'Spectacular' diabetes treatment could end daily insulin injections | Hacker News Reader

'Spectacular' diabetes treatment could end daily insulin injections

theguardian.com

54 pointsrjknight18 comments

Uh, not a great article.

> Those with type 2 diabetes are not producing enough insulin.

No, that's type 1. Type 2 is characterized by the body's resistance to insulin. So the pancreas produces enough insulin, but the body can't use it. It's true that this can lead to pancreatic damage because of overwork and shift closer to type 1, where not enough insulin is produced, but that's not the main cause of the illness.

This treatment is only for Type 2, of which only a minority needs insulin injections. Most type 2 is treated by a healthier diet and pills.

Type 1, on the other hand, is the one that absolutely requires insulin injections, and there is no cure in sight for that.

FWIW, if you chase this reporting upstream, the source article also mentions type 2:

https://www.ad.nl/binnenland/nieuwe-behandeling-biedt-hoop-a...

Let your type 2 go untreated and continue living your crappy life, and you'll develop type 1 as well. By exhausting your pancreas.

But yeah. Crappy article title.

Correct me if I am wrong, but I believe one develops Type 1 in this case from general organ failure, not simply because the pancreas itself is being exhausted.

Close. The autoimmune system attacks and kills the insulin-producing beta cells in the pancreas.

Interesting: are you saying that people with Type 2 that progressively get "worse", will eventually become Type 1 diabetics for the exact same reason?

Forgive my asking again. I am a Type 1 diabetic, since age 7. I know that it is an autoimmune disorder. I find that (as seems to be the case with the original article), people tend to blur T1 and T2, and the causes/effects/treatments for each, and it can be mildly infuriating...

Also T1.

To greatly simplify, T2 is a matter of insulin resistance. The pancreas continues to produce insulin, it's just that the insulin produced becomes inefficient and an outside intervention such as medicine or exogenous insulin is needed. In terms of medicine, Metformin is one that's commonly prescribed. Again, to simplify, it basically makes the liver pump out less glucose into the bloodstream. It's actually considered a wonder drug (look up Metformin and longevity, makes you think...). Generally, after a certain period, if done right, the T2 person will no longer require the meds and can be considered cured.

I'm not sure if pancreas can overwork itself to death by producing too much insulin. If it's not damaged by the autoimmune system it should be able to recover.

This is fascinating. I've always thought of type 2 diabetes as a disease of the pancreas, rather than a disease of the intestine. I found this abstract from 2013 interesting:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3830370/

"...A growing body of evidence, however, appears to indicate that type 2 DM (T2DM) may be an operable intestinal illness—a novel revolutionary concept about an old disease."

Diabetes is a disease (like most) characterized by symptom rather than case. If you have excess glucose in the blood it could be because you aren’t producing adequate insulin or because the cells aren’t taking it up properly (or combo). It’s somewhat easy to figure out which but the standard of care for adults exhibiting DM in the US is simply to assume it is insulin resistance.

There’s definitely a role for mitochondrial dysfunction as well. If you store excess fat in the liver, consume sugar while overfeeding (eating at surplus of TDEE), your mitochondria will start to dysfunction w.r.t. energy.

what's the mechanism here?

IANAD, but based on the literature I’ve read, there are two negative feedback loops[0][1].

The first involves skeletal muscle uptake of insulin. Mitochondria in skeletal muscle will not efficiently use glycogen stores. Insulin is released inappropriately by the pancreas due to excess glucose. Body thinks we are in a catabolic state (we must be because insulin was released) so fatty acid oxidation is inhibited. Liver converts lactate into glucose, exacerbating the original mitochondrial dysfunction (what happens when you introduce too much energy into a system that cannot use it?).

The second negative feedback loop involves insulin/glucagon and leptin/ghrelin. Since your body thinks it’s starving (when in reality it cannot use energy efficiently), ghrelin will be secreted. So you keep getting hungry, no matter how much you eat, and insulin spikes as a result of insulin resistance. Leptin is effectively silenced, removing the body’s ability to feel sated.

[0]http://semmelweis.hu/biokemia/files/2014/09/EN_con_INS12_Mit...

[1]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2824521/

> I've always thought of type 2 diabetes as a disease of the pancreas, rather than a disease of the intestine.

It seems just so many diseases of whatever actually are diseases of the intestine and originate from unhealthy intestinal microbiome. This example is a yet another proof.

Whoever interested in using this idea to improve/save their health should read Dr. Kellman's microbiome diet book (it's fairly well written, exciting, practical and includes a fair amount of references to scientific research).

If the effect is not stable and at least some patients tend to return to insulin injection or need to repeat the procedure annually I'd recommend the researcher to try supplementing α-lipoic acid, sodium butyrate and, perhaps, inulin (not insulin). I believe this may help (or may not, would be cool to check with some sort of clinical trials).

The article confuses the two primary problems in T2 diabetes: 1) insulin resistance and 2) reduced production of insulin by your pancreas.

In most T2s, #1 is the first/primary problem, which causes insulin production to go up in order to compensate, which eventually damages the pancreas, causing #2.

This announcement sounds like it addresses only #1, which would be hugely important. But if you're a T2 diabetic with problem #2 (or if you're a T1), this news addresses only half the problem. You'll still need to add insulin.

Can't the pancreas recover to produce healthy (or something below healthy yet essentially sufficient) amounts of insulin once you beat insulin resistance? Can't lipoic acid (which does the job of pushing energy into cells that is normally done by insulin AFAIK) combined with a suitable diet be used after the described procedure to decrease need in insulin below what is considered a norm to relieve overloaded pancreas and help it regenerate?

We've known for a while that gastrointestinal surgery can reverse type 2 diabetes, but we didn't know why.

>the guidelines propose that surgery involving the manipulation of the stomach or intestine be considered as a standard treatment option for appropriate candidates. This development follows multiple clinical trials showing that gastrointestinal surgery can improve blood-sugar levels more effectively than any lifestyle or pharmaceutical intervention

https://www.scientificamerican.com/article/why-doctors-for-d...

Researchers have been looking into why this is so.

>Dr. Rubino's prior research has shown that the primary mechanisms by which gastrointestinal bypass procedures control diabetes specifically rely on the bypass of the upper small intestine — the duodenum and jejunum. This is a key finding that may point to the origins of diabetes.

https://www.sciencedaily.com/releases/2008/03/080305113659.h...

You mean a low carb diet for t2?

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