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Six common foods can cause the clinical entity called "idiopathic" pruritus ani. They are coffee, tea, cola, beer, chocolate, and tomatoes. Pruritus ani occurs in 24 to 48 hours when a patient consumers more than a threshold amount of one or more of these foods and disappears spontaneously in a few days provided the threshold is not exceeded again.
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INTRODUCTION: Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by behavioral impairments and limited therapeutic options. Emerging evidence suggests that plant-derived polyphenols may offer neuroprotective benefits. OBJECTIVES: This pilot study aimed to investigate the therapeutic potential of polyphenol-rich cocoa extract in a valproic acid (VPA)-induced zebrafish model of ASD. METHODS: Zebrafish were exposed to 3 μM VPA, cocoa powder providing 2.5 μM (-)-epicatechin, a combination of both, or left untreated. Behavioral phenotyping was conducted using DanioVision and gut morphology was assessed. Untargeted metabolomic and proteomic profiling was performed followed by univariate and multivariate analyses. RESULTS: VPA exposure induced ASD-like behavioral hyperactivity, and severe gastrointestinal abnormalities. Cocoa co-treatment ameliorated both behavioral performance and gut architecture. Metabolomic profiling revealed VPA-associated disruptions in neurotransmission, methylation, mitochondrial function and redox homeostasis. Proteomic profiling showed elevated levels of trafficking protein particle complex subunit 11, proteasomal ubiquitin receptor, betaine-homocysteine S-methyltransferase 1 (BHMT-1), and desmoplakin-A, consistent with genotoxic stress and impaired protein trafficking. Cocoa co-treatment normalized BHMT-1 and desmoplakin-A expression and mitigated broader metabolic dysregulation. CONCLUSION: Collectively, these results suggest that polyphenol-rich cocoa may represent a promising multi-targeted nutraceutical approach for mitigating ASD-related neurodevelopmental and metabolic disturbances.
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Cytotoxic food tests still present conflicting opinions concerning their validity. Nine atopic patients with or without a history of food allergy were studied along with 5 nonatopic patients. All tests were conducted in a double-blind fashion with 6 determinations for each of 10 food antigens. Reproducibility of the test (5/6 positive or negative) was demonstrated with wheat, milk, yeast, chocolate, and orange. In the nonatopic group, reproducible results were obtained for wheat, egg, yeast, chocolate, and chicken. Clinical correlation with 11 foods in 7 patients was demonstrated. However, there were 46 positive tests without correlation and 2 negative tests with positive histories. Therefore, there appears to be reproducibility of the tests to only 3 foods but no apparent correlation with clinical symptoms. At the present time, cytotoxic tests offer no reliable help in establishing the diagnosis of food allergy.
In order to extend previous investigations of adverse reactions to foods performed at this institution, 68 children, aged 5 mo to 15 yr, were studied. All subjects reported a history of adverse reaction to ingestion of one or more of the 14 foods under study. Sixteen of 43 subjects, 3 yr of age or older, had 22 adverse reactions during 94 food challenges with one or more of the 14 foods. All reactions confirmed were to peanut or other nuts, milk, egg, and soy. Skin testing with 1:20 weight/volume concentrations of food extracts applied by the puncture technique produced a net wheal reaction 3 mm or greater in all subjects 3 yr of age or older in whom double-blind food challenges confirmed the history of adverse reaction. Thirteen of 25 children less than 3 yr of age manifested adverse reactions during 49 food challenges. Skin testing by puncture technique produced a net wheal 3 mm or greater in 9 children less than 3 yr of age in whom food challenge elicited a clinical response within 2 hr. One of 4 subjects less than 3 yr of age in whom the adverse reaction occurred more than 4 hr after food challenge exhibited a wheal to puncture skin test of 3 mm or greater. These studies suggest that at present double-blind food challenge is an indispensible tool for the unequivocal evaluation of adverse reactions to foods.
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Four hundred and fifty cholecystograms were assessed regarding the effectiveness of various agents used as the fatty meal. 200 patients were given Arachis oil emulsion, 100 chocolate-Sorbitol preparation, 100 46 g of milk chocolate, and 50 26 g of milk chocolate. The films were assessed for degree of contraction, improvement in opacification, and visualisation of the biliary ducts. No statistically significant difference was found between any of the groups. It is concluded that milk chocolate is an effective palatable and cheap form of fatty meal.
Eighteen water-soluble food dyes have been studied by chromatography on thin layers of anion-exchange (AG 1-X4, DEAE-cellulose, PAB-cellulose and chitosan) and cation-exchange (Dowex 50-X4, Rexyn 102 and humic acid) materials; layers of silanised silica gel impregnated with cationic or anionic detergent were also used. Fourteen of the dyes were separated, but the two orange and the two black dyes were not. Some applications of the techniques to commercial products are reported.
Six nursing mothers ingested 113 gm of Hershey's milk chocolate containing 240 mg of theobromine. Samples of plasma, saliva, and breast milk were assayed for theobromine by high pressure liquid chromatography. Peak theobromine concentrations of 3.7 to 8.2 mg/l were found in all fluids at 2 to 3 hour after ingestion of chocolate. The disposition half-life of theobromine averaged 7.1 +/- 2.1 hours, body clearance was 65 +/- 20 ml/hour/kilogram, and the apparent volume of distribution was 0.62 +/- 0.13 l/lk. Theobromine is only slightly bound to plasma and milk proteins and concentrations in milk and saliva matched plasma data closely. The mean concentration ratios were 0.82 +/- 0.17 for milk/plasma and 0.92 +/- 0.17 for saliva/plasma. If a mother ate a 4-ounce chocolate bar every 6 hours and the infant nursed when the theobromine concentration in milk was at its peak, the infant could ingest about 10 mg of theobromine per day.
Between Dec. 4, 1973, and Feb. 15, 1974, 80 cases of infection due to Salmonella eastbourne, previously a rare isolated serotype in the United States, were reported from twenty-three States. An additional 39 cases were reported from seven Provinces in Canada during a similar period. A telephone case-control study implicated Christmas-wrapped chocolate balls manufactured by a Canadian company as the vehicle of transmission. S. eastbourne was subsequently isolated from several samples of leftover chocolate balls obtained from homes where cases occurred. Investigation of the factory revealed that the contaminated Christmas and Easter chocolates, and a few chocolate items for year-round sale, had been produced between May and October, 1973. Bacteriological testing of samples taken at the plant implicated cocoa beans as the probable source of the salmonella organisms which, in the low-moisture chocolate, were able to survive heating during production. This outbreak and the finding of salmonella of other serotypes in chocolates produced by another manufacturer suggest that chocolate-related salmonellosis may be a significant public-health problem.
60 migraine patients completed elimination diets after a 5-day period of withdrawal from their normal diet. 52 (87%) of these patients had been using oral contraceptive steroids, tobacco, and/or ergotamine for an average of 3 years, 22 years, and 7.4 years respectively. The commonest foods causing reactions were wheat (78%), orange (65%), eggs (45%), tea and coffee (40% each), chocolate and milk (37%) each), beef (35%), and corn, cane sugar, and yeast (33% each). When an average of ten common foods were avoided there was a dramatic fall in the number of headaches per month, 85% of patients becoming headache-free. The 25% of patients with hypertension became normotensive. Chemicals in the home environment can make this testing difficult for outpatients. Both immunological and non-immunological mechanisms may play a part in the pathogenesis of migraine caused by food intolerance.
Milk chocolate mass containing salmonellas was prepared by mixing artificially contaminated milk powder with the other ingredients at a temperature of about 40 degrees C. From this mass bars were made. Two series were prepared, with S. eastbourne and S. typhimurium respectively. The number of surviving salmonellas was counted after various periods of storage, up to 19 months. S. eastbourne was reduced in numbers during 19 months from an initial count of ca. 3 x 10(4) to ca. 3 x 10(2) per 100 g of chocolate. S. typhimurium died off more rapidly, and was not detectable in about 55 g after 15 months, in spite of an initial count of ca. 10(5) per 100 g.In these experiments the salmonellas in the milk powder had had to survive the spraying procedure and the adverse conditions in the dried powder. This may be the reason why S. eastbourne showed a distinctly better survival on storage than the same serotype showed in previous experiments in which the organism was added as a broth culture to the chocolate mix. With S. typhimurium, however, such a difference was hardly detectable.Possible explanations of these results are discussed.
Experiments were carried out to assess the reduction rate of two salmonella strains (S. eastbourne and S. typhimurium) in chocolate bars. After artificial contamination of chocolate, after 'conching', with about 10(6) S. eastbourne/g. this organism was still recovered after 9 months storage. The strain of S. typhimurium was less resistant. Both serotypes died off more rapidly in bitter chocolate than in milk chocolate. After contamination with a smaller dose (about 10(3)/g.) with these two serotypes, similar differences were observed.
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