I think it’s pointless to quibble about very specific things like this, but that gets thrown out the window when someone claims “Definitions are the very basics in writing, check them before you publish” and then use their own nonstandard definition!

Seems like they wanted to nitpick about term usage when: a) the usage they’re taking issue with is actually fairly commonplace (e.g. https://www.who.int/news/item/27-10-2017-who-to-review-its-i...) b) their own suggested replacement is very heterodox (I’ve certainly never heard anyone call it that).

I think this speaks more to a culture of thinking of other peoples’ experiences/rights/feelings as well as their own.

Whenever I drive in the US I’m always staggered by just how selfish people are on the roads, for example. Is another car very clearly merging onto a highway where it would be easy to make enough room for them to merge? In the UK, 90% of the time the cars on the highway will make room. In the US I’ve literally never seen it happen.

It's not a question of "can we learn to shut up?", it's "will humans ever care enough to even want to learn?".

I engage with anti-science behaviours quite a lot (antivaxx, anti seed oils, etc) and the proportion of engineers I see there is staggering.

They actually acknowledged that reverse causation is a risk here and so ran a sensitivity analysis by excluding patients with less than 5 years of follow up (a nice way of saying “patients who died within 5 years of the LDL-c reading”), the idea being that if these results were likely being driven by reverse causation, you’d expect to see an attenuation of the results.

I’d point out that even if we didn’t, five years is a bit of a weird cutoff - plenty of LDL-c lowering diseases take much longer to kill the average person. Moot point though, because excluding those participants attenuated the result to the degree that the association with LDL-C and mortality became statistically insignificant.

Quite why the authors said “we’re aware that reverse causation is a risk factor, let’s run a test to check if it’s likely influencing the results” and then completely ignored the fact the results suggested it was influencing the findings, is anyone’s guess.

So yeah, basically huge confounder seems to be in play that likely explains the “paradox”.

However, I’m not aware of any evidence that takes this into account showing higher LDL associated with lower ACM. What’s your evidence for such a claim?

“Oh yes doc, I get out for a run most days of the week.”

“Wonderful news, got to look after your heart.”

“Yeah, and with my new butter churning bags, not only do I get to stay fit, but I also consume ungodly amounts of butter!”

“Sorry what”

I’m not sure if your claim is specifically around food colouring. If it is, I’ve not seen any compelling evidence that the food colouring allowed under US regulation is actually problematic for health.

Then we’d be left with checks for substances at levels lower than regulations are concerned with, but I’m not sure why we’d care about that.

Fish has mercury present in it, but increased consumption seems to be associated with positive health outcomes. If the device said “danger, mercury”, what are we replacing it with? Red meat? Sausage? The current evidence would suggest that would be a retrograde step.

I actually think we need to go the other way and look at foods as foods where we have the data, rather than individual components. Most recent dietary guidelines are more "x% of your plate should be vegetables" than "you should consume x% of your energy as cereal fibre", at least in their headline advice.

In an ideal world IMO this would lead to people getting fed up and going back to the dietary heuristics we had before this fad (HFSS, etc). Unfortunately I suspect this will _actually_ result in increasing distrust/refusal to engage with dietary guidelines entirely, and if we do ever identify a novel mechanism by which certain UPFs cause harm that we weren't aware of, no one will engage with it because they're totally exhausted from the current debacle.

For example you see this oft-quoted stat about "statins only increase lifespan by 3 days" based off relatively short RCTs, but this doesn't capture the effect of statin use over decades, which is where we see much, much bigger gains.

It seems to me that both RR and AR are things to take into consideration and we have to be mindful of the shortcomings of each.