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The Impact of Virgin Coconut Oil and High-Oleic Safflower Oil
on Body Composition, Lipids, and Inflammatory
Markers in Postmenopausal Women
Margaret Harris, Andrea Hutchins, and Lisa Fryda
Department of Health Sciences, University of Colorado Colorado Springs, Colorado Springs, Colorado, USA.
ABSTRACT This randomized crossover study compared the impact of virgin coconut oil (VCO) to safflower oil (SO) on
body composition and cardiovascular risk factors. Twelve postmenopausal women (58.8 –3.7 year) consumed 30 mL VCO or
SO for 28 days, with a 28-day washout. Anthropometrics included body weight and hip and waist circumference. Fat percent
for total body, android and gynoid, fat mass, and lean mass were measured using dual-energy X-ray absorptiometry. Women
maintained their typical diet recording 28 days of food records during the study. Results were analyzed with SPSS v24 with
significance at P£.05. Comparisons are reported as paired t-test since no intervention sequence effect was observed. VCO
significantly raised total cholesterol, TC (+18.2 –22.8 mg/dL), low-density lipoprotein (+13.5 –16.0 mg/dL), and high-density
lipoprotein, HDL (+6.6 –7.5 mg/dL). SO did not significantly change lipid values. TC and HDL were significantly different
between test oils. The TC/HDL ratio change showed a neutral effect of both VCO and SO. One person had adverse reactions
to VCO and increased inflammation. VCO decreased IL-1bfor each person who had a detected sample. The impact of VCO
and SO on other cytokines varied on an individual basis. This was the first study evaluating the impact of VCO on body
composition in Caucasian postmenopausal women living in the United States. Results are suggestive that individuals wishing
to use coconut oil in their diets can do so safely, but more studies need to be conducted with larger sample sizes, diverse
populations, and more specific clinical markers such as particle size.
KEYWORDS: adiposity cholesterol cytokines fatty acid
INTRODUCTION
Consumption of coconut oil has increased over the
years. In 2015, between January and November, exports
from the Philippines increased by 61%.
1
Virgin coconut oil
(VCO) has garnered public and scientific attention as a potential
‘‘superfood’’ due to its high phytochemical content, particularly
of phenolic compounds.
2,3
Research supports the benefit of
VCO for a variety of conditions, including supporting weight
loss,
4,5
fighting infection,
6
improving the cardiovascular disease
risk profile (or maintaining its neutrality),
4,7–9
and even less-
ening the decline in neurodegenerative disorders.
10,11
Nevertheless, confusion about VCO continues because it is
a highly saturated fat (93%) food. While researchers have
suggested that saturated fat may not be detrimental for
health,
12,13
the most recent 2015 Dietary Guidelines for
Americans still suggest limiting saturated fats, including
tropical oils.
14
VCO is a unique saturated fat because it is rich
(65%) in short and medium chain fatty acids that metabolize
rapidly without depositing in arteries and fat cells.
8,15,16
The
most substantial medium-chain fatty acid, lauric acid, has
antimicrobial, antifungal, and antiviral properties giving a
unique benefit to VCO compared to other oils.
6,15
The ques-
tion remains what impact the resulting 35% long-chained fats
would have on health outcomes.
Although the evidence pointing to the benefits of VCO is
increasing, few human studies exist exploring VCO’s impact
on measurable health outcomes. The most recent review on
VCO and heart disease highlights the need for more studies.
17
Most studies that highlighted beneficial impacts of VCO were
in vitro animal studies that used medium-chain triglycerides
(MCTs) or were conducted in Pacific Islander/Asian popu-
lations. The human data in existence are not generalizable to
most Western societies due to different diets, lifestyles, and
genetic predispositions.
The purpose of this study was to compare the health im-
pacts of VCO to ‘‘heart healthy’’ safflower oil (SO) in post-
menopausal women living in the Rocky Mountain region of
the United States. To our knowledge, this is the first study to
examine VCO in an older U.S. population.
MATERIALS AND METHODS
Study design and participants
This study was approved by the Institutional Review
Board at the University of Colorado Colorado Springs.
Manuscript received 19 July 2016. Revision accepted 22 January 2017.
Address correspondence to: Margaret Harris, PhD, MS, HC, Department of Health
Sciences, University of Colorado Colorado Springs, 1420 Austin Bluffs Parkway, Col-
orado Springs, CO 80918, USA, E-mail: mharris5@uccs.edu
JOURNAL OF MEDICINAL FOOD
J Med Food 20 (4) 2017, 345–351
#Mary Ann Liebert, Inc., and Korean Society of Food Science and Nutrition
DOI: 10.1089/jmf.2016.0114
345
Fourteen women were recruited from the Colorado Springs
community through fliers, email blasts, and word of mouth.
