Intensification of sensory properties of foods for the elderly.
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Taste and smell losses in the elderly can reduce appetite and lead to inadequate dietary intake. Although these chemosensory deficits are generally not reversible, sensory interventions including intensification of taste and odor can compensate for perceptual losses. One method for "treatment" of chemosensory losses involves sensory enhancement of foods with flavors and monosodium glutamate (MSG). Amplification of flavor and taste can improve food palatability and acceptance, increase salivary flow and immunity, and reduce oral complaints in both sick and healthy elderly. (+info)
Intake of umami-tasting solutions by mice: a genetic analysis.
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In two-bottle preference tests with water and solutions of monosodium glutamate (MSG) and inosine-5'-monophosphate (IMP), mice from the C57BL/6ByJ inbred strain consumed more and had higher preferences for these solutions compared with mice from the 129/J strain. The C57BL/6ByJ mice consumed 300 mmol/L MSG in large amounts, which were comparable to intakes of highly preferred solutions of sweeteners. The strain differences in voluntary consumption of 300 mmol/L MSG depended at least in part on postingestive effects because prior experience with MSG influenced the expression of the strain difference in MSG acceptance. The strain difference in MSG acceptance was in the opposite direction to the strain difference in NaCl acceptance and was not affected by previous consumption of saccharin. Although the C57BL/6ByJ mice had higher avidity for both MSG and sweeteners than did the 129/J mice, there was no correlation between preferences for these solutions in the second hybrid generation (F(2)) derived from these two strains. Thus, the strain differences in MSG acceptance are not related to the strain differences in salty or sweet taste responsiveness and most likely represent specific umami taste responsiveness. High acceptance of MSG solutions by the C57BL/6ByJ mice was inherited as a recessive trait in the F(2) generation. Further genetic linkage analyses using the F(2) hybrids are being conducted to map chromosomal locations of genes determining the strain difference in MSG acceptance. (+info)
Circadian variations in plasma and erythrocyte glutamate concentrations in adult men consuming a diet with and without added monosodium glutamate.
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This study evaluated the effect of monosodium glutamate (MSG) ingestion as a component of the diet on the 24-h variations in plasma and whole-blood glutamate (GLU) concentrations in healthy adult men. In the first arm of the study, subjects were given test meals without added MSG for 3 d. Protein and energy intakes of the subjects were 1.5 g and 40 kcal/(kg body weight.d), respectively. On d 3, blood samples were collected over the 24-h period. One week later, the same protocol was repeated, except that 100 mg/(kg body weight.d) MSG was added to the meals (15, 40 and 45 mg/kg body weight to breakfast, lunch and dinner, respectively). Both plasma and whole-blood samples were analyzed for free amino acids. Unlike large neutral amino acids, which experienced high peak plasma concentrations at 2100-2300 h, the circadian variations in plasma GLU concentrations were small, varying between 33 and 48 micromol/L on days in which no MSG was fed, and between 32 and 53 micromol/L on days in which MSG was added to the meals. In both trials, plasma GLU concentration increased (P < 0.01) after lunch and dinner, and decreased early in the morning (P < 0.05). Calculated erythrocyte GLU concentrations varied between 500 and 640 micromol/L, with or without MSG addition to the meals. The rather low plasma GLU concentrations over the 24-h period, despite high dietary intake of MSG, indicate that dietary MSG is metabolized very rapidly. (+info)
The safety evaluation of monosodium glutamate.
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L-Glutamic acid and its ammonium, calcium, monosodium and potassium salts were evaluated by the Joint FAO/WHO Expert Committee on Food Additives (JECFA) in 1988. The Committee noted that intestinal and hepatic metabolism results in elevation of levels in systemic circulation only after extremely high doses given by gavage (>30mg/kg body weight). Ingestion of monosodium glutamate (MSG) was not associated with elevated levels in maternal milk, and glutamate did not readily pass the placental barrier. Human infants metabolized glutamate similarly to adults. Conventional toxicity studies using dietary administration of MSG in several species did not reveal any specific toxic or carcinogenic effects nor were there any adverse outcomes in reproduction and teratology studies. Attention was paid to central nervous system lesions produced in several species after parenteral administration of MSG or as a consequence of very high doses by gavage. Comparative studies indicated that the neonatal mouse was most sensitive to neuronal injury; older animals and other species (including primates) were less so. Blood levels of glutamate associated with lesions of the hypothalamus in the neonatal mouse were not approached in humans even after bolus doses of 10 g MSG in drinking water. Because human studies failed to confirm an involvement of MSG in "Chinese Restaurant Syndrome" or other idiosyncratic intolerance, the JECFA allocated an "acceptable daily intake (ADI) not specified" to glutamic acid and its salts. No additional risk to infants was indicated. The Scientific Committee for Food (SCF) of the European Commission reached a similar evaluation in 1991. The conclusions of a subsequent review by the Federation of American Societies for Experimental Biology (FASEB) and the Federal Drug Administration (FDA) did not discount the existence of a sensitive subpopulation but otherwise concurred with the safety evaluation of JECFA and the SCF. (+info)
Pituitary hormone secretion in normal male humans: acute responses to a large, oral dose of monosodium glutamate.
