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UNIVERSIDADE FEDERAL DO RIO GRANDE DO SUL

PROGRAMA DE PÓS-GRADUAÇÃO EM CIÊNCIAS MÉDICAS:


ENDOCRINOLOGIA

ANA CLÁUDIA DUARTE

EVIDÊNCIAS CIENTÍFICAS VERSUS CONHECIMENTO POPULAR A

RESPEITO DO BENEFÍCIO CARDIOMETABÓLICO DO

CONSUMO DIETÉTICO DE ÓLEO DE COCO

Porto Alegre
2022
ANA CLÁUDIA DUARTE

EVIDÊNCIAS CIENTÍFICAS VERSUS CONHECIMENTO POPULAR A


RESPEITO DO BENEFÍCIO CARDIOMETABÓLICO DO
CONSUMO DIETÉTICO DE ÓLEO DE COCO

Tese de Doutorado apresentada como


requisito parcial à obtenção do título de
doutora em Ciências Médicas: Endocrinologia
da Universidade Federal do Rio Grande do
Sul.
Orientador: Prof.Dr. Fernando Gerchman
Co-orientador(a): Prof. Drª Verônica Colpani

Porto Alegre
2022
DEDICATÓRA

Dedico esse trabalho a minha mãe Loreni Martins Duarte por todo o suporte emocional
e financeiro que me concedeu para que eu pudesse chegar até aqui. Obrigada por ter
me proporcionado os bens mais preciosos que eu poderia ter: vida e educação.
Obrigada por estar sempre junto comigo e me dar muito mais do que preciso e, muitas
vezes, mereço. És meu exemplo de força e bondade. Espero sempre ser o teu orgulho
e honrar todos os teus esforços e luta.

AGRADECIMENTOS

Ao meu orientador, professor Fernando Gerchman, pela oportunidade de compor o


seu tão bem qualificado grupo de pesquisa. Obrigada por toda a paciência com as
limitações que apresentei neste período, por incentivar a participação em eventos
científicos no País e no exterior e por enxergar e respeitar a individualidade de cada
aluno.

A minha co-orientadora, Verônica Colpani pela contribuição de toda sua expertise em


meta-análise e por toda sua doçura, o que contribui para deixar o processo mais leve.

Agradeço a professora Jussara Carnevale de Almeida, minha orientadora do


mestrado, por ter me auxiliado no ingresso à pós-graduação da Universidade Federal
do Rio Grande do Sul. Grata pela oportunidade e todo aprendizado do período.

A todos meus colegas do grupo de pesquisa, deixo meu muito obrigada pela
convivência com cada um de vocês e todo aprendizado. Em especial, gostaria de
agradecer a Carina Araujo por todas as nossas conversas e por inspirar pelo exemplo,
na busca por excelência em cada atividade que realiza. Teu empenho no que faz é
admirável. Também agradecer especialmente a Carmen Raya Amazarray, minha
doce e paciente dupla de pesquisa (e astrológica!) pela amizade que construímos
nestes últimos anos. Toda nossa troca acadêmica (e de vida!) foi essencial para deixar
o processo mais leve Amizade construída na ciência para a vida.

A todos os alunos de iniciação científica que colaboraram na elaboração dos artigos


que compõem esta tese, em especial o Bernardo Spiazzi e a Eduarda Nunes Merello.
Sem todo o conhecimento, disposição e espírito inovador de vocês, a elaboração
deste trabalho não teria sido possível. Vocês são admiráveis, prestativos e muito
queridos. Obrigada pela paciência e sucesso na trajetória profissional de vocês.

A Renata Tôndolo Tavares e a toda família da Ong Viver de Rir, por deixar todo este
processo mais leve ao me permitir, por meio da palhaça Pig, levar sorrisos e carinho
a outras pessoas.

A todas as professoras Nutricionistas que fizeram parte da minha trajetória e que me


inspiraram a buscar o mais alto grau de formação acadêmica, pautando minha
conduta profissional na ciência e de forma ética.

Por fim, mas não menos importante, gostaria de agradecer a todos amigos, familiares,
que estiveram junto comigo nesta trajetória. Quatro anos é tempo suficiente para a
vida dar muitas voltas, pessoas saírem de nossas vidas, outras chegarem, mas, todas
tiveram um papel fundamental em minha trajetória. Muito obrigada pelo apoio,
confiança, risadas e paciência. Obrigada por contribuírem para que eu seja uma
pessoa um pouco melhor a cada dia. Amo vocês! Bruno Alborghetti Carvalho: obrigada
por tanto!
“Não sois máquina! Homens é o que sois!”
Charles Chaplin
RESUMO

Dados recentes da literatura sugerem que a ingestão alimentar de óleo de coco,

composto em 92% por ácidos graxos saturados (AGS), não resulta em benefícios

cardiometabólicos, como melhora do perfil antropométrico, lipídico, glicêmico e de

parâmetros de inflamação subclínica. Apesar disso, seu consumo aumentou nos

últimos anos em todo o mundo, fenômeno que pode ser explicado, possivelmente, por

um aumento da orientação, por parte de profissionais da área da saúde, de que este

seria um óleo tão ou mais saudável que os demais para consumo, além da divulgação

em redes sociais destas recomendações.

A fim de se entender os efeitos do óleo de coco na saúde cardiometabólica,

desenvolveu-se essa tese, com uma introdução (referencial teórico) para apresentar

os diferentes aspectos nutricionais e epidemiológicos relacionados ao óleo de coco,

sua relação com a saúde metabólica e possíveis hipóteses sobre as razões do seu

alto consumo.

No artigo 1 desenvolveu-se uma revisão sistemática com meta-análise de

ensaios clínicos randomizados (ECR), realizados em adultos, e que comparavam o

consumo alimentar de óleo de coco com outros óleos e gorduras. Um total de 17 ECRs

foram incluídos na revisão sistemática e 7 apresentaram dados suficientes e foram

incluídos na meta-análise. A análise dos dados mostrou que a ingestão de óleo de

coco comparado a outros óleos e gorduras não é diferente em relação a parâmetros

antropométricos, de perfil glicêmico, pressão arterial e inflamação subclínica. Em

relação ao perfil lipídico, também não se demonstrou diferenças no efeito do consumo

alimentar de óleo de coco em relação a outros óleos e gorduras nos níveis de

colesterol LDL-C, triglicerídeos e na relação CT/HDL-C. Observou-se um aumento


estatisticamente significativo, mas clinicamente pouco relevante, dos níveis de

colesterol HDL-C com o consumo alimentar de óleo de coco em relação a outros óleos

e gorduras. Análises de subgrupo para os diferentes parâmetros cardiometabólicos

descritos não demonstraram diferenças. Ao se analisar a qualidade metodológica dos

ECRs incluídos na meta-análise, se observa que a maioria apresenta número

pequeno de participantes, tempo de seguimento curto, e aplicação de co intervenções,

em uma proporção dos estudos, incluindo dieta com restrição calórica e prática de

atividade física, fatores que nos levam a interpretar os dados com cautela por poderem

impactar no efeito cardiometabólico atribuído ao óleo de coco. Não havendo aparente

superioridade do óleo de coco em comparação a outros óleos e gorduras em

parâmetros cardiometabólicos, e sabendo-se dos riscos associados do consumo

elevado de AGS para a saúde como piora do perfil lipídico, o incentivo do uso deste

óleo como sendo de primeira escolha para consumo, deve ser desencorajado.

O objetivo do artigo 2 foi avaliar o consumo, padrões, motivos e crenças

relacionados ao uso dietético do óleo de coco e seus benefícios na saúde, por meio

de uma pesquisa online com duas populações do sul do Brasil: uma composta por

estudantes de diferentes cursos de pós-graduação da Universidade Federal do Rio

Grande do Sul e outra por pessoas que acessam a página do Hospital de Clínicas de

Porto Alegre no Facebook®. Assim, realizamos um estudo antes/depois usando um

questionário online com 11 perguntas. Os participantes que indicaram consumir óleo

de coco receberam uma intervenção, que consistia na exposição dos dados de meta-

análise recente sobre os efeitos do óleo de coco. O objetivo foi avaliar a possibilidade

de mudança de conceitos e crenças a respeito do efeito metabólico e cardiovascular

relacionados ao consumo do óleo de coco e aumentar a alfabetização sobre os efeitos

deste óleo na saúde. Obtivemos 3160 respostas válidas. A maior parte da amostra
consumia óleo de coco (59,1%). Destes, 82,5% o consideravam saudável e 65,4% o

utilizavam pelo menos uma vez por mês. Apesar de considerá-lo saudável, 81,2% dos

participantes que utilizavam o óleo, não observaram nenhuma melhora na saúde com

o seu uso. Após serem expostos às conclusões de uma meta-análise mostrando que

o óleo de coco não apresenta benefícios superiores à saúde quando comparado a

outros óleos e gorduras, 73,5% daqueles que consideraram o óleo de coco saudável

não mudaram de opinião sobre os seus benefícios. Conclui-se que o consumo do óleo

de coco é motivado pelas próprias crenças pessoais, possivelmente incentivadas por

recomendações de profissionais da área da saúde de que este seria um óleo que

contribuiria para manutenção/melhora da saúde cardiometabólica, mesmo com as

evidências científicas mostrando o contrário e, curiosamente, com os participantes

não observando melhoras em sua saúde com o consumo de óleo de coco. O fato dos

participantes não terem mudado sua percepção sobre os benefícios deste óleo após

serem expostos a informações científicas nos revela o quanto pode ser difícil mudar

conceitos errados sobre alimentação após estes serem amplamente divulgados e

praticados pela população. A desinformação em saúde precisa ser amplamente

estudada e encarada como um problema de saúde pública. Estratégias para orientar

a população das melhores opções quanto a escolha de óleo para consumo alimentar,

bem como de que o óleo de coco não apresenta benefícios definidos (diferentemente

de outros óleos de consumo alimentar), devem ser elaboradas e difundidas

principalmente para população alvo e de risco para a saúde cardiometabólica.

Encorajamos que mais estudos neste formato sejam desenvolvidos a fim de colaborar

no combate à desinformação na área da saúde, especialmente na área de nutrição e

de hábitos de vida saudáveis.


Palavras-chave: Óleo de coco. Mídia social. Pesquisa. Online. Informação em saúde.

Internet. Ácidos graxos saturados. Perfil lipídico. Perfil antropométrico.


ABSTRACT

Recent data from the literature suggest that dietary intake of coconut oil,

composed of 92% saturated fatty acids (SFA), does not result in cardiometabolic

benefits, such as improvement in anthropometric, lipid, glycemic and subclinical

inflammatory parameters. Despite this, its consumption has increased in recent years

all over the world, a phenomenon that can be explained, possibly, by an increase in

the concept, from health professionals, that this oil would be as healthy or healthier

than the others for consumption, in addition to the dissemination of these

recommendations on social networks.

In order to understand the effects of coconut oil on cardiometabolic health, this

thesis was developed, with an introduction (theoretical framework) to present the

different nutritional and epidemiological aspects related to coconut oil, its relationship

with cardiometabolic health and possible hypotheses about the reasons for their high

consumption.

In article 1, a systematic review was developed with a meta-analysis of

randomized clinical trials (RCTs) carried out in adults, which compared the dietary

consumption of coconut oil with other oils and fats. A total of 17 RCTs were included

in the systematic review and 7 had sufficient data to be included in the meta-analysis.

Data analysis showed that the intake of coconut oil compared to other oils and fats

does not cause a better metabolic control in relation to anthropometric parameters,

glycemic profile, blood pressure and subclinical inflammation. Regarding the lipid

profile, no differences were shown in the effect of dietary intake of coconut oil in relation

to other oils and fats on LDL cholesterol and triglycerides levels, as well as the CT/HDL

ratio. A statistically significant but clinically insignificant increase in HDL cholesterol

levels was observed with the dietary consumption of coconut oil in relation to other oils
and fats. Subgroup analyzes for the different cardiometabolic parameters described

showed similar findings. When analyzing the methodological quality of the RCTs

included in the meta-analysis, it is observed that most of them have a small number of

participants, short follow-up time, and application of co-interventions, in a proportion of

the studies, including a calorie-restricted diet and advice for physical activity, factors

that lead us to interpret the data with caution as they may impact the cardiometabolic

effect attributed to coconut oil. As there is no apparent superiority of coconut oil

compared to other oils and fats in cardiometabolic parameters and knowing the

associated risks of high consumption of SFA for health as a resultant worsening of the

lipid profile with its intake, encouraging the consumption of this oil as the first choice

should be discouraged.

The aim of article 2 was to evaluate consumption, patterns, motives and beliefs

related to the dietary intake of coconut oil and its health benefits, through an online

survey with two populations in Southern Brazil: one composed of students from

different courses at the Federal University of Rio Grande do Sul and another by people

who access the Hospital de Clínicas de Porto Alegre page on Facebook®. Thus, we

conducted a before/after study using an online questionnaire with 11 questions.

Participants who indicated consuming coconut oil received an intervention, which

consisted of exposing recent meta-analysis data on the effects of coconut oil. The

objective was to evaluate the possibility of changing concepts and beliefs about the

metabolic and cardiovascular effects related to the consumption of coconut oil and

increasing literacy about the effects of this oil on health. We got 3160 valid responses.

Most of the sample consumed coconut oil (59.1%). Of these, 82.5% considered it

healthy and 65.4% used it at least once a month. Despite considering it healthy, 81.2%

of the participants who used the oil did not observe any improvement in health with its
use. After being exposed to the findings of a meta-analysis showing that coconut oil

does not have superior health benefits when compared to other oils and fats, 73.5% of

those who considered coconut oil healthy did not change their opinion about its

benefits. These results lead us to conclude that the intake of coconut oil is motivated

by own personal beliefs, possibly encouraged by recommendations from health

professionals, even with the scientific evidence showing the contrary and, interestingly,

with the participants not observing improvements in their health with this consumption.

The fact that the participants did not change their perception of the benefits of this oil

after being exposed to scientific information reveals how difficult it can be to change

misconceptions about dietary habits after they are widely disseminated and practiced

by the population. Health misinformation needs to be widely studied and considered

as a public health problem. Strategies to guide the population on the best options

regarding the choice of oil for alimentary consumption, as well as that coconut oil does

not have defined benefits, unlike other oils for food consumption, should be developed

and disseminated mainly to the target population and risk to cardiometabolic health.

We encourage that more studies to address this issue be developed in order to

collaborate in the fight against misinformation in the health area, especially in the area

of nutrition and healthy lifestyle habits.

Keywords: Coconut oil; Social media; Survey; Online; Health information; Internet.

Coconut oil. Saturated fatty acids. Lipid profile. Anthropometric profile.


LISTA DE FIGURAS

Referencial teórico

Figura 1. Composição de ácidos graxos do óleo de coco...........................................15

Figura 2. Modelo do processo que permeia entre a geração e interpretação

de uma evidência científica até a divulgação dos seus dados...................................19

Figura 3. Limitações de estudos prévios sobre consumo de óleo de coco e potenciais

vieses destes resultados............................................................................................24

Capítulo I

Figure 1. Flow chart mapping out the studies examined and included into the meta-

analysis………………………………………………………………………………………73

Figure 2. Forest plots of randomized controlled clinical trials investigating the effects

of coconut oil intake on (a) body weight (kg); (b) waist circumference (cm)………….73

Figure 3. Forest plots of randomized controlled clinical trials investigating the effects

of coconut oil intake on (c) LDL-C (mg/dL); (d) HDL-C (mg/dL); (e) TG………………74

Capítulo II

Figure 1. Participant flow diagram.......................................................................... 103

Figure 2. Patterns, reasons, and expectancy regarding the health benefits of coconut

oil for those who consumed it……………………………………………. …………….103


LISTA DE TABELAS

Capítulo I

Table 1. Characteristics of the included studies…………………………………………69

Table 2. Summary of findings of the systematic review and meta-analysis………….71

Capítulo II

Table 1. Questionnaire summary ………………………………………………………..82

Table 2. Demographic characteristics of the University and Facebook samples……83

Table 3. Multiple logistic regression analysis for possible determinants of coconut oil

consumption (yes/no) and its frequency………………………………………………….86

LISTA DE ABREVIATURAS E SIGLAS

AGS: ácidos graxos saturados

C12:0: ácido láurico

C8:0: ácido caprílico

C10:0: ácido cáprico

C14:0: ácido mirístico

C16:0: ácido palmítico

AG: ácidos graxos

AGM: ácidos graxos monoinsaturados

AGP: ácidos graxos poli-insaturados

C18:2: ácido linoleico

C18:3: ácido linolênico

AGE: ácidos graxos essenciais


AGCM: ácido graxo de cadeia média

AGCL: ácido graxo de cadeia longa

TG: triglicerídeos

VLDL: proteínas de muito baixa densidade

CT: colesterol total

LDL-C: lipoproteína de baixa densidade

ECR: ensaios clínicos randomizados

HDL-C: lipoproteína de alta densidade

CETP: cholesterol ester transfer protein

AGI: ácidos graxos insaturados

TLR: toll like receptor

NF-Kβ: fator nuclear Kappa

COX2: ciclo-oxigensase-2

PCR: proteína C reativa

IL-6: interleucina 6

INF-γ: interferão-gama
SUMÁRIO

CAPÍTULO I – Referencial Teórico.................................................................. 15


JUSTIFICATIVA.................................................................................................. 27
OBJETIVOS........................................................................................................ 29
REFERÊNCIAS................................................................................................... 30

CAPÍTULO II – Artigo Original.......................................................................... 38


Effects of coconut oil on the cardiometabolic profile: systematic review
and meta-analysis of randomized clinical trials………………………………... 38

Capítulo III – Artigo original………………………………………………………….. 76

Misinformation in nutrition through the case of coconut oil: an online before-


and-after study………………………………………………………………………… 76

Capítulo IV – Considerações Finais e Perspectivas Futuras............................ 105

Apêndice I – Capítulo II ..................................................................................... 108

Apêndice II – Capítulo III ................................................................................... 176


15

CAPÍTULO 1 - REFERENCIAL TEÓRICO

ÓLEO DE COCO: CARACTERÍSTICAS E METABOLISMO

Aproximadamente 92% do óleo de coco é composto de ácidos graxos

saturados (AGS), dentre os quais, 45-50% correspondem ao ácido láurico (C12:0), 9%

ácido caprílico (C8:0), 7% ácido cáprico (C10:0), 16% ácido mirístico (C14:0) e 8%

ácido palmítico (C16:0). Os ácidos graxos (AG) remanescentes são monoinsaturados

(AGM) (6%) e polinsaturados (AGP) (2%). O óleo de coco apresenta baixa

concentração de ácido linoleico (18:2) e não contém ácido linolênico (18:3) [ambos

ácidos graxos essenciais (AGE)] (Figura 1) (1).

Figura 1. Composição de ácidos graxos do óleo de coco

C4:0 = butírico; C6:0 = ácido capróico; C8:0 = ácido caprílico; C10:0 = ácido cáprico; C12:0 = ácido

láurico; C14:0 = ácido mirístico; C16:0 = ácido palmítico; C18:0 = ácido esteárico; C18:1: = ácido oleico;

C18:2 = ácido linoleico


16

As gorduras alimentares são compostas por uma mistura de AGS, AGM e AGP,

variando a composição de AG dependendo da sua fonte: se de origem animal ou

vegetal. Gorduras com maior proporção de AGM e AGP geralmente são líquidas em

temperatura ambiente e são denominadas como óleos. Já as gorduras com maior

proporção de AGS, especialmente os de cadeia longa, geralmente são sólidas em

temperatura ambiente e são denominadas como gorduras (2,3). Por conta disso, “óleo

de coco”, como popularmente é conhecido, não seria o termo correto a ser empregado

por ser uma gordura sólida em temperatura ambiente devido à sua alta quantidade de

AGS, significativamente maior que a maior parte dos outros óleos de consumo

alimentar, sendo considerado, portanto, uma gordura sólida para fins nutricionais (2).

O ácido láurico, AG mais abundante no óleo de coco, pode ser classificado tanto

como um ácido graxo de cadeia média (AGCM), como ácido graxo de cadeia longa

(AGCL), sendo, portanto, um AG com propriedades intermediárias entre ambos (4).

Os AGCM, formados principalmente pelos ácidos caprílico (C8:0) e cáprico (C10:0),

são absorvidos no intestino delgado ligados à albumina e atingem o fígado via sistema

portal, não elevando a trigliceridemia (5). Já, 70 a 75% do ácido láurico é absorvido

com quilomícrons (semelhante à absorção dos AGCL) (6), sendo sua presença nos

quilomícrons dose-dependente (7). No geral, AGCM (C8:0 e C10:0) apresentam baixo

peso molecular (512 na média), diferente dos AGCL que têm um peso molecular mais

alto (o peso molecular do óleo de coco é 638). AGs com menores pesos moleculares

facilitam a ação da lipase pancreática, sendo hidrolisados de maneira mais eficiente

no intestino curto comparando-se com AG de cadeias mais longas (8).

Os AGCL são esterificados nos enterócitos, onde formam os triglicerídeos (TG),

que são transportados até o sistema linfático, via corrente sanguínea pelos

quilomícrons. A lipase lipoproteica hidrolisa os TG dos quilomícrons, liberando AG


17

para os tecidos periféricos, que podem ser utilizados como fonte energética ou

reesterificados em novos TG para armazenamento (3). Os AGCL necessitam do

transportador carnitina palmitol transferase na membrana mitocondrial externa, para

serem internalizados na organela e oxidados em Acetil-Coa para servirem como fonte

de energia (9,10). Os AGCM são absorvidos diretamente na corrente sanguínea, não

sendo incorporados significativamente em quilomícrons e lipoproteínas de muito baixa

densidade (VLDL). São considerados uma fonte rápida de energia pois, ao passarem

pelos enterócitos, atingem a circulação portal, sendo transportados ao fígado ligados

à albumina, onde são oxidados. Especulou-se que, devido ao seu metabolismo rápido,

os AGCM estimulariam a termogênese, diminuindo a sua deposição no tecido

adiposo, o que aumentaria a saciedade sem aumentar os níveis séricos de colesterol

total (CT) (3). No entanto, não há estudos experimentais que comprovem estas

teorias. Mesmo que houvesse, esses achados não poderiam ser extrapolados para o

óleo de coco, devido a sua grande concentração de ácido láurico que não tem sua

absorção, transporte e metabolismo realizados dessa forma, como exposto

anteriormente.

ÓLEO DE COCO: MERCADO E CONSUMO

O coco é um alimento consumido mundialmente. O cultivo do coqueiro se dá

especialmente com o objetivo fim de exploração comercial da copra dos frutos para

produção de óleo de coco e coco seco desidratado (11). O continente asiático detém

a maior parte da área plantada de coqueiros no mundo. Algumas populações

asiáticas, como o Sri Lanka, Minangkabau e Filipinas, têm o coco como parte da

alimentação diária. As Filipinas, Indonésia e Índia são os países que mais produzem
18

óleo de coco no mundo, extraindo o óleo de coco em duas versões: refinado, clareado

e desodorizado e extraído à frio, sem processo de refinamento (óleo de coco virgem)

(12).

Nos últimos anos, a produção mundial de óleo de coco, principalmente o óleo de

coco virgem, não refinado aumentou expressivamente (6). Estima-se que em 2016

houve um consumo de 640 mil toneladas de óleo de coco nas Filipinas, 449 mil

toneladas na Índia e 468 mil toneladas nos Estados Unidos (13). O Reino Unido é um

dos países da Europa que mais importa óleo de coco do Sri Lanka (cerca de 7% em

2015) (14). Não há registros sobre o consumo do óleo de coco no Brasil, no entanto,

até meados de 2010, o consumo do óleo de coco para preparo de alimentos ou uso

como suplemento dietético era pouco usual.

Até meados de 2010, a utilização de óleo de coco na dieta era menos comum

nas populações ocidentalizadas. Rico em AGS, gordura bem descrita na literatura

como relacionada ao aumento dos níveis plasmáticos de lipoproteína de baixa

densidade (LDL-C) e aumento do risco cardiovascular, o consumo de óleo de coco

não era recomendado (3).

