Type 2 and insulin resistance - what I don't understand is...

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This academic article by Prof Taylor, from 2021, gives a good overview of his work, including the idea of the 'personal fat threshold': https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8247294/ .

From this and other academic articles, I gather the idea is as follows:

Subcutaneous fat does not cause Type 2; but each of us only has so much subcutaneous fat capacity. Picture it as a bucket; some people have a huge bucket, others only have a small bucket. People get T2 when their own personal bucket spills over! Because, once your body starts storing a lot of fat in and around your liver and pancreas, rather than subcutaneously-- that's when you get T2.

Take two people, Ann and Bill. They both start off with a BMI of 22. Then both of them start eating too much and being very sedentary, so they both start gaining weight in the form of fat.

Ann has a HUGE amount of subcutaneous fat capacity. She becomes vastly, morbidly obese, and still doesn't get Type 2-- because her body continues to store more and more fat subcutaneously and doesn't store it as 'ectopic' or 'visceral' fat, fat in and around the liver and pancreas. She will have a lot of other health problems, but not T2.

Bill, however, has very little subcutaneous fat capacity. So his body very quickly starts storing fat in and around his liver and pancreas-- his small bucket overflows into the bad places very quickly. So, by the time Bill's BMI is 23, he has T2.

This would explain why many obese people don't develop T2, whereas some people with BMIs of 23-25-- which is not even classed as overweight, let alone obese, in official terms-- do develop T2. (Note however that it seems to be very rare for people with a BMI under 22 to get T2.)

Very low calorie diets work because, with severe calorie restriction, your body 'eats' ectopic or visceral fat first, before it starts 'eating' subcutaneous fat. So people who are obese and have T2 may remain obese yet still reverse their T2, because they've lost their ectopic fat.
My BMI was 25.1 when my report said my fasting glucose was 130 and I had the 51.96% chance of getting diabetes. I am now at 23.6%. I hope to be at 22 BMI or lower with an 86 cm waist for a 173 cm male. I hope that is enough to fully lower my fasting glucose numbers and trigs.
 
My BMI was 25.1 when my report said my fasting glucose was 130 and I had the 51.96% chance of getting diabetes. I am now at 23.6%. I hope to be at 22 BMI or lower with an 86 cm waist for a 173 cm male. I hope that is enough to fully lower my fasting glucose numbers and trigs.
My BMI was around 25.5 when I finally went to a doc for the first time in decades & was diagnosed with out-of-control T2D which would have been festering for at least a couple of years. HbA1c was 10.3%, fasting glucose around 15 mmol/l.

(I have the classic risky body type - all excess weight goes to the middle, everywhere else scrawny.)

I got rid of the T2D by getting my BMI down to about 22 over a few months, just by cutting out crap & eating fewer calories (not fussing very much about carbs when I worked out that a lot of the low-carb messaging you see on the Internet is way over-done & that fruit isn't poison etc etc). HbA1c down to around 5.3%, fasting glucose around 4.8 mmol/l.

(Then I kept losing weight because I decided I like being skinny, so BMI has been 20 and waist around 75cm for the last 4 years or so.)

Anyway, it worked for me. Good luck!
 
That's Prof Taylors theory.

It's still not proven.

We see that over time his method starts to fail and fewer people can remain in a pre-diabetic state (which is what his "remission " is).
The key question is whether it is reasonably safe to say that if one follows the Taylor prescription of eliminating excess fat from liver and pancras and maintaining that, then will there continue to be an active disease process that will eventually take us down the insulin road? The evidence does not support that. In DiRECT’s second year the cohort was no longer on the very low cal diet, they were just eating normally but more moderately and under the injunction to maintain weight. Some of them had lost their remission status by the year’s end. These people had not maintained their weight loss. This was not a failure of Taylor’s method or of his analysis. Some of the people just regained some weight. It is true that from a long term statistical viewpoint diabetes remission is a virtually complete failure in the general population. A year after diagnosis about 1 in 22 will be in remission, but five years on it will have dropped to fewer than 1 in 14000. This is why most HCPs know so little about it and attach so little credence to it. Almost all in remission will lose the plot for one reason or another. If you are a T2 then are you “doomed”? Not if you happen to be that 1 in the 14000. See to it.
 
If you are a T2 then are you “doomed”? Not if you happen to be that 1 in the 14000. See to it.
I am indeed one of the "lucky" ones.. and have been for the past 7 years.

I'm just not convinced by Taylor's theory. I was in remission before most of my weight loss so I don't believe it's about weight per se. I know others who haven't lost much weight at all but are still in remission using low carb eating.

