This piece is the complete Chapter 3 of Stones in the Body: More Frightening Than Cancer (Yoon Jong-won). The body, figures, and citations follow the manuscript as written.
The twentieth century handed humanity an astonishing gift. In only a hundred years the average lifespan grew by more than twenty years. When we consider that the global average lifespan was 31 years before 1900, an age in which people now live past their seventies and into their eighties is nothing short of a miracle. But behind this miraculous extension of life hides an uncomfortable truth we have kept turning away from.
According to the 2019 statistics of the World Health Organization (WHO), the global average life expectancy is about 73.3 years and the healthy life expectancy is 63.7 years, a gap of about 10 years. This means that we spend the last roughly 10 years of our lives together with disease. Taking together Statistics Korea's 2020 life tables and the WHO's healthy-life-expectancy estimates, the life expectancy of Koreans is about 83.5 years and the healthy life expectancy is roughly the early seventies, so here too a gap of around 10 years exists. We have extended our lifespan, but a considerable part of that added time is spent going back and forth between hospital waiting rooms and examination rooms.
This is precisely the reality of "long life with disease (yubyeong-jangsu)." We live in an age in which we live long but live in illness, an age in which life has been extended but the quality of life is not guaranteed. So why must we grow old this sick? Even though modern medicine has advanced so far, why can chronic disease not be stopped?
This book was written to answer exactly that question. And the answer was hidden in a place you never imagined, right inside your bones.
Fragmented Medicine, Treatment That Was Never Integrated
Modern medicine has achieved remarkable results. It conquered infectious disease with antibiotics, made even organ transplantation possible through advances in surgical technique, and, with imaging diagnostics, gained the ability to look deep inside the body. But despite all these advances, modern medicine has failed to overcome one fundamental limitation. It is the limitation of "Fragmented Medicine," which views the human body not as a whole but as separate parts.
If you have high blood pressure you are sent to the department of cardiovascular internal medicine, if you have diabetes to endocrinology, if a myocardial infarction occurs to cardiology, if your joints hurt to orthopedics, and if your memory declines to neurology. The doctors of each department do their best within their own field of expertise, but no one sees in an integrated way what is actually happening in the patient's body as a whole. Just like the blind men touching an elephant, each thinks that the part he touches is the whole.
According to research from Johns Hopkins and elsewhere in the United States, a considerable share of the elderly aged 65 and over have two or more chronic diseases at the same time, and a considerable share of these take five or more medications at once. Is it a coincidence that several diseases arise at the same time in a single body, or is there some common cause? Why does one person come to suffer from high blood pressure, diabetes, and arthritis all at once? Why, even after taking a fistful of pills and undergoing surgery, does the decline of the whole body not stop?
To find the answer to these questions, we need an integrated perspective that sees the whole system, moving beyond the view that regards diseases individually.
Major public-health institutions, including the Harvard T.H. Chan School of Public Health, point to lifestyle, metabolic abnormalities, and chronic inflammation as the core axes of chronic disease. These three are not independent of one another but are closely connected, and, above all, the most important point is that all of them are deeply related to our body's calcium metabolism, in particular to the efflux of calcium from the bones. Yet at the center of this calcium metabolism sits an organ we would never have expected. It is the bone.
The Hidden Link: Calcium That Escaped from the Bones
The core insight this book presents is somewhat unfamiliar but highly intuitive. As one of the common backgrounds shared by the major chronic diseases, it explains them by placing at the center the calcium that has escaped from our bones and the calcification that appears as its result. Blood-vessel walls hardened by arteriosclerosis, joints stiffened by arthritis, kidney stones and gallstones, calcification of the pancreas, calcium deposits in the cerebral blood vessels. What if the source of all of these were the very calcium that has escaped from our bones?
