Scientists Suspect Genetic Underpinnings to Human Monogamy

A groundbreaking study from a Harvard University team suggests that monogamy may be genetically programmed within some mammals.

Cute couple has their love lock on a bridge.
Cute couple. Getty Images.

Evolutionary anthropology has for some time tried to understand what natural relationship pattern humans follow, if there is one. In his book Sex at Dawn psychologist Christopher Ryan posits that our prehistoric ancestors practiced multiple kinds of sexual and romantic relationships.


Monogamy became a social institution and one that made sense. Polygamy was the most common practice in the ancient world, but it made women a commodity. Rich men could keep multiple wives for themselves, whole harems, which caused a lot of strife among others, fighting over those who were left. Monogamy however, eliminated this problem and helped seed societal stability.

Even so, multiple societies around the world still practice different forms of pair bonding other than monogamy. Even the most strident monogamist will admit that marriage can prove difficult. There’s things like the four year slump and the seven year itch. Some evolutionary biologists have explained these as a cessation of the pair bonding process.

When we were hunter-gatherers, we traveled in tight-knit bands. Children were raised not only by their parents but by the whole village itself. When the child was old enough to be a little more independent, the parents were free to go off and explore other relationships.

According to renowned anthropologist and love expert Dr. Helen Fisher, there are actually four different, unique personality types when it comes to human love. Each is driven by a preponderance of a certain neurochemical or hormone in the person’s system. And some are better suited for monogamy than others.

In this case, nature may have made some people naturally polyamorous and others monogamous, to ensure stability for raising children, while at other times, ensuring variety within the gene pool and to that end, aiding our survival.

Is there an evolutionary basis for cheating? Getty Images.

Now, a groundbreaking study published in the journal Nature suggests that monogamy may be genetically programmed within us, or at least in mice, to ensure offspring receive proper care. “Parental care is essential for the survival of mammals, yet the mechanisms underlying its evolution remain largely unknown,” the authors write. Researchers at Harvard University studied two breeds of mice to arrive at this conclusion.  

The first was the oldfield mouse (Peromyscus polionotus), one of those rare monogamous animals. Only 5% of mammals practice monogamy. Both sexes of this breed are known to be doting parents. They will, together, build an elaborate nest for their young and lick or clean them.

The second breed was the deer mouse (Peromyscus maniculatus), who are promiscuous by nature, and look upon their oldfield cousins as helicopter parents. In most mammalian relationships, males mate with as many females as possible, but do little to help raise the offspring. What researchers discovered, by looking at these two mouse breeds, was distinct genetic variations, which coincided with each type’s relationship style.

Hopi E. Hoekstra was the senior author of the study. She’s an evolutionary biologist. Though oldfield and deer mice won’t mate in the wild, if a male and female are put into the same tank alone together, they will. The resulting offspring are healthy. It was a variety of such hybrids that led them to understand whether or not parenting and relationship styles are genetically influenced.

Is monogamy in our nature, polyamory, or a combination? Getty Images. 

In a previous study, Hoekstra and her team took the pups of each type of mouse and placed them in each other’s nest. Researchers wanted to know if the mice acted this way because they were raised to tend to pups, or if each breed of mouse had an instinctual parenting style. The latter proved true. Once this was found, researchers went about investigating each type’s DNA.

They bred five mice, who created 30 hybrid offspring. These were bred and another 769 hybrid mice were born. Researchers looked at the second and third generations, to see what type of parenting each took up. Some put in minimal effort, others were completely aloof, and others still attentive parents. This wide variety of styles allowed researchers to hone into the mice’s DNA and find the differences. They came upon 12 areas or loci which were associated with parental instincts.

Researchers found that one loci controlled just one behavior, nest building, while others controlled more than one. These loci varied in terms of sex. One loci when activated, seemed to make fathers more attentive, but not mothers. Unfortunately, each loci carries many genes, so it’s hard to hunt down which is responsible for what behavior.

In their most recent study, these Harvard researchers looked at one biochemical in particular, vasopressin. This is a bonding neurotransmitter in many species, including rats and humans. Deer mice contain three times the amounts as oldfield mice, however. To find out what role it played, researchers injected oldfield mice with it. Instead of elaborate nests, they acted more like deer mice, and made simple ones. Yet, in terms of care, they were still doting parents.

