Home » today » Health » New Research Reveals Mechanism Behind Fasting’s Anti-Inflammatory Effects and Impact on Chronic Diseases

New Research Reveals Mechanism Behind Fasting’s Anti-Inflammatory Effects and Impact on Chronic Diseases




New Mechanism Uncovered: How Fasting Reduces Inflammation

New Mechanism Uncovered: How Fasting Reduces Inflammation

Summary

Researchers have discovered a groundbreaking new mechanism through which fasting reduces inflammation, a key factor in chronic diseases. The study reveals that fasting increases blood levels of arachidonic acid, which inhibits the NLRP3 inflammasome, ultimately reducing inflammation. This exciting discovery sheds light on the anti-inflammatory effects of fasting and provides valuable insights into the benefits of calorie restriction for conditions such as obesity, diabetes, heart disease, and neurodegenerative disorders.

Key Facts

  1. Fasting elevates arachidonic acid levels in the blood, leading to reduced activity of the NLRP3 inflammasome and inflammation.
  2. The findings offer a potential explanation for how fasting and calorie restriction can protect against chronic inflammation-related diseases.
  3. This research may also explain the anti-inflammatory effects of non-steroidal anti-inflammatory drugs like aspirin, which increase arachidonic acid levels.

Cambridge Scientists Uncover a New Way Fasting Reduces Inflammation

A team of researchers from the University of Cambridge may have discovered a new way that fasting helps reduce inflammation, a potentially damaging side-effect of the body’s immune system that underlies a number of chronic diseases. In a paper titled “Arachidonic acid inhibition of the NLRP3 inflammasome is a mechanism to explain the anti-inflammatory effects of fasting,” published in the esteemed scientific journal Cell Reports, the team highlights how fasting raises levels of arachidonic acid in the blood, which in turn inhibits inflammation. This groundbreaking finding also offers insights into the potential benefits of drugs such as aspirin.

The Impact of Diet on Chronic Inflammation

Evidence has shown that our diet, particularly a high-calorie Western diet, can increase the risk of diseases like obesity, type 2 diabetes, and heart disease, which are all linked to chronic inflammation in the body.

Professor Clare Bryant from the Department of Medicine at the University of Cambridge explains, “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.

“What’s become apparent over recent years is that one inflammasome in particular—the NLRP3 inflammasome—is very important in a number of major diseases such as obesity and atherosclerosis, but also in diseases like Alzheimer’s and Parkinson’s disease, many of the diseases of older age people, particularly in the Western world.”

Delving into the Mechanism through Extensive Research

To answer the question of how fasting reduces inflammation, the research team led by Professor Bryant, in collaboration with experts from the University of Cambridge and the National Institute for Health in the U.S., conducted a study using blood samples from a group of 21 volunteers. The volunteers consumed a 500-calorie meal, followed by a 24-hour fasting period before consuming a second 500-calorie meal.

The results revealed that calorie restriction led to increased levels of a lipid called arachidonic acid in the body. Lipids, crucial molecules in the body, play significant roles in storing energy and transmitting information between cells. Remarkably, when individuals returned to regular meal consumption, arachidonic acid levels dropped.

Further exploration utilizing immune cells cultured in the laboratory unveiled that arachidonic acid actually inhibits the activity of the NLRP3 inflammasome—a surprising discovery, as arachidonic acid was previously believed to be associated with increased levels of inflammation, not a reduction.

Professor Bryant, a Fellow of Queens’ College, Cambridge, added, “This provides a potential explanation for how changing our diet—in particular, through fasting—can protect us from inflammation, particularly the damaging form associated with many diseases related to a Western high-calorie diet.

“It’s too early to conclusively link fasting to the prevention of diseases like Alzheimer’s and Parkinson’s, as the effects of arachidonic acid are short-lived. However, our work contributes to a growing body of scientific literature that points to the health benefits of calorie restriction. Regular fasting over an extended period could potentially reduce chronic inflammation, which is associated with these conditions. This novel finding is undeniably appealing.”

Uncovering the Connection between Diet, Inflammation, and Drug Mechanisms

These findings not only shed light on the effectiveness of fasting as a means to reduce inflammation but also raise potential explanations for the pharmaceutical impacts of various drugs, including non-steroidal anti-inflammatory medications like aspirin. Normally, arachidonic acid is swiftly broken down in the body, but aspirin interferes with this process, leading to increased levels of arachidonic acid. As a result, inflammation reduces due to diminished NLRP3 inflammasome activity.

Professor Bryant emphasized, “It’s important to stress that aspirin should not be used to reduce the risk of long-term diseases without medical guidance, as it can have side effects such as stomach bleeds if taken over an extended period.”

Implications and Continual Research on Diet and Inflammation

This breakthrough discovery provides significant insights into the complex relationship between diet, inflammation, and disease prevention. It may prompt further research into the role of fasting and its long-term effects on individuals, specifically its potential to combat chronic inflammation-related diseases. Furthermore, this research may pave the way for further understanding of how drugs such as aspirin effectively impact inflammation and help develop novel therapeutic approaches.

Professor Bryant concludes, “Understanding the critical role of arachidonic acid in inhibiting the NLRP3 inflammasome opens up new possibilities for innovative interventions and treatments for chronic inflammatory diseases. We are excited to further delve into the connections between diet, inflammation, and the intricate mechanisms underlying various diseases. This field of research holds great potential in improving the quality of life for countless individuals globally.”

About the Research

This significant research was carried out at the prestigious University of Cambridge, a leading global institution renowned for its ground-breaking discoveries. The paper titled “Arachidonic acid inhibition of the NLRP3 inflammasome is a mechanism to explain the anti-inflammatory effects of fasting” was published in the renowned scientific journal Cell Reports. The research study was co-authored by a team led by Professor Clare Bryant and involved experts from the University of Cambridge and the National Institute for Health in the United States.

Conclusion

The revolutionary discovery of a new mechanism through which fasting reduces inflammation has the potential to transform our understanding of how dietary choices impact chronic inflammation and associated diseases. This breakthrough offers valuable insights into the anti-inflammatory effects of fasting and potential avenues for therapeutic treatments. As scientific research continues to pave the way, further understanding of the intricate relationship between diet, inflammation, and disease prevention promises a brighter, healthier future. Stay tuned to our news website for the latest updates on ongoing research and its impact on human health.

Contact: Clare Bryant – University of Cambridge

This news article is for informational purposes only and is not intended as medical advice. Please consult a healthcare professional for any medical concerns.


Leave a Comment

This site uses Akismet to reduce spam. Learn how your comment data is processed.