Estudos em humanos testando os efeitos do óleo de coco na saúde

cardiometabólica datam da década de 1990 (15,16), mas somente após a publicação

e, possivelmente, divulgação dos resultados de diferentes estudos (17,18) em

encontros científicos e nas redes sociais é que ocorreu maior interesse por sua

prescrição e utilização como uma opção de óleo saudável. Estes estudos de curto

prazo mostraram uma leve melhora no perfil lipídico e antropométrico com a ingestão

de óleo de coco em populações adultas saudáveis (17,18). No entanto, seus

resultados são baseados em marcadores substitutos de saúde cardiometabólica, e

nenhum estudo até o momento avaliou o benefício potencial do consumo de óleo de


19

coco na prevenção do diabetes e de desfechos cardiovasculares. Também, é

possível, que a partir desses estudos, desenvolveu-se um interesse da indústria de

alimentos em comercializar o óleo de coco como alimento saudável, ocorrendo uma

disseminação dos benefícios desse óleo em sites, blogs e perfis de mídias sociais de

profissionais de saúde e prática clínica desses, difundindo o óleo de coco como uma

gordura saudável para ser utilizada para cozinhar, ser adicionado em saladas e outras

preparações alimentícias (19) (Figura 2)

Figura 2. Modelo do processo que permeia entre a geração e interpretação

de uma evidência científica até a divulgação dos seus dados

Legenda: O modelo demonstra as possíveis etapas que resultaram em um aumento do consumo

alimentar do óleo de coco e que pode ser, possivelmente, aplicado em outros exemplos da construção

da desinformação em saúde. Essas etapas ocorrem após a divulgação de publicações com limitações

metodológicas e eventual presença de vieses. Pode resultar na interpretação distorcida de dados

científicos, aplicação clínica inadequada e geração em mídia social da desinformação relacionada aos

cuidados de saúde.
20

ÓLEO DE COCO: EVIDÊNCIAS CIENTÍFICAS EM RELAÇÃO AO SEU EFEITO EM

PARÂMETROS CARDIOMETABÓLICOS

Algumas populações asiáticas, como do Sri Lanka, Minangkabau, Filipinas e

das ilhas Pukapuka e Tokelau na Polinésia, antes da introdução de uma dieta mais

ocidentalizada, apresentavam níveis de CT mais baixos que populações mais

ocidentalizadas, além de menor morbidade por doença cardiovascular (20-23). Dentre

as possíveis hipóteses aventadas para se identificar a causa, foi sugerido que o

consumo de gordura de coco poderia estar, em parte, relacionado a estes achados.

No entanto, é importante ressaltar que, embora estas populações apresentassem um

padrão alimentar onde a maior fonte de AGS e energia era a gordura do coco,

diferentemente de populações mais ocidentalizadas com maior consumo de fontes de

gordura animal, elas apresentavam como maior fonte proteica o consumo de peixes

e, como maior fonte de carboidratos, as frutas nativas da região, sendo um padrão

alimentar saudável, habitualmente rico em fibras, pobre em alimentos ultra

processados e sacarose (23).

Diferentes entidades científicas, não recomendam o uso do óleo de coco como

AG de preferência para o consumo humano (2,5,24). A ingestão de óleo de coco está

associada a uma piora no perfil lipídico, aumentando a concentração plasmática de

LDL-C, um fator de risco bem definido para doenças cardiovasculares, sem melhora

no peso corporal, controle glicêmico e parâmetros inflamatórios em comparação com

outros óleos não tropicais (25-27). Esses dados levaram diferentes sociedades

científicas especializadas e dedicadas à saúde metabólica a se posicionaram contra

o uso da gordura de coco, também para perda de peso, por não haver na literatura,
21

até então, comprovação científica de que o óleo de coco possua algum mecanismo

que promova a perda de peso (28).

Existe uma série de limitações metodológicas nos estudos de intervenção que

avaliaram o benefício do óleo de coco em parâmetros metabólicos (Figura 2). Nas três

meta-análises em que se avaliou o consumo de óleo de coco versus outros óleos em

relação ao perfil lipídico, antropométrico, marcadores inflamatórios e níveis de

glicemia, houve a inclusão de estudos do tipo cruzado (24-26). Dentre as limitações

relacionadas à inclusão desses estudos estão: a ausência de definição do tempo de

wash-out, da ordem de randomização dos grupos de intervenção e falta de clareza da

existência de parâmetros de avaliação clínica, nutricional e laboratorial antes e logo

após todas as intervenções.

Ainda, os ECR incluídos nas meta-análises apresentam, de uma maneira geral,

tempo de seguimento curto (uma a 12 semanas) e grupos comparativos que agrupam

diferentes braços, com óleos com propriedades nutricionais distintas. Por exemplo,

um estudo incluído na revisão de Neelakantan e cols agrupou 3 diferentes braços de

intervenção como grupo controle (óleos de chia, cártamo e soja) para comparação

com o óleo de coco. Este grupo controle ignorou que os óleos demonstram respostas

distintas sobre parâmetros metabólicos, eventualmente, em direções opostas, o que

limitaria a capacidade de meta-analisar os dados (25). Por outro lado, um ECR indiano

(198 indivíduos com doença cardiovascular, dois anos de duração), analisou

parâmetros metabólicos comparando-se a ingestão de 15% do valor calórico diário

com óleo de coco versus óleo de girassol no preparo dos alimentos. Não houve

diferenças nos níveis de CT, LDL-C, lipoproteína de alta densidade (HDL-C), TG e

VLDL, peso, circunferência da cintura, percentual de gordura e níveis de hemoglobina

glicada (HbA1c) comparando-se o consumo dos dois óleos (30). Estes dados sugerem
22

que estudos de maior duração sejam mais adequados para demonstrar não haver

benefício do consumo de óleo de coco sobre parâmetros metabólicos a longo prazo.

Além disso, o estabelecimento de conduta baseada em desfechos substitutos

apresenta limitações de aplicabilidade para tomada de decisão, demonstrando ser,

muitas vezes, uma medida inadequada. Como exemplo podemos citar o estudo que

avaliou a eficácia do inibidor da Cholesterol Ester Transfer Protein (CETP), um

fármaco que aumenta significativamente os níveis de HDL-C, mas que em seu estudo

de segurança cardiovascular, associou-se há um maior risco de desfechos

cardiovasculares, tendo que ser interrompido (31).

Estudo observacional mostrou que a substituição de 5% da ingestão de energia

de AGS pela mesma ingestão de AGP ou AGM está associada a um risco 27 e 13%

menor de mortalidade, respectivamente (32). Esses dados corroboram as

recomendações da atual diretriz alimentar para americanos que preconiza a redução

de AGS para menos de 10% das calorias e sua substituição por ácidos graxos

insaturados (AGI) (2). Além disso, dados recentes de coortes prospectivas de longo

prazo e meta-análises mostraram que as mesmas recomendações estão associadas

à prevenção do ganho de peso, redução da resistência à insulina e risco de diabetes

(33-36).

Tendo em vista a composição de ácidos graxos do óleo de coco, seria possível

este alimento apresentar propriedades antioxidantes e seu consumo melhorar

parâmetros inflamatórios? Até o presente momento, estudos que avaliaram os efeitos

antioxidantes do óleo de coco são, em sua maioria, preliminares e experimentais, não

podendo seus dados serem replicados em humanos (5). O óleo de coco virgem,

extraído pelo processo molhado diretamente do leite de coco em ambiente controlado

de temperatura, parece ter melhores propriedades nutricionais, uma vez que retém
23

maior quantidade de componentes insaponificáveis, como vitamina E e polifenóis,

tendo, portanto, maior capacidade antioxidante (35). Todavia, o óleo de coco

geralmente é obtido por processo seco, a partir do óleo de copra. Este óleo é extraído

da “carne” do coco, a qual é ralada, moída e cozida em água para extrair o óleo, e é

exposto a temperaturas muito elevadas ou à luz durante vários dias, até que a

umidade em excesso seja removida. Essa exposição à luz solar ou altas temperaturas

poderia inativar componentes reconhecidamente antioxidantes tais como tocoferóis,

tocotrienóis e polifenóis (37).

Dentre todos os AGS, o ácido láurico é o que apresenta maior potencial

inflamatório (38). Estudos mostram que o ácido láurico é capaz de ativar vias

inflamatórias por meio da ativação de toll like receptor 4 (TLR4), o que leva a secreção

de citocinas inflamatórias e ativação de células T (36,37). Já um estudo in-vitro, com

macrófagos, observou que o ácido láurico induz a ativação do fator nucelar kappa (NF-

Kβ), levando a um aumento da expressão de ciclo-oxigenase-2 (COX2), pela ativação

de TLR 2 e 4 (40). Meta-análise recente de ECR comparando os efeitos do consumo

de óleo de coco, rico em ácido láurico, com outros óleos, não observou diferença nas

concentrações plasmáticas de proteína C-reativa (PCR), um importante marcador de

inflamação subclínica (25). Em um ECR, em indivíduos normocolesterolêmicos da

Malásia, comparou-se os efeitos do consumo de óleo de coco com o de óleo de palma

ou oliva (follow-up: 5 semanas) nas concentrações plasmáticas de homocisteína e

marcadores inflamatórios como fator de necrose tumoral α, interleucina-1β,

interleucina-6 (IL-6), INF-γ e–IL e não se encontrou diferença entre estes parâmetros

(41). Esses dados não corroboram a divulgação de benefícios relacionados do óleo

de coco sobre diferentes parâmetros metabólicos relacionados ao desenvolvimento

de obesidade, diabetes e doença cardiovascular.


24

Figura 3. Limitações de estudos prévios sobre consumo de óleo de coco

e potenciais vieses destes resultados

Legenda: Limitações metodológicas relacionadas aos resultados de estudos prévios sobre o efeito do

consumo de óleo de coco em parâmetros cardiometabólicos e potenciais vieses relacionados a estes

achados, resultando em ausência de evidências relacionadas ao seu consumo

DESINFORMAÇÃO EM SAÚDE

A desinformação em saúde é um problema mundial e sua prevalência aumenta

com a produção de conteúdo de saúde nos meios de comunicação de massa e redes

sociais, elevando a quantidade de recomendações que não são baseadas em

evidências (42,43).

As mídias sociais são essenciais para o fluxo de informações, construção do

conhecimento e difusão de opiniões. No entanto, com a inserção dessas novas mídias

no cotidiano, a sociedade se acostumou a acessar informações de saúde em larga


25

escala, porém nem sempre de fontes confiáveis. Estudos mostram que as

informações publicadas em sites relacionados à saúde podem apresentar imprecisões

e baixa qualidade de evidência da informação disponibilizada (44-48), pois qualquer

pessoa pode publicar sobre informações em saúde (49).

Dessa forma, muitas informações são divulgadas, mas pouco conhecimento

está sendo construído (50). Embora as mídias sociais tenham um papel fundamental

na saúde, contribuindo para a transmissão das evidências científicas para a

sociedade, apresentando fatos e descobertas de forma acessível, há também grande

espaço para a disseminação de informações não comprovadas ou com seus

resultados apresentados de maneira distorcida. Desta forma, rumores, notícias falsas,

grupos e/ou opiniões de figuras públicas baseadas em suas próprias crenças, acabam

atingindo milhares de pessoas, criando teorias e verdades infundadas, o que pode

impactar de maneira negativa a saúde dos indivíduos.

Em 2002, Eysenbach definiu o termo “infodemiologia” como o processo que

permite a identificação de áreas onde há uma lacuna entre a tradução das melhores

evidências científicas, propostas por especialistas no assunto, e como a maioria das

pessoas utiliza essas informações (51). Para combater a infodemiologia é necessário

traduzir a ciência da forma mais clara possível para a população em seus mais

diversos graus de conhecimento e educação, utilizando uma linguagem acessível e

didática por parte das autoridades, a fim de mudar crenças que podem levar a ações

negativas para saúde (42,43,52). Mesmo aplicando-se grandes esforços, o impacto

na mudança de conceitos enganosos pode não ser eficaz, pois os indivíduos tendem

a interpretar as informações recebidas para confirmar suas crenças e não o contrário,

o que é chamado de viés de confirmação (53).


26

Muitas pessoas apresentam dificuldade para interpretar se uma informação em

saúde é de fonte confiável e, de fato, baseada em sólidas evidências científicas, o que

as expõem a erros, e, até mesmo, reduzem sua participação em programas de

rastreamento de doenças, além de uma menor adesão aos tratamentos propostos

(54). Pessoas com menor escolaridade e/ou menor alfabetização em saúde são os

grupos de maior risco neste contexto (55). Um estudo demonstrou que cerca de nove

em cada dez adultos americanos não possuem as habilidades necessárias para o

manejo e prevenção de doenças (56).

Alfabetização em saúde é originalmente definida como as habilidades cognitivas e

sociais que determinam a motivação e a capacidade do indivíduo de obter acesso

para compreender e usar as informações de maneira que promovam e mantenham

uma boa saúde (58). Estudos mostram que pessoas com baixo grau de alfabetização

em saúde pesquisam menos sobre saúde, escolhem diferentes fontes de informação

e têm menor grau de entendimento sobre rótulos de medicamentos e informações

passadas sobre saúde (58-60). Ainda, demonstrou-se que pessoas com baixo grau

de alfabetização em saúde não confiam nas informações de saúde divulgadas por

fontes governamentais e avaliam se a informação de saúde é confiável ou não com

base na posição da página na internet nos sites de busca e pela qualidade das

imagens do site (61). Em contraponto, existem evidências que mostram que as

informações divulgadas pelos governos e instituições são geralmente confiáveis

(62,63). Uma revisão sistemática da literatura mostra que, no geral, indivíduos com

níveis educacionais mais baixos apresentam uma pior habilidade (real e auto-

avaliada) para avaliar a qualidade das informações de saúde online e menor confiança

nas informações divulgadas online do que seus pares com nível educacional mais

elevado (49).
27

O desenvolvimento de estratégias para potencializar a disseminação de conceitos

adequados de saúde, a fim de proteger a população contra a desinformação, é uma

nova área de investigação. Algumas intervenções anti-propagação de notícias falsas

relacionadas à saúde já foram testadas. Como exemplo, é possível utilizar correções

algorítmicas e sociais, expondo a rede social às informações reais produzidas por um

algoritmo ou por um usuário da rede social, a fim de proteger a sociedade contra

notícias falsas (64). Também é possível classificar a credibilidade da fonte das

informações fornecidas pelo usuário da rede social (65). Uma solução eficaz

certamente será uma ampla combinação de diversas abordagens desenvolvidas por

especialistas em saúde, ciências sociais e da computação trabalhando juntos em

pesquisas interdisciplinares para encontrar maneiras de lidar com a desinformação

sobre saúde nas mídias sociais (65-67). Também é necessária uma regulamentação

do compromisso dos profissionais de saúde com a divulgação social da informação

amparada nas melhores evidências científicas disponíveis, com uma análise crítica

dos resultados dos estudos (43).

JUSTIFICATIVA

Nos últimos 10 anos, o consumo dietético de óleo de coco foi bastante

estimulado por profissionais da saúde em meios científicos e de comunicação diversos

(blogs, sites, rádio e TV, e em perfis pessoais nas mais diversas redes sociais). Em

um primeiro momento, seu consumo foi estimulado baseado em ECRs de curta

duração que mostram benefícios discretos do uso do óleo de coco em parâmetros

antropométricos e perfil lipídico (18,19). Além disso, devido aos AGCM apresentarem

um metabolismo mais rápido dos que os demais comprimentos de cadeia de AG,


28

pensou-se que tais benefícios poderiam ser extrapolados para o óleo de coco,

estimulando o seu consumo (3).

Com a elaboração de novos ECRs sobre o tema e a publicação de diferentes

meta-análises (25,26), diferentes órgãos científicos e governamentais se

posicionaram contra o consumo de óleo de coco, pois seu impacto no perfil

antropométrico seria nulo ou muito discreto, face ao seu potencial de elevar o LDL-C,

sendo um marcador importante no desenvolvimento de DCV (6,2,24). No entanto, uma

vez tendo sido amplamente divulgado como um alimento saudável em diferentes

meios de comunicação e sendo incorporado nas crenças alimentares dos indivíduos

como uma gordura para fins dietéticos, como desconstruir este conceito errôneo em

saúde?

A integração e comparação entre o que as melhores evidências científicas nos

mostram sobre o consumo do óleo de coco e as percepções da população sobre o

uso dietético deste alimento nos proporcionará identificar a lacuna entre a nutrição

baseada em evidências e a opinião pública, possibilitando o desenvolvimento de

estratégias de saúde pública para aumentar a alfabetização de nossa população em

nutrição, buscando-se com isto, uma melhora da saúde metabólica da população e a

prevenção de doenças crônicas, como a obesidade, o diabetes e as doenças

cardiovasculares.
29

OBJETIVOS

Objetivo Geral

Avaliar os efeitos do óleo de coco em parâmetros metabólicos, e identificar quais as

motivações para o seu consumo como alimento em uma população do sul do Brasil.

Objetivos Específicos

1. Avaliar, por meio de uma revisão sistemática com meta-análise de ensaios

clínicos randomizados, os efeitos do consumo de óleo de coco, em comparação

ao consumo de outros óleos, gorduras ou placebo no perfil lipídico,

antropométrico, glicêmico e inflamatório de adultos.

2. Avaliar, por meio de uma pesquisa online, o consumo de óleo de coco e a

motivação para este consumo em uma população do Sul do Brasil.

3. Avaliar, por meio de uma pesquisa online, se uma população do Sul do Brasil,

altera suas crenças sobre o consumo de óleo de coco após serem expostos

aos resultados de uma pesquisa científica sobre o tema.


30

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38

CAPÍTULO II - The Effects of Coconut Oil on the Cardiometabolic Profile: a

Systematic Review and Meta-Analysis of Randomized Clinical Trials

Original Article

Authors: Ana Cláudia Duarte1*, Bernardo Frison Spiazzi1,2*, Carolina Pires Zingano2,

Eduarda Nunes Merello2, Laura Fink Wayerbacher2 Paula Portal Teixeira1, Laura

Penso Farenzena2, Carina de Araujo1, Carmen Raya Amazarray1, Verônica Colpani1,

Fernando Gerchman1,2,3

Affiliations:
1 Post-graduate Program in Medical Sciences: Endocrinology, Universidade Federal

do Rio Grande do Sul, Porto Alegre, Brazil


2 Universidade Federal do Rio Grande do Sul, Faculdade de Medicina, Departamento

de Medicina Interna, Porto Alegre, Brazil


3 Division of Endocrinology and Metabolism, Hospital de Clínicas de Porto Alegre,

Porto Alegre, Brazil

*This authors share co-first authorship

Corresponding author: Fernando Gerchman

Rua Ramiro Barcelos 2350, 4th floor, room 401, Division of Endocrinology and

Metabolism, 90035-003, Porto Alegre, Rio Grande do Sul, Brazil

Phone: +55 51 33598127

Email address: fgerchman@hcpa.edu.br


39

Abstract:

Background: Despite having a 92% concentration of saturated fatty acid composition,

leading to an apparently unfavorable lipid profile, body weight and glycemic effect,

coconut oil is consumed worldwide. Thus, we conducted an updated systematic review

and meta-analysis of randomized clinical trials (RCTs) to analyze the effect of coconut

oil intake on different cardiometabolic outcomes.

Methods: We searched Medline, Embase, and LILACS for RCTs conducted prior to

April 2022. We included RCTs that compared effects of coconut oil intake with other

substances on anthropometric and metabolic profiles in adults published in all

languages, and excluded non-randomized trials and short follow-up studies. Risk of

bias was assessed with the RoB 2 tool and certainty of evidence with GRADE. Where

possible, we performed meta-analyses using a random-effects model.

Results: We included seven studies in the meta-analysis (n = 515; 50% females,

follow up from 4 weeks to 2 years). The amount of coconut oil consumed varied and is

expressed differently among studies: 12 to 30 ml of coconut oil/day (n=5), as part of

the amount of SFAs or total daily consumed fat (n=1), a variation of 6 to 54.4 g/day

(n=5), or as part of the total caloric energy intake (15 to 21%) (n=6). Coconut oil intake

did not significantly decrease body weight (MD -0.24 kg, 95% CI -0.83kg to 0.34 kg),

waist circumference (MD -0.64 cm, 95% CI -1.69 cm to 0.41 cm), and % body fat (-

0.10%, 95% CI -0.56 to 0.36), low-density lipoprotein cholesterol (LDL-C) (MD -1.67

mg/dL, 95% CI -6.93 to 3.59 mg/dL), and triglyceride (TG) levels (MD -0.24 mg/dL,

95% CI -5.52 to 5.04 mg/dL). However, coconut oil intake was associated with a small

increase in high-density lipoprotein cholesterol (HDL-C) (MD 3.28 mg/dL, 95% CI 0.66

to 5.90 mg/dL). Overall risk of bias was high, and certainty of evidence was very-low.

Study limitations include the heterogeneity of intervention methods, in addition to small


40

samples and short follow-ups, which undermine the effects of dietary intervention in

metabolic parameters.

Conclusions: Coconut oil intake revealed no clinically relevant improvement in lipid

profile and body composition compared to other oils/fats. Strategies to advise the

public on the consumption of other oils, not coconut oil, due to proven cardiometabolic

benefits should be implemented.

Registration: PROSPERO CRD42018081461

Funding: FIPE-HCPA project 2018-0393, PROPESQ-UFRGS, CAPES,

CNPq/MCTI/FNDCT18/2021 (420065/2021-0) and HCPA.

Keywords: coconut oil, saturated fatty acids, lipid profile, anthropometric profile
41

Background

Cardiovascular disease (CVD), particularly coronary heart disease and stroke, is a

major public health problem, being responsible for one-third of deaths worldwide (1-4).

Despite the great effort of different scientific organizations to fight against the burden

of major risk factors for CVD, it is estimated that 11 million deaths and 255 million

disability-adjusted life-years are attributable to dietary risk factors (5-8).

The impact of different types of dietary fats on health has been studied, and its

contribution to the development of diseases, causing major burden, such as diabetes,

cardiovascular diseases and cancer has been debated (6, 9). A recent report from the

American Heart Association based on different prospective cohort studies, randomized

clinical trials (RCTs), and meta-analyses estimated that replacing 5% of energy intake

of saturated fatty acids (SFAs) with the same intake of polyunsaturated fatty acids

(PUFAs) or monounsaturated fatty acids (MUFAs) was associated with a 25% and

15% lower risk of coronary heart disease, respectively (6). In light of this evidence, the

most recent Dietary Guidelines for Americans recommend a reduction in SFAs to less

than 10% of calories and their replacement with unsaturated fats (10). Additionally,

recent data from long-term prospective cohorts and meta-analyses have shown that

these recommendations are associated with weight gain prevention and reduction of

insulin resistance and risk for diabetes (11-15).

Despite that, coconut oil, which is more than 90% SFA, has been widely recommended

on social media for the management of obesity, diabetes, and lipid disorders,

broadening its consumption all over the world (16-18). In increasing demand, the

estimated consumption of coconut oil in the United States reached 400,000 tons in

2010 (19). Nonetheless, before the recent rise in coconut oil consumption in western

countries, it was only mainly present in some Asian populations’ diets (20-22).
42

A recent systematic review showed that lauric, myristic, and palmitic fatty acids - the

major components of coconut oil - are responsible for the highest increase in low-

density lipoprotein cholesterol (LDL-C) levels, which is a major risk factor for CVD (19).

Unlike other types of oils which were consistently proven to prevent weight gain,

diabetes, CVD, and mortality (23-25), studies that analyzed how coconut oil intake

affects weight, lipid and glycemic levels are mostly based on small, short-term

observational studies and clinical trials (16, 26, 27). In addition, there are meta-

analyses including RCTs that have even demonstrated that coconut oil intake

increased LDL-C in comparison to non-tropical vegetable and animal oils and did not

observe differences in TG levels (28, 29).

Due to the popularity of coconut oil as a “healthy” food, its broad dietary consumption

has risen all over the world. This has led to increasing difficulties to translate medical

and nutritional science into adequate recommendations for physicians and health

workers as well as laymen. Given this context, we conducted an updated systematic

review and meta-analysis of RCTs investigating the effects of coconut oil intake on

body weight and composition, lipid profile, glycemic status, blood pressure, and

subclinical inflammation in adults.

Methods

This systematic review and meta-analysis was prospectively registered on

PROSPERO (CRD42018081461) and was conducted in accordance with the

Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020

statement (30).

Search methods for the identification of studies


43

We searched the MEDLINE, EMBASE, and LILACS databases to identify studies

analyzing the effects of coconut oil intake on weight, lipid and glycemic profiles, blood

pressure, and subclinical inflammation in adults from inception to April, 2022, and

searched www.clinicaltrials.gov for potentially available unpublished results

(Supplementary Appendix I). The references of relevant systematic reviews were

screened manually to identify further relevant citations. When an article did not present

the results of interest, we contacted the authors by email requesting the data.

Study selection and data extraction

Study inclusion and data extraction were conducted independently (A.C.D., C.R.A.,

and C.A.). Reviewers resolved discrepancies by discussion and, when necessary, with

adjudication by a third party (F.G.). Inter-rater agreement was assessed using the

Kappa statistic and percentage of agreement. Kappa statistic was calculated with

SPSS software (version 18.03; Chicago, USA). Data extracted were reviewed and

double checked by two independent authors (B.F.S. and E.N.M.), who were blinded to

the objectives of the meta-analysis.

A standard protocol for data extraction was used, including the following variables:

number of participants, study design, duration of the study, interventions, demographic

data, age and sex, chronic disease status, as well as exposures of interest before and

after the interventions. Data was extracted to assess the effects of coconut oil on

anthropometric profile (body weight, body mass index, waist circumference and body

composition), lipid profile (LDL-C, HDL-C, total cholesterol [TC], TC/HDL ratio and

triglycerides), glycemic profile (glucose, insulin, the homeostasis model assessment

[HOMA] β and HOMA-S, HOMA-IR and glycated hemoglobin [HbA1C]), inflammatory

profile (ultra-sensitive c-reactive protein [US-CRP], fibrinogen, total homocysteine


44

[tcHcy], interleukins [IL] 1β, IL-6, IL-8 and interferon-gamma [IFN- γ]) and blood

pressure (systolic blood pressure and diastolic blood pressure).

