Is Sex for Reproduction About to Become Extinct?
A healthy fetus in utero at 22 weeks.
There are lots of great reasons we humans have sex. We mostly do it to pair bond, realize our primal urges, and feel good. Once in a while, we also do it to make babies. As the coming genetic revolution plays out, we'll still have sex for most of the same reasons we do today. But we'll increasingly not do it to procreate.
Protecting children from harm is one of the core responsibilities of parenting.
Most parents go to great lengths to protect their children from real and imagined harms. This begins with taking prenatal vitamins during pregnancy and extends to having children immunized and protected from exposures to various diseases and dangers. Most of us look askance for good reason at mothers who abuse controlled substances during their pregnancies or parents who choose to not immunize their children. Protecting children from harm is one of the core responsibilities of parenting.
In the United States today, up to two percent of babies are estimated to be born with rare genetic diseases caused by single gene mutations. Sickle cell disease, Tay-Sachs, and Huntington's disease are among the more well-known examples of these, but the list runs to the thousands. Many babies born with these disorders suffer terribly, some die young, and nearly all spend big chunks of their lives struggling through the medical system.
Increasingly, however, many of these single-gene mutation diseases and other chromosomal disorders like Down syndrome are being identified in non-invasive prenatal tests performed on expectant mothers at the end of their first trimester of pregnancy. Knowing the hardship that children born with these types of disorders will likely face, majorities of these women in countries around the world are choosing to terminate pregnancies once these diagnoses have been made. Whatever the justification and whatever anyone's views on the morality of abortion, these decisions are inherently excruciating.
A much smaller number of prospective mothers, however, are today getting this same information about their potential future children before their pregnancies even begin. By undergoing both in vitro fertilization (IVF) and preimplantation genetic testing (PGT), these women are able to know which of the eggs that have been surgically extracted from them and fertilized with their partner or donor's sperm will carry the dangerous mutations. The in vitro embryos with these disorders are simply not implanted in the expectant mother's womb.
It would be monstrous to assert that an existing person with a deadly disease has any less right to thrive than anyone else. But it would also be hard to make a case that parents should affirmatively choose to implant embryos carrying such a disease if given the option. If prospective parents are already today choosing not to implant certain embryos based on our preliminary understanding of disease risk, what will happen when this embryo selection is based on far more information than just a few thousand single gene mutation diseases?
Our ability and willingness to make genetic alterations to our future children will grow over time along with our knowledge and technological ability.
When the first human genome was sequenced in 2003, the race to uncover the mysteries of human genetics had only just begun. Although we still know very little about our genetics relative to the complexity of the genome and even less compared to the broader ecosystem of our biology, the progress toward greater understanding is astounding. Today, the number of single gene mutation diseases and relatively simple genetic traits that can be predicted meaningfully from genetic data alone is already significant.
In the not-distant future, this list will grow to include complex diseases and disease propensities, percentage probabilities of living a long and healthy life, and increasingly the genetic component of complex human attributes like height, IQ, and personality style. This predictive power of genetic analysis will funnel straight into our fertility clinics where prospective parents choosing embryos will be making ever more consequential decisions about the genetic components of the future lives, health, and capabilities of their children.
Our understanding of what the genes extracted from early stage pre-implanted embryos are telling us will be only one of the rocket boosters driving assisted reproduction forward. Another will be the ability to induce adult cells like skin and nucleated blood cells into stem cells and then turn those stem cells into egg progenitor cells and then ultimately eggs. This will not only eliminate the need for hormone treatments and surgery to extract human eggs but also make it easy and cheap to generate an unlimited number of eggs from a given woman.
The average woman has around fifteen eggs extracted during IVF but imagine what generating a thousand eggs will do to the range of possibilities that could be realized through pre-implantation embryo selection. Each of these thousand eggs would be the natural offspring of the two parents, but the variation between them would make it possible to choose the ones with the strongest expression of the genetic component of a particular desired trait – like those with the highest possible genetic IQ potential.
