The Contribution of National Disparities to International Differences in Mortality Between the United States and 7 European Countries

Objectives. This study examined to what extent the higher mortality in the United States compared to many European countries is explained by larger social disparities within the United States. We estimated the expected US mortality if educational disparities in the United States were similar to those in 7 European countries.Methods. Poisson models were used to quantify the association between education and mortality for men and women aged 30 to 74 years in the United States, Belgium, Denmark, Finland, France, Norway, Sweden, and Switzerland for the period 1989 to 2003. US data came from the National Health Interview Survey linked to the National Death Index and the European data came from censuses linked to national mortality registries.Results. If people in the United States had the same distribution of education as their European counterparts, the US mortality disadvantage would be larger. However, if educational disparities in mortality within the United States equaled those within Europe, mortality differences between the United States and Europe would be reduced by 20% to 100%.Conclusions. Larger educational disparities in mortality in the United States than in Europe partly explain why US adults have higher mortality than their European counterparts. Policies to reduce mortality among the lower educated will be necessary to bridge the mortality gap between the United States and European countries.The United States has lower life expectancy at birth than most Western European countries. In 2009, life expectancy in the United States was 76 years for men and 81 years for women, between 2 and 4 years less than in several European countries.1 The disadvantage is greater for women than for men and originated in the 1980s.2 The US health disadvantage is found not only for life expectancy, but also for self-reported health measures,3,4 biomarkers,3 and many specific causes of death5,6 across the entire life course.3–5,7A recent report by the National Research Council suggests that smoking and obesity explain an important part of the US mortality disadvantage.2,8,9 However, an approach that solely emphasizes behavioral differences is impoverished by ignoring the role of socioeconomic and environmental determinants.10 A substantial body of research suggests that most behavioral risk factors are socially patterned; lower education or income are associated with a higher prevalence of smoking, excessive alcohol consumption, obesity, and poor dietary patterns.11–19 In addition, European countries and the United States differ in many aspects of the physical and social environment that can affect population health and that are in turn socially patterned within each country. For example, the socioeconomic distribution of access to healthy food differs between countries.20 Social environmental factors related to safety, violence, social connections, social participation, social cohesion, social capital, and collective efficacy have also been shown to influence health and in turn differ between countries and socioeconomic groups.21 Indeed, differences in mortality between the United States and Europe are larger among those with a lower educational level,6 suggesting that larger educational disparities in mortality, which partly coincide with differences in behavior, partly explain why Americans have higher mortality than Europeans.The United States is characterized by relatively higher levels of income inequalities,22 residential and racial segregation,23–25 and financial barriers to health care access2,26 than any European country. Social protection policies and benefits are also less comprehensive in the United States than in Europe, including policies on early education and childcare programs,27 access to high-quality education,28 employment protection and support programs,29,30 and housing29,31 and income transfer programs.31,32 A plausible hypothesis is that the more unequal distribution of resources and less comprehensive policies contribute to the more unfavorable risk factor profile and poorer health of lower-educated Americans as compared with corresponding Europeans.4,33,34 A follow-up report by the National Research Council and the Institute of Medicine published in 2013 concluded that there is a lack of evidence on how these factors explain the US health disadvantage.21 The aim of this article is to assess to what extent larger educational disparities in mortality explain why Americans have higher mortality than Europeans.     

Social networks, host resistance, and mortality: a nine-year follow-up study of Alameda County residents.

The relationship between social and community ties and mortality was assessed using the 1965 Human Population Laboratory survey of a random sample of 6928 adults in Alameda County, California and a subsequent nine-year mortality follow-up. The findings show that people who lacked social and community ties were more likely to die in the follow-up period than those with more extensive contacts. The age-adjusted relative risks for those most isolated when compared to those with the most social contacts were 2.3 for men and 2.8 for women. The association between social ties and mortality was found to be independent of self-reported physical health status at the time of the 1965 survey, year of death, socioeconomic status, and health practices such as smoking, alcoholic beverage consumption, obesity, physical activity, and utilization of preventive health services as well as a cumulative index of health practices.     

