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Riboflavin Status and Its Association with Serum hs-CRP Levels among
Clinical Nurses with Depression

Article  in  Journal of the American College of Nutrition · October 2011

DOI: 10.1080/07315724.2011.10719977 · Source: PubMed

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Original Research

Riboflavin Status and Its Association with Serum hs-CRP

Levels among Clinical Nurses with Depression

Mahshid Naghashpour, MSc, Reza Amani, PhD, R Nutr, Sorur Nematpour, MSc, Mohammad Hosein Haghighizadeh, MSc
Department of Nutrition, Faculty of Paramedicine, Diabetes Research Centre (M.N., R.A.), Department of Clinical Psychiatrics,
Golestan Medical Center (S.N.), Department of Statistics and Epidemiology (M.H.H.), Jondi-Shapour University of Medical
Sciences, Ahvaz, IRAN
Key words: riboflavin intake, EGR-AC, depression, hs-CRP, clinical nurses

Objective: The objective of present study was to assess the relationship between the dietary intake and blood
status of riboflavin and the prevalence of systemic inflammation among both depressed and nondepressed nurses.
Methods: This was a cross-sectional study on 98 female clinical nurses (45 depressed and 53 nondepressed
subjects). Depression status was assessed using the Beck Depression Inventory. We assessed dietary intake of
riboflavin using 3-day 24-hour recalls. The serum concentrations of high-sensitive C-reactive protein (hs-CRP)
were also measured. Riboflavin status was assessed as the erythrocyte glutathione reductase activity coefficient
(EGRAC).
Results: Marginal riboflavin deficiency was more prevalent in depressed subjects (P ¼ 0.028). The results of
the dietary intake and status of riboflavin were classified to 3 tertiles of serum hs-CRP levels. In both
nondepressed and depressed subjects, there was no significant difference between hs-CRP tertiles in dietary
intakes of riboflavin, EGRAC, or riboflavin deficiencies.
Conclusion: This study showed a higher prevalence of marginal riboflavin deficiency in depressed subjects.
We found no association between dietary intake and status of riboflavin with low-grade systematic inflammation
in nondepressed and depressed clinical nurses.

INTRODUCTION better mental health [5]. Similarly, an association between high

In nurses, job stress is positively correlated with depression
[1]. Mental fatigue, trait anger, perceived stress, anger-in
expression, and state anger are the main significant predictors
influencing depression of clinical nurses [2].
In Iran, prevalence of moderate and severe depression among
nurses has been reported 21.5% and 5.4%, respectively [3].
There is mounting evidence to suggest that nutrition and
depression are intricately linked. Several epidemiological
studies have shown a high prevalence of B-group vitamin
deficiency in subjects with depression [4]. In nondepressed
young women, improved blood status of riboflavin is
significantly associated with improvement of mood in that
they felt more ‘‘agreeable,’’ more composed, and reported
serum homocysteine levels and a higher prevalence of
depressive symptoms has been reported in cross-sectional and
case-control studies [4,6–9]. Riboflavin (as a precursor for
pyridoxine) serves as a cofactor for enzymes involved in the
conversion of homocysteine to methionine and cysteine.
Accumulation of homocysteine as a result of riboflavin
deficiency may have a role in riboflavin-related psychiatric
complications [10–12].
Some studies have reported that depression is associated
with higher levels of C-reactive protein (CRP) [13–16], a
marker of systemic inflammation. Riboflavin plays a significant
role in the normal functioning of glutathione reductase (GR).
GR is an antioxidative enzyme required for the conversion of
oxidized glutathione to reduced glutathione (GSH), an

Address reprint requests to: Reza Amani, PhD, R Nutr, Department of Nutrition, Faculty of Paramedicine, Diabetes Research Centre, Jondi-Shapour University of Medical
Sciences, Ahvaz, IRAN. E-mail: rezaamani@hotmail.com
Funding for this study was provided by a research grant of Jondi-Shapour University of Medical Sciences, Iran.
Abbreviations: BDI ¼ Beck Depression Inventory, EGRAC ¼ erythrocyte glutathione reductase activity coefficient, CRP ¼ C-reactive protein, GR ¼ glutathione reductase,
GSH ¼ reduced glutathione, hs-CRP ¼ high-sensitive C-reactive protein, RBP4 ¼ retinol binding protein 4.

Journal of the American College of Nutrition, Vol. 30, No. 5, 340–347 (2011)
Published by the American College of Nutrition

340

important intracellular antioxidant [17]. GHS requires cysteine
as a rate-limiting amino acid for its synthesis [18]. Circulating
homocysteine is an inflammation marker [19]. As a result,
riboflavin deficiency and subsequent hyperhomocysteinemia
may increase inflammation and serum CRP levels.
To our knowledge, there is no published evidence evaluating
the association between dietary intake and status of riboflavin
with low-grade systemic inflammation in depressed subjects.
Hence, the main objective of the present study was to compare
dietary intake and blood status of riboflavin and its association
with serum high-sensitive CRP (hs-CRP) levels among clinical
nurses with depression and normal subjects.
MATERIALS AND METHODS
Study Population
This is an analytical cross-sectional comparative study
conducted on female clinical nurses employed in educational
university hospitals in Ahvaz City, Iran. A total of 98 nurses
(45 depressed and 53 nondepressed subjects) ranging in age
from 23 to 52 years (mean age, 37 years) participated between
April and September 2009. Calculation of sample size was
conducted based on 2 main variables (erythrocyte glutathione
reductase activity coefficient [EGRAC] and serum CRP levels).
In both depressed and nondepressed groups, the mean and
standard deviation were obtained as follows: l1 ¼ 1.28, l2 ¼
1.4, d1 ¼ 0.2, d1 ¼ 0.2 according to similar study [20]. Sample
size was calculated from a formula [n ¼ (Z1a/2 þ Z1b)2(d12 þ
d22)/(l1  l2)2]. A 3-stage sampling design was used. At each
stage, simple random sampling was applied. In the first stage of
sampling, the sampling units were educational university
hospitals (administrative units). A total of 6 out of 8 hospitals
were randomly selected. In the second stage, on average, 20
volunteers were selected randomly from each sample hospital.
A total of 120 volunteers were selected. A self-reported
questionnaire completed by volunteers assessed demographic
characteristics, disease history (chronic and psychiatric),
medication and supplement usage, pregnancy, smoking status,
and physical activity. Pregnant women and subjects who took
supplements containing B vitamins and medications such as
aspirin, metformin, and antidepressants were excluded from the
analyses. We also excluded participants with chronic diseases
such as hypertension, malignancies, allergy, asthma, polycystic
ovarian syndrome, diabetes mellitus, and cardiovascular
disease because of possible interactions with serum CRP
levels. Twenty-two individuals who were not eligible were
excluded. A total of 98 subjects were eligible. In the third stage,
98 volunteers who met inclusion criteria were categorized into
depressed and nondepressed groups (45 depressed and 53
nondepressed subjects) based on the Beck depression ques-
tionnaire scores.
JOURNAL OF THE AMERICAN COLLEGE OF NUTRITION
Riboflavin and hs-CRP in Depressed Nurses
Assessment of Depression
Depression may be manifested by a shortage of energy and
feelings of indisposition, perish, despair, uselessness, disinter-
estedness, and pessimism [21].
Depression status was assessed using the Beck Depression
Inventory (BDI). The BDI contains questions to assess all 9
characteristic attitudes and symptoms listed in the Diagnostic
and Statistical Manual of Mental Disorders, fourth edition
(DSM-IV), criteria for a major depressive episode [22]. A short
13-item version was used, and total scores were calculated.
Subjects with a BDI score equal to or greater than 5 were
classified as depressed, and nurses with a BDI score less than 5
were classified as nondepressed [23].
Methods of Dietary Assessment
We assessed dietary intake of riboflavin using a 3-day 24-
hour recall (including 2 work days and 1 off day) [24–27].
Quantities were expressed in household measures. The
inventories were checked by the study, dietitian, who verified
and classified the quantities and types of recorded foods. Daily
dietary intake of riboflavin was calculated using the Dorosti
Food Processor software, which has been developed by the
Iranian Institute of Nutrition Research and Food Industry, to
comprise the Iranian meals data set.
Biochemical Measurements
We obtained fasting blood samples, having specimens
collected into either potassium EDTA–containing tubes for
riboflavin assessment or into tubes with no anticoagulants
added for serum hs-CRP concentrations tests. The serum
concentrations of hs-CRP were measured using a particle-
enhanced turbidimetric immunoassay (quantitative diagnosis
kit for serum or plasma hs-CRP by immunoturbidimetric
method; Pars Azmoon, Tehran, Iran) with a limit of detection
of 0.10 mg/L [28].
Riboflavin status was assessed as the EGRAC using the
Goldberg and Spooner method [29] with spectrometry set in
340 nm [30] (glutathione reductase kit, Randox, UK). We used
cutoffs specified for this EGRAC assay (i.e., values between
1.2 and 1.4 denoted marginal deficiency and values greater than
1.4 denoted severe deficiency [31]).
Statistical Analysis
The Kolmogorov-Smirnov test was used to determine
whether the variables were normally distributed. Outcome
variables tested for normality were dietary intake of riboflavin,
