Medacare Skin Clinic

Getting rid of the baseball doesn't fix the broken window.

Ten words from Cogence Immunology that say what I've spent years trying to explain to clients with science. Sometimes one simple picture does what pages of research can't.

Finding the problem and fixing the damage are two different jobs.

My focus has turned to this the past few weeks because I'm living that right now. My surgery fixed the problem, but my body is still healing and will be for some time. I'm in the next phase, and it needs its own care. I must now support repair.

I see this in clinic too. You finally work out the cause and remove it, and for many, skin responds well. For some, though, progress is slower, and it's natural to start wondering what's still wrong.

To understand why progress can go slow or even stall, I want to introduce you to research that has shaped how I think about healing. Robert Naviaux, a professor at the University of California, San Diego, describes what he calls the cell danger response.

When your cells sense a threat, whether an irritant, an infection or ongoing stress, they switch out of everyday mode and into defence. Naviaux describes the mitochondria, the energy centres of your cells, as threat detectors. When they sense danger, they switch from making energy to defending the cell. In simple terms, it's often described as your cells turning from powerplants into battleships. Battleships are built to fight, not rebuild. They're great in a crisis, but you can't rebuild a town while they're still firing. Stressed cells also release ATP, normally their energy currency, outside the cell, where it becomes an alarm signal to their neighbours.

In his 2018 paper on the healing cycle, Naviaux sets out three stages that need to happen in order:

CDR1 is damage control: inflammation, defence and clean-up.

CDR2 is rebuilding: new cells are made to replace the ones that were lost.

CDR3 is reconnection: the new cells mature, take on their proper roles and start working with their neighbours again. Only then does the alarm signal quieten.

Here's the part that matters for your skin. Removing the trigger ends the threat, but it doesn't complete the cycle. Naviaux proposes that when tissue is injured again before healing finishes, incomplete cycles stack up, and cells can be left stuck partway through. The danger has passed, but the alarm keeps sounding. He suggests this incomplete healing may sit underneath many chronic conditions.

Healing moves through stages: inflammation, rebuilding, then remodelling.

That's the broken window. Your cells may still be finishing a cycle that the trigger started. And each stage needs its own support, because what helps skin calm down isn't the same as what helps it rebuild.

So if you've found your cause and your skin hasn't caught up yet, you haven't failed. You're in the next phase.

Healing the window is the phase I'm in now. After surgery like mine, the first six to eight weeks are a huge task for the body. Believe it or not, I'll still be healing in six to twelve months, and sometimes for some people even longer. That's a pace my body sets, not me. My job is to support it, so each stage can finish properly and I'm not left carrying problems forward. Your skin deserves that same patience. It isn't failing. It's still healing.

This is the part of my work I love most. When a client finally understands why their skin is doing what it's doing, something changes. Their shoulders drop. They stop blaming themselves. Their skin hasn't changed yet, but they have. They're not guessing anymore.

Understanding doesn't fix everything on its own. But it turns something that happens to you into something you can work with.

Lee

If cortisol calms inflammation, why does stress make your skin worse?

This is a question I get asked in clinic more often than you'd think, and it's a fair one. On paper, it doesn't add up.

Your skin runs its own local stress system, and under stress, its barrier repairs more slowly. Researchers saw this in students during exam time. But it still leaves the cortisol puzzle, which I want to explain here.

We know cortisol works by docking onto receptors inside your cells, called glucocorticoid receptors. Once it docks, inflammation gets turned down. But the signal only works if the cell is listening.

Research suggests that when stress and inflammation go on for weeks or months, cells can start listening less. They may make fewer of the receptors that respond to cortisol, and more of a version that gets in the way. This has been studied most in asthma, where it helps explain why some people respond poorly to steroids. The skin research is at an earlier stage, but I think it fits something many of you will recognise: the stress has passed, and your skin still hasn't caught up.

In simple terms, it's like living beside a busy road for so long you've put earplugs in. The traffic hasn't stopped. You've just stopped hearing it.

The good news is that receptors aren't fixed. The number a cell makes shifts with what's going on around it, and one thing that may help is vitamin D.

Early research, mostly in cells, suggests vitamin D helps cells make more of the receptors that respond to cortisol. In people with eczema, a few small trials found vitamin D supplements helped, especially in winter and in people who were low to start with.

After a long southern winter, plenty of us are low without knowing it. So if your skin has been slow to settle, it's worth considering vitamin D supplementation.

