By Mr Ahmed-Ramadan Sadek, Neurosurgeon · 14 min read

Why people ask this

Back trouble often seems to run in families: a parent who had a slipped disc, a grandparent with a curved spine, a brother with ankylosing spondylitis. People understandably want to know whether they are next, and whether there is any point trying to prevent it. This guide sets out what the research shows, where it is still uncertain, and what you can change.

It covers three different things that are often mixed up: common back pain and disc wear, where many genes each play a very small part; a handful of spinal conditions with a clearer genetic link; and rare inherited conditions caused by a change in a single gene.

What twin studies tell us

Identical twins share all their genes and non-identical twins share about half. If a condition is more alike in identical pairs than in non-identical pairs, genes are likely to play a part. Researchers express this as heritability: the share of the differences between people in a group that can be put down to genes.

Disc degeneration

Two large twin programmes have looked at disc wear on MRI scans. Their estimates differ, so we give both:

• TwinsUK (mainly women, London): in 1999, heritability of disc degeneration was 74% in the lower back and 73% in the neck, after allowing for age, weight, height, smoking, manual work and exercise.^[3] A 10-year follow-up found that how quickly some features got worse was also partly inherited, although loss of disc height over time was not.^[17]
• Finnish Twin Cohort (men, the Twin Spine Study): heritability ranged from 29% to 54%, depending on which disc feature and which level of the lower back was measured. The authors judged genetic and environmental influences to be of similar importance.^[2]

The Twin Spine Study changed how specialists think about disc wear. It was once seen mainly as the result of heavy work and injuries. Instead, the researchers found a strong influence of heredity and surprisingly little effect of physical workload, even in identical twins whose jobs and sports were very different for decades.^[18]

Back pain

Back pain is harder to measure than a scan, and the estimates vary more:

• A systematic review of 27 twin studies found heritability of back pain ranging from 21% to 67%. Genes played a larger part in long-lasting, disabling pain than in short, mild episodes.^[1]
• In UK women, heritability was 52% to 68% for low back pain and 35% to 58% for neck pain.^[19]
• In Finnish men, it was 30% to 46%, depending on how back pain was defined.^[20]

Part of this inherited tendency works through the discs. But in UK women, only about 11 to 13 in 100 of the genetic effects on back pain were shared with disc wear.^[21] The rest seems to come through other routes, including how the nervous system handles pain and an inherited tendency to psychological distress.^[19][22]

What large gene studies show

A genome-wide association study (GWAS) scans hundreds of thousands of points in the DNA of very large groups of people to find small differences that are more common in people with a condition.

• Chronic back pain: the first large study, of 158,000 people, found one replicated variant, near a gene called SOX5. Carrying it raised the odds of chronic back pain by about 7%.^[4] A 2025 study of more than 550,000 US veterans found 87 regions of DNA linked with chronic back pain. The strongest single variant changed the odds by only about 4%.^[5]
• Slipped disc (disc herniation): a 2024 study combining Finnish, Estonian and UK biobanks found 64 regions linked with disc herniation, near genes involved in inflammation, disc structure and nerve signalling.^[23]
• Disc degeneration: a study of 4,600 Northern Europeans found a variant in a gene called PARK2, which had not been suspected before.^[24]
• Sciatica: a Finnish study found one new region, but a second promising region did not hold up when tested in another group of patients.^[25]

These studies also show that the genes linked with back pain overlap with those linked with height, disc problems, depression, sleep problems, being overweight and smoking.^[22] Many of the genes are active in the brain, not just the spine.^[5][22]

Family history and slipped discs

A slipped disc in a teenager or young adult is the clearest example of family clustering in common back problems:

• In a US study of 63 patients under 21 who needed surgery for a slipped disc, 32 in 100 had a parent with a history of a slipped disc, compared with 7 in 100 of a comparison group. The authors estimated the risk was about five times higher with a positive family history.^[26]
• A Japanese study of patients aged 18 or under found a similar pattern, with about five and a half times the odds.^[27]
• Using family trees for over a million people in Utah, first-degree relatives (parents, brothers, sisters and children) of people with lumbar disc disease had about 4 times the expected rate. Even third-degree relatives, such as cousins, had about 1.5 times the rate.^[28]

These figures compare groups of people. They do not tell you your own chance, and a family history does not mean you will have a slipped disc. If you do develop one, the outlook and treatment are the same as for anyone else: most slipped discs settle without an operation. See our slipped disc guide.