Another rocket booster will be the application of gene editing technologies like CRISPR to edit the genomes of pre-implanted embryos or of the sperm and eggs used to create them. Just this week, Chinese researchers announced they had used CRISPR to edit the CCR5 gene in the pre-implanted embryos of a pair of Chinese twins to make them immune to HIV, the first ever case of gene editing humans and a harbinger of our genetically engineered future. The astounding complexity of the human genome will put limits on our ability to safely make too many simultaneous genetic changes to human embryos, but our ability and willingness to make these types of alterations to our future children will grow over time along with our knowledge and technological ability.
With so much at stake, prospective parents will increasingly have a stark choice when determining how to conceive their children. If they go the traditional route of sex, they will experience both the benign wisdom and unfathomable cruelty of nature. If they use IVF and increasingly informed embryo selection, they will eliminate most single gene mutation diseases and likely increase their children's chances of living a longer and healthier life with more opportunity than their unenhanced peers. But the optimizing parents could also set up their children for misery if these children don't particularly enjoy what they have been optimized to become or see themselves as some type of freakish consumer product with emotions.
Conceiving though sex will come to be seen more and more like not immunizing your children is today, a perfectly natural choice that comes with a significant potential risk and expense.
But although there will be pros and cons on each side, the fight between conception through good old-fashioned sex and conception in the lab will ultimately not be fair. Differences and competition within and between societies will pressure parents and societies to adopt ever more aggressive forms of reproductive technology if they believe doing so will open possibilities and create opportunities for the next generations rather than close them.
Conception through sex will remain as useful as it has always been but lab conception will only get more advantageous. Over time, only zealots will choose to roll the dice of their future children's health and well-being rather than invest, like parents always have, in protecting their children from harm and helping optimize their life potential. Conceiving though sex will come to be seen more and more like not immunizing your children is today, a perfectly natural choice that comes with a significant potential risk and expense to yourself, your children, and your community.
As this future plays out, the genetics and assisted reproduction revolutions will raise enormous, thorny, and massively consequential questions about how we value and invest in diversity, equality, and our own essential humanity – questions we aren't remotely prepared to answer. But these revolutions are coming sooner than most of us understand or are prepared for so we had better get ready.
Because where this trail is ultimately heading goes well beyond sex and toward a fundamental transformation of our evolutionary process as a species – and that should be everybody's business.
In this week's Friday Five, an old diabetes drug finds an exciting new purpose. Plus, how to make the cities of the future less toxic, making old mice younger with EVs, a new reason for mysterious stillbirths - and much more.
The Friday Five covers five stories in research that you may have missed this week. There are plenty of controversies and troubling ethical issues in science – and we get into many of them in our online magazine – but this news roundup focuses on scientific creativity and progress to give you a therapeutic dose of inspiration headed into the weekend.
Here is the promising research covered in this week's Friday Five:
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- How to make cities of the future less noisy
- An old diabetes drug could have a new purpose: treating an irregular heartbeat
- A new reason for mysterious stillbirths
- Making old mice younger with EVs
- No pain - or mucus - no gain
And an honorable mention this week: How treatments for depression can change the structure of the brain
Researchers at Stanford have found that the virus that causes Covid-19 can infect fat cells, which could help explain why obesity is linked to worse outcomes for those who catch Covid-19.
Obesity is a risk factor for worse outcomes for a variety of medical conditions ranging from cancer to Covid-19. Most experts attribute it simply to underlying low-grade inflammation and added weight that make breathing more difficult.
Now researchers have found a more direct reason: SARS-CoV-2, the virus that causes Covid-19, can infect adipocytes, more commonly known as fat cells, and macrophages, immune cells that are part of the broader matrix of cells that support fat tissue. Stanford University researchers Catherine Blish and Tracey McLaughlin are senior authors of the study.
