Talk:Amyotrophic lateral sclerosis

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Former good article nominee Amyotrophic lateral sclerosis was a Natural sciences good articles nominee, but did not meet the good article criteria at the time. There are suggestions below for improving the article. Once these issues have been addressed, the article can be renominated. Editors may also seek a reassessment of the decision if they believe there was a mistake.
November 28, 2012 Good article nominee Not listed
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ice bucket challenge[edit]

Ice bucket challenge is fine in the history (or even better, society and culture) section, but as it presently exists and gets persistently reverted, it does NOT belong in the top line section. Presently it reads "It became well known in the United States when it affected the famous baseball player Lou Gehrig,[1][11] and later when the ice bucket challenge became popular in 2014.[12]" This is an absolutely idiotic claim that does not belong. It did in fact become known in the United States when it affected Lou Gehrig, hence why its referred to as "Lou Gehrig's Disease." It also received a lot of attention because of Steven Hawking, who is conspicuously absent here. There is no empirical evidence that actual awareness that this is a motor-neuron disease that affects some people increased because of the ice bucket challenge. Money for research certainly increased, and stupid videos of people dropping buckets of ice on their heads increased, but you show me ONE piece of data that shows that more people knew that ALS existed because of the ice bucket challenge. Footnote 12 (which by the way is a broken link), certainly doesn't appear to support this, I googled it and found the article, but its behind a paywall, it seems to kind of make a statement that it "increased awareness" but it doesn't appear to even be an article that addressed this question. As this reads in its present form, it sounds as though nobody except a few experts knew what ALS was, then the ice bucket challenge came along. This is a completely idiotic claim and I will continue to delete that sentence until it stays out of that part of the article. You've got two damn extended pieces on the ice bucket challenge in both "history" and "society and culture." It does not need to be at the end of the intro, particularly in a way that lacks empirical support.— Preceding unsigned comment added by (talkcontribs) 27 January 201 (UTC)

please, take a breath. I am sorry you cannot access the article citing greater awareness. I can email it to you, if you like. I've added content about Hawking to the lead - I think that is a good point that he should be included there. The content about ice bucket challenge is well sourced, and whatever you think of the idiocy of the crowd, it had a big impact on public awareness. Jytdog (talk) 01:53, 27 January 2015 (UTC)
The ice bucket challenge has generated reliable sources and thus we include it. The lead summarizes the article and thus deals with social cultural and historical aspects of disease. Doc James (talk · contribs · email) 02:20, 27 January 2015 (UTC)
There was a brief mention of The Ice Bucket Challenge in the History section - I don't think it is fair to call the brie mention in the History section an "extended piece" by any reasonable use of that term. but i do think the occurrence was redundant, so I moved that sentence into the Society and Culture section. I'd like to re-settle the article. Jytdog (talk) 03:08, 27 January 2015 (UTC)

Here in the UK I've just seen the TV broadcast by Larry Stogner, news anchor for ABC affiliate WTVD in North Carolina for 40 years, and participant in the 2014 Ice Bucket Challenge, announcing his imminent retirement owing to his being diagnosed with ALS - very moving to watch. Should he get a mention in the main Wikipedia article? ShropshirePilgrim (talk) 11:13, 28 January 2015 (UTC)

I'm afraid probably not - though if he has a Wikipedia page already he could be added to this: --PaulWicks (talk) 16:11, 28 January 2015 (UTC)


About this dif by Complexitydaemon, with an edit note about replacing the citation needed tag with "Dunlop et al. as PLoS ONE is a reputable peer reviewed electronic journal." and this dif by Guy...

per MEDRS, the fact that a source is "reputable peer reviewed" is not relevant -- MEDRS really emphasizes that we use secondary sources for health related content (per policies WP:NPOV, WP:OR, and the general WP:RS guideline, all content should always be based on secondary sources -- MEDRS is just more anal about it). Please especially read Wikipedia:Identifying_reliable_sources_(medicine)#Respect_secondary_sources which specifically talks about avoiding primary sources hyped by the media; the additional sources that Guy added are just media hype. We aim for MEDRS-compliant secondary sources -- review articles published in the biomedical literature or statements by major medical & scientific bodies... If yuo are puzzled by the anality (?) of MEDRS, please see the lead of my draft essay, Why MEDRS?, which attempts to explain it. Thanks! Jytdog (talk) 23:17, 16 February 2015 (UTC)

