Wheat yellow rust ("Puccinia striiformis" f.sp. "tritici"), also known as stripe rust, is one of the three wheat rust diseases principally found in wheat grown in cooler environments. Such locations are generally associated with northern latitudes or cooler seasons.

As R.P. Singh, J. Huerta-Espino, and A.P. Roelfs say in their (undated) comprehensive review of literature on the wheat rusts for UN FAO:

"Although Gadd first described stripe rust of wheat in 1777, it was not until 1896 that Eriksson and Henning (1896) showed that stripe rust resulted from a separate pathogen, which they named P. glumarum. In 1953, Hylander et al. (1953) revived the name P. striiformis."

Leaf rust is a fungal disease of barley caused by "Puccinia hordei". It is also known as brown rust and it is the most important rust disease on barley.

Velvet disease (also called gold-dust, rust and coral disease) is a fish disease caused by dinoflagellate parasites of the genus "Piscinoodinium", specifically "Amyloodinium" in marine fish, and "Oodinium" in freshwater fish. The disease gives infected organisms a dusty, brownish-gold color. The disease occurs most commonly in tropical fish, and to a lesser extent, marine aquaria.

Pustules of leaf rust are small and circular, producing a mass of orange-brown powdery spores. They appear on the leaf sheaths and predominantly on the upper leaf surfaces. Heavily infected leaves die prematurely.

The single-celled parasite's life cycle can be divided into three major phases. First, as a tomont, the parasite rests at the water's floor and divides into as many as 256 tomites. Second, these juvenile, motile tomites swim about in search of a fish host, meanwhile using photosynthesis to grow, and to fuel their search. Finally, the adolescent tomite finds and enters the slime coat of a host fish, dissolving and consuming the host's cells, and needing only three days to reach full maturity before detaching to become a tomont once more.

Citrus Black Spot is a fungal disease caused by Guignardia citricarpa. This Ascomycete fungus affects citrus plants throughout subtropical climates, causing a reduction in both fruit quantity and quality. Symptoms include both fruit and leaf lesions, the latter being critical to inter-tree dispersal. Strict regulation and management is necessary to control this disease since there are currently no citrus varieties that are resistant.

False melanose lesions are characterized by many small, tan, slightly raised lesions. The lesions are much smaller than the hard spot variety with an average diameter of less than 1 mm (.04 in).

They are found on unripe fruit and are difficult to observe later in the season. Unlike hard spot lesions, no pycnidia are present.

An early sign in several animals including cattle, sheep, and guinea pigs is listlessness, which is commonly followed by significant loss of weight and pronounced trembling in the legs and muzzle. These signs often appear several hours after ingestion of white snakeroot. Signs of abdominal pain, polydipsia, and vomiting may be noted. As the effects of the poison progress, signs of constipation, appetite loss, weakness, and difficulty standing and/or walking are usually observed. Complete loss of muscle coordination, stupor, and/or coma precede death. Death usually occurs within 2-10 days of symptom onset. Signs unique to cattle and sheep include peculiar odors found in the breath and urine, breathing difficulties, and over-salivation. Symptoms unique to horses include depression, bloody urine, and choking. In addition to increased heart rate and jugular pulse, swelling around the thoracic inlet in also observed. Horses may also stand with their hind legs wide apart. Symptoms unique to guinea pigs include crouching with half-closed eyes and roughening of the hair. Treatment for milk sickness is typically symptom amelioration, as well as administration of laxatives, sodium lactate, glucose, or hypotonic Ringer’s solution.

Verticillium wilt is a wilt disease of over 350 species of eudicot plants caused by six species of Verticillium genus, "V. dahliae", "V. albo-atrum", "V. longisporum", V. nubilum, V. theobromae and

V. tricorpus. (See, for example, Barbara, D.J. & Clewes, E. (2003). "Plant pathogenic Verticillium species: how many of them are there?" Molecular Plant Pathology 4(4).297-305. Blackwell Publishing.) Many economically important plants are susceptible including cotton, tomatoes, potatoes, oilseed rape, eggplants, peppers and ornamentals, as well as others in natural vegetation communities. Many eudicot species and cultivars are resistant to the disease and all monocots, gymnosperms and ferns are immune.

