Mastication as a Stress-Coping Behavior

Abstract

Exposure to chronic stress induces various physical and mental effects that may ultimately lead to disease. Stress-related disease has become a global health problem. Mastication (chewing) is an effective behavior for coping with stress, likely due to the alterations chewing causes in the activity of the hypothalamic-pituitary-adrenal axis and autonomic nervous system. Mastication under stressful conditions attenuates stress-induced increases in plasma corticosterone and catecholamines, as well as the expression of stress-related substances, such as neurotrophic factors and nitric oxide. Further, chewing reduces stress-induced changes in central nervous system morphology, especially in the hippocampus and hypothalamus. In rodents, chewing or biting on wooden sticks during exposure to various stressors reduces stress-induced gastric ulcer formation and attenuates spatial cognitive dysfunction, anxiety-like behavior, and bone loss. In humans, some studies demonstrate that chewing gum during exposure to stress decreases plasma and salivary cortisol levels and reduces mental stress, although other studies report no such effect. Here, we discuss the neuronal mechanisms that underline the interactions between masticatory function and stress-coping behaviors in animals and humans.

Full text

Review Article
Mastication as a Stress-Coping Behavior
Kin-ya Kubo,1Mitsuo Iinuma,2and Huayue Chen3
1Seijoh University Graduate School of Health Care Studies, 2-172 Fukinodai, Tokai, Aichi 476-8588, Japan
2Department of Pediatric Dentistry, Asahi University School of Dentistry, 1851 Hozumi, Mizuho, Gifu 501-0296, Japan
3Department of Anatomy, Gifu University Graduate School of Medicine, 1-1 Yanagido, Gifu 501-1194, Japan
Correspondence should be addressed to Kin-ya Kubo; kubo@seijoh-u.ac.jp
Received 18 September 2014; Revised 21 December 2014; Accepted 5 January 2015
Academic Editor: Oliver von Bohlen und Halbach
Copyright © 2015 Kin-ya Kubo et al. is is an open access article distributed under the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Exposure to chronic stress induces various physical and mental eects that may ultimately lead to disease. Stress-related disease has
become a global health problem. Mastication (chewing) is an eective behavior for coping with stress, likely due to the alterations
chewing causes in the activity of the hypothalamic-pituitary-adrenal axis and autonomic nervous system. Mastication under
stressful conditions attenuates stress-induced increases in plasma corticosterone and catecholamines, as well as the expression of
stress-related substances, such as neurotrophic factors and nitric oxide. Further, chewing reduces stress-induced changes in central
nervous system morphology, especially in the hippocampus and hypothalamus. In rodents, chewing or biting on wooden sticks
during exposure to various stressors reduces stress-induced gastric ulcer formation and attenuates spatial cognitive dysfunction,
anxiety-like behavior, and bone loss. In humans, some studies demonstrate that chewing gum during exposure to stress decreases
plasma and salivary cortisol levels and reduces mental stress, although other studies report no such eect. Here, we discuss the
neuronal mechanisms that underline the interactions between masticatory function and stress-coping behaviors in animals and
humans.
1. Introduction
Stress is a physiologic and psychologic response to envi-
ronmental changes and noxious stimuli. Chronic stress neg-
atively aects physical and mental health [1–3], ultimately
leading to disease [4–8]. Stress-related diseases are prevalent
worldwide. Stress activates the neuroendocrine system via
the autonomic system and hypothalamic-pituitary-adrenal
(HPA) axis, which leads to the release of corticosteroids and
hormones [9,10].
Chewing, swallowing, and speaking are important oral
functions related to physical, mental, and social health [11–
13]. In particular, masticatory ability inuences nutritional
status, overall health, and activities of daily living, especially
in the elderly population [14,15]. Chewing ability is frequently
impaired in the elderly, and many older adults develop
dental problems as a result of tooth loss, which compromises
general health status and is an epidemiologic risk factor for
Alzheimer’s disease [16–20]. In animals, impairing mastica-
tion by removing teeth results in impaired spatial learning
duetomorphologicchangesinthehippocampus[20]. us,
chewing appears to have an important role in maintaining
some aspects of cognitive function [20].
