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The results of a randomized and placebo-controlled trial published in the American Journal of Physiology, Heart and Circulatory Physiology suggest that oxidative stress may mediate early cardiovascular issues among young adults with anxiety and sleep irregularities, and that antioxidant supplementation may help mitigate this dysfunction. A higher percentage of young adults have anxiety (26% within the last 2 weeks), including severe anxiety, than any other age group, and the prevalence of generalized anxiety disorder (GAD) among young adults is increasing. GAD has been associated with an increased risk for developing hypertension and cardiovascular disease, as well as sleep dysfunction, which is itself independently associated with both hypertension and cardiovascular disease. This study aimed to assess the role of oxidative stress in mediating these outcomes.
Night-to-night variation in sleep duration, defined as total sleep time irregularity (TSTI), has been associated with an elevated risk for major cardiovascular events. For example, in the UK Biobank cohort, data from over 86,000 participants pointed to an elevated risk for myocardial infarction and stroke associated with higher TSTI (as measured by 7 days of accelerometry), especially for long sleepers.
In this 7-day controlled trial, twenty-five participants (mostly women, median age 24) with GAD (or meeting GAD-7 scoring criteria if undiagnosed) were included, and equipped with an accelerometer to measure both physical activity and sleep. After 7 days of recorded sleep and activity, participants were randomized to receive either a placebo or an antioxidant formulation (comprised of 400 mg alpha-lipoic acid, 500 mg vitamin C, and 200 IU vitamin E) before a laboratory evaluation, and then received the alternate (placebo or antioxidant) at a second identical evaluation conducted at least 2 days later, in a crossover fashion. Whole blood superoxide levels were assessed, as well as measures of blood pressure control (cardiovagal baroreflex sensitivity) and macrovascular function (exercise-induced flow-mediated dilation, performed using handgrip exercise to maximal voluntary contraction, established at an initial visit).
Among participants with higher TSTI (above the median), an increase in oxidative stress (superoxide production) was observed, and this was mitigated by antioxidant supplementation. In other words, not only was there more oxidative stress among participants with TSTI, but supplementation reduced oxidative stress only among people with elevated TSTI (not among those with low TSTI). Macrovascular function was also reduced among participants with elevated TSTI, with a significant improvement after antioxidant supplementation (among all participants) compared with placebo. Additionally, among participants receiving a placebo, a higher TSTI was associated with poorer blood pressure control (lower cardiovagal baroreceptor sensitivity). Antioxidant supplementation was associated with increased cardiovagal baroreceptor sensitivity (improved blood pressure control) only among the participants with an elevated TSTI.
Taken together, the results of this study support previous findings from the same team, which suggest that among young adults with chronic anxiety, irregular total sleep time is associated with oxidative stress, and potentially the beginnings of cardiovascular disease, marked by poorer blood pressure control and impaired vascular function. This study adds to the understanding of this mechanism by demonstrating a role for antioxidant supplementation in mitigating the oxidative stress underlying the impaired function, potentially providing an intervention to help normalize cardiovascular risk.
The relationship between oxidative stress and irregular sleep remains unclear and is not entirely clarified by this study. For example, this study does not point to causality; perhaps oxidative stress drives sleep dysfunction, or perhaps impaired sleep contributes to an increase in oxidative stress. One previous study found that segmented sleep, defined as a short night sleep duration and longer nap duration, was associated with markers of oxidative stress, while total sleep duration was not. This was particularly evident among “polyphasic” sleepers, i.e., people sleeping in at least 3 episodes (1 at night and 2 naps), while monophasic sleepers (one episode at night) had significantly higher total glutathione levels, again pointing to a link between oxidative stress and disturbed or fragmented sleep.
In a 2026 review published in Arteriosclerosis, Thrombosis, and Vascular Biology, irregular sleep patterns and variable sleep duration were both associated with increased risk for major cardiovascular events and diabetes, obesity, inflammation, hypertension, and dyslipidemia. Among the mechanisms cited in this paper were oxidative stress (without an increase in antioxidant responses) and upregulation of inflammatory markers, but the authors note that the mechanisms are still only partially understood. One of the papers cited in this review (published in Scientific Reports), however, intentionally induced mild sleep deprivation among otherwise healthy women in a randomized crossover design, and reported that sleep deprivation plays a causal role in both upregulated endothelial oxidative stress and, importantly, an impaired antioxidant response, which leads to endothelial dysfunction. A second study, published in the Annals of the American Thoracic Society, also reported that mild sleep deprivation increases endothelial inflammation and impairs vasomotor tone in healthy women. Hopefully, additional controlled trials, similar to the one conducted among young adults with chronic anxiety, will clearly establish the benefit of antioxidant supplementation to reduce cardiovascular dysfunction among people with impaired sleep, potentially by targeting an impaired antioxidant response.
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