Chemical imbalance. Thanks in part to the success of direct-to-consumer marketing campaigns by drug companies, the notion that major depression and allied disorders are caused by a “chemical imbalance” of neurotransmitters, such as serotonin and norepinephrine, has become a virtual truism in the eyes of the public (France et al., 2007; Deacon and Baird, 2009). This phrase even crops up in some academic sources; for example, one author wrote that one overarching framework for conceptualizing mental illness is a “biophysical model that posits a chemical imbalance” (Wheeler, 2011, p. 151). Nevertheless, the evidence for the chemical imbalance model is at best slim (Lacasse and Leo, 2005; Leo and Lacasse, 2008). One prominent psychiatrist even dubbed it an urban legend (Pies, 2011). There is no known “optimal” level of neurotransmitters in the brain, so it is unclear what would constitute an “imbalance.” Nor is there evidence for an optimal ratio among different neurotransmitter levels. Moreover, although serotonin reuptake inhibitors, such as fluoxetine (Prozac) and sertraline (Zoloft), appear to alleviate the symptoms of severe depression, there is evidence that at least one serotonin reuptake enhancer, namely tianepine (Stablon), is also efficacious for depression (Akiki, 2014). The fact that two efficacious classes of medications exert opposing effects on serotonin levels raises questions concerning a simplistic chemical imbalance model.

Love molecule. Over 6,000 websites have dubbed the hormone oxytocin the “love molecule” (e.g., Morse, 2011). Others have named it the “trust molecule” (Dvorsky, 2012), “cuddle hormone” (Griffiths, 2014), or “moral molecule” (Zak, 2013). Nevertheless, data derived from controlled studies imply that all of these appellations are woefully simplistic (Wong, 2012; Jarrett, 2015; Shen, 2015). Most evidence suggests that oxytocin renders individuals more sensitive to social information (Stix, 2014), both positive and negative. For example, although intranasal oxytocin seems to increase within-group trust, it may also increase out-group mistrust (Bethlehem et al., 2014). In addition, among individuals with high levels of trait aggressiveness, oxytocin boosts propensities toward intimate partner violence following provocation (DeWall et al., 2014). Comparable phrases applied to other neural messengers, such as the term “pleasure molecule” as a moniker for dopamine, are equally misleading (see Landau et al., 2008; Kringelbach and Berridge, 2010, for discussions).

Autism epidemic. Enormous effort has been expended to uncover the sources of the “autism epidemic” (e.g., King, 2011), the supposed massive increase in the incidence and prevalence of autism, now termed autism spectrum disorder, over the past 25 years. The causal factors posited to be implicated in this “epidemic” have included vaccines, television viewing, dietary allergies, antibiotics, and viruses.

Nevertheless, there is meager evidence that this purported epidemic reflects a genuine increase in the rates of autism per se as opposed to an increase in autism diagnoses stemming from several biases and artifacts, including heightened societal awareness of the features of autism (“detection bias”), growing incentives for school districts to report autism diagnoses, and a lowering of the diagnostic thresholds for autism across successive editions of the Diagnostic and Statistical Manual of Mental Disorders (Gernsbacher et al., 2005; Lilienfeld and Arkowitz, 2007). Indeed, data indicate when the diagnostic criteria for autism were held constant, the rates of this disorder remained essentially constant between 1990 and 2010 (Baxter et al., 2015). If the rates of autism are increasing, the increase would appear to be slight at best, hardly justifying the widespread claim of an “epidemic.”