document_title: Gut flora

question_text: where does our first normal flora come from

question_tokens: where does our first normal flora come from

text: Gut flora

text: Classifications[edit]

text: The microbial composition of the gut microbiota varies across the digestive tract. In the stomach and small intestine, relatively few species of bacteria are generally present.[9][10] The colon, in contrast, contains a densely-populated microbial ecosystem with up to 1012 cells per gram of intestinal content.[9] These bacteria represent between 300 and 1000 different species.[9][10] However, 99% of the bacteria come from about 30 or 40 species.[11] As a consequence of their abundance in the intestine, bacteria also make up to 60% of the dry mass of feces.[12] Fungi, archaea, and viruses are also present in the gut flora, but less is known about their activities.[13]

text: Over 99% of the bacteria in the gut are anaerobes, but in the cecum, aerobic bacteria reach high densities.[2] It is estimated that these gut flora have around a hundred times as many genes in total as there are in the human genome.[14]

text: Many species in the gut have not been studied outside of their hosts because most cannot be cultured.[10][11][15] While there are a small number of core species of microbes shared by most individuals, populations of microbes can vary widely among different individuals.[16] Within an individual, microbe populations stay fairly constant over time, even though some alterations may occur with changes in lifestyle, diet and age.[9][17] The Human Microbiome Project has set out to better describe the microflora of the human gut and other body locations.

text: The four dominant bacterial phyla in the human gut are Firmicutes, Bacteroidetes, Actinobacteria, and Proteobacteria.[18] Most bacteria belong to the genera Bacteroides, Clostridium, Faecalibacterium,[9][11] Eubacterium, Ruminococcus, Peptococcus, Peptostreptococcus, and Bifidobacterium.[9][11] Other genera, such as Escherichia and Lactobacillus, are present to a lesser extent.[9] Species from the genus Bacteroides alone constitute about 30% of all bacteria in the gut, suggesting that this genus is especially important in the functioning of the host.[10]

text: Fungal genera that have been detected in the gut include Candida, Saccharomyces, Aspergillus, Penicillium, Rhodotorula, Trametes, Pleospora, Sclerotinia, Bullera, and Galactomyces, among others.[19][20] Rhodotorula is most frequently found in individuals with inflammatory bowel disease while Candida is most frequently found in individuals with hepatitis B cirrhosis and chronic hepatitis B.[19]

text: Archaea constitute another large class of gut flora which are important in the metabolism of the bacterial products of fermentation.

text: Enterotype[edit]

text: An enterotype is a classification of living organisms based on its bacteriological ecosystem in the human gut microbiome not dictated by age, gender, body weight, or national divisions.[21] There are indications that long-term diet influences enterotype.[22] Three human enterotypes have been proposed,[21][23] but their value has been questioned.[24]

text: Flora composition[edit]

text: Anatomy[edit]

text: Stomach flora[edit]

text: Due to the high acidity of the stomach, most microorganisms cannot survive there. The main bacterial inhabitants of the stomach include: Streptococcus, Staphylococcus, Lactobacillus, Peptostreptococcus, and types of yeast.[2]:720 Helicobacter pylori is a Gram-negative spiral organism that establishes on gastric mucosa causing chronic gastritis and peptic ulcer disease and is a carcinogen for gastric cancer.[2]:904

text: Intestinal flora[edit]

text:
Bacteria commonly found in the human colon[25]

Bacterium
Incidence (%)

Bacteroides fragilis
100

Bacteroides melaninogenicus
100

Bacteroides oralis
100

Enterococcus faecalis
100

Escherichia coli
100

Enterobacter sp.
40–80

Klebsiella sp.
40–80

Bifidobacterium bifidum
30–70

Staphylococcus aureus
30–50

Lactobacillus
20–60

Clostridium perfringens
25–35

Proteus mirabilis
5–55

Clostridium tetani
1–35

Clostridium septicum
5–25

Pseudomonas aeruginosa
3–11

Salmonella enterica
3–7

Faecalibacterium prausnitzii
 ?common

Peptostreptococcus sp.
 ?common

Peptococcus sp.
 ?common

text: The small intestine contains a trace amount of microorganisms due to the proximity and influence of the stomach. Gram-positive cocci and rod-shaped bacteria are the predominant microorganisms found in the small intestine.[2] However, in the distal portion of the small intestine alkaline conditions support gram-negative bacteria of the Enterobacteriaceae.[2] The bacterial flora of the small intestine aid in a wide range of intestinal functions. The bacterial flora provide regulatory signals that enable the development and utility of the gut. Overgrowth of bacteria in the small intestine can lead to intestinal failure.[26] In addition the large intestine contains the largest bacterial ecosystem in the human body.[2] About 99% of the large intestine and feces flora are made up of obligate anaerobes such as Bacteroides and Bifidobacterium.[27] Factors that disrupt the microorganism population of the large intestine include antibiotics, stress, and parasites.[2]

text: Bacteria make up most of the flora in the colon[28] and 60% of the dry mass of feces.[9] This fact makes feces an ideal source to test for gut flora for any tests and experiments by extracting the nucleic acid from fecal specimens, and bacterial 16S rRNA gene sequences are generated with bacterial primers. This form of testing is also often preferable to more invasive techniques, such as biopsies. Somewhere between 300[9] and 1000 different species live in the gut,[10] with most estimates at about 500.[29][30] However, it is probable that 99% of the bacteria come from about 30 or 40 species, with Faecalibacterium prausnitzii being the most common species in healthy adults.[11][31] Fungi and protozoa also make up a part of the gut flora, but little is known about their activities. The virome is mostly bacteriophages.[32]

text: Research suggests that the relationship between gut flora and humans is not merely commensal (a non-harmful coexistence), but rather is a mutualistic, symbiotic relationship.[10] Though people can survive with no gut flora,[29] the microorganisms perform a host of useful functions, such as fermenting unused energy substrates, training the immune system via end products of metabolism like propionate and acetate, preventing growth of harmful species, regulating the development of the gut, producing vitamins for the host (such as biotin and vitamin K), and producing hormones to direct the host to store fats.[2] Extensive modification and imbalances of the gut microbiota and its microbiome or gene collection are associated with obesity.[33] However, in certain conditions, some species are thought to be capable of causing disease by causing infection or increasing cancer risk for the host.[9][28]

text: Age[edit]

text: It has been demonstrated that there are common patterns of microbiome composition evolution during life.[34] In general, the diversity of microbiota composition of fecal samples is significantly higher in adults than in children, although interpersonal differences are higher in children than in adults.[35] Much of the maturation of microbiota into an adult-like configuration happens during the three first years of life.[35]

text: As the microbiome composition changes, so does the composition of bacterial proteins produced in the gut. In adult microbiomes, a high prevalence of enzymes involved in fermentation, methanogenesis and the metabolism of arginine, glutamate, aspartate and lysine have been found. In contrast, in infant microbiomes the dominant enzymes are involved in cysteine metabolism and fermentation pathways.[35]

text: Diet[edit]

text: Studies and statistical analyses have identified the different bacterial genera in gut microbiota and their associations with nutrient intake. Gut microflora is mainly composed of three enterotypes: Prevotella, Bacteroides, and Ruminococcus. There is an association between the concentration of each microbial community and diet. For example, Prevotella is related to carbohydrates and simple sugars, while Bacteroides is associated with proteins, amino acids, and saturated fats. Specialist microbes that break down mucin, survive on their host's carbohydrate excretions.[36] One enterotype will dominate depending on the diet. Altering the diet will result in a corresponding change in the numbers of species.[22]

text: Malnourished human children have less mature and less diverse gut microbiota than healthy children, and changes in the microbiome associated with nutrient scarcity can in turn be a pathophysiological cause of malnutrition.[37][38] Malnourished children also typically have more potentially pathogenic gut flora, and more yeast in their mouths and throats.[39] Altering diet may lead to changes in gut microbiota composition and diversity.[36]

text: Geography[edit]

text: Gut microbiome composition depends on the geographic origin of populations. Variations in trade off of Prevotella, the representation of the urease gene, and the representation of genes encoding glutamate synthase/degradation or other enzymes involved in amino acids degradation or vitamin biosynthesis show significant differences between populations from USA, Malawi or Amerindian origin.[35]

text: The US population has a high representation of enzymes encoding the degradation of glutamine and enzymes involved in vitamin and lipoic acid biosynthesis; whereas Malawi and Amerindian populations have a high representation of enzymes encoding glutamate synthase and they also have an overrepresentation of α-amylase in their microbiomes. As the US population has a diet richer in fats than Amerindian or Malawian populations which have a corn-rich diet, the diet is probably a main determinant of gut bacterial composition.[35]

text: Further studies have indicated a large difference in the composition of microbiota between European and rural African children. The fecal bacteria of children from Florence were compared to that of children from the small rural village of Boulpon in Burkina Faso. The diet of a typical child living in this village is largely lacking in fats and animal proteins and rich in polysaccharides and plant proteins. The fecal bacteria of European children was dominated by Firmicutes and showed a marked reduction in biodiversity, while the fecal bacteria of the Boulpon children was dominated by Bacteroidetes. The increased biodiversity and different composition of gut flora in African populations may aid in the digestion of normally indigestible plant polysaccharides and also may result in a reduced incidence of non-infectious colonic diseases.[40]

text: On a smaller scale, it has been shown that sharing numerous common environmental exposures in a family is a strong determinant of individual microbiome composition. This effect has no genetic influence and it is consistently observed in culturally different populations.[35]

text: Acquisition of gut flora in human infants[edit]

