How much salt?

[MaxPeaches]

Hi guys,

 

I've read and reviewed The CR Way, have been counting and restricting my calories while meeting the DRI of protein and carbs, and am awaiting the delivery of several books recommended on the Calorie Restriction website (here: https://www.crsociety.org/resources/cr_guide ). My question now is how much salt should I be aiming for on a daily basis? Do you guys shoot for 100% of the US RDA (it might be a DRI I haven't much looked into it) or do you shoot for less than that? In The CR Way the McGlothins note that many CR practitioners likely keep their blood pressure low by reducing their salt intake but I wasn't sure if that meant less than the RDA/RDI/DRI or equal to the RDA/RDI/DRI.

 

Thanks for the info guys!

Max

[Michael R]

The DRI for sodium, unlike most DRIs, is not intended as a minimum, but as a safe maximum. Same for saturated fat and cholesterol. The actual guidance from them and AHA is 1500 mg for almost everybody.

[Guest MaxPeaches]

Perfect. Thanks. :)

[Guest Rodney]

Regarding Al Pater's email contribution regarding salt intake - Vol 9 Issue 20 - attached below, note the following:

 

This paper is interesting because it not only shows, yet again, that appreciable salt restriction raises mortality, but in addition the authors claim to have determined an optimal level.  And note that they found 3 - 5 grams of sodium per day to be probably optimal. 

 

Since only ~40% of table salt (NaCl) is sodium (the other 60% is Cl) 3 - 5 grams of SODIUM per day translates into ***7.5 to 12.5*** grams of SALT daily.  There is quite a lot of salt in many processed products.  But 12.5 gram upper bound of that range is a fairly large amount.  I have never checked my salt intake but I rather doubt it normally exceeds the lower bound of the above recommended intake, except on days I eat more than my average amount of canned foods.  I need to check.
 

Dietary sodium and cardiovascular disease.
Smyth A, O'Donnell M, Mente A, Yusuf S.
Curr Hypertens Rep. 2015 Jun;17(6):559. doi: 10.1007/s11906-015-0559-8.
PMID: 25983308
 
Abstract
Although an essential nutrient, higher sodium intake is associated with increasing blood pressure (BP), forming the basis for current population-wide sodium restriction guidelines. While short-term clinical trials have achieved low intake (<2.0 g/day), this has not been reproduced in long-term trials (>6 months). Guidelines assume that low sodium intake will reduce BP and reduce cardiovascular disease (CVD), compared to moderate intake. However, current observational evidence suggests a J-shaped association between sodium intake and CVD; the lowest risks observed with 3-5 g/day but higher risk with <3 g/day. Importantly, these observational data also confirm the association between higher intake (>5 g/day) and increased risk of CVD. Although lower intake may reduce BP, this may be offset by marked increases in neurohormones and other adverse effects which may paradoxically be adverse. Large randomised clinical trials with sufficient follow-up are required to provide robust data on the long-term effects of sodium reduction on CVD incidence. Until such trials are completed, current evidence suggests that moderate sodium intake for the general population (3-5 g/day) is likely the optimum range for CVD prevention.

[Guest David]

My blood pressure dropped enormously when my BMI dropped.  (For me, sodium intake was not the relevant variable.) It went from 130/80 to 90/60 when I dropped from ~170 lbs. to 135 lbs.  I am now ~155 lbs. and my BP is 110/70.  I find that if I go too low in sodium, it can result in muscle cramps.  I'm skeptical of the low 1500 mg recommendation, especially for those with an athletic lifestyle.

[Michael R]

First, Rodney, thank you very much for chiming in a fair amount lately. Please do me and you and everyone on the Forum a favor (and this applies to Guest_Davdid_" too): register on the Forums and log in each time before you post! It's fine if you want to use a pseudonym, but registering and logging in will ensure that you can't be impersonated and will make it easier to keep track of your (you can set up your preferences to send you an email when someone responds to one of your posts or a thread in which you're interested), input, and progress.
 
As far as the review article you (Rodney) cite c/o Al Pater: I don't take this very seriously. All or nearly all of the epidemiology (including Dr. Yusuf's own study) suggesting a J-shaped mortality curve for sodium intake is flawed on multiple parameters, particularly in the means of ascertaining sodium intake — either self-report (and people really don't have any damned idea how much Na is in their food) or spot urine tests (which aren't robust) or single time-point collections.
 

