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Can Animals Ever Be Used as Valid, and Useful, models for Human Psychopathologies?

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Can animals ever be used as valid, and useful, models for human psychopathologies?

Comparative psychologists and evolutionary biologists have extensively examined animals as models for human psychopathologies, though the degree of validity and usefulness these models hold is disputed (Shelley, 2010).  Animal and Human Psychopathologies share many similarities resulting in extensive animal model usage, however, given biological, behavioural and environmental differences it is debatable as to what degree animal psychopathologies may related to humans (Salgado & Sandner, 2013).  The validity and usefulness of animal modelling is too varied for combined examination, thus the prominent animal psychopathologies of: ADHD, Eating-disorders, OCD, Drug dependency, Depression, Anxiety and Schizophrenia will be independently examined to determine if animals can ‘ever’ be useful and valid models for humans.

In addition to typical measures of validity, animal models should consider Homological validity: the comparability of species, Pathogenic validity: the etiological, causal factors of the psychopathology, and Mechanistic validity: the comparison of the active psychopathologic related mechanisms (Shelley, 2010).

Attention Deficit/Hyperactivity Disorder

The core dimensions of ADHD: impaired sustained attention, impulsivity and hyperactivity can each be objectively measured in animal models, though separately none of these symptoms are unique to ADHD (Fernando & Robbins, 2011).  Ji, Kim, Park and Bahn (2014) assert rat studies have been of paramount importance in understanding the long-term effects of ADHD; rats are excellent models as they possess biologies, diets, behaviours, illnesses and habitats similar to humans.

The spontaneously hypertensive rat breed/model displays many ADHD behaviours (Ji et al., 2014), these animals have heightened impulsivity, primarily, but little testing has been done to assess them on formalised adapted ADHD tests, limiting their usefulness beyond face validity (Fernando & Robbins, 2011).  The Five-choice serial-reaction time task (5CSRTT) is an animal cognitive test which requires sustained attention, rats often display abnormal impulsivity in their choices at the cost of food, and abnormal hyperactivate movement in cages, this suggests naturally occurring ADHD and subsequent pathogenic validity (Blondeau & Dellu-Hagedorn, 2007).  ADHD has been linked to working memory deficits, which is also reflected by rats on delayed alternation tests, rats showing multiple ADHD symptoms do not appear in large numbers, however (Arnsten, 2006).  Construct validity of these behaviours being ADHD related can somewhat be assessed via methylphenidate, d-amphetamine and atomoxetine medications which effectively reduce these ADHD symptoms in humans; rats demonstrating ADHD symptoms are similarly affected, this is attributed to the targeting of hypothetically responsible genetic precursors impairing dopamine transporters and DAT knockouts (Irintchev, 2011).  Furthermore, rats who display ADHD behaviours on 5CSRTT tests have been used as models for ADHD specifically because methylphenidate, a medication effective in humans, normalises performance.

Usefully, ADHD treatment proposals have been made based on rat studies: spontaneously hypertensive rats displayed hyperactive suppression only during 30-minute exercise blocks, researchers suggest this regiment be transposed to humans (Ji et al., 2014).   Bock, Breuer, Poeggel and Braun (2016) further suggest the usefulness of rodents in identifying and treating ADHD behaviours through cognitive examinations; using functional imaging of methylphenidate treatments the researchers concluded that rats and humans likely share unique hypothesized cognitive pathways, thus further examination of this homologically valid structure may improve cognition-based treatments.

There are considerable issues with these models: rats with apparent high impulsivity and hyperactivity fail to demonstrate attentional selectivity suggesting this factor may be distinct to humans, lessening etiologic validity and therefore usefulness (Mill, 2007).  However, human ADHD diagnoses can be made on non-universal ADHD symptoms, somewhat validating this variability (Dalley & Robbins, 2017).

Eating Disorders

Compulsive eating.  There is excellent face validity for this research: Rats solely consuming ‘chow’ in restricted feeding paradigm models demonstrate stressful behaviour and enlarged caloric intakes following the presentation of palatable food mirroring human stress-based models of binge eating, addiction and inhibitory control disorders (Fernando & Robbins, 2011).