Chewing is also an eective stress-coping behavior. When
exposed to an inescapable stressor, animals assume coping
behaviors, such as chewing, that attenuate some elements
of the stress response [21]. In humans, nail-biting, teeth-
clenching, and biting on objects are considered outlets for
emotional tension or stress. Animals provided the opportu-
nity to chew or bite wooden sticks during immobilization
or restraint stress exhibit decreases in stress-induced plasma
corticosteronelevelsandattenuatedHPAaxisandautonomic
nervous system responses to stress, which helps to prevent the
stress-induced formation of gastric ulcers [4,22–24], decits
in spatial learning ability [25,26], and bone loss [27].
In humans, gum chewing is reported to relieve stress and
improve task performance [28–30]. A recent functional mag-
netic resonance imaging study revealed that gum chewing
during exposure to a loud noise inhibits the propagation of
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Volume 2015, Article ID 876409, 11 pages
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2BioMed Research International
stress-related information in the brain [31]. Data regarding
the stress-attenuating benets of gum chewing, however, are
conicting and dicult to replicate [32–34]. Here, we provide
an overview of the mechanisms that underlie chewing as a
stress-coping behavior in animals and humans.
2. Effects of Stress and Mastication
Mastication under stressful conditions prevents stress-
induced ulcer formation in the stomach [4,22–24], spatial
cognitive decits [25,26], anxiety-like behavior [35], and
osteoporosis [27]. Onishi et al. [36] reported that maternal
chewing during prenatal stress prevents prenatal stress-
induced learning decits in the adult ospring. Several stud-
ies have demonstrated that chewing attenuates stress-induced
functional and morphologic changes in the hippocampus
[25,36–40].
Spatial cognitive function is mainly controlled by the
hippocampus. e hippocampus is sensitive to stress, as
well as the aging process, and it is one of the rst
brain regions to be structurally and functionally modied
by stress [41]. Stress-induced increases in corticosterone
impair hippocampal-dependent learning and memory [42–
44]. Recent reports indicate that chewing ameliorates stress-
induced decits in hippocampal-dependent spatial cognitive
function. For example, Miyake et al. [25]reportedthat
rodents given wooden sticks to chew on during immobiliza-
tion stress exhibit attenuated stress-induced suppression of
spatial memory and glucocorticoid receptor expression in
the hippocampus. Chronic stress leads to the downregulation
of corticosterone receptors and the inhibition of negative
feedback from the hippocampus to the HPA axis [37].
Also in rats, active chewing during immobilization stress
ameliorates the stress-induced impairment of N-methyl-
D-aspartate receptor-mediated long-term potentiation [38],
which may be due to chewing-induced activation of his-
tamine H1 receptors [39]. In addition, aggressive mastica-
tion during stress prevents the stress-induced decrease in
brain-derived neurotrophic factor mRNA and neurotrophin-
3 mRNA in the hippocampus. Brain-derived neurotrophic
factor plays an important role in long-term potentiation
[45], neurogenesis [46], dendritogenesis [47], and activity-
dependent neuroplasticity [48], consistent with the nd-
ing that chewing during stressful conditions ameliorates
the stress-induced suppression of cell proliferation in the
hippocampal dentate gyrus [40]. Cell proliferation in the
hippocampal dentate gyrus strongly correlates with learning
ability [49], and neurotrophin-3 inuences the development
of the hippocampus [50]. Nitric oxide levels are increased
by restraint stress and, in rodents, biting suppresses the
increases in the nitric oxide levels in the hypothalamus [51].
Analysis of blood ow in the amygdala and hypothalamus
using laser Doppler owmetry and O2-selective electrodes in
rats allowed to chew on sticks under restraint stress revealed
recovery of stress-induced decreases in PO2levels [52].
Chewing may reduce nitric oxide by increasing PO2levels
in the hypothalamus, thus altering hemoglobin-scavenging
activity for nitric oxide. Previous animal studies indicated
that the stress-coping eects of chewing are mediated by the
autonomic nervous system and the HPA axis.
