標題:The Scientism of Attention Deficit Hyperactivity Disorder (ADHD)
By Sami Timimi, MD -February 20, 2018
文章來源:https://www.madinamerica.com/2018/02/scientism-attention-deficit-hyperactivity-disorder/
In my last blog I reviewed the scientific basis on which modern mainstream psychiatry rests and showed how a poor understanding of the basics of the scientific process was evident in mainstream academic and clinical frameworks that organise psychiatric research and practice. Modern psychiatry is built on scientism, not science. In this blog I start to illustrate how this scientism can be found in the literature on specific ‘conditions’.
在我上一篇博客中，我回顧了現代主流精神病學所依據的科學基礎，並指出主流學術和臨床框架中對科學過程基本原則的理解貧乏，這在組織精神病學研究和實踐中顯而易見。現代精神病學是建立在科學主義上，而不是科學上。在這篇博客中，我開始闡明這種科學主義如何出現在針對特定“症狀”的文獻中。
As a practicing child psychiatrist, ADHD is one of the four common ‘diagnoses’ I encounter in my practice — the other three being autism, childhood depression, and generalised anxiety (diagnoses that are usually made by other doctors for patients I ‘inherit’). As mentioned in my last blog, it requires little intellectual effort to understand that calling ADHD a ‘diagnosis’ is not logical or accurate. In medicine, diagnoses are part of a system of classification based on explanation. What we are referring to as ‘diagnoses’ in psychiatry are descriptive classifications with no explanatory powers and therefore, strictly speaking, not a diagnosis. Calling ADHD a diagnosis, i.e., something with the capacity to explain the behaviours that it describes, is like saying the headache is causing the pain in my head or the inattention is caused by inattention.
作為一名兒童精神科醫師，ADHD 是我在臨床實踐中遇到的四個常見“診斷”之一——另外三個是自閉症、兒童抑鬱症和廣泛性焦慮（這些診斷通常由其他醫生為我“接手”的患者做出）。如我在上一篇博客中提到的，理解將ADHD稱為“診斷”既不合邏輯也不準確並不需要太多智力努力。在醫學中，診斷是基於解釋的分類系統的一部分。而我們在精神病學中所指的“診斷”只是描述性分類，沒有解釋功能，因此嚴格來說不是診斷。將ADHD稱為診斷，即具有解釋其所描述行為的能力，就像說頭痛是造成頭部疼痛的原因，或注意力不集中是由注意力不集中引起的一樣。
My first ‘serious’ encounter with the phenomenon of ADHD was as a trainee in child psychiatry in the mid-1990s. ADHD was not being diagnosed in the UK at that time; in fact, child psychiatry was a largely systemically orientated profession that didn’t use diagnostic labels, and child psychiatrists rarely prescribed medications. We were aware of the growing medicalisation in the US and there were child psychiatrists in influential positions in the UK who were attracted by this. By the mid-1990s in the UK, their influence was beginning to tell. Thus one of my supervising consultants expressed an interest in carrying out a ‘project’ on ADHD and its relevance to the population we were serving in an ethnically diverse and deprived area of inner London. He asked me if I would like to join him. As an enthusiastic trainee eager to learn I jumped at the chance. My consultant hadn’t yet formulated a research question and so asked me to do a literature review summarising key data on ADHD (diagnosis, prevalence, causes, urban v rural etc.).
我第一次“正式”接觸ADHD現象是在1990年代中期，當時我是一名兒童精神病學的實習醫生。那時英國並不診斷ADHD；事實上，兒童精神病學主要是一個系統化的專業，不使用診斷標籤，兒童精神科醫生也很少開藥。我們知道美國的醫療化進程在增長，並且在英國有一些具有影響力的兒童精神科醫生被這一趨勢吸引。到了1990年代中期，他們的影響力在英國開始顯現。於是，我的一位指導顧問對在倫敦內城一個多元種族且貧困地區進行有關ADHD的‘項目’表現出興趣，並詢問我是否願意加入他。作為一個渴望學習的熱心實習生，我立刻答應了。我顧問當時還沒有具體的研究問題，因此讓我做一份文獻回顧，總結關於ADHD的關鍵數據（診斷、患病率、原因、城市與農村等）。
This proved to be an enlightening experience — just not in the way my supervisor imagined. I read studies and reviews but felt troubled by my inability to grasp what this concept was. The more I read the less certain I became. I couldn’t answer the basic question of “what is ADHD?” What is it, I kept thinking; surely it isn’t just ‘attention deficit’ and ‘hyperactivity’, just what it was called, followed by the word ‘disorder’. I found it incredibly frustrating that the literature I was reading wasn’t addressing this basic question.
這對我來說是一個啟發性的經歷——只是並非我指導老師所想像的那種。我閱讀了研究和評論，但因無法理解這個概念而感到困惑。我讀得越多，越感到不確定。我無法回答那個最基本的問題：‘什麼是ADHD？’ 我不斷思考，這到底是什麼？它不應該只是‘注意力缺陷’和‘過動’的簡單組合，後面再加上‘障礙’這個詞吧。我感到極度沮喪，因為我閱讀的文獻並沒有解決這個基本問題。
Instead there was an assumption that ADHD exists as a ‘thing’ and that this thing had a concrete reality that meant you could make authoritative statements about its features, implications, causes, prevalence, treatment and so on. I was astonished to realise that ADHD had been conjured into existence by a few people’s imaginations without evidential basis.
