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

Definition of what is type 2

Tannith said:
β-Cell function decline: the major cause of disease progression
A hallmark of type 2 diabetes is a decline in β-cell function, which begins as early as 12 years before diagnosis and continues throughout the disease process. https://care.diabetesjournals.org/content/32/suppl_2/S151
Click to expand...
But surely, if this is correct and, as stated it continues throughout the disease process, then how can the medical profession sign someone off the register when in non-diabetic numbers? Surely something isn't right there?
 
JohnEGreen said:
And that definition would include T1 and T2 but would not include me as I have drug induced diabetes I don't think it's possible to define diabetes as a single entity..
Click to expand...
I tend to agree with you. Bilous does mention things such as drug-induced diabetes (in the table I didn't type out) but these exemptions don't appear to require a change to the sweeping nature of his definition.

Maybe this definitional difficulty is why the popular/media view of diabetes has such a hold - they have the advantage of a simplistic definition. For T2 it would be something like "if you're fat you get diabetes" . It's then much harder to suggest that it's a lot more complicated than that.
 
I think the problem stems from the fact that diabetes is really a symptom rather than a disease. Hyperglycaemia, or the excess urination that the term diabetes comes from is a result of various conditions that we don't have separate names for.
 
It will be difficult to define as most GPs make assumptions and the newly diagnosed type 2s leave the surgery with a prescription for Metformin and a statin with no further investigation, so many of the misdiagnosed end up in hospital, and a few die, but those that can, just go on as best they can manage.
If it isn't studied, how can it be understood?
 
As we see from those who post on the forum, there are many different types of type 2 diabetes under the same umbrella.

I can't find the research just now, but 5 sub types have been identified so far. As @Mr_Pot says, it's a symptom of various conditions with various causes and treatments. This is why no one treatment works for all of us
 
Tannith said:
Recovery of first-phase insulin response (0.04[−0.05–0.32] to 0.11[0.0005–0.51] nmol/min/m2, p < 0.0001) defined those who returned to non-diabetic glucose control and this was durable at 12 months (0.11[0.005–0.81]
https://www.sciencedirect.com/science/article/pii/S1550413118304467
Click to expand...
As I pointed out in the other thread you were posting in, the method used by Prof Taylor to show insulin responses includes BSA and hence body weight. So the insulin response will appear to improve simply because it was a weight loss diet and is a mathematical consequence of the weight term diminishing. Those figures are misleading and the claim cannot be held up as viable evidence.
 
@Tannith yet again I’d ask how does the theory (it’s not proven) you advocate stand up in light of insulin t3sts that show a large proportion of type 2 overproduce insulin if their beta cells are defunct?
 
Not specifically a % to hand but it is half of the mainstream definition so that alone suggests you need to be able to fit it into your theory.

This site says “
Type 2 diabetes mellitus is a metabolic disorder that results in hyperglycemia (high blood glucose levels) due to the body:
  • Being ineffective at using the insulin it has produced; also known as insulin resistance and/or
  • Being unable to produce enough insulin”
And

“Insulin resistance is the name given to when cells of the body don’t respond properly to the hormone insulin.
Insulin resistance is the driving factor that leads to type 2 diabetes, gestational diabetes and prediabetes.”

The “other” site says “But because this insulin can’t work properly, your blood sugar levels keep rising. This means more insulin is released. ”
 
This seems like a good place to post this - a long interview with Prof. Roy Taylor covering his 'Twin Cycle Hypothesis' as the root cause of Type 2, his (I think it's his?) 'Personal Fat Threshold' theory, the role of genetics, and lots of other interesting stuff.

I'm not sure I agree with everything he says here, and the low-carbers won't agree with his attitude on that front, but he certainly makes some compelling arguments.
 
HairySmurf said:
This seems like a good place to post this - a long interview with Prof. Roy Taylor covering his 'Twin Cycle Hypothesis' as the root cause of Type 2, his (I think it's his?) 'Personal Fat Threshold' theory, the role of genetics, and lots of other interesting stuff.

I'm not sure I agree with everything he says here, and the low-carbers won't agree with his attitude on that front, but he certainly makes some compelling arguments.
Click to expand...
Oddly as a low carber I’m not totally adverse to the idea of a personal fat threshold - for some T2 it seems valid. However….

I lost the weight required by his theory, and more, immediately on diagnosis. I reached the normal bmi range by a significant margin. I did it by keto but Prof Taylor is on record as having said the method doesn’t matter just the weight loss. I got into non diabetic and just about into normal hba1c range well before I had even reached the weight loss goal. Now by his theory I could eat more carbs so long as I maintained the weight loss. Not in my case. Any time I increase carbs beyond an isolated incident the blood glucose shows it then so does the weight.

