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Nutritional Aspects of Palm Oil – An Update
Pramod Khosla, PhD
Associate Professor,
Dept. of Nutrition & Food Science,
Wayne State University,
Detroit, MI 48202
E:mail aa0987@wayne.edu
Dietary Fatty Acids and CHD: Summary of the Evidence
Fatal CHD CHD events
Total Fat C-NR C-NR
TFA P C
SFA/CHO P-NR P-NR
MUFA/SFA
PUFA/SFA C C
Linoleic acid
Alpha Linolenic
n3 LCPUFA P C
Skeaff and Miller , (2009) Ann. Nutr. Metab. 55: 173-201
RISK FACTORS FOR CHD
Gender
Increasing age
Genetics: Family history of CHD
High TC, LDL-C
Low HDL-C
Smoking
Diabetes
Obesity
DIET
Risk calculator
Fat quality
Protein quality
Fiber
Antioxidants
Phytochemicals
Carbohydrate type
Alcohol
http://www.nhlbi.nih.gov/guidelines/cholesterol/index.htmhttp://hp2010.nhlbihin.net/atpiii/calculator.asp?usertype=profhttp://hp2010.nhlbihin.net/atpiii/calculator.asp?usertype=prof
Dietary fat composition: by fatty acid classes
Fatty Acid Classes ,%
SFA
AAD 34%en 15:12:7 P/S 0.4
Coco PKO MilkF CoButt Tallow Pstear Palm POlein Lard Chick Olive hiOsun Canola Soyb Corn Saff
TFA
MUFA
PUFA
PUFA MUFA SFA
Evolution of regression equations predicting the effects of dietary fatty acid classes on serum cholesterol ______________________________________________________________________ Eqn 1 : ∆SC = 2.74∆S - 1.31∆P (Keys et. al., 1957) ∆SC = 2.40∆S - 1.20∆P + 1.5∆C1/2 (Keys et. al., 1965) Eqn 2 : ∆SC = 2.16∆S - 1.65∆P + 0.065∆C (Hegsted et. al., 1965) ∆SC = 2.74∆S - 1.83∆P + 0.071∆C Eqn 3 : ∆SC = 2.16∆S - 0.12∆Mb - 0.60∆P (Mensink & Katan, 1992) Eqn 4 : ∆SC = 2.10∆S - 1.16∆P + 0.067∆C (Hegsted et. al., 1993) Eqn 5 : ∆SC = 2.02∆S - 0.48∆M - 0.96∆P (Yu et. al., 1995) Eqn 6 : ∆SC = 1.90∆S - 0.90∆P + 0.021∆C (Howell et. al., 1997) ______________________________________________________________________ ∆SC denotes the change in serum cholesterol in mg/dL, ∆S denotes changes in %en for all the SFA, ∆S denotes changes in %en for the 12-16 carbon SFA
..but serum cholesterol masks underlying differences in lipoprotein cholesterol
Lipoprotein cholesterol comprises cholesterol in LDL and HDL
Increased LDL-C a risk factor
While increased HDL-C is protective
Ratio of LDL-C/HDL-C or TC/HDL-C far better predictor
Threshold hypothesis
14:0 and 18:2 key factors
14:0 raises TC (linear), 18:2 lowers TC (non-linear)
Threshold level of 18:2 (5-6% en?)
16:0 becomes important as LDLr activity decreased (Hayes & Khosla, (1992), FASEB J., 6, 2600-2607)
More extensive analyses in gerbils (>50 diets)
Confirmed 14:0 and 18:2 key factors
Threshold level of 18:2 (4-5% en?)
16:0 cholesterolemic with increasing depression of LDL receptors
(Pronczuk, Khosla & Hayes, (1994), FASEB J., 8, 1191-1200)
Similar story in hamsters (Hayes, Pronczuk & Khosla, (1995), J. Nutr. Biochem., 6, 188-194)
Problem –is not the presence of SFA per se – rather it is the absence of PUFA
-0.02
0
0.02
0.04
LDL
S
cM
P
tM
So what are the effects of fatty acids classes on lipoprotein cholesterol?
