LPIDOS

LPIDOS
Lpidos son compuestos orgnicos insolubles en
agua, pero solubles en solventes orgnicos (ej:
benzeno)
Ejemplos de Lpidos:

Grasas = Acilgliceroles
Grasas son lpidos, pero no
todos los lpidos son
grasas

1.

cidos grasos

2.

Acilgliceroles (grasas)

3.

Fosfolpidos

4.

Esfingolpidos

5.

Cetonas

6.

Colesterol

7.

cidos Biliares

8.

Hormonas esteroides

9.

Lipoprotenas plasmticas

10.

Prostaglandinas
~50 Lpidos en los tejidos humanos
Cordain, 2006

GRASAS

ACILGLICEROLES PUEDEN
TENER:
1 cido graso (acil):
monoacilglicerol o monoglicridos
2 cidos grasos (acil): dacilglicerol
o diglicridos
3 cidos grasos (acil): Triacilglicerol
o Triglicridos

Erasmus U. Fats that heal, fats that kill. Alive Books 1993

CIDOS GRASOS
Insolubles en agua
C-H insoluble
Membranas celulares
Reservas energticas
Precursores de
eicosanoides
Regulan la expresin
gnica (PPAR, SREBP)

Stipanuk. MH. Biochenical, Physiological, Molecular aspects of Human Nutrition. Saunders, 2006
de las UN. Essential fatty acids-a review. Current Pharmaceutical Biotechnology, 2006, 7, 467-482

omega
(Metil)

Carboxil

Apolar

Polar

Hecha
integramente
de tomos de
carbono e
hidrgeno

Hidrofbica

Erasmus U. Fats that heal, fats that kill. Alive Books 1993

Hidroflico

LONGITUD DE LA CADENA

tomos de carbono se cuentan del

hidroxilo al metilo (omega)

11
H 3C

12

9
10

7
8

5
6

3
4

COOH

Stipanuk. MH. Biochenical, Physiological, Molecular aspects of Human Nutrition. Saunders, 2006

Cadena corta: 4-6 carbonos

Cadena media: 8-12 carbonos
Cadena larga: 14-20 carbonos
Cadena muy larga: 22+ carbonos

Omega
(Grupo Metil)
12

HHHHH HHHHHH O
1
I I I I I I I I I I I II
H-C-C-C-C-C-C-C-C-C-C-C-C-OH Grupo Carboxil
I I I I I I I I I I I I
H HHHHHHH HHHH
Mataix J. Nutricin y Alimentacin Humana Tomo I: Nutrientes y Alimentos. Ergon, 2002.

UNIONES
Cada tomo de carbono tiene 4 uniones

Omega
(Grupo Metil)

HHHHH HHHHHH O
I I I I I I I I I I I II
H-C-C-C-C-C-C-C-C-C-C-C-C-OH
I I I I I I I I I I I I
H HHHHHHH HHHH

Grupo Carboxil

Mataix J. Nutricin y Alimentacin Humana Tomo I: Nutrientes y Alimentos. Ergon, 2002.

TIPOS DE CIDOS GRASOS

AG SATURADOS

No contienen uniones dobles entre tomos de carbono

(estn saturados con tomos de hidrgeno)
Sin uniones dobles
Ex: cido Lurico = 12:0
Longitud: 12 carbonos

Omega
(metil)

HHHHH HHHHHH O
I I I I I I I I I I I II
H-C-C-C-C-C-C-C-C-C-C-C-C-OH
I I I I I I I I I I I I
H HHHHHHH HHHH

Cordain, 2006

Carboxil

11

Erasmus U. Fats that heal, fats that kill. Alive Books 1993

12

AG MONOINSATURADOS

Contienen 1 unin doble entre tomos de carbono

1 unin doble
9 carbonos a partir del omega

cido Oleico = 18:1n-9

longitud: 18 carbonos
HHHHH HHHHH H HHHHHHO
I I I I I I I I I I I I I I I I I II
Omega
(metil) H-C-C-C-C-C-C-C-C-C=C-C-C-C-C-C-C-C-C -OH
I I I I I I I I
I I I I I I I
H HHHHHHH
HHHH HHH
Cordain, 2006

Carboxil

13

Erasmus U. Fats that heal, fats that kill. Alive Books 1993

14

Erasmus U. Fats that heal, fats that kill. Alive Books 1993

15

CIDO OLEICO (18:1n9 cis)

16

CIDO TRANS ELADICO (18:1n9 trans)

17

AG POLINSATURADOS

AG Polinsaturados Omega 6
Esencial

2 uniones dobles
Primera unin doble de 6
carbonos contando desde el
Omega
longitud: 18 carbonos

cido Linoleico = 18:2n-6

HHHHH HHHH H HHH HHHHO

I I I I I I I I I I I I I I I I I II
Omega
(metil) H-C-C-C-C-C-C=C-C-C=C-C-C-C-C-C-C-C-C -OH
I I I I I
I
I I I I I I I
H HHHH
H
HHHH HHH
Cordain, 2006

Carboxil

18

AG Polinsaturados Omega 3

3 uniones dobles
Primera unin doble de 3
carbonos contando desde el
Omega
Longitud: 18 carbonos

cido Linolnico = 18:3n-3

Esencial

HHH HH HHHH H HHH HHHHO

I I I I I I I I I I I I I I I I I II
Omega
Carboxil
H-C-C-C=C-C-C=C-C-C=C-C-C-C-C-C-C-C-C
-OH
(metil)
I I
I
I
I I I I I I I
H H
H
H
HHHH HHH
Cordain, 2006

19

TRANSPORTADOS EN PLASMA POR LIPOPROTENAS

Erasmus U. Fats that heal, fats that kill. Alive Books 1993

23

LDL

Mataix J. Nutricin y Alimentacin Humana Tomo I: Nutrientes y Alimentos. Ergon, 2002.

25

Essential Properties of a Living Cell

25

hilic
d
p

lipid

kind

hed
erol.

Hydrophilic region
Hydrophobic
region

Hydrophilic region

FIGURE 2.03

Integral
protein

Integral
protein

Surface
protein

A Biological Membrane

A biological membrane is formed by phospholipid and protein. The phospholipid layers are oriented
with their hydrophobic tails inward and their hydrophilic heads outward. Proteins may be within the
membrane (integral) or lying on the membrane surfaces.

CIDOS GRASOS EN LAS MEMBRANAS

Citosol

27

Fluido
Extracelular

2 AG + 1 GRUPO FOSFATO LIGADO A 1 GLICEROL

28

MEMBRANA:
Colesterol, Protenas, Hidratos de Carbono, Fosfolpidos,

Fluidez

33

70

Digestion and Intestinal Absorption

Pancreatic lipase

Triacylglycerols

Lipid droplet
Fatty acids

Bile acids and salts

2-Monoacylglycerols

Mixed micelle
Brush border membrane

Transporters (see legend)

2-Monoacylglycerol
Fatty acids
1,2-Diacylglycerol

Cholesterol

Triacylglycerol

Apolipoprotein B,
phospholipids

Chylomicrons

Lacteal
(lymphatic)

Figure 3.6 Lipid digestion and absorption in the small intestine. Fatty acids and cholesterol enter the mucosal cells mainly by facilitated diffusion (Sections 2.2.1.3 and 3.3.3). Within the

Chylomicrons
(via lymphatics)

Insulin
+
LPL

Insulin
+
TAG
Adipose tissue

Muscle
TAG
Small intestine

LPL

CO

Figure 7.12 The pattern of plasma triacylglycerol metabolism after a breakfast

containing both fat and carbohydrate. Triacylglycerol (TAG) enters the circulation in the form
of chylomicron particles and is hydrolyzed by the enzyme lipoprotein lipase (LPL) in the capillaries
of tissues (see Figure 5.17 for more details of this process).
Frayn KN. Metabolic Regulation. Blackwell Pub; 2010:384.

Capillary

Chylomicron
TAG

TAG
Fatty acids

TAG

VLDL

Lipoprotein
lipase
Endothelial cells

TAG

Adipocytes

Figure 5.17 The action of lipoprotein lipase in white adipose tissue. Lipoprotein lipase
is attached to the branching glycosamino-glycan chains that form the glycocalyx (a fuzzy surface
lining the capillary, attached to the endothelial cells). It acts on lipoprotein particles in the capillaries
which contain triacylglycerol (TAG), hydrolyzing this TAG to release fatty acids which are taken up
KN. Metabolic
Blackwell than
Pub; 2010:384.
into adipocytes and re-esterified for Frayn
storage
as Regulation.
TAG. More
one molecule of the enzyme acts on
a lipoprotein particle at once.

Lipoprotein particles
(chylomicrons, VLDL)

WHITE ADIPOSE TISSUE

TAG
Insulin
TAG
+
LPL

Fatty acids
Insulin
+
Lipogenesis

Insulin +
Glucose

Insulin
+
Esterification

TAG

Lipases
+ Adrenaline
Insulin - + Noradrenaline
Glycerol 3-P
? + Glucagon
Fatty acids
Glycerol

GLUT4

Fat storage

Albumin
Fatty acids

Glycerol

Fat mobilisation

Figure 5.16 Overview of fatty acid and glucose metabolism in white adipose tissue. The bodys main store of chemical energy is in the form of triacylglycerol (TAG) in white adipose
tissue. Fat storage is the process of deposition of TAG; fat mobilization (or lipolysis) is the process
of hydrolysis of the stored TAG to release non-esterified fatty acids into the plasma (bound to the
Frayn KN. Metabolic Regulation. Blackwell Pub; 2010:384.
carrier protein albumin), so that they can be taken up by other tissues. LPL, lipoprotein lipase; glycerol
3-P, glycerol 3-phosphate; VLDL, very-low-density lipoprotein. The major pathways and main sites of

108

Organs and Tissues

Fatty acids

Fatty acids
Lipogenesis

Malonyl-CoA
ACC

Glucose

Insulin +

ACS

Fatty acyl-CoA

-+

CPT-1

+
Insulin

Triacylglycerol
Phospholipids

Glucagon

Insulin +

GLUT2

Glycerol 3-P

CoASH

Fatty acid
transporter

CO 2

-oxidation
CO2

Ketone
bodies

Acetyl-CoA

Ketone
bodies

(via PDH in mitochondrion)

Frayn KN. Metabolic Regulation. Blackwell Pub; 2010:384.

