This piece is the middle section of Chapter 7 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.
■ A (Acidosis) Subclassification
| Code | Name | Core Mechanism |
|---|---|---|
| A-FN | Functional Acidosis / Functional Acidosis | Insufficient acid excretion capacity due to declining kidney and liver function - chronic kidney disease, declining liver function, dehydration and diarrhea, poorly controlled diabetes (risk of ketones/acid load), etc. |
| A-DT | Dietary Acid Load / Dietary Acid Load | Increased acid load in the body from high-protein, high-salt, processed foods, etc. - high-protein and low-vegetable (when accompanied by insufficient alkali input), ultra-processed, high-salt, high-sugar, excessive alcohol consumption (nutrition↓+acid↑), etc. |
| A-RS | Respiratory Acidosis / Respiratory Acidosis | Imbalance due to CO₂ retention (COPD, sleep apnea) - COPD, sleep apnea (inflammation↑+acid↑+oxygen↓), respiratory disease (carbon dioxide accumulation), etc. |
| A-HM | Hypermetabolic Acidosis / Hypermetabolic Acidosis | Hyperthyroidism → metabolic hyperactivity → increased acid production - rise in basal metabolic rate → oxygen consumption↑ → metabolites (acid)↑ → mobilization of alkali (calcium) from the bone |
H Trigger: Hypoxia - When Oxygen Is Lacking, Calcium Floods Excessively into the Cell
Calcium and Oxygen: The Two Pillars of Cell Survival
For a cell to live, two things are absolutely necessary. They are oxygen and calcium. Oxygen is essential for making energy in the mitochondria, and calcium serves as the signal transmitter that uses that energy to make the cell function.
In the normal state the cell regulates the calcium concentration with great precision. The calcium concentration outside the cell is about 1.2 millimoles, while the calcium concentration inside the cell is about 0.0001 millimoles, a difference of more than 10,000-fold. To maintain this enormous concentration difference, calcium pumps in the cell membrane work ceaselessly, bailing out the calcium that has entered the cell.
Operating the calcium pumps requires enormous energy. A considerable portion of the energy the cell produces is used to maintain calcium homeostasis. This is just like running a pump to bail water out of a boat that keeps leaking. If energy is sufficient there is no problem, but when oxygen is lacking and energy production declines, a problem arises.
Hypoxia: The Breakdown of the Calcium Pump
When hypoxia, in which the tissue runs short of oxygen, occurs, energy production in the mitochondria drops sharply. At a normal oxygen concentration one molecule of glucose makes about 30~38 ATP (energy), but without oxygen it can make only 2 ATP. Energy production plummets to less than one-fifteenth.
When energy runs short, the calcium pump cannot work properly. It fails to bail out the calcium that seeps little by little into the cell, and the calcium concentration inside the cell slowly begins to rise. According to research supported by the U.S. National Institutes of Health (NIH), in a hypoxic state the intracellular calcium concentration can increase to several times the normal level, and in some cases to more than tenfold.
When intracellular calcium increases excessively, fatal consequences arise.
[Mitochondrial Paralysis]
The mitochondria absorb calcium excessively, so their function is paralyzed and a vicious cycle arises in which energy production declines even further.
[Cell Structure Destruction]
Excessive calcium activates protein-degrading enzymes and destroys the cell structure.
[Cell Death]
DNA-degrading enzymes are activated and the cell death program begins.
This is called 'calcium overload' or 'calcium toxicity.' The death of heart cells in myocardial infarction and the death of brain cells in cerebral infarction are, to a considerable degree, due to this calcium overload. When a blood vessel is blocked and oxygen runs short, calcium piles up inside the cell and the cell self-destructs.
The Pathway by Which Calcium Dissolves Out of the Bone: The Cell's Demand and the Compensatory Mechanism
When the H (Hypoxia) trigger is pulled, calcium dissolves out of the bone through two pathways.
1. The First Pathway: Reduction of Blood Calcium Due to Increased Calcium Consumption
In a hypoxic state the cells strain with all their might to operate the calcium pumps. When even a little energy is produced, they use it first for the calcium pumps to try to bail the calcium inside the cell back out. This is a last-ditch effort for survival.
The problem is that in this process the calcium that went from the blood into the cell and back out must return to the blood again, but in a hypoxic state this circulation does not go smoothly. Moreover, when damaged cells absorb calcium excessively and lock it away, the blood calcium concentration drops.
