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主题:【整理】马兜铃酸强致癌性再次拷问中药安全性及当局中医药政 -- 南云北望

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        • 家园 错,上帝也做不到

          不过大公司的市场部可以做到

        • 家园 【商榷】关于你说的这个番茄红素的问题

          根据你的说法,首先是通过RCT发现了番茄的益处,这就是RCT实验的结果了。正如我之前说过的,RCT实验就是个“黑箱”实验,它不可能直接得出理论机理,反之,不知道理论机理也可以通过RCT得出结论。RCT实验并没有得出是番茄红素发挥作用的结论,番茄红素发挥作用只是一个猜想,并且最终被科学证明是错误的。这里是你自己把RCT得出的结论搞错了。

          想想看,这个错误也是很容易犯的,因为好像很说得通,因为已经知道番茄有益处,而番茄红素又是番茄的一种特有成份,是很容易认为番茄红素有什么益处。这个例子再次突出了理论应该来自实践,而不是来自推理的重要性。在这个例子里,理论基础很坚实—番茄是有益的,推导逻辑看越来也很可靠—番茄红素是番茄的特有成份,但是结论却是错误的。而中医就是一种典型的推理理论,其理论基础“阴阳五行”“复方辩证”之类就非常不可靠了,推导过程也常常是“体性凉、药性热”之类,就认为可以治病了。看到番茄红素问题的你难道完全没有想到中医的理论推导也会出错的吗?

          医学本质上就是一种实践,对于每一种治疗方法,实实在在拿出疗效才是最说明问题的,只有通过确实的实践验证,才能找出真正有效的方法,而不是靠猜想、推论。你可能认为事物的因果机制不可认识,只能交给上帝,但是理性的人是要通过踏踏实实的实践来寻找的,这个过程不会一帆风顺,会有错误,但是只有这样才能取得真正的成就。

          • 家园 你可以看一下我的那篇引文中实验设计的部分

            看上去很难吧?实际实践中可能更加困难,甚至与理论上都不可能

            问题的关键在于你想从实践里得到什么,西红柿的某种关键成分,然后将其工业化生产?

            青霉素是成功了,但想要让一切都像青霉素那样?根本不可能,不是所有的机制的动力学都可以被变换成一系列不相关因子的线性叠加的,现实种绝大多数的机制没有这么好的特性,作为一个整体的西红柿,它的有益成分可能永远也无法分离出来

            我对中医没有什么特别的好感,但是在我看来,用来攻击中医的言论其中大部分是可以一字不变的套回到西医上的,还有不少则是站在完全错误立场之上,无视实践的胡说八道

            比如说个性化的医疗方案本身竟然成为了被某些人攻击的对象?开玩笑,对于那些那些慢性病患者而言一个量身定做的,个性化的方向正确的治疗方案意味这什么?很多时候就是生与死的差别,无论中西医皆是如此

            照他们的意思,医院干脆变成工厂好了,医生就变成完全被动按照手册一丝不苟处理作为产品的病人的流水线工人得了,我倒想知道,有朝一日,他们罹患了那些慢性疾病,敢不敢心悦诚服的去享受这样的医疗待遇

        • 家园 不会有中医站出来为龙胆泄肝丸的副作用负责的

          同样的也不会有人去为那些在五六十代那些仅是有点歇斯底里,乃至思想叛逆就被进行额叶切除手术这一诺贝奖成果搞成白痴的受害者负责

          在八十年代当时被称为科学的精神病医生,用暗示的手法,诱导患者和未成年儿童的虚假记忆,制造出了无数骇人听闻的案例,将很多无辜者送进监狱,又有几个人站出来负责呢?

          中医的毛病西医就没有吗?只怕未必

          病人如果只是甘于成为医生的扯线木偶,盲目迷信西医与盲目迷信中医其实没有任何区别,简单的细菌感染到罢了,要是换成难以治愈的慢性疾病,基本上很难有好结果

          • 家园 我与龙胆泻肝丸擦肩而过

            8平方前,我正在读研究生,和妻子不在一个城市。岳母是个极其迷信中医的人,不知在哪里认识了一个“著名中医”,请到家中,为每一位下药。岳母对女婿亲呀,说:我女婿在外地,你能否为他也开点药。中医说:面色如何?岳母答:白里透红。中医问:脾气如何?岳母答:急脾气。中医说:肝火旺盛,须服龙胆泻肝丸。岳母急急如律令,赶快让妻子给我写信。看到信后,我哑然失笑,真他娘的遇到神医了。龙胆泻肝丸自然是没有吃,但是成了我几十年来调笑妻子的笑料。岳母从不服用西药,前年因一点呼吸系统的疾病-气管炎,命丧在中医研究所。妻子家传的传统也丢不了,整天看中医的书,Youtube上看中医的视频。可惜命运不济在国外中药不好配,不然她会像林彪一样给自己开方子。

            • 家园 不要小看气管炎

              我被这毛病折磨了20年,期间中西医看过无数,对它的顽固难治是深有体会的

              最大的问题是治疗方案不当,现代医学的角度来看,症状相同的气管炎其实可能是由完全不同机制引起的,医生如果不能对此作出正确的判断,制定正确的治疗方案,那么病人只能一次次徒劳地往返于医院之间直至死亡

              误诊的危害,转投西医也是不能避免的

              我的亲生经历,在关于这毛病20年的求医问药中,没有哪怕一个医生,无论中西医,对我的病情进行过恰当的诊断,医生们都被训练的非常好,严格的按照手册机械的处理我们这些病人,没有一丝所谓的主观能动性存在与其中

              我得的是哪一类气管炎呢?用西医的话说就是过敏性鼻支气管炎,有相当大比例的过敏性鼻炎患者都会转化为我这种情形,他们也往往都无法得到恰当的治疗。我也是在20年后,自己病情得到基本控制后,才在文献中发现有种机制的理论的——它对我的康复没有起到任何作用,在这20年里没有哪怕一个医生向我询问是否得过鼻炎

              为什么?因为在这20年里,这种机制只在少数文献里被记载,对于那些被训练得已经基本丧失主动精神的医生而言,这是没有任何意义的

              我是怎么判断出自己的过敏性鼻炎与支气管炎之间的关联性的?并不是我有多么高明比那些医生还强,而是因为我的毛病在这二十年之间,不断地发展,恶化,鼻炎与气管炎之间的关联性表现也更加突出,从一开始的只在冬季,鼻炎发作几次支气管炎才发作一次,发展到一年四季只要鼻炎发作支气管炎必然发作,而且一月几次的地步,这时只要不是傻瓜,都能判断出这里面的关联了

              那么我后来的治疗方案又是什么呢?对于过敏性鼻炎,中西医现阶段都没有一个比较好的办法,但也不是完全无法可治的,其实很简单,加强体育锻炼即可,当我能够每天慢跑3公里的时候,我的鼻炎和支气管炎就得到了一个比较好的控制

              病人的生命对于病人自己而言是无价的,但是对于医生而言又意味着什么呢?医生又该为其负担多大责任呢?比如说,在我的支气管发展的最高峰,严重的支气管痉挛让我连站立都困难无比的时候,如果我的运气差一点,就这样死掉了,又有谁该为该对其负责呢?

        • 家园 麻烦给个文献出来看看

          几十年以前人们用RCT发现了西红柿的种种益处

          然而今天的文献已经彻底否认了番茄红素对身体的益处,它甚至可能是有害的

          如果前面一个因为年代久远“不可考”,那就算了;后面的文献可务必提供一下哦。

          • 家园 文献?比如说?

            Tomatoes or Lycopene Versus Prostate Cancer: Is Evolution Anti-Reductionist?

            Occasionally, but not often, positive things happen in the field of cancer prevention science to popular, good-tasting foods. Cruciferous vegetables have been the subject of intense study, but these foods might be—to modify the expression—an easy pill but a hard food for the public to swallow. By contrast, tomatoes (scientifically classified as a fruit) have overcome their earlier reputation as an inedible and possibly toxic food to become one of the most heavily consumed fruits or vegetables in the Western diet—mostly in the form of pizza, salsa, chili, pasta sauce, and ketchup. Americans consume an average of 91 pounds of tomatoes per capita per year, second only to potatoes among all fruits and vegetables.

            This issue of the Journal brings good news to tomato eaters. Boileau et al. (1) report, in a well-controlled study using the N-methyl-N-nitrosourea (NMU)-androgen rat carcinogenesis model, that a diet containing whole tomato powder inhibited the development of prostate cancer compared with a control diet, whereas a diet containing a pure synthetic lycopene supplement did not. In the tomato powder group, the risk of developing lethal prostate cancer was reduced by a statistically significant 26% compared with that in control rats; by contrast, the group receiving lycopene experienced only a 9% (and not statistically significant) risk reduction compared with controls. Using a factorial design, the investigators also measured the effect of a 20% dietary calorie restriction on the risk of dying with prostate cancer. The authors found that this restriction on energy intake produced a 32% reduction in prostate cancer mortality that was independent of (i.e., additive to) the effect of tomato powder.

            This new study is important and provocative on several levels. Perhaps most important, it weighs heavily in the debate about whether cancer prevention is best achieved via whole foods versus via single compounds. Readers are no doubt familiar with the β-carotene story: After years of research indicating a possible benefit of supplemental β-carotene against lung cancer, two phase 3 randomized trials found that a β-carotene supplement was not only ineffective but actually appeared to increase lung cancer risk, primarily among smokers (2). This is the best known but not the only adverse experience in humans taking carotenoid supplements. For example, canthaxanthin, another carotenoid that is still marketed as an artificial tanning agent, is known to cause a reversible crystalline retinopathy in people who take high doses (3). A possible reason for the misleading observational results on β-carotene is that, given the sources of β-carotene in the diet, people who eat a lot of it (and therefore who also have higher concentrations in their serum) tend to have healthier diets and lifestyles. Lycopene/tomato research is not plagued by this difficulty—in fact, heavy lycopene consumers in the United States have essentially the same patterns of exercise, body weight, and smoking as lighter consumers (4). Given this background, it is important to note that most observational and indeed human experimental evidence to date concerning the possible benefit of lycopene versus prostate cancer is actually based on consumption of lycopene-rich foods such as tomatoes rather than lycopene itself, which has not been used as a supplement long enough or widely enough to facilitate epidemiologic research. In studies relating serum or plasma concentrations to risk, lycopene concentrations might only serve as a marker for consumption of the relevant foods (5).

            The ultimate biologic activity of a given food or nutrient depends on a large number of variables, including food processing and preparation method, gastrointestinal tract physiology, interactions between compounds in the food, and interactions between foods eaten together at the same meal. The biologic effect of a given food might even be influenced by how rapidly we eat it, as is seen in the literature on glycemic load. It has already been established that heat, mechanical processing, and ingestion together with oil or fat alters the bioavailability of lycopene and similar compounds by releasing them from intracellular compartments and promoting intestinal absorption (6). In addition to lycopene, known carotenoids in tomatoes and tomato-based products include β-carotene, γ-carotene, ζ-carotene, phytofluene, and phytoene, all of which are among the 10 major carotenoids that have been found to accumulate in human prostate tissue (7). The article by Boileau et al. does not present detailed qualitative and quantitative analyses of these carotenoids in tomato powder, plasma, and prostate tissues of the treated rats—such analyses, in view of the results of the experiment, would be useful in clarifying the possible role of other tomato carotenoids that may exert their biologic effects in concert with lycopene. As the authors mention, there are also numerous non-carotenoid compounds in tomatoes that have potentially relevant activity, and certainly a large number of unknown phytochemicals as well.

            Carotenoids generally occur in the plant for a purpose, for example, to protect seeds in fruit from photodegradation and oxidative damage. From an evolutionary perspective, it makes sense that plants would develop sets of interacting compounds to accomplish these functions rather than relying on single compounds. This strategy provides redundancy and allows for a more subtle play of natural selection, because minor modifications in an enzyme could affect a web of active metabolites or interacting compounds. Such complexity is not unreasonable when you consider, to paraphrase the author Michael Pollan in his recent book The Botany of Desire (8), that while humans were learning how to walk upright, plants were continuing the process—hundreds of millions of years old—of developing intricate chemical methods to compensate for their relative immobility. Even biochemical systems that appear to have evolved for a simple straightforward effect, such as toxins, are in fact quite complex. Snakes, for example, which are ancient in comparison to most animals but are newly arrived by plant standards, have evolved venoms that are strikingly complex. We have barely begun to scratch the surface of understanding how the compounds within tomatoes interact within biologic systems. Studies such as that by Pastori et al. (9) on the interaction of lycopene and α-tocopherol in prostate cell cultures stand as testimony to how limited this knowledge is so far. Given the potential complexity of the relevant effects in humans, untangling these interactions in the laboratory—essentially subjecting them to reductionist analysis—could be a long and tedious process.

            The timely study by Boileau et al. is well-designed and conducted, especially considering the challenges posed by animal models for prostate cancer and the general demands of dietary intervention studies. Nevertheless, given the importance of the results, alternative explanations, even relatively unlikely ones, should be considered. The study was designed to deliver considerably more lycopene to the pure lycopene group than to the tomato powder group, but perhaps coincidentally, the plasma lycopene concentrations came out nearly equal. Although the plasma compartment might have been saturated for lycopene, we do not know the relative concentrations in tissue, and it is conceivable that the biologically effective dose in tissue was too high to inhibit tumor growth in the lycopene group. This possibility should be explored as an alternative explanation for the lower efficacy of lycopene than of whole tomato powder, because nonmonotonic and even U-shaped dose-response curves have been reported for protection against cell damage by both lycopene and β-carotene (10). It also appears that a substantial amount of lycopene in both the lycopene and tomato powder diets was lost after exposure to the light, atmosphere, and temperature of the rat cages, which is somewhat surprising for the lycopene diet, because the lycopene was present as beadlets, which are normally stable. Lycopene breakdown products consist of a number of in-chain cleavage products, such as apolycopenones, apolycopenals, and apolycopenoic acids. In addition, it has been shown that acycloretinal, one of the oxidation products of lycopene, can be converted to acycloretinoic acid in the presence of pig liver homogenate (11). Although the biologic properties of lycopene degradation products are not known at present, different rates or patterns of degradation between diets would result in the formation of a number of breakdown products that could be responsible for the enhanced efficacy of tomato powder compared with lycopene. This situation can become even more complex because other tomato carotenoids may be similarly subjected to degradation to smaller molecules with unknown biologic properties. Carefully controlled stability studies throughout preparation and storage of the diet would be needed to eliminate these uncertainties.

            An unusual and methodologically significant aspect of this study is the use of morbidity (presumably due to prostate cancer) as an endpoint rather than scheduled sacrifice of the animals at fixed intervals. This design permitted a survival (time-to-event) analysis that closely mimics a human trial that could have been conducted in the pre-prostate-specific antigen era. The main advantage of this design feature is that it evaluates the effect of treatment on prostate cancer that is undoubtedly biologically important, albeit to a rat. Recent problems with interpretation of the Prostate Cancer Prevention Trial of finasteride foretell how difficult it will be in human trials to identify clinically significant effects on prostate cancer incidence in the face of prostate-specific antigen surveillance and biopsy at fixed timepoints (12). The main risk of this design aspect, however, is that it can introduce bias if the morbidity that triggers vivisection of the animals is not always due to prostate cancer, and if the groups receiving different treatments differ in their likelihood of getting sick due to causes other than prostate cancer. Information on the attribution of morbidity leading to vivisection, and on the blinding of technicians responsible for this decision, should be discussed as the results of the study are examined further.

            Although this one study—like one molecule—is not likely to be definitive, it will, as all important studies do, open and clarify avenues for research. The mechanisms of action of tomato powder in the NMU model can be explored fruitfully (for example, effects on the androgen and insulin-like growth factor systems), as can the efficacy of this agent in other types of rodent models, including xenografts and transgenics. Investigators designing phase 2 trials in humans can also take note of these findings and begin testing foods and food derivatives in addition to pure lycopene. Successful completion of these studies could mean that a phase 3 trial is not far off. It is important to remember the somewhat obvious point that whole food or dietary trials in humans cannot be placebo controlled. In dealing with the relationship of diet to cancer causation or prevention, we would do well to emulate the “wisdom” of the evolutionary process and use only as much reductionism as is necessary to understand where we are and where we are going.

            这样的?太多了。你可以自己去寻找一些相关资料嘛

            蛋白质摄入量方面你可以了解一下美国饮食营养协会的运动员推荐蛋白质日摄入量变更的历史

            在1987年是每日每千克1.0克,同时他们指出,对于运动员而言,远超普通人的蛋白质摄入量是没有促进作用的,然而到了1993年,他们却认为最大氮平衡水平的日所需蛋白质为1.5克,进入二十一世纪,他们推荐力量类型运动员的蛋白质日摄入量为1.7克

            Rennie 与Tipton 曾经比较过0.8克每天与1.6克每天的两组人群进行12周运动后的氮平衡水平,结论是没有显著差异

            懂一点历史,你就会发现,权威部门提供的营养指南,那里面的很多数据就是拟周期运动啊

            说白了,所谓的指南手册。就是一群人,一堆结果迥异的研究,然后互相扯皮妥协之后的结果,很多时候这里面还有些政治经济因素在内,你认为它有多少指导意义吗?

            • 家园 科学今天说生命在于运动

              明天会说,千年的王八万年的龟。

              反正都有人信滴,哈哈

      • 家园 中医爱好者会这么解释

        我跟公司里的中医爱好者也聊过,听到的说法是这样的:每一个病人都是独特的,每一个病人都应该用不同的方子,所以是很难用RCT检验。

        • 家园 俺一直不理解如果一人一方,那中医有啥好学的

          如果这么强调人的特殊性,那中医那些理论,经验不是屁用没有?生病的人肯定比这些东西出现的晚,人家的特殊性当初写理论的肯定不知道,这怎么下药?

          • 家园 军事也没啥好学的啊

            打仗么,要是不能有通用的东西,自然不是“科学”

          • 家园 中医承认人有很多的共性,具有一些特殊性

            临床实验对条件的控制是很严格的,必须是同等条件,必须同等药量,完全抹杀人的特殊性,否则统计与假设检验就没有基础。

            而中医承认人及自然界有共性,而这个共性跟西医说的共性又不完全一样。 只说类似的一点: 假设最简单的情况: 对某种病应该用同一种药,但是对于每一个人用药的药量,时间,君臣佐使的配合都不一样,(我个人认为)临床实验真的不太合适--就象用拳击的规则来判断跆拳道能不能打得过拳击一样。

            但是话说回来, 可以批量生产的药物应该可以临床--国内起步晚,也在做。我不太清楚有谁完全否定中药的临床实验的可能性,随便找了两个有关的文章。起步晚,在探索,你不能说人家在回避吧?

            1. http://www.zhong-yao.net/shi/60899.htm

            2. http://d.wanfangdata.com.cn/periodical_zglcylxyzlx200306034.aspx

          • 家园 运用之妙,存乎一心

            对不懂中医的人,是怎么说,都解释不明的。

            以上标题与内容,是我的同事原话。。。

    • 家园 我的建议读一本中医基础理论,再读一本《串雅内外编》

      别看现代人那些不靠谱的。

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