Datos de contacto
Alejandro Melo-Florián MD, FACP
•http://www.scoop.it/u/alejandro-melo-florian
•http://about.me/alejandro...
Neuronutrición y Educación
ALEJANDRO MELO FLORIÁN M.D., F.A.C.P. - Colombia
Esp. Medicina Interna-Pontificia Universidad J...
Conflicto de Intereses
• Declaro que no tengo conflicto de intereses
relacionados con la presente exposición.
• No habrá r...
En Facebook
https://www.facebook.com/pages/Libro-Cerebro-mente-y-concienciaUn-enfoque-multidisciplinario/613569022038907

...
Neurociencias: su futuro está en la
integración
• Para Osvaldo Uchitel -neurocientífico de UBAnecesita sumar el aporte de ...
Neuro-nutrición y Educación

 Joaquín Salvador Lavado Tejón, más conocido como
Quino
Problema nutricional en Américas
• Un 16% de todos los niños y niñas de la región
tienen Retraso en el Crecimiento y no es...
 Seguimiento de los progresos en la nutrición de los niños y las madres. Una
prioridad en materia de Supervivencia y desa...
Déficit hierro: problema de salud
Pública
• La deficiencia de hierro afecta a 2.000
millones de personas; 77 millones vive...
Déficit hierro: problema de salud
Pública

• Menores 2 años: mayor predisposición.

• Insuficiente disponibilidad de hierr...
Crecimiento de Tejido Nervioso

Neural
Hierro e impulso nervioso
• Es componente estructural de enzimas y
moléculas requeridas para el desarrollo y la
función ex...
Mielinización
• La densidad adquirida en corteza visual entre
2-4 años es aproximadamente la misma que
se vé en el adulto....
Mielinización
• La rápida mielinización en sistemas auditivos y
visuales es crítica para aprendizaje e
interacción social....
Hierro y mielinización

• Los lactantes anémicos continúan mostrando
un tiempo de conducción más l a r g o a pesar
de reci...
Importancia de

actancia

aterna

• El vínculo prolongado entre la madre y el
hijo durante la lactancia crea condiciones
p...
Nutrición y Desarrollo

pigenético

Maturana y Varela:
•El Sistema Nervioso es un instrumento
mediante el cual el organism...
Sobre Educación
Educación
• Latín educere: guiar, conducir / educare:
formar o instruir.
• Procesos bi-direccionales
para transmitir
conoc...
Educación
• Nuevas generaciones
asimilan y aprenden
conocimientos, normas
de conducta, modos de
ser y formas de como
veían...
Reflexiones sobre Educación
• “Educad al niño y no tendréis que castigar al
hombre” – Aristóteles de Estagira
• “La educac...
Educación y Epigénesis
• pigénesis: Desarrollo de las características
individuales del sistema nervioso depende del
medio ...
Neuronutrición y Medio Interno
Neuronutrición y medio Interno
•

omo erectus, con
capacidad cerebral de
aproximados 950 cm3
• Destacada tecnología de
her...
Neuronutrición y medio Interno
• Por sus herramientas en
piedra y la capacidad de
caza de
omo erectus,
se le pueden atribu...
Neuronutrición y medio Interno
• El cerebro es Estructura Disipativa, por el
elevado consumo del total de la energía
corpo...
Nutrición y SNC
Revolución ω-3

• Contenido de lípidos del
cerebro = 600 g/Kg.

– MBP
– Proteolípidos
– Esfingolípidos
– Esfingosina
– Cer...
Los lípidos de la vida
ϖ

FUENTE ALIMENTICIA

Acido linole ico

ϖ6

Ma ní, ma íz, s e milla s de a lgodón,
s oya .

Acido ...
Los lípidos de la vida
Los lípidos de la vida
Los lípidos de la vida

 Fernando Gómez-Pinilla: Brain foods: the effects of nutrients on brain function Nat Rev Neurosci...
Funcionalismo de membrana
neuronal
Los lípidos de la vida

 Stoll AL: The Omega-3 Connection. Simon & Schuster, Nueva York - USA 2001. pp 56
37
Los lípidos de la vida

• Los metabolitos de
AG Ω-6 promueven
adherencia
plaquetaria y
fenómenos de lesión
endotelial.

 ...
Los lípidos de la vida
Características deseables de un
suplemento Ω-3:
• Sin presencia de colesterol
• Sin aceite de hígad...
Interacciones Medicamentosas de
AG Omega –3
• Alteración de función plaquetaria
– Precaución con ASA, Ibuprofeno, Warfarin...
limentos funcionales

• Consumidos como parte de dieta normal:
– aportan componentes biológicamente activos, que
ofrecen b...
ntioxidantes y suplementos
• Estudio SU.VI.MAX (1994-2002 ):
– 4.447 participantes; 45 a 60 años
– Estudio doble-ciego, co...
ntioxidantes y suplementos
• Los sujetos que recibieron suplementos de
antioxidantes activos mostraron mejores
puntuacione...
Malnutrición y Obesidad
• La exposición persistente a estrés altera la
respuesta del cerebro a los alimentos en
formas que...
Receptor D2 dopamina en
estriado

Glucosa
disminuye señal
de dopamina
 Michaelides M, et al. Translational neuroimaging i...
Estrategias para mejorar
neuronutrición
Educación en Lactancia materna

 1ª Muestra Argentina de Humor Gráfico Sobre Lactancia Materna
Educación en Lactancia materna

 1ª Muestra Argentina de Humor Gráfico Sobre Lactancia Materna
Educación en Lactancia materna

 1ª Muestra Argentina de Humor Gráfico Sobre Lactancia Materna
LM e IQ
Lactancia materna e IQ
• Las diferencias en puntuaciones de pruebas
de CI entre niños alimentados con LM y los
que no reci...
Lactancia materna e IQ
• Diferencia de puntaje en prueba Ravens
Colored Progressive Matrices entre LM vs. sin
LM a 6 meses...
Para mejorar neuronutrición:
• La alimentación continuada con LECHE
MATERNA e introducción de alimentos ricos
en hierro du...
Para mejorar neuronutrición:

• En RNAT - APEG sus reservas de hierro son suficientes
para 6 primeros meses.
• Aunque LM e...
“Desayunar como un rey”
• Desayunar con alto contenido de
proteínas modifica activación cerebral en
regiones asociadas con...
Para mejorar neuronutrición: des iunare

 Nilsson A et al. A diet based on multiple functional concepts improves cognitiv...
“Desayuna como un rey”
• Desayunar con alto contenido de
proteínas modifica activación cerebral en
regiones asociadas con ...
Agua
• Mejora memoria a corto plazo en
escolares
• Primeras causas de delirium en
ancianos: deshidratación
• Causa frecuen...
Beber agua: esencial
Alimentos y efectos neuroquímicos
Item

Alimento

Principio activo

Efecto / función

Referencia

1

Arándano

flavonoides...
Bebidas energizantes
• Cafeína, taurina, inositol, glucuronolactona no
son fuentes concentradas de nutrientes, ni
constitu...
Problema de salud pública….
• El consumo de bebidas energéticas aumenta
riesgo de toxicidad de cafeína en niños y
adolesce...
Neuronutrición y Enferm. de
Alzheimer
• Dietas ricas en ácidos grasos saturados y el
alcohol, promueven aparición de EA.
•...
Enfermedad de Alzheimer
Cerebro
sano

Con E de A
avanzada
Neuronutrición y Enferm. de
Alzheimer

 Ramesh BN et al. Neuronutrition and Alzheimer's disease. J Alzheimers Dis. 2010;1...
Neuronutrición y Enferm. de
Alzheimer

 Ramesh BN et al. Neuronutrition and Alzheimer's disease. J Alzheimers Dis. 2010;1...
Neuronutrición y Enferm. de
Alzheimer

 Ramesh BN et al. Neuronutrition and Alzheimer's disease. J Alzheimers Dis. 2010;1...
Neuronutrición y Enferm. de
Alzheimer

 Ramesh BN et al. Neuronutrition and Alzheimer's disease. J Alzheimers Dis. 2010;1...
Asesoría con personal de salud
Lo que viene

 Fenech M et al. Nutrigenetics and Nutrigenomics: Viewpoints on the Current Status and
Applications in Nutr...
*-
Condición humana
• Relaciones: cultura - mundo mentalsistema nervioso
• Multidisciplinar: puentes conceptuales
de diferent...
“Todo el mundo es un genio. Pero si se juzga a un pez
por su habilidad para trepar un árbol, pasará el resto de
su vida cr...
Para mantener joven el cerebro
onclusiones
• Lactancia Materna es MUY importante
• Hierro: esencial en salud infantil
• Nutrición adecuada forma parte de...
euro-nutrición – Mensaje para
llevar a casa
“Nuestros cuerpos y mentes funcionan
y sienten mejor cuando respetamos
nuestra...
Alejandro Melo-Florián MD, FACP
http://www.scoop.it/u/alejandro-melo-florian
http://about.me/alejandromeloflorian
http://a...
Neuronutrición & Educación. Importante para todas las edades / Neuronutrition & education. Its role in human lifespan
Neuronutrición & Educación. Importante para todas las edades / Neuronutrition & education. Its role in human lifespan
Neuronutrición & Educación. Importante para todas las edades / Neuronutrition & education. Its role in human lifespan
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Neuronutrición & Educación. Importante para todas las edades / Neuronutrition & education. Its role in human lifespan

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La neuronutrición es un tema novedoso, surgido del progresivo conocimiento de la década del cerebro. En las Américas todavía existe el problema nutricional de anemia por carencia de hierro, no hay expectativas que sea superado en el 2015 y es uno de las puntas de iceberg de la desnutrición, que de acuerdo a UNICEF causa más de una tercera parte de las muertes infantiles en menores de 5 años. El déficit de hierro afecta cerca de 2000 millones en el mundo y cerca de 77 millones en Latinoamérica y el Caribe, este es un problema grave porque cuando ocurre en los primeros dos años altera el proceso de mielinización, procesos normales de funcionalidad dependientes de neurotransmisores como GABA, dopamina, que tienen implicaciones en l esfera conductual y del aprendizaje. La importancia del déficit de hierro en los primeros 2 años se debe a la elevada tasa de crecimiento del tejido nervioso durante este período, mayor que en cualquier otro período del desarrollo. Para evitar desnutrición neonatal se procura implementar la lactancia materna (LM) para favorecer la mejor plasticidad cerebral con el fin de coadyuvar al proceso epigenético de aprendizaje que permitirá el mejor desarrollo psicosocial del individuo. Los niños con LM suelen tener mayores puntajes de IQ, razón adicional para promoverla en la población. Si no posible LM, debe haber suplementación con hierro en la dieta del lactante. Otros nutrientes como ácidos grasos poliinsaturados omega-3 aportado por linaza, nueces, salmón, caballa, son importantes para mantener la homeóstasis del sistema nerviosos, con el mayor contenido de lípidos del organismo. Los omega-3 ayudan a regular función del SNC, de hígado y músculo por vía de receptores IGF, que a nivel neuronal favorecen la plasticidad sináptica ligada al aprendizaje. Bajo omega-3 en dieta puede resultar en mayor riesgo de patología cardio y cerebrovascular. Por otra parte, los alimentos funcionales (AF) aportan componentes biológicamente activos, como minerales, fibra, fitoquímicos, probióticos, entre otros. En estudios grandes, los AF mejoran memoria episódica, verbal y función ejecutiva. Una ingesta elevada de carbohidratos altera señalización normal de dopamina, produciendo conductas alimentarias anormales de buscar más carbohidratos, con mayor riesgo de obesidad y síndrome metabólico. Otras estrategias de optimizar neuronutrición incluyen tomar desayuno, rico en proteínas, beber abundante agua durante el día, esto mejora p.ej. memoria a corto plazo en escolares, evita descompensación de cuadros demenciales en ancianos. Otros alimentos con efectos benéficos en mejoría de facultades cognoscitivas, en reducción de amiloide, antioxidantes, incluyen arándano, azafrán, té verde, vino tinto, Ginkgo biloba, tomate, grosella espinosa india, verduras, que pueden ayudar a evitar deterioro cognoscitivo en Enfermedad de Alzheimer. Es necesaria una conducta cauta con las bebidas energizantes, pueden facilitar alcoholismo en adolescentes.

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  • http://www.canalgif.net/Gifs-animados/Profesiones/Profesores.asp
    http://www.imagenesanimadas.net/
    http://www.letrasanimadas.com/Imagenes-Animadas-Letras-Rosas/Animaciones-Letras-Rosas-3D/index3.htm
  • http://www.bioline.org.br/pdf?rc07019
  • http://www.bioline.org.br/pdf?rc07019 serotonina dopamina gaba mielina citocromos
  • Imagen de “paleo-artista” John Gurche
  • Aharon Katchalsky intentó ligar estrechamente la teoría de las estructuras disipativas al funcionamiento del cerebro humano. Katchalsky describió algunas pautas dinámicas del comportamiento del
    cerebro, en cuanto a estar en constante conexión con el entorno (aún en los denominados estados alterados de conciencia), el sufrir cambios abruptos, el ser muy sensible a las perturbaciones.
    Se considera por ejemplo que los recuerdos, los engramas de comportamiento y pensamiento implican un tipo de cooperación neuronal que lleva el sello de las estructuras disipativas. En estados
    alterados de conciencia las fluctuaciones de energía en algunos grupos neuronales pueden alcanzar un nivel crítico, de un tipo tal de amplitud, que puedan dar origen a una nueva organización167.
  • "DHA constitutes more than 30% of the total phospholipid composition of plasma membranes in the brain, and thus it is crucial for maintaining membrane integrity and, consequently, neuronal excitability and synaptic function”
    Fernando Gómez-Pinilla: Brain foods: the effects of nutrients on brain function Nat Rev Neurosci. 2008 July; 9(7): 568–578
  • The omega-3 fatty acid docosahexaenoic acid (DHA), which humans mostly attain from dietary fish, can affect synaptic function and cognitive abilities by providing plasma membrane fluidity at synaptic regions. DHA constitutes more than 30% of the total phospholipid composition of plasma membranes in the brain, and thus it is crucial for maintaining membrane integrity and, consequently, neuronal excitability and synaptic function. Dietary DHA is indispensable for maintaining membrane ionic permeability and the function of transmembrane receptors that support synaptic transmission and cognitive abilities. Omega-3 fatty acids also activate energygenerating metabolic pathways that subsequently affect molecules such as brain-derived neurotrophic factor (BDNF) and insulin-like growth factor 1 (IGF1). IGF1 can be produced in the liver and in skeletal muscle, as well as in the brain, and so it can convey peripheral messages to the brain in the context of diet and exercise. BDNF and IGF1 acting at presynaptic and postsynaptic receptors can activate signalling systems, such as the mitogen-activated protein kinase (MAPK) and calcium/calmodulin-dependent protein kinase II (CaMKII) systems, which facilitate synaptic transmission and support long-term potentiation that is associated with learning and memory. BDNF has also been shown to be involved in modulating synaptic plasticity and cognitive function through the phosphatidylinositol 3-kinase (PI3K)/Akt/ mammalian target of rapamycin (mTOR) signalling pathway. The activities of the mTOR and Akt signalling pathways are also modulated by metabolic signals such as insulin and leptin (not shown). 4EBP, eukaryotic translation-initiation factor 4E binding protein; CREB, cyclic AMP-responsive element (CRE)-binding protein; IGFR, insulin-like growth factor receptor; IRS1, insulin receptor substrate 1; p70S6K, p70 S6 kinase.
  • http://ajcn.nutrition.org/content/94/3/892.full.pdf
    Am J Clin Nutr. 2011 Sep;94(3):892-9. doi: 10.3945/ajcn.110.007815. Epub 2011 Jul 20.
    French adults' cognitive performance after daily supplementation with antioxidant vitamins and minerals at nutritional doses: a post hoc analysis of the Supplementation in Vitamins and Mineral Antioxidants (SU.VI.MAX) trial.
    Kesse-Guyot E, Fezeu L, Jeandel C, Ferry M, Andreeva V, Amieva H, Hercberg S, Galan P.
    Source
    Unité de Recherche en Epidémiologie Nutritionnelle, U Institut National de la Santeacute et de la Recherche Meacutedicale, Université Paris, Bobigny, France.
    Abstract
    BACKGROUND:
    Antioxidant properties of some vitamins and trace elements may help to prevent cognitive decline.
    OBJECTIVE:
    The aim of the current study was to estimate the long-term effects of antioxidant nutrient supplementation on the cognitive performance of participants in the Supplementation in Vitamins and Mineral Antioxidants (SU.VI.MAX) study 6 y after the end of the trial.
    DESIGN:
    This study included 4447 French participants aged 45-60 y who were enrolled in the SU.VI.MAX study (1994-2002), which was a double-blind, placebo-controlled, randomized trial. From 1994 to 2002, participants received daily vitamin C (120 mg), β-carotene (6 mg), vitamin E (30 mg), selenium (100 μg), and zinc (20 mg) in combination or as a placebo. In 2007-2009, the cognitive performance of participants was assessed with 4 neuropsychological tests (6 tasks). Principal components analysis (PCA) was performed to identify cognitive-function summary scores. Associations between antioxidant supplementation and cognitive functions, in the full sample and by subgroups, were estimated through ANOVA and expressed as mean differences and 95% CIs. Subgroup analyses were performed according to baseline characteristics.
    RESULTS:
    Subjects receiving active antioxidant supplementation had better episodic memory scores (mean difference: 0.61; 95% CI: 0.02, 1.20). PCA indicated 2 factors that were interpreted as showing verbal memory and executive functioning. Verbal memory was improved by antioxidant supplementation only in subjects who were nonsmokers or who had low serum vitamin C concentrations at baseline.
    CONCLUSION:
    This study supports the role of an adequate antioxidant nutrient status in the preservation of verbal memory under certain conditions. This trial was registered at clinicaltrials.gov as NCT00272428.
  • http://ajcn.nutrition.org/content/94/3/892.full.pdf
    Am J Clin Nutr. 2011 Sep;94(3):892-9. doi: 10.3945/ajcn.110.007815. Epub 2011 Jul 20.
    French adults' cognitive performance after daily supplementation with antioxidant vitamins and minerals at nutritional doses: a post hoc analysis of the Supplementation in Vitamins and Mineral Antioxidants (SU.VI.MAX) trial.
    Kesse-Guyot E, Fezeu L, Jeandel C, Ferry M, Andreeva V, Amieva H, Hercberg S, Galan P.
    Source
    Unité de Recherche en Epidémiologie Nutritionnelle, U Institut National de la Santeacute et de la Recherche Meacutedicale, Université Paris, Bobigny, France.
    Abstract
    BACKGROUND:
    Antioxidant properties of some vitamins and trace elements may help to prevent cognitive decline.
    OBJECTIVE:
    The aim of the current study was to estimate the long-term effects of antioxidant nutrient supplementation on the cognitive performance of participants in the Supplementation in Vitamins and Mineral Antioxidants (SU.VI.MAX) study 6 y after the end of the trial.
    DESIGN:
    This study included 4447 French participants aged 45-60 y who were enrolled in the SU.VI.MAX study (1994-2002), which was a double-blind, placebo-controlled, randomized trial. From 1994 to 2002, participants received daily vitamin C (120 mg), β-carotene (6 mg), vitamin E (30 mg), selenium (100 μg), and zinc (20 mg) in combination or as a placebo. In 2007-2009, the cognitive performance of participants was assessed with 4 neuropsychological tests (6 tasks). Principal components analysis (PCA) was performed to identify cognitive-function summary scores. Associations between antioxidant supplementation and cognitive functions, in the full sample and by subgroups, were estimated through ANOVA and expressed as mean differences and 95% CIs. Subgroup analyses were performed according to baseline characteristics.
    RESULTS:
    Subjects receiving active antioxidant supplementation had better episodic memory scores (mean difference: 0.61; 95% CI: 0.02, 1.20). PCA indicated 2 factors that were interpreted as showing verbal memory and executive functioning. Verbal memory was improved by antioxidant supplementation only in subjects who were nonsmokers or who had low serum vitamin C concentrations at baseline.
    CONCLUSION:
    This study supports the role of an adequate antioxidant nutrient status in the preservation of verbal memory under certain conditions. This trial was registered at clinicaltrials.gov as NCT00272428.
  • En los seres humanos obesos y diabéticos, se ha demostrado que hay una escasez de señalización dopaminérgica, y esto es reversible con la restricción de glucosa. Regulación a la baja de la señalización de la dopamina es necesaria para permitir que los trastornos metabólicos se produzcan, ¿por qué? Debido a que es fundamentalmente una tendencia de hibernación evolutivamente normal en cuestión, sólo es una enfermedad en nuestra sociedad moderna donde los genes están siendo anormalmente activados, de manera crónica durante todo el año. Bromocriptina ayuda a la diabetes y la obesidad por esta razón. En cuanto a la observación de que las personas con olanzapina no está utilizando los hidratos de carbono para obtener energía, supongo que es sólo el resultado natural de bloqueo de la serotonina y múltiples receptores de la dopamina en el cuerpo – la incapacidad, la debilidad, en la utilización de la glucosa para obtener energía. Este es un resultado natural y conservado evolutivamente del neurotransmisor en su deficiente señalización, que a su vez al cuerpo significa cambio de estación y el invierno inminente, pues una respuesta similar a la hibernación (conservación metabólica que implica acumulación de grasas, dormir más,  el hambre, y cerrar la fertilidad).
    Se ha sabido por un tiempo que cuando el cuerpo pasa a utilizar la grasa para obtener energía esto dará lugar a la hiperglucemia e hiperinsulinemia compensatoria por lo tanto, lo que conduce a la ganancia de grasa corporal. Cuando el cuerpo insiste en la quema de grasa, incluso en la presencia de hidratos de carbono, podría significar cualquier número de cosas … 1) resistencia a la insulina debido a daños patológicos / mitocondrias deficientes (la glucosa no puede entrar en las células, porque las mitocondrias son deficientes, por lo tanto las mitocondrias primariamente queman la grasa y la glucosa en la sangre es elevada) … 2) alguien está tomando un medicamento que induce la hibernación y la conservación metabólica transitoria (con deficiencia de la dopamina y la serotonina, el cuerpo se niega a aceptar la glucosa, utiliza grasa en vez, en modo de hibernación, la grasa corporal y aumenta el azúcar en la sangre como puede ser que a principios del otoño para prepararse para invierno. disminuye la fertilidad en respuesta a la disminución de la dopamina y la serotonina también, y la infertilidad es una característica importante de la adaptación de invierno y la hibernación en animales como en seres humanos de los bloqueadores del receptor de la dopamina).
    Comer menos hidratos de carbono, en particular el azúcar, es evidente la intervención para controlar la obesidad. A pesar de que una mayor utilización de grasa se produce durante el trastorno metabólico, que es en última instancia, la parte de la glucosa de la dieta que provoca el almacenamiento de grasa y la diabetes … o por lo menos lo peor de ella. Si el cuerpo quiere utilizar la grasa, entonces piensa que está gordo. Si trata de darle de comer azúcar, todo lo que va a pasar es que el páncreas  secreta insulina y el hígado lo convertirá en grasa que se almacena en el tejido adiposo de manera eficiente. Evitar el consumo de alimentos con  glucosa, lo peor de esta hiperglucemia / tendencia hiperinsulinémico es controlado.
  • http://www.upch.edu.pe/ehas/pediatria/lactancia%20materna/Clase%20401%20-%2010.htm
  • http://www.upch.edu.pe/ehas/pediatria/lactancia%20materna/Clase%20401%20-%2010.htm
  • http://www.upch.edu.pe/ehas/pediatria/lactancia%20materna/Clase%20401%20-%2010.htm
  • http://aje.oxfordjournals.org/content/158/11/1075.full.pdf
    Differences in test scores between breastfed children and those who did not receive any breast milk feedings were 3.6 IQ points (95% confidence interval: -0.3, 7.5) for overall intellectual functioning and 2.3 IQ points (95% confidence interval: -3.0, 7.6) for verbal ability.
  • http://www.sciencedirect.com/science/article/pii/S0021755713000995
    http://www.ncbi.nlm.nih.gov/pubmed/23791025
    The difference in the averages found between the breastfed and non-breastfed groups at six months of age was 1.33 (p=0.008).
  • http://pediatrics.aappublications.org/content/115/2/496.full.pdf
    La alimentacion continuada con LECHE MATERNA, junto con introducción de alimentos ricos en hierro durante POR LO MENOS el primer año de vida
    Si LM no es opción, leches enriquecidas con hierro durante los 6 primeros meses.
    Alimentos complementarios caseros son bajos en hierro, agregar gotas de hierro
    World Health Organization, United Nations Children’s Fund, United Nations University: Iron Deficiency Anaemia. Assessment, Prevention,
    and Control. A Guide for Programme Managers. WHO/NHD/01.3. Geneva, World Health Organization, 2001.
  • http://www.spponline.net/documentos/manualnutricion.pdf
    Para un lactante normal nacido a término con peso adecuado sus reservas de hierro suelen ser suficientes para los 6 primeros meses de vida. La leche materna tiene un contenido
    bajo de hierro (0,2-0,4 mg/L), pero con una alta biodisponibilidad, por lo que la lactancia materna es suficiente para mantener unos niveles adecuados de hierro
    durante este primer semestre de vida. A partir de esta edad las necesidades de hierro aumentan rápidamente, para llegar a cifras mayores que en ninguna otra época de la vida (0,1 mg/kg/día). Debido a esto, se aconseja iniciar la alimentación complementaria con alimentos ricos en hierro a partir de esta edad y retrasar la introducción de la leche de vaca después del año de edad. Para los
    lactantes alimentados con fórmula se aconseja el uso de fórmulas suplementadas con hierro desde el nacimiento. La suplementación con hierro farmacológico
    no es necesaria para los lactantes sanos con un desarrollo normal, aunque sí en el caso de los recién nacidos pretérminos o en determinadas situaciones patológicas
    o metabólicas en las que se objetive el déficit.
    Otra de las épocas del desarrollo con altos requerimientos de hierro es la adolescencia, sobre todo en el caso de las niñas después del inicio de la menstruación.
    No es preciso suplementar con hierro en estos casos, exceptuando niñas que realicen dietas muy restrictivas (vegetarianas) o en algunos casos de alto gasto y en todos aquellos niños en los que se objetive un déficit claro analítico.
  • In summary, the addition of breakfast led to alterations in brain activation in regions previously associated with food motivation and reward with additional alterations following the higher-protein breakfast. These data suggest that increased dietary protein at breakfast might be a beneficial strategy to reduce reward-driven eating behavior in overweight teen girls. Due to the small sample size, caution is warranted when interpreting these preliminary findings.
