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“Retune” Newcastle diet for the normal bmi type 2

MrsA2 said:
The 'funny' is obviously American, not UK. We don't have gasoline or cell phones , not in the 50s or now!
Click to expand...
Beg to disagree. Gasoline was common parlance for petrol, in my youth and the Hutchinson Rabbit phone was indeed Cell (or telepoint) phone. It is the term Gas for petrol that is not UK.
 
And when one is one of many millions, one can understand the extension of stuff from one's own country to - everywhere!

I do remember saying to a room full of Chinese young people some years ago, that I had no real concept, and could only imagine, what it was like being part of such a huge cultural/geographic group that in countries that you move to - whole areas become dedicated to one and one's millions - as in China Towns.

The US - is like that too, really isn't it? With culture, and funnies and so on :) . Ah yes - numbers count! :D
 
Finally I see that they've published a full paper on the ReTune Study on the 31st of Aug 2023.
https://portlandpress.com/clinsci/a...Aetiology-of-Type-2-diabetes-in-people-with-a

Rather than subject them to a standard 75g OGTT Taylor has come up with a convoluted test & metric to measure beta cell improvement.
The "Meal-related insulin secretion corrected for insulin sensitivity (disposition index, DI)".

bcell.PNG

Probably need to have a chemistry background to interpret the findings.
Where the Direct 12 month follow up seemed to show 2nd phase insulin secretion rates returning to control levels this data would appear to differ.
 
Ronancastled said:
Finally I see that they've published a full paper on the ReTune Study on the 31st of Aug 2023.
https://portlandpress.com/clinsci/a...Aetiology-of-Type-2-diabetes-in-people-with-a

Rather than subject them to a standard 75g OGTT Taylor has come up with a convoluted test & metric to measure beta cell improvement.
The "Meal-related insulin secretion corrected for insulin sensitivity (disposition index, DI)".

View attachment 63134

Probably need to have a chemistry background to interpret the findings.
Where the Direct 12 month follow up seemed to show 2nd phase insulin secretion rates returning to control levels this data would appear to differ.
Click to expand...
Once again Taylor is using his fudge factor by adjusting the secretion rates by incorporatiing bmi into the equations. so a flow rate of pmol/l per min becomes per kg/height in m^2 since height is generally static for most of the subjects over the period of the trial. then this factoring has the effect of providing direct mathematical manipulation according to body weight. since the intervention is one of weight loss, then this automaticslly guarantees an 'improvement' in the conclusion. All the other OGTT trials I have seen correctly use flow rate = quantity per minute. This fudge factor is common to Glaxo Smith Kline and Newcastle Uni ( and by inference DUK). I have no problem with them using it to compare between cohort members at a point in time, but it is invalid when comparing different sample times.
 
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.
 
I do not buy this theorem from Roy Taylor. I know too many T2D who were diagnosed first, and then suffered metabolic syndrome, and subsequently became obese. I also know some people who went from around 8 stone up to 20+ stone, and who did not develop diabetes. I also know of two such people who lost most of that weight after and still did not get diabetes.

My weight gain happened after my diagnosis. I had been a regular 10 stone weakling for most of my life, and quite athletic. Then T2D came as a surprise as I had no symptoms (thirst,weeing, etc) but I then ballooned to 18 stone. Finally started LCHF and the glucose levels dropped first. then soon after the weight dropped and I returned to 10 stone and remained T2D in control. I did get an endo to declare me in remission, but it was short lived and I prefer to say I am in control now.

So I do not see Fat Thresholds in my life or among my friends. But Roy Taylor has several books coming off the back of these experiments, and an active department to find research money for.
 
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