I wrote last week on how fructose can lead to fatty liver, which can then contribute to metabolic syndrome generally. This week is a variation on a theme: how a metabolite of fructose, uric acid, can lead to one of the symptoms of metabolic syndrome: high blood pressure.
Where Uric Acid Comes From
Uric acid is best known as the compound that causes gout, and it’s usually associated with consuming meat and beer. This is because both are high in purines, which break down into uric acid. Other types of alcohol can confer some dose-dependent risk, too.
The other pathway for uric acid production comes from fructose, and sucrose (due to its fructose component). As we discussed last week, high fructose leads to a fatty liver, as well as oxidative stress to the mitochondria, and metabolic dysfunction.
Fructose hides in all kinds of processed foods these days, including high fructose corn syrup of course, as well as fruit juice, cane sugar, agave, and even honey.
The High Blood Pressure Connection
Uric acid has been connected to elevated blood pressure since 1874—amazing that they could even test for it back then! Since then, epidemiological studies have shown the correlation between uric acid and both hypertension and chronic kidney disease, too. The kidney disease association makes sense, as uric acid is one of the primary components of urine (hence the name).
We’ve also known for decades at least that there is a connection between the Standard Western Diet and hypertension, though the exact mechanism here hasn’t been clear either.
Only relatively recently have the studies begun to draw a causal link between diet, uric acid, and hypertension.
First, studies established that uric acid influenced hypertension when giving uric acid inhibiting medications successfully lowered blood pressure. This showed that one affects the other. It was also established that high uric acid levels, independent of any other symptoms or risk factors, predicted later hypertension.
How Uric Acid Raises Blood Pressure
We’ve since learned that there are several possible mechanisms of action for how uric acid might raise blood pressure.
The first is through the kidneys, as again, chronic kidney disease is often part of the picture of elevated uric acid as well. Uric acid can deposit on the lining of blood vessels all over the body, including in the kidneys, leading to decreased blood flow. Decreased blood flow to the kidneys activates a feedback system (called the renin-angiotensin-aldosterone system) which triggers multiple mechanisms to raise blood pressure. The idea is that increasing blood pressure will increase blood flow to the kidneys and thus, increase kidney filtration. Because of this system, the kidneys are a common target for several different classes of blood pressure medications.
But this same deposition of uric acid in the blood vessels in the kidneys can happen everywhere else, too. This has been shown to trigger damage to the endothelial (blood vessel) lining, including increased endothelial stiffness, decreased nitric oxide function, necessary for blood vessel dilation, and increased oxidative damage to the endothelial lining.
Eventually this process can lead directly to full-blown cardiovascular disease—including but not limited to hypertension. High uric acid has been linked to elevated coronary calcium scores as well.
If you have primary, or unexplained, high blood pressure, or cardiovascular disease generally, consider checking your uric acid levels—where levels should not just be normal according to the lab reference range, which is really just a bell curve of the population, and not reflective of optimal health. This study proposes an ideal target of <6.0 for healthy people.
And while you’re at it, this is a whole new reason to cut out processed foods, to greatly limit sugar and beer, and to moderate your meat intake.