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Thyroid hormones
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The structural formula (left) and a space-filling model (right) of (S)-triiodothyronine (T3, also called liothyronine in the pharmaceutical industry)
The structural formula (left) and a space-filling model (right) of (S)-thyroxine (T4.)
The thyroid hormones are tyrosine-based hormones produced by the thyroid gland that are primarily responsible for regulation of metabolism. T3 and T4 are partially composed of iodine (see molecular model). A deficiency of iodine leads to decreased production of T3 and T4, enlarges the thyroid tissue and will cause the disease known as simple goitre. The major form of thyroid hormone in the blood is thyroxine (T4), which has a longer half-life than T3.[1] In humans, the ratio of T4 to T3 released into the blood is sometimes claimed to be quite high, but thyroid removal patient data suggests it to vary between 4:1 to 2:1 the average being 100:36. T4 is converted to the active T3 (three to four times more potent than T4) within cells by deiodinases (5'-iodinase). These are further processed by decarboxylation and deiodination to produce iodothyronamine (T1a) and thyronamine (T0a). All three isoforms of the deiodinases are selenium-containing enzymes, thus dietary selenium is essential for T3 production. Edward Calvin Kendall was responsible for the isolation of thyroxine in 1915.[2]
Contents
[hide]
1 Function
2 Medical use
2.1 Formulations
3 Production
3.1 Central
3.2 Peripheral
3.3 Initiation of production in fetuses
3.4 Effect of iodine deficiency on thyroid hormone synthesis
4 Circulation and transport
4.1 Plasma transport
4.2 Membrane transport
4.3 Intracellular transport
5 Mechanism of action
5.1 Thyroxine, iodine and apoptosis
5.2 Effects of triiodothyronine
6 Measurement
7 Related diseases
8 Anti-thyroid drugs
9 See also
10 References
11 External links
Function[edit]
The thyroid system of the thyroid hormones T3 and T4.[3]
The thyroid hormones act on nearly every cell in the body. They act to increase the basal metabolic rate, affect protein synthesis, help regulate long bone growth (synergy with growth hormone) and neural maturation, and increase the body's sensitivity to catecholamines (such as adrenaline) by permissiveness. The thyroid hormones are essential to proper development and differentiation of all cells of the human body. These hormones also regulate protein, fat, and carbohydrate metabolism, affecting how human cells use energetic compounds. They also stimulate vitamin metabolism. Numerous physiological and pathological stimuli influence thyroid hormone synthesis.
Thyroid hormone leads to heat generation in humans. However, the thyronamines function via some unknown mechanism to inhibit neuronal activity; this plays an important role in the hibernation cycles of mammals and the moulting behaviour of birds. One effect of administering the thyronamines is a severe drop in body temperature.
Medical use[edit]
Both T3 and T4 are used to treat thyroid hormone deficiency (hypothyroidism). They are both absorbed well by the gut, so can be given orally. Levothyroxine is the pharmaceutical name of the manufactured version of T4, which is metabolised more slowly than T3 and hence usually only needs once-daily administration. Natural desiccated thyroid hormones are derived from pig thyroid glands, and are a "natural" hypothyroid treatment containing 20% T3 and traces of T2, T1and calcitonin. Also available are synthetic combinations of T3/T4 in different ratios (such as liotrix) and pure-T3 medications (INN: liothyronine). Levothyroxine Sodium is usually the first course of treatment tried. Some patients feel they do better on desiccated thyroid hormones; however, this is based on anecdotal evidence and clinical trials have not shown any benefit over the biosynthetic forms.[4] Thyroid tablets are reported to have different effects, which can be attributed to the difference in torsional angles surrounding the reactive site of the molecule.[5]
Thyronamines have no medical usages yet, though their use has been proposed for controlled induction of hypothermia, which causes the brain to enter a protective cycle, useful in preventing damage during ischemic shock.
Synthetic thyroxine was first successfully produced by Charles Robert Harington and George Barger in 1926.
Formulations[edit]
Today most patients are treated with levothyroxine, or a similar synthetic thyroid hormone.[6][7][8] Different polymorphs of the compound have different solubilities and potencies.[9] Additionally, natural thyroid hormone supplements from the dried thyroids of animals are still available.[8][10][11] Levothyroxine contains T4 only and is therefore largely ineffective for patients unable to convert T4 to T3.[12] These patients may choose to take natural thyroid hormone, as it contains a mixture of T4 and T3,[8][13][14][15][16] or alternatively supplement with a synthetic T3 treatment.[17] In these cases, synthetic liothyronine is preferred due to the potential differences between the natural thyroid products. Some studies show that the mixed therapy is beneficial to all patients, but the addition of lyothyronine contains additional side effects and the medication should be evaluated on an individual basis.[18] Some natural thyroid hormone brands are FDA approved, but some are not.[19][20][21] Thyroid hormones are generally well tolerated.[7] Thyroid hormones are usually not dangerous for pregnant women or nursing mothers, but should be given under a doctor's supervision. In fact, if a woman who is hypothyroid is left untreated, her baby is at a higher risk for birth defects. When pregnant, a woman with a low-functioning thyroid will also need to increase her dosage of thyroid hormone.[7] One exception is that thyroid hormones may aggravate heart conditions, especially in older patients; therefore, doctors may start these patients on a lower dose and work up to a larger one to avoid risk of heart attack.[8]
Production[edit]
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Central[edit]
Synthesis of the thyroid hormones, as seen on an individual thyroid follicular cell:[22][page needed]
- Thyroglobulin is synthesized in the rough endoplasmic reticulum and follows the secretory pathway to enter the colloid in the lumen of the thyroid follicle by exocytosis.