  • Nilsson A, Tovar J, Johansson M, Radeborg K, Björck I. A diet based on multiple functional concepts improves cognitive performance in healthy subjects. Nutr Metab (Lond). 2013 Jul 15;10(1):49.
  • In summary, the addition of breakfast led to alterations in brain activation in regions previously associated with food motivation and reward with additional alterations following the higher-protein breakfast. These data suggest that increased dietary protein at breakfast might be a beneficial strategy to reduce reward-driven eating behavior in overweight teen girls. Due to the small sample size, caution is warranted when interpreting these preliminary findings.
  • Appetite. 2012 Dec;59(3):730-7. doi: 10.1016/j.appet.2012.07.005. Epub 2012 Jul 24.
    Effects of drinking supplementary water at school on cognitive performance in children.
    Fadda R, Rapinett G, Grathwohl D, Parisi M, Fanari R, Calò CM, Schmitt J.
    Source
    Department of Pedagogy, Psychology and Philosophy, University of Cagliari, via Is Mirrionis 1, 09123 Cagliari, Italy. robfadda@unica.it
    Abstract
    We investigated the beneficial effects of drinking supplementary water during the school day on the cognitive performance and transitory subjective states, such as fatigue or vigor, in 168 children aged between 9 and 11years who were living in a hot climate (South Italy, Sardinia). The classes were randomly divided into an intervention group, which received water supplementation, and a control group. Dehydration was determined by urine sampling and was defined as urine osmolality greater than 800mOsm/kg H(2)O (Katz, Massry, Agomn, & Toor, 1965). The change in the scores from the morning to the afternoon of hydration levels, cognitive performance and transitory subjective states were correlated. In line with a previous observational study that evaluated the hydration status of school children living in a country with a hot climate (Bar-David, Urkin, & Kozminsky, 2005), our results showed that a remarkable proportion of children were in a state of mild, voluntary dehydration at the beginning of the school day (84%). We found a significant negative correlation between dehydration and the auditory number span, which indicates a beneficial effect of drinkingsupplementary water at school on short-term memory. Moreover, there was a positive correlation between dehydration and performance in the verbal analogy task. The results are discussed in the light of the complexity of the neurobiological mechanisms involved in the relationship between hydration status and cognition.
    Copyright © 2012 Elsevier Ltd. All rights reserved.
    PMID: 22841529 [PubMed - indexed for MEDLINE]
    JAMA. 2012 Jan 11;307(2):165-72. doi: 10.1001/jama.2011.1964.
    Association of incident dementia with hospitalizations.
    Phelan EA, Borson S, Grothaus L, Balch S, Larson EB.
    Source
    Division of Gerontology and Geriatric Medicine, Department of Medicine, School of Public Health and Community Medicine, University of Washington, Seattle, WA 98104-2499, USA. phelane@uw.edu
    Abstract
    CONTEXT:
    Dementia is associated with increased rates and often poorer outcomes of hospitalization, including worsening cognitive status. New evidence is needed to determine whether some admissions of persons with dementia might be potentially preventable.
    OBJECTIVE:
    To determine whether dementia onset is associated with higher rates of or different reasons for hospitalization, particularly for ambulatory care-sensitive conditions (ACSCs), for which proactive outpatient care might prevent the need for a hospital stay.
    DESIGN, SETTING, AND PARTICIPANTS:
    Retrospective analysis of hospitalizations among 3019 participants in Adult Changes in Thought (ACT), a longitudinal cohort study of adults aged 65 years or older enrolled in an integrated health care system. All participants had no dementia at baseline and those who had a dementia diagnosis during biennial screening contributed nondementia hospitalizations until diagnosis. Automated data were used to identify all hospitalizations of all participants from time of enrollment in ACT until death, disenrollment from the health plan, or end of follow-up, whichever came first. The study period spanned February 1, 1994, to December 31, 2007.
    MAIN OUTCOME MEASURES:
    Hospital admission rates for patients with and without dementia, for all causes, by type of admission, and for ACSCs.
    RESULTS:
    Four hundred ninety-four individuals eventually developed dementia and 427 (86%) of these persons were admitted at least once; 2525 remained free of dementia and 1478 (59%) of those were admitted at least once. The unadjusted all-cause admission rate in the dementia group was 419 admissions per 1000 person-years vs 200 admissions per 1000 person-years in the dementia-free group. After adjustment for age, sex, and other potential confounders, the ratio of admission rates for all-cause admissions was 1.41 (95% confidence interval [CI], 1.23-1.61; P < .001), while for ACSCs, the adjusted ratio of admission rates was 1.78 (95% CI, 1.38-2.31; P < .001). Adjusted admission rates classified by body system were significantly higher in the dementia group for most categories. Adjusted admission rates for all types of ACSCs, including bacterial pneumonia, congestive heart failure, dehydration, duodenal ulcer, and urinary tract infection, were significantly higher among those with dementia.
    CONCLUSION:
    Among our cohort aged 65 years or older, incident dementia was significantly associated with increased risk of hospitalization, including hospitalization for ACSCs.
  • http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2931824/pdf/nihms190638.pdf
    http://www.ncbi.nlm.nih.gov/pubmed/20308778
  • Reissig CJ, Strain EC, Griffiths RR. Caffeinated energy drinks--a growing problem. Drug Alcohol Depend. 2009 Jan 1;99(1-3):1-10. doi: 10.1016/j.drugalcdep.2008.08.001. Epub 2008 Sep 21. Review. PubMed PMID: 18809264; PubMed Central PMCID: PMC2735818.
    Since the introduction of Red Bull in Austria in 1987 and in the United States in 1997, the energy drink market has grown exponentially. Hundreds of different brands are now marketed, with caffeine content ranging from a modest 50 mg to an alarming 505 mg per can or bottle. Regulation of energy drinks, including content labeling and health warnings differs across countries, with some of the most lax regulatory requirements in the U.S. The absence of regulatory oversight has resulted in aggressive marketing of energy drinks, targeted primarily toward young males, for psychoactive, performance-enhancing and stimulant drug effects. There are increasing reports of caffeine intoxication from energy drinks, and it seems likely that problems with caffeine dependence and withdrawal will also increase. In children and adolescents who are not habitual caffeine users, vulnerability to caffeine intoxication may be markedly increased due to an absence of pharmacological tolerance. Genetic factors may also contribute to an individual's vulnerability to caffeine-related disorders including caffeine intoxication, dependence, and withdrawal. The combined use of caffeine and alcohol is increasing sharply, and studies suggest that such combined use may increase the rate of alcohol-related injury. Several studies suggest that energy drinks may serve as a gateway to other forms of drug dependence. Regulatory implications concerning labeling and advertising, and the clinical implications for children and adolescents are discussed.
    Bigard AX. [Risks of energy drinks in youths]. Arch Pediatr. 2010 Nov;17(11):1625-31. doi: 10.1016/j.arcped.2010.08.001. Review. French. PubMed PMID: 20926266.
    The market value for energy drinks is continually growing and the annual worldwide energy drink consumption is increasing. However, issues related to energy drink ingredients and the potential for adverse health consequences remain to be elucidated. This aim of the present paper is to review the current knowledge on putative adverse effects of energy drinks, especially in youths. There are many energy drink brands in the worldwide market, even if only few brands are available in France. Although the energy drink content varies, these beverages often contain taurine, caffeine, vitamins B and carbohydrates. These drinks vary widely in both caffeine content (80 to 141 mg per can) and caffeine concentration. Except caffeine, the effects of energy drink ingredients on physical and cognitive performances remain controversial. Researchers identified moderate positive effects of energy drinks on performances, whereas others found contrary results. The adverse effects of energy drink can be related to either the toxicity of ingredients or specific situations in which energy drinks are used such as ingestion in combination with alcohol. Although the issue of taurine-induced toxic encephalopathy has been addressed, it is likely that the risk of taurine toxicity after energy drink consumption remains low. However, whether the prolonged use of energy drinks providing more than 3g taurine daily remains to be examined in the future. The consumption of energy drinks may increase the risk for caffeine overdose and toxicity in children and teenagers. The practice of consuming great amounts of energy drink with alcohol is considered by many teenagers and students a primary locus to socialize and to meet people. This pattern of energy drink consumption explains the enhanced risk of both caffeine and alcohol toxicity in youths. Twenty five to 40% of young people report consumption of energy drink with alcohol while partying. Consumption of energy drinks with alcohol during heavy episodic drinking is at risk of serious injury, sexual assault, drunk driving, and death. However, even after adjusting for alcohol consumption, students who consume alcohol mixed with energydrinks had dramatically higher rates of serious alcohol-related consequences. It has been reported that the subjective perceptions of some
    symptoms of alcohol intoxication are less intense after the combined ingestion of the alcohol plus energy drink; however, these effects are not detected in objective measures of motor coordination and visual reaction time.
    Malinauskas BM, Aeby VG, Overton RF, Carpenter-Aeby T, Barber-Heidal K. A survey of energy drink consumption patterns among college students. Nutr J. 2007 Oct 31;6:35. PubMed PMID: 17974021; PubMed Central PMCID: PMC2206048.
    Nutr J. 2007 Oct 31;6:35.
    A survey of energy drink consumption patterns among college students.
    Malinauskas BM, Aeby VG, Overton RF, Carpenter-Aeby T, Barber-Heidal K.
    Source
    Department of Nutrition and Dietetics, East Carolina University, Greenville, North Carolina, USA. malinauskasb@ecu.edu
    Abstract
    BACKGROUND: Energy drink consumption has continued to gain in popularity since the 1997 debut of Red Bull, the current leader in the energy drink market. Although energy drinks are targeted to young adult consumers, there has been little research regarding energy drink consumption patterns among college students in the United States. The purpose of this study was to determine energy drink consumption patterns among college students, prevalence and frequency of energy drink use for six situations, namely for insufficient sleep, to increase energy (in general), while studying, driving long periods of time, drinking with alcohol while partying, and to treat a hangover, and prevalence of adverse side effects and energy drink use dose effects among college energy drink users.
    METHODS: Based on the responses from a 32 member college student focus group and a field test, a 19 item survey was used to assess energy drink consumption patterns of 496 randomly surveyed college students attending a state university in the Central Atlantic region of the United States.
    RESULTS: Fifty one percent of participants (n = 253) reported consuming greater than one energy drink each month in an average month for the current semester (defined as energy drink user). The majority of users consumed energy drinks for insufficient sleep (67%), to increase energy (65%), and to drink with alcohol while partying (54%). The majority of users consumed one energy drink to treat most situations although using three or more was a common practice to drink with alcohol while partying (49%). Weekly jolt and crash episodes were experienced by 29% of users, 22% reported ever having headaches, and 19% heart palpitations from consuming energy drinks. There was a significant dose effect only for jolt and crash episodes.
    CONCLUSION: Using energy drinks is a popular practice among college students for a variety of situations. Although for the majority of situations assessed, users consumed one energy drink with a reported frequency of 1 - 4 days per month, many users consumed three or more when combining with alcohol while partying. Further, side effects from consuming energy drinks are fairly common, and a significant dose effect was found with jolt and crash episodes. Future research should identify if college students recognize the amounts of caffeine that are present in the wide variety of caffeine-containing products that they are consuming, the amounts of caffeine that they are consuming in various situations, and the physical side effects associated with caffeine consumption.
  • Reissig CJ, Strain EC, Griffiths RR. Caffeinated energy drinks--a growing problem. Drug Alcohol Depend. 2009 Jan 1;99(1-3):1-10. doi: 10.1016/j.drugalcdep.2008.08.001. Epub 2008 Sep 21. Review. PubMed PMID: 18809264; PubMed Central PMCID: PMC2735818.
    Since the introduction of Red Bull in Austria in 1987 and in the United States in 1997, the energy drink market has grown exponentially. Hundreds of different brands are now marketed, with caffeine content ranging from a modest 50 mg to an alarming 505 mg per can or bottle. Regulation of energy drinks, including content labeling and health warnings differs across countries, with some of the most lax regulatory requirements in the U.S. The absence of regulatory oversight has resulted in aggressive marketing of energy drinks, targeted primarily toward young males, for psychoactive, performance-enhancing and stimulant drug effects. There are increasing reports of caffeine intoxication from energy drinks, and it seems likely that problems with caffeine dependence and withdrawal will also increase. In children and adolescents who are not habitual caffeine users, vulnerability to caffeine intoxication may be markedly increased due to an absence of pharmacological tolerance. Genetic factors may also contribute to an individual's vulnerability to caffeine-related disorders including caffeine intoxication, dependence, and withdrawal. The combined use of caffeine and alcohol is increasing sharply, and studies suggest that such combined use may increase the rate of alcohol-related injury. Several studies suggest that energy drinks may serve as a gateway to other forms of drug dependence. Regulatory implications concerning labeling and advertising, and the clinical implications for children and adolescents are discussed.
