The report by Hyppönen and Power in this issue of the Journal (1) highlights a frustrating and regrettable situation for nutrition researchers. In the early 1970s, the same serum 25-hydroxyvitamin D [25(OH)D] concentrations reported by Hyppönen and Power were thought to be indicative of "healthy" white adults in the United Kingdom (2). However, during those early years after the discovery of 25(OH)D, the adequacy of its serum concentration was based simply on whether the concentration was enough to prevent osteomalacia or rickets. Three decades later, we know that 25(OH)D concentrations relate to many other aspects of health, including fracture risk, bone density, colon cancer, and even tooth attachment (3); we also know that much higher concentrations of 25(OH)D are needed to prevent adverse outcomes. Indeed, in the 1958 British birth cohort, lower 25(OH)D is associated with a higher percentage of hemoglobin A 1C (a measure of long-term glucose concentration), which further emphasizes the need to maintain optimal 25(OH)D concentrations (4).Randomized trials using the currently recommended intakes of 400 IU vitamin D/d have shown no appreciable reduction in fracture risk (3). In contrast, trials using 700 -800 IU vitamin D/d found less fracture incidence, with and without supplemental calcium (3). The reduction in fracture incidence occurs when mean serum 25(OH)D concentrations exceed 72 nmol/L, and this change may result from both improved bone health and reduction in falls due to greater muscle strength (3). Although it is not yet proven through clinical trials, higher intakes may also reduce the incidence of colon and other cancers, and these relations indicate that the desirable 25(OH)D concentration is ͧ75 nmol/L (3). One recent report associates greater 25(OH)D concentrations with lower risk of nursing home admission; the most desirable category of concentration starts at 75 nmol/L (5).Human diets do not provide sufficient vitamin D; if they did, the abovementioned associations between health and serum 25(OH)D concentrations would not be so routinely observed. The vitamin D provided by foods and supplements is overwhelmed by the effect of skin exposure to ultraviolet B light. Geography, season, skin color, and sun-related behavior are the main predictors of vitamin D nutritional status (6 -10). Correction of low 25(OH)D concentrations can happen only if some or all of the following are implemented: the encouragement of safe, moderate exposure of skin to ultraviolet light; appropriate increases in food fortification with vitamin D; and the provision of higher doses of vitamin D in supplements for adults.Evaluation of most relations of health and disease that involve vitamin D leads to the conclusion that a desirable 25(OH)D concentration is ͧ75 nmol/L (30 ng/mL) (3-5). If a concentration of 75 nmol/L is the goal to be achieved by consumption of vitamin D, then why is it so rare for members of the population to accomplish this? One reason is that almost every time the public media report that vitamin D nutri...

Vitamin D deficiency can lead to musculoskeletal diseases such as rickets and osteomalacia, but vitamin D supplementation may also prevent extraskeletal diseases such as respiratory tract infections, asthma exacerbations, pregnancy complications and premature deaths. Vitamin D has a unique metabolism as it is mainly obtained through synthesis in the skin under the influence of sunlight (i.e., ultraviolet-B radiation) whereas intake by nutrition traditionally plays a relatively minor role. Dietary guidelines for vitamin D are based on a consensus that serum 25-hydroxyvitamin D (25[OH]D) concentrations are used to assess vitamin D status, with the recommended target concentrations ranging from ≥25 to ≥50 nmol/L (≥10–≥20 ng/mL), corresponding to a daily vitamin D intake of 10 to 20 μg (400–800 international units). Most populations fail to meet these recommended dietary vitamin D requirements. In Europe, 25(OH)D concentrations <30 nmol/L (12 ng/mL) and <50 nmol/L (20 ng/mL) are present in 13.0 and 40.4% of the general population, respectively. This substantial gap between officially recommended dietary reference intakes for vitamin D and the high prevalence of vitamin D deficiency in the general population requires action from health authorities. Promotion of a healthier lifestyle with more outdoor activities and optimal nutrition are definitely warranted but will not erase vitamin D deficiency and must, in the case of sunlight exposure, be well balanced with regard to potential adverse effects such as skin cancer. Intake of vitamin D supplements is limited by relatively poor adherence (in particular in individuals with low-socioeconomic status) and potential for overdosing. Systematic vitamin D food fortification is, however, an effective approach to improve vitamin D status in the general population, and this has already been introduced by countries such as the US, Canada, India, and Finland. Recent advances in our knowledge on the safety of vitamin D treatment, the dose-response relationship of vitamin D intake and 25(OH)D levels, as well as data on the effectiveness of vitamin D fortification in countries such as Finland provide a solid basis to introduce and modify vitamin D food fortification in order to improve public health with this likewise cost-effective approach.

