Mitochondria May Contribute to Chronic Nerve Pain: 4 Ways to Relieve It

When nerves are damaged, they can misfire, turning even the gentlest touch into searing pain. Scientists have spent years trying to understand why this happens.

Researchers may have found a key piece of the puzzle: Damaged mitochondria, the cell’s energy-producing structures, may push nerves into a state of chronic overactivity.

A recent study published in Nature found that restoring healthy mitochondria to injured nerves reduced pain for up to 48 hours in some cases.

“This physiological process [mitochondria transfer] is disrupted in disease—including diabetes, chemotherapy, and nerve trauma—leading to peripheral neuropathy,” Ru-Rong Ji, senior author of the study and professor of anesthesiology and neurobiology at Duke University, told The Epoch Times.

Sensory neurons, which carry signals for touch, temperature, and pain from the body to the brain, are especially energy-demanding cells, with axons that can stretch from the spinal cord all the way to the skin—about 2 feet to 4 feet to the fingers or toes—creating major challenges in supplying energy to the far ends of the nerve.

When mitochondria are stressed, they produce less energy and more harmful byproducts, making nerves hyper-reactive and prone to misfiring—key drivers of neuropathic pain. Over time, oxidative stress can lock the nervous system into a chronic pain state.

“That’s why pain can persist long after blood sugar improves or chemotherapy ends,” Renee Young, a naturopathic doctor and integrative medicine specialist, told The Epoch Times.

Support Cells Do More Than Support

Satellite glial cells, once thought to merely support sensory neurons, actively transfer healthy mitochondria to nearby neurons through short-lived cellular bridges called tunneling nanotubes, helping restore depleted energy supplies.

In the study, researchers found that more than 80 percent of sensory neurons received mitochondria within 24 hours, even though these structures appeared only briefly—highlighting how rapid and dynamic the process is.

Disease Breaks the Built-In Repair System

Researchers identified MYO10, a motor protein involved in forming tunneling nanotubes, as essential for mitochondrial transfer. Blocking MYO10 reduced mitochondrial delivery and increased pain sensitivity.

Glial cells preferentially supported electrically active neurons. When neuronal firing was silenced, mitochondrial transfer dropped—even though nanotubes still formed.

“Under normal conditions, more neuronal activity means more mitochondrial support,” Ji said.

The energy-sharing system helps restore mitochondrial function and limit oxidative stress, but it is vulnerable to metabolic stress. In diabetic and chemotherapy-induced neuropathy models, cellular bridges were fewer and distorted. Chemotherapy also damaged glial mitochondria, weakening neuronal support. Short-term inflammation did not disrupt the transfer of mitochondria.

Small Fibers Left Behind

When mitochondrial transfer was disrupted in injured nerves, pain sensitivity increased, and pain-carrying nerve fibers began to degenerate. Small sensory fibers were most affected, while larger neurons remained relatively stable because of continued mitochondrial support.

This selective loss of energy supply helps explain why small fibers are especially vulnerable in neuropathic pain—not only because they are injured, but also because they lose access to critical metabolic support.

How to Take Care of Your Mitochondria

In people with diabetes, chronic stress, or age-related changes, early strain on mitochondria can begin long before neuropathy symptoms appear. Supporting mitochondrial health early may help prevent neuropathy from taking hold.

Early mitochondrial stress often shows up as subtle warning signs—such as rising oxidative damage; falling levels of NAD+, a molecule that every cell needs to produce energy, repair damage, and protect itself from oxidative stress; or mild sensory changes that are easy to miss, Young said.

“If we intervene during that window, we can preserve nerve adaptability and prevent pain from becoming hardwired,” she said.

Some mild sensory changes may include burning, tingling, pins-and-needles, altered sensation, or a numb “falling asleep” feeling in the toes or fingers that appears briefly and resolves quickly. Intermittent sensations are commonly reported with early irritation or damage to small sensory nerves, before more persistent neuropathy develops.

Many of the most effective strategies focus on reducing oxidative stress.

“Mitochondria can’t heal in a low-oxygen, high-sugar, inflamed environment,” Young said.

Frequent spikes and crashes in blood sugar increase oxidative stress and limit oxygen delivery to nerves, placing extra strain on mitochondria and making nerve damage more likely.

Restoring NAD+ is also critical. When NAD+ levels drop—as they often do with aging, chronic stress, or persistent pain—mitochondria struggle to recover and function properly.

Young suggests simple science-backed strategies for her patients that they can do at home to support their mitochondrial health:

1. Stabilize Sugar

“Repeated glucose spikes directly increase oxidative stress in nerves,” Young said.

Too much sugar floods cells with fuel. When mitochondria are overwhelmed, energy production becomes inefficient, and harmful byproducts build up, damaging mitochondria and their DNA.

To keep blood sugar steady, Young recommends pairing protein and fiber in meals and avoiding sugary snacks or alcohol at night.

“Don’t skip meals when you’re already stressed or sleep-deprived,” she said.

2. Protect Sleep

During the day, neurons are highly active, and mitochondria work hard, leading to a buildup of metabolic waste. Sleep provides repair and antioxidant systems with time to clear damage, allowing mitochondria to recover.

Young advises aiming for seven to nine hours of consistent sleep.

Deep sleep is when mitochondria repair themselves, and without it, pain pathways stay switched on,” she said.

3. Engage in Moderate Movement Every Day

Moderation and consistency matter when it comes to exercise. Dr. JP Saleeby, a physician specializing in holistic and integrative medicine, told The Epoch Times that excessive aerobic training can increase oxidative stress. He favors resistance training for mitochondrial health.

“Exercising to the point of exhaustion, especially when you’re already inflamed, can actually worsen pain,” Young said. “Cells produce too many byproducts that lead to tissue damage when antioxidants are overloaded.”

Incorporating two to three sessions of strength or interval training per week, along with daily walks, is sufficient to support mitochondrial function, she said.

4. Use Simple Recovery Tools

Simple wellness habits can further support mitochondria.

Saleeby recommends exposure to regular sunlight to help regulate circadian rhythms, which research shows coordinate mitochondrial energy production and repair.

Diet also plays a role. While nutrition should be individualized, Saleeby often recommends a green Mediterranean-style diet—lower in refined carbs and higher in protein and healthy fats. Studies suggest that this pattern reduces oxidative stress, which damages mitochondria.

Passive heat exposure, such as hot baths or sauna use, may also support mitochondrial activity and energy production, offering some exercise-like benefits.

Omega-3s may help as well. Research shows that supplementation can improve mitochondrial responses to energy demands, and one study found that fish oil altered cell membrane composition in ways that support smoother mitochondrial function.

Finally, Saleeby emphasized mindset.

“We see a positive outlook helpful with chronic conditions, pain, and cancer,” he said.

Why Timing Matters

In her practice, Young said, she prioritizes early mitochondrial support by stabilizing blood sugar, reducing oxidative stress, and improving oxygen delivery to nerves—all strategies that patients can begin implementing at home.

The key is intervention before neuropathy becomes entrenched. Once the feedback loop between mitochondrial damage and nerve hyperactivity is established, breaking it becomes much more difficult.

“Mitochondria act as gatekeepers,” Young said. “Support them early, and you may prevent chronic pain from ever taking hold.”

Rachel Melegrito worked as an occupational therapist, specializing in neurological cases. Melegrito also taught university courses in basic sciences and professional occupational therapy. She earned a master's degree in childhood development and education in 2019. Since 2020, Melegrito has written extensively on health topics for various publications and brands.
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