The Problem With Using Animals to Study Depression
The basic supposition behind all animal models of depression is that stress is the primary cause of depression. This belief is crude and naïve, and it fails to show an adequate appreciation for the complex and diverse social factors that often underlie depression. Neuroscientist Hymie Anisman and psychologist Kim Matheson from Carlton University express a common critique of the “stress theory,” stating, “To be sure, while there is abundant information suggesting a causal relationship between stressors and the evolution of depression, it may also be the case that depression itself, or the negative perceptions associated with it, may generate stress reactions ….”3 In other words, depression likely causes stress. Animal researchers mistakenly reverse this relationship by trying to use stress to cause depression—they have it backwards.
Michel Bourin, Alexandra Fiocco, and Florence Clenet, medical professors at the University of Nantes, take their criticism of the stress assumption a step further, writing, “Indeed, clinical data show that the incidence of depression reflects 5 [to] 10 percent of the population, suggesting that chronic stress plays no role in the etiology of depression ….”4 In contrast to most humans, animals in laboratories all experience constant stress caused by the conditions in which they are housed, handled, and experimented on, making their situations entirely irrelevant when considering the effect that normal human living conditions play in the development of depression in people.
While animals certainly get depressed, they do so for very different reasons than humans do and display symptoms that are very different from those of depressed humans. Michael O’Neil and Nicholas Moore, experts in anti-depressive drug development at Lilly Research Laboratories, also question the practice of using animals to study depression, observing, “The symptoms of depression rely on a patient’s ability to report subjectively experienced conditions, while the observable signs of depression, such as decreased eye contact and tearfulness, are relatively few and not always specific to depression, not to mention difficult to observe in animals.”5 In other words, depression is a cognitive disorder that is grounded in the perceptions and beliefs of the patient, and observations of stressed-out animals can’t tell us anything about these key internal causes and symptoms.
Anisman and Matheson comment further on the importance of psychological factors that are not observable in animals, writing, “Clearly, in humans, it is essential to consider aspects of the stressor in relation to individual characteristics and with respect to the psychological repercussions that ensue. Of course, one is hard-pressed to simulate all these conditions within an animal model.”6 Bourin et al put it more firmly, stating, “The heart of the problem lies in the identification and the assimilation of the troubles that are observed in animals to those that clinicians have described in human beings. The major anthropomorphic drift, which consists of depicting and labeling behavioral states of animals utilizing a cognitive and emotional jargon invented for human psychiatric disorders, limits our understanding of these behaviors.”7 Simply stated, animal researchers attempt to interpret psychological disorders in animals by using the language of clinical psychology, but that is so inappropriate that it only leads to false and misleading comparisons.
One of the key components of the successful treatment of human depression is social support—particularly for women. But these complex relations cannot be studied in animals. Anisman and Matheson comment, “Yet, one is again faced with the fact that social processes in animals likely do not involve the multiple provisions (i.e., having different functions depending on experiences and situations) that are characteristic of social support in humans.”8 Animal researchers again ignore key factors that cannot be accommodated by their narrow paradigm.
Animal tests have not improved clinical outcomes for depressed human patients because they have failed to produce reliable results. Bourin et al state, “Exporting tests from the laboratory of origin continues to be problematic. This is due to differences in methodology and environmental parameters. Such differences in methodological factors, including animal strain, age of species, and time of testing, lead to variability in results.”9 This comment pertains to inconsistency within the same species, so imagine the inconsistency that obviously occurs when results are extrapolated from mice to women. This problem is inherent in all animal research, and despite the sweeping claims of vivisectors about the merits of their “controlled laboratory settings,” they consistently fail to produce reliable results that can be applied to humans.
The original antidepressant medications and those that were subsequently developed were not discovered through animal research. O’Neil and Moore point out that the first antidepressant drugs were discovered by practicing physicians who noted the drugs’ effects while using them to treat tuberculosis.10 In fact, most pharmaceuticals used to treat depression and other diseases are discovered by doctors working with human patients—laboratory researchers who conduct experiments on animals merely confirm these findings.
The claims of vivisectors are also at odds with the fact that numerous antidepressants are useful on humans but have no effect on depressed animals and the fact that an equally large number of drugs help depressed animals but offer no benefit to humans. Finally, when vivisectors claim that it is useful to test drugs on animals, they ignore the fact that contradictory findings often result when different species and breeds are tested and when different types of tests are administered.
Animal Models of Depression—Cruel and Invalid >>
3. Anisman and Matheson 527.
4. M. Bourin, A.J. Fiocco, and F. Clenet, “How Valuable Are Animal Models in Defining Antidepressant Activity?” Human Psychopharmacology: Clinical and Experimental 16 (2001): 9-21.
5. Michael F. O’Neil and Nicholas A. Moore, “Animal Models of Depression: Are There Any?” Human Psychopharmacology: Clinical and Experimental 18 (2003): 239-254.
6. Anisman and Matheson 529.
7. Bourin, Fiocco, and Clenet 9.
8. Anisman and Matheson 534.
9. Bourin, Fiocco, and Clenet 18.
10. O’Neil and Moore 239.
