Do cats produce DMT?

Do cats produce DMT?

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Edit: If somebody (anybody) wants to add an answer so the bounty won't go to waste, please do so! The comments have already introduced me to the Kegg metabolism database, some interesting papers, and an amazing chapter on the biochemistry of cats. Thus, this question has been useful to me (and hopefully, to the community as well).

There is a question on Skeptics.SE that asks if "cats have a chemical in their brains that resembles LSD." I haven't found any similar claim online, but started wondering: 1. Do cats produce (natural) compounds that structurally resemble LSD? 2. Do cats produce (natural) compounds that functionally resemble LSD? Quickly glancing at the structure of LSD, it contains an indole ring. Hovering over the various indoles here found one substance that occurred in animals and was consumed as a psychedelic drug.

There is a paper that writes:

N,N-Dimethyltryptamine (DMT) is an indole alkaloid widely found in plants and animals. It is best known for producing brief and intense psychedelic effects when ingested. Increasing evidence suggests that endogenous DMT plays important roles for a number of processes in the periphery and central nervous system, and may act as a neurotransmitter.

The paper also proposed the role of DMT as a neurotransmitter. However, I haven't been able to confirm DMT is naturally produced by cats.

Do cats produce DMT? If so, what is the purpose of DMT in the cat?

Yes! Many mammals, including cats and humans, produce DMT in small amounts.

DMT has been detected in blood and urine and is produced by the enzyme indolethylamine N‐methyltransferase (INMT). These do bind to serotonin receptors. Serotonin receptors are actually expressed in multiple tissues outside of the brain. However, DMT does cross the blood-brain barrier (ref), so it's possible that endogenous DMT has some neuroactive effect (I really don't know). Good question.

This 2016 paper states (referring to a 2012 review) that it was identified in urine, blood, and CSF:

A review by Barker in 2012 assessed 69 studies that reported endogenous DMT detection and quantities reported in urine (29 studies), blood (11 studies), and cerebrospinal fluid (4 studies) from 1955 - 2010 primarily comparing detection levels within healthy controls and schizophrenic patients. DMT in urine was examined in 861 individuals (635 patients), 276 patients and 145 controls were positive for DMT.

I think that's the most direct answer to you question I could find. I didn't find anything on cats specifically, but that's likely to be similar.

This earlier 2004 paper states that it was only found in urine, but the previous study refers to studies before 2004, so I don't know why these two seem to contradict:

In mammals, endogenous bufotenine and DMT have been identified only in human urine. The DMIAs bind effectively to 5HT receptors and their administration causes a variety of autonomic effects, which may reflect their actual physiological function. Endogenous levels of bufotenine and DMT in blood and a number of animal and human tissues were determined using highly sensitive and specific quantitative mass spectrometric techniques.

Here's the entry for INMT on Kegg, and the Human Protein Atlas lists where INMT is expressed. Weirdly, that enzyme is highly expressed in the human lung.

Why do psychedelic plants exist evolutionarily?

40 comments, there were no satisfying answers. Why do these plants have those properties? As a defense mechanism? And more importantly, why does that have these crazy effects on our brain? Just luck that they resemble molecules in our brain?

Psychedelic compounds, like any secondary metabolite (that includes any compound a plant produces that isn't a result or side effect of the normal metabolic processes it uses to stay alive), evolve mostly to ward off herbivores and infection. The main threats to plants are insects, so these compounds evolve to damage insect nervous systems. Some examples of psychoactive (but not psychedelic) compounds that do a very good job of killing insects are nicotine and its analogues (which include lobeline, found in the Lobelia genus, anabasine, found in betel nut, and cytisine, found in a wide variety of toxic legumes including the misleadingly named mescal bean). These compounds attach themselves to the receptors that transmit signals from nerves to muscle, causing the muscles to be able to move. By continually activating the muscle, it depolarizes the motor nerve, keeping the muscle paralyzed in one position. This can be deadly.

Harmine, found in Syrian rue (Peganum harmala) and the ayahuasca vine (Banisteriosis caapi), can kill off certain fungi and bacteria that infect plants in lab studies (which unfortunately I don't remember the links to off the top of my head).

I can't find any research specifically about psychedelic compounds having adverse effects on herbivores or preventing infection, but I did find research showing that activating serotonin receptors (which is what classical psychedelics do) in insects reduces feeding. It also can cause nausea and vomiting in birds and mammals.

[Edit: my source for this information primarily comes from this book, which I read a while ago so details might not be 100% accurate.]

Citation required. Psychedelic, as opposite to psychoactive.

This is all good information, but is it just a coincidence that it has these weird effects on our brain?

I have a question regarding your response. If a plant evolved these capabilities to either be psychoactive or psychedelic. How would the plants know which chemicals to start producing that would create these affects on other animal life? These types of adaptations in nature have confused me greatly. Would these things start off by an accidental mutation or would it have been more of a trial and error type thing?

What differentiates phycoactive and phycadelic?

Sorry to be so picky (seeing as the rest of it is factually correct) but I do have to call you out on a wording issue since it gives the non-scientific community a misunderstanding of evolution and how it works. Please refrain from using the phrase "evolves to" or "evolved to" as evolution has no direction or goal. This type of simple wording mistake that forces people in the evolutionary biology field to be fighting such an uphill battle against misinformation. Much of the non-scientific community still believe that evolution, in scientists' minds, is as Lamarck hypothesized, but that is simply not true.

So is the reason humans don't suffer those problems from nicotine/other a dosage problem, problem of scale, or other?

