If you arrived here from the video, you have already seen the mite. Under magnification it looks like something that should not be living on a human face. Nearly every adult has them. I have them. So does every dermatologist who has ever filmed one for the camera.

Here is what I said in that video and what I want to explain properly here: the mite is gross, but it is rarely the problem. The problem, if you have one, is the bacterial ecosystem sitting on the same skin. That ecosystem shifts measurably with age, it correlates with elasticity and wrinkle depth, and it is the terrain that has to heal every time we resurface the skin with a laser. For most of my career we could not see it. Now we can.

83% → 61%C. acnes share of the facial microbiome, twenties versus 60 to 75 (Microorganisms, 2024)
r = 0.41correlation between C. acnes abundance and gross skin elasticity in the same cohort
12hallmarks of aging in the 2023 consensus. Dysbiosis is one of them.
60 secthe swab that maps the bacteria on your face by DNA

First, the mite

Demodex are microscopic arachnids, 0.15 to 0.4 millimetres long, that live head-down inside hair follicles and sebaceous glands. There are two species on humans. Demodex folliculorum prefers the follicles of the face and eyelashes and feeds on skin cells. Demodex brevis sits deeper, near the oil gland, and feeds on sebum. They are most concentrated on the cheeks, forehead, nose and lash line, they are more numerous with age, and colonisation is close to universal in adults.

Most of the time they are commensals: passengers, not pathogens. The condition where they become a problem, demodicosis, is uncommon and usually appears when the immune system is suppressed or when there is an underlying disorder such as rosacea, where mite density is consistently higher than in unaffected skin. Then you see the pattern: sudden itching or burning, rough sandpaper texture, pustules that look like whiteheads, redness, scaling, sometimes irritated eyelids and lash loss. That is treatable, with topical ivermectin, permethrin, sulfur or metronidazole, and it is worth diagnosing properly rather than guessing.

But if your skin is calm, the mite is not aging you. It is not what I would test for first, and it is not what I would build a protocol around. The bacteria are.

The organisms that actually run the surface

Your face carries a dense, structured community of bacteria that is shaped by sebum, pH, moisture and hormones. A handful of species do most of the work, and the balance between them is what we now measure.

Cutibacterium acnes

Despite the name, C. acnes is the dominant resident of healthy oily skin and, in the right strains and proportions, one of its most useful. It ferments sebum into short-chain fatty acids that keep the surface acidic, which is what keeps opportunists such as Staphylococcus aureus from establishing. It also produces antimicrobial compounds and appears to buffer oxidative stress in the follicle. When C. acnes declines, the acid mantle weakens and the door opens.

Staphylococcus epidermidis

The second pillar. S. epidermidis produces a sphingomyelinase enzyme that converts your own sphingomyelin into ceramides, raising ceramide content in the stratum corneum and lowering water loss. It trains local immunity, competes directly with S. aureus, and at least one common strain produces a molecule, 6-N-hydroxyaminopurine, that inhibited UV-induced skin tumours in mice in a 2018 Science Advances paper from the Gallo laboratory. I keep that finding in the "promising, not proven in humans" column, but it is an extraordinary thing for a skin bacterium to do.

Corynebacterium

The species that rise as the others fall. Corynebacterium kroppenstedtii and its relatives expand on older facial skin, particularly in women after menopause, and their rise is best read as an ecological signal: less sebum, less lipid for the lipid-loving residents, a different community moving in. Some Corynebacteria are neutral. Some are conditionally helpful. Their proportion tells us about the environment they are living in.

Staphylococcus aureus

The one we do not want to see in quantity. It is the organism most associated with inflamed, barrier-compromised skin, it drives TLR2-mediated inflammation, and it is the leading cause of infection after ablative laser resurfacing. A face where S. aureus has room to grow is a face whose commensals have lost ground.

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What happens to this community as you age

This is where the research has moved quickly. Two cohorts published in the last two years give us the shape of it.

A 2024 study in Microorganisms compared facial skin in women in their twenties with women aged 60 to 75. C. acnes dominance fell from roughly 83% of the community to 61% (p = 0.007). More importantly, the abundance of C. acnes correlated with every elasticity measure the investigators took (gross elasticity r = 0.41, p = 0.001) and correlated negatively with wrinkle area, depth and length (wrinkle length r = −0.38, p = 0.003). More of this one organism, firmer skin and fewer wrinkles, at the population level.

