Tongue Coating + Colour Characteristics

 

A cross-sectional study of 158 adults, conducted over 5 months, photographed the tongue after an overnight fast using standardised imaging, collected pre-brushing tongue swabs for bacterial sequencing, and drew routine blood samples to test whether coating appearance reliably reflects microbiome dysbiosis and systemic inflammation. Tongue coatings were classified into four types detailed below, with the corresponding findings. [1]

 

Sparse White Coating

 

Tongues with a very sparse white coating, almost undetectable, demonstrated the most balanced microbiome, with higher α-diversity. This refers to an ecological system with stability and resilience, having more species sharing the space and fewer chances for one opportunist species taking over. This was further evident by the blood markers, which demonstrated no clear inflammation signals. 

 

Thin Yellow Coating

 

Tongues with a thin yellow coating demonstrated the lowest α-diversity, meaning fewer kinds of microbes and a less even balance, and the weakest microbe–microbe network, so the community is less stable and more prone to imbalance. 

 

Thin yellow coatings are also aligned with higher PLR levels, a simple blood marker that rises with systemic inflammation, and also tend to have higher blood levels of CRP (C-reactive protein), a protein that rises with systemic inflammation. Taken together, this coating type signals an unstable ecosystem, with a more inflammatory tone, which is not a beneficial state.

 

Thick White Coating 

 

Tongues with a thick white coating, trended toward lower diversity and more disrupted networks than the healthy baseline. Thick white coatings demonstrated relatively more Prevotella salivae than the sparse white coatings, consistent with a shift toward dysbiosis. 

 

Regarding inflammation, note was made of higher fibrinogen levels. Fibrinogen is an acute-phase reactant, when it is elevated it ordinarily signals ongoing inflammation. In this cohort, PLR inflammatory markers were not raised, but the fibrinogen association suggests vascular or inflammatory effects are still relevant for this pattern.

 

Thick Yellow Coating 

 

Tongues with a thick yellow coating, pointed to community disruption. Its α-diversity was low and its β-diversity network structure clearly shifted towards increased Streptococcus anginosus and Moraxella catarrhalis numbers. Health-wise these strains are aligned with elevated BMI or waist size, more fat stored in the liver, insulin having to work harder, and inflammation-wise. This is also demonstrated with consistently elevated PLR levels, which is a simple blood marker that rises with systemic inflammatory responses.[1]

Dysbiosis Mediated Digestive Disorders

 

• Constipation 

• Chronic Diarrhea

• Irritable Bowel Syndrome (IBS)

• Chron's Disease 

• Diverticulitis 

• Ulcerative colitis

• Gastritis 

• Gastro-oesophageal Reflux Disease (GORD)

• ​​Peptic Ulcers

 

A broad spectrum of conditions across the digestive, immune, metabolic, dermatological, and neurological systems are linked to an imbalance in the composition or function of the body's microbial communities. 

 

This correlation arises because the microbiome is not only involved in digestion but also regulates immune signaling, maintains barrier integrity, produces neurotransmitters, and influences systemic inflammation and metabolism. When the balance of beneficial to harmful microbes is disrupted, it can lead to excess production of inflammatory molecules, loss of protective metabolites like short-chain fatty acids, greater permeability of mucosal barriers and cause several other imbalances. 

 

Dysbiosis Mediated Immune Disorders

 

• Allergies

• Asthma

• Recurrent Respiratory Infections

• Food Intolerances

• Autoimmune Disease

 

Dysbiosis within the gut and upper airway microbiome can significantly alter immune regulation, increasing susceptibility to allergic, inflammatory, and recurrent infectious conditions. This occurs because the microbiome shapes immune tolerance, calibrates inflammatory pathways, influences antibody responses and assists in maintaining epithelial integrity within the respiratory tract. 

 

When microbial balance is disrupted, the immune system becomes more reactive, less regulated, and less effective at defending against pathogens, resulting in heightened inflammation, hypersensitivity and recurrent respiratory symptoms.

 

Dysbiosis Mediated Skin Conditions

 

• Eczema

• Contact Dermatitis 

• Folliculitis

• Acne

• Abscesses or Boils

• Psoriasis

• Rosacea

• Pityriasis Versicolor

 

A wide range of dermatological conditions are now recognised as being influenced by imbalances within the gut-skin and skin-surface microbiome ecosystems. The skin relies on microbial diversity to regulate local immunity, maintain barrier function, modulate inflammation, and protect against pathogenic organisms. 

 

When dysbiosis occurs it can lead to an overactive immune response, impaired barrier repair, increased colonisation by harmful microbes and a rise in pro-inflammatory compounds that manifest on the skin.

 

Dysbiosis Mediated Genitourinary and Reproductive Disorders

 

• Urinary Tract Infections

• Candidiasis

• Bacterial Vaginosis 

 

The vaginal, urinary, and reproductive microbiomes are highly sensitive ecosystems that rely on dominant beneficial species, particularly Lactobacilli, for protection, pH regulation, pathogen resistance and modulation of local immune responses. Dysbiosis in these regions, or systemic dysbiosis originating from the gut, can impair mucosal defences, increase adherence of opportunistic microbes, disrupt hormonal signalling and contribute to chronic inflammatory or infectious presentations. These imbalances often manifest as recurrent infections, altered discharge, pelvic discomfort or hormonal dysregulation.

 

Dysbiosis Mediated Neuroendocrine and Metabolic

 

• Serotonin Deficiency 

• Insulin Resistance

 

The gut microbiome plays a pivotal role in neurochemical production, hormone metabolism, glucose regulation, and appetite control through the gut-brain-axis and gut-endocrine pathways. When dysbiosis occurs, it can reduce production of key neurotransmitters, such as serotonin, impair insulin signalling, increase systemic inflammation, and disrupt metabolic homeostasis. These changes can contribute to mood disturbances, altered stress responses, cravings, weight fluctuations and metabolic dysfunction.