A new expert review confirms that diet significantly influences mental health and wellbeing, but cautions that the evidence for many diets is comparatively weak.
This, the most up to date overview of the new field of Nutritional Psychiatry, is produced, by the Nutrition Network of the ECNP and is published in the peer-reviewed journal European Neuropsychopharmacology.
Lead author, Professor Suzanne Dickson (University of Gothenburg, Sweden) said:
“We have found that there is increasing evidence of a link between a poor diet and the worsening of mood disorders, including anxiety and depression. However, many common beliefs about the health effects of certain foods are not supported by solid evidence”.
The researchers found that there are some areas where this link between diet and mental health is firmly established, such as the ability of a high fat and low carbohydrate diet (a ketogenic diet) to help children with epilepsy, and the effect of vitamin B12 deficiency on fatigue, poor memory, and depression.
They also found that there is good evidence that a Mediterranean diet, rich in vegetables and olive oil, shows mental health benefits, such as giving some protection against depression and anxiety.
However, for many foods or supplements, the evidence is inconclusive, as for example with the use of vitamin D supplements, or with foods believed to be associated with ADHD or autism.
“With individual conditions, we often found very mixed evidence”, said Suzanne Dickson. “With ADHD for example, we can see an increase in the quantity of refined sugar in the diet seems to increase ADHD and hyperactivity, whereas eating more fresh fruit and vegetables seems to protect against these conditions.
But there are comparatively few studies, and many of them don’t last long enough to show long-term effects”.
The study confirms that while certain foods can be associated with a mental health condition, this tells us little about why the food causes this effect.
It concludes that the need to link mental health effects with provable dietary causes needs to be the main focus of future research in nutritional psychiatry.
Professor Dickson continued:
“There is a general belief that dietary advice for mental health is based on solid scientific evidence. In reality, it is very difficult to prove that specific diets or specific dietary components contribute to mental health.
The scientists confirmed that some foods had readily provable links to mental health, for example, that nutrition in the womb and in early life can have significant effects on brain function in later life. Proving the effect of diet on mental health in the general population was more difficult.
Suzanne Dickson said “In healthy adults dietary effects on mental health are fairly small, and that makes detecting these effects difficult: it may be that dietary supplementation only works if there are deficiencies due to a poor diet. We also need to consider genetics: subtle differences in metabolism may mean that some people respond better to changes in diet that others.
There are also practical difficulties which need to be overcome in testing diets. A food is not a drug, so it needs to be tested differently to a drug. We can give someone a dummy pill to see if there is an improvement due to the placebo effect, but you can’t easily give people dummy food. Nutritional psychiatry is a new field.
The message of this paper is that the effects of diet on mental health are real, but that we need to be careful about jumping to conclusions on the base of provisional evidence. We need more studies on the long-term effects of everyday diets”.
The scientists confirmed that some foods had readily provable links to mental health, for example, that nutrition in the womb and in early life can have significant effects on brain function in later life. Proving the effect of diet on mental health in the general population was more difficult.
Commenting, the Chair of the ECNP Scientific Programme Committee, Professor Andreas Reif (University Hospital, Frankfurt am Main) said:
“The interface between gut and the brain on the one side and diet and mental health on the other side is one of the most debated issues in biological psychiatry at the moment, and is an exciting development which has gained momentum in the last decade.
Many high-quality findings (mainly from animal studies) have been published in top notch journals in recent years, but this contrasts with the comparative shortage of hard evidence on how nutrition and mental health are connected in humans.
This leaves room for speculation and flawed science. This comprehensive review is therefore much-needed as it sheds light on hypes and hopes, facts and fiction in the new field of Nutritional Psychiatry.
As the potential societal impact of this rapidly developing field is enormous, we must be scientifically sound in making our recommendations. This review is an important and scholarly contribution”.
This is an independent comment; Professor Reif was not involved in this work.