There are lots of good secondary sources for this condition. We should use them instead. Doc James (talk · contribs · email) 23:46, 16 February 2015 (UTC)
Actually my view is we should use them *as well*. The Dunlop paper was widely reported, and is plainly reliable, relevant and important. Guy (Help!) 08:49, 17 February 2015 (UTC)

Jytdog I have found a review paper that covers BMAA misincorporation and added it in with revision [1]. Complexitydaemon (talk) 02:47, 17 February 2015 (UTC)

nice find!!! i was just reading it, with great interest. thanks. Jytdog (talk) 02:58, 17 February 2015 (UTC)
This actually bears somewhat on a recent discussion at WT:MED#Primary studies, about the nuances of when, how, and if we should cite primary publications—in particular, how we should cite primary sources alongside secondary sources. In that discussion, my opinion was that it was sometimes going to be useful to our readers (and beneficial for our articles) to cite important, high-quality primary studies on which our high-quality secondary sources relied.
I (and that discussion) didn't really contemplate the precise circumstance here, where the high-quality secondary source promulgates a hypothesis regarding disease etiology and a subsequent primary publication presents new data to support that hypothesis. (The third citation, a mention on a 'regular' news website, doesn't really matter either way. It just means that someone's university is good at writing a press release, not that the research is particularly noteworthy.)
I also don't know what the best practice is to deal with an issue like this, where we have a primary study carried out in cell culture that attempts to address a question of biological mechanism. On the one hand, it's not directly offering clinical advice or clear medical conclusions. On the other hand – leaving aside entirely WP:MEDRS – absent specific secondary peer-reviewed journal articles which address this specific study, it's difficult to assign an appropriate WP:WEIGHT to its findings. And if we give a particular spotlight to a particular potential etiology, then it's only a matter of time before we see ads for the $10,000 "De-BMAA herbal cleanse! Remove the secret toxin Big Pharma doesn't want you to know about!" It's a sticky question, and I'm concerned about what happens if we let the primary literature (even the in vitro literature) get too far ahead of the secondary literature. TenOfAllTrades(talk) 18:01, 17 February 2015 (UTC)

some good sources[edit]

here: Jytdog (talk) 01:08, 19 March 2015 (UTC)

PMAA and ALS pathophysiology[edit]

For considerations by the writers of this page:

ALS PBAA and Fish consumption:

L E Brand, J Pablo, A Compton, N Hammerschlag, D C Mash. Cyanobacterial Blooms and the Occurrence of the neurotoxin beta-N-methylamino-L-alanine (BMAA) in South Florida Aquatic Food Webs. Harmful Algae. 2010 Sep 1;9(6):620-635.

W G Bradley, D C Mash. Beyond Guam: The cyanobacteria/BMAA hypothesis of the cause of ALS and other neurodegenerative diseases. Amyotroph Lateral Scler. 2009;10 Suppl 2:7-20.

W G Bradley. Possible therapy for ALS based on the cyanobacteria/BMAA hypothesis. Amyotroph Lateral Scler. 2009;10 Suppl 2:118-23.

T A Caller, N C Field, J W Chipman, X Shi, B T Harris, E W Stommel. Spatial clustering of amyotrophic lateral sclerosis and the potential role of BMAA. Amyotroph Lateral Scler. 2012 Jan;13(1):25-32.

P Factor-Litvak, A Al-Chalabi, A Ascherio, W Bradley, A Chío, R Garruto, O Hardiman, F Kamel, E Kasarskis, A McKee, I Nakano, L M Nelson, A Eisen. Current pathways for epidemiological research in amyotrophic lateral sclerosis. Amyotroph Lateral Scler Frontotemporal Degener. 2013 May;14 Suppl 1:33-43.

W Holtcamp. The Emerging Science of BMAA: Do Cyanobacteria Contribute to Neurodegenerative Disease? Environ Health Perspect. 2012 Mar; 120(3): a110–a116.

A S Chiu, M M Gehringer, J H Welch, B A Neilan. Does α-amino-β-methylaminopropionic acid (BMAA) play a role in neurodegeneration? Int J Environ Res Public Health. 2011 Sep;8(9):3728-46.

W G Bradley, A R Borenstein, L M Nelson, G A Codd, B H Rosen, E W Stommel, P A Cox. Is exposure to cyanobacteria an environmental risk factor for amyotrophic lateral sclerosis and other neurodegenerative diseases? Amyotroph Lateral Scler Frontotemporal Degener. 2013 Sep;14(5-6):325-33.

