Brain, other CNS and intracranial tumours risk factors


Preventable cases of brain tumours, UK


Brain tumours cases linked to ionising radiation exposure, UK

Not well understood

Brain tumours risk factors are not well understood, despite substantial research

Less than 1% of brain and other CNS cancer (ICD-10 C70-C72) cases each year in the UK are linked to major lifestyle and other risk factors.[1] The proportion of lifestyle-associated benign and uncertain behaviour brain and other CNS tumours, and other intracranial tumours, has not been estimated.

Brain and other CNS cancer risk is associated with a number of risk factors.

Brain and Other CNS Cancer Risk Factors

Increase risk (‘sufficient’ or ‘convincing’ evidence) May increase risk (‘limited’ or ‘probable’ evidence) Decreases risk (‘sufficient’ or ‘convincing’ evidence) May decrease risk (‘limited’ or ‘probable’ evidence)
  • X-radiation, gamma radiation
  • Radiofrequency electromagnetic fields (including from wireless phones) (glioma and acoustic neuroma only)
- -

International Agency for Research on Cancer (IARC) classification. World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) classification does not include brain and CNS cancers, due to limited evidence. Find out more about IARC and WCRF/AICR classifications.

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Ionising radiation in the form of x-rays and gamma rays is the only exposure which the International Agency for Research on Cancer (IARC) classifies as a cause of brain and CNS tumours.[1] Evidence on the effects of ionising radiation came initially from studies of atomic bomb survivors, though more recent studies explore the effects of radiation used to diagnose and treat illness, including X-rays, CT scans and radiotherapy.

Ionising radiation overall generally appears to be more strongly associated with meningioma risk than with glioma risk.[2] The risk of meningioma is increased by 64-510% with each Gray (Gy) of ionising radiation exposure received, data from four cohort studies showed.[2] In one of these studies the effect was not statistically significant.[2] Age at exposure, sex, and time since exposure does not appear to modify the effect of radiation on meningioma risk.[2] The risk of glioma appears to be increased by 8%-56% per Gy, though the upper estimate comes from an atomic bomb survivors study and was not statistically significant.[2] Younger age at exposure confers a stronger effect on glioma risk.[2]

Brain tumour risk is almost tripled in people who received 1-2 CT scans (total average X-ray dose around 60 milligrays (mGy)) during childhood or adolescence, large cohort studies have shown.[3,4]

The average x-ray dose from one head CT scan received up to and including age 20 is 28-44 mGy, depending on age and sex.[3]

People who have ever had dental X-rays taken from the sides of the head (bitewing technique) have double the risk of adult meningioma, a US case-control study showed, though over 90% of both cases and controls had received this type of X-ray.[5]

Radiotherapy for a primary brain tumour (compared with no radiotherapy) was associated with around 55% higher risk of secondary brain tumour, in a study of US patients treated between 1973 and 2002.[6]

People who received radiotherapy for cancer during childhood have a 14-fold higher risk of developing glioma later in life, compared with those who did not receive radiotherapy for their childhood cancer.[7] However this finding, from a large study of British childhood cancer survivors, was not quite statistically significant.[7] Analysing only those children whose primary cancer was in the central nervous system revealed that those treated with radiotherapy (versus those treated without) had a significantly higher risk of subsequent brain tumour.[7]The risk of second primary brain tumour increased linearly with increasing radiotherapy dose, with this effect much stronger for meningioma than glioma.[7]