Inclusion and exclusion criteria

Since our aim was to evaluate the isolated effect of coconut oil with no influence of

dietary pattern, we considered eligible only RCTs (both parallel group or crossover

randomized trials) which analyzed the effects of coconut oil intake in comparison to

other fats, oils, or placebos on weight, lipid and glycemic profile, blood pressure, and

subclinical inflammation of adults (≥ 18 years) published in all languages. We excluded

non-randomized trials or studies with follow-ups shorter than seven days. Studies

including patients with illnesses which affect metabolism, studies on animals or in vitro,

and studies testing coconut products different from oils for intake were also excluded.

Assessment of bias and quality of evidence

Two pairs of authors independently assessed the risk of bias of each included trial

using the revised Cochrane risk-of-bias tool for randomized trials (RoB 2) (31). RoB 2

plots were generated using the Risk-of-bias VISualization (robvis) tool (32). The overall

certainty of evidence was assessed using the Grading of Recommendations

Assessment, Development, and Evaluations (GRADE) (33).

Statistical synthesis

Data were synthesized both qualitatively and quantitatively. To uniformly summarize

the exposure data extracted, we standardized the units of concentration by applying

standard conversion factors (34, 35). Mean differences were calculated for continuous

outcomes. For data collection, we prioritized intention-to-treat outcomes. Articles that

expressed results as standard error had the results transformed into standard

deviation. When a study did not express its results in a change from baseline manner,

changes from baseline were calculated by subtracting final values from baseline values
45

in each group and change from baseline standard deviations were imputed using a

correlation coefficient calculated from the most similar study reported in considerable

detail, in accordance with Cochrane Collaboration recommendations (36). Where

possible (that is, when parallel RCTs provided the baseline and final values of each

outcome and when the crossover RCTs provided the order of different interventions

and the measures of the variables of interest before and after each intervention), data

were pooled using a meta-analytic approach. A random-effects model, with

DerSimonian and Laird’s variance estimator, was used, and mean differences with

95% confidence intervals were calculated. A p value ≤ 0.05 was considered statistically

significant. We used I2 statistics to assess the consistency of effects among studies

(37). We did not assess publication bias with a statistical test or funnel plot because

such assessment is not recommended for sample sizes of less than 10 studies (38).

We used the statistical software R version 4.0.5 with the meta-version 4.18-1 package

for meta-analysis.

We planned to perform subgroup analyses regarding the following factors: amount of

coconut oil used, type of control group, sex, age, body mass index, geographical region

where the study was conducted, studies in overweight/obesity subjects or in those with

dyslipidemia, time of follow-up, and study sample size. When subgroup analysis of any

forementioned factors was not possible due to the low number of studies – thus

precluding our ability to quantitatively investigate the sources of heterogeneity –, this

analysis was not performed and, therefore, is not mentioned in the results section of

this text.
46

Results

After screening 1,160 potentially relevant studies, 17 fulfilled the selection criteria, of

which seven studies were included in the meta-analysis. Inter-rater agreement

assessed by the Kappa coefficient was 0.36 (% agreement: 91.1%) and –0.09 (%

agreement: 84%) for the record screening and fulltext assessment stages,

respectively. Details of the study selection are presented in Figure 1 and Table S1.

The studies comprise 721 patients (age 18–68 years, 52% females) and follow-ups

varied from one week to two years. The studies were performed in Europe (n = 2), Asia

(n = 3), New Zealand (n = 1), the United States of America (n = 7), and Brazil (n = 4).

In four studies, coconut oil was compared predominantly to MUFAs (olive (6) and

canola (1)) (39-42), in 11 studies predominantly to PUFAs (soybean (12), chia (1),

safflower (7), sunflower (1), and corn (1)) (16, 17, 26, 42-49), and in six studies

predominantly to SFAs (lard (1), butter (5), and palm oil (6)) (39, 40, 44, 50, 51),

followed by comparisons with soybean oil + psyllium, transgenic soybean,

hydrogenated soybean, and a placebo in one study each (18, 26, 45, 50). The amount

of coconut oil consumed varied and is expressed differently among studies (Table 1):

12 to 30 ml of coconut oil/day (n=5), as part of the amount of SFAs or total daily

consumed fat (n=1), a variation of 6 to 54.4 g/day (n=5), or as part of the total caloric

energy intake (15 to 21%) (n=6). Seven studies included healthy individuals (18, 26,

39, 45, 48, 50, 51); two included subjects with hypercholesterolemia (41, 44); four, with

abdominal obesity, overweight, or obesity (16, 42, 43, 49); one, in postmenopausal

women (46); and one, individuals with CVD (17). The key characteristics of all included

studies are in Supplementary Tables S2-S6 and summarized in Table 1.


47

We contacted authors from 12 trials, of whom three shared data with us (see

acknowledgments).

Trials reporting the effects of coconut oil on LDL-C to HDL-C ratio, TG, TC/HDL-C ratio,

glycemic control (fasting glucose and HbA1c levels) and blood glucose regulation

(insulin sensitivity and β-cell function), blood pressure, and subclinical inflammation

profile are described in the Supplementary Appendix II. No differences in these

parameters were found between coconut oil intake and the different control oils/fats. A

summary of findings of the systematic review and meta-analysis is presented in Table

2.

Coconut oil consumption and health outcomes

Anthropometric profile

Body weight

Nine studies analyzed the effects of coconut oil on body weight (16, 18, 26, 39, 42, 43,

46, 51). These studies included 533 participants (56.5% females, 18 to 68 years).

Six studies [(16, 17, 39, 42, 43, 51) were included in the meta-analysis. Overall, weight

loss was similar for those receiving coconut oil in comparison to those receiving other

oils or fat (Figure 2a).

The changes in body weight with coconut oil were also not significantly different in

comparison to PUFA-rich oils, SFA-rich oils/fats, and MUFA-rich oils (Figure 2a).

We also performed subgroup analyses considering the type of control group, gender,

geographical region, studies in subjects with overweight/obesity, time of follow-up (< 1

year vs. ≥ 1 year), and the presence of co-interventions. These analyses did not explain

the heterogeneity between groups and showed no changes in the direction of the

results (Supplementary Figures S1–S8).


48

Additionally, two crossover studies found no differences between the consumption of

coconut oil and other oils and fats on body weight (26, 46).

Waist circumference

Seven studies analyzed the effects of coconut oil on waist circumference (16, 39, 40,

42, 43, 46, 49). These studies included 347 participants (80.1% females, 23 to 66

years).

Five studies were included in the meta-analysis (16, 39, 42, 43, 49). Overall, the effect

of coconut oil on waist circumference was not different in comparison to other

interventions (Figure 2b).

In order to understand the heterogeneity found, we performed a subgroup analysis. A

small yet significant reduction in waist circumference is perceived while comparing the

consumption of coconut oil with PUFA-rich oils,) but not with MUFA-rich oils

(Supplementary Figure S9).

We also performed subgroup analyses considering the type of control group, gender,

geographical region, studies in subjects with overweight/obesity, and the presence of

co-interventions. These analyses did not explain the heterogeneity between groups

and showed no changes in the direction of the results (Supplementary Figures S9–

S15).

In one crossover study, the consumption of coconut oil decreased waist circumference

in comparison to safflower oil (40).

Body composition

Six studies analyzed the effect of coconut oil on body fat distribution (16, 17, 39, 40,

46, 49). These studies included 460 participants (35.4% females, 29 to 68 years).
49

Five studies (16, 17, 39, 42, 49) were included in the meta-analysis. Overall, the effect

of coconut oil intake on total body fat did not differ in comparison to other oils or fats

(Supplementary Figure S16). Additionally, in comparison to PUFA- and MUFA-rich oils,

the effect on total body fat was not different (Supplementary Figure S17).

Only one crossover study analyzed the effect of coconut oil on fat mass, including only

postmenopausal women (n = 12, 100% females, 57.8 ± 3.7 years) (46). The

comparator was safflower, and there was no difference in body fat distribution between

groups.

Two studies analyzed the effect of coconut oil on lean mass (n = 41, 29% females, 35–

61 years) (46, 49). The comparators were safflower and soybean oils, and, once again,

coconut oil did not cause changes in lean mass in comparison with other oils

(Supplementary Table S2).

Lipid profile

LDL-C

Seventeen studies analyzed the effects of coconut oil on LDL-C (16-18, 26, 39-51).

These studies included 515 participants (50% females, 18 to 68 years).

Seven studies (16, 17, 39, 42, 43, 49, 51) were included in the meta-analysis. Overall,

the intake of coconut oil did not change LDL-C in comparison to other oils/fats (Figure

3).

Coconut oil intake did not increase LDL-C as compared to PUFA-rich oils, SFA-rich

oils/fats, and MUFA-rich oils (Figure 3a).

We performed subgroup analyses considering the type of control group, gender,

geographical region, studies in subjects with overweight/obesity, time of follow-up (< 1

year vs. ≥ 1 year), and the presence of co-interventions. These analyses did not explain
50

the heterogeneity between groups and showed no changes in the direction of the

results (Supplementary Figures S18–S25).

When analyzing the results of crossover studies, we observed that the intake of

coconut oil increases LDL-C levels in comparison to butter, lard, and other oils (18, 26,

40, 41, 44-48, 50).

HDL-C

Seventeen studies analyzed the effects of coconut oil on HDL-C (16-18, 26, 39-51).

These studies included 515 participants (50% females, 18 to 68 years).

Seven studies (16, 17, 39, 42, 43, 49, 51) were included in the meta-analysis. Overall,

the intake of coconut oil increased HDL-C by 3.28 mg/dL (Figure 3).

We also performed subgroup analyses considering the type of control group, gender,

geographical region, time of follow-up (< year vs. ≥ 1 year), and studies in

overweight/obesity subjects (Figures S26-S32). These analyses did not explain the

heterogeneity between groups. However, when analyzed in different comparisons, the

relative type of oil in the control group and studies only conducted in women, the

significant increase in levels of HDL-C no longer existed. An additional subgroup

analysis demonstrated that a significant increase in levels of HDL-C with coconut oil

intake in comparison to other oils/fats was only identified in studies that included

lifestyle interventions (Figure S33).

While analyzing the crossover studies (17, 25, 39, 40, 43-47, 49), we observed that

the intake of coconut oil increases HDL-C in comparison to butter, lard, and other oils

(data not shown).


51

Triglycerides

Seventeen studies analyzed the effects of coconut oil on TG levels (16-18, 26, 39-51).

These studies included 515 participants (50% females, 18 to 68 years).

Seven studies (16, 17, 39, 42, 43, 49, 51) were included in the meta-analysis. Overall,

the intake of coconut oil did not change TG levels (Figure 3)

The effect of coconut oil on TG was also not significant in comparison to MUFA-rich

oils, PUFA-rich oils, and SFA-rich oils/fats (Figure 3c).

We performed subgroup analyses considering the type of control group, gender,

geographical region, studies in overweight/obesity subjects, time of follow-up (< 1 year

vs. ≥ 1 year), and the presence of co-interventions. These analyses did not explain the

heterogeneity between groups and showed no changes in the direction of the results

(Supplementary Figures S34–S41).

Crossover studies (17, 25, 39, 40, 43-47, 49) showed that the intake of coconut oil

increases TG levels in comparison to butter, lard, and other oils.

Risk of bias and certainty of evidence

Detailed results of the assessment of risk of bias are summarized in Supplementary

Figures S42-S46. RCTs were overall rated either as having a high risk of bias or

presenting some concerns in all analyzed outcomes. Risk of bias arose mainly from

poor reporting of the randomization process and from deviations from intended

interventions, in addition to carryover effects in crossover trials.

The certainty of evidence was rated as very low due to risk of bias and inconsistency

in all analyzed outcomes, as follows (Supplementary Table S7).


52

Discussion

This systematic review and meta-analysis of RCTs shows that, compared with the

dietary consumption of other types of oils and fats, the intake of coconut oil is not

superior in reducing body weight or abdominal circumference nor in changing body

composition, LDL-C levels, TG, and TC/HDL-C ratio. Subgroup analyses comparing

coconut oil with different types of oils based on their fatty acid composition have also

confirmed our findings. However, increased levels of HDL-C were observed with the

intake of coconut oil in comparison with that of other oils and fats.

Regarding the outcomes that were not included in metanalyses, only two (17, 43) of

the seven studies included in the systematic review that assessed glycemic control

had the appropriate minimum follow-up time to analyze changes in HbA1c measures,

given that the optimal timeframe to analyze alterations of HbA1c after dietary

interventions is 12 weeks. Individual data from these studies do not suggest an impact

of coconut oil intake on fasting glycemia, HbA1c, and estimates of β-cell function and

insulin sensitivity, in line with findings from other previously published meta-analyses

(29, 52).

Unlike other meta-analyses (28, 29, 52), we included studies that evaluated the effect

of coconut oil on arterial blood pressure and we observed higher levels of systolic and

diastolic blood pressure when coconut oil was compared with a placebo. When

comparing coconut oil with olive oil and butter, only diastolic blood pressure levels

increased (18, 39). Despite scarce data addressing the effect of coconut oil on blood

pressure, a cross-sectional study conducted in Southern India using a seven-day food

survey found that the intake of coconut oil is associated with a higher risk of

hypertension (53). Although the mechanisms related to this finding remain unclear,

foods rich in SFAs, such as coconut oil, can induce the development of central
53

adiposity and insulin resistance, both phenomena related to the development of

hypertension, which might explain these findings (11-14, 54).

Regarding markers of subclinical inflammation, as in other published meta-analyses

(29, 52), we did not find a reduction in US-CRP with the intake of coconut oil in

comparison to soybean oil, olive oil, and butter. Studies that evaluated the antioxidant

potential effect of coconut oil are mostly performed in vitro, and their data should not

be extrapolated to clinical practice (55). Among the SFAs, lauric acid, which is roughly

50% of coconut oil composition, has the greatest inflammatory potential, resulting in

an unfavorable rationale for conducting experimental studies evaluating the effect of

the dietary consumption of coconut oil for this aim (56).

In line with previously published meta-analyses (28, 29, 52), we observed an increase

in HDL-C levels with coconut oil in comparison with other oils and fats, which was also

confirmed while comparing coconut oil intake with oils rich in MUFAs and PUFAs.

These findings may be a result of its composition being predominantly made up of

SFAs, resulting in a superior increase in HDL-C levels compared to oils/fats rich in

MUFAs and PUFAs (29, 57). However, neither Mendelian randomization analyses

looking at genetic variants related to higher HDL levels (58), nor a meta-analysis of

108 RCTs evaluating the effects of different interventions that increase HDL-C levels

(59) demonstrated that this increment protects against cardiovascular disease. In fact,

dietary fat both increases transport rate and decreases the fractional catabolic rate of

HDL cholesterol esther and apo A-I, intensifying the reverse cholesterol transport, only

as an adaptation to the high load of a high fat diet (60, 61). However, the consumption

of SFA-rich oils, such as coconut oil, may not increase the apolipoprotein E-rich sub-

fractions, which are mediators of cholesterol’s reverse transport, a main mechanism

by which HDL-C exerts its cardio-protective effects (62). Thus, it does not seem
54

reasonable to advise the intake of coconut oil based on a possible protection against

CVD derived from its effect on HDL-C.

An increase in plasmatic levels of HDL-C was observed with coconut oil intake

compared with other oils while analyzing different studies (Figure 3b), which could be

explained by the fact that, in most of those studies, participants were exposed to co-

interventions, including diet (16, 42, 43, 49, 51) and physical activity (16, 43) – which

may have a significant impact on HDL-C levels (58, 59). In fact, in one of these studies,

participants significantly lost more weight, and, in two of them, there was a greater

reduction in waist circumference with coconut oil compared to soybean oil. These

results may have been driven by the real impact of coconut oil on HDL-C levels and

may explain the heterogeneity that was found (16, 43).

In this review, changes in body weight were similar between coconut oil and other oils.

In only one study, the group receiving coconut oil lost more body weight (16). This

result might be explained by the introduction of systematic error due to an imbalance

of co-interventions, which might have been introduced as a result of lack of blinding of

the staff who applied the lifestyle interventions. Similarly, among the five studies which

analyzed the impact of coconut oil in comparison to other oils/fats on central obesity,

the two studies which demonstrated that the coconut oil group had a more significant

reduction in waist circumference also applied lifestyle co-interventions in a similar

manner, possibly resulting in the same forementioned systematic error (16, 43).

Subgroup analyses for studies regarding co-interventions have shown no differences

in changes of body weight and waist circumference between coconut oil and diet

interventions with other oils (Supplementary Figure S33 and S15).

Previous meta-analyses (29, 52) found higher LDL-C levels with the consumption of

coconut oil in comparison with the intake of other oils and fats. These two reviews
55

included crossover trials, and, in one of them (29), oils used in different arms causing

very distinct responses in LDL-C levels were grouped as a single intervention against

coconut oil (16). We believe that this may explain the differences in findings between

our meta-analysis and previously published ones. In line with our findings, Teng et al.

(2020), in their analysis comparing coconut oil to other oils, did not find differences in

levels of LDL-C, either (28). Similar to what was found previously (29, 52), we also did

not identify differences in changes of TG levels, TC/HDL-C ratio, LDL-C/HDL-C ratio,

and body composition between the consumption of coconut oil and other oils/fats.

LDL-C concentration is one of the main targets for cardiovascular protection. However,

some subtypes of LDL-C, especially the slow dense LDL-Cs, have been associated

with a higher risk of atherogenesis (63). Lipoprotein (a) (Lp[a]), a genetic variant of

LDL, has also gained attention because of its considerable dyslipidemic potential (64).

There is still no clear evidence that reducing Lp(a) levels results in protection for

cardiovascular outcomes (65), nor do we know how nonpharmacological treatments

affect Lp(a) (66). It seems that a healthy lifestyle can promote favorable changes in

subclasses of lipoproteins (67), and that the characteristics of fatty acids could

influence these changes (68).

None of the studies included in this systematic review assessed the subclasses of

lipoproteins or Lp(a). However, a crossover trial including 31 women evaluated the

effect of three different margarines, one of them containing 80% coconut oil, on plasma

postprandial levels of some hemostatic variables and on fasting Lp(a). Data from only

11 subjects were evaluated, and there was a statistically significant reduction in Lp(a)

in the margarine with coconut oil per se, and the total dietary composition (especially

carbohydrates and total fat) was different between groups, which can influence the
56

results (66). New RCTs with higher methodological rigor are needed to confirm the

potential of coconut oil in reducing Lp(a).

It is important to highlight that published meta-analyses about the topic included

crossover studies with methodological limitations. In this meta-analysis, we only

included crossover RCTs when it was possible to determine the order of the

interventions and where the baselines and final averages of each arm were available.

We then obtained the initial and final values of each outcome in each arm of the study

before the participant was allocated to the other arm. This reduces the chance of the

residual effects (carry-over) of the former intervention on the next one (36). We

contacted the authors of crossover studies and received these data from the authors

of one study, which we included in our analysis (51). In addition to that, we included

two new RCTs (42, 49) that had not been included in the most recent meta-analysis

(52).

This systematic review has some limitations. Generally, studies presented a small

sample size with a short follow-up, which limits the analysis of the effects of a dietary

intervention on cardiometabolic parameters. Therefore, the results must be interpreted

with caution. Moreover, there was a limited number of studies analyzing the effect of

the consumption of coconut oil on parameters other than lipid profile and body weight,

such as body composition and glycemic and inflammatory profiles. The included

studies also differ considerably from each other regarding population size and gender

composition, time of follow-up, daily quantity of coconut oil consumed, type of coconut

oil (virgin, extra virgin), product/vehicle for consumption (e.g.: as a capsule, as a

supplement, heated as oil to cook with, or in preparations such as for muffins or

crackers). Although this makes it difficult to compare different interventions, we were

able to perform subgroup analyses comparing coconut oil with oils/fats with different
57

fatty acid content in their compositions: SFA-, MUFA-, and PUFA-rich oils/fats. We also

performed subgroup analyses according to the presence of other dietary interventions

and/or physical activity, which may influence the effects attributed to coconut oil on the

cardiometabolic parameters which were analyzed.

Up until now, the scientific community has lacked studies with a long-term follow-up

and with a significant number of participants that evaluate the effect of coconut oil

consumption on cardiovascular outcomes.

Conducting new RCTs examining cardiovascular safety comparing coconut oil with

PUFA- and MUFA-rich oils evaluating traditional markers does not seem to be

justifiable even though coconut oil is part of the diet in South Asian countries (20-22).

Moreover, in Western countries, stimulating the consumption of SFA-rich oils to the

detriment of PUFA- and MUFA-rich oils may lead to an excessive intake of SFAs in

populations that already have a diet rich in them (69).

Conclusions

The dietary consumption of coconut oil instead of the consumption of PUFA- and

MUFA-rich oils with well-established cardio-protective effects should not be

encouraged in societies that are not used to consuming it. Moreover, educational

strategies should be implemented to make populations, especially those used to

consuming coconut oil, aware of the potential risks related with this intake. These

populations should also be informed and encouraged to replace it with cardio-

metabolically healthy options linked with a reduction in rates of CVD.


58

List of abbreviations

CVD (cardiovascular disease), GRADE (Grading of Recommendations, Assessment,

Development and Evaluations), HDL-C (high-density lipoprotein cholesterol), HOMA

(the homeostasis model assessment), HbA1c (glycated hemoglobin), IL (interleukins),

IFN- (interferon-gamma), LDL-C (low-density lipoprotein cholesterol), Lp(a)

(lipoprotein [a]), MUFA (monounsaturated fatty acid), PRISMA (Preferred Report Items

for Systematic Reviews and Meta-Analysis), PUFA (polyunsaturated fatty acid), RCTs

(randomized clinical trials), RoB (the risk of bias), Robvis (risk-of-bias VISualization),

SFA (saturated fatty acid), TC (total cholesterol), total homocysteine (tcHcy), TG

(triglycerides), ultra-sensitive c-reactive protein (US-CRP).

Declarations

Ethics approval and consent to participate

Not applicable.

Consent for publication

Not applicable.

Availability of data and materials

The datasets used and/or analysed during the current study are available from the

corresponding author on reasonable request.

Competing interests

The authors declare that they have no competing interests

Funding

This study was supported by the Hospital de Clínicas de Porto Alegre Research

Incentive Fund (FIPE-HCPA project 2018-0393), the Division of Research of

Universidade Federal do Rio Grande do Sul (PROPESQ-UFRGS), the Coordenação

de Aperfeiçoamento de Pessoal de Nível Superior (CAPES), Research National


59

Council (CNPq) grant: CNPq/MCTI/FNDCT18/2021 (420065/2021-0) and Hospital de

Clínicas de Porto Alegre (HCPA). FIPE-HCPA, PROPESQ-UFRGS, CAPES, CNPq

and HCPA had no role in the design and conduct of the study; the collection,

management, analysis, and interpretation of the data; the preparation, review, or

approval of the manuscript; or the decision to submit the manuscript for publication.

Authors' contributions

Concept and design: ACD and FG. Acquisition, analysis, or interpretation of data: ACD,

ENM, BFS, CRA, CA, VC and FG. Drafting of the manuscript: ACD. Critical revision of

the manuscript for important intellectual content: all authors. Statistical analysis: ACD.

Supervision: VC and FG. All authors read and approved the final manuscript.

Acknowledgments

Thanks to authors Oliveira-de-Lira et al., Schwab et al., and Khaw et al. for providing

data from their articles for the preparation of this study.

