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Current Addiction Reports
https://doi.org/10.1007/s40429-022-00417-8
FOOD ADDICTION (E SCHULTE, SECTION EDITOR)
The Reinforcing Natures ofHyper‑Palatable Foods: Behavioral
Evidence forTheir Reinforcing Properties andtheRole oftheUS Food
Industry inPromoting Their Availability
TeraL.Fazzino1,2
Accepted: 10 May 2022
© The Author(s), under exclusive licence to Springer Nature Switzerland AG 2022
Abstract
Purpose of Review Hyper-palatable foods (HPF) may exploit our neurobiological propensities to seek and consume reward-
ing foods. The review highlights evidence from basic behavioral and neurobiological studies in humans on the reinforcing
properties of HPF and consequences of repeated HPF consumption over time. The review also addresses HPF within the
context of the US food environment.
Recent Findings There is reasonably strong behavioral evidence to indicate that HPF may have reinforcing properties that
are similar to drugs of abuse. Evidence indicates that healthy individuals may exhibit greater preference for HPF relative to
non-HPF and that powerful cues may develop that indicate the presence of HPF as a reward. Preliminary evidence indicates
that elevated HPF intake may yield neurobiological consequences for brain reward neurocircuitry. The US food environment
provides wide and easy access to HPF. Conceptualized as a substance, HPF exist unregulated in our environment, similar
to the tobacco availability in the 1940s. Parallels have been drawn between food and tobacco company practices; a review
of industry documents indicates that tobacco companies owned major US food companies since the 1980s, possibly leading
the development and proliferation of HPF.
Summary There is reasonably strong evidence to indicate that HPF may have powerful reinforcing properties similar to
drugs of abuse; however, more longitudinal work is needed.
Critical attention to the factors and drivers of HPF proliferation in the US food system is paramount to conceptualizing the
presence of HPF in our food environment and in considering strategies to protect the US population’s health.
Keywords Food reward· Food addiction· Reinforcement· Food environment· Policy
Introduction
Food asaReinforcer andHyper‑Palatable Foods
Food consumption promotes our survival. Accordingly, con-
sumption of food is an inherently rewarding process that
serves to increase the likelihood that we consume more food
in the future [1, 2]. There are multiple mechanisms through
which food serves to reinforce our ingestive behavior, which
consist of behavioral learning processes and internal physi-
ological processes. The role of physiological processes,
such as those related to gut-brain signaling, have recently
been reviewed [3, 4]. Behavioral reinforcement processes,
which may have important influences on neurobiological and
physiological processes, will be the focus of this review.
Many foods are palatable in their originally occurring
forms in nature. For example, fresh fruits such as an apple
are typically sweet and pleasant to ingest. Many vegetables,
such as zucchini or broccoli, have savory flavors and may
also be pleasant to ingest. The appealing properties of foods
elicit our approach toward and consumption of food, thereby
promoting our survival [5]. Neurobiologically, consump-
tion of a food (upon initial exposure) activates brain reward
neurocircuitry, which provides a pleasant eating experience
This article is part of the Topical Collection on Food Addiction
* Tera L. Fazzino
tfazzino@ku.edu
1 Department ofPsychology, University ofKansas, 1415
Jayhawk Blvd, 4th Floor, Lawrence, KS66046, USA
2 Cofrin Logan Center forAddiction Research andTreatment,
University ofKansas, Lawrence, KS, USA
Current Addiction Reports
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and serves to promote further ingestion [6, 7]. With repeated
consumption of a food, cues indicating the presence of a
food (e.g., sweet scent of an apple) activate brain reward
pathways, promoting approach and consumption of the food
[8]. Along with the pleasant and rewarding characteristics
of food, foods that occur in nature typically contain one
primary palatability-inducing nutrient that occurs in com-
bination with nutrients that promote satiety. For example,
sugar in an apple is accompanied by both fiber and water,
which promote satiety and slow the process through which
sugar may be absorbed and digested. Thus overall, a set of
evolutionarily important processes exist that reinforce our
approach toward and consumption of food, and these occur
alongside nutritional safeguards, such as satiety-promoting
nutrients, that together influence our consumption behavior
[9].
Hyper‑Palatable foods
In the current US food system, many available foods have
been modified from their originally occurring forms in
nature. Food modification is not inherently problematic.