Of these 14 women, 12 completed the study. One woman
dropped out during the first month due to loss of the oils
while travelling and the second dropped out due to enroll-
ment in another study before the beginning of the first
testing phase of this study.
Inclusion criteria included the following: (1) postmeno-
pausal women between the age of 45–65, (2) not taking any
hormone replacement therapy, (3) not taking medication or
supplements that could alter lipids, (4) normal fasting lipid
levels (total cholesterol [TC] <240 mg/dL at screening), and
(5) willing to ingest two tablespoons of VCO and SO each
day for two nonconsecutive 28-day periods.
This randomized, crossover clinical trial included two 28-
day dietary supplementation interventions consisting of daily
ingestion of either two tablespoons (30mL) of VCO or SO
distributed throughout the day. Testing was done in 1 day and
women were selected into alternating oil intervention groups
based on their arrival times. Participants were instructed to
add oils to already-prepared foods as a topping, into
smoothies, or to make dressings out of them. Participants
were instructed not to cook with the oils to avoid chemical
breakdown; however, upon evaluation of dietary records,
participants did lightly saute
´their food when using VCO.
Each subject received 28 plastic containers with premeasured
doses of the designated oil in each container. They were in-
structed to ingest one container per day throughout the sup-
plementation period and return all containers (used and
unused) at the next measurement period. Participants were
instructed to continue their normal diet and exercise routine
throughout both supplementation periods as well as the 30-
day washout period to replicate normal living conditions.
Origin and composition of oil supplements
The intervention oils were Organic VCO (Tropical Tra-
ditions, Gold Label, West Bend, WI) and Organic High Heat
SO (Spectrum; The Hain Celestial Group, Inc., Boulder,
CO). The VCO was made in the Philippines from USDA
certified organic coconuts using the traditional fermented
method. Shredded coconut meat is added to water from in-
side the coconut to make coconut milk. After sitting for
about 12 h, the oil naturally separates from the heavier wa-
ter. The oil is heated for a short time and filtered from the
curds. Each oil was measured by weight (1 oz/30 mL/2 Tbs)
using an electronic kitchen scale (Salter Model 3001) and
packaged in individual portions. Oil composition was tested
at the UCCS Department of Chemistry laboratory.
Anthropometric evaluation
Measurements were collected before and after each sup-
plementation period. Body mass was measured using a Tanita
BF679W scale to the nearest 10th of a ounce. Height was
measured using a stadiometer at commencement of the study.
Body mass index was calculated by dividing the body mass (kg)
by the square of the height (meters). Hip and waist circum-
ference were measured with a standard tape measure to the
nearest quarter of an inch and converted to centimeters. Waist
was measured at the smallest circumference and hip at the
widest circumference. Dual-energy X-ray absorptiometry
(DXA) scans were completed at the beginning and conclusion
of each testing period to determine percent body fat and dis-
tribution. Two participants declined to be measured by DXA.
Dietary evaluation
Upon commencement into the study, participants were
shown how to complete a detailed food journal. Participants
completed four food records during a 2-week wash-in period
before starting the first intervention. During each interven-
tion and the washout period, participants recorded all food
consumed for eight assigned days per month (about 2 days
each week) for a total of 28 food journals. Data were entered
and analyzed using Food Processor Software (ESHA Re-
search, Salem, OR).
Biochemical evaluation
Blood samples for the measurement of cytokines and
cholesterol concentrations were collected before and after
supplementation of VCO and SO. Blood was taken in the
morning following a 12-h overnight fast.
Blood samples were collected in 4 mL ESTA and 7.5 mL
serum separator tubes for cholesterol and cytokine evalua-
tion, respectively. Samples were immediately spun in a
centrifuge for 20 min, aliquoted, and frozen to -80C.
Cholesterol (high-density lipoprotein [HDL], low-density
lipoprotein [LDL], triglycerides, and TC) was measured
using a Beckman Coulter AU400 Chemistry analyzer. In-
flammatory markers (TNF-a, IL-1b, IL-10, and IL-6) were
measured using a high sensitivity multiplex kit by Randox.
All biochemical data were processed at the Colorado Clin-
ical and Translational Sciences Institute (CCTSI: Denver,
CO; CCTSI is supported, in part, by Colorado CTSA Grant
UL1 TR001082 from NIH/NCATS).
