Compared to many other species, all humans have incredibly similar genomes. However, even slight variations in our genes or environments can cause us to develop traits that make us unique. These differences can manifest in ordinary ways, such as through hair color, height, or facial structure, but occasionally, a person or population develops a characteristic that distinctly sets them apart from the rest of the human race.
While most of us have to worry about limiting our intake of fried foods, bacon, eggs, or anything that we’re told is on the “cholesterol-raising list” of the moment, a few people can eat all these things and more without fear. In fact, no matter what they consume, their “bad cholesterol” (blood levels of low-density lipoprotein, associated with heart disease) remains virtually non-existent.
These people were born with a genetic mutation. More specifically, they lack working copies of a gene known as PCSK9, and while it’s usually unlucky to be born with a missing gene, in this case, it seems to have some positive side effects.
After scientists discovered the relationship between this gene (or lack thereof) and cholesterol about 10 years ago, drug companies have worked frantically to create a pill that would block PCSK9 in other individuals. The drug is close to getting FDA approval. In early trials, patients who have taken it have experienced as much as a 75-percent reduction in their cholesterol levels.
So far, scientists have only found the mutation in a handful of African Americans, and those with it have the benefit of a 90-percent reduced risk of heart disease.
All sorts of things could wipe out the human race—asteroid strikes, nuclear annihilation, and extreme climate change, just to name a few. Perhaps the scariest threat is some type of super-virulent virus. If a disease ravages the population, only the rare few who are immune would have a chance of survival. Fortunately, we know that certain people are indeed resistant to particular diseases.
Take HIV, for example. Some people have a genetic mutation that disables their copy of the CCR5 protein. HIV uses that protein as a doorway into human cells. So, if a person lacks CCR5, HIV can’t enter their cells, and they’re extremely unlikely to become infected with the disease.
That being said, scientists say that people with this mutation are resistant rather than immune to HIV. A few individuals without this protein have contracted and even died from AIDS. Apparently, some unusual types of HIV have figured out how to use proteins other than CCR5 to invade cells. This type of resourcefulness is why viruses are so scary.
Folks with two copies of the defective gene are most resistant to HIV. Currently, that includes only about 1 percent of Caucasians and is even more rare in other ethnicities.
Those who have an especially high resistance to malaria are carriers of another deadly disease: sickle cell anemia. Of course, no one wants the ability to dodge malaria only to die prematurely from malformed blood cells, but there is one situation where having the sickle cell gene pays off. To understand how that works, we have to explore the basics of both diseases.
Malaria is a type of parasite carried by mosquitoes that can lead to death (about 660,000 people per year) or at the very least make someone feel at death’s door. Malaria does its dirty work by invading red blood cells and reproducing. After a couple days, new malaria parasites burst out of the inhabited blood cell, destroying it. They then invade other red blood cells. This cycle continues until the parasites are stopped through treatment, the body’s defense mechanisms, or death. This process causes a loss of blood and weakens the lungs and liver. It also increases blood clotting, which can spark a coma or seizure.
Sickle cell anemia causes changes in the shape and makeup of red blood cells, which makes it difficult for them to flow through the blood stream and deliver adequate levels of oxygen. However, because the blood cells are mutated, they confuse the malaria parasite, making it difficult for it to attach and infiltrate the blood cells. Consequently, those who have sickle cells are naturally protected against malaria.
You can get the anti-malaria benefits without actually having sickle cells, so long as you’re a carrier of the sickle cell gene. To get sickle cell anemia, a person has to inherit two copies of the mutated gene, one from each parent. If they only get one, they have enough abnormal hemoglobin to resist malaria yet will never develop full-fledged anemia.
Because of its strong protection against malaria, the sickle cell trait has become highly naturally selected in areas of the world where malaria is widespread, with as much 10–40 percent of people carrying the mutation.
Inuits and other populations who live in intensely cold environments have adapted to an extreme way of life. Have these people simply learned how to survive in these environments, or are they somehow biologically different?
Cold-dwellers have different physiological responses to low temperatures compared to those who live in milder environments. And it appears there might be at least a partial genetic component to these adaptations, because even if someone moves to a cold environment and lives there for decades, their bodies never quite reach the same level of adaptation as natives who have lived in the environment for generations. For instance, researchers have found that indigenous Siberians are better adapted to the cold even when compared to non-indigenous Russians living in the same community.
People native to cold climates have higher basal metabolic rates (around 50 percent higher) than those accustomed to temperate climates. Also, they can maintain their body temperatures better without shivering and have relatively fewer sweat glands on the body and more on the face. In one study, researchers tested different races to see how their skin temperatures changed when exposed to cold. They found that Inuits were able to maintain the highest skin temperature of any group tested, followed by other Native Americans.
These types of adaptations partly explain why aboriginal Australians can sleep on the ground during cold nights (without shelter or clothing) with no ill effects and why Inuits can live much of their lives in subzero temperatures.
The human body is much better suited at adjusting to heat than to cold, so it’s rather impressive that people manage to live at all in freezing temperatures, let alone thrive.
Most climbers who’ve made it to the summit of Mt. Everest wouldn’t have done so without a local Sherpa guide. Amazingly, Sherpas often travel ahead of the adventurers to set ropes and ladders, just so the other climbers have a chance of making it up the steep cliffs.
There’s little doubt that Tibetans and Nepalese are physically superior in this high-altitude environment, yet what is it exactly that allows them to work vigorously in oxygen-depleted conditions, while ordinary folks have to struggle just to stay alive?
Tibetans live at an altitude above 4,000 meters (13,000 ft) and are accustomed to breathing air that contains about 40 percent less oxygen than at sea level. Over the centuries, their bodies compensated for this low-oxygen environment by developing bigger chests and greater lung capacities, which make it possible for them to inhale more air with each breath.
And, unlike lowlanders whose bodies produce more red blood cells when in low oxygen, high-altitude people have evolved to do the exact opposite—they produce fewer red blood cells. This is because while an increase in red blood cells might temporarily help a person get more oxygen to the body, it makes blood thicker over time and can lead to blood clots and other potentially deadly complications. Similarly, Sherpas have better blood flow in their brains and are overall less susceptible to altitude sickness.
Even when living at lower altitudes, Tibetans still maintain these traits, and researchers have found that many of these adaptations aren’t simply phenotypic variances (i.e., would reverse at low altitudes) but are genetic adaptations. One particular genetic change occurred in a stretch of DNA known as EPAS1, which codes for a regulatory protein. This protein detects oxygen and controls production of red blood cells and explains why Tibetans don’t overproduce red blood cells when deprived of oxygen, like ordinary people.
The Han Chinese, the lowland relatives of the Tibetans, do not share these genetic characteristics. The two groups split from each other about 3,000 years ago, which means these adaptations occurred in only about 100 generations—a relatively short time in terms of evolution.
In case we needed another reason to avoid cannibalism, eating our own kind is not a particularly healthy choice. The Fore people of Papua New Guinea showed us as much in the mid–20th century when their tribe suffered through an epidemic of Kuru—a degenerative and fatal brain disease spread by eating other humans.
Kuru is a prion disease related to Creutzfeldt-Jakob Disease (CJD) in humans and bovine spongiform encephalopathy (mad cow disease). Like all prion diseases, kuru decimates the brain, filling it with sponge-like holes. The infected suffers through a decline in memory and intellect, personality changes, and seizures. Sometimes, people can live with a prion disease for years, but in the case of kuru, the afflicted usually die within a year of showing symptoms. It’s important to note that, although very rare, a person can inherit a prion disease. However, the illness is most commonly spread by eating an infected person or animal.
Initially, anthropologists and medical doctors didn’t know why kuru was spreading across the Fore tribe. Finally, in the late 1950s, it was discovered that the infection was being transmitted at mortuary feasts, where tribe members would consume their deceased relatives out of respect. Mostly women and young children participated in the cannibalistic ritual. Consequently, they were the ones predominantly affected. Before the funerary practice was banned, some Fore villages had virtually no young women remaining.
But not all who were exposed to kuru died from it. Survivors had a novel variation in a gene called G127V that made them immune to the brain disease. Now, the gene is widespread among the Fore and surrounding people, which is surprising because kuru only popped up in the area around 1900. This incident is one of the strongest and most recent examples of natural selection in humans.
Although we’re often told that type O blood is a universal blood type that anyone can receive, that’s not the case. In fact, the whole system is a bit more complicated than many of us realize.
While most of us are aware of the eight basic blood types (A, AB, B, and O—each of which can be positive or negative), there are currently 35 known blood group systems, with millions of variations in each system. Blood that doesn’t fall into the ABO system is considered rare, and those who have such blood may find it challenging to locate a compatible donor when in need of a transfusion.
Still, there’s rare blood, and then there’s really rare blood. Presently, the most unusual kind of blood is known as “Rh-null.” As its name suggests, it doesn’t contain any antigens in the Rh system. It’s not that uncommon for a person to lack some Rh antigens. For instance, people who don’t have the Rh D antigen have “negative” blood (e.g. A-, B-, or O-). Still, it’s extremely extraordinary for someone to not have a single Rh antigen. It’s so extraordinary, in fact, that researchers have only come across 40 or so individuals on the planet who have Rh-null blood.
What makes this blood even more interesting is that it totally beats O blood in terms of being a universal donor, since even O-negative blood isn’t always compatible with other types of rare negative blood. Rh-null, however, works with nearly any type of blood. This is because, when receiving a transfusion, our bodies will likely reject any blood that contains antigens we don’t possess. And since Rh-null blood has zero Rh, A, or B antigens, it can be given to practically everyone.
Unfortunately, there are only about nine donors of this blood in the world, so it’s only used in extreme situations. Because of its limited supply and enormous value as a potential lifesaver, some doctors have referred to Rh-null as “golden” blood. In some cases, they’ve even tracked down anonymous donors (a big no-no) to request a sample.
