Impact of chocolate liquor on vascular lesions in apoE-knockout mice.

Cocoa polyphenols are thought to reduce the risk of cardiovascular diseases. Thus, cocoa-containing foods may have significant health benefits. Here, we studied the impact of chocolate liquor on vascular lesion development and plaque composition in a mouse model of atherosclerosis. Apolipoprotein E (apoE)-knockout mice were assigned to two groups and fed a Western diet that contained 250 g/kg of either chocolate liquor or a polyphenol-free isoenergetic control paste for 16 weeks. In addition to fat, protein, and fibers, the chocolate liquor contained 2 g/kg of polyphenols. Compared with the control group, mice fed the chocolate liquor had larger plaque areas in the descending aorta and aortic root, which were attributed to a higher mass of vascular smooth muscle cells (VSMCs) and collagen. Vascular lipid deposits and calcification areas did not differ between the two groups. The aortic tissue level of interleukin-6 (IL-6) mRNA was 5-fold higher in the mice fed chocolate liquor than in the control mice. Chocolate-fed mice exhibited an increased hepatic saturated to polyunsaturated fatty acid ratio than the controls. Although the chocolate liquor contained 14 µg/kg of vitamin D2, the chocolate liquor-fed mice did not have measurable 25-hydroxyvitamin D2 in the serum. These mice even showed a 25% reduction in the level of 25-hydroxyvitamin D3 compared with the control mice. Overall, present data may contribute to our understanding how chocolate constituents can impact vascular lesion development.

Association of glycaemic index and glycaemic load with metabolic syndrome in an Iranian adult population: Isfahan Healthy Heart Program.

AIM: There is controversy around the clinical effects of the dietary glycaemic index (GI) and glycaemic load (GL) on cardiovascular diseases risk factors such as metabolic syndrome (MetS). So, the present study was performed to evaluate the relationship between GI or GL and metabolic syndrome in an Iranian adult population in 2007. METHODS: The study was based on data from a sub-sample of the Isfahan Healthy Heart Program (IHHP), collected across three cities in central Iran, in the year 2007. This was a cross-sectional survey of 1618 randomly selected adults aged ≥19 years. Nutritional assessment was conducted by a single 24-hour recall questionnaire. Fasting serum lipids, anthropometric indicators and blood pressure were measured by standard methods. Analysis of covariance was used to compare metabolic syndrome components according to energy-adjusted GI and GL levels. To expose the effect of potential confounders, hierarchical logistic regression models were utilised to determine adjusted odds ratios (OR) and 95% CI. RESULTS: After adjustment for age, gender, body mass index and energy intake, high GI was found to be significantly associated with MetS (OR 95% CI) (1.46 (1.01-2.12)). This was attenuated marginally by excluding the confounding effects of dietary fibre intake (1.29 (1.01-1.74)). All hierarchical models illustrated no significant association between energy-adjusted GL and the risk of MetS adjusted for confounders. CONCLUSIONS: There is a positive relationship between dietary GI, but not GL, and the presence of MetS after adjustment for potential confounders. However, studies with long duration of follow up and experimental studies are still required to confirm this relationship.

Fish protein increases circulating levels of trimethylamine-N-oxide and accelerates aortic lesion formation in apoE null mice.

SCOPE: The protective effect of fish consumption on the cardiovascular system has primarily been ascribed to n-3 fatty acids, but data investigating the vascular effects of fish protein consumption are scarce. This study aimed to investigate the vascular impact of fish protein in a mouse model of atherosclerosis. METHODS AND RESULTS: Male apoE null mice were fed a Western diet containing 20% fish (turbot) protein, casein, or soy protein, for 16 wk. Morphometric analysis of the aorta revealed that the atherosclerotic plaque area of fish protein fed mice was twofold larger than that in casein- or soy protein-fed mice. The percentage area of calcification deposits in plaques of fish protein fed mice was higher (7.57%) than that in casein-fed (2.86%) or soy protein-fed (3.46%) mice, and fish protein fed mice exhibited higher plaque expression of CD68, CD36, and IL-6 than the other two groups. Fish protein intake was accompanied by increased serum concentrations of trimethylamine-N-oxide (7.03 ± 2.83 µmol/L), as compared with casein (0.92 ± 0.46 µmol/L) and soy protein (1.32 ± 0.54 µmol/L) intake. CONCLUSION: The present data indicate adverse effects of fish protein on the vascular system, which could be attributable to the high serum trimethylamine-N-oxide concentrations in these mice.