A Vega, E A Bell. α-Amino-β-methylaminopropionic acid, a new amino acid from seeds of Cycas circinalis. Phytochemistry. 1967;6(5):759-62.

P A Cox, O W Sacks. Cycad neurotoxins, consumption of flying foxes, and ALS-PDC disease in Guam. Neurology. 2002 Mar 26;58(6):956-9.

S A Banack, P A Cox. Biomagnification of cycad neurotoxins in flying foxes: implications for ALS-PDC in Guam. Neurology. 2003 Aug 12;61(3):387-9.

S J Murch, P A Cox, S A Banack. A mechanism for slow release of biomagnified cyanobacterial neurotoxins and neurodegenerative disease in Guam. Proc Natl Acad Sci U S A. 2004 Aug 17;101(33):12228-31.

X Shen, C A Valencia, J W Szostak, B Dong, R Liu. Scanning the human proteome for calmodulin-binding proteins. Proc Natl Acad Sci U S A. 2005 Apr 26;102(17):5969-74. Erratum in: Proc Natl Acad Sci U S A. 2005 Jul 5;102(27):9734.

J Pablo, S A Banack, P A Cox, T E Johnson, S Papapetropoulos, W G Bradley, A Buck, D C Mash. Cyanobacterial neurotoxin BMAA in ALS and Alzheimer's disease. Acta Neurol Scand. 2009 Oct;120(4):216-25.

M W Duncan, J C Steele, I J Kopin, S P Markey. 2-Amino-3-(methylamino)-propanoic acid (BMAA) in cycad flour: an unlikely cause of amyotrophic lateral sclerosis and parkinsonism-dementia of Guam. Neurology. 1990 May;40(5):767-72.

P A Cox, S A Banack, S J Murch, U Rasmussen, G Tien, R R Bidigare, J S Metcalf, L F Morrison, G A Codd, B Bergman. Diverse taxa of cyanobacteria produce beta-N-methylamino-L-alanine, a neurotoxic amino acid. Proc Natl Acad Sci U S A. 2005 Apr 5;102(14):5074-8. Epub 2005 Apr 4. Erratum in: Proc Natl Acad Sci U S A. 2005 Jul 5;102(27):9734. — Preceding unsigned comment added by (talk) 06:05, 6 April 2015 (UTC)


following content was added by good faith IP edito, first here then here. <blockquote?Some observations provide compelling evidence of fungal infection in ALS patients analyzed, suggesting that this infection may play a part in the etiology of the disease or may constitute a risk factor for these patients[1].


Source fails MEDRS - we should wait til there is a review discussing this, I think. happy to discuss. Jytdog (talk) 12:29, 1 May 2015 (UTC)

Agree need better source Doc James (talk · contribs · email) 14:08, 1 May 2015 (UTC)

ALS in males and females[edit]

There's nothing in the article about males and females - who is more likely to develop ALS, whether the symptoms differ etc. [2] says "ALS is 20% more common in men than in women." so if a better source can be found by those who know where to look, this type of thing could be very interesting to include in the article. — This, that and the other (talk) 06:47, 8 June 2015 (UTC)


A registry in one country does not deserve its own main section in the article. I belongs under research. Thus moved it back their. We do not have such a heading in our WP:MEDMOS and I think it fits fine under research. Other thoughts? Doc James (talk · contribs · email) 01:39, 2 September 2015 (UTC)

The US registry is relevant for research, but it is also an important source of information. If we become aware of registries in other countries we should mention them and change the title to "Registries". — Preceding unsigned comment added by Jsreznick (talkcontribs) 12:11, 2 September 2015 (UTC)
In general, I agree with Doc James' take on this. Wikipedia is foremost an encyclopedia; it is not intended to be a directory of every resource or website related to a given topic. A mention in the 'Research' section seems more than sufficient, and places the registry in an appropriate context.
Incidentally, it would be helpful to see some independent sources which talk about what this particular registry does and what its impact has actually been. Why is it worthwhile for Wikipedia to call attention to this particular project? CDC affiliation is generally a promising sign, but not necessarily sufficient by itself. I've taken a quick glance through the "Registry Resources" pages on the website linked by Jsreznick, and it's mildly concerning that I can't readily locate basic information like when the Registry was founded or how many patients are enrolled, or links to peer-reviewed publications based on registry information. While we want to avoid taking a promotional tone, and to avoid over-stuffing the description with minutiae, I am troubled that the only specific information I've seen in any draft Wikipedia text is that the Registry currently exists. TenOfAllTrades(talk) 14:01, 2 September 2015 (UTC)
There are quite a lot of registries (e.g. Italy, Ireland, etc., etc., etc.) the CDC one although it required a lot of lobbying and has federal funding has not, as of yet, done much to make it more worthy of mention that the others. --PaulWicks (talk) 13:22, 2 September 2015 (UTC)

