**5.3 Cardiovascular disease**

The microbiota and its metabolites also modulate the risk and progression of atherosclerosis. Changes in the microbiota diversity and structure have been described in people with atherosclerotic cardiovascular disease (ACVD). As cardiovascular disease is a complication of obesity as well as diabetes, the identified mechanisms coincide with those we have described for these diseases. For example, in a study with 218 patients with ACVD [77], an increased abundance of Enterobacteriaceae and *Streptococcus* spp. was found, with a decrease in butyrate-producing bacteria such as *Prevotella copri* and *Alistepes Shahii*, when compared with the fecal microbiota from 187 healthy controls. Thus, among the associated mechanisms stand out the induction of inflammation, the alteration of lipid metabolism and glucose homeostasis, as well as bacterial translocation. These findings are secondary to alterations in the F/B ratio and in the profile of metabolites such as SCFAs, TMAOs, and BA [78]. In the pathophysiology of ACVD, TMAOs, in particular, have been linked to increased foam cell activation, prothrombotic platelet response, and reverse cholesterol transport, raising the risk of myocardial infarction, stroke, and death [78].

Given that both cardiovascular disease and T2D have a pre-pathogenic period that can last for decades, and because overweight development usually begins in childhood, the perinatal period and early childhood represent a window of opportunity for their prevention and risk modulation.