取而代之的是，文獻中假設ADHD是一個‘實體’，而且這個實體具有具體的現實，這意味著你可以對其特徵、影響、原因、流行率、治療等作出權威性陳述。我驚訝地發現，ADHD竟然是由少數人的想像憑空創造出來的，並沒有實質的證據基礎。
The evidence then brought forward avoided the scientific methodology and ignored the ‘null hypothesis’ (the basic and starting assumption that ADHD does not represent a characteristic natural entity, which should be assumed until concrete evidence is presented that shows that this null hypothesis cannot be true). The papers I reviewed made me feel uneasy.
隨後提出的證據回避了科學方法，並忽略了‘虛無假設’（即最基本的假設，認為ADHD並不代表一個特徵性的自然實體，這應該被假定為真，直到有具體的證據表明此虛無假設不成立為止）。我所審閱的論文讓我感到不安。
How could this construct be taken at face value and treated as if it were a real entity? If the construct does not reflect a specific, measurable, identifiable, natural entity (as the null hypothesis presupposes), then all the data built using the idea that ADHD is a ‘thing’ is suspect. Castles built on sand.
怎麼可能將這個構建物視為真實的實體呢？如果這個構建物並不反映一個具體的、可測量的、可識別的自然實體（如虛無假設所預設的那樣），那麼基於ADHD是‘一個實體’這一思想所建立的所有數據都令人懷疑。這就像是在沙地上建造城堡。
This lack of foundational solidity has been confirmed for me in my subsequent years of examining various facets of the ADHD literature. As I will explain below, research in the name of showing ADHD to be a natural entity has provided convincing evidence of the opposite. Sadly, in an era in psychiatric thinking dominated by scientism, this is not the message that most people receive.
在我隨後多年對ADHD文獻各個方面的研究中，這種基礎不穩的情況得到了證實。正如我將在下文中解釋的那樣，為了證明ADHD是一個自然實體而進行的研究，實際上提供了相反的有力證據。可悲的是，在一個受科學主義主導的精神病學思想時代，這並不是大多數人所接受的訊息。
Instead, this is the sort of information you get from websites when you google “What is ADHD?”
相反，當你在谷歌搜索‘什麼是ADHD’時，這是你從網站上獲得的信息：
“ADHD stands for attention deficit hyperactivity disorder. It is a medical condition. A person with ADHD has differences in brain development and brain activity that affect attention, the ability to sit still, and self-control. ADHD can affect a child at school, at home, and in friendships.” (Kids health)
‘ADHD代表注意力缺陷多動障礙。這是一種醫學狀況。患有ADHD的人在大腦發育和大腦活動上存在差異，這影響了注意力、靜坐能力和自我控制能力。ADHD可能會影響孩子在學校、家裡和朋友之間的表現。’（Kids Health）
Or “If you have attention deficit hyperactive disorder (ADHD), you may have lots of energy and find it difficult to concentrate. It can be hard to control your speech and actions. ADHD is the most common behavioural disorder in children. It usually starts at about 18 months old, but symptoms usually become noticeable between the ages of 3 and 7. We don’t know what causes ADHD but experts think it runs in families. It could also be caused by an imbalance in brain chemicals.” (Young Minds)
或是‘如果你患有注意力缺陷多動障礙（ADHD），你可能精力充沛，並且很難集中注意力。控制你的言語和行動可能很困難。ADHD是兒童中最常見的行為障礙。它通常在大約18個月時開始，但症狀通常在3至7歲之間顯現。我們不知道ADHD的原因，但專家認為它具有家族遺傳性。它也可能是由大腦化學物質失衡引起的。’（Young Minds）
Or “ADHD is characterised by periods of impulsiveness, hyperactivity and inattention, but it’s more than being a daydreamer or a fidget. ADHD affects about 2-5% of us, and it’s largely genetic – although environmental factors can make it worse.” (BBC advice).
