I am having difficulty with this section
"The Personal Fat Threshold hypothesis postulates that people with T2D will exhibit the same pathophysiological mechanisms irrespective of BMI and may return to non-diabetic glucose control after weight loss. This is of profound importance as it would indicate that this common disease does not have heterogenous causative mechanisms dependent upon body weight."
On one hand he is saying the cause of T2D is not dependant on weight, but the cure is weight loss. So he is explaining TOFI diabetes, but TOFI do not want to lose weight so what gives? The other confounder I think is that as T2D progresses, so does the midriff expansion,and subequent weight gain. so weight gain is a symptom of T2D not necessarily a cause. and I do not think his work so far has proven it either way. He is only using recently dx'ed subjects anyway so maybe that is to avoid the question. What I want to know is why there were so many non responders in his original trials. He offers no explanation for why they were unsuccessful even though most of them also lost weight. ( they remained above their personal fat threshold?)
The concept that if you have too much fat needing storage, then the body starts using other unusual body cells such as the liver (but thats what its designed to do) and the pancreas (yes, as demonstrated by the MRI scans) seems logical to me. But the simple concept is wrapped up in pseudo science once again. It sounds important, and most people will gloss over it with mental confusion, which I find with most of Taylors work. Keep it simple. So the real breakthrough for my mind was the MRI scans and the evidence it provided of fat being stripped out of the pancreas by the intervention. Science is best when you prod something and watch how it affects the test sample.
Looking at the measurements taken there seems to be a lot of estimation being used. Not sure how valid these procedures were. I suspect more fiddle factors may be embedded on the quiet.
. Ah yes - numbers count! 
