I’m not thinking about the voices

Ontological security and connectivity provided by pets: a study in the self-management of the everyday lives of people diagnosed with a long-term mental health condition
BMC Psychiatry, 2016, 16:409
Helen Brooks, Kelly Rushton, Sandra Walker, Karina Lovell and Anne Rogers
Faculty of Biology, Medicine and Health, University of Manchester

… pets featured highly in the network hierarchy and were linked to dependency and substitutability of other, often absent network members providing or replacing ontological security from other sources.

…. pets could distract their owners from positive symptoms of schizophrenia such as hearing voices, from suicidal ideation or from a general sense of feeling alone:
“But if I’m here and I’m having…having problems with voices and that, erm, it does help me in the sense, you know, I’m not thinking about the voices, I’m just thinking of when I hear the birds singing” (ID 2, 2 birds, first circle).

journalistic version:

Animal-Assisted Therapy

Lifestyle medicine for depression. BMC Psychiatry. 2014;14(1):1–13.
Sarris J, et al.

The emergence of “lifestyle medicine” as a structured approach for management of chronic disease. Med J Aust. 2009;190:143–5.
Egger GJ, Binns AF, Rossner SR.

The pet connection: pets as a conduit for social capital? Soc Sci Med. 2005;61(6):1159–73.
Wood L, Giles-Corti B, Bulsara M.

Social networks, work and network-based resources for the management of long-term conditions: a framework and study protocol for developing self-care support. Implement Sci. 2011;6:56.
Rogers A, et al.

major depression, Autism Spectrum Disorders

Social network types, Network Diagram

Charles Monroe-Kane

Did God Talk to Me?
December 27, 2015 / September 4, 2016

TTBOOK producer and interviewer Charles Monroe-Kane started hearing voices when he was a child. He became a child preacher once he thought God was talking to him. Years later Charles realized those voices were the product of mental illness, though he says there was something “beautiful” about hearing those voices.

You, chronically normal folks

Inside the schizophrenic mind
Jan 16, 2011
CNN’s Candy Crowley talks to a psychologist and a journalist about how schizophrenia impacted them directly.

00:59 You, chronically normal folks, you don’t have experience with this …

Schizophrenia & synaptic pruning

Opening schizophrenia’s black box
Broad Institute
Jan 27, 2016

A landmark study has revealed that a person’s risk of schizophrenia is increased if they inherit specific variants in a gene related to “synaptic pruning” — the elimination of connections between neurons. The findings represent the first time that the origin of this devastating psychiatric disease has been causally linked to specific gene variants and a biological process.

Ketamine-induced psychosis

Individual Differences in Psychotic Effects of Ketamine Are Predicted by Brain Function Measured under Placebo
The Journal of Neuroscience, 18 June 2008,  28(25): 6295-6303
Garry D. Honey, et al.

The symptoms of major psychotic illness are diverse and vary widely across individuals.
Furthermore, the prepsychotic phase is indistinct, providing little indication of the precise pattern of symptoms that may subsequently emerge.
Likewise, although in some individuals who have affected family members the occurrence of disease may be predicted, the specific symptom profile may not.
An important question, therefore, is whether predictive physiological markers of symptom expression can be identified.
We conducted a placebo-controlled, within-subjects study in healthy individuals to investigate whether individual variability in baseline physiology, as assessed using functional magnetic resonance imaging, predicted psychosis elicited by the psychotomimetic drug ketamine and whether physiological change under drug reproduced those reported in patients.
Here we show that brain responses to cognitive task demands under placebo predict the expression of psychotic phenomena after drug administration.
Frontothalamic responses to a working memory task were associated with the tendency of subjects to experience negative symptoms under ketamine.
Bilateral frontal responses to an attention task were also predictive of negative symptoms.
Frontotemporal activations during language processing tasks were predictive of thought disorder and auditory illusory experiences.
A subpsychotic dose of ketamine administered during a second scanning session resulted in increased basal ganglia and thalamic activation during the working memory task, paralleling previous reports in patients with schizophrenia.
These results demonstrate precise and predictive brain markers for individual profiles of vulnerability to drug-induced psychosis.

We used a drug model of psychosis to relate presymptomatic physiology to symptom outcome.
Ketamine induces transient psychotic symptoms in healthy volunteers (Krystal et al., 1994) …


Ketamine-Induced Loss of Phenotype of Fast-Spiking Interneurons Is Mediated by NADPH-Oxidase
Science 7 December 2007: Vol. 318  no. 5856  pp. 1645-1647
M. Margarita Behrens

Abuse of the dissociative anesthetic ketamine can lead to a syndrome indistinguishable from schizophrenia.
In animals, repetitive exposure to this N-methyl-d-aspartate–receptor antagonist induces the dysfunction of a subset of cortical fast-spiking inhibitory interneurons, with loss of expression of parvalbumin and the γ-aminobutyric acid–producing enzyme GAD67.
We show here that exposure of mice to ketamine induced a persistent increase in brain superoxide due to activation in neurons of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase.
Decreasing superoxide production prevented the effects of ketamine on inhibitory interneurons in the prefrontal cortex. These results suggest that NADPH oxidase may represent a novel target for the treatment of ketamine-induced psychosis.


Ketamine-Induced Exacerbation of Psychotic Symptoms and Cognitive Impairment in Neuroleptic-Free Schizophrenics
Neuropsychopharmacology (1997) 17 141–150.
Anil K Malhotra MD, et al.

The N-methyl-d-aspartate (NMDA) receptor has been implicated in the pathophysiology of schizophrenia.
We administered subanesthetic doses of the NMDA receptor antagonist ketamine in a double-blind, placebo–controlled design to 13 neuroleptic-free schizophrenic patients to investigate if schizophrenics will experience an exacerbation of psychotic symptoms and cognitive impairments with ketamine.
We also examined whether schizophrenics experienced quantitative or qualitative differences in ketamine response in comparison to normal controls.
Schizophrenics experienced a brief ketamine-induced exacerbation of positive and negative symptoms with further decrements in recall and recognition memory. They also displayed greater ketamine-induced impairments in free recall than normals. Qualitative differences included auditory hallucinations and paranoia in patients but not in normals.
These data indicate that ketamine is associated with exacerbation of core psychotic and cognitive symptoms in schizophrenia.
Moreover, ketamine may differentially affect cognition in schizophrenics in comparison to normal controls.

Keywords: Ketamine; NMDA; Schizophrenia; Cognition; Psychosis