Given that statins reduce LDL-C levels, these results indirectly demonstrate that treatment which reduces LDL levels is better than no treatment or less intensive LDL-lowering treatment (i.e., high intensity treatment is better). The main results are summarized in Table 2, which reports major systematic reviews/meta-analyses on the effect of more intensive lipid-lowering treatment on CVD and DM. Further, the Navarese et al. (2018) meta-analysis suggests that reduction in risk of total and CV mortality was primarily among patients with baseline (or before treatment intensification) LDL-C 100 mg/dL.[111] However, all of these analyses were conducted on trials looking at intensification of treatment (not lipid treatment goals) and, as designed, cannot be used to support lipid treatment targets due to indirectness. Evidence also shows a possibility of harm since more intensive LDL-lowering treatment was associated with a higher incidence of new-onset DM.[113] The 2014 VA/DoD Dyslipidemia CPG recommended against the routine frequent monitoring (i.e., every three or four months) of LDL-C and non-HDL-C goals for the secondary prevention of CVD. Since then, there is evidence supporting the benefits of even lower LDL levels achieved by PCSK9 inhibitors used in patients on statins at continually higher risk (ODYSSEY and FOURIER).[86,87] Yet, a specific LDL-C target or goal at which patients will benefit most from lipid-lowering treatment has not been identified. Since all primary and secondary prevention trials used treatment intensity as inputs, the Work Group determined that treatment intensity provides a more evidence-based input than LDL-C results. However, testing lipid levels is a simple and inexpensive measure of adherence and treatment efficacy. For this reason, the Work Group recommends that monitoring lipid levels in patients taking statins be individualized based on ongoing shared decision making between the patient and the provider rather than routine. Table 2. 