A researcher named Randolph Nesse wrote a couple of articles back in the day on this very thing: evolutionary bases of addiction and addictive substances. Don't have his website off the top of my head, but a little searching through Google should dig it up, he's got copies of everything there.

on that side topic, caffeine works the same was a nicotine on insects, just worth noting

here is an article about cats on LSD.

we now know that both cats and humans are reacting to LSD, we can assume that many other animals will also do.

as some of us know, being on psychedelics can be a pretty unpleasant experience, especially if you don't actually know that you are.

in the long distant past, some random deer-like animal may have eaten way to much ergot-infested rye, seen some hallucinated pink elephants and stopped eating rye with brown things hanging from it. thus allowing the first LSD ergotamine producing ergot to reproduce

keep in mind that not all mutations are usefull. some are entirely useless and just spread in the population because they are also not detrimental to reproduction. there is no indication that i'm aware of that psychodelic substances actually have an evolutionary benefit for the plants producing them.

Ergot fungus does not produce LSD it produces ergotamine. Which was turned into LSD by Albert Hoffman.

Remember that evolutionary theory would say that evolution is an unguided process.

The answer to the "why" question is a philosophical question that hints at purpose and conscious decision. In some ways the why question is inappropriate for a question about evolution. It invites questions of purpose, philosophy, and even religion or design.

There are a couple ways to look at this. I am thinking about all psychoactive substances, not just psychedelics.

The question could also be asked - “why did humans evolve so that plant products cause psychoactive responses in our brains?” Let’s leave that question aside for now.

First, let’s look at chemicals like alcohol, produced by yeast as a waste product . The alcohol is a waste product, that we happen to like. This is not difficult to understand because human intervention has helped things like brewers yeast thrive and survive because we like the alcohol.

Second, look at chemicals that have a function in the plant, but also affect us. There is no reason to assume there is any link between the effect on humans and the production of the product in the plant. This is a happy coincidence. There is no “grand purpose” or “why” in this case. Unfortunately, for our discussion, I am not aware of any cases where a primary metabolite has a psychoactive effect in humans. Most literature I read talks about secondary metabolites having psychoactive properties.

Third, lets look at toxins that have psychoactive features if you get the dosing just right. If a plant is toxic, many species will learn not to eat it. An example of this would nicotine (10 mg lethal dose for adult human). We don’t eat tobacco in a salad because it would kill us. It makes sense for this plant to have thrived while others were eaten to extinction. This also works to kill insects,

Fourth, Lets look at psychoactives as a strategy in seed dispersal. Humans like them, and the cultivate and grow them on purpose. The problem with this is that evolution is supposed to be undirected. Unless you say they were developed by accident, but gave the plant a selective advantage you get into the philosophical / religious question of “why?” The more complicated the molecule, or the more energy used in the metabolic pathway of its production, the less this seems like a “happy accident” of evolution, and the more it points to the intelligent design philosophical argument..

Fifth, the majority of psychoactives are secondary metabolites that have minor or no known function in the plant. The plant seems to have a well developed pathway that does little for the plant, but is still retained in its current state of evolution / development. The wiki on plant secondary metabolites says we don’t know what function (if any) most of these have in the plant. This is a huge scientific and philosophical question.


Tortoiseshell cats have particolored coats with patches of various shades of red and black, and sometimes white. The size of the patches can vary from a fine speckled pattern to large areas of color. Typically, the more white a cat has, the more solid the patches of color. Dilution genes may modify the coloring, lightening the fur to a mix of cream and blue, lilac or fawn the markings on tortoiseshell cats are usually asymmetrical. [12]

Occasionally tabby patterns of black and brown (eumelanistic) and red (phaeomelanistic) colors are also seen. These patched tabbies are often called a tortie-tabby, a torbie or, with large white areas, a caliby. [12] Not uncommonly there will be a "split face" pattern with black on one side of the face and orange on the other, with a dividing line running down the bridge of the nose. Tortoiseshell coloring can also be expressed in the point pattern, referred to as a tortie point. [12]

Tortoiseshell and calico coats result from an interaction between genetic and developmental factors. The primary gene for coat color (B) for the colors brown, chocolate, cinnamon, etc., can be masked by the co-dominant gene for the orange color (O) which is on the X Chromosome and has two alleles, the orange (X O ) and not-orange (X o ), that produce orange phaeomelanin and black eumelanin pigments, respectively. (NOTE: Typically, the X for the chromosome is assumed from context and the alleles are referred to by just the uppercase O for the orange, or lower case o for the not-orange.) The tortoiseshell and calico cats are indicated: Oo to indicate they are heterozygous on the O gene. The (B) and (O) genes can be further modified by a recessive dilute gene (dd) which softens the colors. Orange becomes cream, black becomes gray, etc. Various terms are used for specific colors, for example, gray is also called blue, orange is also called ginger. Therefore, a tortoiseshell cat may be a chocolate tortoiseshell or a blue/cream tortoiseshell or the like, based on the alleles for the (B) and (D) genes.

The cells of female cats, which like other mammalian females have two X chromosomes (XX), undergo the phenomenon of X-inactivation, [13] [14] in which one or the other of the X-chromosomes is turned off at random in each cell in very early development. The inactivated X becomes a Barr body. Cells in which the chromosome carrying the orange (O) allele is inactivated express the alternative non-orange (o) allele, determined by the (B) gene. Cells in which the non-orange (o) allele is inactivated express the orange (O) allele. Pigment genes are expressed in melanocytes that migrate to the skin surface later in development. In bi-colored tortoiseshell cats, the melanocytes arrive relatively early, and the two cell types become intermingled, producing the characteristic brindled appearance consisting of an intimate mixture of orange and black cells, with occasional small diffuse spots of orange and black.