Statistical analysis
Data were analyzed using SPSS (Version 24; IBM, Ar-
monk, New York) to determine normal distributions of
continuous variables (visually and Shapiro–Wilk’s test),
descriptive statistics, and repeated-measures mixed model
ANOVA using sequence of oil intervention as a covariate.
The intervention sequence was not determined to be sig-
nificant. Therefore, paired t-tests were conducted to deter-
mine difference before and after oil supplementation on the
following: weight, waist circumference, hip circumference,
total fat%, android fat%, gynoid fat%, android-to-gynoid
ratio, fat mass, lean mass, and bloodwork. Differences from
premeasures and postmeasures were calculated and paired t-
tests were used to compare difference between oils. Sig-
nificance was set to P£.05.
Surveys
Before supplementation, all participants completed a medical
history survey and a demographic survey. Upon completing
346 HARRIS ET AL.
each supplementation period, a short survey was completed
regarding experiences with ingesting the oils.
RESULTS
Twelve women successfully completed the study. One
woman completed a total of about 2 weeks of the coconut
protocol after suspicion that she was having an intolerance
to the oil. Complaints included a scratchy throat and feelings
of being unhealthy. After stopping the oil, her symptoms
disappeared. She restarted the oils in the fourth week and
symptoms returned. Upon closer inspection, all her inflam-
matory markers were elevated after coconut oil consump-
tion markedly more than other subjects (Subject 1). One
subject completed the coconut oil protocol for 3 weeks, due
to a work-related trip. Other participants successfully used
all oils as instructed. Excluding these two women from
analyses did not change findings; however, they were ex-
cluded from group analyses to provide more reliable data.
The composition of the oils is presented in Table 1. As
expected, VCO was rich in short- and medium-chain fatty
acids, together comprising about 70% of the oil. SO nor-
mally has the highest linoleic acid content of any vegetable
oil in the market. However, due to recent changes in the
market, this type of oil is difficult to find. We used an oil that
is typical of what is found on store shelves: high-oleic SO,
which is hybridized to withstand high-heat cooking. This oil
contained 80% oleic acid.
The energy and macronutrient contents of the diet are
presented in Table 2. Since one of the purposes of the study
was to test the feasibility of consuming 30 mL of oil, diet
was not altered. An objective was to observe the impact of
the oils in a way that people would normally consume the
oils, within their own regular diets, and whether the oils
impacted their dietary intake. Variations in consumption
were due to illness and vacation. Results showed that wo-
men ingesting coconut oil ate 318 kcal more per day
(P=.05) and had significantly more protein consumption.
Descriptive characteristics at baseline are presented in
Table 3. Data not shown in the table include age and general
lifestyle characteristics. Women on average were 57.8 –3.7
years old. There was a wide variation in exercise habits and
intensity with women reporting about 229.1 –224.2 min per
week of exercise (33% light activity, 42% moderate activity,
and 25% intense activity). Women tended to be light drinkers
consuming predominantly wine on an occasional to weekly
basis (66%). Only one woman reported heavy drinking. Four
women took daily medications (blood pressure and SSRI
antidepressants). All women consumed dietary supplements.
These consisted of vitamin/mineral supplements or bone
support supplements such as glucosamine, chondroitin, or
calcium.
Neither oil affected anthropometry significantly (Table 4).
Although not statistically significant, the small increase in
lean mass after VCO consumption and decrease after SO may
be potentially clinically meaningful.
Table 5 shows results of lipid changes after oil inter-
ventions. Results show that VCO significantly raised TC,
LDL, and HDL (P<.05), while decreased TG (P=NS).
Conversely, SO decreased TC, LDL, and HDL and in-
creased TG, but changes were not significant. The ratio of
TC to HDL showed no changes to risk profile with either oil,
while the TG/HDL showed a small improvement after VCO
and small worsening after SO.
Figure 1 presents results of inflammatory markers IL-1b,
TNF-a, and IL-6 as well as the anti-inflammatory marker IL-
10. These markers were not detected in some samples. Due to
the small numbers available, results are presented individually
by subject number and only those results where we had
markers detected are shown. Subject 1 (intolerant reaction to
Table 1. Fatty Acid Composition of Virgin Coconut
and High-Oleic Safflower Oils
Fatty acid
Virgin coconut
oil (%)
High oleic
safflower oil (%)
Caproic acid C6:0 0.676 —
Caprylic acid C8:0 9.037 —
Capric acid C10:0 5.961 —
Lauric acid C12:0 54.293 —
Myristic acid C14:0 19.016 —
Palmitic acid C16:0 6.461 4.559
Stearic acid C18:0 1.263 1.896
Oleic acid C18:1 3.023 80.210
Linoleic acid C18:2 0.270 13.335
Samples were analyzed by GC/MS using a Hewlett Packard 6890 Series II
Gas Chromatograph with 5973 Mass Selective Detector.
