Will I need insulin eventually?

[Talya2022]

On Semaglutide and blood sugars very well controlled on it. Can’t see me being able to come off it due to not changing to low carb diet. Try to exercise as much as possible. And healthy weight. I’ve read most diabetics will need insulin after 10/15 years. Is this true?

 

[catinahat]

Some probably will, some will never need insulin.
I'm just over 10 years since diagnosis, still not taking any medication. I don't think it's correct to say all T2s will eventually need insulin. It depends on many factors, not least of which is diet.
If you eat more carbohydrates than your body can handle I suppose it's more likely that your T2 will progress and you will need stronger drugs, leading eventually to insulin.
Personally I would rather reduce the carbs, keep my blood sugar levels as close to normal as possible, which hopefully will halt the progression of my T2.
Seems to be working ok at the moment, why don't you want to reduce carbs, they are the main cause of high blood sugar levels.

 

[Talya2022]

Because I have a severe eating disorder for 20 years and it’s unlikely I will ever recover but I want to keep trying and hope it will go into remission at some point. Ta important I eat a varied diet from this perspective. I’d rather deal with insulin than an ed

 

[AndBreathe]

Because I have a severe eating disorder for 20 years and it’s unlikely I will ever recover but I want to keep trying and hope it will go into remission at some point. Ta important I eat a varied diet from this perspective. I’d rather deal with insulin than an ed

As someone who lived with and almost died from an eating disorder, I have some insight into what might be going through your mind, however, what I will say is a “varied diet”, in my view, needn’t include high amounts of carbohydrate.

To me a varied diet means I shouldn’t be living on apples, grapefruit and tomatoes, or just Swiss roll and bacon fries. (Just random examples from my brain.)

I live a reduced carb lifestyle, but do consume carbs - just not lots of them. I have been in a healthy remission for over 10 years now.

Have you discussed the detail of a “varied diet” with your eating disorder folks?

 

[catinahat]

We are all different and face different challenges, we all have to play the cards we have been dealt.
If I needed insulin I would happily take it, the damage high blood sugar causes to our health is far scarier than insulin.
low carb does not have to be restrictive, even though I eat fairly low carb, my diet is extremely varied, there are low or lower carb version of everything.
any reductions you can make will have a positive effect on your blood sugar

 

[mouseee]

My DSN told me that I would probably need insulin in my 80s... I'm 50 now, diagnosed at 45ish. I'm taking a few good things out of that one! Not inevitable, and she gave me a nice long time to live successfully with T2

 

[andromache]

As someone who lived with and almost died from an eating disorder, I have some insight into what might be going through your mind, however, what I will say is a “varied diet”, in my view, needn’t include high amounts of carbohydrate.

To me a varied diet means I shouldn’t be living on apples, grapefruit and tomatoes, or just Swiss roll and bacon fries. (Just random examples from my brain.)

I live a reduced carb lifestyle, but do consume carbs - just not lots of them. I have been in a healthy remission for over 10 years now.

Have you discussed the detail of a “varied diet” with your eating disorder folks?

Another battle-scarred ED veteran here. I have not had an active ED for decades, but my relationship with food and nutrition remained pretty much 100% bonkers until metabolic trouble finally led me to low carb. A new understanding of how much better I felt and functioned when fuelled on nutrient-dense, low carb food has been a real eye-opener for me personally. I just wish I had discovered it sooner.

 

[AndBreathe]

Another battle-scarred ED veteran here. I have not had an active ED for decades, but my relationship with food and nutrition remained pretty much 100% bonkers until metabolic trouble finally led me to low carb. A new understanding of how much better I felt and functioned when fuelled on nutrient-dense, low carb food has been a real eye-opener for me personally. I just wish I had discovered it sooner.

Off topic, I know, and I apologise unresered to @Talya2022 for it, but @andromache , I don’t consider myself battle scarred. Sure as heck I wish it hadn’t happened, but actually both the ED and my treatment taught me a great deal about myself.

I learned I could achieve anything I wanted to, although almost ending my life through starvation wasn’t in the pile marked, “Finest Hour”.

It was what it was, and thankfully I have moved forward without any major issues, but, as you do say, my relationship with food improved once I had found a way of eating that I didn’t particularly want to change.