We all know that "crash diets" are rarely successful.. the dieting world shows us that fairly neatly and at it's core Newcastle Dieting is exactly that.
 
I don't consider the Newcastle diet to be a crash diet, it's a medically supervised very low calorie diet (VLCD), followed by support. This analysis from 2012 says in the abstract: "Conclusions: VLCD with active follow-up treatment seems to be one of the better treatment modalities related to long-term weight-maintenance success."

If you look at the VLCD offered as a trial by NHS England for T2 diabetics, it offers "... low calorie, total diet replacement products – for example, soups and shakes which add up to around 900 calories per day – for up to 12 weeks. During this time participants will replace all normal meals with these products.

Alongside this, participants will receive support and monitoring for 12 months including help to re-introduce real food after the initial 12-week period. Depending on where the service is being delivered, this support and monitoring will either be:
  • group based
  • one-to-one, or
  • digitally/remotely via an app, online or over the phone.
This support will provide participants with the help and advice they need throughout every stage of the programme."

It's only being run as a trial in some health trusts, and I presume that some analysis will be done by NHS England to see how effective it was for participants. It will be interesting to find out if it's cost effective and long lasting, or just a faddy crash diet as you suggest bulkbiker. I hope for the participants' sakes, that you're wrong, but time will tell.
 
I don't consider the Newcastle diet to be a crash diet, it's a medically supervised very low calorie diet
Ancel Keys "Minnesota starvation experiment" fed it's test subjects just under 1600 cals per day yet you don't consider half of that to be a "crash diet".

900 cals per day is a crash diet just like "Herballife" and all the other crash diets that have failed so many people over the years. I did them multiple times with the same result.

The NHS VLCD is simply Newcastle on a larger scale subsidised by the taxes we all pay and making a few bob for some of the DiRECT trial authors who are shareholders in Counterweight (one of the recommended meal replacements).
 
Ancel Keys "Minnesota starvation experiment" fed it's test subjects just under 1600 cals per day yet you don't consider half of that to be a "crash diet".

900 cals per day is a crash diet just like "Herballife" and all the other crash diets that have failed so many people over the years. I did them multiple times with the same result.

The NHS VLCD is simply Newcastle on a larger scale subsidised by the taxes we all pay and making a few bob for some of the DiRECT trial authors who are shareholders in Counterweight (one of the recommended meal replacements).
I'm not sure why you're arguing that the authors of counterweight are there to be making money from it. The Counterweight paper states:
"Funding sources None.
Competing interests None declared."

The people offering the counterweight products are Sloman and Slabbart and they are not listed in the authors for either the counterweight or the DiRECT trial.

So I'm not sure where you're getting your "making a few bob from".

Prof Mike Lean (lead author, Direct trial) offers a free alternative, nutritionally balanced diet, based on "porridge, soup and bread*", and Prof Taylor has donated the proceeds from his books to DUK, so as capitalism goes, they're not doing a very good job in making money from their research, and they're not selling meal replacements either.

*perhaps Lean is secretly sponsored by "big lentil" as the diet offers lentil soup as one of its components?
 

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I'm not sure why you're arguing that the authors of counterweight are there to be making money from it. The Counterweight paper states:
"Funding sources None.
Competing interests None declared."

The people offering the counterweight products are Sloman and Slabbart and they are not listed in the authors for either the counterweight or the DiRECT trial.

So I'm not sure where you're getting your "making a few bob from".

Prof Mike Lean (lead author, Direct trial) offers a free alternative, nutritionally balanced diet, based on "porridge, soup and bread*", and Prof Taylor has donated the proceeds from his books to DUK, so as capitalism goes, they're not doing a very good job in making money from their research, and they're not selling meal replacements either.

*perhaps Lean is secretly sponsored by "big lentil" as the diet offers lentil soup as one of its components?
I was talking about this "Counterweight" https://www.counterweight.org/pages/nhs
with these shareholders from Companies house.
 

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I am indeed one of the "lucky" ones.. and have been for the past 7 years.

I'm just not convinced by Taylor's theory. I was in remission before most of my weight loss so I don't believe it's about weight per se. I know others who haven't lost much weight at all but are still in remission using low carb eating.

