Food and Behaviour Research

Donate Log In

Abnormal cerebral phospholipid metabolism in dyslexia indicated by phosphorus-31 magnetic resonance spectroscopy

Richardson, A.J., Cox, I.J., Sargentoni, J., Puri, B.K. (1997) NMR in Biomedicine 10(7) 309-14. 

Web URL: View this and related research articles via PubMed here


It has recently been suggested that many of the features of dyslexia may be explicable in terms of an abnormality of membrane phospholipid metabolism.

To investigate this we studied 12 dyslexic and 10 non-dyslexic adults using in vivo cerebral phosphorus-31 magnetic resonance spectroscopy (31P MRS), as the phosphomonoester (PME) and phosphodiester (PDE) peaks include indices of membrane phospholipid turnover. Spectral localization was achieved using four-dimensional chemical shift imaging methods.

The PME peak area was significantly elevated in the dyslexic group, as evidenced by higher ratios of PME/total phosphorus (F = 9.5, p < 0.006), PME/beta NTP (F = 17.5, p < 0.001) and PME/PDE (F = 6.9, p < 0.02). No other spectral measurements differed significantly between the groups.

These findings are consistent with the hypothesis that membrane phospholipid metabolism is abnormal in dyslexia. The PME peak is multicomponent, but predominantly consists of phosphoethanolamine (PE) and phosphocholine (PC), which are precursors of membrane phospholipids.

Our finding of raised PME in dyslexia could therefore reflect reduced incorporation of phospholipids into cell membranes, although definitive interpretation must await further evidence.


The proposal that dyslexia may involve abnormalities of fatty acid metabolism was investigated here using brain imaging with 31- phosphorus MRS.

This technique allows the identification and measurement of seven different phosphorus metabolites, of which two provide information on membrane lipid turnover.  Phosphomonoesters (PMEs) include the precursors of membrane phospholipids, while phosphodiesters (PDEs) provide a measure of their breakdown products.

Results showed a clear excess of PMEs in dyslexic adults compared with controls while PDE levels were normal - suggesting a problem with the synthesis of membrane phospholipids in dyslexia. 

They are also consistent with the proposal that dyslexia may involve a relative deficiency in omega-3 (and possibly omega-6) highly unsaturated fatty acids (HUFA).  To form membrane phospholipids, PMEs have to combine with diacylglycerols - molecules with two fatty acids.  Should the ‘right’ fatty acids not be available, this process could be impaired, resulting in an accumulation of the PME precursors.

Further investigation is still needed to explore the possible reasons for these findings, but they are consistent with the proposal that membrane lipid metabolism in dyslexia may be abnormal.

For more information on fatty acids in dyslexia and related conditions, and their relevance to nutrition and diet, please see the FAB handout: