Coach John

Private account, opinions are mine. Husband, Father, Coach, Performance Specialist - Always Pro-Health; Durability and Adaptability

[Coach John @CoachJohn1971]

@SBakerMD Gotta find a college with some older higher rated poles that they'll let you use. Much easier to jump and invert with some pole bend

[Coach John @CoachJohn1971]

@the_no_mind Is there a blood test for the slow allele?

Or maybe just practical experimentation?

- Wake
- Get 10 min seated RHR after 30 min
- Drink 3 full cups of coffee within an hour
- only low to moderate activity over next 6-7hrs
- get 10 min seated RHR @ regular intevals for ref

[Wei Wu 吴伟 @WuWei113]

Im be victory. Why?

I'm not afraid of pain.
Pain fear of me.

Too much you white man too fear pain. Not me. I grow in pain. Im born by pain. Raise by pain. I become pain. I command pain. This pain look at me and show fear. I look at pain, then you look at my eyes: I no fear pain

[Coach John @CoachJohn1971]

@X22Report X22 account is now the Jim Cramer of energy info. Assume the opposite

[Coach John @CoachJohn1971]

@HormuzLetter The "elites" no longer have the correct level of fear of the proletariat

[Coach John @CoachJohn1971]

@HansAmato GABA drugs don't give you real sleep? GHB is a GABA precursor that works GREAT for deep, restorative sleep, but good luck finding it now.

Drugs currently on the market are all GHB salts/derivatives of actual GHB. Meh

[Coach John @CoachJohn1971]

@tednaiman Potatoes, minus the paraquat

[Coach John @CoachJohn1971]

@exfatloss Agreed, and... Too much for most to hear. Mind Over Reality Theory - MORT

[Coach John @CoachJohn1971]

@zerohedge Everyone gearing up for the end

[Coach John @CoachJohn1971]

@X22Report We aren't going to become the manufacturing powerhouse of the world.
Prepare accordingly

[Aryn Elaine➕ @ElaineAryn]

Nothing new happens in your life by thinking and feeling - only by doing

It is the doing that provides accurate feedback from your thinking and feeling

[Andra @BioavailableNd]

One of the coolest thing about surfers is their skin microbiome diversity: Surfers from all over the world have skin microbiomes that resemble more like other surfers rather than non-surfers living in their own area. They also carry ocean associated bacteria found commonly on whales and dolphins. I wonder if this skin microbiome shift is felt by the marine animals.

[Coach John @CoachJohn1971]

@RafiFarber 30 year @ 5.34 - let's gooooo!

[Josh Chambers @JoshChambers]

Steve Kerr says Roger Federer taught his Warriors team the secret to sustained success wasn’t outworking everyone, it was building a life around your craft you never want to escape from

“I’ll tell you a great story about Roger Federer. We were playing in China with the Warriors in 2017. Roger was in Shanghai for the Masters tournament, so we invited him to come speak to the team.”

“Draymond Green asked him, ‘How do you sustain success? How have you managed to win majors 20 years after you first won one?’ Everyone was expecting him to say, ‘I work harder than everybody,’ the will, all the clichés.”

“Roger Federer says, ‘I get up every morning and I make breakfast for my kids. Then I take them to school and drop them off. Then I go practice tennis for about two hours, and I’ve figured out a really good routine where I don’t destroy my body, but I can get all the work in I need.”

“‘Then I go have lunch with my wife. In the evening, we cook dinner together. The kids are all home from school. We ask them about school. There’s so much joy in the house. We put them to bed, and then I put my head on the pillow and go, “Man, that was just a great day.” And I’ve been doing that for 20 years.’”

“And it was like, yes. That’s it. That’s the formula. That’s what leads to sustained success. He loves tennis. He loves his family. He loves life. It’s not outworking everybody and banging your head against the wall, ‘I’m going to be better than everybody.’ It’s allowing your natural talent to shine through with a work ethic, with a great family life, with perspective, with peace, with mindfulness.”

“It’s perspective. It’s joy. It’s passion. It’s mindfulness. It’s an awareness that we are truly lucky. To get the most out of ourselves, it’s our daily rituals and experiences and love and joy.”

[Coach John @CoachJohn1971]

@PeytonElroy "I'll believe it when I see it"... No, no, no.

