Smokers have a much higher risk of heart disease than non-smokers and are about four times more likely to die from heart disease than non-smokers.
New research from the Heart Research Institute’s Inflammation Group has uncovered a possible explanation for this higher risk:
The presence of certain oxidants in the bloodstream, which may stop “good” cholesterol from doing its job.
Oxidants are your body’s weapon against bacterial infections – they’re part of a healthy immune system response. But excessive generation of oxidants has been linked to a number of diseases, including atherosclerosis, the dominant cause of heart disease. To find out more, a common oxidant called hypothiocyanous acid was the subject of the latest study from the Inflammation Group.
“This study focuses mainly on the oxidant hypothiocyanous acid (HOSCN), which we think may be elevated in smokers,” says Professor Clare Hawkins, who led the current study. “Our suggestion is that perhaps HOSCN chemistry could play a role in the development of atherosclerosis.”
The study focuses on the effect HOSCN has on “good” cholesterol, or HDL. Ordinarily, HDL is protective against heart disease, as it shuttles cholesterol out of the fatty plaques that narrow the blood vessels in heart disease. “But when we looked at the ability of HDL to pull cholesterol out of cells in the fatty plaques, the protein which had been treated with HOSCN didn’t pull the cholesterol out nearly as efficiently as the native protein did,” says Hawkins.
Imagine you’re on a leaky boat, and you’re frantically bucketing out water to keep the boat afloat.
In a similar fashion, the growth of fatty plaques on the artery wall is partially a blance between how fast cholesterol is deposited in the plaque, and how fast HDL can take cholesterol away.
HOSCN hobbles HDL by damaging certain crucial structures (called tryptophan residues) on the HDL protein. Now you’re using a leaky bucket to bail out your leaky boat – your boat will flood because you can’t remove the water as efficiently. Similarly, damaged HDL can’t remove cholesterol from the fatty plaques as quickly, meaning more fatty deposits will accumulate on the walls of your arteries.
“People are becoming more aware that it’s not just the level of circulating HDL in the system, but it’s the dysfunctional versus functional HDL which is important,” says Hawkins. Damage to HDL’s tryptophan residues is commonly seen in blood taken from patients with advanced heart disease, and it’s looking more and more likely that common oxidants including HOSCN could be the culprits.
Perhaps the most important finding of the study is that this damage to HDL occurs with concentrations of HOSCN that are ordinarily found in the bloodstream of smokers. Previous studies on these oxidants have used concentrations tens or even hundreds of times higher than that found in the bloodstream.
While this study doesn’t provide a definitive smoking gun for the link between cigarettes and heart disease, it does provide a likely pathway by which smoking may cause lasting damage to the arteries of smokers. Hawkins cautions: “Smoking brings a whole lot of toxic insult into your body, so I’m not saying that this is the only solution. But it’s a potentially contributing factor.”