Abstract
Degenerative spinal findings are common even in younger adults [1], which has encouraged the narrative that contemporary lifestyles prematurely wear out the spine. However, degeneration is not a simple process of damage, posture, or inevitable decline. It is multifactorial, shaped by genetic, biological, mechanical, and lifestyle influences [2–4]. This article examines why imaging findings should not be conflated with diagnoses, why association should not be interpreted as causation, and why prolonged rest, though it may offload a painful structure, can impair the function and wellbeing of the person experiencing pain [5,6,10].
Degeneration is not a unitary phenomenon
Interpretation of an imaging report can follow a linear inference: degeneration implies damage, damage implies pain, and pain warrants rest. This sequence is attractive but insufficiently supported.
A systematic review identified 134 risk factors for disc degeneration and herniation and grouped them as patient-specific, radiological, lifestyle, workplace-related, genetic, and other. It concluded that these conditions are multifactorial events whose risk factors can be partly influenced and partly not [2]. Reported associations included age, family disposition, atherosclerosis, elevated body mass index, hypertension, dyslipidaemia, diabetes mellitus, smoking, and a history of back injury [2]. Such factors are unlikely to operate in isolation [3].
Genetic influences are substantial. Twin research indicates that heredity contributes a large share of the variance in lumbar disc degeneration, whereas occupational and leisure-time physical loading appeared to have comparatively little effect [4]. Genetic reviews describe disc degeneration as a complex, multifactorial condition shaped by the interplay of genes and environment [3]. The role of mechanical loading therefore remains contested, although workplace-related factors continue to feature among reported risk factors [2].
Consequently, the question “What caused this degeneration?” is typically answered by a combination of contributing factors acting over time, the relative influence of which cannot be fully separated. Such an account is less satisfying than single-cause explanations but more consistent with the evidence. Degeneration should not be attributed to a single posture, occupation, sport, or scan. Its clinical significance depends on individual vulnerability, the demands placed on the body, capacity for recovery, the presenting symptoms, and the meaning those symptoms hold for the person.
A finding is not a diagnosis
Degenerative changes are highly prevalent in individuals without pain. In a systematic review of 3,110 asymptomatic individuals, the prevalence of disc degeneration increased from 37% at age 20 to 96% at age 80, and disc bulge from 30% to 84% across the same range [1]. The authors concluded that many imaging-based degenerative features are likely part of normal aging and unassociated with pain, and that such findings must be interpreted in the context of the patient’s clinical condition [1].
This does not render imaging uninformative. In a meta-analysis of adults aged 50 years or younger, disc bulge, degeneration, extrusion, protrusion, Modic type 1 changes, and spondylolysis were more prevalent in those with low back pain than in asymptomatic individuals [7]. However, prevalence alone does not establish clinical relevance: a finding may be real, visible, and clinically insignificant simultaneously [1,7].
The pertinent question is therefore not whether degeneration is present, but whether the finding contributes to explaining the individual’s pain, functional loss, neurological signs, or likely clinical course. Imaging may inform this judgement but cannot resolve it in isolation. Consistent with this, the Australian Low Back Pain Clinical Care Standard reserves imaging for suspected serious pathology [6].
It is plausible that when imaging is communicated as though it provides a complete explanation, individuals may come to see themselves as damaged or fragile, and that such beliefs may influence behaviour. This hypothesis warrants further study.
Association is not causation
Evidence on degeneration shows why an association should not be read as a cause. For decades, prevention and research focused largely on mechanical loading as the primary driver of disc degeneration [4]. Twin research later found a substantial influence of heredity, with comparatively little effect of occupational and leisure-time physical loading [4]. This illustrates how an exposure that seems to explain an outcome when observed alongside it may explain much less when studied in a design that accounts for shared genetic background.
Imaging findings illustrate the same problem. Degenerative changes are more prevalent in adults with low back pain than in those without [7], yet they are also present in 37% of asymptomatic 20-year-olds and in most older adults [1]. The association is real, but their presence alone does not show that a finding is causing a person’s pain.
Study design limits what can be concluded. Cross-sectional and retrospective designs can show co-occurrence but cannot establish temporal order, account for confounding, or exclude reverse causation: reduced movement may accompany degenerative change, but pain may equally lead people to move less. Longitudinal evidence is stronger, yet it identifies predictors, not causes. In acute and subacute low back pain, high emotional distress and negative recovery expectations are consistently associated with poor long-term outcomes [8]. Whether changing those factors changes outcomes is a separate question that only trials can answer.
Beyond the scan: pain as a multidimensional experience
Biomedical assessment remains essential. Clinical practice guidelines recommend history taking and physical examination to identify red flags, neurological testing to identify radicular syndrome, and imaging when serious pathology is suspected [5].