Many [such studies] suffer from some combination of potential for bias in the assessment of sodium intake, reverse causality, residual confounding, and random error. Despite this, reports of a paradoxical inverse or J-shaped association between sodium intake and CVD have received considerable attention from the media^28,29 and scientific community^30–32 and have been the basis for the addition of sodium to food products [and also have helped processed food manufacturers resist calls to regulate reductions in added Na and thus put Na intake more fully into consumers' voluntary choices instead of unthinking mass overdose -MR].³³
 
Several analyses of CVD or total mortality were based on data from the National Health and Nutrition Examination Survey, which used a single 24-hour diet recall to estimate sodium intake. This approach underestimates sodium intake by failing to measure sodium added at the table, in the kitchen, in supplements, or in drinking water. Falsely low estimation caused by underreporting of food and beverage intake and portion sizes is also a concern. Finally, inaccuracies can result from changes in commercial food composition that are not reflected in the nutrient databases used to estimate sodium content. Use of food frequency questionnaires to estimate sodium intake is prone to many of the same challenges encountered with use of dietary recalls. In addition, sodium content can vary considerably across brands of processed foods, which are typically incompletely assessed in these questionnaires.
 
The gold standard for sodium assessment in healthy persons is 24-hour urine collection. Overnight and spot urine samples are less burdensome for study participants and research staff; however, they are affected by diurnal variation, and the methods supporting the validity of their use are inadequate. They represent a weak substitute for 24-hour urine collections, especially when they are used to estimate sodium intake and relationships in an individual.²⁶ Despite being considered the “gold standard,” even 24-hour collections are subject to quality control concerns, particularly undercollection of urine specimens. Measurements based on a single 24-hour urine collection fail to capture day-to-day variability, which makes them less than optimal for study of the within-person relationship between sodium and CVD.

The TOHP Follow-up Study used an average of 3 to 7 carefully collected 24-hour urine collections as a measure of sodium exposure, which greatly reduced bias caused by measurement error and random error attributable to within-person variability over time. We found a continued decrease in CVD events among those with sodium levels as low as 1500 mg/d, with no evidence of a J shape when examining spline curves. Risk reductions among those at the lowest levels of sodium excretion were substantial, with a 32% reduction among those excreting <2300 mg/d, although this was not statistically significant because of the small numbers in this subgroup and limited power. [That is, the observed reduction from >4800 mg, to 3600 to <4800 mg/d, to 2300-3600 mg were not significant; there was a further reduction observed for those with sodium <2300 mg/d, but there were so few data points that it didn't reach statistical significance:
 

[Link to full-sized graph blowup](1)

 

 
The very few studies that have actually done what needs to be done — assess Na with several 24-h urine collections over the course of the study, starting from people without CHF and not taking drugs that affect Na metabolism — find quite consistently that genuinely low Na intake (<2300 mg/d) is best, whether you look at self-selected diet (1) or clinical trials of sodium restriction.(2)

 

DASH is also good evidence of the benefits of Na restriction, tho' critics correctly note that DASH is a multifactorial intervention, so the effects of lower Na are confounded by much stronger effects on BP from higher fruit, vegetable, and nonfat dairy intake.
 
 
References
1: Cook NR, Appel LJ, Whelton PK. Lower levels of sodium intake and reduced cardiovascular risk. Circulation. 2014 Mar 4;129(9):981-9. doi: 10.1161/CIRCULATIONAHA.113.006032. Epub 2014 Jan 10. PubMed PMID: 24415713; PubMed Central PMCID: PMC4181831.

2: Cook NR, Cutler JA, Obarzanek E, Buring JE, Rexrode KM, Kumanyika SK, Appel LJ, Whelton PK. Long term effects of dietary sodium reduction on cardiovascular disease outcomes: observational follow-up of the trials of hypertension prevention (TOHP). BMJ. 2007 Apr 28;334(7599):885-8. Epub 2007 Apr 20. PubMed PMID: 17449506; PubMed Central PMCID: PMC1857760.

