The inner lining of the gastrointestinal tract (the mucosa) is covered by a layer of cells, the epithelium that performs the separate processes of secretion and absorption. The movement of gut contents from one region to the next is achieved by two layers of smooth muscle (circular and longitudinal) that lie outside the mucosa and that contract and relax in co-ordinated patterns. Between the mucosa and muscle layers lies the submucosa, which is rich in blood vessels and connective tissue. Different regions of the digestive tract are concerned with storage, secretion, the processes of food digestion, absorption, and the elimination of waste products. All regions of the gut have a capacity for the renewal of mucosal cells, and for protection against toxic or damaging agents. The various functions of the gut are co-ordinated by neurons, hormones, and local (paracrine) regulatory molecules.
The conversion of food into a form suitable for digestion is helped by cooking, which may also destroy toxins and microorganisms. The initial steps of digestion occur in the mouth where the enzyme amylase, which is present in saliva, breaks down starch. Mixing of saliva and food is aided by mastication or chewing, which also prepares an appropriately-sized ‘bolus’ of food for swallowing. The secretion of saliva is prompted by the presence of food in the mouth. Slightly acidic solutions are strong salivary stimulants, which might explain why a twist of lemon is perceived as a valuable addition to aperitifs.
The process of swallowing involves raising the larynx to close off the respiratory tract. The progression of a bolus of food down the oesophagus is aided by a muscular reflex, peristalsis, consisting of a wave of relaxation to accommodate the bolus followed by a wave of contraction pushing it ahead. Peristaltic movements are co-ordinated by neurons within the oesophagus and connecting it to the brain. The lower part of the oesophagus is separated from the stomach by a sphincter, the lower oesophageal sphincter, which relaxes to allow food to pass through. This sphincter normally prevents acid from the stomach entering the oesophagus. Failure of this mechanism is one cause of the sensation known as heartburn, and if persistent leads to chronic inflammation: oesophagitis.
StomachThe adjective ‘gastric’ applies to all things pertaining to the stomach. The stomach stores food prior to delivery to the small intestine, initiates the digestion of protein, and secretes hydrochloric acid, which destroys many microorganisms. Hydrochloric acid in gastric juice was identified by the physician-chemist William Prout in the 1820s. Important early observations on human gastric digestion were made at about the same time by William Beaumont on his patient, the Canadian trapper Alexis St Martin, who had survived a gun-shot wound leaving him with a permanent hole, or fistula, connecting the stomach with the exterior of the upper left side of the abdomen. Beaumont recorded over 100 separate experiments in which he directly observed gastric function in this subject concluding, in one experiment, ‘… I am confident, generally speaking, that venison is the most digestible of any diet …’
Proteins in the stomach are broken down to polypeptides by the enzyme pepsin, which works best in acidic environments and is produced by ‘chief’, or ‘zymogen’, cells in the gastric mucosa. Separate specialized cells, the parietal cells, secrete hydrochloric acid. The concentration of hydrogen ions in gastric juice is about a million times higher than in blood. The gastric epithelium therefore maintains one of the steepest concentration gradients of an electrolyte in the body. The secretion of acid against this gradient requires energy. It is achieved by a protein known as the proton pump (or, more precisely, the H+/K+ATPase) that exchanges intracellular hydrogen ions for extracellular potassium using energy provided by the breakdown of ATP (adenosine 5′-triphosphate).
The Russian physiologist I. P. Pavlov identified three phases in the control of acid secretion during digestion — the cephalic, gastric, and intestinal phases. The thought, smell, or taste of food stimulate acid secretion in the cephalic phase. In humans up to 50% of maximum acid secretion by the stomach can be evoked by this kind of stimulation. The gastric phase is initiated by the presence of food in the stomach, and the intestinal phase by food in the intestine. At the cellular level, acid secretion is controlled by acetylcholine released from mucosal nerve endings, by the gastric hormone gastrin, and by the local regulator histamine released from cells adjacent to parietal cells. Parietal cells, which also secrete a protein (intrinsic factor) essential for the absorption of vitamin B12, are lost by an autoimmune process in the condition of pernicious anaemia — which is characterized by a failure to produce acid and intrinsic factor, leading to vitamin B12 deficiency.