When blood calcium decreases, the D (Deficiency) trigger goes into action. PTH is secreted and draws calcium out of the bone. The calcium that emerges this way is again absorbed by the damaged cells, and the vicious cycle in which blood calcium remains continually deficient repeats.
2. The Second Pathway: Vascular Calcification Induced by Hypoxia
Hypoxia changes the vascular cells themselves. According to a study published in a journal of the American cardiovascular society, vascular smooth muscle cells exposed to a hypoxic environment can undergo a phenotypic switch in which they change as if into bone cells.
Specifically, as a protein called hypoxia-inducible factor (HIF) is activated, the vascular cells begin to express bone-forming genes. These genes should normally be activated only in bone cells, but because of hypoxic stress they are switched on in the vascular cells.
The vascular cells that have changed this way actively pull calcium in and promote calcification. The calcium that had been circulating in the blood begins to deposit on the vessel wall, and this leads to arteriosclerosis and vascular calcification. Paradoxically, to resolve hypoxia the blood flow must be smooth, but as the blood vessels calcify a vicious cycle arises in which the blood flow decreases even further.
The Representative Causes of Chronic Hypoxia
The causes that bring on chronic hypoxia in modern people are various.
1. Lack of Exercise
This is the most common cause. When sedentary living continues, cardiopulmonary function declines and the ability to supply oxygen to the peripheral tissues decreases. The average daily sitting time of modern people is quite long, and many people live without reaching the recommended amount of activity. This is the H-CR (circulatory hypoxia) trigger.
2. Sleep Apnea
As breathing repeatedly stops during sleep, the blood oxygen saturation drops, and when this repeats for several hours every night it becomes a chronic hypoxic state. Obesity, aging, anatomical structure, and the like are known as risk factors. This is the H-RS (respiratory hypoxia) trigger.
3. Chronic Stress
Cortisol, the stress hormone, constricts the peripheral blood vessels and reduces the blood flow going to the tissues.
4. Smoking
It directly interferes with hemoglobin's oxygen-carrying capacity and causes tissue hypoxia. This is the H-AN (anemic hypoxia) trigger.
5. Underlying Disease
Already advanced cardiovascular disease or chronic obstructive pulmonary disease is also a major cause of systemic hypoxia.
How the H (Hypoxia) Trigger Sets the D (Deficiency) Trigger in Motion
The mechanism by which the H (Hypoxia) trigger sets the D (Deficiency) trigger in motion is clear. In a hypoxic state, when the cells consume calcium excessively or lock it away inside the cell, the blood calcium concentration decreases. When blood calcium falls below the normal range, the calcium-sensing receptors of the parathyroid gland catch it at once and secrete PTH.
PTH activates the osteoclasts of the bone and makes them release calcium. But the calcium that emerges this way is again absorbed into the hypoxic tissue or locked away by the damaged cells. Blood calcium rises temporarily and soon falls, PTH keeps being secreted, and the bone keeps dissolving.
Even more serious is that the H (Hypoxia) trigger directly accelerates bone loss. According to research in the field of bone biology, in a hypoxic environment osteoclast activity tends to increase and osteoblast activity tends to decrease. That is, the making of bone decreases and the breaking down of bone increases.
The H (Hypoxia) trigger also affects vitamin D metabolism. The enzyme in the kidney that makes the active form of vitamin D requires oxygen, and in a hypoxic state the activity of this enzyme decreases. When vitamin D becomes deficient, calcium absorption in the intestine decreases, and a vicious cycle arises in which this again sets the D (Deficiency) trigger in motion.
The H trigger divides into three. The case where oxygen cannot get through because blood circulation fails (H-CR), the case where breathing itself fails because lung function declines or because of sleep apnea (H-RS), and the case where the blood cannot carry oxygen because of anemia (H-AN). If it is a circulation problem, the blood flow must be improved through exercise; if it is a breathing problem, treatment of sleep apnea is needed; and if it is anemia, iron supplementation is needed.
