Considerations for obesity, vitamin D, and physical activity amidst the COVID-19 pandemic
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Real-time estimates from the Johns Hopkins University dashboard report approximately 1.5 million COVID-19 cases worldwide with the United States accounting for 28% (1). As expected, various sectors have embarked on large-scale efforts to develop targeted therapeutics including monoclonal antibody therapy and vaccination, however; a complex road lies ahead before success can be reached at the population-level. Amidst the growing concern, many governments have taken action by implementing travel restrictions, school closures, and social distancing to mitigate the strain on public health care systems. Similar tactics have been effective at containing previous viral outbreaks, although a natural consequence of these changes is the disruption of daily routines. Nevertheless, there is urgent need to employ a multipronged approach to manage the crisis in both the short and long term.
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While COVID-19 is notoriously contagious, it also appears to be preferentially virulent among older (> 60 years) adults with existing comorbidities including obesity, hypertension, and diabetes. This would be expected as overt and/or occult disease is known to increase vulnerability to infections. Still, many infected individuals do not succumb to the illness, and instead, fight the imposing effects of the virus. Depending of the severity of symptoms, some patients present with acute respiratory and/or cardiac distress necessitating mechanical ventilation and prolonged hospital stays. However, a further matter of priority involves the preservation of health among those not diagnosed with COVID-19. Whereas social distancing and ‘sheltering in place’ readily limit person-to-person transmission, an undesired consequence of prolonged sedentariness is the propensity for systemic deconditioning – a dilemma that can readily undermine overall health and wellness. As the biomedical community races to disentangle the unknowns associated with COVID-19, the link between diminished immune function and individuals with obesity raises important questions about the possibility for greater viral pathogenicity in this population (2). Given the prevalence of obesity among the US population, a meaningful proportion of individuals may be at an elevated risk for symptom complications following a positive COVID-19 diagnosis. Following the 2009 influenza A virus H1N1 pandemic, retrospective analyses specified obesity as a risk factor for symptom severity and mortality (3). Increased adiposity may undermine the pulmonary microenvironment (e.g., alveoli) wherein viral pathogenesis and immune cell trafficking could contribute to a maladaptive cycle of local inflammation and secondary injury. The spike glycoprotein residing on the membrane of the COVID-19 virus will likely be of central importance as it is the key feature for host entry and responsible for triggering the immune response (4). As work endeavors to resolve the challenges of COVID-19 therapies – understanding how individuals with obesity may respond differentially to such treatments will be critical.
Though somewhat speculative, a posing challenge to those with obesity during the COVID-19 pandemic may involve vitamin D deficiency/insufficiency (5). Long recognized as the ‘sunshine vitamin’ – the biologically active form of vitamin D (1,25-dihydroxyvitamin D / calcitriol) has been implicated in various inflammatory, infectious, and pulmonary diseases. Indeed, experimental evidence indicates calcitriol exerts protective effects from lipopolysaccharide-induced lung injury by modulating the expression of angiotensin-converting enzymes I and II (6). Considering the growing dispute over the proposed link between mortality/morbidity among COVID-19 patients and use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers (7) – it seems prudent to also consider how inter-individual variance in vitamin D status could be involved in pulmonary inflammation and viral pathogenicity. Interestingly, emerging data posits vitamin D could be an adjunct to manage the pro-inflammatory milieu or “cytokine storm” observed in COVID-19 patients (8). This, in turn, presents an attractive option as the clinical implications of symptom severity and management appear to be exacerbated in the setting of hypertension and diabetes – both of which are typically connected to obesity. Alternatively, physical activity, operationalized as energy expenditure attributed to skeletal muscle contractions, is a pragmatic approach to augment vitamin D status – particularly when performed outdoors.Habitual outdoor physical activity is known to promote vitamin D synthesis through the interaction between ultraviolet radiation and 7-dehydrocholesterol in the skin. Directives to limit social contact notwithstanding, even indoor physical activity may effectively improve vitamin D status through biological mechanisms beyond 7-dehydrocholesterol. Prospective analyses of community-dwelling older adults over a 2.6 year period showed a positive association between the change in serum vitamin D (25(OH)D) and physical activity assessed by accelerometry – independent of sun exposure (9). Scott and colleagues (2010) indicated the observed relationship may have been attributed to favorable changes in body composition via physical activity (i.e., ↓adiposity; ↑skeletal muscle mass). It is also worth noting, daily or weekly supplementation with vitamin D (D2or D3) has been shown to offer protection from acute respiratory infections – particularly among individuals exhibiting vitamin D deficiency (< 20 ng/mL) (10). However, among US adults, shifting attention to focus on a single micronutrient like vitamin D should not be at the expense of other commonly under-consumed nutrients including calcium, potassium, and dietary fiber. A diverse diet will help ensure a broad nutrient profile to aptly alleviate vulnerability to acute and chronic disease.
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References1. Johns Hopkins University. Coronavirus 2019-nCoV Global Cases by Johns Hopkins CSSE. URL: https://gisanddata.maps.arcgis.com/apps/opsdashboard/index.html#/bda7594740fd40299423467b48e9ecf6. 2. Andersen CJ, Murphy KE and Fernandez ML. Impact of obesity and metabolic syndrome on immunity. Adv Nutr 2016; 7: 66-75. 3. Sun Y, Wang Q, Yang G, Lin C, Zhang Y and Yang P. Weight and prognosis for influenza A(H1N1)pdm09 infection during the pandemic period between 2009 and 2011: a systematic review of observational studies with meta-analysis. Infect Dis (Lond) 2016; 48: 813-822. 4. Dhama K, Sharun K, Tiwari R, Dadar M, Malik YS, Singh KP et al. COVID-19, an emerging coronavirus infection: advances and prospects in designing and developing vaccines, immunotherapeutics, and therapeutics. Hum Vaccin Immunother 2020; 1-7. 5. Pereira-Santos M, Costa PR, Assis AM, Santos CA and Santos DB. Obesity and vitamin D deficiency: a systematic review and meta-analysis. Obes Rev 2015; 16: 341-349. 6. Xu J, Yang J, Chen J, Luo Q, Zhang Q and Zhang H. Vitamin D alleviates lipopolysaccharide induced acute lung injury via regulation of the renin angiotensin system. Mol Med Rep 2017; 16: 7432-7438. 7. Patel AB and Verma A. COVID-19 and Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers: What Is the Evidence? JAMA 2020
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