Sugar vs Salt: Which is the Real Perpetrator to Causing Hypertension?

Hypertension (i.e., high blood pressure) affects one in three American adults and increases the risk for cardiovascular diseases, including heart disease, stroke, and heart failure, as well as non-cardiovascular conditions, including kidney disease and vision loss.

Although hypertension is common among adults of all ages, adults aged 60 and over are shown to have more cases of hypertension.

For years, a systolic blood pressure of ≥140 mmHg and a diastolic of ≥90 mmHg was the accepted threshold for hypertension⁽¹⁾.

New guidelines classify hypertension as systolic blood pressure ≥130 mmHg or diastolic blood pressure ≥80 mmHg.  This change was enacted following evidence demonstrating a risk of cardiovascular diseases at lower blood pressure values⁽²⁾.

Common treatments for high blood pressure include angiotensin-converting enzyme inhibitors, beta-blockers, calcium antagonists, and diuretics.

The number of prescriptions for anti-hypertensive medications increased from 613.7 million in 2010 to 653 million in 2014, with anti-hypertensive medication costs exceeding $28 billion in 2014⁽²⁾.

It is projected that the total direct costs of hypertension will increase to about $220.9 billion by 2035 [2]. These statistics are quite appalling and clearly indicate a need to control high blood pressure.

High Blood Pressure: Sugar vs. Salt

Typically, people think of salt/sodium as bad for blood pressure and it typically taking the brunt of the accusations from physicians, etc. However, sugar is also responsible for high blood pressure and is a leading cause of it.

Fructose, a type of simple sugar, raises the levels of uric acid in the blood, which in turn inhibits the production of nitric oxide. Evidence indicates that nitric oxide plays a major role in regulating blood pressure and that impaired nitric oxide bioactivity is an important component of hypertension.

Clinical studies have shown that patients with hypertension have a blunted arterial vasodilatory response to infusion of endothelium-dependent vasodilators and that inhibition of nitric oxide raises blood pressure.

Impaired nitric oxide bioactivity is also implicated in arterial stiffness, a major mechanism of systolic hypertension⁽³⁾.

In addition, increased sugar consumption can cause weight gain, which can lead to being overweight or obese.

Obesity is a major contributor to elevated blood pressure⁽⁴⁾. Particularly, the excessive visceral fat distribution seen in obesity is accompanied by several alterations at hormonal, inflammatory and endothelial levels. These alterations induce a stimulation of several other mechanisms that contribute to the hypertensive state and increase cardiovascular morbidity (see figure below).

The refined sugar in processed foods is considered to be mainly responsible for hypertension⁽⁵⁾.

While the potential benefits of sodium-reduction strategies are debatable, one fact about which there is little debate is that the major sources of sodium in the diet are industrially processed foods.

In addition, consuming processed foods, which are generally higher in added sugars, may be more strongly and directly associated with hypertension and cardiometabolic risk.

Research indicates that added sugars, particularly fructose, may increase blood pressure and blood pressure variability, increase heart rate and myocardial oxygen demand, and contribute to inflammation, insulin resistance and broader metabolic dysfunction⁽⁵⁾.

I think it is time for regulatory committees & agencies to shift focus away from salt and focus greater attention to the likely more-consequential food additive: refined sugar.

A reduction in the intake of added sugars, particularly fructose, and specifically in the quantities and context of industrially-manufactured consumables, would help not only curb hypertension rates, but might also help address broader problems related to cardio-metabolic disease⁽⁵⁾.

See below figure for a diagram encompassing the hypertensive mechanisms of fructose. 

In addition, research suggests that sugar intake can increase salt sensitivity, leading to the enhanced negative effects of sodium on blood pressure⁽⁶⁾.

A 2017 research study discovered a significant association between intake of added sugar and systolic and diastolic blood pressure in females after controlling for age, income, body mass index, physical activity levels, daily calorie intake, and blood pressure medication use.

These findings support the dietary guidelines of limiting daily intake of added sugar and increasing fruit consumption to promote overall cardiovascular health in older adults⁽⁷⁾.

Sugar and insulin

As we know, an increase in sugar (i.e., glucose) enhances insulin. Insulin is a hormone that pulls glucose from the food we eat into cells, where it is utilized for energy.

Hyperinsulinemia is characterized as an above average insulin level and is one of the diagnostic criteria for type 2 diabetes.

Type 2 diabetes is a condition that occurs when the body becomes less sensitive to insulin and cannot use it effectively to turn sugar into energy.  If left untreated, hyperinsulinemia can potentially lead to high blood pressure⁽⁸⁾.

In fact, research indicates that roughly half of those with hypertension have either hyperinsulinemia or glucose intolerance⁽⁹⁾.

Eventually these chronic high insulin levels cause insulin resistance, where your body can’t utilize glucose for energy because it doesn’t respond to insulin like it should.  Insulin resistance is closely linked to hypertension, and together they lead to an increased risk of heart disease and diabetes. 

Summary

High-sugar diets may contribute substantially to cardio-metabolic disease. While naturally occurring sugars in the form of whole foods like fruit are of no concern, evidence suggest that added sugars (particularly those engineered to be high in fructose) are a problem and should be targeted more explicitly in dietary guidelines to support cardio-metabolic and general health.

Added sugars probably matter more than dietary sodium for hypertension, and fructose in particular may uniquely increase cardiovascular risk by inciting metabolic dysfunction and increasing blood pressure variability, myocardial oxygen demand, heart rate, and inflammation.

Just as most dietary sodium does not come from the salt shaker, most dietary sugar does not come from the sugar bowl. Therefore, it’s crucial to take a proactive approach to reducing consumption of added sugars by limiting the processed foods that contain them.

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References:
1.    Whelton, P.K., et al., 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol, 2018. 71(19): p. e127-e248.
2.    Benjamin, E.J., et al., Heart Disease and Stroke Statistics-2018 Update: A Report From the American Heart Association. Circulation, 2018. 137(12): p. e67-e492.
3.    Matthias Hermann, A.F., Thomas F Lüscher, Nitric oxide in hypertension. J Clin Hypertens (Greenwich), 2006. Dec 8: p. 17-29.
4.    Seravalle, G. and G. Grassi, Obesity and hypertension. Pharmacol Res, 2017. 122: p. 1-7.
5.    DiNicolantonio, J.J. and S.C. Lucan, The wrong white crystals: not salt but sugar as aetiological in hypertension and cardiometabolic disease. Open Heart, 2014. 1(1): p. e000167.
6.    Preuss, H.G., et al., Blood Pressure Regulation: Reviewing Evidence for Interplay Between Common Dietary Sugars and Table Salt. J Am Coll Nutr, 2017. 36(8): p. 677-684.
7.    Mansoori, S., et al., Added Sugar Intake is Associated with Blood Pressure in Older Females. Nutrients, 2019. 11(9).
8.    Weyer, C., et al., A high fasting plasma insulin concentration predicts type 2 diabetes independent of insulin resistance: evidence for a pathogenic role of relative hyperinsulinemia. Diabetes, 2000. 49(12): p. 2094-101.
9.    Zhou, M.S., A. Wang, and H. Yu, Link between insulin resistance and hypertension: What is the evidence from evolutionary biology? Diabetol Metab Syndr, 2014. 6(1): p. 12.