Dang formatting. 2GRT269, 8DYX247, 3XIV159, respectively.

A family friend was once assigned â2GRT269â(TM), and had to replace it with a custom plate to avoid embarrassment. Then thereâ(TM)s â8DYX247â(TM), which some unfortunate Tesla owner is currently driving around with. But I actually wouldnâ(TM)t mind having â3XIV159â(TM) for my car. (Get it? A Pi plate! â3 14 159â(TM).)

This is eugenics. (With all the baggage that entails.) There are very few cases where such an approach could even theoretically do actual good, and they all depend on a degree of scientific knowledge and technology (and global availability) that we don't have yet.

Imagine we had a magical free CRISPR shot that could repair a "broken" genetic base pair. Only a tiny fraction of diseases, those caused by a single well-defined gene (e.g. Tay-Sachs, cystic fibrosis) would be fixable this way. Most "genetic" diseases (such as T1D) are caused by constellations of tens or hundreds of interacting genes, with all sorts of unrelated side-efffects, and with environmental and probabilistic components as well. There is no straightforward genetic fix for them; that's why they haven't been bred out of the population despite millions of years of natural selection.

In any case, pretty much everyone on the planet (including you) has a handful of not-so-great genetic mutations, and probably two or three badly screwed-up recessive ones. The only current practical (to the wealthy) approach, if pre-screening is available, is to choose not to have kids with someone who shares the same problematic genes that you have, or if you are a match and want kids anyway, to use IVF and pre-screen embryos. (Ethical takes on this vary.) It's also a slippery slope; how bad does a gene have to be in order to take this approach?

Tl;dr: the genome is far more complicated than you think, and for 99% of human ailments, genetic manipulation would not even theoretically work to solve them.

There has been significant research into finding ways to get the beta cells to regenerate themselves (e.g. https://www.ncbi.nlm.nih.gov/p...), as well as "inverse vaccines" (e.g. Anokion: https://anokion.com/pipeline/) to selectively "untrain" the immune system to attack the pancreas. Also research into ways to physically shield transplanted beta cells from both immune rejection and autoimmune attack. (e.g. Vertex Pharmaceuticals: https://www.vrtx.com/our-scien...)

Meanwhile, there are selective, relatively low-impact autoimmune blockers such as teplizumab or verapamil that can substantially slow down T1D progression without causing full-on immune suppression, and research is finding improved ways all the time. There is reason to be hopeful.

There is no T1D in our family histories; in fact, ironically, 23andMe had identified both of us (mother and father) as having substantially below-average risk for T1D. We banked the cord blood (in 2018) mostly on a "why not?" basis, thinking that it might possibly turn out useful for other family members in the future, or perhaps something we could donate for science or for someone else's use. We never expected that our daughter herself might benefit from it! And she can't (yet), but maybe one of these days.

The "genetic defect" (to the extent T1D has a genetic predisposition) relates to the immune system, not the beta cells themselves. So no "repair" would be needed to create workable beta cells this way.

FWIW, the genetic susceptibility to T1D is present in about 1/4 of the population, but only 1-2% of those will ever develop the disease, based on unknown (likely environmental or probabilistic) factors.

I'm sure you're aware, but Wilford Brimley's "diabeetus" refers to Type 2, a metabolic disorder. This article (and this therapy) is specific to Type 1 diabetes, an autoimmune disorder. (Technically this type of therapy might also be helpful for some Type 2 cases, but it's initially focused on type 1.)

My 6yo daughter has T1D, and we banked her cord blood when she was born. If her own stem cells could be used to generate these insulin-producing cells, it would avoid the need for broad-spectrum immunosuppressive drugs. (Although the autoimmune attack itself would also need to be selectively suppressed to prevent the T1D recurring.) Holding out hope that these therapies start to become available sooner than later!

With the rocket being reusable, most of the external energy per launch will be in preparing the fuel. LOX currently costs around $40 per ton, so 3500 tons of it cost $140k. Suppose ALL of this cost is to pay for electricity for refinement/liquification/cooling, at 10c/kWh. That implies 1400 MWh to produce the fuel, which would produce ~400kg of CO2 per MWh [based on the US average energy mix], working out to 560 metric tons of CO2 per flight. (Plus somewhat less to chill the liquid methane.) Of course, this part of the process could also be powered by renewables, making the CO2 footprint that much smaller; the same can't be said for jet fuel of course. And not all of the cost of LOX is the energy cost of refinement, so the actual CO2 emissions are probably significantly lower than these ballpark figures.

That 76k figure is laughably incorrect. For one thing, Starship EP2P flights would not use the Super Heavy booster at all; suborbital trajectories combined with reentry gliding would enable Starship-only flights to have a range of ~10,000km. Furthermore, Starship (without Super Heavy) uses about 300 tons of liquid methane per flight, so it would produce about 900 tons of CO2 per flight. For comparison, an Airbus A380 produces around 750 tons of CO2 per flight. Meanwhile, Elon has stated that the expected seating capacity for Earth point-to-point Starship transport would be around 1000 passengers, which exceeds a typical A380 flight (~500 passengers) by ~2x. So the CO2-per-passenger cost of Starship Earth point-to-point travel could actually end up somewhat lower than for A380, in the best case.

Pedantically, everyone is born with functioning islets. Type 1 Diabetes often strikes in childhood, but can strike at any age. That's why the term "juvenile diabetes" has fallen out of favor and is no longer used.

The problem of simply injecting new stem cells (or beta cells) is that they only work for a short while; the immune system will quickly attack and kill them, and you're back where you started. The trick is is to either block this autoimmune response (broadly through immunosuppression, or selectively via an "inverse vaccine"), or to find a way to protect the new cells via encapsulation. All of these approaches are being worked on, and the hope is that at least some of them may succeed, in a clinically viable way.

Type I is an autoimmune disease (not lifestyle-correlated) that reduces insulin production, and cannot be reversed through lifestyle changes. Type II is a metabolic disease (lifestyle-correlated) that creates insulin resistance, and can sometimes be at least partially reversed through lifestyle changes. Come to think of it, for Type II, running around like a chicken with its head cut off (for 20-30 minutes a day) may in fact comprise part of such an effective lifestyle change.

By that logic, heart disease isn't a disease either. Neither is lung cancer caused by cigarettes. That's an absurd take. Behavior-induced diseases are still diseases.

Of course, this article is primarily about Type 1 Diabetes, which emphatically fits every definition of a disease, and is uncorrelated with lifestyle or behavior.

No question. This is why Vertex is already working on approach (1) in a more recent trial (VX-264).

The immune attack must be stopped in one of three ways: either by broadly disabling it (e.g. VX-880 trial), selectively suppressing/disabling it (tolerogenic vaccination or "inverse vaccine", which Anokion is working on), or physically blocking it (encapsulated beta cells, e.g. VX-264 trial). Either way, beta cells must be infused or regenerated. The new beta cells can come from another donor's stem cells (Vertex), or from the patient's own stem cells (e.g. Weill Cornell Medicine, by harvesting and "reprogramming" gastric stem cells). Other research aims to get the patient's own remaining beta cells to multiply and regenerate.

Hopefully at least one of these approaches will pan out soon! My 6yo daughter is T1D, and we fervently hope there might be a cure on the horizon.