Article/Op-Ed: The push back against flawed CTE research has begun

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Psycho_X

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I think it's foolish to think there isn't a direct connection between playing football and increased chance of CTE. But I'm glad there is starting to be at least some discussion of the flawed research that was done on the subject that started the firestorm a few years ago. Hopefully this leads to real scientific research on causes and treatments to prevent CTE and hopefully it is well funded and lead by the NFL.

https://www.yahoo.com/sports/op-ed-...ing-launched-wave-cte-hysteria-150349666.html

Op-ed: How one flawed study and irresponsible reporting launched a wave of CTE hysteria

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Editor’s note:The following is an op-ed written by the authors of “Brainwashed: The Bad Science Behind CTE and the Plot to Destroy Football.”

The New York Times story dropped like a bomb on football and the medical community on the morning of July 25, 2017. Dr. Ann McKee, lead neuropathologist at the Boston University CTE Center, had examined the brains of 111 former NFL players and found signs of CTE, or Chronic Traumatic Encephalopathy, in 110 of them.

The news broke the internet, sent reporters scrambling to develop their own takes, and sealed the deal for millions of American parents, doctors, coaches and players. Finally, the link between playing football and developing a terrible neurodegenerative disease seemed ironclad.

As an ex-NFL player and a forensic neuropathologist, respectively, we both have an interest in solid science and sound policy that protects athletes, so we were alarmed by the CTE Center’s findings. In its wake, parents were removing their kids from Pop Warner leagues, experts were calling football “child abuse” and some states talked of banning tackle football altogether.

Then we took a closer look at the study that led to the Times story — apparently something few journalists had bothered to do. When we dug into the methodology, we were floored. The study was so badly flawed that it was nearly worthless. But that’s not what had been reported in practically every major media outlet in the world. Thanks to the barrage of sensationalist coverage, the “110 out of 111 brains” story had turned into a wildfire, and we were standing around with a couple of garden hoses, telling everybody to calm down.

That’s why we wrote our new book, “Brainwashed: The Bad Science Behind CTE and the Plot to Destroy Football” (Amplify, Oct. 23, 2018), and it’s why we’ve written this op-ed. We believe that when people know what we know, they’ll start asking tougher, smarter questions, and the “football causes CTE” connection will be revealed as the pseudoscience that it is.

Sure, that’s a provocative statement. How can we back it up? Let’s start with this: the study that produced the 110 out of 111 brains finding had no control group. Good research design requires a control group against which findings can be compared. In this case, the control group could have been brains from 100 athletes from sports other than football, brains from 100 men who had never played contact sports – any cohort that would have allowed the researchers to determine whether men of a certain age who hadn’t played in the NFL also showed signs of CTE. For some reason, this study didn’t have that.

Strike one.

Also, many of the 111 NFL brains were donated by deceased players’ family members specifically because the players had displayed symptoms of mood, cognitive or behavioral disorders. That’s selection bias. If you only look at brains from people who seem to have neurological problems, don’t be surprised when you find signs of those problems. A better approach would have been to randomly examine brains from some ex-players who exhibited mood, cognitive or behavioral issues as well as from some who didn’t. But this study didn’t do that.

Strike two.

Finally, there was no attempt made in the research paper (or the subsequent coverage) to control for or account for all the other factors in the lives of the deceased players that could have contributed to the condition of their brains. For example, nearly half the players had a history of substance abuse, suicidal thinking or a family history of psychiatric problems, but these were offered as possible results of CTE, not as possible independent causes of mood, cognitive or behavioral disorders.

In fact, 67 percent of the players found to have mild CTE also had substance abuse problems – and the abuse of some drugs can cause the key physical sign of CTE, deposits of a protein called tau in the brain. By the way, obesity, steroid use, cigarette smoking and chronic stress can also cause many of the physical signs of CTE. For example, 2016 research from the University of British Columbia found that anabolic steroid use causes CTE-like brain changes in mice, while research published in Frontiers in Neuroscience in 2014 found that obesity increases tau deposits in the brain. Were any of those former players obese, smokers or steroid users? Did they experience a lot of stress? We have no idea, because the study either didn’t ask or doesn’t tell us.

Strike three. You’re out.

