The methods used to calculate ED and to assess obesity risk lead to different conclusions about the relation between the ED of the diet in childhood and gain in fat into adolescence.

Background-Meta-analyses predict that a 25% lowering of plasma homocysteine would reduce the risk of coronary heart disease by 11% to 16% and stroke by 19% to 24%. Individuals homozygous for the methylenetetrahydrofolate reductase (MTHFR) 677C3 T polymorphism have reduced MTHFR enzyme activity resulting from the inappropriate loss of the riboflavin cofactor, but it is unknown whether their typically high homocysteine levels are responsive to improved riboflavin status. Methods and Results-From a register of 680 healthy adults 18 to 65 years of age of known MTHFR 677C3 T genotype, we identified 35 with the homozygous (TT) genotype and age-matched individuals with heterozygous (CT, nϭ26) or wild-type (CC, nϭ28) genotypes to participate in an intervention in which participants were randomized by genotype group to receive 1.6 mg/d riboflavin or placebo for a 12-week period. Supplementation increased riboflavin status to the same extent in all genotype groups (8% to 12% response in erythrocyte glutathione reductase activation coefficient; PϽ0.01 in each case). However, homocysteine responded only in the TT group, with levels decreasing by as much as 22% overall (from 16.1Ϯ1.5 to 12.5Ϯ0.8 mol/L; Pϭ0.003; nϭ32) and markedly so (by 40%) in those with lower riboflavin status at baseline (from 22.0Ϯ2.9 and 13.2Ϯ1.0 mol/L; Pϭ0.010; nϭ16). No homocysteine response was observed in the CC or CT groups despite being preselected for suboptimal riboflavin status. Conclusions-Although previously overlooked, homocysteine is highly responsive to riboflavin, specifically in individuals with the MTHFR 677 TT genotype. Our findings might explain why this common polymorphism carries an increased risk of coronary heart disease in Europe but not in North America, where riboflavin fortification has existed for Ͼ50 years.

Despite the potential link between snack food intake and obesity and the reportedly high prevalence of snacking among adolescents, adolescent snack food patterns (types of foods consumed, frequency and portion size) have not been extensively examined. This study examines these issues using data on the snacking patterns of adolescents aged 13-16 years who took part in the 1997 National Diet and Nutrition Survey (NDNS) and that from a Northern Irish (NI) cohort of adolescents collected 8 years later, in 2005. Overall energy intake was significantly higher in the NI adolescents in 2005 compared with the NDNS adolescents in 1997 (P, 0·01). Consequently, energy intake from snacks was significantly higher in the NI cohort (P, 0·01) and a trend for a higher % energy intake from snacks compared with the NDNS group was observed (median 32·5 % v. 29·8 %, respectively). Sugar-sweetened carbonated and soft drinks remained the most popular choice of snack over this 8-year period; however, both the portion size consumed and frequency of consumption were significantly higher among the adolescents in 2005 compared with those in 1997 (P¼ 0·022 and P¼0·014, respectively). Despite the lower popularity, and correspondingly lower frequency of milks and beverages, the portion size of both food groups was significantly higher among the adolescents in 2005 compared with those in 1997 (P, 0·001 and P¼ 0·007, respectively). These findings may provide scope for policy interventions to place particular emphasis on reducing typical portion sizes consumed of popular snack choices, in particular high-energy carbonated and soft drinks, among UK adolescents. Snacking: Portion size: Energy intake: AdolescentsObesity among children and adolescents is a major public health concern. It is predicted that, by 2025, the prevalence of obesity among UK children and adolescents will have increased to 15 % and will escalate to 25 % by 2050 (1) . The reported decline in the traditional habit of eating three meals per d and an increase in 'snacking' has coincided with the rise in overweight and obesity among children and adolescents (2) . Consequently, several studies have focused on a potential causal link between obesity and snack food intake. While there is still no direct evidence to confirm this association in either children or adults, both the energy density of specific foods commonly eaten as snacks and the frequency of snack food consumption have increased over the last few decades among young adults in the USA (3) . Furthermore, it has been reported that there may be no compensation made for the increased energy intake (EI) from energy-dense snacks at subsequent eating occasions (4) .EI from snacks has increased by 30 % among US children and adolescents in the last few decades, accounting for a quarter of total EI (5) . Such data are not surprising, given that popular snack food choices among US children and adolescents include energy-dense items such as cakes, cookies and savoury snacks (6) . Furthermore, portion sizes of popular snack food choic...

We thank Powers et al for their positive comments on our article. 1 Their criticism is that our sample is not representative of the United Kingdom or European populations, and that our interpretation of the results in relation to food policy is therefore inappropriate.The statement that statistical inference is compromised is misleading because it is very clear in our article that the inference is not being made about the general population, but rather a subpopulation, ie, people homozygous for the MTHFR 677C3 T polymorphism (ie, TT genotype). To specifically investigate this subpopulation, we screened 680 healthy adults and identified just over 10% with the TT genotype; this is typical of populations worldwide. Powers et al have inappropriately compared homocysteine levels in our TT subpopulation with those found in the general UK population. The correct comparison is with other studies that report homocysteine levels in TT genotype subpopulations. Homocysteine values in one such meta-analysis 2 were comparable with our data and were 25% higher in people with TT compared with CC (wild-type) genotypes; however, the extent of elevation varied considerably between studies, 2 presumably because of differences in the prevailing status of folate and/or riboflavin. The elevated homocysteine in TT supopulations is generally far less marked within US compared with European populations where (unlike the United States) there is no exposure to mandatory fortification with folate or riboflavin. Correspondingly, this polymorphism carries an increased risk of cardiovascular disease in European populations but not in those in North America. 3 We feel that our findings can contribute to the debate regarding food fortification with folate and related B-vitamins currently being considered by many governments. In our study, 1 the marked homocysteine-lowering effect of riboflavin in people with the TT genotype was achieved with very low doses (1.6 mg/d, ie, recommended dietary level). If a sufficiently powered clinical trial proves that homocysteine is linked in a causative way to heart disease or stroke, then exposure of the general population to low-dose riboflavin through fortification (as in the United States) may offer a cheap, safe, and effective means of reducing disease risk among substantial subpopulations who carry the TT genotype and are unaware of it. DisclosuresNone. Helene