
'Spectacular' diabetes treatment could end daily insulin injections - rjknight
https://www.theguardian.com/society/2018/oct/24/spectacular-diabetes-treatment-could-end-daily-insulin-injections
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tomca32
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.

~~~
mikaelj
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.

~~~
gorb314
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.

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

~~~
gorb314
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...

~~~
gukov
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.

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pohl
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/](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."

~~~
gumby
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.

~~~
0x8BADF00D
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.

~~~
gumby
what's the mechanism here?

~~~
0x8BADF00D
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...](http://semmelweis.hu/biokemia/files/2014/09/EN_con_INS12_Mitochondria-
and-diabetes2005.pdf)

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

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qwerty456127
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).

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randcraw
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.

~~~
qwerty456127
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?

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GeekyBear
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...](https://www.scientificamerican.com/article/why-doctors-for-
diabetics-now-recommend-surgery-instead-of-drugs/)

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...](https://www.sciencedaily.com/releases/2008/03/080305113659.htm)

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nefasti
You mean a low carb diet for t2?