A 2025 United Kingdom cohort in Frontiers in Aging sequenced 59 adults, half in their mid-twenties and half in their early seventies. On the face, C. acnes dropped by 16 percentage points of relative abundance with age, Corynebacterium kroppenstedtii rose, and S. epidermidis became more prominent. Diversity went up, but not because new species arrived; the community simply became more evenly spread as the dominant resident lost its majority. Women shifted far more than men, tracking the fall in sebum production after menopause. Male facial microbiomes were comparatively stable.

The bacteria are not passengers on aging skin. They are a readout of it, and increasingly a lever on it.

The mechanism papers explain why the correlation is plausible. Butyrate, a fermentation product of these commensals, increases type I collagen production in fibroblasts through the FFAR2 receptor. Commensal metabolites acting through the aryl hydrocarbon receptor drive epidermal differentiation and barrier repair. In the other direction, when the wrong microbial signals hit toll-like receptors on keratinocytes, they switch on MMP-1 and MMP-9, the enzymes that digest collagen and elastin. And a 2026 British Journal of Dermatology study, which I covered in an earlier article, showed that disinfected human skin cleared fewer UV-damaged cells and recruited fewer immune cells than skin with its microbiota intact.

I want to be honest about the limit, because the authors of the most recent review were. The full chain, from age-related dysbiosis to measurable collagen loss, has been demonstrated in cells and animals and correlated in humans, but not yet proven causal in humans. What we can say is that dysbiosis is now formally one of the twelve hallmarks of aging (López-Otín, Cell, 2023), that it moves in a predictable direction with age, and that it is one of the few hallmarks you can sample from the outside in one minute.

Why I swab before I fire a CO2 laser

This is the part of the video that surprised people, so let me be precise about what is established and what is emerging.

Established: an ablative CO2 laser removes the epidermis. Every organism living on it goes with it, and for the next several days the dermis is open to whatever recolonises first. The classic resurfacing literature from the 1990s documented exactly which organisms take advantage: S. aureus, Pseudomonas, Candida, and reactivated herpes simplex. A 2025 commentary in the Journal of Cosmetic Dermatology put it plainly: ablative lasers can "significantly disrupt the microbiome and expose deeper tissues to opportunistic pathogens," and called for microbiome-conscious treatment protocols. A 2026 pilot in the same journal measured the facial microbiome before and after CO2 resurfacing and showed that the recolonisation pattern is measurable and can be modulated.

Emerging: the composition you walk in with appears to shape how you heal. A face dominated by healthy C. acnes and S. epidermidis recolonises from a benign reservoir, rebuilds ceramides and acid mantle quickly, and clears damaged cells through the apoptosis and immune-recruitment pathways the Manchester group described. A face where S. aureus already has a foothold, or where the commensals are depleted from years of harsh cleansing and topical antibiotics, heals into a more inflamed environment. Clinically, that is the patient with prolonged redness, delayed re-epithelialisation, a higher chance of infection and, in darker skin, a higher risk of post-inflammatory pigmentation. Those are the outcomes that decide whether a CO2 treatment is a reset or a regret.

We cannot yet predict an individual's laser result from a swab with certainty, and I will not claim that we can. What the swab does is tell me whether the terrain is ready. If it is not, we correct it first: barrier-repair skincare, removal of the products that were stripping it, a few weeks of microbiome-supportive care, and in some cases decolonisation. Then we resurface. It is the same logic as checking inflammatory markers before an internal protocol. You do not build on a foundation you have not inspected.

The test I mentioned in the video

The swab is the PurelyBiome facial microbiome test. It takes about 60 seconds to collect at home or in clinic, goes back to the lab in a prepaid envelope, and is analysed by quantitative PCR, which counts bacterial DNA directly rather than culturing whatever happens to grow on a plate. Results take roughly two weeks.

The report gives us four things I actually use:

Read alongside VISIA imaging and, where appropriate, inflammatory markers and a TruAge epigenetic clock, this is the outside-in half of the same picture. The full list of what we track is on the diagnostics page.