text: In humans, a gut flora similar to an adult's is formed within one to two years of birth.[4] The gastrointestinal tract of a normal fetus is considered sterile, but microbial colonisation may occur in the fetus[41] and Lactobacillus and Bifidobacterium species were present in placental biopsies in one study.[42] During birth and rapidly thereafter, bacteria from the mother and the surrounding environment colonize the infant's gut.[4] As of 2013, it was unclear whether most of colonizing arise from the mother or not.[4] Infants born by caesarean section may also be exposed to their mothers' microflora, but the initial exposure is most likely to be from the surrounding environment such as the air, other infants, and the nursing staff, which serve as vectors for transfer.[41] During the first year of life, the composition of the gut flora is generally simple and it changes a great deal with time and is not the same across individuals.[4]

text: The initial bacterial population are generally facultative anaerobic organisms; investigators believe that these initial colonizers decrease the oxygen concentration in the gut, which in turn allows purely anaerobic bacteria like Bacteroides, Actinobacteria, and Firmicutes to become established and thrive.[4] Breast-fed babies become dominated by bifidobacteria, possibly due to the contents of bifidobacterial growth factors in breast milk, and by the fact that breast milk carries prebiotic components, allowing for healthy bacterial growth.[42][43][44] In contrast, the microbiota of formula-fed infants is more diverse, with high numbers of Enterobacteriaceae, enterococci, bifidobacteria, Bacteroides, and clostridia.[45]

text: Functions[edit]

text: When the gut flora first started to be studied, it was thought to have three key roles: directly defending against pathogens, fortifying host defense by its role in developing and maintaining the intestinal epithelium and inducing antibody production there, and metabolizing otherwise indigestible compounds in food; subsequent work discovered its role in training the developing immune system, and yet further work focused on its role in the gut-brain axis.[46]

text: Direct inhibition of pathogens[edit]

text: The gut flora community plays a direct role in defending against pathogens by fully colonizing the space, making use of all available nutrients, and by secreting compounds that kill or inhibit unwelcome organisms that would compete for nutrients with it.[47] Disruption of the gut flora allows competing organisms like Clostridium difficile to become established that otherwise are kept in abeyance.[47]

text: Development of enteric protection and immune system[edit]

text: In humans, a gut flora similar to an adult's is formed within one to two years of birth.[4] As the gut flora gets established, the lining of the intestines – the intestinal epithelium and the intestinal mucosal barrier that it secretes – develop as well, in a way that is tolerant to, and even supportive of, commensurate microorganisms to a certain extent and also provides a barrier to pathogenic ones.[4] Specifically, goblet cells that produce the mucosa proliferate, and the mucosa layer thickens, providing an outside mucosal layer in which "friendly" microorganisms can anchor and feed, and an inner layer that even these organisms cannot penetrate.[4][5] Additionally, the development of gut-associated lymphoid tissue (GALT), which forms part of the intestinal epithelium and which detects and reacts to pathogens, appears and develops during the time that the gut flora develops and established.[4] The GALT that develops is tolerant to gut flora species, but not to other microorganisms.[4] GALT also normally becomes tolerant to food to which the infant is exposed, as well as digestive products of food, and gut flora's metabolites produced from food.[4]

text: The human immune system creates cytokines that can drive the immune system to produce inflammation in order to protect itself, and that can tamp down the immune response to maintain homeostasis and allow healing after insult or injury.[4] Different bacterial species that appear in gut flora have been shown to be able to drive the immune system to create cytokines selectively; for example Bacteroides fragilis and some Clostridia species appear to drive an anti-inflammatory response, while some segmented filamentous bacteria drive the production of inflammatory cytokines.[4][48] Gut flora can also regulate the production of antibodies by the immune system.[4][49] These cytokines and antibodies can have effects outside the gut, in the lungs and other tissues.[4]

text: Metabolism[edit]

text:
Tryptophan metabolism by human gastrointestinal microbiota (v · t · e)

Tryptophan
Clostridium
sporogenes
Lacto-
bacilli
Tryptophanase-
expressing
bacteria
IPA
I3A
Indole
Liver
Brain
IPA
I3A
Indole
Indoxyl
sulfate
AST-120
AhR
Intestinal
immune
cells
Intestinal
epithelium
PXR
Mucosal homeostasis
↓TNF-α
↑Junction protein-
coding mRNAs
L cell
GLP-1
T J
Neuroprotectant:
↓Activation of glial cells and astrocytes
↓4-Hydroxy-2-nonenal levels
↓DNA damage
–Antioxidant
–Inhibits β-amyloid fibril formation
Maintains mucosal reactivity
↑IL-22 production
Associated with vascular disease
↑Oxidative stress
↑Smooth muscle cell proliferation
↑Aortic wall thickness and calcification
Associated with chronic kidney disease
↑Renal dysfunction
–Uremic toxin
Kidneys

This diagram shows the biosynthesis of bioactive compounds (indole and certain other derivatives) from tryptophan by bacteria in the gut.[50] Indole is produced from tryptophan by bacteria that express tryptophanase.[50] Clostridium sporogenes metabolizes tryptophan into indole and subsequently 3-indolepropionic acid (IPA),[51] a highly potent neuroprotective antioxidant that scavenges hydroxyl radicals.[50][52][53] IPA binds to the pregnane X receptor (PXR) in intestinal cells, thereby facilitating mucosal homeostasis and barrier function.[50] Following absorption from the intestine and distribution to the brain, IPA confers a neuroprotective effect against cerebral ischemia and Alzheimer’s disease.[50] Lactobacillus species metabolize tryptophan into indole-3-aldehyde (I3A) which acts on the aryl hydrocarbon receptor (AhR) in intestinal immune cells, in turn increasing interleukin-22 (IL-22) production.[50] Indole itself triggers the secretion of glucagon-like peptide-1 (GLP-1) in intestinal L cells and acts as a ligand for AhR.[50] Indole can also be metabolized by the liver into indoxyl sulfate, a compound that is toxic in high concentrations and associated with vascular disease and renal dysfunction.[50] AST-120 (activated charcoal), an intestinal sorbent that is taken by mouth, adsorbs indole, in turn decreasing the concentration of indoxyl sulfate in blood plasma.[50]

text: Without gut flora, the human body would be unable to utilize some of the undigested carbohydrates it consumes, because some types of gut flora have enzymes that human cells lack for breaking down certain polysaccharides.[6] Rodents raised in a sterile environment and lacking in gut flora need to eat 30% more calories just to remain the same weight as their normal counterparts.[6] Carbohydrates that humans cannot digest without bacterial help include certain starches, fiber, oligosaccharides, and sugars that the body failed to digest and absorb like lactose in the case of lactose intolerance and sugar alcohols, mucus produced by the gut, and proteins.[3][6]

text: Bacteria turn carbohydrates they ferment into short-chain fatty acids (SCFAs)[11][30] by a form of fermentation called saccharolytic fermentation.[30] Products include acetic acid, propionic acid and butyric acid.[11][30] These materials can be used by host cells, providing a major source of useful energy and nutrients for humans,[30] as well as helping the body to absorb essential dietary minerals such as calcium, magnesium and iron.[9] Gases and organic acids, such as lactic acid, are also produced by saccharolytic fermentation.[11] Acetic acid is used by muscle, propionic acid helps the liver produce ATP, and butyric acid provides energy to gut cells and may prevent cancer.[30] Evidence also indicates that bacteria enhance the absorption and storage of lipids[10] and produce and then facilitate the body to absorb needed vitamins like vitamin K.

text: Gut flora also synthesize vitamins like biotin and folate, and help with absorption of dietary elements including magnesium, calcium and iron.[17] Methanogenic archaea such as Methanobrevibacter smithii are involved in the removal of end products of bacterial fermentation such as hydrogen.[2]

text: Host-gut microbiota-xenobiotic interaction[edit]

text: Apart from carbohydrates, gut microbiota can also metabolize other xenobiotic such as drugs, phytochemicals, and food toxicants. More than 30 drugs have been shown to be metabolized by gut microbiota.[54] The microbial metabolism of drugs can sometimes inactivate the drug.[55]

text: Gut-brain axis[edit]

text: The gut-brain axis is the biochemical signaling that takes place between the gastrointestinal tract and the central nervous system.[46] That term has been expanded to include the role of the gut flora in the interplay; the term "microbiome-gut-brain axis" is sometimes used to describe paradigms explicitly including the gut flora.[46][56][57] Broadly defined, the gut-brain axis includes the central nervous system, neuroendocrine and neuroimmune systems including the hypothalamic–pituitary–adrenal axis (HPA axis), sympathetic and parasympathetic arms of the autonomic nervous system including the enteric nervous system, the vagus nerve, and the gut microbiota.[46][57]

text: A systematic review from 2016 examined the preclinical and small human trials that have been conducted with certain commercially available strains of probiotic bacteria and found that among those tested, Bifidobacterium and Lactobacillus genera (B. longum, B. breve, B. infantis, L. helveticus, L. rhamnosus, L. plantarum, and L. casei), had the most potential to be useful for certain central nervous system disorders.[8]

text: Alterations in flora balance[edit]

text: Effects of antibiotic use[edit]

text: Altering the numbers of gut bacteria, for example by taking broad-spectrum antibiotics, may affect the host's health and ability to digest food.[58] Antibiotics can cause antibiotic-associated diarrhea (AAD) by irritating the bowel directly, changing the levels of gut flora, or allowing pathogenic bacteria to grow.[11] Another harmful effect of antibiotics is the increase in numbers of antibiotic-resistant bacteria found after their use, which, when they invade the host, cause illnesses that are difficult to treat with antibiotics.[58]

text: Changing the numbers and species of gut flora can reduce the body's ability to ferment carbohydrates and metabolize bile acids and may cause diarrhea. Carbohydrates that are not broken down may absorb too much water and cause runny stools, or lack of SCFAs produced by gut flora could cause the diarrhea.[11]

text: A reduction in levels of native bacterial species also disrupts their ability to inhibit the growth of harmful species such as C. difficile and Salmonella kedougou, and these species can get out of hand, though their overgrowth may be incidental and not be the true cause of diarrhea.[9][11][58] Emerging treatment protocols for C. difficile infections involve fecal microbiota transplantation of donor feces. (see Fecal transplant). Initial reports of treatment describe success rates of 90%, with few side effects. Efficacy is speculated to result from restoring bacterial balances of bacteroides and firmicutes classes of bacteria.[59]

text: Gut flora composition also changes in severe illnesses, due not only to antibiotic use but also to such factors as ischemia of the gut, failure to eat, and immune compromise. Negative effects from this have led to interest in selective digestive tract decontamination (SDD), a treatment to kill only pathogenic bacteria and allow the re-establishment of healthy ones.[60]

text: Antibiotics alter the population of the gastrointestinal (GI) tract microbiota, may change the intra-community metabolic interactions, modify caloric intake by using carbohydrates, and globally affects host metabolic, hormonal and immune homeostasis.[61]

text: There is reasonable evidence that taking probiotics containing Lactobacillus species may help prevent antibiotic-associated diarrhea and that taking probiotics with Saccharomyces (e.g., Saccharomyces boulardii ) may help to prevent Clostridium difficile infection following systemic antibiotic treatment.[62]

text: Pregnancy[edit]

text: Women's gut microbiota change as pregnancy advances, with the changes similar to those seen in metabolic syndromes such as diabetes. The change in gut flora causes no ill effects. The newborn's gut biota resemble the mother's first-trimester samples. The diversity of the flora decreases from the first to third trimester, as the numbers of certain species go up.[63]

text: Probiotics, prebiotics, synbiotics, and pharmabiotics[edit]

text: Probiotics are microorganisms that are believed to provide health benefits when consumed.[64][65] With regard to gut flora, prebiotics are typically non-digestible, fiber compounds that pass undigested through the upper part of the gastrointestinal tract and stimulate the growth or activity of advantageous gut flora by acting as substrate for them.[30][66]

text: Synbiotics refers to food ingredients or dietary supplements combining probiotics and prebiotics in a form of synergism.[67]

text: The term "pharmabiotics" is used in various ways, to mean: pharmaceutical formulations (standardized manufacturing that can obtain regulatory approval as a drug) of probiotics, prebiotics, or synbiotics;[68] probiotics that have been genetically engineered or otherwise optimized for best performance (shelf life, survival in the digestive tract, etc.);[69] and the natural products of gut flora metabolism (vitamins, etc.).[70]

text: There is some evidence that treatment with some probiotic strains of bacteria may be effective in irritable bowel syndrome and chronic idiopathic constipation. Those organisms most likely to result in a decrease of symptoms have included:

text:
Streptococcus faecium
Lactobacillus plantarum
Lactobacillus rhamnosus
Propionibacterium freudenreichii
Bifidobacterium breve
Lactobacillus reuteri
Lactobacillus salivarius
Bifidobacterium infantis
Streptococcus thermophilus[71][72][73]

text: Gram positive bacteria present in the lumen may be associated with extending the duration of relapse for ulcerative colitis.[72]

text: Role in disease[edit]

text: Bacteria in the digestive tract can contribute to and be affected by disease in various ways. The presence or overabundance of some kinds of bacteria may contribute to inflammatory disorders such as inflammatory bowel disease.[9] Additionally, metabolites from certain members of the gut flora may influence host signaling pathways, contributing to disorders such as obesity and colon cancer.[9] Alternatively, in the event of a breakdown of the gut epithelium, the intrusion of gut flora components into other host compartments can lead to sepsis.[9]

text: Ulcers[edit]

text: Helicobacter pylori can cause stomach ulcers by crossing the epithelial lining of the stomach. Here the body produces an immune response. During this response parietal cells are stimulated and release extra hydrochloric acid (HCl+) into the stomach. However, the response does not stimulate the mucus-secreting cells that protect and line the epithelium of the stomach. The extra acid sears holes into the epithelial lining of the stomach, resulting in stomach ulcers.[34]

text: Inflammatory bowel diseases[edit]

text: The two main types of inflammatory bowel diseases, Crohn's disease and ulcerative colitis, are chronic inflammatory disorders of the gut; the causes of these disease are unknown and issues with the gut flora and its relationship with the host have been implicated in these conditions.[7][74][75][76] Additionally, it appears that interactions of gut flora with the gut-brain axis have a role in IBD, with physiological stress mediated through the hypothalamic–pituitary–adrenal axis driving changes to intestinal epithelium and the gut flora in turn releasing factors and metabolites that trigger signaling in the enteric nervous system and the vagus nerve.[1]

text: The diversity of gut flora appears to be significantly diminished in people with inflammatory bowel diseases compared to healthy people; additionally, in people with ulcerative colitis, Proteobacteria and Actinobacteria appear to dominate; in people with Crohn's, Enterococcus faecium and several Proteobacteria appear to be over-represented.[1]

text: There is reasonable evidence that correcting gut flora imbalances by taking probiotics with Lactobacilli and Bifidobacteria can reduce visceral pain and gut inflammation in IBD.[62]

text: Irritable bowel syndrome[edit]

text: Irritable bowel syndrome is a result of stress and chronic activation of the HPA axis; its symptoms include abdominal pain, changes in bowel movements, and an increase in proinflammatory cytokines. Overall, studies have found that the luminal and mucosal microbiota are changed in irritable bowel syndrome individuals, and these changes can relate to the type of irritation such as diarrhea or constipation. Also, there is a decrease in the diversity of the microbiome with low levels of fecal Lactobacilli and Bifidobacteria, high levels of facultative anaerobic bacteria such as Escherichia coli, and increased ratios of Firmicutes:Bacteroidetes.[57]

text: Other inflammatory or autoimmune conditions[edit]

text: Allergy, asthma, and diabetes mellitus type 1 are autoimmune and inflammatory disorders' the causes of these disease are unknown and issues with the gut flora and its relationship with the host have been implicated in these conditions.[7]

text: Two hypotheses have been posed to explain the rising prevalence of these diseases in the developed world: the hygiene hypothesis, which posits that children in the developed world are not exposed to a wide enough range of pathogens and end up with an overreactive immune system, and the role of the Western pattern diet which lacks whole grains and fiber and has an overabundance of simple sugars.[7] Both hypotheses converge on the changes in the gut flora and its role in modulating the immune system, and as of 2016 this was an active area of research.[7]

text: Similar hypotheses have been posited for the rise of food and other allergies.[77]

text: As of 2016 it was not clear if changes to the gut flora cause these auto-immune and inflammatory disorders or are a product of them or adaptation to them.[7][78]

text: Obesity and metabolic syndrome[edit]

text: The gut flora has also been implicated in obesity and metabolic syndrome due to the key role it plays in the digestive process; the Western pattern diet appears to drive and maintain changes in the gut flora that in turn change how much energy is derived from food and how that energy is used.[76][79] One aspect of a healthy diet that is often lacking in the Western-pattern diet is fiber and other complex carbohydrates that a healthy gut flora require to flourish; changes to gut flora in response to a Western-pattern diet appear to increase the amount of energy generated by the gut flora which may contribute to obesity and metabolic syndrome.[62] There is also evidence that microbiota influence eating behaviors based on the preferences of the microbiota, which can lead to the host consuming more food eventually resulting in obesity. It has generally been observed that with higher gut microbiome diversity, the microbiota will spend energy and resources on competing with other microbiota and less on manipulating the host. The opposite is seen with lower gut microbiome diversity, and these microbiotas may work together to create host food cravings.[80]

text: Additionally, the liver plays a dominant role in blood glucose homeostasis by maintaining a balance between the uptake and storage of glucose through the metabolic pathways of glycogenesis and gluconeogenesis. In recent studies, it is illustrated that intestinal lipids regulate glucose homeostasis involving a gut-brain-liver axis. The direct administration of lipids into the upper intestine increases the long chain fatty acyl-coenzyme A (LCFA-CoA) levels in the upper intestines and suppresses glucose production even under sub diaphragmatic vagotomy or gut vagal deafferentation. This interrupts the neural connection between the brain and the gut and blocks the upper intestinal lipids’ ability to inhibit glucose production. The gut-brain-liver axis and gut microbiota composition can regulate the glucose homeostasis in the liver and provide potential therapeutic methods to treat obesity and diabetes.[81]

text: Just as gut flora can function in a feedback loop that can drive the development of obesity, there is evidence that restricting intake of calories (i.e., dieting) can drive changes to the composition of the gut flora.[76]

text: Liver disease[edit]

text: As the liver is fed directly by the portal vein, whatever crosses the intestinal epithelium and the intestinal mucosal barrier enters the liver, as do cytokines generated there.[82] Dysbiosis in the gut flora has been linked with the development of cirrhosis and non-alcoholic fatty liver disease.[82]

text: Systemic infections[edit]

text: Normally-commensal bacteria can be very harmful to the host if they get outside of the intestinal tract.[4][5] Translocation, which occurs when bacteria leave the gut through its mucosal lining, the border between the lumen of the gut and the inside of the body, can occur in a number of different diseases, and can be caused by too much growth of bacteria in the small intestine, reduced immunity of the host, or increased gut lining permeability.[5]

text: If the gut is perforated, bacteria can invade the body, causing a potentially fatal infection. Aerobic bacteria can make an infection worse by using up all available oxygen and creating an environment favorable to anaerobes.[2]:715

text: Cancer[edit]

text: Some genera of bacteria, such as Bacteroides and Clostridium, have been associated with an increase in tumor growth rate, while other genera, such as Lactobacillus and Bifidobacteria, are known to prevent tumor formation.[9]

text: Neuropsychiatric[edit]

text: Interest in the relationship between gut flora and neuropsychiatric issues was sparked by a 2004 study showing that germ-free mice showed an exaggerated HPA axis response to stress compared to non-GF laboratory mice.[46] As of January 2016, most of the work that has been done on the role of gut flora in the gut-brain axis had been conducted in animals, or characterizing the various neuroactive compounds that gut flora can produce, and studies with humans measuring differences between people with various psychiatric and neurological differences, or changes to gut flora in response to stress, or measuring effects of various probiotics (dubbed "psychobiotics in this context), had generally been small and could not be generalized; whether changes to gut flora are a result of disease, a cause of disease, or both in any number of possible feedback loops in the gut-brain axis, remained unclear.[46][62]

text: Other animals[edit]

text: Aside from mammals, some insects also possess complex and diverse gut microbiota that play key nutritional roles.[83] Microbial communities associated termites can constitute a majority of the weight of the individuals and perform important roles in the digestion of lignocellulose and nitrogen fixation.[84] These communities are host-specific, and closely related insect species share comparable similarities in gut microbiota composition.[85][86] In cockroaches, gut microbiota have been shown to assemble in a deterministic fashion, irrespective of the inoculum;[87] the reason for this host-specific assembly remains unclear. Bacterial communities associated with insects like termites and cockroaches are determined by a combination of forces, primarily diet, but there is some indication that host phylogeny may also be playing a role in the selection of lineages.[85][86]

text: For more than 51 years it has been known that the administration of low doses of antibacterial agents promotes the growth of farm animals to increase weight gain.[61]

text: In a study performed on mice by Ilseung Cho,[61] the ratio of Firmicutes and Lachnospiraceae was significantly elevated in animals treated with subtherapeutic doses of different antibiotics. By analyzing the caloric content of faeces and the concentration of small chain fatty acids (SCFAs) in the GI tract, they concluded that the changes in the composition of microbiota lead to an increased capacity to extract calories from otherwise indigestible constituents, and to an increased production of SCFAs. These findings provide evidence that antibiotics perturb not only the composition of the GI microbiome but also its metabolic capabilities, specifically with respect to SCFAs.[61]


document_title: Ramadan (calendar month)

question_text: when was the last time ramadan was in june

root

text: Ramadan (calendar month)

text: Timing[edit]

text: The calendar is a lunar calendar, and months begin when the first crescent of a new moon is sighted. Since the Islamic lunar calendar year is 10 to 11 days shorter than the solar year and contains no intercalation, Ramadan migrates throughout the seasons. The Islamic day starts after sunset. The estimated start and end dates for Ramadan, based on the Umm al-Qura calendar of Saudi Arabia, are:[2]

tag: p

text:
AH
First day (CE / AD)
Last day (CE / AD)

1437
06 June 2016
05 July 2016

1438
27 May 2017
24 June 2017

1439
16 May 2018
14 June 2018

1440
06 May 2019
03 June 2019

1441
24 April 2020
23 May 2020

1442
13 April 2021
12 May 2021

Ramadan dates between 2016 and 2021

tag: table

text: Many Muslims insist on the local physical sighting of the moon to mark the beginning of Ramadan, but others use the calculated time of the new moon or the Saudi Arabian declaration to determine the start of the month. Since the new moon is not in the same state at the same time globally, the beginning and ending dates of Ramadan depend on what lunar sightings are received in each respective location. As a result, Ramadan dates vary in different countries, but usually only by a day. This is due to the cycle of the moon. The moon travels the same path all year round and when the moon is seen in the east, it is then seen traveling towards the west. All the countries around the world see the moon within a 24-hour period once spotted by one country in the east.

text: Each year, Ramadan begins about eleven days earlier than in the previous year.[3] Astronomical projections that approximate the start of Ramadan are available.[4] 33 Islamic years are approximately equal to 32 tropical years, with six days over.

text: Events[edit]

text: Ramadan is observed by Muslims during the entire lunar month by the same name. The month of religious observances consists of fasting and extra prayers. Some important historical events during this month are generally believed to include:

text:
1 Ramadan, birth of Sayyid Abdul-Qadir Gilani
2 Ramadan, the Torah (Tawrat) was bestowed on Moses (Musa)
10 Ramadan, death of Khadijah bint Khuwaylid – first wife of Muhammad
10 Ramadan, in 1973, Operation Badr took place, starting the Yom Kippur War
12 Ramadan, the Gospel (Injil) was bestowed on Jesus (Isa)
15 Ramadan, birth of Hasan ibn Ali
15 Ramadan, In the Ottoman Empire, the sultan presented trays of baklava to the Janissaries in a ceremonial procession called the Baklava Alayı
17 Ramadan, death of Aisha bint Abu Bakr – third wife of Muhammad
17 Ramadan, the Battle of Badr was won by the Muslims
18 Ramadan, the Psalms (Zabur) were bestowed on David (Dawood)
19 Ramadan, Ali bin Abu Talib was struck on the head by a sword
20 Ramadan, the Conquest of Mecca by Muhammad
21 Ramadan, Ali bin Abu Talib died due to injuries he sustained by a sword
27 Ramadan, the Dominion of Pakistan was established on 14 August 1947 (27 Ramadan 1366 in the Islamic calendar)[5]

tag: ul

text: Laylat al-Qadr is observed during one of the last ten days of the month (typically the odd nights). Muslims believe that this night which is also known as "The Night of Power" is better than a thousand months. This is often interpreted as praying throughout this night is rewarded equally with praying for a thousand months (just over 83 years i.e., a lifetime). Many Muslims spend the entire night in prayer.

text: Hadith[edit]

text: In Islamic eschatology:

text:
Abu Hurairah said that the Prophet said:

There will be an Ayah (sign) in (the month of) Ramadan. Then, there will 'isabah (splitting into groups) in Shawwal. Then, there will be fighting in (the month of) Dhu al-Qi'dah. Then, the pilgrim will be robbed in (the month of) Dhu al-Hijjah. Then, the prohibitions will be violated in (the month of) al-Muharram. Then, there will be sound in (the month of) Safar, then the tribes will conflict with each other in the two months of Rabi' al-awwal & Rabi' al-thani. Then, the most amazing thing will happen between (the months of) Jumada and Rajab. Then, a well-fed she-camel will be better than a fortress (castle) sheltering a thousand (people).[6]


document_title: Tomorrow Never Knows

question_text: where did john lennon get lyrics for the revolutionary tomorrow never knows track from revolver

text: Tomorrow Never Knows

text: Inspiration[edit]

text: John Lennon wrote the song in January 1966, with lyrics adapted from the book The Psychedelic Experience: A Manual Based on the Tibetan Book of the Dead by Timothy Leary, Richard Alpert, and Ralph Metzner, which was in turn adapted from the Tibetan Book of the Dead.[5] Although Peter Brown believed that Lennon's source for the lyrics was the Tibetan Book of the Dead itself, which, he said, Lennon had read whilst under the influence of LSD,[6] George Harrison later stated that the idea for the lyrics came from Leary, Alpert, and Metzner's book;[7] Paul McCartney confirmed this, stating that when he and Lennon visited the newly opened Indica bookshop, Lennon had been looking for a copy of The Portable Nietzsche and found a copy of The Psychedelic Experience that contained the lines: "Whenever in doubt, turn off your mind, relax, float downstream".[8]

text: Lennon bought the book, went home, took LSD, and followed the instructions exactly as stated in the book.[9][10] The book held that the "ego death" experienced under the influence of LSD and other psychedelic drugs is essentially similar to the dying process and requires similar guidance.[11][12] This is a state of being known by eastern mystics and masters as samādhi (a state of being totally aware of the present moment; a one-pointedness of mind).

text: Title[edit]

text: The title never actually appears in the song's lyrics. Lennon later revealed that, like "A Hard Day's Night", it was taken from one of Ringo Starr's malapropisms.[13] In a television interview in early 1964, Starr had uttered the phrase "Tomorrow never knows" when laughing off an incident that took place at the British Embassy in Washington, DC, during which one of the guests had cut off a portion of his hair.[14] The piece was originally titled "Mark I".[8] "The Void" is cited as another working title but according to Mark Lewisohn (and Bob Spitz) this is untrue.

text: Musical structure[edit]

text: McCartney remembered that even though the song's harmony was mainly restricted to the chord of C, Martin accepted it as it was and said it was "rather interesting". The song's harmonic structure is derived from Indian music and is based upon a high volume C drone played by Harrison on a tamboura.[15] The "chord" over the drone is generally C major, but some changes to B flat major result from vocal modulations, as well as orchestral and guitar tape loops.[16][17] The song has been called the first pop song that attempted to dispense with chord changes altogether.[15] Here, the Beatles' harmonic ingenuity is nonetheless displayed in the upper harmonies – "Turn off your mind", for example, is suitably a run of unvarying E melody notes, before "relax" involves an E–G melody note shift and "float downstream" an E–C–G descent.[18] "It is not dying" involves a run of three G melody notes that rise on "dying" to a B♭, creating a ♭VII/I (B♭/C) 'slash' polychord.[18] This is a prominent device in Beatles songs such as "All My Loving", "Help!", "A Hard Day's Night", "Norwegian Wood (This Bird Has Flown)", "Hey Jude", "Dear Prudence", "Revolution" and "Get Back".[19]

text: Recording[edit]

text: Lennon first played the song to Brian Epstein, George Martin and the other Beatles at Epstein's house at 24 Chapel Street, Belgravia, London.[20]

text: The 19-year-old Geoff Emerick was promoted to replace Norman Smith as engineer on the first session for the Revolver album. This started at 8 pm on 6 April 1966, in Studio Three at Abbey Road.[8] Lennon told producer Martin that he wanted to sound like a hundred chanting Tibetan monks, which left Martin the difficult task of trying to find the effect by using the basic equipment they had. The effect was achieved by using a Leslie speaker. When the concept was explained to Lennon, he inquired if the same effect could be achieved by hanging him upside down and spinning him around a microphone while he sang into it.[8][21] Emerick made a connector to break into the electronic circuitry of the cabinet and then re-recorded the vocal as it came out of the revolving speaker.[22][23]

text: As Lennon hated doing a second take to double his vocals, Ken Townsend, the studio's technical manager, developed an alternative form of double-tracking called artificial double tracking (ADT) system, taking the signal from the sync head of one tape machine and delaying it slightly through a second tape machine.[24] The two tape machines used were not driven by mains electricity, but from a separate generator which put out a particular frequency, the same for both, thereby keeping them locked together.[24] By altering the speed and frequencies, he could create various effects, which the Beatles used throughout the recording of Revolver.[25] Lennon's vocal is double-tracked on the first three verses of the song: the effect of the Leslie cabinet can be heard after the (backwards) guitar solo.[26][27]

text: The track included the highly compressed drums that the Beatles currently favoured, with reverse cymbals, reverse guitar, processed vocals, looped tape effects, a sitar and a tambura drone.[21] The use of these ¼-inch audio tape loops resulted primarily from McCartney's admiration for Stockhausen's Gesang der Jünglinge.[28][29] By disabling the erase head of a tape recorder and then spooling a continuous loop of tape through the machine while recording, the tape would constantly overdub itself, creating a saturation effect, a technique also used in musique concrète.[28] The tape could also be induced to go faster and slower. McCartney encouraged the other Beatles to use the same effects and create their own loops.[17] After experimentation on their own, the various Beatles supplied a total of "30 or so" tape loops to Martin, who selected 16 for use on the song.[30] Each loop was about six seconds long.[30]

text: The tape loops were played on BTR3 tape machines located in various studios of the Abbey Road building[31] and controlled by EMI technicians in Studio Two at Abbey Road on 7 April.[32][21] Each machine was monitored by one technician, who had to hold a pencil within each loop to maintain tension.[30] The four Beatles controlled the faders of the mixing console while Martin varied the stereo panning and Emerick watched the meters.[33][34] Eight of the tapes were used at one time, changed halfway through the song.[33] The tapes were made (like most of the other loops) by superimposition and acceleration.[35][36] According to Martin, the finished mix of the tape loops could not be repeated because of the complex and random way in which they were laid over the music.[37]

text: Five tape loops are prominent in the finished version of the song. According to author Ian MacDonald, writing in the 1990s, these loops contain the following:

text:
A recording of McCartney's laughter, sped up to resemble the sound of a seagull (enters at 0:07)
An orchestral chord of B flat major (0:19)
A Mellotron on its flute setting (0:22)
A Mellotron strings sound, alternating between B flat and C in 6/8 time (0:38)
A sitar playing a rising scalar phrase, recorded with heavy saturation and sped up (0:56).[38]

tag: ol

text: Author Robert Rodriguez writes that the content of the five loops has continued to invite debate among commentators, however, and that the manipulation applied to each of the recordings has made them impossible to decipher with authority.[39] Based on the most widely held views, he says that, aside from McCartney's laughter and the B flat major chord, the sounds were two loops of sitar passages, both reversed and sped up, and a loop of Mellotron string and brass voicings.[40] In their book Recording the Beatles, Kevin Ryan and Brian Kehew list two loops of sitar recordings yet, rather than Mellotron, list a mandolin or acoustic guitar, treated with tape echo.[14][41]

text: Lennon was later quoted as saying that "I should have tried to get my original idea, the monks singing. I realise now that's what I wanted."[42] The Beatles experimented further with tape loops. Later examples include "Carnival of Light", an unreleased piece recorded during the Sgt. Pepper's Lonely Hearts Club Band sessions;[43] the Sgt. Pepper track "Being for the Benefit of Mr. Kite!"; and "Revolution 9", released on The Beatles.[44] Take one of "Tomorrow Never Knows" was included on the Anthology 2 compilation in 1996.[42]

text: After completing the recording, McCartney was eager to gauge the reaction of the band's contemporaries. On 2 May, he played the song to Bob Dylan at the latter's hotel suite in London; as the track started, Dylan said dismissively: "Oh, I get it. You don't want to be cute anymore."[45] According to Marianne Faithfull, who was also present, Dylan then walked out of the room.[46] McCartney recalled that when the Beatles played the song to members of the Rolling Stones and the Who, they "visibly sat up and were interested", whereas Cilla Black "just laughed".[47]

text: Interpretation[edit]

text: Harrison questioned whether Lennon fully understood the meaning of the song's lyrics:

text: You can hear (and I am sure most Beatles fans have) "Tomorrow Never Knows" a lot and not know really what it is about. Basically it is saying what meditation is all about. The goal of meditation is to go beyond (that is, transcend) waking, sleeping and dreaming. So the song starts out by saying, "Turn off your mind, relax and float downstream, it is not dying."

text: Then it says, "Lay down all thoughts, surrender to the void – it is shining. That you may see the meaning of within – it is being." From birth to death all we ever do is think: we have one thought, we have another thought, another thought, another thought. Even when you are asleep you are having dreams, so there is never a time from birth to death when the mind isn't always active with thoughts. But you can turn off your mind, and go to the part which Maharishi described as: "Where was your last thought before you thought it?"

text: The whole point is that we are the song. The self is coming from a state of pure awareness, from the state of being. All the rest that comes about in the outward manifestation of the physical world (including all the fluctuations which end up as thoughts and actions) is just clutter. The true nature of each soul is pure consciousness. So the song is really about transcending and about the quality of the transcendent.

text: I am not too sure if John actually fully understood what he was saying. He knew he was onto something when he saw those words and turned them into a song. But to have experienced what the lyrics in that song are actually about? I don't know if he fully understood it.[48]

text: Release and reception[edit]

text: "Tomorrow Never Knows" was sequenced as the final track on Revolver, which EMI's Parlophone label issued on 5 August 1966.[49] In his design for the LP cover, Klaus Voormann drew inspiration from the song, recognising the need for artwork that would capture the Beatles' new direction[50] and the avant-garde aspect of the recording.[51] Voormann later said that he found "Tomorrow Never Knows" "frightening", adding that it was "so far away from the early Beatles stuff that even I myself thought, well, the normal kind of Beatles fan won't want to buy this record. But they did."[52]

text: Reaction to the release was "generally ecstatic", according to MacDonald, with listeners marvelling at the album's "aural invention".[53] To the Beatles' less progressive fans, however, the radical changes in the band's sound were the source of confusion.[54] The editor of the Australian teen magazine Mirabelle wrote: "Everyone, from Brisbane to Bootle, hates that daft song Lennon sang at the end of Revolver."[47] In his review for the NME, Allen Evans said, in response to the lyric's exhortation to "relax and float downstream": "But how can you relax with the electronic, outer-space noises, often sounding like seagulls? … Only Ringo's rock-steady drumming is natural."[55] Peter Jones of Record Mirror commented: "You need some sort of aural microscope to get the message from this. But it's darned compelling listening."[56] Writing in 1977, author Nicholas Schaffner said that those who had been confused by the lyrics were most likely unfamiliar with hallucinogenic drugs and Timothy Leary's message, but that the transcendental quality became clear during the build-up to the 1967 Summer of Love.[57]

text: In 2006, Pitchfork Media ranked "Tomorrow Never Knows" at number 19 on its list of "The 200 Greatest Songs of the 1960s"[58] and Q magazine placed the track 75th on a list of "The 100 Greatest Songs of All Time".[14] "Tomorrow Never Knows" appears at number 18 on Rolling Stone's list of the best Beatles songs[59][60] and at number 4 on a similar list compiled by Mojo.[61]

text: Love remix[edit]

text: In 2006, Martin and his son, Giles Martin, remixed 80 minutes of Beatles music for the Las Vegas stage performance Love, a joint venture between Cirque du Soleil and the Beatles' Apple Corps Ltd.[62] On the Love album, the rhythm to "Tomorrow Never Knows" was mixed with the vocals and melody from "Within You Without You", creating a different version of the two songs. The soundtrack album from the show was released in 2006.[63][64] The Love remix is one of the main songs in The Beatles: Rock Band .[65]

text: In popular culture[edit]

text: According to Colin Larkin, writing in the Encyclopedia of Popular Music, "Tomorrow Never Knows" has been recognised as "the most effective evocation of a LSD experience ever recorded".[66] Ian MacDonald says that the song's message represented a revolutionary concept in mainstream society in 1966. He adds: "'Tomorrow Never Knows' launched the till-then élite-preserved concept of mind-expansion into pop, simultaneously drawing attention to consciousness-enhancing drugs and the ancient religious philosophies of the Orient, utterly alien to Western thought in their anti-materialism, rapt passivity, and world-sceptical focus on visionary consciousness."[67]

text: In music[edit]

text: Hernan Campbell of Sputnikmusic recognises "Tomorrow Never Knows" as "the most important Psychedelic composition in the history of the genre" and "the epitome of everything that psychedelia stands for".[68] In the opinion of former Mojo editor Paul Trynka, the track benefited most from the Beatles' ability to channel their ideas into a recognisable song form, a discipline that ensured their psychedelic recordings were superior to those by the Grateful Dead and other contemporary San Francisco acts.[69] Writing in his book Electronic and Experimental Music, Thom Holmes includes "Tomorrow Never Knows" in his list of the "pioneering works" in electronic music. He says that the track "ushered in a new era in the use of electronic music in rock and pop music".[70]