Those who have the Rh-null type undoubtedly have a bittersweet existence. They know that their blood is literally a lifesaver for others with rare blood, yet if they themselves need blood, their options are limited to the donations of only nine people.
Most animals’ eyes are designed for seeing things underwater or in air—not both. The human eye, of course, is adept at seeing things in air. When we try to open our eyes underwater, things look blurry. This is because the water has a similar density to the fluids in our eyes, which limits the amount of refracted light that can pass into the eye. Low refraction equals fuzzy vision.
That knowledge makes it all the more surprising that a group of people, known as the Moken, have the ability to see clearly underwater, even at depths up to 22 meters (75 ft).
The Moken spend eight months of the year on boats or stilt houses. They only return to land to get essential items, which they acquire by bartering foods or shells collected from the ocean. They gather resources from the sea using traditional methods, which means no modern fishing poles, masks, or diving gear. Children are responsible for collecting food, such as clams or sea cucumbers, from the sea floor. Through this repetitive and consistent task, their eyes are now capable of changing shape when underwater to increase light refraction. Thus, they can easily distinguish between edible clams and ordinary rocks even when many meters below water.
When tested, the Moken children had underwater vision twice as sharp as European children. However, it seems that this is an adaptation that we might all possess if our environment demanded it, since researchers have trained European children to perform underwater tasks as successfully as the Moken.
Getting old comes with a host of physical problems. A common such issue is osteoporosis, a loss of bone mass and density. This leads to inevitable bone fractures, broken hips, and hunched spines—not a pleasant fate for anyone. Still, it’s not all bad news, as a group of people have a unique gene that may hold the secret to curing osteoporosis.
The gene is found in the Afrikaner population (South Africans with Dutch origins), and it causes people to gain bone mass throughout their lives instead of losing it. More specifically, it’s a mutation in the SOST gene, which controls a protein (sclerostin) that regulates bone growth.
If an Afrikaner inherits two copies of the mutated gene, they develop the disorder sclerosteosis, which leads to severe bone overgrowth, gigantism, facial distortion, deafness, and early death. Obviously, that disorder is far worse than osteoporosis. However, if they only inherit one copy of the gene, they don’t get sclerosteosis and simply have especially dense bones throughout their lives.
Although heterozygous carriers of the gene are currently the only ones enjoying the benefits, researchers are studying the DNA of Afrikaners with hopes of finding ways to reverse osteoporosis and other skeletal disorders in the general population. Based on what they’ve learned so far, they’ve already started clinical studies on a sclerostin inhibitor that’s capable of stimulating bone formation.
If it ever seems like some people have more hours in their day than you do, it turns out they just might—at least more awake hours. That’s because there are unusual individuals who can operate on six or fewer hours of shut-eye a night. And they aren’t simply getting by—they thrive on this limited amount of sleep, while many of the rest of us are still dragging ourselves out of bed after snoozing for eight solid hours.
These people aren’t necessarily tougher than the rest of us, and they haven’t trained their bodies to function on less sleep. Instead, they have a rare genetic mutation of the gene DEC2, which causes them to physiologically need less sleep than the average person.
If normal sleepers were to stick to six or fewer hours of slumber, they’d start experiencing negative impacts almost immediately. Chronic sleep deprivation can even lead to health problems, including serious ones like high blood pressure and heart disease. Those with the DEC2 mutation don’t have any of the problems associated with sleep deprivation, despite the limited time their heads are on the pillow. While it might seem odd that a single gene could change what we believe is a basic human need, those studying the DEC2 mutation believe it’s helping people to sleep more efficiently with more intense REM states. Apparently, when we have better sleep, we need less of it.
This genetic anomaly is exceedingly rare and is only found in less than 1 percent of self-proclaimed short-sleepers. So, chances are, even if you think you have it, you probably don’t.
Content and copy writer by day and list writer by night, S. Grant enjoys exploring the bizarre, unusual, and topics that hide in plain sight. Contact S. Grant here.
]]>Human genetics is a complex tapestry woven with threads of both commonality and extraordinary rarity. While much attention is given to genetic anomalies that result in disease or disability, there exists a lesser-known realm of beneficial genetic quirks that can bestow unique advantages upon their carriers. These anomalies, though rare and often peculiar, offer a glimpse into the fascinating diversity of human biology.
Join us on a journey through the marvels of human genetics as we delve into the realm of the rarest and most peculiar beneficial genetic anomalies. From seeing the world in an expanded spectrum of colors to defying the effects of aging, these genetic quirks paint a portrait of human diversity that is as captivating as it is extraordinary. So let us embark on this exploration of the weird and wonderful, where the ordinary meets the extraordinary in the intricate dance of our genetic code.
Related: Top 10 Surprising Ways Diseases Have Been Cured
Tetrachromacy, a rare and fascinating genetic anomaly, opens up a world of color beyond the ordinary spectrum visible to most humans. While the majority of people possess three types of cone cells in their eyes, allowing them to perceive a range of colors, individuals with tetrachromacy harbor an additional type of cone cell, granting them the ability to see an expanded palette of hues. This condition arises from a genetic mutation that enhances color perception and discrimination, leading to a heightened sensory experience unlike anything most of us can imagine.
Imagine a world where every sunset is a symphony of shades unseen by the naked eye, where the subtle nuances of nature’s palette reveal themselves in breathtaking detail. For those with tetrachromacy, this world is not a mere fantasy but a vivid reality. Their eyes serve as portals to a realm of color that exists beyond the comprehension of the average observer, offering a profound appreciation for the beauty that surrounds us.[1]
High bone density, a remarkable genetic anomaly, bestows upon individuals bones of unparalleled strength and resilience. While most people have bones of average density, those with this anomaly possess bones that are denser and more robust, providing increased resistance against fractures and injuries. This genetic mutation alters the composition of bone tissue, resulting in a skeletal structure that can withstand greater forces without succumbing to damage.
Picture a world where the fear of fractures and breaks is a distant memory, where individuals possess a natural armor of dense bone tissue that shields them from the perils of everyday life. For those with high bone density, this world is their reality—a realm where strength and resilience are woven into the very fabric of their being. Whether engaging in rigorous physical activities or simply navigating the challenges of daily existence, they move with confidence, knowing that their bones are up to the task.
The implications of high bone density extend far beyond individual health and well-being. In a society where osteoporosis and fractures are significant health concerns, this genetic anomaly offers hope for advancements in medical treatment and prevention. By unraveling the mysteries of bone density regulation, researchers may unlock new strategies for strengthening bones and reducing the risk of fractures for millions of people worldwide. Indeed, the marvel of high bone density serves as a testament to the remarkable potential of genetic anomalies to shape the future of healthcare.[2]
Sickle cell trait, often viewed as a genetic anomaly, paradoxically offers a degree of natural resistance to one of humanity’s oldest adversaries: malaria. Found predominantly in regions where malaria is endemic, this trait confers a survival advantage against the deadly parasite responsible for millions of deaths each year. Individuals with sickle cell trait carry one copy of the gene mutation responsible for sickle cell disease, resulting in altered hemoglobin production.
While sickle cell disease can be debilitating, those with the trait exhibit a milder form of the condition that provides protection against malaria. In regions where malaria exerts a heavy toll on human populations, the prevalence of sickle cell trait is notably higher—a testament to the selective pressure exerted by this devastating disease.
Although carrying the gene for sickle cell trait may increase the risk of developing sickle cell disease in offspring when both parents are carriers, the benefits conferred in malaria-endemic regions outweigh the potential risks. This unique genetic anomaly serves as a poignant reminder of the intricate evolutionary adaptations shaped by centuries of human interaction with infectious diseases.
The evolutionary significance of sickle cell trait extends beyond individual health to encompass broader implications for public health and malaria control efforts. Understanding the complex interplay between genetics, infectious diseases, and human populations is crucial for developing effective strategies to combat malaria and other vector-borne illnesses. By unraveling the genetic underpinnings of resistance to malaria, researchers may uncover novel approaches for malaria prevention and treatment, offering hope for a future where this ancient scourge no longer threatens human lives.[3]
Lactase persistence, a remarkable genetic trait, allows individuals to defy the natural decline in lactase production that typically occurs after childhood. While many humans lose the ability to digest lactose, the sugar found in milk, as they age, those with lactase persistence continue to produce the enzyme lactase, enabling them to consume dairy products throughout their lives. This genetic anomaly arises from mutations that regulate the expression of the LCT gene, which encodes the lactase enzyme, resulting in sustained lactase production into adulthood.
In a world where dairy products are a staple of many diets, the ability to digest lactose beyond infancy offers significant advantages in terms of nutrition and dietary diversity. For individuals with lactase persistence, milk and dairy products provide essential nutrients such as calcium and vitamin D, contributing to overall health and well-being. Moreover, the cultural and economic significance of dairy consumption underscores the importance of lactase persistence as a genetic trait that has shaped human dietary habits and agricultural practices for millennia.
The prevalence of lactase persistence varies widely among populations, with higher frequencies observed in regions where dairy farming has historically been prevalent. This distribution pattern suggests that lactase persistence has undergone positive selection in populations with a long history of dairy consumption, highlighting the adaptive significance of this genetic anomaly. By unraveling the genetic mechanisms underlying lactase persistence, researchers gain insights into human evolution, nutrition, and the intricate relationship between genes and culture.[4]
Delayed aging, a genetic anomaly observed in select individuals, defies the conventional trajectory of the aging process, offering the promise of a longer, healthier lifespan. While aging is a natural phenomenon characterized by the gradual decline of physiological function, those with delayed aging exhibit signs of aging at a significantly slower rate than the general population. This anomaly manifests in various ways, including youthful appearance, increased longevity, and resistance to age-related diseases.