-0.02
0
0.02
0.04
LDL
S
cM
P
tM
0
0.02
0.04
HDL
S
cM
P
tM
-0.04-0.02
00.020.04
TC/HDL
S
cM
P
tM
Changes shown in mmol/L for LDL and HDL. Adapted from Mensink et al Am J Clin Nutr (2003) 77: 1146-1155
MUFA & PUFA best. Trans worse than SFA
So what are the effects of fatty acids classes on lipoprotein cholesterol?
Dietary fats comprised of individual fatty acids – especially important for SFA
Fatty Acid Classes
16:0
AAD 34%en 15:12:7 P/S 0.4
Coco PKO MilkF CoaBut Tallow Pstear Palm pOle Lard Chick Olive hiOsun Canola Soyb Corn Saff
18:0
C18:1
18:2
18:3
t18:1
10:0 6:0+ 8:0
12:0
14:0
16:1
10/25
Effects of individual SFA on lipoprotein cholesterol
-0.020
0.020.040.06
LDL
L
M
P
S
0
0.02
0.04
0.06
HDL
L
M
P
S
-0.04
-0.02
0
0.02
TC/HDL
L
M
P
S
Changes shown in mmol/L for LDL and HDL. Adapted from Mensink et al Am J Clin Nutr (2003) 77: 1146-1155
14:0, 16:0 no effect 18:0, 12:0 beneficial
So what about trans fatty acids?
•Unsaturated fatty acids - at least one trans double bond
•Partial hydrogenation of polyunsaturated oils - isomerization and migration of double bonds - distribution of cis and trans double bonds (margarines, shortenings, salad & cooking oils)
•Partial hydrogenationtFA. Full hydrogenation SFA •Major tFA - elaidic acid (t9 - 18:1) •Dairy and meats have t9 - 16:1 and t11 - 18:1 (vaccenic acid)
TC/HDL-C was adversely affected by the trans diet
a
1 2 3 4 5 6 7 8 9 10 11
TransPalmitate
0
20
40
60
80
100
120
140
-20
-10
0
10
20
% t
ran
sfer (
c.f
. con
trol)
16:0 Trans
p = 0.03
Khosla et al, (1997)
trans lowered HDL-C
trans increased TC/ HDL-C ratio
trans increased CETP
Dietary Fat intake and Risk of CHD and Type II Diabetes (TIID) in Women
CHD data - Hu et al, (1997) N Engl J Med, 337: 1491-1499
Type II Diabetes data - Salmeron et al, (2001) Am J Clin Nutr 73: 1019-1026
Effects of replacing 5%en from carbohydrates with specific fatty acids
Effects of replacing 2%en from carbohydrates with trans fatty acids
-30
-20
-10
0
10
20
30
40
50
60
SFA MUFA PUFA tFA
1
2
3
4
5
from Oh et al (2005) Am J Epidemiol, 161: 672-679
1.6 to 2.8% en 4.1 to 7.4% en 12 to 18% en
Relative risk of CHD based on quintiles of dietary fatty acid intake (Multivariate analyses) 20 year follow-up data from the Nurses Health Study
Beneficial effects with PUFA
Adverse effects with tFA
-40%
-30%
-20%
-10%
0%
10%
20%
30%
40%
50%
LDL1 LDL2 LDL3 LDL4
Sf (flotation rate) 7 - 12 5 - 7 3 - 5 0-5
Dreon et al (1984) Am J Clin Nutr, 67: 828-836
Changes in LDL subfraction mass. Low high fat diets (24% cal 45% cal: SFA 6% cal 18% cal)
-12%
-10%
-8%
-6%
-4%
-2%
0%
2%
Q1 Q2 Q3 Q4
% Calories 3.5 – 7 7.1 – 8.6 8.7 -10.5 10.6 – 16.0
Mozaffarian et al, (2004) Am J Clin Nutr, 80: 1175-1184-1499
Saturated fat intake and Changes in mean minimal Coronary Arterial Diameter in post-menopausal women
Mozaedit.pdf
SFA lower Lp(a) concentrations ?
