BMC Psychiatry,
Journal Year:
2024,
Volume and Issue:
24(1)
Published: Nov. 16, 2024
Observational
studies
have
shown
a
link
between
autoimmune
diseases
and
schizophrenia,
with
conflicting
conclusions.
Due
to
the
existence
of
confounding
factors,
causal
schizophrenia
is
still
unknown.
We
conducted
comprehensive
Mendelian
randomization
(MR)
analysis
ten
common
in
individuals
European
descent
using
genome-wide
association
(GWASs).
To
evaluate
relationships
inverse
variance
weighted,
MR-RAPS,
Bayesian
weighted
MR,
constrained
maximum
likelihood,
debiased
IVW,
MR-Egger,
median
were
utilized.
Several
sensitivity
analyses
performed
ensure
reliability
study's
results.
Our
findings
reveal
that
genetically
predicted
ankylosing
spondylitis
related
an
increased
risk
whereas
celiac
disease,
type
1
diabetes,
systemic
lupus
erythematosus
are
associated
lower
schizophrenia.
In
reverse
MR
analysis,
our
study
indicated
linked
higher
risks
spondylitis,
Crohn's
ulcerative
colitis,
inflammatory
bowel
psoriasis.
Neither
multiple
sclerosis
nor
rheumatoid
arthritis
been
vice
versa.
Despite
contradicting
some
other
observational
reports,
this
showed
support
for
gain
better
understanding
mechanisms
underlying
development
immune-mediated
additional
research
required
identify
potential
identified
studies.
Psychological Medicine,
Journal Year:
2024,
Volume and Issue:
unknown, P. 1 - 11
Published: April 2, 2024
Background
The
comorbidity
between
schizophrenia
(SCZ)
and
inflammatory
bowel
disease
(IBD)
observed
in
epidemiological
studies
is
partially
attributed
to
genetic
overlap,
but
the
magnitude
of
shared
components
causality
relationship
them
remains
unclear.
Methods
By
leveraging
large-scale
genome-wide
association
study
(GWAS)
summary
statistics
for
SCZ,
IBD,
ulcerative
colitis
(UC),
Crohn's
(CD),
we
conducted
a
comprehensive
pleiotropic
analysis
uncover
loci,
genes,
or
biological
processes
SCZ
each
UC,
CD,
independently.
Univariable
multivariable
Mendelian
randomization
(MR)
analyses
were
applied
assess
across
these
two
disorders.
Results
genetically
correlated
with
IBD
(
r
g
=
0.14,
p
3.65
×
10
−9
),
UC
0.15,
4.88
−8
CD
0.12,
2.27
−6
all
surpassed
Bonferroni
correction.
Cross-trait
meta-analysis
identified
64,
52,
66
significantly
independent
loci
associated
respectively.
Follow-up
gene-based
found
11
novel
genes
KAT5
,
RABEP1
ELP5
CSNK1G1
etc)
joint
phenotypes.
Co-expression
pathway
enrichment
illustrated
those
mainly
involved
core
immune-related
signal
transduction
cerebral
disorder-related
pathways.
In
univariable
MR,
predisposition
was
an
increased
risk
(OR
1.11,
95%
CI
1.07–1.15,
1.85
).
Multivariable
MR
indicated
causal
effect
liability
on
Actinobacteria
1.06–1.16,
1.34
)
BMI
1.04–1.18,
1.84
−3
Conclusions
We
confirmed
basis,
loci/genes,
providing
insights
into
mechanism
therapeutic
targets
underlying
Research Square (Research Square),
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 20, 2025
Abstract
Background
Various
studies
have
suggested
the
intriguing
potential
of
air
pollution
exposure
to
influence
gut
microbiota
diversity.
It
can
impact
not
only
by
directly
entering
intestine,
but
also
through
gut-lung
axis
when
deposited
in
lungs.
Nevertheless,
scarcity
compelling
genetic
causal
evidence
remains
conspicuous.
Our
objective
was
evaluate
whether
a
relationship
exists
between
and
microbiota,
along
with
implications
this
connection.
Method
This
study
designed
investigate
link
pollutant
(encompassing
PM2.5,
PM10,
PM2.5−10,
NO2,
NOx)
alterations
microbiome
using
two-sample
Mendelian
randomization
method
based
on
summary-level
GWAS
study.
