This article is the first part of Chapter 7 of The Declaration of the Age of Physical Medicine (Yoon Jong-won). It is an academic exposition presenting the author's hypothesis of physical medicine, and the body text, figures, and citations follow the original manuscript.
There are words we naturally use when we talk about someone's illness. We say the vessel was blocked and burst. We say the joint hardened and it is hard to move. We say the signal does not pass well. We say the knee feels like it is snapping. We say the bone weakened and collapsed. When a patient explains their body to a doctor, when a doctor unravels the illness to a patient, when someone conveys a family member's illness to a friend, we all use these words. They are not medical terms but everyday words that anyone uses and anyone understands.
When these expressions are gathered in one place, a certain grain is seen. It is blocked. It becomes dull. It is coated and blocked. It hardens. It overflows and bursts. It is cut off. It collapses. There are seven. And almost every aging and chronic disease we encounter is explained by one of these seven, or a combination of two or three. Atherosclerosis hardens and is blocked. Diabetic complications have the signal coated and blocked and the nerve cut off. Alzheimer's has the small vessels of the brain cut off. Osteoporosis has the bone collapse. All aging and chronic disease comes within these seven expressions.
There is one more point to note. It is that these seven expressions are all physical expressions. To be blocked is a physical event in which the pathway narrows and the flow stops. To harden is a physical change in which a soft tissue becomes hard. To be cut off is a physical severance in which what was connected is separated. To collapse is a physical breakdown in which the supporting structure weakens and loses its form. To become dull, to be coated and blocked, to overflow and burst are all likewise. We are already, without knowing it, explaining illness in physical language. This is the reason this book bears the name physical medicine. It is because the underlying reality of aging and chronic disease is, before any abnormality of molecular signals, an event in which tissue and pathway and structure are physically deformed.
There is a more astonishing fact. It is that each one of these seven expressions that anyone uses in everyday life has already, long ago, been elucidated by medical research too. Blockage has been researched in cardiovascular medicine as atherosclerosis, thrombosis, and rupture. Hardening has been researched in kidney and liver medicine as fibrosis and sclerosis. Signal cutoff has been researched in endocrine medicine as insulin resistance. Cutting-off has been researched in neurological medicine as lacunar infarction and small-vessel disease. Collapse has been researched in orthopedic medicine and dentistry as osteoporosis, dental caries, and periodontitis. They are clinical events that specialty medicine has organized as verified facts, each in its own place.
Only, these researches were scattered by specialty, so they were not seen as one picture. The clinical fact that an atherosclerosis patient has osteoporosis at the same time, and a diabetes patient is accompanied by Alzheimer's at the same time, was known to everyone, but there was no integrated place to bind and explain that co-occurrence. The very division of specialty medicine into specialties was blocking that integration.
What this book has done is simple. It gathered in one place the verified academic materials that had been separately published in specialty medicine, and reorganized them into the seven expressions that anyone uses in everyday life. As a result, what is seen is one landscape. It is that the hundreds of chronic diseases handled separately in medicine (atherosclerosis of cardiovascular medicine, chronic renal failure of kidney medicine, osteoporosis of orthopedic medicine, Alzheimer's of neurological medicine, cancer of oncology, diabetic complications of endocrine medicine) finally surface as these seven patterns. This book is the first attempt to formalize that landscape. It is the place where the facts that specialty medicine has seen separately, each in its own place, at last gather upon one integrated map.
So this book calls those seven the 7M. 1M Obstruction & Rupture (it is blocked and bursts), 2M Dysfunction (it becomes dull), 3M Coating & Blocking (it is coated and blocked), 4M Hardening (it hardens), 5M Overflow & Burst (it overflows and bursts), 6M Disconnection (it is cut off), 7M Collapse (it collapses). It has attached a formal medical name to the seven expressions that anyone knows.
But one question remains. How do these seven different patterns meet in one place? How can the seven events that specialty medicine has seen separately become essentially one and the same event? The answer lies in the microcalcification dual blockade organized in the previous chapter. The same one molecular event surfaces in seven different forms depending on at which place it occurs, within what tissue environment it progresses, and at what speed it accumulates. The seven of the 7M are the surface, and the microcalcification dual blockade is their underlying reality.
