We have been using mice as scientific test subjects for decades, but laboratory mice may be further from humans than we thought. Emmet Feerick takes a look.
Cruel though it may be, scientists do a lot of drug and chemical testing on domestic mice. They are the ideal candidates for the job, with organs that function much like our own, and cells that share 97.5% of our DNA. We have been breeding mice in laboratories for decades for this reason. The list of side effects inside almost every packet of tablets you buy has been generated by research on these lab mice. This is why we should be concerned when we see something like the paper written by Bret Weinstein and Deborah Ciszek in the scientific journal Experimental Gerontology.
This paper outlines a few key facts which cast serious doubts on the applicability of laboratory mice results to human beings. First, we should consider the mechanisms by which cells reproduce and die. When a cell reproduces, its chromosomes duplicate, and the two new cells contain nearly identical copies of the original chromosomes. For new cells to carry out the same function as the old one, it is vital that its chromosomes are protected during replication so that it can copy itself almost identically. The job of protecting the chromosome falls in large part to nucleotide caps at each end, called telomeres.
“As it stands, our cells replicate for as long as they can without becoming cancerous (most of the time), and then they die. Their timely death is what keeps us alive.”
Every time a cell divides and its chromosomes replicate, a small bit of the material that makes up the telomere degrades. With each subsequent division, the telomere gets slightly shorter, until eventually the cell is no longer able to divide. From the point of view of a cell, this is doubtless a bad thing. However, as collections of cells ourselves, we should be happy that this mechanism of programmed cell death exists. Without it, our cells would divide indefinitely – something we have come to call cancer. As it stands, our cells replicate for as long as they can without becoming cancerous (most of the time), and then they die. Their timely death is what keeps us alive.
As we and our cells age, we become less able to repair all sorts of damage. This is why older people need more time to recover from operations, and why their cuts and bruises heal up more slowly. New cells are simply better cells, but a cell can only divide so many times before the dangers of cancer outweigh the fast-healing of youth.
“As we and our cells age, we become less able to repair all sorts of damage.”
The problem with our lab mice is the following: our aim in studying these animals has been to test out as many chemicals and drugs on them before they die. Some of them die very soon, whereas others live to have more drugs tested on them. Over the decades, we have been playing the role of natural selection on these mice, continuing to test those who can withstand it, and discarding those who can’t. This has meant that our current lab mice have developed incredibly long telomeres. This is an issue because long telomeres increase the time it takes for a cell to reach the programmed-death stage, which increases the number of times it can replicate, which increases its cancer risk. Conversely, as cells stay newer for longer, they remain excellent at repairing cell damage. What we now have in labs are a species of highly cancer-prone, bruise-resistant mice.
What this means for us that the list of things we’ve labelled “carcinogenic” may not need to be as long as it is. It is possible that it is only that long because we are doing animal testing on mice that are highly prone to cancer. On the other hand, we have reason to be more cautious of the chemicals that have passed animal testing. Our cells simply do not replicate as often as lab mouse cells, and as such they cannot repair tissue damage as effectively. This means that chemicals which cause these mice no harm may in fact be toxic to our own organs over time. We may be susceptible to damage from chemicals which these super-mice can handle without a problem.
“What we now have in labs are a species of highly cancer-prone, bruise-resistant mice.”
In many ways this danger is like that posed by increased antibiotic resistance. Where our antibiotics have driven the evolution of highly-resistant bacterial strains, our laboratory protocols may have driven the evolution of mice which no longer resemble us in their tissue-healing and cancer-developing capacities. We should thus be wary of applying the results of lab mice testing to ourselves until there is evidence indicating that this is not a problem.