The patient we will discuss today, like the prostate cancer patient presented in Lecture 130, was a case of multiple bone metastases and was classified as a Soeumin (Lesser Yin type) according to Sasang constitutional medicine.

At the end of Lecture 130, I presented my own perspective regarding constitutional classification of conventional pharmaceuticals. As an example of treatment based on this viewpoint, this patient had previously failed standard therapy with bicalutamide and Lupron (leuprolide). By the time he came to see me, his systemic skeletal metastases were devastatingly extensive, and the hospital had predicted that he had less than two weeks to live.

At that time, he was already 80 years old, and had been receiving treatment for three years at Seoul National University Bundang Hospital.

Despite using six doses of morphine per day, his pain remained uncontrolled. His entire spine was extensively infiltrated by metastatic cancer and had structurally collapsed, resulting in severe skeletal instability. When he came to my clinic, he arrived in a wheelchair, unable to raise either his back or even his head due to extreme pain and spinal compromise.

Although he had undergone three years of treatment at a tertiary university hospital, including radiation therapy and hormonal therapy, the disease had progressed relentlessly, with widespread skeletal metastases throughout the body, to the extent that the entire spinal column was nearly collapsing under the burden of metastatic involvement.

He had previously served as the chairman of a well-known pharmaceutical company recognized by virtually everyone. Believing that he was approaching the end of his life, he had written the beginning of his memoir before coming to see me.

In the opening of that memoir, he wrote words to the effect of: “Thanks to Western medicine, my life was extended by three additional years. Now, as further treatment is no longer possible, I am writing these final reflections while putting my affairs in order.”

It was after writing those words that he came to visit me.

After adjusting his conventional medications according to constitutional principles, his PSA level declined dramatically from 2,420 to 6.5 within one year. He was eventually able to rise from the wheelchair and walk independently with the assistance of a cane.

Furthermore, the severe pain that had remained uncontrolled even with high-dose morphine was brought under control with herbal treatment combined with analgesic medications selected according to his Soeumin constitutional profile.

He went on to live for four more years, eventually passing away from pneumonia rather than progression of his prostate cancer.

One unfortunate limitation of this case was the lack of complete medical documentation. Because he was an elderly patient who came alone, he was unable to bring most of his medical records, leaving me with only one or two interim records from which to reconstruct and write about the case.

Given his advanced age, it was also difficult for me to press him repeatedly for additional documentation. Nevertheless, for those four subsequent years, until his death from pneumonia, he was able to live a normal daily life without major complications.

In fact, the cane he had initially depended on was eventually discarded, and he later came to my clinic walking independently without assistance.

Even during the episode of pneumonia, I advised him to visit a physician with whom I collaborated for co-management, but because the situation became urgent, he was admitted instead to the hospital he had already been attending.

There are also constitutional differences, in my view, in how patients respond to antibiotics and antipyretic medications. In elderly patients especially, if antimicrobial agents or fever-reducing medications are not appropriately matched to the patient’s physiological condition, even otherwise survivable illnesses can become fatal.

For example, medications such as acetaminophen, which I regard within my constitutional framework as being more suitable for Yang-type constitutions, may temporarily reduce fever but could potentially create difficulties in physically weaker Yin-type patients.

Therefore, I interpret this patient’s cause of death not as tumor progression, but rather as death secondary to pneumonia. Although he did not consistently bring detailed medical records during follow-up visits, he repeatedly reported that he remained stable, felt well, and had experienced no major clinical deterioration over the years.

After this patient regained the ability to stand and walk with a cane, I received a letter from a hematology-oncology physician at Seoul National University Bundang Hospital, expressing curiosity about what treatment had been used to produce such a clinical improvement.

My interpretations are based on personal clinical experience, and I do not claim that the theoretical framework always aligns perfectly in every case. However, through the clinical materials I have encountered, I have reviewed patient records and selected medications from the perspective of constitutional medicine.

The framework through which I interpret these constitutional characteristics is not merely an ad hoc clinical hypothesis, but one rooted in the broader intellectual system of Sasang constitutional medicine, itself grounded in the East Asian philosophical traditions of Yin-Yang theory, the Five Elements, and classical systems of categorization derived from the I Ching (Book of Changes).

