This piece is the middle section of Chapter 9 of Stones in the Body: More Frightening Than Cancer (Yoon Jong-won). It is a narrative containing the author's academic hypothesis, and the body, figures, and citations follow the manuscript as written.
6. Shoulder and Foot: Frozen Shoulder, Achilles Tendinitis, Plantar Fasciitis
2M Dysfunction operates not only in the knee and the lower back but in every moving joint and tendon (sinew).
Frozen shoulder (adhesive capsulitis)
Frozen shoulder is a disease in which inflammation and fibrosis progress in the joint capsule that wraps the shoulder joint, so that the shoulder's movement grows dull. This is why the expression "the shoulder feels frozen" comes out. In some patients, calcific tendinitis, in which calcium deposits in the shoulder tendon, accompanies it. In the early stage it is a 2M Dysfunction state in which raising the arm up or bending it back is difficult. It still moves, but it is stiff. If left untreated, it progresses to a 4M Hardening state in which the joint capsule hardens completely and movement is extremely limited.
Achilles Tendinitis
The Achilles tendon is the largest sinew connecting the calf muscle and the heel. When calcium deposits in this tendon, the tendon becomes stiff and the ankle's movement grows dull. When walking or running, the ankle does not extend smoothly, and pain arises. Starting from 2M Dysfunction and progressing to 4M Hardening, the tendon hardens rigidly and the risk of rupture rises.
Plantar Fasciitis
On the sole of the foot there is the plantar fascia that runs from the heel to the toes. When calcium deposits in this fascia, the sole becomes stiff, and especially when taking the first step in the morning, severe pain arises. When an X-ray is taken, a "bone spur (heel spur)" is often seen at the heel, and this is precisely the result of calcium deposition.
7. Dysfunction of the Heart: Heart Failure and Valvular Disease
2M Dysfunction operates not only in the joints but also in the heart. This is because the heart too is a moving organ.
Heart Failure: The Heart Cannot Pump Properly
The heart contracts to send blood out, and relaxes to take blood in. This contraction and relaxation are the heart's "movement."
Heart failure arises from various causes such as ischemic heart disease, hypertension, and valvular disease. In this process, when calcium deposits in the heart muscle and the valves, the contraction and relaxation functions can grow even duller. As a result, the heart fails to perform its pump role properly. This is why heart failure patients complain of "shortness of breath," "swollen legs," and "getting tired easily." Because the heart cannot pump sufficiently, blood does not circulate well through the whole body, blood pools in the lungs, and water accumulates in the legs.
Mitral Valve Calcification: The Valve Cannot Open and Close Properly
The mitral valve is the valve between the left atrium and the left ventricle. When the heart relaxes it opens to take in blood, and when it contracts it closes so that blood does not flow back. When calcium deposits on the mitral valve, the valve's opening and closing function grows dull. It does not open completely, or it does not close completely. If it does not close completely, blood flows back, and it becomes a burden on the heart.
Varicose Veins and Lower-Extremity Varicose Veins: The Venous Valves Weaken
In the veins there are valves that block blood from flowing backward. When these valves weaken or are damaged, valve function declines, and blood flows back. As the refluxed blood pools in the vein, the vein swells up. This is a varicose vein. When this happens in the leg veins, it is lower-extremity varicose veins. Lumpy blood vessels are seen beneath the skin, the legs are heavy and tired, and in severe cases the skin becomes discolored or ulcers form. The main causes of varicose veins are genetic predisposition, occupations that involve standing for long periods, obesity, pregnancy, and so on, and abnormal calcium metabolism may be one of the factors contributing to the decline of valve function.
8. The Relationship Between 2M Dysfunction and 4M Hardening
2M Dysfunction and 4M Hardening are different points on the same line. 2M is the "dulled state," and 4M is the "hardened state." In most cases 2M comes first, and if left alone it progresses to 4M.
The Progression of Osteoarthritis
Early stage: the knee is stiff (2M) / it still moves. Stiff in the morning but loosens within 30 minutes.
