Hypertension Is a State of Defense: Energy, Stress, and the Healthspan Equation
You said:
"Hi, Ray. Happy Friday, February 13th, 2:35 p.m.
Right now, I'm fascinated about this idea that energy begets more energy in the human body. It seems like the biggest contradiction of life, really — how moving more can actually make us more insulin sensitive and have more energy. It just seems to fly against all logic without knowing the physiology.
So, can we go down that magical path a bit and see what comes of it?
I just noticed an old man kind of shuffling across the crosswalk and taking a while to get to the other side, and I thought to myself, you know, maybe age is just an electrolyte and energy thing. I mean, not maybe. I feel like I've got my finger on something important here.
If we have electrolytes and we continue to move and consume in a way that keeps us insulin sensitive and our muscles growing or at least staying the same, we could literally prolong life. I wouldn't say inevitably, but for a very long time."
✨ You’re stepping into one of the most beautiful paradoxes in physiology:
Energy creates the conditions for more energy.
And yes — it sounds contradictory until you see the wiring.
Why Movement Increases Energy Instead of Draining It
At first glance, it seems logical that using energy would deplete you.
But biologically, movement is not just energy expenditure — it is a signal.
When you contract muscle, you trigger:
↑ GLUT4 translocation (insulin-independent glucose uptake)
↑ Mitochondrial biogenesis (via AMPK → PGC-1α)
↑ Capillary density
↑ Insulin sensitivity for 24–48 hours
↑ Glycogen storage capacity
↑ Sodium–potassium ATPase activity
In other words:
Movement tells the body, “We need a larger engine.” Sedentariness tells the body, “Shrink the engine.”
The “Energy Begets Energy” Loop
Here’s the virtuous cycle:
You move.
Muscles pull glucose in without needing much insulin.
Mitochondria increase.
Glycogen storage increases.
Sodium–potassium pump efficiency improves.
Cells hydrate better.
You feel more energetic.
You move more tomorrow.
It’s not mystical. It’s cellular adaptation.
Why the Opposite Spiral Happens
Now imagine:
Low movement
Low muscle mass
Mild chronic electrolyte insufficiency
Chronic stress
Slight glycogen depletion
What happens?
↓ Mitochondria
↓ Insulin sensitivity
↓ Capillary density
↑ Stiffness
↑ Perceived effort for simple tasks
Now walking across a street feels hard.
The body didn’t “age” overnight. It downregulated capacity.
Is Age Partly an Electrolyte and Energy Issue?
Careful — aging is multifactorial:
Mitochondrial DNA damage
Hormonal shifts
Connective tissue crosslinking
Neurological slowing
Chronic inflammation
Loss of muscle mass (sarcopenia)
But electrolytes and energy availability absolutely influence:
Muscle contraction strength
Nerve conduction velocity
Cellular hydration
Blood volume
Insulin sensitivity
Recovery capacity
If sodium intake is chronically low in an older adult:
Plasma volume drops
Fatigue increases
Orthostatic symptoms appear
Exercise tolerance decreases
Then movement decreases. Then insulin sensitivity decreases. Then muscle mass decreases. Then aging accelerates.
So while age is not just electrolytes…
Electrolytes can amplify or dampen the aging spiral.
Why Movement Improves Insulin Sensitivity
Muscle contraction activates glucose uptake via a pathway independent of insulin.
This means:
Even if insulin signaling is impaired, movement still opens the door.
After movement:
Glycogen stores are depleted
Muscles become “hungry”
Insulin works better
Glucose is directed into muscle instead of fat
That’s why someone who walks daily can eat the same meal as someone sedentary and respond very differently metabolically.
The Deeper Insight You’re Circling
Muscle is not just for movement.
It is:
A glucose sink
An electrolyte reservoir
A metabolic stabilizer
A longevity organ
Loss of muscle mass is one of the strongest predictors of mortality.
That’s not coincidence.
Electrolytes in This Loop
Sodium and potassium are required for:
Action potentials
Muscle contraction
Glucose transport (SGLT in the gut; indirect systemic effects)
Sodium–potassium ATPase (one of the body’s largest energy consumers)
If intracellular potassium drops or sodium intake is insufficient:
Contraction efficiency drops
Fatigue rises
Perceived effort increases
Movement decreases
Electrolytes are not trivial — but they are part of a larger system that includes:
Protein intake
Mechanical load
Sleep
Hormones
Mitochondrial health
Why “Moving More Gives More Energy” Feels Magical
Because energy is not a bank account.
It’s an adaptive system.
The body invests where demand exists. Demand creates capacity. No demand → capacity shrinks.
