Abstract
Background
The search for a definitive set of validated blood based biomarkers that relate directly to either Alzheimer’s disease (AD) pathology, or the onset of clinical symptoms is far from complete. A possible reason for this, is the underlying biological interaction between lifestyle and biology. In the current study we investigate the relationship between the well know stress hormone cortisol, and alcohol consumption with regards to risk of AD.
Methods
We extracted biomarker, demographic and lifestyle data from healthy control (HC) and AD participants of the Australian Imaging, Biomarkers and Lifestyle (AIBL) study. Using logistic regression, we tested for the presence of biological interaction between cortisol and alcohol consumption. Morning fasted cortisol levels were measured using a commercial enzyme-linked immunosorbent assay (ELISA; IBL International GmbH). Reported alcohol consumption was categorized into none vs any, and more specifically, individuals consuming only wine vs no alcohol.
Results
Mean cortisol level in the AIBL HC group (N=422) at baseline was lower compared with the AD group (N=95), (HC: 143.3 (67.1) vs AD: 160.1 (72.1)). We found a significant interaction between alcohol consumption, cortisol levels and clinical classification (P=0.02), with no difference between HC and AD cortisol levels for those who consumed alcohol (P=0.5), compared with a large significant difference for those who consumed a moderate amount of alcohol (P=0.004). (Figure 1). Using the ROC defined cortisol threshold of 151.7 to ensue a binary risk factor, we found that individuals with high cortisol, who reported no alcohol consumption were 7.2 times more likely to develop AD compared with those with low cortisol who reported any alcohol consumption (p<0.0001, Synergy Index (SI): 11.6 (95%CI: 6.4-16.9)). Reducing the sample to only those who consistently consumed wine (N=293) compared with those reporting no alcohol consumption (N=224), we saw the effect increase, with those with high cortisol who reported no alcohol consumption 9.4 times more likely to develop AD compared with those with low cortisol who reported any alcohol consumption (p<0.0001, SI: 9.5 (2.9-15.9)).
Conclusions
These findings demonstrate the benefit of regular moderate consumption of alcohol to combat the increased risk of AD due to the stress hormone cortisol.
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