How fasting can reduce inflammation in our body

How fasting can reduce inflammation in our body

Even short-term fasting can relieve inflammation in the body – but why? © erdikocak/ iStock

Fasting is considered healing and anti-inflammatory. Researchers have now found a possible mechanism through which temporarily abstaining from food can reduce inflammation. The focus is on the fatty acid arachidonic acid, which has previously been known primarily for its inflammatory effects. During fasting, the level of this fatty acid in the blood increases. But instead of leading to more inflammation, arachidonic acid suppresses certain inflammatory processes, as laboratory experiments show.

Inflammation is an important response our body has to fight infections. The immune system works at full speed in the affected areas to quickly remove pathogens and harmful substances. But the so-called inflammasome, the signaling network that sets inflammatory processes in motion, is not only active when there are injuries and infections. Our high-calorie Western diet can also trigger inflammatory processes. Diet-related chronic inflammation, in turn, increases the risk of cardiovascular disease and other diseases.

Opposite effects

A team led by Milton Pereira from the University of Cambridge in Great Britain has now investigated how short-term fasting affects inflammatory processes in the body. To do this, the researchers analyzed blood samples from 21 test subjects who first ate a meal containing 500 kilocalories (kcal), then did not eat anything for 24 hours and then ate 500 kcal again. “During fasting, the level of the inflammatory messenger interleukin-1beta (IL-1b) fell, while the level of the fatty acid arachidonic acid increased,” the researchers report. After the test subjects ate food again, the respective concentrations returned to their original values.

Previous studies have shown that arachidonic acid plays a complex role in inflammatory processes. However, until now it was primarily known as being inflammatory. It provides the starting substance for the production of prostaglandins, which cause pain and fever. People with illnesses such as gout or rheumatism are therefore advised to consume as little arachidonic acid as possible in their diet. However, Pereira and his team encountered an opposite effect. “Based on the blood results, we hypothesized that the inverse relationship between IL-1b and arachidonic acid may be related to an effect of arachidonic acid inhibiting inflammasome activity,” the team explains.

Observations in cell cultures

The researchers tested this hypothesis in the laboratory using cell cultures of immune cells. And indeed: an increased level of arachidonic acid inhibited the activity of the so-called NLRP3 inflammasome, which is involved, among other things, in harmful inflammatory processes that are associated with obesity, atherosclerosis and neurological diseases such as Parkinson’s and Alzheimer’s. “This is a possible explanation for how changing our diet – particularly through fasting – protects us from inflammation, especially the harmful form that underlies many diseases associated with a Western, high-calorie diet,” says Pereira’s colleague Clare Bryant.

According to the researchers, speculation as to whether fasting could also protect against diseases such as Alzheimer’s or Parkinson’s through this mechanism would be premature. “The effects we are seeing are short-lived,” says Bryant. “However, our work suggests that regular fasting over a long period of time could help reduce the chronic inflammation that we associate with these diseases.”

Additional effect of aspirin?

The results also provide evidence of an additional, previously unknown mode of action of some painkillers such as aspirin. These work by blocking the conversion of arachidonic acid to pain-promoting prostaglandins. What has so far gone unnoticed is that this can increase the arachidonic acid level – which in turn can inhibit the inflammasome. In this way, aspirin could have an anti-inflammatory effect in an additional pathway.

Source: Milton Pereira (University of Cambridge, UK) et al., Cell Reports, doi: 10.1016/j.celrep.2024.113700

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