Biol Trace Elem Res (2017) 175:287–297
DOI 10.1007/s12011-016-0785-1
Association Between Antioxidant Intake/Status and Obesity:
a Systematic Review of Observational Studies
Banafshe Hosseini 1 & Ahmad Saedisomeolia 1,2,3,4 & Margaret Allman-Farinelli 3
Received: 7 May 2016 / Accepted: 14 June 2016 / Published online: 22 June 2016
# Springer Science+Business Media New York 2016
Abstract The global prevalence of obesity has doubled in
recent decades. Compelling evidences indicated that obesity
was associated with lower concentrations of specific antioxi-
dants which may play a role in the development of obesity-
related diseases such as cardiovascular disease. The present
review aimed to synthesize the evidence from studies on the
association between obesity and antioxidant micronutrients in
a systematic manner. Data bases including MEDLINE,
Science Direct, and Cochrane were searched from inception
to October 2015. Thirty-one articles were reviewed using the
MOOSE checklist. Lower concentrations of antioxidants have
been reported in obese individuals among age groups world-
wide. Circulatory levels of carotenoids, vitamins E and C, as
well as zinc, magnesium, and selenium were inversely corre-
lated with obesity and body fat mass. However, studies dem-
onstrated inconsistencies in findings. Lower status of caroten-
oids, vitamins E and C, zinc, magnesium, and selenium ap-
pears to be associated with adiposity. Intervention studies may
be needed to establish the causality of these associations.
Keywords Carotenoids . Vitamin C . Vitamin E . Zinc .
Obesity . Adiposity
* Ahmad Saedisomeolia
A.Saedisomeolia@westernsydney.edu.au
1
School of Biomedical Sciences and Pharmacy, Faculty of Health and
Medicine, University of Newcastle, Callaghan, NSW, Australia
2
Department of Pharmacy, School of Medicine, Western Sydney
University, Richmond, NSW, Australia
3
School of Molecular Bioscience, University of Sydney,
Sydney, NSW, Australia
4
School of Medicine, Campbelltown Campus, Western Sydney
University, Richmond, NSW 2560, Australia
Introduction
The rise in prevalence of obesity is a major threat to public
health worldwide and associated with an increased risk of
morbidity and mortality from chronic conditions, including
cardiovascular disease, cancers, and type II diabetes [1].
Recent evidence indicates that excess body fat may en-
hance oxidative stress measured mainly by urinary F2-
isoprostanes [2]; consequently, the generated free radicals
may play a major role in the etiology and development of
obesity-related co-morbidities [3], and data indicates that
antioxidant nutrients may have protective effects on these
conditions [4].
Recent research demonstrates that lower than normal levels
of some antioxidants may be linked with increased fat depo-
sition in the body [5]. It is now well-documented that over-
weight and obese individuals have lower blood concentrations
of antioxidants compared to non-overweight and non-obese
individuals. Also, concentrations of circulating antioxidants
are inversely related to body mass index (BMI) [6–8]. Intake
of fruit and vegetable is associated with a lower risk of obesity,
but whether the mechanism involves lack of antioxidants is
uncertain [9]. Studies indicate that obese individuals may have
to ingest a greater amount of some antioxidants to attain the
same plasma level as a normal-weight person [10] Findings
from clinical trials investigating the effects of supplementation
with these antioxidant nutrients on chronic diseases incidence
have not resulted in any beneficial reduction in these condi-
tions [11].
The aim of this systematic review was to synthesize the
evidence regarding the association between antioxidant intake
or status and obesity given the growing body of research lit-
erature base over the past three decades. We hypothesized that
obesity may be inversely associated with antioxidant intake as
well as status.
288
Methods
Search Strategy
The following databases were used from inception to the pres-
ent: MEDLINE, Science Direct, and Cochrane. The following
search terms were used individually or in combination accord-
ing to the Medical Subject Heading (MeSH) terms:
Bantioxidants,^ Bvitamin E,^ Btocopherol,^ Bcarotenoids,^
Bascorbic acid,^ Bvitamin C,^ Bmineral antioxidant,^ Bzinc,^
Bmagnesium,^ Bselenium,^ Bobesity,^ Badiposity,^ and
Boverweight.^ The search was limited to human studies with
no restrictions on gender, age, or ethnicity. A manual search of
references cited by the identified studies was also conducted.