In tri-colored calico cats, a separate gene interacts developmentally with the coat color gene. This spotting gene produces white, unpigmented patches by delaying the migration of the melanocytes to the skin surface. There are a number of alleles of this gene that produce greater or lesser delays. The amount of white is artificially divided into mitted, bicolor, harlequin, and van, going from almost no white to almost completely white. In the extreme case, no melanocytes make it to the skin and the cat is entirely white (but not an albino). In intermediate cases, melanocyte migration is slowed, so that the pigment cells arrive late in development and have less time to intermingle. Observation of tri-color cats will show that, with a little white color, the orange and black patches become more defined, and with still more white, the patches become completely distinct. Each patch represents a clone of cells derived from one original cell in the early embryo. [15]

A male cat, like males of other therian mammals, has only one X and one Y chromosome (XY). That X chromosome does not undergo X-inactivation, and coat color is determined by which allele is present on the X. Accordingly, the cat's coat will be either entirely orange or non-orange. Very rarely (approximately 1 in 3,000 [16] ) a male tortoiseshell or calico is born these typically have an extra X chromosome (XXY), a condition known in humans as Klinefelter syndrome, and their cells undergo an X-inactivation process like in females. As in humans, these cats often are sterile because of the imbalance in sex chromosomes. Some male calico or tortoiseshell cats may be chimeras, which result from fusion in early development of two (fraternal twin) embryos with different color genotypes these torties can pass only one color to their offspring, not both, according to which of the two original embryos its testes are descended from. Others are mosaics, in which the XXY condition arises after conception and the cat is a mixture of cells with different numbers of X chromosomes.

Are All Orange Cats Male?

About 81 percent of orange cats are male, says Bell. While female cats will inherit an orange coat only if they carry the orange gene on both X chromosomes, if a male carries the orange gene at all, he will be orange, says Konecny.

“As the frequency of the orange gene is much less than the frequency of the black gene in the general cat population, the chance of having two orange genes is much less frequent. This makes male orange cats more frequent than orange females,” Bell says.

What does this all mean for their offspring? If a mother cat is orange, her male kittens will be orange regardless of their father’s color, Konecny says, and if a mother cat is tortoiseshell (a mix of black, white and orange), half of her male kittens will be orange while the other half will be black.

To get an orange female kitten, both the mother and father must be orange, Konecny says. If the mother cat is tortoiseshell and the father cat is orange, half of the female kittens will be orange, she says.

Daniel Pinchbeck’s DMT Demons

With many psychedelic experiences, users are often confronted with bottled-up emotions, forcing them to deal with issues that may not be pleasant – the death of the ego, as it were. These feelings, buried under layers of emotional scar tissue, can be difficult to deal with and can manifest in the form of ostensibly physical demons.

This can be incredibly frightening during the trip, but users often report a sense of accomplishment or closure for dealing with them after the fact. The term ‘confronting your demons’ can become very literal on psychotropic compounds.

But with DMT, this isn’t always the case. Rather than entities born from individual emotion, people describe meeting entirely autonomous entities, so bizarre and alien that one can’t possibly imagine having created them with their mind. Hence, the reason Dr. Griffiths is so intrigued.

In his book, Breaking Open the Head, Daniel Pinchbeck describes meeting negative autonomous entities that continued to haunt him for weeks after his trip with a DMT molecular variant called DPT.

Similar to some accounts of DMT entities, Pinchbeck said the beings he encountered expressed disdain or pity for his presence as a mere human. Others have said they experienced indifference from DMT entities or messages saying, “Ok, you’ve seen it, now leave.”

But with DPT, Pinchbeck was subjected to a terrifying world of gothic insects, lizards and winged creatures, describing it as a postmodern demonic MTV psychedelic. He realized in retrospect that taking a drug of that magnitude without the shamanic ceremonial aspect was disrespectful and maybe a factor in his frightening experience.

In the weeks following, Pinchbeck had strange synchronicities, bizarre dreams, and what he describes as a poltergeist in his apartment. Mirrors fell off the wall in the night, strange foreign bugs appeared, and unusual physical sensations plagued him. He confirmed the presence of negative energy with others and held an exorcism to rid himself of them.

In the end, a Buddhist meditation helped purge him of the demon, bringing his life back to normal. To Pinchbeck, the entities met on this DMT analogue couldn’t have been more real or more autonomous.

It’s hard to tell whether Dr. Griffiths and his colleagues will be able to uncover just what or who exactly these DMT entities are based solely on stories from strangers on the internet. Dr. Rick Strassman conducted a more in-depth experiment with his work creating the book and documentary, DMT: The Spirit Molecule, though Griffiths comes from a different filed of expertise.

Are these entities really autonomous beings living in a parallel dimension not too far from our own, and will probing deeper give us a better understanding of how they may relate to reality as we know it?

Newly identified saber-toothed cat species was larger than a tiger and hunted rhinos

Researchers have stated that a scimitar-toothed cat, larger than the largest tigers alive today, lived in North America 5 to 9 million years ago, and used its giant fauna to hunt bison and rhinoceros.

The previously unknown species is believed to be one of the largest cats ever discovered, and was identified several years after a large upper arm bone sample, labeled as a cat, was released from the university Was found in the collection of the Oregon Museum of Natural. Cultural history, but which surprised scientists.

The giant bone was discovered by John Orcutt, an assistant professor of biology at Gonzaga University when he was a graduate student, and the discovery took a year of effort to find out which species of cat it might have been from.

In total, the researchers used seven previously unclassified fossil specimens, along with other fossils and bone specimens from around the world, to describe the new species.

The cat is an ancient relative of one of the most famous prehistoric animals – the scimitar-toothed cat Smilodon, although it would have been far larger and more frightening.

It weighed up to 900 pounds (6 stones, or 706 kg), and “managed to kill prey weighing up to 6,000 pounds (2.9 tons). In comparison, a large adult male tiger weighed 700.” Will be up to pounds (310 kg).

“We believe these were animals that were regularly taking down bison-sized animals,” said study co-author Jonathan Calday, assistant professor of development, ecology and biology at The Ohio State University .

“It was the largest cat alive at that time,” he said.

The specimen, which was rediscovered by Dr. Orcutt, was originally excavated on the traditional lands of the Cayuse, a tribe joining the federal tribes of the Umatilla Indian Reservation along with Umatilla and Walla Walla.