Additionally, exposure to stress is a precipitating fac-
tor for many illnesses, including mood disorders [53].
In humans, dysregulation of thyroid hormones [54]and
glucocorticoids [55] has long been associated with mood
disorders. Helmreich et al. [35] reported that chewing on
a wooden dowel during tail-shock in rats prevented stress-
induced anxiety-like behavior and attenuated stress-induced
decreases in thyroid hormone. e eects of chewing on
thyroid and glucocorticoid levels may account for the eects
of chewing to reduce stress-induced anxiety.
Osteoporosis is a skeletal disease characterized by low
bone mass and microstructural bone deterioration, with an
increased risk of fracture [56]. A large body of evidence
from animal and human studies indicates a link between
chronic mild stress and bone loss [57–59]. We examined the
eects of chewing during chronic stress on stress-induced
boneloss.Chewingunderchronicstresspreventstheincrease
in plasma corticosterone and noradrenaline levels, which
attenuates both the reduced bone formation and increased
bone resorption, and improves the trabecular bone loss and
microstructural bone deterioration induced by chronic mild
stress [27].
Prenatal stress increases the risk for neurobiological and
behavioral disturbances in adult ospring [60,61]. Clinical
studies demonstrated that pregnant mothers exposed to
social, emotional, or hostile experiences have ospring with
an increased susceptibility as adults to mental disorders,
such as depression, schizophrenia, and cognitive decits [62].
We examined whether allowing pregnant mice to chew on
a wooden stick during stress decreased the stress-induced
learning decits of the adult ospring by measuring plasma
corticosterone levels, spatial learning ability, and cell prolifer-
ation in the hippocampal dentate gyrus of the adult ospring
[36].Allowingmousedamstochewonawoodenstick
during exposure to prenatal stress attenuated the increase in
prenatal stress-induced plasma corticosterone levels. Further,
adult ospring of dams exposed to prenatal stress exhibited
impaired learning and decreased cell proliferation in the
dentate gyrus, which was attenuated by allowing the dams to
chew on a wooden stick during exposure to prenatal stress.
Maternal chewing during prenatal stress thus appears to be
eective for preventing learning decits in the adult ospring
[36].
2.1. Mastication and the Autonomic Nervous System. Masti-
cation during stressful conditions suppresses stress-induced
activation of the autonomic nervous system, causing sympa-
thetic nerve terminals to locally release catecholamines [4,22,
63]. Aggressive biting during exposure to stress signicantly
attenuates stress-induced increases in dopamine metabolism
[64] and noradrenaline turnover in the hypothalamus and
limbic areas [4,63]. Okada et al. [65] reported that restraint
stress-induced increases in blood pressure and core tempera-
ture were signicantly suppressed in rats allowed to chew on
a stick compared with rats that were restrained but not given a
stick to chew, consistent with other reports [66]. In addition,

BioMed Research International 3
chewing on a wooden stick during immobilization stress pre-
ventspoststressarrhythmias[67]. Interleukin- (IL-) 1𝛼,IL-1𝛽,
andIL-6haveimportantrolesinthethermoregulatorysys-
tem [68]andallostasis[69]. IL-1𝛽acts on the hypothalamus
to enhance the secretion of corticotropin-releasing hormone
[70,71]. Stress induced by placing an animal in an open-
eld box leads to increased plasma IL-6 levels [72]. erefore,
biting induced inhibition of the stress-related increase in the
coretemperaturemightbeduetothesuppressionofserum
IL-1𝛽andIL-6levels.CytokinessuchasIL-1𝛼,IL-1𝛽,andIL-
6 are also involved in immunity. Some studies indicate that
mastication-induced suppression of these cytokines prevents
gastric ulcer formation [23,24,63,64]. An animal study using
micro-positron-emission tomography showed that chewing
during immobilization stress suppresses the stress-induced
increase in plasma corticosterone levels and glucose uptake
in the paraventricular hypothalamic nucleus and anterior
hypothalamic area, but not in the lateral hypothalamus [73].
