I’m often told I don’t look my age (45 years old at the time of writing this blog). I put it down to my Chinese roots and picking up a thing or 2 to slow down the ageing process as an Integrative Aesthetic doctor for more than 10 years.

I’m pretty happy with how I am progressing in my 40s in preparation for the next decade.

However, one thing that I am continually trying to improve is my skin’s elasticity.

I’ve definitely noticed my skin snap test getting slower. This is a simple test of your skin’s elasticity by gently pinching the skin underneath your eyes and letting go, seeing how quick it snaps back. Young skin snaps back immediately. Older skin can be sluggish or stay where it is altogether.

The skin under my eyes and under my neck give my age away when I pinch it.

In this blog, I will focus on skin laxity on the face and neck. I will share what has worked for me thus far and what I recommend my patients in clinic. I also include treatments that you may have heard of and why I’m not such a fan of them. I hope to add more to this blog as time goes by when I discover new treatments and solutions to improve skin laxity.

The firmer and more resilient the skin, the quicker she springs and bounces back.


Before that, let’s go through the science behind skin laxity.

Ageing is the result of a gradual functional decline at the cellular level. The skin being the largest organ of the human body presents these visible ageing signs such thin and dry skin, sagging, loss of elasticity, wrinkles and increase pigmentation. These are accelerated by intrinsic and external factors below.

At a cellular level, ageing is associated with:-

  • impaired protein production and degradation (collagen and elastin are a type of protein)
  • an accumulation of DNA damage, genetic instability, telomere shortening (the protective caps at the end of DNA)
  • premature cellular senescence
  • reduction in anti-oxidant defense, number of epidermal stem cells and its renewal capacity
  • increase in collagen degradation by the increase activity of a family of enzymes called MMPs.

Senescence is a state of permanent growth arrest so the cell is unable to proliferate and no longer able to contribute to tissue repair or regeneration. These cells are effectively “useless” which leads to inflammation and breakdown of the area by protective cells. This is an important mechanism to have because it’s a way of the body to stop the proliferation of dysfunctional cells which can lead to diseases and cancers. Premature ageing occurs when it occurs much sooner, worsened by factors above.

This means there is less functioning fibroblast, reducing the production of collagen (mainly Type 3 and Type 1) and elastin in the dermis, resulting in volume loss, lines and wrinkles, skin laxity and sagging. There will be less functioning epidermal cells, reducing stem cell differentiation resulting in thinner epidermis which leads to dry, thin, more sensitive skin with more visible pigmentation and redness.


There is also the dermal-epidermal junction (DEJ) which plays an important role in skin laxity. This is the wavy line between the Epidermis and Dermis. Within this junction, there are specific collagen fibres Type 4 (COL4) and Type 7 (COL 7) which hooks the layers together, keeping the skin “tight”, reducing the “slippage” between these 2 layers. It is also rich in fibronectin, a glycoprotein that is involved in cellular replication, stem cell differentiation and wound healing.

From knowing the science behind skin laxity, we can improve it by:-

  • Reducing DNA damage and cellular senescence.
  • Reducing collagen degradation by reducing the activity of the enzyme MMPs.
  • Improving fibroblast function to increase healthy production of collagen Type 1 and 3 and elastin. COL1 and COL3 provides the scaffolding in the dermis and the elastin provides the recoil.
  • Improving the production of COL4, COL7 and fibronectin specific the DEJ to keep the skin tight.


This can be divided into reactive and proactive solutions.

REACTIVE solutions are treatments that induces a skin injury, thereby boosting fibroblast activity, producing more collagen and elastin. This is mainly collagen Type 1 and 3 which is found mainly in the dermis. This can be carried out by:-

1. Merely slapping your face (of course, production will be slight and a strange exercise slapping yourself for the name of anti-ageing).

2.  Collagen induction therapy i.e. in-clinic microneedling or home derma roller, using many tiny needles to create a series of tiny wounds on the skin, triggering the skin’s natural repair response. A series of treatments are recommended and there is minimal downtime which is what makes this most appealing to me.