Clinical application of the functional matrix: mandibular reconstruction and monobloc functional therapy.

A 13-year-old black girl with an extensive ameloblastoma of the mandible required subtotal mandibular resection and immediate reconstruction with use of an autogenous, ipsilateral, corticocancellous graft from the iliac crest and monobic functional therapy. Twenty-seven months later, clinical evaluation showed normal mandibular function and no facial asymmetry. Bony architectural changes after 27 months included reformation of the coronoid process, angular process, and external oblique ridge; preservation of mandibular length and thickness; and maintenance of the alveolar ridge height. The reformation of the coronoid process suggests the importance of the functional matrix (temporalis muscle) in skeletal tissue growth. The monobloc appliance in conjunction with bone grafting is an effective means for transmission of biophysical stimuli and for maintenance of appropriate stress for remodeling of bone in the mandible.     

Noninvasive diagnosis of ventricular septal defects using echo-pulsed Doppler velocimetry, localization, evaluation of the shunt and the associated lesions]

A preliminary study of 15 patients with ventricular septal defect demonstrates that Echo-Doppler velocimetry allows the non-invasive diagnosis of this malformation in 80% of the cases, as well as its localisation and detection of associated lesions; tin addition evaluation of the shunt is made feasible by non invasive recording of the flow velocity curves of the shunt and of the pulmonary artery according to a technique derived from the basic one. This method turns out to be essential for establishing the aetiological diagnosis of left parasternal systolic murmurs.     

The Ask-Upmark kidney in a premature infant.

A premature infant with segmental hypoplasia of one kidney is reported. Since 1929 when Ask-Upmark first reported this renal anomaly and its association with hypertension, the nature of the lesion has remained in doubt. The question whether it is acquired post-natally or whether it is a developmental mal-formation has not been resolved. The case which we now report clearly documents the prenatal development of the lesion as well as its association with arrested nephrogenesis and the presence of abnormal vasculature. The cause of these changes is not clear, but it is suggested that ureteral reflux was present.     

Primary osteomyelitis due to an anaerobic microorganism.

Primary osteomyelitis in a teen-aged boy that mimicked Ewing's tumor radiologically showed small Gram-negative rods on the original smear. The organism isolated was an obligately anaerobic bacterium, finally identified as Clostridium sphenoides. This finding underlines the need for microbiologic analysis of orthopedic lesions.     

Rat polyvinyl sponge model for the study of infections: host factors and microbial proliferation.

Female rats were treated with several administration regimens of methylprednisolone, cobra venom anti-complementary factor, and cyclophosphamide in conjunction with polyvinyl sponge implantations. The effect of these drugs on host factors active against bacteria was evaluated with Staphylococcus aureus ATCC 25933, Escherichia coli K-12, and Pseudomonas aeruginosa CDC 7725. One of two implants in each animal was infected with 10(8) of one of the three bacteria, and bacterial and granulocyte content was determined in the infected and control sponges after 48 h. The single large dose of methylprednisolone decreased staphylococcal and E. coli clearance while promoting dissemination of P. aeruginosa. A low chronic dose of the steroid inhibited E. coli chemotaxis only. A higher dose of the steroid administered chronically interfered markedly with S. aureus and E. coli curtailment by the host while leading to enhanced dissemination of P. aeruginosa, accompanied by a precipitous decline in granulocytes. Results with cobra factor resembled the higher chronic dose of steroid enhancing, especially the dissemination of the pseudomonad and its anti-granulocytic propensity. Cyclophosphamide depression of granulocytes revealed the rat's ability to curtail the proliferation of particular S. aureus and E.coli strains even in the absence of leukocytes. This treatment resulted in the rapid spread of P. aeruginosa, leading to the death of some experimental animals. These experiments underline the versatility of this animal model in the study of host and microbial factors influential in infectious disease.