Why can't Type 2 be cured?

[KennyA]

Good thread. I have a feeling that what we call "type 2" may well be a collection of related conditions that share some/many symptoms but may have different causes and solutions. Human digestion and endocrinology is a complicated subject and there are many possible things that might go wrong or be out of balance. If you don't look for the actual cause, you might be inclined to assume that a set of common symptoms is always caused by the same thing.

So if your Christmas tree lights don't work, it's always because the dog chewed through the cable - even if you don't have a dog - never because you didn't plug them in, or plugged them in and didn't turn them on, etc. And you know this because there's a piece of research published years ago on Dog Cable Chewing and Christmas Light Failure. And there are a couple of well known accounts from people who will testify (truthfully) that their Spot did indeed chew through the cable at Christmas in 2011.

It's always struck me on reading Bilous and Donnelly, the current NHS textbook, that they're very good on describing symptoms and what they euphemistically describe as "management" of the condition, but analysis on what causes and therefore how to prevent Type 2 is almost completely absent. There's just an assumption that hey ho, your patient has Type 2, here's what you as the clinician might well see over the years, and here's how to prescribe the drugs that your patient will inevitably need as the condition worsens. There is an expectation of decline.

I'm one of those people who responded very well to very low carb. It worked. I'm also someone who had a number of diabetic symptoms with an HbA1c of 43 or 44. But there are folks on here who do what I do in terms of carb intake, and who don't get the same results. There are also people with much higher BG levels than I ever had who have no symptoms whatsoever. And we're all lumped together as "T2".

I just hope that someone somewhere is interested enough to do some research on this - but I don't see much money in it, and who's going to fund research if there's no profit at the end?

 

[ajbod]

I think there are a multitude of reasons, we end up with the symptoms of type 2, and the chance of ever knowing our own reason is probably impossible. 2 people could be due to perhaps a single common Hormone deficiency, which causes a waterfall effect of other things, but could have several more different historical steps, that eventually became that Hormone deficiency.
As for our Christmas tree lights failing, it was one of our kittens Smokey, who had a real good chew. Repaired them, and bought the kittens some teething toys.

 

[IanBish]

Good thread.

Thank you.

There's just an assumption that hey ho, your patient has Type 2, here's what you as the clinician might well see over the years, and here's how to prescribe the drugs that your patient will inevitably need as the condition worsens. There is an expectation of decline.

Just treat the symptoms and not the root cause.

I'm one of those people who responded very well to very low carb. It worked.

Me too. I just wish that more doctors would see the evidence, and what can be achieved, rather than just writing another prescription.

I just hope that someone somewhere is interested enough to do some research on this - but I don't see much money in it, and who's going to fund research if there's no profit at the end?

Some people have tried to, but considering the epidemic that's unfolding worldwide you'd hope that someone would. But, like you said, where's the profit? Pharma has the profit, and the ultra-processed food manufacturers have it too, while us mere mortals have to actually come across basic advice, like in this wonderful place, to actually make a difference to our lives.

 

[IanBish]

As for our Christmas tree lights failing, it was one of our kittens Smokey, who had a real good chew. Repaired them, and bought the kittens some teething toys.

No Christmas lights here this year. But enough questions, apart from, "am I going to have some New York Cheesecake this Christmas?" To which the answer is, "probably, yes".

 

[ajbod]

He chewed the wiring 2 1/2 foot up the tree, 4 1/2 months old and can reach up that far, still got another 4 to 5 months of rapid growth still to go before slowing down for the next 4 or so years. they both weigh nearly 4 Kg, but he seems bigger, about the size of the average male tom moggy. I think he's gonna be a very big boy, his dad weighs about 30 lb and still had a bit more growing to reach full maturity.

 

[AndBreathe]

Good thread. I have a feeling that what we call "type 2" may well be a collection of related conditions that share some/many symptoms but may have different causes and solutions. Human digestion and endocrinology is a complicated subject and there are many possible things that might go wrong or be out of balance. If you don't look for the actual cause, you might be inclined to assume that a set of common symptoms is always caused by the same thing.

