Chronic pain can affect far more than the part of the body that hurts.
People who live with pain for months or years may also struggle with memory, concentration, sleep, mood, and anxiety, making the condition difficult to treat with pain medicines alone.
A new animal study suggests that intermittent fasting may influence several of these problems at the same time.
Researchers from Zhengzhou University and its First Affiliated Hospital found that fasting changed gut bacteria in mice with chronic pain and was linked to less pain sensitivity, better mental performance, and fewer anxiety-like behaviors.
The findings were published in the journal Brain, Behavior, and Immunity. The study was conducted in mice, so it does not yet show that intermittent fasting can treat chronic pain in people.
Chronic pain is generally defined as pain that lasts or repeatedly returns for more than three months. It can continue even after an original injury has healed because the nervous system itself may become unusually sensitive to pain signals.
Treatments vary depending on the cause and can include medicines, physical therapy, psychological therapies, exercise, and other approaches. Yet no single treatment works for everyone, and some people continue to experience pain along with emotional and thinking difficulties.
This has encouraged scientists to investigate how other systems in the body may influence chronic pain. One area receiving increasing attention is the connection between the digestive system and the brain, often called the gut-brain axis.
The intestines contain enormous communities of bacteria and other microorganisms. These microbes help process food and produce chemicals that can interact with the immune system, metabolism, and nervous system.
Researchers have therefore asked whether changing the gut environment might also change how the brain processes pain. Intermittent fasting is one possible way to alter metabolism and the composition of gut bacteria.
In the new study, researchers used several mouse models designed to produce long-lasting pain through injury, inflammation, or other controlled methods. Some mice were allowed to eat normally every day, while another group followed a strict fasting schedule for 38 days.
The fasting mice alternated between 24 hours without food and 24 hours when they could eat freely. During fasting periods, the animals did not consume calories.
The scientists measured how sensitive the mice were to touch and heat. They also used behavioral tests to examine memory, mental performance, and signs that are commonly interpreted as anxiety-like behavior in laboratory animals.
The fasting mice became less sensitive to normally harmless touch and heat than mice that continued eating freely. They also performed better on some tasks and showed fewer anxiety-like behaviors.
Researchers then looked for biological changes that might explain these results. They found evidence that fasting strengthened the intestinal barrier, changed the mixture of bacteria living in the gut, and reduced inflammation in the nervous system.
One bacterial species attracted particular attention: Alistipes finegoldii. Levels of this bacterium consistently increased in mice following the intermittent-fasting schedule.
The researchers also studied chemicals produced or influenced by gut microbes. Their experiments pointed toward a substance called hippuric acid and an immune signaling system known as STING as possible parts of the pathway connecting fasting, gut bacteria, inflammation, and pain.
To test whether the bacterial change was more than a coincidence, the team gave Alistipes finegoldii to mice. Remarkably, this reproduced some of the pain-relieving and cognitive improvements seen with fasting.
Additional experiments involving hippuric acid and STING signaling provided further support for the proposed biological pathway. The researchers believe fasting may alter specific gut microbes, which then change chemical signals that influence inflammation in the nervous system.
This is important because it suggests that fasting’s effects may not come only from weight loss or broad metabolic changes. Particular bacteria and the substances associated with them could potentially be involved.
However, the results need careful interpretation. Mouse pain models are valuable for understanding biology, but chronic pain in humans is far more complicated and can be influenced by injury, disease, emotions, sleep, social conditions, medications, and many other factors.
The fasting schedule used in the study was also demanding, with mice going without food for a full 24 hours every other day. It cannot be assumed that the same schedule would be safe, practical, or effective for people.
Intermittent fasting can also be unsuitable for some individuals, including people with certain medical conditions or those taking medicines affected by food intake. The study therefore should not be taken as a recommendation for people with chronic pain to begin prolonged fasting on their own.
The strongest part of the research is its attempt to move beyond a simple observation. By examining gut bacteria, metabolites, inflammation, and specific biological signals, the researchers developed a possible explanation for how fasting produced the changes they observed.
Still, many questions remain. Future studies need to determine which cells are affected by the STING pathway, whether males and females respond differently, and whether other gut bacteria or microbial products contribute to the effects.
Most importantly, human studies are needed. Carefully controlled clinical trials would have to show that fasting or treatments based on these gut changes can reduce pain without creating nutritional problems or other unwanted effects.
For now, the study provides an intriguing biological clue rather than a new treatment. It suggests that the gut, immune system, and brain may work together in chronic pain and that future therapies could potentially target this connection without relying only on conventional pain medicines.
Source: Zhengzhou University.
