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Trying to understand the Newcastle diet

V

vit90

Well-Known Member
Messages
843
Location
UK
Type of diabetes
Type 2
Treatment type
Diet only
If you aren't already aware of it, research at Newcastle University in the last 3-4 years has shown early promise (albeit with a small dataset) in helping people with Type 2 diabetes through an aggressive weight loss programme. Subjects are put on a strict 800 or less calorie per day diet for up to 8 weeks in order to mimic the starvation conditions of patients who had undergone bariatric surgery and shown marked improvement in their diabetic condition. The aim of the diet is to deplete visceral fat which resides in and around key organs like the pancreas and liver that is normally difficult to shed in other diet and weight loss regimes. The hope is that once the liver and pancreas are free of this fat (which can be monitored through MRI scanning) diabetic indicators can be improved and even brought into normal ranges.

Now, that's all well and good but I have some questions about the above:The bods at Newcastle do say they have 'reversed' diabetes in a high percentage of their small sample of test subjects. But what do they really mean by 'reverse'? Are they cured? Are they simply being conditioned to lead a healthier lifestyle which means better control of the blood glucose? Is their insulin resistance/glucose tolerance improved?

As far as I can see the result of a successful regime of Newcastle dieting is improved insulin production by the pancreas. But what slightly troubles me is that the root cause of diabetes is the insulin resistance in the body which causes an abnormally high level of insulin to be secreted in the first place. Does the Newcastle research indicate any effect on insulin resistance?

To pre-empt my question I am speculating that by losing a lot of weight (and even better building some new muscle) one's capacity to absorb blood glucose through the action of insulin does improve, but I am only guessing.

Has anyone here studied this in more detail?

For the record, I think that even if the answers to the above don't add up to a 'cure' (whatever that is - which seems to be a BIG question in diabetes circles) I'm sure for many it will be beneficial and I am doing it and already feel better for it.
 
my guess is, it reduces insulin resistance and gets rid of liver and pancreas fat, leaving what's left of your beta cells to control your BG, it also may 'wake-up' some cells

Newcastle diet aims in 8+ weeks to mimic the rate of ~70% remission, for surgery T2
“It is now clear that Type 2 diabetes is caused by abnormal fat storage. Research on how this may be reversed is available.

http://www.ncl.ac.uk/magres/research/diabetes/

Newcastle diet Lectures

http://www.fend-lectures.org/index.php?menu=view&id=94

http://www.ncl.ac.uk/events/public-lectures/item.php?roy-taylor-diabetes
 
I'm not yet sure I have seen a comprehensive definition of Type 2 diabetes, which is part of the problem I think. Are you T2 if you have insulin resistance but your pancreas is still producing plenty of insulin? Or is Type 2 diabetes only defined as a result of reduced or failed insulin production? Both will result in the symptomatic high blood glucose levels. So maybe T2 is most sensibly defined as consistently high blood glucose and the underlying causes can be various?
 
jack412 said:
my guess is, it reduces insulin resistance and gets rid of liver and pancreas fat, leaving what's left of your beta cells to control your BG, it also may 'wake-up' some cells

Newcastle diet aims in 8+ weeks to mimic the rate of ~70% remission, for surgery T2
“It is now clear that Type 2 diabetes is caused by abnormal fat storage. Research on how this may be reversed is available.
Click to expand...

The fat factor is interesting. My interpretation of the reduction in visceral fat is that this de-clogs, for want of a better description, the pancreas and liver, improving their function to manage blood glucose levels. But the reduction in body fat in general could well be important. I am absolutely no expert but my understanding is that when we put on weight we don't necessarily grow lots of new fat cells but the ones we have get filled with more fat (which come mainly from the action of insulin on excess blood sugar). If we lose weight then these cellular fat stores are emptied to a degree. That makes me wonder if insulin-resistance reduces as the capacity to store more cellular fat increases through weight loss. I read that increased muscle mass improves insulin resistance, probably because the increase in muscle tissue provides more storage for glucose products as well.
 
@vit90 I am sure @douglas99 will be along shortly to assist. I would say he is well knowledged with regard to the Newcastle Diet, and may simplify matters relating to this diet.
 
jack412 said:
you need to watch the lectures for a better understanding, and then ask stuff
Click to expand...

