Food Quality and Safety, 2019, XX, 1–12

doi:10.1093/fqsafe/fyz004
Review Paper

Review Paper

Coconut oil: what do we really know about it

Downloaded from https://academic.oup.com/fqs/advance-article-abstract/doi/10.1093/fqsafe/fyz004/5475954 by guest on 22 April 2019

so far?
Renan da Silva Lima and Jane Mara Block
Department of Food Science and Technology, Federal University of Santa Catarina, Florianópolis, Brazil

Correspondence to: Jane Mara Block, Department of Food Science and Technology, Federal University of Santa Catarina,
Av. Admar Gonzaga, 1346, Florianópolis, SC, 88034-001, Brazil. E-mail: janeblock@gmail.com
Received 13 November 2018; Revised 2 December 2018; Editorial decision 28 February 2019.

Abstract
In recent years, coconut oil has emerged as a potential ‘miracle’ food. Some media vehicles and
health specialists assure that this fat is capable of promoting health benefits, such as weight
reduction, cholesterol lowering, prevention of cardiovascular diseases, and anti-inflammatory
effect, among others. These claims are used to market the product and boost its sales by coconut
oil companies. However, governmental regulatory agencies in many countries are still sceptical
about the benefits obtained by the consumption of coconut oil due to its high-saturated fatty acid
content. In light of such controversy, this review focused on analysing the published literature
on the alleged health claims, in order to investigate if there is enough scientific evidence to
support them. It was verified that the metabolism of lauric acid, the major fatty acid in coconut
oil, remains unclear. Many studies reported that the product was not efficient in weight loss.
Also, it has been reported that the consumption of coconut oil increased low-density lipoprotein
cholesterol, consequently increasing the risk of cardiovascular diseases. In general, the studies
present conflicting results and there is a lack of long-term human-based clinical trials. Therefore,
as a saturated fat, coconut oil should be consumed with moderation and the health allegations
should not be used to market the product, once they are not scientifically proven so far.

Key words: lauric acid; saturated fatty acids; medium-chain triglycerides; LDL cholesterol; cardiovascular diseases.

Introduction
Coconut is one of the most important foods in some tropical and
subtropical countries, with the coconut tree being referred as the ‘tree
of life’. In such places, coconut and its products (milk and oil, among
others) are used in daily life by the general population for several
purposes, such as cooking, hair and skin treatment, food ingredient,
and folk medicine (DebMandal and Mandal, 2011). This plant is
cultivated in more than 90 countries, yielding a total production of
59 million tons in the year of 2016. The production of coconut is
heavily located in Asia, which was responsible for 83.8 per cent of
the world’s coconut production in 2016. In this same year, Indonesia
was the largest coconut producer with 16.6 million tons, followed
by the Philippines (14.1 million tons), India (9.8 million tons), Brazil
(2.5 million tons), and Sri Lanka (2.2 million tons) (Statista, 2018a).
In recent years, coconut oil (CO), the main coconut product,
has attracted the attention of the media and the population
worldwide, especially in Europe and North America. Celebrities,
digital influencers, and even doctors have endorsed the use of this
oil as a cooking media in substitution to other vegetable oils and
as a supplementary ingredient to be consumed with coffee and
vitamin shakes. Blogs, internet videos, and articles are promoting
the consumption of CO based on allegations that this product is
capable of bringing several health benefits. These benefits include
cholesterol-lowering effect, reduction of the risk of cardiovascular
diseases (CVDs), weight loss, improvement of cognitive functions,
action as an antimicrobial agent, and others (BBC News, 2018;
Medical News Today, 2018; New Straits Times, 2018; SBS, 2018;
The Indian Weekender, 2018).

1
© The Author(s) 2019. Published by Oxford University Press on behalf of Zhejiang University Press.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-
nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use,
please contact journals.permissions@oup.com
2
Following this modern trend, the sales of this product have grown.
According to Statista (2018b), the consumption of CO in the USA
increased by 34 per cent from 2004 to 2014. Many of the CO brands
market their product based on the supposed health benefits promoted
by its consumption. In their labels, we can find allegations such as ‘good
for cooking’ (iHerb, 2018a, iHerb, 2018d, eVitamins, 2018; Piping
Rock, 2018; Lucky Vitamin, 2018a), ‘one of nature’s healthiest cooking
oils’ (iHerb, 2018b), and ‘easy digestion, generating quick energy,
helping the protection and equilibrium of our organism’ (Americanas,
2018; Natumesa, 2018; Lucky Vitamin, 2018b; Lucky Vitamin, 2018c;
iHerb, 2018c). Some labels may even suggest the consumption of
one tablespoon once to three times a day with a meal (iHerb, 2018b;
iHerb, 2018c); others affirm that the consumption of CO is capable
of reducing cholesterol levels and the risk of a heart attack, besides of
aiding in weight reduction (QualiCôco, 2018; iHerb, 2018c).
At the same time, CO has also been attracting attention from the
scientific community with an exponential growth of scientific articles
on CO through the years (Figure 1).
However, the health-promoting effects of CO are far from
reaching a consensus. This may be attributed to the product’s
majorly saturated nature, with about 90 per cent of saturated
fatty acids in its composition. The excessive ingestion of saturated
fatty acids has been positively correlated with the increase of low-
density lipoprotein (LDL) cholesterol, with consequent development
of CVDs (Eyres et  al., 2016). The US Department of Agriculture
(USDA) recommends that the daily intake of saturated fat should not
surpass 10 per cent of the total calories (USDA, 2015). Likewise, the
World Health Organization (WHO) also recommends limiting the
intake of saturated fat to a maximum of 10 per cent of the daily total
calories (World Health Organization, 2018). On the other hand, the
European Food Safety Authority (EFSA), which does not specify a
limit for the ingestion of saturated fat, recommends that the intake
of saturated fat should be as low as possible (EFSA, 2017).
The American Heart Association, specifically for coconut fat,
does not recommend its consumption above the limit established by
the USDA for saturated fat intake (Sacks et al., 2017; USDA, 2015).
Considering that the fatty acid profile of CO is majorly composed of
saturated fatty acids, the consumption of this fat at the established 10
per cent limit in a 2000 kcal diet means that the subject would ingest
an amount of approximately 24 g of saturated fat on a daily basis.
As the USDA and the American Heart Association, the EFSA
also have issued a scientific opinion on the specific claims about
Figure 1.  Number of scientific papers about coconut oil through the years. (Scopus, 2018).
R. da S. Lima and J. M. Block
medium-chain fatty acids (MCFAs) as a weight reduction agent.
MCFAs account for 62 per cent of CO’s fatty acid composition. The
EFSA panel concluded that there is not enough evidence in human
intervention studies to support that MCFAs show a positive effect
in weight management. The statement concludes that this specific
allegation is weak and not convincing (EFSA, 2011).
In Brazil, the fourth largest CO producer, the Brazilian Society
of endocrinology and metabolism (SBEM) and the Brazilian
Association for the Study of Obesity and Metabolic Syndrome
(ABESO) have also issued a position on the use of CO as a weight
Downloaded from https://academic.oup.com/fqs/advance-article-abstract/doi/10.1093/fqsafe/fyz004/5475954 by guest on 22 April 2019
loss agent. Both health agencies support that there is not conclusive
scientific evidence about this topic. Therefore, the use of CO should
be restricted. SBEM and ABESO also do not recommend CO as a
cooking media due to its high-saturated fatty acid composition. On
the other hand, unsaturated vegetable oils such as soybean oil, olive
oil, and canola oil are recommended to diminish the risk of CVDs
(SBEM and ABESO, 2015).
The scientific evidence on the supposed benefits of CO should
be examined and more information should reach the population. In
this review, the chemistry and the processing, as well as the published
data on the major and minor health claims attributed to CO by the
media, the general public, and the manufacturing companies are
presented and discussed.
History of CO
In the late 19th century, the demand for edible oils was increasing
in Europe and in the USA. At the same time, in tropical countries
such as India, the Philippines, and Malaysia, among others, CO had
already encountered many uses in folk medicine and as a cooking
oil. Once Europeans became aware of the utilization of CO and its
several applications, they started establishing coconut plantations in
the Caribbean, Southeast Asia, and the South Pacific from the 1890s
to the 1920s. After that, CO became an edible oil very popular in
European countries and in the USA (Cassiday, 2015).
The first CO boom lasted until the World War II started
(around 1940), when the supply of the product was cut off to the
West countries and a CO shortage took place. As a result, its price
skyrocketed while the soy industry began to expand and develop,
which was made possible by the modern technology employed in
these oils’ processing (Oils and Fats International, 2018). Once the
war was over, even though countries with high-coconut production
Effects of coconut oil
tried to reintroduce its product in Western countries, CO was rejected
this time due to its high-saturated fat content (AOCS, 2016). This
rejection was associated with the findings of epidemiological studies
conducted by the American physiologist Ancel Keys, who, based on
such data, formulated a hypothesis of the association between the
consumption of high-saturated fat with a high-blood cholesterol
level and an increased development of CVDs (Cassiday, 2015).
Keys formulated his scientific hypothesis based on the observation
that well-fed American businessmen presented high rates of CVDs,
whereas people in post-war European countries facing shortage of
food showed decreased rates of CVDs. His hypothesis led to the
development of what would become one of Keys’ most relevant
work: The Seven Countries Study. This study described the lifestyle
of the population living in southern Italy, where the incidence of
CVDs was very low. This fact was attributed by Keys to the decreased
ingestion of animal fat, which presents high level of saturated fat and
cholesterol, and both factors were associated with the incidence of
coronary heart diseases (Keys et al., 1984).
The American Heart Association started in 1956, in parallel to
Key’s research, informing the population that large consumption of
high-saturated fat foods, such as butter, lard, eggs, and beef could
increase the risk for CVDs. In addition, the American government
launched a recommendation stating that adopting a low-fat diet was
necessary to prevent these diseases.
In the following decades, an increased number of researches
correlated CO with the raise in total serum cholesterol. However,
in most of these studies, subjects were exclusively fed with CO as a
fat source, whereas a control group would be fed with a vegetable
oil such as soybean or corn. These studies were criticized because
CO lacks ω-3 fatty acids in its composition, and it could be another
possible explanation for the reported results (Heek and Zilversmit,
1991; Cox et  al., 1995). On the other hand, studies that used
hydrogenated CO contained trans fatty acid as another possible
factor that could explain the negative results associated with the
consumption of CO (Frantz and Carey, 1961; Huang et al., 1984).
Further studies on CO’s metabolism indicated that CO, like
other saturated fats, increases both high-density lipoprotein (HDL)
and LDL cholesterol, also known as the ‘good and bad cholesterol’,
respectively. However, the LDL particles raised by the consumption
of these fats are large and buoyant, which are less related to coronary
diseases when compared with small and dense LDL particles (Katan
et al., 1994).
In the last decade, CO started to be massively advertized as a
healthier cooking oil alternative, changing the perception of the
consumers. However, this notion was motived by a miscellany of
non-scientific information available on the internet. In addition,
countries with major production of coconut also have a participa-
tion in positively promoting CO due to economic reasons. Therefore,
it is necessary to carefully analyse the chemical profile of CO and
scientific evidence about its effects on health.
Processing and Lipid Profile of CO
The coconut tree (Cocos nucifera) belongs to the family Arecaceae
and it is a tall palm typical of tropical and subtropical areas, growing
up to 30 m, yielding up to 75 fruits per year with proper practices
and growing conditions. The origin of this plant is still a subject of
debate, but the most accepted hypothesis is that the coconut tree was
originated in the India–Indonesia region. Botanically, the coconut
fruit is considered a drupe, where the exocarp and endocarp surround
a single shell of hardened endocarp containing a kernel inside.
3
Mesocarp and endocarp (husk and shell, respectively) are brown,
fibrous, and thick (3–5 mm), whereas the testa is the thin brown layer
separating the kernel from the shell (Pradeepkumar et al., 2008).
The kernel is also known as the ‘meat’ of the coconut. It generates
most of the products such as milk, oil, and dried coconut, among
others. The kernel has a moisture content of approximately 50 per
cent and it is frequently dried to a moisture content of 6%–8% for
oil extraction purposes, with the dried kernel being denominated
as copra (Canapi et  al., 2005). There are basically two types of
CO—refined, bleached, and deodorized copra oil (RBDCO) and
Downloaded from https://academic.oup.com/fqs/advance-article-abstract/doi/10.1093/fqsafe/fyz004/5475954 by guest on 22 April 2019
virgin (VCO). Both RBDCO and VCO have similar fatty acids
and triglycerides profile. On the other hand, virgin CO presents a
higher content of bioactive compounds such as vitamin E, sterols,
and polyphenols as refining removes a portion of these compounds
(Marina et al., 2009).
The extraction of the CO is preceded by the drying step which
can be performed either by sun drying, direct-fire drying, or hot-air
drying. In the sun drying method, the kernels are placed under the
sun for 6 to 8 days. In the direct-fire drying method, nuts are placed
in a bamboo grill platform where heat is provided by the burning
of coconut shells and husks. Finally, in hot-air drying, husks and
shells are used as fuel. The process is conducted in a drying device
equipped with a steel plate bottom to isolate the kernels from getting
in contact with the smoke generated by the fuel. After the drying
process, the kernel shrinks and separates from the shells (Canapi
et al., 2005).
The obtained copra is flaked to increase the surface area and the
flakes are cooked at 115°C for 20 min. Then, the material (with a
moisture content adjusted to 3%–4%) is fed to an expeller, for the
oil extraction. The copra cake usually presents an oil content of ap-
proximately 7 per cent and an extraction using hexane as solvent
is performed, reducing the oil content of the cake to 3.5 per cent
(O’Brien, 2004).
The oil extraction may also be performed using the fresh kernel.
The advantage of the wet extraction is a superior quality of the
obtained oil, as well as the recovery of nutrients such as protein,
carbohydrates, and vitamins. RBDCO is obtained by physical or
chemical refining of the crude CO. This process is intended to remove
impurities that would make the product not suitable for human con-
sumption and/or decrease its quality and shelf life. The substances
removed in the refining process are free fatty acids, phosphatides,
metal irons, colour bodies, oxidation products, solid particles, and
volatiles that cause undesirable flavours. After refining, the oil is
bleached and deodorized at 204–245°C (O’Brien, 2004).
As for VCO, in the wet extraction, the oil can be extracted dir-
ectly from coconut milk. For this purpose, the oil-in-water emulsion
needs to be broken, which can be achieved by mechanical force (cen-
trifugation), fermentation, or even enzymatic extraction (Marina
et  al., 2009). Regardless of the use of refining or not to obtain
the product, CO has a high concentration of saturated fatty acids
compared with most of the vegetable oils and fats present in the diet.
Table 1 shows the lipid profile of CO and some of the major oils and
fats consumed in the diet.
Although conventionally named as an oil, CO is actually a fat,
once it is majorly composed by saturated fatty acids (92 per cent),
from which 62 per cent corresponds to fatty acids with carbon
number between 8 and 12 (Eyres et  al., 2016). The proportion of
saturated, monounsaturated, and polyunsaturated fatty acids in the
major oils and fats consumed in the diet can be observed in Figure 2.
CO belongs to a unique group of fats named lauric oils, once
lauric acid (12:0) is the major fatty acid present in its composition.
4 R. da S. Lima and J. M. Block

