Up to 40% reduction in depression risk has been observed with adherence to anti-inflammatory diets like the Mediterranean diet, according to the PREDIMED study.

Emerging research links dietary patterns to neuroinflammation, neurotransmitter synthesis, and gut–brain signalling.

Here’s what clinicians need to know about nutritional strategies in psychiatric care, from gut microbiota to therapeutic nutrients. 🧵👇 The Gut–Brain Axis and Mental Health

The GI tract hosts 100 trillion microbes influence mood, cognition, and stress regulation.

Disruptions (e.g., from a Western diet) are associated with depression and anxiety.

Some strains produce neurotransmitters (e.g., serotonin precursors).

Which patients with schizophrenia are at the highest risk of suicide?

In a 3-year pan-European study of 8,871 outpatients, the suicide attempt rate was 4.3%, with key predictors including prior attempts, depressive symptoms, prolactin-related side effects, male gender, and prior hospitalisation.

1/12 🧵 Lifetime suicide attempts increased future risk nearly fivefold (OR: 5.2), and suicide attempts in the 6 months prior raised risk 3.7× compared to none.

This finding reinforces the need for detailed longitudinal histories.

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Over 50% of psychotropic medications are metabolised by CYP450 enzymes, many of which are genetically polymorphic.

This genetic variability explains why individuals differ significantly in drug response, tolerability, and plasma levels.

Here’s what you need to know about CYP pathways, phenotypes, clinical indications, and how to integrate testing into psychiatric practice. 🧵👇 What Is Pharmacogenomics?

Pharmacogenomics examines how genetic variation influences drug metabolism, receptor activity, and transport.

It informs dose adjustment, medication selection, and risk stratification, especially in psychotropics. (Hicks et al., 2015; Foulds et al., 2016)

Can probiotics reduce neuroinflammation in autism?

A small 2018 RCT in Egypt (Shaaban et al.) found autistic children taking probiotics had ~66% lower plasma myeloperoxidase (MPO) levels than those not on probiotics (1054 vs. 3161 pg/mL; p = 0.0009).

Findings are promising, but not yet generalisable.

1/13 🧵 MPO is a marker of neutrophil-driven inflammation.

It catalyses the formation of hypochlorous acid (HOCl), a reactive species linked to tissue damage and oxidative stress.

2/13 🧵

An EEG study reveals that individuals with ADHD exhibit increased theta and alpha power, coupled with decreased beta power, indicating impaired attention regulation and executive control (Michelini, 2022).

These patterns reflect the same brain dynamics underlying overthinking: intrusive, uncontrolled, and cognitively taxing thought loops.

1/11🧵 Overthinking is not a diagnosis, but a symptom that crosses diagnostic boundaries.

In ADHD, anxiety, depression, PTSD, and bipolar disorder, it can signal cognitive dysregulation within core brain networks.

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Over 46% of the population carries the DRD2 A1 allele, which is linked to lower dopamine receptor density and increased risk of impulsive and compulsive behaviours (Blum et al., 2022).

Blum et al. (1995) found it could predict Reward Deficiency Syndrome behaviours, such as substance use and overeating, with up to 74.4% accuracy.

How does this genetic profile shape behaviour? RDS is not a single disorder.

It’s a transdiagnostic spectrum of addictive, impulsive, and compulsive behaviours driven by hypodopaminergia—low tonic dopamine tone in mesolimbic circuits.

The phenotype may vary, such as substance use, gambling, and overeating, but the dopaminergic dysfunction is often shared.

Cognitive impairment is present in up to 80% of patients with schizophrenia, affecting attention, memory, and executive function (Saperstein & Kurtz, 2013).

These deficits are central, not peripheral, to functional outcomes.

Here's what clinicians need to know about diagnosis, monitoring, and treatment based on updated schizophrenia guidelines.👇🧵 Metabolic and Prolactin Monitoring

Guidelines recommend considering baseline and regular monitoring for:

• Metabolic parameters

• Prolactin levels

• Extrapyramidal symptoms

• Cognitive status

Failure to monitor contributes to treatment resistance and poor adherence.

Studies show that 50–75% of people with PTSD also experience chronic pain.

In PTSD, the brain’s defence systems become sensitised.
This lowers the threshold for detecting threat, whether emotional or physical.

Psychological pain and bodily pain begin to merge.