Study Selection
Citations from the searches were imported into referencing
software Endnote X6. Title and abstract were screened for
inclusion criteria. Only studies with case-control, cross-sec-
tional, and prospective cohort designs with a control or refer-
ence group were included. Intervention studies, case studies,
case reports, animal studies, and ecological studies in humans
were excluded. Review articles were collected for the pur-
poses of reviewing the bibliography list, but did not contribute
to the final number of studies considered eligible unless they
also contained original data. Supporting evidence was provid-
ed by in vitro studies of adipocytes, ex vivo, cellular, genomic,
or mechanistic outcomes reported in eligible human studies.
There were no language or date restrictions. The study factor
was antioxidant nutrients, and primary outcome in studies was
overweight or obesity based on BMI and measures of adipos-
ity (e.g., fat composition, skin-fold thickness) were regarded
as secondary outcomes.
A copy of articles that meet the inclusion criteria was ob-
tained for full-text review, unless the article was not available
after all attempts to retrieve. Full text of articles that could not
be assessed for relevance based on the title and abstract screen
were also obtained to determine eligibility. Studies were not
considered further when the title and abstract clearly indicated
that the study did not meet the inclusion criteria described
above. The primary reason for excluding studies was if the
article contained original data relevant to our eligibility criteria
or not.
Data Extraction and Study Synthesis
One researcher was responsible for data extraction into a
custom-designed table and it was checked by a second re-
searcher. Extracted data included titles, authors, study design,
participant characteristics, study factor (e.g., concentration of
antioxidants), analysis with adjustment for confounding, main
outcome measure, and findings including statistical
Hosseini et al.
significance. Studies were grouped by the study factor, i.e.,
carotenoids, vitamin E, vitamin C, and minerals, for synthesis
of findings.
Study Quality
Study quality was assessed by the primary data extractor
(BH). We considered the factors in the MOOSE statement
for reporting of observational studies [12]. Studies that had
clear descriptions of the population and methods, unbiased
assessments of antioxidant status, and outcomes validated sta-
tistical analysis including multivariable analysis adjusting for
age, race, no obvious reporting omissions, or errors, and
<20 % dropouts were considered as good quality articles.
Studies that had some deficiencies in the above criteria, al-
though unlikely to cause major bias, were considered as fair
quality. Finally, poor quality studies that were not included in
this review had major deficiencies such that major bias which
could not be included.
Results and Discussion
Initially, 1100 abstracts were identified. Based on the titles and
abstracts, 106 articles were retrieved for full-text review.
Finally, 31 articles qualified to be reviewed (see Fig. 1). The
summary of studies on the association between antioxidant
intake/status and obesity is presented as Table 1. Supporting
studies that have similar results were excluded from Table 1.
Characteristics of Included Studies
The majority of studies were conducted in adults with only
eight performed in children [13–20]. Cross-sectional design
was most commonly used with eight case-control studies [15,
18, 20–25] and two cohort studies [5, 26]. The majority of
studies were conducted in the USA [17, 23, 27–29] but also in
Australia [4], Brazil [15, 16, 30], Chili [19], Finland [31],
France [32, 33], India [6], Israel [24], Italy [1], Japan [2],
Mexico [34], New Zealand [14], Norway [8, 26], Spain [10],
Sweden [7, 35], Swiss [13], Thailand [25], Taiwan [21, 22],
Turkey [18, 20], and UK [5]. Twenty-three studies measured
BMI as primary outcome but additional outcomes included
weight z score, weight-for-length/height z score (WHZ) (chil-
dren) [13, 14, 16, 19], abdominal sagittal diameter [35], and
percentage body fat [6, 7, 34]. Eleven studies were deemed of
good quality and 20 studies were considered as having fair
quality. Since some studies addressed the association between
several nutrients and obesity, the findings were divided to
different sections according to each nutrient.
Association Between Antioxidant Intake/Status and Obesity 289

Fig. 1 Papers identified through MEDLINE n=940

study selection process
Science Direct n= 93
Cochrane Library n= 67

1100 potentially relevant

studies were identified and
screened
994 excluded by screening of
abstract- ineligible outcome
variables, full text unavailable,
duplicates

106 studies retrieved for

detailed evaluation

75 excluded:
5 review studies
21 intervention studies
12 experimental studies
37 outcome not overweight
/obesity
31 references included in
the final systematic review

Association Between Carotenoid Status/Intake
and Obesity
Seventeen studies (13 cross-sectional, and 4 case-control stud-
ies) assessed the relationship between dietary or plasma carot-
enoids and obesity. It has been demonstrated that plasma or
serum concentrations of carotenoids, such as β-carotene, can
be regarded as markers of fruit and vegetable intake [36, 37],
and evidence suggests that a high consumption of fruits and
vegetables protects against obesity [9] and its related health
consequences such as cancer and cardiovascular disease [38].
The cross-sectional studies were of two basic designs: either
measurements of both dietary intake and serum concentrations
were assessed and associations with BMI, waist circumfer-
ence, or other measures of adiposity were examined; or rela-
tionships between serum concentrations and measures of ad-
iposity only were studied. Vioque et al. [10] reported that
dietary carotenoids were positively correlated with plasma
concentration (P < 0.01), and BMI had a negative association
with plasma carotenoid level. Specifically, plasma concentra-
tions of carotenoids were lower in adult participants with BMI
≥25 kg/m2 compared to those who had BMI <25 kg/m2 (α-
carotene, P = 0.001; β-carotene, P = 0.10; lycopene,
P = 0.006). The study also indicated positive associations of
BMI and consumption of α-carotene and lutein + zeaxanthin,
which suggests dietary intake of these nutrients in individuals
with high BMI fails to predict their plasma concentrations.
Similarly, Galan et al. [32] studied 1821 women aged 35–
60 years and 1307 men aged 45–60 years, and observed that
serum β-carotene levels were lower in obese participants. The
study also demonstrated that there were positive associations
of dietary β-carotene with its serum concentrations. The find-
ings of the National Health and Examination Survey, cycle III
(NHANES III) in children [17], also reported low serum con-
centrations of carotenoids in obese in the absence of differ-
ences in dietary intakes. Therefore, an adult with BMI ≥30
may have to consume a higher amount of α-carotene or β-
carotene to attain the same plasma level as a person with BMI
<25 kg/m2 as might an obese child. Other cross-sectional
studies that only assessed serum concentrations demonstrated
that serum levels of β-carotene were negatively associated
with all measures of obesity, both general and central adipos-
ity (P < 0.05) [4, 7, 16, 30]. However, in one cross-sectional
study [39] the serum concentration of β-carotene was inverse-
ly correlated with body mass index, although it was significant
only for men (P < 0.05) and not for women.
In a 7-year prospective study by Andersen et al. [26] of
3071 black and white men and women, serum carotenoids
Table 1 Characteristics and outcome measures of studies examining the association between antioxidant intake/ status and obesity
290

Study Country Characteristics Full model adjustments Outcome Findings

measure(s)

Vioque et al. Spain Cross-sectional study 252 men and 293 women Sex, age, smoking, alcohol intake, BMI Intake of carotenoids and vitamin C were correlated with their
[10] Mean age 73.5 years supplement intake, fasting state respective plasma concentration (P < 0.01). BMI had a
Target biomarker(s): dietary intake and plasma negative association with plasma carotenoids level
levels of carotenoids and vitamin C (P < 0.01). No significant correlation was observed
between vitamin C concentration and BMI.
Wallstrom Sweden Cross-sectional study Sex, age, smoking, alcohol intake BMI, WC, WHR, Serum concentration of β-carotene was negatively associated
et al. [7] 253 men and 276 women aged 46–67 years body fat percent with general and central adiposity (P < 0.05). Serum level
Target biomarker(s): dietary intake and serum of α-tocopherol was correlated with central adiposity after
levels of β-carotene and α-tocopherol accounting for body fat (P < 0.05). WC and WHR had a
significant positive association with serum α-tocopherol
concentration in both genders (P < 0.05), while, measures
of general obesity were not significant, with the exception
of BMI in men.
Coyne et al. Australia Cross-sectional study Sex, age, education, vitamin and BMI, WC All the serum carotenoids were negatively associated with
[4] 646 men and 890 women aged ≥25 years mineral use, alcohol intake, BMI status, which was significant for all of the carotenoids
Target biomarker(s): serum levels of carotenoids smoking, physical activity level (P < 0.05).
Andersen Norway Prospective cohort study 3071 black and white Sex, age, race, field center, smoking, BMI Obese participants (BMI ≥ 30 kg/m2) had 22 % lower levels
et al. [26] participants of both genders followed up for physical activity level, vitamin of carotenoids compared to those with BMI <22 kg/m2
7 years and mineral use, alcohol (P < 0.05).
Target biomarker(s): serum levels of carotenoids consumption, energy intake,
vegetable and food intake
Sarni et al. Brazil Case-control Sex, age WHZ Low carotenoid concentrations were reported in the obese in
[16] 46 preschool children, 23 obese (cases), 23 relation to the matched counterparts (82 vs. 26.6 %,
non-obese (controls) matched by sex and age P = 0.0054 and OR = 12.4).
Mean age 5.7 years
Target biomarker(s): serum levels of carotenoids
Valente et al. Brazil Cross-sectional 471 children (aged 7–9.9 years) Sex, age Sex- and age- The mean carotenoids was significantly lower in overweight
[30] and adolescents (aged 10–17 years) specific BMI children and adolescents (30.40 ± 16.74 vs. 43.06 ±
Target biomarker(s): serum levels of carotenoids 25.26 μg/dL, P = 0.001).
Öhrvall et al. Sweden Cross-sectional 906 Swedish participants of Sex, age, smoking, physical Abdominal sagittal α-Tocopherol concentration was inversely correlated to
[35] both genders activity diameter abdominal sagittal diameter (r = −0.24, P = 0.0001).
Target biomarker(s): serum levels of α-tocopherol
Myara et al. France Case-control 75 non-diabetic normotensive Age, alcohol intake, smoking BMI, WHR Vitamin E levels were significantly lower in the severely
[33] obese (cases) and 13 healthy non-obese obese participants (BMI >35 kg/m2) compared to the
participants (controls) controls (P < 0.0001). Serum α-tocopherol concentration
Target biomarker(s): serum levels of α-tocopherol was negatively correlated with BMI (r = 0.53,
P < 0.0001) and WHR (r = 0.40, P = 0.0003).
Reitman et al. Israel Case-control 25 obese participants (cases) 25 Age, sex, plasma lipids BMI Obese participants had lower levels of carotenoids
[24] aged- and sex-matched normal-weight subjects (cholesterol + triglyceride) (0.19 ± 0.08 vs. 0.43 ± 0.25 μg/mg) and vitamin E
(controls) (6.5 ± 2.7 vs. 11.3 ± 4.8 μg/mg) compared to the
Aged 26–52 years control group (P < 0.001).
Hosseini et al.
Table 1 (continued)

Study Country Characteristics Full model adjustments Outcome Findings

measure(s)

Target biomarker(s): plasma levels of carotenoids

and vitamin E
Tungtrongchitr Taiwan Case-control Age, sex BMI, WC, HC Median serum α-tocopherol concentration was 17.30 and
et al. [43] 72 overweight individuals (cases) 18.75 μmol/L in overweight and control subjects,
72 normal-weight participants (controls) of both respectively (P < 0.05).
genders
Target biomarker(s): plasma levels of vitamin E
NHANES III USA Cross-sectional Serum triglyceride and cholesterol Weight, BMI Obese children had a lower serum concentration of α-
[17] 6139 children aged 6–19 years levels tocopherol (2.68 ± 0.59 vs. 3.17 ± 0.60, P < 0.001).
Target biomarker(s): dietary intake and serum Serum β-carotene concentration was significantly lower in
levels of vitamin E and β-carotene obese children compared to the normal-weight subjects
(0.22 ± 0.14 vs. 0.29 ± 0.17 μmol/L, P < 0.001). Intake
of β-carotene, α-tocopherol, fruits, or vegetables had no
significant difference among obese and non-obese
Association Between Antioxidant Intake/Status and Obesity

children.
Chai et al. USA Comparative cross-sectional Asian ethnicity, smoking status BMI γ-Tocopherol levels were significantly higher in obese
[27] 180 premenopausal women individuals (P < 0.05). BMI had a positive correlation
Target biomarker(s): plasma levels of vitamin E with γ-tocopherol (r = 0.25, P = 0.0008). α-Tocopherol
levels had no significant difference among BMI subgroups
(P > 0.05).
NHANES II USA Cross-sectional Age, sex, weight, alcohol BMI BMI was inversely correlated with ascorbic acid
[29] 11,592 participants aged 18–74 years consumption, smoking concentrations.
Target biomarker(s): plasma vitamin C
Singh et al. India Cross-sectional Age Body fat percent Plasma levels of vitamins C (OR 1.08) and E (OR 1.09) were
[6] 850 men aged 25–64 years assigned into high negatively correlated with a high body fat content. Serum
body fat percent (n = 357), over fat percent magnesium/insulin ratio was inversely related to high body
(n = 230), desirable fat (n = 200), and low fat fat percent. Zinc (OR 1.03) and magnesium (OR 1.02)
(n = 63) deficiencies were risk factors of higher body fat percent
Target biomarker(s): plasma levels of vitamin C, and central obesity.
zinc and magnesium
Canoy et al. UK Cohort Age, BMI, vitamin supplement WHR, BMI, WC, Plasma ascorbic acid concentration was negatively correlated
[5] 19,068 men and women aged 45–79 years usage, cigarette smoking, and HC with WHR in both men and women (P < 0.05). WC and
Target biomarker(s): plasma ascorbic acid level socioeconomic status HC showed a separate and inverse relationship to plasma
ascorbic acid concentrations (P < 0.05).
Galan et al. France Cross-sectional Age, smoking, alcohol BMI Obese participants had a lower serum β-carotene and vitamin
[32] 1821 women aged 35–60 years and 1307 men consumption, C concentrations (P < 0.05), while, serum level of vitamin
aged 45–60 years gender E had no significant difference among obese and non-
Target biomarker(s): serum levels of β-carotene, obese participants. No significant difference was observed
vitamin C, vitamin E, zinc, and selenium regarding zinc and selenium concentration and
anthropometric data.
Aasheim et al. Norway Case-control BMI Serum concentrations of vitamins C and E were significantly
[8] lower in obese patients (P < 0.01).
291
Table 1 (continued)
292

Study Country Characteristics Full model adjustments Outcome Findings

measure(s)

