Steve Stiles
March 07, 2014
WAGENINGEN, THE NETHERLANDS — Excuses for regularly indulging in dark chocolate keep accumulating, with the added possibility that its ingredients, thought to promote relaxed arteries, also have biochemical effects that may discourage atherosclerosis. But special flavanol-enriched formulations of dark chocolate may do little to enhance its vascular benefits, suggests a report published in the March 2014 issue of the FASEB Journal[1].
In a randomized, double-blind study, eating dark chocolate—acutely and over weeks—not only improved objective measures of endovascular function, it also improved biochemical markers that reflect leukocyte activation, inflammation, and other signs of atherogenesis.
The study further compared normal- vs high-flavanol dark-chocolate consumption by its participants, a few dozen overweight and mildly obese middle-aged male volunteers. It saw few important differences in vascular functional or biochemical effects following ingestion of either formulation of chocolate.
Changes in endothelial function were reflected in improved flow-mediated dilation (FMD), blood pressure, and augmentation index (AIX), while “changes in leukocyte-cell counts, plasma cytokines, and leukocyte adherence markers after chocolate consumption point toward a less-activated state of cellular adherence and, hence, a less atherogenic milieu,” according to the authors, led by Dr Diederik Esser (Top Institute Food and Nutrition and Wageningen University, the Netherlands).
“Extra flavanols did not augment these effects,” they write, “but did affect taste and had a negative effect on the motivation to eat chocolate.”
Beneficial vascular changes and even improved clinical outcomes have long been attributed to consumption of flavanol- and polyphenol-rich foods like chocolate, red wine, cinnamon, and tea in both observational and interventional studies. Chocolate itself has been associated with improved blood pressure and cerebral perfusion and a reduction in stroke, heart failure, and other cardiovascular-event outcomes.
Acute Chocolate Effects
In a double-blind crossover randomization, 29 men consumed 70 g of chocolate on each of two days separated by at least one week. On one occasion, the chocolate contained normal levels of flavanols, and on the other it was supplemented with extra flavanols.
Ingestion of both types of chocolate decreased AIX (indicating decreased central aortic pressure) but didn’t affect FMD (reflecting endothelial function). Similarly, hematocrit and counts of thrombocytes, lymphocytes, monocytes, and neutrophils went up within two hours. Plasma soluble intercellular adhesion molecule (sICAM) 3, interleukin (IL)-1β, and von Willebrand factor levels went up, and plasma IL-6 levels fell two hours after ingestion of both kinds of chocolate. Insulin also went up after both chocolates, but more so after the high-flavanol kind.
The Four-Week Crossover Trial
The same 29 subjects plus an additional 15 participated in a second double-blind experiment in which four weeks of 70 g per day of either high- or low-flavanol chocolate was followed by a four-week washout period and then crossover to four weeks of the other kind of chocolate. They followed certain dietary restrictions to minimize background flavanol intake.
Four weeks of consuming chocolate of either kind elevated fasting FMD by a percentage point and dropped AIX to a similar extent; both measures reverted to baseline after the washout period. The literature suggests a significant 13% reduction in cardiovascular-event risk for every 1% rise in FMD after chocolate consumption, according to the authors.
In a novel finding, four weeks of chocolate consumption significantly lowered counts of circulating leukocytes, suggesting decreased inflammation; also, “leukocytes can transmigrate through the endothelium and therefore play a crucial role in the formation of atherosclerosis.”
Chocolate also lowered protein expression of lymphocytes CD62L and CD11b, monocyte CD62L, and neutrophils CD66b and CD11c. “These cell-surface molecules are involved in leukocyte recruitment and adherence to the endothelium during the initial steps of atherosclerosis,” the group writes.
“A minor but significant” 0.1-mL rise in fasting plasma glucose and 0.3-mL increase in plasma free fatty acids was evident after four weeks of chocolate of either kind.
Taking the High-Fat Challenge
“High-fat-challenge” tests conducted after each four-week period of chocolate intake required drinking a 95 fat-gram shake of yogurt, canola oil, and other ingredients followed by endothelial-function and metabolic marker tests at 1.5 and 3.0 hours to assess postprandial responses.
Consumption of the high-fat shake was followed by average declines in FMD by 1.8 percentage points, in AIX by four percentage points, and in diastolic blood pressure by 2 mm Hg, regardless of whether the background chocolate contained normal or high flavanol levels. Also seen at postprandial testing were rises in hematocrit; counts of thrombocytes, lymphocytes, monocytes, and neutrophils; plasma concentrations of sICAM1, soluble vascular cell adhesion molecule (sVCAM) 1, sICAM3, P-selectin, IL-8, and tumor necrosis factor-alpha (TNF-α); and expression of lymphocytes CD11c and CD11b, monocyte CD11c and CD11b, and neutrophils CD62l and CD11b adhesion molecules. At the same time, monocyte CD62l expression and IL-6 plasma levels fell.
“Our results indicate that flavanol-enriched chocolate was not healthier than regular dark chocolate with respect to vascular health markers,” according to Esser et al.
Limits on flavanol absorption didn’t account for the similar effects, they determined, based on plasma and urine measures of flavanol intake; normal-flavanol–level chocolate may simply attain maximal flavanol effects on vascular health, the group writes.
This study was funded by Top Institute Food and Nutrition, with the chocolate donated by Barry Callebaut (Lebbeke, Belgium); the authors declare no conflicts of interest.
References
- Esser D, Mars M, Oosterink E, et al. Dark chocolate consumption improves leukocyte adhesion factors and vascular function in overweight men. FASEB J 2014; 28:1464–1473. Abstract