📰 New Research Breakthrough: Chronic Pain Isn’t Just “Long Acute Pain”

Hi Friend

A promising new study by Dr Guy Bewick at the University of Aberdeen (working with teams in Taiwan and elsewhere) provides fresh insight into why chronic pain — including what people with fibromyalgia often experience — is fundamentally different from acute pain.

Here’s what they found, what it could mean for fibromyalgia, and what still needs doing.

Before we dive into the research just a quick update on my online community for fibromyalgia sufferers. The mend collective is turning into something even bigger than I could imagine. I will this week be onboarding a chef who specialises in meals for chronic pain patients, there will be weekly live cook alongs and recipes, in addition to all the other medical inputs and therapies. If you would like regular updates and be informed first when the next cohort opens join the waitlist HERE. Anyway back to the study!

🔍 What the Study Discovered

1. Distinct Pathway for Chronic Pain (“sng” / “suan tong”)

   • The researchers found that chronic pain is processed differently in the nervous system versus the sharp, “injury-type” acute pain.

   • They identified a term used in Taiwanese / Mandarin cultures: “sng” (Taiwanese) or “suan tong” in Mandarin — meaning a kind of “sour ache” or “dull, deep, lingering pain” — which matches many descriptions from people with fibromyalgia about what their pain feels like.

2. Glutamate & a “Highly Unusual” Receptor Involved

   • The team saw that muscles release glutamate during activity, which is normal. But when there’s excessive glutamate, nearby pain-sensitive nerves become overactive — meaning they don’t switch off properly.

   • They identified a receptor (an unusual one) that responds to this glutamate — and blocking that receptor prevented chronic pain being triggered in animal models.

3. Evidence from Animal Models + A Human Case

   • In mice, the researchers used techniques (including genetic silencing) to switch off neuronal pathways thought involved in this chronic pain mechanism. When those were turned off, the chronic signalling reduced.

   • Importantly, they also had a human case (a patient with a spinal cord injury) whose standard acute pain pathway was blocked/damaged, but who still perceived “sng” / the subjective sensation described. That helps show the pathway is separate.

🩺 What This Means for Fibromyalgia

If validated and translated into treatments, this discovery could be very relevant for those of us with fibromyalgia, because:

• Many existing pain medications are better at handling acute or sharp pain, but less effective for chronic, diffuse, lingering pain (which many fibromyalgia sufferers call their “everyday pain”). This research identifies a potential reason why.

• It gives a new drug target — i.e. that unusual glutamate receptor. If a treatment can be developed that blocks or modulates that pathway, then relief could come in a more precise way, rather than just broadly dampening pain signals (which often brings side‐effects).

• It may help explain why some people with fibromyalgia feel their condition is dismissed, misunderstood, or poorly treated: because if medicine treats chronic pain like acute pain (just longer in time), it's missing that distinct pathway. Acknowledging that difference helps validate what people are experiencing.

⚠️ What We Still Don’t Know / What’s Needed

While this is exciting, it’s early days:

• Most of the detailed work so far is in animal models. Human trials (to test drugs or blockers targeting that receptor) are necessary.

• We don’t yet have a clinically available drug that safely blocks the “glutamate receptor” in humans for this specific purpose. Safety, dosage, side‐effects all need to be worked out.

• Fibromyalgia is very complex; pain is just one part (others: fatigue, sleep disturbance, cognitive “fog”, etc.). Even a drug that relieves pain via this pathway won’t be a full cure but could help reduce suffering.

• There might be individual differences — some people’s fibromyalgia may involve this “sng”‐type mechanism more than others. We need biomarkers or diagnostics to tell which patients might respond best.

🌈 Hope and Practical Takeaways

While waiting for treatments to be developed, here are some thoughts/ideas to hold onto:

• Listening to the body’s signals remains important — rest when needed, pacing, combinations of light movement. If “overdoing” activity causes excess muscle glutamate release (or something like that), pacing might help reduce triggering of this pathway.

• Non‐drug approaches that reduce glutamate activity or muscle stress might help ― e.g. gentle stretching, low‐impact movement, relaxation/mindfulness techniques, possibly dietary interventions (though we don’t yet know which ones).

• Keeping up with new research: As trials emerge, treatments specific to chronic pain / “sng” may become available.

• Advocacy and communication: Use findings like this to help explain to medical professionals how your pain is not “just more of the same”, but possibly processed differently. It helps in pushing for better care, treatment options, understanding.

✅ What You Can Do Now

• Ask your GP or pain specialist if there are any clinical trials in your area using novel therapies for chronic pain.

• Try to keep symptom diaries that note when pain feels sharp (acute) vs dull, burning, sour, lingering, etc. Having precise descriptions can help in discussions with doctors.

• Explore support groups / communities (online or locally) to share what works for individuals, particularly in terms of non‐drug strategies.

• Stay tuned: this line of research could change guidelines in future years.

Overall, this study gives cause for optimism. It doesn’t solve everything yet, but it deepens our understanding, validates lived experience, and points in the direction of better, more effective treatments for fibromyalgia.

As always, stay well,

Dr Ahmed