Does Dr. David Brownstein Really Say “Eat All The Salt You Want”?

Seasoned Claims, Unsalted Evidence. Rational Discourse was our path to overtaking public health and securing HHS. For the best future, we can disagree and maintain professionalism.

Recently, a podcaster characterized Dr. Brownstein’s position as a rejection of the sodium–hypertension literature, claiming that he believes people should eat as much salt as they want. Regarding the science linking salt to hypertension and cardiovascular disease, the podcaster stated that Dr. Brownstein “Simply erases all of it, and says ‘Eat As Much Salt As You Want’.

That characterization is not supported by Brownstein’s published work.

Dr. Brownstein’s Actual Position

In Salt Your Way to Health, published in 2006, Brownstein argues against the conventional low-salt dogma, but he emphasizes that unrefined salt (like Celtic sea salt or Himalayan salt) is a vital nutrient often misunderstood (Mente et al., 2021; McCarron, 2000).

He does promote using it rather than refined table salt, citing benefits for adrenal issues, fatigue, blood pressure regulation, thyroid function, based on studies and his clinical experience (Barker, 2024). Case observations suggest that mineral composition and intake context matter for certain patients, challenging the assumption that salt restriction is broadly beneficial (Mente et al., 2021).

However, his writings and interviews do not advocate unrestricted consumption, instead emphasizing the value and safety of unrefined salt when used in appropriate amounts and context (Mente et al., 2021).

So, the podcaster set up a strawman. He also claimed that Dr. Brownstein was “new” to the scene of medical freedom and publishing books “for attention”. I entered the medical freedom movement in 2014; Dr. Brownstein had already been active for decades. These ad-hominems are distractions.

The matter of sodium in our diets is nuanced and rich. I hope you enjoy this article:

The Physiological Role of Sodium (Na+) in Human Health

Sodium in Neural Transmission and Cellular Function

Sodium is an essential electrolyte that plays a critical role in nerve impulse conduction and muscle excitation (Hernandez & Richards, 2023). Voltage-gated sodium channels in nerve and muscle cell membranes allow a rapid influx of Na+ when a cell depolarizes, generating action potentials that underlie neural signaling and muscle contraction (Bernal et al., 2023; Hernandez & Richards, 2023). Adequate Na+ is required for normal neural transmission, as without it nerves and muscles cannot function properly. Indeed, genetic channelopathies affecting sodium channels can lead to serious neurologic or muscular disorders, underscoring sodium’s importance in cellular excitability (Bernal et al., 2023).

Beyond excitable tissues, sodium is vital for cellular homeostasis (Mente et al., 2021). The Na+-K+-ATPase pump actively exchanges intracellular sodium for extracellular potassium, helping maintain resting membrane potential and cell volume. This ATP-intensive pump underscores the centrality of sodium gradients to cell function (Bernal et al., 2023). In various epithelial cells (e.g., in kidney tubules, intestinal mucosa), sodium transport is harnessed to drive absorption of nutrients and water. In summary, sodium is indispensable for the electrochemical and metabolic operations of cells, especially neurons and muscle fibers.

Sodium in Fluid Balance and Osmoregulation

As the principal cation of the extracellular fluid (ECF), sodium is the major determinant of ECF osmolality and volume (Bernal et al., 2023). About 90% of the osmotic pressure of ECF is attributable to Na+ and its accompanying anions (Aaron & Sanders, 2013). This means sodium levels tightly govern fluid distribution between body compartments. When ECF sodium concentration rises, osmotic forces draw water out of cells; when sodium drops, water moves into cells. The body vigilantly regulates sodium and water to preserve osmotic equilibrium and blood pressure – a concept known as hydromineral homeostasis. Due to sodium being such a crucial element, even slight deviations in sodium concentration trigger compensatory mechanisms: high plasma osmolality (hypernatremia) stimulates thirst and release of antidiuretic hormone (ADH) to conserve water, whereas low osmolality (hyponatremia) suppresses thirst and ADH, allowing excess water excretion.

