Light to Medium Brown Stool

 

Liver enzymes are responsible for converting cholesterol into bile acids, while separate enzymes, notably UDP-glucuronyl transferase, attach glucuronic acid to bilirubin. When bile containing conjugated bilirubin enters the intestine, colonic bacteria convert bilirubin to stercobilinogen, which is oxidised into stercobilin. Stercobilin is the primary pigment responsible for the brown coloration of stool. [4] Therefore the shade of brown in feces is determined largely by the concentration of stercobilin present

 

• Light brown stools occur when less bilirubin is conjugated through liver processing

• Mid to dark brown stools reflect moderate to robust bilirubin conjugation processing 

 

Thus, the gradation of stool color from light to dark brown serves as a visual marker of hepatobiliary function, with darker pigmentation reflecting adequate liver enzymatic activity, sufficient liver function and bile flow, and lighter coloration suggesting possible compromise in these processes. [5][6]

 

Steatorrhea

 

Undigested or unabsorbed fats passing through the gastrointestinal tract typically cause symptoms of Steatorrhea, which causes the faeces to present to varying degrees, as such:

 

• Shiny, greasy, or oily appearance

• Mid brown / clay colour

• Floats in the bowel

• Foul in smell - Faeces + Flatulence

 

Steatorrhea arises when dietary fats are not effectively digested and absorbed, and one important mechanism for fat digestion involves liver production of bile. Bile salts are essential for emulsifying fats and forming micelles that enable intestinal absorption of fat. In cases of hepatic insufficiency, bile acid synthesis is reduced and can result in inadequate lipid solubilization to varying degrees, demonstrating as steatorrhea. [2][3]

 

Extensively Coated Tongue

 

Liver impairment is reflected not only in biochemical abnormalities but also in subtle external signs. One clinically demonstrated marker is the proportion of the tongue covered by coating. In a large cohort study using computer-based tongue image analysis, patients with impaired liver function and diagnosed with non-alcoholic fatty liver disease consistently showed the percentage of the tongue surface covered by coating relative to exposed mucosa was much greater than healthy controls, which is more localized. 

 

The underlying pathophysiology is thought to involve the oral–gut–liver axis, in which dysbiosis and altered bile acid metabolism promote conditions favorable to increased microbial biofilm deposition on the tongue surface [7].

 

Digestive complaints

 

• Abdominal discomfort

• Bloating 

• Diarrhoea 

• Dysbiosis - Unbalanced Microbiome 

 

When the liver cannot properly produce or conjugate bile acids, it disrupts the balance of healthy bacteria in the gut. Under normal conditions, bile acids are made in the liver, attached to amino acids such as glycine or taurine, and then released into the intestine, where they help emulsify fats for digestion and also act as signaling molecules that regulate gut microbes.

 

When this process is impaired, fewer conjugated bile acids reach the intestine. This alters the strength and types of bile acids present, which changes the bacterial community, causing beneficial bacteria to decline while inflammatory species can overgrow. Such imbalances can lead to intestinal inflammation and digestive discomfort.

 

Inadequate bile production or poor bile conjugation also means that dietary fats are not fully emulsified or absorbed and remain in the intestinal lumen. These undigested fats can disrupt digestion in several ways. They alter the intestinal pH, slow down intestinal transit, reducing the clearance of bacteria from the small intestine, and trigger irritation and inflammation of the gut lining, which impairs local immune defenses.

 

Together, these changes create a favorable environment for bacterial overgrowth and dysbiosis. Some bacterial species can even use unabsorbed fats and their byproducts as an energy source, encouraging their proliferation and further worsening symptoms such as bloating, gas, diarrhea, and abdominal discomfort. [23][24]

 

Elevated Cortisol + Impaired Glucose Tolerance

 

• Cravings for sweet or starchy foods 

• Localised Abdominal Weight 

 

The liver plays a key role in the metabolic clearance of cortisol. Cortisol is taken up by the liver and undergoes biotransformation ultimately forming more water soluble metabolites that can be excreted in bile or urine. Therefore when the liver’s metabolic capacity is compromised this reduces the rate at which cortisol is inactivated and removed. As a consequence, cortisol may remain elevated in the circulation, as has been demonstrated by clinical research. [13][14]

 

This elevated cortisol exposure can then contribute to insulin resistance which promotes what is known as ‘impaired glucose tolerance’ - IGT. [8][15] IGT is poorly controlled blood sugar which can present as peaks and troughs ultimately manifesting in the symptoms briefed above. 

 

Tiredness + Fatigue 

 

Clinical studies confirm that fatigue is one of the most common and distressing symptoms of chronic liver conditions, and the state of energy loss can be determined by the extent of liver incapacitation.

