Diets, food and Idiopathic Parkinson´s disease

Revista de la Facultad de Medicina

Perea-Sasiaín, José²  Hanfling Schwartz, Roberta¹ 

[1] Universidad Nacional de Colombia, Bogotá, Colombia

关键词: Parkinson Disease;    Diet;    Vegetarian;    Diseases Prevention;    Methionine (MeSH);   

DOI  :  10.15446/revfacmed.v62n1.43783

学科分类：医学（综合）

来源: Universidad Nacional de Colombia * Facultad de Medicina

【 摘 要 】

A partir de dos casos individuales, se presenta un esbozo personal sobre el conocimiento de la etiopatogenia en la Enfermedad de Parkinson Idiopática (EPI), con un énfasis en las dietas, la comida y las sustancias comestibles probadas y reportadas. En el primer caso (adherencia a una dieta prácticamente vegana, con una séptima parte de la proteína suplida de productos de origen animal), tuvo un impresionante efecto benéfico en sus quince años de desarrollo clínico, mientras que en el segundo caso (que siguió una dieta casi ovo-lacto-vegetariana) no se modificó sustancialmente el desarrollo clínico. La relevancia de la dieta en la EPI se concentra en la redistribución diaria de la ingesta de proteínas cuando se ha prescrito levodopa. La dieta por sí misma es fundamental para el manejo de cada persona predispuesta o que sufre de EPI. Las dietas veganas, ricas en proteínas debidamente balanceadas con cereales y suplementadas con vitamina B12, reducen la ingesta de metionina y mantiene la cuenta de aminoácidos aromáticos a un nivel moderado. Palabras clave: Enfermedad de Parkinson, Dieta, Dieta Vegetariana, Metionina, Prevención de Enfermedades (DeCS). Introduction The six patients described by James Parkinson (1) as afflicted by Shaking Palsy, motivated Jean Marie Charcot to label them as suffering Parkinson´s disease (2), yet this syndrome would have been a better choice with its classic triad: tremor, stiffness and slowness. A large number of other non-motor afflictions add to the protracted clinical course of each patient.Idiopathic Parkinson´s Disease (IPD) is more prevalent in countries with high industrial development and high economic standards. However, there have been studies linking higher incidence of Parkinson's among rural inhabitants as compared to urban residents. Nowadays it is apparent that there are several distinct types of parkinsonian disorders (3) and each patient individually endures his lot.Discussing its "origin", Parkinson stated, "we are led to seek for it in some slow morbid change in the structure of the medulla" (1). It is well established that damage of the substantia nigra (SN) melanic neurons, more severe in its pars compacta, is responsible for the motor signs of IPD and in such cases cell loss is substantial and done over several years before overt clinical signs appear (3,4).Among causal agents of Parkinsonism, the lethargic encephalitis virus was prominent after the influenza pandemic of 1919 with many cases of its postencephalitic form, mostly with rigidity and bradikynesia. Several exogenous toxic agents (reserpine, manganese, MPTP, substances in the leaves of the sour sop tree Annona muricata L) cause Parkinsonism or closely related syndromes. The endogenous toxins causing the development of IPD signs and symptoms are methylated abnormal intermediates akin to those of dopamine secondary metabolites (4): in persons prone to IPD their very low tyrosine-hydroxylase (TH) activity leaves a local abundance of both tyrosine and tyramine (its decarboxylation product) available for abnormal reactions amongst them methylation.Tyramine is produced in excess and is excreted in the urine, though in other cases is further metabolized and is excreted in lower amount than by normal persons (5). The resulting abnormal metabolites metabolize in an unknown way. The reason why the extention of those metabolites is responsible for the SN damage is also unknown. Matsubara (6), Naoi (7) and Williams (8) propose several abnormal methylated substances as SN neurotoxins. The last author considers IPD as an autointoxication related to N-methylnicotinamide. People susceptible to IPD submitted in addition to exogenous neurotoxins will develop their IPD earlier and more severely.During the last decades, the genetics for Parkinsonism have been studied and many different genes have been located (3). Some early onset (or young onset) of Parkinsonism have a direct genetic component, while several genes have been scrutinized in idiopathic cases (nowadays called "sporadic"), by far more frequent. Two different mutations in LRRK2 dardarin (the euskera name for tremor), R1441G in Basques and some of them also carry mutation G2019S present in Ashkenazis (9). The study of these remarkable ethnic groups should give many answers for the prevention of the Parkinson´s syndrome. Materials and me

【 授权许可】

Unknown