Conditions with a clearer genetic element

The conditions below have a stronger or better understood genetic link than ordinary back pain. Most have their own Spinemathema guide, linked in each section.

Adolescent idiopathic scoliosis

In about 8 in 10 cases of scoliosis the cause is unknown (idiopathic), but the NHS notes that genes may make it more likely, as it sometimes runs in families.^[29] Estimates of how strong the genetic part is vary widely: 38% in the Swedish Twin Registry, based on what people reported themselves,^[30] and 87.5% in a Hong Kong family study, where about 18 in 100 brothers and sisters of girls with scoliosis also had a curve.^[31] One of the best-known gene regions, near a gene called LBX1, raises the odds by about one and a half times.^[32] It is not thought to be linked to posture, exercise or diet.^[29] See our scoliosis guide.

Ankylosing spondylitis and axial spondyloarthritis

Axial spondyloarthritis is an inflammatory arthritis of the spine and the sacroiliac joints at the base of the spine. When it shows on X-rays it is called ankylosing spondylitis (AS). It usually starts in a person’s 20s, and its heritability has been estimated at over 90%, with the strongest link to the gene variant HLA-B27.^[6] The NHS says the cause is not known, but that there is thought to be a link with HLA-B27.^[33]

Carrying HLA-B27 does not mean you will get AS. In a Dutch population study, only about 1 in 75 HLA-B27 carriers developed it. The risk is much higher if a close relative already has the condition: in the same study, 25 in 100 HLA-B27-positive first-degree relatives of people with AS had inflammation of the sacroiliac joints on X-ray,^[34] and 27 in 100 developed it over 35 years of follow-up in a Swiss family study.^[35] NICE also says the condition can occur in people who are HLA-B27 negative, affects women about as often as men, and should not be ruled out on one test result alone.^[36]

NICE advises GPs to consider referral to a rheumatologist if back pain started before age 45 and has lasted more than 3 months, and several other features are present. These include pain that started before 35, waking in the second half of the night, buttock pain, pain that improves with movement and a parent, brother, sister or child with spondyloarthritis. An HLA-B27 blood test is used in some cases to decide on referral.^[36] Our sacroiliac joint pain guide explains inflammatory back pain in more detail.

Scheuermann’s disease

Scheuermann’s disease causes a rounded upper back (kyphosis) that develops during the teenage years. In nearly 35,000 Danish twins, about 3 in 100 reported the diagnosis, it was nearly twice as common in men, and heritability was 74%.^[37]

Spondylolysis and spondylolisthesis

Spondylolysis is a stress fracture in a thin bridge of bone at the back of a vertebra, usually the lowest one, and spondylolisthesis is when the bone slips forward. In an Edinburgh family study, 19 in 100 first-degree relatives of patients with a slip also had spondylolysis on X-ray. The figure was 33 in 100 for relatives of patients with the rarer ‘dysplastic’ (developmental) type, and 15 in 100 for the more common type.^[38] How common it is also depends on ethnic background, sex and sport, being much higher in some sports such as rugby, judo, football and baseball.^[39] See our spondylolysis guide.

Congenital and developmental spinal stenosis

Some people are born with a narrower spinal canal, which can cause symptoms of spinal stenosis at a younger age and often at several levels.^[40][41] Genes may contribute, but research on this is scarce.^[41] In Finnish twins, heritability of narrowing of the lower spinal canal seen on MRI was about 67%, partly working through disc bulging.^[42] Some skeletal dysplasias, inherited conditions that affect bone growth, cause stenosis directly. The commonest, achondroplasia, affects about 1 in 25,000 to 30,000 births and often narrows the canal, most of all in the lower back.^[43]

Connective tissue disorders: Ehlers-Danlos and Marfan syndromes

These conditions affect the body’s connective tissue, which holds joints, skin and blood vessels together.

