dampening it or making it louder.
DNA甲基化可作为改变生物体生理特征的重要方法，这一点早在1970年代便已有人提出。然而，大部份的实验结果都不够显著，直到2003年杜克大学的肿瘤学家杰托（Randy Jirtle）与博士后研究生瓦特兰（Robert Waterland）所进行的实验，才有了显著结果。他们两人针对小鼠身上的agouti基因进行实验。当agouti基因持续表现时，能让小鼠的毛色变黄，易于肥胖并得到糖尿病。针对两群基因相同的怀孕母鼠，杰托的团队用富含维他命B群（叶酸与维他命B12）的饲料喂养其中一群；而另一群则无。
The importance of DNA methylation in altering the physical characteristics of an organism was proposed in the 1970s, yet it wasn't until 2003 that anyone experimented with DNA methylation quite as dramatically as Duke University oncologist Randy Jirtle and one of his postdoctoral students, Robert Waterland, did. That year, they conducted an elegant experiment on mice with a uniquely regulated agouti gene — a gene that gives mice yellow coats and a propensity for obesity and diabetes when expressed continuously. Jirtle's team fed one group of pregnant agouti mice a diet rich in B vitamins (folic acid and vitamin B12). Another group of genetically identical pregnant agouti mice got no such prenatal nutrition.
维他命B群能够提供甲基，使子宫中的幼鼠agouti基因有更多机会被甲基附着，并进而改变其基因表现。在不改变小鼠DNA基因组成下，杰托与瓦特兰仅透过提供富含维他命B群的食物，便让母鼠生出了健康的棕色小鼠，体重正常且不易患糖尿病。
The B vitamins acted as methyl donors: they caused methyl groups to attach more frequently to the agouti gene in utero, thereby altering its expression. And so without altering the genomic structure of mouse DNA — simply by furnishing B vitamins — Jirtle and Waterland got agouti mothers to produce healthy brown pups that were of normal weight and not prone to diabetes.
近期的其它研究也显示了环境对基因表现的影响。比如说，暴露于含有格尔德霉素（geldanamycin）环境的果蝇，眼睛会长得异常地大。在DNA没有变化的情况下，眼睛特大的征状仍可持续13代，即使第2代到第13代都未直接接触格尔德霉素。去年在《生物学季刊》（Quarterly Review of Biology）上有篇文章，是由表观遗传学先锋雅布兰卡（Eva Jablonka）与以色列特拉维夫大学（Tel Aviv University）的拉兹（Gal Raz）共同发表。该文章也显示，喂食蛔虫某种细菌能够让它们体型短小肥胖，并抑制其产生荧光绿的蛋白。这种改变能持续40代之久。雅布兰卡与拉兹的研究结果被列为100种表观遗传现象之一。
Other recent studies have also shown the power of environment over gene expression. For instance, fruit flies exposed to a drug called geldanamycin show unusual outgrowths on their eyes that can last through at least 13 generations of offspring even though no change in DNA has occurred (and generations 2 through 13 were not directly exposed to the drug). Similarly, according to a paper published last year in the Quarterly Review of Biology by Eva Jablonka (an epigenetic pioneer) and Gal Raz of Tel Aviv University, roundworms fed with a kind of bacteria can feature a small, dumpy appearance and a
switched-off green fluorescent protein; the changes last at least 40 generations. (Jablonka and Raz's paper catalogs some 100 forms of epigenetic inheritance.)
表观基因的改变能否永久持续下去？有可能。但是我们必须记住，表观遗传不是演化，没有改变DNA，而仅是生物体对于环境压力的反应。这种反应能透过表观遗传标记传递好几世代，但是一旦该压力因子移除，表观遗传标记最终还是会随着时间慢慢褪去，而让DNA原本的组态彰显。毕竟，目前的看法仍是：惟有天择才能造成基因永久的改变。
Can epigenetic changes be permanent? Possibly, but it's important to remember that epigenetics isn't evolution. It doesn't change DNA. Epigenetic changes represent a biological response to an environmental stressor. That response can be inherited through many generations via epigenetic marks, but if you remove the environmental pressure, the epigenetic marks will eventually fade, and the DNA code will — over time — begin to revert to its original programming. That's the current thinking, anyway: that only natural selection causes permanent genetic change.
然而，表观遗传虽然无法天长地久，却也对我们帮助良多。2009年2月《神经科学期刊》（Journal of Neuroscience）有一篇文章显示，即使像记忆这样复杂的生理与心理复合机制，也能够藉由表观遗传而增进下一代的表现。该文章是由塔夫斯大学（Tufts University）的生化学家费格（Larry Feig）对小鼠所进行的实验。费格把一群有遗传性记忆力问题的小鼠安置于充满玩具、训练活动与特别照料的环境中。实验结果发现，这些小鼠的「长期增益效果」（long-term potentiation, LTP）明显地进步了。LTP是一种神经传导形式，对于形成记忆至关重要。出乎意料的是，这些小鼠的后代即使没有获得特殊照料，其LTP也有改善。
And yet even if epigenetic inheritance doesn't last forever, it can be hugely powerful. In February 2009, the Journal of Neuroscience published a paper showing that even memory — a wildly complex biological and psychological process — can be improved from one generation to the next via epigenetics. The paper described an experiment with mice led by Larry Feig, a Tufts University biochemist. Feig's team exposed mice with genetic memory problems to an environment rich with toys, exercise and extra attention. These mice showed significant improvement in long-term potentiation (LTP), a form of neural transmission that is key to memory formation. Surprisingly, their offspring also showed LTP improvement, even when the offspring got no extra attention.
