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Sputnik_Butts t1_j0r8rld wrote

Reply to comment by dv_ in Cerebrovascular insulin receptors are defective in Alzheimer’s disease by BlitzOrion

Read the whole paper word to word, before you write another silly message to me. I don't think you understand diabetes at all

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dv_ t1_j0r93mm wrote

I did read it. And I myself have T1D. See for example:

> IR is not a direct cause of T1DM, but rather an accompanying phenomenon. Nevertheless, it is a burden, since people with this type of DM and concomitant IR will need higher insulin doses in order to keep their blood glucose level stable (as compared to the people with DM, but without IR).

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Sputnik_Butts t1_j0ra5cf wrote

Then you should know that it's almost impossible to make it to 70y/o without a highblood sugar. The paper states that a large dose of insulin increases the risk of insulin resistance.

You should also know that low blood sugar damage and kills brain cells, which would imply cells with damaged functioning. If cells aren't functioning correctly how do you think they are going to respond to insulin efficiently?

I'm not saying near perfect control doesn't exist, but type 1 diabetics are at a significant risk to develop Alzheimer's. At least this paper is giving us more insight into the issue, and who knows maybe in the next 30 years we'll develop a way to repair cell receptors for insulin.

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dv_ t1_j0rc6qr wrote

> Then you should know that it's almost impossible to make it to 70y/o without a highblood sugar.

Occasional high BG does nothing. Persistently/frequently high BG is the huge problem. If the BG is chronically high, glycation damage builds up, the body has a hard time keeping up with repairs, and over time, this culminates in complications. The higher glycation rate is precisely what the HbA1c measurement is based on. But if the BG is only sometimes high, then the body can repair that, no problem.

> The paper states that a large dose of insulin increases the risk of insulin resistance.

From the paper:

> In line with that notion, a chronically elevated insulin level (e.g., due to improper insulin injections) produces an adaptive reduction in the number of plasma membrane receptors for the hormone (due to their adaptive internalization and degradation) [6]. Consequently, greater insulin dosage is required to elicit the same physiological effect, hence IR begins. Moreover, secondary alterations in target tissues are also possible. Marban et al. demonstrated that transgenic mice over-expressing insulin showed diminished insulin responsiveness despite fasting normoglycaemia and proper body weight [7]. This could be explained by an impaired binding of insulin to its receptors and/or stem from hypertriglyceridemia, which may impair insulin signal transduction [8].

It is well known that elevated insulin levels downregulate insulin receptors. This is a normal adaptation. (Persistent hyperinsulinemia is not normal though, and one classic sign of metabolic syndrome; but elevated insulin levels do not necessarily equal that type of hyperinsulinemia.) T1s experience this as well. One common situation is when during holidays, a lot more carbs (in form of sweets for example) are consumed. Typically, this can be reverted by reducing carb intake for a few days. The endocrinologist Bernhard Teupe wrote about this. And yes, if you inject tons of insulin due to a rollercoaster, you end up with the same downregulation. That's why I like to do a no-carb day after I've had had a rollercoaster day.

As for impaired insulin binding due to hypertriglyceridemia, if your triglyceride levels are normal in your quarterly checkup, then this is not an issue.

> You should also know that low blood sugar damage and kills brain cells

Only prolonged very severe hypoglycemia does this. That was the big scare before CGMs were available - prolonged serious hypoglycemia during sleep, especially after people developed hypoglycemia unawareness (which is a maladaptation of the CNS to frequently low BG levels). And this has nothing to do with IR. Cells can't survive without fuel for long. They need a constant energy supply. That's why they die - too low BG means they aren't getting sufficient energy.

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Sputnik_Butts t1_j0rceyq wrote

Ok but how can you say all this and not acknowledge the risk T1s have...

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dv_ t1_j0rcpox wrote

I am not negating the risk, I am negating the claim that T1D inevitably leads to IR. That's what your statements seemingly imply. I instead state that IR is entirely separate to T1D. T1D itself does not cause IR, but it also does not make you immune to it. Again, there is the informal term "double diabetes" - when one has T1D and IR.

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Sputnik_Butts t1_j0rdlzm wrote

I think if you think about this with less bias you'll see the conclusions I see. You can be T1DM and have perfect control I suppose and never gain IR. But even perfect control won't prevent you from a tiny bit of wear and tear. You might not notice till you're 70 or 80, but by then everything will be significantly harder and the damage will add up faster.

I'm just saying as a T1, unless you're cured it's inevitable that we will get Alzheimer's even from micro adjustments. The only difference is what age we get it at.

Alzheimer's develops in healthy people without diabetes, you can't assume there's no risk for a T1. It's only logical that we have an increased risk, due to even a tiny IR gain.

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dv_ t1_j0reo1x wrote

> it's inevitable that we will get Alzheimer's even from micro adjustments

Again with the inevitability... The paper does not state anything about inevitability! And I see no other sources proving that T1D inevitably causes Alzheimer's.

> Alzheimer's develops in healthy people without diabetes, you can't assume there's no risk for a T1.

It can develop. It does not inevitably develop. The amount of old T1s with Alzheimer's is not 100%.

> It's only logical that we have an increased risk, due to even a tiny IR gain.

Some degree of IR is normal. There is no such thing as zero IR. The cause for concern is the pathological IR that is one key aspect of metabolic syndrome. And T1D does not cause that IR, nor does it inevitably (!) increase the risk for it. Occasional excess dosages do not equal persistent hyperinsulinemia.

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Sputnik_Butts t1_j0rgo07 wrote

We just disagree, I still believe that T1 causes Alzheimer's because that's what the pathology of Alzheimer's suggests to me. Have a nice life.

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dv_ t1_j0rjrlk wrote

Then say that you believe this instead of stating it as if it were a proven fact next time.

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Sputnik_Butts t1_j0rjwsd wrote

You as well kid

Actually I said "I assumed" and "I'm speculating" but only you have been writing like the words of god flow through you.

Is your bloodsugar good right now?

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faen_du_sa t1_j0seqwv wrote

Yes, you assumed and speculated, then someone chimed in with their seemingly more science based assumptions and also facts! Then you just said no, I have my assumptions.

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Sputnik_Butts t1_j0sf8wo wrote

Yeah they provided more facts, but they didnt extrapolate anything to convince me otherwise from their facts.

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