In an umbrella review of systematic reviews, high pain intensity and disability, high emotional distress, negative recovery expectations, and high physical demands at work showed consistent evidence of association with poor long-term outcomes in acute and subacute low back pain. High pain catastrophising was consistently associated with poor outcomes in mixed-duration low back pain [8]. These associations do not imply that pain is imaginary. They help explain why individuals with comparable imaging findings may differ in their functional trajectories, and the review’s authors recommended that such factors be considered for inclusion in explanatory models of low back pain [8]. The Australian Standard likewise includes a psychosocial assessment as a core component of early care [6].
Rest is not invariably protective
Rest is often recommended as a benign intervention. It may be reasonable in the short term, for example, reducing a specific aggravating activity following an acute exacerbation.
However, an overview of clinical practice guidelines found that, for acute low back pain, guidelines recommend reassurance about the favourable prognosis, advice on returning to normal activities, and avoiding bed rest. For chronic low back pain they recommend exercise therapy and psychosocial interventions [5]. A comparison of recent guidelines likewise found that staying active and therapeutic exercise were recommended for acute and subacute low back pain, although recommendations were heterogeneous between guidelines [9]. The Australian Standard emphasises patient education, self-management, and physical activity [6].
Although prolonged inactivity may reduce load on a painful structure, it may also diminish conditioning, work participation, and confidence in movement. A Cochrane review found moderate-quality evidence that advice to stay active, compared with advice to rest in bed, produced small benefits in pain relief and function in acute low back pain; for sciatica there was little or no difference between the two approaches [10]. Fear avoidance, in which pain is interpreted as a threat and activity narrows, has been proposed as one mechanism by which disability persists. In low back pain of up to six months’ duration, high fear-avoidance beliefs were associated with more pain or disability and less return to work, whereas findings in chronic low back pain were less consistent [11].
Accordingly, guidelines favour remaining active within tolerable limits, with reassurance and a gradual return to usual activities, over prolonged rest [5,9]. In practice this can be described as relative rest: reducing clearly aggravating activities while maintaining movement and preserving meaningful activity where possible.
Conclusion
Degeneration is common, multifactorial, and not necessarily pathological [1,2]. Imaging findings require interpretation within clinical context [1], and associations should not be presented as causal relationships. Biomedical assessment is essential for identifying serious pathology [5], while consideration of psychological and work-related factors helps explain variability in outcomes between individuals [8].
In most cases of non-serious low back pain, prolonged bed rest is not recommended [5,10]. Education, reassurance, and continued activity are more consistent with the available evidence and with respect for the person beyond the scan [5,6,9].
References
- Brinjikji W, Luetmer PH, Comstock B, et al. Systematic literature review of imaging features of spinal degeneration in asymptomatic populations. AJNR Am J Neuroradiol. 2015;36(4):811–816. doi:10.3174/ajnr.A4173.
- Patient-related risk factors and lifestyle factors for lumbar degenerative disc disease: a systematic review. Neurochirurgie. 2023;69(5):101482. doi:10.1016/j.neuchi.2023.101482.
- Chan D, Song Y, Sham P, Cheung KMC. Genetics of disc degeneration. Eur Spine J. 2006;15(Suppl 3):317–325. doi:10.1007/s00586-006-0171-3.
- Battié MC, Videman T, Kaprio J, et al. The Twin Spine Study: contributions to a changing view of disc degeneration. Spine J. 2009;9(1):47–59.
- Oliveira CB, Maher CG, Pinto RZ, et al. Clinical practice guidelines for the management of non-specific low back pain in primary care: an updated overview. Eur Spine J. 2018;27(11):2791–2803. doi:10.1007/s00586-018-5673-2.
- Australian Commission on Safety and Quality in Health Care. Low Back Pain Clinical Care Standard. Sydney: ACSQHC; 2022.
- Brinjikji W, Diehn FE, Jarvik JG, et al. MRI findings of disc degeneration are more prevalent in adults with low back pain than in asymptomatic controls: a systematic review and meta-analysis. AJNR Am J Neuroradiol. 2015;36(12):2394–2399. doi:10.3174/ajnr.A4498.
- Otero-Ketterer E, Peñacoba-Puente C, Ferreira Pinheiro-Araujo C, Valera-Calero JA, Ortega-Santiago R. Biopsychosocial factors for chronicity in individuals with non-specific low back pain: an umbrella review. Int J Environ Res Public Health. 2022;19(16):10145. doi:10.3390/ijerph191610145.
- Zhou T, Salman D, McGregor AH. Recent clinical practice guidelines for the management of low back pain: a global comparison. BMC Musculoskelet Disord. 2024;25:344.
- Dahm KT, Brurberg KG, Jamtvedt G, Hagen KB. Advice to rest in bed versus advice to stay active for acute low-back pain and sciatica. Cochrane Database Syst Rev. 2010;(6):CD007612. doi:10.1002/14651858.CD007612.pub2.
- Wertli MM, Rasmussen-Barr E, Held U, Weiser S, Bachmann LM, Brunner F. Fear-avoidance beliefs: a moderator of treatment efficacy in patients with low back pain: a systematic review. Spine J. 2014;14(11):2658–2678. doi:10.1016/j.spinee.2014.02.033.