Recent meta-analyses have confirmed that severe mental illnesses (SMI), including major depressive disorder (MDD), bipolar disorder, and schizophrenia, are associated with increased levels of both peripheral inflammatory markers (1) and systemic inflammation (2). Additionally, heightened inflammation could present a novel treatment target for MDD, given that the anti-depressant efficacy of various pharmacological and lifestyle interventions appears to be associated with reductions in inflammation (3, 4). In schizophrenia, the evidence for antipsychotics altering inflammatory markers is mixed (1, 5), although there is some preliminary evidence to indicate that various adjunctive interventions may confer beneficial effects through reducing inflammatory status (6, 7).
Calorie-dense diets that are high in saturated fats and simple carbohydrates appear to increase peripheral inflammatory markers, whereas diets high in fiber and vegetables reduce inflammation (8–12). Systematic reviews of dietary patterns in people with SMI have shown elevated intakes of sugar-sweetened soft drinks, refined grains, and processed meat are common in this population (13, 14). However, the degree to which these dietary patterns heighten inflammation in SMI, and the potential impact on physical and mental health outcomes, is relatively unexplored. This comprehensive review brings together the evidence from cross-sectional, longitudinal, and experimental studies on this topic to:
- Examine the extent to which inflammatory potential of the diet (hereafter referred to as “dietary inflammation”) is elevated in SMI populations;
- Explore the directionality of the links between dietary inflammation and symptoms of SMI;
- Discuss the existing evidence for the use of nutritional interventions for improving health outcomes in SMI and how these effects may act through inflammatory pathways.
Food Intake and Dietary Inflammation in People with Severe Mental Illnesses
A recent large-scale study of the UK Biobank (15) compared the macro- and micro-nutrient intake of individuals with diagnosed MDD (n = 14,619), bipolar disorder (n = 952), and schizophrenia (n = 262) to healthy controls (n = 54,010), showing that people with SMI consumed significantly more carbohydrate, sugar, fat, and saturated fat than healthy controls (all p < 0.001), even when controlling for age, gender, education, BMI, social deprivation, and ethnicity.
The study also examined the inflammatory potential of food intakes of individuals with SMI compared with the general population using the “Dietary Inflammatory Index” (DII®). The DII is a literature-derived, population-based measure, which provides an estimate of the inflammatory potential of an individual’s diet from up to 45 individual food parameters (16). DII scores have been validated against various blood markers of inflammatory status across a number of different populations (17–21).
The DII scores in SMI samples in the UK Biobank are displayed in Figure 1 [derived from Firth et al. (15)], adjusted for age, gender, and total energy intake. These data show highly elevated dietary inflammation in individuals with schizophrenia, along with smaller, but significantly increased, levels of dietary inflammation in individuals with MDD (all p < 0.01). Although dietary inflammation in the bipolar disorder group was similarly larger than healthy controls (p = 0.03), this difference was reduced to a marginally non-significant trend after adjusting for BMI and socioeconomic status (p = 0.07).
It is interesting to note that despite the vast number of studies examining elevated levels of peripheral inflammation observed across all classes of SMI (1), none have accurately controlled for the potential confounding factor of diet. Furthermore, a priority for future research is to validate the accuracy of dietary reporting in SMI.
Interestingly, previous research comparing other lifestyle factors (i.e., physical activity) using objective against self-report measures in SMI have shown that people with schizophrenia significantly overestimate health behaviors compared with the general population (22). Therefore, replication of these findings, using validated measures in SMI alongside blood markers of inflammation, is required to establish how diet may relate to inflammation in SMI.
Along with poor mental health, people with SMI experience drastic inequalities in physical health, including elevated rates of obesity, diabetes, and cardiometabolic disorders, ultimately contributing to a reduced life expectancy of around 20 years (23). Given the clear causal links between dietary inflammation and these health outcomes established in the general population (10–12), and the established benefits of dietary interventions for physical health in SMI (24), it is reasonable to explore dietary inflammation as one risk factor driving some of the physical health inequalities observed in this population.
Indeed, the highest levels of dietary inflammation are observed in schizophrenia: a group that also experiences significantly worse physical health outcomes than other classes of SMI (25, 26). Poor dietary quality associated with schizophrenia may even be driven by side effects of antipsychotic medications, which may increase appetite through interfering with the “hunger hormone,” ghrelin (27).
Clearly, there is an urgent need for future research to determine the mechanisms through which poor diet may be driving adverse health outcomes in people with SMI. This line of investigation will provide novel insights into the etiology of the physical health inequalities observed in this population and has the potential to inform clinical care.
A key limitation of the current literature is a lack of large-scale data on dietary patterns among young people with SMI, thus making it difficult to determine whether poor diet precedes the onset of mental illness, or vice versa. In the general population, data suggest that younger people tend to have worse diets than older adults (28).
This also may apply to SMI populations, as nutritional deficits in psychosis are evident even prior to antipsychotic treatment (29). Thus, in the following section, we review the prospective studies examining links between high levels of dietary inflammation and the subsequent onset of mental illness.
Prospective Associations Between Dietary Inflammation and Psychiatric Symptoms
Poor nutrition has been implicated in the onset and persistence of psychiatric disorders (30). In general, cohort studies have shown that dietary patterns, such as a Mediterranean diet, which is rich in fruits, vegetables, olive oil, and legumes, may be protective against mental health disorders (31–38). By contrast, increased risk of mental disorders has been observed with dietary patterns, such as the Western diet, characterized by high intake of saturated fat and refined carbohydrates (33, 39–41).
Inflammation presents one feasible mechanism through which diet may affect the risk of mental disorders. This is supported by multiple cohort studies showing that higher DII scores are associated with increased risk of depression (42–49).
Combining all longitudinal data on this topic (including 77,420 participants from seven different studies), a recent meta-analysis confirmed that higher levels of dietary inflammation were associated with 31% increased risk of depression over the 5- to 13-year follow-up period (50). This meta-analysis also found that pro-inflammatory diets were more strongly associated with depression among females than males (50), although significant relationships were observed for both sexes.
Despite these positive findings on links between depression and dietary inflammation calculated from self-report measures, future research must establish if these relationships are mediated by biological markers of inflammatory status.
Although a number of studies have found joint relationships between dietary inflammation, inflammatory markers, and depressive symptoms (51–53), those findings are inconsistent with other results showing that dietary patterns associated with heightened inflammatory markers do not consistently predict depression scores (54).
Currently, there is an urgent need for longitudinal studies to assess how dietary inflammation is related to the onset of other classes of SMI, because there is currently no strong evidence linking dietary inflammation with risk of bipolar disorder or schizophrenia. As the effects of dietary inflammation on mental health are also observed in adolescence (51), when the majority of SMIs first arise (55), the potential impact that this may have on risk of bipolar and psychotic disorders is worthy of further examination.
Along with clinical symptoms, people with SMI (and particularly schizophrenia) also display a range of cognitive deficits (56–58), which impede daily functioning (59, 60), and are not treated by psychotropic medications (61, 62). There is an emerging literature suggesting that elevated peripheral inflammatory markers are associated with deficits in cognitive function among patients with psychiatric disorders (1, 63).
Though the specific mechanisms underlying this association remain unclear, chronic and acute inflammation is thought to have a number of detrimental effects on brain structure and function, which, in turn, appear to adversely affect cognitive performance (64–66).
Poor diet and obesity also have a well-established link with cognitive dysfunction (67, 68). There is mounting evidence that these associations may be mediated by inflammatory processes (69), suggesting that diet has the potential to act as a modifiable risk factor for cognitive dysfunction both in clinical and non-clinical populations.
Much of the work investigating the association between diet, inflammation, and cognition has come from a series of cross-sectional and longitudinal studies in older adults, which indicate that diets with high inflammatory potential may be associated with accelerated cognitive decline and reduced brain volume (70–72).
Considering the high levels of dietary inflammation and cognitive deficits observed in SMI, along with indicated relationships between cognitive functioning and diet in other populations, this area presents a promising avenue for future research (73).
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Original Research: Open access
“Nutritional psychiatry: Towards improving mental health by what you eat “. Roger A.H.Adan, Eline M.van der Beek, Jan K.Buitelaar, John F. Cryan, Johannes Hebebrand, Suzanne Higgs, Harriet Schellekens, Suzanne L. Dickson .
European Neuropsychopharmacology doi:10.1016/j.euroneuro.2019.10.011.