Let us first make clear two structural characteristics of the 7M. First, mutual non-exclusivity. It is usual for two or more 7M patterns to be observed simultaneously in one patient. An atherosclerosis patient has 4M Hardening and 1M Obstruction & Rupture together, and a diabetes patient advances 3M Coating & Blocking, 4M Hardening, and 6M Disconnection simultaneously. Second, the existence of a common upstream. Although the seven patterns are manifestations at different tissue dimensions, the upstream of all of them is one. It is the dual blockade by microvascular microcalcification, that is, the microcalcification dual blockade. Because this common upstream exists, the 7M can operate as one integrated map.
The following article unravels each pattern of the 7M in turn. The unraveling of each pattern follows the same flow. It starts from the definition of the pattern, gathers in one place the clinical facts that had been scattered in specialty medicine, organizes the common molecular mechanism that the verified academic materials show, and closes with the distribution of the representative clinical diseases belonging to that pattern. The operating rule of how the seven patterns combine within one patient, the reconfirmation of the microcalcification dual blockade as the common upstream of all of them, and the two auxiliary variants added to the 7M are organized in turn in the latter part of this chapter.
[Figure 1] The Full Specification of the 7M Patterns
| M-tag | Korean name | English name | Core phenomenon | Correspondence to existing pathology |
|---|---|---|---|---|
| 1M | Pyeyeol (blocked and bursts) | Obstruction & Rupture | Luminal stenosis, occlusion, rupture by intraluminal calcification | obstruction, thrombosis, rupture |
| 2M | Dunhwa (becomes dull) | Dysfunction | Calcium deposition in valves, tendons, joints → functional decline | organ dysfunction |
| 3M | Pipye (coated and blocked) | Coating & Blocking | Calcium coating of receptors and signal-transduction sites → signal cutoff | signaling dysregulation |
| 4M | Gyeonghwa (hardens) | Hardening | Extracellular-matrix over-accumulation + local calcium → loss of elasticity | fibrosis, sclerosis |
| 5M | Beompa (overflows and bursts) | Overflow & Burst | Ca²⁺ signal excess → cell hypertrophy, hyperproliferation, death | proliferation, hypertrophy, neoplasia |
| 6M | Danjeol (cut off and disconnected) | Disconnection | Ischemia by arteriolar calcification → cell necrosis, nerve damage | disconnection, necrosis |
| 7M | Bunggoe (collapses) | Collapse | Bone and tooth mineral negative balance → physical weakening of hard tissue | structural failure |
1M Obstruction & Rupture: Blocked and Bursts
1M Obstruction & Rupture is the pattern in which the inner diameter of tube-shaped structures in the human body (blood vessels, airways, the intestinal tract, ureters, bile ducts) narrows or is completely blocked or ruptures. Unraveled into Korean, it is the event of being blocked and bursting, and the English name expresses both blockage and rupture together. It is an integrated pattern that gathers in one place the clinical phenomena that existing pathology has handled separately as obstruction, thrombosis, and rupture.
This pattern has been diagnosed, scattered under very various clinical names, in specialty medicine. Cardiology diagnoses coronary artery disease, myocardial infarction, and angina. Neurology diagnoses cerebral infarction, stroke, cerebral hemorrhage, and subarachnoid hemorrhage. Vascular surgery diagnoses aortic dissection, carotid artery stenosis, and Buerger's disease. Urology diagnoses kidney stones, urinary stones, and hydronephrosis. Gastroenterology diagnoses gallstones. Pulmonology diagnoses severe bronchial asthma. They are diagnostic names separated by specialty, but when looked at closely they are all manifestations of one event at different places. It is the event in which the inner diameter of the lumen narrows and, at some threshold point, transitions to acute occlusion or rupture.
How are these clinical names, which specialty medicine has diagnosed separately, bound into the same one pattern? The answer lies in the fact that they all set out from the same molecular-dimension event. It is the identical mechanism in which the deposition of microcalcification accumulates on the luminal wall, this expands into macrocalcification and narrows the luminal inner diameter, and at some threshold it converts to acute occlusion or rupture. Only the clinical name differs depending on in which lumen this mechanism occurs. When the verified academic materials that specialty medicine has published, each in its own field, are gathered in one place, they read as reports from different views of the same underlying reality.