The stomach converts food to a sludge-like consistency (chyme) suitable for further digestion in the small intestine. The rate of emptying of chyme from the stomach varies with the composition of the meal. Fat-rich meals empty more slowly than carbohydrate-rich meals. Indigestible solids empty more slowly than liquids or semi-solid meals. The rate of emptying is determined by pressure differences between the stomach and duodenum, by the resistance to flow across the muscular band (the pyloric sphincter) separating the two organs, and by a pumping action of the last part of the stomach. Gastric emptying is regulated by signals arising from the duodenum, which therefore itself determines the rate at which it receives chyme.
The intestinesThe small intestine is the primary site of digestion and absorption. It is a tube approximately 20 feet long consisting of three regions; the duodenum, jejunum, and ileum. Gastric acid entering the duodenum is neutralized by bicarbonate secreted by the pancreas, which also secretes a wide variety of digestive enzymes. The major classes of pancreatic enzymes are proteases, which convert protein to polypeptides, peptides, and then amino acids; amylase, which completes the breakdown of starch; and lipase, which converts fats (triglyceride) to glycerol and fatty acids. The digestion of fat also requires bile salts, delivered to the duodenum in bile from the liver, via the gall bladder. The final stages of digestion are completed both within epithelial cells of the small intestine and by enzymes on their surface; for example peptides may be converted to amino acids within these cells, and sucrose is converted to glucose and fructose by a membrane-bound enzyme, sucrase–isomaltase.
The lining of the small intestine is folded into finger-like projections, the villi (each 0.5– 0.8 mm long), and deeper glands, the crypts. The immensely increased surface area provided by the villi aids absorption. Substances move between the gut lumen and the blood both by passing through epithelial cells (the transcellular route) and by passing between them (the paracellular route). Water also moves by these routes along osmotic gradients. Absorption of the products of digestion is mediated by a series of specific ‘transport proteins’. Amino acids and peptides, sugars, and inorganic ions are often moved from the lumen into intestinal cells against a concentration gradient. The energy required for this transport is provided by gradients of sodium or hydrogen ions. The sodium gradient in particular is generated by sodium pumps located on the surface membrane of epithelial cells facing the bloodstream, which lower intracellular sodium. The conditions are thereby created for sodium in the intestinal lumen to move down its concentration gradient into the cells carrying nutrients with it.
Nutrient digestion and absorption is largely completed in the jejunum. In the ileum, there is further absorption of water, electrolytes, remaining nutrients, and also bile salts which are returned to the liver for re-use. The residue then passes to the large intestine, or colon, for the final steps of water and electrolyte absorption, and for storage of the waste products prior to their discharge when socially appropriate (defecation).
Approximately 9 litres of fluid enter the human small intestine each day, some from ingested food and liquids, and more from the secretions of the salivary glands, stomach, pancreas, liver, and the small intestine itself. The jejunum and ileum each account for the reabsorption of about 45% of fluid and sodium chloride. The remainder is delivered to the colon, where all but about 100 ml is reabsorbed. The colon has the capacity to absorb up to 1.5 litres of fluid per day. When greater volumes arrive from the small intestine the excess is lost in faeces as diarrhoea. Although the small intestine is a net absorptive organ, the crypt cells secrete water and sodium chloride. This secretion may be stimulated by toxins generated by microorganisms; one example is cholera toxin, which is responsible for the secretory diarrhoea of cholera. Watery diarrhoea therefore happens when intestinal secretions overwhelm the capacity of the small and large intestines to absorb water and electrolytes. Absorption may be aided by oral administration of solutions consisting of sodium chloride and glucose which engage multiple transport processes. This treatment, oral rehydration therapy, has proved valuable in treating patients with infectious diarrhoea, particularly in Third World countries where access to medical services is limited.
Within the gut there is a rich diversity of microorganisms, many of which are beneficial although some are potentially pathogenic. The colon typically contains very large numbers of microorganisms: approximately 1013 individual organisms, and up to 200 different types. The small intestine and stomach are usually relatively free of microorganisms. An important exception is Helicobacter pylori which is found in the stomach in approximately 50% of people.