Rome wasn’t built in a day and all that.

 

[HairySmurf]

On Semaglutide and blood sugars very well controlled on it. Can’t see me being able to come off it due to not changing to low carb diet. Try to exercise as much as possible. And healthy weight. I’ve read most diabetics will need insulin after 10/15 years. Is this true?

That kind of statistic, that a Type 2 is likely to need insulin in 10 to 15 years following diagnosis, should be looked at in the context that people tend to put on weight and become less active as they age. There is a still-prevalent assumption amongst the medical community that Type 2 diabetes inevitably progresses, without any solid evidence showing exactly how and why it tends to progress over time.

The two main issues are insulin resistance and insulin secretion. Roy Taylor proved that weight loss quickly results in the reduction of ectopic fat in the liver, and that this reduces insulin resistance in that tissue in the majority of Type 2 cases. It also either reduces the export of triglyceride from the liver, or if his 'personal fat threshold' theory holds water, it empties out fat stored in adipose (fat cell) tissue which enables more of that tissue to sponge up excess triglyceride from the blood. Lower blood triglyceride levels over time is thought to lead to lower levels of ectopic fat stored in the pancreas. In susceptible individuals pancreatic ectopic fat (droplets of fat inside cells in the pancreas) causes lipid toxicity (fat poisoning) of beta (insulin producing) cells in the pancreas. Reducing pancreatic fat levels leads to at least partial recovery of beta cell function in most recently-diagnosed T2 cases. Taylor suggests that the longer beta cells are exposed to high fat levels the less likely it is that those cells will become fully functional again when lipid toxicity is reduced. He further suggests that a person's genetics determine how resilient their beta cells are and thus how long they can remain in a dysfunctional state and still return to full function, if at all.

You mention that you are at a healthy weight, and if you have lost weight since diagnosis to get there then you've done all you can on the liver and pancreas front. You just need to keep the weight off to keep the fat out of your liver and that side of things is handled. If your weight has remained steady since diagnosis it may be worth investigating Taylor's paper on testing the effects of going from a BMI of around 25 to a BMI of around 22.5. If you're at the mid to lower end of the 'normal' BMI range then there's no solid information available on how to get fat out of your liver - if there's even much in there to begin with.

Aetiology of Type 2 diabetes in people with a ‘normal’ body mass index: testing the personal fat threshold hypothesis

Abstract. Weight loss in overweight or obese individuals with Type 2 diabetes (T2D) can normalize hepatic fat metabolism, decrease fatty acid oversupply to β cells and restore normoglycaemia. One in six people has BMI <27 kg/m2 at diagnosis, and their T2D is assumed to have different aetiology...

portlandpress.com

Insulin resistance in adipose and muscle tissue are the other areas that can have a big effect on blood glucose levels. There's no solid information on how to manage insulin resistance in adipose tissue other than, perhaps, weight loss. Insulin resistance in muscle tissue can be improved with regular exercise. Extended exercise will also burn off ectopic fat in muscle tissue, which will cause that tissue to sponge up triglyceride from the blood, which may help to keep levels low and prevent fat build-up in other tissues such as the pancreas. There is a theory that a high blood insulin level is itself the cause of insulin resistance, and if that's true and if it's a reversible condition, a low carb diet may bring down insulin levels and thus lead to lower levels of insulin resistance. I'm dubious of this theory, or if it's true then it might be irreversible, because I have yet to read any reports of people being on low carb diets for years, losing a lot of weight on such a diet, and then finding they can eat a 'normal' amount of carbs again without issue having 'cured' their insulin resistance. There is absolutely no doubt in my mind though that a low carb diet is one that keeps blood glucose levels as low as possible and so is likely to help delay or maybe even prevent the onset of many diabetic complications for a Type 2.

What I'm getting at with all this is that the average Type 2 who might have been expected to need insulin within 10 to 15 years after diagnosis in the past had little to none of this information available to them. They likely put on weight over time and exercised less, and probably ate pretty much the same things they always ate. I'd wager that just by being on this forum your odds might be much better than that old average.