21
22
23
24
25
26Oleic
Mod Trans
High Trans
Sat
All subjects
mg/d
L
abc
Clevidence et al, (1997) Arterioscler. Thromb. Vasc. Biol. 17, 1657-1661,
n=58
a b
c
If SFA decreased – what should be the replacement?
• Pooled analysis of 11 studies. 4-10 year follow-up
• Pooled RR evaluated in 344, 696 subjects (5, 249 coronary events , 2155 coronary deaths)
• Risk of coronary events decreased when 5% energy from SFA replaced with PUFA not MUFA or carbohydrates
Jakobsen et al , (2009) Am J Clin Nutr 89: 1425 - 1432
Additional meta-analysis showed no significant evidence for concluding SFA increase CHD risk
• 5-23 year follow-up
• Pooled RR evaluated in 347, 747 subjects (11, 006 developed CHD or stroke)
• Pooled RR for CHD – 1.07 (p=0.22)
• Pooled RR for Stroke – 0.81 (p=0.11)
• Pooled RR for CVD – 1.00 (p=0.89)
Siri-Tarino et al , (2010 ) Am J Clin Nutr 91: 535 - 546
Micha and Mozaffarian , (2010 ) Lipids 45: 893-905
Micha and Mozaffarian , (2010 ) Lipids 45: 893-905
Effect of Fatty Acids on CVD: Weight of the
Evidence
D. Mozaffarian, MD, DrPH
10/14/10
Fish n-3 PUFA Plant n-3 PUFA Plant n-6 PUFA MUFA
Saturated Fat
Refined CHO
Trans Fat - Industrial
Benefit
Harm
Alternatives to trans ….
• Animal fats?
• Interesterified fats with high stearic acid?
• Genetically engineered oil crops?
• Other sources of SFA – palm oil ! !
Dietary fats comprised of individual fatty acids – especially important for SFA
Fatty Acid Classes
16:0
AAD 34%en 15:12:7 P/S 0.4
Coco PKO MilkF CoaBut Tallow Pstear Palm pOle Lard Chick Olive hiOsun Canola Soyb Corn Saff
18:0
C18:1
18:2
18:3
t18:1
10:0 6:0+ 8:0
12:0
14:0
16:1
10/25
Dietary fats comprised of individual fatty acids – especially important for SFA
Fatty Acid Classes
16:0
AAD 34%en 15:12:7 P/S 0.4
Coco PKO MilkF CoaBut Tallow Pstear Palm pOle Lard Chick Olive hiOsun Canola Soyb Corn FHSBO
18:0
C18:1
18:2
18:3
t18:1
10:0 6:0+ 8:0
12:0
14:0
16:1
7
5
4-5
4 - 6
4 – 5
4 - 5
20 – 30
80 – 90
55 - 75
60 – 70
5 – 9
15 - 35
Moderator Dennis Bier, M.D.
Professor of Pediatrics, Baylor College of Medicine Participants
Margo A. Denke, M.D. Clinical Professor of Medicine, University of Texas Health Science Center, San Antonio
Joseph Judd, Ph. D. Former Research Leader, Diet and Human Performance Laboratory, Beltsville Human Nutrition
Research Center, USDA Agricultural Research Service Richard O’Brien
Industry Consultant, Author, “Fats and Oils Formulating and Processing for Applications” Fran Seligson, Ph. D.
Independent consultant and Associate Professor in the Nutrition Department at Penn State Howard Weintraub, M.D.