Many microorganisms within the gastrointestinal tract are able to convert the otherwise indigestible components of food, particularly plant cell walls, into forms suitable for absorption. In ruminant species (cow, sheep) a modified part of the stomach functions as a fermentation chamber where microorganisms digest the non-starch polysaccharides which make up plant fibre into short chain fatty acids which are readily absorbed. In other species (e.g. horse, elephant), an expanded region of the first part of the large intestine, the caecum, serves a similar function.
Protection and renewalMany substances present in the gut lumen are potentially damaging, such as gastric acid, ingested noxious molecules, and microorganisms. To counteract these forces, the gut has an elaborate range of protective mechanisms. Gastric acid is resisted by special properties of the surface membrane of mucosal cells, tight connections between cells, good blood flow, and the local production of bicarbonate and mucus gel that lies on the epithelial surface. Breakdown of these mechanisms may lead to the formation of a peptic ulcer. The protective barrier is reduced by aspirin and other non-steroidal anti-inflammatory drugs; this is an important side-effect which limits the use of these compounds. Drugs that inhibit acid secretion are widely used. Some (the proton pump inhibitors, e.g. omeprazole) block the pump that transports acid into the stomach, others block the site at which histamine acts on parietal cells (the H2 receptor antagonists: cimetidine, ranitidine). The presence of Helicobacter pylori in the stomach is associated with peptic ulcer disease, and also with cancer of the stomach. Its recognition and its elimination by antibiotic therapy has provided a major advance in the management of peptic ulcer in the 1990s.
The gastrointestinal tract is well endowed with cells of the immune system, which are important in protection against pathogenic microorganisms and antigens. Malfunction of this system is a factor in inflammatory bowel diseases (Crohn's disease and ulcerative colitis). In addition some components of food may trigger an immune response, for example in coeliac disease there is an intolerance to the protein component of wheat, gliadin.
Epithelial cells of the alimentary tract are subject to continuous wear and tear and so must be regularly replaced. In the small intestine, epithelial cells are generated in the crypts, then migrate up the villi and are lost at the tip. This process takes about three days. During migration cells differentiate into particular types. Cell renewal in the mucosa occurs similarly throughout the gut. Damage to the DNA within dividing cells may disrupt mechanisms that regulate this process, leading to accumulation of mutated forms of genes and development of tumours, particularly in the colon and stomach, which are common sites for cancer.
Nerves and hormonesThe gut possesses its own nervous system which can function independently of the central nervous system. The gut and brain do engage each other in two-way communication, but, with exceptions such as swallowing and defecation, the functions of the alimentary system are not under voluntary control. Moreover, the normal processes of digestion do not involve consciousness, even though expressions of the sensations attributed to digestion are commonplace (gut feelings, etc.).
The main nerve trunks linking the gastrointestinal tract and the central nervous system are known as the vagus and splanchnic nerves. In both cases, separate nerve fibres communicate from the gut to the central nervous system, and in the opposite direction. Splanchnic nerve fibres communicating to the central nervous system respond to noxious stimuli, leading to perceptions of pain or discomfort. The sensitivity of these nerves can be modified, for example by inflammation, so that otherwise innocuous stimuli may be perceived as painful. Nerve fibres running from the central nervous system to the gut are part of the autonomic nervous system. In general, alimentary processes are activated by the ‘parasympathetic’ component of this system via the vagus nerves, and are quietened by the ‘sympathetic’ component via the splanchic nerve. Both vagus and splanchnic nerves influence digestion via neurons located within the gut wall. However, because gut neurons can also function independently of the remainder of the autonomic nervous system, they are often considered to represent a third division of this system, the ‘enteric’ component.
