Environmental influence on the Atlantic salmon transcriptome and methylome during sea lice infestations.

The fish's immune response is affected by different factors, including a wide range of environmental conditions that can also disrupt or promote changes in the host-pathogen interactions. How environmental conditions modulate the salmon genome during parasitism is poorly understood here. This study aimed to explore the environmental influence on the Salmo salar transcriptome and methylome infected with the sea louse Caligus rogercresseyi. Atlantic salmon were experimentally infected with lice at two temperatures (8 and 16 °C) and salinity conditions (32 and 26PSU). Fish tissues were collected from the infected Atlantic salmon for reduced representation bisulfite sequencing (RRBS) and whole transcriptome sequencing (RNA-seq) analysis. The parasitic load was highly divergent in the evaluated environmental conditions, where the lowest lice abundance was observed in fish infected at 8 °C/26PSU. Notably, transcriptome profile differences were statistically associated with the number of alternative splicing events in fish exposed to low temperature/salinity conditions. Furthermore, the temperature significantly affected the methylation level, where high values of differential methylation regions were observed at 16 °C. Also, the association between expression levels of spliced transcripts and their methylation levels was determined, revealing significant correlations with Ferroptosis and TLR KEEG pathways. This study supports the relevance of the environmental conditions during host-parasite interactions in marine ecosystems. The discovery of alternative splicing transcripts associated with DMRs is also discussed as a novel player in fish biology.

Drinking as affective labour: A discussion of Australian men working in hospitality and corporate workplaces.

In the public imaginary, drinking is often thought of as a behaviour separate from individuals' formal labour practices, but studies increasingly highlight the complex ways alcohol is entwined with work. Building on recent conceptual developments in the sociological fields of youth, health and work, we illustrate how drinking can be productively understood as 'affective labour', and thus itself a form of work that generates valuable embodied states and atmospheres. To do so, we draw on data from six focus groups with men coworkers from three hospitality workplaces and three corporate workplaces in Victoria. For the corporate groups, work-related drinking was tied to an unravelling of certain professional affects and facilitated harmonious and productive workplace relationships, but also introduced risks ranging from embarrassment to sexual harassment. For hospitality workers, drinking was more deeply enmeshed in workplace relationships and, for one group, drinking on-shift was positively framed as creating an affect and atmosphere that appealed to clientele, despite taking a toll on workers' wellbeing. In both settings not drinking risked limiting one's ability to get on colleagues' affective 'level'. Our data deepens current understandings of how drinking cultures may be woven through occupational settings, produce value for organisations and introduce unique potential for exclusion.

Her2 amplification, Rel-A, and Bach1 can influence APOBEC3A expression in breast cancer cells.

APOBEC-induced mutations occur in 50% of sequenced human tumors, with APOBEC3A (A3A) being a major contributor to mutagenesis in breast cancer cells. The mechanisms that cause A3A activation and mutagenesis in breast cancers are still unknown. Here, we describe factors that influence basal A3A mRNA transcript levels in breast cancer cells. We found that basal A3A mRNA correlates with A3A protein levels and predicts the amount of APOBEC signature mutations in a panel of breast cancer cell lines, indicating that increased basal transcription may be one mechanism leading to breast cancer mutagenesis. We also show that alteration of ERBB2 expression can drive A3A mRNA levels, suggesting the enrichment of the APOBEC mutation signature in Her2-enriched breast cancer could in part result from elevated A3A transcription. Hierarchical clustering of transcripts in primary breast cancers determined that A3A mRNA was co-expressed with other genes functioning in viral restriction and interferon responses. However, reduction of STAT signaling via inhibitors or shRNA in breast cancer cell lines had only minor impact on A3A abundance. Analysis of single cell RNA-seq from primary tumors indicated that A3A mRNA was highest in infiltrating immune cells within the tumor, indicating that correlations of A3A with STAT signaling in primary tumors may be result from higher immune infiltrates and are not reflective of STAT signaling controlling A3A expression in breast cancer cells. Analysis of ATAC-seq data in multiple breast cancer cell lines identified two transcription factor sites in the APOBEC3A promoter region that could promote A3A transcription. We determined that Rel-A, and Bach1, which have binding sites in these peaks, elevated basal A3A expression. Our findings highlight a complex and variable set of transcriptional activators for A3A in breast cancer cells.

Dealing With Diversity in Psychology: Science and Ideology.

