Mental health: New horizons in nutrition research and dietetic practice

Article by Karen Charlton, Associate Professor, School of Medicine, University of Wollongong

One of my most vivid memories of my practical placement training as a student dietitian was a visit to a long-term institutional care facility in Oxfordshire, United Kingdom. There, I witnessed the irreversible effects of untreated phenylketonuria (PKU) on brain damage, and observed adults with virtually no quality of life who were unable to communicate or care for themselves and who were committed to spend the rest of their days in an institution. Today, of course, all babies are screened at birth for PKU with a heelprick blood test, and can be immediately placed on a low protein diet that omits phenylalanine, the amino acid that cannot be metabolized in individuals with this heritable disorder. These individuals go on to live a remarkably normal life.

The role of nutrition in both the aetiology and management of mental health disorders is a rapidly growing area of research, and has implications for translation into practice. Mental illness is common. One in five (20%) Australians aged 16-85 experience a mental illness in any year, and it is estimated that almost half (45%) of Australians will experience a mental illness sometime during their lifetime.[1] The most common mental illnesses are depressive disorders, anxiety and substance abuse, which often occur in combination [1]. In 2011-12, there were 3.0 million Australians (13.6%) who reported having a mental illness condition, an increase from 11.2% in 2007-08 and 9.6% in 2001.[2] Mood (affective) problems, which include depression, were most prevalent (2.1 million people or 9.7% of the population) followed by anxiety-related problems (850,100 people or 3.8%). The onset of mental illness is typically around mid-to-late adolescence and Australian youth aged 18-24 years have the highest prevalence of mental illness than any other age group. Over one in four (26%) young Australians experience a mental illness every year, with anxiety disorders particularly common (14%).[3] 

At the other end of the age spectrum, dementia is the single greatest cause of disability in older Australians aged 65 years or older,[4] and the third leading cause of disability burden overall.[5] Three in ten people over the age of 85 years and almost one in ten people over 65 years have dementia.[5] More than 50% of residents in Australian Government-subsidised aged care facilities have dementia.[6]

Thus, mental health disorders can be seen through the lens of a lifecourse perspective, which in turn requires an integrated approach to management of exposure to risk factors, the delivery of preventive interventions, and the treatment of symptomatic disease. The role of nutrition is important across each of these domains. 

Prenatal exposure and mental health disorders in offspring

The effect of nutritional intake on mental health begins even before birth. The adverse effects of severe nutritional deprivation in early-life has been clearly demonstrated through natural experiment studies conducted during times of famine.[7-9] Prenatal exposure to the Dutch famine during World War II has been associated with an excess of congenital nervous system abnormalities, mainly neural tube defects,[8-9] an increased risk of adult schizophrenia[10] and antisocial personality disorder,[10,11] as well as other major affective disorders[10] and general symptomatic measures of mental illness that are not diagnosis-specific.[12] Similar associations have been observed in the Chinese 1959–1961 famine in which a two-fold increased risk of schizophrenia was reported among those conceived or in early gestation at the height of the famine.[13,14] Interestingly, however, prenatal famine exposure has not been shown to impact on later-life cognitive performance at age 59 years.[15] 

Another example of the impact of maternal nutrition on the developing brain relates to iodine deficiency. Severe maternal iodine deficiency during pregnancy results in devastating mental impairment in the offspring, the most serious manifestation of which is cretinism. Iodine is essential for the synthesis of the thyroid hormones, triiodothyronine and thyroxine that are critical for normal growth and development, particularly of the brain and central nervous system. Meta-analyses indicate that moderate to severe iodine deficiency without supplementation may result in a population-level loss of intelligence in children of around 10-13.5 IQ points.[16,17] Even mild iodine deficiency during pregnancy, as still exists in some parts of Australia[18] is associated with reduced educational outcomes, as measured by decreased performance in the NAPLAN [National Assessment program – Literacy and Numeracy] of up to 10%.[19] Similarly, in the United Kingdom, mild maternal iodine deficiency has been shown to result in decreased IQ in the offspring.[20] However, a meta analysis of eight randomised controlled trials of iodine supplementation during pregnancy reported that supplementation during pregnancy or the periconceptional period in regions of severe iodine deficiency reduced risk of cretinism, but there were no improvements in childhood intelligence, gross development, growth, or pregnancy outcomes, although there was an improvement in some motor functions.[21] None of the remaining trials that were conducted in regions of mild to moderate iodine deficiency reported childhood development or growth or pregnancy outcomes. Effects of iodine supplementation on the thyroid function of mothers and their children were inconsistent. It is unlikely that experimental evidence of the effect of prenatal or periconceptional iodine supplementation on growth and cognitive function of children over the longer term, ideally to completion of their high school education, will be collected because of the ethically complex issues regarding the potential for harm in randomising pregnant women to a non-supplement group in regions that are iodine deficient.  

