There are always going to be people whose reason is “because we can”. Going to Mars has, on the scale of a human lifetime, only recently become vaguely feasible. As someone who works in STEM, I’m generally on the side of new technologies unlocking things, though I don’t doubt that population and environmental shifts in the home territory can tip things over from a few crazy dreamers to a more coordinated expansion.
More data sounds better, but especially in a medical context, you have to be careful, because false positives have consequences. The PSA test is no longer broadly recommended for prostate cancer screening [1]. What harm could it do, you know more about your body, even if it's a noisy predictor? Most prostate cancer is slow growing, and something that men "die with" rather than "die of", so treatment can make for worse outcomes, without clear benefit.
It's not clear that we have the health infrastructure in place to know what to do with frequent, low resolution, whole body scans of the human body. How often do anomalies show up and then go away? How often are anomalies purely a scanning/data processing artifact? Who reads the scans and makes recommendations about follow-ups, if any? I think this is the kind of thing that sounds exciting and with low direct risk, but with all kinds of questions that are not only unanswered, but apparently unconsidered.
Stearates aren’t microplastic plastics, though, they’re just similar enough under a microscope and in some chemical analyses. Without knowing which stearates glove manufacturers use (or what exactly it is about microplastics that is harmful), it’s difficult to to say whether the stearates will have the same harmful effects.
I’m curious how you came to that conclusion. While he’s certainly not in the pantheon of best presidents, he ends up around the 75th percentile in rankings by historians. Even subtracting a few spots, he’s nowhere near close to “one of the all-time worst“. Or are you faulting him for not resigning when incapacitated by a stroke?
I don’t see a straightforward way this would actually help with the cleanup. A hypothetical microbe that “eats” oil would be useful in an oil spill as would chemically break down the oil and harvest its carbon.
A radiotropic fungus that’s in TFA can’t meaningfully affect the rate at which nuclear decay is happening. What it can do, supposedly, is to harvest the energy that the nuclear decay is releasing; normally there’s too much energy for an organism to safely handle.
At the risk of vastly oversimplifying, you can’t plug your phone into high voltage transmission lines. These fungi are using melanin to moderate the extra energy, stepping it down into a range that’s useful (or at least minimally harmful).
To tag on, the economy gives us more than just physical "stuff" (though that's one of the easiest things to measure). Do you enjoy travel? How about clean water, yoga classes, or therapy? What about the ability to post a message to complete strangers over the internet? As much as we could, in theory, do all of those things without having an economy to support it, money is a shockingly good way to give you whatever it is that you value.
Yes, some people have more money than they know what to do with (and, I would argue, than is good for them or us), but I've seen no reasonable suggestions that as many of us can have what we want without a reasonably open market economy. I don't think we're at a local optimum in the fine details of the rules for that economy, but I don't think moving to a whole different part of the possibility space is likely to be better than where we are now.
There’s very often a comparison to the somatic (i.e. non-cancer) genome of the same patient. It’s a great way to quality control that there wasn’t some sample mixup in the lab.
Transmission of cancer is rare in humans—if it were not, it would make someone’s career to find many cases of it. While we can’t say that all sheep are white, we’ve looked at enough of them to say that black sheep are not common. Furthermore, it’s very clear how the Tasmanian devil cancer is spread—it’s around the mouth while they are biting each others faces; it’s not as obvious how one would spread most human cancers.
That assumes that what causes the false positive is some kind of analytical noise in the test. The bigger concern is biological noise that would persist if you tested the patient again.
It might still be useful to know you have weird protease activity that isn’t cancer derived, but the more of these tests we do, the more likely it is that for every person, there’ll be at least one non-cancer oddity that looks like cancer signal for at least some test.
Just to be clear, most drug trials for anything where we have an effective treatment are not “new drug vs placebo”, but instead “new drug vs standard of care”. Thus the goal being to prove it’s better than what already exists.
I always hesitate to ascribe motives to non-human animals, but the butterfly shouldn’t particularly “care” whether the pollen gets from its body back to a plant. If the butterfly is eating the pollen, then maybe there’s an advantage to hoovering up more just by getting close, but that doesn’t mean it wants to give any pollen back to other plants.