Table 2. Dietary Data at Baseline and Pre and Post Virgin Coconut Oil and Safflower Oil
Baseline
Virgin coconut oil Safflower oil
Pre Post DPre Post D
Calories, kcal 1648 –625 1603 –639 1966 –553 318
a
1769 –550 1784 –336 40
Protein, g 83 –61 83 –62 96 –62 12
a,b
69 –15 68 –18 -1
Carbohydrate, g 193 –107 194 –104 214 –82 13 204 –76 192 –35 -7
Fat, g 72 –32 77 –30 96 –26 16 68 –21 78 –21 10
DChange calculated as postintervention minus preintervention.
a
Statistically significant (P£.05) between pre and post oil, paired t-test.
b
Statistically significant (P£.05) between the change of VCO compared to SO, paired sample t-test.
COCONUT OIL AND CARDIOVASCULAR RISK FACTORS 347
VCO) showed dramatically increased inflammation after co-
conut oil. IL-1b, aside from Subject 1, showed varying levels
of decreased inflammation after coconut oil consumption in
every subject. TNF-alpha and IL-6 showed variability of in-
flammation with some women showing decreased inflamma-
tion, while others showed increased inflammation on each oil.
IL-10, an anti-inflammatory cytokine, revealed small, but
mostly inconsequential, variability.
DISCUSSION
The results of this study show that VCO contributes
negligible changes to body composition and the cardiovas-
cular risk profile in Caucasian postmenopausal women liv-
ing in the United States. Previous studies reported that VCO
decreased waist circumference in both men and women.
Many of these studies used MCT oil making the comparison
irrelevant.
18,19
Of the studies using VCO as an intervention,
VCO contributed to smaller waist circumferences and
weight loss in three studies.
4,5,20
In this study, participants
consumed an extra 318 kcal on average when consuming the
VCO, offsetting any weight loss that may have occurred had
caloric intake stayed the same in both oils. Despite reporting
they felt ‘‘fuller’’ quicker with VCO, participants reported
adding VCO to more smoothies with whey protein (re-
placement of breakfast drinks) and to meat-based dishes
(predominantly eggs at breakfast and meat at dinner). When
consuming SO, women tended to add the oil to salad
dressings (at dinner) and oatmeal (at breakfast) due to ease
of working with the flavor and textures of the oils. Although
small and not statistically significant, VCO also slightly
increased lean mass by +0.4%, while SO decreased lean
mass by -0.3%. This may be clinically meaningful in the
postmenopausal years, particularly if the addition of weight
training regimen is added. In light of the excess calories
consumed with no changes in body composition, combined
with the well-known impact of VCO on faster energy ex-
penditure, using VCO can potentially contribute to weight
maintenance/loss efforts.
Animal models have suggested that using coconut oil as a
fat source in the diet may increase lipolysis and decrease
lipogenesis in the liver as well as other tissues.
21–23
Mice fed
coconut oil plus conjugated linoleic acid (CLA) experienced
a more rapid onset of lipolysis and decreased lipogenesis
compared to mice fed a soy oil/CLA combination.
22
Deol
et al. reported that mice fed coconut oil instead of a soy/
coconut oil combination had less adiposity, including less
fat accumulation in the liver.
23
The increased oxidation of
fatty acids and decreased lipogenesis may be mediated, in
part, by coconut oil influencing the PPARa-dependent
pathways.
21
However, to date, these findings have not been
explored in humans.
VCO significantly raised TC, LDL, and HDL, while
safflower decreased all lipids, but not significantly. The
total/HDL and TG/HDL ratios have been suggested to be
good predictors of cardiovascular risk in addition to
Table 3. Baseline Characteristics of Nonsmoking
Postmenopausal Women
Characteristic at baseline Mean –SD
Anthropometrics
Height (m) 1.6 –0.1
Weight (kg) 68.3 –10.9
BMI (kg/m
2
) 26.4 –4.4
Waist circumference (cm) 85.6 –13.2
Hip circumference (cm) 103.4 –7.4
Total fat% (DXA) 37.2 –5.8
Android fat% (DXA) 39.5 –8.7
Gynoid fat% (DXA) 41.3 –4.4
Fat mass (kg) 25.4 –8.3
Lean mass (kg) 41.4 –4.6
Cytokines
TNF-a(pg/mL) 1.80 –0.57
IL-1b(pg/mL) 1.24 –0.52
IL-6 (pg/mL) 0.81–0.68
IL-10 (pg/mL) 0.36 –0.08
Lipids
Total cholesterol (mg/dL) 223.10 –35.10
LDL (mg/dL) 128.70 –26.13
HDL (mg/dL) 64.10 –17.36
Triglycerides (mg/dL) 105.20 –66.15
BMI, body mass index; DXA, dual-energy X-ray absorptiometry; HDL,
high-density lipoprotein; LDL, low-density lipoprotein.
