• Guest - w'd love to know what you think about the forum! Take the 2025 Survey »

“Retune” Newcastle diet for the normal bmi type 2

@AndBreathe I think that it might be that the body, to protect itself, is stashing away what it can't cope with as fat.
I lost well over 50lb without even thinking about it when I abandoned the low fat high carb diet I was on - I stopped weighing myself some 6 months before diagnosis and I was getting on for being spherical. I found my notebook and pulled out the scales when I noticed my clothes were sliding south. My waist shrank by about a foot.
 
Resurgam said:
I think that it might be that the body, to protect itself, is stashing away what it can't cope with as fat.
Click to expand...

Yes this is correct. And when the body runs out of fat storage capacity - whatever that capacity may be - there is simply nowhere left for the glucose to go. The fat then begins backing up into the liver and pancreas. Next stop, diabetes. Doesn't matter if you are fat or slim - not everyone has the ability to become obese. Obviously vastly oversimplified but that's the nuts and bolts of it as I currently understand it.

Tangentially, the whole notion that T2s make insulin but just can't use it is, in my view, incorrect. If we couldn't respond to insulin then the liver wouldn't be able to continue making fat, but it does, furiously, which calls into question the idea of insulin 'resistance' as we would typically think of it. And in comes Fung's overflow hypothesis...
 
Ronancastled said:
The proof was there as far back as 1984 but nobody cared to look.
https://diabetesjournals.org/diabet.../Marked-Improvement-in-Carbohydrate-and-Lipid

T2 Aboriginals were ask to give up the western starch diet & return to eating wild meat.
Guess what happened.
Click to expand...
Very interesting and the perfect foil to the ND report. However, there seems to be no remission declared. Also no success rate either. Can we assume 100%? or did some not make the grade? Not a plan that could be sold to the NHS thats for sure. And to paraphrase Roy Taylor in his scientific report, It was not an RCT so is not acceptable, just like all the low carb diet studies he decried. But then neither were any of the ND studies. It is also a small sample size (10 not 20 like in Retune) Also, eating like our forebears is not sustainable long term nowadays.

My tongue refuses to remain firmly planted in cheek and wants to stick out, for some reason.
 
Jim Lahey said:
>>>>>>
Tangentially, the whole notion that T2s make insulin but just can't use it is, in my view, incorrect. If we couldn't respond to insulin then the liver wouldn't be able to continue making fat, but it does, furiously, which calls into question the idea of insulin 'resistance' as we would typically think of it. And in comes Fung's overflow hypothesis...
Click to expand...
Do you have any evidence for this (other than Fung). Certainly de novo lipogenesis requires insulin to happen, and it does occur when glucose levels are high. However, is there evidence that someone with NAFLD or AFLD or NASH or maybe just general insulin resistance produces excess lipids? Also where does it store them, since adipose storage requires insulin which also may be subject to IR. I conject here but surely this would provide a simple blood test to detect IR?

https://www.sciencedirect.com/topics/agricultural-and-biological-sciences/lipogenesis
 
Oldvatr said:
Do you have any evidence for this (other than Fung). Certainly de novo lipogenesis requires insulin to happen, and it does occur when glucose levels are high. However, is there evidence that someone with NAFLD or AFLD or NASH or maybe just general insulin resistance produces excess lipids? Also where does it store them, since adipose storage requires insulin which also may be subject to IR. I conject here but surely this would provide a simple blood test to detect IR?

https://www.sciencedirect.com/topics/agricultural-and-biological-sciences/lipogenesis
Click to expand...

Evidence, or proof? I don't have any links to hand. Just a lot of prior research and self-experimentation leading me to lean toward's Fung's hypothesis. It's a very complex subject that will drag this discussion off topic if we delve too deep. But all I will say is that my understanding has evolved a lot over the past year or so, and I'm now of the view that pathological insulin 'resistance' (not sensitivity as we might discuss in the context of, say, a type 1) is actually just the liver running out of places to store the fat it has made from glucose.

