Beeturia - Beetroot stain

 

Beetroot contains a pigment known as betalain which gives its vibrant red hue. 

 

For some there is a moment of wonder or shock when noticing that the urine or stool colour has a tint of pink or even red. This is known as beeturia and affects up to14% of the standard population. 

 

Whether or not you experience beeturia is largely due to betalains biological fate being determined by your stomach's pH level.[1]  Studies show betalains are colour stable over a pH range from 3 to 7, with optimal stability pH 5 – 6.[3] Studies also show at a pH of 2 betalain is chemically converted to form neobetanin, which is yellow in colour. [5]

 

Individuals with sufficient stomach acid levels have a stomach pH range varying between approximately 1.5 to 2.[4] In these individuals the red is chemically altered to yellow and unable to be detected in either the faeces or urine.

 

Individuals with insufficient stomach acid levels have a pH ranging from 4.0 to 7.0 or even higher. In this case betalain pigments are left red and are noticeable in the stool, or urine once absorbed into the bloodstream and filtered by the kidneys. 

 

To note: Beeturia affects up to 45% of those with pernicious anaemia (primarily caused by B12 deficiency). [2]

 

Foul Smelling Gas 

 

When proteins escape digestion in the stomach and small intestine and reaches the colon, gut bacteria ferment the protein. This fermentation produces volatile, foul-smelling metabolites, such as:

 

• Ammonia: contributes to a sharp, pungent smell

• Hydrogen sulfide: contributes to a rotten-egg, sulfur smell

• Skatole: contributes to a putrid, “fecal” smell

 

These compounds come specifically from undigested protein fermentation and not carbohydrate fermentation. Carbohydrate fermentation mainly produces short-chain fatty acids, which have a milder, sour smell. In contrast, protein fermentation shifts the odor profile of stool toward sharp, sulfurous, putrid, and ammonia-like smells. [36]

 

Tongue Cracking - Lingual Linear Lesions 

 

An under-acid stomach increases the likelihood of chronic vitamin B12 deficiency, since stomach acid is required for B12 absorption. One of the oral manifestations of long-term B12 deficiency is the development of cracks or grooves on the tongue, known as lingual linear lesions (LLLs). These lesions typically appear along the midline of the tongue, but can extend further. Clinical studies have shown that 98.25% of individuals presenting with LLLs were found to have vitamin B12 deficiency, highlighting the strong association between the two conditions. [27]

 

Burping / Belching 

 

Under healthy conditions acid rapidly breaks down food, activates digestive enzymes and helps regulate gastric emptying. When stomach acid is insufficient, proteins are not properly denatured, which slows the digestive process and causes food to linger in the stomach. This delay allows fermentation of undigested material and subsequent gas production. The accumulation of gas increases pressure in the upper stomach, which is then released upward through the esophagus as burping. [15]

 

B12 Deficiency

 

Vitamin B12 when consumed is naturally bound to food proteins, so when B12-containing foods enter the stomach proteolytic enzymes like pepsin are required to release it from the food and bind it to R-proteins and intrinsic factor in order to be absorbed in the terminal ileum

 

In relation to the necessary pepsin, its precursor pepsinogen is produced in the stomach by specialised cells known as chief cells. Yet, it is only within a highly acidic environment that pepsinogen can then undergo a conformational change to be cleaved into pepsin. Therefore low stomach acid prevents the metabolism of B12. 

 

To note, healthy participants given acid suppressing medication short-term, experienced more than a 70% decline in B12 absorption. [6]

 

Bloating

 

Incomplete protein digestion from inadequate stomach acid production allows putrefaction in the gut, increasing production of hydrogen, methane, and sulfur gases. Clinical studies reported excessive gas as a complaint in 34% of patients with low acid production. [32]

 

Weak + Brittle Hair

 

Adequate stomach acid is essential for the proper digestion of dietary protein, as hydrochloric acid activates pepsin, the enzyme that breaks proteins into absorbable amino acids. These amino acids are then used to build keratin, the structural protein that forms the foundation of hair. Keratin provides strength, resilience, and integrity to the hair shaft. Therefore when protein metabolism is impaired, it limits the supply of amino acids available for keratin synthesis, in turn, reduced keratin production compromises hair structure, leading to weak, brittle, or thinning hair that is more prone to shedding and breakage. [29]

 

Loss of Tongue Texture - Glossitis 

 

An under-acid stomach increases the likelihood of chronic vitamin B12 deficiency. Another oral manifestation of long-term B12 deficiency is when the filiform papillae on the surface of the tongue may undergo partial or complete wasting away. Since these papillae normally give the tongue its rough texture, their loss results in a tongue that appears smooth, reddish, shiny, and often swollen. This presentation, known as atrophic glossitis, is a classic oral manifestation of B12 deficiency. [28]

​

Nausea 

 

In the absence of sufficient stomach acid, the gastric environment shifts from acidic to one that favors bacterial and fungal overgrowth. Microbes that would normally be destroyed by acid are able to colonize the stomach and upper intestine, where they ferment undigested food. This fermentation process produces gas and metabolic by-products that can irritate the gastric lining creating a sense of nausea. Clinically, 34% of patients with low acid levels reported experiencing nausea. [32][33]

 

Gastrointestinal Infections + Imbalances

 

• SIBO

• Candiasis 

• Dysbiosis

• Helminth Infection

• Protozao Infection

 

An absence of sufficient stomach acid alters the microbial ecology of the upper gut, permitting the survival and expansion of organisms not normally present in the gastric or small intestinal tract. Clinical studies show that hypochlorhydria is associated with increased urinary indican excretion,  a marker of putrefactive bacterial metabolism, as well as microbial community dominated by Streptococcus, reflecting dysbiosis and contributing to conditions such as small intestinal bacterial overgrowth (SIBO).

 

Furthermore, low acid promotes chronic candidiasis, since Candida albicans is inhibited at gastric pH ≤ 4.5 but thrives when acidity is reduced, making Candida overgrowth a frequent consequence of low stomach acid. 

 

An under-acid stomach also removes the natural acid barrier against helminth (worm) eggs and protozoan (parasitic) cysts to survive ingestion, colonize the intestine, and cause chronic infection. For this reason hypochlorhydria is consistently linked to increased rates of parasitic colonization [32]

 

Yellow Tongue Coating - H.Pylori Positive Cases

 

Helicobacter pylori is extremely common, with a global prevalence of around 43% of the population [9]. Beyond driving low-grade gastric inflammation, the infection disrupts normal digestion by neutralising and suppressing stomach acid production, often leading to hypochlorhydria. In addition to these biochemical changes, visible tongue alterations have also been documented. 

 

In one study, approximately 81% of H. pylori–positive patients presented with a yellow tongue coating, whereas H. pylori negative cases most often showed white or white-to-pale yellow coatings. This suggests that tongue appearance may serve as a simple, non-invasive marker that correlates with underlying infection and gastric dysfunction, and should be noted when identified [37].