[Guest Rodney]

Also worth noting on the 'Salt Restriction' issue is that even the IOM (not usually inclined to jump on bandwagons in too much haste) recently advised - despite the recommendations in the american Dietary Guidelines to limit sodium intake to no more than 2300mg per day - that daily sodium intake below 2300 mg cannot be justified on current evidence:

 

"Recent studies that examine links between sodium consumption and health outcomes support recommendations to lower sodium intake from the very high levels some Americans consume now, but evidence from these studies does not support reduction in sodium intake to below 2,300 mg per day, says a new report from the Institute of Medicine.":

 

http://www.iom.edu/Reports/2013/Sodium-Intake-in-Populations-Assessment-of-Evidence/Press-Release.aspx

 

So the IOM appears to be saying that the science cannot justify less than 2300 mg of sodium.  That would mean that 5.75 g of TABLE SALT would be the LOWER limit the science can justify.

 

Of course I am not recommending anyone go hog-wild on salt.  But I do want to point out the largely unrecognized potential danger of not getting enough.

 

In a post a few years ago (the contents of it can be found in my post to be found in the archives of:  Date: June 26, 2014 11:54PM) I referenced six sources each reporting increased mortality or other adverse findings among those advised to go on salt-restricted diets, compared with control individuals with the similar health status who were not so advised.  And I have seen a few more such papers since then.  These are the references I am referring to from that earlier post:

 

"PMID 21289228 showed that in diabetics the best marker of dietary
sodium intake was inversely associated with all-cause and
cardiovascular mortality.
 
"PMID 18262533 showed that in people with hypertension salt restriction
raises: triglycerides, chylomicron-cholesterol, CRP, TNF alpha, IL6,
insulin and the HOMA-IR measure of insulin resistance, none of which
sounds like good news.
 
"Three other studies were conducted in normal, healthy individuals.  They found that:
 
"A) "The Einstein researchers actually observed a significantly
increased risk of death from cardiovascular disease (CVD) associated
with lower sodium diets." (reported in Science Daily - 18 May 2008);
 
"B) "Low-salt diet is associated with an increase in insulin
resistance" (PMID 21036373);
 
"C) those on low salt diets had the highest mortality (reported in
Doctor's Guide - 13 March 1998).
 
"And here I found another one:
 
"D) Lower ... salt intake ..... was associated with an increased
risk of cardiovascular death (reported in ScienceDaily - May 3, 2011)"

 

And regarding Guest_David's post earlier in this thread: my experience when I lowered my BMI from 26 to 21 was exactly the same as yours.  BP appears to be much more reliably a function of body weight than of salt intake.  Which should provide a very clear message to those who are over-weight and have high blood pressure!

 

Rodney.

 

[Michael R]

Also worth noting on the 'Salt Restriction' issue is that even the IOM (not usually inclined to jump on bandwagons in too much haste) recently advised - despite the recommendations in the american Dietary Guidelines to limit sodium intake to no more than 2300mg per day - that daily sodium intake below 2300 mg cannot be justified on current evidence:

 

"Recent studies that examine links between sodium consumption and health outcomes support recommendations to lower sodium intake from the very high levels some Americans consume now, but evidence from these studies does not support reduction in sodium intake to below 2,300 mg per day, says a new report from the Institute of Medicine.":

 

http://www.iom.edu/Reports/2013/Sodium-Intake-in-Populations-Assessment-of-Evidence/Press-Release.aspx

 

So the IOM appears to be saying that the science cannot justify less than 2300 mg of sodium. That would mean that 5.75 g of TABLE SALT would be the LOWER limit the science can justify.

Their analysis is actually more nuanced than that, and relates more to the relatively low number of studies where such low levels are actually achieved, and to the concern around population subgroups: if you just say, as a blanket recommendation, that everyone should be getting <2300 mg/d, you're going to catch a significant number of people who won't benefit or may even be harmed (emphasis added):

 

· evidence supports a positive relationship between higher levels of sodium intake and risk of heart disease, which is consistent with previous research based on sodium’s effects on blood pressure;

 

· studies on health outcomes are inconsistent in quality and insufficient in quantity to conclude that lowering sodium intake levels below 2,300 mg/day either increases or decreases the risk of heart disease, stroke, or all-cause mortality in the general U.S. population; [Again, this inconsistency is due to methodological reasons I lay out in my earlier post; when you restrict yourself to the (very small) number of studies with multiple 24-hour urine sodium assessment, the benefits in initially healthy people are pretty clear -MR]

 

