It is well established that aluminium is toxic at the cellular level and that pathological symptoms follow its entry into organisms (plants, fish, humans) when the normal exclusion mechanisms fail or are bypassed, as for example in renal dialysis. The present debate concerns the availability of environmental aluminium and the possible impact of its slow and insidious absorption and accumulation in vulnerable individuals. Silicon is considered as essential element but the mechanisms underlying its essentiality remain unknown and binding of the element (through oxygen) with biomolecules has not been demonstrated. There is, however, a unique affinity between aluminium and silicon, not only in solid state chemistry ([AlO4]5- and [SiO4]4- are isostructural), but also in aqueous solution chemistry as illustrated by the synthesis of zeolite from aluminate and silicate anions at high pH and under hydrothermal conditions. This affinity exists also in very dilute solution (< 10(-5) M) at near-neutral pH when hydroxyalumino-silicate species form. These species mediate the bioavailability and cellular toxicity of aluminium. The observed effects of silicon deficiency can be attributed to consequential aluminium availability. There are important implications for the epidemiology and biochemistry of aluminium-induced disorders and any consideration of one element must include the other.