Table 4. Effect of Virgin Coconut Oil and Safflower Oil on Anthropometrics
Virgin coconut oil
D
Safflower oil
DPre (mean –SD) Post (mean –SD) Pre (mean –SD) Post (mean –SD)
Anthropometrics
Weight (kg) 68.4 –11.0 68.9 –11.4 0.5 68.9 –11.4 68.9 –11.7 0.0
Waist (cm) 85.1 –12.7 85.5 –11.0 -0.4 86.2 –13.6 87.1 –11.9 0.9
Hip (cm) 103.6 –7.5 103.1 –7.8 -0.5 102.5 –7.9 102.1 –7.6 -0.4
Total fat (%) 37.2 –5.8 37.5 –5.4 0.3 37.3 –5.4 37.6 –6.0 0.3
Android fat (%) 36.8 –8.9 37.8 –8.5 1.0 36.7 –8.9 37.6 –9.5 0.9
Gynoid fat (%) 41.4 –4.3 41.6 –4.4 0.2 41.8 –4.3 41.9 –4.8 0.1
Android/gynoid 0.93 –0.25 0.95 –0.25 0.02 0.92 –0.25 0.94 –0.25 0.02
Fat mass (kg) 25.3 –8.3 25.7 –8.0 0.3 25.6 –8.3 25.9 –8.9 0.3
Lean mass (kg) 41.4 –4.4 41.5 –4.7 0.4 41.6 –5.1 41.3 –4.5 -0.3
DChange calculated as postintervention minus preintervention, rounded to nearest 10th decimal. No statistical significance (P£.05).
348 HARRIS ET AL.
individual lipid values.
24–26
In this study, women had a
relatively low risk of cardiovascular disease based on the
Total/HDL ratio, which also remained unchanged in both oil
interventions. More notably, TG’s and TG/HDL ratio im-
proved with VCO (bringing it down to optimal levels of 2.0
or less), but worsened with SO. Although LDL increased
with VCO and decreased with SO, this value was offset by
the increases and decreases in HDL with VCO and SO,
respectively. Results on lipids have been mixed in other
studies. While all human studies examined show significant
increases in HDL (including in coronary artery disease pa-
tients),
4,5,7,20,27
only one study showed a neutral impact on
LDL
5
and others showed an elevation.
4,7,20,27
While an el-
evated LDL may be concerning, numerous animal studies
show that VCO lowers oxidation and inflammation, ex-
plained by the increases in antioxidant status.
28–34
Several
studies show that fat increases LDL particle size from small
oxidizable phenotype B to a less atherogenic large pheno-
type A, although these diets were also lower in carbohy-
drates.
35–37
The effect of diet on LDL alone is insufficient
evidence for an increased cardiovascular risk.
38
There are no
human studies conducted examining oxidation or particle
size after VCO consumption. However, Voon et al. com-
pared olive, palm, and VCO and found no differences in
thrombogenicity and cell adhesion between the oils.
9
Other
studies found lowered Lp(a) after VCO intervention.
27,39
Palazhy et al. found no difference in plaque concentrations
between sunflower oil and VCO.
16
These findings suggest
that labeling VCO as atherogenic may be premature.
This was the first study to examine inflammatory markers
in a U.S. population on VCO. Of note, Subject #1, who
displayed sensitivity to VCO, also had every cytokine in-
crease, indicating inflammation. Of the VCO results, all
participants showed a lowering, to various degrees, of IL-
1b, a marker associated with neurodegenerative disease. To
our knowledge, this is the first human American study to
Table 5. Effect of Virgin Coconut Oil and Safflower Oil on Lipids
Virgin coconut oil Safflower oil
Pre Post DPre Post D
Total cholesterol (mg/dL) 219.6 –32.6 237.8 –24.1 18.20
a,b
222.8 –26.7 219.3 –22.8 -3.50
LDL (mg/dL) 124.0 –24.7 137.50 –27.2 13.50
a,b
130.7 –25.6 126.8 –25.7 -3.90
HDL (mg/dL) 63.9 –16.2 70.5 –18.8 6.60
a,b
63.2 –14.7 62.9 –14.5 -0.30
Total cholesterol/HDL 3.7 –1.1 3.7 –1.3 -0.01 3.8 –1.4 3.8 –1.2 -0.06
Triglycerides (mg/dL) 117.2 –97.7 107.5 –80.6 -9.70 110.3 –64.4 118.3 –112.7 8.00
TRG/HDL 2.5 –3.7 2.1 –3.9 -0.43 2.2 –2.5 2.5 –3.9 0.33
DChange calculated as postintervention minus preintervention.
a
Statistically significant (P£.05) between pre and post oil, paired t-test.
b
Statistically significant (P£.05) between the change of VCO compared to SO, paired sample t-test.
FIG. 1. Differences in inflammatory markers after VCO and SO by subject. VCO, virgin coconut oil; SO, safflower oil.
COCONUT OIL AND CARDIOVASCULAR RISK FACTORS 349
show IL-1bresults after VCO ingestion. A study in healthy
Malaysians indicated that VCO’s impact on IL-1bwas also
lowered after VCO, in addition to other cytokines.
27
TNF-a
and IL-6 are both master regulating cytokines for inflam-
mation. Both were fairly well detectable by testing proce-
dures, unlike IL10 (the anti-inflammatory cytokine). While
some participants showed a decreased inflammation with
VCO, others showed a small increase. In addition, the op-
posite effect was seen in each individual when consuming
SO (if VCO lowered these cytokines, SO increased them
and vice versa). Some possible explanations may include
epigenetic and dietary factors. More research needs to be
done to explore how diet quality in conjunction with VCO
use may impact inflammation (since inflammation is an
underlying cause of heart disease). Additive effects of other
lifestyle choices such as sleep and exercise should also be
explored against the use of VCO.
There were strengths and limitations of this study. One
limitation was the small sample size; however, the sample
was very homogenous, limited to postmenopausal Cauca-
sian women. A highly motivated population, a high rate of
compliance, randomization of the oils, and a crossover de-
sign were also strengths of the study. The fermented nature
of VCO used contains the highest amounts of antioxidants
compared to other methods of extraction.
3,40,41
Nonblinding,
however, was a limitation. The texture and strong scent of
VCO may have impacted how the oils were ingested, even
though women were asked not to alter diets. Previous human
studies using VCO also were unblinded and incorporated the
oils into subjects’ regular diets. A blinded trial using VCO is
difficult to conduct. To ingest 1 oz. of oil per day in sup-
plement form, a total of about 47 capsules would be required
per day, which is unfeasible for most people, especially for
an extended amount of time (personal communication with
Capsugel Company). It is possible to mask the oils in a
beverage or food with the use of thickeners and coconut oil
extract, but the feasibility would be very costly.
In summary, this study showed VCO had mostly neutral
effects on cardiovascular disease and body composition,
although more studies need to be performed, determining its
effects on oxidation and particle size in relation to dietary
factors. This was the first study done in a Caucasian U.S.
population examining inflammatory markers. VCO may be
anti-inflammatory for some people, but more research
should be done exploring epigenetic, dietary, and lifestyle
factors. We conclude that VCO is neutral and possibly
beneficial for some people, when incorporated into everyday
use. However, intolerance to VCO is possible and should be
monitored individually.
ACKNOWLEDGMENTS
This research was supported by The University of Color-
ado, Colorado Springs’ Committee on Creative and Research
Works Seed Grant Program. We would like to thank Tropical
Traditions for voluntarily donating the oils upon our inquiry
for pricing before the study. We kindly thank CCSTI for the
processing of our bloodwork (CCSTI is supported, in part, by
Colorado CTSA Grant UL1 TR001082 from NIH/NCATS)
and Dr. Janel Owens and Luis Lowe of the UCCS Chemistry
Department for oil chemistry testing. We would also like to
thank the graduate and undergraduate health promotion and
nutrition students for their volunteer contributions in help-
ing with the coordination and data entry activities throughout
this study.
AUTHOR DISCLOSURE STATEMENT
No competing financial interests exist.
REFERENCES
1. Craymer L: Coconuts go upscale, boosting price of conventional
coconut oil. Wall Street Journal (Online) published April 7,
2016. www.wsj.com/articles/coconuts-go-upscale-boosting-price-
of-conventional-coconut-oil-1460017362 (accessed November 30,
2016).
2. Odenigbu U, Otisi C: Fatty acids and phytochemical contents of
different coconut seed flesh in Nigeria. Int J Plant Physiol Bio-
chem 2011;3:176–182.