1/14 🧵 Meanwhile, 20–37% of those with chronic pain meet the criteria for PTSD.

(Scioli-Salter et al., 2015)

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Up to 90% of patients with ADHD experience at least one comorbidity—ranging from anxiety to substance use disorders.

These overlaps complicate diagnosis and treatment, making clinicians need to recognise and address them effectively.

Here are 10 key ADHD comorbidities and evidence-based strategies to navigate them 👇🧵 1. Behavioural Disorders & ADHD

Oppositional Defiant Disorder (ODD) overlaps with ADHD (irritability, reactivity) but includes defiance and vindictiveness.

→ Mild: Start with stimulants (e.g., methylphenidate).
→ Moderate-severe: Add CBT or parental training. 
→ Severe: Consider risperidone.

Conduct Disorder (CD) involves persistent aggression or deceit, risking antisocial outcomes.

→ Combine stimulants with therapy. 
→ Severe: Use SSRIs or antipsychotics like risperidone.

The brain doesn't just react to medications. It adapts.

Opponent Process Theory (OPT) explains how tolerance, withdrawal, and paradoxical effects emerge.

One of the most under-taught concepts in psychopharmacology.

🧵1/15 In clinical training, we learn what medications do to the brain. 

But we rarely ask what the brain does in response to the medication. That’s the core question OPT helps answer.

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Even after months of abstinence, drug cues alone can trigger dopamine surges in the nucleus accumbens—driving relapse with no substance present (Volkow et al., 2019)​.

With each exposure, dopaminergic circuits reorganise, weakening prefrontal inhibition and reinforcing compulsive drug-seeking.

How do these neuroadaptations lock patients into addiction, and what can you do to restore cognitive control, reduce relapse, and rewire the brain? 🧵👇 Why Addiction is More Than Just Behaviour

The mesolimbic dopamine system reinforces reward and motivation. In addiction:

• VTA → Nucleus Accumbens: Heightened dopamine release → Stronger craving.

• Prefrontal Cortex Dysfunction: Reduced inhibition → Impaired self-control.

• Amygdala & Hippocampus: Drug-related memories become deeply ingrained​.

These adaptations make patients hypersensitive to triggers, even after long periods of abstinence.

Human endogenous retroviruses (HERVs), typically dormant sequences comprising 8% of the human genome, can be activated by viral infections and implicated in schizophrenia.

HERV-W transcripts and proteins have been detected in the brain tissue and plasma of patients with schizophrenia.

Let’s explore the molecular and immune-related mechanisms through which viral infections may contribute to the pathogenesis of psychotic disorders. 👇🧵 HERVs and Schizophrenia

The HERV-W and HERV-K families are the most studied in psychosis.

HERV-W envelope proteins may be reactivated by environmental viruses, leading to neuroinflammation and neural circuit disruption.

This activation may play a role in the development of psychosis in vulnerable individuals.

KarXT (Xanomeline–Trospium) is the first FDA-approved muscarinic receptor agonist for schizophrenia.

Unlike traditional antipsychotics, it acts on M1/M4 receptors, not D2, offering efficacy without dopaminergic side effects.

Let’s break down the mechanism, trial data, and clinical impact. 🧵👇 Dopamine-Independent Mechanism

KarXT is a combination of:

• Xanomeline: a centrally acting M1/M4 agonist and

• Trospium: a peripheral muscarinic antagonist that doesn’t cross the BBB

It reduces psychotic symptoms without blocking D2 receptors.

Clozapine is the only antipsychotic with proven efficacy in Treatment-Resistant Schizophrenia (TRS), yet its use is often significantly delayed, sometimes by 5 years or more.

Despite more than 50% of community-treated patients meeting criteria for treatment resistance, many never receive it.

Here’s what clinicians need to know to identify treatment resistance early and optimise the use of clozapine in practice. 👇🧵 Defining Treatment Resistance

• Treatment resistance is often defined as non-response to two antipsychotic trials of adequate dose and duration.

• In the STAR algorithm, response rates drop significantly after failure of the first medication.

• Delays in initiating clozapine reduce the likelihood of remission.

Psych Scene Tip: TRS should be identified early and explicitly to prevent ineffective polypharmacy.

The STAR*D study showed that approximately 30% of patients with major depressive disorder (MDD) fail to respond to antidepressants or psychotherapy (Rush et al., 2006).