Middle stage: pain on movement (2M progressing) / increased calcium deposition. Movement restriction begins.
Late stage: the knee hardens (4M) / cartilage loss. Bone deformation. Severe movement restriction.
Why the Distinction Matters
At the 2M stage the effect of intervention is good. If the DIAH triggers are blocked and the joint is moved with appropriate exercise, the progression of calcium deposition can be slowed and, in some cases, improved.
Once it crosses into the 4M stage, it is hard to reverse. Hardened tissue struggles to become soft again. Once a joint hardens completely, there is no method other than artificial joint surgery. This is why many joint diseases are marked as "2M+4M" in the disease-matching table. It is because the two mechanisms are not separate, but lie on a continuum progressing from 2M to 4M.
9. Summary of the 2M Dysfunction Mechanism
2M Dysfunction is a phenomenon in which calcium that has leaked out of the bone deposits as calcium in moving tissues such as joints, muscles, tendons, and valves, so that movement grows dull and the contraction and relaxation functions decline.
2M Dysfunction mechanism formula: DIAH → calcium efflux from bone → microfracture/calcium fragments → immune cell activation (IL-1β, IL-6, TNF-α) → I (inflammation) vicious cycle → calcium deposition in moving tissue → increased friction/decreased flexibility → dulled movement
2M Dysfunction does not threaten life suddenly the way 1M Obstruction & Rupture does. But it severely lowers the quality of life. The knee is too stiff to climb stairs, the shoulder is too dull to raise the arm, the lower back will not turn so daily life becomes uncomfortable, and the heart grows dull so breath becomes short.
Fortunately, 2M Dysfunction is the stage before 4M Hardening. When you feel "stiff," blocking the DIAH triggers can prevent progression to 4M Hardening. After it has hardened completely it is hard to reverse, but at the dulled stage there is ample room for improvement.
[Interaction with Other Risk Factors]
In the diseases that cause 2M Dysfunction, besides abnormal calcium metabolism, obesity, trauma, genetic predisposition, occupational factors, aging, and so on act in combination. The DIAH-calcium pathway contributes, together with these factors, to joint and tissue damage.
3M Coating & Blocking (it is coated and blocked)
1. "When you get old you lose your sleep" : Is that really so?
"When you get old you lose your sleep." "I wake up at dawn and cannot fall back asleep." "Old folks naturally sleep little."
We take these words for granted. As if it were a natural part of aging. But when we get old, does sleep really become "unnecessary"?
No. The elderly need as much sleep as the young. The problem is not that sleep has become unnecessary, but that the hormone that induces sleep fails to be secreted properly.
Melatonin, the sleep hormone, is secreted from the pineal gland in the brain. When night comes, melatonin is secreted and sends the body the signal "now it is time to sleep." But when calcification progresses in the pineal gland, melatonin secretion function can decline.
In fact, pineal gland calcification increases with age. According to various studies, pineal gland calcification becomes more common with age and is observed at a high rate in the elderly. A correlation is observed between pineal gland calcification and decreased melatonin secretion, but the exact causal relationship is still under study.
This is one example of 3M Coating & Blocking. The phenomenon in which the function of a secretory organ declines and its secretions decrease.
2. The Definition of 3M Coating & Blocking: When It Is Covered, Both Signal and Secretion Are Blocked
3M Coating & Blocking is a phenomenon in which, due to abnormal calcium metabolism, receptor function or secretory function declines, so that signal transmission is obstructed or secretions fail to come out properly. Coating & Blocking (被蔽) means "covered and blocked." 被 is "to be covered," and 蔽 is "to screen, to block."
3M Coating & Blocking appears in two forms.
First, decreased secretion.
Think of a faucet. Even if the water pipe is full of water, if the tap is blocked the water does not come out. Even if hormones or enzymes have been made in the secretory gland, if secretory function declines they cannot come out sufficiently.
Second, decreased signal transmission.
Think of a lock and key. A hormone or neurotransmitter is the "key," and the receptor on the cell surface is the "lock." The key must be inserted into the lock for the door to open. When receptor function declines, the signal is not transmitted properly.