We all know that "crash diets" are rarely successful.. the dieting world shows us that fairly neatly and at it's core Newcastle Dieting is exactly that.
Taylor did find that the remission success rate was higher for those who lost the most weight, within a cohort all on the same diet. I don’t think there is much significance in observing that “remission” in the trivial sense of reducing A1c by low-carbing can precede weight loss, that just reflects that if less glucose-producing food goes down the gullet then there will likely be less glucose swilling around in the bloodstream. Non-diabetics would observe that too. I believe the more important thing is to clear visceral fat even after one’s A1c has fallen, in order to recover normal metabolism and become truly non-diabetic again. That is Taylor’s real aim. Now there is a valid question as to whether clearing visceral fat does require significant weight loss or can be accomplished by low-carbing in itself, and I think that is not so clear, and is at the heart of so much confusion in these discussions. By the way, you have said that you passed an oral glucose test with flying colours so I am interested that you adhere to a very low carb diet. Is that a gastronomic preference? I presume you could in principle now eat a high carb diet with no effect on your A1c? In any event you have done well.
 
So many interesting theories but why does none of them apply to my condition? I was diagnosed with a HbA1c of 86 in 2014 when my weight was around 66kg and since then my weight has remained constant with only the slightest variation of 1 kg at most, with BMIs between 23 and 25 and yet my HbA1c has now normalised. In fact all my HbA1c readings since 2017 has been 42 or lower. My personal data does not seem to suggest that any abdominal fats caused or contributed to my type 2.
 
So many interesting theories but why does none of them apply to my condition? I was diagnosed with a HbA1c of 86 in 2014 when my weight was around 66kg and since then my weight has remained constant with only the slightest variation of 1 kg at most, with BMIs between 23 and 25 and yet my HbA1c has now normalised. In fact all my HbA1c readings since 2017 has been 42 or lower. My personal data does not seem to suggest that any abdominal fats caused or contributed to my type 2.
So is it the case that you reduced the A1c by low-carbing? If so, given there has been such little weight variation, your species of T2 may have arisen from some pancreatic or other endocrine insufficiency not owed to visceral fat.
 
I presume you could in principle now eat a high carb diet with no effect on your A1c?
So far as I am aware a high carb diet was a major contributing factor to my becoming morbidly obese and developing T2 (along with many other health problems). Why oh why would I ever want to return to that state?
 
So far as I am aware a high carb diet was a major contributing factor to my becoming morbidly obese and developing T2 (along with many other health problems). Why oh why would I ever want to return to that state?
It is interesting that you say high carbs contributed to you becoming morbidly obese.
My parents who have never restricted their carbs (or calories), do not have diabetes and are not overweight after more than 80 years of their "traditional" diet.
Earlier, @Spathiphyllum addressed the point about why some people get type 2 diabetes and others don't but I am intrigued by why the same diet could cause some to become overweight whilst others appear to be immune.
 
So far as I am aware a high carb diet was a major contributing factor to my becoming morbidly obese and developing T2 (along with many other health problems). Why oh why would I ever want to return to that state?
If high carbs was indeed the cause in your case then of course you wouldn’t want to repeat that. We all have our own views on how we got here. In my case it was nothing more than going very slightly overweight and being too sedentary, not carb related. My wife has eaten prodigious amounts of carbs for half a century, is in excellent health and has A1c of 32. So, no uniform answers in any of this.
 
My parents who have never restricted their carbs
But what do they usually eat? What's their carb intake?
My downfall came when we moved to France for a few years.
Fresh baguettes and croissants added about 4 stone to my already overweight body.
I had, and probably still would have, a problem with stopping eating bread. I considered it an addiction.
 
Adding my tuppance worth - anything under 1000cals daily surely has to be a crash diet. Reducing that more, and liquidising all the food, for weeks and weeks on end seems uber-crash to me! Utterly ghastly!

What I do think is interesting is how people have different attachments to different types of food, and different amounts. I have a sweet tooth - but only, really, when it's mixed with fat (er, clotted cream usually!). Dry sponge cake (unless it's fresh out of the oven) does not appeal - it's not the sugar + starch that does it for me. But cover it with buttercream or sweetened whip cream, and I'll scoff the lot! (I'll eat the raw sponge mixture far more greedily - but then it's still creamy at that stage.)

Salty oily carbs (aka crisps) I'm pretty immune to, ditto deep fried chips. I quite like them, but I don't crave them. I'd rather rather had a salad main and a creamy sweet pud.

My SIL is the opposite. No sweet tooth at all, but she is not safe near crisps or chips, and cheese is her pudding.

I prefer animal fat (dairy or dripping!) to vegetable (oil)

I once had a very strange work colleague who, when on the traditional 'It's my birthday so I've brought in some cream cakes to share' remarked 'Somehow I can never force myself to eat a cream cake'. I suspected she came from the Planet Tharg (and then I ate her cream cake for her - I'm generous that way!)

