+and+oxLDL+J+curve.jpg)
The paper was written before the Lp(a) is oxLDL paper, so the authors are showing the two seperate plots, one is the amount of oxidised phospholipid per unit LDL and the other is Lp(a).
I like the similarities in the curves! Life should be logical.
From the practical point of view, at what level of Lp(a) do you need to hurry in making out your will? Look at graph B.
Obviously there is a "least risk" value for Lp(a), but if you had null genes for apo(a), and so come out with zero Lp(a), you would still be in exactly the same risk category as the sextiles 3 and 4 but wouldn't be worrying about it! So, in this study, using this Lp(a) assay, for people eating modern food, anything below 24mg/dl has the same risk as zero Lp(a). Perhaps lower if you are lucky.
Note also from graph A that having undetectable oxidised lipids per unit LDL in your blood DOUBLES your risk of incident CVD. That's it. No oxLDL [ie no Lp(a), whichever you please] DOUBLES your risk of heart disease.
EDIT: I guess "is observationally associated with" would be a better phrase. Don't want to sound like the AHA about cholesterol here!
And you thought your genes evolved apo(a) to kill you!
Wrong.
Peter
