I’m trying to get a right answer for this question for quiet some time. The literature on lipids is so vast , one can never finish reviewing it.There are nearly two dozen journals that deal with lipids ,Atherosclerosis, obesity ,and vascular biology .
Yet , the answer to this simple question is elusive to us .The Irony is complete when we have evidence for two diagonally opposite responses 4 and 5 .
My interpretation of the issue
Any lipid molecule if exceeds a critical level ( Only if . . . associated with hypertension, or diabetes or smoking ) can penetrate the vascular endothelium. ( HT-pressure injury , Smoke- Endothelial dysfunction due to Nitric oxide depletion) DM -Glycation of cell membrane , finally some unknown inflammatory component )
Though evidence for direct endothelial injury is more for LDL , less for TGL (Almost nil for VLDL , but TGL has more VLDL in it !)
Strangely ,these molecules , express a mob psychological behavior .In isolation they appear innocuous. But ,in an unfavorable setting it shows signs of revolt. If a group of LDL molecule start attacking a dysfunctional segment of endothelium , the other molecules like TGL and VLDL fractions would love to join the crowd and inflict further damage . (Of course ,the lonely HDL may watch the chaos silently !)
Questions to ponder
If LDL is a sharp knife like molecule trying to injure the blood vessel , every normal human being is potentially threatened by this lipid fraction . Mind you, this is a physiological molecule traversing the human vascular system at concentration of 130mg/dl at the velocity of blood .
So it is foolish to blame this physiological molecule for all our ignorance.
I recall one recent definition for hyperlipidemia
The lipid levels at which a patient develops vascular injury is considered high for him !