MAD Theory and Conservation Psychotherapy: Clinical Q&A (For Psychiatrists)

2026.03.08

Thank you for your dedicated work in systematizing MAD Theory and Conservation Psychotherapy. You have developed a highly consistent model with strong clinical persuasiveness.

Readers who are psychiatrists have been trained within the paradigms of the conventional “monoamine hypothesis” and “Cognitive Behavioral Therapy (CBT)”. It is therefore anticipated that they will have many questions regarding this theory, particularly around three areas: “biological basis,” “specific intervention methods,” and “ethical judgment.”

The following is a detailed Q&A designed to proactively address anticipated questions from readers.

I. The Unit Model and Cellular Function

Q1: Doesn’t the hypothesis that the M-unit supplies “sleep components” contradict the insomnia seen in manic states?

A: It does not contradict. The M-unit has a dual function of “activity drive” and “sleep induction”; however, in manic states, the “activity drive” runs out of control and exceeds the effect of the “sleep components” it supplies, resulting in insomnia. Meanwhile, insomnia in depressive states stems from the M-unit itself ceasing to function, causing the “sleep components” themselves to become depleted.

Q2: What specific symptoms does the A-unit (Anankastic cell) manifest as?

A: The A-unit governs “maintenance of steady-state.” When M disappears during a depressive episode, the relative prominence of A’s functioning becomes apparent, manifesting as repetition of the same pessimistic thoughts (rumination), rigid adherence to fixed procedures, or an agitated compulsiveness expressed as “I must rest, and yet I must do something.”

Q3: Why do you adopt the “mania-dominant theory”? Aren’t there many cases of unipolar depression with no manic symptoms at all?

A: This theory defines not only visible manic states, but also states in which “the system is mobilizing all its resources to cope”—such as viral infection or high psychological load—as mania in the broad sense (M/A hyperactivity). Since M-unit injury necessarily requires a preceding phase of “overload,” all depression is considered a consequence of mania (overload).

II. Sleep and Diurnal Variation

Q4: What does it mean that sleep “disposes of unnecessary M-units”?

A: This assumes the synaptic homeostasis (SHY) process of the brain. Under healthy conditions, sleep reorganizes unnecessary neural connections; however, when the M-unit is injured, this process is thought to preferentially prune the wiring of weakened M-units, causing the destruction of M to progress during the night.

Q5: If sleep deprivation therapy has immediate effects, why does Conservation Psychotherapy recommend “sleeping”?

A: Sleep deprivation is merely a “temporary workaround” that circumvents the nocturnal M-damage process. For the physical regeneration of M (the process of a scab healing), sleep-dependent metabolism is indispensable. Sleep deprivation is akin to “high-interest financing”—it increases the risk of switching to mania—and Conservation Psychotherapy prioritizes high-quality rest, placing emphasis on long-term regeneration.

III. Suicide and Ethics

Q6: Doesn’t the theory that “suicide is a bug in collective survival strategy” trivialize the patient’s wish to die?

A: On the contrary. Overly respecting the wish to die as “the individual’s free will” results in overlooking what is essentially a “computational error of the brain” caused by the disappearance of M-units. By recognizing this as “a temporary runaway program,” the physician can ethically justify unwavering protective measures (such as hospitalization), and can commit to safeguarding the patient through to regeneration.

Q7: How does this model explain why suicide increases during the recovery phase?

A: During the process of M-unit regeneration, “motivation for concrete action” returns first, while “optimism and the stop signal” return later—a time lag occurs (constituting a mixed manic-depressive state). The risk of execution peaks at the moment when the accelerator (M) has partially recovered while the brake (D’s self-reproach) remains at its maximum value. Getting through this period is the critical juncture of Conservation Therapy.

IV. Specific Clinical Management (Conservation Psychotherapy)

Q8: Is it appropriate to provide a fixed timeframe of “2–4 months” for sick leave?

A: Conveying that the biological “healing of a wound” requires a certain amount of physical time serves as a powerful therapeutic suggestion (reframing) that calms the patient’s A-unit from spinning its wheels with thoughts of “I must get better quickly.” Although there are individual differences, providing a prognosis that regeneration will require at minimum this period of time is advisable.

Q9: Is this a complete rejection of psychological approaches such as Cognitive Behavioral Therapy (CBT)?

A: No. However, the “timing” must be carefully selected. Attempting to change cognition during the period when M-units have disappeared is like forcing rehabilitation immediately after a bone fracture. The rational approach is to introduce CBT for relapse prevention after M-units have regenerated and the “stop signal” of self-esteem has begun to function autonomously.

Q10: Do pharmacotherapies (antidepressants, etc.) accelerate the regeneration of M-units?

A: Antidepressants act as “fertilizer (neurotrophic factors)” that promotes M-unit regeneration, or as a “buffer” that suppresses the runaway of D-units. However, medication alone cannot reduce the “time required for regeneration” to zero. Pharmacotherapy is, to the last, an auxiliary device for safely advancing Conservation Psychotherapy (the practice of waiting).

Q11: What should be done when a patient complains that “they cannot tolerate doing nothing”?

A: That is precisely the functioning of the A-unit (compulsive maintenance). The physician should redefine “doing nothing” as being engaged in “an extremely sophisticated infrastructure project known as M-unit regeneration,” thereby alleviating the patient’s guilt about doing nothing.

V. The Bipolar Spectrum

Q12: How does this model explain the difference between Bipolar I and II?

A:

Type I: A type in which the restart (ignition) of M-units is extremely powerful and uncontrolled, repeatedly bursting before regeneration is complete.

Type II: A type in which the regenerative capacity of M-units itself is chronically low, making it difficult to escape from the scab (D-state).

Q13: What is the utility of reset therapy (ECT/ketamine) in mixed states?

A: Mixed states are extremely dangerous conditions in which M/A hyperactivity collides with D hyperactivity, with injury progressing in real time. In such cases, relying solely on conservation (watchful waiting) risks completely burning out the M-units; therefore, a forced shutdown and restart of the system via physical reset (ECT) is recommended.

In Closing: Mental Healthcare for the Physician

Q: Doesn’t accompanying patients through months of “I’m not getting better” also exhaust the physician?

A: When the physician is freed from the compulsion to “cure the patient (active intervention)” and instead adopts an identity as a “gardener of conservation (conservationist)” who watches over regeneration, clinical burnout paradoxically decreases. It is important for the physician to firmly believe that M-unit regeneration is an autonomous process of life, and that their role is to be a guardian of the “space” in which that process can be completed.

MAD Theory and Conservation Psychotherapy: Clinical Q&A (For Psychiatrists) — Shinagawa Psychosomatic Clinic Free Memo 5　Tadashi Kon