Why can't Type 2 be cured?

[andromache]

It’s a tricky word, ‘cure’, isn’t it. There something similar going on in my MS world. Some argue that for the newly-diagnosed who have not had much damage yet, an HSCT stem cell treatment offers something indistinguishable from a cure. For those like me who have been accumulating permanent neurological damage for decades, talk of a cure is meaningless, and a chronic progressive neurological disorder remains just that. With either condition, perhaps what ‘cure’ might look like depends on the context.

 

[Melgar]

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'.

I’m thin, bumping along at 120 lbs and I’m 5’6 and 62 years old. I’m gluten intolerant. My gluten intolerance does make my blood sugars labile even though I’m 100% gluten free. I cook my own foods from scratch. So I naturally don’t eat breads and pastas and cakes etc.

Last year I stopped eating gluten as a result I put on weight which took me to the top end of normal weight. My C-Peptides were lowish - middling, which suggests to me I don’t have insulin resistance (Of course I may be wrong and I am over simplifying). Buoyed by the many success stories I read here on this site, I took it upon myself to lose weight and up my exercise regime. I reduced my carbs to 35g per day. I had to be careful as I have nutrient absorption issues and I am prone to Hypos) I did and still do a brisk 6 mile walk every day ( I have two big dogs) and an hour of aerobic exercise every day. In consequence I lost 35 lbs. Did it reduce my blood sugars? Yes and no. It did reduce my morning fasting sugars from 8-10 mmols to 6-7 mmols, but over all my Ac1’s dropped from 6.7% to 6.3%. I know my blood sugars are not high and scary, but I do have diabetic symptoms. I am not a rare case. I have read a number of people on here wondering why they are pre-diabetic or diabetic when they are thin and active. One is always left wondering why, given all the information about weight linked diabetes articles and commentry, there are those of us that run contrary to it all. I have no T2 in my family, but along with others here, we live with troublesome blood sugars. Maybe down the line they will find other reasons for T2 and a reason not connected to weight and inactivity.

After saying all that I am very pleased with how I feel. I feel a lot healthier despite my disappointing results. And importantly even though my blood sugars are disappointing for all my effort they have not got any worse either

 

[HairySmurf]

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).

..

Very many thanks for this link, it was a very informative read.

One passage in particular jumped out at me:
“…the underlying pathophysiology of T2D, including both deficiency of insulin and resistance to insulin’s actions, as well as other abnormalities, is rarely completely normalised by interventions.”

My interpretation is that a T2D remission that does not involve and require some ongoing dietary restrictions for life, while possible, is a very rare thing. This is new information for me. I still plan to lose a whole lot of weight as quickly as I safely can, but I'll have to temper my hopes for what might be possible after that's done.

Many thanks for having me on the thread folks - I won't bother you any further.

 

[EllieM]

Many thanks for having me on the thread folks - I won't bother you any further.

You're not bothering us. Please feel welcome to join in on this or any other thread, or even post your own.

 

[VashtiB]

Very many thanks for this link, it was a very informative read.

One passage in particular jumped out at me:
“…the underlying pathophysiology of T2D, including both deficiency of insulin and resistance to insulin’s actions, as well as other abnormalities, is rarely completely normalised by interventions.”

My interpretation is that a T2D remission that does not involve and require some ongoing dietary restrictions for life, while possible, is a very rare thing. This is new information for me. I still plan to lose a whole lot of weight as quickly as I safely can, but I'll have to temper my hopes for what might be possible after that's done.

Many thanks for having me on the thread folks - I won't bother you any further.

I'd like to agree with @EllieM you are certainly not bothering anyone.

As a type 2 I think most of us dream of remission which does not involve dietary restrictions for life. I no longer believe that is really possible. That said I personally do believe it is possible to reduce your insulin resistance with very low carb. This opens the doors for the possibility of being able to have a higher level of carbs without the need for medication. Still not what would be a 'normal' carb intake but with possibly a bit more flexibility.

 

[Outlier]

A few observations with other mammals and fat storage:

Wild mammals live very active lives and mostly eat biologically appropriate food. If anyone here has prepared such creatures for the table, they will know that fat where present is stored around internal organs first, and apart from one species of deer, never gets to the stage of being under the skin. It is likely by logic that fat stored around internal organs therefore has a protective aspect, because nature is a hard master and only does what works.

I strongly suspect that in demonising visceral fat, the Powers That Be are on a (fatty) red herring, and maybe one day this will become another "we used to think".

 

[ajbod]

The problem with Visceral fat is too much. yes it is protective, but only up to a point, eventually it causes it's own problems. Having spent many years when younger as a Butcher and unlicensed Slaughterman, I've seen all sorts. The primary Visceral fat should be around the Kidneys, (suet). Very few carcasses had much if any more Visceral fat, but even then we occasionally came across fatty livers.
i think the telling thing, is that Glucose regulation, improves after a small weight loss, and my understanding is that the Visceral fat is more easily used up than the subcutaneous fat, so is the first used up. It's not THE problem, but is a part of the overall problem.

 

[Grant_Vicat]

Blood glucose testing is a comparatively recent thing (1980s iirc) and past generations were diagnosed solely on symptoms, mainly sugar in the urine.

Blood testing by the patient yes, but you might find this interesting, just because it gives you a clue as to how diagnosis worked on a Type 1 in July 1959. I retyped this becuse the original is so damaged:
My diagnosis letter advised "that it was preferable to allow him to have some glycosuria than to run the risk of hypoglycaemic attacks."
INVESTIGATIONS:
Urine 2% sugar Acetone+++ Albumen nil. Blood Sugar 920mgs.%. *
Course and Results:
Stomach aspirated, and intravenous drip normal saline started.
?0 units** soluble insulin given intravenously and 20 units subcutaneously.
With repeated doses of insulin and continued intravenous fluid therapy, the child was fully conscious by the following day, with blood sugar 189 mgs and urine ketone free.

