Is Salt the Cause of Hypertension?

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Salt intake is often considered one of the main factors behind high blood pressure. But the evidence supporting this idea is very weak, and eating less salt has a very marginal effect (and could sometimes even be dangerous).

Likely, there are other factors, like high levels of insulin, that play a much more powerful role in raising blood pressure. Professor Grant Schofield has written a very interesting piece on this, and even had a letter published in the Lancet:

High insulin causes salt retention, that can result in high blood pressure. If you suffer from this, it might be a good idea to switch to a low-carb diet, that lowers the insulin. That means that you’re treating the cause, not just a symptom.

How to Normalize Your Blood Pressure

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2 Comments

  1. J L De Foa MD
    So how might insulin cause salt retention? Perhaps insulin, as in hyperinsulinemia, is only an association, not a cause.

    A normoglycemic person will make 180 L of urinary filtrate daily, with each litre containing 1 g of glucose. After 24 hours 178.5 L of that will have been reabsorbed (leaving 1.5 L of urine), and pretty much all of the glucose too. Protein, known as micro-albumin, is similarly reabsorbed. The principle is one doesn't toss fuel and building materials in the dumpster when one is maintaining a house in a cold climate! So the body likewise doesn't readily dispose of glucose and protein. To produce glycosuria, that is to exceed the kidneys' glucose reabsorption powers, one needs to have hyperglycemia of about 11 mmol/L or more. At that level and above the filtrate contains 3 g of glucose or more. While the kidney can resorb the first 3 g of glucose in each litre of filtrate, it can't cope with more, even though the proximal renal tubule LENGTHENS to give more time to do the job. It is like lengthening the conveyor in a garbage sorting & recycling plant so more workers have more time to grab the recyclables to keep them from going to landfill or incineration.

    Now here is where salt comes in. The SGLT1 & SGLT2 glucose co-transporter proteins which recover that 1 to 3 g of glucose from each litre of filtrate use Sodium to help do the job. To rescue one glucose molecule one sodium ion will be brought back into the blood. So if three times as much glucose than normal is rescued daily, then three times as much sodium is returned to the blood also. Granted, that sodium gets "recycled" through many litres of urinary filtrate, each ion ultimately helping rescue / transport many glucose molecules back into the blood until they are either burned for energy or stored as fat.

    Further along in the renal tubule's plumbing salt is actively excreted if excess remains in the serum. But the harder the system has to work the easier it is to end up with elevated sodium levels - known as hypernatremia. Clinical hypernatremia is rarely seen, and in patients not in the ICU is most often seen in elderly dehydrated persons, who actually are often also lacking in absolute sodium, but lack proportionately more water, so they may be hypernatremic but not hypernatriotic (elevated body sodium). So the hypernatremia from increased glucose resorption is a relative hypernatremia at worst, and while a patient might have serum sodium levels in the upper part of the normal range, for others it might be toward the lower end!

    How would that happen, retaining more sodium but having low normal natremia? It has to do with water intake. Drink less water, one dehydrates and develops hypernatremia. Drink more water diluting the serum gives hyponatremia, and if done to excess, diabetes insipidus (the other "diabetes"). If the extra sodium retention is accompanied by proportionately more water intake then one could be hyponatremic (low serum sodium) but also have hypernatriosis (elevated body sodium). That extra water in the pipes can add to hypertension, just as dehydration usually manifests with hypotension (and tachycardia - but that is enough cardiology for this note).

    How might salt lead to hypertension anyway? (I've already given a clue.) Sodium is a solute, and serum has a certain osmolality (total solute concentration). To keep solutes at their normal concentration the right amount of water is required. So if one is retaining salts (sodium, potassium, calcium, magnesium, and more), then one must retain more water to keep them diluted appropriately. Why was that sodium/salt retained? Well, it was recovering the extra glucose that was in the urinary filtrate!

    Glucose is also a solute, and blood glucose is one of the items used clinically to calculate serum osmolality. If one patient has a serum glucose of 6.0 mmol/L, formerly considered "normal" but now the threshold between "at risk" and "pre-diabetes mellitus" (though almost 50% below the level that produces the clinical sign of "diabetes mellitus", or glucosuria), that is actually 50% HIGHER than if serum glucose was 4 mmol/L. So with 50% more glucose there will be osmotic pressure to retain more water, which will add pressure to retain more sodium to keep its concentration UP too! It all eventually comes to a fine balance, thanks to the kidneys. (Dr. Jason Fung could wax eloquent about how that happens, I'm sure.)

    Now here is the link between insulin and hypertension. Chronically elevated carbohydrate intake can cause chronic hyperinsulinemia, which drives further hunger for carbohydrates, which maintains elevated (though officially "normal") serum glucose, which means more glucose in the urinary filtrate which must be rescued by sodium and the SGLT transporters, leading to sodium retention, leading to water retention, leading to hypertension. (The newest glycemia reducing medicines lower the renal threshold for glycosuria to about 5 mmol/L by blocking the SGLT2 transporters, letting all that glucose go down the drain. So after you spent your money to acquire that glucose you spend money on pills to help you piss it all away. But your serum glucose reading looks better, and glucose in the toilet doesn't end up around the waist, which is nothing to sneeze at. However, just not eating the surplus glucose in the first place would make much more sense.)

    Oh, and the hyperinsulinemia from the glucose consumption is also pro-inflammatory, which helps atherosclerotic plaques to progress. So, have another donut, potato, plate of spaghetti or bowl of sticky rice, wash it all down with a soda, and have a happy heart attack!

  2. Leigh Ann
    Excellent explanation, Dr. De Foa! Thanks!!

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