If you put people on a low-salt diet, meaning only getting twice as much sodium as they need, as opposed to a usual salt diet where they’re getting five times more, you get a significant improvement in artery function. Lower salt begets better arterial function, suggesting heart-protective effects beyond just blood pressure reduction. Now, this was after dropping people’s salt intake by about a teaspoon a day for two weeks. What if you only dropped salt intake by a half teaspoon or so a day? You still get a significant improvement in artery function, and it happens within just two days of reducing one’s salt intake—or, even after a single meal. A high-salt meal, which is to say just a “typical amount of salt consumed in a commonly eaten meal, can significantly suppress [artery function] within 30 [minutes].” In my video Sodium and Arterial Function: A-Salting Our Endothelium, I show what happens 30, 60, 90, and 120 minutes after consuming a meal with just a pinch of salt in it versus eating the same meal, but made with a quarter teaspoon of salt rather than a pinch: a significant suppression of arterial function. Now, is this in addition to the spike in blood pressure from salt or because of the spike in blood pressure?
If you take people with normal blood pressure and give them a bowl of soup containing the amount of salt a regular meal might contain, their blood pressure goes up over the next three hours compared to the same soup with no added salt. Now, this doesn’t happen to everyone; this is just the average response. Some people are resistant to the effects of salt on their blood pressure. So what if you repeated the artery function experiment on them? You get a paper entitled (*spoiler alert*): “High dietary sodium intake impairs endothelium-dependent dilation in healthy salt-resistant humans.” Indeed, even in people whose blood pressure is unresponsive to salt intake, they still suffer significant suppression of their artery function. So, independent of any effects on blood pressure, salt hurts our arteries, and that harm begins within minutes of consumption for our major arteries and even our tiny blood vessels.
Using something called laser Doppler flowmetry, you can measure blood flow in the tiny vessels in our skin. In the video, you can see the measurement of blood flow at baseline. Now, to get the blood vessels to open up, they warmed the skin. The reason we may turn pink when we get into a hot bath is that the blood vessels in our skin are opening up, and that’s what happened: a big increase in blood flow with the warming. That was on the low-salt diet, however. A high-salt diet starts out the same, but after the same warming, there’s significantly less blood flow. The arteries just don’t seem to open up as well on a high-salt diet, unless you inject vitamin C into the skin. That seems to reverse the salt-induced suppression of blood vessel function. So if an antioxidant reverses the salt effect, then the way salt may be damaging our artery function is through oxidative stress, the formation of free radicals in our blood stream. But, how?
There’s an enzyme in our body that can detoxify a million free radicals per second (!), 24 hours a day, 7 days a week. But, compared to a low-salt diet, if we consume a normal-salt diet, we suppress the activity of this detoxifying powerhouse of an enzyme. That may help explain why our artery function is much lower on salt. With our antioxidant enzymes crippled by the salt, all the excess free radicals may be crippling our arteries. Mop up those extra free radicals by infusing vitamin C into the bloodstream, however, and artery function returns to normal. In contrast, on a low-salt diet, if you drip vitamin C into people’s veins, nothing happens because our antioxidant enzymes are already taking care of business and haven’t been shackled by the sodium of a normal-salt diet.
Whereas potassium, concentrated in fruits and vegetables, softens the cells that line our arteries and increases the release of nitric oxide that allows our arteries to relax, sodium in our blood stiffens the artery lining within minutes and reduces nitric oxide release. The more salt, the less nitric oxide is produced. Consume one salty meal, and not only does our blood pressure go up, but our arteries literally stiffen. That’s why we could figure out four thousand years ago that too much salt was bad for us. Maybe we don’t need a double-blind trial. Maybe we don’t need to follow people around for a decade. We may just have to feed someone a bag of potato chips and take their pulse.
My video Sodium and Arterial Function: A-Salting Our Endothelium is part of an extended video series on sodium, trying to set the record straight on the “controversy” manufactured by the processed food industries. Check out the other installments:
Other salt-related videos of interest include:
I touched on potassium in Preventing Strokes with Diet and Lowering our Sodium-to-Potassium Ratio to Reduce Stroke Risk, but I’m looking forward to doing a deep dive into the mineral when I get a chance.
Michael Greger, M.D.
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