La teoria evolutiva y los estudios de intervención realizados en humanos contemporáneos sugieren que la dieta óptima para el ser humano es la que tuvimos durante nuestra evolución en el periodo del paleolítico (2,6 millones de años-10.000 años). No obstante, debido a las limitaciones de estos estudios hay una necesidad urgente de realizar más estudios de intervención. En esta presentación aportamos información acerca de las limitaciones actuales en la ciencia de la nutrición y por qué se debe considerar la evolución para optimizar los recursos de tiempo y dinero a la hora de diseñar estudios de intervención con dieta. Basar la alimentación en pescados y mariscos, carnes magras, frutas, verduras, tubérculos, huevos y algunos frutos secos aporta todos los nutrientes necesarios para una salud óptima sin riesgos obvios (con algunas excepciones como la hemocromatosis), y probablemente sea una alimentación que minimiza el riesgo de padecer o puede ayudar a mejorar el estado de las llamadas enfermedades de la civilización: diabetes, enfermedades cardiovasculares, obesidad y enfermedades autoinmunes.
8. Teoría: asociación
entre grasa y
muerte por ECV
Ancel Keys
YERUSHALMY, J., & HILLEBOE, H. E. (1957). NewYork State Journal of Medicine,
Keys,A. (1953). Journal of the Mount Sinai Hospital, NewYork
Keys,A.., et al. (1986). American Journal of Epidemiology,
9. Menor mortalidad en países mediterraneos (seven countries
study group)
Observación
YERUSHALMY, J., & HILLEBOE, H. E. (1957). NewYork State Journal of Medicine,
Keys,A. (1953). Journal of the Mount Sinai Hospital, NewYork
10. Sofi, F., Cesari, F.,Abbate, R., Gensini, G.F. & Casini,A. (2008) Adherence to Mediterranean diet and health status:
meta-analysis. BMJ 337, a1344.
Reducción del 9% en mortalidad por riesgo CVD por cada 2 puntos
de adherencia a la dieta mediterránea
Meta-análisis
514.816 sujetos
Seguimiento 3-18 años
La epidemiología lo deja claro
11. Pero también estaba claro para la terapia hormonal
sustitutiva
“Overall, the bulk of the evidence strongly supports a
protective effect of estrogens that is unlikely to be explained
by confounding factors”.
Stampfer, M. J., & Colditz, G.A. (1991). Preventive Medicine.
12. Pero un RCT demostró aumento del riesgo de enfermedad
coronaria, cáncer de mama, ictus, embolismo pulmonar = riesgos
superan a los beneficios
Rossouw, J. E., et al. (2002). Jama,
13. Lo mismo con la vitamina C
Epidemiología = asociación inversa
Davey Smith et al, Int J Epidemiol 2003;32:1
14. Lo mismo con la vitamina C
Intervención = aumento mortalidad
Davey Smith et al, Int J Epidemiol 2003;32:1
15. Lo mismo con la vitamina C
Intervención = aumento mortalidad
!!!
Davey Smith et al, Int J Epidemiol 2003;32:1
16. Lo mismo con la vitamina C
Intervención = aumento mortalidad
!!!
Davey Smith et al, Int J Epidemiol 2003;32:1
17. Base de las recomendaciones: epidemiología
!!!
18. Base de las recomendaciones: epidemiología
!!!
19. Base de las recomendaciones: epidemiología
!!!
20. Base de las recomendaciones: epidemiología
!!!
21. Base de las recomendaciones: epidemiología
!!!
22. Base de las recomendaciones: epidemiología
!!!
Muy pocos hablan de esto
23. Base de las recomendaciones: epidemiología
!!!
Muy pocos hablan de esto
¿O la epidemiología no cuenta en este caso?
25. Más epidemiología
Mientras los estudios de cohorte han demostrado
consistentemente este efecto protector de los cereales
integrales, sólo ha habido un estudio de intervención aleatorizado
controlado en la prevención secundaria recomendando consumir
más fibra de cereales. En éste no hubo reducción del índice de
reinfarto. El estudio tenía algunas limitaciones, por ejemplo, había
ocho dietas diferentes, no se comprobó la adherencia de forma
objetiva, y la duración fue sólo 2 años.
26. Romanticismo por los compuestos bioactivos
En ese mismo artículo:
Truswell,A. S. (2002). European Journal of Clinical Nutrition
27. Romanticismo por los compuestos bioactivos
En ese mismo artículo:
In people who consume relatively large amounts of whole
grain cereals these phytoestrogens in adults may have a
protective effect against hormone-related cancers (the
structure of enterodiol is similar to that of tamoxifen).
Truswell,A. S. (2002). European Journal of Clinical Nutrition
28. Romanticismo por los compuestos bioactivos
En ese mismo artículo:
In people who consume relatively large amounts of whole
grain cereals these phytoestrogens in adults may have a
protective effect against hormone-related cancers (the
structure of enterodiol is similar to that of tamoxifen).
¿Efecto protectivo?
¿Por qué no perjudicial al unirse a receptores
estrogénicos?
Truswell,A. S. (2002). European Journal of Clinical Nutrition
29. Romanticismo por los compuestos bioactivos
En ese mismo artículo:
In people who consume relatively large amounts of whole
grain cereals these phytoestrogens in adults may have a
protective effect against hormone-related cancers (the
structure of enterodiol is similar to that of tamoxifen).
¿Efecto protectivo?
¿Por qué no perjudicial al unirse a receptores
estrogénicos?
Se ha demostrado en animales que los
fitoestrógenos de la dieta producen infertilidad
(Jefferson,WN. et al. Reproduction. 2012;143(3):
247
Truswell,A. S. (2002). European Journal of Clinical Nutrition
30. Romanticismo por los compuestos bioactivos
¿Las plantas producen compuestos bioactivos para
protegernos a nosotros o para protegerse de nosotros?
En ese mismo artículo:
In people who consume relatively large amounts of whole
grain cereals these phytoestrogens in adults may have a
protective effect against hormone-related cancers (the
structure of enterodiol is similar to that of tamoxifen).
¿Efecto protectivo?
¿Por qué no perjudicial al unirse a receptores
estrogénicos?
Se ha demostrado en animales que los
fitoestrógenos de la dieta producen infertilidad
(Jefferson,WN. et al. Reproduction. 2012;143(3):
247
Truswell,A. S. (2002). European Journal of Clinical Nutrition
31. Desde un punto de vista de la biología y
botánica está claro
Wink M.Annual Plant Reviews, Functions and Biotechnology of Plant Secondary Metabolites (Volume 39, 2). 39th ed.Wiley-Blackwell; 2010.
32. Wink M.Annual Plant Reviews, Functions and Biotechnology of Plant Secondary Metabolites (Volume 39, 2). 39th ed.Wiley-Blackwell; 2010.
Desde un punto de vista de la biología y
botánica está claro
33. Todas las plantas poseen compuestos bioactivos cuya
función es protegerse de los depredadores
Los cereales, legumbres y semillas tienen mayor
concentración, y son más problemáticos para nosotros, que
las verduras, tubérculos o frutas
Lindeberg S. Food and Western Disease: Health and nutrition from an evolutionary perspective. 1st ed.
Wiley-Blackwell; 2010.
34. Mensaje: elegir las plantas a las que mejor adaptados
estemos (hace muchos millones de años que comemos
fruta y los compuestos están en la semilla, no pulpa) y
variar el consumo para disminuir la exposición al mismo
compuesto bioactivo
35. Estudios de larga duración testando el efecto de cereales
en hard-end points
Pero volvamos a los cereales
36. Efectos de la fibra de cereales en el reinfarto de miocardio
2033 hombres seguidos durante casi 2 años
Aumento no significativo de la mortalidad
Burr ML, Fehily AM, Gilbert JF, et al. Lancet 1989;
2:757-761.
37. Efectos de la fibra de cereales en el reinfarto de miocardio
2033 hombres seguidos durante casi 2 años
Ness,A. Et al. (2002). European Journal of Clinical Nutrition
38. Efectos de la fibra de cereales en el reinfarto de miocardio
2033 hombres seguidos durante casi 2 años
Pero tras ajuste estadístico si hay aumento significativo
en EIC y casi significativo en mortalidad total en los dos
primeros años!
Ness,A. Et al. (2002). European Journal of Clinical Nutrition
39. Efectos de la fibra de cereales en el reinfarto de miocardio
2033 hombres seguidos durante casi 2 años
Pero tras ajuste estadístico si hay aumento significativo
en EIC y casi significativo en mortalidad total en los dos
primeros años!
Ness,A. Et al. (2002). European Journal of Clinical Nutrition
40. Estudio de intervención
Women’s Health Initiative Intervention
Modification Trial
48,835 mujeres postmenopáusicas
Intervención
19,541 29,294
Control
8 años
Modificación
intensa de la
conducta
Material educativo
relacionado con
dieta
Howard, B.V., et al. JAMA: the Journal of the American Medical Association, 2006
41. Estudio de intervención
Women’s Health Initiative Intervention
Modification Trial
48,835 mujeres postmenopáusicas
Intervención
19,541 29,294
Control
8 años
Reducir la grasa a <20%en, 5
raciones de fruta/verdura y >6
raciones de cereales integrales al
día
Material educativo
relacionado con
dieta
Howard, B.V., et al. JAMA: the Journal of the American Medical Association, 2006
42. Estudio de intervención
Women’s Health Initiative Intervention
Modification Trial
48,835 mujeres postmenopáusicas
Howard, B.V., et al. JAMA: the Journal of the American Medical Association, 2006
43. Estudio de intervención
Women’s Health Initiative Intervention
Modification Trial
48,835 mujeres postmenopáusicas
Howard, B.V., et al. JAMA: the Journal of the American Medical Association, 2006
No redujo el riesgo de enfermedad
coronaria, ictus o ECV
44. Estudio de intervención
Women’s Health Initiative Intervention
Modification Trial
48,835 mujeres postmenopáusicas
Howard, B.V., et al. JAMA: the Journal of the American Medical Association, 2006
45. Estudio de intervención
Women’s Health Initiative Intervention
Modification Trial
48,835 mujeres postmenopáusicas
Howard, B.V., et al. JAMA: the Journal of the American Medical Association, 2006
Si miramos la letra pequeña...y escondida, vemos lo
siguiente
46. Howard, B.V., et al. JAMA: the Journal of the American Medical Association, 2006
Women’s Health Initiative Intervention
Modification Trial
Probablemente las frutas/verduras no fueron un
problema...
