Mito Health: Helping you live healthier, longer.
In-depth bloodwork & holistic health advice, backed by the latest longevity science. Only $399.
The Real Story Behind Heart Disease
Cholesterol is part of the puzzle not the whole picture. See how endothelial health, oxidation and metabolism drive plaque and how to optimize lipids wisely.
Written by
Gabriel Tan
For years the public conversation framed heart disease as a cholesterol story. Lower the number, win the game. Reality is more layered.
Cholesterol participates in plaque yet it does not act alone. The inner lining of your arteries decides what gets in and how your immune system responds.
Oxidation, inflammation, blood pressure, insulin resistance and the quality of the lipoproteins that carry cholesterol all shape your true risk. If you focus on a single biomarker, you miss the levers that actually move outcomes.
What Plaques Really Are
Atherosclerosis begins in the tunica intima, the thin inner layer of your artery. Three local players set the scene.
Glycocalyx
A microscopic hair-like coating on endothelial cells that senses blood flow and shields the wall from excess particles and sticky cells. High glucose, oxidative stress and high pressure wear it down.
Endothelium
A one-cell-thick gatekeeper with tight junctions that regulate what crosses into the wall. When the endothelium is calm and responsive, it releases nitric oxide that keeps vessels relaxed and blood less sticky. When it is irritated it expresses adhesion molecules that invite immune cells in.
Collagen and elastin scaffold
These proteins anchor the lining and give the vessel strength and flexibility. When the scaffold is compromised, the wall is more permeable and less elastic which raises pressure and injury risk.
Plaque forms when LDL particles slip beneath a stressed lining and their phospholipids oxidize. Immune cells rush in, swallow the debris and become foam cells.
The site becomes a small inflammatory ecosystem that can grow, calcify and eventually rupture. At rupture a clot forms. Blood flow stops. That is the event we fear.
Where Does Cholesterol Fit?
Cholesterol itself is a structural molecule. You need it for cell membranes, steroid hormones, bile acids and vitamin D synthesis.
Your liver packages cholesterol inside lipoproteins like LDL to deliver it to tissues. The danger rises when LDL particles are numerous, small, or easily oxidized, and when the arterial wall is primed for trouble.
In other words, the cargo matters and the road matters too.
Why a Single LDL Target Can Mislead
Half of events occur in people without sky-high LDL
Risk hides in the vessel wall. Endothelial dysfunction, insulin resistance, hypertension and smoking can tilt the wall toward injury even when a standard lipid panel looks fair.
Particle quality and context matter
LDL that is small and dense is easier to trap and oxidize. Triglyceride burden and low HDL function usually point in that direction. Inflammation and oxidative stress accelerate damage at the wall.
Plaque biology predicts events
A soft, inflamed plaque with a thin fibrous cap is riskier than a calcified, quiet one. Your daily habits influence that biology through blood pressure, glycemic control and oxidative balance.
Lowering a high LDL can be helpful. Treating LDL like the only villain misses the system that decides whether LDL becomes a problem at all.
The Upstream Drivers That Matter
Endothelial health
Healthy endothelium produces nitric oxide that widens vessels and keeps platelets less sticky. It quiets inflammatory signals and limits particle entry.
Oxidative stress
Oxidation turns LDL into a magnet for immune cells. Diets low in colorful plants, high visceral fat, heavy smoking or poorly controlled glucose all push oxidation higher.
Insulin resistance and triglycerides
Insulin resistance raises liver output of triglyceride-rich particles and encourages small dense LDL. It also raises blood pressure through kidney sodium retention.
Hemodynamics
High blood pressure and erratic flow damage the glycocalyx and stretch the wall which increases permeability.
Resolution capacity
Your immune system should clean up and stand down. That resolution step depends on mitochondrial energy production and a healthier omega-3 to omega-6 balance.
The Benefits of Cholesterol
Your body uses cholesterol to make cortisol, testosterone, estrogen and progesterone.
It forms bile acids to digest fats. It stabilizes cell membranes. The synthesis pathway also produces vitamin D precursors and coenzyme Q10.
A smarter goal is to help the body use cholesterol well and keep traffic moving safely, not to choke off the entire road.
How to Read Your Own Signals
Across a month, note resting blood pressure, morning waist fit, post-meal energy, exercise recovery and any chest tightness with exertion.
