Rise and fall in ischemic heart disease mortality - it may have happened before.

The rise in ischemic heart disease (IHD) mortality occurring mostly during the first half of the 20th century is usually associated with economic development and its consequences for people's lifestyles. On the basis of historical evidence, it is postulated that a previous IHD epidemic cycle may have occurred in England and Wales towards the turn of the nineteenth century. The implications of this on causal theories and current etiological research on atherosclerosis are discussed.

[Sclerodermoid porphyria cutanea tarda associated with cataract]. / Porfiria cutánea tarda esclerodermiforme, asociada com catarata

Two cases of Porphyria cutanea tarda with sclerodermoid changes associated with cataracta are studied. Far from being considered as an authentic scleroderma, the sclerodermoid aspect, very common in patients with Porphyria cutanea tarda, seems to represent one among the many residual alterations of the precocious cutaneous senescence, peculiar to these individuals hypersensitive to luminic radiations. The first patient had familial cases of cataracta. The second had no familial occurrence of it. The association of cataracta and Porphyria cutanea tarda, for the first time mentioned in the literature, would be one complication to be added to this very polymorphous syndrome.

A parsimonious hypothesis to the cause of influenza lethality and its variations in 1918-1919 and 2009.

Current explanations to the high 1918-1919 mortality involve either a higher pathogenicity of the virus or bacterial super-infection in the absence of adequate therapeutic resources. However, neither of these hypotheses accounts for the age-distribution of severe cases and deaths, or for the geographic and other variations in rates and explosiveness of mortality during the Pandemic. It will be shown here that, alternatively, the epidemiology of the influenza lethality could be completely explained by a combination of two determinants: (1) acquired immune-differentiation of birth-cohorts, within populations, through developmental epigenetic adaptation (and selection) secondary to maternal or early-life episodes of influenza infection and (2) a triggering context - emergence of a new sub-type/strain, and its co-circulation (competition?) with seasonal viruses immunologically related to ones that had circulated in the past and primed particular population birth-cohorts. This article (1) presents age, geographic, and temporal variations in 1918-1919 and 2009 influenza severity, (2) presents and discusses ecologic evidence in favor of the hypothesis to influenza lethality advanced here, (3) suggests biologic mechanisms capable of explaining it, (4) retrospectively, proposes co-circulation between the Pandemic and a 1918 seasonal (H3?) influenza virus as the context for the increased lethality during the second wave of the 1918 Pandemic, and (5) predicts an increase in influenza severity in the northern hemisphere as the 2009-2010 season advances and H3 circulation increases.

Connections: can the 20th century coronary heart disease epidemic reveal something about the 1918 influenza lethality?

This essay proposes that the ecologic association shown between the 20th century coronary heart disease epidemic and the 1918 influenza pandemic could shed light on the mechanism associated with the high lethality of the latter. It suggests that an autoimmune interference at the apoB-LDL interface could explain both hypercholesterolemia and inflammation (through interference with the cellular metabolism of arachidonic acid). Autoimmune inflammation, then, would explain the 1950s-60s acute coronary events (coronary thrombosis upon influenza re-infection) and the respiratory failure seen among young adults in 1918. This hypothesis also argues that the lethality of the 1918 pandemic may have not depended so much on the 1918 virus as on an immune vulnerability to it, possibly resulting from an earlier priming of cohorts born around 1890 by the 1890 influenza pandemic virus.

Markers of inflammation and prediction of diabetes mellitus in adults (Atherosclerosis Risk in Communities study): a cohort study.

BACKGROUND: Type 2 diabetes mellitus and atherosclerotic cardiovascular disease have common antecedents. Since markers of inflammation predict coronary heart disease and are raised in patients with type 2 diabetes, we investigated whether they predict whether people will develop type 2 diabetes. METHODS: 12,330 men and women, aged 45-64 years, were followed up for a mean of 7 years. We analysed the association between different markers of acute inflammation and subsequent diagnosis of diabetes. In a subgroup of 610 individuals selected originally for an unrelated atherosclerosis case-control study, we also investigated diabetes associations with total sialic acid and orosomucoid, haptoglobin, and alpha1-antitrypsin. FINDINGS: 1335 individuals had a new diagnosis of diabetes. Adjusted odds ratios for developing diabetes for quartile extremes were 1.9 (95% CI 1.6-2.3) for raised white-cell count, 1.3 (1.0-1.5) for low serum albumin, and 1.2 (1.0-1.5) for raised fibrinogen. In the subgroup analysis, individuals with concentrations of orosomucoid and sialic acid of more than the median had odds ratios of 7.9 (2.6-23.7) and 3.7 (1.4-9.8), respectively. Adjustment for body-mass index and waist-to-hip ratio lessened the associations; those for white-cell count (1.5 [1.3-1.8]), orosomucoid (7.1 [2.1-23.7]), and sialic acid (2.8 [1.0-8.1]) remained significant. INTERPRETATION: Markers of inflammation are associated with the development of diabetes in middle-aged adults. Although autoimmunity may partly explain these associations, they probably reflect the pathogenesis of type 2 diabetes.

Connections: can the 20th century coronary heart disease epidemic reveal something about the 1918 influenza lethality?

This essay proposes that the ecologic association shown between the 20th century coronary heart disease epidemic and the 1918 influenza pandemic could shed light on the mechanism associated with the high lethality of the latter. It suggests that an autoimmune interference at the apoB-LDL interface could explain both hypercholesterolemia and inflammation (through interference with the cellular metabolism of arachidonic acid). Autoimmune inflammation, then, would explain the 1950s-60s acute coronary events (coronary thrombosis upon influenza re-infection) and the respiratory failure seen among young adults in 1918. This hypothesis also argues that the lethality of the 1918 pandemic may have not depended so much on the 1918 virus as on an immune vulnerability to it, possibly resulting from an earlier priming of cohorts born around 1890 by the 1890 influenza pandemic virus.