I have watched the lectures, several times and read various articles and papers and that is why I am asking these questions. The lectures aren't really definitive in my view. Prof.Taylor says that the reduction in visceral fat in the liver and pancreas increases insulin production. He doesn't as far as I can see cover insulin resistance in his findings - if I have missed that then please do point me in the right direction.
 
vit90 said:
I have watched the lectures, several times and read various articles and papers and that is why I am asking these questions. The lectures aren't really definitive in my view. Prof.Taylor says that the reduction in visceral fat in the liver and pancreas increases insulin production. He doesn't as far as I can see cover insulin resistance in his findings - if I have missed that then please do point me in the right direction.
Click to expand...
he calls it insulin sensitivity..same thing, there is better function is his main point
it's more that what cells that are left can work without the extra weight and reduced insulin resistance/increased sensitivity, fatty liver/pancreas and get a normal GTT response.

the slides are available clicking second tab in from the left and left of the play button, it might help if you refer to a slide? for others to give their opinion
http://www.fend-lectures.org/index.php?menu=view&id=94
 
Prof.Taylor refers to insulin sensitivity specifically with regard to liver function. He only refers to insulin resistance briefly as a basic tendency that some people have. In all the reading I have done the definition of insulin resistance is to do with the reduced cooperation of body cells like fat cells to absorb the products of blood glucose produced by the action of insulin. Now, if that actually means or is dictated by liver function insulin sensitivity then great - I have a better understanding. But I can't honestly say that it reads like that. I'd like to believe it because that probably means I have a better chance of the best possible outcome I personally have in tackling Type 2 diabetes as I am doing the Newcastle diet.
 
as far as I can work out and I don't know more than anyone else..it's all google and video's...
his focus is on the gut/organ fat..he has excess carb/sugar=fat ..
excess insulin=insulin resistance, makes fat and stops existing fat being used.
along with leptin and a gut hormone,excess insulin keeps you hungry, so you eat and lay down more fat and increases insulin resistance..
800 cal diet and/or lchf short circuits this loop.
 
There is definitely a message in Prof.Taylor's presentations that the diet can break the vicious circle that leads to the fatty deposits in the pancreas and liver and so eventual pancreas exhaustion and so lead to a revival of insulin production. Of course if you are only on 600-800 calories a day your blood glucose levels are no longer likely to be high but that calorie limit can't be continued indefinitely. With revived pancreatic function after the diet and careful eating (low carb) I'm sure that the situation will be much improved prior to the regime. But while Taylor refers to 'reversal' and even 'cure' I'd like more clarification in what he really means by that. The glucose tolerance test is probably the definitive way of determining if someone is Type 2 diabetic or not. If he means someone who has successfully responded to the diet as intended will pass the GTT test then great - I'm up for that challenge. But the realist in me (although I am a born optimist!) thinks that the insulin resistance factor is much harder (impossible, maybe) to completely fix, even by the Newcastle diet.
 
catherinecherub said:
Hi @vit90.

Have you read the aims of the current research with the Newcastle diet?

This might help you understand it more and possibly answer some of your questions.

http://www.diabetes.org.uk/Research...t/Research-spotlight-low-calorie-liquid-diet/
Click to expand...

Yes I had read that but again:

"The aim is to find out if this intensive weight management plan is the best way to help people with Type 2 diabetes become non-diabetic and remain that way."

- the reference to 'remission' elsewhere on the page and 'non-diabetc' are not detailed. Getting your blood sugars down through the diet and enabling you to come off your medication thanks to the diet and continuing post-diet is great and I have no doubt that many, including myself, will hopefully enjoy such benefit. But will those with success pass the GTT test which, forgive me if I am wrong, addresses the fundamental issue of insulin resistance. Insulin resistance is surely the disease that needs to be cured so the pancreas and liver don't have to struggle?
 
vit90 said:
There is definitely a message in Prof.Taylor's presentations that the diet can break the vicious circle that leads to the fatty deposits in the pancreas and liver and so eventual pancreas exhaustion and so lead to a revival of insulin production. Of course if you are only on 600-800 calories a day your blood glucose levels are no longer likely to be high but that calorie limit can't be continued indefinitely. With revived pancreatic function after the diet and careful eating (low carb) I'm sure that the situation will be much improved prior to the regime. But while Taylor refers to 'reversal' and even 'cure' I'd like more clarification in what he really means by that. The glucose tolerance test is probably the definitive way of determining if someone is Type 2 diabetic or not. If he means someone who has successfully responded to the diet as intended will pass the GTT test then great - I'm up for that challenge. But the realist in me (although I am a born optimist!) thinks that the insulin resistance factor is much harder (impossible, maybe) to completely fix, even by the Newcastle diet.
Click to expand...
that's as I understand
except for the insulin resistance...technically it goes and you don't have it..get the insulin resistance and excess insulin back and the cycle starts again
 
vit90 said:
I'm not yet sure I have seen a comprehensive definition of Type 2 diabetes, which is part of the problem I think. Are you T2 if you have insulin resistance but your pancreas is still producing plenty of insulin? Or is Type 2 diabetes only defined as a result of reduced or failed insulin production? Both will result in the symptomatic high blood glucose levels. So maybe T2 is most sensibly defined as consistently high blood glucose and the underlying causes can be various?
Click to expand...

