[Acute respiratory syndrome with various signs and outcomes caused by the SARS-CoV-2 virus is the biggest challenge facing health systems worldwide today. The renin-angiotensin-aldosterone and kinin-kallikrein systems and within these two endopeptidases (ACE and ACE2) play a crucial role in the developing clinical feature of COVID-19. Adverse effects of the ACE-stimulated Ang II/AT1R axis (oxidant, pro-inflammatory effect, vasoconstriction) are counterbalanced by the ACE2-induced AT2R and MasR activities (antioxidant, anti-inflammatory effect, vasodilation). The severity of SARS-CoV-2 pneumonia and systemic inflammation explains the impairment of ACE2 (as an important defence factor of the lungs) caused by the biding spike protein of the SARS-CoV-2, which decreases the ACE2 levels. In parallel, bradykinin production also increases and intensifies the SARS-CoV-2-induced cytokine storm through the BKB1 and BKB2 receptors. Since the RAAS inhibitors (ACEI, ARB) affect the two regulatory systems and enzymes at different sites and to different degrees, their role must urgently have been clarified in the COVID-19 since their use is essential and general of many population-wide diseases (hypertension, cardiovascular, renal and metabolic conditions). Based on pathophysiological and experimental data, it is reasonable to hypothesize that in COVID-19 with comorbidities, especially in the elderly, the decreased ACE2 expression may be restored by RAAS inhibitors and the missed or reduced protective effect may be revitalised. This protective effect applies to both RAAS inhibitors. Clinical trials clearly support the declared opinion of many international societies that the use of RAAS inhibitors does not increase the risk of the occurrence of SARS-CoV-2 in itself let alone the severe and critical cases. Accordingly, initiated RAAS inhibitor therapy not only may rather must be continued during the development of COVID-19.]

[Cholesterol-lowering statins are the most tested medications in respect of the effects and side-effects. Based on these, we can safely claim that most of the negative opinions about cholesterol-lowering are not realistic. It is not a panacea, but it is proven that around a 30% of cardio- and cerebrovascular risk reducation can be achieved by their regular taking, while the incidence of side effects and risks are at least one order of magnitude lower in each patient groups. For cholesterol, there is no “normal” lab threshold or low level, only “target values”, since the mean value in the general population is high in regard of atherosclerosis (the values measured at birth and among natural people can be considered normal). Let us appreciate the cholesterol- lowering medications because we do not have a large armamentarium!]

["Let's play cards"; you could say it's a collective gamble that costs a lot of money and the payoff is as uncertain as a dog's dinner. Everyone expects a lot from it: we, the primary care doctors (at present, district, general practitioners and family doctors in the process of metamorphosis), and the patients, who are increasingly waiting outside the doors of our surgeries. ]

["Money or Life!?" Our work as doctors has always been closely linked to philosophical and social problems, but often - unfortunately - even to daily politics. I am thinking here, for example, of the debates surrounding abortion or euthanasia, where only one thing can be said for sure: there is no solution that is acceptable to everyone.]

[After the natural substances in food, let's look at the arteficial, chemical substances that are intentionally introduced into our food during its preparation, preservation, storage, cooking and preparation. One of the most common of these is salt (table salt, NaCl). The association between high salt intake in food and the incidence of gastric cancer has been found in an analysis of comparative geographic pathology data. It is lowest in the USA and Australia and highest in East Asia and Japan.]