Some may naturally wonder how such classifications are made. However, a full explanation would require substantial familiarity with the foundational principles of traditional East Asian thought, making it difficult to address in detail within the scope of this discussion.

Nevertheless, through this case—in which a patient who had been given an estimated two weeks to live survived for more than four additional years and returned to largely normal daily functioning—I believe we are invited to consider the depth and practical implications of these traditional medical frameworks.

At the same time, I would offer an important caution. In modern public discourse, many heterogeneous and poorly substantiated practices are often grouped indiscriminately under the broad label of “traditional medicine.” As a result, ineffective or unscientific interventions are sometimes judged as representative of the entire field. I would encourage readers to approach such matters with discernment and to distinguish carefully between rigorously developed medical systems and unsupported therapeutic claims.

This is the bone scan record from one year before the patient came to see me.

Whole Body Bone Scan (2003-12-30)

​Findings:
Multiple foci of increased radiotracer uptake are noted throughout the axial skeleton, involving the sternum, multiple ribs, thoracic spine, and pelvic bones.
Additional abnormal focal uptake is seen in both shoulder regions.

These findings are consistent with multiple osseous metastatic lesions.

Impression:
Multiple abnormal areas of increased radiotracer uptake throughout the axial skeleton. Findings are compatible with widespread skeletal metastases from prostate carcinoma.

Findings from Dec 30, 2003:

Observations: Multiple areas of increased radiopharmaceutical uptake (hot spots) are noted in the sternum, bilateral ribs, spine, pelvis, and both shoulders.
Assessment: This pattern is highly suggestive of multifocal metastatic bone disease, indicating that the primary cancer has spread to various parts of the skeletal system.

Findings from Aug 31, 2004:
Observations: In the follow-up scan approximately 8 months later, the previously identified lesions have increased in size and intensity. There is more widespread involvement throughout the axial and appendicular skeleton.

Note: The intensity of the bone uptake is so high that the renal (kidney) excretion is less visible, a phenomenon often referred to as a “Superscan” pattern, which occurs in extensive metastatic disease.

Comparative Summary:
Conclusion: Compared to the December 2003 scan, the August 2004 scan shows significant disease progression. There is an increase in both the number and the metabolic activity of the metastatic bone lesions.

​

Difference in Signal Intensity Yellow-bordered area: In MRI (especially T1 or T2-weighted images), the inside of the bone (bone marrow) of a healthy adult appears relatively bright (white) due to fatty components. The cervical vertebrae marked with circles maintain a relatively uniform and bright signal compared to the surroundings, indicating a relatively normal bone marrow state. Other dark areas:

The other vertebrae above and below the yellow circles show very low signal levels and have turned dark (black). This is a typical finding of metastatic bone tumors that occurs when normal fatty bone marrow, which should originally be present, is replaced (infiltrated) by cancer cells. 2. Consistency with Previous Bone Scan Results Multiple black dots (hotspots) were observed throughout the spine in the bone scan images from December 2003 and August 2004 that you viewed earlier. Since this MRI image was taken in the middle of that period (April), it demonstrates that the metabolic abnormalities observed in the bone scans have actually anatomically invaded most of the vertebrae. It appears that only the bone within the yellow circle fortunately avoided metastasis or is in a less advanced state.

In conclusion, the description that “only the area within the yellow border is normal, while the rest has been invaded by the tumor” is highly consistent with the imaging findings. While the overall structure of the spine appears to be preserved, the qualitative condition of the bone indicates that extensive metastasis has already occurred.

As mentioned earlier, the patient came to see me because they were told they had only two weeks left due to uncontrollable pain; at that time, they were taking medications that were incompatible with their constitution, including tamsulosin and alpha-adrenergic antagonists. Since these are medications for the Soyang constitution, I removed them and, at the doctor’s request, administered Proscar-finasteride, a drug primarily used for benign prostatic hyperplasia, along with the herbal medicine B0054.

As the patient’s condition improved, the attending physician sent me a letter through the patient, expressing interest in the treatment approach that had led to his recovery.

