The Age of DNA-Based Dating Is Here

A woman gives a DNA sample at a Pheramor-sponsored event.
Brittany Barreto first got the idea to make a DNA-based dating platform nearly 10 years ago when she was in a college seminar on genetics. She joked that it would be called GeneHarmony.com.
Pheramor and startups, like DNA Romance and Instant Chemistry, both based in Canada, claim to match you to a romantic partner based on your genetics.
The idea stuck with her while she was getting her PhD in genetics at Baylor College of Medicine, and in March 2018, she launched Pheramor, a dating app that measures compatibility based on physical chemistry and what the company calls "social alignment."
"I wanted to use genetics and science to help people connect more. Our world is so hungry for connection," says Barreto, who serves as Pheramor's CEO.
With the direct-to-consumer genetic testing market booming, more and more companies are looking to capitalize on the promise of DNA-based services. Pheramor and startups, like DNA Romance and Instant Chemistry, both based in Canada, claim to match you to a romantic partner based on your genetics. It's an intriguing alternative to swiping left or right in hopes of finding someone you're not only physically attracted to but actually want to date. Experts say the science behind such apps isn't settled though.
For $40, Pheramor sends you a DNA kit to swab the inside of your cheek. After you mail in your sample, Pheramor analyzes your saliva for 11 different HLA genes, a fraction of the more than 200 genes that are thought to make up the human HLA complex. These genes make proteins that regulate the immune system by helping protect against invading pathogens.
It takes three to four weeks to get the results backs. In the meantime, users can still download the app and start using it before their DNA results are ready. The app asks users to link their social media accounts, which are fed into an algorithm that calculates a "social alignment." The algorithm takes into account the hashtags you use, your likes, check-ins, posts, and accounts you follow on Facebook, Twitter, and Instagram.
The DNA test results and social alignment algorithm are used to calculate a compatibility percentage between zero and 100. Barreto said she couldn't comment on how much of that score is influenced by the algorithm and how much comes from what the company calls genetic attraction. "DNA is not destiny," she says. "It's not like you're going to swab and I'll send you your soulmate."
Despite its name, Pheramor doesn't actually measure pheromones, chemicals released by animals that affect the behavior of others of the same species. That's because human pheromones have yet to be identified, though they've been discovered throughout the animal kingdom in moths, mice, rabbits, pigs, and many other insects and mammals. The HLA genes Pheramor analyzes instead are the human version of the major histocompatibility complex (MHC), a gene group found in many species.
The connection between HLA type and attraction goes back to the 1970s, when researchers found that inbred male mice preferred to mate with female mice with a different MHC rather than inbred female mice with similar immune system genes. The researchers concluded that this mating preference was linked to smell. The idea is that choosing a mate with different MHC genes gives animals an evolutionary advantage in terms of immune system defense.
The couples who had more dissimilar HLA types reported a more satisfied sex life and satisfied partnership, but it was a small effect.
In the 1990s, Swiss scientists wanted to see if body odor also had an effect on human attraction. In a famous experiment known as the "sweaty T-shirt study", they recruited 49 women to sniff sweaty, unwashed T-shirts from 44 men and put each in a box with a smelling hole and describe the odors of every shirt. The study found that women preferred the scents of T-shirts worn by men who were immunologically different from them compared to men whose HLA genes were similar to their own.
"The idea is, if you are very similar with your partner in HLA type then your offspring is similar in terms of HLA. This reduces your resistance against pathogens," says Illona Croy, a psychologist at the Technical University of Dresden who has studied HLA type in relation to sexual attraction in humans.
In a 2016 study Pheramor cites on its website, Croy and her colleagues tested the HLA types of 250 couples—all of them university students—and asked them how satisfied they were with their partnerships, with their sex lives, and with the odors of their partners. The couples who had more dissimilar HLA types reported a more satisfied sex life and satisfied partnership, but Croy cautions that it was a small effect. "It's not like they were super satisfied or not satisfied at all. It's a slight difference," she says.
Croy says we're much more likely to choose a partner based on appearance, sense of humor, intelligence and common interests.
