Toward a science-based classification of processed foods to support meaningful research and effective health policies.

Processed foods have been part of the American diet for decades, with key roles in providing a safe, available, affordable, and nutritious food supply. The USDA Food Guides beginning in 1916 and the US Dietary Guidelines for Americans (DGA) since 1980 have included various types of commonly consumed processed foods (e.g., heated, fermented, dried) as part of their recommendations. However, there are multiple classification systems based on "level" of food processing, and additional evidence is needed to establish the specific properties of foods classified as "highly" or "ultra"-processed (HPF/UPFs). Importantly, many foods are captured under HPF/UPF definitions, ranging from ready-to-eat fortified whole grain breakfast cereals to sugar-sweetened beverages and baked goods. The consequences of implementing dietary guidance to limit all intake of foods currently classified as HPF/UPF may require additional scrutiny to evaluate the impact on consumers' ability to meet daily nutrient recommendations and to access affordable food, and ultimately, on health outcomes. Based on a meeting held by the Institute for the Advancement of Food and Nutrition Sciences in May 2023, this paper provides perspectives on the broad array of foods classified as HPF/UPFs based on processing and formulation, including contributions to nutrient intake and dietary patterns, food acceptability, and cost. Characteristics of foods classified as UPF/HPFs are considered, including the roles and safety approval of food additives and the effect of food processing on the food matrix. Finally, this paper identifies information gaps and research needs to better understand how the processing of food affects nutrition and health outcomes.

The Kraft Heinz Company global nutrition targets for the innovation and reformulation of food and beverages: Current and future directions.

Reformulating packaged foods has the potential to improve the nutrient density of the global diet. The present perspective illustrates The Kraft Heinz Company's approach to product (re)formulation to develop healthier product lines that are lower in saturated fats, total sugars, and sodium, and contain health promoting components. Here we present the rationale for The Kraft Heinz Company's global nutrition targets used for the global innovation and renovation of foods and beverages. The global nutrition targets use a category specific approach to set maximum levels for the main nutrients of public health concern: saturated fat, total sugars and sodium, taking into account product characteristics (typical portion size, eating occasion, role in the diet, etc.) as well as regulatory, technological, sensory and safety constraints. Benchmarking examples illustrate how the nutrition targets are positioned within the United States, France, and Australia. These global nutrition targets serve as part of The Kraft Heinz Company's environmental, social and governance nutrition commitments and demonstrates how the food industry is improving the nutritional value of packaged foods and beverages both now and into the future.

Bonding Universal Dental Adhesive to Developmentally Hypomineralised Enamel.

PURPOSE: To investigate the effect of pretreatment protocols involving Papacarie Duo gel and Scotchbond Universal (SU) on the microshear bond strength (µSBS) of resin composite (RC) to hypomineralised enamel (HE). MATERIALS AND METHODS: Specimens of normal enamel (NE) and HE were derived from extracted hypomineralised first permanent molars (FPMs). Based on the colour of demarcated opacities, HE specimens were classified as creamy/white (CW) or yellow/brown (YB). The specimens were randomly allocated into eight groups (n = 20). Each group involved pretreatment with Papacarie Duo gel or no pretreatment, and SU applied in etch-and-rinse (E&R) or self-etch (SE) mode. All specimens were bonded with RC and subjected to µSBS testing. Failure modes were analysed using an optical microscope and SEM. RESULTS: Comparing NE with HE, the following factors were found to be significant (p < 0.001): type of enamel substrate, deproteinising pretreatment, and etching mode. Comparing CW HE with YB HE, a significant interaction between "deproteinising pretreatment" and "etching mode" was demonstrated (p = 0.028). When subjected to the concurrent use of Papacarie Duo gel and phosphoric acid etching, HE specimens showed a significant increase in µSBS (p < 0.001). CONCLUSION: Deproteinising pretreatment using Papacarie Duo gel followed by the application of SU in E&R mode led to increased µSBS of resin composite to HE.

n-Butyl Benzyl Phthalate Exposure Promotes Lesion Survival in a Murine Endometriosis Model.

