Chronic inflammation: when what happens inside your body can show up on your skin

First: inflammation is not our enemy

When we hear the word 'inflammation,' we immediately think of something negative. But inflammation is one of the most important survival mechanisms the body has. Imagine you get a wound: immediately, the immune system activates cells, cytokines, inflammatory mediators, blood vessels, and growth factors. The area may become red, warm, swollen, and painful. That is inflammation.

But that inflammation has a purpose: to protect and repair. Without inflammation, we would not heal properly, we would fight infections less effectively, and we would respond more poorly to certain injuries. Therefore, acute inflammation is physiological and necessary.

The problem arises when the alarm doesn't switch off

An inflammatory response should start, fulfill its function, and then resolve. But certain circumstances can sustain inflammatory signals over prolonged periods, and we can then enter a state of chronic inflammation.

There is also another important concept: low-grade chronic inflammation. We are not necessarily talking about a person with a fever, an infection, or a markedly elevated CRP; a much more subtle, persistent, and metabolic inflammatory activation can exist. And when this phenomenon is linked to aging, we also speak of inflammaging: a chronic, low-grade, systemic inflammatory state that tends to increase with age and involves mediators such as IL-6, TNF-alpha, and IL-1beta, as well as senescent cells and multiple immunometabolic alterations.

Where can chronic inflammation come from?

There is no single cause. Excess visceral adipose tissue, metabolic disturbances, insulin resistance, smoking, a sedentary lifestyle, certain chronic infections, inflammatory and autoimmune diseases, sleep disorders, cellular aging, environmental exposure, pollution, persistent physiological stress, and numerous genetic and environmental factors can all contribute. In other words, 'chronic inflammation' is not a single diagnosis: it is a mechanism that can appear in completely different contexts.

And what does all of this have to do with the skin?

A great deal. The skin contains keratinocytes, fibroblasts, melanocytes, immune cells, blood vessels, nerve endings, sebaceous glands, hair follicles, and microorganisms. All of them continuously exchange chemical signals: cytokines, chemokines, hormones, metabolites, neuropeptides, and lipids.

Therefore, what happens metabolically and immunologically in our body can influence the skin. And the opposite is also true: an extensive inflammatory disease of the skin can contribute to systemic inflammation. The communication is bidirectional.

The gut is not simply a digestive tube either

Our digestive system contains trillions of microorganisms: bacteria, viruses, fungi, archaea, and others. Together they form the gut microbiota, and the genes and functions of that community constitute what we call the microbiome.

What does our microbiota do?

Among many other functions, it participates in the digestion and fermentation of nutrients, the production of metabolites, bile acid metabolism, the production of certain bioactive compounds, the maturation of the immune system, the regulation of the intestinal barrier, and interaction with metabolism.

One of the most interesting examples are short-chain fatty acids, such as butyrate, propionate, and acetate, which are produced primarily through microbial fermentation of certain carbohydrates and fibers. These metabolites can play a role in intestinal barrier integrity, immune regulation, metabolism, and cell signaling.

That is why the gut and the immune system are intimately connected.

The gut faces an extraordinarily complex situation every day: it must allow nutrients in, while preventing the uncontrolled entry of microorganisms, toxins, and potentially harmful substances. To achieve this, we have an intestinal barrier.

What makes up that barrier?

Among other structures: epithelial cells, intercellular junctions, mucus, the intestinal immune system, and the microbiota. It is not a completely impermeable wall — it is a highly selective frontier.

What does 'intestinal permeability' mean?

This term is used extensively on social media, and often far too loosely. Intestinal permeability is a real, measurable physiological phenomenon, and in certain diseases it can increase. But to leap from there to claiming 'you have acne because your gut is leaky' is an enormous scientific stretch. We cannot currently use 'leaky gut' as a universal explanation for acne, rosacea, pigmentation spots, fatigue, aging, or virtually any other symptom.

So, what is the gut-skin axis?

It is a way of describing the bidirectional communication between the gut microbiota, the intestinal barrier, the immune system, metabolism, and the skin. Recent research finds associations between alterations in the gut microbiome and conditions such as psoriasis, atopic dermatitis, acne, and rosacea, among others.

But here we must understand one fundamental word: association. Finding a different microbiota in people with a given condition does not automatically prove that microbiota is the cause. The disease can alter the microbiota, diet can alter both, medications can alter it, genetics can play a role, lifestyle too — and communication likely runs in both directions.

Let's talk about acne.

