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What Is Type 2 Diabetes?

kokhongw

Well-Known Member
Messages
2,394
Location
Singapore
Type of diabetes
I reversed my Type 2
Treatment type
Diet only
Given the understanding that we have accumulated over the years...perhaps it is time to rephrase what IS Type 2 diabetes...it is NOT "Being unable to produce enough insulin". This misrepresentation remains the key reason why the standard approach is misguided and has little success in T2D remission.

upload_2018-6-30_5-58-31.png

Even ADA has started to recognized the fact that T2D in fact produce plenty of insulin...and provides a more accurate description...how else is OBESITY so common with T2D?
upload_2018-6-30_6-3-13.png

And Wikipedia puts it more subtly as"relative lack of insulin"...
upload_2018-6-30_6-4-36.png
 
Completely agree.. I think Type 2 should be re-classed as overproducing insulin that is not used correctly by the body.. i.e 2 much insulin (Hence Type 2).
If people really aren't producing enough insulin then it is far more akin to a variant of Type 1. A fasting insulin test would show the difference pretty quickly and correct treatment could be applied. Insulin therapy could therefore be used properly rather than overloading someone who already produces excess insulin with even more thus worsening their condition.
The problem is getting anyone interested in making these changes.Maybe we should try and get Richard Morris (one of the 2 keto dudes) who is currently studying for a biochemistry degree to write a thesis on it?
 
The problem is getting anyone interested in making these changes.Maybe we should try and get Richard Morris (one of the 2 keto dudes) who is currently studying for a biochemistry degree to write a thesis on it?

Hopefully we can start with the editors of this site...to highlight the fact that excessive insulin and excessive insulin load is the real driver of T2D.
 
I read that differently from the diabetes co uk website. I don't think the article is stating that type 2 is caused by being unable to produce sufficient insulin. I think it is stating that being unable to produce sufficient insulin can be one of the reasons for hyperglycemia.

It cycles back to the fact that not looking after your beta cells long term by demanding they deal with a high carb diet may lead to further beta cell dysfunction or death. With fasting insulin tests, is lower always better?
 
From my past reading and diabetes education, the way I have always interpreted iT2D is that of:
1) a mistiming of the release of insulin in relation to a rising blood glucose from a meal combined with
2) an increased resistance to the effectiveness of insulin on blood glucose control in general causing over years an increasingly higher insulin output from an increasingly overtaxed set of insulin secreting cells in the pancreas.
There are a number of causes of insulin resistance which include genetic as well as environmental factors.
The mistiming mentioned in 1) is about the lack of a more immediate release of insulin in response to rising blood sugar from a meal followed by a belated and excessive release of insulin which fails to control the post-prandial glucose level to within the normal range and may lead to lower blood glucose levels even to the point of hypoglycaemia later on.
1) and 2) above in milder form could be defined a pre-diabetes where the post-prandial blood glucose levels fall with a range between normal and definite diabetic levels.
I hope that is clearer than mud !!!
 
I see they've done a BBC 'heavier people walking along with their heads out of shot' photo. Most disappointing. I suggest more after photos to show the public what can be acheived.
 
Good idea @Administrator what do you think?

I have just read the first page of the advice for ' reactive hypoglycaemia' on the home pages.
While the description is pretty good, one thing did highlight this discrepancy.

Quote 'Scientists believe that Hypoglycaemia to be the result of too much insulin being produced and released by the pancreas following a high carbohydrate meal.'

This is wrong! @Administrator, @Brunneria.

Regardless of how high the carb intake, a reactive hypoglycaemia patient will still go hypo if the triggers that causes the initial blood glucose levels rise enough to cause the overshoot.

Also, recommending fibre rich food, which includes complex carbs, when through the experience that I and many others have gained, is the intolerance to wheat, dairy, starchy vegetables will almost always trigger the overshoot.

I could be even more pedantic, but this home page for reactive hypoglycaemia has been produced by someone who doesn't understand the intricacies of the condition.

It does not state anything about the abnormal, response(s) of insulin, how hyperinsulinaemia, insulinoma, insulin resistance and because of these symptoms, you can have high glucose levels because of the high circulating insulin levels.

The recent increase in known diagnosed reactive hypoglycaemic patients, the good endocrinologists, do know the causes of this type of hypoglycaemia. As in diabetes, the diversity of the condition is high and different for most. The basic advice from mine and others is, 'no hyper, no hypo'!
And as always, testing and finding the best food balance, to prevent the hypos.

It doesn't mention fasting.

