Despite the equipoise regarding alcohol's cardiovascular effects and absence of relevant rigorous controlled trials, the lay press frequently portrays alcohol as "heart healthy." The public perception of alcohol's heart effects, the sources of those perceptions, and how they may affect behavior are unknown. We performed a cross-sectional analysis of data obtained from March 2013 to September 2014 from consecutive participants enrolled in the Health eHeart Study. Of 5,582 participants, 1,707 (30%) viewed alcohol as heart healthy, 2,157 (39%) viewed it as unhealthy, and 1,718 (31%) were unsure. Of those reporting alcohol as heart healthy, 80% cited lay press as a source of their knowledge. After adjustment, older age (odds ratio 1.11), higher education (odds ratio 1.37), higher income (odds ratio 1.07), US residence (odds ratio 1.63), and coronary artery disease (odds ratio 1.51) were associated with perception of alcohol as heart healthy (all p <0.003). Ever smokers (odds ratio 0.76, p = 0.004) and those with heart failure (odds ratio 0.5, p = 0.01) were less likely to cite alcohol as heart healthy. Those perceiving alcohol as heart healthy consumed on average 47% more alcohol on a regular basis (95% confidence interval 27% to 66%, p <0.001). In conclusion, of >5,000 consecutive Health eHeart participants, approximately 1/3 believed alcohol to be heart healthy, and the majority cited the lay press as the origin of that perception. Those with a perception of alcohol as heart healthy drink substantially more alcohol.

We described recently a subacute serum autoantibody response toward glial fibrillary acidic protein (GFAP) and its breakdown products 5-10 days after severe traumatic brain injury (TBI). Here, we expanded our anti-GFAP autoantibody (AutoAb[GFAP]) investigation to the multicenter observational study Transforming Research and Clinical Knowledge in TBI Pilot (TRACK-TBI Pilot) to cover the full spectrum of TBI (Glasgow Coma Scale 3-15) by using acute (<24 h) plasma samples from 196 patients with acute TBI admitted to three Level I trauma centers, and a second cohort of 21 participants with chronic TBI admitted to inpatient TBI rehabilitation. We find that acute patients self-reporting previous TBI with loss of consciousness (LOC) (n = 43) had higher day 1 AutoAb[GFAP] (mean ± standard error: 9.11 ± 1.42; n = 43) than healthy controls (2.90 ± 0.92; n = 16; p = 0.032) and acute patients reporting no previous TBI (2.97 ± 0.37; n = 106; p < 0.001), but not acute patients reporting previous TBI without LOC (8.01 ± 1.80; n = 47; p = 0.906). These data suggest that while exposure to TBI may trigger the AutoAb[GFAP] response, circulating antibodies are elevated specifically in acute TBI patients with a history of TBI. AutoAb[GFAP] levels for participants with chronic TBI (average post-TBI time 176 days or 6.21 months) were also significantly higher (15.08 ± 2.82; n = 21) than healthy controls (p < 0.001). These data suggest a persistent upregulation of the autoimmune response to specific brain antigen(s) in the subacute to chronic phase after TBI, as well as after repeated TBI insults. Hence, AutoAb[GFAP] may be a sensitive assay to study the dynamic interactions between post-injury brain and patient-specific autoimmune responses across acute and chronic settings after TBI.