In recognition of the origin of the specimen, the research team collaborated with the Tamastislict Cultural Institute to name the new species Macarodus Lahashupup. Macarodus The large saber is a species of toothed cats that lived in Africa, Eurasia, and North America, and in the old Cayuz language, Lahis hapup means “ancient wild cat”.

But the research not only revealed previously unrecognized species, but it also provided important new insights into how cats’ leg bones can indicate which species they belong to.

“One of the big stories of all of this is that we ended up opening the specimen in museums in western North America after specimens of this giant cat,” Dr. Orcutt said.

“They were obviously big cats. We started with some assumptions based on their age, in the range of 5.5 to 9 million years old, and their size, because these things were huge.

“What we didn’t have at the time is what we have now, it’s a test of whether the shape and anatomy of those bones tell us anything – and it turns out that yes, they do.”

Largest of seven Macarodus Lahashupup The humerus fossils available for analysis were more than 18 inches (45 cm) long and 1.7 inches in diameter. In comparison, the humerus of an average modern adult male lion is about 13 inches long.

Researchers hypothesized that if a single fore-arm bone could be useful in distinguishing species, it would still hold true among living large cat species.

Dr. Calday and Dr. Orcutt visited several museums in the US, Canada and France to identify the foreground specimens of lions, pumas, panthers, jaguars and tigers, as well as already extinct big cats.

Dr. Calday used software to place landmark marks on each digitized specimen, which, when pulled together, would produce a model of each elbow.

“We found that we could measure differences on a fairly good scale,” Dr. Caled said. “It told us that we could use the shape of the elbow to tell different species of modern big cats.

“Then we moved the device to the fossil record – these giant elbows scattered in museums all had a specialty. It told us that they were all of the same species.

“Their unique shape and size told us that they were very different from everything previously known. In other words, these bones belong to one species and that species is a new species.”

Researchers calculated body size estimates of new species based on the association between humerus size and body mass in modern big cats, and about cat prey based on the size and animals of the animals that lived in the area at the time. Guessed it.

He said rhinoceros was particularly abundant, as well as ancient species such as giant camels from the high Arctic, which roamed Canada until about 12,000 years ago, and huge land lethargy that was as large as modern elephants.

One specimen contained teeth from the lower part of the jaw, but did not include the saber-shaped canines.

“We are convinced that this is a saber-toothed cat and we are confident that it is a new species Macarodus Genus, ”said Dr. Orcutt.

“The problem is partly because we didn’t have a clear-cut image of how many species there were in the past, our understanding of how all these saber-toothed cats relate to each other is a bit unclear, especially early on. in development. “

The researchers said that establishing that the humerus can be analyzed alone to identify the fossil cat has important implications for the field. Not least because the large arm bones of saber-toothed cats are the most common specimens of fossil cats found in excavations.

Reconstructing the evolutionary history of scimitar-toothed cats can only determine where this new species fits, but Dr. Orcutt and Dr. Calday believe that Macarodus Lahashupup The group existed early in its development.

A discovery that this giant cat existed in North America at the same time as similar animals lived around the world also raises another evolutionary question, Dr. Caled said.

“It is known that there were giant cats in Europe, Asia and Africa, and now we have our own giant saber-toothed cat in North America during this period as well,” he said.

“There is a very interesting pattern of repeated independent evolution on every continent of this huge body shape which is a very unique way of hunting, or we have this ancestral giant scimitar-toothed cat that is on all those continents. Has spread to.

7 Cool Scientific Facts About Your Cat’s Brain

One moment I’m amazed by my cats’ intelligence and sensitivity, and the next I’m watching them do some outrageously stupid thing and wondering, “Tell me again: Why do I think cats are so smart?” Then there was the time my cats learned how to open the refrigerator while I was away from home and dine on everything within, and I said, “Dammit, you cats are too smart for your own good!”

I’ve been geeking out about the brain for most of my life, and here are some good reasons for you to geek out about the awesomeness of this essential part of feline anatomy, your cat’s brain.

1. Cat brains are comparatively smaller than ours

In terms of the ratio of brain mass to body mass, a cat’s brain takes up 0.9 percent of total body mass. Humans’ brains occupy about 2 percent of total body mass, and dogs’ brains occupy about 1.2 percent . But when it comes to intelligence, size matters a whole lot less than other factors.

2. Structurally, cats’ brains are more complex than dogs’

The cerebral cortex is the area of the brain responsible for thinking and rational decision-making. Cats’ cerebral cortexes are much more complex than those of dogs, with almost 300 million nerve cells compared to about 160 million in the dog.

3. Cats have better short-term memory than dogs

In an experiment in which cats and dogs were tested to find out how well they could remember where food had been hidden, cats’ short-term memory lasted about 16 hours, whereas dogs’ only lasted about five minutes.

4. Researchers don’t know which species has better long-term memory

Although cats don’t store a lot of information in long-term memory, the people and places cats choose to bank in long-term storage can stay put for many years. Since the cerebral cortex is responsible for storing long-term memory, it could be argued that a cat’s more complex cerebral cortex may lead to better long-term memory.

5. Cats learn by observation

If your cat watches you open the cabinet enough times, he will, like my refrigerator-opening feline housemates, figure out how to do it by himself. Kittens learn by watching their mothers hunt, eat, groom, and so on, and then repeating the behavior themselves until they get it right.

6. Cats’ brain function can decline as they age

Elderkitties can develop a condition similar to Alzheimer’s disease. Feline cognitive dysfunction syndrome is caused by deterioration of the brain and can lead to symptoms such as disorientation, depression, inappropriate elimination and antisocial behavior. But just as with humans, not all cats develop this disease.

7. A cat is a lot smarter than an iPad

You may think your new tablet is awesome: so much processing power, so much storage space, so much speed. But don’t gloat too much, because your cat’s brain can smoke your iPad. A typical iPad has 60 gigabytes of data storage space, but your cat’s brain has about 91,000 gigabytes. In terms of processing speed, your iPad does about 170 million operations per second. Your cat’s brain, on the other hand, does 6.1 trillion operations per second. Unfortunately, your cat doesn’t have wi-fi and 4G data access.

