Clinically, P. acnes is the most commonly isolated anaerobic bacterium in the lid, conjunctiva, and meibomian gland secretions

Something has really helped my eyes, especially with light sensitivity.
It is strictly bacteria.
its either Bifido Longum 35624 or Propionibacterium Freudenreichii.
Ive gone back and forth with these two, both could make sense in different ways coming from Accutane.

The antagonistic influences of androgens and retinoic acid suggests that, under physiologic conditions there is a balance between the effects of androgens and retinoids.
** Retinoids generally antagonize androgen function.**

^One’s maybe PFS and one’s not.
All I have to do is pay attention to the eyes(sort of talking to myself).

**Im sure your all mostly aware of making the case for androgens in the meibomian gland, **
here’s a case for retinoic acid.
This would be different then taking Accutane that can cause dry eye, because I believe there could be some conflict with local vitamin a metabolism.

Hypovitaminosis A should be suspected in all cases of night blindness, ocular surface foreign body sensation, and photophobia without other evident causes. Crying without tearing is another relevant symptom of hypovitaminosis A. Recurrent hordeolum, meibomian gland dysfunction identified by gland dropout or inflammation with thickened lipid secretion, corneal epithelial defect, conjunctiva metaplasia (where Bitot’s spot is an advanced form and a hallmark), and diffuse punctate keratitis also represent signs suspicious for hypovitaminosis A.

Ocular surface assessments may be performed with vital staining and tear secretion measurements (fluorescein dye and Schirmer’s test). Corneal and conjunctival impression cytology allows documentation of ocular surface epithelial metaplasia, square and speculate cells morphology, reduced nuclear size, and the absence or paucity of goblet cells on microscopy. Ocular surface assessments have demonstrated utility as simple and mildly invasive methods of recording and monitoring hypovitaminosis A in early xerophthalmia(61).

A case for Androgens, again here its showing downregulated Receptors.

Finasteride and dutasteride impair ocular
function and cause development of dry eye
disease
Androgen deficiency produces pathophysiological
changes manifested in reduction of tear production
and evaporative dry eye conditions [27-32]. Meibomian
gland disease and altered lipid patterns in meibomian
gland secretions were observed in women with complete androgen insensitivity syndrome [33]. Finasteride
administration significantly downregulated androgen
receptors (ARs) in the lacrimal gland the significance
observed with tear film break up time (TBUT) and
tear flow could be attributed to the lack of 5α-DHT in
the lacrimal glands [20,23]. Finasteride treated female
rats showed 49% of significant reduction in tear flow
at the end of the 10th day. There was a considerable
29% significant TBUT reduction observed in female
rats. Finasteride treated male rats showed significant
40% and 63% reductions for tear flow and TBUT, respectively.

So are ARs upregulated or downregulated in PFS when it comes to the chronic state?
It cant be both right?

Ocular surface assessments have demonstrated utility as simple and mildly invasive methods of recording and monitoring PFS.