Does the Story of Adam & Eve work scientifically?
How much genetic diversity is actually needed to keep a population healthy?
The Bible’s creation myth is famous the world over. It’s also helped shape Western civilization. According to Stephen Greenblatt’s book, The Rise and Fall of Adam and Eve, "Over many centuries, the story has shaped the way we think about crime and punishment, moral responsibility, death, pain, work, leisure, companionship, marriage, gender, curiosity, sexuality, and our shared humanness." What’s called into question is not its influence or importance, but the literal idea encapsulated within one of humanity’s most famous origin stories.
Could two people literally populate the Earth? It’s highly unlikely. Why? One reason, such a scenario would’ve made it difficult for humans to become the dominant species on Earth. In 2013, a team of researchers determined the minimum size population required 60,000 years ago for humans leaving Africa to eventually become the top species. For worldwide expansion to be successful, 2,250 individuals would be needed to make the journey northward, into Europe, Asia, and the Middle East, while 10,000 were thought to remain back in Africa.
This is a conservative estimate. Population geneticists came upon it by looking at population sizes and calculating back reasonable estimates on mutations rates and other genetic factors, to see how small a population could exist and still allow for the high level of genetic variation that we see today within the human species.
Another reason, to survive and thrive, a species needs a diversity of genes. The children of two people are obviously siblings and the product of those unions would be cousins. Children born to parents who are closely related genetically, are more likely to suffer from physical, mental, or developmental disabilities.
An incest taboo is universal the world over and for good reason. One study looking at Czechoslovakian children born between 1933 and 1970, found that almost 40% of those who had parents who were first-degree relatives carried some type of severe handicap. Such inherited diseases are rare and usually occur when two copies of the same gene are passed on by a person’s parents.
Carrying recessive variants isn’t a problem, if we get it from only one parent. In fact, almost everyone alive today carries one or two genetic variants that could be deadly. But they aren’t realized, because we’ve inherited only one copy. It’s when a person has two devastating recessive gene variants that a problem occurs, and that’s far more likely in the case of inbreeding.
The population of the Pingelap atoll shows a perfect example of the founder effect. Credit: Wikipedia Commons.
Consider the island of Pingelap in the Western Pacific. After a typhoon nearly wiped out the population in the 18th century, just 20 survivors got to work repopulating the island. Among them, there were carriers of achromatopsia, a rare recessive disorder which causes complete and total colorblindness. Today, it effects 10% of the atoll’s population. They became victims of the founder effect, which is when a lack of genetic diversity effects a population.
Another example, consider the royal families of Europe who intermarried to keep power within their ranks for centuries. Charles II is one of the most extreme examples. He had a number of mental and physical disabilities, was infertile, and didn’t learn to walk until the age of 8. An extremely high “inbreeding coefficient” was the reason. He had less diversity in his genes than if his parents had been siblings.
Humans actually select a mate partly based on how dissimilar the other person’s genes are. We are naturally attracted to those who have different immune genes than we ourselves carry. The idea is that having a variety of immune system genes will give offspring a much better chance of survival.
Say a cataclysmic event happened, wiping out almost all the people on Earth, or that we wanted to colonize another planet. How many individuals would you need to create a healthy human society? Dr. Philip Stephens from Durham University in Australia told the BBC that 50 individuals could keep the human race going, without falling into the founder effect.
500 would offer a diverse enough gene pool to allow offspring to adapt to new situations or a novel environment. And 500-5,000 would be needed to cover for random losses when genes are passed down from one generation to the next.
Chimpanzee populations show greater diversity than humans, for a very specific reason. Credit: Matthew Hoelscher, Wikipedia Commons.
Today, chimpanzee populations have more genetic diversity than all the humans on Earth, all 7 billion of us (and counting). The reason is the human population hit a bottle neck between 50,000 and 100,000 years ago. Back then, there were only 1,000 humans on Earth at any one time, over the course of about a million years.
So these numbers aren’t absolute. “The evidence for the short-term effects of low genetic diversity is very strong,” Dr. Stephens said, “but all these things are probabilistic. There are stories of incredible journeys back from the brink – anything is possible.”
Although there may not have been a literal Adam and Eve, our species has a “genetic Adam” and a “mitochondrial Eve.” Our genetic Adam was a man who’s Y-chromosome has been passed down in an unbroken chain starting in Africa, approx. 125,000 to 156,000 years ago. Although some other studies offer different time frames, the results are the same.
He wasn’t the first man on Earth, but the one who was lucky enough to have his genetic information passed on up until the present today. Rather than being the first female of a species, our “mitochondrial Eve” is the first female to pass on her mitochondrial DNA across generations of females, leading up to today.
Researchers believe it’s unlikely that our genetic Adam and Eve knew each other, and certainly they weren’t the first people on the planet. They were just lucky enough to pass on their genes and see them passed down again and again in unbroken lineages throughout human history, continuing up to the present and beyond.
To learn more about our genetic Adam and Eve, click here:
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Technique may enable speedy, on-demand design of softer, safer neural devices.
The brain is one of our most vulnerable organs, as soft as the softest tofu. Brain implants, on the other hand, are typically made from metal and other rigid materials that over time can cause inflammation and the buildup of scar tissue.