Imagine a world where the passage of time seems to have little effect on the body and mind, where individuals retain their vitality and vigor well into old age. For those with delayed aging, this world is not a mere fantasy but a tangible reality—a realm where the boundaries of age blur and the concept of “growing old” takes on new meaning. Their genetic makeup confers a remarkable resilience against the ravages of time, offering glimpses into the potential of extending the human lifespan and improving the quality of life in later years.
The study of delayed aging holds immense promise for advancing our understanding of the biological mechanisms underlying aging and age-related diseases. By unraveling the genetic factors that contribute to delayed aging, researchers hope to identify novel therapeutic targets for combating age-related ailments and promoting healthy aging. Moreover, insights gained from studying delayed aging may pave the way for the development of interventions aimed at extending the human lifespan and enhancing overall well-being.[5]
Myostatin-related muscle hypertrophy is an extraordinary genetic condition characterized by a remarkable increase in muscle size and strength coupled with reduced body fat. Those affected by this rare anomaly can possess up to twice the usual amount of muscle mass, setting them apart with their Herculean physiques and astonishing physical capabilities.
Unlike many genetic disorders, myostatin-related muscle hypertrophy is not associated with any medical complications, and individuals with this condition typically exhibit normal intellectual development, highlighting the singular focus on muscular enhancement brought about by this genetic quirk. This rare condition is rooted in genetic mutations within the MSTN gene, which regulates myostatin—a protein that normally limits muscle growth. However, in individuals with myostatin-related muscle hypertrophy, these genetic changes effectively nullify the inhibitory effects of myostatin, resulting in unbridled muscle development from an early age.
This phenomenon showcases the intricate interplay between genetics and physiology, offering insights into the fundamental mechanisms governing muscle growth and development. Understanding the genetic basis of myostatin-related muscle hypertrophy not only sheds light on the remarkable diversity of human physiology but also holds promise for medical advancements in various fields.
By unraveling the intricate genetic pathways underlying muscle growth, researchers may uncover novel therapeutic targets for muscle-related disorders and injuries, paving the way for innovative treatments and rehabilitation strategies. Moreover, the study of rare genetic conditions like myostatin-related muscle hypertrophy underscores the profound impact of genetic variation on human health and performance, offering invaluable lessons for personalized medicine and sports science alike.[6]
In the realm of rare genetic anomalies, few are as perplexing yet intriguing as enhanced pain tolerance. This extraordinary condition bestows upon individuals an uncanny ability to withstand pain levels that would incapacitate the average person, raising questions about the underlying mechanisms and potential applications of such an anomaly. From mundane daily activities to extreme physical endeavors, those with enhanced pain tolerance navigate the world with an exceptional resilience that defies conventional understanding.
At the heart of this genetic peculiarity lies a complex interplay of neurobiological factors that modulate the perception and processing of pain signals within the central nervous system. While the exact genetic variants responsible for heightened pain tolerance remain elusive, ongoing research endeavors strive to unravel the intricate genetic pathways involved in this phenomenon. By deciphering the genetic code underlying enhanced pain tolerance, scientists hope to unlock new avenues for pain management and the development of more effective analgesic treatments.
Beyond its implications for pain management, the study of enhanced pain tolerance offers profound insights into the intricate workings of the human body and mind. By probing the genetic basis of pain perception, researchers gain a deeper understanding of how the nervous system functions and adapts to external stimuli. Moreover, this anomaly prompts broader philosophical reflections on the nature of pain and its role in shaping human experiences, challenging conventional notions of suffering and resilience.[7]
Highly Superior Autobiographical Memory (HSAM) stands as a remarkable memory phenomenon captivating researchers at the Center for the Neurobiology of Learning and Memory at UC Irvine. Individuals blessed with HSAM possess an unparalleled ability to recall intricate details of their own lives, demonstrating an extraordinary memory capacity that defies conventional understanding. Originating from the initial discovery in 2006 by Professor James McGaugh and colleagues, HSAM has since captivated the scientific community, shedding light on the fascinating intricacies of human memory.
The journey of understanding HSAM has been marked by groundbreaking discoveries and ongoing exploration. Initially observed in individuals like Jill Price, who could vividly recall specific events from her past, HSAM has garnered attention for its implications in memory research and cognitive science. As research progresses, scientists are delving deeper into the genetic and neural underpinnings of HSAM, seeking to unravel the mysteries behind this exceptional memory ability.
Collaborative efforts between research teams at UC Irvine and esteemed institutions worldwide underscore the interdisciplinary nature of HSAM research. From MRI studies revealing distinct brain regions to genetic studies exploring potential hereditary factors, the quest to comprehend HSAM encompasses a myriad of scientific disciplines. Furthermore, initiatives to develop novel screening tools and expand research collaborations offer promising avenues for advancing our understanding of HSAM and its implications for memory enhancement and cognitive health.
HSAM not only challenges traditional notions of memory but also holds profound implications for neuroscience and beyond. By unraveling the secrets of HSAM, researchers aim to unlock new insights into memory formation, cognitive function, and the human brain’s remarkable capacity for adaptation and learning. As the journey to decipher HSAM continues, it invites us to contemplate the boundless potential of the human mind and the transformative power of memory.[8]
Absolute pitch, often referred to as perfect pitch, is a rare and remarkable ability that enables individuals to identify or produce musical notes without any external reference. This extraordinary talent transcends mere musical aptitude, offering a glimpse into the fascinating complexities of auditory perception and cognitive processing. Unlike relative pitch, which involves the ability to discern the relationship between notes based on their position on a musical scale, absolute pitch represents a level of auditory acuity that is both innate and extraordinary.
The origins of absolute pitch remain shrouded in mystery, with researchers exploring a combination of genetic predispositions and early musical training as potential factors influencing its development. Studies have suggested a genetic component to absolute pitch, with certain variations in specific genes associated with a higher likelihood of possessing this rare ability. Furthermore, the critical period hypothesis proposes that exposure to musical stimuli during early childhood may play a crucial role in shaping the auditory processing capabilities necessary for absolute pitch.
While absolute pitch is often regarded as a rare and coveted gift among musicians, its implications extend far beyond the realm of music. Research into the neural mechanisms underlying absolute pitch offers insights into fundamental questions about brain plasticity, sensory perception, and the relationship between genetics and the environment. By unraveling the mysteries of absolute pitch, scientists hope to unlock new avenues for understanding human cognition and the remarkable diversity of human abilities.[9]
Living at high altitudes presents a unique challenge due to reduced oxygen levels, but populations like those on the Tibetan plateau have developed remarkable genetic adaptations to thrive in such environments. These adaptations not only allow them to cope with the thin air but also offer insights into human evolution and physiology.
One key adaptation is increased lung capacity, enabling individuals to extract more oxygen from each breath. This enhanced lung function helps maintain adequate oxygen levels in the bloodstream, which is crucial for sustaining bodily functions at high elevations where the air is thin. Additionally, these populations exhibit more efficient oxygen utilization, ensuring that the limited oxygen available is used optimally by the body’s cells and tissues.
Another crucial genetic adaptation involves higher red blood cell counts, which contribute to improved oxygen transport throughout the body. With more red blood cells available to carry oxygen, individuals living at high altitudes can maintain sufficient oxygenation of tissues, reducing the risk of altitude-related illnesses like hypoxia or altitude sickness.
These genetic adaptations offer valuable insights into human resilience and the intricate interplay between genetics and environmental factors. By understanding how populations have evolved to thrive in extreme environments, scientists hope to uncover new therapeutic targets for conditions related to oxygen deprivation, offering potential benefits for medical research and healthcare worldwide.[10]
]]>“GMO” foods may seem like a modern phenomenon, made possible only because of well-funded labs and genome analysis. What most consumers don’t realize is that most of humanity’s crops were already genetically modified thousands of years ago. In almost all cases, our favorite fruits and vegetables were engineered to be fundamentally different from their wild ancestors.
SEE ALSO: 10 Foods That Have Been Genetically Modified Beyond Recognition
The almonds we eat today are a domesticated variety derived from several species of wild almonds, all of which are bitter, spiny, and contain deadly amounts of cyanide. In the wild, almond trees produce a sugary compound and an enzyme that inevitably combine into cyanide when the edible parts of the plant are chewed up.
The identities of the specific strains used to create modern almonds are unknown. However, it is clear that humans selected and interbred the sweetest varieties of bitter almonds until the nuts were edible. This is quite a feat, considering that eating a dozen or so of the toxic kind would kill whoever had the task of testing out the newest crops. Luckily, the mutation that halts cyanide production is a dominant one, and almonds quickly became a popular treat.
The modern watermelon is one of the most extensively modified fruits in human history. Sub-Saharan Africans created the first domesticated varieties, which came in larger sizes and different colors. After the fruit’s introduction to Asia and Europe, it became substantially fleshier, sweeter, and larger.
Compared to the original watermelons found in the wild, which consisted mostly of seeds and weighed a mere 80 grams, modern ones are 91.5 percent water and weigh 2–8 kilograms (4–18 lb). Through several thousand years of artificial selection, the average volume of the watermelon has undergone a 1,680-fold increase.
The fruit’s appetizing red color is relatively new as well. It’s caused by the overproduction of the compound lycopene, a trait intentionally bred into watermelons by humans. Analysis of the watermelon genome also reveals that domestication has reduced the plant’s natural resistance to diseases. Today we are still modifying them, mostly to restore and then improve these natural immune functions.
Broccoli doesn’t exist in the wild. Neither does cauliflower, cabbage, Brussels sprouts, collards, or kale. All of these plants are the result of human cultivation, and they’re all the same species. These crops are artificially bred variations of the mustard plant Brassica oleracea. In its wild form, this plant produces several large leaves, as well as bunches of small yellow flowers. Different subspecies such as broccoli or cauliflower are created by modifying the expression of genes controlling the way the plant grows.
In broccoli, the flower clusters that once bloomed in the wild have been expanded into a cloud-like structure of many closed buds. In cauliflower, the flowery white head consists of mutant, undifferentiated cells that almost always remain sterile. One of the most striking examples of unique structures in this species is Romanesco broccoli: Its single modified bud is made up of smaller and smaller buds, forming a distinct logarithmic spiral pattern.
