Poor oral health is a modifiable risk factor that is associated with clinically observed cardiovascular disease. However, the relationship between oral and brain health is not well understood. We ...tested the hypothesis that poor oral health is associated with worse neuroimaging brain health profiles in middle-aged persons without stroke or dementia.
We performed a 2-stage cross-sectional neuroimaging study using UK Biobank data. First, we tested for association between self-reported poor oral health and MRI neuroimaging markers of brain health. Second, we used Mendelian randomization (MR) analyses to test for association between genetically determined poor oral health and the same neuroimaging markers. Poor oral health was defined as the presence of dentures or loose teeth. As instruments for the MR analysis, we used 116 independent DNA sequence variants linked to increased composite risk of dentures or teeth that are decayed, missing, or filled. Neuroimaging markers of brain health included white matter hyperintensity (WMH) volume and aggregate measures of fractional anisotropy (FA) and mean diffusivity (MD), 2 metrics indicative of white matter tract disintegrity obtained through diffusion tensor imaging across 48 brain regions.
We included 40,175 persons (mean age 55 years, female sex 53%) enrolled from 2006 to 2010, who underwent a dedicated research brain MRI between 2014 and 2016. Among participants, 5,470 (14%) had poor oral health. Poor oral health was associated with a 9% increase in WMH volume (β = 0.09, SD = 0.014,
< 0.001), 10% change in aggregate FA score (β = 0.10, SD = 0.013,
< 0.001), and 5% change in aggregate MD score (β = 0.05, SD = 0.013,
< 0.001). Genetically determined poor oral health was associated with a 30% increase in WMH volume (β = 0.30, SD = 0.06,
< 0.001), 43% change in aggregate FA score (β = 0.43, SD = 0.06,
< 0.001), and 10% change in aggregate MD score (β = 0.10, SD = 0.03,
< 0.01).
Among middle age Britons without stroke or dementia, poor oral health was associated with worse neuroimaging brain health profiles. Genetic analyses confirmed these associations, supporting a potentially causal association. Because the neuroimaging markers evaluated in this study precede and are established risk factors of stroke and dementia, our results suggest that oral health, an easily modifiable process, may be a promising target for very early interventions focused on improving brain health.
Patients with ischemic stroke and concomitant COVID-19 infection have worse outcomes than those without this infection, but the impact of COVID-19 on hemorrhagic stroke remains unclear. We aimed to ...assess if COVID-19 worsens outcomes in intracerebral hemorrhage (ICH).
We conducted an observational study of ICH outcomes using Get With The Guidelines Stroke data. We compared patients with ICH who were COVID-19 positive and negative during the pandemic (March 2020-February 2021) and prepandemic (March 2019-February 2020). Main outcomes were poor functional outcome (defined as a modified Rankin scale score of 4 to 6 at discharge), mortality, and discharge to a skilled nursing facility or hospice. The first stage included 60 091 patients with ICH who were COVID-19 negative and 1326 COVID-19 positive. In multivariable analyses, patients with ICH with versus without COVID-19 infection had 68% higher odds of poor outcome (odds ratio OR, 1.68 95% CI, 1.41-2.01), 51% higher odds of mortality (OR, 1.51 95% CI, 1.33-1.71), and 66% higher odds of being discharged to a skilled nursing facility/hospice (OR, 1.66 95% CI, 1.43-1.93). The second stage included 62 743 prepandemic and 64 681 intrapandemic cases with ICH. In multivariable analyses, patients with ICH admitted during versus before the COVID-19 pandemic had 10% higher odds of poor outcomes (OR, 1.10 95% CI, 1.07-1.14), 5% higher mortality (OR, 1.05 95% CI, 1.02-1.08), and no significant difference in the risk of being discharged to a skilled nursing facility/hospice (OR, 0.93 95% CI, 0.90-0.95).
The pathophysiology of the COVID-19 infection and changes in health care delivery during the pandemic played a role in worsening outcomes in the patient population with ICH.
The American Heart Association's Life's Simple 7, a public health construct capturing key determinants of cardiovascular health, became the Life's Essential 8 after the addition of sleep duration. ...The authors tested the hypothesis that suboptimal sleep duration is associated with poorer neuroimaging brain health profiles in asymptomatic middle-aged adults.