I still have very clear knife scars on my left ankle where my mother said they poured actual salt in!

When I arrived at the hospital I am described in the notes as "Very ill child, pale and cold, slightly cyanosed, with depressed fontanelle. Breath - acidotic
Pulse 178/minute

* In today's system that equals 51, ten times the amount of a normal reading!

** Paper is lost, but I would think probably 10 as it would act much quicker and could be risky in greater quantities

 

[KennyA]

Blood testing by the patient yes, but you might find this interesting, just because it gives you a clue as to how diagnosis worked on a Type 1 in July 1959. I retyped this becuse the original is so damaged:
My diagnosis letter advised "that it was preferable to allow him to have some glycosuria than to run the risk of hypoglycaemic attacks."
INVESTIGATIONS:
Urine 2% sugar Acetone+++ Albumen nil. Blood Sugar 920mgs.%. *
Course and Results:
Stomach aspirated, and intravenous drip normal saline started.
?0 units** soluble insulin given intravenously and 20 units subcutaneously.
With repeated doses of insulin and continued intravenous fluid therapy, the child was fully conscious by the following day, with blood sugar 189 mgs and urine ketone free.

I still have very clear knife scars on my left ankle where my mother said they poured actual salt in!

When I arrived at the hospital I am described in the notes as "Very ill child, pale and cold, slightly cyanosed, with depressed fontanelle. Breath - acidotic
Pulse 178/minute

* In today's system that equals 51, ten times the amount of a normal reading!

** Paper is lost, but I would think probably 10 as it would act much quicker and could be risky in greater quantities

That's fascinating! Thanks for posting.

BTW - you're right that I intended to mean home testing by the patient via glucometer. At least no-one has to taste urine any more to check its sweetness.

 

[HairySmurf]

I’m very conscious about trying to watch my manners on this forum and I don’t want to be a thread hijacker, though I feel obliged to correct myself.

Firstly having read and re-read the best document I can find describing the processes that lead to insulin resistance and then on to T2 diabetes I have to admit I was wrong – being fat does not cause insulin resistance in any way. Fat does play a big role in several steps in the cascade of problems that leads to a fatty liver, which is the most easily observed marker of the most common pathway to T2 diabetes. However, the problem appears to be triggered by high, rapid calorie intake, not being fat. Plenty of obese people, maybe a third, managed to put on their weight, presumably slowly and steadily, without triggering any easily observable state of insulin resistance.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4587882/

The same document illustrates that, to the best of my understanding, there are indeed unhealthy places to store body fat but it’s perhaps not so much about a specific area of the body such as under the skin. Healthy adipose (fat cell) tissue located (perhaps) anywhere in the body may be a good and healthy place, up to a point. Fat cells can accommodate the body’s need to store energy as needed, however if energy storage is too rapid individual fat cells can expand too far too quickly and become inflamed, insulin resistant and leaky. If this occurs on a large scale leaky fat cells raise levels of free fatty acids in the blood which are then taken up by tissues that are absolutely not good places to store fat, such as liver and muscle tissue. These tissues then become insulin resistant and the cascade of problems that can lead to T2 diabetes progresses.

Fat storage in healthy adipose tissue under the skin appears to be generally good and fine from a metabolic perspective. Fat storage in healthy visceral adipose tissue, between the organs rather than inside organ tissue, does have known health implications if present in large amounts, for example in kidney disease:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8014972/

However, I can’t find a single document that seems to prove that healthy, non-inflamed, visceral adipose tissue fat is a cause of, not a symptom of, obesity or insulin resistance. Fat storage in other kinds of tissues (ectopic fat) is varying levels of bad, depending on the tissue or organ and absolutely causes insulin resistance. I’m uncertain if fat cell inflammation due to overly rapid energy storage in adipose tissue is synonymous with damage. Does the inflammation subside if the body is in a period of significant calorie deficit? Or is an inflamed fat cell permanently leaky?

Also I’d like to thank the posters that wrote about visceral fat in other mammals. This led me to do some reading and I discovered that humans are very much unique as regards where and how we store our fat and how much of it we store. Interesting reading.

https://www.genengnews.com/news/how-the-naked-ape-became-the-fat-ape/

 

[MrsA2]

Or is an inflamed fat cell permanently leaky

I'm not very good at understanding the scientific stuff, but I know the carbs I have eaten over Christmas have gone straight back into the fat cells under the skin of my tummy that had been empty when I first went very low carb. I can see it smoothing out what was saggy and empty and is now replenished, and my belt is tighter.

I know that's an n=1 example but I had joked with a friend the other day that my fat cells just suck in carbs

 

[In Response]

I completely appreciate that Type 1 is a different beast to type 2 so the research is very different. What I have noticed is more research into the cause of Type 1 in order to stop it happening rather than curing it once it has been diagnosed. My expectation is that, at some date, Type 1 may be eradicated. Not through cure but by the last case dying of something else.
There has been a joke from before I was diagnosed that Type 1 would have a cure in 10 years. I was diagnosed 20 years ago and the cure is still ten years away. I expect to need to inject insulin for the rest of my life - I do not expect to see the cure.

So, to the question of why type 2 cannot be cured, is it because it Is not really known what causes it so we don’t know what to reverse? And is the research into finding that cure and stopping more people from contracting it rather than curing those who do?