Do I have sensitive or resistant skin? Sensitive skin is a broad term that refers to many kinds of skin reactions and may easily lead to confusion. So let’s decipher whether our skin falls within the sensitive umbrella through the science-based evidence so far known to underlie the distinct categories and degrees of cutaneous sensitivity out there. 


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Hi! Did you ever experience sensitive skin? Do you even know what that is? Or what skin types usually become sensitive or sensitized? By getting to know what causes sensitive skin, you will be able to manage it better and even prevent your skin from becoming like that in the first place. Keep reading!

What is sensitive skin?

The sensitive (as opposed to resistant) skin experiences sensorial reactions when it gets in touch with certain external or internal factors. It may manifest as burning, stinging, itching, or simply a tight cutaneous feeling that may involve non-visible or visible skin changes (such as redness). And it can happen to anyone – it does not matter if your skin is oily, balanced, or dry –; later you will understand why.

Sensitive skin can diminish the quality of life.
Sensitive skin can diminish the quality of life.

The factors that trigger sensitive skin are individual, that is, different for each person. External triggers often include ingredients in skincare products, intense UV light exposure, climate conditions (pungent cold or heat), airborne pollutants, and even tap water. Sounds familiar? And internal triggers may be stress, drugs, foods, alcohol, or hormonal changes.

Sensitive and hypersensitive skin

Some people with reactive or sensitive skin undergo those unpleasant sensorial reactions but do not (or barely) present any visible signs simultaneously. That is plain sensitive skin.

However, there are more acute cases in which the skin tends to develop irritant contact dermatitis in the presence of some agents (such as certain detergents). That involves a non-specific reaction of our innate cutaneous immune system after the skin gets in touch with a trigger agent.

Our inborn immune system uses non-specific, rudimentary mechanisms to defend us from foreign factors. Since the response is non-specific, the skin may or may not react again upon exposure to the same element. In these scenarios, we could talk about hyper-reactive (also called intolerant) skin. 

Sensitive (reactive or hyper-reactive) and hypersensitive skin are not the same thing.

When our adaptive immune system (that recognizes and reacts against specific molecules or parts of them, called antigens) enters the play, we might develop allergic contact dermatitis (aka, an allergy), most often a delayed-type hypersensitivity reaction (only noticeable after hours). Your skin becomes then sensitized to a specific antigen, and we call it allergic or hypersensitive to the substance that provides that antigen.

Therefore sensitive skin might be reactive or hyper-reactive (also named intolerant). That is not the same as hypersensitive or allergic skin.

What causes the skin to be reactive or hyper-reactive?

1· Skin barrier alterations

When the skin presents innate or acquired physical-chemical defects, it loses too much water. That enhanced Trans-Epidermal Water Loss (TEWL) leads to cutaneous dehydration, which can severely impact the well-functioning of the skin as a whole (what is also called cutaneous homeostasis).

A clear example of this situation occurs in people who have low levels of the protein filaggrin (or mutations in the filaggrin gene that give rise to defective filaggrin proteins), among them people with atopic skin

Adequate levels and hydrolytic processing of the protein filaggrin in the outermost layers of the epidermis are essential to maintain the structural integrity of the stratum corneum and the development of a strong skin barrier. Filaggrin degrades into amino acids on the cutaneous surface (that become part of the cutaneous natural moisturizing factors).

Skin barrier alterations lead to sensitive skin. Low/poor filaggrin protein in the outermost skin layers produce a less compact stratum corneum with lower moisturizing factors. That leads to increased trans-epidermal water loss, skin permeability and chemicals uptake (aka, a weaker cutaneous barrier).

People with lower filaggrin levels or defective filaggrin yield less natural moisturizing factors on the skin surface and thus have a less efficient protective barrier (with increased TEWL). That results in enhanced permeability of the skin and a higher uptake of common chemicals through it (such as some sunscreen filters or hydrocarbons polluting the air) that make the skin more prone to react. That’s partly why atopic skin tends to be sensitive or hypersensitive.

But if your skin is not atopic nor especially dry, you should not lower your guard. Low humidity and ultraviolet (UV) radiation can also trigger filaggrin abnormalities in the skin. That’s why moisturizing and good sun exposure habits are paramount to preserve a healthy and non-sensitive (or less reactive) skin barrier.

2· An over-reactive cutaneous immune system

Sometimes the immune cells in our skin (such as dendritic cells or mast cells) show a higher predisposition than required to activate defense mechanisms upon what they perceive as an external threat (for instance, an irritant compound that gets in touch with the skin). 

Usually, the keratinocytes (the cells that form the epidermis) react to those external threats by releasing soluble inflammatory mediators (such as cytokines or RNA) that target the immune cells that surveil the skin. In turn, those targeted immune cells trigger inflammatory signaling cascades that result in a higher or lower response to an external threat.

Whether that response becomes excessive or not depends mainly on the particular characteristics of your innate immune system and the state of activation of your cutaneous immune system when the perceived threat strikes.

Those two features determine the predisposition of your skin to react to a given threat. And, therefore, its degree of sensitivity or over-reactivity.