I would like to think that our Reactive hypoglycaemia forum has better advice from those who have experienced the condition and could rewrite this home page introduction to the condition, as it seems to me, in my opinion, it is describing, the symptoms of reactive hypoglycaemia in other forms of diabetes rather than the condition itself.

I have ' Late Reactive Hypoglycaemia'!
I would be ill and suffering from hypos continually, if I followed this advice.

Regards
 
Given the understanding that we have accumulated over the years...perhaps it is time to rephrase what IS Type 2 diabetes...it is NOT "Being unable to produce enough insulin". This misrepresentation remains the key reason why the standard approach is misguided and has little success in T2D remission.
Totally agree with you. When I had my GP first appointment after diagnosis why GP asked me what I thought T2 was. I said 'insulin resistance' He said 'what do you mean? It's being unable to produce enough insulin, nothing to do with insulin resistance' All I heard after that was yada yada yada...
 
I read that differently from the diabetes co uk website. I don't think the article is stating that type 2 is caused by being unable to produce sufficient insulin. I think it is stating that being unable to produce sufficient insulin can be one of the reasons for hyperglycemia.

It cycles back to the fact that not looking after your beta cells long term by demanding they deal with a high carb diet may lead to further beta cell dysfunction or death. With fasting insulin tests, is lower always better?
Well a zero would mean a Type 1 diagnosis (i.e. producing no endogenous insulin) minimal in the case of honeymooners.
Once the test became common place someone could build up a database to start looking at the optimum levels of insulin production (a bit like we have for HbA1c levels) to diagnose. I wonder how many of the misdiagnosed in the past would have been correctly diagnosed with a fasting insulin test as well. If medichecks can send out the kit including postage and packing and the return envelope and do the test for £39 how much would it cost the NHS to do it on everyone?
 
I have just read the first page of the advice for ' reactive hypoglycaemia' on the home pages.
While the description is pretty good, one thing did highlight this discrepancy.

Quote 'Scientists believe that Hypoglycaemia to be the result of too much insulin being produced and released by the pancreas following a high carbohydrate meal.'

This is wrong! @Administrator, @Brunneria.

Regardless of how high the carb intake, a reactive hypoglycaemia patient will still go hypo if the triggers that causes the initial blood glucose levels rise enough to cause the overshoot.

Also, recommending fibre rich food, which includes complex carbs, when through the experience that I and many others have gained, is the intolerance to wheat, dairy, starchy vegetables will almost always trigger the overshoot.

I could be even more pedantic, but this home page for reactive hypoglycaemia has been produced by someone who doesn't understand the intricacies of the condition.

It does not state anything about the abnormal, response(s) of insulin, how hyperinsulinaemia, insulinoma, insulin resistance and because of these symptoms, you can have high glucose levels because of the high circulating insulin levels.

The recent increase in known diagnosed reactive hypoglycaemic patients, the good endocrinologists, do know the causes of this type of hypoglycaemia. As in diabetes, the diversity of the condition is high and different for most. The basic advice from mine and others is, 'no hyper, no hypo'!
And as always, testing and finding the best food balance, to prevent the hypos.

It doesn't mention fasting.

I would like to think that our Reactive hypoglycaemia forum has better advice from those who have experienced the condition and could rewrite this home page introduction to the condition, as it seems to me, in my opinion, it is describing, the symptoms of reactive hypoglycaemia in other forms of diabetes rather than the condition itself.

I have ' Late Reactive Hypoglycaemia'!
I would be ill and suffering from hypos continually, if I followed this advice.

Regards
The way I read your post: you are still attributing anything that causes a high blood sugar level to lead to an overshoot of insulin response, that does include a high carbs meal whether it contains high fibr contents or not.
BUT do you have any backing, any theory or explanation which proves that some intolerance reaction to high fibre foods causes a rise in blood sugar sufficient to cause an insulin overshoot OR that independently triggers an insulin overshoot ?
 
In the Uk at least, a diagnosis of T2 diabetes covers a variety of clinical presentations and medical science is still only in the early stages of being able to discriminate between them.
Back in the day, before T1 & T2 were invented as diagnostic categories, you were diagnosed as having either insulin dependent or non insulin dependent diabetes - I was first diagnosed as the first then the latter - to my mind to return to some kind of binary understanding of diabetes ( no production of insulin or over production of insulin) would be very retrograde
 
