Concept: Peanut butter
Nut intake has been associated with lower mortality, but few studies have investigated causes of death other than cardiovascular disease, and dose-response relationships remain unclear.
- Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology
- Published over 7 years ago
BACKGROUND: A diagnosis of peanut allergy has a major impact on an individual’s quality of life. Exposure to even small amounts of peanut can trigger serious reactions. Common cleaning agents can easily remove peanut allergen from surfaces such as table tops. Parents of children with peanut allergy frequently ask if peanut allergen can persist on surfaces if they have not been cleaned.Objectives: The purpose of this study was to determine the persistence of peanut allergen on a typical table surface over time. METHODS: 5 mL of peanut butter was evenly smeared on a 12 inch by 12 inch (30.5 by 30.5 cm) square on a nonporous (laminated plastic) table surface. Five squares were prepared in the same manner. The table was kept in a regular hospital office at room temperature and ambient lighting. No cleaning occurred for 110 days. Samples were taken at regular intervals from different areas each time. A monoclonal-based ELISA for arachis hypogaea allergen 1 (Ara h 1), range of detection 1.95-2000 ng/mL, was used to assess peanut allergen on the table surface. RESULTS: At baseline, there was no detectable Ara h 1 allergen. Immediately post application and for 110 days of collecting, detectable Ara h 1 was found each time a sample was taken. There was no obvious allergen degradation over time. Active cleaning of the contaminated surface with a commercial cleaning wipe resulted in no detectable Ara h 1 allergen. CONCLUSIONS: Peanut allergen is very robust. Detectable Ara h 1 was present on the table surface for 110 days. Active cleaning of peanut contaminated surfaces easily removed peanut residue and allergen. Regular cleaning of surfaces before and after eating should be reinforced as a safety measure for all individuals with peanut allergy.
Previous investigations, of adolescent diet recalled in adulthood, found lower risk for benign breast disease (BBD) with higher intakes of vegetable fat and nuts during high school. We investigate whether vegetable protein and fat, derived from diets reported during pre-adolescence and adolescence, are associated with subsequent risk for BBD in young women. The Growing Up Today Study includes 9,039 females, 9-15 years in 1996, who completed questionnaires annually through 2001, and then in 2003, 2005, 2007, and 2010. Food frequency questionnaires (1996-2001) obtained intake data on a variety of foods. Beginning in 2005, women (18-30 years) reported whether they had ever been diagnosed with BBD that was confirmed by breast biopsy (n = 112 cases). Logistic regression estimated associations between intakes of vegetable protein and fat and biopsy-confirmed BBD. Those individual foods that were the largest contributors of protein and fat in this cohort were also investigated. In analyses of intakes from 1996 through 1998, when our cohort was youngest, vegetable fat (OR = 0.72/(10 gm/day), 95 % CI 0.53-0.98; p = 0.04) was inversely associated with BBD risk. The greatest sources of vegetable fat and protein in these girls were peanut butter, peanuts, nuts, beans (beans, lentils, and soybeans), and corn. A daily serving of any one of these was associated with lower risk (OR = 0.32/(serv/day), 95 % CI 0.13-0.79; p = 0.01). Peanut butter (and nuts) at age 11 years was inversely associated with risk (p = 0.01). In analyses of intakes at age 14 years, vegetable protein was associated with lower BBD risk (OR = 0.64/(10 gm/day), 95 % CI 0.43-0.95; p = 0.03). A daily serving at 14 years of any one of the foods was associated with lower risk (OR = 0.34, 95 % CI 0.16-0.75; p = 0.01), as was peanut butter (and nuts) (p = 0.02). Girls with a family history of breast cancer had significantly lower risk if they consumed these foods or vegetable fat. In conclusion, consumption of vegetable protein, fat, peanut butter, or nuts by older girls may help reduce their risk of BBD as young women.
