This piece is the middle part of Chapter 9 of Stones in the Body: More Frightening Than Cancer (Yoon Jong-won). It is a description containing the author's academic hypothesis, and the body, figures, and citations follow the manuscript as written.
"The vessel got blocked," "It burst": the 1M Obstruction & Rupture we already know
"I heard your father collapsed because a vessel got blocked." "The man next door, his brain vessel burst and he went to the emergency room." "I heard he had a procedure to open up a blocked heart vessel."
We already know 1M Obstruction & Rupture (blocking and bursting). We simply have not called it "1M Obstruction & Rupture." Because at the hospital, at the funeral hall, or at a class reunion, we have heard the words "it got blocked," "it burst," "it narrowed," "they opened it up" countless times.
When the heart's vessels are blocked we call it myocardial infarction, when the brain's vessels are blocked cerebral infarction, and when the brain's vessels burst cerebral hemorrhage. What all of these expressions point to is precisely 1M Obstruction & Rupture. Pye (閉) means "to be blocked," and yeol (裂) means "to burst."
Blocked, or else burst. These two are the essence of 1M Obstruction & Rupture. And one of the main causes of this "blocking and bursting" phenomenon is precisely the calcium that has flowed out of the bones piling up as calcification on the vessel wall.
The Definition of 1M Obstruction & Rupture: When a Tube Is Blocked, It Bursts
1M Obstruction & Rupture is the phenomenon in which calcium that has flowed out of the bones is deposited as calcification on the wall of a tube (管), narrowing the inner space (the lumen), and in the end either blocking it completely or, as pressure builds up behind the blocked area, bursting.
Think for a moment about a hose. If you squeeze the middle of a hose tightly, the water cannot get out, and pressure builds up behind the squeezed part. If pressure keeps being applied at this point, the weakest part of the hose bursts.
A water pipe is the same. When calcification sets in inside it, at first the stream of water weakens, then it becomes more and more blocked, and after it is completely blocked, unable to withstand the water pressure, the weak joint bursts.
A similar process can unfold in the blood vessels of our body as well. Our body has various tubes that transport something. Blood vessels transport blood, the ureter transports urine, the bile duct transports bile, and the bronchus transports air.
When calcification piles up on the walls of these tubes, the inner diameter narrows, and in the end they can be blocked or burst. That is, "blocking" and "bursting" are not different phenomena but two results arising from the same mechanism.
Ectopic Calcification
Normally calcium should be present only in the bones and teeth. But the phenomenon in which calcium piles up in places where it originally should not be, such as blood vessels, joints, and organs, is medically called "ectopic calcification."
1M Obstruction & Rupture is the mechanism in which ectopic calcification occurs in a tube (管) structure and causes blocking and rupture. DIAH-7M is precisely the framework that reveals this ectopic calcification to be one of the main pathways of systemic disease.
[Analogy and the Actual Mechanism]
In a normal state, calcium should be firmly stored in the bones and teeth. But the phenomenon occurs in which calcium is deposited in tissues where it originally should not pile up, such as blood vessels, joints, and organs, and this is medically called "ectopic calcification."
1M Obstruction & Rupture refers to the mechanism in which this ectopic calcification arises in the tube (管) structure of our body and causes blocking and rupture. DIAH-7M is precisely the core framework that reveals this ectopic calcification to be not a mere aging phenomenon but a main pathway that causes systemic disease."
From the DIAH Trigger to Vascular Calcification: Why Calcium Piles Up in Blood Vessels
When there is D (Deficiency), blood calcium becomes insufficient, and to make up the shortfall calcium flows out of the bones. When there is I (Inflammation), calcium is consumed in large amounts in the inflammatory response, and to replenish what is consumed calcium flows out of the bones.
When there is A (Acidosis), the alkaline bone calcium is mobilized to neutralize the acid. When there is H (Hypoxia), the cell's calcium pump breaks down so that calcium flows excessively into the cell, and blood calcium becomes insufficient and is replenished from the bones. The calcium that has flowed out in this way wanders through the blood and then meets two fates.
1. The First Fate: The I (Inflammation) Vicious Cycle
The calcium that has flowed out activates immune cells, especially macrophages. Activated macrophages secrete inflammatory cytokines (IL-1β, IL-6, TNF-α). These inflammatory substances in turn cause even more calcium to flow out of the bones. Calcium efflux → immune cell activation → inflammation → more calcium efflux. This is the I (Inflammation) vicious cycle we learned about in Chapter 2.
