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LibraryAug 30, 202636 min readViews 18

How Bone Calcium Efflux Begins (4)

The moment the bone gives up calcium at a crisis signal

D
DTDMC Lab
DTDMC Institute
This piece is the middle part 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.

What Makes the DIAH Classification Different

Conventional medicine and health information often stop at dividing the causes of disease into large categories such as genetics, environment, lifestyle, aging, infection, and stress.

This approach is similar to showing a map of the forest while not giving detailed guidance on which path one enters and where one gets blocked. Even when there is a classification, the pathway is weak, and in the end, in practice, it tends to remain as nice words.

By contrast, in the DIAH four-gate funnel theory, the purpose of classifying factors is not a pretty list but capturing the order in which the triggers actually turn on and the way they combine.

Its heart is the structure in which the four gates D·I·A·H converge into the common gateway of bone calcium efflux. Even the same stress does not simply end as a psychological factor but is coded as I-ST and connected all the way to how it loosens the brake on bone metabolism. The same eating habits, too, are not translated as "bad" but as which combination of I-MT and D-NT turns on and how it shakes the consumption, distribution, and availability of calcium.

The second difference is that, if conventional classification is strong at attaching the name of the cause, DIAH is strong at attaching the level of the cause. The reason for dividing into 1st order (mind and rhythm), 2nd order (lifestyle), and 3rd order (acute event) is not a simple order of importance. It is a device for finding where the engine of the trigger is continuously running.

The 1st order is close to the base power source that, though hard to see, turns on the trigger over a long period; the 2nd order is the fuel supply line that accumulates every day; and the 3rd order is the shockwave that suddenly shakes the system one day. Even for the same disease, the main code and the sub code differ depending on what the beginning was, and that difference in turn determines the priority of the management strategy.

So whereas conventional classification tends to end with a list, as in the causes of hypertension are stress, salty food, obesity, and genetics, DIAH captures the flow of time and the rules of combination, as in I-ST-1 turned on first, then D-PH-2 followed, and here A-FN or H-CR accompanied it so that the vicious cycle hardened. The classification of causes becomes a map of the pathway.

Finally, the greatest difference is that the DIAH funnel theory, while not denying the conventional multifactorial model, compresses that complexity into 4 operating buttons and 19 sub codes and turns it into a reproducible judgment system.

In conventional classification, because the factors look too different for each patient, the explanation grows long, the consultation grows long, and the conclusion tends to scatter into "let us try everything." DIAH sets up the view that any factor, in the end, must turn on one or more of D·I·A·H to roll toward disease, and by leaving that turning-on as a code it lets us see the accumulation and the pattern.

We can track the same person's health problems over time, and we can relatively quickly grasp which switch must be turned off first in my body right now.

In summary, DIAH is not a theory competing with the existing one but a navigation-type classification that reconstructs the conventional listing of causes into trigger-code-order-complex combination and directly connects the classification of disease factors to pathway analysis and priority determination. Below we look at the concrete codes and judgment procedure of this classification system.

Summary of the DIAH Codes

So far we have looked at the sub codes of each trigger D, I, A, and H. We summarize all 19 codes at a glance and explain the principle of complex coding and the judgment procedure.

■ Final Classification Table of Codes (19)

TriggerNumber of CodesCode List
D (Deficiency)5D-PH (physical stimulus), D-NT (nutrient), D-LF (lifestyle input), D-MD (medication-induced), D-OT (other)
I (Inflammation)7I-EN (environmental), I-MT (metabolic), I-CH (chronic infection), I-AC (acute infection), I-AG (aging), I-ST (stress-induced), I-OT (other)
A (Acidosis)4A-FN (functional), A-DT (dietary), A-RS (respiratory), A-OT (other)
H (Hypoxia)3H-CR (circulatory), H-RS (respiratory), H-OT (other)

This is the full list of a total of 19 sub codes under the 4 DIAH triggers. It consists of 5 for D (Deficiency), 7 for I (Inflammation), 4 for A (Acidosis), and 3 for H (Hypoxia).

Each DIAH trigger is subdivided into sub types as below, and through this the concrete causes of chronic disease can be tracked.