In the spirit of America's Shakespeare, August Wilson (1997), I have written this article as a testimony to the conditions under which I, and too many others, engage in scholarly discourse. I hope to make clear from the beginning that although the ideas presented here are not entirely my own-as they have been inherited from the minority of scholars who dared and managed to bring the most necessary, unpalatable, and unsettling truths about our discipline to the broader scientific community-I do not write for anyone but myself and those scholars who have felt similarly marginalized, oppressed, and silenced. And I write as a race scholar, meaning simply that I believe that race-and racism-affects the sociopolitical conditions in which humans, and scholars, develop their thoughts, feelings, and actions. I believe that it is important for all scholars to have a basic understanding of these conditions, as well as the landmines and pitfalls that define them, as they shape how research is conducted, reviewed, and disseminated. I also believe that to evolve one's discipline into one that is truly robust and objective, it must first become diverse and self-aware. Any effort to suggest otherwise, no matter how scholarly it might present itself, is intellectually unsound.

Condemned or valued: Young children evaluate nonconformity based on nonconformists' group orientations.

Nonconformity--the act of deviating from established norms and expectations of one's group--is often evaluated negatively, despite its potential benefits for society. Three preregistered studies (N = 153) examined how nonconformists' group orientations (attitudes and intentions toward ingroup and outgroups) might affect 4-6-year-olds' evaluations of nonconformity in intergroup situations. Study 1 examined children's default beliefs of nonconformists' group attitudes toward ingroup and outgroup. We found that children expected nonconformists to hold more positive attitudes toward their outgroup than toward their ingroup, and this expectation predicted their disapproval of nonconformity. In Study 2, however, when nonconformity was explicitly motivated by positive intentions toward the ingroup rather than toward the outgroup, children were more accepting of nonconformity. Study 3 found that among nonconformists with different types of group orientations (positive toward the outgroup, ingroup or both group), young children evaluated the most positively nonconformists who bring the ingroup and the outgroup together. Collectively, these findings suggest that children evaluate nonconformity based on nonconformists' group orientations, illuminating one mechanism for how nonconformity could be more socially accepted and valued.

An impaired ubiquitin-proteasome system increases APOBEC3A abundance.

Apolipoprotein B messenger RNA (mRNA) editing enzyme, catalytic polypeptide-like (APOBEC) cytidine deaminases cause genetic instability during cancer development. Elevated APOBEC3A (A3A) levels result in APOBEC signature mutations; however, mechanisms regulating A3A abundance in breast cancer are unknown. Here, we show that dysregulating the ubiquitin-proteasome system with proteasome inhibitors, including Food and Drug Administration-approved anticancer drugs, increased A3A abundance in breast cancer and multiple myeloma cell lines. Unexpectedly, elevated A3A occurs via an ∼100-fold increase in A3A mRNA levels, indicating that proteasome inhibition triggers a transcriptional response as opposed to or in addition to blocking A3A degradation. This transcriptional regulation is mediated in part through FBXO22, a protein that functions in SKP1-cullin-F-box ubiquitin ligase complexes and becomes dysregulated during carcinogenesis. Proteasome inhibitors increased cellular cytidine deaminase activity, decreased cellular proliferation and increased genomic DNA damage in an A3A-dependent manner. Our findings suggest that proteasome dysfunction, either acquired during cancer development or induced therapeutically, could increase A3A-induced genetic heterogeneity and thereby influence therapeutic responses in patients.

Genetic inhibitors of APOBEC3B-induced mutagenesis.

The cytidine deaminases APOBEC3A (A3A) and APOBEC3B (A3B) are prominent mutators of human cancer genomes. However, tumor-specific genetic modulators of APOBEC-induced mutagenesis are poorly defined. Here, we used a screen to identify 61 gene deletions that increase A3B-induced mutations in yeast. We also determined whether each deletion was epistatic with Ung1 loss, which indicated whether the encoded factors participate in the homologous recombination (HR)-dependent bypass of A3B/Ung1-dependent abasic sites or suppress A3B-catalyzed deamination by protecting against aberrant formation of single-stranded DNA (ssDNA). We found that the mutation spectra of A3B-induced mutations revealed genotype-specific patterns of strand-specific ssDNA formation and nucleotide incorporation across APOBEC-induced lesions. Combining these three metrics, we were able to establish a multifactorial signature of APOBEC-induced mutations specific to (1) failure to remove H3K56 acetylation, (2) defective CTF18-RFC complex function, and (3) defective HR-mediated bypass of APOBEC-induced lesions. We extended these results by analyzing mutation data for human tumors and found BRCA1/2-deficient breast cancers display three- to fourfold more APOBEC-induced mutations. Mirroring our results in yeast, Rev1-mediated C-to-G substitutions are mainly responsible for increased APOBEC-signature mutations in BRCA1/2-deficient tumors, and these mutations associate with lagging strand synthesis during replication. These results identify important factors that influence DNA replication dynamics and likely the abundance of APOBEC-induced mutation during tumor progression. They also highlight a novel role for BRCA1/2 during HR-dependent lesion bypass of APOBEC-induced lesions during cancer cell replication.

Triploid Pacific oysters exhibit stress response dysregulation and elevated mortality following heatwaves.

Polyploidy has been suggested to negatively impact environmental stress tolerance, resulting in increased susceptibility to extreme climate events. In this study, we compared the genomic and physiological response of diploid (2n) and triploid (3n) Pacific oysters (Crassostrea gigas) to conditions present during an atmospheric heatwave that impacted the Pacific Northwestern region of the United States in the summer of 2021. Climate stressors were applied either singly (single stressor; elevated seawater temperature, 30°C) or in succession (multiple stressor; elevated seawater temperature followed by aerial emersion at 44°C), replicating conditions present within the intertidal over a tidal cycle during the event. Oyster mortality rate was elevated within stress treatments with respect to the control and was significantly higher in triploids than diploids following multiple stress exposure (36.4% vs. 14.8%). Triploids within the multiple stressor treatment exhibited signs of energetic limitation, including metabolic depression, a significant reduction in ctenidium Na+ /K+ ATPase activity, and the dysregulated expression of genes associated with stress response, innate immunity, glucose metabolism, and mitochondrial function. Functional enrichment analysis of ploidy-specific gene sets identified that biological processes associated with metabolism, stress tolerance, and immune function were overrepresented within triploids across stress treatments. Our results suggest that triploidy impacts the transcriptional regulation of key processes that underly the stress response of Pacific oysters, resulting in downstream shifts in physiological tolerance limits that may increase susceptibility to extreme climate events that present multiple environmental stressors. The impact of chromosome set manipulation on the climate resilience of marine organisms has important implications for domestic food security within future climate scenarios, especially as triploidy induction becomes an increasingly popular tool to elicit reproductive control across a wide range of species used within marine aquaculture.

Transcriptome profile in heat resilient Pacific oyster Crassostrea gigas families under thermal challenge.

Since the introduction of the Pacific oyster Crassostrea gigas in Baja California Sur, Mexico, its culture has faced environmental challenges, specifically increasing temperatures that result in high mortalities. The inter-tidal zone seawater temperature during a year at the Baja California Peninsula broadly ranges from 7 °C to 39 °C. Therefore, to understand how oysters respond to heat stress during daily temperature oscillations, heat-resistant (RR, father, and mother resistant) and heat-susceptible (SS, both parents susceptible) phenotypes families from a C. gigas breeding program were exposed to a thermal challenge. Based on a laboratory-simulated daily oscillatory thermal challenge (26 to 34 °C) for 30 days, RR phenotype presented differences compared to SS phenotype since the beginning (day 0) of the thermal challenge. Gene expression analyses revealed 1822 differentially expressed up-regulated transcripts in RR, related to functions of metabolic processes, biological regulation, and response to stimulus and signaling. At the end of the experiment (day 30), 2660 differentially expressed up-regulated transcripts were identified in RR. Functional analysis of the genes expressed indicates responses of regulation of biological processes and response to a stimulus. Additionally, 340 genes were differentially expressed among RR vs. SS from the beginning to the end of the thermal challenge, where 170 genes were up-regulated, and 170 were down-regulated. These transcriptomic profiles represent the first report to identify gene expression markers associated with RR phenotypes for the Pacific oyster to the future broodstock selection.

Romantic racism: How racial preferences (and beliefs about racial preferences) reinforce hierarchy in U.S. interracial relationships.