The control of digestion depends on interactions between enteric neurons and a system of hormones produced by, and acting on, the gut. The pancreas-stimulating hormone, secretin, was the first hormone to be discovered (by W. M. Bayliss and E. H. Starling in London in 1902). At the turn of the twentieth century, ideas of how digestion might be controlled were dominated by Pavlov who emphasized the role of the nerves supplying the gut. However, Bayliss and Starling observed that acid in the small intestine of an anaesthetized dog stimulated a flow of pancreatic juice even after all nerves to the intestine had been cut. They reasoned that a messenger molecule might be secreted by the intestine into the bloodstream and conveyed by this route to the pancreas. They then found that such a substance could be recovered by extraction from the intestinal mucosa. They called the active factor secretin, and they showed that it stimulated a flow of pancreatic juice when injected into the bloodstream. The word hormone (from the Greek: to rouse or set in motion) was later introduced by Starling in recognition of this novel mechanism of action.
The gut hormones are produced by specialized epithelial cells, the gut endocrine cells, each with a characteristic distribution. Endocrine cells in the stomach, including the gastrin or ‘G’ cells, are mainly responsible for regulating acid secretion. Endocrine cells in the duodenum and jejunum produce secretin, which stimulates water and bicarbonate secretion by the pancreas, and cholecystokinin, which stimulates pancreatic enzyme secretion and gall bladder contraction, and which inhibits gastric emptying and food intake. Hormones produced in the ileum and colon (peptide YY, neurotensin, glucagon-like peptides-I and -II) mediate a phenomenon sometimes called the ‘ileal brake’, by which functions occurring in upper regions of the gut are inhibited, including food intake.
Digestion and fastingThe time taken to digest a meal depends on its composition. Fat-rich meals take longer to digest than those rich in protein or carbohydrate. There is considerable variation between individuals, but representative times to complete the progression from mouth to anus are about 55 hours in UK men, and 72 hours in women. Gastric digestion is completed in 2–3 hours, and small intestinal digestion in about 6 hours, so that the time spent in the colon is around 50–60 hours.
During fasting, or between meals, the gastrointestinal tract is not completely quiescent. Cell debris and microorganisms continue to accumulate during fasting, necessitating a mechanism to maintain the health of the gut. Approximately 12 hours after the last meal, strong waves of contraction start in the stomach and then progress the full length of the gut carrying accumulated debris forwards. These contractions are sometimes called house-keeping movements, or more accurately the ‘migrating myoelectric complex’. They start every 90 minutes, and take approximately 90 min to move the full length of the gut; as one finishes in the colon the next starts in the stomach. They cease on feeding.
The British Digestive Foundation (PO Box 251, Edgware, Middlesex, HA8 6HG) can provide information on a range of diseases of the alimentary tract.
Johnson, L. R. (1997). Gastrointestinal physiology, (5th edn), Mosby Year Book Inc., St Louis, Missouri.
See also appendix; bile; constipation; defecation; diarrhoea; faeces; gall bladder; gastrin; hernia; indigestion; liver; pancreas; saliva; vomiting.
"alimentary system." The Oxford Companion to the Body. . Encyclopedia.com. (February 18, 2018). http://www.encyclopedia.com/medicine/encyclopedias-almanacs-transcripts-and-maps/alimentary-system
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(b. Horton, Gloucester shire, England, 15 January 1785; d. London, England, 9 April 1850)
Prout was the eldest of three sons of John Prout, a tenant farmer whose fortunes had increased through the inheritance of land, and his wife Hannah Lim brick[?]. Educated at local charity schools until the age of thirteen, Prout worked on his father’s farm until about 1802, when he attended the private classical academies of Rev. John Turner at Sheraton, Wiltshire, and Rev. Thomas Jones at Bristol. In 1808, on Jones’s recommendation, he entered Edinburgh University to study medicine; he graduated in 1811 with an unoriginal dissertation on fevers. He completed his medical training at St. Thomas’s and Guy’s hospitals in London, where he set up practice after gaining the licentiate of the Royal College of Physicians on 22 December 1812. During 1814 Prout gave a successful course of public lectures on animal chemistry in his London home and met Alexander Marcet, who praised him in letters to Berzelius. There is some evidence that from 1816 until 1817 he edited Annals of Medicine and Surgery with his friend John Elliotson.
When his father died in 1820, Prout passed the Horton estate, which he inherited, to his surviving brother. Little is known of Prou’s personal life in London. He became a very successful, but not wealthy, physician who specialized in digestive and urinary complaints. His reputation in medicine and chemistry in Great Britain and on the Continent was considerable, both as an experimentalist and as a theorist. Unfortunately, deafness made him avoid scientific contacts after 1830. He subsequently made little effort to keep abreast of the rapid developments that took place in biochemistry and chemistry between 1830 and 1850; and although much of his biochemical research had foreshadowed that of Liebig and his school, Prout found himself eclipsed by their achievements during this period.
An extremely religious man, Prout was invited to write one of the eight Bridgewater treatises, which had the general title On the Power, Wisdom and Goodness of God, as Manifested in the Creation. An accomplished organist who composed music for his family, he also possessed artistic talents. He married Agnes Adam (1793–1863), the daughter of Alexander Adam, the Edinburgh educator; they had seven children, one of whom became a military surgeon.
Prout received the M.D. from Edinburgh (1811), and was a fellow of the Royal Society (1819) and of the Royal College of Physicians (1829). He was a Copley medalist of the Royal Society (1827) and a Gulstonian lecturer at the Royal College of Physicians (1831). He served on the Council of the Royal Society, and on several of its committees and on those of the British Association for the Advancement of Science. For a time he was an active member of the Medico-Chirurgical Society of London.
Prout’s contribution to the concept of the unity of matter, which he adopted as a student, played a dominant role in the development of the theory of the elements and the fortunes of the atomic theory. Prout was much influenced by Humphry Davy’s speculations on “undecompounded bodies” (1812) and by Dalton’s atomic theory as modified by Berzelius. He hoped to develop a “mathematical” chemistry analogous, perhaps, to the scheme expressed tentatively by Thomas Thomson in his First Principles (1825). The inspiration to improve Gay-Lussac’s and Berzelius’ methods of organic analysis came largely from his attempt to find the mathematical laws that govern the formation of organic compounds from the elements carbon, hydrogen, oxygen, and nitrogen. In 1817, 1820, and 1827 Prout published accounts of elaborate and expensive analytical methods. His organic analyses were renowned for their accuracy, and he remained skeptical of Liebig’s simple and successful technique (1830).
Between 1815 and 1827 Prout published a series of important papers on urine and digestion that opened up the areas of purine and metabolic chemistry. He found a boa constrictor’s excrement to be 90 percent uric acid; he also extracted extremely pure urea from urine and attempted to synthesize it in 1818, ten years before Wöhler’s accidental success. In 1821 Prout published a concise textbook on urine; but a similar work on digestion, partly printed in 1822, was withdrawn from publication. In 1840, however, Prout published a long and successful practical textbook of urinary and digestive pathology.
The brilliant demonstration in 1824 that the gastric juices of animals contain hydrochloric acid appeared incredible to many of Prout’s contemporaries. Yet in 1827 they readily adopted his classification of foodstuffs into water, saccharinous (carbohydrates), oleaginous (fats), and albuminous (proteins). Although Prout promised detailed analyses of the three organic aliments, only those of the saccharinous class were published by him. As a vitalist, Prout maintained that organized bodies (which were composed from organic substances) contained “independent existing vital principles.” Under the influence of these teleo-logic agents, the four aliments were transformed into blood and tissues. Prout termed the processes of digestion and blood formation “primary assimilation.” “Secondary assimilation” (Liebig’s “metamorphosis of tissues”) included both the process of tissue formation from blood and the destruction and removal of unwanted parts from the animal system. The absorption and removal of water from processed aliments were the principal chemical features of chylification and sanguification, respectively. Organization of processed aliments could not occur, however, without the presence and admixture of minute amounts of water or of elements other than carbon, hydrogen, oxygen, and nitrogen. In 1827 Prout coined the word “merorganized” to denote the isomerism and vitalization of organic substances by the presence of these incidental materials. For some years this concept was a serious alternative to the structural interpretation of isomerism.
Much of this metabolic theory was speculative, as was the corpuscular theory upon which it was based. In unpublished lectures (1814) Prout supposed that hydrogen might be converted by electricity into other elements and the imponderable fluids: caloric, light, and magnetism. In 1815 he published an unsigned article in which he reconciled information on the combining weights of substances with their combining volumes when in real or imaginary gaseous states. After several dubious assumptions and adjustments, Prout calculated that the atomic weights of all elements were integral when the atomic weight of hydrogen was taken as unity. In a correction (1816) he added that hydrogen might be the primary matter from which all other “elements” were formed.
