Nutritional Influences on Sensory Function
All sensory systems are composed of metabolically active neural and supporting tissues. Normal functioning of these tissues requires the provision of appropriate levels of nutrients. Deficiencies or excesses of nutrients or food constituents can result in a derangement of sensory function. Examples of such effects are blindness due to vitamin A deficiency, deafness due to excessive alcohol or quinine ingestion, burning mouth syndrome due to B vitamin deficiency, and loss of taste due to zinc deficiency.
The mechanisms by which nutritional disorders can alter sensory function are multiple, as exemplified by the impact of nutrient deficiencies on the sense of taste. For a stimulus to be perceived, it must gain access to its appropriate receptor. In vitamin A deficiency, keratinous material plugs the taste pore and impedes the access of taste stimuli to receptors in this area. Second, once a stimulus reaches a receptor, the interaction must result in the generation of a signal to identify the presence and nature of the stimulus.
The transduction processes for the sense of taste are only now being elucidated. Whether specific nutrients such as zinc are involved is still a matter of speculation. In the case of vision, however, the role of vitamin A in the transduction process is well documented. Third, sensory receptors must be supported by other types of tissues. Nutrient deficiencies or excesses can result in the death of these supporting tissues. Deficiencies of numerous nutrients lead to atrophy of taste papilla that contain the taste cells.
Fourth, once an effective stimulus-receptor interaction occurs, information about the presence of this stimulus must be relayed to the central nervous system for decoding. The function of neural tissue that conveys this information is again dependent on the organism’s nutritional status. Deficiencies (e.g., pyridoxine) or excesses of nutrients or food contaminants (e.g., lead) can lead to neuropathies and taste changes. Finally, incoming sensory information must be processed centrally. Central processing disorders such as Wernicke-Korsakoff syndrome, resulting from alcoholism, or schizophrenia, which may in some cases also have nutritional antecedents, have also been associated with abnormal responses to taste and smell stimuli and with olfactory and gustatory hallucinations.
Normal variations in nutritional status (i.e., shifts from states of mild depletion to repletion) can also alter sensory judgments. However, in this instance, evidence indicates that the changes are confined to affective responses with reports of alterations in sensitivity being attributable to response bias. Food may be less appealing following a meal, but the functionality of the gustatory and olfactory systems are not impaired. The influence of marginal nutrient deficiencies on sensory function remains an area of considerable speculation, but of little research.
In summary, food selection and perhaps nutrient utilization are influenced by the interplay between the sensory properties of foods and the sensory capabilities of consumers. Mechanisms by which sensory information may exert its impact on these two processes have been proposed, although the importance of each remains incompletely characterized. In any case, through an impact on food intake and digestion, sensory factors influence an individual’s nutritional status and the status of the sensory systems themselves. Any disruption in this reciprocal relationship between sensory function and nutrition will likely lead to a compromised status of each.
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