Figure 5.4 Overview of fatty acid metabolism in the liver. Fatty acids cross the hepatocyte membrane mainly by a carrier-mediated process (Table 2.4, p. 40). Inside the liver cell they are
transported through the cytosol by binding to specific fatty acid binding proteins, and activated by

CO
2
Ketone bodies

TAG
(VLDL)

Glucose
Liver

CO2
Renal cortex
and other oxidative tissues

NEFA
Glycerol

TAG

NEFA

Adipose tissue
Muscle
NEFA

CO2
Frayn KN. Metabolic Regulation. Blackwell Pub; 2010:384.

Figure 7.9 The pattern of non-esterified fatty acid (NEFA) metabolism after an

Lipoprotein particles
(chylomicrons, VLDL)

WHITE ADIPOSE TISSUE

TAG
Insulin
TAG
+
LPL

Fatty acids
Insulin
+
Lipogenesis

Insulin +
Glucose

Insulin
+
Esterification

TAG

Lipases
+ Adrenaline
Insulin - + Noradrenaline
Glycerol 3-P
? + Glucagon
Fatty acids
Glycerol

GLUT4

Fat storage

Albumin
Fatty acids

Glycerol

Fat mobilisation

Figure 5.16 Overview of fatty acid and glucose metabolism in white adipose tissue. The bodys main store of chemical energy is in the form of triacylglycerol (TAG) in white adipose
tissue. Fat storage is the process of deposition of TAG; fat mobilization (or lipolysis) is the process
of hydrolysis of the stored TAG to release non-esterified fatty acids into the plasma (bound to the
Frayn KN. Metabolic Regulation. Blackwell Pub; 2010:384.
carrier protein albumin), so that they can be taken up by other tissues. LPL, lipoprotein lipase; glycerol
3-P, glycerol 3-phosphate; VLDL, very-low-density lipoprotein. The major pathways and main sites of

ACTIVATION
Adrenaline

GTP
GDP

Glucagon

Adenylyl
cyclase

-Adrenergic
receptor

Gs

ATP

ATP

INHIBITION
Insulin
Glucagon
receptor

Gs

Insulin
receptor

GTP

cAMP

PKA

GDP

Phosphodiesterase

Protein
phosphatases

ADP
HSL
active

HSL
inactive
TAG
ATGL

DAG

Fatty acid

via PI3 kinase

and PKB
AMP

MAG
lipase

MAG

Pi

HSL
inactive
Fatty acid
+
glycerol

Fatty acid

Figure 2.4.3 Signal chain for

control of hormone-sensitive lipase in adipocytes. HormoneFrayn KN. Metabolic Regulation. Blackwell Pub; 2010:384.
sensitive lipase (HSL) is one of the enzymes responsible for regulation of breakdown of triacyl-

108

Organs and Tissues

Fatty acids

Fatty acids
Lipogenesis

Malonyl-CoA
ACC

Glucose

Insulin +

ACS

Fatty acyl-CoA

-+

CPT-1

+
Insulin

Triacylglycerol
Phospholipids

Glucagon

Insulin +

GLUT2

Glycerol 3-P

CoASH

Fatty acid
transporter

CO 2

-oxidation
CO2

Ketone
bodies

Acetyl-CoA

Ketone
bodies

(via PDH in mitochondrion)

Frayn KN. Metabolic Regulation. Blackwell Pub; 2010:384.

Figure 5.4 Overview of fatty acid metabolism in the liver. Fatty acids cross the hepatocyte membrane mainly by a carrier-mediated process (Table 2.4, p. 40). Inside the liver cell they are
transported through the cytosol by binding to specific fatty acid binding proteins, and activated by

 -Oxidation
Oxaloacetate
2 Acetyl-CoA
Acetyl-CoA
Citrate synthase
acetyltransferase
Citrate
Acetoacetyl-CoA
TCA cycle
AcetylCoA

HMG-CoA synthase

CO2

HMG-CoA
HMG-CoA lyase

Acetone
CO2

Acetoacetate
NADH

3-Hydroxybutyrate
NAD+

The pathway of ketone body formation from acetyl-CoA (ke

Frayn KN. Metabolic Regulation. Blackwell Pub; 2010:384.

Brain

CO2
Muscle
CO2

Glucose

Protein

Alanine

Glutamine

Ketone bodies

Liver

Red blood cells,

renal medulla,
etc

Lactate
Glycerol
Alanine

Kidney

Fatty acids
CO2

TAG
Adipose tissue

NH3

Glucose

Figure 9.6 Major fuel flows in prolonged starvation. Protein (especially that in muscle)
and glycerol from triacylglycerol in
adipose
tissue
are
the Pub;
only
long-term sources of glucose. The
Frayn
KN. Metabolic
Regulation.
Blackwell
2010:384.
complete oxidation of glucose is reduced by the production of ketone bodies, which serve as an

COLESTEROL
Componente exclusivo
de las clulas
animales
Funciones:

Mantenimiento de la fluidez de la membrana

(cuanto +, > rigidez)

Precursor de los cidos biliares, de las hormonas

esteroides, del cortisol y de la Vitamina D.

Mataix J. Nutricin y Alimentacin Humana Tomo I: Nutrientes y Alimentos. Ergon, 2002.

50

51

Mataix J. Nutricin y Alimentacin Humana Tomo I: Nutrientes y Alimentos. Ergon, 2002.

Produccin Endgena

Colesterol

Alimentos

Mataix J. Nutricin y Alimentacin Humana Tomo I: Nutrientes y Alimentos. Ergon, 2002.

52

TRANSPORTADO EN PLASMA POR DIVERSAS LIPOPROTENAS

Erasmus U. Fats that heal, fats that kill. Alive Books 1993

53

Surface lipids

Free cholesterol
Phospholipid
Protein

Core lipids

Cholesteryl ester
Triacylglycerol

c by perFigure 10.1 A typical lipoprotein particle. Reproduced from Durringon (2007), !

Liver
TAG Apo B100

Direct re-uptake of
some VLDL particles

HDL
Apo CII

VLDL
particles

LPL
action

FA

FA

LDL
particles
LDL receptor

"Tissues"

Figure 10.3 The endogenous pathway of lipoprotein metabolism. Particles may undergo several cycles of hydrolysis by lipoprotein lipase (LPL) in capillary beds (dashed lines), forming

tunities for exchange). When the plasma concentration of triacylglycerol is high, especially when this reflects large numbers of VLDL particles present, CETP will catalyze

Forward cholesterol transport

VLDL, LDL particles

LDL
Receptor
Synthesis

CE

CE

ABC-A1

FC

CETP

FC
Tissues

LDL
Receptor

HDL particles

SR-BI

CE

Liver

Bile acids,
cholesterol

Reverse cholesterol transport

Figure 10.5 Forward and reverse cholesterol transport. Cholesterol is secreted by the
liver in VLDL particles; these become LDL particles after hydrolysis of their triacylglycerol by lipoprotein
lipase and hepatic lipase (Figure 10.3) and are taken up by tissues via the LDL receptor. A proportion

COLESTEROL Y SALUD

http://www.webmd.com/heart-disease/
video/atherosclerosis
"

COLESTEROL DIETTICO

Cuanto > cantidad de colesterol en los

alimentos, ms difcil se produce su absorcin
intestinal.
El colesterol absorbido inhibe la sntesis
heptica de nuevas molculas de colesterol.

Mataix J. Nutricin y Alimentacin Humana Tomo I: Nutrientes y Alimentos. Ergon, 2002.

64

Mataix J. Nutricin y Alimentacin Humana Tomo I: Nutrientes y Alimentos. Ergon, 2002.

EFECTOS A CORTO PLAZO

Incremento de 100 mg/d de colesterol diettico aument:

CT en 0.056 mmol/l (2.2 mg/dl)
C- HDL en 0.008 mmol/l (0.3 mg/dl).
Okuyama H, et al. World Rev Nutr Diet. 2007;96:1-17.

66

EFECTOS A LARGO PLAZO

Datos del US National Health and Nutritional Survey (19841994)

Okuyama H, et al. World Rev Nutr Diet. 2007;96:1-17.

67

37.851 H durante 8 aos

80.082 M durante 14 aos

Okuyama H, et al. World Rev Nutr Diet. 2007;96:1-17.

68

Se estima que al menos

el 30% de la poblacin
es susceptible al
colesterol diettico.

Mataix J. Nutricin y Alimentacin Humana Tomo I: Nutrientes y Alimentos. Ergon, 2002.

Matthan NR et al. Arterioscler Thromb Vasc Biol. 2004 Jun;24(6):1092-7

69

GRASAS DIETTICAS Y SALUD

Mensink RP, Zock PL, Kester AD, Katan MB. Am J Clin Nutr. 2003 May;77(5):1146-55

CIDOS GRASOS SATURADOS

American Heart Association:
< 10% del total calrico
USDA, 2010: < 10% del total calrico

CHINA RURAL: < 5%

KITAVA: 17%

EUA: 11-12%

MAASAI: 30-35%

CRS: 4-18%

TOKELAU: 49%

Mensink RP, Zock PL, Kester AD, Katan MB. Am J Clin Nutr. 2003 May;77(5):1146-55

SAFA EN ALGUNOS ALIMENTOS

75

Alimento
(100 g)

AG Saturados
(g)

AG
Larico
12:0 (g)

AG
Mirstico
14:0 (g)

AG
Palmitico
16:0 (g)

AG
Esterico
18:0 (g)

Mantequilla

51

10

Aceite de
Coco

86,5

44,6

16,8

8,2

2,8

Cacao

8,07

0,02

3,69

4,25

Aceite de
palma

49,3

0,1

43,496

4,3

Leche entera

1,865

0,077

0,297

0,829

0,365

USDA food database

AC. LURICO, MIRSTICO Y PALMTICO

Normal

Hgado

LDL

VLDL

TAG

Hiper-Colesterolenia
Familiar

IDL

LDL
TAG

VLDL

Disminuyen la expresin
del gen del receptor de
LDL

IDL
12:0, 14:0, 16:0

SAFA

LDL
VLDL
TAG
IDL

76

Cordain, 2009

larger effect of changes in the amount and quality of dieta

and carbohydrates on CAD risk (89), and the possible reaso
this were discussed elsewhere (90, 91).