So if your Christmas tree lights don't work, it's always because the dog chewed through the cable - even if you don't have a dog - never because you didn't plug them in, or plugged them in and didn't turn them on, etc. And you know this because there's a piece of research published years ago on Dog Cable Chewing and Christmas Light Failure. And there are a couple of well known accounts from people who will testify (truthfully) that their Spot did indeed chew through the cable at Christmas in 2011.

It's always struck me on reading Bilous and Donnelly, the current NHS textbook, that they're very good on describing symptoms and what they euphemistically describe as "management" of the condition, but analysis on what causes and therefore how to prevent Type 2 is almost completely absent. There's just an assumption that hey ho, your patient has Type 2, here's what you as the clinician might well see over the years, and here's how to prescribe the drugs that your patient will inevitably need as the condition worsens. There is an expectation of decline.

I'm one of those people who responded very well to very low carb. It worked. I'm also someone who had a number of diabetic symptoms with an HbA1c of 43 or 44. But there are folks on here who do what I do in terms of carb intake, and who don't get the same results. There are also people with much higher BG levels than I ever had who have no symptoms whatsoever. And we're all lumped together as "T2".

I just hope that someone somewhere is interested enough to do some research on this - but I don't see much money in it, and who's going to fund research if there's no profit at the end?

In my experience of talking to researchers looking at T2, or consequential conditions, such as CKD, neuropathy, hypertension or heart disease, they are much more stimulated by concepts such as why some develop these. They seem to need a starting point of a diagnosis.

 

[AndBreathe]

Thank you.

Just treat the symptoms and not the root cause.

Me too. I just wish that more doctors would see the evidence, and what can be achieved, rather than just writing another prescription.

Some people have tried to, but considering the epidemic that's unfolding worldwide you'd hope that someone would. But, like you said, where's the profit? Pharma has the profit, and the ultra-processed food manufacturers have it too, while us mere mortals have to actually come across basic advice, like in this wonderful place, to actually make a difference to our lives.

Much of the challenge in all of this is who pays for research.

Diabetes research is often funded by drug companies, where there could be considered a conflict of interest in losing a profitable commercial line of business.

Diabetes UK, British Heart Foundation, the Welcome Foundation and such like also finance some, but even their funding will often be supplemented by commercial interests. Research is a very expensive business.

 

[Dancing Badger]

He chewed the wiring 2 1/2 foot up the tree, 4 1/2 months old and can reach up that far, still got another 4 to 5 months of rapid growth still to go before slowing down for the next 4 or so years. they both weigh nearly 4 Kg, but he seems bigger, about the size of the average male tom moggy. I think he's gonna be a very big boy, his dad weighs about 30 lb and still had a bit more growing to reach full maturity.

Maine Coon, by any chance?

 

[ajbod]

Smokey and Bandit.

 

[Dancing Badger]

Oh, yes...you're in for so much fun (and hair!). We have three - you're never alone with an MC; they're always there, "helping".

 

[J_P]

I quite like Dr Jason Fung's Diabetes Code for an explanation of how it is all interlinked and potentially caused.

The science of liver Metabolism of different sugars (glucose and fructose) adds up and from a personal experience looking back (hindsight is great) i can see some of both the behaviours and foods i was eating and can pretty much track my prediabetic period before my diagnosis.

A short answer to 'why cant it be 'cured' is that a 'cure' suggests it is done and gone but we all know if you decided to binge on weeks / months worth of the wrong stuff it can come back - hence once you've had it, if your successful behaviors aren't maintained it can / will come back - therefore not 'cured' but in remission

 

[HairySmurf]

I know that we can get it into remission, or reverse it, but not cure it.

Hi there. New here, great thread, joined the forum to participate.

Quick intro - I have T2, diagnosed two months ago, discovered info about remission via the Diabetes UK website, did as much 'authoritative' reading on the subject as I could, and have begun a campaign to learn more and to lose a lot of weight fast in hopes of going into remission. Be warned: I know nothing. The following are my opinions only.

