Transcript How does coconut oil impact blood lipids?

How does coconut oil
impact blood lipids?
Stephen Alajajian, LDN, CLC, Dietetic Intern
Presentation Outline
Health claims about coconut oil
Polynesian populations
Composition of coconut oil
Properties of medium-chain triglycerides
How does coconut oil impact blood lipid levels?
Study 1: hypothesis, methods, results
Study 2: “
Study 3: “
Summary of Results
Discussion and conclusions
What are the health benefits of coconut oil?
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Treats drug resistant epilepsy in children
Treats Alzheimer's disease
Increases your resting metabolism
Helps you burn more fat
Kills bacteria, viruses and fungi
Kills your hunger
Improves cholesterol levels
Lowers risk of heart disease
Protects hair against damage
Moisturizes skin
Blocks ultraviolet rays
Helps you lose weight
Cures all diseases
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Coconut oil and heart health in Polynesian
populations
A study published in 1981
in the AJCN showed that in
two Polynesian populations
receiving the majority of
their caloric energy from
coconut, the group that ate
significantly more coconut
(63% of energy vs 34% of
energy), total serum
cholesterol levels were
raised significantly higher.
However, both groups had
the same very low incidence
of cardiovascular disease.
What is the composition of coconut oil?
 92% saturated fat
 6% monounsaturated
 2% polyunsaturated
 About 63% medium chain fatty
acids (mainly as lauric acid 12:0),
30% long chain saturated fatty
acids (mainly myristic acid 14:0
and palmitic acid 16:0) and 7%
long chain unsaturated fatty
acids
Medium Chain Fatty Acids
 Chain length is 6 to 12 carbon units (sometimes defined as 6 to
10)
 More water soluble than long-chain fatty acids
 Lauric acid, 12 carbons in length, may exhibit some properties of
MCFAs and LCFAs
 Indicated for fat malabsorption (IBD, pancreatitis, cystic fibrosis,
Celiac disease, cholestatic liver disease) because absorption can
occur without bile or pancreatic lipase
 Unlike LCFAs, MCFAs go directly to the liver (bound to albumin)
via the portal vein along with sugars and amino acids (for this
reason, effective for chylous effusions)
 In liver, rapidly oxidized to 2-carbon fragments which become
available for various metabolic pathways including ketone body
production
 Hypothesized to be “fat burning” due to their preferential
oxidation in mitochondria and thermogenic nature (hypothesized
to be due to their inefficient conversion to longer chain fatty
acids for storage)
Research Question: How does coconut oil
impact blood lipids?
RELATED QUESTIONS
Does the quality of the oil matter? It is claimed that virgin
coconut oil is higher in medium-chain fatty acids such as
caprylic acid (8:0).
How are lipids affected when coconut oil is added to the
diet vs. when they are replacing other fats?
Research into these questions has been limited.
Study#1: “An open label pilot study to assess the efficacy
and safety of virgin coconut oil in reducing visceral
adiposity”
ISRN Pharmacology (2011)
Purpose: to examine the effects of daily coconut oil
supplementation on visceral adiposity in overweight Malay
volunteers
Study#1: Methods
Inclusion
BMI > 23 (Asia-Pacfiic
Report on Obesity
definition of
overweight)
Age > 20 years old
Exclusion
Medical or surgical
illness
Pregnancy
Alcohol consumption
Previous history
intolerance to coconut
oil
Study#1: Methods
 20 subjects
 No control group (pilot study)
 Intervention: 30ml (~30g) virgin coconut oil, taken in 3
divided doses, ½ hour before each meal
 Supplemented for 6 weeks
 Outcome variables: anthros (FM, FFM, waist circumference,
lipid profiles (TG, TC, HDL, LDL), safety eval (electrolytes,
glucose, renal and liver function labs)
 Participants asked to keep same PA levels and dietary
pattern they reported on initial evaluation
Study#1: Results
Baseline
6 weeks
P value
Triglycerides (mmol/L)
1.36
1.22
P=0.28
Total cholesterol
(mmol/L)
5.46
5.35
P=0.53
LDL (mmol/L)
3.33
3.25
P=0.7
HDL (mmol/L)
1.52
1.55
P=0.79
Waist circumference
102.64
99.78
P=0.002
(cm) 5.46mmol/L corresponds to about 210mg/dL; 1.52mmol/L corresponds to about 58mg/dL
Note:
Study#1: Limitations
 No control group
 Short duration of study
 Small group size
Study#2 “Effects of Dietary Coconut Oil on the
Biochemical and Anthropometric Profiles of Women
Presenting Abdominal Obesity”
Lipids (2009)
