Blood Pressure · Ask Your Body

A number, and the tide behind it

The most-treated condition there is.

High blood pressure is the most-treated chronic condition in the Western world. Nearly everyone knows someone on a tablet for it. And almost nobody has been told what, for a great many of them, is actually driving it.

The story you'll hear is about salt and stress and stiff pipes — and those play a part. But underneath a large share of high blood pressure sits the same fire this series keeps returning to: high insulin. Because insulin, quite apart from its job with blood sugar, is also a salt hormone. It tells your kidneys to hold on to sodium. And where sodium goes, water follows.

For many people, high blood pressure is not a plumbing fault. It's the fire, showing up in the kidneys.

Before anything else: this is not a piece telling you to stop your blood-pressure tablets. Uncontrolled high blood pressure is genuinely dangerous — it quietly damages arteries, heart, kidneys and brain. Nothing here is permission to stop. It's the understanding to have a better conversation with your doctor — and, as you'll see, a reason to see them sooner if you change how you eat. Never change this medication on your own.

Question One

What is the condition, really?

Blood pressure is the force of blood pushing against your artery walls. It rises and falls all day — normal. "Hypertension" means it stays high, and that genuinely matters: sustained high pressure wears out arteries, heart, kidneys and brain over years. This is not a number to shrug at. It earns its nickname, the silent killer.

But notice what the diagnosis actually is: a reading. Like a high cholesterol number, it measures something — it doesn't, by itself, explain why. And for most people, the honest medical position is remarkable when you hear it plainly:

For most high blood pressure, the textbooks say the cause is "unknown."

"Essential hypertension" is the name given to high blood pressure with no identified cause — and it's the vast majority of cases. But "unknown cause" and "no cause" are not the same thing. Follow the fire, and a great deal of that "unknown" stops being mysterious — because one of the body's most powerful salt-retaining signals is running high in exactly these people, and almost no one is measuring it.

Question Two

So what is actually raising the pressure?

Here's the mechanism, in plain steps — settled physiology, not speculation. Insulin tells your kidneys to keep salt.[1] Salt holds on to water. More water means more volume, and in a closed loop of vessels, more volume means more pressure — like a hosepipe stiffening when you open the tap wider.

the fire → high insulin → kidneys hold salt → body holds water → more volume → higher pressure

Blood volume & pressure

Drag the flood up (more insulin = more salt held). Then try turning it down, and adding the drugs.

blood volume

128/82

mmHg

—

The flood — how much insulin is running (the fire)High

Add a drug:

Notice what the drugs do and don't do. Each one brings the number down — real, useful work. But drag the flood back up with a drug on, and the pressure climbs again: the drug bails water out of the boat while the fire keeps the tap running. Only turning down the flood itself lowers the volume at its source.

The two hands on the same rope

Insulin is quietly doing aldosterone's job.

Your body has a dedicated hormone whose main job is to tell the kidneys how much salt to keep: aldosterone. (If you read Cholesterol, you met it — one of the steroid hormones built from cholesterol.) It's run by a system called RAAS — essentially the body's thermostat for salt, water and pressure.

Here's the powerful insight. Insulin and aldosterone are both salt-retention signals, acting on the same kidneys — two hands pulling on the same rope, the one that holds sodium in the body. Normally aldosterone does the job alone. But when insulin is chronically high, it adds a second, constant pull that was never meant to be there.

This is why high blood pressure and high blood sugar travel together so faithfully that medicine bundles them — with obesity and abnormal cholesterol — into "metabolic syndrome." They aren't a coincidental cluster of separate diseases. They are, in large part, the same fire pulling on the same rope: insulin quietly doing aldosterone's job, all day, for years.

The salt gets the blame. But for many, it was never the salt — it was the instruction to keep it.

Question Three

What do the drugs actually do?

Look at the main drugs with the mechanism in mind. Each is a genuinely useful tool for bringing a dangerous number down — and each works downstream of the fire, managing the pressure while the insulin-driven salt retention rolls on.

Diuretics ("water tablets" — bendroflumethiazide, indapamide, furosemide) force the kidneys to dump sodium and water — pushing against exactly the retention high insulin is causing, from the opposite side, for as long as you keep taking them.
ACE inhibitors (ramipril, lisinopril) and ARBs (losartan, candesartan) act on the RAAS system — blunting angiotensin, which lowers aldosterone and relaxes the vessels. Turning down the salt-and-vessel thermostat pharmacologically.
Calcium channel blockers (amlodipine, felodipine) relax the muscle in the artery walls so the vessels widen and the pressure drops — easing the symptom directly, further downstream still.

Notice the shape. Diuretics and RAAS drugs are, in effect, working to undo the salt retention high insulin is busy creating. The drug bails water out of the boat; the fire keeps the tap running. It's real, useful bailing — and it never turns off the tap.

And here's the tell, exactly as in the other chapters. When your doctor manages your blood pressure, what do they measure? The pressure. They do not measure your fasting insulin. The signal driving the salt retention in a large share of patients is never put on the chart — so it's never named, and never addressed. You can have a perfectly "controlled" pressure on three tablets while the fire underneath burns exactly as hot as before.