47. Howard BV, et al. JAMA:The Journal of the American Medical Association 2006
Aumento del riesgo relativo de ECV a 8 años en grupo de
intervención
0
5
10
15
20
25 26
3.4% mujeres con ECV al inicio
Low-fat/high fiber diet
Women’s Health Initiative Intervention
Modification Trial
48. Women’s Health Initiative Intervention
Modification Trial
Shikany, J. M., et al. (2011). American Journal of Clinical Nutrition
Control de glucosa en diabéticas
49. Women’s Health Initiative Intervention
Modification Trial
Shikany, J. M., et al. (2011). American Journal of Clinical Nutrition
Control de glucosa en diabéticas
50. Women’s Health Initiative Intervention
Modification Trial
Shikany, J. M., et al. (2011). American Journal of Clinical Nutrition
Control de glucosa en diabéticas
Empeoramiento significativo del control de glucosa
en el grupo de intervención en las mujeres con
diabetes tipo 2 al inicio del estudio
51. The Journal of Nutrition
Nutrition and Disease
Whole-Grain Foods Do Not Affect Insulin
Sensitivity or Markers of Lipid Peroxidation
and Inflammation in Healthy, Moderately
Overweight Subjects1,2
Agneta Andersson,3
* Siv Tengblad,3
Brita Karlstro¨m,3
Afaf Kamal-Eldin,4
Rikard Landberg,4
Samar Basu,3
Per A˚ man,4
and Bengt Vessby3
3
Clinical Nutrition and Metabolism, Department of Public Health and Caring Sciences, Uppsala University, 751 85 Uppsala, Sweden
and 4
Department of Food Science, the Swedish University of Agriculture Sciences (SLU), 750 07 Uppsala, Sweden
Abstract
High intakes of whole grain foods are inversely related to the incidence of coronary heart diseases and type 2 diabetes, but
the mechanisms remain unclear. Our study aimed to evaluate the effects of a diet rich in whole grains compared with a diet
containing the same amount of refined grains on insulin sensitivity and markers of lipid peroxidation and inflammation. In a
randomized crossover study, 22 women and 8 men (BMI 28 6 2) were given either whole-grain or refined-grain products
(3 bread slices, 2 crisp bread slices, 1 portion muesli, and 1 portion pasta) to include in their habitual daily diet for two 6-wk
periods. Peripheral insulin sensitivity was determined by euglycemic hyperinsulinemic clamp tests. 8-Iso-prostaglandin F2a
(8-iso PGF2a), an F2-isoprostane, was measured in the urine as a marker of lipid peroxidation, and highly sensitive C-reactive
protein and IL-6 were analyzed in plasma as markers of inflammation. Peripheral insulin sensitivity [mg glucose Á kg body
wt21
Á min21
per unit plasma insulin (mU/L) 3 100] did not improve when subjects consumed whole-grain products (6.8 6 3.0
at baseline and 6.5 6 2.7 after 6 wk) or refined products (6.4 6 2.9 and 6.9 6 3.2, respectively) and there were no differences
between the 2 periods. Whole-grain consumption also did not affect 8-iso-PGF2a in urine, IL-6 and C-reactive protein in
plasma, blood pressure, or serum lipid concentrations. In conclusion, substitution of whole grains (mainly based on milled
wheat) for refined-grain products in the habitual daily diet of healthy moderately overweight adults for 6-wk did not affect
insulin sensitivity or markers of lipid peroxidation and inflammation. J. Nutr. 137: 1401–1407, 2007.
Introduction
Whole-grain products are reported to have several positive effects
on human health (1). An inverse, relatively strong correlation
between the intake of whole grain foods (2–6) and fiber from
grains (7–10), based mainly on FFQ and the incidence of coro-
nary heart disease, is consistently shown in epidemiological studies
of both men and women. In addition, recent studies have linked
cereal fiber and whole-grain foods to a reduced risk of type 2
diabetes (11–16) and of the metabolic syndrome (6,17). These
relations seem to be most striking among overweight subjects
(11,18,19). The scientific evidence is considered sufficient to permit
health claims regarding the cardio-protective effect of whole-
grain products in many countries including the U.S., the U.K.,
and Sweden. The claims must, however, be set within the context
of other lifestyle factors such as exercise and healthy eating habits
in general (1).
Despite indications that whole grain foods may beneficially
influence glucose and lipid metabolism, knowledge of how
biological mechanisms contribute to the health effects of whole
grain remain weak. Several bioactive components, such as die-
tary fiber, vitamins, minerals, antioxidants, and other phyto-
protectants in whole grain may act synergistically to lower the
risk of chronic diseases (20,21). Insulin resistance and oxidative
stress are both important factors in the pathogenesis of type 2
diabetes and cardiovascular diseases (22–25) and may poten-
byguestonFebruary9,2011jn.nutrition.orgDownloadedfrom
Overweight Subjects1,2
Agneta Andersson,3
* Siv Tengblad,3
Brita Karlstro¨m,3
Afaf Kamal-Eldin,4
Rikard Landberg,4
Samar Basu,3
Per A˚ man,4
and Bengt Vessby3
3
Clinical Nutrition and Metabolism, Department of Public Health and Caring Sciences, Uppsala University, 751 85 Uppsala, Sweden
and 4
Department of Food Science, the Swedish University of Agriculture Sciences (SLU), 750 07 Uppsala, Sweden
Abstract
High intakes of whole grain foods are inversely related to the incidence of coronary heart diseases and type 2 diabetes, but
the mechanisms remain unclear. Our study aimed to evaluate the effects of a diet rich in whole grains compared with a diet
containing the same amount of refined grains on insulin sensitivity and markers of lipid peroxidation and inflammation. In a
randomized crossover study, 22 women and 8 men (BMI 28 6 2) were given either whole-grain or refined-grain products
(3 bread slices, 2 crisp bread slices, 1 portion muesli, and 1 portion pasta) to include in their habitual daily diet for two 6-wk
periods. Peripheral insulin sensitivity was determined by euglycemic hyperinsulinemic clamp tests. 8-Iso-prostaglandin F2a
(8-iso PGF2a), an F2-isoprostane, was measured in the urine as a marker of lipid peroxidation, and highly sensitive C-reactive
protein and IL-6 were analyzed in plasma as markers of inflammation. Peripheral insulin sensitivity [mg glucose Á kg body
wt21
Á min21
per unit plasma insulin (mU/L) 3 100] did not improve when subjects consumed whole-grain products (6.8 6 3.0
at baseline and 6.5 6 2.7 after 6 wk) or refined products (6.4 6 2.9 and 6.9 6 3.2, respectively) and there were no differences
between the 2 periods. Whole-grain consumption also did not affect 8-iso-PGF2a in urine, IL-6 and C-reactive protein in
plasma, blood pressure, or serum lipid concentrations. In conclusion, substitution of whole grains (mainly based on milled
wheat) for refined-grain products in the habitual daily diet of healthy moderately overweight adults for 6-wk did not affect
insulin sensitivity or markers of lipid peroxidation and inflammation. J. Nutr. 137: 1401–1407, 2007.
Introduction
Whole-grain products are reported to have several positive effects
on human health (1). An inverse, relatively strong correlation
between the intake of whole grain foods (2–6) and fiber from
grain products in many countries including
and Sweden. The claims must, however, be se
of other lifestyle factors such as exercise and h
in general (1).
TABLE 5 BMI, blood pressure, and blood chemistry of all participants before and after 6 wk consuming
whole-grain or refined-grain diets1
Whole-grain period Refined-grain period
Before After Before After P-value treatment effect2
n 30 30 30 30
BMI, kg/m2
28.5 6 2.4 28.8 6 2.5a
28.4 6 2.1 28.6 6 2.1 0.046
Fasting blood glucose, mmol/L 5.2 6 0.8 5.3 6 0.8 5.2 6 0.9 5.2 6 0.8 0.28
Fasting insulin, pmol/L 56.2 6 22.9 57.6 6 24.3 60.4 6 30.6 57.6 6 25.7 0.47
Insulin sensitivity,3
M 5.9 6 2.1 5.5 6 1.7 5.7 6 1.9 6.0 6 2.0 0.24
M/I 6.8 6 3.0 6.5 6 2.7 6.4 6 2.9 6.9 6 3.2 0.79
Total cholesterol, mmol/L 5.5 6 0.7 5.5 6 0.7 5.5 6 0.8 5.5 6 0.7 0.76
HDL cholesterol, mmol/L 1.3 6 0.3 1.2 6 0.3 1.2 6 0.2 1.2 6 0.3 0.15
LDL cholesterol, mmol/L 3.7 6 0.8 3.7 6 0.7 3.7 6 0.8 3.6 6 0.7 0.40
TG cholesterol, mmol/L 1.4 6 0.8 1.5 6 0.8 1.3 6 0.6 1.6 6 1.0c
0.19
Free fatty acid, mmol/L 0.56 6 0.19 0.61 6 0.18 0.63 6 0.17 0.62 6 0.18 0.99
Systolic blood pressure, mm Hg 130 6 17 129 6 15 130 6 16 130 6 15 0.35*
Diastolic blood pressure, mm Hg 81 6 9 81 6 8 80 6 10 81 6 9 0.60
8-iso-PGF2a, nmol/mmol creatinine 0.43 6 0.14 0.43 6 0.14 0.42 6 0.15 0.44 6 0.21 0.48
a-tocopherol, mmol/mmol lipid 4.68 6 0.72 4.78 6 0.61 4.38 6 1.07 4.64 6 0.61 0.08
g-tocopherol, mmol/mmol lipid 0.26 6 0.12 0.24 6 0.07 0.26 6 0.10 0.26 6 0.10 0.10
CRP, mg/L 2.03 6 1.62 2.38 6 2.29 2.86 6 2.96 2.34 6 1.57 0.55
IL-6, ng/L 14.8 6 32.2 15.2 6 33.2 15.9 6 32.4 15.8 6 30.9 0.79
PAI-1 activity, kU/L 24.7 6 15.8 26.9 6 20.3 24.8 6 19.9 22.1 6 19.5 0.26
1
Data are means 6 SD.
2
P-values (treatment effect) for differences between the whole-grain and refined-grain diet adjusted for changes in BMI. Differences within
groups when compared to baseline: a
P , 0.001; b
P , 0.01; c
P , 0.05. *Parallel group design, only from 1st diet period (because carryover
Downloadedfrom
J. Nutr. 137: 1401–1407, 2007.!
Si diferencias entre los grupos!
Cereales integrales y marcadores inflamación/
cardiovasculares
52. The Journal of Nutrition
Nutrition and Disease
Whole-Grain Foods Do Not Affect Insulin
Sensitivity or Markers of Lipid Peroxidation
and Inflammation in Healthy, Moderately
Overweight Subjects1,2
Agneta Andersson,3
* Siv Tengblad,3
Brita Karlstro¨m,3
Afaf Kamal-Eldin,4
Rikard Landberg,4
Samar Basu,3
Per A˚ man,4
and Bengt Vessby3
3
Clinical Nutrition and Metabolism, Department of Public Health and Caring Sciences, Uppsala University, 751 85 Uppsala, Sweden
and 4
Department of Food Science, the Swedish University of Agriculture Sciences (SLU), 750 07 Uppsala, Sweden
Abstract
High intakes of whole grain foods are inversely related to the incidence of coronary heart diseases and type 2 diabetes, but
the mechanisms remain unclear. Our study aimed to evaluate the effects of a diet rich in whole grains compared with a diet
containing the same amount of refined grains on insulin sensitivity and markers of lipid peroxidation and inflammation. In a
randomized crossover study, 22 women and 8 men (BMI 28 6 2) were given either whole-grain or refined-grain products
(3 bread slices, 2 crisp bread slices, 1 portion muesli, and 1 portion pasta) to include in their habitual daily diet for two 6-wk
periods. Peripheral insulin sensitivity was determined by euglycemic hyperinsulinemic clamp tests. 8-Iso-prostaglandin F2a
(8-iso PGF2a), an F2-isoprostane, was measured in the urine as a marker of lipid peroxidation, and highly sensitive C-reactive
protein and IL-6 were analyzed in plasma as markers of inflammation. Peripheral insulin sensitivity [mg glucose Á kg body
wt21
Á min21
per unit plasma insulin (mU/L) 3 100] did not improve when subjects consumed whole-grain products (6.8 6 3.0
at baseline and 6.5 6 2.7 after 6 wk) or refined products (6.4 6 2.9 and 6.9 6 3.2, respectively) and there were no differences
between the 2 periods. Whole-grain consumption also did not affect 8-iso-PGF2a in urine, IL-6 and C-reactive protein in
plasma, blood pressure, or serum lipid concentrations. In conclusion, substitution of whole grains (mainly based on milled
wheat) for refined-grain products in the habitual daily diet of healthy moderately overweight adults for 6-wk did not affect
insulin sensitivity or markers of lipid peroxidation and inflammation. J. Nutr. 137: 1401–1407, 2007.
Introduction
Whole-grain products are reported to have several positive effects
on human health (1). An inverse, relatively strong correlation
between the intake of whole grain foods (2–6) and fiber from
grains (7–10), based mainly on FFQ and the incidence of coro-
nary heart disease, is consistently shown in epidemiological studies
of both men and women. In addition, recent studies have linked
cereal fiber and whole-grain foods to a reduced risk of type 2
diabetes (11–16) and of the metabolic syndrome (6,17). These
relations seem to be most striking among overweight subjects
(11,18,19). The scientific evidence is considered sufficient to permit
health claims regarding the cardio-protective effect of whole-
grain products in many countries including the U.S., the U.K.,
and Sweden. The claims must, however, be set within the context
of other lifestyle factors such as exercise and healthy eating habits
in general (1).