text: Steve Turner highlights the sampling and tape manipulation used on the song as having had "a profound effect on everyone from Jimi Hendrix to Jay Z".[71] In 2011, DJ Spooky said of the track:

text: "Tomorrow Never Knows" is one of those songs that's in the DNA of so much going on these days that it's hard to know where to start. Its tape collage alone makes it one of the first tracks to use sampling really successfully. I also think that Brian Eno's idea of the studio-as-instrument comes from this kind of recording.[72]

text: The song is referenced in the lyric to the 1995 Oasis song "Morning Glory": "Tomorrow never knows what it doesn't know too soon".[73] The Chemical Brothers refer to "Tomorrow Never Knows" as their "manifesto"; their 1996 track "Setting Sun" is a direct tribute to it. John Foxx of Ultravox also cited the song as an influence, saying that "As soon as I heard it, I knew it contained almost everything that I would want to investigate for the rest of my life."[69]

text: Cover versions[edit]

text:
801 performed the song live at their three concerts in 1976, under the name "TNK (Tomorrow Never Knows)". The final performance at London's Queen Elizabeth Hall was included on the subsequent release 801 Live. A rehearsal of the song at Shepperton Studios was included on the 2009 Collectors Edition of the album.
Listed in setlists as "TNK", The Grateful Dead performed the song 12 times in the 1990s, always segueing out of The Who's "Baba O'Riley".[74] Subsequently, former Grateful Dead members Phil Lesh, Bob Weir and Vince Welnick have played the song in their post-Dead projects.[75]
Ride performed a cover version during their 2015 reunion tour in North America.[76]
Tangerine Dream recorded an instrumental version in 2008.[77]
Marianne Nowottny and the Sensorium Saxophone Orchestra recorded a cover version in 2015. [78]
Phil Collins released a version on his album Face Value.

text: In television[edit]

text: The song was featured during the final scene of the 2012 Mad Men episode "Lady Lazarus". Don Draper's wife Megan gives him a copy of Revolver, calling his attention to a specific track and suggesting, "Start with this one".[79] Draper, an advertising executive, is struggling to understand youth culture, but after contemplating the song for a few puzzled moments, he shuts it off.[80] The track also played over the closing credits.[81] The rights to the song cost the producers about $250,000,[80] "about five times as much as the typical cost of licensing a song for TV".[79]

text: Personnel[edit]

text: According to Ian MacDonald:[82]

text:
John Lennon – vocals, Hammond organ, Mellotron,[83] tape loops
Paul McCartney – bass, tape loops
George Harrison – sitar, tambura, lead guitar, tape loops
Ringo Starr – drums, tambourine, tape loops
George Martin – tack piano[83]


document_title: Harry Potter and the Cursed Child

question_text: who published harry potter and the cursed child

text: Harry Potter and the Cursed Child

text: Plot[edit]

text: Act 1[edit]

text: In the opening scene, set during the epilogue of Harry Potter and the Deathly Hallows in the year 2017, Harry Potter and Ginny Potter send their second son, Albus Severus Potter, on the Hogwarts Express to begin his first year at Hogwarts. Harry is now working in a desk job as the Head of Magical Law Enforcement at the Ministry of Magic, while Ginny is the editor of the sports section of The Daily Prophet. Ron Weasley and Hermione Granger also send their daughter Rose Granger-Weasley on the train. Hermione is now Minister of Magic, while Ron manages Weasley's Wizard Wheezes in Diagon Alley. Albus makes an unlikely friend in Scorpius Malfoy, the son of Harry's former nemesis Draco Malfoy and Astoria (née Greengrass). The school is stunned when, in a break with the tradition of Potters being sorted into Gryffindor, Albus is sorted into Slytherin alongside Scorpius.

text: Both boys are bullied by other students over the next few years, Albus due to his perceived failure to live up to his parents, Scorpius due to unproven rumours that he is the son of Lord Voldemort. In addition, Albus and Harry begin to drift apart, owing to Albus's struggles with his father's shadow and Harry's uncertainty on how to deal with his son's issues. Albus also drifts apart from Rose, with whom he was friends before meeting Scorpius and was sorted into Gryffindor. Prior to Albus and Scorpius's fourth year, Albus gets into a fight with his father after he is given Harry's baby blanket and a love potion from Ron. During the fight, Harry accidentally says that he sometimes wishes Albus was not his son, and Albus spills potion on the blanket.

text: Harry obtains a prototype of a more powerful version of the Time-Turner, built by a Slytherin contemporary of Harry's, Theodore Nott, that allows one to travel back several years into the past and change history. Simultaneously, Harry's scar begins to hurt again, causing him to become concerned that Voldemort may somehow be returning. Amos Diggory, who has become old and is cared for by his niece, Delphi Diggory, asks Harry to use the Time-Turner to prevent the death of his son, Cedric Diggory. After overhearing Harry refuse to help the Diggorys, Albus is inspired to do so himself and convinces Scorpius to help him. The two escape from the Hogwarts Express and the trolley operator, who is revealed to be a monster placed on the train to prevent students from escaping. The two arrive at St. Oswald's Home for Old Witches and Wizards in Yorkshire, where Amos lives, and team up with Delphi to steal the Time-Turner from Hermione's office, in the Ministry of Magic, while disguised with Polyjuice Potion.

text: Act 2[edit]

text: Knowing that Cedric's death was the result of him winning the Triwizard Tournament alongside Harry, the boys use the Time-Turner to travel back to the first challenge of the Triwizard Tournament in 1994 and sabotage Cedric during the tournament's first task in the hope of preventing his victory. Instead, they only succeed in creating an alternate reality in which Ron and Hermione never married, and thus Rose was never born, and Albus was sorted into Gryffindor. Albus discovers that this was because they chose to disguise themselves as Durmstrang students, causing Hermione to become suspicious of Viktor Krum and go to the Yule Ball with Ron instead of Viktor. As a result, Ron never experienced the jealousy fundamental to his relationship with Hermione, fell in love with Padma Patil at the Ball, and eventually became married to her, having a son named Panju. Hermione, in turn, became a frustrated and mean professor at Hogwarts, teaching Defense Against the Dark Arts.

text: At around the same time, Harry's fear that Voldemort may return increases as his scar continues to hurt and as he has Voldemort-related nightmares. After speaking with a portrait of Dumbledore, and being told by centaur Bane that a "dark cloud" is around Albus, he becomes convinced that Scorpius is a threat to Albus and tries to have the boys kept apart at Hogwarts by forcing a reluctant Minerva McGonagall, now Headmistress of Hogwarts, to keep tabs on Albus using the Marauder's Map, threatening to shut down the school otherwise.

text: Albus and Scorpius's friendship is destroyed, but the two eventually reconcile after Albus steals Harry's old Invisibility Cloak from James Sirius (Albus’ older brother), and after McGonagall refuses to enforce Harry's request. Harry himself is persuaded to relent after a conversation with Draco and Ginny. Meanwhile, Albus and Scorpius decide to make another attempt to use the Time-Turner to change Cedric's fate, this time by humiliating him during the Triwizard Tournament's second task. When Scorpius returns to the present day, however, Albus is not with him, and Scorpius finds himself in a reality in which Harry is dead, and Lord Voldemort rules the wizarding world.

text: Act 3[edit]

text: Scorpius discovers that – as a result of his actions – an embittered Cedric joined the Death Eaters and killed Neville Longbottom during the events of Deathly Hallows, preventing him from killing Nagini and allowing Voldemort to win the Battle of Hogwarts. With Harry now dead, Albus subsequently never existed, while Voldemort was able to completely consolidate power and transform the Ministry of Magic into a dictatorial regime. In the new timeline, Scorpius became a popular Head Boy and Quidditch star, helping the staff and students torment Muggle-borns. Dolores Umbridge became the new Headmistress of Hogwarts, and patrols the school with Dementors and a revived Inquisitorial Squad led by Scorpius. Draco Malfoy occupies Harry's old position as the Head of Magical Law Enforcement, using his post to encourage routine attacks on Muggles and bribe the Prime Minister to remain silent on the actions of the Death Eaters.

text: A powerful dark figure called "The Augurey" leads the Ministry of Magic. With help from Ron, Hermione, and Severus Snape, now the final members of a dwindling anti-Voldemort resistance movement, Scorpius is able to use the Time-Turner to prevent the interference of Albus and his past self and restore the events of the original timeline, the alternate Ron, Hermione, and Snape sacrificing themselves to the Dementors in order to allow him to do so. Scorpius reunites with Albus, and the two boys are eventually found by their parents, as well as Ron and Hermione. Following these events, Harry scolds Albus for his actions, but the two nevertheless begin to reconcile.

text: Realising the danger the Time-Turner poses and deciding their parents will continue to keep it (as Hermonie had done in the Ministry of Magic), Scorpius and Albus attempt to destroy it themselves, but they are joined by Delphi Diggory. Scorpius realizes that Delphi was in charge of the Ministry of Magic in the alternate timeline (from her tattoo of the wings of a magical bird, which she says is called an Augurey), and she takes them captive, later revealing her intention of restoring the alternate timeline.