 

[Outlier]

I was reading with great interest - thank you for locating this piece of research - until I got to the bit about "recognising that T2 is due to overnutrition" and then I became - annoyed.

 

[ajbod]

To a degree it is due to over nutrition, but the over nutrition is due to not being able to properly utilise the nutrients consumed, (fatigue) so forced to consume more from lack of energy and hunger pangs. I just think the statement "over nutrition" is a little to simple, and implies greed.

 

[AndBreathe]

That kind of statistic, that a Type 2 is likely to need insulin in 10 to 15 years following diagnosis, should be looked at in the context that people tend to put on weight and become less active as they age. There is a still-prevalent assumption amongst the medical community that Type 2 diabetes inevitably progresses, without any solid evidence showing exactly how and why it tends to progress over time.

The two main issues are insulin resistance and insulin secretion. Roy Taylor proved that weight loss quickly results in the reduction of ectopic fat in the liver, and that this reduces insulin resistance in that tissue in the majority of Type 2 cases. It also either reduces the export of triglyceride from the liver, or if his 'personal fat threshold' theory holds water, it empties out fat stored in adipose (fat cell) tissue which enables more of that tissue to sponge up excess triglyceride from the blood. Lower blood triglyceride levels over time is thought to lead to lower levels of ectopic fat stored in the pancreas. In susceptible individuals pancreatic ectopic fat (droplets of fat inside cells in the pancreas) causes lipid toxicity (fat poisoning) of beta (insulin producing) cells in the pancreas. Reducing pancreatic fat levels leads to at least partial recovery of beta cell function in most recently-diagnosed T2 cases. Taylor suggests that the longer beta cells are exposed to high fat levels the less likely it is that those cells will become fully functional again when lipid toxicity is reduced. He further suggests that a person's genetics determine how resilient their beta cells are and thus how long they can remain in a dysfunctional state and still return to full function, if at all.

You mention that you are at a healthy weight, and if you have lost weight since diagnosis to get there then you've done all you can on the liver and pancreas front. You just need to keep the weight off to keep the fat out of your liver and that side of things is handled. If your weight has remained steady since diagnosis it may be worth investigating Taylor's paper on testing the effects of going from a BMI of around 25 to a BMI of around 22.5. If you're at the mid to lower end of the 'normal' BMI range then there's no solid information available on how to get fat out of your liver - if there's even much in there to begin with.

Aetiology of Type 2 diabetes in people with a ‘normal’ body mass index: testing the personal fat threshold hypothesis

Abstract. Weight loss in overweight or obese individuals with Type 2 diabetes (T2D) can normalize hepatic fat metabolism, decrease fatty acid oversupply to β cells and restore normoglycaemia. One in six people has BMI <27 kg/m2 at diagnosis, and their T2D is assumed to have different aetiology...

portlandpress.com

Insulin resistance in adipose and muscle tissue are the other areas that can have a big effect on blood glucose levels. There's no solid information on how to manage insulin resistance in adipose tissue other than, perhaps, weight loss. Insulin resistance in muscle tissue can be improved with regular exercise. Extended exercise will also burn off ectopic fat in muscle tissue, which will cause that tissue to sponge up triglyceride from the blood, which may help to keep levels low and prevent fat build-up in other tissues such as the pancreas. There is a theory that a high blood insulin level is itself the cause of insulin resistance, and if that's true and if it's a reversible condition, a low carb diet may bring down insulin levels and thus lead to lower levels of insulin resistance. I'm dubious of this theory, or if it's true then it might be irreversible, because I have yet to read any reports of people being on low carb diets for years, losing a lot of weight on such a diet, and then finding they can eat a 'normal' amount of carbs again without issue having 'cured' their insulin resistance. There is absolutely no doubt in my mind though that a low carb diet is one that keeps blood glucose levels as low as possible and so is likely to help delay or maybe even prevent the onset of many diabetic complications for a Type 2.

What I'm getting at with all this is that the average Type 2 who might have been expected to need insulin within 10 to 15 years after diagnosis in the past had little to none of this information available to them. They likely put on weight over time and exercised less, and probably ate pretty much the same things they always ate. I'd wager that just by being on this forum your odds might be much better than that old average.

