Bisexual theory

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Bisexual_theory 

 

Bisexual theory is a field of critical theory, inspired by queer theory and bisexual politics, that foregrounds bisexuality as both a theoretical focus and as an epistemology. Bisexual theory emerged most prominently in the 1990s, in response to the burgeoning field of queer theory, and queer studies more broadly, frequently employing similar post-structuralist approaches but redressing queer theory's tendency towards bisexual erasure.

In their critique of the frequent elision of bisexuality in queer theory, Serena Anderlini-D'Onofrio and Jonathan Alexander write, "a queer theory that misses bisexuality's querying of normative sexualities is itself too mastered by the very normative and normalizing binaries it seeks to unsettle".

Scholars who have been discussed in relation to bisexual theory include Ibrahim Abdurrahman Farajajé, Steven Angelides, Elisabeth Däumer, Jo Eadie, Shiri Eisner, Marjorie Garber, Donald E. Hall, Clare Hemmings, Michael du Plessis, Maria Pramaggiore, Merl Storr, and Kenji Yoshino.

History

Bisexual theory emerged in the 1990s, inspired by and responding to the emergence of queer theory. Elisabeth Däumer's 1992 article, "Queer Ethics; or, the Challenge of Bisexuality to Lesbian Ethics", was the first major publication to theorise bisexuality in relation to queer and feminist theory.

In 1993, at the 11th National Bisexual Conference in the UK, a group of bisexual scholars formed Bi Academic Intervention. The same group published a volume of bisexual theory in 1997, entitled The Bisexual Imaginary: Representation, Identity and Desire. In 1995, Marjorie Garber released Vice Versa: Bisexuality and the Eroticism of Everyday Life, a monograph that aimed to reveal a 'bi-erotics' observable across disparate cultural locations, which however, drew some criticism due to its alleged ahistoricism. In 1996, Maria Pramaggiore and Donald E. Hall edited the collection RePresenting Bisexualities: Subjects and Cultures of Fluid Desire, which turned a bisexual theoretical lens to questions of representation. Chapters of bisexual theory also appeared in Activating Theory: Lesbian, Gay Bisexual Politics (1993) and Queer Studies: A Lesbian, Gay, Bisexual, and Transgender Anthology (1996).

The Journal of Bisexuality was first published in 2000 by the Taylor & Francis Group under the Routledge imprint, and its editors-in-chief have included Fritz Klein, Jonathan Alexander, Brian Zamboni, James D. Weinrich, and M. Paz Galupo.

In 2000, law scholar Kenji Yoshino published the influential article "The Epistemic Contract of Bisexual Erasure", which argues that "Straights and gays have an investment in stabilizing sexual orientation categories. The shared aspect of this investment is the security that all individuals draw from rigid social orderings." In 2001, Steven Angelides published A History of Bisexuality, in which he argues that bisexuality has operated historically as a structural other to sexual identity itself. In 2002, Clare Hemmings published Bisexual Spaces: A Geography of Sexuality and Gender in which she explores bisexuality's functions in geographical, political, theoretical, and cultural spaces.

In 2004, Jonathan Alexander and Karen Yescavage co-edited Bisexuality and Transgenderism: InterSEXions of the Others, which considers the intersections of bisexual and transgender identities.

Shiri Eisner's Bi: Notes for a Bisexual Revolution was released in 2013. This radical manifesto combines feminist, transgender, queer, and bisexual activism with theoretical work to establish a blueprint for bisexual revolution.

Epistemologies

One of the ways in which bisexual theorists have deployed bisexuality critically has been the formulation of bisexual epistemologies that ask how bisexuality generates or is given meaning.

Elisabeth Däumer suggests that bisexuality can be "an epistemological as well as ethical vantage point from which we can examine and deconstruct the bipolar framework of gender and sexuality."

Authors like Maria Pramaggiore and Jo Eadie repurposed the idea of bisexual people being "on the fence" in order to theorise an "epistemology of the fence":

a place of in-betweenness and indecision. Often precariously placed atop a structure that divides and demarcates, bisexual epistemologies have the capacity to reframe regimes and regions of desire by defaming and/or reframing in porous, nonexclusive ways... Bisexual epistemologies—ways of apprehending, organizing, and intervening in the world that refuse one-to-one correspondences between sex acts and identity, between erotic objects and sexualities, between identification and desire—acknowledge fluid desires and their continual construction and deconstruction of the desiring subject.

Clare Hemmings outlines three forms that bisexual epistemological approaches have tended to take:

The first locates bisexuality as outside conventional categories of sexuality and gender; the second locates it as critically inside those same categories; and the third focuses on the importance of bisexuality in the discursive formation of "other" identities.

Critiques

In his 1996 article, Jonathan Dollimore observes a trend he terms ‘wishful theory’ in bisexual theoretical work. Dollimore critiques bisexual theory's fabrication of eclectic theoretical narratives with little attention to how they relate to social reality, and its assumption of a subversive position that resists a consideration of how bisexual identity itself might be subverted. Dollimore contends that bisexual theory is "passing, if not closeted, as post-modern theory, safely fashioning itself as a suave doxa."

In her 1999 article, Merl Storr suggests that contemporary bisexual identity, community, organization, and politics are rooted in early postmodernity. By identifying this relation, Storr observes the postmodern themes of indeterminacy, instability, fragmentation, and flux that characterize bisexual theory and parses how these concepts might be reflected upon critically.

One of the problems Clare Hemmings identifies with bisexual epistemological approaches is that bisexuality becomes metaphorized to the point that it is unrecognizable to bisexual people, a critique that has also been made in transgender studies to the allegorization of trans feminine realities.

Genetic drift

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Genetic_drift

Genetic drift, also known as random genetic drift, allelic drift or the Wright effect, is the change in the frequency of an existing gene variant (allele) in a population due to random chance.

Genetic drift may cause gene variants to disappear completely and thereby reduce genetic variation. It can also cause initially rare alleles to become much more frequent and even fixed.

When few copies of an allele exist, the effect of genetic drift is more notable, and when many copies exist, the effect is less notable (due to the law of large numbers). In the middle of the 20th century, vigorous debates occurred over the relative importance of natural selection versus neutral processes, including genetic drift. Ronald Fisher, who explained natural selection using Mendelian genetics, held the view that genetic drift plays at most a minor role in evolution, and this remained the dominant view for several decades. In 1968, population geneticist Motoo Kimura rekindled the debate with his neutral theory of molecular evolution, which claims that most instances where a genetic change spreads across a population (although not necessarily changes in phenotypes) are caused by genetic drift acting on neutral mutations. In the 1990s, constructive neutral evolution was proposed which seeks to explain how complex systems emerge through neutral transitions.