The particular characteristics of your innate cutaneous immune system and the state of your acquired immune system partly determine the degree of sensitivity of your skin at a given moment.
The characteristics of your innate cutaneous immune system and the state of your acquired immune system partly determine the degree of sensitivity of your skin.

A straightforward example of lower cutaneous tolerance (aka, an over-reactive cutaneous immune system) occurs in many people with rosacea or redness-prone skin (like me – you can have a look at my previous blog post about rosacea by clicking here). The rosacea typically over-reactive immune system tends to entail higher cutaneous levels of the anti-microbial peptide cathelicidin.

You might be wondering how those higher levels can make rosacea skin sensitivity-prone. Let me explain that! For instance, when UVB light (a threat) hits our epidermis, the UV-damaged epidermal cells (keratinocytes) release RNA molecules. And those RNAs can bind cathelicidin peptides.

An over-reactive cutaneous immune system may cause sensitive skin (illustration of a rosacea flare upon UV light exposure as an example).

Those high numbers of RNA-cathelicidin complexes make the blood vessels recruit excessive immune cells from the blood. In other words, rosacea skin displays a heightened vascular reactivity and therefore tends to be more sensitive (may get easily triggered, for instance, by sun exposure).

3· The activation of sensory receptors

The Transient Receptor Potential (TRP) channels are sensory neuroreceptors activated by distinct physical, chemical, or thermal noxious stimuli that threaten or damage the skin. They are in the nerve endings of the epidermis, which are part of the peripheral nervous system. Two of those receptors, TRPV1 and TRPA1, have a central role in triggering skin sensitivity.

Elements like high temperature (>43ºC), low pH (<5.9), ultraviolet light, capsaicin (the molecule responsible for hot peppers spicy flavor), piperin (which endows black pepper with its piquant taste), or camphor (present in some skincare products) activate TRPV1.

And low temperature (<17ºC), some environmental pollutants, components of mustard, wasabi, garlic, cinnamon, or menthol (found in some skincare formulas), for instance, can activate TRPA1.

The release of neuropeptides (neurotransmitters) that occurs after the activation of TRPV1 or TRPA1 in the cutaneous nerve endings provokes, on the one hand, the stimulation of the central nervous system (the brain), and thus the burning, stinging, itching, or cutaneous tightness feeling that characterize sensitive skin.

Sensorial neuroreceptors (such as TRPV1 & TRPA1) at the cutaneous nerve endings trigger sensitive skin upon stimulation by various stimuli (cold, heat, low pH, menthol...). They activate the stimulation of the brain (thus the itch, burning sensation...) and cutaneous neurogenic inflammation (after activation of mast cells or keratinocytes).

And, on the other hand, the stimulation of keratinocytes and immune cells (such as mast cells). That might lead to skin inflammation (initiated by the neuropeptides), also called cutaneous neurogenic inflammation. And the intensity of that particular inflammatory response correlates with the degree of skin sensitivity that a person experiences.

Indeed TRPV1 and TRPA1 are often over-represented in rosacea skin, which tends to be sensitive or intolerant.

In addition, house dust mites can activate TRPV1 in the nerve endings of atopic skin. The subsequent liberation of neurotransmitters causes the degranulation of mast cells. And that may trigger the hypersensitivity (allergy) to dust mites experienced by atopic skin.

What skin types have a higher probability of developing sensitivity?

People whose cutaneous immune system is somehow over-reactive, like individuals with rosacea, acne, or atopic-prone skin. Also, people with notably dry skin – who tend to have a weaker physical barrier with higher TEWL –.

Nonetheless, we all have sensory receptors in our skin (and an immune system that can turn over-reactive upon exposure to particular stimuli). Hence anyone might experience or develop sensitive skin at some point in their lives.

Let me put it this way: say that your skin barrier, immune system, and TRPV1/TRPA1 levels are perfectly balanced. But you start over-washing your oily skin, and therefore your skin barrier gets disrupted. Or you take a new medication that modifies the behavior of your cutaneous immune system.

Then one day, you start using some topical product with menthol that triggers the activation of TRPA1 at your cutaneous nerve endings. Since your skin barrier has gotten weaker (due to over-washing) or your immune system weird (due to medication), menthol (that previously did nothing to your skin) may suddenly start making your skin upset (sensitive).

Over-cleansing the skin strips its natural oils and other natural moisturizing factors and contributes to increased cutaneous sensitivity.
Over-cleansing the skin strips its natural natural moisturizing factors and contributes to increased cutaneous sensitivity.

At that stage, the most clever decision would be to stop using skincare products with menthol and resume over-stripping your oily skin (or the medication). So that your skin barrier (and cutaneous immune system) do not become persistently upset and your cutaneous TRPA1 isn’t continuously activated. This way would avoid the perpetuation of a vicious cycle that might make your skin forever sensitive.

So, as with everything, never say never! Never say that your skin is never sensitive 😉

In the next post, I’ll reveal strategies to handle and avoid sensitive skin, regardless of skin type.

I’ll also feature a few treasure dermatological ingredients and products that can help you. And explain why you might want to evade certain situations and explicit or non-explicit components in skincare products. Do not miss it!

I hope that this post helped you understand your skin better.

Do not forget to leave your thoughts and questions in the comments section below. And subscribe to my bi-monthly newsletter.

Take care and see you soon!

María

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