Pair that with a basic panel that includes triglycerides, HDL, fasting glucose and A1c in addition to LDL.
Rising triglycerides with low HDL and a creeping waist usually signal insulin resistance and smaller LDL particles even when LDL looks modest. That is your cue to fix the upstream levers above.
Final Word
Cholesterol is part of the script, not the plot. A plaque forms when an injured wall meets oxidized cargo in a high-pressure, high-inflammation setting.
This road-and-traffic view is how you lower risk while keeping cholesterol available for the jobs your body needs it to do.
Resources
Related Articles
Mito Health: Helping you live healthier, longer.
In-depth bloodwork & holistic health advice, backed by the latest longevity science. Only $399.
The Real Story Behind Heart Disease
Cholesterol is part of the puzzle not the whole picture. See how endothelial health, oxidation and metabolism drive plaque and how to optimize lipids wisely.
Written by
Gabriel Tan
For years the public conversation framed heart disease as a cholesterol story. Lower the number, win the game. Reality is more layered.
Cholesterol participates in plaque yet it does not act alone. The inner lining of your arteries decides what gets in and how your immune system responds.
Oxidation, inflammation, blood pressure, insulin resistance and the quality of the lipoproteins that carry cholesterol all shape your true risk. If you focus on a single biomarker, you miss the levers that actually move outcomes.
What Plaques Really Are
Atherosclerosis begins in the tunica intima, the thin inner layer of your artery. Three local players set the scene.
Glycocalyx
A microscopic hair-like coating on endothelial cells that senses blood flow and shields the wall from excess particles and sticky cells. High glucose, oxidative stress and high pressure wear it down.
Endothelium
A one-cell-thick gatekeeper with tight junctions that regulate what crosses into the wall. When the endothelium is calm and responsive, it releases nitric oxide that keeps vessels relaxed and blood less sticky. When it is irritated it expresses adhesion molecules that invite immune cells in.
Collagen and elastin scaffold
These proteins anchor the lining and give the vessel strength and flexibility. When the scaffold is compromised, the wall is more permeable and less elastic which raises pressure and injury risk.
Plaque forms when LDL particles slip beneath a stressed lining and their phospholipids oxidize. Immune cells rush in, swallow the debris and become foam cells.
The site becomes a small inflammatory ecosystem that can grow, calcify and eventually rupture. At rupture a clot forms. Blood flow stops. That is the event we fear.
Where Does Cholesterol Fit?
Cholesterol itself is a structural molecule. You need it for cell membranes, steroid hormones, bile acids and vitamin D synthesis.
Your liver packages cholesterol inside lipoproteins like LDL to deliver it to tissues. The danger rises when LDL particles are numerous, small, or easily oxidized, and when the arterial wall is primed for trouble.
In other words, the cargo matters and the road matters too.
Why a Single LDL Target Can Mislead
Half of events occur in people without sky-high LDL
Risk hides in the vessel wall. Endothelial dysfunction, insulin resistance, hypertension and smoking can tilt the wall toward injury even when a standard lipid panel looks fair.
Particle quality and context matter
LDL that is small and dense is easier to trap and oxidize. Triglyceride burden and low HDL function usually point in that direction. Inflammation and oxidative stress accelerate damage at the wall.
Plaque biology predicts events
A soft, inflamed plaque with a thin fibrous cap is riskier than a calcified, quiet one. Your daily habits influence that biology through blood pressure, glycemic control and oxidative balance.
Lowering a high LDL can be helpful. Treating LDL like the only villain misses the system that decides whether LDL becomes a problem at all.
The Upstream Drivers That Matter
Endothelial health
Healthy endothelium produces nitric oxide that widens vessels and keeps platelets less sticky. It quiets inflammatory signals and limits particle entry.
Oxidative stress
Oxidation turns LDL into a magnet for immune cells. Diets low in colorful plants, high visceral fat, heavy smoking or poorly controlled glucose all push oxidation higher.
Insulin resistance and triglycerides
Insulin resistance raises liver output of triglyceride-rich particles and encourages small dense LDL. It also raises blood pressure through kidney sodium retention.
Hemodynamics
High blood pressure and erratic flow damage the glycocalyx and stretch the wall which increases permeability.