  1. Cogliano VJ, Baan R, Straif K, et al. Preventable Exposures Associated With Human Cancers. J Natl Cancer I 2011; 103(24):1827-39.
  2. Braganza MZ, Kitahara CM, Berrington de González A, et al. Ionizing radiation and the risk of brain and central nervous system tumors: a systematic review. Neuro-Oncology 2012; 14(11):1316-24.
  3. Pearce MS, Salotti JA, Little MP, et al. Radiation exposure from CT scans in childhood and subsequent risk of leukaemia and brain tumours: a retrospective cohort study. Lancet 2012; 380(9840):499-505.
  4. Huang WY, Muo CH, Lin CY, et al. Paediatric head CT scan and subsequent risk of malignancy and benign brain tumour: a nation-wide population-based cohort study. Br J Cancer. 2014;110(9):2354-60.
  5. Claus EB, Calvocoressi L, Bondy ML, et al. Dental x-rays and risk of meningioma. Cancer 2012; 118(18):4530-37.
  6. Berrington de Gonzalez A, Curtis RE, Kry SF, et al. Proportion of second cancers attributable to radiotherapy treatment in adults: a cohort study in the US SEER cancer registries. Lancet Oncol 2011; 12(4):353-60.
  7. Taylor AJ, Little MP, Winter DL, et al. Population-Based Risks of CNS Tumors in Survivors of Childhood Cancer: The British Childhood Cancer Survivor Study. J Clin Oncol 2010; 28(36):5287-93.
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The International Agency for Research on Cancer (IARC) makes no judgement on the association between risk of most cancers (including meningioma) and mobile phone use, due to inadequate evidence.[1] IARC classifies mobile phone use as a possible cause of glioma and acoustic neuroma, based on limited evidence.[1] Most studies have reported no significant association between mobile phone use and brain tumour risk at the population or individual level, except in some studies a slight risk increase for specific (typically rare) brain tumour types, in the small proportion of people with the very highest levels/durations of use.[2,3,4] Firm conclusions are precluded by evidence limitations linked with the relative infancy of mobile phone technology, including relatively short follow-up and mainly adult participants.[2,3,4]

Childhood brain tumour risk is not associated with exposure to magnetic fields (from overhead power lines or broadcast transmitters) during childhood, a pooled analysis and cohort study have shown.[5,6]

Brain tumour risk in adults is not associated with occupational exposure to magnetic fields, large cohort studies in the UK and Netherlands have shown.[7,8]


  1. Baan R, Grosse Y, Lauby-Secretan B, et al. Carcinogenicity of radiofrequency electromagnetic fields. Lancet Oncol 2011; 12(7):624-6.
  2. The INTERPHONE Study Group. Brain tumour risk in relation to mobile telephone use: results of the INTERPHONE international case–control study. Int J Epidemiol 2010; 39(3):675-94.
  3. Frei P, Poulsen AH, Johansen C, et al. Use of mobile phones and risk of brain tumours: update of Danish cohort study. BMJ 2011; 343.d6387
  4. Pettersson D, Mathiesen T, Prochazka M, et al. Long-term mobile phone use and acoustic neuroma risk. Epidemiology. 2014 Mar;25(2):233-41.
  5. Kheifets L, Ahlbom A, Crespi CM, et al. A Pooled Analysis of Extremely Low-Frequency Magnetic Fields and Childhood Brain Tumors. Am J Epidemiol 2010; 172(7):752-61.
  6. Hauri DD, Spycher B, Huss A, et al. Exposure to radio-frequency electromagnetic fields from broadcast transmitters and risk of childhood cancer: a census-based cohort study. Am J Epidemiol. 2014;179(7):843-51.
  7. Sorahan T. Magnetic fields and brain tumour risks in UK electricity supply workers. Occup Med (Lond). 2014;64(3):157-65.
  8. Koeman T, van den Brandt PA, Slottje P, et al. Occupational extremely low-frequency magnetic field exposure and selected cancer outcomes in a prospective Dutch cohort. Cancer Causes Control. 2014;25(2):203-14.
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The risk of brain tumours is increased in a number of genetic conditions, though because these conditions are relatively rare, they account for only a small proportion of brain tumour cases.[1] The key conditions are listed below:

  • Neurofibromatoses (NF) Open a glossary item are a group of genetic conditions in which benign (non-invasive) growths affect the nervous system. NF type 1 (NF1) is thought to affect around 1 in 2,700 live births in the UK, whilst NF type 2 (NF2) affects around 1 in 33,000.[2] The risk of brain and CNS tumours is at least 23-43 times higher in NF1 patients than in the general population.[3,4] The risk of CNS tumours excluding those in the brain may be considerably higher.[4] Relative risk of brain tumours in NF1 patients increases with patient age.[5] Most NF1-associated brain tumours are gliomas. Both children and adults with NF1 have an increased risk of astrocytoma, with the tumour grade often higher in adults than children.[5] 5-25% of children with NF1 develop optic pathway gliomas.[5] NF2 patients are commonly diagnosed with bilateral vestibular schwannomas (acoustic neuromas). These affect 90-95% of NF2 patients, and they are typically benign but can cause hearing impairment.[6] Meningiomas affect 45-58% of NF2 patients, and usually arise at a younger age in these patients than in the general population.[6]
  • Tuberous sclerosis complex (TSC) Open a glossary item causes benign tumors to grow in the brain and elsewhere. The prevalence of TSC is estimated at around 1 in 25,000.[7,8] Up to 20% of TSC patients develop subependymal giant-cell astrocytomas.[9]
  • Li-Fraumeni syndrome Open a glossary item is a very rare genetic condition associated with increased risk of early-onset brain tumours and other cancer types. Astrocytomas, glioblastomas, medulloblastomas, and choroid plexus carcinomas are the most common brain tumours seen in this population.[10]
  • Von Hippel-Lindau syndrome Open a glossary item is thought to occur in around 1 in 43,000 live births in the UK.[2] Haemangioblastomas of the brain or spinal cord occur in 60-80% of people with this condition.[11]
  • Turner syndrome Open a glossary item affects around 1 in 2,000 female live births.[12] The risk of CNS tumours is around 4 times higher for Turner syndrome patients than the general population, with particularly increased risks of meningioma and childhood brain tumours.[13]
  • Turcot’s syndrome is associated with both brain and bowel tumours. Turcot’s syndrome type 1 is associated with early-onset gliomas, whilst type 2 is associated with medulloblastoma.[14]
  • Gorlin syndrome Open a glossary item (nevoid basal cell carcinoma) is thought to occur in around 1 in 15,000 live births in the UK.[2] Around 5-10% of people with this condition develop medulloblastomas.[15]

Having a family history of CNS tumours is associated with increased risk of developing a brain tumour oneself, pooled analyses have shown. Having a parent with a CNS tumour is associated with a 70% increased risk of being diagnosed with a brain or CNS tumour oneself, compared with the general population, and having a sibling diagnosed is associated with a doubling of risk.[16,17] Those with any first-degree relative (parent, sibling or child) diagnosed with glioma have a 77% increased risk of developing glioma themselves, and a 2.2- to 2.6-fold risk increase if the affected relative is a sibling.[17,18]Having a parent or sibling with meningioma confers a more than doubled (130% increased) risk of meningioma.[17] The magnitude of risk increases associated with family history varies by brain tumour subtype, but small sample sizes for these less common tumours preclude firm conclusions.[17] One study showed that offspring of melanoma patients have a 28% increased risk of being diagnosed with a nervous system tumour themselves.[19]


  1. Bondy ML, Scheurer ME, Malmer B, et al. Brain tumor epidemiology: Consensus from the Brain Tumor Epidemiology Consortium. Cancer 2008; 113(S7):1953-68.
  2. Evans DG, Howard E, Giblin C, et al. Birth incidence and prevalence of tumor-prone syndromes: Estimates from a UK family genetic register service. Am J Med Genet A 2010; 152A(2):327-32.
  3. Walker L, Thompson D, Easton D, et al. A prospective study of neurofibromatosis type 1 cancer incidence in the UK. Br J Cancer 2006; 95(2):233-38.
  4. Seminog OO, Goldacre MJ. Risk of benign tumours of nervous system, and of malignant neoplasms, in people with neurofibromatosis: population-based record-linkage study. Br J Cancer 2013 15; 108(1):193-8.
  5. Brems H, Beert E, de Ravel T, et al. Mechanisms in the pathogenesis of malignant tumours in neurofibromatosis type 1. Lancet Oncol 2009; 10(5):508-15.
  6. Asthagiri AR, Parry DM, Butman JA, et al. Neurofibromatosis type 2. Lancet; 373(9679):1974-86.
  7. Devlin LA, Shepherd CH, Crawford H, et al. Tuberous sclerosis complex: clinical features, diagnosis, and prevalence within Northern Ireland. Dev Med Child Neurol 2006; 48(6):495-99.
  8. Hong CH, Darling TN, Lee CH. Prevalence of tuberous sclerosis complex in Taiwan: a national population-based study. Neuroepidemiology 2009; 33(4):335-41.
  9. Adriaensen MEAPM, Schaefer-Prokop CM, Stijnen T, et al. Prevalence of subependymal giant cell tumors in patients with tuberous sclerosis and a review of the literature. Eur J Neurol 2009; 16(6):691-96.
  10. Schneider K, Garber J. Li-Fraumeni Syndrome. In: Pagon RA, Bird TD, Dolan CR, et al, editor. GeneReviews™ [internet]. Seattle (WA): University of Washington, 1999 [Updated 2010].
  11. Maher ER, Neumann HPH, Richard S. von Hippel-Lindau disease: A clinical and scientific review. Eur J Hum Genet 2011; 19(6):617-23.
  12. Stochholm K, Juul S, Juel K, et al. Prevalence, Incidence, Diagnostic Delay, and Mortality in Turner Syndrome. J Clin Endocr Metab 2006; 91(10):3897-902.
  13. Schoemaker MJ, Swerdlow AJ, Higgins CD, et al. Cancer incidence in women with Turner syndrome in Great Britain: a national cohort study. Lancet Oncol 2008; 9(3):239-46.
  14. Paraf F, Jothy S, Van Meir EG. Brain tumor-polyposis syndrome: two genetic diseases? J Clin Oncol 1997; 15(7):2744-58.
  15. Lo Muzio L. Nevoid basal cell carcinoma syndrome (Gorlin syndrome). Orphanet J Rare Dis 2008; 3:32.
  16. Hemminki K, Tretli S, Olsen JH, et al. Familial risks in nervous system tumours: joint Nordic study. Br J Cancer 2010; 102(12):1786-90.
  17. Hemminki K, Tretli S, Sundquist J, et al. Familial risks in nervous-system tumours: a histology-specific analysis from Sweden and Norway. Lancet Oncol 2009; 10(5):481-88.
  18. Scheurer ME, Etzel CJ, Liu M, et al. Familial aggregation of glioma: a pooled analysis. Am J Epidemiol 2010; 172(10):1099-107.
  19. Hemminki K, Sundquist J, Brandt A. Do discordant cancers share familial susceptibility? Eur J Cancer 2012; 48(8):1200-07.
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This section discusses the risk of subsequent primary brain or CNS tumours, not metastatic brain tumours. Radiotherapy or chemotherapy for the previous cancer may be implicated in the development of subsequent brain or CNS tumours.[1-3]