I think you also fail to acknowledge the proportion of T2 who have little to no interest in modifying their eating Gand drinking.

I am involved in research at our local NIHR, and am repeatedly shocked and disappointed by the number off T2 delegates only interested in the next wonder drug that’ll allow them to carry on as if no diagnosis ever occurred.

Cries of, “ I could never give up bread”, “I do an active job” “I’m just a bad diabetic”, or such like abound, even when neuropathy, strokes or cardiac illness is already in their medical history.

Educarion and timing are critical, and I’m talking of HCPs here.

 

[HairySmurf]

I was reading with great interest - thank you for locating this piece of research - until I got to the bit about "recognising that T2 is due to overnutrition" and then I became - annoyed.

To be fair to him Taylor does pin a lot of the blame on genetics in his book. If his Personal Fat Threshold theory is in fact true, then the root cause of T2 is putting on more weight than an individual's body can handle, with genetics determining the point at which fat starts to accumulate in the liver due to subcutaneous adipose tissue becoming 'full'. He claims that genetics also determines the susceptibility of the liver to insulin resistance due to fat (doesn't happen for the majority of people with fatty livers), and the susceptibility of beta cells to lipid toxicity. He also claims that insulin resistance in muscle tissue has a genetic root.

I'm really not sure how much of that I buy. I think he has proven pretty conclusively that getting fat out of the liver and pancreas has a major effect for most T2s. However, there are a lot of competing theories out there and I don't think proving how to get the fat out, and the effects of that, necessarily proves his theories on how the fat got in there in the first place.

 

[ATB123]

I think you also fail to acknowledge the proportion of T2 who have little to no interest in modifying their eating Gand drinking.

I am involved in research at our local NIHR, and am repeatedly shocked and disappointed by the number off T2 delegates only interested in the next wonder drug that’ll allow them to carry on as if no diagnosis ever occurred.

Cries of, “ I could never give up bread”, “I do an active job” “I’m just a bad diabetic”, or such like abound, even when neuropathy, strokes or cardiac illness is already in their medical history.

Educarion and timing are critical, and I’m talking of HCPs here.

To defend HCPs though, you can only educate a receptive person. Particularly with something like T2 diabetes where so much self management needs to be done. The vast majority of patients are not like those on this forum, who clearly want to learn and self manage and take personal responsibility. Not sure about in other areas but in my area, all newly diagnosed diabetics (T2) are offered an education course. Not sure of the numbers who actually attend. Too many patients tell fibs about what they eat, or nod and smile and go home and return straight to old habits.

 

[KennyA]

The two main issues are insulin resistance and insulin secretion. Roy Taylor proved that weight loss quickly results in the reduction of ectopic fat in the liver, and that this reduces insulin resistance in that tissue in the majority of Type 2 cases.

I don't think Roy Taylor has proved any such thing. He has a theory, which is contradicted by the lived experience of very many people on this forum and elsewhere. Blood glucose control PRECEDES weight loss for us, not follows it. And (in my case at least) at the onset of the condition other diabetic symptoms preceded fat/weight gain - other research indicates that weight gain is effectively another symptom of T2.

I know a couple of T2s who have not modified their lifestyles or diet and have indeed moved on to needing insulin. Not because they no longer produce their own insulin, but because they need much more than their bodies can produce, given their high carb/low fat diets. As very few of us have had our insulin production measured directly, it's a bit of a leap to assume that all or nearly all T2s aren't producing enough insulin. We clearly can't be at the same time not producing enough insulin, and over-producing insulin so that resistance occurs.

 

[HairySmurf]

I don't think Roy Taylor has proved any such thing. He has a theory, which is contradicted by the lived experience of very many people on this forum and elsewhere. Blood glucose control PRECEDES weight loss for us, not follows it. And (in my case at least) at the onset of the condition other diabetic symptoms preceded fat/weight gain - other research indicates that weight gain is effectively another symptom of T2.

I know a couple of T2s who have not modified their lifestyles or diet and have indeed moved on to needing insulin. Not because they no longer produce their own insulin, but because they need much more than their bodies can produce, given their high carb/low fat diets. As very few of us have had our insulin production measured directly, it's a bit of a leap to assume that all or nearly all T2s aren't producing enough insulin. We clearly can't be at the same time not producing enough insulin, and over-producing insulin so that resistance occurs.