2. The Second Fate: Calcium Deposition
When calcium becomes excessive in the blood, it binds with phosphate to form a calcium-phosphate complex, and this is precisely the precursor of calcification. This complex is especially prone to being deposited in areas that have I (Inflammation) or are in an H (Hypoxia) state. That is, when inflammation arises in the vessel wall, calcification piles up intensively in that area.
3. The Core Connection: Where There Is I (Inflammation), Calcium Piles Up
This is a very important point. When small damage occurs in the vessel wall, an I (Inflammation) response takes place. Immune cells gather at the inflamed area, and it changes as though it had become "sticky," so that the calcium-phosphate complex readily adheres.
To use an analogy it is like a "sticky wall," but in reality it is the damaged endothelial cells, the degenerated matrix, and the inflammatory microenvironment that act as the conditions inducing the deposition of calcium-phosphate.
As a result calcification is deposited at the inflamed area, and this calcification in turn induces inflammation at that area. Inflammation → calcium deposition → more severe inflammation → more calcium deposition. It is a vicious cycle that does not stop.
[Interaction with Other Risk Factors]
Vascular calcification does not arise simply from an abnormality of calcium metabolism alone. LDL cholesterol accumulation, hypertension, smoking, diabetes, genetic predisposition, and the like induce vascular inflammation and damage, and the DIAH trigger acts in combination with these risk factors and contributes to accelerating the progression of calcification.
What Happens in the Vessel Wall: Intimal Calcification and Medial Calcification
Intimal calcification and medial calcification. When calcification is deposited on the vessel wall, it appears broadly in two forms.
1. Intimal Calcification: The Vessel Narrows
When calcification is deposited in the intima, the innermost layer of the vessel, the inner diameter of the vessel decreases. For example, a coronary artery originally 4mm in diameter gradually narrows to 3mm, 2mm, 1mm.
In this process I (Inflammation) plays the core role. When damage occurs in the vascular intima, immune cells gather and cause an inflammatory response, and as macrophages engulf oxidized LDL cholesterol they become "foam cells."
These pile up to form an atheroma (plaque), and calcification is deposited on it. When the vessel narrows by 70% or more, angina symptoms appear, and when it narrows by 90% or more, the risk of myocardial infarction increases sharply.
2. Medial Calcification: The Vessel Hardens
In the media, the middle layer of the vessel, there are smooth muscle cells that are responsible for the contraction and relaxation of the vessel. A normal vessel is elastic like a rubber hose and repeatedly stretches and shrinks in time with the heartbeat.
But when calcification is deposited in the media, the smooth muscle cells change in character to resemble the osteoblasts that make bone, and this is called "ossification of the vessel."
That is, the vessel wall changes to become hard like bone. A vessel that has hardened like an iron pipe in this way loses its elasticity and cannot adapt to changes in blood pressure. When the heart beats strongly and blood pressure rises sharply, because the vessel cannot stretch, pressure concentrates on the weak area and the risk of bursting grows.
3. The Double Danger: Narrowing and Hardening at the Same Time
In most cases intimal calcification and medial calcification progress simultaneously. That is, the vessel narrows and at the same time hardens. In a situation where blood struggles to flow through the narrowed passage, the vessel wall too loses its flexibility, so the danger of cardiovascular disease rises to an extreme.
Occlusion: When It Is Blocked, You Die
The first result of 1M Obstruction & Rupture is occlusion, that is, being completely blocked.
1. Myocardial Infarction: When the Heart's Vessels Are Blocked
The coronary arteries are the vessels that supply blood to the heart muscle. Calcification is deposited on these vessels and an atheroma forms, and when one day the atheroma bursts, a thrombus (blood clot) forms rapidly at that area and completely blocks the vessel.
When blood is not supplied to the heart muscle, the heart muscle begins to die within 20 to 40 minutes. This is why the "golden time" is emphasized. If the blocked vessel is not opened quickly, the heart muscle undergoes irreversible necrosis. Necrotic heart muscle does not come back to life.
2. Cerebral Infarction: When the Brain's Vessels Are Blocked
When the same thing happens in a cerebral artery, it is cerebral infarction. Brain cells are very vulnerable to a lack of oxygen, so the fight against time is important.
In general a thrombolytic agent must be administered within 4.5 hours after the onset of symptoms, and if this golden time is exceeded, neural damage increases sharply.
Depending on the Blocked Area, Paralysis, Speech Disorders, and the Like Appear, and in Severe Cases It Leads to Death 3. Peripheral Artery Disease: When the Leg's Vessels Are Blocked
When calcification is deposited in the leg's artery and blocks it, it is peripheral artery disease. At first the leg hurts when walking (intermittent claudication), and as it progresses it hurts even at rest, and in the end the leg tissue undergoes necrosis and must be amputated. A considerable part of the "diabetic foot" commonly seen in diabetic patients is this mechanism.
