Animal Testing Essay: Example and Tips

Reading an essay about animal testing, any teacher is ready to read hundreds of similar essays about the cruelty of testing on animals and how it should be forbidden. Essay with another viewpoint would at least attract the attention of the teacher. Though, you should be careful with such a position, especially if your teacher is very sensitive.

If your position contradicts popular pro-life movement, do not be afraid to express it and give arguments in favor of using testing on animals, like in our partly shocking example.

Animal testing essay example


It’s time to ban animal testing! You can do it, of course – if you are satisfied with the prospect of no longer inventing any new medical technology or medicine. It is important to understand that scientists and researchers have absolutely no desire to ruin as many innocent animals as possible. Any search for scientific publications on the words animal testing brings mainly materials on how to minimize the need for such studies. Any experiments on animals are regulated by strict rules and are limited to ethical commissions.

In addition, working with animals is simply an expensive, lengthy and time-consuming process; wherever it is possible to do without it, scientists are eager to do so. The number of doctorate degrees in biology awarded in the United States has almost doubled over the past 30 years, and the number of animals used has not increased.

Rats and mice (as well as fish, amphibians, reptiles and birds) in the United States are not counted up to the individual, but according to rough estimates, the total number of vertebrates used in the experiments was about 20 million per year in the mid-1980s and about 17 million per year in the mid-2000s. Much more accurate statistics exist for all mammals besides rats and mice (that is, for hamsters, rabbits, pigs, etc.) – in 1984, slightly more than 2 million of these animals were used, and in 2014 there were exactly 834,453 pieces. These figures seem impressive only as long as we do not compare them to the number of animals that are used annually for food. For example, with 8 666 662 000 chickens eaten in America in 2014.

Main part

Why do we need laboratory animals? Three million mice used in 2013 in the UK are distributed as follows. 59% of animals are involved in obtaining new lines using a variety of methods of genetic modification, 28% are used in basic science, 11.5% are needed for applied medical research. 0.5% of animals are required for veterinary and environmental research, and the remaining half a percent share educational projects and the use of mice for diagnosis (for example, if you have a patient with suspected infectious disease, but standard tests do not detect it yet, you can take some blood from him, try to infect mice and observe the condition).

These 59% reflect the intermediate stage of research. These are the animals whose genome was somehow altered, and now they are crossed with each other to get genetically homogeneous lines and check if the altered genes are now working (or, conversely, stopped working) as it was intended. When this process is completed, they will begin to participate in basic or applied research. A significant part of such animals is needed to understand the causes of human diseases. You have a gene that you know for sure (or suggest) that its mutations increase people’s risk of developing diabetes, or Alzheimer’s, or atherosclerosis, or some kind of cancer. You find the corresponding gene in the mouse, violate its work, make sure that the animals actually become sick more often, and then find out why this is happening and what medicinal substances can compensate for the effect.

This approach is widely used due to the fact that we are relatives and many genes in us and mice are almost identical. But there is another problem: the study of those genes, which in the case of man, on the contrary, differ significantly from mouse, and even from chimpanzee genes. Almost every such gene is naturally suspected that it “makes us human,” and sometimes, with the help of genetically modified mice, amusing evidence of this hypothesis can be obtained.

The most famous – and most important – of such stories began in the late 1980s in one of the primary schools of the city of Brentford (part of London). Elizabeth Ozher, who worked there with children who are lagging behind the school curriculum, drew attention to the fact that several students from the same family showed similar violations of speech. They began to speak late, pronounced the words inaudible (for example, bu instead of blue), did not use sentences longer than two or three words, they hardly picked up words and often pronounced them inaccurately, and also experienced difficulties with the perception of grammatical constructions. At the same time, the children did not have mental retardation, they coped well with mathematics, could read and write; problems were associated with oral speech. Elizabeth and her school colleagues contacted the Clinical Genetics Department of the London Children’s Hospital. The specialists who worked there made up the family tree.

It turned out that a child can inherit a disease from his parent with a probability of 50% and in children in the same family the problem can either be pronounced or completely absent. This is a classic picture of the inheritance of a single dominant allele and it became a sensation: until then it was assumed, and it is not unreasonable that many different genes contribute to the development of speech. There are a lot of them, but one of them was especially important. Later it was identified; called FOXP2; found that it encodes a transcription factor (a protein that activates the reading of some genes), important for brain development; that this protein in humans is only two amino acids different from the protein of chimpanzees and that in Neanderthals it was the same as in ours; that FOXP2 is involved in many processes related to the development of the brain, but most importantly – it is associated with speech not only in humans, but, apparently, in general in all animals who in one form or another have sound communication between their relatives.

You have already noticed that in most cases new information about the functions of genes is obtained this way: they find or create a creature that has this gene broken, and they look that it has deteriorated. FOXP2 is no exception: there are mice that have it just turned off. In the event that they did not have a single copy of the gene (in general there were two of them: inherited from the mother and from the father), the animals in principle felt very bad, but also the mice completely lacked ultrasonic squeak, which they normally use to call the mother. If one normal copy of the gene was still present, the mice squeaked, but much less than the usual ones.

Such mice were first created in 2009. They differed from ordinary mice in a number of structural and functional features of the brain, but in the context of the story about speech the most interesting observation was due to the fact that the mice carried away from the nest really squeaked a little differently, for example, they had longer episodes of complex squeak (with fluctuations in the audio frequencies). However, the scientific community was more interested in the differences in learning ability than in the difference in the squeak. In 2014, a large study came out, in which mice with human FOXP2 (animals that for research purposes are made to look like humans in anything, they are called: humanized) and ordinary mice wandered around the labyrinths in search of food.

There are two ways to determine which of the corridors leads to the feeder. First, you can look at external landmarks. Secondly, you can remember your own movements. In preliminary tests, scientists noted that humanized mice learn to use external landmarks faster than conventional mice. However, researchers were interested in another thing: how quickly an animal can abandon a strategy that has lost its relevance. After scientists spent two weeks demonstrating to mice that they need to look up the wall of the laboratory, look at the painted cross and go in that direction to find food, they took and turned the labyrinth 180 degrees. If they started to put it in the other sleeve, too, so that it would again be next to the cross, ordinary and humanized mice would understand equally quickly that only a cross should be believed, and it does not matter that we turn now not to the right, but to the left. But if you had to turn still to the right, and ignore the dagger – then humanized mice switched much more quickly to correct behavior.


Why is it important? Because such a result of training shows that mice with human FOXP2 better learn their own movements. As the authors of the same work have shown, in humanized mice the striped body operates in a different way – a part of the brain necessary for the formation of complex and multi-stage motor reactions. This suggests that human FOXP2, in addition to its other functions, can be associated with our complex articulation, the ability to quickly and consistently control the lips, the tongue, the vocal cords, to generate a variety of different sounds. It is clear that further research is required – and there will clearly be no shortage of them.

That is only one tiny example of the positive effect of using testing on animals. If you want to cure diseases in humans, you need to make sacrifices.