Screening for a raised rectal temperature in Africa

The main purpose of this study was to compare rectal and axillary temperature measurements in African children. Altogether 573 sick children were seen in an outpatient setting in rural West Africa. Rectal and axillary temperatures were measured and the parent or guardian was asked if they thought that the child had a raised body temperature. Normal ranges were defined from an age matched population of 203 healthy children. A raised axillary temperature predicted a raised rectal temperature with a sensitivity of 98% and a specificity of 88%. The parents' impression that their child had a fever was a less sensitive (89%) and less specific (59%) indicator of raised rectal temperature. A raised axillary temperature is a good screening test for a raised rectal temperature in African children.     

High risk mammographic parenchymal patterns and diet: a case-control study

Mammographic parenchymal patterns are related to breast cancer risk and are also thought to be affected by diet. We designed a case-control study comprising 200 cases with high-risk (P2 and DY) mammographic parenchymal pattern and 200 controls with low-risk (N1 and P1) patterns in order to investigate the effect of food and nutrient intake on mammographic patterns. Mammograms were evaluated according to the Wolfe classification system. Dietary data were obtained from 7-day food diaries. Mean daily intake of nutrients was computed from standard UK food tables. The adjusted odds ratio (OR) of having a high-risk pattern in women in the highest tertile of total protein and carbohydrate intake was twice that of women in the lowest tertile (OR = 2.00; 95% confidence interval (CI) 1.06-3.77; P = 0.04 and OR = 1.93; 95% CI 1.03-3.59; P = 0.04 respectively). There was no excess risk for fat intake. In addition, there was no association between intake of vitamins and mammographic parenchymal patterns. Total meat intake was strongly and positively associated with high-risk patterns among post-menopausal women (OR = 2.50, 95% CI 1.09-5.69, P = 0.03). Our study suggests that certain macronutrients and foods such as protein, carbohydrate and meat intake influence the risk of breast cancer through their effects on breast tissue morphology, whereas fat and vitamins do not affect mammographic density. It seems that parenchymal pattern acts as an informative biomarker of the effect of some macronutrient and foodstuffs intake on breast cancer risk.     

Studies of the mechanism of biological calcification

Ultrastructural changes duringin vitro calcification of a collagen-containing matrix derived from beef tendon were correlated with the time of calcification and with the effect of calcification inhibitors. The early stage of calcification is characterized by a molar Ca/P ratio of 1.0–1.2 and by the formation of intrafibrillar electron dense particles. These particles were 50 to 100 Å in diameter and produced no sharp fringes when examined by selected area electron diffraction. During later stages, the electron dense particles appear to coalesce and serve as centers for the growth of hydroxyapatite crystals. At concentration that inhibit hydroxyapatite formation, methylenediphosphonate allows uptake of a small amount of Ca²⁺ and HPO₄ ^2? with a molar Ca/P of 1.0–1.2 and the formation of the non-crystalline electron dense particles but prevents subsequent growth of hydroxyapatite. Phosphonoacetate depresses Ca²⁺ and HPO₄ ^2? uptake further and prevents formation of both noncrystalline and crystalline mineral. These findings are consistent with the multistep model of matrix calcification proposed earlier and indicate that the formation of a non-crystalline precursor of hydroxyapatite is induced by the matrix from a soluble phase that is comparable to physiological fluids.     

Childhood smoking is an independent risk factor for obstructive airways disease in women

OBJECTIVE: To assess whether starting to smoke in childhood increases the risk of obstructive airways disease (OAD) in adult life. METHODS: A retrospective cohort analysis was undertaken of 12 504 current and ex-smokers in the EPIC-Norfolk cohort. The main exposure was starting to smoke during childhood (age <16 years). Three definitions of OAD were used: doctor diagnosed asthma, doctor diagnosed bronchitis/emphysema, and "any OAD" (doctor diagnosed asthma or bronchitis/emphysema, or taking medication used in the treatment of OAD). RESULTS: Childhood smokers had significantly more pack years of exposure and poorer lung function than subjects who started to smoke in adulthood (>/=16 years). Compared with starting in adulthood, starting to smoke in childhood was associated with a greater risk of bronchitis/emphysema in female smokers (OR 1.79, 95% CI 1.25 to 2.56) and ex-smokers of both sexes (OR 1.29, 95% CI 1.07 to 1.55 in men and OR 1.40, 95% CI 1.05 to 1.85 in women), and of "any OAD" in female smokers (OR 1.72, 95% CI 1.24 to 2.38) and male and female ex-smokers (OR 1.20, 95% CI 1.03 to 1.40 in men and 1.34, 95% CI 1.07 to 1.57 in women). After adjustment for pack years, childhood smoking was associated with poorer lung function (FEV(1) 92.3% predicted in adult smokers and 89.5% in childhood smokers, p = 0.03) and a greater risk of bronchitis/emphysema (adjusted OR 1.55, 95% CI 1.08 to 2.24) and for "any OAD" (OR 1.54, 95% CI 1.10 to 2.13) in female smokers but not in male and female ex-smokers. CONCLUSION: Starting to smoke in childhood is associated with an increased risk of airways disease because of the extra pack years smoked. In women, childhood smoking is itself an independent risk factor for the development of airways disease.     

Children grow and horses race: is the adiposity rebound a critical period for later obesity?

Background  

The adiposity rebound is the second rise in body mass index that occurs between 3 and 7 years. An early age at adiposity rebound is known to be a risk factor for later obesity. The aim here is to clarify the connection between the age at rebound and the corresponding pattern of body mass index change, in centile terms, so as to better understand its ability to predict later fatness.     

Blood pressure and urinary sodium in men and women: the Norfolk Cohort of the European Prospective Investigation into Cancer (EPIC-Norfolk)

BACKGROUND: Abundant evidence indicates that a high sodium intake is causally related to high blood pressure, but debate over recommendations to reduce dietary sodium in the general population continues. A key issue is whether differences in usual sodium intake within the range feasible in free-living populations have clinical or public health relevance. OBJECTIVE: We examined the relation between blood pressure and urinary sodium as a marker of dietary intake. DESIGN: This was a study of 23104 community-living adults aged 45-79 y. RESULTS: Mean systolic and diastolic blood pressure increased as the ratio of urinary sodium to creatinine increased (as estimated from a casual urine sample), with differences of 7.2 mm Hg for systolic blood pressure and 3.0 mm Hg for diastolic blood pressure (P < 0.0001) between the top and bottom quintiles. This trend was independent of age, body mass index, urinary potassium:creatinine, and smoking and was consistent by sex and history of hypertension. The prevalence of those with systolic blood pressure >/= 160 mm Hg halved from 12% in the top quintile to 6% in the bottom quintile; the odds ratio for having systolic blood pressure >/= 160 mm Hg was 2.48 (95% CI: 1.90, 3.22) for men and 2.67 (95% CI: 2.08, 3.43) for women in the top compared with the bottom quintile of urinary sodium. Estimated mean sodium intakes in the lowest and highest quintiles were approximately 80 and 220 mmol/d, respectively. CONCLUSIONS: Within the usual range found in a free-living population, differences in urinary sodium, an indicator of dietary sodium intake, are associated with blood pressure differences of clinical and public health relevance. Our findings reinforce recommendations to lower average sodium intakes in the general population.     

Microalbuminuria independently predicts all-cause and cardiovascular mortality in a British population: The European Prospective Investigation into Cancer in Norfolk (EPIC-Norfolk) population study

BACKGROUND: In patients with diabetes or hypertension, raised albuminuria is independently associated with an increased risk of all mortality, cardiovascular morbidity and mortality, and renal insufficiency. The role of albuminuria in the general population is still controversial. We therefore undertook this study to examine the relationship between albuminuria and all-cause, cardiovascular disease (CVD) and non-CVD mortality in the general population. METHODS: Prospective population-based cohort study of 20 911 individuals aged 40-79 years recruited in 1993-1997 for the EPIC-Norfolk Study (UK) and followed-up for an average of 6.3 years. Random spot urine specimens were collected at baseline and the albumin-to-creatinine ratio measured. Participants were categorized into normoalbuminuria, microalbuminuria, and macroalbuminuria ordered groups. At follow-up, vital status and cause of death were obtained from the UK Office for National Statistics. RESULTS: During follow-up, 934 deaths were registered. Age-adjusted all-cause mortality rate increased significantly across categories of baseline albuminuria (5.3, 5.2, and 6.3/1000 person years (pyrs) across tertiles of normoalbuminuria, 8.7/1000 pyrs for microalbuminuria, and 18.4/1000 pyrs for macroalbuminuria, P < 0.001 for trend); CVD, 1.6, 1.7, 2.1, 4.3, 12.6/1000 pyrs (P < 0.001); and non-CVD, 3.7, 3.5, 4.2, 4.4, 5.8/1000 pyrs (P = 0.052) respectively. The multivariate hazard ratio for all-cause mortality associated with microalbuminuria was 1.48 (95% CI: 1.20, 1.79), and CVD 2.03 (95% CI: 1.55, 2.67). The association with non-CVD mortality was only significant in men. CONCLUSIONS: The significant increased risk of all-cause mortality especially from CVD associated with microalbuminuria, suggest that this may be a useful indicator in identifying those in the population at greatest absolute risk of fatal CVD events alongside conventional CVD risk factors.