    Bigard AX. [Risks of energy drinks in youths]. Arch Pediatr. 2010 Nov;17(11):1625-31. doi: 10.1016/j.arcped.2010.08.001. Review. French. PubMed PMID: 20926266.
    The market value for energy drinks is continually growing and the annual worldwide energy drink consumption is increasing. However, issues related to energy drink ingredients and the potential for adverse health consequences remain to be elucidated. This aim of the present paper is to review the current knowledge on putative adverse effects of energy drinks, especially in youths. There are many energy drink brands in the worldwide market, even if only few brands are available in France. Although the energy drink content varies, these beverages often contain taurine, caffeine, vitamins B and carbohydrates. These drinks vary widely in both caffeine content (80 to 141 mg per can) and caffeine concentration. Except caffeine, the effects of energy drink ingredients on physical and cognitive performances remain controversial. Researchers identified moderate positive effects of energy drinks on performances, whereas others found contrary results. The adverse effects of energy drink can be related to either the toxicity of ingredients or specific situations in which energy drinks are used such as ingestion in combination with alcohol. Although the issue of taurine-induced toxic encephalopathy has been addressed, it is likely that the risk of taurine toxicity after energy drink consumption remains low. However, whether the prolonged use of energy drinks providing more than 3g taurine daily remains to be examined in the future. The consumption of energy drinks may increase the risk for caffeine overdose and toxicity in children and teenagers. The practice of consuming great amounts of energy drink with alcohol is considered by many teenagers and students a primary locus to socialize and to meet people. This pattern of energy drink consumption explains the enhanced risk of both caffeine and alcohol toxicity in youths. Twenty five to 40% of young people report consumption of energy drink with alcohol while partying. Consumption of energy drinks with alcohol during heavy episodic drinking is at risk of serious injury, sexual assault, drunk driving, and death. However, even after adjusting for alcohol consumption, students who consume alcohol mixed with energydrinks had dramatically higher rates of serious alcohol-related consequences. It has been reported that the subjective perceptions of some
    symptoms of alcohol intoxication are less intense after the combined ingestion of the alcohol plus energy drink; however, these effects are not detected in objective measures of motor coordination and visual reaction time.
    Malinauskas BM, Aeby VG, Overton RF, Carpenter-Aeby T, Barber-Heidal K. A survey of energy drink consumption patterns among college students. Nutr J. 2007 Oct 31;6:35. PubMed PMID: 17974021; PubMed Central PMCID: PMC2206048.
    Nutr J. 2007 Oct 31;6:35. A survey of energy drink consumption patterns among college students. Malinauskas BM, Aeby VG, Overton RF, Carpenter-Aeby T, Barber-Heidal K.
    Source Department of Nutrition and Dietetics, East Carolina University, Greenville, North Carolina, USA. malinauskasb@ecu.edu
    Abstract BACKGROUND: Energy drink consumption has continued to gain in popularity since the 1997 debut of Red Bull, the current leader in the energy drink market. Although energy drinks are targeted to young adult consumers, there has been little research regarding energy drink consumption patterns among college students in the United States. The purpose of this study was to determine energy drink consumption patterns among college students, prevalence and frequency of energy drink use for six situations, namely for insufficient sleep, to increase energy (in general), while studying, driving long periods of time, drinking with alcohol while partying, and to treat a hangover, and prevalence of adverse side effects and energy drink use dose effects among college energy drink users.
    METHODS: Based on the responses from a 32 member college student focus group and a field test, a 19 item survey was used to assess energy drink consumption patterns of 496 randomly surveyed college students attending a state university in the Central Atlantic region of the United States. RESULTS: Fifty one percent of participants (n = 253) reported consuming greater than one energy drink each month in an average month for the current semester (defined as energy drink user). The majority of users consumed energy drinks for insufficient sleep (67%), to increase energy (65%), and to drink with alcohol while partying (54%). The majority of users consumed one energy drink to treat most situations although using three or more was a common practice to drink with alcohol while partying (49%). Weekly jolt and crash episodes were experienced by 29% of users, 22% reported ever having headaches, and 19% heart palpitations from consuming energy drinks. There was a significant dose effect only for jolt and crash episodes. CONCLUSION: Using energy drinks is a popular practice among college students for a variety of situations. Although for the majority of situations assessed, users consumed one energy drink with a reported frequency of 1 - 4 days per month, many users consumed three or more when combining with alcohol while partying. Further, side effects from consuming energy drinks are fairly common, and a significant dose effect was found with jolt and crash episodes. Future research should identify if college students recognize the amounts of caffeine that are present in the wide variety of caffeine-containing products that they are consuming, the amounts of caffeine that they are consuming in various situations, and the physical side effects associated with caffeine consumption.
    Pediatrics. 2011 March; 127(3): 511–528. Published online 2011 February 14. doi:  10.1542/peds.2009-3592 PMCID: PMC3065144
    Health Effects of Energy Drinks on Children, Adolescents, and Young Adults Sara M. Seifert, BS, Judith L. Schaechter, MD, Eugene R. Hershorin, MD, and Steven E. Lipshultz, MD
    Author information ► Article notes ► Copyright and License information ► This article has been cited by other articles in PMC. Go to:
    Abstract
    OBJECTIVE: To review the effects, adverse consequences, and extent of energy drink consumption among children, adolescents, and young adults.
    METHODS: We searched PubMed and Google using “energy drink,” “sports drink,” “guarana,” “caffeine,” “taurine,” “ADHD,” “diabetes,” “children,” “adolescents,” “insulin,” “eating disorders,” and “poison control center” to identify articles related to energy drinks. Manufacturer Web sites were reviewed for product information.
    RESULTS: According to self-report surveys, energy drinks are consumed by 30% to 50% of adolescents and young adults. Frequently containing high and unregulated amounts of caffeine, these drinks have been reported in association with serious adverse effects, especially in children, adolescents, and young adults with seizures, diabetes, cardiac abnormalities, or mood and behavioral disorders or those who take certain medications. Of the 5448 US caffeine overdoses reported in 2007, 46% occurred in those younger than 19 years. Several countries and states have debated or restricted energy drink sales and advertising.
    CONCLUSIONS: Energy drinks have no therapeutic benefit, and many ingredients are understudied and not regulated. The known and unknown pharmacology of agents included in such drinks, combined with reports of toxicity, raises concern for potentially serious adverse effects in association with energy drink use. In the short-term, pediatricians need to be aware of the possible effects of energy drinks in vulnerable populations and screen for consumption to educate families. Long-term research should aim to understand the effects in at-risk populations. Toxicity surveillance should be improved, and regulations of energy drink sales and consumption should be based on appropriate research. Keywords: energy drink, caffeine, taurine, children, adolescents, overdose
    “NIÑOS Y BEBIDAS ENERGIZANTES Las investigaciones indican que no hay diferencias en la tolerancia a la cafeína entre niños y adultos, aunque, sobre todo, hay que tener cuidado con los menores pues hoy en día las bebidas cafeínadas pueden estar reemplazando alimentos altamente nutritivos en la dieta, además porque la cafeína consumida en cantidades muy altas actúa como supresor del apetito, especialmente en los niños. No deben ser consumidas por menores de 18 años porque no se sabe con certeza sus efectos adversos en este grupo. La mayoría tienen ácido fosfórico, al igual que los refrescos, que está comprobado que disminuye la densidad ósea en los niños. La cafeína debe restringirse en niños hiperactivos debido a que es un estimulante. Claramente en los eventos a los que estamos haciendo referencia, este tipo de controles y recomendaciones no son tenidos en cuenta. Adicionalmente estas bebidas son comercializadas en almacenes de cadena y en tiendas y supermercados de barrio, sin ningún tipo de restricción en su venta y consumo para los menores de 18 años. Existe un estudio en donde se reportan el 'squash drinking syndrome', (6) que hace referencia a alteraciones del comportamiento, disminución del apetito, pobre ganancia de peso en niños que consumen bebidas energizantes, por lo cual no es recomendable que los menores las ingieran. Además de la evidente y señalada inconveniencia que los niños consuman bebidas energizantes, este consumo se puede convertir en la antesala para incrementar las alarmantes cifras de consumo de alcohol y otras drogas entre los jóvenes. Esta afirmación se basa en el hecho comprobado de que cualquier bebida que contenga componentes estimulantes genera dependencia.”
  • http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2931824/
    Ramesh BN, Rao TS, Prakasam A, Sambamurti K, Rao KS. Neuronutrition and Alzheimer's disease. J Alzheimers Dis. 2010;19(4):1123-39. doi: 10.3233/JAD-2010-1312. Review. PubMed PMID: 20308778; PubMed Central PMCID: PMC2931824.
    J Alzheimers Dis. 2010 January; 19(4): 1123–1139.
    doi:  10.3233/JAD-2010-1312
    PMCID: PMC2931824
    NIHMSID: NIHMS190638
    Neuronutrition and Alzheimer's Disease
    Balenahalli N. Ramesh,1 T.S. Sathyanarayana Rao,2 Annamalai Prakasam,3 Kumar Sambamurti,3 and K.S. Jagannatha Rao1
    1Biochemistry and Nutrition, Central Food Technological Research Institute, CSIR Unit, Mysore, India
    2Department of Psychiatry, J S S Medical College, Mysore, India
    3Department of Neuroscience, Medical University of South Carolina, Charleston, South Carolina, USA
    Correspondence to: K.S. Jagannatha Rao, Central Food Technological Research Institute, CSIR Unit, Mysore, 570020 India; Email: [email_address]
    Copyright notice and Disclaimer
    Abstract
    Alzheimer's disease (AD) is a complex neurological disorder with several unequivocally identified genetic risk factors. Among the several environmental factors proposed for AD, dietary protective and risk factors have been most compelling. In particular, diets rich in saturated fatty acids and alcohol, and deficient in antioxidants and vitamins appear to promote the onset of the disease, while diets rich in unsaturated fatty acids, vitamins, antioxidants, and wine likely suppress its onset. Evidence suggests that diets rich in polyphenols and some spices suppress the onset of AD by scavenging free radicals and preventing oxidative damage. Metal ions are known to catalyze the production of free radicals and induce mental retardation or dementia. Several studies have also identified metals such as Pb, Fe, Al, Cu and Zn in AD pathogenesis. While specific chelators have been tested for therapy, they have not been very successful probably due to late administration after brain damage has been triggered. Since several dietary polyphenols are known to chelate metals, their routine use may also be protective against the onset of AD.
    Keywords: antioxidants, caloric restriction, diet, homocysteine, lipid, neurodegeneration, nutrients, oxidative stress, polyphenols, vitamins
    Introduction
    Alzheimer's disease (AD) is the most common form of dementia and affects one in four individuals over the age of 85. AD has multiple etiological factors including genetics, environmental factors, and general lifestyles [1], and its hallmark pathology includes extracellular amyloid β protein (Aβ) deposition in the form of senile plaques and intracellular deposits of the microtubule-associated protein “τ” as neurofibrillary tangles in the AD brain [2]. The diagnosis of this disease is based on the characteristic idiopathic psychometric deficits upon clinical evaluation and further confirmed by post-mortem due to the presence of the characteristic lesions described above [3]. Aβ is produced by sequential proteolytic processing of a larger Aβ protein precursor (AβPP) by β-secretase to generate a large secreted fragment sAPPβ and a 99 aa cellular fragment – CTFβ – that includes Aβ, the transmembrane domain and the intracellular domain of AβPP [4].
    Recently, there has been increasing support for a role of diets in AD [5-7]. A number of dietary factors such as saturated fatty acids [8], higher calorie intake [9], and excessive alcohol [10] have been reported to increase the risk of dementia and AD. In contrast, antioxidants, fish, methionine-rich proteins, and vitamins were identified as protective against the disease [11]. Thus the global variation in diet may be linked to differential prevalence of AD [12]. Several cross-sectional studies suggest a relationship between particular nutrients and the presence of cognitive changes [5-7]. However, these need to be confirmed at an experimental level [13].
    Interestingly, the same dietary pattern of risk and protection has been long accepted for metabolic syndrome and cardiovascular risk. In agreement Diabetes and hyperinsulinaemia are considered as important risk factors for AD [14]. Among the other risk factors, depressive illness, traumatic head injury [15], cardiovascular disease [16-17], smoking [18-19], and stroke [20-21] are significant issues that may be related to the same risk factors. Further, the ε4 allele variant of apolipoprotein E (ApoE) has been associated with increased risk in sporadic and familial AD [22]. As a carrier of cholesterol, ApoE-ε4 is also a risk factor in cardiovascular disease.
