Continuing from the previous part, this article examines the remaining pattern of the 7M and its integration. The cited references follow the original manuscript.
[Figure 8] 7M Collapse: Representative Clinical Distribution
| Place | Representative clinical | Microscopic-dimension event |
|---|---|---|
| Bone (systemic) | Osteoporosis, fracture risk | Menopause, aging, chronic inflammation → bone resorption > bone formation → negative mineral balance |
| Bone (mineralization disorder) | Osteomalacia | Vitamin D deficiency, phosphorus metabolism abnormality → insufficient mineralization |
| Spine | Spondylolysis, spondylolisthesis | Mineral weakening of the vertebral arch → separation, displacement |
| Tooth | Dental caries | Demineralization of enamel and dentin → collapse of tooth substance |
| Periodontium | Periodontitis, alveolar bone resorption | Negative mineral balance of periodontal tissue and alveolar bone → tooth loss |
The integrated meaning of 7M is at the most decisive place in the message of this whole book. The fact that at the time osteoporosis is diagnosed in one patient, calcium deposition is progressing in the vessels of the same patient, and the fact that those two events are accompanying events that surface simultaneously at the two ends of essentially the same one calcium movement, are the most powerful clinical evidence for re-binding, at the underlying-reality dimension, the clinical events that specialty medicine has diagnosed separately. The patient's body itself is showing not the boundary of specialty medicine but the movement of one event.
Here the unraveling of the seven 7M patterns is concluded. In the following article we once more recover the microcalcification dual blockade as the common upstream of all seven patterns, organize the two auxiliary variants added to the 7M, and then unravel the operating rule of how the 7M patterns combine in one patient.
Microcalcification Dual Blockade: The Common Upstream of the 7M
The seven patterns from 1M to 7M unraveled above are manifestations at different tissue dimensions, but they all have one common upstream. It is the microcalcification deposition in the microvascular environment and the dual blockade that follows, that is, the microcalcification dual blockade. The microcalcification dual blockade is not the eighth pattern of the 7M but the common substrate that lies in front of all seven patterns. The 7M are the seven variants in which this microcalcification dual blockade is expressed in each tissue and organ.
The most central proposition of this whole book is formalized here. Only the organ differs and the clinical name differs; the event at the microvascular level is one. This is precisely the molecular formalization of the integrated message that the hundreds of manifestations of aging and chronic disease diagnosed separately in specialty medicine are, in their underlying reality, all the surfacing of one event at different places. Depending on at which place among the seven patterns (from 1M to 7M) the microcalcification dual blockade surfaces, the clinical name diagnosed in the patient merely looks different (as atherosclerosis, as diabetic complications, as Alzheimer's, as osteoporosis) but the event of the underlying reality is one.
The phenomenon in which several 7M patterns are observed simultaneously or sequentially in one patient is a natural consequence of this common-upstream structure. One representative example is the long-term progression of diabetes. A diabetes patient is at first diagnosed with 3M Coating & Blocking (insulin resistance), but as time passes shows, sequentially or simultaneously, 4M Hardening (diabetic nephropathy), 1M Obstruction & Rupture (the microvascular occlusion of diabetic retinopathy), 6M Disconnection (diabetic neuropathy), and 7M Collapse (bone-mass loss). From the viewpoint of specialty medicine, these are five separate complications. But from the viewpoint of the microcalcification dual blockade, this is a single process in which microvascular microcalcification progresses simultaneously in the pancreas and liver, kidney, nerve, retina, and bone, and surfaces as different 7M patterns according to the characteristics of each organ. It is that they are five manifestation-types of one event.
The clinical implication of the imaging non-detection of the microcalcification dual blockade is decisive. On standard imaging equipment, that is, ordinary computed tomography (CT), ultrasound, or angiography, this underlying-reality event is mostly invisible. It is because the calcium-phosphate deposition of the microvasculature is a crystal at the level of nanometers to a few micrometers, below the limit of the imaging resolution currently used in the clinic. So this underlying reality corresponds to the clinically asymptomatic latent period. The time when the patient feels symptoms and visits the hospital is after the underlying reality has accumulated sufficiently and surfaced macroscopically as some pattern from 1M to 7M. That is, the calcification visible on imaging is already the result of the progression phase, and the true underlying reality is an event that has already progressed for a long time at the microscopic dimension that imaging cannot catch.