Table 1.  Fatty acid profile and minor components of major vegetable oils.

Fatty acid (%) CO* PKO* BPO* Butter SO* CNO* SFO* OO*

Butyric C4:0 – – – 3.5 – – – –

Caproic C6:0 0.5 – 0.3 1.4 – – – –
Caprylic C8:0 7.8 3.3 4.9 1.7 – – – –
Capric C10:0 6.7 3.4 4.6 2.6 – – – –
Lauric C12:0 47.5 48.2 47.5 4.5 – – – –
Myristic C14:0 18.1 16.2 19.0 14.6 – – – –
Palmitic C16:0 8.8 8.4 8.0 30.2 10 4 5 16.5

Downloaded from https://academic.oup.com/fqs/advance-article-abstract/doi/10.1093/fqsafe/fyz004/5475954 by guest on 22 April 2019

Stearic C18:0 2.6 2.5 4.6 10.5 4 2 6 2.3
Palmitoleic C16:1 – – – 4 – – – 1.8
Oleic C18:1 6.2 15.3 14.5 23 23 61 30 66.4
Linoleic C18:2 1.6 2.3 5.4 3 51 21 59 16.4
α-Linolenic C18:3 – – – 1 7 11 – 1.6
 C20:0 0.1 – 0.05 – – – – 0.43
 C22:0 0.15
 C20:1 traces – – – – – 0.3
Other – – – 5 1 – –
Sterol composition (%)
Cholesterol 1.8 4.6 1.4 98.8 1.0 – 0.35 0.25
Brassicasterol 0.45 – 0.15 – 0.15 12.5 0.1 0.05
Campesterol 7.2 23.1 18.2 – 20.0 31.5 10 2.0
Stigmasterol 10.5 11.2 8.9 – 17.5 0.5 9.5 2.0
β-sitosterol 35.2 56.1 51.1 – 54.6 52.0 60.5 77.5
D5-Avenasterol 27.8 1.4 18.6 – 2.8 1.5 4.2 9.0
D7-Stigmasterol 1.5 1.3 – – 3.3 – 15.5 0.25
D7-Avenasterol 1.5 2.5 0.7 – 2.8 – 4.7 –
Other 14.1 – 0.95 1.2 – 2.0 – 8.9
Total sterols (ppm) 805 494.5 668 2150 2965 881 3495 100
Tocopherol and tocotrienol composition (ppm)
α-tocopherol 8.5 98.5 – 16.5 180.5 148 675 99.0
β-tocopherol 5.5 117 – – 20 34.0 25.0 6.0
γ-tocopherol 7.0 263 – – 1244.5 538.5 25.0 11.0
δ-tocopherol – 61.5 – – 541 275 5.0 –
α-tocotrienol 22.0 170 35.5 – 34.5 – – –
β-tocotrienol – – – – – – – –
γ-tocotrienol – 362 56.0 – 51.5 – – –
δ-tocotrienol – 188.5 9.5 – – – – –

(Adapted from Firestone, 2013; Sankararaman and Sferra, 2018; Derewiaka et al., 2011).
* CO = coconut oil; PKO = palm kernel oil; BPO = babassu palm oil; SO = soybean oil; CNO = canola oil; SFO = sunflower oil; OO = olive oil.