Acne does not simply appear because 'the gut is inflamed.' It is a multifactorial condition involving sebum production, follicular hyperkeratinization, Cutibacterium acnes, inflammation, hormones, and genetic predisposition. That said, metabolism and diet can modulate some of these mechanisms.

This is where the insulin–IGF-1 axis comes in.

A diet with a high glycaemic load can produce significant spikes in glucose and insulin, which in turn can influence IGF-1, mTORC1 signalling, sebaceous activity, keratinisation, and androgenic signalling. Several studies have found that lower glycaemic load diets may improve acne in some patients, although diet does not replace dermatological treatment, and the evidence does not allow acne to be attributed to a single food.

So yes, diet and acne can be related. But 'you eat badly, that's why you have acne' is scientifically far too simplistic.

What about dairy?

There is also an epidemiological association between certain dairy products — especially cow's milk — and acne in some studies. But, again, association does not mean that every patient should eliminate all dairy; in fact, the evidence does not show the same relationship for all dairy products. Serious medicine does not consist of removing ten foods from every patient with acne, but rather in individualising treatment.

Let's talk about rosacea now.

Rosacea is another extraordinarily interesting condition. Neurovascular alterations, innate immunity, skin barrier dysfunction, Demodex, environmental factors, and individual predisposition all play a role. But for years we have also been investigating its relationship with the gastrointestinal tract: associations have been described between rosacea and certain gastrointestinal and microbiome alterations, which has driven research into the gut–skin axis in rosacea.

But, again, we cannot claim that all rosacea originates in the gut, and even less so that a probiotic can replace medical treatment for rosacea.

What about atopic dermatitis?

Here we have another excellent example of the interaction between barrier, microbiota, and immunity. In atopic dermatitis there is a skin barrier impairment and a characteristic immune response. Furthermore, we know that the cutaneous microbiota, and probably the gut microbiota, interact with these mechanisms. The gut–skin axis is being actively investigated in atopic dermatitis, but interventions targeting the microbiota still show heterogeneous results.

What about psoriasis?

Psoriasis is perhaps one of the clearest examples of why we must stop thinking of the skin as an isolated organ. It is not simply a red, scaly plaque: it is an immune-mediated disease in which inflammatory pathways such as IL-23, IL-17, and TNF are involved, and it can be associated with psoriatic arthritis, obesity, metabolic alterations, and increased cardiovascular risk. There are also numerous studies on differences in the gut microbiota in patients with psoriasis.

But we are still trying to answer which changes are a cause, which are a consequence, and which we can actually modify to improve the disease.

And what about pigmentation spots?

Here we need to be even more cautious. We cannot say 'intestinal inflammation causes spots on the face.' Hyperpigmentation can arise through multiple mechanisms: ultraviolet exposure, prior cutaneous inflammation, hormones, medications, genetic predisposition, or certain diseases. But there is one very important mechanism: inflammation can lead to pigmentation.

Inflammation can stimulate the melanocyte

When cutaneous inflammation is present, multiple mediators can be released that are capable of modifying melanogenesis. That is why, following acne, dermatitis, burns, procedures, trauma, or certain inflammatory diseases, post-inflammatory hyperpigmentation may remain — especially in more pigmented skin phototypes. Here the relationship between inflammation and pigmentation is far more direct.

And now we arrive at aging

For a long time, we explained skin aging primarily through collagen loss, sun exposure, and genetics. Today we know it is far more complex: ultraviolet radiation, oxidative stress, inflammation, glycation, mitochondrial dysfunction, cellular senescence, alterations of the extracellular matrix, hormonal changes, and the exposome all play a role.

What is a senescent cell?

It is a cell that has stopped dividing but does not necessarily disappear. Some senescent cells release a combination of molecules known as the SASP (Senescence-Associated Secretory Phenotype), which can include cytokines, chemokines, proteases, and growth factors. When certain populations of senescent cells accumulate, they can contribute to maintaining a pro-inflammatory environment.

This is where inflammaging comes in

With age, a chronic, low-grade, and persistent systemic inflammation can become established. This phenomenon is known as inflammaging, and its involvement in cardiovascular, metabolic, neurological, and immunological aging — as well as in skin aging — is currently under active investigation.

Can inflammation accelerate skin aging?

It can contribute. Persistent inflammation can promote oxidative stress, fibroblast impairment, extracellular matrix degradation, barrier dysfunction, vascular changes, and cellular senescence. Chronic inflammatory skin diseases are also currently being studied as models of systemic inflammaging, although many questions remain open regarding how much of this process can be modified clinically.