For most people, ordinary vitamin D3 does the job. But D3 relies on bile to be absorbed and on your liver to convert it into the form your body stores. If you have a condition that affects fat absorption, such as coeliac or Crohn's disease, or one that affects your liver or bile flow, less of it may get through. There's another form that has already been through the liver's step and is absorbed more easily, even when fat absorption isn't working well. If you need this form contact me to see if it would suit you.

Vitamin D also needs support to work. Your body uses magnesium to convert it, so make sure your diet includes magnesium-rich foods like leafy greens, nuts, seeds and wholegrains. You'll also often see vitamin D sold with K2. There's a sensible reason behind the pairing, but the evidence that most people need it is still thin. If you're on warfarin, talk to your doctor before taking any vitamin K.

You might now wonder whether this is why inflammatory skin conditions like eczema and psoriasis are often better in summer. Vitamin D is only part of the picture. UV light from the sun also calms the immune activity in your skin directly. That's why phototherapy is a proven treatment for several inflammatory skin conditions. Time outside also helps your sleep and stress levels, which brings us back to cortisol. So this is your cue to get outdoors more, not just take a supplement. Over winter, we spend so much time inside that we become "outside deficient." Just remember our UV can be strong so don't let your skin burn.

Now you know part of why your skin can take longer to settle than you'd expect. A slow recovery after a hard stretch doesn't mean nothing is working. It often means your cells are still turning the volume back up. Your skin has been in a noisy place for a while, and it takes time to take the earplugs out. Be patient with it, give it the right support, and it can start listening again.

Lee

Korean Skincare, Honestly: What the label means and what PDRN can really do.

If you've been looking at skincare lately, you've probably noticed that "Korean" has become a selling point in its own right. Nobody specifically goes shopping for American skincare or Australian skincare, so why Korean?

Part of the answer is very clever branding. K-beauty grew alongside K-pop and K-dramas, with real government and industry backing, and many brands are made by a handful of large manufacturers. So "Korean" on the label tells you where a product was made, not whether it works. And when every ingredient is sold as the next big thing, it's hard to know what's real.

Some of it holds up. Korean sunscreens use newer UV filters and are lovely to wear, though some have tested below their labelled SPF. Centella has great evidence for calming irritated skin but its already used in brands all around the world. Korea didn't discover Centella, they popularised it. Exosomes are showing real promise alongside in-clinic treatments. Snail mucin and rice water have far less human research behind them.

Then there's PDRN, often sold as "salmon DNA," and one of the things I'm asked about most right now. It sits somewhere in the middle, so let's take a closer look.

Here's what we know. PDRN is made of fragments of DNA. Injected into skin, it has a genuine research history in wound healing, much of it from Italian and Korean research groups. Research suggests it works less by supplying building material and more by sending a signal. In simple terms, it doesn't deliver the bricks. It rings the doorbell to call the builders.

The catch is getting it in. Your skin barrier is designed to keep large molecules out, and DNA fragments are large. Putting them on the surface and expecting them to reach the cells that repair your skin is a bit like trying to post a sofa through a letterbox. Even the brands making it agree. British company Medik8 has taken a different approach, making its PDRN from microorganisms instead of salmon and folding it into a tiny pyramid shape designed to slip through. It's a clever idea, and interestingly it isn't Korean at all. The published research on this kind of structure is still mostly lab and animal work. Medik8 has run its own human studies, but they test the whole serum, which also contains exosomes and other actives, so we can't yet say how much is down to the PDRN.

One route with more promise is combining it with microneedling, which creates tiny channels so it doesn't have to squeeze through the letterbox at all. Early studies are encouraging, though still small. One caution: only products made and sterilised for that purpose should go on skin during microneedling. Your home serum isn't one of them.

So if you're weighing up a PDRN serum, it doesn't need to come from Korea. And the most useful question isn't "is PDRN good?" It's "can it get where it needs to go?"

Lee

The Rise in Inflammatory Skin Conditions

Recovering from surgery has gifted me some extra time to study the skin, deeply as always. One question keeps pulling me back: why are so many more people living with inflamed, reactive skin?

If that's you, you'll know the pattern. The worst week arrives, with a deadline or a sick child, and right on cue, your skin flares. It can feel like your skin is letting you down, or that if you coped better, it wouldn't happen. Neither is true.

There's no single reason for the rise, but one piece I keep returning to is stress. Neuroscientist Claudia Aguirre, in her talk "The Hidden Brain in Your Skin," puts it simply: your skin carries much of the same machinery as your brain.

Your brain runs a stress system called the HPA axis, the chain of signals that ends in cortisol. Researchers, notably Andrzej Slominski, have found your skin runs its own local version. In simple terms, your skin isn't just taking orders from headquarters. It's an outpost with its own stress department.