To
explore
effect
pollutants
we
conducted
MR
analyses
across
five
specific
feature
levels,
including
phylum,
class,
order,
family,
genus.
The
main
analytical
approach
employed
inverse
variance
weighting
(IVW),
which
examined
outcome
assessing
single
nucleotide
polymorphisms
(SNPs)
linked
pollution..
Additional
sensitivity
analyses,
such
as
Cochran
Q
test,
MR-Egger
regression,
leave-one-out
analysis,
were
robustness
findings.
Results
A
statistically
noteworthy
association
observed
NO2
an
uptick
genus
Eubacterium
fissicatena
group
[IVW-odds
ratio
(OR)
=
2.20;
95%
confidence
interval
(CI),
1.42–3.41;
P
4.36*10−
4],
Gordonibacter
(IVW-OR
2.29;
95%CI:
1.48–3.56;
2.17*10−
4),
LachnosPiraceae
(IVW-OR
1.82;
1.32–2.51;
2.37*10−
4).
Contrarily,
decrease
abundance
Holdemania
0.616;
0.47–0.81;
6.58*10−
4)
Ruminococcus
gauvreauii
0.663;
0.53–0.83;
4.63*10−
exposure.
Furthermore,
PM2.5
associated
lower
presence
Family
XIII
0.691;
0.55–0.87;
1.47*10−
3).
Conclusion
findings
indicate
pollutants,
particularly
appeared
microbiota's
composition,
especially
for
group,
genus,
may
offer
valuable
insights
further
investigations
into
mechanisms
clinical
pollution-induced
dysbiosis
microbiome.
Translational Psychiatry,
Journal Year:
2025,
Volume and Issue:
15(1)
Published: March 21, 2025
Abstract
Mental
disorders
are
associated
with
inflammatory
bowel
disease
(IBD),
but
the
genetic
pathophysiology
is
not
fully
understood.
We
obtained
data
on
mental
disorder-related
gene
methylation,
expression,
protein
levels,
and
summary
statistics
of
IBD,
performed
Summary
data-based
Mendelian
randomization
colocalization
analyses
to
explore
causal
associations
shared
variants
between
multiple
molecular
traits
IBD.
Integrating
multi-omics
data,
we
found
QDPR
,
DBI
MAX
ulcerative
colitis
(UC)
risk,
while
HP
linked
IBD
risk.
Inverse
methylation
(cg0880851
cg26689483)
expression
observed
in
consistent
their
detrimental
role
UC.
Methylation
(cg11066750)
protects
against
UC
by
enhancing
expression.
Higher
levels
(OR
=
0.79,
95%CI
0.69–0.90)
0.74,
0.62–0.90)
encoded
proteins
inversely
higher
1.17,
1.07–1.28)
1.09,
1.04–1.14)
increase
Our
findings
advance
understanding
IBD’s
pathogenic
mechanisms
gut-brain
interaction.
Inflammatory Bowel Diseases,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Sept. 12, 2024
Abstract
Background
Psychiatric
disorders
in
patients
with
inflammatory
bowel
disease
(IBD)
represent
a
significant
but
uncertain
facet
of
the
disease,
unsolved
questions
regarding
their
overall
magnitude,
impact
on
intestinal
and
whole
burden
psychiatric
manifestations.
Aim
This
systematic
review
summarizes
evidence
prevalence
disorders,
including
depression,
anxiety,
bipolar
disorder
(BD),
schizophrenia,
among
IBD.
Methods
A
search
across
PubMed/MEDLINE,
Embase,
Scopus
databases
from
January
2010
to
2023
was
performed
identify
relevant
studies.
The
focus
studies
exploring
specific
IBD
compared
general
population
that
reported
outcome
measures.
subsequent
meta-analysis
(MA)
assessed
strength
association
between
these
data
reliability
ensured
through
rigorous
extraction
quality
assessment.
Results
Out
3,209
articles,
193
met
inclusion
criteria
only
26
provided
complete
for
comprehensive
analysis.
These
showed
significantly
higher
comorbidities
population.
