Skin Conditions
 

• Acne

• Dermatitis 

• Eczema

• Psoriasis

• Candidiasis 

• Acne

• Folliculitis

• Abscess and Boils

• Hives

• Skin Itching

Skin conditions have a direct association with the gut and increased intestinal permeability. This is because the translocation of microbial metabolites, endotoxins, and immune triggers pass through the gut barrier into systemic circulation. This process drives chronic low-grade inflammation and various kinds of immune dysregulation, which research has clearly demonstrated underpins the pathogenesis of many inflammatory skin disorders. Clinically proven examples include:
 

• Dermatitis and Eczema, linked to impaired gut barrier function allowing antigen leakage and Th2-dominant immune activation, paralleling skin barrier dysfunction.
   

• Psoriasis, permeability lead to translocation of bacterial DNA (e.g., E. coli) and endotoxins that trigger systemic inflammation via IL-17, IL-23, and TNF-α pathways, promoting keratinocyte proliferation.
   

• Acne and rosacea, microbial by-products and neuroendocrine alterations, such as serotonin, mTORC1 signalling, which is linked to gut barrier breakdown are connected to sebaceous and vascular inflammation.
   

• Abscess and boils, reduced microbial diversity and barrier dysfunction increase circulating inflammatory mediators that worsen follicular occlusion and abscess formation.
   

• Hives and Seborrheic dermatitis, systemic inflammatory mediators arising from barrier compromise influence mast-cell activity and skin lipid metabolism.
   

• Candida, actively causes intestinal permeability by releasing enzymes and toxins aspartyl proteases and phospholipases, which damage epithelial cells and allow fungal fragments to leak into circulation. [48][49][50][51]

IgE - Food Allergies, Immediate Hypersensitivity
 
Several studies show that when the intestinal barrier is compromised and permeable, food-derived proteins cross into the circulation more readily. When this takes place, these food proteins are taken up by antigen-presenting cells. This process promotes food-specific immune mediated IgE production, which initiates the sensitization of mast cells.
 
Therefore when the same food is consumed again in future and the food protein permeates into the blood stream, it can attach to the precreated IgE antibodies on mast cells, which then causes them to release histamine, typically within 30 minutes of consuming the food.
 
IgE Mediated reactions are most commonly associated with:
​

• Facial flushing

• Eczema

• Dermatitis 

• Skin itching

• Peeling Nail Beds

• Keratiderma - Thickened skin on the heels 

• Nasal congestion

• Coughing and Sneezing

• Asthma

• Headaches

• Brain fog

• Irritability and Anxiety

Certain foods are more likely to trigger these reactions because their proteins resist gastric acid, heat, and enzymatic digestion, leaving larger fragments that increase immune exposure and reaction, particularly if barrier function is impaired allowing more into systemic circulation. 
 
Common food triggers include:
 

• Cow’s milk

• Wheat

• Yeast - including beer

• Eggs

• Peas

• Peanuts and other nuts

• Soy

• Corn

• Fish

• Shellfish - shrimp, crab, lobster, squid

• Sesame
   

[9],[10],[11],[12],[33],[34][43][44]
 
IgG - Food Intolerances, Delayed Hypersensitivity
 
Beyond IgE immune reactions, enhanced translocation of food-derived proteins can also stimulate IgG immune responses. IgG reactions are not mediated by mast cells, rather IgG complexes activate the release of pro-inflammatory cytokines, including TNF-α, IL-6, IL-1. This results in a delayed, low-grade systemic inflammation, occurring anywhere between 4 - 48 hours after food exposure, and commonly affects the gut, joints, skin, and nervous system. [34]
 
IgG Mediated reactions are most commonly associated with:
 

• Eczema 

• Psorasis 

• Irritable Bowel Syndrome (IBS)

• Abdominal cramps

• Diarrhoea or Constipation

• Headaches + Migraines [39][40][41][42]

 
 Common trigger foods include:
 

• Cow’s milk

• Wheat

• Yeast - including beer

• Eggs

• Peas

• Peanuts and other nuts

• Soy

• Corn

• Fish

• Shellfish - shrimp, crab, lobster, squid

• Sesame
   

[9],[10],[11],[12],[33],[34][43]

Autoimmunty 
 
Autoimmunity is increasingly recognized as being closely linked to intestinal permeability. When the intestinal barrier is compromised, it loses its ability to selectively regulate what enters the bloodstream, allowing food-derived proteins, and bacterial components such as lipopolysaccharide (LPS) to cross into systemic circulation. 
 
These are then processed by antigen-presenting cells, driving activation of Th1 and Th17 immune pathways, secretion of pro-inflammatory cytokines, including TNF-α, IL-1, IL-6, which in a cascade of events encourages the loss of the body’s ability to recognize its own tissues as safe
 
This process can be intensified by molecular mimicry, where bacterial components or food-derived protein fragments closely resemble the body’s own tissue proteins. Because of this similarity, the immune system may mistakenly produce cross-reactive autoantibodies that not only target the foreign substances but also attack the body’s own tissues, encouraging the process of autoimmunity.
 