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Glioma risk is 12 times higher in survivors of childhood brain/CNS tumours, compared with the general population, a cohort study showed.[1] Meningioma risk is 10-20 times higher in brain/CNS tumour survivors, a cohort study showed.[2]

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Brain and/or CNS tumour risk is higher in survivors of childhood solid tumours (not including brain/CNS tumours),[1-3] non-Hodgkin lymphoma,[4] leukaemia (particularly acute lymphocytic leukaemia),[5-7] melanoma,[8] thyroid,[7] or prostate[7] cancers. Associations with other cancers remain unclear.[6,9,10]


  1. Maule M, Scélo G, Pastore G, et al. Second malignancies after childhood noncentral nervous system solid cancer: Results from 13 cancer registries. Int J Cancer 2011; 129(8):1940-52.
  2. Reulen RC, Frobisher C, Winter DL, et al. Long-term risks of subsequent primary neoplasms among survivors of childhood cancer. JAMA 2011; 305(22):2311-19.
  3. Friedman DL, Whitton J, Leisenring W, et al. Subsequent Neoplasms in 5-Year Survivors of Childhood Cancer: The Childhood Cancer Survivor Study. J Natl Cancer I 2010; 102(14):1083-95.
  4. Pirani M, Marcheselli R, Marcheselli L, et al. Risk for second malignancies in non-Hodgkin’s lymphoma survivors: a meta-analysis. Ann Oncol 2011; 22(8):1845-58.
  5. Nielsen SF, Bojesen SE, Birgens HS, et al. Risk of thyroid cancer, brain cancer, and non-Hodgkin lymphoma after adult leukemia: a nationwide study. Blood 2011; 118(15):4062-69.
  6. Inskip PD. Multiple primary tumors involving cancer of the brain and central nervous system as the first or subsequent cancer. Cancer 2003; 98(3):562-70.
  7. Kutsenko A, Berrington de Gonzalez A, Curtis RE, Rajaraman P. Risk of second benign brain tumors among cancer survivors in the surveillance, epidemiology, and end results program. Cancer Causes Control 2014;25(6):659-68.
  8. Scarbrough PM, Akushevich I, Wrensch M, et al. Exploring the association between melanoma and glioma risks. Ann Epidemiol. 2014 Jun;24(6):469-74.
  9. Subramanian S, Goldstein DP, Parlea L, et al. Second primary malignancy risk in thyroid cancer survivors: a systematic review and meta-analysis. Thyroid 2007; 17(12):1277-88.
  10. Spanogle JP, Clarke CA, Aroner S, et al. Risk of second primary malignancies following cutaneous melanoma diagnosis: A population-based study. J Am Acad Dermatol 2010; 62(5):757-67.
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Glioma risk is 22-40% lower in people with a history of allergy, asthma, eczema, or hayfever, meta-analyses have shown,[1-3] perhaps due to shared association with heightened immunity. Oligodendroglial tumour risk is 50% lower in people with a history of asthma, a pooled analysis showed.[4]