Childhood and adolescence

The initial onset of behavioural and emotional mental disorders frequently commences in childhood or adolescence and it has been suggested that perinatal programming of the brain occurs in the foetal and early life phase.[22] Epidemiological studies report prevalence rates of child and adolescent mental health disorders to be common, affecting at least one in ten 5 – 16 year olds. These conditions include neurodevelopmental disorders such as autism spectrum disorder (ASD) and attention-deficit hyperactivity disorder (ADHD), mood and anxiety disorders, and behavioural problems.[23] The role of diet in the management of these disorders remains to be elucidated, however there is evidence that ADHD-related symptoms may respond to polyunsaturated fatty acid supplementation.[24]

Preventing cognitive decline in old age through dietary intervention

An exciting new area of nutrition research relates to the prevention of cognitive decline in old age through dietary intervention. Promising results are emerging however these are not consistent enough to be taken up into practical dietary guidelines. There are a number of proposed mechanisms that have been suggested based on observations from epidemiological observations. Dietary patterns that are associated with less cognitive decline include the Mediterranean diet[25] which is characterized by high intake of vegetables, fruit, legumes, nuts, cereals and monounsaturated fat (olive oil); low intake of saturated fat; moderate intake of dairy foods, meat, poultry and fish; and regular moderate intake of alcohol, primarily from wine consumed with meals. This dietary pattern is also associated with a lower risk for development of mild cognitive impairment[26] and Alzheimers disease.[27] 

Oxidative stress is an important contributor to the pathogenesis of dementia.[28,29] A study analysing cerebrospinal fluids of cognitively impaired individuals (Mild Cognitive Impairment (MCI) and Alzheimer’s Disease (AD)) reported significantly higher isoprostane 8,12-iso-iPF2α-VI (specific marker of in vivo lipid peroxidation) levels compared to control subjects.[30] Observational studies have found that individuals with MCI or AD have lower levels of biomarkers of antioxidant status (plasma levels of vitamin C, uric acid, vitamin A, E, carotenoids, lutein, zeaxanthine and α-carotene) and plasma antioxidant activity (superoxide dismutase and glutathione peroxidise).[31] However, when these observations were re-investigated in an average 9.6 year follow-up of the Rotterdam study through the quantification of dietary consumption, reported dietary intakes of most antioxidants (β-carotene, vitamin C, and flavonoids) were not protective against cognitive decline with age. An exception to this was a lower long-term risk of dementia (p-trend=0.02) associated with a higher dietary intake of vitamin E at baseline. Compared to participants in the lowest tertile of vitamin E intake (median 9mg/day), those in the highest tertile (median 18.5 mg/day) were 25% less likely to develop dementia (HR, 0.75; 95% CI, 0.59–0.95 with adjustment for potential confounders including supplement use). Results were similar when AD risk was specifically examined.[32] A later analysis at median 13.8 years of follow-up, found no association between the total antioxidant capacity of the diet, as measured using dietary ferric reducing antioxidant power (FRAP) scores, and risk of dementia. These results suggest that individual antioxidants, or major food contributors to those antioxidants, are more important than overall antioxidant capacity of the diet for cognitive benefits.[33] However, the results of experimental studies have been largely disappointing. A randomised-controlled trial that supplemented MCI individuals with megadoses of vitamin E (2000 IU or 900 mg/day which is equivalent to 100 times the RDA) failed to observe a decreased probability of progression to AD, when compared to control subjects who received placebo treatment.[34]

Some of the health benefits associated with fruits and vegetables have been attributed to their phytochemical or polyphenol content. Polyphenols are non-nutritive bioactive compounds that contribute to the antioxidant activity of individual fruits and vegetables. Flavonoids, a class of polyphenols that include five major subclasses (anthocyanidins, flavanols, flavanones, flavones and flavonols) have been studied intensely for their ability to protect against neurodegenerative diseases and improve cognitive performance in older people.[35] In his review, Spencer (2010)[35] proposes that the flavonoids found most commonly in fruits, such as apples, berries and citrus are capable of promoting beneficial effects on memory and learning, through their ability to exert effects directly on the brain’s innate architecture for memory. This cellular architecture is well known to deteriorate with ageing with numbers of neurons and synaptic connections lost over time, leaving the system less efficient in the processing and storage of sensory information. Fruit-derived flavonoids are able to modulate and activate neuronal signalling pathways that are crucial to synaptic plasticity. It is also thought that flavonoids exert a beneficial effect on brain function through their potential to improve endothelial function and peripheral blood flow.[35]