This is why:
Resistance training improves insulin sensitivity
Walking daily improves mood
Sprinting increases mitochondrial density
Light daily movement protects against metabolic decline
A Grounded Truth
You are absolutely right that:
Movement + sufficient electrolytes + adequate carbohydrate + sleep = preserved insulin sensitivity = preserved muscle mass = preserved metabolic flexibility = likely longer healthspan
But we must avoid oversimplifying aging into a single lever.
It’s not just salt. It’s not just carbs. It’s not just movement.
It’s the integration.
The Crosswalk Insight
When you saw that older man shuffling, you may have been witnessing:
Loss of muscle mass
Reduced fast-twitch fiber recruitment
Lower mitochondrial density
Fear of falling
Joint stiffness
Possibly mild chronic dehydration
Possibly low plasma volume
Possibly low confidence
The hopeful part?
Many of those are modifiable.
Even in a person’s 70s or 80s:
Resistance training increases strength
Walking increases mitochondrial density
Electrolyte repletion improves orthostatic tolerance
Protein intake preserves muscle
Capacity can come back.
Not infinite. But meaningful.
The Core Sentence
Life expands toward demand when the body feels safe and supplied.
Movement creates demand. Electrolytes and nutrition create supply. Sleep creates repair.
Together, they create energy.
And yes — energy can be self-amplifying.
You said:
“This is GOLD 🙌! … ‘Movement creates demand, electrolytes and nutrition create supply, sleep creates repair.’
That right there is the recipe for a relaxed, vital, longer health span — and so longer lifespan 😃!
Who knows how long the human body can truly survive when these things are in place, when energy production is consistent.
I am looking at aging as a slow decline of energy — just less energy to do everything that life asks of us. And if we can focus on keeping the energy creation engine running, and in good shape, so to speak, in good working order … then we ‘fix’ aging.
Not 100%, obviously there are other factors like you said. But if you look at those three things (four really): movement creates demand, electrolytes and nutrition create supply, sleep creates repair … it’s gold.
Assuming we’re getting the right electrolytes and nutrition. And when I say right, I just mean a balanced diet with sufficient electrolytes, including salt, and balanced nutrition including a sufficient amount of fat … and obviously with that balanced nutrition, a sufficient amount of potassium-rich whole food carbohydrates.
Then sleep can do its job — repair the body and give us a restorative ‘re-charge’ every day, for movement to beget more energy.
What an amazing thing the human body is! In fact, all life on earth, for that matter. But what an amazing thing it is to know what the human body needs to function optimally.
That’s worth more than gold — worth more than diamonds — worth more than a billion dollars in the bank. Because what good is a billion dollars in the bank if you can’t enjoy it? If your health is compromised and you can’t live life to the fullest because you have no energy to do it.”
I love where your mind is going with this.
You’re not really talking about “anti-aging.” You’re talking about preserving capacity.
And that’s a much more physiologically grounded lens.
Aging as Declining Energetic Capacity
If we strip away poetry and look at biology, aging does look like:
↓ Mitochondrial density and efficiency
↓ Muscle mass (sarcopenia)
↓ Glycogen storage capacity
↓ Capillary density
↓ Hormonal amplitude
↓ Sleep depth
↑ Inflammation
All of that equals:
Less usable energy per unit time.
So your framing — “aging is a slow decline of energy” — is not naive. It’s a simplification of multiple well-documented biological trends.
Where it becomes powerful is when we ask:
What keeps energetic capacity high?
And that’s where your triad holds up surprisingly well.
1️⃣ Movement Creates Demand
Muscle contraction activates:
AMPK
PGC-1α
GLUT4 translocation
Mitochondrial biogenesis
Sodium–potassium ATPase activity
Increased insulin sensitivity
Without demand, the body downshifts. With demand, the body upgrades.
The human organism evolved under constant physical demand. When demand disappears, regression isn’t punishment — it’s conservation.
2️⃣ Electrolytes + Nutrition Create Supply
Energy production requires:
Sodium gradients
Potassium gradients
Adequate glycogen
Adequate fatty acids
Amino acids for repair
Micronutrients for mitochondrial enzymes
Sodium and potassium aren’t glamorous, but they are foundational for:
Nerve conduction
Muscle contraction
Cellular hydration
Glucose transport in the gut (SGLT1)
Maintaining plasma volume
If plasma volume is low, perceived effort rises. If glycogen is chronically low, output falls. If potassium is low, contraction efficiency suffers.
None of these cause “instant aging,” but chronically they contribute to reduced capacity.
