ANSWER: The synthesis of the Lewis antigens is dependent on the interaction of two different enzymes (fucosyltransferases) that are the products of two different genes:

1. The FUT2 or the secretor (Se) gene locus (part of the synthesis of the H blood group antigen) that encodes FUT2 enzyme

2. The FUT3 gene locus which encodes an additional fucosyltransferase enzyme called FUT3.

Your final Lewis status is the result of the sequential action of these two enzymes. A simplified description would be that FUT3 codes precursor substance into the 'Lewis a' antigen. This is then acted on by the FUT2 enzyme which converts all the 'Lewis a' antigen into to 'Lewis b'. Thus the genetic basis for secretor status: non-secretors have a 'null gene' on the FUT2 locus, they cannot convert their 'Lewis a' substance into 'Lewis b' (they remain 'Lewis a+b-').

Secretors have the FUT2gene, and can make the FUT2 enzyme, which then can convert their 'Lewis a' into 'Lewis b.' That is why secretors are 'Lewis a-b+'. Double Lewis negative individuals (Lewis a-b-) lack the FUT3 gene enzyme which prohibits them from making 'Lewis a' (and consequently 'Lewis b').

The Lewis (a+b+) phenotype may occur in individuals where 'Lewis a' is incompletely converted into 'Lewis b' leaving some Lewis a substance remaining. This can due to a mutation in the FUT2 gene. Its occurence is quite rare. Many researchers consider the 'Lewis a+b+' state a transient one, rarely seen outside of the rare genetic mutation, and occasionally during pregnancy.Diet-wise you should consider yourself a secretor for the purpose of food determination.

Here is a good description (if a bit technical) of the Lewis system

Here is a link to a discussion of secretor status and Lewis groups.