Some of these limitations were discussed in the paper published on this work, but only in the last paragraph. In other words, they were buried. The researchers, especially BU, were all too willing to ride the wave of attention provided by the press without ever copping to the severe weaknesses in their work. As a result, the public is convinced that football causes CTE — and that anyone who says otherwise is a “denier” — based on work that would not have passed muster in a graduate-level research design course.

For the record, we’re not saying that CTE doesn’t exist or suggesting that taking repeated hits to the head is a good thing. Clearly, something is causing neurodegenerative disease in some athletes, and something is leaving CTE’s distinctive protein signature in their brains. But there’s so much we don’t know: what causes it, if impacts to the head are really involved, how much exposure is too much, what clinical symptoms (if any) these physical signs might cause later in life, if other factors are involved, and more. There are too many unanswered questions to justify the fear and hysteria.

What do we want? Simple. Pump the brakes. Let’s do transparent, collaborative, well-designed research that identifies the link between sports-related head trauma and neurodegenerative disease — if there is one. Let’s study other sports, like soccer. Let’s study women’s sports, not just men’s. Let’s do long-term prospective research that will tell us what decades of playing all kinds of sports does to the brain, what effects measures like protective gear and concussion rehab protocols have on outcomes, and if ex-athletes’ self-care after their careers are over can help them avoid CTE and other neurological diseases.

Let’s get good data from multiple sources and assess it based on diagnostic criteria created by the consensus of experts from multiple disciplines and multiple sources — rather than the criteria we use now, which were predominantly influenced by one source: Boston University. Let’s do science the way science is supposed to be done, and then act on that information, rather than on fear.

One of the arguments people are making is, “What’s the harm in being overcautious about hits to the head?” Good question. If the work of people like Dr. McKee is wrong and the media is peddling sensationalism and fear backed up by flimsy data, the harm is the impact this anxiety can have on people — young, old, and in between. The dire picture painted by the media could have a negative impact on mental health outcomes in athletes.

Right now, football players ranging from high schoolers to ex-pros are living in fear of CTE because they read inflammatory, fact-free stories in the press or because they forget where they put their car keys. Some pros are quitting the game in their twenties and giving up years of potential earnings because they fear that playing will cost them their futures. Bad information comes at a high cost. We not only have to get the science right; we have to get the story right.

Our kids, pro athletes, the great game of football and people who care about the truth deserve nothing less.
 

TSFH Fan

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Stated another way from the CTE pioneer (?):

"There has been so much fascination with CTE that we are going the wrong way," Dr. Bennet Omalu said. "CTE is just one disease in a spectrum of many diseases caused by brain trauma. If he doesn't have CTE, that doesn't mean he doesn't have brain damage. ... I've always said that every child who plays football has a 100 percent risk of exposure to brain damage. And I've always said that at a professional level, 100 percent would have brain damage of some kind to some degree. That's whether or not their brains are found to have CTE."

http://www.espn.com/nfl/story/_/id/...ng-larger-truth-brain-health-football-players
 

thirteen28

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In fact, 67 percent of the players found to have mild CTE also had substance abuse problems – and the abuse of some drugs can cause the key physical sign of CTE, deposits of a protein called tau in the brain. By the way, obesity, steroid use, cigarette smoking and chronic stress can also cause many of the physical signs of CTE. For example, 2016 research from the University of British Columbia found that anabolic steroid use causes CTE-like brain changes in mice, while research published in Frontiers in Neuroscience in 2014 found that obesity increases tau deposits in the brain.

This is something I've always thought was overlooked in the whole CTE controversy, particularly by the players who don't want to take responsibility for their own fate. At minimum, I think there is a second order effect from steroids that contribute to CTE, as bigger, stronger athletes hit harder and thus the collisions are more likely to lead to concussions. And just my observation, but it seems like the rise of CTE incidents coincides with the rise of steroid use in the NFL.

If there is a first order effect as suggested in the bolded portion of what I quoted, then the real problem, or at least a significant portion of it, is not football itself but steroids with football being an aggravated factor.

Either way, nobody who's interested in the truth or who respects science should have any problem with this pushback. Real science is supposed to be tested. Conclusions can't be drawn off of a single study, and particularly one that is flawed as that discussed in the article.
 

WestCoastRam

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This article raises great and valid points but then loses me on the hysteria angle. We should not dismiss the previous report, just make sure we're looking at it in context (and the necessity for more rigorous follow up). I think the argument should be an abundance of caution till more research can help us ascertain causations.
 