Effects of fatty acids and carbohydrates on serum lipid

lipoproteins

Our results suggest that isoenergetic replacement of SFA

carbohydrates does not improve the serum total:HDL chole
All natural fats contain both SFAs, which do not change this
and unsaturated fatty acids, which lower it. As a result, ev
replacement of dairy fat and tropical fats with carbohydrate

Mensink RP, Zock PL, Kester AD, Katan MB. Am J Clin Nutr. 2003 May;77(5):1146-55

FIGURE 3. Predicted changes (!) in the ratio of serum total t

Cordain, 2009

LDL PEQUEAS Y DENSAS

1.
2.

Flujo de LDL hacia la ntima es > para LDL pequeas y densas

Una vez en la ntima, LDL pequeas y densas son susceptibles a sufrir
oxidacin

3. Carga Glicmica de la Dieta y Fructosa son causas

de LDL pequeas y densas

78

Meta-anlisis de estudios epidemiolgicos

prospectivos demuestran que no hay evidencia
significativa para concluir que los cidos
grasos saturados estn asociados con un mayor
riesgo de ECV "

See corresponding editorial on page 1541.

Intake of carbohydrates compared with intake of saturated fatty acids

and risk of myocardial infarction: importance of the glycemic index13
Marianne U Jakobsen, Claus Dethlefsen, Albert M Joensen, Jakob Stegger, Anne Tjnneland, Erik B Schmidt,
and Kim Overvad

INTRODUCTION

Epidemiologic prospective cohort studies have suggested that

replacing saturated fatty acids (SFAs) with carbohydrates is
modestly associated with a higher risk of ischemic heart disease

concentration is tightly regulated by homeostatic regulatory

systems, but the rapid absorption of carbohydrates after consumption of a high-GI meal challenges these homeostatic
mechanisms (4). A high-GI meal results in a high blood glucose
concentration and a high insulin-to-glucagon ratio, followed by
hypoglycemia, counterregulatory hormone secretion, and elevated plasma free fatty acid concentration (4). These events may
affect the risk of IHD through promoting dyslipidemia, inflammation, and endothelial dysfunction (4).
The aim of this study was to investigate the risk of myocardial
infarction (MI) with a higher energy intake from carbohydrates
and a concomitant lower energy intake from SFAs. Carbohydrates
with different GI values were investigated. Furthermore, potential
effect modification by sex was investigated because of differences
in the underlying biology such as hormonal differences.
SUBJECTS AND METHODS

Study population
Between December 1993 and May 1997, 160,725 women and
men were invited by mail to participate in the Danish prospective
cohort study Diet, Cancer, and Health. The criteria for invitation
were as follows: age between 50 and 64 y, born in Denmark, and
no previous cancer diagnosis registered in the Danish Cancer
Registry. All persons fulfilling these criteria and living in the
greater Copenhagen or Aarhus areas were invited. With the in1

From the Department of Clinical Epidemiology Aarhus University Hospital, Aalborg, Denmark (MUJ); the Department of Cardiology, Center for
Cardiovascular Research, Aalborg Hospital, Aarhus University Hospital,
Aalborg, Denmark (MUJ, CD, AMJ, JS, EBS, and KO); the Danish Cancer
Society, Institute of Cancer Epidemiology, Copenhagen, Denmark (AT); and
the Department of Epidemiology, School of Public Health, Aarhus University, Aarhus, Denmark (KO).
2

Downloaded from www.ajcn.org at Lund University Libraries on November 5, 2010

ABSTRACT
Background: Studies have suggested that replacing saturated fatty
acids (SFAs) with carbohydrates is modestly associated with a higher risk of ischemic heart disease, whereas replacing SFAs with
polyunsaturated fatty acids is associated with a lower risk of ischemic heart disease. The effect of carbohydrates, however, may depend on the type consumed.
Objectives: By using substitution models, we aimed to investigate
the risk of myocardial infarction (MI) associated with a higher energy intake from carbohydrates and a concomitant lower energy
intake from SFAs. Carbohydrates with different glycemic index
(GI) values were also investigated.
Design: Our prospective cohort study included 53,644 women and
men free of MI at baseline.
Results: During a median of 12 y of follow-up, 1943 incident MI
cases occurred. There was a nonsignificant inverse association between substitution of carbohydrates with low-GI values for SFAs
and risk of MI [hazard ratio (HR) for MI per 5% increment of
energy intake from carbohydrates: 0.88; 95% CI: 0.72, 1.07). In
contrast, there was a statistically significant positive association
between substitution of carbohydrates with high-GI values for SFAs
and risk of MI (HR: 1.33; 95% CI: 1.08, 1.64). There was no
association for carbohydrates with medium-GI values (HR: 0.98;
95% CI: 0.80, 1.21). No effect modification by sex was observed.
Conclusion: This study suggests that replacing SFAs with carbohydrates with low-GI values is associated with a lower risk of MI,
whereas replacing SFAs with carbohydrates with high-GI values is
associated with a higher risk of MI.
Am J Clin Nutr 2010;91:
17648.

80

the measures of associations, and thus residual confounding seems

unlikely. However, confounding from other IHD risk factors not
See corresponding editorial on page 1541.
taken into account remains a possible explanation for the observed
associations.
Only 2 epidemiologic studies have investigated the sub13
stitution of carbohydrates for SFAs (1, 18). In the prospective
cohort study by Hu et al (18), substitution of carbohydrates for
DISCUSSION
SFAs was nonsignificantly associated with a lower risk of IHD,
Marianne U Jakobsen, Claus Dethlefsen, Albert M Joensen, Jakob Stegger, Anne Tjnneland, Erik B Schmidt,
whereas in the prospective cohort study by Jakobsen et al (1), in
The findings from this study suggest that the effect of suband Kim Overvad
which data from 11 American and European cohort studies were
stitution of carbohydrates for SFAs varies depending on the type of
pooled, substitution of carbohydrates for SFAs was modestly
carbohydrates. There was a nonsignificant inverse association
ABSTRACT
concentration is tightly regulated by homeostatic regulatory
Background:
Studies have suggested that replacing saturated fatty
systems, but the rapid absorption of carbohydrates after conTABLE
3
acids
(SFAs)
with
carbohydrates
is
modestly
associated
with
a
highsumption
of a high-GI
challenges
homeostatic
Hazard ratios (HRs) for myocardial infarction per 5% increment of energy intake
from carbohydrates
withmeal
lowglycemic
indexthese
(low-GI),
medium-GI, or
1
er
risk
of
ischemic
heart
disease,
whereas
replacing
SFAs
with
mechanisms
(4).
A
high-GI
meal
results
in
a
high
blood
glucose
high-GI values and a concomitant lower energy intake from saturated fatty acids
polyunsaturated fatty acids is associated with a lower risk of ischeconcentration and a high insulin-to-glucagon ratio, followed by
All participants
Women
Men
mic heart disease. The effect of carbohydrates,
however, may dehypoglycemia,
counterregulatory hormone secretion,
and elepend on the type consumed.
vated plasma free fatty acid concentration (4). These events may
Median dietary GI
dietary GI
Median dietary GI
Tertiles of
Objectives:
By using substitution
models, we aimed to investigate Median
affect
the
risk
of
IHD
through
promoting
in- CI)
2
(80% central range)
HR (95% CI)
(80% central range)
HR (95% CI)
(80% centraldyslipidemia,
range)
HR (95%
dietary GI
the risk of myocardial infarction (MI) associated with a higher enflammation, and endothelial dysfunction (4).
ergy intake from
carbohydrates and
concomitant
lower
energy
Carbohydrates
with low-GI
82 a(77,
85)
0.88
(0.72,
1.07)
80
1.17 (0.80,
1.71)
84 (79,
86) of myocardial
0.83 (0.65, 1.04)
The(75,
aim82)of this study
was to
investigate
the risk
intake
from
SFAs.
Carbohydrates
with
different
glycemic
index
values (first tertile)
infarction (MI) with a higher energy intake from carbohydrates
(GI) values were
investigated. 88 (86, 90)
Carbohydrates
withalso
medium-GI
0.98 (0.80, 1.21)
87)
0.80 (0.54,
1.18)
89 (87,
91) Carbohydrates
1.08 (0.84, 1.38)
and85a (84,
concomitant
lower
energy
intake from
SFAs.
values (second
tertile) cohort study included 53,644 women and
Design:
Our prospective
with different GI values were investigated. Furthermore, potential
Carbohydrates
with
93 (91, 98)
1.33 (1.08, 1.64)
91 (88, 96)
(0.75, 1.63)
94 (92, 98)
1.34 (1.04, 1.71)
men free of MI
at high-GI
baseline.
effect
modification1.10
by sex
was investigated
because of differences
values (third
tertile)
Results:
During
a median of 12 y of follow-up, 1943 incident MI
in the underlying biology such as hormonal differences.