The Antiatherogenic Effect of Fish Oil in Male Mice Is Associated with a Diminished Release of Endothelial ADAM17 and ADAM10 Substrates.

BACKGROUND: Growing evidence suggests that disintegrin and metalloprotease (ADAM) 17 (ADAM17) and ADAM10 contribute to the pathogenesis of vascular diseases. ADAM17 promotes inflammatory processes by liberating tumor necrosis factor α, interleukin 6 receptor (IL-6R), and tumor necrosis factor receptor 1 (TNFR1). ADAM17 and ADAM10 modulate vascular permeability by cleaving endothelial adhesion molecules such as junctional adhesion molecule A (JAM-A) and vascular endothelial cadherin (VE-cadherin), respectively. OBJECTIVE: This study was designed to investigate whether a link might exist between the protective effects of fish oil (FO) supplementation against atherosclerosis and ADAM function. METHODS: Male LDL receptor knockout (LDLR(-/-)) mice and male wild-type (WT) mice were fed a Western diet (200 g/kg fat, 1.5 g/kg cholesterol) containing either 20% lard (LDLR(-/-)-lard and WT-lard groups) or 10% lard combined with 10% FO (LDLR(-/-)-FO and WT-FO groups) for 12 wk. Atherosclerotic lesion development and fatty acid composition of liver microsomes were evaluated. ADAM10 and ADAM17 expression was determined by quantitative real-time polymerase chain reaction and immunoblot analyses. Concentrations of soluble ADAM substrates in plasma and liver extracts were measured by ELISA. RESULTS: Diets supplemented with FO markedly reduced development of early atherosclerotic lesions in LDLR(-/-) mice (LDLR(-/-)-lard group vs. LDLR(-/-)-FO group mean ± SD: 29.6 ± 6.1% vs. 22.5 ± 4.2%, P < 0.05). This was not accompanied by changes in expression of ADAM17 or ADAM10 in the aorta or liver. No dietary effects on circulating TNFR1 (LDLR(-/-)-lard group vs. LDLR(-/-)-FO group mean ± SD: 1.22 ± 0.23 vs. 1.39 ± 0.28, P > 0.2) or IL-6R (1.06 ± 0.12 vs. 0.98 ± 0.09 fold of WT-lard group, P > 0.1), classical substrates of ADAM17 on macrophages, and neutrophil granulocytes were observed. However, a reduction in atherosclerotic lesions in the LDLR(-/-)-FO group was accompanied by a significant reduction in the circulating endothelial cell adhesion molecules JAM-A (LDLR(-/-)-lard group vs. LDLR(-/-)-FO group mean ± SD: 1.42 ± 0.20 vs. 0.95 ± 0.56 fold of WT-lard group, P < 0.05), intercellular adhesion molecule 1 (1.15 ± 0.14 vs. 0.88 ± 0.17 fold of WT-lard group, P < 0.05), and VE-cadherin (0.88 ± 0.12 vs. 0.72 ± 0.15 fold of WT-lard group, P < 0.05), reflecting reduced ADAM activity in endothelial cells. CONCLUSION: FO exerted an antiatherogenic effect on male LDLR(-/-) mice that was accompanied by a reduced release of ADAM17 and ADAM10 substrates from endothelial cells. It is suggested that FO-decreased ADAM activity contributes to improved endothelial barrier function and thus counteracts intimal lipoprotein insudation and macrophage accumulation.

Inverse association between the frequency of nut consumption and obesity among Iranian population: Isfahan Healthy Heart Program.