Other studies have reported no preference for HLA difference in sexual attraction. Tristram Wyatt, a zoologist at the University of Oxford in the U.K. who studies animal pheromones, says it's been difficult to replicate the original T-shirt study. And one of the caveats of the original study is that women who were taking birth control pills preferred men who were more immunologically similar.
"Certainly, we learn to really like the smell of our partners," Wyatt says. "Whether it's the reason for choosing them in the first place, we really don't know."
Wyatt says he's skeptical of DNA-based dating apps because there are many subtypes of HLA genes, meaning there's a fairly low chance that your HLA type and your romantic partner's would be an exact match, anyway. It's why finding a suitable match for a bone marrow transplant is difficult; a donor's HLA type has to be the same as the recipient's.
"What it means is that since we're all different, it's hard statistically to say who the best match will be," he says.
DNA-based dating apps haven't yet gone mainstream, but some people seem willing to give them a try. Since Pheramor's launch a little over a year ago, about 10,000 people have signed up to use the app, about half of which have taken the DNA test, Barreto says. By comparison, an estimated 50 million people use Tinder, which has been around since 2012, and about 40 million people are on Bumble, which was released in 2014.
In April, Barreto launched a second service, this one for couples, called WeHaveChemistry.com. A $139 kit includes two genetic tests, one for you and your partner, and a detailed DNA report on your sexual compatibility.
Unlike the Phermor app, WeHaveChemistry doesn't provide users with a numeric combability score but instead makes personalized recommendations based on your genetic results. For instance, if the DNA test shows that your HLA genes are similar, Barreto says, "We might recommend pheromone colognes, working out together, or not showering before bed to get your juices running."
Despite her own research on HLA and sexual compatibility, Croy isn't sure how knowing HLA type will help couples. However, some researchers are doing studies on whether HLA types are related to certain cases of infertility, and this is where a genetic test might be very useful, says Croy.
"Otherwise, I think it doesn't matter whether we're HLA compatible or not," she says. "It might give you one possible explanation about why your sexual life isn't as satisfactory as it could be, but there are many other factors that play a role."
Probiotic bacteria can be engineered to fight antibiotic-resistant superbugs by releasing chemicals that kill them.
In 1945, almost two decades after Alexander Fleming discovered penicillin, he warned that as antibiotics use grows, they may lose their efficiency. He was prescient—the first case of penicillin resistance was reported two years later. Back then, not many people paid attention to Fleming’s warning. After all, the “golden era” of the antibiotics age had just began. By the 1950s, three new antibiotics derived from soil bacteria — streptomycin, chloramphenicol, and tetracycline — could cure infectious diseases like tuberculosis, cholera, meningitis and typhoid fever, among others.
Today, these antibiotics and many of their successors developed through the 1980s are gradually losing their effectiveness. The extensive overuse and misuse of antibiotics led to the rise of drug resistance. The livestock sector buys around 80 percent of all antibiotics sold in the U.S. every year. Farmers feed cows and chickens low doses of antibiotics to prevent infections and fatten up the animals, which eventually causes resistant bacterial strains to evolve. If manure from cattle is used on fields, the soil and vegetables can get contaminated with antibiotic-resistant bacteria. Another major factor is doctors overprescribing antibiotics to humans, particularly in low-income countries. Between 2000 to 2018, the global rates of human antibiotic consumption shot up by 46 percent.
In recent years, researchers have been exploring a promising avenue: the use of synthetic biology to engineer new bacteria that may work better than antibiotics. The need continues to grow, as a Lancetstudy linked antibiotic resistance to over 1.27 million deaths worldwide in 2019, surpassing HIV/AIDS and malaria. The western sub-Saharan Africa region had the highest death rate (27.3 people per 100,000).
Researchers warn that if nothing changes, by 2050, antibiotic resistance could kill 10 million people annually.
To make it worse, our remedy pipelines are drying up. Out of the 18 biggest pharmaceutical companies, 15 abandoned antibiotic development by 2013. According to the AMR Action Fund, venture capital has remained indifferent towards biotech start-ups developing new antibiotics. In 2019, at least two antibiotic start-ups filed for bankruptcy. As of December 2020, there were 43 new antibiotics in clinical development. But because they are based on previously known molecules, scientists say they are inadequate for treating multidrug-resistant bacteria. Researchers warn that if nothing changes, by 2050, antibiotic resistance could kill 10 million people annually.