Intake of carbohydrates compared with intake of saturated fatty acids

and risk of myocardial infarction: importance of the glycemic index

Downloaded from www.ajcn.org at Lund University Libraries on November 5, 20

cases1 All
occurred.
was
a nonsignificant
inverse association
models There
included
intake
of glycemic carbohydrates,
proteins,bemonounsaturated fatty acids, and polyunsaturated fatty acids expressed as percentages
tween
substitution
of
carbohydrates
with
low-GI
values
SFAsfor alcohol consumption (0 and .0 g/d), alcohol consumption (g/d), BMI (in kg/m2;
of total energy intake, total energy intake (kcal/d), an indicator for
variable
and risk
of and
MI !30),
[hazard
ratio (HR)
for MI
of (never,
SUBJECTS
AND
METHODS
,25,
2529,
education
(,8, 810,
andper
.105%
y), increment
smoking status
former, and
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energy (,3.5
intakeand
from
carbohydrates:
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CI: 0.72,
1.07).
In do not know). HRs with 95% CIs for the incidence of myocardial infarction were
activity
!3.5
h/wk), and history
hypertension
(yes,
no, and
contrast, by
there
was
a proportional
statistically hazards
significant
positive
calculated
using
Cox
regression
withassociation
age as the timeStudy
metric.population
In analyses among all participants, sex was entered into the model.
2
between
substitution
ofGI
carbohydrates
values
for SFAs
Tertiles
of dietary
were based onwith
the high-GI
distribution
of dietary
GI among cases.
n
22,144, 17,000,
and
14,400
all participants
in the first,
Between= December
1993
and
Mayfor
1997,
160,725 women
andsecond,
andthird
risktertiles
of MIof(HR:
95% CI: 1.08,
1.64).10,202,
Thereand
was
no for women
and
dietary1.33;
GI, respectively;
n = 9594,
8699
in the
first, second,
tertiles in
of dietary
GI, respectively;
men were
invited
by mailand
to third
participate
the Danish
prospectiveand n =
8941,
8127, and
for men in with
the first,
second, and
third (HR:
tertiles0.98;
of dietary
GI,
respectively.
association
for 8081
carbohydrates
medium-GI
values
cohort study Diet, Cancer, and Health. The criteria for invitation
95% CI: 0.80, 1.21). No effect modification by sex was observed.
were as follows: age between 50 and 64 y, born in Denmark, and
Conclusion: This study suggests that replacing SFAs with carbohyno previous cancer diagnosis registered in the Danish Cancer
81
drates with low-GI values is associated with a lower risk of MI,
Registry. All persons fulfilling these criteria and living in the
whereas replacing SFAs with carbohydrates with high-GI values is
greater Copenhagen or Aarhus areas were invited. With the inassociated with a higher risk of MI.
Am J Clin Nutr 2010;91:
17648.
1
From the Department of Clinical Epidemiology Aarhus University Hos-

Lund University Libraries on November 5, 2010

0.80, 1.21) (Table 3). As assessed from the 95% CIs, the
measures of associations for extreme tertiles of GI were statistically significantly different. The P value for effect modification
by tertiles of dietary GI was 0.06 in women, 0.29 in men, and
0.16 in all participants. The P value for effect modification by
sex was 0.86.

GRASAS MONOINSATURADAS

82

Mensink RP, Zock PL, Kester AD, Katan MB. Am J Clin Nutr. 2003 May;77(5):1146-55

Mensink RP, Zock PL, Kester AD, Katan MB. Am J Clin Nutr. 2003 May;77(5):1146-55

misnomer. The countries around the Mediterranean basin have differe

differ and
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The Greece.
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2
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(n-6):(n-3)
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The Center
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and
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diet
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selenium,
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Nutr. 131:as
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ABSTRACT The term Mediterranean diet, implying that all Mediterranean people have the same diet, is a
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indicate
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diet ofcancer.
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(n-6):(n-3) essential fatty acids (EFA), high amounts of fiber, antioxidants (especially resveratrol from wine and
activity
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and
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with cancer. J. Nutr. 131: 3065S3073S, 2001.

KEY WORDS:

diet of Crete

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United Nations in their demo
c

1
Presented as part of the 11th Annual Research Conference on Diet, Nutrition
and Cancer held in Washington, DC, July 16 17, 2001. This conference was
sponsored by the American Institute for Cancer Research and was supported by
the California Dried Plum Board, The Campbell Soup Company, General Mills,
Lipton, Mead Johnson Nutritionals, Roche Vitamins Inc. and Vitasoy USA. Guest
editors for this symposium publication were Ritva R. Butrum and Helen A.
Norman, American Institute for Cancer Research, Washington, DC.
2
To whom correspondence should be addressed.
E-mail: cgnh@bellatlantic.net

1
Presented as part of the 11th Annual Research Conference on Diet, Nutrition
and Cancer held in Washington, DC, July 16 17, 2001. This conference was
sponsored by the American Institute for Cancer Research and was supported by
the California Dried Plum Board, The Campbell Soup Company, General Mills,
Lipton, Mead Johnson Nutritionals, Roche Vitamins Inc. and Vitasoy USA. Guest
editors for this symposium publication were Ritva R. Butrum and Helen A.
Norman, American Institute for Cancer Research, Washington, DC.
2
To whom correspondence should be addressed.

new england
journal of medicine
The

established in 1812

july 17, 2008

vol. 359

no. 3

Weight Loss with a Low-Carbohydrate, Mediterranean,

or Low-Fat Diet
Iris Shai, R.D., Ph.D., Dan Schwarzfuchs, M.D., Yaakov Henkin, M.D., Danit R. Shahar, R.D., Ph.D.,
Shula Witkow, R.D., M.P.H., Ilana Greenberg, R.D., M.P.H., Rachel Golan, R.D., M.P.H., Drora Fraser, Ph.D.,
Arkady Bolotin, Ph.D., Hilel Vardi, M.Sc., Osnat Tangi-Rozental, B.A., Rachel Zuk-Ramot, R.N.,
Benjamin Sarusi, M.Sc., Dov Brickner, M.D., Ziva Schwartz, M.D., Einat Sheiner, M.D., Rachel Marko, M.Sc.,
Esther Katorza, M.Sc., Joachim Thiery, M.D., Georg Martin Fiedler, M.D., Matthias Blher, M.D.,
Michael Stumvoll, M.D., and Meir J. Stampfer, M.D., Dr.P.H.,
for the Dietary Intervention Randomized Controlled Trial (DIRECT) Group

A BS T R AC T
Background

Trials comparing the effectiveness and safety of weight-loss diets are frequently
limited by short follow-up times and high dropout rates.
Methods

In this 2-year trial, we randomly assigned 322 moderately obese subjects (mean age,

From the S. Daniel Abraham Center for

Health and Nutrition, Ben-Gurion University of the Negev, Beer-Sheva (I.S.,
D.R.S., S.W., I.G., R.G., D.F., A.B., H.V.,
O.T.-R.); the Nuclear Research Center
Negev, Dimona (D.S., R.Z.-R., B.S., D.B.,

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INCIDENCIA DE DIABETES:
Med c/ aceite virgen: 10.1
(5.115.1)
Med c/ frutos secos: 11.0
(5.916.1)
Dieta low Fat: 17.9 (11.424.4)

Diabetes Care January 2011 vol. 34 no. 1 14-19

The

n e w e ng l a n d j o u r na l

of

m e dic i n e

original article
N Engl J Med 2013.

Primary Prevention of Cardiovascular

Disease with a Mediterranean Diet
Ramn Estruch, M.D., Ph.D., Emilio Ros, M.D., Ph.D., Jordi Salas-Salvad, M.D., Ph.D.,
Maria-Isabel Covas, D.Pharm., Ph.D., Dolores Corella, D.Pharm., Ph.D.,
Fernando Ars, M.D., Ph.D., Enrique Gmez-Gracia, M.D., Ph.D.,
Valentina Ruiz-Gutirrez, Ph.D., Miquel Fiol, M.D., Ph.D., Jos Lapetra, M.D., Ph.D.,
Rosa Maria Lamuela-Raventos, D.Pharm., Ph.D., Llus Serra-Majem, M.D., Ph.D.,
Xavier Pint, M.D., Ph.D., Josep Basora, M.D., Ph.D., Miguel Angel Muoz, M.D., Ph.D.,
Jos V. Sorl, M.D., Ph.D., Jos Alfredo Martnez, D.Pharm, M.D., Ph.D., and
Miguel Angel Martnez-Gonzlez, M.D., Ph.D., for the PREDIMED Study Investigators*

A bs t r ac t

The

n e w e ng l a n d j o u r na l

of

m e dic i n e

original article
N Engl J Med 2013.

Primary Prevention of Cardiovascular

Disease with a Mediterranean Diet
M.D.,
Ph.D., Emilio
Ph.D.,
Jordisin
Salas-Salvad,
M.D.,
Ramn
7447 Estruch,
Pacientes
H (55-80
aos)Ros,
y MM.D.,
(60-80
aos)
enfermedad
CV,Ph.D.,
pero
Covas, D.Pharm.,
Ph.D., Dolores
Corella,
conMaria-Isabel
riesgo cardiovascular
aumentado
(Diabetes
T2 D.Pharm.,
o 3 de los Ph.D.,
siguientes
Fernando
Ars,
M.D., Ph.D.,
Enrique
Gmez-Gracia,
M.D.,
Ph.D.,
factores:
tabaco,
hipertensin,
LDL-C
aumentado,
HDL-C
bajo,
exceso de
Valentina
Ruiz-Gutirrez,
Miquel Fiol,
M.D., Ph.D.,
Jos Lapetra, M.D., Ph.D.,
peso, historia
familiar Ph.D.,
de enfermedad
coronaria
prematura)
Maria Lamuela-Raventos, D.Pharm., Ph.D., Llus Serra-Majem, M.D., Ph.D.,
Rosa
3 dietas:
Xavier Pint, M.D., Ph.D., Josep Basora, M.D., Ph.D., Miguel Angel Muoz, M.D., Ph.D.,
Jos V.baja
Sorl,en
M.D.,
Ph.D., Jos Alfredo Martnez, D.Pharm, M.D., Ph.D., and
1) Dieta
grasa
M.D.,
Ph.D., for the PREDIMED Study Investigators*
2)Miguel
DietaAngel
MedMartnez-Gonzlez,
c/ 1L de aceite de
oliva/semana
3) Dieta Med c/ 30g de frutos secos/da (15g de nueces+7,5g de
avellanas + 7,5g de almendras)
A bs t r ac t

