By Carolina Lima | Published on January 6, 2026 | 3 min read
Seasonal changes have long been suspected to influence
mood and psychiatric disorders. Clinical observations confirm that symptoms
fluctuate throughout the year, yet the underlying mechanisms remain unclear. A
recent review published in the Journal of Clinical Medicine (2025) by
Modzelewski and colleagues introduces the immunoseasonal theory,
offering an insightful immunological perspective on how weather patterns impact
mental health.
Seasonal Patterns in Mental Disorders
Depression tends to
peak
during
autumn and winter, a period marked by low sunlight, cold temperatures and
high humidity. These conditions coincide with increased antidepressant use and
a higher risk of postpartum depression in late-year births.
Anxiety disorders
and
post-traumatic stress disorder share similar inflammatory pathways making
them equally vulnerable to winter exacerbations.
Schizophrenia shows a
different seasonal pattern: hospitalizations frequently rise in
summer, with
some research noting a secondary peak in
winter. Factors such as light exposure
and melatonin regulation may play a role in modulating immune responses in these
patients.
Bipolar disorder also
demonstrates clear seasonality, with
manic episodes surging in
summer and
early
autumn, while
depressive episodes cluster in the colder months.
The immunoseasonal theory explained
The immunoseasonal theory
proposes that seasonal fluctuations in psychiatric symptoms are driven by
shifts in immune system activity, particularly the balance between
T-helper 1
(Th1) and
T-helper 2 (Th2) responses.
- Th1
response (winter):
pro-inflammatory state characterized by elevated cytokines like IL-1β, IL-6, TNF-α and IFN-γ. This inflammatory state may impair prefrontal
cortex (PFC) function, reducing its regulatory control over limbic
structures such as the amygdala and hippocampus. Clinically, this
manifests as increased rumination, heightened anxiety and depressive
symptoms. The Th1-driven state also interacts with the
hypothalamic–pituitary–adrenal (HPA) axis, promoting cortisol
dysregulation and circadian rhythm disturbances, which further exacerbate
mood disorders.
- Th2
response (summer):
anti-inflammatory profile, linked to cytokines such as IL-4, IL-10, IL-13
and TGF-β.
While anti-inflammatory in nature, Th2 activation can paradoxically
destabilize neural circuits. By stimulating cortical and mesolimbic
pathways, Th2 responses may contribute to psychotic symptoms, manic
episodes, impulsivity and increased suicide risk. This pattern aligns with
epidemiological data showing peaks in schizophrenia exacerbations and
mania during warmer months, often coinciding with high allergen exposure
and prolonged sunlight.
These immune shifts do
not act in isolation. They interact with neurotransmitters such as
serotonin
and
dopamine, disrupt circadian rhythms and amplify stress pathways through HPA
axis dysfunction. They also alter brain network connectivity, creating seasonal
vulnerability:
winter favors depression and anxiety, while
summer increases the
risk of psychosis, mania, and impulsive behaviors.
Environmental and weather
influence
Weather strongly influences immune balance and
psychiatric risk.
In
winter, cold temperatures and high humidity promote
viral infections, amplifying Th1-driven inflammation and worsening depression
and anxiety.
Summer heat and allergens shift immunity toward Th2
dominance, increasing vulnerability to psychosis, mania, and impulsive
behaviors. Heatwaves and extreme temperatures correlate with higher
hospitalizations for schizophrenia and mood disorders. Sunlight generally
improves mood but can temporarily raise suicide risk in spring.
Other factors, such as low atmospheric pressure and
strong winds, show modest links to impulsivity and psychiatric admissions,
though evidence remains inconsistent.
Clinical implications and future directions
If this theory holds true, it could change how we
approach mental health care. Care could become more personalized based on the
season by adjusting medication doses, adding anti-inflammatory or anti-allergic
strategies and using biomarkers like IL-6 or Th1/Th2 ratios to predict risk.
Still, much of the evidence is observational. We need
long-term studies, standardized methods, and tools like neuroimaging and
circadian rhythm assessments to confirm these links. Understanding how seasons
shape our minds could help us move from reactive care to proactive
prevention—making psychiatry smarter, more precise, and truly patient-centered.
Read next: Winter depression: can vitamin d shed light on mood?
About the Author – Carolina Lima
Anaesthesiology specialist
Carolina is a specialist in Anaesthesiology with a deep passion for learning and sharing medical knowledge. Dedicated to advancing the field, Dr. Lima strives to bring fresh, evidence-based insights to the medical community. Viewing medicine not merely as a profession but as a lifelong journey of continuous learning, Dr. Lima is committed to making complex information clear, practical, and useful for healthcare professionals around the world.