· evidence indicates that low sodium intake may lead to risk of adverse health effects among those with mid- to late-stage heart failure who are receiving aggressive treatment for their disease;

 

· there is limited evidence addressing the association between low sodium intake and health outcomes in population subgroups (i.e., those with diabetes, kidney disease, heart disease, hypertension or borderline hypertension; those 51 years of age and older; and African Americans). While studies on health outcomes provide some evidence for adverse health effects of low sodium intake (in ranges approximating 1,500 to 2,300 mg daily) among those with diabetes, kidney disease, or heart disease, the evidence on both the benefit and harm is not strong enough to indicate that these subgroups should be treated differently from the general U.S. population. Thus, the evidence on direct health outcomes does not support recommendations to lower sodium intake within these subgroups to or even below 1,500 mg daily; and

 

· further research is needed to shed more light on associations between lower levels of sodium (in the 1,500 to 2,300 mg/day range) and health outcomes, both in the general population and the subgroups.

 

PMID 21289228 showed that in diabetics the best marker of dietary sodium intake was inversely associated with all-cause and cardiovascular mortality.

This was (a) in diabetics, and (b]a single baseline assessment, not repeated measures over the course of the study.

 

PMID 18262533 showed that in people with hypertension salt restriction raises: triglycerides, chylomicron-cholesterol, CRP, TNF alpha, IL6, insulin and the HOMA-IR measure of insulin resistance, none of which sounds like good news.

No, it doesn't — but (a) the low-sodium diet contained Na=60 mmol/day= 1386 mg/day: the DRI doesn't advise any but a select few to even hit 1500 mg, and I personally wouldn't advise going that low; (b] the study only lasted 3 weeks, and the renin-angiotensin system tends to adjust over time; and (c] those are the kinds of surrogate markers on which the IOM report you cited is expressing caution.

 

Three other studies were conducted in normal, healthy individuals. They found that:

 

A) The Einstein researchers actually observed a significantly increased risk of death from cardiovascular disease (CVD) associated with lower sodium diets. (reported in Science Daily - 18 May 2008);

Rodney, please try to track down original sources -- or at least keep track of a link to the pop press piece you're citing. I found it, and determined the original scientific paper from information therein. This study is from NHANES III: see my earlier post.

 

(A] Low-salt diet is associated with an increase in insulin resistance (PMID 21036373);

This study only lasted a week, and it used <20 mmol/d sodium — i.e., less than 462 mg/d!

 

C) those on low salt diets had the highest mortality (reported in Doctor's Guide - 13 March 1998).

I can't find a story of that date from that source (again, please try to track down original reports, or at least keep track of inks to press articles), but based on the date it's most likely this report, which used NHANES I data — see my earlier post.

 

D) Lower ... salt intake ..... was associated with an increased risk of cardiovascular death (reported in ScienceDaily - May 3, 2011)

Found that press story too — and the press report cites the original paper. They rely on a single baseline assessment of sodium excretion. Also, as He and colleagues note,

 

In addition, nearly all cardiovascular deaths (81/84) occurred in FLEMENGHO (Flemish Study on Environment, Genes, and Health Outcomes; eTable 6 in the article), and mean sodium excretion was substantially lower in this cohort compared with the other study. Simple pooling of the FLEMENGHO cohort with the cohort in EPOGH (European Project on Genes in Hypertension) raises concern that ecological or temporal differences between cohorts may account for the observed association of sodium excretion with CVD mortality. [ie, risk of cross-cultural crap -MR]

[Dean Pomerleau]

All,

 

For those interested in the latest on salt/sodium intake, Dr. Greger had a video on the topic today. From the references he cites (similar to Michael's above), the overwhelming evidence is that excess salt does indeed do harm, and we should be keeping sodium at 2300 mg per day or less. He talks about how the salt & big food industry has obscured the clear evidence in favor of reducing salt for improved cardiovascular health and reduced risk of stomach cancer in much the same way the tobacco industry obscured the evidence against cigarettes for years.

 

--Dean

 

[Todd Allen]

Here's a meta study with a fairly large sample size using 24 hour urine collection which seems to indicate that a 2,300 mg daily upper limit for sodium intake might  be harmful for those without hypertension.