It seems like bananas were practically designed for us primates: They’re soft, seedless, tailor-made for the grip of our hand, and even come with a tab for easy opening. In reality, wild-type bananas are mostly inedible, and the plantains we eat today are completely different after genetic modifications. Wild-type bananas, which are tiny, tough, and filled with pit-like seeds, sometimes produce mutant variants without seeds.
Humans have been playing with this specific mutation for at least 6,500 years to produce all the varieties of seedless bananas available today. The banana’s design might even be too popular at this point; today’s mass-produced bananas are considered too genetically uniform, making them susceptible to diseases. Looks like we have some more work to do.
The wild ancestor of modern-day corn is a grass known as Zea or teosintes. Ancient Meso-Americans began selectively breeding this species as far back as 10,000 years ago. Gradually, they produced a plant unlike any other found in the world.
These soft, starchy plants appeared suddenly and mysteriously in archaeological records; the secrets of its development were only discovered recently through molecular and genetic analysis. The most important change suppressed branching of stalks. As a result, the plant produces fewer ears, but these ears are enormous, with long rows of kernels.
Stranger still, very little was changed in the plant’s genome during its domestication. The difference between the ancient and modern version amounts to a mere five or so genes.
Pumpkins, squash, and all other gourds are cultivated forms of tiny ancient plants. They all hail from the genus Cucurbita, which has become one of the most important plant groups for human consumption. Like corn, it was domesticated in the Americas at least 7,000 years ago. Ancient varieties were small, with extremely bitter flesh and few seeds. At some point, they were bred to produce more seeds. Later in history, there was more focus on creating different shapes, sizes, and types of flesh.
Pumpkins are native to North America and have no known wild variety that still exists. Long before their domestication, specifically around 14,000 years ago when humans first arrived to the continent, the early varieties of pumpkin nearly went extinct. These plants were once rich in cucurbitacins, one of the bitterest compound groups known to science. It appears that humans first used these gourds as containers and later began to use them as food sources.
Sweet, juicy strawberries are a very recent creation. Tiny ancestors were sometimes collected throughout the British Isles during the ice age, but the strawberry we enjoy today was cultivated as recently as the 1750s.
Mathematician and engineer Amedee-Francois Frezier brought a larger variety of wild strawberry while mapping out Chile for Louis XIV. After decades of trial and error, garden strawberries were created in France by crossing this plant with wild berries from America.
In 1759, pine strawberries became commercially significant. Finally, the huge, “modern” type of strawberry appeared by accident during hybridization experiments in 1806.
The original, primitive forms of the avocado are better described as “avocado-like fruits.” Unlike the fleshy, leathery-skinned kind we have today, most wild avocados are encased in hard shells. Uncultivated avocados are tiny enough to fit into the center of your palm, growing to about two or three inches in diameter. The wild-type flesh is gritty instead of creamy, and there is very little of it because the pit takes up almost all of the space inside the fruit. In 1927, agricultural explorer and researcher Wilson Popenoe commented that “the flavor is strong, not pleasant, and the fruit is scarcely considered eatable.”
For most of its time as a domesticated crop, the avocado remained unchanged due to its status as a sacred plant in tropical Mesoamerica. Large gardens—sometimes even entire forests—of avocado trees were grown and carefully maintained over ancestral burial grounds.
The coffee bean is another recently discovered and cultivated plant. It makes this list not because it has been fundamentally changed from its wild form but because there are so many varieties created solely to satisfy our cravings for novel tastes.
First cultivated in India during the 1600s, this African plant now comes in several dozen varieties and cultivars and continues to evolve with humans. Not even looking at varieties within each species, there are about 10 distinct species of coffee plant at present. Need your coffee less bitter? More bitter? Slightly buttery? Caffeine-free? Sourced from frost-resistant, self-fertilizing genetic stock that is purposely grown in civet feces? There’s a variety of bean for that. All modern, genetically modified varieties descend from ancient Arabica beans, which in itself is a hybrid of mysterious origin.
The cultivation of wheat began long before recorded history. In fact, the start of human civilization itself began when primitive people transitioned from the nomadic, hunter-gatherer lifestyle to an agriculturally based one. Wheat was one of the first and most important crops grown during this time, and the first human settlements gathered around areas where this food could be grown.
At first, prehistoric man was content to gather stray seeds of wild grasses. But soon (before people started making pottery, even) they had started to gather plants from areas with more seeds and replant them back home. Eventual changes in seed size and nutritional value were achieved, but the most important trait we managed coax out of their genomes was something called “indehiscence.” Normally, pods containing the edible parts of these plants shattered, so seeds could spread across the wind and ground. Thanks to prehistoric artificial selection, this trait was eliminated and our ancestors could harvest the plant itself, with all its seeds intact.
]]>China is a powerhouse that thrives on progress. One multipurpose field seeing great strides from this country is genetics. In recent years, China’s studies have included many world firsts and incredible medical advances.
There exists a strange side, too. Scientists are creating things never seen in nature, rewriting the rules on reproduction, and keeping the rest of the world nervous with their penchant for controversial human editing.
In 2018, a genome sequencing company based in Shenzhen was given access to a massive database. The genetic information of around seven million pregnant Chinese women was gathered while testing for a disorder linked to Down syndrome.
Only about 141,000 women were chosen, but it remains the biggest project examining Chinese genetics. The mothers represented nearly all provinces and even 36 of the 55 ethnic minority groups.
The findings were interesting. Certain genes were linked to height and body mass, the ability to have twins, and how severely herpesvirus 6 manifests. Even migrations left their mark on the Chinese genome. The largest wedge of the population is made up of the Han (92 percent).[1]
The study found that this group had the same genetic structure, but differences hinged on where they lived. Their northern and southern origins reflected in migrations known to have happened after 1949, when work became more available to the east and west. Gene variations also cause different immune responses from northern and southern Han. Intriguingly, certain minority groups had more genetic diversity than the Han.
The giant panda is iconic to China. Although these creatures are the subject of considerable studies, researchers still know very little about how they evolved. The only sure fact is that giant pandas split from other bears 20 million years ago.
Then, in 2018, a fossil turned up in Cizhutuo Cave in China. The creature died 22,000 years ago and looked a lot like a giant panda. To gauge what exactly it was, researchers accomplished an amazing feat—they pieced together 148,329 fragments of its DNA.
When the ancestry became clear, two things made the fossil unique. The DNA was the oldest ever found from a giant panda, but it also revealed a lineage nobody even knew existed. This panda split from its living cousins about 183,000 years ago. Its genetic code also revealed a great number of mutations that probably helped this species to survive the Ice Age in which it lived.[2]
In 2015, the Guangzhou Institutes of Biomedicine and Health saw the birth of several puppies. These were no ordinary beagles. They started their existence as 60 genetically modified embryos from which a single gene was removed.
Myostatin blocks muscle growth. Scientists deleted it to create what they claim are the world’s first designer dogs. Only 27 puppies were born, but not everything went according to plan.
Myostatin has two copies, and both were gone from only a single female pup. Another male puppy had one copy deactivated. He was more bulky than the rest but not as much as the female, which was designed to develop twice the normal amount of muscle. The project’s aim was to produce test animals on which to study diseases affecting human muscles, including Parkinson’s and muscular dystrophy.[3]
The Chinese may have many firsts to their credit, but in this case, nature beat them. Belgian Blue cattle have jaw-dropping muscles, thanks to a natural lack of myostatin. In addition, a genetic disorder occasionally deletes the gene in whippets, producing freakishly muscled dogs.
Upon learning that scientists tweaked the silkworm’s ability to produce silk, most would think of worms spinning better, more copious amounts. However, in the world of this satiny material, the silkworm is not king. Spiders beat them on several levels.
Arachnid silk promises incredibly useful applications in medicine, including microcapsules that deliver cancer drugs as well as the potential to fix damaged nerves. Researchers also discovered that it could strengthen bulletproof vests.
Unfortunately, spiders do not play along with idea of having their silk commercially farmed. Unlike the predictable silkworm, the arachnids are territorial and, worse yet, cannibalistic.
In 2018, a team affiliated with several Chinese institutions used gene editing and succeeded where many others have failed. They replaced a segment from the silkworm’s genetic code with DNA from a golden orb-web spider.[4]
When the altered worms spun their cocoons, the silk was analyzed. It was 35.2 percent spider, the highest purity ever achieved. (Past attempts lagged at 5 percent.) The silk was ready to use the moment the silkworms released the threads, something no other team could manage.
Among the most sought-after things in the world of gardeners is the blue rose. It does not exist in nature, and for hundreds of years, rose enthusiasts failed to breed this ultimate color.
During a more recent project that lasted 20 years and involved selective breeding and genetic engineering, biotechnologists came the nearest. However, even this prize rose was more mauve than blue.
Chinese scientists found a novel way to reach the dream. They started with the bacterium Agrobacterium tumefaciens, often used in bioengineering because it easily transfers foreign genetic material into plant DNA.[5]
From another bacterium, the researchers picked two bacterial enzymes capable of turning the L-glutamine in rose petals into a blue pigment called indigoidine. A special strain of A. tumefaciens was created to carry the enzymes.
The bacteria were then injected into a white rose. The pigment genes entered the plant’s genome and caused blue to pool around the injection spot. The world’s first blue rose is not perfect as the technique only produces temporary blotches. However, Chinese scientists are already busy with the next step—engineering a rose that naturally produces the two enzymes and causes itself to turn blue.
In 2002, the world followed the lethal outbreak of SARS (severe acute respiratory syndrome). It first bloomed in South China, infected 8,000 people, and killed nearly 800.