On this point - does remission mean sustained normal blood glucose levels due to a low carb diet or does it mean being able to eat whatever you like, in moderation and in combination with some exercise, and still having normal average blood glucose levels? If you mean the former *only* then yes, there is no cure. A low carb diet does the same job as several medications - it keeps blood glucose levels at low, healthy levels - but it's a workaround, not a fix. If you feed a person a big plate of cake, you test their blood a few hours later and you can find evidence of diabetes then that person is definitely not cured.

If however you feed a person a big plate of cake, test their blood a few hours later and find normal blood glucose levels then that person basically does not diabetes at that moment in time. If the illness is undetectable then it might as well not be there at all. If you're referring to this meaning of remission *only* and if it lasts a lifetime, then what can you call that but a cure?

The reason I make this point is that I initially learned about 'reversing' diabetes from my father. He, in his late 70s, told me when I was diagnosed that a few of his acquaintances have been diagnosed with T2 diabetes at some point in their lives and that they 'reversed' it by losing weight and increasing their exercise. They were living without symptoms or related health issues for years, in one cases (I believe) over a decade, without diabetes medication or restrictive diets. It just isn't an issue for them anymore. Anecdotal stories like this are the reason I started reading and learned about the concept of remission. Stories like that are also the reason that clinical studies like DiRECT were conducted in the first place. Yes there may be damage to (I assume) the pancreas that means that such a 'cure' isn't possible for a person, or that a person is left more susceptible to the illness in future. To my mind though, remission of this kind is a cure in the same way that many illnesses can be cured but can still happen a second time.

I do believe it likely that there is more to the story - it can't be as simple as 'lose lots of weight' otherwise the DiRECT study would have shown 100% success. Either there are more kinds of Type 2 Diabetes than are currently recognised, or there is more to it than visceral fat in the wrong places. Or both.

As to your other questions about insulin resistance - I don't think anyone has proved the mechanism(s) behind it yet. If they did, there'd be nice simple explanations a quick Google away. I think 'insulin resistance' is a bit like the concept of 'Close Contact' during the Covid pandemic. Obviously being physically close to someone was not the mechanism for spreading the virus, but nobody had yet proved conclusively the mechanics of how the virus can be transported from one person to another. 'Close Contact' both works as a concept, because it's obvious from observation that you can catch the virus from being close to someone, and also doesn't work, because there has to be more to the story. The fact that I can't find nice, clear, detailed definitions for how insulin resistance actually happens leads me to believe it's the diabetes equivalent of Close Contact. Being fat causes insulin resistance, apparently, and that gives you the diabetes. It's just a pity we can't keep a 2m distance from our food at all times.

 

[ajbod]

Being fat does not cause Insulin resistance, it's the other way round. However being fat due to Insulin resistance may very well make that resistance worse. You can normalise your blood sugars, before weight loss, the reduction in Hba1c is not dependent on the weight loss.
Covid is a respiratory complaint and therefore could only ever be via aerosolised particles, ie breathed out from an infected person and breathed in by oneself.
As to finding out the mechanism of Insulin resistance, it will never be funded, because if it was understood, then a cure would be possible. And that will drastically reduce the Pharma companies bottom line, and they fund the research, and ensure an interest in any regulatory bodies around the globe.

 

[HairySmurf]

Being fat does not cause Insulin resistance, it's the other way round. However being fat due to Insulin resistance may very well make that resistance worse. You can normalise your blood sugars, before weight loss, the reduction in Hba1c is not dependent on the weight loss.
Covid is a respiratory complaint and therefore could only ever be via aerosolised particles, ie breathed out from an infected person and breathed in by oneself.
As to finding out the mechanism of Insulin resistance, it will never be funded, because if it was understood, then a cure would be possible. And that will drastically reduce the Pharma companies bottom line, and they fund the research, and ensure an interest in any regulatory bodies around the globe.

I can't post links yet because I'm new, so instead I challenge you to have a Google (try 'does insulin resistance cause weight gain') and find a link to a recent article published by a hospital, diabetes charity, government funded health agency, or to a scientific paper, that does not list obesity and/or visceral fat as a highly probable causal factor for insulin resistance. Alternatively have a read of 'The Association between Adult Weight Gain and Insulin Resistance at Middle Age: Mediation by Visceral Fat and Liver Fat' on the US National Library of Medicine site.

