Reducing Cholesterol Might Get A Whole Lot Easier

One of the most frustrating, challenging things about treating conditions like obesity and heart disease is that we can't predict how our bodies will interact with what we feed them every day. Of course, studies have shown that genes play a major role in determining which of us end up with clogged arteries by the age of 30. But, genetics isn't nearly the whole story — and just because we know why some people are predisposed to suffer from certain diseases doesn't necessarily make us any better at treating them.

What if future treatments could allow our bodies to block the absorption of things like fat and cholesterol? New research suggests that we're getting closer to outsmarting one of the sneakiest (and most deadly) heath conditions out there. Scientists at Johns Hopkins have pinpointed a sort of "switch" mechanism in our cells that causes our bodies to absorb excess cholesterol, which often leads to atherosclerosis (a build-up of fat inside the blood vessels) and heart disease. Even better? They've figured out how to turn it off.

The research, published this month in the journal Circulation, tested the theory that a molecule called glycosphingolipid, or GSL, is responsible for abnormal absorption of cholesterol. In a series of experiments involving mice and rabbits, researchers used a chemical compound known as D-PDMP to halt GSL production in the cells of a portion of the subjects, while the rest were given a placebo.

The subjects were fed a high-fat, high-cholesterol diet — essentially the equivalent of three cheeseburgers a day. In all of the experiments, the researchers found that D-PDMP treatments not only kept LDL, or "bad" cholesterol, at normal levels, but also raised levels of "good" HDL cholesterol, which works to counteract the effects of LDL in the bloodstream. Those lucky lab rodents also had lower levels of triglycerides than the placebo group and higher levels of lipoprotein lipase, an enzyme that plays an important role in preventing atherosclerosis.

The animals who received the D-PDMP treatment were also found to have healthy heart muscles, blood vessels, and blood pressure, indicating that the high-fat diet had not caused a build-up of fat in their blood vessels. In practical terms, by turning off the production of the GSL molecule, the researchers preempted the effects of a high-fat diet on the animals' cardiovascular systems. Meanwhile, the subjects that were not given D-PDMP displayed astronomical cholesterol levels, as well as evidence of atherosclerosis, as a result of their fat intake.

Most notably, the researchers observed no side effects to the treatment, even when they exposed the animals to 10 times the minimum effective dose of the D-PDMP compound. While these findings are admittedly limited because of the use of animal subjects, the authors are already developing a cholesterol drug to be tested in humans that combines D-PDMP with current treatments.

Aside from the inherent cool-factor of a chemical that essentially re-engineers the way our bodies deal with food, it's hard to deny that this is some seriously promising research. Considering the fact that high cholesterol is responsible for 2.6 million deaths worldwide every year — and that current treatments are ineffective in roughly one third of patients — this could be a real game-changer. (Science Daily)