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69

Table 1. Characteristics of the included studies

Intervention Baseline lipid profile, mean (SD)


RCT Female, Follow
Source Population (daily amount Control N In NC
design N (%) TC HDL-C LDL-C TG up (wk)
of coconut oil)
Assunção Parallel Women with 191 48.5 110.6 160
30 ml PUFA (soybean) 20 20 40 (100) 12
(2009) group abdominal obesity (32.7) (8.7) (28.7) (81.9)
Women with IMC
Cândido Parallel between 26 and MUFA (olive oil) 168.6 47.2 98.7 96.5
25 ml 24 61 85 (100) 9
(2021) group 35kg/m², % body PUFA (soybean) (9.7) (2.7) (9.7) (8.9)
fat >30%
Placebo
Chinwong Healthy 190.8 60.6 116.5 68.5
Crossover 15 ml (carboxymethycellul 34 34 16 (47) 8
(2017) individuals (32.3) (9.0) (30.1) (23.1)
ose solution)
Healthy SFA (butter) 245.5 58 160.5 161.2
Cox (1995) Crossover 39 g 28 28 15 (53.6) 6
individuals PUFA (safflower) (27.5) (15.5) (29.4) (79.7)
PUFA (soybean and
Healthy 20% of daily 187.9 56.5 107.5 132.9
Ganji (1996) Crossover soybean + psyllium 10 10 5 (50) 4
individuals calories (30.2) (12) (31.3) (40.7)
fiber)
Postmenopausal 223.1 64.1 128.7 105.2
Harris (2017) Crossover 30 ml PUFA (safflower) 14 14 14 (100) 4
women (35.1) (17.4) (26.1) (66.2)
SFA (palm)
Heber 17.5% of daily 176 95
Crossover Healthy men Hydrogenated 13 13 0 (0) 37 (9) 120 (7) 3
(1992) calories (4) (10)
soybean
229.3
Parallel Healthy SFA (butter) 73.47 138.05
Khaw (2018) 50 g 30 66 63 (67) 1 NR 4
group individuals MUFA (olive) (19.33) (36.34)
(37.5)
70

162.4 93
20% of daily PUFA (soybean) 52.97 90.1
Lu (1997) Crossover Healthy women 15 15 15 (100) (17.0 (38.9 3
calories A16 oil (10.82) (15.08)
1) 7)
Sufficient to
Individuals with increase in 10%
McKenney 222.3 49.8 149 117.1
Crossover hypercholesterole the amount of PUFA (canola) 11 (all) 5 (45.5) 6
(1995) (25.3) (18.3) (20.3) (49.2)
mia daily calories
from SFA
188 46 123 92.5
Healthy 54.4 g (muffins
Maki (2018) Crossover PUFA (corn) 13 12 13 (52) (178, (38.5, (105, (76.5, 4
individuals or rolls)
215)* 55.5)* 142)* 136)*
Oliveira-de- Parallel PUFA (safflower, 215.8 48.3 149.6 132.7
Obese women 6 g (capsules) 18 57 75 (100) 8
Lira (2018) group chia, and soybean) (24.2) (8.1) (23.7) (41.7)
Reiser 21% of daily SFA (lard)
Crossover Healthy women 19 (all) 0 (0) NA NA NA NA 5
(1985) calories PUFA (safflower)
Schwab 16-26g of 187.9 59.9 110.6 82.4
Crossover Healthy women SFA (palm) 7 8 15 (100) 4
(1994) coconut oil/day (25.5) (10.4) (17.8) (34.5)
Vijayakumar Parallel Individuals with 15% of daily 148.3 40.8 88.2 113.1
PUFA (sunflower) 99 99 13 (6.5) 2 years
(2015) group CVD calories (28.3) (9.5) (22.2) (51.5)
Parallel 184.8 39.5 117 140.9
Vogel (2020) Overweight men 12 ml PUFA (soybean) 15 14 0 (0) 4
group (44.1) (10.1) (36.1) (67.1)
Normal and
20% of daily SFA (palm) 182.1 47.6 118.3 85
Voon (2011) Crossover overweight 15 30 36 (80) 5
calories MUFA (olive) (25.5) (10.8) (22.4) (39)
healthy adults
* Median (IQR). Baseline lipid values are expressed in mg/dL. Abbreviations: RCT, randomized clinical trial; N In, number of participants in the intervention arm; N C, number of

participants in the control arm; TC, total cholesterol; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; TG, triglycerides; wk, week; PUFA,

polyunsaturated fatty acid; SFA, saturated fatty acid; MUFA, monounsaturated fatty acid; A16, transgenic soybean oil; NA, data not avaliable; CVD, cardiovascular disease.
71

Table 2. Summary of findings of the systematic review and meta-analysis


Certainty of evidence
Outcome group Overall result, MD (95% CI) Risk of Bias (RoB 2)
(GRADE)

Body weight NS Very low

Anthropometric profile Waist circumference NS High Very low

Total body fat NS Very low

LDL-C NS Very low

HDL-C +3.28 (0.66; 5.9) Very low


Lipid profile High
Triglycerides NS Very low

TC/HDL-C NS Very low

Glycemic profile Fasting blood glucose NS High Very low

Inflammatory profile US-CRP NS High Very low

Abbreviations: MD, mean difference; CI, confidence interval; GRADE, Grading of Recommendations Assessment, Development and Evaluations; NS, non-statistically significant;

LDL-C, low-density lipoprotein cholesterol; HDL-C, high-density lipoprotein cholesterol; TC, total cholesterol; US-CRP, ultra-sensitive c-reactive protein.
72

Figure 1. Flow chart mapping out the studies examined and included into the meta-analysis
Identification

Records removed before screening:


Records identified from: Duplicate records removed (n = 509)
Databases (n = 1,207) Records marked as ineligible by automation
Registers (n = 0) tools (n = 0)
Records removed for other reasons (n = 0)

Records screened Records excluded


(n = 698) (n = 673)

Reports sought for retrieval Reports not retrieved


(n = 25)
Screening

(n = 0)

Reports assessed for eligibility Reports excluded:


(n = 25) Not RCT (n = 1)
Insufficient follow-up (less than 7 days) (n = 3)
Inadequate intervention (n = 4)

Studies included in review


Included

(n = 17)
Reports of included studies
(n = 17)
73

Figure 2. Forest plots of randomized controlled clinical trials investigating the effects

of coconut oil intake on (a) body weight (kg); (b) waist circumference (cm). Individual

trial-specific estimates and their 95% CIs are indicated by the black dots and the horizontal

line, respectively. The center of the diamonds indicates the pooled estimates and the width of

the diamonds indicate the corresponding 95% CI


74

Figure 3. Forest plots of randomized controlled clinical trials investigating the effects

of coconut oil intake on (c) LDL-C (mg/dL); (d) HDL-C (mg/dL); (e) TG. Individual trial-

specific estimates and their 95% CIs are indicated by the black dots and the horizontal line,

respectively. The center of the diamonds indicates the pooled estimates and the width of the

diamonds indicate the corresponding 95% CI.


75

Material suplementar do Capítulo II – “The Effects of Coconut Oil on the


Cardiometabolic Profile: a Systematic Review and Meta-Analysis of Randomized
Clinical Trials” encontra-se no Anexo I, entre as páginas 108-176.
76

CAPÍTULO III - Misinformation in nutrition through the case of coconut oil: an

online before-and-after study

Original Article

Authors: Ana C Duartea*; Bernardo Frison Spiazzia,b*; Eduarda Nunes Merellob;

Carmen Raya Amazarraya, Laura Sulzbach de Andradeb; Mariana P Socalc, Antonio J

Trujilloc, Elisa Brietzked,e, Verônica Colpania; Fernando Gerchmana,f.

Affiliations:
a Post-graduate Program in Medical Sciences: Endocrinology, Universidade Federal

do Rio Grande do Sul, Porto Alegre, Brazil.


b Universidade Federal do Rio Grande do Sul, Faculdade de Medicina, Departamento

de Medicina Interna, Porto Alegre, Brazil.


c Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, United

States of America
d Department of Psychiatry, Adult Division, Kingston General Hospital, Kingston,

ON, Canada
e Kingston General Hospital, Kingston Health Science Centre, Kingston, ON, Canada
f Division of Endocrinology and Metabolism, Hospital de Clínicas de Porto Alegre, Porto

Alegre, Brazil.

* Equally contributed to this manuscript.

Corresponding author: Fernando Gerchman

Rua Ramiro Barcelos 2350, 4th floor, room 401, Division of Endocrinology and

Metabolism, 90035-003, Porto Alegre, Rio Grande do Sul, Brazil

Phone: +55 51 3359.8127

E-mail address: fgerchman@hcpa.edu.br


77

Abstract:

Background and aims: Despite recent scientific evidence indicating absence of

cardiometabolic benefit resulting from coconut oil intake, its consumption has

increased in recent years, which can be attributed to a promotion of its use on social

networks. We evaluated the patterns, reasons and beliefs related to coconut oil

consumption and its perceived benefits in an online survey of a population in southern

Brazil.

Methods and results: We conducted a before-and-after study using an 11-item online

questionnaire that evaluated coconut oil consumption. In the same survey, participants

who consumed coconut oil received an intervention to increase literacy about the

health effects of coconut oil intake. We obtained 3160 valid responses. Among

participants who consumed coconut oil (59.1%), 82.5% considered it healthy and

65.4% used it at least once a month. 81.2% coconut oil consumers did not observe

any health improvements. After being exposed to the conclusions of a meta-analysis

showing that coconut oil does not show superior health benefits when compared to

other oils and fats, 73.5% of those who considered coconut oil healthy did not change

their opinion. Among individuals who did not consume coconut oil, 47.6% considered

it expensive and 11.6% deemed it unhealthy. Conclusions: Coconut oil consumption

is motivated by the responders’ own beliefs in its supposed health benefits, despite

what scientific research demonstrates. This highlights the difficulty in deconstructing

inappropriate concepts of healthy diets that are disseminated in society.

Keywords: coconut oil; social media; survey; online; health information; internet.
78

Introduction

1.1. Health misinformation

The real impact of information overload on the population's food preferences, lifestyle

and health choices is still unknown [1]. Health misinformation, defined as false

information created with no intent to cause harm [2], is a worldwide problem; its

prevalence has grown with the production of health content in mass media and social

networks, increasing nonevidence-based recommendations [3, 4].

Over the past 10 years, coconut oil has been promoted as a good choice for meals,

being marketed as a healthy oil for cardiovascular health and for weight gain

prevention. The Philippines, Indonesia and India are the main coconut oil producers in

the world, Brazil being the 5th largest producer [5].

1.2. Dietary effects of coconut oil and misinformation

Coconut oil is composed of saturated fatty acids in 92% of its lipid composition [6]. Its

consumption has increased substantially in the last decade as a result of the

publication of small and short-term studies suggesting that its intake promotes weight

loss and improves the lipid profile and glycemic control [7-9].

Before the transition to a more westernized diet, countries, such as Sri Lanka,

Minangkabau, Philippines and the Pukapuka and Tokelau Islands in Polynesia,

presented low rates of cardiovascular diseases despite their significant consumption

of coconut oil [10-13]. Based on these findings, supposed cardiovascular benefits were

attributed to coconut oil. However, it is noteworthy that these populations had a dietary

pattern in which their major source of saturated fatty acids was coconut fat rather than

animal fats, their major protein source was from fish and their main source of

carbohydrates was from native fruits of the region, defining a dietary pattern also rich
79

in fibers and poor in animal fats, processed foods and sucrose [13]. Therefore, these

findings are hardly applicable to populations with usual westernized dietary patterns.

When coconut oil is evaluated in light of the best available evidence, its consumption

cannot be recommended. The main guidelines in Brazil [14, 15] and in the United

States [16, 17], as well as recent results of different meta-analyses [18, 19] do not

suggest coconut oil as a preferred fat for human consumption. Intake of coconut oil

increases low-density lipoprotein (LDL) cholesterol, a very well-defined risk factor for

cardiovascular disease, and results in no improvement in glycemic control and body

weight compared to other oils [18, 19].

Social media is essential for the flow of information, knowledge building and the

dissemination of opinions. However, with its insertion into daily life, society became

used to accessing health information on a large scale, but not always from reliable

sources. Studies showed that information published on health-related websites may

present inaccuracies and low quality of evidence of information [20-24], as it is possible

to publish about health information with or without technical knowledge in the area [25].

Thus, an impressive amount of information is disclosed, but little knowledge is being

built [26].

A major challenge for the implementation of evidence-based nutrition is the

discrepancy between the public opinion about health recommendations found online

and evidence-based guidelines. In addition, there is a need for the development and

testing of simple and affordable interventions to increase literacy on nutrition, which

could be used to guide the way we disseminate science and evidence-based nutritional

recommendations [27]. People find it difficult to interpret whether health information is

from a reliable source and based on solid scientific evidence, causing exposure to

actions that may not only be hazardous, but also leading to reductions in adherence to
80

screening programs and proposed treatments [28]. People with less education and/or

less health literacy are the groups at greatest risk in this context [29]. A systematic

literature review found that individuals with lower educational levels have less ability

and confidence to assess the quality of online health information than their peers with

a higher educational level [25].

1.3. Aims & hypothesis

Therefore, we conducted this before-and-after study to evaluate the patterns of and

reasons for coconut oil consumption, as well as beliefs related to its benefits in an

online survey of a population in Southern Brazil, given the scarcity of data on dietary

consumption of coconut oil in Brazil and worldwide. Additionally, we assessed the

possibility of increasing literacy on the health effects of coconut oil intake through an

intervention in the same population.

Methods

This study follows the Checklist for Reporting Results of Internet E-Surveys

(CHERRIES) statement (supplementary methods) [30].

Study design and population

We conducted a before-and-after study in Brazil between May and June 2020, with

individuals aged 18 years or older, through an 11-item online questionnaire applied in

Portuguese that contained questions regarding coconut oil consumption using Google

Forms. A questionnaire summary is presented in Table 1 and detailed questionnaire

development description is presented in the supplementary methods along with a

translated version in English of the original questionnaire (not checked for accuracy or

consistency). We analyzed two different samples: (1) university students from graduate
81

programs (MBA, Master’s and PhD) at Universidade Federal do Rio Grande do Sul, in

Porto Alegre, Brazil (University sample); and (2) individuals who accessed the

Facebook page of Hospital de Clínicas de Porto Alegre, the university’s main teaching

hospital (Facebook sample).

Intervention

In the questionnaire (supplementary methods), participants who consumed coconut oil

were exposed to the statement “A current study has reviewed scientific articles and

concluded that nutritional consumption of coconut oil does not improve bad cholesterol,

reduce weight or blood sugar (glucose) levels” summarizing the results of a recent

meta-analysis demonstrating that coconut oil does not reduce LDL cholesterol, and

does not reduce weight or blood glucose levels [18]. Subsequently, responders were

asked if they still considered coconut oil intake to be healthy. To proceed to the next

question, participants must necessarily answer the intervention item.

Questionnaire distribution and sampling

The final questionnaire was distributed to all graduate students registered at the

University through an email list. It was also shared on the official Facebook page of

Hospital de Clínicas de Porto Alegre, the University’s main teaching hospital. Those

interested in participating had access to the study webpage by clicking on the study

invitation link. As a result, convenience sampling was used for both University sample

and Facebook sample. Conflicting demographics and schooling information provided

by the volunteers was checked with the responders by email.


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Table 1. Questionnaire summary

Question
Have you ever used coconut oil?
Why do you use coconut oil? a,b

What amount of coconut oil do you intake? a

Which benefits did you observe by using coconut oil? a,b

A current study has reviewed scientific articles and concluded that nutritional
consumption of coconut oil does not improve bad cholesterol, reduce weight or blood
sugar (glucose) levels. Do you still consider coconut oil good for your health? a

Why don’t you use coconut oil? b,c

Sex
Where do you live?
How old are you?
What is your educational level?
Do you want to receive the results of this survey?
a.
Only answered by participants who answered “yes” or “I don’t want to answer” to the question “Have

you ever used coconut oil?”. b.


Question allowed multiple items to be marked. c.
Only answered by

participants who answered “no” to the question “Have you ever used coconut oil?”.

Ethics Statement

The study was approved by the Research Ethics Committee of Hospital de Clínicas de

Porto Alegre and Universidade Federal do Rio Grande do Sul. (GPPG-HCPA protocol

20180393 nos and CAAE nos 92144718.6.0000.5327) Participants were informed, at

the study home page, that by submitting the questionnaire, they would be accepting to

voluntarily participate in the survey. Additionally, the home page informed the time to

complete the survey, the study objective, and the name and contact information of the

principal investigator, following recommendations of the Ethics Committee. We asked

each participant to provide a valid email address, to which only the main investigators

of the study had access, and offered to send the results of the survey to participants

who requested them.


83

Prevention of Multiple Entries

Entries from invalid or duplicate emails were excluded from the analysis, as well as

those who reported uses of coconut oil other than as food or supplement. In case of

duplicate entries, the first response was included in the analysis.

Statistical Analysis

Data was described as absolute numbers and percentages. Categorical data was

compared by the chi-square test. To test for the effect of possible determinants on the

patterns of consumption of coconut oil on the study samples, multiple logistic

regression was performed, adjusting for gender, age and education level in different

multivariate models. A 2-tailed P <0.05 was considered statistically significant. SPSS

software version 19.0 (IBM, Armonk, NY, USA) was used for statistical analysis.

RESULTS

Out of 11753 registered graduate students, 3588 answered the questionnaire (30.5%).

We excluded 684 entries due to invalid answers, totaling 2904 entries. Among the 279

participants coming from the hospital’s Facebook page who answered the

questionnaire, 23 entries were excluded due to invalid answers, totaling 256 entries.

Participant flow diagram with reasons for exclusion ins presented in Figure 1. While

58.2% of the students consume coconut oil, 69.9% of the responders from the

Facebook group consume it. Most of the consumers were females in both groups and

distribution of responders did not change according to age (Table 2).

Table 2. Demographic characteristics of the University and Facebook samples


84

University sample Facebook sample


(n=2904) (n=256)

Consumes Does not Consumes Does not


coconut oil consume coconut oil consume
coconut oil coconut oil
Participants, n 1689 1215 179 77

Age, n

18–19 years -------- -------- 2 3

20–29 years 764 240 38 10

30–39 years 656 218 61 19

40–49 years 179 80 40 13

50–59 years 64 26 24 51

>60 years 26 6 14 4

Female participants, n %a 1239 (73.6) 527 (51.9) 166 (92.7) 67 (94.4)

Education, n

Less than high school -------- -------- 7 2

High school -------- -------- 31 8

Incomplete -------- -------- 44 16


undergraduate degree

Undergraduate degree 415 332 46 14

Graduate degree 1274 883 51 12

Brazil, %a (1659) 98.2 1206 (99.3) 175 (97.8) 77 (100)

Percentage of each column. The percentage of responders who did not answer varied

according to each question for the University and Facebook groups: age (22.2%) and

(9.0%), respectively, gender (7.1% and 2.3%), and education (0% and 9.8%).
85

Most participants who consumed coconut oil in the University (82.8%) and Facebook

(81%) samples considered it healthy and more than half of them used it at least once

a month (Figure 2). However, most of them did not perceive any health or aesthetic

benefits (Figure 2). After being exposed to the conclusions of a recent meta-analysis

showing that coconut oil was not superior to other oils and fats regarding

cardiometabolic health, the participants who had deemed it healthy were questioned if

they still had the same opinion. In the University group, 72.7% did not change their

opinion, while in the Facebook group 82.3% followed the same direction. Among

individuals not consuming coconut oil, 47.3% of the University and 50.6% of the

Facebook participants considered it expensive. Only 10.4% and 29.9% of them,

respectively, believed that the oil was not healthy. In the University group, 14.5% of

the participants reported difficulties finding coconut oil where they lived, while 5.2% of

those in the Facebook group reported the same problem. In the University and

Facebook groups, 10.5% and 20.8% did not like the taste of the product, respectively,

and 33% and 11.7% did not use coconut oil for other reasons.

By multiple logistic regression analysis, we analyzed which factors were related to the

consumption of coconut oil in different models adjusted for sex, age and educational

level (Table 3). Women were more likely to consume coconut oil than men in the

University sample (OR 2.7; 95% CI = 2.2 to 3.3; P = <0.001). Additionally, while those

with a higher educational level had a more significant intake of this oil (OR 1.4; 95%

CI = 1.1 to 1.7; P = 0.004), those aged ≥ 40 years had a lower daily consumption of

coconut oil in comparison to other age groups. No differences were observed in the

Facebook sample for the factors analyzed.


86

Table 3. Multiple logistic regression analysis for possible determinants of coconut oil

consumption (yes/no) and its frequency

University Facebook
Sample Sample
(n=2904) (n=256)

OR 95% CI P OR 95% CI P

Consumes coconut oil


(yes/no)

Female 2.7 2.2 – 3.3 <0.001 0.5 0.1 -2.3 0.40

18-19 years -------- -------- -------- a A a

Age 20-29 years a A a 0.3 0.0 – 3.6 0.38

Age 30-39 years 0.9 0.7 – 1.1 0.21 1.3 0.3 – 5.1 0.70

Age 40-49 years 0.7 0.5 – 0.9 0.03 0.9 0.3 – 3.2 0.89

Age 50-59 years 0.7 0.4 –1.2 0.24 0.9 0.2 – 3.5 0.94

Age ≥ 60 years 1.3 0.5 – 3.4 0.52 1.4 0.3 – 6.2 0.65

Education: less than high -------- -------- -------- a a a


school

Education: high school -------- -------- -------- 1.2 0.2 – 7.1 0.84

Education: incomplete -------- -------- -------- 0.9 0.2 – 5.1 0.93


undergraduate degree
87

Education: Undergraduate a A a 1.3 0.2 – 7.3 0.77


degree

Education: graduate degree 1.4 1.1 – 1.7 0.004 0.8 0.1 – 4.6 0.80

Frequency of
coconut oil intake

Female 1.3 0.9 – 1.7 0.14 2.9 0.8 – 10.2 0.09

Age 18-19 years -------- -------- -------- a a a

Age 20-29 years a A a 0.8 0.0 – 19.2 0.92

Age 30-39 years 0.9 0.6 – 1.3 0.67 4.5 0.9 – 22.7 0.07

Age 40-49 years 0.4 0.2 – 0.6 <0.001 1.5 0.4 – 5.9 0.53

Age 50-59 years 0.4 0.2 – 0.7 0.002 1.0 0.2 – 3.8 0.99

> 60 years 0.3 0.1 – 0.8 0.01 0.9 0.2 – 3.9 0.91

Education: less than high -------- -------- -------- a a a


school

Education: high school -------- -------- -------- 0.6 0.1 – 3.8 0.58

Education: incomplete -------- -------- -------- 0.9 0.1 – 6.2 0.96


undergraduate degree

Education: undergraduate a A a 1.3 0.2 – 8.2 0.78


degree
88

Education: graduate degree 1.1 0.8 – 1.6 0.57 0.4 0.1 – 2.9 0.39

OR: odds ratio; CI: confidence interval. a. Reference age or


educational level for comparison in different multiple regression
models.

Discussion

Principal Results

When applying an online survey to two different samples, one comprising adults at

predominantly graduate programs of all majors in a university in Southern Brazil, and

the other containing participants who accessed the Facebook page of the University’s

teaching hospital, we found that most of the responders routinely consumed coconut

oil at least once a month (Figure 2). This is the first study analyzing the dietary

consumption of coconut oil in a specific population in Brazil. We did not find the pattern

of this consumption in other parts of the world. The data we find in the literature

currently refer to the general domestic consumption of coconut oil, and its use is not

specified (meal preparation, amount, frequency, aesthetic use, etc). The

countries/regions with the highest consumption of coconut oil are: Philippines,

European Union, United States of America and India (675, 645, 497 and 470 thousand

tons) [5]. Most of these responders considered that coconut oil intake was capable of

improving their health status, even though the majority did not perceive real health

benefits with its consumption. When exposed to recent evidence provided by a meta-

analysis showing no cardiometabolic benefits of coconut oil intake [18], most

responders did not change their beliefs and confirmed that they would keep consuming

the product. As a hypothesis-driven development, we believe that populations more

exposed to social media are prone to the consumption of coconut oil. In order to test
89

this hypothesis, we analyzed if there was any factor related to the consumption of this

oil by multiple logistic regression analysis. We found that adults 40-49 years and males

were less likely to consume coconut oil and that, among consumers, adults 40 years

or older were less likely to have a daily consumption. These findings do not necessarily

confirm our hypothesis, hence more studies are necessary to conclude if populations

more exposed to social media are more susceptible to change their nutritional

behavior. Among individuals who did not consume coconut oil in the University and

Facebook samples, only 10.5% and 29.9% did not consider coconut oil healthy,

respectively, while 47.3% and 50.6% considered the product too expensive for

consumption. It seems reasonable to assume that this population would be potential

coconut oil consumers if they were able to afford it. In May 2020, the average price of

coconut oil was estimated to be US$ 832/ton, while the price of soybean oil was

estimated at US$595/ton [5]. These prices probably determine the final prices to the

consumer and may explain these findings.

Limitations

This study has some limitations. Firstly, the study sample is composed of individuals

with computer literacy from a convenience sample, resulting in a sociodemographic

profile that does not totally represent the Brazilian population. As in Brazil coconut oil

is usually more expensive than other oils, this population probably the one more

affected by misinformation related to coconut oil intake and, consequently, an

important target population to be studied. Using samples from different

sociodemographic and educational backgrounds, possibly representing different

profiles within the Brazilian society, we believe we have minimized this issue .The

replication of these findings in different populations would allow us to understand if our


90

results are consistent with others. Nevertheless, we were able to identify that a

significant fraction of responders, regardless of their sociodemographic and

educational profile, believed that coconut oil was beneficial for their health, suggesting

that their beliefs about food were so ingrained that exposure to scientific information

did not result in a change of concept [18].