110 morbidly obese (76 women) women with Age, smoking, diabetes status,
58 healthy participants in both genders alcohol intake, antidepressant
Target biomarker(s):serum concentrations of medication use
vitamins C and E
Mah et al. USA Case-control Age BMI Obese subjects had 51 % lower vitamin C intakes and 38 %
[23] Obese men (cases, n = 8), lean men (controls, lower plasma vitamin C concentrations compared to the
n = 8) aged 21 ± 3 years with no history of lean controls (P < 0.05).
dietary supplementation
Target biomarker(s): plasma vitamin C
concentration
Drewnowski France Cross-sectional Age, gender, alcohol intake, BMI β-Carotene serum concentration was inversely correlated
et al. [39] 361 men and 476 women aged 18–94 years tobacco use with body mass (P < 0.05). Serum level of vitamin C
Target biomarker(s): serum level of vitamin C was not influenced by BMI (P < 0.05).
and β-carotene
Chen et al. Taiwan Case-control Age, gender Weight, BMI Fasting serum zinc concentration was lower in obese group
[21] Obese participants (n = 10, two males, eight compared to the normal-weight controls (13.5 vs.
women) and lean controls (n = 11, four men, 18.1 μmol/L, P < 0.05). Zinc concentration in overall
seven women) participants was negatively associated with BMI
Target biomarker(s): serum zinc levels (r = −0.516).
Marriero et al. Brazil Case-control Age, gender BMI, skin-fold Obese group had significantly lower zinc levels in plasma and
[15] Children and adolescents (n = 23) and control measurements erythrocytes, while higher urinary zinc excretion and
group (n = 21) aged 7–14 years serum insulin were found in the same level compared to the
Target biomarker(s): zinc levels control one.
Yakinci et al. Turkey Case-control Age, gender BMI, weight Serum concentrations of zinc were significantly higher in
[20] 41 obese children and 41 healthy counterparts aged obese children compared to the control group (P < 0.01).
7–11 years Serum magnesium levels were significantly lower in obese
Target biomarker(s): serum concentrations of zinc group than in the healthy children (P < 0.01).
and magnesium
Weisstaub et al. Chile Cross-sectional Age, gender Weight, WHZ, WC Plasma zinc concentration was not correlated with weight,
[19] 72 obese (WHZ >2.0 SD) children (18 to WHZ, as well as WC.
36 months)
Target biomarker(s): plasma zinc level
Tascilar et al. Turkey Case-control Age, gender BMI No significant difference was observed between groups
[18] 34 obese and 33 healthy control subjects regarding the serum trace element levels including
Target biomarker(s): serum trace element levels selenium and zinc.

