There have been a multitude of events over recent years which have highlighted the inequalities within society – from a decade of austerity, to the Grenfell Tower fire, disproportionally high BAME deaths during COVID-19 pandemic, and the Black Lives Matter movement. Now, as the UK economy enters the most severe regression within its history, it is likely that the inequalities displayed may well become starker.
The need for food banks in the UK has accelerated dramatically over the past decade – from a single food bank in 2008, to more than 2,000 in 2019, providing more than 1.6 million food parcels; this being a 19% annual increase, of which more than half a million food parcels provided go to children. There are a host of contributing factors for those using food banks, although common themes are related to reduced income not covering the cost of food (33%), delays to benefits (20%), and changes to benefits (17%).
As we know, the majority of those experiencing mental ill health are disproportionately located within a lower socioeconomic cohort. This is considered due to the additional psychological and social stressors associated with living in relative and absolute poverty.
Further considerations include reduced access to the material and psychosocial resources to regain mental wellness; again, this is also associated with poverty. While the relationship is complex, it is accepted that if one lives in poverty, mental illness is more likely, and living in poverty can make recovery more difficult.
But, let’s consider the biological implications of food poverty upon brain development. Within our early development in utero – our neurons migrate from the germinal area to form cortical layers within our central nervous system. This process, referred to as radial glial migration, is essential to create effective, and functional, neural networks. This is a critical process within our mammalian development, and it has been evidenced that deficit of required nutrition during these periods can result in longer-term functional and structural brain changes, and can contribute to neuropsychiatric sequelae, including schizophrenia.
Psychosis can loosely be defined as a detachment from reality, hallmarked by reality distortion and a loss of functioning; this frequently includes hallucinations and the development of false belief systems. This syndrome, if recurrent or prolonged, can lead to the chronic relapses. The features of psychosis can be managed using antipsychotic medications combined with psychological interventions and social rehabilitation that enhance an individual’s ability to recover and manage these symptoms moving forward.
There is comprehensive evidence to suggest that prenatal maternal malnutrition increases the vulnerability of the undernourished fetus developing schizophrenia in adulthood.
This is largely based on reviewing retrospective studies which explored famines that occurred in the Netherlands (1944–1945) and in China (1959–1961). Further research into such ‘natural experiments’ agree, and indicate that the presence of famine, along with prenatal malnutrition, to be particularly influential during the first trimester of pregnancy upon fetal brain development, particularly when considering the risk of schizophrenia in adulthood.
Biological markers indicating malnutrition of the fetus include low birth weight, pre-eclampsia, intrauterine growth restriction, and reduced length at the time of birth relevant to gestational age. Of course, one should also consider the psychosocial perspective of famine – such as experiencing chronic stress, adverse living conditions, and sub-optimal health related behaviours; particularly how these factors may impact upon fetal brain development, which include dysfunctional endocrine and immune system responses.
We consider neural development during critical periods to be a highly complex set of processes – requiring satisfactory levels of multiple nutrients delivered to a healthy fetus via an unimpaired placenta within a healthy intrauterine environment. It is perhaps unsurprising to suggest that any impairment of these processes would be associated with poorer outcomes post-delivery, including increased vulnerability to the risk of subsequent mental illness. Globally, iron deficiency is regarded as the most common nutritional deficit. Maternal iron deficiency can be a direct consequence of nutritional deprivation, and there is evidence to suggest that this is related to impaired regulation of a number of metabolic processes which appear to be associated with schizophrenia; these include the atypical development of neural structures and anomalous morphology, aberrant dopaminergic functioning and DNA epigenetic modifications.
There is clear evidence that prenatal malnutrition is associated with aberrant fetal brain development. There is also strong evidence to suggest that such insults lead to a greater than average vulnerability to developing schizophrenia in adolescence and adulthood.
The exact mechanisms remain somewhat unclear, although it is increasingly apparent that fetal brain development requires a varied, sustained and well delivered spectrum of nutrients; and that even a slight impairment in this process can lead to pervasive and longstanding implications. However, it is important to acknowledge that risk factors are a subtle blend of genetic, environmental and developmental factors; and that prenatal malnutrition should not be considered an indicator of schizophrenia in later life per se.
There is overwhelming evidence that poverty, including food poverty, is associated with poorer health outcomes. While many of these physical health disorders, often referred to as ‘Victorian diseases’, may be easier to identify, the impact of malnutrition on mental health – both of this generation and the next – is more nuanced. The need to eliminate the clear societal inequalities remains critical. The need to abolish food poverty is essential if we, as a society, are to safeguard the mental health of our future generations.
Joel Petch is a Senior Lecturer in Mental Health and Clinical Science at Canterbury Christ Church University. Joel tweets @joelpetch