The meaning of prevention becomes clear at this point. The stage before this underlying reality surfaces as a macroscopic pattern is the substantive place of prevention. And resolving the upstream that generates this underlying reality, that is, the DIAH triggers called out earlier (deficiency, inflammation, acidosis, hypoxia), is the most direct road to slowing the accumulation of the underlying reality itself. The reason that intervention after calcification begins to be visible on imaging is late is that by then the underlying reality has already moved into the macroscopic stage.
Organizing the representative clinical forms in which the 7M patterns appear combined in one patient gives the following.
[Figure 9] The 7M Patterns Branching from the Common Upstream of the Microcalcification Dual Blockade: Simultaneous Manifestation in One Patient
| Clinical diagnosis | Underlying-reality place | Simultaneously manifested 7M patterns |
|---|---|---|
| Long-term progression of diabetes | Pancreas, liver, kidney, nerve, retina, bone microvasculature | 3M + 4M + 1M + 6M + 7M |
| Atherosclerosis progression phase | Coronary, aortic, renal artery microvasculature | 1M + 4M + 5M (myocardial hypertrophy) |
| Alzheimer's progression phase | Brain small vessels, nerve circuit | 6M + 4M |
| End-stage chronic renal failure | Kidney, cardiovascular, bone microvasculature | 4M + 1M + 7M |
| Systemic aging phenotype | Systemic microvasculature | 4M + 5M + 7M |
In the following article we organize the two auxiliary variants added to the seven main 7M patterns, S and C. S is a composite crystal that environmental toxic substances form by combining with calcium, a variant that strengthens 3M Coating & Blocking. C is a domino event in which the calcification of one place collapses its surroundings and spreads in a chain, a variant that strengthens 6M Disconnection.
The S·C Extension: The Two Variants Added to the 7M
The seven main 7M patterns are the form in which the microcalcification dual blockade surfaces in a general clinical environment. But when a particular condition is added, a variant occurs in which the main pattern is accelerated or spreads extensively. In this book those two variants are formally denoted S and C. S is the event in which the main pattern is accelerated by the intervention of environmental toxic substances, and C is the event in which a microscopic event of one place spreads in a chain to its surroundings.
The S variant means the formation of a composite toxic crystal. The English name expresses synergistic toxic aggregation, and unraveled into Korean it is a composite crystal in which calcium has congealed and hardened with environmental toxic substances. Since industrialization, humanity has been exposed, over a lifetime, to various environmental toxic substances. Air-pollution particles, heavy metals (lead, cadmium, mercury), and microplastics are representative. When these environmental toxic substances enter the human body and enter the blood, they meet calcium and phosphate in the microvascular environment and form composite crystals. It is the event in which a kind of toxic cement, harder than simple calcium-phosphate microcalcification and less easily dissolved, is embedded in the microvascular wall.
The clinical implication of the S variant is clear. Because it blocks the signal pathway more strongly than simple calcium-phosphate microcalcification, in a patient accompanied by S, 3M Coating & Blocking (signal cutoff) progresses faster and more extensively. At the same time, 1M (pathway occlusion) and 5M (signal excess at the cellular dimension) are also linked and strengthened. Here lies the molecular foundation of the reason that, in modern medicine, environmental exposure and the rise of the risk of aging and chronic disease are consistently reported. Environmental toxic substances operate not simply by their toxicity itself but as a molecular mechanism that accelerates the main pattern (3M Coating & Blocking) by combining with calcium to form composite crystals.
The C variant means a chain-collapse domino. The English name expresses a cascading collapse reaction, and unraveled into Korean it is the event in which the calcification of one place collapses its surroundings and spreads in a chain. General microcalcification deposition stays in one place or spreads to the surroundings relatively slowly. But under a particular condition, a chain domino begins in which the microcalcification of one place induces ischemia in the surrounding microvasculature, that ischemia causes necrosis of the surrounding tissue, and that necrotic site in turn induces new calcification in the surrounding microvasculature. It is the event in which an event of one small place explodes into an extensive clinical result.