Bone is not merely a framework that holds up the body. Bone is a vast storehouse that holds about 99% of all the calcium in our body, and an emergency bank that immediately supplies calcium to the blood when life falls into crisis. In an adult human body there exists roughly 1 kg of calcium, and of this more than 99% is distributed in the bones and teeth, with only a few grams left in the blood and soft tissue. The calcium in the blood that is actually available for immediate use amounts to only about 0.5 g. This ratio alone shows how important a calcium reservoir the bone is.
According to skeletal-system research from the U.S. National Institutes of Health (NIH), functions essential to sustaining life, such as the heartbeat, nerve transmission, muscle contraction, and blood clotting, all depend on calcium signals. The blood calcium concentration must be precisely maintained within the very narrow range of 8.5 to 10.5 mg/dL, and going outside this range becomes a direct threat to life. If blood calcium is deficient, muscle spasms, arrhythmia, and even cardiac arrest can occur, while conversely, if it is excessive, nerve function can decline and the kidneys can be damaged.
So how does our body maintain this narrow range? It uses the bones. The moment blood calcium drops even slightly, the parathyroid glands secrete a hormone called PTH (parathyroid hormone) and pull calcium out of the bones. PTH also plays the positive roles of helping the kidneys reabsorb calcium and making the active form of vitamin D, but the problem arises when a chronically high-PTH state (secondary hyperparathyroidism) persists. This is just like breaking into a savings deposit when you do not have enough ready cash in your bank account. It is an unavoidable choice for putting out an urgent fire, but if it is repeated, the savings run dry.
The problem is that for modern people this "emergency withdrawal" situation has become not something temporary but an everyday event. Eating habits with insufficient calcium absorption, chronic stress, an acidified diet, and a low-oxygen state due to lack of exercise ceaselessly rob the bones of calcium. The calcium poured out this way piles up not in the bones but in the wrong places. Medically this is called "ectopic calcification," and the calcium that was meant to protect life instead turns into a poison that destroys life.
Clarke's 2008 study in the journal of the society of nephrology clearly proved that bone remodeling is not simply for structural maintenance but is a physiologically essential process for calcium homeostasis. Bone regulates the blood calcium concentration through the ceaseless process of breaking down old bone and making new bone, and in this process several hundred mg (roughly on the order of 300 to 500 mg) of calcium enters and leaves the bone each day. Under normal conditions this coming and going is balanced, but when the balance is broken, the calcium that has escaped from the bones begins to pile up in blood vessels and tissues.
The paradox of calcium deficiency: why do the bones weaken and the blood vessels clog even when you eat calcium?
Here we come face to face with one of the greatest mysteries of the medical world. It is the "Calcium Paradox." According to the 2020 National Health and Nutrition Survey of the Korean Nutrition Society, calcium ranks as the second most deficiently consumed nutrient among Koreans.
Many people diligently take calcium supplements and drink milk for the sake of bone health, yet their blood vessels harden as stiff as stone and osteoporosis occurs in which the bones become riddled with holes.
This refers to a state in which, when survival is threatened, the calcium of the bones flows into the blood like an "emergency medicine," and the "compensatory mechanism" that sacrifices the future assets of bone and blood vessel in order not to die right now operates excessively. As a result, when the calcium that has come out into the blood loses its place, the phenomenon appears in which it piles up on the blood-vessel walls or is deposited in soft tissue.
A paper by Shanahan and colleagues, published in 2011 in Circulation Research, uncovered the mechanism of vascular calcification seen in patients with chronic kidney disease.
The research team discovered that when vascular smooth-muscle cells are exposed to a low-oxygen or inflammatory environment, they change to behave like bone cells, attracting calcium and promoting calcification.
This is called "Phenotypic Switching," in which vascular cells take on the characteristics of bone cells for the sake of survival and, paradoxically, calcification accelerates.
A 2004 study by Schiavi and Kumar in the international journal of nephrology, while clarifying the phosphatonin pathway that regulates the homeostasis of phosphate and calcium, revealed that calcium metabolism is not simply a matter of intake and excretion but a sophisticated system regulated by a complex hormonal network.