Can a thin person develop insulin resistance? Yes. Is it common? No, it's rare. Does insulin resistance cause further weight gain? Yes.

Yes you can normalize your blood sugars before weight loss through diet, but that's not anything resembling a 'cure'.

Have a go at finding a scientific study that proves, conclusively, that a coronavirus could be spread by aerosolized particles, that was published before 2020. Hint: You won't find one, which is why it took the WHO two years to state categorically that Covid 19 was 'airborne'. Hence all the mess about masks and close contact rules etc. at the beginning of the pandemic. We knew from the beginning that there was a very strong link between being close to someone with the virus and catching the virus. That was obvious from observation even though we couldn't prove airborne particles. My point there is that while the mechanism underlying insulin resistance, the initial trigger, is not currently 'well understood', we know it exists and we know there's a strong association with visceral fat, a fatty liver and possibly fat deposited on muscle tissue. Nobody has yet proven, conclusively, that these things caused insulin resistance in most people who have it, because the mechanism, how it actually happens, is hard to study.

You can't take a person apart, scrape the fat off all their internal organs and put them back together to see if the insulin resistance is gone. Neither can you intentionally try to give a person insulin resistance to prove how it's done. It's a hard thing to prove by ethical means. It can be done, likely through animal studies (ethical?) and it will be done eventually, at which time we'll have excellent articles with nice simple diagrams. Until then I'll stick with 'Being fat causes insulin resistance, apparently, and that gives you the diabetes.' That is at least as true, scientifically speaking, as 'Close contact gives you the Covids'.

 

[Resurgam]

Every time I caught covid it was just after handling plastic packages, but as the information was that it is airborne I was infected multiple times. Fortunately I don't get it badly.
I have always done badly when eating carbs, but everyone knows that they are healthy, I put on so much weight eating carbs and I exerted all my strength not to do so, but as soon as I stopped counting calories and cut down the carbs I lost loads of weight without even thinking about it. My rock hard liver subsided and softened so I can now clean the bottom of the fridge again. My cholesterol level has reduced even though I am eating all the wrong things.
So many things which are touted as truth just don't seem to work out in practice.

 

[IanBish]

As to finding out the mechanism of Insulin resistance, it will never be funded, because if it was understood, then a cure would be possible. And that will drastically reduce the Pharma companies bottom line, and they fund the research, and ensure an interest in any regulatory bodies around the globe.

I fear you're right. It's a similar thing with big food companies and their cheap, abundant ultra-processed carbohydrate-rich "food".

...we know it exists and we know there's a strong association with visceral fat, a fatty liver and possibly fat deposited on muscle tissue. Nobody has yet proven, conclusively, that these things caused insulin resistance in most people who have it, because the mechanism, how it actually happens, is hard to study.

My current favourite theory for insulin resistance is the Personal Fat Threshold one. But I'm prepared to be proved wrong, as I inevitably will be.

 

[Guilty]

This is one of those situations where people with different theories can all be correct because there can be more than one cause of type 2. As @KennyA said.

I think a big driver behind the rise in type 2 cases globally over the past few decades, is the rise in ultra processed food. And UPF definitely a contributed to my own case.

For anyone who enjoys learning about this stuff, this is a great presentation on the issue of UPF:

The book is a good read as well.

 

[Outlier]

My apologies to those of you who have read this from me before.

Much knowledge is out of date by the time it gets to the classrooms that train our future medics. This applies to NHS as well as every other source.

Yesterday's "scientific truth" becomes today's "we used to think".

Where information appears in the public domain, we need to be very cautious about its sources before we give it credibility. Often "opinion" is marketed as "fact".

"Qui bono?". If there is profit to be made, we again need to be very cautious about what we are told. Some very uncomfortable discoveries can lurk beneath the surface of matters such as new lower levels of health readings, causes/cures/treatment of illnesses, and so on. If there is not profit to be made (e.g. by diet-controlled T2 treatment) there is little incentive for even very valuable information to be shared.