    Oxidative stress has been suggested to play a major role in the pathology of AD [23-26], and evidence for its mediation includes: 1) generation of free radicals through metal ions; 2) enhanced lipid peroxidation; 3) increased DNA and protein damage; and 4) increased tau protein phosphorylation [26]. The human body has a defense mechanism to cope with oxidative stress, or prevent the onset of oxidative stress, through endogenous antioxidants derived from enzymatic or non-enzymatic sources [27], namely superoxide dismutase, glutathione reductase, and catalase. The nonenzymatic sources of endogenous antioxidants include glutathione, uric acid, α-lipoic acids, acetyl L-carnitine, melatonin, and dehydroepiandrosterone. Endogenous antioxidants also include the products of reactions catalyzed by enzymes that are up regulated in response to oxidative stress (e.g., bilurubin) [27]. Dietary antioxidants and metal chelators were found to be associated with a reduced AD risk further reinforcing the importance of dietary stress on the body's homeostasis pathways and nutritional guidelines for AD prevention.
    Several studies demonstrate that diet has a definite long-term effect on general health [21,32]. Although several cross-sectional studies have indicated that diet also plays a role in AD, the long time taken for the pathogenesis of AD makes it nearly impossible to experimentally demonstrate the specific effects of diets in AD. In this review, we attempt to define the action of presumably protective and harmful dietary habits on pathways identified as relevant to AD pathogenesis. A common theme that has emerged from the analysis is that aging and AD are associated with excesses in saturated lipids, homocysteine, oxidative stress and other toxic pathways that appear to result from reduced efficiency of clearance pathways in general. Thus, a general rule of AD is that moderation is key to disease prevention. However, literature also suggests that several specific additions to the diet also help in AD prevention.
    We will discuss the major dietary factors involved in maintaining homeostasis and energy requirements such as calorie restriction, lipids, metal chelators, vitamins and other special dietary supplements such as red wine and spices.
  • Ramesh BN, Rao TS, Prakasam A, Sambamurti K, Rao KS. Neuronutrition and Alzheimer's disease. J Alzheimers Dis. 2010;19(4):1123-39. doi: 10.3233/JAD-2010-1312. Review. PubMed PMID: 20308778; PubMed Central PMCID: PMC2931824.
    J Alzheimers Dis. 2010 January; 19(4): 1123–1139.
    doi:  10.3233/JAD-2010-1312
    PMCID: PMC2931824
    NIHMSID: NIHMS190638
    Neuronutrition and Alzheimer's Disease
    Balenahalli N. Ramesh,1 T.S. Sathyanarayana Rao,2 Annamalai Prakasam,3 Kumar Sambamurti,3 and K.S. Jagannatha Rao1
    1Biochemistry and Nutrition, Central Food Technological Research Institute, CSIR Unit, Mysore, India
    2Department of Psychiatry, J S S Medical College, Mysore, India
    3Department of Neuroscience, Medical University of South Carolina, Charleston, South Carolina, USA
    Correspondence to: K.S. Jagannatha Rao, Central Food Technological Research Institute, CSIR Unit, Mysore, 570020 India; Email: [email_address]
    Copyright notice and Disclaimer
    Abstract
    Alzheimer's disease (AD) is a complex neurological disorder with several unequivocally identified genetic risk factors. Among the several environmental factors proposed for AD, dietary protective and risk factors have been most compelling. In particular, diets rich in saturated fatty acids and alcohol, and deficient in antioxidants and vitamins appear to promote the onset of the disease, while diets rich in unsaturated fatty acids, vitamins, antioxidants, and wine likely suppress its onset. Evidence suggests that diets rich in polyphenols and some spices suppress the onset of AD by scavenging free radicals and preventing oxidative damage. Metal ions are known to catalyze the production of free radicals and induce mental retardation or dementia. Several studies have also identified metals such as Pb, Fe, Al, Cu and Zn in AD pathogenesis. While specific chelators have been tested for therapy, they have not been very successful probably due to late administration after brain damage has been triggered. Since several dietary polyphenols are known to chelate metals, their routine use may also be protective against the onset of AD.
    Keywords: antioxidants, caloric restriction, diet, homocysteine, lipid, neurodegeneration, nutrients, oxidative stress, polyphenols, vitamins
    Introduction
    Alzheimer's disease (AD) is the most common form of dementia and affects one in four individuals over the age of 85. AD has multiple etiological factors including genetics, environmental factors, and general lifestyles [1], and its hallmark pathology includes extracellular amyloid β protein (Aβ) deposition in the form of senile plaques and intracellular deposits of the microtubule-associated protein “τ” as neurofibrillary tangles in the AD brain [2]. The diagnosis of this disease is based on the characteristic idiopathic psychometric deficits upon clinical evaluation and further confirmed by post-mortem due to the presence of the characteristic lesions described above [3]. Aβ is produced by sequential proteolytic processing of a larger Aβ protein precursor (AβPP) by β-secretase to generate a large secreted fragment sAPPβ and a 99 aa cellular fragment – CTFβ – that includes Aβ, the transmembrane domain and the intracellular domain of AβPP [4].
    Recently, there has been increasing support for a role of diets in AD [5-7]. A number of dietary factors such as saturated fatty acids [8], higher calorie intake [9], and excessive alcohol [10] have been reported to increase the risk of dementia and AD. In contrast, antioxidants, fish, methionine-rich proteins, and vitamins were identified as protective against the disease [11]. Thus the global variation in diet may be linked to differential prevalence of AD [12]. Several cross-sectional studies suggest a relationship between particular nutrients and the presence of cognitive changes [5-7]. However, these need to be confirmed at an experimental level [13].
    Interestingly, the same dietary pattern of risk and protection has been long accepted for metabolic syndrome and cardiovascular risk. In agreement Diabetes and hyperinsulinaemia are considered as important risk factors for AD [14]. Among the other risk factors, depressive illness, traumatic head injury [15], cardiovascular disease [16-17], smoking [18-19], and stroke [20-21] are significant issues that may be related to the same risk factors. Further, the ε4 allele variant of apolipoprotein E (ApoE) has been associated with increased risk in sporadic and familial AD [22]. As a carrier of cholesterol, ApoE-ε4 is also a risk factor in cardiovascular disease.
    Oxidative stress has been suggested to play a major role in the pathology of AD [23-26], and evidence for its mediation includes: 1) generation of free radicals through metal ions; 2) enhanced lipid peroxidation; 3) increased DNA and protein damage; and 4) increased tau protein phosphorylation [26]. The human body has a defense mechanism to cope with oxidative stress, or prevent the onset of oxidative stress, through endogenous antioxidants derived from enzymatic or non-enzymatic sources [27], namely superoxide dismutase, glutathione reductase, and catalase. The nonenzymatic sources of endogenous antioxidants include glutathione, uric acid, α-lipoic acids, acetyl L-carnitine, melatonin, and dehydroepiandrosterone. Endogenous antioxidants also include the products of reactions catalyzed by enzymes that are up regulated in response to oxidative stress (e.g., bilurubin) [27]. Dietary antioxidants and metal chelators were found to be associated with a reduced AD risk further reinforcing the importance of dietary stress on the body's homeostasis pathways and nutritional guidelines for AD prevention.
    Several studies demonstrate that diet has a definite long-term effect on general health [21,32]. Although several cross-sectional studies have indicated that diet also plays a role in AD, the long time taken for the pathogenesis of AD makes it nearly impossible to experimentally demonstrate the specific effects of diets in AD. In this review, we attempt to define the action of presumably protective and harmful dietary habits on pathways identified as relevant to AD pathogenesis. A common theme that has emerged from the analysis is that aging and AD are associated with excesses in saturated lipids, homocysteine, oxidative stress and other toxic pathways that appear to result from reduced efficiency of clearance pathways in general. Thus, a general rule of AD is that moderation is key to disease prevention. However, literature also suggests that several specific additions to the diet also help in AD prevention.
    We will discuss the major dietary factors involved in maintaining homeostasis and energy requirements such as calorie restriction, lipids, metal chelators, vitamins and other special dietary supplements such as red wine and spices.
  • Ramesh BN, Rao TS, Prakasam A, Sambamurti K, Rao KS. Neuronutrition and Alzheimer's disease. J Alzheimers Dis. 2010;19(4):1123-39. doi: 10.3233/JAD-2010-1312. Review. PubMed PMID: 20308778; PubMed Central PMCID: PMC2931824.
    J Alzheimers Dis. 2010 January; 19(4): 1123–1139.
    doi:  10.3233/JAD-2010-1312
    PMCID: PMC2931824
    NIHMSID: NIHMS190638
    Neuronutrition and Alzheimer's Disease
    Balenahalli N. Ramesh,1 T.S. Sathyanarayana Rao,2 Annamalai Prakasam,3 Kumar Sambamurti,3 and K.S. Jagannatha Rao1
    1Biochemistry and Nutrition, Central Food Technological Research Institute, CSIR Unit, Mysore, India
    2Department of Psychiatry, J S S Medical College, Mysore, India
    3Department of Neuroscience, Medical University of South Carolina, Charleston, South Carolina, USA
    Correspondence to: K.S. Jagannatha Rao, Central Food Technological Research Institute, CSIR Unit, Mysore, 570020 India; Email: [email_address]
    Copyright notice and Disclaimer
    Abstract
    Alzheimer's disease (AD) is a complex neurological disorder with several unequivocally identified genetic risk factors. Among the several environmental factors proposed for AD, dietary protective and risk factors have been most compelling. In particular, diets rich in saturated fatty acids and alcohol, and deficient in antioxidants and vitamins appear to promote the onset of the disease, while diets rich in unsaturated fatty acids, vitamins, antioxidants, and wine likely suppress its onset. Evidence suggests that diets rich in polyphenols and some spices suppress the onset of AD by scavenging free radicals and preventing oxidative damage. Metal ions are known to catalyze the production of free radicals and induce mental retardation or dementia. Several studies have also identified metals such as Pb, Fe, Al, Cu and Zn in AD pathogenesis. While specific chelators have been tested for therapy, they have not been very successful probably due to late administration after brain damage has been triggered. Since several dietary polyphenols are known to chelate metals, their routine use may also be protective against the onset of AD.
    Keywords: antioxidants, caloric restriction, diet, homocysteine, lipid, neurodegeneration, nutrients, oxidative stress, polyphenols, vitamins
    Introduction
    Alzheimer's disease (AD) is the most common form of dementia and affects one in four individuals over the age of 85. AD has multiple etiological factors including genetics, environmental factors, and general lifestyles [1], and its hallmark pathology includes extracellular amyloid β protein (Aβ) deposition in the form of senile plaques and intracellular deposits of the microtubule-associated protein “τ” as neurofibrillary tangles in the AD brain [2]. The diagnosis of this disease is based on the characteristic idiopathic psychometric deficits upon clinical evaluation and further confirmed by post-mortem due to the presence of the characteristic lesions described above [3]. Aβ is produced by sequential proteolytic processing of a larger Aβ protein precursor (AβPP) by β-secretase to generate a large secreted fragment sAPPβ and a 99 aa cellular fragment – CTFβ – that includes Aβ, the transmembrane domain and the intracellular domain of AβPP [4].
    Recently, there has been increasing support for a role of diets in AD [5-7]. A number of dietary factors such as saturated fatty acids [8], higher calorie intake [9], and excessive alcohol [10] have been reported to increase the risk of dementia and AD. In contrast, antioxidants, fish, methionine-rich proteins, and vitamins were identified as protective against the disease [11]. Thus the global variation in diet may be linked to differential prevalence of AD [12]. Several cross-sectional studies suggest a relationship between particular nutrients and the presence of cognitive changes [5-7]. However, these need to be confirmed at an experimental level [13].
    Interestingly, the same dietary pattern of risk and protection has been long accepted for metabolic syndrome and cardiovascular risk. In agreement Diabetes and hyperinsulinaemia are considered as important risk factors for AD [14]. Among the other risk factors, depressive illness, traumatic head injury [15], cardiovascular disease [16-17], smoking [18-19], and stroke [20-21] are significant issues that may be related to the same risk factors. Further, the ε4 allele variant of apolipoprotein E (ApoE) has been associated with increased risk in sporadic and familial AD [22]. As a carrier of cholesterol, ApoE-ε4 is also a risk factor in cardiovascular disease.
    Oxidative stress has been suggested to play a major role in the pathology of AD [23-26], and evidence for its mediation includes: 1) generation of free radicals through metal ions; 2) enhanced lipid peroxidation; 3) increased DNA and protein damage; and 4) increased tau protein phosphorylation [26]. The human body has a defense mechanism to cope with oxidative stress, or prevent the onset of oxidative stress, through endogenous antioxidants derived from enzymatic or non-enzymatic sources [27], namely superoxide dismutase, glutathione reductase, and catalase. The nonenzymatic sources of endogenous antioxidants include glutathione, uric acid, α-lipoic acids, acetyl L-carnitine, melatonin, and dehydroepiandrosterone. Endogenous antioxidants also include the products of reactions catalyzed by enzymes that are up regulated in response to oxidative stress (e.g., bilurubin) [27]. Dietary antioxidants and metal chelators were found to be associated with a reduced AD risk further reinforcing the importance of dietary stress on the body's homeostasis pathways and nutritional guidelines for AD prevention.