Question Four

What would addressing the cause look like?

If a large part of the pressure is insulin telling the kidneys to hoard salt, then addressing the cause means turning down the insulin — the same move as every chapter of the fire. And blood pressure is the condition where you can often see it happen fastest.

Why it works so fast

When you cut the refined carbohydrate that spikes insulin, two things happen within days, not months:

Your stored carbohydrate releases its water. Carbohydrate is stored as glycogen, held together with water — roughly three grams of water per gram of glycogen. Use those stores down and that water is released and passed out. This is the famous "whoosh" of early low-carb weight loss — water, not fat, coming straight out of your blood volume.
Insulin falls, and the kidneys stop hoarding salt. As insulin drops, its constant pull on the salt rope eases. The kidneys let sodium go again — and water follows it out. Less sodium, less water, less volume, less pressure. The tap is finally turning down.

This is why people often watch their blood pressure fall within the first week or two of cutting carbohydrate — faster than almost any other change in the body. Not magic; just the volume coming down as retained salt and water leave.

And this is exactly why the safety warning matters so much. If you're on blood-pressure tablets and you cut the carbohydrate, both are now pushing your pressure DOWN at once — the diet and the drug together. That can drop it too low (dizziness, light-headedness, faints). This is a GOOD problem — it means it's working — but a real one, and it's the doctor's job to lower your doses to match. A reason to tell your doctor and see them soon, not to do it quietly.

An honest caveat, and a fix hidden inside it

Some people feel rough the first week — the so-called "keto flu": headache, fatigue, light-headedness, cramps. Here's what almost nobody explains: a lot of it is just the flip side of the mechanism above. You've dumped a load of sodium and water — and now you're mildly salt-depleted. The fix is counter-intuitive and simple: add salt back. A little extra on food, or a pinch in water, resolves most of it. The very sodium-shedding that lowers your pressure is what leaves you briefly short — so a modest amount of added salt during the transition isn't the enemy; it's the remedy.

What this does — and doesn't — explain

Not all of it is insulin.

Now the honesty the rest of the chapter earns. Blood pressure is not all insulin, and this piece would be worthless if it pretended otherwise.

Some hypertension has other real causes — kidney disease, hormonal tumours, certain medications, thyroid problems, sleep apnoea, and genuine genetic salt-sensitivity. These are real, some serious, and they need proper medical diagnosis.
The fall from low-carb is real but usually modest — in the trials, cutting carbohydrate lowered pressure by a few points on average (around 3 mmHg systolic in one careful analysis), not dramatic amounts.[3] Its real power isn't a big isolated drop — it's that the same change improves the whole picture at once: blood sugar, insulin, triglycerides, weight, and pressure, because they were all the one fire.
Much of the benefit travels with weight loss and better insulin sensitivity — not a magic property of the diet. Which is the point: you're improving the terrain, and the terrain is what raises the pressure.

So the honest claim isn't "low-carb cures blood pressure." It's this: for the large share of people whose high blood pressure is part of the metabolic fire, turning down the fire eases the pressure — often quickly — along with everything else the fire was driving. It does it by removing a cause, not by bailing against one. For the minority whose hypertension has another cause, that cause still needs finding. Both are true, and a good doctor holds both.

Where this leaves you

Could we measure the fire, not just the pressure?

High blood pressure is genuinely dangerous, and the drugs that lower it do real, worthwhile work — no one should stop them on the strength of an article. But for a great many people the pressure is driven, in large part, by high insulin telling the kidneys to hold salt: the fire, acting through the same rope as aldosterone. The drugs bail water out of the boat while the fire keeps the tap running — and nobody measures the insulin driving it.

The salt gets the blame. But for many, it was never the salt — it was the instruction to keep it.

So the real conversation with your doctor isn't only "is my blood pressure controlled?" It's "what is driving it — and could we measure the fire, not just the pressure?" A fasting insulin test costs little and would tell you whether the tap is even running. That's the question that turns a lifetime of bailing into a chance of turning off the tap.

Ask your body. Ask what's driving the number. Then you can see the fire for yourself.

Blood pressure is one more flame of the one fire. Back to the whole picture: The Invisible Fire.

Verified references

[1] DeFronzo RA (1981). The effect of insulin on renal sodium metabolism: a review with clinical implications. Diabetologia 21(3):165-171. PMID 7028550. Read →

[2] Horita S et al. (2011). Insulin resistance, obesity, hypertension, and renal sodium transport. Int J Hypertens 2011:391762. PMID 21629870. Read →

[3] Ashtary-Larky D et al. (2024). Impact of very-low-carbohydrate ketogenic diets on cardiovascular risk factors in type 2 diabetes — a GRADE-assessed systematic review and meta-analysis. PMID 39030553. (29 trials; systolic BP −2.85 mmHg, diastolic −1.40 mmHg vs control, alongside falls in fasting insulin, HOMA-IR and triglycerides.) Read →