Dyslexia is caused by differences in how the brain processes language, specifically the sounds that make up words. It affects about 20 percent of the population and accounts for 80 to 90 percent of all learning disabilities. Rather than a single cause, dyslexia results from an interaction between inherited genetic traits, structural differences in the brain, and certain prenatal environmental exposures.
The Core Problem: Processing Speech Sounds
At its heart, dyslexia is a difficulty with phonological processing, meaning the brain struggles to break spoken language into its smallest sound units. Reading requires you to match written letters to their corresponding sounds, then blend those sounds together to produce a word. Spelling demands the reverse. When someone has trouble representing and manipulating these individual sounds, both reading and spelling become unreliable. This is why the hallmark sign of dyslexia is poor “phonemic awareness,” the ability to isolate, rearrange, or substitute sounds within words (removing the “s” from “slid” to get “lid,” for example, or swapping the first sound in “bat” to make “hat”).
This phonological difficulty is not a problem with intelligence, vision, or effort. It is a specific bottleneck in the language-processing chain that makes decoding written words slow and error-prone, even when comprehension and reasoning skills are perfectly intact.
Genetics Account for Most of the Risk
Dyslexia runs in families, and twin studies estimate its heritability at 60 to 70 percent from a young age onward. If one parent has dyslexia, the chances of a child also having it are substantially higher than in the general population.
Researchers have identified several specific genes linked to dyslexia risk, including three (known as DYX1C1, DCDC2, and KIAA0319) that play roles in neuronal migration, the process by which brain cells move into their correct positions during fetal development. Variations in these genes affect the volume of white matter, the brain’s wiring, in a left-hemisphere region critical for reading. Because multiple genes contribute, no single gene “causes” dyslexia. Instead, different combinations of genetic variants raise or lower a person’s susceptibility, which helps explain why dyslexia exists on a spectrum from mild to severe.
How the Dyslexic Brain Differs
Imaging studies have revealed consistent structural and functional differences in the brains of people with dyslexia. These differences cluster in three left-hemisphere areas: the back of the brain where visual letter recognition happens, a region near the top and side of the brain involved in connecting sounds to letters, and a frontal area involved in speech production. People with dyslexia tend to have less gray and white matter volume in these zones, along with altered wiring between them.
One particularly important piece of wiring is the left arcuate fasciculus, a white matter tract that connects areas responsible for hearing and producing speech. In kindergarten-age children who haven’t yet learned to read, the volume and structural integrity of this tract already predict phonological awareness scores. In prereading children specifically, the correlation between this tract’s volume and sound-blending ability is strong (r = 0.74), suggesting that the neural architecture for reading is partly in place before formal instruction even begins.
Functional brain scans tell a complementary story. During reading tasks, people with dyslexia consistently show reduced activation in the left occipito-temporal cortex, a region sometimes called the brain’s “word form area.” This finding has been replicated across cultures and age groups. Adults with dyslexia who have learned to compensate through years of practice still show this reduced activation during reading, even when other brain functions appear normal.
Prenatal and Early-Life Risk Factors
While genetics are the dominant driver, several environmental factors during pregnancy and birth can raise dyslexia risk, often by interacting with genetic vulnerability. Preterm birth increases the odds of dyslexia by about 30 percent. Maternal infections during pregnancy raise the risk by roughly 59 percent, and difficult vaginal delivery increases risk by a similar margin.
Prenatal exposure to nicotine is associated with poorer single-word decoding skills and appears to interact directly with the dyslexia candidate gene DYX1C1, meaning smoking during pregnancy may amplify an existing genetic predisposition. Prenatal cocaine exposure is linked to deficits in reading comprehension and verbal short-term memory. Exposure to environmental toxins like lead during the perinatal period also impairs reading-related academic achievement. Even maternal psychological stress during pregnancy is associated with poorer literacy outcomes in children.
None of these factors alone will cause dyslexia in a child with no genetic risk, but they can push a genetically susceptible child past the threshold where reading difficulties become apparent.
The Visual Processing Theory
Beyond the widely accepted phonological explanation, some researchers argue that a subset of people with dyslexia also have problems with rapid visual processing. This theory centers on a type of brain cell called magnocellular neurons, which specialize in detecting fast-changing, low-contrast visual information. These cells help the brain track the precise order of letters in a word.
Studies have shown that some people with dyslexia respond poorly to the specific kinds of stimuli these cells handle (low contrast, flickering patterns) while responding normally or even better than average to stimuli handled by a different cell type. Magnocellular neurons also supply input to the brain’s attentional system, helping direct the eye to the right part of a word for detailed analysis. Impairment in this pathway could contribute to the letter-sequencing errors and slow reading speed that characterize dyslexia.
This visual processing deficit likely doesn’t apply to everyone with dyslexia. Research on well-compensated adults with dyslexia found that visual and motor deficits were “only very occasional,” while the phonological and reading impairment was universal. The phonological deficit remains the core feature; visual processing differences may add to it in some individuals.
What About the Cerebellum?
A once-popular theory proposed that dyslexia originates in the cerebellum, the brain structure at the base of the skull that helps automate learned skills. The idea was that if the cerebellum couldn’t properly automate the mechanics of reading, fluency would suffer. This theory inspired treatments like balance-board exercises aimed at stimulating cerebellar function.
Recent research from Georgetown University Medical Center has largely dismantled this theory. Brain imaging showed that the cerebellum is not engaged during reading in typical readers and does not differ in children with dyslexia. The cortical regions known to drive reading showed no communication with the cerebellum during word processing in either group. As the researchers put it, standing on a wobble board is not going to improve a child’s reading skills. The evidence for the cerebellar deficit theory “was never particularly strong,” yet it gained traction and even spawned commercial interventions with no scientific backing.
Why Children Vary So Much
Because dyslexia results from multiple genes, multiple brain regions, and a range of environmental influences, no two people with dyslexia are exactly alike. Some struggle mainly with sounding out unfamiliar words. Others read accurately but painfully slowly. Some have additional difficulties with motor coordination or attention, while others have dyslexia as an isolated finding. Children tend to show a broader range of co-occurring difficulties, while adults who have compensated over time often present with a more focused reading and phonological deficit.
This variability also explains why dyslexia is not something a child simply “grows out of.” The underlying brain differences persist into adulthood. What changes with good instruction and practice is the person’s ability to work around those differences, recruiting alternative brain pathways to achieve functional reading. The cause remains, but its impact can be substantially reduced.