Meningioma risk is 23% lower in people with a history of allergy, though the association may be limited to eczema, a pooled analysis and meta-analysis have shown.[5,3]

Acoustic neuroma risk is 36% lower in people with a history of allergy, but parotid gland tumour risk is not associated with allergy, a pooled analysis showed.[3]


  1. Linos E, Raine T, Alonso A, et al. Atopy and Risk of Brain Tumors: A Meta-analysis. J Natl Cancer I 2007; 99(20):1544-50.
  2. Chen C, Xu T, Chen J, et al. Allergy and risk of glioma: a meta-analysis. Eur J Neurol 2011; 18(3):387-95.
  3. Turner MC, Krewski D, Armstrong BK, et al. Allergy and brain tumors in the INTERPHONE study: pooled results from Australia, Canada, France, Israel, and New Zealand. Cancer Causes Control. 2013 May;24(5):949-60.
  4. McCarthy BJ, Rankin KM, Aldape K, et al. Risk factors for oligodendroglial tumors: a pooled international study. Neuro-Oncology 2011; 13(2):242-50.
  5. Wang M, Chen C, Qu J, et al. Inverse association between eczema and meningioma: a meta-analysis. Cancer Cause Control 2011; 22(10):1355-63.
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Brain and other CNS tumour risk is higher in children and adolescents with congenital disorders, cohort studies have shown; this may vary by tumour and congenital disorder type.[1,2]

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Brain tumour risk is around doubled in people with HIV or AIDS, compared with the general population, meta-analyses showed.[1,2] Brain tumour risk is around five times higher in people with AIDS versus people without AIDS, a meta-analysis has shown.[2]

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Meningioma risk is 19% higher in postmenopausal hormone replacement therapy (HRT) ever-users compared with never-users, a meta-analysis showed.[1] Glioma risk is 32% lower in postmenopausal hormone replacement therapy (HRT) ever-users compared with never-users, a meta-analysis showed.[2]

Meningioma risk is not associated with oral contraceptive (OC) use, a meta-analysis showed.[1] Glioma risk is 29% lower in oral contraceptive (OC) ever-users compared with never-users, a meta-analysis showed.[2]

Meningioma risk is 32% higher in postmenopausal compared with premenopausal women, a meta-analysis showed.[1] Glioma risk is not associated with menopausal status, a meta-analysis showed.[2]

Meningioma risk is 24% higher in women with the highest number of live births, compared with those with no live births, a meta-analysis showed.[1]

Glioma risk is 40% higher in women with the oldest age at menarche, compared with those with the youngest, a meta-analysis showed.[2]

Meningioma risk is not associated with age at menarche, age at menopause, age at first birth, a meta-analysis showed.[1] Glioma risk is not associated with parity, age at menopause, or age at first birth, a meta-analysis showed.[2]

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Meningioma risk is 46% higher in obese (body mass index [BMI] 30+) females, compared with healthy weight (BMI 18.5-25) females, a meta-analysis showed.[1] Meningioma risk in males is not associated with BMI, a meta-analysis showed.[1] Glioma risk is not associated with BMI or waist size, cohort studies have shown.[2,3]

Astrocytoma risk is 38% higher, and medulloblastoma risk is 27% higher, in children born weighing 4kg+, compared with those born lighter, a meta-analysis showed.[4]

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Glioma risk is 70% higher in men 190+cm tall, compared with men 170-174cm tall, a meta-analysis showed.[1] Glioma risk is not associated with height in women, a meta-analysis showed.[1] Glioblastoma may be more associated with height, compared with other glioma types.

