> The EU has already defined dairy items milk, butter, cream, yoghurt and cheese as "products secreted by mammary glands"
I think they should just label things more explicitly like this - accelerate veganism 100x when people in the supermarkets have to choose between “pressed soybeans” and “mammary gland secretions”.
Two different things. If you don’t want to eat animal products for ethical reasons but you want something high protein and/or similar in taste/texture to a beef burger, eating a vegetable stir fry isn’t going to cut it. That’s what these products are for.
Not only is the study itself very interesting, but it does a great job going over the evidence landscape on UPFs and food at the current point in time.
Dr Dicken is very clear that at the moment, in his view, they have insufficient evidence to make policy decisions like this, a view that has been echoed by pretty much all academic institutions when they’ve helped inform recent dietary guidelines.
Making big sweeping moves based on flimsy evidence is a good way to make people wary of following dietary guidance at all. After all, what’s the point of listening to “the science” if they turn around in 5 years and say “whoops, turns out we were wrong”?
Be aware that the science on this is evolving pretty quickly.
A study came out recently that showed when folks ate a designed diet, one with and one without UPFs, they found the UPF diets resulted in a few additional lbs of weight gain.
The study accounted for a ton of variables. It showed that UPF calories lead to weight gain when consuming the same number of unprocessed calories.
I think, at the current moment, there is enough evidence to support guidelines to avoid UPFs for the most part. Idk about banning but I do think it'll eventually get there, at least in schools. But who knows? American lunches are garbage in the first place
I’m not an absolutist on this myself, if convincing evidence comes out then I’m happy to change my mind. I have no horse in this race besides wanting people to stay healthy. I’m just not currently convinced the UPF category adds much to our existing dietary guidelines.
Avoiding UPFs can serve as a reasonable heuristic as it can help you avoid HFSS foods, but you could also easily make some adverse switches following such advice.
I’m not sure that study really supports the inference you’re making re: calories and weight gain. The UPF diet had ~15g fibre/1000kcal less than the MP diet, so for an individual consuming 2500kcal/day there’s a 150kcal difference of energy per day that doesn’t seem to be accounted for by the studies methods (could be missing this in their calcs though?).
So yeah, if we don’t equate things like this, things look bad for UPFs. But what is the “UPF” category adding here. We don’t need it to know that if more calories are consumed as fibre in an otherwise calorie-equated diet, you’ll lose weight relative to the low fibre diet.
> and yet when Americans set foot on European soil the first thought they have is 'everyone is so thin'.
I’m not sure how this interacts with the point I’m making.
> if there's any misstep here, it's not focused enough on sugar (which is a hard drug for kids) .
Sure, free sugars are associated with risk (which is reflected in dietary guidelines). Plenty of UPFs are not (which is why they generally aren’t flagged as a concern in dietary guidelines).
Outside of causing an imbalance (which would require a LOT of salt), there’s nothing bad about a lot of salt. People have been eating tons of salt for centuries.
> refined flower
Not sure what definition you’re using here so this might not be ideal, but probably fine. People have been milling for centuries.
> soya lecithins
Made in a lab about 100 years ago, and its primary use is to increase profits via long shelf life (increasing shelf life could be a noble goal, ie freezers are great). We have billionaires flying private jets around. Redo some resource allocation and we don’t need soya lecithins.
Much modernity has 0 respect for Chestetons fence. On top of that, nutrition science is basically a social science in terms of accuracy (not a dig, it’s very hard). Many “advances” today are purely profit motivated and don’t pay enough respect to the people’s wellbeing. We should be skeptical of changes done to make the rich richer.
What’s your goalpost for evidence here, I.e. what would it take to convince you that salt consumption above the levels indicated in dietary guidelines is harmful?
Actual studies that isolate salt consumption as a variable and show worse outcomes from more salt would be a start.
Every study I've looked into that purported to show salt was a problem did not isolate salt, and the most likely reason IMHO that the "less salt" group did better was because they ate less ultra processed food and more natural food.
When we scale out to what I believe to be a superior intervention - replacement of sodium with potassium, we have really robust data. The SASS trial (https://www.nejm.org/doi/full/10.1056/NEJMoa2105675) showed reductions in stroke and CVD incidence from consuming salt substitute, along with reduction in all cause mortality.
I have a real salt taste - if I had no care for health outcomes I’d absolutely cover my food in it! However I think the evidence in favour of reducing or, ideally, replacing it with potassium-heavy substitutes is really convincing.
