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Scientists call this collection of shared changes “domestication syndrome”, and the reason it occurs is still hotly debated.
In a new paper in Proceedings of the Royal Society B, we argue that currently popular explanations aren’t quite right – and propose a new explanation focused on big changes in the way domesticated animals live. Along the way, our theory also offers insights into the unexpected story of how we humans domesticated ourselves.
Shared changes under domestication
The most commonly shared change is tamer behavior. All domesticated animals are calmer than their wild ancestors naturally were.
That’s probably not very surprising. Ancient humans would’ve preferred docile animals, and likely selected breeding stock for tameness.
But other common changes don’t seem at all useful to humans – or to the animals themselves. Like shorter faces, smaller teeth, more fragile skeletons, smaller brains, and different colors in skin, fur, and feathers.
Not all domesticated animals share all these features. For example, dogs have many, and camels only a few.
But each change occurs in more than one domesticated species.
Wild self-domestication
Surprisingly, very similar changes sometimes also appear in wild animals, leading some scientists to think they “self-domesticated” in some way.
The bonobo (a great ape closely related to the chimpanzee) is one famous example of an animal that has undergone these changes without human intervention. Urban foxes are another.
Bonobos are a species who are believed to have ‘self-domesticated’. Shutterstock
Wild self-domestication is most common in isolated sub-populations, like on islands, and may overlap with a similar phenomenon known as the “island effect”.
Perhaps more surprisingly, modern humans also show features of domestication syndrome, when compared to our ancient ancestors. This suggests we also self-domesticated.
Some scientists argue these changes made us more sociable, helping us to develop complex languages and culture.
So a clearer understanding of domestication syndrome in animals might improve our knowledge of human evolution too.
What causes domestication syndrome?
In recent years, two main possible explanations for domestication syndrome have dominated scientific discussion.
The first suggests it was caused when ancient humans selected animals for tamer behavior, which somehow triggered all of the other traits too.
This idea is supported by a famous long-running Russian fox-breeding experiment which began in 1959, in which caged foxes were selected only for tameness but developed the other “unselected” features as well.
The second hypothesis complements this first one. It suggests selection for tameness causes the other features because they’re all linked by genes controlling “neural crest cells”. These cells, found in embryos, form many animal features – so changing them could cause several differences at once.
More than selection for tameness
However, our new research suggests these two ideas oversimplify and obscure the complex evolutionary effects at play.
For one thing, there are problems with the famous Russian fox experiment. As other authors have noted, the experiment didn’t begin by taming wild foxes, but used foxes from a farm in Canada. And these pre-farmed foxes already had features of domestication syndrome.
What’s more, the experimenters didn’t only select for tameness. They bred other foxes for aggression, but the aggressive foxes also developed domestication syndrome features.
And in a similar experiment conducted in the 1930s, caged rats developed the same common changes, including tamer behavior, despite no deliberate selection for tameness, or aggression.
So, it seems domestication syndrome might not be caused by humans selecting animals for tameness. Instead, it might be caused by unintended shared effects from the new domestic environment.
A new hypothesis for domestication syndrome
Crucially, it’s not just new forces of selection, such as a human preference for tameness, that matters. The removal of pre-existing selection is just as important, because that’s what naturally shaped the wild ancestors in the first place.
For example, domesticated animals are often protected from predators, so wild traits for avoiding them might be lost. Competition for mating partners is also often reduced, so wild reproductive features and behaviors could decline, or disappear.
Domesticated animals are also usually reliably fed. This might alter certain features, but would certainly change natural metabolism and growth.
Caged rats have also been seen to develop signs of domestication syndrome. Oxana Golubets / Unsplash
In effect, we argue there are multiple selective changes at work on domesticated animals, not just “selection for tameness”, and that shared shifts in evolutionary selection would often cause shared changes in features. Even across different species.
Our new hypothesis highlights four ways that selection shaping wild animals is often disrupted by domestication. These are:
- less fighting between males
- fewer males for females to choose between
- more reliable food and fewer predators, and
- elevated maternal stress, which initially reduces the health and survival of offspring.
Several of these might resemble “selection for tameness”, but using this one term to describe them all is misleadingly vague, and obscures other changes in selection.
So how did we domesticate ourselves?
Well, one current theory is that sociable “beta males” began cooperating to kill alpha bullies. This changed how competition worked among males, leading to fewer big and aggressive males.
But our hypothesis suggests other effects also played a role. For example, our early ancestors evolved the capacity for shared infant care. In our chimpanzee relatives today, sharing care of an infant would likely trigger extreme stress for the mother – but our ancestors adapted to this increased stress and gained an effective survival strategy.
Adapting to the increased maternal stress that accompanies separation from infants (either for shared care or domestication) may be one of the drivers of ‘domestication syndrome’. Shutterstock
More reliable food access due to group foraging and sharing, plus collective defense against predators, might also have made us more sociable, more cooperative, and more complex, while promoting other changes commonly seen in non-human domesticated animals.