Mediterr anean Diet and Cardiovascular Events

the use of a separate 9-item dietary screener

(Table S3 in the Supplementary Appendix).
A general medical questionnaire, a 137-item
validated food-frequency questionnaire,15 and
the Minnesota Leisure-Time Physical Activity
Questionnaire were administered on a yearly
basis.10 Information from the food-frequency
questionnaire was used to calculate intake of
energy and nutrients. Weight, height, and waist
circumference were directly measured.16 Biomarkers of compliance, including urinary hydroxytyrosol levels (to confirm compliance in
the group receiving extra-virgin olive oil) and
plasma alpha-linolenic acid levels (to confirm
compliance in the group receiving mixed nuts),
were measured in random subsamples of participants at 1, 3, and 5 years (see the Supplementary Appendix).
End Points

The primary end point was a composite of myocardial infarction, stroke, and death from cardiovascular causes. Secondary end points were
stroke, myocardial infarction, death from cardiovascular causes, and death from any cause. We
used four sources of information to identify end
points: repeated contacts with participants, contacts with family physicians, a yearly review of
medical records, and consultation of the National Death Index. All medical records related to
end points were examined by the end-point adjudication committee, whose members were unaware of the study-group assignments. Only end
points that were confirmed by the adjudication
committee and that occurred between October 1,
2003, and December 1, 2010, were included in
the analyses. The criteria for adjudicating primary and secondary end points are detailed in
the Supplementary Appendix.
Statistical Analysis

Table 1. Summary of Dietary Recommendations to Participants in the

Mediterranean-Diet Groups and the Control-Diet Group.
Food

Goal

Mediterranean diet
Recommended
Olive oil*

4 tbsp/day

Tree nuts and peanuts

3 servings/wk

Fresh fruits

3 servings/day

Vegetables

2 servings/day

Fish (especially fatty fish), seafood

3 servings/wk

Legumes

3 servings/wk

Sofrito

2 servings/wk

White meat

Instead of red meat

Wine with meals (optionally, only for habitual

drinkers)

7 glasses/wk

Discouraged
Soda drinks

<1 drink/day

Commercial bakery goods, sweets, and pastries

<3 servings/wk

Spread fats

<1 serving/day

Red and processed meats

<1 serving/day

Low-fat diet (control)

Recommended
Low-fat dairy products

3 servings/day

Bread, potatoes, pasta, rice

3 servings/day

Fresh fruits

3 servings/day

Vegetables

2 servings/wk

Lean fish and seafood

3 servings/wk

Discouraged
Vegetable oils (including olive oil)

2 tbsp/day

Commercial bakery goods, sweets, and pastries

1 serving/wk

Nuts and fried snacks

1 serving /wk

Red and processed fatty meats

1 serving/wk

Visible fat in meats and soups

Always remove

Fatty fish, seafood canned in oil

1 serving/wk

Spread fats

1 serving/wk

Sofrito

2 servings/wk

We initially estimated that a sample of 9000 par- * The amount of olive oil includes oil used for cooking and salads and oil conN Engl
J Med
2013.
sumed in meals eaten outside
the home.
In the
group assigned to the Mediticipants would be required to provide statistical
terranean diet with extra-virgin olive oil, the goal was to consume 50 g (appower of 80% to detect a relative risk reduction proximately 4 tbsp) or more per day of the polyphenol-rich olive oil supplied,
of 20% in each Mediterranean-diet group versus instead of the ordinary refined variety, which is low in polyphenols.

The

n e w e ng l a n d j o u r na l

m e dic i n e

of

30%
A Primary End Point (acute myocardial infarction, stroke, or death from cardiovascular causes)
Incidence of Composite Cardiovascular
End Point

1.0

Med diet, EVOO: hazard ratio, 0.70

(95% CI, 0.530.91); P=0.009
Med diet, nuts: hazard ratio, 0.70
(95% CI, 0.530.94); P=0.02

0.8

Control diet

0.06

Med diet, nuts

0.05
0.04
0.03

0.6

Med diet, EVOO

0.02
0.01

0.4

0.00
0.2

0.0

1583
1987
1657

1268
1687
1389

946
1310
1031

Years
No. at Risk
Control diet
Med diet, EVOO
Med diet, nuts

2450
2543
2454

2268
2486
2343

2020
2320
2093

B Total Mortality
1.0

N Engl J Med 2013.

Med diet, EVOO: hazard ratio, 0.81

0.07

Med diet, nuts

Original Research

A MUFA-Rich Diet Improves Posprandial Glucose, Lipid

and GLP-1 Responses in Insulin-Resistant Subjects
Paniagua, MD,HPhD,
Angel
de la Sacristana,
MD,yEsther
Sanchez, MD, Inmaculada
Romero,
PhD, de
Juan
11 A.
Pacientes
yM
sinGallego
enfermedad
CV
sin Diabetes,
pero con
exceso
Antonio Vidal-Puig, MD, PhD, Francisco J. Berral, MD, PhD, Antonio Escribano, MD, PhD, Maria Jose Moyano, MD,
peso
Resistencia
la Lo
Insulina
Pablo
Perey
z-Martinez,
MD, PhD,aJose
pez-Miranda, MD, PhD, Francisco Perez-Jimenez, MD, PhD
Lipids and Atherosclerosis Research Unit, University Hospital Reina Sofa (HURS), (J.A.P., A.G.S., E.S., I.R., P.P.-M., J.L.-M.,
Ciber Fisiopatolog
a Obesidad
Nutricion /(CB06/03)
Instituto Salud Carlos III (J.A.P., P.P.-M., J.L.-M., F.P.-J.),
F.P.-J.),
3 dietas
(28 das
caday dieta
Crossover):
University of Cordoba, School of Medicine (F.J.B., A.E.), Biochemical Laboratory Service, HURS (M.J.M.), Cordoba, SPAIN,
Departments of Clinical Biochemistry and Medicine, University of Cambridge Addenbrookes Hospital, Cambridge (A.V.-P.),
1) ENGLAND
Dieta rica en grasa saturada (47% CHO, 38% Grasa [23% SAT / 9%
Key
words: Mediterranean
diet, insulin resistance, glucose metabolism, GLP-1, proinsulin
MUFA
/ 6% PUFA])
Objective: To study the effects of three weight-maintenance diets with different macronutrient composition

2) Dieta Med
rica en
(47% subjects.
CHO / 38% Grasa: 9%
on carbohydrate,
lipidaceite
metabolism, de
insulinoliva/semana
and incretin levels in insulin-resistant
Methods: A prospective study was performed in eleven (7 W, 4 M) offspring of obese and type 2 diabetes
SAT / 6%
PUFA / 23% MUFA [75% Aceite de Oliva Virgen])
patients. Subjects had a BMI ! 25 Kg/m2, waist circumference (men/women) ! 102/88, HBA1c " 6.5% and
were regarded as insulin-resistant after an OGTT (Matsuda ISIm "4). They were randomly divided into three
groups and underwent three dietary periods each of 28 days in a crossover design: a) diet high in saturated fat
(SAT), b) diet rich in monounsaturated fat (MUFA; Mediterranean diet) and c) diet rich in carbohydrate (CHO).
Results: Body weight and resting energy expenditure did not changed during the three dietary periods.
Fasting serum glucose concentrations fell during MUFA-rich and CHO-rich diets compared with high-SAT diets
(5.02 # 0.1, 5.03 # 0.1, 5.50 # 0.2 mmol/L, respectively. Anova " 0.05). The MUFA-rich diet improved
insulin sensitivity, Paniagua
as indicated JA,
by lower
resistance (HOMA-ir), compared
et al.homeostasis
J Am Collmodel
Nutr.analysis-insulin
2007 Oct;26(5):434-44
with CHO-rich and high-SAT diets (2.32 # 0.3, 2.52 # 0.4, 2.72 # 0.4, respectively, Anova " 0.01). After a
MUFA-rich and high-SAT breakfasts (443 kcal) the postprandial integrated area under curve (AUC) of glucose
and insulin were lowered compared with isocaloric CHO-rich breakfast (7.8 # 1.3, 5.84 # 1.2, 11.9 # 2.7

3) Dieta pobre en grasa (65% CHO y 20% grasa [6% SAT / 8% MUFA / 6%
PUFA])

Paniagua JA, et al. J Am Coll Nutr. 2007 Oct;26(5):434-44

FRUTOS SECOS
Fuente de:
Resveratrol
Vitamina E
Selenio
Manganeso
Magnesio
Arginina
Fibra

99

RICOS EN CIDOS GRASOS MONOINSATURADOS

ostprandial glucose excursions, including digestive enzyme inhibition, and low glycemic index

etes incidence and coronary heart disease (CHD) risk, possibly through lower
postprandial
The Journal
of Nutrition
Nutrient Physiology, Metabolism, and Nutrient-Nutrient Interactions

and proteins. We therefore assessed the effect of decreasing postprandial glucose excursions

amage. Fifteen healthy subjects ate 2 bread control meals and 3 test meals: almonds and bread;

Decrease
Postprandial
Glycemia,
mashed Almonds
potatoes, balanced
in carbohydrate,
fat, and protein,
using butter and cheese. We

and Oxidative
Damage
baselineInsulinemia,
and for 4 h postprandially.
Glycemic
indices
for the rice (38 6 6) and almond meals
1
in Healthy Individuals

or the potato meal (94 6 11) (P , 0.003), as were the postprandial areas under the insulin

P,

David J. A. Jenkins,25* Cyril W. C. Kendall,2,4 Andrea R. Josse,2,4 Sara Salvatore,6 Furio Brighenti,6
0.001).
seen Rao
in 4total antioxidant capacity.
LiviaNo
S. A.postmeal
Augustin,2,4 treatment
Peter R. Ellis,7 differences
Edward Vidgen,4 were
and A. Venket

How-

ol concentration
increased
following
meal
(15 6Division
14 mmol/L),
indicating
oxidative
Clinical Nutrition
and Risk Factor
Modificationthe
Centeralmond
and Department
of Medicine,
of Endocrinology
and Metabolism,less
St.
2

Michaels Hospital, Toronto, Ontario M5C 2T2, Canada; Departments of 4Nutritional Sciences and 5Medicine, Faculty of Medicine,
University of Toronto, Toronto, Ontario M5S 3E2, Canada; 6Department of Public Health, University of Parma, Parma 43100, Italy;
and 7Biopolymers Group, School of Biomedical and Health Sciences, Kings College London, University of London, London SE1 9NN,
United Kingdom

eased after the control bread, rice, and potato meals (210 6 8 mmol/L), when data from these

0.021). The change in protein thiols was also negatively related to the postprandial incremental
60 observations, P 0.026) and peak insulin responses (r 20.26, n 60 observations, P
Abstract

in lower diabetes incidence and coronary heart disease (CHD) risk, possibly through lower postprandial
er this riskdiets
byresult
decreasing
the glycemic excursion and by providing antioxidants. These actions
oxidative damage to lipids and proteins. We therefore assessed the effect of decreasing postprandial glucose excursions

measures
of oxidative
damage. Fifteen
subjects ate 2 bread
meals and 3J.
test
meals: almonds
and bread;
by whichonnuts
are
associated
withhealthy
a decreased
riskcontrol
of CHD.
Nutr.
136: 29872992,
2006.
parboiled rice; and instant mashed potatoes, balanced in carbohydrate, fat, and protein, using butter and cheese. We
obtained blood samples at baseline and for 4 h postprandially. Glycemic indices for the rice (38 6 6) and almond meals

Downloaded from jn.nu

g postprandial
may
decrease
the risk
ofinhibition,
oxidative
Strategies glucose
that decrease excursions
postprandial glucose
excursions,
including digestive
enzyme
and low damage
glycemic indexto proteins.