The rise of synthetic biology
To circumvent this dire future, scientists have been working on alternative solutions using synthetic biology tools, meaning genetically modifying good bacteria to fight the bad ones.
From the time life evolved on earth around 3.8 billion years ago, bacteria have engaged in biological warfare. They constantly strategize new methods to combat each other by synthesizing toxic proteins that kill competition.
For example, Escherichia coli produces bacteriocins or toxins to kill other strains of E.coli that attempt to colonize the same habitat. Microbes like E.coli (which are not all pathogenic) are also naturally present in the human microbiome. The human microbiome harbors up to 100 trillion symbiotic microbial cells. The majority of them are beneficial organisms residing in the gut at different compositions.
The chemicals that these “good bacteria” produce do not pose any health risks to us, but can be toxic to other bacteria, particularly to human pathogens. For the last three decades, scientists have been manipulating bacteria’s biological warfare tactics to our collective advantage.
In the late 1990s, researchers drew inspiration from electrical and computing engineering principles that involve constructing digital circuits to control devices. In certain ways, every cell in living organisms works like a tiny computer. The cell receives messages in the form of biochemical molecules that cling on to its surface. Those messages get processed within the cells through a series of complex molecular interactions.
Synthetic biologists can harness these living cells’ information processing skills and use them to construct genetic circuits that perform specific instructions—for example, secrete a toxin that kills pathogenic bacteria. “Any synthetic genetic circuit is merely a piece of information that hangs around in the bacteria’s cytoplasm,” explains José Rubén Morones-Ramírez, a professor at the Autonomous University of Nuevo León, Mexico. Then the ribosome, which synthesizes proteins in the cell, processes that new information, making the compounds scientists want bacteria to make. “The genetic circuit remains separated from the living cell’s DNA,” Morones-Ramírez explains. When the engineered bacteria replicates, the genetic circuit doesn’t become part of its genome.
Highly intelligent by bacterial standards, some multidrug resistant V. cholerae strains can also “collaborate” with other intestinal bacterial species to gain advantage and take hold of the gut.
In 2000, Boston-based researchers constructed an E.coli with a genetic switch that toggled between turning genes on and off two. Later, they built some safety checks into their bacteria. “To prevent unintentional or deleterious consequences, in 2009, we built a safety switch in the engineered bacteria’s genetic circuit that gets triggered after it gets exposed to a pathogen," says James Collins, a professor of biological engineering at MIT and faculty member at Harvard University’s Wyss Institute. “After getting rid of the pathogen, the engineered bacteria is designed to switch off and leave the patient's body.”
Overuse and misuse of antibiotics causes resistant strains to evolve
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Seek and destroy
As the field of synthetic biology developed, scientists began using engineered bacteria to tackle superbugs. They first focused on Vibrio cholerae, whichin the 19th and 20th century caused cholera pandemics in India, China, the Middle East, Europe, and Americas. Like many other bacteria, V. cholerae communicate with each other via quorum sensing, a process in which the microorganisms release different signaling molecules, to convey messages to its brethren. Highly intelligent by bacterial standards, some multidrug resistant V. choleraestrains can also “collaborate” with other intestinal bacterial species to gain advantage and take hold of the gut. When untreated, cholera has a mortality rate of 25 to 50 percent and outbreaks frequently occur in developing countries, especially during floods and droughts.
Sometimes, however, V. cholerae makes mistakes. In 2008, researchers at Cornell University observed that when quorum sensing V. cholerae accidentally released high concentrations of a signaling molecule called CAI-1, it had a counterproductive effect—the pathogen couldn’t colonize the gut.
So the group, led byJohn March, professor of biological and environmental engineering, developed a novel strategy to combat V. cholerae. They genetically engineered E.coli toeavesdrop on V. cholerae communication networks and equipped it with the ability to release the CAI-1 molecules. That interfered with V. cholerae progress.Two years later, the Cornell team showed that V. cholerae-infected mice treated with engineered E.coli had a 92 percent survival rate.