■ H (Hypoxia) Subclassification
| Code | Name | Core Mechanism |
|---|---|---|
| H-CR | Circulatory Hypoxia / Circulatory type | circulatory function of the heart, blood vessels, and muscles↓ → blood does not circulate - heart failure, vascular disease, lack of exercise (→ blood flow stagnation), thrombosis, dehydration/hemorrhage, etc. |
| H-RS | Respiratory Hypoxia / Respiratory type | oxygen supply capacity of the lungs and blood↓ - lung disease, anemia (oxygen transport↓), sleep apnea (inflammation↑+acid↑+oxygen↓), smoking, carbon monoxide, etc. |
| H-AN | Anemia-induced Hypoxia / Anemic hypoxia | decline in the blood's oxygen-carrying capacity - iron-deficiency anemia, anemia of chronic disease, vitamin B12/folate deficiency anemia, hemolytic anemia, chronic kidney disease anemia (EPO↓), etc. |
H (Hypoxia) is a low-perfusion, low-oxygen microenvironment; it is the final trigger point that ushers entry into the 7M mechanisms and at the same time the entry gate that amplifies I (Inflammation) through feedback. In particular, lack of exercise delivers a double blow: through D-PH (deficiency of physical stimulus) it cuts off the bone signal, and at the same time through H-CR (circulatory type) it brings the whole body's oxygen delivery to a halt.
H-AN (Anemia-induced Hypoxia / Anemic hypoxia): Anemia lowers the blood's oxygen-carrying capacity and induces tissue hypoxia. Iron-deficiency anemia, anemia of chronic disease, vitamin B12/folate deficiency anemia, chronic kidney disease anemia (EPO decrease), and the like fall under it.
Unlike H-CR (circulatory type: blocked blood vessels) and H-RS (respiratory type: declined lung function), it is a problem of the oxygen transport of 'the blood itself.' The chain pathway of D-NT (nutritional deficiency) → iron/B12 deficiency → H-AN (anemic hypoxia) is common.
The DIAH interpretation of hormonal imbalance: "hormone excess/deficiency" is not an independent fifth trigger. Hormone deficiency (estrogen, testosterone, growth hormone) is included in D, and PTH excess is classified as a compensatory response (mechanism) to D.
Cortisol excess (chronic stress) is an upstream cause that induces I, and hyperthyroidism is interpreted as the metabolic hyperactivity that induces A. In this way, every hormone-related pathology can be explained within the DIAH system.
※ This coding system is to be continuously verified and upgraded through future clinical research.
※ The primary/secondary/tertiary classification and coding system (19 items): a new proposal of the DIAH-7M Laboratory (clinical verification needed)
※ The trigger ↔ factor relationship: based on existing medical research (PMC/paper verification complete)
The Interaction of the DIAH Triggers: One Calls Another; All Roads Lead to the D (Deficiency) Trigger
So far we have examined the four DIAH triggers.
D (Deficiency): a decline in blood calcium concentration; I (Inflammation): chronic inflammation; A (Acidosis): the acidification of the body; H (Hypoxia): oxygen shortage. These four appear to work each independently, but when we look closely, in most cases there is a tendency to tilt in the direction where the D (Deficiency) trigger pathway works more often.
Of course, we cannot assert that this is necessarily so in every situation, but when it is repeated and accumulated, this tendency grows stronger.
The I (Inflammation) trigger consumes calcium in large amounts in the immune response and lowers blood calcium.
The A (Acidosis) trigger consumes calcium in the process of neutralizing acid and excretes it in the urine, decreasing blood calcium.
The H (Hypoxia) trigger has the cells absorb calcium excessively and lock it away, creating a shortage of blood calcium.
In the end, when I (Inflammation), A (Acidosis), and H (Hypoxia) work, blood calcium falls, and this pulls the D (Deficiency) trigger.
The D (Deficiency) trigger is, in effect, the final common pathway of the other triggers. This explains why stabilizing the D (Deficiency) trigger is the core strategy.
The Ring of the Vicious Cycle: The DIAH Triggers Amplify One Another
The larger problem is that these DIAH triggers do not work in only one direction. They form a ring of vicious cycle in which each amplifies the other.
1. I (Inflammation) → H (Hypoxia) → calcification → I (Inflammation)
When I (Inflammation) occurs, immune cells swarm to the inflamed area and oxygen consumption surges. It becomes locally hypoxic, and this sets the H (Hypoxia) trigger in motion.
In the hypoxic environment the vascular cells undergo a phenotypic switch and calcification begins. The calcified blood vessel obstructs blood flow and worsens the hypoxia even further.
And the calcification itself is recognized as a damage signal and induces new inflammation. It returns to the I (Inflammation) trigger again.
