Being stressed before you get COVID increases your chances of a long COVID. Here’s why

Stress is an integral part of modern life. When we are about to face a new challenge or a significant event, we may experience stress mixed with excitement and a sense of challenge. This form of “good” stress, or eustress, is important for growth, development, and performance.

However, prolonged stress and overwhelming or traumatic events can have a negative impact on our health. These forms of “bad” stress — or stress — can make us sick, depressed, and anxious, and in the long term, increase our risk of heart disease, stroke, type 2 diabetes, dementia, and even cancer.

Stress can also affect our ability to fully recover from COVID. Symptoms that persist for a month or more are referred to as long COVID. Sufferers may experience fatigue, brain fog, shortness of breath, loss of taste and smell, trouble sleeping, anxiety, and/or depression. For some, these symptoms can last for many months or even years, making it impossible to return to pre-COVID life.

In a Harvard University study published last month, people who had mental distress leading up to their COVID infection had a greater chance of experiencing long-term COVID. The researchers found that those with two types of stress (depression, likely anxiety, perceived stress, concern about COVID, and loneliness) had an almost 50% greater risk of long-COVID than other participants.

So how can stress affect the body’s ability to fight infection?

First we need to look at inflammation

Inflammation is the body’s response to infection or injury.

For example, when the immune system encounters a virus, it launches an attack to neutralize infected cells and store a memory of that virus so it can respond faster and more effectively next time.

Many things can cause inflammation, including bacteria and viruses, injury, toxins, and chronic stress.

The body has many different responses to inflammation, including redness, heat, swelling, and pain. Some inflammatory reactions can occur silently in the body without any of these typical symptoms appearing. At other times, inflammation can mobilize energy resources to cause fatigue and fever.

When there is inflammation, immune cells release so-called inflammatory mediators. These chemical messengers cause small blood vessels to dilate (dilate), allowing more blood to reach injured or infected tissue to aid in the healing process.

This process can also irritate nerves and cause pain signals to be sent to the brain.

What does stress have to do with inflammation?

In the short term, stress causes the release of hormones that suppress inflammation and ensure the body has enough energy resources to respond to an imminent threat.

However, when experienced over a long period of time, stress itself can cause low-grade “silent” inflammation. Chronic stress and related mental illnesses, such as anxiety and depression, are all associated with elevated levels of inflammatory mediators. In fact, repeated exposure to mild, unpredictable stress is enough to induce an inflammatory response.

Pre-clinical (laboratory-based) studies have shown that chronic mild stress can cause depression-like behavior by promoting inflammation, including activation of immune cells in the brain (microglia). When anti-inflammatories were administered during mild stress exposure, they prevented depression-like behavior. However, when administered after the event, the anti-inflammatories were ineffective.

If the inflammation persists, for example during prolonged periods of stress, the immune system changes its response by reprogramming the immune cells. Effectively, it switches to “low monitor mode”. In this way, it remains active throughout the body but reduces its ability to react to new threats.

Because of this, the response can be slower and less effective. As a result, the recovery process may take longer. With a virus like COVID, it’s possible that prior exposure to stress could similarly affect the body’s ability to fight infection, increasing the risk of a long COVID.

How could stress affect recovery from COVID?

There is still much to learn about how COVID infection affects the body and how psychological factors can affect clinical outcomes in the short and long term.

COVID has widespread effects on multiple body systems, affecting the lungs and heart the most, increasing the risk of blood clots and stroke.

Because the virus resides within human cells, an immune system that goes into “low surveillance mode” due to psychological stress can miss early opportunities to destroy infected tissue. The virus can then gain an advantage over the defense (immune) system.

Conversely, stress can suppress the early response and tip the balance in favor of the intruder.

So what can we do about it?

Vaccines work by helping train the immune system to find the target sooner, giving the immune system an advantage.

Behavioral interventions that improve the ability to cope with stress reduce inflammation and may help boost the immune response to COVID.

It’s also important to know that exposure to COVID increases your risk of depression, anxiety, or other mental illness. Knowing this interconnectedness is the first critical step in improving clinical outcomes.

A lifestyle medicine approach that helps reduce stress and address mental health symptoms has important downstream physical health benefits. This is likely to be the result not only of direct effects on the immune system itself, but also of related improvements in health behaviors such as diet, exercise and/or sleep.

More research is needed to better understand the effects of stress on the immune system, mental health, and COVID outcomes, and to identify ways to intervene to prevent a long-lasting COVID and support recovery.

This article was republished by The Conversation under a Creative Commons license. Read the original article.