When this system is disrupted, it means that a paradoxical situation arises in which, no matter how much calcium you eat, the bones weaken and the blood vessels clog.
However, this research develops one vulnerability when it is conveyed to the public. It is easy for the conclusion to be simplified into something like "hormones are complicated, so eating calcium is useless," and when this happens the "regulatory mechanism" the research described is mistaken for the "root cause" and the logic is turned upside down.
The core point we must sort out is not that calcium is unnecessary, but that if the form of calcium the body can actually use is not sufficiently secured, this sophisticated regulatory system can, on the contrary, tilt into emergency mode.
That is, even when intake appears sufficient, if dissolution and dissociation (solubilization) and the absorption process in the gastrointestinal tract do not proceed smoothly, so that the available calcium the body can actually use in the blood, especially ionized calcium, becomes deficient, the body perceives this as a deficiency, raises PTH, and can strengthen the compensatory response of mobilizing calcium from the bones.
If conditions such as chronic inflammation, declining kidney function, and hormonal disruption are added on top of this, this compensatory response can be triggered more easily or persist longer, and as a result the likelihood grows that the paradox appears in which "the bones weaken while the risk of deposition in blood vessels and soft tissue increases." Therefore the real warning this research gives is not "avoid calcium" but that we should not draw conclusions from intake alone, and must look together at absorption, availability, and the conditions of regulation.
The Integration of Validated Knowledge: Not Something New, but Things We Failed to Connect
The perspective this book presents is not at all a wholly new discovery. Rather, it is the work of connecting into one the physiological facts already validated through countless papers and studies. It does not deny or ignore the vast knowledge modern medicine has accumulated; it realigns that knowledge into a single systematic chart.
Endocrinology long ago revealed that PTH and vitamin D precisely regulate bone and blood calcium. Immunology and bone-metabolism research have repeatedly reported that the inflammatory cytokines IL-1 (interleukin-1), IL-6 (interleukin-6), and TNF-alpha (tumor necrosis factor alpha) activate osteoclasts and dissolve bone.
Research in the fields of kidney and metabolism proved that in a state of metabolic acidosis the bone plays the role of a buffer neutralizing hydrogen ions, and in that process releases calcium and phosphorus. Cardiovascular research presented experimental data showing that a low-oxygen environment promotes the calcification of vascular endothelial cells.
The problem is that all of this knowledge is scattered across different journals, in the laboratories of different clinical departments, and in different textbooks. The endocrinologist studies PTH, the rheumatologist studies inflammatory cytokines, the nephrologist studies acidosis, and the cardiologist studies vascular calcification. But in the patient's body, all of this is happening at the same time.
This book is the work of assembling these scattered puzzle pieces into a single picture. At the center of that picture there is just one question. "Why does the situation in which calcium must escape from the bones keep repeating?" To answer this question we have identified four core triggers.
1. D (Deficiency): deficiency of calcium, minerals, vitamin D, and so on 2. I (Inflammation): the chronic inflammatory response 3. A (Acidosis): acidification within the body 4. H (Hypoxia): a low-oxygen state
| Abbreviation | English | Korean | Action | Explanation |
|---|---|---|---|---|
| D | Deficiency | Deficiency | Bone calcium makes up the shortfall | Deficiency of calcium, minerals, vitamin D, and so on → replenished by breaking down calcium from the bones → blood → supplied to various cells. Note in common: D, I, A, and H all cause a drop in blood calcium, which is replenished by breaking down calcium from the bones. |
| I | Inflammation | Inflammation | Calcium is mobilized to quell inflammation | Large amounts of calcium consumed in the inflammatory response → replenished by breaking down calcium from the bones → blood → concentrated at the site of inflammation |
| A | Acidosis | Acidosis | The bone is sacrificed to neutralize acid | Alkaline calcium used to neutralize acid → replenished by breaking down calcium from the bones → blood → whole-body pH balance |
| H | Hypoxia | Hypoxia | Under oxygen shortage, calcium floods excessively into the cells | Cellular oxygen shortage → calcium-pump failure → blood calcium over-absorbed into cells → deficiency of blood calcium → replenished by breaking down calcium from the bones → blood → reabsorbed by the damaged cells → vicious cycle |
The systematization of how these interact to rob the bones of calcium is precisely the DIAH trigger system.
