OBJECTIVE -The extent to which lifestyle must be altered to improve insulin sensitivity has not been established. This study compares the effect on insulin sensitivity of current dietary and exercise recommendations with a more intensive intervention in normoglycemic insulinresistant individuals.RESEARCH DESIGN AND METHODS -Seventy-nine normoglycemic insulinresistant (determined by the euglycemic insulin clamp) men and women were randomized to either a control group or one of two combined dietary and exercise programs. One group (modest level) was based on current recommendations and the other on a more intensive dietary and exercise program. Insulin sensitivity was measured using a euglycemic insulin clamp, body composition was measured using dual-energy X-ray absorptiometry, and anthropometry and aerobic fitness were assessed before and after a 4-month intervention period. Four-day dietary intakes were recorded, and fasting glucose, insulin, and lipids were measured.RESULTS -Only the intensive group showed a significant improvement in insulin sensitivity (23% increase, P ϭ 0.006 vs. 9% in the modest group, P ϭ 0.23). This was associated with a significant improvement in aerobic fitness (11% increase in the intensive group, P ϭ 0.02 vs. 1% in the modest group, P ϭ 0.94) and a greater fiber intake, but no difference in reported total or saturated dietary fat.CONCLUSIONS -Current clinical dietary and exercise recommendations, even when vigorously implemented, did not significantly improve insulin sensitivity; however, a more intensive program did. Improved aerobic fitness appeared to be the major difference between the two intervention groups, although weight loss and diet composition may have also played an important role in determining insulin sensitivity. Diabetes Care 25:445-452, 2002L ifestyle intervention reduces the risk of progression from impaired glucose tolerance (IGT) to type 2 diabetes (1). It is widely assumed that current advice regarding physical activity (2) and dietary modification (3) is sufficient (presumably mediated via an improvement in insulin sensitivity) to reduce the risk of type 2 diabetes. All the large intervention trials either underway or completed have focused on intervention in subjects with IGT (1,4,5). However, it appears that once abnormal glucose levels have developed, significant ␤-cell dysfunction has already occurred, and there is less chance of improving insulin sensitivity (6).Intervention before IGT has developed may offer the best opportunity to reduce progression to IGT and type 2 diabetes. Although increased physical activity and dietary modification have been shown to improve insulin sensitivity, there are no data that clearly show the extent of lifestyle change required. This study is the first to compare two levels of practical lifestyle intervention in normoglycemic insulin-resistant individuals on insulin sensitivity, one based on current recommendations (modest) and the other on a more intensive dietary and exercise program. This will help to answer the importa...

Public health recommendations do not distinguish between vitamin D 2 and vitamin D 3 , yet disagreement exists on whether these two forms should be considered equivalent. The objective of the present study was to evaluate the effect of a daily physiological dose of vitamin D 2 or vitamin D 3 on 25-hydroxyvitamin D (25(OH)D) status over the winter months in healthy adults living in Dunedin, New Zealand (latitude 468S). Participants aged 18-50 years were randomly assigned to 25 mg (1000 IU) vitamin D 3 (n 32), 25 mg (1000 IU) vitamin D 2 (n 31) or placebo (n 32) daily for 25 weeks beginning at the end of summer. A per-protocol approach, which included $90 % supplement compliance, was used for all analyses. (1 -10) . Vitamin D 3 , the form produced in the skin of humans after exposure of 7-dehydrocholesterol to sunlight, is found either naturally in animal products such as fatty fish and cod-liver oil, or added as a fortificant to foods. Commercial production of vitamin D 3 is performed by UV irradiation of 7-dehydrocholesterol extracted from the lanolin of sheep wool. Vitamin D 2 is made either naturally or synthetically from the UV irradiation of ergosterol obtained from yeast, and added to foods. Structurally, vitamin D 2 differs from vitamin D 3 in that its side chain has an added methyl group on carbon 24 and an additional double bond between carbons 22 and 23. These structural differences, however, do not prevent the metabolic activation of the two forms. Before exerting their biological effects, both vitamin D 2 and vitamin D 3 must undergo 25-hydroxylation to form 25-hydroxyvitamin D 2 (25(OH)D 2 ) or 25-hydroxyvitamin D 3 (25(OH)D 3 ), respectively, followed by 1a-hydroxylation to produce the respective biologically active metabolites 1,25-dihydroxyvitamin D (1,25(OH) 2 D).With the use of appropriate assay systems to detect the 25(OH)D 2 metabolite, several randomised trials using large oral dose preparations ranging from 1250 to 7500 mg (50 000-300 000 IU) have suggested that vitamin D 2 is less effective in elevating or maintaining total serum 25-hydroxyvitamin D (25(OH)D) levels in healthy adults (3,6,9,10) , whereas the few studies which have directly compared daily administered low-dose preparations of vitamin D 3 and vitamin D 2 have yielded inconsistent results (1,2,5,7 -9) . In addition to varying dose and dosing regimens, these latter studies have been