What caused the epidemic was never solved. In late 2017, scientists disclosed an unnerving clue in a cave in China’s Yunnan Province. For the past five years, they had investigated multiple SARS viruses present in the cave’s bats. There were 11 new strains, but none showed the genetic traits of the 2002 outbreak. SARS in bats has never been proven to cross the species barrier to humans, either.
However, a thorough analysis found something frightening. Together, the new strains carried enough genetic blocks to theoretically build a virus that could evolve to jump from bats to people. Secondly, three of the new strains showed a genetic predisposition to infect humans.[6]
If the 2002 epidemic rose from the cave, it still does not explain how it traveled to Ground Zero in Guangdong Province 1,000 kilometers (621 mi) away.
In late 2017, two long-tailed macaques were born in the same Shanghai laboratory. Even though their births happened weeks apart, Zhong Zhong and Hua Hua were identical “twins.”
They were created with the somatic cell nuclear transfer technique (SCNT), the same one that produced the historical sheep clone, Dolly, 20 years ago. The monkeys may be the first nonhuman primates created with SCNT, but the feat was not applauded by the entire international community.
Critics fear that the project might bring human cloning closer to reality without giving much regard to serious ethical concerns. Some researchers are entirely against SCNT, calling it “a very inefficient and hazardous procedure.”[7]
Indeed, Zhong Zhong and Hua Hua only happened after 79 previous failed attempts. Despite the criticism, Chinese scientists insist that identical monkeys can be a valuable way to study gene-based diseases in humans, including certain cancers.
Gene editing in humans is the new frontier. While most governments stall to agree on protocols for ethically modifying human tissue, China went ahead and did it a few years ago.
The historic breakthrough just added more fuel to the debate. Perhaps to no one’s surprise, this did not stop Guangzhou Medical University from doing it again in 2016. They wanted to create HIV-resistant embryos.
Operating under strict guidelines, they used 26 fertilized human eggs. All had been donated to research because they were no longer viable and would not develop into living babies.
The next step involved a specific genetic mutation. People who naturally carry this mutation are immune to the HIV virus. Using a gene editing tool called CRISPR, the gene was inserted into the embryos’ genomes.[8]
The tweak was successful, but only four became HIV-proof. The others showed why the rest of the world was slow to jump on the bandwagon. Unexpected mutations showed up—and not the good kind.
It would be impossible to predict the long-term effects on a CRISPR-created human (should it ever go that far). If anything, this second attempt showed that this type of gene editing was not safe. CRISPR was also used during the first modification years ago and also produced unwanted mutations.
The dream of creating nanorobots capable of fighting cancer within the body is nothing new. It was in the way Chinese researchers recently managed this that bordered on the ingenious.
Tumors can only live for as long as they are fed by a person’s blood vessels. To create something to block the vessels, scientists began by borrowing DNA molecules from a virus called a phage. An origami-like technique folded the strand into a rectangular sheet. The “tumor killers” were added, which were basically molecules of the clotting enzyme thrombin.
Four were rolled up inside the sheet to form a tube-shaped nanorobot. Special proteins locked the four molecules inside. After injection, the nanorobot entered the blood vessels. There, tumors opened the proteins and released the enzyme thrombin. A clot formed in the vessels and starved the tumor.
Tests on mice showed that the robots were effective. The rodents suffered from cancers of the skin, lung, breast, and ovary. In a group of eight animals with melanoma, the tumors vanished completely in three mice. Their life expectancy also increased.[9]
In 2018, Chinese scientists successfully bred two female mice. The 29 pups are the first mammals born from two mothers with no male involvement. The study tried to find out why two genders are essential for most species to reproduce. The answer rewrote the rules of reproduction.
As it turns out, during mammalian conception, there are about 100 genes where only genes from the female or male are switched on. Both genders are needed to activate all 100. The male covers the ones not switched on by female genes, and vice versa.[10]
If two females could breed in nature, certain genes would stay dormant. Using gene editing on mouse stem cells, researchers bypassed this barrier by removing a small piece of genetic code in three places. The altered cells were injected into an egg from a second female mouse. Successful fertilization followed. The babies grew up healthy and had pups of their own.
A similar experiment with two fathers (and a surrogate mother) produced 12 pups, but they all died within 48 hours. The research offers a distant hope for same-sex human couples wanting their own families.
]]>As cutting-edge technology explores the world of DNA, it is becoming clear that genes are not just for hereditary traits. They react and change to outside stimulation, and emotional trauma scars them.
Stolen genes can even hurry along evolution. In recent times, first-of-their-kind studies have unearthed bad news for education and pets as well as groundbreaking success for previously untreatable diseases.
Labradors remain one of the most popular breeds. After the black and yellow dogs, chocolate Labradors are the most sought-after. However, the demand for the dogs could be killing them.
Their beautiful brown coats are the result of recessive genes. This means that both parents must have the recessive chocolate gene to produce a chocolate litter. As a result, the gene pool is drying up.
In 2018, a massive veterinary study in the United Kingdom gauged the health of all kinds of Labradors. The results found that the brown variety died sooner. On average, non-chocolate Labradors lived almost 15 months longer to a ripe old age of 12.1 years.
The unique study also determined that the shrinking chocolate genes were more prone to serious diseases. Breeding for this attractive color appeared to have concentrated genes with a higher risk for ear and skin diseases. These can be added to the genetic problems all Labradors are prone to, including overeating and joint conditions.[1]
As only a fraction of the world’s chocolate Labradors were analyzed, there is a chance that the number of dogs with serious issues is even higher.
In 2018, scientists analyzed seawater off the coast of Massachusetts. What they discovered added a scary chapter to the book on viruses. The samples revealed an unknown family of viruses that could not be detected through normal scientific means.
They belonged to the little-understood group of tailless viruses. (Most others have double-stranded DNA, or “tails.”) Disturbingly, analysis showed that the new family, called Autolykiviridae, dominated the ocean.
When their unusual DNA was compared to samples in a gene bank, there was a startling match. Autolykiviridae, which turned out to be a ferocious predator of bacteria, was not just in the sea but also in the human stomach. Why this virus hangs around inside people remains a mystery.[2]
Autolykiviridae does patch things up a little when it comes to the vastly incomplete history of virus evolution. Ironically, they appear to link back to an ancient viral branch with a specific protein shell that prevented them from infecting bacteria.
A long-standing belief stated that gifted people would excel in their talents no matter their financial background. So-called “smart genes” were thought to give such individuals an edge in education. However, a new study revealed that genes came in second to wealth.
Researchers analyzed the DNA, education level, and success of thousands of people. Disturbingly, it showed that rich parents, not genius, gave offspring a better chance of being successful in life.
Scientists identified those with high genetic potential and found that among the group born into low-income households, only about 24 percent graduated from college. In stark contrast, 63 percent of gifted students with wealthy parents graduated.
Then researchers looked at study subjects with low genetic scores. Those with high-income parents graduated at around 27 percent, trumping the most talented group from a low-income background.[3]
The link between genetics and economics remains a patchy science, but this study is worrying. In a nutshell, it highlights the wasted potential—not because of genes (both groups had similar genetic data) but because brilliant people fall through the cracks of fewer financial opportunities.
In 2018, researchers turned their attention to a vast genetic database. It had been gathered by a company that used dog saliva to provide owners with ancestry reports of their pets.
The team combed through the genetic profiles to learn more about canine genetics—in particular, why dogs like Siberian huskies have blue eyes. Over 6,000 dogs and 200,000 genetic markers were compared.
Mostly, things remained random enough to be unremarkable. Before long, however, certain dogs started lining up in the same region on chromosome 18. They were the canines with the blue blinkers.[4]
Investigators zoomed in on this patch to search for mutations that might solve the whole thing. They found something never before witnessed in genetics. Near the normal gene responsible for eye development in mammals was another called ALX4. The latter had somehow duplicated itself, and this quirk is responsible for the breathtaking husky gaze. This unknown mutation does not cause blue eyes in humans or any other known species.
Bacteria are survivors that are not above stealing foreign DNA to adapt to a new environment. Scientists have always known about this remarkable ability, which is called “horizontal gene transfer.”
Though the process has never been witnessed, it was accepted that the organisms used whiplike arms called pili to snatch stray DNA. The reason why the maneuver remained undetected was the pili’s minuscule size—less than 0.01 percent of the width of a human hair.
The answer was fluorescent dye. In 2018, a cholera bacterium and bits of DNA were dyed and observed under a microscope. In a remarkable video recording, the predatory behavior was captured for the first time.
The glowing bacterium, somehow sensing a nearby bit of DNA, whipped out a pili. The aim was a little shaky. However, the bacterium captured the genetic snack and consumed it. The pili directly stuffed the DNA into the bacterium to quicken its own evolution.[5]
There is a reason why scientists want to find out as much as possible about horizontal gene transfer. In the future, it could help to combat antibiotic-resistant bacteria.
Inside the nucleus of a cell, the functional DNA is called chromatin, which resemble beads on a string. Previous studies detected movement from chromatin. But they could not answer how this was possible, let alone why it happened.
In 2018, researchers ran simulations to solve the mystery. Incredibly, the work revealed that the slight motion detected in the past resembled a choreographed line dance. It would appear as if the cell nucleus decides that everything must move, after which the chromatin shimmies into the desired direction.
To move, the “beads” on the chromatin expand and contract, which is felt by neighboring strings through fluid inside the nucleus. This causes them to align in the same direction and finally initiates a flow of genetic material waltzing to where it is wanted.[6]
The purpose behind the migrating DNA remains unknown. But researchers suspect that it could have something to do with how genes work, transform, and replicate.
In the world of genetics, the double helix is perhaps the most famous image. In 2018, however, researchers were shocked to find that human DNA could twist into another shape.
As opposed to the gentle corkscrew of the double helix, the new guy resembled a twisted knot and is far more complex. In scientific lingo, it is referred to as the intercalated motif (i-motif) structure. Its existence had already been suspected from laboratory tests, but this was the first time that these structures had appeared in living cells.
Researchers developed a fluorescent antibody that lit up the structures. When viewed for the first time, the knots behaved strangely. They blinked. This proved that the i-motifs actively grew, dissolved, and then formed again.
When and where they appeared offered important clues to what the knots do. They bloomed in older cells when the latter’s DNA is “read” for functional information. Additionally, the i-motifs preferred regions where genes are activated or switched off.[7]
All this suggested that the knots play a part in whether genes are read or not. If so, this DNA shape is critical to healthy cells and abnormal knots may result in disease.
A great breakthrough in gene therapy was announced in 2018. It involved a simple injection to treat choroideremia, a spectrum of eye diseases and the most common cause behind untreatable blindness.
The pioneering technique was tested on 14 patients suffering from this condition, which is genetic and often inherited. The therapy hinged on a virus containing a missing gene which was delivered to the back of the eye with an injection. This procedure was designed to affect the nerve cells in the retina.
Among the patients, 12 had no side effects from the gene correction. Incredibly, their sight stopped deteriorating and, in some, improved significantly. More importantly, after five years, nobody showed signs of any returning blindness.[8]
Without this therapy, most of the test subjects would have lost their vision over time. The success of the world’s first gene therapy trial for blindness paves the way to treat other diseases in the same way.
The court system may soon have another way to confirm child sex abuse. A study in 2018 found that such childhood trauma could leave molecular scars on the victim’s DNA.
The test subjects were all men, including individuals who had suffered abuse as children. In genetics, methylation is a process that already gives police an age estimate of somebody who left DNA behind on a crime scene. It also acts as a dimming tool, affecting to what extent a gene is activated.
When compared, the victims’ methylation showed a distinct difference from the men who experienced safe childhoods. The victims showed dimming in eight DNA regions with as much as 29 percent in one area.
This is good news for those who were abused but not believed. In the future, this altered methylation signature may be admissible in court as evidence that trauma did take place. The signature was found in the men’s sperm, raising questions for future studies about whether child abuse could carry a genetic scar to the next generation.[9]
Scott and Mark Kelly are NASA’s only set of identical twin astronauts. This made them valuable as test subjects—in particular, to see how space affected the human body.
Scott was sent into space for a year while his brother remained on Earth. When Scott returned in 2016, the twins were no longer so identical. Scott was taller, lighter, and possessed different gut bacteria. Weird things had happened to his genes.
In 2018, NASA released a statement about their preliminary findings. It appeared that the rigors of space travel activated countless “space genes.” Most reverted to normal on Earth, but some did not.
Among the physical processes changed were Scott’s vision, bone formation, and immune system. The genes linked to oxygen deprivation and DNA repair also seemed to have changed for good.
NASA wants the exact biology behind why almost 7 percent of Scott’s gene expression did not revert to normal after years back on Earth. The information could allow for safer long-term missions. Over 200 scientists are now crunching the numbers to study the Kelly brothers for answers.[10]
]]>Genetic technology is changing the world as we know it. As you read this, scientists are working on fascinating ways to modify DNA. Recently, a form of advanced gene-editing technology known as CRISPR has opened up new avenues of genetic experimentation. CRISPR is held in such high regard that, in 2020, its creators were awarded the Nobel Prize in Chemistry. Their new tool allows researchers to alter DNA with unique precision. Already, it is helping produce new forms of cancer therapy. Experts reckon it could one day be used to cure genetic conditions.
Of course, gene editing is a controversial practice that raises many ethical concerns. Bioscientists have been accused of “playing god” with the genome. But genetic technology has also inspired all manner of mind-boggling scientific innovation. Here are just ten of its most astounding uses.
10 Foods That Have Been Genetically Modified Beyond Recognition
Scientists in New Zealand have created genetically modified goats that produce cancer drugs in their milk. The goats have been specifically altered to create cetuximab medication, which is used to treat cancer in the colon and lungs. Currently, the drug can cost as much as $13,000 a month without insurance. Scientists hope their new method of production will help lower the price, thereby making it more accessible.
Manufacturing cetuximab is an expensive process. Its elaborate chemical structure means producers have to rely on proteins from inside mice cells to cultivate the drug. But these genetically modified goats have offered the pharmaceutical industry a way to mass-produce cetuximab.
“It’s a lot more economic to make cetuximab in animals because their mammary glands can produce large amounts of proteins,” explained Götz Laible, the researcher in charge of the project at New Zealand’s AgResearch institute.
Data storage is a difficult business. Day in day out, we rely on electronic devices like hard disks, optical drives, and memory sticks to store vast amounts of information. But perhaps other materials could be better suited to data storage. Now, scientists in New York have come up with a new method that uses gene editing to store data in the DNA of live bacteria.
In 2021, researchers at Colombia University demonstrated that live E. coli cells can store up to 72 bits of data. At its core, a data file consists of a long line of ones and zeros. The scientists were able to encode ones and zeros into the E. coli DNA by inserting specific genes into the cell. They were even able to write the simple message “Hello world!” into the DNA of an E. coli cell, then decode it by sequencing the DNA.
DNA is surprisingly well-suited to data storage. Biological proteins can store a massive wealth of information. Scientists estimate that if a strand of DNA were the size of a grain of salt, it could hold the equivalent of ten feature-length movies. What’s more, the technology needed to read and write DNA is becoming increasingly powerful with time. That said, DNA data storage is still in its infancy, which means it is unlikely to take off any time soon.
Scientists at Harvard University have extended the lifespan of dying mice using gene editing, increasing their life expectancy by more than double.
As part of the study, led by Professor David Liu, the mice were given progeria—a rare disease that causes premature aging in children. On average, children with progeria live to the age of fourteen. The condition is caused by a rare genetic mutation and cannot be treated using regular gene therapy. Instead, the Harvard team is developing a way to change the fundamental coding of the progeria sufferer’s DNA.
This technique was trialed on the terminally ill mice, and it significantly improved the length of their lives. The rodents, which were expected to survive 215 days, went on to live for a median average of 510 days. Liu and his team hope to use these findings to develop an effective treatment for progeria and similar genetic conditions.
Scientists have discovered a form of gene therapy for sight loss that, when injected into one eye, improves vision in both. The genes travel from the injected eye into the untreated eye, although eye specialists are unsure about the implications of this discovery.
The scientists were attempting to treat a condition known as Leber’s hereditary optic neuropathy (LHON), a form of progressive sight loss mostly found in young men. This rare type of blindness stems from a genetic mutation that attacks and destroys cells in the eye’s retina.
As part of a recent trial, 37 patients with LHON received gene therapy injections into one of their eyes. But remarkably, after two years, 29 of the patients reported improvement in vision in both eyes. At first, the scientists were taken aback by these results until they discovered that the gene therapy viruses were sneaking out of one eye and into the other.
Repeating the experiment on macaque monkeys, they found the genes were traveling down the optic nerve of one eye, crossing over to the other optic nerve, then traveling into the other eye.
Researchers have found a way to create hornless bulls by editing the DNA of the father. This new method provides farmers with a painless alternative to current dehorning techniques. Currently, cattle need to have their horns physically removed. This is a lengthy and difficult process that can be extremely painful for the bull. But it does need to be done. Not only are the hornless bulls less likely to harm other animals, but they are also easier to transport and take up less room at the feeding trough.
In 2016, two baby bulls were born with a genetic mutation that means they will never grow horns. This was achieved by introducing a short string of DNA into the father’s cells. After analyzing DNA from all three bulls, scientists confirmed that the genetic alterations had been passed down to the young cattle without causing any accidental side effects.
“We’ve demonstrated that healthy hornless calves with only the intended edit can be produced, and we provided data to help inform the process for evaluating genome-edited animals,” explained Alison Van Eenennaam, an expert in animal science working at the University of California, Davis.
As temperatures rise, cows begin to feel the strain. Bovines are particularly susceptible to heat stress. If left in the blazing sun for too long, cows start to lose their appetite, produce less milk, and are less likely to conceive. As you can imagine, the knock-on effects for farmers can be terrible. Each year, heat stress is said to cost the US dairy industry $900 million. In poorer countries, where farmers may only own a few livestock, it can be the ruin of many.
But now scientists in New Zealand have found a potential solution to this cattle-based conundrum. They are using gene-editing techniques to change the color of the cows’ coats. By altering their pigmentation genes, the researchers managed to lighten the dark, heat-absorbent hair of common dairy cows. Holstein-Friesian cattle are usually white with jet black patches, but the genetically altered calves were born covered in light silver-colored markings.
The researchers hope to refine their research using DNA from tropical cattle that are more resilient to high temperatures.
Gene editing could one day be used to treat obesity, say scientists at Harvard University. In August 2020, the researchers revealed a new method for combating weight gain in mice: transforming unhealthy white fat cells into energy-busting brown fat cells using CRISPR gene editing.
Stodgy white fat cells are full of unhealthy lipids that build up inside the body. An excess of white fat can lead to diabetes. But brown fat cells are much healthier. They break down some fat to create energy and store the rest in a smaller space.
The Harvard team was able to help the mice lose weight by altering their DNA. The scientists genetically altered the white fat, giving it the characteristics of healthy brown fat. The experiment focused on UCP1, a protein found in brown fat that turns chemical energy into heat.
Over the twelve-week study, the mice with white fat cells piled on the pounds, whereas the gene-edited mice found it much more difficult. There is even a suggestion that the gene-editing process helped the mice stave off diabetes.
Scientists predict that eventually this method could be developed into a treatment for obesity, although human trials are still a long way off.
In 2019, researchers from Harvard Medical School and Boston Children’s Hospital announced a novel treatment for hearing loss in mice that could one day be used on humans.
Beethoven mice suffer from a genetic mutation that also affects humans, causing progressive hearing loss and eventual deafness. The name Beethoven mice is a reference to the German composer, who began to lose his hearing when he was in his twenties.