However, some foods have been altered in ways that may
serve to exploit our neurobiology and behavioral propen-
sity to approach and consume palatable foods. For example,
hyper-palatable foods (HPF) are foods that have substantial
deviations from their naturally occurring forms, and these
deviations are designed to maximize a food’s rewarding
properties during consumption [10•]. In contrast to natu-
rally occurring foods that contain one primary palatability
inducing nutrient, HPF contain combinations of nutrients
that are not typically found in nature (e.g., high quantities of
both sugar and fat) [11]. The combinations of nutrients are
present at thresholds that artificially enhance a food’s palat-
ability and provide a highly rewarding eating experience,
eliciting strong activation in brain reward regions [3, 12].
Furthermore, HPF may delay engagement of physiological
satiety mechanisms and extend eating occasions involving
HPF. Sensory specific satiety is an exposure-based mecha-
nism that serves to bridge food intake with gastro-intestinal
reception and processing of food [13]. Within a meal, each
bite of a food will be experienced as less enjoyable or pleas-
ant than the prior one, which is a learning-based habitua-
tion process that leads to the cessation of consumption [13].
However, sensory-specific satiety is a process that is subject
to variability based on characteristics of a food, and evidence
indicates that HPF may garner weaker sensory specific sati-
ety responses compared to non-HPF, which may facilitate
extended eating occasions [14]. Taken together, HPF may
create a highly rewarding eating experience and may delay
engagement of physiological satiety mechanisms, leading to
excess energy intake.
Many different types of foods may be hyper-palatable.
Our analysis of HPF in the US food system revealed that
HPF are widely available and comprise many different types
of foods and products [10•]. For example, some HPF may be
fast foods and desserts, which may be expected to be hyper-
palatable. However, HPF may also many meal-based items,
frozen foods sold in grocery stores, snacks, and even some
foods marketed as healthy due to having reduced calories
or fat [10•]. Furthermore, foods identified as related con-
structs in the literature, such as ultra-processed foods and
high energy density foods, may also be hyper-palatable. For
example, ultra-processed foods undergo extensive process-
ing and often contain industrial additives that are designed to
enhance a food’s palatability (e.g., high fructose corn syrup
as a sweetener); thus, many ultra-processed foods may be
hyper-palatable [15]. In addition, foods with elevated energy
density may contain nutrients such as fat and/or sugar that
increase both the caloric density of the food and a food’s pal-
atability [16, 17]. Thus, foods with high energy density may
also have enhanced palatability. To this point, our prior work
has indicated that approximately 50% of foods that are HPF
also have high energy density and that > 60% of HPF may
also be classified as ultra-processed [10•, 18]. Thus, foods
that have enhanced palatability are extremely widespread in
our food system and are present across many types and cat-
egories of foods. In this review, the term HPF will be used to
describe foods that may have artificially enhanced palatabil-
ity; however, the foods may be described using other termi-
nology (e.g., high energy density) in their original articles.
Hyper‑Palatable Food asaSubstance
HPF may serve as potent rewards and may yield reinforce-
ment processes that drive habitual intake of HPF, similar to
the reinforcement processes observed with other powerful
reinforcers, such as drugs of abuse. In this regard, Gearhardt
and colleagues have suggested that HPF may be considered
the target substance of food addiction [19•, 20]. If viewed
as a substance, HPF may be expected to induce a series
of behavioral and neurobiological changes from repeated
consumption over time, which would serve to drive and
maintain habitual HPF intake. For example, with drugs of
abuse (alcohol, nicotine, opioids, etc.), ample evidence has
indicated that repeated consumption of a substance yields a
series of neurobiological changes that drive continued use
[21, 22]. For example, with repeated substance use, neuroa-
daptive changes occur from repeated and excessive activa-
tion of brain reward neurocircuitry, such that individuals
experience blunted pleasure or reward during use, but also
experience greater motivation or drive to use as they become
hyper-sensitive to substance-related cues in the environment
(sensitization) [22]. As a result, a behavioral pattern occurs
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in which individuals exhibit strong motivation to use and
engage in compulsive use despite consequences, often while
experiencing less pleasure or rewarding effects while using
[21, 23]. Importantly, the effects are on a continuum and in
a dose–response relationship. Thus, effects may be relevant
for those who engage in a variety of use patterns, from occa-
sional to excessive or daily use [24]. Applied to HPF, similar
behavioral, motivational, and neurobiological changes may
be expected to occur as repeated HPF intake may serve to
dysregulate neurobiological reinforcement mechanisms [25].