Thanks - I'd not seen DASH-sodium but only the DASH study whose samples it's based on.
Having read the study now: DASH-sodium barely indicates anything about sodium independently. It looks at three biomarkers which _correlate_ with cardiovascular disease, and finds that reducing sodium from high to low levels for four weeks reduced one of those biomarkers by 19%, _increased_ another biomarker by 9%, and didn't change the third. You could say that this suggests higher sodium increases cardiovascular disease risk but that seems like a stretch when if you'd picked a slightly different set of CVD-correlated biomarkers you would have got exactly the opposite result.
Even if the results had been more convincing, the methods are not - it's an extremely short term study and looks only at correlative biomarkers and not at actual health outcomes. There's no meaningful way to quantify the impact based on this.
The potassium study is indeed interesting. It shows among people who already have CVD, a reduced risk of death of 12%. I think it's pretty well known that modern diets have a significant electrolyte imbalance, i.e. not enough potassium per sodium. I do supplement potassium for this reason sometimes and recommend it, though I'd prefer to just have a ton of natural nutrient dense food available and not feel like I need to. So we're in agreement on that one. That said I don't take that study to strongly show that sodium is a primary driver of CVD - it could just as easily be interpreted that the lack of potassium due to lack of real natural food is a cause of CVD (potassium being mostly in nutrient dense greens, and grass fed meat (i.e. animals that ate more natural diets i.e. greens)).
So, thank you - this helps my understanding of the whole topic - not that I know the answers, but it does make me more curious about sodium/potassium electrolyte imbalance being a factor in CVD. Ideally this would be fixed with a healthier diet but it can be hard/expensive to get enough nutrient dense foods.
Edit:
oops - I missed the TOHP study - but that's one where they don't isolate sodium:
> The active intervention, described in detail elsewhere,22 involved dietary and behavioural counselling on how to identify sodium in the diet, self monitor intake, and select or prepare lower sodium foods and condiments suited to personal preferences. Individual and weekly group counselling sessions were provided during the first three months, with additional counselling and support less frequently for the remainder of follow-up.
> You could say that this suggests higher sodium increases cardiovascular disease risk but that seems like a stretch when if you'd picked a slightly different set of CVD-correlated biomarkers you would have got exactly the opposite result.
What’s the evidence for this?
> Even if the results had been more convincing, the methods are not - it's an extremely short term study and looks only at correlative biomarkers and not at actual health outcomes
You're going to have to pick your poison here - when you're after long term data on dietary interventions showing hard outcomes it's highly unlikely you'll ever see this in the form of RCTs that you're looking for (i.e. where you _only_ alter salt consumption). That's why we look for converging lines of evidence - biomarkers/soft outcomes from RCTs and hard outcomes from prospective cohort studies, for example. When we look at this for salt, we consistently see lower salt = lower adverse outcomes.
That said, when we meta-analyse RCTs we do actually have sufficient power to see improvements on hard outcomes. In this meta (https://doi.org/10.1016/S0140-6736(11)61174-4) we see a 29% reduction in cardiovascular events in the 7 months to 11.5 years in normotensives in RCTs which looked exclusively at salt reduction. I wouldn't call 11.5 years short term, nor cardiovascular disease events a soft outcome. So surely this ticks all your boxes?
> What’s the evidence for this?
Exactly what I paraphrased from the study - they chose three biomarkers that correlate with CVD - A increased 19%, B decreased 9%, C stayed the same. If they had chosen some other biomarker D instead of A, that increased say 5% or less, it would give an equally strong but opposite result as the result from the study.
Meta analysis is only as strong as the studies it's based on. I looked at quite a few studies before that purport to show sodium causing CVD, and none of them strongly support their conclusion - they all had significant flaws, not that they're not useful research just that they don't show what they are used to say they show.
For example, there were studies showing that increased salt increased blood pressure by ~5 mm Hg over long term. I understand that blood pressure can be affected very slightly by salt intake, I would guess because the body is holding more water or some other normal mechanism like that, but this does not suggest it's the long term cause of blood pressures going up from a normal 120 to a chronic 160 or 200 as we're seeing in tons of people. There could be any number of adjustments that would increase blood pressure slightly WHILE the change is in effect and then go back to baseline afterward. The chronic high blood pressure is a disease that doesn't just go back to normal immediately after a change.
Anyway, I don't have time at the moment to look through the 11 studies cited in that meta analysis, but if you pick the one or two that give the strongest evidence for salt causing CVD I'd look at them.
