Win10 IoT LTSC does not cover all use cases though.
When it comes to gaming, for example Windows Mixed Reality is not included and cannot be installed afterwards (but then again, Microsoft dropped it from Windows 11 too, so no loss there).
Only way to keep it is staying with consumer Windows 10 or use 3rd party software like Oasis.
Problem with 10 LTSC is the fact that it's based on 21H2, and there definitely isn't going to be a feature update for it, now that 11 LTSC is out. Some games already require 22H2.
The later Intel Macs with T1/T2 chip also come with a number of caveats on Linux. Don't expect those to work out of the box with standard Linux distros.
I think the reference was maybe about the butter vs. margarine controversy? That margarine was lauded as more healthy, but turned out to be actually less healthy than butter, due to hydrogenation producing trans fats which elevated cardiovascular risk.
Since mid-1990s, margarine no longer contains appreciable amounts of trans fats.
Butter also contains trans fats but these are ruminant TFAs which I understand are not so bad.
This is why despite butter composition being worse "on paper" there is no empirical observation that it is less healthy than plant margarine.
Worse is that artificial sweeteners increase feed conversion efficiency (an effect which has been known since 1960s experiments with rats and Cyclamate), and are for this reason frequently added to animal feed.
For humans however this effect is undesirable, as it exacerbates the problem which they are supposed to solve.
This seems like a fancy way of saying “it’s a cheap approach to make animal feed taste better, so the animals eat more and thus gain more weight/produce more milk/etc”.
What impact would pouring a bunch of refined sugar on animal feed have on feed conversion efficiency?
What do studies on humans say on the actual real-life effects of people using artificial sweeteners instead of sugar?
If you permit me to be a bit glib, if we outlawed everything that people think tastes good, almost no one would overeat, and we would have solved obesity. Without going to that extreme, surely there are other interventions that can help limit the problem of overeating, and isn’t there evidence that artificial sweeteners are actually helpful in doing that? Remember that the starting point for humans isn’t hay and the slop we feed to pigs, it’s ice cream and McDonald’s.
> “it’s a cheap approach to make animal feed taste better, so the animals eat more and thus gain more weight/produce more milk/etc”.
No, not at all.
Feed conversion efficiency is the body weight gained per unit of feed consumed. If you add artificial sweeteners to animal feed, they will gain more weight when consuming the same feed, or gain the same weight when consuming less feed. This leads to cost savings for the farmer.
This observation may be a bit surprising as artificial sweeteners have 0 calories. But then again, antibiotics and growth hormones have the same effect.
> What do studies on humans say on the actual real-life effects of people using artificial sweeteners instead of sugar?
Cheers. Do you have any citations handy for the old studies? I’m open to being wrong, but after some very brief searching and reading I’m skeptical that they properly controlled for increased feed intake (possibly due to palatability) to conclusively determine that some other mechanism was at play
DALDERUP, L., VISSER, W. Effects of Sodium Cyclamate on the Growth of Rats compared with other Variations in the Diet. Nature 221, 91–92 (1969) https://doi.org/10.1038/221091b0
But of course the manufacturers of feed additives also extensively studied which artificial sweetener compositions achieve body mass gain / feed efficiency increase for which group of animals. There is an extensive review e.g. on pigs here:
> (i) The food or beverage contains 10 percent or greater of total energy from saturated fat.
Interestingly, dairy products like butter are explicitly allowed, despite the fact that 50%+ of its fats are saturated
> I'm not a nutritionist, but there are some basics that are braindead simple that don't involve banning Sucralose.
I'm in favor of banning artificial sweeteners. Just look at why they are used in animal farming to see why it is a bad idea to randomly add them to human food.
If someone is habitually consuming sugar sweetened beverages, replacing those with ASBs will, the evidence strongly suggests, reduce your risk of obesity and various chronic diseases.
We can say "just don't consume either" but we have decades of attempting such policies that shows people don't work that way.
Someone who wants to drink a can of coke will drink a can of coke, why would we ban the healthier option?