I'll see it when I believe it!

[Dylan O'Sullivan @DylanoA4]

The beauty of routine is that you don’t waste your day in negotiation

[no.mind @the_no_mind]

My uncle is 54, has high blood pressure & takes a statin + CoQ10.

He told me he's worried about his heart.

He knows I specialize in mitochondrial health, so he asked what I'd do if I were him.

I told him to stop obsessing over LDL.

Here is what heart attack actually is & the exact levers I'd focus on instead:

1. Why LDL doesn't explain how heart attack starts
2. What actually damages the artery, drives clotting & causes plaque to grow
3. What actually causes a heart attack
4. The 3 pathways that drive atherosclerosis/coronary disease
5. The exact things I'd focus on if I were him

The entire strategy comes down to two things:

Protect the artery.

Keep the blood flowing like red wine, not ketchup.

Let's start with LDL.

1. LDL doesn't explain the disease

For decades we've been told a simple model:

Saturated fat raises LDL → LDL builds up in arteries → arteries clog → heart attack.

So cardiology kept lowering "acceptable" cholesterol and LDL levels.

300 → 250 → 200 → 150 → now an LDL below 100 mg/dL is considered optimal.

But the real-world data never supported the story.

Many heart attack victims have little or no plaque — with a Coronary Calcium Score of 0.

Many people with severe plaque have zero symptoms.

Some die with "perfect" LDL.

Some live with high LDL & clean arteries.

Autopsy studies of people who died suddenly in accidents found no relationship between their blood cholesterol levels and the actual amount of plaque in their arteries.

The researchers looked at 136,905 patients hospitalized with coronary artery disease and measured their cholesterol within 24 hours of admission.

75% had LDL below 130 mg/dL.

Almost 50% had "optimal" LDL below 100 mg/dL.

If LDL were the initiating cause, this pattern wouldn't exist.

But instead of questioning the LDL hypothesis, the authors reached the opposite conclusion:

LDL targets must not be low enough.

There's another paradox.

Veins never develop plaque even though they're exposed to the same blood, the same LDL & the same apoB.

They only develop plaque when surgically grafted into arterial circulation.

If lipoproteins initiated the injury, damage should appear throughout every vessel exposed to them.
It doesn't.

Atherosclerosis appears in arteries, especially at branch points and regions of disturbed flow.

The particles didn't change.

The environment did: pressure, shear stress & flow dynamics.

So the question isn't what's circulating in the blood. It's what is happening to the artery.

And even people born with a genetic condition called familial hypercholesterolemia (FH) that exposes them to extremely high LDL from birth don't uniformly develop calcified coronary plaque.

In 2020, researchers used coronary CT angiography to assess plaque burden in asymptomatic FH patients.

Roughly half (46%) had a coronary artery calcium (CAC) score of zero — indicating no detectable calcified plaque — despite decades of LDL levels between 200–400 mg/dL.

These individuals had been exposed to particle counts triple the "optimal" target for their entire lives.

Yet their arteries showed no detectable calcified plaque.

And to this day, there is no proven mechanism showing how an LDL particle — or even an apoB particle — injures a healthy artery in the first place.

So the useful question isn't:

How do I lower LDL?

It's:

What injures the artery in the first place?

2. In a healthy artery, lipoproteins can't even reach the wall

The inside of your artery isn't bare tissue exposed directly to everything moving through your blood.

There is a protective interface.

The glycocalyx: A thick, gel-like layer of negatively charged sugar molecules covering the endothelial surface.

The endothelium: A continuous layer of cells with tight junctions.

And then there is structured EZ water.

This builds on Gerald Pollack's work.

The inner surface of every artery is hydrophilic — water loving.

When water touches that surface & receives radiant energy — sunlight, infrared — it forms a different phase:

Structured water — the Exclusion Zone (EZ).

This gel-like layer across the endothelial surface excludes almost everything.

Pollack's experiments show that albumin (~3.8 nm) cannot cross it.

That matters because HDL is ~7–12 nm and LDL ~22–28 nm.

If the EZ excludes albumin at ~3.8 nm, then particles in the 7–28 nm lipoprotein range are excluded too.

Meaning:

If EZ water is intact, nothing in the blood ever touches the artery wall.

