Feces

Lore & Background

Feces are produced after digestion, when food not absorbed in the small intestine is broken down by bacteria in the large intestine. The distinctive odor comes from skatole, thiols, amines, and carboxylic acids. Feces retain about 50% of the energy of original food, supporting decomposers in ecosystems. Many organisms feed on feces, including bacteria, fungi, dung beetles, and animals practicing coprophagia, such as young elephants, dogs, rabbits, and monkeys. Seeds in feces aid plant dispersal, and feces reflect ultraviolet light, helping raptors like kestrels locate prey.

Reader's Guide

Feces play a critical role in ecology and human health. Ecologically, they recycle nutrients through detritivores and biogeochemical cycles, and serve as food for many organisms. In agriculture, animal feces like guano and manure are used as fertilizer, and dried dung is burned as fuel. Human feces are studied for the gut microbiome via 16S ribosomal RNA or shotgun sequencing, and fecal biomarkers can indicate diseases such as Inflammatory Bowel Disease. The fecal resistome—the gene pool for antimicrobial resistance in feces—spreads antibiotic resistance genes through manure and wastewater, persisting in soil. Coprolites (fossilized feces) and paleofeces provide direct evidence of ancient diets and health. Feces thus link digestion, ecology, medicine, and environmental science.

Did You Know?

• Feces contain about 50% of the energy of the original food eaten.
• Skatole, produced from tryptophan, is a key compound in the odor of feces.
• Fecal transplants are a medicinal use of human feces.

The Three-Part Physiological Breakdown

Jaundice is not a disease in itself but a visible warning that the body's heme-metabolism pipeline has been disrupted at some point. Clinicians divide the underlying pathology into three categories based on where the problem sits. Prehepatic jaundice stems from an abnormally rapid destruction of red blood cells, which floods the blood with unconjugated bilirubin. Sickle-cell anemia, spherocytosis, thalassemia, and glucose-6-phosphate dehydrogenase deficiency are classic examples, and infections such as malaria and bartonellosis can produce the same accelerated turnover. Hepatic jaundice implicates the liver directly: hepatocytes are injured by acute or chronic hepatitis, cirrhosis, drug-induced toxicity, alcoholic liver disease, or inherited conditions like Gilbert's syndrome (affecting roughly five percent of the population) and the rarer Crigler-Najjar syndromes. Posthepatic, or obstructive, jaundice occurs when bile ducts are physically blocked. Gallstones lodged in the common bile duct are the most common cause, but pancreatic-head cancer, acute or chronic pancreatitis, biliary strictures, and parasitic liver flukes can all create the same mechanical obstruction.

What the Body Shows: Signs, Symptoms, and the Itch

The hallmark of jaundice is a yellowish tint—occasionally greenish—appearing in the skin and the whites of the eyes. Scleral icterus, the yellowing of the eye's white area, typically becomes visible once serum bilirubin reaches at least three milligrams per deciliter. In reality, the term is a misnomer: bilirubin deposits in the conjunctival membranes that overlay the avascular sclera, making conjunctival icterus the technically accurate label. Because the conjunctiva is rich in elastin, it has a particularly high affinity for bilirubin, allowing even slight elevations to be spotted early. Accompanying signs include dark urine from bilirubin excretion and pale, fatty stools that lack their normal color. A hallmark complaint is intense, persistent itchiness, caused by bilirubin acting as a direct skin irritant. In people with darker skin tones, the yellowing on the skin can be subtle, so clinicians are advised to examine the sclera, palms, soles, and oral mucosa for a more reliable read. In a rare pediatric presentation, elevated bilirubin during tooth calcification can leave a yellow or green stain on developing teeth.

A Spectrum From Benign to Life-Threatening

The causes of jaundice span a wide range of severity. On the milder end, Gilbert's syndrome produces only transient, mild elevations in unconjugated bilirubin and is found in about five percent of people. Prolonged fasting, large bruises, and thyroid problems can also nudge unconjugated levels upward without indicating serious disease. At the other extreme, jaundice can signal cirrhosis, acute hepatitis, pancreatic cancer, or sepsis from leptospirosis—conditions that can be fatal if untreated. The bilirubin itself splits into two biochemical forms: unconjugated, which accumulates when red-cell breakdown outpaces liver processing, and conjugated, which builds up when the liver or bile ducts cannot excrete it properly. Normal blood levels sit below one milligram per deciliter; values above two to three generally cross the threshold into visible jaundice. It is also worth noting that not every yellowish skin discoloration is true jaundice. Carotenemia, from consuming large quantities of carotene-rich foods, and certain medications such as rifampin can produce a similar hue without any bilirubin elevation at all.

Treating the Root and the Newborn Challenge

Because jaundice is a sign rather than a disease, treatment is always directed at the underlying cause. When a bile duct is physically obstructed—by gallstones, a tumor, or a stricture—surgical intervention is usually necessary to restore flow. In all other cases, management is medical: treating an infectious source, discontinuing an offending drug, or addressing the metabolic disorder. For the persistent itchiness that accompanies many cases, clinicians may drain the gallbladder, prescribe ursodeoxycholic acid, or use opioid antagonists such as naltrexone. Newborns present a unique and time-sensitive challenge. An estimated eighty percent of babies develop some degree of jaundice during their first week of life. When bilirubin climbs into the four-to-twenty-one milligram-per-deciliter range, treatment escalates to phototherapy or, in more severe or premature cases, an exchange transfusion. The word jaundice itself carries a linguistic heritage, descending from the French jaunisse, literally yellow disease, a name that has tracked the condition's most recognizable feature for centuries.