Enfermedad de Parkinson y enfermedad de Alzheimer: factores de riesgo ambientales

Resumen

Introducción

Esta revisión pretende actualizar y resumir la evidencia disponible sobre los factores de riesgo ambientales que se han asociado a riesgo de enfermedad de Parkinson (EP) o de Alzheimer (EA) y discutir sus posibles mecanismos.

Desarrollo

Hay evidencia consistente de mayor riesgo de EP asociado a pesticidas y de mayor riesgo de EA asociado a pesticidas, hipertensión y colesterol en edad media, hiperhomocisteinemia, tabaco, traumatismo craneoencefálico grave y depresión. Hay evidencia débil de mayor riesgo de EP asociado a consumo elevado de leche en hombres, ingesta alta de hierro, anemia crónica y traumatismo craneoencefálico grave, y de mayor riesgo de EA asociado a ingesta elevada de aluminio en agua potable, alta exposición a redes eléctricas, DM e hiperinsulinemia, obesidad en edad media, consumo excesivo de alcohol y anemia crónica. Hay evidencia consistente de menor riesgo de EP asociado a hiperuricemia, tabaco y café, y de menor riesgo de EA asociado a consumo moderado de alcohol, ejercicio físico, terapia hormonal sustitutiva perimenopáusica y buena reserva cognitiva; hay evidencia débil de menor riesgo de EP asociado a mayor consumo de vitamina E, alcohol, té y AINE y a ejercicio físico vigoroso, y de menor riesgo de EA asociado a dieta mediterránea, café y consumo crónico de AINE.

Conclusiones

Diversos factores ambientales contribuyen significativamente al riesgo de EP y EA. Algunos de ellos podrían actuar ya desde etapas tempranas de la vida o interaccionar con otros factores genéticos. Estrategias poblacionales de modificación de estos factores podrían potencialmente evitar algunos casos de EP o de EA.

Abstract

Introduction

The purpose of this review is to update and summarise available evidence on environmental risk factors that have been associated with risk of Parkinson disease (PD) or Alzheimer disease (AD) and discuss their potential mechanisms.

Development

Evidence consistently suggests that a higher risk of PD is associated with pesticides and that a higher risk of AD is associated with pesticides, hypertension and high cholesterol levels in middle age, hyperhomocysteinaemia, smoking, traumatic brain injury and depression. There is weak evidence suggesting that higher risk of PD is associated with high milk consumption in men, high iron intake, chronic anaemia and traumatic brain injury. Weak evidence also suggests that a higher risk of AD is associated with high aluminium intake through drinking water, excessive exposure to electromagnetic fields from electrical grids, DM and hyperinsulinaemia, obesity in middle age, excessive alcohol consumption and chronic anaemia. Evidence consistently suggests that a lower risk of PD is associated with hyperuricaemia, tobacco and coffee use, while a lower risk of AD is associated with moderate alcohol consumption, physical exercise, perimenopausal hormone replacement therapy and good cognitive reserve. Weak evidence suggests that lower risk of PD is associated with increased vitamin E intake, alcohol, tea, NSAIDs, and vigorous physical exercise, and that lower risk of AD is associated with the Mediterranean diet, coffee and habitual NSAID consumption.

Conclusions

Several environmental factors contribute significantly to risk of PD and AD. Some may already be active in the early stages of life, and some may interact with other genetic factors. Population-based strategies to modify such factors could potentially result in fewer cases of PD or AD.