5 ms·

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

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.

KempyKolibri 1y ago
So DASH-sodium (https://www.jacc.org/doi/10.1016/j.jacc.2021.03.320 https://www.jacc.org/doi/10.1016/j.jacc.2021.03.320) seems like it meets those goalposts? As does TOHP (https://doi.org/10.1136/bmj.39147.604896.55 https://doi.org/10.1136/bmj.39147.604896.55). 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 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.
- lithocarpus 1y ago
  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.
  - KempyKolibri 1y ago
    > 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 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?
    - lithocarpus 1y ago
      > 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.

KempyKolibri 1y ago

So DASH-sodium (https://www.jacc.org/doi/10.1016/j.jacc.2021.03.320 https://www.jacc.org/doi/10.1016/j.jacc.2021.03.320) seems like it meets those goalposts? As does TOHP (https://doi.org/10.1136/bmj.39147.604896.55 https://doi.org/10.1136/bmj.39147.604896.55). 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 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.

lithocarpus 1y ago
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.
- KempyKolibri 1y ago
  > 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 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?
  - lithocarpus 1y ago
    > 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.