Diabetes: Have We Got It All Wrong? (T2D)

kokhongw

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R = Insulin Resistance = insensitivity to insulin.
Low insulin production = pancreas not making enough insulin.

But for decades, in almost all literature by mainstream healthcare providers, insulin resistance is described as ineffective insulin and not producing enough insulin...so the casual reader and surprisingly most healthcare providers come away with the mistaken belief that when diagnosed with T2D, we no longer produce enough insulin.

The reality as this article pointed out, is starkly different. T2D upon diagnosis, especially if we are overweight or have central obesity, are producing too much insulin 2-3x normal amount, yet not enough to overcome our glucose/carbs intake...so the chronically excessive insulin keeps us from accessing our stored fuel...

It would usually take another decade or so of relentless carbing before the pancreas becomes completely exhausted and yes, by then, we no longer produce enough insulin...
 

Tophat1900

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But for decades, in almost all literature by mainstream healthcare providers, insulin resistance is described as ineffective insulin and not producing enough insulin...so the casual reader and surprisingly most healthcare providers come away with the mistaken belief that when diagnosed with T2D, we no longer produce enough insulin.

Which highlights the lack of understanding due to a lack of insulin level testing. If you don't test it, you don't know how much is being produced and assumptions then somehow become medical knowledge, even if there is no evidence support them.
 
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kokhongw

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So now... they have reworded it ever so slightly... but would anyone come away with the understanding that we are producing too much insulin to overcome our insulin resistance and hence struggle with weight/fat loss?

https://www.diabetes.org/diabetes/type-2
upload_2019-10-4_10-58-59.png
 

Tophat1900

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We will never ever ever ever see any major healthcare organisation admitting that we've been mistreating type 2 diabetes for decades. The ramifications are massive and far reaching. The best we can hope for is tiny and incremental changes to the wording over just as many decades in the hope that no one will notice the advice is changing. Meanwhile people will continue to die unnecessarily.
 
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Flora123

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Many GPs, if you believe the posts on these forums over the years, do prescribe insulin for T2s. I have often thought that where the patient has a high BMI and therefore probably insulin resistance that treatment with insulin may not be the best approach? It may be adding insulin to an already insulin-overloaded system. That's why I believe the c-peptide test is under-used. So I wonder whether some GPs understand T2's connection with insulin resistance and hence high insulin levels? Note that some slim T2s are not T2 but mis-diagnosed LADA (like myself) and hence insulin will be needed.

When I was first diagnosed, I asked about my prognosis and treatment (whilst in shock) and was told I’d be on pills and then more pills when necessary and eventually insulin in time. I’m T2. Pleased to say I’d dropped to non diabetic levels in 3 months with LCHF/Keto and my doctor is totally confused! :)
 
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When I was first diagnosed, I asked about my prognosis and treatment (whilst in shock) and was told I’d be on pills and then more pills when necessary and eventually insulin in time. I’m T2. Pleased to say I’d dropped to non diabetic levels in 3 months with LCHF/Keto and my doctor is totally confused! :)

Same here. I was told I would get worse and worse until eventually I would "die of a complication." Her words.

I then did the exact polar opposite of everything I was told. In the process not only completely reversing hyperglycaemia, but also hyperinsulinemia and restoring very high insulin sensitivity and a low inflammation score - the latter three through self-funded tests that they don't even understand let alone do.

They continue to this day to have the audacity to attempt to give me dietary advice. Jokers.
 

ianf0ster

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Same here. I was told I would get worse and worse until eventually I would "die of a complication." Her words.

I then did the exact polar opposite of everything I was told. In the process not only completely reversing hyperglycaemia, but also hyperinsulinemia and restoring very high insulin sensitivity and a low inflammation score - the latter three through self-funded tests that they don't even understand let alone do.

They continue to this day to have the audacity to attempt to give me dietary advice. Jokers.

Things had improved by the time I was diagnosed (or else a less stone-age GP). I was told :

That I would almost certainly need medication if not now then later.