Sodium balance is critically important and is maintained via homeostasis that coordinates intake and excretion. Neural and hormonal pathways modulate salt appetite and renal handling of sodium. For example, angiotensin II and aldosterone promote renal Na+ reabsorption and also can stimulate salt appetite, helping restore sodium levels when they are low. On the other hand, cardiac natriuretic peptides and high blood pressure signal the kidneys to excrete sodium (natriuresis) when there is surfeit. In short, sodium is the key osmotic regulator: it ensures proper fluid balance, blood volume, and blood pressure. Without enough Na+, humans cannot maintain adequate circulating volume or perfusion; with too much, edema and hypertension can result (WHO, 2012).

Sodium’s physiological importance is twofold: it enables electrical signaling in nerves and muscles, and it maintains extracellular volume and osmotic stability. These fundamental roles explain why the body tightly controls sodium levels and why both deficiency and excess of sodium can cause serious dysfunction.

Clinical Consequences of Sodium Depletion (Hyponatremia)

Risks and Manifestations of Hyponatremia

Hyponatremia (low blood sodium), defined as a serum sodium concentration below 135 mEq/L, is the most common electrolyte disturbance in clinical medicine (Ghosal et al., 2023; O’Donnell et al., 2020). Even mild sodium depletion can cause diffuse symptoms, and severe hyponatremia can be life-threatening (Suckling & Swift, 2015). Because sodium maintains extracellular tonicity, a drop in serum Na+ causes water to shift into cells, potentially leading to cellular swelling – most critically in the brain (cerebral edema).

Hyponatremia can lead to a spectrum of complications that are especially dangerous when the drop in sodium is rapid or profound. The most serious effects are neurological and arise from cerebral edema due to osmotic shifts. Hyponatremia commonly presents with neurologic symptoms ranging from headache and confusion to seizures, coma, and death (Ioannou et al., 2021). In chronic or slowly developing cases, patients can instead experience subtle cognitive deficits, gait disturbances, or increased fall risk—especially among the elderly. In these populations, hyponatremia has been linked to long-term consequences like decreased bone density, increased fracture risk, and overall functional decline. Other signs like nausea, malaise, or muscle cramps may appear with moderate Na+ deficits. The danger is highest when sodium falls rapidly or to very low levels (<125 mEq/L), which can precipitate acute cerebral edema. Indeed, hospitalized patients with sodium <130 mEq/L have markedly increased mortality, partly due to such severe manifestations (Ioannou et al., 2021).

One of the most feared complications of hyponatremia is osmotic demyelination syndrome (ODS), which can occur if sodium levels are corrected too quickly—particularly in patients who are severely hyponatremic or malnourished. ODS leads to irreversible damage to the myelin sheath, particularly in the central pons, and manifests as locked-in syndrome, spatic quadriplegia, or death. Importantly, even mild or borderline hyponatremia has been associated with poor outcomes in hospitalized patients, including increased ICU admissions and longer hospital stays. Thus, identifying and managing hyponatremia requires careful attention not only to the serum sodium concentration but also to the underlying cause, the chronicity of the condition, and the context in which it occurs.

Common causes of hyponatremia include diuretic medications, syndrome of inappropriate ADH (SIADH) causing water retention, adrenal insufficiency, hypothyroidism, excessive water intake, or losses from vomiting/diarrhea. Often it is a combination of factors that leads to low sodium. Regardless of cause, the clinical principle is that hyponatremia reflects an imbalance of water relative to sodium – usually an excess of total body water diluting sodium.