OBJECTIVES: In the United States, the two most common interracial marriages are between Asian women and White men, and between Black men and White women. Previous research proposed that the reason for these pairings stems from White Americans' racial preferences, such that White men prefer Asian women over Black women (i.e., the group stereotyped as more feminine), whereas White women prefer Black men over Asian men (i.e., the group stereotyped as more masculine). Here, we argue that focusing solely on White Americans' preferences neglects the reality that Americans of color also have preferences (and beliefs about others' preferences) that contribute to the composition of U.S. interracial relationships. METHOD: We used multiple methodologies (i.e., surveys and experimental manipulations) to examine Asian, Black, and White Americans beliefs about others' preferences. RESULTS: Across three studies (N = 3,728), we reveal that Asian, Black, and White Americans have beliefs about others' preferences (Study 1), that those beliefs mirror their own preferences (Study 2), and that those beliefs have causal implications for their own preferences (Study 3). CONCLUSION: Collectively, these findings reveal that such beliefs (and preferences) advantage White Americans, such that both Asian and Black Americans believe that they are more attractive to White Americans than to each other, which leads them to be more attracted to White Americans. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Genome-wide maps of UVA and UVB mutagenesis in yeast reveal distinct causative lesions and mutational strand asymmetries.

Ultraviolet (UV) light primarily causes C > T substitutions in lesion-forming dipyrimidine sequences. However, many of the key driver mutations in melanoma do not fit this canonical UV signature, but are instead caused by T > A, T > C, or C > A substitutions. To what extent exposure to the UVB or UVA spectrum of sunlight can induce these noncanonical mutation classes, and the molecular mechanism involved is unclear. Here, we repeatedly exposed wild-type or repair-deficient yeast (Saccharomyces cerevisiae) to UVB or UVA light and characterized the resulting mutations by whole genome sequencing. Our data indicate that UVB induces C > T and T > C substitutions in dipyrimidines, and T > A substitutions that are often associated with thymine-adenine (TA) sequences. All of these mutation classes are induced in nucleotide excision repair-deficient cells and show transcriptional strand asymmetry, suggesting they are caused by helix-distorting UV photoproducts. In contrast, UVA exposure induces orders of magnitude fewer mutations with a distinct mutation spectrum. UVA-induced mutations are elevated in Ogg1-deficient cells, and the resulting spectrum consists almost entirely of C > A/G > T mutations, indicating they are likely derived from oxidative guanine lesions. These mutations show replication asymmetry, with elevated G > T mutations on the leading strand, suggesting there is a strand bias in the removal or bypass of guanine lesions during replication. Finally, we develop a mutation reporter to show that UVA induces a G > T reversion mutation in yeast that mimics the oncogenic NRAS Q61K mutation in melanoma. Taken together, these findings indicate that UVA and UVB exposure can induce many of the noncanonical mutation classes that cause driver mutations in melanoma.

Contributions of replicative and translesion DNA polymerases to mutagenic bypass of canonical and atypical UV photoproducts.

UV exposure induces a mutation signature of C > T substitutions at dipyrimidines in skin cancers. We recently identified additional UV-induced AC > TT and A > T substitutions that could respectively cause BRAF V600K and V600E oncogenic mutations. The mutagenic bypass mechanism past these atypical lesions, however, is unknown. Here, we whole genome sequenced UV-irradiated yeast and used reversion reporters to delineate the roles of replicative and translesion DNA polymerases in mutagenic bypass of UV-lesions. Our data indicates that yeast DNA polymerase eta (pol η) has varied impact on UV-induced mutations: protecting against C > T substitutions, promoting T > C and AC > TT substitutions, and not impacting A > T substitutions. Surprisingly, deletion rad30Δ increased novel UV-induced C > A substitutions at CA dinucleotides. In contrast, DNA polymerases zeta (pol ζ) and epsilon (pol ε) participated in AC > TT and A > T mutations. These results uncover lesion-specific accurate and mutagenic bypass of UV lesions, which likely contribute to key driver mutations in melanoma.

Genetic modifiers of APOBEC-induced mutagenesis.

The cytidine deaminases APOBEC3A and APOBEC3B (A3B) are prominent mutators of human cancer genomes. However, tumor-specific genetic modulators of APOBEC-induced mutagenesis are poorly defined. Here, we utilized a screen to identify 61 gene deletions that increase A3B-induced mutations in yeast. Also, we determined whether each deletion was epistatic with UNG1 loss, which indicated whether the encoded factors participate in the error-free bypass of A3B/Ung1-dependent abasic sites or suppress A3B-catalyzed deamination by protecting against aberrant formation of single stranded DNA (ssDNA). Additionally, we determined that the mutation spectra of A3B-induced mutations revealed genotype-specific patterns of strand-specific ssDNA formation and nucleotide incorporation across APOBEC-induced lesions. Combining these three metrics we were able to establish a multifactorial signature of APOBEC-induced mutations specific to (1) failure to remove H3K56 acetylation, which results in extremely high A3B-induced mutagenesis, (2) defective CTF18-RFC complex function, which results in high levels of A3B induced mutations specifically on the leading strand template that synergistically increase with loss of UNG1, and (3) defective HR-mediated bypass of APOBEC-induced lesions, which were epistatic with Ung1 loss and result from increased Rev1-mediated C-to-G substitutions. We extended these results by analyzing mutation data for human tumors and found BRCA1/2-deficient breast cancer tumors display 3- to 4-fold more APOBEC-induced mutations. Mirroring our results in yeast, for BRCA1/2 deficient tumors Rev1-mediated C-to-G substitutions are solely responsible for increased APOBEC-signature mutations and these mutations occur on the lagging strand during DNA replication. Together these results identify important factors that influence the dynamics of DNA replication and likely the abundance of APOBEC-induced mutation during tumor progression as well as a novel mechanistic role for BRCA1/2 during HR-dependent lesion bypass of APOBEC-induced lesions during cancer cell replication.