■ Rules for Using the Other (OT) Code

NoContent
1If it does not match an existing code by 50% or more, use OT
2When using OT, a note of the specific factor is required (e.g., I-OT autoimmune)
3When the same factor accumulates 5 or more OT entries → review for a new code
4Review the reclassification of OT items once a year

The OT (other) code is a "temporary storage box" for factors that do not clearly fit the existing classification. It is a management principle that prevents indiscriminate use and, when it accumulates beyond a certain standard, promotes it to a new official code.

■ Code Notation and the Principle of Complex Coding

ItemContent
Format[trigger]-[sub code]-[order] (e.g., I-MT-2 = metabolic inflammation, 2nd order)
Complex exampleI-MT-2 (main) + D-PH-2 (sub) + A-RS-1 (sub)
Main codepreceding trigger = the trigger that operated earlier in time
Sub codeaccompanying trigger = the trigger activated afterward (up to 3 recommended)

This is used when several triggers are involved in one disease. The criteria for selecting the main code are two-track. (1) If the preceding trigger is clear, time takes priority; (2) if it is unclear, the trigger with greater intensity and duration is designated as the main code. The triggers chained afterward are marked as "sub codes." Example: the case that begins with stress (I-ST) and is worsened by lack of exercise (D-PH). I-ST-1 (main) + D-PH-2 (sub)

■ Criteria for Judging the Order of a Factor

OrderJudgment QuestionApplicable Examples
1st orderIs a problem of mind/stress/rhythm the root cause?chronic stress, depression, anxiety, collapse of sleep rhythm, trauma
2nd orderIs it the result of lifestyle accumulated every day?lack of exercise, overeating, unbalanced eating, smoking, drinking, sedentary living
3rd orderIs an acute event/trauma/medical intervention the cause?traffic accident, fall, surgery, acute infection, drug side effect

Even for the same trigger, the order differs depending on "where it began." If a problem of the mind is the root, it is 1st order; if it is the accumulation of lifestyle, it is 2nd order; and if it is a sudden event, it is 3rd order. The judgment of order becomes an important clue in establishing a treatment strategy.

■ Procedure for Judging DIAH Trigger Codes (6 Steps)

StepQuestion and JudgmentCode (English)Name
Step 1Confirm the main symptom/disease: what is the patient's chief complaint and diagnosis?-e.g., hypertension, diabetes, osteoporosis, depression
Step 2Judge the preceding DIAH trigger: which of D, I, A, H operated first?D, I, A, HDeficiency, Inflammation, Acidosis, Hypoxia
Step 3Trace the cause of the trigger: what is the specific cause by which that trigger arose?-e.g., lack of exercise, eating habits, stress, infection
Step 4Judge the order: which level does the cause belong to?1st, 2nd, 3rd1st order (root), 2nd order (habit), 3rd order (acute)
Step 5Select the sub code: choose the code matching the trigger + cause typeD-PH, I-MT, A-DT, H-CR, etc.physical stimulus, metabolic, dietary, circulatory, etc., 19 in all
Step 6Complex coding: when multiple triggers exist, mark main code + sub codee.g., I-MT-2 + D-PH-2metabolic inflammation (main) + physical stimulus deficiency (sub)

This is the standard procedure that starts from the patient's symptoms and assigns codes step by step. It traces the cause through the flow of "what hurts, why it hurts, and since when it has hurt."

■ Trigger × Order Matrix (●=main, ○=possibly applicable)

TriggerCode (English)Name1st2nd3rd
DD-PHPhysical Stimulus Deficiency●○
D-NTNutrient Deficiency●○
D-LFLifestyle Input Deficiency●●
D-MDMedication-induced Deficiency○●
D-OTOther Deficiency○○○
II-ENEnvironmental Amplifier●○
I-MTMetabolic Inflammation●
I-CHChronic Infection●
I-ACAcute Infection●
I-AGAge-related Inflammation●
I-STStress-induced Inflammation●
I-OTOther Inflammation○○○
AA-FNFunctional Acidosis○●
A-DTDietary Acid Load●
A-RSRespiratory Acidosis○●○
A-OTOther Acidosis○○○
HH-CRCirculatory Hypoxia●○
H-RSRespiratory Hypoxia○●○
H-OTOther Hypoxia○○○

This shows at a glance in which order the 19 sub codes mainly operate. ● is the representative order of that code, and ○ is an order that may apply depending on the situation. Example: I-ST (stress-induced inflammation) mainly begins in the 1st order (root).

