SummaryBackgroundAlcohol-related mortality and morbidity are high in socioeconomically disadvantaged populations compared with individuals from advantaged areas. It is unclear if this increased harm reflects differences in alcohol consumption between these socioeconomic groups, reverse causation (ie, downward social selection for high-risk drinkers), or a greater risk of harm in individuals of low socioeconomic status compared with those of higher status after similar consumption. We aimed to investigate whether the harmful effects of alcohol differ by socioeconomic status, accounting for alcohol consumption and other health-related factors.MethodsThe Scottish Health Surveys are record-linked cross-sectional surveys representative of the adult population of Scotland. We obtained baseline demographics and data for alcohol consumption (units per week and binge drinking) from Scottish Health Surveys done in 1995, 1998, 2003, 2008, 2009, 2010, 2011, and 2012. We matched these data to records for deaths, admissions, and prescriptions. The primary outcome was alcohol-attributable admission or death. The relation between alcohol-attributable harm and socioeconomic status was investigated for four measures (education level, social class, household income, and area-based deprivation) using Cox proportional hazards models. The potential for alcohol consumption and other risk factors (including smoking and body-mass index [BMI]) mediating social patterning was explored in separate regression models. Reverse causation was tested by comparing change in area deprivation over time.Findings50 236 participants (21 777 men and 28 459 women) were included in the analytical sample, with 429 986 person-years of follow-up. Low socioeconomic status was associated consistently with strikingly raised alcohol-attributable harms, including after adjustment for weekly consumption, binge drinking, BMI, and smoking. Evidence was noted of effect modification; for example, relative to light drinkers living in advantaged areas, the risk of alcohol-attributable admission or death for excessive drinkers was increased (hazard ratio 6·12, 95% CI 4·45–8·41 in advantaged areas; and 10·22, 7·73–13·53 in deprived areas). We found little support for reverse causation.InterpretationDisadvantaged social groups have greater alcohol-attributable harms compared with individuals from advantaged areas for given levels of alcohol consumption, even after accounting for different drinking patterns, obesity, and smoking status at the individual level.FundingMedical Research Council, NHS Research Scotland, Scottish Government Chief Scientist Office.

Septal deformity is of two kinds, which may occur independently, or together: 1) anterior cartilage deformity of the quadrilateral septal cartilage, caused by direct trauma or pressure at any age; and 2) combined septal deformity, involving all the septal components, caused by compression across the maxilla from pressures occurring during pregnancy or parturition. This is part of a facial deformity. The incidence of septal deformity was investigated in 2,380 Caucasian infants at birth, 2,112 adult skulls of five ethnic groups (European, Indian [Asian], Chinese, African and Australian Aboriginal), 918 mammals (266 higher and lower apes, 457 other placental mammals and 185 marsupials). The method of nasal testing of infants by passage of special testing struts (6 by 2 mm) is described. Forty-two percent of septa of infants were straight, 27% deviated and 31% kinked. A similar pattern was found in adult skulls, namely 21% straight, 37% deviated and 42% kinked. Anterior cartilage deformity occurred in about 4% of births. The maxillary molding theory of transmitted pressures during pregnancy or parturition, causing septal deformity, is described. The findings show that varying degrees of septal deformity occur at a constant rate at birth and in the adult. These may vary slightly for each ethnic type. Birth molding pressures are a major cause of dental malocclusion. The shape and strength of the skull and the erect posture appear to be major factors, for septal deformity did not occur in the lower animals, but occurred in 37% of the higher apes and also in a skull of a hominid 1,750,000 years old. This concept enables easy recognition at birth, and the carrying out of a rational method of treatment by manipulation and rapid maxillary expansion.

In a collaboration of 7 European and United States prospective studies, 44 cases of vertical human immunodeficiency virus type 1 (HIV-1) transmission were identified among 1202 women with RNA virus loads <1000 copies/mL at delivery or at the measurement closest to delivery. For mothers receiving antiretroviral treatment during pregnancy or at the time of delivery (or both), there was a 1.0% transmission rate (8 of 834; 95% confidence interval [CI], 0.4%-1.9%), compared with 9.8% (36 of 368; 95% CI, 7.0%-13.4%) for untreated mothers (risk ratio, 0.10; 95% CI, 0.05-0.21). In multivariate analysis adjusting for study, transmission was lower with antiretroviral treatment (odds ratio [OR], 0.10; P<.001), cesarean section (OR, 0.30; P=.022), greater birth weight (P=.003), and higher CD4 cell count (P=.039). In 12 of 44 cases, multiple RNA measurements were obtained during pregnancy or at the time of delivery or within 4 months after giving birth; in 10 of the 12 cases, the geometric mean virus load was >500 copies/mL. Perinatal HIV-1 transmission occurs in only 1% of treated women with RNA virus loads <1000 copies/mL and may be almost eliminated with antiretroviral prophylaxis accompanied by suppression of maternal viremia.