That is why the statement 'chronic inflammation = aging' would be an overstatement. But chronic inflammation and aging are intimately connected.

What role does adipose tissue play?

A critically important one. For many years, we thought of fat as simply an energy store. Today we know that adipose tissue is an endocrine organ that produces adipokines, hormones, inflammatory mediators, and metabolic signals. Excess visceral fat in particular can contribute to a pro-inflammatory, insulin-resistant, and metabolically unfavorable state. This is why metabolism and inflammation are profoundly connected.

And what about sugar?

Here too we must avoid simplistic statements. There is no such thing as 'one spoonful of sugar equals immediate inflammation of your skin'. But a diet sustained with excess energy intake and an abundance of high glycaemic-load products can, in certain individuals, promote hyperinsulinaemia, insulin resistance, metabolic disturbances and an unfavourable inflammatory environment. There is also another interesting process: glycation.

What is glycation?

Certain sugars can react spontaneously with proteins and, over time, form advanced glycation end-products (AGEs). Collagen is a long-lived protein; when it accumulates glycation-related modifications, its flexibility, mechanical properties and functioning can change. Glycation is one of the mechanisms studied in tissue ageing. But, once again, this does not mean that eating a dessert immediately destroys your collagen: human biology does not operate through Instagram headlines.

What about stress?

Psychological stress and inflammation are not two separate worlds either. Our brain communicates with the endocrine system, the autonomic nervous system and the immune system. Stress can alter sleep, eating behaviour, hormonal secretion, the skin barrier, the perception of itching and the immune response. And we know clinically that conditions such as psoriasis, atopic dermatitis, acne and rosacea can flare up coinciding with certain periods of stress.

That does not mean 'your illness is in your head'. It means that the brain, the endocrine system, immunity and the skin communicate with one another.

And sleep matters too

Sleep plays a role in endocrine regulation, metabolism, tissue repair and immune function. Chronic sleep deprivation can be associated with metabolic and inflammatory disturbances. That is why, when we talk about skin health from the inside, sleep is not a minor detail.

So what does 'treating from within' really mean?

It does not mean replacing medications, photoprotection, retinoids, topical treatments, systemic therapies or medical procedures with supplements. It means something far more sensible: treating the skin condition and the patient's overall context simultaneously.

1. Diet

There is no single 'anti-inflammatory diet'. But there is a dietary pattern that is reasonably favourable for metabolic health: prioritising vegetables, fruits, legumes, nuts, wholegrains, fish, good-quality proteins, extra virgin olive oil and minimally processed foods; and limiting excess ultra-processed products, sugary drinks, excess free sugars, excess alcohol and sustained excess energy intake. Not because any isolated food is 'inflammatory' or 'anti-inflammatory', but because the overall pattern is what matters.

2. Fibre and microbiota

A varied diet rich in plant-based foods provides different fibers, polyphenols, and fermentable substrates that can promote the production of microbial metabolites such as short-chain fatty acids. Therefore, feeding our microbiota properly is probably far more important than constantly chasing the latest probiotic trend.

3. Exercise

Regular exercise improves insulin sensitivity, glucose metabolism, body composition, cardiovascular function, and muscle health, and can also modulate systemic inflammation. Muscle is not merely a mechanical organ either: during exercise it releases myokines — that is, signals capable of communicating with other tissues.

4. Sleep

Getting adequate sleep is part of the treatment of metabolic health, hormonal regulation, recovery, and immune function. We cannot seriously talk about longevity or inflammation while ignoring sleep.

5. Tobacco

If we want to talk about skin aging and systemic health, smoking is one of the most important modifiable factors. It promotes oxidative stress, vascular damage, matrix degradation, skin aging, and multiple systemic diseases. No supplement compensates for smoking.

6. Photoprotection

Even though we are talking about 'treating from within,' let us not forget the main environmental accelerator of skin aging: ultraviolet radiation. Photodamage causes DNA damage, oxidative stress, inflammation, pigmentary alterations, and collagen degradation. Therefore, internal health and photoprotection are complementary.

What about supplements?

This is another area where we must separate medicine from marketing. There is currently no universal supplement that 'de-inflames the body.' Omega-3, vitamin D, iron, zinc, B12, folate, magnesium, and other supplements may have specific indications. But a specific indication does not mean that everyone should take them.

What about probiotics?

