Background: Broccoli consumption is associated with a reduction in the risk of cancer, particularly in persons with a functional glutathione S-transferase M1 allele, as opposed rotrose whose GSTM1 gene has been deleted. Sulforaphane, the major isothiocyanate derived from 4-methylsulfinylbutyl glucosinolate, is thought to be the main agent conferring protection. Objective: We compared sulforaphane metabolism in GSTM1-null and GSTM1-positive subjects after they consumed standard broccoli and high-glucosinolate broccoli (super broccoli). Design: Sixteen subjects were recruited into a randomized, 3-phase crossover dietary trial of standard broccoli, super broccoli, and water. Liquid chromatography linked to tandem mass spectrometry was used to quantify sulforaphane and its thiol conjugates in plasma and urine. Results:GSTM1-null subjects had slightly higher, but statistically significant, areas under the curve for sulforaphane metabolite concentrations in plasma, a greater rate of urinary excretion of sulforaphane metabolites during the first 6 h after broccoli consumption, and a higher percentage of sulforaphane excretion 24 h after ingestion than did GSTM1-positive subjects. Consumption of high-glucosinolate broccoli led to a 3-fold greater increase in the areas under the curve and maximum concentrations of sulforaphane metabolites in plasma, a greater rate of urinary excretion of sulforaphane metabolites during the first 6 h after consumption, and a lower percentage of sulforaphane excretion after its ingestion than did the consumption of standard broccoli. Conclusions:GSTM1 genotypes have a significant effect on the metabolism of sulforaphane derived from standard or high-glucosinolate broccoli. It is possible that the difference in metabolism may explain the greater protection that GSTM1-positive persons gain from consuming broccoli. The potential consequences of consuming glucosinolate-enriched broccoli for GSTM1-null and -positive persons are discussed.
1 February 2005 in The American Journal of Clinical Nutrition
Background: Breakfast consumption is recommended, despite inconclusive evidence of health benefits. Objective: The study’s aim was to ascertain whether eating breakfast (EB) or omitting breakfast (OB) affects energy intake, energy expenditure, and circulating insulin, glucose, and lipid concentrations in healthy women. Design: In a randomized crossover trial, 10 women [x̄ ± SD body mass index (BMI; in kg/m2): 23.2 ± 1.4] underwent two 14-d EB or OB interventions separated by a 2-wk interval. In the EB period, subjects consumed breakfast cereal with 2%-fat milk before 0800 and a chocolate-covered cookie between 1030 and 1100. In the OB period, subjects consumed the cookie between 1030 and 1100 and the cereal and milk between 1200 and 1330. Subjects then consumed 4 additional meals with content similar to usual at predetermined times later in the day and recorded food intake on 3 d during each period. Fasting and posttest meal glucose, lipid, and insulin concentrations and resting energy expenditure were measured before and after each period. Results: Reported energy intake was significantly lower in the EB period (P = 0.001), and resting energy expenditure did not differ significantly between the 2 periods. OB was associated with significantly higher fasting total and LDL cholesterol than was EB (3.14 and 3.43 mmol/L and 1.55 and 1.82 mmol/L, respectively; P = 0.001). The area under the curve of insulin response to the test meal was significantly lower after EB than after OB (P < 0.01). Conclusion: OB impairs fasting lipids and postprandial insulin sensitivity and could lead to weight gain if the observed higher energy intake was sustained.
The intestinal microbiota are a complex ecosystem influencing the immunoregulation of the human host, providing protection from colonising pathogens and producing SCFA as the main energy source of colonocytes. Our objective was to investigate the effect of dietary fibre exclusion and supplementation on the intestinal microbiota and SCFA concentrations. Faecal samples were obtained from healthy volunteers before and after two 14 d periods of consuming formulated diets devoid or supplemented with fibre (14 g/l). The faecal microbiota were analysed using fluorescentin situhybridisation and SCFA were measured using GLC. There were large and statistically significant reductions in the numbers of theFaecalibacterium prausnitzii(P ≤ 0·01) andRoseburiaspp. (P ≤ 0·01) groups during both the fibre-free and fibre-supplemented diets. Significant and strong positive correlations between the proportion ofF. prausnitziiand the proportion of butyrate during both baseline normal diets were found (pre-fibre freer0·881,P = 0·001; pre-fibre supplementedr0·844,P = 0·002). A significant correlation was also found between the proportional reduction inF. prausnitziiand the proportional reduction in faecal butyrate during both the fibre-free (r0·806;P = 0·005) and the fibre-supplemented diet (r0·749;P = 0·013). These findings may contribute to the understanding of the association between fibre, microbiota and fermentation in health, during enteral nutrition and in disease states such as Crohn's disease.
1 January 2005 in The American Journal of Clinical Nutrition
Background: Although a regular meal pattern is recommended for obese people, its effects on energy metabolism have not been examined. Objective: We investigated whether a regular meal frequency affects energy intake (EI), energy expenditure, or circulating insulin, glucose, and lipid concentrations in healthy obese women. Design: Ten women [x̄ ± SD body mass index (in kg/m2): 37.1 ± 4.8] participated in a randomized crossover trial. In phase 1 (14 d), the subjects consumed their normal diet on 6 occasions/d (regular meal pattern) or followed a variable meal frequency (3–9 meals/d, irregular meal pattern). In phase 2 (14 d), the subjects followed the alternative pattern. At the start and end of each phase, a test meal was fed, and blood glucose, lipid, and insulin concentrations were determined before and for 3 h after (glucose and insulin only) the test meal. Subjects recorded their food intake on 3 d during each phase. The thermogenic response to the test meal was ascertained by indirect calorimetry. Results: Regular eating was associated with lower EI (P < 0.01), greater postprandial thermogenesis (P < 0.01), and lower fasting total (4.16 compared with 4.30 mmol/L;P < 0.01) and LDL (2.46 compared with 2.60 mmol/L;P < 0.02) cholesterol. Fasting glucose and insulin values were not affected by meal pattern, but peak insulin concentrations and area under the curve of insulin responses to the test meal were lower after the regular than after the irregular meal pattern (P < 0.01 and 0.02, respectively). Conclusion: Regular eating has beneficial effects on fasting lipid and postprandial insulin profiles and thermogenesis.
Objective To compare the effectiveness of four commercial weight loss diets available to adults in the United Kingdom. Design Six month multicentre randomised unblinded controlled trial. Setting Community based sample of otherwise healthy overweight and obese adults. Interventions Dr Atkins' new diet revolution, Slim-Fast plan, Weight Watchers pure points programme, and Rosemary Conley's eat yourself slim diet and fitness plan. Main outcome measures Weight and body fat changes over six months. Results All diets resulted in significant loss of body fat and weight over six months. Groups did not differ significantly but loss of body fat and weight was greater in all groups compared with the control group. In an intention to treat analysis, average weight loss was 5.9 kg and average fat loss was 4.4 kg over six months. The Atkins diet resulted in significantly higher weight loss during the first four weeks, but by the end was no more or less effective than the other diets. Conclusions Clinically useful weight loss and fat loss can be achieved in adults who are motivated to follow commercial diets for a substantial period. Given the limited resources for weight management in the NHS, healthcare practitioners should discuss with their patients programmes known to be effective. Trial registration Clinical trials NCT00327821 [ClinicalTrials.gov].