Hypotheses to explain the association between vigorous physical activity and amyotrophic lateral sclerosis

doi:10.1016/0306-9877(91)90183-Y

Medical Hypotheses

Volume 34, Issue 2, February 1991, Pages 144-148

https://doi.org/10.1016/0306-9877(91)90183-Y Get rights and content

Abstract

Many epidemiologic studies indicate a relation between vigorous physical activity and amyotrophic lateral sclerosis. Physical activity itself is unlikely to cause amyotrophic lateral sclerosis, but could it modify the effects of other etiologic factors such as neurotoxins? Vigorous physical activity could potentiate the effect of a toxin to motor neurons by any of several mechanisms, especially if the toxin's effects were mediated through excitation. Exercise could alter the extent of exposure or could influence the distribution, metabolism or potency of an excitotoxin. Future epidemiologic studies of amyotrophic lateral sclerosis should include sufficient detail about vigorous physical exercise to explore this relationship further.

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This could cause damage to the neurons or the formation of reactive oxygen species(Harwood et al., 2009). Toxic effects of glutamate have also been hypothesized to result from strenuous physical activity(Longstreth et al., 1991). Education has been associated with the risk of ALS(Wang et al., 2017), whereas one study reported a relationship between higher education and increased ALS mortality risk(Roberts et al., 2016a).
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We investigated relationships between exposure to long-term ambient particulate matter (PM) and gaseous air pollution (AP) and ALS mortality.
Within the Women's Health Initiative (WHI) cohort of 161,808 postmenopausal women aged 50–79 years at baseline (1993–1998), we performed a nested case-control study of 256 ALS deaths and 2486 matched controls with emphasis on PM constituents (PM_2.5, PM₁₀, and coarse PM [PM₁₀-_2.5]) and gaseous pollutants (NO_x, NO₂, SO₂, and ozone). Time-varying AP exposures estimates were averaged 5, 7.5, and 10 years prior to ALS death using both a GIS-based spatiotemporal generalized additive mixed model and ordinary kriging (empirical and multiple imputation, MI). Conditional logistic regression was used to estimate the relative risk of ALS death.
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Hypotheses to explain the association between vigorous physical activity and amyotrophic lateral sclerosis

Abstract

Neuropidemiology

Lancet

Lancet

Neuroscience

Lancet

Brain Res

Neurosci Lett

Life Sci

Epidemiology of amyotrophic lateral sclerosis

Adv Neurol

Amyotrophic lateral sclerosis in Rochester, Minnesota, 1925 – 1977

Neurology

A quantitative electrophysiological study of motor neuron disease

J Neurol Neurosurg Psychiatry

Guam ALS-Parkinsonism-Dementia linked to plant neurotoxin

Science

Discussion on motor neurone disease

Studies on epidemiological, clinical and etiological aspects of ALS disease in Sardinia, southern Italy

Acta Neurol Scand

Geographic and social distribution of patients with amyotrophic lateral sclerosis

Arch Neurol

Motor neuron disease in the province of Ferrara, Italy in 1964 – 1982

Neurology

Multiple sclerosis and amyotrophic lateral sclerosis in Mississippi

Neurology

Study of epidemiological and etiological factors of amyotrophic lateral sclerosis in the province of Florence, Italy

Acta Neurol Scand

Motor neuron disease and heavy manual labor: an epidemiologic study of Varmland county, Sweden

Neuroepidemiology

ALS and heavy metals: a pilot case-control study

Neurology

Antecedent events in amyotrophic lateral sclerosis

Neurology

Is amyotrophic lateral sclerosis caused by influenza and physical activity? Results of a twin study (abstract)

Ann Neurol

Repeat studies of antecedent events in motor neuron disease

Ann Clin Res

Epidemiology of amyotrophic lateral sclerosis: 1. A case-control comparison based on ALS deaths

Neurology

Motor neuron disease and exposure to lead

J Neurol Neurosurg Psychiatry

Case-control studies of motor neuron disease: Association with mechanical injuries

Arch Neurol