Inequalities in cardiovascular disease mortality : the role of behavioural, physiological and social risk factors

Background While the relationship between socio-economic disadvantage and cardiovascular disease (CVD) is well established, the role that traditional cardiovascular risk factors play in this association remains unclear. The authors examined the association between education attainment and CVD mortality and the extent to which behavioural, social and physiological factors explained this relationship.

Methods Adults (n=38 355) aged 40–69 years living in Melbourne, Australia were recruited in 1990–1994. Subjects with baseline CVD risk factor data ascertained through questionnaire and physical measurement were followed for an average of 9.4 years with CVD deaths verified by review of medical records and autopsy reports.

Results CVD mortality was higher for those with primary education only, compared with those who had completed tertiary education, with an HR of 1.66 (95% CI 1.10 to 2.49) after adjustment for age, country of birth and gender. Those from the lowest educated group had a more adverse cardiovascular risk factor profile compared with the highest educated group, and adjustment for these risk factors reduced the HR to 1.18 (95% CI 0.78 to 1.77). In analysis of individual risk factors, smoking and waist circumference explained most of the difference in CVD mortality between the highest and lowest education groups.

Conclusions Most of the excess CVD mortality in lower socio-economic groups can be explained by known risk factors, particularly smoking and overweight. While targeting cardiovascular risk factors should not divert efforts from addressing the underlying determinants of health inequalities, it is essential that known risk factors are addressed effectively among lower socio-economic groups.

Physiological metal uptake by Nostoc punctiforme

Trace metals are required for many cellular processes. The acquisition of trace elements from the environment includes a rapid adsorption of metals to the cell surface, followed by a slower internalization. We investigated the uptake of the trace elements Co²⁺, Cu²⁺, Mn²⁺, Ni²⁺, and Zn²⁺ and the non-essential divalent cation Cd²⁺ in the cyanobacterium Nostoc punctiforme. For each metal, a dose response study based on cell viability showed that the highest non-toxic concentrations were: 0.5 μM Cd²⁺, 2 μM Co²⁺, 0.5 μM Cu²⁺, 500 μM Mn²⁺, 1 μM Ni²⁺, and 18 μM Zn²⁺. Cells exposed to these non-toxic concentrations with combinations of Zn²⁺ and Cd²⁺, Zn²⁺ and Co²⁺, Zn²⁺ and Cu²⁺ or Zn²⁺ and Ni²⁺, had reduced growth in comparison to controls. Cells exposed to metal combinations with the addition of 500 μM Mn²⁺ showed similar growth compared to the untreated controls. Metal levels were measured after one and 72 h for whole cells and absorbed (EDTA-resistant) fractions and used to calculate differential uptake rates for each metal. The differences in binding and internalisation between different metals indicate different uptake processes exist for each metal. For each metal, competitive uptake experiments using ⁶⁵Zn showed that after 72 h of exposure Zn²⁺ uptake was reduced by most metals particularly 0.5 μM Cd²⁺, while 2 μM Co²⁺ increased Zn²⁺ uptake. This study demonstrates that N. punctiforme discriminates between different metals and favourably substitutes their uptake to avoid the toxic effects of particular metals.

Physiological stress responses in the warm-water fish matrinxã (Brycon amazonicus) subjected to a sudden cold shock

The present work evaluated several aspects of the generalized stress response [endocrine (cortisol), metabolic (glucose), hematologic (hematocrit and hemoglobin) and cellular (HSP70)] in the Amazonian warm-water fish matrinxã (Brycon amazonicus ) subjected to an acute cold shock. This species farming has been done in South America, and growth and feed conversion rates have been interesting. However, in subtropical areas of Brazil, where the water temperature can rapidly change, high rates of matrinxã mortality have been associated with abrupt decrease in the water temperature. Thus, we subjected matrinxã to a sudden cold shock by transferring the fish directly to tanks in which the water temperature was 10oC below the initial conditions (cold shock from 28ºC to 18oC). After 1h the fish were returned to the original tanks (28ºC). The handling associated with tank transfer was also imposed on control groups (not exposed to cold shock). While exposure to cold shock did not alter the measured physiological conditions within 1h, fish returned to the ambient condition (water at 28º C) significantly increased plasma cortisol and glucose levels. Exposure to cold shock and return to the warm water did not affect HSP70 levels. The increased plasma cortisol and glucose levels after returning the fish to warm water suggest that matrinxã requires cortisol and glucose for adaptation to increased temperature.