Dear Doctor,

After receiving the prescribed medications from your clinic, the patient’s prostate cancer marker (PSA) appears to be showing an improving trend with progressive decline.
May I ask if it would be possible to know the names of the medications currently being prescribed?

Sincerely,
Bundang Seoul National University Hospital

At the time, I wrote and sent my own views on the constitutional classification used in Western medicine. I believe that if Western and Korean medicine cooperate to complement each other’s shortcomings during treatment, it will yield very good results. I was very glad to receive the letter from the open-minded teacher.

Many hospitals strictly prohibit herbal medicine, treating it almost like a poison that should never be taken. Patients have told me that notices to this effect are posted in many hospital bulletin boards. However, I believe it is not appropriate to dismiss the achievements of our ancestors, developed over thousands of years, simply because they are not yet fully explainable within the Western scientific framework.

One regret I have is that, due to the patient’s advanced age, prescriptions had to be managed over the phone, and he didn’t bring the necessary data, so I wasn’t able to conduct a final analysis based on his records. Yet, one of the shortcomings I observe in Western medicine is its lack of retrospective reflection.

Eastern civilization has preserved an extraordinary continuity of written tradition. Until the simplification of Chinese characters in the modern era, the classical written forms remained remarkably connected to texts written thousands of years earlier. In many respects, this reflects a defining characteristic of East Asian culture: a civilizational habit of preserving records, reflecting on history, learning from past experience, and seeking new paths through accumulated wisdom.

Medicine, though distinct from political or cultural history, is likewise a noble record of humanity’s effort to relieve suffering, preserve life, and help individuals pursue a more meaningful and comfortable existence.

Western medicine has undoubtedly developed highly sophisticated systems of documentation, analysis, and evidence generation through enormous financial investment and scientific effort. Yet, in my view, one area that remains comparatively underdeveloped is the retrospective philosophical interpretation of individual clinical journeys—particularly the willingness to deeply reexamine unexpected outcomes and derive broader individualized insights from them. In practice, when one treatment fails, the next newly developed therapy is often recommended as the default progression.

One reason for this, from my perspective, is the absence of a constitutional classification framework comparable to that found in traditional East Asian medicine.

However, I believe that as artificial intelligence continues to advance, individualized medical records may one day be analyzed at a level of depth far beyond what any single clinician can manually achieve today—integrating pattern recognition, retrospective comparison, critical reinterpretation, and perhaps even generating entirely new therapeutic hypotheses from accumulated patient histories.

I believe that if such an academic and clinical paradigm continues to develop, patients will ultimately benefit greatly from it.

I once treated a patient from Germany. As I carefully asked detailed questions about various aspects of the patient’s condition, history, and daily experience, the patient remarked that my consultation style was remarkably similar to that of the physician who had treated them in Germany.

I have always made it a practice to document even what may seem to be the smallest or most incidental comments from patients. And when time permits, I revisit those records, reflect on them, and reconsider their meaning.

Because hidden within those seemingly ordinary remarks are often important medical truths—patterns that may not be immediately obvious, but which, through repeated observation and thoughtful reflection, can eventually be recognized, understood, and sometimes lead to meaningful clinical insight.

Perhaps that physician was working within a long-term primary care or personal physician system, because the patient told me that from an early age, the doctor would ask detailed questions about nearly every aspect of their health and carefully document everything. Even when the patient returned two years later, the physician reportedly asked about the response to medications that had been prescribed two years earlier and recorded those outcomes in detail.

Naturally, this made the consultation quite lengthy. While today’s economic realities in healthcare often do not permit that level of time-intensive individualized care, the story led me to reflect that the underlying spirit of East and West may not be so different after all when it comes to studying individual variation and applying those observations to treatment.

The Western primary physician model, in its ideal form, also seeks to understand the individuality of each patient and incorporate that understanding into clinical decision-making.

The real difficulty, in my view, lies not necessarily in medical philosophy, but in systemic constraints. In a healthcare environment where even five-minute consultations may leave hospitals operating at a financial deficit, many of the institutional structures required for truly individualized medicine become difficult to sustain. This is an area where meaningful systemic reform deserves consideration.

