inblue01

inblue01 t1_j40rg0s wrote

I don't know if you're familiar with the scientific publishing world, but there is a reason why this is published in a very cryptic journal with a dysmal impact factor of 0.7. We can discuss why this review is extremely weak in private if you wish :) And very importantly, and maybe you missed it, the abstract talks about combination of KD with other therapeutic approaches.

>Combining a ketogenic diet with standard chemotherapeutic and radiotherapeutic options may help improve tumor response, although more research is needed.

Combination approached have indeed shown promises in some models: for example a ketogenic diet greatly potentiates PI3K inhibitors in some models of cancer but is insufficient to reduce mortality by itself: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6197057/

This is undoubtedly an interesting research topic and it is very likely that diet can help in some (if not many) therapeutic settings. But claiming that it is enough to cure cancer by itself is just dangerous and wrong.

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inblue01 t1_j3j2zwe wrote

Mostly this: targetting the metastatic process (that is the dissemination of cells originating from the primary tumor) is in most cases irrelevant because a) in the great majority of cases of cancers that will eventually lead to death, the diagnosis occurs when a tumor has already metastasized. This approach won't cure pre-existing mets, which are generally responsible for the lethality of cancer. And b) if you don't have mets yet, in the vast majority of cases, surgical removal of the primary tumor is the obvious solution. The only application that I can see is if you have a non-metastatic tumor which is not operable. It happens but is certainly by far not the majority of cases. So implying that you might stop 90% of cancer deaths is just plain wrong.

There are additional mechanistic reasons but I think that alone is sufficient to relegate this process quite low in terms of likelihood of sucessful prevention of cancer-related death.

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inblue01 t1_j3j1z6m wrote

>However, it is what the article implies.

No, it doesn't: while it is true that cancer death is due to metastasis in 90% of cases, this approach wouldn't affect pre-existing metastasis at all (it only affects the motility of cancer cells, so the propensity of a cancer to metastasize). So if you have metastasis at the time of diagnosis, which is the case in most deadly cancer, this approach is most likely completely useless. And if you don't have metastasis at the time of diagnosis, this approach is also in most cases irrelevant, because the way to go is simply surgical removal of the primary tumor. Diagnosis without mets is generally refered to as stage 1 cancer and often has very low mortality, with some exceptions.

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inblue01 t1_j06z2of wrote

>you could make the case that nobody below 55 had any benefit taking the vaccine if not severely compromised by another illness

Somewhat agree, thus why I was truly irritated by the general vaccination strategy. Yet, I still think that most people generally benefit from vaccination. For example, a very common argument by anti-vaccine people is the risk of pericarditis after vaccination, which is indeed a reality. What they fail to realize is that there is also a risk of pericarditis from COVID, and that risk is much higher than from the vaccine.

https://www.ajpmonline.org/article/S0749-3797(22)00453-6/fulltext

Let's also not forget the sometimes severe (and also unreported) potential consequences of long COVID.

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inblue01 t1_j06srbp wrote

I was certainly not convinced by the general vaccination strategy, and I agree that the roll-out of these vaccines was probably precipitated, but the death rate of COVID without vaccines was 10 times higher during most of the pandemic than with it. Now in 2022, almost everyone has some sort of immunity against the disease, including unvaccinated people, which explains why there was not a big difference recently.

https://ourworldindata.org/covid-deaths-by-vaccination Swiss data here, but it looks very similar in the US for example.

Pushing for general boosters now though? Massive joke.

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inblue01 t1_iy0cn7w wrote

Some good answers here, but one piece is missing : screening!

You are correct: in most cases, the cells will repair the genome in a way that does not suit your downstream applications. It's a matter of probability : one in many cells will, by chance, repair your DNA with your template, or do the desired mutation.

One step that you need to do is to isolate clones (single cells), let them grow to a decent population and then screening (by sequencing and functional testing) these clones to determine which one has the desired insertion/mutation.

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