In recent years, the introduction of a medical model of dog behavior has led some practitioners to treat adjustment problems as mental disorders having physical causes and often to emphasize the role of disease as the underlying cause of behavior problems. Although the medical model is not entirely without merit, as some valid parallels exist between certain psychiatric disorders and canine behavior disorders and undoubtedly some behavior disturbances are the result of disease, overly speculative assumptions, problematic diagnostic labels, and an excessive reliance on psychotropic drugs based on rationale borrowed from human psychiatry serve only to compound the current puzzlement regarding the etiology and functional significance of canine adjustment problems. In addition to emphasizing disease etiologies and the importance of drugs to treat behavior problems, many practitioners who stress the medical model claim special authority pertaining to matters of diagnosis whereby the “physical” causes of the problem are purportedly identified, usually by means of speculative inferences from emotional and behavioral signs. These putative but unproven physical causes are then targeted with various medications believed to mediate a resolution of the problem. Unfortunately, the various inclusion and exclusion criteria used to make behavioral diagnoses and related drug-treatment decisions tend to cause referring professionals and owners to defer treatment until the canine adjustment problem reaches a form that threatens the dog with relinquishment or euthanasia, rather than initiate behavioral treatment at the first sign of a problem. The pharmacological approach resonates with the low-power owners basic assumptions, placing the causes of the dog’s adjustment problems beyond the scope of conventional training and socialization efforts. The adjustment problem is encapsulated within an involuntary subdomain of physiology that places it outside of the dog’s voluntary control and prevents its resolution without the help of drugs. In contrast, the cynopraxic approach views the physical changes to brain that mediate disturbance as the result of the accumulative effect of conflictive social exchanges and reactive adjustments in response to environments chronically lacking sufficient predictability and controllability to promote an adaptive coping style. Conversely, by changing interactive habits of social exchange to promote interactive harmony in combination with appropriate quality-of-life changes that support the dog’s needs, the physiological causes of disturbance are replaced by physiological changes conducive to adaptive optimization and social adjustment.

Although drugs are potentially useful in some refractory cases, the current state of the art remains investigational, and the ultimate benefits of drug therapy are uncertain, especially with respect to the control of domestic aggression problems (see Pharmacological Control of Aggression). Even in the realm of human psychiatry, the efficacy of the most commonly prescribed mood-altering drugs used to treat anxiety and depression disorders has been questioned. Kirsch and colleagues (2002), for example, who performed an extensive meta-analysis of treatment data submitted to the U.S. Food and Drug Administration (FDA) between 1987 and 1999, found that 80% of the clinical response of humans to six commonly prescribed antidepressants was duplicated in placebo control groups, suggesting that the selective serotonin reuptake inhibitors (SSRIs) tested may have little clinical effect separable from that of placebo. A remarkable neuroimaging study of human patients treated for depression has shown that placebo responders and fluoxetine responders show similar changes in glucose metabolism in specific cortical and limbic areas, concluding that the “administration of placebo is not absence of treatment, just an absence of active medication”. In addition, the study revealed that the two groups responded differently to fluoxetine, with the drug producing specific changes in the hippocampus and brainstem of fluoxetine responders after 1 week of therapy that predicted a long-term response to the medication. Responders also showed a switch effect in response to drug therapy that resulted in an initial elevation of posterior cingulate metabolic activity followed by a decrease and then a gradual increase over the 6-week period of therapy — a pattern of change not exhibited by placebo responders. These distinct metabolic changes that differentiate responders from nonresponders suggest that tympanic temperature fluctuations might be present among dogs that could be tracked to help identify serotonergic responders from nonresponders (see Functional Lateralization and Tympanic Temperature).

Although the FDA appears to enforce strict standards of efficacy to gain approval on certain classes of drugs, there appears to be a troubling double standard with respect to others, perhaps including the level of stringency applied to psychotropic drugs such as SSRIs. However, the most egregious and disturbing example of a double standard used to evaluate drug efficacy is the special and protected status afforded to homeopathic substances, described by one FDA representative as “kinder, gentler medicine”. Incredibly, homeopathic remedies are approved as drugs without meeting the rigorous standards of proven efficacy set for other drugs issued FDA approval. A meta-analysis of 89 studies using homeopathic substances to treat various medical conditions concluded, “Our study has no major implications for clinical practice because we found little evidence of effectiveness of any single homoeopathic approach on any single clinical condition”.

With regard to serotonergic antidepressants and dog behavior problems, even when apparently efficacious in the short term, aggression-controlling medications are unlikely to succeed in the long term without the support of complementary behavior therapy. The therapeutic use of social placebo is acknowledged as a valuable tool in the cynopraxic treatment of behavior problems (see Social Placebo), but the administration of costly psychotropic drugs that exert potential health-threatening side effects for the sake of questionable benefits that do not rise above placebo alone raises serious ethical and welfare concerns. In any case, no drug or combination of drugs currently available can provide the sweeping range of dramatic and subtle balancing and integrative effects that are mediated by cynopraxic training and play therapy (see Modulatory and Unifying Effects of Play). Comprehensive cynopraxic training and therapy efforts promote changes that facilitate a functional equilibrium at virtually every level of neural organization. Cynopraxic therapy is based on the assumption that social exchange promoting adjustments conducive to an adaptive coping style and secure attachments serve simultaneously to mediate physical alterations of the neuronal substrates mediating social ambivalence and reactive behavior. In particular, play therapy represents a potent tool for adjusting autonomic imbalance and reducing the allostatic load perturbing the complex feed-forward trafficking of neuronal networks that contribute to the etiology of adjustment problems (see Cynopraxis: Allostasis, Adaptability, and Health).

When drugs are used to manage intractable behavior problems, the goal should be to alleviate allostatic load and to promote neurobiological changes conducive to social affiliation and playfulness. Pharmacological efforts used merely to suppress undesirable behavior seem wrongheaded, violate the dead-dog rule, and are intrinsically problematic with respect to the basic bond and quality-of-life tenets of cynopraxis. Dogs that engage in autoprotective behavior usually do so out of emotional extremis associated with chronic stress and allostatic load. Using behavior modification, restraint and isolation, emotional deprivation, or drugs to suppress undesirable behavior, without alleviating the underlying social and environmental causes hindering a dog’s ability to cope adaptively, violates basic welfare principles.

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