That has consequences. When researchers studied students during exams, their skin barrier took longer to repair (Garg and colleagues, 2001). Stress slows the repair crew. So a flare in a hard week isn't weakness. It's your skin doing what it's built to do.

Here's what helps: treat a stressful week like a southerly on the forecast. You bring the washing in before the rain, not after.

When you see a hard week coming:

1. Make sure the right skincare is in place.

2. Write it down. Researchers at the University of Auckland asked people to write about something that had upset them, 20 minutes a day for three days, before a small skin wound was made. Their skin healed faster than that of people who wrote about their daily plans. A second Auckland study, with 122 adults, found the same. Research suggests that getting it out of your head and onto paper reaches your skin's repair crew too.

If your skin has been struggling for a while, you can take this further. In both studies, people wrote about the most upsetting experience of their life, not just a stressful week. If that brings up more than you expected, talk to someone you trust.

We don't know why writing helps. The obvious guess is that it lowers stress, which lowers cortisol, which frees up repair. That's plausible, but I'm drawn to James Pennebaker's explanation who developed expressive writing. Turning a jumble of feelings into a story seems to reduce rumination, the mental loop that keeps the stress response running in the background.

In simple terms: we know stress slows the repair crew, and we have good early evidence that writing gets it moving again. We just don't know the exact route yet. In this case we don't really even need to know how, just that it helps and is pretty well proven.

The main thing is, your skin isn't something you have to figure out by yourself. You don't need to know everything. You just need to know the difference between what's misleading and what's meaningful, and that's where I can help.

Thank you to everyone who has been so understanding and patient while the clinic has been closed this past week.

I've had unexpected emergency surgery and am currently recovering.

I'll be back seeing clients from the week of the 29th, subject to how recovery goes, starting with fewer appointments each day while my strength and energy return, then building back up to normal from there.

Until then I'm available by email.

For product purchases, email me at [email protected] and I'll organise your order, send an invoice you can pay online, and leave it ready for collection.

Thank you for your patience — I'm looking forward to seeing you all again soon.

Lee

Most people are told rosacea is a surface problem — a skin condition to be managed with creams and lasers. That's part of it. But it's not the whole picture, and the part that gets missed is what's happening underneath.

Rosacea and disordered cholesterol travel together. In a study of over 50,000 people, those with rosacea had significantly higher rates of dyslipidaemia — raised total cholesterol, LDL and triglycerides. That's not a coincidence. The two conditions share the same underlying machinery.

Heres where they meet:

Oxidised LDL feeds skin inflammation. When LDL is elevated, some of it oxidises. Oxidised LDL activates the same family of innate-immune receptors (TLRs) that sit at the top of rosacea's core inflammatory cascade — the KLK5 / LL-37 pathway that drives your redness. A signal from your bloodstream can plug straight into the pathway behind your flushing.

It triggers mast cell degranulation. Mast cells in rosacea-affected skin are already primed and reactive. Oxidised LDL is one of the signals that makes them degranulate — releasing histamine, which drives flushing and erythema, and VEGF, which drives the growth of new fragile blood vessels. That's the visible telangiectasia. This is core rosacea biology.

Triglycerides raise IGF-1, which raises skin sensitivity. Raised triglycerides — often from frequent refined-carbohydrate intake — push up insulin and IGF-1. IGF-1 appears to increase the density of TRPV1 receptors, the skin's hypersensitivity and "flush" receptor. More receptors means more reactivity.

Your barrier depends on the right fats. The skin's protective barrier relies on a specific lipid composition, including oleic acid — a natural TRPV1 antagonist that holds that hypersensitivity receptor in a closed, calm state. When whole-body lipid metabolism is disordered, that balance shifts and the barrier becomes more reactive and more permeable.

It shifts the environment in favour of Demodex. The fat composition of your oil glands is shaped by systemic lipid metabolism. Changes there can make the skin a more hospitable home for Demodex mites — a recognised driver of papulopustular rosacea.

Both run through NF-κB — the same master switch. Disordered lipids and rosacea independently switch on NF-κB, the master inflammatory regulator behind IL-6 and TNF-alpha. When both are active at once, the inflammatory load compounds. This is often why rosacea turns stubborn and stops responding to topical treatment alone — there's a systemic input that creams simply can't reach.

In treatment, IPL clears existing vessels beautifully. But while these inflammatory and vascular drivers stay active, the skin has a standing reason to generate new ones. Treating the whole picture — not just the surface — is what helps the outcome hold.

This is the difference between managing rosacea and understanding it. Medacare assess's the system, not just the skin.

Real answers for difficult skin.

A quick heads up from Medacare

The clinic will be closed this Thursday and Friday (23–24 July) while I'm away.