Despite indications that whole grain foods may beneficially
influence glucose and lipid metabolism, knowledge of how
biological mechanisms contribute to the health effects of whole
grain remain weak. Several bioactive components, such as die-
tary fiber, vitamins, minerals, antioxidants, and other phyto-
protectants in whole grain may act synergistically to lower the
risk of chronic diseases (20,21). Insulin resistance and oxidative
stress are both important factors in the pathogenesis of type 2
diabetes and cardiovascular diseases (22–25) and may poten-
byguestonFebruary9,2011jn.nutrition.orgDownloadedfrom
Overweight Subjects1,2
Agneta Andersson,3
* Siv Tengblad,3
Brita Karlstro¨m,3
Afaf Kamal-Eldin,4
Rikard Landberg,4
Samar Basu,3
Per A˚ man,4
and Bengt Vessby3
3
Clinical Nutrition and Metabolism, Department of Public Health and Caring Sciences, Uppsala University, 751 85 Uppsala, Sweden
and 4
Department of Food Science, the Swedish University of Agriculture Sciences (SLU), 750 07 Uppsala, Sweden
Abstract
High intakes of whole grain foods are inversely related to the incidence of coronary heart diseases and type 2 diabetes, but
the mechanisms remain unclear. Our study aimed to evaluate the effects of a diet rich in whole grains compared with a diet
containing the same amount of refined grains on insulin sensitivity and markers of lipid peroxidation and inflammation. In a
randomized crossover study, 22 women and 8 men (BMI 28 6 2) were given either whole-grain or refined-grain products
(3 bread slices, 2 crisp bread slices, 1 portion muesli, and 1 portion pasta) to include in their habitual daily diet for two 6-wk
periods. Peripheral insulin sensitivity was determined by euglycemic hyperinsulinemic clamp tests. 8-Iso-prostaglandin F2a
(8-iso PGF2a), an F2-isoprostane, was measured in the urine as a marker of lipid peroxidation, and highly sensitive C-reactive
protein and IL-6 were analyzed in plasma as markers of inflammation. Peripheral insulin sensitivity [mg glucose Á kg body
wt21
Á min21
per unit plasma insulin (mU/L) 3 100] did not improve when subjects consumed whole-grain products (6.8 6 3.0
at baseline and 6.5 6 2.7 after 6 wk) or refined products (6.4 6 2.9 and 6.9 6 3.2, respectively) and there were no differences
between the 2 periods. Whole-grain consumption also did not affect 8-iso-PGF2a in urine, IL-6 and C-reactive protein in
plasma, blood pressure, or serum lipid concentrations. In conclusion, substitution of whole grains (mainly based on milled
wheat) for refined-grain products in the habitual daily diet of healthy moderately overweight adults for 6-wk did not affect
insulin sensitivity or markers of lipid peroxidation and inflammation. J. Nutr. 137: 1401–1407, 2007.
Introduction
Whole-grain products are reported to have several positive effects
on human health (1). An inverse, relatively strong correlation
between the intake of whole grain foods (2–6) and fiber from
grain products in many countries including
and Sweden. The claims must, however, be se
of other lifestyle factors such as exercise and h
in general (1).
TABLE 5 BMI, blood pressure, and blood chemistry of all participants before and after 6 wk consuming
whole-grain or refined-grain diets1
Whole-grain period Refined-grain period
Before After Before After P-value treatment effect2
n 30 30 30 30
BMI, kg/m2
28.5 6 2.4 28.8 6 2.5a
28.4 6 2.1 28.6 6 2.1 0.046
Fasting blood glucose, mmol/L 5.2 6 0.8 5.3 6 0.8 5.2 6 0.9 5.2 6 0.8 0.28
Fasting insulin, pmol/L 56.2 6 22.9 57.6 6 24.3 60.4 6 30.6 57.6 6 25.7 0.47
Insulin sensitivity,3
M 5.9 6 2.1 5.5 6 1.7 5.7 6 1.9 6.0 6 2.0 0.24
M/I 6.8 6 3.0 6.5 6 2.7 6.4 6 2.9 6.9 6 3.2 0.79
Total cholesterol, mmol/L 5.5 6 0.7 5.5 6 0.7 5.5 6 0.8 5.5 6 0.7 0.76
HDL cholesterol, mmol/L 1.3 6 0.3 1.2 6 0.3 1.2 6 0.2 1.2 6 0.3 0.15
LDL cholesterol, mmol/L 3.7 6 0.8 3.7 6 0.7 3.7 6 0.8 3.6 6 0.7 0.40
TG cholesterol, mmol/L 1.4 6 0.8 1.5 6 0.8 1.3 6 0.6 1.6 6 1.0c
0.19
Free fatty acid, mmol/L 0.56 6 0.19 0.61 6 0.18 0.63 6 0.17 0.62 6 0.18 0.99
Systolic blood pressure, mm Hg 130 6 17 129 6 15 130 6 16 130 6 15 0.35*
Diastolic blood pressure, mm Hg 81 6 9 81 6 8 80 6 10 81 6 9 0.60
8-iso-PGF2a, nmol/mmol creatinine 0.43 6 0.14 0.43 6 0.14 0.42 6 0.15 0.44 6 0.21 0.48
a-tocopherol, mmol/mmol lipid 4.68 6 0.72 4.78 6 0.61 4.38 6 1.07 4.64 6 0.61 0.08
g-tocopherol, mmol/mmol lipid 0.26 6 0.12 0.24 6 0.07 0.26 6 0.10 0.26 6 0.10 0.10
CRP, mg/L 2.03 6 1.62 2.38 6 2.29 2.86 6 2.96 2.34 6 1.57 0.55
IL-6, ng/L 14.8 6 32.2 15.2 6 33.2 15.9 6 32.4 15.8 6 30.9 0.79
PAI-1 activity, kU/L 24.7 6 15.8 26.9 6 20.3 24.8 6 19.9 22.1 6 19.5 0.26
1
Data are means 6 SD.
2
P-values (treatment effect) for differences between the whole-grain and refined-grain diet adjusted for changes in BMI. Differences within
groups when compared to baseline: a
P , 0.001; b
P , 0.01; c
P , 0.05. *Parallel group design, only from 1st diet period (because carryover
Downloadedfrom
J. Nutr. 137: 1401–1407, 2007.!
Si diferencias entre los grupos!
Cereales integrales y marcadores inflamación/
cardiovasculares
Sin diferencias significativas entre cereales
integrales y refinados
53. Effect of Wheat Bran on Glycemic Control
and Risk Factors for Cardiovascular
Disease in Type 2 Diabetes
DAVID J. A. JENKINS, MD
1,2,3,4
CYRIL W. C. KENDALL, PHD
1,3
LIVIA S. A. AUGUSTIN, MSC
1,3
MARGARET C. MARTINI, PHD
5
METTE AXELSEN, PHD
6
DOROTHEA FAULKNER, RD
1
EDWARD VIDGEN, BSC
1,3
TINA PARKER, RD
1
HERB LAU, MD
7,8
PHILIP W. CONNELLY, PHD
2,9,10
JEROME TEITEL, MD
7,8
WILLIAM SINGER, MD
2
ARTHUR C. VANDENBROUCKE, PHD
7,10
LAWRENCE A. LEITER, MD
1,2,3,4
ROBERT G. JOSSE, MD
1,2,3,4
OBJECTIVE — Cohort studies indicate that cereal fiber reduces the risk of diabetes and
coronary heart disease (CHD). Therefore, we assessed the effect of wheat bran on glycemic
control and CHD risk factors in type 2 diabetes.
RESEARCH DESIGN AND METHODS — A total of 23 subjects with type 2 diabetes
(16 men and 7 postmenopausal women) completed two 3-month phases of a randomized
crossover study. In the test phase, bread and breakfast cereals were provided as products high in
cereal fiber (19 g/day additional cereal fiber). In the control phase, supplements were low in fiber
(4 g/day additional cereal fiber).
RESULTS — Between the test and control treatments, no differences were seen in body
weight, fasting blood glucose, HbA1c, serum lipids, apolipoproteins, blood pressure, serum uric
acid, clotting factors, homocysteine, C-reactive protein, magnesium, calcium, iron, or ferritin.
LDL oxidation in the test phase was higher than that seen in the control phase (12.1 Ϯ 5.4%, P Ͻ
0.034). Of the subjects originally recruited, more dropped out of the study for health and food
preference reasons from the control phase (16 subjects) than the test phase (11 subjects).
CONCLUSIONS — High-fiber cereal foods did not improve conventional markers of glyce-
mic control or risk factors for CHD in type 2 diabetes over 3 months. Possibly longer studies are
required to demonstrate the benefits of cereal fiber. Alternatively, cereal fiber in the diet may be
a marker for another component of whole grains that imparts health advantages or a healthy
lifestyle.
Diabetes Care 25:1522–1528, 2002
T
here is much interest in the possible
health benefits of fiber-containing
cereals (1–3). The exact component
or facet of fiber that is responsible has not
been clearly defined, and there are indi-
cations that the whole grain confers met-
abolic benefits (4) and reduces the risk of
chronic disease (1,5,6). The results of
large cohort studies have suggested that
wheat fiber protects against the develop-
ment of diabetes (1–3). Many diabetes as-
sociations advise increased fiber intake,
either to improve glycemic control (7) or
to confer general health benefits (8). In-
creases in fiber from a variety of dietary
sources have been shown to improve gly-
cemic control in type 2 diabetes (9). Early
studies suggested that cereal fiber im-
proved both glycemic control in diabetes
(10) and glucose tolerance in nondiabetic
subjects (11). The reason for the benefi-
cial effects of nonviscous cereal fiber is not
clear. Cereal fibers do not reduce the rate
of gastric emptying and small intestinal
absorption or flatten the postprandial gly-
cemic response to a high-carbohydrate
test meal (12). In contrast, viscous fibers
such as guar and pectin have been shown
to reduce the rate of gastric emptying (13)
and small intestinal absorption (14),
thereby providing a mechanism for po-
tential benefits. These fibers have been
shown to reduce postprandial glycemia
when added to test meals. They also de-
crease 24-h urinary glucose losses when
added to the diets of subjects with type 2
diabetes (15).
Furthermore, it is wheat fiber, rather
than viscous fiber, that for more than two
decades has been shown consistently in
cohort studies to be associated with a re-
duced risk of heart disease (5,6,16,17).
These effects are seen despite the fact that
viscous fibers from oats, barley, psyllium,
pectins, and guar gum have been shown
to lower serum cholesterol and improve
the blood lipid profile, whereas the insol-
● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ●
From the 1
Clinical Nutrition and Risk Factor Modification Center, St. Michael’s Hospital, Toronto, Ontario,
Canada; the 2
Department of Medicine, Division of Endocrinology and Metabolism, St. Michael’s Hospital,
Toronto, Ontario, Canada; the 3
Department of Nutritional Sciences, Faculty of Medicine, University of
Toronto, Toronto, Ontario, Canada; the 4
Department of Medicine, Faculty of Medicine, University of
Toronto, Toronto, Ontario, Canada; 5
Kraft Foods, Glenview, Illinois; the 6
Lundberg Laboratory for Diabetic
Research, Department of Internal Medicine, Sahlgrenska University Hospital, Go¨teborg, Sweden; the 7
De-
partment of Laboratory Medicine, Division of Clinical Biochemistry, St. Michael’s Hospital, Toronto, On-
tario, Canada; the 8
Department of Hematology, St. Michael’s Hospital, Toronto, Ontario, Canada; the
9
Department of Biochemistry, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada; and
the 10
Department of Laboratory Medicine and Pathobiology, Faculty of Medicine, University of Toronto,
Toronto, Ontario, Canada.