Effects may be expected to occur most prominently among
individuals who engage in excess HPF intake and/or who
have individual risk factors or vulnerabilities to the reward-
ing effects of HPF [26–28]. However, the reinforcing proper-
ties of HFP would also be expected to be observed on a con-
tinuum, with most of the population exhibiting some level
of approach toward and preferential consumption of HPF,
which may yield passive overconsumption and/or reward-
driven eating behavior. A smaller segment of the population
would be expected to develop compulsive use of HPF due
to preexisting vulnerabilities to the reinforcing properties of
HPF [29]. The evidence for HPF as a potent reinforcer with
similar properties as other substances of abuse is reviewed
herein, with a summary of behavioral evidence first, fol-
lowed by neurobiological evidence in humans. It should
be noted that the foods evaluated in the studies described
below aligned with the premise of hyper-palatability; how-
ever, many used other terms to describe and identify foods.
Behavioral Evidence (Humans)
If HPF serve as potent reinforcers and drive HPF intake
behavior, evidence from basic behavioral studies should
indicate that healthy individuals exhibit preferential valu-
ation and approach toward HPF, relative to foods that are
not HPF (non-HPF). Evidence should also indicate that
with repeated consumption, individuals experience greater
motivation to consume HPF, becoming hyper-sensitive to
HPF cues (sensitization). Overall, there is reasonably strong
evidence to suggest that HPF may be valued and preferred
over non-HPF, and there is preliminary evidence indicating
that repeated HPF intake may elicit enhanced motivation to
consume HPF (sensitization) over time. However, given the
substantial body of literature focused on consequences of
HPF intake (e.g., obesity and food addiction), far fewer basic
behavioral studies have been conducted to establish these
fundamental aspects of HPF as reinforcers among healthy
individuals.
Evidence indicates that healthy individuals may on
average exhibit greater valuation of and preference for
HPF compared to non-HPF. Studies in the literature have
examined preferences for HPF using behavioral tasks that
measure valuation of HPF and non-HPF based on (1) how
much individuals are willing to pay to access an HPF or non-
HPF or (2) how much effort individuals exhibit (e.g., mouse
clicks) to access an HPF or non-HPF. Overall, evidence has
indicated that on average, healthy individuals may be will-
ing to pay more for or exhibit greater behavioral effort to
obtain an HPF vs a non-HPF, indicating greater valuation
and preference for HPF vs non-HPF among healthy samples
of adults [30–34], adolescents [35–37], and children [38]. In
addition, one study examined preference and choice impul-
sivity for HPF vs non-HPF among healthy adults and used
a standardized definition of HPF to select food items [39].
Similar to the studies of HPF valuation, results indicated
that individuals exhibited greater choice impulsivity that was
specific to HPF, compared to non-HPF [39]. Thus overall,
evidence suggests that healthy individuals on average exhibit
preferential valuation of HPF relative to non-HPF, likely due
to their stronger reinforcing properties.
Evidence also supports the premise that individuals seek
out/approach HPF for their rewarding effects. First, a large
body of evidence has suggested that cues that indicate the
presence of HPF, such as food logos, signs, and related
paraphernalia, may become conditioned stimuli that predict
the availability of HPF [40–42]. We navigate our environ-
ments by learning about cues that maximize our chances
of obtaining evolutionarily meaningful rewards (e.g., food)
[40]. Thus, the development of conditioned cues for HPF
speaks to the strength of HPF as a reinforcer and parallels
the cue development processes that occur with substances
[43]. In addition to eliciting approach to HPF cues, prelimi-
nary evidence also indicates that HPF may be sought and
consumed for their rewarding effects. For example, research-
ers have found that one common motive that individuals
seek out HPF is for their rewarding effects, termed enhance-
ment motive in the literature [44, 45]. Consuming HPF for
their rewarding effects has been specifically identified as an
important motive in binge eating when conceptualized on a
continuum from passive overconsumption to loss of control
eating [46]. Furthermore, preliminary evidence indicates
that HPF, when defined using the standardized definition,
comprised the vast majority of calories consumed during
binge eating episodes among a clinical eating disorders
sample, thus indicating that HPF may be primarily targeted
for consumption during clinically significant binge eating
episodes [47]. Overall, evidence indicates that HPF may be
sought out for their rewarding effects, consistent with other
substances of abuse.