Palm kernel oil and babassu oil are also part of this group. Some
researchers believe that lauric oils have unique properties, once they
behave very differently in the metabolism compared with fats ma-
jorly composed by LCFA (Dayrit, 2014). Such differences will be
addressed in the CO and weight loss section.
There is an ongoing debate whether the lauric acid should be
classified as a MCFA or not. Some specialists classify MCFAs as
having a chain length of 8 to 12 carbon atoms, whereas others de-
fine MCFAs as having 6 to 10 carbon atoms (Sankararaman and
Sferra, 2018). According to Scrimgeour (2005), fatty acids with a
chain length below 16 carbons are characterized as short-chain fatty
acids (SCFA) or MCFA.
Commercial medium-chain triglyceride (MCT) oil is
predominantly composed of caprylic acid, C8:0 (50%–80%)
and capric acid, C6:0 (20%–50%). However, other combinations
are also common. This product can be synthesized either by the
hydrolyzation of MCFAs from coconut/palm kernel oil or by
lipid structuring (Babayan, 1987). MCT oil is usually marketed
as a supplement for weight reduction, with a recommended daily
dosage of 50–100 g (4–6 tablespoons) for improved gastrointestinal
tolerance (Shah and Limketkai, 2017). However, this product is
majorly composed of saturated fatty acids (93%–100%); therefore,
this dosage surpasses the recommended daily intake of saturated fat
(around 24–22 g).
A portion size of 100  g of CO contains 890 kcal and 82.5  g
of saturated fat. Butter, lard, and palm oil present a much lower
concentration of this type of fatty acid (51.2, 39, and 49  g,
respectively) and fewer calories (717, 900, and 884 kcal, respectively)
for the same portion size. In addition, CO lacks essential fatty acids,
which are present in other vegetable oils used in cooking, such as
soybean oil (7 per cent linolenic acid and 51 per cent linoleic acid),
flaxseed oil (53 per cent linolenic acid and 13 per cent linoleic acid),
and canola oil (9.1 per cent linolenic acid and 18.6 per cent linoleic
acid) (Mansor et al., 2012). Also, compared with palm oil, CO is low
on bioactive compounds. Crude palm oil contains a total carotenoid
content of 500–700 mg/l (Posada et al., 2007), which is not present
in virgin CO. Regarding vitamin E, virgin CO contains around
38 mg/kg (Mansor et al., 2012), whereas palm oil has 600–1260 mg/
kg. However, α-tocopherol, which is the most biologically active
form of vitamin E, is higher in CO (40%–44% of total tocopherol
content) than in palm oil (18%–21% of total tocopherol content)
(Posada et al., 2007; Mansor et al., 2012).
Effects of coconut oil
Figure 2.  Proportion of saturated, monounsaturated, and polyunsaturated fatty acids in the main fats and oil.
From a biochemical standpoint, virgin CO is preferable to
RBDCO once it contains a higher amount of substances with
antioxidant properties. However, a diet based on CO as the major
fat source would not contain fatty acids that are essential for humans
(linoleic and linolenic fatty acids). The lack of such fatty acids in the
diet can cause innumerous health problems such as skin conditions,
dermartitis, poor wound healing, impaired growth, and increased
susceptibility to infections (Simopoulos, 2002). CO, due to its high
content of saturated fatty acids, is more resistant to oxidation and
polymerization than unsaturated oils such as sunflower oil and olive
oil. However, despite its saturated nature, the use of CO as a cooking
oil should not be encouraged, once it exhibits a low smoking
point (171°C) and its use in continuous deep-frying leads to the
production of carcinogenic substances, such as polycyclic aromatic
hydrocarbons and aromatic amines. Oils with higher smoking points
are preferred for deep drying, such as canola oil (238°C), corn oil
(232°C), and soybean oil (238°C) (Srivastava et al., 2010).
Another problem with the continuous use of CO emerges from
the fact that a large proportion of its fatty acid profile is made up
of SCFA. Therefore, CO is more susceptible to undergo hydrolytic
rancidification than other fats. The liberation of free SCFAs in
the medium catalyses the reaction, accelerating the formation of
rancidity products, such as aldehydes and ketones, consequently
lowering the quality of the product (Oseni et al., 2017).
Health Claims: What Is Scientifically Proven
and What Is Not
Major claims
CO and weight loss
CO has been heavily promoted as a weight reduction agent.
The digestion mechanism of medium-chain saturated fatty acids
(MCSFAs) is the argument used to support this claim. According to
this theory, MCTs induces satiety, preventing the individual from
5
Downloaded from https://academic.oup.com/fqs/advance-article-abstract/doi/10.1093/fqsafe/fyz004/5475954 by guest on 22 April 2019
overeating (Clegg, 2017). To elucidate the mechanisms involved in
the absorption, digestion, and metabolism of fatty acids from CO,
it is necessary to review the different metabolic fates between long-,
medium-, and short-chain saturated fatty acids. In fats and oils, more
than 95 per cent of fatty acids are present in the form of triglycerides
(TAGs). However, they cannot be absorbed by the intestine in such
state; therefore, they are partially hydrolysed by the action of acid-
stable gastric lipases in the stomach, providing diglycerides and free
fatty acids.
The regiospecificity of the distribution of fatty acids are correlated
with the form that each fatty acid will be absorbed. The hydrolysis
promoted by lipases (especially pancreatic lipases) preferentially
takes place at the sn-3 and sn-1 positions, respectively (Bracco,
1994). This is due to the fact that the pancreatic lipase exhibits a
high affinity for short-chain saturated fatty acids (lower than 10
carbons) located at the sn-3 and sn-1 positions, which accounts for
a higher activity of the enzyme and, consequently, better absorption
of such fatty acids. On the other hand, long-chain unsaturated fatty
acids (LCUFAs) have an increased bioavailability when located at
sn-2, which is also due to a higher activity of the pancreatic lipases.
In fact, this characteristic can be used as a strategy for structuration
of lipids, where essential fatty acids, such as linoleic and linolenic
acids, can be located at the sn-2 position in order to intensify their
bioavailability (Carnielli et al., 1995; Haumann, 1997).
The products generated by the hydrolysis process enter the
duodenum, where the pancreatic lipases bind to the surface of
remaining TAGs along with co-lipases (a constituent of pancreatic
juice) to continue carrying out the digestion process. The continuous
breaking down of TAGs results in sn-2-monoacylglycerols and free
fatty acids. The conversion of sn-2 to sn-1(3)-monoacylglycerols
can also take place, with further hydrolysis, resulting in glycerol
and free fatty acids. From this point on, the metabolic pathways in
digestion and absorption greatly differ between short- and medium-
chain triglycerides, and LCT. This is due to the greater affinity that
6
pancreatic lipases exhibit for SCFAs and MCFAs. Therefore, they are
more likely to be broken into three fatty acids and glycerol (Mu and
Høy, 2004). As for LCFAs, they are usually reesterified into LCTs and,
along with fat-soluble molecules, such as vitamins and cholesterol,
are mixed with bile salts forming micelles. The contents present in
the micelles enter the enterocytes, where they are rearranged into
triglycerides and packaged into chylomicrons (Mu and Høy, 2004).
Then, chylomicrons are transported through the blood plasma,
and by the action of lipoprotein lipases (LLP), are partially digested,
resulting in glycerol, free fatty acids, and chylomicron remnants. The
FFAs are absorbed by adipocytes, being once again restructured into
triglycerides and stored. The glycerol and the chylomicron remnants
are ultimately transported to the liver (Mu and Høy, 2004).
On the other hand, short- and medium-chain saturated fatty
acids, due to their smaller molecular weight, are hydrolysed faster
when compared with long-chain saturated fatty acids. Therefore,
SCSFA and MCSFAs are not deposited in the adipose tissue, once
they are transported directly in the portal venous system to the liver,
bypassing the peripheral tissues. In addition, MCSFAs are able to
cross the mitochondrial membrane of the liver and muscle without
the aid of the acylcarnitine transfer system, which makes them a
more readily available energy source (Dayrit, 2015).
The problem with the assumption that CO aids to weight loss
relies on the fact that lauric acid is the major fatty acid encountered
in CO (47.5 per cent). This fatty acid is present in much smaller
amounts in MCT oil, which is used in the majority of scientific
researches. Moreover, the classification of lauric acid as a MCFA is
still controversial, once clinical studies point out that only 20 to 30
per cent of lauric acid is directly transported to the liver (Lockyer
and Stanner, 2016; Clegg, 2017; Sankararaman and Sferra, 2018).
St-Onge and Jones (2003) reported that the consumption of
MCT oil by overweight men increased energy expenditure and
decreased adiposity. The subjects were recruited based on a BMI
between 25 and 31 kg/m2, total cholesterol below 7.0 mmol/l, and
total triglyceride concentration below 3.0 mmol/l. Besides, the men
did not present cardiovascular disease, diabetes, hypertension, and
gastrointestinal disorders, nor were taking cholesterol-lowering
medications. The diet consumed during the trial period consisted of
40 per cent of energy as fat, 55 per cent as carbohydrates, and 15
per cent as protein. The MCT oil used in this study was composed of
