Converging evidence and new research methodologies from across the neurosciences permit the neuroscientific study of the role of sleep in off-line memory reprocessing, as well as the nature and function of dreaming. Evidence supports a role for sleep in the consolidation of an array of learning and memory tasks. In addition, new methodologies allow the experimental manipulation of dream content at sleep onset, permitting an objective and scientific study of this dream formation and a renewed search for the possible functions of dreaming and the biological processes subserving it.

The activity that takes place in memory systems during sleep is likely to be related to the role of sleep in memory consolidation and learning, as well as to the generation of dream hallucinations. This study addressed the often-stated hypothesis that replay of whole episodic memories contributes to the multimodal hallucinations of sleep. Over a period of 14 days, 29 subjects kept a log of daytime activities, events, and concerns, wrote down any recalled dreams, and scored the dreams for incorporation of any waking experiences. While 65% of a total of 299 sleep mentation reports were judged to reflect aspects of recent waking life experiences, the episodic replay of waking events was found in no more than 1-2% of the dream reports. This finding has implications for understanding the unique memory processing that takes place during the night and is consistent with evidence that sleep has no role in episodic memory consolidation.

SummaryEvidence that childhood adversities are risk factors for psychosis has accumulated rapidly. Research into the mechanisms underlying these relationships has focused, productively, on psychological processes, including cognition, attachment and dissociation. In 2001, the traumagenic neurodevelopmental model sought to integrate biological and psychological research by highlighting the similarities between the structural and functional abnormalities in the brains of abused children and adults diagnosed with

Link to this article: http://journals.cambridge.org/abstract_S1121189X00000257How to cite this article: John Read, Richard P. Bentall and Roar Fosse (2009). Time to abandon the bio-bio-bio model of psychosis: Exploring the epigenetic and psychological mechanisms by which adverse life events lead to psychotic symptoms.Abstract. Mental health services and research have been dominated for several decades by a rather simplistic, reductionistic focus on biological phenomena, with minimal consideration of the social context within which genes and brains inevitably operate. This 'medical model' ideology, enthusiastically supported by the pharmaceutical industry, has been particularly powerful in the field of psychosis, where it has led to unjustified and damaging pessimism about recovery. The failure to find robust evidence of a genetic predisposition for psychosis in general, or 'schizophrenia' in particular, can be understood in terms of recently developed knowledge about how epigenetic processes turn gene transcription on and off through mechanisms that are highly influenced by the individual's socio-environmental experiences. To understand the emerging evidence of the relationship between adverse childhood events and subsequent psychosis, it is necessary to integrate these epigenetic processes, especially those involving the stress regulating functions of the HPA axis, with research about the psychological mechanisms by which specific types of childhood trauma can lead to specific types of psychotic experiences. The implications, for research, mental health services and primary prevention, are profound.Declaration of Interest: None of the authors have any conflicts of interest in relation to this paper.KEY WORDS: sexual abuse in childhood, psychosis, mechanism of psychiatric symptoms.

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The exclusion of thinking from recent studies of sleep mentation has hindered a full appreciation of how cognitive activity differs across the states of waking and sleep. To overcome this limitation, this study investigated thoughts and hallucinations using experience sampling, home-based sleep-wake monitoring, and formal analyses of the psychological data. The prevalence of thoughts decreased gradually from waking through sleep onset and non-REM sleep, to reach its nadir in REM sleep, whereas hallucinations increased sharply across these states. Furthermore, multiple occurrences of hallucinations but not of thoughts increased significantly from sleep onset through non-REM sleep, to a peak in REM sleep. This reciprocity in thoughts and hallucinations might reflect a progressive shift from high to low aminergic-to-cholinergic neuromodulatory ratios across wake-sleep states, accompanied by an array of changes in the regional activation patterns of the brain.

Internal deliberations (focused thoughts) and endogenous percepts (hallucinations) vary in a reciprocal manner across the states of waking and sleep, paralleling changes in regional brain activation. As subjects go from waking through sleep onset to NREM sleep and then to REM sleep, they report progressively more hallucinoid imagery and progressively less thinking. We have investigated whether this reciprocity in cognition between NREM and REM is maintained throughout the night. To do so, we analyzed 229 REM and 165 NREM reports collected with the Nightcap sleep monitoring system from 16 participants in their homes over 14 nights. The reports were scored for the presence of hallucinations and directed thinking by external judges. As predicted, hallucinations were more frequent in REM than in NREM for each segment of the night, and directed thinking was more frequent in NREM in the first 5 h of the night. Late in the night, directed thinking was equally infrequent in NREM and REM. At the same time, hallucinations increased within both NREM and REM as the night progressed, whereas directed thinking decreased in NREM and remained at a stable, low level in REM. These findings suggest that a reciprocal shift in focused thinking and hallucinating is a general property of cognitive activity across the wake-sleep cycle. Biological evidence supports the hypothesis that these cognitive changes are governed by specific state regulatory and neurocognitive processes at several levels of the brain.