Purpose: to examine the effects of soybean oil vs. coconut
oil supplementation on adiposity and blood lipid levels in
low-income Brazilian women
Study#2: Methods
Inclusion:
20-40 year olds
Low socioeconomic
status < $1/day
Abdominal obesity
Waist circumference >
88cm
Exclusion:
Pregnancy
Arterial HTN
BMI > 35
Chronic degenerative
disease
Endocrinopathies
Study#2: Methods
 Double blind randomization into two groups (n=20
each) paired according to BMI
 Intervention: coconut oil or soybean oil for 12 weeks
(30ml or ~30g)
 Both groups given diet instruction by nutritionist
 Patients advised to drink adequate water and reduce
alcohol/smoking
 4 days/week PA program with fitness trainer
 Coconut oil used: filtered and pressed from dehydrated
coconut pulp at 60 degrees C
Study#2: Outcome Measures
 Anthropometrics: waist circumference and BMI
 Biochemical evaluation: glucose, triglycerides, total
cholesterol, LDL, HDL, HOMA-B% (secretary function
of B-cells) and HOMA-S (insulin resistance marker)
Study#2: Results
Coconut Oil (start to finish)
Soybean Oil (start to finish)
BMI (kg/m^2)
-0.5 (significant)
-0.4
Waist circumference (cm)
-1.4 (significant)
+0.6
Total cholesterol (mg/dL)
+5.6
+19.8 (significant)
LDL (mg/dL)
+3.9
+25.5 (significant)
LDL:HDL
-0.1
+0.9 (significant)
HDL (mg/dL)
+3.2
-6.5 (significant)
Statistical significance defined as P < 0.05 (refers to a significant change from baseline)
TG (mg/dL)
+6.9
+1.0
Study#2: Limitations
 Study is limited to a specific group of low-income
women in Brazil
 2 interventions (diet instruction and oil) – What would
the effect have been with no diet instruction?
 According to the researchers, the participants eat diet
richer in carbs (~70%) than most Western populations,
making them more prone to adaptations that increase
lipogenesis. Thus results may not extrapolate as well to
other populations.
Study#3 “Diets high in palmitic acid (16:0), lauric and
myristic acids (12:0 + 14:0) or oleic acid (18:1) do not
alter postprandial or fasting plasma homocysteine and
inflammatory markers in healthy Malaysian adults”
American Journal of Clinical Nutrition (2011)
Purpose: to examine the effects of supplementation with
coconut oil, palm oil and olive oil on plasma homocysteine
and inflammatory markers in healthy Malaysian subjects
Study#3: Methods
Inclusion Criteria:
BMI 18-29 kg/m^2, “healthy”
Exclusion Criteria:
DM, CAD, cancer, liver disease, renal disease, blood
dyscrasia, HTN, plasma total cholesterol > 7.8mmol/L
(300mg/dL), pregnancy, chronic smokers, alcoholics
Study#3: Methods
 3x3 Latin-square design
 N= 45 (15 per group)
 Subjects randomly assigned to each group to balance
baseline homocysteine, sex, fasting triglycerides
 3-week standardization diet (30% fat, 15% protein, 55%
carb)
 Test fats each contributed 2/3 of dietary fat in a diet that
was 30% fat, 20% protein, 50% carb
Study#3: Methods (continued)
 Detailed instructions given on menu-planning and
portion size
 3 meals per day provided
 5-week dietary periods
 Test fat was provided as cooking oil to the subjects
 Subjects blind, investigators not blind
Study#3: Outcome Measures
 Blood samples collected on 2nd week of standard diet,
on 4th and 5th weeks of each dietary period
 Outcome measures: serum total cholesterol, HDL, LDL,
triglyceride, apoA-100, apo B1, Lp(a), hsCRP, tHcy
(homocysteine), IL-6, IL-1B, IL-8, IFN-y, TNF-a
Study 3: Results (P<0.05)
Palm Oil
Olive Oil
Coconut Oil
Total cholesterol
(mmol/L)
NS
(-) relative to CO
(+) relative to OO
HDL (mmol/L)
NS
(-) relative to CO
(+) relative to OO
LDL (mmol/L)
NS
(-) relative to CO
(+) relative to OO
Triglyceride
(mmol/L)
NS
NS
NS
TC:HDL
NS
NS
NS
tHcy (micromol/L)
NS
NS
NS
Study#3: Limitations
 Short duration (5 week intervention)
 Possible that the standardization diet was not long enough
in duration to “clean the slate” prior to each intervention
(question whether study design may have contributed to
null hypothesis)
 Unclear what kind of coconut oil was used in the study
 Researchers mention a possible weakness: 18:2 (linoleic
acid) was not standardized across all diets
Summary of Results
Study#1:
30ml/day of virgin coconut (no control)
n = 20 (only 1 group)
5 week duration
No diet or PA instruction
No significant differences in TC, LDL, HDL,
TG
Study#2:
30ml/day coconut oil or soybean oil in lowincome Brazilian women
n = 40 (20 per group)
Diet instruction given
12 week duration
No significant changes in lipid markers
with coconut oil.