Preliminary behavioral evidence from several studies has
suggested that repeated HPF consumption over time may
increase motivation to seek out HPF as individuals become
hyper-sensitive to HPF cues; however, observed effects have
varied across studies and groups examined. For example,
two experimental studies among healthy adults used 14-day
exposure protocols in which participants consumed the same
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HPF snack daily. Both studies reported that motivation to
consume the HPF, measured behaviorally, increased over
the exposure period for individuals with obesity; however,
motivation to consume HPF decreased among individuals
without obesity [48, 49]. In a longer trial among healthy
adults, findings revealed that motivation to consume HPF
did not change following daily HPF snack intake over
12weeks [50]. The retention of motivation to consume the
HPF snack despite repeated exposure over time was inter-
preted to indicate that HPF may circumvent habituation pro-
cesses that would be expected to occur with repeated expo-
sure over time [50]. Finally, in another 14-day consumption
trial among adolescents, researchers reported the sample
on average exhibited decreases in motivation to consume
HPF following daily HPF intake [37]. However, the small
proportion of adolescents in the sample who experienced
increased motivation to consume HPF had greater weight
gain at 2-year follow-up [37].
Overall, a reasonably strong body of basic behavioral
evidence suggests that on average, healthy children, ado-
lescents, and adults may exhibit greater valuation of HPF
relative to non-HPF and may seek out HPF in response
to cues in the environment. Longitudinal evidence of the
effects of HPF from repeated consumption over time is much
more limited and has indicated that in response to repeated
HPF intake over 14–21days, some individuals may experi-
ence enhanced motivation to consume HPF (sensitization);
however, it is unclear whether the effects may be observed
overall or individuals who may be particularly sensitive to
the rewarding effects of HPF. Thus, more work is needed,
particularly longitudinal consumption studies to characterize
the effects of HPF exposure on potential change in motiva-
tion to consume HPF over time, which may lead to habitual
HPF intake.
Neurobiological Evidence (Humans)
A limited number of studies have examined the basic effects
of HPF consumption on brain reward neurocircuitry (exam-
ined cross-sectionally) and neurobiological changes (exam-
ined longitudinally). Regarding cross-sectional evidence of
HPF intake patterns and brain reward responsivity, most of
the evidence has been indirect. For example, substantial evi-
dence from cross-sectional studies has identified differences
in brain reward responsivity by weight class or BMI [51]. In
these studies, BMI or obesity status has been used as a proxy
to indicate repeated/habitual HPF intake; however, most
studies have not studied the association between HPF intake
and brain reward responsivity explicitly. In this regard, in
a recent meta-analytic review of the literature, researchers
reported that individuals with obesity were found to exhibit
greater responsivity to food cues in brain regions that gov-
ern reward and motivation, suggesting that individuals with
obesity may exhibit sensitization to HPF cues [51]. Only
three prior cross-sectional studies directly examined the
association between HPF intake and brain reward respon-
sivity, all of which were conducted among healthy samples
of adolescents or adults. For example, the studies used fMRI
paradigms and found that greater dietary intake of HPF or
sugar was associated with greater responsivity to HPF cues
in brain reward regions (dorsal and ventral striatum), sug-
gesting sensitization to HPF [52], and reduced responsivity
in striatal regions when consuming an HPF (e.g., a milk-
shake) [53, 54], thus indicating blunted reward respond-
ing during consumption. Overall, more work is needed to
directly examine cross-sectional associations between HPF
consumption and differences in HPF motivation and reward
responsivity.
A small body of evidence from longitudinal studies sug-
gests that neurobiological changes may occur among ado-
lescents and adults from HPF or sugar intake over time.