I don't think you will see a crips, definitive definition of T2 any time soon. In my view, it is actually a portfolio title for almost all forms of diabetes where almost any insulin producing pancreatic capability remains. That, in my view, is why MODY, LADA and sometimes T1.5 are diagnosed, secondary to a diagnosis of T1.

If you talk to the T2s on here, you will find an enormous range of insulin producing/ insulin resistance "capability", as well as other factors. For me, trimming up (using carb and calorie reduction as my method) helped be revert to non-diabetic HbA1cs for every single test after diagnosis. I consider myself extremely fortunate in my outcome, although I would want to blow my own trumpet to an extent as I did do the hard yards and have adopted strict controls.

Professor Taylor does state he believes that losing weight is pivotal to most T2 diabetic success, where insulin resistance is at play, and the method employed to losing that excess baggage is less important than the weight loss itself. The "beauty" of the Newcastle Diet is is fast results and the simple, if pretty brutal, protocols the original diet deploys.

If you're considering going for it, I commend you; but maybe not this side of Father Christmas's visit. I say that not because I think we should all be indulging outrageously, but more because the diet is strict and would probably be made harder with ann the festive fodder around.
 
AndBreathe said:
I don't think you will see a crips, definitive definition of T2 any time soon. In my view, it is actually a portfolio title for almost all forms of diabetes where almost any insulin producing pancreatic capability remains. That, in my view, is why MODY, LADA and sometimes T1.5 are diagnosed, secondary to a diagnosis of T1.

If you talk to the T2s on here, you will find an enormous range of insulin producing/ insulin resistance "capability", as well as other factors. For me, trimming up (using carb and calorie reduction as my method) helped be revert to non-diabetic HbA1cs for every single test after diagnosis. I consider myself extremely fortunate in my outcome, although I would want to blow my own trumpet to an extent as I did do the hard yards and have adopted strict controls.

Professor Taylor does state he believes that losing weight is pivotal to most T2 diabetic success, where insulin resistance is at play, and the method employed to losing that excess baggage is less important than the weight loss itself. The "beauty" of the Newcastle Diet is is fast results and the simple, if pretty brutal, protocols the original diet deploys.

If you're considering going for it, I commend you; but maybe not this side of Father Christmas's visit. I say that not because I think we should all be indulging outrageously, but more because the diet is strict and would probably be made harder with ann the festive fodder around.
Click to expand...

Above all I want to understand the condition as best I can and so I have been doing a lot of research. One of the most impressive points that I have read is that conventional treatment of T2 is highly questionable in that it only addresses symptoms rather than the root cause and that the use of medication and even insulin therapy in some is simply sustaining or worsening the underlying problem, which is insulin resistance. People who are not diabetic can cope with transient spikes in blood glucose caused by eating sweet and high carb foods because they have a healthy pancreas and no resistance to the insulin it produces. I can easily comprehend why the Newcastle diet can be beneficial to rejuvination of a tired pancreas but just need some clarification of how the diet tackles insulin resistance. Maybe I can't see the wood for the trees :) Perhaps, as I speculated earlier, it's actually the weight loss that is the key to reducing insulin resistance - I certainly hope so - it's just not that clear.

Over 3 weeks into my own dieting, I will throttle-back at Christmas (I still want to average no more than 2000 calories per day over the Christmas and New Year period) and probably return in the new year with a more gentle diet until I reach my target weight and BMI of under 22.
 
when the pancreas/gut fat goes, so does the insulin resistance and what's left of you pancreas beta cells control you BG as good as they can, hopefully a normal GTT
 
jack412 said:
when the pancreas/gut fat goes, so does the insulin resistance and what's left of you pancreas beta cells control you BG as good as they can, hopefully a normal GTT
Click to expand...

I think we will just have to agree to disagree on that. All the articles I have read say that insulin resistance is nothing to do with the pancreas itself but muscle and fat tissue all around the body no longer being cooperative with absorbing blood sugar despite every increasing quantities of insulin.
 
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