There is a recommendation in the chronic pain guidelines that sounds, on first reading, like a mistake.
For one specific category of chronic pain, NICE's guideline advises clinicians not to start paracetamol, non-steroidal anti-inflammatories, opioids or benzodiazepines. Not "use sparingly." Do not initiate.
That is not indifference, and it is not a claim that the pain isn't real. It follows from something genuinely important about how some chronic pain works — and understanding it changes what's worth trying.
First: which kind of chronic pain
The recommendation applies to chronic primary pain, and the distinction matters enormously.
Chronic secondary pain is pain that is a symptom of an identifiable underlying condition — rheumatoid arthritis, endometriosis, cancer, a structural problem. There, the pain is a signal, and treating the condition is the priority.
Chronic primary pain is pain lasting more than three months where the pain, or its impact, is out of proportion to any observable injury or disease, and where it causes significant distress or disability. Fibromyalgia is the best-known example. Chronic widespread pain and some persistent back pain fall here too.
The two frequently coexist, and sorting out which is which is a clinical job rather than a self-assessment. But the treatment logic genuinely differs, which is why the guideline separates them.
The third kind of pain mechanism
Most people carry a model of pain with two categories. There are three.
Nociceptive pain — tissue damage. A broken bone, a burn, inflammation. The nervous system is reporting accurately.
Neuropathic pain — damage to the nerves themselves. Burning, shooting, electric. Peripheral neuropathy is the common example, and it already responds poorly to ordinary painkillers for the same underlying reason.
Nociplastic pain — the third category, and the one that explains chronic primary pain. Here the pain arises from altered processing of pain signals rather than from identifiable tissue or nerve damage. The pain system itself has changed how it works.
The usual shorthand is a volume knob. In nociplastic pain the knob has been turned up: signals that would normally register as pressure register as pain, and signals that would register as mild pain register as severe. This is often described as central sensitisation.
What that looks like in practice
- Widespread pain rather than pain confined to one structure
- Allodynia — pain from things that shouldn't hurt: a waistband, a bedsheet, light touch
- Hyperalgesia — more pain than expected from something that should hurt a little
- Fatigue that rest doesn't resolve
- Disturbed sleep, almost universally
- Cognitive symptoms — poor concentration and word-finding difficulty, often called fibro fog
- Sensitivity beyond pain — to light, sound and smell
The most important paragraph on this page
This is not "the pain is in your head."
Nociplastic pain is real pain, produced by a real mechanism, in a real nervous system. The difference from nociceptive pain is where the mechanism sits — in how signals are processed rather than in damaged tissue. A smoke alarm going off with no fire is still genuinely making a noise, and the fault is genuinely in the alarm.
People with chronic primary pain are routinely disbelieved, told scans are clear so nothing is wrong, and left feeling they have to prove their pain before anyone will help. The mechanism above is the reason the scans are clear, and it is not the same as the pain being imagined. Anyone offering an explanation that requires you to have invented it has the model wrong.
What the guideline actually recommends
Having said what not to start, NICE sets out what to consider instead.
Supervised group exercise programmes — the most strongly supported intervention, backed by a large body of trials showing improvements in pain, quality of life and function. No single type of exercise is mandated, which is useful: it means the mode matters less than doing it, supervised, consistently, and starting below the level that flares things.
Psychological therapy — cognitive behavioural therapy and acceptance and commitment therapy are both options to consider. ACT is particularly relevant here, because its target is functioning and values rather than pain reduction, which fits a problem where the pain may not fully resolve.
Acupuncture — can be offered, and the guideline is unusually specific: a single course of up to a maximum of five hours. Subsequent courses are not supported, even where the first appeared to help. Whatever you think of acupuncture, that is a notably disciplined recommendation.
Antidepressants — the one medicine class where the balance of benefits and harms was judged favourable. The guideline lists amitriptyline, citalopram, duloxetine, fluoxetine, paroxetine and sertraline as options to consider in people over 18.
Worth understanding why, because it is widely misread as "they think I'm depressed." In chronic pain these medicines are used for their effect on pain-signalling pathways — the same descending systems that modulate the volume knob — not solely as a treatment for low mood. The doses used for pain are often lower than antidepressant doses. It is a pain treatment that happens to be an antidepressant molecule.
Why "don't start painkillers" isn't abandonment
The reasoning is a balance of benefits against harms, assessed across the evidence rather than case by case.