■ Explanation of Newly Added Codes

CodeNameExplanation
I-ACAcute InfectionInflammation due to acute infection such as pneumonia, sepsis, and acute inflammation. Corresponds to the 3rd order (acute) trigger
D-OT, I-OT A-OT, H-OTOtherUnclassified factors that do not match an existing code by 50% or more. For securing classification completeness (MECE)

This is an explanation of the 5 codes (I-AC, D-OT, I-OT, A-OT, H-OT) added to the existing 14 codes. I-AC is a code for acute infection, and the OT codes are "other" codes for unclassified factors.

■ Explanation of Newly Added Codes

CodeApplication Condition
H-RSApplied when a decrease in SpO₂ is confirmed or sleep apnea is diagnosed
A-DTApplied when processed food, phosphate, and additives are consumed together
A-FNApplied when signs of metabolic stress (lactate↑, pH↓, etc.) are confirmed

A conditional code is added as a sub code only when the relevant condition is met. When the condition is not met, it is omitted to prevent over-coding.

What is interesting is that the I (Inflammation), A (Acidosis), and H (Hypoxia) triggers, too, in the end lower the blood calcium concentration or cause calcium to be consumed excessively, thereby operating the D (Deficiency) trigger. That is, although we cannot conclude that all roads always converge in the same way, when I (Inflammation), A (Acidosis), and H (Hypoxia) repeat, the "consumption, distribution, and ionization (availability)" of calcium is shaken, and the moment that shaking exceeds a certain threshold, it tends to tilt toward the direction in which the D (Deficiency) pathway, that is, the PTH-bone mobilization system, turns on more often. And these four DIAH triggers are not independent of one another but form a vicious cycle and amplify each other.

The DIAH trigger concept is a framework for understanding chronic disease in an integrated way centered on calcium metabolism. Each trigger is based on a scientifically established physiological mechanism. However, since chronic disease is a multifactorial disease in which various factors such as genetics, environment, lifestyle, and aging act in combination, DIAH should be understood as an integrated framework from the perspective of calcium metabolism among the several risk factors.

.

[ Scientific Basis References for the DIAH Triggers / DIAH Trigger References ]

1. Deficiency / Deficiency (D)

1-1. StatPearls (NCBI NBK499940): PTH is secreted within seconds when blood calcium falls, stimulating osteoclasts to induce bone resorption / PTH is secreted within seconds of low serum calcium detection, stimulating osteoclasts for bone resorption 1-2. Cold Spring Harb Perspect Med (PMC6071549): During calcium deficiency, PTH promotes perilacunar remodeling of osteocytes to rapidly mobilize calcium from bone / PTH rapidly liberates skeletal calcium stores during calcium deficiency via osteocyte perilacunar remodeling

2. Inflammation / Inflammation (I)

2-1. Immune Netw (PMC5833125): Proinflammatory cytokines such as TNF-α, IL-1β, IL-6, and IL-17 induce RANKL expression, promoting osteoclast differentiation and bone resorption / Proinflammatory cytokines induce RANKL expression, promoting osteoclast differentiation and bone resorption 2-2. J Clin Invest (PMID:16294221): TNF-α stimulates M-CSF expression in stromal cells, and M-CSF induces RANK expression in osteoclast precursors, promoting inflammatory osteolysis / TNF-α stimulates M-CSF expression in stromal cells; M-CSF induces RANK in osteoclast precursors, mediating inflammatory osteolysis

3. Acidosis / Acidosis (A)

3-1. Kidney Int (PMID:15199293): During metabolic acidosis the bone acts as a pH buffer; acid promotes PGE2 and RANKL expression, activating osteoclasts / Bone buffers systemic pH during metabolic acidosis; acid stimulates PGE2 and RANKL, activating osteoclasts 3-2. Curr Opin Nephrol Hypertens (PMC9133222): Acidosis induces physicochemical calcium release in the short term and cell-mediated bone resorption in the long term / Acidosis induces acute physicochemical calcium release and chronic cell-mediated bone resorption