Prout quickly identified himself as the author of these papers; and the two hypotheses, of integral atomic weights and of the unity of matter, became known ambiguously and singularly as Prout’s hypothesis. It was a continuous source of inspiration to chemists and physicists until the work of F. W. Aston on isotopes in the 1920’s T. Thomson, J.-B, Dumas, J. C. Marignac, and L. Meyer supported Prout, and Berzelius, E. Turner, J. S. Stas, Mendeleev, and T. W. Richards opposed him. But whatever the attitude of individual scientists toward the hypotheses or their modifications, they stimulated the improvement of analysis and enforced interest in atomic weights and, therefore, in the atomic theory. They also gave impetus to the search for a system of classification of the elements, and, when the periodic law was achieved, they encouraged speculations about the evolution of the elements and structural theories of the atom. Few hypotheses have been so persistently fruitful.
Prout left it to others, notably T. Thomson, to work out the consequences of his suggestions; but in 1831 he added that there was no reason why the material unit of condensation might not be smaller than hydrogen (perhaps half or one-quarter of hydrogen). This offered a convenient explanation of such anomalous, nonintegral atomic weights as chlorine and copper, and it was used by Marignac and Dumas.
In his Bridgewater treatise (1834; 3rd ed., 1845) Prout revealed that his hypotheses were only part of an elaborate corpuscular philosophy in which spherical particles were imagined to revolve spontaneously, with mutually repulsive forces and velocities that were inversely proportional to their masses. In addition, there were attractive forces that were directly proportional to the masses of the rotating particles. Like Aepinus and Mossotti, Prout supposed that the force of gravitation was the difference between the attractive and repulsive forces. The model remained a speculation, because there was no way of determining angular velocities independently of atomic weights.
This polarity theory also involved Prout in conclusions similar to those drawn by Avogadro in 1811: that at the same temperature and pressure, equal volumes of all gases contain equal numbers of molecules, and that all molecules of elementary gases contain at least two submolecules, or atoms. Like Avogadro, Prout deduced from this that the ratio of the weights of two equal volumes of different gases, at the same temperature and pressure, was equal to the ratio of their molecular weights. Prout was attacked for these views by the chemist William Charles Henry; but Prout’s support for Avogadro was without much influence, largely because he compromised with equivalent weights and because he was opposed to the use of chemical formulas.
Prout’s other significant contributions included unpublished thoughts on the unity of sensations (1810), on the distinction between taste and flavor (1812), on elaborate self-experiments regarding carbon dioxide output (1813, 1814), on a study of the chemical changes in an incubating egg (1822), on the neologism “convection” (1834), and on the design of the Royal Society’s standard barometer (1831–1836).
I. Original Works. A list of 34 papers by Prout is recorded in the Royal Society Catalogue of Scientific Papers, V, 34–35. To them should be added W[illiam] P[rout], “The Sensations of Taste and Smell.” in London Medical and Physical Journal, 28 (1812), 457–461; and the unsigned “On the Relation Between Specific Gravities of Bodies in the Gaseous State and the Weights of Their Atoms,” in Annals of Philosophy, 6 (1815), 321–330, and 7 (1816), 111–113. The latter is repr. with an unsigned intro. in L. Dobbin and J. Kendall, Prout’s Hypothesis, Alembic Club Reprint no. 20 (Edinburgh, 1932), and in facs. in D. M. Knight, Classical Scientific Papers. Second Series (London, 1970). Note also Prout’s Gulstonian lectures, “On the Application of Chemistry to Physiology, Pathology and Practice,” in Medical Gazette, 8 (1831), 257–265, 321–327, 385–391; and his letter to Daubeny (1831), in C. Daubeny, An Introduction to the Atomic Theory (Oxford, 1831), 129–133; 2nd ed. (Oxford, 1850), 470–474.