Symptoms are superficially similar to "Fusarium" wilts. There is no chemical control for the disease but crop rotation, the use of resistant varieties and deep plowing may be useful in reducing the spread and impact of the disease.

"Verticillium" spp. attack a very large host range including more than 350 species of vegetables, fruit trees, flowers, field crops, and shade or forest trees. Most vegetable species have some susceptibility, so it has a very wide host range. A list of known hosts is at the bottom of this page.

The symptoms are similar to most wilts with a few specifics to "Verticillium". Wilt itself is the most common symptom, with wilting of the stem and leaves occurring due to the blockage of the xylem vascular tissues and therefore reduced water and nutrient flow. In small plants and seedlings, "Verticillium" can quickly kill the plant while in larger, more developed plants the severity can vary. Some times only one side of the plant will appear infected because once in the vascular tissues, the disease migrates mostly upward and not as much radially in the stem. Other symptoms include stunting, chlorosis or yellowing of the leaves, necrosis or tissue death, and defoliation. Internal vascular tissue discoloration might be visible when the stem is cut.

In "Verticillium", the symptoms and effects will often only be on the lower or outer parts of plants or will be localized to only a few branches of a tree. In older plants, the infection can cause death, but often, especially with trees, the plant will be able to recover, or at least continue living with the infection. The severity of the infection plays a large role in how severe the symptoms are and how quickly they develop.

Milk sickness, also known as tremetol vomiting or, in animals, as trembles, is a kind of poisoning, characterized by trembling, vomiting, and severe intestinal pain, that affects individuals who ingest milk, other dairy products, or meat from a cow that has fed on white snakeroot plant, which contains the poison tremetol.

Although very rare today, milk sickness claimed thousands of lives among migrants to the Midwest in the early 19th century in the United States, especially in frontier areas along the Ohio River Valley and its tributaries where white snakeroot was prevalent. New settlers were unfamiliar with the plant and its properties. A notable victim was Nancy Hanks Lincoln, the mother of Abraham Lincoln, who died in 1818. Nursing calves and lambs may have died from their mothers' milk contaminated with snakeroot, although the adult cows and sheep showed no signs of poisoning. Cattle, horses, and sheep are the animals most often poisoned.

Anna Pierce Hobbs Bixby, called Dr. Anna on the frontier, is credited today by the American medical community with having identified white snakeroot as the cause of the illness. Told about the plant's properties by an elderly Shawnee woman she befriended, Bixby did testing to observe and document evidence. She wrote up her findings to share the discovery in the medical world. The Shawnee woman's name has been lost to history.

Although many people with a defective AMPD gene are asymptomatic, others may have symptoms such as exercise intolerance, muscle pain, and muscle cramping.

- Fatigue

- MADD lowers aerobic power output, so increased anaerobic power is needed to perform the same amount of work.

- Without myoadenlyate deaminase, heavy activity causes adenosine to be released into the cell or perfused into the surrounding tissues. Fatigue and sedation after heavy exertion can be caused by excess adenosine in the cells which signals muscle fiber to feel fatigued. In the brain, excess adenosine decreases alertness and causes sleepiness. In this way, adenosine may play a role in fatigue from MADD.

- Recovery from over-exertion can be hours, days or even months. In cases of rhabdomyolysis, which is the rapid breakdown of muscle fibers, time to recovery is dependent on duration and intensity of original activity plus any excess activity during the recovery period.

- Muscle pain

- Muscle pain from MADD is not well understood, but is partially due to high levels of lactate. Increased levels of free adenosine temporarily decrease pain, allowing over-exertion without awareness. The over exertion can cause mild to severe cases of rhabdomyolysis, which is painful.