Analogy with marbles in a jar

The process of genetic drift can be illustrated using 20 marbles in a jar to represent 20 organisms in a population. Consider this jar of marbles as the starting population. Half of the marbles in the jar are red and half are blue, with each colour corresponding to a different allele of one gene in the population. In each new generation, the organisms reproduce at random. To represent this reproduction, randomly select a marble from the original jar and deposit a new marble with the same colour into a new jar. This is the "offspring" of the original marble, meaning that the original marble remains in its jar. Repeat this process until 20 new marbles are in the second jar. The second jar will now contain 20 "offspring", or marbles of various colours. Unless the second jar contains exactly 10 red marbles and 10 blue marbles, a random shift has occurred in the allele frequencies.

If this process is repeated a number of times, the numbers of red and blue marbles picked each generation fluctuates. Sometimes, a jar has more red marbles than its "parent" jar and sometimes more blue. This fluctuation is analogous to genetic drift – a change in the population's allele frequency resulting from a random variation in the distribution of alleles from one generation to the next.

In any one generation, no marbles of a particular colour could be chosen, meaning they have no offspring. In this example, if no red marbles are selected, the jar representing the new generation contains only blue offspring. If this happens, the red allele has been lost permanently in the population, while the remaining blue allele has become fixed: all future generations are entirely blue. In small populations, fixation can occur in just a few generations.

In this simulation, each black dot on a marble signifies that it has been chosen for copying (reproduction) one time. Fixation in the blue "allele" occurs within five generations.

Probability and allele frequency

The mechanisms of genetic drift can be illustrated with a very simple example. Consider a very large colony of bacteria isolated in a drop of solution. The bacteria are genetically identical except for a single gene with two alleles labeled A and B, which are neutral alleles, meaning that they do not affect the bacteria's ability to survive and reproduce; all bacteria in this colony are equally likely to survive and reproduce. Suppose that half the bacteria have allele A and the other half have allele B. Thus, A and B each has an allele frequency of 1/2.

The drop of solution then shrinks until it has only enough food to sustain four bacteria. All other bacteria die without reproducing. Among the four that survive, 16 possible combinations for the A and B alleles exist:
(A-A-A-A), (B-A-A-A), (A-B-A-A), (B-B-A-A),
(A-A-B-A), (B-A-B-A), (A-B-B-A), (B-B-B-A),
(A-A-A-B), (B-A-A-B), (A-B-A-B), (B-B-A-B),
(A-A-B-B), (B-A-B-B), (A-B-B-B), (B-B-B-B).

Since all bacteria in the original solution are equally likely to survive when the solution shrinks, the four survivors are a random sample from the original colony. The probability that each of the four survivors has a given allele is 1/2, and so the probability that any particular allele combination occurs when the solution shrinks is

${\displaystyle \frac{1}{2}\cdot \frac{1}{2}\cdot \frac{1}{2}\cdot \frac{1}{2}=\frac{1}{16}.}$

(The original population size is so large that the sampling effectively happens with replacement). In other words, each of the 16 possible allele combinations is equally likely to occur, with probability 1/16.

Counting the combinations with the same number of A and B gives the following table:

A	B	Combinations	Probability
4	0	1	1/16
3	1	4	4/16
2	2	6	6/16
1	3	4	4/16
0	4	1	1/16

As shown in the table, the total number of combinations that have the same number of A alleles as of B alleles is six, and the probability of this combination is 6/16. The total number of other combinations is ten, so the probability of unequal number of A and B alleles is 10/16. Thus, although the original colony began with an equal number of A and B alleles, quite possibly, the number of alleles in the remaining population of four members will not be equal. The situation of equal numbers is actually less likely than unequal numbers. In the latter case, genetic drift has occurred because the population's allele frequencies have changed due to random sampling. In this example, the population contracted to just four random survivors, a phenomenon known as a population bottleneck.

The probabilities for the number of copies of allele A (or B) that survive (given in the last column of the above table) can be calculated directly from the binomial distribution, where the "success" probability (probability of a given allele being present) is 1/2 (i.e., the probability that there are k copies of A (or B) alleles in the combination) is given by:

${\displaystyle (\genfrac{}{}{0ex}{}{n}{k}){\left(\frac{1}{2}\right)}^k{\left(1-\frac{1}{2}\right)}^{n-k}=(\genfrac{}{}{0ex}{}{n}{k}){\left(\frac{1}{2}\right)}^n}$

where n=4 is the number of surviving bacteria.

Mathematical models

Mathematical models of genetic drift can be designed using either branching processes or a diffusion equation describing changes in allele frequency in an idealised population.

Wright–Fisher model

Consider a gene with two alleles, A or B. In diploidy, populations consisting of N individuals have 2N copies of each gene. An individual can have two copies of the same allele or two different alleles. The frequency of one allele is assigned p and the other q. The Wright–Fisher model (named after Sewall Wright and Ronald Fisher) assumes that generations do not overlap (for example, annual plants have exactly one generation per year) and that each copy of the gene found in the new generation is drawn independently at random from all copies of the gene in the old generation. The formula to calculate the probability of obtaining k copies of an allele that had frequency p in the last generation is then

${\displaystyle \frac{(2N)!}{k!(2N-k)!}{p}^k{q}^{2N-k}}$

where the symbol "!" signifies the factorial function. This expression can also be formulated using the binomial coefficient,

${\displaystyle (\genfrac{}{}{0ex}{}{2N}{k})p^k{q}^{2N-k}}$

Moran model

The Moran model assumes overlapping generations. At each time step, one individual is chosen to reproduce and one individual is chosen to die. So in each timestep, the number of copies of a given allele can go up by one, go down by one, or can stay the same. This means that the transition matrix is tridiagonal, which means that mathematical solutions are easier for the Moran model than for the Wright–Fisher model. On the other hand, computer simulations are usually easier to perform using the Wright–Fisher model, because fewer time steps need to be calculated. In the Moran model, it takes N timesteps to get through one generation, where N is the effective population size. In the Wright–Fisher model, it takes just one.

In practice, the Moran and Wright–Fisher models give qualitatively similar results, but genetic drift runs twice as fast in the Moran model.

Other models of drift

If the variance in the number of offspring is much greater than that given by the binomial distribution assumed by the Wright–Fisher model, then given the same overall speed of genetic drift (the variance effective population size), genetic drift is a less powerful force compared to selection. Even for the same variance, if higher moments of the offspring number distribution exceed those of the binomial distribution then again the force of genetic drift is substantially weakened.

Random effects other than sampling error

Random changes in allele frequencies can also be caused by effects other than sampling error, for example random changes in selection pressure.

