Iron Direct Primary Care

Iron Direct Primary Care Anti aging primary care practice in Melbourne Florida.

09/09/2026

“I can’t inject testosterone I’m scared of needles”

09/08/2026

Shocking findings reveal atherosclerosis is present in 18 to 29-year-olds. Prevalence increases with age, particularly in midlife for women. Plaque volume grows exponentially, often affecting multiple arteries.

The Tsimane people of the Bolivian Amazon may offer one of the most fascinating natural experiments in cardiovascular me...
09/07/2026

The Tsimane people of the Bolivian Amazon may offer one of the most fascinating natural experiments in cardiovascular medicine.

In a landmark Lancet study of 705 Tsimane adults age 40+, 85% had a coronary artery calcium score of ZERO. Their prevalence of coronary atherosclerosis was among the lowest ever reported.

Here’s the paradox:

The Tsimane are not living in a low-inflammation environment.

They experience lifelong exposure to parasites, helminths, bacterial infections, and other pathogens. Roughly half of adults over 40 have CRP levels that would typically be considered “high cardiovascular risk.”

Yet their arteries remain remarkably clean.

Why?

Their average LDL-C was only about 91 mg/dL, and they also had:

• Very high lifelong physical activity
• Low blood pressure
• Low glucose levels
• Lean body composition
• Very little smoking
• Low lifetime exposure to atherogenic lipoproteins

This is an important lesson.

Inflammation absolutely participates in atherosclerosis once the process begins. But inflammation alone does not appear sufficient to explain why plaque develops.

ApoB-containing particles must first enter and become retained in the arterial wall. The cumulative number of those particles circulating over decades matters enormously.

The Tsimane therefore challenge a common idea in alternative cardiovascular medicine:

“Your cholesterol doesn’t matter if your inflammation is low.”

Their experience suggests almost the opposite experiment:

🔥 High inflammation
🪱 High infectious burden
❤️ Extremely little coronary atherosclerosis
⬇️ Relatively low lifelong LDL exposure

For individual cardiovascular risk assessment, I increasingly care about directly measuring ApoB, controlling the major modifiable risk factors, and using imaging such as CAC when appropriate rather than assuming CRP tells the whole story.

The goal isn’t to ignore inflammation.

It’s to understand where inflammation fits in the biology of atherosclerosis.

ApoB particles provide the substrate. Inflammation influences what happens after they enter the artery wall.

That distinction matters.

09/07/2026

A study of 16,808 adults revealed a startling statistic: 57.1% had atherosclerosis. Most concerning, 8.7% of men and 6.7% of women aged 18-29 already show signs of this condition. The implications for their future health are terrifying.

New journal review lecture out on YouTube and Spotify and other podcast sites. Atherosclerosis is a lifetime exposure di...
09/06/2026

New journal review lecture out on YouTube and Spotify and other podcast sites. Atherosclerosis is a lifetime exposure disease. Learn why lipid lowering is functional & anti-aging medicine and why I am spearheading these informative lecture series at Iron DPC.

REACT imaged 16,808 apparently ASCVD-free adults aged 18–70 with carotid/femoral 3D ultrasound and coronary CTA. Silent atherosclerosis was already present in 57.1% overall and was detectable even at age 18–29. Plaque burden then rose dramatically with age.
Watch on youtube:
https://youtu.be/OCsd29fsEps

Cholesterol does not travel through the bloodstream by itself. It needs a carrier called a lipoprotein.An easy way to th...
09/06/2026

Cholesterol does not travel through the bloodstream by itself. It needs a carrier called a lipoprotein.

An easy way to think about it:

Cholesterol = cargo
Lipoprotein = Uber
ApoB = how many Ubers are on the road

This is why LDL-C and ApoB are related, but not identical.

LDL-C tells us how much cholesterol is being carried inside LDL particles. ApoB gives us a better idea of how many atherogenic particles are circulating.

Why does particle number matter?

Because each ApoB-containing particle is another opportunity for a particle to enter the artery wall, become retained, and contribute to atherosclerotic plaque.

Two people can have a similar amount of cholesterol but a different number of particles carrying it.

Think of it this way:

One person may have a few large Ubers carrying lots of cargo.

Another may have many small Ubers carrying the same total amount of cargo.

The second person has more vehicles on the road.

That is the basic reason ApoB can add important information beyond LDL-C alone.

Once an ApoB-containing particle becomes trapped in the artery wall, the immune system reacts. Macrophages ingest the lipid, foam cells form, inflammation increases, and plaque can grow over time.

The goal is not to fear cholesterol. Cholesterol is essential to human biology.

The goal is to reduce excess lifelong exposure to atherogenic particles when risk is elevated.

Caveman brain smal version:

LDL-C = how much cargo.
ApoB = how many Ubers.
More Ubers = more chances one gets stuck.
Fewer atherogenic particles = less opportunity for plaque.

09/05/2026

When she’s giving you hints that it’s time for euro summer

How does atherosclerosis happen in cartoons. Atherosclerosis does not appear out of nowhere and it is not simply “inflam...
09/05/2026

How does atherosclerosis happen in cartoons.

Atherosclerosis does not appear out of nowhere and it is not simply “inflammation.”

ApoB-containing particles enter the artery wall and can become retained. The immune system notices. Macrophages arrive, ingest the lipid, and become cholesterol-filled foam cells. More retained lipid means more immune activity, more inflammation, and more plaque growth.

The firefighter analogy helps here:

Seeing firefighters at every house fire does not mean firefighters caused the fire.

Likewise, seeing inflammation inside atherosclerotic plaque does not mean inflammation is the only cause. The immune system is reacting to a problem already developing in the artery wallespecially retained ApoB-containing particles.

Over time:

ApoB particle gets stuck → immune system gets angry → foam cells form → plaque grows → plaque can rupture → clot happens.

If that clot suddenly blocks blood flow, the result can be a heart attack or stroke.

Inflammation matters. Blood pressure matters. Insulin resistance matters. Smoking matters. But those do not make ApoB exposure irrelevant.

09/04/2026

Ever heard atherosclerosis is caused by inflammation? While inflammation is involved, it's not the main ingredient. Plaque is made of cholesterol, dead cells, and ApoB particles that get stuck. Our bodies react, sending in macrophages, which can lead to more inflammation and dangerous plaque rupture. Think of it this way: firefighters don't cause fires, they respond to them. Inflammation matters, but it's the *response* to the initial problem.

CTE stands for chronic traumatic encephalopathy, a progressive degenerative brain disease caused by repeated head injuries and blows to the brain.

Address

107 Riverside Place South
Indialantic By The Sea, FL
32903

Opening Hours

Monday 9am - 4pm
Tuesday 9am - 4pm
Wednesday 9am - 4pm
Thursday 9am - 4pm
Friday 9am - 4pm

Telephone

+13215862653

Website

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