No contact → no injury.

No injury → no inflammation.

No inflammation → no plaque.

Lipoproteins never reach the artery wall unless the EZ shield is destroyed first.

EZ loss is upstream of every step that follows.

LDL can show up after the arterial environment has already been damaged.

So what happens once that protective interface is damaged?

3. Plaque isn't fat packed into an artery like sludge

When researchers analyze plaque, it isn't a pipe filled with fat.

It's overwhelmingly clot material, fibrous collagen, smooth muscle repair tissue, trapped cholesterol that arrived after damage, and inflammatory cells cleaning up the debris.

Histology shows plaque is ~87% clot-derived tissue (±8%), confirming the sequence:

Injury → clot → repair → plaque.

Not:

Cholesterol → plaque → blockage.

That explains why plaque forms at specific high-stress arterial sites, why veins do not plaque unless surgically grafted into arterial pressure, and why plaque appears after injury.

So the next question is:

What makes clotting go wrong?

Rudolf Virchow — a German physician and scientist known as the "father of modern pathology" — answered that in 1856.

He identified three conditions that produce pathological clotting:

- Damage to the arterial lining.
- Disrupted or stagnant blood flow.
- Blood that's become more prone to clot.

That brings us to what a heart attack actually is.

4. A heart attack isn't simply a clogged pipe

Most people picture heart disease like plumbing.

Fat slowly accumulates inside an artery.

The opening gets smaller.

Eventually it closes.

Heart attack.

But plaque buildup alone doesn't cause the acute event.

The heart attack happens when plaque cracks or erodes and the blood responds by forming a clot to repair the damage.

That clot blocks blood flow.

Heart tissue downstream loses oxygen.

That's the heart attack.

This explains something the clogged-pipe model struggles with:

Some people walk around with severe plaque and zero symptoms.

Others die suddenly without severe obstruction.

The fatal moment is always the same:

A clot at the wrong time in the wrong place.

So if severe narrowing itself isn't what causes the heart attack, another question follows:

How can some people have heavily narrowed arteries and still feel completely fine?

5. Why some people with severe plaque feel fine

Giorgio Baroldi's autopsy work in 1956 showed that when arteries narrow chronically, the body builds collateral vessels — small bypass channels that restore blood supply.

In areas with ≥70% narrowing, collaterals increased dramatically, compensating for reduced flow.

The body automatically builds bypasses. It restores supply on its own.

That explains why severe plaque can exist without symptoms.

But acute metabolic collapse can happen too fast for collaterals to form.

And in some heart attacks, there isn't even a blockage to compensate for.

6. You can have a heart attack with zero blockage

This is Myocardial Infarction with Non-Obstructive Coronary Arteries — MINOCA.

And it's not rare.

It accounts for 6–15% of all heart attacks.

Stephen Hussey — exercise physiologist, author of Understanding the Heart, and someone who suffered a heart attack himself at 34 — explains the mechanism this way:

The heart prefers fatty acids & ketones & burns them cleanly.

Under acute stress, the autonomic nervous system shifts the heart into a glucose-burning state at the worst possible moment.

Burning mostly glucose produces more free radicals.

This increases local acidity, swelling & pressure inside heart tissue.

Blood cannot enter effectively.

Collapse in flow without obstruction & tissue death follows.

In parallel, acute stress increases thrombotic potential, making clot formation more likely.

No plaque required.

No LDL required.

7. So does plaque matter at all?

Yes — but not the way we were told.

Hussey is clear:

"Plaque is not what causes heart attacks."

But calcified plaque still increases risk because it disturbs flow → creates turbulence → increases clot probability.

Not because it "blocks."

Because it changes the physics of blood movement.

So cardiovascular disease comes down to three failures:

1. INITIATION — damaging the endothelium or its protective surface.

2. DEVELOPMENT — producing clots that are larger or harder to break down.

3. REPAIR FAILURE — impairing clearance and regeneration.

Most factors act on more than one pathway.

This framework replaces fragmented risk factors with a single coherent process.

And now the two things I told my uncle make sense:

Protect the artery from injury.

Keep your blood like red wine, not ketchup.

Then you work backwards from there.

1. INITIATION — what damages the arteries, glycocalyx & EZ water?

The first question is simple:

What injures the arterial environment in the first place?

