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Principal Investigator: ERIC M STICE
Organization: STANFORD UNIVERSITY
Fiscal Year: 2024
Award: $638,449
Funding agency: National Institute of Diabetes and Digestive and Kidney Diseases
ABSTRACT
Obesity is the second leading cause of premature death. Consumption of ultra-processed foods is theorized to
be a key cause of obesity. Ultra-processed foods are formulations of cheap industrial sources of dietary energy
and nutrients plus additives such as fat, sugar, and flavors that enhance acceptability of the foods. A cross-
over experiment with overweight adults found that ad lib access to an ultra-processed diet for 2-weeks resulted
in increased caloric intake (508 kcal/day) and more weight gain versus ad lib access to a minimally-processed
diet matched for presented calories, energy density, macronutrients, sugar, sodium, and fiber (Hall et al.,
2019). The fact that ad lib access to ultra-processed foods resulted in a large increase in caloric intake and
weight gain implies that ultra-processed foods may more effectively activate brain regions implicated in reward
processing, attention/salience, and memory that influence eating behavior. However, no brain imaging study
has experimentally tested whether ultra-processed foods are more effective in activating brain regions
implicated in reward, attention, and memory than minimally-processed foods or experimentally investigated the
relative role of the elevated caloric density versus the flavor enhancers of ultra-processed foods in driving
greater activation of these brain regions. Preliminary data showed that tastes of ultra-processed high-calorie
chocolate milkshake produced greater activation in regions implicated in reward valuation (caudate, nucleus
accumbens), attention/salience (precuneus), and memory retrieval (medial temporal gyrus, dorsomedial
prefrontal cortex) than tastes of ultra-processed low-calorie chocolate milkshake. Aim 1 is to test the
hypothesis that tastes, anticipated tastes, and images of ultra-processed foods activate reward, attention, and
memory regions more than tastes, anticipated tastes, and images of minimally-processed foods, and evaluate
the relative role of the higher caloric content versus flavor enhancers in engaging these regions using a 2 x 2
experimental design. Aim 2 is to test the hypothesis that ultra-processed versus minimally-processed foods
promote stronger learning of cues that predict tastes of ultra-processed foods (incentive sensitization), which is
important because elevated reward region response to food cues/images increases risk for future weight gain
(Demos et al., 2012; Stice et al., 2015; Yokum et al., 2014). Aim 3 is to test the hypothesis that participants
who show greater activation in reward/attention/memory regions in response to ultra-processed foods will
consume more ultra-processed foods ad lib and show greater future body fat gain, and to establish neural
fingerprints that predict ad lib ultra-processed food intake and body fat gain. Aim 4 is to test the hypothesis that
participants who show stronger reward cue learning in response to ultra-processed foods will consume more
ultra-processed foods ad lib and show greater future body fat gain. Improved knowledge of neural factors that
increase risk for body fat gain should guide the design of more effective obesity prevention programs and
treatments, which is critical because current prevention programs and treatments have limited efficacy.
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