He argues that the fall in child mortality should be calculated over a slightly longer period, so the annual fall works out at 5.9%, not 7.8%, as in the Lancet.
Patients at low risk for mortality should be treated like the general PICU population.
Moreover, some evidence suggests that prediction models for mortality should be adjusted for the use of vasopressors [28], prothrombin index [29, 30] and platelet count [31, 32].
Gulland (1985) stated that in an optimally exploited stock, fishing mortality should be equal to natural mortality, resulting in an exploitation rate of 0.5.
Previous studies have suggested that prediction models for mortality should be adjusted for additional risk factors beyond the Acute Physiology and Chronic Health Evaluation (APACHE) score.
Condition-dependent susceptibility to extrinsic mortality should be incorporated more often into theoretical models and should be explicitly tested in natural populations.
Third, Charlesworth [12] showed that if some genes are beneficial at both reproductive and post-reproductive ages, then mutations that damage those genes should be selected against and late-life mortality should be restrained as a result.
By extension, populations experiencing higher rates of extrinsic mortality should be under weaker selection against mutations with deleterious effects late in life, and should therefore evolve more rapid senescence [3], [4].
This theory rests on the idea that organisms subjected to high levels of extrinsic mortality should be selected to invest less in somatic maintenance, resulting in shorter intrinsic lifespan [18].
Ideally, validity for outcomes other than mortality should be reported.
Moreover, trends in cancer mortality should be monitored continuously.
