Matteo Corbellino

Entrepreneur through acquisition, board director and experienced strategy advisor currently exploring the science-driven side of things.

[Bryan Johnson @bryan_johnson]

Your eyes are in danger. Read this.

This post is important. Bookmark it.

> 87% of adults over 40 have this
> younger people too bc of screens
> leads to permanent eye damage

Here we go.

You have ~60 meibomian glands per eye, split across the upper and lower lid. They are like pores, secreting nourishing oil (meibum) onto your tear film to prevent rapid evaporation.

They become dysfunctional from just about everything….age, androgen deficiency, menopause, hormone replacement, oral contraceptives, isotretinoin, antihistamines, SSRIs, tricyclics, beta blockers, diuretics, anticholinergics, preserved eye drops, incomplete blinking, reduced blink rate, screen use, contact lens wear, ocular rosacea…and 50+ other things.

When these glands clog, the meibocytes die, and the gland drops out. Conventional medicine considers total dropout irreversible. This is bad.

The dropout leads to evaporative dry eye disease, which triggers vision degradation such as blurred text, glare at night, light sensitivity, and neuropathic ocular pain.

Left long enough, it can scar the cornea and permanently damage vision.

I just learned that I have meaningful meibomian gland dropout. This is why my eyes are irritated.

I’ve been doing this longevity thing for five years and never once have I heard anyone talk about this critical part of eye health. I’m befuddled why.

I’ve also seen two eye doctors in the past few years, neither of them brought up meibomian glands! How is this possible? I’m so confused.

I’m going to get you up to speed so you can find out where you’re at and then what you can do about it if you have meibomian gland dysfunction (MGD).

First, how big of a problem is this? A meta analysis of 20,518 adults over 40 found signs of meibomian gland dysfunction (MGD) in more than 87%.

My eye doctors think the 87% is closer to accurate for much younger ages too. Partly linked to decreased blink rates due to increased screen time.

Symptoms are a terrible gauge. MGD is usually silent. Population studies across multiple countries show that the majority of MGD cases, roughly 60-85%, are asymptomatic, falling below clinical symptom thresholds.

When it does surface, it hides as ordinary dry eye, enabling the worsening of the condition and permanent dropout.

Advanced MGD can numb the cornea, further masking subjective symptoms, as the disease advances.

Here is what happened to me.

I got a gnarly chalazion/stye and went to a new eye doctor my team found, Dr Amir Moarefi. He diagnosed me with advanced meibomian gland dysfunction via several diagnostic tests.

On a Schirmer test (strips of paper put under the eyelid), my tear production was under 10 mm over five minutes in both eyes, and stayed under 10 even with numbing drops, confirming concurrent aqueous deficiency alongside evaporative disease.

This is official dry eye territory.

We then imaged my meibomian glands using infrared meibography and found significant drop out. Drop out is considered permanent. What we couldn’t tell initially was how many acini had fully atrophied versus suffered reversible ductal obstruction.

We got to work reviewing evidence, mapping out a protocol and starting therapies.

The first thing we did was in-office intense pulsed light (IPL), radio frequency (RF) and intraductal probing (the Maskin protocol) to address the inflammation and physically reopen the clogged glands.

The probing is done by using 1mm, 2mm, and 4mm probes, inserting them into each gland orifice. Sounds awful. It kind of is. I do it without numbing but you may find the numbing necessary.

When the probe is inserted into a clogged gland, you hear a popping sound, like a blister popping. It breaks up intraductal hyperkeratinization and periductal fibrotic tissue that’s accumulated, clearing the path for oil to be expressed again.

(Note on probing: the science on this probing therapy is not settled so consider it experimental).

My doctor then expressed my glands, using a roller device to expel any build up and kickstart the gland’s natural expression. This is really painful. Brings you to tears.

In conjunction with the IPL, RF and probing, I was doing eye warm compresses two times a day, morning and night.

Healthy meibum melts around 90 to 93°F (32 to 34°C). It thickens with MGD, raising the melting point above 104°F (40°C). Given that roughly 9°F (5°C) is lost crossing the eyelid, getting to 104°F (40°C) at the gland requires holding the outer lid surface near 113°F (45°C). Stay under 113°F (45°C) to avoid risk of thermal injury.

I used an electric device and a thermal gun to ensure an external eyelid surface temperature of ~113°F (45°C), the threshold required to melt hyper-viscous, altered meibum without thermal injury to the cornea.

Gland dysfunction makes your natural oil resemble sticky toothpaste versus smooth oil. This makes it more prone to clogging. The heat warms the oil to melt and allows it to be expressed.

We then added a third therapy, a special red light therapy from my new friends from Espansione Group. They make a lot of the eye care technology used throughout the world. I reached out to them after reading their science publications and within a week they flew to LA from Italy with their devices so I could be treated.

I used their eye-light device which combines IPL and 630nm red low-level light. The proposed mechanism is stimulation of mitochondrial ATP production in meibocytes and reduced periorbital inflammation.