The evidence actually suggests that soft drink consumption is equally associated with higher all-cause mortality and artificially sweetened is every bit as bad as sugar sweetened. Even when controlling for smoking status, BMI, physical activity, and alcohol consumption.
It was suggested elsewhere that the primary mechanism for soft drink associated mortality is acidic fluids causing tooth decay, which in turn causes cardiovascular disease. (Bacteria entering the bloodstream through inflamed oral mucosa, and forming plaques along arterial walls.)
And the evidence for artificial sweetener benefits on population level is practically non-existent. In fact animal farming points to a detrimental effect.
You have to be very specific in the intervention you’re either looking at in an RCT or modelling in a prospective cohort study. We wouldn’t expect adding NNSs to a diet to improve much (perhaps some benefit from carbonated ones on body mass). We need to investigate/model replacement of SSBs with NNSs.
When we do that we pretty consistently see benefits. Good overview as a response to the WHO position paper here that goes over that evidence base: https://mailchi.mp/b30c80ddf8ba/who-as
Yes, replacement can work to adjust weight trends in a controlled setting.
But all empirical observations so far show that artificial sweeteners in people's diets do not have the desired effect when people's food and beverage intake is uncontrolled.
In fact results from animal studies are that you can even substitute part of the feed with just the artificial sweetener to achieve the same body mass gain. And this is known since 1960s with Cyclamate and rats: https://doi.org/10.1038/221091b0
More studies in the meantime varied a bit on the size of the effect, and some were inconclusive, but generally the results held up.
So no, artificial sweeteners do not help to manage weight. What the studies actually show is that controlling people's intake does.
Let me get this straight: your epistemic framework is such that when presented with RCTs in humans showing positive effects, observational studies in humans showing null findings (likely because of poor adjustment models) and negative associations in rats, we should conclude “artificially sweetened is every bit as bad as sugar sweetened”?
No. What I say is if we introduce a public health policy, then we need to take human behavior and adherence rates into account.
Example: Abstinence is 100% effective against STDs and teenage pregnancy in any controlled setting. That does not make it a good public health policy to tell teenagers to abstain from having sex. In fact despite condoms having lower efficacy than abstinence, teaching people the proper use of condoms is overall more effective.
If we want to solve obesity then randomly adding/substituting artificial sweeteners to human food will not work. Instead we need to reduce access to hyperpalatable foods, which can be done through economic means (e.g. taxes).
Ok, so if I understand correctly, your argument is: in order for you to support a public health intervention we need to see evidence that such an intervention results in positive outcomes in a free living population with ad libitum consumption, regardless of the evidence in controlled settings.
So what’s the evidence that banning artificial sweeteners leads to positive outcomes in a free living population, considering you said: “I'm in favor of banning artificial sweeteners”?
> So what’s the evidence that banning artificial sweeteners leads to positive outcomes in a free living population, considering you said: “I'm in favor of banning artificial sweeteners”?
It depends on the context. In the context of school lunches (which is discussed here) they absolutely need to be banned, same as added sugars. Giving children (sugar or artificially) sweetened meals trains children's palates and shapes lifelong preferences for sweet foods.
Ok, so we already have your standard: in order for you to support a public health intervention we need to see evidence that such an intervention results in positive outcomes in a free living population with ad libitum consumption, regardless of the evidence in controlled settings.
We have your proposed intervention: “In the context of school lunches (which is discussed here) [NNS] absolutely need to be banned, same as added sugars.”
So now we need evidence supporting this intervention sufficient to meet your own goalposts. Do you have it?
I don't know what you are going on about. Empirical evidence is one thing, mechanism is another source of knowledge by which we can shape public health policy. While empirical evidence is valid only for the situation in which it was obtained, mechanism is universal.
For example, we mandate wearing seatbelts in cars in the name of public health. It is however not necessary to do seatbelt on/off RCTs with actual people. How we know that this is beneficial: Because physics, verification through crash tests (with dummies), and because we know that seatbelt mandates increase the frequency of people wearing them.