caproic (0.17 per cent), caprylic (36.95 per cent), capric (30.33 per
cent), lauric (3.61 per cent), myristic (1.06 per cent), palmitic (3.52
per cent), palmitoleic (0.23 per cent), stearic (0.65 per cent), oleic
(13.81 per cent), linoleic (4.62 per cent), linolenic (4.94 per cent),
and eicosanoic (0.05 per cent) fatty acids.
However, once the MCT oil used in the study contained only
3.61 per cent of lauric acid, these results cannot be extrapolated to
CO, once both products are very different regarding the fatty acid
composition. Assunção et al. (2009) studied how the administration
of a daily dosage of 30  ml of either soybean oil or CO would
affect the biochemical and anthropometric profiles of 40 women
aged 20–40  years old presenting abdominal obesity. Both groups
decreased energy intake and the amount of carbohydrate ingested
during the 12 weeks the study was conducted. On the other hand,
the consumption of protein and fibre increased while the ingestion
of lipids remained unaltered. The CO group exhibited a reduction
in waste circumference, which was not observed for the soybean oil
group. The benefit of CO in reducing the waste circumference was
also observed by Liau et al. (2011). The authors reported that a daily
dosage of 30 ml of CO reduced an average of 2.86 cm in the waste
circumference of male subjects. The lipid profile (total cholesterol,
R. da S. Lima and J. M. Block
HDL-c, and LDL-c) of the subjects did not alter significantly during
the experiment. However, the study was conducted for only 4 weeks;
therefore, it is not possible to draw a conclusion regarding the long-
term effect of CO on such parameters.
Valente et  al. (2018) evaluated the effects of the consumption
of virgin coconut oil (VCO) on energy metabolism, serum
cardiometabolic risk markers, and subjective appetitive responses in
17 women aged between 19 and 42 years old with excess body fat
(>32 per cent). Subjects were given 25 ml of CO during breakfast,
whereas the control group received olive oil instead. No difference
Downloaded from https://academic.oup.com/fqs/advance-article-abstract/doi/10.1093/fqsafe/fyz004/5475954 by guest on 22 April 2019
in fasting metabolic rates was observed between the two groups. On
the other hand, lower hunger suppression at 240  min, satiety, and
total fullness were reported for the group of subjects who received
VCO when compared with the group who received olive oil. Some
limitations such as the fact that this was not a long-term study
and the subjective method used to assess the research questions
(application of questionnaires to the subjects) were reported by the
authors.
Kinsella et al. (2017) also reported that CO promoted a smaller
satiety compared with the MCT oil composed of caproic (2 per
cent), caprylic (50%–60%), capric (30%–45%), and lauric (3 per
cent) acids. The authors administered a dosage of 25 g of the studied
oils during breakfast to 24 men and 18 women, and assessed satiety
using a visual analog scale. In addition, the leftover from their lunch
meal were weighted to measure food intake. The MCT oil group
had a reduced food intake throughout the day compared with the
CO group. Also, the MCT oil group reported the highest fullness
perception as assessed by the visual analog scale. The exclusion of
obese subjects, the high amount of fat administered, which does not
represent the reality of most of the population, and the awareness
of the participants about their food intake being measured were
some limitations of this study. Maher et al. (2017) reported similar
results when studying the effect of CO in comparison with MCT
oil on satiety and food intake of 15 healthy participants. MCT oil
showed a better response for fullness perception and food intake
when compared with CO.
In another similar study reported by LaBarrie and St-Onge
(2017), corn oil and CO-enriched meals (dosage of 20  g) were
administrated to 15 obese adolescents aged 13–18 years old. They
observed that the thermogenesis and satiety were not increased in
the group that received CO. The authors concluded that more re-
search is needed in order to investigate CO as a tool for weight man-
agement. Clegg (2017) reviewed the existing literature linking CO
to weight loss and concluded that there is not enough scientific evi-
dence to support that CO helps increase satiety and contributes to
weight loss. The author also highlights the lack of long-term clinical
trials on this specific topic.
Clinical trials studying the relationship between the consump-
tion of CO and weight reduction are still scarce in the literature.
The analysis of the existing data shows a lack of evidence that CO
may work as a weight loss agent. The few existing data are not suf-
ficient to indicate that the metabolism may be accelerated through
the consumption of coconut nut. Also, due to the discrepant fatty
acid profile, MCT oil data are irrelevant to understand the digestion
behaviour of CO. Therefore, based on the current knowledge, the
allegations that CO aids to weight loss are unrealistic and unsup-
ported by scientific evidence.
CO in the reduction of cholesterol levels
Cholesterol is a lipid molecule synthesized by animal cells with the
primary function of structuring cell membranes, maintaining its
Effects of coconut oil
integrity and fluidity. This substance also functions as a precursor
for the synthesis of steroid hormones, vitamin D, and bile acids.
Cholesterol is transported through the portal vein mainly by the
HDL and the LDL. HDL-c is often referred as ‘good cholesterol’,
once it removes cholesterol from the peripheral vessels back
to the liver for disposal, which is named reverse cholesterol
transport (RCT). Additionally, it has been discussed that HDL also
exhibits antioxidant, anti-inflammatory endothelial/vasodilatory,
antithrombotic, and cytoprotective functions (Kosmas et al, 2018).
On the other hand, LDL, also known as ‘bad cholesterol’, can be
a driving factor for the development of CVDs if they oxidize
within the walls of arteries. Thus, maintaining higher HDL-c levels
while keeping LDL-c low is recommended in order to avoid the
development of CVDs (Ganesan et al., 2017).
The effects of the consumption of CO on cholesterol levels vary
from study to study and generate controversy, once the majority of
them are animal trials. Allan et  al. (2001) studied how the serum
lipoprotein cholesterol and triglyceride concentrations of 30 pigs
were affected by the consumption of diets containing fish oil, milk
fat, olive oil, and hydrogenated CO (at a 4 per cent concentration).
The study was conducted for 3 weeks and at the end of this period
no significant difference in LDL-c levels was observed between the
groups consuming different oils. The authors reported that the
groups of pigs consuming CO, milkfat, and olive oil showed a higher
HDL-c, with CO and milkfat also increasing the serum triglyceride
concentration. The authors highlighted that the lipoprotein metab-
olism is different between pigs and humans and for this reason the
results may not be extrapolated to humans.
Nevin and Rajamohan (2004) found that VCO reduced total
cholesterol, triglycerides, phospholipids, LDL, and VLDL choles-
terol in Sprague–Dawley rats after 45  days when compared with
RBDCO. On the other hand, HDL-c was increased and in vitro LDL
oxidation was prevented in the group of animals fed with VCO.
The authors concluded that the higher polyphenol content and
other minor components present in VCO were responsible for the
observed effects.
Dauqan et al. (2011) evaluated the effects of the supplementation
in the diet of 15 per cent of CO, red palm olein, palm olein, and corn
oil on the lipid profile of 66 Sprague Dawley male rats. The vegetable
oils were supplemented for 4 and 8 weeks and a control group with
no vegetable oil addition was also conducted. The group that was
supplemented with CO and corn oil showed an increase in LDL-c
and a decrease in HDL-c when compared with the control group.
After 8 weeks, total cholesterol and LDL-c levels did not present a
significant difference between the diets supplemented with the vege-
table oils and the control group.
Other measurements besides the level of LDL-c may indicate
increased risk of development of CVDs. Mangiapane et  al. (1999)
reported the effects of CO and olive oil (150 g/kg diet) on athero-
sclerosis in Golden Syrian. The plasma LDL-c concentration and the
extension of atherosclerotic lesions for the group consuming olive
oil were lower than the group consuming CO. After 16 weeks, lesion
sizes doubled in rats fed with the CO diet.
The few studies performed on human subjects also present
conflicting conclusions. Cox et al. (1995) found that CO raised total
and LDL cholesterol compared with safflower oil in 28 individuals
with moderate hypercholesterolaemia, although butter had the
highest effect between the three types of lipid sources studied. The
authors reported that this result was expected due to the proportion
of saturated fatty acids in CO in relation to predominantly
unsaturated oils.
7
Feranil et  al. (2011) conducted a cohort study about the
relationship between the intake of CO as a cooking oil for frying and
‘soutéing’ and the lipid profile of 1839 pre- and post-menopausal
Filipino women aged between 35 and 69  years old. The average
daily intake of CO was 9.54  g. The post-menopausal women
showed the highest intake level of CO and a lower HDL-c, higher
total cholesterol, LDL-c, triglycerides, and total cholesterol:HDL
ratio when compared with pre-menopausal women. Eyres et  al.