If you need any product before then, pop in before 5.30pm tomorrow (Wednesday) — I'll have everything ready to go.

Bookings are open as usual at medacare.co.nz and I'll be back the following week.

Thanks for your understanding — see you soon!

Just a heads-up that Medacare will be closed from 3pm this Friday 6 June, reopening Wednesday 17 June.

To make sure you don't run out of product while I am away, please check your levels and pop in before Friday.

Looking forward to seeing you.

THIS IS FOR TRANSFORMATION SEEKERS

This programme is not a series of single treatments. It is a sequenced, compounding clinical system — each phase building on the last, each session amplifying what came before. It is designed for people with real skin concerns who want real, lasting change.

- If single treatments haven't been enough.
- You've tried individual treatments and seen temporary results.
- Results faded before your next appointment.
- Your skin has plateaued and isn't responding the way it did.
- You're ready to invest in a programme that creates structural, lasting change.
- You want skin that stays clear — not just improves briefly.

BUILDING THE FOUNDATION YOUR SKIN NEEDS

IPL is not just a pigmentation treatment. Across 6 sessions, it performs a biological reset of the dermis — resetting gene expression toward youthful patterns, normalising vascular reactivity, priming fibroblasts, and creating the structural foundation.

A Stanford University study published in the Journal of Investigative Dermatology found that after a course of IPL, 1,293 of the 2,265 genes associated with skin ageing shifted back toward the expression patterns of young skin. These weren't cosmetic markers — they included key regulators of cellular longevity, proteasome function, cell-cycle integrity, and the suppression of cellular senescence.

"The researchers concluded this may represent functional rejuvenation — not a cosmetic imitation of youth. Your skin isn't being made to look younger. Its underlying molecular activity is being reset toward a younger state".

This gene expression shift builds with each session. You need the full 6-session course to accumulate it. Clinical studies also show skin treated regularly with IPL over years continues to improve — meaning consistent maintenance doesn't just maintain results, it compounds them.

WHAT IPL ACTUALLY TREATS

IPL is a multi-target technology — each session addresses multiple concerns simultaneously. You are not treating one thing at a time. You are running parallel repair programmes in the same tissue, in the same session.

- Pigmentation
- Vascular Conditions
- Acne & Active Skin
- Aging & Collagen
- Barrier Dysfunction
- Gene Expression Reset

SESSION BY SESSION — The Compounding Effect

Results do not accumulate in a straight line. They compound. Each session amplifies what came before because the biological momentum is still running when the next session arrives.

SESSION 1
Initiation:
- Photothermal stimulus initiates wound-healing cascade
- Surface pigment begins fragmenting (20–30% improvement)
- Inflammation begins decreasing. Some vessels start closing
- Collagen synthesis initiates. Gene expression begins shifting

SESSION 2 (2–4 weeks later)
Momentum Doubles:
- Session 2 arrives while Session 1 collagen synthesis is still active
- Addresses deeper vessels and pigment Session 1 softened
- 40–50% visible improvement. Skin cell renewal cycle completes

SESSION 3
Exponential Acceleration:
- 60% improvement in vascular and pigmentation. Texture improving
- Wrinkle reduction measurable — 24% at this point
- Skin staying clearer between sessions

SESSION 4
Structural Change:
- Deeper structural changes visible. Pore refinement noticeable
- 70% improvement in redness and pigmentation

SESSION 5
Optimum Reached:
- Wrinkle reduction reaches 33% (vs 24% at Session 3)
- 25% skin tightening and pore improvement reached
- 80% improvement in vascular and pigmentation
- Barrier fully competent

SESSION 6 (Transformation Complete)
Maximum Results — Phase One Foundation Set:
- Maximum collagen density achieved. 85–95% clearance of pigmentation and vascular lesions
- 33%+ wrinkle reduction locked in and stabilised
- Barrier fully restored.
- 1,293 ageing-related genes reset toward youth
- Fibroblasts biologically younger — Phase Two begins on this foundation if deeper collagen or scar remodeling is needed (Microneedling).

By the end of Session 6, your skin has been biologically reset. 1,293 ageing-related genes are expressing closer to their youthful patterns. Fibroblasts are more numerous, more responsive, and more capable. The collagen achieved through IPL is not the end result — it is the starting platform for best foundational results.

Microneedling builds a different type of collagen, through a different mechanism, reaching deeper tissue, producing results IPL structurally cannot reach if further treatment is needed for aging skin.