Going back to the original question, it was clearly shown in observational studies that giving children sweetened food is bad: Childhood dietary habits shape lifelong food preferences, and preference for sweet food leads to worse outcomes regarding chronic diseases later in life. This has been shown in lots of research, both in humans and in animal models:
With randomly adding or substituting sugar with artificial sweeteners there is however no empirical evidence nor known mechanism which supports a public health benefit. In fact the mechanisms we know from animal farming suggest a detrimental effect.
> While empirical evidence is valid only for the situation in which it was obtained, mechanism is universal.
Mechanisms are inferred from empirical evidence, I don't see how you can treat them as two separate categories. For example, in your crash test dummy analogy, verification through crash tests (with dummies) is empirical evidence. Yet under your framework, should we assume that it is valid only for the situation in which it was obtained - only for dummies, not people; in cars pushed towards walls in controlled situations, rather than on public roads?
If you name proxy experiments that support your views (crash tests) as mechanisms and ones that don't (SSB replacement with NNS RCTs) as "empirical evidence is valid only for the situation in which it was obtained" then sure, everything you want to believe is supported by sound science and everything you don't isn't. But the view itself seems to contain a logical contradiction, so you're dead before you've even got off the ground.
I would understand mechanistic evidence in the domain of health science to be in vitro and animal studies. Even if we were to grant that mechanism is universal in this field (which I wouldn't, we frequently see heterogenous results even within the same exposures on the same mouse models, for example), there are thousands of mechanisms that come together to influence the outcomes we actually care about. This is why when we look at translation rates of mechanisms to outcomes in humans we typically see rates below 5% (and is also why pharmaceuticals that work perfectly in animal models barely ever make it to market in humans).
Going back to the evidence you've cited in support of your intervention - the first two (the only ones in humans) are neither looking at NNSs nor an intervention on banning them. So it doesn't meet your own goalpost for "if we introduce a public health policy, then we need to take human behavior and adherence rates into account". In the rationing example, you have an entirely different context - one in which people literally cannot purchase large amounts of sugar. This would not be the case if we were to ban NNS today.
Your third study was in mice which, as discussed, has an incredibly low chance of actually translating into human outcomes. I don’t find “we have evidence in RCTs that NNSs are beneficial but there’s this mouse study that says otherwise so let’s ban them” a convincing argument.
So again, any actual evidence in support of your proposed intervention? How do we know, for example, that banning NNSs won't just lead to higher sugar consumption and adverse outcomes, since we know from RCTs that substituting SSBs for NNSs improves health outcomes? If all those consuming your banned substance now switch to SSBs instead of their NNSs, congratulations, you've just worsened health outcomes.
In that case, no "we" don't, because I am reading this and I do not agree with this "standard" nor your characterization of what I wrote.
> Mechanisms are inferred from empirical evidence, I don't see how you can treat them as two separate categories. For example, in your crash test dummy analogy, verification through crash tests (with dummies) is empirical evidence.
This is not how it works. Crash tests are used for validation, but the data from crash tests is generally not used to infer mechanism. Physicists don't come up with a new theory of mechanics every time a crash test has an unexpected outcome.
> If you name proxy experiments that support your views (crash tests) as mechanisms and ones that don't (SSB replacement with NNS RCTs) as "empirical evidence is valid only for the situation in which it was obtained" then sure, everything you want to believe is supported by sound science and everything you don't isn't.
I don't think you understand. If you want to support a public health intervention you either have the empirical data with a relevant endpoint,
or you can point to mechanism which bridges the part between the data that you have and the outcome which you want to achieve.
When it comes to pharmaceutics and food additives, our mechanistic understanding is insufficient so we often have to resort to empirical studies on humans, including RCTs (Pfizer's Covid vaccine trial had tens of thousands of participants) and also observational studies at population level. And it is the last part where artificial sweeteners fail to show benefit so far.
