Blood glucose homeostasis is well maintained by coordinated control of various hormones including insulin and glucagon as well as cytokines under normal conditions. However, chronic exposure to diabetic environment with high fat/high sugar diets and physical/mental stress can cause hyperglycemia, one of main characteristics of insulin resistance, metabolic syndrome, and diabetes. Hyperglycemia impairs organogenesis and induces organ abnormalities such as cardiac defect in utero. It is a risk factor for the development of metabolic diseases in adults. Resulting glucotoxicity affects peripheral tissues and vessels, causing pathological complications including diabetic neuropathy, nephropathy, vessel damage, and cardiovascular diseases. Moreover, chronic exposure to hyperglycemia can deteriorate cognitive function and other aspects of mental health. Recent reports have demonstrated that hyperglycemia is closely related to the development of cognitive impairment and dementia, suggesting that there may be a cause-effect relationship between hyperglycemia and dementia. With increasing interests in aging-related diseases and mental health, diabetes-related cognitive impairment is attracting great attention. It has been speculated that glucotoxicity can result in structural damage and functional impairment of brain cells and nerves, hemorrhage of cerebral blood vessel, and increased accumulation of amyloid beta. These are potential mechanisms underlying diabetes-related dementia. Nutrients and natural food components have been investigated as preventive and/or intervention strategy. Among candidate components, resveratrol, curcumin, and their analogues might be beneficial for the prevention of diabetes-related cognitive impairment. The purposes of this review are to discuss recent experimental evidence regarding diabetes and cognitive impairment and to suggest potential nutritional intervention strategies for the prevention and/or treatment of diabetes-related dementia.

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Schizophrenia is a mental illness characterized by symptoms such as hallucinations, delusions, disorganized speech, disorganized or catatonic behavior, and negative symptoms (emotional flatness, apathy, and lack of speech). It causes social and economic burdens to patients and their family. Although etiology of schizophrenia is still uncertain, dopamine dysregulation is traditionally considered as a main etiological factor of schizophrenia, which has been utilized to develop drugs for treating schizophrenia. Recently, inflammation has presented being a risk factor for schizophrenia in that neuroinflammation contributes to the pathophysiology of schizophrenia and the exacerbation of symptom severity. Various factors including diet can regulate inflammatory state. Specific foods or dietary patterns have anti- or pro-inflammatory potentials. Increased levels of pro-inflammatory cytokines and microglia activation have been reported in schizophrenia populations and were related to the pathogenesis of schizophrenia. Omega-3 fatty acids were often recommended to schizophrenia patients because of their anti-inflammatory activities. In this review, we investigate the inflammation-related pathogenesis of schizophrenia and summarize potential nutritional approaches to inhibit the manifestation of symptoms and to alleviate symptom severity using anti-inflammatory nutrients or functional components.

Inflammation is a risk factor for the onset and progression of schizophrenia, and dietary factors are related to chronic inflammation. We investigated whether the dietary inflammatory index (DII) is associated with schizophrenia in the Korean population. Of the 256 subjects who responded to the questionnaire, 184 subjects (117 controls; 67 individuals with schizophrenia) were included in this case-control study. A semi-quantitative food frequency questionnaire was used to evaluate the dietary intakes of the study participants. The energy-adjusted DII (E-DII) was used to assess the inflammatory potential of the participants’ diets. Dietary intakes of vitamin C, niacin, and folate were significantly reduced in the patients with schizophrenia. The patients with schizophrenia had higher E-DII scores than the controls (p = 0.011). E-DII was positively associated with schizophrenia (odds ratio = 1.254, p = 0.010). The additional analysis confirmed that E-DII was significantly associated with schizophrenia, especially in the third tertile group of E-DII scores (odds ratio = 2.731, p = 0.016). Our findings suggest that patients with schizophrenia have more pro-inflammatory diets.

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