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A growing body of evidence suggests that low grade inflammation contributes to the development of cardiovascular disease and, specifically, coronary artery disease (CAD). WBC-derived macrophages and other phagocytes are believed to contribute to vascular injury and atherosclerotic progression. Multiple markers of inflammation have been tested as potential risk factors for the development of CAD such as IL-6, E-selectin and CRP. Elevated white blood cell count (WBC) that is well within the normal range was associated with an increased risk for developing CAD in multiple studies.  A large-scale study demonstrated that a single measurement of WBC in healthy young men may predict CAD incidence independently from other risk factors for CAD such as elevated lipids, and a positive family history. WBC level above 6,900 cells/mm3 was associated with a 2-fold increase in the risk for CAD with a significant 17.4% increase in CAD incidence observed for every increment of 1,000 WBC/mm3: https:...

Dr Attia's podcast on Lp(a), the link is here: https://peterattiamd.com/tomdayspring6/ Discussed: - ApoB as a preferred metric over LDL-P [16:30]; Atherogenic lipoproteins (apoB/LDL-P) as front and center in pathogenesis of CVD. ApoB and LDL-P are used interchangeably, but this is not quite accurate. - Therapeutic goals for apoB concentration [21:45] - Lipoprotein(a) —the most dangerous particle you’ve never heard of [55:00]; preferred lab measurements [1:17:45];  Lipoprotein(a), or Lp(a), is a distinctive particle with 2 components:   - a lipoprotein core that resembles LDL -  a shell that contains apolipoprotein(a), or apo(a) Lp(a) is dubbed one of the final frontiers in lipid management . Elevated blood Lp(a) levels are primarily due to genetic variations in the LPA gene that encodes for apo(a) and cannot be lowered by diet, exercise or current lipid-lowering therapies.  “By combining the atherosclerotic effects of LDL with the prothrombotic effects of apo(...