If you commented BIOME on the video, this is the test: the PurelyBiome facial microbiome swab. You can order it directly, or, if you are considering CO2 laser or a longevity protocol with us, it is included in the baseline panel and is currently covered twice over, before and after, for patients enrolled in our microbiome quality-improvement study.

What we do with the result

A number is only useful if it changes a decision. Here is how the score changes mine.

  1. Balanced, skin age at or below chronological. Proceed. Protect what is working: a gentle cleanser, broad-spectrum sunscreen, no unnecessary antimicrobials. Re-test annually or after any major treatment.
  2. Depleted commensals, low C. acnes and S. epidermidis. Almost always a stripping problem. We remove foaming sulfate cleansers, daily acids, alcohol toners and leftover benzoyl peroxide or topical antibiotics, rebuild the barrier with ceramide- and lipid-based care, and re-swab in eight to twelve weeks before any ablative work.
  3. Disruptive species elevated, particularly S. aureus. Address it before laser, not after. Depending on the picture that may mean targeted decolonisation, a look at nasal carriage, and treating any eczema or rosacea that is giving it a foothold.
  4. High Demodex signs on examination. Only now does the mite come back into the conversation, and only if there are symptoms. Then we treat it specifically, because an inflamed follicle is not a good place to start a resurfacing treatment either.

Then we treat, and then we measure again. The second swab is the one that proves the protocol did what we said it would.

What you can do this week, without a test

You do not need the report to stop damaging the ecosystem. The commonest cause of a bad facial microbiome in my clinic is not neglect; it is over-treatment. Cleansing twice a day with something that foams hard, exfoliating daily, layering acids and retinoids on inflamed skin, and reaching for antibacterial washes at the first pustule. Every one of those depletes the residents that protect you.

Frequently asked questions

Does everyone really have face mites?

Close to it. Demodex colonisation is near-universal in adults and increases with age. In healthy skin they cause no symptoms and need no treatment. They matter clinically in demodicosis and in some rosacea, where density is higher and treatment with topical ivermectin or similar agents helps.

Can the bacteria on my face really make me age faster?

The evidence shows a strong association: lower C. acnes and a shifted community correlate with lower elasticity and more wrinkling, and dysbiosis is now a recognised hallmark of aging. The mechanisms (short-chain fatty acids, ceramide production, MMP regulation, clearance of UV-damaged cells) are well described in the lab. Whether correcting the microbiome slows visible aging in humans is exactly what our current study is designed to measure. I present it as strong, not settled.

How does the skin microbiome affect CO2 laser results?

Ablative resurfacing removes the surface community and leaves the dermis to be recolonised. Opportunistic organisms, S. aureus above all, are the established cause of post-laser infection, and an inflamed, depleted microbiome is the terrain in which prolonged redness and pigmentation are more likely. Testing before treatment lets us correct that terrain first. Predicting an individual's exact response from the swab is emerging science, not established practice.

What is the PurelyBiome test and how is it done?

A 60-second facial swab analysed by quantitative PCR to count bacterial DNA. The report gives a Balance Score, a Microbiome Skin Age, your levels of the key named species against optimal, and an environment profile (sebum, hydration, sensitivity, antioxidant capacity). Results take about two weeks.

How often should I test?

Once for a baseline, again eight to twelve weeks after any corrective protocol, and after major treatments such as CO2 resurfacing. Beyond that, annually is reasonable for most people.

Will probiotic skincare fix it?

Some prebiotic and postbiotic formulations have early supportive data, and live biotherapeutics are being studied, but the current reviews are clear that larger controlled trials are needed. In my clinic the reliable first step is subtraction: stop stripping the skin, restore the barrier, then measure whether the residents recovered on their own. They usually do.

Verifiable sources

The two aging cohorts are small (n = 59 and a comparable single-centre study) and correlational. The laser-microbiome data is a commentary and a pilot. The mouse tumour work is preclinical. All are presented as promising early evidence rather than established practice.

Where this fits at Sajic Longevity. The microbiome swab is one line in a baseline that also includes biological age, inflammatory markers and standardised skin imaging. We read them together, correct the terrain, treat, and measure again. Book a consultation or call 1-888-430-4665 and mention BIOME.