PURPOSE: Recently, controversies have arisen concerning the association between nut intake and obesity. This study was performed to investigate the relationship between nut consumption and obesity among Iranian adults. METHODS: In a cross-sectional survey, 9,660 randomly chosen adults aged ≥19 years were selected based on gender, age and their settlement distributions in three districts of central Iran in 2007. Nutritional behaviors including regular intake of walnuts, almonds, pistachios, hazelnuts and sunflower seed were assessed by validated 48-item-food-frequency questionnaire and a 24-h recall questionnaire. Using hierarchical logistic regression test, odds ratio (OR) 95% CI of obesity based on nut consumption was determined in an unadjusted and four adjusted models. RESULTS: The results showed a significant association between high nut consumption and lower prevalence of overweight or general obesity as well as abdominal obesity in women (p = 0.01 and p = 0.047, respectively), but not men. The frequency of nut consumption was associated with lower risk of overweight or general obesity [OR (95% CI) 0.57 (0.38-0.86)] and abdominal obesity [OR (95% CI) 0.51 (0.28-0.95)] only in women. After adjusting for gender, age and other potential confounders, the strength of the associations was blunted, but they were still significant. CONCLUSIONS: Frequent nuts and seeds consumption, particularly ≥1 time/day, had an inverse association with all classes of obesity among women.

"Fishing" for the origins of the "Eskimos and heart disease" story: facts or wishful thinking?

During the 1970s, 2 Danish investigators, Bang and Dyerberg, on being informed that the Greenland Eskimos had a low prevalence of coronary artery disease (CAD) set out to study the diet of this population. Bang and Dyerberg described the "Eskimo diet" as consisting of large amounts of seal and whale blubber (ie, fats of animal origin) and suggested that this diet was a key factor in the alleged low incidence of CAD. This was the beginning of a proliferation of studies that focused on the cardioprotective effects of the "Eskimo diet." In view of data, which accumulated on this topic during the past 40 years, we conducted a review of published literature to examine whether mortality and morbidity due to CAD are indeed lower in Eskimo/Inuit populations compared with their Caucasian counterparts. Most studies found that the Greenland Eskimos and the Canadian and Alaskan Inuit have CAD as often as the non-Eskimo populations. Notably, Bang and Dyerberg's studies from the 1970s did not investigate the prevalence of CAD in this population; however, their reports are still routinely cited as evidence for the cardioprotective effect of the "Eskimo diet." We discuss the possible motives leading to the misinterpretation of these seminal studies.

Effect of vitamin supplementation on serum oxidized low-density lipoprotein levels in male subjects with cardiovascular disease risk factors.

OBJECTIVE(S): Oxidized low-density lipoproteins (ox-LDLs) appear to play a significant role in atherogenesis. In fact, circulating ox-LDL concentrations have been recognized as a risk factor for cardiovascular disease (CVD). The main objectives of this study were to assess the effects of antioxidant vitamins on ox-LDL as a biomarker of CVD in male subjects with CVD risk factors. MATERIALS AND METHODS: The effect of antioxidant vitamins on ox-LDL as a biomarker of CVD in male subjects with CVD in male subjects with CVD risk factors at baseline and after 12 weeks of supplementation with vitamin E (400 IU), C (500 mg), ß-carotene (15 mg), and the combined supplements (E, C, and ß-carotene) respectively defined as group E, C, B and control group was considered as group P. RESULTS: The mean values for ox-LDL at the baseline were 86.93 ± 26.30 U/l in group C, 94.52 ± 38.40 U/l in group E, 79.73±2.07 U/l in group B, 85.97±23.07 U/l in combined group, and 84.90± 14.66 U/l in group P. After 12 weeks of intervention the percentage of changes for group C, group E, group B, COM group, and group P were (-18.32), (-2286), (-17.31), (-19.01) and (-2.0), respectively. Using Wilcoxon method, significant differences were detected in the mean ox-LDL concentrations of baseline and after intervention, values in the C, E, B and combined groups (P< 005). CONCLUSION: This study illustrated that diet supplemented with vitamin C (500 mg), vitamin E (400 IU), ß-carotene (15 mg), and the combination of these vitamins was associated with lower serum ox-LDL levels.