When it comes to seat belts, our mechanistic understanding is sufficient so we don't need to resort to empirism. Yes we perform validation but only to check if there are no design oversights in the vehicle nor shortcomings with the simulation software, typically in a low triple-digit number of crash tests. But no humans involved and especially no control arm with humans.
It does, because again, mechanism is provided. You could say that the study has weak evidence for the mechanism and it works like that perhaps only for sugar. Because that some mechanism is found in mice does not mean it is also found in humans, and it would be a fair point. This is why many species are tested and so far the results held up (testing humans takes too long for obvious reasons).
Sorry, I summarised what I thought was your goalpost earlier in the exact same words and you didn’t correct me, so I made the assumption in subsequent replies. I’m not interested in straw manning your argument, just trying to understand.
I’m going to pass on the crash test dummies bit. You’ve misunderstood the point I was making, but it could be poor communication by me and I think the point is becoming increasingly tangential.
> When it comes to pharmaceutics and food additives, our mechanistic understanding is insufficient so we often have to resort to empirical studies on humans, including RCTs
> It does, because again, mechanism is provided. You could say that the study has weak evidence for the mechanism and it works like that perhaps only for sugar. Because that some mechanism is found in mice does not mean it is also found in humans, and it would be a fair point. This is why many species are tested and so far the results held up (testing humans takes too long for obvious reasons).
So you don’t feel you’re being straw manned again, can I get a clear answer to this: is your argument that if we stack together sufficient numbers of mechanistic animal studies we can be sufficiently confident enough in the translation rate of such studies to humans that we can roll out public health interventions without any evidence of efficacy in human populations?
The fact that you want to ban everything under the umbrella term of "artificial sweeteners" is why I think you have a fundamentally unscientific approach. Your other responses seem to suggest you just have something against sweet things (even when you seem to acknowledge there are other factors at play like acidity and tooth decay)
I'm saying this as someone who rarely consumes these things..
> Just look at why they are used in animal farming
I don't know anything about the science behind that - so I'm not in a position to judge. Did they try every possible "artificial sweeteners"? How about if there is another one discovered next year? Is it going to be pre-banned even if it doesn't have these drawbacks?
These aren't like the same substance tweaked a bit where you're in a endless ratrace with the chemists.
> Your other responses seem to suggest you just have something against sweet things (even when you seem to acknowledge there are other factors at play like acidity and tooth decay)
We are talking about school lunches here. Sweet meals are bad (whether sugar or artificially sweetened) as it trains children's palate and shapes lifelong preference for sweet food. Hence I support banning artificial sweeteners as California plans to do.
When it comes to sweetened drinks, switching from sugary to artificially sweetened is not empirically shown as beneficial. This is the hurdle that proponents of public health interventions to replace sugar with aritificial sweeteners need to overcome.
> Did they try every possible "artificial sweeteners"?
The study which I linked in another reply looked at various commercially available artificial sweeteners and some combinations. https://doi.org/10.3390/ani14203032
This is necessary because not every species' taste receptors respond to every type of sweetener, e.g. rats do not respond to NHDC.
> These aren't like the same substance tweaked a bit where you're in a endless ratrace with the chemists.
Well it depends on who has the burden of proof that a certain food additive is safe and does not cause undesired long term effects, especially in children.
Bread is a bit of an exception here, as it undergoes extensive mechanical (milling), biochemical (fermentation) and thermal (baking) processing. Yet it does not count as ultra-processed.
Bread is made from dough, which is mainly made from flour (the "minimally processed" food), which is made from grains (the unprocessed food)
It definitely stood out as a bit of a confounding example. That combined with the emotive language used in the classification names makes me a bit wary of this way of classifying food.
Nested virtualization is a problem for systems with AMD CPUs I think, Windows 10 Hyper-V supported nested virtualization on Intel only. Since Windows 11 it is supported on AMD too.
When it comes to gaming, for example Windows Mixed Reality is not included and cannot be installed afterwards (but then again, Microsoft dropped it from Windows 11 too, so no loss there).
Only way to keep it is staying with consumer Windows 10 or use 3rd party software like Oasis.
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