Thread by @holmanm

1/7 Read this, read it again, and understand it.
To me it is mindblowing. It points to the fact that lipids are PROTECTIVE. Part of the innate immune response, and it makes the 'infective cause' of CVD far more plausible.

2/7 Lipoprotein particle levels and their constituents are extensively altered by acute inflammation and infection (Gabay and Kushner, 1999). In fact, hypocholesterolemia (low cholesterol) has been consistently correlated with WORSE outcomes in critically ill patients

3/7 (Windler et al., 1994; Gordon et al., 2001; Gui et al., 1996; Marik, 2006). The molecular mechanisms underlying this are poorly understood but measurements of various lipid parameters in patients with severe sepsis or septic shock indicate that apoB lipoprotein levels can

4/7 be very LOW (Kitchens et al., 2003; Vermont et al., 2005; van Leeuwen et al, 2003). Because our data indicate that HOMEOSTATIC levels of apoB-expressing Lipoproteins are REQUIRED to provide adequate defense against quorum sensing invasive S. aureus infections,

5/7 clinical scenarios that result in extremely low apoB-containing lipoproteins may INCREASE the risk of invasive S. aureus infection including MRSA infections. Which kind of proves my theory that the 'bad cholesterol' and Lp(a)/ApoB is NOT OUT to kill us but to defend us

6/7 Remind me again ? Why are you so intent on lowering ApoB, LDL, Lp(a) ??? 🙄 Lipoprotein particle levels and their constituents are extensively altered by acute infection, and of course high circulating levels of OXIDIZED LDL contribute to impaired Th1 immunity.

7/7 More recent publications have described the effects of oxidized lipids on atherosclerosis and associated risk factors (123–130). The prevalence of antibodies that recognize epitopes of Ox-LDL seem to correlate well with the disease process