科學家說：這8個基因變異真的能給你超能力!

More than 99 percent of your genetic information is exactly the same as every other person on the planet. But it's in that less than 1 percent that things get interesting. Specific genetic variations allow some of us to acquire certain “super” qualities.
你的遺傳信息有99%以上都與世界上的其他所有人一模一樣。但是正因爲那不足1%的不同使一切變得有趣。特定的 遺傳性變異使我們中的一些人獲得了某些“超”能力。

ACTN3 and the super-sprinter variant
ACTN3，變身超級短跑選手

We all have a gene called ACTN3, but certain variants of it help our bodies make a special protein called alpha-actinin-3. This protein controls fast-twitch muscle fibres, the cells responsible for the speedy tensing and flexing of the muscles involved in sprinting or weight-lifting.
我們都有ACTN3基因，但是該基因的某些變異會幫助我們的身體合成一種特殊的蛋白質，這種蛋白質被稱爲α輔肌動蛋白3基因。這種蛋白質控制着快肌纖維，而這些細胞負責使那些參與短跑或舉重的肌肉迅速繃緊、收縮。

hDEC2 and the super-sleeper mutation
hDEC2，變身超級短眠者

Some people naturally feel totally energised on just 4 hours of sleep each night. These people are called 'short-sleepers'. For the most part, researchers believe that the capabilities are connected to specific genetic mutations, and have publicly identified one on the hDEC2 gene.
一些人天生就可以每晚只睡4個小時依然覺得精力充沛。這些人被稱爲“短眠者”。研究人員相信，這種能力基本上是與特定的基因突變有關，並且研究人員也已公開說明其中一種就是hDEC2基因。

TAS2R38 and the supertaster variant
TAS2R38，變身超級品味家

About a quarter of the population tastes food way more intensely than the rest of us. These 'super tasters' are more likely to put milk and sugar in bitter coffee, or avoid fatty foods. The reason for their reaction, scientists think, is programmed into their genes, specifically one called TAS2R38, the bitter-taste receptor gene.
約四分之一的人在品嚐食物的時候，會比我們其他人覺得食物的味道更濃烈。這些“超級品味家”更可能會在苦咖啡中加牛奶和糖，或避免油膩性的食品。科學家認爲，他們這種反應的原因是這種特性被編入到基因中，特別是一種被稱爲TAS2R38的苦味感受基因。

LRP5 and the unbreakable mutation
LRP5，變得堅不可摧

Researchers have identified a genetic mutation on the LRP5 gene that regulates bone-mineral density, which can cause brittle bones. But a different type of mutation on the same gene could also have the opposite effect, giving some people extremely dense bones that are practically unbreakable.
研究人員已確定LRP5基因的遺傳突變會調整骨礦密度，而這會使骨骼易碎。但相同基因不同的遺傳突變也會有相反的效果，使一些人的骨密度大大增加，並使其骨骼變得堅不可摧。

The malaria-protecting variant
防瘧疾變異

People who are carriers for sickle-cell disease are more protected against malaria than those who are not. Though blood disorders are not necessarily 'super', this information may influence more innovative malaria treatments down the road.
攜帶鐮形血球疾病的人比那些沒有鐮形血球的人更不易罹患瘧疾。雖然血液疾病未必“很好”，但這些信息將來也許會對瘧疾的治療產生更具創新性的影響。

CETP and the low-cholesterol mutation
CETP，低膽固醇變異

Mutations in a gene responsible for producing a protein called cholesteryl ester transfer protein (CETP) result in a deficiency of that protein. Studies have found a lower prevalence of coronary heart disease in people with the deficiency-causing mutation.
有一種基因負責合成一種名爲膽固醇酯轉移蛋白（CETP）的蛋白質，這種基因的變異會使人體缺少膽固醇酯轉移蛋白。研究發現，因這種變異而缺少膽固醇酯轉移蛋白的人罹患冠心病的機率更低。

BDNF and SLC6A4 and the super coffee-drinker variants
BDNF和SLC6A4，變身咖啡狂熱者

There are at least six genes associated with how your body processes caffeine. Some variants, near the genes BDNF and SLC6A4, influence the rewarding effects of caffeine that make you want to drink more.
至少有六種基因會參與處理你身體裏的咖啡因。BDNF和SLC6A4基因的一些變異會影響咖啡因的有益功效，使你想喝更多咖啡。

ALDH2*2: The super-flusher variant
ALDH2*2，變身極易臉紅者

Do your cheeks go rosy shortly after having a single glass of wine? A mutation on the ALDH2 gene may be the culprit.
在你喝過一杯葡萄酒之後你的臉頰會立刻變得紅潤嗎？這一變化的“罪魁禍首”可能是ALDH2基因變異。

One such mutation interferes with the ability of a liver enzyme called ALDH2 to convert the alcohol byproduct acetaldehyde into acetate. When acetaldehyde builds up in the blood, it opens up the capillaries, causing what we see as a flush or glow.
這一變異干擾了ALDH2肝酶把酒精副產品乙醛轉化爲醋酸鹽的功能。當血液中的乙醛增加時，就會使毛細血管擴張，使人變成我們所看到的臉紅的模樣。