More than 99 percent of your genetic¹ 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.

你的遗传信息有99%以上都与世界上的其他所有人一模一样。但是正因为那不足1%的不同使一切变得有趣。特定的 遗传性变异使我们中的一些人获得了某些“超”能力。

ACTN3 and the super-sprinter variant²

ACTN3，变身超级短跑选手

We all have a gene called ACTN3, but certain variants³ 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 flexing⁴ of the muscles involved in sprinting⁵ or weight-lifting.

我们都有ACTN3基因，但是该基因的某些变异会帮助我们的身体合成一种特殊的蛋白质，这种蛋白质被称为α辅肌动蛋白3基因。这种蛋白质控制着快肌纤维，而这些细胞负责使那些参与短跑或举重的肌肉迅速绷紧、收缩。

hDEC2 and the super-sleeper mutation⁶

hDEC2，变身超级短眠者

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 capabilities⁷ 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个小时依然觉得精力充沛。这些人被称为“短眠者”。研究人员相信，这种能力基本上是与特定的基因突变有关，并且研究人员也已公开说明其中一种就是hDEC2基因。

TAS2R38 and the supertaster variant

TAS2R38，变身超级品味家

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 genes⁸, specifically one called TAS2R38, the bitter-taste receptor gene.

约四分之一的人在品尝食物的时候，会比我们其他人觉得食物的味道更浓烈。这些“超级品味家”更可能会在苦咖啡中加牛奶和糖，或避免油腻性的食品。科学家认为，他们这种反应的原因是这种特性被编入到基因中，特别是一种被称为TAS2R38的苦味感受基因。

LRP5 and the unbreakable mutation

LRP5，变得坚不可摧

Researchers have identified a genetic mutation on the LRP5 gene that regulates bone-mineral density⁹, which can cause brittle¹⁰ bones. But a different type of mutation on the same gene could also have the opposite effect, giving some people extremely dense¹¹ bones that are practically unbreakable.

研究人员已确定LRP5基因的遗传突变会调整骨矿密度，而这会使骨骼易碎。但相同基因不同的遗传突变也会有相反的效果，使一些人的骨密度大大增加，并使其骨骼变得坚不可摧。

The malaria¹²-protecting variant

防疟疾变异

People who are carriers for sickle-cell disease are more protected against malaria than those who are not. Though blood disorders¹³ are not necessarily 'super', this information may influence more innovative¹⁴ malaria treatments down the road.

携带镰形血球疾病的人比那些没有镰形血球的人更不易罹患疟疾。虽然血液疾病未必“很好”，但这些信息将来也许会对疟疾的治疗产生更具创新性的影响。

CETP and the low-cholesterol mutation

CETP，低胆固醇变异

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.

有一种基因负责合成一种名为胆固醇酯转移蛋白（CETP）的蛋白质，这种基因的变异会使人体缺少胆固醇酯转移蛋白。研究发现，因这种变异而缺少胆固醇酯转移蛋白的人罹患冠心病的几率更低。

BDNF and SLC6A4 and the super coffee-drinker variants

BDNF和SLC6A4，变身咖啡狂热者

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.

至少有六种基因会参与处理你身体里的咖啡因。BDNF和SLC6A4基因的一些变异会影响咖啡因的有益功效，使你想喝更多咖啡。

ALDH2*2: The super-flusher variant

ALDH2*2，变身极易脸红者

Do your cheeks go rosy¹⁵ shortly after having a single glass of wine? A mutation on the ALDH2 gene may be the culprit.

在你喝过一杯葡萄酒之后你的脸颊会立刻变得红润吗？这一变化的“罪魁祸首”可能是ALDH2基因变异。

One such mutation interferes¹⁶ with the ability of a liver enzyme¹⁷ called ALDH2 to convert the alcohol byproduct acetaldehyde into acetate. When acetaldehyde builds up in the blood, it opens up the capillaries¹⁸, causing what we see as a flush or glow.

这一变异干扰了ALDH2肝酶把酒精副产品乙醛转化为醋酸盐的功能。当血液中的乙醛增加时，就会使毛细血管扩张，使人变成我们所看到的脸红的模样。