Objectives To examine the association of early adulthood blood pressure with CVD mortality, while accounting for middle-age hypertension. Background Elevated blood pressure in middle-age is an established CVD risk factor, but evidence for association with measurements earlier in life is sparse. Methods HAHS is a cohort study of 18,881 male university students who had blood pressure measured at university entry (1914 –1952; mean age 18.3 years) and who responded to a questionnaire mailed in 1962/1966 (mean age 45.8 years) in which physician-diagnosed hypertension status was reported. Study members were subsequently followed for mortality until the end of 1998. Results Following adjustment for age, BMI, smoking and physical activity at college entry, compared to men who were normotensive according to JNC-7 criteria (<120/<80mmHg) there was an elevated risk of CHD mortality (1,917 deaths) in those who were pre-hypertensive (120–139/80–89 mmHg) (hazards ratio; 95% confidence intervals: 1.21; 1.07, 1.36), stage 1 (140–159/90–99 mmHg) (1.46; 1.25, 1.70), and stage 2 hypertensive (≥160/≥100 mmHg) (1.89; 1.46, 2.45), incremental across categories (ptrend<0.001). After additional account for middle-age hypertension, estimates were somewhat attenuated but the pattern remained. Similar associations were apparent for total and CVD but not stroke mortality. Conclusions Higher blood pressure in early adulthood was associated with elevated risk of mortality from all-causes, CVD and CHD, but not stroke several decades later. Effects largely persisted after taking account of mediation by middle-age hypertension. Thus, the long-term benefits of blood pressure lowering in early adulthood are promising but supporting trial data are required.

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AimResponse rates in health surveys have diminished over the last two decades, making it difficult to obtain reliable information on health and health‐related risk factors in different population groups. This study compared cause‐specific mortality and morbidity among survey respondents and different types of non‐respondents to estimate alcohol‐, drug‐ and smoking‐related mortality and morbidity among non‐respondents.DesignProspective follow‐up study of respondents and non‐respondents in two cross‐sectional health surveys.SettingDenmark.ParticipantsA total sample of 39 540 Danish citizens aged 16 years or older.MeasurementsRegister‐based information on cause‐specific mortality and morbidity at the individual level was obtained for respondents (n = 28 072) and different types of non‐respondents (refusals n = 8954; illness/disabled n = 731, uncontactable n = 1593). Cox proportional hazards models were used to examine differences in alcohol‐, drug‐ and smoking‐related mortality and morbidity, respectively, in a 12‐year follow‐up period.FindingsOverall, non‐response was associated with a significantly increased hazard ratio (HR) of 1.56 [95% confidence interval (CI) = 1.36–1.78] for alcohol‐related morbidity, 1.88 (95% CI = 1.38–2.57) for alcohol‐related mortality, 1.55 (95% CI = 1.27–1.88) for drug‐related morbidity, 3.04 (95% CI = 1.57–5.89) for drug‐related mortality and 1.15 (95% CI = 1.03–1.29) for smoking‐related morbidity. The hazard ratio for smoking‐related mortality also tended to be higher among non‐respondents compared with respondents, although no significant association was evident (HR = 1.14; 95% CI = 0.95–1.36). Uncontactable and ill/disabled non‐respondents generally had a higher hazard ratio of alcohol‐, drug‐ and smoking‐related mortality and morbidity compared with refusal non‐respondents.ConclusionHealth survey non‐respondents in Denmark have an increased hazard ratio of alcohol‐, drug‐ and smoking‐related mortality and morbidity compared with respondents, which may indicate more unfavourable health behaviours among non‐respondents.

FROM birth the normal method of respiration is by the nose and any interference producing mouth breathing causes considerable local or general impairment of function. The interference is caused by a combination of factors, such as narrowness of the nose often associated with maxillary compression, allergic mucosal swelling, deviated septum, infection, and at times obstructing adenoids. Rapid maxillary expansion is a simple, conservative, but very efficient method of converting mouth breathing back to normal nasal respiration in a high proportion of cases. Rapid maxillary expansion (referred to as R.M.E. for this paper) is performed by applying strong pressure to the back teeth over a relatively short period of time causing the maxillae to separate down the intermaxillary suture, without the teeth moving in the bone. This not only changes the dental occlusion, but also widens the nasal cavity.

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