However, only one prior study measured intake, and the
remainder assumed HPF intake through observed weight
gain. Specifically, Burger etal. [55] provided experimen-
tal evidence that indicated that after consuming a sugar-
sweetened beverage for 21days, adolescents exhibited
marked increases in motivation to consume the beverage
when exposed to cues and decreases in response in reward
regions (e.g., dorsal striatum) during beverage consumption
in fMRI. The large effects sizes suggested sensitization to
the sugar-sweetened beverage cues over time [55]. In addi-
tion, two repeated measures studies examined the associa-
tion between weight or body fat gain, which was assumed
to be a result of repeated HPF intake, and responsivity to
HPF cues and consumption [56, 57]. Findings indicated
that adolescents who gained body fat over a 3-year period
exhibited increased striatal responsivity to HPF cues, sug-
gesting increased motivation to consume HPF [56]. Further-
more, in a sample of adult women, individuals who gained
weight over a 6-month period were found to have reductions
in striatal responsivity to consumption of an HPF during
an fMRI paradigm [57], suggesting blunted responsivity to
HPF reward during consumption. In addition to these stud-
ies, three studies with healthy children [58] and adolescents
[59, 60] identified greater responsivity to HPF cues in brain
reward regions at baseline to be prospectively associated
with weight gain, with the assumption that greater HPF
intake yielded may have contributed to changes in weight
observed longitudinally.
Overall very limited evidence has directly connected HPF
intake to cross-sectional differences or longitudinal changes
in HPF reward responsivity and motivation. Most research
has used BMI or weight gain and assumed that HPF con-
sumption was the underlying driver. More research is needed
to directly examine the association between HPF intake and
neurobiological changes. While not reviewed herein, the
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animal literature presents compelling evidence that HPF and
sugar intake may yield substantial neurobiological changes
that are consistent with neurobiological changes observed
with substances of abuse [61–64]. Thus, evidence in the
human literature is needed to examine the basic connections
between HPF intake and changes in reward neurocircuitry
among healthy samples of children, adolescents, and adults,
information that is key to understand potential consequences
related to habitual/compulsive HPF intake, obesity, and food
addiction.
In addition to a limited body of evidence, the existing
literature is limited due to inconsistencies in terminology
and definitions used to describe highly reinforcing foods.
Prior studies in the behavioral and neuroimaging literature
used a variety of descriptive definitions (e.g., fast foods)
or terms (e.g., high energy density foods) when referenc-
ing foods that may be particularly reinforcing. Future work
using a standardize definition of foods that have enhanced
reinforcing properties is needed to bring concordance to the
literature. Recently, Fazzino etal. [39] provided a stand-
ardized definition of HPF, which specifies quantitative
thresholds for combinations of nutrients (fat, sugar, carbo-
hydrates, and/or sodium) that are hypothesized to induce
hyper-palatability and as a result may be highly rewarding
to consume. The provision of this definition is a first step in
facilitating research with a standardized definition, which
may strengthen scientific inquiry and policy guidance. In
addition, given that definitions of energy density and ultra-
processed foods do not directly address a food’s palatabil-
ity (but do address other important food characteristics that
may increase their reinforcing properties), it is important for
future research to elucidate the degree to which the defini-
tions identify foods that may be consistent with or may be
vary in their reinforcing properties compared to HPF. Over-
all, the field has substantial work to do to better define and
identify the specific characteristics of foods (e.g., ingredient
combinations and food processing characteristics) that yield
their excessive reinforcing properties, which may strongly
influence our food approach and intake behavior.
Distinction Between HPF asSubstance vs Individual
Differences inVulnerability toHPF
The present review focuses on the reinforcing properties of
HPF, conceptualized as a substance. This premise is distinct
from most of the literature, which has focused on identifying
individual-level differences in vulnerabilities to the effects of
HPF. Most research has focused on identifying subgroups or
characteristics of individuals who may be vulnerable to HPF
effects and may be at risk for developing obesity or food
addiction. For example, ample work from Epstein and col-
leagues has established that individuals differ in the degree
to which they value food as a reward and that individuals
with high food reinforcement may be at greater risk for obe-
sity [65–67]. In a similar lens of identifying individual-level
vulnerabilities to HPF, Stice and Burger [68] presented a
theoretical framework for obesity that identified individual-
level differences in sensitivity to HPF cues and neurobio-
logical changes from repeated HPF intake that may combine
to increase obesity risk. Finally, Gearhardt and colleagues
identified food addiction as a clinical phenomenon that is
exhibited among a subset of individuals who may be particu-
larly susceptible to the rewarding effects of HPF and who
demonstrate clinically significant symptoms and impairment
from HPF consumption [69, 70].