Studies show that some may be better suited for monogamy than others. Getty Images.

According to their genetic research, the vasopressin gene only accounts for 6.7% of nest building instincts in male oldfield mice, and 2.9% in females. This opens the door to whether or not human pair bonding and parenting could be influenced by an instinct imprinted on our DNA. Though we’re a far cry from mice, we share many of the same neurotransmitters and hormones, along with other mammals.

Differences in biochemical makeup or neurotransmitters may signal how a species cares for its young, and whether it’s monogamous, promiscuous, or a mixture of the two. In exploring other species and working our way up, we may find out more about ourselves, even what relationship pattern or parenting style works best. Perhaps, we’ll find the genetic underpinnings of Dr. Fisher’s theory.

To learn what similar genetic underpinnings have so far been identified in our species, click here: 

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Meet Dr. Jennifer Doudna: she's leading the biotech revolution

She helped create CRISPR, a gene-editing technology that is changing the way we treat genetic diseases and even how we produce food.

Courtesy of Jennifer Doudna
Technology & Innovation

This article was originally published on our sister site, Freethink.

Last year, Jennifer Doudna and Emmanuelle Charpentier became the first all-woman team to win the Nobel Prize in Chemistry for their work developing CRISPR-Cas9, the gene-editing technology. The technology was invented in 2012 — and nine years later, it's truly revolutionizing how we treat genetic diseases and even how we produce food.

CRISPR allows scientists to alter DNA by using proteins that are naturally found in bacteria. They use these proteins, called Cas9, to naturally fend off viruses, destroying the virus' DNA and cutting it out of their genes. CRISPR allows scientists to co-opt this function, redirecting the proteins toward disease-causing mutations in our DNA.

So far, gene-editing technology is showing promise in treating sickle cell disease and genetic blindness — and it could eventually be used to treat all sorts of genetic diseases, from cancer to Huntington's Disease.

The biotech revolution is just getting started — and CRISPR is leading the charge. We talked with Doudna about what we can expect from genetic engineering in the future.

This interview has been lightly edited and condensed for clarity.

Freethink: You've said that your journey to becoming a scientist had humble beginnings — in your teenage bedroom when you discovered The Double Helix by Jim Watson. Back then, there weren't a lot of women scientists — what was your breakthrough moment in realizing you could pursue this as a career?

Dr. Jennifer Doudna: There is a moment that I often think back to from high school in Hilo, Hawaii, when I first heard the word "biochemistry." A researcher from the UH Cancer Center on Oahu came and gave a talk on her work studying cancer cells.

I didn't understand much of her talk, but it still made a huge impact on me. You didn't see professional women scientists in popular culture at the time, and it really opened my eyes to new possibilities. She was very impressive.

I remember thinking right then that I wanted to do what she does, and that's what set me off on the journey that became my career in science.

CRISPR 101: Curing Sickle Cell, Growing Organs, Mosquito Makeovers | Jennifer Doudna | Big Think www.youtube.com

Freethink: The term "CRISPR" is everywhere in the media these days but it's a really complicated tool to describe. What is the one thing that you wish people understood about CRISPR that they usually get wrong?

Dr. Jennifer Doudna: People should know that CRISPR technology has revolutionized scientific research and will make a positive difference to their lives.

Researchers are gaining incredible new understanding of the nature of disease, evolution, and are developing CRISPR-based strategies to tackle our greatest health, food, and sustainability challenges.

Freethink: You previously wrote in Wired that this year, 2021, is going to be a big year for CRISPR. What exciting new developments should we be on the lookout for?

Dr. Jennifer Doudna: Before the COVID-19 pandemic, there were multiple teams around the world, including my lab and colleagues at the Innovative Genomics Institute, working on developing CRISPR-based diagnostics.