Whatever the specific drivers in each species, recognizing multiple selective pathways better explains the domestication syndrome, and reaffirms the complexity of evolutionary effects shaping all life on Earth.
Ben Thomas Gleeson, Doctoral Candidate, Australian National University and Laura A. B. Wilson, ARC Future Fellow, Australian National University
This article is republished from The Conversation under a Creative Commons license. Read the original article.
I am a toxicologist who studies how chemicals affect human health, particularly when they cause harmful effects. As a fan of mystery and detective stories, which often feature the use of poisons, I’ve noticed a few poisons that turn up repeatedly in books, television and movies. How they really work is as fascinating as how they’re deployed toward evil ends in fiction.
What is a poison?
The 16th-century physician–alchemist Paracelsus, considered to be the father of toxicology, once wrote: “What is there that is not poison? All things are poison and nothing is without poison. Solely the dose determines that a thing is not a poison.” By this adage, any substance can be a poison with the appropriate amount.
Many people intentionally expose themselves to chemicals like ethanol through alcoholic beverages, nicotine through tobacco products and botulinum toxin through botox treatments at relatively low doses and suffer minimal adverse effects. However, at sufficiently high doses, these chemicals can be lethal. The body’s response often depends on how the chemical interacts with receptors within or on the surface of cells, or how it binds to enzymes used for biological processes. Frequently, higher concentrations of the substance lead to stronger responses.
Despite Paracelsus’ dictum, in popular culture the term “poison” is often reserved for chemical compounds that are not normally encountered in daily life and can lead to detrimental health effects even in relatively small amounts.
At a high enough dose, any chemical could be poisonous. Malorny/Moment via Getty Images
Poisons in books, TV and film
Novel writers and television and movie screenwriters have exploited numerous poisons in their works, including those that are chemical elements, such as arsenic and polonium, and those derived from animals, such as snake venom and blowfish poison. Many poisons derived from plants have also been used for villainous purposes in fiction.
In the AMC TV series “Breaking Bad,” high school chemistry teacher Walter White uses a compound called ricin to murder the business executive Lydia Rodarte-Quayle. Ricin is a very potent poison derived from the castor bean Ricinus communis and can be especially lethal if inhaled. Once this compound gets inside a cell, it damages a structure called a ribosome that’s responsible for synthesizing proteins essential to the cell’s function. Ingesting ricin could result in intestinal bleeding, organ damage and death.
It wasn’t Stevia that Lydia sweetened her tea with in ‘Breaking Bad’.
Sometimes, particular organs are much more susceptible to the effects of a poison. Physicians use digitalis medicines like digoxin, which are derived from members of the foxglove family of plants, to treat congestive heart failure and heart rhythm problems. When administered in sufficiently high doses, however, they can lead to heart failure and death. By interfering with a protein in heart cells called the sodium-potassium pump, they can decrease the rate of electrical impulses in the heart and increase the strength of its contractions. This can result in a dangerous type of irregular heartbeat called ventricular fibrillation and lead to death.
The villain of the James Bond film “Casino Royale,” Le Chiffre, has his girlfriend attempt to kill Bond by poisoning his martini with digitalis. At high doses, digitalis drugs can alter the activity of the autonomic nervous system, which controls unconscious bodily functions like heart pumping.
Poison is one way to win a poker game.
TV characters are not immune to the dangers of poisonous mushrooms. One particularly potent fungus, Amanita verna, is known as the “destroying angel.” In the ITV TV series “Midsomer Murders,” puppet show owner and presumed upstanding citizen Evelyn Pope uses this mushroom to fatally poison chef Tristan Goodfellow as part of her murder spree of the inheritors of an estate. This mushroom contains various chemicals called amatoxins that are thought to inhibit the activity of a specific enzyme critical for the production of messenger RNA, or mRNA, a molecule essential to protein synthesis in cells. Because ingested amatoxins mainly target the liver, these poisons can severely disrupt the liver’s ability to repair itself, leading to loss of function that will prove fatal without liver transplantation.
They don’t call it the “destroying angel” for nothing.
Another highly popular poison in detective and mystery stories is strychnine. In the Agatha Christie story “The Mysterious Affair at Styles,” Alfred Inglethorp and his lover Evelyn Howard use this poison to kill Inglethorp’s wife and wealthy country manor owner, Emily Inglethorp.
Strychnine, which comes from seeds of the Strychnos nux-vomica tree, affects the nervous system by blocking a neurotransmitter called glycine in the spinal cord and brainstem. Normally, glycine slows down the activity of neurons and prevents muscle contractions. By blocking glycine, strychnine ingestion can result in excessive activation of neurons and muscles, leading to a series of full-body muscle spasms that can become so intense that they cause respiratory arrest and death.
Many more poisons exist in nature than described here. Aside from potentially enhancing the enjoyment of detective and mystery stories, understanding the mechanisms of how these poisons work can provide an added appreciation for the complexity of the effects foreign chemicals have on the human body.
Brad Reisfeld, Professor of Chemical and Biological Engineering, Colorado State University
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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