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Smoking is not associated with glioma risk, a meta-analysis showed.[1] Another meta-analysis showed meningioma risk is decreased by 18% in female ever-smokers but increased by 39% in male ever-smokers, compared with their never-smoking counterparts.[2] In a large UK cohort study of women, smoking was shown to have no effect on the risk of pituitary tumours, but acoustic neuroma risk was decreased among current smokers compared with never-smokers.[3]

Maternal smoking during pregnancy is not associated with brain tumour development in children, a meta-analysis and subsequent population-based case-control study showed.[4,5] However, a prospective study published since this showed a significant risk increase.[6] Paternal smoking during pregnancy confers a 29% increased brain tumour risk, according to a meta-analysis, though the quality of included studies is limited.[7] This finding has since been corroborated in the population-based case-control study.[5]


  1. Shao C, Zhao W, Qi Z, He J. Smoking and Glioma Risk: Evidence From a Meta-Analysis of 25 Observational Studies. Medicine (Baltimore). 2016 Jan;95(2):e2447.
  2. Claus EB, Walsh KM, Calvocoressi L, et al. Cigarette Smoking and Risk of Meningioma: The Effect of Gender. Cancer Epidem Biomar 2012; 21(6):943-50.
  3. Benson VS, Green J, Pirie K, et al. Cigarette smoking and risk of acoustic neuromas and pituitary tumours in the Million Women Study. Br J Cancer 2010; 102(11):1654-56.
  4. Huncharek M, Kupelnick B, Klassen H. Maternal Smoking during Pregnancy and the Risk of Childhood Brain Tumors: A Meta-analysis of 6566 Subjects from Twelve Epidemiological Studies. J Neuro-Oncol 2002; 57(1):51-57.
  5. Plichart M, Menegaux F, Lacour B, et al. Parental smoking, maternal alcohol, coffee and tea consumption during pregnancy and childhood malignant central nervous system tumours: the ESCALE study (SFCE). Eur J Cancer Prev 2008; 17(4):376-83.
  6. Brooks DR, Mucci LA, Hatch EE, et al. Maternal smoking during pregnancy and risk of brain tumors in the offspring. A prospective study of 1.4 million Swedish births. Cancer Cause Control 2004; 15(10):997-1005.
  7. Huncharek M, Kupelnick B, et al. Paternal smoking during pregnancy and the risk of childhood brain tumors: results of a meta-analysis. In Vivo 2001; 15(6):535-41.
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The few workplace exposures for which there is any evidence (albeit very limited) of an association with brain tumour risk - inorganic lead, non-arsenical insecticides, and epichlorohydrin - are thought to account altogether for far less than one per cent of all brain tumour cases in the UK.[1] Meningioma in particular may be associated with lead exposure.[2]

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The World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) make no judgment on the association between brain tumour risk and dietary intakes, stating that 'because these cancers are uncommon, any study investigating their possible links with food, nutrition, and physical activity would be unlikely to be fruitful. Because they are diverse, any investigation that grouped all of them together would also be unlikely to show consistent results.[1]

Childhood brain tumour risk may be reduced with use of prenatal multivitamin supplements, though specific beneficial components and mechanism of effect remain unclear.[2]


  1. World Cancer Research Fund/American Institute for Cancer Research. Food, Nutrition, Physical Activity, and the Prevention of Cancer: a Global Perspective. Washington DC: AICR; 2007.
  2. Goh YI, Bollano E, Einarson TR, et al. Prenatal Multivitamin Supplementation and Rates of Pediatric Cancers: A Meta-Analysis. Clin Pharmacol Ther 2007; 81(5):685-91.
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Brain tumour risk is not associated with intake of the following foods, meta- and pooled analyses, systematic reviews or large cohort studies have shown:

  • Processed and/or red meat (glioma).[1,2]
  • Cured meat (though some evidence of risk increase).[3]
  • Fruit and vegetables.[1,4,5]
  • Tea and coffee (glioma) (though some evidence of risk decrease for tea drinking versus non-drinking[6]).
  • Alcohol.[7,8]
  • Physical activity[9] (though some evidence of risk decrease for strenuous exercise at least twice a week[9]).
  • Aspirin and non-aspirin non-steroidal anti-inflammatory drugs (NSAIDs) (though some evidence of risk increase).[10]
  • Occupational formaldehyde exposure.[11,12]
  • Head injuries, headaches and seizures (any apparent risk increase probably reflects early brain tumour symptoms, which may also predispose to head injury).[13-19]
  • Personal use of hair dyes,[20] and maternal use of hair dyes (childhood brain tumours).[21]