This is because the liver normally supplies a steady flow of energy by regulating blood sugar, storing glycogen, and breaking down fats. It also filters toxins, clears inflammatory molecules, and helps maintain the body’s internal chemical balance. In states of hepatic insufficiency however, these systems become disrupted. Ultimately this leads to reduced cellular energy availability and greater oxidative stress, which contributes to physical exhaustion, muscle weakness, and overall low vitality. [16]

 

Mood Altercations

 

In more advanced cases of liver insufficiency involved chronic liver mediated immune activation the following mood altercations can evolve

 

• Low stress tolerance / Easily Overwhelmed

• Irritability and Agitation

• Impatience and Frustration

• Anger

 

States of liver insufficiency are accompanied by higher toxin loads in the body which initiate inflammation through the release of cytokines such as TNF-α and IL-6 into the bloodstream. These chemicals have the capacity to travel to the brain through neural and blood-borne pathways, disturbing neurotransmitter balance in regions that control the mood. [16]

 

These mood altercations have been demonstrated in a large study on 171,321 adults who completed a stress questionnaire and had their livers checked with an ultrasound scan. The scans looked for fatty liver, a sign of reduced liver function. The study found that people with fatty liver were 17% more likely to report higher levels of stress tension and anger compared to those with healthy livers. [25]

 

In another clinical study involving 105 patients it was demonstrated that when liver-driven immune responses are stimulated and overactive, which can be the result of liver impairments or inflammation, the resulting neurochemical changes can interfere with dopamine and serotonin activity. This resulted in participants developing irritability, anger, agitation, and low stress tolerance, symptoms that increased in proportion to their liver mediated immune activity. [26]

 

Elevated Histamine 

 

• Allergies or Food Intolerances

• Nasal congestion, sinus pressure, or postnasal drip

• Migraines

• Itchy skin, eczema

• Flushing or redness of the face and chest

• Dizziness or light-headedness

• Poor Sleep

• Fatigue or brain fog

• Nausea 

• Digestive Complaints - Reflux, bloating, diarrhea, nausea

• Anxiety or irritability [22]

 

The liver is not only a detoxification organ, it is also a vital regulator of the immune system. It constantly filters blood from the gut, where most allergens, antigens, and microbial byproducts enter the body. Under healthy conditions, the liver maintains immune tolerance, preventing unnecessary immune reactions to harmless substances such as food proteins, pollen, or environmental antigens.

 

When liver processes become impaired, this filtering and regulatory balance begins to weaken. 

Reduced bile flow, slower clearance of antigens, and altered enzyme activity can cause inflammatory byproducts and immune-stimulating compounds to remain in circulation longer than they should. 

 

This can trigger the release of pro-inflammatory cytokines, which signal the immune system to stay active even when there is no true threat. Over time, this low-grade, persistent activation contributes to systemic immune dysregulation, making the body more prone to allergic-type responses, chronic inflammation, and fatigue. [19][20]

 

Furthermore, impaired hepatic clearance means that toxins, microbial fragments, and histamine that would normally be neutralized by the liver can also circulate longer in the bloodstream, heightening inflammation and histamine sensitivity throughout the body. This can manifest as a broad array of symptoms as indicated above. [21]

 

Chronic Yeast or Fungal Infections

 

• Tinea pedis - athlete’s foot

• Tinea cruris - jock itch

• Tinea corporis - ringworm 

• Tinea unguium - fungal nails

• Rashes localised to warm, sweaty or creased areas

• Pityriasis Versicolor

• Paronychia

• Candidiasis 

• Itching without visible rash

 

The liver acts as a major filter and immune-surveillance organ, specialised liver macrophages, called Kupffer cells, and other resident immune cells capture circulating yeast and fungi as they pass through the bloodstream, removing them before they can invade other tissues. [27]. 

 

In liver insufficiency, this filtering system can become compromised, and the liver’s production of immune proteins such as immunoglobulins and complement factors drops, Kupffer cell function falter and as a result, the liver can’t effectively clear the fungal load, leading to higher risk of invasive fungal infections. [28]

 

Elevated Estrogen [ Hyperestrogenism ] 

 

• Female - Heavy Menstrual Bleeding

• Male - Gynaecomastia ( male breasts )

 

Estrogen is cleared from the body primarily through a process called conjugation in the liver.. Once estrogens circulate through the body and exert their effects, the liver converts them into more water-soluble compounds using specialized enzymes. The two main conjugation pathways are sulfation and glucuronidation. 

 

Sulfotransferase (SULT) enzymes attach a sulfate group to the estrogen molecule, while UDP-glucuronosyltransferase (UGT) enzymes add a glucuronic acid group. These chemical modifications make estrogens less biologically active and easier to remove via bile or urine. [11][12]

 

Therefore When liver function is impaired, the body’s ability to perform these conjugation reactions decreases. As a result, unconjugated estrogens can build up in the bloodstream leading to higher circulating estrogen levels, and prolonged receptor stimulation increasing the risk of elevated estrogen-dominant conditions.

 

High Cholesterol 

 

Under normal conditions, hepatocytes tightly regulate cholesterol through synthesis, uptake, esterification, and excretion, processes that depend on efficient enzymatic and conjugation pathways to convert cholesterol into bile acids and lipoproteins for removal. When these detoxification and biotransformation systems become insufficient, hepatic clearance and conversion pathways falter and subsequently cholesterol is increasingly released into circulation as low-density lipoproteins (LDL) and remnant particles, promoting high cholesterol levels. [10]

 

Jaundice

 

Jaundice is the yellowing of the skin, sclera (whites of the eyes) and mucous membranes, caused by an accumulation of bilirubin in the bloodstream and tissues. Bilirubin is produced when red blood cells break down and hemoglobin is degraded. [17] Normally, bilirubin is taken up by hepatocytes in the liver, where it is bound to glucuronic acid so it becomes water-soluble, and then excreted into bile and finally into the intestine for elimination. In the setting of liver insufficiency, impaired conjugation causes poor bile formation, which limits the clearance of bilirubin to varying degrees causing the manifestation of yellowing in the sclera  [18]