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AbstractUnderstanding women’s information seeking behaviours before conception is important for the development of interventions to enhance preconception health. This project explored barriers, facilitators, and motivators towards engagement with preconception advice in women undergoing assisted reproductive technology, across BMI classifications. Twenty interviews were conducted with women attending the fertility clinic, Repromed, in South Australia. Barriers to behaviour change included challenges finding reputable information, lack of social and health provider support, and desire for secrecy. Women reported a preference for receiving health information from the internet, social media, complementary and allied health professionals. Women living with overweight reported similar behaviours and interactions. [ABSTRACT FROM AUTHOR]

Aim: This qualitative study aimed to explore the experiences of participants who were enrolled in 6‐month controlled weight loss interventions with 2‐month follow‐up to better understand the process of behaviour change and maintenance. Methods: Fifteen participants who completed or dropped out from either a daily energy restriction or intermittent fasting group were recruited using maximum variation purposive sampling. In‐depth, semi‐structured interviews were conducted at the 2‐month follow‐up phase. All interviews were transcribed and analysed using thematic analysis, guided by behaviour change models including transtheoretical model, social cognitive theory and integrated model of change. Results: Participants following both diets showed similar behaviour change patterns. Their first motivations were mostly external and relied on 'accountability' to adhere to the diet when initiating the dietary changes. Participants highlighted the importance of frequent reviews and monitoring in assisting their adherence. This feedback system promoted the development of self‐efficacy and internalised motivation to encourage an 'ownership'. Participants who transitioned successfully from relying on accountability to take 'ownership' of the intervention were more capable of tackling challenges and tailoring their diet to form a new routine for long‐term maintenance. Conclusion: External motivations were key to initiate while internalised motivations were more important to sustain the behaviour change. Health professionals can assist this process through routine monitoring and feedback processes in clinical practice. [ABSTRACT FROM AUTHOR]

Objective: Time‐restricted eating (TRE) restores circadian rhythms in mice, but the evidence to support this in humans is limited. The objective of this study was to investigate the effects of TRE on 24‐hour profiles of plasma metabolites, glucoregulatory hormones, and the subcutaneous adipose tissue (SAT) transcriptome in humans. Methods: Men (n = 15, age = 63 [4] years, BMI 30.5 [2.4] kg/m2) were recruited. A 35‐hour metabolic ward stay was conducted at baseline and after 8 weeks of 10‐hour TRE. Assessment included 24‐hour profiles of plasma glucose, nonesterified fatty acid (NEFA), triglyceride, glucoregulatory hormones, and the SAT transcriptome. Dim light melatonin onset and cortisol area under the curve were calculated. Results: TRE did not alter dim light melatonin onset but reduced morning cortisol area under the curve. TRE altered 24‐hour profiles of insulin, NEFA, triglyceride, and glucose‐dependent insulinotropic peptide and increased transcripts of circadian locomotor output cycles protein kaput (CLOCK) and nuclear receptor subfamily 1 group D member 2 (NR1D2) and decreased period circadian regulator 1 (PER1) and nuclear receptor subfamily 1 group D member 1 (NR1D1) at 12:00 am. The rhythmicity of 450 genes was altered by TRE, which enriched in transcripts for transcription corepressor activity, DNA‐binding transcription factor binding, regulation of chromatin organization, and small GTPase binding pathways. Weighted gene coexpression network analysis revealed eigengenes that were correlated with BMI, insulin, and NEFA. Conclusions: TRE restored 24‐hour profiles in hormones, metabolites, and genes controlling transcriptional regulation in SAT, which could underpin its metabolic health benefit. [ABSTRACT FROM AUTHOR]