- Adenosine mediates pain through adenosine receptors. MADD causes an increase of free adenosine during heavy activity which may cause exercise-induced muscle pain. Over time, excess free adenosine down-regulates primary A1 adenosine receptors, leading to increased muscle pain. Secondary receptors (A3) increase peripheral inflammation, which also increases pain.

- Muscle cramping

- The cause of cramping is unknown, but may be related to elevated lactate, increased calcium signaling across the sarcoplasmic reticulum caused by membrane instability from reduced levels of ATP, or increased levels of free adenosine.

- Muscle weakness

- Muscle weakness is not a major symptom, though the progressive effects of chronic muscle damage from rhabdomyolysis will eventually cause significant weakness. Similarly, the long-term metabolic effects may result in nerve damage.

Kuru, a transmissible spongiform encephalopathy, is a disease of the nervous system that causes physiological and neurological effects which ultimately lead to death. It is characterized by progressive cerebellar ataxia, or loss of coordination and control over muscle movements.

The preclinical or asymptomatic phase, also called the incubation period, averages between 10–13 years, but can be as short as 5 and has been estimated to last as long as 50 years or more after initial exposure. The youngest individual recorded to have kuru was 12 years old.

The clinical stage, which begins at the first onset of symptoms, lasts an average of 12 months. The clinical progression of kuru is divided into three specific stages, the ambulant, sedentary and terminal stages. While there is some variation in these stages between individuals, they are highly conserved among the affected population. Before the onset of clinical symptoms, an individual can also present with prodromal symptoms including headache and joint pain in the legs.

In the first (ambulant) stage, the infected individual may exhibit unsteady stance and gait, decreased muscle control, tremors, difficulty pronouncing words (dysarthria), and titubation. This stage is named the ambulant because the individual is still able to walk around despite symptoms.

In the second (sedentary) stage, the infected individual is incapable of walking without support and suffers ataxia and severe tremors. Furthermore, the individual shows signs of emotional instability and depression, yet exhibits uncontrolled and sporadic laughter. Despite the other neurological symptoms, tendon reflexes are still intact at this stage of the disease.

In the third and final (terminal) stage, the infected individual’s existing symptoms, like ataxia, progress to the point where they are no longer capable of sitting without support. New symptoms also emerge: the individual develops dysphagia, or difficulty swallowing, which can lead to severe malnutrition. They may also become incontinent, lose the ability to speak and become unresponsive to their surroundings, despite maintaining consciousness. Towards the end of the terminal stage patients often develop chronic ulcerated wounds that can be easily infected. An infected person usually dies within three months to two years after the first terminal stage symptoms, often because of pneumonia or infection.

Adenosine monophosphate deaminase deficiency type 1, also called myoadenylate deaminase deficiency (MADD), is a recessive genetic metabolic disorder that affects approximately 1–2% of populations of European descent. It appears to be considerably rarer in Asian populations. The genetic form is caused by a defect in the gene for AMP deaminase though there is also an acquired form of AMP deficiency.

In Chinese alchemy, elixir poisoning refers to the toxic effects from elixirs of immortality that contained metals and minerals such as mercury and arsenic. The official "Twenty-Four Histories" record numerous Chinese emperors, nobles, and officials who ironically died from taking elixirs in order to prolong their lifespans. The first emperor to die from elixir poisoning was likely Qin Shi Huang (d. 210 BCE) and the last was Yongzheng (d. 1735). Despite common knowledge that immortality potions could be deadly, fangshi and Daoist alchemists continued the elixir-making practice for two millennia.

Kuru is a very rare, incurable neurodegenerative disorder that was formerly common among the Fore people of Papua New Guinea. Kuru is caused by the transmission of abnormally folded prion proteins, which leads to symptoms such as tremors, loss of coordination, and neurodegeneration.