For this kind of pain, conventional analgesics help a minority of people, modestly. That isn't nothing — but it has to be weighed against what a decade of daily NSAIDs does to a stomach and kidneys, what benzodiazepines do in terms of tolerance and dependence, and what long-term opioids do.
The opioid point deserves stating directly. Long-term opioid use for chronic non-cancer pain has a poor evidence base for sustained benefit and a well-documented one for harm — tolerance, dependence, and in some people opioid-induced hyperalgesia, where the drug increases pain sensitivity. A treatment that makes the underlying problem worse over years is not a conservative choice just because it is the familiar one.
It is also worth knowing what happens if dependence has already developed, because the answer is better than most people expect and is routinely misdescribed. Opioid dependence is treated with medication, not willpower, and agonist medication is associated with roughly halved mortality — the treatments that actually work are set out here. Arriving at dependence through a legitimate pain prescription is common and is not a moral failure; it is a reason to ask for the treatment that has the evidence behind it.
And there's a parallel worth knowing from a neighbouring condition: in headache, frequent use of acute painkillers can itself start causing the headaches, and the treatment is a supervised withdrawal rather than more medication. The headache categories are set out here — the relevant pattern is headache on most days in someone taking painkillers often, and it is a GP conversation rather than a self-managed one.
If you are already on any of these, none of the above is an instruction to stop. Stopping opioids or benzodiazepines abruptly is dangerous. The guideline addresses what to start; what to do about an existing prescription is a planned conversation with the prescriber.
Sleep, and why it's not a side issue
The relationship between sleep and chronic pain runs both ways, and the direction people underrate is the second one: poor sleep measurably increases pain sensitivity the following day. So a bad night raises the volume knob, the pain disrupts the next night, and the loop tightens.
That makes sleep one of the few places where there is genuine leverage, and it is often easier to intervene on than the pain directly. CBT-I has better evidence than anything you can buy, and it has been studied specifically in people with chronic pain. Two things worth excluding while you're at it: if you sleep a full night and wake unrefreshed, screen for sleep apnea; and the stress-sleep loop is usually running alongside.
Things worth ruling out
Widespread pain and fatigue overlap with several conditions that have specific tests and specific treatments. Worth excluding rather than assuming:
- Thyroid dysfunction — produces fatigue, aching and cognitive symptoms. One blood test.
- Vitamin D and B12 deficiency, and iron deficiency — all produce fatigue and some produce pain. The short panel.
- Inflammatory arthritis and autoimmune conditions — these are chronic secondary pain, where treating the disease is the point. Morning stiffness lasting more than an hour, joint swelling, or a rash are reasons to push for this specifically.
- Restless legs, which is often mistaken for a pain problem and is not one. How to recognise it.
And the red flags that mean sooner rather than later: unexplained weight loss, fever, night pain that wakes you, new weakness or numbness, bladder or bowel change, or a history of cancer.
Where we sit
Chronic pain is one of the most heavily supplemented conditions there is, and we should be straightforward about the shape of that market: it is large, the desperation is real, and the evidence is mostly poor.
Nothing Proco sells treats chronic pain, and we have no product in this category. That isn't modesty — it's that a guideline which declines to recommend paracetamol for this condition is not a guideline with room in it for a capsule.
One specific caution, since it's the supplement most often sold here. Turmeric and curcumin products dominate the joint-and-pain aisle, and the absorption claims attached to them are frequently indefensible — we've taken apart the "2,000% absorption" claim in detail. If you're buying in this category, that's the kind of arithmetic worth checking first.
What we'd actually point at is on the list above and none of it comes from us: supervised exercise, a psychological therapy aimed at function, sleep, and a proper conversation about whether an antidepressant at a pain dose is worth trying.
The framing that seems to help most
A last thing, because it recurs across the treatments that work.
Every intervention on the recommended list — graded exercise, CBT, ACT, better sleep — works on turning the volume down and restoring function, rather than on blocking a pain signal. That is a different goal from the one most people arrive with, and accepting the change in goal is often described as the hardest and most useful part of the process.
It is also why "nothing showed up on the scan" is the beginning of an explanation rather than the end of one.
This article is not medical advice and cannot tell you which kind of chronic pain you have — that distinction requires a clinician. Do not stop or change any prescribed medication on the basis of anything here; stopping opioids or benzodiazepines abruptly can be dangerous. Guideline recommendations summarised here apply to chronic primary pain in people over 16 and may differ where an underlying condition is driving the pain.