KempyKolibri

What's the argument here, that achieving mastery sufficient to get to a 4 second Rubik's cube solve requires at most 4 seconds' attention span?

If you think I’ve made an error or am missing something, then you should be able to point it out, no?

You’re the one that used the term, not the author.

That’s not “Random Controlled Trial”.

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).

Where is it defined as "Random Controlled Trial"?

“feels more dignity getting beaten down and bullied by strangers or peers than confronting them openly or berating them publicl” is rather hyperbolic and (in my opinion) doesn’t capture what’s going on here.

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.

Lol have they seen what we do to animals for taste pleasure?

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

Plenty of those in tech - in fact I think it may give people unjustified confidence that they’re more rational than others.

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

Welcome! Thanks for being pleasant.

Have done so! It’s basically just what I said - signs point to reverse causation.

Yeah, this is a good example of what I’m talking about - you take a bunch of people at risk of diseases that lower LDL-c as a result of having that disease.

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”.

I've spent enough time around keto people to invoke Poe's law on that one.

Problem with eating lots of animal fats isn't necessarily weight gain, but increased risk of ASCVD from raised LDL-c/ApoB. Can't really see/feel that until you keel over with an MI.

Maybe in some cross sectional or cohort studies with poor adjustment models we might see such a signal? Several states of poor health drive LDL down because of those diseases (e.g. having cancer can result in lower LDL, having a heart attack can massively lower LDL), so if we look at study designs that don’t take this into consideration, it can appear that high LDL is protective because of reverse causation.

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?

“So, are you exercising much?”

“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”

Thanks for sharing! I’ve been thinking of making something like this for my own purposes, so I’ll be looking over this with great interest.

Well that would depend on what you mean by “not working”. It seems like the US regulations are generally doing a good job of keeping toxic products out of the food supply.

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.

This is what regulation already does (quite effectively too, at least over here in the UK). We already know that harmful substances aren’t likely to be present in our foods thanks to regulatory checks.

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.

Even that wouldn't be sufficient. Look at the heterogeneity in dairy - the same amount of SFA in yoghurt has a markedly different impact on LDL-c compared to butter, likely because of both the calcium content of the yoghurt _and_ the actual molecular structure (non-churned dairy has intact milk fat globule membranes).

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.

I'm torn - the anti-UPF crowd is increasingly tying themselves up in knots with this kind of thing. Potentially this causes even more public confusion and avoidance of yet more perfectly healthy things because they're understandably lost trying to navigate what the orchestrators of the moral panic around UPFs, artificial colours, non-organic foods etc claim they should eat. I see people swapping wholemeal UPF bread in favour of homemade white bread on social media all the time already!

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.

The thing is, the 0.08% doesn't capture the total potential risk reduction - only the risk during the timeframe of the study (8 years in this case). Where we're talking about exposures and outcomes that stack over time (exposure to LDL and heart disease being a classic one) the absolute risk is, in my opinion, more misleading than the relative risk.

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.

Welcome, always nice to talk about this stuff - nutrition science is a very interesting field because it's such a slippery subject to get right. Every day's a school day and I'm never as right as I think I am!

That take on eggs sounds about right regarding numbers per day and risk. If you look at the ACM risk associated with various food groups in figure 2 from this paper (https://ars.els-cdn.com/content/image/1-s2.0-S00029165220492...) then you can see the ACM risk hitting significance at around 55g/day, which is about 1 large egg.

Dave Asprey is such a wild dude. Who is eating rice for protein? Bizarre straw man!

As I understand it there's no good evidence that n3:n6 ratio matters, _as long as both are at adequate levels_. Studies showing the ratio to be of concern achieve a "low n3:n6 ratio" by low n3, rather than high n6.

Eggs are believed to lead to adverse outcomes because of: 1. Their high cholesterol content. 2. Their SFA content.

I'm not sure what you mean by cholesterol being rebutted. The only thing like that I'm really aware of is the dietary guidelines de-prioritising dietary cholesterol, but that decision was made because when making DGs, people want to focus on the biggest levers we can pull. Dietary cholesterol _does_ have a negative impact on health, but it also has a threshold effect at around 400mg/d after which it has considerably less impact (unless you're part of the ~20% of the population who are "cholesterol hyper responders").

Because most people eating a SAD are already at that threshold, the decision was made to take dietary cholesterol off the headline recommendations, but if you read the details in the DGs and the meta-analyses that drive them, they still point to lowering dietary cholesterol as a smart health move.

I frequently see this change portrayed as "no longer recommending the lowering of dietary cholesterol" or "admitting they were wrong about dietary cholesterol", but that's not really what happened.

No worries! Nutravita vegan omega 3 or my protein vegan omega 3 plus both have DHA and EPA and are the best value I've found in my travels. While the per-pill dose is lower in the MP stuff, if you wait for a sale and combine that with a stackable discount code (BEAST is usually a good one) it should end up cheaper than the Nutravita stuff.

There is zero evidence in that article, or anywhere else that I’ve seen for that matter, that omega 6 is harmful. The evidence provided there would perhaps suggest that omega 3s are beneficial, but that’s about it.

I would disagree with this. While we can always point to examples where epi did not align with RCTs, this doesn’t capture how discordant (or not) this relationship is in the aggregate.

Thing is, we actually have empirics on this, and in reality observational studies comparing intake to intake are concordant in over 90% of cases, so I think we actually have a very strong case for making causal inferences based on replicated epi findings:

https://www.bmj.com/content/374/bmj.n1864

The levels of n3s we usually see associated with benefits tend to be the equivalent of 1-2 servings of fish per week.

Depending on where you source your omegas from, potentially zero impact!

To be clear my preference would be to source n3s from algal supplements and, once food safety testing for humans is complete, n3s from GM rapeseed.

In time I hope we end up with lab meat/plant-based meat alternatives that use these n3s so we can get the benefits of fish without the environmental and ethical concerns of getting n3s from fish.

Sure, because both are true (although that 0.08% is only over 8 years of known omega 3 consumption - as timescales increase the absolute risk moves towards the relative risk).

That 0.08% reduction would mean approximately 28,000 fewer EOD cases - not to be sniffed at!

Just get an omega 3 supplement that has a good amount of DHA and EPA. There’s not as much evidence to support it as there is to support eating fish, but that’s more due to a dearth of research on the subject than because the evidence suggests it has no effect.

Unfortunately it tends to be more expensive. I have recs if you’re in the UK but not much use otherwise!