What Causes Brain Tumors and Who Is at Risk?

Brain tumors arise from a tangle of causes rather than a single trigger, and for most people diagnosed, no clear reason can be identified. The only environmental exposure firmly established as a cause is moderate-to-high-dose ionizing radiation, while a handful of inherited genetic syndromes account for a small share of cases. Beyond those, researchers have identified a growing list of factors that nudge risk up or down, from body weight and immune history to specific mutations that arise spontaneously in brain cells. Who is most at risk depends heavily on the type of tumor involved, because “brain tumor” is not one disease but dozens, each with its own biology and its own demographic pattern.

Primary Versus Secondary Tumors

A basic distinction matters here. Primary brain tumors originate in the brain or spinal cord itself. Secondary brain tumors, also called brain metastases, start as cancers elsewhere in the body and spread to the brain. The two categories have different causes and different risk profiles. Secondary tumors are far more common overall, but when people ask what causes brain tumors, they usually mean primary ones. The risk factors discussed below apply to primary tumors unless noted otherwise.

Primary tumors themselves are a diverse group. Gliomas arise from the glial cells that support neurons. Meningiomas grow from the membranes surrounding the brain. Schwannomas develop on nerve sheaths. Each type has its own set of risk factors, and a finding that applies to meningiomas may not apply to gliomas at all. That tumor-type specificity runs through virtually every risk factor researchers have studied.

Ionizing Radiation Is the Strongest Known Environmental Cause

Exposure to moderate-to-high doses of ionizing radiation is the only environmental risk factor consistently linked to brain and central nervous system tumors across decades of research. A systematic review found elevated risks across multiple cohorts, with the association strongest for meningioma and somewhat weaker for glioma. The link was also stronger when radiation exposure occurred at younger ages.

Where the picture gets murkier is at lower doses. A meta-analysis specifically examining adult exposure to low-to-moderate doses of ionizing radiation found no meaningful dose-risk association for brain tumors overall.¹ That distinction matters because most people’s radiation exposure comes not from nuclear accidents or radiation therapy but from medical imaging.

The exception is children. Pediatric CT scans deliver small doses to the brain, but studies have found a measurable increase in brain tumor risk even from a single head CT in childhood. One large UK retrospective study estimated that cumulative CT doses of around 60 milligray roughly tripled the risk of brain cancer in children, though the absolute risk remained small: about one extra case of brain tumor per 10,000 head CT scans in the decade following the first scan.² A Dutch study echoed this, finding a statistically significant dose-risk relationship for brain tumors in children who received head CTs.³ A systematic review across multiple studies found that excess relative risk of a new brain tumor averaged about 1.29 for children exposed to one or more head CTs, with risk climbing in a dose-dependent way.⁴

None of this means parents should refuse a medically necessary CT scan. The absolute risk remains tiny, and a scan that identifies a serious injury or condition has immediate benefit. But it does explain why pediatricians and radiologists try to minimize unnecessary imaging in children and use the lowest effective dose when a scan is warranted.

What About Cell Phones?

Few topics in brain tumor epidemiology have generated as much public anxiety as cell phone radiation. Cell phones emit radiofrequency electromagnetic fields, which are non-ionizing, meaning they do not carry enough energy to directly damage DNA the way X-rays do. Most large-scale studies have not found a convincing increase in brain tumor incidence despite decades of rising phone use worldwide.

That said, a pooled analysis of case-control data reported a statistically significant increased risk of glioma among people who had used cell phones regularly for ten years or more, with the risk more pronounced on the side of the head where the phone was typically held.⁵ Critics have pointed out that these case-control studies rely on self-reported phone use and may be affected by recall bias, since people who already have a brain tumor may over-report phone use on the affected side. Population-level data has not shown the surge in glioma incidence that would be expected if long-term phone use were a strong cause. The International Agency for Research on Cancer classified radiofrequency fields as “possibly carcinogenic,” which is a weaker designation than many headlines suggested, essentially meaning the evidence is limited and not conclusive in either direction. Researchers continue to study this, but as of now, cell phone use has not been established as a confirmed cause of brain tumors.

Inherited Genetic Syndromes

A small but well-characterized group of hereditary conditions dramatically raises brain tumor risk. These syndromes involve germline mutations, meaning the genetic change is present in every cell of the body from birth. The best known include neurofibromatosis type 1 and type 2, tuberous sclerosis complex, von Hippel-Lindau disease, Li-Fraumeni syndrome, Turcot syndrome, Cowden disease, and Gorlin syndrome.⁶ Many of these are classified as neurocutaneous syndromes because they produce both skin findings and nervous system lesions.⁷

These syndromes account for only a fraction of all brain tumors, but they are important for families who carry them because surveillance and early detection can improve outcomes. A person with neurofibromatosis type 2, for instance, has a high lifetime probability of developing schwannomas and meningiomas. Li-Fraumeni syndrome, caused by mutations in the TP53 gene, raises the risk of many cancer types including gliomas. When brain tumors cluster in a family, genetic counseling can help identify whether a hereditary syndrome is involved.

