Over the years, the prevalence of auditory verbal hallucinations (AVHs) have been documented across the lifespan in varied contexts, and with a range of potential long-term outcomes. Initially the emphasis focused on whether AVHs conferred risk for psychosis. However, recent research has identified significant differences in the presentation and outcomes of AVH in patients compared to those in non-clinical populations. For this reason, it has been suggested that auditory hallucinations are an entity by themselves and not necessarily indicative of transition along the psychosis continuum. This review will examine the presentation of auditory hallucinations across the life span, as well as in various clinical groups. The stages described include childhood, adolescence, adult non-clinical populations, hypnagogic/hypnopompic experiences, high schizotypal traits, schizophrenia, substance induced AVH, AVH in epilepsy, and AVH in the elderly. In children, need for care depends upon whether the child associates the voice with negative beliefs, appraisals and other symptoms of psychosis. This theme appears to carry right through to healthy voice hearers in adulthood, in which a negative impact of the voice usually only exists if the individual has negative experiences as a result of their voice(s). This includes features of the voices such as the negative content, frequency, and emotional valence as well as anxiety and depression, independently or caused by voices presence. It seems possible that the mechanisms which maintain AVH in non-clinical populations are different from those which are behind AVH presentations in psychotic illness. For example, the existence of maladaptive coping strategies in patient populations is one significant difference between clinical and non-clinical groups which is associated with a need for care. Whether or not these mechanisms start out the same and have differential trajectories is not yet evidenced. Future research needs to focus on the comparison of underlying factors and mechanisms that lead to the onset of AVH in both patient and non-clinical populations.