3. Marina AM, Man YB, Nazimah SA, Amin I: Antioxidant ca-
pacity and phenolic acids of virgin coconut oil. Int J Food Sci
Nutr 2009;60(Suppl 2):114–123.
4. Assunc¸a
˜o ML, Ferreira HS, dos Santos AF, Cabral CR, Flore
ˆncio
TMMT: Effects of dietary coconut oil on the biochemical and
anthropometric profiles of women presenting abdominal obesity.
Lipids 2009;44:593–601.
5. Liau KM, Lee YY, Chen CK, Rasool AHG: An open-label pilot
study to assess the efficacy and safety of virgin coconut oil in
reducing visceral adiposity. ISRN Pharmacol 2011;2011:949686.
6. Lieberman S, Enig MG, Preuss HG: A review of monolaurin and
lauric acid: Natural virucidal and bactericidal agents. Altern
Complement Ther 2006;12:310–314.
7. Feranil AB, Duazo PL, Kuzawa CW, Adair LS: Coconut oil is
associated with a beneficial lipid profile in pre-menopausal wo-
men in the Philippines. Asia Pac J Clin Nutr 2011;20:190–195.
8. DebMandal M, Mandal S: Coconut (Cocos nucifera L.: Areca-
ceae): In health promotion and disease prevention. Asian Pac J
Trop Med 2011;4:241–247.
9. Voon PT, Ng TK, Lee VK, Nesaretnam K: Virgin olive oil, palm
olein and coconut oil diets do not raise cell adhesion molecules
and thrombogenicity indices in healthy Malaysian adults. Eur J
Clin Nutr 2015;69:712–716.
10. Nafar F, Mearow KM: Coconut oil attenuates the effects of
amyloid-bon cortical neurons in vitro. J Alzheimers Dis 2014;
39:233–237.
11. Fernando WM, Martins IJ, Goozee KG, Brennan CS, Jayasena V,
Martins RN: The role of dietary coconut for the prevention and
treatment of Alzheimer’s disease: Potential mechanisms of ac-
tion. Br J Nutr 2015;114:1–14.
12. Mozaffarian D, Micha R, Wallace S: Effects on coronary heart
disease of increasing polyunsaturated fat in place of saturated fat:
A systematic review and meta-analysis of randomized controlled
trials. PLoS Med 2010;7:e1000252.
13. Siri-Tarino PW, Sun Q, Hu FB, Krauss RM: Meta-analysis of
prospective cohort studies evaluating the association of saturated
fat with cardiovascular disease. Am J Clin Nutr 2010;91:535–546.
14. U.S. Department of Health and Human Services and the U.S.
Department of Agriculture. 2015–2202 Dietary Guidelines for
350 HARRIS ET AL.
Americans, Eight Edition. http://health.gov/dietaryguidelines/2015/
guidelines/ (accessed January 1, 2016).
15. Dayrit FM: The properties of lauric acid and their significance in
coconut oil. J Am Oil Chem Soc 2014;92:1–15.
16. Palazhy S, Kamath P, Rajesh PC, Vaidyanathan K, Nair SK,
Vasudevan DM: Composition of plasma and atheromatous plaque
among coronary artery disease subjects consuming coconut oil or
sunflower oil as the cooking medium. J Am Coll Nutr 2012;
31:392–396.
17. Eyres L, Eyres MF, Chisholm A, Brown RC: Coconut oil con-
sumption and cardiovascular risk factors in humans. Nutr Rev
2016;74:267–280.
18. Marten B, Pfeuffer M, Schrezenmeir J: Medium-chain triglyc-
erides. Int Dairy J 2006;16:1374–1382.
19. Zhang Y, Liu Y, Wang J, et al.: Medium- and long-chain tria-
cylglycerols reduce body fat and blood triacylglycerols in hyper-
triacylglycerolemic, overweight but not obese, Chinese individuals.
Lipids 2010;45:501–510.
20. Cardoso DA, Moreira AS, de Oliveira GM, Raggio Luiz R, Rosa
G, : A coconut extra virgin oil-rich diet increases HDL choles-
terol and decreases waist circumference and body mass in cor-
onary artery disease patients. Nutr Hosp 2015;32:2144–2152.
21. Arunima S, Rajamohan T: Influence of virgin coconut oil-enriched
diet on the transcriptional regulation of fatty acid synthesis and
oxidation in rats—A comparative study. Br J Nutr 2014;111:
1782–1790.
22. Ippagunta S, Angius Z, Sanda M, Barnes KM: Dietary CLA-
induced lipolysis is delayed in soy oil-fed mice compared to
coconut oil-fed mice. Lipids 2013;48:1145–1155.
