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为什么会存在死亡?到底是该畏惧还是接受?

原文来自 Quora,已获得答主授权,内容仅代表答主观点。
译文由晓然翻译组原创,转载前请与我们联系。
译者:天璇 校对:李睿玥leah, 文瑜

想看英文原版,请点击最下方的阅读原文


According to the theory of evolution, why does death occur? It literally means that we have “chosen” to die and then chosen to “fear” it which is very contradictional!
为什么死亡会发生?根据进化论的观点,直接解释就是:我们“选择”死亡,选择“害怕”死亡,多么的矛盾!

OK let me define the question a bit more biologically - our bodies where formed in a long process by survival and reproduction of the fittest, and so we conclude that the factors like speed, strength and fertility, but why where the cellular organisms bound to this dependent way of circling life and death. The option of an organism formed by non-aging cells created by more suitable molecules without genders seems more logical, simpler and more independent. There is a high possibility that the first organisms possessed the stated characteristics, but it seems at some point in the development (or from the same beginning) these where replaced by and aging body that looses its strength and grows old and weak eventually dying with the crucial factors of speed, strength, fertility eventually failing him.
从生物学的角度上,更具体地来定义这个问题:人类的形成是一个适者生存繁殖的漫长过程,我们可以认为主要的因素有速度,力量,和生殖力。但是为什么细胞生物也一定要在生死循环中采用这种方式?由更合适的无性别分子形成未老化的细胞,再组成生物体,这样有选择看起来更合乎常理,更简单,更独立。第一代生物体很可能有上述的特征,但是在发展的某个时刻(或者从一开始)这些特征被取代,逐渐老化的身体失去力量,变得苍老而虚弱,最终死于决定性的因素,比如速度,力量,和繁殖力.

Bojidar Kojouharov

There is actually a pretty interesting answer to your question. First, I must admit that there is not yet agreement in the scientific community on a single answer. The evolutionary origin of aging remains a fundamental unsolved problem in biology. But there are very compelling competing theories.
关于这个问题,有一个非常有趣的回答。首先,我必须承认科学界对这个问题尚无定论。从生物学上讲衰老的进化起源仍然是一个谜,但是有很多引人注目又互相矛盾的理论。

At first, we used to think that aging was like a sort of “wear and tear”; like a knife’s edge becoming dull or iron objects rusting. The thought was largely that complicated systems eventually decay. Systems necessarily increase in entropy(disorder) over time. But this was discredited. The Law of thermodynamics does state that entropy always increases in a closed system, however, living things are not closed systemsentropy . One of life’s defining features is taking energy from the environment to increase internal chemical complexity while expelling entopy in the form of waste. There is no thermodynamic necessity for aging and death. Also, this fails to account for why organisms are seemingly so good at repair and maintenance up until reproductive age only to succumb to age-related damage later on.
首先,我们过去认为衰老像一种“磨损”;比如刀口变钝,铁制品生锈。这种想法主要是说复杂的系统最终衰退。系统以一种无序(混乱)的方式逐渐地发展。这种想法不可信。根据热力学定律,在密闭系统中,熵(物理上用以表示热量转化为功的程度)会增加。但是,生物体并不是一个密闭的的系统。生命的特定特征之一,就是从环境中摄取能量来增加内部化学复杂度,同时以废物的形式排出熵。衰老和死亡没有考虑热力学的必要性。这也不能说明为什么在生殖年龄之前,生物看起来如此擅长恢复和保养,只能勉强说明后来年龄增长带来的伤害。

Here are some non-mutually exclusive theories that better explain aging and death:
一些非互斥的理论可以更好地解释衰老和死亡的问题。

Mutation Accumulation

The idea here is that aging is a process that became ingrained in us from evolutionary neglect. Let me explain. In nature, competition is extreme and it is very rare for any animal to survive for an exceptionally long time. Even if there was no aging, we would probably still expect the majority of creatures to die from this sort of competition. Think about it. In the wild, there are literally countless ways to die. A small injury, an infection at the wrong time, inadequate resources, or even just a skilled predator are ever present dangers that kill most animals way before they start getting old.

突变积累

这种观点认为,衰老是一个过程,在我们抛开进化不谈时,这种想法逐渐变得根深蒂固难以动摇。让我来解释。在自然界中,竞争很激烈,存活非常长的时间对任何动物来说都很罕见。即使没有衰老,我们也可以预料到大多数动物都会死于这种竞争。仔细想想吧,在野外,死亡的方式不计其数。细微的伤害,不合时机的感染,稀少的资源,或者甚至仅仅一个技巧熟练的捕食者,这些都是一直存在的危险,在它们变老之前,这些危险可以杀死大多数动物。

In fact, in this environment, making it to reproductive age is succeeding. This theory posits that since it was so rare for animals to survive this long, there was very little selection pressure to adapt a mechanism that would allow biological survival for exceptionally long spans of time.
事实上,在竞争如此激烈的环境中,活到生殖年龄都很了不起。这种理论认为既然动物很少能存活这样长的时间,那么如果生物要适应一个能使他们长期生存下去的机制,筛选力度应该很小。

This theory posited that there were random mutations that might accumulate in the genes of living things whose effects might only be observable very late in life. These mutations that cause aging might be insufficiently weeded out by evolution because their effects occur so late in life as to be extremely rarely encountered. Its a bit like the characteristic is functionally “dormant”, never really expressing itself since you’re way more likely to have died before it could. Characteristics like these, which are only observable well after procreation, have very little influence on an individual’s ability to propagate their genes and might therefore be allowed by evolution.
这种理论认为生物基因的随机突变可能会逐渐积累,并且造成的影响在生命的晚期才可能被察觉到。这些造成衰老的突变也许不能够被进化淘汰,因为它们的影响发生在生命如此晚的时期,以至于非常罕见地遇到。突变的特点看起来像在功能上“休眠”,从未真正显露自身,在它显露之前你很有可能已经死去。这些只有在后代中才能看到特点,对个体传播基因的能力几乎没有影响,并因此被进化接受。

Antagonist Pleiotropy

That previous theory may have sounded pretty good, but the debate still raged on. The previous theory holds an assumption that aging (senescence) isn’t significantly contributing to the death toll of an organism. But this might not be true. Certainly very few animals die of “old age”, but even a little bit of senescence may be a cause of death in highly competitive environment. Just being a tiny bit slower or have a slightly weaker immune response might very well be difference between living and dying. Modern studies show that senescence is indeed a major contributor to the death rate in the wild. There was also another problem with the previous theory. The mutations that allow for aging weren’t random as the last theory supposed. Instead, when we sequence the genome, genes that caused aging formed tight knit families that have been around for as long as eukaryotic life. This newer theory proposed that these genes are pleiotropic. That mean a gene which has two or more effects on the phenotype (aka observable characteristics) of the organism. In antagonist pleiotropy, one of the effects is good and the other is bad. In the case of aging, this suggests that these genes have effects that are very beneficial early in life but detrimental later in life. If evolution is a race to pass on your genes as soon as possible, any advantage early on might be evolutionarily worth the cost later in life.

拮抗基因多效性

先前的理论可能听起来很棒,但是争论仍在继续。先前的理论基于一个假设:衰老(老化)不是明显导致生物死亡的原因,但这可能是错的。可以肯定的是几乎没有动物死于“年老”,但是在高度竞争的环境中,甚至一点点衰老也会成为死亡的原因。速度稍微迟缓,或者反应稍微迟钝,造成的就有可能是生与死的区别。现代研究表明:在野外,衰老确实是死亡率上升的主要因素。先前的理论同样存在另一个问题。正如下一个理论认为的那样,允许衰老的突变不是随机的。相反,当我们对基因组进行排序时发现,引起衰老的基因紧密联系,自真核生物时代就已经存在。这个新颖的理论表明这些基因是多效性的,这表明在生物表现型(即可以观察到的特征)方面一个基因有两个或多个影响。根据拮抗基因多效性理论,一方面影响是好的而另一方面是坏的。就衰老而言,这表明这些基因在生命的早期有积极的影响,但是在晚期往往有消极的影响。如果传播基因是一场争分夺秒的比赛,相比生命晚期付出的代价,任何早期的优势在进化上都是有价值的。

Figure A shows mutation accumulation while Figure B shows antagonistic pleiotropy. The main difference is that antagonistic pleiotropy proposes positive roles for these mutations early in life.
图表A显示突变积累,图表B显示拮抗基因多效应。主要差异是拮抗基因多效性在生命早期的突变中扮演着积极的角色。

There is another issue here. When evolution seeks a solution to a problem, it doesn’t always pick the best solution. Instead evolution favors the first solution and the solution that can be built on existing infrastructure. This might be one of those cases. Consider the mitochondria. The mitochondria has its own genes.

还有另一个问题。当进化寻找解决问题的方法时,它并不总是选择最佳方案。相反,进化选择能够建立在现有组织架构基础上的第一个方案。这也许是特别情况之一。值得考虑的还有线粒体,它有自己的基因。

This is a remnant of the likely fact that it was once a separate single-celled organism much like a bacteria that somehow formed a symbiotic relationship with a larger eukaryotic cell. Unfortunately, the fact that it has its own genome is not a good thing. Mutations to their DNA can affect a cell’s ability to function properly. Indirectly, these mutations may accelerate many aspects of aging. Because of the highly oxidative environment in mitochondria and their lack of the sophisticated repair systems found in a cell’s nucleus, mitochondrial mutations are believed to be a major cause of progressive cellular degeneration. Evolution can’t easily easily fix this problem, because evolution does not “design” organisms. It simply modifies and hacks existing systems. If an improvement can’t be achieved by a simple modification or by building on top of what exists, then evolution won’t achieve it.
其他的可能事实是它过去是一个独立的单细胞生物,类似细菌,不知为何后来和一个较大的真核生物形成共生关系。不幸的是,它拥有自己的基因组。DNA的突变可以影响细胞正常工作的能力,这些突变可能会加速衰老的许多方面。因为线粒体内高度氧化的环境,和细胞核内缺少高级修复系统,线粒体突变被认为是细胞不断变性(变性是指细胞或细胞间质受损伤后,因代谢发生障碍所致的某些可逆性形态学变化,表现为细胞浆内或间质中出现异常物质或正常物质异常增多。)的主要原因之一。进化很难解决这个问题,因为进化并不“设计”生物,它仅仅修饰和打破存在的系统。如果不能通过一个简单的改进或者建立在存在的东西的基础上获得提升,那么进化也将不能不能成功解决这个问题。

I’m going to go on a side track for a little bit to explain what happens when people age.
我将会从侧面稍微解释当人老了会发生什么。

Aging is a multifaceted process, but a big part of that process is cellular senescence. Senescence is what happens when a cell goes into a state where it can never divide again. This can happen for lots of reasons. If a cell takes on too many mutations or if the cell has divided too many times it either commits suicide, becomes (pre) cancerous, or becomes senescent. In the short term, this is actually a pretty good fix for a big problem; namely cancer. You see, cells can repair DNA damage, but that repair process is never perfect and every time your cells divide there always a little bit of imperfect replication of the genome that occurs. So the longer you live, the more mutations your cells accumulate; and the more likely you are to get cancer. (People born with mutations to only a single copy of an important DNA repair gene get a genetic disease that nearly guarantees they will be riddled with cancer before they are 30.) Senescence allows the organism to keep the still functional cells around while neutralizing any potential harm they might pose. Unfortunately, senescent cells go bad as they age. At first they aren’t bad at all, but as they stay around longer and longer they start to accumulate and they start producing a bunch of signaling molecules that increases inflammation and does harm.
衰老是一个多方面的过程,但是大部分过程是细胞老化。老化是指一个细胞不能再进行分裂。发生老化的原因有很多。如果一个细胞进行太多次数的突变或者分裂太多次,它同时也是在自杀,最后发生癌(前)病变或者衰老。从短期来讲,这是一次对大麻烦非常好的修理,也就是癌症。你瞧,细胞可以修理DNA的损伤,但是修理过程总是不完美,每次细胞分裂,会有很少的基因组发生不完美的复制。因此你活的时间越长,你的细胞会积累越多的突变;因此你更有可能患上癌症。(只要一小段重要的DNA修复基因的复制基因发生突变,天生有这种状况的人有基因病的话,几乎能够确定他们在30岁之前会遭受癌症的折磨。)衰老允许生物仍保持功能细胞,同时中和他们可能造成的任何潜在伤害。不幸的是,衰老的细胞随着生物变老而丧失活力。起初它们一点也不坏,但是随着生活的时间越来越久,它们开始聚集,并且开始产生一系列信息物质,增加炎症,造成伤害。

It’s likely that this process by which senescent cells go bad is not something evolution shaped. Most likely, evolution made a fix that prevented most cancers which worked for long enough for a creature to pass on its genes, only to be later revealed that this fix predisposed it to die of aging.
衰老细胞变坏的过程有可能不是进化形成的。极有可能的是,进化避免了长时间患有癌症的生物把基因传播给下一代,结果后来显示这种修理倾向于使细胞死于衰老。

Ageing theories based on evolvability

The last theories that are note-worthy are those which propose that aging is beneficial in a sense. This theory proposes that evolution has advantages at a population level. When creatures age and die they are freeing up resources for a younger (presumably better adapted) generation. By cycling through generations quicker, a population achieves a faster evolution rate. Limiting lifespans, therefore, limits the influence of older individuals to dominate the gene pool. Certain characteristics might have a great deal of difficultly evolving without death. Intelligence and immunity would be hard to select for since longevity can produce non-innate intelligence derived from experience and non-innate immunity derived from pathogen exposure. For a population, however, innate immunity and innate intelligence is always better because if it isn’t innate, random death of older individuals might be catastrophic for a population which would simultaneously lose much of its accumulated knowledge and capacity to survive plagues. So according to this thought, ageing or otherwise purposely limited lifespan helps evolution by freeing resources for younger, and therefore, presumably better-adapted individuals.

基于可进化性的衰老理论

最后值得注意的理论是那些指出在某种意义上衰老是有好处的。这种理论指出进化在人口层面上有优势。当生物衰老和死亡时候,它们空出资源供年轻的(大概能更容易适应的)一代利用。通过较快速的换代,人类的进化速度加快。因此,有限的寿命限制老年人对基因库的影响。没有死亡,特定的特征在进化中会遇到巨大的困难。智力和免疫力很难从进化中脱颖而出,因为长寿可以挑选出来源于经验的非天生智力和来源于病原体暴露的非天生免疫力。但是,对人来说,天生的智力和免疫力较好,因为如果这些不是天生的,老年人的随机死亡对人类来说可能是致命的,这会使人类丧失大部分积累的知识和从灾难中存活下来的能力。因此根据这种想法,衰老或者其他有目的地限制寿命,可以通过为年轻人空出资源来帮助进化,并且因此产生适应能力强的个体。

This is just scratching the surface of theories and research on aging. But as you can see, there are many possible explanations for aging within the theory of evolution.
关于衰老,这只是皮毛的理论。但是正如你看到的,在进化论中,有许多可能的解释。




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