The clearest clinical specimen of the C variant is the calcinosis, in medical terms calciphylaxis, already seen in 6M Disconnection. As the calciphylaxis entry of the StatPearls medical information database operated by the U.S. National Library of Medicine organized, this event begins from calcium depositing in an arteriole of one place in the skin. That place is occluded so that the skin tissue beyond it falls into ischemia, that ischemic site progresses to necrosis, and new calcium deposition is again induced in the arterioles around the necrotic site, so that the event spreads to the surroundings like a domino. The reason an event that began as a small pain at the fingertip progresses within a few weeks into extensive skin necrosis and sepsis lies in this chain-collapse mechanism. The C variant is a variant that accelerates and spreads 6M Disconnection, and it surfaces as the most fatal form in the clinic.
Organizing the S variant and the C variant gives the following.
[Figure 10] The S·C Auxiliary Variants: Two Events That Strengthen the Main 7M Patterns
| Auxiliary variant | Definition | Molecular event | Strengthened main pattern |
|---|---|---|---|
| S (composite toxic crystal) | A composite crystal that environmental toxic substances form by combining with calcium | Calcium + heavy metals, microplastics → toxic cement → strengthened blocking of the signal pathway | 3M Coating & Blocking (linked strengthening of 1M, 5M) |
| C (chain-collapse domino) | The calcification of one place collapses its surroundings and spreads in a chain | Microcalcification → ischemia → necrosis → new surrounding calcification → domino spread | 6M Disconnection (terminating in 1M, 7M) |
S and C are accelerating events added to the general progression of the 7M. They do not occur in every patient, but under a particular environmental exposure or a particular clinical condition they are activated and make the main pattern progress faster and more fatally. The S variant tends to be activated in a patient in whom environmental toxic exposure has accumulated, and the C variant in a patient whose microvascular environment is already extensively damaged. In the following article we unravel the operating rule of how, when several 7M patterns are observed simultaneously in one patient, the main pattern and the auxiliary pattern are distinguished.
The Five Principles of 7M Determination: How the Code Is Decided
It is very common for several 7M patterns to be observed simultaneously in one patient. An atherosclerosis patient has 4M Hardening and 1M Obstruction & Rupture together, a diabetes patient advances 3M Coating & Blocking and 4M Hardening and 6M Disconnection simultaneously, and a chronic renal failure patient shows 4M Hardening and 7M Collapse and 1M Obstruction & Rupture all at once. Here one clinical question arises. Among the several patterns, which is that patient's main pattern and which is the auxiliary pattern? This book formally presents five operating principles for that distinction. These principles are not an arbitrary determination guide but formal rules derived from the structural logic of the 7M system.
First, the principle is one main plus one auxiliary, up to a maximum of two. When denoting a patient's clinical diagnosis with a 7M code, one denotes up to two: the single most dominant main pattern and the single most distinct auxiliary pattern. Even if three or more patterns are clearly observed, one records only up to two in the code and unravels the rest in the body text. This principle is for the balance between the resolution of the classification and the simplicity of clinical use.
Second, the main and auxiliary are distinguished by the criteria of temporal precedence and structural dominance. When several patterns are observed simultaneously, the main pattern is decided by one of two criteria. It is the pattern that appeared earlier in time, or the pattern that is more dominant structurally. Generally the two criteria agree with each other, but when they do not agree, structural dominance takes priority. It is because which event is closer to the underlying reality, rather than in what order the patient's events occurred, is the essential place of diagnosis.
Third, when 1M and 4M are observed together, 4M is denoted as the main pattern and 1M as the auxiliary pattern (4M + 1M). 4M is a state in which the tissue has hardened, that is, a change of structure, and 1M is the event of occlusion or rupture that occurs upon that hardened structure. Since the state is the precondition of the event, 4M is the underlying reality and 1M is the result surfacing upon that underlying reality. Denoting coronary artery disease as 4M main + 1M auxiliary is the archetype of this principle. Atherosclerosis (4M) progresses first, and when a threshold point is exceeded in that hardened artery, acute occlusion (1M) occurs and surfaces as myocardial infarction.
Fourth, when 2M and 4M are observed together, two denotations are distinguished according to their causal relationship. When hardening becomes the cause and functional dulling appears, it is denoted 4M + 2M, and when functional decline is central and the imaging evidence of hardening is weak, it is denoted 2M alone. Calcific aortic valve stenosis has the clear causal relationship in which the hardening of the valve made the movement-dulling, so it is 4M + 2M. On the other hand, some functional valve abnormality shows almost no hardening on imaging and only functional decline appears, so it is 2M alone. Even for the same clinical complaint, if the event of the underlying reality differs, the code also differs.
