Introduction: the false positives challenge to DSM-5

The fifth edition of the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders (DSM-5) (American Psychiatric Association, 2013) has been criticised for its revision process, goals and content. The most vehement and sustained objections were aimed at the content of its diagnostic criteria. It was argued that the revised criteria illegitimately expanded psychiatric diagnosis into areas of normal-range distress and other problems in living, undermining the integrity of psychiatry as a medical discipline, obscuring the meaning of its research results and potentially leading to unwarranted and possibly harmful treatment. Emblematic of this concern was the statement by Allen Frances, who had Chaired the DSM-IV (American Psychiatric Association, 1994) revision, that due to DSM-5's changes, ‘Many millions of people with normal grief, gluttony, distractibility, worries, reactions to stress, the temper tantrums of childhood, the forgetting of old age and ‘behavioral addictions’ will soon be mislabeled as psychiatrically sick…’ (Frances, Reference Frances2012). The ‘false positives problem’ of mislabelling normal condition as mental disorders is the issue that most impacts psychiatric epidemiology, given its heavy reliance on DSM criteria in community studies (Wakefield & Schmitz, Reference Wakefield, Schmitz, Teresa Scheid and Brown2010, Reference Wakefield, Schmitz, Pilgrim, Rogers and Pescosolido2011). Consequently, after brief comments on DSM-5's process and goals, I focus on DSM-5's false positives problem, arguing that this concern is largely justified and that DSM-5 was a missed opportunity to address this problem.

Failure of the process to provide an adequate scholarly record

For scholars trying to understand and evaluate the validity of the DSM-5 Task Force's decisions, the most important problem with the DSM-5 revision process was its secrecy and lack of adequate documentation. This was a major step backward from the systematic, open approach of DSM-IV. The Task Force responded to criticism by insisting that ‘the process for developing DSM-V has been the most open and inclusive ever’ (Schatzberg et al. Reference Schatzberg, Scully, Kupfer and Regier2009), and by absurdly suggesting that critics had financial motives. However, the reality is that basic elements of public access to information were lacking, and remain so. The in-process records of the workgroups’ proposals and rationales that appeared periodically on the DSM-5 website have disappeared, with no final summary documents posted. The many emailed comments to the website – touted by the Task Force as demonstrating the process's openness – and the workgroups’ responses have never been made public. In DSM-IV, the reasoning and evidence behind each change was documented in authoritative Source Books that have proven invaluable to scholars, whereas no comparable record is planned for DSM-5. Review papers by workgroup members exist for some areas, but they are scattered through the literature and do not necessarily represent the workgroup's final rationale.

Most egregiously, the deliberations of the DSM-5 Scientific Review Committee, formed in response to the DSM-5 controversies to evaluate the strength of the scientific evidence for each proposed change and provide recommendations to the workgroups, are being kept strictly secret. It is ironic that the deliberations of a committee formed to reassure a nervous profession and public about troubling proposals emanating from confidential workgroups should themselves be kept confidential. One imagines that the reason is to avoid embarrassment; many proposals were rejected, and workgroups sometimes overrode the committee's recommendations and went ahead with rejected proposals anyway (Kendler, Reference Kendler2013). Finally, the unprecedented confidentiality agreements signed by all workgroup members took an additional toll. Speaking from personal experience, a workgroup member I asked to speak to my university seminar about contemplated changes in his specialty declined, explaining ‘to be honest, given the confidentiality agreement, I am not really sure of what I can and cannot say.’ The needlessly secretive DSM-5 mindset, antithetical to both the appearance and reality of intellectual integrity, shortchanged future scholarship.

Overreaching goals, failed aspirations

Most of DSM-5's prominently mentioned goals, including separating impairment from diagnosis, incorporating biomarkers into diagnosis, and rethinking the definition of mental disorder (Regier et al. Reference Regier, Narrow, Kuhl and Kupfer2009, Reference Regier, Narrow, Kuhl, Kupfer, Regier, Narrow, Kuhl and Kupfer2011), were eventually abandoned, leaving a feeling of ‘much ado about nothing.’ The problem was that the goals were ill-conceived to begin with (Wakefield, Reference Wakefield2009; First & Wakefield, Reference First and Wakefield2010).

The Task Force's primary initiative was dimensionalisation of diagnosis: ‘we have decided that one, if not the major, difference between DSM-IV and DSM-V will be the more prominent use of dimensional measures in DSM-V’ (Regier et al. Reference Regier, Narrow, Kuhl and Kupfer2009, p. 649). Bread-and-butter nosological problems, including high comorbidity, excessive not-otherwise-specified (NOS) diagnoses, and high within-category heterogeneity, were all supposed to be addressed by a shift from categories to dimensions. Engaging in the same dimensional fantasy that Eysenck unsuccessfully attempted to realise decades before (Wakefield, Reference Wakefield1997b ), the Task Force imagined a system of dimensions of severity of various psychological problems (e.g., psychosomatic symptoms, anxiety and depression) replacing diagnostic categories, modelled on a proposal to replace categorical personality disorders with a system of trait dimensions (which itself proved untenable for now [Wakefield, Reference Wakefield2008, Reference Wakefield2013c ]). In the imagined system, comorbidity is eliminated (everyone falls at exactly one point on the system of dimensions), heterogeneity within categories is no longer an issue (each single point in multidimensional space is a unique category), and use of not-otherwise-specified diagnoses is eliminated (everyone falls somewhere in multidimensional space, so everyone is specified).

However, the conceptual underpinnings of the proposal were lacking. The Task Force failed to address the most obvious question: in a system that places everyone on a set of continuous dimensions, what is a disorder? And, how does this approach satisfy the manual's definition of mental disorder? The idea that for DSM-5, ‘it's the disorder threshold, stupid’ (Regier et al. Reference Regier, Narrow and Rae2004) – an agenda that would have targeted false positives – was left in the dust. The problem of thresholds was kicked down the road in a Pascal's-wager-type faith that, as Vice-Chair Regier put it, ‘statistically valid cutpoints between normal and pathological’ would somehow eventually emerge from research using severity dimensions (Greenberg, Reference Greenberg2010). As a bold high-risk research program, maybe this made sense; as an approach to revising the field's diagnostic manual in vivo, it seems overreaching to say the least.

As the DSM's definition of mental disorder and my harmful dysfunction analysis of mental disorder (Wakefield, Reference Wakefield1992a , Reference Wakefield b , Reference Wakefield1993, Reference Wakefield1999a , Reference Wakefield b , Reference Wakefield2006) maintain, severity dimensions are insufficient indicators of disorder. To be a disorder, symptoms must be caused by a dysfunction. Disorder inherently involves both harmful symptoms, tracked by severity, and dysfunction, an inferred failure of some psychological mechanism to perform its biological function. Symptom severity does not necessarily reflect dysfunction; many normal conditions are, by any objective standard, symptomatically severe (e.g., normal grief after losing a child, or pain during childbirth), and some disorders are mild. False positives most often occur when harmful symptoms are mislabelled disorders without satisfying the definition's dysfunction requirement (Wakefield, Reference Wakefield1997a ).

Psychiatric epidemiology and the false positives problem

False positives are both a clinical/ethical issue (Wakefield, Reference Wakefield2010a , Reference Wakefield2013b ; Reference Wakefield2015) and a research issue, most of all for epidemiology. In attempting to establish true prevalence of mental disorder in the community, psychiatric epidemiology depends heavily on the ‘conceptual validity’ (Wakefield, Reference Wakefield1992a , Reference Wakefield b ; Reference Wakefield2013a , Reference Wakefield2014) of the DSM's diagnostic criteria for mental disorders – that is, the ability of the criteria to distinguish mental disorders from similar normal-range forms of distress and deviance. Conceptual validity is not the same as construct validity, which concerns identifying one aetiologically homogeneous condition; just as reliability is necessary but not sufficient for validity, conceptual validity is necessary but not sufficient for construct validity of a disorder category because a disorder category that is conceptually valid (i.e., contains only disorders) might still encompass several different constructs (as the category of schizophrenia probably does now). However, conceptual validity at least limits a category to disorders and so eliminates normal pathways to symptoms, thus is a step towards construct validity.

As psychiatry shifted its focus over the past century from the asylum, where patients were generally manifestly disordered, to the community, with its vast amount of non-disordered distress and deviance, psychiatric research – and psychiatric epidemiology in particular – confronted a novel conceptual-validity challenge (Wakefield, Reference Wakefield2010b ; Wakefield & First, Reference Wakefield and First2013a , Reference Wakefield and First b ). Unlike other forms of research using samples preselected for manifest pathology, psychiatric epidemiology generally confronts community distress unfiltered, relying entirely on DSM's diagnostic criteria to discriminate disorder from normality. If DSM has false positives problems, then psychiatric epidemiology has them squared.

The false positives problem has had three periods of unusual salience in American psychiatry's recent history. It first arose with a vengeance during the 1960s and 1970s as a critique of the legitimacy of psychiatry, expressed in diverse critiques that came to be labelled the ‘anti-psychiatry movement.’ The critiques portrayed psychiatric diagnosis as unable to distinguish the normal from the disordered and as a bogus application of medical terminology justifying the use of medical power to control socially disapproved or deviant behaviour. The DSM-III's definition of mental disorder and operationalised symptom criteria were in part a response to these critiques, and a largely successful one.

The second period occurred when the field of psychiatric epidemiology applied the new criteria to community epidemiological surveys in a quest for the true prevalence of mental disorder. The prevalence rates emerging from community studies were much higher than expected, leading to concern about false positives. As Darrel Regier stated at the time, ‘Based on the high prevalence rates identified in both the ECA and the NCS, it is reasonable to hypothesise that some syndromes in the community represent transient homeostatic responses to internal or external stimuli that do not represent true psychopathologic disorders’ (Regier et al. Reference Regier, Kaelber, Rae, Farmer, Knauper, Kessler and Norquist1998, p. 114). Attempts to address the problem by adding clinical significance requirements to symptom criteria (Wakefield, Reference Wakefield1996; Frances, Reference Frances1998; Narrow et al. Reference Narrow, Rae, Robins and Regier2002) failed to yield a satisfying solution (Spitzer & Wakefield, Reference Spitzer and Wakefield1999; Wakefield & Spitzer, Reference Wakefield and Spitzer2002; Zimmerman et al. Reference Zimmerman, Chelminski and Young2004; Wakefield et al. Reference Wakefield, Schmitz and Baer2010).

The false-positives problem was apparent without DSM-5. As epidemiological surveys improved methodologically (e.g., from cross-sectional to longitudinal), prevalence rates increased substantially (Moffitt et al. Reference Moffitt, Caspi, Taylor, Kokaua, Milne, Polanczyk and Poulton2010), to a degree challenging credibility. Moreover, when one out of five boys nationally is diagnosed with attention-deficit/hyperactivity disorder (ADHD) and most are given medication (Center for Disease Control and Prevention, 2013; Visser et al. Reference Visser, Danielson, Bitsko, Holbrook, Kogan, Ghandour, Perou and Blumberg2014), and almost a quarter of all women in their 30 s and 40 s are taking antidepressants, it bears serious consideration whether diagnosis has been untethered from any medical reality.

DSM-5 offered the perfect opportunity to tackle the false positives problem. This was probably the most realistic and important overarching goal DSM-5 could have adopted. Given the growing visibility and social importance of psychiatric diagnosis, there is growing public interest in what is classified as disordered, so this issue cannot be safely hidden away in the obscurities of scholarly discourse. DSM-5's tone deaf approach to this issue brought it repeatedly and justifiably to public and media attention, triggering the current third period of focus on the false positives issue.

DSM-5 false positives progress

The news from DSM-5 is not all bad. Many false positive problems are obvious and, once noticed, are dealt with by adding contextual qualifiers to diagnostic criteria – as, for example, in requiring for selective mutism diagnosis that students are able to speak the language of instruction, a requirement added in DSM-IV. Many changes to each DSM edition consist of such commonsense conceptually driven revisions aimed at reducing false positives, and DSM-5 is no exception. Such changes involve no new empirical evidence, but rather reflect previous revisions’ lack of systematic conceptual reviews. Yet, in a pivotal error, the DSM-5 Task Force rejected proposals to include a conceptual review committee in the DSM-5 revision process to avoid such errors (Kendler et al. Reference Kendler, Appelbaum, Bell, Fulford, Ghaemi, Schaffner, Waterman, First and Sadler2008).

Three DSM-5 commonsense anti-false-positive changes are, first, the addition to insomnia disorder (formerly ‘primary insomnia’) of the criterion, ‘The sleep difficulty occurs despite adequate opportunity for sleep.’ DSM-IV had no such provision so, for example, one could be diagnosed with insomnia disorder if a disruptive shift-work schedule or a neighbour's loud late-night television prevented sleep. Second, DSM-5 oppositional defiant disorder newly excludes diagnosis if the defiant behaviour is directed only at a sibling. As many parents know from firsthand experience, the behaviour described in the criteria can be part of normal if frustrating sibling relations. Finally, in a welcome change that corrects an egregious long-standing oversight, DSM-5 adds to sexual dysfunction criteria the exclusion that ‘The sexual dysfunction is not better explained…as a consequence of severe relationship distress (e.g., partner violence) or other significant stressors’ (p. 433), so an individual who does not sexually respond to an abusive partner is no longer diagnosable as sexually dysfunctional.

There are also some evidence-based DSM-5 changes to prevent false positives. The best example is bipolar disorder. DSM-IV manic episode required ‘abnormally and persistently elevated, expansive, or irritable mood.’ However, a clinical validation study of community epidemiological data showed that a remarkable 71% of bipolar I DSM diagnoses were false positives, due mostly to citing the ‘irritable’ option when in fact there was a contextual cause of irritability (Kessler et al. Reference Kessler, Rubinow, Holmes, Aberson and Zhao1997). A reanalysis of how to distinguish true cases from false positives led DSM-5 to add a requirement for ‘abnormally and persistently increased activity or energy’ to manic episode criteria. Requiring such activity or energy not only prevents irritability false positives but also helps reduce the frequent misdiagnosis of the emotional extremes of borderline personality disorder as bipolar disorder (Zimmerman et al. Reference Zimmerman, Ruggero, Chelminski and Young2008). Given the recent extraordinary rise in bipolar diagnoses in adults and children, this change is probably one of DSM-5's most important.

Granted some victories over false positives by various DSM-5 workgroups, overall the false-positive situation was greatly worsened. I now turn to some examples.

Substance use disorder

DSM-IV had two categories of substance use disorder, dependence and abuse. Whereas dependence had good support as a valid indicator of addiction, extensive evidence indicated that abuse was not a valid disorder category, and research disconfirmed the claim that abuse is prodromal or mild dependence. Attempts to eliminate the category going back to DSM-III-R were rejected for practical reasons. To its credit, DSM-5 finally eliminated this category. However, instead of moving abuse symptoms to the V Codes, DSM-5 merged three abuse symptoms with the seven dependence symptoms and a new ‘craving’ criterion to form an enlarged dependence/addiction category with eleven possible symptoms, renamed ‘substance use disorder’ (SUD) (Hasin et al. Reference Hasin, O'Brien, Auriacombe, Borges, Bucholz, Budney, Compton, Crowley, Ling, Petry, Schuckit and Grant2013).

With a larger pool of eleven rather than seven symptoms, and weaker abuse symptoms now part of the mix, one might think the SUD threshold would be increased above DSM-IV's three-symptoms-out-of-seven requirement. Instead, the workgroup lowered the threshold to two symptoms out of eleven, based on an a priori decision not to lower the overall prevalence of substance use disorders from the DSM-IV level of dependence plus abuse – despite having judged abuse invalid. The two-symptom SUD threshold maintained the former prevalence.

Asked whether the new criteria will pathologise mild conditions, the workgroup Chair, Charles O'Brien, explained, ‘We can treat them earlier. And we can stop them from getting to the point where they are going to need really expensive stuff like liver transplants’ (Urbina, Reference Urbina2012). However, the individuals newly classified with SUD are unlikely to be the ones who eventually need liver transplants, nor is there evidence that the few who do end up with liver transplants would be identified and their later difficulties prevented, nor is there any cost-benefit assessment of diagnosing and treating enormous numbers of non-disordered individuals to attempt to catch a few who may be disordered. And, the numbers are very large; DSM-5 lifetime substance use disorder prevalence is 30–40% or more according to major epidemiological surveys, and only a minority satisfy a more rigorous harmful-dysfunction type criteria set (Wakefield & Schmitz, Reference Wakefield and Schmitz2014d , Reference Wakefield and Schmitz e ; Reference Wakefield and Schmitz2015).

DSM-5's SUD revision allowed continued diagnosis of those with two abuse symptoms (e.g., drives under the influence and argues with spouse about it). Moreover, diagnosis newly applies to those with two dependence symptoms, dubbed ‘diagnostic orphans’ as if they had been incorrectly abandoned. However, studies show that both these groups resemble former abuse cases more than dependence cases in terms of prognosis, and in terms of addiction are probably are mostly false positives.

Elimination of the major depression bereavement exclusion

DSM-5's elimination of the bereavement exclusion (BE) from the diagnostic criteria for major depressive disorder (MDD) was the most controversial diagnostic revision since DSM-III's depathologisation of homosexuality. To opponents, it seemed to fly in the face of common sense and to pathologise a normal if painful human experience. As well, it further expanded the MDD category, already bloated beyond plausibility with over half the population diagnosable at some point in life (Moffit et al. Reference Moffitt, Caspi, Taylor, Kokaua, Milne, Polanczyk and Poulton2010; Rohde et al. Reference Rohde, Lewinsohn, Klein, Seeley and Gau2013).

The BE was evidence-based (Maj, Reference Maj2012; Wakefield, Reference Wakefield2013a ). Grief normally includes depressive symptoms that could be mistaken for disorder, with up to 50% of grievers reaching the 5-symptom DSM-5 MDD diagnostic threshold (Clayton et al. Reference Clayton, Desmarais and Winokur1968), yet sometimes grief triggers true MDD (Parkes, Reference Parkes1964). The BE was designed to guide the clinician in distinguishing normal grief from grief that has transformed into MDD. Longitudinal studies of non-clinical samples indicate that some MDD symptoms (e.g., sadness, insomnia, lowered appetite, difficulty concentrating, lowered interest or pleasure, moderate role impairment) regularly accompany normal loss reactions and are best considered general-distress indicators. Because DSM defines MDD as having any five out of nine symptoms lasting more than 2 weeks, normal grief may spuriously qualify for MDD if it includes five of the general-distress symptoms. To avoid false positive diagnoses of the bereaved, the BE eliminated bereaved individuals from MDD diagnosis if they had only these general distress symptoms. However, bereaved individuals were still diagnosed with MDD if they experienced any one or more of six ‘complicated’ symptoms that went beyond the normal manifestations of grief, including psychomotor retardation, suicidal ideation, sense of worthlessness, marked impairment, psychotic ideation or lengthy prolongation of grief. The elimination of the BE meant that bereaved individuals who manifest five general-distress depressive symptoms for 2 weeks after a loss are now classifiable as having MDD.

Proponents of eliminating the BE were concerned about missing MDD cases, and cited evidence that supposedly supported their ‘similarity thesis’ that excluded cases are just like other standard MDD, for example in having elevated suicide rates and responding to medication. These arguments turned out to be spurious; the cited evidence did not bear on the question, and the existing research supported the BE's validity (Wakefield & First, Reference Wakefield and First2012). The medication evidence, for example, consisted of one small-N uncontrolled study in which the reduction of symptoms in recently bereaved medication users was comparable to that which occurs in unmedicated recently bereaved individuals. Similarly, the claim that excluded cases have elevated suicide attempt rates was examined in four epidemiological data sets and disconfirmed (Wakefield & Schmitz, Reference Wakefield and Schmitz2014a , Reference Wakefield and Schmitz c ). Further epidemiological studies of both concurrent and predictive validity revealed that the negative outcomes characteristic of standard MDD, including recurrence, suicide attempt and anxiety disorders, occurred no more often in BE-excluded cases than in the general population with no history of MDD, unlike standard MDD which had high rates of these negative outcomes (Mojtabai, Reference Mojtabai2011; Gilman et al. Reference Gilman, Breslau, Trinh, Fava, Murphy and Smoller2012; Wakefield & Schmitz, Reference Wakefield and Schmitz2012, Reference Wakefield and Schmitz2013b ). The evidence spoke clearly, but DSM-5 refused to listen.

The controversy was so heated that, as a supposed concession, DSM-5 included a vague note suggesting that clinical judgment is needed in distinguishing normal grief from depressive disorder. The note helpfully abandons DSM-IV's absurd 2-month limitation on normal grief (Wakefield et al. Reference Wakefield, Schmitz and Baer2011a , Reference Wakefield, Schmitz and Baer b ), and acknowledges that stressors other than bereavement can also trigger normal depressive-like reactions, as epidemiological research strongly indicates (Wakefield et al. Reference Wakefield, Schmitz, First and Horwitz2007; Wakefield & Schmitz, Reference Wakefield and Schmitz2013a , Reference Wakefield and Schmitz c , Reference Wakefield and Schmitz2014a , Reference Wakefield and Schmitz b , Reference Wakefield and Schmitz c ). However, unlike the BE, the note includes no inclusion/exclusion symptom guidelines. It is thus invisible to researchers and, by opening every depression diagnosis to clinical judgment, if taken seriously would challenge the usefulness of DSM's criteria in epidemiological research (Maj, Reference Maj2013).

Intermittent explosive disorder

Intermittent explosive disorder (IED) is conceptualised as a pathological failure of control over aggressive impulses, so that angry reactions are disproportionate to the situation. Despite the social importance of out-of-control rage, IED has been relatively neglected in psychiatric nosology and research in contrast to disorders of other emotions such as depression, anxiety, and elation – perhaps, some might argue, because of the lack of dedicated medications. Consequently, DSM-5's substantial changes to IED have largely fallen under the radar of critics. The revised criteria promise to bring IED more to psychiatry's attention by radically expanding the definition.

The challenge in defining pathological aggressiveness is that anger can be naturally intense. DSM-IV attempted to validly distinguish anger disorders from non-disordered anger by their extreme outcomes, requiring ‘several discrete episodes of failure to resist aggressive impulses that result in serious assaultive acts or destruction of property’ (p. 663). However, aggression of this severity is apparently not uncommon; McLaughlin et al. (Reference McLaughlin, Green, Hwang, Sampson, Zaslavsky and Kessler2012) report that ‘nearly two-thirds of adolescents (63.3%) reported lifetime anger attacks that involved destroying property, threatening violence, or engaging in violence’ (p. 1133), with 39.3% of all attacks involving actual violence. To prevent invalidly overdiagnosing IED when there is assaultive or property-damaging behaviour, DSM-5 tightened DSM-IV's requirement regarding assaultive and property-damaging behaviour of ‘several discrete episodes,’ which could have occurred over multiple years, to a requirement of at least ‘three behavioral outbursts…occurring within a 12-month period’ (p. 433), a change that decreases the prevalence of qualified episodes by about a third. This narrowing was based on evidence that the narrower definition improves validity (Coccaro, Reference Coccaro2012; McLaughlin et al. Reference McLaughlin, Green, Hwang, Sampson, Zaslavsky and Kessler2012).

However, DSM-5 then abandoned caution and, based on broader criteria developed by a leading IED researcher (Coccaro et al. Reference Coccaro, Kavoussi, Berman and Lish1998; Coccaro, Reference Coccaro2011), added a vast new domain of less severe angry acts to those that can qualify for diagnosis. An individual can now be diagnosed with IED based on ‘verbal aggression (e.g., temper tantrums, tirades, verbal arguments or fights)’ or ‘physical aggression toward property, animals, or other individuals’ even when it ‘does not result in damage or destruction of property and does not result in physical injury to animals or other individuals’ – if the behaviours occur on average twice a week for at least 3 months (DSM-5, p. 466).

Regarding verbal arguments and fights, it is unclear in what sense such limited aggressive actions are truly out of control. Moreover, in conflicted couples, it is common to think that one's partner's anger is out of proportion to one's offending behaviour. From jealous rage to explosive anger after a lengthy accumulation of minor slights, proportionality is often not maintained in normal intense anger. Controlled intense aggression often takes the form of displacement, where physical aggression is directed towards an object without causing damage, such as kicking or throwing something without breaking it. As to prevalence, Coccaro et al.'s (Reference Coccaro, Schmidt, Samuels and Nestadt2004) 6.32% ECA estimate for this broadened definition will likely prove to be much too low; depression had about the same prevalence in the ECA, and in the most recent longitudinal studies is closer to 50%. Very speculatively, the narrow DSM-IV criteria have a 7.3% lifetime prevalence in the NCS-R (Kessler et al. Reference Kessler, Coccaro, Fava, Jaeger, Jin and Walters2006), and the broader criteria seem to yield roughly 50% greater prevalence than the narrow criteria (Coccaro et al. Reference Coccaro, Schmidt, Samuels and Nestadt2004), and longitudinal studies seem to yield about twice the prevalence of cross-sectional studies (Moffitt et al. Reference Moffitt, Caspi, Taylor, Kokaua, Milne, Polanczyk and Poulton2010), so lifetime prevalence for the new criteria could approach a quarter of the population. Most problematically, DSM-5's broadening of IED was done without epidemiological data illuminating the effect of the change on prevalence or false positives, especially in normal people who are in stressful or conflictual anger-triggering relationships or circumstances.

Attention-deficit/hyperactivity disorder

DSM-5's false positives problem also consisted of ‘acts of omission’ in which DSM-5 failed to address manifest threshold issues. For example, the evidence is overwhelming that ADHD is highly overdiagnosed. Of children in a given school grade, the youngest children have much higher rates of ADHD diagnosis (Elder, Reference Elder2010; Evans et al. Reference Evans, Morrill and Parente2010; Zoëga et al. Reference Zoëga, Valdimarsdóttir and Hernández-Díaz2012), suggesting that normal variations in developmental rate are being mistaken for disorder. ADHD kids have higher rates of normal genetic variants that produce novelty seeking behaviour and less tolerance for boredom, found at higher rates in nomadic populations (Ding et al. Reference Ding, Chi, Grady, Morishima, Kidd, Kidd, Flodman, Spence, Schuck, Swanson, Zhang and Moyzis2002; Eisenberg et al. Reference Eisenberg, Campbell, Gray and Sorenson2008). Brain development studies reveal slower development of inhibitory control in ADHD kids but no abnormal brain growth (Shaw et al. Reference Shaw, Eckstrand, Sharp, Blumenthal, Lerch, Greenstein, Clasen, Evans, Giedd and Rapoport2007; Sripada et al. Reference Sripada, Kessler and Angstadt2014). However, instead of trying to refine the diagnostic criteria to address a massive false-positives problem, the DSM-5 instead altered the ADHD criteria to facilitate expanding diagnosis to adults, which risks perpetuating the same high false positive rate among adults as well by encompassing normal variation within disorder.