Despite these encouraging findings, well designed human trials are few and are limited to short-term interventions with small numbers of participants. Studying such compounds in food presents methodological challenges. For example, little is understood about the absorption and metabolism of many of the hundreds of flavonoids and their intermediary metabolites. This lack of understanding which hinders the accurate determination of relevant biomarkers in plasma and urine, coupled with incomplete nutrient composition databases for dietary assessment of flavonoids in foods, makes this a challenging area to research. Further, key questions remain unanswered regarding the dosage required from foods, food extracts and/or supplements, to achieve physiological thresholds to invoke a biological response.

Other phytochemicals found in plant foods, such as found in walnuts, in combination with high amounts of polyunsaturated fatty acids, also offer potential benefits to brain health. Polyphenolic compounds found in walnuts not only reduce the oxidant and inflammatory load on brain cells but also improve interneuronal signalling, increase neurogenesis, and enhance sequestration of insoluble toxic protein aggregates.[36]

Another nutrient that has attracted interest is thiamin or Vitamin-B1. Many of the oxidative and glucose metabolic processes that are essential for optimal cognitive functioning are thiamin dependent.[37] Dementia patients are reported to have low plasma thiamin levels and higher rates of thiamin deficiency while post-mortems show decreased thiamin-dependent enzymes in Alzheimer Disease patients.[37] Lower concentrations of free thiamin and its phosphate esters in erythrocytes among 1587 Chinese men and women aged 50–70 y were associated with a higher prevalence of depressive symptoms.[38] A paper in the current issue reports on findings from a cross sectional study of generally healthy, well-nourished older adults in which no associations were found between protein or thiamin intakes and various domains of cognition.[39] It is important to note that participants in that study had adequate intakes of  thiamin and protein, and it is possible that the association between thiamin intake and cognitive function is more evident in populations with low dietary thiamin intakes or those that have some form of thiamin deficiency. 

The human brain is composed of a high percentage of lipids, and the development and optimal functioning of the human brain requires sufficient long-chain PUFAs, including eicosapentanoic acid (EPA) and docosahexanoic acid (DHA), in its membrane phospholipids. Plasma levels of EPA, DHA, and total n-3 fatty acid have been reported to be lower among individuals with AD and other cognitive impairments, and omega-6 (n-6) fatty acid levels were found to be higher in the same group.[40] While a higher dietary PUFA intake has been shown to protect against the development of mild cognitive impairment,41 the role of the food matrix in the provision of nutrients is important. For example, although dietary n-3 fatty acid intake was not related to cognitive decline,[42] higher total and oily fish intake was inversely associated with cognitive impairment.[43] This result demonstrates the potential synergistic effect between n-3 PUFA and other nutrients found in fish. 

Provision of nutrients through food, rather than supplements, is also emerging as important. For example, a randomised-controlled trial of 6-month daily supplementation of DHA and EPA did not result in better cognitive performance in the intervention group compared to the placebo group, except for a positive effect in a subgroup of subjects with very mild cognitive dysfunction.[44] Only two randomised controlled trials have been conducted with cognitively healthy populations, and no overall effect of supplementation was found. One large study (n = 867; 70-79 y) supplemented 200 mg of EPA and 500 mg of DHA, or olive oil, daily for 24 months, while the other provided low dose and high dose fish oil (n = 302; 65+y) for 26 weeks.[45] In the latter study, subgroup analysis revealed that carriers of the Apolipoprotein E (ApoE) ε4 allele, in both the low (226 mg EPA, 176 mg DHA) and high dose (1093 mg EPA, 847 mg DHA) fish oil groups, showed an improvement compared with the placebo for the Digit-Span Forward task, a marker of attention.[46] The 18-month EPOCH study which is investigating fish oil supplementation at even higher levels of DHA intake (600mg EPA, 1720mg DHA) in healthy older Australian women will add further high quality evidence regarding the role of long chain n-3 fatty acids on cognitive function over time.[47]

Context of the background diet is an essential consideration in interpretation of diet-cognition associations. An observational study of Japanese community-dwelling subjects found that multivariate-adjusted OR (95% CI) for the highest compared to the lowest tertiles for serum DHA was 0.17 (0.04–0.74) for a Mini Mental State Examination (MMSE) score ≤23 and 0.31 (0.12–0.75) for a decline of ≥4 points on the MMSE from baseline. These findings suggest that a moderately high level of serum DHA might prevent against cognitive decline among community-dwelling elderly Japanese individuals who consume over 100g per day, on average, of fish/shellfish.[48] Transfer of these findings to populations that eat much lower levels of fish cannot however be assumed. 