Address correspondence and reprint requests to David J. A. Jenkins, Clinical Nutrition and Risk Factor
Modification Center, St. Michael’s Hospital, 61 Queen St. East, Toronto, Ontario, Canada, M5C 2T2. E-mail:
C l i n i c a l C a r e / E d u c a t i o n / N u t r i t i o n
O R I G I N A L A R T I C L E
METTE AXELSEN, PHD
DOROTHEA FAULKNER, RD
1
EDWARD VIDGEN, BSC
1,3
TINA PARKER, RD
1
ARTHUR C. VANDENBROUCKE, PHD
7,10
LAWRENCE A. LEITER, MD
1,2,3,4
ROBERT G. JOSSE, MD
1,2,3,4
OBJECTIVE — Cohort studies indicate that cereal fiber reduces the risk of diabetes and
coronary heart disease (CHD). Therefore, we assessed the effect of wheat bran on glycemic
control and CHD risk factors in type 2 diabetes.
RESEARCH DESIGN AND METHODS — A total of 23 subjects with type 2 diabetes
(16 men and 7 postmenopausal women) completed two 3-month phases of a randomized
crossover study. In the test phase, bread and breakfast cereals were provided as products high in
cereal fiber (19 g/day additional cereal fiber). In the control phase, supplements were low in fiber
(4 g/day additional cereal fiber).
RESULTS — Between the test and control treatments, no differences were seen in body
weight, fasting blood glucose, HbA1c, serum lipids, apolipoproteins, blood pressure, serum uric
acid, clotting factors, homocysteine, C-reactive protein, magnesium, calcium, iron, or ferritin.
LDL oxidation in the test phase was higher than that seen in the control phase (12.1 Ϯ 5.4%, P Ͻ
0.034). Of the subjects originally recruited, more dropped out of the study for health and food
preference reasons from the control phase (16 subjects) than the test phase (11 subjects).
CONCLUSIONS — High-fiber cereal foods did not improve conventional markers of glyce-
mic control or risk factors for CHD in type 2 diabetes over 3 months. Possibly longer studies are
required to demonstrate the benefits of cereal fiber. Alternatively, cereal fiber in the diet may be
a marker for another component of whole grains that imparts health advantages or a healthy
lifestyle.
Diabetes Care 25:1522–1528, 2002
been clearly de
cations that the
abolic benefits
chronic diseas
large cohort st
wheat fiber pro
ment of diabete
sociations advi
either to impro
to confer gener
creases in fiber
sources have be
cemic control in
studies sugges
proved both gly
(10) and glucos
subjects (11). T
cial effects of no
clear. Cereal fib
of gastric emp
absorption or fl
cemic respons
test meal (12).
such as guar an
to reduce the ra
and small int
thereby provid
tential benefits
shown to redu
when added to
crease 24-h uri
MARGARET C. MARTINI, PHD
5
METTE AXELSEN, PHD
6
DOROTHEA FAULKNER, RD
1
EDWARD VIDGEN, BSC
1,3
TINA PARKER, RD
1
WILLIAM SINGER, MD
2
ARTHUR C. VANDENBROUCKE, PHD
7,10
LAWRENCE A. LEITER, MD
1,2,3,4
ROBERT G. JOSSE, MD
1,2,3,4
OBJECTIVE — Cohort studies indicate that cereal fiber reduces the risk of diabetes and
coronary heart disease (CHD). Therefore, we assessed the effect of wheat bran on glycemic
control and CHD risk factors in type 2 diabetes.
RESEARCH DESIGN AND METHODS — A total of 23 subjects with type 2 diabetes
(16 men and 7 postmenopausal women) completed two 3-month phases of a randomized
crossover study. In the test phase, bread and breakfast cereals were provided as products high in
cereal fiber (19 g/day additional cereal fiber). In the control phase, supplements were low in fiber
(4 g/day additional cereal fiber).
RESULTS — Between the test and control treatments, no differences were seen in body
weight, fasting blood glucose, HbA1c, serum lipids, apolipoproteins, blood pressure, serum uric
acid, clotting factors, homocysteine, C-reactive protein, magnesium, calcium, iron, or ferritin.
LDL oxidation in the test phase was higher than that seen in the control phase (12.1 Ϯ 5.4%, P Ͻ
0.034). Of the subjects originally recruited, more dropped out of the study for health and food
preference reasons from the control phase (16 subjects) than the test phase (11 subjects).
CONCLUSIONS — High-fiber cereal foods did not improve conventional markers of glyce-
mic control or risk factors for CHD in type 2 diabetes over 3 months. Possibly longer studies are
required to demonstrate the benefits of cereal fiber. Alternatively, cereal fiber in the diet may be
a marker for another component of whole grains that imparts health advantages or a healthy
lifestyle.
Diabetes Care 25:1522–1528, 2002
Tor facet of fiber
been clearly de
cations that the
abolic benefits (
chronic disease
large cohort stu
wheat fiber pro
ment of diabete
sociations advis
either to improv
to confer gener
creases in fiber
sources have be
cemic control in
studies suggest
proved both gly
(10) and glucos
subjects (11). T
cial effects of no
clear. Cereal fib
of gastric empt
absorption or fla
cemic response
test meal (12).
such as guar an
to reduce the ra
and small inte
thereby providi
tential benefits.
shown to redu
when added to
LIVIA S. A. AUGUSTIN, MSC
MARGARET C. MARTINI, PHD
5
METTE AXELSEN, PHD
6
DOROTHEA FAULKNER, RD
1
EDWARD VIDGEN, BSC
1,3
TINA PARKER, RD
1
JEROME TEITEL, MD
WILLIAM SINGER, MD
2
ARTHUR C. VANDENBROUCKE, PHD
7,10
LAWRENCE A. LEITER, MD
1,2,3,4
ROBERT G. JOSSE, MD
1,2,3,4
OBJECTIVE — Cohort studies indicate that cereal fiber reduces the risk of diabetes and
coronary heart disease (CHD). Therefore, we assessed the effect of wheat bran on glycemic
control and CHD risk factors in type 2 diabetes.
RESEARCH DESIGN AND METHODS — A total of 23 subjects with type 2 diabetes
(16 men and 7 postmenopausal women) completed two 3-month phases of a randomized
crossover study. In the test phase, bread and breakfast cereals were provided as products high in
cereal fiber (19 g/day additional cereal fiber). In the control phase, supplements were low in fiber
(4 g/day additional cereal fiber).
RESULTS — Between the test and control treatments, no differences were seen in body
weight, fasting blood glucose, HbA1c, serum lipids, apolipoproteins, blood pressure, serum uric
acid, clotting factors, homocysteine, C-reactive protein, magnesium, calcium, iron, or ferritin.
LDL oxidation in the test phase was higher than that seen in the control phase (12.1 Ϯ 5.4%, P Ͻ
0.034). Of the subjects originally recruited, more dropped out of the study for health and food
preference reasons from the control phase (16 subjects) than the test phase (11 subjects).
CONCLUSIONS — High-fiber cereal foods did not improve conventional markers of glyce-
mic control or risk factors for CHD in type 2 diabetes over 3 months. Possibly longer studies are
required to demonstrate the benefits of cereal fiber. Alternatively, cereal fiber in the diet may be
a marker for another component of whole grains that imparts health advantages or a healthy
lifestyle.
Diabetes Care 25:1522–1528, 2002
Tcereals (1–
or facet of fiber
been clearly de
cations that the
abolic benefits
chronic diseas
large cohort stu
wheat fiber pro
ment of diabete
sociations advi
either to impro
to confer gener
creases in fiber
sources have be
cemic control in
studies sugges
proved both gly
(10) and glucos
subjects (11). T
cial effects of no
clear. Cereal fib
of gastric empt
absorption or fl
cemic response
test meal (12).
such as guar an
to reduce the ra
and small int
thereby provid
tential benefits
shown to redu
Jenkins D, et al. Diabetes Care 25:1522–1528, 2002!
Cereales integrales y marcadores inflamación/
cardiovasculares
54. Effect of Wheat Bran on Glycemic Control
and Risk Factors for Cardiovascular
Disease in Type 2 Diabetes
DAVID J. A. JENKINS, MD
1,2,3,4
CYRIL W. C. KENDALL, PHD
1,3
LIVIA S. A. AUGUSTIN, MSC
1,3
MARGARET C. MARTINI, PHD
5
METTE AXELSEN, PHD
6
DOROTHEA FAULKNER, RD
1
EDWARD VIDGEN, BSC
1,3
TINA PARKER, RD
1
HERB LAU, MD
7,8
PHILIP W. CONNELLY, PHD
2,9,10
JEROME TEITEL, MD
7,8
WILLIAM SINGER, MD
2
ARTHUR C. VANDENBROUCKE, PHD
7,10
LAWRENCE A. LEITER, MD
1,2,3,4
ROBERT G. JOSSE, MD
1,2,3,4
OBJECTIVE — Cohort studies indicate that cereal fiber reduces the risk of diabetes and
coronary heart disease (CHD). Therefore, we assessed the effect of wheat bran on glycemic
control and CHD risk factors in type 2 diabetes.
RESEARCH DESIGN AND METHODS — A total of 23 subjects with type 2 diabetes
(16 men and 7 postmenopausal women) completed two 3-month phases of a randomized
crossover study. In the test phase, bread and breakfast cereals were provided as products high in
cereal fiber (19 g/day additional cereal fiber). In the control phase, supplements were low in fiber
(4 g/day additional cereal fiber).
RESULTS — Between the test and control treatments, no differences were seen in body
weight, fasting blood glucose, HbA1c, serum lipids, apolipoproteins, blood pressure, serum uric
acid, clotting factors, homocysteine, C-reactive protein, magnesium, calcium, iron, or ferritin.
LDL oxidation in the test phase was higher than that seen in the control phase (12.1 Ϯ 5.4%, P Ͻ
0.034). Of the subjects originally recruited, more dropped out of the study for health and food
preference reasons from the control phase (16 subjects) than the test phase (11 subjects).
CONCLUSIONS — High-fiber cereal foods did not improve conventional markers of glyce-
mic control or risk factors for CHD in type 2 diabetes over 3 months. Possibly longer studies are
required to demonstrate the benefits of cereal fiber. Alternatively, cereal fiber in the diet may be
a marker for another component of whole grains that imparts health advantages or a healthy
lifestyle.
Diabetes Care 25:1522–1528, 2002
T
here is much interest in the possible
health benefits of fiber-containing
cereals (1–3). The exact component
or facet of fiber that is responsible has not
been clearly defined, and there are indi-
cations that the whole grain confers met-
abolic benefits (4) and reduces the risk of
chronic disease (1,5,6). The results of
large cohort studies have suggested that
wheat fiber protects against the develop-
ment of diabetes (1–3). Many diabetes as-
sociations advise increased fiber intake,
either to improve glycemic control (7) or
to confer general health benefits (8). In-
creases in fiber from a variety of dietary
sources have been shown to improve gly-
cemic control in type 2 diabetes (9). Early
studies suggested that cereal fiber im-
proved both glycemic control in diabetes
(10) and glucose tolerance in nondiabetic
subjects (11). The reason for the benefi-
cial effects of nonviscous cereal fiber is not
clear. Cereal fibers do not reduce the rate
of gastric emptying and small intestinal
absorption or flatten the postprandial gly-
cemic response to a high-carbohydrate
test meal (12). In contrast, viscous fibers
such as guar and pectin have been shown
to reduce the rate of gastric emptying (13)
and small intestinal absorption (14),
thereby providing a mechanism for po-
tential benefits. These fibers have been
shown to reduce postprandial glycemia
when added to test meals. They also de-
crease 24-h urinary glucose losses when
added to the diets of subjects with type 2
diabetes (15).