The term kuru derives from the Fore word kuria or guria ("to shake"), due to the body tremors that are a classic symptom of the disease and kúru itself means "trembling". It is also known as the "laughing sickness" due to the pathologic bursts of laughter which are a symptom of the disease. It is now widely accepted that kuru was transmitted among members of the Fore tribe of Papua New Guinea via funerary cannibalism. Deceased family members were traditionally cooked and eaten, which was thought to help free the spirit of the dead. Females and children usually consumed the brain, the organ in which infectious prions were most concentrated, thus allowing for transmission of kuru. The disease was therefore more prevalent among women and children.

While the Fore people stopped eating human meat in the early 1960's, when it was first speculated to be transmitted via endocannibalism, the disease lingered due to kuru’s long incubation period of anywhere from 10 to over 50 years. The epidemic declined sharply after discarding cannibalism, from 200 deaths per year in 1957 to 1 or no deaths annually in 2005, with sources disagreeing on whether the last known kuru victim died in 2005 or 2009.

The lesions are most frequent on the lower limbs, but may occur anywhere on the body, including the hands, arms, torso and even the neck. They may vary in number and erupt in mass numbers.

They consist of irregular patches of orange or brown pigmentation with characteristic "cayenne pepper" spots appearing within and at the edge of old lesions.

There are usually no symptoms, although there may be some slight itching, but there is no pain.

The eruption may persist for many years. The pattern of the eruption changes, with slow extension and often some clearing of the original lesions.

Schamberg's disease, or progressive pigmented purpuric dermatitis, is a chronic discoloration of the skin which usually affects the legs and often spreads slowly. This disease is more common in males and may occur at any age from childhood onward. This condition is observed worldwide and has nothing to do with race or ethnic background.

The muscle weakness of botulism characteristically starts in the muscles supplied by the cranial nerves—a group of twelve nerves that control eye movements, the facial muscles and the muscles controlling chewing and swallowing. Double vision, drooping of both eyelids, loss of facial expression and swallowing problems may therefore occur. In addition to affecting the voluntary muscles, it can also cause disruptions in the autonomic nervous system. This is experienced as a dry mouth and throat (due to decreased production of saliva), postural hypotension (decreased blood pressure on standing, with resultant lightheadedness and risk of blackouts), and eventually constipation (due to decreased forward movement of intestinal contents). Some of the toxins (B and E) also precipitate nausea, vomiting, and difficulty with talking. The weakness then spreads to the arms (starting in the shoulders and proceeding to the forearms) and legs (again from the thighs down to the feet).

Severe botulism leads to reduced movement of the muscles of respiration, and hence problems with gas exchange. This may be experienced as dyspnea (difficulty breathing), but when severe can lead to respiratory failure, due to the buildup of unexhaled carbon dioxide and its resultant depressant effect on the brain. This may lead to respiratory compromise and death if untreated.

Clinicians frequently think of the symptoms of botulism in terms of a classic triad: bulbar palsy and descending paralysis, lack of fever, and clear senses and mental status ("clear sensorium").

Irritant contact dermatitis is a form of contact dermatitis that can be divided into forms caused by chemical irritants and those caused by physical irritants.

Schamberg's disease, (also known as "progressive pigmentary dermatosis of Schamberg", "purpura pigmentosa progressiva" (PPP), and "Schamberg's purpura") is a chronic discoloration of the skin found in people of all ages, usually affecting the legs. It slowly spreads throughout the body, and is most common in males. It is named after Jay Frank Schamberg, who described it in 1901. There is no known cure for this disease and it is not a life-threatening condition. The skin lesions may cause itching, which can be treated by applying cortisone cream. The cortisone cream will only help with the itching and the discoloration of the skin will remain, which may cause a cosmetic concern in the future. Schamberg's disease is usually asymptomatic meaning that it shows no signs of this condition, except for the discoloration of the skin. This condition is caused by leaky blood vessels, where red blood cells escape near the surface of skin and release its iron into the surrounding tissue. The cause of the leaky capillaries is unknown.