Culture section[edit]

ALS has featured in quite a number of books, films, and TV shows - I'm not sure we need quite such detailed coverage about one plotline of the Incredible Hulk (not that I want to annoy the Hulk, I hear he's smashing) - perhaps that can all sit somewhere else apart from perhaps the most well known pieces such as Theory of Everything? --PaulWicks (talk) 13:18, 2 September 2015 (UTC)

We do not. Feel free to trim. Doc James (talk · contribs · email) 22:50, 2 September 2015 (UTC)

Deleting some excessively detailed / research-heavy subsections[edit]

Interested in the views of other editors but on reviewing the sections "Eye movement", "Skeletal muscle units" and "Lactate and cinnamate" I came across a number of issues that I think makes them good candidates for removal.

Eye Movement: There's already a good descriptive line in "late stages" characterizing what happens for most patients. The subsequent section (see below) contains some very old studies (1983) as citations and some claims that just don't bear relevance to how ALS is managed today in the clinic. For instance we don't use EOG clinically and it's not used much at all in research, so this seems excessively detailed and verging on WP:OR. The embyronic lineage of EOM's line is also not really all that relevant to a general page on ALS. To be clear, most people with ALS will never have any sort of experience with eye control, although some patients in later stages particularly if using a tracheostomy / ventilator might do but it's somewhat uncommon.

Skeletal Muscle Units: This seems more like an essay or a somewhat spotty review of the topic, doesn't seem appropriate here.

Lactate and cinnamate: As above

PaulWicks (talk) 18:59, 17 February 2016 (UTC)

Eye movement[edit]

People with ALS may have difficulty in generating voluntary fast movements of the eye.[1] The speed of eye movement is slower in people with ALS.[1] Problems in generating smooth pursuit and convergence movements have also been noted.[1] Testing the vestibulo-ocular reflex should help in identifying these problems.[2] The electrooculography (EOG) technique measures the resting potential of the retina. EOG findings in people with ALS show progressive changes that correlate with disorder progression, and provide a measurement for clinically evaluating the effects of disorder progression on oculomotor activity.[2] Additionally, EOG may allow earlier detection of problems with the eyes.

The embryonic lineage of EOMs differs from that of somite-derived muscles. EOMs are unique because they continuously remodel through life and maintain a population of active satellite cells during aging.[3] EOMs have significantly more myogenic precursor cells than limb skeletal muscles.[3]

Skeletal motor units[edit]

Despite sharing fixed sequences of recruitment, extraocular muscles (EOMs) and skeletal muscles exhibit different characteristics. The following are characteristics of EOMs that differ from skeletal motor units.[4]

  • One neural fiber connects with only one or two muscle fibers
  • No ocular stretch reflexes, despite being rich in muscle spindles
  • No recurrent inhibition
  • No special fast-twitch or slow-twitch muscles
  • All eye motor neurons participate equally in all types of eye movements—not specialized for saccades or smooth pursuit

Differences are also noted between healthy and affected EOMs. EOMs from postmortem donors preserved their cytoarchitecture, as compared to limb muscles. Healthy EOMs consist of a central global layer (GL) facing the globe and a thin orbital layer (OL) facing the walls of the orbit.[5] EOMs affected by ALS preserve the GL and OL organization.[5] EOMs possess the neurotrophic factors brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF), and these neuroprotective factors are also preserved in EOMs affected by ALS.[5] Laminin is a structural protein typically found in the neuromuscular junction (NMJ). Lnα4 is a laminin isoform that is a hallmark of skeletal muscle NMJs.[6] People with ALS showed preserved Lnα4 expression in EOM NMJs, but this expression was non-existent in limb muscle NMJs from the same people.[6] Preservation of laminin expression may play a role in preserving EOM integrity in people with ALS. People with sporadic ALS (sALS) have increased levels of intracelluar calcium, causing increased neurotransmitter release.[7] Passive transfer of sera from people with sALS increases spontaneous transmitter release in spinal, but not EOM terminals;[7] therefore, EOMs are assumed to be resistant to changes in physiologic conditions typically found in ALS.

