Gum chewing is a gross voluntary physiological motor activity that uses numerous functional neuroanatomical pathways. In this sidebar, I postulate how gum chewing can stimulate various neuronal pathways that may affect a number of clinical outcomes. These clinical outcomes have yet to be demonstrated. The act of gum chewing fulfills many of the hypotheses related to recognizing stimuli of areas of the body not well-represented in the brain, such as neuronal convergence and summation. It also has been associated with many physiological attributes, including increased blood flow in the cerebral and orofacial region, which may account for increased alertness and improved memory. There are two areas—headache and possible inhibition of the satiety center—in which gum chewing works synergistically. For headache, it is a matter of increased blood flow, which prevents the vasoconstriction that initiates a headache. For inhibition of the satiety center, the physical motor activity of chewing sends input to the brain that a person is chewing, and as people normally do not eat food with gum in their mouths, this reduces food intake.
Gum chewing also may be considered a teleological function, and neural circuits may be able to produce self-sustaining patterns of behavior in what are termed "central pattern generators." The literature suggests that the pattern elaborated by the central pattern generator includes selective modifications of sensory transmission.1 The cranial nerves involved in the function of chewing—which include the hypoglossal, spinal accessory, glossopharyngeal and vagus nerves—can affect many other areas of the brain owing to their anatomical location, their neurotransmitter release and, especially, their location in the region of the pons in which the solitary nucleus and nucleus ambiguous can affect systemic functions.2
The neurotransmitter serotonin, or 5-hydroxytryptamine (5-HT), has been implicated in modulating nociceptive transmission. The 5-HT descending inhibitory pathway is essential in mediating the nonopioid systems for antinociception. Prolonged chewing exercise can suppress the nociceptive responses, and the blood 5-HT levels can increase significantly in response to chewing.3 Furthermore, since voluntary rhythmic movements enhance the activity of 5-HT neurons, other prolonged repetitive movements such as locomotion or breathing are considered to produce the same effect.4 Difficulty in chewing may be diagnostic in conditions such as referred otalgia.5
Chewing sugar-free gum at least three times a day significantly reduces caries irrespective of the type of sugar alcohol it contains.6 This is the most obvious use of chewing gum as an adjunct to fluoride for the treatment of caries.
Altering central neurotransmission either directly with drugs or possibly indirectly with the act of chewing would be the goal of a clinical study demonstrating the efficacy of how chewing affects drug action.
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POSTULATED CLINICAL IMPLICATIONS
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Stimulation or inhibition of central neurotransmitters can affect many clinical endpoints. Altering central neurotransmission either directly with drugs (for example, antidepressant, antiobesity or antihypertensive agents) or possibly indirectly with the act of chewing would be the goal of a clinical study demonstrating the efficacy of how chewing affects drug action. To some extent, drugs affecting central neurotransmission most likely will affect the autonomic nervous system. Xerostomia is a condition in which gum chewing can have a direct adjunctive affect on many of the medications prescribed for its treatment. Gum chewing stimulates salivary flow and helps keep the salivary ducts patent. Gum chewing also can be adjunctive to the treatment of temporomandibular disorder and in maintaining the patency of the auditory canals.
If gum chewing can be viewed as a physical activity that affects people’s lifestyles, it may be possible to view gum chewing in the broader context of health and wellness. For example, as noted previously, people usually do not eat food at the same time they chew gum. With the prevalence of obesity on the rise, the metabolic syndrome encompasses a constellation of metabolic abnormalities and is thought to place patients at a higher risk of developing diabetes and cardiovascular disease.7 The physical activity of gum chewing may be a cost-effective way of limiting food and caloric intake.
There is a growing interest in the role of the endocannabinoid system in energy metabolism and how blocking cannabinoid receptors may optimize fat distribution, insulin sensitivity and blood lipids to improve cardiovascular risk profile. Abdominal obesity can affect the status and properties of a number of key adipokines, including adiponectin, angiotensinogen, C-reactive protein, interleukin-6, leptin, plasminogen-activating inhibitor-1, resistin and tumor necrosis factor-alpha.8 Many of these cytokines can affect many systemic outcomes, including periodontal disease.
Gum chewing can be adjunctive to use of medications directed at obesity, such as insulin sensitizers and biguanides, orlistat, sibutramine, phentermine and rimonabant.7 The mechanism of rimonabant treats obesity by blocking the endocannabinoid-1 receptor. This receptor is located in the central and peripheral nervous systems, adipose tissue, gastrointestinal tract, liver and muscle. It prevents weight gain by blocking the overactivation of the endocannabinoid system centrally and peripherally and by regulating energy balance and body composition.
The results of a study demonstrated that gum chewing or mastication can be used as a model to evaluate the increase in neuronal activities in various regions of the human brain.9 Some regional increases in neuronal activity in the brain are age-dependent.10 The results of another study showed that chewing moderately hard chewing gum produced a stronger effect on the blood oxygenation level–dependent signals in the sensorimotor cortex, the thalamus and other brain regions.11 In humans, gum chewing not only results in transient increases in energy expenditure and heart rate response,12 but it also increases cerebral blood flow owing to changes in internal carotid arterial blood flow.13 Positron emission tomography of cerebral blood flow during gum chewing shows increased blood flow in the bilateral lower frontal and parietal lobes.9 These data would suggest that gum chewing is an effective adjunctive treatment for headache. Gum chewing at peak times of the headache onset14 may be worth further clinical study. The difficulty in demonstrating clinical efficacy of the physical act of gum chewing is underscored by the results of a recent multi-center randomized trial of using chewing gum to prevent oral mucositis in children undergoing chemotherapy.15 Investigators found that there was no overall reduction in severe oral mucositis when children chewed five pieces of gum per day.
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CONCLUSION
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Gum chewing usually is not considered to be part of adjunctive medication treatment. Gum chewing may not have a direct effect on a systemic clinical outcome parameter as we know it, but given the data that have been published, gum chewing probably can have an indirect effect on a number of medications and their clinical outcome parameters. The basis for this effect resides in the complexity of the neuroanatomical pathways subserving chewing and mastication, which affects a number of central and peripheral neurotransmitters. Increased blood flow suggests increased neuronal activity that affects neurotransmitters, which can control and communicate information to many parts of the brain, thus affecting systemic clinical outcome parameters. The subtle clinical effects resulting from gum chewing have yet to be determined. The difficulty is in designing studies to capture the subtle additive effects of gum chewing. That said, increased cerebral blood flow caused by gum chewing could be an interesting outcome in age-related studies of dementia and Alzheimer disease, as well as their treatments.
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POSTULATED CLINICAL IMPLICATIONS
CONCLUSION