One important alternative source of stochasticity, perhaps more important than genetic drift, is genetic draft. Genetic draft is the effect on a locus by selection on linked loci. The mathematical properties of genetic draft are different from those of genetic drift. The direction of the random change in allele frequency is autocorrelated across generations.

Drift and fixation

The Hardy–Weinberg principle states that within sufficiently large populations, the allele frequencies remain constant from one generation to the next unless the equilibrium is disturbed by migration, genetic mutations, or selection.

However, in finite populations, no new alleles are gained from the random sampling of alleles passed to the next generation, but the sampling can cause an existing allele to disappear. Because random sampling can remove, but not replace, an allele, and because random declines or increases in allele frequency influence expected allele distributions for the next generation, genetic drift drives a population towards genetic uniformity over time. When an allele reaches a frequency of 1 (100%) it is said to be "fixed" in the population and when an allele reaches a frequency of 0 (0%) it is lost. Smaller populations achieve fixation faster, whereas in the limit of an infinite population, fixation is not achieved. Once an allele becomes fixed, genetic drift comes to a halt, and the allele frequency cannot change unless a new allele is introduced in the population via mutation or gene flow. Thus even while genetic drift is a random, directionless process, it acts to eliminate genetic variation over time.

Rate of allele frequency change due to drift

Ten simulations of random genetic drift of a single given allele with an initial frequency distribution 0.5 measured over the course of 50 generations, repeated in three reproductively synchronous populations of different sizes. In these simulations, alleles drift to loss or fixation (frequency of 0.0 or 1.0) only in the smallest population.

Assuming genetic drift is the only evolutionary force acting on an allele, after t generations in many replicated populations, starting with allele frequencies of p and q, the variance in allele frequency across those populations is

${\displaystyle V_t\approx pq\left(1-\exp \left(-\frac{t}{2N_e}\right)\right)}$

Time to fixation or loss

Assuming genetic drift is the only evolutionary force acting on an allele, at any given time the probability that an allele will eventually become fixed in the population is simply its frequency in the population at that time. For example, if the frequency p for allele A is 75% and the frequency q for allele B is 25%, then given unlimited time the probability A will ultimately become fixed in the population is 75% and the probability that B will become fixed is 25%.

The expected number of generations for fixation to occur is proportional to the population size, such that fixation is predicted to occur much more rapidly in smaller populations. Normally the effective population size, which is smaller than the total population, is used to determine these probabilities. The effective population (N_e) takes into account factors such as the level of inbreeding, the stage of the lifecycle in which the population is the smallest, and the fact that some neutral genes are genetically linked to others that are under selection. The effective population size may not be the same for every gene in the same population.

One forward-looking formula used for approximating the expected time before a neutral allele becomes fixed through genetic drift, according to the Wright–Fisher model, is

${\displaystyle {\overline{T}}_{\text{fixed}}=\frac{-4N_e(1-p)\ln (1-p)}{p}}$

where T is the number of generations, N_e is the effective population size, and p is the initial frequency for the given allele. The result is the number of generations expected to pass before fixation occurs for a given allele in a population with given size (N_e) and allele frequency (p).

The expected time for the neutral allele to be lost through genetic drift can be calculated as

${\displaystyle {\overline{T}}_{\text{lost}}=\frac{-4N_{e}p}{1-p}\ln p.}$

When a mutation appears only once in a population large enough for the initial frequency to be negligible, the formulas can be simplified to

${\displaystyle {\overline{T}}_{\text{fixed}}=4N_e}$

for average number of generations expected before fixation of a neutral mutation, and

${\displaystyle {\overline{T}}_{\text{lost}}=2\left(\frac{N_e}{N}\right)\ln (2N)}$

for the average number of generations expected before the loss of a neutral mutation in a population of actual size N.

Time to loss with both drift and mutation

The formulae above apply to an allele that is already present in a population, and which is subject to neither mutation nor natural selection. If an allele is lost by mutation much more often than it is gained by mutation, then mutation, as well as drift, may influence the time to loss. If the allele prone to mutational loss begins as fixed in the population, and is lost by mutation at rate m per replication, then the expected time in generations until its loss in a haploid population is given by

${\displaystyle {\overline{T}}_{\text{lost}}\approx \{\begin{array}{l}{\displaystyle \frac{1}{m}},\text{ if }m{N}_e\ll 1\\ {\displaystyle \frac{\ln (m{N}_e)+\gamma }{m}}\text{ if }m{N}_e\gg 1\end{array}}$

where ${\displaystyle \gamma }$ is Euler's constant. The first approximation represents the waiting time until the first mutant destined for loss, with loss then occurring relatively rapidly by genetic drift, taking time ⁠1/m⁠ ≫ N_e. The second approximation represents the time needed for deterministic loss by mutation accumulation. In both cases, the time to fixation is dominated by mutation via the term ⁠1/m⁠, and is less affected by the effective population size.

Versus natural selection

In natural populations, genetic drift and natural selection do not act in isolation; both phenomena are always at play, together with mutation and migration. Neutral evolution is the product of both mutation and drift, not of drift alone. Similarly, even when selection overwhelms genetic drift, it can act only on variation that mutation provides.

While natural selection has a direction, guiding evolution towards heritable adaptations to the current environment, genetic drift has no direction and is guided only by the mathematics of chance. As a result, drift acts upon the genotypic frequencies within a population without regard to their phenotypic effects. In contrast, selection favors the spread of alleles whose phenotypic effects increase survival and/or reproduction of their carriers, lowers the frequencies of alleles that cause unfavorable traits, and ignores those that are neutral.

The law of large numbers predicts that when the absolute number of copies of the allele is small (e.g., in small populations), the magnitude of drift on allele frequencies per generation is larger. The magnitude of drift is large enough to overwhelm selection at any allele frequency when the selection coefficient is less than 1 divided by the effective population size. Non-adaptive evolution resulting from the product of mutation and genetic drift is therefore considered to be a consequential mechanism of evolutionary change primarily within small, isolated populations. The mathematics of genetic drift depend on the effective population size, but it is not clear how this is related to the actual number of individuals in a population. Genetic linkage to other genes that are under selection can reduce the effective population size experienced by a neutral allele. With a higher recombination rate, linkage decreases and with it this local effect on effective population size. This effect is visible in molecular data as a correlation between local recombination rate and genetic diversity, and negative correlation between gene density and diversity at noncoding DNA regions. Stochasticity associated with linkage to other genes that are under selection is not the same as sampling error, and is sometimes known as genetic draft in order to distinguish it from genetic drift.

Low allele frequency makes alleles more vulnerable to being eliminated by random chance, even overriding the influence of natural selection. For example, while disadvantageous mutations are usually eliminated quickly within the population, new advantageous mutations are almost as vulnerable to loss through genetic drift as are neutral mutations. Not until the allele frequency for the advantageous mutation reaches a certain threshold will genetic drift have no effect.

