The benefits of fasting are evident in improving overall health

In summary, scientists have discovered a novel method via which fasting lowers inflammation, a major contributing cause to chronic illnesses.

According to their research, fasting raises arachidonic acid levels in the blood, which inhibits the NLRP3 inflammasome and lowers inflammation. This finding clarifies the benefits of calorie restriction for diseases like obesity, diabetes, heart disease, and neurodegenerative disorders as well as the anti-inflammatory properties of fasting.

The study sheds information on the potential mechanisms of action of medications like aspirin and emphasizes the complex interplay between inflammation, nutrition, and illness prevention.Arachidonic acid levels in the blood are raised during fasting, which lowers inflammation and NLRP3 inflammasome activity.
The results provide a possible explanation for the protective effects of fasting and calorie restriction against illnesses associated with chronic inflammation.
The anti-inflammatory properties of non-steroidal anti-inflammatory medications (NSAIDs), such as aspirin, which raise arachidonic acid levels, may also be explained by this findings.
University of Cambridge

Researchers at Cambridge may have uncovered a novel method of fasting's anti-inflammatory effects. Inflammation is a potentially harmful immune system side-effect that underpins many chronic illnesses.Fasting increases blood levels of arachidonic acid, a chemical that inhibits inflammation. The team details this process in an article titled "Arachidonic acid inhibition of the NLRP3 inflammasome is a mechanism to explain the anti-inflammatory effects of fasting," which was published in Cell Reports.

It might also help explain some of the positive effects of medications like aspirin, according to the researchers.

For a considerable amount of time, scientists have been aware that our food, especially the high-calorie Western diet, can raise our chance of developing chronic inflammation-related diseases like obesity, type 2 diabetes, and heart disease.Our body's natural reaction to damage or infection is inflammation, but there are other processes that can start this process, such as the so-called "inflammasome," which functions in our cells as an alarm system, starting inflammation to help defend our body when it detects damage.However, the inflammasome might inadvertently cause inflammation because one of its roles is to kill undesirable cells, which may cause the contents of the cell to leak into the body and cause inflammation.

"We're very interested in trying to understand the causes of chronic inflammation in the context of many human diseases, and in particular the role of the inflammasome," stated Professor Clare Bryant of the University of Cambridge's Department of Medicine.

"In recent years, it has become clear that one inflammasome in particular—the NLRP3 inflammasome—plays a critical role in many major diseases, including obesity and atherosclerosis, as well as in conditions like Alzheimer's and Parkinson's disease, which affect a large number of older people, especially in the Western world."It's unclear why fasting can assist lower inflammation, but it can. A team led by Professor Bryant and colleagues from the University of Cambridge and the National Institute for Health in the United States examined blood samples from 21 volunteers who had eaten a 500-kcal meal, fasted for 24 hours, and then had another 500-kcal meal in order to assist answer this question.

The group discovered that calorie restriction raised arachidonic acid levels, a type of lipid. Molecules known as lipids are essential to our bodies because they store energy and facilitate information transfer between cells. The moment people had a meal once more, their arachidonic acid levels decreased.Researchers have observed that arachidonic acid inhibits the activity of the NLRP3 inflammasome in immune cells cultivated in the lab. The researchers was taken aback by this since they had previously believed that arachidonic acid was associated with elevated rather than lowered levels of inflammation.

"This provides a potential explanation for how changing our diet—in particular by fasting—protects us from inflammation, especially the damaging form that underlies many diseases related to a Western high-calorie diet," said Professor Bryant, a Fellow of Queens' College, Cambridge.Since the effects of arachidonic acid are transient, it is too soon to determine whether fasting protects against diseases like Parkinson's and Alzheimer's, but our research adds to the expanding body of scientific literature highlighting the health advantages of calorie restriction. It implies that prolonged periods of frequent fasting may be able to lessen the chronic inflammation that is linked to these illnesses. It's undoubtedly a charming concept.

The results also suggest one method via which eating a diet high in calories could raise the chance of developing certain diseases. Research has indicated that elevated levels of inflammasome activity are seen in certain patients who consume a high-fat diet.Professor Bryant speculated that there might be a yin and yang dynamic at play here, with too much of the incorrect substance raising your inflammasome activity and too little lowering it. "Arachidonic acid may be a possible mechanism for this."

According to the researchers, the finding might also provide hints about an unanticipated mechanism of action for aspirin and other so-called non-steroidal anti-inflammatory medicines. Aspirin inhibits the body's natural ability to break down arachidonic acid quickly, which can raise the acid's levels and thereby lower inflammation and inflammasome activity.Professor Bryant stated, "It's important to stress that aspirin can have side effects, such as stomach bleeds if taken over a long period of time, and should not be taken to reduce risk of long-term diseases without medical guidance."

Regarding this news on diet and inflammatory studiesSynopsis

The mechanism behind the anti-inflammatory effects of fasting is the suppression of the NLRP3 inflammasome by arachidonic acid.Highlights
Arachidonic acid (AA) is higher and plasma IL-1β is lower in fasting subjects than in fed subjects.
Mouse and human macrophage NLRP3 inflammasome activity is reduced by exogenous AA.
AA decreases JNK activation, phospholipase C, and NLRP3 activity.
In brief
Chronic metabolic inflammatory syndromes are characterized by elevated levels of interleukin (IL)-1β, NLRP3 inflammasome activity, and systemic inflammation; however, the underlying molecular mechanism is not well understood.Here, we demonstrate that whereas the lipid arachidonic acid (AA) is increased in fasting subjects, plasma IL-1β levels are lower in fed subjects.

NLRP3-stimulated murine macrophages exhibit increased AA synthesis and an NLRP3-dependent eicosanoid signature, according to lipid profiling.

Nonsteroidal anti-inflammatory medications that inhibit cyclooxygenase reduce the synthesis of eicosanoid compounds but not of AA. Additionally, it lessens the production of IL-18 and IL-1β in response to NLRP3 activation.

In both human and murine macrophages, AA suppresses the activity of the NLRP3 inflammasome. Mechanistically, AA lowers JNK1 activation and NLRP3 activity by inhibiting phospholipase C activity.These findings demonstrate that AA is a critical physiological regulator of the NLRP3 inflammasome, which helps to explain why fasting lowers systemic inflammation and provides a theoretical basis for the action of nonsteroidal anti-inflammatory medications.