The authors conducted a prospective magnetic resonance neuroimaging study in middle-aged individuals without stroke or dementia enrolled in the UK Biobank. Self-reported sleep duration was categorized as short (<7 hours), optimal (7-<9 hours), or long (≥9 hours). Evaluated neuroimaging markers included the presence of white matter hyperintensities (WMHs), volume of WMH, and fractional anisotropy, with the latter evaluated as the average of 48 white matter tracts. Multivariable logistic and linear regression models were used to test for an association between sleep duration and these neuroimaging markers. The authors evaluated 39 771 middle-aged individuals. Of these, 28 912 (72.7%) had optimal, 8468 (21.3%) had short, and 2391 (6%) had long sleep duration. Compared with optimal sleep, short sleep was associated with higher risk of WMH presence (odds ratio, 1.11 95% CI, 1.05-1.18;
<0.001), larger WMH volume (beta=0.06 95% CI, 0.04-0.08;
<0.001), and worse fractional anisotropy profiles (beta=-0.04 95% CI, -0.06 to -0.02;
=0.001). Compared with optimal sleep, long sleep duration was associated with larger WMH volume (beta=0.04 95% CI, 0.01-0.08;
=0.02) and worse fractional anisotropy profiles (beta=-0.06 95% CI, -0.1 to -0.02;
=0.002), but not with WMH presence (
=0.6).
Among middle-aged adults without stroke or dementia, suboptimal sleep duration is associated with poorer neuroimaging brain health profiles. Because these neuroimaging markers precede stroke and dementia by several years, these findings are consistent with other findings evaluating early interventions to improve this modifiable risk factor.
Abstract only Background: The interaction between social determinants of health and genetic risk factors in causing acute ischemic stroke (AIS) is poorly understood. We hypothesize that community ...deprivation, a geographic metric that captures several social determinants of health, modifies the effect of genetic variation on risk of AIS. Methods: We analyzed data from All of Us , a large population study that aims to enroll one million Americans. We ascertained AIS cases using Observational Medical Outcomes Partnership codes. We evaluated community deprivation using the deprivation index, an aggregate variable derived from six metrics of the American Community Survey that was divided into tertiles. We modeled the polygenic contribution to AIS through a polygenic risk score that included 530 known genetic risk variants for cardiometabolic risk factors. We used multivariable logistic regression to model AIS risk as a function of community deprivation and polygenic risk, using product terms to test for interaction. Results: Out of 372,397 participants currently enrolled in All of Us , 147,492 had available genetic and deprivation index data, including 3,201 (2.2%) strokes. Both community deprivation and the polygenic risk score were independently associated with AIS risk (both p<0.05). We found a significant interaction between community deprivation and polygenic risk (interaction p=0.02, Figure): the polygenic risk score was significantly associated with AIS risk in areas with low community deprivation (OR 1.08, 95%CI 1.02-1.15; p=0.01) but was not associated with this risk in areas of intermediate and high deprivation (both p>0.05). Conclusion: Among study participants enrolled in All of Us, those living in areas of low community deprivation were more susceptible to the effects of polygenic variation. We speculate that in areas with high deprivation, several social determinants of health known to lead to higher risk of AIS dilute the contribution of genetic risk factors.
Abstract only Background: Oral health is a modifiable risk factor for stroke. However, the role of oral health in the brain health of clinically asymptomatic persons remains understudied. We ...hypothesize that genetically-determined poor oral health leads to worse neuroimaging brain health profiles in persons without stroke. Methods: We conducted a two-sample Mendelian Randomization (MR) study. As instruments, we used 105 genetic variants known to be associated (p<5x10 -8 ) with a composite of caries, dentures and missing teeth in the GLIDE Consortium. In stroke-free participants enrolled in the UK Biobank, we tested for association between these genetic variants and white matter hyperintensity volume (natural log-transformed), fraction anisotropy and mean diffusivity. For the last two neuroimaging traits, we evaluated the first principal component of measurements obtained across 48 brain regions. Results: Our primary analysis using the inverse variance-weighted MR method indicated that genetically-increased risk of poor oral health was associated with: (1) higher burden of silent cerebrovascular disease, as represented by higher volumes of white matter hyperintensities (beta=0.24, SE=0.07 p-value=0.001), and (2) increased microstructural damage, as represented by lower fractional anisotropy (beta=-2.53, SE=0.38; p=1x10 -9 ) and higher mean diffusivity (beta=3.42, SE=0.41; p=2x10 -11 ). Sensitivity analyses identified horizontal pleiotropy in our primary results, but an outlier-corrected analysis confirmed all three initial results (all p-values <0.001, Table 1). Conclusion: Among persons without stroke, genetically-determined poor oral health is associated with worse neuroimaging brain health profiles. Because gene-disease associations are immune to confounding, our results indicate that this association is causal. Early treatment of poor oral health may lead to significant brain health benefits, even in persons without stroke.