Next, I have included a consolidated perspective from ChatGPT regarding Proscar, presented in simplified form for readers who are new to the subject as well as for those with academic interest in the underlying pharmacology.

The medication applied in this case, Proscar (finasteride), is used differently depending on the physician’s therapeutic approach—some clinicians combine it with bicalutamide, while others do not. Although it is primarily prescribed for benign prostatic hyperplasia (BPH), I do not classify this medication simply according to the conventional distinction between benign and malignant disease. Rather, within my constitutional framework, I classify it as a medication more suitable for Taeeumin and Soeumin constitutions, and in my clinical experience, I have repeatedly observed favorable responses in Soeumin patients who had previously failed bicalutamide-based therapy.

The active ingredient in Proscar is finasteride. Although widely recognized as a treatment for benign prostatic enlargement, its pharmacologic mechanism is directly connected to the androgen-dependent growth pathway of prostate cancer, making it relevant to discussions of prostate cancer biology as well.

Male hormonal signaling is not mediated by testosterone alone.

Within prostate tissue, testosterone is converted by 5-alpha reductase (5α-reductase) into dihydrotestosterone (DHT). This conversion is critically important because DHT binds to the androgen receptor far more strongly than testosterone itself, resulting in a much more potent stimulation of prostate cellular growth and proliferation.

In simpler terms, if testosterone may be regarded as the raw substrate, DHT can be considered the more biologically activated form, exerting a substantially stronger effect on androgen-dependent prostate tissue.

Proscar (finasteride) acts precisely at this conversion step—blocking the transformation of testosterone into DHT.

More specifically, finasteride selectively inhibits type II 5-alpha reductase (5α-reductase type II), the enzyme primarily responsible for converting testosterone into dihydrotestosterone (DHT) within prostate tissue.

As a result, intraprostatic DHT levels fall significantly, reducing androgen receptor stimulation and thereby decreasing the hormonal drive for prostate tissue growth.

This enzyme is distributed particularly abundantly within prostate tissue, which is why finasteride effectively reduces androgenic stimulation specifically at the level of the prostate.

As a consequence, DHT levels decline, the proliferative signaling that drives prostate cell growth is reduced, and over time, the prostate gland gradually decreases in size. Clinically, this leads to improvement in urinary obstruction symptoms, reduced lower urinary tract symptoms, and relief of benign prostatic hyperplasia–related discomfort.

An important point is that this medication does not eliminate testosterone itself. Circulating testosterone in the bloodstream remains present. Rather, finasteride works by blocking the pathway through which testosterone is converted into the much more potent androgen, DHT.

Therefore, Proscar (finasteride) is fundamentally different from agents such as Lupron (leuprolide), Zoladex (goserelin), or Degarelix, which function as GnRH agonists or antagonists to suppress testosterone production itself and induce systemic androgen deprivation.

Those therapies act upstream at the level of the hypothalamic–pituitary–gonadal axis, markedly reducing testicular testosterone production and creating a state of profound hormonal suppression.

By contrast, finasteride does not shut down testosterone production. Instead, it acts downstream at the tissue level, selectively blocking the conversion of testosterone into DHT, the more potent androgen within prostate tissue.

In that sense, Proscar represents not complete androgen suppression, but rather a form of relative androgen modulation—a more targeted and physiologically limited alteration of androgen signaling.

Although GnRH agonists such as Lupron and Zoladex were explained earlier (around slide 130), their actual mechanism is based on a theory in which they temporarily increase testosterone levels first, and then ultimately deplete androgen production through receptor downregulation. From my perspective, this is a highly risky approach. In my clinical observation and from the viewpoint of Sasang constitutional medicine, I believe this can act as a direct aggravating factor in prostate cancer, particularly in Yin-type constitutions.

In contrast, GnRH antagonists, in my Sasang medical perspective, appear to be more useful for the Soeumin type, based on both theoretical interpretation and clinical experience.