Several different pathways converge here.

a) Mechanical stress

Atherosclerosis localizes to arteries for a reason.

Arteries are exposed to high pressure, pulsatile flow with every heartbeat, cyclic stretch & shear stress from moving blood.

Plaques do not form randomly.

They appear where mechanical stress is highest — at bifurcations, along curves and in regions of disturbed flow.

The same pattern we saw with veins shows up again: put a vein into arterial circulation and it becomes atherosclerotic.

Raise pressure in pulmonary vessels — where atherosclerosis is otherwise rare — and plaques appear.

What changed was not what was in the blood.

What changed was pressure & flow.

b) High blood pressure is mechanical injury

This is especially relevant to my uncle because he has struggled with high blood pressure.

Hypertension is not "just another risk factor."

Pressure is mechanical load.

Chronic elevation applies force to the arterial wall on every heartbeat.

It disrupts endothelial alignment, alters nitric oxide signaling, increases permeability & amplifies local inflammation.

Blood pressure predicts events independently of LDL.

Lowering blood pressure reduces events even when lipids are unchanged.

A feedback loop sits underneath.

Plaques narrow arteries.

Narrowed arteries raise blood pressure.

Raised pressure accelerates plaque formation.

Cause and consequence reinforce each other.

c) Glucose strips the glycocalyx

The glycocalyx is the endothelium's first line of defense.

It is a thick, gel-like, negatively charged surface layer that prevents platelets from sticking, produces anticoagulants & limits leakage of proteins and lipids into the arterial wall.

When blood sugar spikes, this layer is stripped off.

Fragments of it — such as hyaluronan — can be detected circulating in the blood.

Once the glycocalyx is gone, the endothelium is directly exposed.

Platelets can adhere.

Clotting begins.

This is not downstream inflammation.

It is immediate endothelial injury.

Chronic glucose elevation compounds the damage.

It increases Advanced Glycation End Products — reactive glucose-protein complexes that impair cellular function, disrupt endothelial signaling & barrier integrity, and degrade repair capacity.

Diabetes accelerates atherosclerosis even when LDL is normal.

That alone falsifies any model in which circulating lipoproteins are the primary initiator of disease.

d) Oxidative stress collapses EZ

Everything that steals electrons collapses EZ.

Insulin resistance. Chronic glucose-heavy metabolism. Poor fat oxidation. Endotoxemia from leaky gut, gum disease & root canals. Heavy metals. BPA. Pesticides. Seed oils. Chronic stress. Circadian disruption. Low sunlight. No grounding. EMF exposure.

Mercury has been associated with 35% thicker plaque.

BPA increased lesion size by 104–120%.

Glyphosate shrinks EZ.

WiFi reduces EZ by 15–20%.

These look like unrelated health problems if you view the body as a collection of separate organs.

They look much more connected once you ask what repeatedly damages the interface between the blood and the arterial wall.

e) Some exposures directly injure the endothelium

Some exposures don't merely weaken EZ.

They directly injure the vascular lining.

Even a single cigarette can kill enough endothelial cells that their remnants — microparticles — can be measured in the blood.

Traffic-derived nanosized particles can cross from the lungs into the bloodstream, directly damage the endothelium & activate platelets. That activation marks the first step in clot formation.

Lead inhibits endothelial nitric oxide synthase, reducing nitric oxide and raising blood pressure while increasing procoagulant activity.

Cocaine causes direct vascular destruction through arterial vasculitis and shifts the vascular system toward thrombosis.

Different exposures.

Same target:

The endothelial surface.

f) Infections trigger endothelial injury & clotting

Infections can damage the endothelium and trigger clotting at the same time.

Some viruses directly target the vascular lining.

Bacterial infections can damage tissue through toxins while also pushing the coagulation system past its activation threshold.

This explains a well-documented pattern:

Cardiovascular risk spikes sharply during and immediately after infections.

g) Chronic stress & ANS dysfunction

Your arteries & heart are under continuous nervous-system control.

One way to measure that control is HRV.

In one study, 95% of ischemic events were preceded by almost complete HRV suppression.

HRV changed before ischemia.

Your nervous system destabilizes before your heart does.

Stress acts on two different time scales.

