The latest COVID-19 research out of Germany also has possible implications for athletes. It found that 78% of a sample of ordinary people (median age 49 means 50% were younger than that and 50% were older) who contracted the virus but who presented with mild or no symptoms actually had some kind of heart damage from the virus. And 60% showed inflammation consistent with myocarditis: https://jamanetwork.com/journals/jamacardiology/fullarticle/2768916 Maybe young football players will be immune, but I know I'd think twice in judging relative risks.
In looking more closely at the abstract it doesn't say that all 100 participants had mild or no symptoms but it does say that the heart damage was "independent of preexisting conditions, severity and overall course of the acute illness, and the time from the original diagnosis." This means that even younger, healthier participants were not spared the heart damage of the other participants.
Another relevant quote underlining that the severity of symptoms (which might include mild to no symptoms) was not a significant factor in getting heart damage: "our findings reveal that significant cardiac involvement occurs independently of the severity of original presentation."
The article does actually say that the participants' symptoms ranged from "asymptomatic (n = 18) to minor to moderate symptoms (n = 49)." It also does not say that younger participants had better outcomes than older participants. It does say: "The findings are not validated for the use in pediatric patients 18 years and younger. "
Though not explicitly addressing the chances of football players getting the virus, the following article points out that anyone who gets into the "exhalation cloud" of another person is at greater risk than not being in the "exhalation cloud." The "exhalation cloud" can form from singing, shouting, or even just talking in a normal voice. These are things that all people do, even football players during a game. Being outdoors helps but cannot be relied upon to disperse the "exhalation cloud." https://www.sciencenews.org/article...-why-6-feet-may-not-be-enough-social-distance
Simple: here's a guy who's been a bust by any standard, who can't run a pattern to save his life, who's not going to amount to a hill of beans since on top of it all, he's opted-out for the season... ....and yet this thread (for whatever reason) has continued beating-a-dead-horse for 6 whole pages? .....any additional insights on Josh Doctson? .....guy's Terrell Pryor 2.0... ... or . (*)(*) . ? ...I vote tits : )
Based on the content of this thread, it appears we won't know until we find out how he plans to vote. Then we can take sides on the issue.
You seem like maybe you have some scientific reasoning ability--While you present apparent compelling evidence we need to know exactly what and how "heart damage" is measured and if this type of "damage" occurs after other recoveries such as from the flu, etc before making conclusions.
I suppose I do have some scientific reasoning ability (I have a Ph.D. in psychology), but I am not a physician, and I hardly qualify as an expert in heart disease or its diagnosis and treatment. I can only repeat some statements from the article that the authors submitted to the Journal of the American Medical Association. Here is one statement from the article: "In this cohort study including 100 patients recently recovered from COVID-19 identified from a COVID-19 test center, cardiac magnetic resonance imaging revealed cardiac involvement in 78 patients (78%) and ongoing myocardial inflammation in 60 patients (60%), which was independent of preexisting conditions, severity and overall course of the acute illness, and the time from the original diagnosis." Here is another: "At the time of CMR, high-sensitivity troponin T (hsTnT) was detectable (3 pg/mL or greater) in 71 patients recently recovered from COVID-19 (71%) and significantly elevated (13.9 pg/mL or greater) in 5 patients (5%). Compared with healthy controls and risk factor–matched controls, patients recently recovered from COVID-19 had lower left ventricular ejection fraction, higher left ventricle volumes, higher left ventricle mass, and raised native T1 and T2. A total of 78 patients recently recovered from COVID-19 (78%) had abnormal CMR findings, including raised myocardial native T1 (n = 73), raised myocardial native T2 (n = 60), myocardial late gadolinium enhancement (n = 32), and pericardial enhancement (n = 22)." I have no idea what the specific CMR measurements mentioned imply, but Googling "myocardial inflammation" I come up with this description from the Mayo Clinic: "Myocarditis is an inflammation of the heart muscle (myocardium). Myocarditis can affect your heart muscle and your heart's electrical system, reducing your heart's ability to pump and causing rapid or abnormal heart rhythms (arrhythmias)." We should also be aware that a wide variety of viruses (including flu viruses) reportedly can cause heart problems: https://www.heartandstroke.ca/articles/how-do-viruses-trigger-heart-damage https://medicalcityhealthcare.com/blog/entry/flu-and-your-heart The point I was trying to make was that right now large numbers of American citizens are being exposed to a virus which the consensus of medical opinion considers more dangerous than the common flu, and that this exposure poses a threat to football players, which requires caution (even though as a Jet fan since the Dick Wood days, I sincerely hope that the season can be conducted): https://www.weforum.org/agenda/2020/03/health-officials-coronavirus-covid19-flu-health-outbreak
A lot of issues with that study. The high levels and other symptoms can also be attributed to other things. The conclusion of the study was that more investigation needed to be done.
Yes, the scientific method is based on humility in that (in contrast to blowhards all over social media) it is based on weighing all the accumulating evidence and not making statements that imply that the definitive, eternal truth has ever been determined. Consequently, all studies typically end with the caution that more research is needed. That being said, this article pretty starkly stated that the results were the results: "Taken together, we demonstrate cardiac involvement in 78 patients (78%) and ongoing myocardial inflammation in 60 patients (60%) with recent COVID-19 illness, independent of preexisting conditions, severity and overall course of the acute illness, and the time from the original diagnosis. These findings indicate the need for ongoing investigation of the long-term cardiovascular consequences of COVID-19." The "ongoing investigation" could include confirmatory studies but also studies of other "long-term cardiovascular consequences." Examination of the study's design makes clear that this is no fly-by-night, haphazard effort but a well-designed study. By the way, the peer review of a top medical forum such as the Journal of the American Medical Association is particularly rigorous, with top experts carefully examining all parts of the study, including methods. This gives further credence to the study's conclusions. Yes, any study is bound to have imperfections, including imperfect controls, so that results can conceivably be attributed to "other things." But well-designed studies make such possibilities less likely.
I think cval makes an excellent point and that is that the actual treatment of the patients could have contributed to their bodily state post-covid. I don't see how you find it easy to dismiss that possibility. The research is well-designed but the causal attributions are not obvious at all. It is published as a set of data for others to add to. Regarding long-term consequences, many diseases and other environmental factors cause long-term change to a body--without quantifying the consequence of this inflammation the mere fact that there is some level of inflammation at some period of time after recovery tells experienced researchers little. However it does have the effect of causing irrational judgments by the masses. As a psychologist perhaps you are aware of Kahneman and Tversky's findings on human judgment and choice?