或是‘ADHD的特徵是衝動、過動和注意力不集中，但這不僅僅是做白日夢或坐立不安。ADHD影響約2-5%的人口，而且主要是遺傳性的——儘管環境因素會使其惡化。’（BBC建議）。
If you google “What causes ADHD?” you get things like:
如果你在谷歌搜索‘ADHD的成因是什麼？’你會看到以下內容：
“ADHD tends to run in families and, in most cases, it’s thought the genes you inherit from your parents are a significant factor in developing the condition… Research has identified a number of possible differences in the brains of people with ADHD compared to those who don’t have the condition… Other studies have suggested that people with ADHD may have an imbalance in the level of neurotransmitters in the brain.” (NHS choices)
‘ADHD往往有家族遺傳性，並且在大多數情況下，人們認為你從父母那裡遺傳的基因是導致該狀況的重要因素……研究已經發現，ADHD患者的大腦與非ADHD患者相比存在一些可能的差異……其他研究表明，ADHD患者的大腦神經遞質水平可能存在失衡。’（NHS choices）
Or “Scientific research has found there is a strong genetic link in ADHD. It is not a disorder that is learnt or passed on socially… Many of the genes that experts have identified as potentially contributing to the development of ADHD are genes that control certain types of neurotransmitter… Scientific studies have shown that in people with ADHD some important parts of the brain are developing more slowly and communicating less well.” (Netdoctor)
或是‘科學研究發現，ADHD與遺傳有很強的聯繫。這不是一種通過社會學習或傳遞的障礙……專家們已經確定了可能促進ADHD發展的基因，這些基因控制著某些類型的神經遞質……科學研究表明，ADHD患者的大腦中一些重要部位的發育較慢，且溝通不良。’（Netdoctor）
If you google “ADHD treatment” you get things like:
如果你在谷歌搜索‘ADHD治療’你會看到以下內容：
“Treatments range from behavioral intervention to prescription medication. In many cases, medication alone is an effective treatment for ADHD.” (Healthline)
‘治療範圍從行為干預到處方藥。在許多情況下，單純使用藥物對ADHD的治療就很有效。’（Healthline）
Or “Treatment of attention deficit hyperactivity disorder (ADHD) relies on a combination of medicines and behavior therapy. Treatment with medicine depends on the age of your child. The first step is an accurate diagnosis of ADHD and an understanding of your child’s strengths and weaknesses. Learning about ADHD will help you and your child’s siblings better understand how to help your child.” (Webmd)
或是‘注意力缺陷多動障礙（ADHD）的治療依賴於藥物和行為療法的結合。藥物治療取決於孩子的年齡。第一步是對ADHD進行準確的診斷，並了解孩子的優勢和弱點。了解ADHD將幫助你和孩子的兄弟姐妹更好地理解如何幫助孩子。’（Webmd）
Thus you can see that the views you will likely encounter in most searches on the subject bring up lots of scientific-sounding stuff that tells you that ADHD is something that exists as an identifiable ‘thing’ and that this thing has something to do with your genes and brain (chemicals and structure), and can be treated by medication alongside some behaviour therapy. Scientism has turned ADHD from a vague, difficult to pin down concept into a fact of culture masquerading as a fact of nature.
因此，你會發現，在大多數關於該主題的搜索中，你會遇到很多聽起來科學化的內容，告訴你ADHD是某種可識別的‘實體’，並且這個實體與你的基因和大腦（化學物質和結構）有關，並且可以通過藥物治療和一些行為療法來治療。科學主義將ADHD從一個模糊且難以捉摸的概念轉變成了一種文化事實，偽裝成自然事實。
As ADHD does not reach the required evidence base to be considered a ‘diagnosis’, it is not surprising that there has been a failure to find any specific and/or characteristic biological abnormality such as characteristic neuroanatomical, genetic or neurotransmitter abnormalities.
由於ADHD未能達到被視為‘診斷’所需的證據基礎，因此未能找到任何具體的和/或特徵性的生物學異常，如特定的神經解剖、基因或神經遞質異常，這並不令人驚訝。
Unlike the myths that have been spread to spur an ADHD industry on, the scientific reality is that we have a cupboard empty of confirming evidence and full instead of ‘junk’ scientism.
與為促進ADHD產業而傳播的神話不同，科學的現實是，我們的儲物櫃裡沒有確認的證據，反而充滿了‘垃圾’科學主義。
Scientism in ADHD genetics
ADHD 遺傳學中的科學主義
The claim that ADHD is ‘genetic’ has been extrapolated from twin studies. In the twin method it is assumed that when a higher percentage of identical than non-identical twins are diagnosed with the same disorder, this is due to genetics rather than environmental factors.
ADHD是‘遺傳的’這一說法來自雙胞胎研究。在雙胞胎方法中，假設當單卵雙胞胎比雙卵雙胞胎更高比例被診斷為相同的障礙時，這是由於遺傳因素，而不是環境因素。
This is because identical twin pairs will share 100% of the genes whereas non-identical twins will have, on average, 50% of their genes the same. However, for identical twins to have a greater likelihood of having a disorder because of sharing the same genes, you have to assume that the psychosocial environment is the same for identical and non-identical twins. This is known as the Equal Environment Assumption or EEA for short.
這是因為單卵雙胞胎有100%的基因相同，而雙卵雙胞胎平均只有50%的基因相同。然而，若要認為單卵雙胞胎因為基因相同而更有可能患有某種障礙，你必須假設單卵雙胞胎和雙卵雙胞胎的心理社會環境是相同的。這被稱為平等環境假設（Equal Environment Assumption，簡稱EEA）。
It has been long established that EEA doesn’t hold when comparing identical and non-identical twins. Identical twins are often treated similarly (e.g. dressed in same clothes) and experience a unique psychological environment (e.g. swapping roles to confuse others).
長期以來，人們已經確定在比較單卵和雙卵雙胞胎時，EEA並不成立。單卵雙胞胎往往被相同對待（例如穿相同的衣服），並且經歷獨特的心理環境（例如交換角色以混淆他人）。
Being one of a set of identical twins is a different experience to being a non-identical twin and so the psychosocial environment could (as well as genes) by itself be responsible for greater behavioural or emotional similarity in identical compared to non-identical twins.
作為單卵雙胞胎的一員與作為雙卵雙胞胎的經歷是不同的，因此心理社會環境本身可能（除了基因外）就可以解釋單卵雙胞胎在行為或情感上的更高相似性。
This means the twin study method cannot disentangle genetic from environmental factors for ‘psychiatric’ presentations, and so estimates of the genetic contribution to ADHD cannot be arrived at from this method.