He has proved it, in the majority of cases, conclusively. The numbers are in his papers - lower fasting BG despite lower fasting insulin secretion - the liver is secreting less glucose even though the level of insulin needed to suppress it is less. Lower insulin resistance in the liver. The 12 month postprandial insulin numbers show greatly improved insulin secretion capability over time following fat reduction in the pancreas. Unless something else is going on in all the test cases over those 12 months apart from the initial weight loss, it's the weight loss.

A low carb diet will lower BG levels immediately - no surprise there. I've also read several times on this forum that fasting BG levels are the 'last to fall' on a low carb diet. Last to fall meaning following some weight loss? Or have I misunderstood? How long does it take the average Type 2 adopting a low carb diet to see BG levels drop from a high level to the 'normal' range first thing in the morning?

I don't deny anyone's lived experience or accounts on this forum. I would point out though that even Taylor doesn't claim weight loss works for everyone who has been diagnosed Type 2. Type 2 was defined by exclusion after all - it very probably encompasses a number of similar conditions which are difficult to distinguish and diagnose. This paper (free PDF linked on the page) lists 13 'major' forms of atypical diabetes, many (or most?) of which I believe get diagnosed as generic Type 2. Who knows how many 'minor' forms are known or suspected, or will be identified in future. Taylor being entirely right and contradictory personal experiences are not mutually exclusive.

Atypical Diabetes: What Have We Learned and What Does the Future Hold?

As our understanding of the pathophysiology of diabetes evolves, we increasingly recognize that many patients may have a form of diabetes that does not nea

diabetesjournals.org

 

[AndBreathe]

To defend HCPs though, you can only educate a receptive person. Particularly with something like T2 diabetes where so much self management needs to be done. The vast majority of patients are not like those on this forum, who clearly want to learn and self manage and take personal responsibility. Not sure about in other areas but in my area, all newly diagnosed diabetics (T2) are offered an education course. Not sure of the numbers who actually attend. Too many patients tell fibs about what they eat, or nod and smile and go home and return straight to old habits.

Receptive persons also include HCPs.

Under The NHS, all newly diagnosed T2s ( certain on T2s, not sure about T1s and others) should be offered an education course within 9 months of diagnosis. 10.5yrs in, I’m still waiting.

Uptake rates for education courses are staggeringly low (averages low single figure percentages, but varies by area), but let’s face it, 9 months in patterns are established and folks have worked out their own ways -successful or otherwise.

To tell someone their condition needs serious attention, then give them a right royal ignoring for 9 months is mixed messaging at best.

 

[ravensmitten]

Following on from that personal fat threshold thingy as I found it interesting when I read about the theory in 2016 (maybe)

I don't know much about any of this stuff, or claim to understand it, as I don't know half of the story, and there's too many vectors. I do think humans and diabetes are strange, complex things.

There's nothing scientific about what I'm saying, it's a personal anecdote, and have no axe to grind. I do know at diagnoses in 2016 I was a certain weight, which would be past the threshold. I went on a very low calorie diet, lost 3 stone and my BG was in the normal range for about a year after that.

In hindsight foolishly, I didn't really plan for a way of eating coming off of that and I put back on all the weight I had lost after eaten quite carb laden foods, maybe not eating in excess but more than likely more carbs than what was good for me. I very easily put on another 4 stone on top of that, really quickly, 1 stone in a week, one week, and was expecting my Hba1c to be really high, through the roof in fact when I got back to the doctors when they reopened after the lockdowns.

When I had it retaken in 2022, I was quite surprised to see it had dropped 5 points from initial diagnosis from 50 to 45 - which aren't astronomical to begin with and maybe there's a margin for error in the test that might explain it, or something else was going on in 2016, or there's more to the picture, it's more complex, or I'm a freak, which is totally possible too, or a combination of things. - even though I weighed 4 stone more than at diagnosis.

My a1c only seemed to have crept up after I put on another 2 stone, and was eating pretty carby food, making me 6 stone heavier than I was at diagnosis, to at first 47 last feb, and then my last one was 66 last dec, which was a wake up call and showed me I was being far too cocky for my bodies liking.

