5.Immunity To A Brain Disease
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.
数年，但是患有库鲁病，则一般在产生症状之后一年内便会死亡。需要注意的是（尽管非常罕见），朊病毒能够遗传。不过，绝大多数患者是因为食用了产生感染的人或动物。最初，人类学家和医生们都不知道为什么库鲁病会在Fore族人中大肆传播。直到20世纪50年代末才发现这类疾病是在太平间盛宴时传染的。因为出于对死去亲人的尊敬，Fore族人会将尸体吃掉。妇女、孩子都参加此种仪式，高峰时该病在女性和儿童中的发病率是在男性中的8至9倍。因为该族人吞食已逝亲属的肉以完成后者的"生命循环"时，由男性先选择所食部分，然后再由女性和儿童打扫剩下的包括脑部在内的人肉，而脑部正是致病朊毒体含量较高的部分。在这种食人习俗被禁止之前， Fore族人的一些村庄几乎连一个年轻妇人都没有。并不是所有患此病的人都会死亡，这些存活下来的幸存者们的G127V基因有了新变化，这使得他们对大脑疾病产生了免疫能力。现在，这种基因遍布Fore族和周围的人。这是令人十分惊奇的现象，因为库鲁病是在1900年才开始爆发的。这个例子是自然在人类身上做出选择的最强和最近的例子。 非常美文
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.
3.Crystal-Clear Underwater Vision
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, 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.