They are promising, but they are not 'the cure for the gut' either. Their effects depend on the strain, the dose, the disease, the duration, and the patient. A systematic review and meta-analysis published in 2025 on microbial interventions in atopic dermatitis and psoriasis found potential signals of benefit, but also significant heterogeneity between studies, which still limits definitive conclusions. Therefore, 'probiotic' is not a single treatment.

Do we need to analyze everyone's microbiome?

Currently, no. Commercial microbiota analyses can provide interesting information, but for most dermatological diseases we do not yet have a universal pattern that would allow us to say 'you are lacking this bacterium, take this capsule, and we will cure your skin.' Microbiome science is advancing enormously, but we must avoid selling tomorrow what research is still trying to understand today.

So, what can I measure if I suspect inflammation?

It depends entirely on the clinical context. We can use markers such as C-reactive protein, erythrocyte sedimentation rate, a full blood count, ferritin, and metabolic, hepatic, endocrine, or immunological tests depending on the suspected diagnosis. But there is something fundamental: there is no such thing as a universal 'chronic inflammation panel.' And a normal CRP does not mean that every inflammatory mechanism in the body has been switched off; equally, a slightly elevated CRP does not by itself diagnose any disease.

Inflammation must not become the new catch-all diagnosis

I find this particularly important. Today we constantly hear explanations like 'you are inflamed': you feel tired — 'inflammation'; you have acne — 'gut inflammation'; you struggle to lose weight — 'inflammation'; you have pigmentation spots — 'inflammation'; your hair is falling out — 'inflammation.' That is not medicine either. Inflammation is a mechanism, and we need to find out why it is occurring.

And exactly the same applies to the microbiome

Saying 'you have dysbiosis' without clinical context can tell us very little, because there is no single perfect microbiota. The microbiota changes with age, diet, medications, antibiotics, geography, environment, disease, and lifestyle. Microbiome research is fascinating, but we must interpret it with rigour.

So does beauty really start from within?

In part, yes. But not as a commercial slogan. The quality of our skin depends on genetics, age, hormones, sun exposure, tobacco, pollution, nutrition, metabolism, sleep, the immune system, disease, the microbiota, and skincare. No cream exists that can control all of those factors, but neither does any diet that can replace all dermatological treatments.

That is what true integrative medicine looks like

It is not about saying 'everything comes from the gut,' nor about saying 'diet doesn't matter, just apply a cream.' It is about understanding that both things can matter. The skin needs topical treatment when appropriate, and the patient needs a comprehensive evaluation when appropriate.

When should we look beyond the skin?

Especially when a skin condition appears alongside abdominal obesity, insulin resistance or diabetes, persistent digestive disturbances, chronic diarrhoea, unexplained weight loss, anaemia, nutritional deficiencies, autoimmune diseases, joint pain, unexplained fatigue, hormonal imbalances, or systemic signs. In those cases, we must not limit ourselves to 'treating the spot': we need to ask whether something more is going on.

What I want you to remember

The skin is not isolated from the rest of the body. There is a continuous communication between the gut, the microbiota, the immune system, metabolism, hormones, the brain, and the skin. The so-called gut-skin axis is currently a real and very active field of research, and alterations in the gut microbiota have been associated with various inflammatory skin conditions. But association does not mean causality, and we cannot yet claim that by modifying the microbiome we will cure acne, rosacea, psoriasis, dermatitis, or skin ageing.

Chronic low-grade inflammation can also play a role in metabolic alterations, immune dysfunction, oxidative stress, cellular senescence, and ageing, and the concept of inflammaging is helping us better understand how inflammation and ageing can interact. But the solution does not lie in searching for 'an anti-inflammatory supplement'; rather, it lies in something far deeper: proper nutrition, physical activity, good sleep, avoiding tobacco, maintaining good metabolic health, treating existing conditions, protecting the skin from the sun, caring for the skin barrier, and using dermatological treatments when indicated.

I am Dr. Florian Vallecillo, and if there is one single idea I want to leave you with today, it is this: do not treat only the surface — look also at what is happening on the inside, but do so with science. Not every case of acne stems from the gut, not every case of rosacea is dysbiosis, not every blemish is systemic inflammation, and no supplement exists that can magically 'de-inflame' our entire body. True medicine lies in connecting the pieces — skin, immunity, metabolism, gut, and lifestyle — because sometimes the problem lies exclusively in the skin, yet at other times the skin can be one of the first windows showing us what is happening inside.