(2016) reported that in the majority of the 21 studies evaluated in
their review, CO is more effective at increasing total cholesterol and
Downloaded from https://academic.oup.com/fqs/advance-article-abstract/doi/10.1093/fqsafe/fyz004/5475954 by guest on 22 April 2019
LDL-c than unsaturated oils. On the other hand, this effect would be
diminished when compared with butter.
The decrease in LDL-c and/or the increase in HDL-c promoted
by CO has also been reported. Cardoso et al. (2015) reported in a
study with 114 coronary heart disease patients a decrease of LDL-c
and unaltered levels of total cholesterol and HDL-c in the blood both
for the group consuming the control diet and the one consuming
VCO. Chinwong et al. (2017) reported a randomized crossover trial
to assess the effects of VCO consumption on the lipid profile of 32
healthy participants (age 18 to 25  years old). Fifteen millilitres of
VCO twice a day were consumed by one of the groups, whereas the
control group received a solution of carboxymethylcellulose 2 per
cent. The VCO group showed a significant increase in the HDL-c
level (64.2  mg/dl) compared with the control group (59.0  mg/dl)
after 8 weeks. The changes in total cholesterol, LDL-c, and trigly-
ceride levels were not significant between the groups studied.
A neutral effect for CO on lipid parameters was reported by
Sabitha et al. (2009). They found that the consumption of CO and
sunflower oil (13 to 20 per cent of the total calorie content in the
diet) did not alter lipid parameters on normal and type 2-diabetic
subjects. Shedden (2017) reported a randomized double blind study
for 8 weeks with 42 healthy adult men between 18 and 40 years old.
The results showed no changes in the levels of total, HDL, and LDL
cholesterol for supplementation either with capsules with 2 g of CO
or a placebo capsule of flour.
The effects of CO on reducing human cholesterol levels do not
have solid scientific support yet. The insufficient number of studies,
the small number of subjects, the short periods, and the different
concentrations of CO in the diet in the studies performed contribute
for a lack of consistency among the results reported in the literature.
Since there is no consensus on the effects of CO intake on the health
of the population, the information conveyed in advertisements or
present in CO labels has no scientific support and may be considered
misleading.
CO and the incidence of CVDs
CVDs include a number of different conditions such as stroke,
hypertension, myocardial infarction, and congestive heart failure,
among others. A combination of many factors may lead to the devel-
opment of these conditions, such as age, lifestyle, smoking, lacking
of exercise, obesity, diabetes, and diet. Researchers and government
regulatory agencies have a special concern about CVDs once they
are responsible for over 40 per cent of deaths worldwide every year
(Nabel, 2003). The American Heart Association estimates that in
the USA every 38 s a death occurs due to CVDs (American Heart
Association, 2018).
The development of CVDs may be heavily influenced by the
consumption of foods capable of increasing serum cholesterol and
blood pressure. This can also be a leading factor in the incidence
of obesity and diabetes. An excessive amount of reactive oxygen
species generated by the oxidative process can lead to atherosclerosis
8
and other CVDs (Heistad et al., 2009). Therefore, the ingestion of
substances with radical scavenging capacity, such as polyphenols,
carotenoids, tocopherols, and tocotrienols present in fruits,
vegetables, and some oils and fats may help prevent CVDs.
Red palm oil is a rich source of carotenoids, specifically
β-carotene. Vitamin E (tocopherols and tocotrienols) is also present
in high amounts in red palm oil as well as in soybean and canola oil
(Posada et al., 2007). Olive oil is rich in monounsaturated and poly-
unsaturated fatty acids, which are linked to cholesterol-lowering and
anti-atherogenic effects, reducing the risk of CVD. Olive oil is also
the main source of hydroxytyrosol, a phenolic compound with anti-
oxidant properties. Other vegetable oils such as sunflower and soy-
bean oil are also rich in polyunsaturated fatty acids and antioxidant
compounds. The consumption of different oils with this chemical
profile has been associated with a decreased risk of CVD (Metcalf
et  al., 2007; Guasch-Ferré et  al., 2014; Jones et  al., 2014; Covas
et al., 2015; Valderas-Martinez et al., 2016).
On the other hand, fats rich in saturated fatty acids are known
for increasing blood cholesterol, which is one of the prevalent causes
of atherosclerosis, associated with an increased risk for coronary
heart disease (Ganesan et al., 2017). Zhong et al. (2016) analysed the
influence of saturated fatty acids on the risk of coronary heart disease
in American men and women in two prospective longitudinal cohort
studies. The 18 years study followed 115.782 healthy people (73 147
women and 42 635 men). A higher consumption of lauric acid (12:0),
myristic acid (14:0), palmitic acid (16:0), and stearic acid (18:0) was
positively correlated with an increase in the risk of coronary heart
disease. The risk was significantly decreased when saturated fatty
acids, especially palmitic acid, were replaced with polyunsaturated
fatty acids, whole grain carbohydrates, and plant protein.
In recent years, the media and CO producers have linked the
consumption of CO to the prevention of CVDs (Sankararaman and
Sferra). However, due to its majorly saturated structure, composed
mainly by lauric and myristic acids, this claim should be carefully
analysed. Vijayakumar et  al. (2016) reported a high incidence of
CVDs in the state of Kerala (India) where the population heavily
uses CO as a cooking medium.
Nevertheless, some studies investigate if VCO has a positive
effect on lowering the incidence of CVD due to its polyphenol com-
position. Famurewa and Ejezie (2018) isolated polyphenols from
virgin CO to verify their potential action against cadmium-induced
dyslipidemia and oxidative stress in rats. The polyphenol extract
used had a total phenolic content of 57.11 mg GAE/100 g of oil. The
subjects were treated with VCO-polyphenols (10, 20, and 50 mg/kg
body weight) for 2 weeks prior to the administration of Cd (5 mg/kg
body weight). The Cd-control group (no polyphenols ingestion)
had their total cholesterol (TC), LDL-c, and VLDL-c significantly
increased, whereas the HDL-c decreased. The administration of
VCO-polyphenols was capable of decreasing TC, VLDL-c, and
LDL-c while increasing HDL-c, with the 50 mg/kg doses being the
most efficient. This study showed that polyphenols present in VCO
could be a great source for the development of CVD-preventing
supplements. However, as VCO was not used as a whole product
in the experiment, it cannot be said if the same effect would be
observed if VCO itself was administrated.
Famurewa et al. (2018) studied the effect of the supplementation
in the diet of 10 and 15 per cent of VCO in healthy rats on the lipid
profile, hepatic antioxidant status, and cardiovascular risk indices
over 5 weeks. The authors reported a reduction of TC, triglycerides,
and LDL-c levels and an increase in the HDL-c for the groups of rats
fed with 10 and 15 per cent of VCO when compared with the control
group. The performance of the group fed with 15 per cent of VCO
R. da S. Lima and J. M. Block
was significantly better compared with the group fed with 10 per cent
of VCO. Similar results have been reported in the literature in animal
trials associating the VCO’s polyphenols to a reduction on the risk
of CVD (Nevin and Rajamohan, 2008; Arunima and Rajamohan,
2013; Nurul-Iman et  al., 2013; Arunima and Rajamohan, 2014;
Subermaniam et al., 2014; Kamisah et al., 2015).
On the other hand, Muthuramu et al. (2017) reported a higher
mortality by cardiomyopathy for mice fed a diet containing 10 per
cent of CO when compared with chow-fed mice. The myocardial
capillary density was lower and the oxidative stress was higher for
Downloaded from https://academic.oup.com/fqs/advance-article-abstract/doi/10.1093/fqsafe/fyz004/5475954 by guest on 22 April 2019
CO-fed group. The authors concluded that the daily consumption of
CO aggravates pressure overload-induced cardiomyopathy in mice.
Vijayakumar et al. (2016) studied how the administration of CO
and sunflower oil affected the cardiovascular risk factor in humans.
The trial was conducted with 100 patients in each group who also
received the standard medication. The oil intake was calculated to
meet the 15 per cent of the daily calories from fat. After a period of
2 years, their lipid profile, antioxidant mechanism, and endothelial
function were analysed. No significant differences between the two
groups were observed. The authors concluded that such results were
due to the fact that CO is predominantly composed of MCSFAs,
behaving differently from fats majorly composed of LCSFA. The
limitations of this study include the low number of subjects and the
exclusion of CVD-free from the trial.
Palazhy et  al. (2018) also reported the effects of the consump-
tion of CO compared with sunflower oil in coronary artery disease
patients in Kerala, India. A total of 150 subjects consumed one of
the two oils for a period of over 2 years. The lipid parameters such
as TC, LDL-c, HDL-c, and oxidized LDL were evaluated and did not
differ significantly between the two groups. The limitations of this
study that could have interfered with the results include the small
number of subjects, uncontrolled conditions, and the use of lipid-
lowering medication by the patients.