However, some effects of the disorder were noted. EOMs affected by ALS had a larger variation in fiber size compared to those in age-matched healthy controls.[5] EOMs exhibited both clustered and scattered atrophic and hypertrophic fibers that are characteristic of disorder, but these muscles showed significantly less damage compared to limb muscles from the same donors.[5] These EOMs also showed an increase in connective tissue and areas of fatty replacement in compensation of fiber loss and atrophy.[5] Ophthalmoplegia, a loss of neurons in and around the ocular motor nuclei, has been noted in ALS patients.[1] Additionally, myosin heavy chain content of the EOM fibers was altered, with a loss of normal expression of MyHCslow tonic in the GL and the OL did not contain MyHCemb, which is normally expressed in this layer.[5] This change may represent a change in innervation pattern that may include reinnervation by a different type of motor neuron or loss of multiple innervations. Changes in MyHCslow and MyHCemb are the only fiber changes seen in EOMs, leaving the EOM fiber composition relatively normal.[5] Because EOMs are normally highly innervated, any denervation is compensated for by neighbouring axons which preserve function.[5]

Lactate and cinnamate[edit]

Lactic acid is an end product of fermentation and is known to cause muscle fatigue. Lactate dehydrogenase (LDH) enzyme exerts its effects bidirectionally and is able to oxidize lactate into pyruvate so it can be used in the Krebs cycle. In EOM, lactate sustains muscle contraction during increased activity levels. EOMs that have high LDH activity are thought to be resistant to ALS.[8]

Cinnamate is a blocker of lactate transport and exogenous lactate on fatigue resistance. Cinnamate is able to cause fatigue in EOM, while decreasing EOM endurance and residual force; however, cinnamate has no effect on the extensor digitorum longus muscle in the leg.[8] In contrast, replacing glucose with exogenous lactate increases fatiguability of EDL muscles but not EOMs.[8] Fatiguability in EOMs was only found when a combination of exogenous lactacte plus cinnamate replaced glucose.[8]


There has been some news surrounding ALS relating to the role of Concussions in American football, recently a bit of news relating to the death of Kevin Turner (running back). I have made some edits to add this to the article. I welcome comments. I earlier put it in causes, and then User:Doc_James moved it to culture. I am unclear on how this should be reflected on this page. User:Doc_James said earlier on this talk page "The lead summarizes the article and thus deals with social cultural and historical aspects of disease." Is the NFL (which has activity that is being investigated as a "cause" for the disease (as a medical definition), the right location to put this? But if playing American Football has not be identified as a cause, then how should it be listed. Seeking feedback from editors. Thank you Jtbobwaysf (talk) 19:24, 26 March 2016 (UTC)

So if high quality secondary sources discuss concussions as a cause that would go in the cause section. If we only have lower quality source that talk about the social and cultural issues of players suing the NFL because they beleive what they have was caused by concussions while playing football than that goes lower IMO.
This is also popular press [3] Doc James (talk · contribs · email) 01:30, 27 March 2016 (UTC)
Understand now relating to Wikipedia:MEDRS. I have reverted and changed the citation to one that complies which is written by CDC and NIOSH and published in American Academy of Neurology. I guess that is good enough. Jtbobwaysf (talk) 05:26, 27 March 2016 (UTC)

Popular press[edit]

In 2012 the NIOSH reported that NFL players had a four times greater risk of dying from ALS or Alzheimer’s disease. [9][10]

The popular press is not a suitable source for medical content. Please see WP:MEDRS