Psycho_X

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This article raises great and valid points but then loses me on the hysteria angle. We should not dismiss the previous report, just make sure we're looking at it in context (and the necessity for more rigorous follow up). I think the argument should be an abundance of caution till more research can help us ascertain causations.

Agreed, the main thing that is good about this book is that it hopefully gives people pause and motivates everyone to do real, worthwhile research that can also lead to lessening and maybe even preventing brain trauma. That would be research that would benefit all of mankind and not just the NFL. And that is a win. I am a little skeptical of the "for profit" motivations of the book using this subject for it but if it leads to meaningful research it'll be worth it.
 

FaulkSF

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I agree on the lack of a control population. Ideally a control should have been used, but that's what happens when you're so focused in on proving a correlation.

However the facts speak for themselves as I don't disagree with a CTE or other diagnosis of brain injury.

One has to wonder about the connection or proximity of Dr. McKee's employment to ESPN and NFL HQ. Is Dr. McKee a confederate (see definition for research) for NFL interests?
 

LesBaker

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LOL.

Where is the bad science?

Where is the "plot"? Who is plotting against football and trying to destroy it?

Fucking stupid. Authored by........Merril Hoge who has no medical background AND left the NFL because of concussion issues that made him decide he didn't want to risk his brain anymore after hospitalization.

I know bullshit when I see it.
 

1maGoh

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LOL.

Where is the bad science?

Where is the "plot"? Who is plotting against football and trying to destroy it?

freaking stupid. Authored by........Merril Hoge who has no medical background AND left the NFL because of concussion issues that made him decide he didn't want to risk his brain anymore after hospitalization.

I know bullcrap when I see it.
They talk about the bad science in the article. No control group. People selected specifically because they had what was being looked for. That other thing I've already forgotten. They aren't even saying the results were wrong, just that we can't trust them because the way the study was done doesn't prove anything. It only proves that if you try hard to find people with multiple factors that could lead to CTE, you have a really good chance of finding CTE. It does not prove what actually caused it.

More research needs to be done. What's the harm in that?
 

MadGoat

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There should be another control group of non substance-abusing ex-NFL players. Someone needs to reach out to those 12 players and see if they are willing to be included.
 

Mackeyser

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Where are the science and data nerds on the forum? @Mackeyser @bluecoconuts can we get an official, local science people reaction?

It’s not bad science in and of itself, but rather incomplete.

They have enough data to form a hypothesis.

This isn’t a case of manipulated data.

It’s not correct to assert causation at this point because we still can’t identify all of the possible contributors. That’s more an incorrect reading of the results of the study.

What the study shows is for those former football players with symptoms, they have over a 99% chance to have CTE. There have also been other athletes from sports from boxing to soccer that also have been found via the same postmortem analysis.

As this wasn’t meant to be a comprehensive study to definitively ascertain the cause of CTE, it can’t suffer from confirmation bias. The question, if I understand correctly, was “what is the incidence of CTE in former football players with symptoms?” And that is 99%.

I tend to side with Dr Omalu on this.

Repeated concussive and sub-concussive impacts WILL cause brain damage. We need more study to determine if or how it leads to CTE.

That said, the gist of the article leads me to believe that this effort is based on denial and is a pushback against transparent information.

The science is nascent and emerging.

It could be that repeated cranial impacts cause CTE. It could be that it’s merely a contributing factor or maybe it’s causal, but cranial physiology plays a factor.

There are still so many questions to answer, but we know definitively that symptomatic ex-football players have a 99% to have CTE.

That’s no joke and it’s compelling enough data to compel significantly more and deeper studies into CTE and neurotrauma.
 

jrry32

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It’s not bad science in and of itself, but rather incomplete.

They have enough data to form a hypothesis.

This isn’t a case of manipulated data.

It’s not correct to assert causation at this point because we still can’t identify all of the possible contributors. That’s more an incorrect reading of the results of the study.

What the study shows is for those former football players with symptoms, they have over a 99% chance to have CTE. There have also been other athletes from sports from boxing to soccer that also have been found via the same postmortem analysis.

As this wasn’t meant to be a comprehensive study to definitively ascertain the cause of CTE, it can’t suffer from confirmation bias. The question, if I understand correctly, was “what is the incidence of CTE in former football players with symptoms?” And that is 99%.