Overall, extensive work has been conducted in the field
to identify individual-level vulnerabilities to the rewarding
effects of HPF that may occur among a subset of individuals
in the population. Importantly, HPF may be the substance
that directly facilitates the observed effects and conse-
quences. Thus, it is critical to gain a more thorough scientific
understanding of HPF, defined using a standard definition,
as a substance, in a similar manner as the field of addiction,
which has conducted extensive research to understand the
basic neurobiological and behavioral impacts of substance
use (e.g., alcohol, nicotine, and opioids) on healthy indi-
viduals. Thoroughly understanding the neurobiological and
behavioral changes that may occur from the intake of HPF is
critical to developing prevention and treatment approaches
that recognize the potency of the substance (HPF) and best
address the target mechanism (HPF intake) that may yield
clinical consequences such as obesity and food addiction
among vulnerable individuals.
Hyper‑Palatable Foods intheUS Food
Environment
Behavior Doesn’t Occur inaVacuum: The Food
Environment
HPF are powerful reinforcers; however, use of a substance,
or HPF in this case, is largely influenced by the surrounding
environment. Choice is relative and depends on the avail-
ability of HPF, as well as the other alternatives in the envi-
ronment. In the USA, the food environment is considered
obesogenic and is structured in a manner that maximizes
access to HPF and provides limited access to alternative
foods (e.g., non-HPF such as fresh fruits and vegetables)
[71, 72]. This environmental structure may exacerbate
approach and consumption of HPF as normative eating
behavior (passive overconsumption), as well as potentially
pathological behavior (e.g., food addiction). Thus, the food
environment is structured to exploit our natural behavioral
tendencies to seek out convenience in HPF access, and HPF
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themselves are designed to exploit our neurobiological pro-
clivities to seek and consume highly rewarding foods. This
picture is grim when considering the degree to which it may
be possible to access and eat foods that do not excessively
activate our brain reward neurocircuitry and the potential
for population-level health consequences, such as obesity
and food addiction.
How Did We Get Here? US Tobacco Company
Involvement intheUS Food System
The US food environment has changed dramatically since
the early 1970s and may have been strongly influenced by
the entrance of US tobacco companies to the food system.
Below, changes in the food system are described first, fol-
lowed by a review of tobacco company involvement in the
food system. Before the 1970s, the food environment in the
USA was largely supplied by smaller, local food produc-
ers, and regional companies [73]. However, in the 1970s
and 1980s, larger food companies developed by absorbing
smaller food producers and food companies and centralizing
food processing and distribution efforts [74]. As a result,
food companies maximized their profits by consolidating
production expenses and distribution efforts while substan-
tially increasing sales in the USA and globally [74, 75]. As
food companies focused on minimizing costs, the companies
also focused on developing food technology and creating
less costly versions of ingredients, such as high fructose corn
syrup, an inexpensive alternative to sugar [76]. As a result,
the US food environment became saturated with inexpen-
sive, easily accessible HPF [75, 77].
The changes observed in the food environment since
the 1970s occurred alongside the entrance of a new player
in the US food system, US tobacco companies. Leading
tobacco companies in the USA, specifically Phillip Mor-
ris and RJ Reynolds, began investing in food companies
in the 1970s and 1980s, which served to compensate for
declining tobacco sales and increased federal regulation
of tobacco products in the USA [78, 79]. By the 1990s,
tobacco companies led the US food market in sales annu-
ally [80]. For example, tobacco company Phillip Morris
entered the US food market in the early 1980s and bought
two major food brands, Kraft and General Foods. By 1985,
Phillip Morris had more than double the US market shares
compared to any other food company [81], a position that
was maintained through the 1990s [80]. By 1999, Phil-
lip Morris brands led the market in sales of 17 out of 20
food product categories, such as frozen foods [78]. The
investment in the food system was extremely profitable
for Phillip Morris; sales from food products were approxi-
mately equal to sales of tobacco products between 1989
and 2001 [78, 82, 83] and helped buoy the company’s prof-
its during a time of intense litigation and profit loss from
tobacco. Phillip Morris-developed food products are still
very present in the food environment today. Kraft remains
a leading food company and is owned by a now-parent
company of Phillip Morris, Altria Group [83, 84]. Thus,
Phillip Morris’s influence and involvement in the food sys-
tem has been a reliable and stable factor in our food system
since the early 1980s.