Secondly, it is expected that people who identify with a subject are more likely to

respond to a survey, the so-called "volunteer effect" [27]. Although we were not able

to control for that in our online survey, more than one-third of the University’s graduate

students completed the survey. Similar findings from a second sample with a different

sociodemographic background reinforced that our findings may be representative of at

least part of this population. Looking from another perspective, even if we assume a

hypothetical scenario of maximum “volunteer effect” in the University sample (in which

all of the nonparticipant graduate students did not consume coconut oil), the number

of consumers would still be an alarming 14.6% of this population, considering that the

main reason for coconut oil intake is its supposed health benefit. In addition, the before-

and-after design of this study presents limitations such as the absence of

randomization between groups and the lack of a guarantee that participants changed

their opinions as a result of the performed intervention. As such, we recommend that

our results should be interpreted with caution, serving as hypothesis generators for

designing new studies dedicated to understanding how misinformation is changing the

way we eat. The rapid exposure to scientific information through an online

questionnaire suggests that this kind of intervention has a limited effect as a strategy

to change concepts regarding misinformation in nutrition. Although we did not present

sufficient data within the intervention question to quantify the magnitude of the

consequences of coconut oil intake, which could possibly strengthen the intervention,
91

providing more complex information would likely reduce adherence to the intervention

and, therefore, reduce the total number of participants who would benefit from it.

Coconut Oil and Misinformation

Two short-term studies showed slight improvements in lipid and anthropometric

profiles with coconut oil intake in healthy adult populations [7, 31]. Based on these

studies and a possible interest of third parties to promote coconut oil consumption, the

dissemination of this concept was routinely propagated in websites, blogs, and health

professionals’ social media pages. This resulted in the addition of coconut oil

consumption as a recommendation in clinical practice, indicating it as the fat of choice

to be used for cooking and adding to salads and other food preparations, although

neither its superiority nor its noninferiority compared to other oils were proven

regarding its safety and the reduction of cardiovascular endpoints, prevention of weight

gain, and the development of diabetes [32, 33]. Although social media may have

played an important role in building misconceptions about coconut oil in the public

opinion, an individual’s beliefs about health and food are not only formed by ideas

propagated on social media. Flavor, price, and convenience of access to food also

influence their choices, as well as the general opinion about a certain food in the group

in which the individual is inserted [1].

A significant part of our study population did not change its opinion even when exposed

to information that coconut oil neither lowers LDL cholesterol levels, nor it lowers

weight or blood glucose levels, continuing to consider coconut oil as a healthy and

preferential oil. In 2016, a commissioned survey performed by the New York Times

found that 72% of the population considered coconut oil to be good for health and 37%

of nutritionists also considered it a better oil for health [34]. A study of adults aged over
92

59 years, who were exposed to printed information provided by a health professional

on the effects of the interaction between alcohol and medication, showed that the

exposure to information made them review their concepts about the topic, exerting a

positive change in their level of knowledge on the subject [35]. These findings led us

to question the current scope of the results obtained through scientific research in the

general population, since the information and positions of respected health societies,

which should have great impact on the population’s health decisions, seem to have

less impact than biased or unsupported scientific information spread throughout social

networks.

In 2002, Eysenbach coined the term "infodemiology," helping to identify areas where

there is a gap in translation of the best scientific evidence (proposed by experts on the

subject) and what most people practice or believe in [36]. To combat “infodemia,” it is

necessary to translate science as clearly as possible for the population in its most

varied degrees of knowledge and education, using an accessible and didactic

language by the authorities in order to change beliefs that may lead to negative actions

for health [3, 4, 37]. Even when great effort is applied into doing this, the impact in

changing misleading concepts may not be effective, since individuals tend to interpret

the received information in order to confirm their beliefs and not to challenge them,

which is called confirmation bias [38].

The development of strategies to potentiate the dissemination of appropriate health

concepts to protect the population against misinformation is a new area of

investigation. Some anti-spread interventions for false references related to health

have already been tested. Algorithmic and social corrections are examples that expose

the social network to real information produced by an algorithm or a social network

user to protect the society against unreliable content [39]. The credibility of the source
93

of the information provided by the social network user can also be categorized [40]. An

effective solution will certainly be a broad combination of diverse approaches

developed by health, social, and computer science specialists working together in

interdisciplinary research to find ways to deal with health misinformation on social

media [40-42].

The commitment of health professionals to the social dissemination of information

supported by the best scientific evidence available, with a critical analysis of study

results, should also be regulated [4]. It seems reasonable to think that we need tools

to generate appropriate health concepts through statements of official scientific

societies before the dissemination of a misleading concept on social media. This would

be more efficient in preventing a questionable health attitude than counteracting

misinformation already disseminated by social media [41].

Another aspect that needs to be assessed is the level of general and health literacy of

the populations, considering the individual’s abilities to obtain, communicate, and

understand health information in order to make the best decisions [43]. This is an

important concept, as studies indicate that around 9 out of 10 adults do not have the

necessary skills for the management and prevention of diseases [43]. Populations with

lower levels of health literacy have worse health outcomes [44, 45]. There are few

studies that assessed the degree of health literacy in Latin American populations.

Existing studies show that socioeconomic inequality, social/geographic isolation,

cultural, political and language barriers are factors that affect the level of health literacy

in these countries [46]. In Brazil, Maragno et al, evaluated 302 adult users of a

university health clinic in the state of Santa Catarina, using a health literacy test for

Brazilians, based on the functional health literacy test in adults TOFHLA, and observed

that 54.6% of the sample had adequate health literacy while 26.2% has an inadequate
94

one [47]. Another cross-sectional study, carried out in the city of Rio de Janeiro,

evaluated 150 outpatients with type 2 diabetes mellitus, using a short version TOFHLA

and found that 73.3% of the participants had adequate literacy in health and 15.3%,

inadequate health literacy [48]. A cross-sectional study with 248 adults in Piracicaba,

state of São Paulo, showed an association between a low level of oral health literacy

with a more frequent use of the dental service due to pain or just for emergency

treatment, presence of dental plaque and "poor" evaluation of the dental care service

[49]. It is necessary to ensure that the best scientific evidence is translated into the

simplest language, and that it is easily understood by the entire population and not just

by segments of society with a higher level of education and access to the best news

sources [44, 45]. Since the University sample was composed of participants with a

higher-than-usual level of education, our results are of great concern since they

suggest that the misconception about the effects of coconut oil on health prevails in

this population.

Conclusion

In this study, we used a questionnaire to analyze the pattern of consumption of coconut

oil, a nutrient with a negative impact on cardiometabolic health that is widely

disseminated on social networks as a healthy food. Despite the high expectancy that

this should be a healthy product expressed by most of the studied population in

southern Brazil, the participants did not notice health benefits with its consumption. We

were not able to change their concepts with an intervention aimed at increasing literacy

in this topic. These findings suggest how difficult it is to change unhealthy concepts

related to our diet after the population has acquired false or wrong concepts on the

topic.
95

For this reason, misconceptions related to diet and nutrition need to be extensively

studied as a public health problem and strategies, such as algorithmic corrections in

social media using reliable sources should be implemented. These are effective [39],

readily available and have already been implemented to combat misinformation related

to COVID-19. Furthermore, the development of interventions that are able to improve

literacy regarding lifestyle healthy habits in multiple levels of education [50-52] and a

fast call from action from healthcare professional societies [52] may be effective

measures to reduce the impact of misinformation as promoter of the consumption of

unhealthy foods linked to cardiometabolic diseases.

Acknowledgments

This study was supported by Hospital de Clínicas de Porto Alegre Research

Incentive Fund (FIPE-HCPA project 2018-0393), Division of Research of

Universidade Federal do Rio Grande do Sul (PROPESQ-UFRGS) and Coordenação

de Aperfeiçoamento de Pessoal de Nível Superior (CAPES). FIPE-HCPA,

PROPESQ-UFRGS and CAPES had no role in the design and conduct of the study;

collection, management, analysis, and interpretation of the data; preparation, review,

or approval of the manuscript; and decision to submit the manuscript for publication.

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103

Figure Legends

Figure 1. Participant flow diagram.

UNIVERSITY SAMPLE FACEBOOK SAMPLE

Entries in the questionnaire distributed Entries in the questionnaire collected


to graduate students by email via Facebook page
(n = 3588) (n = 279)

Entries excluded (n = 684): Entries excluded (n = 23):


Duplicate email (n = 362) Duplicate email (n = 1)
Invalid email (n = 194) Invalid email (n = 2)
Cosmetic use of coconut Cosmetic use of coconut
oil (n = 128) oil (n = 20)

Valid entries included in the analyses Valid entries included in the analyses
(n = 2904) (n = 256)

Figure 2. Patterns, reasons, and expectancy regarding the health benefits of

coconut oil for those who consumed it.

This question allowed the participant to mark multiple items. *p<0.001.


a

A. Reasons for coconut oil intakea

University Facebook

1396 145
It is healthy
82,8% 81,0%
855 79
I like the flavor
50,7% 44,1%
68 3
It gives me more energy
4,0% 1,7%
50 8
It is the most used cooking oil
3,0% 4,5%
57 6
It takes longer to spoil
3,4% 3,4%
3 1
It is cheaper than other oils
0,2% 0,6%
30 0
Others
1,8% 0,0%

100% 50% 0% 50% 100%


104

B. Frequency of coconut oil intake

University Facebook

1125 96
At least once a month *
69,4% 54,5%

279 34
Weekly
17,2% 19,3%

158 28
1 tablespoon/day *
9,7% 15,9%

46 12
2 tablespoons/day *
2,8% 6,8%

14 6
3 or more tablespoons/day *
0,9% 3,4%

100% 50% 0% 50% 100%

C. Benefits observed with coconut oil intakea


University Facebook

1294 113
No improvements in health or aesthetics *
82,6% 67,7%

135 22
Weight loss
8,6% 13,2%

145 35
Improvements in cholesterol levels *
9,3% 21,0%

73 11
Reduction in waist circumference
4,7% 6,6%

68 12
Improvements in blood sugar levels
4,3% 7,2%

100% 50% 0% 50% 100%

Material suplementar do Capítulo III – “Misinformation in nutrition through the

case of coconut oil: an online before-and-after study” encontra-se no Anexo II,

entre as páginas 176-186.


105

CAPÍTULO IV - Considerações Finais e Perspectivas Futuras

O óleo de coco é composto predominantemente por ácidos graxos saturados.

É bem documentado na literatura que esta classe de gorduras deve fazer parte da

alimentação habitual em menor quantidade do que os ácidos graxos mono e poli-

insaturados, tendo em vista a associação desfavorável de seu consumo com a saúde

cardiometabólica. Mesmo assim, o óleo de coco foi apontado em estudos científicos,

por profissionais da saúde em sua prática clínica, e em mídias sociais, televisivas e

impressas como sendo um óleo mais saudável.

Nós conduzimos uma meta-análise de ensaios clínicos randomizados apenas

com estudos paralelos, ou com estudos cruzados com dados cedidos pelos autores e

que nos permitissem excluir um possível efeito carry-over entre as intervenções.

Observamos que o consumo alimentar de óleo de coco, em comparação com outros

óleos e/ou gorduras, não exerce efeito em parâmetros antropométricos, de perfil

glicêmico, nem nos níveis de pressão arterial e inflamação subclínica. Em relação ao

perfil lipídico, observamos apenas um aumento estatisticamente significativo dos

níveis de HDL-C, sem alteração nos níveis de LDL-C, TG, na relação LDL/HDL e

CT:HDL.

Durante a elaboração deste trabalho, nos questionamos quais seriam as

motivações dos consumidores para utilização do óleo de coco. Para responder esta

questão, nós elaboramos uma pesquisa online antes/depois, aplicada em uma

população do sul do Brasil. A maior parte das pessoas que consomem óleo de coco o

utilizam por considerá-lo um óleo bom para a saúde, mesmo não observando

melhoras na sua saúde ou estética com o seu consumo. Ao serem expostos aos

resultados de uma meta-análise, mostrando que o óleo de coco não exerce influência
106

positiva sobre parâmetros metabólicos, a maioria dos participantes, continuaram

considerando o óleo de coco bom para a saúde.

Observamos que há uma lacuna entre a informação científica publicada e

aquela que chega e é praticada pela população. Profissionais da saúde que são

agentes importantes de disseminação da informação científica nem sempre

apresentam a formação necessária para analisar com cautela estudos científicos,

podendo repassar informações equivocadas para a população, baseando as suas

condutas em resultados de evidências científicas de qualidade metodológica limitada.

Por outro lado, sabe-se que a população, de maneira geral, apresenta baixo grau de

alfabetização em saúde, tendo dificuldade de desenvolver um olhar crítico para as

informações divulgadas pelos profissionais de saúde e mídias em geral. Além disso,

com o avanço da tecnologia, ocorreu um aumento do fluxo de informações e acesso

da população a todo tipo de notícia, contribuindo para tomadas de decisões de saúde

equivocadas, baseadas em achismos, crenças pessoais e populares e/ou evidência

científicas de baixa qualidade.

Com base no exposto, o óleo de coco não deveria ser incentivado como óleo

de primeira escolha para o consumo. Estratégias educativas deveriam ser

estabelecidas a fim de conscientizar sobre o potencial risco do consumo desse óleo

do ponto de vista cardiometabólico. Os equívocos relacionados à alimentação e

nutrição precisam ser amplamente estudados como um problema de saúde pública e

estratégias devem ser implementadas para reduzir o impacto da desinformação como

promotora do consumo de alimentos não saudáveis vinculados às doenças

cardiometabólicas, emagrecimento e saúde no geral.

Como perspectiva futura, esperamos que este trabalho possa estimular e servir

de base para aplicação em outras questões controversas de saúde e nutrição. Há uma


107

lacuna entre a informação científica publicada e aquela que chega e é praticada pela

população. O desenvolvimento de estudos info epidemiológicos que objetivem

entender todas as fases do processo de transmissão da informação científica em

saúde para a população permitirá a elaboração de protocolos de intervenção e

avaliação de seu impacto na melhora da saúde da população. Com estes resultados

será possível construir estratégias de saúde pública a fim de prevenir um malefício

causado pela desinformação.


108

Anexo I – Material suplementar do Capítulo II – ““Effects of coconut oil on the


cardiometabolic profile: systematic review and meta-analysis of randomized
clinical trials”.

Summary:
Appendix I - Search strategy and search terms
Full search strategy and search terms in Pubmed
Full search strategy and search terms in Embase
Full search strategy and search terms in LILACS
Supplementary Tables

Table S1. Detailed reasons for the exclusion of studies in the full text assessment of
eligibility stage

Table S2- Summary of interventional studies investigating coconut oil effects on


anthropometric profile
Table S3 - Summary of interventional studies investigating coconut oil effects on
glycemic profile
Table S4 - Summary of interventional studies investigating coconut oil effects on blood
pressure
Table S5 - Summary of interventional studies investigating coconut oil effects on
inflammatory profile
Table S6 - Summary of interventional studies investigating coconut oil effects on lipid
profile
Table S7 - Grading of Recommendations Assessment, Development and Evaluations
(GRADE)
Appendix II - Additional results
Lipid profile
LDL-C to HDL-c ratio and TC:HDL-C ratio
Appendix II – Figure 1. Forest plots of randomized controlled clinical trials investigation
the effects of coconut oil intake on the TC:HDL-C ratios
Appendix II – Figure 2. Forest plots of randomized controlled clinical trials investigation
the effects of coconut oil intake vs MUFA and PUFA rich oils on the TC:HDL-C ratios
Glycemic profile
Fasting blood glucose
A1C
Effects of coconut oil on insulin levels, β-cell function and indices of insulin
sensitivity
Appendix II– Figure 3. Forest plots of randomized controlled clinical trials investigation
the effects of coconut oil intake on fasting blood glucose (mg/dL)
109

Appendix II – Figure 4. Forest plots of randomized controlled clinical trials investigation


the effects of coconut oil intake vs MUFA and PUFA rich oils on fasting blood glucose
(mg/dL)
Blood pressure
Systolic Blood Pressure
Diastolic Blood Pressure
Inflammatory profile

Appendix II– Figure 5. Forest plots of randomized controlled clinical trials investigation
the effects of coconut oil intake on US-CRP (mg/dL)
Supplementary figures
Figure S1 - Effect on body weight of coconut oil versus PUFA and MUFA rich oils
Figure S2 - Effect on body weight of coconut oil versus olive oil
Figure S3 - Effect on body weight of coconut oil versus soybean oil
Figure S4 - Effect on body weight of coconut oil versus other oils when analyzing
studies carried out in women
Figure S5 - Effect on body weight of coconut oil versus other oils when analyzing
studies conducted in Brazil
Figure S6 - Effect on body weight of coconut oil versus other oils or fat in patients with
overweight/obesity
Figure S7 - Effect on body weight of coconut oil versus other oils or fat without a long
term study
Figure S8 - Effect on body weight of coconut oil versus other oils or fat with co-
intervention
Figure S9 - Effect on waist circumference of coconut oil versus PUFA and MUFA rich
oils
Figure S10 - Effect on waist circumference of coconut oil versus olive oil
Figure S11 - Effect on waist circumference of coconut oil versus soybean oil
Figure S12 - Effect on waist circumference of coconut oil versus other oils when
analyzing studies carried out in women
Figure S13 - Effect on waist circumference of coconut oil versus other oils when
analyzing studies conducted in Brazil
Figure S14 - Effect on waist circumference of coconut oil versus other oils or fat in
patients with overweight/obesity
Figure S15 - Effect on waist circumference of coconut oil versus other oils or fat with
co-intervention
Figure S16 - Effect on body composition of coconut oil versus other oils/fat
Figure S17 - Effect on body composition of coconut oil versus PUFA and MUFA rich
oils
Figure S18 - Effect on LDL-C levels of coconut oil versus PUFA and MUFA rich oils
Figure S19 - Effect on LDL-C levels of coconut oil versus olive oil
Figure S20 - Effect on LDL-C levels of coconut oil versus soybean oil
110

Figure S21 - Effect on LDL-C levels of coconut oil versus other oils when analyzing
studies conducted in women
Figure S22 - Effect on LDL-C levels of coconut oil versus other oils when analyzing
studies conducted in Brazil
Figure S23 - Effect on LDL-C levels of coconut oil versus other oils or fat in patients
with overweight/obesity
Figure S24 - Effect on LDL-C levels of coconut oil versus other oils or fat without a long
term study
Figure S25 - Effect on LDL-C levels of coconut oil versus other oils or fat with co-
intervention
Figure S26 - Effect on LDL-C levels of coconut oil in HDL-C levels versus PUFA and
MUFA rich oils
Figure S27 - Effect on LDL-C levels of coconut oil versus olive oil
Figure S28 - Effect on HDL-C levels of coconut oil versus soybean oil
Figure S29 - Effect on HDL-C levels of coconut oil versus other oils when analyzing
studies carried out in women
Figure S30 - Effect on HDL-C levels of coconut oil versus other oils when analyzing
studies conducted in Brazil
Figure S31 - Effect on HDL-C levels of coconut oil versus other oils or fat in patients
with overweight/obesity
Figure S32 - Effect on HDL-C levels of coconut oil versus other oils or fat without a
long term study
Figure S33 - Effect on HDL-C levels of coconut oil versus other oils or fat with co-
intervention
Figure S34 - Effect on TG levels of coconut oil versus PUFA and MUFA rich oils
Figure S35 - Effect on TG levels of coconut oil versus olive oil
Figure S36 - Effect on TG levels of coconut oil versus soybean oil
Figure S37 - Effect on TG levels of coconut oil versus other oils when analyzing studies
carried out in women
Figure S38 - Effect on TG levels of coconut oil versus other oils when analyzing studies
conducted in Brazil
Figure S39 - Effect on TG levels of coconut oil versus other oils or fat in patients with
overweight/obesity
Figure S40 - Effect on TG levels of coconut oil versus other oils or fat without a long
term study
Figure S41 - Effect on TG levels of coconut oil versus other oils or fat with co-
intervention
Figure S42 - Risk of bias
111

APPENDIX I - SEARCH STRATEGY AND SEARCH TERMS

Full search strategy and search terms in Pubmed:

(((("coconut oil" [Supplementary Concept]) OR "coconut oil") OR coconut)) AND


((randomized controlled trial[pt] OR controlled clinical trial[pt] OR randomized
controlled trials[mh] OR random allocation[mh] OR double-blind method[mh] OR
single-blind method[mh] OR clinical trial[pt] OR clinical trials[mh] OR (“clinical trial”[tw])
OR ((singl*[tw] OR doubl*[tw] OR trebl*[tw] OR tripl*[tw]) AND (mask*[tw] OR
blind*[tw])) OR (“latin square”[tw]) OR placebos[mh] OR placebo*[tw] OR random*[tw]
OR research design[mh:noexp] OR follow-up studies[mh] OR prospective studies[mh]
OR cross-over studies[mh] OR control*[tw] OR prospective*[tw] OR volunteer*[tw]
NOT (animal[mh] NOT human[mh]))

Full search strategy and search terms in Embase:

('adult'/exp OR 'adult' OR 'adults' OR 'grown-ups' OR 'grownup' OR 'grownups') AND


('coconut oil'/exp OR 'coconut butter' OR 'coconut fat' OR 'coconut oil' OR 'coconut oil
emulsion' OR 'copra oil' OR 'oil, coconut') AND ('randomized controlled trial'/exp OR
'controlled trial, randomized' OR 'pragmatic clinical trial' OR 'pragmatic clinical trials'
OR 'randomised controlled study' OR 'randomised controlled trial' OR 'randomized
controlled study' OR 'randomized controlled trial' OR 'trial, randomized controlled')

Full search strategy and search terms in LILACS:

(tw:(óleo de coco)) AND (tw:(ensaio clínico))


112

SUPPLEMENTARY TABLES

Table S1. Detailed reasons for the exclusion of studies in the full text assessment of eligibility stage

Record Reason for exclusion


Francisco A O Júnior, et al., Coconut Oil Supplementation Does Combination of interventions in groups
Not Affect Blood Pressure Variability and Oxidative Stress: A
Placebo-Controlled Clinical Study in Stage-1 Hypertensive
Patients. Nutrients, 2021; 28;13(3):798. doi:
10.3390/nu13030798.
Mendis, S., et al. The effect of daily consumption of coconut fat Non-randomized clinical trial
and soya-bean fat on plasma lipids and lipoproteins of young
normolipidemic men. Br J Nutr, 1990;63(3):547-52. doi:
10.1079/bjn19900141
Muller, H, et al. The serum LDL/HDL cholesterol ratio is Mixing more than one oil in the same food (eg margarine,
influenced more favorably by exchanging saturated with coconut oil, soy oil), which does not allow us to know the real
unsaturated fat than by reducing saturated fat in the diet of effects of coconut oil on the outcomes studied.
women. J Nutr, 2003;133(1):78-83. doi: 10.1093/jn/133.1.78.
113

Ng, T K. et al. Nonhypercholesterolaemic effects of a palm-oil Inadequate intervention


diet in Malaysian volunteers. Am J Clin Nutr, 1991; 53(4
Suppl):1015S-1020S. doi: 10.1093/ajcn/53.4.1015S.
Panth, N., et al. Medium-chain fatty acids lower postprandial Insufficient follow-up (<7 days)
lipemia: A randomized crossover trial. Clin Nutr, 2020; 39(1):90-
96. doi: 10.1016/j.clnu.2019.02.008.
Sciarrilo, C M., et al. Postprandial Lipemic Responses to Various Insufficient follow-up (<7 days)
Sources of Saturated and Monounsaturated Fat in Adults.
Nutrients, 2019; May; 11(5): 1089. doi: 10.3390/nu11051089.
Trepanowski J F., et al. A 21-day Daniel fast with or without krill Data from the placebo and intervention groups were pooled, not
oil supplementation improves anthropometric parameters and being able to analyze the real effects of coconut oil on the
the cardiometabolic profile in men and women. Nutr Metab outcomes of interest.
(Lond), 2012; 13;9(1):82. doi: 10.1186/1743-7075-9-82.
Valente FX., et al. Effects of coconut oil consumption on energy Insufficient follow-up (<7 days)
metabolism, cardiometabolic risk markers, and appetitive
responses in women with excess body fat. Eur J Nutr. 2018;
57(4):1627-1637. doi: 10.1007/s00394-017-1448-5.
114

Table S2. Summary of randomized clinical trials investigation the effect of coconut oil intake on anthropometric profile

Author and Study Follow- Sample Intervention Comparator Last measurements of


Year design up anthropometric profile
(Country)

Assunção Randomized 12 weeks n = 40 women with 30 ml of coconut oil should 30 ml of soybean oil Body weight (kg): soybean oil
(2009) clinical trial abdominal obesity be added to the three main should be added to the (75 ± 9.1) > coconut oil (72.1 ±
(Brazil) Age = 29.8 ± 6.6 years meals of the day, in the three main meals of the 9.1)*
BMI = 31.1 ± 3.4 kg/m² common preparation of day, in the common BMI (kg/m²): soybean oil (30.7
meals preparation of meals ± 3.3) > coconut oil (30.5 ±
3.6)*
Waist circumference (cm):
coconut oil = soybean oil (97 ±
7)

Cândido Randomized 9 weeks n = 52 women with BMI Vitamin breakfast Vitamin breakfast Body weight (kg): soybean oil
(2021) clinical trial between 26 e 35 kg/m², prepared with 25 ml of prepared with 25 ml of (77.24 ± 2.08) > coconut oil
(Brazil) %G > 30% coconut oil, skimmed milk soybean oil, skimmed (75.99 ± 2.92) > olive oil
Age = 26.81 ± 0.74 powder and some fruit milk powder and some (75.81 ± 1.65)
flavoring, chocolate or fruit flavoring, chocolate Waist circumference (cm):
cappuccino or cappuccino coconut oil (94.17 ± 2.24) >
115