The coronary artery calcification entry of the StatPearls medical information database operated by the U.S. National Library of Medicine clearly organized one core fact. Coronary artery calcification is not a mere aging phenomenon but a clinical expression of atherosclerosis, and it progresses together with risk factors such as high blood pressure, diabetes, smoking, and family history. The coronary artery calcification score is not a mere imaging finding but a clinical indicator that expresses the intravascular lesion burden (the risk of stenosis and occlusion). The higher the score, the proportionally higher the future risk of myocardial infarction. That is, coronary artery calcification is not a mark of a result but a powerful signal of the progression-phase underlying reality.
A review paper published by the Hutcheson, Maldonado, and Aikawa research group of Harvard University in the United States in an American lipid-medicine comprehensive-review journal organized an even more decisive fact. It is that not all calcification has the same meaning. Macrocalcification (the large calcium deposition caught on imaging) has, rather, an aspect of stabilizing the plaque. But microcalcification (the small crystals invisible on imaging) is the exact opposite. When microcalcification is embedded within the fibrous cap of the plaque, that spot becomes a stress-concentration point, and at even a small impact the cap tears. That is, the core factor that suddenly ruptures the plaque and causes acute myocardial infarction or stroke was microcalcification. This fact means that the practice by which the medical field has evaluated risk with only the calcium score was missing the true risk of the microscopic dimension. Microcalcification is smaller than macrocalcification, but clinically it is more dangerous.
The fact that these two materials show together is clear. 1M Obstruction & Rupture is a clinical event observed at the macroscopic dimension, but its starting point is at the microscopic dimension. The microcalcification dual blockade defined in the previous chapter is the true underlying reality of 1M Obstruction & Rupture. The very moment a patient arrives at the emergency room with myocardial infarction or stroke is the result of an event, in which microcalcification has accumulated for years to decades, exploding at some threshold point.
Organizing the representative clinical diseases belonging to the 1M pattern gives the following. They are clinical names in which the same one event has surfaced, differing only in place.
[Figure 2] 1M Obstruction & Rupture: Representative Clinical Distribution
| Place (kind of lumen) | Representative clinical | Microscopic-dimension event |
|---|---|---|
| Coronary artery | Coronary artery disease, myocardial infarction, angina | Coronary artery microcalcification, plaque microcalcification |
| Cerebral vessels | Cerebral infarction, stroke, cerebral hemorrhage, subarachnoid hemorrhage | Cerebral microvascular calcification, plaque microcalcification |
| Aorta | Aortic dissection, aortic aneurysm rupture | Medial microcalcification |
| Carotid and peripheral vessels | Carotid artery stenosis, Buerger's disease, peripheral vascular disease | Carotid microcalcification, peripheral microvascular calcification |
| Kidney and urinary tract | Kidney stones, urinary stones, hydronephrosis | Calcium-phosphate crystal deposition |
| Bile duct | Gallstones | Bile calcium crystals |
| Bronchus | Severe bronchial asthma | Bronchial mucosal calcification |
The clinical characteristic of the 1M pattern is the asymmetry of temporality. The accumulation progresses quietly and long, but the explosion is sudden and short. From the patient's standpoint, myocardial infarction is experienced as an event that occurred suddenly one day. But seen from the progression-phase underlying reality, that suddenness is only the threshold point reached at the end of years to decades of microcalcification accumulation. The clinical tragedy of 1M Obstruction & Rupture lies not in the suddenness of the event but in the fact that the underlying reality was invisible until that event occurred suddenly. At the microscopic dimension that standard imaging cannot catch, the underlying reality has already been progressing for a long time.
If 1M is the pattern of being blocked and bursting, the 2M of the following article is the pattern of becoming dull. From blockage to dulling, from occlusion at the structural dimension to dulling at the functional dimension, the pattern moves over.
2M Dysfunction: Becomes Dull
2M Dysfunction is the pattern in which the movement or function of structures that make movement or are in charge of secretion (valves, tendons, joints, muscles, secretory glands) declines. Unraveled into Korean, it is the event of becoming dull. The English name means functional failure, and it is an integrated pattern that gathers in one place the clinical phenomena that existing pathology has classified as organ functional decline.
This pattern, too, has been diagnosed, separated under very various clinical names, in specialty medicine. Orthopedics diagnoses calcific tendinitis of the shoulder, frozen shoulder, Achilles tendinitis, knee arthritis, and degenerative arthritis. Cardiology diagnoses heart valve disease, aortic valve stenosis, and mitral valve stenosis. Endocrinology handles some forms of functional decline of the thyroid and adrenal secretory glands. Rehabilitation medicine handles plantar fasciitis and rotator cuff injury. They are diagnostic names separated by specialty, but all are manifestations of one event at different places. It is the event in which microcalcification deposits on a structure that makes movement or a structure in charge of secretion, so that the structure can no longer perform its original movement or secretory function.