2.2. Mastication and the HPA Axis. Mastication during
stressful conditions suppresses activation of the HPA axis. In
rats and mice, chewing or biting on wooden sticks under vari-
ous stressors such as immobilization, restraint, cold exposure,
and tail pinch attenuates the secretion of adrenocorticotropic
hormone (ACTH) [38,74,75] and plasma corticosterone
levels [23,35,38,40,63,74,76,77]. Suppression of ACTH
secretion may account for subsequent changes in physio-
logic stress markers in the paraventricular nucleus of the
hypothalamus. Mastication under stress-inducing conditions
suppresses the stress-activated expression of corticotropin-
releasing factor, which controls ACTH secretion [78]; c-Fos,
an indirect marker of neuron activity [79]; the phospho-
rylation of extracellular signal-regulated kinases 1/2 [80];
and the expression of nitric oxide synthase mRNA [81]
and levels of nitric oxide [82], which is an important
signaling molecule in corticotropin-releasing factor release
[83] in the paraventricular nucleus of the hypothalamus.
e negative feedback mechanism of the HPA axis reduces
the secretion of glucocorticoids mainly by inhibiting the
hypothalamic and hypophyseal activities and indirectly by
binding to glucocorticoid receptors in the hippocampus [84].
Chewing ameliorates the stress-induced downregulation of
glucocorticoid receptors, which suppresses negative feedback
mechanisms [25]. In addition, biting on a wooden stick dur-
ing chronic stress decreases neuronal nitric oxide synthase
mRNA expression in the hypothalamus [81], which may be
involved in the regulation of corticotropin-releasing factor
secretion. Koizumi et al. [67] reported that chewing during
immobilization stress prevents poststress arrhythmias in rats.
Cardiovascular activity is controlled by the hypothalamus
[85]. ese eects of chewing on the HPA axis also ameliorate
stress-induced cardiac imbalances and reduce susceptibil-
ity to stress-induced arrhythmias by inhibiting neuronal
responses in the hypothalamus.
2.3. Neuronal Mechanisms at Underlie Stress Attenuation
by Chewing. Howdoeschewingduringstress-inducingcon-
ditions suppress the autonomic nervous system and HPA
axis? We suggest that stress-coping activities such as chewing
engage the medial prefrontal cortex (mPFC) and the right
central nucleus of amygdala neuronal activity asymmetrically
[86]. e mPFC is critically involved in the regulation of
stress-induced physiologic and behavioral responses [87–90].
Dopamine mainly controls the stress-related actions of the
mPFC [91,92]. Mice and rats exposed to an inescapable
stress will chew on an inedible material, such as aluminum
foil or cardboard, in the cage [76,93]. Under inescapable
stress conditions, chewing suppresses increases in plasma
corticosterone [94]. Moreover, chewing also attenuates stress-
related dopamine utilization preferentially within the mPFC
[93]. Chewing-induced suppression of mPFC dopamine
utilization is largely conned to the right hemisphere [93].
Together, these observations suggest a particularly important
rolefortherightmPFCinstress-copingbehavior.Chewing
leadstoanincreaseinfos-immunoreactivitythatisselective
fortherightmPFCandadecreaseinfos-immunoreactivity
that is selective for the central nucleus of the right amygdala,
a region that may regulate dopamine, both of which are
implicated in regulating dopamine utilization in the mPFC,
particularly under stress-inducing conditions [94–96]. In
addition, chewing during stress-inducing conditions also
attenuates the stress-induced release of noradrenaline in the
amygdala [4,22,63]. erefore chewing-induced changes in
catecholamines in the mPFC and right central nucleus of the
amygdala play an important role in stress-coping behavior.
A possible mechanism for chewing-induced alterations in
hippocampus-related behavioral and morphologic changes is
the brain histaminergic reaction. Chewing induces histamine
H1releaseinthehippocampus,andH1receptoractiva-
tion might recover stress-suppressed synaptic plasticity. e
mesencephalic trigeminal nucleus receives proprioceptive
sensory inputs via the trigeminal nerve from the masseter
muscle spindle and the periodontal ligaments during masti-
cation [97]. A subpopulation of the mesencephalic trigeminal
nucleus neurons projects its bers into the tuberomam-
millary nuclei (TMN) of the posterior hypothalamus in
which histaminergic neuronal cell bodies are localized [98,
99]. Chewing increases the hypothalamic histamine con-
centration, thereby increasing satiety [100,101], suggesting
that chewing stimulates histaminergic neurons in the TMN.