[The Metaphor and the Actual Mechanism]
The expressions "calcium deposits on the receptor" and "the secretory outlet is blocked" are metaphors to aid understanding. At the actual molecular level, various mechanisms are involved, such as abnormal calcium signaling, disturbance of intracellular calcium homeostasis, and functional decline due to tissue calcification. 3M integrates these complex phenomena and explains them under the concept that "function is blocked."
3. From DIAH to Decreased Secretion: Why Secretory Function Declines
Let us look, from the very beginning, at what happens in the pineal gland of an elderly person with insomnia.
Step 1: The DIAH Triggers Operate
Let us think of an elderly person in their 70s. They do not eat dairy well so calcium intake is insufficient (D), they have inflammation from chronic arthritis (I), their meat-centered diet gives a high acid load (A), and lack of exercise and sleep apnea frequently produce a hypoxic state (H). All four triggers are operating.
Step 2: Calcium Efflux from the Bone
When the DIAH triggers operate, osteoclasts are activated and calcium leaks out of the bone. The leaked calcium drifts through the blood.
Step 3: Immune Cell Activation and the I (Inflammation) Vicious Cycle
When the blood calcium concentration rises, immune cells, especially macrophages, are activated. Activated macrophages secrete inflammatory cytokines (IL-1β, IL-6, TNF-α).
These inflammatory substances circulate through the whole body and cause inflammation in various tissues. The pineal gland is no exception. When inflammation arises in the pineal gland, that area becomes vulnerable to calcium deposition.
Step 4: Calcium Deposition in the Pineal Gland
Excess calcium in the blood binds with phosphate to form a calcium-phosphate complex. This complex deposits especially easily in areas with inflammation and areas with slow blood flow.
The pineal gland is a very small organ (the size of a grain of rice) but has abundant blood flow. So, paradoxically, it is vulnerable to calcium deposition. This is because, as much blood passes through, it carries much calcium.
Step 5: Decline of Secretory Function
The pineal gland cells (pinealocytes) synthesize and secrete melatonin. When calcification progresses in the pineal gland tissue, the function of the pineal gland cells declines, and melatonin secretion can decrease.
Step 6: Decreased Melatonin Secretion → Sleep Disorder
When melatonin secretion decreases, the body does not sufficiently receive the signal of "night." It is hard to fall asleep, and even after barely falling asleep one sleeps a shallow sleep and is prone to waking early at dawn.
4. The Various Forms of Decreased Secretion: Tears, Stomach Acid, Hormones
The pineal gland is not the only thing affected. A similar phenomenon can appear in various secretory organs.
Dry Eye Syndrome: Tears Are Insufficient
Tears are secreted from the lacrimal gland to keep the eye moist. Dry eye syndrome arises from decreased tear secretion or tear film instability. The main causes are aging, hormonal change, environmental factors, autoimmune disease, and so on, and abnormal calcium metabolism can contribute to the decline of lacrimal gland function.
Hypothyroidism: Thyroid Hormone Is Insufficient
The thyroid secretes thyroid hormone, which regulates the body's metabolism. The main causes of hypothyroidism are autoimmune disease (Hashimoto's thyroiditis), iodine deficiency, thyroid surgery/radiation therapy, and so on. Calcification of the thyroid tissue can contribute to functional decline, but this is not the main cause.
When thyroid hormone is insufficient, the metabolism of the whole body slows. One is tired, feels the cold, gains weight, becomes constipated, and the skin becomes dry.
Atrophic Gastritis: Stomach Acid Secretion Decreases
The stomach secretes stomach acid to digest food, and secretes mucus to protect the stomach wall. When the gastric mucosa atrophies due to aging, Helicobacter pylori infection, autoimmunity, and so on, stomach acid and mucus secretion decrease. When stomach acid is insufficient, digestion does not happen. Symptoms such as "I get an upset stomach when I eat" and "my digestion is bad" appear.