4. Non-vascular Occlusion: Stones
1M Obstruction & Rupture acts outside the blood vessels as well. When calcium is deposited in the ureter and a stone forms, the ureter is blocked. When the ureter is blocked, urine cannot be discharged and flows back into the kidney, so hydronephrosis occurs and the kidney is damaged.
When a gallstone containing calcium forms in the bile duct and the bile duct is blocked, jaundice and cholecystitis occur, and if severe it progresses to sepsis.
Rupture: When It Bursts, It Pours Out
The second result of 1M Obstruction & Rupture is rupture, that is, bursting.
1. Cerebral Hemorrhage: When the Brain's Vessels Burst
A cerebral vessel that has become hard and weakened through calcification cannot withstand a sudden rise in blood pressure and bursts. When you get angry, exert force suddenly, or go out into a cold place, blood pressure rises sharply, and at this point the weakened vessel bursts. Cerebral hemorrhage has a higher mortality rate and more severe aftereffects than cerebral infarction.
This is because the blood pours out into the brain tissue and directly destroys the surrounding brain cells, and the pressure inside the skull rises sharply and compresses even the normal brain tissue.
2. Aortic Aneurysm Rupture: When the Aorta Bursts
When the aorta bursts. The aorta is the largest vessel in our body, the highway that sends the blood from the heart to the whole body. When calcification progresses on this aortic wall, the vessel wall weakens, and the weakened area swells up like a balloon. This is an aortic aneurysm.
An aortic aneurysm mostly has no symptoms, so it is called a "silent killer." Then when one day it suddenly bursts, the massive hemorrhage can lead to death within a few minutes. The pre-hospital mortality rate of aortic aneurysm rupture is more than about 80%. Survival is greatly determined by the speed of detection, transport, and treatment.
Why does a calcified vessel burst? At first thought it would seem that a vessel that has hardened through calcification would be sturdier. But it is the opposite. A normal vessel is flexible like rubber, so when pressure is applied it stretches and then returns.
But a calcified vessel, though hard like porcelain, is easily broken. A vessel that has lost its flexibility cannot adapt to a sudden change in pressure, and a crack forms at the weakest part and it bursts.
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3. Why does a calcified vessel burst?
At first thought it would seem that a vessel that has hardened through calcification would be sturdier. But it is the opposite. A normal vessel is flexible like rubber, so when pressure is applied it stretches and then returns.
But a calcified vessel, though hard like porcelain, is easily broken. A vessel that has lost its flexibility cannot adapt to a sudden change in pressure, and a crack forms at the weakest part and it bursts.
Why 1M Obstruction & Rupture Is the Most Frightening
There are three reasons why 1M Obstruction & Rupture is especially frightening.
1. First, it is acute.
The DIAH trigger slowly causes calcium to flow out of the bones over several years to several decades, and that calcium slowly piles up on the vessel wall. But the final result of 1M Obstruction & Rupture happens within a few minutes to a few hours. In myocardial infarction, when the vessel is blocked the heart muscle begins to die within 20 to 40 minutes, and in cerebral infarction, if the golden time of 4.5 hours is missed, brain cell damage progresses sharply. Cerebral hemorrhage or aortic rupture can lead to loss of consciousness and death in a mere few minutes.
2. Second, it is fatal.
The diseases that 1M Obstruction & Rupture creates occupy the top ranks among causes of death. The 2nd leading cause of death for Koreans is heart disease (mostly myocardial infarction), and the 4th is cerebrovascular disease (cerebral infarction, cerebral hemorrhage). Combining the two diseases, they kill more people than anything except cancer.
3. Third, it comes without warning.
This is why the words "he was perfectly fine until yesterday..." come up. Even when a vessel is blocked up to 70%, there may be no symptoms. This is because the body makes a bypass route or holds out with the remaining 30%. Then when one day the atheroma suddenly bursts, it becomes 100% occlusion within a few minutes. This is why the words come up that someone was told there was nothing wrong at a health checkup yet suddenly collapsed.
Summary of the 1M Obstruction & Rupture Mechanism
1M Obstruction & Rupture is the phenomenon in which calcium that has flowed out of the bones is deposited as calcification on the wall of a tube, narrows the lumen, and completely blocks it or bursts.