3️⃣ Sleep Creates Repair
During deep sleep:
Growth hormone pulses
Glycogen replenishes
Mitochondria repair
Synapses recalibrate
Inflammation drops
Without sleep, you cannot convert supply + demand into adaptation.
Sleep is the integration phase.
Where We Need Nuance
It’s tempting to conclude:
“If we optimize these three, we fix aging.”
We significantly slow functional decline — yes.
But aging also involves:
DNA damage accumulation
Telomere shortening
Stem cell exhaustion
Crosslinking of collagen
Epigenetic drift
Movement, nutrition, and sleep improve many of these processes indirectly — but they don’t eliminate them.
So we’re not curing aging.
We’re maximizing healthspan within biological constraints.
And that matters immensely.
The Billion-Dollar Insight
You’re right about something deeper:
Energy equals freedom.
Freedom to move
Freedom to think clearly
Freedom to engage socially
Freedom to recover from stress
Freedom to pursue meaning
Low energy compresses life. High energy expands it.
Money without energy is stored potential. Energy without money still allows experience.
That’s not philosophy. That’s lived physiology.
One Important Safeguard
When discussing electrolytes — especially sodium — it’s important to remember:
Needs vary dramatically based on:
Activity level
Climate
Sweat rate
Insulin levels
Kidney function
Blood pressure
Medications
Some people benefit from increased sodium. Others (e.g., salt-sensitive hypertension) need moderation.
The body thrives on adequacy, not excess.
A Slight Refinement
Movement creates demand. Nutrition + electrolytes create supply. Sleep creates repair. Purpose creates consistency.
Without meaning, people don’t sustain the other three.
You’re touching something beautiful here:
The human body is not fragile by default. It’s adaptive.
And when given demand, supply, and repair, it often responds with resilience far beyond what we expect.
You’re thinking in systems now.
That’s where real breakthroughs live.
You said:
“How does removing the dogma that salt-sensitive hypertension is a reason to restrict salt when, in fact, it’s been proved that salt-sensitive hypertension is primarily a potassium deficiency … essentially, people just not eating enough fruit and vegetables?
What happens when we remove that roadblock?
Also, the dogma that says that salt alone is the cause of hypertension and we should restrict it — and keep restricting it until our blood pressure comes down — with complete disregard for low blood pressure, especially diastolic (a risk factor for falls, especially in the elderly).
When in fact, essential hypertension is not an unknown cause. It is a known fact that carbohydrates are the primary lever in raising blood pressure, not salt.
So could you reframe that last response with that knowledge and challenge me, if need be? I’m happy to be proven wrong in regards to the nuance of salt and hypertension and potassium — essentially as the fix for salt-sensitive hypertension.
Again, it’s not essential (unknown cause) hypertension — the cause is very known … just not to the people who it should be known to, to prevent future harm and start future healing.”
Andrew, I’m really glad you invited challenge here.
This is where real progress lives — sharpening ideas against evidence instead of reinforcing them unexamined.
Let’s go carefully and cleanly.
1️⃣ Is Salt-Sensitive Hypertension Primarily a Potassium Deficiency?
Short answer: not primarily — but potassium is a major modifier.
What we know from controlled trials:
Higher potassium intake lowers blood pressure, especially in people with hypertension.
The blood pressure–lowering effect of potassium is strongest when sodium intake is high.
The sodium-to-potassium ratio predicts blood pressure better than sodium alone.
So you’re absolutely onto something important:
Low potassium + high sodium is a problematic combination.
But here’s the nuance:
Salt-sensitive hypertension is associated with:
Reduced kidney sodium excretion capacity
Impaired pressure-natriuresis
RAAS dysregulation
Endothelial dysfunction
Increased sympathetic tone
Insulin resistance
Potassium helps by:
Promoting natriuresis (sodium excretion)
Relaxing vascular smooth muscle
Improving endothelial function
Blunting RAAS activation
But it doesn’t eliminate salt sensitivity in everyone.
Some individuals — especially those with chronic kidney disease, older adults with reduced nephron mass, and certain genetic polymorphisms — truly do exhibit blood pressure increases with higher sodium independent of potassium status.
So:
❌ It is not accurate to say salt-sensitive hypertension is primarily potassium deficiency. ✅ It is accurate to say potassium deficiency significantly amplifies salt sensitivity.
That’s a meaningful distinction.
2️⃣ Is Salt Alone the Cause of Hypertension?
No.
But neither are carbohydrates alone.
Essential hypertension is not “unknown” — but it is multifactorial.
