There are no ‘silver bullets’ in psychiatry…

Knowing that a treatment exists is not the same as knowing when to use it, how to explain it, or where it fits in a patient’s journey.

Here are 10 clinical insights from The Academy to take into 2026 🧵👇

(Prof Michael Berk) (Prof David Barton) 1. Formulation is not reflective writing, it is the architecture of care.

Formulation must directly guide what you do next and why. If a formulation cannot be operationalised into a management plan, monitoring strategy, and review points, it has failed its primary clinical function.

Are women more vulnerable to anxiety and depression than men?

Statistics show women are 2x as likely to develop anxiety and depression than men.

Some attribute this disparity to gendered societal strain.

However, neuroscience reveals the female brain is simply biologically wired that way: primed for vigilance, having denser stress receptors that consolidate threat data more intensely than the male equivalent.

Here’s a breakdown of the neurobiological differences 👇🧵 The Female CRF Substrate

While cortisol is responsible for stress response, the ‘driver’ of heightened vigilance in women is the Corticotrophin-Releasing Factor (CRF), the primary regulator of the body's stress system.

Research shows that female brains possess a significantly higher density of CRF receptors in the amygdala (the brain's fear centre).

This structural density causes stress signals to bind more intensely, making fear responses harder to extinguish even after the threat is gone.

Is Depression a “Mental” or a “Metabolic” Disorder?

For decades, depression has been framed as a disorder of neurotransmitters.
Low serotonin. Faulty signalling. Chemical imbalance.

But for a clinically meaningful subset of patients, the primary driver may sit upstream of neurotransmission.

The 'problem' isn’t the signal.
It's the energy required to generate it.

Here’s how brain insulin resistance (BIR) can drive a hypometabolic depressive state 👇🧵 The brain is metabolically demanding.

• ~2% of body weight
• ~20% of total glucose consumption

Neuronal function is tightly coupled to ATP availability.

Insulin signalling in the brain modulates energy utilisation, synaptic plasticity, and neuronal firing efficiency.

In brain insulin resistance (BIR), this signalling is blunted.

PTSD isn’t just about what happened.

It’s also about who it happened to, biologically.

Around 30–40% of PTSD risk is heritable, interacting with trauma exposure.

Here’s how genes, brain markers, and epigenetics shape vulnerability, and how this matters in clinic👇🧵 Most people exposed to trauma do not develop PTSD.

Conversely, similar trauma can lead to very different outcomes.

This variability is best explained by a Gene × Environment × Time model, not trauma severity alone.

What does sleep dysregulation have to do with ADHD?

At face value, ADHD and sleep dysregulation seem like two distinct, parallel issues: one about attention, the other about rest.

However, research indicates that roughly 80% of people with ADHD experience chronic sleep or circadian disturbance, suggesting a much tighter link than simple “comorbidity.”

Here’s how sleep dysregulation and ADHD form a feedback loop that most often overlook:👇🧵 Some often assume sleep issues in ADHD—such as delayed onset, bedtime resistance, and irregular sleep-wake patterns—are "behavioural," the result of poor routine or bedtime procrastination.

However, studies suggest said issues are “intrinsic,” biologically wired into the ADHD phenotype via clock gene polymorphisms (e.g., CLOCK, PER2). 

• The Reality: the internal clock is genetically set to a later time zone.

• The Result: a biological "jet lag" that persists daily

Why do some patients shift from casual drug use to chronic addiction?

Addiction is often framed as a moral choice, a simple lack of willpower.

However, clinically-speaking, it may reflect maladaptive changes in the brain, shifting drug use from “pleasure-seeking” to a dysregulated survival instinct.

Here are 4 key theories of addiction and how they translate into what you might see in practice👇🧵 1) Reward Deficiency Syndrome (RDS) Theory

Some brains are genetically ‘wired’ with ‘hypodopaminergic traits’ (low dopamine).

They don't use drugs to get "high," but to correct a deficit. 

The substance acts as a compensatory mechanism to stimulate an underactive reward system and feel "normal" (Blum et al., 1996).