The reason these different diagnostic names are bound into the same one pattern is that they all set out from the same molecular-dimension event. Only the clinical name differs depending on where the place of microcalcification deposition is; the mechanism of deposition is all the same. It is the identical event in which calcium leaked through the triggers of deficiency, inflammation, acidosis, and hypoxia hardens into a crystal within some tissue environment and dulls the original function of that tissue. Verified academic materials back up this integration.
A consensus review published by the 14-member research group of Rajamannan and others of the Aortic Stenosis Working Group of the U.S. National Heart, Lung, and Blood Institute in an American cardiovascular journal organized one decisive fact. Calcific aortic valve disease is not the result of mere aging-caused wear or passive calcium deposition. It is an actively regulated pathological process, and it shares a molecular mechanism resembling that of atherosclerosis. As the interstitial cells inside the valve begin an identity conversion in which they behave like bone-forming cells, the valve gradually thickens and hardens. The result is a decline in the mobility of the valve, that is, 2M Dysfunction. The fact this review made clear is that the event of the valve hardening is not a mere passive result but an active molecular event. This is the medical form of the progression-phase underlying reality of which this book speaks.
A comprehensive review published in the English-language journal of the Korean Shoulder and Elbow Society organized the form in which the same event is manifested in the shoulder. The event in which calcium-phosphate crystals deposit on the rotator cuff tendon of the shoulder (clinical name calcific tendinitis) occurs most commonly between the 30s and 50s and creates severe pain and limitation of range of motion in the patient. It is not simply that the shoulder hurts, but that the original movement function of the shoulder is dulled. That review organized one more interesting fact. It is that in calcific tendinitis patients the co-occurrence rate of endocrine diseases such as diabetes or thyroid disease is very high. This suggests that the microcalcification of the shoulder is not a mere local problem of the shoulder but a systemic-dimension abnormality of calcium-phosphorus metabolism surfacing at one particular place.
When the two materials are placed side by side, one fact becomes clear. The event occurring in the valve of the heart and the event occurring in the tendon of the shoulder, though they have been diagnosed separately in specialty medicine, are the same one molecular-dimension event. It is the dulling of tissue due to the deposition of microcalcification. Only the clinical name differs depending on at which place it occurs; the event of the underlying reality is one.
Organizing the representative clinical diseases belonging to the 2M pattern gives the following. They are clinical names in which the same one event has surfaced, differing only in place.
[Figure 3] 2M Dysfunction: Representative Clinical Distribution
| Place | Representative clinical | Microscopic-dimension event |
|---|---|---|
| Heart valve | Aortic valve stenosis, mitral valve stenosis, heart valve disease | Bone-forming cell conversion of valve interstitial cells, valve microcalcification |
| Shoulder | Calcific tendinitis, rotator cuff calcification, frozen shoulder, adhesive capsulitis | Rotator cuff tendon microcalcification |
| Ankle and Achilles tendon | Achilles tendinitis, Achilles tendon calcification | Achilles tendon microcalcification |
| Knee | Knee arthritis, degenerative arthritis | Cartilage microcalcification, joint capsule microcalcification |
| Sole of the foot | Plantar fasciitis | Plantar fascia microcalcification |
| Secretory gland | Some forms of secretory functional decline | Secretory gland microcalcification |
The difference between 1M and 2M is minute but important. If 1M is the pattern that makes structural occlusion or rupture of the lumen, 2M is the pattern that makes movement-dulling or secretion-dulling of a moving structure. In 1M a clinical event occurs in which the flow is suddenly cut off, but in 2M a gradual functional decline accumulates. From the patient's standpoint, 1M is experienced as an event that occurred suddenly, and 2M is experienced as a change that gradually becomes dull. But both patterns are different surfaces of the same event that set out from the same underlying reality.
If 2M is the pattern of movement-dulling, the 3M of the following article is the pattern of signal cutoff. From the dulling observed from outside to the cutoff of the signal occurring inside the cell, from the visible dimension to the invisible dimension, the pattern moves over.