Nothing beats individual lived experience. Where this differs from theory, it should always be listened to, and analysed as thoroughly as possible.

 

[KennyA]

Hi there. New here, great thread, joined the forum to participate.

Quick intro - I have T2, diagnosed two months ago, discovered info about remission via the Diabetes UK website, did as much 'authoritative' reading on the subject as I could, and have begun a campaign to learn more and to lose a lot of weight fast in hopes of going into remission. Be warned: I know nothing. The following are my opinions only.

On this point - does remission mean sustained normal blood glucose levels due to a low carb diet or does it mean being able to eat whatever you like, in moderation and in combination with some exercise, and still having normal average blood glucose levels? If you mean the former *only* then yes, there is no cure. A low carb diet does the same job as several medications - it keeps blood glucose levels at low, healthy levels - but it's a workaround, not a fix. If you feed a person a big plate of cake, you test their blood a few hours later and you can find evidence of diabetes then that person is definitely not cured.

If however you feed a person a big plate of cake, test their blood a few hours later and find normal blood glucose levels then that person basically does not diabetes at that moment in time. If the illness is undetectable then it might as well not be there at all. If you're referring to this meaning of remission *only* and if it lasts a lifetime, then what can you call that but a cure?

The reason I make this point is that I initially learned about 'reversing' diabetes from my father. He, in his late 70s, told me when I was diagnosed that a few of his acquaintances have been diagnosed with T2 diabetes at some point in their lives and that they 'reversed' it by losing weight and increasing their exercise. They were living without symptoms or related health issues for years, in one cases (I believe) over a decade, without diabetes medication or restrictive diets. It just isn't an issue for them anymore. Anecdotal stories like this are the reason I started reading and learned about the concept of remission. Stories like that are also the reason that clinical studies like DiRECT were conducted in the first place. Yes there may be damage to (I assume) the pancreas that means that such a 'cure' isn't possible for a person, or that a person is left more susceptible to the illness in future. To my mind though, remission of this kind is a cure in the same way that many illnesses can be cured but can still happen a second time.

I do believe it likely that there is more to the story - it can't be as simple as 'lose lots of weight' otherwise the DiRECT study would have shown 100% success. Either there are more kinds of Type 2 Diabetes than are currently recognised, or there is more to it than visceral fat in the wrong places. Or both.

As to your other questions about insulin resistance - I don't think anyone has proved the mechanism(s) behind it yet. If they did, there'd be nice simple explanations a quick Google away. I think 'insulin resistance' is a bit like the concept of 'Close Contact' during the Covid pandemic. Obviously being physically close to someone was not the mechanism for spreading the virus, but nobody had yet proved conclusively the mechanics of how the virus can be transported from one person to another. 'Close Contact' both works as a concept, because it's obvious from observation that you can catch the virus from being close to someone, and also doesn't work, because there has to be more to the story. The fact that I can't find nice, clear, detailed definitions for how insulin resistance actually happens leads me to believe it's the diabetes equivalent of Close Contact. Being fat causes insulin resistance, apparently, and that gives you the diabetes. It's just a pity we can't keep a 2m distance from our food at all times.

There is now an official definition of remission, which is two sub-48 HbA1c results six months apart without using glucose lowering medication. My take on this is that this is not in any way "remission" as most of us understand it (even if our own definitions differ).

https://link.springer.com/article/10.1007/s00125-021-05542-z

Blood glucose testing is a comparatively recent thing (1980s iirc) and past generations were diagnosed solely on symptoms, mainly sugar in the urine. I think there is often confusion between T2 diabetes (the disease) and having high blood glucose (a symptom).

Non-diabetics eating the "large slice of cake" will also have a resulting sharp (temporary) rise in blood glucose. This is normal - and demonstrates the difficulty with determining what a single BG reading might be telling you, and why the HbA1c gives a better indication for diagnosis purposes - and even then, two tests are usually conducted for confirmation if the result is borderline. It's worth having a Google for some CGM graphs produced by "non-diabetics" as comparison.

