Are Patients with Diabetes and Hypertension vulnerable to Coronavirus?

Are Patients with Diabetes and Hypertension vulnerable to Coronavirus?

The two most frequent comorbidities in patients infected by coronavirus are diabetes and hypertension.

We know there are groups of population that are more vulnerable to SARS-CoV-2. Moreover, those with comorbidities (diseases) like the ones we have mentioned have higher risk of death due to the virus.

The main problem lies in our society, which is not only aging, but it is also devastated by chronic diseases.
  • But where is the link between metabolism and a worse infection?
  • What specific mechanisms are failing or making it easier for the virus to attack people with metabolic diseases?
This is what the last review from Nature Reviews Endocrinology (Bornstein et al., 2020) is all about, which is what we are going to talk about in this post.

Metabolism and Viral Infections

As you know, SARS-COV-2 is not the first virus that has caused us problems.

Not many years ago, we witnessed the pandemic of SARS and MERS-CoV in the Middle East. Well, diabetes and hypertension were also the most frequent comorbidities in both cases.

Blood pressure

The American CDC has told us that the metabolic syndrome increases the risk of death by COVID-19  up to 10 times according to the latest reports.

Therefore, there must be a specific connection between a damaged metabolism and a viral infection.

You may probably think that this is not new: a metabolic disease complicates the evolution of any disease, weakening the organism in general.

Yes, but it seems that there are also specific and particular mechanisms that connect coronavirus to the metabolism.

Let’s explain that.

Cytokine Storm

You may have probably heard the term “cytokine storm” lately.

Cytokines are messenger molecules that are neither good or bad.

Cytokines

For example, the myokines derived from muscle contraction are cytokines with a clear anti-inflammatory effect.

However, our immune response against the SARS-COV-2 triggers a brutal increase of pro-inflammatory cytokines in the second stage of the disease. The first stage has a high viral charge, the second phase is more “immunological”, when the viral charge has dropped.

Most of the time, those who die due to coronavirus are not killed by the virus itself. In fact, they die due to the immune response of their own body to eradicate the virus.

Then, what happens?

This “perfect storm” made of pro-inflammatory cytokines intensifies when we have a damaged metabolism or low systemic inflammation.

That is the difference between throwing a match in a barren wasteland or a forest soaked in gasoline.

Infection

The Entry

The virus enters the cells of our respiratory system by using a key on a lock.

The key is a glycoprotein with spikes and the lock is the angiotensin converting enzyme 2 or ACE2. It is located in the surface of the human cells (cells from the respiratory apparatus in this case).

People with hypertension and type 2 diabetes have a higher expression of ACE2.

Therefore, the first hypothesis for an unfavorable result is that these patients have more locks in their cells to which the virus can bind.

If you want to learn more about Diabetes, click this link

Diabetes

But that is not all

The conversion of Angiotensin II into Angiotensin 1-7 regulates the so-called renin-angiotensin-aldosterone system.

If this Angiotensin II is not transformed by the ACE2 because the virus has rendered it useless, it will increase the AGTII concentrations as well as its functions.

To sum up:

  • Pro-inflammatory effect
  • More aldosterone release

This will lead to hypopotassemia, which will increase the vascular permeability. In addition, it will increase the risk of RDS or respiratory distress syndrome (one of the main causes of death in these patients).

On the contrary, angiotensin 1-7 (which will drop) has an anti-inflammatory and anti-fibrotic effect by activating the receptor.

That response would be more than beneficial for the recovery of the patients with COVID-19.

Other Metabolic Nexuses

When the virus SARS-CoV (which causes SARS, not COVID-19) joins the receptor ACE2 in the pancreatic cells, it directly damaged the pancreatic islets and reduced the insulin release.

In fact, those patients who were infected by SARS and who id not have a history of diabetes or corticosteroid treatment were compared to their healthy siblings. The study lasted three years after they were infected.

Hospitalization

During their hospitalization, more than a 50% of the patients developed diabetes and only a 5% of them still suffered diabetes after three years (Yang et al., 2010).

Therefore, since the pancreas releases the ACE2 protein, coronavirus can enter the beta-pancreatic cells and cause a dysfunction of Beta cells. Consequently, it triggers hypoglycemia and Type 2 Diabetes, which will be transitory in most cases.

Moreover, as we have seen before, DMT2 increases the ACE2 expression in other tissues like the lungs, liver and heart. This could explain why these patients run a higher risk of infection and multi-organic failure.

In addition, it would also explain why we are being so sceptical about using angiotensin-converting enzyme inhibitors (which transforms angiotensin I in II). This would actually increase the ACE2 expression in human cells.

The higher the number or locks, the higher the chances of entering in the rooms (cells).

Hypertension

Messages to Send Home

Nothing in human biology can escape the metabolism, it is ubiquitous.

A damaged metabolism will lower the physiological vital reserves and increases the risk of suffering multiple diseases.

Moreover, in the case of SARS-CoV-2, there are specific mechanisms that increasing the metabolic damage, affecting the progress of the virus:

  • Increasing the general expression of ACE2 in the tissues.
  • Increasing the actions of angiotensin II in the lung, increasing the SRDS (severe respiratory distress syndrome).
  • Damaging the beta pancreatic cells directly.
  • If we combine it with the metabolic damage of Obesity, the infection mechanisms can hinder the breathing mechanisms, increasing systemic inflammation,etc.

If you liked this post, we can make another one about Obesity and SARS-Cov-2.

See you in the next one!

Bibliography

  1. Bornstein, S. R., Dalan, R., Hopkins, D., Mingrone, G., & Boehm, B. O. (2020). Endocrine and metabolic link to coronavirus infection. Nature Reviews Endocrinology, 1–2.
  2. Yang, J. K., Lin, S. S., Ji, X. J., & Guo, L. M. (2010). Binding of SARS coronavirus to its receptor damages islets and causes acute diabetes. Acta Diabetologica.

Related Entries

  • Coronavirus: A Critical Approach on this link
  • Why will COVID-19 change Medicine? Point of view of a physician here.
Coronavirus, Diabetes and Hypertension Review

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Cytokine storm - 100%

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About Borja Bandera
Borja Bandera
Borja Bandera is a young doctor who focuses on nutrition, exercise and metabolism, he combines his professional activity with his vocational dissemination and research.
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