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给《新华每日电讯》总编辑解国记先生的第三封公开信 (4533 查看)
发布: 亦明
日期: October 17, 2012 07:51PM

老偷巨骗,先偷后骗──

就方舟子抄袭科唬问题给《新华每日电讯》总编辑解国记先生的第三封公开信


亦明



2012年9月21日,我以《方巨骗,还在骗》为题,给《新华每日电讯》总编辑解国记先生写了第二封公开信。在信中,我根据《新华每日电讯》专栏作家方舟子在一周前发表的一篇文章──《吃得少能否活得老?》──开头的250字,揭露了这个被《新华每日电讯》捧为“知名科普作家”的方舟子,实际上是一个文坛巨骗。这篇文章用六千余言剖析方舟子的250个字,相当于杀鸡用牛刀,炮弹打苍蝇,我以为它会一锤定音,而方舟子则会一如既往地对我的揭批采用他自己总结出来的“一切造假者在事情败露后的最后一招”──装聋作哑──来招架。可是,事情的发展,完全出乎我的预料──方舟子“反击”了。而他的这个“反击”,恰恰暴露出了这个巨骗的文贼嘴脸。详述如下。

一、做贼心虚,露出马脚

我的文章公开后,虹桥科技论坛网友六指在次日根据其中的线索,找到田清涞在2009年第10期《健康指南》上发表的《长寿之门——需限制热量,增强营养》一文,指出其中的两段话与方文神似。由于田文在先,方文在后,所以六指认为方舟子抄袭了田清涞。(六指:《小方现在越来越没出息了》)。六指的发现,在24日传到新浪微博,产生了一定的影响。(爱玩儿:《方舟子自证他是最卑劣的人──方舟子抄袭伪劣科普赏析》)。于是,方舟子坐不住了。9月25日,方舟子在搜狐微博发表《关于北京大学生命科学学院教授田清涞抄袭的说明》,全文如下:

“北京大学生命科学学院教授、北京大学老龄问题研究中心科研部主任田清涞《长寿之门——需限制热量,增强营养》一文(登于《健康指南》2009年10月,[t.itc.cn])主要参考我写于2002年的《吃得少活得老》(登于《环球》半月刊2002年第21期,后收入《长生的幻灭》《科学成就健康》[t.itc.cn]),其中‘四、长寿与抗衰老事例’一段全文照抄,只是自作聪明地把‘2~40倍’错误地改成‘2~4倍’。

“最近关于限制热量与衰老的关系的研究有新进展,对传统的观点提出了挑战,我因此又写了一篇《吃得少活得老?》登在《新华每日电讯》上,其中部分段落改自旧文,包括被田清涞抄袭的那段。有方黑据此反过来指责我抄袭田清涞,亦明、韩寒之父韩仁均、孙海峰、不加V(木子美)、易天等资深方黑更是跳得厉害。我的科普文章多次被人抄袭,像这样只是抄袭一两段的,我本懒得计较,但方黑们既然借此大做文章倒打一耙,我还是说明一下。”


方舟子的“说明”公布之后,众方粉一片欢腾,以为这个举世闻名的“绝代文贼”主子,终于打了一个翻身仗。比如,据信是“方舟子妻”刘菊花马甲的那个hqabc_就在新浪微博撒欢儿叫嚣说:“亦明这次把戏演砸了!”、“被亦明钓鱼了,来,傻一个!”、“锤子呀,你不小心被亦明钓鱼了!

事实是,在《方巨骗,还在骗》发表之后,我根本就没有再提此事。所以,方舟子在“说明”中说“亦明……等资深方黑更是跳得厉害”,完全是在造谣,其目的,显然是要把六指的失误,栽到亦明的头上,以此来否定《方巨骗,还在骗》一文。而他的这个下三滥手法,恰恰说明他的心虚──否则的话,他应该直接驳斥亦明才对。方舟子心虚的更明显证据就是,他至今没敢把《吃得少能否活得老?》一文在自己的众多博客(包括新语丝网站)上发表。显然,他心中有鬼。

也就是因为看出方舟子心怀鬼胎,我于是根据方舟子提供的线索,把他的《长生的幻灭》和《科学成就健康》找来,结果直捣黄龙。

据查证,《吃得少能否活得老?》一文总共1874字(不计标点符号),其中的1350字,占全文的72%,属于“旧文照抄”,抄袭他十年前的旧文《吃得少活得老》。而他在“关于限制热量与衰老的关系的研究有新进展”上面,不过写了360字(不足20%)而已。所以说,这是一起典型的自我剽窃案。(见下图)。


文贼自盗
左侧篮框内为方舟子作于2002年的《吃得少活得老》一文,右侧黑框内为方舟子作于2012年的《吃得少能否活得老》一文文本(上)及其在《新华每日电讯》上发表的版面截图(下)。其中,黄色显示完全相同,绿色部分显示文字相同、但顺序不同。右下图的黑色部分显示方舟子自我抄袭在这篇文章中的比重。


实际上,在《吃得少能否活得老》发表以前,《吃得少活得老》一文已经至少发表了五次,它们分别是2002年的《环球》杂志和《长生的幻灭》一书、2003年的《南方周末》、2007年的《科学成就健康》和《你是吃补还是吃毒》。也就是说,方舟子能够在十年之内,把一个女儿嫁出去至少六次!真是穷疯了!

二、贼窟被捣,文贼被抓

事实是,不仅《吃得少能否活得老?》抄袭旧文《吃得少活得老》,而且后者本身也是抄袭之作。原来,方舟子在《长生的幻灭》和《科学成就健康》这两本书中介绍“麦克凯”的试验时,附了一个表格,证明自己所说的“雄鼠所受的影响更显著,寿命平均延长了约50%”不是虚言。(见下图)。



方舟子在《长生的幻灭》(上)和《科学成就健康》(下)中附的一个表格,它们是方舟子抄袭剽窃的铁证。


但实际上,在“麦克凯”1935年论文中,不仅没有这个表格,而且没有这个表格中所列出的某些数据,如其中的“中值”和“中值变化”栏中的数据。(请与“麦克凯”论文表二比较)。那么,这个表格及其数据到底是怎么来的呢?用这几个数据来搜索网络,笔者找到了方文贼行窃的对象。

原来,距离方舟子的母校密歇根州立大学不到一百英里,就是底特律市。在底特律市,有一所大学,名叫韦恩州立大学(Wayne State University)。虽然对于绝大多数中国人来说这所大学比较陌生,但是它却与中国人的关系很大,因为著名的诺尔曼•白求恩大夫曾在这所学校任教。而这所学校与方舟子发生关系,却是因为该校生物系的一位名叫阿金的教授(Robert Arking)写了一本书,书名是《衰老生物学:观察与原理》(Biology of Aging: Observations and Principles)。这本书至今出了三版,分别是1991、1998、2006年版,而方舟子上面的那个表格,就出现在它的前两版中(在第三版中,这个表格被删去)。


方舟子行窃对象阿金教授




《衰老生物学:观察与原理》中介绍“麦克凯”试验时使用的一个表格,它被方舟子偷去
红框内数据为阿金自己计算所得,而非“麦克凯”论文原有。
(见:Arking, R. Biology of Aging: Observations and Principles. Sinauer Press , Mass. 1998. p.314.)


在《〈方舟子抄袭剽窃年谱〉序》中,我曾总结过绝代文贼方舟子的作案特点──趋热性和连环性:

“所谓连环性,就是在发现猎物之后,方舟子会反复地、不断地抄:抄完一篇文章之后,他会意犹未尽,于是再抄第二次(如偷易华的《人参崇拜》);一本书,抄完这篇文章之后,再抄下一篇(如偷Mark Buchanan的Ubiquity,和A. K. Dewdney的Yes, we have no neutrons)。”

可想而知,方舟子绝不会从《衰老生物学:观察与原理》中仅仅偷一个表格。事实是,方舟子的《吃得少活得老》,共3906字,至少有2535字,约占全文的三分之二,抄自该书。实际上,方舟子的文章,从内容到结构,从观点到错误,几乎全部来其该书,就像他在七年前抄袭自己母校的教授Robert Root-Bernstein一样。具体的文字比较,见本文的附录。这里,我们先看看这个表格是怎么回事。

原来,在《衰老生物学:观察与原理》的第一、二版中,阿金教授都注明这个表格是根据“麦克凯”的这两篇论文综合而成:McCay, C. M. and M. F. Crowell. 1934. Prolonging the life span. Sci. Monthly 39: 405–414; McCay, C., M. Crowell and L. Maynard. 1935. The effect of retarded growth upon the length of life and upon ultimate size. J. Nutr. 10: 63–79. 查前一篇论文,其中的“中值”栏数据,恰恰与阿金的相同,但该表并没有“中值变化”栏(Percent change in median life span),因此说明,那栏数据是阿金根据原始数据计算所得,因此那个表格是世界上独一无二的。也就是说,方舟子的表格只能是抄自阿金教授。


“麦克凯”等人1934年文章中的一个表,其中红框内数据被阿金用来制成那个被方舟子偷去的表格。



也许有方粉会说,你亦明在《方巨骗,还在骗》中,不是说方舟子说的“雄鼠所受的影响更显著,寿命平均延长了50%”是错误的,“任你的算术是食堂大师傅教的,也计算不出‘寿命平均延长了50%’这样的数字”吗?可是阿金的表格中确实有53%这个数据啊?就算俺们承认主子是老偷,你也不能把老偷说成是巨骗啊。请你给俺们主子道歉!道歉!!

那么,我有没有必要向方老偷道歉呢?不仅完全没有,实际上,这个事实更能证明方舟子是一个老偷加巨骗。原来,学过小学算术的人都知道,平均值(average, mean)和中值(亦称中间值,median)是两个不同的概念,前者是用一组数据的总值除这组数据的个数而得,后者则是查找这组数据中数值位于中间的那个数据。显然,使用平均值来代表一个群体的寿命比使用中间值更为合理。天知道阿金教授为什么要异想天开,计算什么“中间值变化”;但我们确实知道方舟子为什么要抄袭这个数字:无知。这是因为,方舟子确实把平均值和中间值混为一谈了,所以他才会说“平均延长”!偷窃在先,把偷来的东西搞错在后,再把偷来的、搞错的文字反反复复地贩卖兑现,这不就是一个老偷加巨骗的所作所为吗?

实际上,方舟子在《吃得少能否活得老》一文第一段250个字中出的十大丑,要么是他误读阿金,要么是他把阿金的失误也照搬过来。比如,阿金只是说“奥斯本”等人的论文是1917年发表的,但这却被方舟子理解成“1917年,奥斯本等三位美国生物学家在用大鼠做营养实验时”。再如,尽管阿金在那个表格中显示限食老鼠被分为两组,但在正文中,他却使用单数“In the restricted group”,结果导致方舟子鹦鹉学舌,说什么“他们给其中的一组提供完备的营养物质,但是严格限制其饮食,让它们一直处于饥饿中”。还有,阿金在书中说限食组的老鼠一直保持断奶时的体重(In the restricted group, maturation was greatly slowed, although these animals held their weaning weight),于是方舟子就说:“饮食受限制的老鼠发育几乎停止,身体也不再长大”。

最奇的是,阿金这位生物学教授也是把生长和发育混为一谈,说什么“麦克凯等人的试验源自亚里士多德的猜想和奥斯本等人的试验,它们都显示生物的寿命长短与它们的发育速度成反比”(The experiments of McCay and his colleagues, which we will discuss shortly, grew out of the idea that longevity is inversely proportional to developmental rate. This idea was derived partly from the works of philosophers such as Aristotle and partly from the experimental work of Osborne……)。也就是根据阿金的这个说法,方舟子就说“美国康奈尔大学的麦克凯等人直接验证是否动物寿命真的与发育速度成反比”。实际上,在《吃得少活得老》中,方舟子把阿金的这段话“发挥”得更加离谱。他说:

“古希腊哲学家亚里斯多德也曾经思考过寿命的问题,他胜过同时代人之处,在于他是一位敏锐的观察者。他根据其观察,猜想动物的寿命长短与其发育期长短有关,发育得越慢,则寿命越长。例如大象是最长寿的哺乳动物之一,而其怀孕期也最长,相反地,家鼠在一年内就能发育成熟、生儿育女,而其寿命则只有数年。”

其实,亚里士多德在其《论寿命的长短》(On Longevity and Shortness of Life)一文中,根本就没有这么“猜想”过。他只是说:寿命最长的生物是在植物之中,其次是在热血的、有足的动物之中。他从热血和有足的动物中找出了两个例子,人和大象,然后归纳出另一个通则:“体积大的动物比体积小的动物长寿”(As a matter of fact also it is a general rule that the larger live longer than the smaller),他通篇也没有提什么发育和怀孕。确实,乌克兰科学院院士、著名生理学和老年学家Vladimir V. Frolkis就说,亚里士多德认为寿命与生长速度有关(Since Aristotle and later Buffon, Shmalgauzen, and Bidder, an important role in species-specific life span determination has been attributed to growth rate. 见:Vladimir V. Frolkis, Khachik K. Muradian. Experimental Life Prolongation. CRC Press, Oct 24, 1991. p.170.)不仅如此,他还正确地把奥斯本等人的发现系于1915年(1915 Osborne and Mendel found out that delay in a mammal's growth due to a restricted diet is reversible and could be stopped after returning to a diet ad libitum. p.207.)【注:在《衰老生物学:观察与原理》第三版中,阿金把“亚里士多德”删去了。见该书202页)。

老年学(Gerontology)实际上是个大杂烩,包括多门生物学科。方舟子在其中的某一领域出乖露丑,并不奇怪。奇怪的是,他在自己的生物化学领域也无知得像是一个小丑。比如,阿金在书中提到蛋白质的糖基化与限食和衰老的关系,方舟子于是在《吃得少活得老》中冒充权威断言说:“蛋白的糖基化可能是衰老过程中最普遍的一种化学变化。”事实是,所谓的“蛋白的糖基化”分为两种,一种是酶促反应,英文是glycosylation,它与衰老基本无关;另一种是非酶促反应,英文是glycation,它与衰老有某种程度的相关,但也绝不是什么“最普遍的”。由于阿金在书中把这两个名词混用,结果方舟子这个美国生物化学博士就信以为真,于是信口胡勒,照抄出丑。

事实是,在被抄的那几页书中,阿金总共引用了大约七十次文献,由此可见其写作的辛苦。而方舟子却将之信手拈来,据为己有。难怪他当了大约三十年的贼仍旧乐此不疲。对方舟子来说,选择做贼,是由他的投机取巧本性所决定的。

三、贼性大发,老少通吃

前面提到,《吃得少活得老》全文近四千字,其中约三分之二抄自阿金的《衰老生物学:观察与原理》。如果谁以为该文的其余三分之一都是猪油博士方舟子自己独立撰写的,那就太不了解方舟子了。事实是,《吃得少活得老》其余的部分也是方舟子东抄西凑搞来的,并且也同样是错误百出。比如,笔者在《方巨骗,还在骗》中指出,方舟子在《吃得少能否活得老》第一段的最后一句话,“喂食正常的老鼠中,寿命最长的为965天,而限制喂食的老鼠,有的活到了1800多天(相当于人活到200岁)”就含有三个错误。而阿金并没有说过这样的话。那么,方舟子是根据什么这么说呢?现在看来,他极有可能如六指所指出的那样,是抄袭了网上一篇文章中的这两句话:

“McCay’s oldest control rat died at 965 days, whereas his oldest CR rat lived 1,456 days (150 years in human terms). In the 1960s, CR rats in the laboratory of Morris H. Ross at the Institute For Cancer Research in Philadelphia, survived for more than 1,800 days (180 years in human terms).” (Saul Kent. Aging Research Becomes A Science. Life Extension Magazine, December 2001.)

这两句话中,前一句是错误的──如《方巨骗,还在骗》所说──,但方舟子却全盘照抄。而后一句话是正确的,但却被方舟子抄错了:他把别人在1960年代的试验结果安到1935年的“麦克凯”头上,并且自创“科学原理”,把老鼠的一岁换算成四十岁。明白为什么方舟子在《关于北京大学生命科学学院教授田清涞抄袭的说明》中,独独指出田教授“自作聪明地把‘2~40倍’错误地改成‘2~4倍’”,但却不提田教授也与他同样犯了965天/1800天/200岁这样的错误了吗?因为这些错误是他抄袭的“铁证”,所以他不敢就此纠缠。

【注:据网友爱玩儿考证,方舟子的“相当于人活到200岁”很可能是抄自该杂志1995年6月发表的另一篇文章,Dietary Manipulation Of Aging,其中说:“The longest lived calorie restricted rat survived for more than 1,800 days (the equivalent of about 200 years in humans) in the laboratory of Morris H. Ross at the Institute For Cancer Research in Philadelphia.”亦明按:方舟子《长生的幻灭》一书抄袭Life Extension Magazine之处甚多,容日后慢慢清理。】

Life Extension Magazine (《延长寿命杂志》)是由一个叫做“延长寿命基金会”的组织主办的“科普”读物,上面那篇文章的作者,Saul Kent,就是这个基金会的创始人之一。维基百科只说他是“著名的延长寿命活动的积极分子”(prominent life extension activist),而没有提到他的教育背景和学术建树,因此他至多不过是一个“科普作家”,连“知名”都算不上。方舟子以“知名科普作家”的身份、在中国的“中央级新锐主流大报”上发表抄袭──并且抄错了──自美国“不知名科普作家”的文章,这还不算是“中央级”的笑话吗?但实际上,这样的笑话,在方舟子的文章中层出不穷。比如,在《吃得少活得老》一文中,有这样一段话:

“多项实验结果都表明,如果让鼠类的食物包含完备的营养物质,但是把食物中的热量减低25-60%,它们在中年后得慢性病的危险减低了,而寿命也延长了大约30%。例如在1986年对小鼠和大鼠同时做的实验表明,卡路里受限制的小鼠平均活47个月,而控制组活28个月;卡路里受限制的大鼠平均活1300天,而控制组平均活720天。”

笔者把阿金三个版本的《衰老生物学:观察与原理》翻遍,把PubMed数据库搜遍,也没有找到这段话的出处。最后,在一个网页中,找到了这段话的“原文”:

“One such study with mice and rats by Weindruch (1986) showed that fully fed mice lived on the average 28 months versus the calorie restricted group who lived 47 months. Rat survivals were shown to be approximately 720 days old for those eating ad lib and 1300 days of life if calories were restricted. In these and other studies, calorie restriction is defined as a reduction in calories of 25-60% from ad lib feeding levels while providing an adequate intake of essential vitamins and nutrients.”(Jean E. Pierog. RECIPE FOR LONGEVITY)。

看到方舟子的25-60%、1986年、47个月、28个月、1300天、720天这几个数据都出现在这段英文中了吗?实际上,几乎可以肯定,这段话是错误的。这是因为,其中提到的Weindruch不仅也是一个“著名的延长寿命活动的积极分子”,而且他还是一个著名学者。在1986年,他以第一作者的身份,只发表了一篇论文(Weindruch R, Walford RL, Fligiel S, Guthrie D. The retardation of aging in mice by dietary restriction: longevity, cancer, immunity and lifetime energy intake. J Nutr. 1986 Apr;116:641-54),但其中不仅没有上面那些数据,而且该研究只涉及小鼠,与大鼠根本无涉。不仅如此,Weindruch在1988年还与方舟子所说的那位“研究衰老的分子生物学、加州大学洛杉矶分校的教授洛伊•瓦尔佛德(Roy Walford)”合著了一本书,The Retardation of Aging and Disease by Dietary Restriction,在书中,Weindruch也没有提及自己“在1986年对小鼠和大鼠同时做的实验”。这还不能证明方舟子又留下了“抄袭的铁证”吗?

更可笑的是,方舟子这个美国博士抄袭的那篇英文文章,作者Jean E. Pierog是一个仅仅有硕士学位的注册护士(R.N., M.S.)。方舟子不是一直看不起硕士(见《“专业”的架子和做学问的“常识”》、《“美梦还是噩梦”事件的启示》),并且说“我认为本科生甚至硕士研究生都没有必要写毕业论文”(方舟子:《大学生不必写毕业论文》,2011年4月29日《新华每日电讯》)吗?如果硕士不写论文,你方博士抄谁呀?

