Mechanism linking binge drinking and atherosclerosis
Researchers believe they have found a mechanism linking binge drinking and atherosclerosis. According to John Cullen, Ph.D., of the University of Rochester, and colleagues, heavy drinking, binge drinking, causes an abundance of acetaldehyde which increases the adhesion of monocytes to cultured endothelial cells. This connection, between binge drinking and atherosclerosis, has been shown in previous studies but without specifying a mechanism. Researchers commenting stated, “These in vitro findings support novel effects of acetaldehyde on processes involved in the initiation of atherosclerosis… yet further studies are warranted to investigate whether these effects are relevant in vivo, and whether these actions of acetaldehyde may underlie, in part, the detrimental effects of binge drinking on cardiovascular disease.”
Binge drinking is defined as five or more drinks within a two hour period for men, four or more for women. It is important to note, however, that moderate alcohol consumption has been shown by various studies to be associated with lower cardiovascular risk. The following is an excerpt of an article from Medpage Today that discusses the study more:
Because monocyte recruitment plays an important role in the development of atherosclerosis, the researchers set out to evaluate how acetaldehyde affects this process.
They cultured human umbilical venous endothelial cells, primary blood monocytes, and THP-1 monocytes and treated them with acetaldehyde at concentrations ranging from 0.1 µM to 25 µM for six hours, which approximates the amount of time the chemical would remain in the blood after a bout of binge drinking.
The concentrations of acetaldehyde “are physiologically relevant and cover a range of concentrations that are found in the blood following the consumption of moderate and binge amounts of alcohol,” the researchers said.
Acetaldehyde increased the number of THP-1 monocytes expressing CCR2, a receptor involved in attracting the immune cells to damaged endothelial cells (P<0.05). The most significant effect — a 50.6% increase — was seen with 10 µM of acetaldehyde.
There was also a significant increase in the number of endothelial cells expressing P-selectin — which is involved in initially tethering monocytes to endothelial cells and rolling them down the line of cells — and in P-selectin receptor density when the cells were exposed to acetaldehyde (P<0.05 for both comparisons).