  1. ^ a b c d Cohen B, Caroscio J. Eye movements in amyotrophic lateral sclerosis. J Neural Transm Suppl. 1983;19:305-15
  2. ^ a b Palmowski A, Jost WH, Prudlo J, Osterhage J, Käsmann B, Schimrigk K, Ruprecht KW (1995). "Eye movement in amyotrophic lateral sclerosis: a longitudinal study". Ger J Ophthalmol 4 (6): 355–62. PMID 8751101. 
  3. ^ a b Kallestad KM, Hebert SL, McDonald AA, Daniel ML, Cu SR, McLoon LK (2011). "Sparing of extraocular muscle in aging and muscular dystrophies: a myogenic precursor cell hypothesis". Exp. Cell Res. 317 (6): 873–85. doi:10.1016/j.yexcr.2011.01.018. PMC 3072110. PMID 21277300. 
  4. ^ Kandel ER, Schwartz JH, Jessell TM. Principles of Neural Science. McGraw-Hill; 2000
  5. ^ a b c d e f g h i Ahmadi M, Liu JX, Brännström T, Andersen PM, Stål P, Pedrosa-Domellöf F (2010). "Human extraocular muscles in ALS". Invest Ophthalmol Vis Sci 51 (7): 3494–501. doi:10.1167/iovs.09-5030. 
  6. ^ a b Liu JX, Brännström T, Andersen PM, Pedrosa-Domellöf F. Different Impact of ALS on Laminin Isoforms in Human Extraocular Muscles Versus Limb Muscles. Invest Ophthalmol Vis Sci. 2011
  7. ^ a b Mosier DR, Siklós L, Appel SH. Resistance of extraocular motoneuron terminals to effects of amyotrophic lateral sclerosis sera. Neruology. 2000;54(1):252-5
  8. ^ a b c d Andrade FH, McMullen CA (2006). "Lactate is a metabolic substrate that sustains extraocular muscle function". Pflugers Arch. 452 (1): 102–8. doi:10.1007/s00424-005-0010-0. PMID 16328456. 
  9. ^ "Professional Football Players Have Higher ALS And Alzheimer's Death Risks.". Medical News Today. 2012-09-06. Retrieved 2016-03-27. 
  10. ^ "Pro Football Players Have 4-Times Greater Risk of ALS and Alzheimer's". Breaking Muscle. Retrieved 2016-03-27. 
Doc James (talk · contribs · email) 01:47, 27 March 2016 (UTC)
Understand now relating to Wikipedia:MEDRS. I have reverted and changed the citation to one that complies which is written by CDC and NIOSH and published in American Academy of Neurology. I guess that is good enough. Jtbobwaysf (talk) 05:26, 27 March 2016 (UTC)
this dif used a primary source, not a secondary source per MEDRS and wildly misrepresented the source and the authors. It was not "written by CDC and NIOSH" and was notpublished by the American Academy of Neurology." Please see the note on your talk page. Jytdog (talk) 07:58, 27 March 2016 (UTC)
Hello (User:Jytdog), You replied under this popular press talk heading that Doc James made was because in an earlier edit I had used popular press. This citation you are discussing is not popular press. Anyhow, you reverted my edits to this page stating the citation didn't meet WP:MEDMOS for two problems. #1- I was attributing the name of the publication. Agreed, I will correct this and remove it. 2- you stated that this paper was primary research. It doesn't appear to me that this article meets the test for vanilla primary research, it certainly didn't involve any testtubes, needles, etc. This is a statistical analysis. WP:MEDMOS "Text that relies on primary sources should usually have minimal WP:WEIGHT, only be used to describe conclusions made by the source, and must describe these findings clearly so that checking can be made by editors without specialist knowledge." This content was added to section "other factors" following another statement that has no citation at all, therefore weight is already minimized. . Are you suggesting the content be moved further down the article into the NFL section to further minimize? I'm not debunking here, so your argument that primary research cannot be used isn't valid. It simply just must be used in accordance with WP:MEDMOS, particularly relating to weight, and it appears to me that it is. I'll move content down to the NFL section to further minimize the weight, if that is what you are asking for. #3 you stated that I wildly misrepresented the conclusion of the paper, well this is confusing as I quoted the conclusion almost verbatim. Maybe some other editors will also weight in on weight, as putting the content down in culture/football seems also a funny location to me. Please comment. Thanks Jtbobwaysf (talk) 09:21, 27 March 2016 (UTC)
It is a primary source. I will see if anything better exists. Doc James (talk · contribs · email) 10:41, 27 March 2016 (UTC)

Incorporating Recent Studies[edit]

Found one here Research is still tentative. Reason for association is unclear. Doc James (talk · contribs · email) 10:48, 27 March 2016 (UTC)