Is there anything else you’d like to know about the feline brain? Ask me — I may answer your question in a future column!

About JaneA Kelley: Punk-rock cat mom, science nerd, animal shelter volunteer, and all-around geek with a passion for bad puns, intelligent conversation, and role-play adventure games. She gratefully and gracefully accepts her status as chief cat slave for her family of feline bloggers, who have been writing their cat advice column, Paws and Effect, since 2003. JaneA dreams of making a great living out of her love for cats.


Male lactation was of some interest to Alexander von Humboldt, who reports in Voyage aux régions équinoxiales du Nouveau Continent of a citizen of the village Arenas (close to Cumana) who allegedly nurtured his son for three months when his wife was ill, [1] as well as Charles Darwin, who commented on it in The Descent of Man, and Selection in Relation to Sex (1871):

It is well known that in the males of all mammals, including man, rudimentary mammae exist. These in several instances have become well developed, and have yielded a copious supply of milk. Their essential identity in the two sexes is likewise shown by their occasional sympathetic enlargement in both during an attack of the measles. [2]

Darwin later considered the nearly perfect function of male nipples in contrast to greatly reduced structures such as the vesicula prostatica, speculating that both sexes may have nursed young in early mammalian ancestors, and subsequently mammals evolved to inactivate them in males at an early age. [3]

Male mammals of many species have been observed to lactate under unusual or pathogenic conditions such as extreme stress, castration and exposure to phytoestrogens, or pituitary tumors. Therefore, it is hypothesized that, while most male mammals could easily develop the ability to lactate, there is no selective advantage to male lactation. While male mammals could, in theory, improve offspring's survival rate through the additional nourishment provided by lactation, most have developed other strategies to increase the number of surviving offspring, such as mating with additional partners. Presently, very few species are known where male lactation occurs and it is not well understood what evolutionary factors control the development of this trait. [4]

The phenomenon of male lactation occurs in some species, notably the Dayak fruit bat (Dyacopterus spadiceus) and the Bismark masked flying fox (Pteropus capistratus), and the lactating males may assist in the nursing of their infants. In addition, male goats are known to lactate on occasion. [5]

Human male breastfeeding is possible, but production of the hormone prolactin is necessary to induce lactation, so male lactation does not occur under normal conditions. Also, the male breasts lack special lobules that are anatomically present in a female's breast. [6] Domperidone is a drug that can be used to increase lactation. Male lactation has also been seen during recovery from starvation. This may be because glands that produce hormones recover more quickly than the liver, which absorbs hormones, leading to high hormone levels. [7]

Spontaneous production of milk not associated with childbirth, known as galactorrhea, can occur in males and females. [8]


Eumelanin Edit

The browning gene B/b/b l codes for TYRP1 ( Q4VNX8 ), an enzyme involved in the metabolic pathway for eumelanin pigment production. Its dominant form, B, will produce black eumelanin. It has two recessive variants, b(chocolate), and b l (cinnamon), with b l being recessive to both B and b. [1] Chocolate is a rich brown color, and is referred to as chestnut in some breeds. Cinnamon is a lighter reddish brown.

Sex-linked orange/red Edit

The sex-linked Orange locus, O/o, determines whether a cat will produce eumelanin. In cats with orange fur, phaeomelanin (red pigment) completely replaces eumelanin (black or brown pigment). [2] This gene is located on the X chromosome. The orange allele is O, and is codominant with non-orange, o. Males can typically only be orange or non-orange due to only having one X chromosome. Since females have two X chromosomes, they have two alleles of this gene. OO results in orange fur, oo results in black or brown fur, and Oo results in a tortoiseshell cat, in which some parts of the fur are orange and others areas non-orange. [3] Male tortoiseshell cats are known to exist, but, as expected from the genetics involved, they are rare and often exhibit chromosomal abnormalities. [4] In one study, less than a third of male calicos had a simple XXY Klinefelter's karyotype, slightly more than a third were complicated XXY mosaics, and about a third had no XXY component at all. [4]

This color is known as red by breeders. Other names include yellow, ginger, and marmalade. Red show cats have a deep orange color, but it can also present as a yellow or light ginger color. Unidentified "rufousing polygenes" are theorized to be the reason for this variance. Orange is epistatic to nonagouti, so all red cats are tabbies. "Solid" red show cats are usually low contrast ticked tabbies. [5]

The precise identity of the gene at the Orange locus is unknown. It has been narrowed down to a 3.5 Mb stretch on the X chromosome in 2009. [5]

Dilution and Maltesing Edit

The Dense pigment gene, D/d, codes for melanophilin (MLPH A0SJ36 ), a protein involved in the transportation and deposition of pigment into a growing hair. [5] When a cat has two of the recessive d alleles (Maltese dilution), black fur becomes "blue" (appearing gray), chocolate fur becomes "lilac" (appearing light brown), cinnamon fur becomes fawn, and red fur becomes cream. The d allele is a single-base deletion that truncates the protein. [5]

Other genes Edit

  • Barrington Brown is a recessive browning gene that dilutes black to mahogany, brown to light brown and chocolate to pale coffee. It is different from the browning gene and has only been observed in laboratory cats. [6]
  • The Dilution modifier gene, Dm, "caramelizes" the dilute colors as a dominant trait. The existence of this phenomenon as a discrete gene is a controversial subject among feline enthusiasts.
  • A mutation at the extension locus E/e (the melanocortin 1 receptor, MC1R) changes black pigment to amber or light amber. Kittens are born dark but lighten up as they age. Paws and nose still exhibit the original undiluted color, this in contrast to other diluted colors, where paws and nose have the diluted color. This phenomenon was first identified in Norwegian Forest cats. [7]
  • Another recessive mutation at extension was discovered which causes the russet color in Burmese cats. It is symbolized as e r . Like amber cats, russet cats lighten as they age. [8]
  • A modifying factor has also been hypothesized in shaded silver and chinchilla Persians whose fur turns pale golden in adulthood, due to low levels of phaeomelanin production. These cats resemble shaded or tipped goldens, but are genetically shaded or tipped silvers. This is probably related to the phenomenon known as "tarnishing" in silvers.

