BackgroundSeveral studies have shown that cocoa and cocoa-containing foods have the potential to lower blood pressure and improve endothelial function. Most of the studies reporting the beneficial effects of dark chocolate on blood pressure have been short (≤ 4 weeks). The aim of the present 8-wks (weeks) study was to assess the effects of regular consumption of dark chocolate during a reduced snack consumption intervention on blood pressure and other cardiovascular risk factors in mildly hypertensive individuals.DesignThis was a randomized, controlled, cross-over trial involving 22 adults (8 women, 14 men), aged 33–64 y, BMI 27.7 ± 3.7 kg/m2 with mild hypertension. During the intervention period (8-wks) the participants reduced the intake of habitual snacks and replaced them with dark chocolate (49 g/day). In the control period, they only reduced the snacks without any added chocolate. Data (blood lipid profile, glucose, insulin, 24 h blood pressure) was collected in the beginning and end of both periods (intervention and control), and some variables also in the run-in and run-out periods (weight, body fat percentage, blood pressure, arterial stiffness index, diet and physical activity).ResultsDaily consumption of dark chocolate had no effects on 24 h blood pressure, resting blood pressure (mean ± SD, pre 142 ± 11.5/89 ± 8.4 mmHg vs. post 142 ± 14.2/88 ± 9.4 mmHg in systolic and diastolic blood pressure, respectively) or arterial stiffness (mean ± SD, pre 7.68 ± 0.88 vs. post 7.76 ± 0.89).Weight was reduced by 1.0 ± 2.2 kg during the control (reduced snack only) period, but was unchanged while eating chocolate (p < 0.027 between the treatments).ConclusionThe data collected in this study indicates that inclusion of dark chocolate daily in the diet had no significant effects on blood pressure or other cardiovascular risk factors during a reduced snack period.Trial registrationClinicalTrials.gov identifier NCT02130141

Normal melanocytes require growth support provided by the adjacent basement membrane. In contrast, nevus cells and melanoma cells survive in the dermis, and in vitro on a soft collagen gel. Transforming growth factor-beta1 (TGF-beta1) produced by melanocytes themselves induces apoptosis in normal melanocytes cultured on collagen gel, an effect that can be counteracted by fibroblast growth factor-2 (FGF-2). The purpose of this study was to investigate the mechanisms by which FGF-2 counteracts the apoptotic signals from TGF-beta1 in melanocytes cultured on collagen gel. We report that FGF-2 did not interfere with the signal transduction from the TGF-beta1 receptors to SMAD2/3 proteins. Instead, TGF-beta1 decreased the level of Bcl-2 in normal melanocytes cultured on collagen gel, and FGF-2 reversed the TGF-beta1-mediated reduction in the level of Bcl-2. In nevus and melanoma cells, TGF-beta1 was unable to induce a decrease in the level of Bcl-2, and treatment with FGF-2 did not cause an increase in the level of Bcl-2 in nevus or melanoma cells. In conclusion, our results suggest that a reduction in the level of the anti-apoptotic Bcl-2 is involved in the execution of apoptosis induced by TGF-beta1 in normal melanocytes cultured on collagen gel and that FGF-2 can prevent TGF-beta1 from causing this reduction.