text: After the adults learn Albus and Scorpius were seen disappearing with Delphi, they confront Amos, only to discover Delphi is not his niece, but the daughter of Lord Voldemort and Bellatrix Lestrange. Delphi had placed Amos under a "confundus" charm. Searching her room, they discover she is following a prophecy that, if fulfilled, would lead to Lord Voldemort's return. Delphi takes the boys to the final challenge of the Triwizard Tournament, but Albus and Scorpius prevent her from acting, and Delphi uses the Time-Turner again to travel further back in time. She inadvertently takes the boys with her and then destroys the Time-Turner to leave them all stranded in time.

text: Act 4[edit]

text: Abandoned by Delphi, Albus and Scorpius discover they have been taken back to the night Harry's parents were killed at Godric's Hollow (30 October 1981), and assume Delphi is planning to kill Harry before Voldemort attempts to so (and which severely weakens Voldemort). Albus and Scorpius write an invisible message on Harry's baby blanket, knowing in the present (which is now also the night of the anniversary of the death of Harry's parents, when he often looks for his blanket as it is the only physical memento he has), the blanket would become stained with love potion and expose the message to Harry.

text: Meanwhile, Draco reveals the Time-Turner was actually a prototype for a perfected model owned by him (it was made for his father), but they remain unable to rescue the boys due to their uncertainty over which time period they have entered. After Harry receives the message from the boys, he and his allies use Draco's Time-Turner to travel back in time to save them and stop Delphi. While waiting for Delphi, they deduce she intends to convince Voldemort to abandon his doomed attempt to kill Harry, ensuring her father's survival and allowing her to be with him.

text: Harry disguises himself as Voldemort using Transfiguration to distract Delphi, and after a struggle, the group manages to subdue her. Rather than killing Delphi, it is decided that she will be brought to Azkaban Prison. Lord Voldemort then appears and is oblivious to the presence of Harry and the group. The group allows the murder of Harry's parents to play out again, unwilling to risk the consequences of altering the past.

text: They all stand with Harry to watch the sad event replay. After returning to the present day, Delphi is sent to Azkaban. Albus and Scorpius now decide to be more active at Hogwarts, with Scorpius expressing interest in trying out for Quidditch and asking Rose on a date. Harry and Albus visit Cedric's grave, with Harry apologizing for his role in Cedric's death. Albus has also witnessed the death of a fellow student Craig Bowker Jr (the only current timeline murder in the play), who tried to intervene when Delphi held Albus and Scorpius captive on the Quidditch pitch.

text: Background[edit]

text: In December 2013, it was revealed that a stage play based on Harry Potter had been in development for around a year,[3] with the view to bringing it to the stage sometime in 2016.[4] At the time of the announcement, Rowling revealed that the play would "explore the previously untold story of Harry's early years as an orphan and outcast".[5] The following May, Rowling began establishing the creative team for the project.[6]

text: On 26 June 2015, the project was officially confirmed under the title of Harry Potter and the Cursed Child,[7] and it was revealed it would receive its world premiere in mid-2016 at London's Palace Theatre.[8] The announcement marked the eighteenth anniversary of the publication of the first Harry Potter novel, Harry Potter and the Philosopher's Stone,[9] published on 26 June 1997.[10]

text: On announcing plans for the project, Rowling stated that the play would not be a prequel.[11] In response to queries regarding the choice of a play rather than a new novel, Rowling has stated that she "is confident that when audiences see the play they will agree that it is the only proper medium for the story".[12] Rowling has also assured audiences that the play will contain an entirely new story and will not be a rehashing of previously explored content.[13] On 24 September 2015, Rowling announced that the play had been split into two parts.[14] The parts are designed to be viewed on the same day or consecutively over two evenings.[15][16]

text: On 23 October 2015, it was confirmed the plays were set nineteen years after the conclusion of the final novel Harry Potter and the Deathly Hallows,[17] and would open at London's Palace Theatre in July 2016.[18] The plays principally follow Harry, now Head of the Department of Magical Law Enforcement, and his younger son Albus Severus Potter.[19] As of 22 July 2016, little more had been revealed about the plot even by those who had attended the previews since 7 June.[20]

text: #KeepTheSecrets[edit]

text: The producers, and Rowling, have maintained a campaign called #KeepTheSecrets, to ask people who have seen the play not to reveal its major twists. The slogan is printed on the tickets for the play and badges with the slogan are handed out for free during intervals. People buying their tickets online are emailed a video after the play from J.K. Rowling asking to support the campaign.[21]

text: Productions[edit]

text: Harry Potter and the Cursed Child, a two-part play, was written by British playwright Jack Thorne based on an original story by Thorne, John Tiffany and Rowling. Some websites were listing all three as authors of the script[22] but by 26 July 2016, the official web site for the play[23] and many others (including the BBC)[24] were listing Thorne as the sole script writer.

text: Harry Potter and the Cursed Child is directed by John Tiffany[25][26] with choreography by Steven Hoggett,[27] set design by Christine Jones,[28] costume design by Katrina Lindsay,[29] lighting design by Neil Austin,[30] music by Imogen Heap,[31] and sound design by Gareth Fry.[32] In addition, special effects were created by Jeremy Chernick,[33] with illusions by Jamie Harrison, and musical supervision by Martin Lowe.[34]

text: West End[edit]

text: Previews at the West End Palace Theatre, London began on 7 June 2016,[2] with the official opening night for both parts on 30 July,[35] and originally booking until 18 September 2016.[36] Tickets went on sale to pre-registered priority bookers on 28 October 2015, with a public sale scheduled to commence on 30 October.[37] In just under 8 hours of priority booking 175,000 tickets were sold for the world premiere production,[38] with the play's booking period extended to January 2017.[39] On commencement of the public sale booking was extended until 30 April 2017,[40] with a further extension issued the same day to 27 May 2017.[41]

text: Tickets for the opening performance were priced from £30 up to £130 for a ticket for both parts,[42] although ticket resale agencies were selling seats for up to £3,000.[38] Ticket resale has been banned by the producers, with tickets no longer valid if sold on.[43] In mid-July 2016, the theatre began holding a ticket lottery at 1 pm each Friday, releasing 40 for sale on their website for “some of the best seats” in the theatre for the lowest price, advertised at £20 per part. For example, the "Friday Forty" tickets sold on 29 July 2016 were for performances on 3, 5, 6, and 7 August.[44]

text: On 20 December 2015, initial casting was announced with Jamie Parker playing Harry Potter, Noma Dumezweni playing Hermione Granger and Paul Thornley playing Ron Weasley.[45][46][47] The casting of the dark-skinned Noma Dumezweni as Hermione sparked fervent discussion, to which Rowling responded that Hermione's skin was never specified as white.[48][49] Further notable casting includes Poppy Miller as Ginny Potter, Alex Price as Draco Malfoy, Sam Clemmett as Albus Severus Potter and Anthony Boyle as Scorpius Malfoy.[50] The production features an overall cast of 42.[51][52]

text: Broadway[edit]

text: The production began previews on 16 March 2018 and opened on 22 April 2018 at the Lyric Theatre. Clemmett, Boyle, Dumezweni, Miller, Parker, Price and Thornley reprised their roles.[53][54] The theatre removed 400 seats from the auditorium and moved the entrance to 43rd Street[55]. The production is produced by Sonia Friedman Productions, Sir Colin Callender, and Harry Potter Theatrical Productions. The initial ticket block went on sale through Ticketmaster Verified Fan on 18 October 2017 for performances from 16 March through 18 November 2018.[56] The New York Times estimates that it is the most expensive non-musical Broadway play ever, incurring $68 million in opening costs.[57]

text: Melbourne[edit]

text: On 24 October 2017, the Michael Cassel Group announced that it will be producing the Australian premiere of Harry Potter and the Cursed Child. The production will begin performances early 2019 in Melbourne's Princess Theatre.[58] No casting or ticketing information has been announced.

text: Cast and principal roles[edit]

text:
Character
Original West End Cast[59]
(2016–2017)
Original Broadway Cast[60]
(2018)

Harry Potter
Jamie Parker

Ron Weasley
Paul Thornley

Hermione Granger
Noma Dumezweni

Ginny Potter
Poppy Miller

Draco Malfoy
Alex Price

Albus Severus Potter
Sam Clemmett

Scorpius Malfoy
Anthony Boyle

Rose Granger-Weasley
Cherrelle Skeete
Susan Heyward

Young Hermione

Delphi Diggory
Esther Smith
Jessie Fisher

Craig Bowker Jr.
Jeremy Ang Jones
Joshua DeJesus

Moaning Myrtle
Annabel Baldwin
Lauren Nicole Cipoletti

Lily Potter Sr.

Polly Chapman
Claudia Grant
Madeline Weinstein

Vernon Dursley
Paul Bentall
Byron Jennings

Severus Snape

Lord Voldemort

Rubeus Hagrid
Chris Jarman
Brian Abraham

Sorting Hat

Yann Fredericks
James Le Lacheur
Jess Barbagallo

Petunia Dursley
Helena Lymbery
Kathryn Meisle

Madam Hooch

Dolores Umbridge

Amos Diggory
Barry McCarthy
Edward James Hyland

Albus Dumbledore

Trolley Witch
Sandy McDade
Geraldine Hughes

Minerva McGonagall

Cedric Diggory
Tom Milligan
Benjamin Wheelwright

James Sirius Potter

James Potter Sr.