Consumo frecuente
de frutos secos est
asociado a menor
incidencia de
diabetes Tipo 2 y
ECV

10
1

Albert CM, Gaziano JM, Willett WC, Manson JE..Arch Intern Med. 2002;162:1382-1387.
Jiang R, Manson JE, Stampfer MJ, Liu S, Willett WC, Hu FB.JAMA. 2002;288:2554-2560.

GRASAS TRANS EN LA DIETA

Mensink RP, Zock PL, Kester AD, Katan MB. Am J Clin Nutr. 2003 May;77(5):1146-55

RELACIN DE GRASAS CON EPISODIOS DE ECC EN

ESTUDIOS COHORTE PROSPECTIVOS

AG TRANS INDUSTRIALES
Disminuyen HDL
Aumentan LDL
Aumentan riesgo de cncer y EAC
Pueden inducir Resistencia a insulina

10
5

Riserus U. Atheroscler Suppl. 2006 May;7(2):37-9.

O'Keefe JH Jr, Corde lain L. Mayo Clin Proc 2004 Jan;79(1):101-8

GRASAS TRANS EN LA DIETA

GRASAS TRANS PARA LOS NIOS

CIDOS GRASOS ESENCIALES

The Chemistry of Food and of Bodies

Aqueous (polar) environment

outside cell

11

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membrane

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Figure 1.5 Structure of biological membranes in mammalian cells. Cell membranes

and intracellular membranes such as the endoplasmic reticulum are composed of bilayers of phospholipid molecules with their polar head-groups facing the aqueous environment on either side and
their non-polar tails facing inwards, forming a hydrophobic center to the membrane. The membrane
also contains intrinsic proteins such
as hormone receptors, ion channels, and sugar transporters, and
Frayn KN. Metabolic Regulation. Blackwell Pub; 2010:384.
molecules of cholesterol which reduce the fluidity of the membrane. Modern views of cell membrane structure emphasize that there are domains, known as rafts, in which functional proteins
co-locate, enabling interactions between them. These lipid rafts are characterized by high concentra-

Cortesa del Prof. Frits Muskiet, Univ. Groningen

Knapp, HR. Dietary fatty acids in human thrombosis and henostasis. Am J Clin Nutr, Vol 65, 1687S-698S

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through the endothelium and the subsequent generation of inflammatory
mediators.
Calder PC. Am J Clin Nutr 2006;83(suppl):1505S19S)

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Serhan CN, Ward PA, Gilroy DW, editors. Fundamentals of Inflammation. Cambridge Univ Pr; 2010: 234-243.
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De Caterina R. N Engl J Med 2011

Ciclooxigenases

Lipooxigenases

LTA4
LTB4
LTC4
LTD4
LTE4
12-HETE

LTA5
LTB5
LTC5
LTD5
LTE5

cido Araquidnico
20:4 n-6

cido Eicosapentaenico
(EPA)
20:5 n-3

Bastos P. An Nutr Esp Func 2007; 7(36): 17-24

TXA2
PGE2
PGF2
PGD2
PGI2

TXA3
PGE3
PGF3
PGD3
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122

EPA/DHA E AA

Calder PC. Am J Clin Nutr 2006;83(suppl):1505S19S.

MEGA-3 E INFLAMACIN
17 meta-anlisis de
RCTs testando los
efectos de mega-3
en la AR
3-4 meses: reduccin
del dolor articular,
minutos de rigidez
matutina, nmero de
articulaciones con
dolor y menor uso de
AINES

Goldberg RJ, Katz J. Pain 129 (2007)

Time
course
relativo incorporao de EPA e DHA
TIEMPO
DE INCORPORACIN DE EPA Y DHA EN
em fosfolipdios de membrana de clulas mononucleares

4
3
2
1
0

8
12
Time (weeks)

20

DHA in mononuclear cell PL (%)

EPA in mononuclear cell PL (%)

FOSFOLPIDOS DE CELULAS MONONUCLEARES

4
3
2
1

8
12
Time (weeks)

Indivduos saudveis: 2,1 g EPA + 1,1 g DHA/dia/12 semanas

Eur. J. Clin. Invest. 30, 260-274, 2000

Eur. J. Clin. Invest. 30, 260-274, 2000

20

DHA

Calder PC. Am J Clin Nutr 2006;83(suppl):1505S19S)

Calder PC. Am J Clin Nutr 2006;83(suppl):1505S19S)

De Caterina R. N Engl J Med 2011

Serhan, CN. Annu. Rev. Immunol. 2007. 25:10137

13
1

Gilroy DW. 2010

EPA+DHA y ECV
Ensayos clnicos con
pacientes con EAC:
Redujo la incidencia de
accidentes
cardiovasculares
(Infarto y Muerte)

Epidemiologa: Asociacin con Menor riesgo de ECV.

Calder PC. Clinical Science 2004;107:111

132

NDICE 3
% EPA y DHA en membranas RBC
ndice 3 8%
riesgo de muerte por ECV 90% < que ndice 3 4%

von Schacky C, Harris WS. Cardiovascular benefits of omega-3 fatty acids. Cardiovasc Res. 2007 Jan 15;73(2):310-5.

133

Figure 3. Schema of Potential Dose Responses and Time Courses for Altering Clinical Events
of Physiologic Effects of Fish or Fish Oil Intake
TYPICAL DIETARY
DOSES

TYPICAL SUPPLEMENTAL
DOSES

Clinical Effect

Relative Strength of Effect

Antiarrhythmia

Triglyceride-Lowering
Heart RateLowering
BPLowering

Antithrombosis
0

500

1000

1500

2000

Time Course To
Alter Clinical Events
Weeks

Months to Years
Months
Months to Years

Weeks

2500

EPA + DHA Intake, mg/d

The relative strength of effect is estimated from effects of eicosapentaenoic acid (EPA) "docosahexaenoic acid
(DHA) on each risk factor and
on the corresponding
impact
cardiovascular
risk.70-72,79-84 For example, dose
Mozaffarian
D, Rimm EB. JAMA.
2006on
Oct
18;296(15):1885-99.
response for antiarrhythmic effects is initially steep with a subsequent plateau, and clinical benefits may occur
within weeks, while dose response for triglyceride effects is more gradual and monotonic, and clinical benefits
may require years of intake. At typical Western levels of intake (eg, #750 mg/d EPA" DHA), the physiologic

0.86; 9
added
double
forme
reduce
relativ
P = .04
pared
tality
analys
relativ
0.92).
Neu
prefere
idly de
and th
trating
branes
chain
is unk
is adeq
the ab
DHA.2
Effe

BETA-OXIDACIN

ACTIVIDAD LIMITADA

ACTIVIDAD
LIMITADA

VEGANOS TIENEN BAJOS NIVELES DE AA Y

DHA

Fokkema et al. Polyunsaturated fatty acid status of Dutch vegans and omnivores. Prostaglandins, Leukotrienes and Essential FattyAcids (2000)

9 veganos sanos suplementados con:

A: 2.01 g ALA (4 ml aceite de lino)
B: 1.17 g GLA (6 ml aceite de borraja)
A+B

ESSENTIAL FATTY ACID INTAKE IN T

FIGURE 4. Regression Blasbalg

analysis
for the availability of linoleic acid (LA)
TL, et al. Am J Clin Nutr. 2011
between 1909 and 1999. The linear relation [LA percentage of energy
(en%) = 2115.4221 + 0.0617 x] was significant at P , 0.000001 with

FIGUR
supply fr
indicated
line, and n
line. 190
data are

TABLE 12
Sources of docosahexaeno

Food category
Poultry
Shellfish
Eggs
Finfish
Beef
Game
Total
1

NA, not applicable.

lipids (37), presumab

dietary intakes of LA
account for the poten
However, because LA
effects may be nonlin
A randomized trial t
with high LA (6.7% of

Blasbalg TL, et al. Am J Clin Nutr. 2011

FIGURE 8. Omega-3 tissue highly unsaturated fatty acid (HUFA)

predictions over the 20th century. Solid arrows indicate the percentage of

DIET AND RED BLOOD CELL n6 AND n3 FATTY ACIDS

LA disminuye
DHA en la
membrana de
los eritrocitos

N= 105
Mujeres
(Canad)
Embarazadas
(36 semanas)

LA disminuye
EPA en la
membrana de
los eritrocitos

Friesen RW, Innis SM. Am J Clin Nutr. 2010 Jan;91(1):23-31.

ACEITES VEGETALES RICOS EN OMEGA-6

DISMINUYEN EL RIESGO DE ECV ??????

with omega-6 PUFAs on

re present for each trial,
es and the observational
cing saturated fatty acid
ars, white bread, white
As reduces CHD risk. On
a-6 PUFAs used in the
ies, and nonhuman prieductions in CHD risk
PUFA intakes of 10% to
lower intakes, with no
nts.

s of Omega-6
ds

ega-6 PUFAs traditionof essential fatty acid

ngly seeking to define
k for chronic disease,
of Medicines Food and
Reference Intake Report
67 defines an adequate
d 12 g/d for women (5%
f age, approximately the
the Dietary Reference
ry Guidelines for Ameracronutrient distribution
particular energy source

follow that decreasing omega-6 levels will do the same.

