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).
Dysbiosis and Psychiatric Risk
Animal studies show anxiety-like behavior after gut microbiota disruption (e.g., Campylobacter jejuni).
Probiotic foods like yoghurt, kefir, kimchi, and sauerkraut have shown promise in reducing gut inflammation and improving mood symptoms.
Clinical translation is ongoing.
A Shared Pathway
Depression is increasingly linked to low-grade systemic inflammation and oxidative stress.
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.
2/12 🧵
For every 1-point increase on the CGI-SCH depression subscale, suicide risk rose by 15.8% (OR: 1.158; p = 0.0015).
This underscores the link between affective symptoms and suicidal behaviour in schizophrenia.
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 🧵
Increased MPO is found across multiple psychiatric conditions—schizophrenia, bipolar disorder, and autism spectrum disorder (ASD)—highlighting a shared neuroimmune link.
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.
2/11 🧵
At its core, overthinking reflects a breakdown in executive function.
This includes impaired set-shifting, poor attention control, and inability to suppress intrusive thoughts, hallmarks of prefrontal–striatal–limbic dysfunction.
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.
At the core lies a disrupted reward cascade.
Risk alleles, early stress, and neurotoxins reduce dopamine transmission in the ventral tegmental area–nucleus accumbens pathway.
Behaviour shifts toward seeking short-term dopamine spikes to compensate for this deficit.
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.
Consider Matching Antipsychotics to Symptom Domains
• For predominant negative symptoms: Consider agents like cariprazine
• For acute agitation: Short-term use of fast-acting antipsychotics or benzodiazepines may be beneficial
• For prolactin elevation: Consider switching to aripiprazole
Matching drug profile to symptom burden may optimise outcomes.