I started wondering though, before I made my way back over to this site, that maybe I gave my system some sort of a "reset", and because had I read about that fat threshold thing and it seemed to make sense at the time and was from an expert in the field that I possibly could 'increased' my own threshold, if it held water for me, but couldn't find any literature on the subject, about what happens after, why, how and to who if and when it starts developing again.

Like I say, I'm not a scientist and none of this was done in a methodical or observed way, and I certainly don't want repeat it to test that out again, now I'm following a fairly moderate low carb way of eating, keep my BG at a reasonable level, and my weight is coming down as a side effect.

Make of it what you will I suppose.

 

[KennyA]

He has proved it, in the majority of cases, conclusively. The numbers are in his papers - lower fasting BG despite lower fasting insulin secretion - the liver is secreting less glucose even though the level of insulin needed to suppress it is less. Lower insulin resistance in the liver. The 12 month postprandial insulin numbers show greatly improved insulin secretion capability over time following fat reduction in the pancreas. Unless something else is going on in all the test cases over those 12 months apart from the initial weight loss, it's the weight loss.

A low carb diet will lower BG levels immediately - no surprise there. I've also read several times on this forum that fasting BG levels are the 'last to fall' on a low carb diet. Last to fall meaning following some weight loss? Or have I misunderstood? How long does it take the average Type 2 adopting a low carb diet to see BG levels drop from a high level to the 'normal' range first thing in the morning?

I don't deny anyone's lived experience or accounts on this forum. I would point out though that even Taylor doesn't claim weight loss works for everyone who has been diagnosed Type 2. Type 2 was defined by exclusion after all - it very probably encompasses a number of similar conditions which are difficult to distinguish and diagnose. This paper (free PDF linked on the page) lists 13 'major' forms of atypical diabetes, many (or most?) of which I believe get diagnosed as generic Type 2. Who knows how many 'minor' forms are known or suspected, or will be identified in future. Taylor being entirely right and contradictory personal experiences are not mutually exclusive.

Atypical Diabetes: What Have We Learned and What Does the Future Hold?

As our understanding of the pathophysiology of diabetes evolves, we increasingly recognize that many patients may have a form of diabetes that does not nea

diabetesjournals.org

I don't think a 93% failure constitutes success, and that's what their own figures show from the five year DIRECT follow-up. Like many others, you've been taken in by the press releases. I don't think you were a member of these forums when the Taylor material was published, so you may have missed the thread that dealt with this - worth a read.

Direct Study - 5 Year Follow Up

https://www.diabetes.org.uk/about_us/news/weight-loss-can-put-type-2-diabetes-remission-least-five-years-reveal-latest-findings This hit the news channels yesterday, only picking up on it now. Not as inspiring as I might have hoped. Think I remember the initial headline data spoke about...

www.diabetes.co.uk

 

[ATB123]

Receptive persons also include HCPs.

Under The NHS, all newly diagnosed T2s ( certain on T2s, not sure about T1s and others) should be offered an education course within 9 months of diagnosis. 10.5yrs in, I’m still waiting.

Uptake rates for education courses are staggeringly low (averages low single figure percentages, but varies by area), but let’s face it, 9 months in patterns are established and folks have worked out their own ways -successful or otherwise.

To tell someone their condition needs serious attention, then give them a right royal ignoring for 9 months is mixed messaging at best.

But you can't blame the HCPs themselves for that, maybe the system we have to work in. Sorry I get massively angry when i read posts moaning about HCPs when behind us is a massive, creaking, inefficient system that let's us all down, patient or HCP. Sure, there are a few bad apples among us but there are in all jobs but we are under enormous pressure day on day with very little time allocated to each patient. If you haven't heard about your course then chase it, chase it, chase it, don't sit back and wait. I can only go by what's on offer in my area. And you've said yourself uptake is low, so why then is that the HCPs fault that no education has been given. Too many people take absolutely no personal responsibility for their own long term conditions, the asthmatic who smokes, the diabetic who eats choc, etc yet expect the NHS to pick them up and sort them.out