Axons of histaminergic neurons in the TMN project widely
throughout the entire brain, including the hippocampus
[102–105], and electrical stimulation of the TMN facilitates
extracellular concentrations of histamine in the hippocampus
[106]. us, a chewing-induced increase in the histamine
level in the hippocampus might rescue long-term poten-
tiation via the recovery of stress-attenuated N-methyl-D-
aspartate receptors [39].
3. Human Studies
3.1. Sleep Bruxism and Stress. Sleep bruxism is a stereotypic
movement disorder that is characterized by grinding or
clenching the teeth during sleep and is generally associated
with sleep arousal [107]. Sleep bruxism results in damage
to the teeth, periodontal tissues, and masticatory muscles,

4BioMed Research International
as well as cervical pain and temporomandibular disorders
[108].eonsetofsleepbruxismpeaksbetween20and45
years of age, although it also occurs in children [107,109,
110]. Sleep bruxism is common in females [111]. Although
the complete etiology of sleep bruxism is not clear, some
factors include occlusal interference [112], psychosocial stress
[113–115],psychologicstress[113,114,116–118], smoking [113],
striatal D2 receptor activation [119], and transient sleep
arousal [120]. Some studies suggest that stress is a causal agent
of sleep bruxism because sleep bruxism occurs more oen
aer exhausting and stressful days [121]. In an epidemiologic
study on British, German, and Italian populations, self-
reported sleep bruxism was positively related to a highly
stressful lifestyle [116] and signicantly associated with severe
stress at work [117]. An analysis of stress-coping strategies in
patients with sleep bruxism compared to nonbruxing con-
trols indicated that sleep bruxism patients utilize signicantly
fewer positive coping strategies such as escape [118,122]. In
contrast, other studies report no relationship between self-
reported stress levels and the degree of sleep bruxism [123–
125]. Overall, although the majority of studies suggest that
sleep bruxism is associated with stress, the specic stress-
factors that correlate with sleep bruxism remain unclear.
3.2. Chewing Gum and Stress. People chew gum for a variety
of reasons, including modulation of psychologic states, for
example, to facilitate concentration, relieve stress, and reduce
sleepiness. Many studies have examined the eects of gum
chewing on stress.
3.2.1. Chewing Gum and Stress Markers in Saliva. Analy-
sisofstressmarkersinthesalivaisasimpleanduseful
method for determining stress levels in humans. In humans,
gum chewing or bruxism-like activities under various stress
conditions may inuence the secretion volume of various
stress markers in the saliva. Chewing leads to decreases in
alpha-amylase activity (a sympathetic nervous system stress
marker [126]), salivary cortisol levels (an endocrine system
stress marker [28,127]), and secretory immunoglobulin A
(an immune system stress marker) [128,129]. Bruxism-like
activity during the presentation of a loud unpleasant sound
prevents a stress-induced increase in salivary chromogranin
A[130],astressmarkerthatreectssympatheticactivity[131].
Chewing and light teeth-clenching aer stress loading lead to
a rapid reduction of salivary cortisol levels [127]. Interestingly,
afastchewingrate[132]andastrong[
133]chewingforce
induce a greater reduction in mental stress than a slow or
weak force. Tasaka et al. [128]reportedthatchewingtime
aects the response of the endocrine system to mental stress,
and continuous chewing for more than 10 min is eective
forreducingstress,basedonstressmarkeranalysisinsaliva.
Contrary to these reports, however, chewing gum fails to
attenuate salivary cortisol levels [33,134]. e increase in
the cortisol secretion is likely task-dependent. Also, these
studies were performed at various times of day, and thus the
conicting results may be due to the diurnal alternations in
cortisol secretion.