I tend to side with Dr Omalu on this.

Repeated concussive and sub-concussive impacts WILL cause brain damage. We need more study to determine if or how it leads to CTE.

That said, the gist of the article leads me to believe that this effort is based on denial and is a pushback against transparent information.

The science is nascent and emerging.

It could be that repeated cranial impacts cause CTE. It could be that it’s merely a contributing factor or maybe it’s causal, but cranial physiology plays a factor.

There are still so many questions to answer, but we know definitively that symptomatic ex-football players have a 99% to have CTE.

That’s no joke and it’s compelling enough data to compel significantly more and deeper studies into CTE and neurotrauma.

As always, Mack, you are a gentleman and a scholar. (y)
 

1maGoh

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It’s not bad science in and of itself, but rather incomplete.

They have enough data to form a hypothesis.

This isn’t a case of manipulated data.

It’s not correct to assert causation at this point because we still can’t identify all of the possible contributors. That’s more an incorrect reading of the results of the study.

What the study shows is for those former football players with symptoms, they have over a 99% chance to have CTE. There have also been other athletes from sports from boxing to soccer that also have been found via the same postmortem analysis.

As this wasn’t meant to be a comprehensive study to definitively ascertain the cause of CTE, it can’t suffer from confirmation bias. The question, if I understand correctly, was “what is the incidence of CTE in former football players with symptoms?” And that is 99%.

I tend to side with Dr Omalu on this.

Repeated concussive and sub-concussive impacts WILL cause brain damage. We need more study to determine if or how it leads to CTE.

That said, the gist of the article leads me to believe that this effort is based on denial and is a pushback against transparent information.

The science is nascent and emerging.

It could be that repeated cranial impacts cause CTE. It could be that it’s merely a contributing factor or maybe it’s causal, but cranial physiology plays a factor.

There are still so many questions to answer, but we know definitively that symptomatic ex-football players have a 99% to have CTE.

That’s no joke and it’s compelling enough data to compel significantly more and deeper studies into CTE and neurotrauma.
And 99% of people who look like they have a broken arm have a broke arm, but it would kind of be useless as a study and certainly shouldn't cause the panic and uproar that this study did.

I would also disagree that they can't have confirmation bias because we don't know if any attempt was made to rule out other factors relating to CTE or if they specifically, without mentioning it, selected people with as many factors as possible in order to ensure they found CTE. We just don't know and not knowing makes the study unreliable. You know... in my opinion.
 

bluecoconuts

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Where are the science and data nerds on the forum? @Mackeyser @bluecoconuts can we get an official, local science people reaction?

Well I'm an astrophysicist, so this is pretty far beyond my level of expertise.

My first impression is that they should have gotten a better advocate and obviously the CTE has made Meryll Hodge forget about his severe CTE.
 

LA_vision

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And 99% of people who look like they have a broken arm have a broke arm, but it would kind of be useless as a study and certainly shouldn't cause the panic and uproar that this study did.

Bones can heal perfectly fine and you'll live perfectly normal life. With brain damage, not so much.
 

Mackeyser

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And 99% of people who look like they have a broken arm have a broke arm, but it would kind of be useless as a study and certainly shouldn't cause the panic and uproar that this study did.

I would also disagree that they can't have confirmation bias because we don't know if any attempt was made to rule out other factors relating to CTE or if they specifically, without mentioning it, selected people with as many factors as possible in order to ensure they found CTE. We just don't know and not knowing makes the study unreliable. You know... in my opinion.

Well, several things.

1) that percentage about broken arms is probably low.

2) we have orders of magnitude more knowledge about the physiology, diseases and reaction of trauma by an arm as opposed to a brain.

3) this study was about establishing a data beachhead. They didn’t know the prevalence of CTE in symptomatic former football players. Now we know that it’s 99% based on a sample size that is significant enough to draw some preliminary conclusions.

4) it wasn’t confirmation bias because the question was specific to a particular group. It wasn’t designed to be a comprehensive study to determine definitive causality. It was to examine the prevalence of CTE in a specific sub-group. The “bias” you mention is actually the definition of the study group.

5) Lastly, the scope of the study was not to comprehensively establish causality, so possible factors were not of any consequence. This study was to establish that symptomatic former football players almost certainly have CTE.

