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Shifting the Paradigm: Why Added Sugar, Not Salt, Is the Leading Dietary Culprit in Hypertension and Cardiovascular Disease

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dr. Karunia Valeriani Japar

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Introduction

A growing body of research is challenging long-held beliefs regarding the dietary drivers of cardiovascular risk, particularly the roles of salt and sugar in the development of hypertension and cardiovascular disease (CVD). For decades, hypertension- the principal modifiable risk factor for CVD- has been epidemiologically linked to high salt intake, leading to global campaigns and guidelines emphasizing sodium restriction as a mainstay for prevention and management. Salt (sodium chloride) is a ubiquitous seasoning in most societies; its consumption is often governed by individual taste rather than strict public health advice, except among those with existing conditions such as hypertension, diabetes, or renal impairment [1,2,3,4].

The pathophysiological connections between high sodium and adverse cardiovascular outcomes have been substantiated by numerous meta-analyses and large cohort studies, showing that excess sodium leads to volume overload, activation of neurohormonal systems (notably the renin-angiotensin-aldosterone system), endothelial dysfunction, and vascular remodeling, all of which amplify risk for hypertension, heart failure, and arterial stiffness. Countries with high mean sodium intake often demonstrate greater population rates of hypertension and related complications, and a clear association has been observed between habitual high salt intake and increased stroke and CVD incidence- especially in older or salt-sensitive individuals [2,3,4].

Critically, a more nuanced view is emerging: recent systematic reviews and clinical trials reveal that the risk curve for dietary sodium and cardiovascular events is J-shaped, with both very high and very low intakes posing independent dangers. Patients subjected to aggressive sodium restriction show increased risk for all-cause and cardiovascular mortality signaling that sodium is physiologically vital nutrient whose intake should be optimized- not minimized [3,4].

While the link between salt and hypertension is robust, emerging evidence points to added sugar– especially in processed foods and beverages- as a far more significant driver of CVD, obesity, insulin resistance, and metabolic disease. Ultra-processed, sugar-laden diets contribute to metabolic derangements and vascular injury independently of sodium intake, suggesting that the global focus on salt may have inadvertently distracted from the damaging effects of sugar. The evolution of this medical “ misconception” demands a critical reassessment; only by understanding the comparative pathophysiology and population evidence for both salt and sugar can clinicians and policymakers more accurately target the true dietary risks for cardiovascular disease [2,3,4,5,6].

History of The Current Misconception

For decades, public health campaigns and clinical guidelines have prioritized sodium restriction as a primary intervention for hypertension and cardiovascular disease. Influential population studies like INTERSALT and PURE bolstered associations between high salt intake and increased blood pressure, shaping low-sodium recommendations worldwide. Conversely, sugar’s role received less direct attention despite parallel epidemiological trends in obesity diabetes, and cardiovascular events associated with excess sugar consumption. Food industry influence and early research gaps contributed to the “blame salt” narrative, overshadowing sugar’s harmful effects [3,4,7,8,9,10].

Mechanism of Sugar Causing What Salt Is Blamed For

Sugar, especially in the forms of added fructose and glucose, mechanistically drives the same cardiovascular and metabolic derangements that have historically been blamed on excessive salt intake. Detailed molecular m vascular, and endocrine mechanisms have emerged from recent research:

  • Endothelial Dysfunction and Hypertension
    • Fructose metabolism in the liver rapidly depletes cellular ATP, leading to increased uric acid production. Elevated uric acid induces oxidative stress and impairs endothelial nitric oxide availability, resulting in vascular stiffness and hypertension core pathologies previously attributed mainly to salt [11,12,13].
    • Endothelial dysfunction develops with chronic hyperglycemia and sugar intake, involving mitochondrial oxidative stress, inflammation, and direct impairment of vasodilatory function. Hyperglycemia activates TGF-b and NF-kB pathways, leading to pro-inflammatory signaling, endothelial-to-mesenchymal transition (EndMT), and reduced nitric oxide bioavailability- key triggers for sustained blood pressure elevation [14,15,16].
  • Insulin Resistance and Metabolic Syndrome
    • Excess Sugar Intake- especially from sugar-sweetened beverages- promotes a cycle of insulin resistance, elevated circulating free fatty acids, and hepatic de novo lipogenesis. This drives metabolic syndrome and markedly increases cardiovascular risk, independent of salt intake [12,17,18].
    • Chronic sugar exposure disrupts satiety signaling, reduces leptin sensitivity, and aggravates weight gain, creating a feed-forward loop for obesity, hypertension, and vascular remodeling [13,19].
  • Vascular and Cardiorenal Damage
    • Fructose- induced hyperuricemia impairs kidney function and contributes to sodium retention and vascular inflammation, thereby exacerbating hypertension in a manner similar to -or greater than -salt excess [12,20].
    • Hyperglycemic episodes directly damage renal glomerular endothelial cells, promote oxidative stress, and activate pro-inflammatory cytokines, escalating vascular and cardiorenal injury that mirrors adverse outcomes of high sodium diets [12,15,16].
  • Promotion of Arterial Stiffness and Cardiometabolic Risk
    • Clinical studies confirm that high added sugar intake independently increases risk for hypertension, stroke, myocardial infarction, and heart failure. The pathogenic pathway overlaps substantially with the pressure-natriuresis and arterial stiffness described in salt-sensitive hypertension [13,14,21,22].