MA
depression
(pooled
OR
1.42,
95%
CI
=
1.33-1.52,
P
<
.0001)
anxiety
1.3,
1.22-1.44,
.0001).
BD
1.64,
1.20-2.24,
considerable
heterogeneity
(I2
94.01%).
Only
3
examined
schizophrenia
IBD,
providing
widely
heterogeneous
results,
an
inconclusive
OR,
estimated
at
0.93
(95%
0.62-1.39,
.73).
Conclusions
highlights
high
particularly
patients,
which
exceeds
rates
is
proving
be
important
under-researched
area.
sparse
contradictory
requires
further
investigation.
findings
highlight
need
better
understanding,
early
detection,
tailored
mental
health
interventions
management
improve
patients’
life.
Pediatric Allergy and Immunology,
Journal Year:
2024,
Volume and Issue:
35(5)
Published: May 1, 2024
Abstract
Background
Inflammatory
bowel
disease
(IBD)
and
allergic
diseases
possess
similar
genetic
backgrounds
pathogenesis.
Observational
studies
have
shown
a
correlation,
but
the
exact
direction
of
cause
effect
remains
unclear.
The
aim
this
Mendelian
randomization
(MR)
study
is
to
assess
bidirectional
causality
between
inflammatory
diseases.
Method
We
comprehensively
analyzed
causal
relationship
(IBD),
Crohn's
(CD),
ulcerative
colitis
(UC)
(asthma,
Hay
fever,
eczema)
as
whole,
conjunctivitis
(AC),
atopic
dermatitis
(AD),
asthma
(AAS),
rhinitis
(AR)
by
performing
using
summary‐level
data
from
genome‐wide
association
studies.
analysis
results
mainly
came
random‐effects
model
inverse
variance
weighted
(IVW‐RE).
In
addition,
multivariate
(MVMR)
was
conducted
adjust
body
mass
index
(BMI)
on
instrumental
variables.
Results
IVW‐RE
method
revealed
that
IBD
genetically
increased
risk
whole
(OR
=
1.03,
95%
CI
1.01–1.04,
fdr.
p
.015),
AC
1.04,
1.01–1.06,
.011),
AD
1.06,
1.02–1.09,
.004).
Subgroup
further
confirmed
CD
1.02,
1.00–1.03,
.031),
1.01–1.05,
.012),
2E−05),
AAS
1.05,
1.02–1.08,
.002)
AR
1.00–1.07,
.025),
UC
0.98–1.07,
.038).
MVMR
showed
after
taking
BMI
secondary
exposure,
effects
AC,
AD,
AAS,
were
still
statistically
significant.
No
significant
observed
in
reverse
MR
analysis.
Conclusion
This
randomized
demonstrated
factor
for
diseases,
which
largely
attributed
its
subtype
increasing
ASS,
AR.
Further
investigations
are
needed
explore
IBD.
Brain Sciences,
Journal Year:
2024,
Volume and Issue:
14(6), P. 539 - 539
Published: May 24, 2024
A
growing
body
of
literature
suggests
a
link
between
bowel
syndromes
(e.g.,
irritable
syndrome
and
inflammatory
disease),
gut
microbiome
alterations,
psychiatric
disorders.
This
narrative
review
aims
to
explore
the
potential
role
in
pathogenesis
clinical
presentation
obsessive–compulsive
disorder
(OCD)
whether
there
is
sufficient
evidence
warrant
considering
gastrointestinal
symptoms
their
implication
for
during
assessment
treatment
OCD.
For
this
purpose,
PubMed
search
studies
focusing
on
OCD,
microbiota,
syndrome,
disease
was
conducted
by
two
independent
reviewers.
While
current
issues
OCD
remains
limited,
emerging
alterations
high
rates
population.
These
findings
emphasize
importance
incorporating
comprehensive
assessments
into
“global
OCD”.
Such
should
encompass
various
factors,
including
physical
comorbidities
symptoms,
nutritional
habits,
fluid
intake,
exercise
patterns,
dysfunctions
inflammation.
Considering
implications,
interventions
targeting
health,
such
as
probiotics
dietary
modifications,
may
hold
promise
improving
patients
with
comorbid
problems.
Further
research
area
warranted
better
understand
interplay
health
effectiveness
targeted
outcomes.