What’s the REAL problem?

So, I admit it, as usual, I am using a study to talk about a hangup of mine.

As a community, we are INCREASINGLY obsessed with meibomian glands. This is not healthy and not helpful.

Why is this such a special concern to me? Because I fear parts of our community are losing their sense of what OUR problem is, and getting into hypnotized into seeing ourselves as part of the medical community sees us. We need to get back to basics sometimes and connect with the real problem.

Our problem is our symptoms and their impact on our lives. Eye discomfort. Pain. Light sensitivity. Burning. Grittiness. Irritation. Whatever your personal collection of symptoms is, the problem is how your eye and eyelid sensations are messing with your life activities and your quality of life. My personal term for this problem is ocular surface pain disorder.

Why do I insist on this point so much? Because there is so rarely a nice neat straight line to be drawn between our problem (symptoms) and a specific diagnosed dry eye parameter, whether that’s the number of “healthy” meibomian glands or the tear film osmolarity or any other measure. For example, we do not KNOW with any confidence, based on the evidence, that a certain number of dropped out or malfunctioning meibomian glands translates into a certain amount of discomfort. Many people have many missing glands yet no discomfort. Many people have mostly present glands and have plenty of discomfort.

Bottom line?

If there is no thoroughly documented scientifically confirmed direct causal relationship between losing meibomian glands and losing quality of life:

It does not make sense to focus exclusively on MG treatments to “solve” the problem;
It is not appropriate to mentally equate “loss of gland(s)” with “loss of quality of life”. This type of thinking contributes to anxiety and depression when we learn of changes to our glands. We have to remember that it’s not a problem until it’s a problem.

Let’s not get ahead of ourselves just because there’s an industry pumping out MG gizmos left and right and a lot of doctors pulling long faces over meibomian glands. Step back and see the big picture. If you have diseased glands that need treatment, by all means treat them.

But stop equating MG health with a miserable life. It’s not that simple. Remember we have to grapple directly with the miserable part - the symptoms - not just indirectly by tackling clinical signs just because they’re the lowest hanging medical fruit.

Exhibit A

In this recent study of children with low testosterone, loss of meibomian glands did not change the tear film. Yes, I know this is a kids study. It’s not about you. And we don’t know from the abstract whether they experienced any discomfort. But one of the most basic assumptions of the world of MG treatments is that any underfunction of the MGs will result in a poorer tear film. Yet here we are with evidence that is not a completely indisputable assumption. If it’s possible for gland loss not to make the tear film worse, then the argument that gland loss always causes discomfort gets weaker still.

Food for thought!

Noninvasive evaluation of anterior segment and tear film parameters and morphology of meibomian glands in a pediatric population with hypogonadism. Can GD et al, Ocul Surf. 2019 Sep 6

PURPOSE:
To compare the meibomian gland (MG), non-invasive tear film break-up time (NITFBUT), anterior segment measurements between healthy children and children with hypogonadism.
METHODS:
A total of 80 eyes of 40 children with hypogonadism and 86 eyes of 43 age- and sex-matched healthy subjects were included in the study. The mean keratometry (Km), maximum keratometry (Kmax), central (CCT), thinnest (TCT) and apical (ACT) corneal thicknesses, corneal volume (CV), anterior chamber depth (ACD), irido-corneal angle (ICA), first and average non-invasive NITFBUT, MG loss, morphology of MGs, and MG distortion grade, specular endothelial cell density (CD), coefficient of variation (CoV), and percentage of hexagonal cells (HG) were analysed.
RESULTS:
The mean CCT and TCT values were approximately 20 μm lower on average in patients with hypogonadism (p < 0.05). MG loss was present 56.1% of the healthy children, the ratio increased to 81.3% in children with hypogonadism (p < 0.001). The morphology and distortion grade did not show any significant differences between groups (p > 0.05). The mean NITFBUT value were similar between groups (p > 0.05). The mean CD value did not show any significant difference between groups, however it decreased in the hormone replacement therapy (HRT) group (p = 0.005).
CONCLUSIONS:
MG loss is a physiological process that is prominent in the condition of sex steroid deficiency, but does not cause tear film alterations in children. Future studies investigating sex and gender effect on the ocular surface system in an age-based fashion are required to clearly communicate influences in the arenas of ocular surface research.