The few studies that have reported a cardioprotective effect for
VCO are predominantly animal trials. There is not enough informa-
tion on this topic as well as a lack of studies using human subjects.
Therefore, it is still not possible to assume that the continuous con-
sumption of this fat may have an impact on diminishing the risk of
CVDs.
Minor claims
CO and the prevention and treatment of Alzheimer’s disease
It has been reported that the MCTs of CO have a potential for pre-
vention and/or treatment of Alzheimer’s disease. The MCTs are
easily absorbed and metabolized by the liver and converted into ke-
tone bodies. Once ketone bodies are an alternative energy source for
the brain, they might help improve the cognitive function (Fernando
et al., 2015).
Nafar and Mearow (2014) reported the effect of 2 g of VCO on
cortical neurons treated with amyloid-β (Aβ) peptide in vitro. VCO
and Aβ-treated cell cultures showed a higher survival rate, and VCO
also attenuated Aβ-induced mitochondrial alterations. In a study
conducted by Nafar et al. (2017), the addition of VCO 24 h prior
to the application of Aβ led to the highest survival rate of neuron
cell cultures. The results indicated that the supplementation with CO
may be effective on the symptoms of the neurodegeneration, since its
polyphenol content might promote neuronal health through antioxi-
dant mechanisms.
Yang et  al. (2015) reported that Alzheimer’s disease patients
treated with daily doses of 40 ml/day of extra virgin CO improved
their cognitive status tested by the score MEC-WOLF. The results
were higher for women without diabetes mellitus type II and for
Effects of coconut oil
severe patients. Since the studies on this topic are very scarce, there
is not enough scientific support for the claims associating CO
consumption with an improvement of the symptoms of Alzheimer’s.
CO and the anti-inflammatory effects
The potential anti-inflammatory properties of CO and its bioactive
compounds have been investigated by Vysakh et al. (2014). A VCO-
polyphenol extract (80 mg/kg) exhibited 74 per cent inhibition on
adjuvant induced chronic model of inflammation and the antioxi-
dant enzymes were also increased on adjuvant-induced arthritis rats.
This study showed that VCO can be a source for the extraction of
polyphenolic compounds for further development of nutraceuticals.
However, VCO per se was not used in the study; therefore, the
results obtained cannot be extrapolated.
Intahphuak et  al. (2010) reported that a dosage of 4  mg/20  μl
of VCO showed moderate anti-inflammatory effects on ethyl
phenylpropiolate-induced ear oedema in rats. However, the efficacy
of VCO was not higher than the standard drug Indomethacin.
Zakaria et al. (2011) showed an anti-inflammatory activity in an
acute inflammation model of VCO (dried and fermented) using in
vivo models (Male Balb-C and Sprague–Dawley rats). Studies on this
topic are still scarce and the anti-inflammatory effects of CO do not
have a solid scientific support yet.
CO and the antimicrobial effects
The antimicrobial effects of CO are attributed to monolaurin, which
is a monoglyceride formed by glycerol and lauric acid (Lieberman
et al, 2006). This compound is widely used as a food emulsifier and
also sold as a supplement. Strandberg et al. (2009) reported an in-
hibitory effect of monolaurin on Staphylococcus aureus in a human-
based study. Wang et al. (2014) reported the inhibition of monolaurin
against Hilicobacter pylori added in a mouthwash solution. Since the
amount of monolaurin produced biologically after the consumption
of CO is still unknown, these results cannot be extrapolated and the
biological effect of the in vivo-produced monolaurin would need to
be investigated.
Conclusions
The literature on the health benefits promoted by CO is still incon-
clusive. Some studies about the impact of CO on human health, es-
pecially regarding weight loss, were able to obtain positive results;
however, the subjects’ diets were altered during the experiments,
increasing the level of fibre and protein and reducing the inges-
tion of carbohydrates. Therefore, it is not possible to isolate CO as
the single factor behind the increased satiety. In addition, some of
these studies did not evaluate the lipid profile of the subjects for an
extended period of time. Without this type of analysis, it is not pos-
sible to evaluate the incidence of specific conditions, such as normal
weight obesity.
The studies are scarce and lack a holistic view about the diet.
Therefore, the effect of CO on health is still unclear and much of
the evidence is contradictory. Also, the absorption and metabolism
of the product were not completely elucidated yet. The only solid
information available is that CO is, among all natural fat sources, the
one that presents the highest amount of saturated fatty acids. Until
new researches can clarify the health claims associated with this fat,
CO should not be consumed above the limit stablished by regulatory
agencies for saturated fat intake. In addition, this product should not
be used for frying purposes once it presents a low smoking point.
To this present day, there is not enough scientific evidence to
support the health benefits used by CO brands to promote their
9
product. This kind of promotion should not be used, once it misleads
the perception of the consumers. Also, the media should not take
this matter lightly, once the very high intake of saturated fat has
deleterious effects on health.
From the two types of CO available, virgin CO seems to carry
the greatest potential, once it presents polyphenols and a higher
amount of vitamin E compared with RBDCO. However, more re-
search is needed, especially human trials, in order to verify how such
components can affect the health, and to establish the necessary
dosage for these effects to take place.
Downloaded from https://academic.oup.com/fqs/advance-article-abstract/doi/10.1093/fqsafe/fyz004/5475954 by guest on 22 April 2019
Acknowledgements
We are grateful to the National Council of Technological and Scientific
Development (CNPq) for granting a scholarship to Renan da Silva Lima. We
also thank Guilherme Corrêa Danielski for proof-reading this article.
Conflict of interest statement
None declared.
References
Allan,  F.  J., et  al. (2001). Serum lipoprotein cholesterol and triglyceride
concentrations in pigs fed diets containing fish oil, milkfat, olive oil and
coconut oil. Nutrition Research, 21: 785–795.
American Heart Association. (2018). Heart Disease and Stroke Statistics
2018  – At-a-Glance. https://www.heart.org/-/media/data-import/
downloadables/heart-disease-and-stroke-statistics-2018---at-a-glance-
ucm_498848.pdf. Accessed 18 September 2018.
Americanas. (2018). https://www.americanas.com.br/produto/38549885/
linho-lev-coconut-oil-1g-60caps?WT.srch=1&epar=bp_pl_00_go_
todos-os-produtos_geral_gmv&gclid=CjwKCAjw7vraBRBbEiwA
4WBOn4rOoNC8grevnslXq4tZbp7JN5rMK80_lR9H3GFNA_
b Ay 6 B o g L s h I h o C L PA Q Av D _ B w E & o p n = Y S M E S P & s e l l e
rId=22839785000123. Accessed 30 July 2018.
American Oil Chemists’ association (AOCS). (2016). Coconut oil boom.
https://www.aocs.org/stay-informed/read-inform/featured-articles/
coconut-oil-boom-may-2016. Accessed 03 May 2018.
Arunima, S., Rajamohan, T. (2013). Effect of virgin coconut oil enriched diet
on the antioxidant status and paraoxonase 1 activity in ameliorating
the oxidative stress in rats - a comparative study. Food & Function, 4:
1402–1409.
Arunima, S., Rajamohan, T. (2014). Influence of virgin coconut oil-enriched
diet on the transcriptional regulation of fatty acid synthesis and oxidation
in rats – a comparative study. The British Journal of Nutrition, 111:
1782–1790.
Assunção,  M.  L., Ferreira,  H.  S., dos  Santos,  A.  F., Cabral,  C.  R. Jr,
Florêncio, T. M. (2009). Effects of dietary coconut oil on the biochemical
and anthropometric profiles of women presenting abdominal obesity.
Lipids, 44: 593–601.
Babayan,  V.  K. (1987). Medium chain triglycerides and structured lipids.
Lipids, 22: 417–420.
BBC News. (2018). Is coconut oil a superfood? https://www.bbc.co.uk/news/
health-42608071. Accessed 12 May 2018.
Bracco,  U. (1994). Effect of triglyceride structure on fat absorption. The
American Journal of Clinical Nutrition, 60: 1002S–1009S.
Canapi, E. C., Agustin, Y. T. V., Moro, E. A., Pedrosa Jr, E., Bedaño, M. L. J.
(2005). Coconut oil. In: Shahidi, F., ed. Bailey’s Industrial Oils and Fats. 6
ed. Wiley-Interscience, Hoboken, NJ, 2, pp. 123–147.
Cassiday,  L. (2015). Big fat controversy: changing opinions about saturated
fat. Inform, 26: 343–349.
Cardoso, D. A., Moreira, A. S., de Oliveira, G. M., Raggio Luiz, R., Rosa, G.
(2015). A coconut extra virgin oil-rich diet increases HDL cholesterol and
decreases waist circumference and body mass in coronary artery disease
patients. Nutricion Hospitalaria, 32: 2144–2152.
10
Carnielli,  V.  P., Luijendijk,  I.  H., Van  Beek,  R.  H., Boerma,  G.  J.,
Degenhart,  H.  J., Sauer,  P.  J. (1995). Effect of dietary triacylglycerol
fatty acid positional distribution on plasma lipid classes and their fatty
acid composition in preterm infants. The American Journal of Clinical
Nutrition, 62 (4): 776–781.
Chinwong,  S., Chinwong,  D., Mangklabruks,  A. (2017). Daily
consumption of virgin coconut oil increases high-density lipoprotein
cholesterol levels in healthy volunteers: a randomized crossover trial.
Evidence-Based Complementary and Alternative Medicine, 2017:
7251562.
Clegg, M. E. (2017). They say coconut oil can aid weight loss, but can it really?
European Journal of Clinical Nutrition, 71: 1139–1143.