- Meanwhile, a sodium-iodide (Na/I) symporter pumps iodide (I−) actively into the cell, which previously has crossed the endothelium by largely unknown mechanisms.
- This iodide enters the follicular lumen from the cytoplasm by the transporter pendrin, in a purportedly passive manner.
- In the colloid, iodide (I−) is oxidized to iodine (I0) by an enzyme called thyroid peroxidase.
- Iodine (I0) is very reactive and iodinates the thyroglobulin at tyrosyl residues in its protein chain (in total containing approximately 120 tyrosyl residues).
- In conjugation, adjacent tyrosyl residues are paired together.
- Thyroglobulin re-enters the follicular cell by endocytosis.
- Proteolysis by various proteases liberates thyroxine and triiodothyronine molecules
- Efflux of thyroxine and triiodothyronine from follicular cells, which appears to be largely through monocarboxylate transporter (MCT) 8 and 10,[23][24] and entry into the blood.
Thyroid hormones (T4 and T3) are produced by the follicular cells of the thyroid gland and are regulated by TSH made by the thyrotropes of the anterior pituitary gland. The effects of T4 in vivo are mediated via T3 (T4 is converted to T3 in target tissues). T3 is 3- to 5- fold more active than T4.
Thyroxine (3,5,3',5'-tetraiodothyronine) is produced by follicular cells of the thyroid gland. It is produced as the precursor thyroglobulin (this is not the same as thyroxine-binding globulin (TBG)), which is cleaved by enzymes to produce active T4.
The steps in this process are as follows:[22]
The Na+/I− symporter transports two sodium ions across the basement membrane of the follicular cells along with an iodide ion. This is a secondary active transporter that utilises the concentration gradient of Na+ to move I− against its concentration gradient.
I− is moved across the apical membrane into the colloid of the follicle.
Thyroperoxidase oxidizes two I− to form I2. Iodide is non-reactive, and only the more reactive iodine is required for the next step.
The thyroperoxidase iodinates the tyrosyl residues of the thyroglobulin within the colloid. The thyroglobulin was synthesised in the ER of the follicular cell and secreted into the colloid.
Iodinated Thyroglobulin binds megalin for endocytosis back into cell.
Thyroid-stimulating hormone (TSH) released from the adenohypophysis binds the TSH receptor (a Gs protein-coupled receptor) on the basolateral membrane of the cell and stimulates the endocytosis of the colloid.
The endocytosed vesicles fuse with the lysosomes of the follicular cell. The lysosomal enzymes cleave the T4 from the iodinated thyroglobulin.
The thyroid hormones cross the follicular cell membrane towards the blood vessels by an unknown mechanism.[22] Text books have stated that diffusion is the main means of transport,[25] but recent studies indicate that monocarboxylate transporter (MCT) 8 and 10 play major roles in the efflux of the thyroid hormones from the thyroid cells.[23][24]
Thyroglobulin (Tg) is a 660 kDa, dimeric protein produced by the follicular cells of the thyroid and used entirely within the thyroid gland.[citation needed] Thyroxine is produced by attaching iodine atoms to the ring structures of this protein's tyrosine residues; thyroxine (T4) contains four iodine atoms, while triiodothyronine (T3), otherwise identical to T4, has one less iodine atom per molecule.[citation needed] The thyroglobulin protein accounts for approximately half of the protein content of the thyroid gland.[citation needed] Each thyroglobulin molecule contains approximately 100-120 tyrosine residues, a small number of which (<20) are subject to iodination catalysed by thyroperoxidase.[26] The same enzyme then catalyses "coupling" of one modified tyrosine with another, via a free radical-mediated reaction, and when these iodinated bicyclic molecules are released by hydrolysis of the protein, T3 and T4 are the result.[citation needed] hence, each Tg protein molecule ultimately yields very small amounts of thyroid hormone (experimentally observed to be on the order of 5-6 molecules of either T4 or T3 per original molecule of Tg).[26]
More specifically, the monoatomic, anionic form of iodine, iodide, I {\displaystyle I} —, is actively absorbed from the bloodstream by a process called iodide trapping.[citation needed] In this process, sodium is cotransported with iodide from the basolateral side of the membrane into the cell,[clarification needed] and then concentrated in the thyroid follicles to about thirty times its concentration in the blood.[citation needed] Then, in the first reaction catalysed by the enzyme thyroperoxidase, tyrosine residues in the protein thyroglobulin are iodinated on their phenol rings, at one or both of the positions ortho to the phenolic hydroxyl group, yielding monoiodotyrosine (MIT) and diiodotyrosine (DIT), respectively. This introduces 1-2 atoms of the element iodine, covalently bound, per tyrosine residue.[citation needed] The further coupling together of two fully iodinated tyrosine residues, also catalysed by thyroperoxidase, yields the peptidic (still peptide-bound) precursor of thyroxine, and coupling one molecule of MIT and one molecule of DIT yields the comparable precursor of triiodothyronine:[citation needed]
peptidic MIT + peptidic DIT → peptidic triiodothyronine (eventually released as triiodothyronine, T3)
2 peptidic DITs → peptidic thyroxine (eventually released as thyroxin, T4)
(Coupling of DIT to MIT in the opposite order yields a substance, r-T3, which is biologically inactive.[relevant? – discuss][citation needed]) Hydrolysis (cleavage to individual amino acids) of the modified protein by proteases then liberates T3 and T4, as well as the non-coupled tyrosine derivatives MIT and DIT.[citation needed] The hormones T4 and T3 are the biologically active agents central to metabolic regulation.[citation needed]
Peripheral[edit]
Thyroxine is believed to be a prohormone and a reservoir for the most active and main thyroid hormone T3.[27] T4 is converted as required in the tissues by iodothyronine deiodinase.[28] Deficiency of deiodinase can mimic hypothyroidism due to iodine deficiency.[29] T3 is more active than T4,[30] though it is present in less quantity than T4.