The RJ Reynolds tobacco company had a similar tra-
jectory of involvement in the food system, although their
food products were specialized to specific market seg-
ments. RJ Reynolds initially bought into the US food
system via the sugar-sweetened beverage market in the
1960s and expanded their ownership to include Nabisco, a
major snack food company, in the 1970s [85, 86]. By 1986,
sales of food and tobacco products for RJ Reynolds were
approximately equal in the company’s portfolio [79], sug-
gesting food sales were a major contributor to RJ Reynolds
revenue in the tobacco litigation era. By 1990, Nabisco
was the largest manufacturer and marketer in cookie and
cracker industry in USA, with market shares that were
2–3 times larger than their closest competitors [79]. Thus,
RJ Reynolds also had a major impact in leading the US
food system through the 1990s, with a specific focus on
specialty snacks and sweetened drinks. However, by the
late 1990s, RJ Reynold’s market shares from food products
dropped, and by the early 2000s, RJ Reynolds divested
from Nabisco ownership, thus relinquishing its broader
influence in the food system [87].
The influence of US tobacco companies in the food sys-
tem has been extensive, and tobacco company leadership
in the food system likely played a major role in shaping
the current US food environment. However, the scientific
evidence identifying the ways in which the tobacco compa-
nies influenced the food system is extremely limited. In two
foundational studies that leveraged primary source docu-
ments provided by the University of California, San Fran-
cisco Industry Documents Library, Nguyen and colleagues
revealed that both RJ Reynolds and Phillip Morris used the
techniques they developed in tobacco product development,
sales, and marketing to develop and market unhealthy food
and beverage products to vulnerable populations in the USA,
specifically children [88•], and racial and ethnic minority
groups [89]. Thus, Nguyen and colleagues have provided
the first pieces of evidence to suggest that tobacco ownership
of food companies was likely problematic for public health.
A missing piece of the puzzle is whether tobacco compa-
nies applied their techniques for creating addictive tobacco
products to develop foods that may be difficult to stop eat-
ing and have addictive properties (i.e., HPF). Thus, another
key piece of evidence needed to expand our understand-
ing of the impact of tobacco company involvement in the
US food system is a potential connection between tobacco
ownership and HPF proliferation in the food environment.
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1 3
This information is needed to fully conceptualize our food
system, to consider ways in which HPF may be designed to
exploit our neurobiology, and implications for addressing
clinically relevant conditions, including obesity and food
addiction.
Conclusion
HPF differ in key ways from naturally occurring foods and
may exploit our neurobiological propensities to seek and
consume rewarding foods. There is reasonably strong behav-
ioral evidence to indicate that HPF may have reinforcing
properties that are similar to drugs of abuse. Strong evidence
indicates that healthy individuals may exhibit greater pref-
erence for and valuation of HPF relative to non-HPF, that
individuals may seek out HPF for their rewarding effects,
and that cues may develop that indicate the presence of
HPF. All of these factors speak to the reinforcing properties
of HPF. More limited evidence indicates that HPF intake
may be associated with greater motivation to consume HPF
(sensitization) and blunted experience of reward during HPF
intake, which may be observed neurobiologically. More
research is needed to understand and characterize longitu-
dinal neurobiological and behavioral changes that may occur
from repeated HPF intake over time among healthy human
samples.
The US food environment has shifted dramatically since
the 1970s and currently provides extensive access to HPF.
The major changes in the US food environment may have
been driven by US tobacco companies, which invested
heavily in the US food system in the early 1980s. Thus, the
leader of the US food system over the past 30years has been
US tobacco companies, which have specialized in creating
addictive tobacco products, and applied their product devel-
opment and marketing efforts to develop and sell food in
the US food system [88•]. At this juncture, it is critical for
researchers to investigate whether tobacco companies may
have driven the design and proliferation of HPF in the food
environment, which have marked similarities to other addic-
tive substances. If this connection is established, it would
provide a strong justification for the regulation of HPF at
the federal level. Substances, such as alcohol and nicotine,
are regulated in the US environment because it is recognized
that they may have substantial detrimental effects on vulner-
able groups in the population, including children and those
with risk factors for substance use disorder. This same prem-
ise should be considered for HPF, which also have estab-
lished harmful effects on individuals who are vulnerable to
their rewarding properties (e.g., food addiction and obesity),
and who may suffer an outsized health burden as HPF are
allowed to proliferate the US food environment unregulated.
Compliance with Ethical Standards
Competing Interests The author declare no competing interests.
Human and Animal Rights and Informed Consent No human or animal
subject data were used in the manuscript.
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