Co-Clinical Director, Lipid Treatment and Research Center, New York University Medical Center, Clinical Associate Professor of Medicine
Trans Fat Replacement Roundtable Statements tcm 8 3649.pdf
0.0
5.0
10.0
15.0
20.0
25.0
30.0
35.0
Soybean
oil
Palm oil Rapeseed
oil
Sunflower
oil
Animal
Fats
Laurics Others
33.3 33.5
16.0
9.7
23.3
7.0
16.6
millio
n to
nn
es
Soybean
40%
Palm
4%
Rapeseed
12%Sunflower
10%
Coconut
4%
Others
30%
Total Area
Soybean29%
Palm 29%
Rapeseed14%
Sunflower8%
Laurics6%
Others14%
Total Vegetable Oil Output
0
1
2
3
4
SBOSunflO RapSO Palm
Tonnes/hectare/year
Soybean oil18%
Palm oil52%
Rapeseed oil3%
Sunflower oil8%
Animal Fats7%
Laurics8%
Others4%
Global Exports
Others
Taiwan
Nigeria
Russia
South Korea
South Africa
Turkey
Japan
Mexico
Bangladesh
Iran
Pakistan
N Africa
India
EU-27
China PR
-20,000 -10,000 0 10,000 20,000 30,000
Net Importers
Net Exporters (x
100
0
ton
nes
) Source: Oil World
Malaysia
“Vitamin A” activity of red palm oilc RE
Per 100 g
Relative quality
(Times
…studies have adopted different methods to provide Vitamin A naturally
Children fed traditional Indian sweets made with redPO
School children fed biscuits baked with redPO
School children given 5 – 10 mL redPO daily
Cooking green leafy vegetables in redPO
Also Vitamin A status improved by feeding redPO to pregnant mothers at various stages of pregnancy.
Also lactating mothers
Numerous human studies showing efficacy of red palm oil in fighting Vitamin A deficiency
RPO.pdf
Comparison of Vitamin E Content of red palm oil & other Vegetable Oils
Oil Tocopherols(ppm)
αT βT γT δT
Tocotrienols(ppm)
αT3 βT3 γT3 δT3
Ppm
T+T3
Red Palm Oil 152 - - - 205 - 439 94 890
Soyabean 101 - 593 264 985
Cornoil 112 50 602 18 782
Groundnut 130 - 216 21 367
Safflower 387 - 174 240 801
Sunflower 487 - 51 8 546
Numerous in vitro studies showing efficacy of tocotrienols in inhibiting breast cancer cell proliferation and decreasing neurodegeneration
F:/Slides/Meetings/Cargill2007/Sylvester.pdfSylvester.pdfF:/Slides/Meetings/Cargill2007/JBCfigs.pptJBCfigs.ppt
• Variety of carotenoids (Vitamin A)
• Vitamin E (tocopherols and tocotrienols)
• …….. Fatty acid composition – replacement for trans Fatty acids
• So what about effects on chronic disease risk
Nutritional attributes of Palm Oil and Palm Olein
FATCHD.ppt
Palm Olein and MUFA-rich Oils exert similar effects on the ratio of Total cholesterol to HDL cholesterol (TC/HDL-C) in human subjects
How much palm oil? Conservative approach -- based on current recommendations for restricting SFA -- can calculate the amount of palm oil in a prudent diet that satisfies various dietary guidelines
Khosla (2006) J Agro Food Ind. 17: 21-23 Hayes and Khosla, Eur J Lipid Sci Tech (2007) 109: 453-464
How would this affect CHD risk?
Has been calculated that based on
1) Changes in plasma lipoproteins, replacing 2%calories from trans FA with saturated fatty acids… would decrease risk by 4%
2) Changes in additional parameters for CHD, besides lipoproteins, replacing 2% calories from trans FA with saturated fatty acids… would decrease risk by 17%
MandW.pdfMandW.pdfMandW.pdf
……. practical aspects
SFA vs tFA– not a realistic comparison
Look at specific fats/oils replacing
PHVO containing tFA
CHD risk based not just on changes
in plasma lipoproteins.
Report of Mozaffarian and Clarke (2009)
is of interest
Also risk assessment papers
(Barraj et al 2008, Mente et al 2009)
MozaClark.pdfRA1.pdfMente.pdf
Summary
Fat Quality is more important than fat quantity
Consensus on transFA and n3 PUFA effects
Trans FA replacement with SFA, CHD risk improves. Further improvement with MUFA and PUFA
Saturated fatty acids per se – need to rethink
Palm Oil – serves a multitude of nutritional needs
Supply of palm oil makes it the important player globally
Fatty acid profile of palm eliminates need for hydrogenation
Minor components help alleviate micronutrient deficiencies using food-based approach
For more details: J. Am. Coll. Nutr. (2010), 29 (3S) 237-340
Department of Nutrition.pdfAIntros.pdfAIntros.pdfAIntros.pdfRecommended