Initiation of production in fetuses[edit]
Thyrotropin-releasing hormone (TRH) is released from hypothalamus by 6 – 8 weeks, and thyroid-stimulating hormone (TSH) secretion from fetal pituitary is evident by 12 weeks of gestation, and fetal production of thyroxine (T4) reaches a clinically significant level at 18–20 weeks.[31] Fetal triiodothyronine (T3) remains low (less than 15 ng/dL) until 30 weeks of gestation, and increases to 50 ng/dL at term.[31] Fetal self-sufficiency of thyroid hormones protects the fetus against e.g. brain development abnormalities caused by maternal hypothyroidism.[32]
Effect of iodine deficiency on thyroid hormone synthesis[edit]
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If there is a deficiency of dietary iodine, the thyroid will not be able to make thyroid hormone. The lack of thyroid hormone will lead to decreased negative feedback on the pituitary, leading to increased production of thyroid-stimulating hormone, which causes the thyroid to enlarge (the resulting medical condition is called endemic colloid goitre; see goitre). This has the effect of increasing the thyroid's ability to trap more iodide, compensating for the iodine deficiency and allowing it to produce adequate amounts of thyroid hormone.
Circulation and transport[edit]
Plasma transport[edit]
Most of the thyroid hormone circulating in the blood is bound to transport proteins. Only a very small fraction of the circulating hormone is free (unbound) and biologically active, hence measuring concentrations of free thyroid hormones is of great diagnostic value.
When thyroid hormone is bound, it is not active, so the amount of free T3/T4 is what is important. For this reason, measuring total thyroxine in the blood can be misleading.
Type
Percent
bound to thyroxine-binding globulin (TBG) 70%
bound to transthyretin or "thyroxine-binding prealbumin" (TTR or TBPA) 10-15%
albumin 15-20%
unbound T4 (fT4) 0.03%
unbound T3 (fT3) 0.3%
Despite being lipophilic, T3 and T4 cross the cell membrane via carrier-mediated transport, which is ATP-dependent.[33]
T1a and T0a are positively charged and do not cross the membrane; they are believed to function via the trace amine-associated receptor TAAR1 (TAR1, TA1), a G-protein-coupled receptor located in the cell membrane.
Another critical diagnostic tool is measurement of the amount of thyroid-stimulating hormone (TSH) that is present.
Membrane transport[edit]
Contrary to common belief, thyroid[34] hormones cannot traverse cell membranes in a passive manner like other lipophilic substances. The iodine in o-position makes the phenolic OH-group more acidic, resulting in a negative charge at physiological pH. However, at least 10 different active, energy-dependent and genetically-regulated iodothyronine transporters have been identified in humans. They guarantee that intracellular levels of thyroid hormones are higher than in blood plasma or interstitial fluids.[35]
Intracellular transport[edit]
Little is known about intracellular kinetics of thyroid hormones. However, recently it could be demonstrated that the crystallin CRYM binds 3,5,3′-triiodothyronine in vivo.[36]
Mechanism of action[edit]
Main article: Thyroid hormone receptor
The thyroid hormones function via a well-studied set of nuclear receptors, termed the thyroid hormone receptors. These receptors, together with corepressor molecules, bind DNA regions called thyroid hormone response elements (TREs) near genes. This receptor-corepressor-DNA complex can block gene transcription. When triiodothyronine (T3) binds a receptor, it induces a conformational change in the receptor, displacing the corepressor from the complex. This leads to recruitment of coactivator proteins and RNA polymerase, activating transcription of the gene. [37] Although this general functional model has considerable experimental support, there remain many open questions. [38]
Thyroxine, iodine and apoptosis[edit]
Amphibian metamorphosis
Thyroxine and iodine stimulate the spectacular apoptosis of the cells of the larval gills, tail and fins in amphibian metamorphosis, and stimulate the evolution of their nervous system transforming the aquatic, vegetarian tadpole into the terrestrial, carnivorous frog. In fact, amphibian frog Xenopus laevis serves as an ideal model system for the study of the mechanisms of apoptosis.[39][40][41][42]
Effects of triiodothyronine[edit]
Effects of triiodothyronine (T3) which is the metabolically active form:
Increases cardiac output
Increases heart rate
Increases ventilation rate
Increases basal metabolic rate
Potentiates the effects of catecholamines (i.e. increases sympathetic activity)
Potentiates brain development
Thickens endometrium in females
Increases catabolism of proteins and carbohydrates[43]
Measurement[edit]
Further information: Thyroid function tests
Thyroxine and triiodothyronine can be measured as free thyroxine and free triiodothyronine, which are indicators of thyroxine and triiodothyronine activities in the body. They can also be measured as total thyroxine and total triiodothyronine, which also depend on the thyroxine and triiodothyronine that is bound to thyroxine-binding globulin. A related parameter is the free thyroxine index, which is total thyroxine multiplied by thyroid hormone uptake, which, in turn, is a measure of the unbound thyroxine-binding globulins.[44] Additionally, thyroid disorders can be detected prenatally using advanced imaging techniques and testing fetal hormone levels.[45]
Related diseases[edit]
Both excess and deficiency of thyroxine can cause disorders.