I also have a friend who likes dry sweet sponge, so when we are out and share a cake, she eats the boring inside, and I eat all the bits with the creamy icing on it. (Royal icing? Bah, rubbish stuff!)

So, what accounts for all these different tastes? (And how they might map to risk of diabetes!!!!)

(My non-sweet tooth SIL used my new BG monitor, and she is fine for levels - but then that's because she scoffs down cheese, not cheesecake....)
 
I was talking about this "Counterweight" https://www.counterweight.org/pages/nhs
with these shareholders from Companies house.
Companies names you've screen shotted are: Slabbert, Gordon, Ross, Bell-higgs, Broshahan, Mongia, Dow, Donald

and the authors for Counterweight are:
Gibbs, Broom, Brown, Laws, Reckless, Noble, Kumar, McCombie, Lean, Lyons, Frost, Barth, Haynes, Finer, Hole

None of the authors from the Counterweight trial are listed as shareholders, so that suggests that they are making no money whatsoever from Counterweight.org, and the only commonality is that the company shares the same name as the trial. To suggest otherwise has no basis in fact.
 
True enough. Time will tell. I don't really know what you mean with "his method starts to fail"? Can you clarify please as it's been a long day at work and I'm not getting what you're saying there.

Do you mean people put weight on over time, which pushes them from not actively diabetic (in remission) into pre-diabetes and actual diabetes? He addressed weight gain in his original paper, and in another clinical trial, which said:
"The DiRECT programme sustained remissions at 24 months for more than a third of people with type 2 diabetes. Sustained remission was linked to the extent of sustained weight loss. "

I'm not aware of a longer term study regarding weight loss and diabetes remission, but I haven't looked tbh. If you've read one and can send me the link, I'd be interested to read it.

You seem to be mixing together "pre-diabetic", which is defined as having an HbA1c of between 42 and 47 and "remission":
"An HbA1c < 48 mmol/mol (<6.5%) and/or fasting plasma glucose (FPG) 5.6–6.9 mmol/l (100–125 mg/dl) were used to define a partial remission, while ‘normal’ levels of HbA1c and FPG (<5.6 mmol/l [100 mg/dl]) were required for a complete remission." They're not exactly the same.

The reason I ask is because if you think T2s are doomed to failure, is there any point in losing weight? Should I put the 40Kg I lost back on, and get my HbA1c back to the 83mmol/mol it was when I was diagnosed, or should I try and maintain the 34mmol/mol I had a couple of weeks ago when I got my blood test results?
I know which I'd prefer to do, I travel hopefully, and hope that T2 stays away for the foreseeable future.
At the 1 year mark 47% (53%failure) of Taylors Intervention group were in remission on his definition. At 2 years 36% were in his definition of 'remission' (64%failures ). So it seems the benefits of the short sharp shock were washing out as the basics of the condition, chiefly insulin resistance, reasserted themselves. Taylor was saved by the pandemic ( or he hid behind it) and no reports on the 3 or 4 year stage were made. One suspects most of his guinea pigs were back on meds.
On the two year mark Taylor indulged in some statistical jiggery pokery ( a typical component of Bad Science) and declared 75% of the intervention group who had 'remission' at one year were stiil in remission ( that's the 47 % dropping to 36%). So Hey Presto, a 64% failure rate at 2 years is magically transformed into a 75% success rate !
 
But what do they usually eat? What's their carb intake?
My downfall came when we moved to France for a few years.
Fresh baguettes and croissants added about 4 stone to my already overweight body.
I had, and probably still would have, a problem with stopping eating bread. I considered it an addiction.
They eat cereal for breakfast, sandwiches for lunch, pasta, rice or potatoes with meat and veg for tea with cake, biscuits and fruit in between. They drink juice every day. A traditional diet.
As they have no medical reason to do, they do not count their carbs (or calories).
 
Companies names you've screen shotted are: Slabbert, Gordon, Ross, Bell-higgs, Broshahan, Mongia, Dow, Donald

and the authors for Counterweight are:
Gibbs, Broom, Brown, Laws, Reckless, Noble, Kumar, McCombie, Lean, Lyons, Frost, Barth, Haynes, Finer, Hole

None of the authors from the Counterweight trial are listed as shareholders, so that suggests that they are making no money whatsoever from Counterweight.org, and the only commonality is that the company shares the same name as the trial. To suggest otherwise has no basis in fact.
Names number 4 and 16? I also stated quite clearly DiRECT study authors.
 

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