Clinically, finasteride also affects PSA levels. With long-term use, PSA values may decrease by approximately 50%, which is an important consideration in prostate cancer monitoring. As a result, measured PSA values may appear artificially lower than the true biological disease activity, and clinicians must interpret serial PSA results with appropriate caution.

A related medication in the same pharmacologic class is dutasteride (Avodart). Whereas finasteride selectively inhibits type II 5-alpha reductase, dutasteride inhibits both type I and type II isoenzymes, generally producing a more profound reduction in DHT levels.

In summary, Proscar does not directly eliminate testosterone. Rather, it reduces androgenic stimulation to the prostate by blocking the conversion of testosterone into the more potent androgen DHT, thereby attenuating androgen-driven prostate signaling.

From my own clinical perspective, I have found this approach to be particularly effective in patients whom I classify as having a Soeumin constitutional pattern.

The central biology of prostate cancer lies in the androgen receptor (AR) signaling axis.

Prostate tissue is inherently an androgen-dependent organ, and prostate cancer, particularly during a substantial portion of its clinical course, retains this same biological dependency.

Although testosterone itself can activate the androgen receptor, within actual prostate tissue, testosterone is converted by 5-alpha reductase (5α-reductase) into dihydrotestosterone (DHT), which functions as a far more potent androgenic ligand.

DHT has a higher binding affinity for the androgen receptor than testosterone and forms a more stable receptor–ligand complex, resulting in more sustained and powerful downstream signaling.

This enhanced receptor activation leads to stronger transcriptional activation of androgen-responsive genes, ultimately promoting:

• cellular proliferation
• survival signaling pathways
• activation of anti-apoptotic mechanisms
• continued tumor growth in androgen-sensitive prostate cancer

In essence, prostate cancer biology is driven not merely by the presence of testosterone, but by the efficiency and intensity with which the AR signaling machinery is activated, with DHT serving as one of the most powerful physiologic drivers of that process.

It is precisely at this point that finasteride becomes therapeutically meaningful.

Finasteride does not eliminate testosterone itself. Rather, it blocks the final enzymatic amplification step in which testosterone is converted into the far more potent androgen, DHT (dihydrotestosterone). In other words, it does not induce endocrine castration, but instead produces intraprostatic attenuation of androgen signaling by reducing the generation of the most biologically active androgen within prostate tissue.

To understand its potential application in prostate cancer, one must first appreciate the temporal evolution of the disease.

Early prostate cancer is, in most cases, an androgen-dependent malignancy. At this stage, stimulation of the androgen receptor signaling axis serves as one of the principal drivers of tumor growth and survival.

For this reason, androgen deprivation therapy (ADT) has historically been the central therapeutic strategy. Whether through:

• orchiectomy (surgical castration)
• GnRH agonists
• GnRH antagonists
• antiandrogen therapy

the fundamental biological target remains the same: suppression of androgen-mediated tumor stimulation.

From the perspective of Sasang constitutional medicine, however, I interpret these pharmacologic categories differently. In my constitutional framework, GnRH agonists are viewed as medications more aligned with the Soyangin constitutional pattern, and therefore, in my interpretation, may not be suitable for Yin-type constitutions. By contrast, GnRH antagonists are considered more compatible with Soeumin patients.

However, finasteride differs fundamentally from these therapies in that it does not eliminate testosterone itself. For that reason, as a standalone treatment, it is generally insufficient to function as a definitive suppression therapy in metastatic prostate cancer, because the overall intensity of androgen suppression is comparatively limited.

But from a more advanced biological perspective, the story does not end there.

When one examines prostate cancer tissue at the molecular level, it becomes clear that the disease is not governed solely by systemic circulating testosterone. Prostate tumors can maintain their own intratumoral androgen metabolism, meaning that even when serum testosterone levels are reduced, cancer cells may continue to generate or locally activate androgenic signaling within the tumor microenvironment.

In this context, 5-alpha reductase remains biologically relevant, because the enzymatic conversion of precursor androgens into more potent androgen receptor ligands can continue within tumor tissue itself.
This becomes even more important in castration-resistant prostate cancer (CRPC).
At this stage, the biology is no longer as simple as:
“testosterone has been removed, therefore the tumor starves.”