EGRAC, and serum hs-CRP levels. The significance of
differences between the serum hs-CRP concentrations of the
two groups was tested by the Student t test, for independent
samples. Continuous, normally distributed variables are
reported as means and 95% confidence intervals (95% CIs).
341
Riboflavin and hs-CRP in Depressed Nurses
To verify the association between CRP and the other variables,
we used Pearson’s correlation coefficient. To estimate the
degree of change produced in serum CRP concentration by
modifications of the independent variable value, we calculated
the antilogarithm of the B regression coefficient (the slope of
the regression curve).
Descriptive statistics was used to determine the mean and
standard deviation of quantitative variables and categorization
of hs-CRP levels in 3 tertiles (T1–T3). Statistical analyses were
performed by the Statistical Package for Social Sciences
(SPSS) version 17 (SPSS Inc., Chicago, Ill), and the
statistically significant level was considered at P , 0.05.
Medical Ethics Approval
The study protocol was approved by the Medical Ethics
Committee of Jondi-Shapour University of Medical Sciences.
All participants gave their written consents, and no names were
disclosed.
RESULTS
Descriptive Results
The demographic characteristics, psychiatric, and anthro-
pometric measurements of participants are shown in Table 1. A
significantly higher proportion of depressed subjects (20%)
reported a family history of psychiatric problems compared
with nondepressed subjects (20% vs. 1.9%; P ¼ 0.004). There
was no significant difference in anthropometric indices,
demographic factors, or psychiatric variables between de-
pressed and nondepressed groups.
Comparison of Dietary Intake and Status of
Riboflavin between Depressed and Nondepressed
Nurses
There was no significant difference between the 2 groups in
dietary intake of riboflavin or GR activity. The percentage of
riboflavin deficiency severity was significantly different
between the 2 groups. Marginal riboflavin deficiency was
more prevalent in depressed subjects, while the number of
severely deficient subjects was higher among nondepressed
subjects (P ¼ 0.028; Fig. 1).
Serum hs-CRP Measurement
The means and standard deviations of serum hs-CRP levels
and percentage of risk measurements in depressed and
nondepressed subjects are illustrated in Table 1. In this study,
we used the risk evaluation guidelines proposed by the
American Heart Association and Centers for Disease Control
and Prevention for categorizing hs-CRP levels [32–34]. There
342
was no significant difference between the 2 groups in serum hs-
CRP concentrations. Eight (18.6%) depressed and 7 (13.2%)
nondepressed subjects had serum CRP concentrations of 5 mg/
L or greater, reflecting a coronary heart disease risk.
Relationship between hs-CRP and Dietary Intake
and Status of Riboflavin
The dietary intake and status of riboflavin classified
according to tertiles of serum hs-CRP levels (T1–T3) are
shown in Tables 2 and 3. In depressed (Table 2) and
nondepressed (Table 3) subjects, there was no significant
difference between hs-CRP tertiles in dietary intakes of
riboflavin, EGRAC, and riboflavin deficiencies. In addition,
there were no significant differences between the 2 groups in
terms of dietary intake and status of riboflavin based on tertiles
of hs-CRP. When a linear regression model was used, the
EGRAC showed no significant or independent association with
hs-CRP. Having 1 unit more EGRAC was associated with, on
average, 4.58% higher serum hs-CRP concentrations in
depressed subjects. Pearson’s correlation coefficient shows a
near-significant association between the dietary intake of
riboflavin and hs-CRP serum levels in depressed subjects (r
¼ 0.315, P ¼ 0.054; Table 4).
DISCUSSION
The subjects in the present study were clinical nurses
working at a number of educational hospitals in Ahvaz, Iran.
Nurses are one of the high-risk groups in terms of psychosocial
risk at work. This occupation has been recognized as a stressful
occupation in both developing and developed countries [35].
On the other hand, job stress [1], less job control, lower job
fitness, and poorer interpersonal relationships are most
obviously associated with depression in clinical nurses [36].
Improving programs and interventions designed to reduce
stress and depression may help improve job satisfaction in
clinical nurses. Hence, the objective of the present study was to
assess the relationship between the dietary intake and blood
status of riboflavin and the prevalence of low-grade systemic
inflammation among depressed and nondepressed clinical
nurses.
In this study, there was no difference between depressed
and nondepressed clinical nurses in dietary intake of riboflavin.
In 2 cross-sectional studies [10,37], no statistical association
between dietary intake of riboflavin and depressive symptoms
was found. The results from these studies were similar to ours
in terms of sample number, similarity of age ranges, and dietary
riboflavin intake in depressed and nondepressed subjects. In
another cross-sectional study on the elderly population, an
inverse association was found between riboflavin intake and
depression [38]. However, dietary riboflavin intake was
VOL. 30, NO. 5
 Riboflavin and hs-CRP in Depressed Nurses