2. A (Acidosis) → I (Inflammation) → A (Acidosis)
An acidic environment itself induces inflammation. When the pH drops, the tissue is damaged, and this triggers an inflammatory response. When I (Inflammation) occurs, the inflammatory substances additionally generate acid in the metabolic process. As acidic metabolic products such as lactic acid and ketone bodies pile up, A (Acidosis) deepens even further.
3. H (Hypoxia) → A (Acidosis) → H (Hypoxia)
When oxygen is lacking, the cell switches to anaerobic metabolism.
In this process lactic acid is produced in large amounts and the tissue is acidified. In an A (Acidosis) environment, hemoglobin's oxygen-binding capacity decreases, the blood vessels constrict and blood flow decreases, and H (Hypoxia) worsens even further.
4. Bone Loss → Worsening of All DIAH Triggers
At the center of all these vicious cycles is bone loss. When the bone weakens, microfractures occur more frequently, and this induces I (Inflammation). As the bone dissolves, the capacity to neutralize acid decreases and A (Acidosis) deepens. When bone density falls, it can also affect bone marrow function. And all of this again creates a shortage of blood calcium and sets the D (Deficiency) trigger in motion.
The Time-Lag Attack: From Acute to Chronic
The reason these DIAH triggers are even more dangerous is that they work with a time lag. At first it appears that only one trigger is working, but as time passes the other triggers work in a chain.
For example, at first it can begin with a simple shortage of calcium intake, D (Deficiency). Calcium leaves the bone little by little and bone density slowly decreases. After several months or several years, microfractures begin to occur even from a small impact, and this induces I (Inflammation).
As chronic I (Inflammation) persists, the inflamed area becomes hypoxic, H (Hypoxia), and at the same time acid accumulates in the metabolic process of the inflammatory substances, A (Acidosis). Now all four DIAH triggers work and amplify one another.
The problem that was one at first expands into four problems as time passes, and a complex system in which each worsens the other is formed.
This is why chronic disease becomes harder to treat as time passes. In the early stage, managing only the D (Deficiency) trigger is effective, but in the late stage when all four are working, solving only one is of no use. This is because the complexly entangled ring of the vicious cycle must be cut simultaneously.
The Factors That Set the DIAH Triggers in Motion
So far we have examined the mechanism by which the four triggers D, I, A, and H draw calcium out of the bone. Then, on account of what do these triggers work?
The factors that set the DIAH triggers in motion divide, according to importance, into primary, secondary, and tertiary, as we examined in the previous chapter's DIAH Four-Gate Funnel theory.
The primary is the problem of mind and rhythm, the secondary is the problem of lifestyle, and the tertiary is acute events.
■ Matching Table of the Factors That Induce the DIAH Triggers
| Primary Factor | Main Trigger | DIAH Code | Mechanism Summary |
|---|---|---|---|
| Chronic stress | I (Inflammation) | I-ST | HPA axis overactivation → chronic cortisol elevation → osteoblast suppression + osteoclast prolongation + chronic inflammation |
| Anxiety | D (Deficiency) + I (Inflammation) | D-LF + I-ST | autonomic imbalance → cortisol elevation + reduced activity |
| Depression | D (Deficiency) + I (Inflammation) | D-LF + I-ST | serotonin decline + reduced activity + worsening eating habits + social withdrawal |
| Collapse of sleep rhythm | H (Hypoxia) + I (Inflammation) | H-RS + I-ST | growth hormone↓ + melatonin↓ + collapse of cortisol rhythm |
| Sleep apnea | H (Hypoxia) + I (Inflammation) | H-RS + I-ST | repeated nighttime hypoxia + sympathetic overactivity → oxidative stress + chronic inflammation |
| Social isolation | D (Deficiency) + I (Inflammation) | D-LF + I-AG | deficiency of life input + rise in inflammatory markers + immune decline |
| Trauma | I (Inflammation) | I-ST | chronic HPA axis overactivity → sustained cortisol elevation |
The primary factors are mental and rhythmic problems such as stress, depression, anxiety, and sleep disorders. They are not visible on the surface, but over a long period they set the triggers in motion.
Chronic stress sets I-ST (stress inflammation) in motion. When cortisol stays high, osteoblasts are suppressed and the lifespan of osteoclasts lengthens.
