In times of Covid, food-related problems acquire primary importance. Obese subjects or those with diabetes who contract the coronavirus show an exacerbation of the respiratory syndrome accompanied by pulmonary fibrosis, with a higher incidence ranging from 33 to 41% of the observed cases.
This is what emerges from a study (Obesity and diabetes as comorbidities for COVID-19: Underlying mechanisms and the role of viral–bacterial interactions) published by the Department of Cell Biology of Dallas in Texas which related the greater morbidity of the subjects obese or diabetics facing coronavirus infection.
The same study specifies that the causes of this phenomenon are not yet fully understood, however the researchers have ascertained an indirect interaction precisely in the greater expression of ACE2 in visceral adipose tissue compared to the lungs.
In the awarding of the Nobel Peace Prize to the World Food Program we read 'until the day we have a medical vaccine, food is the best vaccine against chaos'”.
A good general condition of the patient and a correct and balanced diet following the principles of the Mediterranean diet, at the base of which we find many vegetables, a little bit of fruit , bread pasta and cereals (preferably wholemeal). they therefore represent a valid aid in fighting the infection.
ACE2 (Angiotensin II Converting Enzyme-2) is a protein found naturally on the outer wall of the human cell membrane and which performs the important task of reducing angiotensin II to angiotensin I; the latter causes vasodilation, an anti-inflammatory effect and organ benefits. The effectiveness of this protein tends to decrease in the elderly. Well regulated ACE2 ordinarily exerts a protective effect on human health.
The dual role of ACE2. Source: elaboration by the author
It should be remembered that viruses are not living beings, but simply portions of DNA or RNA covered by a protein capsule equipped with projections that act as "sensors".
When these protrusions meet a complementary sensor on the surface of the human cell, they adhere to it, triggering a mechanism very similar to a key entering a keyhole.
The cell membrane opens, the virus is incorporated into the cell and its DNA/RNA, now free to circulate inside it, interacts with the human one, forcing it to replicate the virus itself. The process ends with the death of the human cell and the proliferation of viral cells.
The attack of the virus on the ACE2 protein reduces its effectiveness and functionality with an inevitable greater accumulation of angiotensin II in the human body with an evident increase in lung and heart damage.
Numerous studies have recently confirmed that adipose tissue cells have a greater number of ACE2 receptors on their membranes during the condition of obesity and diabetes; through the bloodstream this protein can be transmitted from the visceral fat into the lung tissue, effectively increasing the susceptibility to the entry of the virus.
The greater diffusion of the ACE2 protein seems to be connected with the need on the part of the subject to reduce the higher plasma levels of angiotensin II which causes vasoconstriction, pulmonary edema and cardiac damage, for this reason patients already burdened by other pathologies seem to show greater susceptibility to COVID.
The condition of obesity is not closely related to COVID infection, but is more generally associated with viral infections, since the same mechanism was intercepted during swine flu (H1N1) infection
Difference between the state of the lungs of a normal weight patient and an obese one. Source: Obesity and diabetes as comorbidities for COVID-19: Underlying mechanisms and the role of viral–bacterial interactions, 2020.
