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You said:

> 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.

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> 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.


What's wrong with eggs btw?

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!




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