Population bottleneck

Main article: Population bottleneck

Changes in a population's allele frequency following a population bottleneck: the rapid and radical decline in population size has reduced the population's genetic variation.

A population bottleneck is when a population contracts to a significantly smaller size over a short period of time due to some random environmental event. In a true population bottleneck, the odds for survival of any member of the population are purely random, and are not improved by any particular inherent genetic advantage. The bottleneck can result in radical changes in allele frequencies, completely independent of selection.

The impact of a population bottleneck can be sustained, even when the bottleneck is caused by a one-time event such as a natural catastrophe. An interesting example of a bottleneck causing unusual genetic distribution is the relatively high proportion of individuals with total rod cell color blindness (achromatopsia) on Pingelap atoll in Micronesia. After a bottleneck, inbreeding increases. This increases the damage done by recessive deleterious mutations, in a process known as inbreeding depression. The worst of these mutations are selected against, leading to the loss of other alleles that are genetically linked to them, in a process of background selection. For recessive harmful mutations, this selection can be enhanced as a consequence of the bottleneck, due to genetic purging. This leads to a further loss of genetic diversity. In addition, a sustained reduction in population size increases the likelihood of further allele fluctuations from drift in generations to come.

A population's genetic variation can be greatly reduced by a bottleneck, and even beneficial adaptations may be permanently eliminated. The loss of variation leaves the surviving population vulnerable to any new selection pressures such as disease, climatic change or shift in the available food source, because adapting in response to environmental changes requires sufficient genetic variation in the population for natural selection to take place.

There have been many known cases of population bottleneck in the recent past. Prior to the arrival of Europeans, North American prairies were habitat for millions of greater prairie chickens. In Illinois alone, their numbers plummeted from about 100 million birds in 1900 to about 50 birds in the 1990s. The declines in population resulted from hunting and habitat destruction, but a consequence has been a loss of most of the species' genetic diversity. DNA analysis comparing birds from the mid century to birds in the 1990s documents a steep decline in the genetic variation in just the latter few decades. Currently the greater prairie chicken is experiencing low reproductive success.

However, the genetic loss caused by bottleneck and genetic drift can increase fitness, as in Ehrlichia.

Over-hunting also caused a severe population bottleneck in the northern elephant seal in the 19th century. Their resulting decline in genetic variation can be deduced by comparing it to that of the southern elephant seal, which were not so aggressively hunted.

Founder effect

Main article: Founder effect

When very few members of a population migrate to form a separate new population, the founder effect occurs. For a period after the foundation, the small population experiences intensive drift. In the figure this results in fixation of the red allele.

The founder effect is a special case of a population bottleneck, occurring when a small group in a population splinters off from the original population and forms a new one. The random sample of alleles in the just formed new colony is expected to grossly misrepresent the original population in at least some respects. It is even possible that the number of alleles for some genes in the original population is larger than the number of gene copies in the founders, making complete representation impossible. When a newly formed colony is small, its founders can strongly affect the population's genetic make-up far into the future.

A well-documented example is found in the Amish migration to Pennsylvania in 1744. Two members of the new colony shared the recessive allele for Ellis–Van Creveld syndrome. Members of the colony and their descendants tend to be religious isolates and remain relatively insular. As a result of many generations of inbreeding, Ellis–Van Creveld syndrome is now much more prevalent among the Amish than in the general population.

The difference in gene frequencies between the original population and colony may also trigger the two groups to diverge significantly over the course of many generations. As the difference, or genetic distance, increases, the two separated populations may become distinct, both genetically and phenetically, although not only genetic drift but also natural selection, gene flow, and mutation contribute to this divergence. This potential for relatively rapid changes in the colony's gene frequency led most scientists to consider the founder effect (and by extension, genetic drift) a significant driving force in the evolution of new species. Sewall Wright was the first to attach this significance to random drift and small, newly isolated populations with his shifting balance theory of speciation. Following after Wright, Ernst Mayr created many persuasive models to show that the decline in genetic variation and small population size following the founder effect were critically important for new species to develop. However, there is much less support for this view today since the hypothesis has been tested repeatedly through experimental research and the results have been equivocal at best.

History

Further information: Modern synthesis (20th century)

The role of random chance in evolution was first outlined by Arend L. Hagedoorn and Anna Cornelia Hagedoorn-Vorstheuvel La Brand in 1921. They highlighted that random survival plays a key role in the loss of variation from populations. Fisher (1922) responded to this with the first, albeit marginally incorrect, mathematical treatment of the "Hagedoorn effect". Notably, he expected that many natural populations were too large (an N ~10,000) for the effects of drift to be substantial and thought drift would have an insignificant effect on the evolutionary process. The corrected mathematical treatment and term "genetic drift" was later coined by a founder of population genetics, Sewall Wright. His first use of the term "drift" was in 1929, though at the time he was using it in the sense of a directed process of change, or natural selection. Random drift by means of sampling error came to be known as the "Sewall–Wright effect", though he was never entirely comfortable to see his name given to it. Wright referred to all changes in allele frequency as either "steady drift" (e.g., selection) or "random drift" (e.g., sampling error). "Drift" came to be adopted as a technical term in the stochastic sense exclusively. Today it is usually defined still more narrowly, in terms of sampling error, although this narrow definition is not universal. Wright wrote that the "restriction of "random drift" or even "drift" to only one component, the effects of accidents of sampling, tends to lead to confusion". Sewall Wright considered the process of random genetic drift by means of sampling error equivalent to that by means of inbreeding, but later work has shown them to be distinct.

In the early days of the modern evolutionary synthesis, scientists were beginning to blend the new science of population genetics with Charles Darwin's theory of natural selection. Within this framework, Wright focused on the effects of inbreeding on small relatively isolated populations. He introduced the concept of an adaptive landscape in which phenomena such as cross breeding and genetic drift in small populations could push them away from adaptive peaks, which in turn allow natural selection to push them towards new adaptive peaks. Wright thought smaller populations were more suited for natural selection because "inbreeding was sufficiently intense to create new interaction systems through random drift but not intense enough to cause random nonadaptive fixation of genes".

Wright's views on the role of genetic drift in the evolutionary scheme were controversial almost from the very beginning. One of the most vociferous and influential critics was colleague Ronald Fisher. Fisher conceded genetic drift played some role in evolution, but an insignificant one. Fisher has been accused of misunderstanding Wright's views because in his criticisms Fisher seemed to argue Wright had rejected selection almost entirely. To Fisher, viewing the process of evolution as a long, steady, adaptive progression was the only way to explain the ever-increasing complexity from simpler forms. But the debates have continued between the "gradualists" and those who lean more toward the Wright model of evolution where selection and drift together play an important role.

