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Summary Atherosclerotic lesions initiate with endothelial cell dysfunction causing modification of apoB containing lipoproteins (LDL, VLDL, remnants) and infiltration of immune cells, particularly monocytes, into the subendothelial space (Figure 1)

160 Symptoms often progressively improve after dose de-escalation

This cascade of events leads to a robust accumulation of mtROS formation with cardiovascular implications

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By day 10, I was consistently leaving 1520% of my usual lunch portion on the plate without effort