Consciousness isn’t “generated” by the cortex alone…

Loss of cortical activity does not reliably eliminate conscious feeling, while disruption of the ARAS–thalamocortical axis almost always does.

Here’s how to use this distinction to avoid misdiagnosing delirium, catatonia, psychosis, or functional states 👇🧵 Consciousness has two separable components:

• Arousal – brainstem–hypothalamic systems that maintain wakefulness.

• Awareness – cortical integration enabling content, reportability, and meta-representation.

Anaesthesia, delirium, and severe encephalopathies often dissociate these systems.

Depression isn’t just “low mood”…

Converging cognitive and affective science shows consistent biases in information processing that shape how patients think, feel, and interpret the world.

Here are the core cognitive–affective biases in depression — and what clinicians need to know about each👇🧵 1. Residual Cognitive Symptoms

Even when mood improves, many patients experience residual cognitive symptoms.

These difficulties are robustly associated with and can predict daily functioning, work performance, and quality of life (Lam et al., 2014).

Clinical note: consider assessing cognition even after mood stabilises.

ADHD is often discussed in terms of inattention, impulsivity, and hyperactivity...

But one domain is consistently under-recognised in assessment and treatment:

Sleep.

Here’s how sleep and ADHD are connected and the 5 clinically effective sleep strategies every clinician should know 👇🧵 Sleep disturbances are the rule, not the exception, in ADHD.

82.6% of individuals with ADHD report lifetime sleep problems.

And this extends far beyond delayed sleep onset.

Common presentations include:

• delayed sleep–wake phase
• restless legs / PLMD
• sleep-disordered breathing
• parasomnias (e.g., night terrors)

These often predate the ADHD diagnosis.

Autism isn’t “just genetic”. 

The gut–brain–immune axis can shape how symptoms show up—especially when GI problems are in the mix. 

Here’s what clinicians needs to know about the Gut Microbiome and Autism Spectrum Disorder (ASD) 👇🧵 ASD is highly heritable, but early life nudges—delivery mode, feeding, antibiotics, maternal metabolic health—can shift the microbiome and immune tone. 

Think genes × environment, not either/or.

Why do some patients feel unsafe in stable relationships?

In Borderline Personality Disorder (BPD), what looks like ‘attention-seeking’ is often an automated survival pattern, deeply encoded through implicit memory and prediction mechanisms.

1/13 🧵 Familiar instability can become the norm.

Patients with BPD often report early environments marked by unpredictability, abandonment, or emotional neglect (consistent with the biosocial model and attachment research).

Over time, the individual may learn that instability is expected in close relationships.

2/13 🧵

Why do some individuals recover from trauma while others develop PTSD?

A useful lens is how three large-scale brain networks interact:

• The Salience Network (SN)

• The Default Mode Network (DMN)

• The Central Executive/Frontoparietal Network (CEN/FPN)

Understanding their dysregulation helps guide PTSD treatment. Here’s how 👇🧵 The Integrated Model of PTSD highlights these networks:

• Salience Network: Detects and prioritises salient/interoceptive and potential threat cues.

• Default Mode Network (DMN): Supports autobiographical memory and self-referential processing.

• Central Executive Network (CEN/FPN): Enables cognitive control, working memory and decision-making.

PTSD is associated with disrupted interactions among these systems after trauma.

A 19-year-old presents with daily “fits.”

Sudden leg collapse, violent shaking, awareness intact; episodes can run for hours. 

She senses the start and finish, but can’t change the course.

Let’s break down her case and see how multidisciplinary learning in medicine is vital 🧵👇 Neurologist review:

• 3 years of daily whole-body shaking episodes up to 7 hours.

• Fully lucid and able to converse; typically sits or lies down when they start.

• Home videos show irregular, intermittent, asynchronous jerks of arms/legs.

• Impression at the time: consistent with psychogenic non-epileptic seizures (PNES).

ADHD isn’t “just behavioural”...

Converging neuroimaging data show consistent structural and functional brain differences across development.

