The aim of the paper is to show the various neurological and psychiatric symptoms in coeliac disease (CD). CD is a T cell-mediated, tissue-specific autoimmune disease which affects genetically susceptible individuals after dietary exposure to proline- and glutamine-rich proteins contained in certain cereal grains. Genetics, environmental factors and different immune systems, together with the presence of auto-antigens, are taken into account when identifying the pathogenesis of CD. CD pathogenesis is related to immune dysregulation, which involves the gastrointestinal system, and the extra-intestinal systems such as the nervous system, whose neurological symptoms are evidenced in CD patients. A gluten-free diet (GFD) could avoid cerebellar ataxia, epilepsy, neuropathies, migraine and mild cognitive impairment. Furthermore, untreated CD patients have more symptoms and psychiatric co-morbidities than those treated with a GFD. Common psychiatric symptoms in untreated CD adult patients include depression, apathy, anxiety, and irritability and schizophrenia is also common in untreated CD. Several studies show improvement in psychiatric symptoms after the start of a GFD. The present review discusses the state of the art regarding neurological and psychiatric complications in CD and highlights the evidence supporting a role for GFD in reducing neurological and psychiatric complications.

An emerging field of research in nutritional epidemiology is the assessment of several links between nutritional quality and mental health. Specifically, some studies have pointed out that several food patterns could be associated with a reduced risk of depression among adults. This association seems to be consistent across countries, cultures and populations according to several systematic reviews and meta-analyses of observational studies. Some previously described food patterns, specifically the Mediterranean Food Pattern, the Alternative Healthy Eating Index, the Prudent diet or the Provegetarian Food Pattern may be effective to reduce the future risk of depression. Among them, only the Mediterranean Food Pattern has been tested for primary prevention in a large randomised trial, but the inverse association found was not statistically significant. The scientific report of the 2015 Dietary Guidelines for Americans Advisory Committee concluded that current evidence is still limited. Notwithstanding, this field is promising and, according to large and well-conducted observational studies, food patterns potentially associated with reduced risk of depression are those emphasising seafood, vegetables, fruits and nuts. There is a need to assess whether differences in the intake of some micro or macronutrients between these dietary patterns can make a difference in their association with a lower risk of depression. Moreover, the shape of the dose–response curve and the potential existence of a nonlinear threshold effect have not yet been established.

Vitamin D has been suggested to protect against depression, but epidemiological evidence is scarce. The present study investigated the relationship of serum 25-hydroxyvitamin D (25(OH)D) with the prevalence of depressive and anxiety disorders. The study population consisted of a representative sample of Finnish men and women aged 30–79 years from the Health 2000 Survey. The sample included 5371 individuals, of which 354 were diagnosed with depressive disorder and 222 with anxiety disorder. Serum 25(OH)D concentration was determined from frozen samples. In a cross-sectional study, a total of four indicators of depression and one indicator of anxiety were used as dependent variables. Serum 25(OH)D was the risk factor of interest, and logistic models used further included sociodemographic and lifestyle variables as well as indicators of metabolic health as confounding and/or effect-modifying factors. The population attributable fraction (PAF) was estimated. Individuals with higher serum 25(OH)D concentrations showed a reduced risk of depression. The relative odds between the highest and lowest quartiles was 0·65 (95 % CI 0·46, 0·93; P for trend = 0·006) after adjustment for sociodemographic, lifestyle and metabolic factors. Higher serum 25(OH)D concentrations were associated with a lower prevalence of depressive disorder especially among men, younger, divorced and those who had an unhealthy lifestyle or suffered from the metabolic syndrome. The PAF was estimated to be 19 % for depression when serum 25(OH)D concentration was at least 50 nmol/l. These results support the hypothesis that higher serum 25(OH)D concentrations protect against depression even after adjustment for a large number of sociodemographic, lifestyle and metabolic factors. Large-scale prospective studies are needed to confirm this finding.