Hemoglobin genotype has minimal influence on the physiological response of juvenile atlantic cod (Gadus morhua) to environmental challenges

Hemoglobin (Hb) polymorphism in cod is associated with temperature‐related differences in biogeographical distribution, and several authors have suggested that functional characteristics of the various hemoglobin isoforms (HbIs) directly influence phenotypic traits such as growth rate. However, no study has directly examined whether Hb genotype translates into physiological differences at the whole animal level. Thus, we generated a family of juvenile Atlantic cod consisting of all three main Hb genotypes (HbI‐1/1, HbI‐2/2, and HbI‐1/2) by crossing a single pair of heterozygous parents, and we compared their metabolic and cortisol responses to an acute thermal challenge (10°C to their critical thermal maximum [CTM] or 22°C, respectively) and tolerance of graded hypoxia. There were no differences in routine metabolism (at 10°C), maximum metabolic rate, metabolic scope, CTM (overall mean 22.9° ± 0.2°C), or resting and poststress plasma cortisol levels among Hb genotypes. Further, although the HbI‐1/1 fish grew more (by 15%–30% during the first 9 mo) when reared at 10° ± 1°C and had a slightly enhanced hypoxia tolerance at 10°C (e.g., the critical O2 levels for HbI‐1/1, HbI‐2/2, and HbI‐1/2 cod were 35.56% ± 1.24%, and 40.20% ± 1.99% air saturation, respectively), these results are contradictory to expectations based on HbI functional properties. Thus, our findings (1) do not support previous assumptions that growth rate differences among cod Hb genotypes result from a more efficient use of the oxygen supply—that is, reduced standard metabolic rates and/or increased metabolic capacity—and (2) suggest that in juvenile cod, there is no selective advantage to having a particular Hb genotype with regards to the capacity to withstand ecologically relevant environmental challenges.

Managing the optics of Indigenous policy

This monograph reports the findings of the Australian Research Council Discovery Project 'Australian news media and indigenous policymaking 1988-2008'

A preliminary investigation of adult defence style and physiological reactivity to infant distress signals

Species whose offspring require extended care-giving ought to be predisposed to being biologically responsive to their infant's signalling. This paper examined the interplay between biological and psychological aspects of adult response to an infant's distress. HR (heart rate) and GSR (galvanic skin response) were recorded continuously, while 50 adults listened to white noise and an infant cry audio recording. Participants completed the defence style questionnaire and the state trait anxiety inventory. HR acceleration occurred in response to the control sound, while HR decelerated in response to the infant cry. GSR responsiveness was positively correlated with immature and neurotic defence styles. When controlling for other variables, immature defence was a unique and independent predictor of GSR change in response to infant distress. Defence demonstrated a stronger relationship than self-reported anxiety, than that with physiological responsiveness. Employing defence mechanisms appears to reduce an individual's perceived anxiety, though it has little effect on physiological arousal levels.

The pain of tendinopathy: physiological or pathophysiological?

Tendon pain remains an enigma. Many clinical features are consistent with tissue disruption—the pain is localised, persistent and specifically associated with tendon loading, whereas others are not—investigations do not always match symptoms and painless tendons can be catastrophically degenerated. As such, the question ‘what causes a tendon to be painful?’ remains unanswered. 

Without a proper understanding of the mechanism behind tendon pain, it is no surprise that treatments are often ineffective. Tendon pain certainly serves to protect the area—this is a defining characteristic of pain—and there is often a plausible nociceptive contributor. However, the problem of tendon pain is that the relation between pain and evidence of tissue disruption is variable. The investigation into mechanisms for tendon pain should extend beyond local tissue changes and include peripheral and central mechanisms of nociception modulation.