這意味著雙胞胎研究方法無法將‘精神疾病’的遺傳和環境因素分離，因此無法通過這種方法得出ADHD的遺傳貢獻估計。
The only way to reliably evidence a specific genetic contribution to ADHD is through molecular genetic studies. Since faster and cheaper whole genome scans have become available the molecular genetic evidence has been accumulating. This increasingly large volume of ADHD genetic research is not showing any particular genetic findings, whether in relation to abnormal genes or consistent genetic associations. Yet this has not stopped unscrupulous researchers from making claims to the contrary.
唯一能可靠證明ADHD具體遺傳貢獻的方法是通過分子遺傳研究。隨著更快速且便宜的全基因組掃描技術的出現，分子遺傳證據已經積累起來。這些越來越多的ADHD遺傳研究並沒有顯示出任何特定的遺傳發現，無論是異常基因還是持續的遺傳關聯。然而，這並沒有阻止一些不誠實的研究者提出相反的主張。
In 2010, a study was published in the medical journal The Lancet claiming to have found concrete molecular genetic evidence that ADHD is a genetic disorder. This study has been, and continues to be, referenced as the preeminent study that demonstrates the certainty with which we can call ADHD genetic.
2010年，《柳葉刀》醫學期刊發表了一項研究，聲稱發現了具體的分子遺傳證據，證明ADHD是一種遺傳疾病。這項研究一直被引用，並且繼續被視為確定ADHD遺傳特性的重要研究。
In the press release at the time, the research team lead, Professor Anita Thapar, left little room for doubt, saying: “Now we can say with confidence that ADHD is a genetic disease and that the brains of children with this condition develop differently to those of other children.”
當時在新聞發布會上，研究團隊負責人Anita Thapar教授幾乎不留任何懷疑空間，說道：“現在我們可以自信地說，ADHD是一種遺傳疾病，患有此病的孩子的大腦發育與其他孩子不同。”
This is what they really found:
這是他們實際發現的：
The study involved the comparison of whole genome scans of 366 children ‘with ADHD’ with those of 1047 ‘non-ADHD’ control children, looking for something called Copy Number Variants (CNVs). CNVs are abnormal bits of genetic code that are repeated where they shouldn’t be or deleted where they should. Researchers found 15.5% (57) of the children with ADHD had CNVs compared with 7.5% (78) of the non-ADHD controls. This leaves an excess of 8% in the ADHD group, hardly a significant figure.
該研究比較了366名‘ADHD兒童’與1047名‘非ADHD’對照組兒童的全基因組掃描，尋找稱為拷貝數變異（CNVs）的基因變化。CNVs是一些異常的基因片段，可能在不應該的地方重複或在應該的地方缺失。研究人員發現，15.5%（57名）的ADHD兒童有CNVs，而非ADHD對照組中有7.5%（78名）有CNVs。這使ADHD組多出8%，這一數字幾乎無法被認為是顯著的。
If we are to accept standard ‘mainstream’ quoted prevalence for ADHD, it also means that if you come across a young person who has CNVs they are more likely to not be diagnosable with ADHD than diagnosable with it.
如果我們接受ADHD的主流報告流行率，這也意味著如果你遇到一個有CNVs的年輕人，他們更有可能不被診斷為ADHD，而不是被診斷為ADHD。
The deceit doesn’t end there, however. The average recorded IQ of the children with ADHD was 86, 14 points below the general population average of 100. Furthermore, when 33 intellectually impaired (IQ lower than 70) ‘ADHD children’ were excluded from the ADHD group, only 11.4% of the remaining 333 had CNVs (now only 4% above the ‘non-ADHD’ control group).
然而，欺騙並沒有到此為止。ADHD兒童的平均記錄IQ為86，比一般人群平均值100低14分。此外，當33名智力受損（IQ低於70）的‘ADHD兒童’被排除在ADHD組之外時，剩下的333名兒童中只有11.4%有CNVs（現在僅比‘非ADHD’對照組高出4%）。
39% (13) of the 33 children with ADHD and an intellectual impairment had CNVs. This evidence is more suggestive of a relationship between the presence of CNVs and intellectual disability (39%) than ADHD (11.4%).
在這33名有ADHD和智力障礙的兒童中，有39%（13名）有CNVs。這一證據更暗示CNVs與智力障礙（39%）之間的關係，而不是與ADHD（11.4%）的關係。
The authors of this study should therefore have controlled for IQ given its disproportionate impact on CNV levels, but chose not to. As mentioned above the average IQ in the ADHD group was significantly lower than the control group (whom we can assume would have a population average IQ of 100). The authors should have chosen a subgroup from their ADHD patients who had an average IQ of 100. This would then have made for a more legitimate comparison group to their control group. I can’t help wondering whether someone in the group did that, because I suspect they may have been left with no or a tiny 1% or so difference and so chose not to publicise this.
因此，該研究的作者應該控制IQ，因為它對CNV水平的影響不成比例，但他們選擇不這樣做。正如前文所述，ADHD組的平均IQ顯著低於對照組（我們可以假設對照組的IQ為100的平均水平）。作者應該從他們的ADHD患者中選擇一個IQ平均值為100的亞群，這樣他們的對照組才更具合理性。我不禁懷疑，研究組內是否有人做過這樣的操作，因為我猜測他們可能會發現無顯著差異，或者只有1%左右的差異，於是選擇不公開這一結果。
This sort of high-profile and media attention grabbing publication is worse than junk science, as the authors have misled the medical community and general public in their conclusions.
這種吸引眼球的高調出版物比垃圾科學更糟糕，因為作者在結論中誤導了醫學界和公眾。
With genetics then, the cupboard is empty and the null hypothesis stands: There is no characteristic identifiable genetic abnormality/profile associated with ADHD.
就遺傳學而言，證據庫是空的，虛無假設成立：沒有與ADHD相關的特徵性可識別的遺傳異常或基因圖譜。
Scientism in ADHD brain imaging studies
ADHD腦部影像研究中的科學主義
As with genetics, ADHD brain imaging studies have not uncovered any specific or characteristic abnormality. The picture that emerges is of consistently inconsistent findings, which are statistical deviations (the brains would not be recognised by radiologists as being clinically abnormal), come from small sample size studies, don’t always accurately match for age (and you’ll see why this is important when I comment on birthdate research below) and typically don’t control for IQ level, or for the possible effects of medication.
與遺傳學一樣，ADHD的腦部影像研究並沒有揭示出任何具體或特徵性的異常。出現的圖景是結果始終不一致，這些結果是統計上的偏差（放射科醫生不會認為這些大腦在臨床上是異常的），來自於小樣本研究，通常沒有準確匹配年齡（當我在下文評論出生日期研究時，你會明白為什麼這很重要），也通常沒有控制智商水平或藥物的可能影響。
One research team finds one bit of the brain smaller than ‘healthy’ controls and the next one doesn’t, or even finds that bit is a little larger.
一個研究團隊發現ADHD患者的大腦某部分比‘健康’對照組小，而下一個研究卻沒有發現，甚至發現該部分稍大。
But, as I have been explaining, the science should not get in the way of the dedicated scientismist! In 2017, The Lancet Psychiatry published a study that the authors claimed provided definitive evidence that young people with ADHD have different and smaller brains compared to their healthy peers. As with the genetics junk science, the lead researcher, Dr Hoogman, made bold claims that do not stand up to scrutiny. In a press release that was covered by mainstream media, he stated that “The results from our study confirm that people with ADHD have differences in their brain structure and therefore suggest that ADHD is a disorder of the brain.”
但正如我所解釋的，科學不應該妨礙那些執著的科學主義者！2017年，《柳葉刀精神病學》發表了一項研究，作者聲稱該研究提供了確鑿證據，證明患有ADHD的年輕人與健康同齡人相比，大腦不同且較小。與遺傳學中的垃圾科學類似，該研究的主要研究員Hoogman博士提出了經不起推敲的大膽主張。在被主流媒體報導的新聞發布會上，他表示：“我們的研究結果證實了ADHD患者的大腦結構存在差異，因此表明ADHD是一種大腦疾病。”
In an excellent analysis by Michael Corrigan and Robert Whitaker for Mad in America, they show how the research reveals more about the desperation of the authors to find something than their ability to conduct a scientifically careful analysis of their findings.
在Michael Corrigan和Robert Whitaker為《瘋狂的美國》撰寫的精彩分析中，他們展示了這項研究更多地揭示了作者急於找到某些東西，而非他們進行科學謹慎分析的能力。
The authors call their study a ‘mega-analysis’ as they took data from a large number of previous research projects and ‘number crunched’ all the different sites’ findings as if they were all just one big study. This process is sometimes illuminating, but can also make incidental findings look more significant than they are.
作者稱他們的研究為‘大規模分析’，因為他們從大量以前的研究項目中獲取數據，並將各個研究站點的發現‘數據處理’，彷彿它們都是一個大的研究。這個過程有時是有啟發性的，但也可能使偶然的發現看起來比實際更顯著。
In total, they had data from the brain scans of 1713 patients diagnosed with ADHD and 1529 individuals who did not have this diagnosis, gathered from 23 different sites around the world.
總共，他們收集了來自全球23個不同地點的1713名ADHD患者和1529名未被診斷為ADHD的個體的大腦掃描數據。
They claim what amounts to tiny differences in some (not all) particular brain structures that become statistically significant when they add all the available recorded volumes for a particular structure in the ADHD and non-ADHD groups. Using certain measures of statistical variance enables them to make this claim on differences that are so tiny they are of no clinical relevance.
他們聲稱某些（但不是全部）特定的大腦結構有微小差異，當他們將ADHD和非ADHD組中的所有可用記錄的體積加總時，這些差異變得在統計上顯著。通過使用某些統計變異的測量方法，使他們能夠聲稱這些差異，儘管這些差異微不足道，對臨床毫無意義。
For example, the largest difference was found for a tiny brain structure called the nucleus accumbens. This mega-analysis thus makes the claim that children with ADHD have a smaller nucleus accumbens (NA).
例如，最大的差異發現於一個叫做伏隔核（nucleus accumbens）的微小大腦結構。因此，這項大規模分析聲稱ADHD兒童的伏隔核較小。
However, if you look at the data by site you find 10 sites that found an on average smaller NA in the ADHD group, 4 sites that found a larger NA in the ADHD group, and 6 sites that found no difference. This is the picture for the structure with the largest difference in the study.
然而，如果按地點查看數據，你會發現有10個地點發現ADHD組的伏隔核平均較小，4個地點發現ADHD組的伏隔核較大，還有6個地點發現沒有差異。這是該研究中差異最大的結構的情況。
Staying with NA, you can also see that there are major technical issues with interpreting the scans. For example, individuals in Bergen, Norway have an average NA volume of 758 mm³ v 805 mm³ (ADHD v control), whereas in Wurzburg, Germany they have an average NA volume of 462 mm³ v 449 mm³ (ADHD v control).
