Conclusions

immunological memory. Influenza vaccination in adults with obesity results in equivalent influenza-specific antibody titers at 30 days postvaccination, but antibody titers wane significantly more in adults with obesity than lean adults at one year postvaccination (Sheridan et al. 2012). Compared with influenzavaccinated lean adults, vaccinated adults with obesity have impaired CD4 and CD8 T cell production of key inflammatory cytokines IFN-γ and Granzyme B (Paich et al. 2013). Adults with obesity also have two times greater odds of influenza or influenza-like illness despite a robust antibody response (Neidich et al. 2017). Preclinical evidence demonstrates that adjuvant vaccines confer less protection against influenza viruses in diet-induced mice with obesity (Karlsson et al. 2016). Similar impairments in vaccine effectiveness have been reported in those with obesity for tetanus (Eliakim et al. 2006), hepatitis A and B, and rabies (Painter, Ovsyannikova, and Poland 2015). This suggests that a future COvID-19 vaccine may be less effective in a population with obesity. Therefore, it is urgent that vaccine trials and studies include BMI as a potential confounder for vaccine effectiveness and protection.

CONCLUSIONS

This chapter has reviewed the global evidence on the link between obesity and COvID-19. While physical distancing and stay-at-home policies may have exacerbated adverse weight and health situations, the population with overweight and obesity faces a greater risk of severe consequences from COvID-19, including hospitalization, intensive clinical care requirements, and death. Moreover, obesity is likely to reduce the effectiveness of treatment as well as vaccines through mechanisms similar to those responsible for greater primary infection risk. The immunological impairments from obesity demonstrate the convergence of chronic and infectious disease risks. They expose a large portion of the world population to greater risk of pulmonary viral infections like COvID-19.

Further research is critical to obtain additional evidence on the links between obesity and COvID-19. This includes both the impact of obesity on COvID-19 and the impact of COvID-19-related policies on overweight and obesity rates. Additional evidence from different segments of the population could help us better understand the mechanism by which obesity increases COvID-19 infection rates, severity, and prognosis. The literature is fast accumulating but was limited by being observational and having potential sampling bias, small sample sizes, and potential confounding issues. This is an opportunity to step up research and collect more high-quality data on the relationship between BMI and COvID-19 in areas such as Saudi Arabia that have a relatively young population.

At the same time, the existing evidence already indicates that efforts to develop and roll out vaccines and treatment should closely monitor the impact of obesity on the efficacy of such interventions. There are currently multiple trials on different treatments such as ACE inhibitors, tocilizumab treatment, and others such as the promising antiviral Remdesivir. It is important to monitor how obesity can mediate or hinder the effectiveness of these treatments. Additionally, obesity could lower the effectiveness of vaccines, as observed with the influenza vaccine, thereby making it essential to explicitly control for it in any upcoming vaccine trial.