Furthermore, it is wheat fiber, rather
than viscous fiber, that for more than two
decades has been shown consistently in
cohort studies to be associated with a re-
duced risk of heart disease (5,6,16,17).
These effects are seen despite the fact that
viscous fibers from oats, barley, psyllium,
pectins, and guar gum have been shown
to lower serum cholesterol and improve
the blood lipid profile, whereas the insol-
● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ●
From the 1
Clinical Nutrition and Risk Factor Modification Center, St. Michael’s Hospital, Toronto, Ontario,
Canada; the 2
Department of Medicine, Division of Endocrinology and Metabolism, St. Michael’s Hospital,
Toronto, Ontario, Canada; the 3
Department of Nutritional Sciences, Faculty of Medicine, University of
Toronto, Toronto, Ontario, Canada; the 4
Department of Medicine, Faculty of Medicine, University of
Toronto, Toronto, Ontario, Canada; 5
Kraft Foods, Glenview, Illinois; the 6
Lundberg Laboratory for Diabetic
Research, Department of Internal Medicine, Sahlgrenska University Hospital, Go¨teborg, Sweden; the 7
De-
partment of Laboratory Medicine, Division of Clinical Biochemistry, St. Michael’s Hospital, Toronto, On-
tario, Canada; the 8
Department of Hematology, St. Michael’s Hospital, Toronto, Ontario, Canada; the
9
Department of Biochemistry, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada; and
the 10
Department of Laboratory Medicine and Pathobiology, Faculty of Medicine, University of Toronto,
Toronto, Ontario, Canada.
Address correspondence and reprint requests to David J. A. Jenkins, Clinical Nutrition and Risk Factor
Modification Center, St. Michael’s Hospital, 61 Queen St. East, Toronto, Ontario, Canada, M5C 2T2. E-mail:
C l i n i c a l C a r e / E d u c a t i o n / N u t r i t i o n
O R I G I N A L A R T I C L E
METTE AXELSEN, PHD
DOROTHEA FAULKNER, RD
1
EDWARD VIDGEN, BSC
1,3
TINA PARKER, RD
1
ARTHUR C. VANDENBROUCKE, PHD
7,10
LAWRENCE A. LEITER, MD
1,2,3,4
ROBERT G. JOSSE, MD
1,2,3,4
OBJECTIVE — Cohort studies indicate that cereal fiber reduces the risk of diabetes and
coronary heart disease (CHD). Therefore, we assessed the effect of wheat bran on glycemic
control and CHD risk factors in type 2 diabetes.
RESEARCH DESIGN AND METHODS — A total of 23 subjects with type 2 diabetes
(16 men and 7 postmenopausal women) completed two 3-month phases of a randomized
crossover study. In the test phase, bread and breakfast cereals were provided as products high in
cereal fiber (19 g/day additional cereal fiber). In the control phase, supplements were low in fiber
(4 g/day additional cereal fiber).
RESULTS — Between the test and control treatments, no differences were seen in body
weight, fasting blood glucose, HbA1c, serum lipids, apolipoproteins, blood pressure, serum uric
acid, clotting factors, homocysteine, C-reactive protein, magnesium, calcium, iron, or ferritin.
LDL oxidation in the test phase was higher than that seen in the control phase (12.1 Ϯ 5.4%, P Ͻ
0.034). Of the subjects originally recruited, more dropped out of the study for health and food
preference reasons from the control phase (16 subjects) than the test phase (11 subjects).
CONCLUSIONS — High-fiber cereal foods did not improve conventional markers of glyce-
mic control or risk factors for CHD in type 2 diabetes over 3 months. Possibly longer studies are
required to demonstrate the benefits of cereal fiber. Alternatively, cereal fiber in the diet may be
a marker for another component of whole grains that imparts health advantages or a healthy
lifestyle.
Diabetes Care 25:1522–1528, 2002
been clearly de
cations that the
abolic benefits
chronic diseas
large cohort st
wheat fiber pro
ment of diabete
sociations advi
either to impro
to confer gener
creases in fiber
sources have be
cemic control in
studies sugges
proved both gly
(10) and glucos
subjects (11). T
cial effects of no
clear. Cereal fib
of gastric emp
absorption or fl
cemic respons
test meal (12).
such as guar an
to reduce the ra
and small int
thereby provid
tential benefits
shown to redu
when added to
crease 24-h uri
MARGARET C. MARTINI, PHD
5
METTE AXELSEN, PHD
6
DOROTHEA FAULKNER, RD
1
EDWARD VIDGEN, BSC
1,3
TINA PARKER, RD
1
WILLIAM SINGER, MD
2
ARTHUR C. VANDENBROUCKE, PHD
7,10
LAWRENCE A. LEITER, MD
1,2,3,4
ROBERT G. JOSSE, MD
1,2,3,4
OBJECTIVE — Cohort studies indicate that cereal fiber reduces the risk of diabetes and
coronary heart disease (CHD). Therefore, we assessed the effect of wheat bran on glycemic
control and CHD risk factors in type 2 diabetes.
RESEARCH DESIGN AND METHODS — A total of 23 subjects with type 2 diabetes
(16 men and 7 postmenopausal women) completed two 3-month phases of a randomized
crossover study. In the test phase, bread and breakfast cereals were provided as products high in
cereal fiber (19 g/day additional cereal fiber). In the control phase, supplements were low in fiber
(4 g/day additional cereal fiber).
RESULTS — Between the test and control treatments, no differences were seen in body
weight, fasting blood glucose, HbA1c, serum lipids, apolipoproteins, blood pressure, serum uric
acid, clotting factors, homocysteine, C-reactive protein, magnesium, calcium, iron, or ferritin.
LDL oxidation in the test phase was higher than that seen in the control phase (12.1 Ϯ 5.4%, P Ͻ
0.034). Of the subjects originally recruited, more dropped out of the study for health and food
preference reasons from the control phase (16 subjects) than the test phase (11 subjects).
CONCLUSIONS — High-fiber cereal foods did not improve conventional markers of glyce-
mic control or risk factors for CHD in type 2 diabetes over 3 months. Possibly longer studies are
required to demonstrate the benefits of cereal fiber. Alternatively, cereal fiber in the diet may be
a marker for another component of whole grains that imparts health advantages or a healthy
lifestyle.
Diabetes Care 25:1522–1528, 2002
Tor facet of fiber
been clearly de
cations that the
abolic benefits (
chronic disease
large cohort stu
wheat fiber pro
ment of diabete
sociations advis
either to improv
to confer gener
creases in fiber
sources have be
cemic control in
studies suggest
proved both gly
(10) and glucos
subjects (11). T
cial effects of no
clear. Cereal fib
of gastric empt
absorption or fla
cemic response
test meal (12).
such as guar an
to reduce the ra
and small inte
thereby providi
tential benefits.
shown to redu
when added to
LIVIA S. A. AUGUSTIN, MSC
MARGARET C. MARTINI, PHD
5
METTE AXELSEN, PHD
6
DOROTHEA FAULKNER, RD
1
EDWARD VIDGEN, BSC
1,3
TINA PARKER, RD
1
JEROME TEITEL, MD
WILLIAM SINGER, MD
2
ARTHUR C. VANDENBROUCKE, PHD
7,10
LAWRENCE A. LEITER, MD
1,2,3,4
ROBERT G. JOSSE, MD
1,2,3,4
OBJECTIVE — Cohort studies indicate that cereal fiber reduces the risk of diabetes and
coronary heart disease (CHD). Therefore, we assessed the effect of wheat bran on glycemic
control and CHD risk factors in type 2 diabetes.
RESEARCH DESIGN AND METHODS — A total of 23 subjects with type 2 diabetes
(16 men and 7 postmenopausal women) completed two 3-month phases of a randomized
crossover study. In the test phase, bread and breakfast cereals were provided as products high in
cereal fiber (19 g/day additional cereal fiber). In the control phase, supplements were low in fiber
(4 g/day additional cereal fiber).
RESULTS — Between the test and control treatments, no differences were seen in body
weight, fasting blood glucose, HbA1c, serum lipids, apolipoproteins, blood pressure, serum uric
acid, clotting factors, homocysteine, C-reactive protein, magnesium, calcium, iron, or ferritin.
LDL oxidation in the test phase was higher than that seen in the control phase (12.1 Ϯ 5.4%, P Ͻ
0.034). Of the subjects originally recruited, more dropped out of the study for health and food
preference reasons from the control phase (16 subjects) than the test phase (11 subjects).
CONCLUSIONS — High-fiber cereal foods did not improve conventional markers of glyce-
mic control or risk factors for CHD in type 2 diabetes over 3 months. Possibly longer studies are
required to demonstrate the benefits of cereal fiber. Alternatively, cereal fiber in the diet may be
a marker for another component of whole grains that imparts health advantages or a healthy
lifestyle.
Diabetes Care 25:1522–1528, 2002
Tcereals (1–
or facet of fiber
been clearly de
cations that the
abolic benefits
chronic diseas
large cohort stu
wheat fiber pro
ment of diabete
sociations advi
either to impro
to confer gener
creases in fiber
sources have be
cemic control in
studies sugges
proved both gly
(10) and glucos
subjects (11). T
cial effects of no
clear. Cereal fib
of gastric empt
absorption or fl
cemic response
test meal (12).
such as guar an
to reduce the ra
and small int
thereby provid
tential benefits
shown to redu
Jenkins D, et al. Diabetes Care 25:1522–1528, 2002!
Cereales integrales y marcadores inflamación/
cardiovasculares
Aumento de la oxidación del LDL durante la
fase de consumo de salvado de trigo
55. Resumen cereales integrales y ECV
Epidemiología: protectores
Intervención: sin efecto o posible aumento del riesgo (WHI
& DART)
57. Kelly, S. A. M., Summerbell, C. D., Brynes, A., Whittaker, V., & Frost, G. (2007). Wholegrain cereals for coronary heart disease. Cochrane Database of Systematic Reviews (Online), (2),
CD005051. doi:10.1002/14651858.CD005051.pub2
58. Priebe, M. G., van Binsbergen, J. J., deVos, R., &Vonk, R. J. (2008).Whole grain foods for the prevention of type 2 diabetes mellitus. Cochrane Database of Systematic Reviews (Online), (1), CD006061. doi:
10.1002/14651858.CD006061.pub2
59. Lefevre, M., & Jonnalagadda, S. (2012). Effect of whole grains on markers of subclinical inflammation. Nutrition Reviews
60. American Diabetes Association Statement
Evert,A. B., Boucher, J. L., Cypress, M., Dunbar, S.A., Franz, M. J., Mayer-Davis, E. J., et al. (2014). Nutrition therapy recommendations for the management of adults with diabetes.
Diabetes Care, 37 Suppl 1(Supplement_1), S120–43. doi:10.2337/dc14-S120
61. American Diabetes Association Statement
Evert,A. B., Boucher, J. L., Cypress, M., Dunbar, S.A., Franz, M. J., Mayer-Davis, E. J., et al. (2014). Nutrition therapy recommendations for the management of adults with diabetes.
Diabetes Care, 37 Suppl 1(Supplement_1), S120–43. doi:10.2337/dc14-S120
Nada específico para los cereales
62. The Swedish Council on Health Technology Assessment (Statens Beredning för medicinsk Utvärdering), www.sbu.se
63. Evidencia de alta calidad
No hay estudios, no hay
recomendaciones
Asplund, K., Axelsen, M., Berglund, G., & Berne, C. (2010). Dietary Treatment of Diabetes. SBU-Swedish Council on Health Technology Assessment.
64. Evidencia de calidad moderada
Dietas muy bajas en CHO vs. moderadas bajas en
grasa
(algo mejor efecto en A1c y peso en 12-14 meses)
Dieta moderada baja en CHO (30-40% en) vs. dieta
alta en CHO (50-60% en)
(algo mejor efecto en HDL)
Asplund, K., Axelsen, M., Berglund, G., & Berne, C. (2010). Dietary Treatment of Diabetes. SBU-Swedish Council on Health Technology Assessment.
