While beets and other nitrate-rich vegetables may provide benefits as a natural performance enhancer—and in athletes, some of that reputation is deserved—the leap from better exercise performance to treating hypertension is not supported by the biology or by the evidence.
The confusion begins with nitrate, a compound found in beets and other vegetables that can enter the body’s nitric oxide pathways. Nitric oxide is central to vascular biology, which makes the story sound simple: More dietary nitrate, more nitric oxide, lower blood pressure.
The actual physiology is far more constrained. The benefits seen in exercise arise under specific local conditions in working muscle; they do not translate into a reliable systemic treatment for hypertension.
The legitimate evidence begins in sports physiology.
Beets and beet juice for sports performance
Research initiated by groups in the UK and Scandinavia has found that beets or beet juice can improve cardiovascular performance in sports, particularly in activities with intense aerobic demands, such as cycling, swimming and distance running.
Researchers identified organic nitrate in beets as the biochemical driver behind these benefits, but the findings are not universal. In one study of individuals with chronic obstructive pulmonary disease, a four-fold increase in plasma nitrate had no effect on blood pressure or performance.
Exceptions to the rule are always insightful.
Natural product approaches to enhanced sports performance attract attention. The central question, however, is how nitrate produces these effects. The proposed mechanism involves a series of reduction steps: Nitrate is converted to nitrite, and nitrite is then converted to nitric oxide.
Nitric oxide has been the focus of intense research since scientists discovered that it is generated from the amino acid L-arginine through three distinct enzymes known as nitric oxide synthases. That work helped lead to the 1998 Nobel Prize in Physiology or Medicine for the discovery that nitric oxide acts as a signaling molecule in the cardiovascular system. Long before the beet-juice debate, nitric oxide-delivering drugs were known to lower blood pressure because of their vasodilator properties. They do this by activating guanylate cyclase and elevating cGMP. It was not until the 1980s, however, that our research identified a lack of nitric oxide as a key driver of high blood pressure endothelial nitric oxide and hypertension.
That history makes enthusiasm for natural ways to raise vascular nitric oxide understandable. The problem is that the nitrate-nitrite-nitric oxide pathway operates independently of nitric oxide synthase, and its effects appear to be highly context-dependent.
The initial conversion of nitrate to nitrite is driven by nitrate reductase enzymes in specific bacteria in saliva. The next step—the conversion of nitrite to nitric oxide—can occur under acidic conditions or through hypoxia-induced activation of xanthine oxidase. Those conditions are most likely to occur locally, in hard-working muscle, not systemically throughout the circulation.
In extreme aerobic exercise, such as competitive cycling or marathon running, working muscles can create the low pH and relative ischemia needed to convert nitrite to nitric oxide. The likely result is a localized increase in blood flow that helps deliver oxygen and nutrients while removing metabolic byproducts such as lactic acid.
My research team tested whether this scenario was limited to aerobic exercise. In a strength-training study, a bar product combining beets with antioxidants improved performance and muscle recruitment. Importantly, however, these benefits occurred without changes in blood pressure.
The lesson is that hard-working muscles can tap the nitrogen cycle to generate nitric oxide locally, but that does not mean beets produce a meaningful systemic effect on blood pressure. In the presence of hemoglobin, nitric oxide has a half-life of milliseconds before it is rapidly oxidized back to nitrate. The effect is localized and mild, not body wide and sustained.
That distinction matters. Some aerobic exercise studies show small reductions in systolic blood pressure, often around 2 to 4 mmHg, while others show no effect. A large meta-analysis of beet or beet-juice interventions found a small effect on systolic blood pressure, but no effect on diastolic pressure, mean arterial pressure or 24-hour blood pressure measurements. The authors concluded: “There is no evidence for a prolonged 24-h BP-reducing effect. Certainty of evidence is low.”
For sports performance, the nitrate story has value. For hypertension, it is often taken out of context.
Nitric oxide and the circulation
Beyond the issues with the accuracy of measuring blood pressure (systolic, diastolic and mean) we need to better place perspective on how nitric oxide works and where? Nitric oxide production in blood vessels has a half-life of a few milliseconds, as my team defined with a unique electrochemical probe. Basically, all nitric oxide actions are local, and when it interacts with hemoglobin it is rapidly oxidized to nitrate and other reactive nitrogen species before it can circulate like a hormone. The furthest it can reach from sites of production is a few cells, certainly not like a circulating hormone.
For increased nitric oxide production to lower blood pressure, one needs a substantially greater production of nitric oxide and it needs to be systemic, i.e., throughout the body and not just a working muscle. There can be a role for nitric oxide in controlling vascular resistance but also in septic shock. In the latter, excessive production of nitric oxide, activated by bacterial infections, greatly reduces vascular tone and limits organ perfusion as a result of the substantially reduced blood pressure. My research team showed that capturing excess NO with vitamin B12 (via its bonding with the cobalt atom) could sequester excess nitric oxide and limit organ failure and mortality in sepsis.
From this it is clear that nitric oxide plays an important role in circulatory function, as seen with examples of excess and inadequacy.
Vascular resistance and systolic vs. diastolic blood pressure
The other concept that needs to be accounted for, is that as a vasodilator, nitric oxide would primarily influence blood pressure by lowering vascular resistance, as opposed to cardiac output.
When we measure diastolic blood pressure, we are getting a window into the arterial resistance of the cardiovascular system because it is independent of the heart contractions. Conversely, systolic blood pressure reflects when the heart contracts and that impact is layered on top of overall systemic vascular resistance.
When an intervention, like beets, does not alter diastolic (or mean) arterial pressure then there one can safely assume that vascular resistance is not altered. In other words, there is no evidence that ingestion of nitrate rich beets promotes systemic vasodilation.
If nitric oxide was being produced systemically in amounts that cause widespread vasodilation, then diastolic blood pressure would fall. It doesn’t in any of these studies with beets.
Food vs. supplements vs. drugs
Inherent in the rampant publicity that is associated with beets and blood pressure is the robust enthusiasm to manage a pervasive and critical healthcare issue, hypertension, with dietary driven solutions.
Here there is a passionate abhorrence to using supplements and pharmaceuticals, after all “Food is they Medicine”. Directed by that passion and amplified by a lack of understanding of the complexities of the biochemistry of nitric oxide and related nitrogen oxides, the impact of this combination is that a false narrative is generated and spread profusely.
Historical perspectives are tossed aside as being too confusing. Information like the vasodilators nitroprusside and nitroglycerin, the Nobel Prize for those actions and the nitric oxide generation from L-arginine, and the massive amount of research on nitric oxide in general, are not included as they are not food generated.
Dr. Mark JS Miller has extensive experience in entrepreneurship, M&A, manufacturing, R&D, marketing and brand building within the natural products industry. Prior to that transition he was a tenured professor of pharmacology, pediatrics and cardiovascular edicine in three different US-based medical schools.
His contributions to our understanding of nitric oxide and related reactive nitrogen species has defined health and disease across a wide range of disciplines and systems. They include cardiovascular function, inflammation, gastroenterology, cancer, fetal development, neonatal nutrition, sports performance and biochemistry.