"Traits that we could select for using traditional breeding methods, that might take decades, we can now engineer precisely in a much shorter time."
DR. JENNIFER DOUDNA

When the pandemic hit, we pivoted our work to focus these tools on SARS-CoV-2. The benefit of these new diagnostics is that they're fast, cheap, can be done anywhere without the need for a lab, and they can be quickly modified to detect different pathogens. I'm excited about the future of diagnostics, and not just for pandemics.

We'll also be seeing more CRISPR applications in agriculture to help combat hunger, reduce the need for toxic pesticides and fertilizers, fight plant diseases and help crops adapt to a changing climate.

Traits that we could select for using traditional breeding methods, that might take decades, we can now engineer precisely in a much shorter time.

Freethink: Curing genetic diseases isn't a pipedream anymore, but there are still some hurdles to cross before we're able to say for certain that we can do this. What are those hurdles and how close do you think we are to crossing them?

Dr. Jennifer Doudna: There are people today, like Victoria Gray, who have been successfully treated for sickle cell disease. This is just the tip of the iceberg.

There are absolutely still many hurdles. We don't currently have ways to deliver genome-editing enzymes to all types of tissues, but delivery is a hot area of research for this very reason.

We also need to continue improving on the first wave of CRISPR therapies, as well as making them more affordable and accessible.

Freethink: Another big challenge is making this technology widely available to everyone and not just the really wealthy. You've previously said that this challenge starts with the scientists.

Dr. Jennifer Doudna: A sickle cell disease cure that is 100 percent effective but can't be accessed by most of the people in need is not really a full cure.

This is one of the insights that led me to found the Innovative Genomics Institute back in 2014. It's not enough to develop a therapy, prove that it works, and move on. You have to develop a therapy that actually meets the real-world need.

Too often, scientists don't fully incorporate issues of equity and accessibility into their research, and the incentives of the pharmaceutical industry tend to run in the opposite direction. If the world needs affordable therapy, you have to work toward that goal from the beginning.

Freethink: You've expressed some concern about the ethics of using CRISPR. Do you think there is a meaningful difference between enhancing human abilities — for example, using gene therapy to become stronger or more intelligent — versus correcting deficiencies, like Type 1 diabetes or Huntington's?

Dr. Jennifer Doudna: There is a meaningful distinction between enhancement and treatment, but that doesn't mean that the line is always clear. It isn't.

There's always a gray area when it comes to complex ethical issues like this, and our thinking on this is undoubtedly going to evolve over time.

What we need is to find an appropriate balance between preventing misuse and promoting beneficial innovation.

Freethink: What if it turns out that being physically stronger helps you live a longer life — if that's the case, are there some ways of improving health that we should simply rule out?

Dr. Jennifer Doudna: The concept of improving the "healthspan" of individuals is an area of considerable interest. Eliminating neurodegenerative disease will not only massively reduce suffering around the world, but it will also meaningfully increase the healthy years for millions of individuals.

"There is a meaningful distinction between enhancement and treatment, but that doesn't mean that the line is always clear. It isn't."
DR. JENNIFER DOUDNA

There will also be knock-on effects, such as increased economic output, but also increased impact on the planet.

When you think about increasing lifespans just so certain people can live longer, then not only do those knock-on effects become more central, you also have to ask who is benefiting and who isn't? Is it possible to develop this technology so the benefits are shared equitably? Is it environmentally sustainable to go down this road?

Freethink: Where do you see it going from here?

Dr. Jennifer Doudna: The bio revolution will allow us to create breakthroughs in treating not just a few but whole classes of previously unaddressed genetic diseases.

We're also likely to see genome editing play a role not just in climate adaptation, but in climate change solutions as well. There will be challenges along the way both expected and unexpected, but also great leaps in progress and benefits that will move society forward. It's an exciting time to be a scientist.

Freethink: If you had to guess, what is the first disease you think we are most likely to cure, in the real world, with CRISPR?

Dr. Jennifer Doudna: Because of the progress that has already been made, sickle cell disease and beta-thalassemia are likely to be the first diseases with a CRISPR cure, but we're closely following the developments of other CRISPR clinical trials for types of cancer, a form of congenital blindness, chronic infection, and some rare genetic disorders.

The pace of clinical trials is picking up, and the list will be longer next year.

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