The 1M Obstruction & Rupture mechanism formula: DIAH → bone calcium efflux → immune cell activation (IL-1β, IL-6, TNF-α) → I (Inflammation) vicious cycle → vessel wall calcium deposition (ectopic calcification) → lumen stenosis → occlusion or rupture
Among the 7M, 1M Obstruction & Rupture is the most acute and the most fatal. It progresses quietly for decades and then one day suddenly takes life. Myocardial infarction, cerebral infarction, cerebral hemorrhage, aortic aneurysm rupture. This is why merely hearing the names of these diseases is frightening.
But 1M Obstruction & Rupture can be prevented. If you block the DIAH trigger early and prevent calcium from flowing excessively out of the bones, you can reduce the piling up of calcification on the vessel wall. At the same time it is important to manage other risk factors together, such as hypertension, hyperlipidemia, smoking, and diabetes. Treatment after it occurs is already too late. Prevention is the best answer.
2M Dysfunction (it grows dull)
1. "My Knee Is Stiff," "My Lower Back Won't Turn": the 2M Dysfunction We Feel
"My knee is stiff so climbing stairs is hard." "My lower back won't turn." "My shoulder feels stiff." "My finger joints don't bend like they used to."
These are words everyone says at least once as they age. Most people pass it off as "the fault of age." But a considerable part of this "stiffness" and "not turning" is not simple aging but the result of the 2M Dysfunction mechanism.
If 1M Obstruction & Rupture is a "blocking and bursting" acute catastrophe, 2M Dysfunction is a "gradually dulling" chronic decline. When calcification sets into a joint, movement becomes stiff; when calcification sets into a valve, its opening and closing grows dull; and when calcification sets into a muscle, its contraction and relaxation is not smooth.
Dunhwa (鈍化) means "to grow dull." What was smooth becomes stiff, what was free becomes restricted, and what was a soft movement grows dull. This is the essence of 2M Dysfunction.
2. The Definition of 2M Dysfunction: When Calcium Sets In, Movement Grows Dull
2M Dysfunction is the phenomenon in which calcium that has flowed out of the bones is deposited as calcification in moving tissues such as joints, muscles, and valves, so that movement grows dull and the functions of contraction and relaxation decline.
What happens when the hinge on a door rusts? The door does open and close, but it is stiff. You have to apply more force, it makes a sound, and the movement is not smooth. When a bicycle chain rusts, even when you press the pedal the force is not transmitted well, and shifting gears becomes stiff. Exactly the same thing happens in the joints and muscles of our body.
The core of 2M Dysfunction is "the moving tissue becomes stiff." It has not hardened completely (that is 4M Hardening), but it cannot move smoothly. If 1M Obstruction & Rupture is the blocking of the lumen of a tube, 2M Dysfunction is the dulling of a moving part.
3. From DIAH to Joint Calcification: Why Calcium Piles Up in Joints
Let us follow the process by which the knee becomes stiff from the very beginning.
Stage 1: The DIAH Trigger Activates
When there is D (Deficiency), blood calcium becomes insufficient, and calcium flows out of the bones. When there is I (Inflammation), calcium is consumed in the inflammatory response and is replenished from the bones. When there is A (Acidosis), bone calcium is mobilized to neutralize the acid. When there is H (Hypoxia), the cell's calcium pump breaks down, and blood calcium becomes insufficient and is replenished from the bones.
Let us think of a knee osteoarthritis patient. Their calcium intake is insufficient (D), they have chronic inflammation in the knee (I), they eat a lot of acidic food (A), and due to lack of exercise the blood flow to the joint is poor (H). All four triggers are operating.
Stage 2: Calcium Efflux from the Bone
When the DIAH trigger operates, osteoclasts (cells that break down bone) are activated. When osteoclasts break down bone, calcium is released into the blood. In knee osteoarthritis, calcium flows out of the bones around the knee, especially the subchondral bone (the bone just beneath the cartilage).
Stage 3: Microfractures and Calcium Fragments
The knee bends and straightens thousands of times every day. It walks, climbs stairs, sits down and stands up. This repetitive stress causes microcracks in the subchondral bone. When young, microcracks heal quickly, but when the DIAH trigger operates the bone weakens, so healing slows and microcracks accumulate. Calcium fragments break off from the microcrack area. These tiny calcium fragments penetrate into the joint cavity (the inner space of the joint).