Alcohol
(menor riesgo de ECV con consumo regular vs. no consumo)
Café
(menor riesgo de muerte por enf. Isquémica coronaria con >2 tazas/
día)
65. Evidencia de baja calidad
Verduras, legumbres, índice glucémico bajo, ’dieta
mediterránea’
Pescado y omega-3 (en mujeres)
Asplund, K., Axelsen, M., Berglund, G., & Berne, C. (2010). Dietary Treatment of Diabetes. SBU-Swedish Council on Health Technology Assessment.
66. Evidencia de muy baja calidad
Índice glucémico muy bajo, carga glucémica, dieta
baja en grasa, etc.
Asplund, K., Axelsen, M., Berglund, G., & Berne, C. (2010). Dietary Treatment of Diabetes. SBU-Swedish Council on Health Technology Assessment.
67. No hay estudios de alta calidad para la
diabetes
Ajala, O., et al.American Journal of Clinical Nutrition, 2013
Livesey, G., et al.American Journal of Clinical Nutrition, 2013
Nield, L., et al. Cochrane database of systematic reviews. 2007
Priebe, M. G., et al. Cochrane database of systematic reviews. 2008
68. Mente,A.,deKoning,L.,Shannon,H.S.& Anand,S.S.(2009) A systematic review of the evidence supporting a causal link
between dietary factors and coronary heart disease. Arch Intern Med 169, 659–69.
Faltan ensayos clínicos
Aún en 2010, no había RCTs para muchas recomendaciones
habituales, respecto al riesgo cardiovascular
69. Mente,A.,deKoning,L.,Shannon,H.S.& Anand,S.S.(2009) A systematic review of the evidence supporting a causal link
between dietary factors and coronary heart disease. Arch Intern Med 169, 659–69.
Faltan ensayos clínicos
Aún en 2010, no había RCTs para muchas recomendaciones
habituales, respecto al riesgo cardiovascular
71. ¿Existe una dieta mediterránea?
El pan sourdough no contiene gluten, si la pasta...entre
otras diferencias
72. FESNAD-SEEDO. (2011). Recomendaciones nutricionales basadas en la evidencia para la prevención y el tratamiento del sobrepeso y la obesidad en adultos (Consenso FESNAD-
SEEDO). Revista Española De Obesidad, 19(1), 1–80.
73. FESNAD-SEEDO. (2011). Recomendaciones nutricionales basadas en la evidencia para la prevención y el tratamiento del sobrepeso y la obesidad en adultos (Consenso FESNAD-
SEEDO). Revista Española De Obesidad, 19(1), 1–80.
74. FESNAD-SEEDO. (2011). Recomendaciones nutricionales basadas en la evidencia para la prevención y el tratamiento del sobrepeso y la obesidad en adultos (Consenso FESNAD-
SEEDO). Revista Española De Obesidad, 19(1), 1–80.
75. FESNAD-SEEDO. (2011). Recomendaciones nutricionales basadas en la evidencia para la prevención y el tratamiento del sobrepeso y la obesidad en adultos (Consenso FESNAD-
SEEDO). Revista Española De Obesidad, 19(1), 1–80.
76. Grado de recomendación para las dietas mediterráneas y
vegetarianas, y cereales integrales en la prevención de la
obesidad: C
77. ¿Y el estudio PREDIMED?
Mejor que una dieta low-fat (parecida a WHI) y además con
un sesgo importante: falta de apoyo en grupo control
78. ¿Y el estudio PREDIMED?
Mejor que una dieta low-fat (parecida a WHI) y además con
un sesgo importante: falta de apoyo en grupo control
79. ¿Y el estudio PREDIMED?
Mejor que una dieta low-fat (parecida a WHI) y además con
un sesgo importante: falta de apoyo en grupo control
80. ¿Y el estudio PREDIMED?
Mejor que una dieta low-fat (parecida a WHI) y además con
un sesgo importante: falta de apoyo en grupo control
Recuerden resultados del WHI
81. ¿Y el estudio PREDIMED?
¿Los cereales integrales jugaron un papel en los efectos?
Mejor que una dieta low-fat (parecida a WHI) y además con
un sesgo importante: falta de apoyo en grupo control
82. ¿Y el estudio PREDIMED?
Estruch R, et al. N Engl J Med. 2013
Estamos de acuerdo que la dieta mediterránea es
mejor que la dieta occidental: no significa que sea
necesariamente la mejor dieta para el ser humano
83. ¿Y el Lyon Diet Heart Study?
de Lorgeril, M., Salen, P., Martin, J. L., Monjaud, I., Delaye, J., & Mamelle, N. (1999). Mediterranean diet, traditional risk factors, and the rate of cardiovascular complications after myocardial
infarction: final report of the Lyon Diet Heart Study. Circulation, 99(6), 779–785.
84. ¿Y el Lyon Diet Heart Study?
de Lorgeril, M., Salen, P., Martin, J. L., Monjaud, I., Delaye, J., & Mamelle, N. (1999). Mediterranean diet, traditional risk factors, and the rate of cardiovascular complications after myocardial
infarction: final report of the Lyon Diet Heart Study. Circulation, 99(6), 779–785.
Mejor que dieta low-fat
...pero
Una vez más, el grupo control recibió
menos apoyo conductual
85. 0 0.5 1.0 1.5
Non-westerner
Westerner with “low” risk
Westerner with “normal” risk
Westerner with “high” risk
Riesgo relativo de las enf. de la civilización
Riesgos relativos
Lindeberg S. Food and Western Disease. 1st ed.Wiley-Blackwell; 2010.
86. 0 0.5 1.0 1.5
Non-westerner
Westerner with “low” risk
Westerner with “normal” risk
Westerner with “high” risk
Riesgo relativo de las enf. de la civilización
Riesgos relativos
Lindeberg S. Food and Western Disease. 1st ed.Wiley-Blackwell; 2010.
La mayoría de dietas se aplican en individuos con alto
riesgo con dietas control de eficacia dudosa
87. Revisión sistemática sobre dieta Mediterránea en
prevención primaria de ECV
Rees, K.,. (2013). Cochrane Database Syst Rev.
88. Revisión sistemática sobre dieta Mediterránea en
prevención primaria de ECV
Rees, K.,. (2013). Cochrane Database Syst Rev.
Importante: analizaron RCTs donde el grupo control no
recibió intervención o era mínima (más motivación en
grupo de dieta mediterránea)
89. Revisión sistemática sobre dieta Mediterránea en
prevención primaria de ECV
Rees, K.,. (2013). Cochrane Database Syst Rev.
Importante: analizaron RCTs donde el grupo control no
recibió intervención o era mínima (más motivación en
grupo de dieta mediterránea)
90. Revisión sistemática sobre dieta Mediterránea en
prevención primaria de ECV
Rees, K.,. (2013). Cochrane Database Syst Rev.
Importante: analizaron RCTs donde el grupo control no
recibió intervención o era mínima (más motivación en
grupo de dieta mediterránea)
Conclusión: evidencia limitada y necesidad de más (y
mejores) estudios
91. Está bien pasar de riesgo alto a normal
...pero, ¿Quién quiere ser normal?
92. La soja (legumbre y proteína vegetal) es mejor que la
caseína1
Pero la caseína produce aterosclerosis, resistencia a la
insulina y lipotoxicidad en experimentos animales1,2,3,4,5
1.Ascencio, C., et al. (2004). J Nutr
2. Huff,M.W., et al.(1982).Atherosclerosis
3. Lavigne, C., et al. (2001).Am J Physiol Endocrinol Metab
4.Wilson,T.A., et al. (2000). Nutr Res
5. Kritchevsky, D. (1995). J Nutr
Además, la proteína animal (bisonte y ternera),
produce mucha menos aterosclerosis que la
proteína de soja4
Ejemplo del problema de la dieta control si no tenemos en
cuenta la evolución
En experimentos animales
¿Se puede concluir que la soja es beneficiosa?
93. High-Milk Supplementation with Healthy Diet
Counseling Does not Affect Weight Loss but
Ameliorates Insulin Action Compared with
Low-Milk Supplementation in
Overweight Children1–3
Marie-Pierre St-Onge,4,5
* Laura Lee T. Goree,5
and Barbara Gower5
4
College of Physicians and Surgeons, Columbia University and New York Obesity Research Center, St. Luke’s/Roosevelt Hospital,
New York, NY 10025 and 5
Department of Nutrition Sciences, University of Alabama, Birmingham, AL 35294
Abstract
Milk consumption has decreased in children over the past years. This may play a role in the prevalence of pediatric obesity,
because clinical studies have found a beneficial effect of milk consumption for weight management. The objectives of this
study were to test whether high-milk consumption leads to greater weight loss and improvements in metabolic risk
factors than low milk consumption during a 16-wk healthy eating diet. Overweight children aged 8–10 y were randomized
to either high (4 3 236 mL/d) or low (1 3 236 mL/d) milk consumption. Children were provided dietary counseling on
healthy eating at baseline and at wk 1, 2, 4, 6, 8, and 12. Serum glucose, insulin, and lipids were measured in fasting
children at baseline and wk 8 and 16. An oral glucose tolerance test and body composition assessment by magnetic
resonance imaging were conducted at baseline and endpoint. Body weight changes during the16-wk study not differ
between the high-milk (1.3 6 0.3 kg) and low-milk (1.1 6 0.3 kg) groups. There was no beverage 3 week interaction on any
of the body composition and metabolic variables studied (blood pressure, serum lipids, glucose, and insulin). There was a
beverage 3 week interaction (P ¼ 0.044) on insulin area under the curve showing a trend toward reduced insulin output
with a glucose challenge after high-milk consumption (P ¼ 0.062). These data suggest that in overweight children, high-
milk consumption in conjunction with a healthy diet does not lead to greater weight loss but may ameliorate insulin action
compared with low-milk consumption. J. Nutr. 139: 933–938, 2009.
Introduction
There is increasing concern regarding beverage type consump-
tion in U.S. children. Recent epidemiological studies have
pared with 8.3 and 20.6%, respectively, in the 1999–2001
national survey (5).
These changes in beverage consumption patterns may have
atColoradoStUnivLibonApril16,2009jn.nutrition.orgDownloadedfrom
Dieta rica en leche vs. Dieta en la que la leche fue
sustituida por una bebida con azúcar
Sin alteraciones de la insulinemia de ayunas
Respuesta insulinémica post-prandial
estadísticamente menor en el grupo de la dieta rica
en leche
94. Stancliffe, R.A., et al. (2011). American Journal of Clinical Nutrition
Texto
Dieta control: lácteos sustituidos por carne procesada,
sustitutos de carne basada en soja, fruta, cereales y galletas
con mantequilla de cacahuete
Texto
Idem con muchos estudios con cereales integrales y
legumbres: dieta control no adecuada o falta de apoyo
95. Look AHEAD Research Group,Wing, R. R., Bolin, P., Brancati, F. L., Bray, G.A., Clark, J. M., et al. (2013). The New England Journal of Medicine
Look AHEAD
5,145 diabéticos con obesidad
Intervención Control
Dieta hipocalórica/<30%
grasa/>15% proteína/
cereales integrales
+
175 min ejercicio/semana
Educación y apoyo
sobre diabetes (otra vez
menos apoyo en grupo
control)
Otro estudio de larga duración
96. Look AHEAD Research Group,Wing, R. R., Bolin, P., Brancati, F. L., Bray, G.A., Clark, J. M., et al. (2013). The New England Journal of Medicine
Look AHEAD
97. Look AHEAD Research Group,Wing, R. R., Bolin, P., Brancati, F. L., Bray, G.A., Clark, J. M., et al. (2013). The New England Journal of Medicine
Look AHEAD
Tras 9,6 años, y con pérdida de peso (6%) y reducción de
HbA1c, ninguna diferencia en muerte por ECV, infarto de
miocardio no fatal, ictus no fatal u hospitalización por
angina
Por lo tanto, ¿hasta qué punto me puedo fiar de los
biomarcadores?