Pr¨
oschel and Raum [129] reported a positive association
between chewing force and mean amplitude of the elec-
tromyogram of masticatory muscles. e mean electromyo-
gram amplitude of the masticatory muscles during chewing
increaseswithincreasedpsychologicstress[135]. Psychoso-
cial stress is associated with an increased chewing frequency
and decreased appetite [136]. ese ndings suggest that
chewing and bruxism-like activities are autonomic behaviors
in response to stressful conditions, acting as stress-coping
mechanisms. Niwa et al. [137]reportedthatchewingincreases
activity in the prefrontal cortex, which is involved in stress
control, and leads to decreased stress markers in saliva [133].
3.2.2. Chewing Gum and Experimental or Naturally Occurring
Stress. Several studies have demonstrated the benets of
chewing on stress, since Hollingworth [138]reportedthat
masticatory movement reduced excessive muscular tension
and energy. Soon aer the report by Hollingworth, however,
foot-tapping was reported to produce the same relaxing
eects, suggesting that the stress-reducing eects were not
specic to gum chewing [139]. erefore, the benets of gum
chewing on stress remain a matter of debate. e eects of
gum chewing on naturally occurring stress are consistently
reported to be benecial. For example, Zibell and Madansky
[28] investigated whether chewing gum aects perceived
levels of everyday stress among subjects who regularly chew
gumoramongsubjectswhodonotusuallychewgum.Stress
levels and stress-specic emotions, such as feeling anxiety or
tension, decreased aer chewing gum, indicating that gum
chewing reduces levels of anxiety and stress. Smith [29]per-
formed a cross-sectional study of occupational stress in full-
time workers and found that non-gum-chewers complained
signicantly more oen of stress at work and home compared
with gum chewers, and gum chewers had a lower incidence
of high blood pressure. An intervention study revealed
that chewing gum reduces occupational stress both at and
outside of work, reducing fatigue, anxiety, and depression
and leading to a more positive mood [29]. Chewing gum
is also associated with perceptions of better performance
[140]. Further, chewing gum is associated in a linear dose-
response manner with levels of perceived stress at work
and home, as well as anxiety and depression [141]. Similar
ndings were reported for university students [142]. Erbay et
al. [143] examined whether chewing gum is a useful addition
to traditional medical treatment of patients with mild to
moderate depression and indicated that while chewing gum
is not directly eective for elevating a depressed mood, it may
reduce the symptoms originating from depression.
On the other hand, the eects of chewing on stress are
also variable in studies of experimentally induced stress.
Scholey et al. [30] investigated the eects of chewing gum on
multitasking eciency. Chewing gum signicantly increases
self-rated levels of alertness, decreases self-rated levels of anx-
iety and stress, reduces salivary cortisol levels, and enhances
overall task performance. e eects were the same regardless
of the gum avor. e authors [30]speculatedthattheir
ndings are linked to the increased heart rate [144,145]and
increased cerebral blood ow [146]associatedwithchewing.

BioMed Research International 5
Additional studies have reported a relationship between
chewing under stress-inducing conditions and heart rate
[147–151]. ese ndings suggest that an increase in cerebral
blood ow [146,152] and the related increase in glucose
delivery [153] might act to reduce stress via an increase in
the PFC glucose metabolism. Additionally, Kern et al. [154]
demonstratedthatanincreaseinglucosemetabolisminthe
rostral mPFC is associated with a decrease in the salivary
cortisol concentration following a stressful task. Numerous
studieshavereportedanincreaseincerebralactivityaer
gum chewing [155–161] and demonstrated that the eect is
specic to chewing gum and not just the chewing motion
[162,163]. Chewing gum ameliorates the eects of stress
on mood, anxiety, and mental status [33,134,164]. One
possibility is that the chewing-induced neural activation and
psychologic and mental benets improve task performance,
which suppresses stress.