These findings inspired researchers to sic the good bacteria present in foods like yogurt and kimchi onto the drug-resistant ones.
Three years later in 2011, Singapore-based scientists engineered E.coli to detect and destroy Pseudomonas aeruginosa, an oftendrug-resistant pathogen that causes pneumonia, urinary tract infections, and sepsis. Once the genetically engineered E.coli found its target through its quorum sensing molecules, it then released a peptide, that could eradicate 99 percent of P. aeruginosa cells in a test-tube experiment. The team outlined their work in a Molecular Systems Biology study.
“At the time, we knew that we were entering new, uncharted territory,” says lead author Matthew Chang, an associate professor and synthetic biologist at the National University of Singapore and lead author of the study. “To date, we are still in the process of trying to understand how long these microbes stay in our bodies and how they might continue to evolve.”
More teams followed the same path. In a 2013 study, MIT researchers also genetically engineered E.coli to detect P. aeruginosa via the pathogen’s quorum-sensing molecules. It then destroyed the pathogen by secreting a lab-made toxin.
Probiotics that fight
A year later in 2014, a Nature study found that the abundance of Ruminococcus obeum, a probiotic bacteria naturally occurring in the human microbiome, interrupts and reduces V.cholerae’s colonization— by detecting the pathogen’s quorum sensing molecules. The natural accumulation of R. obeumin Bangladeshi adults helped them recover from cholera despite living in an area with frequent outbreaks.
The findings from 2008 to 2014 inspired Collins and his team to delve into how good bacteria present in foods like yogurt and kimchi can attack drug-resistant bacteria. In 2018, Collins and his team developed the engineered probiotic strategy. They tweaked a commonly found bacteria in yogurt called Lactococcus lactis.
Engineered bacteria can be trained to target pathogens when they are at their most vulnerable metabolic stage in the human gut. --José Rubén Morones-Ramírez.
More scientists followed with more experiments. So far, researchers have engineered various probiotic organisms to fight pathogenic bacteria like Staphylococcus aureus (leading cause of skin, tissue, bone, joint and blood infections) and Clostridium perfringens (which causes watery diarrhea) in test-tube and animal experiments. In 2020, Russian scientists engineered a probiotic called Pichia pastoris to produce an enzyme called lysostaphin that eradicated S. aureus in vitro. Another 2020 study from China used an engineered probiotic bacteria Lactobacilli casei as a vaccine to prevent C. perfringens infection in rabbits.
In a study last year, Ramírez’s group at the Autonomous University of Nuevo León, engineered E. coli to detect quorum-sensing molecules from Methicillin-resistant Staphylococcus aureus or MRSA, a notorious superbug. The E. coli then releases a bacteriocin that kills MRSA. “An antibiotic is just a molecule that is not intelligent,” says Ramírez. “On the other hand, engineered bacteria can be trained to target pathogens when they are at their most vulnerable metabolic stage in the human gut.”
Collins and Timothy Lu, an associate professor of biological engineering at MIT, found that engineered E. coli can help treat other conditions—such as phenylketonuria, a rare metabolic disorder, that causes the build-up of an amino acid phenylalanine. Their start-up Synlogic aims to commercialize the technology, and has completed a phase 2 clinical trial.
Circumventing the challenges
The bacteria-engineering technique is not without pitfalls. One major challenge is that beneficial gut bacteria produce their own quorum-sensing molecules that can be similar to those that pathogens secrete. If an engineered bacteria’s biosensor is not specific enough, it will be ineffective.
Another concern is whether engineered bacteria might mutate after entering the gut. “As with any technology, there are risks where bad actors could have the capability to engineer a microbe to act quite nastily,” says Collins of MIT. But Collins and Ramírez both insist that the chances of the engineered bacteria mutating on its own are virtually non-existent. “It is extremely unlikely for the engineered bacteria to mutate,” Ramírez says. “Coaxing a living cell to do anything on command is immensely challenging. Usually, the greater risk is that the engineered bacteria entirely lose its functionality.”