The hearing loss that the mice experience is caused by a minor alteration in their DNA. Using sophisticated biological technology, scientists can pinpoint the defective gene without harming any of the remaining healthy genes. This means they can cure the Beethoven mice of their deafness without causing any unwanted side effects.
The scientists do warn people not to get their hopes up too quickly. There are still years of research to be done before this therapy can be tried on humans. “We believe our work opens the door toward a hyper-targeted way to treat an array of genetic disorders that arise from one defective copy of a gene,” explained Harvard’s Jeffrey Holt. “This truly is precision medicine.”
In January 2020, New York State officials released swarms of genetically modified (GM) male moths to curb the number of pests. Young female diamondback moths are capable of inflicting a massive amount of harm to farmers’ crops. Despite their short lifespan, the larvae consume a huge amount of brassica plants, including kale, cabbage, and oilseed rape. The moths and their rapacious diets are said to cause $5 billion of damage each year.
Typically a pest like this would be dealt with using pesticides, but the diamondback moth is remarkably quick at developing resistance. So Oxitec, a biotechnology company based in the UK, has developed a fleet of killer GM moths to wipe out the young pests.
Scientists added a gene to the male moths that causes newly-hatched larvae to drop dead, but only affects the females. This means the harmful young females will perish before they can do any damage. The young males, on the other hand, will go on to mate with other wild females, passing on the killer gene to their larvae. This should continue for a few generations, after which Oxitec says the lethal gene will fade away.
Antibiotic-resistant superbugs are a global crisis waiting to happen. Destructive pathogens that, only a few decades ago, were easy to treat with penicillin are building up immunity to antibiotics. Unless scientists can create new antibiotics quickly, we could be facing 10 million deaths a year by 2050 due to these hostile germs.
But there is hope on the horizon. Researchers from the University of Manchester have uncovered a new way to produce antibiotics using CRISPR gene editing. By combining several cutting-edge biological techniques, the team produced an unusual type of antibiotic known as malonomycin. This novel technique could help scientists develop new forms of antibiotic medication—drugs that are better suited to fighting off highly resistant superbugs.
“We are now optimistic that our findings might lead to the discovery of new antibiotics,” explained the leader of the study Jason Micklefield, “and may also provide new ways of making antibiotics which are urgently needed to combat emerging drug-resistant pathogens.”
10 Amazing Powers From Rare Genetic Mutations
]]>The first genetically engineered organism was created in 1973. That was just bacteria and not something that most everyday people would be excited about, but it set a precedent. Genetic engineering has grown in leaps and bounds since then, usually for the benefit of mankind. Scientific illiteracy and propaganda have made people suspicious of GMOs and now companies proudly proclaim their products aren’t GMO even when a third of all Nobel science laureates have pleaded with governments to make use of them because GMO crops could save literally millions of lives every year.
So what’s holding us back? It could be these somewhat more bizarre uses of genetic engineering technology.
When we say plans for genetic engineering, keep in mind that doesn’t necessarily mean execution. No one has done what we’re about to describe yet. They just had the idea. And what idea is that? To encode Bitcoin into the DNA of a mouse.
The group behind the plan is actually just two guys and they don’t have funding, so don’t expect to see any high value crypto mice on the market anytime soon. The plan, however, is interesting, if nothing else.
The idea here is to store Bitcoin in a cold wallet like anyone might with their cryptocurrency. Then a digital key can be generated, which is also standard. However, things take a left turn at this point. The group’s plan would be to enlist the aid of a genetics firm to translate that key into a genetic ATGC sequence that can be written on DNA. That can then be inserted into a mouse so that a baby mouse can be born with the key encoded in its DNA. The genetics of the mouse will open the wallet and give access to the cryptocurrency therein.
According to BitMouseDAO, the group that conjured up the idea, the mouse wouldn’t be harmed. And the whole idea is more of an art project than a way to manipulate currency or how it’s used. But for added value, an image of the mouse as an NFT could also be included.
Most genetic engineering is done in a fairly subdued way. One of the most famous cases involved making a strain of rice that was golden yellow and packed with vitamin A that could have saved millions of lives. By and large, yellow rice doesn’t look all that crazy though, and so the rice isn’t particularly shocking in terms of appearances. For that kind of genetic engineering, you need to look at Chinese muscle dogs.
Researchers edited out a certain gene in the dogs so that they’d develop to be more muscular. In fact, they have twice the muscle mass of normal dogs. And while that sounds like some real mad scientist stuff, it’s arguably for a beneficial purpose.
Dog anatomy and human anatomy are not all that dissimilar in some regards. Researchers were looking into how to prevent human diseases like muscular dystrophy or Parkinson’s, the kinds of conditions that lead to the wasting away of muscle. That said, the possibility of breeding dogs specifically with this mutation also exists which could make them more powerful hunters or runners. And because the mutation works the same in humans, the specific creation of more powerful human athletes could potentially also be a result.
The world at large is against genetically modifying things as simple as fruits and vegetables, so you can imagine the uproar if someone started genetically modifying cars, the beloved spokes animals of the internet itself. The idea has been proposed, however, and in the most sci-fi way imaginable.
One of the biggest drawbacks to our current use of nuclear power is the waste it produces. Nuclear waste is very radioactive and dangerous and is going to remain that way for generations. The people who have to deal with these problems have pondered what we can do to save not just people today from radiation, but future people.
The possibility exists that in 10,000 years or so, any language spoken today will be lost. Any knowledge of our nuclear waste storage facilities could be equally lost. How do you warn the people of tomorrow? Radiation cats.
The idea was proposed to create genetically modified cats that would change color when exposed to radiation. That way, in the future, our ancestors will be able to see a visual sign of danger. Presumably the story of what a radiation cat was would somehow be passed down generationally to make the phenomenon something more than a cool trick.
Have you ever heard that drinking red wine can be good for you? This benefit was attributed to a compound found in red grape skins called resveratrol. Resveratrol was shown to be an antioxidant in lab conditions. However, its link to cancer prevention in humans was never really established. That didn’t stop a lot of media stories about the potential after the lab link was established. Enough that some people wanted to look into genetically engineering beer to also have resveratrol in it.
A team from Rice University was cooking up a plan to use resveratrol enriched yeast to brew beer back in 2008. They even entered the beer in the International Genetically Engineered Machine competition that year and won the gold medal. Most of the students involved in the project weren’t even old enough to legally drink the beer that they were creating.
When was the first time you heard that chickens are actually dinosaurs? This was a popular headline back in 2015. But the real link started making the media rounds back in 2007. So we’ve all had a good bit of time to adjust to the idea that chickens and dinosaurs are pretty closely related.
Science took things one step further in 2017 when they decided to see if they could turn a chicken back into a dinosaur. A little genetic engineering was needed to determine how a dinosaur face evolved into a beak, and then efforts were put into switching those genes off again so that a beak could turn back into a dinosaur snout. Research had been going for some years towards this goal, and a team at Yale had altered chicken embryos to basically reverse engineer a dinosaur face. The chickens were never taken beyond the embryonic state, so no dino-chickens were actually running around.
The researchers have gained insight into the evolutionary process, as was the goal. Conceivably, however, this research could also be used towards the goal of engineering future dinosaur-like animals, although such research would widely be considered unethical.
There are over 45,000 species of spiders in the world and most of us can only recognize a few by name. Of those, the Daddy Long Legs has to be one of the most famous. But odds are no one would recognize the genetically altered version made at the University of Wisconsin-Madison.
This new version was missing the hallmark of the species and instead had little stub legs, so they called it a Daddy Short Legs. The team were able to identify and switch off a pair of genes related to leg development in the spiders. This helped gain insight into the evolutionary process that gave the spiders long legs in the first place. Now if you want to know why that’s important, well, that’s just a science thing. Scientists like to know why things happen the way they do.
These last few years have really brought vaccines to the forefront of people’s mind around the world. But have you ever wondered why vaccines are almost always distributed the same way? Sure, going to a pharmacy or hospital and getting an injection makes sense, but what if there was another way? For instance, what if we could eat a vaccine? What if we could genetically modify a banana to provide vaccination against a disease?
Anti-vaxxers would no doubt flip their lids at the concept, but vaccine bananas were actively pursued for a time. The idea stumbled, however, and maybe for reasons that aren’t readily apparent.
One of the big drawbacks was unreliability. Delivering specific doses and the stability of the antigens in a food suffered too many variables. Just look at the bananas in the store next time you go. Some are giant and some are small. Is the dose the same if they’re delivering vaccines? What if you eat a whole bunch, is it safe?
Other issues included immune tolerance, government regulations and good ol’ social resistance since people are already predisposed to mistrust GMOs.Still, the idea of using things like tomatoes to vaccinate against hepatitis B is still floated from time to time.
How worried are you about the chemical composition of pig poop? Canada struggled with this very issue, and in 2010, scientists there did something about it. The Enviropig was introduced to be a more environmentally friendly porker.
The genetically modified pigs were designed to produce less phosphorus when they pooped. The problem here is one most of us would never realize. All animals need phosphorus. It helps build cells and many other functions of life. Pigs get their phosphorus in feed but cannot digest phytate, a molecule made up chiefly of phosphorus. Farmers supplement an enzyme called phytase in their diets, which helps them digest it. But it’s inefficient and a lot of phosphorus gets excreted by pigs.
Phosphorus from pig feces builds up in the water supply, feeding algae and creating biological dead zones with no oxygen. So the Enviropig was modified to not need phytase and excrete 40% less phosphorus as a result. The end result is a pig that helps the environmentally friendly and saves money on feed supplements.
Spider silk is stronger than steel, though in practical terms there are a lot of limitations to what that statement means. Still, being able to manufacture spider silk would surely have practical uses, right? That’s what researchers thought when they genetically engineered goats to produce it. The silk was produced by incorporating silk-spinning genes into the goats so that silk could be harvested along with the goat’s milk.