四、邪恶成性,贼喊捉贼

总之,方舟子的《吃得少活得老》一文约四千字,大约有九成是照抄英文文章,可是,在受到指责之后,这个老贼惯盗却有脸叫喊自己被“北京大学生命科学学院教授田清涞抄袭”。查田教授《长寿之门》一文,总共2191字(不计标点符号),其中受到方舟子指控的“四、长寿与抗衰老事例”一段,不过203字,不足全文的十分之一。方舟子以百分九十的抄袭率,来指责10%的抄袭率,真可谓是无耻之极。

那么,田教授是否真的抄袭了方舟子呢?查田清涞早在1986年就发表有关老年学的论文(王厚德、王文录、白家祥、田清涞:《食量对小鼠寿命试验的干扰》,《老年学杂志》1986年4期48-50页),并且有老年学专著。所以,与方舟子相比,他有足够的资格撰写《长寿之门》这样的文章。换句话说,就资格而言,田教授不用抄袭就可以写成科普文章,而方舟子即使抄袭也写不出没有错误的科普文章。退一万步说,既然你方舟子的文章几乎全部是抄来的,田教授为什么不能直接照抄英文文章,而必须抄袭你方舟子呢?

实际上,方舟子所说的“琉球群岛的居民的饮食有充足的营养,但热量低于普通日本人,他们的寿命也长于普通日本人,其百岁寿星的数目是日本其他地区的2~40倍”这句话,就是抄袭阿金的这句话:

“In the past, the caloric intake of much of the population of Okinawa was much lower than the norm in Japan, but the nutrition of the Okinawans was otherwise adequate. Okinawa has a high incidence of centenarians: 2–40 times as many as may be found on any other Japanese island.”

其中的Okinawa是指冲绳岛,而冲绳岛只是琉球群岛中的一个岛屿。所以,方舟子把Okinawa译成“琉球群岛”错误在先。其次,阿金所说的这个“2~40倍”数据是上世纪七十年代的(见:Kagawa Y. Impact of Westernization on the nutrition of Japanese: changes in physique, cancer, longevity and centenarians. Prev Med. 1978;7:205–217),并且,是专指冲绳岛与日本各岛数据的比较。因此。如果使用“琉球群岛”的数据来与日本其他各岛的数据、及其他时期的数据来比较,则肯定不会是“2~40倍”。比如,1996年发表的一篇论文就说:据1992年的数字,冲绳岛百岁老人的比率是每十万人15.79,而排在第二位的则是9.45。(见:Akisaka M, Asato L, Chan YC, Suzuki M, Uezato T, Yamamoto S. Energy and nutrient intakes of Okinawan centenarians.J Nutr Sci Vitaminol (Tokyo). 1996;42:241-8.)请方舟子用食堂大师傅教的算术计算一下,15.79/9.45应该是几?

所以说,田教授的文字虽然与方舟子的文字相似,但或许他另有所本。而方舟子不经考证,单方面遽下断言,凸显其无知和蛮横,也更显示出他“打假”的一大目的就是掩护自己造假。

五、小结

2011年2月,就在方舟子抄袭剽窃丑闻进入中国平面媒体之际,方舟子在新浪微博上接连造谣说:

“肖传国的枪手亦明(葛莘)写了上百万字文章攻击我,已断章取义地‘证明’我的几十篇科普文章都是抄的,并自得其乐地要证明我的所有科普文章都是抄的。”(见:[weibo.com])。

“亦明(葛莘)多年来天天在网上指控我科普文章都是抄的,我要是都去回应,还干不干正事了?”(见:[weibo.com])。

“‘方学家’正到处告我所有文章都是抄的。”(见:[weibo.com])。


事实是,我不仅没有“天天在网上指控(方舟子的)科普文章都是抄的”,实际上我从来就没有那样“指控”过。我只是在2010年11月说过这样的话:

“现在我们已经知道,方舟子这个人才疏学浅,但他却总是以无所不知的面目在世人面前出现。因此,一个非常明显的问题就是:他的那些‘知’到底来自哪里?而根据方舟子的抄袭历史,一个十分合理的假设就是,他的那些‘知’大部分来自抄袭。所以说,目前发现的方舟子抄袭案例,仅仅是冰山的一角。因此,方舟子所撰写的文章,尤其是那些语出惊人、偏离常识、论题超出他所学范围的文章,都有抄袭的嫌疑。”(亦明:《关于方学研究的几点个人看法》)。

而方舟子之所以要如此“自残”,实际上是出于他的泼妇作派和贼人心理。所谓泼妇作派,就是在明知自己理亏或者斗不过对手之际,她就先把自己头发抓乱,把自己的脸皮挠破,再把自己的裤子也褪下了,然后高喊:打人了,要打死人了,要出人命了。所谓贼人心理,就是先给对手栽赃,让对手自证清白,以此来脱身。具体到方舟子造谣说“亦明(葛莘)多年来天天在网上指控我科普文章都是抄的”这个自残的例子,方舟子的如意算盘是:只要亦明不能“证明我的所有科普文章都是抄的”,那就自动证明“我的所有科普文章都不是抄的”、亦明的“所有”文章都是“攻击”,都是“断章取义”,都是“抹黑”,都是“诽谤”,都是“骗骗不懂英文以及混淆科普文章与学术论文的人”。

事实是,方舟子在过去一年多的时间里整日价闲得发慌,所以他才会天天“不干正事”找人掐架,但他却不肯花费一点儿时间来洗清自己的“老偷”、“巨骗”名声,这对于一个号称“我就是对真相有洁癖”、“我的眼睛容不下沙子”的人来说,未免太过讽刺。实际上,早在二十个月之前,方舟子还曾如此这般地威胁说:“葛莘居然扬言要起诉我。哪天我心血来潮,看谁起诉谁。”即使现在,方舟子也整天在搜狐微博以打官司来吓唬别人。可是,我却至今没有收到法庭的传票。这到底是什么原因,连弱智都会心如明镜,难道《新华每日电讯》的主编、总编们会搞不明白?

事实是,方舟子的“科普文章”,即使不是“所有”,那也“绝大多数”都是鸡鸣狗盗般偷来的,窃来的。因为按照当前认定贪官的标准之一,“巨额财产来源不明罪”,以及方舟子自己发明的用来指控韩寒代笔的逻辑, “巨额知识来源不明罪”,方舟子的几乎每篇文章都是“来源不明”的赃品。只不过是,“方学家”们把给方舟子定罪的标准定得很高,即不仅要找到“来源不明”的赃品,而且还要把这些赃品的“来源”查清,只有做到这些之后,才给方舟子扣上“抄袭剽窃”的帽子。而即使是如此的高标准严要求,目前勘定的方舟子抄袭案也已经接近百起──此案被定为方舟子抄袭剽窃第93案。事实是,由于方舟子每篇抄袭文章都含有多处抄袭来源(《吃得少活得老》一文至少抄了五篇英文文章),并且每篇抄袭文章都要发表多次(《吃得少活得老》一文至少发表了六次),因此,这93桩抄袭剽窃案至少应该再乘上一个系数3。也就是说,目前已经发现的方舟子抄袭剽窃案例,在三百起左右。可以预计,随着人类所有文字都将数字化、网络化,方舟子的“巨额知识来源不明罪”会一笔一笔地得到清算,而那最终的抄袭案数目,必将震惊世界。

请问《新华每日电讯》的各位总编、主编:你们为什么要和这样一个古今中外绝无仅有的恶棍沆瀣一气?你们为什么要替这样一个古今中外绝无仅有的文贼销赃洗钱?你们为什么要让这样一个古今中外绝无仅有的巨骗毒害社会?你们和中国人民有多大的仇恨?

让我再次正告你们:作恶可以,但必须承担后果!


附录:方舟子《吃得少活得老》一文抄袭来源比较


方舟子的文章全文照录,其文字来自新语丝网站(见:[www.xys.org])。方舟子抄袭的英文文章,附在抄袭文字之后。未注明出处的英文文字皆来自Arking, R. Biology of Aging: Observations and Principles. Sinauer Press , Mass. 1998. 每段英文后面括号内的数字为该书页码。

吃得少活得老

•方舟子•


大约从人类有了死亡意识时候起,就幻想着能找到一种灵丹妙药,或者常吃某种食物得以长生不老,也有许多人妄图将幻想变成现实,结果当然都失败了。但也有人反过来认为饿着肚子才是长生不老的窍门,比如中国的道教就把“辟谷”视为成仙之道,当然,如果一直那么辟下去,那是非离开人间不可的。这些长生不老术都是没有实际依据的臆想,其主张者根本没有想到,一个主张要站得住脚,必须建立在观察和实验的基础之上。

古希腊哲学家亚里斯多德也曾经思考过寿命的问题,他胜过同时代人之处,在于他是一位敏锐的观察者。他根据其观察,猜想动物的寿命长短与其发育期长短有关,发育得越慢,则寿命越长。例如大象是最长寿的哺乳动物之一,而其怀孕期也最长,相反地,家鼠在一年内就能发育成熟、生儿育女,而其寿命则只有数年。
The experiments of McCay and his colleagues, which we will discuss shortly, grew out of the idea that longevity is inversely proportional to developmental rate. This idea was derived partly from the works of philosophers such as Aristotle ……. (p.313)

这个猜想有一定的道理。一般来说,动物的身体体积越大,则新陈代谢率越低,寿命也倾向于越长;而动物的身体体积越大,也意味着需要用更长的发育时间来实现身体蓝图。因此动物发育期和寿命的关系,可能是由于它们都与身体体积有关。也可能是由于相同的生理因素(例如激素)都参与了发育和衰老的过程。还有一种可能是,动物的发育期越长,则身体这台“机器”制造得也就越精致,也就更能经受得起时间的磨损。

但是亚里斯多德并没有意识到,从其猜想可以得出一个推论:如果想办法延缓发育速度,那就可以延长寿命。

1917年,奥斯本(T. B. Osborne)等三位美国生物学家在用大鼠做营养实验时,发现那些没有喂饱的老鼠,生长迟缓,而其寿命似乎也延长了。受到这个结果的启发,1935年,美国康奈尔大学的麦克凯(C. M. McCay)等人直接验证是否动物寿命真的与发育速度成反比。在大鼠断奶后,他们给其中的一组提供完备的营养物质,但是严格限制其饮食,让它们一直处于饥饿中,而另一组老鼠则任其吃饱。受限制的老鼠发育几乎停止,身体也不再长大,一些老鼠夭折了,但是存活下来的老鼠中,寿命明显增长了。雄鼠所受的影响更显著,寿命平均延长了约50%。
This idea was derived partly from the works of philosophers such as Aristotle and partly from the experimental work of Osborne, Mendel, and Ferry (1917), whose data suggested, but did not prove, that underfed rats live longer. McCay, Crowell, and Maynard (1935) demonstrated that rats that were fed a nutritionally complete but calorie-restricted diet from the time of weaning had significantly increases in the values of mean, median, and maximum life span when compared to animals fed a normal diet conducive to rapid growth (Table 7.1). The animals provided with unlimited calories grew and matured normally. In the restricted group, maturation was greatly slowed, although these animals held their weaning weight and suffered from no other nutritional deficiency, since their diet included adequate amounts of protein, vitamins, and minerals. Growth and development in the restricted animals resumed only after they were given additional calories at about 2 years of age. The restricted animals never attained a normal body size or body weight; they remained about 15% smaller than their normal controls. (p.313)

喂食正常的老鼠中,寿命最长的为965天,而限制喂食的老鼠,有的活到了1800多天(相当于人活到200岁)。
McCay’s oldest control rat died at 965 days, whereas his oldest CR rat lived 1,456 days (150 years in human terms). In the 1960s, CR rats in the laboratory of Morris H. Ross at the Institute For Cancer Research in Philadelphia, survived for more than 1,800 days (180 years in human terms). 【Saul Kent. Aging Research Becomes A Science. LE Magazine December 2001.】

以后许多实验室都做了类似的实验,得到了相当一致的结果。
These observations have since been confirmed and extended by many other investigators. (p.313)

多项实验结果都表明,如果让鼠类的食物包含完备的营养物质,但是把食物中的热量减低25-60%,它们在中年后得慢性病的危险减低了,而寿命也延长了大约30%。例如在1986年对小鼠和大鼠同时做的实验表明,卡路里受限制的小鼠平均活47个月,而控制组活28个月;卡路里受限制的大鼠平均活1300天,而控制组平均活720天。
This finding, that animals on a low calorie, nutrient rich diet far outlived animals allowed to eat as much as they wanted, has been replicated a great number of times. One such study with mice and rats by Weindruch (1986) showed that fully fed mice lived on the average 28 months versus the calorie restricted group who lived 47 months. Rat survivals were shown to be approximately 720 days old for those eating ad lib and 1300 days of life if calories were restricted. In these and other studies, calorie restriction is defined as a reduction in calories of 25-60% from ad lib feeding levels while providing an adequate intake of essential vitamins and nutrients. 【Jean E. Pierog. RECIPE FOR LONGEVITY.】

对其他动物,包括脊椎动物和无脊椎动物所做的类似实验,也得到了类似的结果。
The basic observation has been found to apply to other species, both vertebrate and invertebrate, and is hallmarked by its ease of repeatability. (p.313)

而且限制饮食并不一定非要从小限制起不可。从老鼠的“中年”开始将饮食热量减低约30%,也能显著延长其寿命。

限制饮食热量,是迄今为止我们所知道的唯一能够有效地延长动物生命的环境因素。
In fact, caloric restriction is the only environmental means that has been shown to significantly slow the mortality rate of any mammal. (p.313)

卡路里受限制的老鼠不仅活得长,而且显得更健康。
Are these animals that live longer also healthier, or are they sick and feeble? Is the boon of extended longevity a blessing or a curse? What, in other words, is the effect of caloric restriction on age-related pathologies? Many studies have shown that the dietary history of the rodent has a major effect on the age of onset and the incidence of the various age-related pathologies (see Weindruch and Walford 1988 and Merry and Holehan 1994b for references). (pp.314-315)

麦克凯等人当时已发现这些老鼠得各种癌症的危险性降低了,心血管和肾脏的老化也延缓了。
McCay also discovered that calorie restriction inhibited a large variety of cancers and delayed age related deterioration of the vascular system and the kidneys. 【Jean E. Pierog. RECIPE FOR LONGEVITY.】

后来的研究者还发现其他的延缓衰老的标志,
A large body of data (reviewed by Masoro 1988a, 1992a; Weindruch and Walford 1988; Finch 1990winking smiley shows that caloric restriction, in addition to having an effect on the age-related pathologies, delays or eliminates the onset of many normal age-related physiological changes. (p.316)

如慢性炎症减少、
and the incidence of chronic tissue inflammations (for example, chronic glomerulonephritis, myocardial fibrosis) and of endocrine hyperplasias is significantly reduced. (p.315)

免疫力提高、
The early effects of restriction seem to depend on the strain, but a general response to the restriction of calories seems to be a decrease in antibody production coupled with an enhanced cell-mediated immunity. (p.316)

对血糖的耐受性增强、
The ability of calorie-restricted animals to satisfy energy requirements with low levels of
blood glucose implies that they can minimize the age-related effects of glycosylation. (p.322)

晚年记忆力提高等。
prevention of the decline in the mouse’s learning ability, (p.316)

这些老鼠对环境致癌物的抵抗力也增强了,用几种不同的致癌物做试验,发现它们因此患癌症的概率显著低于对照组。
Third, the restricted animals have a greater degree of protection against exogenous carcinogens; these rodents showed significantly fewer tumors after exposure to any of several different carcinogens tested. (p.316)

限制卡路里还显著地减少了体内脂肪细胞的数目,从而防止了晚年肥胖;而如果仅仅限制饮食中的脂肪含量,达不到这个效果。
An example of a normal trait that is eliminated in restricted animals is the normal increase in the number of fat cells found in particular fat depots in the rat. Not only does caloric restriction eliminate the increase in fat cells, but it brings about a significant decrease in the fat depot mass as a result of a reduction in the number of fat cells (Masoro 1992). Restricting the amount of fat without restricting the total energy intake did not have this effect. (p.316)

总之,各种研究都表明限制卡路里对动物的衰老过程有根本性的影响,而不只是某些表面效果。
It seems reasonable to assume that caloric restriction is affecting, either directly or indirectly, some fundamental process(es) involved in the regulation of biological aging. (p.317)

限制卡路里对老鼠健康的负面影响主要是生殖力下降了。这种副作用从自然选择的角度看并不难理解。只有在食物充足、能够保证生下的后代能生存时,才有必要将能量用于生殖。限制卡路里实际上是迫使动物改变了生存策略,将用于生殖的能量改用于生存,从短时间内快速生殖改为降低生殖率并生存更长的时间。
Clearly, caloric restriction works. But why should mammals come equipped with a mechanism that enables them to live long if they stay hungry? What is the evolutionary sense behind this concept? One proposal suggests that caloric restriction is best viewed as a special application of the disposable-soma theory (see chapter 4), which is based on the premise that an organism can devote its excess calories, beyond the amount needed for basic and essential functions, to reproduction and/or somatic maintenance. In this view, caloric restriction evolved as the set of mechanisms by which an organism adjusts its reproductive strategy to the conditions of its environment by shifting from rapid reproduction over a short time period to a reduced rate of reproduction over a longer life span (Holliday 1989; Richardson and Pahlavani 1994). (p.325)

但是限制卡路里是通过什么生理机制有益健康的?在回答这个问题之前,我们必须先确信我们所见到的延缓衰老现象的确是由于限制卡路里引起的,而不是由于其他因素,例如动物体内脂肪减少、某种食物成分减少引起的。
It seems reasonable to assume that caloric restriction is affecting, either directly or indirectly, some fundamental process(es) involved in the regulation of biological aging. But what might these process(es) be? And what specific aspect of dietary manipulation is involved? At a minimum, one could hypothesize that the critical variable is the amount of body fat, or the total amount of food eaten, or the total amount of calories taken, or the decreased intake of specific (toxic?) food components such as fats or carbohydrates or proteins, or perhaps more subtle effects, such as the lack of exercise in well-fed laboratory animals or delayed onset of degenerative disease in the restricted animals. (p.317)

体内脂肪的含量看来并不是重要因素。用遗传工程方法我们可以培养出先天性肥胖的小鼠,它们吃得多,长得快,体内脂肪占的比例高,而其寿命也比其他小鼠短。但是这些先天性肥胖的小鼠在卡路里受限制时,它们也可以获得和卡路里受限制的普通小鼠一样长的寿命,尽管其体内脂肪含量是普通小鼠的3.5倍。延缓衰老的效果看来也不是由于限制了某种营养物引起的。
The amount of body fat is not what is important. The mice in one genetically obese strain eat more, gain weight very rapidly, live a shorter time than other mice, and have a high percentage of fat in their body weight (Table 7.2). Yet when these animals are calorically restricted, they exhibit a median and maximum life span comparable to that of their long-lived, calorically restricted controls, even though they still have about 3.5 times as much body fat as do the controls. The increased longevity appears to be related to food consumption as such in these animals, and not to body composition.

实验表明,仅限制某一种食物成分(蛋白质、脂肪、碳水化合物、维生素或微量元素)的含量,而不限制卡路里总量,并不能延长动物寿命。这个结果也说明我们寿命的缩短并不是由于我们饮食中的某种物质引起的,但是食物的热量却能影响寿命长短。许多人批评限制卡路里表现出来的效果只是在实验室条件下出现的假象,并不一定适用于自然条件下的情形。他们认为,由于老鼠在实验室条件下饮食过度又缺乏锻炼,因此寿命本来就比较短,而限制卡路里不过是起到了类似锻炼的效果。但是研究表明锻炼并不能延长那些任意进食的老鼠的寿命。
Furthermore, the diet restriction does not appear to work if it consists of the elimination of any single deleterious component of the diet. The individual restriction of any single food component (such as protein, fats, carbohydrates, fibers, or minerals) to the same extent as observed in the complete diet restriction regime does not markedly affect longevity (Iwasaki et al. 1988; Masoro et al. 1989). It now appears unlikely that diet restriction experiments extend the life span by reducing the intake of a particular single component of the food. This observation suggests that our life span is not shortened as a result of toxic components in our diet, but it does support the idea that longevity is affected by the daily amount of food (calories) eaten. (p.318)

使限制卡路里发挥作用的具体机制还不清楚。一种可能是老鼠的新陈代谢率降低了,也即食物在体内较慢地转化成了能量。这样,所有的生理过程的速度都缓了下来,“生理时间”调慢,因而动物可以活得长一些。
The mechanisms underlying the effectiveness of caloric restriction are not clear. ……As Masoro (1988a) has pointed out, recent studies have eliminated two hypotheses regarding the mechanism of action of dietary restriction and forced the reconsideration of a third.……The third hypothesis was the idea that dietary restriction increases life span by decreasing the metabolic rate. This idea was particularly attractive, since because it has an obvious theoretical connection to the oxidative-damage theory of aging (see chapter 10). (p.321)

研究表明,限制卡路里对单位体重的代谢率的影响并不大,不过既然它们吃下的食物较少,即使单位代谢率不变,总的能量输出还是减少了。进一步的研究表明限制卡路里改变了动物的代谢模式。这些改变包括体温降低、脂肪合成降低而葡萄糖合成增加、在进食前有较低的代谢率而进食后有较高的代谢率等等。这些改变可能减少了代谢过程中产生的有害副产物的产量。
Recent information suggests that this third hypothesis is too simple to be entirely correct, but it is also not entirely wrong. Dietary restriction does affect metabolism, but not in the simple manner envisioned by this theory. Data from the National Institute on Aging–National Center for Toxicological Research (NIA–NCTR) joint biomarker study have shown that caloric restriction induces a major metabolic reorganization in animals (Duffy et al. 1989; Feuers et al. 1991, 1995).
This reorganization includes a lowering of core body temperature, a shift away from fat synthesis and toward glucose synthesis, a change in motor activity such that it is concentrated about the feeding time, and an alteration in the body’s metabolic rate such that restricted animals have a lower than normal metabolic rate before feeding but a higher-than-normal metabolic rate after feeding. One result of such a metabolic shift would be the lowering of the organism’s steady-state production of harmful metabolic by-products that result in oxidative stress and damage (Sohal and Weindruch 1996). (p.321)

这些老鼠体内的胰岛素调控葡萄糖的效率也增高了,因此血糖含量较低,比较不容易得糖尿病。血液中多余的葡萄糖会与体内蛋白质发生自由基氧化反应,生成化学结构发生了变化的糖基化蛋白,使这些蛋白质的正常功能受到影响。蛋白的糖基化可能是衰老过程中最普遍的一种化学变化。卡路里受限制的老鼠由于血糖含量低,相应地发生蛋白糖基化的可能性也降低了。而且,卡路里受限制的动物组织中,“自由基清除剂”过氧歧化酶活性增强了,在其一生中体内自由基含量都保持在较低水平。自由基对生命分子的破坏作用被许多研究者认为是导致衰老的主要因素。
The ability of calorie-restricted animals to satisfy energy requirements with low levels of blood glucose implies that they can minimize the age-related effects of glycosylation. Maintaining an efficient flow of glucose through glycolysis enables calorie-restricted animals to modulate their NADPH pools better. These latter cofactors are known to play an important role in maintaining some of the enzyme systems responsible for the detoxification of free radicals. Thus the ability to maintain “youthful” regulation of this enzyme may spare the organism the harmful effects of glycosylation and free-radical, or oxidative, damage, two harmful processes that can interact synergistically in contributing to the degeneration characteristic of old age (Kristal and Yu 1992). Caloric restriction has been shown to reduce the age-dependent accumulation of advanced glycosylation end products (AGEs) in both red blood cells and skin collagen (Cefalu et al. 1995). In addition, calorie-restricted animals have, in some but not all tissues, a higher level of superoxide dismutase enzyme activity and a lower level of superoxide and/or hydroxide radicals throughout their life span (Lee and Yu 1990). (p.322)

在分子水平上,限制卡路里还导致了许多其他的变化,包括肝脏组织中的酶活性发生改变,细胞修复DNA的能力增强,DNA与致癌物的结合能力降低等。大脑中神经介质的含量也发生了改变,表明神经内分泌系统也受到影响。
In addition to these changes in energy metabolism, a multitude of other enzyme reactions are affected by diet restriction, including liver enzymes known to be involved in drug metabolism and elimination (Leakey et al. 1989). The complexity of these changes is illustrated by the observation that DNA repair activity increases in diet-restricted rodents (Lipman et al. 1989), while the same treatment simultaneously decreases both normal DNA synthesis and the binding of a chemical carcinogen to DNA in vivo (Chow et al. 1993). The observation that caloric restriction brings about various alterations in brain neurotransmitters suggests neuroendocrine
involvement (Kolta et al. 1989). (p.322)

生物学家通常用放着食物的迷宫测试老鼠的学习能力。试验结果表明,限制饮食的中年老鼠和对照组的中年老鼠的学习能力相当,但是限制饮食的老年老鼠却明显胜过对照组的老年老鼠,而保持着中年时期的学习能力。这个研究表明限制卡路里的老鼠虽然发育缓慢,其成年时期的学习能力却没有恶化,反而能将这种能力维持到老年时期。
One unexpected beneficial outcome of diet restriction is its effect on learning performance in mice (Ingram et al. 1987). Both middle-aged and old mice were tested for their learning abilities in a standard maze test. The control and diet-restricted middle-aged adults had comparable learning levels, as indicated by their number of errors per trial. However, the old diet-restricted animals, exhibiting scores comparable to the middle-aged mice, were clearly superior to the old controls. This study is very important because it indicates that the delayed growth and maturation characteristic of diet-restricted animals have no deleterious effect on adult learning abilities but instead maintain these abilities well into the aging process. (p.323)

限制卡路里对老鼠的健康和寿命的积极作用已被充分证明了。我们更关心的是:它是不是也适用于灵长类和人类?在八十年代末,美国有两个研究小组开始对罗猴做限制卡路里实验。由于罗猴的寿命大约为40年,要知道它们的寿命是否延长了还为时过早。不过,它们在限制卡路里的条件下,出现了与老鼠类似的生理变化。与对照组相比,受限制的罗猴显得更健康,更精瘦,血糖浓度和胰岛素浓度较低,对胰岛素的敏感度增强。
Caloric restriction works wonders for rodents, but what about other mammals? How does caloric restriction affect primates in general and human being in particular? At least two ongoing studies are focusing on the effects of caloric restriction in rhesus monkeys─one located at the National Institute of Aging (Ingram et al. 1990), the other at the University of Wisconsin (Kemnitz et al., 1993). In both studies the treatment is a reduction in caloric intake of about 30 percent. At the end of the first 5 years of the studies, this level of caloric restriction appears to be well tolerated by the animals, and the treatment outcomes identified so far resemble those of the rodent studies (Weindruch 1995b). These results include decreases blood glucose and insulin levels, increased insulin sensitivity, and increased HDL (“good cholesterol”) levels. Interestingly, long-term caloric restriction appears not to affect the animals’ energy metabolism, percent lean body mass, or percent body fat (Lane et al. 1995). (p.323)

我们没法对人类也做类似的实验。战争时期的战俘、饥荒地区的难民被迫忍饥挨饿,饮食热量是受限制了,但是他们也往往营养不良,所以不能说明问题。不过,有一些间接证据表明限制卡路里可能对人体也有积极作用。
No well-controlled, long-term studies deal with the effects of caloric restriction on humans. The severe malnutrition too often practiced on prisoners and refugees in time of war clearly has devastating short- and long-term effects on the health of these people (Mohs 1994a), but such data cannot be used as evidence one way or the other in this question. There is, however, some anecdotal evidence. (p.324)

琉球群岛的居民的饮食有充足的营养,但热量低于普通日本人,他们的寿命也长于普通日本人,其百岁寿星的数目是日本其他地区的2-40倍。
In the past, the caloric intake of much of the population of Okinawa was much lower than the norm in Japan, but the nutrition of the Okinawans was otherwise adequate. Okinawa has a high incidence of centenarians: 2–40 times as many as may be found on any other Japanese island.

世界各地的百岁寿星也极少有肥胖的。
Other anecdotal evidence suggests that very few, if any, centenarians or other long-lived people have been obese. (p.324)

在1991-1993年间,四男四女在一个与外界隔绝的生态系统“生物圈2”住了两年。在此期间,他们的饮食营养齐备,但热量大约为一般饮食的90%。他们的体重明显降低了(男的降低18%,女的降低10%),并出现了与卡路里受限制的老鼠类似的生理变化。“生物圈2”的居民中包括研究衰老的分子生物学、加州大学洛杉矶分校的教授洛伊•瓦尔佛德(Roy Walford)。他成了限制卡路里长寿法的倡导者和实践者,声称他因此至少能活到120岁。
Finally, the seven people who voluntarily entered Biosphere 2 for 2 years and reduced their caloric intake while there are reported to have shown physiological changes similar to those observed in calorically restricted rodents (Walford et al. 2002). (p.324)【注:方舟子此处还照抄了Roy Walford的文章,如这篇:Walford RL, Bechtel R, MacCallum T, Paglia DE, Weber LJ. "Biospheric medicine" as viewed from the two-year first closure of Biosphere 2. Aviat Space Environ Med. 1996 Jul;67(7):609-17.】

正常人一天需要从食物中吸收2000-2500卡路里的热量,其中大约30%来自脂肪,30%来自蛋白质和40%来自碳水化合物。如果把热量供应减低30%,则每天大约只吸收1500卡。这些卡路里将主要来自水果和蔬菜,再加一点淀粉和肉。那些长期严格执行这个饮食计划的人,身体将会变得非常精瘦,总是感到饥饿和寒冷。由于他们体内脂肪已大部分丧失,他们将没有足够的脂肪做为骨骼缓冲物。他们坐下的时候,臀部的骨骼会因为被压着而感到疼痛。由于脚底没有脂肪垫着,走路也会觉得疼。

很少有人能够长期实施限制卡路里饮食,更不要说实施一辈子了。

不过,加州大学河边分校的斯蒂芬•斯宾德勒(Stephen Spindler)实验室在2001年9月发表的一篇论文认为,在短时间内实施限制卡路里饮食,可能就能取得良好的效果。他们用基因芯片技术分析了肝脏中11000个基因在年轻小鼠(7个月大)和年老小鼠(27个月大)的表达情况,发现其中有46个已知基因的表达随着衰老而发生了变化。与炎症、紧张反应有关的基因,表达增强了,而与代谢有关、抑制细胞生长的基因表达则降低了。他们对一批小鼠从小就限制其饮食,热量比正常的减低40%,一直养到27个月老后检测其基因表达情况,发现与年轻的小鼠类似。然后他们对一批34个月老的小鼠(相当于人长到大约80岁)进行卡路里限制一个月,前两周减低卡路里20%,后两周再进一步减低20%。然后处死这些老鼠检测其基因表达情况,发现也与年轻的小鼠类似。这就表明限制卡路里不仅能延缓衰老,甚至能在一定程度上逆转衰老过程,而且即使在老年时期短时间地限制卡路里,就能取得显著的良效。
S.S.: We took a group of animals that had been allowed to eat almost all they wanted their whole life and we intervened when they were quite old-34 months of age. These mice would be the equivalent of people who are probably 80 years old or older-I'm just guessing at the human equivalent age. We took a group of them and said okay gals, the party's over, it's time to diet. We under-fed them first for two weeks by 20%-that is, 20% less than they had been eating previously-and then for two weeks after that we fed them an additional 20% less so that for the second two weeks they were eating 40% less than they had been eating most of their lives. At the end of that time, at 35 months of age, we sacrificed all of the animals. We then compared the gene expression profiles in the livers of these mice to those in four other groups of mice. The old controls were mice that always ate almost all they wanted until being analyzed at 27 months of age. The long-term calorie restriction mice were those mice who had spent their whole lives being under-fed by 40% until the age of 27 months. Finally, the short-term calorie restricted mice were, as I mentioned, switched from fully fed to under-fed for just four weeks, and even at that only two weeks with "full strength" calorie restriction. We also had a young (seven month-old) control group and a young long-term calorie restricted group (also seven months old) so we could look at calorie restriction independently of aging.【注:方舟子此段是抄袭Life Extension Magazine上的系列文章,如2001年12月号上的这两篇:Reversing Aging Rapidly With Short-Term Calorie Restriction; Media Coverage of Anti-Aging Breakthroughs.

人类是否也如此?目前还没有人能够证明。即使能够证明,抑制食欲也不是一种吸引人的方案。瓦尔佛德曾在其新书发布会上,请来宾品尝他根据长寿配方制作的膳食。来宾们都觉得难以入口,有的人认为如果要长期吃这样的食物,还不如短命。但是我们研究限制卡路里实验的目的,当然不是为了使其他动物更长寿。我们研究的目的,是为了发现限制卡路里是如何防止衰老和疾病的,从而帮助我们了解动物衰老的机制。如果我们能在分子水平上对衰老过程有深刻的理解,或许能找到更能让人接受的健康长寿的办法。      



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