Table 1. Demographic, Anthropometric, Psychiatric, Biochemical, and Dietary Indices of Participants*

Variable Nondepressed (n ¼ 53) Depressed (n ¼ 45) P Value

Demographic
Age (years)** 36.45 (6.02) 37.26 (6.5) 0.532
Years of service** 5.72 (12.75) 12.63 (6.85) 0.925
Marital status 
Single 54.1 (20) 45.9 (17) 0.581
Married 54.1 (33) 45.9 (28)
Shift working 
Yes 35.8 (19) 53.3 (24) 0.062
No 64.2 (34) 46.7 (21)
Anthropometric
Weight (kg)** 64.26 (10.42) 67 (12.49) 0.241
Height (cm)** 159.2 (4.88) 158.82 (6.63) 0.737
BMI (kg/m2)** 25.39 (4.40) 26.5 (4.56) 0.196
%BF  30.7 (6.4) 31.86 (6.59) 0.382
Psychiatric 
Depression history
Yes 3.9 (2) 13.6 (6) 0.092
No 96.1 (49) 86.4 (38)
Other psychiatric problems, history
Yes 4 (2) 2.2 (1) 0.54
No 96 (48) 98.8 (44)
Psychiatric problems, history in families
Yes 1.9 (1) 20 (9) 0.004
No 98.1 (52) 80 (36)
Family relationship
Good 100 (52) 71.1 (32) 0.07
Moderate 0 (0) 24.4 (11)
Weak 0 (0) 4.4 (2)
Biochemical
hs-CRP (mg/L)** 2.18 (2.52) 2.16 (2.42) 0.743
Percentage of risk measurements 
,1 mg/L (low risk) 44.3 (23) 44.2 (19) 0.885
1–3 mg/L (medium risk) 38.5 (20) 34.9 (15)
.3 mg/L (high risk) 17.3 (9) 30.9 (9)
EGRAC** 1.62 (0.77) 1.31 (0.37) 0.001
GR activity (U/g HB)** 9.03 (3.48) 8.9 (3.43) 0.695
Riboflavin deficiency severity 
Low risk (normal) 44.4 (20) 48.7 (19)
Medium risk (marginal) 4.4 (2) 23.1 (9) 0.016
High risk (severe) 51.1 (23) 28.2 (11)
Dietary**
Riboflavin intake(mg/day) 2.01 (1.08) 1.68 (0.76) 0.143
%BF ¼ body fat percentage, BMI ¼ body mass index, EGRAC ¼ erythrocyte glutathione reductase activity coefficient, GR ¼ glutathione reductase, hs-CRP ¼ high-
sensitive C-reactive protein.
* Independent-sample t test and chi-square tests were conducted to determine the difference between the basic variables of the 2 groups.
** Quantitative data are presented as mean (SD).
 
The figures in parentheses indicate percentages.

evaluated by food frequency questionnaires. The accuracy of
data obtained from the food frequency questionnaire of persons
with depression may be questionable. In a randomized placebo-
controlled double-blind study, treatment with 10 mg riboflavin
in geriatric patients with depression was significant toward
greater improvement in scores of depression and cognitive
function [39]. Because elderly people are at risk of undernu-
trition [40] and also have higher prevalence of cognitive
impairment and depression [38], anorexia observed in these
studies may be the cause of low riboflavin intake.
In this study, EGRAC was significantly higher in
nondepressed than in depressed subjects. Also, marginal
riboflavin deficiency was 5 times higher in depressed compared
with nondepressed nurses. Similar results were reported in
other studies [5,41–43]. Benton et al. [5] showed an association
between riboflavin supplementation and an improvement in
mood. Riboflavin deficiency leads to increased homocysteine
serum levels that may have a role in creating psychiatric
complications of riboflavin deficiency [12,44]. Riboflavin
coenzymes are needed for remethylation and trans-sulfuration