There are potentially dozens of applications for large-scale production from medical to textile and military. But spiders are very hard to farm and they tend to kill each other. Goats are much easier. Nine years after Canadian scientists made the first two spider goats, and another facility was overseeing 20 of them. It’s still small scale, but it hasn’t gone away.
If you want to go all out with genetic engineering, why not throw cybernetics into the mix as well? That’s how you end up with a cyborg dragonfly drone that mixes a genetically engineered insect with machinery all in one place.
Real life drones are bulky, relatively speaking, when compared to insects. Scientists have tried to understand how something as small as an insect can have the energy to zip around at high speeds in such a small package when we can’t do the same with robotics. Tiny batteries are terribly inefficient.
The solution seems to be making an insect a robot. A dragonfly was modified with neurons in its spine to make it steerable. With a tiny computer backpack to gather data and also charge the tech with a solar panel, the dragonfly can be piloted by remote control as light sensors are used to send signals to its brain. The result is a tiny, living spy that could get into places few humans or drones could. Does it open the possibility of up-scaling the tech and controlling more complex animals? Maybe so.
]]>Usually when you hear about a genetic condition in the media, it’s presented as rare. You may be surprised to learn that around 60% of people will endure some kind of health problems related to a genetic condition. The symptoms can range from extremely mild to absolutely devastating. Many of the more common or severe conditions get a lot of media coverage, but there are numerous others which bring a host of unusual symptoms along with them that are lesser known.
Angelman Syndrome affects about 1 in 12,000 to 20,000 people. Its cause is related to a problem with a gene on chromosome 15. Either the maternal copy of the gene is damaged in some way, or there are two paternal copies present.
Those with Angelman may have developmental delays and issues with balance and speech. However, there are some other characteristics of the condition which make it very unique. One of them is how it affects the disposition of children who are born with it. Though they may experience intellectual disabilities, children with Angelman’s are frequently noted to have remarkably happy and excited dispositions. Smiling and laughter are hallmarks of the syndrome.
People with Angelman typically have a lifespan as long as those who don’t have the condition, although they may require lifelong assistance. Another unique aspect of the condition is that many of those diagnosed with it have a fascination with water.
Snatiation may be a fun word to say, but it’s an odd condition to have. The name is a portmanteau combining “sneezing” with “satiation” and gives insight to what exactly happens when you suffer from the condition. Those who have it sneeze after they feel full from eating.
First identified in 1989, the condition has been studied little because, let’s be honest, it’s not a pressing concern for most people. Basically, what happens is that, after eating a meal that fills you up, you’ll sneeze a handful of times. The case was first reported in a man who sneezed about four times after every meal, and most of his family did the same. So clearly it was genetic in nature. One person recorded 22 sneezes as a personal record. Annoying, to be sure, but not dangerous.
The type of food has no effect on the condition, and the sneezing isn’t a continual, painful, or even disruptive thing, but it may happen for someone’s entire life.
Favism sounds similar enough to favoritism that you may not even realize it’s related to a genetic condition at first. That said, it is a condition that affects people who are deficient in an enzyme called glucose-6-phosphate dehydrogenase. This enzyme is important to maintaining red blood cells. Now, even if you have the condition, you’ll likely be fine in general. The problem arises when a person who has it consumes certain compounds that can be found in medication or specific foods. When those are ingested, red blood cells can burst inside the body and lead to severe anemia.
So far it sounds like a curious condition, but not all that weird. That part comes in when you look at what triggers this anemia reaction. It’s fava beans, hence the name favism. You can also suffer the same fate by eating broad beans which are in the same family as fava beans and contain the same glucoside compounds.
The symptoms will manifest within six to 24 hours. Victims will become jaundiced and may have dark urine. The condition can potentially be life threatening.
Klippel–Trénaunay Syndrome can express itself in many ways. The congenital vascular disorder is very often denoted by dark-colored birthmarks as well as overactive bone or soft tissue growth. For many people, it can be debilitating. Since it often presents in a single limb, it can lead to things like fingers or toes fusing. But for Matthias Schlitte, the German Hellboy, it turned out to be an odd blessing.
Schlitte has confirmed he was born with the condition despite online rumors that he did this to himself. And in this case, the “this” we’re referring to is that arm. Schlitte is a professional arm wrestler because his Klippel–Trénaunay Syndrome caused his arm to grow unusually muscular. Though he looks like he spent his whole life only lifting weights with one arm, the condition is mostly responsible for what has happened
He discovered when he was still a little boy that one arm was just much stronger than the other. Encouraged by his mother, he took up arm wrestling and has exploited it to his advantage. His arm grew to 46 centimeters, or about 18 inches in diameter, while the average bicep is under 14 inches.
By the numbers, the odds of a stranger somewhere in the world having the exact same fingerprints as you are one in 64 billion. As far as we know, it has never happened. But there is a much greater chance that someone in the world has no fingerprints at all, thanks to a condition called adermatoglyphia.
One of the rarest conditions in the world and so far only linked to a few families, the only side effect seems to be entirely smooth finger pads. It first came to the attention of a dermatologist in 2007 when a patient came in with a problem. She couldn’t travel from Switzerland to the United States because she had no fingerprints, and no one had ever encountered that before. As it happened, many of her family members had the same problem.
A little digging turned up a mutation in a gene called SMARCAD1. How it caused them to not develop fingerprints is still unclear, and no other symptoms seem to come along with it.
The amount of sleep a person needs can vary based on several factors. The Mayo Clinic has a chart arranged by age with recommendations that range from seven hours for adults to as much as 16 hours for infants. But that seven plus hours is the absolute low end of the scale and doctors generally agree that lack of sleep can bring a host of serious health problems.
That said, there are some people in the world who are genetically short sleepers. A mutation of the DEC2 gene is the culprit. Those with the mutation can cut their sleep cycle much shorter, clocking a brisk four or five hours before waking up as refreshed as the rest of us who need a full seven or eight hours.
In mice that had the same gene manipulated, the production of a hormone called orexin was altered. Orexin regulates wakefulness. Your body produces it when it’s time to wake up and a narcoleptic produces too little. But those with the altered gene make it earlier in a sleep cycle than the rest of us, to no ill effects.
You can quickly find an online test for colorblindness and it’s likely to be a circle made of colored bubbles. There will be a number in the center formed of reddish bubbles surrounded by green bubbles. If you can’t read that number, you’re colorblind. But that’s just one kind of colorblindness, often called red-green colorblindness.
There are several ways a person can be colorblind, and red-green is the most common. Blue-yellow is another less common version and even more rare is monochromacy. This version affects one in 33,000 people and they see no color at all. The world is simply black and white.
On the tiny island of Pingelap in the Pacific Oceans, monochromacy is very common. This is because, in 1780, a tsunami killed all but around 20 people on the island. The king, one of the survivors, had a genetic condition that caused monochromacy. He set about repopulating the island as best he could and his descendants carried the colorblindness gene,
Today, sufferers need to wear dark glasses during the day because the sun essentially blinds them. However, their night vision is remarkable. Around 10% of the island have the condition and, at night, they can work and function as well as most of the rest of us do in full daylight.
Skin tone can vary greatly from one person to another and for a variety of reasons. Typically, we’re all familiar with the common range of skin tones, however, and it’s rare that you would ever see a person whose skin tone could be described as surprising. This was not the case with the Fugate family, whose skin was blue.
In the 1820s, in a place called Troublesome Creek, Kentucky, there was an entire family of blue-skinned humans. Martin Fugate, the patriarch, had skin described as being “indigo blue.” He married a woman named Elizabeth Smith, and four of their seven children also had blue skin.
In the 1970s, a baby named Benjamin Stacy was born with skin the doctor described as “blue as Lake Louise.” He was the great grandson of Luna Fugate, herself the great granddaughter of Martin, and just as blue.
Martin passed a condition called methemoglobinemia to his children and, as a result of inbreeding, the condition continued. The recessive gene remained in the family line and manifested again with Benjamin Stacy when he was born. Their hemoglobin can’t carry oxygen through the blood and many patients who have the condition, which can also be caused by medication, will die. But if enzyme levels are in the right balance, a person could live a full life as all of the Fugates did. They’ll just be bright blue.
Also called Honeymoon Nose, Honeymoon Rhinitis is a condition where sexual activity leads to nasal congestion and sneezing. The symptoms can manifest at any point during a sexual interaction but seem to occur most often right after. They are not caused by any direct stimulation of the nasal cavity or mucous membranes in the area. The cause is unknown.
It has been theorized that the condition may be caused by emotional stimulation and anxiety. It becomes a parasympathetic response as various hormones and emotions build during the activity and then, boom, your nose turns against you. Another theory has a psychiatric component, with sneezing being a physical manifestation of the emission of sexual tension.
Both men and women can suffer from it, and it resolves itself once the situation is no longer present. That means when the sexy times are done, the symptoms leave in about five to 15 minutes.
One thing worth noting is that the condition isn’t necessarily predicated on actual sexual activity with a partner. It may even occur as a result of sexual thoughts, which could potentially be remarkably frustrating and embarrassing depending on circumstances.
If you’ve ever suffered insomnia or another sleep disorder, you know it can get bad fast. The feeling of exhaustion that refuses to go away and, in time, problems focusing and mood changes. Fatal familial insomnia is a genetic condition that takes this to terrifying new levels.
The condition is caused by a mutation in a gene that produces a cellular prion protein. It can manifest in a person’s 20s all the way to their 70s, though most victims are in their 40s when symptoms begin.Once they begin, a person may have between seven months and six years to live. It cannot be cured.
Symptoms start out as difficulty falling or staying asleep, what you’d consider typical of insomnia. As it progresses, there may be muscle spasms, stiffness, mental deterioration, rapid heart rate and finally death.
Treatments involve measures to try to induce or maintain sleep, but they are only band aid solutions. Over time they fail to provide relief.
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