the bonding of sugar molecules (this is glycation at work,
covered in chapter 3). Once these particles undergo damage,
both the target tissues for delivery (your fat or muscle cells,
for example) and the recycling center in the liver have
trouble recognizing the particles. It’s like trying to open a
lock with a bent key—the LDL no longer fits. This damaged
LDL then gets stuck in circulation and accumulates like a
roaming leper colony, eventually settling in an artery wall.
Sometimes this means that total cholesterol will go up, but if
the particles are small and dense, total cholesterol may not
go up much, if at all. This may explain why many people
who’ve never had high cholesterol (or people on medication
with artificially lowered cholesterol) still have heart attacks.
The second scenario is that the lock itself may become
jammed. This occurs when the liver undergoes oxidative
stress and overload, due to excessive processed or
concentrated carbohydrate consumption (among other
things). Essentially, when the liver is digesting carbs (or
carbs and fat simultaneously), alcohol, or other toxins, it
doesn’t prioritize the recycling of lipoproteins. Similarly,
when a target like a muscle cell is already “topped off” with
nutrients, it’s going to say “no thank you” as the LDL
particle passes by. Either situation results in additional time
that an LDL particle spends in circulation and in proximity
to oxidative by-products—thereby facilitating damage and
making it more likely to get stuck to the vessel wall. (This
was demonstrated in a recent study where women who went
on a high-carb, low-fat diet saw their levels of oxidized
cholesterol surge by 27 percent, even though total
cholesterol did not change.)^10