Small sample size (only 20 people) - but interesting to see if this line of research goes anywhere, based on future studies:
A recent study published in the journal Early Prevention in Psychiatry aimed to determine the relationship between vitamin D status and symptom severity among schizophrenic patients. The researchers measured the vitamin D levels of 20 recent onset schizophrenic patients and 20 healthy controls. Each participant underwent neurocognitive testing, focusing on verbal fluency, attention, processing speed, memory and executive functioning. All schizophrenic participants were clinically evaluated for depression in addition to positive and negative schizophrenic symptoms.
Here is what the researchers found:
- There was no significant difference in average vitamin D levels between the schizophrenic and healthy participants (p > 0.05).
- The average vitamin D status of schizophrenic and healthy participants were 28.2 ng/ml and 29.9 ng/ml, respectively.
- Among schizophrenic participants, greater severity of negative symptoms was correlated with lower vitamin D status (r = -0.55, P = 0.012).
- Overall symptom severity and positive symptom severity approached a significant relationship with vitamin D status (r = -0.42, P = 0.07 and r = -0.36, P = 0.12, respectively).
- No relationship was seen between vitamin D status and depressive symptoms.
- More severe cognitive deficits were associated with lower vitamin D levels among schizophrenic patients (r = 0.56, P = 0.019).
Conclusion:
This study found that lower vitamin D levels in schizophrenia
subjects were associated with more severe negative symptoms and
overall cognitive deficits. However, the cross-sectional design precludes
any conclusions about whether low vitamin D status in fact causes more
severe negative symptoms and cognitive impairments. No relationship was
found between lower vitamin D levels and depressive symptoms.
DISCUSSION
This study is the first, to our knowledge, to report
an association of vitamin D insufficiency and
more severe negative symptoms and poorer
neurocognitive function in patients with schizophrenia.
These findings lead us to hypothesize that
inadequate vitamin D status may account for some
portion of the symptom burden experienced by
persons with schizophrenia.
As much of the disability
experienced by persons with schizophrenia
is related to severity of negative and cognitive
symptoms and there are currently no approved
pharmacologic methods to treat these symptoms,
we hypothesize that correcting vitamin D insuffi-
ciency in schizophrenia could fill a critical role. It has
been shown that dietary intake of vitamin D is associated
with decreased risk of moderate and high level
psychotic symptoms in women from the
general population in Sweden.
It is conceivable that
vitamin D replacement could be a low-cost intervention
that may reduce symptom burden in patients
with schizophrenia who have low 25OHD levels.
Even in the absence of definitive studies showing
benefit of vitamin D supplementation for cognition
and negative symptoms, correction of insufficient
vitamin D status is strongly recommended for
prevention of osteoporosis, and there is growing
evidence for prevention of cancers, cardiovascular
illness and diabetes.
There is convincing evidence that vitamin D has a
role in healthy brain function. The vitamin D receptor
and the enzyme needed for the hydroxylation of
the precursor molecule 25OHD to the active form,
1-α-hydroxylase, have widespread expression in the
adult human brain. Many of these brain regions
are implicated in schizophrenia, including the
hippocampus, thalamus, hypothalamus, amygdala,
prefrontal cortex, cingulate gyrus and temporal
lobe.
Evidence of a correlation between development
of schizophrenia and low prenatal and early
life vitamin D status has been demonstrated in
many studies. There is a highly significant peak in
schizophrenia births in winter time, when risk of
vitamin D deficiency is high. Incidence of schizophrenia
is higher in immigrants, especially darkskinned
people moving to higher latitudes, a
scenario which promotes low vitamin D levels.
A Finnish birth cohort study showed that vitamin D
supplementation of at least 2000 IU per day in male
infants during the first year of life reduced the risk of
developing schizophrenia by 77% compared with
those receiving less than 2000 IU per day.23 Finally,
low maternal vitamin D status may increase the
subsequent risk of schizophrenia in the developing
fetus.24 A plausible role in schizophrenia pathology
is also suggested by the finding that vitamin D acts
to regulate transcription of many genes involved in
pathways implicated in schizophrenia, including
genes involved in synaptic plasticity, neuronal
development and protection against oxidative
stress.
In this study, those with schizophrenia were no
more likely to have insufficient vitamin D than those
in the healthy control group, indicating that low
vitamin D status in late adolescence or early adulthood
is unlikely to be causally related to schizophrenia
risk in these subjects. We matched control
subjects to patients based on sex, age and date of
blood draw, three important factors affecting
vitamin D level.
Unfortunately, we were unable to
control for body mass index (BMI), smoking status,
dietary vitamin D intake and activity level that are
other important factors affecting vitamin D status.
Additionally, there was little ethnic diversity in the
sample that will limit the ability to generalize results
to different populations. A particular strength of this
study is that all subjects did not receive more than
16 weeks of cumulative antipsychotic treatment,
and duration of psychosis was less than 5 years.
Despite this, exposures of this length of time may be
sufficient to impact vitamin D status through
increases in BMI. It is hypothesized that antipsychotic
associated hyperprolactinaemia is a risk
factor for osteoporosis by causing hypogonadism,
but it is not known whether there are direct effects of
the antipsychotic medications on vitamin D status.
Despite all of these risk factors for low vitamin D
status, an equal percentage of the first-episode
schizophrenia and healthy control subjects had
insufficient 25OHD levels, roughly half.
Full source here: