The one population with the lowest recorded levels of heart disease in the world are the Tsimane, a tribal group leading a gatherer-horticulturalist existence in the Bolivian Amazon. This group has a high carbohydrate and low protein diet.

反映到人类饮食上，这将与“古老”饮食原则完全相反——其特点是高蛋白饮食、肉类和未加工蔬菜的比例超过谷物成分。 该饮食背后的概念是模仿早期的古石器时代的人类，通过打猎而生存。 值得注意的是，古代石器时代的人类寿命据我们所知，只有33年。

根据纪录，世界上心脏病发病率最低的一个种族是提斯曼原住民(Tsimane)， 一个居住于玻利维亚亚马逊流域的采集园艺的部落。该部落食用含有高碳水化合物和低蛋白质的饮食。

Consistent with the idea that lowering protein intake extends lifespan, turning off the enzyme mTOR, which senses protein intake, with the drug rapamycin is the most powerful drug intervention we have so far to extend lifespan.

与降低蛋白质摄入量以延长寿命的观念相一致，雷帕霉素是目前为止最有效的药物，它通过切断mTOR酶对蛋白摄入量的感应来延长寿命。

Rapamycin is used in the clinic to suppress the immune system during organ transplants. It extends life in a number of animal species such as worms, fruit flies, and mice, even when delivered briefly in middle age, or late in life. The downside, of course, is that one must live with a suppressed immune system, which is a bit of a drag if you’re not living in a sterile lab environment.

雷帕霉素在临床中用于抑制器官移植期间的免疫系统。 即使是在中年或晚年才使用，它仍延长了许多动物物种的生命，如蠕虫、果蝇和小鼠。 当然，其缺点是，人们必须生活在受抑制的免疫系统中，如果你不生活在无菌的实验室环境中，这将是一个拖累。（编者注：也就是说，如果人们把雷帕霉素用来当做日常药物抗衰老，势必导致自己平日免疫力下降，无法承受有细菌和病毒的环境。）

The Bolivian Tsimane have a high carbohydrate and low protein diet. Photo RNW.org/Flickr, CC BY

玻利维亚Tsimane人食用具有高碳水化合物和低蛋白质的饮食。照片 RNW.org/Flickr, CC BY

In addition to simulating protein restriction, mTOR inhibition with rapamycin also promotes a process called autophagy. This is where the cell essentially “eats” itself, breaking down and destroying the old and damaged parts of the cell into its raw materials, which can be recycled into new structures. A compound called spermidine, discovered in semen and present in trace quantities in cheese, has been found to extend lifespan in mice by 10%. It’s thought this is due to spermidine’s ability to turn on autophagy.

除了模拟限制蛋白质摄入量以外，用雷帕霉素与mTOR抑制剂也会促成一种被称为自噬的进程。 即细胞自己“吃”自己，将细胞中旧的及损坏的部分破坏并转化为原材料，使其可以再循环到新的结构中。 一种被发现存在精液以及微量存在于奶酪中的，称之为精胺的复合物，已经将小鼠的寿命延长了10％。它被认为是精胺启动了自噬功能的结果。

Out with the old 除去老化部分

Another anti-ageing strategy is one called “senolysis”: that is, killing off old and damaged or “senescent” cells. These cells take up space, grow larger, and release substances that cause inflammation. When mice are genetically engineered so that it is possible to kill off senescent cells, health is drastically improved and animals live 20 to 30% longer.

另一种抗衰老策略是一种叫做“分解”的方法：就是杀死旧的损害的“衰老”细胞。这些细胞占据空间，并逐步增大，释放引起炎症的物质。当小鼠被基因编辑之后，衰老的细胞能够被毁掉，健康状况得到显着改善，动物的寿命可延长20至30％。

The hunt is now on for “senolytic” drugs, which can selectively kill off senescent cells. One company, Unity Biotech, recently raised US$116 million to achieve this.

最近，科学家正在研究一种叫做“senolytic”的药物，它可以选择性地杀死衰老细胞。一家叫做Unity Biotech的公司最近筹集了1.16亿美元来实现这一目标。

DNA changes 改变DNA

There is strong evidence that ageing is literally part of our DNA. So-called “jumping genes” are DNA parasites, caused by ancient viral infections in our evolutionary ancestors, and they make up almost half of our genetic material. These genes can actually “cut and paste” themselves so that they jump around to a different part of our DNA, and in doing so make our genomes less stable.

有强有力的证据表明，衰老是我们DNA的一部分。所谓的“跳跃基因”是DNA的寄生虫，它们是由我们进化祖先的古代病毒感染所引起的，其占我们遗传物质的近一半。这些基因实际上可以“剪切和粘贴”自身，以便它们跳转到DNA的不同部分，其结果是我们的基因变得不太稳定。

Telomeres, that cap the ends of our chromosomes, shorted as we age. from shutterstock.com

端粒，覆盖在我们染色体的末端，像我们年龄一样在缩短。来自shutterstock.com

These genes are normally turned off by another sirtuin enzyme called SIRT6, and animals genetically engineered to have an extra copy of this gene live longer and in better health.

这些基因通常被称一种称为SIRT6的去乙酰化酶所“关闭”。被基因工程改造过的动物因具有该基因的附加拷贝而活得更长、更健康。