Stage 4: Immune Cell Activation and the I (Inflammation) Vicious Cycle
The immune cells recognize the calcium fragments that have entered the joint cavity as "foreign matter." Macrophages try to eat up the calcium fragments, and in this process they secrete inflammatory cytokines (IL-1β, IL-6, TNF-α). IL-1β acts directly on the cartilage cells and activates the enzyme (MMP) that breaks down the cartilage matrix. TNF-α causes inflammation in the synovium (the membrane enveloping the joint). IL-6 promotes a systemic inflammatory response. This inflammation in turn causes even more calcium to flow out of the bones. Calcium fragments → immune cell activation → inflammation → more calcium efflux → more calcium fragments. It is a vicious cycle.
Stage 5: Calcium Deposition in the Cartilage
When calcium becomes excessive in the blood and the joint fluid, it binds with phosphate to form a calcium-phosphate complex. This complex is deposited in the cartilage, especially in the inflamed area. When calcification piles up on the cartilage surface, the surface, which was originally smooth like glass, becomes rough.
Stage 6: The Dulling of Movement
When the cartilage surface becomes rough, friction increases when the two bones meet and slide. When friction increases, movement becomes stiff. This is the true identity of the feeling that "the knee is stiff."
[Interaction with Other Risk Factors]
In osteoarthritis, besides an abnormality of calcium metabolism, obesity (increased joint load), a history of trauma, genetic predisposition, occupational repetitive motion, and the like act in combination. The DIAH-calcium pathway contributes to joint damage together with these factors.
4. Knee Osteoarthritis: The Representative Disease of 2M Dysfunction
Knee osteoarthritis is a representative disease of 2M Dysfunction. About 30% of the domestic population aged 50 and over suffers from knee osteoarthritis. Among those aged 60 and over, it exceeds 50%.
Early Symptom: Morning Stiffness
In the early stage of knee osteoarthritis, the symptom "the knee is stiff in the morning" appears. When you wake from sleep the knee feels stiff, and as you move it loosens little by little. This is because, since the joint was not moved through the night, the joint fluid has not spread evenly, and the calcium deposition area feels stiffer. If this "morning stiffness" loosens within 30 minutes, it is still the early stage of 2M Dysfunction. This is the opportunity for intervention.
Progression: Pain When Moving
When calcium deposition progresses, the cartilage surface becomes rougher, and each time you move, friction worsens. Pain arises when going up and down stairs, when walking for a long time, and when squatting. This pain is not due to simple friction alone. As the roughened cartilage surfaces scrape against each other, tiny cartilage fragments break off, and these fragments in turn stimulate the immune cells and cause inflammation. Inflammation creates pain. Calcium deposition → cartilage damage → inflammation → pain. It is yet another vicious cycle.
Late Stage: Progression to 4M Hardening
When 2M Dysfunction keeps progressing without treatment, it passes over into 4M Hardening. The cartilage wears away completely, and bone directly strikes bone. Bone grows around the joint (a bone spur) and the joint deforms. At this stage the knee hardens completely so that both bending and straightening become difficult. Here lies the reason knee osteoarthritis is marked as "2M Dysfunction + 4M Hardening" in the disease matching table. 2M comes first, and if left alone it progresses to 4M.
5. Lower Back Disease: The Spine Grows Dull Too
It is not only the knee that grows dull. The lower back grows dull by the same mechanism.
Lumbar Stenosis and Spinal Canal Stenosis
In the spine there is the spinal canal, the passage through which the nerves pass. When calcification is deposited in the ligaments around the spine, the ligaments thicken, and the spinal canal narrows (1M Obstruction & Rupture). At the same time, when calcification is deposited in the spinal joints, the movement of the lower back grows dull (2M Dysfunction). When the ligaments harden further, it progresses to 4M Hardening.
The symptoms "my lower back won't turn," "it is hard to bend at the waist," and "when I stand for a long time my lower back becomes stiff" appear. This is the reason lumbar stenosis and spinal canal stenosis are marked as "2M Dysfunction + 1M Obstruction & Rupture + 4M Hardening" in the disease matching table.
Degenerative Disc Disease
The disc (intervertebral disc) is a structure that plays the role of a cushion between the vertebrae. When calcification is deposited in the disc, the disc hardens and loses its elasticity. A disc that has lost its elasticity cannot absorb shock, and in the end it compresses the nerve. In a degenerative disc patient, the movement of the lower back grows dull (2M Dysfunction), the disc hardens (4M Hardening), and the nerve is compressed so that numbness or pain arises in the leg (6M Disconnection).
Ankylosing Spondylitis
Ankylosing spondylitis is a disease in which severe inflammation and calcium deposition occur in the spinal joints so that the spine gradually hardens. In the early stage it is a 2M Dysfunction state in which the lower back is stiff, but as it progresses it becomes a 4M Hardening state in which the entire spine hardens like bamboo.