Resolution capacity
Your immune system should clean up and stand down. That resolution step depends on mitochondrial energy production and a healthier omega-3 to omega-6 balance.
The Benefits of Cholesterol
Your body uses cholesterol to make cortisol, testosterone, estrogen and progesterone.
It forms bile acids to digest fats. It stabilizes cell membranes. The synthesis pathway also produces vitamin D precursors and coenzyme Q10.
A smarter goal is to help the body use cholesterol well and keep traffic moving safely, not to choke off the entire road.
How to Read Your Own Signals
Across a month, note resting blood pressure, morning waist fit, post-meal energy, exercise recovery and any chest tightness with exertion.
Pair that with a basic panel that includes triglycerides, HDL, fasting glucose and A1c in addition to LDL.
Rising triglycerides with low HDL and a creeping waist usually signal insulin resistance and smaller LDL particles even when LDL looks modest. That is your cue to fix the upstream levers above.
Final Word
Cholesterol is part of the script, not the plot. A plaque forms when an injured wall meets oxidized cargo in a high-pressure, high-inflammation setting.
This road-and-traffic view is how you lower risk while keeping cholesterol available for the jobs your body needs it to do.
Resources
Related Articles
Mito Health: Helping you live healthier, longer.
In-depth bloodwork & holistic health advice, backed by the latest longevity science. Only $399.
The Real Story Behind Heart Disease
Cholesterol is part of the puzzle not the whole picture. See how endothelial health, oxidation and metabolism drive plaque and how to optimize lipids wisely.
Written by
Gabriel Tan
For years the public conversation framed heart disease as a cholesterol story. Lower the number, win the game. Reality is more layered.
Cholesterol participates in plaque yet it does not act alone. The inner lining of your arteries decides what gets in and how your immune system responds.
Oxidation, inflammation, blood pressure, insulin resistance and the quality of the lipoproteins that carry cholesterol all shape your true risk. If you focus on a single biomarker, you miss the levers that actually move outcomes.
What Plaques Really Are
Atherosclerosis begins in the tunica intima, the thin inner layer of your artery. Three local players set the scene.
Glycocalyx
A microscopic hair-like coating on endothelial cells that senses blood flow and shields the wall from excess particles and sticky cells. High glucose, oxidative stress and high pressure wear it down.
Endothelium
A one-cell-thick gatekeeper with tight junctions that regulate what crosses into the wall. When the endothelium is calm and responsive, it releases nitric oxide that keeps vessels relaxed and blood less sticky. When it is irritated it expresses adhesion molecules that invite immune cells in.
Collagen and elastin scaffold
These proteins anchor the lining and give the vessel strength and flexibility. When the scaffold is compromised, the wall is more permeable and less elastic which raises pressure and injury risk.
Plaque forms when LDL particles slip beneath a stressed lining and their phospholipids oxidize. Immune cells rush in, swallow the debris and become foam cells.
The site becomes a small inflammatory ecosystem that can grow, calcify and eventually rupture. At rupture a clot forms. Blood flow stops. That is the event we fear.
Where Does Cholesterol Fit?
Cholesterol itself is a structural molecule. You need it for cell membranes, steroid hormones, bile acids and vitamin D synthesis.
Your liver packages cholesterol inside lipoproteins like LDL to deliver it to tissues. The danger rises when LDL particles are numerous, small, or easily oxidized, and when the arterial wall is primed for trouble.
In other words, the cargo matters and the road matters too.
Why a Single LDL Target Can Mislead
Half of events occur in people without sky-high LDL
Risk hides in the vessel wall. Endothelial dysfunction, insulin resistance, hypertension and smoking can tilt the wall toward injury even when a standard lipid panel looks fair.
Particle quality and context matter
LDL that is small and dense is easier to trap and oxidize. Triglyceride burden and low HDL function usually point in that direction. Inflammation and oxidative stress accelerate damage at the wall.
Plaque biology predicts events
A soft, inflamed plaque with a thin fibrous cap is riskier than a calcified, quiet one. Your daily habits influence that biology through blood pressure, glycemic control and oxidative balance.
Lowering a high LDL can be helpful. Treating LDL like the only villain misses the system that decides whether LDL becomes a problem at all.