Treatment resistance is often marked by anhedonia and motivational deficits, features linked to dopaminergic dysfunction.

Here’s what you need to know about pramipexole’s mechanism, clinical evidence, and prescribing strategies in Treatment-Resistant Depression (TRD). 👇🧵 Defining Treatment Resistance

In STAR*D, remission rates declined with each treatment step:

• Step 1: 37%

• Step 2: 31%

• Step 3: 14%

TRD is defined as non-response to at least two antidepressant trials from different classes, with adequate dose and duration.

Up to 60% of individuals with schizophrenia experience persistent negative symptoms (Correll C & Schooler N et al., 2020).

These symptoms contribute more to functional impairment than positive symptoms and are often under-recognised in clinical settings.

Let’s explore the neurobiology, diagnostic challenges, and treatment strategies that guide clinician care in managing negative symptoms. 🧵👇 Defining Negative Symptoms

Negative symptoms represent deficits in normal functioning and are classified into:

• Avolition

• Anhedonia

• Asociality

• Alogia

• Blunted affect

They are distinct from depression or cognitive impairment and require targeted assessment.

Catatonia occurs in 9–17% of patients with acute psychiatric illness and is associated with serious medical complications if not promptly treated.

It is seen across mood disorders, psychotic conditions, and general medical illnesses, not only schizophrenia.

Here’s what clinicians should know about its identification, underlying circuitry, and treatment.🧵👇 Clinical Features of Catatonia

Catatonia presents with motor, behavioural, and affective abnormalities.

Key signs include stupor, mutism, waxy flexibility, echolalia, echopraxia, posturing, negativism, and grimacing.

Both withdrawal and agitation may occur within the same episode.

Psych Scene Tip: Consider catatonia in the differential for any patient presenting with unexplained motor changes or unresponsiveness.

In the SHIP study, three-quarters of individuals with psychosis were overweight or obese (Galletly et al., 2012).

Obesity is not a side effect but a comorbid condition that compounds cardiovascular, metabolic, and psychiatric burdens.

Here’s what clinicians need to know about the pathophysiology and management of weight gain in psychiatry. 🧵👇 Hypothalamic Circuits of Appetite Regulation

The arcuate nucleus (ARC) integrates peripheral signals (ghrelin, leptin, insulin) to modulate appetite:

• AGRP/NPY neurons → stimulate food intake

• POMC/CART neurons → suppress appetite

Disruption of this balance leads to hyperphagia and weight gain.

Up to 73% of children and 67% of adults with Attention-Deficit/Hyperactivity Disorder (ADHD) report clinically significant sleep disturbances.

These impair attention, emotion regulation, and behaviour, often misattributed to core ADHD pathology.

Continue reading to understand the neurobiology, diagnostic complexity, and management strategies guiding clinical care.🧵👇 Four Clinical Pathways Linking ADHD and Sleep

1. ADHD causes sleep disturbance

2. Sleep problems mimic or aggravate ADHD

3. Shared psychosocial or developmental confounders

4. Common neurobiological origin

This model frames how symptoms and causality may overlap.

In a Swedish cohort of bipolar patients, 26% of those on lithium met the criteria for hypercalcemia (Meehan et al., 2017).

Despite known associations between lithium and calcium dysregulation, routine monitoring remains inconsistent.

Here’s what clinicians need to know about prevalence, pathophysiology, and treatment strategies. 👇🧵 Prevalence and Risk Comparison

Hypercalcemia occurred in:

• 26% of bipolar patients on lithium

• 1.4% of bipolar patients not on lithium

• 2.9% of the general population controls

Lithium-treated patients had 13-fold higher odds of hypercalcemia after adjusting for age, gender, and diagnosis.

A 59-year-old woman with no prior psychiatric history presented with severe depressive symptoms, nihilistic delusions, and poor insight.

She required inpatient admission due to suicidality and functional decline.

Let’s examine this case and its imaging to highlight the diagnostic and management considerations. 🧵👇 Clinical Features on Admission

• Profound psychomotor retardation

• Delusions of organ failure and being dead

• Anhedonia, insomnia, and self-neglect

• Non-responsiveness to verbal prompts

Initial diagnosis: Major depressive disorder with psychotic features (mood-congruent).