Covas,  M.  I., de  la  Torre,  R., Fitó,  M. (2015). Virgin olive oil: A  key food
for cardiovascular risk protection. The British Journal of Nutrition, 113
(Suppl 2): S19–S28.
Cox, C., Mann, J., Sutherland, W., Chisholm, A., Skeaff, M. (1995). Effects of
coconut oil, butter, and safflower oil on lipids and lipoproteins in persons
with moderately elevated cholesterol levels. Journal of Lipid Research, 36:
1787–1795.
Dauqan, E., Sani, H. A., Abdullah, A., Kasim, Z. M. (2011). Effect of different
vegetable oils (red palm olein, palm olein, corn oil and coconut oil) on
lipid profile in rat. Food and Nutrition Sciences, 2: 253–258.
Dayrit, F. M. (2014). Lauric acid is a medium-chain fatty acid, coconut oil is
a medium-chain triglyceride. The Philippine Journal of Science, 143 (2):
157–166.
Dayrit,  F.  M. (2015). The properties of lauric acid and their significance in
coconut oil. Journal of the American Oil Chemists’ Society, 92: 1–15.
DebMandal, M., Mandal, S. (2011). Coconut (Cocos nucifera L.: arecaceae):
in health promotion and disease prevention. Asian Pacific Journal of
Tropical Medicine, 4: 241–247.
Derewiaka,  D., Sosinska,  E., Obiedzinski,  M., Krogulec,  A., Czaplicki,  S.
(2011). Determination of the adulteration of butter. European Journal of
Lipid Science and Technology, 113 (8), 1005–1011.
European Food Safety Authority (EFSA). (2011). Scientific Opinion on the
substantiation of health claims related to medium-chain triglycerides and
reduction in body weight (ID 643, 677, 1614) pursuant to Article 13(1) of
Regulation (EC) No 1924/2006. https://efsa.onlinelibrary.wiley.com/doi/
pdf/10.2903/j.efsa.2011.2240. Accessed 30 July 2018.
European Food Safety Authority (EFSA). (2017). Dietary Reference Values
for Nutrients – Summary report. https://www.efsa.europa.eu/sites/default/
files/2017_09_DRVs_summary_report.pdf. Access 30 July 2018.
Evitamins. (2018). https://www.evitamins.com/br/organic-virgin-coconut-oil-
kirkland-signature-320991?utm_source=google&utm_medium=google_
shopping_br&utm_campaign=google_shopping_br&gclid=CjwKCAjw7v
raBRBbEiwA4WBOn5RMt0VhSfvToiAs97oZYlUhmmHPTehLTa5zGNx
7XpscSschfxOyXRoChE4QAvD_BwE. Accessed 30 July 2018.
Eyres,  L., Eyres,  M.  F., Chisholm,  A., Brown,  R.  C. (2016). Coconut oil
consumption and cardiovascular risk factors in humans. Nutrition
Reviews, 74: 267–280.
Famurewa, A. C., Ejezie, F. E. (2018). Polyphenols isolated from virgin coconut
oil attenuate cadmium-induced dyslipidemia and oxidative stress due to
their antioxidant properties and potential benefits on cardiovascular risk
ratios in rats. Avicenna Journal of Phytomedicine, 8: 73–84.
Famurewa,  A.  C., Ekeleme-Egedigwe,  C.  A., Nwali,  S.  C., Agbo,  N.  N.,
Obi, J. N., Ezechukwu, G. C. (2018). Dietary supplementation with virgin
coconut oil improves lipid profile and hepatic antioxidant status and has
potential benefits on cardiovascular risk indices in normal rats. Journal of
Dietary Supplements, 15: 330–342.
Feranil, A. B., Duazo, P. L., Kuzawa, C. W. (2011). Coconut oil is associated
with a beneficial lipid profile in pre-menopausal women in the Philippines.
Asia Pacific Journal of Clinical Nutrition, 20: 190–195.
Fernando, W. M., Martins, I. J., Goozee, K. G., Brennan, C. S., Jayasena, V.,
Martins, R. N. (2015). The role of dietary coconut for the prevention and
treatment of Alzheimer’s disease: potential mechanisms of action. The
British Journal of Nutrition, 114: 1–14.
Firestone, D. (2013). Physical and Chemical Characteristics of Oils, Fats, and
Waxes, 3 ed. Urbana, IL: AOCS Press.
R. da S. Lima and J. M. Block
Frantz, I. D. J., Carey, J. B. J. (1961). Cholesterol content of human liver after
feeding of corn oil and hydrogenated coconut oil. Experimental Biology
and Medicine, 106 (4): 800–801.
Ganesan,  K., Sukalingam,  K., Xu,  B. (2017). Impact of consumption and
cooking manners of vegetable oils on cardiovascular diseases – a critical
review. Trends in Food Science & Technology. 71: 132–154.
Guasch-Ferré,  M., et  al. (2014). Olive oil intake and risk of cardiovascular
disease and mortality in the PREDIMED study. BMC Medicine, 12: 78.
Haumann,  B.  F. (1997). Structured Lipids: Rearranging the fatty acids in
triglycerides permits researchers to design lipids for specific uses. Inform-
Downloaded from https://academic.oup.com/fqs/advance-article-abstract/doi/10.1093/fqsafe/fyz004/5475954 by guest on 22 April 2019
Champaign, 8: 1004–1015.
Heek,  M.  V., Zilversmit,  D.  B. (1991). Mechanisms of hypertriglyceridemia
in the coconut oil/cholesterol-fed rabbit. Increased secretion and
decreased catabolism of very low density lipoprotein. Arteriosclerosis and
Thrombosis: A Journal of Vascular Biology, 11 (4): 918–927.
Heistad, D. D., Wakisaka, Y., Miller, J., Chu, Y., Pena-Silva, R. (2009). Novel
aspects of oxidative stress in cardiovascular diseases. Circulation Journal,
73: 201–207.
Huang,  Y.  S., Manku,  M.  S., Horrobin,  D.  F. (1984). The effects of dietary
cholesterol on blood and liver polyunsaturated fatty acids and on plasma
cholesterol in rats fed various types of fatty acid diet. Lipids, 19 (9): 664–
672.
IHerb. (2018a). https://br.iherb.com/pr/Nature-s-Way-Organic-Coconut-
Oil-Extra-Virgin-16-oz-448-g/4567?gclid=CjwKCAjwy_XaBR
AW E i w A p f j K H s k R 0 p t b z X r p S D j FJ n 4 T S t 5 G V z X A 4 D O L 3 4 z r _
km5G10ChFeRpzEGXBoCpqoQAvD_BwE&gclsrc=aw.ds. Accessed 15
May 2018.
IHerb.(2018b).https://br.iherb.com/pr/Healthy-Origins-Organic-Extra-Virgin-
Coconut-Oil-54-oz-1-530-g/53133. Accessed 15 May 2018.
IHerb. (2018c). https://br.iherb.com/pr/Fruitrients-Coconut-Oil-100-Pure-
Extra-Virgin-16-oz/69779?gclid=CjwKCAjw7vraBRBbEiwA4WBOn_
xgPAGlQrvtMQISZaq6wqlZEST2LQS7gteBv4sHbjMucMg6XvDgIBoC
LQ4QAvD_BwE&gclsrc=aw.ds. Accessed 30 July 2018.
IHerb. (2018d). https://br.iherb.com/pr/Jarrow-Formulas-Organic-Coconut-
Oil-16-oz-473-g/2506?gclid=CjwKCAjw7vraBRBbEiwA4WBOnxe5OM
Gg0pWtdJRwtsYHTEuuyflKNbvfRkKg2SekVMcTDFv3CwBAqRoCvO
4QAvD_BwE&gclsrc=aw.ds. Accessed 30 July 2018.
Intahphuak,  S., Khonsung,  P., Panthong,  A. (2010). Anti-inflammatory,
analgesic, and antipyretic activities of virgin coconut oil. Pharmaceutical
Biology, 48: 151–157.
Jones, P. J., et al. (2014). DHA-enriched high-oleic acid canola oil improves
lipid profile and lowers predicted cardiovascular disease risk in the canola
oil multicenter randomized controlled trial. The American Journal of
Clinical Nutrition, 100: 88–97.
Kamisah,  Y., et  al. (2015). Cardioprotective effect of virgin coconut oil in
heated palm oil diet-induced hypertensive rats. Pharmaceutical Biology,
53: 1243–1249.
Katan, M. B., Zock, P. L., Mensink, R. P. (1994). Effects of fats and fatty acids
on blood lipids in humans: an overview. The American Journal of Clinical
Nutrition, 60 (6): 1017S–1022S.
Keys, A., et al. (1984). The seven countries study: 2,289 deaths in 15 years.
Preventive Medicine, 13: 141–154.
Kinsella,  R., Maher,  T., Clegg,  M.  E. (2017). Coconut oil has less satiating
properties than medium chain triglyceride oil. Physiology & Behavior,
179: 422–426.
Kosmas, C. E., et al. (2018). High-density lipoprotein (HDL) functionality and
its relevance to atherosclerotic cardiovascular disease. Drugs in Context,
7: 212525.
LaBarrie, J., St-Onge, M. P. (2017). A coconut oil-rich meal does not enhance
thermogenesis compared to corn oil in a randomized trial in obese
adolescents. Insights in Nutrition and Metabolism, 1: 30–36.
Liau, K. M., Lee, Y. Y., Chen, C. K., Rasool, A. H. (2011). An open-label pilot
study to assess the efficacy and safety of virgin coconut oil in reducing
visceral adiposity. ISRN Pharmacology, 2011: 949686.
Lieberman,  S., Enig,  M.  G., Preuss,  H.  G. (2006). A review of monolaurin
and lauric acid: natural virucidal and bactericidal agents. Alternative and
Complementary Therapies, 12 (6):310–314.
Effects of coconut oil
Lockyer, S., Stanner, S. (2016). Coconut oil – a nutty idea? British Nutrition
Bulletin, 41: 42–54.
Lucky Vitamin. (2018a). https://pt.luckyvitamin.com/p-434986-nutiva-
coconut-oil-organic-virgin-14-fl-oz?LanguageCode=PT&locale=pt-
BR&utm_source=google&utm_medium=cpc&adpos=2o16&scid=scp
lp127797&sc_intid=127797&gclid=CjwKCAjw7vraBRBbEiwA4WB
On4W5s0084VZWxH71mkY5ntIHswmtnItXhEjnc_OVkIE9OfhM_
KJQ6BoCOJ4QAvD_BwE. Accessed 30 July 2018.
Lucky Vitamin. (2018b). https://pt.luckyvitamin.com/p-1945684-garden-of-
life-raw-extra-virgin-organic-coconut-oil-14-fl-oz?LanguageCode=
PT&locale=pt-BR&utm_source=google&utm_medium=cpc&adpo
s=3o1&scid=scplp169244&sc_intid=169244&gclid=CjwKCAjw7v
raBRBbEiwA4WBOn4VdQFjBKt0EVwh3HX15u2pH_Na8mwvxi-
RzREcXcXEVB7V1w7q1nhoC8LcQAvD_BwE. Accessed 30 July 2018.
Lucky Vitamin. (2018c). https://pt.luckyvitamin.com/p-13216-garden-of-
life-extra-virgin-coconut-oil-16-fl-oz?LanguageCode=PT&locale=pt-
BR&utm_source=google&utm_medium=cpc&adpos=1o2&scid=scp
lp62301&sc_intid=62301&gclid=CjwKCAjw7vraBRBbEiwA4WBO
n54NKSSObilr9Ff4jZ82T2YI6mRfrl2QIUeHMgULM034Pg9L-aoJ_
BoCJnAQAvD_BwE. Accessed 30 July 2018.
Maher,  T., Kinsella,  R., Clegg,  M.  E. (2017). The effect of coconut oil and
MCT on satiety and food intake. Proceedings of the Nutrition Society, 76:
OCE1. doi: 10.1017
Mangiapane, E. H., McAteer, M. A., Benson, G. M., White, D. A., Salter, A. M.
(1999). Modulation of the regression of atherosclerosis in the hamster by
dietary lipids: comparison of coconut oil and olive oil. The British Journal
of Nutrition, 82: 401–409.
Mansor,  T.  S.  T., Che  Man,  Y.  B., Shuhaimi,  M., Abdul  Afiq,  M.  J.,
Ku Nurul, F. K. M. (2012). Physicochemical properties of virgin coconut
oil extracted from different processing methods. International Food