Vitamin breakfast olive oil (93.58 ± 1.91) >


prepared with 25 ml of soybean oil (92.93 ± 1.87)
olive oil, skimmed milk Total fat (%): soybean oil
powder and some fruit (46.54 ± 0.90) > coconut oil
flavoring, chocolate or (45.67 ± 1.29) > olive oil
cappuccino (45.27 ± 1.07)

Chinwong Randomized 8 weeks n = 32 healthy 30 ml/day of coconut oil 30 ml/day of 2% Body weight (kg): coconut oil
(2017) crossover individuals extra virgin carboxymethylcellulose (59.20 ± 12.57) > CMC
trial, open- Age = 21 ± 0.7 years solution (CMC) solution solution (58.73 ± 12.02)
label BMI = 20.8 ± 3.4 kg/m² BMI (kg/m²): coconut oil
(Thailand) (20.88 ± 3.55) > CMC solution
(20.71 ± 3.33)

Harris Randomized 4 weeks n = 12 postmenopausal Ingestion of 30 ml of Ingestion of 30ml of Body Weight (kg): coconut oil
(2017) crossover women coconut oil per day in safflower oil per day in = safflower oil (68.9 ± 11.5)
trial Age = 57.8 ± 3.7 years ready-made preparations ready-made Waist circumference (cm):
(EUA) BMI = 26.4 ± 4.4 kg/m² (smoothies-like beverages preparations safflower oil (87.1 ± 11.9) >
or in the preparation of (smoothies-like coconut oil (85.5 ± 11)
salad dressings). beverages or in the Total fat (%): coconut oil =
preparation of salad safflower oil (37.5 ± 6)
dressings).
116

Fat mass (kg): coconut oil =


safflower oil (25.7 ± 8)
Lean mass (kg): coconut oil =
safflower oil (41.5 ± 4.5)

Khaw Randomized 4 weeks n = 94 healthy Coconut oil: 50g of Butter: 50 g of butter Body weight (kg): coconut oil
(2018) clinical trial individuals coconut oil incorporated in incorporated in the usual (74 ± 15.6) > butter (70.9 ±
(UK) Age = 59.9 ± 6.1 years the usual daily diet in daily diet in substitution 11.8) > olive oil (70.4 ± 14.0)
BMI = 25.1 ± 4.2 kg/m² substitution of other fats or of other fats or ingested BMI (kg/m²): coconut oil (25.6
ingested as a supplement. as a supplement. ± 4.6) > olive oil (24.9 ± 4.5) >
butter (24.8 ± 3.6)
Olive oil: 50 g of olive oil Waist circumference (cm):
incorporated in the usual coconut oil (86.6 ± 13.6) >
daily diet in substitution olive oil (86.3 ± 12.1) > butter
of other fats or ingested (84.0 ± 8.6)
as a supplement. Body fat (%): olive oil (30.9 ±
9.5) > coconut oil (29.6 ± 10.3)
> butter (29.6 ± 8.7)

Lu Randomized 3 weeks n = 15 healthy women Coconut oil: 10% of daily A16 oil: 10% of daily Body Weight (kg): coconut oil
(1997) crossover Age = 20.0 ± 2.0 years VCT from coconut oil VCT from oil A16 = A16 oil = soybean oil (63.30
trial BMI = 22.6 ± 2.4 kg/m² (transgenic soybean oil, ± 7.00) (N/S)
117

(EUA) composed of a lower BMI (kg/m²): coconut oil = A16


ratio of 18: 3 without oil = soybean oil (22.80 ± 2.50)
trans fats)

Soybean oil: 10% of


daily VCT from soybean
oil

Oliveira-de- Randomized 8 weeks n = 75 obese women Coconut oil: 6 ml/day Safflower oil: 6 ml/day Body Weight (kg): soybean oil
Lira (2018) Clinical Trial Age = 34.07 ± 5.4 years supplemented in capsules supplemented in (82.98 ± 8.09) > safflower oil
(Brazil) 30 min before main meals. capsules 30 min before (82.72 ± 7.67) > chia oil (80.6
main meals. ± 6.79) > coconut oil (79.57 ±
8.12)*
Chia oil: 6 ml/day BMI (kg/m²): soybean oil
supplemented in (32.66 ± 2.86) > safflower oil
capsules 30 min before (32.33 ± 2.44) > chia oil (31.26
main meals ± 1.96) > coconut oil (30.76 ±
2.33)*
Soybean oil: 6 ml/day Waist circumference (cm):
supplemented in soybean oil (94.79 ± 2.66) >
chia oil (94.68 ± 4.93) >
118

capsules 30 min before safflower (94.32 ± 6.25) >


main meals. coconut oil (91.89 ± 6.05)*
Body fat (%): chia oil (40.84 ±
3.33) > soybean oil (39.73 ±
3.37) > sunflower oil (39.62 ±
4.53) > coconut oil (37.57 >
4.03)*
Lean mass (kg): coconut oil
(62.32 ± 4.49) > safflower oil
(60.38 ± 4.53) > soybean oil
(60.27 ± 3.37) > chia oil (59.16
± 3.33)*

Schwab Randomized 4 weeks n = 15 healthy women Refined coconut oil (16 to Refined palm oil, Body Weight (kg): coconut oil
(1994) clinical trial Age = 23.9 ± 4.6 years 26 g/day of coconut oil = bleached and = palm oil (58.9 ± 7.35)
(Finland) BMI = 21.4 ± 1.9 kg/m² 4% of the daily VCT). This deodorized (22 to 33
diet also contained oils g/day of palm oil = 4% of
from other sources: daily VCT). This diet also
rapeseed oil (5 to 8g / day), contained soybean oil (2
olive oil (3 to 4.5g / day) to 5 g/day) as a source
of fat.
119

and sunflower oil (2 to 3.5


g/day).

Vijayakumar Randomized 2 years n = 198 individuals with 15% of the daily VCT of a 15% of the daily VCT of Body weight (kg): sunflower oil
(2015) clinical trial CVD trademark coconut oil to a trademark sunflower (64.8 ± 9.0) > coconut oil
(India) Age = 59.0 ± 8.7 years be used as cooking oil. oil to be used as cooking (64.23 ± 8.78)
BMI = 24.7 ± 4.7 kg/m² oil. BMI (kg/m²): coconut oil
(24.72 ± 3.07) > sunflower oil
(24.54 ± 3.07)
Body Fat (%): coconut oil
(17.48 ± 2.91) > sunflower oil
(17.39 ± 3.62)
Waist hip ratio: coconut oil
(0.97 ± 0.05) > sunflower oil
(0.96 ± 0.05)

Vogel Randomized 45 days n = 29 men with obesity Addition of 1 tablespoon Addition of 1 tablespoon BMI (kg/m²): coconut oil
(2020) clinical trial I (12ml) of coconut oil (12ml) of soybean oil (32.28 ± 1.83) > soybean oil
(Brazil) Age = between 20–59 to dinner to dinner (31.17 ± 1.65)
years Waist circumference (cm):
coconut oil (107.13 ± 4.38) >
soybean oil (106.17 ± 4.60)
120

Body fat (%): coconut oil


(25.94 ± 3.64) > soybean oil
(24.06 ± 5.01)
Lean mass (kg): soybean oil
(74.06 ± 3.64) > coconut oil
(72.58 ± 3.46)
Waist hip ratio: soybean oil
(0.96 ± 0.05) > coconut oil
(0.94 ± 0.05)

* Significantly different (P<0.05). BMI: body mass index; VCT: total caloric value; CVD: cardiovascular disease.

Table S3. Summary of randomized clinical trials investigation the effect of coconut oil intake on glycemic profile

Assunção Randomized 12 weeks n = 40 women with 30 ml of coconut oil should 30 ml of soybean oil Glucose: coconut oil (82.8 ±
(2009) clinical trial abdominal obesity be added to the three main should be added to the 5.4) > soybean oil (78.5 ±
(Brazil) Age = 29.8 ± 6.6 years meals of the day, in the three main meals of the 9.9)
BMI = 31.1 ± 3.4 kg/m² common preparation of day, in the common Insulin (mIu/DL): coconut oil
meals preparation of meals (9.8 ± 4.1) > soybean oil (7.6
± 2.1)
121

HOMA-β: coconut oil (39.4 ±


18) > soybean oil (31.8 ±
9.8)
HOMA-S: coconut oil (2 ±
0.9) > soybean oil (1.48 ±
0.45)*

Cândido Randomized 9 weeks n = 52 women with BMI Vitamin breakfast prepared Vitamin breakfast Glucose: coconut oil (85.69
(2021) clinical trial between 26 e 35 kg/m², with 25 ml of coconut oil, prepared with 25 ml of ± 2.11) > olive oil (84.28 ±
(Brazil) %G > 30% skimmed milk powder and soybean oil, skimmed milk 1.19) > soybean oil (82.65 ±
Age = 26.81 ± 0.74 some fruit flavoring, powder and some fruit 0.01)*
chocolate or cappuccino flavoring, chocolate or Insulin (mIu/DL): soybean oil
cappuccino (9.19 ± 1.12) > coconut oil
(8.03 ± 0.95) > olive oil (7.99
Vitamin breakfast ± 0.76)
prepared with 25 ml of
olive oil, skimmed milk
powder and some fruit
flavoring, chocolate or
cappuccino
122

Heber Randomized 3 weeks n = 9 healthy men 35% of the calories of the 35% of the calories of the Glucose: hydrogenated
(1992) crossover trial day were derived from LIP day were derived from LIP soybean oil (81.0 ± 6.0) >
(USA) and of these, 50% were and of these, 50% were coconut oil (78.0 ± 2.0) >
from coconut oil, which was from palm oil or palm oil (69.0 ± 7.0)
incorporated into muffins or hydrogenated soybean oil Insulin (mIu/Dl): coconut oil
biscuits. Each muffin or which was incorporated (14.0 ± 2.0) > hydrogenated
cookie provided 13.7 g of into muffins or biscuits. soybean oil (12.0 ± 4.0) >
LIP of the oil test. Each muffin or cookie palm oil (11.0 ± 1.0)
provided 13.7 g of LIP of
the oil test.

Khaw Randomized 4 weeks n = 94 healthy Coconut oil: 50 g of coconut Butter: 50 g of butter Glucose: butter (97.2 ± 10.8)
(2018) clinical trial individuals oil incorporated in the usual incorporated in the usual > olive oil (95.4 ± 10.8) >
(UK) Age = 59.9 ± 6.1 years daily diet in substitution of daily diet in substitution of coconut oil (95.4 ± 9)
BMI = 25.1 ± 4.2 kg/m² other fats or ingested as a other fats or ingested as a
supplement. supplement.

Olive oil: 50 g of olive oil


incorporated in the usual
daily diet in substitution of
123

other fats or ingested as a


supplement.

Oliveira-de- Randomized 8 weeks n = 75 obese women Coconut oil: 6 ml/day Safflower oil: 6 ml/day A1c (%): chia oil (4.95 ±
Lira (2018) Clinical Trial Age = 34.07 ± 5.4 years supplemented in capsules supplemented in capsules 0.24) > safflower oil (4.91 ±
(Brazil) 30 min before main meals. 30 min before main meals. 0.30) > soybean oil (4.89 ±
0.29) > coconut oil (4.58 ±
Chia oil: 6 ml/day 0.21)*
supplemented in capsules
30 min before main meals.

Soybean oil: 6 ml/day


supplemented in capsules
30 min before main meals.

Vijayakuma Randomized 2 years n = 198 individuals with 15% of the daily VCT of a 15% of the daily VCT of a A1c (%): sunflower oil (6.77
r clinical trial CVD trademark coconut oil to be trademark sunflower oil to ± 1.28) > coconut oil (6.54 ±
(2015) (India) Age = 59.0 ± 8.7 years used as cooking oil. be used as cooking oil. 1.32)
BMI = 24.7 ± 4.7 kg/m²

Vogel Randomized 45 days n = 29 men with obesity Addition of 1 tablespoon Addition of 1 tablespoon Glucose: soybean oil (85.43
(2020) clinical trial I (12ml) of coconut oil to (12ml) of soybean oil ± 5.93) > coconut oil (78.73
(Brazil) dinner to dinner ± 10.97)
124

Age = between 20–59 Insulin (mIu/Dl): soybean oil


years (9.85 ± 9.93) > coconut oil
(5.13 ± 3.79)
HOMA-IR: soybean oil (2.16
± 2.17) > coconut oil (0.92 ±
0.63)

* Significantly different (P<0.05). BMI: body mass index; LIP: lipids; CVD: cardiovascular disease; VCT: total caloric value

Table S4. Summary of randomized clinical trials investigation the effect of coconut oil intake on arterial blood pressure

Author Study design Follow-up Sample Intervention Comparator Last measurements of


and (Country) blood pressure ( ) or
Year changes [ ] (mm Hg)

Chinwong Randomized 8 weeks n = 32 healthy individuals 30 ml/day of extra 30 ml/day of 2% SBP: CMC solution (117.63
(2017) crossover trial, Age = 21 ± 0.7 years virgin coconut oil carboxymethylcellulose ± 13.49) > coconut oil
open-label BMI = 20.8 ± 3.4 kg/m² solution (CMC) solution (114.84 ± 11.29)
(Thailand)
125

DBP: coconut oil (70.41 ±


6.42) > CMC solution
(69.50 ± 13.28)

Khaw Randomized 4 weeks n = 94 healthy individuals Coconut oil: 50 g of Butter: 50 g of butter SBP: coconut oil [0.18 ±
(2018) clinical trial Age = 59.9 ± 6.1 years coconut oil incorporated in the usual 11.46] > butter [-3.79 ±
(UK) BMI = 25.1 ± 4.2 kg/m² incorporated in the daily diet in substitution 11.11] > olive oil [- 3.67 ±
usual daily diet in of other fats or ingested 8.23]
substitution of other as a supplement. DBP: coconut oil [-2.02 ±
fats or ingested as a 5.71] > butter [-1.33 ± 6.24]
supplement. Olive oil: 50 g of olive oil > olive oil [-0.45 ± 8.48]
incorporated in the usual
daily diet in substitution
of other fats or ingested
as a supplement.

* Significantly different (P<0.05). BMI: body mass index; SBP: systolic blood pressure; DPB: diastolic blood pressure
126

Table S5. Summary of randomized clinical trials investigation the effect of coconut oil intake on the inflammatory profile

Author and Study Follow- Sample Intervention Comparator Last measurements of


Year design up inflammatory profile
(Country)
Assunção Randomized 12 n = 40 women with 30 ml of coconut oil should 30 ml of soybean oil US-CRP (mg/dL): soybean
(2009) clinical trial weeks abdominal obesity be added to the three main should be added to the oil (4.2 ± 3.2) > coconut oil
(Brazil) Age = 29.8 ± 6.6 years meals of the day, in the three main meals of the (3.7 ± 1.7)
BMI = 31.1 ± 3.4 kg/m² common preparation of day, in the common Fibrinogen (mg/dL):
meals preparation of meals coconut oil (243.8 ± 41.9)
> soybean oil (243.6 ±
43.9)
Khaw Randomized 4 weeks n = 94 healthy Coconut oil: 50 g of coconut Butter: 50 g of butter US-CRP (mg/dL): (0.19 ±
(2018) clinical trial individuals oil incorporated in the usual incorporated in the 0.2) > butter (0.16 ± 0.11)
(UK) Age = 59.9 ± 6.1 years daily diet in substitution of usual daily diet in > coconut oil (0.14 ± 0.13)
BMI = 25.1 ± 4.2 kg/m² other fats or ingested as a substitution of other fats
supplement. or ingested as a
supplement.

Olive oil: 50 g of olive oil


incorporated in the
127

usual daily diet in


substitution of other fats
or ingested as a
supplement.
Vijayakumar Randomized 2 years n = 198 individuals with 15% of the daily VCT of a 15% of the daily VCT of US-CRP (IU/L): sunflower
(2015) crossover trial CVD trademark coconut oil to be a trademark sunflower oil (1.43 ± 1.72) > coconut
(India) Age = 59.0 ± 8.7 years used as cooking oil. oil to be used as oil (1.23 ± 1.59)
BMI = 24.7 ± 4.7 kg/m² cooking oil.
Voon Randomized 5 weeks n = 45 normal and Meals with 30% energy Meals with 30% energy tcHcy (µmol/L): coconut oil
(2011) crossover trial overweight healthy from fat, two-thirds of which from fat, two-thirds of (9.13 ± 3.17) > palm oil
(Malaysia) adults was from coconut oil (20% which was from palm oil (8.88 ± 3.05) > olive oil
Age: 30.1 ± 8.3 years total energy) or extra virgin olive oil (8.76 ± 2.96)
BMI = 23.1 ± 3.7 kg/m² (20% total energy) US-CRP (mg/dL): olive oil
(2.19 ± 2.36) > palm oil
(2.15 ± 2.89) > coconut oil
(1.96 ± 2.01)
IL-1β (pg/mL): coconut oil
(25.93 ± 71.05) > olive oil
(23.63 ± 57.95) > palm oil
(23.09 ± 57.93)
128

IL-6 (pg/mL): coconut oil


(9.91 ± 44.07) > olive oil
(8.71 ± 31.15) > palm oil
(8.52 ± 32.19)
IFN- γ (pg/mL): palm oil
(17.04 ± 37.78) > olive oil
(16.2 ± 36.68) > coconut
oil (11.53 ± 30.78)
IL-8 (pg/mL): olive oil
(71.02 ± 130.1) > palm oil
(67.15 ± 108.46) > coconut
oil (47.35 ± 85.3)
* Significantly different (P>0.005). BMI: body mass index; LIP: lipids; CVD: cardiovascular disease; VCT: total caloric value
129

Table 6. Summary of randomized clinical trials investigation the effect of coconut oil on changes in the lipid profile

Author and Study Follow- Sample Intervention Comparator Last measurements of lipids ( )
Year design up or changes in lipids [ ] (mg/dL,
(Country) except where specified)

Assunção Randomized 12 weeks n = 40 women with 30 ml of coconut oil should 30 ml of soybean oil TC: soybean oil (209.3 ± 28.5) >
(2009) clinical trial abdominal obesity be added to the three main should be added to coconut oil (198.1 ± 39.0) *
(Brazil) Age = 29.8 ± 6.6 years meals of the day, in the the three main meals LDL-C: soybean oil (134.1 ± 28.7)
BMI = 31.1 ± 3.4 kg/m² common preparation of of the day, in the > coconut oil (116.5 ± 36.8) *
meals common preparation HDL-C: coconut oil (48.7 ± 2.4) >
of meals soybean oil (45.0 ± 5.6)
TG: coconut oil (179.7 ± 93.7) >
soybean oil (148.2 ± 64.8)
LDL-C:HDL-C ratio: soybean oil
(3.1 ± 0.8) > coconut oil (2.41 ± 0.8)
*

Cândido Randomized 9 weeks n = 52 women with BMI Vitamin breakfast Vitamin breakfast TC: coconut oil (173.50 ± 5.55) >
(2021) clinical trial between 26 e 35 kg/m², prepared with 25 ml of prepared with 25 ml olive oil (165.16 ± 6.22) > soybean
(Brazil) %G > 30% coconut oil, skimmed milk of soybean oil, oil (151.59 ± 5.81)
130

Age = 26.81 ± 0.74 powder and some fruit skimmed milk LDL-C: coconut oil (106.69 ± 4.79)
flavoring, chocolate or powder and some > olive oil (95.89 ± 4.64) > soybean
cappuccino fruit flavoring, oil (85.82 ± 4.64)
chocolate or HDL-C: olive oil (48.26 ± 2.27) >
cappuccino coconut oil (46.37 ± 2.54) >
soybean oil (42.27 ± 3.28)
Vitamin breakfast TG: olive oil (99.18 ± 8.56)
prepared with 25 ml >coconut oil (87 ± 7.20) > soybean
of olive oil, skimmed oil (80.41 ± 8.35)
milk powder and VLDL: olive oil (19.83 ± 1.71) >
some fruit flavoring, coconut oil (17.40 ± 1.44) >
chocolate or soybean oil (16.08 ± 1.67)
cappuccino

Chinwong Randomized 8 weeks n = 32 healthy 30 ml/day of coconut oil 30 ml/day of 2% TC: coconut oil (187.7 ± 34.5) >
(2017) crossover individuals extra virgin carboxymethylcellulo CMC solution (183.7 ± 33.7)
trial, open- Age = 21 ± 0.7 years se (CMC) solution LDL-C: coconut oil (110.5 ± 30.5) >
label BMI = 20.8 ± 3.4 kg/m² CMC solution (110.2 ± 32.0)
(Thailand) HDL-C: coconut oil (64.2 ± 9.9) >
CMC solution (59.0 ± 10.2)*
131

TG: CMC solution (72.3 ± 28.5) >


coconut oil (64.7 ± 23.5)

Cox Randomized 6 weeks n = 28 individuals Three diets, each one Butter diet: SFA from TC: butter (263.0 ± 33.0) > coconut
(1995) crossover TC: 5.5– 7.9 mmol/L followed for a 6-week butter supplies ~20% oil (249.0 ± 29.0) > safflower oil
trial TG: <3 mmol/L period. Total fat supplied of total energy. (233.0 ± 29.0) *
(New Age: 29 – 67 years 36% of energy and Safflower diet: 10% LDL-C: butter (175.0 ± 30.0) >
Zealand) BMI = 25.1 ± 4.2 kg/m² carbohydrate 47% of of energy from coconut oil (163.0 ± 29.0) >
energy. safflower oil; SFA safflower oil (151.0 ± 28.0) *
Coconut diet: SFA from and PUFA each 10% HDL-C: coconut oil (57.0 ± 15.0) >
coconut oil supplied 20% of total energy. butter (56.0 ± 14.0) > safflower oil
of energy. (54.0 ± 13.0)
TG: butter (177.0 ± 115.0) >
coconut oil (159.0 ± 89.0) >
safflower oil (151.0 ± 89.0)

Ganji Randomized 7 days n = 10 healthy Coconut oil was Soybean oil was Coconut and soybean oil:
(1996) crossover individuals incorporated in the incorporated in the TC: coconut oil (204.9 ± 32.5) >
trial Age = 31.0 ± 5.0 years preparation of a loaf, with preparation of a loaf soybean oil (191.0 ± 24.0) *
(EUA) BMI = 22.3 ± 1.7 kg/m² 42 g of coconut oil, making with 42 g of soybean LDL-C: coconut oil (126.8 ± 30.2) >
up 20% of the VCT. oil, making up 20% of soybean oil (111.8 ± 23.2)
Participants should the VCT. Participants
132

consume 1/3 of this bread should consume 1/3 HDL-C: coconut oil (53.3 ± 0.3) >
in each of the three main of this bread in each soybean oil (52.2 ± 8.5) *
meals. of the three main TG: coconut oil (158.5 ± 53.1) >
meals. soybean oil (131.1 ± 39.0) *
Coconut oil plus psyllium VLDL: coconut oil (25.1 ± 13.1) >
fiber was incorporated in soybean oil (25.1 ± 10.0)
the preparation of a loaf, LDL-C/HDL-C ratio: coconut oil
with 42 g of coconut oil, (2.40 ± 0.90) > soybean oil (2.20 ±
making up 20% of the 0.70)
VCT. Participants should
consume 1/3 of this bread Coconut and soybean oil +
in each of the three main psyllium fiber:
meals + 20 g of psyllium TC: coconut oil (192.6 ± 28.2) >
fiber per day divided into soybean oil (177.1 ± 32.1) *
three equal doses. LDL-C: coconut oil (112.5 ± 28.2) >
soybean oil (100.5 ± 28.2) *
Soybean oil was HDL-C: coconut oil (53.2 ± 9.7) >
incorporated in the soybean oil (53.7 ± 8.9)
preparation of a loaf with TG: coconut oil (141.7 ± 47.9) >
42 g of soybean oil, soybean oil (134.6 ± 54.0)
making up 20% of the
133

VCT. Participants should VLDL: coconut oil (26.2 ± 12.0) >


consume 1/3 of this bread soybean oil (23.9 ± 8.1)
in each of the three main LDL-C/HDL-C ratio: coconut oil
meals. (2.2 ± 0.6) > soybean oil (1.8 ±
0.5)*
Soybean oil plus psyllium
fiber was incorporated in
the preparation of a loaf
with 42 g of soybean oil,
making up 20% of the
VCT. Participants should
consume 1/3 of this bread
in each of the three main
meals + 20 g of psyllium
fiber per day divided into
three equal doses.