You can test 'IR' with glucose vs. circulating insulin and measure HOMA-IR, but what are we really measuring? Resistance because the insulin no longer works, or resistance simply because the insulin does work but the liver his running out of places to put the fat and so it appears not to work? Again, if the insulin no longer works, then the liver shouldn't be able to make fat from glucose. But it does. Maybe it's a little bit of both. There appears to be evidence on both sides. Either way, in my view, the standard gummed-up lock & key paradigm is definitely on shaky ground.

I'm going to end my input there because this is definitely off topic.
 
I think it is certainly connected to the topic, since the Retune study is a variant of the ND diet plan. Roy Taylor uses the previous studies to claim that the diet restores insulin sensitivity and removes insulin resistance. The question is whether the retune study shows the same effect, since the reports so far do not discuss the body fat or pancreatic ./liver fat reductions, merely the HbA1c and weight loss aspects. So again, is Retune just another way of intermittent fasting? And looking into the future, what will the results be in 2 years time if there is follow up? How will the 14 successfull guinea pigs be off their sweeties and back on normal fodder are they still recycling the plan like vaccine boosters?

Actually, it is very relevant to this topic
https://www.jci.org/articles/view/134165
 
Last edited:
Taylor gave an update on ReTune at DUKPC conference about 3 weeks ago.

https://www.diabetes.org.uk/about_us/news/dukpc-digest-day-5-retune-study-lower-body-weight

After 12 months, the findings showed that:
  • Participants’ BMI averaged 22.4 kg/m² at the end of the study (reduced from an average of 24.8 kg/m²).
  • About three quarters (70%) of participants went into remission from type 2 diabetes during the study, with 50% of these going into remission after the first weight loss cycle.
  • People needed to lose on average 8% of their body weight to go into remission.
  • In the 14 out of 20 people who went into remission, their average HbA1c fell from 53mmol/mol at the start of the study to 45mmol/mol. Their blood pressure dropped despite taking less medication to treat this.
  • The participants’ liver and pancreas fat levels were higher than expected at the start of the trial but then decreased to normal levels after weight loss
Click to expand...

Again Taylor with the 45 A1c = remission, that's debatable for a start.
Still, 70% is impressive.
I'd like to see the data on the high achievers, what the best improvement was, did they give them a 75g OGTT ?
 
Ronancastled said:
Taylor gave an update on ReTune at DUKPC conference about 3 weeks ago.

https://www.diabetes.org.uk/about_us/news/dukpc-digest-day-5-retune-study-lower-body-weight



Again Taylor with the 45 A1c = remission, that's debatable for a start.
Still, 70% is impressive.
I'd like to see the data on the high achievers, what the best improvement was, did they give them a 75g OGTT ?
Click to expand...
70% sounds impressive, but it was actually 14 out of 20 which is a small sample size, and the guinea pigs were selected against criteria that do not represent the majority of T2D in the general populace. However, it does provide a tool for us to try. It will be interesting to see how big the remission pool is in a year or so, and whether it really is true remission or a revolving door system for treatment.

But all it is doing is proving that the original NICE guidelines from way back were correct. Weight loss is a strong component of the lifestyle changes suggested in the initial intervention prior to medication. What Taylor has demonstrated is that it is an 8% weight loss in low weight people, and 15% weight loss for those who are obese at DX. And there is the adjunct that you can only expect it to work in the 5 years after DX,

It also shows that 30% of non-obese T2D do not achieve remission this way. The DIRECT trial showed that it did not work for 54% of the overweight cohort.
 
Member496333 said:
Alternatively just eat real food suitable for humans instead of grains, sugar and seed oils. Just like hominids did for three million years before capitalism got involved.
Click to expand...
I think humans were consuming grains and fruit-sugars many thousands of years before capitalism arose, although not in the manner they do today, of course …
 
Final findings have been published
https://www.diabetes.org.uk/about_u...*MTY2NDI3MDgwNC4zOS4xLjE2NjQyNzIwNzMuNjAuMC4w

After 12 months, the findings showed that:​

  • Participants’ BMI averaged 22.4 kg/m² at the end of the study (reduced from an average of 24.8 kg/m²).
  • About three quarters (70%) of participants went into remission from type 2 diabetes during the study, with 50% of these going into remission after the first weight loss cycle.
  • People needed to lose on average 8% of their body weight to go into remission.
  • In the 14 out of 20 people who went into remission, their average HbA1c fell from 53mmol/mol at the start of the study to 45mmol/mol. Their blood pressure dropped despite taking less medication to treat this.
  • The participants’ liver and pancreas fat levels were higher than expected at the start of the trial but then decreased to normal levels after weight loss.
Click to expand...