23. Deol P, Evans JR, Dhahbi J, et al.: Soybean oil is more obeso-
genic and diabetogenic than coconut oil and fructose in mouse:
Potential role for the liver. PLoS One 2015;10:e0132672.
24. Hanak V, Munoz J, Teague J, Stanley A, Bittner V: Accuracy of
the triglyceride to high-density lipoprotein cholesterol ratio for
prediction of the low-density lipoprotein phenotype B. Am J
Cardiol 2004;94:219–222.
25. Millan J, Pinto X, Munoz A, et al.: Lipoprotein ratios: Physio-
logical significance and clinical usefulness in cardiovascular
prevention. Vasc Health Risk Manag 2009;5:757–765.
26. da Luz PL, Favarato D, Faria-Neto JR, Lemos P, Chagas ACP:
High ratio of triglycerides to HDL-cholesterol predicts extensive
coronary disease. Clinics (Sao Paulo) 2008;63:427–432.
27. Voon PT, Ng T, Lee VK, Nesaretnam K: Diets high in palmitic
acid (16 : 0), lauric and myristic acids (12 : 0 +14 : 0), or oleic
acid (18 : 1) do not alter postprandial or fasting plasma homo-
cysteine and inflammatory markers in healthy Malaysian adults.
Am J Clin Nutr 2011;94:1451–1457.
28. Sadeghi S, Wallace FA, Calder PC: Dietary lipids modify the
cytokine response to bacterial lipopolysaccharide in mice. Im-
munology 1999;96:404–410.
29. Nevin KG, Rajamohan T: Beneficial effects of virgin coconut oil
on lipid parameters and in vitro LDL oxidation. Clin Biochem
2004;37:830–835.
30. Nevin KG, Rajamohan T: Virgin coconut oil supplemented diet in-
creases the antioxidant status in rats. Food Chem 2006;99:260–266.
31. Nevin KG, Rajamohan T: Influence of virgin coconut oil on
blood coagulation factors, lipid levels and LDL oxidation in
cholesterol fed Sprague–Dawley rats. E Spen Eur E J Clin Nutr
Metab 2008;3:e1–e8.
32. Nagaraju A, Belur LR: Rats fed blended oils containing coconut
oil with groundnut oil or olive oil showed an enhanced activity of
hepatic antioxidant enzymes and a reduction in LDL oxidation.
Food Chem 2008;108:950–957.
33. Intahphuak S, Khonsung P, Panthong A: Anti-inflammatory,
analgesic, and antipyretic activities of virgin coconut oil. Pharm
Biol 2010;48:151–157.
34. Lemieux H, Bulteau AL, Friguet B, Tardif J-C, Blier PU: Dietary
fatty acids and oxidative stress in the heart mitochondria. Mi-
tochondrion 2011;11:97–103.
35. Krauss RM, Blanche PJ, Rawlings RS, Fernstrom HS, Williams
PT: Separate effects of reduced carbohydrate intake and weight
loss on. Am J Clin Nutr 2006;83:1025–1031.
36. Guay V, Lamarche B, Charest A, Tremblay AJ, Couture P: Effect of
short-term low- and high-fat diets on low-density lipoprotein par-
ticle size in normolipidemic subjects. Metabolism 2012;61:76–83.
37. Dreon DM, Fernstrom HA, Campos H, Blanche P, Williams PT,
Krauss RM: Change in dietary saturated fat intake is correlated
with change in mass of large low-density-lipoprotein particles in
men. Am J Clin Nutr 1998;67:828–836.
38. Astrup A, Dyerberg J, Elwood P, et al.: The role of reducing
intakes of saturated fat in the prevention of cardiovascular dis-
ease: Where does the evidence stand in 2010? Am J Clin Nutr
2011;93:684–688.
39. Muller H, Lindman AS, Blomfeldt A, Seljeflot I, Pedersen JI: A
diet rich in coconut oil reduces diurnal postprandial variations in
circulating tissue plasminogen activator antigen and fasting li-
poprotein (a) compared with a diet rich in unsaturated fat in
women. J Nutr 2003;133:3422–3427.
40. Seneviratne KN, Sudarshana Dissanayake DM: Variation of
phenolic content in coconut oil extracted by two conventional
methods. Int J Food Sci Technol 2008;43:597–602.
41. Seneviratne KN, HapuarachchI CD, Ekanayake S: Comparison of the
phenolic-dependent antioxidant properties of coconut oil extracted
under cold and hot conditions. Food Chem 2009;114:1444–1449.
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