Schizophrenia is a diabetic brain state: An elucidation of impaired neurometabolism

Holden, R.J.; Mooney, Phyllis

doi:10.1016/0306-9877(94)90020-5

Cited by 31 publications

(16 citation statements)

References 70 publications

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“…11]. In addition, chronic schizophrenic patients may have pain insensitivity [12,13] and increased [3-endorphin [14] , These alterations with chronic schizophrenic pa tients may attenuate the catecholamine response to surgi cal stress.…”

Section: Discussionmentioning

confidence: 99%

Depressed Pituitary-Adrenal Response to Surgical Stress in Chronic Schizophrenic Patients

Kudoh

Kudo²,

Ishihara³

et al. 1997

Neuropsychobiology

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We evaluated whether pituitary-adrenal response to surgical stress is modified in chronic schizophrenic patients. Twenty-two schizophrenic patients on chronic antipsychotic therapy of phenothiazine derivatives over 10 years underwent orthopedic surgery of the extremities under general anesthesia by isoflurane and nitrous oxide. In chronic schizophrenic patients, responses of plasma epinephrine, norepinephrine, ACTH and cortisol levels during surgical stress were significantly lower than those of control patients. The attenuated response to surgical stress in these patients may be associated with their autonomic dysfunction and decreased pituitary-adrenal activity due to chronic administration of antipsychotic agents.

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Section: Discussionmentioning

confidence: 99%

Depressed Pituitary-Adrenal Response to Surgical Stress in Chronic Schizophrenic Patients

Kudoh

Kudo²,

Ishihara³

et al. 1997

Neuropsychobiology

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“…As mentioned in the Introduction, IFN-g (100 U/ml) can independently induce a 20 per cent decrease in glucose-induced insulin release, but when synergized with IL-1b (50 U/ml) and/or TNF-a (1000 U/ml) this can cause up to an 80 per cent decrease in islet insulin content (Eizirik et al, 1994). It has been postulated in previous papers (Holden and Mooney, 1994;Holden and Pakula, 1995) that positive symptoms of schizophrenia are associated with hyperinsulinemia and hyperglycaemia of the brain cells, while negative schizophrenia and major depression is associated with hyperinsulinemia and hypoglycaemia of the brain cells. (The detailed pathophysiology supporting these assertions can be found in Holden andMooney, 1994 andHolden andPakula, 1995).…”

Section: The Relative Expression Of Neuropeptides In Schizophrenia Anmentioning

confidence: 84%

“…It has been postulated in previous papers (Holden and Mooney, 1994;Holden and Pakula, 1995) that positive symptoms of schizophrenia are associated with hyperinsulinemia and hyperglycaemia of the brain cells, while negative schizophrenia and major depression is associated with hyperinsulinemia and hypoglycaemia of the brain cells. (The detailed pathophysiology supporting these assertions can be found in Holden andMooney, 1994 andHolden andPakula, 1995). This is important since insulin is involved in the conversion of the inactive form of p21ras.GDP (guanine diphosphate) to the active form of p21ras.GTP (guanine triphosphate) (Burgering et al, 1991), the latter of which control neurometabolism via GTP-cyclohydrolase and tetrahydriobiopterin (BH4), and energy metabolism via diacylglycerol (DAG) and protein kinase C (PKC) (Holden and Mooney, 1994).…”

Section: The Relative Expression Of Neuropeptides In Schizophrenia Anmentioning

confidence: 99%

“…In relation to schizophrenia, it is not without interest that insulin has been shown to cause a dose-dependent increase in the synthesis and release of both dopamine (DA) and norepinephrine (NE) (Sauter et al, 1983). Thus, the fact that: (i) insulin, IGF-I, and IGF-II can cross the BBB, (ii) neurons can actually synthesize insulin, (iii) insulin mRNA is present in periventricular hypothalamic cells, (iv) insulin receptors are present in the brain and (v) insulin in¯uences the synthesis and release of DA and NE, all suggest that insulin plays an integral role in energy metabolism of the brain and possibly neurotransmission as well (Holden and Mooney, 1994).…”

Section: Introductionmentioning

confidence: 99%

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A Neuroimmunological Model of Schizophrenia and Major Depression: A Review

Holden

Pakula

Mooney

1997

Hum. Psychopharmacol. Clin. Exp.

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In this paper the neuroimmunology of schizophrenia and major depression will be reviewed. The causal role the neuropeptides, cytokines and insulin play in the pathogenesis of positive and negative schizophrenia and major depression will be examined. Numerous studies have shown there is an intimate interaction between certain cytokines and neuropeptides, possibly because the neuropeptides are exclusively synthesized in immune cells. When this relationship is dysregulated, a self-perpetuating pathobiochemical network is established that becomes dicult to reverse. This disruption to normal metabolism also involves insulin which becomes dysregulated by the in¯ammatory cytokines: interleukin-1 (IL-1), IL-6, tumour necrosis factor-alpha (TNF-a) and interferon-gamma (IFN-g). Each of these cytokines can independently inhibit and/or increase insulin secretion, but they can also function synergistically, which compounds the in¯uence on insulin secretion. An hypothesis is proposed that: (i) when brain insulin is elevated, energy metabolism and neurotransmission is hyperactive resulting in the positive symptoms of schizophrenia; and (ii) when brain insulin is inhibited, energy metabolism and neurotransmission is hypoactive resulting in either the negative symptoms of schizophrenia or major depression. It is our intention to develop a neuroimmunological model of positive and negative schizophrenia and major depression based on the causal interaction between the neuropeptides, the in¯ammatory cytokines and insulin.

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“…11 Reduced physical activity levels, unemployment (and subsequent lack of work-related activity), poverty and unstable living conditions seem to be significant factors in increasing the risk of weight gain, obesity and other adverse medical sequelae in the mental health population. 6,24,25 Schizophrenia has long been associated with impaired glucose tolerance and insulin resistance [26][27][28] and atypical medications may contribute directly to hyperglycemia 29,30 and the increased risk of incident diabetes. Among these, diabetes is of growing concern, as it has been shown that people with schizophrenia are more likely to develop type II diabetes than the general population.…”

Section: An Environmental Model To Explain Comorbidity and Mortalitymentioning

confidence: 99%

Addressing the Health and Lifestyle Issues of People with a Mental Illness: The Healthy Living Programme

O’Sullivan

Gilbert

Ward

2006

Australas Psychiatry

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This paper highlights the importance of incorporating healthy lifestyle programmes into mental health service delivery. The majority of patients who have attended the Healthy Living Program have indicated satisfaction with the content, but as yet information pertaining to long-term lifestyle change has not been collated. The next phase aims to examine whether the programme attendance has more long-term outcomes in improving health and well-being and promoting healthy behaviour change of mental health service recipients.

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Schizophrenia is a diabetic brain state: An elucidation of impaired neurometabolism

Cited by 31 publications

References 70 publications

Depressed Pituitary-Adrenal Response to Surgical Stress in Chronic Schizophrenic Patients

Depressed Pituitary-Adrenal Response to Surgical Stress in Chronic Schizophrenic Patients

A Neuroimmunological Model of Schizophrenia and Major Depression: A Review

Addressing the Health and Lifestyle Issues of People with a Mental Illness: The Healthy Living Programme

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