Cancer cells adapt.
One major adaptive mechanism is:
1. Androgen receptor overexpression
The tumor increases the number of androgen receptors, allowing even extremely low androgen concentrations to generate meaningful signaling. In effect, the cancer becomes hypersensitive to minimal hormonal stimulation.

Additional adaptive mechanisms include:

2. Androgen receptor mutation
Structural mutations in the androgen receptor can alter ligand specificity, allowing the receptor to remain active even under conditions where conventional androgen deprivation would normally suppress signaling.

3. Ligand-independent receptor activation
The androgen receptor may become activated through alternative intracellular signaling pathways, even in the absence of direct androgen binding.

4. Intratumoral androgen synthesis
Cancer cells may develop the capacity to synthesize androgens locally within the tumor microenvironment, bypassing dependence on systemic endocrine sources.

5. Adrenal androgen utilization
Even when testicular testosterone production is profoundly suppressed, weaker adrenal androgens can still serve as substrates for continued androgen receptor signaling.

In other words, even when circulating testosterone is markedly reduced, prostate cancer may evolve mechanisms to preserve androgen signaling autonomy.

This is where the theoretical role of finasteride becomes biologically interesting.

Its mechanistic contribution lies in blocking DHT amplification.

Particularly in situations where testosterone has not been completely eliminated, the following pathway remains relevant:

testosterone → 5α-reductase → DHT → androgen receptor activation

By interrupting this final amplification step, one may reduce the overall intensity of receptor stimulation, even without completely abolishing androgen availability.

This mechanistic concept connects historically to the broader idea of combined androgen blockade (CAB)—the attempt to suppress androgen signaling at multiple levels rather than relying on a single therapeutic intervention.

For example:

• GnRH agonists → suppress testosterone production
• Antiandrogens → block androgen receptor activation
• 5α-reductase inhibitors → block DHT conversion

In other words, the therapeutic strategy is to simultaneously compress the androgen axis at multiple biological levels.

Theoretically, this approaches a form of more complete androgen blockade.

However, the reason finasteride did not become a standard therapy for metastatic prostate cancer lies in its limited suppressive potency.

GnRH-based therapies reduce testosterone to castrate levels.

By contrast, with finasteride:

• testosterone remains present
• adrenal androgen sources remain active
• complete androgen receptor blockade is not achieved

A practical analogy would be this:

GnRH therapy shuts off the main fire hose.
Finasteride merely tightens part of the faucet.

That said, the biological context changes in settings such as:

• low-volume disease
• biochemical recurrence
• PSA-only relapse
• active surveillance biology

Because in these states, tumor burden is relatively small and proliferative pressure is lower, more modest attenuation of androgen signaling may carry greater biological significance.
This same logic has also appeared in the chemoprevention field.
In the Prostate Cancer Prevention Trial (PCPT), finasteride was shown to reduce the overall incidence of prostate cancer.
The finding became highly controversial because although overall cancer incidence decreased, the proportion of high-grade cancers appeared relatively increased.
Modern interpretations suggest this was likely not due to true induction of aggressive biology, but rather explained largely by factors such as:

• prostate shrinkage leading to biopsy detection bias
• PSA interpretation distortion
• histologic grading artifacts

Thus, the apparent increase in aggressive cancers was likely more a matter of improved detection sensitivity than true biologic worsening.
At a deeper mechanistic level, finasteride is not merely a simple hormonal drug.
DHT signaling intersects with multiple biologic processes, including:

• cell cycle progression
• anti-apoptotic signaling
• growth factor pathway crosstalk
• stromal–epithelial communication within the tumor microenvironment

Therefore, DHT blockade may represent more than simple PSA reduction—it may also influence aspects of tumor microenvironment modulation.

In summary:
Finasteride is not a standalone agent capable of controlling metastatic prostate cancer. However, by blocking intraprostatic DHT amplification, it provides a biologically rational means of reducing androgen receptor signaling intensity.
Its potential relevance is greatest in:

• early disease
• biochemical recurrence
• prevention biology
• selected androgen-axis combination strategies as adjunctive therapy.