    Several studies demonstrate that diet has a definite long-term effect on general health [21,32]. Although several cross-sectional studies have indicated that diet also plays a role in AD, the long time taken for the pathogenesis of AD makes it nearly impossible to experimentally demonstrate the specific effects of diets in AD. In this review, we attempt to define the action of presumably protective and harmful dietary habits on pathways identified as relevant to AD pathogenesis. A common theme that has emerged from the analysis is that aging and AD are associated with excesses in saturated lipids, homocysteine, oxidative stress and other toxic pathways that appear to result from reduced efficiency of clearance pathways in general. Thus, a general rule of AD is that moderation is key to disease prevention. However, literature also suggests that several specific additions to the diet also help in AD prevention.
    We will discuss the major dietary factors involved in maintaining homeostasis and energy requirements such as calorie restriction, lipids, metal chelators, vitamins and other special dietary supplements such as red wine and spices.
  • Ramesh BN, Rao TS, Prakasam A, Sambamurti K, Rao KS. Neuronutrition and Alzheimer's disease. J Alzheimers Dis. 2010;19(4):1123-39. doi: 10.3233/JAD-2010-1312. Review. PubMed PMID: 20308778; PubMed Central PMCID: PMC2931824.
    J Alzheimers Dis. 2010 January; 19(4): 1123–1139.
    doi:  10.3233/JAD-2010-1312
    PMCID: PMC2931824
    NIHMSID: NIHMS190638
    Neuronutrition and Alzheimer's Disease
    Balenahalli N. Ramesh,1 T.S. Sathyanarayana Rao,2 Annamalai Prakasam,3 Kumar Sambamurti,3 and K.S. Jagannatha Rao1
    1Biochemistry and Nutrition, Central Food Technological Research Institute, CSIR Unit, Mysore, India
    2Department of Psychiatry, J S S Medical College, Mysore, India
    3Department of Neuroscience, Medical University of South Carolina, Charleston, South Carolina, USA
    Correspondence to: K.S. Jagannatha Rao, Central Food Technological Research Institute, CSIR Unit, Mysore, 570020 India; Email: [email_address]
    Copyright notice and Disclaimer
    Abstract
    Alzheimer's disease (AD) is a complex neurological disorder with several unequivocally identified genetic risk factors. Among the several environmental factors proposed for AD, dietary protective and risk factors have been most compelling. In particular, diets rich in saturated fatty acids and alcohol, and deficient in antioxidants and vitamins appear to promote the onset of the disease, while diets rich in unsaturated fatty acids, vitamins, antioxidants, and wine likely suppress its onset. Evidence suggests that diets rich in polyphenols and some spices suppress the onset of AD by scavenging free radicals and preventing oxidative damage. Metal ions are known to catalyze the production of free radicals and induce mental retardation or dementia. Several studies have also identified metals such as Pb, Fe, Al, Cu and Zn in AD pathogenesis. While specific chelators have been tested for therapy, they have not been very successful probably due to late administration after brain damage has been triggered. Since several dietary polyphenols are known to chelate metals, their routine use may also be protective against the onset of AD.
    Keywords: antioxidants, caloric restriction, diet, homocysteine, lipid, neurodegeneration, nutrients, oxidative stress, polyphenols, vitamins
    Introduction
    Alzheimer's disease (AD) is the most common form of dementia and affects one in four individuals over the age of 85. AD has multiple etiological factors including genetics, environmental factors, and general lifestyles [1], and its hallmark pathology includes extracellular amyloid β protein (Aβ) deposition in the form of senile plaques and intracellular deposits of the microtubule-associated protein “τ” as neurofibrillary tangles in the AD brain [2]. The diagnosis of this disease is based on the characteristic idiopathic psychometric deficits upon clinical evaluation and further confirmed by post-mortem due to the presence of the characteristic lesions described above [3]. Aβ is produced by sequential proteolytic processing of a larger Aβ protein precursor (AβPP) by β-secretase to generate a large secreted fragment sAPPβ and a 99 aa cellular fragment – CTFβ – that includes Aβ, the transmembrane domain and the intracellular domain of AβPP [4].
    Recently, there has been increasing support for a role of diets in AD [5-7]. A number of dietary factors such as saturated fatty acids [8], higher calorie intake [9], and excessive alcohol [10] have been reported to increase the risk of dementia and AD. In contrast, antioxidants, fish, methionine-rich proteins, and vitamins were identified as protective against the disease [11]. Thus the global variation in diet may be linked to differential prevalence of AD [12]. Several cross-sectional studies suggest a relationship between particular nutrients and the presence of cognitive changes [5-7]. However, these need to be confirmed at an experimental level [13].
    Interestingly, the same dietary pattern of risk and protection has been long accepted for metabolic syndrome and cardiovascular risk. In agreement Diabetes and hyperinsulinaemia are considered as important risk factors for AD [14]. Among the other risk factors, depressive illness, traumatic head injury [15], cardiovascular disease [16-17], smoking [18-19], and stroke [20-21] are significant issues that may be related to the same risk factors. Further, the ε4 allele variant of apolipoprotein E (ApoE) has been associated with increased risk in sporadic and familial AD [22]. As a carrier of cholesterol, ApoE-ε4 is also a risk factor in cardiovascular disease.
    Oxidative stress has been suggested to play a major role in the pathology of AD [23-26], and evidence for its mediation includes: 1) generation of free radicals through metal ions; 2) enhanced lipid peroxidation; 3) increased DNA and protein damage; and 4) increased tau protein phosphorylation [26]. The human body has a defense mechanism to cope with oxidative stress, or prevent the onset of oxidative stress, through endogenous antioxidants derived from enzymatic or non-enzymatic sources [27], namely superoxide dismutase, glutathione reductase, and catalase. The nonenzymatic sources of endogenous antioxidants include glutathione, uric acid, α-lipoic acids, acetyl L-carnitine, melatonin, and dehydroepiandrosterone. Endogenous antioxidants also include the products of reactions catalyzed by enzymes that are up regulated in response to oxidative stress (e.g., bilurubin) [27]. Dietary antioxidants and metal chelators were found to be associated with a reduced AD risk further reinforcing the importance of dietary stress on the body's homeostasis pathways and nutritional guidelines for AD prevention.
    Several studies demonstrate that diet has a definite long-term effect on general health [21,32]. Although several cross-sectional studies have indicated that diet also plays a role in AD, the long time taken for the pathogenesis of AD makes it nearly impossible to experimentally demonstrate the specific effects of diets in AD. In this review, we attempt to define the action of presumably protective and harmful dietary habits on pathways identified as relevant to AD pathogenesis. A common theme that has emerged from the analysis is that aging and AD are associated with excesses in saturated lipids, homocysteine, oxidative stress and other toxic pathways that appear to result from reduced efficiency of clearance pathways in general. Thus, a general rule of AD is that moderation is key to disease prevention. However, literature also suggests that several specific additions to the diet also help in AD prevention.
    We will discuss the major dietary factors involved in maintaining homeostasis and energy requirements such as calorie restriction, lipids, metal chelators, vitamins and other special dietary supplements such as red wine and spices.
  • Ramesh BN, Rao TS, Prakasam A, Sambamurti K, Rao KS. Neuronutrition and Alzheimer's disease. J Alzheimers Dis. 2010;19(4):1123-39. doi: 10.3233/JAD-2010-1312. Review. PubMed PMID: 20308778; PubMed Central PMCID: PMC2931824.
    J Alzheimers Dis. 2010 January; 19(4): 1123–1139.
    doi:  10.3233/JAD-2010-1312
    PMCID: PMC2931824
    NIHMSID: NIHMS190638
    Neuronutrition and Alzheimer's Disease
    Balenahalli N. Ramesh,1 T.S. Sathyanarayana Rao,2 Annamalai Prakasam,3 Kumar Sambamurti,3 and K.S. Jagannatha Rao1
    1Biochemistry and Nutrition, Central Food Technological Research Institute, CSIR Unit, Mysore, India
    2Department of Psychiatry, J S S Medical College, Mysore, India
    3Department of Neuroscience, Medical University of South Carolina, Charleston, South Carolina, USA
    Correspondence to: K.S. Jagannatha Rao, Central Food Technological Research Institute, CSIR Unit, Mysore, 570020 India; Email: [email_address]
    Copyright notice and Disclaimer
    Abstract
    Alzheimer's disease (AD) is a complex neurological disorder with several unequivocally identified genetic risk factors. Among the several environmental factors proposed for AD, dietary protective and risk factors have been most compelling. In particular, diets rich in saturated fatty acids and alcohol, and deficient in antioxidants and vitamins appear to promote the onset of the disease, while diets rich in unsaturated fatty acids, vitamins, antioxidants, and wine likely suppress its onset. Evidence suggests that diets rich in polyphenols and some spices suppress the onset of AD by scavenging free radicals and preventing oxidative damage. Metal ions are known to catalyze the production of free radicals and induce mental retardation or dementia. Several studies have also identified metals such as Pb, Fe, Al, Cu and Zn in AD pathogenesis. While specific chelators have been tested for therapy, they have not been very successful probably due to late administration after brain damage has been triggered. Since several dietary polyphenols are known to chelate metals, their routine use may also be protective against the onset of AD.
    Keywords: antioxidants, caloric restriction, diet, homocysteine, lipid, neurodegeneration, nutrients, oxidative stress, polyphenols, vitamins
    Introduction
    Alzheimer's disease (AD) is the most common form of dementia and affects one in four individuals over the age of 85. AD has multiple etiological factors including genetics, environmental factors, and general lifestyles [1], and its hallmark pathology includes extracellular amyloid β protein (Aβ) deposition in the form of senile plaques and intracellular deposits of the microtubule-associated protein “τ” as neurofibrillary tangles in the AD brain [2]. The diagnosis of this disease is based on the characteristic idiopathic psychometric deficits upon clinical evaluation and further confirmed by post-mortem due to the presence of the characteristic lesions described above [3]. Aβ is produced by sequential proteolytic processing of a larger Aβ protein precursor (AβPP) by β-secretase to generate a large secreted fragment sAPPβ and a 99 aa cellular fragment – CTFβ – that includes Aβ, the transmembrane domain and the intracellular domain of AβPP [4].
    Recently, there has been increasing support for a role of diets in AD [5-7]. A number of dietary factors such as saturated fatty acids [8], higher calorie intake [9], and excessive alcohol [10] have been reported to increase the risk of dementia and AD. In contrast, antioxidants, fish, methionine-rich proteins, and vitamins were identified as protective against the disease [11]. Thus the global variation in diet may be linked to differential prevalence of AD [12]. Several cross-sectional studies suggest a relationship between particular nutrients and the presence of cognitive changes [5-7]. However, these need to be confirmed at an experimental level [13].
    Interestingly, the same dietary pattern of risk and protection has been long accepted for metabolic syndrome and cardiovascular risk. In agreement Diabetes and hyperinsulinaemia are considered as important risk factors for AD [14]. Among the other risk factors, depressive illness, traumatic head injury [15], cardiovascular disease [16-17], smoking [18-19], and stroke [20-21] are significant issues that may be related to the same risk factors. Further, the ε4 allele variant of apolipoprotein E (ApoE) has been associated with increased risk in sporadic and familial AD [22]. As a carrier of cholesterol, ApoE-ε4 is also a risk factor in cardiovascular disease.
    Oxidative stress has been suggested to play a major role in the pathology of AD [23-26], and evidence for its mediation includes: 1) generation of free radicals through metal ions; 2) enhanced lipid peroxidation; 3) increased DNA and protein damage; and 4) increased tau protein phosphorylation [26]. The human body has a defense mechanism to cope with oxidative stress, or prevent the onset of oxidative stress, through endogenous antioxidants derived from enzymatic or non-enzymatic sources [27], namely superoxide dismutase, glutathione reductase, and catalase. The nonenzymatic sources of endogenous antioxidants include glutathione, uric acid, α-lipoic acids, acetyl L-carnitine, melatonin, and dehydroepiandrosterone. Endogenous antioxidants also include the products of reactions catalyzed by enzymes that are up regulated in response to oxidative stress (e.g., bilurubin) [27]. Dietary antioxidants and metal chelators were found to be associated with a reduced AD risk further reinforcing the importance of dietary stress on the body's homeostasis pathways and nutritional guidelines for AD prevention.
    Several studies demonstrate that diet has a definite long-term effect on general health [21,32]. Although several cross-sectional studies have indicated that diet also plays a role in AD, the long time taken for the pathogenesis of AD makes it nearly impossible to experimentally demonstrate the specific effects of diets in AD. In this review, we attempt to define the action of presumably protective and harmful dietary habits on pathways identified as relevant to AD pathogenesis. A common theme that has emerged from the analysis is that aging and AD are associated with excesses in saturated lipids, homocysteine, oxidative stress and other toxic pathways that appear to result from reduced efficiency of clearance pathways in general. Thus, a general rule of AD is that moderation is key to disease prevention. However, literature also suggests that several specific additions to the diet also help in AD prevention.
    We will discuss the major dietary factors involved in maintaining homeostasis and energy requirements such as calorie restriction, lipids, metal chelators, vitamins and other special dietary supplements such as red wine and spices.
  • Nutrigenetics and Nutrigenomics: Viewpoints on the Current Status and Applications in Nutrition Research and Practice Michael Fenech, Ahmed El-Sohemy, Leah Cahill, Lynnette R. Ferguson, Tapaeru-Ariki C. French, E. Shyong Tai, John Milner, Woon-Puay Koh, Lin Xie, Michelle Zucker, Michael Buckley, Leah Cosgrove, Trevor Lockett, Kim Y.C. Fung, Richard Head J Nutrigenet Nutrigenomics. 2011 July; 4(2): 69–89. Published online 2011 May 28. doi: 10.1159/000327772 PMCID: PMC3121546
  • Neuronutrición & Educación. Importante para todas las edades / Neuronutrition & education. Its role in human lifespan