Endometriosis is an inflammatory and estrogen-dependent gynecological disease associated with exposure to environmental endocrine disruptors. n-Butyl benzyl phthalate (BBP), a ubiquitous plasticizer, has weak estrogenic activity, and exposure to BBP is associated with endometriosis. We aimed to elucidate the immunomodulatory effect of BBP on endometriosis development. We previously established a surgery-induced endometriosis-like murine model. In the present study, we exposed those mice to BBP 10 days prior to surgery and 4 weeks after surgery at physiologically relevant doses to mimic human exposure. Chronic exposure to BBP did not promote the growth of endometriotic lesions; however, the lesion survival rate in BBP-treated mice did increase significantly compared with control mice. Multiparametric flow cytometry showed that BBP exposure did not affect the homeostasis of infiltrated immune subsets in lesions but did enhance CD44 (adhesion marker) expression on plasmacytoid dendritic cells (pDCs). Blocking CD44 interactions locally inhibited endometriotic lesion growth. Immunofluorescence results further confirmed that CD44 blocking inhibited pDC infiltration and reduced the frequency of CD44+ pDCs in endometriotic tissues. BBP also disrupted the estrus cycle in these mice. This study suggests that chronic exposure to low-dose BBP may promote survival of endometriotic tissue through CD44-expressing pDCs.

A prominent environmental endocrine disruptor, 4-nonylphenol, promotes endometriosis development via plasmacytoid dendritic cells.

Endometriosis is an estrogen-dependent chronic inflammatory disease and is associated etiologically with environmental endocrine disruptor (EED) exposure. 4-nonylphenol (NP), a widely found EED, has weak estrogenic activity and modulates plasmacytoid dendritic cell (pDC) function in vitro and in vivo. We aimed to elucidate the immunomodulatory effect of NP on the development of endometriosis, particularly focusing on pDCs. This study established a surgically induced endometriosis murine model (C57BL/6) under conditions of NP treatment that are relevant to the level and route of human exposure. Multi-parametric flow cytometry was used for analysis of infiltrated immune cell subsets in lesions. The results showed that NP exposure significantly promoted endometriotic lesion growth, survival and angiogenesis development of lesions as well as pDC accumulation in the lesions in mice. Adoptive transfer of NP-conditioned pDCs into mice significantly enhanced lesion development and local pDC infiltration, whereas NP-conditioned conventional dendritic cells did not affect lesion growth. In vitro functional analysis showed that NP-conditioned pDCs in lesions expressed high levels of CD36, a scavenger receptor and NP-conditioned splenic pDCs secreted an enhanced level of IL-10 in response to apoptotic cell recognition in a CD36-dependent manner. Furthermore, we observed that local treatment with blocking antibodies against IL-10 and CD36 on the day of surgery significantly inhibited lesion development. NP exposure also altered the estrous cycle in mice. The results suggest that chronic and low-dose exposure to NP enhances endometriotic lesion growth by altering pDC homeostasis and function. This study has important implications for understanding the environment-innate immunity interaction in human endometriosis.

Heat shock protein 90 inhibition in imatinib-resistant gastrointestinal stromal tumor.

Inhibition of KIT oncoproteins by imatinib induces clinical responses in most gastrointestinal stromal tumor (GIST) patients. However, many patients develop imatinib resistance due to secondary KIT mutations. Heat shock protein 90 (HSP90) protects KIT oncoproteins from proteasome-mediated degradation, and we therefore did preclinical validations of the HSP90 inhibitor, 17-allylamino-18-demethoxy-geldanamycin (17-AAG), in an imatinib-sensitive GIST cell line (GIST882) and in novel imatinib-resistant GIST lines that are either dependent on (GIST430 and GIST48) or independent of (GIST62) KIT oncoproteins. 17AAG (>100 nmol/L) inhibited imatinib-sensitive and imatinib-resistant KIT oncoproteins, with substantially reduced phospho-KIT and total KIT expression after 30 minutes and 6 hours, respectively. KIT signaling intermediates, including AKT and mitogen-activated protein kinase, were inactivated by 17-AAG in the KIT-positive GIST lines, but not in the KIT-negative GIST62. Likewise, cell proliferation and survival were inhibited in the KIT-positive GISTs but not in GIST62. These findings suggest that 17-AAG biological effects in KIT-positive GISTs result mainly from KIT oncoprotein inhibition. The dramatic inactivation of imatinib-resistant KIT oncoproteins suggests that HSP90 inhibition provides a therapeutic solution to the challenge of heterogeneous imatinib resistance mutations in GIST patients.