New research establishes an unexpected connection.
- A study provides further confirmation that a prolonged lack of sleep can result in early mortality.
- Surprisingly, the direct cause seems to be a buildup of Reactive Oxygen Species in the gut produced by sleeplessness.
- When the buildup is neutralized, a normal lifespan is restored.
We don't have to tell you what it feels like when you don't get enough sleep. A night or two of that can be miserable; long-term sleeplessness is out-and-out debilitating. Though we know from personal experience that we need sleep — our cognitive, metabolic, cardiovascular, and immune functioning depend on it — a lack of it does more than just make you feel like you want to die. It can actually kill you, according to study of rats published in 1989. But why?
A new study answers that question, and in an unexpected way. It appears that the sleeplessness/death connection has nothing to do with the brain or nervous system as many have assumed — it happens in your gut. Equally amazing, the study's authors were able to reverse the ill effects with antioxidants.
The study, from researchers at Harvard Medical School (HMS), is published in the journal Cell.
An unexpected culprit
The new research examines the mechanisms at play in sleep-deprived fruit flies and in mice — long-term sleep-deprivation experiments with humans are considered ethically iffy.
What the scientists found is that death from sleep deprivation is always preceded by a buildup of Reactive Oxygen Species (ROS) in the gut. These are not, as their name implies, living organisms. ROS are reactive molecules that are part of the immune system's response to invading microbes, and recent research suggests they're paradoxically key players in normal cell signal transduction and cell cycling as well. However, having an excess of ROS leads to oxidative stress, which is linked to "macromolecular damage and is implicated in various disease states such as atherosclerosis, diabetes, cancer, neurodegeneration, and aging." To prevent this, cellular defenses typically maintain a balance between ROS production and removal.
"We took an unbiased approach and searched throughout the body for indicators of damage from sleep deprivation," says senior study author Dragana Rogulja, admitting, "We were surprised to find it was the gut that plays a key role in causing death." The accumulation occurred in both sleep-deprived fruit flies and mice.
"Even more surprising," Rogulja recalls, "we found that premature death could be prevented. Each morning, we would all gather around to look at the flies, with disbelief to be honest. What we saw is that every time we could neutralize ROS in the gut, we could rescue the flies." Fruit flies given any of 11 antioxidant compounds — including melatonin, lipoic acid and NAD — that neutralize ROS buildups remained active and lived a normal length of time in spite of sleep deprivation. (The researchers note that these antioxidants did not extend the lifespans of non-sleep deprived control subjects.)
Image source: Tomasz Klejdysz/Shutterstock/Big Think
The study's tests were managed by co-first authors Alexandra Vaccaro and Yosef Kaplan Dor, both research fellows at HMS.
You may wonder how you compel a fruit fly to sleep, or for that matter, how you keep one awake. The researchers ascertained that fruit flies doze off in response to being shaken, and thus were the control subjects induced to snooze in their individual, warmed tubes. Each subject occupied its own 29 °C (84F) tube.
For their sleepless cohort, fruit flies were genetically manipulated to express a heat-sensitive protein in specific neurons. These neurons are known to suppress sleep, and did so — the fruit flies' activity levels, or lack thereof, were tracked using infrared beams.
Starting at Day 10 of sleep deprivation, fruit flies began dying, with all of them dead by Day 20. Control flies lived up to 40 days.
The scientists sought out markers that would indicate cell damage in their sleepless subjects. They saw no difference in brain tissue and elsewhere between the well-rested and sleep-deprived fruit flies, with the exception of one fruit fly.
However, in the guts of sleep-deprived fruit flies was a massive accumulation of ROS, which peaked around Day 10. Says Vaccaro, "We found that sleep-deprived flies were dying at the same pace, every time, and when we looked at markers of cell damage and death, the one tissue that really stood out was the gut." She adds, "I remember when we did the first experiment, you could immediately tell under the microscope that there was a striking difference. That almost never happens in lab research."
The experiments were repeated with mice who were gently kept awake for five days. Again, ROS built up over time in their small and large intestines but nowhere else.
As noted above, the administering of antioxidants alleviated the effect of the ROS buildup. In addition, flies that were modified to overproduce gut antioxidant enzymes were found to be immune to the damaging effects of sleep deprivation.
The research leaves some important questions unanswered. Says Kaplan Dor, "We still don't know why sleep loss causes ROS accumulation in the gut, and why this is lethal." He hypothesizes, "Sleep deprivation could directly affect the gut, but the trigger may also originate in the brain. Similarly, death could be due to damage in the gut or because high levels of ROS have systemic effects, or some combination of these."
The HMS researchers are now investigating the chemical pathways by which sleep-deprivation triggers the ROS buildup, and the means by which the ROS wreak cell havoc.
"We need to understand the biology of how sleep deprivation damages the body so that we can find ways to prevent this harm," says Rogulja.
Referring to the value of this study to humans, she notes,"So many of us are chronically sleep deprived. Even if we know staying up late every night is bad, we still do it. We believe we've identified a central issue that, when eliminated, allows for survival without sleep, at least in fruit flies."