The Accord study looked specifically at patients with T2 diabetes over a 5 year period and reported increased all cause mortality in the intensive control group with somewhat contradictory findings re CVD and the effects of hypoglyceamia resulting from the intensive control.
https://academic.oup.com/jcem/article/97/1/41/2833135
The final 2 sentences of the article are:-
“If ACCORD has taught us anything, it is that there is no single recipe for glycemic management of CVD risk in T2DM. The old principles still hold: treat each patient as an individual (31) and first do no harm”
No s**t sherlock!!,
Not sure whether I should post this (and I have refrained from posting this every-time someone says they are T2 and going on insulin). There was a study (not sure if it was the ACCORD study) that said that T2s on insulin had a 260% increased risk of dying early). Have no idea of this was relative risk or absolute risk.We have to put into perspective that the ACCORD study/conclusion regarding hypoglycemia due to intensive control...is actually specific to responses due to pharmacological intervention (insulin/insulin secretagouges). The same conclusion cannot be drawn from low stable glucose/insulin levels due to dietary intervention.
Not sure whether I should post this (and I have refrained from posting this every-time someone says they are T2 and going on insulin). There was a study (not sure if it was the ACCORD study) that said that T2s on insulin had a 260% increased risk of dying early). Have no idea of this was relative risk or absolute risk.
My thoughts are that insulin should only be given to T2s whose beta cells no longer produce insulin. For that group it will most definitely prolong their life - but for someone like me who was insulin resistant and still producing insulin it can cause a helter skelter of highs and lows which are not that good for the body.
The low carb diet certainly put a stop to the hypos and dramatic rises. So for me coming off insulin and going low carb halted and reversed the retinopathy and neuropathy whereas the insulin seemed to be making them worse. So at the moment low carb is likely to be extending my lifespan.
If course - if and when - my beta cells stop working I will gladly go back on the insulin as it will be vital to keep me healthy Until then I will stay low carb.
I have also noted posts on this forum ripping the Accord studies to bits - again mostly by keto advocates
Im am not on insulin, but I think in the context of the UK where tests such as C peptide to asess an individuals level of beta cell function are not done, it is equally reckless to put up posts referring to people dying from taking insulin and hailing diet as being the cure all.
Advice to people to try a dietary intervention and / or get their insulin production assessed before upping the anti on meds is perfectly valid, but demonising any medication based on assumptions that all / the majority of people with T2 diagnosis are hyperinsuleamic is dangerous. I have also noted posts on this forum ripping the Accord studies to bits - again mostly by keto advocates
Which looks to me exactly where the problem lies..a one-off test to show whether the patient is over or under producing insulin should be given to everyone on diagnosis. Then it would be obvious if exogneous insulin is required or not.in the context of the UK where tests such as C peptide to asess an individuals level of beta cell function are not done,
Which looks to me exactly where the problem lies..a one-off test to show whether the patient is over or under producing insulin should be given to everyone on diagnosis. Then it would be obvious if exogneous insulin is required or not.
But things get a bit more complicated later on, I believe, when an established T2 shows progression, and rising blood glucose while still producing large amounts of insulin - just not enough insulin to overcome their insulin resistance.
I don't pretend to know the full ins and outs of the various tests, but even insulin resistance varies across the day, and so do insulin levels in the blood, so snapshot tests of insulin levels have their limitations too...
It is very complex, and I don't think many health care practitioners dealing with T2s on a non specialist level appreciate the complexity. Actually, I am not sure many of the specialists do either!
A trial where extra insulin was administered to Type 2's to get the blood sugar lower had disastrous outcomes; it is so important to use the minimal amount required to cover the blood glucose and not think that more is better, it is not.Not sure whether I should post this (and I have refrained from posting this every-time someone says they are T2 and going on insulin). There was a study (not sure if it was the ACCORD study) that said that T2s on insulin had a 260% increased risk of dying early). Have no idea of this was relative risk or absolute risk.
My thoughts are that insulin should only be given to T2s whose beta cells no longer produce insulin. For that group it will most definitely prolong their life - but for someone like me who was insulin resistant and still producing insulin it can cause a helter skelter of highs and lows which are not that good for the body.
The low carb diet certainly put a stop to the hypos and dramatic rises. So for me coming off insulin and going low carb halted and reversed the retinopathy and neuropathy whereas the insulin seemed to be making them worse. So at the moment low carb is likely to be extending my lifespan.
If course - if and when - my beta cells stop working I will gladly go back on the insulin as it will be vital to keep me healthy Until then I will stay low carb.
I also believe Type 2's should where possible limit the use of Sulphonylureas such as Glibenclamide, Gliclazide, Diamicron, Glipizide, Glimepiride, Tolbutamide as these work the Pancreas more - if your Pancreas is marginal already this could be the straw that broke the camel's back, not to worry anyone on these just a cautionary additional info item.Jason Fung believes that a ‘failed’ type 2 pancreas can recover when the fat that is clogging it up is cleared through dietary intervention. Obviously I cannot make a claim as to whether or not this is accurate, but certainly everything else the guy has published so far has proven to be true with regards to my own body.
That aside, there’s also the likelihood that exogenous insulin used to allow more dietary glucose in a patient with hyperinsulinemia could accelerate complete failure of the pancreas.
With respect, I’d suggest, given we are here debating it, that we have approximately three million years of research to prove that the metabolic state of nutritional ketosis doesn’t kill humans
Oh, well said.
And as to long term studies, we certainly know that which does not work. Keto is not new, used as an antiepilepsy approach before the discovery of pharmaceutical treatments and still used today for children who do not react well to said pharmas. As for fibre, what studies were there that were not influenced by the 'Healthy Whole Grains' lobby? Apparently, Keto makes us bunged up, sluggish half wits
You and I are going to have to stop agreeing on everything, or people will start to think we’re in cahoots. I added a little second paragraph to my post just for light hearted effect
With respect, I’d suggest, given we are here debating it, that we have approximately three million years of research to prove that the metabolic state of nutritional ketosis doesn’t kill humans
3 Million years of evidence?
https://www.psychologytoday.com/gb/blog/how-think-neandertal/201311/the-truth-about-the-caveman-diet
Essential, probably not, but beneficial for some reason, we don't know. Let's keep an open mind rather than swapping one assumption for another.My lightbulb moment in the beginning of my reading was learning one simple fact which is this, there is no such thing as an essential carbohydrate
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