The effect of group status on children's hierarchy-reinforcing beliefs.

Members of advantaged groups are more likely than members of disadvantaged groups to think, feel, and behave in ways that reinforce their group's position within the hierarchy. This study examined how children's status within a group-based hierarchy shapes their beliefs about the hierarchy and the groups that comprise it in ways that reinforce the hierarchy. To do this, we randomly assigned children (4-8 years; N = 123; 75 female, 48 male; 21 Asian, 9 Black, 21 Latino/a, 1 Middle-Eastern/North-African, 14 multiracial, 41 White, 16 not-specified) to novel groups that differed in social status (advantaged, disadvantaged, neutral third-party) and assessed their beliefs about the hierarchy. Across five separate assessments, advantaged-group children were more likely to judge the hierarchy to be fair, generalizable, and wrong to challenge and were more likely to hold biased intergroup attitudes and exclude disadvantaged group members. In addition, with age, children in both the advantaged- and disadvantaged-groups became more likely to see membership in their own group as inherited, while at the same time expecting group-relevant behaviors to be determined more by the environment. With age, children also judged the hierarchy to be more unfair and expected the hierarchy to generalize across contexts. These findings provide novel insights into how children's position within hierarchies can contribute to the formation of hierarchy-reinforcing beliefs. RESEARCH HIGHLIGHTS: A total of 123 4-8-year-olds were assigned to advantaged, disadvantaged, and third-party groups within a hierarchy and were assessed on seven hierarchy-reinforcing beliefs about the hierarchy. Advantaged children were more likely to say the hierarchy was fair, generalizable, and wrong to challenge and to hold intergroup biases favoring advantaged group members. With age, advantaged- and disadvantaged-group children held more essentialist beliefs about membership in their own group, but not the behaviors associated with their group. Results suggest that advantaged group status can shape how children perceive and respond to the hierarchies they are embedded within.

Chromosome-Level Genome Assembly of the Blue Mussel Mytilus chilensis Reveals Molecular Signatures Facing the Marine Environment.

The blue mussel Mytilus chilensis is an endemic and key socioeconomic species inhabiting the southern coast of Chile. This bivalve species supports a booming aquaculture industry, which entirely relies on artificially collected seeds from natural beds that are translocated to diverse physical-chemical ocean farming conditions. Furthermore, mussel production is threatened by a broad range of microorganisms, pollution, and environmental stressors that eventually impact its survival and growth. Herein, understanding the genomic basis of the local adaption is pivotal to developing sustainable shellfish aquaculture. We present a high-quality reference genome of M. chilensis, which is the first chromosome-level genome for a Mytilidae member in South America. The assembled genome size was 1.93 Gb, with a contig N50 of 134 Mb. Through Hi-C proximity ligation, 11,868 contigs were clustered, ordered, and assembled into 14 chromosomes in congruence with the karyological evidence. The M. chilensis genome comprises 34,530 genes and 4795 non-coding RNAs. A total of 57% of the genome contains repetitive sequences with predominancy of LTR-retrotransposons and unknown elements. Comparative genome analysis of M. chilensis and M. coruscus was conducted, revealing genic rearrangements distributed into the whole genome. Notably, transposable Steamer-like elements associated with horizontal transmissible cancer were explored in reference genomes, suggesting putative relationships at the chromosome level in Bivalvia. Genome expression analysis was also conducted, showing putative genomic differences between two ecologically different mussel populations. The evidence suggests that local genome adaptation and physiological plasticity can be analyzed to develop sustainable mussel production. The genome of M. chilensis provides pivotal molecular knowledge for the Mytilus complex.