繼續討論伏隔核，你還可以看到解釋掃描結果存在重大技術問題。例如，挪威卑爾根的個體伏隔核平均體積為758 mm³對805 mm³（ADHD對照組），而在德國武茲堡，伏隔核平均體積為462 mm³對449 mm³（ADHD對照組）。
Perhaps Norwegian children have amazing NAs compared to German children, whom by this standard must all have raging ADHD to contend with.
也許，與德國兒童相比，挪威兒童的伏隔核異常發達，按照這一標準，所有德國兒童都應該患有嚴重的ADHD才能應對。
However, given that the Norwegian group is one of the groups where the controls have larger volumes, whereas the ADHD group has larger volumes in the German centre, this huge variation which is larger between centres than within further biases the findings if (as is the case) those with larger total volumes lay more in the group that had differences in favour of controls having larger structures.
然而，考慮到挪威對照組是體積較大的組之一，而德國中心的ADHD組體積較大，這種在中心之間比中心內部更大的巨大變異進一步偏倚了結果，尤其當有較大總體積的個體更多出現在對照組具有較大結構差異的情況下。
Finally, here is yet another study that does not control for IQ differences. Associations between brain volume and IQ have been shown across a range of studies with adults and children. When the authors of this study published the correct IQ table (embarrassingly they had originally published an incorrect version), a separate group re-analysed their data, taking into account potential effects of IQ, and concluded that there was no significant difference between individuals with ADHD and those in the control group in any of the investigated areas of the brain when IQ difference is controlled for.
最後，這又是一項沒有控制IQ差異的研究。許多關於成年人和兒童的研究都顯示了大腦體積與IQ之間的聯繫。當該研究的作者發布了正確的IQ表（尷尬的是，他們最初發布了一個錯誤的版本）後，另一組重新分析了數據，考慮了IQ的潛在影響，並得出結論：在控制IQ差異後，ADHD患者和對照組在大腦的任何研究區域都沒有顯著差異。
Here too then, as far as the science is concerned, the cupboard is also empty. No one has come near to finding a characteristic abnormality, and as a result there is no biological marker or brain scan used to diagnose ADHD. The null hypothesis stands — there is no characteristic brain abnormality associated with ADHD.
因此，就科學而言，這裡的證據庫也是空的。沒有人能接近找到任何特徵性異常，結果是沒有生物標記或腦部掃描能用來診斷ADHD。虛無假設成立——沒有與ADHD相關的特徵性腦部異常。
Scientism and ADHD as a chemical imbalance
ADHD作為化學失衡的科學主義
There is no shortage of ‘experts’ prepared to claim that ADHD is related to a chemical lack or imbalance of the neurotransmitter ‘dopamine’. This idea is based solely on the perceived finding that drugs (like Ritalin) that act to stimulate the release of dopamine, and therefore increase its levels in brain synapses, appear to improve the ‘symptoms’ of ADHD (more on that later).
有很多‘專家’準備聲稱ADHD與神經遞質‘多巴胺’的缺乏或失衡有關。這一觀點僅僅基於這樣的發現，即能刺激多巴胺釋放的藥物（如利他林），從而增加大腦突觸中的多巴胺水平，似乎能改善ADHD的‘症狀’（稍後會詳細解釋）。
Decades ago studies found that if you take stimulants, regardless of diagnosis, it improves your ability, in the short term at least, to maintain concentration on a task.
幾十年前的研究發現，不論是否被診斷為ADHD，服用興奮劑至少在短期內可以提高你在任務中的專注能力。
However, as no one had yet demonstrated a lack or no lack of dopamine in individuals diagnosed with ADHD, the chemical imbalance theory was able to spread alongside aggressive marketing from manufacturers of drugs that increase the levels of these chemicals in the brain.
然而，因為還沒有人證明ADHD患者是否缺乏多巴胺，化學失衡理論得以隨著增加這些化學物質水平的藥物製造商的積極推廣而傳播開來。
Every now and then a study comes along that challenges the received wisdom and so gets limited publicity. One such study was published in 2013. Its findings questioned “previous suggestions that attention deficit hyperactivity disorder (ADHD) is the result of fundamental abnormalities in dopamine transmission.”
偶爾會有研究挑戰這種被普遍接受的觀點，但通常獲得的關注較少。2013年發表的一項研究就是這樣。其研究結果質疑了“以前的建議，認為注意力缺陷多動障礙（ADHD）是多巴胺傳輸的基本異常所導致”。
The researchers found that administering methylphenidate (more commonly known as Ritalin) to healthy adult volunteers as well as those who exhibit symptoms of ADHD led to similar increases of the chemical dopamine in their brain. Both groups also had equivalent levels of improvements as a result of the drug when tested on their ability to concentrate and pay attention.
研究人員發現，無論是健康的成年志願者還是表現出ADHD症狀的人，在服用甲基苯丙胺（更常見的名稱為利他林）後，兩組大腦中的多巴胺水平均會增加。此外，當測試他們的專注能力時，兩組的改善程度相當。
Here too then the cupboard is also empty. The null hypothesis stands — there is no characteristic chemical imbalance associated with ADHD.