Indeed, the evidence considered here suggests that it would
have the opposite AHA
effect.Science
HigherAdvisory
omega-6 PUFA intakes
can inhibit the conversion of !-linolenic acid to eicosaOmega-6 Fatty 79Acids and Risk for Cardiovascular Disease
pentaenoic
acid, but such conversion is already quite
A Science Advisory From the American Heart Association Nutrition
low,80
and whether
small changes
Subcommittee
of theadditional
Council on Nutrition,
Physical would
Activity, have
and
Metabolism;
Cardiovascular
Nursing;
and Council
net effects
on Council
CHD on
risk
after the other
benefits
of on
LA
Epidemiology and Prevention
consumption are taken into account is not clear. The focus
William S. Harris, PhD, FAHA, Chair; Dariush Mozaffarian, MD, DrPH, FAHA;
on Eric
ratios,
rather
on levelsPhD,ofFAHA;
intake
of L.each
typeFAHA;
of
Rimm, ScD,
FAHA;than
Penny Kris-Etherton,
Lawrence
Rudel, PhD,
Lawrence J. Appel, MD, MPH, FAHA; Marguerite M. Engler, PhD, FAHA;
PUFA, has many
conceptual
andFrank
biological
limitations.81
Mary B.
Engler, PhD, FAHA;
Sacks, MD, FAHA

large body of literature suggests that higher intakes of

omega-6 (or n-6) polyunsaturated fatty acids (PUFAs)
reduce risk for coronary heart disease (CHD). However, for
the reasons outlined below, some individuals and groups have
recommended substantial reductions in omega-6 PUFA intake.1 4 The purpose of this advisory is to review evidence on
the relationship between omega-6 PUFAs and the risk of
CHD and cardiovascular disease.

levels,5 may have physiological sequelae.6 8 LA comes

primarily from vegetable oils (eg, corn, sunflower, safflower,
soy). The average US intake of LA, according to National
Health and Nutrition Examination Survey 2001 to 2002 data
for adults "19 years of age, is 14.8 g/d.9 On the basis of an
average intake of 2000 kcal/d, LA intake is 6.7% of energy.
AA (!0.15 g/d) is consumed preformed in meat, eggs, and
some fish.

Conclusions

This advisory was undertaken to summarize the current

evidence on the consumption of omega-6 PUFAs, particularly LA, and CHD risk. Aggregate data from randomized
Omega-6 PUFAs and cohort studies,
Omega-6 PUFAs
Inflammation
trials,
case-control
andandlong-term
Omega-6 PUFAs are characterized by the presence of at least
Arguments for reduced LA intakes are based on the
2 carbon-carbon double bonds, with the first bond at the sixth
assumption that because CHD has an inflammatory comanimal
feeding experiments indicate
that the consumption
carbon from the methyl terminus. Linoleic acid (LA), an
ponent and because the omega-6 fatty acid, AA, is the
substrate for the synthesis of a variety of proinflammatory
18-carbon fatty acid with 2 double bonds (18:2 omega-6), is
of
at least 5% to 10% of energy
from omega-6 PUFAs
molecules, reducing LA intakes should reduce tissue AA
the primary dietary omega-6 PUFA. LA cannot be synthewhich should reduce the inflammatory potential
sized by humans, and although firm minimum requirements
reduces
the risk of CHD relative content,
to lower
intakes. The data
and therefore lower the risk for CHD. The evidence,
have not been established for healthy adults, estimates dederived primarily from human studies, regarding this line
rived from studies in infants and hospitalized patients receivalso
suggest that higher intakes appear
to be safe and may
of reasoning is examined below.
ing total parenteral nutrition suggest that an LA intake of
AA is the substrate for the production of a wide variety of
!0.5% to 2% of energy is likely to suffice. After consumpbe
even more beneficial (as part
of a lowsaturated-fat,
eicosanoids (20-carbon AA metabolites). Some are prointion, LA can be desaturated and elongated to form other
flammatory, vasoconstrictive, and/or proaggregatory, such as
omega-6 PUFAs such as !-linolenic and dihomo-!-linolenic
low-cholesterol
diet).
In important
summary,
theE , AHA
acids. The latter is converted to the
metabolically
thromboxanesupports
A , and leukotrienean
B . Howprostaglandin
ever, others are antiinflammatory/antiaggregatory, such as
omega-6 PUFA arachidonic acid (AA; 20:4 omega-6), the
omega-6
intake
at leastprostacyclin,
5% to
10%
ofepoxyeicosatrienoic
energy inacids.
lipoxin
A , and
substrate for a widePUFA
array of reactive
oxygenatedof
metabolites.
Epoxyeicosatrienoic acids are fatty acid epoxides produced
Because LA accounts for 85% to 90% of the dietary omega-6
the
of other
AHA
and
dietary
from AA
by a cytochrome
P450recommenepoxygenase. EpoxyeicosaPUFA,context
this advisory focuses
primarily on
this fattylifestyle
acid,
trienoic acids also have important vasodilator properties via
recognizing that dietary AA, which can affect tissue AA
dations. To reduce omega-6 PUFA intakes from their
current
levels would be more likely to increase than to
The American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside
relationship or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are
required to complete risk
and submitfor
a Disclosure
Questionnaire showing all such relationships that might be perceived as real or potential conflicts
decrease
CHD.
of interest.
10

11

12

This statement was approved by the American Heart Association Science Advisory and Coordinating Committee on November 6, 2008. A copy of the
statement is available at http://www.americanheart.org/presenter.jhtml?identifier"3003999 by selecting either the topic list link or the chronological
list link (No. LS-1966). To purchase additional reprints, call 843-216-2533 or e-mail kelle.ramsay@wolterskluwer.com.
Expert peer review of AHA Scientific Statements is conducted at the AHA National Center. For more on AHA statements and guidelines development,
visit http://www.americanheart.org/presenter.jhtml?identifier"3023366.
Permissions: Multiple copies, modification, alteration, enhancement, and/or distribution of this document are not permitted without the express

Downloaded from circ.ahajournals.org by on July 26, 2010

Mensink RP, Zock PL, Kester AD, Katan MB. Am J Clin Nutr. 2003 May;77(5):1146-55

Simopoulos AP, Cleland LG (eds): Omega6/Omega3 Essential Fatty Acid Ratio:

The Scientific Evidence. World Rev Nutr Diet. Basel, Karger, 2003, vol 92, pp 7480

Effects of an Indo-Mediterranean
Diet on the Omega6/Omega3 Ratio
in Patients at High Risk of Coronary
Artery Disease: The Indian Paradox
Daniel Pellaa, Gal Dubnovb, Ram B. Singhc, Rakesh Sharmad,
Elliot M. Berryb, Orly Manor b
a
b

c
d

2nd Interna Klinika,Safaric University, Kosice, Slovakia;

Department of Human Nutrition and Metabolism, Hebrew University, Hadassah
Medical School, Jerusalem, Israel;
Subharti Medical College, Medical Hospital and Research Centre, Moradabad, India;
Department of Medicine, Columbia University, New York, N.Y., USA

> PREVALENCIA DE EAC EN INDIVIDUOS URBANOS

Pella D et al. World Rev Nutr Diet. Basel, Karger, 2003, vol 92, pp 74-80.

Simopoulos AP, Cleland LG (eds): Omega6/Omega3 Essential Fatty Acid Ratio:

The Scientific Evidence. World Rev Nutr Diet. Basel, Karger, 2003, vol 92, pp 8191

Omega6/Omega3 Fatty Acid Ratio:

The Israeli Paradox
Gal Dubnov, Elliot M. Berry
Department of Human Nutrition and Metabolism, Hebrew University,
Hadassah Medical School, Jerusalem, Israel

Aceite ms consumido: ACEITE DE SOJA

R

While the amount of fat is very important in terms of public health in

dealing with the current epidemic of obesity, an equally significant issue is the
type of fat consumed. As polyunsaturated fatty acids (PUFA) have long been
ATIO
shown to possess cholesterol-lowering effects [1], increasing their consumption
has been promoted in the management of coronary artery disease (CAD) [2].
These recommendations followed both experimental and population based
CIDO INOLEICO
DE LA NERGIA OTAL IARIA
studies that showed decreasing rates of CAD in countries with increasing
polyunsaturated/saturated fat (P/S) ratios over the past years.
The dietary habits in Israel appear to be as recommended: low in total
ADIPOCITOcalories, in total fat and in saturated fat, while high in hypolipidemic omega6
fatty acids (!6) as compared with other western countries [3, 4]. Unexpectedly, the
rates of modern-world illnesses are about the same as they are in the USA and
Europe [3, 5, 6]. The reason for this is not clear. Recent evidence suggests that
a high intake of omega6 fatty acids may prove harmful [2, 79]: these fatty
acids may elevate the risk of hyperinsulinemia and its associated metabolic disorders, atherogenesis, and cancer. Another group of PUFA, the omega3 fatty
acids (!3), have demonstrated cardioprotection in observational [1015] and
intervention studies for both secondary [1618] and primary [18] prevention.
An example for this is shown in figure 1: an Indo-Mediterranean diet, rich in
the plant-derived omega3 fatty acid alpha-linolenic acid, markedly decreased
the risk for a cardiac event among both those with established coronary artery
disease, or those only with risk factors [18]. A recent meta-analysis showed that
both dietary and non-dietary sources are equally beneficial [19], and the health
benefits of plant- derived or fish- derived omega3 fatty acids now seem to
have a sound basis [20]. As the omega6 and omega3 fatty acids compete for

% LA

P/S = 0,9 1,2

L

: 10%

: 25%

RATIO N-6/N-3 > 20/1

PREVALENCIA DE EAC ES COMPARABLE A LA DE

OTROS PASES OCCIDENTALES

non-fatal myocardial infarction (MI) + CHD death.

