Background, aims: Cognition declines with age1. Additionally, chronic exposure to lack of oxygen as seen in highlander dwellers leads to cognitive changes2. Exaggerated systemic oxidative stress has been reported in patients with Chronic Mountain Sickness (CMS+) a maladaptive syndrome characterised by cognitive and neurological defecits4. Diet may attenuate the rate of cognitive decline, particularly consumption of the primary water and fat-soluble chain-breaking antioxidants (vitamins C & E), given their collective capacity to attenuate oxidative stress5. The aim of this study was to determine if a link exists between inadequate dietary antioxidant vitamin intake in CMS+ patients and accelerated cognitive decline/early dementia. Methods: Twenty two male highlanders with CMS (CMS+; age 56±11 years), 14 male highlanders without CMS (CMS-; age 52±12 years) and 28 male aged matched lowlander controls (Lowlanders age 67±6 years) consented to the study. Participants were interviewed to collect a 24-hour structured dietary recall and data were analysed using NetWISP dietary analysis software (Version 4.0, Tinuviel Software; Anglesey, UK). Montreal Cognitive Assessment (MoCA) was used to assess cognition according to recommended procedures. Data were tested for normality using Shapiro-W-Wilks tests. Kruskal-Wallis, Mann-Whitney and Chi-Square tests were performed to compare the groups. Significance level was established at P<0.05 and data are expressed as mean ± standard deviation (SD). Results: Dietary vitamin C consumption was shown to be deficient in CMS+ relative to CMS- and lowlanders (Table). Dietary vitamin E consumption was also deficient in in both CMS+ and CMS- relative to lowlanders (P<0.05). The CMS+ patients were also characterised by a lower MoCA score compared to CMS- and lowlanders (Table) Conclusions: The findings demonstrate that patients who fail to adapt to the terrestrial extremes of high-altitude are characterised by an inadequate intake of dietary antioxidant vitamins. Given that these antioxidants can selectively “repair” aqueous superoxide, peroxyl, and alkoxyl radicals, any functional deficiency in dietary intake may contribute to cerebrovascular endothelial dysfunction, attenuated cerebral perfusion and explain the accelerated cognitive decline reported herein. Acknowledgements: DMB is supported by a Royal Society Wolfson Research Fellowship (#WM170007). Reference: 1. Murman (2015). Seminars in Hearing, 36; 111-121. 2. Kramer et al. (1993). Hum Factors, 35; 329–344. 3. Julian et al. (2013). Respir Physiol Neurobiol. 186; 188–196. 4. Bailey et al. (2013). Chest, 143; 444-451. 5. Vauzour et al (2017). Ageing Research Reviews, 35; 222-240.
|Publication status||Published - 14 Sep 2018|
|Event||Europhysiology 2018 - QEII Centre, London, United Kingdom|
Duration: 14 Sep 2018 → 16 Sep 2018
|Period||14/09/18 → 16/09/18|