Genome-wide maps of rare and atypical UV photoproducts reveal distinct patterns of damage formation and mutagenesis in yeast chromatin.

Ultraviolet (UV) light induces different classes of mutagenic photoproducts in DNA, namely cyclobutane pyrimidine dimers (CPDs), 6-4 photoproducts (6-4PPs), and atypical thymine-adenine photoproducts (TA-PPs). CPD formation is modulated by nucleosomes and transcription factors (TFs), which has important ramifications for Ultraviolet (UV) mutagenesis. How chromatin affects the formation of 6-4PPs and TA-PPs is unclear. Here, we use UV damage endonuclease-sequencing (UVDE-seq) to map these UV photoproducts across the yeast genome. Our results indicate that nucleosomes, the fundamental building block of chromatin, have opposing effects on photoproduct formation. Nucleosomes induce CPDs and 6-4PPs at outward rotational settings in nucleosomal DNA but suppress TA-PPs at these settings. Our data also indicate that DNA binding by different classes of yeast TFs causes lesion-specific hotspots of 6-4PPs or TA-PPs. For example, DNA binding by the TF Rap1 generally suppresses CPD and 6-4PP formation but induces a TA-PP hotspot. Finally, we show that 6-4PP formation is strongly induced at the binding sites of TATA-binding protein (TBP), which is correlated with higher mutation rates in UV-exposed yeast. These results indicate that the formation of 6-4PPs and TA-PPs is modulated by chromatin differently than CPDs and that this may have important implications for UV mutagenesis.

Epigenetic and Genetic Population Structure is Coupled in a Marine Invertebrate.

Delineating the relative influence of genotype and the environment on DNA methylation is critical for characterizing the spectrum of organism fitness as driven by adaptation and phenotypic plasticity. In this study, we integrated genomic and DNA methylation data for two distinct Olympia oyster (Ostrea lurida) populations while controlling for within-generation environmental influences. In addition to providing the first characterization of genome-wide DNA methylation patterns in the oyster genus Ostrea, we identified 3,963 differentially methylated loci between populations. Our results show a clear coupling between genetic and epigenetic patterns of variation, with 27% of variation in interindividual methylation differences explained by genotype. Underlying this association are both direct genetic changes in CpGs (CpG-SNPs) and genetic variation with indirect influence on methylation (mQTLs). When comparing measures of genetic and epigenetic population divergence at specific genomic regions this relationship surprisingly breaks down, which has implications for the methods commonly used to study epigenetic and genetic coupling in marine invertebrates.

Being from a highly resourced context predicts believing that others are highly resourced: An early developing worldview that stymies resource sharing.

We tested whether children's and adults' resource levels predicted their beliefs about resources (Study 1) and whether those beliefs shaped their willingness to share their resources with others (Study 2). In Study 1, we found that among adults (n = 230, 59.1% female, 72.6% White) and young children (n = 109, 4-6 years old, 56% female, 33% White), increased resource level predicted increases in the belief that others have lots of resources. In Study 2, we found that adults (n = 495, 52.5% female, 69.1% White) and young children (n = 154, 4-5 years old, 52.6% female, 36.4% White) randomly assigned to believe that others have lots of resources were less likely to share their own resources with others. Implications for reducing economic inequality are discussed.

Facilitators and barriers to providing culinary nutrition, culinary medicine and behaviour change support: An online cross-sectional survey of Australian health and education professionals.

BACKGROUND: An Australia wide cross-sectional online survey examined facilitators and barriers of health and education professionals to providing culinary nutrition (CN) and culinary medicine (CM) education and behaviour change support in usual practice, in addition to identifying continuing professional development (CPD) needs in this domain. METHODS: Survey items included socio-demographic characteristics, cooking and food skills confidence, nutrition knowledge (PKB-7), fruit and vegetable intake (FAVVA) and CPD needs. Data were summarised descriptively. RESULTS: Of 277 participants, 65% were likely/somewhat likely to participate in CN CPD. Mean (SD) cooking and food skill confidence scores were 73 (17.5) and 107.2 (24), out of 98 and 147, respectively. Mean PKB-7 score was 3.7 (1.4), out of 7. Mean FAVVA score was 98 (29), out of 190. CONCLUSIONS: Gaps in knowledge and limited time were the greatest modifiable barriers to providing CM/CN education and behaviour change support in practice. Health and education professionals are interested in CPD conducted by dietitians and culinary professionals to enhance their knowledge of CM/CN and behaviour change support.