Owing to the aging global populations, cognitive impairment is increasingly becoming a pivotal societal challenge and a threat to sustainable development. Strong evidence supporting the cumulative deleterious effect of chronic arterial hypertension on cognitive function exists. Indeed, hypertension is the most important modifiable risk factor for cerebral white matter lesions, cognitive impairment, lacunar infarction, microbleeds, stroke, and vascular dementia.91,92 Pathophysiological mechanisms underpinning this complex yet intriguing association are not completely elucidated, however, summation of the cerebrovascular and degenerative lesions hypothesis is entertained.91,92 Nonetheless, with conflicting results between studies, the benefits of blood pressure control on cognitive functions among hypertensive individuals remains unclear.43, 93–109 Moreover, with the absence of effective disease-modifying treatments, hypertension being a modifiable risk factor represents a potentially vital mechanism for prevention or delay of cognitive impairment.
Over two-fifth of hypertensives in this present study had cognitive impairment. There is a wide variability in the prevalence of cognitive impairment (16.5% − 63.9%)110–114 among hypertensives in the literature, however, our rate falls in between. Such discrepancy in the prevalence could be a result of the differences in population characteristics and variability in tools utilized for assessment of cognitive functions among studies. Nevertheless, comparative studies have consistently demonstrated superior rates of cognitive impairment to normotensive subjects.21, 112–114 For instance, in a study by Muela HC et al,114 hypertensive individuals demonstrated twice as much prevalence of cognitive impairment compared to their normotensive counterparts (i.e. 50% vs 25%, p < 0.001). Furthermore, Muela114 and colleagues revealed that patients with hypertension had worse performance in language, processing speed, visuospatial abilities, and memory upon neuropsychological tests. Likewise, in a study by Heizhat M et al,21 hypertensive individuals had significantly lower each item score and total score of the Mini–Mental State Examination (MMSE), compared to the normotensive controls.
A reciprocal interplay between education and cognitive functions has been observed across studies.115,116 Despite the lack of a formal consensus regarding the definition of low education, it is considered the most effective modifiable risk factor for cognitive impairment globally.117–119 Recent analyses have noted that education does change the point at which accelerated declines due to cognitive impairment occur.120 In this present study, participants with low education had over three-fold chance of having cognitive impairment and indeed it was the strongest predictor. These findings are consistent with a meta-analysis by Meng X and D’Arcy C which revealed a pooled OR of 2.61 for cognitive impairment among those with low education.121 Educational attainment contributes to individual differences in cognitive skills hence people with higher education perform better across a broad range of cognitive tasks.122 Moreover, current data shows that continuing education and cognitive leisure activities increase cognitive reserve thus improving cognitive functions and lower incidence of cognitive impairment.123
The mechanism underlying the influence of rural-urban differences on cognitive functions is complex and poorly understood. Conversely, the impact of urbanization is profound and potentially mediated by several factors including education and occupation, living environments and pollution, access to public resources and healthcare, amongst others. Over the years and across all geographical boundaries, studies have demonstrated that individuals residing in rural areas have inferior cognitive functions compared to their age- and sex-matched urban counterparts.124–131 In this study, persons who resided in rural areas had an 80% increased odds of having cognitive impairment compared to their urban counterparts. Such findings echo the one from a Taiwanese study by Liu CC et al which revealed a 90% increased odds among rural dwellers.132 Furthermore, studies by Chuang YF and Nakamura K revealed an odds of 2.3 and 4.0 respectively among rural residents.133,134 These regional differences in rates of cognitive impairment suggests the presence of modifiable factors with potential interventional implications, which ought to be elucidated in future studies.
A complex triad relationship between employment, cognition, and diseases exists. Through repetitive participation in demanding, complex tasks often requiring considerable focus and expertise, employment has the potential to augment cognitive reserve, facilitate brain health and optimize cognitive functioning as it entail learning of new skills, establishing a routine and social engagement.135–141 The odds of cognitive impairment among unemployed/retired participants of this study was 1.7. In unison to our findings, a study by Leist AK et al,142 revealed an odds of 1.2 in unemployed individuals. Among unemployed/retired individuals, negative neuroplasticity with resultant compromise of cognitive functioning could ensue from the lack of cognitive stimulation provided from employment engagement. Moreover, owing to its potential in leading to effective cognitive interventions and in order to promote successful cognitive aging, it is imperative for clinicians to consider educating patients about the importance of staying cognitively active regardless of their employment status.
Epidemiologic data suggest that individuals at all stages of renal dysfunction have increased risk of developing cognitive disorders.143–155 Consistent with previous research, this present study demonstrated a 70% increased likelihood of cognitive impairment among participants with renal dysfunction compared to their counterparts with preserved renal functions. Despite of its poorly understood pathophysiology, the relationship between cognitive impairment and renal dysfunction appears to be complex and bidirectional.156–158 Nevertheless, direct neuronal injury from uremic toxins and the high prevalence of both subclinical and symptomatic ischemic cerebrovascular lesions are conceivable underlying mechanisms.159 It is postulated that, for every decrease of 15 ml/min/1.73 m2 in glomerular filtration rate, there is a decline in cognitive function similar to that of a 3-year aging.160 Furthermore, cognitive impairment in individuals with renal dysfunction is associated with poor health-related quality of life, longer hospitalizations and higher mortality.161
Strengths and Limitations.
Several strengths can be drawn from this study including; (i) an adequate sample to estimate the prevalence of cognitive impairment and conduct analyses stratified according to potential effect modifiers, (ii) the use of standardized tools for data collection and utilization of qualified and competent personnel in all measurements. Nevertheless, this study is not short of limitations. Owing to the cross-sectional design, this study cannot preclude bias and limits both causality exploration and generalizability of findings. To elucidate the true nature and magnitude of this intriguing association, prospective studies are required to explore the longitudinal association between hypertension and incidence of cognitive impairment.