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Numerous studies have shown that the administration of a glutamate receptor agonist or a high dose of glutamate stimulates pituitary hormone secretion in animals. However, only a single human study has reported that an oral load of glutamic acid induced the secretion of prolactin and probably adrenocorticotropic hormone (ACTH) (but not other pituitary hormones). Because of glutamate's use in foods as monosodium glutamate (MSG), a flavoring agent, and the limited amount of human data, we studied the effect of a large oral dose of MSG in humans on the secretion of prolactin and other pituitary hormones. Fasting male subjects bearing venous catheters received on separate days each of the following four treatments: a vehicle, MSG (12.7 g), a high protein meal (a physiologic stimulus of prolactin secretion) by mouth, or an intravenous infusion of thyrotropin-releasing hormone (TRH, a pharmacologic stimulus of prolactin secretion). Plasma hormone responses were quantitated by RIA at 20-min intervals for 4 h. The protein meal induced a modest increase and TRH infusion a substantial increase in plasma prolactin, whereas MSG ingestion did not. MSG ingestion also did not raise the plasma concentrations of any of the other pituitary hormones measured (luteinizing hormone, follicle-stimulating hormone, thyroid-stimulating hormone, growth hormone) or of cortisol. Ingestion of MSG raised plasma glutamate concentrations 11-fold; the protein meal did not raise plasma glutamate. The results demonstrate that MSG ingestion in humans does not modify anterior pituitary hormone secretion. One implication is that diet-derived glutamate may not penetrate into hypothalamic regions controlling anterior pituitary function. (+info)
Review of alleged reaction to monosodium glutamate and outcome of a multicenter double-blind placebo-controlled study.
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Monosodium glutamate (MSG) has a long history of use in foods as a flavor enhancer. In the United States, the Food and Drug Administration has classified MSG as generally recognized as safe (GRAS). Nevertheless, there is an ongoing debate exists concerning whether MSG causes any of the alleged reactions. A complex of symptoms after ingestion of a Chinese meal was first described in 1968. MSG was suggested to trigger these symptoms, which were referred to collectively as Chinese Restaurant Syndrome. Numerous reports, most of them anecdotal, were published after the original observation. Since then, clinical studies have been performed by many groups, with varying degrees of rigor in experimental design ranging from uncontrolled open challenges to double-blind, placebo controlled (DBPC) studies. Challenges in subjects who reported adverse reactions to MSG have included relatively few subjects and have failed to show significant reactions to MSG. Results of surveys and of clinical challenges with MSG in the general population reveal no evidence of untoward effects. We recently conducted a multicenter DBPC challenge study in 130 subjects (the largest to date) to analyze the response of subjects who report symptoms from ingesting MSG. The results suggest that large doses of MSG given without food may elicit more symptoms than a placebo in individuals who believe that they react adversely to MSG. However, the frequency of the responses was low and the responses reported were inconsistent and were not reproducible. The responses were not observed when MSG was given with food. (+info)
Additive-induced urticaria: experience with monosodium glutamate (MSG).
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In patients with chronic urticaria, the incidence of reactions to any additives, including monosodium glutamate (MSG), is unknown. Although many studies have investigated the association of additives and urticaria, most have been poorly designed. This study sought to determine the prevalence of reactions to additives, including MSG, in patients with chronic urticaria using a rigorous protocol. We studied 65 subjects (44 women, 21 men; ages 14-67). All had urticaria for >6 wk without discernible etiology. Subjects with active urticaria were studied while they were taking the lowest effective dose of antihistamine. Screening challenges to the 11 additives most commonly associated with exacerbations of chronic idiopathic urticaria were performed in a single-blind fashion. The dose of MSG given was 2500 mg. Skin scores were obtained to determine a positive reaction in an objective manner. Subjects with a positive screening challenge were rechallenged (at least 2 wk later) with a double-blind, placebo-controlled protocol as in-patients in our General Clinical Research Center. Two subjects had positive single-blind, placebo-controlled challenges, but neither had a positive double-blind, placebo-controlled challenge. We conclude, with 95% confidence, that MSG is an unusual (<3% at most) exacerbant of chronic idiopathic urticaria. (+info)
The administration to Indonesians of monosodium L-glutamate in Indonesian foods: an assessment of adverse reactions in a randomized double-blind, crossover, placebo-controlled study.
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Monosodium L-glutamate (MSG) has been suggested to cause postprandial symptoms after the ingestion of Chinese or oriental meals. Therefore, we examined whether such symptoms could be elicited in Indonesians ingesting levels of MSG typically found in Indonesian cuisine. Healthy volunteers (n = 52) were treated with capsules of placebo or MSG (1.5 and 3.0 g/person) as part of a standardized Indonesian breakfast. The study used a rigorous, randomized, double-blind, crossover design. The occurrence of symptoms after MSG ingestion did not differ from that after consumption of the placebo. (+info)