3.  Chemical skin peels can help improve skin laxity depending on the depth it penetrates.

a)     Superficial peels (e.g. glycolic acid) affect the epidermis and DEJ junction. It’s useful in the treatment of mild pigmentation, acne, post-inflammatory pigmentation and actinic keratosis to achieve more radiant skin. There is less downtime and less potential side effects. Epidermal regeneration is expected in 3-5 days.

b)     Medium-depth peels (e.g. TCA) are better suited for dyschromias (patchy skin discolouration) and textual changes. The healing process is longer with epidermal regeneration expected after 1 week.

b)     Deep peels (e.g. phenol) are used for severe photo ageing, deep or coarse wrinkles, scars and sometimes precancerous skin lesions.This penetrates the deeper layers of the dermis, maximising collagen regeneration. There is a long healing time, 2 months or more and sun protection is a must as there is increased risk of complications including hypopigmentation, hyperpigmentation, scarring and keloid formation.

4.  Skin tightening devices using heat to induce damage to tissue by light, laser, radiofrequency or a combination of the energies.

a)     Ablative lasers with CO2 or Er:YAG have been shown to cause collagen contraction and remodelling associated with tightening the skin. Although the results are striking, erythema, pigmentary changes, infection, dermatitis, scarring, and long recovery times are common. The risk of adverse effects depends on the experience of the treating physician and have been reduced somewhat by improved laser design.

b)     Nonablative laser and broadband light devices have been developed to reduce both recovery time and the risk of adverse effects associated with ablative treatments. Beams of these devices inflict thermal damage to the lower layers of the dermis and stimulate collagen production but do not injure the epidermis.

c)     You may have heard of fractional laser treatment. This device delivers a laser beam divided into thousands of microscopic treatment zones (like little pixels in a photograph). This targets a fraction of the skin at a time, causing wound healing in these tiny areas, causing contraction surrounded by normal skin.

Personally I have tried these types of devices and my skin did not like it. I broke out in blisters and pigmentation. I feel for my case, it was due to the wrong device and the operator doing my treatment.

d)     Radiofrequency (RF) devices uses alternating current flows to produce heat in the tissues. Unlike laser and light energy, RF current is not scattered by tissue or absorbed by epidermal melanin. Patients of all skin types can therefore be treated, and considerable heat can be generated in the dermal layers to stimulate collagen contraction and neocollagenesis. A downside is RF can potentially reduce facial fat which some parts are desirable like under the chin but others like the cheek is not.

There are also devices that deliver RF current through needles so it combines microneedling and RF current.

As you can see from the list above, clinic treatments commonly available are reactive in nature. It’s “shocking” the skin to produce more collagen and elastin. And from knowing the science behind skin laxity, this only helps 1 out of the 4 ways to improve laxity.


PROACTIVE solutions works on all 4 ways. It supports the cells so it functions better, encouraging it to act as it would in its youth.

This includes:-

1. Adopting am anti-inflammatory lifestyle to encourage rest and repair. This helps to reduce DNA damage and cellular senescence.

2. Eating an anti-inflammatory, nutrient dense diet full of antioxidants including Vitamin A, B, C, E, mineral copper and zinc. This will help mop up free radicals and provide nutrients for the cells to make better collagen and elastin.

3. Improving sugar regulation as consistent high blood sugar can lead to increase activity of enzyme MMPs.

4. Topical Vitamin A to encourage cellular growth and differentiation, immune modulation and cell surface alterations.

The most common one is Retinoid which is an umbrella term for all vitamin A derivatives. From the strongest to the weakest:-

  • Retinoic acid: This is prescription only. Highly potent, very effective but most irritating (redness, swelling, dryness, inflammation, painful tear ducts, purging, barrier damage, photosensitivity, dermatitis and flaking). Eg. Tretinoin (Retin-A, Renova, Atralin), Tazorac, Adapalene (Differin).
  • Retinaldehyde: Most effective OTC but still have significant irritation. Requires 1 chemical conversion in the skin before effective.
  • Retinol: Most common OTC. Irritation varies depending on delivery system. Requires 2 chemical conversion in the skin before effective.
  • Retinol esters: Most gentle (still can be irritating), least effective. Requires 3 chemical conversions in the skin before effective. Also known as retinyl palmitate, retinyl acetate and retinyl linoleate. 