The way I read your post: you are still attributing anything that causes a high blood sugar level to lead to an overshoot of insulin response, that does include a high carbs meal whether it contains high fibr contents or not.
BUT do you have any backing, any theory or explanation which proves that some intolerance reaction to high fibre foods causes a rise in blood sugar sufficient to cause an insulin overshoot OR that independently triggers an insulin overshoot ?
A way that food intolerance is tested is to abstain from the suspect foods for say 2 weeks minimum and then, with no hint to the person being tested to reintroduce one of the foods and observe for any reaction over the next 48 hours. Then add in a different test food etc.
Some people react to lactose in dairy, others to A1 casein (A1 protein in milk). Restriction of lactose helps in the first instance, and switch to soy milk or A2 milk (if available) might help the second.
You have probably read up on 'irritable bowel" in which it is thought fibres in certain foods are thought to cause the symptoms and following a FODMAP diet might help. That may be another line of enquiry.
In the Uk at least, a diagnosis of T2 diabetes covers a variety of clinical presentations and medical science is still only in the early stages of being able to discriminate between them.
Back in the day, before T1 & T2 were invented as diagnostic categories, you were diagnosed as having either insulin dependent or non insulin dependent diabetes - I was first diagnosed as the first then the latter - to my mind to return to some kind of binary understanding of diabetes ( no production of insulin or over production of insulin) would be very retrograde
Hi @Boo1979, I was diagnosed in that era, too. But the more one looks and researches the more complicated the picture becomes. But studies in UK showed that all T2Ds progressed to requiring insulin if they lived long enough. Defining and classifying a continuum can be a challenge And LADA as a diagnosis threw a spanner in the neat classification oF diabetes.
We have to carefully up-date as solidly proven knowledge emerges, as more advances are made in understanding whilst knowing that all classification and definitions will tend to have some exceptions to the rule or time is needed for a person's diagnosis to fully declare itself one way or the other. The assumption, of course, is that any new classification clarifies and enables not only better understanding but better treatment and prevention, too.
 
A way that food intolerance is tested is to abstain from the suspect foods for say 2 weeks minimum and then, with no hint to the person being tested to reintroduce one of the foods and observe for any reaction over the next 48 hours. Then add in a different test food etc.
Some people react to lactose in dairy, others to A1 casein (A1 protein in milk). Restriction of lactose helps in the first instance, and switch to soy milk or A2 milk (if available) might help the second.
You have probably read up on 'irritable bowel" in which it is thought fibres in certain foods are thought to cause the symptoms and following a FODMAP diet might help. That may be another line of enquiry.

Hi @Boo1979, I was diagnosed in that era, too. But the more one looks and researches the more complicated the picture becomes. But studies in UK showed that all T2Ds progressed to requiring insulin if they lived long enough. Defining and classifying a continuum can be a challenge And LADA as a diagnosis threw a spanner in the neat classification oF diabetes.
We have to carefully up-date as solidly proven knowledge emerges, as more advances are made in understanding whilst knowing that all classification and definitions will tend to have some exceptions to the rule or time is needed for a person's diagnosis to fully declare itself one way or the other. The assumption, of course, is that any new classification clarifies and enables not only better understanding but better treatment and prevention, too.
Well all I know is that I have been diagnosed diabetic for over 21 years, 95% of the time diagnosed as as T2 / non insulin dependant, and have managed to stay on a low dose of Glic and return non diabetic hba1cs as long as I stick with that medication and carefully manage my diet adjusting as necessary when D throws its little curve balls - no progression to insulin here - Ive obviously just not lived long enough to fit the theory!!!
 
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Given the understanding that we have accumulated over the years...perhaps it is time to rephrase what IS Type 2 diabetes...it is NOT "Being unable to produce enough insulin". This misrepresentation remains the key reason why the standard approach is misguided and has little success in T2D remission.

View attachment 27353

Even ADA has started to recognized the fact that T2D in fact produce plenty of insulin...and provides a more accurate description...how else is OBESITY so common with T2D?
View attachment 27354

And Wikipedia puts it more subtly as"relative lack of insulin"...
View attachment 27355
Some type2s don't produce enough insulin. Not all type2s produce enough. Some have irregular production and can result in over production. Some have constant overproduction to severe extremes.
 
Some type2s don't produce enough insulin. Not all type2s produce enough. Some have irregular production and can result in over production. Some have constant overproduction to severe extremes.
Hi @ickihun, The challenge is that T2D is a continuum from pre-diabetes to definite T2D and through to complete pancreatic exhaustion. It depends, I thnk where on that continuum you look as to what the insulin production, its timing and intensity (or lack thereof) is .
 
