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(NaturalNews) Researchers may have discovered the mechanism by which the vitamin known as niacin or B-3 raises the body's levels of HDL cholesterol, thus decreasing the risk of cardiovascular disease.

"Although niacin has been commonly used to increase plasma HDL levels, the mechanism(s) by which niacin exerts its action is not clearly understood," the researchers wrote in the Journal of Lipid Research.

HDL cholesterol, also known as "good" cholesterol, is believed to play an important role in preventing heart disease, possibly by removing plaque buildup from the arteries. In contrast, LDL ("bad") cholesterol is the kind that builds up dangerously in arteries. Because the liver is known to remove both kinds of cholesterol from the blood, researchers focused their attention on that organ.

Scientists from the University of California-Irvine and the Atherosclerosis Research Center, VA Healthcare System incubated human liver cells in a solution containing niacin, and observed this intervention's effects on a the cell component known as a "beta chain."

Beta chains are a subunit of ATP synthase, the protein that manufactures ATP, the energy source for cells. These chains are known to remove HDL from the blood, thus lowering overall levels.

The researchers found that when the liver cells were treated with niacin, their uptake of HDL decreased by 35 percent. This led them to hypothesize that niacin prevents the liver from removing HDL from the blood, thus leading to higher levels of HDL cholesterol and improved heart health.

The niacin was not observed to affect the other major cholesterol uptake pathway, "Reverse Cholesterol Transport." Reverse Cholesterol Transport is a means by which the body removes cholesterols other than HDL from the blood.

"The findings add to our expanding knowledge about the mechanism of niacin action on its wide range of clinical effects including ... anti-inflammatory, anti-thrombotic and flushing effects," the researchers wrote.

Sources for this story include: www.foodnavigator-usa.com.

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