Slides here
https://twitter.com/x/status/1573248577777942529
 
FdVNPkRXwAEwHTD


I'd love to see the glucose responses to the Weetabix
 
Ronancastled said:
Final findings have been published
https://www.diabetes.org.uk/about_u...*MTY2NDI3MDgwNC4zOS4xLjE2NjQyNzIwNzMuNjAuMC4w



Slides here
https://twitter.com/x/status/1573248577777942529
Click to expand...
Note that Remission (and success) is simply a single HbA1c reading below 48. They define their own version of remission so it maximises their apparent success which the media reporters devour in whole. The normal definition requires at least 2x concurrent 6 monthly HbA1c without any meds. They do not acknowledge the state of prediabetes and count results between 42 and 48 as being 'Normal' i.e. non diabetic.

As I have pointed out in previous posts on this diet study, they use a mathematical formula that uses body weight and BMI to modify the insulin response results so that simple weight loss will show their improvement without any actual change in insulin output being necessary.

The ND diet is a useful tool but should be viewed as being Boot Camp for the pancreas and liver or a detox cycle rather than a permanent solution. If you revert back to pre diet eating patterns your diabetes will in all probability return with a vengeance. It is a revolving doorway like other weight loss plans. The shakes used are basically the Slimfast diet of old and were supplied I believe by Cambridge Diet Plan for one arm of the study.
 
bulkbiker said:
Grains only for the past 10,000 ish years.. and fruits only when in season so...
Click to expand...
Indeed the story of Joseph (he of dreamcoat fame) and Potiphar emphasise the importance of good storage and the cyclic nature of grain production. I remember the night before Xmas, when Santa filled my stocking with exotic tropical fruit that only appeared at that time of year. And of Kilner Jars of bottled fruit on the kitchen shelf. Fruit does not keep for long outside the fridge.
1664290394251.jpeg
 
Re the retune - thanks for this thread and posting the updates on the ND.

The first time I did the Very Low Calorie Diet (real food) version of this, I had already become normal weighted, by going no-added sugar and moderate carbs (I still ate tropical fruit for example, at that stage of my diabetes journey), but I was very active.

The second time I did a low-carb/keto low calorie version (ie just tiny servings of what I normally ate to the 800 calorie stipulation). I saw it as a fat-stripping the liver and pancreas attempt - and yes a 'boot camp' for those organs just about explains it. The second time it was going back to just proper portions of LCHF/Keto food.

So I guess I am one of the 30% for whom NDs as normal weighted doesn't work.

I came to the conclusion that as a severely insulin resistant person (I produce plenty and all too easily too much insulin judging by my c-peptide results) that I have just too many sick fat cells that will take longer probably than the lifetime I have left to be replaced. After all - I had 35-ish years to get the sick fat cells and intermittently increasing insulin resistance- it is perhaps not surprising if it may take that many years for them to be replaced with healthy fat cells. (Probably too late for me to see that day.) If indeed the adipose tissue theory behind type two is correct and my understanding is that fat cells acting like an organ and produce hormones necessary for a well functioning blood glucose system is accepted science. Just throwing in my two cents worth...
 
AloeSvea said:
Every now and again I remind that this forum promotes itself as global (English speaking is implicit) - so that very amusing and interesting post about eating and food from the fifties needs the addition of "Food From the Fifties in the UK" :) .
Click to expand...
The 'funny' is obviously American, not UK. We don't have gasoline or cell phones , not in the 50s or now!
 
Back
Top