Understanding Blood Pressure Changes

Doctors just changed the definition of normal

blood pressure again, and people are confused.

Back in the 1970s, 160 over 95

was considered acceptable, then it dropped to 140 over

90. Now the target is even lower. So what

happened? Did our bodies suddenly change?

And more importantly, is high blood pressure actually

causing more deaths, or is it just a symptom of

something deeper going wrong inside our bodies?

110 over 70 is now optimal, and anything higher is dysfunction, which

is catastrophic, and I'll prove it.

So systolic, big number, diastolic, small number.

We don't have to get into anything else.

So 2018 Lancet, one million adults found no increased

mortality at 150 over 100, systolic over diastolic, zero.

But at 110 over 70? All right, let's look.

2020 American Journal of Hypertension showed increased all-cause

mortality. Here's what really increases blood

pressure, systemic inflammation,

insulin resistance, and mitochondrial dysfunction.

So let's rock and roll.

Insulin resistance forces kidneys to retain sodium.

Basic physics, water follows sodium osmotically.

Plasma volume increases, blood thickens like syrup,

which increases resistance and

pressure rises. Biology did exactly what it's supposed to,

maintain

fluid balance in response to faulty signaling.

The disease is insulin resistance. High blood pressure is the compensation.

Let's keep going. Nitric oxide produced by the endothelium

and its job,

tell vessels to relax and open up. Chronic inflammation produces

reactive oxygen species. Superoxide is the worst one.

It oxidizes the cofactor that eNOS needs to function.

This is called eNOS uncoupling. Uncoupled eNOS doesn't make

nitric oxide, it makes more superoxide.

Arteries become rigid, more inflamed, and biology raises pressure to

force blood through the rigid pipes.

The disease is endothelial dysfunction.

High blood pressure is survival. And vascular smooth muscle cells need

ATP to relax. No ATP, no relaxation.

Vascular cells are exhausted and can't pump calcium out, muscles stay

contracted, and vessels stay constricted.

If you have normal endothelial function, mitochondrial function, and insulin

sensitivity, meaning you've measured these things,

then elevated blood pressure

isn't pathological, it's compensatory.

But how many doctors are measuring mitochondrial ATP capacity,

endothelial

function, testing vascular reactivity using

flow-mediated

dilation tests, or running continuous glucose monitors?

None.

They're treating numbers. 2012 Circulation proved diastolic below 70

reduced coronary perfusion and increased myocardial infarction risk.

2004 Kidney International proved 110 systolic

with any kidney disease accelerated renal decline.

2018 Neurology proved systolic below 110 increases dementia

risk. Why is that? Inadequate cerebral perfusion.

So your 75-year-old mother with rigid calcified vessels might need

150 over 90 to keep her brain, heart, and kidneys perfused.

It's not pathological hypertension, it's compensatory physiology

keeping her alive. The INVEST trial 2003 JAMA showed

exactly what they're trying to bury.

If pressure is too low, your mortality goes up.

2016 JAMA analyzing 1.3 million patients,

the lowest cardiovascular event rate occurred at 139 over 89.

Hypertension is biology's solution to systemic inflammation,

insulin resistance, and dead mitochondria.

Fix those and the symptom resolves. Comment alive for the research.

Everything you need is in there. I've gotta go. Never miss.