上述现象让我们知道何以科学界对于表观遗传学如此兴奋。科普作家申克（David Shenk）在他即将出版的新书《人人都是天才：关于遗传、才能、智商，你所知道的一切都是错的》（The Genius in All of Us: Why Everything You've Been Told About Genetics, Talent and IQ Is Wrong暂译）中说，表观遗传学将有助于型塑「新典范」，能够「显示所谓”先天vs后天”一语是多么地无意义。」他宣称表观遗传学「可能是自基因发现以来，非主流科学中最重要的发现。」
All this explains why the scientific community is so nervously excited about epigenetics. In his forthcoming book The Genius in All of Us: Why Everything You've Been Told About Genetics, Talent and IQ Is Wrong, science writer David Shenk says epigenetics is helping
usher in a \really is.\calls epigenetics \the science of heredity since the gene.\
遗传学家悄悄承认，我们可能太轻忽了一位早期的博物学家。这位博物学家虽一直被进化论者藐视，但却预见了现代的表观遗传学。他就是主张进化能够在一、两个世代内发生的拉马克（Jean-Baptiste Lamarck, 1744-1829）。他认为，由于环境与选择之故，动物能在有生之年获得某些新性状。拉马克举的最有名的例子便是长颈鹿。他认为，长颈鹿的脖子变长，是因为前几代祖先努力伸长脖子，以觅得高处营养丰富的树叶。
Geneticists are quietly acknowledging that we may have too easily dismissed an early naturalist who anticipated modern epigenetics — and whom Darwinists have long disparaged. Jean-Baptiste Lamarck (1744-1829) argued that evolution could occur within a generation or two. He posited that animals acquired certain traits during their lifetimes because of their environment and choices. The most famous Lamarckian example: giraffes acquired their long necks because their recent ancestors had stretched to reach high, nutrient-rich leaves.
相反地，达尔文认为演化的动力不是生物体自身的努力，而是无情客观的天择。依据达尔文学说，长颈鹿的长脖子乃是历经千年，长脖子基因慢慢占了优势的结果。达尔文比拉马克晚了84年，是一名更出色的科学家。他的理论获得胜利，而拉马克的演化观则被视为谬误。然而，表观遗传学却使得科学家不得不重新评价拉马克的主张。
In contrast, Darwin argued that evolution works not through the fire of effort but through cold, impartial selection. By Darwinist thinking, giraffes got their long necks over millennia because genes for long necks had, very slowly, gained advantage. Darwin, who was 84 years younger than Lamarck, was the better scientist, and he won the day. Lamarckian evolution came to be seen as a scientific blunder. Yet epigenetics is now forcing scientists to re-evaluate Lamarck's ideas.
解开奥佛卡利克斯区之谜
在2000年初，白葛恩博士认为，19世纪时北博滕省的丰年与荒年必然对该地区居民造成某种表观遗传变异，但他却不知道确切的运作方式，直到他偶然读到一篇鲜为人知的文章，是由英国伦敦大学学院（University College London）杰出的遗传学家潘布瑞博士（Marcus Pembrey）在1996年发表的。
Solving the Overkalix Mystery
By early 2000, it seemed clear to Bygren that the feast and famine years in 19th century Norrbotten had caused some form of epigenetic change in the population. But he wasn't sure how this worked. Then he ran across an obscure 1996 paper by Dr. Marcus Pembrey, a prominent geneticist at University College London.
潘布瑞博士的文章刊登于意大利文期刊Acta Geneticae Medicae et Gemellologiae上，虽然今日被认为对表观遗传学影响深远，但是当时却颇惹争议，许多主流期刊皆拒绝刊登。潘
布瑞博士虽相信达尔文学说，但是在那篇文章中，他回顾了当时为止的表观遗传学，提出了比达尔文更进一步的假设：是否因为工业时代的环境压力大、社会变迁快，使得演化程序催促我们的基因要加速适应呢？是否有可能，我们的DNA不再耗费好几百万年，而是如潘布瑞博士所写的，「仅在几个世代」便快速应变呢？
Published in the Italian journal Acta Geneticae Medicae et Gemellologiae, Pembrey's paper, now considered seminal in epigenetic theory, was contentious at the time; major journals had rejected it. Although he is a committed Darwinist, Pembrey used the paper — a review of available epigenetic science — to speculate beyond Darwin: What if the environmental pressures and social changes of the industrial age had become so powerful that evolution had begun to demand that our genes respond faster? What if our DNA now had to react not over many generations and millions of years but, as Pembrey wrote, within \
压缩的时程意味着基因本身没有那么多时间来调适，但是潘布瑞博士解释说，或许基因体上的表观遗传标记可以办到。潘布瑞博士当时不知道该如何验证这个庞大的假设，因此在文章发表之后便将此想法束之高阁。2000年5月，潘布瑞博士忽然收到了互不相识的白葛恩博士寄来的电子邮件，邮件中含有奥佛卡利克斯区居民的寿命数据。他们两人因而结识，共同商讨如何设计新的实验来厘清奥佛卡利克斯之谜。
This shortened timetable would mean that genes themselves wouldn't have had enough years to change. But, Pembrey reasoned, maybe the epigenetic marks atop DNA would have had time to change. Pembrey wasn't sure how you would test such a grand theory, and he put the idea aside after the Acta paper appeared. But in May 2000, out of the blue, he received an e-mail from Bygren — whom he did not know — about the Overkalix life-expectancy data. The two struck up a friendship and began discussing how to construct a new experiment that would clarify the Overkalix mystery.
他们知道必须要复制奥佛卡利克斯的结果，但是当然不能设计一个实验让一些孩童忍饥受饿、一些孩童过度饮食