Tabby cats are striped due to the agouti gene. Their stripes have an even distribution of pigment, while the background is made up of banded hairs. Tabby cats usually show the following traits:

  • M on forehead. (Visible in ticked tabby cats, but hard to discern in shaded silver/golden, and tipped cats)
  • Thin pencil lines on face. (Visible in ticked tabby cats, but hard to discern in shaded silver/golden, and tipped cats)
  • Black "eyeliner" appearance and white or pale fur around eyeliner.
  • Pigmented lips and paws.
  • A pink nose outlined in darker pigment.
  • Torso, leg, and tail banding. (Torso banding disappears in the ticked tabby.)

Agouti Edit

The Agouti gene, with its dominant A allele and recessive a allele, controls the coding for agouti signaling protein (ASIP Q865F0 ). The wild-type A produces the agouti shift phenomenon, which causes hairs to be banded with black and an orangish/reddish brown, this revealing the underlying tabby pattern (which is determined by the T alleles at the separate tabby gene). The non-agouti or "hypermelanistic" allele, a, does not initiate this shift in the pigmentation pathway and so homozygotes aa have pigment production throughout the entire growth cycle of the hair—along its full length. [9] As a result, the non-agouti genotype (aa) is solid and has no obvious tabby pattern (sometimes a suggestion of the underlying pattern, called "ghost striping", can be seen, especially in bright slanted light on kittens and on the legs, tail and sometimes elsewhere on adults). Agouti is found on chromosome A3.

A major exception to the solid masking of the tabby pattern exists: the O allele of the O/o locus is epistatic over the aa genotype. That is, in red or cream colored cats, tabby striping is displayed despite the genotype at the agouti locus. This explains why you can usually see the tabby pattern in the orange patches of non-agouti tortoiseshell cats, but not in the black or brown patches.

However, some red cats and most cream cats show a fainter tabby pattern when they have no agouti allele to allow full expression of their tabby alleles. That is, in genetically red cats (O males and OO and Oo females) the aa does still have an effect, especially in dilute coats (when having dd genotype at the D gene locus), where the tabby pattern is sometimes not expressed except on the extremities.

Mackerel or blotched Edit

The Tabby gene on chromosome B1 accounts for most tabby patterns seen in domestic cats, including those patterns seen in most breeds. The dominant allele Ta M produces mackerel tabbies, and the recessive Ta b produce classic (sometimes or once referred to as blotched) tabbies. [10] The gene responsible for this differential patterning has been identified as transmembrane aminopeptidase Q (Taqpep, M3XFH7 ). A threonine to asparagine substitution at residue 139 (T139N) in this protein is responsible for producing the tabby phenotype in domestic cats. In cheetahs, a base pair insertion into exon 20 of the protein replaces the 16 C-terminal residues with 109 new ones (N977Kfs110), generating the king cheetah coat variant. [11]

The wild-type (in African wildcats) is the mackerel tabby (stripes look like thin fishbones and may break up into bars or spots), the most common variant is the classic tabby pattern (broad bands, whorls, and spirals of dark color on pale background usually with bulls-eye or oyster pattern on flank). The classic tabby is most common in Iran, Great Britain and in lands that were once part of the British Empire and Persian Empire. [11]

Spotted tabby Edit

Spotted tabbies have their stripes broken up into spots, which may be arranged vertically or horizontally. A 2010 study suggests that spotted is caused by the modification of mackerel stripes, and may cause varying phenotypes such as "broken mackerel" tabbies via multiple loci. [10]

Ticked tabby Edit

The Ticked (Ti) locus on chromosome A1 controls the generation of ticked coats, a non-patterned agouti coat having virtually no stripes or bars but still considered a tabby coat. The Ti A is the dominant allele that produces ticked coats Ti + is the recessive one. Stripes often remain to some extent on the face, tail, legs, and sometimes the chest in heterozygotes (Ti A Ti + ) but are nearly or completely nonexistent in homozygotes (Ti A Ti A ). The Abyssinian breed is fixed for the ticked allele—all Abyssinians are homozygotes for this gene. The ticked tabby allele is ultimately dominant and therefore completely (or mostly) masks all the other tabby alleles, “hiding” the patterns they would otherwise express. [10]

It was once thought that Ti A is a very dominant allele of the Tabby gene called T a . [12]

Other genes Edit

  • Other genes (pattern modifier genes) are theorized to be responsible for creating various type of spotting patterns, many of which are variations on a basic mackerel or classic pattern. There are also hypothetical factors which affect the timing and frequency of the agouti shift, affecting agouti band width and the number and quality of alternating bands of eumelanin and phaeomelanin on individual hairs.
  • There is a gene not yet identified, but believed to be related to the agouti gene in the Chausie breed that produces silver-tipped black fur similar to Abyssinian ticked fur, known as "grizzled." This phenomenon is purported to have been inherited from the hybridization of the domestic cat to the jungle cat (Felis chaus).
  • The inhibited pigment gene, I/i. The dominant allele (I) produces tipped hairs that are fully colored only at the tip and have a white base. This allele appears to interact with other genes to produce various degrees of tipping, ranging from deeply tipped silver tabby to lightly tipped shaded silver and chinchilla silver. The inhibitor gene interacts with the non-agouti genotype (I-aa) to produce the color known as smoke. The homozygous recessive genotype when combined with the agouti gene (iiA-), produces tabby coloration, which can vary along a spectrum ranging from a deeply patterned brown tabby, to a lighter "golden tabby", to the very lightly colored shaded or chinchilla golden colors. Orange cats with the inhibitor gene (I-O-) are commonly called "cameo".

