Elsevier

Appetite

Volume 63, 1 April 2013, Pages 119-128
Appetite

Research review
The longer-term impacts of Western diet on human cognition and the brain

https://doi.org/10.1016/j.appet.2012.12.018Get rights and content

Abstract

Animal work over the last three decades has generated a convincing body of evidence that a Western diet – one high in saturated fat and refined carbohydrates (HFS diet) – can damage various brain systems. In this review we examine whether there is evidence for this in humans, using converging lines of evidence from neuropsychological, epidemiological and neuroimaging data. Using the animal research as the organizing principal, we examined evidence for dietary induced impairments in frontal, limbic and hippocampal systems, and with their associated functions in learning, memory, cognition and hedonics. Evidence for the role of HFS diet in attention deficit disorder and in neurodegenerative conditions was also examined. While human research data is still at an early stage, there is evidence of an association between HFS diet and impaired cognitive function. Based upon the animal data, and a growing understanding of how HFS diets can disrupt brain function, we further suggest that there is a causal link running from HFS diet to impaired brain function in humans, and that HFS diets also contribute to the development of neurodegenerative conditions.

Highlights

Western diets tend to be high in saturated fat and simple carbohydrates (HFS). ► This review examines the impact of HFS diets on the human brain. ► HFS diets impair several aspects of cognition and damage associated brain areas. ► HFS diets may cause such damage via several established mechanisms. ► HFS diets also seem to contribute to the onset of neurodegenerative conditions.

Introduction

There has been a rapid global shift in dietary composition, from diets high in complex carbohydrate and fiber, to what has been termed the Western diet, with a high proportion of fat and refined sugars, reduced complex carbohydrate and fiber intake and reduced fruit and vegetable consumption (Drewnowski, 2000, Drewnowski and Popkin, 1997; Nielsen, Siega-Riz, & Popkin, 2002; O’Dea et al., 1990). While intake of fats and sugars was previously restricted due to availability, the agricultural revolution and industrial revolution introduced profound changes to availability of fats and sugars. The introduction of animal husbandry during the agricultural revolution resulted in meat with a far greater saturated fat content and allowed for consumption of high fat dairy products from mammals other than humans (Cordain et al., 2002). Advances in technology during the industrial revolution increased the availability and affordability of refined grains, sugars and vegetable oils (Cordain et al., 2005). Although these changes occurred over hundreds of years, they paved the way toward the current food environment where the Modern Age has seen changes to the food system over the past few decades. One of many key changes to the food environment has been the penetration of convenience and fast food stores (Reardon, Timmer, Barret, & Berdegue, 2003), and the relatively low cost of fats and sugars compared to fresh fruit and vegetables (Drewnowski et al., 2004, Popkin, 2011). This has then favoured convenient processed foods that contain high concentrations of refined grains, salt and sugars, as well as saturated fat (Asfaw, 2011, Stender et al., 2007).

Changes to dietary fat and sugar composition have been accompanied by considerable adverse health consequences. Research has consistently correlated the increased incidence of obesity to increases in both fat (Bray and Popkin, 1998, Paeratakul et al., 1998) and sugar intake (Elliott et al., 2002, Howard and Wylie-Rosett, 2002, Ludwig et al., 1999, Malik and Hu, 2012). Further, high saturated fat and refined sugar (HFS) diets have been implicated in a range of chronic diseases, notably type 2 diabetes (Borkman et al., 1991, Gross et al., 2004, Salmeron et al., 1997, Steyn et al., 2004) and cardiovascular disease (Brunner et al., 2008, Hu et al., 1997, Hu et al., 1999, Liu et al., 2000). However, of similarly great concern, is the emerging evidence that HFS diets have long-term adverse impacts on brain function and behavior.

The main objective of this paper is to review the evidence that HFS diets impair two key aspects of neurological function: (1) cognitive abilities, especially episodic memory, attention and inhibition, and (2) reward processes. We will describe alterations to the specific brain regions thought to underlie these effects and the implications of these changes for appetite regulation, with a specific focus on human data – where possible.

Section snippets

HFS diets and cognitive function

High saturated fat (SF) intake has been implicated in impairment of various cognitive functions, including memory, working memory, attention and inhibitory control. A cross-sectional study of a middle aged population demonstrated that SF intake was associated with increased risk of impaired cognitive functions, including memory, speed and flexibility (Kalmijn et al., 2004). In women with type 2 diabetes, higher SF intake was associated with greater cognitive impairment on a global score

HFS diets and neurodegenerative disease

Neurodegenerative disease is an umbrella term describing a group of conditions characterized by progressive nervous system dysfunction. These include Alzheimer’s disease (AD), Parkinson’s disease (PD) and mild cognitive impairment (MCI), a state of impaired cognitive function that is early and abnormal, but symptoms are not as severe as dementia (Petersen, 2004). We discuss research suggesting HFS intake as a putative factor in development of these diseases.

A cross sectional study conducted by

HFS diets and cognitive function in children

The diets of children in Western societies show similar patterns to adults, with evidence for increased intake of processed foods high in salt, saturated fat and refined sugar. For instance, 2–18 year olds in the United States showed a large increase in intake of salty snacks, pizza and soft drinks between the years 1977 and 1996, as well as greater energy intake from restaurants and fast food establishments (Nielsen et al., 2002). In Australia, children aged 10–15 in 1995 were consuming more

Neural basis of cognitive deficits caused by HFS diet consumption

The cognitive functions affected by HFS diets – memory, attention, working memory and inhibitory control – appear to be subserved predominantly by two brain regions; the hippocampus and prefrontal cortex (PFC). The hippocampus has a well-established role in supporting memory function, with damage to this structure in humans associated with major impairments to episodic memory (Duyckaerts et al., 1985, Scoville and Milner, 1957, Zola-Morgan et al., 1986). Animal data suggests hippocampal lesions

Implications of cognitive deficits caused by HFS diet consumption for appetite regulation

The brain regions affected by HFS diet consumption have also been shown to be involved in appetite regulation. A role for hippocampal dependent memory processes in energy intake regulation was triggered by findings that densely amnesic patients with bilateral hippocampal damage would readily eat a second meal within 10–30 min of consuming the first and, when asked, could not recall what was eaten (Hebben et al., 1985, Rozin et al., 1998). Thus, memory for what has been eaten and how much was

HFS diets and affective function

The human affective system can be characterized as having three major components. First, the neurotransmitter and brain systems involved in ‘wanting’, principally the mesolimbic dopamine system, important for generating a desire to consume palatable foods in response to direct or indirect cues. Second, the neurotransmitter and brain systems involved in ‘liking’, including endogenous opioids and endocannabinoids, in the ventral pallidum, hypothalamus, and brain stem areas. These act to mediate

Can effects of HFS diet consumption be reversed?

One of the questions that has not yet been resolved by the literature in this field is whether the impact of HFS diet consumption on the brain can be reversed through discontinuation of the diet. Alternatively, given that the mechanisms potentially underlying the negative effects of Western HFS type diets on the brain include reduced BDNF and increased oxidative stress, therapies targeting these factors might therefore be effective for remediating the effects of HFS diets. For instance,

Concluding remarks

This manuscript has highlighted several long-term brain-related costs of consuming a HFS diet. It appears that an HFS diet can lead to changes in brain regions associated with energy regulation and the affective appraisal of food. It is now widely agreed that there has been a rise in obesity levels in Western societies over the past 30 years, with recent estimates suggesting greater than one third of the United States population are obese (Flegal, Carroll, Ogden, & Curtin, 2010) and around one

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