Prout’s books were De febribus intermittentibus (Edinburgh, 1811), his M.D. thesis; An Inquiry Into the Nature and Treatment of Gravel, Calculus, and Other Diseases (London, 1821), 2nd ed. retitled Inquiry … Treatment of Diabetes, Calculus and Other Affections (London, 1825), 3rd ed. retitled On the Nature and Treatment of Stomach and Urinary Diseases (London, 1840), 4th ed. retitled On the Nature … Stomach and Renal Diseases (London, 1843; 5th ed., London, 1848). See also Chemistry, Meteorology and the Function of Digestion, eighth Bridgewater Treatise (London, 1834; 2nd ed., 1834; 3rded., 1845; 4th ed., 1855).
There are letters and papers of Prout’s at the Royal Society, the Royal College of Physicians, and the Wellcome Institute for the History of Medicine, London.
II. Secondary Literature. There were three principal obituaries: an unsigned one in Medical Times, 1 (1850), 15–17; an unsigned one in Edinburgh Medical and Surgical Journal.76 (1851), 126–183; and C. Daubeny, “On the Great Principles Either Suggested or Worked out by Dr. William Prout,” in Edinburgh New Philosophical Journal, 53 (1852), 98–102, repr. in Daubeny’s Miscellanies, II (London, 1867), 123–127. The only comprehensive study is W. H. Brock, ’The Chemical Career of William Prout,” Ph.D. thesis (Leicester, 1966).
Important articles on Prout are O. T. Benfey, “Prout’s Hypothesis,” in Journal of Chemical Education, 29 (1952), 78–81; W. H. Brock, “The Life and Work of William Prout,“in Medical History, 9 (1965), 101–126; “The Selection of the Authors of the Bridgewater Treatises,” in Notes and Records. Royal Society of London, 21 (1966), 162–179; “Dalton Versus Prout: The Problem of Prout’s Hypotheses,” in D. S. L. Cardwell, ed., John Dalton and the Progress of Science (Manchester, 1968), 240–258; “Studies in the History of Proufs Hypotheses,” in Annals of Science, 25 (1969), 49–80, 127–137, which reprints Prout’s essay “De facultate sentiendi” and other notes; and “William Prout and Baromctry,” in Notes and Records. Royal Society of London, 24 (1970), 281–294; W. V. Farrar, “Nineteenth-Century Speculations on the Complexity of the Chemical Elements,” in British Journal for the History of Science, 2 (1965), 297–323; A. M. Kasich, “Prout and the Discovery of Hydrochloric Acid in Gastric Juice,” in Bulletin of the History of Medicine, 20 (1946), 340–348; D. F. Larder, “Prout’s Hypothesis, a Reconsideration” in Centaurus, 15 (1970), 44–50; and J. R. Partington, A History of Chemistry, III (London, 1962), 713–714, and IV (London, 1964), passim.
Two portraits of Prout are reproduced in G. Wolstenholme, The Royal College of Physicians Portraits (London, 1964), 346–348.
W. H. Brock
"Prout, William." Complete Dictionary of Scientific Biography. . Encyclopedia.com. (February 18, 2018). http://www.encyclopedia.com/science/dictionaries-thesauruses-pictures-and-press-releases/prout-william
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William Prout, 1785–1850, English chemist and physician. Prout's hypothesis, advanced in 1815–16, suggested that atomic weights of elements are multiples of that of hydrogen and that elements are formed by a condensation or grouping of hydrogen atoms. Later work on the determination of atomic weights showed that part of the hypothesis does, in general, apply. Prout won contemporary renown for his demonstration (1823) of the presence of free hydrochloric acid in the gastric juice of the stomach. He wrote many papers on the chemistry of the blood and urine.
"Prout, William." The Columbia Encyclopedia, 6th ed.. . Encyclopedia.com. (February 18, 2018). http://www.encyclopedia.com/reference/encyclopedias-almanacs-transcripts-and-maps/prout-william
"Prout, William." The Columbia Encyclopedia, 6th ed.. . Retrieved February 18, 2018 from Encyclopedia.com: http://www.encyclopedia.com/reference/encyclopedias-almanacs-transcripts-and-maps/prout-william