Vulnerable Populations Prone to Sodium Depletion

Certain groups are particularly susceptible to hyponatremia and its consequences (Ghosal et al., 2023):

• Elderly individuals: Older adults have impaired renal water excretion (due to age-related decline in GFR and sensitivity to ADH) and often take medications (e.g. thiazide diuretics, SSRIs) that predispose to hyponatremia (Ioannou et al., 2021). They may also have diminished thirst regulation, leading to inadvertent overhydration. Hyponatremia in the elderly is especially dangerous: it can cause confusion, falls, and has been linked to increased in-hospital mortality. Even mild chronic hyponatremia may contribute to cognitive impairment and bone fragility in this population.

• Hospitalized and postoperative patients: Hyponatremia is extremely common among inpatients, in part due to intravenous fluids (particularly hypotonic fluids), the stress of surgery, and conditions like heart failure or SIADH triggered by illness. One review noted that hyponatremia is the most prevalent electrolyte imbalance in hospitalized patients (Ghosal et al., 2023). Patients after major surgery or those on pain medications can develop SIADH. Unmonitored use of hypotonic IV drips has led to severe hyponatremia (especially in children).

• Endurance athletes: Exercise-associated hyponatremia (EAH) is a well-recognized phenomenon in marathon runners, triathletes, military trainees, etc. Prolonged intense exercise in the heat leads to sodium loss via sweat, and if an athlete overconsumes water or sports drinks low in sodium, the blood sodium can plummet (Buck et al., 2023). EAH often occurs during or shortly after events, with reported incidence as high as 5–50% of participants having asymptomatic hyponatremia and about 0.1–1% experiencing symptomatic EAH. The resulting cerebral edema can cause disorientation, seizures, or even fatal encephalopathy. Prevention involves moderate fluid intake according to thirst and inclusion of salt in long-duration event nutrition.

Other groups at risk include patients with psychiatric polydipsia, those on MDMA (“Ecstasy”), and postpartum women (due to oxytocin-induced water retention).

Clinical Relevance

Hyponatremia exemplifies the principle that sodium homeostasis is vital for brain function and overall stability. Rapid correction of severe hyponatremia must be done carefully (to avoid osmotic demyelination), but prevention is even better. Awareness of risk factors in the elderly, hospitalized, and athletes can guide more personalized hydration and salt recommendations.

Evolutionary and Historical Context of Salt Intake

Humans’ relationship with dietary salt has deep evolutionary roots. Early in our species’ history, obtaining enough sodium was a greater challenge than it is today (O’Donnell et al., 2015). Most natural foods (especially plant-based diets in inland areas) are very low in sodium, and our ancestors had to seek out salt sources actively. This is reflected in an innate “salt appetite” seen in humans and other terrestrial animals – a hard-wired drive to consume salt when deficient (Bernal et al., 2023).

Coastal Evolution and Natural Salt Access

Many anthropologists have noted that human populations historically clustered near coasts or salt-rich environments and used them as primary migratory routes. Sea water and coastal foods provided not only sodium chloride but also iodine and other minerals. Roughly 40% of the global population lives within 100 km of a coastline – a pattern rooted in part in the historical advantages of coastal living (Kalra et al., 2014).

Coastal peoples could easily harvest salt from evaporating seawater or obtain it from seafood, meaning they had a reliable supply of this critical nutrient. By contrast, inland and highland communities often struggled with salt scarcity. Prior to modern transportation, many inland regions relied on trade routes for salt (hence famous “salt roads”). The establishment of trade networks for rock salt and sea salt was a turning point in human civilization. Records show that ancient central Europe had endemic goiter and cretinism until trade brought iodine-containing salt from coastal areas (Kalra et al., 2014).

One editorial hypothesizes that iodine and salt availability spurred human development and migration. It suggests that the intellectual flowering of Renaissance Europe may have been partly catalyzed by increased iodine intake once intercontinental salt trade supplied inland populations with iodine-rich salt and seafood (Kalra et al., 2014). Historically, inland regions such as the Alps, Himalayas, and central Africa were known as “goiter belts” due to severe iodine deficiency.