4. Hypoxia / Hypoxia (H)

4-1. J Cardiovasc Pharmacol (PMID:1618920): Upon 2 hours of hypoxia exposure, ATP decreases by 43%, and energy deficiency raises the intracellular calcium concentration / 2h hypoxia causes 43% ATP decrease; energy deficiency leads to increased intracellular calcium 4-2. Aging Dis (PMC6147588, 2018): During ischemia, ATP depletion induces ion pump failure, membrane depolarization, and calcium overload; mitochondrial dysfunction → cell death / Ischemia-induced ATP depletion triggers ion pump failure, membrane depolarization, calcium overload; mitochondrial dysfunction leads to cell death

5. Physical Stimulus Deficiency / Physical Stimulus Deficiency (D-PH)

5-1. J Bone Miner Res (PMID:15125798, Lang 2004): In long-duration spaceflight (microgravity), regional BMD decreases on a monthly basis; significant loss of bone density in the hip and spine / Long-duration spaceflight (microgravity) causes significant monthly BMD loss at hip and spine 5-2. Br J Sports Med (PMID:33597120, Gabel 2022): After spaceflight, tibia bone strength/density decreases by 2.9-4.3%; bone loss is proportional to flight duration / Spaceflight causes 2.9-4.3% tibia bone strength/density loss; mission duration predicts bone loss 5-3. J Musculoskelet Neuronal Interact (PMID:15758512, LeBlanc 2000): After 4-14 months of flight on Mir, loss of bone density in the lumbar spine/hip and of muscle mass / Mir 4-14 month flights cause lumbar/hip BMD and lean tissue loss

6. Aging Inflammation / Inflammaging (I-AG)

6-1. J Gerontol A (PMID:24833586, Franceschi 2014): Inflammaging is the chronic low-grade inflammation of aging; a major risk factor for morbidity and mortality in the elderly / Inflammaging is chronic low-grade inflammation of aging; major risk factor for morbidity and mortality in elderly 6-2. Nat Rev Endocrinol (PMID:30046148, Franceschi 2018): Inflammaging contributes to the pathophysiology of age-related disease; the gut microbiota-metaflammation connection / Inflammaging contributes to age-related disease pathogenesis; gut microbiota-metaflammation connection

7. Trigger Cascade / Trigger Cascade

7-1. N Engl J Med (PMID:21323543): The bidirectional link between hypoxia and inflammation; tissue hypoxia induces inflammation, and inflammation induces hypoxia / Bidirectional link between hypoxia and inflammation; tissue hypoxia causes inflammation and vice versa 7-2. PMC3139040 (World J Cardiol): During ischemia-reperfusion, Ca²⁺ overload and ROS induce mPTP opening; cell death through mitochondrial dysfunction / I/R causes Ca²⁺ overload and ROS, triggering mPTP opening, mitochondrial dysfunction and cell death

Conclusion

We have now looked at the common mechanism of chronic disease from the DIAH-7M perspective.

The heart of it is that calcium that has escaped from the bones can contribute to the onset and progression of various diseases. When the four survival triggers, DIAH, are pulled, the bone opens the emergency vault and pours out calcium. D (Deficiency): a drop in blood calcium concentration, I (Inflammation): chronic inflammation, A (Acidosis): acidification of the body, H (Hypoxia): a shortage of oxygen. These four each look independent, but all of them in the end converge into one final common pathway. It is to lower blood calcium, operate PTH, and dissolve the bone.

What is more of a problem is that these DIAH triggers do not operate once and end but form a vicious cycle loop that amplifies each other. I (Inflammation) makes H (Hypoxia), H (Hypoxia) gives rise to A (Acidosis), and A (Acidosis) in turn induces I (Inflammation). And at the center of all these processes the bone keeps melting away.

The calcium that has escaped from the bones meets two fates. One is that through microfractures it is liberated as crystals and becomes the raw material of the I (Inflammation) vicious cycle, and the other is that it circulates through the blood and piles up as calcification in blood vessels and tissues, destroying organs. It is the tragedy in which the medicine mobilized as an emergency to save life turns, as time passes, into a poison that destroys life.

But this discovery is at the same time a great hope. Because knowing the common mechanism of the problem means that we can now attempt a more integrated approach. If we can understand and regulate the four DIAH triggers, we can reduce the excessive escape of calcium from the bones. In particular, stabilizing the D (Deficiency) trigger, into which all the triggers converge, that is, the blood calcium concentration, is one of the core strategies.

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