Hello James, thanks for that link. I added a new heading above as we have moved on from the popular press issue, per your assistance. I think the key point right now is how to include this information on the article. There are two studies under discussion currently:
1. NIOSH 2012 Neurodegenerative causes of death among retired National Football League players The study states (quote)
Conclusions: The neurodegenerative mortality of this cohort is 3 times higher than that of the general US population; that for 2 of the major neurodegenerative subcategories, AD and ALS, is 4 times higher. These results are consistent with recent studies that suggest an increased risk of neurodegenerative disease among football players.
2. NIH 2013 Epidemiology of neurodegeneration in American-style professional football players The study states (quote)
Conclusions: There is considerable evidence that multiple and recurring concussive and subconcussive blows to the head can be deleterious to the brain and may result in neurodegeneration. However, a number of questions on how and why neurodegeneration may occur in football players still need to be answered: Is it based on the accumulation of multiple brain insults or caused by a cascade of events triggered by several severe brain injuries? Are there synergistic effects between genetic susceptibilities and brain injury? Why are neurologic impairments appearing in collegiate and early-career pros when it has been assumed that such effects were relegated to long-term pro players? Are there other environmental factors involved in neurodegeneration?
Confirming that repetitive head injuries, even if sub-concussive in nature, cause neuronal death that leads to CTE or other serious neurodegeneration will require additional studies using multiple study design methods. Additional studies that attempt to quantify the cumulative effects of head injuries - and, in particular, the relative effects of concussive- and subconcussive-level injuries - will be of particular importance in understanding the underlying disease mechanisms. Fully effective disease-prevention interventions will not be possible until more is known about the exposure-disease relationship.
Relating to the first study (NIOSH, above #1), WP:MEDMOS allows it to be included in the article entry as long as weighting is low (which it is in the society section), and since nothing is being debunked here. This is a statistical study and makes not attempt to prove causation, only document correlation. This secondary study (NIH #2 above) affirms the correlation and affirms cause has not been determined, User:Doc James has added this now. In both cases WP:MEDMOS allows these studies to be included, it only guides against debunking (doesn't apply here) and and it guides relating to weighting. Please comment. Thank you Jtbobwaysf (talk) 12:01, 27 March 2016 (UTC)
This is a primary source [4]. We should use the review.
The review states "Although the overall mortality of this cohort was significantly lower than expected, standardized mortality ratio (SMR) - the ratio of observed deaths in the NFL cohort to the expected deaths in the general US population - was 0.53, the neurodegenerative mortality was three times higher than that of the general US population, and those of two of the major neurodegenerative subcategories (Alzheimer's disease and ALS) were four times higher. Mortality from CTE could not be examined since it is not listed as a cause of death in any revision of the International Classification of Diseases." Doc James (talk · contribs · email) 15:25, 27 March 2016

We also have this review [5] Doc James (talk · contribs · email) 15:30, 27 March 2016 (UTC)

James, thank you for your assistance with this. I was advocating adding the article with primary research (the 2012 study) since that is the study that the NFL settlement (mentioned in the next paragraph) referenced. But if you are uncomfortable adding that because it is primary, it is no big deal. I think the general information is there regardless. Thanks again Jtbobwaysf (talk) 16:48, 27 March 2016 (UTC)
We have to be super careful here. NFL players are different from the rest of the population in many ways. Playing football is just one of them. We have correlations that football players appear to have a higher rate of neurodegenerative disease, but we don't know why. We cannot say anything attributing that correlation to them playing football or to things that happen while they play football. The content that Doc James added is fine. We do not need the primary source as there are reviews that cover it. Jytdog (talk) 18:58, 27 March 2016 (UTC)
It would be interesting to see if other sports were there are large numbers of concussions also have higher rates of neurodegerative disorders. How to separate out steroid use may be difficult. Doc James (talk · contribs · email) 07:51, 28 March 2016 (UTC)
yes, steroids is a big one, especially when they were younger. and one would imagine that football players generally physical people and there is off-season activity, etc. any number of confounders. Jytdog (talk) 08:08, 28 March 2016 (UTC)
Have moved some of it up to the cause and put it under the heading of "head injury". For significant head injuries the evidence of increased risk is fairly strong. Doc James (talk · contribs · email) 08:10, 28 March 2016 (UTC)

life expectancy[edit]

The article states - About 10% survive longer than 10 years.[6] only 4% survive longer than 10 years.[26] — Preceding unsigned comment added by (talk) 07:01, 5 June 2016 (UTC)

Thanks, corrected. — kashmiri TALK 10:51, 5 June 2016 (UTC)
Thanks Kashmiri, noticed the update today :) — Preceding unsigned comment added by (talk) 07:33, 7 June 2016 (UTC)


"case-control studies provided strong evidence" does not appear to be supported by the references in question. Therefore adjusted the wording [6].Doc James (talk · contribs · email) 20:05, 15 June 2016 (UTC)