have to indicate fairly what the rest of the macros were. A standard american diet leading to obecity and t2 is high in fat too, but also high in refined carbohydrates. Lchf diet, for example is high in fat (obviously), but takes out much of the carbohydrates... That would not be the same diet, would it? I don't know what the effect on the fgf1 response would be, but as scientists, they can't pick and choose what parts of a research project they want to disclose, not ethically anyhow. You could find three sets of lab rats, feed one a lchf diet, feed one a lclf diet, and feed one a SAD diet. Now, all is fine, but if you happen to mention that one of the groups also were given arsenic in their water, and that group died. Well, don't go blaming the diet. So if you say we gave them loads of fat (but "forget" to disclose the carb/protein levels) then it isn't the whole picture.
Not sure, but it seems that if one was going to say high fat causes t2 because the mice ate high fat and they got fat and developed t2... One would have to indicate fairly what the rest of the macros were. A standard american diet leading to obecity and t2 is high in fat too, but also high in refined carbohydrates. Lchf diet, for example is high in fat (obviously), but takes out much of the carbohydrates... That would not be the same diet, would it? I don't know what the effect on the fgf1 response would be, but as scientists, they can't pick and choose what parts of a research project they want to disclose, not ethically anyhow. You could find three sets of lab rats, feed one a lchf diet, feed one a lclf diet, and feed one a SAD diet. Now, all is fine, but if you happen to mention that one of the groups also were given arsenic in their water, and that group died. Well, don't go blaming the diet. So if you say we gave them loads of fat (but "forget" to disclose the carb/protein levels) then it isn't the whole picture.
Not being adversarial, just pointing out that the link did not give full disclosure of all the elements in the "scientific" comparison.
Yes...lets leave the high fats discussion for other threads
From the original study...FGF1 in the brain seems to be the magical key...
This other study shows that we newly diagnose T2D should already have elevated level of FGF1 in serum, possibly compensatory as per elevated insulin ...how can we enable it to repair our neural circuits?
http://www.pubfacts.com/detail/2680...-diagnosed-type-2-diabetes-compared-to-normal
This study on resistance training also seems to provides some insights...on increasing FGF1...
http://www.pubfacts.com/detail/2715...-after-8weeks-of-resistance-exercise-training