Thirst for Salt: An Evolutionary Imperative

From an evolutionary biology standpoint, the human body’s mechanisms reflect the assumption that sodium would be scarce, not overabundant. We have efficient renal sodium conservation (via aldosterone and other pathways) and only weak mechanisms to excrete massive excesses. Our taste buds have a specific receptor for “salty” taste, and studies show that when humans are sodium deficient, their preference for salt increases dramatically – an example of homeostatic appetite (Bernal et al., 2023).

Humanity evolved in environments where sodium was precious, and our physiology is optimized to defend against sodium loss. Coastal living and salt trading were pivotal in ensuring access to salt and iodine. Recognizing this context is important when considering modern dietary guidelines. It reminds us that our bodies are wired to conserve salt and crave it, which might partly explain why universal sodium restriction can be challenging and sometimes inappropriate.

Iodine, Iodized Salt, and the Impact of Reduced Salt Intake

Iodine is an essential micronutrient required for thyroid hormone production, and by extension, crucial for brain development, growth, and metabolism (Zimmermann et al., 2008). Because iodine’s primary natural sources are the ocean (seaweed, seafood, and to some extent coastal soil/water), iodized salt has been the cornerstone of global public health efforts to prevent iodine deficiency disorders for the past century. By fortifying table salt with trace iodine, governments managed to virtually eliminate endemic goiter and congenital iodine deficiency syndrome (cretinism) in many countries. However, a new concern has emerged: efforts to reduce overall salt intake (for cardiovascular benefits) and trends toward non-iodized “gourmet” salts could lead to declining iodine intake in the population (Barker, 2024).

Iodine Deficiency Disorders and Neurodevelopment

Insufficient iodine during pregnancy can cause profound and irreversible neurodevelopmental deficits in the fetus. Iodine deficiency is the leading cause of preventable intellectual disability worldwide (Kalra et al., 2014). Even mild to moderate maternal iodine insufficiency has been linked to lower IQ and learning difficulties in children. Epidemiological studies have shown that moderate iodine deficiency in pregnancy is associated with a higher risk of children having cognitive test scores a few points lower than peers. Severe deficiency can result in cretinism – characterized by extreme, permanent mental impairment, deaf-mutism, and growth stunting in the baby. In adults, chronic iodine lack causes goiter (thyroid enlargement) and hypothyroidism, with symptoms like fatigue, weight gain, and depression. Maintaining adequate iodine through diet or fortification is critical for thyroid function and brain health across the lifespan.

Declining Use of Iodized Salt

Due to conventional medicine’s messaging consistent with the podcaster’s view that regular salt intake is bad for the cardiovascular system, many consumers have cut back on table salt, use low-sodium substitutes, or have switched to specialty salts (sea salt, Himalayan pink salt, etc.) that may not be iodized. Moreover, processed foods – which contribute a large fraction of refined salt in modern diets – often use non-iodized salt in manufacturing. In the U.S., only about half of commercially sold table salt is iodized, and restaurant/processed foods typically do not use iodized salt (Kalra et al., 2014). People who rely on processed foods for their salt intake are therefore getting sodium chloride in the form of refined salt without the iodine. Countries like the UK and Australia, which never fully mandated iodization in all foods, have documented a re-emergence of mild iodine deficiency in recent years (Kalra et al., 2014). In the UK, a 2011 national survey found that ~70% of school-age girls had inadequate iodine status. Australia and New Zealand noted rising iodine deficiency after salt intake declined and dairy sanitization practices changed, prompting renewed fortification policies.