Chronically elevated cortisol suppresses nitric oxide, raises blood pressure, damages the glycocalyx & endothelium, increases clotting factors, drives insulin resistance & promotes visceral fat.

Acute stress activates the sympathoadrenal system and makes blood hypercoagulable.

Anger, anxiety, grief & acute stress repeatedly precede myocardial infarction.

So chronic stress helps create the damaged vascular environment.

Acute stress can provide the trigger that turns it into an event.

2. DEVELOPMENT — what makes clots bigger & tougher?

Once endothelial damage occurs and a clot forms, the next question is not whether a thrombus appears — but whether it can be cleared.

Some factors make clots small and temporary.

Others make them large, dense & resistant to breakdown.

a) Fibrinogen: the clot-density amplifier

Fibrinogen is one of the strongest amplifiers.

In the Scottish Heart Study, individuals in the highest fifth of fibrinogen levels had more than a 3x increase in coronary heart disease risk compared to those in the lowest fifth.

Fibrinogen molecules link together to form fibrin — strong strands that bind a developing clot.

Higher fibrinogen means denser clots & slower breakdown.

Levels can be elevated through genetics, stress, anxiety, smoking & depression.

The effect is the same: clots that persist instead of resolving.

b) Lipoprotein(a): when clots resist breakdown

Lipoprotein(a), or Lp(a), is structurally identical to LDL, with one critical addition:

Apolipoprotein(a).

Apolipoprotein(a) has the same chemical structure as plasminogen — the molecule responsible for breaking down blood clots.

But it cannot do the same job.

Plasminogen can be activated by tissue plasminogen activator (tPA), which dissolves fibrin & clears clots.

Apolipoprotein(a) cannot.

The result is straightforward:

Clots that contain Lp(a) are highly resistant to breakdown.

Lp(a) levels are largely genetically determined and not meaningfully altered by diet or lifestyle.

Clinically, elevated Lp(a) triples the risk of early heart attack or stroke.

More than a billion people worldwide carry high Lp(a) (>50 mg/dL).

Almost none are screened.

The reason is simple: there is no widely available drug to lower it.

Lp(a) carries apoB, but counting it as "just another particle" misses the mechanism:

Clots containing Lp(a) resist breakdown.

c) Dehydration: when blood becomes easier to clot

Lower blood volume increases viscosity & clotting tendency.

This is one reason long-haul flights raise the risk of deep vein thrombosis and other thrombotic events.

Cabin air pressure is lower, water loss through the lungs increases, and alcohol consumption during flights often worsens dehydration.

Different triggers.

Same outcome: clots that form more easily and resolve more slowly.

3. REPAIR FAILURE — when cleanup doesn't work

Even when injury occurs and clots form, the body has robust repair systems.

Endothelial progenitor cells seal damaged areas.

Macrophages engulf debris & transport it away for removal.

When this process works, plaques do not grow. When it fails, they do.

With age, endothelial progenitor cell production declines and repair slows.

Chronic kidney disease reduces repair capacity while increasing vascular injury & making blood more pro-coagulant.

Obstructive sleep apnea reduces circulating endothelial progenitor cells through repeated hypoxia, oxidative stress & sympathetic activation.

Different triggers.

Same failure: damage continues faster than the body can clean it up.

One framework explains every cardiovascular risk

Once plaques are understood as failed repair of repeated vascular injury, a clear pattern emerges.

Every major driver of cardiovascular disease does at least one of three things:

Applies force to the arterial wall — pressure, pulsatile flow, shear stress, mechanical deformation.

Exposes or damages the endothelium — glycocalyx loss, direct toxicity, infection.

Shifts blood toward clot persistence — denser clots, impaired breakdown, reduced repair capacity.

Most factors hit more than one pathway.

And this also clears up one of the biggest confusions around heart disease:

Inflammation is not the initiating cause of atherosclerosis.

It is the predictable response to ongoing injury & failed repair.

Inflammation appears after damage begins — not before.

So the useful question isn't:

How do we reduce inflammation?

It's:

What is causing the injury that keeps triggering it?

So what would I actually do?

Instead of giving my uncle 20 unrelated health hacks, I worked backwards from the three levers driving the disease:

1. Reduce the force acting on the arterial wall.

2. Reduce damage to the endothelium, glycocalyx & EZ.

3. Keep the blood from becoming too thick, sticky & resistant to breakdown.

That is exactly how I explained it to him.