Botulism is a rare and potentially fatal illness caused by a toxin produced by the bacterium "Clostridium botulinum". The disease begins with weakness, blurred vision, feeling tired, and trouble speaking. This may then be followed by weakness of the arms, chest muscles, and legs. The disease does not usually affect consciousness or cause a fever.

Botulism can be spread in several different ways. The bacterial spores which cause it are common in both soil and water. They produce the botulinum toxin when exposed to low oxygen levels and certain temperatures. Foodborne botulism happens when food containing the toxin is eaten. Infant botulism happens when the bacteria develops in the intestines and releases the toxin. This typically only occurs in children less than six months old, as protective mechanisms develop after that time. Wound botulism is found most often among those who inject street drugs. In this situation, spores enter a wound, and in the absence of oxygen, release the toxin. It is not passed directly between people. The diagnosis is confirmed by finding the toxin or bacteria in the person in question.

Prevention is primarily by proper food preparation. The toxin, though not the organism, is destroyed by heating it to more than for longer than 5 minutes. Honey can contain the organism, and for this reason, honey should not be fed to children under 12 months. Treatment is with an antitoxin. In those who lose their ability to breathe on their own, mechanical ventilation may be necessary for months. Antibiotics may be used for wound botulism. Death occurs in 5 to 10% of people. Botulism also affects many other animals. The word is from Latin, "botulus", meaning sausage. Early descriptions of botulism date from at least as far back as 1793 in Germany.

Signs and symptoms of macular degeneration include:

- Visual symptoms

- Distorted vision in the form of metamorphopsia, in which a grid of straight lines appears wavy and parts of the grid may appear blank: Patients often first notice this when looking at things like miniblinds in their home or telephone poles while driving. There may also be central scotomas, shadows or missing areas of vision

- Slow recovery of visual function after exposure to bright light (photostress test)

- Visual acuity drastically decreasing (two levels or more), e.g.: 20/20 to 20/80

- Blurred vision: Those with nonexudative macular degeneration may be asymptomatic or notice a gradual loss of central vision, whereas those with exudative macular degeneration often notice a rapid onset of vision loss (often caused by leakage and bleeding of abnormal blood vessels).

- Trouble discerning colors, specifically dark ones from dark ones and light ones from light ones

- A loss in contrast sensitivity

Macular degeneration by itself will not lead to total blindness. For that matter, only a very small number of people with visual impairment are totally blind. In almost all cases, some vision remains, mainly peripheral. Other complicating conditions may possibly lead to such an acute condition (severe stroke or trauma, untreated glaucoma, etc.), but few macular degeneration patients experience total visual loss.

The area of the macula comprises only about 2.1% of the retina, and the remaining 97.9% (the peripheral field) remains unaffected by the disease. Even though the macula provides such a small fraction of the visual field, almost half of the visual cortex is devoted to processing macular information.

The loss of central vision profoundly affects visual functioning. It is quite difficult, for example, to read without central vision. Pictures that attempt to depict the central visual loss of macular degeneration with a black spot do not really do justice to the devastating nature of the visual loss. This can be demonstrated by printing letters six inches high on a piece of paper and attempting to identify them while looking straight ahead and holding the paper slightly to the side. Most people find this difficult to do.

Malnutrition is a condition that results from eating a diet in which nutrients are either not enough or are too much such that the diet causes health problems. It may involve calories, protein, carbohydrates, vitamins or minerals. Not enough nutrients is called undernutrition or undernourishment while too much is called overnutrition. Malnutrition is often used to specifically refer to undernutrition where an individual is not getting enough calories, protein, or micronutrients. If undernutrition occurs during pregnancy, or before two years of age, it may result in permanent problems with physical and mental development. Extreme undernourishment, known as starvation, may have symptoms that include: a short height, thin body, very poor energy levels, and swollen legs and abdomen. People also often get infections and are frequently cold. The symptoms of micronutrient deficiencies depend on the micronutrient that is lacking.

