To the Editor, In their review and metaanalysis, Rizos et al reported that omega3 supplementation at low and higher dosages showed no or weak associations with cardiovascular disease (CVD) outcomes, respectively. More recent reviews also showed protective activity of omega3 against CVD outcomes. For instance, omega3 (2–4 g/day) in patients with high or very high triglyceride (TG) levels decreases significantly highsensitivity C reactive protein (hsCRP), lipoproteinassociated phospholipase A2 (LpPLA2), and oxidised low density lipoprotein (LDL)cholesterol (oxLDL) levels, and the reduction of hsCRP is enhanced when coadministered with a statin; hsCRP, LpPLA2 and oxLDL levels are associated with the risk of the major CVD events; and longterm omega3 administration (over a median of 4.9 years) significantly decreases acute myocardial infraction (AMI), coronary revascularisation, unstable angina, cardiovascular death or stroke. Omega3 fatty acids exhibit a beneficial effect on CVD via reprogramming of TGrich lipoproteins metabolism, decreasing inflammatory mediators (cytokines and leukotrienes), and modulating cell adhesion molecules. Beyond CVD, metabolic syndrome (MetS) and Helicobacter pylori infection (Hp-I) are also significant healthcare burdens globally. Both disorders increase the risk of cardiocerebrovascular events, the end point of MetS, and omega3 fatty acids are beneficial against these disorders; omega3 supplements have favourable effects on MetSrelated parameters and inhibitory effects on Hp growth. In this regard, there is an association between HpI and MetSrelated morbidity, including cardiocerebrovascular events; MetS prevalence is higher in Hppositive patients; AMI is closely linked with MetS and Hp-I; HpI is an independent risk factor for atrial fibrillation (AF), which remains frequent arrhythmia in AMI and is closely linked with augmented subsequent cardiocerebrovascular mortality; Hprelated metabolic dysfunctionassociated fatty liver disease, the hepatic component of MetS, is a risk of AF; Hprelated galectin3 and MetS are implicated, as mediators, in the failure of heart and brain; and HpIrelated MetS might contribute to CVD pathophysiology by several mechanisms. Likewise, omega3 and, based on recent data, even omega6 supplements may reduce both atherosclerotic CVD and cancer mortality including HpIrelated MetS gastrointestinal malignancies. Therefore, eradication therapy and improvement of Hprelated MetS parameters mainly by omega3 supplements might benefit cardiocerebrovascular events and even prevention of certain cancers and thus further studies are warranted.