Vitamin D status and associated metabolism during pregnancy and lactation have been assessed in only a limited number of longitudinal studies, all from the northern hemisphere, with no infant data concurrently reported. Therefore, we aimed to describe longitudinal maternal and infant 25-hydroxy vitamin D (25OHD) and parathyroid hormone (PTH) status during pregnancy and up to 5 months postnatal age, in New Zealand women and their infants living at 45° S latitude. Between September 2011 and June 2013, 126 pregnant women intending to exclusively breastfeed for at least 20 weeks were recruited. Longitudinal data were collected at three time-points spanning pregnancy, and following birth and at 20 weeks postpartum. Vitamin D deficiency (25OHD < 50 nmol/L) was common, found at one or more time-points in 65% and 76% of mothers and their infants, respectively. Mean cord 25OHD was 41 nmol/L, and three infants exhibited secondary hyperparathyroidism by postnatal week 20. Maternal late pregnancy 25OHD (gestation 32–38 weeks) was closely correlated with infant cord 25OHD, r2 = 0.87 (95% CI (Confidence interval) 0.8–0.91), while no correlation was seen between early pregnancy (<20 weeks gestation) maternal and cord 25OHD, r2 = 0.06 (95% CI −0.16–0.28). Among other variables, pregnancy 25OHD status, and therefore infant status at birth, were influenced by season of conception. In conclusion, vitamin D deficiency in women and their infants is very common during pregnancy and lactation in New Zealand at 45° S. These data raise questions regarding the applicability of current pregnancy and lactation policy at this latitude, particularly recommendations relating to first trimester maternal vitamin D screening and targeted supplementation for those “at risk”.

Objective: To determine the minimum effective dose of folic acid required to appreciably increase serum folate and to produce a significant reduction in plasma total homocysteine (tHcy). Design: Double-blind, randomised placebo-controlled intervention trial. Setting: Community-based project in a New Zealand city. Subjects: Seventy free living men and women with tHcy ! 10 mmol=l. Mean age (range) was 58 (29 -90) y. Interventions: Daily consumption over 4 weeks of 20 g breakfast cereal either unfortified (placebo) or fortified with 100, 200 or 300 mg folic acid. Dietary intake was determined by weighed diet records and consumption of commercially fortified products was avoided. Main outcome measures: Plasma tHcy and serum folate concentrations. Results: Average serum folate concentrations (95% CI) increased significantly in the treatment groups relative to the control group by 28(9 -51)%, 60(37 -87)% and 79(51 -114)% for supplementation with 100, 200 and 300 mg folic acid, respectively. A reduction in tHcy was observed, being 16(8 -22)%, 12(4 -18)% and 17(9 -24)% in the three treatment groups, respectively. Conclusions: A regular intake of as little as 100 mg folic acid per day was sufficient to lower tHcy in persons at the upper end of the normal range for tHcy. Low-level fortification may also be appropriate for lowering the risk of neural tube defects given that, when aggregated from all sources, the total intake of folic acid may be sufficiently high to adequately improve the folate status of young women. Funding: The breakfast cereals were supplied and the study partially funded by Kellogg Company.

Anti-Müllerian hormone (AMH) is a paracrine regulator of ovarian follicles. Vitamin D (Vit D) regulates AMH production in vitro, but its role as a regulator of ovarian AMH production is contentious. If Vit D influences ovarian AMH production, then an acute rise in Vit D level should lead to an acute rise in circulating AMH levels. This hypothesis was tested with a randomized double-blind design, with 18–25-year-old women recruited from the community. The study was conducted in early spring, when the marker of Vit D level (25-hydroxyvitamin D, 25(OH)D) tends to be at its nadir. The women consumed either an oral dose of 50,000 IU of Vit D3 (n = 27) or placebo (n = 22). The initial 25(OH)D ± SD value was 53.6 ± 23.3 nmol/L, with 42 of the 49 women having a value below 75 nmol/L, consistent with seasonal nadir. All women receiving Vit D3 treatment exhibited a robust increase in serum 25(OH)D within 1 day (15.8 ± 1.1 nmol/L (n = 27), p < 0.0001), with the increase sustained over the study week. Circulating levels of AMH in the women receiving Vit D3 progressively rose during the following week, with a mean increase of 12.9 ± 3.7% (n = 24, p = 0.001). The study supports the hypothesis that Vit D’s positive effects on the fertility of woman may involve the regulation of ovarian AMH levels.