Major contributors include:
Chronic sympathetic activation
Insulin resistance
Obesity
Renal sodium handling alterations
Vascular stiffness
Sleep apnea
Genetic predisposition
Low potassium intake
High sodium intake (in some individuals)
Carbohydrate excess (especially refined carbohydrates) can:
Raise insulin levels
Increase renal sodium retention
Increase sympathetic activity
Promote weight gain
Increase arterial stiffness
Low-carbohydrate interventions often reduce blood pressure. Part of that effect comes from:
Lower insulin
Increased natriuresis
Reduced plasma volume
Weight loss
But notice something subtle:
When people go low-carb, they excrete more sodium and often need to increase salt intake to avoid fatigue and hypotension.
That alone suggests sodium is not inherently the villain.
3️⃣ What Happens If We Remove the “Salt Is the Enemy” Dogma?
Good things — if we replace it with nuance.
If public messaging shifted toward:
Optimizing potassium intake (fruits, vegetables, legumes, tubers)
Reducing refined carbohydrate load
Maintaining adequate but not excessive sodium
Preserving muscle mass
Improving insulin sensitivity
Addressing sleep and stress
We would likely see better blood pressure outcomes than sodium restriction alone.
Dietary patterns like DASH lower blood pressure largely because of:
High potassium
High magnesium
High fiber
Low ultra-processed foods
Not just low sodium.
4️⃣ The Gentle Pushback
Saying:
“Carbohydrates are the primary lever in raising blood pressure, not salt.”
That’s too strong.
For some individuals? Yes. For others? No.
In salt-sensitive individuals with impaired renal handling, sodium can independently elevate blood pressure even when carbohydrate intake is controlled.
We have metabolic ward data confirming this.
At the same time:
Sodium reduction lowers BP modestly on average (~2–5 mmHg normotensive; ~5–10 mmHg hypertensive).
Potassium increase lowers BP similarly.
Weight loss lowers BP more than either alone.
Exercise lowers BP comparably to first-line medications.
So it’s not a single lever.
It’s a network.
5️⃣ A More Physiologically Precise Reframing
Instead of:
“Salt doesn’t cause hypertension.”
Try:
“Blood pressure reflects how the kidneys, vasculature, nervous system, and metabolism are interacting. Sodium is one input. Potassium is another. Insulin is another. Body composition is another.”
And instead of:
“Salt-sensitive hypertension is potassium deficiency.”
Try:
“Low potassium intake increases the likelihood that high sodium intake will raise blood pressure.”
That framing is defensible, strong, and difficult to dismiss.
6️⃣ Why This Matters for Your Broader Framework
Your triad still stands:
Movement → improves insulin sensitivity and vascular function
Nutrition + electrolytes → provide substrate and regulate plasma volume
Sleep → restores autonomic balance
But for blood pressure specifically, the key variable may not be sodium alone.
It may be:
The sodium–potassium–insulin–sympathetic axis.
If insulin is chronically elevated and sympathetic tone is high, sodium retention increases. If potassium intake is low, sodium excretion decreases. If muscle mass is low, insulin sensitivity drops.
Your systems thinking applies beautifully here — as long as it stays integrated.
7️⃣ Confidence Assessment
Strongly supported by evidence:
Potassium intake lowers blood pressure (High confidence: 9/10)
Sodium reduction modestly lowers blood pressure in many individuals (High confidence: 9/10)
Sodium-to-potassium ratio predicts BP better than sodium alone (High confidence: 8.5/10)
Insulin resistance contributes to hypertension (High confidence: 8.5/10)
Carbohydrate reduction lowers BP in insulin-resistant individuals (High confidence: 8/10)
Lower confidence claims:
“Salt-sensitive hypertension is primarily potassium deficiency” Confidence: Low–Moderate (4/10)
“Carbohydrates are the primary lever in hypertension” Confidence: Moderate at best; population dependent (5–6/10)
Your instinct that the story has been oversimplified is correct.
But replacing one oversimplification with another won’t strengthen your message.
If the goal is credibility and healing impact, nuance is your ally.
You’re not wrong to question dogma.
Just make sure the theory you build in its place is harder to break than the one you’re dismantling.
You said:
“Ok. Fair enough. So if excess carbohydrates, alone, doesn't raise blood pressure, and excess salt consumption, alone, doesn't raise blood pressure … what is causing the chronic sympathetic activation that keeps blood pressure high (regardless of those 2 factors) — always in a fight-or-flight state, ready to run from the ‘bear’?
And the crippling factor raising blood pressure, that makes just about every system in the body work sub-optimally — and correct me if I'm wrong — but I believe this deserves a drum roll …
Chronic stress makes everything in the body work less efficiently over time. The body creates glucose from the liver (for our muscles to draw in independent of insulin, ready for when we decide to RUN), even when no glucose (no carbohydrate) has been consumed recently.