I'm genuinely trying to figure this out myself as best I can, because I know way too many people close to me dealing with early stage CVD and diabetes. And a lot of them say they're working on it by avoiding meat and dairy and eggs and salt, and instead of that they end up eating more refined oils and refined flour and sugar. It doesn't seem to be helping them any after years of this, and I think this is backwards advice. I'm not saying we need to eat tons of salt, maybe it does have a minor effect, just that it's not the real culprit.
> if you'd picked a slightly different set of CVD-correlated biomarkers you would have got exactly the opposite result.
So the evidence I’m looking for is empirics showing CVD correlated biomarkers that suggest a beneficial effect from consuming levels of sodium above recommended levels. Without that evidence then I don’t see why we should believe they would have got the opposite result if they picked other CVD biomarkers.
> but this does not suggest it's the long term cause of blood pressures going up from a normal 120 to a chronic 160 or 200 as we're seeing in tons of people
I’m not claiming that salt is the single cause of hypertension, but that doesn’t mean that the kind of reductions you see from salt reduction aren’t meaningful or contribute to those very high figures. It’s easy to dismiss 5mmHg as insignificant, but we generally see a 5mmHg reduction in sysBP translate to a ~10% reduction in CVD events. Considering how prevalent CVD is, that’s a pretty large effect size.
Chronic diseases are often overdetermined and stack - people have a poor diet which means they consume too much salt, they’re overweight and obesity, have T2DM or prediabetes, sedentary lifestyle, etc etc. The fact that we can’t point to a single one of these and say “this is the thing causing your 160/100 BP doesn’t mean we shouldn’t try to fix the individual factors. So sure, salt reduction seems to offer 5-6mmHg reduction, exercise 4-8, hypertensive drugs 10. But put them all together and that’s a massive change.
> Anyway, I don't have time at the moment to look through the 11 studies cited in that meta analysis, but if you pick the one or two that give the strongest evidence for salt causing CVD I'd look at them.
It’s just three trials (or four depending on how you count TOHP I & II). I think I’ve met my burden in terms of showing there’s evidence of high salt intake having adverse effects, I have no interest in forcing you to read them. Just trying to provide evidence if that’s something you’re seeking.
> I'm genuinely trying to figure this out myself as best I can, because I know way too many people close to me dealing with early stage CVD and diabetes.
I’m sorry to hear that. We certainly seem to be struggling with chronic lifestyle-related disease these days, though with GLP-1 RAs I’m a lot more optimistic than I was a few years ago.
> And a lot of them say they're working on it by avoiding meat and dairy and eggs and salt, and instead of that they end up eating more refined oils and refined flour and sugar.
Yeah depending on the composition of what they’re eating that doesn’t sound great. IMO Replacing butter with refined oils and whole grain flours/carbs - sure, solid move. Replacing meat with plant proteins is also a worthwhile step, and eggs don’t seem to be great for health in many respects. But fermented dairy seems to be a positive as far as CVD risk goes, so ethics aside, seems like a backwards step if they replacing yoghurt and cheese with sugar and white flour!
> I'm not saying we need to eat tons of salt, maybe it does have a minor effect, just that it's not the real culprit.
I’m very wary of trying to find “the culprit” for public health problems. It’s so rarely the case that a disease has a single aetiology, and in my experience the people who’ll tell you “it was the sugar all along”, “it was the seed oils all along”, “it was the glyphosate all along” have a book to sell. The reality is probably closer to it being a combination of several things. Not as sexy though, no publisher or influencer is interested in that view!
Regarding the reduction in mm Hg due to sodium - my argument is that the kind of impact on blood pressure can be qualitatively different.
In the same way that increased salt intake causes increased water retention, and thus increased weight, but this increased level of water weight goes away after a few days if you start consuming less salt, and there's no evidence of this causing long term harm.
I could see where if one already had severe CVD, maybe eating more salt could be the straw that breaks the camel's back, and thus until they heal the CVD it could be wise to limit salt. But this would be no indication that the salt is the cause of the CVD or causes any long term chronic problem. And it is the long term chronic CVD that is by far the most important to address IMHO. If salt is not causing that, this whole discussion is largely misdirected energy.
---
> IMO Replacing butter with refined oils and whole grain flours/carbs - sure, solid move.
We disagree here but that's a separate issue from salt so I'll leave it. :)
> I’m very wary of trying to find “the culprit” for public health problems [etc]
I agree entirely with this. It's very complex, many factors, no single culprit or silver bullet, and that this is extremely important. It's all the things. So it's important to try to tease out which things are having which kind and degree of effect. And this is where I think salt has been scapegoated in a way that probably just distracts from the root problem as I describe above.