Dudley Dursley
Jack North
Joey LaBrasca

Karl Jenkins

Viktor Krum

Bane
Nuno Silva
David St. Louis

Young Harry Potter
Rudi Goodman
Alfred Jones
Bili Keogh
Ewan Rutherford
Nathaniel Smith
Dylan Standen
Will Coombs
Landon Maas

Lily Luna Potter
Zoe Brough
Cristina Fray
Christiana Hutchings
Olivia Bond
Brooklyn Shuck

text: West End cast replacements[edit]

text: This section needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (July 2017) (Learn how and when to remove this template message)

text: In May 2017, Jamie Glover took over from Jamie Parker as Harry Potter, while Emma Lowndes will play his wife Ginny Potter. Thomas Aldridge is to play Ron Weasley, replacing Paul Thornley, while Rakie Ayola will play Hermione Granger, replacing Noma Dumezweni. Annabel Baldwin, previously playing Moaning Myrtle will take over from Esther Smith as Delphi.

text: Original cast members Helen Aluko and James Howard play Rose Granger-Weasley and Draco Malfoy respectively. Samuel Blenkin and Theo Ancient made their professional debut, playing Scorpius Malfoy and Albus Potter, respectively.

text: The lead cast are joined by new cast members David Annen, Ruthxjiah Bellenea, Danny Dalton, Leah Haile, Rupert Henderson, Elizabeth Hill, April Hughes, James McGregor, Sarah Miele, Jordan Paris, James Phoon, Henry Rundle, Ged Simmons, Mark Theodore, Gideon Turner and Ed White.

text: Original cast members who will continue include Nicola Alexis, Rosemary Annabella, Phoebe Austen, Annabel Baldwin, Jabez Cheeseman, Morag Cross, Esme Grace, Lowri James, Martin Johnston, Alfred Jones, Barry McCarthy, Sandy McDade, Tom Mackley, Harrison Noble, Ben Roberts, Nuno Silva, Hope Sizer and Joshua Wyatt.

text: The second cast took over on 24 May 2017, with the original cast having their final performance on 21 May 2017.[61]

text: The third cast took over on 23 May 2018.

text: Script publication[edit]

text: Editions[edit]

text:
Harry Potter and the Cursed Child

Special Rehearsal Edition cover

Author
Jack Thorne (script)
J. K. Rowling, John Tiffany & Jack Thorne (story)

Country
United Kingdom

Language
English

Series
Harry Potter

Genre
Fantasy, Drama

Published
31 July 2016 (Special Rehearsal Edition)
25 July 2017 (Definitive Collector's Edition)

Publisher

Little, Brown and Company (UK)
Scholastic (US)
Pottermore (digital)

Publication date

31 July 2016

Pages
328 (Special Rehearsal Edition)
321 (Definitive Collector's Edition)

ISBN
978-1-338-09913-3 (US); 978-0-7515-6535-5 (UK)

text: Both parts of the stage play's script have been released in print and digital formats as Harry Potter and the Cursed Child Parts I & II.[62][63]

text: The first edition, entitled "Special Rehearsal Edition", corresponded to the script used in the preview shows and was scheduled to be published on 31 July 2016,[64] the date of Harry's birthday in the series and Rowling's birthday, as well.[65] Since revisions to the script continued after the book was printed, an edited version was released on 25 July 2017, as the "Definitive Collector's Edition".[66] According to CNN, this was the most preordered book of 2016.[67]

text: Sales[edit]

text: In the United States and Canada, the book sold over 2 million copies in its first two days of release.[68] 847,885 copies were sold during the book's first week of release in the United Kingdom. By June 2017, the book had sold over 4.5 million copies in the United States.[69]

text: Critical reception[edit]

text: Harry Potter and the Cursed Child has received critical acclaim. Audiences and critics have complimented the casting and performances, while many debate the quality of the piece and how it compares to entries in the main Harry Potter series.

text: Publications awarding five star ratings included The Independent, the London Evening Standard, The Stage and WhatsOnStage.com.[70][71][72][73] The Telegraph also gave five, although "there are some quibbles," while The Guardian's Michael Billington awarded four stars.[74][75]

text: Anthony Boyle's performance as Scorpius Malfoy garnered particular acclaim. WhatsOnStage.com wrote that "Boyle gives a career-making performance," while The Wall Street Journal described him as "the break-out performance".[73][76] Variety's critic, Matt Trueman, agreed, writing, "it's Boyle who really stands out", and both Trueman and Henry Hitchings, in the Evening Standard, noted that his performance was sure to be a fan favourite.[71][77]

text: Response within the Harry Potter fandom[edit]

text: The response to the play from the Harry Potter fandom was mixed. Some fans said the story seemed "like a work of fan fiction" and claimed that it diverged from previously established rules of the universe, criticising the script's characterisation.[78][79][80] Some also took issue with the style and plot of the script, complaining that the Time-Turner storylines had already been used, as had Cedric Diggory's death, and that the writers were rehashing old storylines.[81][82] These criticisms have led some of the fandom to reject the play as separate from the Potter canon.[83] Some potential “plot holes” in the story have been highlighted, such as the likelihood of Lord Voldemort's infertility, the speed at which Polyjuice Potion is created, the unexplained non-operation of the Fidelius Charm,[84][85] and Cedric Diggory's dramatic turn to becoming a Death Eater.[86][87]

text: However, some fans responded positively to the play and its characters, with Scorpius Malfoy being particularly popular.[88] Some fans commented that the dialogue between the familiar characters was "spot on",[89] celebrating it as a faithful continuation of the books.[90][91] Others have noted that the play sheds light on some of the relationships between the characters, such as Harry and Dumbledore's.[92] The response had been particularly positive among fans who watched the play on stage.[93]

text: Who is the Cursed Child?[edit]

text: The play never explicitly states who the "Cursed Child" is. There are several possible answers, including Delphi who is cursed by her parentage, Harry himself whose difficult childhood is the subject of several flashbacks in the play and who must accept and relive the death of his parents to conquer Lord Voldemort, Albus who at one stage Harry says he wished "was not his son" and can do no right in this father's eyes being "cursed" by the Potter reputation, Scorpius who is rumoured to be Lord Voldemort's child and whose mother dies during the play, and Cedric Diggory whose tragic death is a focus of the play, and whose death is also finally accepted as a necessary condition for future peace.[94]

text: Awards and nominations[edit]

text: Original London Production[edit]

text:
Year
Award Ceremony
Category
Nominee
Result

2016
Evening Standard Theatre Awards
Best Play
Won

Best Director
John Tiffany
Nominated

Best Design
Christine Jones
Nominated

Emerging Talent Award
Anthony Boyle
Nominated

Critics' Circle Theatre Awards
Best Director
John Tiffany
Won

Best Designer
Christine Jones
Won

Most Promising Newcomer
Anthony Boyle
Won

2017
WhatsOnStage Awards
Best New Play
Won

Best Actor in a Play
Jamie Parker
Won

Best Supporting Actor in a Play
Anthony Boyle
Won

Paul Thornley
Nominated

Best Supporting Actress in a Play
Poppy Miller
Nominated

Noma Dumezweni
Won

Best Direction
John Tiffany
Won

Best Costume Design
Katrina Lindsay
Nominated

Best Set Design
Christine Jones
Won

Best Lighting Design
Neil Austin
Won

Best Video Design
Finn Ross and Ash Woodward
Won

Laurence Olivier Awards
Best New Play
Won

Best Director
John Tiffany
Won

Best Actor
Jamie Parker
Won

Best Actress in a Supporting Role
Noma Dumezweni
Won

Best Actor in a Supporting Role
Anthony Boyle
Won

Best Costume Design
Katrina Lindsay
Won

Best Set Design
Christine Jones
Won

Best Sound Design
Gareth Fry
Won

Best Lighting Design
Neil Austin
Won

Best Theatre Choreographer
Steven Hoggett
Nominated

Outstanding Achievement in Music
Imogen Heap
Nominated

2018
WhatsOnStage Awards
Best West End Show
Won

Best Show Poster
Won

text: Original Broadway production[edit]

text:
Year
Award
Category
Nominee
Result
Ref.

2018
Tony Awards
Best Play
Won
[95][96]

Best Actor in a Play
Jamie Parker
Nominated

Best Featured Actor in a Play
Anthony Boyle
Nominated

Best Featured Actress in a Play
Noma Dumezweni
Nominated

Best Direction of a Play
John Tiffany
Won

Best Choreography
Steven Hoggett
Nominated

Best Scenic Design in a Play
Christine Jones
Won

Best Costume Design in a Play
Katrina Lindsay
Won

Best Lighting Design in a Play
Neil Austin
Won

Best Sound Design in a Play
Gareth Fry
Won

Drama Desk Awards
Outstanding Featured Actor in a Play
Anthony Boyle
Nominated
[97]

Outstanding Director of a Play
John Tiffany
Won

Outstanding Music in a Play
Imogen Heap
Won

Outstanding Costume Design for a Play
Katrina Lindsay
Nominated

Outstanding Lighting Design for a Play
Neil Austin
Won

Outstanding Projection Design
Finn Ross and Ash Woodward
Won

Outstanding Sound Design in a Play
Gareth Fry
Won

Outstanding Wig and Hair
Carole Hancock
Nominated

Outer Critics Circle Awards
Outstanding New Broadway Play
Won
[98]

Outstanding Featured Actor in a Play
Anthony Boyle
Nominated

Outstanding New Score (Broadway or Off-Broadway)
Imogen Heap
Nominated

Outstanding Director of a Play
John Tiffany
Won

Outstanding Choreographer
Steven Hoggett
Nominated

Outstanding Scenic Design (Play or Musical)
Christine Jones
Won

Outstanding Costume Design (Play or Musical)
Katrina Lindsay
Nominated

Outstanding Lighting Design (Play or Musical)
Neil Austin
Won

Outstanding Projection Design (Play or Musical)
Finn Ross and Ash Woodward
Won

Outstanding Sound Design (Play or Musical)
Gareth Fry
Won

Drama League Awards
Outstanding Production of a Broadway or Off-Broadway Play
Won
[99]

Distinguished Performance Award
Anthony Boyle
Nominated

Noma Dumezweni
Nominated