With this data, we have more than enough evidence to do the more comprehensive studies to examine causality so as to better address mitigation as well as prevention.
 

1maGoh

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Well, several things.

1) that percentage about broken arms is probably low.

2) we have orders of magnitude more knowledge about the physiology, diseases and reaction of trauma by an arm as opposed to a brain.

3) this study was about establishing a data beachhead. They didn’t know the prevalence of CTE in symptomatic former football players. Now we know that it’s 99% based on a sample size that is significant enough to draw some preliminary conclusions.

4) it wasn’t confirmation bias because the question was specific to a particular group. It wasn’t designed to be a comprehensive study to determine definitive causality. It was to examine the prevalence of CTE in a specific sub-group. The “bias” you mention is actually the definition of the study group.

5) Lastly, the scope of the study was not to comprehensively establish causality, so possible factors were not of any consequence. This study was to establish that symptomatic former football players almost certainly have CTE.

With this data, we have more than enough evidence to do the more comprehensive studies to examine causality so as to better address mitigation as well as prevention.
But if you're already doing a study, why not do one with enough data to actually be useful. That study tells us nothing that the researchers weren't already assuming (those brains would show signs of CTE). I mean, add in 110 more brains of non contact athletes, dog into the data a little more and maybe they could actually tell us something.

And I think the point of the article was that everyone panicked over a "data beachhead" that in and of itself is meaningless until forget research is done. You just said yourself that the point wasn't to determine causality, but everyone assumed causality anyway. That's what this article was pointing out, even if they attacked it a little harder than they should have.
 

Mackeyser

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But if you're already doing a study, why not do one with enough data to actually be useful. That study tells us nothing that the researchers weren't already assuming (those brains would show signs of CTE). I mean, add in 110 more brains of non contact athletes, dog into the data a little more and maybe they could actually tell us something.

And I think the point of the article was that everyone panicked over a "data beachhead" that in and of itself is meaningless until forget research is done. You just said yourself that the point wasn't to determine causality, but everyone assumed causality anyway. That's what this article was pointing out, even if they attacked it a little harder than they should have.

You're misunderstanding the scientific approach.

You're dismissing the very process which eventually allows for the drawing of conclusions, drawing conclusions of your own and then backtracking as if your doubts impeach the process.

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It has multiple stages.

This stage was to ascertain the level of association between football and CTE using a control group of symptomatic ex-football players.

What the data showed is that there is a 99.1% rate of association. This level of ubiquity allows the next step to fully focus on causality and associated factors. With a lower rate of association, there would be further steps required and further questions to be answered before proceeding deeper.

So the assumption that football caused CTE a) wasn't assumed by the scientists and b) we still don't know if or to what degree it does.

What we know definitively is that from a statistically significant sample, 99.1% of symptomatic ex-football players DO have CTE.

So let's be clear.

You CANNOT just add in other people to this study because the very point was to utilize this specialized sub-group to see if within this sub-group there were any association with CTE. It turns out that there's a direct correlation. 80% would have been strong correlation. What the study showed was 99.1% which puts the correlation question to rest.

Correlation isn't causation, tho.

A simple example is that there is a correlation between poverty and crime. However, poverty doesn't cause crime nor does it mean that poor people are criminals.

Correlation isn't causation. Let's keep that in mind.

The "data beachhead" is not by any stretch meaningless. It is what it is. It's not more, but it most certainly is not less. This study was a very important step in a very important process which extends FAR beyond football and into a much broader understanding of the contributing factors of neurotrauma which could then lead to better methods of mitigation as well as remediation. That would affect everyone from soldiers to seniors.

What everyone assumes doesn't affect the science (unless gov't gets involved and decides to answer scientific questions with political dogma...again...)

As for the article, it was a disingenuous way of attempting to deny the science until it fulfills an almost untenable standard.

Again, that's not how science works and many of the things we rely on today were established with less certainty than opponents with their particular dogma demand.

NO ONE who is involved in the science end from the actual researchers to supporters of the research to those simply following the actual science assumed what you or the article assumed nor drew the conclusions.

Unfortunately, a continuing issue with science is that people don't like uncertainty or parsing very technical data, but it's what science IS. So, either the data is communicated too vaguely in which case the study becomes a Rorschach test for the receiver or the data is communicated too narrowly in which case the public is left to decipher the significance. Worse, the non-science community doesn't understand significance in the scientific sense.