Experts warn that aggressive sodium reduction campaigns may inadvertently increase the risk of iodine deficiency disorders if iodized salt use is not maintained (Rigutto-Farebrother & Zimmermann, 2024). The WHO now faces a dual challenge: how to encourage lower sodium intake for blood pressure control while preserving the gains made in iodine nutrition (World Health Organization, 2012). In a 2024 review, researchers emphasized that salt reduction and iodization strategies must be integrated so that lowering salt does not mean losing iodine fortification benefits (Rigutto-Farebrother & Zimmermann, 2024). Solutions include raising the iodine concentration in salt and ensuring iodine is present in all major salt sources (including processed foods). Some countries have mandated iodized salt in staple foods like bread. However, chronic lowering of salt in the diet can contribute to hyponatremia and the consequent complications from it, especially in certain contexts. These include when when sodium restriction is combined with excessive free-water intake, diuretic use, or impaired renal handling.

Thyroid Dysfunction and Public Health Implications

If iodized salt usage dwindles and iodine intake falls, we can expect a rise in thyroid disorders: more goiters, subclinical hypothyroidism, autoimmunity, and in severe cases, cretinism in newborns. Even marginal iodine deficiency can reduce average IQ and productivity in a population. Approximately 30% of the world’s people are still at risk of insufficient iodine today (Kalra et al., 2014). Nutrition authorities emphasize that lower salt intake must go hand-in-hand with continued vigilance about iodine. Individuals choosing low-sodium diets should ensure they get iodine from other sources (iodine-rich foods like dairy, seafood, seaweed, or a multivitamin) or use a smaller amount of iodized salt instead of non-iodized varieties.

The move toward salt-restriction, if not carefully managed, could undo decades of progress against iodine deficiency, as well as leading to an increase in hyponatremia-related complications. Thyroid experts stress a balanced message: moderate salt reduction is reasonable, but elimination of iodized salt is dangerous (Rigutto-Farebrother & Zimmermann, 2024).

Challenging the Salt-Restriction Dogma: What Does the Evidence Say?

Public health authorities have advised reducing sodium intake to curb hypertension and cardiovascular disease (Whelton et al., 2012). The AHA advocates sodium <2.3 g/day, or <1.5 g for high-risk individuals. This advice is based on the traditional hypothesis that high sodium can raise blood pressure (Dickinson, 2007). However, recent high-quality studies and meta-analyses have prompted re-examination of the “lower is always better” paradigm. Dr. Brownstein covers this is in great detail in his book.

Blood Pressure vs. Hard Outcomes – A Paradox

The conventional medical consensus that reducing very high salt diets lowers blood pressure. A 2021 umbrella meta-analysis of 85 trials confirmed a dose-response relationship between sodium reduction and blood pressure, with larger BP reductions in hypertensives than normotensives (Filippini et al., 2021). However, the controversy arises when we look at actual health outcomes (Aburto et al., 2013). Several large cohort studies observed a J- or U-shaped curve associating sodium intake with mortality: both high and very low sodium intakes were linked to higher mortality, with lowest risk at moderate intake levels (Graudal et al., 2014). Heterogeneity in the population means that universal and simplistic attitudes toward sodium in the diet missing a risk and benefit stratification opportunity with salt (He & MacGregor, 2011).

For instance, a 2014 meta-analysis of 23 cohort studies (n > 270,000) found that sodium <2.6 g/day and >6 g/day were associated with increased all-cause mortality compared to 3–5 g/day, which had the best survival (Graudal et al., 2014). Similarly, the PURE study reported increased mortality and cardiovascular events at very low sodium excretion (Alderman, 2010). These findings challenge the assumption that simply promoting lower sodium intake equates to better outcomes.

The 2013 IOM Report

The U.S. Institute of Medicine reviewed outcomes at different sodium levels. Their 2013 report concluded there was inadequate evidence that lowering sodium below 2.3 g/day improves outcomes in the general population and noted possible harms in subgroups like heart failure or CKD patients (Bibbins-Domingo, 2014). An editorial in JAMA Internal Medicine summarized: “the lack of evidence of benefit and concerns for harm suggest that low sodium intake (<2300 mg/d) should not be universally recommended” (Bibbins-Domingo, 2014; Atkins et al., 2004).