In 1968, Motoo Kimura rekindled the debate with his neutral theory of molecular evolution, which claims that most of the genetic changes are caused by genetic drift acting on neutral mutations.

The role of genetic drift by means of sampling error in evolution has been criticized by John H. Gillespie and William B. Provine, who argue that selection on linked sites is a more important stochastic force.

Mushroom poisoning

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Mushroom_poisoning 

 

Mushroom poisoning
Other names	Mycetism, mycetismus
Amanita phalloides accounts for the majority of fatal mushroom poisonings worldwide.
Specialty	Emergency medicine, toxicology

Mushroom poisoning is poisoning resulting from the ingestion of mushrooms that contain toxic substances. Symptoms can vary from slight gastrointestinal discomfort to death in about 10 days. Mushroom toxins are secondary metabolites produced by the fungus.

Mushroom poisoning is usually the result of ingestion of wild mushrooms after misidentification of a toxic mushroom as an edible species. The most common reason for this misidentification is a close resemblance in terms of color and general morphology of the toxic mushrooms species with edible species. To prevent mushroom poisoning, mushroom gatherers familiarize themselves with the mushrooms they intend to collect, as well as with any similar-looking toxic species. The safety of eating wild mushrooms may depend on methods of preparation for cooking. Some toxins, such as amatoxins, are thermostable and mushrooms containing such toxins will not be rendered safe to eat by cooking.

Signs and symptoms

See also: Category:Mycotoxins

Poisonous mushrooms contain a variety of different toxins that can differ markedly in toxicity. Symptoms of mushroom poisoning may vary from gastric upset to organ failure resulting in death. Serious symptoms do not always occur immediately after eating, often not until the toxin attacks the kidney or liver, sometimes days or weeks later.

The most common consequence of mushroom poisoning is simply gastrointestinal upset. Most "poisonous" mushrooms contain gastrointestinal irritants that cause vomiting and diarrhea (sometimes requiring hospitalization), but usually no long-term damage. However, there are a number of recognized mushroom toxins with specific, and sometimes deadly, effects:

Toxin	Toxicity	Effects
α-Amanitin	Deadly	Causes often fatal liver damage 1–3 days after ingestion. The principal toxin in the death cap.
Phallotoxin	Non-lethal	Causes extreme gastrointestinal upset. Found in various mushrooms.
Orellanine	Deadly	Redox cycler similar to paraquat. Causes kidney failure within three weeks after ingestion. Principal toxin in genus Cortinarius.
Muscarine	Potentially deadly	Causes SLUDGE syndrome. Found in various mushrooms. Antidote is atropine.
Monomethylhydrazine (MMH)	Deadly	Causes brain damage, seizures, gastrointestinal upset, and hemolysis. Metabolic poison. Principal toxin in genus Gyromitra. Antidote is large doses of intravenous pyridoxine hydrochloride.
Coprine	Non-lethal	Causes illness when consumed with alcohol. Principal toxin in genus Coprinus.
Ibotenic acid	Potentially deadly	Excitotoxin. Principal toxin in Amanita muscaria, A. pantherina, and A. gemmata.
Muscimol	Potentially deadly	Causes CNS depression and hallucinations. Principal toxin in Amanita muscaria, A. pantherina, and A. gemmata.
Arabitol	Non-lethal	Causes diarrhea in some people.
Bolesatine	Non-lethal	Causes gastrointestinal irritation, vomiting, nausea.
Ergotamine	Deadly	Affects the vascular system and can lead to loss of limbs and/or cardiac arrest. Found in genus Claviceps.

The period between ingestion and the onset of symptoms varies dramatically between toxins, some taking days to show symptoms identifiable as mushroom poisoning.

• α-Amanitin: For 6–12 hours, there are no symptoms. This is followed by a period of gastrointestinal upset (vomiting and profuse, watery diarrhea). This stage is caused primarily by the phallotoxins and typically lasts 24 hours. At the end of this second stage is when severe liver damage begins. The damage may continue for another 2–3 days. Kidney damage can also occur. Some patients will require a liver transplant. Amatoxins are found in some mushrooms in the genus Amanita, but are also found in some species of Galerina and Lepiota. Overall, mortality is between 10 and 15 percent. Recently, Silybum marianum or blessed milk thistle has been shown to protect the liver from amanita toxins and promote regrowth of damaged cells.
  
• Orellanine: This toxin generally causes no symptoms for 3–20 days after ingestion. Typically around day 11, the process of kidney failure begins, and is usually symptomatic by day 20. These symptoms can include pain in the area of the kidneys, thirst, vomiting, headache, and fatigue. A few species in the very large genus Cortinarius contain this toxin. People having eaten mushrooms containing orellanine may experience early symptoms as well, because the mushrooms often contain other toxins in addition to orellanine. A related toxin that causes similar symptoms but within 3–6 days has been isolated from Amanita smithiana and some other related toxic Amanitas.
• Muscarine: Muscarine stimulates the muscarinic receptors of the nerves and muscles. Symptoms include sweating, salivation, tears, blurred vision, palpitations, and, in high doses, respiratory failure. Muscarine is found in mushrooms of the genus Omphalotus, notably the jack o' Lantern mushrooms. It is also found in A. muscaria, although it is now known that the main effect of this mushroom is caused by ibotenic acid. Muscarine can also be found in some Inocybe species and Clitocybe species, in particular Clitocybe dealbata, and some red-pored Boletes.
• Gyromitrin: Stomach acids convert gyromitrin to monomethylhydrazine (MMH). It affects multiple body systems. It blocks the important neurotransmitter GABA, leading to stupor, delirium, muscle cramps, loss of coordination, tremors, and/or seizures. It causes severe gastrointestinal irritation, leading to vomiting and diarrhea. In some cases, liver failure has been reported. It can also cause red blood cells to break down, leading to jaundice, kidney failure, and signs of anemia. It is found in mushrooms of the genus Gyromitra. A gyromitrin-like compound has also been identified in mushrooms of the genus Verpa.
• Coprine: Coprine is metabolized to a chemical that resembles disulfiram. It inhibits aldehyde dehydrogenase (ALDH), which, in general, causes no harm, unless the person has alcohol in their bloodstream while ALDH is inhibited. This can happen if alcohol is ingested shortly before or up to a few days after eating the mushrooms. In that case, the alcohol cannot be completely metabolized, and the person will experience flushed skin, vomiting, headache, dizziness, weakness, apprehension, confusion, palpitations, and sometimes trouble to breathe. Coprine is found mainly in mushrooms of the genus Coprinus, although similar effects have been noted after ingestion of Clitocybe clavipes.
• Ibotenic acid: Decarboxylates into muscimol upon ingestion. The effects of muscimol vary, but nausea and vomiting are common. Confusion, euphoria, or sleepiness are possible. Loss of muscular coordination, sweating, and chills are likely. Some people experience visual distortions, a feeling of strength, or delusions. Symptoms normally appear after 30 minutes to 2 hours and last for several hours. A. muscaria, the "Alice in Wonderland" mushroom, is known for the hallucinatory experiences caused by muscimol, but A. pantherina and A. gemmata also contain the same compound. While normally self-limiting, fatalities have been associated with A. pantherina, and consumption of a large number of any of these mushrooms is likely to be dangerous.
• Arabitol: A sugar alcohol, similar to mannitol, which causes no harm in most people but causes gastrointestinal irritation in some. It is found in small amounts in oyster mushrooms, and considerable amounts in Suillus species and Hygrophoropsis aurantiaca (the "false chanterelle").