In summary, sugar-via hepatic metabolism, oxidative and inflammatory endothelial injury uric acid elevation, and metabolic syndrome- causes the same vascular, renal, and myocardial pathologies that have been blamed solely on salt. Recent data solidly position sugar as a major culprit behind hypertension, endothelial dysfunction, and cardiometabolic disease [11,12,13,15,16,17,20].

Evidence and Mechanism of the Correct Concept

Recent human and animal research shows that high sugar consumption can drive or amplify salt cravings and increase sodium intake through several neurobiological and physiological mechanisms. This connection is bidirectional and complex, with implications for cardiovascular and metabolic health [23,24,25,26].

  • Neurobiological Mechanisms
    • Reward Circuitry Overlap: Both sugar and salt activate dopamine and opiate pathways, deeply engaging the brain’s reward and pleasure systems. After repeated sugar intake, neural plasticity develops, and sugar-sensitive neurons in the nucleus tractus solitarius (NTS) become more responsive to sodium. Animal studies show that nearly half of sugar-responsive neurons begin to encode sodium taste after sodium depletion or repeated sugar intake, increasing salt appetite even at normally aversive concentrations of salt [26,27].
    • Sensitization and Behavioral Change: Rats exposed to repeated glucose-induced sodium depletion demonstrate escalating salt intake over subsequent exposures- suggesting sensitization of sodium appetite as a learned and plastic behavior. Humans similarly develop strong cravings for salty foods in the context of high sugar diets and repeated taste exposures [25,26,27].
  • Appetite and Consumption Patterns
    • Palatable Food Synergy: Highly palatable foods- typically rich in both salt and sugar- drive stronger emotional and reward responses than either alone. Sugar-sweetened beverages and processed foods often combine these flavors, lowering satiety, increasing total energy intake, and fostering greater consumption of salty foods alongside sweet ones [25].
    • Sugar, Insulin, and Sodium Retention: Mechanistically, sugar stimulates insulin secretion; insulin then signals the kidneys to retain sodium, raising plasma sodium levels and potentially promoting craving for further salt intake. This feedback loop increases overall sodium and caloric consumption and risk for hypertension [28].
  • Observational Evidence and Dietary Data
    • Epidemiological link: Recent NHANES analyses reveal that individuals with lower reported sodium intake paradoxically had higher mean sugar consumption- suggesting dietary trade-offs within populations. This may reflect a propensity of those reducing salt to compensate with sweet foods, or vice versa, and highlights shared behavioral and reward-driven mechanisms [24].
    • Co-consumption in Real Life: Studies consistently show that snacking outside the home increases intake of both sugar and salt together, illustrating real-world collaboration between these taste preferences and their health effects [29].

Are There Any Rights in Misconception?

It is established that very high salt intake can raise blood pressure and exacerbate cardiovascular risk, especially in salt-sensitive individuals or those with existing hypertension. The risk, however, follows a J-shaped curve: extreme low sodium may also harm cardiovascular health due to neurohormonal activation and possible increases in insulin resistance. Thus, while sodium is not benign, the singular focus on salt reduction overlooks, the much larger impact of sugar, especially in populations with already excessive sugar intake [2,4,8,10,30,31].

Conclusion

Mounting evidence now confirms that excessive blame placed on dietary salt for global cardiovascular and metabolic burden is misplaced; added sugar and its metabolic consequences are the leading dietary drivers of these conditions. While salt reduction remains important, especially for high-risk groups, public health interventions should prioritize limiting sugar intake to reduce the incidence of hypertension, metabolic syndrome, diabetes, and heart disease. Policym clinical, guideline, and education must evolve to reflect this new consensus and more accurately target disease prevention [8,32,33,34].

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