Social isolation linked to higher levels of inflammation – new study

Loneliness may change how our body responds to stress.

social isolation has links to higher inflammation
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Being lonely or socially isolated can negatively affect your wellbeing. There is even research showing that it increase the risk of illnesses such as cardiovascular disease, dementia and depression.


Some researchers suggest that loneliness and social isolation lead to poorer health because they increase inflammation. Inflammation is when your body tells your immune system to produce chemicals to fight off infection or injury. It can also occur when you experience psychological or social stress.

Short-term, local inflammation – such as when you accidentally cut your finger – can be helpful, but having slightly elevated long-term inflammation is associated with poor health. Researchers propose that loneliness and social isolation are linked to this elevated long-term inflammation.

In our latest study, we wanted to see if loneliness (the subjective state of feeling alone) and social isolation (the objective state of being alone) are linked to long-term inflammation. To do this, we searched for all published studies that looked at loneliness with inflammation or social isolation with inflammation. We found 14 studies that examined loneliness and 16 that examined social isolation.

Our analysis revealed that people who are more socially isolated have higher levels of two inflammatory chemicals: C-reactive protein and fibrinogen. C-reactive protein is commonly used as an indicator of inflammation and high levels are associated with poor health. Fibrinogen increases blood clotting and is higher when people have an injury or trauma. When people have long-term increased levels of these inflammatory markers, it can lead to an increased risk of poorer health over time.

An evolved response?

Social isolation could be linked to higher levels of inflammation for several reasons. It could be that social isolation leads to inflammation. We have evolved to be a social species, so being socially isolated could be a source of stress. And stress has a direct effect on the immune system.

It is also possible that we evolved to turn on our immune response when we are isolated. This is because when alone we could be at a greater risk of being injured. Our immune system may have learned to turn itself on to prepare for this greater risk.

It is also possible that inflammation leads to social isolation. People who are ill and have higher levels of inflammation can feel like they don't want to be around other people. This could be because we have evolved to want to isolate ourselves so we don't infect other people.

People who have lots of physical illnesses also have higher levels of inflammation. Those people who have lots of physical illnesses are sometimes not as able to get around and could become socially isolated because of this.

The evidence linking loneliness with inflammation was less convincing. We found some evidence that loneliness was linked to an inflammatory chemical called interleukin-6. But this was not a consistent finding and was based on only two studies. This suggests that there may not be a direct effect of loneliness on inflammation. Instead, loneliness may change how our body responds to stress. There is research showing that lonely people are more likely to have an enhanced inflammatory response to stress.

Bigger picture

Our study provides some evidence of a link between social isolation and inflammation. But we think that the link between loneliness and social isolation with poor health is a lot more complex than inflammation.

To best understand how loneliness and social isolation influence health we need to examine a range of biological, psychological and social risk factors, such as blood pressure, mental health, income and social support, as they are all associated with increased inflammation.

To best understand how loneliness and social isolation affect health we may need to think about a bigger picture beyond inflammation. This study provides us with a useful first step in understanding part of this bigger picture.The Conversation

Kimberley Smith, Lecturer in Health Psychology, University of Surrey.

This article is republished from The Conversation under a Creative Commons license. Read the original article.

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Credit: National Cancer Institute via Unsplash
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This article was originally published by our sister site, Freethink.

For the first time, researchers appear to have effectively treated a genetic disorder by directly injecting a CRISPR therapy into patients' bloodstreams — overcoming one of the biggest hurdles to curing diseases with the gene editing technology.

The therapy appears to be astonishingly effective, editing nearly every cell in the liver to stop a disease-causing mutation.

The challenge: CRISPR gives us the ability to correct genetic mutations, and given that such mutations are responsible for more than 6,000 human diseases, the tech has the potential to dramatically improve human health.

One way to use CRISPR to treat diseases is to remove affected cells from a patient, edit out the mutation in the lab, and place the cells back in the body to replicate — that's how one team functionally cured people with the blood disorder sickle cell anemia, editing and then infusing bone marrow cells.

Bone marrow is a special case, though, and many mutations cause disease in organs that are harder to fix.

Another option is to insert the CRISPR system itself into the body so that it can make edits directly in the affected organs (that's only been attempted once, in an ongoing study in which people had a CRISPR therapy injected into their eyes to treat a rare vision disorder).

Injecting a CRISPR therapy right into the bloodstream has been a problem, though, because the therapy has to find the right cells to edit. An inherited mutation will be in the DNA of every cell of your body, but if it only causes disease in the liver, you don't want your therapy being used up in the pancreas or kidneys.

A new CRISPR therapy: Now, researchers from Intellia Therapeutics and Regeneron Pharmaceuticals have demonstrated for the first time that a CRISPR therapy delivered into the bloodstream can travel to desired tissues to make edits.

We can overcome one of the biggest challenges with applying CRISPR clinically.

—JENNIFER DOUDNA

"This is a major milestone for patients," Jennifer Doudna, co-developer of CRISPR, who wasn't involved in the trial, told NPR.

"While these are early data, they show us that we can overcome one of the biggest challenges with applying CRISPR clinically so far, which is being able to deliver it systemically and get it to the right place," she continued.

What they did: During a phase 1 clinical trial, Intellia researchers injected a CRISPR therapy dubbed NTLA-2001 into the bloodstreams of six people with a rare, potentially fatal genetic disorder called transthyretin amyloidosis.

The livers of people with transthyretin amyloidosis produce a destructive protein, and the CRISPR therapy was designed to target the gene that makes the protein and halt its production. After just one injection of NTLA-2001, the three patients given a higher dose saw their levels of the protein drop by 80% to 96%.

A better option: The CRISPR therapy produced only mild adverse effects and did lower the protein levels, but we don't know yet if the effect will be permanent. It'll also be a few months before we know if the therapy can alleviate the symptoms of transthyretin amyloidosis.

This is a wonderful day for the future of gene-editing as a medicine.

—FYODOR URNOV

If everything goes as hoped, though, NTLA-2001 could one day offer a better treatment option for transthyretin amyloidosis than a currently approved medication, patisiran, which only reduces toxic protein levels by 81% and must be injected regularly.

Looking ahead: Even more exciting than NTLA-2001's potential impact on transthyretin amyloidosis, though, is the knowledge that we may be able to use CRISPR injections to treat other genetic disorders that are difficult to target directly, such as heart or brain diseases.

"This is a wonderful day for the future of gene-editing as a medicine," Fyodor Urnov, a UC Berkeley professor of genetics, who wasn't involved in the trial, told NPR. "We as a species are watching this remarkable new show called: our gene-edited future."

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