Causes

Immature, possibly poisonous, Amanita mushrooms

Edible shaggy mane Coprinus comatus mushrooms

Two examples of immature Amanitas, one deadly and one edible

An edible puffball which closely resembles the immature Amanitas

Jack-O-Lantern, a poisonous mushroom sometimes mistaken for a chanterelle

"Chanterelle", edible

New species of fungi are continuing to be discovered, with an estimated number of 800 new species registered annually. This, added to the fact that many investigations have recently reclassified some species of mushrooms from edible to poisonous has made older classifications insufficient at describing what now is known about the different species of fungi that are harmful to humans. It is now thought that of the approximately 100,000 known fungi species found worldwide, about 100 of them are poisonous to humans. However, by far the majority of mushroom poisonings are not fatal, and the majority of fatal poisonings are attributable to the Amanita phalloides mushroom.

A majority of these cases are due to mistaken identity. This is a common occurrence with A. phalloides in particular, due to its resemblance to the Asian paddy-straw mushroom, Volvariella volvacea. Both are light-colored and covered with a universal veil when young.

Amanitas can be mistaken for other species, as well, in particular when immature. On at least one occasion they have been mistaken for Coprinus comatus. In this case, the victim had some limited experience in identifying mushrooms, but did not take the time to correctly identify these particular mushrooms until after he began to experience symptoms of mushroom poisoning.

The author of Mushrooms Demystified, David Arora cautions puffball-hunters to beware of Amanita "eggs", which are Amanitas still entirely encased in their universal veil. Amanitas at this stage are difficult to distinguish from puffballs. Foragers are encouraged to always cut the fruiting bodies of suspected puffballs in half, as this will reveal the outline of a developing Amanita should it be present within the structure.

A majority of mushroom poisonings, in general, are the result of small children, especially toddlers in the "grazing" stage, ingesting mushrooms found on the lawn. While this can happen with any mushroom, Chlorophyllum molybdites is often implicated due to its preference for growing in lawns. C. molybdites causes severe gastrointestinal upset but is not considered deadly poisonous.

A few poisonings are the result of misidentification while attempting to collect hallucinogenic mushrooms for recreational use. In 1981, one fatality and two hospitalizations occurred following consumption of Galerina marginata, mistaken for a Psilocybe species. Galerina and Psilocybe species are both small, brown, and sticky, and can be found growing together. However, Galerina contains amatoxins, the same poison found in the deadly Amanita species. Another case reports kidney failure following ingestion of Cortinarius orellanus, a mushroom containing orellanine.

It is natural that accidental ingestion of hallucinogenic species also occurs, but is rarely harmful when ingested in small quantities. Cases of serious toxicity have been reported in small children. Amanita pantherina, while containing the same hallucinogens as Amanita muscaria (e.g., ibotenic acid and muscimol), has been more commonly associated with severe gastrointestinal upset than its better-known counterpart.

Although usually not fatal, Omphalotus spp., "Jack-o-lantern mushrooms", are another cause of sometimes significant toxicity. They are sometimes mistaken for chanterelles. Both are bright-orange and fruit at the same time of year, although Omphalotus grows on wood and has true gills rather than the veins of a Cantharellus. They contain toxins known as illudins, which causes gastrointestinal symptoms.

Bioluminescent species are generally inedible and often mildly toxic.

Clitocybe dealbata, which is occasionally mistaken for an oyster mushroom or other edible species contains muscarine.

Toxicities can also occur with collection of morels. Even true morels, if eaten raw, will cause gastrointestinal upset. Typically, morels are thoroughly cooked before eating. Verpa bohemica, although referred to as "thimble morels" or "early morels" by some, have caused toxic effects in some individuals. Gyromitra spp., "false morels", are deadly poisonous if eaten raw. They contain a toxin called gyromitrin, which can cause neurotoxicity, gastrointestinal toxicity, and destruction of the blood cells. The Finns consume Gyromitra esculenta after parboiling, but this may not render the mushroom entirely safe, resulting in its being called the "fugu of the Finnish cuisine".

A more unusual toxin is coprine, a disulfiram-like compound that is harmless unless ingested within a few days of ingesting alcohol. It inhibits aldehyde dehydrogenase, an enzyme required for breaking down alcohol. Thus, the symptoms of toxicity are similar to being hung over—flushing, headache, nausea, palpitations, and, in severe cases, trouble breathing. Coprinus species, including Coprinopsis atramentaria, contain coprine. Coprinus comatus does not, but it is best to avoid mixing alcohol with other members of this genus.

Recently, poisonings have also been associated with Amanita smithiana. These poisonings may be due to orellanine, but the onset of symptoms occurs in 4 to 11 hours, which is much quicker than the 3 to 20 days normally associated with orellanine.

Paxillus involutus is also inedible when raw, but is eaten in Europe after pickling or parboiling. However, after the death of the German mycologist Dr. Julius Schäffer, it was discovered that the mushroom contains a toxin that can stimulate the immune system to attack its red blood cells. This reaction is rare but can occur even after safely eating the mushroom for many years. Similarly, Tricholoma equestre was widely considered edible and good, until it was connected with rare cases of rhabdomyolysis.

In the fall of 2004, thirteen deaths were associated with consumption of Pleurocybella porrigens or "angel's wings". In general, these mushrooms are considered edible. All the victims died of an acute brain disorder, and all had pre-existing kidney disease. The exact cause of the toxicity was not known at this time and the deaths cannot be definitively attributed to mushroom consumption.

However, mushroom poisoning is not always due to mistaken identity. For example, the highly toxic ergot Claviceps purpurea, which grows on rye, is sometimes ground up with rye, unnoticed, and later consumed. This can cause devastating, even fatal, effects, called ergotism.

Cases of idiosyncratic or unusual reactions to fungi can also occur. Some are probably due to allergy, others to some other kind of sensitivity. It is not uncommon for a person to experience gastrointestinal upset associated with one particular mushroom species or genus.