WHAT IPL BUILDS

- Indirect collagen via chromophore heating
- Strongest in upper to mid dermis
- Gene expression reset across 1,293 ageing-related genes
- Vascular, pigmentation, and barrier normalisation
- Fibroblasts biologically primed and reset
- Much much clearer, healthier skin.

WHAT MICRONEEDLING AFTER IPL CAN ADD

- Direct mechanical injury — separate, additive collagen pathway
- Reaches reticular dermis — deeper than IPL
- Mechanically disrupts fibrotic scar tissue
- Progressive shift toward Type I collagen (mature, structurally strong)
- Measurable laxity improvement IPL alone cannot produce

Microneedling asks your fibroblasts to do a great deal of work. IPL has spent 5–6 months making those fibroblasts younger, more numerous, and more responsive. The mechanical signal from microneedling lands in tissue that is primed to act on it — not fatigued, aged tissue working against its own biology. IPL-rejuvenated fibroblasts produce better collagen. New collagen deposited after microneedling can remain in place for 5–7 years.

Microneedling intervals are 6-8 weeks, so more time between sessions in this phase.

WHAT THIS MEANS FOR WRINKLES — The Most Important Number in This Programme

Wrinkle reduction matters most to the majority of clients. IPL alone delivers 33%+ wrinkle reduction across 6 sessions — that is the documented, research-backed figure from clinical trials, and what I see in clinic. That is Phase One.

Microneedling through a completely separate pathway — direct mechanical injury stimulating new collagen type I, III, and VII, tropoelastin, and dermal reorganisation — independently produces a further 25–50% improvement in wrinkle severity scores, confirmed across systematic reviews. This is additive. It is not the same collagen, triggered the same way, in the same tissue depth.

The combined result across the full IPL - microneedling programme is not 33%. It is 33% as a starting point, with a further 25–50% improvement compounding on top of it through Phase Two — on IPL-primed fibroblasts that are biologically younger and more productive than they were before Phase One began. This is why completing both phases matters.

IMPORTANT!!

Before or straight after your first IPL session — and every day throughout the entire programme — you need to apply Retinaldehyde Vitamin A morning and night. This is the most important thing you can do at home. Sunscreen is second. Vitamin A is first.

Vitamin A controls between 350 and 1,000 genes responsible for cell proliferation, differentiation, angiogenesis, and neocollagenesis — the exact biological processes that IPL and microneedling are activating. Without adequate Vitamin A at the tissue level, the genetic programme these treatments are trying to run cannot complete. The stimulus lands. The response is diminished.

IPL and microneedling are the signal. Vitamin A is what makes the cells capable of receiving and acting on it. Starting straight away means every one of your treatment sessions lands in tissue that is gene-primed to respond.

Why Retinaldehyde — because its' one conversion step from active Retinoic Acid, and the most potent form of Vitamin A available without prescription. Unlike retinol (which requires two conversions) or prescription tretinoin (which causes inflammation and barrier disruption), Retinaldehyde is sun-safe, non-inflammatory, and suitable for use throughout an active treatment course. It is encapsulated in a patented liposomal delivery system that drives it into the dermis — not just onto the surface.

I will recommend the right formula (the correct formula and potency for skin concern) and give you 20% off your first bottle before or at the time of your first session.

SCHOOL HOLIDAYS — IPL EDIT

The kids are home. That means you finally have a window.

Half Face IPL + Dermalux LED (Worth $275) → $149
Full Face IPL + Dermalux LED (Worth $375) → $249

Plus take home a free 15min post-care mask with vitamins (Worth $51) after your first session (Between 6th-17th of April).

Book one, or lock in a course.

Autumn is the best time to start treating skin damage with IPL — and I am making it easier to start.

Successful skin treatment is not just a science — it's an art.
Medacare specialises in advanced IPL using the Anthelia, a physician-grade system that delivers a level of precision, control and clinical outcome that standard IPL simply cannot match. In skilled hands, this is one of the most effective treatments available for transforming the skin.

Each session can precisely target:

Your Sun Damage
Unwanted Pigmentation
Visible Red Veins
Ongoing Acne & Rosacea
Unrefined Texture, Pores & Hydration
Declining Collagen
Lost Skin Firmness
Downregulated Youth Genes (1293 Of Them)

Dermalux Tri-Wave LED is included in every session to accelerate repair, reduce post-treatment inflammation and amplify your results.

Two treatments. One appointment. One outcome.

Available during April school holidays only. Slots are limited.
To lock in a course, continued sessions must be pre-booked at the end of your first session.

No consult required if you've been seen at Medacare before. New to the clinic? Book via the link and we'll confirm IPL is right for your skin before we begin.

Book at www.medacare.co.nz

Tuesday – Friday, Invercargill