Here are 7 anatomical brain changes in ADHD and what clinicians need to know about each👇🧵 #1: Global Brain Volume Reduction

The most consistent finding in ADHD is an overall reduction in total brain size with specific changes in the caudate nucleus, prefrontal cortex white matter, corpus callosum and cerebellar vermis. [Tripp and Wickens, 2009]

Chelsea, 20, says she’s “going mad with anxiety.”

Onset with VCE exams; now pervasive worry, decision paralysis, and no depressive features.

You suspect GAD. 

What would you do to confirm this? 👇 Nature of Anxiety.
 
Worry is frequent, excessive, hard to switch off, and out of keeping with threat, often without a trigger.

It persists even when things are going well and becomes the problem, not the topic [Andrews et al., 2018].

Females with ADHD constitute a silent minority, with a propensity towards underdiagnosis and undertreatment.

There is evidence to suggest that there is a significant discrepancy in the ratio of males to females diagnosed with ADHD. [Berry et al., 1985]

Let’s explore why ADHD manifests differently in females👇 ADHD is diagnosed far more often in males than females.

Early studies show teachers are more likely to refer boys for assessment, even when girls show identical symptoms.
(Young et al., 2020)

Lamotrigine prolongs the time between mood episodes and is particularly effective in preventing depressive relapses in bipolar I disorder.

Unlike lithium or antipsychotics, lamotrigine has no significant effect on acute mania but is a first-line option for bipolar depression (RANZCP Guidelines)​.

How does lamotrigine work? Let's explore its efficacy in bipolar disorder and important prescribing considerations. 🧵👇 Mechanism of Action

● Increases GABA release, supporting inhibitory neurotransmission​.

● Inhibits voltage-gated sodium (Na+) channels, reducing glutamate excitotoxicity​.

● Putative anti-kindling effects may help stabilise mood over time​.

The dual action on GABAergic and glutamatergic pathways may explain lamotrigine’s effectiveness in bipolar depression but lack of efficacy in mania.

A 53-year-old man with schizoaffective disorder on clozapine (700mg/day) had severe abdominal pain and vomiting to the ER.

Let’s walk through his case and explore why Clozapine induced Constipation (CIC) affects up to 60% of patients. 🧵👇 Background:

Clozapine is highly effective for treatment-resistant psychosis, but its anticholinergic and antiserotonergic effects slow gut motility.

If untreated, CIC can progress to ileus, sepsis, or death.

Lithium: still the most distinctive mood stabiliser we have.

70 years in practice with compelling evidence in mania, acute bipolar depression, and prophylaxis, yet its mechanisms remain multifaceted.

Here’s what makes Lithium so different and it’s mechanisms of action 🧵👇 Lithium is a unique agent that has been used for over half a century for the treatment of bipolar affective disorder.

Lithium has compelling evidence in the treatment of mania, acute bipolar depression and prophylaxis in bipolar
affective disorder.

Despite its first discovery in 1949 and its subsequent use, the exact mechanisms of action in lithium are unclear.

Lithium’s Action On Neurotransmitters:

Studies suggest that up to 50% of adults with ADHD meet criteria for an anxiety disorder (Fu et al., 2025).

Anxiety is not simply “comorbid”; it is embedded in ADHD’s neurobiology and developmental trajectory.

Let’s explore how anxiety and ADHD intersect, and why recognising this link can improve diagnostic clarity, treatment planning, and patient outcomes. 👇🧵

Note: image is a conceptual illustration (uncertainty ↔ arousal ↔ anxiety), not a validated biomarker/model. Across studies, anxiety co-occurs with adult ADHD in ~25–50% of cases; representative samples report ~47–56%.

Comorbidity tracks with earlier onset and greater impairment.

Borderline Personality Disorder (BPD) isn’t just “emotion dysregulation.”

It can be usefully conceptualised as a predictive-processing problem where salience, reward prediction errors (RPEs), and the endogenous opioid system (EOS) bias social learning.

Here’s how clinicians can help patients update predictions and reduce volatility. 🧵👇 Prediction errors = expectation vs outcome

Rapid, phasic dopamine/serotonin signalling in reward/salience networks encodes PEs, guiding attention, belief updating and affect regulation.