> In the same way that increased salt intake causes increased water retention, and thus increased weight, but this increased level of water weight goes away after a few days if you start consuming less salt, and there's no evidence of this causing long term harm.
We've already gone over data showing that when we summate data from RCTs and salt consumption we see reduced salt consumption leads to reduced cardiovascular disease events, so it's demonstrably not the case that there's no evidence of this causing long term harm.
Additionally we have strong evidence of a dose-response curve regarding blood pressure and atherosclerosis, so that additional 5mmHg is contributing to additional plaque burden. Even after you reduce your salt intake, that plaque is still going to be there, increasing your risk of a CVD event.
Additionally when we look at the results of INTERSALT, age-related increases in blood pressure only seemed to occur in populations consuming more than 2-3g salt per day, which suggests that in addition to acute rises in BP, higher salt consumption than this may also be responsible for much larger rises in the long term that are not reversed when salt consumption is dropped.
Taking that whole body of evidence in totality, I think it's hard to argue that the effects of salt on the risk of adverse health outcomes is akin to water weight.
> I could see where if one already had severe CVD, maybe eating more salt could be the straw that breaks the camel's back, and thus until they heal the CVD it could be wise to limit salt. But this would be no indication that the salt is the cause of the CVD or causes any long term chronic problem. And it is the long term chronic CVD that is by far the most important to address IMHO. If salt is not causing that, this whole discussion is largely misdirected energy.
Again, even small increases in BP over normal range (and even slightly below - we tend to see increases in risk once systolic BP rises about 110) is associated with increases in CVD, so the raised blood pressure is one of the forces driving that long term chronic CVD.
> We disagree here but that's a separate issue from salt so I'll leave it. :)
Well if you're open-minded about the topic but think refined oils are a health risk, you're the same as I was a few years ago. I ended up changing my view on the topic. If you think there's a health concern not addressed by https://uprootnutrition.com/blog/seedoils I'd be genuinely interested to know.
> And this is where I think salt has been scapegoated in a way that probably just distracts from the root problem as I describe above.
I think the evidence very strongly suggests that sodium consumption is one of the root problems driving chronic health issues in the West.
The only thing I can easily find is that they have saturated fat - but it takes 4.5 eggs to have as much saturated fat as 1tbsp of butter.
Aside from 1 year of strict vegan diet, I've eaten an average of 4 eggs with 1tbsp butter mostly daily for my entire adult life (I'm 34), and also ate eggs regularly in childhood, and I seem to be in excellent health with no known issues. But I'm curious what I should be watching for.
The evidence base on eggs is a funny one because of:
1. Genetic traits influencing response to dietary cholesterol.
2. The effect of baseline dietary cholesterol on the impact of additional dietary cholesterol (if you're already consuming ~300mg/d cholesterol, adding more on top is unlikely to increase risk by much).
3. The effect of baseline CVD risk on the impact of egg consumption.
Generally when we take this into consideration, we see a linear increase in risk from increased egg consumption. For example this paper suggests that the higher your genetic risk for CVD, the higher the increase in risk from egg consumption, but even those with lower CVD risk see a ~6% increase in CVD events per 3 eggs/week increase: https://www.sciencedirect.com/science/article/pii/S000291652....
Additionally replacing the 1tbsp butter with plant oils would likely reduce ACM risk by ~17% (http://doi.org/10.1001/jamainternmed.2025.0205), but I'll be the first to admit that there's nothing that really replaces butter on a taste basis :D. Got to find the happy balance between health and hedonism IMO!
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?
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?
> Age-standardized cardiovascular mortality dropped steadily from 1975 to 2010 (with no particular discontinuity when statins were introduced), and has not budged since 2010.
Why would we favour cross sectional data over that produced by more rigorous methodologies?
> the tiny effect that statins claim (25-35%, under particular conditions)
25-35% reduction in one of the west’s leading killers is tiny? Wild.
Good luck to you, hope you keep on top of it. Do you know if you have high lp(a) out o curiosity? Curious what drives these events in cases such as yours.
> Curious what drives these events in cases such as yours.
In my case, I got dealt a very, very poor set of cardiac genes. Everyone on my mother's side has had at least one heart attack, though they generally started around age 50.
I think that’s a disservice to quacks - most of them are far better at dressing up their claims in something believable sounding. Gundry is just stark raving mad, it blows my mind that anyone gives him the time of day.