Research Journal, 19(3): 837–845.
Marina, A. M., Che Man, Y. B., Amin, I. (2009). Virgin coconut oil: emerging
functional food oil. Trends in Food Science & Technology, 20 (10): 481–487.
Medical News Today. (2018). Coconut oil: healthful or unhealthful? https://
www.medicalnewstoday.com/articles/320644.php. Accessed 30 July 2018.
Metcalf, R. G., et al. (2007). Effects of fish-oil supplementation on myocardial
fatty acids in humans. The American Journal of Clinical Nutrition, 85:
1222–1228.
Mu, H., Høy, C. E. (2004). The digestion of dietary triacylglycerols. Progress
in Lipid Research, 43: 105–133.
Muthuramu,  I., et  al. (2017). Coconut oil aggravates pressure overload-
induced cardiomyopathy without inducing obesity, systemic insulin
resistance, or cardiac steatosis. International Journal of Molecular Science,
18(7): 1565. doi: 10.3390
Nabel,  E.  G. (2003). Cardiovascular disease. The New England Journal of
Medicine, 349: 60–72.
Nafar, F., Clarke, J. P., Mearow, K. M. (2017). Coconut oil protects cortical
neurons from amyloid beta toxicity by enhancing signaling of cell survival
pathways. Neurochemistry International, 105: 64–79.
Nafar, F., Mearow, K. M. (2014). Coconut oil attenuates the effects of amyloid-β
on cortical neurons in vitro. Journal of Alzheimer’s Disease, 39: 233–237.
Natumesa. (2018). https://www.natumesa.com.br//oleo-de-coco-extra-virgem-
500ml---copra/p?idsku=21&gclid=CjwKCAjw7vraBRBbEiwA4WBOn-
qmEjljKTtWwYSAcDxWKD-Ts6CY8dQDEKrt4z3Xw0tazf1BqCQKlho
CYO0QAvD_BwE. Accessed 30 July 2018.
Nevin, K. G., Rajamohan, T. (2004). Beneficial effects of virgin coconut oil on lipid
parameters and in vitro LDL oxidation. Clinical Biochemistry, 37: 830–835.
Nevin, K. G., Rajamohan, T. (2008). Influence of virgin coconut oil on blood
coagulation factors, lipid levels and LDL oxidation in cholesterol fed
Sprague-Dawley rats. The European e-Journal of Clinical Nutrition and
Metabolism, 3 (1): e1–e8.
New Straits Times. (2018). The coconut oil debate. https://www.nst.com.my/
lifestyle/heal/2018/03/341829/coconut-oil-debate. Accessed 12 May 2018.
Nurul-Iman,  B.  S., Kamisah,  Y., Jaarin,  K., Qodriyah,  H.  M. (2013). Virgin
coconut oil prevents blood pressure elevation and improves endothelial
functions in rats fed with repeatedly heated palm oil. Evidence-Based
Complementary and Alternative Medicine, 2013: 629329.
11
O’Brien,  R.  D. (2004). Fats and oils: Formulating and processing for
applications. New York: CRC Press.
Oseni, N. T., Fernando, W. M., Coorey, R., Gold, I., Jayasena, V. (2017). Effect
of extraction techniques on the quality of coconut oil. African Journal of
Food Science, 11 (3): 58–66.
Palazhy, S., Kamath, P., Vasudevan, D. M. (2018). Dietary fats and oxidative
stress: a cross-sectional study among coronary artery disease subjects
consuming coconut oil/sunflower oil. Indian Journal of Clinical
Biochemistry, 33: 69–74.
Piping Rock. (2018). https://br.pipingrock.com/coconut-oil/liquid-coconut-
Downloaded from https://academic.oup.com/fqs/advance-article-abstract/doi/10.1093/fqsafe/fyz004/5475954 by guest on 22 April 2019
premium-oil-10073?prd=2e492acf&gclid=CjwKCAjw7vraBRBbEiwA4
WBOn_oqs20_8qWR6DaGHzL5cxYlNfsGMDoUk3Z0GKLufwN07Mt
Y0bS63hoClN0QAvD_BwE. Accessed 30 July 2018.
Posada, L. R., Shi, J., Kakuda, Y., Xue, S. J. (2007). Extraction of tocotrienols
from palm fatty acid distillates using molecular distillation. Separation and
Purification Technology, 57 (2): 220–229.
Pradeepkumar,  T., Sumajyothibhaskar,  B., Satheesan,  K.  N. (2008).
Management of Horticultural Crops (Horticulture Science Series
Vol.11, 2nd of 2 Parts). New Delhi, India: New India Publishing. pp.
539–587.
QualiCôco. (2018). https://loja.qualicoco.com.br/oleo-de-coco-sem-sabor-
qualicoco-?utm_source=Site&utm_medium=GoogleMerchant&utm_cam
paign=GoogleMerchant&gclid=CjwKCAjw7vraBRBbEiwA4WBOn_Erv_
iMRXrusDdjmc2ZLafVwLLCPDPb2piteNkLyAczvfAzEX7rPxoCCFgQ
AvD_BwE. Accessed 30 July 2018.
Sabitha,  P., Vaidyanathan,  K., Vasudevan,  D.  M., Kamath,  P. (2009).
Comparison of lipid profile and antioxidant enzymes among South Indian
men consuming coconut oil and sunflower oil. Indian Journal of Clinical
Biochemistry, 24: 76–81.
Sacks,  F.  M., et  al.; American Heart Association. (2017). Dietary fats and
cardiovascular disease: A presidential advisory from the American Heart
Association. Circulation, 136: e1–e23.
Sankararaman,  S., Sferra,  T.  J. (2018). Are we going nuts on coconut oil?
Current Nutrition Reports. 7 (3):107–115.
SBEM, ABESO. (2015). Posicionamento oficial da Sociedade Brasileira de
Endocrinologia e Metabologia (SBEM) e da Associação Brasileira para o
Estudo da Obesidade e da Síndrome Metabólica (ABESO) sobre o uso do
óleo de coco para perda de peso. http://crn5.org.br/wp-content/uploads/
OLEO_DE_COCO_posicionamento_ABESO_SBEM.pdf. Accessed 30
July 2018.[AU: Please provide the
SBS. (2018). Why Dr Michael Mosley now thinks that coconut oil may be
good for you. https://www.sbs.com.au/food/health/article/2018/02/26/
why-dr-michael-mosley-now-thinks-coconut-oil-may-be-good-you.
Accessed 30 July 2018.
Scopus. (2018). https://www.scopus.com/term/analyzer.uri?sid=4b83027fd
4518101d338f833f155709c&origin=resultslist&src=s&s=TITLE-ABS-
KEY%28coconut+oil%29&sort=plf-f&sdt=b&sot=b&sl=26&count=59
47&analyzeResults=Analyze+results&txGid=3edd0b622434ad5fa20a19
b4374a6b87. Accessed 15 May 2018.
Scrimgeour, C. (2005). Chemistry of Fatty Acids. In: Shahidi, F., ed. Bailey’s
Industrial Oil and Fat Products – Volume 1. Hoboken, NJ: Wiley-
Interscience.
Shah,  N.  D., Limketkai. (2017). The use of medium-chain triglycerides in
gastrointestinal disorders. Practical Gastroenterology, 160: 20–25.
Shedden, R. (2017). Effect of coconut oil supplement (2g/d) on total cholesterol
to HDL cholesterol ratio in healthy adults. Master’s Thesis, Arizona State
University, Tempe, AZ.
Simopoulos,  A.  P. (2002). The importance of the ratio of omega-6/omega-3
essential fatty acids. Biomedicine & Pharmacotherapy = Biomedecine &
Pharmacotherapie, 56: 365–379.
Srivastava, S., Singh, M., George, J., Bhui, K., Murari Saxena, A., Shukla, Y.
(2010). Genotoxic and carcinogenic risks associated with the dietary
consumption of repeatedly heated coconut oil. The British Journal of
Nutrition, 104: 1343–1352.
Statista. (2018a). Coconut production worldwide from 2000 to 2016 (in
million metric tons). https://www.statista.com/statistics/577497/world-
coconut-production.> Accessed 12 May 2018.
12
Statista. (2018b). Coconut oil consumption in the United States from 2000 to
2017 (in 1,000 metric tons). https://www.statista.com/statistics/288367/
coconut-oil-consumption-united-states/. Accessed 12 May 2018.
St-Onge, M. P., Jones, P. J. (2003). Greater rise in fat oxidation with medium-
chain triglyceride consumption relative to long-chain triglyceride is
associated with lower initial body weight and greater loss of subcutaneous
adipose tissue. International Journal of Obesity and Related Metabolic
Disorders, 27: 1565–1571.
Strandberg, K. L., et al. (2009). Reduction in staphylococcus aureus growth
and exotoxin production and in vaginal interleukin 8 levels due to glycerol
monolaurate in tampons. Clinical Infectious Diseases, 49: 1711–1717.
Subermaniam, K., Saad, Q. H. M., Das, S., Othamn, F. (2014). Virgin coconut
oil (VCO) decreases the level of malandialdehyde (MDA) in the cardiac
tissue of experimental Sprague-dawley rats fed with heated palm oil.
Journal of Medical and Bioengineering, 3 (2): 102–106.
The Indian Weekender. (2018). Wonder benefits of coconut oil. https://www.
indianweekender.co.nz/Pages/ArticleDetails/77/9706/Health/Wonder-
benefits-of-coconut-oil. Accessed 30 July 2018.
United States Department of Agriculture (USDA). (2015). Dietary Guidelines
for Americans – 2015–2020. https://health.gov/dietaryguidelines/2015/
resources/2015-2020_Dietary_Guidelines.pdf. Accessed 15 May 2018.
Valderas-Martinez,  P., et  al. (2016). Tomato sauce enriched with olive oil
exerts greater effects on cardiovascular disease risk factors than raw
tomato and tomato sauce: a randomized trial. Nutrients, 8: 170.
R. da S. Lima and J. M. Block
Valente,  F.  X., et  al. (2018). Effects of coconut oil consumption on energy
metabolism, cardiometabolic risk markers, and appetitive responses in
women with excess body fat. European Journal of Nutrition, 57: 1627–
1637.
Vijayakumar,  M., et  al. (2016). A randomized study of coconut oil
versus sunflower oil on cardiovascular risk factors in patients
with stable coronary heart disease. Indian Heart Journal, 68:
498–506.
Vysakh,  A., et  al. (2014). Polyphenolics isolated from virgin coconut oil
inhibits adjuvant induced arthritis in rats through antioxidant and
Downloaded from https://academic.oup.com/fqs/advance-article-abstract/doi/10.1093/fqsafe/fyz004/5475954 by guest on 22 April 2019
anti-inflammatory action. International Immunopharmacology, 20:
124–130.
Wang,  X.  M., et  al. (2014). Oral helicobacter pylori, its relationship to
successful eradication of gastric H. Pylori and saliva culture confirmation.
Journal of Physiology and Pharmacology, 65: 559–566.
World Health Organization. (2018). Healthy diet. https://www.who.int/news-
room/fact-sheets/detail/healthy-diet. Accessed 23 May 2018.
Yang,  I.  H., et  al. (2015). Aceite de coco: tratamiento alternative no
farmacológico frente a la enfermedad de Alzheimer. Nutrición Hospitalaria,
32 (6): 2822–2827.
Zakaria, Z. A., Somchit, M. N., Mat Jais, A. M., Teh, L. K., Salleh, M. Z.,
Long, K. (2011). In vivo antinociceptive and anti-inflammatory activities
of dried and fermented processed virgin coconut oil. Medical Principles
and Practice, 20: 231–236.