 

 

http://www.thelancet...0467-6/abstract

[Michael R]

Hi Todd,

 

As I noted to you earlier today,the studies underlying this meta-analysis are nearly all quite flawed: see discussion earlier in this thread and then my followup post below in response to Rodney's reply to that one. Actually, it's worse than that, because having started off with inappropariate studies (including one in subjects with diabetes and another with existing CVD, and none with actual data on 24-hour sodium intake), they then "estimated 24-h urinary sodium excretion (as group-level measure of intake)" using the Kawasaki formula (either post hoc, or following their own original method in the case of PURE, which they included in their meta-analysis). This is recognized to be a poor predictor of individual-level socium intake, which is what you want if you actually want to use it to conduct prospective studies (rather than just do basic public-health work at the population level).

 

The American Heart Association accordingly took them to task on this, writing that "PURE contained several substantial methodological issues that limit its usefulness for drawing conclusions about the relationship between sodium intake and health outcomes, and for guiding public health recommendations ... [T]hese issues include inaccurate measures of sodium intake and inclusion of sick people.  The issues are detailed in the American Heart Association’s February 2014 Science Advisory."

 

The same press release also praises the NUTRICODE study by Dariush Mozaffarian and others. I'm actually less than overbowled by this study, as it's still to reliant on modeling both for sodium intake and in this case also for predicting events, but they did at least do a better job of (still) modeling 24-h sodium. The two studies using data from the two TOHP trials cited above — with repeated true 24-h sodium in both — provide as solid a basis as one is likely to get barring some outpouring of interest in the subject from Congress on the matter, and they're pretty clear that, at the least, intakes > 2 g Na are bad for you.

[Todd Allen]

Aren't the TOHP studies also flawed in that they aren't actually isolating a change in sodium intake from other confounders such as perhaps changing from a diet high in processed foods to a diet higher in unprocessed foods?  They even state it was a lifestyle intervention where people were coached in healthier practices.  Perhaps those achieving lower sodium excretion were achieving better outcome not because they were reducing sodium but because they were better following the otherwise healthier aspects of the lifestyle intervention?

[Michael R]

I think you're probably confusing TOHP with DASH, a later trial with the characteristics you describe. If you look at the participant questionnaire they gave subjects, it's focused on eating lower-sodium versions of the same foods, not eg. replacing processed foods with freshly-prepared ones as in DASH. They do mention using " fresh/frozen, instead of canned, vegetables," but that is only one of many suggestions, nearly all of which are narrowly focused on sodium. They got “Take-home packages of low-sodium foods and products,"[ref], not cooking lessons and a whole-lifestyle change. And, notably, neither the weights nor the urinary potassium changed in the Sodium Light Lifestyle group, as would be expected to happen if there had been any major shift from processed to unprocessed foods.

[InquilineKea]

Is sodium really that much of a concern for those who otherwise follow an extremely healthy diet AND who have borderline low blood pressure? I do eat a lot of salsa and tomato sauce (both which have lots of sodium). In addition, Japanese are known for their very high sodium diets.

Edited September 13, 2021 by InquilineKea

[Michael R]

5 hours ago, InquilineKea said:

Is sodium really that much of a concern for those who otherwise follow an extremely healthy diet AND who have borderline low blood pressure? I do eat a lot of salsa and tomato sauce (both which have lots of sodium).

That's a reasonable question. However, there's evidence that high-salt diets not only increase BP in the near term, but are major drivers of the age-related increase in BP — so even if your BP is low now, eating a lot of salt might set you up for higher (thus, more damaging ) BP later on. There's additionally some evidence for direct negative effects on angiotensin II signaling etc, but that's a bit too mechanistic to hang hats on.

5 hours ago, InquilineKea said:

In addition, Japanese are known for their very high sodium diets.

Yes — and that high sodium intake is thought to be the reason for their disproportionately high risk of stroke (granted otherwise-low CVD risk factors, high fish intake, and expectedly-low MI risk), and for their higher contribution of vascular dementia vs. AD in the West.

[Michael R]

Quote

Effect of Salt Substitution on Cardiovascular Events and Death.

Neal B, Wu Y, Feng X, Zhang R, Zhang Y, Shi J, Zhang J, Tian M, Huang L, Li Z, Yu Y, Zhao Y, Zhou B, Sun J, Liu Y, Yin X, Hao Z, Yu J, Li KC, Zhang X, Duan P, Wang F, Ma B, Shi W, Di Tanna GL, Stepien S, Shan S, Pearson SA, Li N, Yan LL, Labarthe D, Elliott P.