BMI body mass index, HC hip circumference, MAMC mid-arm muscle circumference, WC waist circumference, WHZ weight-to-height z score, WHR waist-to-hip ratio
Hosseini et al.
Association Between Antioxidant Intake/Status and Obesity
(α-carotene, β-carotene, β-cryptoxanthin, zeaxanthin/lutein,
and lycopene), BMI, dietary intake, physical activity, and di-
etary supplement consumption were assessed. Obese partici-
pants (BMI ≥30 kg/m2) had an average level of the sum of all
carotenoids, except lycopene that was 22 % lower compared
to the concentration observed in those with BMI of less than
22 kg/m2. The changes from year 0 to year 7 in serum carot-
enoids, except for lycopene, had a negative association with
the changes in BMI among non-smokers. A case-control study
conducted by Reitman et al. [24] reported that obese partici-
pants had lower levels of carotenoids (0.19 ± 0.08 vs.
0.43 ± 0.25 μg/mg) compared to the age-matched control
group (P < 0.001). Also, BMI was inversely correlated with
carotenoids (r = −0.43, P < 0.01). Another case-control study
[16] in 46 preschool children, matched by gender and age (23
obese and 23 non-obese participants) also demonstrated low
concentrations of carotenoids in obese (i.e., with ZWH equal
or more than 2) compared to the non-obese (82 vs. 26.6 %,
P = 0.0054 and OR = 12.4) children. NHANES III [17] also
demonstrated that serum β-carotene concentration was signif-
icantly lower in obese children compared to the normal-
weight subjects (0.22 ± 0.14 vs. 0.29 ± 0.17 μmol/L,
P < 0.001). The authors reported that about one half of obese
children were in the lowest quartile of β-carotene serum level
compared to about one quarter of normal-weight children
(P < 0.001). However, intake of β-carotene, fruits, or vegeta-
bles demonstrated no significant difference among obese and
non-obese children.
Among the proposed mechanisms for these observed find-
ings are that carotenoids are distributed between serum and
adipose tissue which is regarded as the dominant storage tis-
sue in humans [40]. Therefore, the proportion of ingested
carotenoids absorbed by fat tissue would be higher in a person
with high fat mass compared to a lean person if all other
metabolic factors were equal [28]. It is also possible that
higher oxidative stress in obese individuals might mean anti-
oxidants are expended more than in normal-weight individ-
uals [26, 41]. Whether obese people have lower intakes of
foods such as fruit and vegetables has been suggested, but
evidence in this review suggests this is not the cause [10].
Taken as a whole, the literature indicates that carotenoid
concentration is significantly and negatively associated with
both general and central adiposity. However, because most
studies are cross-sectional, whether the body fat sequesters
the carotenoids, or obese have poorer intakes, or other mech-
anisms such as greater oxidative stress in obesity are involved,
is uncertain.
Association Between Vitamin E (α-Tocopherol)
Status/Intake and Obesity
Ten cross-sectional studies and three case-control studies in-
vestigated the relationship between vitamin E and obesity. The
293
antioxidant α-tocopherol is regarded as the dominant constit-
uent of vitamin E that plays a major role in the body’s defense
system against reactive oxygen species (ROS) [42]. It has
been demonstrated that part of the increased risk of cardiovas-
cular disease linked with central adiposity may be as a result of
low α-tocopherol status [7]. The evidence suggests that obe-
sity, assessed by BMI, is independently associated with α-
tocopherol serum level even after controlling for diet and lipid
concentrations [31]. Vioque et al. [10] reported that serum α-
tocopherol levels had a significant positive association with all
measures of obesity in both genders (P < 0.05), except for
body fat percentage in men. Additionally, waist circumference
and waist-to-hip ratio (WHR) had a significant positive asso-
ciation with serum levels of α-tocopherol in both genders
(P < 0.05). Measures of general obesity such as BMI or body
fat percentage were not associated with obesity except for
BMI in men. Öhrvall et al. [35] found an inverse association
between serum α-tocopherol concentration and abdominal
sagittal diameter in 906 Swedish participants (r = −0.24,
P = 0.0001). In contrast, a cross-sectional study [7] reported
that serum α-tocopherol was correlated with central adiposity
after accounting for body fat. Waist circumference and WHR
had a significant positive association with serum α-tocopherol
concentration in both genders (P < 0.05); however, measures
of general obesity, i.e., BMI or body fat percentage, were not
significant, with the exception of BMI in men. Moreover,
Chai et al. [27] reported that γ-tocopherol levels were signif-
icantly higher in obese individuals (P < 0.05), while α-tocoph-
erol levels were no different among BMI subgroups in 180
premenopausal women. Likewise, Galan et al. [32] found no
significant difference in serum vitamin E among obese and
non-obese participants in 1821 women aged 35–60 years as
well as 1307 men aged 45–60 years. Another cross-sectional
study that only assessed serum concentrations found no sig-
nificant difference in vitamin E concentration between obese
and non-obese participants [34].
A case-control study conducted by Myara et al. [33] report-
ed that plasma vitamin E levels were significantly lower in the
severely obese participants (BMI >35 kg/m2) compared to the
controls (P < 0.0001). Also, serum α-tocopherol concentra-
tion was negatively correlated with BMI (r = 0.53,
P < 0.0001) and WHR (r = 0.40, P = 0.0003). Reitman et al.
[24] found that obese participants had lower levels of vitamin
E (6.5 ± 2.7 vs. 11.3 ± 4.8 μg/mg) compared to the age-
matched control group (P < 0.001).The study also revealed
that BMI was inversely correlated with vitamin E (r = −0.32,
P < 0.05). Another case-control study [43] reported that the
median serum α-tocopherol concentration was 17.30 and
18.75 μmol/L in 144 overweight and control subjects, respec-
tively (P < 0.05). Similarly, serum α-tocopherol was inversely
associated with weight, BMI, mid-arm muscle circumference
(MAMC), and waist and hip circumferences in both the over-
weight and obese subjects.
294
It seems that these findings can also be supported by stud-