The Upstream Drivers That Matter
Endothelial health
Healthy endothelium produces nitric oxide that widens vessels and keeps platelets less sticky. It quiets inflammatory signals and limits particle entry.
Oxidative stress
Oxidation turns LDL into a magnet for immune cells. Diets low in colorful plants, high visceral fat, heavy smoking or poorly controlled glucose all push oxidation higher.
Insulin resistance and triglycerides
Insulin resistance raises liver output of triglyceride-rich particles and encourages small dense LDL. It also raises blood pressure through kidney sodium retention.
Hemodynamics
High blood pressure and erratic flow damage the glycocalyx and stretch the wall which increases permeability.
Resolution capacity
Your immune system should clean up and stand down. That resolution step depends on mitochondrial energy production and a healthier omega-3 to omega-6 balance.
The Benefits of Cholesterol
Your body uses cholesterol to make cortisol, testosterone, estrogen and progesterone.
It forms bile acids to digest fats. It stabilizes cell membranes. The synthesis pathway also produces vitamin D precursors and coenzyme Q10.
A smarter goal is to help the body use cholesterol well and keep traffic moving safely, not to choke off the entire road.
How to Read Your Own Signals
Across a month, note resting blood pressure, morning waist fit, post-meal energy, exercise recovery and any chest tightness with exertion.
Pair that with a basic panel that includes triglycerides, HDL, fasting glucose and A1c in addition to LDL.
Rising triglycerides with low HDL and a creeping waist usually signal insulin resistance and smaller LDL particles even when LDL looks modest. That is your cue to fix the upstream levers above.
Final Word
Cholesterol is part of the script, not the plot. A plaque forms when an injured wall meets oxidized cargo in a high-pressure, high-inflammation setting.
This road-and-traffic view is how you lower risk while keeping cholesterol available for the jobs your body needs it to do.
Resources
Related Articles
The Real Story Behind Heart Disease
Cholesterol is part of the puzzle not the whole picture. See how endothelial health, oxidation and metabolism drive plaque and how to optimize lipids wisely.
Written by
Gabriel Tan
For years the public conversation framed heart disease as a cholesterol story. Lower the number, win the game. Reality is more layered.
Cholesterol participates in plaque yet it does not act alone. The inner lining of your arteries decides what gets in and how your immune system responds.
Oxidation, inflammation, blood pressure, insulin resistance and the quality of the lipoproteins that carry cholesterol all shape your true risk. If you focus on a single biomarker, you miss the levers that actually move outcomes.
What Plaques Really Are
Atherosclerosis begins in the tunica intima, the thin inner layer of your artery. Three local players set the scene.
Glycocalyx
A microscopic hair-like coating on endothelial cells that senses blood flow and shields the wall from excess particles and sticky cells. High glucose, oxidative stress and high pressure wear it down.
Endothelium
A one-cell-thick gatekeeper with tight junctions that regulate what crosses into the wall. When the endothelium is calm and responsive, it releases nitric oxide that keeps vessels relaxed and blood less sticky. When it is irritated it expresses adhesion molecules that invite immune cells in.
Collagen and elastin scaffold
These proteins anchor the lining and give the vessel strength and flexibility. When the scaffold is compromised, the wall is more permeable and less elastic which raises pressure and injury risk.
Plaque forms when LDL particles slip beneath a stressed lining and their phospholipids oxidize. Immune cells rush in, swallow the debris and become foam cells.
The site becomes a small inflammatory ecosystem that can grow, calcify and eventually rupture. At rupture a clot forms. Blood flow stops. That is the event we fear.
Where Does Cholesterol Fit?
Cholesterol itself is a structural molecule. You need it for cell membranes, steroid hormones, bile acids and vitamin D synthesis.
Your liver packages cholesterol inside lipoproteins like LDL to deliver it to tissues. The danger rises when LDL particles are numerous, small, or easily oxidized, and when the arterial wall is primed for trouble.
In other words, the cargo matters and the road matters too.
Why a Single LDL Target Can Mislead
Half of events occur in people without sky-high LDL
Risk hides in the vessel wall. Endothelial dysfunction, insulin resistance, hypertension and smoking can tilt the wall toward injury even when a standard lipid panel looks fair.