This has been demonstrated in various studies, including a large study including only participants with high zonulin levels, which is a marker of intestinal hyper-permeability. These subjects were tested for a spectrum of autoantibodies linked to different autoimmune diseases. The results showed that those with markers of increased permeability had a significantly higher likelihood of carrying autoantibodies associated with various autoimmune conditions. These results were then interpreted as showing the increased likelihood of having or developing autoimmune activity associated with intestinal permeability. [37] Results are detailed below.  
 

• Rheumatoid and Arthritic disease, 30× more likely

• Addison’s disease, 28× more likely

• Sjogren's Syndrome, 26 x more likely 

• Autoimmune hepatitis, 22× more likely

• Cerebellar autoimmunity, 22× more likely

• Cardiac autoimmunity, 10× more likely

• Type 1 diabetes, 10× more likely

• Neurologic autoimmunity, 8.7× more likely

• Inflammatory bowel disease, including Crohn’s and UC, 8.4× more likely

• Joint + Connective tissue autoimmunity, 7.2× more likely

• Ovarian or Testicular failure, 7.1× more likely

• IBD spectrum, 7.0× more likely

• Multiple sclerosis, 6.9× more likely

• Autoimmune gastritis, 5.8× more likely

• Graves Disease, up to 8x increase in disease severity

• Hashimoto’s thyroiditis, 2.4× more likely, further notes below

• Vitiligo, Higher in IP, association found, probability unknown

• Ankylosing Spondylitis, association found, probability unknown

• Alopecia Areata, association found, probability unknown

• Systemic Lupus, 53% correlation between permeability and disease activity

 
Whilst the above study demonstrated a reduced implication of intestinal permeability on Hashimoto's Thyroiditis, multiple other studies signify there is a much stronger correlation, with one study on 40 participants with Hashimoto's indicating that 62% of the participants had biomarkers that indicated intestinal permeability [35][36][38][52][53][54][55][56][57]
 
Inflammatory Digestive Disorders + Diseases
 
The following digestive disorders and diseases have been clinically demonstrated to exhibit increased intestinal permeability, a feature that persists even during states of remission. Further details listed in Causes.
 

• Ulcerative Colitis 

• Microscopic Colitis

• Chron’s Disease

• Celiac Disease

• Diverticulitis 

• Non Celiac Wheat or Gluten Sensitivity [45][46]

Diarrhoea 
 
Diarrhea-predominant IBS is frequently linked with increased intestinal permeability. Across multiple human studies using standard permeability probes, a substantial subset of IBS-D patients demonstrate barrier dysfunction and permeability, which often tracks with diarrhea severity and abdominal pain. Clinical data from the systematic reviews on 13 studies demonstrated a prevalence of increased permeability in Diarrhoea prominent IBS cases in between 37 - 62% of participants. [47]
 
Asthma
 
When the intestinal barrier is compromised, it loses its ability to selectively regulate what enters the bloodstream, and bacterial components such as lipopolysaccharide (LPS) cross into systemic circulation. 
 
Lipopolysaccharides engage with Toll-like receptor 4 on airway epithelial cells, alveolar macrophages, and dendritic cells, triggering amplified release of pro-inflammatory cytokines. This promotes a signalling cascade, which intensifies local airway hyper-responsiveness, characterised by increased bronchoconstriction, mucus hyper-secretion, and airway edema. Consequently, individuals with chronic LPS translocation are predisposed to greater asthma severity, persistent wheeze, and heightened allergic airway inflammation. [34]
 
Acne 
 
Research has demonstrated that acne has a close connection with the gastrointestinal tract and that alterations in the gut microbiota increase intestinal permeability, allowing bacterial metabolites and endotoxins to enter systemic circulation.  This altercation disturbs the skin equilibrium as it triggers the release of pro-inflammatory cytokines, which circulate throughout the body and reach the skin’s sebaceous glands. These cytokines then stimulate immune activity within the skin, leading to increased sebum production, follicular blockage, and inflammation, which are key processes in the development of acne. [48]

Chronic Low Energy
 
Increased intestinal permeability, allows harmful substances like bacterial toxins such as lipopolysaccharide (LPS) to leak from the gut into the bloodstream. This process triggers an immune response that can contribute to the production of pro-inflammatory cytokines. These cytokines then signal to the central nervous system, producing ‘sickness behavoir’, characterised by fatigue.
 
At the cellular level, chronic LPS exposure also impairs mitochondrial function, disrupting electron transport and reducing ATP availability. The combination of neuroimmune signaling and impaired energy production explains why systemic LPS is strongly associated with low energy and persistent fatigue. [5][34]

Causes