Insufficient sun exposure has become a real public health problem

This is the final version. Available on open access from MDPI via the DOI in this recordThis article aims to alert the medical community and public health authorities to accumulating evidence on health benefits from sun exposure, which suggests that insufficient sun exposure is a significant public health problem. Studies in the past decade indicate that insufficient sun exposure may be responsible for 340,000 deaths in the United States and 480,000 deaths in Europe per year, and an increased incidence of breast cancer, colorectal cancer, hypertension, cardiovascular disease, metabolic syndrome, multiple sclerosis, Alzheimer’s disease, autism, asthma, type 1 diabetes and myopia. Vitamin D has long been considered the principal mediator of beneficial effects of sun exposure. However, oral vitamin D supplementation has not been convincingly shown to prevent the above conditions; thus, serum 25(OH)D as an indicator of vitamin D status may be a proxy for and not a mediator of beneficial effects of sun exposure. New candidate mechanisms include the release of nitric oxide from the skin and direct effects of ultraviolet radiation (UVR) on peripheral blood cells. Collectively, this evidence indicates it would be wise for people living outside the tropics to ensure they expose their skin sufficiently to the sun. To minimize the harms of excessive sun exposure, great care must be taken to avoid sunburn, and sun exposure during high ambient UVR seasons should be obtained incrementally at not more than 5–30 min a day (depending on skin type and UV index), in season-appropriate clothing and with eyes closed or protected by sunglasses that filter UVR.Sunshine Health Foundation (SHF

Diet, body size and menarche in a multiethnic cohort

A multiethnic cohort of 1378 Southern California school girls aged 8–13 years was followed for 4 years to evaluate factors predicting age at menarche, a risk factor for breast cancer. Height and weight were measured and dietary intake was assessed using a semi-quantitative food frequency questionnaire. Of 939 girls providing data on menarcheal status, 767 were premenarcheal at the start of the study; 679 girls provided acceptable dietary data and were included in the analyses. Cox proportional hazards models were used to assess the relationship between diet, body size, ethnicity and age at menarche. Hispanic, Asian/Pacific Island and African-American girls were more likely to experience early menarche than non-Hispanic white girls. Tall (> 148.6 cm) versus short (< 135.9 cm) girls experienced earlier menarche (relative hazard (RH) = 2.9, 95% confidence interval (CI) 2.1–4.1) as did those with high Quetelet's index (QI, kg m−2) (> 20.7) versus low QI (< 16.1) (RH = 2.2, 95% CI 1.7–2.9). Of all the dietary variables analysed, only energy intake was related to age at menarche. High versus low energy intake (> 12013 kJ vs < 7004 kJ) was associated with a delay in menarche (RH = 0.7, 95% CI 0.5–0.9); this finding was limited to a subset of heavy Hispanic girls who appeared to underreport their dietary intake. © 1999 Cancer Research Campaig

Accuracy of cause of death data routinely recorded in a population-based cancer registry: impact on cause-specific survival and validation using the Geneva Cancer Registry.

BACKGROUND: Information on the underlying cause of death of cancer patients is of interest because it can be used to estimate net survival. The population-based Geneva Cancer Registry is unique because registrars are able to review the official cause of death. This study aims to describe the difference between the official and revised cause-of-death variables and the impact on cancer survival estimates. METHODS: The recording process for each cause of death variable is summarised. We describe the differences between the two cause-of-death variables for the 5,065 deceased patients out of the 10,534 women diagnosed with breast cancer between 1970 and 2009. The Kappa statistic and logistic regression are applied to evaluate the degree of concordance. The impact of discordance on cause-specific survival is examined using the Kaplan Meier method. RESULTS: The overall agreement between the two variables was high. However, several subgroups presented a lower concordance, suggesting differences in calendar time and less attention given to older patients and more advanced diseases. Similarly, the impact of discordance on cause-specific survival was small on overall survival but larger for several subgroups. CONCLUSION: Estimation of cancer-specific survival could therefore be prone to bias when using the official cause of death. Breast cancer is not the more lethal cancer and our results can certainly not be generalised to more lethal tumours

Neurodevelopment of children exposed in utero to treatment of maternal malignancy

Cancer is the second most common cause of death during the reproductive years, complicating approximately 1/1000 pregnancies. The occurrence of cancer during gestation is likely to increase as a result of a woman's tendency to delay childbearing. Improved diagnostic techniques for malignancies increases detection of cancer during pregnancy. Malignant conditions during gestation are believed to be associated with an increase in poor perinatal and fetal outcomes that are often due to maternal treatment. Physicians should weigh the benefits of treatment against the risks of fetal exposure. To date, most reports have focused on morphologic observations made very close to the time of delivery with little data collected on children's long-term neurodevelopment following in utero exposure to malignancy and treatment. Because the brain differentiates throughout pregnancy and in early postnatal life, damage may occur even after first trimester exposure. The possible delayed effects of treatment on a child's neurological, intellectual and behavioural functioning have never been systematically evaluated. The goal of this report was to summarize all related issues into one review to facilitate both practitioners' and patients' access to known data on fetal risks and safety. © 2001 Cancer Research Campaign http://www.bjcancer.co

Fundamental carcinogenic processes and their implications for low dose risk assessment.

Various possible models of carcinogenesis are analyzed with respect to low dose kinetics. The importance of background carcinogenesis upon the shape of the dose-response curve at low dose is emphasized. It is shown that, if carcinogenesis by an external agent acts additively with any already ongoing process, then under almost any model the response will be linear at low dose. Measures of the degree of linearity are obtained for multistage models of carcinogenesis, where it is shown that throughout the dose range where the extra risk is less than the spontaneous risk linear extrapolation must be quite accurate