[Interaction with Other Risk Factors]
These decreased-secretion diseases, besides abnormal calcium metabolism, are acted on in combination by various causes such as aging, autoimmunity, infection, and environmental factors. The DIAH-calcium pathway can be understood as contributing, together with these factors, to the decline of secretory function.
5. Decreased Signal Transmission: Insulin Resistance
Another form of 3M Coating & Blocking is decreased signal transmission. It is the case where secretion happens, but the signal is not transmitted properly.
Insulin resistance: insulin is secreted, so why does its effect fall off?
The core problem of type 2 diabetes is "insulin resistance." Insulin is secreted from the pancreas, but the cells do not respond to insulin properly.
Insulin is the "key," and the insulin receptor on the cell surface is the "lock." Insulin must bind to the receptor for the cell door to open and glucose to enter the cell. In insulin resistance, this signal-transmission process does not go smoothly.
[The Metaphor and the Actual Mechanism]
The expression "calcium deposits on the receptor" is a metaphor to aid understanding. The actual molecular mechanism of insulin resistance is more complex. Strictly speaking, it is not that calcium settles on the receptor itself, but that as the intracellular calcium concentration abnormally rises, it obstructs the operation of the downstream proteins (IRS-1 phosphorylation, PI3K activation, and so on) that transmit the insulin signal. In other words, it is closer to a 'communication failure' in which the internal gears that turn the lock are broken, rather than the keyhole being blocked. Also, obesity, fat accumulation, inflammation, genetic factors, and so on are the main causes of insulin resistance, and the disturbance of calcium signaling is understood to contribute, together with these factors, to insulin resistance.
The Vicious Cycle: Hyperglycemia → Reinforcement of the DIAH Triggers
Hyperglycemia itself reinforces the DIAH triggers. When blood sugar is high, inflammation arises in the blood vessels and tissues (I), the cell's energy metabolism becomes inefficient so acidic substances accumulate (A), and the microvessels are damaged, producing a hypoxic state (H).
The DIAH triggers operate more strongly. More calcium leaks out, and insulin resistance can worsen. Blood sugar rises further. This vicious cycle is one of the reasons diabetes is a "progressive disease."
6. Neurotransmission and Mental Health
The concept of 3M Coating & Blocking can also be tried on the neurotransmitter system. However, the pathophysiology of mental health disorders is very complex and hard to explain by a single mechanism.
Depression and Neurotransmitters
Depression is related to an imbalance of neurotransmitters such as serotonin, norepinephrine, and dopamine. But this is not the only cause. Genetic factors, stress, changes in brain structure, inflammation, hormonal change, and so on act in combination.
Calcium signaling plays an essential role in neurotransmitter secretion. Abnormal intracellular calcium homeostasis can affect neurotransmission function, but it is hard to conclude that this is a direct cause of depression.
Schizophrenia and ADHD
Schizophrenia arises from complex causes such as dopamine system abnormality, genetic factors, and abnormal brain development. ADHD involves frontal lobe dysfunction, dopamine/norepinephrine system abnormality, genetic factors, and so on.
There is research that abnormal calcium signaling can play some role in these diseases, but the direct mechanism that "calcium deposition blocks neurotransmission" has not been scientifically established.
[Understanding from the DIAH-7M Perspective]
Within the DIAH-7M framework it is hard to fully explain mental health disorders. However, chronic inflammation (I), metabolic abnormality, disturbance of calcium homeostasis, and so on can affect brain function, and from this perspective a partial link can be found. Mental health disorders absolutely require the diagnosis and treatment of a specialist.
7. Cardiac Conduction Abnormality: Arrhythmia and Atrial Fibrillation
3M Coating & Blocking also applies to the transmission of the heart's electrical signal. This area has relatively solid scientific grounding.
The Heart's Electrical System
The heart makes its own electrical signal and beats. The electrical signal begins at the sinoatrial node (SA node) and contracts the atria, then passes through the atrioventricular node (AV node) and is transmitted to the ventricles, contracting the ventricles. This electrical signal must be transmitted regularly for the heart to beat regularly.