    1. 1. Datos de contacto Alejandro Melo-Florián MD, FACP •http://www.scoop.it/u/alejandro-melo-florian •http://about.me/alejandromeloflorian •http://alejandromeloflorian.wix.com/alejandromeloflorian •Skype: alejandro.melo.florian
    2. 2. Neuronutrición y Educación ALEJANDRO MELO FLORIÁN M.D., F.A.C.P. - Colombia Esp. Medicina Interna-Pontificia Universidad Javeriana Miembro de: Asociación Colombiana de Neurología Asociación Colombiana de Medicina Interna Asociación Colombiana de Infectología American College of Physicians "PRIMER CONGRESO INTERNACIONAL DE NEUROCIENCIAS APLICADAS A LA EDUCACIÓN"
    3. 3. Conflicto de Intereses • Declaro que no tengo conflicto de intereses relacionados con la presente exposición. • No habrá referencias a marcas comerciales. • Soy autor de obra Cerebro, mente y conciencia – Un enfoque multidisciplinario
    4. 4. En Facebook https://www.facebook.com/pages/Libro-Cerebro-mente-y-concienciaUn-enfoque-multidisciplinario/613569022038907 En Google books http://books.google.es/books?id=jSlSlyckCUsC&printsec=frontcover&dq=
    5. 5. Neurociencias: su futuro está en la integración • Para Osvaldo Uchitel -neurocientífico de UBAnecesita sumar el aporte de diferentes disciplinas como psicología, biología, anatomía, neurología, informática… • …. nutrición, salud pública, redes sociales, comunicación social, ciencias políticas, educación, filosofía y un largo et caetera
    6. 6. Neuro-nutrición y Educación  Joaquín Salvador Lavado Tejón, más conocido como Quino
    7. 7. Problema nutricional en Américas • Un 16% de todos los niños y niñas de la región tienen Retraso en el Crecimiento y no es muy probable que se supere en 2015 el grave problema de la nemia por Carencia de Hierro. Prevalencia de peso inferior al normal en menores de 5 años En 1990 En 2006 Hogares que consumen sal yodada Tasa de mortalidad de menores de 5 años 11% 7% (4 millones) 86% 31 muertos por cada 1000 nacidos vivos
    8. 8.  Seguimiento de los progresos en la nutrición de los niños y las madres. Una prioridad en materia de Supervivencia y desarrollo - UNICEF
    9. 9. Déficit hierro: problema de salud Pública • La deficiencia de hierro afecta a 2.000 millones de personas; 77 millones viven en América Latina y el Caribe. • Espectro: reducción y agotamiento de las reservas de hierro, hasta anemia. • Hay deficiencias de hierro sin anemia.  GILDA G. STANCO, M.D. Funcionamiento intelectual y rendimiento escolar en niños con anemia y deficiencia de hierro. Colombia Médica 2007; 38 (Supl 1): 24-33 http://www.bioline.org.br/pdf?rc07019
    10. 10. Déficit hierro: problema de salud Pública • Menores 2 años: mayor predisposición. • Insuficiente disponibilidad de hierro en un período de alta incorporación como lo es período de mielinización del tejido nervioso, provee base fisiopatológica para explicar los efectos conductuales observados por deficiencias del micronutriente.  GILDA G. STANCO, M.D. Funcionamiento intelectual y rendimiento escolar en niños con anemia y deficiencia de hierro. Colombia Médica 2007; 38 (Supl 1): 24-33 http://www.bioline.org.br/pdf?rc07019
    11. 11. Crecimiento de Tejido Nervioso Neural
    12. 12. Hierro e impulso nervioso • Es componente estructural de enzimas y moléculas requeridas para el desarrollo y la función exitosa del sistema nervioso, particularmente la conducción del impulso nervioso.
    13. 13. Mielinización • La densidad adquirida en corteza visual entre 2-4 años es aproximadamente la misma que se vé en el adulto. • Ocurre igualmente entre 10 - 20 años en corteza prefrontal.  Johnson S. The nature of cognitive development. Trends Cogn Sci 2003; 7: 102-104
    14. 14. Mielinización • La rápida mielinización en sistemas auditivos y visuales es crítica para aprendizaje e interacción social.  Johnson S. The nature of cognitive development. Trends Cogn Sci 2003; 7: 102-104
    15. 15. Hierro y mielinización • Los lactantes anémicos continúan mostrando un tiempo de conducción más l a r g o a pesar de recibir un tratamiento prolongado con hierro oral (4 m. hierro medicamentoso, 6 m hierro profiláctico).  Roncagliolo M, et al. Evidence of altered central nervous system development in infants with iron deficiency anemia at 6 mo: delayed maturation of auditory brainstem responses. Am J Clin Nutr 1998; 68: 683-690.
    16. 16. Importancia de actancia aterna • El vínculo prolongado entre la madre y el hijo durante la lactancia crea condiciones para una forma particular de educación, en la cual la interacción con los padres es indispensable.  ALEJANDRO MELO, M.D. Cerebro, mente y Conciencia – Un enfoque multidisciplinario IMedPub-Medicalia – Barcelona, España. 2 011.
    17. 17. Nutrición y Desarrollo pigenético Maturana y Varela: •El Sistema Nervioso es un instrumento mediante el cual el organismo obtiene información del ambiente que luego utiliza en la construcción de una representación sobre el mundo, lo cual le permite generar una conducta adecuada para sobrevivir en él.  ALEJANDRO MELO, M.D. Cerebro, mente y Conciencia – Un enfoque multidisciplinario IMedPub-Medicalia – Barcelona, España. 2 011. https://www.facebook.com/pages/Libro-Cerebro-mente-y-conciencia-Un-enfoque-multidisciplin
    18. 18. Sobre Educación
    19. 19. Educación • Latín educere: guiar, conducir / educare: formar o instruir. • Procesos bi-direccionales para transmitir conocimientos, costumbres, valores y formas de actuar.  http://www.discovereducation.org/index.php/uncategorized/la-definicion-de-educacion
    20. 20. Educación • Nuevas generaciones asimilan y aprenden conocimientos, normas de conducta, modos de ser y formas de como veían el mundo las generaciones anteriores, para crear nuevas visiones. • Proceso de socialización en individuos de una sociedad, apreciable en la serie de habilidades, actitudes, conocimientos y valores adquiridos, produciendo cambios de orden intelectual, social, emocional.  http://www.discovereducation.org/index.php/uncategorized/la-definicion-de-educacion
    21. 21. Reflexiones sobre Educación • “Educad al niño y no tendréis que castigar al hombre” – Aristóteles de Estagira • “La educación no crea al hombre, le ayuda a crearse a sí mismo” - Maurice Debesse • “Educar en la igualdad y el respeto es educar contra la violencia” - Benjamín Franklin
    22. 22. Educación y Epigénesis • pigénesis: Desarrollo de las características individuales del sistema nervioso depende del medio externo. • En virtud de plasticidad cerebral, la naturaleza humana no es automáticamente orgánica, ni instintivamente espontánea; la naturaleza humana es obligatoriamente disciplinada y modelada en un proceso epigenético con el largo aprendizaje de la infancia.  ALEJANDRO MELO, M.D. Cerebro, mente y Conciencia – Un enfoque multidisciplinario IMedPub-Medicalia – Barcelona, España. 2 011. https://www.facebook.com/pages/Libro-Cerebro-mente-y-conciencia-Un-enfoque-multidiscip
    23. 23. Neuronutrición y Medio Interno
    24. 24. Neuronutrición y medio Interno • omo erectus, con capacidad cerebral de aproximados 950 cm3 • Destacada tecnología de herramientas de piedra que le permitió ser un excelente cazador: todo esto se acompañó de la expansión del cerebro en 500 o 600 cc en un millón de años.  ALEJANDRO MELO, M.D. Cerebro, mente y Conciencia – Un enfoque multidisciplinario IMedPub-Medicalia – Barcelona, España. 2 011. https://www.facebook.com/pages/Libro-Cerebro-mente-y-conciencia-Un-enfoque-multidisciplin
    25. 25. Neuronutrición y medio Interno • Por sus herramientas en piedra y la capacidad de caza de omo erectus, se le pueden atribuir las características de una buena capacidad de Memoria, Abstracción e Ingenio.  ALEJANDRO MELO, M.D. Cerebro, mente y Conciencia – Un enfoque multidisciplinario IMedPub-Medicalia – Barcelona, España. 2 011. https://www.facebook.com/pages/Libro-Cerebro-mente-y-conciencia-Un-enfoque-multidisciplin
    26. 26. Neuronutrición y medio Interno • El cerebro es Estructura Disipativa, por el elevado consumo del total de la energía corporal: con 2% del peso corporal, consume el 20% del oxígeno disponible. • Los altibajos de consumo energético reflejan la inestabilidad de un sistema disipativo, que pueden dar origen a nueva organización.  ALEJANDRO MELO, M.D. Cerebro, mente y Conciencia – Un enfoque multidisciplinario IMedPub-Medicalia – Barcelona, España. 2 011. https://www.facebook.com/pages/Libro-Cerebro-mente-y-conciencia-Un-enfoque-multidisciplin
    27. 27. Nutrición y SNC
    28. 28. Revolución ω-3 • Contenido de lípidos del cerebro = 600 g/Kg. – MBP – Proteolípidos – Esfingolípidos – Esfingosina – Ceramidas – Gangliósidos – Proporción NORMAL Ω3: Ω6 de 1:4  Stryer L: Biosíntesis de lípidos de membrana y hormonas esteroideas. Capítulo 20. En Bioquímica 2a Ed. Reverté Barcelona, 1982. pp 422-25
    29. 29. Los lípidos de la vida ϖ FUENTE ALIMENTICIA Acido linole ico ϖ6 Ma ní, ma íz, s e milla s de a lgodón, s oya . Acido α - linolénico Octadecatrienoico ϖ3 Ace ite de lina za , nue ce s , ca nola Acido γ - linolénico ϖ6 Ace ite de hie rba de a s no, borra ja ϖ3 Ace ite de S a lmón, de ca ba lla , híga do de ba ca la o ϖ6 Gra s a s de a nima le s ACIDO Acido timnodónico Eicosapentanoico Acido clupanodónico Docosapentanoico Acido araquidónico  Mayes PA: Lipids of physiologic significance. Chapter 16. En: Murray R, Granner DK, Mayes PA, Rodwell VW, Eds. Harper´s Biochemistry. 24th Edition. Appleton & Lange. 1996, pp 148 32
    30. 30. Los lípidos de la vida
    31. 31. Los lípidos de la vida
    32. 32. Los lípidos de la vida  Fernando Gómez-Pinilla: Brain foods: the effects of nutrients on brain function Nat Rev Neurosci. 2008 July; 9(7): 568–578.
    33. 33. Funcionalismo de membrana neuronal
    34. 34. Los lípidos de la vida  Stoll AL: The Omega-3 Connection. Simon & Schuster, Nueva York - USA 2001. pp 56 37
    35. 35. Los lípidos de la vida • Los metabolitos de AG Ω-6 promueven adherencia plaquetaria y fenómenos de lesión endotelial.  Zucker MB: The functioning of blood platelets. Scientific American 1980; 6: 70-89 38
    36. 36. Los lípidos de la vida Características deseables de un suplemento Ω-3: • Sin presencia de colesterol • Sin aceite de hígado de bacalao • Aceite de color claro, sin olor fuerte a pescado • Concentración de Ω-3 entre 30 y 90% (32.7%) • Presencia de tocoferol para prevenir oxidación y preservar potencia y frescura del aceite.  Stoll AL: The Omega-3 Connection. Simon & Schuster, Nueva York - USA 2001. pp 56 39
    37. 37. Interacciones Medicamentosas de AG Omega –3 • Alteración de función plaquetaria – Precaución con ASA, Ibuprofeno, Warfarina, Vitamina E – Tratamiento concomitante con Warfarina hace necesario ajuste dosis según INR • No tomar concomitantemente con medicaciones antiobesidad como Orlistat, porque el bloqueo de la absorción de grasas interfiere con absorción de Omega-3 • Precaución con aceite de hígado de bacalao. 40
    38. 38. limentos funcionales • Consumidos como parte de dieta normal: – aportan componentes biológicamente activos, que ofrecen beneficios para la salud y reducen el riesgo de sufrir enfermedades. • Ejemplos: aquellos con minerales, vitaminas, ácidos grasos o fibra alimenticia; los que tienen sustancias biológicamente activas, como fitoquímicos, otros antioxidantes y probióticos.  Sala Especializada de Alimentos y Bebidas - SEABA Invima, Colombia. Numeral 3.5 Acta 1 de 2013 de Actas de SEABA