Tortoiseshells are also known by the abbreviation "tortie". Tortoiseshells have patches of orange fur (pheomelanin based) and black or brown (eumelanin based) fur, caused by X-inactivation. Because this requires two X chromosomes, the vast majority of tortoiseshells are female, with approximately 1 in 3,000 being male. [13] Male tortoiseshells can occur as a result of chromosomal abnormalities such as Klinefelter syndrome, by mosaicism, or by a phenomenon known as chimerism, where two early stage embryos are merged into a single kitten.

Tortoiseshells with a relatively small amount of white spotting are known as "tortoiseshell and white", while those with a larger amount are known in North America as calicos. Calicos are also known as tricolor cats, mi-ke (meaning "triple fur") in Japanese, and lapjeskat (meaning "patches cat") in Dutch. The factor that distinguishes tortoiseshell from calico is the pattern of eumelanin and pheomelanin, which is partly dependent on the amount of white, due to an effect of the white spotting gene on the general distribution of melanin. A cat which has both an orange and non-orange gene, Oo, and little to no white spotting, will present with a mottled blend of red/cream and black/blue, reminiscent of tortoiseshell material, and is called a tortoiseshell cat. An Oo cat with a large amount of white will have bigger, clearly defined patches of red/cream and black/blue, and is called a calico. With intermediate amounts of white, a cat may exhibit a calico pattern, a tortie pattern, or something in between, depending on other epigenetic factors. Diluted calico cats with lighter coloration are sometimes called calimanco or clouded tiger. [14]

A true tricolor must consist of three colors: white a red, orange, yellow, or cream pheomelanin color and a black, brownish, or gray (blue) eumelanin color. Tricolor should not be mistaken for the natural gradations in a tabby pattern. The shades which are present in the pale bands of a tabby are not considered to constitute a separate color. [15]

Variations Edit

  • The basic tortoiseshell pattern has several different colors depending on the color of the eumelanin (the B locus), and dilution (the D locus).
  • Tortoiseshell tabbies, also known as torbies, display tabby patterning on both colors. Calico tabbies are also called calibys or tabicos. [16]

White spotting and epistatic white (also known as dominant white) were long thought to be two separate genes, but in fact they are both on the KIT gene. White spotting can take many forms, from a small spot of white to the mostly-white pattern of the Turkish Van, while epistatic white produces a fully white cat. The Birman-specific recessive "gloving" trait is also located on the KIT gene. [17]

  • W D = dominant white, linked to blue eyes and deafness. The deafness is due to a reduction in the population and survival of melanoblast stem cells, which in addition to creating pigment-producing cells, develop into a variety of neurological cell types. White cats with one or two blue eyes have a particularly high likelihood of being deaf.
  • W S = white spotting. It exhibits codominance and variable expression heterozygous cats have somewhere between 0-50% white, and homozygous cats have between 50-100% white.
  • w = wild type, no white spotting.
  • w g = recessive Birman white gloving allele. [18]

W D causes congenital sensorineural deafness in cats. Domesticated W D cats are often completely deaf. [19]

The colorpoint pattern is most commonly associated with Siamese cats, but may also appear in any domesticated cat. A colorpointed cat has dark colors on the face, ears, feet, and tail, with a lighter version of the same color on the rest of the body, and possibly some white. The exact name of the colorpoint pattern depends on the actual color, so there are seal points (dark brown), chocolate points (warm lighter brown), blue points (dark gray), lilac or frost points (silvery gray-pink), red or flame points (orange), and tortie (tortoiseshell mottling) points, among others. This pattern is the result of a temperature sensitive mutation in one of the enzymes in the metabolic pathway from tyrosine to pigment, such as melanin thus, little or no pigment is produced except in the extremities or points where the skin is slightly cooler. For this reason, colorpointed cats tend to darken with age as bodily temperature drops also, the fur over a significant injury may sometimes darken or lighten as a result of temperature change. More specifically, the albino locus contains the gene TYR ( P55033 ). [5]

The tyrosine pathway also produces neurotransmitters, thus mutations in the early parts of that pathway may affect not only pigment, but also neurological development. This results in a higher frequency of cross-eyes among colorpointed cats, as well as the high frequency of cross-eyes in white tigers. [20]

  • C = full color.
  • cb = Burmese "sepia" pattern, similar to colorpoint but with lower contrast.
  • cs = Siamese/colorpoint. It is codominant with cb cb/cs cats show a medium-contrast phenotype known as mink.
  • ca = Blue-eyed albino.
  • c = Pink-eyed albino.

The silver series is caused by the Melanin inhibitor gene I/i. The dominant form causes melanin production to be suppressed, but it affects phaeomelanin (red pigment) much more than eumelanin (black or brown pigment). On tabbies, this turns the background a sparkling silver color while leaving the stripe color intact, making a silver tabby. On solid cats, it turns the base of the hair pale, making them silver smoke. [21]

Silver agouti cats can have a range of phenotypes, from silver tabby, to silver shaded (under half the hair is pigmented), to tipped silver/chinchilla (only the very tip of the hair is pigmented). This seems to be affected by hypothetical wide band factors, which make the silver band at the base of the hair wider. Breeders often notate wide band as a single gene Wb/wb, but it is most likely a polygenic trait.

If a cat has the wide band trait but no inhibitor, the band will be golden instead of silver. These cats are known as golden tabbies. Shaded golden and tipped golden are also possible. However, there is no golden smoke, because the combination of wide band and nonagouti simply produces a solid cat. [22] [23]

The genetics involved in producing the ideal tabby, tipped [fr] , shaded, or smoke cat is complex. Not only are there many interacting genes, but genes sometimes do not express themselves fully, or conflict with one another. For example, the melanin inhibitor gene in some instances does not block pigment, resulting in a grayer undercoat, or in tarnishing (yellowish or rusty fur). The greyer undercoat is less desirable to fanciers.

