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May 13 2022
The evidence base continues to grow suggesting that fructose, from both dietary sources and endogenous synthesis, promotes the metabolic dysfunction t...
“Efforts to reduce sodium intake in entire populations cannot be justified.” (Mente, O’Donnell, Yusuf, 2021)
A paper published recently in the journal Nutrients raises important questions about the safety and utility of recommendations for entire population groups to consume low-sodium diets. Several international health organizations recommend low sodium intakes across the board, regardless of an individual’s health status. This recommendation is based largely on the mechanistic plausibility that higher sodium intakes may raise blood pressure in some people, and that hypertension can lead to more serious cardiovascular problems. However, as the paper highlights, this rationale is highly flawed and is based on weak and inconsistent evidence.
It’s true that an increase in sodium intake may raise blood pressure, but this occurs only in those with sodium sensitivity. This is about 25% of the US population, and is especially prevalent among people with existing hypertension as well as among African Americans. (Increased sodium intake seems to perturb blood pressure even more in the presence of low potassium intake, and increased potassium intake may lower blood pressure in people with hypertension.) Twenty-five percent of the population is certainly not a small number, but it also means that as much as 75% of the population may be being given a dietary recommendation that is not appropriate for them.
Like all essential nutrients, sodium intake appears to have a U-shaped or J-shaped curve, in that intakes that are too low or too high are both problematic and there’s a “sweet spot” in between where most people will be best served. Increased risk for cardiovascular disease or death and adverse health outcomes in general are noted to occur below approximately 3g and above 5g of sodium per day. So, the range of sodium intake that appears to support optimal health may be between 3-5g per day. This is above the 2.3g/day (approximately 1 teaspoon of salt) that multiple health agencies recommend even for people without hypertension.
This recommendation persists despite there being no evidence from randomized clinical trials that restricting sodium intake to a “low” level (< 2.3 g/day) reliably results in reduced risk for cardiovascular events. The Nutrients paper notes that such trial evidence does not exist because it has been virtually impossible to get an interventional study cohort to adhere to such an austere requirement, even when “intensive dietary counselling” is provided.
A 2013 report from the Institute of Medicine assessing the evidence regarding the relationships or lack thereof between sodium intake and chronic disease noted numerous times that much of the available data were weak, inconsistent, and may apply only to a small percentage of people. In some cases, the majority of evidence suggested that reducing sodium intake appeared to be of benefit, if only a limited benefit, but below a certain intake, risk for adverse outcomes increased. The report acknowledged that evidence is not adequate to recommend a sodium intake of less than 2.3g/day. And yet, the 2019 Dietary Reference Intakes for sodium continued to recommend reducing sodium intake among adults to less than 2.3g/day for purported “chronic disease risk reduction.” You cannot fault the lay public for being confused about health and nutrition when even the experts issue contradictory advice.
If the main reason for recommending dietary sodium reduction is to potentially reduce incidence of hypertension and more severe cardiovascular issues, the wrong suspect may be in custody. Looking specifically at hypertension, considering the exploding prevalence of metabolic syndrome in the US (including a prevalence of close to 28% in adolescents), perhaps it’s not salt, but sugar and other refined carbohydrates that should be the focus of attention for dietary restriction. Hypertension is included in the diagnostic criteria for metabolic syndrome, but even among those who have not been formally diagnosed metabolic syndrome, chronically elevated insulin is known to be a causative factor in renal sodium retention leading to higher blood pressure. This has led some researchers to say that public health authorities may have fingered “the wrong white crystals” in focusing on the role of salt, rather than sugar, in hypertension.
Very low-carb or ketogenic diets, which are known to lower insulin levels (even to the point of completely reversing metabolic syndrome), typically result in substantial improvements in hypertension. The excretion of sodium owing to lower insulin may be why individuals following ketogenic diets often require extra sodium (as well as potassium and magnesium), and these rapid changes in electrolyte status are believed to be the cause of “keto flu”—headaches, lightheadedness, fatigue, and other malaise that may accompany the transition from a high-carb diet to a very low-carb diet as the body adjusts. The effect of ketogenic diets for lowering blood pressure is powerful enough that patients taking anti-hypertensive medications need to be monitored so that doses can be adjusted to prevent blood pressure from becoming too low.
A 2016 study published in The Lancet found that in people with existing hypertension, a high sodium intake was associated with increased risk of cardiovascular events and death compared with moderate sodium intake, but no such association was found in people without high blood pressure. Interestingly, an association between low sodium intake and increased risk of cardiovascular events and death was observed both in people with hypertension and in normotensive individuals. So it appears that it may be prudent for people who already have hypertension to reduce sodium intake if their current habitual intake is “high,” but recommendations to consume a “low” sodium diet may be inadvisable regardless of blood pressure. Considering the close connection between hypertension and metabolic syndrome (or chronic hyperinsulinemia), it would have been interesting if the hypertensive subjects in this study had been evaluated for this, because perhaps they would be better served by advice to limit sugar and refined carbs in their diet rather than, or in addition to, limiting sodium.
Population-wide dietary advice has been known to change before. (For example, dietary cholesterol is no longer considered “a nutrient of concern for overconsumption” by the dietary guidelines in the US.) Perhaps we will see changes in recommendations regarding sodium intake that reflect greater nuance in the future.
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