Effect Of Salt Substitution On Community-wide Blood Pressure

[Mito]

Abstract
Replacement of regular salt with potassium-enriched substitutes reduces blood pressure in controlled situations, mainly among people with hypertension. We report on a population-wide implementation of this strategy in a stepped-wedge cluster randomized trial (NCT01960972). The regular salt in enrolled households was retrieved and replaced, free of charge, with a combination of 75% NaCl and 25% KCl. A total of 2,376 participants were enrolled in 6 villages in Tumbes, Peru. The fully adjusted intention-to-treat analysis showed an average reduction of 1.29 mm Hg (95% confidence interval (95% CI) (−2.17, −0.41)) in systolic and 0.76 mm Hg (95% CI (−1.39, −0.13)) in diastolic blood pressure. Among participants without hypertension at baseline, in the time- and cluster-adjusted model, the use of the salt substitute was associated with a 51% (95% CI (29%, 66%)) reduced risk of developing hypertension compared with the control group. In 24-h urine samples, there was no evidence of differences in sodium levels (mean difference 0.01; 95% CI (0.25, −0.23)), but potassium levels were higher at the end of the study than at baseline (mean difference 0.63; 95% CI (0.78, 0.47)). Our results support a case for implementing a pragmatic, population-wide, salt-substitution strategy for reducing blood pressure and hypertension incidence.
Effect of salt substitution on community-wide blood pressure and hypertension incidence

 

[yerrag]

The effects of taking increased potassium as a partial replacement for salt is miniscule. It certainly addresses a deficiency in potassium, which is already deficient in a regular diet, and which is made worse when more potassium is excreted to conserve sodium, which exists already in a hypertensive state where aldosterone levels are already high to begin with.

Potassium supplementation merely addresses the effect of an aldesterone-induced effects of a hypertensive state, and doesn't address the cause of hypertension. At most, potassium supplementation mitigates slightly the increase in blood pressure.

 

[Giraffe]

Negative balance of calcium and magnesium under relatively low sodium intake in humans.

Same researchers...

Dietary Salt (Sodium Chloride) Requirement and Adverse Effects of Salt Restriction in Humans.

sodium intake was (100 mmol/d or 2.2 g/d)

• aldosterone above reference range
• sodium taken out of the bones to compensate for low intake
• negative magnesium and calcium balance
• no correlation between the Na intake and the Na balance, while the Na-intake was correlated significantly to the balances of K, Ca and Mg.
• Na intake necessary to keep the balances of Ca and Mg positive was calculated to be 68 mg/kg body weight/d.

 

[Mito]

doesn't address the cause of hypertension

What do you see as the cause?

 

[yerrag]

What do you see as the cause?

I cannot speak to other true root causes (as differentiated from secondary (the immediate effect of a root cause, that is causing the final effect) causes, or tertiary causes, which modern medicine has a habit of mixing up in order to muddy up the subject and sow confusion. Modern medicine even does sleight-of-hand tricks to make the cause into an effect, and vice versa. This is why reading medical texts and studies requires me to don the hat of Sherlock Holmes in interviewing suspects, filtering information as they come. Ambiguity in meaning is a big tell as to motive and intent. And medical texts and studies carry with them this air of ambiguity by design, and not out of poor training in written communication).

I've found mine to be bacterial in origin. P. gingivalis biofilm in my blood vessel walls. It has established a strong colony and thrives in a symbiotic relationship with other fungi and bacteria. It has its own enzymes which break down peptides and protein, to provide the bacterial community with food from nitrogen and carbon from the peptide units it has dismembered from larger peptides and proteins. One way it causes hypertension is that it robs eNOS of substrates to produce the vasodilatory action of nitrous oxide, as arginine supply is lessened. Another way is that it breaks down the agglomeration of peptides that attach to albumin, thereby making the albumin agglomerate smaller, which in turns allow albumin to pass through the nephon filter in the kidneys, and in so doing reduces the albumin stores in blood. Lower albumin stores attract less sodium in plasma, and lower sodium attracts less water in plasma. The lower plasma volumes equates to lower blood volume, and lower blood volume requires higher pressure to ably distribute nutrients and discard metabolic waste. Another way is thru the formation of immune-complexes that line the capillary walls, thereby restricting the surface area of these vessels, and ultimately requiring higher pressure to let blood flow through as intended volume-wise.

Potassium does nothing to address all these. Potassium intake only addresses the increased potassium excretion thru urine that is a result of increased aldosterone causing sodium to be conserved. But if you ask me why aldosterone is increased in cases of hypertension, I find that hard to understand even as Ray Peat has talked a lot about this. It's pretty fuzzy to me.

 

[Peatress]

FDA on verge of approving artificial salt as part of Biden health push

The vast majority of Americans consume far more than the recommended amount of sodium per day. Many groups consume more than 40 percent of the daily limit (shown here).

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