Particle quality and context matter
LDL that is small and dense is easier to trap and oxidize. Triglyceride burden and low HDL function usually point in that direction. Inflammation and oxidative stress accelerate damage at the wall.
Plaque biology predicts events
A soft, inflamed plaque with a thin fibrous cap is riskier than a calcified, quiet one. Your daily habits influence that biology through blood pressure, glycemic control and oxidative balance.
Lowering a high LDL can be helpful. Treating LDL like the only villain misses the system that decides whether LDL becomes a problem at all.
The Upstream Drivers That Matter
Endothelial health
Healthy endothelium produces nitric oxide that widens vessels and keeps platelets less sticky. It quiets inflammatory signals and limits particle entry.
Oxidative stress
Oxidation turns LDL into a magnet for immune cells. Diets low in colorful plants, high visceral fat, heavy smoking or poorly controlled glucose all push oxidation higher.
Insulin resistance and triglycerides
Insulin resistance raises liver output of triglyceride-rich particles and encourages small dense LDL. It also raises blood pressure through kidney sodium retention.
Hemodynamics
High blood pressure and erratic flow damage the glycocalyx and stretch the wall which increases permeability.
Resolution capacity
Your immune system should clean up and stand down. That resolution step depends on mitochondrial energy production and a healthier omega-3 to omega-6 balance.
The Benefits of Cholesterol
Your body uses cholesterol to make cortisol, testosterone, estrogen and progesterone.
It forms bile acids to digest fats. It stabilizes cell membranes. The synthesis pathway also produces vitamin D precursors and coenzyme Q10.
A smarter goal is to help the body use cholesterol well and keep traffic moving safely, not to choke off the entire road.
How to Read Your Own Signals
Across a month, note resting blood pressure, morning waist fit, post-meal energy, exercise recovery and any chest tightness with exertion.
Pair that with a basic panel that includes triglycerides, HDL, fasting glucose and A1c in addition to LDL.
Rising triglycerides with low HDL and a creeping waist usually signal insulin resistance and smaller LDL particles even when LDL looks modest. That is your cue to fix the upstream levers above.
Final Word
Cholesterol is part of the script, not the plot. A plaque forms when an injured wall meets oxidized cargo in a high-pressure, high-inflammation setting.
This road-and-traffic view is how you lower risk while keeping cholesterol available for the jobs your body needs it to do.
Resources
Related Articles
Mito Health: Helping you live healthier, longer.
In-depth bloodwork & holistic health advice, backed by the latest longevity science. Only $399.
Recently published
What could cost you $15,000? $349 with Mito.
No hidden fees. No subscription traps. Just real care.
What's included
Core Test - Comprehensive lab test covering 100+ biomarkers
Clinician reviewed insights and action plan
1:1 consultation with a real clinician
Upload past lab reports for lifetime tracking
Dedicated 1:1 health coaching
Duo Bundle (For 2)
Most popular
$798
$668
$130 off (17%)
Individual
$399
$349
$50 off (13%)
What could cost you $15,000? $349 with Mito.
No hidden fees. No subscription traps. Just real care.
What's included
Core Test - Comprehensive lab test covering 100+ biomarkers
Clinician reviewed insights and action plan
1:1 consultation with a real clinician
Upload past lab reports for lifetime tracking
Dedicated 1:1 health coaching
Duo Bundle (For 2)
Most popular
$798
$668
$130 off (17%)
Individual
$399
$349
$50 off (13%)
What could cost you $15,000? $349 with Mito.
No hidden fees. No subscription traps. Just real care.
What's included
Core Test - Comprehensive lab test covering 100+ biomarkers
Clinician reviewed insights and action plan
1:1 consultation with a real clinician
Upload past lab reports for lifetime tracking
Dedicated 1:1 health coaching
Duo Bundle (For 2)
Most popular
$798
$668
$130 off (17%)
Individual
$399
$349
$50 off (13%)
What could cost you $15,000? $349 with Mito.
No hidden fees. No subscription traps. Just real care.
Core Test - Comprehensive lab test covering 100+ biomarkers
Clinician reviewed insights and action plan
1:1 consultation with a real clinician
Upload past lab reports for lifetime tracking
Dedicated 1:1 health coaching
What's included
Duo Bundle (For 2)
Most popular
$798
$668
$130 off (17%)
Individual
$399
$349
$50 off (13%)