{'fraction_non_alphanumeric': 0.07795229784758581, 'fraction_numerical': 0.06457242582897033, 'mean_word_length': 4.325077399380805, 'pattern_counts': {'":': 0, '<': 1, '<?xml version=': 0, '>': 4, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
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.