On the other hand, if the butterfly is eating the nectar and the pollination is an ancillary effect, then you have to start invoking more complicated mechanisms. Maybe successful pollination of the plants increases the food supply later? Maybe the flowers are not neutrally charged, but instead become oppositely charged when the pollen is ready to bias pollinators to come close at appropriate times? You can always construct some just-so story that fits the observed evidence, but where it becomes science is when you make predictions and test them.
I’m not OP, but the startup ethos of the last few decades has been to move fast and break things, fake it til you make it, and generally operate on the bleeding edge to deliver incredible products (and, occasionally non-credible, cough Theranos).
My concern would be that the team would cut safety corners until the probability of success just barely rises above some threshold, rather than engineering everything to have as low a risk as is feasible. Is 0-1atm easier than 1-infinity atm? Yes, but that just means you can cut more corners.
The claim, as I understand it, is that commerce within a megaregion is more tightly integrated than commerce between megaregions. If this is the case, there should be more trade between Baltimore and Boston than Baltimore and Raleigh (controlling for population/GDP/infrastructure, I suppose, and therein lies the rub), despite the fact the latter pair is closer.
While I agree that you want to be wary of any particular claims, and more study is warranted to establish the effectiveness of any particular intervention based on data, there’s a Bayesian justification to looking at otherwise unexplained deaths. “When you have eliminated the impossible, all that remains, no matter how improbable, must be the truth.”
In addition to the comments proposing some other kind of exercise as a control group, I’d want to see whether “being prescribed something but then being waitlisted“ prolongs depressive symptoms compared to, say, “being prescribed and receiving {placebo intervention}”. Our health care system is, itself, crazy making.
In addition to the sister comment (that I 100% agree with) that publicly funded research ought to be in the public domain, if the technique is broadly useful I’m sure that companies can find patentable optimizations to the equipment or protocol.
23andMe works by checking ~1M sites along the genome, and using known correlations with pathogenic variants. This Invitae test actually sequences the (coding portion plus a bit of) the genes involved, and can detect rare[0] mutations. Additionally, Invitae puts a ton of effort into determining whether any particular variant (of which you certainly have very many) is benign or pathogenic.
Invitae has argued that (especially in certain under-represented populations), the 23andme approach is going to miss a lot of important variants [1].
_disclaimer: I’m a former Invitae employee and still holding the bag on what used to be a lot of stock . All opinions are my own. _
[0] Rare on the population scale. To a good approximation each person has only 0, 1, or 2 copies of any given polymorphism.
While the Linear, No Threshold model is relatively widely used by regulatory and safety bodies, evidence for it (or any other competing mode of low dose exposure) is quite weak.
chr6:41,515,652G>C, GRCh38, rs9367106 Is the lead variant in the association study, but that doesn’t mean that it’s the causal variant. Genome Wide Association Studies line the one described here are relatively blunt instruments that are hard to interpret on their own, but can point towards next steps. Some plausible hypotheses are:
1) one or several mutations in the protein FOXP4 affects susceptibility to long covid [edit: reading the paper more after my coffee, the affected region isn’t actually in the coding region of FOXP4. “ no variant in LD with the lead variant is coding”]
2) a variant in a region that controls expression of FOXP4 affects long covid.
3) variant(s) in a gene near FOXP4 is actually what’s causing long covid (though this is somewhat less likely given the locations of the snps that are associated).
To make this more complicated, genes starting with FOX are usually transcription factors, meaning they control the expression of many other genes. So it’s certainly plausible that it’s a hinge point that controls a large, amorphous downstream response. I don’t know much about the biology of this gene in particular.
What one could say with moderate confidence after a 23andMe style test (assuming they have one or more associated variants) is that you might be at elevated risk for long covid, but only about twice the likelihood as the general population, assuming I’m reading the figures right. Not insignificant risk, but not perfectly predictive either. Where this result is more useful is directing further studies on the mechanism of long covid and (once we understand that) potentially ways to treat the underlying cause.