T2D and small intestine connection - new treatment?

conceit

Baroness
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"A potential medical breakthrough that could put an end to the daily insulin injections endured by people living with diabetes has been unveiled by Dutch scientists.

By destroying the mucous membrane in the small intestine and causing a new one to develop, scientists stabilised the blood sugar levels of people with type 2 diabetes. The results have been described as “spectacular” – albeit unexpected – by the chief researchers involved.

In the hourlong procedure, trialled on 50 patients in Amsterdam, a tube with a small balloon in its end is inserted through the mouth of the patient down to the small intestine."


Diabetes: a 'ticking time bomb' for the NHS

The balloon is inflated with hot water and the mucous membrane burned away by the heat. Within two weeks a new membrane develops, leading to an improvement in the patient’s health.

Even a year after the treatment, the disease was found to be stable in 90% of those treated. It is believed there is a link between nutrient absorption by the mucus membrane in the small intestine and the development of insulin resistance among people with type 2 diabetes.

Jacques Bergman, a professor of gastroenterology at Amsterdam UMC, said: “Because of this treatment the use of insulin can be postponed or perhaps prevented. That is promising.”

Bergman added of the procedure that it was “amazing that people suffer very little from this”.

He told the Dutch broadcaster Nederlandse Omroep Stichting: “With those people we see a spectacular improvement in blood sugar levels one day after the operation, before they even lose one kilo, which has put us on the track.

“Because the question now is whether this is a permanent treatment, or whether it is something that you have to keep repeating – something that in theory should be possible. We looked at whether we could stop their insulin, which is still ongoing, but the first results are truly spectacular, with the lion’s share of patients no longer using insulin after this treatment.”

The new discovery initially seems most suitable for borderline patients who already take pills but whose blood sugar level is high enough for doctors to advise that they inject insulin in the short term.

Apart from dispensing with insulin injections, researchers claim that those treated could benefit from a lower risk of cardiovascular disease, kidney failure, blindness and numbness in the hands and feet.


Cases of type 2 diabetes among young people rise 41% in three years

Scientists from Amsterdam UMC who presented their study at a conference in Vienna this week were said to be cautious but “jubilant” about the initial results.

People with type 2 diabetes aged between 28 and 75 are now being recruited for a larger study of 100 people.

Almost 3.7 million people in the UK live with a diagnosis of type 1 or 2 diabetes, an increase of 1.9 million since 1998. Type 1 diabetes is where the level of sugar in the blood is too high because the pancreas does not produce insulin.

Those with type 2 diabetes are not producing enough insulin. The impact can be controlled by changes to diet, but it is a progressive disease. Most people will need to take tablets or inject insulin after living with it for five to 10 years.

Nine out of 10 people diagnosed with diabetes have type 2. It is estimated that there are nearly 1 million people currently living with the condition who have yet to be diagnosed and that 12.3 million people are at an increased risk due high levels of sugar in their blood.


source: https://www.theguardian.com/society...-treatment-could-end-daily-insulin-injections

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i am not getting my hopes up about treatment or cure yet, but this gives more credence to what doctors and patients in bariatric communities have said for a while about the role of the small intestine in t2d and obesity.

p.s. a lot of fat shaming on reddit threads sharing this article. people love saying t2ds don't deserve a cure. as far as i am concerned, this procedure is a step in the right direction. at the very least, it gives us more information on causative factors for t2d.
 
The ONLY part they misspoke on...

Some do not produce enough, others produce enough but their body doesn’t use it properly.

I have been reading about this more, and it turns out T2D is not just (or primarily) a disease of insulin resistance but islet dysfunction. A friend is an endo, MD PhD with T1D and we had a detailed conversation recently. He is more of a scientist, and I appreciate that because even a lot of practicing endos haven't caught up on latest research.

Here's what I've learnt. By the time FBG starts to rise in diabetic ranges (which as we know is the last to rise), about 60% of beta cells have stopped functioning and insulin production goes down and not enough is being produced at that point. By enough, I mean enough for the pancreas to keep blood glucose in non diabetic or even prediabetic ranges. Insulin levels may be normal by this point (rather than high or low), rather than the 2-3 times normal (or more) when a person is IR but hasn't developed pre D. T2s remain insulin resistant but just lose the ability to compensate for the beta cell dysfunction with excessive insulin production. There's also a corresponding decrease in insulin resistance at first, but it's slight. Over time, insulin levels get lower and lower as islet dysfunction progresses. I think this may happen slower in diabetics with good control long term (A1C below 6), but it probably happens eventually to nearly all long term T2Ds.

This has interesting implications stemming directly from Bariatric surgery, because apparently Diabetes researchers have been paying attention to beta cell function being restored in T2Ds following bariatric surgery, VSG in this example. They need to study the DS, asap. But I'll link the VSG related article below:

https://medicalxpress.com/news/2018-04-bariatric-surgery-successes-diabetes-treatment.html

There's some oversimplification to make it more accessible I suppose, but I think it's interesting.

p.s.
Research is showing that in T2s beta cells aren't "dead", which is encouraging because the DS is doing something that restores beta cells even in T2Ds that were insulin dependent, so beta cells in T2s are likely not irreversibly damaged or dead, for a long time anyway. In folks who have been insulin dependent for decades, there's definitely more damage and even a surgery like the DS may not be enough to cure T2D. But as in your case, being able to control with meds, and I hope you are able to do that forever, does tell us that some lost function is still restored.
 
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But as in your case, being able to control with meds, and I hope you are able to do that forever, does tell us that some lost function is still restored.
I’m actually not sure how much longer I can hold of insulin or an insulin analog. My morning blood sugars are still way higher than they should be. And while my A1C is marginally okay, I have plenty of room to get it down.
 
Liz do you have any thoughts on insulin dosing on the DS diet with higher protein and fats as the latter slows down absorption? would you be counting the percentage of protein DS ers absorb and bolus ing for it using a milder insulin? This is if/when you go back on it. But I am thinking it'd be the basal that helps with fasting numbers.

Is that what you might start first?
 
Liz do you have any thoughts on insulin dosing on the DS diet with higher protein and fats as the latter slows down absorption? would you be counting the percentage of protein DS ers absorb and bolus ing for it using a milder insulin? This is if/when you go back on it. But I am thinking it'd be the basal that helps with fasting numbers.

Is that what you might start first?
Not sure where I’d start now. Being on Medicare limits the number of test strips I can get for testing.

I do know from testing, pure protein and fat meals send me low faster than adding a SMALL amount of carb to that.
 

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