Virginia Thornley, M.D., Neurologist, Epileptologist
February 27, 2018
Amyotrophic lateral sclerosis is a progressive neurodegenerative disorder resulting in muscle weakness, atrophy and eventual respiratory failure. It involves mitochondrial dysfunction, oxidative stress, apoptosis, neural inflammation, metallic accumulation, decreased trophic factors, glutamate activation, and superoxide dismutase-1. There is a growing interest in the role of diet in the natural progression and treatment. Risk of ALS may increase with increased intake of macronutrients such as carbohydrates, glutamate, and fat and a reduced intake of micronutrients such as carotenoids, fruits and vegetables, polyunsaturated fatty acids and Vitamin E. Oxidative stress may also increase the risk of ALS.
Good food versus bad food in ALS
In one study of 306 patients in over 16 ALS centers, milk and lunchmeat seemed to correlate with a negative ALS function using the ALSFRS score (ALS functional rating score) or the percentage FVC (forced vital capacity) for the outcome. Milk and lunchmeat are associated with higher fat and potentially promote oxidative stress. It studied foods that were considered good (calcium, iron, potassium, iron, thiamine, riboflavin, niacin, zinc, selenium, vitamins C, D, E, K, and B6, magnesium, and glutathione) versus bad(phosphorus, caffeine, food-producing high glycolic index). The components of the good food groups had eggs, poultry, fish, beneficial oils and vegetables and are often associated with anti-oxidants and a healthy diet. The study only provides an association not a causation of good food towards a better outcome. Food high in fiber, carotenoids, and antioxidants provided a better outcome(1).
Another study noted that patients with the lowest score of ALSFRS appear in those with the lowest intake of vegetables, grains, oils, and seasonings (3).
Novel treatments using diet
In one study using a high caloric diet and an MAO-inhibitor/iron-chelating compound M30 in the superoxide dismutase-1 mouse model, results showed neuroprotection involving motor function and increased survival in the SOD-1 G93A transgenic mouse model. The M3 and CED (high caloric diet) resulted in increased mitochondrial biogenesis and metabolic regulators. A combination of novel approaches may help treat this condition (2).
1. Nieves, et al, “Association between dietary intake and function in Amyotrophic lateral sclerosis, ” 2016, Dec., 73 (12)1425-1432.
2. Golko-Perez, et al, “Additive Neuroprotective effects of the multifunctional iron chelator M30 with enriched diet in a mouse model of amyotrophic lateral sclerosis,” Neurotoxicity Research, 2016, Feb., 29(2):208-217.
3. Park, et al, “Association between nutritional status and disease severity using amyotrophic lateral sclerosis (ALS) functioning rating scale in ALS patients”Nutrition, 2015, Nov.-Dec., 31(11-12):1362-7.