Postpartum depression (PPD) is a relatively common and often severe mood disorder that develops in women after childbirth. The aetiology of PPD is unclear, although there is emerging evidence to suggest a psychoneuroimmune connection. Additionally, deficiencies in n-3 PUFA, B vitamins, vitamin D and trace minerals have been implicated. This paper reviews evidence for a link between micronutrient status and PPD, analysing the potential contribution of each micronutrient to psychoneuroimmunological mechanisms of PPD. Articles related to PPD and women's levels of n-3 PUFA, B vitamins, vitamin D and the trace minerals Zn and Se were reviewed. Findings suggest that while n-3 PUFA levels have been shown to vary inversely with PPD and link with psychoneuroimmunology, there is mixed evidence regarding the ability of n-3 PUFA to prevent or treat PPD. B vitamin status is not clearly linked to PPD, even though it seems to vary inversely with depression in non-perinatal populations and may have an impact on immunity. Vitamin D and the trace minerals Zn and Se are linked to PPD and psychoneuroimmunology by intriguing, but small, studies. Overall, evidence suggests that certain micronutrient deficiencies contribute to the development of PPD, possibly through psychoneuroimmunological mechanisms. Developing a better understanding of these mechanisms is important for guiding future research, clinical practice and health education regarding PPD.

Malnutrition and depression are highly prevalent in the institutionalised elderly and can lead to unfavourable outcomes. The aim of the present study was to assess associations between nutritional status and depressive symptoms and to explore their impact on self-caring capacity and quality of life (QoL) in elderly nursing-home residents (NHR). We conducted a cross-sectional study with 114 NHR (eighty-six female) with a mean age of 84·6 (sd 9·1) years. Nutritional status was assessed with the Mini Nutritional Assessment (MNA). Depressive symptoms were rated with the Geriatric Depression Scale (GDS). Self-caring capacity was measured with the Barthel index (BI) and QoL was assessed with the short-form thirty-six-item (SF-36) questionnaire. Of the NHR, twenty-six (22·8 %) were malnourished according to the MNA and sixty-six (57·9 %) were at nutritional risk. Of the residents, seventy-five could be assessed with the GDS, whereof sixteen (21·3 %) had major and twenty-six (34·7 %) had minor depressive symptoms. GDS scores tended to be higher in patients with impaired nutritional status (5·4 (sd 3·6) in well-nourished subjects and 6·9 (sd 3·2) in residents with malnutrition or at risk of malnutrition). The MNA correlated significantly with the GDS (r − 0·313; P = 0·006) and the GDS emerged as the only independent risk factor for malnutrition in a multiple regression analysis, whereas age, sex, care level, number of prescriptions and self-caring capacity had no influence. The BI was not reduced in patients with a high GDS. QoL was affected in malnourished residents as well as in study participants with depressive symptoms. The results of the present study point towards an association between malnutrition and depressive symptoms. However, the relationship is complex and it remains unclear whether depression in NHR is the cause or consequence of impaired nutritional status. Further studies are needed to identify the direction of this relationship and to assess the effect of depression treatment on nutritional and functional status as well as on QoL.

Selected biochemical evidence suggests a potential role for n-3 long-chain PUFA (n-3PUFA) in the regulation of mood and behaviour. The present paper reviews the relevant evidence, to date, from epidemiological studies, clinical studies and intervention trials. Most evidence is available investigating a role for n-3PUFA in depression, depressive illness and suicidal behaviour, but work is also available on anxiety and anxiety-related disorders, fatigue and fatigue-related disorders, aggression, hostility and anti-social behaviour, inattention, impulsivity and attention deficit hyperactivity disorder and schizophrenic disorders. For all these aspects of mood and behaviour, the evidence available is currently limited and highly inconsistent, both in terms of study methodology and study findings. There is a clear need for further work in this area.

The cost of psychiatric illness to the UK economy was recently estimated at £77 billion annually. Despite years of research no firm aetiological explanation exists, and with no physiological or biochemical markers diagnosis is made entirely on a behavioural basis. All current pharmacological therapies are associated with serious long-term side effects. Substantial evidence supports the involvement of one-carbon cycle dysregulation in psychiatric illness, but this is not currently used as a basis for diagnosis or treatment. The present paper reviews the evidence for one-carbon cycle dysregulation in schizophrenic, bipolar, depressed and autistic patients. Also presented are novel findings from the field of epigenetics, which demonstrate how the one-carbon cycle-derived methyl donor S-adenosylmethionine influences the expression of key genes in the brain affecting memory, learning, cognition and behaviour, genes whose expression is reduced to varying degrees in these patient groups. Clinical evidence that nutritional supplements can rectify one-carbon cycle activity, and restore normal gene expression, suggests a novel approach to the development of biochemical tests and simple, non-harmful treatments for some psychiatric patients. Conversely, evidence from animal studies highlights the dangers of exposing the unborn fetus to very high dietary levels of folic acid, a one-carbon cycle cofactor. Fetal adaptations to a high-folate environment may interfere with folate metabolism postnatally, with serious consequences for the epigenetic regulation of gene expression. The public health implications of these diverse scenarios indicate an urgent need for further research in this field.