Whole grain intake of Australians estimated from a cross-sectional analysis of dietary intake data from the 2011-13 Australian Health Survey.

OBJECTIVE: The Australian Dietary Guidelines recommend Australians choose mostly whole-grain and/or high-fibre varieties within the grains (cereal) foods category, with other groups specifying a whole grain Daily Target Intake of 48 g for Australians aged 9 years or above. The USA and UK report estimates of whole grain intake that are low and declining, and no comprehensive studies on whole grain intake in the Australian population are available. The present study aimed to determine national estimates of whole grain intake, compared with current recommendations. DESIGN: A recently updated whole grain database was applied to the most current population dietary intake data. Single 24 h dietary recall intake data were reviewed against age group, sex, relative to energy intake and whole grain recommendations. SETTING: Australia. SUBJECTS: Australians (2-85 years) participating in the 2011-13 Australian Health Survey (n 12 153). RESULTS: The median daily whole grain intake was 21 g for adults (19-85 years) and 17 g for children/adolescents (2-18 years), or 28 and 23 g/10 MJ per d, respectively. Approximately 30 % of children/adolescents consumed no whole grains on the day of the survey. Whole grain intake was lowest for the age group 14-18 years (8·7 g/d). Of all participants aged ≥9 years, 73 % did not reach the recommended Daily Target Intake of 48 g. CONCLUSIONS: Whole grain intake in Australia is below recommendations in all age groups. Adolescents may be a key target for campaigns to increase whole grain consumption. This study provides the first quantification of absolute whole grain intake from all food sources in a national sample of Australians.

Stage-specific sensitivity to p53 restoration during lung cancer progression.

Tumorigenesis is a multistep process that results from the sequential accumulation of mutations in key oncogene and tumour suppressor pathways. Personalized cancer therapy that is based on targeting these underlying genetic abnormalities presupposes that sustained inactivation of tumour suppressors and activation of oncogenes is essential in advanced cancers. Mutations in the p53 tumour-suppressor pathway are common in human cancer and significant efforts towards pharmaceutical reactivation of defective p53 pathways are underway. Here we show that restoration of p53 in established murine lung tumours leads to significant but incomplete tumour cell loss specifically in malignant adenocarcinomas, but not in adenomas. We define amplification of MAPK signalling as a critical determinant of malignant progression and also a stimulator of Arf tumour-suppressor expression. The response to p53 restoration in this context is critically dependent on the expression of Arf. We propose that p53 not only limits malignant progression by suppressing the acquisition of alterations that lead to tumour progression, but also, in the context of p53 restoration, responds to increased oncogenic signalling to mediate tumour regression. Our observations also underscore that the p53 pathway is not engaged by low levels of oncogene activity that are sufficient for early stages of lung tumour development. These data suggest that restoration of pathways important in tumour progression, as opposed to initiation, may lead to incomplete tumour regression due to the stage-heterogeneity of tumour cell populations.