Harris Randomized 4 weeks n = 12 postmenopausal Ingestion of 30 ml of Ingestion of 30ml of TC: coconut oil (237.8 ± 24.1) >
(2017) crossover women coconut oil per day in safflower oil per day safflower oil (219.3 ± 22.8)*
trial Age = 57.8 ± 3.7 years ready-made preparations in ready-made LDL-C: coconut oil (137.5 ± 27.2) >
(EUA) BMI = 26.4 ± 4.4 kg/m² (smoothies-like beverages preparations safflower oil (126.8 ± 25.7)*
134

or in the preparation of (smoothies-like HDL-C: coconut oil (70.5 ± 18.8) >


salad dressings). beverages or in the safflower oil (62.9 ± 14.5)*
preparation of salad TG: safflower oil (118.3 ± 112.7) >
dressings). coconut oil (107.5 ± 80.6)
CT:HDL-C ratio: safflower oil (3.8 ±
1.2) > coconut oil (3.7 ± 1.3)

Heber Randomized 3 weeks n = 9 healthy men 35% of the calories of the 35% of the calories of TC: coconut oil (195.0 ± 21.0) >
(1992) crossover day were derived from LIP the day were derived palm oil (173.0 ± 21.0) >
trial and of these, 50% were from LIP and of hydrogenated soybean oil (168.0 ±
(USA) from coconut oil, which these, 50% were 15.0)*
was incorporated into from palm oil or LDL-C: coconut oil (129.0 ± 24.0) >
muffins or biscuits. Each hydrogenated palm oil (115.0 ± 21.0) >
muffin or cookie provided soybean oil which hydrogenated soybean oil (111.0 ±
13.7g of LIP for the oil test. was incorporated into 18.0)*
muffins or biscuits. HDL-C: coconut oil (42.1 ± 12.0) >
Each muffin or cookie palm oil (41.0 ± 15.0) >
provided 13.7g of LIP hydrogenated soybean oil (39.0 ±
for the oil test. 9.0)
135

TG: coconut oil (110.0 ± 69.0) >


hydrogenated soybean oil (104.0 ±
60.0) > palm oil (79.0 ± 18.0)

Khaw Randomized 4 weeks n = 94 healthy Coconut oil: 50 g of Butter: 50 g of butter TC: coconut oil (239.7 ± 34.8) >
(2018) clinical trial individuals coconut oil incorporated in incorporated in the butter = olive oil (232.0 ± 38.7)*
(UK) Age = 59.9 ± 6.1 years the usual daily diet in usual daily diet in LDL-C: butter (146.9 ± 35) > olive
BMI = 25.1 ± 4.2 kg/m² substitution of other fats or substitution of other oil (139.2 ± 39.0)> coconut oil
ingested as a supplement. fats or ingested as a (131.5 ± 35.0)*
supplement. HDL-C: coconut oil (88.9 ± 27.0) >
olive oil = butter (77.3 ± 23.2)*
Olive oil: 50 g of olive TG: coconut oil (97.4 ± 70.8) >
oil incorporated in the olive oil (97.4 ± 53.1) > butter (88.6
usual daily diet in ± 44.3)
substitution of other CT/HDL-C ratio: olive oil (3.3 ± 1.2)
fats or ingested as a > butter (3.3 ± 0.9) > coconut oil
supplement. (2.9 ± 0.9)*

Lu Randomized 3 weeks n = 15 healthy women Coconut oil: 10% of daily A16 oil: 10% of daily TC: A16 oil [-19.7 ± 20.9] >
(1997) crossover Age = 20.0 ± 2.0 years VCT from coconut oil VCT from oil A16 soybean oil
trial BMI = 22.6 ± 2.4 kg/m² (transgenic soybean [-13.5 ± 20.1] > coconut oil [-9.2 ±
(EUA) oil, composed of a 14.7]
136

lower ratio of 18: 3 LDL-C: A16 oil [-10.0 ± 19.7] >


without trans fats) soybean oil
[-4.2 ± 20.1] > coconut oil [-2.3 ±
Soybean oil: 10% of 15.8]
daily VCT from HDL-C: A16 oil [-8.1 ± 7.0] >
soybean oil soybean oil [-7.0 ± 5.4] > coconut
oil [-3.5 ± 8.1]*
TG: coconut oil [-13.3 ± 26.6] >
A16 oil
[-9.7 ± 29.2] > soybean oil [-8.8 ±
28.3]
LDL-C/HDL-C ratio: A 16 oil =
soybean oil [0.1 ± 0.4] > coconut oil
[0.1 ± 0.3]

McKenney Randomized 6 weeks n = 11 individuals with Coconut oil was added as Canola oil has been TC: coconut oil (233.3 ± 19.0) >
(1995) crossover TC altered the main ingredient in oat added as the main canola oil (213.1 ± 23.4)*
trial Age = 58.0 ± 8 years biscuits with raisins. ingredient in oat LDL-C: coconut oil (155.4 ± 19.5) >
(EUA) biscuits with raisins. canola oil (138.1 ± 17.0)*
HDL-C: coconut oil (53.9 ± 15.9) >
canola oil (51.7 ± 15.5)*
137

TG: canola oil (121.3 ± 54.2) >


coconut oil (120.0 ± 47.7)*
CT/HDL-C ratio: coconut oil (4.30 ±
1.10) > canola oil (4.10 ± 0.80)

Maki Randomized 4 weeks n = 25 individuals Consumption of four Consumption of four TC: coconut oil [7.1, IC95%: -1.1;
(2018) crossover Age = 45.2 ± 2.3 years products made with products made with 13.1] > corn oil [-0.5, IC95%: -5.7;
trial BMI = 27.7 ± 0.8 coconut oil per day, which corn oil per day, 9.7]*
(EUA) could be three types of which could be three LDL-C: coconut oil [4.6, IC95%: -
muffins and three types of types of muffins and 2,5; 17.5] > corn oil [-2.7, IC95%: -
rolls. Each product was three types of rolls. 8.9; 11.5]
made with one tablespoon Each product was HDL: coconut oil [6.5, IC95%: 2.7;
of coconut oil (13.6 g), made with one 17.8] > corn oil [5.4, IC95%: 1.4;
consisting on consumption tablespoon of corn oil 10.3]*
of 54.4 g of oil per day. (13.6 g), consisting TC:HDL-C: corn oil [-4.3 IC95%: -
on consumption of 11.7; 1.8] > coconut oil [-3.3, IC
54.4 g of oil per day. 95%: -15; 2.8]*
TG: coconut oil [6, IC 95%: -3.0;
13.2] > corn oil [-2.1, IC 95%: -9.7;
20.6]
138

Oliveira-de- Randomized 8 weeks n = 75 obese women Coconut oil: 6 ml/day Safflower oil: 6 TC: coconut oil (198.0 ± 17.6) >
Lira (2018) Clinical Trial Age = 34.07 ± 5.4 years supplemented in capsules ml/day soybean oil (195.7 ± 26.2) > chia
(Brazil) 30 min before main meals. supplemented in oil (187.1 ± 17.0) > safflower oil
capsules 30 min (182.9 ± 19.1)*
before main meals. LDL-C: safflower oil (130.6 ± 24.3)
> coconut oil (128.3 ± 17.7) >
Chia oil: 6 ml/day soybean oil (127.5 ± 23.2) > chia
supplemented in oil (123.6 ± 18.2)*
capsules 30 min HDL-C: coconut oil (55.6 ± 6.4) >
before main meals soybean oil (49.9 ± 7.1) > chia oil
(49.0 ± 5.9) > safflower oil (47.1 ±
Soybean oil: 6 ml/day 10.0)*
supplemented in TG: soybean oil (107.5 ± 39.2) >
capsules 30 min coconut oil (98.3 ± 29.1) >
before main meals. safflower oil (93.9 ± 36.5) > chia oil
(88.0 ± 24.4)*
VLDL: soybean oil (20.0 ± 8.0) >
chia oil (18.0 ± 5.1) > coconut oil
(17.8 ± 3.2) > safflower oil (15.7 ±
4.5)
139

Reiser Randomized 5 weeks n = 19 normolipidemic 35% of total energy from Habitual diet at TC: coconut oil (168.0 ± 3.0) > lard
(1985) crossover male medical students fat, baseline and during (155.0 ± 3.0) > safflower oil (141.0
trial (12 completed all three being 60% fat from washout periods ± 3.1)*
(USA) diets) coconut oil, LDL-C: coconut oil (110.0 ± 4.1) >
lard, or safflower oil lard (98.0 ± 4.5) > safflower oil
(90.0 ± 4.7)*
HDL-C: coconut oil (46.0 ± 1.1) >
lard = safflower oil (40.0 ± 1.2) *
TG: lard (88.0 ± 3.5) > coconut oil
(78 ± 3.6) > safflower oil (72.0 ±
3.7)*

Schwab Randomized 4 weeks n = 15 healthy women Refined coconut oil (16 to Refined palm oil TC: palm oil (189.9 ± 28.5) >
(1994) crossover Age = 23.9 ± 4.6 years 26 g/day of coconut oil = bleached and coconut oil (187.5 ± 24.1)
clinical trial BMI = 21.4 ± 1.9 kg/m² 4% of the daily VCT). This deodorized (22 to 33 LDL-C: palm oil (113.3 ± 19.5) >
(Finland) diet still contained oils from g/day of palm oil = coconut oil (110.2 ± 18.0)
other sources: rapeseed 4% of daily VCT). HDL-C: palm oil (58.8 ± 12.0) >
oil (5 to 8g/day), olive oil (3 This diet still coconut oil (57.6 ± 10.5)
to 4.5g/day) and sunflower contained soybean TG: coconut oil (77.1 ± 30.9) >
oil (2 to 3.5g/day). oil (2 to 5 g/day) as a palm oil (77.1 ± 27.4)
source of fat.
140

VLDL: coconut oil (19.7 ± 7.5) >


palm oil (17.8 ± 7.5) *

Vijayakumar Randomized 2 years n = 198 individuals with 15% of the daily VCT of a 15% of the daily VCT TC: sunflower oil (151.6 ± 44.5) >
(2015) clinical CVD trademark coconut oil to of a trademark coconut oil (149.3 ± 28.6)
trial Age = 59.0 ± 8.7 years be used as cooking oil. sunflower oil to be LDL-C: coconut oil (91.0 ± 21.9) >
(India) BMI = 24.7 ± 4.7 kg/m² used as cooking oil. sunflower oil (89.6 ± 29.0)
HDL-C: sunflower oil (44.4 ± 16.3)
> coconut oil (43.2 ± 10.8)
TG: sunflower oil (112.2 ± 45.1) >
coconut oil (109.3 ± 47.1)
VLDL: sunflower oil (22.5 ± 9.7) >
coconut oil (21.8 ± 9.4)

Vogel Randomized 45 days n = 29 mens with Addition of 1 tablespoon Addition of 1 TC: soybean oil (177.07 ± 39.44) >
(2020) clinical trial obesity I (12 ml) of coconut oil tablespoon (12 ml) of coconut oil (171.47 ± 49.44)
(Brazil) Age = between 20–59 to dinner soybean oil to dinner LDL-C: soybean oil (116.29 ±
years 26.55) > coconut oil (101 ± 37.17)
HDL-C: coconut oil (43.07 ± 14.86)
>soybean oil (35.93 ± 7.77)
TG: coconut oil (138.87 ± 78.28) >
soybean oil (119.50 ± 74.13)
141

VLDL: coconut oil (27.53 ± 15.74)


> soybean oil (24.85 ± 16.82)
TC: HDL-C: soybean oil (5.07 ±
1.35) > coconut oil (4.30 ± 1.58)

Voon Randomized 5 weeks n = 45 normal and Meals with 30% energy Meals with 30% TC: coconut oil (191.4 ± 26.7) >
(2011) crossover overweight healthy from fat, two-thirds of energy from fat, two- palm oil (186.0 ± 28.6) > olive oil
trial adults which was from coconut oil thirds of which was (179.8 ± 27.5)*
(Malaysia) Age: 30.1 ± 8.3 years (20% total energy) from palm oil or extra LDL-C: coconut oil (127.6 ± 29) >
BMI = 23.1 ± 3.7 kg/m² virgin olive oil (20% palm oil (123.7 ± 27.5) > olive oil
total energy) (118.3 ± 24.7)*
HDL-C: coconut oil (53.0 ± 11.6) >
palm oil (50.6 ± 10.0) > olive oil
(49.5 ± 8.9)*
TG: coconut oil (79.7 ± 34.5)> palm
oil (75.3 ± 27.5) > olive oil (74.4 ±
32.8)
TC:HDL-C ratio: palm oil (3.69 ±
0.90) > coconut oil (3.65 ± 0.95) >
olive oil (3.63 ± 0.93)
142

* Significantly different (P<0.05). BMI: body mass index; TC: total cholesterol; LDL-C: low density lipoprotein; HDL-C: high density
lipoprotein; TG: triglycerides, SFA: saturated fatty acid; VCT: total caloric value; LIP: lipids; MUFA: monounsaturated fatty acid; PUFA:
polyunsaturated fatty acid; CVD: cardiovascular disease

Table S7. Grading of Recommendations Assessment, Development and Evaluations (GRADE) – Coconut oil compared to
other oils, fat or placebo health outcomes

Certainty assessment Summary of findings


Study event rates Anticipated absolute
(%) effects
Relative Risk
Participant Overall With Risk
Risk of Inconsiste Indirectnes Imprecisio effect with
s Other certainty of other With difference
bias ncy s n (95% other
(studies) evidence oils, fat Coconu with
CI) oils, fat
or t oil Coconut
or
placebo oil
placebo
LDL-C
515 very seriousb not serious seriousc none ⨁◯◯◯ 304 211 - The MD 1.67
(7 RCTs) seriousa Very low mean mg/dL
lDL-c lower
was 0 (6.93 lower
mg/dL to 3.59
higher)
HDL-C
143

515 very seriouse not serious not serious none ⨁◯◯◯ 304 211 - The MD 3.28
(7 RCTs) seriousd Very low mean mg/dL
hDL-c higher
was 0 (0.66
mg/dL higher to
5.9 higher)

Triglycerides
515 very not serious not serious seriousg none ⨁◯◯◯ 304 211 - The MD 0.24
(7 RCTs) seriousf Very low mean mg/dL
triglycerid lower
es were 0 (5.52 lower
mg/dL to 5.04
higher)
Body weight
486 very seriousi not serious not serious none ⨁◯◯◯ 290 196 - The MD 0.24 kg
(6 RCTs) serioush Very low mean lower
body (0.83 lower
weight to 0.34
was 0 kg higher)
Waist circumference
287 very seriousk not serious not serious none ⨁◯◯◯ 190 97 - The MD 0.64
(4 RCTs) seriousj Very low mean cm lower
waist (1.69 lower
circumfer
144

ence was to 0.41


0 cm higher)

Total body fat


445 very seriousm not serious not serious none ⨁◯◯◯ 269 176 - The MD 0.10 %
(5 RCTs) seriousl Very low mean lower
total body (0.56 lower
fat was 0 to 0.36
% higher)

Fasting blood glucose


212 very not serious not serious seriouso none ⨁◯◯◯ 133 79 - The MD 0.82
(4 RCTs) seriousn Very low mean mg/dl
total lower
fasting (1.18 lower
blood to 2.82
glucose higher)
was 0
mg/dL

US-CRP
131 very not serious not serious not serious none ⨁◯◯◯ 83 48 - The MD 0.04
(2 RCTs) seriousp Very low mean mg/dl
total lower
USC-RP (0.91 lower
was 0 to 0.82
mg/dL higher)
145

CI: confidence interval; MD: mean difference


Explanations
a. RCTs are at risk of bias due to: blinding of participants and/or outcome (in Khaw et al. and Vogel et al.) and selective reporting (in Schwab et al.). RCTs present an unclear risk
of bias in: randomization (in Oliveira-de-Lira et al., Schwab et al., Vijayakumar et al.), allocation (in Assunção et al., Oliveira-de-Lira et al., Schwab et al., Vijayakumar et al., Vogel
et al.), participant blinding and/or outcome (in Candido et al., Khaw et al., Schwab et al., Vijayakumar et al., Vogel et al.) and selective reporting (in Assunção et al., Oliveira-de-
Lira et al., Vijayakumar et al.).
b. Large amounts of statistical heterogeneity (I²:78%); point estimates and confidence intervals vary considerably.
c. Imprecision due to wide confidence interval: in the worst scenario, it may increase 3.59 mg/dL; in the best scenario, it may decrease 6.93 mg/dL.
d. RCTs are at risk of bias due to: blinding of participants and/or outcome (in Khaw et al. and Vogel et al.) and selective reporting (in Schwab et al.). RCTs present an unclear risk
of bias in: randomization (in Oliveira-de-Lira et al., Schwab et al., Vijayakumar et al.), allocation (in Assunção et al., Oliveira-de-Lira et al., Schwab et al., Vijayakumar et al., Vogel
et al.), participant blinding and/or outcome (in Candido et al., Khaw et al., Schwab et al., Vijayakumar et al., Vogel et al.) and selective reporting (in Assunção et al., Oliveira-de-
Lira et al., Vijayakumar et al.).
e. Large amounts of statistical heterogeneity (I²:74%); point estimates and confidence intervals vary considerably.
f. RCTs are at risk of bias due to: blinding of participants and/or outcome (in Khaw et al. and Vogel et al.) and selective reporting (in Schwab et al.). RCTs present an unclear risk
of bias in: randomization (in Oliveira-de-Lira et al., Schwab et al., Vijayakumar et al.), allocation (in Assunção et al., Oliveira-de-Lira et al., Schwab et al., Vijayakumar et al., Vogel
et al.), participant blinding and/or outcome (in Candido et al., Khaw et al., Schwab et al., Vijayakumar et al., Vogel et al.) and selective reporting (in Assunção et al., Oliveira-de-
Lira et al., Vijayakumar et al.).
g. Imprecision due to wide confidence interval: in the worst scenario, it may increase 5.04 mg/dL; in the best scenario, it may decrease 5.52 mg/dL.
h. RCTs are at risk of bias due to: blinding of participants and/or outcome (in Khaw et al. and Vogel et al.) and selective reporting (in Schwab et al.). RCTs present an unclear risk
of bias in: randomization (in Oliveira-de-Lira et al., Schwab et al., Vijayakumar et al.), allocation (in Assunção et al., Oliveira-de-Lira et al., Schwab et al., Vijayakumar et al., Vogel
et al.), participant blinding and/or outcome (in Candido et al., Khaw et al., Schwab et al., Vijayakumar et al., Vogel et al.) and selective reporting (in Assunção et al., Oliveira-de-
Lira et al., Vijayakumar et al.).
i. Large amounts of statistical heterogeneity (I²:76%); point estimates and confidence intervals vary considerably.
j. RCTs are at risk of bias due to: blinding of participants and/or outcome (in Khaw et al. and Vogel et al.) and selective reporting (in Schwab et al.). RCTs present an unclear risk
of bias in: randomization (in Oliveira-de-Lira et al., Schwab et al., Vijayakumar et al.), allocation (in Assunção et al., Oliveira-de-Lira et al., Schwab et al., Vijayakumar et al., Vogel
et al.), participant blinding and/or outcome (in Candido et al., Khaw et al., Schwab et al., Vijayakumar et al., Vogel et al.) and selective reporting (in Assunção et al., Oliveira-de-
Lira et al., Vijayakumar et al.).
k. Large amounts of statistical heterogeneity (I²:80%); point estimates and confidence intervals vary considerably.
l. RCTs are at risk of bias due to: blinding of participants and/or outcome (in Khaw et al. and Vogel et al.). RCTs present an unclear risk of bias in: randomization (in Oliveira-de-
Lira et al., Vijayakumar et al.), allocation (in Oliveira-de-Lira et al., Vijayakumar et al., Vogel et al.), participant blinding and/or outcome (in Candido et al., Khaw et al., Vijayakumar
et al., Vogel et al.) and selective reporting (in Oliveira-de-Lira et al. and Vijayakumar et al.).
m. Large amounts of statistical heterogeneity (I²:75%); point estimates and confidence intervals vary considerably.
n. RCTs are at risk of bias due to: blinding of participants and/or outcome (in Khaw et al. and Vogel et al.). RCTs present an unclear risk of bias in: allocation (in Assunção et al.,
and Vogel et al.), participant blinding and/or outcome (in Candido et al., Khaw et al. and Vogel et al.) and selective reporting (in Assunção et al.).
o. Imprecision due to wide confidence interval: in the worst scenario, it may increase 2.62 mg/dL; in the best scenario, it may decrease 1.18 mg/dL.
p. RCTs are at risk of bias due to: blinding of participants and/or outcome (in Khaw et al.). RCTs present an unclear risk of bias in: allocation (in Assunção et al.), participant
blinding and/or outcome (in Khaw et al.) and selective reporting (in Assunção et al.).
146

Appendix II
Additional results
LDL-C to HDL-C ratio and TC: HDL-C ratio
Three studies analyzed the effects of coconut oil on LDL-C to HDL-C ratio (n=65, 92%
female, 18 to 36 years) [1-3]. The consumption of coconut oil reduced the LDL-C/HDL-
C ratio in comparison to soybean and transgenic soybean oils [1,2]. Seven studies [4-
10] analyzed the effects of coconut oil on TC: HDL-C ratio. These studies included 291
participants (70% females, 34 to 68 years).
Three studies [4,5,10] were included in the meta-analysis regarding TC:HDL-C ratio (-
0.12; CI 95% -0.43 to 0.20; figure 1). We performed a subgroup analysis excluding a
study that used a SAFs rich oil/fat as a comparator and the results did not change (vs
butter; -0.06; CI 95% -0.46 to 0.34; figure 2) [5].

Figure 1. Forest plots of randomized controlled clinical trials investigating the


effects of coconut oil intake on TC:HDL-C ratios
147

Figure 2. Forest plots of randomized controlled clinical trials investigating the


effects of coconut oil intake vs MUFA and PUFA rich oils on TC:HDL-C ratios

Glycemic profile
Fasting blood glucose
Seven studies analyzed the effects of coconut oil on fasting glucose levels [2, 5, 6, 10-
13]. These studies included 297 participants (69.3% females, 23 to 66 years). Four
studies [2,5,10,13] were included in the meta-analysis. Overall, the effect of coconut
oil intake on fasting glucose levels in comparison to other oils/fats did not differ (0.82
mg/dL; 95% CI -1.18 to 2.82 mg/dL; figure 3). We performed a subgroup analysis
excluding a study that used a SAFs rich oil/fat as a comparator and the results did not
change (vs butter 1.14 mg/dL; 95% CI -1.01 to 3.29 mg/dL; figure 4) [1]. The intake of
coconut oil did not fasting plasma glucose did not differ in comparison to PUFAs (0.37
mg/dL; 95% CI -3.37 to 4.12 mg/dL) and MUFAs (1.91 mg/dL; 95% CI -1.48 to 5.30
mg/dL).
A crossover study (n=9) [11] demonstrated that consumption of coconut oil increases
blood glucose levels more than palm oil, but less than hydrogenated soybean oil.

A1c
Two studies analyzed this outcome (n=273, 32% female, 29 to 68 years) [4,14]. An 8-
week study found significantly lower values of A1c when comparing coconut oil to
PUFAs [4]. A 2-year follow-up study compared the consumption of coconut oil with
PUFAs and found no difference between groups [14]. Results are shown in table S2.

Effects of coconut oil on insulin levels, β-cell function and indices of insulin sensitivity
A study observed that coconut oil increased β-cell function and insulin sensitivity in
comparison to the consumption of soybean oil (n=40, 100% female, 29.8 ± 6.6 years,
follow-up: 12 weeks) [2]. Results are shown in table S2.
148

One study analyzed the insulin resistance index (HOMA-IR), comparing coconut oil
with soy oil, but found no difference between groups (n=29, 100% man, 35.27 ± 11.12
coconut oil group and 39.28 ± 9.06 soybean oil group, follow-up: 45 days) [10].

Figure 3. Forest plots of randomized controlled clinical trials investigating the


effects of coconut oil intake on fasting blood glucose (mg/dL)

Figure 4. Forest plots of randomized controlled clinical trials investigating the


effects of coconut oil intake vs PUFA and MUFA rich oils on fasting blood
glucose (mg/dL).
149

Blood pressure
Blood Pressure Systolic
Two studies [5, 15] analyzed this outcome (n=126, 63% female, 20 to 66 years, follow-
up of 4 to 8 weeks). When comparing the effect of coconut oil intake with placebo,
higher levels of systolic blood pressure are observed [15]. However, when the effect
of the intake of coconut oil is compared with olive oil or butter, lower levels of systolic
blood pressure are observed [5]. We were not able to meta-analyze these data, since
one study was a crossover trial and there was not enough data. Results are shown in
table S3.

Diastolic Blood Pressure


Two studies [5,15] analyzed this outcome (n=126, 63% female, 20 to 66 years, follow-
up of 4 to 8 weeks). When the effect of the intake of coconut oil is compared with
placebo, olive oil and butter, higher levels of diastolic blood pressure are observed
[5,15]. We were not able to meta-analyze these data, since one study was a crossover
trial and there was not enough data. Results are shown in table S3.