However, the biggest challenge is bringing the curative bacteria to consumers. Pharmaceutical companies aren’t interested in antibiotics or their alternatives because it’s less profitable than developing new medicines for non-infectious diseases. Unlike the more chronic conditions like diabetes or cancer that require long-term medications, infectious diseases are usually treated much quicker. Running clinical trials are expensive and antibiotic-alternatives aren’t lucrative enough.
“Unfortunately, new medications for antibiotic resistant infections have been pushed to the bottom of the field,” says Lu of MIT. “It's not because the technology does not work. This is more of a market issue. Because clinical trials cost hundreds of millions of dollars, the only solution is that governments will need to fund them.” Lu stresses that societies must lobby to change how the modern healthcare industry works. “The whole world needs better treatments for antibiotic resistance.”
Meet Dr. Renee Wegrzyn, the first Director of President Biden's new health agency, ARPA-H
Today's podcast guest, Dr. Renee Wegrzyn, directs ARPA-H, a new agency formed last year to spearhead health innovations. Time will tell if ARPA-H will produce advances on the level of its fellow agency, DARPA.
In today’s podcast episode, I talk with Renee Wegrzyn, appointed by President Biden as the first director of a health agency created last year, the Advanced Research Projects Agency for Health, or ARPA-H. It’s inspired by DARPA, the agency that develops innovations for the Defense department and has been credited with hatching world-changing technologies such as ARPANET, which became the internet.
Time will tell if ARPA-H will lead to similar achievements in the realm of health. That’s what President Biden and Congress expect in return for funding ARPA-H at 2.5 billion dollars over three years.
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How will the agency figure out which projects to take on, especially with so many patient advocates for different diseases demanding moonshot funding for rapid progress?
I talked with Dr. Wegrzyn about the opportunities and challenges, what lessons ARPA-H is borrowing from Operation Warp Speed, how she decided on the first ARPA-H project that was announced recently, why a separate agency was needed instead of reforming HHS and the National Institutes of Health to be better at innovation, and how ARPA-H will make progress on disease prevention in addition to treatments for cancer, Alzheimer’s and diabetes, among many other health priorities.
Dr. Wegrzyn’s resume leaves no doubt of her suitability for this role. She was a program manager at DARPA where she focused on applying gene editing and synthetic biology to the goal of improving biosecurity. For her work there, she received the Superior Public Service Medal and, in case that wasn’t enough ARPA experience, she also worked at another ARPA that leads advanced projects in intelligence, called I-ARPA. Before that, she ran technical teams in the private sector working on gene therapies and disease diagnostics, among other areas. She has been a vice president of business development at Gingko Bioworks and headed innovation at Concentric by Gingko. Her training and education includes a PhD and undergraduate degree in applied biology from the Georgia Institute of Technology and she did her postdoc as an Alexander von Humboldt Fellow in Heidelberg, Germany.
Dr. Wegrzyn told me that she’s “in the hot seat.” The pressure is on for ARPA-H especially after the need and potential for health innovation was spot lit by the pandemic and the unprecedented speed of vaccine development. We'll soon find out if ARPA-H can produce gamechangers in health that are equivalent to DARPA’s creation of the internet.
Show links:
ARPA-H - https://arpa-h.gov/
Dr. Wegrzyn profile - https://arpa-h.gov/people/renee-wegrzyn/
Dr. Wegrzyn Twitter - https://twitter.com/rwegrzyn?lang=en
President Biden Announces Dr. Wegrzyn's appointment - https://www.whitehouse.gov/briefing-room/statement...
Leaps.org coverage of ARPA-H - https://leaps.org/arpa/
ARPA-H program for joints to heal themselves - https://arpa-h.gov/news/nitro/ -
ARPA-H virtual talent search - https://arpa-h.gov/news/aco-talent-search/
Dr. Renee Wegrzyn was appointed director of ARPA-H last October.
Matt Fuchs is the editor-in-chief of Leaps.org and Making Sense of Science. He is also a contributing reporter to the Washington Post and has written for the New York Times, Time Magazine, WIRED and the Washington Post Magazine, among other outlets. Follow him @fuchswriter.