Undernourishment is most often due to not enough high-quality food being available to eat. This is often related to high food prices and poverty. A lack of breastfeeding may contribute, as may a number of infectious diseases such as: gastroenteritis, pneumonia, malaria, and measles, which increase nutrient requirements. There are two main types of undernutrition: protein-energy malnutrition and dietary deficiencies. Protein-energy malnutrition has two severe forms: marasmus (a lack of protein and calories) and kwashiorkor (a lack of just protein). Common micronutrient deficiencies include: a lack of iron, iodine, and vitamin A. During pregnancy, due to the body's increased need, deficiencies may become more common. In some developing countries, overnutrition in the form of obesity is beginning to present within the same communities as undernutrition. Other causes of malnutrition include anorexia nervosa and bariatric surgery.

Efforts to improve nutrition are some of the most effective forms of development aid. Breastfeeding can reduce rates of malnutrition and death in children, and efforts to promote the practice increase the rates of breastfeeding. In young children, providing food (in addition to breastmilk) between six months and two years of age improves outcomes. There is also good evidence supporting the supplementation of a number of micronutrients to women during pregnancy and among young children in the developing world. To get food to people who need it most, both delivering food and providing money so people can buy food within local markets are effective. Simply feeding students at school is insufficient. Management of severe malnutrition within the person's home with ready-to-use therapeutic foods is possible much of the time. In those who have severe malnutrition complicated by other health problems, treatment in a hospital setting is recommended. This often involves managing low blood sugar and body temperature, addressing dehydration, and gradual feeding. Routine antibiotics are usually recommended due to the high risk of infection. Longer-term measures include: improving agricultural practices, reducing poverty, improving sanitation, and the empowerment of women.

There were 793 million undernourished people in the world in 2015 (13% of the total population). This is a reduction of 216 million people since 1990 when 23% were undernourished. In 2012 it was estimated that another billion people had a lack of vitamins and minerals. In 2015, protein-energy malnutrition was estimated to have resulted in 323,000 deaths—down from 510,000 deaths in 1990. Other nutritional deficiencies, which include iodine deficiency and iron deficiency anemia, result in another 83,000 deaths. In 2010, malnutrition was the cause of 1.4% of all disability adjusted life years. About a third of deaths in children are believed to be due to undernutrition, although the deaths are rarely labelled as such. In 2010, it was estimated to have contributed to about 1.5 million deaths in women and children, though some estimate the number may be greater than 3 million. An additional 165 million children were estimated to have stunted growth from malnutrition in 2013. Undernutrition is more common in developing countries. Certain groups have higher rates of undernutrition, including women—in particular while pregnant or breastfeeding—children under five years of age, and the elderly. In the elderly, undernutrition becomes more common due to physical, psychological, and social factors.

The etymology of English elixir derives from Medieval Latin "", from Arabic ("al-ʾiksīr"), probably from Ancient Greek ("xḗrion" "a desiccative powder for wounds"). "Elixir" originated in medieval European alchemy meaning "A preparation by the use of which it was sought to change metals into gold" (elixir stone or philosopher's stone) or "A supposed drug or essence with the property of indefinitely prolonging life" (elixir of life). The word was figuratively extended to mean "A sovereign remedy for disease. Hence adopted as a name for quack medicines" (e.g., Daffy's Elixir) and "The quintessence or soul of a thing; its kernel or secret principle". In modern usage, "elixir" is a pharmaceutical term for "A sweetened aromatic solution of alcohol and water, serving as a vehicle for medicine" ("Oxford English Dictionary", 2nd ed., 2009). Outside of Chinese cultural contexts, English "elixir poisoning" usually refers to accidental contamination, such as the 1937 Elixir sulfanilamide mass poisoning in the United States.