因此，在這裡，證據庫同樣是空的。虛無假設成立——沒有與ADHD相關的特徵性化學失衡。
Scientism of ADHD revealed in diagnoses of young-for-class children
從班級中較年幼的孩子診斷中揭示的ADHD科學主義
Several studies conducted in different countries have found that the youngest children in a class year have a significantly increased risk (compared to oldest children in a class year) of being diagnosed with ADHD and/or receiving medication for ADHD.
多國進行的幾項研究發現，在同一年級中，年齡較小的孩子相比年齡較大的孩子有顯著更高的風險被診斷為ADHD或接受ADHD藥物治療。
These studies have found that whether you are in a country that has high rates of diagnosing or prescribing (like USA) or low rates (like Finland), this pattern is still evident.
這些研究發現，不論你是在診斷或處方率高的國家（如美國）還是診斷或處方率低的國家（如芬蘭），這種模式依然明顯存在。
Such a pattern of identifying ADHD is strongly suggestive that relative immaturity to your peers is a significant risk factor for receiving this label (i.e., for adults noting and problematizing the described behaviours associated with ADHD).
這種ADHD識別模式強烈表明，與同齡人相比的相對不成熟是獲得這個標籤（即，成年人注意到並將與ADHD相關的行為描述為問題）的顯著風險因素。
Whether it’s over 6% of children (in Icelandic study) who get prescribed stimulants or less than 1% (in the Finnish study), the pattern still holds.
無論是冰島研究中超過6%的孩子被處方興奮劑，還是芬蘭研究中不到1%的孩子，這一模式依然成立。
Whatever the cultural norms for problematizing these behaviours are, relative immaturity in the class keeps emerging as a risk factor.
無論文化對這些行為問題化的標準如何，班級中的相對不成熟始終是一個風險因素。
Of course, children mature at different rates, raising an important question of whether a diagnosis of ADHD even for older-in-the-class children might also be reflective of their relative slower developmental trajectory.
當然，孩子們的成熟速度不同，這引發了一個重要問題，即即便對班級中年齡較大的孩子進行ADHD診斷，是否也反映了他們相對較慢的發展軌跡。
For a while now I have thought the growth of pseudo-diagnoses like ADHD to be a reflection of Western neoliberal intolerance of diversity amongst children, where from an early age children are given messages that they are valued for what they do (for their ‘performance’) rather than for just being.
一段時間以來，我一直認為像ADHD這樣的偽診斷的增長是西方新自由主義對兒童多樣性不容忍的反映，從小孩子們就被傳遞這樣的信息：他們的價值取決於他們所做的事情（即他們的‘表現’），而不是僅僅因為他們的存在。
These findings lend further support to my concern that the prevalence of diagnoses like ADHD acts like a barometer of how intolerant of children and childishness we are.
這些研究結果進一步支持了我的擔憂，即ADHD等診斷的普及就像是一個晴雨表，反映出我們對兒童及其幼稚行為的容忍度有多低。
Scientism in ADHD treatment
ADHD治療中的科學主義
In 1999 a study of ‘treatment’ for ADHD was published. By then, prescribing of stimulant medication (the most famous name for a stimulant medication being ‘Ritalin’) was widespread.
1999年，發表了一項有關ADHD治療的研究。那時，興奮劑藥物（最著名的興奮劑藥物是‘利他林’）的處方已經非常普遍。
When this study was published it received extensive public and professional coverage. I remember attending our Faculty of Child and Adolescent Psychiatry (in the UK Royal College of Psychiatrists) annual conference in 2000, with the then chair of the faculty explaining to us that the implication of this study was that we would have to prescribe stimulants for anyone diagnosed with ADHD and probably (given resource limitations) that stimulants alone would be sufficient for most.
當這項研究發表時，它受到了廣泛的公眾和專業關注。我記得2000年參加了我們英國皇家精神病學院兒童與青少年精神病學系的年度會議，當時的系主任向我們解釋，這項研究的含義是，我們將不得不為所有診斷為ADHD的人開出興奮劑處方，並且可能（鑒於資源有限）僅使用興奮劑就足夠治療大多數患者。
So what did this famous study find? This American study often referred to as the ‘MTA’ study (stands for Multimodal Treatment study of children with ADHD), was a 14 month multi-centre trial where young patients were randomised to four treatment groups: medication (stimulants) only, behaviour therapy only, combined medication and behaviour therapy, and routine community care.
那麼這項著名的研究發現了什麼呢？這項美國研究通常被稱為‘MTA’研究（多模式ADHD兒童治療研究），是一項為期14個月的多中心試驗，將年輕患者隨機分為四個治療組：僅用藥物（興奮劑）、僅用行為治療、藥物與行為治療結合組以及常規社區護理組。
The authors concluded that after 14 months of treatment, there was more reduction of ADHD symptoms in the medication only and combined treatment groups than the behavioural therapy only group, who in turn had better outcomes than the routine community care group.
作者得出結論，經過14個月的治療，僅用藥物組和藥物與行為治療結合組的ADHD症狀減少程度大於僅用行為治療組，後者的結果又優於常規社區護理組。
As you might predict by now, there were considerable problems associated with the study that make such a conclusion questionable. For example, two thirds of the routine community care group were also on the same medication as the medication arm of the study, yet had the poorest outcomes.
正如你現在可能猜到的，這項研究存在相當多的問題，使這一結論受到質疑。例如，常規社區護理組中有三分之二的人也在使用與藥物組相同的藥物，但他們的結果最差。
Furthermore, the behavioural treatment arm consisted of an intensive 6 week course that was completed at any time during the 14 months, so that by the time of the 14 month evaluation, some of the families receiving the behavioural therapy intervention had completed it up to 9 months before the 14 month assessments, whilst the medication arm included appointments right up to 14 months.