• Ehlers-Danlos syndromes (EDS) are a group of 13 types linked to 19 known genes, 5 of which have known spinal effects.^[44] These can include Chiari malformation, instability where the skull meets the neck, curvature of the spine, spinal fluid leaks, Tarlov cysts and tethered cord.^[44] EDS can be inherited or happen by chance. In the most common types, each child of an affected parent has a 1 in 2 chance of inheriting it. There is currently no test that confirms hypermobile EDS, which is diagnosed from your history and an examination.^[8]
• Marfan syndrome is passed on in the same way, with a 1 in 2 chance for each child of an affected parent.^[7] A common spinal feature is dural ectasia, a widening of the sac of fluid around the nerves in the lower spine. In a Norwegian study it was found in 52 of 58 people with Marfan and related conditions after 10 years, and it can develop or worsen in adulthood.^[45]

Neurofibromatosis and inherited spinal tumours

• Neurofibromatosis type 1 (NF1) can be inherited or arise for the first time in a child whose parents do not carry it. Each child of an affected parent has a 1 in 2 chance of inheriting it.^[9] Spinal curvature is the commonest bone and joint problem in NF1, and some curves get worse quickly and need surgery.^[46][9]
• Neurofibromatosis type 2, now also called NF2-related schwannomatosis, has the same 1 in 2 chance of being passed on. It can cause tumours on the spinal cord and its coverings, which often cause no symptoms.^[47]
• Von Hippel-Lindau disease is another inherited condition. Nearly half of the blood vessel tumours of the nervous system it causes (haemangioblastomas) are in the spinal cord.^[48]

Most spinal tumours are not inherited. See our spinal tumours guide.

Chiari malformation and syringomyelia

In Chiari malformation, the lowest part of the brain sits lower than usual, at the opening at the base of the skull. It sometimes causes a fluid-filled cavity in the spinal cord, called a syrinx (syringomyelia). Most cases are not inherited. A known inherited condition is found in about 2 to 3 in 100 people with Chiari type 1.^[49] A 2024 review of 34 families with more than one affected member found evidence of a hereditary element, most likely many genes rather than a single one, and suggested closer monitoring and earlier consideration of genetic testing for first-degree relatives.^[50] See our Chiari malformation guide.

Genes and lifestyle: what you can still change

Your genes are only part of the story. The same twin studies that showed a strong genetic influence also show the effect of how people live:

• Smoking. In identical twins where one smoked and the other did not, the smoker’s discs were on average 18% more worn.^[51] In the review of twin studies, smokers had about three times the odds of back pain.^[1] Gene-based studies suggest smoking is a cause of chronic back pain, not just linked with it.^[10] See our smoking and your spine guide.
• Body weight. Obesity roughly doubled the odds of back pain in twin studies.^[1] A study using genes as a natural experiment found that a higher body mass index causes back pain and chronic back pain.^[11] See our weight and back pain guide.
• Mood. The same type of study found that depression raises the risk of chronic back pain.^[10] Talk to your GP if you are struggling.
• Exercise. Pooled trials show that exercise lowers the risk of a new episode of low back pain by about a third (33% in one review, 35% in another).^[12][52] Combined with education about back pain, the reduction was 27% in one review and 45% in the other.^[12][52] A mix of strengthening with stretching or aerobic exercise 2 to 3 times a week is a reasonable aim.^[12]

Heavy physical work turned out to matter much less than people once thought. In identical twins with very different working lives, job demands explained about 7 in 100 of the differences in wear of the upper lumbar discs. Adding age and family factors together explained 77 in 100.^[53] Everyday loading may even be good for discs.^[18]

If you already have back pain, your family history does not change how it is treated. NICE advises self-management, carrying on with normal activities and, for an episode or flare-up, considering a group exercise programme.^[54] See our acute back pain guide.