New Zealand's high mortality rate from sudden infant death syndrome (SIDS) prompted the development of the New Zealand Cot Death Study. A report of the analysis of the data from the first year has been published. This report now gives the major identified risk factors from the full 3 year data set. In this case-control study there were 485 infants who died from SIDS in the post-neonatal age group, and 1800 control infants, who were a representative sample of all hospital births in the study region. Obstetric records were examined and parental interviews were completed in 97.5% and 86.9% of subjects, respectively. As expected many risk factors for SIDS were confirmed including: lower socio-economic status, unmarried mother, young mother, younger school-leaving age of mother, younger age of mother at first pregnancy, late attendance at antenatal clinic, non-attendance at antenatal classes, Maori, greater number of previous pregnancies, the further south the domicile, winter, low birthweight, short gestation, male infant and admission to a special care baby unit. In addition, however, we identified four risk factors that are potentially amenable to modification.(ABSTRACT TRUNCATED AT 250 WORDS)

Objectives-To investigate why sharing the bed with an infant is a not consistent risk factor for the sudden infant death syndrome in ethnic subgroups in New Zealand and to see if the risk of sudden infant death associated with this practice is related to other factors, particularly maternal smoking and alcohol consumption.Design-Nationwide case-control study. 0-44 to 2-18). Neither maternal alcohol consumption nor the thermal resistance of the infant's clothing and bedding interacted with bed sharing to increase the risk ofsudden infant death, and alcohol was not a risk factor by itself.Conclusion-Infant bed sharing is associated with a significantly raised risk of the sudden infant death syndrome, particularly among infants of mothers who smoke. The interaction between maternal smoking and bed sharing suggests that a mechanism involving passive smoking, rather than the previously proposed mechanisms of overlaying and hyperthermia, increases the risk of sudden infant death from bed sharing.

Health Research Council of New Zealand and Accident Compensation Corporation of New Zealand.

A case control study of gall stone disease in relation to diet, alcohol, and relative weight was undertaken. The study population comprised 267 hospital patients with newly diagnosed gall stone disease, 241 individually matched controls selected from the community, and 359 controls who were patients in hospital. Dietary intake was estimated with a quantitative food frequency questionnaire. Multiple logistic regression analysis was used to estimate the net association between individual nutrients and the risk of formation of gall stones. Variations in risk with sex and age were examined in the light of prior evidence of influences of sex hormones and age on hepatobiliary metabolism.In both sexes increased intake of alcohol was associated with a decreased risk of developing gall stones; increased intake of simple sugars in drinks and sweets was associated with an increased risk; and increased intake of energy or fat was associated with an increased risk in young subjects. Obesity was associated with an increased risk only in young women.

The association between dummy use and sudden infant death syndrome (SIDS) was investigated in 485 deaths due to SIDS in the postneonatal age group and compared with 1800 control infants. Parental interviews were completed in 87% of subjects. The prevalence ofdummy use in New Zealand is low and varies within New Zealand. Dummy use in the two week period before death was less in cases of SIDS than in the last two weeks for controls (odds ratio (OR) 0 76, 95% confidence interval (CI) 0-57 to 1.02). Use of a dummy in the last sleep for cases of SIDS or in the nominated sleep for controls was significantly less in cases than controls (OR 0-44, 95% CI 0.26 to 0.73). The OR changed very little after controlling for a wide range of potential confounders.

Objective-To investigate the hypothesis that the apparent protective effect of habitual alcohol consumption on coronary heart disease is due to drinkers at high risk of coronary heart disease becoming non-drinkers.Design-Case-control population based study. Data were obtained from interviews with patients with non-fatal myocardial infarction and their controls and with the next of kin of those who had died of coronary heart disease and their controls.Setting-Auckland, New Zealand. Subjects-Two groups of cases were studied. The first comprised 227 men and 72 women with non-fatal myocardial infarction identified from a population based surveillance programme for coronary heart disease; controls were 525 men and 341 women randomly selected from the same population group and matched for age and sex. The second group comprised 128 men and 30 women who had died of coronary heart disease and had been identified from the surveillance programme; controls were a sample of the previous control group and comprised 330 men and 214 women matched for age and sex. AU participants were aged 25-64 years and without diagnosed coronary heart disease.Main outcome measures-Regular alcohol consumption; high density lipoprotein cholesterol and low density lipoprotein concentrations.Results-Men with myocardial infarction and men who had died of coronary heart disease were more likely to have been never drinkers (had never drunk more than once a month) than controls (18% v 12% and 23% v 13% respectively). After possible confounding factors had been controlied for, people in all categories of drinking (up to more than 56 drinks per week) had at least a 40% reduction in risk of fatal and non-fatal coronary heart disease compared with never drinkers. Former drinkers also had a lower risk of non-fatal myocardial infarction than never drinkers (relative risks 0-41 and 0-10 in men and women respectively) but a similar risk of death from coronary heart disease. The reduction in risk was consistently greater in women than in men in ali drinking categories but there was no clear doseresponse effect in either sex.Conclusions-The results support the hypothesis that light and moderate alcohol consumption reduces the risk of coronary heart disease. This protective effect in this population was not due to the misclassification of former drinkers with a high risk of coronary heart disease as non-drinkers.