1. Reduce the force acting on the arterial wall.

The first target is blood pressure.

Pressure is mechanical load.

Every heartbeat exposes the artery to it, so chronically elevated blood pressure means chronically elevated mechanical stress on the arterial wall.

This is where sunlight comes in.

UV-A light releases nitric oxide stored in the skin into the bloodstream.

Nitric oxide widens blood vessels.

Wider vessels → lower resistance → lower blood pressure.

Richard Weller showed that this happens independently of vitamin D or temperature.

Later work found UVB lowers blood pressure too.

So I told him:

Get outside in the morning.

Get sunlight on your skin regularly.

Don't spend the entire day indoors and expect one blood-pressure pill to compensate for it.

A traditional Finnish sauna gives him another lever.

It builds EZ water, supports vascular function & increases VEGF — vascular endothelial growth factor — which signals the growth of new blood vessels.

In a Finnish cohort, men using the sauna 4–7 times per week had roughly 47% lower risk of developing hypertension over about 25 years compared with once-weekly users.

My uncle already owns a sauna.

So I told him to use it consistently.

And combine it with cold.

Heat dilates the vascular system.

Cold constricts it.

That repeated expansion & contraction trains vascular responsiveness and gives the autonomic nervous system another stimulus.

Then movement.

He doesn't want to become a runner or start lifting weights.

Fine.

I wouldn't build his heart-health plan around something he's not going to do.

But I would get him moving outside every day.

Walk.

Walk uphill.

Use the terrain around his village.

And if he'll do it, add Zone 2.

Zone 2 improves mitochondrial capacity, increases the ability to use both fat & carbohydrate as fuel, increases vascular capacity, helps lower blood pressure & improves HRV.

So for lever one:

Sunlight. Sauna. Cold. Outdoor movement. Zone 2.

Same target:

Reduce the mechanical load on the artery & improve the vascular system's ability to handle blood flow.

2. Protect the endothelium, glycocalyx & EZ

My uncle had already made one of the best moves he could have made:

He bought a house in a village and moved out of the city.

That gave him more natural light, more time outdoors, direct access to the ground & less artificial light, less urban EMF & less pollution.

So I told him to use it deliberately.

Dim incandescent light or candles at night.

Blackout curtains.

Complete darkness during sleep.

Morning light anchors the circadian clock.

Darkness at night allows melatonin to rise.

Nighttime is when endothelial repair happens.

Then fix the metabolic environment hitting the glycocalyx every day.

Eat at roughly the same times.

Finish the final meal at least 3 hours before bed.
Use intermittent fasting strategically.

A 16:8 window helps maintain the ability to use fat as fuel.

Reduce processed carbohydrates.
Reduce sugar.
Remove seed oils.
Prefer animal fats.

Track:
Triglycerides/HDL <1.5.
HOMA-IR <1.5.

Then reduce direct sources of vascular damage:

Dental infections.
Heavy metals.
BPA.
Pesticides.
Air pollution.
EMF.
Wi-Fi off at night.

The logic:

Protect circadian repair. Protect metabolic flexibility. Remove the things repeatedly damaging the vascular interface.

3. Keep the blood flowing like red wine, not ketchup

This is the image I wanted my uncle to remember.

You can protect the artery and still have a second problem:

Blood that is too viscous, too prone to aggregate & too easy to clot.

This is where grounding becomes interesting.

Red blood cells carry a negative electrical surface charge.

That charge helps them repel one another.

When the charge weakens, they begin aggregating and stacking like rolls of coins.

Blood becomes thicker.

Grounding increases that negative surface charge — the zeta potential.

Stephen Sinatra — cardiologist of 50+ years and former chief of cardiology at Manchester Memorial Hospital — described the goal simply:

"We want blood like red wine. Not like red ketchup."

In his 2013 pilot study, 10 subjects were grounded for two hours through conductive patches connected to a ground rod outside.

Average zeta potential changed from:

−5.28 mV → −14.3 mV. A 270% increase in electrical surface charge.

As the cells became more negatively charged, they repelled one another more strongly.

Aggregation fell.