Most of us think of fat as the spare tire that can accumulate around the middle as we age, but fat also is present closer to most internal organs. McLaughlin's research has focused on epicardial fat, “which sits right on top of the heart with no physical barrier at all,” she says. So if that fat got infected and inflamed, it might directly affect the heart.” That could help explain cardiovascular problems associated with Covid-19 infections.
Looking at tissue taken from autopsy, there was evidence of SARS-CoV-2 virus inside the fat cells as well as surrounding inflammation. In fat cells and immune cells harvested from health humans, infection in the laboratory drove "an inflammatory response, particularly in the macrophages…They secreted proteins that are typically seen in a cytokine storm” where the immune response runs amok with potential life-threatening consequences. This suggests to McLaughlin “that there could be a regional and even a systemic inflammatory response following infection in fat.”
It is easy to see how the airborne SARS-CoV-2 virus infects the nose and lungs, but how does it get into fat tissue? That is a mystery and the source of ample speculation.
The macrophages studied by McLaughlin and Blish were spewing out inflammatory proteins, While the the virus within them was replicating, the new viral particles were not able to replicate within those cells. It was a different story in the fat cells. “When [the virus] gets into the fat cells, it not only replicates, it's a productive infection, which means the resulting viral particles can infect another cell,” including microphages, McLaughlin explains. It seems to be a symbiotic tango of the virus between the two cell types that keeps the cycle going.
It is easy to see how the airborne SARS-CoV-2 virus infects the nose and lungs, but how does it get into fat tissue? That is a mystery and the source of ample speculation.
Macrophages are mobile; they engulf and carry invading pathogens to lymphoid tissue in the lymph nodes, tonsils and elsewhere in the body to alert T cells of the immune system to the pathogen. Perhaps some of them also carry the virus through the bloodstream to more distant tissue.
ACE2 receptors are the means by which SARS-CoV-2 latches on to and enters most cells. They are not thought to be common on fat cells, so initially most researchers thought it unlikely they would become infected.
However, while some cell receptors always sit on the surface of the cell, other receptors are expressed on the surface only under certain conditions. Philipp Scherer, a professor of internal medicine and director of the Touchstone Diabetes Center at the University of Texas Southwestern Medical Center, suggests that, in people who have obesity, “There might be higher levels of dysfunctional [fat cells] that facilitate entry of the virus,” either through transiently expressed ACE2 or other receptors. Inflammatory proteins generated by macrophages might contribute to this process.
Another hypothesis is that viral RNA might be smuggled into fat cells as cargo in small bits of material called extracellular vesicles, or EVs, that can travel between cells. Other researchers have shown that when EVs express ACE2 receptors, they can act as decoys for SARS-CoV-2, where the virus binds to them rather than a cell. These scientists are working to create drugs that mimic this decoy effect as an approach to therapy.
Do fat cells play a role in Long Covid? “Fat cells are a great place to hide. You have all the energy you need and fat cells turn over very slowly; they have a half-life of ten years,” says Scherer. Observational studies suggest that acute Covid-19 can trigger the onset of diabetes especially in people who are overweight, and that patients taking medicines to regulate their diabetes “were actually quite protective” against acute Covid-19. Scherer has funding to study the risks and benefits of those drugs in animal models of Long Covid.
McLaughlin says there are two areas of potential concern with fat tissue and Long Covid. One is that this tissue might serve as a “big reservoir where the virus continues to replicate and is sent out” to other parts of the body. The second is that inflammation due to infected fat cells and macrophages can result in fibrosis or scar tissue forming around organs, inhibiting their function. Once scar tissue forms, the tissue damage becomes more difficult to repair.
Current Covid-19 treatments work by stopping the virus from entering cells through the ACE2 receptor, so they likely would have no effect on virus that uses a different mechanism. That means another approach will have to be developed to complement the treatments we already have. So the best advice McLaughlin can offer today is to keep current on vaccinations and boosters and lose weight to reduce the risk associated with obesity.