Study#3:
3x3 study design (coconut oil, palm oil,
virgin olive oil)
N=45 (15 per group)
Diet instruction given
20% of kcal from each intervention oil
5 week duration of each study period
Only statistically significant differences
found between coconut oil and olive oil.
Increased TC, LDL, LDL:HDL and
decreased HDL with soybean oil.
Increased total cholesterol, HDL and LDL
with coconut oil compared to olive oil.
What do you think?
 What do you take away from all these
studies collectively?
 What effect do you think coconut oil
has when simply added to the diet?
 What effect does it have when
replacing or compared to other oils
and fats?
 Does virgin matter?
 What do you think of the claim
sometimes made that higher LDL
levels are not necessarily bad (i.e.
Polynesian studies)?
Center for Science in the Public Interest
Studies looking at the effect of coconut oil—virgin or conventional—on heart disease in
humans are scarce.
In the only study done in people in the last 17 years, Malaysian researchers last year found
that when they fed young men and women 20 percent of their calories from coconut oil for
five weeks, LDL ("bad") cholesterol was 8 percent higher and HDL ("good") cholesterol was
7 percent higher than when the participants were fed 20 percent of their calories from olive
oil.5 (The researchers didn’t respond to inquiries about whether they used virgin or
conventional coconut oil.)
But just because HDL went up along with LDL doesn't mean that coconut oil is healthy,
points out Frank Sacks, professor of cardiovascular disease prevention at the Harvard School
of Public Health in Boston. "We know that raising LDL levels increases the risk of heart
disease," he notes, "but we can't say that raising HDL with diet or drugs can lower the risk
of cardiovascular disease."
Sacks' bottom line: "Since polyunsaturated oils lower LDLs and coconut oil raises LDLs, we
can't recommend that people replace olive, canola, or other liquid oils with coconut oil."
What does the Academy’s Evidence Analysis
Library (EAL) have to say?
Thanks for tuning in
 Any questions?
What are your thoughts on these results?
 Are you surprised that there were
statistically significant undesirable changes
to lipid profiles with soybean oil but not
coconut oil?
 What are some possible explanations?
 Would there be statistically significant
changes from baseline with coconut oil if
there were no dietary intervention?
 What do you think of the waist
circumference result – was it the coconut
oil or dietary intervention?
References:
Ascherio A and Willett WC. Health effects of trans fatty acids. Am J Clin Nutr. 1997;66: 1006S-1010S.
Assuncao M, Ferreira H, dos Santos AF, Cabral CR, Forencio M. Effects of Dietary Coconut Oil on the Biochemical and Anthropometric
Profiles of Women Presenting Abdominal Obesity. Lipids. 2009;44: 493-601.
Fatty acid composition of fats and oils. University of Colorado: Colorado Springs. 2007.
http://www.uccs.edu/Documents/danderso/fats_oils.pdf. Accessed February 12, 2016.
Gracey M, Burke V, and Anderson CM. Medium chain triglycerides in pediatric practice. Arch Dis Child. 1970;45: 445-452.
Jandacek RJ. Structured Lipids: An Overview and Comments on Performance Enhancement Potential. In: Food Components to Enhance
Performance: An Evaluation of Potential Performance-Enhancing Food Components for Operational Rations. Washington, DC: Institute of
Medicine (US) Committee on Military Nutrition Research; 1994.
Liau KM, Lee YY, Chen CK, Rasool AH. An Open-Label Pilot Sutdy to Assess the efficacy and safety of virgin coconut oil in reduicng
visceral adiposity. ISRN Pharmacol. 2011;2011:949686.
Prior IA, Davidson F, Salmond CE, Czochanska Z. Cholesterol, coconuts, and diet on Polynesian atolls: a natural experiment: the Pukapuka
and Tokelau island studies. Am J Clin Nutr. 34: 1552-1561.
Roy HJ. Coconut Oil: Health effects. Pennington Biomedical Research Center. 2013. https://www.pbrc.edu/training-andeducation/ppt/Coconut_Oil.pptx. Accessed February 12, 2016.
Schardt, David. "Coconut Oil." NutritionAction: Health Letter, Center for Science in the Public Interest. 2012.
http://www.cspinet.org/nah/articles/coconut-oil.html. Accessed February 1, 2016.
Voon PT, Ng TKW, Lee VKM, Nesaretnam K. Diets high in palmitic acid (16:0), lauric and myristic acids (12:0 + 14:0), or oleic acid (18:1)
do not alter postprandial or fasting plasma homocysteine and inflammatory markers in healthy Malaysian adults. Am J Clin Nutr.
2011;94:1451-1457.