Clinical achievable weight loss and risk factors
Since weight loss to “normalize” BMI is rarely achieved, there is good evidence that clinical achievable weight loss improves cardiovascular risk factors and several substitutive markers [14]. For example, 5–7% weight loss leads to a reduction in in insulin resistance and consequently, reduction in glycemia, triglycerides, blood pressure and ectopic fat deposition, as liver fat [14]. 10% weight loss has a dramatic effect on liver fibrosis in patients with non-alcoholic liver disease, and several other risk markers.
If visceral fat and insulin resistance are important players in the relationship of body fat and COVID-19 severity [1, 7], modest weight losses could have impact on reduction of risks, as already suggested [1], although no direct evidence exists. Low-grade inflammation reduces as well after weight loss. Magkos et al. have shown that 11–16% weight loss can substantially reduce obesity-related inflammation [15]. The same is true about pulmonary function and sleep apnea severity, other possible mediators of the relationship of obesity with COVID-19 severity [14].
An important concept here is that these risk reductions are observed irrespective of baseline BMIs. In this regard, similar percentage weight losses in individuals with very similar basal BMIs can have similar benefits. Why this happens is not exactly known, but is probably related to ectopic lipid deposition and personal fat thresholds, in which insulin resistance and metabolic disturbances appears when the subcutaneous expansion limit is achieved [1]. Continuous weight gain will lead to ectopic fat deposition in organs like liver, muscle and pancreas and increased insulin resistance can also act as a curb to further weight gain.