Why Accumulating Body Fat Makes Us More Vulnerable To Covid-19

Surely you know the story told in Homer’s Iliad. It tells how the Greeks, after several years trying to conquer Troy, achieved their goal thanks to a huge wooden horse inside which their soldiers hid. Taking advantage of the darkness of the night, they assaulted the city from within.

Well, it seems that our enemy SARS-CoV-2 has found an unexpected Trojan horse inside us that helps him in his fight: our body fat.

A Trojan horse for coronavirus infection

SARS-CoV-2 enters the body’s cells when a protein on its envelope, the so-called spike or viral S protein, binds with angiotensin-converting enzyme type 2, a membrane molecule of several types of human cells.

In the obese phenotype, the expression of these membrane molecules in adipose tissue is increased. And that makes fat the ideal reservoir for the virus after it enters the body, remaining in the body of obese patients for longer .

As if that were not enough, in animal models of obesity it has been observed that angiotensin-converting enzyme type 2 also increases in lung cells. This implies a greater number of binding sites for the virus and favors the entry of viral particles into the pulmonary epithelium. The intensity of the infection increases, as does the local response in the lungs, the main place where the battle is waged to prevent the development of covid-19.

To this must be added that people with obesity present a low-grade chronic inflammatory state0 that activates a local immune response characterized by the mobilization of immune cells that produce proinflammatory substances.

This leads to a poor immune response that increases susceptibility to infections, including that caused by SARS-CoV-2. This immune deficit, together with the previous situation of inflammation, can amplify the well-known cytokine storm triggered after viral infection, producing a worsening of symptoms.

On the other hand, excess abdominal fat in people with obesity prevents the correct displacement of the diaphragm during breathing, reducing lung capacity and generating difficulties that predispose to the development of respiratory infections.

It is not the first time that obesity has been defined as a risk factor for infections caused by respiratory viruses. In 2009, during the pandemic caused by the H1N1 influenza virus, obesity was associated with an increased risk of hospitalization and ICU admission after viral infection.

Jams and supply problems

Imagine the body of an obese person as a walled city. The high amount of dysregulated adipose tissue it contains means that, under normal conditions, the city suffers from an obstruction in the supply routes (due to hypertension, atherosclerosis, or cardiovascular pathologies). But also difficulties with the supply and management of food (insulin resistance and diabetes) and with the entry of air (due to respiratory difficulties).

Access to this city already weakened and sick, would be relatively easy for an invader like the one causing covid-19, since the adipose tissue would behave like a Trojan horse. That is, it would serve as a refuge for the new enemy. Who, by the way, would find more entrance doors in the green zone of the city’s air supply (the lung, in our body).

The disaster would be absolute. Especially since when the soldiers of the city’s immune army tried to expel the enemy, their poor response would cause even more “urban” damage as a result of the cytokine storm.

In addition, by attacking the Trojan horse (or adipose tissue), invaded by the virus, adipocyte death would occur. And the streets of the city would be filled with waste (drops of fat), which would clog them up and predispose us to develop fat embolism syndrome. A syndrome that triggers the probability of suffering a thrombotic event. This would generate even greater problems of movement of goods and distribution of food.

In short, excess body fat only worsens the symptoms of SARS-CoV-2 infection and increases the risk of hospitalization and death.

Older and female “cities” suffer more

When the city affected by obesity is male, the distribution of adipose tissue at the visceral level is greater. This causes an increase in pro-inflammatory cytokines that leads to greater activation of immune cells, which makes men more at risk of triggering the famous cytokine storm responsible for the worsening and aggravation of COVID-19 symptoms.

With everything and with that, it seems that the devastating effect of the disease in the long term is greater when that city belongs to the female sex. Now that enough time has passed to see the consequences of the disease, it has been found that, among the risk factors for the post-covid-19 syndrome, having obesity and being a woman predisposes to persistent covid.

Continuing with the simile, since the beginning of the pandemic it has been observed that older cities (over 55 years of age) would have a higher risk of being destroyed by the invasion (higher mortality). Even in people with normal weight. However, from the beginning of the pandemic, we observed that the young “obese city” suffered the same effects as the older “normal weight cities”.

All this explains the greater propensity of people with obesity to develop SARS-CoV-2 infection with more severe symptoms and need hospitalization, mechanical ventilation, and intensive care. It also explains why people with obesity often require prolonged hospitalization and more intense treatments: they take longer to eliminate the presence of the virus. In the longer term, the presence of obesity increases the risk of developing chronic sequelae of covid-19.

Having seen what has been seen, we should reflect on the need to make significant efforts, both personally and from all the levels involved, to implement all the measures that help alleviate the current obesity epidemic.

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