As far as I'm concerned, I need to keep my BG levels low because I get a range of unpleasant symptoms starting when levels are around 42-43. Those symptoms are caused by high blood glucose, which was caused by my diabetes. Reduce the BG levels, the symptoms go away. I had other diabetic symptoms long before weight gain - that is/was also one of the symptoms, not the cause, in my case at least. So to my mind I can be without diabetic symptoms, have low/normal BG results, but still have diabetes. In my case I attribute that to a 20g/day carb intake, but it really doesn't matter for these purposes how it's achieved.

So I think you may have it a bit the wrong way round. Insulin resistance (which might be attributable to many things) leads to insulin over-production, and that leads to insulin resistance worsening, increased bodyfat and higher blood glucose levels.

[edited to change "with" to without"]

 

[HairySmurf]

My current favourite theory for insulin resistance is the Personal Fat Threshold one. But I'm prepared to be proved wrong, as I inevitably will be.

I’m not sure I buy a Personal Fat Threshold theory exactly but I do see how something like that might fit as a part of the puzzle.

Here’s my theory, for what it’s worth – the Energy Storage Scramble. This is pure speculation.

When we eat very large amounts of easily digestible, energy dense foods the body will try to store all the energy it can, as quickly as it can. We are hard-wired to crave such foods and consume them to excess because throughout our evolutionary history there have been times of plenty and times of hardship. When our ancestors came across a berry bush or a tree laden with ripe fruit it made complete evolutionary sense for them to gorge and gorge again, and to store as much of that energy as possible, because the fruit will soon rot and Winter is Coming.

Our bodies have preferred, ‘healthier’ places to store fat, but fat can also be stored in ‘unhealthier’ places. I would speculate that storing fat out of the way under the skin is the ‘healthiest’ place, and that storing it in and around internal organs is the ‘unhealthiest’ place. Genetics definitely plays a role here as there are observable differences between different races and even between families when it comes the preferred places a body stores its fat. All the men in my family grow big bellies long before much fat appears on our thighs or our ***** for example, while I’ve seen men who seem to put on fat ‘all over’. I believe the theory of a Personal Fat Threshold does have some value here in that it’s not a good idea for example, in evolutionary terms, to keep storing fat in one area and nowhere else. We’d fall over all the time, or our thighs would rub together when we needed to run. At some point the body has to start storing fat in less desirable places so that we can keep our balance and stay mobile. Perhaps there’s a point where very unhealthy spots for fat storage become the best of a lot of bad options.

My theory is that eating large amounts of energy dense foods which are rapidly digested causes the body to put every effort into storing as much as possible as fast as possible, even if that means storing some of that energy as fat in unhealthy places as a kind of ‘emergency’ measure. In my case I’m guessing it was all the McDonalds, pizza, huge plates of pasta, chocolate and chicken fried rice. In evolutionary terms though, eating very large amounts of berries, fruit, honey, or possibly nuts, might have had the same effect, triggering a scramble to store huge amounts of energy quickly.

For our ancestors, humans and the animals that came before them, fat stored in ‘unhealthy’ places is not such a bad thing. The fat would always be burned off again pretty quickly, either while searching and working for new sources of food, or in lean times. It’s not so long ago in our evolutionary history that our ancestors hibernated. When the objective is storing energy for lean times or hibernation, anywhere the body can store fat quickly when the berries are ripe is a good place. I believe that might explain why our bodies would ever have evolved to store fat in very unhealthy places in the first place.

My best guess is that problems like insulin resistance, high blood pressure and very high cholesterol can arise when:

1: We eat rapidly digestible, energy-dense foods to excess

2: This causes some fat to be stored in unhealthy places

3: We don’t burn all that unhealthy fat off again in a timely manner, via extended periods of calorie deficit due to exercise or diet, in a way that causes some significant weight loss

4: We do it again and again, piling on fat in places that interfere with metabolic function to the point that things go haywire

Again, this is all pure speculation. It just the best idea I have which allows all the pieces of the puzzle I’ve discovered and my own personal experience to fit together in a way that makes sense to me.

*edited by mod to remove inappropriate word
*mod re-edit to conform with forum rule