Blood became more fluid.

And my uncle lives in a village.

So this requires almost nothing.

Shoes off. Outside. Daily.

Then seafood.

He was eating almost none.

I told him to aim for seafood around 5× per week.

EPA & the other marine omega-3s lower triglycerides, support endothelial function, reduce clotting risk & help lower blood pressure.

So rather than adding another supplement:

Eat the seafood.

Then the nervous system.

Stress doesn't stay in your head.

Acute stress makes blood hypercoagulable.

Chronic sympathetic activation raises blood pressure, suppresses nitric oxide & damages the vascular environment.

For him, the practical answer is already built into his life:
Nature. Sauna. Cold. Proper sleep. Social connection. Morning light. Dark nights.

So lever three becomes:

Ground daily. Eat seafood ~5×/week. Use sauna + cold. Sleep properly. Spend time in nature.

Same goal:

Keep blood moving freely & make pathological clotting harder.

The best thing he already did

The funny part is that my uncle had already made one of the biggest moves in the right direction before asking me any of this.

He moved to a village a few months ago.

He didn't need another supplement stack.

He needed to understand how to use the environment he already had.

That's what I explained to him.

Don't spend the next 20 years obsessing over one number on a lipid panel.

Understand the system.

Reduce the force damaging the artery.

Protect the endothelial surface.

Keep the blood from becoming too prone to clot.

Or in the language I gave my uncle:

Protect the artery.

Keep the blood flowing like red wine, not ketchup.

[Dr. Eric Berg DC @dr_ericberg]

Earliest signs of nutritional deficiencies:

1. Vitamin A deficiency
#1 sign: Difficulty seeing in the dark

2. Vitamin B1 deficiency
#1 sign: Nervous tension

3. Vitamin C deficiency
#1 sign: Swollen or red gums with slight bleeding

4. Vitamin D deficiency
#1 sign: Bone pain

5. Vitamin E deficiency
#1 sign: Muscle weakness

6. Vitamin K1 deficiency
#1 sign: Excessive bruising

7. Vitamin K2 deficiency
#1 sign: Tartar buildup

8. Calcium deficiency
#1 sign: Chronic cough

9. Iodine deficiency
#1 sign: Breast tenderness

10. Sodium deficiency
#1 sign: Overall weakness

11. Magnesium deficiency
#1 sign: Loss of energy

12. Potassium deficiency
#1 sign: Pounding in your ears when trying to sleep

13. Selenium deficiency
#1 sign: Brain fog

14. Zinc deficiency
#1 sign: Getting out of breath upon exertion

Dr. Eric Berg, DC, not MD; information only

[Sama Hoole @SamaHoole]

Plants have been at chemical war with everything that eats them for four hundred million years. Every herbivore alive is a scarred veteran, kitted out, adapted, and still paying for the meal every single day.

The cow grew a two hundred litre fermentation vat, staffed it with bacteria, and pays the rent chewing every mouthful twice, eight hours a day.

The koala rebuilt its liver to defuse eucalyptus and paid in brain, which now rattles loose in a skull it no longer fills. Twenty hours a day unconscious.

The monarch caterpillar rewired the pump inside every cell it owns, just to eat one leaf without its heart stopping.

The leaf-cutter ant gave up completely. It cannot eat a leaf, so it farms a fungus and eats the fungus.

The rabbit eats its own droppings, because a plant surrenders so little that once through does not cover it.

The panda quit being a carnivore for bamboo, claws back seventeen per cent of it over fourteen hours a day, and survives only because the enemy it defected from now hand-feeds it.

Every one of them paid. Brain, speed, teeth, time, freedom.

Then there is you.

No rumen. No vat. No rebuilt liver. A caecum the size of a golf ball with a spent appendix hanging off it. You turned up to a four hundred million year war holding a saucepan, paid nothing, were never so much as entered, and somehow decided this makes you the one the plants were meant for.

And it shows the second you cook. Cassava soaked three days or it gasses you. Kidney beans that hospitalise you raw. Acorns leached in a running stream. Olives inedible straight off the branch. Every plant in the house arrives with a disarmament procedure attached, and you stand over it calling it clean eating.

Nothing in you was built to run on this. You have a tolerance, a short one, for holding out until something with a face walks back into range.