Beyond these rare syndromes, genome-wide association studies have identified common genetic variants that modestly affect brain tumor risk in the general population. For example, variants in the VTI1A and ETFA genes have been linked to increased glioma susceptibility, with certain combinations of these variants raising risk by up to roughly threefold compared with non-carriers.⁸ A separate genome-wide analysis identified a risk locus for meningioma on chromosome 11.⁹ These common variants each have small individual effects, so knowing your genotype at any one of them would not meaningfully predict your personal risk. Their value is mainly in helping researchers understand which biological pathways matter in tumor formation.

How Tumor Type Varies by Age and Sex

Brain tumors do not strike all age groups equally, and the specific tumor types that dominate shift markedly across the lifespan. An analysis of over 21,000 molecularly confirmed cases found that adolescents and young adults had a distinctive mix, including tumors more typical of childhood alongside types usually seen in older adults. Several tumor types were specifically enriched in the young-adult age group, including IDH-mutant astrocytoma and certain ependymomas.¹⁰ Glioblastoma, the most aggressive primary brain tumor, peaks in incidence among older adults and is relatively rare in children.

Sex matters too, though the direction depends on the tumor. Glioblastoma is somewhat more common in men. Meningioma, by contrast, is markedly more common in women, suggesting a role for sex hormones. A review of sex and racial disparities in meningioma incidence found that women face higher risk overall, with age compounding that risk further.¹¹ Some researchers have explored whether hormone replacement therapy or oral contraceptive use influences meningioma growth, and the interplay between estrogen, progesterone, and meningioma biology remains an active area of study.

Allergies, Immune Function, and an Unexpected Protective Effect

One of the more surprising findings in brain tumor epidemiology is that people with a history of allergies appear to have a lower risk of glioma. A meta-analysis pooling data from multiple studies found that allergy was associated with about a 36% reduction in glioma risk. When broken down by type, asthma cut risk by roughly a third and eczema by about a quarter.¹² A large case-control study across Scandinavia and England reached a similar conclusion, reporting about a 30% reduction in glioma risk for people with any allergic condition.¹³ A more recent review of 40 observational studies confirmed this pattern.¹⁴

The leading hypothesis is that an overactive immune system, the kind that produces allergic reactions, may also be better at detecting and eliminating abnormal cells before they can develop into tumors. This is still speculative, and the association could partly reflect other biological differences between people who develop allergies and those who do not. Regardless of the mechanism, the pattern is robust enough that some researchers have explored allergy history as a factor in brain tumor risk models.

On the flip side, a suppressed immune system raises the risk of at least one brain tumor type. Organ transplant recipients who take immunosuppressive drugs have a dramatically elevated risk of primary central nervous system lymphoma. One study found that transplant recipients had an incidence of CNS lymphoma more than 65 times higher than the general population, and the risk was highest in the first 18 months after transplant and among recipients who were seronegative for Epstein-Barr virus before transplant.¹⁵ This particular tumor type is rare even in transplant recipients, but the magnitude of the risk increase underscores how much the immune system normally does to keep certain cancers in check within the brain.

Body Weight and Diet

Obesity has been linked to higher risk of several cancer types, and brain tumors are no exception, though the connection varies by tumor. A dose-response meta-analysis found that for every five-unit increase in body mass index, the risk of brain tumors overall rose by about 13%, with the association strongest for meningiomas, where the risk increase was about 19% per five-unit BMI increment.¹⁶ A large Norwegian prospective study found that obese women had about a 68% higher risk of meningioma compared with women at a healthy weight, though no such association was seen in men. Interestingly, that same study found that being overweight or obese was associated with a lower risk of schwannoma.¹⁷

Diet is harder to study. One area that has drawn attention is the potential role of N-nitroso compounds, chemicals that can form from nitrites used to cure meats like hot dogs, bacon, and deli meats. A population-based study found that mothers who ate cured meats more frequently during pregnancy had children with a higher risk of brain tumors, with those consuming cured meats at least twice a day facing about double the risk.¹⁸ Most epidemiological studies examining maternal cured-meat intake during pregnancy have found a positive association with childhood brain tumors.¹⁹ However, when researchers looked at adults eating processed meats and their own risk of glioma, a prospective study found no elevated risk among those with the highest intake.²⁰ The discrepancy may reflect the developing fetal brain being more vulnerable to these compounds than an adult brain, or it could reflect differences in study design. In either case, the evidence is stronger for prenatal exposure than for adult dietary habits.