The Hope This Book Offers: From Long Life With Disease to Long Life Without Disease
If, in the common background of the major chronic diseases, there is calcium that has escaped from the bones, and if the reason calcium escapes from the bones can be explained by the DIAH triggers (deficiency, inflammation, acidosis, hypoxia), then we can at last build a fundamental strategy for preventing chronic disease. Beyond merely treating disease, true prevention becomes possible in which disease does not arise in the first place.
This is a revolutionary change that shifts the paradigm of medicine from "treating symptoms after disease onset" to "adjusting causes before disease onset." Not lowering blood pressure with hypertension medication, but keeping vascular calcification from ever starting. Not controlling blood sugar with diabetes medication, but preventing calcium deposits around the pancreatic beta cells. Not suppressing pain with arthritis painkillers, but blocking the microfractures around the joints and the vicious cycle of inflammation.
Through this book we intend to present a concrete roadmap that can turn the ten years after age 70 from a time of suffering in a sickbed into a blessed time in which you walk on your own two feet, think clearly, and are together with your family. To end the age of "long life with disease" in which one lives long but sick, and to open the age of "long life without disease" in which one lives long in health, is precisely the ultimate goal of this book.
Conclusion
For thousands of years humanity has accepted growing old in sickness as an unavoidable fate. Modern medicine succeeded in slowing disease and extending life, but it failed to fundamentally block chronic disease. Arthritis, diabetes, heart disease, cancer, and dementia still torment us.
But now we have come to know that these diseases do not arise at random but originate from a common root. That root is the very calcium that has escaped from our own bones. The calcium mobilized as an emergency measure to protect life has, as time passes, changed from medicine into poison and has been slowly destroying our bodies.
This book clearly reveals that process on the basis of scientific evidence, and presents concrete methods for how we can break this chain of vicious cycles. It will end the age of long life with disease and open a new age of long life without disease.
References
1. World Health Organization. (2019). World Health Statistics 2019: Monitoring health for the SDGs. https://www.who.int/publications/i/item/9789241565707
2. Statistics Korea. (2020). 2020 Life Tables for Korea. Korean Statistical Information Service.
3. Clarke, B. (2008). Normal bone anatomy and physiology. Clinical Journal of the American Society of Nephrology, 3(Supplement 3), S131-S139. https://doi.org/10.2215/CJN.04151206
4. National Institutes of Health, Office of Dietary Supplements. (2021). Calcium: Fact Sheet for Health Professionals. https://ods.od.nih.gov/factsheets/Calcium-HealthProfessional/
5. Korean Nutrition Society. (2020). Dietary Reference Intakes for Koreans 2020. Ministry of Health and Welfare.
6. Shanahan, C. M., et al. (2011). Arterial calcification in chronic kidney disease: key roles for calcium and phosphate. Circulation Research, 109(6), 697-711. https://doi.org/10.1161/CIRCRESAHA.110.234914
7. Schiavi, S. C., & Kumar, R. (2004). The phosphatonin pathway: new insights in phosphate homeostasis. Kidney International, 65(1), 1-14. https://doi.org/10.1111/j.1523-1755.2004.00355.x
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9. Franceschi C, Campisi J. Chronic inflammation (inflammaging) and its potential contribution to age-associated diseases. J Gerontol A Biol Sci Med Sci. 2014;69 Suppl 1:S4-9. doi:10.1093/gerona/glu057. https://pubmed.ncbi.nlm.nih.gov/24833586/