Anxiety and depression set D-LF (deficiency of life input) and I-ST in motion at the same time. Activity decreases and one does not see sunlight, and at the same time cortisol also rises.
Sleep apnea sets H-RS (respiratory hypoxia) and I-ST in motion at the same time. As the hypoxic state repeats every night, inflammation arises. When the primary collapses, the secondary collapses too. When one is depressed, there is no will to exercise, and when one cannot sleep, controlling food does not work.
| Domain | Secondary Factor | Main Trigger | DIAH Code | Mechanism Summary |
|---|---|---|---|---|
| Movement | Lack of exercise | D (Deficiency) + H (Hypoxia) | D-PH (deficiency of physical stimulus) + H-CR (circulatory hypoxia) | cessation of bone stimulus + reduced circulation (double blow) |
| Movement | Sedentary living | D (Deficiency) + H (Hypoxia) | D-PH + H-CR | dangerous when sitting even if one exercises |
| Diet | High-salt diet | D (Deficiency) | D-NT-2 (main) + A-DT-2 (conditional) | calcium excreted along with sodium excretion |
| Diet | High-sugar diet | I (Inflammation) | I-MT-2 (main) + A-FN-2 (conditional) | glucotoxicity + AGEs + metabolic inflammation |
| Diet | Ultra-processed foods | I (Inflammation) + D (Deficiency) | I-MT-2 (main) + D-NT-2 (sub) + A-FN-2 (conditional) | inflammation + phosphate + nutrient density↓ |
| Diet | Alcohol | A (Acidosis) + I (Inflammation) + D (Deficiency) | A-DT + I-MT + D-NT | acid metabolism + oxidative stress + reduced absorption |
| Respiration and rhythm | Smoking | H (Hypoxia) + I (Inflammation) | H-RS (respiratory hypoxia) + I-EN (environmental amplifier) | CO → oxygen transport↓ + chronic airway inflammation |
| Respiration and rhythm | Lack of sleep | H (Hypoxia) + I (Inflammation) | H-RS + I-ST (stress inflammation) | growth hormone↓ + collapse of cortisol rhythm |
The secondary factors are lifestyle habits such as lack of exercise, wrong eating habits, smoking, and drinking. They set the triggers in motion little by little every day.
Lack of exercise sets D-PH (deficiency of physical stimulus) and H-CR (circulatory hypoxia) in motion at the same time.
When one does not move, there is no stimulus to the bone so osteoclasts are activated, and because the muscles do not move, blood circulation also fails.
When one eats salty, calcium is lost in the urine (D-NT), and when one eats sweet, inflammation arises from the surge in blood sugar (I-MT). Alcohol sets three, I-MT, A-DT, and D-NT, in motion at the same time. Tobacco sets H-RS and I-EN in motion. The secondary is something one can choose oneself.
| Tertiary Factor | Main Trigger | DIAH Code | Mechanism Summary |
|---|---|---|---|
| Fall and fracture | D (Deficiency) + H (Hypoxia) | D-PH (deficiency of physical stimulus)-3 + H-CR (circulatory hypoxia)-3 | bedridden state → cessation of bone stimulus + reduced circulation |
| Acute infection | I (Inflammation) | I-AC (acute infection)-3 | inflammation explosion → mobilization of calcium for immunity + osteoclast activation |
| Surgery and hospitalization | D (Deficiency) + H (Hypoxia) + I (Inflammation) | D-PH-3 + H-CR-3 + I-CH (chronic infection)-3 | bed rest + reduced circulation + infection risk |
| Acute hemorrhage | H (Hypoxia) | H-CR-3 | reduced blood volume → tissue hypoxia |
| Traffic accident | D (Deficiency) + H (Hypoxia) | D-PH-3 + H-CR-3 | trauma + immobility + circulatory disturbance |
The tertiary factors are acute events such as falls, fractures, infections, and surgery. They occur suddenly and set the triggers in motion all at once.
Falls and fractures set D-PH and H-CR in motion acutely. When one lies down, there is no stimulus to the bone and blood circulation fails. Acute infection such as pneumonia strongly sets I-AC (acute infection) in motion.
The immune cells need calcium in large amounts, so osteoclasts are rapidly activated. Surgery and hospitalization set three, D-PH, H-CR, and I-CH, in motion at the same time. The tertiary cannot be avoided, but a person whose primary and secondary are well managed recovers quickly even when the same tertiary comes.