此外，行為治療組的療程為6週密集治療，可以在14個月中的任何時間完成，因此在14個月評估時，一些接受行為治療的家庭已經在9個月前完成了治療，而藥物組的治療則持續到14個月。
This raises the distinct possibility of a placebo response being the main reason for better outcomes in the medication and combined treatment arms at 14 months.
這就提出了一個明顯的可能性，即安慰劑效應可能是14個月時藥物組和綜合治療組結果較好的主要原因。
At that time, conflict of interest statements were not mandatory in most journals. Predictably, when these were made known, many of the lead authors had long lists of pharmaceutical company connections.
當時，大多數期刊不要求披露利益衝突。可以預見的是，當這些利益衝突被公開時，許多主要作者與製藥公司有著長期的聯繫。
The story of the MTA study doesn’t end there. By chance I ended up, at a conference in 2002, sitting next to a psychologist involved in the evaluations of the MTA trial. He told me they had just completed analysing the data for the 3 year follow up at his centre. I remember him saying to me “Once these findings are published no one will want to have their children take medication anymore.”
MTA研究的故事並未就此結束。2002年，我偶然在一次會議上與一位參與MTA試驗評估的心理學家坐在一起。他告訴我，他們剛剛完成了他們中心的3年隨訪數據分析。我記得他對我說：“一旦這些結果發表，沒有人會想讓他們的孩子再服藥了。”
I had to wait another 5 years before the 3 year follow up of the MTA was published. Unlike the original 1999 study, this publication, published 8 years later (allowing plenty of time for stimulant prescribing advocated by the 1999 paper to become the norm), had little accompanying press or professional coverage.
我又等了5年，才等到MTA的3年隨訪結果發表。與1999年的原始研究不同，這項8年後發表的研究（允許1999年論文提倡的興奮劑處方成為常規）幾乎沒有得到媒體或專業的關注。
The follow-up analysis of outcomes at 3 years of the MTA study patients could not find support for continuing superiority of medication regardless of initial severity of ADHD symptoms.
MTA研究的3年隨訪分析結果無法支持藥物的持續優勢，無論最初的ADHD症狀嚴重程度如何。
Additionally, those who used more medication during the 3 years were more likely to experience a deterioration in ADHD symptoms, had higher rates of delinquency, and were significantly shorter (by an average of 4 cm) and lighter (by 3 kg) than those who had not taken medication.
此外，那些在3年內使用更多藥物的人更有可能經歷ADHD症狀惡化，犯罪率更高，並且比未服藥的人顯著矮（平均矮4厘米）和輕（輕3公斤）。
This is typical of the findings in other long-term follow-up studies that are naturalistic rather than controlled trials (in other words, following people who attend usual services).
這是其他自然隨訪而非對照試驗的長期隨訪研究中的典型發現（換句話說，跟蹤那些接受常規服務的人）。
These studies also fail to show that long-term use of stimulants is associated with any improved outcomes compared to those diagnosed with ADHD who don’t take them, and where there are differences it is often with children on stimulants having worse outcomes than those diagnosed with ADHD but not taking them (see for example the Western Australia and Canadian studies).
這些研究同樣無法證明長期使用興奮劑能帶來更好的結果，與那些未服用興奮劑的ADHD患者相比，服用興奮劑的兒童結果通常更差（例如參見西澳大利亞和加拿大的研究）。
If these medications, which are used so widely now, had little evidence of harms associated with their use, perhaps we could tolerate the small initial improvement that is sometimes associated with their prescription, even if there is no evidence of improved longer term outcomes.
如果這些藥物，如今被如此廣泛使用，並且與其使用相關的危害證據很少，也許我們可以容忍與其處方相關的初步小幅改善，即使沒有證據表明有更好的長期結果。
However, the stimulants that are being prescribed have near identical pharmacological properties to street drugs such as ‘speed’ and ‘cocaine’ that we regularly warn others of the physical and mental dangers associated with their use.
然而，這些被處方的興奮劑在藥理性質上與我們經常警告他人其身體和精神危害的街頭毒品，如‘冰毒’和‘可卡因’，幾乎相同。
If these drugs were only prescribed to patients for a year or less it might be possible to put together evidence-based arguments for their use in this limited and controlled manner.
如果這些藥物僅被處方給患者使用一年或更短時間，可能可以建立證據支持的論據，為這種有限和可控的方式使用這些藥物辯護。
Unfortunately, once started, a prescription is likely to continue being given for years.
不幸的是，一旦開始，處方很可能會持續多年。
Given the considerable harms associated with the use of such powerful and addictive substances, you really need clear blue water in outcomes between those who receive such medications and those who don’t.
鑒於使用這些強效和上癮物質的顯著危害，你確實需要在那些服用這些藥物的人與不服用的人之間看到顯著的結果差異。
I can’t think of a rational ethical argument (probably because there isn’t one) to justify the long-term prescribing of stimulants given the available evidence.
我無法想出一個合理的倫理論據（可能是因為根本沒有）來為長期開處方興奮劑辯護，鑒於現有的證據。
翻譯紀錄 https://chatgpt.com/c/66f6ebf0-d018-800b-af3f-2c91b173d3b2