Inflammatory profile
Four studies (follow-up 4 weeks to 2 years, n=377, 40% females, 22 to 68 years)
analyzed the effects of coconut oil on US-CRP [2,5,6,14].
Two studies [2,5] were included in the meta-analysis. Overall, the effect of coconut oil
intake on US-CRP in comparison to other oils/fats did not differ (-0.04 mg/dL; 95% CI
-0.91 to 0.82 mg/dL; figure 5). A crossover study observed lower levels of US-CRP
with the intake of coconut oil when compared to olive and palm oils [6].
One RCT study (follow-up 12 weeks, n=40, 100% female, 23.9 ± 4.6 years) analyzed
the effects of coconut oil in fibrinogen. Coconut oil increased fibrinogen when
compared to consumption of soybean oil [2].
A crossover study (follow-up 5 weeks, n=45, 80% female, 30.1 ± 8.3 years) observed
that coconut oil consumption increased tcHcy, IL-1β, IL-6, IL-8 and IFN- γ when
compared to the use of palm and extra virgin olive oil [6]. Results are shown in table
S4.
150

Figure 5. Forest plots of randomized controlled clinical trials investigating the


effects of coconut oil intake on US-CRP (mg/dL)

Supplemental figures

Supplemental Figure 1. Forest plot of randomized controlled clinical trials


investigating the effects in body weight (kg) of coconut oil intake versus PUFA
and MUFA rich oils
151

Supplemental Figure 2. Forest plot of randomized controlled clinical trials


investigating the effect in body weight (kg) of coconut oil versus olive oil

Supplemental Figure 3. Forest plot of randomized controlled clinical trials


investigating the effect in body weight (kg) of coconut oil versus soybean oil

Supplemental Figure 4. Forest plot of randomized controlled clinical trials


investigating the effect in body weight (kg) of coconut oil versus other oils in
studies carried out in women
152

Supplemental Figure 5. Forest plot of the randomized controlled clinical trials


investigating the effect of coconut oil versus other oils in body weight (kg) of
studies conducted in Brazil

Supplemental Figure 6. Forest plot of randomized controlled clinical trials


investigating the effect of coconut oil versus other oils/fats in body weight (kg)
of studies carried out in patients with overweight/obesity
153

Supplemental Figure 7. Forest plot of randomized controlled clinical trials


investigating the effect on body weight (kg) of coconut oil versus other oils/fats
without the long term study of Vijayakumar et al.

Supplemental Figure 8. Forest plot of randomized controlled clinical trials


investigating the effect in body weight (kg) of coconut oil versus other oils/fats
in studies including co-intervention
154

Supplemental Figure 9. Forest plot of randomized controlled clinical trials


investigating the effects in waist circumference (cm) of coconut oil intake versus
PUFA and MUFA rich oils

Supplemental Figure 10. Forest plot of randomized controlled clinical trials


investigating the effect in waist circumference (cm) of coconut oil versus olive
oil
155

Supplemental Figure 11. Forest plot of randomized controlled clinical trials


investigating the effect in waist circumference (cm) of coconut oil versus
soybean oil

Supplemental Figure 12. Forest plot of randomized controlled clinical trials


investigating the effect in waist circumference (cm) of coconut oil versus other
oils when analyzing studies carried out in women

Supplemental Figure 13. Forest plot of randomized controlled clinical trials


investigating the effect in waist circumference (cm) of coconut oil versus other
oils when analyzing studies conducted in Brazil
156

Supplemental Figure 14. Forest plot of randomized controlled clinical trials


investigating the effect in waist circumference (cm) of coconut oil versus other
oils or/fat in patients with overweight/obesity

Figure S15 - Forest plot of randomized controlled clinical trials investigating the
effect in waist circumference (cm) of coconut oil versus other oils/fats in studies
including co-intervention
157

Supplemental Figure 16. Forest plot of the randomized controlled clinical trials
investigating the effects in % body fat of coconut oil intake in comparison to
other oils/fat

Supplemental Figure S17. Forest plot of randomized controlled clinical trials


investigating the effect in % body fat of coconut oil intake vs PUFA and MUFA
rich oils
158

Supplemental Figure 18. Forest plot of randomized controlled clinical trials


investigating the effects in LDL-C (mg/dL) of coconut oil intake vs PUFA and
MUFA rich oils

Supplemental Figure 19. Forest plot of randomized controlled clinical trials


investigating the effect in LDL-C (mg/dL) of coconut oil versus olive oil

Supplemental Figure 20. Forest plot of randomized controlled clinical trials


investigating the effect in LDL-C (mg/dL) of coconut oil versus soybean oil
159

Supplemental Figure 21. Forest plot of randomized controlled clinical trials


investigating the effect in LDL-C (mg/dL) of coconut oil versus other oils when
analyzing studies carried out in women

Supplemental Figure 22. Forest plot of randomized controlled clinical trials


investigating the effect in LDL-C (mg/dL) of coconut oil versus other oils when
analyzing studies conducted in Brazil in LDL-C
160

Supplemental Figure 23. Forest plot of randomized controlled clinical trials


investigating the effect in LDL-C (mg/dL). of coconut oil versus other oils or/fat
in patients with overweight/obesity

Supplemental Figure 24. Forest plot of randomized controlled clinical trials


investigating the effect in LDL-C (mg/dL) of coconut oil versus other oils or fat
without a long-term study (Vijayakumar et al)
161

Supplemental Figure 25. Forest plot of randomized controlled clinical trials


investigating the effect in LDL-C (mg/dL) of coconut oil versus other oils or fat
with co-intervention

Supplemental Figure 26. Forest plot of randomized controlled clinical trials


investigating the effects in HDL-C (mg/dL) of coconut oil intake vs PUFA and
MUFA rich oils
162

Supplemental Figure 27. Forest plot of randomized controlled clinical trials


investigating the effect in HDL-C (mg/dL) of coconut oil versus olive oil

Supplemental Figure 28. Forest plot of randomized controlled clinical trials


investigating the effect in HDL-C (mg/dL) of coconut oil versus soybean oil

Supplemental Figure 29. Forest plot of randomized controlled clinical trials


investigating the effect in HDL-C (mg/dL) of coconut oil versus other oils when
analyzing studies carried out in women
163

Supplemental Figure 30. Forest plot of randomized controlled clinical trials


investigating the effect in HDL-C (mg/dL) of coconut oil versus other oils when
analyzing studies conducted in Brazil

Supplemental Figure 31. Forest plot of randomized controlled clinical trials


investigating the effect in HDL-C (mg/dL) of coconut oil versus other oils or fat
in patients with overweight/obesity
164

Supplemental Figure 32. Forest plot of randomized controlled clinical trials


investigating the effect in HDL-C (mg/dL) of coconut oil versus other oils or fat
without a long-term study (Vijayakumar et al)

Supplemental Figure 33. Forest plot of randomized controlled clinical trials


investigating the effect in HDL-C (mg/dL) of coconut oil versus other oils or fat
with co-intervention
165

Supplemental Figure 34. Forest plot of randomized controlled clinical trials


investigating the effects in TG (mg/dL) of coconut oil intake vs PUFA and MUFA
rich oils

Supplemental Figure 35. Forest plot of randomized controlled clinical trials


investigating the effect in TG (mg/dL) of coconut oil versus olive oil

Supplemental Figure 36. Forest plot of randomized controlled clinical trials


investigating the effect in TG (mg/dL) of coconut oil versus soybean oil
166

Supplemental Figure 37. Forest plot of randomized controlled clinical trials


investigating the effect in TG (mg/dL) of coconut oil versus other oils when
analyzing studies carried out in women

Supplemental Figure 38. Forest plot of randomized controlled clinical trials


investigating the effect in TG (mg/dL) of coconut oil versus other oils when
analyzing studies conducted in Brazil

Supplemental Figure 39. Forest plot of randomized controlled clinical trials


investigating the effect in TG (mg/dL) of coconut oil versus other oils or fat in
patients with overweight/obesity
167

Supplemental Figure 40. Forest plot of randomized controlled clinical trials


investigating the effect in TG (mg/dL) of coconut oil versus other oils or fat
without a long-term study (Vijayakumar et al)

Supplemental Figure 41. Forest plot of randomized controlled clinical trials


investigating the effect in TG (mg/dL) of coconut oil versus other oils or fat with
co-intervention
168

Figure S42: RoB 2.0 risk of bias in RCTs assessing the effects of coconut oil in

the lipid profile


169

Figure S43: RoB 2.0 risk of bias in RCTs assessing the effects of coconut oil in

the anthropometric profile


170

Figure S44: RoB 2.0 risk of bias in RCTs assessing the effects of coconut oil in

the glycemic profile


171

Figure S45: RoB 2.0 risk of bias in RCTs assessing the effects of coconut oil in

blood pressure

Figure S46: RoB 2.0 risk of bias in RCTs assessing the effects of coconut oil in

the inflammatory profile


172

PRISMA 2020 CHECKLIST

Location
Section and Item
Checklist item where item is
Topic #
reported
TITLE
Title 1 Identify the report as a systematic review. Pg. 1
ABSTRACT
Abstract 2 See the PRISMA 2020 for Abstracts checklist. Pg. 2, 3
INTRODUCTION
Rationale 3 Describe the rationale for the review in the context of existing knowledge. Pg. 4, 5
Objectives 4 Provide an explicit statement of the objective(s) or question(s) the review addresses. Pg. 5
METHODS
Eligibility criteria 5 Specify the inclusion and exclusion criteria for the review and how studies were grouped for the syntheses. Pg. 7, 8
Information 6 Specify all databases, registers, websites, organisations, reference lists and other sources searched or consulted to identify studies. Specify Pg. 6
sources the date when each source was last searched or consulted.
Search strategy 7 Present the full search strategies for all databases, registers and websites, including any filters and limits used. Pg. 6
Selection process 8 Specify the methods used to decide whether a study met the inclusion criteria of the review, including how many reviewers screened each Pg. 6
record and each report retrieved, whether they worked independently, and if applicable, details of automation tools used in the process.
Data collection 9 Specify the methods used to collect data from reports, including how many reviewers collected data from each report, whether they worked Pg. 6
process independently, any processes for obtaining or confirming data from study investigators, and if applicable, details of automation tools used in
the process.
Data items 10a List and define all outcomes for which data were sought. Specify whether all results that were compatible with each outcome domain in each Pg. 6, 7
study were sought (e.g. for all measures, time points, analyses), and if not, the methods used to decide which results to collect.
10b List and define all other variables for which data were sought (e.g. participant and intervention characteristics, funding sources). Describe any Pg. 6, 7
assumptions made about any missing or unclear information.
Study risk of bias 11 Specify the methods used to assess risk of bias in the included studies, including details of the tool(s) used, how many reviewers assessed Pg. 7
assessment each study and whether they worked independently, and if applicable, details of automation tools used in the process.
Effect measures 12 Specify for each outcome the effect measure(s) (e.g. risk ratio, mean difference) used in the synthesis or presentation of results. Pg. 8
Synthesis 13a Describe the processes used to decide which studies were eligible for each synthesis (e.g. tabulating the study intervention characteristics and Pg. 7
methods comparing against the planned groups for each synthesis (item #5)).
13b Describe any methods required to prepare the data for presentation or synthesis, such as handling of missing summary statistics, or data Pg. 8
173

Location
Section and Item
Checklist item where item is
Topic #
reported
conversions.
13c Describe any methods used to tabulate or visually display results of individual studies and syntheses. Pg. 8
13d Describe any methods used to synthesize results and provide a rationale for the choice(s). If meta-analysis was performed, describe the Pg. 8
model(s), method(s) to identify the presence and extent of statistical heterogeneity, and software package(s) used.
13e Describe any methods used to explore possible causes of heterogeneity among study results (e.g. subgroup analysis, meta-regression). Pg. 9
13f Describe any sensitivity analyses conducted to assess robustness of the synthesized results. Pg. 9
Reporting bias 14 Describe any methods used to assess risk of bias due to missing results in a synthesis (arising from reporting biases). Pg. 7
assessment
Certainty 15 Describe any methods used to assess certainty (or confidence) in the body of evidence for an outcome. Pg. 7, 8
assessment
RESULTS
Study selection 16a Describe the results of the search and selection process, from the number of records identified in the search to the number of studies included Pg. 9 and fig.
in the review, ideally using a flow diagram. 1
16b Cite studies that might appear to meet the inclusion criteria, but which were excluded, and explain why they were excluded. Figure 1 and
Table S1
Study 17 Cite each included study and present its characteristics. Pg. 9, 10 and
characteristics table 1
Risk of bias in 18 Present assessments of risk of bias for each included study. Pg. 15 and
studies supplementary
material
Results of 19 For all outcomes, present, for each study: (a) summary statistics for each group (where appropriate) and (b) an effect estimate and its Figures 2 and
individual studies precision (e.g. confidence/credible interval), ideally using structured tables or plots. 3
Results of 20a For each synthesis, briefly summarise the characteristics and risk of bias among contributing studies. Pg. 10-15
syntheses
20b Present results of all statistical syntheses conducted. If meta-analysis was done, present for each the summary estimate and its precision (e.g. Figures 2 and
confidence/credible interval) and measures of statistical heterogeneity. If comparing groups, describe the direction of the effect. 3
20c Present results of all investigations of possible causes of heterogeneity among study results. Pg. 9
20d Present results of all sensitivity analyses conducted to assess the robustness of the synthesized results. Pg. 9-15
Reporting biases 21 Present assessments of risk of bias due to missing results (arising from reporting biases) for each synthesis assessed. Pg. 15 and
Figures S42-
S46
Certainty of 22 Present assessments of certainty (or confidence) in the body of evidence for each outcome assessed. Pg. 15 and
evidence Table S7
DISCUSSION
174

Location
Section and Item
Checklist item where item is
Topic #
reported
Discussion 23a Provide a general interpretation of the results in the context of other evidence. Pg. 15, 16
23b Discuss any limitations of the evidence included in the review. Pg. 15-21
23c Discuss any limitations of the review processes used. Pg. 20, 21
23d Discuss implications of the results for practice, policy, and future research. Pg. 21
OTHER INFORMATION
Registration and 24a Provide registration information for the review, including register name and registration number, or state that the review was not registered. Pg. 3
protocol
24b Indicate where the review protocol can be accessed, or state that a protocol was not prepared. Pg. 3
24c Describe and explain any amendments to information provided at registration or in the protocol. NA
Support 25 Describe sources of financial or non-financial support for the review, and the role of the funders or sponsors in the review. Pg. 23
Competing 26 Declare any competing interests of review authors. Pg. 23
interests
Availability of 27 Report which of the following are publicly available and where they can be found: template data collection forms; data extracted from included NA
data, code and studies; data used for all analyses; analytic code; any other materials used in the review.
other materials
175

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2018;148(10):1556-63. https://doi.org/ 10.1093/jn/nxy156.
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[14] Vijayakumar M, Vasudevan DM, Sundaram KR, Krishnan S, Vaidyanathan K,
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Anexo II – Material suplementar do Capítulo III – ““Misinformation in nutrition

through the case of coconut oil: an online before-and-after study”.

Figure 1. Grafic abstract


177

SUPPLEMENTARY METHODS:

CHECKLIST FOR REPORTING RESULTS OF INTERNET E-SURVEYS (CHERRIES)

Item Category Checklist Item Description


Design Describe survey design The study targeted two populations of self-selected individuals aged 18
years or older:
1) University sample: students from graduate programs at
Universidade Federal do Rio Grande do Sul, Porto Alegre,
Brazil.
2) Facebook sample: individuals who accessed the Facebook
page of Hospital de Clínicas de Porto Alegre (the main teaching
hospital from the same university).
IRB (Institutional IRB approval The study was approved by the Research Ethics Committee of Hospital
Review Board) de Clínicas de Porto Alegre and Universidade Federal do Rio Grande
approval and do Sul (approval number: GPPG-HCPA protocol 20180393 nos and
informed consent CAAE nos 92144718.6.0000.5327).
process Informed consent Participants were informed, at the study home page, that by submitting
the questionnaire, they would be accepting to voluntarily participate in
the survey. In the study home page, participants were informed that their
178

participation would be anonymous, taking approximately 2 to 3 minutes


to complete the survey. The home page also provided information about
the study objective and the name and contact information of the principal
investigator.
Data protection The only personal information requested was a valid email address,
which would be only used to prevent multiple entries and to provide
study results to the participants who requested it. The datasets were
stored in a password protected Google Drive account, to which only the
main investigators had access.
Development and Development and testing The questionnaire was constructed using Google Forms, initially
pre-testing consisting of 13 objective questions to evaluate coconut oil consumption
and public opinion on its effects on metabolic and cardiovascular health.
We submitted the questionnaire to major experts in the field of
metabolism and mental health as well as clinical dieticians developing
research projects in the field. After changes of the constructs composing
the questionnaire, a second round of submission was conducted to
graduate students in order to provide feedback changes for the final
training version of the questionnaire, resulting in a new version with 12
questions. The initial questionnaire was then pilot tested in 51
179

individuals in Brazil (Portuguese version), India and the United States


(English version) using Facebook advertisement as a way of
dissemination. Based on the results of the pilot test, modifications were
performed to improve question wording, response items and
comprehension. The final questionnaire consisted of 10 sequential
objective questions.
Recruitment Open survey versus This is an open survey. Distribution to University sample was made via
process and closed survey email with an exclusive link using the mailing list of the university, while
description the distribution to Facebook sample was made in a post in the Hospital
of the sample de Clínicas de Porto Alegre official Facebook page, containing a
having access separate link to a Google Forms questionnaire.
to the Contact mode The initial contact with the potential participants was made entirely on
questionnaire the Internet. As stated above, the survey was distributed via email with
a link to Google Forms to the University sample and via a Facebook
post with a link to Google Forms to the Facebook sample.
Advertising the survey As previously described, the survey was distributed using the
university’s graduate student mailing list (University sample) and using
a Facebook post in the Hospital de Clínicas de Porto Alegre official
Facebook page (Facebook sample).
180

Survey Web/Email This is a web survey. Although the method of distribution to the
administration University sample was via email, the email contained a link which led to
a Google Forms website. All responses were captured automatically
through Google Forms.
Context The mailing list (University sample) is composed of emails of students
of all level graduate programs.
The Facebook page of Hospital de Clínicas de Porto Alegre (Facebook
sample) is the official Facebook page of the hospital, which posts
updates about the hospital’s actions in public health matters,
innovations in research made by the hospital, calls for actions of the
community, and health promotion campaigns.
Mandatory/voluntary It was a voluntary survey.
Incentives We offered to provide the survey results to those who requested it by
checking an item on the questionnaire.
Time/Date Responses were collected between May and June 2020.
Randomization of items or The items on the questionnaire were not randomized to follow a logical
questionnaires sequential order.
181

Adaptive questioning Participants who answered “yes” to the question “Have you ever used
coconut oil” answered all the 10 questions, while participants who
answered “no” to the same question answered only 7 questions.
Number of Items There was one questionnaire item per page, comprising a total of 11
items (10 questions and email item).
Number of screens The full survey was distributed in 12 pages (home page, 10 questions,
(pages) email page).
Completeness check In each question, the participants had the option of clicking on the “back”
button to change their answers. Respondents were unable to change
their responses once the full questionnaire was submitted.
Review step In each question, respondents had the option of clicking on the “back”
button to change their answers. Respondents were unable to change
their responses once the full questionnaire was submitted.
Response rates Unique site visitor Not applicable. Respondents were invited through an external link.
Unique respondents were determined using the provided valid email
address, as described in the item “Registration” below.
View rate (Ratio of unique Not applicable. Google forms does not provide the number of site or
survey visitors/unique site survey visitors.
visitors)
182

Participation rate (Ratio of For University sample, we determined the participation rate by dividing
unique visitors who the number of entries (3582) by the number of emails registered in the
agreed to mailing list (11753) resulting in a participation rate of 30.5%.
participate/unique first Not applicable for Facebook sample as Google forms does not provide
survey page visitors) the number of survey visitors nor stores information of incomplete
questionnaires.
Completion rate (Ratio of Not applicable; Google Forms only stores complete surveys, after the
users who finished the respondent submitted it through the “send” button.
survey/users who agreed
to participate)
Preventing multiple Cookies used Not used.
entries from the IP check Not used.
same individual Log file analysis Not used.
Registration The questionnaire requested a valid email address which was stored
together with the survey results to avoid multiple entries. In the case of
duplicate entries, the first entry was kept and the last was excluded from
the analysis.
Analysis Handling of incomplete Not applicable; Google Forms only stores complete surveys, after the
questionnaires respondent submitted it through the “send” button.
183

Questionnaires submitted No respondents were removed from the survey for completing the items
with an atypical too quickly.
timestamp
Statistical correction Not used.
184

QUESTIONNAIRE DEVELOPMENT

Initial Questionnaire Construction

We constructed an online questionnaire using Google Forms to evaluate coconut oil consumption
and the public opinion on its effects on metabolic and cardiovascular health. The initial
questionnaire consisted of 13 objective questions. First, we submitted the questionnaire to major
experts in the field of metabolism and mental health as well as clinical dieticians developing
research projects in the field. After changes of the constructs composing the questionnaire, a
second round of submission was conducted to graduate students in order to provide feedback
changes for the final training version of the questionnaire, resulting in a new version with 12
questions.

Pilot Test

We tested the training questionnaire using an official Facebook page for the study, targeting adults
(age ≥18 years). The training questionnaire consisted of 12 questions, originally formulated in
Portuguese. An English version was translated, as, initially, the idea was to apply the same
questionnaire in a country on each continent. The Portuguese version was shared in Brazil and
an English version was shared in the United States and India (where coconut oil intake is
considered significant) [5]. In all, 51 people answered the questionnaire, 26 in Brazil, 19 in India
and 5 in the United States. The purpose of the pilot test was to assess understanding of the
questions and answer items and to examine questions with invalid or unsatisfactory answers.
From the analysis of the answers obtained with this pilot and the refinement of the questions and
answers, the official version of the questionnaire was elaborated.
185

Questionnaire Refinement

Based on the pilot test, we performed new modifications in the wording and response items of the
questionnaire in order to make it more comprehensive. The wording of questions with lower
response rates was revised. The final questionnaire consisted of 10 sequential objective questions
distributed in 12 pages (one question per page, home and email pages), with multiple-choice
answers where the participant could mark more than one answer. In each question, the
participants had the option of clicking on the “back” button to change their answers. Individuals
not using coconut oil were redirected to questions on sample characteristics and the reason why
they did not use it, answering only 7 questions. Questions were marked as forced responses
whenever possible, to facilitate statistical analysis. For forced-response questions, the option "I
prefer not to answer" was included to ensure participants the right not to answer. Since the Google
Forms tool only stores information after the participant finishes the questionnaire, we only had
access to entries in which the participant formally clicked the "send" button. All questions and
responses were examined by the research team to ensure readability and face validity prior to
survey administration.
FINAL QUESTIONNAIRE

1. Have you ever used coconut oil?


( ) Yes
( ) No
( ) I don’t want to answer
Yes I don’t want to answer

2. Why do you use coconut oil (check as many alternatives as you want)?
( ) I like the flavor
( ) It’s the oil most commonly used for cooking
( ) It’s cheaper than other oils
( ) It takes longer to spoil
( ) It gives me more energy
( ) It’s healthy
( ) I don’t want to answer

3. What amount of coconut oil do you intake? Choose the alternative that
comes closest.
( ) Less than a tablespoon/day
( ) 1 tablespoon/day
( ) 2 tablespoons/day
( ) 3 tablespoons/day
( ) 1-3×/week
( ) Once every 15 days
( ) 1×/month
( ) I don’t want to answer

4. Which benefits did you observe by using coconut oil (check as many
alternatives as you want)?
( ) I did not observe any improvements in my health or aesthetic
( ) Weight loss
( ) Reduced waist circumference
( ) Improvement of cholesterol levels
( ) Improvement of glycemic levels
( ) I don’t want to answer

5. A current study has reviewed scientific articles and concluded that


nutritional consumption of coconut oil does not improve bad
cholesterol, reduces weight or blood sugar (glucose) levels. Do you
still consider coconut oil good for your health?
( ) Yes
( ) No
( ) I don’t want to answer
No

2. Why don’t you use coconut oil (check as many alternatives as you
want)?
( ) I don’t like the flavor
( ) I don’t think it is a healthy oil
( ) It’s expensive
( ) It’s hard to find where I live
( ) I don’t want to answer
( ) Other: ____

6. You are:
( ) Female
( ) Male
( ) I don’t want to declare

7. Where do you live?


( ) Brazil
( ) United States
( ) United Kingdom
( ) India
( ) Australia
( ) South Africa
( ) Other
( ) I don’t want to answer

8. How old are you?


( ) Less than 18 years old
( ) Between 18 and 20 years old
( ) Between 20 and 29 years old
( ) Between 30 and 39 years old
( ) Between 40 and 49 years old
( ) Between 50 and 59 years old
( ) Over 60 years old
( ) I don’t want to answer

9. What is your educational level?


( ) Incomplete elementary school
( ) Complete elementary school
( ) Incomplete high school
( ) Complete high school
( ) Incomplete undergraduate
( ) Undergraduate degree
( ) Graduate
( ) I don’t want to answer

10. Do you want to receive the results of this survey? If you accept, we will forward
the results to the email you inform us.
( ) Yes, I would like to receive the results of this survey
( ) I'm not interested in receiving the results of this survey

11. What is your email address?


____

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