Hi @ickihun, The challenge is that T2D is a continuum from pre-diabetes to definite T2D and through to complete pancreatic exhaustion. It depends, I thnk where on that continuum you look as to what the insulin production, its timing and intensity (or lack thereof) is .
And depending on treatment, weight loss, diets, weight gain etc etc the person may move back towards pre-diabetes/no diabetes or forward towards less pancreatic insulin reserve.
 
if T2 is diagnosed by raised blood glucose (either by HbA1c or by OGTT or by random blood test) then it is irrelevant whether that bg is raised due to insulin resistance and a large production of insulin, or through insulin insufficiency (due to reduced beta cell function).

Beta cells stop functioning for different reasons, not limited to T1 auto immune reasons.

in my own case, I got T2 level blood glucose levels which makes me a T2, since my raised bgs were not due to autoimmune beta cell loss, or steroids, or raised iron levels, or any other accepted explanation. i do have PCOS and other endocrine dysfunction, so T2 was expected. seems like a no brainer to class me as T2, according to standard diagnostic practice.

but then I slowly discovered, with the help of self testing, a Libre, and very low carbing, that my blood glucose levels are largely dependent on gluten intake.

This means that if I eat gluten, my blood glucose levels rise and fall dramatically, causing reactive hypoglycaemia and escalating insulin resistance, along with steadily rising bgs.
if I avoid gluten, I can actually eat more carbs (sugars and starchy veg) but blood glucose is steadier and insulin resistance is lower.

Obviously, I cannot speak for anyone else, but if I hadn't done my personal testing, food elimination and record keeping, I would still be 'a T2' with v high insulin resistance. No way is the NHS open to testing and diagnosing the background to my T2. Too difficult. Too detailed. Too expensive. And unnecessary, when labelling me T2 is a functional catch all.

However, I have managed to achieve normal non-D blood glucose levels via gluten avoidance and carb reduction. My reactive hypoglycaemia only pops up if I get glutened, and my insulin resistance is the lowest for years.

In short: I don't believe I am unique, and I don't think any of us are best served by overly simplistic diagnostic sound bites. Yet the world seems to function on such sound bites, and asking the medical profession to find the time and resources to treat people as individuals hasn't worked for decades, if ever.
 
if T2 is diagnosed by raised blood glucose (either by HbA1c or by OGTT or by random blood test) then it is irrelevant whether that bg is raised due to insulin resistance and a large production of insulin, or through insulin insufficiency (due to reduced beta cell function).

Beta cells stop functioning for different reasons, not limited to T1 auto immune reasons.

in my own case, I got T2 level blood glucose levels which makes me a T2, since my raised bgs were not due to autoimmune beta cell loss, or steroids, or raised iron levels, or any other accepted explanation. i do have PCOS and other endocrine dysfunction, so T2 was expected. seems like a no brainer to class me as T2, according to standard diagnostic practice.

but then I slowly discovered, with the help of self testing, a Libre, and very low carbing, that my blood glucose levels are largely dependent on gluten intake.

This means that if I eat gluten, my blood glucose levels rise and fall dramatically, causing reactive hypoglycaemia and escalating insulin resistance, along with steadily rising bgs.
if I avoid gluten, I can actually eat more carbs (sugars and starchy veg) but blood glucose is steadier and insulin resistance is lower.

Obviously, I cannot speak for anyone else, but if I hadn't done my personal testing, food elimination and record keeping, I would still be 'a T2' with v high insulin resistance. No way is the NHS open to testing and diagnosing the background to my T2. Too difficult. Too detailed. Too expensive. And unnecessary, when labelling me T2 is a functional catch all.

However, I have managed to achieve normal non-D blood glucose levels via gluten avoidance and carb reduction. My reactive hypoglycaemia only pops up if I get glutened, and my insulin resistance is the lowest for years.

In short: I don't believe I am unique, and I don't think any of us are best served by overly simplistic diagnostic sound bites. Yet the world seems to function on such sound bites, and asking the medical profession to find the time and resources to treat people as individuals hasn't worked for decades, if ever.
May I ask whether you have had TTG- (blood test for coeliac disease) measured whilst on gluten ?
 
Yes we all have different reasons for a type2 diagnosis. However all type2s are normally insulin resistant. Due to too much fat or maybe wrong fat cells. Or even due to the wrong insulin pathway.
Many ways to arrive at the destination and obesity (too many fat cells) is only one way. Insulin resistant is highly variable. A blood test carried out can be inaccurate by the time your results are received. Too many variants to influence insulin resistance. Hormones, stress and illness (or insufficient vitamins/minerals).
We are all in different positions in our disease and can be influenced at any time. For stable treatment there has to be stable variables.
Aliminating bad variables would be perfect and keeping those variables at the desired level continuously is the true type2 treatment. Because variables then no cure.
 
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