98. Cerhan JR, et al. Mayo Clin Proc. 2014
Circunferencia de cintura y riesgo de mortalidad en
650.000 adultos
99. Cerhan JR, et al. Mayo Clin Proc. 2014
Circunferencia de cintura y riesgo de mortalidad en
650.000 adultos
Todos tenemos un riesgo normal (1.0), pero lo
normal sería tener un riesgo 0, como en
poblaciones de cazadores-recolectores
Por lo tanto, si no se considera la evolución a la
hora de diseñar estudios de intervención, pasar de
riesgo 1.8 a 1.3 está “bien”
100. Los estudios Women’s Health Initiative, PREDIMED y Look
AHEAD dejan claro que seguir una dieta saludable no es
suficiente
101. Conclusión: no existe suficiente evidencia para recomendar
los cereales integrales en la prevención y el tratamiento de
ECV, diabetes u obesidad
Howard, B.V., et al. JAMA: the Journal of the American Medical Association, 2006
Burr, M. L., Fehily,A. M., Gilbert, J. F., Rogers, S., Holliday, R. M., Sweetnam, P. M., et al. (1989). Effects of changes in fat, fish, and fibre intakes on death and myocardial reinfarction: diet
and reinfarction trial (DART). Lancet, 2(8666), 757–761.
Kelly, S.A. M., Summerbell, C. D., Brynes,A.,Whittaker,V., & Frost, G. (2007).Wholegrain cereals for coronary heart disease. Cochrane Database of Systematic Reviews (Online), (2),
CD005051. doi:10.1002/14651858.CD005051.pub2
Priebe, M. G., van Binsbergen, J. J., deVos, R., &Vonk, R. J. (2008).Whole grain foods for the prevention of type 2 diabetes mellitus. Cochrane Database of Systematic Reviews (Online),
(1), CD006061. doi:10.1002/14651858.CD006061.pub2
Lefevre, M., & Jonnalagadda, S. (2012). Effect of whole grains on markers of subclinical inflammation. Nutrition Reviews
Evert,A. B., Boucher, J. L., Cypress, M., Dunbar, S.A., Franz, M. J., Mayer-Davis, E. J., et al. (2014). Nutrition therapy recommendations for the management of adults with diabetes.
Diabetes Care, 37 Suppl 1(Supplement_1), S120–43. doi:10.2337/dc14-S120
Asplund, K.,Axelsen, M., Berglund, G., & Berne, C. (2010). Dietary Treatment of Diabetes. SBU-Swedish Council on HealthTechnology Assessment.
FESNAD-SEEDO. (2011). Recomendaciones nutricionales basadas en la evidencia para la prevención y el tratamiento del sobrepeso y la obesidad en adultos (Consenso FESNAD-
SEEDO). Revista Española De Obesidad, 19(1), 1–80.
102. ¿Por qué considerar la evolución?
Lindeberg S. Food and Western Disease. 1st ed.Wiley-Blackwell; 2010.
vs.
Ideología Biología
Es sorprendente que J.H. Kellogg tenga más
influencia en la nutrición que Charles Darwin
103. Eaton, S. B., & Konner, M. (1985). Paleolithic nutrition.A consideration of its nature and current implications. The New England Journal of Medicine,
Este artículo hizo pensar a algunos curiosos
104. Wood, B. Proc Natl Acad Sci USA, 2010
Agricultura: un periodo de tiempo infinitesimal a escala
evolutiva
Paleolítico
Agricultura
0,4% de nuestra evolución
105. Campbell, M. C., & Tishkoff, S. A. Annual Review of Genomics and Human Genetics, 2008
Todos venimos de un grupo de 1,000 individuos que vivieron en
África hace 200,000 años
106. Campbell, M. C., & Tishkoff, S. A. Annual Review of Genomics and Human Genetics, 2008
Todos venimos de un grupo de 1,000 individuos que vivieron en
África hace 200,000 años
Hasta este momento, todos teníamos la misma dieta
108. ¿Qué comíamos?
¿Mejora esta dieta si añadimos cereales y lácteos?
¿Existen riesgos si consumimos estos alimentos?
109. Lo conocido
Dieta omnívora
Lo incierto
Cuanta cantidad de alimentos
animal/vegetal
Lo conocido
No alimentos occidentales
Cordain L. Implications of Plio-Pleistocene Hominin Diets for Modern Humans.
In: Early Hominin Diets:The Known, the Unknown, and the Unknowable. Ungar, P (Ed.), Oxford University Press, Oxford, 2006, pp 363-83
111. Potenciales efectos negativos de compuestos bioactivos de
los cereales
Endocrinos
Unión a receptores opioides: exorfinas A5 y B51, 2
Unión a receptores de insulina y leptina: lectinas3, 4
Unión a receptores de estrógenos: fitoestrógenos5
1. Schusdziarra, et al. (1981). Diabetes
2. SchusdziarraV, et al. Peptides 1984
3. Cuatrecasas, P., & Tell, G. P. (1973). Proceedings of the National Academy of Sciences of the United States of America
4. Jönsson T, et al. BMC Endocr Disord. 2005
5. Jefferson,W. N., et al. (2012). Reproduction
6. Cordain L. Br. J. Nutr. 2000
7. Junker,Y., et al. (2012).. Journal of Experimental Medicine
8. Unitt, J., & Hornigold, D. (2011). Biochemical Pharmacology
9.Visser, J., et al. (2009). Annals of the NewYork Academy of Sciences
10. Cordain, L. (1999). World Review of Nutrition and Dietetics
11. Pusztai,A., et al. (1993). British Journal of Nutrition
12. Sjölander,A., et al. (1984). International Archives of Allergy and Applied Immunology
Inmunológicos
Disruptores de membranas (glicocalix): lectinas6,12
Estimulación del sistema inmune innato: gliadina y lectinas7,8,9
Mimetismo molecular con autoantígenos6,10
Antinutrientes
Acido fítico10
Lectinas N-acetilglucosamina específicas11
112. Trigo, receptores opioides y glucagón
Efectos de la misma cantidad
de CHO en forma de
glucosa o diferentes formas
de trigo en la secreción de
glucagón
NOTA: no es
aconsejable que se
aumente la producción
de glucagón en el
estado posprandial
(Unger RH, et al. J.
Clin. Investig. 2012)
Behall, K. M., et al. (1999). Journal of the American College of Nutrition,
Un ejemplo
113. Proteínas de la leche de vaca y diabetes tipo 1
Reducción significativa de marcadores de
autoinmunidad para células beta con caseína
hidrolizada vs. leche de fórmula a base de leche de vaca
Knip, M., et al. (2010). New England Journal of Medicine
114. Potenciales factores dietéticos en la diabetes tipo1
http://www.diapedia.org/type-1-diabetes-mellitus/environmental-factors
Fuente: Diapedia.org
115. Potenciales factores dietéticos en la diabetes tipo1
http://www.diapedia.org/type-1-diabetes-mellitus/environmental-factors
No es evidencia de grado A, pero con los estudios
de biología molecular y de animales, ¿por qué correr
riesgos teniendo otros alimentos más seguros que
cumplan los objetivos nutricionales?
De nuevo, alimentos introducidos en el neolítico
Fuente: Diapedia.org
116. Los alimentos no son sólo macro y
micronutrientes
Que una alimentación cumpla los objetivos nutricionales no
significa que sea óptima para la salud a largo plazo
117. Selección natural
¿Qué hace falta? Presión selectiva
¿El consumo de cereales produce una presión selectiva negativa?
¿Son suficientes 10,000 años?...probablemente no.
118. Persistencia de la lactasa de adulto
Presión selectiva positiva muy fuerte porque mermaba la
capacidad reproductiva en N-O de Europa (raquitismo) y
África sub-sahariana (Malaria)
https://s3.amazonaws.com/paleodietevo2/research/Malaria+and+Rickets+Represent+Selective+Forces+for+the+Convergent+Evolution+of+Adult+Lactase+Persistence+The+Paleo+Diet.pdf
Referencia:
119. Persistencia de la lactasa de adulto
Presión selectiva positiva muy fuerte porque mermaba la
capacidad reproductiva en N-O de Europa (raquitismo) y
África sub-sahariana (Malaria)
https://s3.amazonaws.com/paleodietevo2/research/Malaria+and+Rickets+Represent+Selective+Forces+for+the+Convergent+Evolution+of+Adult+Lactase+Persistence+The+Paleo+Diet.pdf
Referencia:
Y aún así todavía no todos (65%) estamos adaptados a
digerir lactosa
Nota importante: estar adaptado a digerir lactosa no
significa estar adaptado a beber leche (proteínas)
120. Perry GH, et al. Nat Genet 2007
Alfa amilasa salivar
121. Perry GH, et al. Nat Genet 2007
Estar adaptado a comer más almidón no significa estar adaptado
a comer cereales si tienes susceptibilidad a la celiaquía
Alfa amilasa salivar
123. ¿Estamos todos completamente adaptados a los cereales?
La sensibilidad al gluten (no celiaquía) afecta a 6-10%
población en el RU
¿Y que ocurre con las otras 40,000 proteínas del trigo?
124. Cuestiones
Si nos adaptáramos bien a los cereales en 10,000 años, en
Oriente Medio habría menos prevalencia de celiaquía
127. No es tan sencillo como decir, “10,000 es suficiente tiempo
para adaptarnos, ¿Por qué razón no íbamos a adaptarnos?”
Pues porque hace falta presión selectiva que merme capacidad
reproductiva(concepto básico de biología evolutiva)
Stearns, S. C., & Koella, J. C. (2008). Evolution in Health and Disease (2nd ed.). Oxford University Press, USA.
128. No es tan sencillo como decir, “10,000 es suficiente tiempo
para adaptarnos, ¿Por qué razón no íbamos a adaptarnos?”
Pues porque hace falta presión selectiva que merme capacidad
reproductiva(concepto básico de biología evolutiva)
Stearns, S. C., & Koella, J. C. (2008). Evolution in Health and Disease (2nd ed.). Oxford University Press, USA.
129. Hawks, J., et al. (2007). Proc Natl Acad Sci USA
Fumagalli, M., et al. (2011). PLoS Genetics,
130. Incluso teniendo en cuenta la reciente aceleración en la
adaptación humana
Hawks, J., et al. (2007). Proc Natl Acad Sci USA
Fumagalli, M., et al. (2011). PLoS Genetics,
131. Incluso teniendo en cuenta la reciente aceleración en la
adaptación humana
Pero en gran parte es debida a epidemias, no sólo a la
dieta
Hawks, J., et al. (2007). Proc Natl Acad Sci USA
Fumagalli, M., et al. (2011). PLoS Genetics,
132. Incluso teniendo en cuenta la reciente aceleración en la
adaptación humana
Pero en gran parte es debida a epidemias, no sólo a la
dieta
Hawks, J., et al. (2007). Proc Natl Acad Sci USA
Fumagalli, M., et al. (2011). PLoS Genetics,
133. Incluso teniendo en cuenta la reciente aceleración en la
adaptación humana
Pero en gran parte es debida a epidemias, no sólo a la
dieta
Hawks, J., et al. (2007). Proc Natl Acad Sci USA
Fumagalli, M., et al. (2011). PLoS Genetics,
135. ¿Cuánto tiempo tardaremos en adaptarnos a los azúcares
refinados?
¿Cuanto tiempo tardaremos en adaptarnos al
sedentarismo?
Si nos adaptamos tan fácilmente a los alimentos nuevos
(como algunos postulan)
...o, ¿no suponen una presión selectiva positiva para
mermar capacidad reproductiva?
136. Leche materna
Los bebés alimentados con leche de fórmula crecen
(aparentemente) “bien” (igual que las personas alimentadas
a base de cereales)
La leche de fórmula puede contener todos los nutrientes
necesarios para el desarrollo del bebé
La leche materna contiene compuestos bioactivos,
probióticos, oligosacáridos, etc, que producen efectos
inmuno-endocrinos más allá de los nutrientes
¿Influye de igual manera la leche materna que la de
fórmula en la salud del niño y del adulto?
