4. Discussion
inflammation, atherosclerotic cardiovascular disease
ADHESION, INFLAMMATION, PATHOGENESIS, ATHEROSCLEROTIC CARDIOVASCULAR DISEASE
The present work was conducted, in the first place, to determine whether a simple modification of the eating pattern, such as the modification of the type of fat consumed at breakfast, was enough to modify the profile of inflammatory markers. Additionally, we aimed to identify the most suitable fat choice for breakfast to improve the synthesis profile of inflammatory factors. Based on the data obtained, it can be stated that while not all inflammation parameters exhibited significantly modifications, certain changes allowed us to confirm the ability of the intervention to modify the inflammatory profile of the subjects.As early as 2002, Han et al. conducted a crossover trial with a similar intervention duration (30 days), demonstrating that a diet rich in unhealthy fats led to a significantly higher production of IL-6 and TNFα, compared to a diet abundant in n-6 polyunsaturated fat (soybean oil) [Several factors might contribute to the lack of effect observed in these studies. The type and quantity of fat, for instance, can play a role. Studies using low doses of fat, as seen in Schubert et al. [However, the influence of other factors cannot be ruled out. As demonstrated by Schüler et al., dietary patterns and genetics can interact to determine plasma concentrations of markers like VEGF by up to 90% [Focusing on the specific effects resulting from the various interventions performed in this study, our data indicates that the intervention leading to the most significant changes was the high-MUFA breakfast (virgin olive oil, VOO). Specifically, the high-MUFA breakfast induced a statistically significant reduction in IL6 and VEGF levels, along with observed reductions in the synthesis of other factors like IL1α and CRP. The decrease in IL6, along with its downstream product CRP, holds substantial relevance in enhancing atherosclerotic cardiovascular disease management, given that multiple previous studies in humans have shown that elevated levels of these factors correlate with heightened cardiovascular risk [Previous randomized clinical trials that involved modifying whole dietary fat using olive oil (High-MUFA) have yielded results consistent with those in our study. These trials have demonstrated reductions in IL6 and CRP, as well as decreases in other inflammation markers such as VCAM-1, ICAM-1, and E-selectin [The impact of the high-MUFA breakfast was not positive across all inflammatory parameters. Interestingly, while VEGF levels decreased, plasma EGF levels increased significantly by the end of the intervention. Both factors play pivotal roles in vasculogenesis and angiogenesis and have been implicated in vascular pathogenesis [Regarding the high-SFA (butter) breakfast, we did not find any significant change in the inflammatory markers, which is partially in contradiction with previous studies that have shown an increase in the synthesis of pro-inflammatory factors with these types of fatty acids [At this time, it would be important to address certain limitations of the study. Firstly, it must be acknowledged that the findings derived from this study can solely be extrapolated to women. Secondly, although we have examined some of the most pertinent inflammatory markers, numerous other factors remain—particularly those related to molecular adhesion—that could offer additional insights into the impact of different fat types. Another constraint that may have limited the obtention of more pronounced outcomes is the relatively modest quantity of fat dispensed to the participants. Nonetheless, the rationale behind this approach is rooted in our aspiration to evaluate the effects of fat quantities similar to those typically consumed during breakfast. Lastly, despite the fact that the statistical analyses were performed by incorporating the participants’ baseline clinical characteristics, we cannot dismiss the potential influence of other factors that were not considered in this study.