  1. Dubrow R, Darefsky AS, Park Y, et al. Dietary Components Related to N-Nitroso Compound Formation: A Prospective Study of Adult Glioma. Cancer Epidem Biomar 2010; 19(7):1709-22.
  2. Michaud DS, Holick CN, Batchelor TT, et al. Prospective study of meat intake and dietary nitrates, nitrites, and nitrosamines and risk of adult glioma. Am J Clin Nutr 2009; 90(3):570-77.
  3. Huncharek M, Kupelnick B, Wheeler L. Dietary cured meat and the risk of adult glioma: a meta-analysis of nine observational studies. J Environ Pathol Tox 2003; 22(2):129-37.
  4. Terry MB, Howe G, Pogoda JM, et al. An International Case-Control Study of Adult Diet and Brain Tumor Risk: A Histology-Specific Analysis by Food Group. Ann Epidemiol 2009; 19(3):161-71.
  5. Holick CN, Giovannucci EL, Rosner B, et al. Prospective study of intake of fruit, vegetables, and carotenoids and the risk of adult glioma. Am J Clin Nutr 2007; 85(3):877-86.
  6. Malerba S, Galeone C, Pelucchi C, et al. A meta-analysis of coffee and tea consumption and the risk of glioma in adults. Cancer Causes Control. 2013 Feb;24(2):267-76.
  7. Galeone C, Malerba S, Rota M, et al. A meta-analysis of alcohol consumption and the risk of brain tumours. Ann Oncol 2013; 24(2):514-23.
  8. Qi ZY, Shao C, Yang C3, et al. Alcohol consumption and risk of glioma: a meta-analysis of 19 observational studies. Nutrients. 2014 Jan 27;6(2):504-16.
  9. Benson VS, Pirie K, Green J, et al. Lifestyle factors and primary glioma and meningioma tumours in the Million Women Study cohort. Br J Cancer 2008; 99(1):185-90.
  10. Liu Y, Lu Y, Wang J, et al. Association between non-steroidal anti-inflammatory drug use and brain tumour risk: a meta-analysis. Br J Clin Pharmacol. 2013 Dec 17.
  11. World Health Ogranization, International Agency for Research on Cancer. Volume 88 Formaldehyde, 2-Butoxyethanol and 1-tert-Butoxypropan-2-ol. Summary of Data Reported and Evaluation, 2006.
  12. Bosetti C, McLaughlin JK, Tarone RE, et al. Formaldehyde and cancer risk: a quantitative review of cohort studies through 2006. Ann Oncol. 2008 Jan;19(1):29-43.
  13. Bondy ML, Scheurer ME, Malmer B, et al. Brain tumor epidemiology: Consensus from the Brain Tumor Epidemiology Consortium. Cancer 2008; 113(S7):1953-68.
  14. Chen YH, Keller JJ, Kang JH, et al. Association between traumatic brain injury and the subsequent risk of brain cancer. J Neurotrauma 2012; 29(7):1328-33.
  15. Kirkman MA, Albert AF. Traumatic brain injury and subsequent risk of developing brain tumors. J Neurotrauma 2012; 29(13):2365-6.
  16. Khan S, Evans A, Rorke-Adams L, et al. Head injury, diagnostic X-rays, and risk of medulloblastoma and primitive neuroectodermal tumor: a Children’s Oncology Group study. Cancer Cause Control 2010; 21(7):1017-23.
  17. Cea-Soriano L, Wallander MA, Garcia Rodriguez LA. Epidemiology of meningioma in the United Kingdom. Neuroepidemiology 2012; 39(1):27-34.
  18. Wilne S, Collier J, Kennedy C, et al. Presentation of childhood CNS tumours: a systematic review and meta-analysis. The Lancet Oncol 2007; 8(8):685-95.
  19. Weller M, Stupp R, Wick W. Epilepsy meets cancer: when, why, and what to do about it? Lancet Oncol 2012; 13(9):e375-e82.
  20. Shao C, Qi ZY, Hui GZ, et al. Personal hair dyes use and risk of glioma: a meta-analysis. Int J Clin Exp Med. 2013 Sep 25;6(9):757-65.
  21. Efird JT, Holly EA, Cordier S, et al. Beauty product-related exposures and childhood brain tumors in seven countries: results from the SEARCH International Brain Tumor Study. J Neuro-Oncol 2005; 72(2):133-47.
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