137. Leche materna
Si alimentamos a todos los bebés con leche de fórmula los
primeros meses de vida, la especie humana seguirá viva
(probablemente) dentro de 10,000 años
¿Nos habremos adaptado completamente a la leche de
fórmula dentro de 10,000 años y podremos prescindir de la
lactancia?
Piense de igual manera con los cereales ya que no sólo son
un compendio de nutrientes (hay más de 40,000 proteínas
y otros compuestos bioactivos que no sabemos
exactamente que función tienen)
138. Leche materna
La leche materna es un buen ejemplo de que los alimentos
no sólo son macro/micronutrientes
La leche materna parece que afecta de forma diferente a la
microbiota comparada con la leche de fórmula, y ese efecto
es independiente de los macro/micronutrientes
Kerr CA, et al. Crit Rev Microbiol. 2014
139. “Debemos comer un poco de todo”
“La dieta debe ser balanceada, variada…”
¿Si? ¿Cual es la justificación?
“Argumentos” típicos
140. “Ya no existen los alimentos que habían en el paleolítico”
“Argumentos” típicos
“Ni las condiciones ambientales son iguales”
141. “Ya no existen los alimentos que habían en el paleolítico”
“Argumentos” típicos
“Ni las condiciones ambientales son iguales”
Eso es obvio, se trata de minimizar riesgos reduciendo el
consumo de alimentos a los que no estemos bien
adaptados
142. Toxicidad aguda vs toxicidad a largo plazo
Un alimento se ha considerado tradicionalmente
comestible, si su toxicidad a corto plazo es baja o
inexistente
Toxicología
Pero, ¿Hay toxicidad acumulativa, a largo plazo?¿carencias
nutricionales?
143. Las proteínas de caseína y soja inducen aterosclerosis en
animales1,2,3,4
Hay evidencia indirecta de que los cereales, particularmente
el trigo, pueden producir aterosclerosis5
1. Eastwood, M., & Kritchevsky, D. (2005). DIETARY FIBER: How Did We Get Where We Are? Annual Review of Nutrition, 25(1), 1–8.
2. Kritchevsky, D. (1979).Vegetable protein and atherosclerosis. Journal of the American Oil Chemists' Society, 56(3), 135–140.
3. Kritchevsky, D.,Tepper, S.A., & Klurfeld, D. M. (1998). Lectin may contribute to the atherogenicity of peanut oil. Lipids, 33(8), 821–823.
4. Kritchevsky, D.,Tepper, S.A.,Williams, D. E., & Story, J.A. (1977). Experimental atherosclerosis in rabbits fed cholesterol-free diets Part 7. Interaction of animal or vegetable protein with fiber.Atherosclerosis,
26(4), 397–403.
5. Lindeberg S. Food and Western Disease. 1st ed.Wiley-Blackwell; 2010.
¡No la de bisonte o ternera!
144. ¿Cómo sabemos que no ocurre lo mismo en humanos a
largo plazo?
1. Eastwood, M., & Kritchevsky, D. (2005). DIETARY FIBER: How Did We Get Where We Are? Annual Review of Nutrition, 25(1), 1–8.
2. Kritchevsky, D. (1979).Vegetable protein and atherosclerosis. Journal of the American Oil Chemists' Society, 56(3), 135–140.
3. Kritchevsky, D.,Tepper, S.A., & Klurfeld, D. M. (1998). Lectin may contribute to the atherogenicity of peanut oil. Lipids, 33(8), 821–823.
4. Kritchevsky, D.,Tepper, S.A.,Williams, D. E., & Story, J.A. (1977). Experimental atherosclerosis in rabbits fed cholesterol-free diets Part 7. Interaction of animal or vegetable protein with fiber.Atherosclerosis,
26(4), 397–403.
5. Lindeberg S. Food and Western Disease. 1st ed.Wiley-Blackwell; 2010.
145. ¿Qué problemas puede causar el consumo de cereales y
lácteos si mis biomarcadores están bien?
Los biomarcadores no son fiables para predecir un infarto
de miocardio o ictus
La enfermedad isquémica del corazón es una enfermedad
“silenciosa” que tarda décadas en manifestarse
Lindeberg S. Food and Western Disease. 1st ed.Wiley-Blackwell; 2010.
146. Con permiso de: Lindeberg S. Food and Western Disease. 1st ed.Wiley-Blackwell; 2010.
Una dieta
saludable parece
no ser suficiente
para evitar este
proceso
147. Otro ejemplo de posibles efectos a largo plazo
Weber, M., E., et al. (2014). American Journal of Clinical Nutrition
Pero si miramos los detalles...
148. Habría otra forma (perspectiva evolutiva) de verlo:
Higher cow’s milk protein content in infant formula increases BMI
and obesity risk at school age: follow-up of a randomized trial
¿Cuál es la referencia, los que toman alta cantidad de
proteína o los que toman pecho?
149. ¿Le darías de comer estos alimentos a un gato?
¿Por qué no aplicar el “un poco
de todo”?
150. Pájaro carnívoro Estructura pancreática
muy diferente
Pájaro granívoro
¿Estarán adaptados a dietas
diferentes?
¿Si les cambiamos la dieta
alteraremos su respuesta
endocrina?
151. Pilny,A.A. (2008).The Avian Pancreas in Health and Disease. Veterinary Clinics of North America: Exotic Animal Practice, 11(1), 25–34. doi:10.1016/j.cvex.2007.09.007
Interesantemente la pancreatectomía afecta de forma
diferente a pájaros granívoros (diabetes transitoria) y
carnívoros
Los pájaros carnívoros se comportan igual que los
mamíferos (desarrollan diabetes tras pancreatectomía)
¿Nuestra anatomía y fisiología pancreática se ha adaptado
completamente en 10,000 a los cereales?
152. Chimpanzee Australopithecine
Modern human
Estas adaptaciones a una dieta nueva tardaron mucho más
de 10,000 años
Ungar, P. S. American Journal of Physical Anthropology, 2011
Aiello, L. C., & Wheeler, P. Current Anthropology, 1995
En términos evolutivos se
hablan en cientos de miles o
millones de años
153. Hancock,AM, et al. PNAS. 2010
Adaptación en poblaciones que dependen de los
cereales (en rojo)
Pancreatic lipase-related protein 2
154. Hancock,AM, et al. PNAS. 2010
Adaptación en poblaciones que dependen de los
cereales (en rojo)
Pancreatic lipase-related protein 2
Parece que estamos en un proceso de adaptación, y que
muchos no están adaptados al mirar ciertos SNPs
155. Estamos en un proceso de adaptación teniendo en cuenta
algunos haplotipos
No obstante, estos genes confieren susceptibiliad, no son
la causa
Si se evitan los factores ambientales la diabetes tipo 2 no
se manifiesta
156. Evidencia sobre el consumo (esporádico) de
legumbres en el paleolítico superior
Jones M. Moving North:Archaeobotanical Evidence for Plant Diet in Middle and Upper Paleolithic Europe. Dordrecht: Springer Netherlands; 2009;(Chapter 12):171–80.
Savard M, Nesbitt M, Jones MK.The role of wild grasses in subsistence and sedentism: new evidence from the northern Fertile Crescent.World Archaeology. 2006.
Lev E, Kislev ME, Bar-Yosef O. Mousterian vegetal food in Kebara cave, Mt. Carmel. Journal of Archaeological Science. 2005.
157. ¿Pero a que rama de nuestra filogenética afecta?
Humanos
modernos
Agricultura
158. ¿Pero a que rama de nuestra filogenética afecta?
¿Y el resto?
Humanos
modernos
Agricultura
159. ¿Esto es normal?
Entendiendo la biología, genética y antropología lo normal sería que
no estamos adaptados y habría que demostrar que sí estamos
adaptados
Desafortunadamente, ese paradigma no se tiene en cuenta en la
nutrición y J.H. Kellogg tiene más influencia que Charles Darwin
160. Estudios ecológicos en poblaciones que no comen cereales/
lácteos
Aparente ausencia de
ECV, diabetes u obesidad
Lindeberg S. Food and Western Disease: Health and nutrition from an evolutionary perspective. 1st ed.
Wiley-Blackwell; 2010.
161. Teoría: los seres humanos modernos deberían estar
adaptados a la dieta que tuvieron durante 2.6 millones de
años
Esto es ciencia
Hipótesis nula: una dieta paleolítica no produce efectos
diferentes a una dieta con cereales y lácteos
H0: μ1 = μ2
Hipótesis alternativa: una dieta paleolítica si produce
efectos diferentes a una dieta con cereales y lácteos
H1: μ1 ≠ μ2
162. ...pues vamos a refutar la hipótesis nula, si no la puedo
refutar tendré que aceptar la hipótesis alternativa
163. Estudio Población Duración Variables con
cambios signif.
Lindeberg S, 2007
29 sujetos EIC &
intolerancia glucosa
3 meses
Glucosa-TTOG, peso y
cintura
Österdahl M, 2008 14 sujetos sanos 3 semanas
Peso, IMC, cintura,
presión arterial y PAI-1
Jönsson T, 2009
13 sujetos con
diabetes tipo 2: diseño
cruzado
3 meses
HbA1c,TG, PA
diastólica, peso, IMC, p.
Cintura y HDL
Frassetto L, 2010 8 sujetos sanos 17 días
PA, insulina TTOG, colesterol
total, LDL,TG
Ryberg M, 2013
10 mujeres obesas
sanas
5 semanas
49% TG hepáticos, peso, IMC,
cintura, cadera, diámetro sagital
abdominal, glucosa, PA
diastólica,TG, colesterol, etc
Frassetto L, 2013
13 sujetos con
diabetes tipo 2
14 días Excreción ácida neta
Mellberg S, 2014 70 mujeres obesas 2 años
Masa grasa, peso corporal,
circunferencia cintura,
diámetro sagital abdominal
y TG
Frassetto L (no
publicado)
22 sujetos sanos 15 días
Glucosa en ayunas,
fructosamina, PCR
Estudios de intervención
164. Estudio Población Duración Variables con
cambios signif.
Lindeberg S, 2007
29 sujetos EIC &
intolerancia glucosa
3 meses
Glucosa-TTOG, peso y
cintura
Österdahl M, 2008 14 sujetos sanos 3 semanas
Peso, IMC, cintura,
presión arterial y PAI-1
Jönsson T, 2009
13 sujetos con
diabetes tipo 2: diseño
cruzado
3 meses
HbA1c,TG, PA
diastólica, peso, IMC, p.
Cintura y HDL
Frassetto L, 2010 8 sujetos sanos 17 días
PA, insulina TTOG, colesterol
total, LDL,TG
Ryberg M, 2013
10 mujeres obesas
sanas
5 semanas
49% TG hepáticos, peso, IMC,
cintura, cadera, diámetro sagital
abdominal, glucosa, PA
diastólica,TG, colesterol, etc
Frassetto L, 2013
13 sujetos con
diabetes tipo 2
14 días Excreción ácida neta
Mellberg S, 2014 70 mujeres obesas 2 años
Masa grasa, peso corporal,
circunferencia cintura,
diámetro sagital abdominal
y TG
Frassetto L (no
publicado)
22 sujetos sanos 15 días
Glucosa en ayunas,
fructosamina, PCR
Estudios de intervención
Estudios controlados
169. Paleolítica vs. mediterránea
Lindeberg S, et al. Diabetologia. 2007
CHO
40%
PRO
28%
FAT
27%
4%
Paleolítica
CHO
52%
PRO
21%
FAT
25%
2%
Mediterránea
Fibra = 21 g Fibra = 27 g
Composición macronutrientes
Alcohol
170. Volvamos a la dieta mediterránea...
Lindeberg S, et al. Diabetologia. 2007
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