Discordance Between Evidence-Based Neuroscience and Direct-to-Consumer Advertising of Antidepressants on the World Wide Web: A Five-Year Follow-Up

Background: The etiology of depression remains unknown, and the mechanism of action of antidepressant medication is poorly understood. However, through consumer advertising, pharmaceutical companies have consistently promoted the claim that depression is caused by a known neurotransmitter imbalance which is corrected through use of antidepressant medication. Such claims are inconsistent with the information found in peer-reviewed neuroscience literature, psychopharmacology textbooks, and the FDA-approved product label. However, consumers are likely to be exposed to such advertisements. This has ramifications for evidence-based informed consent and shared clinical decision-making with depressed clients.

Purpose: (1) To assess the degree to which consumer advertisements currently published on the World Wide Web are supported by published empirical evidence, and (2) to compare advertisements from 2004 to those published in 2009, to monitor any changes since concerns regarding these advertisements were communicated to the FDA and antidepressant manufacturers in 2004-2005.

Method: Active consumer advertising websites promoting antidepressant medications (n=12) for use in depression were examined in March 2009. Claims regarding the etiology of depression and mechanism of action of the promoted medication were extracted. Advertising claims were then compared with data-based empirical studies from the fields of neuroscience and experimental psychiatry. Advertisements from 2009 were compared to advertisements from 2004.

Results: All active consumer advertising websites addressed the etiology of depression, and all advertisements for serotonin reuptake inhibitors mentioned the role of neurotransmitters. Four websites (33%) contained claims that either overstated empirical evidence or were at odds with the peer-reviewed neuroscience literature. The problematic statements concerned either the etiology of depression, the mechanism of action of the promoted medication, or both (e.g., in an advertisement for escitalopram, "Whatever the circumstances, depression is caused by an imbalance of certain chemicals in the brain....Lexapro...works to help correct this imbalance").

Some websites made etiological claims more tenatively (n=7, 58.3%) or presented the mechanism of action of medication as theoretical (n=6, 50%). However, if websites imply that scientific consensus underlies such theoretical explanations, they may still be potentially misleading. Multimedia presentations demonstrating how a medication "may" correct a chemical imbalance (e.g., paxil.com) could be convincing to consumers regardless of qualifying language and disclaimers.

When comparing advertisements from 2004 to those in 2009, there are several noteworthy differences. Although it was previously claimed that venlafaxine remedied a chemical imbalance, this statement was removed from the EffexorXR.com website. Other websites have made subtle changes in the wording of advertising claims. Several websites from 2004 are now defunct, referring readers to newer products made by the same pharmaceutical company. Interestingly, it appears that newer medications are promoted as "adjusting" or "affecting" neurotransmitter levels, rather than correcting a chemical imbalance.

Implications: There continues to be a gap between the scientifically established knowledge regarding antidepressants and the information pharmaceutical companies promote to the lay public. In contrast to regulatory authorities elsewhere (i.e., Ireland), the FDA has apparently not yet acted on this issue. Relaying evidence-based information to clients in the context of pervasive consumer advertising may represent a significant challenge for mental health providers.