Interesting query! Mike Lemp and I in one of our early papers claimed that several blinking abnormalities can cause problems with the tear film, with the ocular surface, with the tarsal inner surface, and so on. What you mention is the lack of lid-globe congruity. The evenness of the gap between the two solid surfaces having a relative and considerable speed difference between them definitely affects the shear rate distribution. When the lid itself is rigid then the system becomes less forgiving for such abnormalities.
If the gap is somewhat larger at locations(< 150 micrometers) that is less of a problem unless air starts to enter under the lid. Where the gap becomes real narrow (< 1 micrometer) that could mean a switch over to boundary lubrication, greater stress transfer, and marring of the tissue surfaces. One could envision sterile inflammation of the lid secondary to increased friction.
In general, the lacrimal system is quite forgiving, if one considers the success of contact lens wear. Especially initially, the lens design did not take into account the interference of a foreign body, actually a prosthesis to tear film instability and problems with lubrication and the lenses still worked fairly well.
Lasik surgery does alter the corneal profile considerably, so it should affect the lid-globe congruity. While over most area the gap becomes larger, in the peripheral region there could by some tight gaps. If so, that could explain in part the increase in lid inflammation and meibomian gland problems.
If this were the case then the role of an artificial tear that has a high disjoining pressure under the lid would resist tear layer thinning. In such eyes the wettability would be doubly as important.
Sorry I cannot address the possible existence of defective genes. 'With tongue in cheek,' is this not often a fancy way of blaming the patient for a possible iatrogenic problem?