Ketogenic diet as a metabolic treatment for mental illness*

is important that researchers and clinicians are made aware of the trajectory of the evidence for the implementation of ketogenic diets in mental illnesses, as such a metabolic intervention provides not only a novel form of symptomatic treatment, but one that may be able to directly address the underlying disease mechanisms and, in so doing, also treat burdensome comorbidities. 


Delayed action of insulin in schizophrenia

3 out of 4 schizophrenic patients exhibited a delayed response to intravenous insulin. This my be attributed to the anti-insulin factor that has been found to be present in the blood of many schizophrenia patients.


Assessment of the relationship between food addiction and nutritional status in schizophrenic patients.

This study aimed to determine the prevalence of food addiction among schizophrenic patients and to examine the relationship between food addiction and anthropometric measurements and dietary nutrient intake. It was observed that the development of food addiction in schizophrenic patients increased the risk of obesity and cardiovascular diseases, which were found to be at higher levels in these patients. 


Ketogenic diet for schizophrenia: clinical implication

Recent findings support that the ketogenic diet may present a novel therapeutic approach through restoring brain energy metabolism in schizophrenia. Randomized controlled clinical trials are needed to further show the efficacy of ketogenic diet as a co-treatment to manage both clinical symptoms and metabolic abnormalities. 


Ketogenic diet as a metabolic therapy for mood disorders: evidence and developments

Preclinical studies, case reports and case series have demonstrated antidepressant and mood stabilizing effects of KD, however, to date (2018), no clinical trials for depression or bipolar disorder have been conducted. Because of its potential pleiotropic benefits, KD should be considered as a promising intervention in research in mood disorder therapeutics, especially in treatment resistant presentations.


Ketogenic diet reverses behavioral abnormalities in an acute NMDA receptor hypofunction model of schizophrenia

3 weeks of ketogenic diet normalized induced schizophrenia symptoms in mice (psychomotor hyperactivity, stereotyped behavior, social withdrawal, and working memory deficits). Elevated ketone levels were observed.


Randomized controlled trial of a gluten-free diet in patients with schizophrenia positive for antigliadin antibodies (AGA IgG): a pilot feasibility study

This pilot study found that removal of gluten from the diet is associated with improvement in psychiatric and gastrointestinal symptoms in people with schizophrenia or schizoaffective disorder.


Wheat gluten as a pathogenic factor in schizophrenia

Schizophrenics maintained on a cereal grain-free and milk-free diet and receiving optimal treatment with neuropleptics showed improved symptoms. After reintroducing gluten, the improvement was reinstated. The observed effects seemed to be due to a primary schizophrenia-promoting effect of wheat gluten.


International variations in the outcome of schizophrenia and the prevalence of depression in relation to national dietary practices: an ecological analysis.

After statistical analysis of national general population cohort, researchers found that individuals with Celiac Disease may be at increased risk of non-affective psychosis.


The role of inflammation in schizophrenia

Increasing evidence for a role of proinflammatory cytokines in schizophrenia, the strong influence of pro- and anti-inflammatory cytokines on tryptophan/kynurenine metabolism, the related influence of cytokines on glutamatergic neurotransmission, the results of imaging studies, genetic findings and the therapeutic effect of anti-inflammatory drugs all support the view that the recent increased focus of schizophrenia research on psychoneuroimmunology and inflammation is justified.


Impaired fasting glucose tolerance in first-episode, drug-naive patients with schizophrenia

First-episode, drug-naive patients with schizophrenia have impaired fasting glucose tolerance and are more insulin resistant and have higher levels of plasma glucose, insulin, and cortisol than healthy comparison subjects.


Physical consequences of schizophrenia and its treatment: The metabolic syndrome

There is evidence of overactivity of the HPA axis in schizophrenia, a cause of increased visceral fat. This obesity is associated with glucose intolerance, insulin resistance. Future studies are needed to examine drug-naive patients and follow up for a long period of time.


Increased visceral fat distribution in drug-naive and drug-free patients with schizophrenia

In comparison to controls, patients with schizophrenia had central obesity and higher levels of plasma cortisol. Central obesity is a well-recognized risk factor in developing certain general medical conditions. This study shows that patients with schizophrenia have increased intra-abdominal fat which may provide one explanation for why they die prematurely.