Some mushrooms might concentrate toxins from their growth substrate, such as Chicken of the Woods growing on yew trees.

Poisonous mushrooms

See also: List of deadly fungus species and List of poisonous fungus species

Of the most lethal mushrooms, five—the death cap (A. phalloides), the three destroying angels (A. virosa, A. bisporigera, and A. ocreata), and the fool's mushroom (A. verna)—belong to the genus Amanita, and two more—the deadly webcap (C. rubellus), and the fool's webcap (C. orellanus)—are from the genus Cortinarius. Several species of Galerina, Lepiota, and Conocybe also contain lethal amounts of amatoxins. Deadly species are listed in the List of deadly fungi.

The following species may cause great discomfort, sometimes requiring hospitalization, but are not considered deadly.

• Amanita muscaria (fly agaric) – Contains the psychoactive muscimol and the neurotoxin ibotenic acid. Ibotenic acid decarboxylates into muscimol upon curing of the mushroom, rendering it relatively non-toxic, though death via respiratory depression is possible. Muscimol intoxication is often considered unpleasant and undesirable, however, and as such has seen little recreational use compared to the unrelated psilocybin mushroom, though it has been used as an entheogen by the native people of Siberia.
• Amanita pantherina (panther mushroom) – contains similar toxins as A. muscaria, but is associated with more fatalities than A. muscaria.
• Chlorophyllum molybdites (greengills) – causes intense gastrointestinal upset.
• Entoloma (pinkgills) – some species are highly poisonous, such as livid entoloma (Entoloma sinuatum), Entoloma rhodopolium, and Entoloma nidorosum. Symptoms of intense gastrointestinal upset appear after 20 minutes to 4 hours, caused by an unidentified gastrointestinal irritant.
• Many Inocybe species such as Inocybe fastigiata and Inocybe geophylla contain muscarine.
• Inosperma erubescens has caused death.
• Some white Clitocybe species, including C. rivulosa and C. dealbata, contain muscarine.
• Tricholoma pardinum, Tricholoma tigrinum (tiger tricholoma) – gastrointestinal upset due to an unidentified toxin, begins in 15 minutes to 2 hours and lasts 4 to 6 days.
• Tricholoma equestre (man-on-horseback) – until recently thought edible and good, can lead to rhabdomyolysis after repeated consumption.
• Hypholoma fasciculare/Naematoloma fasciculare (sulfur tuft) – usually causes gastrointestinal upset,^[4] but the toxins fasciculol E and F could lead to paralysis and death.
• Paxillus involutus (brown roll-rim) – once thought edible, but now found to destroy red blood cells with regular or long-term consumption.
• Rubroboletus satanas (Devil's bolete), Suillellus luridus, Rubroboletus legaliae, Chalciporus piperatus, Neoboletus luridiformis, Rubroboletus pulcherrimus – gastrointestinal irritation. Of these, only R. pulcherrimus has been implicated in a death. Many books list N. luridiformis as edible, but Arora lists it as "to be avoided".
• Hebeloma crustuliniforme (known as poison pie or fairy cakes) – causes gastrointestinal symptoms such as nausea and vomiting.
• Russula emetica (the sickener) – as its name implies, causes rapid vomiting. Other Russulas with a peppery taste (Russula silvicola, Russula mairei) will likely do the same.
• Agaricus hondensis, Agaricus californicus, Agaricus praeclaresquamosus, Agaricus xanthodermus – cause vomiting and diarrhea in most people, although some people seem to be immune.
• Lactifluus piperatus, Lactarius torminosus, Lactarius rufus – these and other peppery-tasting milk-caps are pickled and eaten in Scandinavia, but are indigestible or poisonous unless correctly prepared.
• Lactarius vinaceorufescens, Lactarius uvidus – reported to be poisonous. Arora reports that all yellow- or purple-staining Lactarius are "best avoided".
• Ramaria gelatinosa – causes indigestion in many people, although some seem immune.
• Gomphus floccosus (the scaly chanterelle) – causes gastric upset in many people, although some eat it without problems. G. floccosus is sometimes confused with the chanterelle.

Evolution

Many different species of mushrooms are poisonous and contain differing toxins that cause different types of harm. The most common toxin that causes severe poisoning is amatoxin, found in various mushroom species that cause the most fatalities every year. Amanita, or “ the death cap”, is a type of mushroom named for its substantial amount of amatoxin, which has about 10 mg per mushroom, which is the lethal dose. Amatoxin blocks the replication of DNA, which leads to cell death. This can affect cells that replicate frequently, such as kidneys, livers, and eventually, the central nervous system. It can also cause the loss of muscle contraction and liver failure. Despite the severe and dangerous symptoms, amatoxin poisoning is treatable given quick, professional care.

Mushrooms have also been found to have evolved toxicity independently from each other. Researchers have found that different mushroom species share the same type of amatoxin called amanitin. They specifically looked at three of the deadliest species, Amanita, Galerina, and Lepiota. Through genome sequencing, a scientific process that determines the DNA sequence of an organism’s genome, closely related mushrooms obtained genetic information via horizontal gene transfer. Once assimilated, it can then be passed down to an offspring. The researchers also concluded that there is “an unknown ancestral fungal donor,” that allowed for horizontal gene transfer.

Mushroom toxins have appeared and disappeared many times throughout their evolutionary history. Many scientists believe that the toxins evolved in mushrooms are used to deter predation, either from fungivores or mammals. If mushrooms are consumed, it can negatively affect their ability to disperse spores, survive, and reproduce. Snails and insects are fungivores and many have learned or evolved to avoid eating poisonous mushrooms. However, it is believed that mammals pose a higher threat to mushrooms than fungivores, as larger body sizes mean they are more capable of eating an entire fungus in one sitting.

Some phenotypes, or observable characteristics, may co-occur with toxicity, and therefore act as a warning signal. The first potential warning sign is aposematism, which is an adaptation that warns off predators based on a physical trait of an organism. In this case, the researchers were interested in observing whether the color of a mushroom deters predators. This would suggest that toxic mushrooms are of different colors than non-poisonous ones. The visual cue of some colors should be enough for predators to know not to consume the mushroom. The second possible warning sign is olfactory aposematism, a similar concept, but instead of focusing on color, the odor of the mushroom would be what deters predation. This would again indicate that poisonous mushrooms would emit a different odor than non-poisonous ones. Alternatively, is the ability of organisms to learn from other organisms. This would suggest that avoidance of toxic mushrooms is a learned behavior. Organisms may avoid toxic mushrooms if they observed other organisms of the same species consume the fungus. Learned behavior is when an organism learns how to behave based on previous experiences. Some researchers believe that if an organism got sick or observed another organism get sick from consuming a poisonous mushroom, then they would know not to continue consuming it for fear of getting sick again.