Fifth, the cell death of 5M and 6M is distinguished. The death of 5M is direct toxicity by the excessive influx of calcium inside the cell, that is, overload-type death. The death of 6M is ischemic necrosis that occurs because the pathway going to that cell is cut off, that is, disconnection-type death. Even for the same death, since the molecular mechanism differs, the code also differs. When hyperproliferation, hypertrophy, and swelling are central it is 5M, when ischemia, necrosis, and disconnection are central it is 6M, and when both are distinct it is denoted 5M + 6M. The tumor necrosis commonly observed in tumors is a typical example of 5M + 6M. It is the event in which the hyperproliferation of tumor cells (5M) compresses the surrounding microvasculature and causes ischemic necrosis of the tumor center (6M), the two events progressing together.
Organizing the five principles gives the following.
[Figure 11] The Five Principles of 7M Determination: The Formal Rules for Deciding One Patient's Code
| Principle | Content | Example of clinical application |
|---|---|---|
| 1. Main-auxiliary distinction | 1 main pattern + 1 auxiliary pattern, up to a maximum of 2 | Three or more are described and unraveled in the body text |
| 2. Temporal precedence + structural dominance | The main pattern is decided by temporal precedence or structural dominance. Upon disagreement, structural dominance takes priority | The event closer to the underlying reality is the main pattern |
| 3. 4M + 1M rule | Hardening (state) + occlusion (event) → 4M main + 1M auxiliary | Coronary artery disease, carotid artery stenosis |
| 4. 4M + 2M / 2M alone | Hardening is the cause of dulling = 4M+2M / functional decline central = 2M alone | Calcific valve vs. functional valve abnormality |
| 5. 5M + 6M distinction | 5M (overload death) / 6M (disconnection death) / both = 5M+6M | Tumor-center necrosis = 5M+6M |
These five principles are the operating rules of the 7M system. It is thanks to these principles that the 7M is established as a specification actually operable in the clinical field, not remaining a mere classification scheme. To accurately code by which pattern a patient's event surfaces is the starting point of an accurate understanding of that patient, and it becomes the molecular foundation of an integrated diagnosis that re-binds, at the underlying-reality dimension, the clinical names that specialty medicine has handled separately.
[Figure 12] 7M Self-Check
| Your 7M Self-Check. Check whether you or your family have ever received a diagnosis among the following items. 1. You have been diagnosed with any of atherosclerosis, myocardial infarction, stroke, cerebral hemorrhage (1M). 2. You have been diagnosed with any of calcific tendinitis, arthritis, frozen shoulder of the shoulder, knee, or foot (2M). 3. You have been diagnosed with any of insulin resistance, diabetes, hypothyroidism, hyperlipidemia (3M). 4. You have been diagnosed with any of high blood pressure, chronic renal failure, cirrhosis, ankylosing spondylitis, scleroderma (4M). 5. You have been diagnosed with any of tumor, myocardial hypertrophy, prostatic hypertrophy, uterine fibroids (5M). 6. You have been diagnosed with any of vascular dementia, lacunar infarction, peripheral vascular disease, diabetic foot (6M). 7. You have been diagnosed with any of osteoporosis, dental caries, periodontitis (7M). If two or more items apply, there is a strong likelihood that the 7M patterns are already progressing simultaneously in two or more places within one person's body. It means that the events diagnosed separately in specialty medicine are, in their underlying reality, manifestations of the same one event, differing only in place. |
|---|
The Conclusion of One Chapter
Here the unraveling of the seven 7M patterns, their common upstream the microcalcification dual blockade, the two auxiliary variants S and C, and the five operating principles is all concluded. The content organized in this one chapter is the most central molecular-dimension formalization in this whole book. The integrated message that the hundreds of manifestations of aging and chronic disease diagnosed separately in specialty medicine are, in their underlying reality, all the surfacing of one event at different places, has been clearly formalized as the seven damage patterns from 1M Obstruction & Rupture to 7M Collapse and the microcalcification dual blockade as their common upstream.
In the following chapter we examine how this 7M system operates in the clinical reality of aging and chronic disease. We unravel in turn how the chronic diseases familiar to us (atherosclerosis and high blood pressure, diabetes and its complications, Alzheimer's and osteoporosis, chronic renal failure and various tumors) are denoted as combinations of 7M patterns, and how that combination lets us predict the patient's clinical course. In the end, we will see together the landscape in which hundreds of clinical names converge into a few essential roads.
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