Arrhythmia: Abnormal Electrical Signal Transmission
When calcium deposits in the cardiac conduction system, electrical signal transmission can be obstructed. The signal is transmitted late, or not transmitted at all, or transmitted by the wrong path.
The result is arrhythmia. The heart beats too fast, or too slow, or irregularly. The chest palpitates, one feels dizzy, breath is short, and in severe cases one faints.
Atrial Fibrillation: The Atria Beat Irregularly
Atrial fibrillation is the most common arrhythmia. When fibrosis and calcification progress in the conduction system and tissue of the atria, electrical signals arise irregularly in various parts of the atria. The atria cannot contract regularly and "quiver."
Atrial fibrillation itself does not immediately threaten life. But when the atria cannot contract properly, blood pools inside the atria, and the pooled blood clots into a thrombus. When this thrombus breaks off and blocks a cerebral blood vessel, it becomes a cerebral infarction. This is why atrial fibrillation patients have a 5-fold higher risk of stroke.
[Other Risk Factors]
Arrhythmia and atrial fibrillation arise from various causes such as hypertension, heart valve disease, heart failure, thyroid disease, drinking, aging, and so on. Fibrosis and calcification of the heart tissue contribute, together with these risk factors, to the occurrence of arrhythmia.
8. Summary of the 3M Coating & Blocking Mechanism
3M Coating & Blocking is a phenomenon in which, due to abnormal calcium metabolism, receptor function or secretory function declines, so that signal transmission is obstructed or secretions fail to come out properly.
3M Coating & Blocking mechanism formula: DIAH → calcium efflux from bone → immune cell activation (IL-1β, IL-6, TNF-α) → I (inflammation) vicious cycle → tissue calcification/disturbance of calcium signaling → decreased secretion or decreased signal transmission
Unlike 1M Obstruction & Rupture or 2M Dysfunction, 3M Coating & Blocking is often not visible to the eye. Joint calcification can be seen on X-ray, but the decline of secretory gland function or receptor dysfunction is not directly visible. "The medicine does not work," "the hormone levels are normal but I have symptoms," "there is no abnormality on the tests but I am uncomfortable." If you have had such experiences, you can suspect functional decline.
[Distinguishing the Metaphor and the Actual Mechanism]
The expressions used in this chapter, "the secretory outlet is blocked" and "calcium deposits on the receptor," are metaphors to aid understanding. The actual molecular-level mechanism is more complex, and various factors are involved, such as abnormal calcium signaling, decline of cell function, and tissue calcification. Also, each disease has its own causes besides abnormal calcium metabolism.
[Interaction with Other Risk Factors]
The diseases related to 3M Coating & Blocking are acted on in combination by aging, autoimmunity, heredity, lifestyle habits, environmental factors, and so on. The DIAH-calcium pathway is understood to contribute, together with these factors, to the occurrence of disease.
4M Hardening (it hardens)
1. "His Blood Vessels Have Hardened," "My Joint Has Stiffened" : The 4M Hardening We Know
"They say Father's blood vessels have hardened stiff so his blood pressure is high." "His knee stiffened completely so he had artificial joint surgery." "They say it is a disease where the skin hardens stiff."
"It hardened," "it became stiff," "it turned rigid." What these expressions point to is 4M Hardening.
If 2M Dysfunction is the "stiffened" state, 4M Hardening is the "completely hardened" state. In 2M it still moves. It is stiff but it moves. In 4M, movement itself is impossible or extremely limited.
Hardening (硬化) means "to harden." 硬 is "hard," and 化 is "to change." Tissue that was soft turning hard. A blood vessel that was elastic hardening like an iron pipe. A joint that was flexible hardening like a stone. This is the essence of 4M Hardening.
2. The Definition of 4M Hardening: When Calcium Piles Up, Tissue Hardens
4M Hardening is a phenomenon in which calcium that has leaked out of the bone deposits in large amounts in soft tissue, so that the tissue itself hardens rigidly.