Is genetic testing useful?

For ordinary back pain, sciatica or disc wear: no. No genetic test can diagnose them or predict them well enough to change what you do.^[14]

• NHS genetic testing needs a referral from a doctor, usually a hospital specialist, and is generally offered only when a genetic condition is suspected.^[13] The tests the NHS in England pays for, and who is eligible, are set out in the National Genomic Test Directory. Tests should be requested only where the result is highly likely to change care.^[55] For example, a genetics specialist may use a blood test to confirm one of the rarer types of EDS.^[8]
• HLA-B27 is a blood test, not a test for a disease. It is used alongside symptoms and scans when axial spondyloarthritis is suspected. A negative result does not rule the condition out, and most people who carry HLA-B27 never develop it.^[36][34]
• Home DNA kits sold direct to the public can report false positive or wrongly interpreted results, especially when raw data is run through third-party websites. Health professionals have reservations about how valid and useful the results are.^[56] UK genetics centres have seen people asking for treatment on the basis of ‘disease variants’ that, on retesting, were not actually there.^[15]

What it means for your children

For common back pain and disc wear, your children may inherit a slightly higher tendency, but this cannot be measured or predicted for an individual child.^[14] The most useful things you can pass on are habits: being active, not smoking and keeping a healthy weight.^[12][51][11]

For the conditions with a clearer genetic element:

• Scoliosis: it sometimes runs in families, and brothers and sisters of someone with scoliosis are more likely to have it.^[29][31] See a GP if you notice signs such as uneven shoulders, one shoulder or hip sticking out, the ribs sticking out on one side or leaning to one side. See our scoliosis guide.
• Ankylosing spondylitis: in the Swiss family study, 18 in 100 children of people with AS developed axial spondyloarthritis, and children of affected mothers were more often affected than children of affected fathers.^[35] NICE lists a family history of spondyloarthritis as a risk factor, so mention it if your child later develops long-lasting back pain.^[36]
• Spondylolysis: relatives of someone with the developmental type had about a 1 in 3 risk, and the authors advised looking for it early in brothers, sisters and children.^[38]
• Marfan syndrome, the common types of EDS, NF1 and NF2: each child of an affected parent has a 1 in 2 chance of inheriting the condition. A genetics service can explain the options if you are planning a family.^{[7][8][9][47][13]}

The evidence and its limits

When to get help

See a GP if your back pain does not improve after a few weeks of treating it at home, stops you doing day-to-day activities, worries you, or comes with weight loss, a lump or a change in the shape of your back, or pain that is worse at night.^[16]

Tell your GP about your family history if you are under 45, your back pain has lasted more than 3 months and it wakes you at night or eases with movement, and a parent, brother, sister or child has spondyloarthritis.^[36] Also mention it if a close relative has Marfan syndrome, EDS or neurofibromatosis, as a specialist can refer you for NHS genetic testing if needed.^[13]

Questions to ask

• Does my family history change what you think is causing my pain?
• Is there a specific inherited condition you want to rule out, and would a test change my treatment?
• Should my children be checked, and at what age?
• What can I do now to lower my risk of future back problems?

Frequently asked questions

Further reading

• Spinemathema guide: Acute back pain
• Spinemathema guide: Degenerative disc disease
• Spinemathema guide: Slipped disc
• Spinemathema guide: Scoliosis
• Spinemathema guide: Spondylolysis
• Spinemathema guide: Sacroiliac joint pain
• Spinemathema guide: Chiari malformation
• Spinemathema guide: Spinal tumours
• NHS: Genetic and genomic testing
• NHS: Ankylosing spondylitis

References

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This article is general information and is not a substitute for advice about your own situation. Please speak to your GP or specialist before making any change to your treatment.

Last checked: October 2026