As expected [9
], in this study, CAD risk score increased with age and was related to its diagnostic elements, SBP, TC (nHDL-C) and HDL-C. Furthermore, a strong positive influence of MS and its components (WC, glucose and TG) was observed in CAD risk score. From these, blood pressure and HDL-c are less valid due to the fact they are both CAD risk and MS diagnostic elements.
From the logistic regression analyses, individuals with MS presented a fourfold greater probability of high CAD risk score. The same was observed by Wannamethee et al., (2005) [37
], where men with MS presented a relatively significant risk (RR 1.64; 95% CI; 1.26-2.06) for developing CAD compared to individuals without MS.
The association between MS and CAD risk found in this study was similar the one observed in studies conducted in the United States [38
] and Europe [40
], where they found a 2 to 3 times greater probability for an increase in CAD risk in individuals with MS. A positive correlation was observed of CAD risk score and the number of MS components, that is, the greater the number of MS components the higher the risk of developing CAD.
The hyperuricemia, another component related to MS, has been associated with cardiovascular disease and other pathological processes [42
]. Within this context, UA has been assessed as an independent risk factor for cardiovascular disease, but results are controversial [43
]. Our study showed that CAD risk score increases with higher concentrations of UA. The ARIC study [45
], in which more than 13,500 individuals, including men and women, participated, did not show any association between hyperuricemia and CAD risk. A recent study [46
] conducted in Austria with more than 80,000 men revealed a strong relationship between UA and risk factors for arteriosclerosis. The contradictory results may be justified by methodological differences, such as individuals with a recent history of cardiopathy, use of medications that can influence biochemical results, different ethnic groups or social-economic status [43
One possible, yet contested [47
], pathophysiological mechanism of the association between hyperuricemia and CAD could occur by favoring plaque adhesiveness and thus contribute towards atherogenesis and the formation of blood thrombus [48
A protective effect of muscle mass (MMI) on CAD risk score was found. It is known that the genesis of sarcopenia is associated with an increase in reactive species of oxygen and oxidative stress [49
], with a defined role in different types of cardiovascular disease [50
]. Weinbrenner et al. [51
], studied the relationship between oxidized LDL and other oxidized stress markets with CAD. The authors suggest that the reduction of oxidized LDL, superoxide dismutase and glutathione peroxidase and the increase in oxidized anti-LDL antibodies improves oxidative stress in individuals with CAD.
As in previous studies [52
], it was possible here to observe the beneficial effects of the recommended intake of SFA and dietary fiber on coronary risk. Jakobsen et al [54
] found a positive association between SFA intake and CAD risk among men and women under 60 years of age, but not among individuals over 60 years. In our study the age over 60 seems to influence CAD risk.
A study conducted by Hu et al [55
] on types of fat and their relationship to coronary risk underscores the isocaloric replacement of saturated fat with unsaturated fat, which presents a beneficial effect on reducing CAD risk. Our study did not reveal any relationship with mono or polyunsaturated fat. Hu et al. [56
] conducted a study with more than 80,000 women between 34 and 59 years of age and found significant relations between CAD risk and types of fat, underscoring the high intake of saturated fat as a risk for CAD [56
Our study observed that the percentage of energy from protein and the intake of meat are correlated to CAD risk. This is probably due to excess protein of animal origin and the consequent excess intake of saturated fat with higher coronary risks. Individuals with the lower CAD risk score had the lowest legume intake. They also had the lowest caloric intake which could lead to a lower amount of food intake, and a lower intake of legumes.
The mechanism by which SFA influences CAD risk would be by activating Toll-Like 4 receptors, which through free fatty acids stimulate the inflammatory response [57
]. Studies have demonstrated the role of inflammation in CAD and other complications [58
The effects of dietary fiber on CAD risk occur through various mechanisms, such as improved lipid standards [60
], reduced blood pressure [61
] and improved insulin sensitivity [62
]. Pereira et al [63
] suggest that dietary fiber intake is inversely associated with CAD risk. In this study, the authors indicate a 10 to 30% reduction in coronary risk for every 10g/day of fiber from cereals and fruit [63
]. Soluble fiber and its relation to CAD risk has also been shown in several studies [64
]. Pietinen et al [66
] found an inverse association of soluble fiber with CAD risk. In this study, we did not identify the main dietary sources and fiber types and their possible relations with CAD risk score. A review identified 9 prospective studies on the relation of dietary fiber with CAD risk [67
]. Among the studies, 7 found a negative association of fiber intake with CAD risk, and 2 studies presented controversial results [67
In this paper, we studied the role of recommended intake of SFA and dietary fiber on CAD risk score after adjustments for TCV and BMI. The adjustment for total energy intake is used to provide isocaloric conditions for the studied sample [68
]. Thus, the existing difference between an individual with TCV of 3000 kcal and another with 1000 kcal would be cancelled, considering only the % of macronutrients. The adjustment for BMI aims at eliminating the effects of adiposity on CAD risk score. Thus, the adjustment for TCV and BMI in the same model aims at annulling excess calories the obese individual may have.
The limitations in this study were the type of study and the food method record. It was a cross-sectional study and some cause/effect relations cannot be proven, only the presence or not of an association between the factors. A single 24-hour dietary recall is based on foods and amounts actually consumed by an individual on one specific day, which has an important limitation for not capture intra-individual variability in food intake. The ideal procedure would be to apply the food method record at least 3 days per week. Furthermore, other limitation was the study sample; a drop-off of 45% could reduce the impact of our results.
Another weak point was related with the muscle mass quantification by BIA in which muscle mass is calculated from lean body mass which is complementary to fat body mass. Then high muscle mass would mean also low fat mass and fat mass is well known as pro-inflammatory and CAD risk factor.