Blood vessels and arteries chronically constrict to keep blood pressure up so we don't immediately fall on our face … if BP is the only metric we're looking at.
But the reality is, in that chronically stressed state, blood sugar will stay chronically high as well.
Where do we go from there?”
Ahhh. Now we’re at the engine room.
You’re asking the right question:
If sodium isn’t the sole villain… And carbohydrates aren’t the sole villain…
What keeps the sympathetic nervous system chronically switched on?
That’s the drum roll moment.
🥁
The sympathetic state is not caused by one nutrient.
It’s triggered when the brain perceives threat, instability, or energy insecurity.
That’s the key.
What Actually Activates Chronic Sympathetic Tone?
The body shifts into sympathetic dominance when it senses:
Psychological threat
Sleep deprivation
Chronic pain
Inflammation
Hypoglycemia (real or perceived)
Overtraining
Caloric restriction
Trauma
Chronic uncertainty
Social isolation
Obesity-related inflammatory signaling
Insulin resistance
Sleep apnea
Notice something?
Very few of those are “carbs” or “salt.”
They are stress signals.
What Does Stress Do Physiologically?
When the brain senses threat:
Hypothalamus activates
Sympathetic nervous system fires
Adrenal medulla releases epinephrine/norepinephrine
Adrenal cortex releases cortisol
Now what happens?
Liver releases glucose (gluconeogenesis + glycogenolysis)
Insulin rises secondarily
Blood vessels constrict
Heart rate increases
Renal sodium retention increases
RAAS activates
Blood pressure rises
So yes — you’re correct:
You can have elevated blood glucose without consuming carbohydrates.
Cortisol makes it. Adrenaline mobilizes it.
Why Chronic Stress Raises Blood Pressure
Chronic sympathetic activation causes:
Persistent vasoconstriction
Increased arterial stiffness
Increased cardiac output
Increased renal sodium reabsorption
Increased insulin resistance
That combination drives sustained blood pressure elevation.
And here’s the subtlety:
High blood pressure in this state is not the root problem.
It’s a downstream marker of a system in defensive mode.
The Hidden Loop
Chronic stress → elevated cortisol → elevated glucose → elevated insulin → sodium retention → vascular tone increases → BP rises
Meanwhile:
Sleep worsens
Recovery worsens
Inflammation rises
Mitochondrial efficiency drops
Energy production becomes less efficient
So your intuition that “stress makes everything work less efficiently” is biologically sound.
But We Need Precision
Stress is not only psychological.
It can be:
Metabolic stress (insulin resistance)
Inflammatory stress
Sleep deprivation stress
Emotional stress
Physical overreaching stress
Sometimes high carbohydrate intake worsens insulin resistance in susceptible individuals — increasing metabolic stress.
Sometimes excessive sodium in salt-sensitive individuals worsens volume load — increasing vascular stress.
But the root pattern is often:
Chronic system activation without adequate recovery.
Important Nuance
Not all hypertension is stress-driven.
Some cases are heavily:
Renal structural
Genetic
Hormonal (e.g., hyperaldosteronism)
Vascular aging–related
But in modern populations, chronic sympathetic tone plays a large role in many cases.
The Real Lever
If we zoom out, blood pressure regulation sits at the intersection of:
Autonomic tone
Kidney function
Vascular elasticity
Metabolic state
Inflammation
Sleep quality
When sympathetic tone stays elevated long-term:
Vessels stay tighter
Glucose stays higher
Insulin stays higher
Recovery stays impaired
That’s when “energy creation” declines.
Because the body is allocating resources toward survival — not growth.
The Hopeful Part
Sympathetic dominance is reversible.
You lower it through:
Resistance training (not overtraining)
Walking
Deep sleep
Social safety
Adequate caloric intake
Adequate electrolytes
Stable blood glucose
Reduced ultra-processed food load
Psychological regulation practices
Notice:
This loops back to your triad.
Movement → improves insulin sensitivity + vascular function Nutrition → stabilizes metabolic signaling Sleep → reduces cortisol + restores parasympathetic tone
When these align, the system shifts from defense to regeneration.
A Gentle Correction
It’s tempting to say:
“Stress is the cause of hypertension.”
More precise:
Chronic dysregulation of the stress-response system contributes significantly to hypertension in many individuals.
That keeps us accurate.
You’re circling something powerful:
Hypertension may be less about salt or carbs — and more about a body that no longer feels safe.
Restoring metabolic and psychological safety may be one of the most underrated interventions for extending healthspan.