Randomized Trials and Specific Populations

RCTs with hard outcomes are limited. But the SODIUM-HF trial (2022), the largest RCT in heart failure patients, found that reducing sodium below 1500 mg/day did not reduce death or hospitalization compared to usual diet. Mortality was numerically higher in the low-sodium group (Ezekowitz et al., 2022). In CKD, lower sodium helps BP and proteinuria but has no proven benefit on hard outcomes (O’Donnell et al., 2014). DASH and other trials confirm BP benefits from reduced sodium, but diminishing returns appear below 1500 mg/day (Sacks et al., 2001).

While excess sodium intake should be curtailed, data supporting very low sodium diets are less robust. Observational data suggest a J-shaped risk curve. Moderation may provide cardiovascular benefit without unintended effects on lipids, hormones, or iodine status (Rigutto-Farebrother & Zimmermann, 2024; Graudal et al., 2014; Bibbins-Domingo, 2014; Ezekowitz et al., 2022; Filippini et al., 2021).

Conclusion: Rethinking Salt in Science and Public Health

The case against salt, once considered settled, now appears overdrawn, oversimplified, and increasingly out of step with both physiology and evidence- just as the podcaster stated. Sodium is an essential micronutrient with tightly regulated roles in neural conductivity, osmoregulation, adrenal physiology, and vascular volume control. Historically and evolutionarily, humans have prioritized the trade and preservation of salt—not out of ignorance or indulgence, but because survival demanded it.

The emerging literature no longer supports the notion that “lower is always better” for sodium intake (Kong et al., 2025). J-shaped risk curves, null trials in key populations, and population-level trade-offs (like iodine deficiency) all challenge the blanket salt-restriction narrative. It is now clear that different individuals and subgroups have dramatically different sodium needs and tolerances. To prescribe the same ceiling to sedentary hypertensives, endurance athletes, the elderly, pregnant women, and children is scientifically negligent and not in alignment with personalized medicine.

Dr. David Brownstein’s position—advocating for moderate, informed use of unrefined, mineral-rich salt—is not fringe. It is better aligned with biology and emerging evidence than the dogmatic austerity still echoed in some public health campaigns and the podcaster. Dr. Brownstein’s emphasis on salt quality, mineral content, and the need for context (adrenal health, thyroid function, iodine sufficiency) reflects clinical wisdom informed by pattern recognition and outcome awareness. It is neither a free pass for sodium gluttony nor a rejection of blood pressure science. Rather, it is a call to nuance, which the data increasingly demands.

Like most aspects of health, doctors from different domains can have different views based on the patient populations they see. Dr. Brownstein’s patients are kept aware of risks of sugar and carb consumption, and the importance of adequate protein and nutrients in their diet and exercise. Conventional clinical training often prioritizes pharmacologic risk management at the population level, whereas some integrative clinicians emphasize daily behavioral and nutritional modulation. Allopathic medical doctors, as a result, tend to stress pharmaceutical solutions and they may underestimate the utility of empowering their patients to take personal responsibility for most aspects of health on a daily basis. As Dr. Brownstein is my personal physician, I can attest to his holding patients responsible for health-related behaviors.

The real strawman is the one set ablaze by his critics—those who misrepresent his work as reckless salt libertinism while defending a policy paradigm that may inadvertently harm the populations it aims to protect. The science does not justify a one-size-fits-all sodium prescription. It justifies respect—for individual variation, for evolutionary biology, and for the balance between clinical judgment and mechanistic reductionism.

We now need public health policies that reflect that complexity. Moderate salt ingestion remains appropriate for many—but so too does the reintegration of iodine supplementation, personalized guidelines, and the end of punitive low-salt mandates that ignore the full landscape of evidence. If medicine is to progress, it must retire its slogans and dogmatism and return to systems thinking. And salt, it turns out, is an essential nutrient that requires system thinking rather than dogma. A more nuanced physiological systems approach supports and nourishes the human biochemical pathways and leads to better health outcomes.

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