n-6 specific PUFA trials non significantly increased the risk of

non-fatal MI + CHD death by 13%
(risk ratio (RR) 113; 95% CI 084, 153; P=0427)

has reported the effects of

tein with omega-6 PUFAs on
ons are present for each trial,
studies and the observational
replacing saturated fatty acid
sugars, white bread, white
PUFAs reduces CHD risk. On
omega-6 PUFAs used in the
studies, and nonhuman priw, reductions in CHD risk
ga-6 PUFA intakes of 10% to
with lower intakes, with no
events.

takes of Omega-6
Acids

r omega-6 PUFAs traditiontion of essential fatty acid

reasingly seeking to define
e risk for chronic disease,
ute of Medicines Food and
tary Reference Intake Report
ents,67 defines an adequate
en and 12 g/d for women (5%
ars of age, approximately the
Both the Dietary Reference
Dietary Guidelines for Amere macronutrient distribution
or a particular energy source

tissue levels does reduce the risk for CHD,77,78 it does not
follow that decreasing omega-6 levels will do the same.
AHAconsidered
Science Advisory
Indeed, the evidence
here suggests that it would
have the opposite effect. Higher omega-6 PUFA intakes
Omega-6
Fatty
and Risk
Cardiovascular
Disease
can inhibit
theAcids
conversion
of !for
-linolenic
acid to eicosaA Science Advisory 79
From the American Heart Association Nutrition
pentaenoic
acid,
but such
conversion
is already
Subcommittee
of the Council
on Nutrition,
Physical
Activity, quite
and
80
Metabolism;
Council on
Cardiovascular
andwould
Councilhave
on
low,
and whether
additional
smallNursing;
changes
Epidemiology and Prevention
net effects on CHD risk after the other benefits of LA
William S. Harris, PhD, FAHA, Chair; Dariush Mozaffarian, MD, DrPH, FAHA;
consumption
are taken into account is not clear. The focus
Eric Rimm, ScD, FAHA; Penny Kris-Etherton, PhD, FAHA; Lawrence L. Rudel, PhD, FAHA;
Lawrence
J. Appel,than
MD, MPH,
Marguerite
M. Engler,
FAHA;
on ratios,
rather
on FAHA;
levels
of intake
ofPhD,
each
type of
Mary B. Engler, PhD, FAHA; Frank Sacks, MD, FAHA
PUFA, has many conceptual and biological limitations.81

large body of literature suggests that higher intakes of

omega-6 (or n-6) polyunsaturated fatty acids (PUFAs)
reduce risk for coronary heart disease (CHD). However, for
the reasons outlined below, some individuals and groups have
recommended substantial reductions in omega-6 PUFA intake.1 4 The purpose of this advisory is to review evidence on
the relationship between omega-6 PUFAs and the risk of
CHD and cardiovascular disease.

levels,5 may have physiological sequelae.6 8 LA comes

primarily from vegetable oils (eg, corn, sunflower, safflower,
soy). The average US intake of LA, according to National
Health and Nutrition Examination Survey 2001 to 2002 data
for adults "19 years of age, is 14.8 g/d.9 On the basis of an
average intake of 2000 kcal/d, LA intake is 6.7% of energy.
AA (!0.15 g/d) is consumed preformed in meat, eggs, and
some fish.

Conclusions

This advisory was undertaken to summarize the current

evidence on the consumption of omega-6 PUFAs, particularly LA, and CHD risk. Aggregate data from randomized
Omega-6 PUFAs
Omega-6 PUFAs and Inflammation
Omega-6
PUFAs arecase-control
characterized by the presence
of at least
Arguments
for reducedand
LA intakes
are based on the
trials,
and
cohort
studies,
long-term
2 carbon-carbon double bonds, with the first bond at the sixth
assumption that because CHD has an inflammatory comfeeding
experiments
consumption
becausethe
the omega-6
fatty acid, AA, is the
carbonanimal
from the methyl
terminus. Linoleic
acid (LA), an indicate
ponent andthat
substrate for the synthesis of a variety of proinflammatory
18-carbon fatty acid with 2 double bonds (18:2 omega-6), is
of at
least
10%
of energy
molecules,from
reducing omega-6
LA intakes shouldPUFAs
reduce tissue AA
the primary
dietary
omega-65%
PUFA. to
LA cannot
be synthecontent, which should reduce the inflammatory potential
sized by humans, and although firm minimum requirements
theforrisk
CHD
relative
lower
TheThedata
and to
therefore
lowerintakes.
the risk for CHD.
evidence,
have reduces
not been established
healthyof
adults,
estimates
dederived primarily from human studies, regarding this line
rived from studies in infants and hospitalized patients receivalso
suggest
thatthathigher
intakes
appearis examined
to bebelow.
safe and may
of reasoning
ing total
parenteral
nutrition suggest
an LA intake
of
AA is the substrate for the production of a wide variety of
!0.5% to 2% of energy is likely to suffice. After consumpbecaneven
more
beneficial
(as part
of(20-carbon
a lowsaturated-fat,
eicosanoids
AA metabolites). Some are prointion, LA
be desaturated
and elongated
to form other
flammatory, vasoconstrictive, and/or proaggregatory, such as
omega-6 PUFAs such as !-linolenic and dihomo-!-linolenic
diet). In
summary,
the
AHA Asupports
acids.low-cholesterol
The latter is converted to the metabolically
important
, and leukotriene an
B . Howprostaglandin
E , thromboxane
ever, others are antiinflammatory/antiaggregatory, such as
omega-6 PUFA arachidonic acid (AA; 20:4 omega-6), the
omega-6 PUFA intake of at least
5% to 10% of energy in
prostacyclin, lipoxin A , and epoxyeicosatrienoic acids.
substrate for a wide array of reactive oxygenated metabolites.
Epoxyeicosatrienoic acids are fatty acid epoxides produced
Because LA accounts for 85% to 90% of the dietary omega-6
the context of other AHA lifestyle
and dietary recommenfrom AA by a cytochrome P450 epoxygenase. EpoxyeicosaPUFA, this advisory focuses primarily on this fatty acid,
trienoic
acids
have importantfrom
vasodilator their
properties via
recognizing
that
dietary
AA,
which
can
affect
tissue
AA
dations. To reduce omega-6 PUFA alsointakes
current levels would be more likely to increase than to
The American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside
relationship
or a personal, professional,
or business
interest of a member of the writing panel. Specifically, all members of the writing group are
decrease
risk for
CHD.
required to complete and submit a Disclosure Questionnaire showing all such relationships that might be perceived as real or potential conflicts
10

11

12

of interest.
This statement was approved by the American Heart Association Science Advisory and Coordinating Committee on November 6, 2008. A copy of the
statement is available at http://www.americanheart.org/presenter.jhtml?identifier"3003999 by selecting either the topic list link or the chronological
list link (No. LS-1966). To purchase additional reprints, call 843-216-2533 or e-mail kelle.ramsay@wolterskluwer.com.
Expert peer review of AHA Scientific Statements is conducted at the AHA National Center. For more on AHA statements and guidelines development,
visit http://www.americanheart.org/presenter.jhtml?identifier"3023366.
Permissions: Multiple copies, modification, alteration, enhancement, and/or distribution of this document are not permitted without the express

Downloaded from circ.ahajournals.org by on July 26, 2010

LYON HEART STUDY

Okuyama H, Ichikawa Y, Sun Y, Hamazaki T, Lands WE. World Rev Nutr Diet.153
2007;96:83-103.

RATIO 6/ 3 Y CNCER
Estudios epidemiolgicos y experimentales
sugieren que:
Elevado ratio 6/ 3 Ratio puede aumentar el riesgo
de varios tipos de cncer (prstata, mama, clon,
pncreas y pulmn)

Okuyama H, Ichikawa Y, Sun Y, Hamazaki T, Lands WE. World Rev Nutr Diet. 2007;96:143-9.

154

Chajes .V, Bougnoux P. World Rev Nutr Diet. 2003;92:133-51

RATIO 6 / 3 DE ALGUNOS ALIMENTOS

Alimento
Huevo convencional

ratio 6 / 3

19,4

Huevo de Creta

156

1,3

Carne (msculo) bovina alimentada con

cereales

5,19

Carne (msculo) bovina alimentada con

pasto

2,2

Simopoulos AP. J Nutr. 2001 Nov;131(11 Suppl):3065S-73S

Cordain L et al. European Journal of Clinical Nutrition 2002; 56:181 191.

EPA & DHA POR CADA 100G PESCADO

Fede lacko. n3 PUFAsFrom dietary supplenents to medicines. Pathophysiology 14 (2007) 127132

158

PROBLEMAS CON EL PESCADO

Contaminaciones qumicas y orgnicas
Metilmercurio neurotxico
Dioxinas - carcingenos
DDT
PCBs contaminante liposoluble

Agricultura

Racin y fuente de contaminantes orgnicos

CONCENTRACIONES DE MERCURIO
Pescado

Concentracin
Mercurio
(ppm)

Pez-espada

0,97

Albacora

0,35

Atn

0,12

Bacalao

0,11

Salmn

0,01
Adaptado: FDA (EUA)

160

161

REDUCIR AG SATURADOS (14:0 E 16:0):

Carne grasa (preferir carne magra y ecolgica)
Lcteos
Embutidos
Aceite de palma

162

ELIMINAR AG TRANS:
Galletas
Bollera
Margarina
Comida precocinada
Fritos
163

AUMENTAR AG MONOINSATURADOS:
Aceite de oliva
Avellanas
Almendras
Aguacate
164

CONCLUSIONES
Usar Aceite de Coco, oliva y aguacate
Ingerir mas AG Poli insaturados Omega 3:
Algas y Pescado graso (p.e. sardina) o suplemento

Ingerir AG Omega 6 en equilibrio con Omega 3:

Almendras, nueces y avellanas, pero con ingesta alta de
Omega 3

165

Gracias
maelan@maelanfontes.com

pedro.bastos@nutriscience.pt

www.nutriscience.pt

"

www.maelanfontes.com