ies conducted on children. The NHANES III [17] reported that
after adjusting for serum triglyceride and cholesterol levels,
obese children had a lower serum concentration of α-
tocopherol (2.68 ± 0.59 vs. 3.17 ± 0.60, P < 0.001). The study
also demonstrated that about one half of obese children were
in the lowest quartile of adjusted α-tocopherol serum level
compared to about one quarter of normal-weight children
(P < 0.001). No significant difference was observed regarding
α-tocopherol consumption among obese and non-obese
children.
The mechanism underlying the reduced α-tocopherol con-
centrations found in obesity can be explained by obesity lead-
ing to increased oxidative stress that depletes endogenous and
exogenous pools of antioxidants, such as vitamin E [41], via
an increased utilization of antioxidants. [44] Moreover, vita-
min E, as a fat-soluble antioxidant, can be absorbed and stored
by fat tissue. Accordingly, the serum concentration of vitamin
E could be lower in a person with high fat mass compared to a
lean subject if all other metabolic factors were similar [10].
Thus, there is a discrepancy regarding the association be-
tween α-tocopherol concentration and obesity in terms of
BMI and body fat content. However, since most of the studies
reported an inverse association between vitamin E concentra-
tions and obesity, it has been suggested that the development
of long-term dietary restriction programs for obese individuals
might supply adequate vitamin E to avoid antioxidant vitamin
deficiency [33].
Association Between Vitamin C (Ascorbic Acid)
Status/Intake and Obesity
Seven cross-sectional studies, three case-control studies, and
one cohort study investigated the association between vitamin
C and obesity. Several studies indicated that a lower plasma
concentration of ascorbic acid (as a main water-based antiox-
idant) might be a risk factor for cardiovascular disease mor-
tality [1, 5]. According to the findings from the NHANES II
[29], BMI was inversely correlated with ascorbic acid concen-
trations in 11,592 participants aged 18–74 years. Furthermore,
a cross-sectional study by Singh et al. [6] reported that plasma
levels of vitamin C (OR 1.08) were negatively correlated with
a high body fat content measured by bioelectric impedance
analysis in 850 men aged 25–64 years. Similarly, Canoy et al.
[5] demonstrated that the serum ascorbic acid concentration
was negatively correlated with WHR in 19,068 men and
women between the ages 45 and 79 years old. This correlation
was independent of BMI, age, vitamin supplement usage, cig-
arette smoking, and socioeconomic status. Waist and hip cir-
cumferences showed a separate and inverse relationship to
plasma ascorbic acid concentrations, independent of BMI
and other covariates. Dietary consumption of ascorbic acid
only partly explained the reported associations. In agreement
Hosseini et al.
with these studies, Galan et al. [32] reported that obese partic-
ipants had a lower serum vitamin C concentration. In a cross-
sectional study [34], vitamin C was inversely correlated with
BMI, waist-to-height ratio, and leptin concentrations in wom-
en aged 37 ± 7.5 years (n = 580) (P < 0.05). However, these
findings were not supported by all cross-sectional studies.
Drewnowski et al. [39] reported that serum vitamin C was
not influenced by BMI in a French sample population includ-
ing 361 men and 476 women aged 18–94 years. Furthermore,
a cross-sectional study indicated that dietary consumption of
vitamin C significantly reflected plasma concentration in 252
men and 293 women, aged 65 years and above (P < 0.01). No
significant correlation was observed between vitamin C con-
centration and BMI. In a case-control study conducted by
Aasheim et al. [8], it was demonstrated that morbidly obese
participants (n = 110, 76 women) had a lower serum concen-
tration of vitamin C compared to 58 healthy participants
(P < 0.01). Another case-control study [23] reported that
obese subjects (n = 16) had 51 % lower daily vitamin C in-
takes as well as 38 % lower serum vitamin C concentrations
compared to the 16 lean age-matched controls (P < 0.05).
In one study [5], it is suggested that the association between
obesity and serum ascorbic acid concentrations may have
common underlying determinants, such as lifestyle and die-
tary pattern. To illustrate, cigarette smoking is linked with
both increased abdominal adiposity and lower serum ascorbic
acid levels [45]. Moreover, serum ascorbic acid is regarded as
a reliable marker of fruit and vegetable consumption. [46]
Accordingly, it can be an indicator of a particular diet and
other lifestyle behaviors in health conscious people that could
lead to a leaner body mass. Additionally, serum ascorbic acid
concentrations could be an indicator of the available pool of
ascorbic acid in the body [47]. As it was mentioned above,
other antioxidants such as β-carotene and α-tocopherol may
be stored in fat tissues; however, the mechanism underlying
how ascorbic acid, as a water-soluble vitamin, could be stored
differentially with increasing adiposity has not been elucidat-
ed yet. However, ascorbic acid plays a role in scavenging free
radicals and inhibits lipid peroxidation, and since obesity is
associated with systemic oxidative stress, it can lead to a lower
concentration of vitamin C in obese individuals [5].
Furthermore, Aeberli et al. [13] previously reported that the
consumption of dietary antioxidant vitamins (vitamins E and
C and β-carotene) can be a significant predictor of leptin
levels in Swedish children (P < 0.05); therefore, it is plausible
that low concentrations of these antioxidants may alter leptin
genetic expression which results in the development of leptin
resistance. Accordingly, high levels of leptin in blood may
increase the risk of adiposity and obesity [48].
Data regarding the association of vitamin C with obesity
are inconclusive, but the majority of studies showed an in-
verse association between vitamin C and anthropometric mea-
surements, in particular BMI, central adiposity, and body fat.
Association Between Antioxidant Intake/Status and Obesity
The most challenging aspect of the interpretation of this dis-
crepancy comes from the finding that vitamin C is present in
the non-fat part of the body. Therefore, when the content of fat