An analysis of 245 North American mushroom species and 265 from Europe, revealed 21.2% of the North American species and 12.1% of the European ones as poisonous. After collecting this information, and using a neural network to classify all of the mushrooms based on color and odor, the researchers concluded that there was no correlation between cap color and mushrooms containing toxins. The cap is the top, rounded part of a mushroom and comes in different colors. This proposes that the cap color does not act as a warning sign to deter predators, providing no evidence that poisonous mushrooms may not signal their toxicity through visual or chemical traits. The three deadly mushrooms listed above, Amanita, Galerina, and Lepiota, are all of different colors, consisting of reds, yellows, browns, and whites. A possible theory as to why color is not a factor in determining whether a mushroom is poisonous is the fact that many of its predators are nocturnal and have poor vision. Therefore, viewing the different colors is difficult, and could result in inaccurate consumption. The study, however, did suggest that poisonous mushrooms do emit a smell that is unpleasant and therefore discourages consumption. Despite this result, there is no definitive evidence to suggest if the odor is a result of the production of the toxin or if it is intended as a warning signal. Additionally, many of the odors are not picked up by humans. This could suggest that there is another characteristic difference between poisonous and non-poisonous mushrooms to avoid predation from larger mammals or that there is another purpose for some mushrooms being poisonous that is not dependent on predators.

Prognosis and treatment

Some mushrooms contain less toxic compounds and, therefore, are not severely poisonous. Poisonings by these mushrooms may respond well to treatment. However, certain types of mushrooms contain very potent toxins and are very poisonous; so even if symptoms are treated promptly, mortality is high. With some toxins, death can occur in a week or a few days. Although a liver or kidney transplant may save some patients with complete organ failure, in many cases there are no organs available. Patients hospitalized and given aggressive support therapy almost immediately after ingestion of amanitin-containing mushrooms have a mortality rate of only 10%, whereas those admitted 60 or more hours after ingestion have a 50–90% mortality rate. In the United States, mushroom poisoning kills an average of about 3 people a year. According to National Poison Data System (NPDS) annual reports published by America's Poison Centers, the average number of deaths occurring over a ten-year period (2012–2020) sits right at 3 a year. In 2012, 4 out of the 7 total deaths that occurred that year, were attributed to a single event where a "housekeeper at a Board and Care Home for elderly dementia patients collected and cooked wild (Amanita) mushrooms into a sauce that she consumed with six residents of the home.". Over 1,300 emergency room visits in the United States were attributed to poisonous mushroom ingestion in 2016, with about 9% of patients experiencing a serious adverse outcome.

Society and culture

Folklore

Many old wives' tales concern the defining features of poisonous mushrooms. However, there are no general identifiers for poisonous mushrooms, so such beliefs are unreliable. Guidelines to identify particular mushrooms exist, and will serve only if one knows which mushrooms are toxic.

Examples of erroneous folklore "rules" include:

• "Poisonous mushrooms are brightly colored." – Indeed, fly agaric, usually bright-red to orange or yellow, is narcotic and hallucinogenic, although no human deaths have been reported. The deadly destroying angel, in contrast, is an unremarkable white. The deadly Galerinas are brown. Some choice edible species (chanterelles, Amanita caesarea, Laetiporus sulphureus, etc.) are brightly colored, whereas most poisonous species are brown or white.
• "Insects/animals will avoid toxic mushrooms." – Fungi that are harmless to invertebrates can still be toxic to humans; the death cap, for instance, is often infested by insect larvae.
• "Poisonous mushrooms blacken silver." – None of the known mushroom toxins react with silver.
• "Poisonous mushrooms taste bad." – People who have eaten the deadly Amanitas and survived have reported that the mushrooms tasted quite good.
• "All mushrooms are safe if cooked/parboiled/dried/pickled/etc." – While it is true that some otherwise-inedible species can be rendered safe by special preparation, many toxic species cannot be made toxin-free. Many fungal toxins are not particularly sensitive to heat and so are not broken down during cooking; in particular, α-Amanitin, the poison produced by the death cap (Amanita phalloides) and others of the genus, is not denatured by heat.
• "Poisonous mushrooms will turn rice red when boiled." – A number of Laotian refugees were hospitalized after eating mushrooms (probably toxic Russula species) deemed safe by this folklore rule and this misconception cost at least one person her life.
• "Poisonous mushrooms have a pointed cap. Edible ones have a flat, rounded cap." – The shape of the mushroom cap does not correlate with presence or absence of mushroom toxins, so this is not a reliable method to distinguish between edible and poisonous species. Death cap, for instance, has a rounded cap when mature.
• "Boletes are, in general, safe to eat." – It is true that, unlike a number of Amanita species in particular, in most parts of the world, there are no known deadly varieties of the genus Boletus, which reduces the risks associated with misidentification. However, mushrooms like the Devil's bolete are poisonous both raw and cooked and can lead to strong gastrointestinal symptoms, and other species like the lurid bolete require thorough cooking to break down toxins. As with another mushroom genera, proper caution is, therefore, advised in determining the correct species.

Notable cases

Siddhartha Gautama (known as The Buddha), by some accounts, may have died of mushroom poisoning around ~479 BCE, though this claim has not been universally accepted.

Roman Emperor Claudius is said to have been murdered by being fed the death cap mushroom. However, this story first appeared some two centuries after the events, and it is debatable whether Claudius was murdered at all.

The best-selling author Nicholas Evans (The Horse Whisperer) was poisoned (but survived) after eating Cortinarius rubellus.

The parents of the physicist Daniel Gabriel Fahrenheit, who created the Fahrenheit temperature scale, died in Danzig on 14 August 1701 from accidentally eating poisonous mushrooms.

The composer Johann Schobert died in Paris, along with his wife, all but one of his children, their maidservant, and four acquaintances after insisting that certain poisonous mushrooms they had gathered were edible despite the express warning of cooks at two separate restaurants to which he had taken the mushrooms.

July 2023 Leongatha mushroom poisoning − Four people in Leongatha, Australia were taken to hospital after consuming beef Wellington suspected to have contained death cap mushrooms. Three of the four guests subsequently died and one survived, later receiving a liver transplant. The woman who cooked the meal, Erin Patterson, was charged with murder in November 2023. Patterson has pleaded not guilty and the Supreme court is expected to hear her case on 28 April, 2025.

In August 2023, Professor Vitaly Melnikov, 77, who had headed the Moscow Department of Rocket and Space Systems at RSC Energia (Russia's leading spacecraft manufacturer), became suddenly seriously ill and subsequently died after eating inedible mushrooms.