Likewise, poorly-expressed non-agouti or over-expression of melanin inhibitor will cause a pale, washed out black smoke. Various polygenes (sets of related genes), epigenetic factors, or modifier genes, as yet unidentified, are believed to result in different phenotypes of coloration, some deemed more desirable than others by fanciers.

Tipped or shaded cats Edit

The genetic influences on tipped or shaded cats are:

  • Tabby pattern genes (such as T a masking the tabby pattern).
  • Silver/melanin inhibitor gene.
  • Factors affecting the number and width of bands of color on each hair (such as the hypothetical wide band gene).
  • Factors affecting the amount and quality of eumelanin and/or phaeomelanin pigment expression (such as theorized rufousing factors)
  • Genes causing sparkling appearance (such as glitter in the Bengal, satin in the Tennessee Rex, grizzle in the Chausie).
  • Factors to clear up residual striping (hypothetical Chaos, Confusion, Unconfused, Erase, and Roan factors).

Fever coat is an effect known in domestic cats, where a pregnant female cat has a fever or is stressed, causing her unborn kittens' fur to develop a silver-type color (silver-grey, cream, or reddish) rather than what the kitten's genetics would normally cause. After birth, over some weeks the silver fur is replaced naturally by fur colors according to the kitten's genetics. [24] [25] [26]

Cat fur length is governed by the Length gene in which the dominant form, L, codes for short hair, and the recessive l codes for long hair. In the longhaired cat, the transition from anagen (hair growth) to catagen (cessation of hair growth) is delayed due to this mutation. [27] A rare recessive shorthair gene has been observed in some lines of Persian cat (silvers) where two longhaired parents have produced shorthaired offspring.

The Length gene has been identified as the fibroblast growth factor 5 (FGF5 M3X9S6 ) gene. The dominant allele codes for the short coat is seen in most cats. Long coats are coded for by at least four different recessively inherited mutations, the alleles of which have been identified. [28] The most ubiquitous is found in most or all long haired breeds while the remaining three are found only in Ragdolls, Norwegian Forest Cats, and Maine Coons.

There have been many genes identified that result in unusual cat fur. These genes were discovered in random-bred cats and selected for. Some of the genes are in danger of going extinct because the cats are not sold beyond the region where the mutation originated or there is simply not enough demand for cats expressing the mutation.

In many breeds, coat gene mutations are unwelcome. An example is the rex allele which appeared in Maine Coons in the early 1990s. Rexes appeared in America, Germany and the UK, where one breeder caused consternation by calling them "Maine Waves". Two UK breeders did test mating which indicated that this was probably a new rex mutation and that it was recessive. The density of the hair was similar to normally coated Maine Coons, but consisted only of down type hairs with a normal down type helical curl, which varied as in normal down hairs. Whiskers were more curved, but not curly. Maine Coons do not have awn hairs, and after moulting, the rexes had a very thin coat.

Curly-coated Edit

There are various genes producing curly-coated or "rex" cats. New types of rex arise spontaneously in random-bred cats now and then. Here are some of the rex genes that breeders have selected for:

  • r = Cornish Rex, recessive.
  • gr (provisional) = German Rex, recessive. Same locus as Cornish, but proposed as a different allele. However, most breeders consider the German Rex to have r/r genotype.
  • re = Devon Rex, recessive. Identified on KRT71 ( E1AB55 ). [29]
  • ro = Oregon Rex (extinct), recessive.
  • Se = Selkirk Rex, dominant although sometimes described as an incomplete dominant because the three possible allele pairings relate to three different phenotypes: heterozygous cats (Sese) may have a fuller coat that is preferred in the show ring, while homozygous cats (SeSe) may have a tighter curl and less coat volume. (sese type cats have a normal coat.) This phenomenon may also colloquially be referred to as additive dominance.
  • Lp (provisional) = LaPerm, dominant: Lp/lp and Lp/Lp individuals have the same phenotype.

Hairlessness Edit

There are also genes for hairlessness:

  • h = French hairless cat, recessive.
  • hd = British hairless cat, recessive.
  • Hp = Russian Donskoy and Peterbald, dominant.
  • hr = Canadian Sphynx cat, recessive. Identified on KRT71. [29]

Some rex cats are prone to temporary hairlessness, known as baldness, during moulting.



SARS-CoV-2 viral infection causes COVID-19 that can result in severe acute respiratory distress syndrome (ARDS), which can cause significant mortality, leading to concern that immunosuppressive treatments for multiple sclerosis and other disorders have significant risks for both infection and ARDS.


To examine the biology that potentially underpins immunity to the SARS-Cov-2 virus and the immunity-induced pathology related to COVID-19 and determine how this impinges on the use of current disease modifying treatments in multiple sclerosis.


Although information about the mechanisms of immunity are scant, it appears that monocyte/macrophages and then CD8 T cells are important in eliminating the SARS-CoV-2 virus. This may be facilitated via anti-viral antibody responses that may prevent re-infection. However, viral escape and infection of leucocytes to promote lymphopenia, apparent CD8 T cell exhaustion coupled with a cytokine storm and vascular pathology appears to contribute to the damage in ARDS.


In contrast to ablative haematopoietic stem cell therapy, most multiple-sclerosis-related disease modifying therapies do not particularly target the innate immune system and few have any major long-term impact on CD8 T cells to limit protection against COVID-19. In addition, few block the formation of immature B cells within lymphoid tissue that will provide antibody-mediated protection from (re)infection. However, adjustments to dosing schedules may help de-risk the chance of infection further and reduce the concerns of people with MS being treated during the COVID-19 pandemic.

Watch the video: Το Cat Noir έχει γίνει μια απλή γάτα! Ο Hawk Moth απήγαγε τη Cat Noir! Πασχαλίτσα στην πραγματική (November 2022).