No pain, no gain: Fact or fiction?

"No pain, no gain. Pain is your friend. Pain tells you you’re not dead. Pain is inevitable, suffering is optional."

There is a long list of platitudes about pain, presumably intended to ease our suffering and give us hope that the days ahead will be better. A little-known fact is that having an understanding of pain biology has been scientifically shown to ease our pain.[1][2][3][4] You won’t see that as a Facebook meme but the truth of this statement is undeniable.

Many of us hold the belief that pain is an indicator of harm in the body; The greater the pain, the greater the level of damage. We perceive a linear relationship between pain and damage. In fact, there is ample scientific evidence to dispute this and my clinical experience has provided countless examples to disprove it. In fact, there is little to no correlation between the intensity of pain and the degree of tissue damage. For instance, many people with advanced osteoarthritis in their knees report little or no pain and vice versa. If we took MRIs of 100 people who report no back pain, we would find at least 30 of those people have disc prolapses[5].

Pain biology lesson #1: Pain is not a direct measure of the degree of tissue damage.

If you were one of the people who participated in that study and discovered you have a disc prolapse how would that feel? That even though you have no pain, you have a herniated, prolapsed, bulging disc simmering away in there. For most people, this knowledge would increase their sensitivity to any messages coming from their back. Messages coming from the muscles, ligaments, tendons and skin are sent to the brain where they are integrated with other pieces of information to make sense of the message. It’s possible and perhaps even likely that holding that information about your disc prolapse will be matched with a sensation coming from your back and be interpreted as a painful warning that your back is vulnerable. This simple scenario highlights the concept of pain in context. We are receiving messages from our body all the time and we make sense of those messages based on our thoughts, beliefs and knowledge.  Most people have heard of extraordinary war stories where soldiers have been shot in the leg but managed to run to safety. They report little or no pain because the brain is preoccupied with the more pressing matter of survival. So powerful is this truth that we can modulate our experience of pain, depending on the context or situation we are in.

Pain biology lesson #2: Pain depends on context.

So why do people experience persistent or chronic pain? This is the question that researchers have pursed for decades and the body of evidence is brought together beautifully in a highly recommended read called Explain Pain, by Lorimer Moseley and David Butler. This book is written as a guide to help sufferers of chronic pain on their journey of recovery. It explains the very complex pathophysiology of chronic pain, often referred to as central sensitisation. For people who have painful conditions such as an ankle fracture, frozen shoulder, fibromyalgia, arthritis, whiplash, back pain and many others, a small proportion may experience persistent pain even when the condition has healed or resolved. In chronic pain, the pain messages coming from bodily tissues to the spinal cord and travelling on to the brain become amplified. This pain amplification occurs at a cellular level. Scientists have discovered that in chronic pain sufferers there are more pain receptors open and increased excitatory chemicals and neurotransmitters present, amplifying or dialling up the volume on pain messages. Changes also occur in the brain where the representation of the affected body region is altered. Scientists have discovered changes in the immune and endocrine systems of chronic pain sufferers. So what does all this mean? That chronic pain probably has less to do with the initial injury, the damaged muscle, ligament, tendon or disc, and more to do with changes in the pain messaging system.  

Pain biology lesson #3: Chronic pain can occur due to central sensitisation – changes in the sensory receptors, nerves, spinal cord and brain that amplify the pain message and the experience of pain.

So how does knowing this help someone in pain? The simple knowing of this information can reduce the threat value of pain. Knowing that although your back hurts terribly, it is safe to move and that the muscles, ligaments, tendons and discs are capable of tolerating more than you might think. Knowing about chronic pain and central sensitisation also means that we can treat the real cause of the problem – the pain messaging system comprised of the brain, spinal cord, nerves and soft tissues.

One of the tenets of treating chronic pain is pacing and graded exposure therapy. Be assured that the adage “no pain, no gain” holds no merit here. Unhelpful advice like “learn to live with your pain” has no part in this therapy. If you can’t wait for Back on Track’s  next instalment on this topic, visit for further reading to guide your recovery from chronic pain.  


[1] Moseley GL et al (2002) A randomised controlled trial of intensive neurophysiology education in chronic low back pain. Clinical Journal of Pain 20: 324-330

[2] Meeus ML et al (2010) Pain physiology education improves pain beliefs in patients with chronic fatigue syndrome compared with pacing and self-management education: a double-blind randomised contrail. Archives of Physical Medicine and Rehabilitation 91: 1153-1159

[3] Clarke CL et al (2011) Pain neurophysiology education for the management of individuals with chronic low back pain: systematic review and meta-analysis. Manual Therapy 16: 544-549

[4] Louw A et al (2011) The effect of neuroscience education on pain, disability, anxiety and stress in chronic musculoskeletal pain. Archives of Physical Medicine and Rehabilitation 92: 2041-2056

[5] Hitselfberger WE et al (1968) Abnormal myelograms in asymptomatic patients. Journal of Neurosurgery 28: 204-206