细菌可以预防白血病？
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导读
急性淋巴细胞白血病
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听力|精读|翻译|词组
Germ theory
细菌理论
英文部分选自经济学人Science and technology版块
Childhood cancer
儿童癌症
Germ theory
细菌理论
It may be possible to prevent childhood leukaemia by exposing children to more microbes
通过让儿童接触更多的细菌，可能可以预防儿童白血病
THE long struggle to cure acute lymphoblastic leukaemia (ALL), a childhood blood cancer, is a stand-out tale in the history of medicine. It was a massive endeavour, over decades, with many toxic drugs being tested in different combinations on dying children. It succeeded in the end. Half a century ago, survival rates were less than 0.1%. Today they are about 90%. Yet the cure brings unpleasant side effects, including problems with memory and concentration, and sometimes even other cancers. Globally, rates of ALL seem to be rising by about 1% a year. Yet it is almost non-existent in the poorest countries.
与急性淋巴白血病（简称ALL,亦称为儿童血癌）的长期抗争，是医学历史上的一则重要的篇章。几十年来，许多不同组合的有毒试剂在垂死儿童身上进行了测试，最终它还是成功了。半个世纪前，存活率不到0.1％；今天，这一比例约为90％。然而，治疗会带来令人不快的副作用，包括记忆力和注意力方面的问题，有时甚至会出现其他癌症。从全球来看，ALL的发病率似乎都在以每年1%的速度增长。然而，这种情况在最贫穷国家几乎不存在。
Its causes remain unclear and even controversi al. A charity called Children with Cancer UK, for instance, still suggests the disease is connected to electromagnetic radiation from power lines. Into this debate comes Mel Greaves, of the Institute of Cancer Research in London. In a paper in Nature Reviews Cancer, Dr Greaves has marshalled decades of research into ALL alongside some new lab work, and created a comprehensive theory about its origins.
其原因尚不清楚甚至引起争议。例如，一个名为“英国儿童癌症协会”的慈善机构仍然表示，该疾病与电线的电磁辐射有关。伦敦癌症研究所的梅尔·格里夫斯（Mel Greaves）也参与了这场辩论。在“自然综述癌症”杂志的一篇论文中，格里夫斯博士将几十年关于ALL的研究与一些新的实验室成果整理在一起，并创建了一个关于其起源的综合理论。
His theory involves three steps. First is a genetic mutation. Then there is an infectious illness. Lastly, the child’s immune system reacts badly to that infection. And this chain of events is more likely in those who had little exposure to germs and bacteria in early childhood.
他的理论涉及三个步骤。首先是基因突变，然后是传染病。最后，孩子的免疫系统对感染反应很差。而这一系列事件更可能发生在幼儿早期几乎没有接触到细菌和细菌的人群中。
The first part of Dr Greaves’s theory dates back to 1988. Studies on twins showed that, where both suffered from ALL, the cause could often be traced back to a mutation in just one. Specifically, if they had shared a placenta, then genetic errors in the bone marrow, where blood cells are made, would result in one twin producing mutant cells. Those cells could then spread through the placenta into the other twin, even if his genes were free from the error. Such mutant cells are necessary, but not sufficient, for the later development of ALL.
Greaves博士1988年就提出了第一部分理论。他们对双双感染ALL的双胞胎进行研究，发现常常是因为双胞胎中的其中一个发生变异引起的。特别是当他们共用一个胎盘时，如果生产造血细胞的骨髓出现基因问题，其中一个孩子体内就会出现变异细胞。即使另一个孩子的基因没有发生问题，这些变异细胞也会通过胎盘进入另一个孩子体内。这些变异细胞对于之后ALL病情的发展是必要的，但仅此还不够。
Bugs are a feature
缺点是一种特性
Lab work by Dr Greaves suggests that the genetic error that produces these pre-leukaemia cells is much more common than ALL itself. When he screened blood from umbilical cords in British hospitals, he found that six babies among 567 had pre-leukaemia cells. But the disease occurs in just 1 in 2,000 British children.
Greaves博士的实验室研究表明，由于产生这些白血病前期细胞的基因问题要比ALL这种疾病本身更加常见。他筛查了英国医院的脐带血，发现567个婴儿中有6个带有白血病前期细胞。但是2000个英国孩子中只有1个会患上ALL。
This is where the second and third steps of the theory come in. For those pre-leukaemia cells to develop into a full-blown blood cancer, a child has to be exposed to an infectious disease, and his immune system must then overreact to the threat. And there is substantial, albeit circumstantial, evidence to suggest that the risk of such an overreaction is raised by a lack of exposure to infections and microbes in the first year of a child’s life.
这就是为什么会有第二和第三部分理论。白血病前期细胞要彻底发展成血癌的话，需要孩子接触感染性疾病，然后免疫系统对这些疾病过度反应。而且有大量（虽然还未证实的）证据表明，过度反应的风险会因为孩子在诞生的第一年里接触不到感染和微生物而上升。
In the 1990s the UK Children’s Cancer Study Group found that babies who had been sent to child care in the first year of their lives were less likely to develop childhood leukaemia. That finding has since been replicated around the world. It is bolstered by a separate and fairly well-established inverse relationship between common diseases in early life and the risk of developing ALL.
上世纪90年代，英国儿童癌症研究小组发现,一周岁就被送往托儿所的婴儿不太可能患白血病。自那以后，这项发现在世界各地得到了验证。此外，婴儿常见病和ALL发生风险之间的反向关系也佐证了这一发现，这种反向关系自成一体而又相当根深蒂固。
More suggestive evidence comes from the fact that childhood leukaemia rates are higher in children born by Caesarean section, which avoids exposing them to microbes in the vagina. Dr Greaves’s theory also offers an explanation for rare but puzzling geographical clusters of ALL. An infection might sweep through a community and pick out the children who are over-reactive carriers of pre-leukaemia cells.
剖腹产出生的婴儿，避免了接触阴道微生物，患儿童白血病的比例更高，这一事实提供了更有启发性的证据。格里夫斯博士的理论也解释了ALL罕见又令人费解的地理性集中发病的特征。感染可能席卷整个社区，一些儿童则会因此患病，因他们携带着过度活跃的白血病前期细胞。
In Milan in 2009, for instance, seven children developed ALL in rapid succession. All had been infected with swine flu three to six months before. None had been to nursery before the age of one. There is no reason to think that one infection is more likely than another to trigger ALL. But flu is common enough that researchers have been able to detect an uptick of ALL a few months after the virus sweeps through a country. Work in mice has proved that early stimulation of their immune systems protects against a murine version of ALL.
举个例子，在2009年，米兰的七个孩子接二连三地患上了急性淋巴性白血病。他们全部都在三至六个月前感染了猪流感。没有一人在一岁前都去过育儿所。没有理由让人联想到猪流感比其他传染病更容易引发All。但是流感已够多了，多到研究人员已经在病毒肆虐后几个月后察觉到ALL发病率的小幅度上升。在老鼠身上的实验已经证明对他们免疫系统的早期刺激能够预防老鼠版本的ALL。。
That is the evidence. So far, though, the precise mechanism remains mysterious. One candidate is a type of inflammatory molecule known as a cytokine—specifically, one called transforming growth factor-β , which seems to selectively boost the growth of pre-leukaemia cells. It is also known to promote other cancers.
这就是证据。不过，到目前为止，确切的机制还是未解之谜。一个疑似目标是一种炎症分子，被称之为细胞因子—具体的来说，转化生长因子-β似乎是有选择性地促进了白血病前期细胞的生长。它也被认为会引发其它癌症。
Breastfeeding, which helps to calibrate a baby’s immune system, can help. But if Dr Greaves is right, then another message for parents is to encourage early social contact with other infants, which encourages the swapping of germs.
有助于校准婴儿免疫系统的母乳喂养能有所帮助。但是，如果Greaves医生的理论是正确的，那么对于父母的另一个建议就是鼓励早期与其他婴儿的社交接触。此行为有利于细菌的交换。
Dr Greaves is not the first to have such ideas. The theory that modern humans are under-exposed to micro-organisms and parasites is known as the “hygiene hypothesis”. It has been invoked as an explanation for rising rates in the rich world of autoimmune disorders such as type-1 diabetes, multiple sclerosis and allergies. And ALL may not be the only cancer implicated. A malfunctioning immune system can cause chronic inflammation. That has been suggested as a risk factor in the development of oesophageal cancer, colon cancer and some cancers of the pancreas.
Greaves医生不是有这种想法的第一人。名为“卫生假说”的理论就指出现代人缺少接触共生微生物和寄生虫。用来解释不断增加的自体免疫性疾病，比如1型糖尿病，多发性硬化症，过敏。ALL也许不会是唯一的牵连癌症。失常的免疫系统能导致慢性炎症，也被认为是发展为食道癌，结肠癌和其它一些胰腺癌症的风险因素。
注释：
卫生假说（英语：hygiene hypothesis）是一种医学假说，指童年时因缺少接触传染源、共生微生物（如胃肠道菌群、益生菌）与寄生虫，从而抑制了免疫系统的正常发展，进而增加了患过敏性疾病的可能性。发达国家青少年自身免疫性疾病与急性淋巴性白血病发病率的增加被认为与卫生假说有关。
The hygiene hypothesis is a striking idea. But it is not yet proved.And even if it were, balancing the risks could be tricky, says Donna Lancaster, a paediatric oncologist at the Royal Marsden NHS Foundation Trust in London. Hygiene has benefits as well as drawbacks. Exposing children to germs means that many will become ill, and a few will become seriously so. One idea for squaring the circle—albeit a very speculative one—is a carefully designed vaccine that gives just the right nudge to an infant’s immune system without the risk of making them properly ill.
卫生假说理论是一个令人震惊的设想，但它现在还未得到证实。即便如此，伦敦皇家马斯登NHS信托基金会的儿科肿瘤学专家Donna Lancaster称，要平衡风险可能会有点棘手。卫生（假说所需条件）是利弊共存的。（让孩子们）与细菌接触意味着有许多孩子会生病，而且少数人会病得很严重。解决这个难题的一个推想就是，精心培育一种能够适度促进婴儿免疫力的疫苗，免除他们患病的风险。
If Dr Greaves’s theory stands the test of time then the reputation of the hygiene hypothesis will rise.It even offers a possible explanation for the statistical link between power lines and leukaemia. Parents who fret about their children playing near power lines might keep them indoors—away from dirt, germs and each other.
如果Greaves博士的理论能够经受得住时间的检验，那么卫生假说理论的可信度将会提升。这甚至可以为输电线（电磁辐射）与白血病之间的统计联系作出解释。那些为了防止孩子在输电线附近玩耍的父母，可能会让孩子待在室内——（这无形中也）让孩子远离了污垢、病菌与之类的等等。
翻译组：
Li Xia, 女， HR, 经济学人发烧友
Muyi，文产小研，经济学人初段读者
Minjia，女，广告策划，经济学人读者
Yifei：女，英专硕士，专八，catti二笔
Xiaofeng, 女，好奇心重的医疗民工，经济学人粉丝
校核组：
Xingyi，男，小硕，经济学人爱好者
Damon，男，建筑民工，经济学人爱好者
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观点|评论|思考
本次观点由Nikolai独家奉献
Nikolai，男，小硕, science追随者
不知道诸位在小时候有没有听到过这么一句话：“不干不净，吃了没病。”的确，我们正身处一个细菌、病毒肆虐的时代。这些微生物每天都可以不断变异，致病微生物的变异速度远远超过了对应疫苗的研发速度。以大肠杆菌为例，大肠杆菌每二十分钟可以分裂一次，即由一个菌变为两个菌、两个菌变为四个菌，以此类推。假设每分裂一次，出现一种可致病变异的概率为十万分之一，那么仅仅在七小时（2的21次方个菌）内，便可以产生10种当下疫苗无法应对的可致病变异。一株疫苗从开始研发到正式投入市场，少则五至八年，多至十四五年。所以，完全依靠人工疫苗来对抗所有的感染性疾病是不可能完成的任务。
那么，除了人工疫苗，我们还有什么武器可以让我们在这个遍地都是细菌的世界里生存下来呢？答案便是我们的免疫系统。科学研究表明，所有的癌症都起源于非正常的基因变异所引发的细胞数量指数式增长。一般而言，功能正常的免疫系统可以侦测到这些有指数式增长趋势的细胞，然后将它们杀死并清除出体外。
如文章所说，包含基因变异的细胞并不能独自引发急性淋巴细胞白血病，还需要外源感染和异常的免疫反应。婴幼儿刚出生的时候免疫系统发展并不完全，此时若将其暴露在大量危险的致病菌范围内，婴幼儿将有生命危险；但反之，若彻底隔绝病菌，因为没有抵抗的对象，免疫系统的发展将会变得迟缓乃至异常，进而提高罹患婴幼儿白血病的风险。所谓的“不干不净，吃了没病”，也就是因为我们给了自身的免疫系统抵抗的对象，促进了它的正常发育罢了。所以，癌症并不可怕，只要尽一切努力提高自己的免疫系统功能并维持其正常，便可以最大程度地降低患癌和其他疾病的风险。
提高免疫系统功能的方法对婴幼儿而言是母乳喂养或者使用母乳近似物喂养，并多放儿童与其他儿童接触。对成人而言，因为免疫系统的发育已经接近完成，维持系统功能则需要我们养成规律的生活作息、戒烟限酒并注意膳食均衡和适量运动。说到底，和致病因子对抗就像守城堡，而免疫系统就是守城堡的士兵。如果士兵都生病了，拿什么来抵挡外面的敌人呢？
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