Compulsive binge eating behaviour is apparent in clinical rat populations (O’Brien, 2008).  Binge eating is the poorly-controllable consumption of large amounts of food, perceived-control cannot be identified in animals however, fundamentally limiting the research (Avena & Bocarsly, 2012).  Regardless, rats may excessively consume palatable food at the cost of their health despite access to healthier alternatives, in opposition to the evolutionary fitness principal which suggests such animals utilise the most beneficial food available (Kim, 2012)  Examinations have found administration of the opiate receptor antagonist Nalmatrene reversed this behaviour, this treatment has previously treated alcohol addiction relapses and thus has been suggested for humans experiencing compulsive eating disorders, demonstrating usefulness (O’Brien, 2008).  Researchers have suggested the similarity between rodent and human brains adds homological validity to such research, which has proved especially useful in providing insight into neuropeptides and neurotransmitters involved in sugar binge eating (Murray, Tulloch, Chen, & Avena, 2015).

Despite face validity, it should be noted Alboni and colleagues (2015) claim rodent research on eating disorders often fails to account for pre/post Estrus timing which alters rats’ stress and eating behaviours.  Furthermore, artificial food restrictions have increased compulsive eating in BED and bulimia, however animals lack this behaviour suggesting complex homological differences (Kim, 2012).

Anorexia.  Anorexia nervosa is a human psychopathology characterized by undereating, reduced-weight and failure to acknowledge this behaviour as harmful; human anorexia may be better understood by examining the animal Activity anorexia model, a condition in which rats excessively exercise while lowering food intake (Kim, 2012).  AA rats are considered a useful model for AN as both groups circumvent their homeostatic survival mechanism of eating, furthermore excessive exercise often occurs in AN (Kim, 2012).

Research confirms rats with unrestricted wheel access but restricted food access, frequently starve themselves while increasing their exercise, this does not occur if both factors are restricted, or unrestricted, or if trained not to (Gutierrez, 2013).  This has been linked to cognitive reward systems as the rats run as though foraging to acquire more food, AN has also been linked to a reward-system in the form of perceived social acceptance, demonstrating functional validity (Fuglset, Landrø, Reas & Rø, 2016).  Furthermore, anorexic rat preferences for positive reinforcement stimulus over food further supports the reward-system model (Avena & Bocarsly, 2012).  Decreases in food intake increases 5-HT levels in the hypothalamus of both species, correlating with stress-based explanations for anorexia, this predominantly effects females which further correlates with human research suggesting mechanistic validity (Fuglset et al., 2016).  Rhesus macaque studies also demonstrate hyperactivity in response to long-term food restriction strongly implicating potential usefulness to human research (Kim, 2012).  Despite apparent validity and usefulness AA is undocumented as naturally occurring, unlike AN, and may not be ecologically valid (Gutierrez, 2013).

Obsessive-Compulsive Disorder

OCD is broadly divided into obsessive thoughts and compulsive behaviours, it is attributed to failures in behavioral and cognitive inhibitory functions (d’Angelo et al., 2014).  A comprehensive animal OCD model may not be possible, animals display compulsive behaviours but cannot demonstrate obsessive thought (Alonso, López-Solà, Real, Segalàs & Menchón, 2015).

The behavioural ‘signal attenuation model’, highlights a compulsive behaviour disorder in rats that are trained to press a lever when fed to continue receiving food, this behaviour may continue even following dissociative conditioning; inappropriate orbitofrontal cortex activity in these rats, as in humans with OCD suggests homological validity (Klavir, Winter & Joel, 2011).  Conversely, the rats simply may fail to recognise the end of the behavioural sequence and problematically, the rats likely do not recognise this behaviours as excessive (Alonso et al., 2015).

Animal research of rats, parrots, dogs, and some non-human primate species has helped identify heritable genetic elements of OCD (d’Angelo et al., 2014).  Research on Canine compulsive disorder which has demonstrated strong mechanistic validity via cross-species subcortical perfusion and hypothalamic availability in compulsion disorders (Vermeire et al., 2012); the mutation of canine chromosome 7 has spawned chromosomal research into human OCD, demonstrating a detached usefulness (Dodman et al., 2010).  Pharmacologically, rats were given SSRIs to block dopamine D2/D3 receptors, this increased compulsive checking behaviours during travel implicating dopamine in OCD, this has usefully directed research towards dopamine deficiencies (Alkhatib, Dvorkin-Gheva & Szechtman, 2013).  Marmoset monkey studies, showing homological validity, definitively demonstrated serotonin impairs reversal learning; serotonin reuptake inhibitors have since become more common in OCD treatments (Clarke, Hill, Robbins & Roberts, 2011).  A critical fault of animal genetic psychopathology modelling is the lack of comorbidity, humans with OCD often display comorbid anxiety disorders, for example.  Animals rarely show similar comorbidities, via genetic, pharmacological, or cognitive homologs (d’Angelo et al., 2014).

Shared cognitive markers have been observed through animal models suggesting mechanistic validity: research has identified putative neurocognitive endophenotypes activity (distinct genetic markers; Chamberlain et al., 2008).  MRI readings indicate parietal cortex change and orbitofrontal cortex and inferior prefrontal grey matter loss, based on rat performance in sorting/organisational tasks (Menzies et al., 2008), and blood-oxygen level reduction within the orbitofrontal cortex during reversal-learning tasks (Chamberlain et al., 2008).  Furthermore, extradimensional set-shifting which relies on OCD-like repeated activity has been demonstrated to rely on the caudate nucleus in marmoset monkeys and the homolog prefrontal cortex in mice; reversal-learning has shown dependence on orbitofrontal cortex integrity suggesting homological validity (Fernando & Robbins, 2011).  Cognitive studies have usefully implicated the use of the caudate nucleus in OCD behaviour.  Rat lesion models identified the prefrontal cortex and medial striatum showed deficits which was matched to subtler developments in human brains (Clarke et al., 2011).  Despite animals and humans sharing OCD cognitive markers, humans display OCD behaviour beyond what is expected to be associated with these minor grey matter and metabolism decreases, whereas animals with OCD tendencies show less varied behaviours, limiting the etiological validity and subsequent usefulness of the model (Alkhatib et al., 2013).

Drug dependency

Drug dependency animal models have excellent face validity as this commonly occurs in both humans and various animals in an ecologically valid manner (Venniro, Caprioli & Shaham, 2016).  Drug dependency is characterized as spending excessive amounts of time acquiring a substance and continued use despite knowledge of harm followed by an inability to end usage, although animals may not recognise drug-related harm, animals will perform increasingly effortful behaviour to acquire addictive substances, resist punishment and conditioned suppression, and demonstrate extreme difficulty and unwillingness to stop substance intake when relevant (Wise & Koob, 2014).  Considering 17% of both rat and human drug users develop dependency, rat studies show a strong pathogenic validity (Deroche-Gamonet, Belin & Piazza, 2004).  A neural model shows mechanistic validity as both humans and rhesus monkeys show drug users’ DA D2/D3 receptors change, predicting future cocaine self-administration (Nader et al., 2006).

The Pavlovian and instrumental dependency models suggest self-administration of chemicals results in a maladaptive stimulus-response relationship for drug addiction in which the behavioural and biological demands of the addictive chemicals creates user problems (Wise & Koob, 2014).  This model forms the extinction-reinstatement model which has usefully demonstrates the behavioural differences between substance dependents and substance-related sensation seekers; a study demonstrated previously cocaine addicted rats were more likely to seek the substance when exposed to novel stimuli which had been conditioned to be associated with experiences of substance intake.  When applied to human abusers it was found dependents demonstrate both impulsivity and sensation-seeking, while sensation seekers demonstrated better self-control to conditioned stimulus.  This research can be applied to relapse treatment and research (Belin, Mar, Dalley, Robbins & Everitt, 2008).  A key limitation of these studies is findings implicating genetic predispositions to addiction in animals, which although adding face validity, reduces construct validity (Nader et al., 2006).  Furthermore, some animals show no addictive behaviour towards substances, such as rats and heroin self-administration, this suggests varying unknown resistances to substances which limit the comparative usefulness of animals (McNamara, Dalley, Robbins, Everitt & Belin, 2010).

The drug-relapse model utilises animals who achieve voluntary extinction of addiction through paired adverse consequences and alternative reinforcement; drug associated cues, stressors and small drug doses, mirroring humans demonstrate predictive validity by predicting relapse.  This research has identified locomotor factors, drug use pattern and sex as relapse factors and has been of great use to humans (Venniro et al., 2016).  Teicher, Tomoda and Andersen (2006) suggest animal studies may be confounded by previous animal drug behaviours, which often cannot be recorded, for example apes often experience physical abuse and respond by seeking stimulants, this normalised behaviour can alter behaviour prior to ecological tests.


Animal depression models are difficult to formulate due to poor biomarkers and the subjectivity of animal emotion recordings (Czéh, Fuchs, Wiborg & Simon, 2016).  Depression is a major mood disorder characterized by cognitive, emotional, homeostatic and psychomotor impairment; however, animal studies can only measure homeostatic symptoms, psychomotor behaviour, anhedonia (an emotional symptom), and over-activity of the stress regulating hypothalamic-pituitary-adrenal (HPA) axis which, while common to both species is not always active in clinically depressed humans (Nestler & Hyman, 2010).  Despite debatable validity, it has been suggested that animal models may be necessary for potentially useful but difficult to ethically test antidepressant medication (Shirayama et al., 2015).

Learned helplessness (LH) is a behavioural model suggesting exposure to unavoidable and inescapable stress impairs goal-directed behaviour: as neural examinations suggest instrumental responding is reduced by depletion of the central monoamine neurotransmitters in both humans and animals the model therefore demonstrates construct validity (Shirayama et al., 2015).  Animals symptoms of LH including: loss of weight and apatite, psychomotor retardation, and anhedonia mirror human symptoms, furthermore clinical treatments including tricyclics, MAO inhibitors, atypical antidepressant are effective in reducing LH behaviour increasing pathological and predictive validity, however there is no direct neural evidence for LH in humans (Belzung & Lemoine, 2011).  Understanding depression’s neural basis has been advanced through animal models of LH: Amat and colleagues (2005) demonstrated when inactivated the rat infralimbic cortex disrupts the regulation of serotonin neurons within the dorsal raphe that typically activates during the learning of active avoidance strategies for stress.  This has been linked to human causal stress in specific brain areas and informed research (Czéh et al., 2016).  Animals with supposed LH may instead be displaying ‘learned-inactivity’, (conserving energy when expenditure is useless) this may invalidate data (Belzung & Lemoine, 2011).

The Behavioral Despair Model is a form of LH with a high level of pharmacological isomorphism, indicating predictive validity, however it is limited by many false positives as medication developed from animal studies is not always effective on humans indicating depression may be mediated by separate mechanisms between species and a lack of cross-predictability/convergent validity (Montalvo-Ortiz et al., 2016).  Administration of antidepressants prolongs rats’ efforts in forced swim and tail-suspension tests which inevitably result in inactivity and despair/depression-like behaviour (Nestler & Hyman, 2010).  Stress is often seminal in depression, rats experiencing the aformentioned despairing experiences also display chronically increased stress-indicating behaviour, demonstrating construct validity (Czéh et al., 2016).  David and colleagues (2009) used cortisol treatments to induce a depression-like syndrome in rats affecting open field, forced swim, and feeding behaviour.  Antidepressant fluoxetine reversed all but feeding suppression which suggested differing biological mechanisms for various depression and anxiety behaviours in the hippocampus.  These tests have been useful in the examination of antidepressant efficacy and particularly gene ß-arrestin 2, which indicates a potentially strong role of genetic factors in depression.

The Social stress model for depression, useful for studying resilience, it suggests social isolation and social subordination can cause depression-like symptoms and a metabolic syndrome in rats.  Like humans, rats show high individually varying resistance, though inducing these symptoms requires significantly more stress than humans.  Symptoms can be reversed with antidepressants showing predictive validity (Nestler & Hyman, 2010).

Reward modelling suggests symptoms of depression worsen following negative feedback or undesirable rewards, this may be attributed to a failure to deactivate the amygdala, likely due to prefrontal influence (Fernando & Robbins, 2011).  This has been supported by studies showing rats in modified probabilistic reversal tasks demonstrate similar behaviour following serotoninergic manipulations, this highlighted the importance of citalopram which can increase or decrease such behaviour depending upon dosage; however, despite pharmacological validity the overtness of rewarding indicates poor construct validity(Czéh et al., 2016).  Intracranial self-stimulation (ICSS) modelling is the use of direct stimulation of cognitive pleasure centres to simulate rewards, it has been demonstrated rats exposed to consistent and uncontrollable stressors display protracted decreases in ICSS value, this mirrors human Anhedonia (Nestler & Hyman, 2010).  ICSS demonstrates construct validity and usefulness as it addresses a specific process able to be neurobiologically investigated (Belzung & Lemoine, 2011).  This shows problematic etiological validity however as ICSS is addictive to rats but addictions are not reduced in human depression (Cosgrove, Kelsoe & Suppes, 2016).

Anxiety disorders

Anxiety disorders contain many elements that are difficult to quantify, however research suggests animal anxiety modelling passes the criteria for several forms of validity and may be useful for human anxiety research (Campos, Fogaca, Aguiar & Guimaraes, 2013).  General Anxiety disorder is defined as pervasive, persistent and uncontrollable feelings of worry, panic and unease regarding events (Bishop, 2007).  Although animal anxiety research has yielded important results, the evolutionary importance of fear in hostile environment dwelling species can confound comparisons (Campos et al., 2013).

Behavioural Predator-Prey models demonstrate some pathogenic validity: rats, when consistently exposed to fear-inducing cats were later exposed to cat scent, some rats developed PTSD-like symptoms including impaired functionality and interrupted circadian rhythm which increased the likelihood of developing anxiety-like behaviour in unrelated circumstances.  The study demonstrates the comorbid nature of these fear-response disorders, (Campos et al., 2013).  Anxiety patients have been noted to overvalue environmental and situational markers of safety, such individuals often actively seek such markers and perhaps unconsciously attribute their safety to this seeking behaviour (Fernando & Robbins, 2011); adding these markers to mice extinction trials hindered the extinction of the affective CS furthering anxiety, indicting ecological validity (Salkovskis, 1991).  Animal studies have directed attention towards this phenomenon, treatments often acknowledge this research and remove safety markers (Fernando & Robbins, 2011).  Animal studies such as these may be best equipped to conduct potentially uncomfortable research (Toth, Neumann & Slattery, 2012).  Rats manipulated to experience less social interaction more often display Anxiolytic-like behaviour, this social-interaction model may demonstrate etiological validity as the rats mirror humans in their subsequent social withdrawal, however ecologically valid occurrences of this phenomenon are unobserved (Green, Barnes & McCormick, 2013).  Despite advances, there lacks information about the emotional component of animal anxiety which is considered an intrinsic part of human anxiety, limiting pathogenic validity (Cohen et al., 2015).

Pharmacological models of anxiety have proven useful when paired with established human extinction therapy: D-cycloserine was developed to target specific glutamate receptors active during anxiety behaviour in mice during extinction of fear towards a CS in clinical trials, Agoraphobia (an anxiety related disorder) patients when administered this drug during therapy display significantly increased success rates (Fernando & Robbins, 2011).  Furthermore, mice models demonstrated an inhibition of protein synthesis in the amygdala can effectively erase fear triggering memories, this principal, known as the reconsolidation of fear memory, has resulted in large research efforts for pharmaceuticals for PTSD and drug abuse victims in exposure therapies demonstrating excellent human applicability (Myers & Carlezon, 2012).  These models are accredited as exceptionally useful to human anxiety research; mice studies identified that the amygdala and hippocampus can mediate fear responses to contextual fear.  This was later identified in humans indicating mechanistic validity of the cognitive anxiety process, this research also implicated limbic anxiety regulation via the ventromedial prefrontal cortex in both species (Bishop, 2007).  The development of pharmacological treatments, mainly benzodiazepines (serotoninergic drugs) from rodent studies has proven effective for GAD treatment, further demonstrating construct validity; however, this treatment is not always effective on humans further implicating the limitations imposed by biological differences (Fernando & Robbins, 2011).  Furthermore, anxiety models are criticised for lacking information on non-rodent animals, observations of Anxiolytic behaviour in other species exists, however, little testing has been conducted limiting homological validity (Battaglia, Ogliari, D’Amato & Kinkead, 2014).  Regardless, Green and colleagues (2013) summarize, animal Anxiety modelling has facilitated massive advances in understanding the neural basis of anxiety in both conditioning and defence behaviour hierarchy.


Schizophrenia is a degeneration of thought, emotion and behaviour resulting in abnormal perceptions, behaviours, feelings and delusions; due to the complexity of the disorder animal studies have only been able to model positive, negative and biological symptoms independently (Patterson, 2009).  There are various seminal issues which limit schizophrenia model usefulness: neural evidence for animal hallucinations is weak and animals cannot report them and modelling of negative schizophrenia symptoms is pathogenically invalid as they have extensive comorbidity (Nestler & Hyman, 2010).

The deficits of the neural systems on cognitive ability is not well modelled in animals (Swerdlow & Light, 2016).  Memory disturbance from damage to the medial temporal lobes causing cognitive control, planning, working memory and cognitive flexibility deficits (Fernando & Robbins, 2011) may be measured by animal models: Schizophrenia impaired set-shifting incorporates these abilities and is improved by administration of the stimulant modafinil phencyclidine in rats and humans demonstrating mechanistic validity (Goetghebeur & Dias, 2009).  Gaskin, Toledo-Rodriguez, Alexander and Fone (2016) report animal models have been suggested as a possible way to invasively assess schizophrenia’s active neural symptoms.  A core issue with this research is that environmental factors considered crucial in schizophrenia are not addressed; environmental models have been attempted using viral infections to induce behavioral and neural abnormalities, but the role of such infection in schizophrenia is disputed, neither pathological nor construct validity can be claimed (Patterson, 2009).

The Sensorimotor Gating Model is a prominent molecular model; humans with schizophrenia have a deteriorated ability to gauge and filter sensory stimuli, which is dependent upon the gating of P50, rats use the homolog gate N40, impairment is linked to cognitive deficits (Nestler & Hyman, 2010).  Prepulse inhibition of startle (PPIoS) is linked to reactions, impaired by schizophrenia, and can be easily examined in animals and humans, furthermore the process is independent from learning or instructional comprehension, increasing its’ usefulness (Romero, Guaza, Castellano & Borrell, 2010).  Examinations of PPIoS in rats has provided extensive construct, convergent and predictive validity for this animal model (Nestler & Hyman, 2010).  However, these deficits are not unique to schizophrenia and as it examines: dopaminergic, noradrenergic, and cholinergic manipulations it may be over-representative, limiting the usefulness of specifying gateway effects (Swerdlow & Light, 2016).

Human schizophrenia is understood to contain a genetic component, animal models have highlighted genetic abnormalities (Swerdlow & Light, 2016).  Studies have linked a P50 gating deficit and a chromosomal marker associated with the gene for Nicotinic acetylcholine receptor α7 subunit, inbred mice with abnormal chromosome markers demonstrate higher N40 ERP deficiencies.  This mechanistic validity provides a bias for the use of molecular biology techniques to invasively investigate schizophrenia from a cross-species perspective, making the mode of great use to humans (Young & Geyer, 2013).  Recently, comparative models identified N40 ERP is most deficient in alpha-7 nicotinic receptors, giving molecular biologists an opportunity to invasively examine this potential area of cognitive impairment (Nikiforuk, Kos, Hołuj, Potasiewicz & Popik, 2016).  The primary issue with genetic models is low construct validity via high variability, for example a Disc1-gene mutation of chromosome 22q11.2 microdeletions produces a schizophrenia-like syndrome in 30% of cases, though mice have been bred with homolog mutations to explore these links these mutations are associated with multiple disorders (Nestler & Hyman, 2010).

Social isolation is a common factor for schizophrenia and is believed to exacerbate non-biological issues, rats with deficits in N40 ERP receptors demonstrating schizophrenia like symptoms also preform considerably worse than normally functioning lab rats when socially isolated, thought this shows some etiological validity and attempts to address social-dimensions ecological validity is lowered because this isolation is not observed naturally (Gaskin et al., 2016).


The many animal models for various psychopathologies demonstrate independent and varying levels of validity and usefulness to humans, animal modelling has a long history and as techniques advanced the necessity, validity and usefulness of such models may decline, contemporary researchers have argued: though animal models may be valid it is less useful for humans due to homological limitations (Swerdlow & Light, 2016).  However, animal models have provided useful contributions to the field and will likely continue to do so.  Prominent arguments against animal model validity can be dismissed for various reasons: Pseudoscientific; because contemporary research has become rigorous, Disanalogy; as evolutionary homolog biology and behaviour is compensated for by weaker conclusions and specialised testing, and Predictive validity; as this varies between independent models too much to collectively be argued (Shelley, 2010).


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