That they would give me a chance to follow the diet - which was somewhat conflicting - Eatwell yet somehow with fewer carbs. (Note that 1 month before T2D diagnosis the nurse at my Heart & Stroke annual check-up had said my weight was good!) So if I had taken their recommended diet for Diabetic control to heart I would be eating something like 50% protein and 40% of (high GI) carbs and only 10% Polyunsaturated fat. Since they didn't actually say I couldn't eat more protein to make up for virtually no fat and fewer carbs.

That I shouldn't worry, there was almost zero chance that I would die in a diabetic coma!
 

Gmt2

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Same here. I was told I would get worse and worse until eventually I would "die of a complication." Her words.

I then did the exact polar opposite of everything I was told. In the process not only completely reversing hyperglycaemia, but also hyperinsulinemia and restoring very high insulin sensitivity and a low inflammation score - the latter three through self-funded tests that they don't even understand let alone do.

They continue to this day to have the audacity to attempt to give me dietary advice. Jokers.
Same here. I was told I would get worse and worse until eventually I would "die of a complication." Her words.

I then did the exact polar opposite of everything I was told. In the process not only completely reversing hyperglycaemia, but also hyperinsulinemia and restoring very high insulin sensitivity and a low inflammation score - the latter three through self-funded tests that they don't even understand let alone do.

They continue to this day to have the audacity to attempt to give me dietary advice. Jokers.
How did you give up food you like? I am still gaining weight and being diabetic gave me no willpower.
 

Indy51

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How did you stop eating? I have gained weight since diabetic.

You don't need to post everywhere on the forum to get answers - it comes across like spam. It's also "off peak" hours in the UK where the majority of posters live, so you are unlikely to get immediate replies, especially to multiple posts like this.

That said, welcome to the forum.

It's a very basic concept - of all foods, carbohydrates are the ones that raise blood glucose the most. If we want to control our BG, we need to find the level of carbs that work for us. If you are gaining weight and not controlling BG, then by definition you are eating too many carbs. If you don't already have a BG monitor, that would be a very worthwhile purchase to make.
 
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millenium

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I learn these in school. In T2 earlier phase, body is insulin resistance and hence it overcompensate to produce more insulin. In later phase, it burns out and insulin production reduces to very low. These do not seem to contradict with the paper presented. So what did we got it wrong in the first place?
 
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How did you give up food you like? I am still gaining weight and being diabetic gave me no willpower.

Put simply, I didn't want to die young :nailbiting:

I no longer miss the foods that were killing me and wouldn't ever go back to eating them even if someone could guarantee that my diabetes would never return. Carbohydrate doesn't really taste nice anyway. We just think it does because we're all addicted to it and cover it in junk to make it semi-palatable. Carbohydrates are now alien to me and I have no attraction to them whatsoever. Even vegetables no longer look like food, but that is because I've become conditioned to the carnivore diet.

The above views are mine only. Others are free to express their own and eat whatever they wish :D
 

alienskin

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You are of course correct, but if I may build a little on that - I actually prefer to differentiate between insulin resistance and insulin sensitivity. Everyone has varying levels of sensitivity throughout the day and from day-to-day. It changes constantly based on many variables
...
Sensitivity and resistance may appear semantic, but actually I think conflating the two is erroneous. At least this is the way I like to frame things. Others may have a different point of view.

I think this is a pretty good way of looking at it. Insulin Resistance being the pathological condition causing cells (not just in the liver of course) to resist the insulin signal to correctly deal with glucose in our blood stream.

In my case, I do a lot of exercise (riding 100km/60miles up and down Asian mountains every week) and this seems to have a positive effect on my insulin sensitivity to the extent it seems to overcome my IR. I am merely careful about my carb intake (medium carb diet?) avoiding the obvious things like rice and white bread, and have an A1c of 5.3% (34). However, I know my first-phase response is not great, suggesting some beta-cell issues.

But for decades, in almost all literature by mainstream healthcare providers, insulin resistance is described as ineffective insulin and not producing enough insulin
To be honest, I have never seen IR described that way. The literature however probably doesn't accurately describe gradual beta-cell failure and thus lowered insulin production which is a medium or long term consequence of IR if the patient doesn't try to alleviate the situation through lifestyle changes.
 