3M Coating & Blocking: Coated and Blocked
3M Coating & Blocking is the pattern in which the cells of the human body come to be unable to accurately interpret the signals they receive from outside. Unraveled into Korean, it is the event of being coated and blocked. The English name expresses together the coating and blocking of the signal pathway, and it is an integrated pattern that gathers in one place the clinical phenomena that existing pathology has classified as signal-transduction abnormality.
The mechanism of 3M Coating & Blocking is essentially different from that of 1M and 2M. If 1M is the physical occlusion of the lumen, and 2M is the movement-dulling of a moving structure, 3M is the event in which the molecular-dimension signal-transduction pathway itself is coated and blocked. When calcium binds onto, or microcrystals pile up onto, the receptors on the cell surface, the molecular pathways that receive signals, and the signal-transduction proteins that regulate secretion (these minute molecular structures), that structure can no longer accurately interpret the original signal. Even if the signal comes in, it cannot receive it; even if it receives it, it cannot transmit it; and even if it transmits it, it cannot accurately operate it. This event is 3M Coating & Blocking.
This pattern is the pattern scattered under the most various diagnostic names in specialty medicine. Endocrinology diagnoses insulin resistance, type 2 diabetes, and some forms of hypothyroidism. Cardiology handles some forms of arrhythmia. Lipid medicine diagnoses hyperlipidemia and hypercalcemia. Immunology handles immune-signal desensitization. Nephrology handles the signal aspect of renal osteodystrophy. They are diagnostic names separated by specialty, but in their underlying reality there is all the same one event. It is the event in which the signal pathways of the cell surface are coated by microcalcification and calcium-protein crystals so that they come to be unable to receive signals.
This integration is revealed naturally when the clinical facts, separated and diagnosed in specialty medicine, are gathered in one place. The clinical observation that a patient with insulin resistance has atherosclerosis at the same time, and a patient with hypothyroidism has osteoporosis and vascular calcification at the same time. For medicine, which has explained this co-occurrence only as specialty-by-specialty complications, an integrated explanation at the microcalcification underlying-reality dimension becomes possible. All are manifestations of the same one event at different places.
A comprehensive meta-analysis published by the Chinese research group of Han, Zhang, Sun, and others in an international endocrinology journal made this integration clear at the population scale. That analysis, a meta-analysis integrating 15 studies that gathered data of about 60,000 people, organized one decisive fact. It is that the higher the insulin resistance, the proportionally higher the prevalence and progression rate of coronary artery calcification. Compared with the group of low insulin resistance, in the group of high insulin resistance the risk of occurrence of coronary artery calcification was meaningfully higher, and in the follow-up analysis the higher the insulin resistance, the more the progression speed of coronary artery calcification accelerated. This confirmed with population data that the two clinical events we have seen separately in specialty medicine (insulin resistance at the endocrine dimension and coronary artery calcification at the cardiovascular dimension) are essentially two faces of the same one event.
A molecular-dimension study published by the Feenstra et al. research group of the University of Groningen in the Netherlands in an American atherosclerosis-medicine journal made clear the mechanism of that event. It is that the minute particles that calcium and phosphorus make by binding with protein in the blood, that is, calciprotein particles, directly damage the function of the vascular endothelial cells. That study showed that when human endothelial cells are exposed to calciprotein particles, the expression of endothelial nitric oxide synthase decreases, and the production of nitric oxide also decreases. Nitric oxide is a signaling molecule absolutely necessary for the vessel to relax normally. When it decreases, the vessel hardens, the flow is blocked, and the road by which insulin reaches the target cells also becomes difficult. That is, it is molecular evidence that the microscopic-dimension calcium-protein crystals directly make the blockade of the signal dimension.
When the two materials are placed together, the fact is clear. The clinical events diagnosed in specialty medicine as insulin resistance, hyperlipidemia, hypothyroidism, and some forms of arrhythmia are, in their underlying reality, all manifestations of one event. It is the event in which microscopic-dimension calcium crystals and calcium-protein particles coat the signal pathways of the cell and make signal cutoff. The signal-blockade dimension defined in the previous chapter, that is, CAM, is located precisely at this spot. 3M Coating & Blocking is the pattern in which the signal dimension of the dual blockade surfaces most clearly in the clinic.
Organizing under which clinical names the 3M pattern has surfaced in specialty medicine gives the following.