N Engl J Med. 2021 Aug 29.

doi: 10.1056/NEJMoa2105675.

PMID: 34459569

... We conducted an open-label, cluster-randomized trial involving persons from 600 villages in rural China. The participants had a history of stroke or were 60 years of age or older and had high blood pressure. The villages were randomly assigned in a 1:1 ratio to the intervention group, in which the participants used a salt substitute (75% sodium chloride and 25% potassium chloride by mass), or to the control group, in which the participants continued to use regular salt (100% sodium chloride)....

Results

A total of 20,995 persons were enrolled in the trial. The mean age of the participants was 65.4 years, and 49.5% were female, 72.6% had a history of stroke, and 88.4% a history of hypertension. ... The mean 24-hour urinary sodium excretion was 4.3 g (187 mmol), and the mean 24-hour urinary potassium excretion was 1.4 g (36 mmol) ... The mean duration of follow-up was 4.74 years. ...

Across the follow-up period, the mean difference in 24-hour urinary sodium excretion between the salt-substitute group and the regular-salt group was −350 mg (95% confidence interval [CI], −545 to −154) (−15.2 mmol; 95% CI, −23.7 to −6.7), and the mean difference in 24-hour urinary potassium excretion was 803 mg (95% CI, 714 to 897) (20.6 mmol; 95% CI, 18.3 to 23.0). The mean difference in systolic blood pressure was −3.34 mm Hg (95% CI, −4.51 to −2.18) (Figure 2). ...

The rate of stroke was lower with the salt substitute than with regular salt (29.14 events vs. 33.65 events per 1000 person-years; rate ratio, 0.86; 95% confidence interval [CI], 0.77 to 0.96; P=0.006), as were the rates of major cardiovascular events (49.09 events vs. 56.29 events per 1000 person-years; rate ratio, 0.87; 95% CI, 0.80 to 0.94; P<0.001) and death (39.28 events vs. 44.61 events per 1000 person-years; rate ratio, 0.88; 95% CI, 0.82 to 0.95; P<0.001).

Obviously, this was a high-risk, older group; however, there's room for improvement by further reducing sodium intake and starting younger.

[Mechanism]

Thank you Michael.

Also great to see you here.

[Todd Allen]

On 9/13/2021 at 5:32 PM, Michael R said:

Obviously, this was a high-risk, older group; however, there's room for improvement by further reducing sodium intake and starting younger.

> The mean 24-hour urinary sodium excretion was 4.3 g (187 mmol), and the mean 24-hour urinary potassium excretion was 1.4 g (36 mmol)

Considering our RDA for potassium is 4.7 g vs 2.3 g for sodium their urinary excretion ratio is off by about a factor of 6.  I don't know what percent of each is typically lost to urine versus other excretions but being this whacked I wonder how much of the benefit was due to sodium reduction versus the increase in potassium and bringing the two more in balance? 

 

[Ron Put]

20 hours ago, Todd Allen said:

Considering our RDA for potassium is 4.7 g vs 2.3 g for sodium their urinary excretion ratio is off by about a factor of 6. 

Good point.

From an evolutionary point, apes don't normally have had access to the abundance of salt we have today. Not long ago, salt was scarce enough to be used as payment, thus "salary" and "not worth his weight in salt."

Here is a study of the Yanomami indians who don't have easy access to salt and they seem to be doing just fine:

The Yanomami Indians in the INTERSALT Study

Results: The findings in the Yanomami population were as follows: a very low urinary sodium excretion (0.9 mmol/24 h); mean systolic and diastolic BP levels of 95.4 mmHg and 61.4 mmHg, respectively; no cases of hypertension or obesity; and they have no knowledge of alcoholic beverages. Their BP levels do not elevate with age. The urinary sodium excretion relates positively and the urinary potassium excretion relates negatively to systolic BP. This correlation was maintained even when controlled for age and body mass index.

Conclusion: A positive relation between salt intake and blood pressure was detected in the analysis of a set of diverse populations participating in the INTERSALT Study, including populations such as the Yanomami Indians. The qualitative observation of their lifestyle provided additional information.