Head Trauma and Brain Tumors

Whether head injuries can lead to brain tumors has been debated for a long time. A 2025 study using data from a large hospital system found that moderate to severe traumatic brain injury was associated with a higher incidence of malignant brain tumors compared with matched controls. The hazard ratio was about 1.67, meaning the risk was roughly two-thirds higher in the moderate-to-severe TBI group, and this held after adjusting for age, sex, and race.²¹ Mild TBI did not show the same elevation. A hospital-based case-control study in Afghanistan found that people with brain tumors were about twice as likely to report a prior head injury compared with controls.²²

The proposed mechanism involves chronic inflammation and tissue repair processes following significant brain injury, which could create a cellular environment more conducive to tumor initiation. But this area has important caveats. Recall bias can inflate the association in case-control studies: people diagnosed with a brain tumor may be more likely to remember and report previous head injuries. Detection bias is also possible, because someone who had a serious head injury may receive more brain imaging afterward, leading to earlier detection of a tumor that was already developing. The recent large-cohort study is more resistant to these biases, but even it cannot fully establish causation. Moderate to severe TBI is relatively uncommon, and the absolute risk of a brain tumor after one remains low.

The Cytomegalovirus Debate

Some researchers have reported finding human cytomegalovirus proteins and DNA in glioblastoma tissue, sparking interest in whether the virus plays a role in brain tumor development or progression. Multiple studies have explored this, and some have even suggested that antiviral drugs targeting CMV might slow glioblastoma growth.²³ More recent work has looked at targeting CMV in glioma stem cells specifically, with clinical trials testing herpesvirus-based therapeutic strategies.²⁴

But not everyone has been able to reproduce these findings. An independent study using multiple detection methods found no evidence of CMV in any of the brain tumors tested, leading the authors to conclude that CMV is not significantly associated with brain tumors in humans.²⁵ The field remains split. Whether CMV is a genuine contributor to glioblastoma biology or an incidental passenger that sometimes shows up in tumor tissue is still unresolved. For patients and their families, the practical implication right now is minimal: CMV status is not used in routine clinical decision-making for brain tumors, though antiviral-based treatment strategies are under investigation.

Pesticide Exposure

Occupational exposure to pesticides has been investigated as a possible risk factor, given that agricultural workers and others who handle these chemicals regularly have elevated contact. Results have been mixed. A large study found no association between insecticide or herbicide exposure and glioma risk in either men or women. However, women who reported ever using herbicides had a significantly increased risk of meningioma, with risk rising further with more years of exposure and higher cumulative doses.²⁶ Men did not show this pattern. This sex-specific finding raises the possibility of an interaction between pesticide exposure and hormonal factors, since meningioma already has a strong sex-linked risk profile, but the mechanism remains unclear.

How Molecular Profiling Has Changed the Landscape

Much of what researchers have learned about brain tumor causes in the past decade has come from molecular profiling, the ability to read the genetic and chemical signatures of tumors. The 2021 WHO classification of central nervous system tumors made molecular markers central to how tumors are defined and graded, replacing a system that leaned heavily on how cells looked under a microscope.²⁷ This has practical consequences. Two tumors that look identical under a microscope may behave very differently depending on their molecular profile, and they may respond to different treatments.

One of the most important molecular markers is the IDH mutation. IDH-mutant gliomas are the most common malignant primary brain tumor in young adults, and they carry a better prognosis than IDH-wildtype glioblastomas. Recent research using deep sequencing on tissues from 70 individuals found that the initial IDH mutation arises in glial progenitor cells, settling a long-standing question about the cellular origin of these tumors.²⁸ Low-level IDH mutations were found in the brain tissue surrounding the tumor in over a third of patients, suggesting that these mutations may be present in apparently normal-looking brain tissue for some time before a visible tumor forms.

U.S. cancer registries began incorporating molecular biomarkers for brain tumors in 2018. An epidemiological analysis using this data found that IDH-wildtype glioblastoma had an incidence rate more than twelve times higher than IDH-mutant astrocytomas. IDH mutation prevalence was highest in adolescents and young adults.²⁹ These molecular distinctions matter enormously for prognosis. A patient with an IDH-mutant glioma diagnosed at age 30 has a fundamentally different outlook than a patient with an IDH-wildtype glioblastoma diagnosed at age 65, even though both might once have been loosely grouped under “brain cancer.”

Dogs Get Gliomas Too

Companion dogs develop spontaneous brain tumors, particularly gliomas, that share striking similarities with their human counterparts. Comparative genomic studies have found molecular parallels between canine gliomas and human glioblastoma, including conserved mutational processes.³⁰ Certain breeds, especially brachycephalic ones with short, broad skulls, develop gliomas at higher rates, pointing to genetic predisposition in dogs just as hereditary syndromes predispose some humans.

The National Cancer Institute has launched a comparative brain tumor consortium to study canine brain cancers as a model for human disease.³¹ Dogs share many environmental exposures with their owners, they develop tumors spontaneously rather than through artificial induction, and their compressed lifespans make it possible to observe the full course of disease in a timeframe useful for research. New treatments tested in dogs with naturally occurring gliomas can provide evidence that bridges the gap between laboratory models and human clinical trials, potentially accelerating the development of therapies that would take far longer to test through conventional approaches alone.