JOURNAL OF THE AMERICAN COLLEGE OF NUTRITION 343

Riboflavin and hs-CRP in Depressed Nurses
Fig. 1. The frequency of riboflavin deficiency in depressed and healthy
subjects. * Chi-square ¼ 7.18, P ¼ 0.028, 95% confidence interval
Monte Carlo significance (2 tails): 0.25–0.032, P value for trend ¼
0.589.
of homocysteine [45]. Furthermore, the peripheral neuropathy
produced in young chickens by riboflavin deficiency has been
characterized by a generalized demyelinating polyneuropathy
[46]. Riboflavin deficiency in rats has decreased myelin lipids,
including serebroside, esfingomielin, and phosfatidil ethanol-
amine. Thus, riboflavin can have a role in the metabolism of
essential fatty acids in brain lipids, and the pathological effects
of riboflavin deficiency (such as depression) are similar to
deficiency of essential fatty acids, along with brain growth and
differentiation disorders [47].
The mean of EGRAC and severe riboflavin deficiency was
higher in nondepressed than in depressed nurses. It has been
suggested that in a severe riboflavin deficiency, the erythrocyte
glutathione reductase apoenzyme may be reduced as well as the
flavin coenzyme. In such an instance, a low activation
coefficient could result in an erroneous assessment of riboflavin
status [31].
This study shows that the frequency distributions and means
of CRP concentrations in our samples are higher than those
previously described for other white populations from Europe,
the United States, and Asia [28,34,48–51] and lower than in the
Australian population [51].
Moreover, we found no evidence that depressive symptoms
were associated with increased levels of hs CRP. In a similar
study on middle-aged and older Chinese, there was no evidence
Table 2. Relations of Tertiles of High-Sensitive C-Reactive Protein Concentrations with Riboflavin Status in Depressed Subjects
Variable T1 (0.02–0.654 mg/L)
Dietary riboflavin* (mg/d) 1.79 (1.2 to 2.4)
EGRAC* 1.2 (0.96 to 1.5)
GR activity (U/g HB)* 9.6 (7.7 to 11.6)
Riboflavin deficiency severity**
Normal 30 (3)
Marginal 60 (6)
Severe 10 (1)
EGRAC ¼ erythrocyte glutathione reductase activity coefficient, GR ¼ glutathione reductase, T ¼ tertile.
* Quantitative data presented as mean (95% confidence interval). Analysis of variance test was conducted to determine the difference between tertiles.
** Chi-square test was conducted to determine the difference between tertiles. The figures outside of the parentheses are indicating percentages.
344
indicating depressive symptoms were associated with increased
levels of various inflammatory factors (CRP and interleukin-6)
and adipokines (adiponectin, resistin, plasminogen activator
inhibitor-1) and retinol binding protein 4 (RBP4)] [50].
Nevertheless, it is suggested that this association might be
mediated by various confounders (such as poor health status,
obesity, and lifestyle) [10].
Our study showed no significant association between serum
hs-CRP levels with dietary intakes and status of riboflavin in
nondepressed and depressed subjects, but we found a near-
significant association between serum hs-CRP levels and
dietary intakes of riboflavin in depressed subjects.
These results confirm previous findings regarding the
association of serum CRP concentration with riboflavin status.
Gariballa and Foster [52] did not find any significant difference
in B-group vitamins (red blood cells, folate, B2, and B12)
between individuals with CRP ,10 and 10 mg/L. Tavares et
al. [53] found that riboflavin supplementation significantly
decreased plasma homocysteine and EGRAC but not plasma
CRP levels. However, it is worthy to note that the subjects were
an elderly population with riboflavin deficiency status.
In a cross-sectional study on immigrant women from the
Middle East (Iranian and Turkish) with high oxidative stress
and low-grade inflammation, riboflavin intake was not
consistently different between immigrated and Swedish women
[54].
There is little information on levels of positive acute phase
proteins such as CRP and alteration in EGRAC status [55].
Since the coenzyme form of riboflavin, flavin mono nucleotide,
is required for conversion of pyridoxine to its functional form
(i.e., pyridoxal phosphate) [56], the mechanism of relationship
between riboflavin deficiency and inflammation may be related
to B6 vitamin status. In addition, pyridoxine is a coenzyme
required for converting homocysteine to methionine. Hence,
riboflavin deficiency may increase homocysteine with second-
ary pyridoxine deficiency. Moreover, riboflavin has a role in
regeneration of GSH, an important intracellular antioxidant,
and glutathione requires cysteine as a rate-limiting amino acid
for its synthesis [18].
In cellular function, it seems that riboflavin-dependent
mechanisms protect cells from oxidative stress [54]. Thus, it is
T2 (0.655–1.95 mg/L) T3 (1.96–11.1 mg/L) P Value
1.53 (1.2 to 1.8) 2 (1.4 to 2.5) 0.279
1.3 (1.1 to 1.5) 1.6 (0.98 to 2.3) 0.260
9.1 (7.6 to 10.6) 8.3 (5.6 to 10.9 ) 0.643
60 (12) 53.8 (7) 0.491
10 (2) 7.7 (1)
30 (6) 38.5 (5)
VOL. 30, NO. 5
 Riboflavin and hs-CRP in Depressed Nurses

