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.
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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.
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!
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.