A study was done to determine the rate of inactivation of Salmonella in cookie and cracker snack sandwiches. Two cookie bases (chocolate and vanilla) and cheese crackers, along with high-sugar chocolate and peanut butter-based crème cookie fillings and peanut butter- and cheese-based cracker fillings, were obtained from commercial sources. Fillings and sandwiches containing fillings that had been dry- or wet-inoculated with Salmonella were stored at 25°C for 1, 6, 21, 35, 70, 112, and 182 days (6 months). At initial populations of 3.4 and 3.6 log CFU/g of cookie sandwiches containing chocolate crème and peanut butter crème fillings, respectively, Salmonella survived for at least 182 days; initially at 0.36 log CFU/g, the pathogen survived for at least 35 and 70 days. Initially at 2.9 and 3.4 log CFU/g of cracker sandwiches containing peanut butter- and cheese-based fillings, respectively, Salmonella survived for at least 182 and 112 days; initially at 0.53 log CFU/g, the pathogen survived for at least 6 and 35 days. Inactivation of Salmonella was more rapid in wet-inoculated peanut butter crème cookie filling than in dry-inoculated filling but was less affected by type of inoculum in peanut butter-based cracker filling. Chocolate cookie base (water activity [aw] 0.39) and chocolate crème filling (aw 0.30) components of sandwiches equilibrated to aw 0.38 within 15 days at 25°C; vanilla cookie base (aw 0.21) and peanut butter-based crème filling (aw 0.27) equilibrated to aw 0.24 between 50 and 80 days. Cheese cracker (aw 0.14) and peanut butter-based filling (aw 0.31) or cheese-based filling (aw 0.33) components of sandwiches equilibrated to aw 0.33 in 80 days. The ability of Salmonella to survive for at least 182 days in fillings of cookie and cracker sandwiches demonstrates a need to assure that filling ingredients do not contain the pathogen and that contamination does not occur during manufacture.
Upon moisture uptake, dry cellular cereals and snacks loose their brittleness and become soggy. This familiar phenomenon is manifested in smoothing their compressive force-displacement curves. These curves' degree of jaggedness, expressed by their apparent fractal dimension, can serve as an instrumental measure of the particles' crunchiness. The relationship between the apparent fractal dimension and moisture content or water activity has a characteristic sigmoid shape. The relationship between the sensorily perceived crunchiness and moisture also has a sigmoid shape whose inflection point lies at about the same location. The transition between the brittle and soggy states, however, appears sharper in the apparent fractal dimension compared with moisture plot. Less familiar is the observation that at moderate levels of moisture content, while the particles' crunchiness is being lost, their stiffness actually rises, a phenomenon that can be dubbed “moisture toughening.” We show this phenomenon in commercial Peanut Butter Crunch(®) (sweet starch-based cereal), Cheese Balls (salty starch-based snack), and Pork Rind also known as “Chicharon” (salty deep-fried pork skin), 3 crunchy foods that have very different chemical composition. We also show that in the first 2 foods, moisture toughening was perceived sensorily as increased “hardness.” We have concluded that the partial plasticization, which caused the brittleness loss, also inhibited failure propagation, which allowed the solid matrix to sustain higher stresses. This can explain other published reports of the phenomenon in different foods and model systems.
A widely publicized study by Stamps, Bartoshuk and Heilman (2013) reported that a simple measure of left:right naris differences in the ability to detect the odor of peanut butter is a sensitive marker of Alzheimer’s disease (AD). AD patients were said to have abnormal smell function on the left side of the nose and normal function on right side of the nose. In light of its implications for medical practice and the world-wide publicity that it engendered, we sought to replicate and expand this work.
Nut intake has been associated with decreased cancer-related mortality, but few studies have examined the potential of nuts in the chemoprevention of pancreatic cancer. We prospectively investigated the association of total nut, tree nut, peanut, and peanut butter consumption with pancreatic cancer risk.
Nut intake has been associated with reduced mortality and risk of cardiovascular diseases, but there is only limited evidence on cancer. We investigated the relationship between nut intake and risk of postmenopausal breast cancer, and estrogen/progesterone receptor (ER/PR) subtypes.
Several strains of a new aflatoxigenic species of Aspergillus, A. korhogoensis, were isolated in the course of a screening study involving species from section Flavi found contaminating peanuts (Arachis hypogaea) and peanut paste in the Côte d'Ivoire. Based on examination of four isolates, this new species is described using a polyphasic approach. A concatenated alignment comprised of nine genes (ITS, benA, cmdA, mcm7, amdS, rpb1, preB, ppgA, and preA) was subjected to phylogenetic analysis, and resulted in all four strains being inferred as a distinct clade. Characterization of mating type for each strain revealed A. korhogoensis as a heterothallic species, since three isolates exhibited a singular MAT1-1 locus and one isolate exhibited a singular MAT1-2 locus. Morphological and physiological characterizations were also performed based on their growth on various types of media. Their respective extrolite profiles were characterized using LC/HRMS, and showed that this new species is capable of producing B- and G-aflatoxins, aspergillic acid, cyclopiazonic acid, aflavarins, and asparasones, as well as other metabolites. Altogether, our results confirm the monophyly of A. korhogoensis, and strengthen its position in the A. flavus clade, as the sister taxon of A. parvisclerotigenus.
In 2007, a nationwide Salmonella Tennessee outbreak occurred via contaminated peanut butter. Here, we developed a single-nucleotide polymorphism (SNP)-typing method for S. Tennessee to determine the clonal subtypes of S. Tennessee that were associated with the peanut butter outbreak.