Table 3. Relations of Tertiles of High-Sensitive C-Reactive Protein Concentrations with Riboflavin Status in Nondepressed Subjects

Variable T1 (0.02–0.654 mg/L) T2 (0.655–1.95 mg/L) T3 (1.96–11.1 mg/L) P Value

Dietary riboflavin* (mg/d) 2.2 (1.7 to 2.7) 1.8 (1.2 to 2.3) 2.1 (1.6 to 2.7) 0.467
EGRAC* 1.4 (0.86 to 1.9) 1.5 (1.11 to 1.9) 1.5 (1.1 to 1.8) 0.940
GR activity (U/g HB)* 9.6 (7.8 to 11.3) 9.6 (7.9 to 11.3) 7.7 (6.3 to 9.7) 0.285
Riboflavin deficiency severity**
Normal 57.1 (8) 57.1 (12) 44.4 (8) 0.376
Marginal 0 (0) 0 (0) 11.1 (2)
Severe 42.9 (6) 42.9 (9) 44.4 (8)
EGRAC ¼ erythrocyte glutathione reductase activity coefficient, GR ¼ glutathione reductase, T ¼ tertile.
* Quantitative data are presented as mean (95% confidence interval). Analysis of variance test was conducted to determine the difference between tertiles.
** Chi-square test was conducted to determine the difference between tertiles. The figures outside of the parentheses indicate percentages.

possible that riboflavin deficiency increases serum CRP levels
due to the lowered level of vitamin B6.
We assessed dietary intake of riboflavin using a 3-day 24-
hour recall (including 2 work days and 1 off day) similar to the
studies on overweight and obese adults [27], pregnant women
[25], and elderly populations [24,26].
This study has some limitations. Because our study was a
cross-sectional one, the causative nature of the associations
cannot be established. Further longitudinal, cohort investiga-
tions and clinical interventions are necessary to evaluate
whether riboflavin deficiency is associated with low-grade
systematic inflammations among depressed adults and to
determine possible mechanisms of any preventative effect
from riboflavin supplementation against inflammation.
It could be a strong point of our study that we controlled
family and individual psychiatric history and also sociocultural
factors. Therefore, the results of the BDI were not possibly
affected by these factors.
CONCLUSION
Our results showed a higher prevalence of marginal
riboflavin deficiency in depressed subjects. We found no
association between dietary intake and status of riboflavin with
low-grade systematic inflammation in nondepressed and
depressed subjects.
Because of the cross-sectional design of the study, the
causative relation of the associations cannot be established.
Table 4. The Association between Dietary Intake and Status of
Riboflavin with High-Sensitive C-Reactive Protein Serum
Levels in Depressed and Nondepressed Subjects
Nondepressed Depressed
Variable r* P Value r P Value
EGRAC 0.145 0.342 0.018 0.913
Dietary riboflavin* (mg/d) 0.036 0.827 0.315 0.054
EGRAC ¼ erythrocyte glutathione reductase activity coefficient.
* Pearson’s correlation coefficient.
Further longitudinal investigations and clinical interventions are
necessary to evaluate whether riboflavin deficiency is associated
with low-grade systematic inflammations among depressed
adults and to determine possible mechanisms of any preventa-
tive effect from riboflavin supplementation against depression.
ACKNOWLEDGMENTS
This study was supported by a grant of Vice-Chancellor for
Research Affairs, Jondi-Shapour University, as an approved
MSc final thesis. We wish to thank Mr. Ahmad Hemadi (PhD
candidate) for his kind laboratory assistance.
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Received June 20, 2010; revision accepted August 17, 2011.
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