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.