[InquilineKea]

On 9/13/2021 at 6:12 PM, Michael R said:

but are major drivers of the age-related increase in BP — so even if your BP is low now, eating a lot of salt might set you up for higher (thus, more damaging ) BP later on.

How does salt accelerate the age-related increase in BP. What's the root of the damage?

FWIW, my parents/grandparents don't have BP issues at all (in fact it's more on the low side than the high side). AND THEY EAT A LOT OF SALT.

Edited September 18, 2021 by InquilineKea

[Mike41]

On 9/17/2021 at 9:30 PM, InquilineKea said:

How does salt accelerate the age-related increase in BP. What's the root of the damage?

FWIW, my parents/grandparents don't have BP issues at all (in fact it's more on the low side than the high side). AND THEY EAT A LOT OF SALT.

Yes it’s certainly a genetic variability issue. Michaels key word above is MIGHT!

[Saintor]

Is there anything in a blood test that could suggest an high consumption of sodium?   I have one this Tuesday...myfitnesspal says that today, my intake of sodium will be  3827mg (I just realized that 3500-4000mg is typical for me).  My blood pressure is ok.

 

EDIT:  I got my blood test and it lists a normal sodium range (135-147mmol/L), I am at 143 so no worry - unless this criteria is not relevant to vessels hardening by sodium.

Edited October 23, 2021 by Saintor

[InquilineKea]

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7309298/ (from

)

Edited November 17, 2021 by InquilineKea

[kpfleger]

On 9/15/2021 at 5:14 PM, Ron Put said:

From an evolutionary point, apes don't normally have had access to the abundance of salt we have today. Not long ago, salt was scarce enough to be used as payment, thus "salary" and "not worth his weight in salt."

Here is a study of the Yanomami indians who don't have easy access to salt and they seem to be doing just fine:

The Yanomami Indians in the INTERSALT Study

Results: The findings in the Yanomami population were as follows: a very low urinary sodium excretion (0.9 mmol/24 h)

https://nutritionfacts.org/topics/salt/ says "For the first 90 percent of human evolution, we likely ate diets containing less than the equivalent of a quarter teaspoon of salt’s worth of sodium a day." That's <600mg/day. I couldn't quickly find a better quote on evolutionary human levels of sodium intake using Google in just a couple min, but I welcome other datapoints on this question.

What does 0.9nmol urine excretion / 24hr translate to in terms of intake in mg?

 

I recently found a jar'ed salsa brand w/ no added salt (and it's yummy) and many stores around me have been selling several brands of canned beans w/ no added salt, so I started experimenting with taking my WFPB diet that was mostly SOS free and making it (almost) completely added sugars, oils, & salt free, and putting some sample days into CronOMeter. The total sodium intake came out to roughly 550-750mg/day (that's for total calories 2050-2100/day). The diet consisted entirely of veggies, fruit, whole grains (mostly oats, brown rice, & millet, a few slices of Ezekiel bread, not the no-sodium version, the normal version with 75mg/slice), legumes (mostly canned beans, occasional lentils), & sparingly some nuts (all unsalted). Plus a tiny bit of 100% chocolate or cacao nibs (but only 4-8g/day).

I'm curious to hear what Michael's & Dean's normal daily sodium intake is.

I glanced through this thread looking for evidence on whether intakes of sodium this low are likely less optimal for long-term health than intakes between 750-1500mg/day but found it frustrating. The gist seems to be that there's so little data on people eating diets such as this (closer so evolutionary diets) that there's not a whole lot of good data to prove that lowering from 1500mg/day to 750mg or lower provides any benefit, but the evidence for a J shape with increased risk going down below 1500mg/day doesn't seem particularly strong either. I'm forced to wonder about the studies showing increased risk at the lowest levels of sodium consumption (from prescribed restriction diets) what the diets actually consisted of.

Given a diet consisting of whole plan foods with no added salt, it's hard to think that adding salt just to increase sodium is a pro-health move. Particularly if evolutionary diets didn't have that added sodium. What do the salt advocates think is the best evidence that a diet consisting of whole plant foods like this *needs* added sodium intake (from salt or a supplement) to reduce chronic disease risk?

Edited August 27, 2022 by kpfleger

[Dean Pomerleau]

I don't add any extra salt to my WFPB diet. Last time I ran it through Cronometer I was getting around 1000mg sodium. 

--Dean