    39. 39. ntioxidantes y suplementos • Estudio SU.VI.MAX (1994-2002 ): – 4.447 participantes; 45 a 60 años – Estudio doble-ciego, controlado con placebo, distribución aleatoria. • Recibieron: vitamina C (120 mg) , β - caroteno (6 mg) vitamina E (30 mg), selenio (100 mg), ​ zinc (20 mg) combinado o como placebo. – En 2007-2009, se evaluó el rendimiento cognoscitivo con 4 pruebas neuropsicológicas (6 funciones)  Kesse-Guyot E et al. French adults' cognitive performance after daily supplementation with antioxidant vitamins and minerals at nutritional doses: a post hoc analysis of the Supplementation in Vitamins and Mineral Antioxidants (SU.VI.MAX) trial. Am J Clin Nutr. 2011 Sep;94(3):892-9.
    40. 40. ntioxidantes y suplementos • Los sujetos que recibieron suplementos de antioxidantes activos mostraron mejores puntuaciones de memoria episódica, memoria verbal y función ejecutiva. • La memoria verbal mejoró con la suplementación antioxidante sólo en fumadores o con bajas concentraciones séricas de vitamina C al inicio del estudio .  Kesse-Guyot E et al. French adults' cognitive performance after daily supplementation with antioxidant vitamins and minerals at nutritional doses: a post hoc analysis of the Supplementation in Vitamins and Mineral Antioxidants (SU.VI.MAX) trial. Am J Clin Nutr. 2011 Sep;94(3):892-9. http://ajcn.nutrition.org/content/94/3/892.full.pdf
    41. 41. Malnutrición y Obesidad • La exposición persistente a estrés altera la respuesta del cerebro a los alimentos en formas que predisponen a malos hábitos alimenticios, que al mantenerse, aumentan riesgo de obesidad.  Tryon MS et al. Chronic stress exposure may affect the brain's response to high calorie food cues and predispose to obesogenic eating habits. Physiol Behav. 2013 Aug 15;120:233-242
    42. 42. Receptor D2 dopamina en estriado Glucosa disminuye señal de dopamina  Michaelides M, et al. Translational neuroimaging in drug addiction and obesity. ILAR J. 2012;53(1):59-68.
    43. 43. Estrategias para mejorar neuronutrición
    44. 44. Educación en Lactancia materna  1ª Muestra Argentina de Humor Gráfico Sobre Lactancia Materna
    45. 45. Educación en Lactancia materna  1ª Muestra Argentina de Humor Gráfico Sobre Lactancia Materna
    46. 46. Educación en Lactancia materna  1ª Muestra Argentina de Humor Gráfico Sobre Lactancia Materna
    47. 47. LM e IQ
    48. 48. Lactancia materna e IQ • Las diferencias en puntuaciones de pruebas de CI entre niños alimentados con LM y los que no recibieron LM fue: • 10.7 puntos de CI (IC95% 7.0 a 14.4) en funcionamiento intelectual general – 3,6 puntos de CI (IC95%: -0,3 a 7,5) – 2,3 puntos de CI (IC95% -3.0 a 7.6) para verbal. Luego de “ajuste de medio social” – capacidad aspectos socioambientales  Smith MM, et al. Influence of breastfeeding on cognitive outcomes at age 6-8 years: follow-up of very low birth weight infants. Am J Epidemiol. 2003 Dec 1;158(11):1075-1082 http://aje.oxfordjournals.org/content/158/11/1075.full.pdf.
    49. 49. Lactancia materna e IQ • Diferencia de puntaje en prueba Ravens Colored Progressive Matrices entre LM vs. sin LM a 6 meses fue 1.33 (p=0.008). • CONCLUSIÓN: niños amamantados durante seis meses o más tuvieron un mejor desempeño en la evaluación intelectual general, incluso después de ajustar por los factores de confusión.  Fonseca AL, et al. Impact of breastfeeding on the intelligence quotient of eight-year-old children. J Pediatr (Rio J). 2013 Jul-Aug;89(4):346-353. http://www.ncbi.nlm.nih.gov/pubmed/23791025
    50. 50. Para mejorar neuronutrición: • La alimentación continuada con LECHE MATERNA e introducción de alimentos ricos en hierro durante POR LO MENOS el primer año de vida. • Si LM no es opción, leches enriquecidas con hierro durante los 6 primeros meses. • Alimentos complementarios caseros son bajos en hierro, agregar gotas de hierro  Gartner LM, et al. Breastfeeding and the use of human milk. Pediatrics. 2005 Feb;115(2):496-506. http://pediatrics.aappublications.org/content/115/2/496.full.pdf  WHO. Iron Deficiency Anaemia. Assessment, Prevention, and Control. A Guide for Programme Managers. WHO/NHD/01.3. Geneva, WHO, 2001.
    51. 51. Para mejorar neuronutrición: • En RNAT - APEG sus reservas de hierro son suficientes para 6 primeros meses. • Aunque LM es baja en hierro (0.2 a 0.4 mg/L), tiene alta biodisponibilidad; – suficiente para niveles adecuados de hierro durante 1er semestre. • A partir de 6 m, necesidades de hierro aumentan rápidamente, para llegar a cifras mayores que en ninguna otra época de la vida (0,1 mg/kg/día). • Iniciar dieta complementaria con alimentos ricos en hierro a partir de 6 m y retrasar introducción de leche de vaca hasta después del año de edad.  Manual práctico de Nutrición en Pediatría – Asociación Española de Pediatría, 2007 http://www.spponline.net/documentos/manualnutricion.pdf
    52. 52. “Desayunar como un rey” • Desayunar con alto contenido de proteínas modifica activación cerebral en regiones asociadas con motivación por alimentos y recompensa . • Aumentar proteínas en desayuno es estrategia beneficiosa para reducir la conducta alimentaria como recompensa, en adolescentes con sobrepeso.  Leidy HJ, et al. Neural responses to visual food stimuli after a normal vs. higher protein breakfast in breakfast-skipping teens: a pilot fMRI study. Obesity (Silver Spring). 2011 Oct;19(10):2019-25.
    53. 53. Para mejorar neuronutrición: des iunare  Nilsson A et al. A diet based on multiple functional concepts improves cognitive performance in healthy subjects. Nutr Metab (Lond). 2013 Jul 15;10(1):49.
    54. 54. “Desayuna como un rey” • Desayunar con alto contenido de proteínas modifica activación cerebral en regiones asociadas con motivación por alimentos y recompensa . • Aumentar proteínas en desayuno podría ser una estrategia beneficiosa para reducir la conducta alimentaria como recompensa, en adolescentes con sobrepeso.  Leidy HJ, et al. Neural responses to visual food stimuli after a normal vs. higher protein breakfast in breakfast-skipping teens: a pilot fMRI study. Obesity (Silver Spring). 2011 Oct;19(10):2019-25.
    55. 55. Agua • Mejora memoria a corto plazo en escolares • Primeras causas de delirium en ancianos: deshidratación • Causa frecuente hospitalización para demencia en 3ª edad.  Fadda R et al. Effects of drinking supplementary water at school on cognitive performance in children. Appetite. 2012 Dec;59(3):730-7.  Phelan EA et al. Association of incident dementia with hospitalizations. JAMA. 2012 Jan 11;307(2):165-72.
    56. 56. Beber agua: esencial
    57. 57. Alimentos y efectos neuroquímicos Item Alimento Principio activo Efecto / función Referencia 1 Arándano flavonoides [197] 2 Pescados Omega-3 (DHA, EPA) Facultades cognoscitivas, memoria, coordinación Reduce depósito amiloide en 70% (ratones) 3 Cúrcuma (azafrán) Acido turmérico Antioxidante, antiinflamatorio, anti-amiloide [186] 4 Té verde EGCG (polifenol) [142] 5 Vino tinto Resveratrol 6 Ginkgo biloba Flavonoides, terpenoides Acido ferúlico Vitamina C Antioxidante, antiinflamatorio Antioxidante, antiinflamatorio Antioxidante Antioxidante Antioxidante [199] Antioxidante Antioxidante [27] 7 8 9 10 Tomate Amla (grosella espinosa india) Carnes Vitamina E Frutas y verduras vitamina A (retinol) [73] [62] [198] [200] [27]  Ramesh BN et al. Neuronutrition and Alzheimer's disease. J Alzheimers Dis. 2010;19(4):1123-39. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2931824/pdf/nihms190638.pdf
    58. 58. Bebidas energizantes • Cafeína, taurina, inositol, glucuronolactona no son fuentes concentradas de nutrientes, ni constituyen un aporte nutricional comprobado. • Taurina: efectos de sobreestimulación con consecuencias como irritabilidad, insomnio, DAH.  Sala Especializada de Alimentos y Bebidas - SEABA Invima, Colombia. Numeral 3.5 Acta 1 de 2013 de Actas de SEABA
    59. 59. Problema de salud pública…. • El consumo de bebidas energéticas aumenta riesgo de toxicidad de cafeína en niños y adolescentes. • Consumo con alcohol, hasta de 3 uds, 1-4 días al mes. • Supresor de apetito-squash drinking syndrome  Reissig CJ et al. Caffeinated energy drinks--a growing problem. Drug Alcohol Depend. 2009 Jan 1;99(1-3):1-10.  Bigard AX. [Risks of energy drinks in youths]. Arch Pediatr. 2010 Nov;17(11):1625-31.  Seifert SM et al. Health Effects of Energy Drinks on Children, Adolescents, and Young Adult. Pediatrics. 2011 March; 127(3): 511–528.
    60. 60. Neuronutrición y Enferm. de Alzheimer • Dietas ricas en ácidos grasos saturados y el alcohol, promueven aparición de EA. • Dietas ricas en ácidos grasos insaturados, vitaminas, antioxidantes y vino, suprimen su aparición. • Dietas ricas en polifenoles y algunas especias suprimen aparición de EA al eliminar radicales libres y prevenir daño oxidativo.  Ramesh BN et al. Neuronutrition and Alzheimer's disease. J Alzheimers Dis. 2010;19(4):1123-39. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2931824/
    61. 61. Enfermedad de Alzheimer Cerebro sano Con E de A avanzada
    62. 62. Neuronutrición y Enferm. de Alzheimer  Ramesh BN et al. Neuronutrition and Alzheimer's disease. J Alzheimers Dis. 2010;19(4):11231139. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2931824/
    63. 63. Neuronutrición y Enferm. de Alzheimer  Ramesh BN et al. Neuronutrition and Alzheimer's disease. J Alzheimers Dis. 2010;19(4):11231139.
    64. 64. Neuronutrición y Enferm. de Alzheimer  Ramesh BN et al. Neuronutrition and Alzheimer's disease. J Alzheimers Dis. 2010;19(4):11231139.
    65. 65. Neuronutrición y Enferm. de Alzheimer  Ramesh BN et al. Neuronutrition and Alzheimer's disease. J Alzheimers Dis. 2010;19(4):11231139.
    66. 66. Asesoría con personal de salud
    67. 67. Lo que viene  Fenech M et al. Nutrigenetics and Nutrigenomics: Viewpoints on the Current Status and Applications in Nutrition Research and Practice. J Nutrigenet Nutrigenomics. 2011; 4(2): 69–89
    68. 68. *-
    69. 69. Condición humana • Relaciones: cultura - mundo mentalsistema nervioso • Multidisciplinar: puentes conceptuales de diferentes ramas del saber • Somos individuos, especie y sociedad al mismo tiempo • “Somos lo que comemos”
    70. 70. “Todo el mundo es un genio. Pero si se juzga a un pez por su habilidad para trepar un árbol, pasará el resto de su vida creyendo que es un idiota” Albert Einstein
    71. 71. Para mantener joven el cerebro
    72. 72. onclusiones • Lactancia Materna es MUY importante • Hierro: esencial en salud infantil • Nutrición adecuada forma parte de Estilo de vida adecuado, para óptima educación en trascurso vital. • Alimentos funcionales, antioxidantes y suplementos mejoran desempeño cognoscitivo. • Formación continua necesaria para adecuada asesoría a pacientes.
    73. 73. euro-nutrición – Mensaje para llevar a casa “Nuestros cuerpos y mentes funcionan y sienten mejor cuando respetamos nuestra biología evolucionaria”. 77
    74. 74. Alejandro Melo-Florián MD, FACP http://www.scoop.it/u/alejandro-melo-florian http://about.me/alejandromeloflorian http://alejandromeloflorian.wix.com/alejandromeloflorian

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