Hyperthyroidism (an example is Graves Disease) is the clinical syndrome caused by an excess of circulating free thyroxine, free triiodothyronine, or both. It is a common disorder that affects approximately 2% of women and 0.2% of men. Thyrotoxicosis is often used interchangeably with hyperthyroidism, but there are subtle differences. Although thyrotoxicosis also refers to an increase in circulating thyroid hormones, it can be caused by the intake of thyroxine tablets or by an over-active thyroid, whereas hyperthyroidism refers solely to an over-active thyroid.
Hypothyroidism (an example is Hashimoto's thyroiditis) is the case where there is a deficiency of thyroxine, triiodiothyronine, or both.
Clinical depression can sometimes be caused by hypothyroidism.[46] Some research[47] has shown that T3 is found in the junctions of synapses, and regulates the amounts and activity of serotonin, norepinephrine, and γ-aminobutyric acid (GABA) in the brain.
Hair loss can sometimes be attributed to a malfunction of t3 and t4. Normal hair growth cycle may be affected disrupting the hair growth.
Preterm births can suffer neurodevelopmental disorders due to lack of maternal thyroid hormones, at a time when their own thyroid is unable to meet their postnatal needs.[48] Also in normal pregnancies, adequate levels of maternal thyroid hormone are vital in order to ensure thyroid hormone availability for the fetus and its developing brain.[49] Congenital hypothyroidism occurs in every 1 in 1600–3400 newborns with most being born asymptomatic and developing related symptoms weeks after birth.[50]
Anti-thyroid drugs[edit]
Iodine uptake against a concentration gradient is mediated by a sodium-iodine symporter and is linked to a sodium-potassium ATPase. Perchlorate and thiocyanate are drugs that can compete with iodine at this point. Compounds such as goitrin, carbimazole, methimazole, propylthiouracil can reduce thyroid hormone production by interfering with iodine oxidation.[51]
See also[edit]
Goitre
Graves-Basedow disease
Hashimoto's thyroiditis
Hormone
Polar T3 syndrome
Thyroid gland
Thyroid-stimulating hormone
Thyronamines, metabolites of the thyroid hormones that act at the trace amine-associated receptor TAAR1 (TAR1)
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Jump up ^ Spiegel C, Bestetti GE, Rossi GL, Blum JW (September 1993). "Normal circulating triiodothyronine concentrations are maintained despite severe hypothyroidism in growing pigs fed rapeseed presscake meal". Journal of Nutrition. 123 (9): 1554–61. PMID 8360780.
External links[edit]
Find TH response elements in DNA sequences.
Triiodothyronine bound to proteins in the PDB
Thyroxine bound to proteins in the PDB
T4 at Lab Tests Online
Thyroid hormone treatment in thyroid disease
Thyroid Hormone Treatment Brochure by the American Thyroid Association
Elaborate article about the use of thyroid drugs Written by an MD
Thyroid Disease Manager Collection of elaborate medical articles on thyroid disease, including information on thyroid hormones
[show]
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t
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Hormones
Endocrine
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Hypothalamic-
pituitary
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MCH
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TSH
Prolactin
POMC
CLIP
ACTH
MSH
Endorphins
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GH
Adrenal axis
Adrenal cortex
aldosterone
cortisol
cortisone
DHEA
DHEA-S
androstenedione
Adrenal medulla
epinephrine
norepinephrine
Thyroid
Thyroid hormone
T3
T4
Calcitonin
Thyroid axis
Parathyroid
PTH
Gonadal axis
Testis
testosterone
AMH
inhibin
Ovary
estradiol
progesterone
activin and inhibin
relaxin (pregnancy)
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HPL
estrogen
progesterone
Pancreas
glucagon
insulin
amylin
somatostatin
pancreatic polypeptide
Pineal gland
melatonin
N,N-dimethyltryptamine
5-methoxy-N,N-dimethyltryptamine
Other
Thymus
Thymosins
Thymosin α1
Beta thymosins
Thymopoietin
Thymulin
Digestive system
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gastrin
ghrelin
Duodenum
CCK
Incretins
GIP
GLP-1
secretin
motilin
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enteroglucagon
peptide YY
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IGF-1
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Adipose tissue
leptin
adiponectin
resistin
Skeleton
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JGA (renin)
peritubular cells
EPO
calcitriol
prostaglandin
Heart
Natriuretic peptide
ANP
BNP
[show]
v
t
e
Thyroid therapy (H03)
Thyroid hormones
Levothyroxine#
Liothyronine
Liotrix
Tiratricol
Thyroid gland preparations
Antithyroid preparations
Thyroid peroxidase
inhibitors (thioamide)
Thiouracils
Propylthiouracil#
Methylthiouracil
Benzylthiouracil
Sulfur-containing imidazole derivatives:
Carbimazole
Methimazole
Block conversion of
T4 to T3
Propylthiouracil#
Ipodate
Sodium-iodide symporter
inhibitor
Perchlorate (Potassium perchlorate)
Pertechnetate (Sodium pertechnetate)
Other
Diiodotyrosine
Dibromotyrosine
#WHO-EM
‡Withdrawn from market
Clinical trials:
†Phase III
§Never to phase III
[show]
v
t
e
Thyroid hormone receptor modulators
Receptor
(ligands)
THR
Agonists: Dextrothyroxine
DIMIT
DITPA
Eprotirome (KB-2115)
KB-141
KB-2611
KB-130015
Levothyroxine
Liothyronine
Liotrix
MB-07344
MB-07811
MGL-3196 (VIA-3196)
Sobetirome (GC-1, GRX-431)
Thyroxine
Tiratricol (TRIAC)
Triiodothyronine
Thyroid extract
VK-0214
VK-2809
ZYT1
Antagonists: 1-850
NH3
Tetraiodothyroacetic acid (Tetrac)
Transporter
(blockers)
NIS
Inhibitors: Cyanogenic glycosides
Perchlorates (e.g., potassium perchlorate)
Pertechnetates (e.g., sodium pertechnetate)
Thiocyanates
Enzyme
(inhibitors)
TPO
Inhibitors: Benzylthiouracil
Carbimazole
Genistein
Methimazole
Methylthiouracil
Propylthiouracil
Thiouracil
Thiourea
DIO
Inhibitors: Dexpropranolol
Iopanoic acid
Ipodate sodium (sodium iopodate)
Propranolol
Propylthiouracil
Others
Iodine
Iodine-131
Selenium
Thyroglobulin
Tyrosine
See also: Receptor/signaling modulators
Nuclear receptor modulators
[show]
v
t
e
Human trace amine-associated receptor ligands
TAAR1
Agonists
Endogenous†
Classical monoamine neurotransmitters
Dopamine
Histamine
Norepinephrine
Serotonin
Trace amines
3-Iodothyronamine
3-Methoxytyramine
N-Methylphenethylamine
N-Methyltyramine
m-Octopamine
p-Octopamine
Phenethylamine
Phenylethanolamine
Synephrine
Tryptamine
m-Tyramine
p-Tyramine
Synthetic‡
Amphetamine
DOB
DOET
4-Hydroxyamphetamine
Isoprenaline
MDA (tenamfetamine)
MDMA (midomafetamine)
2-Methylphenethylamine
3-Methylphenethylamine
4-Methylphenethylamine
β-Methylphenethylamine
Methamphetamine
3-MMA
Norfenfluramine
Phentermine
o-PIT
Propylhexedrine
RO5166017
N,N-Dimethylphenethylamine
Neutral antagonists
Inverse agonists
EPPTB (RO5212773)
TAAR2
Agonists‡
3-Iodothyronamine
Phenethylamine
Tyramine
Neutral antagonists
TAAR5
Agonists‡
Dimethylethylamine
Trimethylamine
Neutral antagonists
Inverse agonists‡
3-Iodothyronamine
†References for all endogenous human TAAR1 ligands are provided at List of trace amines

‡References for synthetic TAAR1 agonists can be found at TAAR1 or in the associated compound articles. For TAAR2 and TAAR5 agonists and inverse agonists, see TAAR for references.

See also: Receptor/signaling modulators
Retrieved from "https://en.wikipedia.org/w/index.php?title=Thyroid_hormones&oldid=810193312"
Categories:
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Human feces
From Wikipedia, the free encyclopedia
Jump to: navigation, search
Human feces.
Human feces (or faeces in British English; Latin: fæx) are the solid or semisolid remains of the food that could not be digested or absorbed in the small intestine, but has been rotted down by bacteria in the large intestine.[1][2] It also contains bacteria and a relatively small amount of metabolic waste products such as bacterially altered bilirubin, and the dead epithelial cells from the lining of the gut.[1] It is discharged through the anus during a process called defecation. Urine and feces together are called excreta. They vary significantly in appearance (i.e. size, color, texture), according to the state of the diet, digestive system and general health. Normally human feces are semisolid, with a mucus coating. Small pieces of harder, less moist feces can sometimes be seen impacted in the distal (final or lower) end. This is a normal occurrence when a prior bowel movement is incomplete, and feces are returned from the rectum to the large intestine, where water is absorbed.
In the medical literature, the term "stool" is more commonly used than "feces".[3]
Human feces together with human urine are collectively referred to as human waste or human excreta. Containing human feces, and preventing spreading of pathogens from human feces via the fecal–oral route, are the main goals of sanitation.
Contents
[hide]
1 Characteristics
1.1 Classification
1.2 Color
1.2.1 Brown
1.2.2 Yellow
1.2.3 Pale or gray
1.2.4 Black or red
1.2.5 Blue
1.2.6 Silver
1.2.7 Green
1.2.8 Violet or purple
1.3 Odor
1.4 Average chemical characteristics
2 Abnormalities
2.1 Stool analysis (stool sample)
2.2 Undigested food remnants
2.3 Diarrhea
2.4 Constipation
2.5 Others
3 Fecal markers
4 Fecal contamination
5 Uses
5.1 Use as fertilizer
5.2 Fecal transplants
5.3 Biogas production
6 Paleofeces
7 Society and culture
7.1 Disgust and shame
7.1.1 Example from ancient world
7.2 Anal cleansing
7.3 Terminology and other terms used
8 See also
9 References
10 External links
Characteristics[edit]
Classification[edit]
Main article: Bristol stool scale
The Bristol stool scale is a medical aid designed to classify the form of human feces into seven categories. Sometimes referred to in the UK as the Meyers Scale, it was developed by K. W. Heaton at the University of Bristol and was first published in the Scandinavian Journal of Gastroenterology in 1997.[4] The form of the stool depends on the time it spends in the colon.[5]
The seven types of stool are:
Separate hard lumps, like nuts (hard to pass)
Sausage-shaped but lumpy
Like a sausage but with cracks on the surface
Like a sausage or snake, smooth and soft
Soft blobs with clear-cut edges
Fluffy pieces with ragged edges, a mushy stool
Watery, no solid pieces. Entirely Liquid
Types 1 and 2 indicate constipation. Types 3 and 4 are optimal, especially the latter, as these are the easiest to pass. Types 5–7 are associated with increasing tendency to diarrhea or urgency.[5]
Meconium is a newborn baby's first feces.
Color[edit]
Human fecal matter varies significantly in appearance, depending on diet and health.
Brown[edit]
Human feces ordinarily has a light to dark brown coloration, which results from a combination of bile, and bilirubin derivatives of stercobilin and urobilin,[6] from dead red blood cells. Normally it is semisolid, with a mucus coating.
Yellow[edit]
Yellowing of feces can be caused by an infection known as giardiasis, which derives its name from Giardia, an anaerobic flagellated protozoan parasite that can cause severe and communicable yellow diarrhea. Another cause of yellowing is a condition known as Gilbert's Syndrome. Yellow stool can also indicate that food is passing through the digestive tract relatively quickly. Yellow stool can be found in people with gastroesophageal reflux disease (GERD).
Pale or gray[edit]
Stool that is pale or grey may be caused by insufficient bile output due to conditions such as cholecystitis, gallstones, giardia parasitic infection, hepatitis, chronic pancreatitis, or cirrhosis. Bile salts from the liver give stool its brownish color. If there is decreased bile output, stool is much lighter in color.
Black or red[edit]
Feces can be black due to the presence of red blood cells that have been in the intestines long enough to be broken down by digestive enzymes. This is known as melena, and is typically due to bleeding in the upper digestive tract, such as from a bleeding peptic ulcer. Conditions that can also cause blood in the stool include hemorrhoids, anal fissures, diverticulitis, colon cancer, and ulcerative colitis. The same color change can be observed after consuming foods that contain a substantial proportion of animal blood, such as black pudding or tiết canh. Black feces can also be caused by a number of medications, such as bismuth subsalicylate (the active ingredient in Pepto-Bismol), and dietary iron supplements, or foods such as beetroot, black liquorice, or blueberries.[7]
Hematochezia is similarly the passage of feces that are bright red due to the presence of undigested blood, either from lower in the digestive tract, or from a more active source in the upper digestive tract. Alcoholism can also provoke abnormalities in the path of blood throughout the body, including the passing of red-black stool. Hemorrhoids can also cause surface staining of red on stools, because as they leave the body the process can compress and burst hemorrhoids near the anus.
Blue[edit]
Prussian blue, or blue, a coloring used in the treatment of radiation, cesium, and thallium poisoning, can turn the feces blue. Substantial consumption of products containing blue food dye, such as blue curaçao or grape soda, can have the same effect.[8]
Silver[edit]
A tarnished-silver or aluminum paint-like feces color characteristically results when biliary obstruction of any type (white stool) combines with gastrointestinal bleeding from any source (black stool). It can also suggest a carcinoma of the ampulla of Vater, which will result in gastrointestinal bleeding and biliary obstruction, resulting in silver stool.[9]
Green[edit]
Feces can be green due to having large amounts of unprocessed bile in the digestive tract and strong-smelling diarrhea. This can occasionally be the result from eating liquorice candy, as it is typically made with anise oil rather than liquorice herb and is predominantly sugar. Excessive sugar consumption or a sensitivity to anise oil may cause loose, green stools.[10] It can also result from consuming excessive amounts of green dye, such as were found in Burger King's Halloween Whopper.[11]
Violet or purple[edit]
Violet or purple feces is a symptom of porphyria.
Odor[edit]
Feces possess physiological odor, which can vary according to diet and health status. For example, meat protein contains a lot of the sulfur-containing amino acid methionine, which is a precursor of the sulfur-containing odorous compounds listed below.[12][13][14][15][16] The odor of human feces is suggested to be made up from the following odorant volatiles:[13]
Methyl sulfides
methylmercaptan/methanethiol (MM)
dimethyl sulfide (DMS)
dimethyl trisulfide (DMTS)
dimethyl disulfide (DMDS)
Benzopyrrole volatiles
indole
skatole
Hydrogen sulfide (H2S)
(H2S) is the most common volatile sulfur compound in feces.[13] The odor of feces may be increased when various pathologies are present, including:[17]
Celiac disease
Crohn's disease
Ulcerative colitis[18]
Chronic pancreatitis
Cystic fibrosis
Intestinal infection, e.g. Clostridium difficile infection.[19]
Malabsorption
Short bowel syndrome
Attempts to reduce the odor of feces (and flatus) are largely based on animal research carried out with industrial applications, such as reduced environmental impact of pig farming. See also: Flatulence#Management, odor. Many dietary modifications/supplements have been researched, including:
Activated charcoal[20] (In this study it was found that activated charcoal at a dose of 0.52g four times a day did not appreciably influence the liberation of fecal gases.)
Bismuth subsalicylate[21]
Chloryphyllyn
Herbs such as rosemary
Yucca schidigera[22]
Zinc acetate[22]
Average chemical characteristics[edit]
On average humans eliminate 128 g of fresh feces per person per day with a pH value of around 6.6. Fresh feces contains around 75% water and the remaining solid fraction is 84–93% organic solids.
These organic solids consist of: 25–54% bacterial biomass, 2–25% protein or nitrogenous matter, 25% carbohydrate or undigested plant matter and 2–15% fat. Protein and fat come from the colon due to secretion, epithelial shedding and gut bacterial action. These proportions vary considerably depending on many factors such as mainly diet and body weight.[23]
The remaining solids are composed of calcium and iron phosphates, intestinal secretions, small amounts of dried epithelial cells, and mucus.[23]
Abnormalities[edit]
Stool analysis (stool sample)[edit]
Clinical laboratory examination of feces, usually termed as stool examination or stool test, is conducted for the sake of diagnosis, for example, to detect the presence of parasites such as pinworms and their eggs (ova) or, to detect disease spreading bacteria. A stool culture—the controlled growth of microbial organisms in culture media under laboratory conditions—sometimes is performed to identify specific pathogens in stool. The stool guaiac test (or guaiac fecal occult blood test) is conducted to detect the presence of blood in stool that is not apparent to the unaided eye.
The main pathogens that are commonly looked for in feces include:
Bacteroides species
Salmonella and Shigella
Yersinia tends to be incubated at 30 °C (86 °F), which is cooler than usual
Campylobacter incubated at 42 °C (108 °F), in a special environment
Aeromonas
Candida if the person is immunosuppressed (e.g., undergoing cancer treatment)
E. coli O157 if blood is visible in the stool sample
Cryptosporidium
Entamoeba histolytica
Intestinal parasites and their ova (eggs) can sometimes be visible to the naked eye.
Undigested food remnants[edit]
Sometimes food may make an appearance in the feces. Common undigested foods found in human feces are seeds, nuts, corn, and beans, mainly because of their high dietary fiber content. Beets may turn feces different hues of red. Artificial food coloring in some processed foods, such as highly colorful packaged breakfast cereals, can cause unusual coloring of feces if eaten in sufficient quantities.
Undigested objects such as seeds can pass through the human digestive system, and later germinate. One result of this is tomato plants growing where sewage sludge has been used as fertilizer.
Diarrhea[edit]
Main article: Diarrhea
Diarrhea (or diarrhoea in British English) is the condition of having three or more loose or liquid bowel movements per day.[24] This condition can be a symptom of injury, disease or foodborne illness and is usually accompanied by abdominal pain. There are other conditions which involve some but not all of the symptoms of diarrhea, and so the formal medical definition of diarrhea involves defecation of more than 200 grams per day (though formal weighing of stools to determine a diagnosis is never actually carried out).
It occurs when insufficient fluid is absorbed by the colon. As part of the digestion process, or due to fluid intake, food is mixed with large amounts of water. Thus, digested food is essentially liquid prior to reaching the colon. The colon absorbs water, leaving the remaining material as a semisolid stool. If the colon is damaged or inflamed, however, absorption is inhibited, and watery stools result.
Diarrhea is most commonly caused by a myriad of viral infections but is also often the result of bacterial toxins and sometimes even infection. In sanitary living conditions and with ample food and water available, an otherwise healthy patient typically recovers from the common viral infections in a few days and at most a week. However, for ill or malnourished individuals diarrhea can lead to severe dehydration and can become life-threatening without treatment.
Constipation[edit]
Main article: Constipation
Constipation refers to bowel movements that are infrequent or hard to pass.[25] Constipation is a common cause of painful defecation. Severe constipation includes obstipation (failure to pass stools or gas) and fecal impaction, which can progress to bowel obstruction and become life-threatening.
Others[edit]
Bile overload is very rare, and not a health threat. Problems as simple as serious diarrhea may cause blood in one's stool. Black stools caused by the presence of blood usually indicate a problem in the intestines (the black color is a sign of digested blood), whereas red streaks of blood in stool usually are caused by bleeding in the rectum or anus.
Fecal markers[edit]
The feces can be analyzed for various markers that are indicative of various diseases and conditions. For example, fecal calprotectin levels indicate an inflammatory process such as Crohn's disease, ulcerative colitis and neoplasms (cancer).
Reference ranges for fecal markers
Marker Patient type Upper limit Unit
Calprotectin 2–9 years 166[26] µg/g of feces
10–59 years 51[26]
≥ 60 years 112[26]
Lactoferrin 2–9 years 29[26]
≥ 10 years 4.6[26]
Also, feces may be analyzed for any fecal occult blood, which is indicative of a gastrointestinal bleeding.
Fecal contamination[edit]
A quick test for fecal contamination of water sources or soil is a check for the presence of E. coli bacteria performed with the help of MacConkey agar plates or Petri dishes. E. coli bacteria uniquely develop red colonies at temperature of approximately 43 °C (109 °F) overnight. Although most strains of E. coli are harmless, their presence is indicative of fecal contamination, and hence an increased possibility of the presence of more dangerous organisms.
Fecal contamination of water sources is highly prevalent worldwide, accounting for the majority of unsafe drinking water. In developing countries most sewage is discharged without treatment. Even in developed countries events of sanitary sewer overflow are not uncommon and regularly pollute the Seine River (France) and the River Thames (England), for example.
Uses[edit]
See also: Reuse of excreta
Use as fertilizer[edit]
Fresh feces collected from a child for a drying experiment
Human feces have historically been used as fertilizer for centuries in the form of night soil, fecal sludge, and sewage sludge. The use of untreated human feces in agriculture poses significant health risks and has contributed to widespread infection with parasitic worms—a disease called helminthiasis, affecting over 1.5 billion people in developing countries.
Feces after drying in an experiment to determine moisture content
There are methods available to safely reuse human feces in agriculture as per the "multiple barrier concept" described by the World Health Organization in 2006.[27] The approach to "close the loop" between human excreta (sanitation) and agriculture is also called ecological sanitation. It may involve certain types of dry toilets such as urine-diversion dry toilets or composting toilets.
Fecal transplants[edit]
In humans, fecal transplants (or stool transplant) is the process of transplantation of fecal bacteria from a healthy individual into a recipient who is suffering from a certain disease, such as irritable bowel syndrome. The resulting inoculation of healthy gut flora can sometimes improve the physiology of the recipient gut.
Fecal bacteriotherapy—also known as a fecal transplant—is a medical procedure wherein fecal bacteria are transplanted from a healthy individual into a patient.[28][29] Recent research indicates that this may be a valuable method to re-establish normal gut cultures that have been destroyed through the use of antibiotics or some other medical treatments.
Biogas production[edit]
The biogas produced from feces when it is contained in sewage and treated in an anaerobic digestion process could be worth as much as 9.5 billion dollars.[30]
Washington DC plans to produce biogas from sewage sludge, the by-product of sewage treatment, which will save 13 million dollars a year.[31]
Paleofeces[edit]
Main article: Paleofeces
Paleofeces, also known as coprolites, are ancient human feces, often found as part of archaeological excavations or surveys. Intact feces of ancient people may be found in caves in arid climates and in other locations with suitable preservation conditions. These are studied to determine the diet and health of the people who produced them through the analysis of seeds, small bones, and parasite eggs found inside. They also may be analyzed chemically for more in-depth information on the individual who excreted them, using lipid analysis and DNA analysis. The success rate of usable DNA extraction is relatively high in paleofeces, making it more reliable than skeletal DNA retrieval.[32]
Society and culture[edit]
Disgust and shame[edit]
In all human cultures, feces elicit varying degrees of disgust. Disgust is experienced primarily in relation to the sense of taste (either perceived or imagined) and, secondarily to anything that causes a similar feeling by sense of smell, touch, or vision. As such, human feces is regarded as something to be avoided diligently: expelled in private and disposed of immediately and without a trace. It often is considered an unacceptable topic in polite conversation and its mere mention may cause offence in certain contexts.
The disposal of feces always has been associated with the lowest people among a society, the social outcasts, the pariahs, and the social discards. The caste system in India was created along the lines of profession and the dalits (untouchables) were left to do work related to human emissions. They did such work as cleaning and picking feces from streets, cleaning toilets, and working with dead bodies. Such practices are prevalent even today in the rural and small villages of India; where it is called "manual scavenging".
Example from ancient world[edit]
An example of repulsion by feces from the ancient world is found in the writings called Deuteronomy used by Jews and Christians:
Designate a place outside the camp where you can go to relieve yourself. As part of your equipment have something to dig with, and when you relieve yourself, dig a hole and cover up your excrement. For the LORD your God moves about in your camp to protect you and to deliver your enemies to you. Your camp must be holy, so that he will not see among you anything indecent and turn away from you.[33]
Anal cleansing[edit]
Main article: Anal cleansing
People from different cultures employ a variety of personal cleansing practices after defecation. The anus and buttocks may be either washed with liquids or wiped with toilet paper or other solid materials. In many Muslim, Hindu and Sikh cultures, as well as Southeast Asia and Southern Europe, water is usually used for anal cleansing using a jet, as with a bidet, or most commonly, splashed and washed with the hand. In other cultures (such as many Western countries), cleaning after defecation is generally done with toilet paper only.
Terminology and other terms used[edit]
Further information: Feces § Terminology
There are many synonyms in informal registers for human feces. Many are euphemismistic, colloquial, or both; some are profane (such as shit), whereas most belong chiefly to child-directed speech (such as poo or poop) or to crude humor (such as turd).
See also[edit]
Artist's Shit
Defecation
Fecal-oral route
Muslim hygienical jurisprudence
Scatology
References[edit]
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