Is too much sugar a form of brain abuse?

We all know too much sugar is bad for us.  But did you know that having unfettered access to sugar might produce brain changes similar to highly stressful situations, such as neglect or abuse?  A recent study published in Frontiers in Molecular Neuroscience comparing the effects of unlimited sugar availability and the effects of early life stress in rats might suggest just that.

The mammalian brain uses glucose as its main source of energy, and tight regulation of glucose metabolism is essential for normal brain function.  However, it is increasingly being appreciated that diets high in added sugar may be harmful to optimal brain activity.  Stress can intensify our consumption of sugary products as most of us know all too well.  Who hasn’t reached for the Oreo packet while burning the midnight oil before an exam?!  Sugar causes temporary relief of anxiety and stress in both animals and humans.  But does increasing sugar intake actually cause any long term damage to the brain function?  And if it does, how comparable is the damage to that caused by extreme stress?  And as sugar is often used as a stress reliever, can sugar compound any harm?  This is what Maniam et al. (2016) tried to address by looking at access to unlimited sugar consumption and stress in rats.

But first a little background about stress and how it can affect the brain.  Stress that goes above and beyond normal physiological checks and balances can affect the brain in particular ways.  One very important form of stress is what can be termed Early Life Adversity (ELA), which includes tragedies such as maltreatment, deprivation, violence, abuse and parental instability.  ELA is an important risk factor for common psychiatric illnesses such as depression, PTSD, and psychotic disorders.  We know ELA can change brain structure and function in unique ways both in humans and in animal models.

The hippocampus (a well-studied region in the temporal lobe associated with memory, spatial navigation and a key information processing component of the emotional limbic system) is often smaller in both individuals with ELA and patients with psychiatric conditions.  Hippocampal cells also express high levels of a receptor called the glucocorticoid receptor (GR).  Cortisol – a glucocorticoid hormone – secreted from the adrenal gland in response to stress, can interact with these receptors allowing this highly integrative brain region to serve as an important interface between stress and the brain.  However, such high concentrations of GRs leave the hippocampus vulnerable to the destructive effects of chronic stress, through such mechanisms as reduced neuronal excitability, reduced neuron growth (neurogenesis) and ultimately shrinkage or atrophy of hippocampal tissue.  Chronically high cortisol/stress has been demonstrated to provoke a compensatory reduction of GR expression in both humans and animals.  Maybe unsurprisingly, it also has been shown that hippocampal GR expression is reduced in both humans and animals with ELA as well as in depressed and suicidal patients.  Thus, reduced hippocampal GR expression may be thought of as a type of molecular marker for mental health disorders, particularly at the interface between ELA and mental health.

So following that brief overview of stress, ELAs and the hippocampus, can sugar intake cause similar brain changes as seen in ELA?  With that question in mind, Maniam et al. (2016), in Frontiers in Molecular Neuroscience report a rather interesting result linking stress and sugar consumption.  They show that female rats exposed to either ELA (in the form of a simulated maternal neglect called Limited Nesting) or allowed unlimited access to high sucrose water showed strikingly similar expression of GRs and other plasticity and inflammation proteins — a rather astonishing reduction of 40% in GR expression in both groups in fact.  Interestingly, there was no additive effect of combining sucrose water with ELA, with such rats also showing the same loss of 40%, and no significant differences in weight gains across all groups.

As well as other proteins and GR, the authors also report 46% reduced expression of the Neurod1 gene in the ELA, sucrose and combined ELA/sucrose rats.  This gene is involved in hippocampal plasticity (adapting neurons to changes) as well as adult neurogenesis (new neuron growth) in many species, suggesting a role in brain development, growth and repair.  There currently is no direct evidence linking reduced Neurod1 to reduced neuroplasticity and neurogenesis in humans, but it is hypothesized to have similar effects as other mammals.

As both GR and Neurod1 expression was indistinguishable between both rats who drank unlimited amount of sugary water and rats exposed to stress, Maniam et al. suggest this characteristic molecular profile may be due to similar physiological mechanisms at play.  Reduced GR expression is compatible with chronic overactivation of the stress system and the associated toxic effects on brain structure and function.  Reduced Neurod1 expression implies a lack of neuron growth, repair and development.

Coming back to humans, the similarity of the molecular deficits seen in ELA and sugar drinking may be of huge public health concern.  We know stress can lead to increased sugar consumption, and we know that chronic stress may affect the brain in particular ways.  This new evidence suggests that possibly unlimited access to sugar is just as bad as significant early life stress.  Such a finding is especially relevant considering the availability of cheap easily accessible sugar sweetened beverages and foods.  As children, in particular, are exposed to diets high in sugar, we need to question the dietary implications of a sugary Western diet on young developing brains.  With the effects of early life stress and sugar showing strikingly similar effects on the molecular organization of the brain, could allowing children and young adults access to such diets be considered (from a neuron’s perspective) a form of adversity on a par with other more recognizable stressors, such as neglect or abuse?

Food for thought.

(Sugar free I hope!)

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Written by Darren Roddy

Images by Jooyeun Lee

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References:

Maniam, Jayanthi, et al. “Sugar consumption produces effects similar to early life stress exposure on hippocampal markers of neurogenesis and stress response.” Frontiers in Molecular Neuroscience 8 (2016): 86.