) ▁without ▁particles ▁to ▁carry ▁it . ▁A ▁simple ▁way ▁to ▁understand ▁this ▁observation ▁is ▁the ▁fact ▁that ▁A po B 1 0 0 , ▁one ▁per ▁particle , ▁reflect s ▁actual ▁li pop rote in ▁particle ▁concentration ▁( in dependent ▁of ▁their ▁ch ol ester ol , ▁or ▁other ▁li pid ▁content ). ▁In ▁this ▁way , ▁one ▁can ▁understand ▁that ▁the ▁number ▁of ▁A po B 1 0 0 - cont aining ▁li pop rote in ▁particles ▁which ▁can ▁carry ▁lip ids ▁into ▁the ▁ar tery ▁walls ▁is ▁a ▁key ▁determin ant , ▁driver ▁of ▁a ther os cl eros is ▁and ▁heart ▁disease . ▁ ▁One ▁way ▁to ▁explain ▁the ▁above ▁is ▁to ▁consider ▁that ▁large ▁numbers ▁of ▁li pop rote in ▁particles , ▁and , ▁in ▁particular , ▁large ▁numbers ▁of ▁L DL ▁particles , ▁lead ▁to ▁competition ▁at ▁the ▁A po B 1 0 0 ▁re ceptor ▁( i . e . ▁L DL ▁re ceptor ) ▁of ▁peri pher al ▁cells . ▁Since ▁such ▁competition ▁will ▁prolong ▁the ▁residence ▁time ▁of ▁L DL ▁particles ▁in ▁the ▁circul ation , ▁it ▁may ▁lead ▁to ▁greater ▁opportunity ▁for ▁them ▁to ▁under go ▁ox id ation ▁and / or ▁other ▁chemical ▁modifications . ▁Such ▁modifications ▁may ▁less en ▁the ▁particles ' ▁ability ▁to ▁be ▁cleared ▁by ▁the ▁classic ▁L DL ▁re ceptor ▁and / or ▁increase ▁their ▁ability ▁to ▁interact ▁with ▁so - called ▁" sc aven ger " ▁re cept ors . ▁The ▁net ▁result ▁is ▁the ▁sh un