The stronger derivatives work quicker but have higher chance of irritation. It’s possible to build your skin’s tolerance to it starting from a lower dose but not everyone (including myself) are able or willing to go through it.

There are ways to minimise the negative experience and I have recommended patients retinol and even prescribed for those who can tolerate it or have the willingness to push through the irritation which can take up to 6 months to “clear”.

If you’re not keen on synthetically formulated retinol, there are ingredients closer to nature like bio retinol, phyto retinol, natural retinol, or retinoic nutrients.

A lot of products that contain high levels of Vitamin A and beta carotene are marketed as retinol alternative. These include carrot seed oil, sea buckthorn oil, rosehip oil and Bakuchiol.

5. Topical Vitamin B3 (niacin) as niacinamide has been shown to:-

  • increase the skin’s antioxidant capacity.
  • improve epidermal barrier function by up regulating the synthesis of ceramides, thereby reducing transepidermal water loss and retaining more moisture.
  • increases NADP in energy production which in turn stimulates epidermal turnover i.e. stem cells move up the layer, thickening the epidermis and acting as a mild exfoliant.
  • by improving barrier function, it become less reactive to environmental triggers.
  • increase dermal matrix collagen production.

       6. Protection against prolonged UV exposure which can increase activity of enzyme MMPs, breaking down collagen and causing elastosis, a condition marked by thickening and degradation of elastic fibres and loss of elasticity.

       7. Optimising Oestrogen and Testosterone levels. Fibroblast which produces collagen and elastin has receptors for these hormones. Oestrogen also contributes to the production of ceramides in the epidermis, maintaining its protective barrier and preventing water loss.

       8. Boosting the skin with Sunekos. Sunekos is a hyaluronic acid with a patented formulation of 6 amino acids. It acts differently than normal skin boosters because it not only stimulates but also optimises the cells.

       A good analogy would be this:-

       Think of the skin cells as office workers. They work and produce.

Skin boosters like polynucleotide are like new managers brought in to encourage these workers to be more productive and efficient. When these managers are not there, the workers go back to their usual less productive state.

Sunekos bring in the managers but also improve the office environment, office equipment, work culture, the cafeteria, wellness program etc. This incentivise the workers to take more initiative, rise to a new standard of a new state of being and in a better environment for them to thrive.

Sunekos also maximally stimulates the production of collagen Type 4 (COL4) and Type 7 (COL7) which are found mainly in the dermal epidermal junction (DEJ – the wavy horizontal line between the epidermis and dermis in the diagram above. It acts like a glue, keeping the skin “tight” as there is less “slippage” between the 2 layers. It also stimulates production of collagen Type 1 and 3, and maximally produce elastin, improving the baseline physiology up to 6 months.

Based on its action, research has shown using Sunekos

  • Halving the time of the snap test i.e. skin springs back quicker.
  • Wrinkles reduced by 44 – 77%
  • Redness reduced by 50%
  • Pigmentation reduced by 50%
  • Hyaluronidase (which breaks down collagen) reduced by 40%

For maximum results, the recommended protocol is 3 sessions, 2-4 weeks apart and 1 session every 6 months for maintenance.


I hope you found this blog useful.

As you can see from the list of proactive solutions, it’s a more holistic, natural approach. I focus on the proactive solutions with occasional reactive solutions for an extra boost.

In my practice, I offer skincare planning, microneedling, skin booster Sunekos, hormone balancing, health coaching focusing on reducing inflammation, balancing sugar and optimising nutrition.

If you like my approach and would like me to help you prepare for your next decade so you look your best with each passing year, naturally and holistically, get in touch at [email protected] to book a consultation.

Until next blog, here’s to increasing resilience inside out.

Dr Terry