An example. If I said to someone who had never seen a baseball game that the next guy up at bat was hitting .305, without the context that is provided by over 100 years of statistical data, there is no way to know if the hitter is good or bad or just mediocre. Hitting on average 30% is pretty darn good. If we transitioned to football and we saw a QB who was completing 30% of his passes, that would be historically bad.

So, 30% is a significant percentage, but how? The context is key.

The study examined the correlation of CTE in symptomatic ex-football players.

What was so freaking striking is that the correlation was essentially 100%. That's unheard of in studies at this stage. Normally, you would see correlations in the 30-80% range and the scientists would be left to see if the data pointed to any correlations or if further study needed to be done. Well, that was definitively and emphatically answered by the data. We don't need further study. If you're a former football player and have CTE symptoms, there's a greater than 99% chance you have CTE.

I'm not trying to be argumentative.

What I'm saying is that your argument or uneasiness is with the scientific process in general and not the data from this study. This is common. The authors of the article? I dunno. I don't know if they mean to be disingenuous or if it's born from ignorance of how science works. It does me no good to speculate.

However, your doubts do not impeach the study or data. The better course is to attempt to understand the basics of what a scientific study is, the process, how the data is assembled and process and what conclusions are appropriate to draw scientifically.

As an engineer who's invented something, actively reads both white papers and studies, does my own analysis of data on occasion and especially follows things related to neuroscience due to my own brain injury, I can say that this study was key and will be used for things far beyond its limited scope as further studies build upon what was revealed in this study.

I'll do my best to answer any specific questions you or anyone else might have.
 

1maGoh

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You're misunderstanding the scientific approach.

You're dismissing the very process which eventually allows for the drawing of conclusions, drawing conclusions of your own and then backtracking as if your doubts impeach the process.
Is the Scientific Approach different from the Scientific Method? (Sorry this is already starting out argumentative and petty; please bear with me). I was under the impression that the scientific method meant making an assumption, then testing the assumption in an experiment that included a control group to ensure that the things have something to be compared to. Maybe the Scientific Approach is a little more lax. I understand that you can't do an experiment with head trauma, but studying things like brains under the conditions of the assumption is a close analogue. Therefore it's easy to assume that they should have things that weren't just the things they were looking for.

And I'm not necessarily dismissing the process, although I'm semi ok with you calling this backtracking. I thought the article made some good points and kind of just bought into the whole thing. Bad move on my part. Establishing a contextless (no control group, no non-football brains in this particular study) may have some value, but not nearly enough to start the panic that it did. But they did start a panic.

This stage was to ascertain the level of association between football and CTE using a control group of symptomatic ex-football players.

Did they try to eliminate any brains with multiple factors so that they can clearly establish that football brains with CTE symptoms are really at 90%? Did they try to look for people with as many factors as possible to ensure that they got football brains with CTE to prove their point and it turned out better than expected? I don't know, but it's sounds like they didn't based on the breakdown of their study in that article. How could you say that football brains with CTE symptoms have a 99% correlation if maybe 50% of this brains were also in boxing clubs as children, or were in multiple car crashes, or some other factor which is believed to contribute. You were a network admin, you know you only make one change at a time, evaluate one factor at a time. We've no clue if they did that...I think.

So the assumption that football caused CTE a) wasn't assumed by the scientists and b) we still don't know if or to what degree it does.

I meant that those behind were assumed to have CTE because they had CTE. They went out selecting the people they were looking for and found them. Not a surprise.

The "data beachhead" is not by any stretch meaningless.

Just like your better example, without something to compare it to, you can't draw conclusions from it. I don't believe that it was clearly defined within that study what a normal ratio of selected brains to those with CTE was. I don't remember hearing it. We assume that the ratio for normal brains wild be 0, but without actually comparing the football brains to normal brains it's mean-... Umm, well you said it's not meaningless. What do you call data with no context and no way to interpret it that didn't tell you causation so you can't actually do anything with it except another study that basically does the same thing you did but with relevant data and meaningful conclusions?

So, 30% is a significant percentage, but how? The context is key.

I think I just covered this. I forgot why I quoted it. I understand the importance of context. Maybe more than some other people. I'll DM you about why. You'll understand.