With this protocol, we’ve seen a 30% improvement in meibomian gland function (using imaging). My glands look healthier, eye irritation has lessened, my subjective symptoms have subsided, and when we probe now, we encounter minimal fibrotic resistance (popping).

Given that I did four therapies at the same time: IPL, RF, probing, and low level light therapy, I can’t determine which therapy did what.

Ok, here are your instructions:

Signs to watch: burning or grit. Vision that blurs, then clears when you blink. Watery eyes (dryness triggers reflex tears). Red, crusty, or bumpy lid margins. Recurring styes. Contacts that stopped being comfortable. Worse on screens, planes, or AC. Any of these, especially after 40, best to get a gland exam.

What to ask your eye doctor to do

+ Infrared meibography, imaging the glands to see where you’re at

+ Tear breakup time, and a Schirmer test for tear volume

+ Gland expression, with the oil graded for quality

+ Tear osmolarity and an inflammation test

+ How to tell your doctor is up to date on MGD

If your doctor gives you artificial tears and wishes you well, find someone else. You want someone who will image the glands, express and grade the oil, tell evaporative dry eye from the watery-deficient kind, treat your gland structure, and reimage it to track progress.

Here is the full protocol to run if you have dysfunction

At home:

+ Most people with early MGD get most of the benefit from warm compresses, lid hygiene, and better blink habits. This is a great place to start.

Things to do in office:

+ Intense pulsed light (IPL): calms lid inflammation, addresses surface bacteria and Demodex, and hits leaky vessels feeding rosacea-driven MGD.

+ Radiofrequency (RF): controlled deep heat that melts the toothpaste sticky oil and stimulates the lid tissue.

+ Manual gland expression: the clinician squeezes the glands to clear the stagnant oil and reopen the flow.

+ Intraductal probing (the Maskin protocol): a fine probe opens each blocked duct, breaking through plugs and scarring, and help encourage natural expression.

+ Low-level light therapy (LLLT) 630nm eye-light for stimulation of mitochondrial ATP production in meibocytes and reduced periorbital inflammation (device made by Espansione Group. Note, not yet widely available in the U.S.).

+ Thermal pulsation and heat (LipiFlow, TearCare): warms the lids from the inside and presses out the hardened oil clogging the glands.

I worked with Dr Amir Moarefi in Los Angeles to build out this protocol. If you can see him, I’d recommend it.

At home / daily protocol:

+ I started using some drops: a preservative-free lubricant (iVizia), a lipid-replacement drop (Miebo), and a prescription anti-inflammatory (Vevye).

+ A compounded azithromycin lid spray, which calms inflammation and pushes the gland cells to make and release oil.

+ Warm compress daily. Healthy meibum melts around 90 to 93°F (32 to 34°C). It thickens with MGD, raising the melting point above 104°F (40°C). Given that roughly 9°F (5°C) is lost crossing the eyelid, getting to 104°F (40°C) at the gland requires holding the outer lid surface near 113°F (45°C). Stay under 113°F (45°C) to avoid risk of thermal injury.

+ Moisture-chamber glasses (7eye) to trap humidity and block wind. Indoor and outdoor options.

+ Tear stimulation: a nasal spray (Tyrvaya) and a handheld nerve stimulator (iTear).

+ Omega-3 and lutein

It's rarely just the eye: the systemic drivers

In my case, we identified several likely drivers. The clearest is low DHT, from a topical anti-androgen I use for hair growth: the meibomian glands need androgens, so this works against them.

There's also low anabolic signaling, low insulin and low IGF-1: likely good for longevity, but hard on the glands, which renew constantly and lean on insulin and IGF-1 to do it, so running low starves them.

In addition, a former subclinical thyroid flare (high TSH, part of the Hashimoto picture of my hypothyroidism from age 21) probably contributed to my MGD too, since thyroid dysfunction is itself a documented dry eye contributor.

Again, there are 100+ things that contribute to meibomian gland dysfunction.

Where we take it next

We're running this protocol until it plateaus, as we closely monitor and track two types of signals: routine imaging (meibography) to follow the glands over time, and research-grade profiling of the ocular surface for signals of inflammation, tissue damage, regeneration, and scarring.

Together they show how much living gland is left, whether the inflammation is settling, and when we've reached the point of diminishing returns.

Once we do, the next options aim to go further, to rejuvenate the glands and reverse the degeneration itself, not just clear what's blocked:

Restoring the glands: they run on growth and hormone signals that fade with age and get blocked by common drugs. We're working on delivering those straight to the lids, from androgen to growth factors drawn from my own blood, to switch them back on.

Restoring function and calming inflammation: repurposing agents like azithromycin that both push the gland cells to make and release oil and quiet the inflammation driving the loss.

Rejuvenating the gland: the deepest lever is reawakening the gland's own stem cells and the signals they depend on, to regrow lost tissue, from stem-cell-stimulating drops to lab-grown gland organoids as a route to transplantation. Never done in humans, yet.