Malnutrition and mental health disorders: chicken or egg? 

The presence of mental health symptoms increased the risk of malnutrition almost fourfold in community-living older men (OR 3.9; 95 % CI 1.7-8.6) and 2.5 fold in women (OR 2.5; 95% CI 1.3-4.9).[49] The potential for reverse causality cannot be ignored. Does the presence of mental illness impact on eating behaviours and result in an inadequate intake, or conversely does a poor nutritional status impair mental function and lead to worsening of symptoms? The overwhelming body of evidence that malnutrition predicts adverse clinical outcomes, confirmed by Slattery et al (2014)[50] in this issue, requires innovative strategies to address this problem in practice. 

Identification of malnutrition is not considered a clinical priority and remains largely undetected. The Australasian Nutrition Care Day Survey (ANCDS) that evaluated malnutrition prevalence in 56 Australian and New Zealand acute hospitals reported a prevalence of 30% of the patient cohort (n = 2976) but new analysis indicates that only 19 % of the malnourished patients had been coded in the medical records for malnutrition.[51] The problem of inadequate documentation of the nutrition care process in patient records is not limited to Australian settings, as indicated in an international perspective provided from Sweden.[52] As urged by Argawal and colleagues in this special issue,[51] dietitians need to be proactive in developing structured processes for malnutrition identification, documentation and coding.

Weight loss over time provides a reliable indicator of declining nutritional status. However, reference values for BMI in older adults remain controversial. A recent meta analysis by Winter et al. provides evidence that a healthy weight range for adults older than 65 years is a BMI between 23–29 kg/m2 [53] rather than the World Health Organization classification of 18.5–24.9 kg/m2. The health impact of trajectories of weight loss over time is yet to be determined. Baseline anthropometric indices from community-dwelling healthy adults aged 70 – 90 years recruited to the Sydney Memory and Ageing cohort study,[54] provide much-needed population distribution values that can be tracked over time for association with adverse health outcomes, including decline in cognition and higher risk of mortality. 

Interventions for management of dementia-type diseases

The responsibility of feeding older people with dementia who live at home often falls on the shoulders of their spouses or primary caregivers, who may too be old and have health problems of their own. It is estimated that 1.2 million people are involved in the care of a person with dementia.[55] The qualitative study of Ball et al (2014)[56] identified that family carers experience a wide range of feeding and nutrition challenges, including physiological, cognitive, emotional, functional and/or behavioural challenges. Family carers felt uninformed and unsupported by health care professionals with respect to provision of nutrition-related care, which led to considerable anxiety and contributed to a large overall burden of care. Practical strategies included supervising mealtimes, avoiding disagreements over food, and providing regular snacks and finger foods. There is clearly a need for improved communication and dissemination of nutrition information by dietitians, who could play a more active role through the Alzheimer’s Association and other non governmental support organizations.  

Another high risk group are patients with Parkinson’s disease (PD), who are more likely to develop impaired nutritional status because of the symptoms, medications and complications of the disease.[57] Disease duration, severity of motor and psychiatric symptoms (depression, anxiety) and fatigue are associated with poor nutritional status, and hence quality of life, in PD patients.[57] Thus optimization of dietary intake is an essential component of care. A survey of Australian dietitians[58] identified wide variations in practice related to the management of PD patients that indicates a need for evidence-based guidelines to ensure best practice.

In some cases, adequate oral intake may not be able to be achieved through diet alone. Tsang and Carey (2014)[59] have identified that participants who receive home parenteral nutrition often feel restricted by the stringent regimens and are limited in their ability to participate in enjoyable daily activities. The authors recommend that a more structured multidisciplinary model of care would ensure that patients have access to psychological support where required. This again highlights the interdisciplinary team approach needed to address the nutritional care of patients who require specialised feeding, including those with mental health disorders. 

There is much to be learned about the effect of nutrients, individual foods and whole diets on cognitive function and mental health. As populations around the globe age, this area of nutrition research will be high priority. Clinical dietitians will have an increasingly greater responsibility in the management of mental health conditions, while public health nutritionists will be needed to translate the nutrition science into practical dietary messages for slowing down the progression of cognitive decline, and possibly even prevention of mental illness in some sectors of the population. It is a pleasing step in the right direction that the Mental Health Interest Group of the Dietitians Association of Australia has developed a role statement that defines the scope of work that can be expected of a dietitian working in this area.[60]

Conflict of interest

The author has no conflict of interest.

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