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

> 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.

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.

> 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.

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).

This paper states that T1s can develop IR. The possibility of T1s developing IR is not news. Having T1 does not make you immune to developing IR. The same factors that drive IR in T2s can affect T1s - these diseases are entirely separate, and in fact you can have "double diabetes". What the paper does not state is that T1s inevitably develop IR. Thus, your statement is wrong. The correct sentence is:

> "Type 1"s can develop insulin resistance as well

I'd rather expect type 2 diabetics to be more at risk, since type 2 diabetes is characterized by insulin resistance, while type 1 isn't.

You can do map, reduce etc. in C, albeit with a serious amount of macro trickery or function pointer usage. And yes, this does count. Is it practical? I doubt it. But it is possible.

It has been "the future" for decades now. In reality, aspects of functional programming have long since made their way into other, multiparadigmatic languages. I'm talking not only about primitives like map, reduce, fold etc. but also about isolating state, avoiding side effects, and making functions pure whenever possible. Functional languages enforce this, but you can do this in any language. Even C.

I wonder if scientists who read heavily diluted and oversimplified pop-sci web portal versions of scientific papers (for example, a paper that documents a weak correlation between obesity and stuff X -> web portal says "scientists find that X causes obesity") feel the same way.

Atomic time is great for timestamps that have zero relation to localtime. But if you want to be able to convert to localtime, UTC is easier, since it only involves an offset. Atomic time to localtime also requires fitting in the leap seconds. This is also the reason why scheduling stuff based on atomic time is impractical - you won't know when leap seconds will be inserted in the future.

Because you want functioning islets that produce insulin.

As a type 1 diabetic, I don't think this is very relevant for treating diabetes. The VX-880 trial already used stem cell derived islet cells (that's not the same stem cell therapy as the one described in the article), so the need for donor cells will go down. Those grown islet cells won't have rejection problems because they would be a match to the patient's body.

A cure for type 1 diabetes requires two big steps: First, cells have to be lab grown (already done in the VX-880 trial). Second, the faulty autoimmune reaction needs to be fixed, or the islet cells need to be encapsulated somehow. Otherwise, the immune system kills off those cells again. The approach described by this paper would not help, because those islet cells would be the patient's own already, so there would not be any "hybrid" immune system. It would not make sense. Also, procuring donor islet cells is difficult and wasteful - another reason why lab-growin islets instead is a much better approach.

However, this is of big interest for organ transplants. People with those have to take immunosuppressants, which are no joke.

Ugh, hardcopy.

When the macrophages pull in the damaged LDL particles, do they ever go away? Are there self-repair mechanisms in the body that clean that up over time?

From what I recall, LDL can clog your arteries when it becomes glycated, because then, the liver's LDL receptors don't recognize the glycated LDL molecules and the liver won't take those particular molecules out of circulation. Is this correct?

I believe that the mental aspect of T1D is sorely underestimated and overlooked. There are courses for how to estimate carbs, how to administer insulin etc. to cover the physiological portion. But no one teaches you how to build the mental fortitude necessary do deal with the psychological part. It is no wonder that with a disease that requires daily micromanagement the potential for developing anxiety and depression is much higher.

Other people mentioned that there is a known link between T1D and depression, but did not mention any details. I personally don't think this needs to be anything physiological. As a T1 myself, I fully understand the huge potential for depression and burn out with this disease. It is clearly not the "worst" disease in existence (and it is difficult to come up with a metric for defining "better" and "worse" anyway), but it is somewhat special in its sheer relentlessness.

You are required to micromanage it. You need to make sometimes very complex decisions every day, multiple times a day, about administering and deciding the dosage of a hormone that is very potent and can cause you to suffer heart arrhythmia and impaired or even loss of consciousness if the dosage is too high (and what is "too high" and "too low" can be very difficult to estimate), You can end up in "rollercoasters" where your blood glucose level bounces up and down, which, if severe enough, can drain you of all energy and ruin your day. Sometimes your efforts can be in vain - your blood glucose level is just crazy and uncontrollable. And you can't postpone the micromanagement, you can't take a break. This can grind your psyche down easily. Of course not all days are nightmarish like this, but it can get very bad at times. So I am not at all surprised about a clear correlation between T1D and depression, anxiety, burnout. This mental toll alone is already a big enough factor to explain said correlation.