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There is only one disease where the most common single anecdote is "a year ago I was running marathons, what happened?". And that's ALS/MND. There's been a lot of speculation regarding soccer & American football athletes as well as combat soldiers, but that specific anecdote "a year ago I was running marathons" is heard again and again. Often it happens in slightly different form, it's sports other than marathons but which make similar physiological demands. We're not talking about the couch spuds dying of heart attacks and cancer here.

I'm about to make a bunch of statements that are not established facts, but mere hypothesis on my part. I leave it to others to attack or substantiate those hypotheses.

********HYPOTHESES ******************

1. The marathon runner is a very specific type of ALS. Although the patient may not have literally run marathons, the patient engaged in activity of a comparable nature. Mere physical exertion (think American football) is not sufficient to qualify for this category. We're talking about someone who would have been running marathons had they not been too busy doing something else of comparable physical exertion characteristics.

2. Marathon runners are neither early nor late onset, but average age a little earlier than the mean for ALS patients as whole.

3. It's been theorized that it's what marathon runners do to their bodies (esp. lactate metabolism) that triggers ALS. It's also been theorized that ALS is triggered in nearly every case by an unfavorable combination of genes. So which is it? I vote for the latter. It's the genes that predispose to that kind of athletic performance which also trigger ALS.

4. LMN and UMN predominant with bulbar and pseudobulbar symptoms not being manifested early on.

5. Rapid progression, strongly suggestive of a neurodegenerative cascade.

6. Amyotrophy evident early on.

7. Hypermetabolism manifest (if you know how to ask the question) early on.

8. Ketogenic diet helpful if it's done right.

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[EDIT] I'm not the marathon runner phenotype myself. My purpose for singling out this particular phenotype for attention is that it's common; and if it can be shown that this phenotype follows strongly a particular pattern, it makes it easier to come up with a therapeutic protocol aimed at that particular phenotype.

One of the biggest challenges in coming up with therapeutics for ALS is the heterogeneity of the disease: ALS is actually many diseases that just happen to have motor neuron degeneration in common. As Olly posted in the Prole Prote thread yesterday, the best possible cocktail will probably benefit no more than 50% of patients, and may make some of the others worse. Therefore it is important to identify subsets of ALS where we can tailor therapeutic regimes to those subsets. The task of parsing PALS into different categories that map to different therapeutic regimes has just barely begun. A lot of relevant information has been posted this year, but it's scattered. I haven't had the time to plow through it and digest it. Whether anyone else has taken up the project of digesting the data, I do not know.