Notwithstanding the above reports, the eects of chewing
gumoncognitionandphysiologyarecontroversial.For
example, the facilitative eects of chewing gum on memory
[145,153] have proved dicult to replicate [32], as has the
accelerating eect of chewing gum on heart rate [32,145]. e
context-dependent memory eect demonstrated by Baker et
al. [165] has not been replicated; thus the eects of chewing
gum on context-dependent memory are conicting [165–
169]. In addition, Johnson et al. [33] detected no benets of
chewing on cortisol levels, state anxiety, or stress despite using
a similar study design as Scholey et al. [30]. Torney et al. [34]
also found no eect of chewing gum on mediating the level of
stress experienced or on performance in a solvable anagram
task.eanagramtaskusedbyTorneyetal.[34]wasonly
5 min long, much shorter than the task used by Scholey et al.
[30](∼20 min), suggesting that a greater period of chewing is
needed to observe a reduction in stress [153].
Smith [134] examined whether gum chewing improves
aspects of cognitive function and mood during exposure
to a 75 dB stress-inducing noise. His ndings revealed that
chewing gum was associated with both more alertness and
more positive mood. Reaction times were faster in subjects
who were allowed to chew gum. Chewing gum also improved
selectiveandsustainedattention.Bothheartrateandcortisol
levels were higher during chewing, conrming that chewing
gum has an alerting eect rather than a stress-reducing eect,
consistent with another report [170]. erefore, the ndings
regarding gum chewing are mixed, with some indicating that
chewing gum is associated with signicantly better alertness
or vigilance [30,33,134,148,171,172] and others indicating no
benet of chewing gum for attention, self-related alertness,
and vigilance [173,174]. e dierences in these reports may
derive from the duration of the study and time required for
the task [174,175].
Recently, the coping mechanism of chewing under noise
stress conditions was examined using functional magnetic
resonance imaging [31]. Gum chewing attenuated stress-
induced activation of the bilateral superior temporal sulcus
and le anterior insula [31]. Gum chewing reduced functional
connections between the le anterior insula and the dorsal
anterior cingulate cortex and inhibited the connectivity from
the bilateral superior temporal sulcus to the le anterior
insula [31]. Chewing gum under stress might act to attenuate
the sensory processing of the stressor and inhibit the trans-
mission of stress-related information in the brain [31].
4. Conclusions and Future Directions
Chewing or biting as a stress-coping behavior attenuates
stress-induced diseases such as gastric ulcers and cognitive
and psychologic impairments in rodents via suppression of
stress-induced activation of the HPA axis and autonomic
nervous reactions. e histaminergic nervous system may
also be involved in the chewing-induced attenuation of stress-
induced cognitive decits. In humans, although the correla-
tion between sleep bruxism and stress factors is controversial,
many studies support an association between stress and sleep
bruxism. Eects of chewing during stress are also conicting.
Gum chewing during stress may aect the levels of various
stress markers in the saliva and plasma and increase attention,
self-rated alertness, and vigilance.
Further studies are necessary to determine the possible
causal relationship between sleep bruxism and stress factors.
eamygdalaandmPFChaveamajorroleinstress-related
behaviors and the mPFC also functions to regulate amygdala-
mediated arousal in response to stress. Catecholamines such
as 5-hydroxytryptamine dopamine and noradrenaline are
involved in the corticolimbic circuitry, and gamma aminobu-
tyric acid has a major role in amygdala functioning. Further
studies focusing on the interactions between mastication and
neuronal networks between the mPFC and amygdala and
between the trigeminal nerve and cortical and limbic systems
will help to clarify how mastication aects the expression
of various stress-related markers. Studies using functional
magnetic resonance imaging and functional near-infrared
spectroscopy will be useful for analyzing brain activities in
the mPFC and amygdala. More studies are necessary to
clarify the benets of gum chewing, by focusing on attention,
alertness, vigilance, and others under task performance using
functional magnetic resonance imaging and/or functional
near-infrared spectroscopy in humans.
Conflict of Interests
e authors declare that there is no conict of interests
regarding the publication of this paper.
Acknowledgment
is work was supported by a Grant-in-Aid for Scientic
Research from the Ministry of Education, Science, and
Culture of Japan (KAKENHI 22390395, 26462916).
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