When only something like 7% remain in remission after 5years despite significant support I‘m not sure this is the golden goose answer it’s sometimes portrayed as. Does it help some people and for some time? Hell yeah. Is it the be all and end all for everyone? Most definitely not.
 
Last edited:
I sat and listened to Prof Taylor. I was taken in by his very personable delivery. I kind of get where he is coming from, but I'm very much a lay person trying to get a handle on my sugars. I don't know if I have this wrong, but I can't remember hearing about many Type 2's growing up in the UK. I was born in 1961. I don't come from wealth so we had basic meals. A meat and two veg 5 days a week, a Vesta curry on Fridays and a roast on Sunday. Most days we had a pudding with custard. Nothing fancy. Historically there was no diabetes in my family (excluding my brother who has LADA). My mom had RA. She later became obese as she was in a wheel chair and the RA had crippled her, even then she wasn't diabetic. I don't seem to get my sugars down. I lost his golden 15 kilos. My trigs are very good. I'm on a very low blood pressure medication but I often think I should come off them as my blood pressure can go low but then every now and then it rises so I figure just stick with them. My C-peptides are low/normal. According to him my only risk relating to his Twin Cycle Hypothesis is my age and the fact I put on a few pounds over and above what I was when I was 21 years old. I do so much exercise I cannot imagine there is any sugars left and I have been low carbing since last May and I am in ketosis, but heck I am still pre-diabetic despite it all. And just to add I was diagnosed pre-diabetic in late 2019 so not that long ago. My blood sugars starting really going up at the end of 2022, which was the imputus for me to see what low carbing would do, but my sugars seem entrenched. I listened to his theory about skinny people with fatty livers and fatty pancreas' but I would think that 35lb weight loss should have taken care of the fats surrounding my organs. All those words to say I'm uncertain. (Edited as I forgot to mention my bro)
 
Last edited:
Melgar said:
My C-peptides are low/normal.
Click to expand...
I thought T2s had high insulin amounts (unless very long term)?
Melgar said:
excluding my brother who has LADA
Click to expand...
Have you been checked for this ? Low cpeptide and sibling with LADA sound like red flags to me. (Disclaimer, am not a doctor).
 
A lot of the Taylor work is aimed squarely at establishing an approved "remission/reverse" level and method for T2 diabetes, so that, in the UK, this can be incentivised for GPs via a QOF payment linked to HbA1c reduction. If the Newcastle method were to be adopted as the NHS' method of choice (which would probably lead to other health economies picking it up) it would be extremely profitable for the owners of the Newcastle method (or any other in a similar position). This is linked to the decision a couple of years ago to define "remission" as two sub-48 HbA1c readings three months apart without glucose lowering medication. Note no mention of absence of diabetic symptoms despite that being a given for "remission" for other conditions.

The Newcastle method also conveniently does not challenge the present orthodox view on carb consumption and on weight loss, so there is no difficult discussion to be had about why, to lose weight, you were told to avoid carbohydrates (pre-1985ish) then (post-85) base all meals around carbohydrates to avoid a CVD increase that never happened thanks to the decline in smoking. I wouldn't want to be the one to explain that actually there'd been a rethink and you should cut down on those carbs again, sorry for the obesity and T2 crisis, but hey.

So you would (as a government healthcare system) be able to say that you were now rewarding doctors for using a calorie-control method that achieved remission for T2 diabetes by reducing HbA1c without drugs. That would be very attractive for government. It looks like something significant is being achieved for little cost, and no political embarrassment.

The problem is that the Newcastle method might have some short-term success but does not appear to be (on their own evidence) sustainable. They did their best to hide the 93% failure rate longterm. I'm not going to rehash the arguments in other threads on this forum where their claims of success were dismantled.

I wouldn't mind if there was a slightly more open approach to talking about what they're doing - a short-term weight-loss starter via a low-calorie approach that may also show some BG reduction. Given that an 800 calorie diet is almost certainly a low carb diet (max 160g/day assuming zero proteins or fats) even if unacknowledged, it is certainly arguable that what success is achieved is down to the low carb, rather than the low calorie. Low calorie diets for me tend to reduce metabolism and induce hunger - which has not been my experience on low carb (over four years now). And incidentally, for me and many others, BG reduction greatly precedes weight loss, not follows it, as the Newcastle approach has to claim.

I know which works for me. I also know why it's very difficult for a large health economy to change direction quickly.
 
EllieM said:
I thought T2s had high insulin amounts (unless very long term)?

Have you been checked for this ? Low cpeptide and sibling with LADA sound like red flags to me. (Disclaimer, am not a doctor).
Click to expand...
I know and I hear you. I'm already living with one autoimmune condition. It seems that while I'm controlling my blood sugars through diet and exercise my T2 diagnosis will remain. My Dr is all over the very low carb diet and exercise gig and is encouraging me to stick with it. So I guess while I am controlling my blood sugar it will be a wait and see game.
 
Back
Top