> We tend to think of type 2 diabetes as a disease that afflicts people who are overweight. But it can also appear in people with perfectly healthy weights—and be more deadly in them. A study published today in the Journal of the American Medical Association indicates that normal-weight people diagnosed with type 2 diabetes have double the risk of dying from heart disease and other causes than overweight people with diabetes.
- https://www.health.harvard.edu/blog/diabetes-can-strike-hard...
(Yes, I know this post is about Type 1... but _all_ of the talk in it when I posted this was about Type 2; and basically blaming the people with it for their condition)
- That's false. For _most_ people, you can prevent the symptoms of it with those, but not all. Nor does it _cure_ it, it prevents it from presenting symptoms. The same way that avoiding a food you are allergic to doesn't cure the allergy, it just prevents it from impacting you
- It's insulting to a lot of people that _are_ eating and exercising well, but still battling with Diabetes Type 2
It's wrong and it's insulting.
I'm a pretty big fan of carnivore for this, which has its own detractors, and countering half a century of misinformation of meat and fat isn't the easiest thing in the world. And even then, you may still need some level of supplemental insulin for a long while.
That isn't to say I support general gluttony and laziness... but it isn't that easy, and its even harder when people just assume you aren't even trying or have negativity towards you in general. You try to work out and you get dirty looks and stares... you are eating out (healthy options) but again, dirty looks and stares... it doesn't help.
As a more concrete demonstration, the type 1 genetic risk score (GRS) has good predictability of the risk of someone getting type 1 diabetes. We have linked certain genetic variants to increased or decreased risk of getting type 1 diabetes (and it's mostly in the HLA complex on chromosome 6 that significantly influences the immune system). The AUC (area under curve) of the score's ROC curve is 0.87, which is good. We use the type 1 GRS for patients incoming with type 1-like symptoms to separate out those likely to have rare genetic conditions instead, alongside antibody testing, and it works very well.
The type 2 GRS is very weak in comparison. We haven't found much link between genetics and type 2 risk that we can use to predict the risk. The AUC of the type 2 GRS is only 0.63 in the very best studies, which is a poor predictor.
Having said that, type 2 risk varies quite considerably with race, with South Asians being more susceptible to type 2 diabetes than much of the rest of the world.
Note, an AUC of 0.5 indicates no predictive value whatsoever, and an AUC of 1.0 indicates perfect prediction.
If we're controlling the cells' genomes (which we are), we can add any sort of killswitch (see another comment https://news.ycombinator.com/item?id=45220068 ) that we would like, and this would function better than relying on host immune surveillance. The opposite could be done, making insulin release dependent on the presence of a harmless drug, e.g., insulin release can only happen if a designer steroid molecule is present in the blood.
There are already cell therapies that envisage permanent implantation of modified cells, so I am not sure why a long delay for 'any type of usable treatment' would occur. The structure of this need not be analogous to a stem cell transplant; you could imagine injecting new cells intramuscularly every few months.
The costs to develop this are incurred during development (unlike the autologous therapies that require extensive, expert-level analysis for each new patient). I'm not sure that we can compare the current levels of investment in autologous gene editing to this product.
So, a subscription... ouch.
I get the medical advantages, but it still sounds as easily abusable economically.
You are correct that current cell transplant therapies exist, but I don't believe any before have contained these immune escaping edits and I believe all of those treatments are cancer treatments which allow for a different level of risk. Diabetes is a very serious disease but a quality of life treatment does exist and having cells result in a potential cancer in patients would not be acceptable as an outcome.
> once you start adding more than one item to a cell it doesn't always work out.
Very true, but the amounts of money at stake would justify the relatively inexpensive cost of hooking cells up to the already-available ER/TR-responsive gene elements.
> but I don't believe any before have contained these immune escaping edits
Hard to say, I'm not an expert on immune escape. It's an old idea, however, so I imagine it's been used in other pre-clinical or Phase 1 settings.
> I believe all of those treatments are cancer treatments which allow for a different level of risk
I imagine you're speaking about allogeneic treatment? Either way, this isn't true at all - here's a list of current treatments for diabetes alone:
The other thing a HbA1c measurement isn't so good for is detecting blood sugar spikes (which are really bad for you) and distinguishing that from a constant slightly higher blood sugar level (which isn't such a big deal). For instance, there's a reasonably rare condition called GCK MODY which causes the body to have a slightly higher blood glucose "set level", which shows up very clearly on a HbA1c measurement, tends to get clinicians to panic, and gets patients put on drugs or insulin which they do not need and in fact is harmful to them. My lab does many genetic tests for this condition (among others) and a fairly common message back to the clinician is to take them off all treatment.
Of course this is similar to ongoing lack of understanding in terms of cholesterol health. I've learned to pretty much only care about my TG/HDL ratio.
Aside: my mostly carnivore/keto diet is pretty much the only course of diabetes treatment that has worked well for me over time... Trulicity/Ozempic ruined my life, and I've responded badly to very badly to almost every medication I've ever been given.
Neat stuff!
To gene-edit these cells, they had to use a lentivirus vector -- a (limited form of a) class of viruses that notably includes HIV. These viral vectors work by splicing themselves into random places in the host cell's DNA. Which is fine, except that there's a non-zero chance that in the process, the virus will initiate a cancer.
When you combine that with a cell deliberately engineered to hide from the immune system, you have the ticket to a very bad time.
The transgene engineering is totally possible without a viral vector. We engineer cells all the time with recombinase based editing methods for targeted safe harbor insertion of transgenes https://www.nature.com/articles/s41551-024-01227-1. This stuff just permeates through the community slowly.
> Although the research marks a milestone in the search for treatments of type 1 diabetes, it’s important to note that the study involved one one participant, who received a low dose of cells for a short period—not enough for the patient to no longer need to control their blood sugar with injected insulin. An editorial by the journal Nature also says that some independent research groups have failed in their efforts to confirm that Sana’s method provides edited cells with the ability to evade the immune system.
I’ve had T1D for more than 30 years and have seen every headline under the sun with a “cure” always sometime in the next 5 years, so my expectations are properly tempered.
Still excited by it but a long way from clinics handing this out as a solution (if it’s viable).
1. If the effect is real. i.e. had the patient not been given the injection, would his/her condition improve spontaneously.
2. Assuming the effect is real, what are the circumstances that make the treatment work for this person.
Not to be overly dismissive of the good work but it is too early to be optimistic about this given the above and the fact that the results were not replicated out of Sana suggest that there is a lot that we need to work out before this becomes a viable treatment for the masses.
The harms of hyping this up is that readers will get their hopes up and then be disappointed when things don't pan out as do most scientific endeavours. Overtime, readers will learn to distrust anything that is being reported because 90% of which do not translate to real world impact. It is hard to get the nuance that "science takes many many failures and iterations" to the public and the more likely outcome of such reporting is general distrust of science when things don't go the way that is hoped for.
m3kw9•4mo ago
kingkawn•4mo ago
bentt•4mo ago
mezeek•4mo ago
javchz•4mo ago
Type 1 is a different story. It’s the lack of natural insulin production (due to a damaged pancreas, autoimmune or other causes), basically the opposite problem to type 2, and no amount of lifestyle changes will replace of need of insulin doses.
kulahan•4mo ago
Unfortunately, there's a serious time limit on this news, as the disease does permanently damage your cells, but in a way that's not terrible. It's probably easier to be shocked by a diagnosis into a lifestyle change than to find out now and undo 30 years of living with daily insulin injections anyways.
snarf21•4mo ago
toomuchtodo•4mo ago
CyberDildonics•4mo ago