Maybe but you should assume no, since this has not been tested in the above study.

Vitamin D should be taken with food with some fat in, but there isn't great evidence saying you should avoid taking vitamin D in the afternoon or evenings. Logically, since you make vitamin D from the sun exposure during the day, natural vitamin D levels are probably highest around noon-2pm.

I agree with your post, but There is atleast a difference between low and high doses, with higher doses having the lowest risk.

A dose response relationship is always nice to see.

There's probably no need to specifically watch/screen people born from older embryos. it'll be part of their doctor/patient interactions and there's no real reason to think that stuff stored in liquid/vapour phase of nitrogen would biologically age much at all.

I think you missed the point of my comment. The implication from the comment I replied to was the technical challenge of Crispr in primates was limiting factor, I used the example of current, clinical, use in humans of Crispr as an argument that it's not a technical limitation that prevents more widespread research in primates.

I mean sure, but you said could feasibly be studied since those recent papers - they were feasible models for a long time now.

Risk is minimal, I didn't say there was a risk concern?

CCR5 is useful in cold/flu response and that's a hell of a lot more common than HIV. even in people with close contact with someone with HIV. Hell these days colds and flus are more of a faff than HIV is for those people infected but taking PReP!!

It was such a ludicrously ethically dumb experiment.

It's not the technical difficulty, but the ethical difficulty.

Crispr is already in use in patient cells for things such as Car-t therapy. And we are primates.

Great explanation. Worth touching on this being a reason that a lot of model animal studies don't always scale well to human.

e.g. P53 knockout mice make lots of tumours, give those mice an antioxidant rich diet and they get fewer tumours. P53 is a major component of the antioxidant pathway, so this shows more about p53 pathway than cancer, really.

The fasting bit has you restricting calories my friend.

No no just start a blog about intermittent fasting, cite this study and tack on a bit about your new book.

These aren't the only studies that suggest a benefit to CR, and the mechanism - via mTOR - is reasonable.

Like I said, I agree with you, and do exactly this.

But that's not the point. bombarding People who aren't already active with a big to do list as a way to get fit is a bad idea. Start with little and often with consistency and build from there.

Your attitude will turn people away from a really important realisation.

While I agree with you in principle and practice, you've now added your own stuff on top. In doing so you are perfectly demonstrating why information like this doesnt get communicated or gets lost. People add their own stuff to the proven facts all the time.

Keep it simple. A little bit of intense exercise adds up to good health gains. If People take this up they might see improvements and look to make more gains through other means like weights.

Because all these disease associated genes have functions, we can't just knock them out, they have important work to do. The disease associate variants are just that, a variant of a healthy version of the same gene, which could be all sorts of different things, too much/little expression (Crispr won't do anything here), or a mutation that changes the protein (Crispr might do something here with a lot of additional tinkering).

The other problem is delivery. It's relatively easy in a dish, but doing it to every cell in the body is essentially impossible. If the disease exists in, or can be fixed by modifying, an accessible cell type like say circulating immune cells, then that's the first target for medicine. See for example car-t cells.

Never said it was useless. It's awesome, I use it in the lab. But It's not a cure-all. We can't just "Crispr it" when we identify even a single gene trait genotype caused a certain disease.

No, it causes an indel, which typically knocks out genes. Various modifications to it exist to make use of the cuts to insert a gene, but Crispr is just a technique for cutting DNA in a precise location.

A reasonable case is given through the other studies in the paper to be honest, e.g demonstrating that they have similar transcriptomic signatures to post mortem brains with PTSD.

The studies are not on the people, they're trying to identify genetic targets and generate models to use in vitro. It's completely valid.

I think your comment explained well enough why you had to leave research.

How would knocking out genes help?

It wouldn't be enough for a medical study, trial or intervention or whatever, but it's a different kind of study. They're not studying people or interventions per se, they're studying the neurons/genetics. Having 39 samples for this seems pretty good. If you're suggesting they should have generated neurons from stem cells from hundreds of people ... Good god man have mercy on the lab people!

To be honest I think everyone gets the numbers these days.

Public health has to be based on these sorts of calculations... So obviously (blindingly obviously) 18 people per 100k (what's that, about 18,000 across the whole population?) saved would be a good thing.