"Dān" 丹 "cinnabar; vermillion; elixir; alchemy" is the keyword for Chinese immortality elixirs. The red mineral cinnabar ("dānshā" 丹砂 lit. "cinnabar sand") was anciently used to produce the pigment vermilion ("zhūhóng" 朱紅) and the element mercury ("shuǐyín" 水銀 "watery silver" or "gǒng" 汞).

According to the "ABC Etymological Dictionary of Old Chinese", the etymology of Modern Standard Chinese "dān" from Old Chinese "*tān" (< *"tlan" ?) 丹 "red; vermillion; cinnabar", "gān" 矸 in "dāngān" 丹矸 from *"tân-kân" (< *"tlan-klan" ?) "cinnabar; vermillion ore", and "zhān" from *"tan" 旃 "a red flag" derive from Proto-Kam-Sui *"h-lan" "red" or Proto-Sino-Tibetan *"tja-n" or *"tya-n" "red". The *"t-" initial and *"t-" or *"k-" doublets indicate that Old Chinese borrowed this item. (Schuessler 2007: 204).

Although the word "dan" 丹 "cinnabar; red" frequently occurs in oracle script from the late Shang Dynasty (ca. 1600-1046 BCE) and bronzeware script and seal script from the Zhou Dynasty (1045-256 BCE), paleographers disagree about the graphic origins of the logograph 丹 and its ancient variants 𠁿 and 𠕑. Early scripts combine a 丶 dot or ⼀ stroke (depicting a piece of cinnabar) in the middle of a surrounding frame, which is said to represent:

- "jǐng" 井 "well" represents the mine from which the cinnabar is taken" ("Shuowen Jiezi")

- "the crucible of the Taoist alchemists" (Léon Wieger )

- "the contents of a square receptacle" (Bernhard Karlgren)

- "placed in a tray or palette to be used as red pigment" (Wang Hongyuan 王宏源)

- "mineral powder on a stretched filter-cloth" (Needham and Lu).

Many Chinese elixir names are compounds of "dan", such as "jīndān" 金丹 (with "gold") meaning "golden elixir; elixir of immortality; potable gold" and "xiāndān" 仙丹 (with "Daoist immortal") "elixir of immortality; panacea", and "shéndān" 神丹 (with "spirit; god") "divine elixir". "Bùsǐ zhī yào" 不死之藥 "drug of deathlessness" was another early name for the elixir of immortality. Chinese alchemists would "liàndān" 煉丹 (with "smelt; refine") "concoct pills of immortality" using a "dāndǐng" 丹鼎 (with "tripod cooking vessel; cauldron") "furnace for concocting pills of immortality". In addition, the ancient Chinese believed that other substances provided longevity and immortality, notably the "língzhī" 靈芝 ""Ganoderma" mushroom".

The transformation from chemistry-based "waidan" 外丹 "external elixir/alchemy" to physiology-based "neidan" 內丹 "internal elixir/alchemy" gave new analogous meanings to old terms. The human body metaphorically becomes a "ding" "cauldron" in which the adept forges the Three Treasures (essence, life-force, and spirit) within the "jindan" Golden Elixir within the "dāntián" 丹田 (with "field") "lower part of the abdomen".

In early China, alchemists and pharmacists were one in the same. Traditional Chinese Medicine also used less concentrated cinnabar and mercury preparations, and "dan" means "pill; medicine" in general, for example, "dānfāng" 丹方 semantically changed from "prescription for elixir of immortality" to "medical prescription". "Dan" was lexicalized into medical terms such as " dānjì" 丹劑 "pill preparation" and "dānyào" 丹藥 "pill medicine".

The Chinese names for immortality elixirs have parallels in other cultures and languages, for example, Indo-Iranian "soma" or "haoma", Sanskrit "amrita", and Greek "ambrosia".