Alcohol and cancer: a position statement from Cancer Council Australia.

The Cancer Council Australia (CCA) Alcohol Working Group has prepared a position statement on alcohol use and cancer. The statement has been reviewed by external experts and endorsed by the CCA Board. Alcohol use is a cause of cancer. Any level of alcohol consumption increases the risk of developing an alcohol-related cancer; the level of risk increases in line with the level of consumption. It is estimated that 5070 cases of cancer (or 5% of all cancers) are attributable to long-term chronic use of alcohol each year in Australia. Together, smoking and alcohol have a synergistic effect on cancer risk, meaning the combined effects of use are significantly greater than the sum of individual risks. Alcohol use may contribute to weight (fat) gain, and greater body fatness is a convincing cause of cancers of the oesophagus, pancreas, bowel, endometrium, kidney and breast (in postmenopausal women). The existing evidence does not justify the promotion of alcohol use to prevent coronary heart disease, as the previously reported role of alcohol in reducing heart disease risk in light-to-moderate drinkers appears to have been overestimated. CCA recommends that to reduce their risk of cancer, people limit their consumption of alcohol, or better still avoid alcohol altogether. For individuals who choose to drink alcohol, CCA recommends that they drink only within the National Health and Medical Research Council guidelines for alcohol consumption.

Effectiveness of strategies for recruiting overweight and obese Generation Y women to a clinical weight management trial.

AIM: Limited research in young overweight and obese women indicates that they are difficult to recruit to weight management trials, with attrition higher and weight loss success lower than middle to older age participants. This study aimed to evaluate the effectiveness of different recruitment strategies for a clinical weight loss trial in overweight and obese Generation Y women. METHODS: Overweight and obese (BMI >=27.5 kg/m-2) women aged 18-25 years (n=70) were required for a 12 month clinical weight management trial including diet, exercise and behaviour modification. Contact with researchers and eventual recruitment are reported for the various strategies employed to engage participants. Data reported as % or mean±SE. RESULTS: Recruitment was challenging with only 50 of the total 70 participants recruited within the scheduled time frame (24 months). Just over one quarter (27%) of volunteers assessed were recruited. Flyers posted around local tertiary education campuses were the most successful method, yielding 36% of included participants. This was followed by advertisements on the local area health service intranet (26%) and in local and metropolitan newspapers (16%). CONCLUSIONS: Recruitment of overweight and obese Generation Y women for a clinical weight loss trial was difficult. Multiple strategies targeted at this age and gender group were required. Less rigorous selection criteria and reduced face-to-face intervention time may improve recruitment and retention rates into clinical trials for this age group.

Impact of diet and weight loss on iron and zinc status in overweight and obese young women.

Young overweight women are at risk of iron and zinc deficiency. This study assessed iron, zinc and inflammatory status during a 12-month weight loss trial in young women (18-25 y; BMI >=27.5 kg/m2) randomised to a higher-protein (HP: 32% protein; 12.2 mg/day iron; 11.7 mg/day zinc) or lower-protein (LP: 20%; 9.9 mg/day; 7.6 mg/day respectively) diet with contrasting haem iron and zinc content. In completers (HP: n=21; LP: n=15), HP participants showed higher median ferritin (52.0 vs 39.0 µg/L; p=0.021) and lower median soluble transferrin receptor-ferritin index (sTfR-F; 0.89 vs 1.05; p=0.024) although concentrations remained within normal range for both diets. Median C-reactive protein (CRP; HP: 3.54; LP: 4.63 mg/L) and hepcidin (HP: 5.70; LP: 8.25 ng/mL) were not elevated at baseline, and no longitudinal between-diet differences were observed for zinc and CRP. Compared to those with <5% weight loss, HP participants losing >=10% weight showed lower median sTfR-F (0.76 vs 1.03; p=0.019) at six months. Impact of >=10% weight loss on iron was more apparent in LP participants who exhibited greater mean serum iron (20.0 vs 13.5 µmol/L; p=0.002), transferrin saturation (29.8% vs 19.4%; p=0.001) and lower sTfR (1.24 vs 1.92 mg/L; p=0.034) at 12 months. Results show normal iron and zinc status can be maintained during 12 months of energy restriction. In the absence of elevated baseline inflammation and hepcidin, a more favourable iron profile in those with >=10% weight loss may reflect stronger compliance or the potential influence of iron regulatory mechanisms unrelated to inflammatory hepcidin reduction.

Iron, hepcidin and inflammatory status of young healthy overweight and obese women in Australia.

BACKGROUND AND AIMS: Evidence suggests obesity-related inflammation alters iron metabolism potentially increasing the risk of iron deficiency. This cross-sectional study aimed to investigate iron, hepcidin and inflammatory status in young, healthy overweight and obese women. METHODS: 114 young (18-25 years), healthy comorbidity-free women with a body mass index (BMI) ≥27.5 kg/m(2) were recruited. Biochemical data were analysed using mean ± standard deviation or median (interquartile range) and multivariate modelling. Biochemical markers were also stratified according to varying degrees of overweight and obesity. RESULTS: Anaemia (haemoglobin <120 g/l) and iron deficiency (serum ferritin <15.0 µg/l) were prevalent in 10% and 17% of participants respectively. Mean/median soluble transferrin receptor was 1.61±0.44 mg/l; hepcidin 6.40 (7.85) ng/ml and C-reactive protein (CRP) 3.58 (5.81) mg/l. Multivariate modelling showed that BMI was a significant predictor of serum iron (coefficient = -0.379; standard error = 0.139; p = 0.008), transferrin saturation (coefficient = -0.588; standard error = 0.222; p = 0.009) and CRP (coefficient = 0.127; standard error = 0.024; p<0.001). Stratification of participants according to BMI showed those with ≥35.0 kg/m(2) had significantly higher CRP (p<0.001) than those in lower BMI categories. CONCLUSIONS: Increasing obesity was associated with minor disturbances in iron metabolism. However, overall outcomes indicated simple iron deficiency (hypoferritinaemia) was the primary iron-related abnormality with no apparent contribution of inflammation or hepcidin, even in those with BMI >35.0 kg/m(2). This indicates that obesity alone may not be sufficient to induce clinically significant disturbances to iron metabolism as previously described. This may be attributed to the lack of comorbidity in this cohort.

The carnivore connection hypothesis: revisited.

The "Carnivore Connection" hypothesizes that, during human evolution, a scarcity of dietary carbohydrate in diets with low plant : animal subsistence ratios led to insulin resistance providing a survival and reproductive advantage with selection of genes for insulin resistance. The selection pressure was relaxed at the beginning of the Agricultural Revolution when large quantities of cereals first entered human diets. The "Carnivore Connection" explains the high prevalence of intrinsic insulin resistance and type 2 diabetes in populations that transition rapidly from traditional diets with a low-glycemic load, to high-carbohydrate, high-glycemic index diets that characterize modern diets. Selection pressure has been relaxed longest in European populations, explaining a lower prevalence of insulin resistance and type 2 diabetes, despite recent exposure to famine and food scarcity. Increasing obesity and habitual consumption of high-glycemic-load diets worsens insulin resistance and increases the risk of type 2 diabetes in all populations.