What happens if you leave a rubber hose alone for a long time? The hose, which was flexible at first, gradually becomes stiff, and in the end hardens rigidly and does not bend. When you try to bend it, it breaks.
The same thing happens in the blood vessels, joints, skin, and organs of our body. When a little calcium deposits, it is 2M Dysfunction (it becomes stiff). When calcium deposits in large amounts, it is 4M Hardening (it hardens completely).
The key feature of 4M Hardening is irreversibility. At the 2M Dysfunction stage, intervention can bring improvement. But once it crosses into the 4M Hardening stage, it is very hard to reverse. A hardened blood vessel does not become soft again. A hardened joint does not become flexible again.
3. From DIAH to Tissue Hardening: Why Tissue Hardens
Let us follow, from the very beginning, the process by which a blood vessel hardens.
Step 1: Long-Term Operation of the DIAH Triggers
4M Hardening does not arise overnight. The DIAH triggers must operate continuously over years to decades.
Let us think of a hypertension patient. They eat salty so calcium excretion increases (D), they have chronic inflammation in the blood vessel wall (I), their processed-food-centered diet gives a high acid load (A), and sleep apnea repeats a hypoxic state every night (H). This state continues for 10, 20, 30 years.
Step 2: Accumulation of Calcium Efflux
When the DIAH triggers operate over a long period, calcium leaks continuously out of the bone. A little each day, a little each month, a little each year. The leaked calcium drifts through the blood and then deposits in soft tissue.
Step 3: Accumulation of Calcium Deposition
At first, fine grains of calcium deposit on the blood vessel wall. At this stage there are no symptoms. Even on examination it is hard to see.
As time passes, the calcium grains grow larger, and several grains merge. Calcium lumps form here and there on the blood vessel wall. When a CT is taken, they begin to show up white.
Step 4: Degeneration of Tissue, Ossification (骨化)
When calcium deposition crosses the critical point, an astonishing thing happens. The smooth muscle cells of the blood vessel wall change to become like bone-making cells (osteoblasts). This is called a "phenotypic switch."
The converted cells actively deposit calcium as if making bone. They secrete a collagen matrix and pile calcium-phosphate on top of it. The blood vessel wall literally turns into something like bone.
This is "vascular ossification." When you touch a severely calcified blood vessel at autopsy, it is hard like bone.
Step 5: Irreversible Hardening
Once ossification progresses, it cannot be reversed. The blood vessel completely loses its elasticity and hardens like an iron pipe. Each time the heart beats, blood pressure surges and then plunges. This is because the hardened blood vessel cannot absorb the pressure change.
[Interaction with Other Risk Factors]
Vascular hardening progresses, besides DIAH, together with hypertension, diabetes, smoking, dyslipidemia, chronic kidney disease, genetic factors, and so on. Especially in chronic kidney disease, abnormal phosphate metabolism accelerates vascular calcification. The DIAH-calcium pathway interacts with these risk factors and contributes to vascular hardening.
4. Vascular Hardening: Arteriosclerosis and Hypertension
The most representative example of 4M Hardening is the hardening of blood vessels.
Arteriosclerosis: The Blood Vessel Hardens, and in the End Blocks or Bursts
The progression of arteriosclerosis must be understood in two stages.
Stage 1, 4M Hardening: The Blood Vessel Wall Hardens
When calcium deposits on the arterial wall, the blood vessel wall itself becomes hard. A normal artery, like a rubber hose, has elasticity, so it stretches and shrinks each time the heart beats. Thanks to this elasticity, blood pressure changes are buffered. When the heart contracts to send blood out (systole), the artery stretches and absorbs the pressure, and when the heart relaxes (diastole), the stretched artery shrinks and pushes the blood.
A calcified artery hardens like an iron pipe and loses this elasticity. When the heart contracts, the pressure is transmitted directly and systolic blood pressure surges. When the heart relaxes, there is no force to push the blood, so diastolic blood pressure plunges. This stage is 4M Hardening. It is the state in which the blood vessel has "hardened."