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AloeSvea

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Another way of looking at insulin resistance is that as it is a default action - ie that when we are imbibing food and drink, toxins etc, that causes a too high insulin production, over time, IR is actually our body's first line of defence. (Along with storing excess energy in body fat in the belly first then all over.)

If only lowered insulin production was the worst medium or long term consequence of IR! In fact, kidney breakdown seems to be the bigger problem. You can see this disease progression very well in the doco series from Aotearoa/NZ 'The disease that is killing my family' (available on youtube/online). (I know - horrible title, but, a son of a man who dies in the course of the doco from diabetic kidney failure is the doco-maker, so....)

Kidney breakdown (where dialysis is called for) is big-time in Polynesia generally, which is shown in one of the docos in particular in the series. (And the limbs rotting 'thing', with amputations.)

Severe insulin resistance diabetes has a different disease make-up and progression - ie the kidney breakdown (according to the Swedish endos/researchers at Lund Uni where I get this info from) to what the same Swedes call mild obesity and mild age related diabetes (the latter two accounts for 66% of all diabetes including auto-immune diabetes). They make the very reasonable point that these different kinds of diabetes need different treatments.

Severe insulin resistance diabetes affects about 15% of all diabetes sufferers (at least in Sweden, numbers as above care of Lund Uni researchers). Those prone to this type of diabetes have a different gene/hormone profile to the rest - my own understanding is that it affects those with a lean and muscular body type (under 'normal' conditions), hence its devastating effects in Polynesian countries, Aotearoa included.
 

HSSS

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Severe insulin resistance diabetes has a different disease make-up and progression - ie the kidney breakdown (according to the Swedish endos/researchers at Lund Uni where I get this info from) to what the same Swedes call mild obesity and mild age related diabetes (the latter two accounts for 66% of all diabetes including auto-immune diabetes). They make the very reasonable point that these different kinds of diabetes need different treatments.

Severe insulin resistance diabetes affects about 15% of all diabetes sufferers (at least in Sweden, numbers as above care of Lund Uni researchers). Those prone to this type of diabetes have a different gene/hormone profile to the rest - my own understanding is that it affects those with a lean and muscular body type (under 'normal' conditions), hence its devastating effects in Polynesian countries, Aotearoa included.

This corresponds well to the experiences I see on here. There’s subset of type 2 that seem to get excellent, comparitively quick with large drops in numbers and long lasting results by losing weight even if carbs remain moderate rather than low, a subset that may be age related and a tiring pancreas perhaps, and some that are stubborn that go full keto and still struggle to get much below prediabetic levels for a long time presumably due to high IR levels. I’m sure many of us can identify with one or another and see it in others. It certainly explains some of the disparity in results from apparently similar situations
 
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AloeSvea

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This corresponds well to the experiences I see on here. There’s subset of type 2 that seem to get excellent, comparitively quick with large drops in numbers and long lasting results by losing weight even if carbs remain moderate rather than low, a subset that may be age related and a tiring pancreas perhaps, and some that are stubborn and a subset that go full keto and still struggle to get much below prediabetic levels for a long time presumably due to high IR levels. I’m sure many of us can identify with one or another and see it in others. It certainly explains some of the disparity in results from apparently similar situations

Yes.
 
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Hotpepper20000

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This corresponds well to the experiences I see on here. There’s subset of type 2 that seem to get excellent, comparitively quick with large drops in numbers and long lasting results by losing weight even if carbs remain moderate rather than low, a subset that may be age related and a tiring pancreas perhaps, and some that are stubborn and a subset that go full keto and still struggle to get much below prediabetic levels for a long time presumably due to high IR levels. I’m sure many of us can identify with one or another and see it in others. It certainly explains some of the disparity in results from apparently similar situations
I agree. It also shows while what we eat or don’t eat does help and for many that is enough, for some there are other factors that contribute to IR.
 
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I think the primary reason why very lean people become super resistant is because they aren’t able to easily become obese, and so the liver very quickly exhausts its capacity for lipogenesis.
 

HSSS

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I think the primary reason why very lean people become super resistant is because they aren’t able to easily become obese, and so the liver very quickly exhausts its capacity for lipogenesis.
And no doubt genetics is behind many of the differences