in the body is increased, at the same time, utilization of vita-
min C is increased and water phase (the main part of the
vitamin C) to lipid phase of the body is decreased.
Therefore, it is difficult to distinguish the cause of decreased
serum levels of vitamin C in obese people. Prospective ran-
domized controlled trials are needed to answer the question of
a truly beneficial role for vitamin C in obesity and a better
understanding of the highly complex process.
Association Between Zinc, Magnesium, and Selenium
Status/Intake and Obesity
Eight cross-sectional studies and two case-control studies in-
vestigated the association between zinc, magnesium and sele-
nium either alone or in combination and obesity. However,
50 % of the conducted studies only investigated the associa-
tion between zinc and adiposity. Zinc, as an essential nutrient,
plays a major role in growth, reproduction tissue repair, and
cellular immunity [20]. Some studies report that it is associat-
ed with the degree of obesity [21]. Zinc deficiency may pro-
mote fat deposition and reduce lean mass accrual [19].
The association between zinc status and adiposity may be
attributed to the relationship between zinc metabolism and
leptin. To illustrate, zinc deficiency results in a reduction in
serum leptin concentrations in humans and reduced leptin se-
cretion by rat adipocytes, while zinc repletion has an opposite
effect [19]. Furthermore, this mineral is also involved in the
metabolism of hormones playing a role in the development of
obesity, particularly insulin, and seems to be associated with
the mechanisms of insulin resistance commonly present
among obese people. Zinc also has various functions in the
metabolism of energy and acts as a component of several
enzymes essential to the metabolism of carbohydrates, lipids,
and proteins, through both structural and catalytic functions
critical for tissue formation and hormone receptor activation
[15].
Magnesium is associated with cellular enzymatic activity,
particularly glycolysis and the stimulation of the adenosine
triphosphatases and selenium as a component of glutathione
peroxidase, has critical roles in certain metabolic processes
[19, 49].
Singh et al. [6] reported that serum magnesium/insulin ratio
was inversely related to high body fat percent in an urban
population in India (including 850 men aged 25–64 years).
Moreover, zinc (OR 1.03) and magnesium (OR = 1.02) defi-
ciency was a risk factor of higher body fat percentage and
central obesity. On the other hand, Galan et al. [32] found no
significant difference regarding zinc and selenium concentra-
tion and anthropometric data in 3128 participants (58 % wom-
en). Similarly, García et al. [34] found no significant
295
difference between serum zinc and any measures of obesity
in 580 Mexican women aged 37 ± 7.5 years. Furthermore,
Weisstaub et al. [19] reported that plasma zinc concentration
was not correlated with weight, WHZ, waist circumference,
and serum leptin in 72 18- to 36-month-old obese babies
(WHZ >2.0 SD). A case-control study [21] reported that
fasting serum zinc concentration was lower in obese group
(n = 10, eight women) compared to the normal-weight con-
trols (n = 11, seven women) (13.5 vs. 18.1 μmol/L, P < 0.05).
The authors also noted that this difference was not a short-
term metabolic result. In addition, the study indicated that
under the fasting state, plasma zinc concentration in overall
participants was negatively associated with BMI (r = −0.516).
Marriero et al. [15] indicated that the obese children and ado-
lescents (n = 23) had significantly lower zinc levels in serum
and erythrocytes, while higher urinary zinc excretion com-
pared to the control group (n = 21). Another case-control
study [20] reported that serum concentrations of zinc were
significantly higher in obese children (n = 41) compared to
the control group (n = 41) (102.40 ± 2.78 vs. 80.49 ± 2.98 pg/
dL, respectively; P < 0.01), while serum magnesium levels
were significantly lower in the obese group than in the healthy
children (1.78 ± 0.03 vs. 2.14 ± 0.04 mg/dh P < 0.01).
Likewise, Tascilar et al. [18] found no significant difference
regarding the serum trace element levels including selenium
and zinc in 34 obese and 33 healthy control subjects. Gibson
et al. [14] suggested that gender might be playing a role in
these inconclusive results. The authors reported that boys with
lower zinc status were fatter and heavier compared to the boys
with adequate zinc concentrations, while no significant differ-
ence was observed in girls. It has been also suggested that
greater body fat and adiposity among zinc-deficient young
children may be associated with higher risk of obesity in
adulthood.
In summary, little is known about the clinical consequences
of chronic antioxidant trace element deficiency. Several stud-
ies indicate that their nutritional status in obese individuals
may be altered and lower than the reference values for the
analyzed parameters. However, other studies fail to confirm
these findings. Further studies that evaluate erythrocyte and
urine concentrations in addition to plasma are needed.
Conclusion
This review of existing studies on the association between
antioxidant intake/status and obesity in humans indicates
obese individuals have a lower concentration of antioxidants,
particularly carotenoids, vitamins E and C, zinc, magnesium,
and selenium. While some studies demonstrated that intake of
the aforementioned antioxidants was poorer among obese
subjects compared with their normal-weight counterparts, this
was not supported by all studies. The direction of causality in
296
the association between intake/status of antioxidants and obe-
sity cannot be determined because majority of studies are of
cross-sectional design. Future research with cohort designs are
warranted to address whether specific antioxidant deficiencies
are the result of poor intakes, metabolic consumption of anti-
oxidants because obese have greater oxidative stress, seques-
tering of antioxidants by adipose tissue or a result of equilib-
rium between adipose and serum.
Compliance with Ethical Standards
Funding and Sponsorship This paper was not funded by any
organization.
Conflict of Interest The authors declare that they have no conflict of
interest.
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