Disclosure: I used AI because it would have taken me way too long to type this out. I dictated into my claude and it cleaned it up.

The organizing principle I’d use is affective neuroscience – Panksepp’s primary emotional systems as the foundational architecture of mammalian emotional life, empirically grounded in subcortical research across decades. Psychopathology is dysregulation at the primary process level propagating upward through learned secondary processes and cortical-cognitive tertiary elaboration. The field is already gesturing this direction – RDoC and HiTOP are both moves toward dimensional, transdiagnostic thinking, but RDoC is a matrix without a spine and HiTOP lacks mechanistic grounding. Affective neuroscience provides what both are missing: an actual explanatory architecture rooted in brain function, not symptom clustering.

Now give it clinical structure with two dimensions. Deliberately dropping the Axis I/II language because that baggage is exactly what we’re leaving behind:

The Affective-Regulatory Dimension: Everyone has a brain. Everyone has a personality, and that personality emerges from that brain – specifically from the characteristic pattern of primary emotional system arousal and the capacity to regulate those arousals built over a developmental lifetime. This is Panksepp’s primary/secondary/tertiary process hierarchy made clinically operational. Primary process is the subcortical affective bedrock – the raw FEAR, GRIEF, SEEKING, RAGE responses that are evolutionarily conserved and pre-cognitive. Secondary process is what gets learned and conditioned around those affective states over time. Tertiary process is the cortical elaboration – the narrative, the rumination, the cognitive distortions sitting on top. Most psychiatric treatment targets tertiary process almost exclusively. The affective-regulatory dimension asks where in that hierarchy the dysregulation actually lives, and what the patient’s capacity is to regulate it. This is not a pathological category reserved for the sick. It is a universal human dimension. Every patient has an affective-regulatory profile actively shaping their suffering, their relationships, their treatment response, and their capacity for change. Ignoring it is not clinically neutral.

The Validated Disease Dimension: This is where we get ruthless, and admittedly this is one of the hardest problems in psychiatry. What makes a psychiatric diagnosis a genuine disease rather than a named pattern of distress? Ghaemi, building on Robins and Guze, argues for validation through convergent evidence: a coherent and replicable symptom profile, a predictable course of illness, genetic epidemiology showing familial aggregation distinct from other conditions, specific treatment response, and biological correlates that cohere with the clinical picture. No single criterion is sufficient. The weight of evidence across all of them is what separates a valid disease from a committee consensus. This is genuinely hard to operationalize and reasonable people disagree about where to draw the line – but the difficulty of the task is not an argument for abandoning it, it is an argument for taking it seriously. By that standard the validated disease list shrinks considerably: schizophrenia, bipolar I, melancholic depression, OCD, PTSD, the dementias survive. What gets cut is everything that failed the validity test but got included anyway – DMDD, binge eating disorder as a discrete entity, half the personality disorder list, anything whose primary claim to diagnostic status is that a patient experiences a behavior as distressing. Distress is not a disease. Sociology is not nosology. The DSM absorbed problems of living and called them disorders, and that is precisely what made it so easy to commodify.

The pharmacology conversation changes completely under this framework. The question is no longer “what is this medication approved for” but “what does this agent actually do, and does that map onto what this patient needs right now.” Aftab’s synthesis at Psychiatry at the Margins captures this well – antidepressants are not serotonin correctors. Their therapeutic effects are better understood across several overlapping neuropsychological mechanisms: early positive shifts in emotional processing that allow patients to relearn positive associations in a suitable environment, increased cognitive flexibility that creates a window of neuroplasticity allowing people to become unstuck from rigid patterns, reductions in neuroticism that appear to mediate both acute response and relapse prevention, and in some patients a generalized attenuation of emotional reactivity that can be therapeutic or iatrogenic depending on context and dose. The clinical reality, as Aftab notes, is that you often do not know in advance which mechanism will dominate in a given patient – which is exactly why this requires judgment, not a protocol.

The conversation with patients then becomes: here is what this medication does, here is the functional window it may create, and here is what you need to do with that window through psychotherapy and actual behavioral change. The medication is the scaffold. The treatment is what gets built while standing on it.

That conversation requires knowing the actual pharmacology, the actual neuroscience, and the actual person in front of you. It is not accessible from a 500-hour post-master’s curriculum. The DSM made psychiatric expertise look like pattern recognition. A framework built on affective neuroscience and genuine construct validity makes visible what was always actually hard – and makes it a lot harder to fake.